Title: Part One
Tags: cvs pharmacology neuro haeme metabolism equipment git obs immune definition cellphys acid-base pharm msk anaes volatile micro nmbd opioid cvspham autonomic electrical resp localanaes renal respiratory endo analgesics equation neuropharm

Q: Normal Bicarb
A: 24 (22-26)

Q: Acute Respiratory Acidosis Compensation
A: The [HCO3] will increase by 1 mmol/l for every 10 mmHg elevation in pCO2 above 40 mmHg

Q: Chronic Respiratory Acidosis compensation
A: The [HCO3] will increase by 4 mmol/l for every 10 mmHg elevation in pCO2 above 40mmHg

Q: Acute Respiratory Alkalosis compensation
A: The [HCO3] will decrease by 2 mmol/l for every 10 mmHg decrease in pCO2 below 40 mmHg

Q: Chronic Respiratory Alkalosis compensation
A: The [HCO3] will decrease by 5 mmol/l for every 10 mmHg decrease in pCO2 below 40 mmHg

Q: Renal Blood Flow (Proportion of CO)
A: 22%

Q: Normal GFR
A: 125ml/min

Q: Methods of Renal Autoregulation
A: Myogenic
Tubuloglomerular Feedback

Q: Describe the mechanism of myogenic autoregulation
A: Increase wall tension stimulates vasoconstriction, increasing resistance proprotional to the increase in pressure

Q: Control of Renal Blood Flow
A: Local (myogenic, tubuloglomerular feedback)
Neuronal (SNS)
Hormonal (RAAS)

Q: Boyle's Law
A: PV = K, i.e. pressure and volume are inversely related at constant temperature

Q: Charle's Law
A: V = KT, i.e. volume and temperature are linearly related when pressure is constant.

Q: Henry's Law
A: The number of molecules of dissolved gas is equal to the partial pressure of the gas at the surface of the liquid

Q: Graham's Law
A: Diffusion rates through orifices are inversely proportional to the square root of the molecular weight

Q: Dalton's Law
A: In a mixture of gases, each gas exerts the pressure that it would exert if it occupied the volume alone

Q: Respiratory Quotient
A: Ratio of CO2 eliminated/O2 consumed; usually 0.8, varies with metabolic substrates. Carbs - higher, fats - lower.

Q: Reynolds Number - Definition
A: Dimensionless index which predicts liklihood of turbulent flow. Represents the ratio of inertial to viscous forces.
>2000 = likely turbulent

Q: Bohr Effect
A: Increased PaCO2 decreases Hb affinity for O2

Q: Phases of the Cardiac Cycle
A: Slow Vent Filling
Atrial Contraction
Isovolumetric Ventricular Contraction
Ejection
Isovolumetric Ventricular Relaxation
Rapid Vent. Filling

Q: Effect of atrial kick
A: 10% extra filling at rest, up to 40% extra filling in tachycardic states

Q: Peripheral chemoreceptors - stimuli
A: Low PaO2
High PaCO2
Acidaemia

Q: Peripheral chemoreceptors - location
A: Carotid body, aortic bodies

Q: Carotid body innervation
A: Glossopharyngeal nerve

Q: Aortic body innervation
A: Vagus nerve

Q: Ventral Respiratory Group - Function
A: Controls the the intercostal muscles, involved with inspiration and expiration

Q: Apneustic Centre - Function
A: Prevents overexpansion by modulating DRG
- Via afferent feedback from stretch receptors

Q: Pneumotaxic Centre function
A: Modulates the DRG:
- ↑ RR and ↓ Vt by inhibiting inspiratory ramp of action potentials

Q: Absolute Humidity
A: Mass of water in a volume of air g/m^3

Q: Addiction
A: Behavioural pattern characterised by compulsive use and fixation on acquiring and using a drug

Q: Affinity
A: Ability of a drug to bind to a receptor.
Described by the association constant, Ka

Q: Afterload
A: Sum of forces, elastic and kinetic, opposing ventricular ejection

Q: Agonist
A: Drug which produces a maximal response at receptor site. i.e. high affinity and an activity of 1.

Q: Alveolar Dead Space
A: Dead Space occurring due to ventilated but not perfused alveoli. <1ml in normal individuals.

Q: Anatomical Dead Space
A: Volume of the conducting zone of the respiratory tree. Equal to 2.2ml/kg.

Q: Antagonist
A: Drug which produces no response at the receptor, but prevents other ligands binding. i.e. High affinity but activity of 0.

Q: Anxiolysis
A: Where a drug reduces anxiety without impairing other CNS or MSK function

Q: Autoregulation
A: Ability of an organ to regulate blood flow over a range of perfusion pressures and changes in demand, by means of local mechanisms only

Q: Beer's Law
A: Amount of light absorbed is proportional to the concentration of the absorbing substance

Q: Beer-Lambert Law
A: Summation of Beer and Lambert's laws. Amount of light absorbed is proportional to both the concentration of the absorbing substance and the distance it travels through it.

Q: Bernoulli Principle
A: In order to maintain a constant flow, a fluid must increase its velocity as it flows through a constriction. This increase in kinetic energy is offset by a decrease in potential energy, causing a decrease in fluid pressure.

Q: Bioavailability
A: Proportion of administered drug reaching systemic circulation unchanged.

Q: Bowman's Principle
A: Less potent agents have a quicker onset. This is because a greater dose is required (low potency) and so a greater concentration gradient exists (favouring diffusion to the effect site).

Q: Buffer
A: Solution containing weak acids and/or weak bases that will tend to resist a change in [H+] when an acid or base is added.

Q: Calorie
A: Amount of heat energy required to raise the temperature of 1g of water by 1°C

Q: Central Anticholinergic Syndrome
A: Cerebral excitation or depression, characterised by somnolence, confusion, amnesia, agitation, hallucinations, dysarthria, ataxia, delirium.

Q: Clearance
A: The volume of plasma which is cleared of a drug per unit time (ml/min). Cl = k.Vd
Sum of clearance by individual organ systems (renal, hepatic, lung, independent, etc)

Q: Closing Capacity
A: The volume at which basal airways begin to close. Sum of the Closing Volume and Residual Volume. If CC > FRC, then this may cause gas trapping, atelectasis, and subsequent hypoxia.
This is not a problem provided FRC>CC. However, CC>FRC if FRC is small (neonates, children, pregnancy, disease), or if CC is increased (in age).

Q: Commensal
A: Organism that colonises a host without causing disease

Q: Competitive Antagonist
A: High affinity but activity of 0. Displace other ligands from a binding site. Can be overriden by increasing the dose of agonist.

Q: Contractility
A: Determinants of myocardial performance, independent of preload and afterload.

Q: Critical Pressure
A: Pressure required to liquefy a vapour at its critical temperature.

Q: Critical Temperature
A: Temperature above which a substance cannot be liquefied, regardless of pressure.

Q: Cyanosis
A: When capillary blood contains >5g/dl of DeoxyHb.

Q: Dead Space
A: Volume of respiratory system not participating in gas exchange.
Physiological Dead Space = Alveolar Dead Space + Anatomical Dead Space.

Q: Desensitisation
A: Loss in response over a long time period, usually due to change in receptor morphology or loss in receptor numbers

Q: Define Digestion
A: Process of breaking down macromolecules into readily absorbed compounds.

Q: Essential Fatty Acid
A: Fat required in the diet for normal health, but may also be used as an energy substrate (which vitamins cannot)

Q: Ester hydrolysis
A: The breakdown of a drug due to nonspecific circulating plasma esterases.
It is accelerated in acidosis.

Q: Equilibrium
A: In a closed system, where there is no net movement of particles from one place to another, or no net change in state. Different from steady-state, which is an open system.

Q: Exponential Function
A: Where the rate of change is proportional to the current value.

Q: Fick Principle
A: Blood flow to an organ is equal to uptake of a tracer substance by that organ, divided by the arterio-venous concentration difference

Q: Gauge Pressure
A: Pressure relative to atmospheric pressure

Q: General Anaesthesia
A: Drug induced state of reversible unconsciousness which creates amnesia, anaesthesia, and decreased muscular tone.

Q: Half-life
A: Time taken for process to decrease by 50% from the starting value. At 5 half-lives, a process is ~97% complete.

Q: Heat
A: Kinetic energy content of a body, measured in Joules. Related to temperature via the Specific Heat Capacity.

Q: Hofmann Elimination
A: The spontaneous breakdown of a drug at normal body temperature and pH.
Slowed with acidosis and hypothermia.

Q: Hypnosis
A: Where a drug creates a near-natural sleep state on the ECG, though REM sleep is suppressed.

Q: Hypoxia
A: Where tissue oxygenation falls below the level required for oxidative phosphorylation.

Q: Hypoxaemia
A: Low PaO2 (<60mmHg).

Q: Hysteresis
A: A type of system which is dependent on its present state as well as its past state. Typically occurs when there is a dynamic lag between input and output.

Q: Idiosyncrasy
A: Individual patient response to a drug. It is typically mediated by a reactive metabolite rather than the drug itself.

Q: Isomer
A: Isomerism describes groups of compounds which have the same chemical formula but different arrangement of atoms

Q: Impedance
A: Effective resistance of an electrical circuit or component to alternating current, arising from the combined effect of ohmic resistance and reactance (impedance).
Unlike resistance, varies with frequency.

Q: Induction Agent
A: Agent which will induce loss of consciousness in 1 arm-brain circulation time.

Q: Intrinsic Activity
A: Size of effect a drug has when bound to a receptor.

Q: Lambert's Law
A: Amount of light absorbed is proportional to the length of the path light has to travel in the absorbing substance.

Q: Define Laminar Flow
A: Fluid moving in a steady manner without turbulence.

Q: Law of Mass Action
A: Rate of a chemical reaction is proportional the product of the concentrations of the reactants.

Q: Mean Arterial Pressure
A: Average arterial pressure over a single cycle. MAP = CO * SVR, and (for normal heart rates, as MAP will generally increase with HR (greater systolic time)) = DBP + SBP/3.

Q: Meniscus
A: Curvature of a liquid surface at its contact with a container wall, which occurs as a consequence of the surface tension of that liquid.

Q: Mineral
A: Inorganic substance requried in the diet to maintain health.

Q: Resonant Frequency
A: Frequency at which a system tends to oscillate when disturbed and left alone.
If the system is minimally damped, this will be close to the natural frequency.

Q: Non-competitive Antagonist
A: High affinity but activity of 0. Typically cause conformational change in a receptor, preventing ligand binding. Cannot be overidden by increasing the dose of agonist

Q: Osmolarity
A: The number of osmoles per litre of solution. Changes with amount of solute added as well as temperature and pressure.

Q: Osmolality
A: Number of osmoles per kg of solvent. Unaffected by changes in temperature and pressure.

Q: Osmosis
A: Movement of solvent molecules across a semi-permeable membrane from a dilute solution to a concentrated one, in order to equalise concentrations on each side.

Q: Define p50, and it's values in Hb, HbF, and myoglobin
A: The partial pressure at which an oxygen-carrying protein is 50% saturated.
A marker of affinity of Hb for O2.
HbA = 27mmHg; HbF = 18mmHg, Myoglobin = 2.7mmHg.

Q: Pain
A: Unpleasant sensory and emotional experience associated with actual or potential tissue damage

Q: Partial Pressure
A: Pressure exerted by each component of a gas mixture.

Q: Pasteur Point
A: PO2 at which oxidative phophorylation cannot continue; ~1mmHg

Q: Pathogen
A: Disease-causing organism.

Q: Pathogenicity
A: Ability of an organise to cause disease.

Q: Peristalsis
A: A propagating wave of radial symmetrical contraction and relaxation of a muscular tube

Q: pH
A: Stands for the power of hydrogen.
Negative log to the base 10 of the hydrogen ion concentration, i.e. pH = -Log10([H+])

Q: Potency
A: Dose of drug required to produce a certain effect.
Given by the ED_50.

Q: Preload
A: Average myocardial sarcomere length at the onset of systole, which is typically approximated with End Diastolic Volume.

Q: Define Relative Humidity
A: Ratio of mass of water vapour in a volume of air to the mass required to saturate that volume at the same temperature

Q: Resonance
A: Tendency of a system to oscillate at increasing amplitude at certain (i.e. resonant frequency and it's harmonics) frequencies

Q: Respiratory Exchange Ratio
A: Ratio of volume of CO2 produced to volume O2 consumed per unit time, at any given instant (whether or not steady-state has been reached).
Normal value: 0.8
Approaches 1.0 during aerobic exercise
May reach 1.2 during anaerobic exercise.

Q: Saturated Vapour Pressure
A: Pressure exerted by a vapour in equilibrium with its liquid state

Q: Second Messenger
A: Intracellular protein which acts as an intermediate compound in a signal transduction cascade, and include cAMP, cGMP, and calcium.

Q: Sensitivity definition
A: Ability of a test to exclude disease, i.e. false negative rate.

Q: Specificity definition
A: Ability of a test to confirm disease present, i.e. false positive rate.

Q: Shear Rate
A: Speed of deformation of a shearing force. Proportional to flow (N.s/m^2)

Q: Sleep
A: Naturally occurring state of reversible unconsciousness from which a person may be roused by external stimuli.

Q: Specific Heat Capacity
A: How much energy (in Joules) that must be applied to 1kg of a substance to raise its temperature from 14°C to 15°C, without a change in state.

Q: Tachyphylaxis
A: Rapid decrease in response to repeated dosing over a short time period, usually due to depletion of transmitter

Q: Gas Tension
A: Gas pressure that must be exerted on a liquid to keep gas molecules in solution

Q: Temperature
A: Thermal state of a substance which determines whether it will give or recieve heat energy to another body.
Measured in degrees.

Q: Thermoneutral Zone
A: The ambient temperature range across which normal core temperature can be maintained without increasing metabolic rate above the resting level.

Q: Venturi Effect
A: The reduction in fluid pressure that occurs when fluid flows through a narrowed section of pipe. A particular application of the Benoulli principle.

Q: Virulence
A: Severity of disease caused by a pathogen.

Q: Viscosity
A: Tendency of fluids to resist flow, given by shear rate (speed of deforming forces, given in Pascal-seconds) between layers in a flowing gas.

Q: Vitamin
A: Organic substance required in the diet to maintain health

Q: Withdrawal
A: Pathological response when a drug is ceased.
During administration receptors may be up-regulated in the continued presence of an antagonist, or down-regulated in the continued presence of an agonist.

Q: Windkessel Effect
A: Elastic distension of large arteries during systole, limiting the pressure (and therefore afterload) increase with ejection of stroke volume. Additionally, diastolic recoil maintains constant flow at capillary level.

Q: Define EBM
A: The conscientious, explicit, and judicious use and appraisal of current best evidence in making decisions about the care of individual patients.

Q: Stages of EBM
A: 1. Ask an answerable question
2. Search
3. Critically appraise the evidence
4. Integrate the evidence with the patients unique circumstances and values
5. Evaluate the result

Q: NHMRC Levels of Evidence - Level I
A: Systematic review of RCTs

Q: NHMRC Levels of Evidence - Level II
A: At least one good RCT

Q: NHMRC Levels of Evidence - Level III
A: III-1: a pseudo-RCT
III-2: Comparative study with concurrent controls (e.g. cohort)
III-3: Comparative study without concurrent controls, such as a cohort study with historical controls

Q: NHMRC Grades of Evidence - Grade A
A: Trusted to guide practice

Q: NHMRC Grades of Evidence - Grade B
A: Trusted to guide practice in most situations

Q: NHMRC Grades of Evidence - Grade C
A: Evidence provides some support, care should be taken in the application of it

Q: NHMRC Grades of Evidence - Grade D
A: Evidence is weak and recommendation is with caution

Q: Systematic Review
A: Process of evaluating all of the (quality) literature to answer a specific clinical question

Q: Meta Analysis
A: Mathematical technique of combining the results of different trials to derive a single pooled estimate of effect

Q: Data Types
A: Qualitative, quantitative ( categorical, ordinal, numeric (discrete, continuous (interval, ratio)))

Q: Qualitative Data
A: Uses words rather than numbers

Q: Quantitative Data
A: Uses numbers, or is coded numerically

Q: Categorical data
A: Where data exist in discrete categories without intrinsic order

Q: Ordinal data
A: Where data exist in categories with an intrinsic order (e.g. age group)

Q: Numerical Data
A: Where the data is an actual number. Can be continuous or discrete.

Q: Continuous data
A: Where the data can assume any value, including fractions (e.g. Hb). Continuous data may be ratio or interval.

Q: Interval data
A: Where the difference between two values is meaningful, but without a rational zero.

Q: Ratio Data
A: Form of continuous data where '0' means no measurement

Q: Bias
A: Systematic deviation from truth

Q: Selection bias
A: Where subject allocation results in treatment groups that are systematically different, apart from in the intervention being studied

Q: Detection bias
A: Where measurements are taken differently between groups

Q: Observer bias
A: Where the data collector adjudicates outcomes

Q: Publication bias
A: Where negative studies are less likely to be submitted or published than positive ones

Q: Recall bias
A: Altered reporting of symptoms by patients depending on which group they have been allocated to

Q: Response bias
A: When patients who enroll for a trial differ from the population, limiting generalisability

Q: Hawthorne Effect
A: Where the process of actually doing the study improves the outcome, independent of the intervention

Q: Confounding factor - definition and requirements
A: A variable which, if removed, changes the outcome by a clinically significant amount.
Associated with the exposure but not a consequence of it. An independent predictor of outcome.

Q: Methods of controlling for confounding - by design
A: Randomisation
Restriction
Matching

Q: Methods of Controlling for Confounding - By Analysis
A: Standardisation, Stratification

Q: Central Limit Theorem
A: The sample means of multiple random samples of a population will follow a normal distribution, even if the characteristic is not normally distributed

Q: Measures of Central Tendency
A: Quantifies degree of clustering of a sample. Can be mean, mode, or median.

Q: Mode
A: Most common value in a sample

Q: Median
A: Middle value when a sample is ranked lowest to highest. Best measure of central tendency when data are skewed.

Q: Mean
A: The average.
Best measure when data are not skewed.

Q: Measures of Deviation
A: Measurement of dispersion around the central value. Include range, percentiles, IQR, variance, and standard deviation.

Q: Range (Data)
A: The highest and lowest values. Highly influence by outliers.

Q: Percentiles
A: Observations ranked into 100 equal parts, i.e. the median is the 50th centile.

Q: IQR
A: The 25th-75th centile

Q: Variance
A: Measure of dispersion. Evaluates how far each value is from the mean, penalising those which are further from the mean.

Q: Standard Deviation
A: The positive square root of the variance. It is used because it has a number of useful properties with respect to the normal distribution. i.e. u+/- 1 STD contains 68% of results, 2 STD 95% of results, 3 STD 99.7% of results

Q: Standard Error of the Mean
A: Measure of the precision of the estimate of the mean

Q: Confidence Interval
A: Range in which the true population parameter is likely to lie

Q: Absolute Risk
A: Risk of an event occurring in the exposed group

Q: Relative Risk
A: Risk of an event occurring in the exposed group relative to the unexposed group

Q: Absolute Risk Reduction
A: Decrease in risk provided by an exposure

Q: Relative Risk Reduction
A: Proportional decrease in incidence provided by treatment

Q: Odds
A: Probability of an event happening compared to the probability of it not happening.

Q: Odds Ratio
A: Ratio of the odds of the outcome occurring in the exposed compared to the odds of it occurring in the unexposed. OR>1 suggests risk is higher in exposed. OR=1 suggests the risk is equivalent.

Q: Drug Development - Phase 0
A: Pre-clinical R&D, in vitro and animal testing

Q: Drug Development - Phase I
A: First human administration. Pharmacokinetic and tox data. 20-100 subjects.

Q: Drug Development - Phase II
A: Administration to select groups. Aim to establish dose-response curve and demonstrate efficacy

Q: Drug Development - Phase III
A: Full-scale evaluation of benefits and risks. 2000-3000 subjects.

Q: Drug Development - Phase IV
A: Post-marketing surveillance. May reveal uncommon/long-term risks.

Q: Volume of Distribution
A: Theoretical volume into which an amount of drug would distribute to produce the identified plasma concentration

Q: Rate Constant for Elimination
A: k. Fraction of the Vd from which the drug is removed per unit time

Q: Rate of Elimination is equal to
A: Product of clearance and the current concentration

Q: First Order Kinetics
A: A constant proportion of the drug is eliiminated per unit time. i.e. the elimination of a drug is dependent on its current plasma concentration

Q: Zero Order Kinetics
A: A constant amount of drug is eliminated per unit time.

Q: Properties of Oral Route of Administration
A: Lowest bioavailability due to first past metabolism, gut metabolism, bacterial metabolism.
Absorption via uptake of polar molecules, or diffusion of lipid-soluble molecules

Q: Onset of epidurally administered drugs
A: Speed of onset determined by unionised portion of drug available

Q: Properties of Intrathecal Administration
A: Small dosing.
Minimal systemic effects.
Position affects spread

Q: Properties of Rectal administration
A: Slow/incomplete/erratic absorption.
~50% of drug will bypass portal circulation.

Q: Properties of a molecule which will affect its distribution
A: Molecule size
Ionisation
Protein binding

Q: Phase I reactions
A: Oxidaiton, reduction, or hydrolysis, typically via CYP450 enzymes

Q: Phase II reactions
A: Glucoronidation
Sulfation
Acetylation
Methylation

Q: High Extraction Ratio
A: Rapid uptake/high capacity. I.e. metabolism is independent of protein binding and limited by hepatic flow

Q: Low Extraction Ratio
A: Amount of free drug dependent on protein binding and hepatocyte function. Metabolism is independent of flow.

Q: Michaelis Constant
A: Concentration of a substrate which causes an enzyme to work at 50% of maximum capacity

Q: Method of drug secretion at the proximal tubule
A: Active against [gradient]. Separate mechanisms for acidic and alkaline substances

Q: Properties of drugs excreted in the distal tubule
A: Passive diffusion down concentration gradient.
Therefore acidic drugs have increased elimination in an alkalinle urine.

Q: Enterohepatic Recirculation
A: Excretion of drug into bile, followed by bacterial metabolism and reabsorption

Q: Infusion kinetics - Loading dose
A: Loading dose = Vd x [Target]

Q: Indications for drug monitoring
A: Avoid toxicity
Adjust dosing for efficacy
Monitor compliance or determine failure of therapy

Q: Characteristics of drugs that require monitoring
A: Narrow target range, Significant pharmacokinetic variability, Relationship between the concentration in plasma and clinical effects, Determined concentration range, Validated monitoring assay

Q: Timing of sampling for toxicity
A: At peak concentration. Determined by absorption, distribution, and dosing schedule

Q: Timing of sampling for monitoring
A: At steady state, i.e. 4-5 half-lives

Q: Timing of levels for drugs with short half-lives
A: Trough levels (least variable)

Q: Factors which affect interpretation of drug levels
A: Timing of sample
Dosing schedule
Patient factors
Protein binding
Active metabolites

Q: Receptor
A: Component of a cell which interacts with a ligand and initiates a sequence of events which lead to an observed change in function

Q: Chemical Antagonist
A: When a drug binds directly to another, e.g. protamine/heparin

Q: Physiologic antagonist
A: When a countering effect is produced by agonism of other pathways, e.g. GTN and noradrenaline

Q: Receptor types
A: Intracellular (cytoplasmic, intranuclear)
Enzyme-linked
Ion-channel
GPCR

Q: Intracellular Receptors activation
A: Activated by lipid-soluble molecules which pass through the cell membrane

Q: Enzyme-linked receptors
A: Activated by an extracellular ligand, causing enzymatic activity on the intracellular side

Q: Ion-channel receptors
A: Create a channel in the membrane in response to either ligand binding, or a change in transmembrane voltage

Q: Methods of enzyme interaction
A: Enzyme antagonism
False substrate

Q: Enzyme antagonism mechanisms, consequences, and types
A: Prevents enzyme activity, increasing [substrate] and decreasing [product].
May be competitive (ACE-I), non-competitive, or irreversible (aspirin)

Q: False substrate
A: A drug which competes for an enzyme binding site, and produces a product.

Q: Physicochemical action
A: Where the mechanism of action is due to physicochemical properties, e.g. mannitol

Q: Methods of drug action
A: Receptor
Enzyme interaction
Physicochemical interaction

Q: Graded response to drug administration
A: Continuous increase in effect with dose

Q: Quantal response to drug interaction
A: Demonstrate a response once a certain proportion of receptors are occupied (e.g. death with LD50)

Q: Adverse effect
A: Noxious or unintended effect associated with administration of a drug at the normal dose

Q: Type A Adverse Reaction
A: Related to the pharmacological action. Common, dose-response, predictable

Q: Type B Adverse Reaction
A: Patient specific/idiosyncratic, poor response relationship, not predictable

Q: Type C Adverse Reaction
A: Statistical effect associated with monitoring. Typically identification of a background disease which would otherwise go unnoticed.

Q: Mechanisms of Drug Interaction
A: Pharmaceutic
Pharmacokinetic
Pharmacodynamic

Q: Pharmacokinetic interaction
A: Drug interaction affecting A/D/M/E

Q: Drug Interactions - Absorption
A: Affected by:
Changed pH of environment
Gastric emptying time

Q: Drug Interactions - Distribution
A: Competition for protein binding
Altered cardiac output
Displacement from tissue binding sites
Chelation

Q: Drug Interactions: Metabolism
A: CYP450 interaction/induction
Competition for enzymatic pathways

Q: Drug Interactions: Elimination
A: Changes in urinary pH, competition for active transport mechanisms

Q: Drug Interactions - Pharmacodynamic (3 types)
A: Additive (summation), antagonistic, synergystic (multiplicative). May be evaluated using an isobologram.

Q: Isobologram
A: Graph which plots a line of equal activity between the concentrations of two drugs. Linear = additive interaction, concave = synergistic, convex = antagonistic.

Q: Alterations in Drug Response: Pharmacokinetics affecting placental transfer
A: Drug factors:
- pKa
- lipid solubility
- molecular weight (<600 Daltons will freely diffuse)
- protein binding
- plasma concentration
Maternal factors:
- Uteroplacental perfusion
- Placental transport out and placental metabolism
Fetal factors:
- pH (ion trapping)
- Protein binding

Q: Pharmacokinetics of Neonates: Absorption
A: Prolonged gastric emptying time, reduced pancreatic and bile salt secretion
Higher bioavailability due to reduced first pass metabolism

Q: Pharmacokinetics of Neonates - Distribution
A: 70-75% TBW (compared to 50-60% for adult) increases V_D
Less plasma protein (and see effect of pH)
Low pH
- Affects ionized fraction of drugs
- Affects protein binding
Very small body fat %

Q: Pharmacokinetics of Neonates - Metabolism
A: Reduced enzymatic capacity of all pathways
- low plasma cholinesterase
- larger yet less metabolically active liver
    - P450 not matured

Q: Pharmacokinetics of Neonates - Elimination
A: Proportionally lower GFR - adult equivalence at 6-12 months

Q: Continous infusion rate calculation
A: Infusion rate = [Target] x Clearance

Q: Intracellular/Extracellular [Na]
A: 15mmol/l, 140mmol/l

Q: Intracellular/Extracellular K
A: 150mmol/L, 4.5mmol/L

Q: Intracellular/Extracellular [Cl]
A: 10mmol/L, 100mmol/L

Q: Gradients affecting diffusion of ions
A: Hydrostatic gradients
Concentration gradients
Electrical gradients

Q: Nernst Equation calculates:
A: The equilibrium potential for the ion, i.e. the potential difference produced by an ion with differing concentrations on either side of the membrane.

Q: Primary Active Transport
A: Movement of a substance against its concentration gradient at the cost of ATP

Q: Secondary Active Transport
A: Where a substance moves against a concentration gradient with another molecule that had a gradient established by active transport

Q: Gibbs-Donnan Effect
A: Uneven electrical charge on either side of a membrane, caused by uneven distribution of particles as some may not be permeable

Q: Functions of the placenta
A: Transport of gases and nutrients
Immunological barrier
Endocrine
Metabolic

Q: Normal placental blood flow
A: 600ml/min

Q: PO2 and SpO2 in the umbilical vein
A: 28mmHg
70%

Q: Changes that facilitate foetal oxygenation despite low PaO2
A: Foetal Hb has inc. O2 affinity
Increased level of foetal Hb (~50%>than mothers)
Double-Bohr effect
Increased CI
High foetal oxygen extraction

Q: Double-Bohr Effect
A: Foetal CO2 diffuses to maternal, alkalinising foetal blood whilst acidifying maternal blood, therefore favouring foetal O2 loading and maternal O2 unloading

Q: Double-Haldane effect
A: Haldane Effect:
- DeoxyHb has a higher affinity for CO2 than oxyHb.
Double Haldane Effect:
- Maternal Hb releases O2, increasing its affinity for CO2
- This favours foetal CO2 release and O2 loading
- Foetal O2 loading favours further maternal O2 release, and therefore further maternal CO2 loading
Accounts for ~45% of CO2 transfer.

Q: Glucose diffusion across placenta
A: Faciliated diffusion

Q: Molecules actively transported across placenta
A: Ca, Fe, vitamins A & C

Q: Development of the placenta
A: Maternal blood sinuses at trophoblastic cords, which send out placental villi. These sinuses become invaginated by multiple foetal villi, supplied by 2x umb. arteries & 1x umb. vein.

Q: Properties of the developing placenta
A: Thick(er) membrane reduces permeability. Placental permeability peaks @ 34 weeks.

Q: Properties of mature placenta
A: 3.5μm thick membrane, large surface area ~14m^2, ~500g, blood flow of 600ml/min

Q: Functions of nose breathing
A: Humidification
Filtration
Warming

Q: Properties of the nose which facilitate filtration
A: Turbinates increase surface area and turbulent flow

Q: Advantages of mouth breathing
A: Minimises resistance at high MV

Q: Functions of the larynx
A: Airway protection
Speech
Effort closure

Q: Define effort closure
A: Tighter occlusion of the laryngeal inlet due to constriction of the aryepiglottic muscles, allowing the airway to withstand up to 120cmH2O

Q: Number of airway divisions
A: 23

Q: Conducting Zone
A: First 16 divisions of the airway.
No gas exchange.
Supplied by bronchial circulation.
Volume is the anatomical dead space.

Q: Anatomy of the trachea
A: D shaped, avg. 1.8cm diameter, 11cm long

Q: Properties of the respiratory zone
A: Slow flow due to high x-sectional area. Majority of lung volume (i.e. all non-anatomical-dead-space).

Q: Alveolar Surface Area
A: 50-100m^2

Q: Alveolar Wall Thickness
A: 0.2-0.3um

Q: Alveolar Capillary diameter
A: 7-10um

Q: Type II Alveolar cells
A: Secrete surfactant to reduce surface tension and improve alveolar recruitment
May become Type I Alveolar cells

Q: Type I Alveolar Cells
A: Pneumocytes, make up 90% of alveolar surface area and are optimised for gas exchange

Q: External Intercostal Function
A: Inspiration

Q: Internal Intercostal Function
A: Expiration

Q: Accessory Muscles
A: SCM: Elevates sternum
Scalene: Elevates sternum and first two ribs
Pec major
Serratius anterior

Q: Muscles of active expiration
A: Abdominal wall (rectus, obliques, transversus abdominus), internal intercostals

Q: Effect of lung volume on PVR
A: Optimised at FRC. Large lung volumes stent open extra-alveolar vessels but compress smaller vessels. Vise-versa at small lung volumes.

Q: Critical opening pressure
A: Pressure required to create flow in small pulmonary vessels, above that which would be expected for vascular pressure gradients.

Q: West Zone 1
A: PA>Pa>Pv. No flow, alveolar deadspace.

Q: West Zone 2
A: Pa > PA > Pv. Flow determined by Pa-PA pressure gradient rather than the A-V gradient. I.e. Starling Resistor - flow is independent of downstream pressure

Q: West's Zone 3
A: Pa>Pv>PA. Blood flows, dependent on a-v gradient.

Q: West's Zone 4
A: Collapse of extra-alveolar vessels at low lung volumes.
Pa > Pint > Pv > PA

Q: Hypoxic Pulmonary Vasoconstriction
A: Low PAO2 causes arteriolar constriction, diverting blood from poorly oxygenated alveoli and improving V/Q matching

Q: Inputs to Respiratory Centre
A: Peripheral & Central chemoreceptors Mechanoreceptors
Irritant receptors
Limbic system
Executive function input

Q: Central chemoreceptor location
A: Ventral medulla

Q: Central Chemoreceptor stimulus
A: Fall in pH

Q: Central Chemoreceptor Characteristics (compared to peripheral receptors)
A: Stronger (80% of total response), but slower (due to time taken for diffusion)
Increased sensitivity (as no protein buffering).
Respond only to respiratory acidosis (as only CO2 crosses BBB to become bicarb + H)

Q: Mechanism of CO2 Retention
A: Prolonged respiratory acidosis (i.e. prolonged CSF acidosis) stimulates active secretion of bicarbonate into the CSF, causing normalisation of pH and decreased stimulation of central chemoreceptors.

Q: Hering-Breuer Reflex
A: Overinflation stimulating bronchial muscle to stimulate the apneustic centre and limit further inspiration

Q: Non-chemoreceptor inputs to the respiratory centre
A: Mechanoreceptors (stretch receptors)
J-receptors
Irritant receptors
Pain receptors
Thalamic temperature
Limbic
Cerebral cortex (conscious control)

Q: Dorsal Respiratory Group
A: Controls diaphgram - i.e. inspiratory only

Q: Abneusis
A: Long, deep breaths caused by loss of apneustic centre

Q: Compliance
A: Change in volume for a change in pressure

Q: Pressure gradient for lung compliance
A: Alveolar-Intrapleural

Q: Static Compliance
A: Compliance of the system at a given volume when there is no flow, and therefore no pressure component due to resistance

Q: Causes of Increased Lung Compliance
A: Normal aging
Acute asthma
Emphysema

Q: Causes of Decreased Lung Compliance
A: Alterations in lung volume and consolidation
- Reduced at extremes of lung volume, and is highest at FRC.
Increased surface tension.
Alveolar
- Increased pulmonary blood volume/venous congestion.
Interstitial
- Loss of elasticity

Q: Causes of Decreased Chest Wall Compliance
A: Restriction, structural abnormalities (obestity, paralysis, ossification, kyphosis, constriction), positioning

Q: Calculation of an inspiratory time-constant
A: Resistance x Compliance (with a constant inflation pressure)

Q: Importance of respiratory time-constants
A: Time constants determine rate of filling, final volume is determined by compliance.
At high RR, a greater proportion of Vt will be distributed to low-time constant alveoli, reducing dynamic compliance and creating shunt.

Q: Fast alveoli
A: Low time constant, poor compliance, empty and fill rapidly

Q: Slow alveoli
A: High time constant, high resistance, slow filling and emptying

Q: Pendelluft
A: Redistribution of gas between alveoli with uneven time constants

Q: Phases of the (Peripheral nerve) Action Potential
A: Rising
Peak
Falling
Hyperpolarisation
Resting

Q: Rising phase of the Action Potential mechanism
A: Stimulus above the threshold pot. opens voltage gated Na channels, causing rapid rise in intracellular Na, further channel opening, and depolarisation

Q: Opening potential of voltage-gated Na channels in peripheral nerve
A: -55mV

Q: Voltage at which fast Na channels change from inactive to closed in the ventricle
A: -50mV

Q: Resting membrane potential of a peripheral nerve
A: -70mV

Q: Peak membrane potential during a peripheral nerve Action Potential
A: 30mV

Q: Saltatory conduction
A: Conduction in myelinated cells, where the AP jumps between gaps in myelin sheath called nodes of ranvier

Q: Function of myelin
A: Increases nerve conduction velocity and reduces energy expenditure

Q: Amount of CO2 in the body
A: 120L

Q: Normal CO2 production
A: 200ml/min

Q: Time-variable distribution of CO2
A: Three-compartment model with variable time constants

Q: Effect of hyperventilation on CO2
A: Decrease in CO2 in all compartments (though most rapidly in blood), causing a drop in PCO2

Q: Effect of hypoventilation on CO2
A: Gradual rise in PaCO2, as CO2 levels rise across all compartments

Q: Effect of apnoea on CO2
A: CO2 increases by 3-6mmHg/min

Q: Hamburger Shift
A: Exchange of intracellular bicarb with extracellular Cl via the BAND3 protein, which facilitates ongoing bicarb production in the RBC.

Q: CO2 output equation
A: PACO2 = CO2 output / alveolar ventilation

Q: Normal mixed venous PCO2
A: 46mmHg

Q: Normal PACO2
A: 40mmHg

Q: Normal PaCO2
A: 40mmHg

Q: Normal mixed expired PCO2
A: 27mmHg

Q: Types of Hypoxia
A: Hypoxic
Anaemic
Histiotoxic
Ischaemic

Q: Hypoxic Hypoxia
A: Hypoxia due to low PaO2 (<60mmHg)

Q: Physiological causes of hypoxic hypoxia
A: Decreased alveolar ventilation
Diffusion limitation
Shunt
Dead space
Low FIO2

Q: Anaemic hypoxia
A: Hypoxia due to low Hb. Usually asx at rest but limits exercise tolerance.

Q: Compensation for anaemic hypoxia
A: Increased 2,3-DPG, causing R-shift in HbO2 curve to favour oxygen offloading at tissues

Q: Ischaemic hypoxia
A: Impaired CO causing impaired O2 delivery

Q: Histotoxic hypoxia
A: Impaired tissue oxidative processes, preventing utilisation of delivered O2

Q: PO2 at 3000m
A: 60mmHg

Q: Altitude at which LoC occurs in unacclimatised individuals
A: 5,400m

Q: Armstrong limit
A: 19,200m

Q: Causes of iPEEP
A: Incomplete exhalation due to:
- High RR
- High airways resistance

Q: Sinuses of Valsalva
A: Outpouchings of the aortic wall which produce eddy currents preventing valve leaflets occluding the coronary os during systole

Q: LAD territory
A: LA, Anteroseptal, anterior, anterolateral wall segments

Q: Branches of the LAD
A: Diagonal or septal perforators

Q: LCx territory
A: Lateral and posterior (inferolateral) LV

Q: LCx Branches
A: Obtuse Marginal x3

Q: RCA territory
A: RA and RV, and inferoseptal and inferior segments

Q: LAD course
A: Anterior IV groove to the apex, where it anastomoses with the PDA

Q: LCx course
A: L AV groove

Q: RCA course
A: Vertically downward in the R AV groove. Branches to the posterior IV artery which anastomses with the LAD

Q: Coronary Dominance
A: The artery which supplies the PDA. RCA supplies SA node in 60% and AV in 90%

Q: Cardiac venous drainage
A: Majority coronary sinus, 1/3 via anterior cardiac veins directly into the RA, some via the thebesian veins to the left sided chambers

Q: Coronary Blood Flow Equation
A: (Pressure(aortic) - cavity pressure)/Coronary Vascular Resistance

Q: Normal coronary blood flow
A: 250ml/min (5% of CO), increases up to 4x during exercise.

Q: Coronary flow during systole
A: LV CBF minimal during systole due to high CVR and cavity pressure.
RV CBF less affected, as cavity pressure is lower.
Tachycardia reduces diastolic time and therefore LV CBF.

Q: Normal myocardial O2 extraction
A: 70%

Q: Control of coronary blood flow
A: Autoregulation (myogenic, hypoxia), and direct PNS or SNS activation.

Q: Events in Slow Ventricular Filling
A: Arterial pressure falling, CVP slowly rising (post y-descent), ECG shows P wave

Q: Events in Atrial Contraction
A: Arterial pressure falling, CVP shows a wave, ECG shows PR interval

Q: Events in Isovolumetric Ventricular Contraction
A: AV valves close, arterial pressure falling, CVP shows c wave, ECG shows QRS or QT

Q: Events in Ejection
A: Semilunar valves open, arterial pressure rises rapidly, CVP shows x descent (shortening RV pulls RA down), ECG shows ST segment

Q: Events in Isovolumetric Relaxation
A: Semilunar valves close, arterial pressure falls (dicrotic notch shows valve closure), CVP shows v wave, ECG shows T wave

Q: Events in Rapid Ventricular Filling
A: AV valves open, arterial pressure falling, CVP shows y descent as there is a rapid drop in CVP, ECG shows TP interval

Q: Determinants of CO
A: HR, preload, afterload, contractility

Q: Equation for cardiac chamber wall stress
A: Wall Stress = Pressure x radius / 2x Wall thickness

Q: Causes of increased end-diastolic filling pressure
A: Inc. circulating volume, inc VR, dec. venous compliance, atrial kick, inc. TPR, dec. intrathoracic pressure

Q: Determinants of systemic arterial impedance
A: Resistance
Inertia
Compliance

Q: Determinants of myocardial O2 demand
A: Heart rate, contractility, ventricular wall tension.
Minor include external work and basal O2 consumption.

Q: Equation for Wall Tension
A: WT = Pressure x radius / 2

Q: Effect of preload and afterload on MVO2
A: Both increase wall tension and therefore MVO2, though preload has a proportionally smaller effect (preload inc. EDV, which is not directly proportional to radius, whilst afterload inc. EDP, which is directly proportional to pressure)

Q: Normal Cerebral Blood Flow
A: 750ml/min (~15% of resting CO)

Q: Normal Cerebral metabolic rate for oxygen
A: 50ml/min

Q: Hagan-Poiseuille Equation
A: Flow = Driving pressure x pi x r^4 / (8 x viscosity x length)

Q: Normal Cerebral Perfusion Pressure
A: ~80mmHg

Q: Cerebral Perfusion Pressure equation
A: CPP = MAP - ICP

Q: Range at which CPP is autoregulated
A: 60-160mmHg, via myogenic means

Q: Causes of left-shift in the cerebral blood flow autoregulation curve
A: Neonates, children

Q: Causes of right-shift of the cerebral blood flow autoregulation curve
A: Chronic hypertension
Acute sympathetic stimulation

Q: Effect of CO2 on cerebral vessels
A: Vasodilatation

Q: Baroreceptors
A: Stretch receptors in the aortic arch and carotid sinus which are vital in the autonomic control of blood pressure

Q: Volume receptors
A: Low-pressure stretch receptors in the SVC, IVC, pulmonary circulation, and atrial walls

Q: Innervation of the carotid sinus
A: Glossopharyngeal nerve

Q: Innervation of aortic baroreceptors
A: Vagus nerve

Q: Integration of baroreceptor control
A: Afferent fibres to the NTS and RVLM are GABA (inhib), resulting in decreased SNS tone and increased PNS tone

Q: Effects of baroreceptor activation
A: Arteriolar and venous vasodilatation, hypotension, bradycardia, decreased CO, decreased RR

Q: Range over which the carotid sinus is active
A: 50-200mmHg

Q: ANP secretion
A: In the atria on activation of stretch receptors

Q: Effects of ANP
A: Increased GFR
Decreased aldosterone secretion
Vasodilatation

Q: α1-receptors
A: Smooth muscle - agonism causes:
- Vasoconstriction
- Relaxation of GIT muscle (via presynaptic receptors)
- Constriction of GU muscle

Q: α2-receptors
A: CNS, arterioles, pancreas. Agonism results in sedation, analgesia, vasodilatation, and inhibition of insulin release.

Q: β1-receptors
A: Cardiac muscle and the JGA.
Cardiac agonism causes increased inotropy, chronotropy, and dromotropy.
JGA agonism results in increased renin release

Q: β2-receptors
A: Present in skeletal, vascular and bronchial smooth muscle, and the liver.
Agonism causes vasodilation, bronchodilation, glycogenolysis, and increased activity of the Na+-K+ ATPase pump, increasing intracellular potassium.

Q: β3-receptors
A: Fat. Agonism causes lipolysis and thermogenesis.

Q: Class I Antiarrhythmics Mechanism
A: Block active and refractory voltage-gated Na+ channels (use-dependent blockade), prolonging phase 0 of the AP.
Inc. pacing threshold and defib. energy requirement

Q: Class I antiarrythmics subtypes
A: Ia - intermediate dissociation, Ib - fast dissociation, Ic - slow dissociation

Q: Class II antiarrythmics
A: β-Blockers, reducing proarrythmic effects of beta stimulation (which inc. pacemaker current, inc. Ca current, inc. repol K and Cl currents, Inc. Ca storage, reduced serum K)

Q: Class III antiarrhythmics MoA
A: Block outward K channels slowing repolarisation and prolonging the cardiac refractory period

Q: Class IV antiarrhythmics MoA
A: L-type Ca channel antagonists, inhibit slow inward Ca current, slowing nodal conduction and decreasing inotropy

Q: Bainbridge Reflex
A: Atrial Stretch Reflex: increased CVP is relayed by vagus to vasomotor centre. Causes increased SA nodal activity - isolated sinus tachycardia

Q: Set point of baroreceptors
A: 100mmHg, which may be R or L shifted

Q: Bezold-Jarisch Reflex
A: Chemo/mechanoreceptors in LV sense noxious stimuli and cause hypotension, bradycardia, and apnoea followed by rapid shallow breathing

Q: Oculocardic Reflex
A: Pressure applied to globe generates PNS response

Q: Lambert Law
A: Absorption of radiation is proportional to the distance it travels through the solution

Q: Lung function: Filtration
A: Entire CO passes through 7um capillary beds which sieve emboli and protect systemic circulation

Q: Lung Function: Activated substances
A: Angiotensin I
Arachidonic acid

Q: Lung function: Inactivated substances
A: 5HT, NA, bradykinin, ANP, PGs, lignocaine, fentanyl

Q: Lung functions: Blood resevoir
A: Highly compliant vasculature holding 500ml volume reserve for the LV

Q: Lung functions: Drug delivery
A: Organ optimised for gas exchange is also optimised for delivery of inhaled agents.
Drugs absorbed are lipophilic and alkaline.

Q: Lung functions: Endocrine
A: Release of inflammatory mediators and NO
Metabolises angiotensin I to angiotensin II

Q: Strengths of Meta-analyses
A: Enhanced precision of estimate of effect, useful when large trials are not feasible, clinically relevant outcome (e.g. NNT)

Q: Weaknesses of meta-analyses
A: Publication bias
Duplicate publication
Heterogeneity
Inclusion of outdated studies

Q: Types of Nephron
A: Superficial, midcortical, juxtamedullary

Q: Characteristics of superficial cortical nephrons
A: Short loops of henle

Q: Characteristics of Juxtamedullary nephrons
A: Long loops of henle
Efferent arteriole forms vasa recta of the kidney
Flow is not autoregulated

Q: Kidneys, proportion of resting cardiac output
A: 22%

Q: Kidney oxygen extraction
A: 10%. High renal blood flow required for filtration rather than oxygenation.

Q: Renal autoregulation range
A: 60-160mmHg

Q: Myogenic autoregulation
A: Intrinsic constriction of the afferent arteriole in response to an increased transmural pressure. Resistance therefore increases proportionally to pressure.

Q: Tubuloglomerular feedback
A: Constriction or dilatation of the afferent arteriole in response to adenosine or NO (respectively) release from the macula densa, which monitors flow in the ascending limb. Increased driving pressure increases flow and prompts adenosine release, whilst a decrease in flow stimulates NO release.

Q: Neuronal control of glomerular filtration
A: SNS innervation cause afferent and efferent arteriolar constriction, increasing capillary hydrostatic pressure but decreasing oncotic pressure.
The overall effect is a slight reduction in GFR.

Q: Renal hormonal response to a fall in GFR
A: Renin is released by the JGA in response to B1 stimulation, which catalyses angiotenin I production from angiotensinogen.

Q: Effect of Angiotensin II
A: Stimulates aldosterone release.
Vasoconstricts afferent and efferent arterioles (preserved GFR at a reduced renal blood flow).
Reduces Kf by constricting glomerular mesangial cells.
Increases SNS activity and generalised vasoconstriction (5x more than NA).
Increases thirst.
Stimulates ADH release.

Q: Value for NFP and changes across capillary
A: Average 17mmHg.
Falls across capillary as capillary hydrostatic pressure falls and interstitial oncotic pressure rises (protein free-fluid is filtered, increasing [protein] of remaining fluid)

Q: Molecular weight below which molecules are freely filtered
A: <7000 Da

Q: Normal Filtration Fraction
A: Filtration fraction = proportion of RPF that is filtered. Normally ~20% (Normal RBF 1100ml/min, therefore RPF 600ml/min, normal GFR 125ml/min).

Q: Proximal Tubule Absorbs:
A: Basically everything, including protein

Q: Proximal Tuble Excretes
A: H+, organic ions, ammonium

Q: Ascending limb absorbs and excretes
A: Common ions (Na, K, Cl), and excretes H+

Q: Countercurrent Mechanism
A: NaCl is actively removed from thick ascending limb, increasing interstitial osmolality. Increased osmolality causes water to diffuse in from the descending limb.
Fluid in the descending limb is now more concentrated. As it travels around the loop, more NaCl is removed from the thick ascending limb, and the osmolality is increased further.
The end result is that the:
- Interstitium is maximally concentrated at the tip of the loop of henle
- Filtrate is hypotonic at the end of the loop of henle

Q: Substances reabsorbed from the distal tubule
A: Na, Cl, HCO3, Ca

Q: Substances secreted from the distal tubule
A: K, H+

Q: Role of the collecting ducts
A: Concentration and dilution of urine.
Collecting ducts run through concentrated interstitium. Release of ADH increases no. of aquaporins, causing water to flow into interstitium and urine to become concentrated.

Q: Distribution of Potassium
A: 90% in ICF
8% in bone
2% in ECF

Q: Roles of potassium
A: Regulation of cellular pH
Control of cellular volume
DNA/protein synthesis
Enzymatic function
Resting membrane potential

Q: Symptoms of hyperkalaemia
A: Weakness, paralysis, parasthesias

Q: ECG findings of hyperkalaemia
A: 5.5-6.5: Tall tented T waves
6.5-7.5: Loss of P wave, long PR interval
7.5-8.5: Widening QRS
>8.5: Sine-wave QRS

Q: ECG findings of hypokalaemia
A: Long PR, long QT, flat T waves/TWI, U waves, ST depression

Q: Classify determinants of serum potassium
A: Dependent on intake, sequestration, and elimination

Q: Potassium elimination is affected by
A: Plasma [K]
Tubular flow rates
Aldosterone
Sodium and water balance
Alkalosis

Q: Formula for renal clearance
A: Cl = Urinary concentration x Urinary Flow / Plasma concentration

Q: Properties of Creatinine
A: Produced at a relatively constant rate, not metabolised, freely filtered, minimally excreted, not rebsorbed

Q: Factors affecting creatinine production
A: Race, muscle mass (affected by age, sex), diet

Q: Use of plasma creatinine as an indicator of renal failure
A: Inversely proportional to GFR at steady state. During acute changes, plasma creatinine will underestimate GFR as it is not yet at steady state

Q: How does plasma creatinine estimate GFR
A: Plasma [Cr] is inversely proportional to GFR at steady state

Q: Use of CrCl to estimate GFR
A: Better approximation of GFR than Plasma [Cr] alone. Requires 24 hour urine collection.

Q: Cockroft-Gault formula
A: CrCl ~= (140 - Age) x weight x sex coefficient (Male=1, Female=0.85) / (72 x Cr)

Q: Weaknesses of GFR/CrCl estimators
A: Dependent on plasma [Cr], which is variable and unreliable at extremes of: age, muscle mass, critical illness, malignancy, diet

Q: Determinants of efficacy of a buffer system
A: pKa of the buffer (80% of buffering occurs within 1 pH unit)
Amount of the buffer
Whether the system is open or closed

Q: Important buffer systems
A: Bicarbonate
Protein (including Hb)
Phosphate

Q: Isohydric principle
A: All buffer systems are in equilibrium with the same amount of H+

Q: pKa of the HCO3-/H+ <=> H2CO3 reaction
A: 6.1

Q: The bicarbonate buffer is open because...
A: CO2 can be exhaled, and bicarbonate can be renally excreted

Q: Protein buffering
A: Via H+ binding to histidine residues of imidazole groups.
Important in intracellular buffering as pH there is 6.8 and closer to protein buffer pKa.
Includes Hb.

Q: Hb buffering
A: Quantitatively most important non-bicarb buffer. Due to large (38) no. of histidine residues and large amount of Hb.

Q: pKa of Hb
A: DeoxyHb: 8.2, OxyHb: 6.6

Q: Phosphate buffering
A: Optimal pKa (6.8) but small quantity and closed system limit ECF buffering. High phosophate concentrations in urine and ICF make it a significant contibutor there.

Q: Normal Tidal Volume
A: 7ml/kg or 500ml

Q: Normal Inspiratory Reserve Volume
A: 45ml/kg or 2500ml

Q: Normal Expiratory Reserve Volume
A: 15ml/kg or 1500ml

Q: Normal Residual volume
A: 20ml/kg or 1500ml

Q: Normal FRC
A: 30ml/kg or 3L

Q: Normal PA pressures
A: 25/8 mmHg (MAP 15 mmHg)

Q: Normal RV pressures
A: 25/0 mmHg

Q: Normal LA pressures
A: 5 mmHg

Q: Normal LV pressures
A: 120/0 mmHg

Q: Ages at which CC exceed FRC
A: Supine at 45, Erect at 60

Q: Diagnosis of obstructive airway disease
A: FEV1 <80% predicted, FEV1/FVC <0.7

Q: Restrictive lung disease spirometry characteristics
A: FEV1 <80%, FVC <80%, FEV1/FVC >0.7

Q: CVS changes in pregnancy
A: ↑ Intravascular volume (oestrogen ↑ plasma, EPO - ↑ RBC) with ↓ oncotic pressure, ↑ VR, ↑ CO, ↑ HR, ↑ SV, ↓ SVR (progesterone), ↓ SBP, ↓ DBP, ↓ MAP

Q: Plasma volume changes in pregnancy by trimester
A: ↑ in all; 35% in 1st, 45% in 2nd, 50% in 3rd

Q: HR changes by trimester
A: ↑ in all, 15% in 1st, 18% in 2nd, 25% in 3rd

Q: SV changes by trimester
A: ↑ in all, 20% in 1st, 25% in 2nd, 30% in 3rd

Q: CO changes in pregnancy by trimester
A: Increased in all, 20% in 1st, 40% in 2nd, 45% in 3rd

Q: Shunt
A: Blood reaching the systemic circulation without being oxygenated via passage through the lung

Q: Types of physiological shunt
A: Anatomical
- Bronchial circulation
- Thebesian veins
Functional (V/Q scatter)

Q: Functional shunt
A: Blood passing through alveolar capillaries with inadequate ventilation, I.e V/Q mismatch/scatter but not true shunt.
Partial shunts cannot be modelled by venous admixture, so is calculated as a virtual or functional shunt.

Q: Normal physiological shunt fraction
A: 2-5%

Q: PO2 Dry Atmospheric Gas
A: 160mmHg (0.21 * 760mmHg)

Q: PO2 Humidified Tracheal Gas
A: 149mmHg (760 - 47 [humidification]) * 0.21

Q: PO2 Alveolar Gas
A: 105mmHg (PAO2 = 149mmHg - 40/0.8)

Q: PO2 Arterial Blood
A: 100mmHg (Different from alveolar due to A-a gradient)

Q: PO2 Capillary Blood
A: 45mmHg

Q: PO2 Mitochondria
A: 5mmHg

Q: PO2 Mixed Venous Blood
A: 40mmHg (75%)

Q: VO2 Max
A: Limit of O2 consumption, where metabolism switches to anaerobic

Q: Role of Surfactant
A: Decrease alveolar surface tension
Stabilise small alveoli
Prevent fluid transudation

Q: Valsalva Manouvere
A: Forced expiration against a closed glottis. Performed by increasing Paw to 40cmH2O for 10-15s.

Q: Valsalva Phase I
A: Paw to 40cmH20, ↑ P thoracic, ↑SBP and ↑ DBP due to aortic compression and increased LV preload from squeezing pulmonary vasculature

Q: Valsalva Phase II
A: ↓ VR due to high thoracic pressure, ↓ CO, ↓ SBP & DBP.
Baroreceptor activation, ↑ SNS activation causing ↑ HR and ↑ SVR, with ↑ BP in late phase II

Q: Valsalva Phase III
A: Paw returns to 0. PVR rapidly ↓, with a subsequent fall in LV preload causing ↓
HR and ↓ BP

Q: Valsalva Phase IV
A: VR normalises, CO normalises, SBP and DBP overshoot due to normal CO entering high SVR.
Baroreceptors respond and HR, SBP and DBP return to normal.

Q: Valsalva: Response in CCF/Volume overload
A: Square wave. ↑ Paw causes sustained ↑ in SBP and DBP. Only mild drop when pressure is released.

Q: Valsalva: Reponse in autonomic neuropathy
A: Minimal baroreceptor response.
No increased SNS outflow in phase II, so BP falls whilst Paw is high.
No increased vagal tone in phase IV, so no overshoot.

Q: Bowditch Effect
A: Increase in myocardial contractility with increased heart rate

Q: Determinants of Contractility
A: SNS outflow
Tachycardia (bowditch/treppe effect)
Afterload (Anrep effect)
Drugs
Disease states
Almost all act by changing levels of intracellular calcium

Q: Anrep effect
A: Increased afterload causes an increase in contractility

Q: Mechanism of the Bowditch Effect
A: Increased Ca influx due to more frequent depolarisations cannot be met with increasing activity of the Na/K and Na/Ca exchange pumps, leading to an increased intracellular Ca.

Q: CSF is...
A: Transcellular fluid in the subarachnoid space. ~2ml/kg, split evenly between the skull and spine.

Q: Functions of CSF
A: Mechanical protection (reduce effective weight)
Buffering ICP
Stable extracellular environment
pH regulation
Nutrition

Q: Formation of CSF
A: Ultrafiltration and secretion. Active Na transport, faciltated glucose transport.
70% produced in choroid plexus, 30% in brain capillary endothelium
500ml/day.

Q: Factors affecting CSF formation
A: Constant within normal parameters, though is decreased at CPP <70mmHg due to less choroidal blood flow.

Q: CSF contents relative to plasma
A: Na unchanged.
Increased Mg and Cl.
Decreased K, glucose, protein, Ca.

Q: CSF circulation is due to:
A: Respiratory oscillations, arterial pulsation, ongoing production

Q: CSF circulation route
A: Lateral ventricles
Third ventricle, via foramen of Munro
Fourth ventricle, via Aqueduct of Sylvius
Cisterna Magna, via Foramina of Luschka and Foramen of Magendie
Then, cranially to basilar cisterns via the Sylvian fissure
OR
Caudally, to the spinal subarachnoid by central canal

Q: CSF reabsorption: requirements and location
A: Pressure-dependent - CSF pressure 1.5mmHg > venous pressure facilitates reabsorption by arachnoid villi, in dural walls of sagittal and sigmoid sinuses. Linear increase in reabsorption until ICP 22.5mmHg.
85% in intracranial villi, 15% in spinal villi.

Q: Corticospinal tract: function and crossing
A: Motor function. Crosses at the brain stem.

Q: Dorsal columns: function and crossing
A: Light touch and proprioception. Crosses at the brain stem.

Q: Spinothalamic tract: function and crossing
A: Pain and temperature. Crosses within two vertebral segments of the spinal root.

Q: Spinocerebellar tract: function and crossing
A: Unconscious proprioception. Does not cross.

Q: Complete cord transection: Findings
A: Loss of motor and sensation below the level.
Initially flaccid paralysis, progressing to spastic after a few weeks. Double incontinence.

Q: Central cord syndrome
A: Flaccid paralysis and loss of sensation, in the upper limbs greater than the lower limbs

Q: Anterior cord syndrome
A: Motor, pain, and temperature loss below the level of the lesion (only dorsal columns are spared)

Q: Brown-Sequard syndrome
A: Cord hemisection, causing:
- Ipsilateral loss of motor function below the level
- Ipsilateral loss of light touch and proprioception below the level
- Contralateral loss of pain and temperature below the level
- Ipsilateral loss of pain and temperature AT the level

Q: Normal ICP
A: <13mmHg

Q: ICP Waveform: P1
A: First peak, represents arterial pulsation

Q: ICP waveform: P2
A: Second peak, represents intracranial compliance

Q: ICP waveform, P3
A: Third peak, dicrotic wave representing valve closure

Q: Lundberg A Waves
A: A wave: Square wave up to 50mmHg lasting 5-20 minutes.

Q: Lundberg B waves
A: Variable spikes in ICP at 30-120s intervals, suggestive of vasospasm

Q: Lundberg C waves
A: Benign oscillations at 4-8/min

Q: Monroe Kellie Doctrine
A: The skull is a rigid box of fixed volume and dismal elastance. Therefore, any increase in volume of one substance must be met with a decrease in volume of another or a rise in ICP.

Q: Physiological reponse to an increased ICP
A: Displacement of CSF to the spinal subarachnoid
Compression of vascular bed
Increased CSF reabsorption
Increase in MAP to maintain CPP

Q: Classification and methods of treating ICP
A: Brain: Osmotic agents
Blood: Evacuation of haemorrhage, sedation (reduced dyssynchrony and increased venous pressure, minimises seizure risk), hypocarbia (reduced blood volume), barbiturates (reduced flow and blood volume), hypothermia (reduced flow)
CSF: EVD

Q: Stimulators of nociceptors
A: H+, K+, ACh, histamine, 5HT, bradykinin

Q: Sensitisers of nociceptors
A: Prostaglandins, leukotrienes, substance P, neurokinin A, calcitonin GRP

Q: Pain fibres
A: Aδ, C

Q: Aδ fibres size and speed
A: 2-5um diameter myelinated fibres, conduct at 40m/s

Q: C fibres
A: <2um unmyelinated fibres, conduct at 2m/s

Q: Gate theory
A: Aβ 'touch' fibres stimulate inhibitory interneurones in the dorsal horn, which inhibit signals from peripheral C fibres from rising to the thalamus

Q: Opiates
A: Naturally occurring substance with morphine like properties

Q: Opioids
A: General term for all substances with an affinity for opioid receptors

Q: Opioid receptor: activation and chemistry
A: Gi receptor. Activation causes:
Presynaptically: Closes voltage-gated Ca channels, reducing neurotransmitter release
Postsynaptically: ↑ K efflux causing subsequent membrane hyperpolarisation

Q: Opioid receptor classification
A: MOP, KOP, DOP, NOP

Q: MOP receptor effects
A: Respiratory depression
Bradycardia
Analgesia, euphoria, miosis (Edinger-Westphal nucleus)
Constipation. Notably the only receptor to cause nausea & vomiting

Q: KOP receptor
A: Less respiratory depression than MOP
Analgesia (predominantly spinal), sedation, meiosis, dysphoria

Q: DOP receptor effects
A: Analgesia, respiratory depression, urinary retention, physical dependence
Notably minimal constipation

Q: NOP receptor
A: Anxiety, depression, appetite change.
Hyperalgesia at low doses, analgesic at high doses.

Q: Distribution of blood in circulation
A: 15% in arteries
65% in veins
10% in pulmonary circulation
5% in cardiac chambers
5% in capillaries

Q: Central control of the ANS
A: Hypothalamus: Anterior, medial, lateral, posterior

Q: Anterior hypothalamus regulates
A: Controls PNS and thermoregulation.

Q: Medial hypothalamus
A: Satiety (in reponse to high BSL)

Q: Lateral hypothalamus
A: Contains thirst centre and hunger drive

Q: Posterior hypothalamus
A: Controls vasomotor centres, modulates sympathetic vasoconstriction, positive and negative inotropy/chronotropy

Q: SNS: spinal and ganglion anatomy
A: Efferent nerve synapse with two others in series, maintaining tonic outflow.
Efferent sympathetics form the ventral root ganglion
Afferents form the dorsal root ganglion

Q: Sympathetic trunks run:
A: Run T1 to L2.
Divided into cervical, thoracic (upper and lower), lumbar, and pelvic parts.

Q: Effect of SNS activation
A: Bronchial smooth muscle relaxation
Inotropy/chronotropy
Peripheral vasodilatation
Mydriasis
Piloerection & sweating
Ejaculation

Q: Cranial parasympathetic innvervation
A: CN III, VII, IX, and X (predominantly vagus)

Q: Sacral parasympathetic innervation
A: Hypogastric plexus from S2-4 innervating colon, rectum, bladder, and uterus

Q: Enteric plexus
A: GIT ANS free of CNS control. Contains its own sensory and integrative neurons, as well as excitatory and inhibitory neurons to coordinate muscle activity

Q: Normal total body water %
A: ~60% of total mass
~15% of this is in kinetically slow compartments (connective tissue and bone) and does not play much of a role in fluid redistribution.

Q: Contents of Normal Saline
A: 154mmol Na
154mmol Cl

Q: Contents of Hartmann's
A: 130mmol Na
109mmol Cl
28mmol bicarb (as lactate)
4mmol K
3mmol Ca

Q: Contents of Plasmalyte
A: 140mmol Na
98mmol Cl
27mmol Acetate
23mmol Gluconate
5mmol K
1.5mmol Mg

Q: Stewart-Hamilton Equation
A: CO = amount of indicator / area under the concentration-time graph

Q: Modified Stewart-Hamilton Equation
A: CO = V(Tb-Ti)k1k2 / area under concentration-time graph
Where, k1 = density constant, k2 = computation constant

Q: Functions of the Kidney
A: Waste elimination
Volume control
Osmolarity and electrolyte control
Acid-Base
Blood pressure
Endocrine function
Gluconeogenesis

Q: Endocrine functions of the kidney
A: RAAS
Vitamin D
EPO
Prostaglandins

Q: Renin-Angiotensin System Pathway
A: Angiotensinogen secreted by liver
Cleaved to angiotensin I by renin
Angiotensin I cleaved to angiotensin II by ACE
Angiotensin II - exerts effects

Q: Stimulators to release of angiotensinogen
A: Glucocorticoids
Thyroid hormones
Oestrogens
Angiotensin II
Inflammatory proteins

Q: Renin production
A: By JGA in response to:
- β1
- ↓ Renal perfusion
- ↓ Na^+ load at the macula densa

Q: Vitamin D - Renal metabolism
A: 25 hydroxy vitamin D converted in proximal tubule to calcitriol (active)

Q: Stimulants to EPO release
A: Hypoxia
Hypotension
Low Hct

Q: Inhibitors of glucagon release
A: Somatostatin
Secretin
Free fatty acids
α-agonists
Insulin
Ketones
GABA

Q: Effect of hepatic disease on BSL
A: Fluctuating BSL as glycogenesis and glycolysis (stimulated by insulin and glucagon) are impaired

Q: Platelet lifespan
A: 7-10 days
Removed by reticuloendothelial system in liver and spleen

Q: Platelet Ib/IIb/IIIa and IIb/IIIa function
A: Bind vWF, which also binds to collagen
IIb & IIIa also bind fibrin, encouraging aggregation

Q: Acute immunological transfusion reactions
A: ABO mismatch
Acute haemolysis
Febrile non-haemolytic
Urticaria
Anaphylaxis
TRALI

Q: ABO mismatch incidence
A: 1:40,000

Q: Acute haemolytic reaction incidence
A: 1:76,000

Q: Acute haemolytic reaction mechanism
A: Type II hypersensitivity: immunological destruction of transfused cells

Q: Febrile non-haemolytic reaction incidence
A: 1:100

Q: Febrile non-haemolytic reaction mechanism
A: Mild inflammatory reaction secondary to cytokine release. Fever >1ºC above baseline OR 38ºC

Q: TRALI mechanism
A: Donor plasma HLA activates receipient leukocyte antigen, in turn activating pulmonary neutrophils
Causes fever, shock, and pulmonary oedema

Q: Non-immunological acute transfusion reactions
A: Massive transfusion complications
Non-immune mediated haemolysis
Sepsis
Transfusion Related Circulatory Overload (TACO)

Q: Delayed Immunological transfusion reactions
A: Delayed haemolytic transfusion reaction
Post-transfusion purpura
TA-GVHD
Alloimmunisation
Transfusion-related Immune Modulation

Q: Delayed Non-immunological transfusion reactions
A: Iron Overload

Q: Massive transfusion
A: Greater than 50% of circulating volume in 4 hours, or whole circulating volume in 24 hours

Q: Complications from a massive transfusion dependent on:
A: No. of units
Rate of transfusion
Patient

Q: Massive transfusion complications
A: Air embolism
Hypothermia
Hypocalcaemia
Hypomagnesaemia
Citrate toxicity
Lactic acidosis
Hyperkalaemia

Q: Basal Metabolic Rate definition
A: Energy output required to sustain life at rest, which is:
- Fasted for 12 hours
- In a comfortable environment
- At mental and physical rest

Q: Basal metabolic rate normal value
A: 100W/day

Q: Factors affecting BMR
A: Age
- Dec. with age
Body fat
GIT
- Inc. with digestion, dec with starvation
Environment
Physiological states
- Hyperthyroid, catechols, corticosteroids
Disease states

Q: Indirect calorimetry method
A: Relaxed and fasted pt
Take FiO2, MVO2, MVCO2 at steady state
Use abbreviated weir equation

Q: Abbreviated Weir Equation
A: REE = 3.94 x (FiO2 - ETO2) + (1.1 x VCO2)

Q: Thermoneutral Zone in Neonates
A: 32-34°C

Q: Mechanisms of heat exchange
A: Radiation
Conduction
Convection
Evaporation

Q: Interthreshold range
A: Range of core temperatures which will not trigger an ANS response
0.2-0.4°C

Q: Peripheral temperature sensation
A: Cold and Warm type receptors

Q: Cold type receptors
A: Beneath epidermis
Active 10-40°C
Static maxima 25°C
Excited by cooling

Q: Warm receptors
A: Lie deep to the dermis
Excited by warming
Active from 30-50°C
Static maxima at 44°C

Q: CNS responses to hyperthermia
A: Remove clothing, sprawl, reduce activity

Q: CNS responses to hypothermia
A: Huddle, seek shelter, add clothing

Q: CVS responses to hyperthermia
A: Peripheral vasodilation and AV shunting, increase CO to improve cutaneous flow

Q: MSK responses to hyperthermia
A: Sweating

Q: MSK responses to hypothermia
A: Piloerection, shivering

Q: Metabolic responses to hypothermia
A: Increased BMR, non-shivering thermogenesis

Q: Method by which Hb binds oxygen
A: Cooperative binding.
Cooperativity is a phenomenon displayed by systems with (near)identical elements which act non-independently of each other.
This can be seen with enzymes or receptors with multiple binding sites where the affinity of the binding sites for a ligand is increased (positive cooperativity), or decreased (negative cooperativity), when a ligand is bound.

Q: Normal CSF pH
A: 7.33

Q: Normal CSF pCO2
A: 50mmHg

Q: Hypersensitivity reaction
A: Exaggerated immune response which causes host injury

Q: Type I hypersensitivity reaction mechanism
A: IgE mediated 'immediate hypersensitivity' reaction
Antigen stimulates B lymphocyte to produce IgE. On re-exposure, antigen cross links IgE causing mast cell degranulation, releasing massive amounts of histamine, leukotrienes, and prostaglandins.

Q: Type I hypersensitivity reaction example
A: Anaphylaxis

Q: Anaphylaxis is a ... hypersensitivity reaction
A: Anaphylaxis is a Type I hypersensitivity reaction

Q: Type II hypersensitivity reaction mechanism
A: Cellular hypersensitivity, mediated by IgM & IgG
Antibody binding to cell surface antigen, with immune response against affected cell & phagocytosis

Q: A transfusion reaction is a ... hypersensitivity reaction
A: Type II

Q: Type III hypersensitivity reaction mechanism
A: Immune complex deposition, mediated by IgM, IgG, IgA
Tissue deposition of Ab-Ag complexes

Q: Type IV hypersensitivity reaction mechanism
A: Delayed hypersensitivity reaction, T-cell mediated
T-cell induced mononuclear cell accumulation. Release of monokines and lymphokines.

Q: Necrotising vasculitis is a ... hypersensitivity reaction
A: Type III

Q: Granulomatous vasculitis is a ... hypersensitivity reaction
A: Type IV

Q: Subtypes of type III hypersensitivity
A: Formation of complexes in circulation, with subsequent tissue deposition
e.g. Serum sickness
Formation of complexes directly in tissues
e.g. Arthus reaction

Q: Changes in pulmonary blood pressures with exercise
A: Sight increase in MPAP, limited due to distension and recruitment of pulmonary capillaries.
Improves V/Q matching, bringing it closer to 1 and reducing baseline mismatch

Q: Respiratory consequences of spinal injury
A: Above C3: Complete respiratory paralysis
Below C5: Complete loss of IC tone, paradoxical breathing reducing VC by 50%. Significant impediment to forced expiration.
C5 - T8: Intercostal weakness, reducing IC tone and FRC. Impaired forced expiration - low FEV1, poor cough, atelectasis, dec compliance, inc. WoB.

Q: Cardiovascular effects of spinal injury
A: Above T5: Interrupted SNS outflow to heart, causing unopposed parasympathetic activity & bradycardia. CO maintained by SV, which must be maintained by high preload.
Below T5: Interrupted SNS outflow to arterioles, causing decreased SVR and hypotension. Also causes venous pooling with increased DVT risk.

Q: Neurogenic Shock
A: Cardiovascular collapse that occurs with spinal injury, due to impaired SNS outflow

Q: Spinal shock
A: Flaccid paralysis and areflexia below the level of the spinal cord lesion. Priapism may occur.

Q: GI effects of spinal injury
A: Unopposed parasympathetic input:
Delayed gastric emptying
Gastric ulceration (unopposed acid secretion)
Constipation

Q: Thermoregulatory effects of spinal injury
A: Impaired thermoregulation
- Vasodilation causes increased heat loss
- Impaired sweating may prevent heat loss

Q: RMP effects of hyperkalaemia
A: Depolarises the RMP, bringing it closer to threshold potential and increasing ease at which AP are generated
Also known as increasing irritability

Q: RMP effects of hypokalaemia
A: Hyperpolarises the RMP, making it harder for the cell to generate and propagate AP

Q: RMP effects of hyponatraemia
A: Hyponatraemia = reduced osmolarity, therefore intracellular hypokalaemia, causing a 'relative' hyperkalaemia, bringing RMP closer to threshold potential.

Q: RMP effects of hypocalcaemia
A: Lowers the threshold potential, bringing it closer to RMP and causing membrane instability.

Q: Phases of the Pacemaker Potential
A: Phase 0, 3, 4

Q: Pacemaker cell threshold potential
A: -40mV

Q: Pacemaker maximal diastolic potential
A: -65mV

Q: Peak pacemaker potential
A: 20mV

Q: Pacemaker potential phase 4
A: Mixed Na/K 'funny' current which causes gradual depolarisation.
Sympathetics increase the funny current.
Parasympathetics increase K permeability, flattening the gradient.

Q: Changes in ion permeability in phase 3 of the pacemaker potential
A: Ca channels close, K channels open causing repolarisation.

Q: Ventricular muscle absolute refractory period
A: 250ms

Q: Ventricular muscle relative refractory period
A: 50ms

Q: Ventricular action potential: Phase 0
A: Depolarisation: at the threshold potential (-70mV), voltage gated fast Na channels briefly open, causing depolarisation.

Q: Ventricular action potential: Phase 1
A: Partial repolarisation
Closure of Na channels results in K efflux down its electrochemical gradient, causing a slight drop in voltage

Q: Ventricular action potential: Phase 2
A: Plateau phase
L-type calcium channels open, causing a slow inward Ca current which maintains depolarisation and facilitates muscle contraction

Q: Ventricular action potential: Phase 3
A: Repolarisation
Membrane permeability normalises - outward K current normalises RMP

Q: Ventricular action potential: Phase 4
A: Resting phase
Membrane potential is at -85mV

Q: Ventricular muscle RMP
A: -85mV

Q: Peak ventricular membrane potential during phase 0
A: 30mV

Q: When does the absolute refractory period of a peripheral neuron end?
A: When the membrane potential becomes -ve (fast Na channels go from refractory to closed)

Q: Four characteristics of a neurotransmitter
A: Synthesised or stored within a neuron
Released from the pre-synpatic membrane to trigger an effect at the post-synaptic membrane
Gives the same physiological effect when administered exogenously
Mechanism for removing it from the synapse

Q: Excitatory Post Synaptic Potential effects
A: Na and K diffuse down gradients - however movement of Na is greater and depolarisation occurs.
Size of potential is related to the number of vesicles released from the pre-synaptic cell

Q: Inhibitory Post-Synaptic Potential mechanism
A: May be either K or Cl mediated.
K: Binding opens K channels, which diffuse down gradients hyperpolarising the membrane
Cl: Binding opens Cl channels. the nernst potential for Cl is ~-70mV, so the membrane potential doesn't change, however it increases the amount of Na/K movement required to depolarise a cell and therefore inhibits the cellular AP.

Q: Methods of removal of neurotransmitter
A: Reuptake into presynaptic membrane (NA)
Degradation (e.g. ACh)
Diffusion (minor)

Q: Motor units
A: Consist of an α-motor neuron and the muscle cells it innervates
Gross movement muscles have many (quadriceps has ~1000) muscle cells per neuron
Fine movement muscles have few (extraocular has ~10-25) muscle cells per neuron

Q: Tetany
A: When frequent action potentials result in accumulation of Ca in cytoplasm, causing increased and sustained muscle tension

Q: Define reflex
A: Automatic predictable response to a stimulus

Q: Classes of Inotrope
A: Class I: Increase intracellular Ca (Adrenaline, milrinone, glucagon, digoxin)
Class II: Calcium sensitisers (Levosimendan)
Class III: Endocrine/metabolic (T3)

Q: Distribution of Ventilation
A: Right lung better than left
Bases better than apices, at low flow rates in the erect position
Dependent lung better in the lateral position when spont venting

Q: Distribution of perfusion in the lung
A: Bases better than apices
More pronounced at TLC, slightly reversed at RV

Q: V/Q = 0
A: Shunt

Q: V/Q > 1
A: Dead space

Q: V/Q 0-1
A: V/Q scatter

Q: Bohr Equation
A: Vd/Vt = (PaCO2 - PECO2) / PaCO2

Q: Effect of dead space on gas tension
A: PaCO2 rises, increasing MV to increase Va
No change in PaO2

Q: Effect of Shunt on PCO2
A: CO2 content rises, but PCO2 does not rise unless the shunt fraction is large and the patient is unable to increase Va.

Q: Effect of shunt on PaO2
A: PaO2 falls proportionally to the shunt fraction, as given by the isoshunt diagram.

Q: Effect of VQ scatter on gas tension
A: PaO2 falls, but can be improved with increasing PAO2

Q: Normal Thermoneutral Zone in Adults
A: 27-31°C.

Q: Variables affecting distribution of potassium
A: Insulin
Aldosterone
β-agonism
Acid-base status
Cell lysis
Exercise
ECF osmolarity

Q: Stages of platelet plug formation
A: Adhesion
Activation
Aggregation
Contraction

Q: Platelet plug formation: Adhesion
A: To subendothelial connective tissue by vWF

Q: Platelet plug formation: Activation mechanism
A: Exocytosis of granules:
- Promotion of the coagulation cascade
Platelet deformation:
- Activation of membrane phospholipase A2 to form thromboxane A2
- Contractile proteins deform platelet into a disc with long projections
Aggregation:
- ADP changes GP expression
 - GP bind vWF (vWF binds sub-endothelial connective tissue), and fibrinogen (which activates more platelets)

Q: Platelet plug formation: Aggregation
A: Platelets adhere together by fibrin forming a plug
Stimulated by ADP and thromboxane A2 from other platlets

Q: Platelet plug formation: Contraction
A: After some time platelets contract, retracting clot and sealing the vessel wall

Q: Ventricular Threshold Potential
A: -70mV

Front: Number of alveoli in the human lung
Back: About 500 million

Front: Describe Weibel's idealized model of human airways

Front: How far into the airway tree does air flow by bulk flow?
Back: Around 16 generations (or the terminal bronchioles)

Front: What is the dominant mechanism of gas movement in the respiratory zone?
Back: Diffusion

Front: Where in the airway tree do inhaled particles typically deposit and why?
Back: Terminal bronchioles because bulk flow gas velocity approaches zero here.

Front: What is the mechanism of gas movement in the respiratory zone?
Back: Diffusion

Front: What layers does an oxygen molecule cross when moving from alveolus to haemoglobin molecule
Back: surfactant
alveolar epithelial cell
interstitium
endothelial cell
plasma
erythrocyte membrane

Front: At approximately what airway generation does the respiratory zone begin?
Back: 17 (according to Weibel)

Front: What is an acinus?
Back: The anatomical unit of lung consisting of structures distal to the terminal bronchiole

Q: Stages of haemostasis
A: Vessel constriction
Platelet plug formation
Fibrin formation
(Fibrinolysis)

Q: Factors in the extrinsic pathway
A: Tissue Factor
Factor VII

Q: (Non-contact) Factors in the Intrinsic Pathway
A: Factor VIII
Factor IX
Factor XI

Q: (Contact) factors in the intrinsic pathway
A: HMWK
Factor XII

Q: Factors in the common pathway
A: Factor X
Factor V
Factor II (prothrombin)
Factor I (fibrinogen)

Q: Prothrombin time measures (pathway and factors)
A: Extrinsic pathway (requires addition of tissue factor)
Factor VII
Factor X
Factor V
Factor II (prothrombin)
Factor I (fibrinogen)

Q: APTT measures (pathway and factors)
A: Intrinsic pathway
Factor XI
Factor IX
Factor VIII
Factor X
Factor V
Factor II (prothrombin)
Factor I (fibrinogen)

Q: Activated Clotting Time Measures
A: Intrinsic pathway
Used to monitor anticoagulation for extracorporeal circuits

Q: Inactivation of circulating endogenous catecholamines
A: Extraneuronal uptake (lungs, liver, kidney, gut), with inactivation by COMT in the liver and kidney
Neuronal uptake by SNS endings, with inactivation by MAO in nerve cytoplasm

Front: What are the lung volumes making up TLC?
Back: RV
IRV
ERV
TV

Front: Which lung "volumes" can be measured with simple spirometry?
Back: expiratory reserve
tidal
inspiratory reserve

Front: Which lung "capacities" cannot be measured with simple spirometry?
Back: Total lung
Functional residual

Front: Describe the plethysmograph method of FRC measurement
Back: Subject is placed in a closed box and breathes on a mouthpiece.

Front: What is the limitation of the helium dilution method of total lung capacity measurement?
Back: It does not measure lung volume distal to closed airways (relevant in diseased lung).

Front: State the alveolar ventilation equation. What is its significance?
Back: [$]\dot{V}_A=\frac{\dot{V}co_2}{Pco_2}\cdot K[/$]
Significance is the inverse relationship between alveolar ventilation and Pco_2

Q: Composition of triglycerides
A: Glycerol and 3x fatty acids

Q: Digestion and Absorption of fat
A: Emulsification by bile salts, partially digested fats, mechanical action of the stomach
Facilitated diffusion of mixed micelles, FFA, and glycerol into enterocyte
- Short chain (<12 C) diffuse into portal circulation
- Others packaged into chylomicrons and excreted into lymphatics

Q: Production of ATP from FFA
A: β-oxidiation to acetyl CoA. Acetyl CoA enters citric acid cycle and produces ATP

Front: Describe Fowler's method for measuring anatomical dead space
Back: Following a single inspiration of pure oxygen, expired nitrogen content is sampled continuously. The nitrogen content rises as nitrogen-containing alveolar gas washes out dead space gas. Expired volume is measured, and the anatomic dead space is found by plotting expired volume against nitrogen content. (This method takes advantage of the fact that the conducting airways move gas via bulk flow, whereas in the respiratory zone, diffusion is the primary method of gas flow.)

Front: What is the normal ratio of physiological dead space to tidal volume ratio at rest?
Back: 0.2 to 0.35

Front: What is the difference between anatomical and physiological dead space?
Back: Anatomical is the volume of the conducting airways.
Physiological is the volume of gas not participating in gas exchange, and is the sum of alveolar and anatomical dead space

Q: Classification of microorganisms
A: Prokaryotes (bacteria)
Viruses
Eukaryotes (fungi, helminths, protozoa)

Front: How can anatomic dead space be measured?
Back: Fowler's method (measure expired nitrogen following a single inspiration of pure oxygen).

Front: How can physiologic dead space be measured?
Back: Bohr's method, involving measurements of arterial (so-called Enghoff modification) and expired CO_2 (and the Bohr equation).
[$]\frac{V_d}{V_t} = \frac{PaCO_2 - P_ECO_2}{PaCO_2}[/$]
Reference: West, Brandis

Q: Classification of Bacteria
A: By gram stain and morphology

Q: Gram stain method
A: Crystal violet solution
iodine solution
Washed with solvent - gram +ve retain the stain due to thick peptidoglycan wall
Safarin stain is applied which stains the gram -ve bacteria pink

Q: Classification of viruses
A: DNA/RNA
Double-stranded/Single Stranded
Negative-sense or Positive Sense (RNA only)
Capsid symmetry
Enveloped or non-enveloped

Q: Viruses: Negative-sense vs. Positive-sense
A: Positive sense may be translated directly into protein, negative sense requires RNA-polymerase to transcript to positive sense

Q: Antimicrobial Resistance
A: When the maximal tolerable level of an agent is insufficient to inhibit growth

Q: Volume of bile produced per day
A: 1L

Q: Haemoglobin metabolism pathway
A: Circulating erythrocytes and haptoglobin-Hb complexes are phagocytosed by splenic macrophages
Hb metabolised to:
- Globin: To amino acids
- Iron: Re-used to synthesise Hb
- Haeme:
Metabolised to biliverdin by splenic macrophages
Biverdin reduced to unconjugated bilirubin, bound to albumin
Unconjucated bilirubin conjugated in liver
Conjugated bilirubin actively excreted in bile
Conjugated bilirubin metabolised to urobilinogen by gut bacteria
Urobilinogen then:
- Enterohepatically recirculated and eliminted in faeces or bile or urine
- Metabolised to stercobilinogen and then sterobilin by gut bacteria

Q: Volume of gastric secretions produced per day
A: 2L

Q: Phases of gastric secretion
A: Cephalic
Gastric
Intestinal

Q: Cells which secrete gastric acid
A: H+/K pump in parietal cells

Q: Substances which cause gastric acid secretion
A: ACh (vagal)
Histamine
Gastrin

Q: Physiological inhibitors of gastric acid secretion
A: Low gastric pH
Somatostatin

Q: Secretion of pepsin
A: Pepsinogen secreted by chief cells in response to ACh or β stimulation
Cleaved to pepsin in gastric lumen

Q: Intrinsic factor secretion
A: From parietal cells

Q: Gastric mucous: Secreted by which cells in response to what stimulus
A: By neck cells in response to prostaglandins

Q: Volume of pancreatic secretion produced
A: 1.5L per day

Q: Stimulants to pancreatic exocrine secretion
A: CCK
Gastrin
Secretin
Vagal innervation

Q: Contents of exocrine pancreatic secretions
A: HCO3
Water
Enzymes
- Trypsinogen
- Amylase
- Lipase

Q: CCK secretion and function
A: Secreted from pancreatic acinar cells
Stimulates:
- GB
- Duodenal secretions
Regulates satiety and leptin release from fat

Q: Secretin release and function
A: From proximal duodenum in reponse to low pH
- Slows gastric emptying
- Stimulates pancreatic exocrine secretion

Q: Motilin release and function
A: Released cyclically from M cells in the small bowel
Stimulates the migrating motor complex

Q: Determinants of gastric emptying
A: Function of antral pressure vs pyloric resistance
Subdivide into:
Stomach
Duodenal
Systemic
Drugs

Q: Stomach factors which affect gastric emptying​
A: Distension
- Release of gastrin
Contents
- Liquids faster than solids
- Protein stimulates release

Q: Gastric half-time of liquids
A: ~20 minutes, empty in an exponential fashion

Q: Gastric half time of solids
A: ~2 hours. Dwell time of 30mins. Empty in a linear fashion

Q: Duodenal factors which affect gastric emptying
A: All negative feedback mechanisms:
- Duodenal distension
- Hypo/hyperosmolar chyme
- Acidic chyme
- Composition (carbs quicker than protein quicker than fat)

Q: Systemic factors which infuence gastric emptying
A: Motilin levels
SNS/PNS input
Pregnancy
- Smooth muscles relaxed
- Incompetent LoS
- Inc. gastrin production
- Inc. gastric acid production

Q: Drugs which increase gastric emptying
A: Metoclopramide
Erythromycin

Q: Drug classes which impede gastric emptying
A: Opioids
Alcohol
Anticholinergics

Q: Frequency range for US waves
A: 2-15 MHz

Front: What is the function of the conducting airways?
Back: To move gas to and from the respiratory zone.

Q: Spatial resolution
A: How close two objects can be and still be distinguishable. Two types:
- Axial resolution: How far they can be apart in the direction of the beam
- Lateral resolution: How far they can be apart when side by side

Q: Relationship between frequency and resolution and penetration
A: High frequency = high resolution, low penetration
Low frequency = low resolution, high penetration

Q: Effect of tissue interfaces on US waves
A: Absorbed
Reflected
Transmitted
Scattered

Q: Absorbance of US waves
A: Sound lost as heat
Inversely proportional to water content of tissues

Q: Reflection of US waves depends on
A: Reflected at interface, sound returns to the probe
Dependent on:
- Difference in sound conduction between the tissues
- Angle of incidence
- Smoothness of the plane

Q: Time-Gain compensation
A: Amplification of signals which have taken longer to return, aiming to nullify the fact that weaker signals are returned from deeper tissues.

Q: B-Mode
A: Standard 2D US mode

Q: Doppler equation
A: V = ΔF x s/(2 x Fo x cosθ), where:
ΔF= Frequency shift
s = Speed of sound
Fo = Emited Frequency
θ = Angle between sound wave and object

Q: Direction of the doppler effect
A: Reflected frequencies are higher towards and lower away

Q: Pulse oximetry light wavelengths used
A: 660nm (deoxyHb)
940nm (oxyHb)

Q: Pulse oximeter components
A: Two diodes
Photocell
Microprocessor

Q: Pulse oximetry mechanism
A: Absorbance of red and infrared light
Relative absorption related to oxygenation of Hb
Pulsatile flow allows (constant) tissue component to be subtracted

Q: Methods of measuring ETCO2
A: Infrared spectroscopy
Colourimetric methods
Rayman Scattering
Gas Chromatography

Q: Principles of infrared spectroscopy (not specific to CO2)
A: Gases with two or more different atoms will absorb infrared radiation to varying degrees
Knowledge of the likely components of a gas mixture allows an appropriate wavelength to be selected

Q: CO2 measurement using infrared spectroscopy: components and process
A: Requires:
4.28um light
Sapphire sampling chamber
Emitter
Lens
Detector
Chamber allows one wavelength of light through. Levels are measured on the other side, and correspond to gas content in the sample. Wavelength is plotted of partial pressure over time.

Q: Colourimetric methods of CO2 measurement
A: Litmus paper which changes colour when exposed to H+ (produced by CO2)

Q: Sources of error (and corrective techniques) in infrared capnography
A: Errors intrinsic to method:
Wavelength overlap (N_2O and CO peak absorbances are very close; 4.5 and 4.7 µm, respectively)
Collision Broadening Effect
- Widened absorbance spectra in the presence of other gasses—O_2, N_2, N_2O—due to intermolecular forces.
Errors of equipment:
Variable amount of radiation
Variable detector sensitivity
Variable efficacy of the crystal window and lens
Correction:
Mainstream capnographs use a double-beam capnometer (uses a reference chamber.
Side-stream capnographs use parallel narrow-band filters and photodetectors for CO and N_2O plus external measurement of pO_2

Q: Collision Broadening Effect
A: Intermolecular forces depend on their proximity to other molecules in the mixture.
Presence of other molecules alters the absorption spectra and therefore the amount of radiation absorbed.
Can be corrected for by compensating against measured or predicted values.

Q: Causes of high ETCO2
A: Decreased MVa (including incomplete exhalation of lungs with long time constants)
Increased CO2 producution
Increased inspired CO2

Q: Causes of a rapid drop in ETCO2
A: Failure of ventilation
Failure of circulation

Q: Causes of a gradual drop in ETCO2
A: Decreased CO2 production
Increased Vd
Increased Va (decreased PaCO2)
Sampling error

Q: Liquid Expansion Thermometry Method
A: Requires:
- Graduated evacuated capillary of negligible volume
- Mercury/alcohol resevoir
- Constriction ring (prevents capillary action/mercury falling back down)
When heated, kinetic energy content of mercury increases and it expands up the capillary. Rate is related to the time-constant of the system, typically 30s.

Q: Wet and Dry Bulb Mechanism
A: Two thermometers, one is wrapped in a wick attached to a water resevoir.
The dry thermometer measures surrounding air temperature.
The wet thermometer is cooled by evaporative cooling. The temperature difference is a function of the latent heat of vaporisation of water and how much evaporative cooling is occurring (and therefore humidity).

Q: Course of the SCV
A: Continuation of the axillary vein over the upper surface of the first rib.
Travels poteriorly to the clavicle.
Separated from the SCA by the anterior scalene
Joints with the IJV to form the brachiocephalic vein

Q: Anterior border of the SCV
A: Clavicle, subclavius, pec major

Q: Posterior borders of the SCV
A: Anterior scalene, SCA

Q: Inferior border of the SCV
A: First rib, apex of lung

Q: Superior border of the SCV
A: Skin, subcut tissue, platysma

Q: Borders of the safe triangle
A: Anteriorly by pectoralis major
Posteriorly by latissimus dorsi
Superiorly by the base of the axilla
Inferiorly by the 5th intercostal space

Q: Lateral borders of the trachea
A: Carotid sheaths
Thyroid lobes and inferior thyroid artery
Recurrent laryngeal nerves

Q: Posterior borders of the trachea
A: Oesophagus
Vertebral column

Q: Surface anatomy relevant for tracheosomy
A: Laryngeal structures (hyoid, thyroid cartiledge, cricothyroid, cricoid), sternal notch, thyroid lobes

Front: Describe the general arrangement of the phospholipid bilayer
Back: hydrophilic heads facing out, lipophilic chains facing inwards, creating central hydrophobic layer, forms a "fluid mossaic" with no fixed positions of individual molecules
Reference: Peck and Hill (3e) pp. 1

Q: [...] is the transport process where [...]
A: Pinocytosis; an area of cell membrane invaginates around a large target molecule

Front: Factors influencing rate of diffusion across a cell membrane (often determines time to drug effect)
Back: Molecular size
Concentration gradient
Protein binding
Ionization
Lipid solubility

Front: Methods of crossing the cell membrane
Back: Passive diffusion
Facilitated diffusion
Active transport
Pinocytosis
Ion channel

Q: SNS neurotransmitters
A: Nicotinic ACh at the ganglion, NA at the effect site.

Front: What factors determine the ionization of a drug?
Back: Molecular structure
pH of solution

Q: The [...] is the [...]
A: pK_a; pH at which 50% of a weakly ionic molecule is ionized.
Reference: Peck & Hill

Q: A weak acid is mostly [...] at pH [...] than its pK_a
A: unionized; less

Q: Specificity: Equation
A: Spec = true neg / disease neg = true neg/(true neg + false pos)

Q: Sensitivity: Equation
A: Sens = true pos / disease pos = true pos/(true pos + false neg)

Q: [...] are mostly [...] at pH [...] than their pK_a
A: Weak bases; unionized; greater

Q: In general, [...] binds [...] molecules in plasma
A: albumin; neutral or acidic

Q: Normal A-a gradient
A: Age/4 + 4 in mmHg
Increases with age due to fall in closing capacity.

Q: In general, [...] bind [...] drug molecules
A: globulins; basic

Front: What are the main plasma proteins involved in drug binding?
Back: Albumin
Globulins

Q: In acute inflammation, the plasma albumin level [...]
A: falls

Q: Anti-asthma drug classes
A: Oxygen
β2-agonists
Corticosteroids
Muscarinic antagonists
Methylxanthines
Ketamine
Volatile anaesthetic agents
Leukotriene antagonists
Magnesium
Heliox

Q: Mechanisms for renal elimination of non-volatile acid
A: Reabsorption of HCO3-
Bound to filtered buffers
As ammonium

Q: Lower limit of urinary pH
A: 4.4
Active transport of H+ is inhibited at this level

Q: Sites of bicarbonate elimination and reabsorption
A: Freely filtered
Reabsorbed in PCT (90%), thick ascending limb, DCT, and CT

Q: Process of bicarbonate reabsorption
A: H+ secreted into lumen
Secreted H+ combines with filtered HCO3- to produce CO2
CO2 diffuses into tubular cell
CO2 converted into HCO3- and H+
HCO3 reabsorbed
H+ secreted back into lumen (may be used to reabsorb more bicarb OR bind to a filtered base)

Q: Process of acid elimination using glutamine and ammonia
A: Glutamine metabolised in proximal tubular cells to produce NH4+ and HCO3-
HCO3- diffuses into blood
NH4+ secreted into tubule by NH4+-Na+ antiporter

Q: Non volatile acids
A: Lactate
Sulphate
Phosphate
Ketones

Q: Number of H+ ions excreted with each PO4 in urine
A: 2

Q: Protein binding is clinically relevant above a binding level of [...]
A: approximately 90%

Q: For drugs without specific transport mechanisms only [...] forms are absorbed in the gut
A: unionized

Q: Even acidic drugs are primarily absorbed in the small bowel due to the presence of [...]
A: mucosal villi.

Front: Factors influencing oral bioavailability
Back: Pharmaceutical preparation
Physicochemical interactions (food, other drugs)
Patient factors (impaired absorption or motility)
Gut pharmacokinetic interactions
First pass metabolism

Q: [...] is [...]
A: Extraction ratio; the fraction of drug removed from blood by an organ of elimination following a single pass through that organ

Drugs with rapid hepatocyte uptake and high metabolic capacity have metabolism independent of protein binding and highly dependent on hepatic blood flow.

Front: Advantages of IV route
Back: direct plasma delivery independent of absorption or tissue perfusion

Front: Disadvantages of IV route
Back: Initially high plasma concentration with risk of side effects

Front: Disadvantages of oral route
Back: lowest bioavailability due to:
Physicochemical interactions (food, other drugs)
Patient factors (impaired absorption or motility)
Gut pharmacokinetic interactions
First pass metabolism
Strong ions without specific transport mechanisms not absorbed

Front: Advantages of mucosal routes (i.e., sublingual, nasal, buccal)
Back: Rapid onset
Bypass first pass metabolism

Front: Advantages of intramuscular route
Back: near total bioavailability
onsent more rapid than oral

Front: Disadvantages of intramuscular route
Back: dependent on muscle perfusion - may result in "delayed bolus" effect
local damage to tissues (pain, abscess, haematoma)
inadvertant IV injection

Front: Attributes of drugs readily crossing the blood brain barrier (when intact)
Back: Have specific mechanism (predominant)
- active transport
- facilitated diffusion
Able to passively diffuse
- unionised
- highly lipid soluble
- low molecular weight
Are not metabolised by the BBB
- counter-example: monoamines are highly metabolised by BBB monoamine oxidase

Q: [...] protein binding in the fetus [...] drug transfer across the placental membrane
A: High; increases

Q: [...] have [...]
A: Prodrugs; no inherent activity prior to metabolism

Front: Organs containing cytochrome P450 enzymes
Back: Brain
Lung
Liver
Gut
Kidney

Front: Phase II reactions typically occur in
Back: Liver (but also acetylation in lung and spleen)

Front: Acetylation occurs in which tissues
Back: Lung
Liver
Spleen

Q: A change in pH of 0.3 is equivalent to a change in [H+] of:
A: 2 (either doubling or halving)

Q: Tolerance
A: Requirement for a larger dose to achieve the same effect

Q: Mechanisms of tolerance
A: Change in receptor morphology
Loss of receptors
Enzymatic induction
Physiological compensations
Change in response to drug receptor activation

Q: Osmoreceptor location and function
A: Hypothalamus
Respond to changes (1-2%) in ECF tonicity

Q: Stimulators of thirst
A: Hypertonicity
Hypovolaemia
Hypotension
Angiotensin II

Q: Double Donnan Effect
A: Competing Gibbs-Donnan Equilibriums between:
- Extracelluar Na
- Intracellular protein

Q: Effects of NaHCO3
A: Hypertonic (2000mosm/L)
- Increased ECF volume
- Increased ADH from tonicity/may also decrease ADH (from volume)
Alkalinising
- Metabolic alkalosis
- Hypokalaemia

Q: Change in tonicity required to alter ADH secretion
A: 1-2%

Q: Change in volume required to cause ADH release
A: 7-10%

Q: [...] is calculated by [...]
A: pK_a; taking the negative log of the acid or base dissociation constant
Extra: pK_a = -log([proton acceptor]/[proton donor])

Q: Total body Na content
A: 60mmol/Kg
70% exchangeable

Q: Sodium distribution
A: 50% ECF
45% bone
5% ICF

Q: Functions of sodium
A: Regulation of ECF volume
Osmolarity
Acid-base balance
Resting Membrane Potential
Major ion driving many primary and secondary active transport systems

Q: Reabsorption of Sodium
A: 90% in PCT and ascending LOH  (bulk reabsorption)
10% in DCT and CT (effect of aldosterone)

Q: Principal cells: Location and pump
A: DCT
Na/K ATPase

Q: Intercalated Cells: Pump and Function
A: Na/H
Collecting tubule

Q: Clarke electrode measures
A: Oxygen tension

Q: Clarke electrode components
A: Blood Chamber
Measuring chamber, containing:
- KCl solution
- Platinum cathode
- Ag/Ag-Cl anode
Oxygen permeable membrane separating each chamber
Battery

Q: Clarke electrode mechanism
A: 0.6V applied across the electrodes
Anode: Ag and Cl react, producing electrons
Cathode: O2 combines with (4) electrons and produces (4) hydroxyl ions.
Current (electron flow) is proportional to O2 available at the cathode.

Q: Limitations of Clarke electrode
A: Clean from protein, not damaged
Kept at 37 degrees
May read falsely high with halothane

Q: Stimulants to vomiting (classes)
A: Central
- Direct
- CTZ
GIT stimulation

Q: Direct central (e.g. cerebral) stimulants of vomiting
A: Emotion
Pain
Olfactory
Visual

Q: CTZ stimulants of vomiting
A: Vestibular acting on:
- H1
- ACh
Drugs/Toxins acting on:
- 5-HT3
- D2
- μ-opioid receptors

Q: GIT stimulation of vomiting
A: Distension
Toxins

Q: Neurotransmitters used (and site) in GIT stimulation of vomiting
A: 5-HT3 in mucosal stretch receptors
ACh and H1 in NTS afferents

Q: Process of vomiting
A: Coordinated by vomit center in medulla:
- Prodromal nausea
- Salivation
- Deep inspiration, soft palate elevation, and epiglotic closure
- Relaxation of oesophageal sphincters
- Retrograde intestinal contraction
- Violent contraction of the diaphragm and abdominal muscles

Q: Anatomical respiratory changes in pregnancy
A: Diaphragm pushed upwards by ~4cm
Increased AP and transverse diameter of the chest wall (~2-3cm)
Large airway dilation, reducing airway resistance by ~35%

Q: Pregnancy, changes in MV, RR, VT:
A: MV increases by 50%
RR increases by 10%
VT increases by 40%

Q: Changes in lung volumes with pregnancy
A: ERV decreases
RV decreases
IRV increases
TV increases

Q: Percentage change in lung capacities with pregnancy
A: FRC decreases
- By 20% erect
- By 30% supine
Expiratory capacity decreases by 30%
Total lung capacity decreases by 5%
Inspiratory capacity increases by 10%
VC unchanged

Q: PCO2 and HCO3 changes in pregnancy
A: Compensated respiratory alkalosis
PCO2 26-32mmHg
HCO3- 18-21mmol/L

Q: Weaknesses of RCTs
A: Costly
Time-consuming
Not appropriate for all study designs

Front: State Fick's law of diffusion

Q: Regarding transfer in the lung, Carbon monoxide is [...]
A: diffusion limited

Q: In the lung, the transfer of nitrous oxide is [...]
A: perfusion limited

Q: Principles of Pulse Oximetry
A: Beer-Lambert Law
Different absorption spectra of OxyHb and DeoxyHb
Requires pulsatile flow to calculate "R", and compare it to known values

Front: Normal transit time of a red cell in the pulmonary capillaries at rest
Back: 0.75 seconds

Front: Transit time of red cell in alveolar capillaries during severe exercise
Back: 0.25 seconds

Q: Factors that decrease FRC
A: Height (being short)
Chest wall:
- Supine position (falls by 1L)
- Weight
- Muscle relaxation
- Pregnancy
- Obesity
- Disease
Lung:
- Alveolar (surfactant, consolidation)
- Interstitial (ILD)
- Pleural (PThx)

Front: How is it possible to determine the volume of blood in pulmonary capillaries?
Back: By determining the uptake of carbon monoxide at varying FiO_2. This will vary due to competitive binding with O_2.

Front: How is equation describing diffusing capacity in the lung derived?
Back: Derived from Fick's Law:
given impossible to measure A and T:
arranged as:
since the venous partial pressure of CO is extremely small:

Front: Difference between elimination and excretion
Back: Elimination refers to removal from plasma via:
- excretion
- metabolism
Excretion refers to removal from body

Front: Routes of excretion
Back: Lungs
Tears
Sweat
Urine
Bile
Faeces
Breast milk
Reference: Peck & Hill

Q: [...] are preferentially excreted in [...] urine where they are trapped as [...]
A: Basic drugs; acidic; cations

Q: [...] are selectively secreted in [...]
A: High molecular weight compounds; bile

Q: [...] involves [...]
A: Enterohepatic circulation; drug conjugates being metabolised by bacterial enzymes in the gut and then reabsorbed

Q: In renal disease, volume of distribution is often [...]
A: increased

Front: Differences in pulmonary vs. systemic circulation
Back: Pulsatile vs. continuous flow
Low vs. high resistance
Accepts the entire blood volume vs. directs flow
- therefore, thin walled arterial tree with minimal smooth muscle
Constricts in response to hypoxaemia
Reference: Brandis
Other fields (not shown on cards):
Comment: this needs work

Front: Describe the relationship between pulmonary vascular pressure and resistance
Back: PVR falls as arterial OR venous pressure increases.

Front: State the equation used to calculate pulmonary blood flow using the Fick principle
Back: [$]\dot{Q}=\frac{\dot{V}o_2}{C_ao_2-C_{\bar{V}}o_2}[/$]
Reference: West

Front: Mechanism of hypoxic pulmonary vasoconstriction
Back: Dependent on alveolar Po_2
Intermediate steps unclear
Final path involves increased intracellular Ca^2+ resulting in constriction of pulmonary arterioles

Front: Describe the relationship between alveolar hypoxia and pulmonary vasoconstriction
Back: non-linear
plateau when Po_2 > 100
marked when Po_2 <70

Front: Situations involving hypoxic pulmonary vasoconstriction
Back: Regional:
- disease states
   - airway obstruction
   - atelectasis
Global:
- low Po_2 at altitude
- fetal to neonatal transition

Q: Mechanisms of Antimicrobial Resistance
A: Modification or Inactivation of Drug
e.g. β-lactamases
Modification to Target Site
Modification to Membrane permeability
e.g. Anaerobes have no O2-transport channel - prevents aminoglycosides
Removal or Sequestration of Antimicrobial Agent
e.g. glycopeptide resistance in VRSA.
Modification of Metabolic Pathways

Q: Cough Reflex process
A: Touch and irritant receptors in the upper airways
Vagal afferents to the medulla cough centre in nucleus ambiguus
Three phases:
1. Inspiratory
- Large inspiration
2. Compressive
- Effort closure
- Contraction of abdominal and internal intercostal muscles, raising intrapleural pressure to >100mmHg
3. Expulsive
- Wide opening of the cords and epiglotis
- Compression of noncartilagenous airways and high turbulent flow assists removal of debris

Q: RBC lifespan
A: 120 days

Q: RBC: Unique characteristics
A: - Anucleate
- No ribosomes
- No mitochondria

Q: RBC: Shape and advantages (of the shape)
A: Biconcave disc
Maximal surface area for gas exchange
Deformable to pass through capillary beds

Q: RBC function
A: Gas transfer
Acid-Base
Metabolism

Q: Components (e.g. bands, etc) in a sarcomere
A: A-band
I-band
H-band
Z-line
M-line

Q: Z-line
A: End of the sarcomere

Q: M-line
A: Band of connection between myosin filaments

Q: Actin
A: Protein which is drawn into the thick filament during contraction.
Has tropomyosin attached, which in turn attaches troponin

Q: Myosin
A: Large double-headed protein which binds actin and ATP

Q: Tropomyosin
A: Long filament that runs in a groove along actin, binds troponin

Q: Troponin
A: Protein which reveals the myosin binding site on actin when activated by Ca2+

Q: Electrical process of excitation-contraction coupling
A: Nicotininc receptors stimulated by ACh
End-plate potential spreads along T tubules
Ca2+ is released from the SR

Q: Process of contraction during excitation-contraction coupling
A: Actin and myosin cross-link, ADP is released
Myosin head rotates, moving to a new actin binding site
ATP binds to the myosin head
ATP hydrolysed, and the head pulls and 'recocks', binding to a new actin site and resuming its position
This process continues as long as their is calcium causing troponin to reveal the myosin binding site on actin

Q: Changes in band lengths during excitation-contraction coupling
A: The A-band is unchanged
The H-band shortens
The I-band shortens

Q: Process of relaxation in excitation-contraction coupling
A: Ca2+ is pumped back into the SR (using ATP - hence active process)
Troponin releases Ca2+
Binding sites are occluded by troponin, and no further contraction occurs

Front: State the alveolar gas equation

Q: Before reaching steady state, [...] [...] the value of the respiratory exchange ratio due to [...]
A: hyperventillation; increases; the difference between O_2 and CO_2 reserves
Extra: Remember,
R = Vco_2 / Vo_2

Front: State the shunt equation
Back: rearranged:
Reference: West

Q: The respiratory exchange ratio is [...] at the [...] of an erect lung
A: higher; apex
Extra: Due to higher, steeper CO_2 dissociation curve compared with O_2, combined with reduced perfusion at the apex.
Remember,
[$]R=\frac{\dot{V}co_2}{\dot{V}o_2}[/$]
Reference: West

Front: Typical VQ ratio at the lung apex
Back: 3.3
Reference: West

Front: Typical VQ ratio at the lung base
Back: 0.63
Reference: West

Q: Optimal damping coefficient
A: D = 0.64
Optimal compromise between speed and accuracy. Overshoot is small (~7%) and response is rapid

Q: PaCO2 between which cerebral blood flow is linear
A: 20mmHg to 80mmHg

Q: Flow-metabolism coupling describes
A: Linear association between CMRO2 and CBF

Q: Dynamic compliance deviates from static compliance when:
A: High RR
Lung units with unequal time constants (less filling, therefore more pressure to overcome resistance)

Front: Forms of O_2 carriage in blood
Back: Dissolved
Bound to Hb

Front: Solubility of oxygen in blood
Back: 0.003 mL/100mL/mmHg

Q: The haemoglobin molecule consists of [...] and [...]
A: four haem molecules; four polypeptide chains

Q: Normal haem contains [...] ([...]) iron
A: ferrous; Fe^II+

Q: Methaemoglobin contains [...] ([...]) iron
A: ferric; Fe^III+

Front: Equation describing oxygen content of blood
Back: [$]Ca_{O_2}=1.34 \cdot Hb \cdot Sp_{O_2} + 0.003 \cdot P_{O_2}[/$]
Hb in g/100 mL
gives answer in mL/100 mL
Note: Huffner's constant is 1.39mls/g  in vitro, but in vivo it is 1.34 due to the effect of methaemoglobin.

Front: Describe the effect of polycythaemia and anaemia on oxygen carrying capacity
Back: Normal oxygen saturations despite marked increase/decrease in oxlygen concentration

Q: [...] allows [...]
A: The steep lower portion of the oxyhaemoglobin curve; a large transfer of oxygen to the tissues for a small drop in Po_2

Q: [...] allows for [...]
A: The flat upper portion of the oxyhaemoglobin dissociation curve; small drops in alveolar Po_2 while maintaining a high oxygen content

Front: Causes of increased 2,3-diphosphoglycerate
Back: Pregnancy
Hypoxia
Hyperthyroidism
Alkalaemia
Due to increased activity of diphosphoglycerate mutase (Rapoport-Luebering shunt)

Front: Effect of 2,3-diphosphoglycerate on haemoglobin
Back: binds beta subunits of deoxy-Hb and reduces oxygen affinity

Q: Affinity of CO for haemoglobin compared with O_2
A: 240 times

Front: Effect of carbon monoxide (CO) on oxy-haemoglobin dissociation at low concentrations
Back: Left-shift of oxyhaemoglobin dissociation curve resulting in poor O_2 delivery at the tissues
Reference: West

Front: Solubility of CO_2 in blood
Back: 0.067 ml/100mL/mmHg

Front: Proportion of total CO_2 dissolved in mixed venous blood
Back: Approximately 10%

Q: Properties of drugs which determine GIT absorption
A: Molecular Weight
Concentration Gradient
Lipid solubility
Ionisation
Pharmaceutical Preparation
Physiochemical interactions

Q: Patient factors affecting GIT absorption
A: GIT blood flow
Surface Area
pH
Motility
Digestive Enzymes
GIT bacteria and subsequent metabolism
Disease

Q: Filtration coefficient is a function of
A: Membrane permeability
Membrane surface area

Front: Muscles involved in inspiration
Back: Diaphragm
External intercostals
Accessory muscles (including):
- Scalenes (elevate ribs 1-2)
- Sternomastoids (elevate sternum)

Q: At rest, expiration is a [...] process due to [...]
A: passive; elastic recoil of lung and chest wall tissues

Q: Due to [...], the lung volume at any given intrapleural pressure is [...] during [...]
A: hysteresis; less; inspiration

Front: Normal compliance of the human lung
Back: 200mL/cmH_2O ( this is "lung in a bottle" compliance)

Q: Intrapleural pressure is [...] due to [...]
A: negative; elastic recoil of the lung

Front: State the Laplace equation as it applies to a bubble
Back: [$]P=\frac{4\cdot surface\: tension}{r}[/$]

Front: State the Laplace equation as it applies to the alveolus
Back: [$]P=\frac{2\cdot surface\: tension}{r}[/$]
Reference: West

Front: Regarding the pressure-volume relationship in the airways, what factors cause hysteresis?
Back: Surface tension (note hysteresis is almost abolished during saline inflation)
Dynamic airway compression
Reference: West

Front: Functions of surfactant
Back: Reduces surface tension, causing:
- stabilises relative alveolar volumes
- increases lung compliance
- keeps alveoli dry by contributing to interstitial hydrostatic pressure
Reference: Brandis

Q: Secreted by [...], [...] is the major [...]
A: type II alveolar cells; dipalmitoyl phosphatidylcholine (DPPC); surfactant in the lung

Front: Consequences of lost surfactant in the lung
Back: increased surface tension, therefore:
reduced lung compliance
areas of atelectasis
alveolar odema (surfactant reduces hydrostatic pressure gradient)

Front: Mechanisms of alveolar stability
Back: Surfactant
Alveolar interdependence (alveoli are supported by surrounding structures, including adjacent alveoli)

Q: [...] is [...] at the lung bases due to [...]
A: Intrapleural pressure; less negative; the weight of the lung

Q: The [...] of the lung has an [...] resting volume due to [...]
A: apex; increased; greater negative transpleural pressure

Q: The relaxation pressure of the lung and chest wall are [...] at [...]
A: equal and opposite resulting in an airway pressure of zero; FRC

Q: Regarding the relaxation pressure-volume curve, the [...] is atmospheric at [...]
A: chest wall pressure; 75% of vital capacity
Extra: Recall that the chest wall pressure here is analagous to a subject with a normal chest wall but no lungs

Q: Relationship between a primary change in HR and CO
A: CO is independent of HR between 40-50 to 180bpm

Q: Substrates used by the heart
A: Whatever is available:
Glucose, lactate, ketones, fatty acids in proportion to their arterial concentration

Q: Overweight BMI
A: >25

Q: Obese BMI
A: >30

Q: Morbidly Obese BMI
A: >40
>35 with obesity-related disease

Q: Normal O2 content of blood
A: 20.4ml/100ml of blood:
- 20.1ml bound to Hb
- 0.3ml dissolved

Q: Daily water losses due to humidification
A: 150ml
(300 ml without reabsorption due to condensation in trachea)

Q: dP/dT max is:
A: An index of myocardial contraction: Maximum rate of change in LV pressure during isovolumetric contraction
It is preload dependent and afterload independent

Q: If air flows through a tube, a [...] exists along it
A: pressure gradient

Laminar flow is inversely proportional to viscocity while turbulent flow is inversely proportional to density

Q: In laminar conditions, when tube radius is [...] resistance [...]
A: halved; increases 16-fold
Extra: Described by Hagen-Poiseuille equation:
[$]R = \frac{8 \eta l}{\pi r^4}[/$]
Reference: West

Q: [...] flow occurs at [...] Reynolds numbers
A: Laminar; low
Extra: Typically below 2000
For fluid flow in a tube:
[$]Re=\frac{\rho vd}{\eta}[/$]
Where:
ρ = density
v = velocity
d = tube diameter
η = viscosity

Front: State the equation giving Reynold's number for flow in a tube
Back: [$]Re=\frac{2rv\rho}{\eta}[/$]
where:
v = average velocity (cm/s)
ρ = density
r = radius (cm)
η = viscocity (poise) - note that viscocity is proportional to temperature in gasses, and inversely proportional to temperature in liquids
Reference: West, Guyton & Hall

Q: At most airway generations, flow is [...], while flow is turbulent in [...], and probably laminar in [...]
A: transitional; the trachea; only the most distal airway generations

Q: Under [...] conditions, driving pressure is approximately proportional to [...]
A: turbulent; flow^2

Front: Equation describing airway driving pressure
Back: P = K_1V+K_2V^2
where:
K_1 and _2 are constants
V = flow

Q: [...] are the [...]
A: Medium caliber bronchi; chief site of airway resistance

Front: Factors affecting airway radius
Back: Extraluminal factors:
- Compression:
    - Haemorrhage, tumour, dynamic hyperinflation, atelectasis compressing airways, etc.
- Lung volume
    - Radial traction tents open airways as lung volume increases
Luminal constriction:
- Bronchospasm, bronchoconstriction
Intraluminal obstruction:
- Sputum plugging, aspiration

Q: Regarding airway resistance, gas [...] has a [...] effect than gas [...].
A: density; greater; viscocity
Extra: This is evidence that flow is not laminar in the medium-sized airways (the site of most airway resistance).

Q: At [...] lung volumes, expiratory flow is [...]
A: low to moderate; effort independent
Extra: This is due to dynamic airway compression

Q: During expiration, the equal pressure point moves distally as [...]
A: airway resistance increases as lung volume falls

Q: During dynamic airway compression, flow is dependent on [...]
A: the alveolar-intrapleural gradient

Front: Factors worsening dynamic airway compression
Back: Bronchoconstriction
Low lung volume
Reduced lung elasticity (emphysema, ageing) - reduces driving pressure and elastic recoil

Front: How is FEV_1 calculated
Back: The volume of air exhaled from vital capacity with maximum effort in 1 second

Front: Causes of unequal ventilation
Back: Topographical:
- Dependent greater than uppermost (uppermost regions have higher resting volume and therefore sit on a flatter part of the pressure-volume curve)
Time constant inequality:
- Increased respiratory rate exacerbates this
Proximal to distal along lung unit:
- Due to dilatation of distal airways increasing distance covered by diffusion

Q: In lung units with a long time constant, ventilation will be [...] with [...]
A: reduced; increased respiratory rate
Extra: Note: time constant = compliance x resistance

Q: Anterior Border of the IJV
A: SCM

Q: Posterior border of the IJV
A: Lateral mass of C1, scalene muscles, lung pleura

Q: Medial border of the IJV
A: ICA

Q: Surface anatomy/landmark approach to IJV cannulation
A: Identify the triangle formed by the two heads of SCM and the clavicle.
Palpate the artery, and ensure the site of entry is lateral to the carotid. Aim:
- Caudally, at a 30 degree angle to the frontal plane
- Parallel to the sagittal plane
- Towards the ipsilateral nipple

Q: Borders of the ACF
A: Medially by pronator teres
Laterally by brachioradialis
Superiorly by an imaginary line between the medial and lateral epicondyles

Q: Contents of the ACF
A: Median nerve
Brachial artery
Biceps tendon and aponeurosis
Radial and posterior interosseous nerves
Veins (basilic, cephalic)

Q: Venous variations in the ACF
A: 1. Median cubital vein connecting the basilic and cephalic veins
2. Median vein of the forearm, which divides into a median basilic and median cephalic vein which drain into the basilic and cubital veins

Q: ECG effects of Class Ia antiarrhythmics
A: Increase QRS duration and QT interval
Due to both slowed conduction and prolonged refractory period

Q: ECG effects of Class Ib antiarrhythmics
A: Nil significant changes
Due to little effect on normal tissues at therapeutic doses

Q: ECG effects of Class Ic antiarrhythmics
A: Prolong QRS duration
Due to decreased conduction velocity.

Q: ECG effects of Class II antiarrhythmics
A: PR prolongation

Q: ECG effects of Class III antiarrhythmics
A: Prolonged QT

Q: ECG effects of Class IV antiarrythmics
A: Prolonged PR interval

Q: Methods for transport across cell membranes
A: Diffusion
Active/passive Transport
Exo/endocytosis

Q: List the plasma proteins
A: Albumin
Globulins
-α1/α2
- β globulins (β2-microgolbulin, CRP, transferrin)
- Gamma-globulins (IgG, IgM, IgE...)
Fibrinogen
Coagulation factors
Complement

Q: α1 globulins in blood
A: α1 anti trypsin
α1-fetoprotein
Serum amyloid A

Q: α2 globulins in blood
A: Haptoglobin
Ceruloplasmin
Protein C
Thyroxin-binding globulin

Q: β globulins in blood
A: Transferrin
Plasminogen
β2 microglobulin
CRP

Q: γ globulins in blood
A: IgG
IgA
IgM
IgE
IgD

Q: Work of breathing can be calculated from [...]
A: pressure x volume
Extra: Work measured in Joules

Q: During quiet breathing, the work of breathing is performed by [...]
A: the inspiratory muscles (entirely)
Extra: Potential energy of deformed elastic tissues is available as potential energy during expiration

Q: [...] is a measure of [...]
A: Power; the rate at which work is performed
Extra: Units: Watt (Joules/second)
Regarding "work" of breathing, power is the correct term when referring to the energy consumed by ventilation per unit of time, while "work" is appropriately applied to a single event, such as one breath

Q: Regarding "work" of breathing, power is the correct term when referring to [...], while "work" is appropriately applied to [...]
A: the energy consumed by ventilation per unit of time; a single event, such as one breath
Extra: In this context,
Work = volume x pressure
Power = work/unit time

Front: Components of total work of breathing
Back: Work against elastic recoil
~ 65% of work
Work against resistance to gas flow
~ 35% of work
Reference: Nunn

Q: For a constant minute volume in a state of increased elastic recoil, the work of breathing is [...] with [...] respiratory rate
A: reduced; increased

Q: For a constant minute volume in increased air flow resistance, the work of breathing is [...] with a [...] respiratory rate
A: decreased; decreased
Reference: Nunn

Front: Normal efficiency of work of breathing
Back: 5-10%

Front: What is the area representing work done to overcome viscous forces (airway and tissue resistance) in the diagram?
Back: ABCEA

Front: What are the basic elements of the respiratory control system?

Front: Brainstem components controlling respiration
Back: Pons
- pneumotaxic centre (upper pons)
- apneustic centre (lower pons)
Medulla
- dorsal respiratory group
- ventral respiratory group
- central chemoreceptors

Q: Controlling respiration, the [...] is located in [...]
A: pneumotoxic centre; the upper pons
Reference: West

Q: [...] associated with a rise in [...] results in [...]
A: Cerebral vasodilation; Pco_2; enhanced diffusion of CO_2 into the CSF

Front: Describe the activity of peripheral chemoreceptors to PO2
Back: Begins at PO2 of 500
Rapidly increases below 100

Q: [...] are the only cells which [...]
A: Peripheral chemoreceptors; directly respond to hypoxaemia

Q: [...] bodies but not [...] bodies respond to [...]
A: Carotid; aortic; pH
Reference: West

Front: Hering-Breuer reflexes are relevant only in which situations?
Back: Animals
Neonates
In adults, tidal volumes >1L

Q: Juxtacapillary receptors (J receptors) are located in [...]
A: the alveolar walls
Extra: Stimulation causes rapid shallow breathing.
Reference: West

Front: Stimuli to J receptor activation
Back: Pulmonary capillary engorgement
Increased interstitial fluid volume
Irritants in pulmonary circulation
(causes rapid, shallow breathing)

Q: As Po_2 [...], the response to hypercapnoea is [...]
A: increases; reduced

Front: Effects of chronic hypercapnoea on control of respiration
Back: Loss of CO_2 stimulus (central/peripheral)
- near normalisation of CSF pH
- near normalisation of plasma pH
Oxygen tension becomes primary driver of ventilation (acts at peripheral chemoreceptors)

Front: Changes to ventilation and blood gases with exercise
Back: Respiratory rate and tidal volume increase, but mechanism is unclear as:
Pco_2 remains the same or decreases slightly
Po_2 decreases only at very high workloads
pH decreases only at high workloads

Front: At what Po2 does response to hypoxia inflect?
Back: Po2 ~50mmHg

Q: [...] Pco_2 [...] the response to hypoxia
A: Decreased; decreases

Front: Changes to respiratory exchange ratio during exercise
Back: ~ 1.0 in aerobic conditions
 - reflects increased carbohydrate metabolism
> 1.0 in anaerobic conditions
 - due to lactate production (which liberates bicarbonate)

Front: Changes to diffusing capacity during exercise and their causes
Back: Increased 3x due to distension of pulmonary capillaries, causing:
- Increased pulmonary capillary volume
- Increased D_M
Reference: West

Front: Pulmonary vascular changes during exercise
Back: Increased pulmonary blood flow
Decreased pulmonary vascular resistance
 - recruitment and distension due to raised arterial and venous pressures and increased flow
Slightly decreased V/Q inequality (especially at the apices)
(V/Q inequality may increase with severe workload due to alveolar oedema)

Front: At 5800m, where atmospheric pressure is half that at sea level, what is the Po2 of inspired air?
Back: P_Ao_2 = (380 - 47) x 0.2093
          = 70mmHg

Front: Adaptations to altitude
Back: Hyperventilation (2-3 days to maximize)
 - due to hypoxic ventilatory drive
 - initially inhibited by increased CSF pH, which then normalises
 - maximum breathing capacity increases due to reduced gas density
Polycythaemia (months to maximise)
Oxyhaemoglobin P_50
 - increased at moderate altitude (due to increased 2,3-DPG levels)
 - decreased at extreme altitude (reduces diffusion limitation of O_2 transfer)
Increased capillary concentration
Altered oxidative enzymes
Natural selection of certain traits among long-term altitude populations
Reference: West

Q: Cofactors in the clotting cascade
A: Va
VIIIa

Q: Action of Protein C
A: Destroys Va and VIIIa

Q: Action of Protein S
A: Enhances the action of Protein C

Q: Action of antithrombin III
A: Inhibits serine proteases (non-cofactors) in all three pathways
- IIa
- VIIa
- IXa
- Xa
- XIa
- XIIa
Potentiated by heparin

Q: Normal daily production of lactate
A: 1400mmol/day

Q: Cori Cycle
A: 1. Lactate Production
- Fementation of pyruvate to lactate by LDH, regenerating NAD+
2. Lactate metabolism (gluconeogenesis)
- Lactate → pyruvate → glucose in liver

Q: Rate of urea production
A: 30g/day of 100g protein diet

Q: [...] occurs [...] rapidly when breathing pure O_2 because [...]
A: Absorption atelectasis; more; the total partial pressure of mixed venous gas becomes less

Front: Effects of liquid breathing
Back: Increased work of breathing
Reduced CO2 elimination
- slower rate of diffusion in liquid phase

Front: How is closing capacity measured?
Back: By measuring closing and residual volume
Closing volume can be measured with single breath nitrogen test
During inspiration, apical lung expanded less and received less O2
As basal airway closure occurs, nitrogen concentration rises due to apical alveolar gas containing less O_2 indicating the start of closing volume
Reference: Brandis

Q: Response to loss of 1L of blood
A: Venoconstriction
Transcellular fluid shift
Decreased RBF
Decreased urine volume
Mobilisation of resevoir volumes
Increased muscle pump
Vasoconstriction
Tachycardia

Q: Normal blood urea concentration
A: 3-6mmol/L

Q: Determinants of Preload
A: Heart rate (+ filling time)
Atrial Contraction
Ventricular Compliance
Afterload (change end systolic volume)
Valvular disease
External compression (pericardium)
Venous return

Q: Borders of the Femoral Triangle
A: Lateral: Sartorius
Superior: Inguinal ligament
Medial: Adductor Longus
Roof: Fascia lata
Floor: Iliopsoas

Q: Location of MOP receptors
A: Cerebral cortex, spinal cord, periaqueductal grey matter, peripheries

Front: In health, what is the normal end-tidal to P_a difference in CO_2?
Back: 2-5mmHg
Caused by physiological dead space (physiological dead space = alveolar dead space + anatomical dead space)

Front: Expiratory reserve volume in mL/kg
Back: 15mL/kg
Reference: Brandis

Front: Vital capacity in mL/kg
Back: 60-70 mL/kg
Reference: Brandis

Front: Functional residual capacity in mL/kg
Back: 30 mL/kg
Reference: Brandis

Front: Methods for measuring functional residual capacity (FRC)
Back: Gas dilution (e.g., helium)
Body plethysmography

Front: How is lung compliance measured?
Back: Static compliance test.
Patient inspires in small volumes and pauses (so that alveolar pressure is equal to mouth pressure). With the glottis open, oesophageal pressure is transduced (assumed to be proportional to intrapleural pressure).
A pressure-volume curve is plotted, and the slope of the line is lung compliance (remember, C=∆V/∆P).
By convention, compliance is slope of line between FRC and FRC + 1L

Q: Eponymous name for the atrial stretch reflex
A: Bainbridge reflex

Front: What is specific compliance? What is the normal value?
Back: Lung compliance per unit of volume. By convention, given at functional residual capacity (FRC).
Normal 0.05 /cmH2O
(note units as compliance is given in volume/pressure units, volume cancels out)

Front: What is the term F in the alveolar gas equation?
Back: [$]F = P_Aco_2\cdot F_io_2\cdot \frac{1-R}{R}[/$]
Normal value 2mmHg
Increases with increased F_io_2

Front: What is Hufner's number?
Back: Millilitres of oxygen that combine with 1g of fully saturated haemoglobin.
Equal to 1.34 in vivo
Reference: Brandis, West

Front: Differences between HbA and HbF curves
Back: HbF is left shifted due to reduced 2,3 DPG binding. (HbF consists of two alpha chains, and two gamma chains which have less affinity.)
P_50 is about 18mmHg (vs. 27 for HbA)
Reference: Brandis

Q: Mild Hypothermia
A: 32-35°C

Q: Moderate Hypothermia
A: 28-32°C

Q: Severe Hypothermia
A: <28°C

Q: Stages of compatibility testing
A: 1. Typing
- ABO
- Rhesus
2. Antibody screening
- For minor antibodies (e.g. Kell, Duffy)
3. Crossmatching
- Saline test: Donor RBC and recipient serum mixed together and observed
- Coombs test: Evaluate for IgG Ab

Q: Respiratory changes during labour
A: 70% increase in MV during contractions
Hypoventilatory period post contraction

Q: Components of the Innate Immune System
A: Physicochemical barriers
Humoral mechanisms
Cellular mechanisms

Q: Physiochemical barriers
A: Skin
Mucous membranes
- Ciliary elevator
Gastric acid
Urination
- High flow, low residual volumes

Q: Components of innate humoral immunity
A: Complement
Acute-Phase proteins
Proteolytic enzymes

Q: Complement system can be activated by
A: Ab-Ag complexes (classical)
Substances in bacterial cell wall (alternate)

Q: Complement system functions
A: Opsonisation
Chemotaxis
Phagocyte and macrophage activation
Mast cell degranulation
Destruction via the membrane attack complex
Vasodilation

Q: Acute-Phase protein function
A: Opsonisation
Inflamation:
- Capillary dilatation and increased permeability
- Endothelial activation
- Monocyte and neutrophil attraction

Q: Components of innate cellular immunity
A: Mast cells
Natural killer cells
Leukocytes

Q: Types of leukocyte
A: Neutrophils
Monocytes
Eosinophils
Basophils
Lymphocytes

Q: Neutrophil: Process of activation
A: Margination
Chemotaxis
Phagocytosis of opsonised bacteria
Respiratory burst

Q: Types of adaptive immunity
A: Active
Passive

Q: Components of the active immune system
A: Cellular
Humoral

Q: Components of the adaptive cellular immune system
A: B cells
T cells

Q: Role of B cells
A: Produce antibody
Present antigen to T cells
Form memory cells

Q: Role of T helper cells
A: Activate cytotoxic T cells
Active B cells and macrophages to produce antibody when stimulated by APCs

Q: Role of cytotoxic T cells
A: Destruction of virally infected and tumour cells
Transformation to memory cells

Q: Functions of the cardiovascular system
A: Gas transport/exchange
Waste transport
Nutrient transport
Fluid homeostasis
Endocrine
Immunological
Thermoregulation

Q: In the systemic circulation, the chief site of resistance is the [...]
A: arteriole

Front: Describe the pressure, cross sectional area and velocity relationships moving through the systemic circulation
Reference: Power and Kam

Q: Normal blood volume
A: 70 mL.kg^–1

Q: Resting kidney blood flow
A: 1100mL/min

Q: Resting skeletal muscle blood flow
A: 750mL/min

Q: Resting skin blood flow
A: 500mL/min

Q: Difference between true and functional syncitium
A: A true sycytium consists of a protoplasm containing many nuclei surrounded by single cell membrane
Cardiac muscle is a functional syncitium as cells are connected by intercalated discs with gap junctions

Q: On exertion, cardiac efficiency [...]
A: improves
Extra: True as cardiac output rises more than oxygen consumption during exercise
Reference: Power and Kam

Q: Describe the sympathetic innervation of the heart
A: Fibers from the mediolateral columns of thoracic spinal cord synapse in the sympathetic chain
Second order neurones from the upper thoracic sympathetic trunk form a plexus around heart

Front: What are the phases of the cardiac action potential?
Back: 0 - depolarization
1 - partial repolarization
2 - plateau
3 - repolarisation
4 - resting potential
Reference: Guyton & Hall

Front: Describe the changes occuring in phase 2 of the cardiac action potential
Back: Plateau phase occurs due to:
slow voltage gated calcium channel opening
fast potassium channels closing
Reference: Guyton & Hall

Front: Describe the changes during Phase 4 of the cardiac action potential
Back: Minimal membrane permeability
Negative charge mainly due to K gradient
Reference: Guyton & Hall

Front: Normal intracellular and extracellular [Na^+]
Back: 10 mEq/L
142 mEq/L
Reference: Guyton & Hall

Q: The [...] equation describes [...]
A: Goldman-Hodgkin-Katz; the membrane potential of a cell involving two cations and one anion
Extra: where RT/F = -61
Reference: Guyton & Hall

Front: When a membrane is permeable to several ions, what determines the membrane potential?
Back: Of each ion:
- charge
- permeability
- concentration gradient
This is encapsulated by the Goldman-Hodgkin-Katz equation in scenarios involving two cations and one anion:
where RT/F = -61
Reference: Guyton & Hall

Q: Latent Heat of Vaporisation
A: Amount of heat energy required to convert 1g of a substance from the liquid phase to the gaseous phase, at a given temperature.

Q: Relative humidity achieved via nose breathing
A: 90%

Q: Relative humidity achieved via mouth breathing
A: 60%

Q: Laryngeal muscle which opens cords
A: Cricoarytenoid
Rotates the arytenoid cartilage, abducting vocal cords and reducing inspiratory resistance

Q: Laryngeal muscles of expiration
A: Thyroarytenoid
Adduct the cords and increase resistance

Q: Effect of plasma [K] on potassium elimination
A: Stimulates aldosterone release
Stimulates Na/K pump action

Q: Effect of tubular flow rate on potassium elimination
A: Elimination from principal cells is passive, occurs down concentration gradient. Therefore increased flow increases elimination

Q: Effect of sodium on potassium elimination
A: High Na inhibits aldosterone release

Q: Effect of water on potassium elimination
A: High water content inhibits ADH secretion

Q: Effect of alkalosis on potassium elimination
A: Increased elimination as hydrogen ions are reabsorbed over potassium ions

Q: List the cardiac reflexes
A: Bainbridge
Cushing
Baroreceptor
Oculocardic
Bezold-Jarisch

Q: Cushing reflex
A: Stimulated by ischaemia of the vasomotor centre due to high ICP
Triad of:
- HTN
- Bradycardia
- Irregular respirations (due to respirtory centre ischaemia)
SNS activation: ↑ SVR and BP, with ↑ HR. Aortic baroreceptors cause a PNS response, then causing bradycardia.

Q: Respiratory effects of hypothermia
A: L shift of O2-Hb dissociation curve
Impaired HPV, causing shunt

Q: CVS effects of hypothermia
A: Peripheral vasoconstriction, causing ↑ VR, ↑ CO, ↑ MVO2 (followed by ↓ CO, ↓ BP as CVS function worsens)
Bradycardia
Arrhythmia

Q: Haeme effects of hypothermia
A: Coagulopathy
Platelet sequestration in liver and spleen

Q: Renal effects of hypothermia
A: Cold diuresis due to reduced solute resorption in LoH

Q: Pharmacological effects of hypothermia
A: Prolonged onset and offset of NMBR
Increased solubility of volatile agents in tissues

Q: Conduction velocity of myocardium
A: 0.5 m/sec

Q: Rate of conduction of Purkinje fibres
A: 4 m/s

Q: Compared with skeletal muscle, myocardial contraction is more dependent on [...] due to [...]
A: extracellular calcium; larger T tubules and smaller sarcoplasmic reticulum
Reference: Guyton & Hall

Q: Equation for ejection fraction
A: EF = (EDV-ESV)/EDV

Q: Factors modifying the Frank-Starling relationship
A: Inotropy
Afterload

Q: Effect of hypocalcaemia on myocardium
A: Reduced inotropy due to reduced effect of calcium on myofilaments

Q: Intrinsic AV node rate
A: 40-60 bpm

Q: Intrinsic rate of purkinje fibre firing
A: 15-40 bpm

Q: Mechanism of vagal stimulation on heart
A: Acetylcholine stimulates the Gi coupled M2 and also increase K permeance via the gamma delta subunit of the K channel.
This causes increased potassium permeance and hyperpolarisation of the cell membrane:
- Prolonged phase 4 of the pacemaker potential
The end result is:
Reduced SA nodal rate
Slowed or failed AV nodal conduction

Front: Effect of sympathetic stimulation on cardiac function
Back: Increased rate of SA nodal discharge
Increased AV nodal conduction
Increased myocardial contractility
Reference: Guyton & Hall
Other fields (not shown on cards):
Comment: this should be heavily updated

Front: Regarding the vasculature, turbulence occurs in:
Back: great vessels
branch points of larger arteries
Reference: Guyton & Hall

Front: Convert mmHg to cmH_2O
Back: 1 mmHg = 1.36 cmH_2O

Front: Describe the pressure-flow relationship in passive vascular beds
Back: Flow increases non-linearly due to decreases in vascular resistance through distension.
This effect is greater than would be expected according to the Hagen-Poiseuille equation.
The effect is modified by sympathetic stimulation.
Reference: Guyton & Hall

Front: Factors regulating pacemaker activity in the heart
Back: Net autonomic input
Drugs
Circulating hormones
- adrenaline
- thyroid hormones
Serum K
- high: bradycardia
- low: tachycardia (increased phase 4 hyperpolarisation)
Hypoxia
- Resting membrane potential less negative, funny current not generated as not hyperpolarized in phase 3
- Vagal stimulation from carotid body in hypoxia
Reference: Klabunde (cvphysiology.com)

Q: Roles of the diaphragm
A: Inspiration
Coughing/vomiting/sneezing
Maintaining LoS tone

Q: Ionised calcium reference range
A: 1.1-1.3mmol/L

Q: Calcium regulation
A: Vitamin D
PTH
Calcitonin

Q: Actions of calcitonin
A: Inhibits GIT Ca absorption
Inhibits osteoclast activity
Stimulates osteoblast activity
Inhibits renal resorption of Ca

Q: Actions of PTH
A: Increases osteoclastic activity
Inhibits osteoblastic activity
Increase renal reabsorption of Ca in the DCT
Increase GIT Ca absorption

Q: Actions of calcitriol
A: Improves calcium absorption in intestine

Q: Monosaccharides produced by digestion
A: Glucose (80%)
Galactose
Fructose

Q: Factors affecting mixed venous P_CO2
A: CO2 production
Ventilation (i.e. PaCO2)
Cardiac output
CO2 dissociation curve: HbO2 state, haldane effect

Q: Medullary Concentration Gradient
A: Physiological process producing a concentration gradient of up to 1400mmol/Kg from cortex to medulla
Allows kidney to concentrate urine to differing extents

Q: Components of the counter-current multiplier system
A: Na and Cl move from the thick ascending limb into interstitium
H2O moves from the descending limb into interstitium down osmotic gradient
Net result:
- Interstitial osmolality increases
- Descending limb osmolality increases
- Ascending limb osmolailty decreases
The effect is multiplied by the shape of the loop (counter current), with effect being multiplied with increasing depth down the loop.

Q: Properties of the vasa recta
A: Supply renal medulla
Slow blood flow
Permeable to water and solutes

Q: Mechanism of counter-current exchange
A: Vasa recta follow the loop of henle
Solutes and water diffuse as per the changing medullary gradient - moving in on the descent and out on the ascent.
Therefore, at normal rates of blood flow vasa recta do not wash away the concentration gradient

Q: Role of urea in counter-current mechanism
A: Filtered urea is reabsorbed in the thick ascending limb and with water in the DCT/CT
Contributes ~50% of the medullary concentration gradient

Q: Maximal renal concentrating ability
A: 1400mmol/kg

Q: Difference between distensibility and compliance
A: Distensibility = compliance / original volume

Front: Compare arterial and venous pressure-volume curves at normal sympathetic tone
Back: x intersects at 400 and 2200mL
normal values: 100mmHg at 500mL (arterial) and 6mmHg at 2500mL (venous)
compliance: 1 mL•mmHg^-1 (arterial) and 50 mL•mmHg^-1 (venous)
Reference: Guyton & Hall

Front: Effect of sympathetic tone on arterial and venous compliance

Front: Factors affecting pulse presure
Back: Stroke volume
Ejection character
Arterial compliance
Reference: Guyton & Hall

Q: Normal RAP
A: 0-3 mmHg

Q: Minimum right atrial pressure
A: -3 to -5 mmHg

Q: Functions of the venous system
A: Conduit for blood returning to heart
 - passively via pressure gradient
 - actively via venous pump mechanism
Variable blood reservoir

Q: Maximum cell to capillary distance
A: 20 - 30 µm

Front: Constituents of the interstitum
Back: Collagen fibres
Proteoglycan filaments:
 - hyaluronic acid (98%)
 - protein (2%)
Fluid (similar to plasma except less proteins)
 - "tissue gel" (>99%; bound to proteoglycans)
 - free fluid (<1%)
Reference: Guyton & Hall

Front: Net filtration for total capillary circulation
Back: 2 mL•min^-1 outwards to interstitium for whole body
Fluid is absorbed into circulation via lymphatics. Due to net outward force of 0.3 mmHg for total capillary system.
Reference: Guyton & Hall

Front: Describe the pathway of nitric oxide production by endothelial cells resulting in smooth muscle relaxation
Reference: Guyton & Hall

Q: Factors exposed when vascular endothelium is damaged
A: Collagen
vWF
Tissue Factor

Q: Actions of thrombin (IIa)
A: Cleaves fibrinogen to fibrin
Activates factor V, VIII, IX, creating positive feedback which accelerates Xa production

Q: Anticoagulant factors
A: Tissue Factor Pathway Inhibitor
Antithrombin III
Protein C
Protein S

Q: Mechanism of clot regulation
A: Dilution of factors
Activation of anticoagulant factors

Q: Mechanism of clot lysis
A: tPA binds to fibrin and cleaves plasminogen to plasmin
Plasmin cleaves fibrin into FDPs

Q: Action of FDPs
A: Inhibit thrombin and fibrin formation

Q: Classify failures of Action Potential Propagation
A: Failure of AP to reach terminal
Presynaptic inhibition
Failure of synthesis of neurotransmitter
Failure of exocytosis
Failure to remove/excessive breakdown of neurotransmitter
Antagonism at postsynaptic receptor
Loss of post-synaptic receptor
Post-synaptic inhibition (IPSP)
Refractory period (Absolute, relative)

Q: Manometer vs Tonometer
A: Manometer: Gas Pressure
Tonometer: Liquid Pressure

Q: Gas vs. Vapour
A: Gas: Gaseous form of a substance above its critical temperature - cannot be liquified.
Vapour: Gaseous component of a substance below its critical temperature. Can be liquified.

Q: Avogadro's Law
A: Equal volumes of gas at the same temperature and pressure contain the same number of molecules

Q: Starling Equation
A: Kf(Pch - Pih - σ(Pco - Pio))

Q: Reflection coefficient
A: σ
Protein will leak from capillary as fluid travels along it, slightly increasing interstitial oncotic pressure and slightly decreasing capillary oncotic pressure.

Q: Typical arteriolar capillary hydrostatic pressure
A: 25mmHg

Q: Typical value for venous hydrostatic pressure
A: 10mmHg

Q: Typical value for interstitial hydrostatic pressure
A: -6mmHg

Q: Typical value for capillary oncotic pressure
A: 25mmHg

Q: Typical value for interstitial oncotic pressure
A: 5mmHg

Q: Causes of oedema (by starling forces)
A: Increased filtration pressure
Decrease oncotic pressure gradient
Increased capillary permeability
Inadequate lymph flow

Q: Features of REM sleep
A: EEG activity resembling that of awake individuals
Lasts 5-30 minutes
Frequency of REM sleep decreases with age
Dreaming occurs
Irregular HR and RR
May be:
- Tonic (occasional muscle twitches)
- Phasic (bursts of rapid eye movements)

Front: Effect of age on functional residual capacity
Back: None in absence of disease at both extremes of age
Reference: Brandis

Front: Explain the relationship between FRC, closing capacity, and V/Q mismatch
Back: V/Q inequality is minimised at functional residual capacity if it is greater than closing capacity
Reference: Brandis

Q: Describe the metabolic functions of the lung
A: Synthesises:
- Proteins
- Surfactant
- Platelets
Activates:
- Angiotensin II (from angiotensin I)
Inactivates:
- Proteases
- Vasoactives (some)
Consumes:
- Carbohydrate

Q: Functions of ACE
A: Converts angiotensin I to II
Inactivates bradykinin

Front: Vasoactive substances unaffected by pulmonary circulation
Reference: Brandis

Front: Effect of pulmonary circulation on amines
Reference: http://ceaccp.oxfordjournals.org/content/13/3/98

Front: Describe the "defence" mechanisms protecting the lung?
Back: Physical:
- Upper airway filtering and particle impaction
- Airway reflexes (cough, sneeze)
- Mucociliary escalator
- Bronchoconstriction slows flow and enhances deposition.
Cellular:
- Alveolar macrophages phagocytose particles in the respiratory zone.
Chemical:
- Immune mediators in secretions (especially IgA)
Reference: Brandis

Q: Define central blood volume
A: Volume of blood in heart and lungs

Front: Functions of the nose
Back: Respiratory:
- Gas flow
- Humidification
- Filtration
Smell
Phonation

Front: Mechanisms of particle removal in the upper airways
Back: Filtration (nasal hairs)
Impaction (due to changes in flow direction)
Sedimentation (due to force of gravity, trachea>nasal passage)
All facilitated by turbulent flow
Reference: Brandis

Front: Advantages of locating haemoglobin in erythrocytes
Back: Isolates Hb from general circulation to:
- avoid glomerular filtration
- maintain tetrameric structure (free Hb dissociates into dimers)
- reduce plasma oncotic pressure
Increased efficiency (by co-location with):
- 2,3 DPG
- carbonic anhydrase
- mehaemoglobin reductase
Reference: Brandis

Front: Mechanisms of the Haldane effect
Back: Due to features of deoxyhaemoglobin:
Forms carbamino compounds 3.5 times more than oxyhaemoglobin (70% of effect)
Buffers H+ better (30% of effect)
Reference: Brandis

Front: Functions of red cell membrane
Back: Transfer:
- gasses
- bicarbonate
- chloride
Protects:
- promotes tetramer structure of haemoglobin
- prevents glomerular filtration
Immunological
- red cell antigens
Reference: Brandis

Q: Alterations to drug response: Cardiac disease
A: A: Decreased CO decreases PO absorption
D: Prolonged arm-brain circulation time
    Increased a1 glycoprotein, increasing binding of basic drugs
    Decreased Vd
M: Change in CO will affect metabolism of drugs with a high ER
E: Decreased RBF decreases clearance

Q: Saturated vapour
A: Vapour which is in equilibrium with its own liquid state

Q: CNS effects of hypothermia
A: CMRO2 falls by 6% per 1 degree fall in temp
Antiinflammatory
Amnesia, apathy, dysarthria

Q: Portal venous SpO2
A: 85% in resting gut
75% in active gut

Q: Hepatic Arterial Buffer Response
A: Hepatic arterial resistance is proportional to portal venous flow

Q: Autoregulation of liver blood flow
A: Myogenic
Hepatic arterial buffer response

Q: External determinants of hepatic blood flow
A: Venous return:
- Thoracic pressure
- Cardiac tamponade/failure
ANS tone
- Exercise
- D/α/β receptors in hepatic artery
- α receptors in portal vein

Q: Myocardial changes with ageing
A: Decreased receptor density and number
Decreased maximum heart rate
Decreased inotropy
- Mild
Decreased diastolic compliance
Increased reliance on atrial kick

Q: Vascular changes with ageing
A: Increased SVR
Reduced compliance
Reduced catecholamine receptor density
Reduced endothelial cell function (decreased NO)

Q: Normal hepatic blood flow
A: 1500ml/min, 25% of CO
- 1/3rd from hepatic artery
- 2/3rd from portal vein
- Join to form a sinusoid, which drains to the central vein
Each supplies ~50% of hepatic O2 requirements.

Q: Renal O2 consumption
A: 6ml/100g/min

Q: Hepatic O2 consumption
A: 2ml/100g/min

Front: Equation giving rate of forward ligand-receptor reaction
Reference: Peck & Hill

Front: State equation giving equilibrium dissociation constant. State units and meaning.
Back: units:
mmol • L^-1
^
Represents concentration of ligand achieving 50% receptor occupancy.
Reference: Peck & Hill

Front: State equation giving drug-ligand association constant. State units.
Back: K_A = 1 / K_D
_
where:
_
_
Units:
L • mmol^-1
Reference: Peck & Hill

Front: Define efficacy
Back: Absolute magnitude of drug response. Used to compare response between drugs acting on a given receptor
Note potencies (given by ED50) relate to each drug individually.
Reference: http://ceaccp.oxfordjournals.org/content/4/6/181

Q: When [...], [...] must be present.
A: maximum response in a system in produced at low receptor occupancy; reserve receptors ("spare receptors")
Reference: http://ceaccp.oxfordjournals.org/content/4/6/181

Front: Effect of competitive antagonist on dose-response curve
Back: Right shift of dose response curve
No change in maximum response
Effect is dependent upon the relative concentrations and receptor affinities of agonist and antagonist.
Reference: http://ceaccp.oxfordjournals.org/content/4/6/181

Front: Effect of non-competitive antagonist on dose-response curve
Back: Right shift of dose-response curve
Depressed maximum response
Reference: http://ceaccp.oxfordjournals.org/content/4/6/181

Front: Chief site of vasomotor system in the CNS
Back: Vasomotor centre located at junction of pons and medulla
Reference: Guyton & Hall

Q: Relationship of cardiac contraction to AP propagation
A: Begins shortly after depolarisation, continues ~50ms after repolarisation is complete.

Q: Cardiac PNS innervation
A: SA by R vagus
AV by L vagus
Atria is innervated, ventricle is not: therefore ↑ PNS tone will ↓ chronotropy and have no effect on inotropy

Q: Cardiac SNS innervation effects
A: β1 stimulation:
↑ Inotropy
↑ Chronotropy
↓ AP duration (inc. K rectifier channel opening)

Q: Normal P wave duration
A: <0.1s

Q: Normal PR interval
A: 0.12-0.2s

Q: Normal QRS duration
A: <0.12s

Q: ST segment represents
A: Phase II of the cardiac AP

Q: QT interval represents
A: Time of onset of depolarisation to the completion of repolarisation - i.e. duration of the cardiac AP
Shortens with increasing HR

Q: Bazett's Formula (for QTc)
A: sqrt(QT)/RR
Should be <0.44s

Q: Daily protein requirement
A: 1g/kg

Q: Daily water requirement
A: 30ml/kg

Q: Daily Na requirement
A: 2mmol/kg

Q: Daily K requirement
A: 1mmol/kg

Q: Daily Ca/Mg/PO4 requirement
A: 0.1 mmol/kg

Q: Trace elements
A: Fe
Zn
Cu
Iodine
Chromium
Manganese
Selenium

Q: Effects of hypercapnoea
A: Increased CBF
Increased ICP
Hyperventilation (~1L/min per mmHg above 40mmhG)
Central depression (PaCO2 > 100mmHg)

Q: Normal O2 flux
A: Flux = delivery to tissues (not extraction):
Normal flux 1L/min

Q: Normal range of [H+]
A: 36-44nmol/L

Q: Normal myocardial O2 consumption
A: 21-27ml/min

Q: Daily saliva production
A: 1L

Q: Contents of saliva
A: Water (98%)
Amylase
Lipase
Mucin
Haptocorrin
Lysozyme
Lactoferrin
IgA

Q: Functions of saliva
A: Lubrication
Digestion
Neutralisation of acid
Antibacterial

Q: Functions of the Stomach
A: Digestive
- Temporary food storage
- Secretion of enzymes
- Mixing
- Acid secretion
- Intrinsic factor secretion
- Gastric endocrine (gastrin)

Q: CVS responses to standing
A: ↓ VR causing ↓ CO causing baroreceptor activation and compensatory:
↑ TPR and venoconstriction
↑ HR
↑ contractility

Q: Duration of hyperventilation (to reduce CO2) of effect on ICP
A: 4-12 hours
CSF HCO3 decreases in response to continual hyperventilation, and vasoconstriction decreases as CSF pH normalises

Front: Mechanism of inverse agonism
Back: Some receptors demonstrate a low level of "constitutive" activity in the absence of a ligand. Inverse agonists reduce this activity when bound to the receptor.
e.g. flumazenil.
Reference: Peck & Hill

Front: Define potentiation, in the context of drug-drug interaction
Back: An interaction where a drug has no intrinsic action in a system, but increases the action of another drug. Interaction mechanisms are diverse.
Example:
probenecid reduces renal excretion of penicillin, but does not itself have antibiotic activity
Reference: Peck & Hill

Front: Define isomerism and its two main categories
Back: Molecules of the same atomic formulae having different structural arrangements.
Two classes:
Structural isomerism
- differing order of atomic bonds
Stereoisomers
- same atomic bonds but different three-dimensional configuration
Reference: Peck & Hill

Front: Define tautomerism
Back: Property whereby a molecule undergoes spontaneous interconversion between structural isomers depending upon the prevailing milieu (e.g., pH of solution)
Reference: Peck & Hill

Front: Define geometric isomerism
Back: Form of stereoisomerism (same chemical bonds, different three-dimensional configuration).
Occurs where dissimilar groups are attached to atoms linked in a way which prevents free rotation (e.g., carbon-carbon double bond, or ring structure).
Reference: Peck & Hill, http://www.chemguide.co.uk/basicorg/isomerism/geometric.html

Front: Define optical isomerism
Back: Molecules that differ three-dimensionally by the placement of atoms or groups around a chiral centre, such that they cannot be superimposed.
Named because they were distinguished by how they rotated in polarised light.
Reference: Peck & Hill, http://www.chemguide.co.uk/basicorg/isomerism/optical.html

Front: Define enantiomer
Back: A single optical stereoisomer (mirror image) of a molecule possessing exactly one chiral centre.
Example:
S-warfarin and R-warfarin
Reference: Peck & Hill, http://www.chemguide.co.uk/basicorg/isomerism/optical.html

Regarding isomerism, a molecule posessing no plane of symmetry is chiral. A molecule posessing a plane of symmetry is achiral
Reference: http://www.chemguide.co.uk/basicorg/isomerism/optical.html

Front: Define diastereoisomer
Back: A single isomer of a molecule posessing multiple chiral centres (and therefore n^2 maximum possible isomers, where n = number of chiral centres).
Equivalent in a molecule with a single chiral centre is an enantiomer.
Reference: Peck & Hill, http://www.chemguide.co.uk/basicorg/isomerism/optical.html

Q: Coronary sinus pO2
A: 20mmHg

Q: Oxygen debt
A: Oxygen required post exercise to:
- Metabolise lactate
- Replenish ATP
- Replenish Phosphocreatine
- Replenish Oxymyoglobin

Q: Mean portal venous blood pressure
A: 10mmHg

Q: Measurement of hepatic blood flow
A: Indocyanine green & Fick Principle
- Indicator which has uptake only by the liver, is eliminated in bile (with no enterohepatic recirculation)
Infuse until steady state is reached (therefore rate of infusion = rate of uptake). Sample hepatic vein blood and any peripheral arterial blood.

Q: Measurement of Renal Blood Flow
A: Use Para-aminohippurate (PAH) & Fick Principle
- Plasma is completely cleared of PAH at low concentrations
 - Therefore renal art. [PAH] = peripheral art. [PAH] = peripheral v. [PAH]
Therefore, renal tubular plasma flow = (urine [PAH]/plasma [PAH]) x urine flow
- RBF can be calculated from plasma flow & haematocrit
 - Underestimates as 10% of RBF goes to parenchyma and not tubules

Q: Mechanisms of fluid and solute movement across capillary membranes
A: Diffusion
(Ultra)Filtration

Q: Characteristics of diffusion (across capillary membranes)
A: Large volumes
Bidirectional
Net movement affected by concentration gradient - Starling forces are not involved
Responsible for movement of gases, nutrients, wastes

Q: (Ultra)filtration (across capillary membranes) is
A: May be into or out-of capillary (but not both)
Governed by starling forces
Important for the movement of water, and solute (not colloid) via bulk flow

Q: Digestion of carbohydrates
A: Mouth + duodenum: Amylase
Brush-border: Sucrase/maltase/lactase hydrolyse carbohydrate to monosaccharides
Enterocyte: Absorption
- Glucose/Galactose: Na co-transporter
- Fructose: Facilitated diffusion

Q: Gastrin secretion and function
A: G cells of stomach in response to distension
Stimulates:
- Gastric acid secretion
- Panreatic exocrine secretion

Q: Effect of high renal perfusion pressure
A: Tubular damage due to high pressure
Pressure diuresis due to inability to reabsorb large volume of filtrate

Q: Cells damaged with low renal blood flow
A: Ischaemia of poorly-vascularised medulla and metabolically active tubular cells

Q: Gram +ve cocci (examples)
A: Staph. Aureus
Strep. Pneumoniae
Enterococcus faecalis

Q: Gram +ve rods (examples)
A: Listeria
C. difficile

Q: Gram -ve cocci (examples)
A: N. meningitidis
N. gororrhoea

Q: Gram -ve rods (examples)
A: Escherichia Coli
Pseudomonas Aeruginosa

Q: Amount of CO2 in alveolar dead space
A: Contain some CO2 as they will be partially ventilated from anatomical dead space (which contains mixed-expired CO2)

Q: Factors decreasing oedema in lungs
A: Low PAP
Low alveolar oncotic pressure
Respiratory pump improves lymph flow
Hydrostatic pressure is more negative closer to the hilum, improving lymph absorption
One-way valves in lymphatic system

Q: Function of fibrous atrioventricular rings
A: Insulation
Physical structure

Q: Gas dilution method of measuring FRC
A: Subject breaths known volume and concentration of helium from a circuit. After rebreathing, concentration of helium is measured:
V1 x [He]1 = (V1 + FRC) x [He]2

Q: Difference between gas dilution and body plethysmography for measuring FRC
A: Gas dilution only includes volume of communicating airways
Body plethysmography will measure non-communicating alveoli & also PTHx

Q: Functions of FRC
A: Oxygen Store
- Buffer for continual oxygenation of blood, even in respiration
- Only clinically modifiable store of O_2
Optimise compliance
- Minimise WoB
- Prevent atelectasis
Minimise PVR
Minimise V/Q mismatch
- Maintain lung volume above closing capacity

Q: Estimated plasma osmolarity equation
A: Est. Osmolarity = 2[Na] + [glucose] + [urea]

Q: Osmolarity vs. molarity
A: Osmolarity = number of osmoles (particles that are able to exert an osmotic pressure) per litre.
Molarity = number of moles of solute per litre.

Q: Concentration-dependent killing antibiotics
A: Aminoglycosides
Daptomycin
Metronidazole

Q: Time-dependent killing antibiotics
A: Beta-lactams
Carbapenems
Monobactams
Clindamycin
Macrolides

Q: Concentration and time-dependent killing antibiotics
A: Fluoroquinolones
Azithromycin
Tetracyclines
Vancomycin
Tigecycline
Linezolid

Q: Change in pH per degree decrease below 37
A: Increases by 0.015

Q: Endothelial regulation of haemostasis
A: Secretion of substances
- NO
- Prostacyclin
- Adenosine diphosphate
- tPA
Anticoagulant proteins
- Heparan
- Thrombomodulin

Q: Action of thrombomodulin
A: Binds thrombin, removing it from circulation.
Thrombin-thrombomodulin complex also activates protein C

Q: Production and effects of thromboxane A2
A: Produced in platelets from membrane phospholipid by COX
Potent vasoconstriction and platelet activator

Q: Proportion of population who are Rhesus positive
A: 85%

Q: Characteristics of the innate immune system
A: Immediacy
Non-specific
Not modified by repeat exposures

Q: Classical signs of inflammation
A: Pain
Heat
Redness
Swelling
Loss of function

Q: Functions of antibody
A: Opsonisation
Agglutination
Inactivation of pathogen
Activation of complement

Q: Mechanism of action of cytotoxic T cells
A: Induce apoptosis in target
Rapid division & inspection of other cells for infection

Q: Primary immune response process
A: APCs phagocytose pathogen
APC express antigen
APC present to B and T cells in lymph nodes
T cell becomes activated
- Clonal expansion
- Portion become memory cells
B cell becomes activated by APC and T cell
- Clonal expansion
- Portion become memory cells
- Portion become plasma cells
  - Plasma cells produce 2000 Ab molecules/second

Q: Secondary immune response process
A: ABC phagocytose pathogen
ABC express and present antigen
Memory T and memory B cells rapidly divide and produce Ab

Q: Myoglobin - difference from Hb
A: 1 haeme group and 1 globin chain binding 1 oxygen molecule
No cooperative binding
- Curve has rapid upstroke and an early plateau
p50 2.7mmHg
Allows myoglobin to rapidly uptake O2 from blood, and unload it into the cell

Q: Carboxyhaemoglobin vs. carbaminiohaemoglobin
A: CarboxyHb: COHb
CarbaminoHb: CO2Hb

Q: Types of oxygen saturation
A: Functional
Fractional

Q: Functional saturation
A: OxyHb expressed as a fraction of OxyHb and DeoxyHb

Q: Fractional saturation
A: OxyHb expressed as a fraction of DeoxyHb, OxyHb, MetHb, and COHb

Q: Effort-independent portion of flow-volume loop
A: The linear descending part of the expiratory curve.
Rate of expiration cannot be exceeded due to dynamic airways compression

Q: Organs where Starling resistors are important
A: Lung (alveolar, interstital pressure)
Heart (Cavity pressure, pericardium, pneumothoraces)
Brain (ICP)
Eye (Intraocular pressure - glaucoma)
Uterus (contractions)
Any capsulated organ
Muscle pump
Compartment syndromes, plaster cast

Q: Surfactant composition
A: Phospholipid (80%)
Lipid (10%)
Proteins (8%)

Q: Structure of surfactant phospholipid
A: Amphipathic
- Hydrophilic and hydrophobic end orientate it at the air-liquid interface

Q: Define the 'ideal' alveolar PO2
A: PO2 in the alveoli of there was:
- No V/Q mismatch in any region
- The respiratory exchange ratio is correct
It is calculated from the alveolar gas equation

Q: Type I hypersensitivity timing
A: Immediate up to typically 20-30mins

Q: Type II hypersensitivity timing
A: 5-8 hours

Q: Type III hypersensitivity timing
A: 2-8 hours

Q: Type IV hypersensitivity timing
A: 24-72 hours

Q: ATP requirement of urea cycle
A: 3 ATP

Q: Characteristic of essential amino acids
A: Cannot be produced by transamination from other aminoacids - must be supplied in diet.

Q: Catabolism of amino acids
A: Oxidative deamination
- Remove amino group to form ammonia and ketoacid
Transamination
- Transfer amino group to another amino acid/ketoacid

Q: Hepatic lipogenesis stimulus and process
A: Occurs when insulin levels are high and hepatic glycogen stores are full.
Excess carbs and AAs are converted to FFAs and glycerol, and esterified to form TGs.

Q: Liver glycogen stores
A: 100g

Q: Skeletal muscle glycogen stores
A: 200g
For muscle use only

Q: Actions of insulin (broad overview - not by time)
A: Facilitation of glucose uptake
Increased storage of metabolic substrates
- Hepatic glycogenesis
- Lipogenesis
- AA uptake - protein synth
Inhibition of gluconeogenesis

Q: Starvation
A: The failure to absorb sufficient calories to sustain normal body function

Q: Refeeding syndrome definition and pathogenesis
A: Deranged metabolic state occuring following reinstitution of feed following a prolonged period of fasting
Pathogensis:
- Large increase in insulin
- Sodium and water retention
- Increased CO2 production increases WoB

Q: Electrolyte derangements with refeeding syndrome
A: Hypomagnesaemia
Hypophosphataemia
Hypokalaemia
Increased ECF volume/oedema

Q: Minimum urine concentration
A: 50mmol/L

Q: Effect of immersion on urine output
A: CVP rises due to an ↑ in central blood volume
RA stretch stimulates ANP release and subsequent ↑ in UO

Q: Normal calcium level in blood
A: 2.20 - 2.55 mmol/L

Q: Parietal cells secrete
A: Acid
Intrinsic factor

Q: Alkaline tide refers to
A: Gastic venous blood becomes alkaline following a meal due to acid secretion.
Gastic respiratory quotient is negative due to CO2 consumption

Q: Primary bile acids
A: Cholic acid
Chenodeoxycholic acid

Q: Electrolyte derangements with persistent vomiting
A: Hypochloraemia
Hyponatraemia
Hypokalaemia
Metabolic alkalosis
Hypovolaemia

Q: Blood-brain barrier composition
A: Physical barrier: Capillary endothelium, basement membrane, astrocyte foot processes
- Tight-junctions between capillary endothelial cells, preventing non-lipid soluble molecules crossing without a transport protein
- Capillary endothelium contains large number of mitochondria due to high ATP requirements of active transport
Chemical barrier: Enzymes in endothelial cells and astrocytes degrade some toxic substances

Q: Blood-CSF barrier composition
A: Tight junctions between choroid plexus epithelium, preventing polar molecules crossing directly into CSF

Q: Circumventricular organs
A: Areas of the brain outside the blood brain barrier:
- Chemoreceptor trigger zone
- Subfornical organ
- Organum vasculosum
- Pineal gland
- Pituitary gland
- Median eminence of the hypothalamus

Q: Role of ?HCG
A: Prolong life of corpus luteum

Q: Rate of rise of ?HCG
A: Doubles every two days until 10 weeks

Q: Main pregnancy hormones
A: ?HCG
HPL
Progesterone
Oestrogen
Prolactin
PTH
Thyroid hormones

Q: Foetal respiratory changes at birth
A: Transition to pulmonary ventilation
FRC established

Q: Cardiovascular changes at birth
A: Loss of umbilical circulation
Closure of the ductus venous, ductus arteriosus, and foramen ovale
Drop in PVR and establishment of pulmonary circulation
Rise in SVR due to loss of placental circulation

Q: hPL (human placental lactogen) function
A: Insulin antagonist, secreted in response to a fall in maternal blood glucose.
Encourages maternal lipolysis, maintaining maternal blood glucose (and therefore foetal blood glucose)

Q: Transport functions of the placenta
A: Gas exchange
Delivery of nutrients
Waste removal

Q: Immunologic functions of the placenta
A: Isolates foetus from maternal immune system, preventing rejection

Q: Metabolic functions of the placenta
A: Synthesises:
- Glycogen
- Cholesterol
- Fatty acids

Q: Endocrine function of the placenta
A: Synthesises:
- βHCG
- hPL
- Oestriol
- Progesterone

Q: Purpose of maternal respiratory alkalosis
A: Increases gradient for CO2 diffusion from foetus

Q: Factors assisting CO2 transfer across the placenta
A: Low maternal pCO2
Double Haldane effect

Q: Formation of amniotic fluid
A: Early pregnancy: Ultrafiltrate of foetal plasma
Late pregnancy: Foetal urine

Q: Functions of amniotic fluid
A: Decrease effective weight of foetus
Recycle foetal urine output
Distributes pressure of contractions evenly over the foetus (Pascal principle)

Q: Types of calibration of a cathether-transducer system
A: Static calibration
Dynamic calibration

Q: Steps of static calibration
A: Zero
Check and adjust gain
Check time stability

Q: Damping coefficient represents
A: Value which describes to what extent the magnitude of an oscillation falls with each successive oscillation
Calculated from the ratio of the magnitude of consecutive oscillations.

Q: Critical Damping
A: When the damping coefficient is equal to 1
This is the value of damping which is just enough to prevent an overshoot

Q: Overdamped
A: Damping coefficient > 1
Will not overshoot but will take even longer than a critically damped signal to reach the final rest position

Q: Advantages of optimal damping
A: Maximal range of frequency responses
- Accuracy is maintained frequencies up to 2/3rds of the resonant frequency - greater than other values of D
Minimal phase distortion
- Same time delay for all harmonics
Minimal amplitude distortion

Q: Dynamic calibration is required for accurate measurement of
A: Systolic and diastolic blood pressures

Q: Principle of a strain gauge
A: Increased stretch on a resistor causes a change in electrical resistance

Q: Basic principle of clark electrode
A: Amount of current flowing in the circuit is proportional to oxygen tension in electrolyte solution

Q: Phases of a capnograph
A: 1. Inspiratory baseline
2. Expiratory upstroke
3. Expiratory plateau
4. Inspiratory downstroke

Q: Increase in phase 1 of capnograph due to
A: Inspired CO2

Q: Decrease in phase 3 of capnogram due to
A: Increased dead space
- Incomplete expiration
Increased Va: Low PaCO2
Leak

Front: Abnormal responses to valsalva manoeuvre
Back: Autonomic dysfunction (absent overshoot)
- blood pressure falls in phase 1 and does not improve until phase 3
- absent phase 4 and no HR response
Raised CVP (square wave)
- observed in CCF, tamponade, constrictive pericarditis, valvulopathy
- occurs as venous return not affected by raised intrathoracic pressure and afterload is reduced
Reference: http://www.frca.co.uk/article.aspx?articleid=100372

Front: Cardiovascular effects of central neuraxial blockade
Back: Blockade of thoracolumbar sympathetic outflow dependent upon height of block (sacral: no effect; upper lumbar: partial sympatholysis; T1-4: loss of cardioaccelerator fibres; brainstem: vasomotor centre—life-threatening).
May result in:
- reduced total peripheral resistance
- reduced venous return
- reduced cardiac output
Compensatory mechanisms (which may be partially ablated):
- baroreceptor reflex increasing sympathetic outflow
- low pressure receptors (maladaptive response of bradycardia and inhibition of renin-angiotensin-aldosterone system)
Reference: NYSORA

Front: Normal cardiac index in adults
Back: 3 L•min^-1•m^-2
^
^
Reference: Guyton & Hall

Front: Normal cardiac index in a 10 year old
Back: 4 L•min^-1•m^-2
^
^
Reference: Guyton & Hall

Front: Describe the effect of intrapleural pressure on cardiac output
Back: Increased: right shift (i.e., reduced output for given RAP)
Decreased: left shift (i.e., increased output for a given RAP)
Reference: Guyton & Hall

Front: Describe the relationship between right atrial pressure and venous return in the absence of nervous circulatory reflexes
Back: Plateau (<4mmHg) due to venous collapse
x intercept at 7mmHg due to:
- insufficient pressure gradient to generate flow
- absence of cardiac output at steady state
Reference: Guyton & Hall

Front: Define mean systemic filling pressure
Back: The pressure measured anywhere in the systemic circulation when all flow of blood is stopped.
Reference: Guyton & Hall

Front: State equation giving venous return
Back: where (normal value):
VR = venous return (5 L/min)
Psf = systemic filling pressure (7mmHg)
PRA = right atrial pressure (0mmHg)
RVR = resistance to venous return (1.4mmHg/L/min)
This is a derivation of Ohm's law.
Reference: Guyton & Hall

Front: Describe effect of resistance to venous return on the RAP-VR relationship
Back: Slope inversely proportional to resistance
Psf (x intercept) unchanged

Front: Describe effect of increased vascular compliance on RAP-venous return relationship
Back: Downward vertical shift resulting in movement of x intercept
Increased compliance results in decreased Psf
Same effect as decreased intravascular volume
Reference: Guyton & Hall

Front: Describe immediate effect of increased intravascular volume on RAP-venous return relationship
Back: Upward vertical shift resulting in changes in Psf
Increased volume increases Psf
Same effect as decreased vascular compliance
Over time, compensatory mechanisms will result in cardiac output and venous return returning to baseline
Reference: Guyton & Hall

Front: Effects of maximal sympathetic stimulation on cardiac output, according to RAP-cardiac output/venous return relationships
Back: Increased cardiac output (point D compared with point A)
Due to:
- Increased cardiac performance
- Vertical shift of VR curve and increased Psf due to reduced vascular compliance
- Reduced slope of VR curve due to increased resistance to venous return
Reference: Guyton & Hall

Front: Effects of spinal anaesthesia on cardiac output, according to RAP-cardiac output/venous return relationships
Back: Reduced cardiac output (point B compared with point A)
Due to:
- increased slope of venous return curve due to reduced resistance to venous return
- down shift of venous return curve (and lower Psf) due to increased vascular compliance
- reduced cardiac performance due to reduced sympathetic tone
Reference: Guyton & Hall

Front: Describe the compensatory cardiovascular mechanisms in a healthy person moving from sitting to standing
Back: Carotid MAP must be maintained above the lower limit of cerebral autoregulation (~60 mmHg), in order to prevent reduced cerebral blood flow and the faint reflex. Note that there is approximately a 20mmHg drop between aortic root and carotid artery pressure in an erect subject.
Standing causes:
1. reduced venous return due to hydrostatic effects resulting in venous pooling
2. reduced cardiac output (transiently 20%) and blood pressure
3. high pressure baroreceptor firing is reduced resulting in sympathetic stimulation (and parasympathetic inhibition)
4. restoration of cardiac output and blood pressure by:
- increased venous return (reduced capacitance)
- increased heart rate
- increased stroke volume (sympathetic contractility and increased preload)
- increased PVR
Reference: Guyton & Hall

Front: Factors determining venous return
Back: VR = (P_SF - P_RA) / R_VR
P_SF
- venous capacitance
- systemic volume
P_RA
- proportional to venous return/cardiac output
- intrapleural pressure
R_VR
- 1/3 arteriolar resistance
- 2/3 venous resistance

Front: Effect of general anaesthesia on venous return
Back: [$]VR = \frac{P_{SF} - P_{RA}}{R_{VR}}[/$]
P_SF
- reduced circulating volume: haemorrhage, fasting, 3rd spacing, insensible losses
- increased venous capacitance: drugs, inflammation
P_RA
- increased intrapleural pressure due to IPPV
R_VR
- reduced arteriolar resistance due to direct effect and sympatholysis: increases venous return, but P_SF effect dominantes
- pneumoperitoneum increases R_VR
- positioning variable modifier of R_VR

Front: How is cardiac output measured using a thermodilution technique
Back: Via a PA catheter:
Cold saline is injected via a proximal (RA) port.
Distal thermistor records change in temperature.
Area under temperature-time curve is inversely proportional to cardiac output (Stewart-Hamilton equation).
Reference: derangedphysiology.com

Q: Sources of error in PAC CO measurement
A: Variability
- Normal to observe up to 10% variability between given measurements
Tricuspid regurgitation
- Results in indicator recycling, and low-amplitude thermodilution curve (similar to low cardiac output)
- common in PPV
Intracardiac shunts
- R to L: Indicator bypasses thermistor, resulting in spuriously high CO
Incorrect injectate volume
Warm fluid
- Colder fluid gives more precise measurements but increases risk of bradycardia, arrhythmia
Poorly positioned PAC
- Must be in West zone 3

Front: What is represented by the slope of the curve in this diastolic volume-pressure curve?
Back: ∆P/∆V = elastance
Note:
compliance = 1/elastance
Reference: Brandis

Q: [Which area] represents [...] on the LV pressure-volume loop
A: Area ABCD; external pressure-volume work
Extra: Under normal conditions, this is 99% of useful work performed, the other component being kinetic work of blood flow.
Reference: Brandis, Guyton & Hall

Q: Comparing these LV pressure-volume loops, loop 2 has [changed factor], while [...] and [...] remain unchanged.
A: increased preload; contractility; afterload
Extra: Preload is best represented by LV end-diastolic volume. (This has clearly changed.)
Afterload is best measured by the slope of the line between LV end-diastolic volume and LV end-systolic point. (These lines are parallel.)
Contractility is best measured by changes in the slope of the LV endsystolic pressure-volume relationship.
Reference: Brandis
Other fields (not shown on cards):
Comment: convert to cloze

Front: Outline the relevant CNS physiological differences of pregnancy and their implications for anaesthesia
Reference: CEACCP

Front: Outline the relevant haematological differences of pregnancy and their implications for anaesthesia
Reference: CEACCP

Front: Outline the relevant gastrointestinal differences of pregnancy and their implications for anaesthesia
Back: Reduced oseophageal barrier pressure due to effects of gravid uterus and hormonal changes, reduced gastric emptying.
Antacid prophylaxis and rapid sequence induction should be performed after 18 weeks gestation to preven aspiration.
Reference: CEACCP

Front: Important side effects of inhalational anaesthetics in pregnancy
Reference: CEACCP

Front: Important side effects of neuromuscular blocking agents in pregnancy
Reference: CEACCP

Front: Important side effects of opioids in pregnancy
Reference: CEACCP

Front: Important side effects of NSAIDs in pregnancy
Back: Premature duct closure: avoid >28/40
Reference: CEACCP

Front: Maximum dose of lignocaine (with and without adrenaline)
Back: 3 mg•kg^-1
7 mg•kg^-1 (with adrenaline)

Front: Maximum dose of ropivacaine (with and without adrenaline)
Back: Dose is the same regardless of adrenaline
3 mg•kg^-1

Front: Outline the principles of pulse contour analysis for cardiac output measurement
Back: Cardiac output ≈ AUC (systolic pressure-time curve) x heart rate x calibration factor
Calibrated:
- transpulmonary thermodilution (PiCCO — pulse induced contour cardiac output)
- lithium dilution (LiDCO)
Uncalibrated:
- "compliance" based on demographics, biometrics and waveform characteristics (FloTrak/Vigileo)
Reference: doi:10.1093/bjaceaccp/mkr044

Front: Outline the principles of doppler measurement of cardiac output
Back: PW doppler used to measure aortic VTI.
- VTI x aortic cross sectional area (CSA) = SV
- SV x HR = CO
Reference: doi:10.1093/bjaceaccp/mkr044

Front: Speed of ultrasound in tissue
Back: 1540 m•s^-1
Reference: doi:10.1093/bjaceaccp/mkr044

Front: What factors determine the resonant frequency of a system?
Back: Defined by:
[$]f_0=\frac{1}{2}\pi\sqrt{\frac{k}{m}}[/$]
Where:
ƒ_0 = resonant frequency
k = elasticity/spring constant
m = system mass
Reference: Miller

Front: Explain how amplification artefact occurs in biomedical pressure transduction systems
Back: Amplification artefact "overshoots" pressure measurements due to resonance.
As the waveform consists of a summation of sine waves with differing frequencies (a Fourier series), any coincidence with a resonant frequency of the system will cause resonance.
Reference: Miller, doi:10.1093/bjaceaccp/mkm022

Front: Essential components of an invasive arterial pressure measurement system
Back: 1. intra-arterial cannula
2. tubing (incorporating an infusion system)
3. transducer
4. microprocessor and display screen
5. mechanism for zeroing and calibration
Reference: doi:10.1093/bjaceaccp/mkm022

Front: Describe the Von Recklinghausen oscillotonometer
Back: Configuration:
Two cuffs (one sensing, one occluding)
Two separate bellows
Pressure guage
Operation:
Occluding cuff inflated above systolic then slowly deflated
Sensing cuff begins oscillating when systolic pressure reached
Peak oscillation at MAP
Diastolic calculated
Relevance:
NB: DINAMAP^®) uses a one-cuff system
Reference: doi:10.1093/bjaceaccp/mkm022

Front: Describe the oscillometer method of blood pressure measurement
Back: Stepwise cuff deflation from pressure above systolic. Observed oscillations due to pulse increase then decrease in amplitude.
Systolic pressure:
maximum rate of amplitude increase
Mean pressure:
maximum amplitude
Diastolic pressure:
maximum rate of amplitude decrease
Reference: doi:10.1093/bjaceaccp/mkm022

Front: Requirements for accurate cuff blood pressure measurements
Back: Cuff:
- appropriately fitting cuff (small cuff overestimates)
- at heart level
- free of external compression
Patient:
- regular pulse between 30-300 beats/min
- blood pressure not severely low
- compressible arteries (calcified arteries overestimate)
- still (initial measurement may be painful)
Reference: doi:10.1093/bjaceaccp/mkm022

Front: Sources of artefact/error in pulse oximetry
Back: Venous pulsation (typically due to patient movement)
Poor perfusion (resulting in low signal:noise)
Additional absorbance in blood
- CarboxyHb reads artifically high (high 660nm absorption)
- Methaemoglobinaemia causes trend towards 85%
- Methylene blue causes SpO2 <65% for several minutes
- Ambient light
Low saturation
- Machines calibrated on healthy individuals at SpO2 75%
Reference: Miller

Front: What is the function of a Thorpe tube? How does it work?
Back: Measures gas flow
Consists of:
- vertical, open-ended tube with calibrated markings
- bobbin (or bobbin rotameter)
- gas flow source at bottom
Mechanism:
- gas flow causes bobbin to rise
- as bobbin rises, aperture around it increases
- comes to rest at point where force of gravity balances force due to gas flow
- change from laminar to turbulent flow at higher gas flow rates changes the equation describing the system
Reference: Miller

Q: [...] = [...]τ
A: t_½; 0.693
Q: where:
τ = [...] in the equation y=e^-^kt
A: 1/k
Reference: Cross & Plunkett
Other fields (not shown on cards):
Comment: cloze field in extra

Q: An exponential process is said to be complete after [...]. At this point, [...]% of the process has occurred.
A: three time constants; 94.9
Reference: Cross & Plunkett

Front: Define accuracy
Back: The ability of a measuring device to match the actual value of the quantity being measured
Reference: Cross & Plunkett

Front: Define precision
Back: The ability of a measurement device to provide reproducible results upon repeated measurement.
Reference: Cross & Plunkett

Front: Define drift, in the context of measurement
Back: A fixed deviation from the true value at all points in the measured range
Reference: Cross & Plunkett

Front: Define zeroing, in the context of measurement
Back: The removal of any fixed drift from a measurement system.
Reference: Cross & Plunkett

Front: Define calibration, in the context of measurement
Back: A process of checking a monitoring device for linearity of correlation between actual and measured values over a given measurement range.
Reference: Cross & Plunkett

Front: Name the base SI units
Back: "SMMACKK"
Reference: Cross & Plunkett

Front: State the universal gas equation
Back: PV = nRT
where:
P = pressure
V = volume
n = moles of gas
R = 8.3145 J/mol K
T = absolute temperature
Reference: Cross & Plunkett

Front: Define dew point
Back: Point at which the temperature of a cooling vapour reaches a relative humidity of 100%, causing vapour to condense as dew.
Reference: Cross & Plunkett

Front: Draw a diagram of a defibrillator circuit
Back: Charging:
Discharging:
Inductor modifies the current-time waveform:
Reference: Cross & Plunkett

Front: Constituents of soda lime
Back: 4% sodium hydroxide (NaOH)
15% bound water
81% calcium hydroxide (Ca(OH)_2)
Traces:
pH indicators:
- phenolphthalein (red to white), ethyl violet (white to purple)
Silicates (harden granules)
KOH
Reference: Cross & Plunkett; examiner reports

Front: State the reaction between soda lime and CO_2
Back: Overall:
CO_2 + Ca(OH)_2 → CaCO_3 + H_2O + Heat
Constituent reactions:
1.
CO_2 + H_2O → H_2CO_3
2.
2NaOH + H_2CO_3 (KOH catalyses)→ Na_2CO_3 + 2H_2O + heat
3.
Na_2CO_3 + Ca(OH)_2 → CaCO_3 + 2NaOH + heat
4.
Ca(OH)2 + heat → CaO + H_20
Reference: Cross & Plunkett
Examiner reports

Front: Hazards of soda lime
Back: Contains traces of volatile:
- Must be replaced in patients at risk of MH
Decomposes volatiles:
Sevoflurane produces compound A , which may cause renal, hepatic and neurological damage (some jurisdictions dictate a minimum fresh gas flows)
Carbon monoxide production:
- from R-CHF2 containing molecules (e.g., isoflurane)
- Especially with dry soda lime ("Monday morning effect", and at low or high flows)
Trichloroethylene (old school volatile) produces neurotoxin
Indicator dye colours may be confused
- Phenolphthalein (red to white), ethyl violet (white to purple)
Reference: examiner reports

Front: What is the size of soda lime granules? Why?
Back: 4-8 mesh (passes through seive with four holes per square inch, but not a seive 8 holes per square inch)
Reasons:
- optimal balance between surface area and gas flow
- uniformity gives uniform gas flow
Reference: examiner reports

Q: When a substance has increased internal energy without increased temperature, it must [...]
A: have undergone a phase transition
Reference: examiner reports

Front: What is the Seebeck effect
Back: Effect where, at the junction of two dissimilar metals, a voltage will be produced, the magnitude of which will be in proportion to the temperature difference between the two metals.
Thermocouple devices operate on this principle.
Reference: Cross & Plunkett

Front: Electrical methods of measuring temperature
Back: Voltage proportional to temperature:
- Thermocouple (Seebeck effect)
Resistance correlated to temperature:
- Resistance wire (most metals, direct correlation)
- Thermistor (inverse correlation; semiconductor material)
Reference: Cross & Plunkett

Front: Why does a N_2O cylinder get warmer when not in use? How does this relate to the pressure on the cylinder guage, and how does it compare with a bedside oxygen cylinder?
Back: At room temperature, nitrous oxide exists below its critical temperature, and so the cylinder contains both liquid and vapour.
When in use, the latent heat of vaporization cools the remaining liquid. This in turn reduces saturated vapour pressure, which is reflected by the reduced pressure of the Bourdon guage.
When not in use, the liquid is no longer being cooled, and it is warmed by the ambient environment. This increases the saturated vapour pressure in the cylinder, which is reflected as increased pressure on the Bourdon guage.
As a bedside oxygen cylinder is above the critical temperature of oxygen, it contains gas and vapour or liquid. The Bourdon guage therefore correlates with the total number of oxygen molecules in the cyclinder.
Reference: tutorial

Front: How does a bourdon gauge work?
Back: Measures pressure.
Hollow, flattened metal cylinder mechanical connection to a guage
Analagous to a children's party whistle
Reference: tutorial

Front: Define the Avogadro constant
Back: 6.02 x 10^23 mol^-1
Number of atoms in 12g of ^12C
Number of atoms in 1 mole
Reference: Cross & Plunkett

Front: Difference between serum and plasma
Back: Plasma is cell free blood
Serum is clotting factor free blood
Reference: tutorial

Front: How does an osmometer work
Back: Colligative properties:
- Presence of solute changes the melting point (as well as SVP, osmotic pressure and boiling point)
- Osmotic pressure is directly proportional to the depression of melting point.
- 1osm of solute will change the freezing point by 1.86ºC
Reference: Cross & Plunkett

Front: How does the thermodilution curve change with cardiac output?
Back: increased: earlier onset, smaller AUC
decreased: later, larger AUC
Reference: Deranged Physiology

Front: Effect of reduced volume of cold mass in thermodilution measurement of cardiac output
Back: Overestimation of cardiac output
Reference: Miller

Front: Define thermistor
Back: Device for measuring temperature, consisting of a semi-conductor material whose electrical resistance changes in inverse proportion to its temperature
Cheap, quick to respond, but deteriorate over time.

Front: Define transducer
Back: Device which converts one form of energy to another

Front: Define mixed venous blood
Back: Contains blood from:
- IVC, SVC and coronary sinus (mixing occurs in RV)
Sampled from PA

Q: Amount of H+ buffered per mmol of Hb reduced
A: 0.7mmol
This facilitates haldane effect and why venous blood is only slightly more acidic than arterial blood.

Front: Define context sensitive half time
Back: The time taken for the plasma concentration to fall to half of the value at the time of stopping an infusion of that drug, with regards to the duration of the infusion (the "context").
Note:
Half-time is not a constant (compared with half-life), and the time taken for plasma concentration to halve again may be much longer.
Reference: Peck & Hill

Front: Anaesthetic machine safety requirements (gases)
Back: Supply lines:
- pin indexed connectors for cylinders
- non-interchangeable gas hose connectors
- pressure guages for supply lines and cylinders
Oxygen:
- reserve O_2 supply
- O_2 failure alarm
- O_2 must enter back bar last (to prevent proximal leak)
- exactly one touch-coded O_2 flow knob
Vaporiser:
- Vaporiser interlock system to prevent more than one vaporiser being turned on
- Vaporisers must increase delivery when dial rotated in an anti-clockwise direction

Front: Operating principles of an out of circuit variable bypass vaporizer
Back: Located between flowmeters and common gas outlet
Controlled splitting of fresh gas flow into vaporizer and bypass streams
Full saturation in vaporizer chamber ( achieved with wicks and baffles)
Compensates for:
- temperature with bimetallic strip and heat sink (given saturated vapour pressure changes with temperature)
- high and low gas flow (ensuring reliable splitting)

Front: Safety features of variable bypass plenum vaporizer (headings only)
Back: Agent specificity
- key indexed filling
- pin indexed safety system connectors
- colour coding of unit and agent containers
Single agent administration
- interlock mechanism
- single cartridge slot (Aladdin system)
Temperature management (heat of vaporization and changes in ambient temperature necessary as SVP changes will affect agent partial pressure)
- heavy construction with materials of high specific heat capacity and thermal conductivity
- dynamic temperature adjustment via a thermally expanding element, a bimetallic strip or an electronic control system
Flow management
- baffles and wicks increase the liquid/gas surface area and the rate of vaporization (which may still be exceeded by the gas flow rate)
Tipping and overfilling
- long vaporization chamber inflow
- heavy-based construction
- transport modes
- side filling and overflow ports
Anti-pumping
- check valves and long vaporization chamber inflow prevent entrainment of vaporizer gas in the inflow of the bypass channel
Agent depletion
- filling gauges
- low pressure alarms (Tec 6)
Reference: CEACCP, Miller

Front: General operating principle of gas blender (desflurane)
Back: Typically used only for desflurane (as it has a low boiling point of 23ºC)
Desflurane is heated to 39ºC giving vapour pressure of 2atm
Pressure of fresh gas flow proximal to flow restrictor and desflurane is equalized by variable resistor and differential pressure transducer mechanism
Adjustable resistance downstream of pressure equalizer device gives desflurane gas concentration

Front: Describe the general operation of a vacuum insulated evaporator oxygen supply
Back: Oxygen below its critical temperature in gas/vapour equilibrium in insulated chamber
Vapour drawn off and heated
In high demand situation, pressure-raising vaporiser increases vapourisation
Pressure regulator lowers pressure to pipeline
System sits on scales to measure oxygen supply

Front: Classify Mapleson circuits
Back: Mapleson system
- Only A has FGF distant from patient
- A, B & C have valves close to the patient
- Only D has release valve distant from patient
- E and F have NO release valve
- Only E has no reservoir
- Only variants of D (Bain) and E (Jackson-Rees, so-called "F") are used in modern practice

Front: Types of Mapleson A circuits
Back: Fresh gas flow is at end of reservoir tubing
Magill - the original
Lack - coaxial configuration

Front: Describe Mapleson B & C systems
Back: Fresh gas flow between bag and valve
Inefficient - once the bag is full, fresh gas is vented
Rebreathing is inevitable unless FGF > peak inspiratory flow rate (typically 3 x MV)

Front: What is the common feature of Mapleson D, E and F systems?
Back: Fresh gas enters at patient end

Front: Describe the components of a circle breathing circuit
Back: Fresh gas flow
Unidirectional (check) valves
Patient Y connector
Heat/moisture exchange filter
Inspiratory and expiratory tubing
Adjustable pressure limiting (APL)
valve
Reservoir bag
CO_2 absorber

Q: Define Colligative Properties
A: Properties of a solution that depend on the ratio of solute to solvent, and not on the type of molecules present

Q: Colligative Properties - Examples
A: Vapour pressure
Boiling point
Freezing point
Osmotic pressure

Q: Raoults Law
A: The vapour pressure of a solute above a solution is equal to the vapour pressure of the solvent (at the same temperature), multiplied by the mole fraction of the solute present

Front: What is the rate limiting step of endogenous catecholamine synthesis?
Back: Tyrosine conversion to dihydroxyphenylalanine in the cytoplasm, catalyzed by tyrosine hydroxylase
Reference: Peck & Hill

Q: Plasma Mg < 0.7 mmol/L may cause:
A: Arrhythmia

Q: Plasma Mg 4-6mmol/L
A: Nausea, hyporeflexia, speech impairment

Q: Plasma Mg 6-10mmol/L
A: Weakness, respiratory depression, bradycardia

Q: Plasma Mg >10mmol/L
A: Cardiac arrest

Q: Determinants of PVR
A: Lung volume
Hypoxic Pulmonary Vasoconstriction
PAP (recruitment and distension)
Minor factors (which increase PVR) include:
- Hypercarbia
- Hypothermia
- Acidaemia
- Pain

Q: Dialysis
A: Separation of particles in a liquid based on their ability to pass through a membrane

Q: Diffusion
A: Spontaneous movement of substances from a higher concentration to a lower concentration

Q: Determinants of solute movement in haemodialysis
A: Ficks law:
Concentration gradient between blood and dialysate
- Flow rate of blood and dialysate
Solubility and availability of the solute:
- Mass
- Charge
- Protein binding
Membrane permeability

Q: Laws relevant to solute movement in haemofiltration
A: By Starling Forces:
Transmembrane pressure generated
- Blood flow
- Oncotic pressure gradient
Porosity of membrane
Note elimination is independent of solute concentration gradients.

Q: Determinants of drug elimination in RRT
A: Drug Factors:
- Free drug in plasma
- Protein binding
- Vd
- Size of drug
- Ionisation/solubility
RRT factors:
- Dose/flow rates
- Membrane permability
Patient factors:
- Residual renal function
- Timing of RRT related to administration

Front: What is the relationship between saturated vapour pressure and temperature?
Back: SVP is dependent upon temperature, it displays a non-linear relationship to increasing temperature.
Note: SVP does not change with atmospheric pressure.
Reference: Miller

Q: Normal body oxygen stores
A: 1.5L, split between:
- 850ml in blood
- 450ml in FRC
- 250ml bound to myoglobin

Q: PO2 and SpO2 in the umbilical artery
A: 18mmHg
SpO2 45%

Q: Normal foetal HR
A: 120-140

Q: Normal neonatal HR
A: 120-160

Q: Three basic renal excretory processes
A: Filtration
Secretion
Reabsorption

Q: Factors determining a substance's glomerular filtration
A: Molecular weight
- Proxy for molecular diameter, which determines how easily it passes between podocytes
Charge
 - GBM is negatively charged and repels negatively charged molecules
Protein binding
- Bound molecules cannot be filtered

Front: What is the innervation of the intrinsic muscles of larynx?
Back: All supplied by recurrent laryngeal nerves except cricothyroid, which is supplied by external branch of superior laryngeal nerve (also a branch of vagus).
Reference: Netter

Arm veins
1 - axiallary (from brachial and basilic)
2 - cephalic
3 - cephalic
4 - median cubital
5 - basilic

Regarding blood gas analysis:
Measuring O_2:
Clarke (polarographic) electrode
or
Hersh (galvanic) fuel cell:
Measuring CO_2:
Severinghaus electrode
Measuring pH:
Glass electrode
Reference: derangedphysiology.com; Dr Podcast

Q: All relevant gasses used in anaesthesia can be analysed using infrared absorbance, except [...].
A: oxygen
Reference: CEACCP

Front: Define therapeutic index. What does it describe?
Back: [$]Therapeutic\:Index=\frac{LD_{50}}{ED_{50}}[/$]
Measures drug safety by describing the difference between minimum effective and minimum toxic doses.
ED50
- Median drug dose producing pre-defined threshold of response in a population of subjects
LD50
- Median drug dose producing death in a given population of subjects
Reference: Miller

Q: Storage functions of the liver
A: Glycogen
TGs
Vitamins (ADEK, folic acid, B12)
Fe
Cu

Q: Synthetic functions of the liver
A: Bile
Plasma proteins
- Clotting factors
- Albumin

Q: Metabolic functions of the liver
A: Carbs
Fats
Protein
Bilirubin
Acid-base
- Lactate
Drugs and toxins

Q: Endocrine functions of the liver
A: Produces angiotensinogen
Produces IGF-1
Converts T4 to T3

Q: Immune functions of the liver
A: Kupffer cells
- Endotoxin
- Bacteria/viruses, etc

Q: Acid-Base functions of the liver
A: May consume or produce large numbers of H+:
- CO2
- Organic acid anion metabolism:
 - Lactate
 - Ketones
 - AAs
- Ammonium
- Plasma protein production (albumin)

Q: Henderson-Hasselbalch Equation
A: pH = pKa + log10 ([A-]/[HA])

Q: Structural difference of foetal haemoglobin
A: Beta subunits replaced with gamma subunit, which prevents binding of 2,3-DPG and therefore left-shifts the curve.

Q: Driver of maternal respiratory alkalosis
A: Progesterone affects central chemoreceptors, left-shifting O2 and CO2 response curves causing hyperventilation

Q: Storage Lesion
A: Decay of stored blood over time:
- Loss of 2,3 DPG
- Haemolysis
- Hyperkalaemia
- Acidaemia
- Hyponatraemia

Q: Location of EPO production in the adult
A: 85% in the peritubular cells kidney
15% in the liver

Q: Clark electrode formula
A: O_2 + 4e^- + 2H_2O -> 4OH^-

Q: Pneumotacograph
Operating Principle:
[...]
A: - resistance is placed in the gas flow
- pressure drop across resistance is measured
Reference: Anaesthesia UK

Q: Relaxed conformation is
A: When a Hb molecule has 4 O2 bound to it

Q: Haemoglobin species
A: Physiological:
- HbA
- HbA2
- HbF
Pathological:
- MetHb
- HbS
- COHb
- CyanoHb

Q: Methaemoglobinaemia consequences
A: MetHb molecules cannot bind O2
MetHb molecules left-shift remaining (normal) O2, reducing O2 offloading at tissues

Q: Methaemoglobinaemia protective mechanisms
A: Glutathione in RBC reduces oxidising agents prior to oxidisation of Fe occurring
Methaemoglobin reductase uses NADH to reduce ferric iron

Q: Causes of methaemoglobinaemia
A: Oxidising agents:
- SNP
- NO
- Amide local anaesthetics
- Sulphonamides
Failure of methaemoglobin reductase
- G6PD

Q: Myoglobin structure and oxygen binding
A: Contains one globin chain and one haeme group
Does not exhibit cooperative binding
Oxy-Myoglobin dissociation curve has a rapid upstroke and early plateau

Q: Form of carbon dioxide in arterial blood
A: Bicarbonate (90%)
Dissolved (5%)
Carbamino compounds (5%)

Q: Form of additional carbon dioxide in venous blood
A: Bicarbonate (60%)
Dissolved (10%)
Carbamino compounds (30%)

Q: Carbon dioxide solubility relative to oxygen
A: 20x

Q: Formation of carbamino compounds
A: CO2 binds to HB, displacing a H+ ion
H+ ion is then buffered to another protein (also commonly Hb)
Carbamino compounds form ~1/3 of the arterio-venous CO2 difference
- Large proportion due to the Haldane effect

Q: A-a gradient equation:
A: = PAO2 - PaO2
Where:
- PAO2 calculated by alveolar gas equation
- PaO2 measured by arterial blood gas

Q: Classify mechanisms of decreased alveolar ventilation
A: Respiratory centre depression
Nerve dysfunction
NMJ dysfunction
Muscular dysfunction
Chest wall abnormalities

Q: Diffusion limitation
A: When gas transfer across a membrane does not result in an equilibrium of partial pressures gradients

Q: Perfusion limitation
A: When gas transfer across a membrane results in equal partial pressure gradients, such that the amount of gas transferred is dependent on solvent flow

Q: Normal oxygen diffusion time across alveolar membrane
A: 0.25s

Q: Factors which may result in oxygen becoming diffusion limited:
A: Decreased alveolar SA
Increased thickness
High cardiac output
Deceased PAO2 (e.g. altitude)

Q: DLCO is
A: Diffusion capacity of the lung for carbon monoxide
Measurement of the lungs ability to transfer gases

Q: DLCO method
A: Vital capacity breath of 0.3% CO is held for 10s
Difference in inspired and expired CO concentration is proportional to diffusion capacity

Q: DLCO must be corrected for:
A: Age
Sex
Hb

Q: CVS effects of hypocapnoea
A: Myocardial depression
Peripheral vasoconstriction
- Decreased CBF
Pulmonary vasodilation

Q: Isobestic point
A: Wavelength at which light is absorbed equally by both haemoglobin species
Absorption at the isobestic point is independent of saturation, and is a function of haemoglobin concentration

Q: Isobestic points (wavelengths)
A: 590nm
805nm

Cerebral circulation/Circle of Willis
1 - anterior communicating artery
2 - anterior cerebral arteries
3 - middle cerebral artery
4 - internal carotid (small branch is opthalmic)
5 - posterior communicating artery
6 - posterior cerebral arteries
7 - superior cerebellar arteries
8 - basilar artery (giving pontine arteries)
9 - anterior inferior cerebellar arteries
10 - vertebral arteries
11 - posterior inferior cerebellar arteries
12 - anterior spinal artery
Reference: Brandis, Vander's

Front: Alterations to drug response: Hepatic disease
Back: Absorption:
- Portosystemic shunting produces higher oral bioavailability
- Reduced absorption of lipid soluble vitamins and other substances (e.g., vitamin K, resulting in reduced synthesis of clotting factors dependent upon Vitamin K)
Distribution:
- Reduced protein binding
- Metabolic acidosis affecting ionised drug fraction
- Increased total body water giving higher volumes of distribution
Metabolism:
- Reduced phase I > phase II
Elimination:
- Reduced enterohepatic circulation in obstructive pathologies (redcued effectiveness of OCP and other steroid-based compounds)
- Increased clearance of ordinarily highly protein bound drugs due to reduced protein binding
PD: Hepatic encephalopathy increases sensitivity to opioids and BZDs
Reference: Peck & Hill

Front: Alterations to drug response: Renal failure
Back: Absorption:
- Altered gastric pH
- Altered gut motility as symptom of uraemia (i.e., N/V/D)
Distribution:
- ↑ V_D
- Acidosis altering protein binding and ionization of weak ions
- ↓ protein binding capacity
Metabolism:
- ↓ Renal metabolism of drugs (e.g., prilocaine)
- Uraemia ↓ hepatic reductive and hydrolytic processes (relative sparing oxidation)
Elimination:
- ↓ Renal clearance of active drug, active metabolites and toxic metabolites
Reference: Peck & Hill; CEACCP

Front: Define hormone
Back: Chemical messenger secreted from ductless endocrine glands acting on a remote target organ.
Reference: Power & Kam

Front: Functions of the hypothalamus
Back: Control of autonomic functions
- cardiovascular
- temperature
- feeding
- water balance
- stress response (regulates sympathetic activation of adrenal medulla)
- sexual behaviours
Regulation of pituitary hormones
- direct neural control of the posterior pituitary hormones
- indirect control of anterior pituitary via hypophyseal portal system
Reference: Power & Kam

Front: Factors determining extent of injury following electrocution
Back: Current and current type:
- Current inversely proportional to impedance (dry skin 10^6 Ω.cm^–2)
- Threshold for VF: 100 mA AC, 500 mA (DC)
Frequency:
- Determines fibrillatory potential
- Greatest danger at 50 Hz
- No risk of VF above 100 Hz
Current pathway
Duration of application
Reference: Dr Podcast

Front: Drugs metabolized by CYP2C19
Back: Diazepam
Phenytoin
Omperazole
Clopidogrel (pro-drug)
This enzyme is polymorphic, with no clopidogrel activity in some individuals, and slow hydroxylation of phenytoin.
(note: nomenclature is CYP (family: 45% similarity)(subfamily: 55% similarity)(isoform)
Reference: Peck & Hill

Front: Drugs metabolized by CYP2E1
Back: volatiles
paracetamol
(note: nomenclature is CYP (family: 55% similarity)(subfamily: 45% similarity)(isoform)
Reference: Peck & Hill

Front: Drugs metabolized by CYP3A4
Back: benzodiazepines
fentanil and derivatives
lignocaine
vecuronium
(note: nomenclature is CYP (family: 45% similarity)(subfamily: 55% similarity)(isoform))
Reference: Peck & Hill

Front: What are the volumes of the components of the ECF?
Back: By %TBW (Total 45%):
- Interstitial 20%
- Intravascular 8%
- Transcellular fluid 2%
- Kinetically inactive 15%
-> Dense connective tissue 7.5%
-> Bone 7.5%
Reference: Brandis

Front: What fluids are trancellular?
Back: (fluids surrounded by epithelium)
- CSF
- aqueous humour
- joint fluid
- bile
- bowel fluid
- bladder urine
- peritoneal and pleural fluid
Reference: Brandis

Front: What factors control the distribution of water between ECF and ICF?
Back: Systemic factors:
- Anything which adjusts ECF osmolality
Local factors:
- Many cells have the ability to alter their solute concentration, and/or generate osmoles (idiogenic osmoles; e.g., brain neurones)
Reference: Brandis

Front: Outline the control of total body water
Back: Thirst-ADH mechanism
Sensors:
- osmoreceptors, low and high pressure baroreceptors
Controller:
- hypothalamus
Effectors:
- thirst
- ADH
Reference: Brandis

Front: Define thirst
Back: Conscious sensation of the physiological urge to drink
Reference: Brandis

Front: What is the difference between venous and whole body haematocrit? Why does this difference exist?
Back: Whole body Hct = 0.91 x venous Hct
Due to Hamburger effect (osmotic swelling from chloride shift into cells as a result of H+ production due to carbon dioxide buffering).
Remember, haematocrit = cellular blood volume/total blood volume
Reference: Brandis

Front: What is osmotic pressure?
Back: The pressure which must be applied to a test solution to prevent the net movement of water across a semi-permeable membrane, where the reference solution (on the other side of the membrane) is pure water.
Osmotic pressure of plasma is 5545 mmHg.
Reference: Brandis

Front: How can osmotic pressure be calculated?
Back: With the van't Hoff equation
Osmotic pressure = n x (c/M) x RT
Where:
n = number of particles
c = concentration in g/L
M = molecular weight of molecules
R = 0.082 (universal gas constant in litre.atm K-1 mol-1)
T = absolute temperature (ºK)
Remember:
osmotic pressure is the pressure which must be applied to a test solution to prevent the net movement of water from a reference solution of pure water on the other side of semi-permeable membrane.
Osmotic pressure of plasma (287 mOsm.L^–1) is 5545 mmHg!
Reference: Brandis

Front: Functions of the liver
Back: (SMIDGES)
Synthesis
- All plasma proteins except for VW factor and immunoglobulins
- Esp. coagulation factors
Metabolism (anabolic, catabolic processes)
- Protein
   - ornithine cycle produces ammonia which is critical for the excretion of fixed acids
- Fat
- Carbohydrates
- Steroids
Immune
- Reticuloendothelial system - removal of red cells, encapsulated organisms
- Kupffer cells activate complement, accumulate ferritin, activate other cells
Drug metabolism
- Phase I and Phase II
diGestion
- Bile production
Excretion
- Esp. bilirubin
Storage
- Glycogen
- Fat soluble vitamins
- blood reservoir (450mL, 350ml of which can be mobilised)

Front: Classify antiplatelet drugs
Back: 1. Adhesion
Von Willebrand Inhibitors
- dextran
2. Activation
Prostacyclin (PG I_2)
- epoprostenol directly inhibits platelet activation
Platelet phosphodiesterase inhibition (increase cAMP—paradoxical as platelets are activated by Gs coupled beta-1 adrenoceptors also)
- dipyridamole (also inhibits platelet ADP response)
Cyclooxygenase inhibitors (prevent thromboxane A_2 production needed for activation of further platelets)
- aspirin
3. Aggregation
ADP receptor antagonists (ADP receptors activate GP IIb/IIIa receptors)
- clopidogrel irreversibly binds ADP P2Y_12 receptor
Glycoprotein IIb/IIIa receptor antagonists (prevents platelet aggregation via fibrin linkages between GP IIb/IIIa receptors)
- abciximab (mAB)
- tirofiban, eptifibatide
Remember: platelets adhere, activate, aggregate and stabilize
Reference: Cross & Plunkett

Front: Classify anti-coagulants
Back: Inhibit factor production
- warfarin (inhibits F II, VII, IX and X; proteins C and S)
Inhibit Xa
- LMWHs >> UFH
- direct Xa inhibitors (rivarox-, apix- and edoxaban)
Direct thrombin inhibitors
- dabigatran
Promote anti-thrombin III activity
- UFH (LMWHs do not act via this pathway)
Reference: Peck & Hill

Front: Minimum concentration of adrenaline in ligocaine to reduce systemic absorption
Back: must be >1:200 000 (i.e., 5 µg/mL)
Reference: Examiner Reports

Front: Define emulsion
Back: A fine dispersion of minute droplets of one liquid in another in which it is not soluble or miscible.
By contrast, a suspension is particles of any phase dispersed in a liquid.

Q: Proportion of an acid/base ionised with respect to pKa?
A: Per pH unit change from pKa:
+2   99%
+1   90%
 0    50%
–1   10%
–2   1%

Front: Correspond volume of distribution to fluid compartmental model of the body
Back: 70 mL.kg–1    intravascular (large molecules; e.g., heparin)
200 mL.kg–1 ECF (charged particles, e.g., muscle relaxant)
600 mL.kg–1 total body water (drugs can enter cells; e.g., alcohol)
≥1 L.kg–1 more than total body weight (drug must be highly lipid soluble)

Front: ABCD of enzyme inducers
Back: Alcohol
Barbiturates
Carbamazepine/Cigarettes
Dilantin (phenytoin)

Front: ABCD of low extraction ratio drugs
Back: Asthma drugs (theophylline)
Blood (warfarin)
Carbamazepine
Dilantin (phenytoin)/Diazepam
Reference: Peter Howe

Front: Equation calculating volume of distribution
Back: V_D = Dose/C_0
_
Where C_0 is calculated.
Reference: Cross & Plunkett

Front: Differences in neonatal cardiac physiology
Back: Neonatal heart is:
- Non-compliant
- At higher tension (therefore reduced contractile reserve)
Consequences:
- Excessive preload of minimal consequence
- Reduced preload will impair cardiac output
- Afterload sensitive
Therefore:
- Avoid hypovolaemia (fluid boluses unlikely to harm)
- Avoid bradycardia—CPR if rate <60 BPM
Reference: Ian McKenzie

Q: Define an acid
A: Bronsted and Lowry: Substance which donates a hydrogen ion to solution
Stewart: Substance which increases the hydrogen ion concentration in solution

Q: What is the fixed acid production per day?
A: 10 mmol/kg/day

Front: Define nausea
Back: Unpleasant subjective sensation associated with urge to vomit

Front: Define central sensitization
Back: Increased responsiveness of nociceptive neurons in the central nervous system (i.e., post-synaptic) to their normal or subthreshold afferent input.
Reference: IASP

Front: Mechanisms of central sensitization
Back: Windup
- activity dependent activation mediated by release of additional neurotransmitters (not just glutamate but substance P and cGRP) resulting in prolonged EPP allowing temporal summation
Changes to signal transduction
- phosphorylation of receptor proteins increase activaiton in presence of neurotransmitters
Changes in gene expression
- slow onset, long-lasting, maintained by inflammation and nerve damage
Connections between A beta and C fibres
- producing allodynia

Front: Define neuropathic pain
Back: Pain caused by a lesion or disease of the somatosensory nervous system
Reference: IASP

Front: Describe the course of the internal jugular vein
Back: Origin:
jugular foramen
Course
- travels inferiorly in the carotid sheath (with internal carotid and vagus nerve)
- initially posterior to, then lateral and then anterolateral to the carotid artery during its descent
Termination:
joins subclavian vein at sternoclavicular joint
Reference: FRCA

Front: Structures penetrated during insertion of epidural needle
Back: Skin
Subcutaneous tissue
Supraspinous ligament
Interspinous ligament
Ligamentum flavum

Front: Contents of epidural space
Back: Fat
- Varies in direct proportion to the rest of the body
- Not uniform in distribution; exists in bands at level of intervertebral foramina
Dural sac
- Ends at approximately S2. Contains the spinal cord (to the lower border of L1) and cauda equina
Spinal nerves
- In pairs
- Dorsal root ganglia in lateral recesses
Vessels
- anterior > posterior venous plexus (engorged in pregnancy)
Connective tissue
- Variable dorsomedian folds, median fold
- After leakage of nucleus pulposus, surgery or previous epidural catheterization may be heavy scar tissue
Reference: CEACCP

Front: Obligate glucose utilizers
Back: Brain (can use other substrates in addition)
Red cells (exclusively)
Reference: Adam Skinner

Front: List quantity and potency of hormones secreted by the thyroid
Back: Thyroxine (T4) 80mcg – 1/3 converted peripherally by deiodination
Triiodothyronine (T3) 4 mcg (5 times potency)
Reverse T3 (inactive)
Reference: Adam Skinner

Front: Characterize the structure and secretions of the adrenal gland
Back: Cortex, consisting of 3 zones (GFR):
- glomerulosa - aldosterone, corticosterone
- fasciculata - cortisol, corticosterone, sex steroids
- reticularis - cortisol, corticosterone, sex steroids
Medulla
- catecholamine
Reference: Adam Skinner

Q: What is the role of the liver in acid-base homeostasis
A: Buffer production
- Albumin
Production of volatile acid
Metabolism of acids and bases
- Intrinsic
    - Lactate
- Extrinsic
    - Drugs
Production of fixed acids
- Urea

Front: Compare Static and Dynamic compliance
Back: Static
- measured at static volumes to exclude non-elastic resistance
- V_T/(P_plat – PEEP)
Dynamic
- measured during normal breathing at points of no flow (end expiratory, end inspiratory)
- includes airway resistance
- V_T/(P_max – PEEP)
Remember:
1/total compliance = 1/chest wall + 1/lung (compliance = 1/elastance)
Compliance measurements (remember, always inside - outside)
lung: alveolar - pleural
chest wall: pleural - atmospheric
total: alveolar - atmospheric
Reference: Stan Tay

Front: Renal handling of glucose
Back: - Freely filtered
- Secondary active co-transport with Na+ by S-GLUT transporter
- Totally reabsorbed in PCT if BSL <11 mM
- BSL >11 saturates transporter, causing glycosuria + osmotic diuresis

Front: Renal hormones which affect blood pressure
Back: EPO
- Red cell mass
RAAS
- ECF volume
- SVR

Front: At what point does hypoxaemia produce hypoxia?
Back: Hypoxaemia = arbitrarily defined as pO2 of 60mmHg
Hypoxia = inadequate oxygenation of tissues resulting in anaerobic metabolism
Occurs at delivery of <500mL per minute (50% of normal O2 delivery) indicated by lactaemia
Reference: Stan Tay

Front: Define drug
Back: Substance administered to cause a change in a physiological system

Front: Mechanisms of drug action
Back: Interact with body systems to cause a physiological change via:
- Receptor-ligand
- Ion channel
- Enzyme
- Physicochemical

Front: Define ageing
Back: Universal and progressive physiological (as opposed to pathological) phenomenon characterized by degenerative changes in the structure and functional reserve in organ systems.
Major processes:
1. senescence - apoptosis
2. changed cellular architecture - fibrosis

Front: Respiratory system changes during normal ageing
Back: Chest wall
↓ Compliance due to muscle weakness and joint degeneration
Restrictive functional impairment
Leads to an ↑ reliance on diaphragmatic breathing
Lung parenchyma
↓ Elastin-producing cells, replaced by collagen
↓ Alveolar surface area, ↓ bronchial calibre, decreased recoil and increased distensibility
Spirometry
↓ VC
↑ RV
↑ CC
Gas exchange
↑ A-a gradient due to ↑ CC relative to FRC
Central control
↓ Responsiveness to CO_2 and O_2

Front: Thermoregulatory changes in normal ageing
Back: Increased variance of core temp at rest
- lower heat production
- lower set point
Response to cold
- reduced response due to decreased BMR and muscle mass
Response to heat
- reduced response due to less sweating, and elevated core temp at which responses are triggering

Front: Nervous system changes in ageing
Back: Loss of nerve fibres (both centrally and peripherally) AND depletion of neurotransmitters (reduced synthesis and increased destruction), resulting in:
Central:
Reduced cognition
- short term memory capacity reduced >40% after 60 years old
Reduced CBF and CMRO2 proportionally to reduced neural density
Pre-disposition to post operative delirium and cognitive impairment (POCD)
Peripheral:
Reduced conduction velocities due to loss of myelin
Muscle atrophy due to denervation
Loss of response of autonomic organs despite increased catecholamine levels

Front: Pain changes in normal ageing
Back: Patient report
- ↓ Reporting (verbal descriptors better than VAS)
Clincal reponse
- ↑ Threshold in response to thermal pain
- Equivocal threshold in response to mechanical pain
Microscopic changes:
Peripheral nervous system
- ↓ Unmyelinated>myelinated fibres
- ↑ Damaged or degenerative nerve fibres
- ↓ Number and function of peripheral nociceptors
Central nervous system
- ↓ Myelin in dorsal horn
- ↓ Number of opioid receptors
- ↓ Neurotransmitter synthesis/transport/receptor binding throughout CNS

Front: Pharmacokinetic changes in ageing
Back: Absorption
- largely unchanged in normal ageing
Distribution
- larger volume of distribution of lipid soluble drugs (greater % fat)
- reduced albumin (implications for acidic, neutral drugs)
- increased a1ACP (implications for basic drugs)
Metabolism:
- decreased hepatorenal function (start with lower doses of organ-dependently cleared drugs)
- paracetamol clearance and metabolism preserved
- organ independent processes largely unchanged
Excretion:
age-related decline in GFR

Front: Pharmacodynamic changes in ageing
Back: "More sensitive" due to reduced functional reserve of all organ systems
Hyporesponsiveness to catecholamines
Impaired compensatory mechanisms

Front: What is INR?
Back: Laboratory test of the extrinsic and common pathways.
Involves the addition of tissue factor and calcium to citrated, platelet poor plasma at 37ºC.
Time to clot formation gives prothrombin time, then adjusted by calibration factor to give INR.
Only test sensitive to factor VII deficiency.

Front: Prevalence of ABO groups
Back: A 45%
B 9%
AB 3%
O 43%

Front: Describe the immunogenic components of red cells
Back: Universal antibody expression:
- ABO - most immunogenic, on H antigen stem
Inconsistent antibody expression:
- Rhesus - antibodies dependent upon previous exposure
- Kell system - antibodies results from previous exposure to multiple blood products

Front: Define shivering
Back: Involuntary, oscillatory, muscular activity that augments metabolic heat production

Front: Typical ABG at term pregnancy
Back: PaCO_2 30
PaO_2 103
pH 7.44
HCO_3^– 20

Front: Factors affecting gravid uterine blood flow
Back: No placental autoregulation, so flow is a function of myometral and placental flow:
- Uterine artery pressure
- Uterine venous pressure (IVC compression may significantly decrease perfusion pressure)
-Ri_N-PL (non-placental intrinsic resistance), responds to vasoactive drugs
- Ri_PL (placental intrinsic resistance), spiral arterioles, respond to vasoactive drugs
- IUP (contractions cause starling resistor behaivour)
- Extrinsic vascular resistance (contractions cause reduced placental and myometrial flow)

Front: Categorize tocolytics
Back: Calcium channel blockers (e.g., nifedipine—first line)
Beta_2-adrenoceptor agonists
Oxytocin antagonists (i.e., atosiban)
NSAIDs (e.g., indomethacin)
Glyceryl trinitrite
Inhalational agents
Acidosis, hypoxia

Front: Outline the treatment of hypertension during pregnancy
Back: Methyldopa (first line)
- centrally acting alpha-adrenergic agonist
Labetalol (additional, second-line agent)
- non-selective beta-blocker and alpha-1 blocker
- preserves uterine blood flow (minimal fetal transfer—unique among beta blockers as most cause fetal bradycardia)
Hydralazine
- direct arteriolar vasodilator (minimal venodilation and therefore reduced postural hypotension)
- tachycardia and flushing
Nifedipine (third-line)
Outpatient
- methyldopa > labetalol > nifedipine
Inpatient
- labetalol or hydralazine > nifedipine
NOTE:
- angiotensin-related drugs contraindicated—TERATOGENIC
- MgSO4 is not anti-hypertensive but is fetally neuroprotective and anti-convulsant specifically in eclampsia
- general anaesthetics, opioids and regional anaesthetic techniques have an important role

Front: Factors affecting VD
Back: Drug
- lipid solubility
- plasma protein binding
- molecular size
- pKa
Patient
(all affect pH, protein binding, total body water and/or body composition)
Physiological
- pregnancy
- age (neonates are acidaemic and wet; elderly have reduced vessel rich tissue)
Pathological
- renal failure
- liver failure
- obesity
- acid-base disturbance

Front: Outline the events during and following NA release from a nerve terminal
Back: (1) NA synthesised and stored in neuronal vesicles
(2) Action potential permits Ca2+ entr y stimulating
(3) Exocytosis of NA into synaptic gap.
(4) NA binds to receptors on effector cell.
(5) Three things can happen:
- NA binds to presynaptic α-2 receptor, inhibiting further NA release
- NA binds to presynaptic β-receptor to enhance reuptake of NA
- Extraneuronal uptake absorbs NA into effector cell (7), where it is metabolized by COMT/MAO with overflow occurring systemically (8).
Reference: Stoelting

Front: Why are humidification devices required during mechanical ventilation?
Back: Airway devices bypass the humidifying effect of the upper airways resulting in dry, cold supply line gas being delivered directly to the lower airways.
This increases the viscocity of the mucous which is essential for the functioning of the mucociliary elevator.
This dessication occurs until the isothermic saturation boundary is reached, which is the airway level at which body temperature and 100% relative humidity is achieved.
Reference: BJA/CEPD Reviews/Vol 1 No 2 2001

Front: What is the operating principle of a heat and moisture exchange filter?
Back: Inline breathing circuit device, consisting of:
- moisture exchange layer
- filter layer
Moisture exchange layer
Consists of a pleated, hygroscopically coated foam or paper
Expired gas cools as it passes, condensing onto the foam, with condensation promoted by hygroscopic coating (usually this is NaCl). The latent heat of vaporization is released to the substrate.
Inspired gas is heated and humidified when it passes in the opposite direction. Therefore, the gas is heated and moistened dependent upon the patient's core temperature and the condition of the airways.
Filter layer
Typically a electrostatic or hydrophobic material
Reference: BJA/CEPD Reviews/Vol 1 No 2 2001

Front: What are the levels of machine check?
Back: Level one:
- performed by service personnel
- performed for systems being placed into service (new or following service)
- detailed, ensures calibration, electrical safety testing, comprehensive leak testing
Level two:
- performed prior to starting each list by the anaesthetist or an appropriately trained delegate
- ensures servicing date and functioning of gas supply, vaporizers, breathing circuit, scavenging and alternative means of ventilation
Level three:
- performed by the anaesthetist prior to every anaesthetic
- involves full check of any equipment which has been changed (which if almost anything has been, will effectively be a level two check)
Reference: ANZCA PS31 (2014)

Front: What components commonly contribute to surgical fire?
Back: Fire triad required to cause fire—oxidizer, fuel and ignition source.
Oxidizer:
Substance which contributes to combustion more than air does (generally by supplying oxygen)
- O_2, NO, N_2O and H_2O_2
_
Ignition source:
Anything capable of producing a spark or flame.
Electrical
- defibrillator, diathermy, faulty/inappropriate equipment, static build-up
Friction
- drills, burrs
Heat/Light
- LAZER devices, argon beam coagulators, heated probes
Fuel:
Store of potential energy capable of participating in a reaction with an oxidizer
- Equipment
- Preparation solutions
- Patient sources (e.g., bowel gas)
Reference: CEACCP

Front: Outline the management of a surgical fire
Back: - sound alarm
- stop all gases
Involving patient:
- quench or smother with anything immediately at hand—consider CO2 extinguisher if this is not successful
- remove all fuels (including endotracheal tube if any suggestion of airway fire)
Involving equipment:
- stop medical gas supply
- attempt to extinguish
- evacuate
Reference: CEACCP

Front: What are the components of a scavenging system?
Back: Note: 4 and 5 are often combined; typically only open scavenging interface with active disposal is used in Aus.

Front: Define scavenging. Why is it necessary?
Back: Scavenging is the removal and safe disposal of waste anaesthesia gasses from the breathing circuit to avoid contaminating the theatre environment.
Hazards of poor scavening to staff are:
- impaired cognition and fatigue
- spontaneous abortion and reduced fertility in females
- reduced fertility and female>male offspring in males
- ?haematological malignancy
- ?hepato-renal dysfunction

Front: Describe the washout of a volatile anaesthetic
Back: Characterized in terms of F_A/F_A0
Initial phase:
- washout of circle circuit and FRC
- this establishes wash-out concentration gradient
Terminal phase:
- washout of tissues via central compartment
- compartmental washout determined largely by tissue:blood coefficients, which calculate time constants (=T:B/perfusion)—remember 3x time constant ~ 95% of exponential process
- most modelling consists of VRG (including brain) which accounts for 75% of cardiac output, large fat and muscle groups (with much, much longer time constants—not saturated until >24 hours) and smaller vessel-poor group (e.g., bone)
Note: obese individuals have unusually large volumes of well-perfused fat tissue in the omentum and peri-viscera, resulting in dramatic increase in time to MAC_AWAKE

Front: Describe the synthesis of haem
Back: Occurs in mitochondria.
Protoporphyrin + Fe^2+ ––> haem
Reference: Kam & Power (3e)

Front: How can humidity be measured?
Back: Relative:
Hair hygrometer
Wet and dry bulbs
Relative and absolute:
Regnault's hygrometer
Absolute:
resistance and capacitance transducers
mass spectrometry
ultraviolet spectrophotometry

Front: Michaelis-Menten equation. What does it describe?
Back: Describes the transition from non-linear to linear kinetics as drug concentration increases.
V = C_outflow / (Km + C_outflow)
where: Km = concentration of drug at 50% enzyme capacity
Metabolism increases proportionally with concentration as long as the metabolic organ outflow concentration is less than half Km, which corresponds to a metabolic rate that is roughly one-third of the maximal rate.
Metabolism is proportional to concentration, meaning that clearance is constant, for typical doses of all intravenous drugs used in anesthesia.
Reference: Stoelting

Front: What is glomerulo-tubular balance? What are the causative mechanisms?
Back: Phenomenon of sodium and water reabsorbtion in the PCT matching increases in GFR.
Occurs via two mechanisms:
1. Increased glucose and amino acid load results in increased co-transport of sodium
2. When GFR is increased, glomerular capillary oncotic pressure is increased, enhancing reabsorbtion in proximal convoluted tubule
Reference: Kam & Power

Front: What is the mechanism of pressure diuresis?
Back: Autoregulation via myogenic and tubuloglomerular feedback operate only in cortical nephrons. Juxta-medullary nephrons are not autoregulated myogenically.
At high MAP, perfusion to this small population of nephrons (10% of total) increases dramatically, resulting in a disproportionate increase in filtration and a dissipation of the medullary hyperosmolarity via vasa recta flow, resulting in an increased urinary loss of water and solutes.
Reference: Kam & Power

Front: Effects of the transfusion of 1000mL of autologous blood
Back: 20% increase in vascular volume resulting
Haemodynamics
- increased cardiac output, raised MAP
Baroreceptor response
- venodilation and pooling of venous blood
- reduced ADH secretion (threshold for low-pressure baroreceptors is 8-10%)
No osmoreceptor response as fluid is isotonic
Autoregulatory response
- constant organ perfusion maintained, preventing sustained increase in cardiac output due to increased afterload
Capillary dynamics
- increased hydrostatic pressure causing increase in interstitial water (modest)
Renal response
- increased urine output due to reduced ADH and pressure diuresis
Reference: Brandis

Front: Effects of rapid transfusion of 1000mL of 5% dextrose
Back: Initial intravascular effects rapidly dissipated across total body water
ECF:ICF volume = 1:2
ISF:IVF volume = 3:1
Therefore, only 85 mL increase in IVF
No baroreceptor response
Osmoreceptor response:
- osmotic pressure decreased by 7 mOsm (2.5%) so threshold achieved leading to:
  - decreased ADH resulting in renal output of dilute urine
  - suppression of thirst
Reference: Brandis

Front: Effect of rapid infusion of 1000mL of 4% albumin
Back: Fluid remains intravascular resulting in increased cardiac output, increased MAP resulting in high- and low-pressure baroreceptor responses and autoregulatory response of tissues preventing further increases in MAP.
No osmoreceptor response.
Reference: Brandis

Front: Describe the EEG changes associated with non-REM
Back: Wakefulness - Beta waves
Drowsiness - Alpha waves
 Stages 1-2
- High-frequency, low amplitude EEG
   - stages 3-4 ("slow wave sleep"; high amplitude, low-frequency EEG)

Front: How do damping and resonant frequency affect the reproduction of an arterial waveform?
Back: Note that as natural frequency increases, the acceptable range of damping coefficients increases
Reference: McLintic

Front: The van't Hoff equation
Back: Osmotic pressure = n x (c/M) x RT
n = no. of dissociated particles
c = conc. In g/L
M = molecular weight
R = Universal Gas Constant (0.082)
T = absolute temperature (K)
Remember: osmotic pressure is the hypothetical pressure which must be applied to a test solution when placed opposite pure water across a semi-permeable membrane.
Reference: Brandis

Front: Define the doppler effect
Back: The difference in sound frequency between emitter and observer as a result of relative velocity between the two bodies.

Front: Describe the intracranial elastance relationship
Back: Remember, elastance is change in pressure per change in volume (inverse of compliance which is change in volume per change in pressure).
Reference: Cross & Plunkett

Front: Properties favouring transdermal administration
Back: (a) combined water and lipid solubility
(b) molecular weight of <1,000
(c) pH 5 to 9 in a saturated aqueous solution
(d) absence of histamine-releasing effects
(e) daily dose requirements of <10 mg

Front: Mass spectrometer: operating principles
Back: "Scans" spectrum of mass:charge by altering the deflection force of the magnetic fields.
Reference: Aston

Front: Function of thromboxane
Back: Vasoconstriction
Binds TP receptor (GPCR) causing platelet activation

Front: Role of prostacyclin (PGI_2)
Back: Binds IP1, IP2 causing:
- Vasodilation
- Platelet inhibition
- Bronchodilation

Front: Role of PGE_2
Back: Vasodilation (including afferent arteriole)
Bronchodilation
Gastric mucous production
Impairs platelet aggregation

Front: Role of PGF_2α
Back: - Bronchoconstriction
- Pulmonary vasoconstriction
- Uterine contraction

Q: Expected PaCO2 in metabolic acidosis
A: CO2 should be close to the last two digits of the pH

Q: Acids are ionised ... their pKa
A: Above

Q: Bases are ionised ... their pKa
A: Below

Q: LCx territory
A: Inferolateral wall segment

Q: Change in gas solubility with a decrease in temperature
A: Gas solubility increases as temperature falls.
This is due to reduced kinetic energy of molecules, preventing dissociation.

Q: pH-stat method
A: CO_2 is added to the circuit so that pH and PaCO_2 are normal when corrected for temperature

Q: alpha-stat method
A: pH and CO_2 are maintained at 'normal for 37°C'.
This means patient will have a measured:
- Increased pH
- Decreased pCO2

Q: Lower Oesophageal Sphincter is
A: The distal 2-4cm of oesophagus
Macroscopically indistinguishable from the rest
Higher nerve cell density and can constrict at a higher pressure
Important in maintaining barrier pressure

Q: Barrier Pressure is
A: The pressure difference between the LoS and the stomach
Typically~20mmHg

Q: Classify the things affecting barrier pressure
A: Changes in:
- LoS pressure
- Gastric pressure

Q: Factors affecting LoS pressure
A: Swallowing
- Decreased during, transiently increased post
Age
- Decreased at extremes of age
Diaphragm
- Pinchcock action exerted by diaphragm
- Lost in hiatus hernia
Stomach
- Flap valve formed by stomach occludes GOJ at high gastric pressures
Hormonal
Drugs

Q: Hormones increasing LoS tone
A: Increased tone:
- Gastrin
- Motilin
- α-agonists

Q: Hormones decreasing LoS tone
A: Progesterone
Glucagon
Vasoactive intestinal peptide (VIP)

Q: Drugs decreasing LoS tone
A: ETOH
IV and volatile anaestetic agents
Anticholinergics

Q: Drugs increasing LoS tone
A: Suxamethonium
Metoclopramide
Anticholinesterases

Q: Gastric pressure is a function of
A: Intraabdominal pressure
 - e.g. obesity, pregnancy)

Q: Unit of airways resistance
A: cmH_2O/L/sec

Q: Solubility of CO2 compared to O2
A: 20x

Q: Changes in BP waveform at different sites
A: Waveform becomes more exaggerated, with greater gradients.
SBP increases, DBP decreases. MAP is constant.
The dicrotic notch appears later and is less sharp.

Q: Half-life of warfarin dependent clotting factors
A: Protein C: 8 hours
Protein S: 30 hours
II: 24 hours
VII: 4-6 hours
IX: 24 hours
X: 48-72 hours

Q: Classify the factors relating to local anaesthetic toxicity
A: Drug factors
Block factors
Patient factors

Q: Local Anaesthetic Toxicity: Drug Factors
A: Drug used
- CC/CNS ratio of the drug
- Racemic vs. entantiopure preparations
- pKa
- Lipid solubility
- Protein binding
Dose used
- Infusions more likely than single shot
- Rate of administration vs. clearance

Q: Block factors affecting LA toxicity
A: Site
Use of adjuncts
Technical factors

Q: Patient factors affecting LA toxicity
A: Blood flow to affected area
α1-acid glycoprotein level
- Deceased level increases free drug fraction, increasing toxicity
Hepatic disease
Age
- Clearance reduced in children and elderly
Acidosis
- Increased unionised portion

Q: Mechanism of cardiac toxicity of LAs
A: Blocking of the Na^+ (and potentially the K^+ and Ca^2+ channels)
- Toxicity related to time that LA spends bound to receptor
Direct myocardial depressant effect
- Reduces cAMP via action on metabotropic receptors

Q: Phases of cardiac LA toxicity
A: Initial phase:
- HTN
- Tachycardia
Intermediate phase:
- Myocardial depression
- Hypotension
Terminal phase:
- Severe hypotension
 - Vasodilation
- Arrythmias
 - Bradycardia
 - Heart block
 - VT, VF, asystole

Q: Phases of CNS toxicity of LAs
A: Initial excitatory phase (interneurone blockade):
- Perioral tingling
- Slurred speech
- Tremulousness
- Confusion
- Convulsions
Inhibitory phase:
- Coma
- Apnoea

Q: Additives to Propofol
A: - 10% soya bean oil (protein free)
- 1.2% egg lecithin (emulsifier, not allergenic)
- 2.5% glycerol (for tonicity)
- Trace NaOH
- Bacteriostatic agents:
   - Generics: sodium metabisulphate
   - Diprivan: disodium edetate (less allergenic)

Q: Propofol: MoA
A: Positive allosteric modulator at:
- GABA_A
- Glycine receptors
Antagonist of:
- Neuronal nicotinic ACh receptors
- D2 receptors (anti-emetic)

Q: Propofol: Induction Dose
A: 2.5-3.5 mg.kg^-1 (children)
1-2 mg.kg^-1 (adults)

Q: Propofol: Effect site concentration to maintain anaesthesia
A: 4-8 µg.mL^-1 plasma concentration

Q: Gay-Lussac's Law
A: Pressure exerted by a gas is proportional to temperature
(For a given mass and constant volume)

Q: The shunt equation is only valid when:
A: The shunt is from mixed venous blood

Q: Renal handling of urea
A: 100% filtered
- 50% reabsorbed in the PCT
- 50% secreted into the loop of Henle
- 50% reabsorbed in CD (augmenting the counter-current mechanism)
Net result is approximatey 20-50% is excreted, depending upon hydration status.

Q: Ticagrelor: MoA
A: Reversible non-competitive antagonist of ADP at P2Y_12 receptor, preventing activation of Gp IIb/IIIa receptor

Q: Daily bicarbonate load filtered by the kidney
A: 4 to 5 mol.day^–1
Filtered load = [HCO3–] x GFR = 24 mmol x 180 L.day^–1 = 4 000 to 5 000 mM
- Once plasma bicarbonate exceeds approximately 28 mmol.L^–1, it appears in the urine

Q: Adrenal gland is different from other sympathetically innervated organs because
A: It is a modified sympathetic ganglion
Innervated by pre-ganglionic fibres, and stimulated by ACh

Q: Synthesis of ACh
A: Produced in nerve cytoplasm from choline and Acetyl-CoA by acetyltransferase
Choline from diet and recycled ACh.
Acetyl-CoA produced in mitochondria

Q: Amount of ACh per vesicle
A: ~10,000

Q: Number of vesicles released per action potential
A: ~200

Q: How is ACh broken down by AChE
A: Anionic site binds quaternary ammonium moity
Esteratic site binds ester group
Once bound, ACh is acetylated then hydrolysed to acetic acid

Q: Structure and location of the nicotinic ACh receptor
A: Ionotropic (Na+, K+, Ca2+)
Five subunits (Two α, one β, one γ, one δ (ε in the foetus))
Located in:
- Post-synaptic NMJ
- Preganglionic ANS
- Brain

Q: Muscarinic ACh receptor properties and subtypes
A: Metabotropic (GPCR) - Subtypes:
 - M1: Secretory and CNS
 - M2: Heart
 - M3: Bronchi and arterioles
 - M4 & 5: CNS

Q: G-protein receptor properties, subunits, and function
A: - Metabotropic
- Membrane bound protein with 7 helical regions traversing the membrane and a selective ligand binding site
- Hetreotrimeric (three units; α, β, γ)
- Bind GDP - on activation replaced by GTP and the α-GTP subunit dissociates
- Activate second-messenger proteins, causing a cascade

Q: G-protein receptor subtypes
A: Gs
- Stimulatory
- Increase cAMP, leading to a biochemical effect
Gi
- Inhibitory
- Inhibit adenylyl cylase, reducing cAMP
Gq
- Variable effect
- Activate phospholipase C. Affects:
 - IP3, and therefore Ca2+ release
 - DAG, protein kinase C, with variable effect

Q: Factors in sample size calculation
A: - Acceptable Type I error (α)
- Acceptable Type II error (β)
- Effect size
- Population variance
- Study design
- Cost
- Participant availability

Q: Methods to assess neuromuscular blockade
A: Clinical
- Head lift >5s
- > 10ml/kg Vt
- Tongue protrusion
Electrical
- Uses a nerve stimulator
- Tactile/visual
- Electrical
 - Accelerometer
 - Force transduction
 - EMG

Q: Properties of a nerve stimulator
A: Consists of two electrodes, power supply, controls
Produces a:
- Monophasic
- Square wave
- Constant current lasting <0.3ms
- Supramaximal stimulus (25% greater than maximum required)

Q: Neuromuscular stimulation patterns
A: ToF
Tetantic stimulation
PTC
Double Burst
Single Twitch

Q: Define Fade and why it occurs
A: Reduction of twitch height with repeated stimuli during a partial neuromuscular block.
Occurs due to the effect of non-depolarising agents on the presynaptic membrane, reducing ACh production.

Q: Process of ToF monitoring
A: Four identical 2Hz stimuli 0.5Hz apart (1.5s total)
Number and amplitude of observed twitches indicate degree of blockade.
Can be measured using either total number of twitches or ToF ratio.
Can repeat up to every 10s.

Q: Tetanic stimulation process
A: High frequency (50-200Hz) stimulation for 5s
Normal muscle: tetanic contaction
Partially blocked muscle: fade (proportional to degree of blockade)

Q: Post Tetanic Count process
A: Tetanic stimulus is given, followed 3s later by single twitches at 1Hz.
Response seen prior to return of twitches on ToF.
Typically, a ToF of 1 will occur when the PTC ≈ 9.
Should not be repeated faster than every 6 minutes.

Q: Define Post Tetanic Facilitation
A: Increase in neuromuscular response following a tetanic stimulus.
Duue to the tetanic stimulus mobilising ACh vesicles into the prejunctional area.

Q: Double burst process
A: Two 0.2ms 50Hz (tetanic) stimuli are applied 750ms apart.
Identical contractions in normal muscle.
Reduced amplitude of second contraction in partially paralysed muscle.

Q: Single twitch stimulation process
A: A single stimulus lasting ~0.2ms is applied.
> 75% blockade causes a depressed response.
Twitch must be assessed prior to blockade to establish baseline.

Q: Changes to sleep with age
A: Neonate: 16-18 hours/day (50% REM)
Infant: 10 hours/day (20-25% REM)
Adult: 6-8 hours/day (15-20% REM)

Q: Purpose of Sleep
A: - Energy conservation
- Preservation of cognitive function (deprivation results in decline)
- Memory formation

Q: Endocrine changes during sleep
A: Endo:
- Increased ADH secretion
- Melatonin at onset of darkness (inhibited by bright light) induces sleep
- Growth hormone during first episode of slow-wave sleep (stage III-IV)
- Cortisol troughs early in the morning and peaks rapidly after waking

Q: CVS changes during sleep
A: - NREM: Reduced CO/SVR
- REM: Normal CO/SVR

Q: Resp changes during sleep
A: - Decreased MV due to decreased Vt
- Loss of airway tone

Q: Nervous and MSK changes during sleep
A: NREM:
- Reduced SNS activity
REM:
- Paralysis (tonic REM)
- Twitches (phasic REM)

Q: Classify devices for measurement of cardiac output
A: Invasive:
- Thermodilution
- PiCCO
- TOE
- Fick
Non-invasive:
- TTE
- MRI
- Thoracic impedance

Q: Optimal features of a pressure transduction system
A: Resonant frequency 30x that of the frequency to be measured
Optimally damped

Q: Irritant receptors in the lung cause
A: Bronchoconstriction and hyperpnoea

Q: Clopidogrel: Indications
A: - Prevent thrombosis in PVD
- Combined therapy in MI
- Combined therapy post-PCI to prevent stent failure

Q: Dantrolene: Uses
A: - Malignant hyperthermia
- Neuroleptic malignant syndrome
- Ecstasy intoxication
- Chronic muscle spasticity

Q: Dantrolene: Pharmaceutics
A: - 20 mg sodium salt as orange lyophilized powder
- Excipients: 3g mannitol, sodium hydroxide
- Reconstituted with 60 mL water
- pH 9.5

Q: Dantrolene: MoA
A: Blocks ryanodine receptor preventing sarcoplasmic release of calcium

Q: Define capacitance
A: Ability of a system to store electrical charge.
Measured in Farads.

Q: Capacitor properties:
A: - Oppose DC flow (no electrons can actually flow unless breakdown voltage is reached)
- Allow AC flow

Q: Define inductance
A: Property of a conductor by which a change in current induces an electromotive force in the conductor and any nearby conductors.
Measured in Henry's.

Q: Properties of inductors
A: - Resist rate of change of current flow (e.g., high frequency AC)
- Permit constant flow (constant DC)

Q: Sugammadex: MoA
A: Forms complex with aminosteroid muscle relaxants (particularly rocuronium)

Q: Sugammadex: Dosing
A: PTC 0/post RSI: 16mg/kg
PTC > 1: 4mg/kg
ToF > 2: 2mg/kg

Q: Sugammadex: Adverse effects
A: Bradycardia (rare)
Hypersensitivity

Q: Mapleson D Circuit structure
A: - FGF at patient end
- Release valve and reservoir at other end of tubing

Q: Mapleson D circuit flow requirements
A: Required flow to prevent re-breathing:
- 2 - 4 times minute ventillation (spontaneous breathing)
- 1 - 2 times minute ventillation (controlled breathing)

Q: Mapleson D circuits: Advantages
A: - Low resistance
- Tubing can be of infinite length (increases resistance)
- Efficient for controlled breathing

Q: Factors affecting re-breathing in Mapleson circuits
A: - Circuit design
- Fresh gas flow
- Minute ventillation
- Spontaneous vs. controlled ventillation

Q: Semi-closed circuits:
A: Do not entrain room air

Q: IgA function
A: Dimers in mucous, acts to opsonize pathogen

Q: IgE function
A: Binds to Fc receptors on mast cells and basophils, and triggers degranulation in response to antigen binding

Q: IgG function
A: Mediates secondary immune response
75% of total immunoglobulin.

Q: IgM function
A: Immediate immune response

Q: Normal gastric pH
A: 1.4

Q: Define fasting
A: Metabolic state achieved after complete digestion and absorption of a meal prior to the onset of starvation

Q: Define voltage
A: Potential difference which dissipates 1 W of energy per 1 A of current

Q: Types of electrical injury
A: VF
- Function of current density and frequency
Burns
Tetanic contraction
- Can cause asphyxiation due to sustained muscle contraction

Q: Microshock
A: Current required to induce VF when applied directly to myocardium
0.05-1mA
Requires skin breach
- Guidewire
- Pacing lead
- Conducting fluid

Q: Macroshock
A: Induces VF from surface contact
100mA

Q: Methods of electrical safety
A: Insulation
Fuses
Residual Current Devices
Line isolation supply with a line isolation monitor
Equipotential earthing

Q: How does a fuse work
A: Ceases all current flow when current exceeds threshold (typically 20A)
Requires:
- A fault that causes a high current to flow
- A working fuse

Q: How does a RCD work?
A: Measures the current difference between the active and neutral lines, and will disconnect power within 10ms if a >10mA difference exists.
Non-fault: No current difference
Fault: Current difference, as current delivered via active will not be returned via neutral.

Q: Pros and cons of RCDs
A: Pros: Safe
Cons: Will shut off power to device when a fault occurs (bad for devices without a battery backup)

Q: How does a Line Isolation Supply work?
A: Line isolated supply: 'Transformed' supply creating an earth-referenced floating supply.
Two faults are required to complete a circuit:
- Active wire to fault to ground
- Neutral wire to fault to ground

Q: How does a line isolation monitor work?
A: Safety device for a line isolation supply.
LIM alarms if the prospective hazard current exceeds 20mA. This is the amount of current that could flow IF a second fault completed the circuit.
LIM checks the impedance between the active wire and the ground, and the neutral wire and ground.
No fault: Both impedances should be the same and close to infinite
Single fault: Calculated impedance of one line will be significantly lower, and therefore the prospective hazard current increases.

Q: Electrically safe equipment classifications:
A: I: Earthed
- Any part that can contact the user is earthed to ground
II: Double-insulated
- All parts of the device that the user can touch have two layers of insulation
III: Low-voltage
- Device is <40V DC, 24V AC

Q: Classification of Electrically Safe Areas:
A: B areas: Macroshock protection
- RCD
- LIM
BF areas: Cardiac protection
- Equipotential earthing
Z areas: No particular protection

Q: State the Fick Equation solved for MVO2
A: CMVO2 = CaO2 - VO2/Q

Q: Platelet Plug Formation: Activation stimulants
A: Collagen
Adrenaline
ADP
Thrombin

Q: Rate of onset of a volatile anaesthetic agent is dependent on (headings only)
A: Uptake of agent into:
- Alveoli
- Blood
- CNS

Q: Define MAC
A: The minimum alveolar concentration at steady state which prevents a movement response to a standard surgical stimulus (midline incision) in 50% of a population.
- Does not reflect lack of awareness (reflects action on spinal reflexes)
- Only valid at 1atm
- Unpremedicated patient

Q: Properties of MAC
A: - Inversely proportional to agent potency (as per Meyer-Overton hypothesis)
- Normally distributed
- Additive (use of multiple agents is additive)
- Estimated clinically with end-tidal gas measurement

Q: Variations of MAC
A: MAC awake
- Typically 1/3rd of MAC for most agents
MAC-BAR
- Minimum alveolar concentration required to block adrenergic response, i.e. to prevent a rise in HR or BP following skin incision.
MAC95
- The MAC required to prevent a movement response to a standard surgical stimulus in 95% of the ppulation.
MAC.hr-1
- The amount of time a patient is exposed to 1 MAC of an agent. Used to compare different agents.

Q: Factors decreasing MAC
A: Physiological factors:
- Age (decreases ~6% per decade over 40)
- Hypothermia
- Hypocapnoea
- Hyponatraemia
- Hypothyroidism
- Hypovolaemia
- Hypotension
- Hypoxia
- Pregnancy
- Anaemia
Pharmacological factors:
- Acute ETOH and CNS depressant intoxication
- Lithium
- Chronic amphetamine use

Q: Factors increasing MAC
A: Physiological factors:
- Youth
- Hyperthermia
- Hypercapnoea
- Hypernatraemia
- Hyperthyroidism
- SNS tone
- Increased Patm
Pharmacological factors:
- Chronic ETOH and CNS depressant abuse
- Acute amphetamine intoxication

Q: Define partition coefficient
A: Describe the relative affinity of an agent for two phases.
Defined as the ratio of the concentration of agent in each phase, when both phases are of equal volume and the partial pressures are in equilibrium at STP

Q: Define blood:gas partition coefficient
A: Describes the solubility of the agent in blood relative to air, when the two phases are of equal volume and in equlibrium at STP.

Q: Significance of a low blood:gas partition coefficient
A: Agents with a low blood:gas partition coefficient are poorly soluble in blood.
They have a rapid onset and offset because only a small number of molecules in blood are required to generate a high partial pressure, which creates a steep gradient for diffusion into the CNS.

Q: Define the oil:gas partition coefficient
A: Describes the solubility of the agent in fat relative to air, when both phases are of equal volume and in equilibrium at STP

Q: Significance of the oil:gas partition coefficient
A: High oil:gas partition coefficient indicates a greater potency, and therefore a low MAC

Q: Delivery of a volatile anaesthetic agent to the alveolus is dependent on:
A: Inspired concentration
- High Fi increases the rate of increase of Fa
- Fi is dependent on:
 - FGF
 - Concentration of agent in FGF
 - Volume of the breathing system
 - Absorption of agent by circuit
Alveolar ventilation
- Increased VA increases Fi
FRC
- A greater Vt/FRC ratio increases onset
Second gas effect

Q: Factors affecting uptake of volatile agent from lungs
A: Blood:gas partition coefficient. Affected by:
 - Temperature (BG coefficients ↓ as temperature ↑)
 - Haematocrit (variable effect, depending on plasma vs. RBC solubility)
 - Fat (↑ with lipaemia)
Alveolar blood flow
- Function of CO and shunt fraction
- Increased alveolar blood flow increases uptake
Alveolar-venous pressure gradient
- Dependent on:
 - Uptake of agent in tissues
 - Blood:tissue solubility coefficients

Q: Pharmacokinetic differences of volatile agents in children
A: Increased rate of induction due to:
- Increased VA/FRC ratio
- Lower albumin and cholesterol
- Increased proportion of CO going to head

Q: Pharmacokinetic differences of volatile agents in the elderly
A: Increased rate of induction due to:
- Lower MAC requirement
- Lower albumin

Q: Mechanism of Action of Volatile Anaesthetics (headings only)
A: Macroscopic
Microscopic
Molecular

Q: Macroscopic actions of volatile anaesthetics
A: Spine:
 - Decreasing transmission of noxious signals
 - Inhibition of spinal efferents
Brain:
 - Global CBF depression

Q: Microscopic mechanism of inhalational anaesthetic agents:
A: Presynaptic inhibition of:
- 5HT
- ACh
- Glutamine
Postsynaptic augmentation of:
- GABA_A

Q: Molecular actions of inhalational anaesthetic agents:
A: Alteration of α-subunits of GABA_A, increasing opening time
Enhance the activity of two-pore K+ channels, hyperpolarising pre- and post-synaptic CNS neurons

Q: Molecular weight of a volatile anaesthetic affects
A: ↓ MW ↓ boiling point, and therefore ↑ SVP

Q: Increased H^+ content of a volatile anaesthetic:
A: ↑ Potency
↑ Flammability

Q: Increased F^- content of a volatile anaesthetic
A: ↓ Flammability
↓ Potency
↓ Oxidative metabolism, ↓ toxicity

Q: Increased Cl^- content of a volatile anaesthetic
A: ↑ Potency

Q: A Di-fluor-methyl (-CHE_2) group on a volatile anaesthetic
A: Produces CO in the presence of dry soda lime

Q: Amount of potassium excreted from the kidneys
A: 30-100 mmol/day

Q: Sources of error peculiar to side-stream capnography
A: Sample line blockage:
- Water vapour
Sampling delay

Q: Twitch vs tetany
A: Twitch is the response to a single stimulus
Tetany is the sustained contraction occurring due to repetetive simulation occuring before relaxation

Q: Mechanism of tetany
A: Stimulus must be above critical frequency
- Critical frequency is dependent on the AP duration of the cell
Occurs due to repeated stimulus causing Ca2+ release to exceed uptake into SR

Q: Force of tetanic contraction
A: Up to 4x greater than single twitch

Q: Mechanism of Ca2+ release from SR
A: AP spreads down T-tubules deep into myocyte and close to SR, causing depolarisation of SR membrane
Dihydropyridine receptor is activated, releasing a small amount of Ca2+.
Dihydropyridine receptor activates ryanodine receptor, causing greater release of Ca2+.

Q: Minimising work of breathing
A: Elastic:
- Optimise lung volume with PEEP
- Minimise surface tension with surfactant
- Optimise RR
Resistive work:
- Decrease RR
- Increase laminar flow
 - Increase radius
  - Increase lung volume
  - Bronchodilators
 - Reduce density
  - Heliox

Q: Cholinesterase subtypes
A: Acetylcholinesterase
Butylcholinesterase

Q: Acetylcholinesterase location
A: RBC membrane
NMJ
Cholinergic synapses

Q: Suxamethonium Apnoea: Definition
A: Congenital or acquired deficiency of butylcholinesterase, causing prolongation of the action of suxamethonium

Q: Suxamethonium Apnoea: Genetics
A: 4 alleles:
- u (usual/normal)
- s (silent)
- a (atypical, dibucaine resistant)
- f (fluoride resistant)

Q: Causes of acquired butylcholinesterase deficiency
A: Pregnancy
Disease:
- Liver disease
- Renal failure
- Cardiac failure
- Thyrotoxicosis
- Malignancy
Drugs

Q: Drugs causing butylcholinesterase deficiency
A: - Ketamine
- Anticholinesterases (e.g., neostigmine)
- Lignocaine and ester local anaesthetics
- Lithium
- Metoclopramide
- Cytotoxics
- OCP

Q: Esmolol: MoA
A: β_1 >> β_2 adrenoceptor antagonist

Q: Esmolol: Distribution
A: 60% protein bound
VD_SS 3.5 L.kg^–1

Q: Malignant Hyperthermia: Definition
A: Pharmacogenetic disease of skeletal muscle induced by exposure to volatile anaesthetic agents.
Prolongs ryanodine receptor activation, causing extensive Ca release from the SR and tetanic muscle contraction, with corresponding hyperthermia, increased VO2, lactic and respiratory acidosis, leading to rhabdomyolysis, DIC, and death.

Q: Treatment of MH
A: Switch off volatiles
Hyperventilate
Dantrolene (see "Dantrolene")
Bicarbonate (consider)
Glucose
Iced fluids (and cavity lavage if possible)
Fast — anticipate ventricular arrhythmias

Q: Sugammadex: Interactions
A: Antibiotics
flucloxacillin, fusidic acid:
- bind to sugammadex and reduce its effectiveness
Toremifene (SERM)
- bind sugammadex and reduce its effectiveness
Oral contraceptive pill
- treat as for "missed pill" as reduces progesterone availability

Q: Benzodiazepines: Absorption
A: High PO bioavailability

Q: Define: TD_50, LD_50, LC_50
A: TD_50:
- Median dose reaching a pre-defined threshold of toxicity
LD_50:
- Median dose causing death
LC_50:
- Median lethal concentration of drug

Q: Stucture of Voltage-gated Ion Channels
A: Common 4-unit (each with 6 transmembrane segments) around a central pore (selective for the ion)
S4 helix senses transmembrane potential

Q: Activation of voltage gated ion channels
A: - S4 helix senses change in transmembrane voltage
- Opens the channel when threshold potential is reached
On activation:
- Channel goes from resting to active state
- Then to inactive state (absolute refractory period)
- Then to resting state

Q: Formula for hepatic clearance
A: Cl = Hepatic Blood Flow x Extraction Ratio

Q: Anaesthetic machine: Gas supply safety
A: 1. Pin indexed connections for medical gas cylinders
2. A reserve supply of O2
3. Non-interchangeable gas hose connectors
4. Pressure gauge for gas supply line and cylinder pressures

Q: Anaesthetic Machine: Oxygen Safety
A: - Supply failure alarm
- O2 enters backbar last
- Only one way to adjust O2
- O2/N2O proportioning system

Q: Anaesthetic machine: Gas outlet safety
A: - Fresh gas outlet must be 22mm OD, 15mm ID, and visible
- High pressure relief valve
- Gas scavenging system connections must be of a different diameter

Q: Anaesthetic machine: Other safety requirements
A: - Each functional sub-system of the machine must automatically activate its alarms when activated
- Adequate maintenance of the machine

Q: Atracurium: Elimination
A: Independent of hepatic and renal function

Q: Cisatracurium: Pharmaceutics
A: R-Cis, R'-Cis isomer of atracurium
Colourless solution at 2-5mg.ml-1
Store at 4°C

Q: Cisatracurium: Dose
A: 0.15-0.2mg/kg

Q: Cisatracurium: Duration
A: 25-30 minutes

Q: Cisatracurium: Onset
A: 60-180s

Q: Cisatracurium: Class
A: Benzolisoquinolonium

Q: Paracetamol: Class
A: NSAID, acetanilide derivative

Q: Paracetamol: CNS
A: Analgesia.
- Synergism with other analgesics (e.g., NSAIDs, tramadol, opioids) resulting in agent-sparing effect and reduced side-effects
Antipyretic

Q: Paracetamol: Resp
A: May precipitate/exacerbate analgesic asthma due to glutathione depletion

Q: Paracetamol: Haeme
A: Cytopaenia

Q: Classification of opioids
A: Naturally occuring:
- Endogenous (endorphins, encephalins, dynorphins)
- Opium derivatives
- Phenanthrenes (morphine, codeine)
Semi-synthetic (simple modifications to morphine):
- Diacetylmorphine
- Buprenorphine
- Oxycodone
Synthetic:
- Phenylpiperidines (fent, alf, remi, pethidine)
- Diphenylpropylamines (methadone)

Q: How do opioids cause respiratory depression
A: Right shift of CO2 response curve

Q: Morphine: Intrathecal dosing
A: 100-300µg once only
Must be preservative free.
No further opioids for 24/24

Q: Morphine: Unique CVS/Resp
A: More histamine release, therefore more:
- Bronchospasm and raised PVR
- Bradycardia and hypotension
- Pruritis

Q: Opioid: Uses
A: Analgesia
Premedication
Anxiolysis
Cough suppression
LV failure
Rigors:
- Pethidine
- Alfentanil
- Tramadol

Q: Fentanyl: Class
A: Synthetic phenylpiperidine

Q: Fentanyl: MoA
A: Pure µ opioid receptor agonist
(minimal histamine release compared with phenanthrenes)

Q: Fentanyl: V_D and protein binding
A: Vd 4L/kg
80% protein bound

Q: Fentanyl: Relative lipid solubility to morphine
A: 600x

Q: Alfentanil: Relative lipid solubility to morphine
A: 90x

Q: Remifentanil: Relative lipid solubility to morphine
A: 20x

Q: Oxycodone: Relative lipid solubility to morphine
A: 1x

Q: Alfentanil: V_D and protein binding
A: 0.6L/kg
90% protein bound

Q: Remifentanil: Protein binding and V_D
A: 70% protein bound
VD 0.5L/kg

Q: Pethidine: Unique CVS
A: ↓ Inotropy

Q: Morphine: t_1/2β
A: 160 minutes

Q: Fentanyl: t_1/2β
A: 190 minutes

Q: Alfentanil: t_1/2β
A: 100 minutes

Q: Remifentanil: t_1/2β
A: 10 minutes

Q: Oxycodone: t_1/2β
A: 200 minutes

Q: Tramadol: Distribution
A: V_D 4 L.kg^–1

Q: Local Anaesthetic Toxicity: Block Factors
A: Site
Use of adjuncts
- Adrenaline
Technique
- Aspiration
- Test dose
- Use of ultrasound

Q: Local Anaesthetic Toxicity: Patient Factors
A: Blood flow to area
α1-acid glycoprotein levels
- Low level inc. free drug
- Neonates and infants 50% that of adults
Hepatic disease
- Reduces amide clearance
Age
Organ blood flow
- Clearance
Pharmacokinetic interactions
Extremes of age
- Clearance reduced in children and elderly
pH (acidosis)
- Increases unionised portion
- Increases cerebral blood flow

Q: Advantages and Disadvantages of transdermal administration
A: Advantages:
- Compliance
- Easy
- Painless
- No first pass metabolism
- Stable [plasma] when established
Disadvantages:
- Slow onset
- Variable [plasma] in first 24/24
- OD and abuse potentials

Q: CYP450 enzymes named after:
A: Wavelength of light they absorb when:
- In reduced form
- Combined with CO

Q: Classification of CYP450 enzymes
A: Families:
- CYP1 vs CYP2
Subfamilies:
- CYP1A vs CYP1B
Isoforms:
- CYP1A1 vs CYP1A2

Q: Speed of onset of LA is affected by
A: Drug factors:
- Dose
- Lipid solubility
- Ionised portion (pKa, tissue pH)
Patient factors:
- Nerve activity (frequency dependent blockade)
- Nerve fibre size
- Hyperkalaemia (↓ speed of onset)
Technical factors:
- Proximity to nerve
- Use of adjuncts

Q: Categorise the factors affecting duration of neuromuscular blocking drugs
A: Technical Factors
Drug Factors
Patient Factors

Q: Technical factors affecting duration of action of NMBD
A: Dose
Drug error

Q: Patient factors affecting duration of NMBD
A: Age
Acidosis
- Potentiates blockade
Hyperthermia
- Reduced hepatic and renal clearance, reduced Hoffman degradation
Renal impairment
- Prolonged duration of aminosteroids
Hypo/hyperkalaemia
- RMP more/less negative
Hypermagnesaemia
- Decreased sensitivity of post synaptic membrane
Hypocalcaemia
- Decreased presynaptic membrane sensitivity
Disease:
- Myasthenia Gravis (Increased sensitivity to ND NMBDs)
- Eaton-Lambert Syndrome (increased sensitivity to all NMBDs)
- Pseudocholinestease deficiency

Q: Drug interactions affecting duration of NMBD:
A: Frusemide
- Potentiates blockade at low dose, reduces blockade at high dose
– Indirect effect on K^+; may effect cAMP resulting in altered RMP
Volatile anaesthetics
- Potentiate blockade by stabilising post junctional membrane
Antibiotics
- Potentiate blockade
– Aminoglycosides: Competition with P-type voltage-gated Ca^2+ channels
Local anesthetics & lithium
- Potentiate blockade
Anticholinesterases:
- Reduce blockade by increase ACh concentration at the NMJ
OCP:
- Potentiates blockade by competing for plasma cholinesterase binding sites
Ca2+ channel blockers:
- Potentiate blockade by inhibiting Ca release

Q: Histamine: Production
A: Amine produced by decarboxylation of histidine

Q: Histamine: Location
A: All tissues, particular those exposed to outside environment:
- Lungs
- Gut
- Skin

Q: Histamine: Receptors
A: H1 receptors:
- Gq
- Inflammation
H2 receptors:
- Gs
- Gastric acid secretion
H3 receptors:
- Presynaptic Gi in CNS
H4 receptors:
- Gi in bone marrow and other solid haematological organs (spleen, liver, thymus)

Q: Alterations in drug response: Obesity
A: Absorption:
- ↓ gastric emptying
- ↓ SC blood flow
Distribution:
- ↑ Vd of fat soluble drugs
- ↑ CO
- ↑ α1-glycoprotein
- ↑ blood volume
Metabolism:
- ↑ Plasma and tissue esterase levels
- Normal or ↑ hepatic enzymes
Elimination:
- ↑ GFR due to ↑ RBF due to ↑ CO

Q: Factors Affecting Metabolic Rate
A: Age
- Neonate BMR 2x that of adults
- Declines by 2% each decade of life
Body composition
- ↑ lean muscle mass ↑ MR
Diet
- Digestion ↑ BMR by ~10% (Specific Dynamic Action of food)
- Starvation ↓ BMR
Exercise
- Greatest and most variable source of energy consumption
Environment:
- MR ↑ in cool environments, ↓ up to 10% in temperate environments
Physiological states ↑  BMR:
- Pregnancy (up to 20%)
- Lactation
- SNS tone
- Corticosteroids
Disease states ↑ BMR:
- Malignancy
- Sepsis
- Hyperthyroidism

Q: Specific Dynamic Action
A: Amount of energy required to assimilate nutrients.
Protein > carb > fat.

Q: Components of a pH electrode
A: Blood chamber
Measuring chamber, which:
- Separated from blood by H+ permeable glass
- Contains buffer solution
- Contains Ag/AgCl measuring electrode
Reference chamber, which:
- Separated from blood by H+ permeable glass
- Contains KCl solution
- Contains Hg/HgCl reference electrode

Q: Principle of pH electrode
A: Two solutions with different H+ activities will develop a potential difference between them (proportional to the concentration gradient)

Q: Method of pH electrode
A: H+ passes through the glass along a concentration gradient:
- Generates variable PD in measuring chamber, as H+ ions are buffered and gradient is maintained
- Generates constant PD in reference chamber, as there is no buffer of H+ ions in the KCl solution
Once H+ has equilibrated between blood and the KCl solution, the potential difference between the measuring and reference electrodes is proportional to the H+ concentration in blood

Q: Limitations of pH electrode
A: Requires regular two-point calibration
Kept at 37 degrees
Electrodes clean from protein

Q: Severinghaus electrode contains:
A: Blood Chamber
Bicarbonate chamber, which:
- Contains bicarb in a nylon mesh
- Separated from blood by CO2 permeable membrane
- Separated from reference and measuring chambers by H+ permeable glass
Measuring chamber, containing:
- Buffer solution
- Ag/AgCl measuring electrode
Refrence chamber, containing:
- KCl solution
- Hg/HgCl reference electrode

Q: Severinghaus electrode method
A: CO2 diffuses from blood into the bicarbonate chamber
CO2 reacts with water in the bicarbonate chamber to produce H+ ions
From here, the process is identical to the pH electrode, except bicarbonate chamber takes the place of blood chamber

Q: Mechanism of Hersch Fuel Cell:
A: - Oxygen is reduced at the cathode, promoting spontaneous current flow
- Oxidation of Pb provides the source of electrons
- Flow of current is calibrated to the pO_2

Q: Reactions of Hersch Fuel Cell
A: Anode: Pb + 2OH^– → PbO + H_2O + 2e^–
^
Cathode: O_2 + 2H_2O + 4e^– → 4OH^–

Q: Pros/Cons of Hersch Fuel Cell
A: Pros:
- Compact
- Temp compensated
- Faster than Clarke electrode (20 vs. 60s; but still slower than paramagnetic analyser)
Cons:
- Expensive
- Reacts with NO to produce oxidation at Pb anode which gives falsely high pO2
- Short operating life 6-12 months

Q: Operating principle of surgical diathermy
A: Cuts and coagulates tissues by passing an AC current through them.
Works on Current Density (current/area):
- High density causes tissue heating and destruction (at electrode)
- Low density causes safe levels of tissue heating and no destruction (at the plate)

Q: Modes of Diathermy
A: Cutting
- Constant 0.5MHz operation maximizes focal tissue destruction
Coagulation
- Damped sine save causes heating and coagulation with minimal destruction
Blended
- Intermittent 1:1 operation at 1.5 MHz provides intermediate heating and destruction

Q: Diathermy risks
A: Burns
Electrocution (injuring patient or personnel, damaging implants)
Interference (triggering pacemakers, ICDs (may result in electrocution)
Smoke production (possible respiratory irritant/carcinogen)
Tissue dissemination (possible source of metastatic seeding)

Q: Oxygen: Pharmaceutics
A: Molecular weight 32 g.mol^-1
Boiling point:–182ºC

Q: Oxygen: Uses
A: Treatment and prevention of hypoxaemia
- e.g. preox
Displacement of gas (e.g. PTHx)
Hyperbaric O2 therapy
Cluster headache

Q: The major inhibitory neurotransmitter in the spine and brainstem is:
A: Glycine

Q: Atmospheric pressure in mmHg, kPa, bar, and PSI
A: 760 mmHg
101.3 kPa
1.013 bar
14.7 PSI

Q: Net water reabsorption in the kidney (as a percentage of filtered volume)
A: Proximal tubule 65% (fixed)
Loop of Henle 15% (fixed)
Distal tubule 8% (complete absence of ADH) to >19% (maximal ADH level)

Q: Maximal urine volume
A: 22L.day^–1 if intake is maintained:
- In the absence of ADH, only 8% of water reabsorbed in the DCT
- The remaining 12% of total filtered water is passed in the urine

Q: Minimal urine volume per day
A: ~500ml/day.
- Daily solute load is approximately 700mOsm.day^–1
- Maximum urinary osmolality is about 1400mOsm.kg^–1

Synthesis of prostanoids

Q: Prostanoids are
A: Diverse subgroup of eicosanoids (20-carbon molecules) derived from fatty acids. Include:
- Thromboxane
- Prostacyclin
- Prostaglandins

Q: Determinants of afterload
A: Afterload = ventricular wall stress, therefore:
Afterload = Ventricular cavity pressure x ventricular cavity radius / ventricular wall thickness

Q: Determinants of ventricular transmural systolic pressure
A: Intrathoracic Pressure
Ventricular Cavity Pressure

Q: Determinants of ventricular cavity pressure
A: Outflow tract impedance
- Valvular disease (e.g. AS)
- HOCM
Systemic arterial impedance
- Resistance
- Inertia
- Compliance

Q: Determinants of Systemic Arterial Resistance (SVR)
A: As per Hagan-Poiseuille Equation:
Radius
- Greatest determinant
- Related to degree of vasoconstriction
Viscosity
- Affected by haematocrit
Length
- Essentially fixed

Q: Determinants of systemic arterial inertia
A: Mass of blood
Heart rate

Q: List the hormones regulating tubular reabsorption
A: Angiotensin II
Aldosterone
ADH
ANP
Parathyroid hormone

Q: A-band
A: Myosin filaments

Q: H-band
A: Gap between actin filaments

Q: I-band
A: Gap between myosin filaments

Q: Skeletal muscle cell diameter
A: 10-100μm

Q: Muscle fibre subtypes
A: Slow oxidative fibres (red fibres)
- Multiple mitochondria
- Sutained fatigue-resistant contraction
Fast glycolytic fibres (white fibres)
- Fewer mitochondria
- More glycogen
- Strong but easily fatigued

Q: Skeletal muscle cell contents
A: Several hundred nuclei
Multiple mitochondria
Sarcoplasmic reticulum
Glycogen
Myoglobin
Myofilaments

Q: Myofibrils are formed from
A: Myofilaments arranged in parallel
Myofilaments are formed from sarcomeres arranged in series

Q: Respiratory effects of acidosis
A: Increased MV
- Peripheral and central chemoreceptors
Right shift of oxy-Hb curve
Bronchoconstriction

Q: CVS effects of acidosis
A: ↓ Inotropy
↓ Response to catecholamines
Arrhythmia
↓  SVR

Q: CNS effects of acidosis
A: Confusion, obtundation

Q: Electrolyte effects of acidosis
A: Hyperkalaemia
- K^+ ↑ by 0.6mmol/L for every 0.1 fall in pH
- Due to impaired Na^+/K^+ ATPase
(Ionised) hypercalcaemia
- H^+ displaces Ca2+ from binding site on albumin

Q: Cellular effects of acidosis
A: Impaired enzyme function
Molecular ionisation
- Alter ability to cross cell membranes
- Affect function
Altered cellular RMP

Q: Classify the factors affecting recovery from inhalational anaesthesia
A: Drug Factors
Patient Factors
Machine Factors

Q: Drug factors affecting recovery from inhalational anaesthesia
A: B:G and T:G partition coefficients
- More soluble agents will have a greater resevoir of drug in tissue
Metabolism
- Metabolised agents (e.g. halothane) are eliminated more rapidly
Absorption into breathing system

Q: Patient factors affecting recovery from inhalational anaesthesia
A: V_A
- ↑ VA ↑ elimination
CO
- ↑ CO ↑ elimination
Loss from tissue beds

Q: Machine and case factors affecting recovery from anaesthesia
A: Fresh gas flow rate
Duration of anaesthesia
- ↑ Duration ↑ time for elimination
Depth of anaesthesia

Q: Define allosteric modulator
A: Substance which binds a receptor distant to the ligand-binding site, and modifies (positively or negatively) the effect of the ligand.
Has no activity in absence of a ligand.

Q: Define oncotic pressure
A: Osmotic pressure exerted by colloid particles

Q: Effects of aldosterone
A: Increased Na^+ reabsorption
Increased water reabsorption (due to Na^+ reabsorption)
Increased K^+ elimination
Increased H^+ elimination

Q: Albumin: Half-Life
A: ~20 days

Q: Albumin: Normal Range
A: 28-58 g/L

Q: Transaminases: Normal Range
A: ALT: < 54 U/L
AST: <35 U/L

Q: Tests of liver function:
A: Synthetic
- Albumin
- Clotting assay (INR, APTT)
Metabolic:
- ALT
- AST
Obstructive:
- GGT
- ALP
- Bilirubin

Q: Current solution for blood storage
A: SAGM:
- Saline
- Adenine (ATP substrate)
- Glucose (for RBC glycolysis)
- Mannitol
Kept at 4°C to minimise metabolic requirement and inhibit bacterial growth, but not freeze blood.

Q: PRBC storage time
A: 35 days
- 70% survival

Q: Platelet storage (ex vivo)
A: - Kept at 22°C (below this, platelets become non-functional)
- Bag allows gas exchange to occur
- Agitated to prevent clotting and facilitate gas exchange
- pH kept between 6.2 and 7.8

Q: Additional changes with stored whole blood
A: WBC nonfunctional after 4-6 hours
Platelets nonfunctional within 48 hours if stored at 4°C
Factor levels significantly decrease after 21 days

Q: Reduction in core body temp with general anaesthesia
A: 1-3°C

Q: Phases of heat loss in general anaesthesia
A: 1. Rapid reduction
2. Gradual reduction
3. Plateau

Q: Rapid reduction phase of heat loss
A: Core temp falls by 1-1.5°C in 30mins
Due to:
- Vasodilation (SVR)
- Heat redistribution to peripheries (total body heat content only decrases slightly)
- Impaired thermoregulatory responses (wider interthreshold range)

Q: Interthreshold range in general anaesthesia
A: 4°C

Q: Gradual reduction phase of heat loss in general anaesthesia
A: Core temp falls 1°C over following 2-3 hours
- Heat loss exceeds heat production
- Non-shivering thermogenesis is only option for paralysed patient

Q: Plateau phase of heat loss in general anaesthesia
A: Thermoregulatory responses activated, further loss attenuated by increased heat production

Q: Heat loss in neuraxial anaesthesia
A: - Typically less exteme (0.5°C) than GA
- Plateau does not occur as vasoconstrictive responses inhibited by blockade

Q: Alterations to Drug Response: Absorption in pregnancy
A: - ↓ Gastric emptying
- N/V, GORD
- ↑ CO (↑ IM/SC absorption)
- Volatiles (↑ MV & ↓ FRC causes ↑ alveolar uptake; ↑ CO ↓ establishment of blood partial pressure gradient)

Q: Alterations to Drug Response: Distribution in pregnancy
A: - ↑ CO, ↑ TBW, plasma volume, fat mass
- ↓ albumin, ↓ α1-glycoprotein
- ↓ pH

Q: Alterations to Drug Response: Metabolism in pregnancy
A: No change to HBF
Progesterone induces enzymes
Oestrogen competes for enzymes
Decreased plasma cholinesterase activity

Q: Alterations to Drug Response: Elimination in pregnancy
A: - ↑ RBF, ↑ GFR

Q: Pharmacodynamic changes in pregnancy
A: - ↑ LA sensitivity
- ↓ MAC

Q: Define critical length with respect to nerve fibres
A: Length of axon which must be blocked in order to prevent action potential transmission.
Dependent on myelination and fibre diameter.

Q: Concentration effect
A: Phenomenon where the rise in alveolar partial pressure of inhaled gas is disproportionately rapid when administered in high concentrations.

Q: List classes of vasodilators
A: Nitrates and nitrate-precursors
Potassium channel activators
Calcium channel blockers
Miscellaneous
 - volatiles
 - intravenous anaesthetics
ACE-Is and A2RBs
alpha blockers
centrally acting agents

Q: Class Ia antiarrhythmic example
A: Procainamide

Q: Class Ib antiarrhythmic example
A: Lignocaine
Phenytoin

Q: Class Ic antiarrhythmic example
A: Flecainide

Q: Sotalol: Indications
A: Treatment of ventricular tachyarrhythmias
Rhythm control of atrial fibrillation (particularly post DC cardioversion)

Q: Sotalol: MoA
A: Non-selective beta-blocker (L-sotalol only)
Class III antiarrhythmic (both stereoisomers)

Q: Sotalol: Kinetics
A: 90% oral bioavailability
No protein binding
Not metabolised
Renal elimination of active drug (>90%)

Q: Renal/electrolyte effects of hypocapnoea
A: Decreased serum K
Decreased serum Ca
- Ca binds to H+ binding site on albumin
- Causes paresthesias and twitches

Q: Local Anaesthetics Duration: Patient factors
A: Tissue pH
↓ Duration with ↓ tissue pH
Metabolic impairment
- Hepatic failure increases duration of action of aminosteroids
- Butylcholinesterase deficiency increases duration of ester local anaesthetics
Site of administration
- Well vascularised tissue (e.g. intercostal area) has greater systemic uptake

Q: Properties of Schneider TCI model
A: Typically targets effect site
(Plasma targeting inconsistent due to fixed V1: identical bolus for every patient)
Uses:
- Age
- Height (for lean body weight)
- Weight
Fixed V_1 (4.2 L) and V_3 (238 L), age-based V_2
Smaller induction boluses, slower onset mainly due to small V_1 (useful in elderly, frail patients). Reduced adverse events, less propofol used.

Q: Properties of Marsh model
A: Typically targets plasma concentration
Requires TBW, age (not used in calc)
Fixed rate constants
Variable compartment sizes (but larger V_1 than Schneider)
Delivers larger induction bolus, with rapid onset mainly due to larger V_1 — safe in robust, young patients
- Weight used to calculate all compartment volumes
Modified Marsh:
- Uses a keo of 0.2L.min-1 instead of 0.26L.min-1
- Gives a smaller induction

Q: Bombay blood group
A: Lack H-antigen stem:
- Do not express A or B antigen (so are universal PRBC donors)
- Express anti-H antibody (H-antigen is present in all A, B, O groups, so Bombay phenotype can only accept blood from other Bombay phenotype pts)

Q: Scavenging: Open vs closed
A: Structure of the scavenging interface depends on the type of scavenging system:
Open interface:
- Used by active scavenging systems
- Active systems use a pump to generate a pressure gradient drawing gas to the disposal assembly
- Interface is open to air to prevent negative pressure being transmitted to the patient
Closed interface:
- Used by passive scavenging systems
- When gas pressure in the collection assembly exceeds 5cmH_2O, the positive relief valve opens and gas enters a resevoir bag
- When gas pressure in the disposal assembly falls below 0.5cmH_2O, the negative relief valve opens and gas enters the disposal assembly

Q: Define surface tension
A: Tendency of a fluid to minimise it's surface area

Q: Data requirements for parametric tests:
A: Continuous and numerical
Normally distributed
- Large (n > 100) is okay (central limit theorem)
Random samples
Samples have same variance
Observations are independent

Q: Parametric test examples
A: Z test
Student's T Test
F Test
ANOVA

Q: Non-parametric test properties
A: Don't require data to follow any particular distribution
Are not as powerful as parametric tests
More broadly applicable than parametric test

Q: Non-parametric test examples
A: Mann-Whitney U Test (Wilcoxon Rank Sum Test)
Wilcoxon Signed Ranks Test

Q: Principles of paramagnetic analysis
A: Oxygen is attracted by magnetic fields (paramagnetic)
- Due to unpaired electrons in the outer shells of oxygen atoms spinning in the same direction
Most other gases weakly repelled by magnetic fields (diamagnetic)
The attaction of a gas mixture to a magnetic field is therefore proportional to its oxygen content

Q: Method of paramagnetic analysis
A: Test gas flows into a tube
Reference gas flows into a parallel tube
Both gases pass through:
- Flow restrictors
- Magnetic field (turning off and off at ~100Hz)
Gases combine in the magnetic field
- Greater oxygen content -> greater movement into the magnetic field
This movement creates a negative pressure behind the gas.
The pressure difference between the tested gas and the reference gas is proportional to the oxygen content of the test gas.

Q: Pros of Paramagnetic analyser
A: Accurate
Fast
- Breath-to-breath analysis
Doesn't require regular calibration

Q: Cons of paramagnetic analyser
A: Water vapour reduces accuracy
Interference from other paramagnetic gases
- Nitric oxide (effect is minimal as nitric is given in far smaller volumes than oxygen, and is only weakly paramagnetic)

Q: Plenum Vaporiser
A: Requires supra-atmospheric pressure to operate

Q: Define Boiling Point
A: Temperature where the SVP equals atmospheric pressure.
Bubbles because the substance enters a vapour phase within the liquid, which then rise to the surface and break free.
At temperatures lower than the boiling point, bubbles form and are then crushed by the greater surrounding pressure.

Q: Immunity: Definition
A: Recognition of self vs. non-self in order to identify and eliminate pathogen

Q: Normal plasma [Mg]
A: 0.7 - 1mmol/L

Q: DINAMAP stands for:
A: Device for Indirect Non-invasive Automated Mean Arterial Pressure monitoring

Q: Total body calcium content
A: 1-1.3kg

Q: Enzyme which converts noradrenaline to adrenaline
A: Phenylethanolamine N-methyltransferase (PNMT)
Located in adrenal medulla.

Q: The heart is less tolerant of anaemia due to:
A: A high O2 extraction ratio (70%)

Q: Reduction in FRC with induction of anaesthesia
A: 10-20%
Irrespective of: IV (excluding ketamine as it does not reduce muscle tone) vs inhalational, relaxant vs. spont vent

Q: Percentage of airways resistance due to small (<2mm) airways
A: 20% in adults
40% in neonates

Q: Moles of volatile acid produced per day
A: 13-20mol

Q: Abnormal factor in haemophila A
A: Factor VIII

Q: Abnormal factor in haemophilia B
A: Factor IX

Q: Peripheral nerve action potential duration
A: 1-2ms

Q: Muscle cell action potential duration
A: 5-10ms

Q: Important ketone bodies
A: Acetoacetate
β-Hydroxybutyrate

Q: Embden–Meyerhof–Parnas pathway describes
A: Glycolysis (Glucose to pyruvate)

Q: Why is ammonia an ineffective urinary buffer
A: The NH_3 + H^+ ⇋ NH_4 reaction has a pKa of 9.2

Q: Substances specifically excluded by the BBB
A: Catecholamines
- Neurotransmitter action
Amino Acids
- Neurotransmitter action
Ammonia
- Neurotoxin

Q: Brown fat: Importance and difference from white fat
A: Vital for nonshivering thermogenesis, especially in the neonate
- Located in neck, interscapula region, suprarenal, supraclavicular
Produces heat via uncoupled oxidative phosphorylation

Q: Nerve fibre classification
A: Type A: Myelinated, large, fast (up to 120m/s). Include:
- Aα: Motor fibres.
- Aβ: Touch fibres.
- Aγ: Intrafusal (proprioceptive) muscle fibre.
- Aδ: Pain fibres
Type B: Myelinated, <3μm, conduct up to 30m/s. Innervate pre-ganglionic neurons.
Type C: Unmyelinated, 1μm, conduct at 0.5-2m/s. Pain fibres.

Q: Release of CRH
A: Response to stress
Circadian rhythm
- Peaks before waking
- Troughs during sleep

Q: Structure of mitochondria
A: Inner and outer membrane
- Inner membrane permeable to pyruvate, amino acids, fatty acids
Intermembrane space collects H+ ions produced in the mitochondrial matrix
Mitocondrial matrix
- Conducts metabolic function

Q: Processes completed in mitochondrial matrix
A: - Oxidative metabolism via citric acid cycle/electron transport chain
- Fatty acid metabolism
- Urea cycle
- Haeme synthesis

Q: Neonatal respiratory rate
A: 25-40

Q: Neonates: Changes to compliance
A: Increased CW compliance
Decreased lung compliance

Q: Changes to ventilation in neonates
A: Obligate nose breathers
Increased MV due to high metabolic rate, met with an increased RR

Q: Neonatal respiratory pattern
A: Periodic breathing: Slowly oscillating RR and Vt
Periodic apnoea: Normal breathing with intermittent apnoeas

Q: Changes to neonate volume and capacities
A: Increased closing capacity
Unchanged FRC
Unchanged Vt and dead space

Q: Daily energy requirement
A: 40kcal/m^2/hr

Q: HbA vs HbA_2
A: A: Two alpha and two beta subunits
A_2: Two alpha and two delta subunits

Q: 2-3 DPG and blood transfusion
A: 2-3 DPG totally depleted after ~2 weeks in storage
Takes ~24/24 following transfusion for 2-3DPG to return to normal

Q: Causes of increased physiological dead space
A: Upright posture
Low PAP or impaired pulmonary blood flow
- PE
Increased airway pressure
COAD

Q: Difference between SpO2 and SaO_2
A: SpO_2: O_2 saturation as measured by pulse oximeter
SaO_2: O_2 saturation as measured by ABG
Should usually correlate. Differences typically due to weaknesses of either measuring system, e.g.:
- Poor peripheral perfusion, haemaglobinopathy with pulse ox
- Venous sample, massive leukocytosis with ABG

Q: Causes of pathological shunt
A: Intracardiac
- e.g. VSD
Vascular
- e.g. PDA
Intrapulmonary
- e.g. Pulmonary oedema

Q: Propofol: CSHT at 30 minutes
A: ~6 minutes

Q: Context-Sensitive Decrement Time is
A: The time it takes for a drug level to fall to a particular percentage of its starting value following cessation of an infusion

Q: Drug factors affecting duration of local anaesthetic agents
A: - Vasodilator properties
- Use of additives
- Lipid solubility (↑ duration of action as drug remains at nerve for longer)
- Protein binding (↑ binding ↑ duration)

Q: Define ED95
A: The median dose of a neuromuscular blocking drug required to produce a 95% depression of twitch height

Q: Features of graduated log-dose response curve for NDMB
A: Initial plateau:
- Minimal effect at low doses due to spare receptors
Steep slope:
- Rapid increase in receptor occupancy with relatively small increase in drug increases blockade
Plateau:
- >95% receptor occupancy: nil further reduction in twitch height with increasing dose

Q: Stages of Sleep
A: Classified by EEG findings:
REM
Non-REM (further divided into)
- Stage 1: Drowsy (θ-waves replace α-waves)
- Stage 2: Sleep spindles
- Stage 3: δ waves appear
- Stage 4: Deep sleep (δ waves become synchronised)

Q: Define turbulent flow
A: Irregular movement in radial, axial, and circumferential axes

Q: BIS: Signal processing
A: Sensors:
4 forehead electrodes measure frontalis EMG and EEG
Processing:
EEG
- compressed spectral array (CSA)—Fourier transformation of raw signal to produce histogram of frequencies (median frequency is reduced under GA)
- biocoherence—phase coherence of brain regions decreases under GA
- burst suppression (periods of isoelectric EEG activity)
Combines with EMG and "other parameters"

Q: BIS: Outputs
A: BIS
Number between 0 and 100 (<40: increasing BS; 40-60: GA, 60-85: sedation; >85: awake)
EMG
activity in 70-110Hz range (may hint at interference)
Signal quality index
- "higher the better"
Suppression ratio (percentage of last 63 seconds where EEG is isoelectric

Q: BIS: Definition
A: Proprietary method of signal processed EMG and EEG to estimate depth of anaesthesia.

Q: Halothane: MAC
A: 0.75

Q: Enflurane: MAC
A: 1.7

Q: Non-respiratory functions of the lung
A: FIRMTITS:
Filtration
- Of blood
Immune
- IgA
- Macrophages
Resevoir
- Blood vol for the LV
Metabolic
- ATI to ATII
Temperature
Inhalational
Taking up drugs
Synthetic
- Surfactant
- Platelets

Q: Neonatal airway differences
A: Head and neck:
- Obligate nose breathers
- Proportionally enlarged head and occiput
- Proportionally short neck
Laryngeal changes:
- Disproportionately large tongue
- Epiglottis is u-shaped, longer, and stiffer
- Larynx lies at C4 (rather than C6 in adults)
- Narrowest part of the upper airway is at the cricoid
Intrathoracic changes
- Intrathoracic trachea is also shorter
- Left and right bronchi arise at similar angles
- Airways themselves are narrower, and have a higher resistance to flow

Q: Autonomic changes of ageing
A: Impaired autonomic function
Impaired baroreceptor response
Decreased exercise tolerance

Q: The VIE stores oxygen:
A: - As a liquid at 700kPa
- Above its boiling point
- Below its critical temperature

Q: Risk of left IJ (relative to R IJ) cannulation
A: Damage to the thoracic duct

Q: Respiratory changes of obesity
A: Airway:
- Difficult BMV
- Potentially difficult airway
- Increased GORD
- Increased OSA/OHS
Respiratory pattern:
- Increased MV
- ↑ Airway reactivity (TNF-α, IL-6, leptin)
Volumes:
- Decreased ERV, FRC
- CC > FRC
- Decreased oxygenation store and apnoea time
Work of breathing:
- Increased elastic WoB due to poor compliance due to reduced FRC
- Increased resistive WoB due to lower lung volumes
- Decreased CW compliance
Blood gases:
- Increased A-a gradient due to basal collapse and shunt
Circulatory:
- Increased PVR due to reduced FRC
- PHTN and R heart dysfunction

Q: Order nerves are blocked by local anaesthetic
A: Mostly (though not entirely) a function of critical length:
1. Aγ (proprioceptive)
2. Small myelinated Aδ (sharp pain, cold)
3. Large myelinated fibres: Aα (motor) and Aβ (touch)
4. Unmyelinated C (dull pain, heat) fibres

Q: Stimulation of aldosterone release
A: Increased K+
Increased ATII
Increased ACTH
Increased H+ (Decreased pH)

Q: Amount of cortisol produced per day
A: 15-30mg

The R equation is (for SpO2 monitors)

Q: CVS effects of obesity (classify):
A: Hormonal
CVS parameters
Cardiac

Q: CVS hormonal changes in obesity
A: Secreted from abdominal visceral fat:
- Leptin: Cardiac remodelling and LVH
- Angiotensinogen: HTN, LV remodelling
- Plasminogen activator inhibitor-1: Predisposes to VTE
- Inflammatory adipokines: Impair endothelial fn, increasing SVR
Catecholamines: ↑ inotropy, ↑ SVR, worsen endothelial fn

Q: Cardiovascular parameter changes in obesity
A: ↑ VO2
- ↑ LBM
↑ Blood Volume
- ↑ ATI
- ↑ Aldosterone
↑ Stroke Volume
- ↑ Preload (blood volume)
- ↑ Inotropy (catechols)
↑ CO
- To maintain DO2

Q: Cardiac muscle changes in obesity
A: Diastolic dysfn
- Myocardial fibrosis
Fatty infiltration of myocardium and conducting system
- Arrythmia
BiV hypertrophy due to ↑ afterload:
- LV due to systemic HTN
- RV due to:
 - LV diastolic failure
 - ↑ PVR (hypoxia, acidosis)

Q: Variables in IPPV which determine its physiological effects
A: - Mode of ventilation
- Vt, Pip, plateau pressure
- Respiratory rate
- I:E ratio
- PEEP (much more important than the other factors)

Q: Respiratory effects of PEEP/IPPV
A: ↓ WoB
- ↓ VO2
Changes anatomical/apparatus dead space:
- ETT: ↓ dead space as volume is less than anatomical dead space
- NIV: ↑ dead space
↑ Lung volume/FRC:
- ↑ Alveolar recruitment and oxygenation
- ↑ Lung compliance, ↓ WoB
- May ↑ dead space if PA > Pa (West Zone 1)
↓ Airway resistance:
- Resistance ↓ as lung volume ↑

Q: CVS effects of PEEP/IPPV
A: Alteration in CO:
- ↑ Intrathoracic pressure ↓ VR and CO
 - More marked in hypovolaemia
 - Less marked when lung compliance is poor
- ↓ LV preload due to ↑ RV afterload (↑ RV EDV, ↓ LV EDV)
- ↓ LV afterload due to ↓ LV transmural pressure
↓ MAP
Altered O2 flux:
- PaO2 ↑ but CO ↓
PVR
- Will ↑ if above FRC, ↓ if below FRC

Q: End-Organ effects of PEEP and IPPV
A: ↓ UO due to ↓ CO and RBF
ADH release
- Oedema
↓ Hepatic blood flow due to ↓ pressure gradient for hepatic flow

Q: Platelet α-granules contain
A: Contain fibrin, vWF, PDGF

Q: Platelet δ-granules contain
A: Contain 5-HT, ATP, ADP, and Ca^2+.

Q: Classify the factors affecting volatile washout
A: Brain-Blood and Tissue-Blood
Blood-Alveolus
Alveolus-Air
Other

Q: Factors affecting washout of volatile from brain-blood and tissue-blood
A: T:B coefficients
Duration
Depth

Q: Factors affecting washout of volatile from blood-alveolus
A: B:G coefficient
Alveolar CO
- Elimination increased with decreased CO (to a point)
- Shunt

Q: Factors affecting washout of volatile from alveolus-air
A: MV_A and VA/FRC

Q: Other factors affecting washout of volatile
A: Metabolism
Absorption into circuit
Percutaneous losses

Q: Key advantages of circle system
A: Preserves gases
- Anaesthetic
- Oxygen
Preserves heat and moisture
Reduces fire risk

Q: Pros of circle system
A: Cheaper to operate
Conserves gases/heat/moisture
Low dead space
Reduced greenhouse effects

Q: Cons of circle system
A: FGF is not directly delivered to the patient
- More difficult to titrate
Nitrogen may build up in the circuit
Less portable
Increased resistance of circuit
Requires soda lime

Q: How much CO<sub>2</sub> absorbed by 100g of soda-lime?
A: 26L

Q: Define cleaning
A: Physical removal of foreign material

Q: Define decontamination
A: Destruction of contaminants such that they cannot reach a susceptible site in sufficient number to cause harm

Q: Disinfection
A: Elimination of all pathological organisms, excluding spores.

Q: Sterilisation
A: Elimination of all microbial life, including spores