PhysiologyVIVA’sApril2013 April 2009 - · PDF fileBy Ku, Shanmuganathan, Hollingworth...

By Ku, Shanmuganathan, Hollingworth

Physiology VIVAs Apr 13-09 - 1

Physiology VIVA’s April 2013 – April 2009

Table of Contents Apr 2013 ........................................................................................................................................ 2 September 2012 .......................................................................................................................... 8 April 2012 .................................................................................................................................... 27 September 2011 ........................................................................................................................ 58 April 2011 .................................................................................................................................... 83 September 2010 ..................................................................................................................... 103 April 2008 ................................................................................................................................. 111 April 2009 ................................................................................................................................. 112

Please ignore highlighted colours. They were used while we made the document together and would be a bit too time consuming to remove.



Apr 2013 (By Ku)

1. Blood Pressure Measurement

Shown a picture of a monitor screen with IA line and NIBP. How is the blood pressure monitored in this case? (two ways IA line and NIBP).

Q What are the causes for inaccuracies in each?

• NIBP: o cuff size (widths ~ 40% of arm circumference) o tube o patient movement, dysrhythmias, hypotension. o intrinsic inaccuracy with DBP as it’s a derived value. o Too frequent measure = impedes BF; aim >2min o Intermittent. o Haematoma, obesity, lymphedema.

• IABP: o Static: zeroing, equipment calibration o Dynamic: damping, resonance o Damping: tendency for oscillation to minimise through

frictional/viscous forces. o Fn: frequency of oscillation when a system is disturbed. o Fn needs to be at least 10x above natural frequency (ie. Above 10th

harmonic) to minimise inaccuracy from resonance. Eg. Fn1-3 Hz, so Fn = 30Hz.

o Damping optimal at coefficient: 0.63. ie. Minimal overshoot and rapid response of oscillation wave, provides optimal condition for rapid changing IABP.

Q How is intra-arterial BP monitored? (explained where SBP and DBP and MAP was) You have shown me where the lines are, but how does the IA line get these numbers?

• By pressure transducer with zeroing to atmospheric pressure then algorithm to transducer pressure detected by strain gauge to number, based algorithm.

Q How is NIBP measured? talked about oscillotonometry and drew the graph of oscillation vs time and marked out sbp and map and dbp and explained that DBP can be calculated?

• MAP = point of max. oscillation. • SBP = point when oscillation starts • DBP = point where sudden drop of oscillation amplitude, or when amplitude

plateaus. Or derived from MAP / SBP value.



Q What is the formula for this calculation?

• MAP = DBP + 1/3 PP.

2. Oxygen Stores

Q Name the sources of oxygen in the body.

• FRC = 270 mls • myoglobin = 200 • blood = 820 • dissolved in tissue fluids. = 45

Q How much does the Lung store?

• FRC = 30ml/kg. So 70kg = 2100mls. • (work out PAO2 using gas equation) PAO2 = ~100mmHg when FiO2 = 21%. • (divide by atmospheric pressure) FAO2 = 100/760 = 13%, so = 273ml. so only

for ~1 min of supply. • If FiO2 = 100%, gets ~7mins.

Q How much does Hb store?

= sats % * Hufner’s (1.36 /g 1.34 ml/g) * [Hb] in g/dL = ml / dL.

Q Oxygen flux equation and of each variable.

= CO * chemical component * dissolved component = 1L/min.

Q So how much is in the body in total?

• Blood: 20ml/100ml, so 5L = 20*50 = ~1000ml. • Mb: 200ml • Tissue = 50ml, • So total = 270+1000+200+50 = ~1520 mls.

Q Oxygen consumption in neonate versus adult.

Adult = 250ml/min = 3.5ml/kg/min; neonate = 7ml/kg/min. ie 2x adult.

3. BP & exercise

Draw the SBP DBP and MAP change for mild moderate and severe exercise.

• See pic

Why does the SBP line rise faster than the DBP line?

• ↑↑CO



• ↓↓TPR – recruitment of skel mm capillary beds • ∴ ↑↑pulse pressure

What about MAP, why does it rise as such? (explained its due to the contribution of SBP and DBP).

What happens when exercise stops (BP dips the rises again due to baroreceptor reflex)

• Sudden dec in SV, as muscle pump dec, SNS dec. then an exponential fall in CO. (see Adams Answer)

What is the role of oxygen in this? (aerobic respiration in the mitochondria, final step in electron transport chain').

Write the formula for final step (formula for metabolic water).

• ½ O2 + 2H+ + 2e- ! H2O

What does oxygen do in this step? (electron acceptor)

You mentioned oxygen debt, when does it happen? whats the difference between oxygen debt and deficit?

• Oxygen debt happens when there’s oxygen deficit from increased metabolism eg. Exercise.

• Oxygen deficit = difference between O2 demands and O2 consumption of the muscle during inc metabolism eg exercise, 2nd to anaerobic met.

• O2 debt = when exercise ceases, a period of increased O2 consumption = O2 debt, repays the O2 deficit.

4. Nerve Action Potential

• Name some excitable cells in the body. o Myocardiocyte, neurons, skeletal muscle cells, SM cells.

• Draw a nerve action potential. What is happening at the upstroke? What is happening at the downstroke? where is there an overshoot for potassium? (the channels open longer).

• What is the resting membrane potential. What is it due to? How can this be determined (Nernst equation).

• What is the membrane potential if it was due solely to potassium? • What about if the RMP was due solely to sodium? Which direction do Na

and K move in? o Sodium EP =

• Why does action potential travel only forward? (due to refractory periods) • What is the refractory period of nerve?

o When nerve is resistant to further depolarisation, either absolute or relative.



o total AP = 1-2msec. ARP until 1/3 through repolarisation, RRP thereon until back to baseline

• Draw the graph for ion conductance for Na and K in a nerve.

• Draw a muscle action potential. No after hyperpolarisation. • mechanical response = 7.5 – 100msec depending on fibre type • What is the refractory period of muscle? markedly smaller than

mechanical response ∴ why tetany possible

Examiner 1: 1. Flow

• what kinds of flow are there? o Laminar, turbulent, transitional

• what are their differences? o Laminar: flow proportional to pressure; parallel to edge of a concentric

tube, parabolic flow front, centre = 2x average flow velocity. o Turbulent: flow square related to pressure; disorganised, eddies, square

front. • what is the flow within alveoli?

o diffusion • what factors would contribute to different kinds of flow? • if you want to flush an anesthetic circuit, which kind of flow would you

use? o To flush, need high volume of gas and velocity ie high flow rate. o High volume depends on diameter. o So higher diameter, higher velocity ! turbulent flow likely.

• draw a graph with Y axis being AWR and X-axis being from "mouth to alveoli"



2. RMP

What is resting membrane potential?

Steady state potential exists across the cell membrane.

Complete a form for various extra- and intra-cellular ion concentrations

• Extra: o Na 135-145 o K 3.5-5 o Cl 100 o Mg 0.75-1 mmol o Ca 2.2-2.5 corrected; (ionised Ca: 1.15-1.3) o HCO3 20-30 o pH 7.4

• Intra: o Na 10 o K 150 o Cl 9 o Mg 10 mmol o Ca 100 nanomol o HCO3 10 mmol o pH 7.1

•

What are the factors contributing to RMP? ‘/

• Differential membrane permeability to Na and K (100x) • Na/K ATPase slightly electrogenic (3Na vs 2K) • Gibbs-Donnon effect = presence of impermeable charged molecule affects the

distribution of other permeable, charged molecules at equilibrium.

‘Pump-leak hypothesis’

Derive the nernst equation, explain each item in the formula.



What will the membrane potential be like if solely due to potassium? it will be more negative, why? -90mV, as this is the equilibrium potential for potassium.

3 factors are: large conc, high permeability, high transmembrane conc gradient.

Tell me the goldman form of the equation.

= includes conc + permeabilities of all charged species present.

Examiner 2: 3. Coronary blood supply

anatomy of coronary arteries.

• Aortic sinus!LCA! o LAD (septal front, base, anterior) + o L circumflex (lateral/back + LA)!coronary sinus!RA.

• Aortic sinus!RCA (RA, RV, some LV base) o !R marginal (R base) + o Post descend (septal back)

• 70% R dominant • 20% codominant • 10% L dominant

draw curves of left and right coronary arteries flow vs time.

what happens to coronary blood flow with sympathetic stimulation?

• inc CBF as inc metabolic demand w inc HR, contractility. • Metabolic auto overrides SNS vasoconstrict.

what are the regulating factors for coronary blood flow?

• Autoregulation (myogenic/metabolic vs. systemic) • CorPP • CVR

4. Placenta

functions of placenta? (TIME)

• Gas transport • Endocrine role: progesterone • Transport: gas, nutrients, waste, water/electrolytes, drug, heat • Immune: maternal IgG to fetus. • Metabolic: glycogen, cholesterol, FFA, enzymes synthesis • Endocrine

o B-HCG (human chorionic growth): maintains corpus luteum. o HPL (human placento-lactogen): insulin antagonist, inc maternal BSL o Oestrogen



o progesterone

tell me about gas transport across placenta, do you know any equation governing it?

• FIck’s Law of diffusion: sol / √MW * conc grad * SA / T

tell me about double Bohr effect, draw curves.

• Bohr = right shift of OHDC in presence of CO2, H, (23DPG, temp) • Double Bohr = combined effect of enhanced O2 transport as HbA right shift

inc offload, HbF left shift inc uptake.

tell me about the endocrine functions of the placenta.

September 2012 (By Lord Hollingworth & Ku)

My viva September 2012 Monday 1. Venous return & cardiac output etc

• What is VR? What is CO? How are they related? I drew the guyton curve. see april

• If contractility is suddenly increased, what happens to VR? equilibrium movement to ↑VR

• To CO? To RA pressure? RAP ↓s • Where does the blood go? Into the arterial system • What is the compliance of venous vs arterial system? venous compliance is

x30 arterial

2. What is clearance?

volume of plasma cleared of drug per unit of time, ml/kg/min

• How can any substance be used to measure this? Using derivative of Fick principle. Ux.V/Px

• What substances do we use? Inulin and creatinine • Why do we not use inulin clinically?

o requires infusion and steady state which practically not useful • Why is cr inaccurate? secreted as well as filtered • Do we need to measure urine cr to calculate this? yes need urinary

concentration & volume • So what formula do we use to find GFR from serum cr? GFR = Ux.V/P • Draw a graph of relationship between serum cr and Gfr.



• How much renal function do you have to lose before rise in serum cr? 50% drop in GFR

• What substances what zero clearance? Albumin and glucose which are fully reabsorbed

• How to calculate renal plasma flow? What to use? o use para-amino-hippurate (PAH) o 90% filtered ∴ need to correct by dividing by 0.9 o need to factor in RBF is diff to RPF o RBF = RPF/(1-HCT)

3. Draw pleural pressure time curve for normal tidal breath



• Are the pleural pressure the same in the upright lung? • What is the pressure in the apex? more –ve in apex as does not have weight of

lung on it. • How would this change when the person is supine? less difference between

dependant and non dependant part as less effect of gravity



• How would the curve change for gasping breaths? ↑in negative pressure to drive inspiration

• What explains the difference in the curves?

4. Draw nerve action potential

• What causes the depolarization/ repol? dep Na;; repol K • Where in the graph do the K channels start to open to begin repol?

• What is RMP for nerve? -70mV • What determines this? Nernst potential for Na and K? Na +60, K -90 • nernst equation:

58 = RT/F R = ideal gas constant; T = temp; F = faraday constant



• How would this potential change with increase in temperature? will cause ↓in equilibrium potentials due to changes which will cause smaller and quicker AP

• Goldman equation? summation of all channels as prev in Apr 2012 • Effects of protein? Donnan effect is contribution to RMP of non diffusable

intracellular anions • Gibbs donnan. What is the size of effect of Gibbs donnan? -17mV

contribution • What about Na/K ATPase? - Is this important? Size of this effect? -10mV

contribution. essential to prevent cellular swelling and lysis (double donnan

Sept 2012 Day 3

1. Heart and oxygen

• What is O2 consumption of heart, 25mlO2/min (10% basal VO2 ie 20mlO2/min – despite only 5% CO)

%basal VO2 %CO Brain 20 15 Heart 10 5 Liver 20 30 Renal 7 25 Resting mm 20 15-20 Skin 5 5 basal VO2 = 250mls/min basal CO = 5000ml/min

• What is total body O2 consumption, • What percentage of CO does heart receive? • - what does this imply about oxygen use by the heart (high myocardial

extraction ratio). • What does the heart use the energy for? myocardial contraction?? • What determines coronary perfusion pressure (

o starling resistor: " LV corP = aortic DP – (LVP or RAP) " RV cor P = aortic SP or DP – (RVP or RAP)

• Why did you use diastolic pressure in the formula?

2. Pulmonary Defences

• What are the pulmonary defence mechanisms? o filtration - nose o irritant receptors – cough o cilia – escalator to remove o pulmon macrophages o secretion IgA

• Tell me about cilia, where are the cilia. trachea • what is the role of mucus,

o trapping of foreign particles



o moisturising inhaled air o prevent drying of epithelial surfaces

• what do alveolar macrophages do – o APC o phagocytosis of foreign pathogens and dead tissues o coordination of immune system by release of cytokines/chemokines, o remodelling of tissues

• how do they interact with the other components of the immune system, • where does complement come from.

o series of 25 plasma proteins from liver • which of the polymorphonuclear leucocytes is most important in fighting a

pneumonia? neutrophils??

3. Types of flow.

• What types of flow do you know, laminar, turbulent, transitional • What determines the rate of laminar flow and how is turbulent flow

o laminar = p = k.v & R = 8nl/pie r4 o turbulent: p = k.v2 & R = dl/pie r5 o transitional: p = k.v + k.v2 o P = F x R

• What does the wavefront of laminar flow look like (parabola), • What about turbulent flow (straight line), • What type of flow occurs in the alveoli (trick question, diffusion is the correct

answer), • If I was to flush gas out of an anaesthetic circuit, which type of flow would I

want to use (turbulent, think about the wavefront).

4. Acid base.

• Interpret these figures from a blood gas (metabolic acidosis with resp compensation).

• What is the normal pH range? (35-45nM H+/L) • If the pH was 7.4, what would the H+ concentration be? pH = -log [H] • pH 7.4 is 40 nanoMoles/L • pH 7.0 is 100 nM • pH 7.35 is 45 nM • pH 7.45 is 35 nM • What quantity of fixed acids does the body produce in a day?

o daily production of " volatile acid (resp) – CO2 20,000mmol/d " fixed:

" lactate 2000mmol/day " H+ 100 mmol/d

o fixed acid excreted o acid-base balance – acid made = acid excreted

• Where do they come from (incomplete metab of CHO (lactate), fats (ketones), protein (sulphate, phosphate).

• If I infused someone with HCl, how would the body respond? o 1st = buffering



o 2nd = resp excretion of volatile acid o 3rd = renal retention of HCO3

• Name some buffer systems ( o HCO3 (HCO3=/H2CO3)

" pH = 6.1 + log [HCO3]/[CO2] o Hb (Hb-/HHb) o proteins (P-/HP) o phosphates (HPO4

2-/H2PO4-)

o ammonium (NH3/NH4 ) • Which is most important? in order of importance! • What makes a good buffer system. Closed system = buffer pK should be +/- 1

from 7.4. Open system no problem • Why is the HCO3 system so important if the pKa is so far from 7.4? (quantity

of HCO3 and it is an open ended buffer system ie can be continually adjusted by resp and kidney variables

• What is the kidney's role in acid base balance? o longer term equilibrium – days/weeks o method:

" ↑ reabsorbtion of HCO3 " excrete titratable acid (phosphates, creatinine, ketoacids " exceret ammonium

o upregulate above systems buffers to ↑ability to excrete acid load

1. Draw the Left ventricular pressure-volume loop.

What are each of the events in this cycle? Quantify the volumes.

Why does the pressure not change much during diastole?

• Because LV is easy to fill, has high compliance at physiological range ie low elastance. P/V

What will happen if you rapidly infuse one litre of normal saline into a healthy, young person? (Drew the curve with increased pre-load.)

• Inc filling, inc preload+

What will the curve look like in a healthy geriatric patient? (Struggled a bit to understand what they were getting at... Some hints: is atrial contraction more or less important in the elderly? More. Guessed that they were referring to some diastolic dysfunction, and shifted the diastolic elastance curve.) Move on...

• Reduced EF: loss of elasticity of muscle fibre. • ↓ventricular compliance • Reduced contractility: reduction of intrinsic contractile ability of heart • Inc afterload: fibrotic changes to aortic root, higher MAP, • Inc peak pressure • diastolic dysfunction – LVEDV ↑steepness elastance curve



NB know how curve changes with preload, afterload, contractility.

2. Outline the Autonomic Nervous System.

Outline the receptors at each point.

• SNS: Spinal level ! Sym chain ! pre fibre synapse with post fibre ! nAChR with Ach ! post glanglionic fibre to effector organ ! adrenoceptor + NorAdr.

o T1-L3 of SC o Synapse in paravertebral or prevertebral ganglia o Postganglionic, nonmyelinated fibre on organs.

• PSNS: brain and pelvis ! preganglionic fibre, long, synapse close to the effector organ ! Ach ! muscarinic.

o Pregang fibre leave CNS via cranial N (3, 7, 9, 10) – 1973! + some sacral N roots

o Ganglion synapse either on organ directly, or close to organ. • Exception = adrenal - ACh; sweat & skeletal capillary beds – muscarinic

Where else in the body do you see acetyl choline? (5)

• All pregang • Post gang PSNS • NMJ • Sweat / adrenal medulla • Some neuron in CNS.

NB all pre = myelinated in ANS; and has nAChR.

Which cranial nerves are parasympathetic? (Started to slowly outline pupil innervation...' I'll just move you on, which is the main one? Vagus What does the Vagus n. innervate? (I was far too slow through this whole section and probably should've got further.)

• cranial N (3, 7, 9, 10) – 1973! + some sacral N o vagus: heart, lung, gut, pancreas, o 3 eye, lacrimal gland o 9 salivary gland

Extra: What are some drugs that work on ANS:

• Ganglionic: o Trimetaphan o Hexamethonium

• Non-selective alpha o Phentolamine, shorter 3x 1>2 o Phenoxamine; phenoxybenzamine, longer 100x 1>2

• More selective alpha: o antagonists: prazocin α1



o Agonist: Clonidine (200:1), dexmedetomedine (2000:1), methy-DOPA (10:1)

• ß blockers • Adrenergic agonists • Cholinergic:

o non selective antagonists – " atropine, glyco, hyoscine, scopolamine

o selective antagonists " M1 pirenzipine - stomach " M2 ipratropium bromide

o indirect agonists – edro, neo, organophospates o agonists – nicotine (cigarette smoke)

3. Draw a graphs of (?intrathoracic) pressures during normal tidal respiration.

What would change if the patient was pregnant? (I don't think I'd seen or thought of this before and struggled. Thinking aloud... FRC reduced, increased WOB if CC above FRC... increased intrathoracic pressures. Drew a graph.)

• dec FRC, higher atelectasis incidence



• decr compliance of chest wall ∴ decr angle of line • Work = to overcome friction/viscous force of airway + elastic recoil of lung. • decr AWR by 35% – skinnier • 40% higher VT

What would change if you inhaled as hard as you could, paused, then blew out as hard as you could?

• Bulging R of upstroke ie high –ve IPP • L side would bulge cross axis as exceeds passive recoil energy needs • may not return to baseline – see below – trapping

• DAC effect may cause early closure of airway ! inc RV (KB112) • ‘in nitrogen washout method measurement of FRC, a forced expiration should

be avoided because it may not reduce the volume of gas in the lungs to the true RV because of gas trapping due to DAC’.

Draw the flows. I commented that forced expiratory flows would be effort independent.

Why? Explained dynamic airway closure.

What is the limiting factor in inspiration? Airway calibre...

• To flow? Pressure gradient? Resistance (typically low); compliance (typically high).



• (No, the airways are pretty large. What sort of flow will there be?) Oh, turbulent flow.

And what is the relation between resistance and turbulent flow?

• R in turbulent flow = dl/pie r5 • Resistance markedly inc in turbulent flow, hence higher WoB. • As flow is unpredictable, there’s no single equation to define rate of turbulent

flow hence its resistance.

4. What would happen if I somehow managed to infuse an acid into your veins without harming you?

• Buffering (mins-hrs) • respiratory compensation (hrs-days) • renal correction. (days – weeks)

Tell me about the buffers in the body. buffer = solution containing weak acid & conjugate base. resists pH change by accepting/donating H ions

Extra: HCO3/Hb Intra: Protein/phosphate (pKa close to intracellular pH ~6.8) Urine tract: phosphate/ammonium

Tell me about the respiratory response.

o Inc H+ ! CO2, sensed by chemoreceptors both peripheral / central ! inc MV and dec CO2

How do your kidneys compensate?

o HCO3 reabsorbed. o H+ secreted by renal tubular cells, excreted. Each H+ results in HCO3

resynthesised, up HCO3 o Phosphate buffer and ammonium excretion (formed by glumate)

Started talking about bicarbonate filtration and resorption... How much bicarbonate is filtered every day? GFR 180 L/day, plasma HCO3 is 24 mmol/L... OK, we won't do the maths. 4000-5000mmol/d

1. Cardiac Action Potentials

Draw the action potential of a cardiac myocyte.

o (easy)

Number the phases. What is happening in each phase? (changes in ion permeability and ion fluxes)

o 4 = K



o 0 = upstroke: Na fast o 1 = spike = dec of Na conductance + inc K o 2 = plateau = inc Ca L + inc K o 3 = repolarisation: inc K, dec Na, Ca.

Mark on the absolute and relative refractory periods. What causes these?

o 200ms / 50ms o Fast Na channel closure. 0,1,2,early 3 o Relative: late 3 (partial recovery of inactivated fast Na channel)

What happens if a suprathreshold stimulus is delivered to the cell in the relative refractory period, how does this change as the period progresses

o phase 0 starts off with a shallower gradient and shorter peak ------ o can becomes steeper with a higher peak as the number of Na channels

available for activation increases - p21 Levy and Pappano)

What is meant by the terms excitability:

o Ease of cell to depolarise in response to a stimulus.

irritability

o (size of stimulus required to bring the membrane potential to threshold, dependent on resting membrane potential and threshold potential). More irritable = diminished potential and arrhythmia more likely.

What causes the resting membrane potential?

o (Leakage of K from the cell, Na/K/ATPase pump, small contribution from Na leakage in to the cell, Gibbs-Donnan equilibirium - luckily did not ask me to explain Gibbs-Donnan in great depth).

o Gibbs-Donnon effect = presence of impermeable charged molecule affects the distribution of other permeable, charged molecules at equilibrium, across a membrane.

What happens to the resting membrane potential in hyperkalaemia? (Becomes less negative).

• Can you draw an action potential in hyperkalaemia? 5mins up after I said Ummmm? a few times!

o Amplitude smaller o RMP less negative o Duration shorter o Steepness less

2. Body water & osmolality

How much water is present in the body



o (42L in a 70kg male).

How is this water distributed?

o Simple: o 2/3 ICF o 1/3 ECF ! ¼ intravascular, ¾ ISF.

o complicated: o ICF as above o ECF =

" 20% interstitial " 7.5% intravascular " 7.5% dense connective tissue " 7.5% bone " 2.5% transcellular fluid

What are the compartments of the ECF?

What do we mean by the term functional ECF?

o (Water that is readily exchangeable between fluid compartments).

What are the sources of non-functional ECF?

o (Water held within bone matrix, dense CT).

What is an osmole?

o 1 osmole = 1 mole of molecule present in 1 kg of solvent. o 1 mole = 6 * 10^23 = avogardro’s number.

What is osmolality? What is osmolarity?

o Lality = expressed in kg of solvent; temp independent o Larity = expressed in volume (L) of solvent; temp dependent o NB: tonicity: effective osmolarity of solution. Ineffective = urea/glucose

(except at BBB or in diabetic)

How can osmolality be measured? (I said freezing point depression but they looked like they wanted more than this)

How else can osmolality be measured? (I said calculated via 2Na + Glucose + Urea, they stared at my equation and gave me a look that suggested that was wrong - I checked it wasn't, maybe they were looking for something else).

o Calculated osmolarity = 2 Na + 2 K + Glucose + Urea ( all in mmol/L).

Have you heard of an osmometer? (Honesty being the best policy I said No! I have since heard that this seems to come up every year for a few people so might be worth spending a few minutes on). 5mins up so moved on.



o Osmometer = equipment for measurement of osmolality that relies on fact that osmotic pressure is related to the change in freezing point or vapour pressure of the solution.

o Osmotic P = hydrostatic P that just stops osmosis. o Osmotic P estimated by van’t Hoff equation: n x (c/M) x RT

o n = no. of particle dissociate into o c = concentration in g/L; M = MW o R, T = constants Universal Gas constant 0.08; T = absolute temp

o Osmolarity estimated by dividing Pressure by RT.

3. Gas exchange - lungs & placenta

Compare the lungs with the placenta as gas exchange organs

o Both involve diffusion of gases down partial pressure gradient, obeying Fick’s Law.

o Lung more efficient than placenta (3) o Bigger SA: 60m2 vs 16m2 o Thinner: 0.5 mic m v 3.5 mic m o Higher permeability at blood/gas interphase than blood/blood.

o But placenta blood flow larger in proportion to body surface area o Also high UBF 750ml/min to placenta (10=15% CO), maintains p gradient.

600ml v 300ml. o Also HbF allows double Bohr + double Haldane. So uptake O2, removal CO2

enhanced. o HbF at term = 50% 80% ! <5% at 6 months. Down to <5% by 6 months of

age.

What are the adaptations of the placental and uterine circulations that promote transfer of oxygen?

How do we measure the affinity of Hb for oxygen? (p50 value).

o By comparing the p50 value

What is the value for adult Hb? (26mmHg).

What is the value for fetal Hb? (18mmHg).

What is the saturation of blood in the umbilical artery and vein? (Unfortunately I knew the pO2 values but not the sats - I'd recommend learning these if poss. I estimated what the sats would be from the values I knew for pO2, they seemed relatively happy with this).

o pCO2 fetal 55 mmHg (!40) ! maternal 30 (!45) mmHg o PO2: maternal 100 mmHg (!40) ! fetal 15 (!30) mmHg. I o Sats: HbF sats 40%!80%; Maternal sats: 98% ! 75%



4. Flow, pressure & volume during breathing

Draw graphs of the changes in gas flow, alveolar pressure and intrapleural pressure during QUIET TIDAL BREATHING. Include units. (West 8ed p111).

o See graphs

How do these graphs change in IPPV?

o invert alveolar pressure graph o IPP would also be ↑+ve with insp ie opposite – depending on insp pressure

from vent



1. Change in position

What happens when a person stands from a supine position?

• Venous pool • Tendency to drop cerebral perfusion pressure transiently by 22mmHg

at carotids – CBF ↓20% o Compensate: baroceptor o Muscle pump / venous valve o Drop in cerebral venous pressure, so tends to maintain

perfusion pressure gradient

Various questions relating to site and function of baroreceptors, effect on SVR, MAP, HR

• High baroceptors: carotid sinus, aortic body. o Inc SVR, venoconstriction so VR, SV, CO. o Inc HR, maintains CO.

• Low baroceptors: RA, great veins in pulm system. o Inc RAAS tone, AT2 vasoconstrict. ADH volume retain.

How much blood pools in the lower limbs?

o 500-700mls. o % distribution of blood in norm vasculature:

o veins 65, o arteries/arterioles 15 (13+2), o cap 5, o central 15. (↑ 25% when supine)

2. Flow

• Tell me about flow • Laminar flow, hagan poiseuille, examples of laminar flow • Turbulent flow, Reynolds number, examples of which. Effect of increasing

viscosity/density on the flow type, tube length. • How do we measure flow in Anaesthesia? Rotameters, pneumotachograph

o Where would you find a pneumotachograph. o at various points in the breathing system or ventilator o pair of sensors is often used: I & E measured independently.

• How does it work. What are important principles in its use? o Fixed orifice with known fixed resistance, o Pressure drop measured across resistor and transduced into flow

measure. o Volume derived from flow v time. o Laminar flow maintained so P related to flow; eg. Mesh screen.

3. What are the respiratory changes with aging?

• Various questions on the decreases, effect that Anaesthesia could have.



• Significance of FRC/closing capacity, significant ages- 45 supine, 65 erect

• ↓alveolar surface area • ↑dead space : tidal volume • Compliance:

o Lung - ↑ due to loss of elasticity o chest wall compliance decrease – stiffening of joints across chest wall o C TOTAL = unchanged

• TLC – normal only due to air trapping • FVC, FEV1 all reduced • RV increases • FRC unchanged. • ↑shunt due to ↑closing capacity – loss of lung elastic tissue ⇒ IPP more +ve

⇒ atelectasis dependant parts of lung • These changes occur as a result of reduction in elastic support of the airways

and leads to increased collapsibility of alveoli and terminal conducting airways.

• 65: CC=FRC erect ! V/Q mismatch, dec PaO2. Estimated by:

PaO2=100 – (age/4) mmHg

• PaCO2 not altered by age. • Atelectasis, pulmonary emboli and pneumonia more common • These complications are increased in smokers, COPD, abdo/thoracic surgery • loss of elastic tissue around the oropharynx with aging ! prone to OSA. • No teeth!BMV difficult • OA limit C-spine, TMJ movement.

Made up:

o CVS changes with aging? o HR dec o Preload o Contractility dec o Afterload inc ! LVH, LV strain

" Ventricular wall tension: as dec compliance, dec radius, inc T. " Aortic root pressure: aortic sclerosis " Aortic compliance dec, loss of Windkessel effect " Inc SVR " HTN

o Rhythm: HB, ectopic, AF more prevalent (atrial kick 1/3 LVEDV, so AF get 1/3 drop CO)

o CO dec by 3% per decade (FRCA) o SNS tone

" Dec 2nd down regulate adreneoceptor " Global impair of ANS, so baroceptor reflex

o Polypharmacy so o BP drop: diuretic, antihypertensives o Confusion/sedation: TCA, opioid,



o Interaction: o Renal System

o GFR dec 1% per year over the age of 20 (loss of renal cortical glomeruli)

o Dec RBF (atherosclerosis, dec CO) o DM, NSAID, ACEi. o Prostatism, dehydration

o CNS: o Atherosclerosis/HTN, inc CVA/TIA. o Neuronal density is dec 30% by the age of 80 years. o Cognitive impair, dementia, Parkinsonism. o Confusion often caused by: change of environment, medication,

electrolyte imbalance, cerebral emboli and sepsis. o Visual and hearing impairment o ANS impair, haemodynamic instability, delayed gastric emptying o Don’t give details in neurontransmission pathway

Endocrine / Metabolic

o BMR dec 1% per year after the age of 30 o may cause impaired thermoregulatory control o Hypothermia ! shivering ! inc O2 MR o Inc risk of DM, thyroid disease, osteoporosis, malnutrition

Pharmacology

o Dec CO o Dec TBW o Inc adipose tissue o Plasma proteins are o MAC decreases by ~6% per decade for all inhaled anaesthetics. o MAC (age)can be calculated by the following equation:

MAC(age) = a x 10bx

x = Age – 40years

b = - 0.00269

a = MAC at age 40years ( halothane 0.75%, isoflurane1.17%, enflurane1.63%, sevoflurane1.8%, desflurane 6.6%)

4. Temperature regulation

What is thermoneutral zone?

• Ambient temp associated with minimal metabolic rate / o2 consumption.



• Ie no need to inc metabolism for thermoregulation.

Other than adult male are there any different groups? what affects the thermoneutral zone?

• Dressed or not • Neonate; 32-34 • Adult: 22-28. • Acclimatisation.

What is normal body temperature?

• 36.5-37.5

What is the interthreshold range? How is this affected by Anaesthesia?

• = core body temp range when there’s no autonomic thermoregulatory response.

Draw me a graph of heat loss during general Anaesthesia, explain each step.

• Know the 3 phases: o Redistribution o Ongoing heat loss (pre-equilibrium) o equilibrium

What ways can heat be lost in theatre?

• Radiation 40% • Convection 30% • Evaporation skin 15% • Evaporation lung 10% • Conduction 5%

What is the main way?

• radiation

How does this occur?

• Heat transfer down temperature gradient. • Phase 3 can’t be normally maintained by DM neuropathy, neonates / elderly.



April 2012 (by Hollingworth)

1. Vascular function

what are the functions of the venous system?

o return of blood to heart o reservoir of blood (capcitance vessels) ∴ regulation of CO

what factors affect venous return?

• VR = MSFP – RAP / RVR (resistance to venous return) o MSFP = blood volume, venous tone/capacitance, calf muscle pump o RAP = thoracic pump, RV function, tricuspid valve function o RVR = venous tone, caval compression o other: haematocrit, body posture,

what is the shape of veins? (wanted to hear depends on filling)

o depends on perfusion. collapsed > elipsoid > circular

Draw a vascular function curve. what is this point? (MSFP)

draw how the curve changes with loss of 1.5 litres of blood?

superimpose cardiac output curve? what happens with increased SNS activity?

o SNS inc both vaso and veno tone, overall there’s inc VR. (PK161)

2. Thermoregulation

mechanisms of heat loss in an awake patient in theatre at 20 degrees? which is most important?

o radiation 55%, E 30%, CC 15% o rad 40, convect 30, evap skin/wound 15, evat lung 10, conduct 5.

what is radiation heat loss?

o IR electromagnetic wave transfer of heat from warm object to distant cooler one. dependant on 4th power temp diff

how does the patient compensate?

o Vasomotor: vasoconstriction (1st), o Behaviour change: activity, behaviour, o Heat production: shiver, NST



now the patient is anaesthetized and paralyzed, what happens?

(drew the temp vs time graph) what is happening here? (rapid decline in temp due to redistribution)

• 1 = vasoD & loss of core:periphery gradient – 1st hr. 1-1.5degC heat loss • 2 = heat loss>heat production due to ↓VO2, ↓BMR, paralysis. not reached

effector threshold. 1-4hrs & lose another 1 deg • 3 = effector threshold – vasoC. equilibrium

now outside at 40 degrees?

• evapouration = only way to lose heat if ambient temp > body temp. depends on relative humidity. latent heat of vap of water = 0.58kcal/g water. sweat = external fluid.

now in a sauna at 70 degrees? same

asked something about does sweating alone cause heat loss or does having the fluid on the skin help? same

3. Compliance

What is laplaces law?

o The pressure inside a sphere (or hollow tube) is directly proportional to the surface tension and indirectly proportional to the radius.

o P = T/r (cylinder) o sphere with 1 fluid lined surface: P = 2T/r (eg = alveolus or heart) o sphere with 2 fluid lined surfaces: P = 4T/r ( eg a soap bubble) o For heart: P = T * thickness / r or (T = p*r/2*thickness)

(quite detailed here)



o Also note: Tension (T) = wall Stress(S) x wall thickness (w) ( for a thin walled sphere, T is thus ~ S )

o In the heart, an increased afterload causes an increase in wall stress (and hence O2 demand). For a given wall tension (T), an increase in wall thickness (w), will decrease the wall stress (S) ( ie compensatory ventricular hypertrophy)

o wall tension = P.r/2.w (thus, increased O2 demand with ↑ arterial pressure and ↑ ventricular radius, and ↓ demand with ↑ w)

- but shouldn’t inc wall thickness (hypertrophy), actually means inc O2 demand?

where does it apply?

o lung & heart, blood vessels (bladder, stomach, bowel)

anywhere else?? above

you mentioned surface tension why is it important in the lung?

• impt variable in p-v curve o good: ?keeps lung connected to throacic cage ??? o bad:

" surface tension ⇒ tendancy for small alveoli to collapse: if r ↓s ⇒ p ↑s ∴ pressure gradient for flow out of alveoli to bigger alveoli.

• It’s important factor of lung compliance. High ST, low compliance, implicated in infant resp distress syndrome.

how does the body reduce ST?

• Surfactant ↓ST (3 functions) ∴ o ↓atelectasis o ↓pulmon oedema - ↓reabsorption of fluid into alveoli from capillaries

by ↓ing alveolar lining pressure ⇒ ↓ed movement of fluid " ST is like ‘sucking force’, larger ST, larger sucking force into

alveoli. o ↑compliance of lung esp at small lung volumes (surfactant molecules

repel each other – charged molecule). ! think infant resp distress: stiff, pulmon oedema, atelectasis

how does the body reduce ST? what is surfactant?

• = mixture of:

o 90% lipids – mostly phospholipid (of which 80% DPPC) o proteins o CHOs

where is it produced? type II alveolar epithelial cells

what are the functions?(wanted to hear increased compliance) how does it have an anti-wetting function? above



other functions of type 2 cells?

• creation & replacement of type I cells, epithelial barrier (NB make up 60% of epithelial cells but only cover 5% epithelial surface)

function of type 1 cells?

• thin epithelial barrier to facilitate gas exchange. 95% of of epithelial surface (no organelle, don’t divide)

draw a compliance curve ? (i didnt draw inspiration and expiration) is that for inspiration or expiration?

what is hysteresis?

• Hysteresis is the dependence of a system not only on its current environment but also on its past environment: in lung = higher expanding pressures are needed for a given lung volume during inspiration compared to expiration

o common to all elastic bodies, elastic recoil on shortening is less than pressure needed to stretch due to energy loss

o due to presence of viscous resistance to changes in lung volume = frictional resistance in 2 forms:

" air in & out " surfactant

Hystersis: in lung = = higher expanding pressures are needed for a given lung volume during inspiration compared to expiration. This is considered to be due to higher pressure required to overcome surface tension at onset of inspiration.

4. Cells What is a cell?

• The structural, functional and biological unit of all organisms

How is a RBC different from other cells?

• does not contain a nucleus • no organelles: no mitochondria, no ribosomes, golgi ie sparse cytoplasm



• high conc of Hb, CA, HCO3, O2, CO2

how do they generate energy?

• aerobic (mitochondira) vs anaerobic (cytoplasm) • obligate glucose user; by glycolysis of glucose (Embden Myerhoff Pathway),

produce lactate. • Lactate formed fom pyruvate, catalysed by lactate dehydrogenase, to allow

regeneration of NAD from NADH, which is essential for Embden-Meyerhof pathway (a form of anaerobic glycolysis) to proceed in anaerobic conditions or in cells with no mitochondria eg. RBC.

• in glycolysis: glucose units are broken down to pyruvate. 2 ATP molecules are used, but four are produced, resulting in net gain of 2 ATP.

what is the fate of lactate? role of NAD+? (Embden myerhoff pathway)

• NAD+ cofactor for glycolysis and allows (ineffieicnt) ATP creation to continue

• Lactate: o locally oxidised when O2 reavailable (not in rbc) o to liver for metab:

" gluconeogenesis ⇒ store as glycogen (needs g6P) " transaminated to alanine " in liver cori cycle – able to lactate ⇒ (Embden myerhoff

pathway) o moved to organ metabolisers as direct energy substrate - heart, kidney,

liver. • Manson’s take on Lactate fate

It can be reutilised by the cells it is formed in(when pyruvate is able to enter the citric acid cycle the equilibrium shifts to allow lactate -> pyruvate) when oxygen is resupplied or can diffuse out of cells into the plasma and go:

1. Liver, to under go gluconeogensis(from pryuvate), this glucose can a. enter into the ATP inefficient cori cycle for further energy production during

anaerobic conditions in the muscle. (Cori cycle picture). PK367 b. be stored as glycogen and c. enter the citric acid cycle

2. heart as an energy substrate.

what else? what else is produce in the RBC?

• (23DPG) function? made by side shunt of glycolysis pathway

what else does RBC contain?

o specifically lack organelles incl mitochondria ie ATP from glucose glycolysis only (embden Meyerhoff) ⇒ lactate producers

" ATP runs NaKATPase " NADH used by metHb reductase to keep Hb reduced

o sparse cytoplasm



o Hb o structural membrane proteins

tell me more about haemoglobin

• = tetramer of 4 globin chains, each with own haem in hydrophobic pocket o x 4 haem ⇒ O2 (made by condensation of glycine & succinyl CoA) o x 4 globin ⇒ Co2 (bind to lysine/argine aa at amine part of Hb) & H

(bind to imidazole group on histidine, 38/Hb molecule; pKa 6.8 deoxy, 7.9 oxy)

o adult: 97.5% HbA (α2ß2), 2.5% HbA2 (α2δ2) and small amounts other eg HbA1c

o foetal = 97.5% HbF (2α, 2γ) – completely gone by 6/12

• HbF at term = 80% ! <5% at 6 months

Examiners were not particularly friendly, I left feeling pretty average, but I passed

1. Draw lead II of an ECG, describe what is happening at each stage.

• Lead 2 lies in axis of heart • P wave: atrial depolarisation SAN ⇒ AVN which is down & Left (ie dep toward = upward) • Small initial Q wave: depolarization starting in IV septum spreading down & right (ie dep

away = downward) • Large R wave = depolarisation spreads endo ⇒ epicardial & larger bulk of LV means net

effect is down & left (ie dep toward = upward) • Small S wave = activation of remaining ventricle, wave spreading upwards ie (dep away =

downwards) • T wave = ventricular repolarisation moving from epicardial to endocardial (ie repol away =

upward)

Identify diastole and systole.

• (PK p. 130 power kam)

Why do we use lead II in anaesthetic practice for monitoring (described direction of current across the heart but they wanted more).

o ischaemia – ideally placed for inf ischaemia o arrhythmias – most prominent deflection of p & QRS waves

What is the ECG monitoring for (rate, rhythm, ST changes).

• (rate, rhythm, ST changes). 25mm/sec 1small block = 0.04sec, 1 large block = 0.20 sec, 1mV = 1cm

Why is lead II better for this. Other people got asked about calibration.

o square wave calibration to prove 1mV = 1cm o all leads present o stable baseline with no interferance



2. Tell me about the organs that receive the most blood flow.

o 30% liver o 25% kidney o 15-20% skel muscle @ rest o 15% brain o 5% coronary

Since you started with the liver (!) tell me about the circulation to and from the liver.

• 1000ml from portal venous, 500ml hep artery, out via hep vein

What feeds into the portal system.

• Just say: SI, spleen, pancreas, gall bladder, colon.

Autoregulation.

• autoreg of hep artery, not portal vein. • hep arterial buffer response exists i.e metabolic autoregulate of HBA dilate

when PV flow dec. o dec PV, inc HB o inc PV, dec HB o but not the other way round.

• extrinsic regulation by SNS

What would happen in hypotension.



• Dec HBF; O2 delivery met by ↑extraction • ↑SNS ⇒

o mobilisation of blood from hepatic system ~500ml blood) o ↓portal venous flow

Portal triad:

• portal vein, • hepatic artery, • bile duct;

• Bile canaliculi →interlobular bile ducts → intrahepatic bile ducts → left and

right hepatic ducts merge to form → common hepatic duct exits liver and joins → cystic duct (from gall bladder) forming → common bile duct → joins with pancreatic duct →forming ampulla of Vater → enters duodenum

Where does it drain – to sinusoids then central vein (wanted direction on a diagram).

• ie blood & bile drain in diff directions

Describe La Place’s law and when it might be applied in the body.

o The pressure inside a sphere (or hollow tube) is directly proportional to the surface tension and indirectly proportional to the radius.

o P = T/r

Tell me more about alveolar compliance. ??



What would have to an alveoli if there was no surfactant. collapse

What is the advantage of having a partially open alveoli. gas exchange ie open to atmosphere, closer to steep slope of compliance curve

Draw the compliance curve for the lung (explain hysteresis).

• (repeat)

Is this static or dynamic compliance? can see both

o dynamic – effects on high airflow rate at beginning or insp & expiration

o static: " always lower than dynamic " doesn’t include airflow effect " even if remove surfactant (with saline) still see some hysteresis

due to viscous resistance of lung parenchyma

How do you measure static compliance.

• breath out in series of steps, hold position for as long as possible. pressure drop to 70-80% initial value

• Pressure: ITP indicated by transoesophageal probe. • Volume measured by spirometry

4. Tell me about EEG changes during sleep.

" BATD. " A when close eyes, drowsy " stage 1 = T " stage 2 = T with sleep spindles & K complexes " stage 3&4 = D waves " tendancy to ↑amplitude & ↓frequency " cycle up to REM which rapid irreg low amplitude waves

similar to awake EEG

What are sleep spindles;

• generated in reticular nucleus of thalamus;

what do they look like,

• = bursts of higher frequency activity

what do they represent

• brain inhibiting processing to keep sleeper in tranquil state. seen in stage 2 sleep



K complex = largest event in normal EEG. function = suppress cortical arousal response to stimuli & aiding sleep based memory consolidation

What is sleep vs what is anaesthesia.

• sleep = natural occuring state of reversible unconsiousness which person is rousable from by external stimuli. necessary for life.

• GA = pharmacologically induced state of reversable unconciousness which creates amnesia, ↓mm tone, analgesia; not necessary for life, not rousable unless drug is turned removed from the system.

Why don’t we see REM pattern EEG in anesthesia.

• REM = state of ↑ brain activity. GA agents cause global suppression of brain activity via GABA agony

What is burst suppression, why does it occur.

• pattern of alternating no brain activity and high voltage electrical activity. • burst episodes assoc with excitatory cortical activity & depletion of

extracellular Ca & ability of neurones to restore concentration. • bursts ⇒ ↓Ca ⇒ inhibition of synaptic transmission ⇒ suppression periods ⇒

time for pumps to restore Ca concs. • As deeper unconciousness: shorter bursts & longer suppression

How can we use EEG to monitor anaesthesia

• (BIS, entropy, evoked potentials ..what else?)

What are the principles of BIS monitoring.

o processing: " fourier anaylsis: raw EEG to component sine waves of specific

frequency & amplitude " power analysis: amplitude of EEG at each frequency at given

point in time o incidence of burst suppression o (Bispectral analysis) coherence - ↓conciousness ⇒ more coherant EEG

! combines 3 with multivariate analysis & proprietary alorgithm to give BIS number using reference trials on healthy volunteers.

• Problems: o agent dependent o poor PPV and NPV for awareness o inter-individual variation.

• Not fully validated in paeds. • Others eg.: Auditory Evoked potentials: response of brainstem/mid

brain/cortex to acoustic stimulus of the auditory nerve. • Entropy: describes order of chaotic wave pattern of EEG.



1. Cardiac Action Potential

Draw the SA node AP on these axes.

• Where does the ventricular AP occur - draw it on the same axes.

How long after the SA node AP does the ventricular AP commence?

• 3-5 squares, 0.12-0.2secs ie = PR interval.

What is occuring in that time? (transmission of AP across atria. AV conduction delay.)

• Point to different parts of the AP phases - what channels are open here? • Can we tetanize cardiac muscle? – Nope. As ARP of cardiac muscle is longer

than the contractile mechanism of vent muscle

2. Thermoregulation

• What is your body temp right now? 36.5-37.5 • What controls it? sensor, central control, effector mechanism. CAP (Cold, A

delta, Post hypo), WCA (Warm, C fibre, Ant hypo) • You mentioned inter-threshold range - what is that? ITR = (range of core

temp’s at which no autonomic thermoregulatory response triggered. (normally 0.2 – 0.5 degrees). Sweating occurs at the upper border and vasoconstriction at the lower border of this range – GA ↑s size to 5deg 20x 4 degree. 0.2!4

• TNZ = temp range over which VO2 is minimized. o adult 25-30, o neonate 32-34, o prem 34-36

• Where are your afferent receptors? skin



• What are your efferent mechanisms - i.e. How do you lose heat? vasoD, sweating, behavioural

• What if the ambient temp > skin temp? sweat > evap • You mentioned thermoneutral zone - tell me about it, draw graph? Is this

graph the same for everyone (ie: right shift in neonates, prems)

CT = critical temperature

• Do neonates lose/gain heat the same ways you do? o heat loss = vasoD, behaviour ie crying, limited sweating (prems

cannot) o heat gain = behaviour ie crying, skin vasoC, NST (shivering not

possible until >3/12) ! problems =

• large BSA – so lose heat quickly with radiation. • little fat – little insulation • flaccid posture - • large head with ↑blood flow: • ↓central control of temp: • large MV: so lose heat via evaporation from airway and contact

with cool air • ↓behavioural response

• You mentioned non-shivering thermogenesis – o uncoupling of oxidative phosphorylation to produce heat instead of

ATP o occurs mostly in brown fat but also elsewhere o brown fat = cells with multicuclei, high SNS innervation, lot mitochon,

good blood supply. usually perinephritic, peri large blood vessels, interscapula, base of neck (2-6% body weight neonate)

• Which nerves innervate brown fat? symp Moving on...

3. Pneumothorax

• What would happen if I had an apical bleb that burst? = small air filled lesion just under pleual surface. correlation with primary spont PTX



• You mentioned pneumothorax (PTX)- what is that? = abnormal collection of air or gas in between parietal and visceral pleura

• What are the consequences of a PTX? removal of –ve IPP uncoupling movement of chest wall & underlying lung ⇒

o ↓VA (alveolar ventilation) o atelectasis o shunt

• with significant PTX ⇒ obstruction & tension to VR, shock. • You mentioned impaired gas exchange/atelectasis/HPV/impaired VR - tell us

about it? • What happens to the air? air will be slowly reabsorbed over time • You mentioned 100% O2 helping - why?

o hypoxaemia due to large amounts of shunt ⇒ methods to correct incl ↑MV, ↑FiO2 ⇒ ↑gradient for absorption of O2 from other units with better VQ match

o also denitrogen blood, favouring gradient for resorption of N2 in PTX to blood. Venous O2 not much inc with 100% O2.

(correct hypoxaemia, de-N2 blood, maintain O2 gradient) Fine, moving on...

4. Renal dysfunction

• What is GFR? 125ml/min or 180L/day • How does lab calculate this - eGFR?

o (MDRD formula) Modification of Diet in Renal Disease; uses estimation from creatinine clearance adjusted for age, weight, gender

o Or Cockcroft Gault formula. " Cockcroft-Gault CrCl = (140-age) * Wt* (0.85 if female) / (72

* Cr) • You mentioned Cockcroft Gault formula - can you show us? no STUPID

o Also = estimation from creatinine clearance adjusted for age, weight, gender

• Why is it different for females/males? (Muscle bulk) • This patient is in ICU - is there another way to measure their GFR?

o (24hr urinary creatinine clearance) Ux.V/Px • How does this work? modified version of Fick principle (Renal clearance

formula) • creatinine by product of muscle metab. filtered (but also secreted – thus GFR

will be overestimated). See inverse log relationship – GFR needs to be ½ norm before abnormal serum creatinine

• Do you know any other tests for renal dysfunction - have you heard of cystatin C or something else...DING!

o GFR by inulin technique, is complicated, costly, time-consuming and have potential side-effects.

o Creatinine on other hand is inaccurate at detecting mild renal impairment, and levels vary with muscle mass, protein intake.

o Cockcroft and Gault formula and the MDRD formula try to adjust for these variables.

o Cystatin C has a low MW, and it is GFR filtered. Serum cystatin C may be more precise than creatinine levels.



o Cystatin C levels are less dependent on age, sex, race and muscle mass compared to creatinine.

1. LV Pressure-volume loop

• Can you please draw a LV PV loop?

• Now you cross clamp the aorta, draw this? Ie inc afterload.

• What is afterload? impedance to ejection of blood from the LV. Includes SVR,

aortic compliance, aortic valve pathology, ventricular wall tension…etc. • What other changes occur with increasing afterload?

o (Law of Leplace can define afterload: wall Tension= P.r/wall thickness,

o viscosity of blood affecting afterload – 8nl/π r4 ∴ ↓viscocity via ↓HCT



o dec stroke volume o inc myocardial work, MRO2.

• How do we change the loop for increasing preload,

• now contractility?

• What is elastance? = pressure/volume relationship ie inverse of compliance • How does the curve change with diastolic dysfunction?

would see more steep curve



• How does the curve change with aortic incompetence? What phase is this (isovolumetric relaxation?) see R) sloping D ⇒ A vertical line

• Why have you drawn that line on an angle (volume change with leaking of blood through incompetent valve)

2. Temperature Regulation

• Tell me about the ways we lose heat in theatre? • Tell me about convection, conduction, radiation, evaporation etc?

o 55% radiation = IR electromagnetic transfer of heat from warm surface to distant cool object. proportional to diff to power 4

o 30% evapouration = loss of enery by change of phase from liquid to vapour as defined by latent heat of vaoprisation (0.58kcal/kg water)

o 15% C&C " conduction = 2 material objects in direct contact and temp flow

from high heat to low heat until equlibirum " convection = motion of gas/liquid carrying away heat from

warm surface

Manson’s no.: again: 40% rad, 30% convec, 15% eva skin, 10% eva from lung, 5% conduct

• Is there a graph you know? Explain it? ??? o Temp changes under GA: redistribution; pre-equilibrium, equilibrium

• What ways can we prevent acute heat loss in theatre? o minimise heat redistribution:

" pre warming periph compartment – needs to be 1hr " preop pharm vasoD – eg nifedipine. autoreg processes maintain

norm core o cutaneous warming

" passive " forced air blanket – should be direct next to skin for best effect

o internal warming – 1 litre room temp ⇒ ↓0.25deg core o peritoneal lavage & warming o CPB o amino acid infusion ⇒ ↑metabolic rate

• How does a Bair hugger work? When should it be turned on? convection & conduction of warm air. turn on at beginning of case.

• What are the consequences of hypothermia for the patient? o cardiac morbidity x3 - ↑SNS o perioop wound infections x3 – tissue ↓oxygen due to vasoC & direct

impaired immune system o periop blood loss ↑30% - impaired platelet function & slower clotting

enzyme synthesis



3. Capnpography

• Can you draw a normal capnograph for me? Explain it?

• Where does inspiration start? phase 4 prior to downstroke. = washing out of sample chamber

• In phase 3 of the graph, where is this gas coming from? mixed alveolar gas o Mixed alveolar ! end tidal plateau.

• What are time constants? o = used to describe the rate of change of an exponential process o time taken for process to complete if initial rate of change of

exponential process was allowed to continue o 95% complete after 3 time constants (1 = 63%)

• Do you know an equation? Tau = compliance x resistance • Now your patients cardiac output has dropped by 50% ... can you superimpose

the curve? ??? o Ie = alveolar dead space increased, so end tidal CO2 value lower.

• Why did you draw that shape (dec delivery of CO2 back to the lungs due to dec cardiac output)... any other reasons?? Eventually realised they wanted me to talk about west zones of the lung, in particular zone 1 changes with decreased CO.

o zone 1(A>a>v) = pathological o zone 2 (a>A>v) = apex to 10cm above heart. flutter flow o zone 3 (a>v>A) = 10cm above to base o zone 4 = low lung volumes, weight ⇒ compression extra-alveolar

vessels

4. Blood pressure measurement

• Can you please tell me about the oscillometric blood pressure monitor and how it works?

o Senses oscillations to detect SBP, MAP, DAP o quick inflation to >50mmHg above SBP (adaptive) o deflation in increments slowly o <2mins repeat ⇒ ↑error; due to blood flow impedence.

• Can you draw a graph for me showing the oscillations detected as it deflates? Where is sys, MAP, diastolic? What is the most accurate? MAP most sensitive

3

2 4

1



• Can you tell me about an invasive blood pressure monitor? What components are involved?

o transducer = device which converts energy from one form to another o list others: saline filled pressured tubing, IA cannula, processor,

display. • Quickly moved me onto resonance and damping? • What is resonance?

o process whereby amplitude amplification occurs when frequency of oscillating signal approaches the natural reasonant frequency of a measuring system

o minimised by keeping reasonant frequency of measuring system >10th harmonic of measured variable

o bp F0 = 60-180bpm = 1-3Hz ∴ >10th harmonic = 30Hz • What is damping?

o force which has a tendancy to decrease movement within a system – due to inertia & frictional resistance; viscous/friction force

• Why are the systems calibrated to have such a high resonant frequency ( o allow for increased HR o ↑dynamic accuracy

• Do you think the systems are optimally damped? No ....... How can you increase the damping of your system?

o overdamped = bubbles, clot in cannula, excessive tubing o underdamped = taps, ↑tube length

• Do you know an equation that relates resonance and damping? I said there was a complicated graph but I didnt know an equation relating them ...

1. Oxygen carriage

• Tell me how Oxygen is carried in the blood? o combined to Heam in Hb



o dissolved • Write the oxygen flux equation. Do2 = CaO2 x CO (HbxSO2x1.34)/100 +

0.03 x PO2 o For arterial blood. = 50 x 20 = 1000ml/min o For venous blood = 50 x (15+1.2) = 800ml/min

• What does each part of this equation mean. • What is Hufner's number. =amount of O2 which can bind with 1 gram. • Why is it not 1.39. abnormal forms of Hb eg HbCO or MetHb • How much O2 do you require? 250mls/min basal demand • What happens if patient's Hb is 50. What happens if they have no Hb. What do

you do? o transfuse – although lack of 2,3DPG mean actual O2 delivery to

tissues will not improve immediately o place in hyperbaric chamber at 3 atmos ⇒ dissolved O2 to 6ml/100ml

• Draw rough outline of Hb.

• Where does O2 bind on Hb. haem



Draw OHDC for HbA. What about HbF. Why is it different. How is that an advantage.

HbF p50 = 18 ie L shift. ↑uptake O2

2. Blood gases

• Shown a blood gas - analyse this. • Mine was a pretty straight forward one, something like this (don't remember

exact numbers) o pH 7.32, pCO2 80, pO2 350, BE -20 (HCO3 not given) = mixed

metabolic & resp acidosis ie sepsis or MH • Discuss causes of metabolic acidosis and types

• • Anion Gap discussion = (Na + K) – (Cl + HCO3) norm 8-16mmol/L.

o rasied gap = MUDPILES



" (methanol, " uremia, " diabetic ketoacidosis, " propylene glycol, " isoniazid, " lactic acidosis, " ethylene glycol, " salicylates

o normal gap = USED CARP ie hyperchloraemic met acidosis " Ureteroenteric fistula " saline admin " endocrine – addisons/spironlactone, primary

hyperparathyroidism " diarrhoea " carbonic anhydrase inhibitors " ammonium chloride " renal tubular acidosis " pancreatitis

Where is lactate formed?

o Wherever anaerobic metabolism occurs: RBC, muscle.

3. Draw Ventricular Action Potential

• Explain each phase • Discuss RMP

o defined by ↑permeability of K > Na o Double Donnan effect –

" non diffusable intracellular anions (proteins & phosphates) " NaKATPase creates external Na as nondiffusable

o vent mm -80mV RMP, threshold -70mV

Ion Inside Cell Outside Cell Equilibirum Potential mV

Na+ 15 150 +60

K+ 150 5.5 -90

Cl- 9 125 -70

• Write Nernst equation and discussion with regards to the ventricular AP

Goldman Hodge Katz form:



gK = K conductance gT = total conductance • Nernst potentials of Na +60 , Cl -70, K -90

4. Gastric physiology

• Draw stomach and discuss hormones SECRETED by the stomach

• Discuss hormones ACTING on the stomach and what each one does o Gastrin –

" +ve input to ECL cell, chief & parietal " ↑growth GI mucosa " ↑antral pump contraction

o CCK – inhibit gastric emptying o Secretin – inhibit gastrin ⇒ ↓gastric acid secretion o GIP – inhibit gastric acid secretion & motility o motilin – regulation of migrating motor complexes



o GIH – (from D cells in GI mucosa & pancreas): inhibits all other hormones ⇒ ↓motility, ↓absorption products of digestion

• Discuss anatomy (muscle layers) of the stomach o muscularis externa: outisde > inside: (LCO)

" longitudinal " circular " oblique " mucosa incl rugae

• Discuss peristalsis details - [drew a food bolus in oesophagus] - discuss what happens to this food bolus - ie. what makes it progress and what happens at each stage

o peristalsis " radially symetrical contraction & relaxation of mm propogating

wave in muscular tube in aterograde fashion " controlled by medulla oblongata

o primary peristalsis – " occurs when bolus enters oesophagus during swallow " bolus into stomach in 8-9secs

o secondary peristalsis – " activated by stretch receptors showing bolus stuck " local reflex

Manson:

• Cephalic phase • Gastric phase • SI phase.

I think there was discussion on gastric mucous too but don't remember secreted from goblet cells under the action of prostaglandins. trefoil peptides

1. Exercise physiology

• O2 consumption at rest for adult and neonate in ml/kg/min 3.5 vs 7 • O2 consumption when riding bike up hill.

o O2 consumption can inc up to 15x ie 250ml/min to 4L/min.



• Draw graphic trend of SBP and DBP as exercise progresses from light to mod to heavy

• Explain trend o SBP ↑ing due to ↑CO driven by SNS o DBP ↑ing but by less due to falling SVR

• What happens to SBP and DBP when you stop o ↓SNS activity ⇒ ↓CO ⇒ ↓SVR to other tissues o ∴ on top of ongoing skel muscle vasoD may see ↓↓bp until

baroreceptor system kicks in o VO2 remains elevated after severe ex for ~90mins

• Overall physiological response to exercise o CVS:

" demand led system " ↑metabolic build up in muscles ⇒ ↓TPR ⇒ ↑CO to meet

demands of tissues " ↑VR – mm pump, thoracic pump " targetted blood flow to muscles – splachinc vasoC

o tissues: " ↑O2 extraction " ↑2,3 DPG " recruitment of capillaries



o Resp: " ↑MV instantly & linear ↑with ↑ing exercise " ↑CO:MV 1:4 (easier to move air than blood) " R shift OHDC in tissues " mod ex: little chage in ABG " severe exercise ↓Pco2, ↑PO2, ↓pH lactic acid

2. Osmolality and osmolarity

osmolality = number of osmoles of solute / kg of solvent (indep temp & volume of solvent) ! mosm/kg osmolarity = number of osmoles of solute / litre of solvent (dep on temp & volume) ! mosm/L

• Given diagram of two solutions separated by semi-perm membrane (one w higher solute concentration than the other. What happens next

o solvent will move from area of low solute conc to area of high solute concentration

• Define osmotic pressure. Hydrostatic pressure applied to prevent movement of solvent molecules by osmosis across a semipermeable membrane

• If pressure is applied on one side will it stop the water movement? yup = osmotic pressure: p=nrt/V

• Colligative properties - name all 4 o bp elevation o osmotic pressure o freezing point depression o SVP depression

How do you measure osmolality

• measured: Osmolality can be measured on an analytical instrument called an osmometer. It works on the method of depression of freezing point.

• calculated: osmolal gap ie 2x(Na+K) + urea + glucose. o measured – calculated should be <10. o causes of ↑ed osmolal gap = DM (ketones), ethanol, methanol,

mannitol, ethylene glycol

• Osmolality vs tonicity tonicity = effective osmolality of a solution ie particles actually exerting a force across a membrane eg effective = solutes (most) which don’t cross the membrane. eg ineffective glucose in presence of insulin

• Tonicity of hartmann's. tonicity for D5%. o Hartmans osmolality = 280 o D5W initially osmolality = 282 then metab to water & ⇒ ∴ zero

! ∴ slightly hypotonic thus gradient for movement out of plasma • What happens when there is a insulin deficit?

o D5W – high glucose load will make glucose an effective solute in skel mm & adipose beds ⇒ incr tonicity of D5W

3. Respiratory



• Normal MV for 70kg man. 5-8L/min or 110ml/kg; • Scenario of asthmatic pt in ICU with MV of 10L/min but PaCo2 is still raised.

o What could be the reason? o asthma = hyperreactive airways, ↑bronchial secretions, gas trapping o therefore cause

" physiological dead space specifically proportionally increased anatomical dead space ( in relation to rapid shallow breathing)

" shunt – gas trappping – blood moving through areas V/Q <1 o supplemental FiO2 is supporting life o hypercarbia causes:

" incr FiCO2 " hypoventilation " V/Q mismatch & shunt – shunt ie V/Q <1 being major cause

due to gas trapping " incr CO2 production – incr MV " rapid shallow breathing thus MV does not = VA ‘wasted vent’

" ie MV – anatomical DS = VA • Discussion of physiological (anatomical, alveolar) and apparatus dead space

o anatomical dead space " = 2.2mlkg adult & child " measure with N2 washout

o alveolar dead space: norm = 0.3 " Bohr eq = VD/Vt = PACO2 – PECO2/PACO2 " usually minimal in healthy lung; NB above = end tidal not

mixed expiratory; if mixed expiratory = measure of physio DS. • How do you measure physiological dead space

o Bohr method breathing into a douglas bag to measure mixed expired CO2. PACO2 is measured via arterial PaCO2

• How to measure alveolar dead space. • How do you get each component in Bohr eqn

o PACO2 = arterial sample o PECO2 can be measured by Douglas bag or in theatre substituted for

PETCO2 (with correction factor) • What could be the cause of increased DS in the abovementioned pt?

o anatomical o (alveolar)

4. General/Sleep physiology

• Physiological changes in recovery – o CNS – PONV, delirium, reduced LOC if residual anaesthetic effect o respi – hypoxia: alveolar hypovent, VQ mismatch (atelectasis), pulmon

oedema (diffusion limitation), upper airway obstruction, dec resp drive o thermoregulatory changes – shivering o CVS instability – high SNS drive post extubation/awakening before

examiners switched focus to CNS • EEG for asleep pt. delta waves • What happens in a very deep GA - burst supp and isoelectric waveform • Draw waveform for burst supp. burst of high frequency, lower amplitude

waves



• What is the normal amplitude for an ECG? how abt EEG? o EEG 50uV ie v small o ECG 2000uV

• EEG for awake state • Frequencies for various EEG waveforms

o beta 13-30 Hz , o alpha 8-13, o theta 4-8Hz, o delta <4Hz

• Which part of brain is involved in control of sleep - said RAS • Which neurotransmitters are involved when you are waking up? Mentioned

NA acting on locus ceruleus, Ach, glutamate, dopamine • Which part of the brain produces noradrenaline? bell rang before answering

locus cereuleus, nucleus raphe magnus, PAG

Viva on 16/04/12

1. Myocardial Action Potentials

• Draw me a X and Y axis, then examiner put a dot on X axis: start from here draw me a SA node AP and don’t worry about the voltage, I just want the shape of it. Finished.

• Then draw me a LV myocardial AP starting from where you think it should be, following the SA node AP transmission. Finished.

• Why did you choose to start from here? o Coz the SA node AP takes about 0.15s which falling in the range of PR

interval 0.12-0.2s. • Tell me what’s happening in the phases of the LV AP. • Does myocardium get tetany? Why not? nope • Where is absolute and relative refractory period on your graph?

o ARP 200ms, RRP 50ms. 1/3 through repolarisation (late 3 to 4)



• Why is it refractory? Na channels are in an inactive state • What happens to make it become relatively refractory?

o movement of Na channels back to closed active state o Relative: late 3 (partial recovery of inactivated fast Na channel)

• What happens in hyperkaelemia of 8mmol/l? o incr irritability of myocardial cells. chance of arrhytmias but as K rises

eventually heart will stop in diastole.

ECG changes = loss P wave, wide QRS, tall Ts for (High K), short QTc

ECG change with low K:

o Prolongation of the PR interval o T wave flattening and inversion o ST depression o Prominent U waves (best seen in the precordial leads) o Apparent long QT interval due to fusion of the T and U waves (= long QU

interval) o Frequent supraventricular and ventricular ectopics o AF, atrial flutter, atrial tachycardia o VT, VF and Torsades de Pointes

2. Stomach

• What’s the function of the stomach? o immune – HCL – innate immune system o mixing of food stuffs & formation of chyme o storage of food and emptying of food o absorption

" of acid based drugs " acidification of Fe into absorpable state " lipase " pepsinogen ⇒ pepsin

o secretion of hormones – IF - needed for B12 absorption in ilieum • Draw me a picture of the stomach.

o • Where are the cells secreting HCl? from crypts in body & fundus



• How many layers of smooth muscle does stomach have? 3= long, circle, oblique

• Tell me how stomach moves? o cephelad phase: receptive relaxation – vagally mediated o coordinated Peristalsis waves – begins in lower body. controlled by

gastric basal electrical rhythm o coordinated contractions – antral systole ⇒ movement towards

antrum • But how? What’s controlling the movement of it?

o hormonal " ↑emptying – H, motilin, gastrun, Ach " ↓emptying – PGs, GIP, secretin, CCK, GIH

o neural: " local autononic reflexs " vagal

o local sensing: " osmolality in duodenum " fats, CHO, acid in duodenum

• What does the stomach secrete? It’s components? o see prior

• Draw me a picture of a parietal cell and illustrate the mechanism of grastric

production.

• Is gastric acid continuous in 24 hours? What happens to the parietal cell to increase acid production? no. related to ingesiton of food (via ECL cells)

NB gastric emptying, gastric secretions can both be summarised by 3 phases (cephalic, gastric, intestinal); but different for:

Mechanism of peristalsis: as above

Or Manson’s alternative resource:

Peristalsis



• Initiated near the fundus and the body, progressing towards the pylorus, producing a peristaltic wave.

• Velocity of 1cm/sec, at a frequency of 3 per minute. • Inc Frequency by Vagal • Inc force by: gastrin, ACh.

Swallowing

3. Calnography

• Draw me a normal capnography trace. o repeat

• Where do inspiration and expiration start? o repeat

• Why does expiration starts from the flat part? o no Co2 in resp anatomical dead space, by end of inspiration.

• Tell me about those phases? o upstroke (2) = transition from dead space to alveolar gas

• Then different disease/situations. o obstructive pattern – sloping exp trace – due to impaired wash out

from alveoli • If a person have an arterial pCO2 of 80 mmgh what’s the physiological

effects? o hypercarbia effects:

" CNS: " ↑CBF



" narcotic effect at high levels – LOC & resp suppression " CVS

" ↑central SNS output " but direct –ve effects on heart eg ↓inotrop, ↓chronotrope, vessels ! balance depends on level of PCO2

" ↑arrhytmias " ↑coronary blood flow " periph vasoD

" resp: " ↑MV – depending on drugs eg opiates, Vas " alveolar hypoxia " pulmonary HTN

" thermoreg - ↑heat loss 2nd to vasoD effects " metabolic – inhibition of metabolic pathways " renal – attempts to buffer & reabsorb more HCO3

• What the blood PH is likely to be if it’s acute and uncompensated? I said 7.0 -> He asked if I guessed or worked out from an equation. I said guess.

o Acute respiratory acidosis: HCO3− increases 1 mEq/L for each 10 mm Hg rise

inPaCO2. o Chronic respiratory acidosis: HCO3

− rises 3.5 mEq/L for each 10 mm Hg rise inPaCO2.

The expected change in pH with respiratory acidosis can be estimated with the following equations:

• Acute respiratory acidosis: Change in pH = 0.008 X (40 − PaCO2) • Chronic respiratory acidosis: Change in pH = 0.003 X (40 − PaCO2)

4. Calcium

• What’s the plasma concentration of Ca++? o normal total = 2.2-2.6 mmol/L o normal ionised Ca 1.15-1.3 mmol/L o acidosis ⇒

" ↓calcium binding to albumin " ↑ionised Ca

• What does Ca++ combine in plasma? o albumin – causes variation in total amount of Ca. does not effect

ionised Ca o corrected Ca – corrects total calcium level if albumin level abnormal

• Tell me the functions of Ca++?. o cell signalling

" neurotransmitter – release of Ach " secondary cell messenger

o cell membrane – NMDA, DHPR o muscle contration – all mm types o enzyme function - coagulation o 99% total body Ca involved in structural support – bones o intracellular Ca = 100nanomoles

• How does Ca++ make muscle contract?



o skel mm & cardiac: presence of Ca interacts with Trop C causing removal of Trop I from actin-myosin binding site. presence of Ca allows ongoing excitation contraction coupling

o smooth mm: Ca binds to calmodulin ⇒ activation of calmodulin dependant myosin light chain kinase

• What’s tetany? tetany is incomplete relaxation of mechanical mechanism between summated stimuli

• What causes it? o high frequency external stimulation o hypocalcaemia – low ECF Ca ⇒ ↓threshold to activation of volatge

gated Na channels ie more irritable⇒ progressive depolarisation ⇒ ↑possibility of Aps

" 50% ↓Ca level ⇒ spont AP generation • How is Ca++ regulated by body?

o Parathyroid gland – releases PTH o 1,25-OH2D (calcitrol) o (calcitonin)

• What’s the function of PTH? o ↑active vit D in kidney ⇒ ↑Ca absorb from gut o ↑reabsorp Ca in kidney, ↑excretion phosphate o ↑bone Ca release

• When do you see increased PTH? o hyperparathyroidism:

" primary = patholological high release eg tumour " secondary = physiological ↑ due to ↓Ca eg end stage RF " tertirary = unregulated ↑PTH release after persistent

parathyroid stimulation • What condition may cause secondary PTH?-end stage RF. • Why does it cause increased PTH? lack ability to 1 hydroxylate 25-(OH)2D

and work to rebaorb Ca

September 2011 (By Shanmuganathan)

Monday am phys:

1. Afterload/Cardiac output

• Determinants of cardiac output? Equation for cardiac output? Draw LV pressure volume loop with AL line explaining all the phases of systole and diastole. Things that affect afterload? How does viscosity affect afterload?

CO = HR × SV SV determined by Preload, afterload and contractility Graph



Afterload is the imepedence to the ejection of blood from the heart into arterial circulation. Affected by: i) Ventricular wall tension ii) aortic root pressure iii) Aortic wall compliance iv) SVR – viscosity increases afterload by virtue of the HG-equation. 2. ICF/ECF concentrations of Na, K and Cl

[Na]i: 10mmol/l [Na]o: 140mmol/L, [K]i: 135mmol/l [K]o: 4mmol/l, [Cl]i: 10 [Cl]o: 110mmol/l

• What determines these? Nearnst equation with figures for the differents constants. Goldman-Field and cord conductance. Gibbs Donnan effect.

For a single ion distribution across the semi-permeable membrane is determined by opposing factors – i) diffusion down chem gradient ii) Electrical force trying to achieve electrical neutrality.

𝐸 = 𝑅𝑇 ÷ 𝑧𝐹 ln 𝑖𝑜𝑛 𝑜 ÷ 𝑖𝑜𝑛 𝑖 room temp = E = 58

Gibbs Donnan Effect – whereby the presence of non diffusible intracellular anion proteins directly influence the movement of diffusible ion. Has a small effect on RMP

3. Temperature and GA

• What is heat? Heat loss when in a fridge, then how this is accelerated by a GA. Different percentages for different mechanisms? Then heat gain in a sauna (well, a sauna with no humidity, so I guess a desert). How heat can be lost with/without humidity in this example.

Heat is the kenetic energy possesed by the molecules of a substance. Temperature is the thermal state of an object that determines whether it receives or donate heat. Heat travels down a temperature gradient (woolly defination – sorry – I cant find the exact statements I had writen down) GA i) Intial rapid phase: Redistribution, 1st hr temp decreases 0.5-1C due to decrease MR and increased heat loss from skin. Dependent on core to periphery temp gradient ii) Linear phase: Slow decline for 2-4hrs. Loss > metabolic heat production. (Rad: 40%, Convec: 30%, Conduc: 5% & Evap: 15%) iii) Plataeu phase: 3-4hrs. Heat production = heat loss. Metabloic heat resistricted to the core.



Heat loss mechanism like Conduc, convec and radiation require a thermal gradient to transfer heat –hot to cold. This is lost in a sauna – ambient temp > body temp. Only mecahnism to loss heat is via evaporation. 0.58kCal dissapated/gram of sweat. Evapouration is dependent on humidity.

4. Capnography

• Draw a normal capnogram. Then went through several examples - bronchospasm (with explanation of dynamic airways compression and differing resistances with long time constants), decreased cardiac output, rebreathing, recovery from muscle relaxant, then a weird one about a partially loose sidestream CO2 catheter

?? Can discuss as a group.

1. FRC

• What is the FRC.

FRC = ERV + RV or equilibrium point of opposing elastic forces of the chest wall and lung. FRC = 30mls/kg

• What changes FRC?

Height, weight, position, disease & anaesthetic & muscle relaxation

• Does it change with age? Height? Anaesthesia?

Does not change with age in the absence of condition that alter recoil of the lung or chest wall. Changes with height proportionally Decreases with anaesthesia 15-20%

• What are the functions of FRC? How much O2 within it?

i) O2 Store, ii) Buffer to maintain steady PaO2 iii) Prevent atelectasis iv) Minimise work of breathing v) Minimise PVR vi) Minimise V/Q mismatch vii) keep airways resistance low

O2 stores:

• 270 in FRC (13%) • 800 in blood • 200 myoglobin • 50 tissues



2. Pituitary hormones

• Tell me about the pituitary gland. What is it anatomically. What are the embryological derivations. Is there a third lobe? What hormones does it produce (wanted all 8).

Comprised of 2 lobes, anterior and posterior. ?? Pars intermedius as the 3rd lobe Anterior pituatry is derived from the ectodermal outpouching – Rathke Pouch. Consists of 2 cell types – chromophils (granular secretory, either acidophils orbasophils) & chromophobes (agranular secretory) Protein hormones (acidophils): GH & PRL Glycoproteins (basophils): FSH, LH, TSH Polypeptides (basophils): ACTH Posterior pit is an extesion of the hypothalamus Scecretes ADH and oxytocin. Synthesized in the SupraOpticalNucleus & ParaVentricularNucleus and stored in the posterior pit.

• Tell me about ADH. What are the triggers for release?

Nonapeptide produced in the SON & PVN. T1/2 16-20mins. Metabolised by tissue peptidases ADH released by i) increases in osmolarity. Threshold starting at 280mOsm/l. ii) Hypovolemia sensed by baroreceptors. Rate of ADH secretion is 1/∝ to baroreceptor firing. iii) Pain, stress, emotion, exercise & drugs

• Where are the hypothalamic osmoreceptors? Are they within or without the BBB? What are the receptors? Other than V1 & V2, are there any others? Is it a weak or strong vasoconstrictor?

In the hypothalamus as part of the AV3V - Organum Vasculosum, of the Lamina Teminalis (OVLT) and Subfornical Organ (SFO). They lack BBB. Strong vasoconstrictor.

?? just V1 & V2. Sound like a leading question.

3. Venous return

• What is venous return? What factors determine venous return?

Is the quantity of blood flowing from the veins into the R) atrium/min

VR = (MSFP – RAP) ÷ RVR

• What is the mean systemic filling pressure? Draw the graph.



MSFP ~ 7mmHg. Is the degree of filling of the systemic circulation that forces blood back to the heart. Pressure measured in the systemin circulation at circulatory arrest. Represents a degree of over filling.

• Why the plateau at negative pressures?

At -2mmHg the large vessel collapse preventing VR producing a plateau.

• Is the linear component of the line really linear? Why?

Yes it is linear as the VR decreases linearly with increases in RAP between 0 and MSFP. Hydrostatic gradient promotes venous return.

• How does the curve change if 1 litre of fluid is rapidly infused?

Parallel displacement to the right therefore enhanced VR at any given RAP. 15% increase in blood vol will double MSFP. 15% decrease in blood vol will drop MSFP to 0

• What are the normal values?

RAP: 0mmHg = VR: 5L RAP: 7mmHg = VR: 0L

4. Temperature & regulation

• What is heat? What is temperature?

See above for def

• What is the normal body temperature? What changes this? How is it detected?

37C ± 0.4C. Posterior hypothalamus esthablishes the set point. Na & Ca ion ratio and neurotransmittors determine the set point. Detected by skin receptors (Krause and Ruffini) intergrated in the hypothalamus.

• Where are the bulbs of Krause, and where do they send their signals to?

Located in the dermis and transmit info via Aδ fibres. Produce static discharge which increases when temp drops below 25C.

Kraus = cold (santa Kraus)

Ruffini = warm (roof is on fire)

• Other than the skin and the hypothalamus, where else is temperature detected?

The core ie deep body thermal receptors

• What is the response to cold, and when does it 'kick in'?



Interthreshold range: The range of core temps at which no autonomic thermoregulatory responses occur (37C ± 0.2C). Vasoconstriction 36.6C, Non shivering thermogenesis 36C and shivering 35.5C

• At what temperature do you shiver?

35.5C

Monday pm Room 1:

1. Cardiovascular changes with ageing

• Changes in SBP, DBP, MAP.

Increase in SBP and MAP due to reduced elasticity in the large arteries. DBP may increase because of increased peripheral resistance. Age >75 have a decreased DBP due to rapid run off of blood in the stiffer large arteries. Baroreceptor response is imparied. β-R repsonse is imparied due to reduced receptor numbers, receptor affinity or decreased cAMP.

• Why does conduction system slow down? Reflected pressure waves contribute to increased afterload.

Due to fibrous infiltration of the SA node = loss of pacemaker cells

• Draw radial pulse waveform for old -versus- young person • Ventricular and aortic compliance are reduced. • Slower up stroke due to decreased myocardial performance. • Higher peak pressure during systole due to decreased compliance. • Increased transmission velocity because of increased aortic wall stiffness. • Slower HR

2. Fick's Law

• What describes diffusion (Ficks law), write the equation

Flux = (A/T) × (Sol/√MW) ×(P1-P2)

• How does this apply to gas exchange across placenta? (diff gradient incl. Bohr and Haldane effects, diff surface area, thickness)

Blood/blood interface. Large SA 10-15m2, 3.5µm thick Fetal Hb has higher affinity for O2. Fetal Hb has a high conc. Encouraging diffusion. Double Bohr and Haldane effect Maternal Hyperventilation High rate of placental blood flow. Diffusion is flow limited



3. Pulmonary vascular resistance

• Why is pulmonary arteral pressure so low compared to systemic? • Explain West zones of lung. Does recruitment or distension contribute more? • Explain hypoxic pulmonary vasoconstriction.

See previous PHSL VIVA

• Draw graph of pulmonary vascular resistance Vs. lung volume.

U- shaped with nadir at FRC

4. Hyponatraemia

• Main physiological causes (relative volume deficit, excess water). How do you calculate osmolarity? What's the difference between mmol and mEq? Explain how massive hyperglycaemia and lipidaemia cause hyponatraemia. Something about urea being an ineffective osmole. Why have hypo-, not hyper-natraemia in large volume deficit?

Osmolarity = 2[Na+ + K+] + Urea + Gluose

An equvilant is the amount of the substance × by its valancy

Pseudohyponatraemia due to increase in tonicity from glucose and lipids drawing more H20 and diluting Na+

Urea is an ineffective osmole as it will diffuse across all fluid compartments equally without isolated compartmental increases in tonicity.

1. Adrenal Medulla

• What does the adrenal medulla produce?

Synthesizes + secretes bioamines ie mainly Adrenaline, Norad (minimal -mainly peripheries)

• What are the steps for synthesis?

Tyrosine (hydroxylated by tyrosine hydroxlase, rate limiting step)# L-dopa (converted by Dopa carboxylase) # Dopamine (taken up by chromaffin cells and converted by dopamine-β-hydroxylase) # Norad. Norad (N-methylated by PNMT) # adrenaline

• Where does the tyrosine come from?

Diet or dereived from hydroxylation of L-phenylalanine in the liver.



• What are the enzymes required? What do they act on?

?? See above

• What are the receptor subtypes? What does each receptor subtype do?

α1 – Vasoconstrict, Relax GI smooth muscle, contract GU smooth muscle. α2 - Inhibition of norad release, Plt aggregation, VSM contraction β1 – Increase HR,contractility, relaxation of GI smooth muscle β2 – Bronchodilation, vasodialtion, glycogenolysis, muscle tremor β3 – Lipolysis of fat 2. Coronary circulation

Draw the graph of flow in the left and right coronary arteries. Explain the differences.

Why does this occur? What dictates coronary blood flow? What is it normally?

250ml/min. 5% of CO. Subendocardial flow in the LV ceases during systole. Pressures are a lot lover in the RV

What would happen during exercise?

Myocardial O2 extraction (55-65%) is flow dependent, with exercise CoBF inceases to match demand. Increases 4-5× 1000-1250ml/min. Heart cannot develop O2 debt.

Would anything during exercise have a negative effect on coronary blood flow?

Increase in HR reducing diastolic time

What would happen if pulmonary vascular resistance increases? decrease

3. Upper Airway

• What are the functions of the upper airway?

See previous viva

• Explain how a cough occurs.

Cough reflex applies to the lower repiratory tracts. Larynx, carnia terminal bronchial and alv are sensitive to noxcious stimuli. Afferent impulses travel via Aδ fibres then up the vagus to the medulla for intergration. Autonomic sequence of event is triggered by neural circuits.

i) 2.5L rapid inspired. ii) epiglottis closes and vocal cords shut tight, trapping air with in the lungs. iii) Abdominal & expiratory muscles contract increasing the pressure



with in the lungs rapidly to 100mmHg. iv) vocal cords and epiglottis suddenly open so air explodes out, 100mile/hr. the strong compression of the lung causes the non-cartilaginous part to invaginate producing slits. Foreign material is carried away with the moving air.

• Explain humidification of inspired air. • Where does this occur? • Explain how the anatomy assists this. • How does the water in air change if the inspired air was 20 degrees compared

to 37? o 37 = 47mmhg o 20 = 14.5mmhg

See previous VIVA

• What about the vapour pressure? Describe turbulent flow.

Turbulant flow is a square wave front with eddies and swirls. Re > 4000 often occuring in branched or uneven tubes. P = kv2 Turbulent flow is proportinal to the r5 and inversely proportional to fluid density. 4. Gas flow measurement

• How do you measure gas flow on an anaesthetic machine?

i) Mechanical – Dry gas meter, Wright spirometer & peak flow meter, Strain gauge, Pilot tube. ii) Pressure drop – Pneumotachograph, Venturi, Oriface, Rotameter iii) Ultrasound iv) Thermal conductivity

• Draw a pneumotachograph. Explain how it works.

A known/fixed resistance to flow and causes a pressure drop measured by a differential pressure transducer. Q = P/R

• What do the capillary tubes do?

Produce laminar flow and a known resistance to gas flow.

• Why is a heating element included and what does this achieve?

To prevent condensation which encourages turbulent flow and to ensure that viscosity of gas is maintianed. Increase temp = decrease viscosity.

• Why would a wheatstone bridge be used with this? (Specifically told to not draw it).



Adam and KB says it increases sensitivity of a circuit

Tuesday PM, room 1

1. Capnography

• Draw a capnogram. Show the phases. What is happening at each phase? Identify the alpha and beta angles. What causes the angles to change? What are the sources of error in the capnogram? How is the CO2 measured? What would be the effect of rebreathing CO2 on the capnogram? On the baseline? On the plateau?

Methods of measurement i) Infrared, ii) Photoacoustic spectrometry, iii) Laser spectrometry, iv) Mass spectrometry, v) Chemical colourimety, vi) Ramen Scattering Capnogram - Phase 0: Inspiratory phase, P1: Dead space (apparatus and anatomical) gas, free of CO2, P2: Mixture of alv and dead space gas, P3: Alv plateau. Peak represents PECO2.

Increased α angle = V/Q mismatch ie astham, bronchospasm Increased β angle occurs with rebreathing of excessive dead space 2. Oxygen cascade

• Draw the oxygen cascade. Explain how the value at each step is derived.

Dry room air: 159mmHg Saturated room air: 149mmHg – humdification of dry inspired gas Alveolar gas: 100mmHg – gas exchange in alv Arterial blood: 95mmHg – venous admixture End capillary blood: 40mmHg – duffision of O2 to cells Mitoc: 4- 22mmHg



• Explain venous admixture.

Amount of mixed venous blood that needs to be added to the pulmonary end capillary blood to produce the observed arterial partial pressure of O2

• Explain physiological causes for a change in diffusing capacity.

Increased diffusing capacity: i) Exercise ii) Increased capillary blood volume (recruitment) Decreased diffusing capacity: i) $ capillary transit time, ii) $ capillart blood volume iii) pulmonary congestion iv) alv capillary blockage

• Explain shunt. Write the shunt equation.

Shunt refers to blood that enters the aretrial system without going thru ventilated areas.

QS/QT = (CcO2 – CaO2) / (CcO2 – CvO2)

• Explain diffusion and perfusion limitation. Is oxygen diffusion or perfusion limitated? Under what circumstance does oxygen exchange become diffusion limited? Transit time for RBCs in pulmonary capillary? Effect of exercise on RBC transit time?

Perfusion limited: Gas transfer between alv & cap is dependent on the amount of blood flowing thru the capillary. Dependent on partial pressure build up. Diffusion limited: Gas transfer is independent on partial pressure. Gas transfer is limited by diffusion. O2 NORMALLY PERFUSION LIMITED Oxygen becomes diffusion limited in severe exercise where transit time of RBC < 0.25sec and at altitude. Normal transit time in 0.75sec.

3. Temperature regulation

What are the mechanisms of heat loss? What mechanisms of heat loss are active in a room in which the ambient temperature is 38.0 degrees?

• Vasodilation, inc blood flow to skin. Heat loss via radiation, conduction, convection

• Sweating + heat loss via evaporation • Higher than core temp, so only way = evaporation via sweat. Lose 0.5kcal/g of

water. o 4.18 kJ/kg/C = specific heat of water o ~0.58kcal/g H2O or 2.5kJ/ml o NB: caloric value of glucose: 4.18 kcal/g



Draw the graph of temperature changes in GA? What is happening in each phase of the graph?

• Redistribution: 1st hour: vasodilation to peripheral, equilibration of core / peripheral temp.

• Ongoing heat loss: 2nd – 3rd hours o Rad: 60% 40% o Convect: 15% 30% o Evap: from skin, wound: 15% o Evap: from lung 10% o Conduct: 10% 5%

• Plateau phase: heat loss = heat gain via thermogenesis. o NB: DM, neonate, elderly.

What is the interthreshold range? What happens to the interthrehold range in GA?

= range of core body temperature where there’s no autonomic thermoregulatory response (sweat, vasoactivity…etc) think of that graph

Widens:

What happens to temperature regulation in pregnancy? In a menstruating woman?

• Vasodilate, higher heat loss, met by higher MR in pregnancy • Core temperature inc in menstruation. 2nd progesterone rise

What is the the thermoneutral zone for adults and neonates?

• Adult: 22-28C • Neonate: 28-32; 32-34

4.LV Pressure-volume loop

• Draw the pressure-volume loop for an adult left ventricle. • Identify the valve events. • Identify diastole and systole. • Identify stroke volume. Draw the changes be if the abdominal aorta was

clamped. • Draw the changes that cause stroke volume to be maintained. • Show the gradient on the curve that reflects left ventricular elastance. Explain

the relationship between elastance and compliance. • Explain lusitrophy. Show how the curve would be altered if lusitrophy was

impaired.

1. Shunt



• Define shunt. causes, • Derive shunt equation,how can me measure each component, • What happens to Pao2 and O2 content during shunt, why?(flat part and steep

part of ODC ),

At the top/flat of the curve – a small drop in O2 content = a large drop in PaO2 Mid/steep portion of the curve – a small drop in PaO2 = a large drop in O2 content

• Cardiac causes of shunt, what happens to shunt during PE.

Thebesian veins, R to L shunt. PE causes a shift to a high V/Q ratio producing alv dead space. Is not a problem with shunt!!! 2. Foetal circulation

• Describe fetal circulation, saturation at IVC, why high PVR, why IVC blood goes to brain,

Saturations –

• Ductus venosus: 80%, • IVC:67%, • LV:65% • Systemic cir: 60%, • RV:50% • SVC:32%

High PVR – non aerated lung with intact HPV

IVC has the highest O2 saturation

• What happens at birth- only cardiac changes

Afterload increases closing the Foramen ovale when LAP > RAP. PVR drops allowing flow from RA to RV to LA. Ductus arteriosus closes with exposure to high PaO2. Closure of ductus venosus. Closure of the shunts the LV & RV goes into a series circuit.

3. Capillaries

• Diameter of capillary,diameter of RBC, Starlings forces,

5-10µm in dia and 1mm long. RBC diam 7µm. Starling forces NFP = [Pc - Pif] – [πp – πif] Pc: 35mmHg (arterial end), 15mmHg (venous end) Pif: 0, πc: 28mmHg, πif:3mmHg NFP arterial end: 10mmHg, venous end: -10mmHg

• why capillaries have high pressure, Law of Laplace,



T = P × r Because of their small radius the wall tension required to prevent rupture is low so they can withstand relatively high intravascualr pressures.

• how substances cross capillary, formula for diffusion

Diffusion for nutrients and metabolites. Bulk flow for fluid

• describe how a capillary looks like under a microscope

Thin walled vessels made up of tubes of endothelial cells lying on a basement membrane

4. Kidney & acid-base

• How does kidney handle hydrogen ion, how much HCO3- is filtered, what happens to H + when all HCO3- is absorbed, titratable acidity,

H+ is freely filtered, 0.684mmol/day. 4320mmol/day of HCO3- is freely flitered.

• Write the equation for H+ combining with HPO4-,

H+ + HPO42- = H2PO4

-

• How much H+ is produced per day, how much of H+ is excreted by HPO4-.

• 100mmol/d H+ • 40mmol/day of H+ can be excreted/day with HPO4-

• what is body's normal phosphate level, what % of HPO4- is excreted as H2PO4,

Plasma PO4- level is 1mmol/L

• How much PO4 is filtered per day, do we excrete all PO4 as H2PO4(I said no)- they asked me why?.

90% freely filtered, 160mmol/day. 75% reabsorbed thus 40mmol/day available for buffering.

• Other methods of H+ excretion- glutamine to NH4 and HCO3-, in what condition does glutamine broken excessively....

?? acidosis

ding ding ding...



PHYSIOLOGY

Examiner 1

1. Control of ventilation

• Describe for me the control of ventilation?

Sensor: chemoreceptors, lung and other receptors Central controller: Medulla, pons, brain Effector: resp muscles

• What areas of the brain are involved?

Medullary resp centre – reticular formation. Pre-botzinger complex: resp rhythm generation. DRG: inspiration. VRG: expiration.

• Are there any other areas?

Pneumotaxic center: Upper pons ⇒ ↑RR. Regulates inspiratory volume and RR. Fine tunes the resp rhythm Apneustic center: Lower pons ⇒ ↓RR. Excitatory effect on inspiration and prolong ramp potential.

• What types of chemoreceptors are involved?

Central and Peripheral

• Where are the chemoreceptors?

A chemorecptor is a receptor that responds to change in the chemical composition of blood or fluid around it.

• Which (peripheral or central) are more important?

Central chemo-R are most important, involved in min to min ventilation.

• Which are more sensitive?

Peripheral as it matches ventilation to abrupt changes in PCO2

• Can you draw a CO2 vs. minute ventilation curve? • What is the slope of the line?

?? Gain of the system ie respiratory drive

• Can you demonstrate what would happen to the curve in an elderly smoker?



COPD: CO2 response to ventilation is reduced. pH of brain ECF has returned to near normal thus have lost most of their stimulus to ventilate.

2. Liver failure & anaesthesia

• What are the implications of a patient in severe liver failure requiring anaesthesia?

• What are the functions of the liver?

Protective functions: i) Blood reservior ii) macrophage system iii) Drug metabolism iv) coagulation v) urea synthesis

Regulatory functions: i) Glucostat (CHO metabolism) ii) Fat metabolism iii) protein metabolism iii) bile production iv) storage of vitamins

• What functions are most affected in liver failure? • What plasma proteins are made by the liver? • Phase I reactions>phase II • coagulation system • ↓PPB • ↓plasma cholinesterase • Albumin, ? fibrinongen • Are there any plasma proteins that are not made by the liver?

Immunoglobulins

• Tell me about the role of the liver in coagulation?

Produce coagulation factors and bile, required for absorption of vit K

• Which coagulation factors are made by the liver? Which ones aren't?

Liver makes, fibrinogen (I), prothrombin (II), V, VII, IX, X, XI, Protein C & S + Antithrombin

∴ NOT made 3,4,6,8,12,13

• Which coagulation tests will be affected in liver failure?

INR

• Tell me about the liver and carbohydrate metabolism?

Liver contains 100g of glycogen which can be released s free glucose. Uptake into hepatocytes is not a energy dependent process. Glucokinase coverts glucose to G6P and stored as glycogen. Glycogen synthetase builds glycogen stores and glycogen phosporylase breaks its down. Gluconeogenesis is facilitated by glucagon Insulin :



• enhances glucose phosphorylation, glycogen synthase, increases glycolysis, • inhibits gluconeogenesis and glycogenolysis.

• What are the roles of insulin?

Anabolic hormone CHO metabolism – i) Increase glucose transport via GLUT4 ii) increase glycogen synthase iii) reduce glycogenolysis iv) reduce gluconeogenesis v) reduce glucose release by the liver. Protein metabolism – i) increased tissue uptake of aa ii) increase protein synthesis iii) decreased protein breakdown. Fat metabolism – i) increased fat synthesis ii) clearance of fat in blood by lipoprotein lipases iii) increased fatty acid synthesis, stored as TAG iv) decreased ketogenesis v) inhibition on hormone sensitive lipase Electrolytes – decreases membrane permeability to Na+ = hyperpolarization which shift K+ into cells lowering plasma K+.

• What are the actions of glucagon?

liver effects: Hepatic glycogenolysis, gluconeogensis & lipolysis and protein catabolism

• Describe the process of gluconeogenesis?

Glucose is synthesised from non CHO precursors, derived form fat and protein metabolism. Occurs in the cytoplasm of the liver Hydrolytic rxn converting

• G6P to glucose, • fructose-1-6diphosphate to fructose-6-phosphate & • conversion of pyruvate to phosphoenolpyruvate (2 enzyme step)

In the liver alanine and lactate derived from muscle is converted to pyruvate. Glucagon and glucocorticoids promote gluconeosis. Insulin has an inhibitory effect.

• What is glycogen?

Synthesised from glucose in liver and muscle when excess glucose is available. Requires glycogen synthase

• What happens in end-stage liver failure? • What are the CNS effects? • What causes them? • Can you describe the urea cycle?



Nitrogenous end-products of aa degradation is ammonia. Surplus ammonia is toxic and is converted to urea for excretion by the kidneys. Urea cycle is an enegry dependetn cycle using 3 ATPs. Ornithine combines with NH3 & CO2 to form citrulline which combines with a 2nd NH3 to form arginine which is hydrolysed to form ornithine, H2O and urea. 2H+ are produced for each urea molecule formed – 1000mmol formed. H+ may be impt for neutralising the alkali load from the metabolism of neutral aa.

• What does the urea cycle produce and consume? • How does the urea cycle link into carbohydrate metabolism?

Examiner 2

3. Coronary circulation

• Can you describe for me the anatomy of the coronary circulation?

Arise from the aortic root. RCA and LCA. LCA ÷ into LAD & circumflex.

• What are the branches of the marginal artery?

?? there are non

• What is the venous drainage of the coronary circulation?

Coronary sinus recieves blood from the small, middle, great and oblique cardiac veins + left marginal and left posterior ventricular vein.

• Where does the coronary venous drainage go to?

Right atrium

• Which part of the venous drainage is most important? • Can you draw for me a graph of Left vs. Right coronary artery flow vs. time? • What is the total coronary flow per minute?

250ml/min

• What percentage of this goes to Left vs. Right?

L > R

• So can you quantify flow to the right coronary during systole in mL/min? o total =250ml/min. o 180 to L, o 70 to R

• What colour is the venous blood from the coronary circulation? • What does this mean? I think he was getting at that it is dark blue due to high

O2 extraction



4. Oxygen measurement

• In what forms can we measure oxygen?

Tension, content & saturation

• List ways to measure O2 tension

i) paramagnetic ii) fuel cell iii) clark electrode iv) USS v) raman scattering vi) mass spec, vii) gas chromatography

• List ways to measure O2 content?

i) calculation from saturation ii) Van slyke apparatus iii) Lex O2 Con

• List ways to measure saturation?

i) pulse oximetry ii) co-oximetry

• What does paramagnetic mean?

A substance when directed into a magnetic field, locates itself with the strongest part of the field due to the unparied electrons on the outer shell of the molecules

• Other than oxygen do you know of any other paramagnetic gases?

Nitric Oxide

• What does diamagnetic mean?

Repelled from field

• What diamagnetic gases do you know of?

N2O, N2, CO2

• Can you describe paramagnetic gas analyisis?

Dumbell on filament – O2 attacted into a non uniform magnetic field due to unpaired electrons. Displaces nitrogen filled dumbells on filament. Mirror on dumbell swivels and reflected light beam moves on a scale.

• Are there different types of paramagnetic analyser?

Null displacement – reflected light detected by a photocell causes current to flow in a coil around the dumbell and stabilses the mirror current required measured. Differential pressure transducer – sample gas & reference gas sucked thru anaylser. Magnet switched on and off rapidly. O2 is held by the magnetic field thus creating a



difference in tension between the 2 gasses. The diff is transduced andrelated to O2 tension.

• Which one do you have in the machines in your hospital? • Can you explain how it works? -I drew the diaphragm analyser diagram • What is the diaphragm connected to? - I said a strain gauge, and maybe a

wheatstone bridge • What is a strain gauge? Can you draw one?

Wheatstone bridge

• Can you explain the other (dumbell) paramagnetic analyser? • What detects the movement of the dumbells? • What converts the light signal to our screen display? -I started to talk about

transducers and the bell rang

1. Saline & osmolality

• What is in a litre bag of normal saline?

H2O, Na & Cl: 154mmol

• Why is it called “normal”.

Osmolarity is near the same as blood Historical term = used to think blood was 0.9% salt. Near normal osmolality

• Difference between osmolarity and osmolality

Osmolality: number of osmoles of solute/kg of solvent. Independent of temp & pressure. Osmolarity: number of osmoles of solute/L of solution. Altered by temp because of the expansion of the soultion.

• How is osmolality calculated

Osmometer. Works on the method of depression of freezing point.

• What is the clinical use of calculating serum and urine osmolality • What is the anion gap

The diff in the measure cation and the meausre anions in the plasma, urine or serum. Used in attempting to identify the cause of metabolic acidosis. Anion gap = (Na + K) – (HCO3 – Cl). norm= 8-16

• Where is ADH produced. How does it act.



SON + PVN & stored in the posterior pituatry. Act on the V2 receptors on the basolateral membrane of collecting duct cells to enhance luminal expression of AQP2

• What are collegiative properties of fluids.

Properties of a solution that depend only on the particle concentration (osmolality). The number of particles present per unit volume is impt

• Why do people put antifreeze in their car

Drops the freezing point

2. Cut to Hand - Responses

• What happens if I cut my hand. They wanted to hear in general, withdrawl reflex, pain, bleeding.

• Further detail on withdrawl reflex, and then what happens to the other arm. (I bombed this part).

o sensory input of pain from periphery o afferent pain via A delta. Polysynaptic mediation in spinal cord o efferent Aα to flexors to withdraw (inhibition to antagonists ie to relax

& allow withdrawal) o crossed extension reflex =

" coactivation of contralateral Aα extensor motor neurone (allows fixation of other side of body to allow withdrawal from pain)

• Describe the anatomy of the sympathetic nervous system

Arise from preganglionic neurons in the grey matter of the lateral horn of the spinal cord from T1 – L2/3 Synapse with the post ganglionic neurons within the sympathetic chain. Pre ganglionic fibres are myleinated B fibres. Post ganglionic fibres are unmyelinated C fibres. Cervical part – Sup middle and inf ganglia Thoracic part – T1-T5 Lumbar part Pelvic part Adrenal medullary 2. Arterial pCO2

• What determines C02 tension in arterial blood.

PaCO2 = VCO2 ÷ VAlv

• Define minute ventilation

MV = RR × TV



• What would happen to paC02 in ventilated patient if resp rate was halved and tidal volume remained constant.

PaCO2 doubles

• Difference between alveolar ventilation and minute ventilation.

Alv ventilation = MV – dead space – the volume of fresh gas flow entering the respiratory zone each minute. Represents the amount of gas available for gas exchange MV is the total voulme entering the lung.

• Graph of paCO2 vs alveolar ventilation. Then how does this graph change with a large dose of opioid (in an unventilated patient).

Graph right shifted and gradient decreased. Gain and sensitivity redeuced.

4. Cerebral Blood Flow

• Normal cerebral blood flow (for adult and also per 100g of tissue)

• Draw graph of cerebral blood flow vs pa02. They wanted to know exactly how quickly CBF rises when pa02 drops below 50mmHg.

• How is cerebral blood flow measured. (They didn’t seem to mind when I told them that I didn’t know more apart from nitrous, and that somehow Fick’s principle is involved).

cerebral blood flow measurement: - fick principle - nitrous oxide or xenon 133 - carotid angio - transcranial dopplirometry - cerebral Spo2 Ketty Schmidt : - N2O using Fick. 10% N2O over 20mins, map arterial & venous conc 2 sigmoid curves seen on graph & gap in middle = CO

• What happens to cerebral blood flow when you’re dropped onto Mount Everest.

Hyperventilation leading to vasoconstriction leading to decreased CBF. Death will ensue as resp alkalosis will brake hyperventilation + over ride peripheral chemoreceptos and urge to breath is abolished leading to apnea



Physiology

1. Hypoxaemia types and details about each type they did ask me about how each one produces the hypoxemia in detail and I had to write down shunt equation as well as alveolar gas equation

i) Hypoventilation ii) Diffusion limitation iii) Shunt iv) V/Q mismatch v) low FiO2

2. Hypothalamo-pit axis, post pit, details about ADH mech of axn

went in to details about ADH , all its effects like thirst, water rentention vasoconstriction and also the intracellular signal pathway GPCR

1. LV pressure loop, contractility - had to draw the loop, how it changes with contractility, definition of contractility, how to measure it I said slope of IABP line , they asked more and I mentioned echocardiogram seemed to be satisfied with that, stroke volume, ejection fraction, frank starling law , graph

2. Immune system : natural, acquired and details about complement - they seemed to be satisfied with my superficial knowledge about this, but I did know a bit on the complement cascade

Innate – non specific defence that doesn’t require prior exposure to pathogen. i) Physical barrier ii) Complement iii) phagocytes

Complement is a group of 25 heat labile of which C1-C9 are impt. Produces an amplification cascade. Classical pathway and alternative pathway ending in the common pathway. Function of complement i) Chemotaxis (C3a C5a) ii) Opsonisation (C3b), iii) MAC (C6-9) iv) degranualtion of mast cells (C3a Ca5) v) vasodialtion and increased permeability (C3a C5a)

Phagocytes derived from pluripotent haemopoietic stem cells

Acquired – specific defence targeted at pathogens following exposure. T Cells – made in the thymus. Each T clone respond to 1 antigen. T-Helper (CD4) – bind to MHCII antigen complex and release cytokines which activate CD8 and increase production. T-Cytotoxic (CD8) – Bind MHCI antigen complex, releases perforin which lyse cell membrane B lymphocytes – activated by T cells which produce antibodies. 1st exposure takes 10-14 days. Second exposure = rapid productions

Physiology 1: ADH

• Tell me about the production, transport and secretion of ADH. • What Receptors does it act on?



V2 receptor on the basolateral membrane

• Are the 2nd messengers in the vasculature the same as in the kidney?

No V1 is Gq. V2 is Gs

• What are the effects of alcohol on ADH release?

Suppresses ADH release

• What are its overall effects on the kidney- wanted dec UO? • What are the effects on the splanchnic system?

Vasoconstriction

• What are the effects on the lung- I said vasoconstriction?

↑PVR

• How is it metabolised?

Tissue peptidases and 1/3 secreted by the kidney.

• Extras- are there any hormones that inhibit its secretion

ANP

Physiology 2: Pulse oximetry

• Tell me how a pulse oximeter works?

Light shine at 2 wave lenghts red (660nm) – Hb and infrared (940nm) – HbO2. Activated sequentially followed by an off period at 100Hz. Intenstity of radiation from the 2 LEDs measured.

• Can you draw the graph? • What is this point?(isobestic point)

Absorbance of light by Hb and HbO2 is the same at 805nm. The absorbance at any of these points depends only on the Hb Conc

• What is its significance? - -used to be used in older oximeters as reference point, now no longer used

Earlier models used wavelenghts at isobestic points to compensate for Hb conc

• How does it tell it is arterial blood?

By selecting out the pulsatile component only



• What does the R value mean?

Ratio of the amplitude of the red and infrared signals. Has a non linear relationship with saturation.

• Any conditions that could alter this?

Most calibration points are between 80-100. Values below this are extrapolated from higher readings and are subject to much error.

• How accurate is it?

>70% accuracy of ± 2% 50-70% accuracy of ± 3%

• What can effect the pulse oximeter accuracy?

Patient – i) vasocontriction ii) movement, shivering iii) malpositioning iv) dyes (methylene blue, idocyanine green underestimate) Environment – Light flickering at same frequency, infrared heaters Delay – Due to siganl average time, necessary to reduce motion and other artefacts LB Law – i)wavelenght not monochromatic ii) scattering iii) length of light path vaires Physiology 3: Saline and osmolality

• Tell me about normal saline? • Why is it called normal? • What is normal osmolality in the blood?

280-295

• So why is this normal and not hypertonic?

we measure it via freezing point depression rather than calculated value, so it is isoosmolar with blood when measured by freezing point depression

• Why is that?

We have extra unmeasured ions

• What is Osmolar gap(if they didn’t volunteer the above.) • What conditions tend to cause a high osmolar gap?

Alcohol, methanol, ketones, mannitol, ethylene glycol

• What is the difference between osmolality, what is osmolarity? • You mentioned ethylene glycol that is also known as antifreeze – could we use

salty water instead in our engines? • What are collegitive properties of fluids?



• What happens to SVP when osmolaRity is increased?

it decreases

Physiology 4: Starling's curve for LV

• Can you draw a Starlings curve for the Left ventricle (SV vs sarcomere length) • What is the peak you have drawn there? 2.2um • What else can you put on the x-axis apart from sarcomere length? ( LVEDP,

LVEDV, CVP) • What happens either side of the peak?

Decrease in SV or force of contraction

• What is this? – pulled out a pressure transducer. • If I attached this to a CVL and measured the pressure what does this tell me

about the RV.

indication of preload but very limited clinical application.

• If I took this as being a measure of LV preload what assumptions would I be making for this to be correct?

There there is no valvular pathology, pulmonary pathology cardiac compliance and no arrthyrmias.

• How does this pressure transducer work? • What is a Wheatstone bridge? How does it make your reading more accurate.

What are the two ways that it can work (resistance and current sensors)

The bridge changes the reference level to zero so that any changes is essentially an infintie gain.

April 2011 (By Shanmuganathan)

THE FOUR STEMS: 1. LV pressure time CURVE, 2. ARTERIAL PRESSURE 3. Pulm circulation 4. Blood gas (the stem looks easy/straight-forward.. was quite a sweat they twist it but lovely duo examiners.. who guided me through).

1. LV PRESSURE CURVE:

• draw the lv pressure time curve, LAP tracing, when does the lv filling start (after IVR), EXPLAIN DIASTOLIC PHASES.."She WANTED ME TO DRAW DIASTOLIC FLOW time curve and the area under the diastolic curve and what it represents". no idea ..



2. BP

• You talked about pressure : how to measure arterial pressure .. I classified.. talk about electromanometer assembly.. I went thro.. can u explain the way the diaphragm operates.. ( detail of moving plastic on stretched wire that alters resistance and then the amplification..) phew.. lucky i crammed it prev night

Classification of BP Measurement Manual – Cuff + Mercurey manometer + Palpation / Korotkoff method / Doppler

• Single cuff, tubing + bulb, mercury manometer and detector (stethoscope, doppler etc)

• Width 40% circumference of arm or 20% length of arm • Korotkoff sounds – I) sound appears II) quieter III) rise in vol IV) muffling V)

loss of sound • Inaccuracies - i) SBP slightly lower then direct measuurement and DBP not

good correlation ii) leaks iii) wrong cuff size iv) AF, HoTN (over estaimates SBP), obesity, shivering, movement

Automated – Automated oscillometric, Arterial tonometry and Penaz technique

• Single cuff which occludes artrial flow and then deflated • SBP – Sudden increase in magnitude of oscillations • MAP – Lowest pressure at which max amplitude obtained • DBP – Abrupt decrease in amplitude • Inaccuracies – i) SBP accurate, MAP & DBP not so good ii) unable to follow

rapid changes in pressure iii) Obesity, AF, HoTN

??Invasive

3. Pulmonary Circulation Examiner 2: tell me whats the PA pressure

25/8mmHg (mean 15mmHg), Pulsatile flow

(25/10 mean 12).. why do u think the mean is so low. i went blah blah.. he jus wanted LA PRESSURE is 5mmhg.. so no need for the RV to sweat it out !!.

Lung accepts the whole blood vol and not concerned with directing blood from region to region. Keeps the work of the right heart as small as possiible for efficient gas exachange

THEN HE GOES.. I DOUBLE THE CARDIAC OUTPUT.. how will it alter the PVR ( reduced)

PVR: 2mmHg/L/min Presure increases i) Recruitment is the chief mechanism for fall in PVR - Zone 1 & 2. ii) Distension – Zone 2 & 3



why/ ( recruitment and distention) .. which one of the vessels collapsed vessel/ parlty opened vessel requires higher pressure to recruit..

Reason some vessels are unperfused at low pressures is no fully understood. Perhaps random differences in geometry of complex networks resulting in preferential flow - West

dint approve of my guess.. .. West zones.. when do u see zone 1.. pa occlusion.. he wanted hypotension.. i dint volunteer,, then he goes.. why dosent hypotension produce zone 1.. ?

Zone 1 may be present in severe hemorrhage/HoTN or Alv presure raised ie IPPV (over all )= alv dead space

Zone1 – PA > Pa > Pv Zone 2 – Pa > PA > Pv Zone 3 – Pa > Pv > PA

4. Blood Gas Interpretation

• OK here is a blood gas (pH 7.5, HCO3 35, pO2 75, CO2 45 ) ; metab alkalosis, eg: vomiting. etc..

• compensation.. he goes: o --> "WHY doesn't the kidney try sincerely to correct though the pH is

alkalotic?"..[Clue: any hormone that does it?] .. At last i said it "Aldosterone mediated paradoxical aciduria in a effort to conserve volume as vomiting is continuing... "

o also prox mechanism – attempt to conserve Na but loss of H

Other questions: spinal anesthesia and pulmonary circulation, the resisters and formula and example the autonomic influence to the pacemaker potential, ions involved.. compliance curve for COAD and resistive disease



1. Oxygen cascade

• Can you draw the oxygen cascade?

Picture

• How is the alveolar value measured/calculated?

??

• Is there a different or better form of this equation (alv. gas eqn) and what is it?

PAO2 = PIO2 – (PAO2/R) + F

• Why is there a correction factor? What is it for?

F is a correction factor. Typically 2mmHg. Alv Gas equation is valid under steady state conditions with no inspired CO2. As FIO2 approaches 1 a correction factor is applied to allow for diff in inspired and expired vols

F = PACO2 × FIO2 ×[(1-R)/R]

• Why is there a drop from alveolar to arterial?

Shunted blood from bronchial artery and thebesian veins

• How is shunt written/expressed?

2. Ultrasound

• Tell me about ultrasound

Ultrasound: Sound waves with frequency (2-15MHZ) above the threshold for human hearing Sound: Longitudinal pressure waves that travel through a medium causing its molecular density to compress and rarefraction

• How are ultrasound waves produced?

Piezoelectric crystal which expands and contracts when a AC current is passed thru it

• How are they received?

Reflected waves return to the probe where they hit the piezoelectric crystal and are converted back to a current. Crystals spend 1% of time producing sound waves and 99% of time listening for their return.

• What is doppler ultrasound?

Doppler measures velocity from change in frequency (Δ in frequency ∝ velocity)



• What is the equation for doppler shift?

V = C×Fd÷ (2F0×cosΘ) V = velocity, C = speed of sound thru tissues, Fd = fre shift, F0 = fre emitted, Θ = angle between emitted sound and moving object.

• Why choose one frequency over another?

Increase frequency decreases depth of image. Superficial structures : 10-15Mhz, Deeper structures: 5-7MHz and Heart: 2.5-7.5MHz

• What is attenuation?

Loss of amplitude or power of the signal as it travels thru the tissues. Caused by absorption, reflection, refraction and scattering. Higher fre = more attenuation and less penetration. For 1MHz, 1dB is lost per cm traveled.

3. Smooth muscle vs skeletal muscle

• What are the differences between smooth muscle and skeletal muscle?

Insert table

• What do they look like under a microscope? • What is the tension length relationship for smooth muscle?

Max length and force of contraction of smooth muscle is greater then that of skeletal muscle because of prolonged attachement of myosin cross bridges to the actin filaments. Cross bridge cycling rate is reduced – ‘latch state’

• What is actually happening at the bottom and top of the curve? • What is the optimal overlap value? • How is smooth muscle contraction different from skeletal muscle (excitation-

contraction coupling and in the nature of the contractile force)?

Smooth muscle isnt under voluntary control. Has different isoforms of actin myosin. Less sacroplasmic reticulum and few mitoc. Fluctuating RMP (-20 to -65mV) Smooth muscle contain calmodulin (no troponin). Ca2+ + calmodulin = activation of MLCK, which phosphylates the myosin light chain # increase ATPase activity and cross bridge cycling. Occurs at a slower rate. MLC phosphatase dephosphorylates MLC. Relaxation occurs with dissociation of Ca2+/Calmodulin complex

• Is their a length-tension relationship for smooth muscle?

No – ‘Plasticity of Smooth Muscle’. Stretching increases tension and if held at the greater length then tension falls. Smooth mucle behaves like a viscous mass and not a rigid tissue.

4. LV Pressure-time trace



• Draw a LV pressure-time trace • Superimpose the Aortic pressure -They were meticulous about the detail, ie

were the lines perfectly superimposed in the upper portion, or offset, where and by how much

• When does the mitral valve open? (I said when the atrial pressure is higher than ventricular, they wanted to hear at the end of isovolumetric relaxation)

• When does blood stop flowing out of the aorta? • Why does the aortic pressure drop before blood stops flowing?

Wiggers Diagram

1. What is the normal Systolic and diastolic BP?

• What BP is in the elderly? In the child?

Elderly (70y): 140/75mmHg MAP - % moderately due to %in TPR. SBP - % > MAP due to $ compliance of elastic vessels DBP - $ declines beyond 60 Child (10y): 105/65mmHg

• How do you defined SBP and DBP? Draw Aortic root pressure.

SBP: Reflects max LVSP exerted on the walls of the arteries during contraction phase of the heart. DBP: Relates the level of vessel recoil or amount of vasoconsrtiction in the arterial system or the lowest arterial BP reached during the ventricular cycle.

• What determines SBP? and DBP? and What is MAP?

MAP: average pressure in the arterial system during the cardiac cycle.

MAP = DBP + 1/3PP

MAP = CO x SVR

• What value can BP drops to if HR is very low? -- (I think the answer is MSFP)

?? With minimal blood flow or with no blood flow the pressure within the circulation reaches an equilibrium called MSFP – 7mmHg

2. What is the SI unit of Temperature? How do you define Kelvin?

K = 1/273.16 of the thermodynamic temperature of the triple point of water



= temp and pressure at which ice, water and water vapor are in thermodynamic equilibrium

Kelvin is an absolute scale in that there is a theoretical true zero where molecular activity ceases

• what classification of thermometers do you know? Explain principles of electrical thermometers

Non Electrical: i) Liquid filled ii) Dial – Bourdon gauge or bimetallic strip iii) chemical Electrical: i) Resistance thermometer ii) Thermistor iii) Thermocouple iv) Infrared i) resistance of metal increases linearly with increase in temp ii) small bead of metal oxide, the resistance of which falls exponentially as temp rises iii) Seebeck effect – voltage is produced at the junction of two dissimilar metals and the magnitude varies linearly with temperature at the junction

• How do you calibrate it? (shocker)

Need a reference thermometer + multimeter to measure thermister resistance

Q1: tell me about the hepatic circulation, where does blood flow in portal circulation come from? what factors affect hepatic blood flow, autoregulation, what happens after meal

Derived from both the hepatic artery and portal vein. 1.5L/min or 25% of CO. Both contribute to hepatic oxygenation.

Hepatic Art: 30% of total blood flow + 40-50% of O2 supply. Hepatic arteriolar pressure is 35mmHg. Portal vein: Valveless vein and drains blood from the intestines, stomach, spleen, pancrease and liver. 70% of total blood flow & 50-60% O2 supply. O2 sat is 85% due to mesenteric arterial shunting. Portal system is low resistance, low pressure and low flow

Intrinsic – i) Autoregulation, Some degree within the hepatic artery. Flow is maintained untilSBP < 80mmHg. Portal system has no autoregulation and flow is linear to pressure. ii) Semireciprocal interrelationship ‘hepatic arterial buffer’ between portal venous & arterial flows. $ portal = %artery flow due to a bulid up of adenosine that dilates the artery. No change in portal flow (not autoregulated) when arterial flow is altered.

Extrinsic – Hepatic artery has α, β & Da receptors. Portal vein has only α receptors. Glucagon increases HBF by vasodialtion. VIP & secretin vasodilates the artery but minimal effect on the portal vein.



Feeding increases intestinal blood flow and increases HBF.

Q2: draw the pressure time tracing obtained from the PA catheter when it's in RV, then PA, then wedged.

• difference between RV and PA tracing

RV: Small peak followed by a large peak due to atrial contraction followed by ventricular contraction. RV – systolic: 15-30mmHg, diastolic: 0-8mmHg. PA: Large peak due to ventricular ejection with small dicrotic notch due to closure of pulmonary valves. PA – systolic: 15-30mmHg, diastolic: 5-15mmHg. Distingush by i) no initial peak ii) dicrotic notch iii) small diff between peak and trough preassures iv) wave form less symmetrical.

• what assumptions made for wedged pressure to reflect LV preload

PAOP reflects LAP in the absence of abnormal mitral valve, norm atrial compliance and LVEDP

Q3: O2 cascade similar to the question above

Q4: what is monroe kellie doctrine, draw intracranial compliance curve, CSF production and absorption curve.

Monroe Kellie – states that the cranial compartment is icompressible and the volume inside the cranium is fixed. The cranium and its constituents create a state of volume equilibrium so that an increase of one constituent is compensated by a decrease in another

85% brain; 5-10% blood, 5-10% CSF (both = 75mls) ! (CSF has another 75mls in spinal cord)

This is my viva as best I can recall. It was much more stop-start than I expected. Examiners were very calm, friendly and professional.

1. Pulmonary circulation/HPV/West zones

• What is normal pulmonary artery pressures and MAP? • Why is it so low?

See above

• What are the determinants of PVR?

Follows Hagen Poiseuille equation



Lung volume: @ RV resistance increases as extra alv vessels collapse. @ TLC resistance increases due to compression of alv vessels. Resistance is lowest @ FRC Pressure: recruitment and distension $ PVR Viscocity: %HCT # %PVR HPV: %HPV # %PVR NO production by shear stress # vascular relaxation. Neural: α1 vasoconstricts, β2 vasodialtes Humoral: Histamine, 5HT, TXA all vasoconstrict

• HPV what determines it? Is it present in the denervated lung?

Occurs in isolated lungs. Mediated by PAO2 (major influence) & PVO2.

• What’s the mechanism of HPV?

Mechanism is not known.

• When PA pressure rises what happens to PVR? How does this occur? • West zones – describe the characteristics of each one. • Is West zone 1 present in a normal healthy person? What situations can cause

West zone 1 to be present?

See above

2. GFR/Starling/measurement

• Say I’m given a drug that changes GFR. By what possible mechanisms could this be achieved? (Break up the Starling equation, changes in aff/eff art. tone, MAP, mesangial cell tone

• Write out the Starling equation, explain all the terms.

GFR = Kf × NFP NFP = PGC – PBC – πGC σ is ignored as assumed 1 for kidney ie not permeable Kf dependent on surface area & hydraulic permeability. Mesangial cell: contraction (ATII, histamine, NA, TXA2, Endothelin & ADH) relaxation (ANP, PGE2 & cAMP) PGC: Most impt determinant. Determined by MAP, Afferent arteriolar resistance & Efferent arteriolar resistance. Increase afferent arteriolar resistance = $PGC # $GFR (ATII = $GFR, PGE2 = % GFR). Increase efferent aretiolar resistance = %PGC # %GFR (biphasic response with severe arteriolar vasoC = $GFR due to πGC > PGC PBC: Obstruction of urinary tract will %PBC # $ GFR



πGC: influenced by colloid osmotic pressure, flitration fraction

• Why is the oncotic pressure in Bowman space so low?

There is no protein within the Bowmen capsule

• How large does a molecule have to be to NOT be freely filtered? I said 7000 Daltons, they seemed happy

> 7000Da. Between 7000 & 70000Da the amount filter becomes progressively smaller with increasing molecular size

4-8nm!!!!! with ↓for –ve charged particles

• Why is haemoglobin with a molecular weight of 69 kD filtered yet albumin with a weight of 70 kD not filtered? charge

Charge is the 2nd determinant of filtration of macromolecules. –ve molecules are filtered to a lesser extent & +ve charge to a greater extent then neutral molecules

• How is GFR measured in the lab? Why is it not done in day to day practice? • How is it measured in day to day practice? Cr clearance or estimations based

on age, sex and spot creatinine • What is the relationship between plasma creatinine and GFR? Draw a graph

describing this relationship.

3. RBC structure/Hb/breakdown of RBC

• Describe the structure of haemoglobin. How many Fe ions per Hb molecule?

Hb is a metalloprotein. 65kDa. Each Hb has 4 polypeptide chains. Each globin chain has its own haem group in a hydrophobic pocket.

• What binds to Hb

O2, CO2, H+ & 2,3-DPG

• What is the lifespan of the RBC?

120 days

• Where is it broken down? IV and RES Proportion broken down in each?

Removed by the reticuloendothelial cells, esp the spleen.

• In the liver what cells are responsible for RBC break down, by what process do they take up the RBC?



Phagocytosed by Kupffer cells of the liver

• Describe the process of RBC breakdown in IV compartment and RES. • What happens to the protein chains? • What happens to the Fe? • What happens to the haem ring? I basically regurgitated the paragraph from

Kerry’s book plus talked about uro- and stercobilin and how they’re excreted

Metabloic systems become less active as they age leading to fragility. Fragile membranes rupture during passage thru the trabeculae of the spleen. Hb is phagocytised by macrophages. Globin: globin chains are broken down into aa for protein synthesis & gluconeogensis Iron: released from macrophages and carried back to bone marrow for production of RBC or storage in the liver as ferritin Protoporhyrin: Protoporphyrin ring opened to biliverdin + carbon monoxide. Biliverdin converted to bilirubin, bound to alb and carried to the liver where its conjugated with glucuronic acid and excreted in bile. In the gut bili is converted to stercobilin and in the kidney converted to urobilinogen

4. LV/ aortic pressure traces. I got hammered in this question, it went for AGES

• Draw the LV pressure vs time trace (Hint: Draw it BIG, take up a whole page) • Mark where the MV opens and closes • What is happening when the MV opens? End of isovolumetric relaxation, LV

pressure drops below RA pressure • Can LV pressure ever be less than 0? yes with severe stenosis of mitral valve!! • Is ventricular relaxation in diastole an active or passive process? active -

lusitropy • Superimpose the LV pressure vs time trace for a failing LV. I Struggled BAD • How is the gradient of the upslope different? How about the down slope?

o decr upstroke gradient o slow downslope gradient o starting at higher pressures o longer in systole, less in diastole

Define contractility

Is the factor that is responsible for changes in the myocardial performance which is independent of HR, preload and afterload.

• What features of the curve are sometimes used as an index of contractility? dP/dt At what part of the curve is it measured?

(dp/dt)max refers to max rate of change of pressure in the L) ventricle during isovolumetric contraction. Increase in contractility will increase rise of pressure. This index does correlate with contractility but the problem is that it is not independent of myocardial loading factors.



• What is used as an index of contractility clinically. I floundered here but I guess an answer would be pulse pressure

• What is the Treppe phenomenon? What is the mechanism?

Is a staircase effect. A series of maximal stimuli is delivered to skeletal muscle at a frequency below the the tetanising frequency leading to increase in tension developed by each twist until a uniform tension per contraction is reached. Due to increased Ca2+ availability

• Superimpose the aortic pressure vs time curve on the LV trace. Make sure you draw it exactly to-the-millimetre perfect. I was hassled about which curve was on top and at what point they cross because I didn’t draw it exactly perfectly

• Mark the points where the AV opens and closes. • When is the rapid ejection phase, when is the slow ejection phase, why are

they rapid/slow respectively?

Rapid ejection phase: associated with an abrupt rise in the ventricular pressure which acc’n the bolus of blood Slow ejection: contractile and pressure within the ventricle is decreasing during this phase. Flow continues due to the momentum of the blood bolus. ! ∴ when LV pressure > aortic = rapid, when underneat = slow

• Definition of DBP

See above

DING DING DING

Questions others got:

• ECG • Pain – definition, mechanism of referred pain from uterus, pain pathways • Flow vs volume loops – mechanism of dynamic airway compression • Electrical resistance – in series, in parallel, examples of each in the body • Control of body water • Potassium • Resonance and damping • Exponential functions, time constants • Physiological changes in exercise • Bile – components and function:

o water o bile salts = steroid compounds from liver as cholesterol o bile acids = cholic acid & others o bile pigments o electrolytes

My vivas:



Blood Pressure

• What would be a normal BP for a healthy adult? • You are in PAC – nurse tells you a patient’s BP is 200/100. How is this likely

to have been measured? • What are the sources of error with automated NIBP.

Techincal: i) unable to follow rapid changes in presure ii) cuff – misplaced, wrong size, deflated to fast Patient: i) Patient movement ii) Obesity iii)AF iv) HoTN – overestimates SBP & underestimates DBP v) HTN – underestimates

• Why does irreg HR mean automated NIBP may struggle?

Oscillations with each ventricluar contraction is variable and the machine can’t provide reliable determination of blood pressure.

• What is most accurate –

MAP>SBP>DBP

• Auscultatory method – what is measured? How could we estimate MAP?

Korotkoff sounds – I) sound appears II) quieter III) rise in vol IV) muffling V) loss of sound MAP = DBP + 1/3(SBP – DBP)

• When should we use 5th sound over 4th sound? In what sort of patient do we not get 5th sound? exercise & children. Controversy over this

• What is normal BP in children cf adults?

Pregnancy

• CV changes with pregnancy

Increases: i) HR(1st:17% 2nd & 3rd:25%) ii)SVR (1st:30%) iii) CO (50% by 36wk) due to % inVR, uteroplacental circulation, breast & skin blood flow. iv) Blood volume (term:40%) + plasma vol (term:50%) + RBC vol (term:20% due to erythropoietin)

Decreases: i) Hct (33%) ii) PVR (35% 20wks due to progesterone & prostaglandin mediated vasodilation) iii) MAP (10% nadir at 20wk) iv) colloid oncotic pressure

No change: i) CVP ii) capillary wedge pressure

• Why is SV increased? Why is SVR decreased?

Increase in SV due to increased preload and increase vascular volume.



Decreased due to placenta blood flow 750ml/min. Placenta acts as an AV shunt + vasodilation of many tissues ie kidney, gut, heart, breast and skin.

• When during labour is the greatest strain on the heart? – which stage? What happens when the placenta is delivered?

post delivery - CO increases

• 15% latent phase, • 30% active phase, • 45% expulsive phase of labour, • post delivery 60-80% due to autotransfusion and increased VR from uterine

involution. Return to normal in 2 weeks. Water

• How is water distributed in the body?

Intracellular fluid: 55% Extracellular fluid: 45% (ISF:20%, Intravascular:7.5%, Transcellular:2.5%, Dense CT:7.5%, Bone:7.5%)

• How could we determine the size of the ICF?

No tracer is available for the ICF so its determined indirectly by TBW – ECF. ICF declines with age. TBW measured by Tritium Oxide which mixes within all compartments and is a weak β emitter and measured by a scintillation counter. ECF meaured by ionic ie 82Br. Over estimates ECF as it enters the cells.

• TBW – heavy water – how do we do it? How could we account for loss of indicator in urine (conc v time curve)

• ECF? – inulin • How is water movement regulated between ICF and ECF?

Water movements until osmolality is the same on both sides of the membrane. ECF:ICF distribution is dependent on osmolality. ECF osmolality controls H2O & cell volume. Na+ contributes 86% of ECF osmolality and 92% tonicity

• And between ISF and PV – he wanted Starling equation

Filtration pressure = Kf [(Pc-Pi) – σ(Oc-Oi)]

• What is the reflection coefficient? What capillary bed in body has very low reflection coefficient? – liver

Measures the leakiness of the capillary. Is a correction factor applied to the measured oncotic gradient across the capillary wall to take account of the effective oncotic pressure. Value from 0-1.



Flow-volume loop (Manson)

• Draw a flow volume loop – max expiratory effort o KB p 138 = Forced VC breath

• Draw flow volume loop from FRC

• Explain dynamic airways compression o Starling Resistor mechanism o Inc ITP transmitted to alveoli, inc PA ! Pmouth P gradient. o But inc ITP also compress airway; when ITP > airway P ! DAC. o Equal-pressure point beyond = airway collapse. o Driving force remains same even with inc expiratory effort.

• Draw flow volume loop for obstructive airway disease • why is curve dished out?

o DAC more pronounced in " Inc airway resistance eg asthma/bronchitis " Inc compliance eg emphysema " Initial low lung volume eg restrictive lung dx (as dec drive P).

• Explain dynamic airway compression – draw picture of alveolus/airway and show pressures, Starling resistor

o repeat • What happens to expiratory graph with extra-thoracic compression?

o Pronounced DAV.



o

A B C

A: Variable extrathoracic obtxn: eg vocal cord paralysis, extrathoracic goiter and laryngeal tumours; inspiration affected.

B: Variable intrathoracic obtxn; expiration affected.

C: fixed large airway obtxn: tracheal stenosis caused by intubation and a circular tracheal tumour.

NB: Effort independent = part of descending limb of expiratory curve from onset of airway closure down to residual volume. (KB138)

Flow-volume loop

• Draw a flow volume loop – max expiratory effort • Draw flow volume loop from FRC • Explain dynamic airways compression

Starling resistor mechanism. Driving pressure for flow is now the diff in pressure between alv pressure and intrapleural pressure. The driving force remains the same even with increased expiratory effort. Flow is constant.

• Draw flow volume loop for obstructive airway disease • why is curve dished out?

Scooped out pattern due to compression of major airways leading to premature closure + disproportionate decrease in flow latter in expiration due to heterogencity of lung disease resulting in earlier and rapid emptying of fast alv units compared with slow alv units.

• Explain dynamic airway compression – draw picture of alveolus/airway and show pressures, Starling resistor



• • High lung volume Medium lung volume Low lung volume

• What happens to expiratory graph with extra-thoracic compression?

Physiology Viva -April/2011

Q1: Upper Respiratory Tract

• Tell me about the functions of upper respiratory tract.

i) Pathway for inspired and expired gas. ii) Conditioning of gas – assisted by the turbulent flow and increased surface area of the turbinates. Humidification, warming and removal of particulate matter & minimising H2O loss iii) Olfaction

• How does air get humidified?

Humdification is assisted by the turbulent flow and increased surface area due to turbinates which are cover by a rich supply of vessels.

• What is saturated vapour?

Is the vapour pressure at a given temp where the vapour of a substance is in equilibrium with the surface of that’s substance in liquid phase.

• Where does the air get fully saturated? • Why is upper respiratory tract effective at humidification?

without it would markedly incre insensible losses by >50%

• Does all water vapour get lost on expiration? • At 20C, is vapour pressure lower or higher comparing to at 37C?

20C = 17.5mmHg, 37C = 47mmHg



Q2; Blood pressure

• How does BP measured in theatre?

Non invasive: i) manual ii) automated Invasive

• Tell me about invasive BP measurement. • What are the components of the measuring system? • Tell me about transducer. How does it work?

A transducer is a device that converts a signal in one form of energy to another form of energy ie electrical, mechanical chemical. Accompanied by a sensor and display.

• Why is Wheatstone bridge used?

Wheatstone brigde is a method of measuring electrical resistance. A pressure transducers contain a strain gauge whos resistance varies and a wheatstone bridge allows such change in resistance to be calculated.

R1/R2 = R3/R4 – null deflection system (no current flows thru the galvanometer.)

• Indications of invasive BP measurement. • How do you assess accuracy?

i) Dynamic ii) Static – Zeroing, gain and time stability

• Tell me about dynamic accuracy?

i) Resonant frequency (Fn) – Fn should be higher then the natural frequency of the biological system otherwise the latter will cause the system to resonate and distort. The Fn has to be high enough to ensure the flat frequency response produced by optimal damping encompasses the 1st 10 harmonics. Use stiff, short and wide tubing and stiff diaphragm + low density fluids ii) Damping coefficient – D=0.64 with 7% overshoot

• What is natural frequency?

Is the frequency at which a system tends to oscillate in the absence of a driving or damping force

• What is resonance?

Is the tendency of a system to oscillate with greater amplitude at certain frequencies ie resonant frequencies. The system stores vibrational enegry.



• What will change in natural frequency when column of water is connected to diaphragm?

Natural frequency of the system drops towards the natural frequency of the biological system

• Draw an art BP waveform. • What happens with this waveform when resonance happens? • Which part is amplified the most?

?? Large highs and lows

Q3: Nutrition

• What is TPN?

Total Parentaral Nutrition

• Have you prescribed TPN before? • What are the components?

CHO(70% of calories), lipids (30% of calories), aa, electrolytes, vitamins, trace elememts and volume/fluid

• What is the daily requirement of Na, K, and Energy?

Na: 1mmol/kg/day, K:1mmol/kg/day REE:20-30kcal/kg/day

• Why CHO is prescribed?

Stimulates insulin production (anabolic hormone), decreases gluconeogensis and lipolysis

• We are able to making proteins from CHO, why do we still prescribe protein?

To prevent breakdown of endogenous proteins for gluconeogensis

• What types of amino acid are there?

Essential and non essential

• What is essential amino acid?

9 of 22 aa are essential as they cannot be created from other compounds and have to be taken in.

• What is respiratory quotient?

Is a dimensionless number used in calculations of metabolic rate estimated from CO2 production



RQ = CO2 eliminated / O2 consumed

• What is RQ for CHO, protein and fatty acid?

Proteins:0.8-0.9, CHO:1.0, Fats:0.7

• Who needs TPN? • Which group of patients need high energy requirement?

TPN is indicated when the GIT is not working, not available or not appropirate ie short bowel sysndrome, mucositis Trauma, septic and burns need high energy requirements What trauma group especially?

• What group of patients do you need to modify RQ?

?? hypermetabolic states, ie MH, thyrotoxicosis

Q4: Blood Bank

• How is blood collected?

Whole blood is collected and centrifuged into its components (RBC, FFP, Cryo, Plts

• What is in the bag? • Platelets get centrifuged. What temp is it stored? What is the half life of stored

platelets? Half life of platelets in the body?

Stored at 4C to decerease risk of bacterial growth. Should be used with in 24-48hours. Normal life span of plt is 8-12days. T1/2 is 4 days

• How is plasma stored?

Frozen within 8hrs of storage at -30C from a single donor.

• What does citrate do?

Is an anticoagulant – by binding Ca2+

• What happens to RBC in stored blood?

Na/K-ATPase dysfunction = osmotic fragility which increases with storage time. Spherical and rigid, leading to lysis.

• Potassium, PH, calcium, 2,3 DPG.

K+:19-30mmol/L,



pH:7.1 with addition of presevative then down to pH:6.6-6.9 at 21days due to accumulation of CO2 thru cellular respiration that cant be vented thru the bag. Blood transfusions provide citrate in large quantities for endogenous generation of HCO3

- = metabloic alkaosis. 2,3-DPG: 50% at day 14, 5% at day 28. Returns to normal with 24-48hrs of trnsfusion

• Why is K+ high in stored blood? • Why is pH low? • What are the complications of massive blood transfusion?

Transfussion of volume of stored blood > then the recipients blood in 24hrs i) Citrate toxicity – involutary tremor, decrease HR, widening of QRS and prolongation of QT. ii) HyperK+ - due to Na/K-ATPase dysfunction. iii) Acidosis – pH of stored blood 6.6-6.9 iv) Depletion of 2,3-DPG v) Dilutional coagulopathy – FV & VIII are labile vi) Microaggregates – can get lodged in the microvasculature and release lysosome causing ARDS vii) Volume overload viii) Infections

• O negative blood is reserved for what group of patient? Why?

Universal donor. PRBC are plasma depleted and therefore don’t contain any antibodies. The O –ve RBC have H suface antigens which donot elicit a response from the host antibodies.

September 2010 (By Ku)

1. Could you tell me about cardiovascular changes with aging (debatable viva)

So let's talk about HR. Why does that reduce

o Dec, secondary to: o vagal predominance o fibrotic changes in pacemaker cell o dec beta adrenoceptor sensitivity to SNS stimulation.

Could you draw a lead 2 ECG and show me some changes

o Slower HR o QRS long o PR long o QTc long



What happens to QRS with aging

o = ventricular depolarisation; could widen, if there’s dec conduction along ventricular muscles, due to fibrotic changes in aging in bundle of his / purkinje fibres.

o ? related to an increase in L-type Ca++ current and slowing of the L-type Ca++ inactivation so that longer Ca++ influx occurs with each heartbeat.[8]

So you mentioned compliance reduce, what's the result of that

o Dec arterial compliance ! inc SVR, afterload, HTN o Dec ventricular wall compliance ! inc vent wall tension, afterload,

myocardial work. o LV hypertrophy; which couples with decreased DBP ! risk ischemia

What happens to diastolic pressure

o stiffer aorta, more rapid drop of pressure, lower diastolic pressure, increase in pulse pressure.

What implication does increased MAP and systolic have

o Could have end organ damage eg. Renal failure, CNS damage, pulm oedema. o Could have reset of baroceptor reflex, cerebral perfusion pressure

autoregulation.

Why does contractility reduce

o There is a dropout of myocytes with aging o increasing fibrotic changes in ventricular myocyte.

o CVS changes with aging? o HR dec o Preload o Contractility dec o Afterload inc ! LVH, LV strain

" Ventricular wall tension: as dec compliance, dec radius, inc T. " Aortic root pressure: aortic sclerosis " Aortic compliance dec, loss of Windkessel effect " Inc SVR " HTN

o Rhythm: HB, ectopic, AF more prevalent (atrial kick 1/3 LVEDV, so AF get 1/3 drop CO)

o CO dec by 3% per decade (FRCA) o SNS tone

" Dec 2nd down regulate adreneoceptor " Global impair of ANS, so baroceptor reflex

2 What is a resting membrane potential?



• Steady state potential (charge) exists across the cell membrane.

What's typical value for skeletal muscle

• -90mV

What causes that

• Pump-leak hypothesis: o Na/K ATP generate concentration gradient o Membrane has different permeability to K and Na (higher with K) o Gibbs-Donnan effect:

" Gibbs-Donnon effect = presence of impermeable charged molecule affects the distribution of other permeable, charged molecules at equilibrium, across a membrane.

Can you write an equation to calculate potential for ions (Adam’s answer copy/paste)

Goldman Hodge Katz form:

gK = K conductance gT = total conductance • Nernst potentials of Na +60 , Cl -70, K -90

Ie ln RT/F = log 58

Why is universal gas constant in the equation

•

Why does RMP deviate from Vk

• summation of all channels

What else contribute to rmp



• Na/K ATPase o -10mV contribution. essential to prevent cellular swelling and lysis

(double donnan • Gibbs Donnan

What's Gibbs Donna effect

• Gibbs-Donnon effect = presence of impermeable charged molecule affects the distribution of other permeable, charged molecules at equilibrium, across a membrane.

What happens to cell if only Gibbs Donna is in effect

• Hypopolarised, only: • -17mV contribution

What happens if ECF k was to go up ;

- Ie hyperkalaemia, the RMP would go down ie less -ve.

3. What is FRC?

= volume of lungs at end of normal expiration

• Balancing point between outward force of CW and inward of lung • Also = starting lung volume for tidal volume respiration • Also = point where PVR is at its lowest • = RV + ERV

• What's typical values o 30ml/kg; ie ~2100ml in 70kg man.

• What's functions of FRC o Oxygen store o Minimise WOB:

" Reduce atelectasis " Steepest part of compliance curve " Minimise PVascularR " Reduce Airway resistance

o Minimise V/Q mismatch o Buffer to maintain steady arterial pO2

• How much oxygen is there at FRC o 2100ml o PAO2 = FIO2 – PACo2 / R

" = (760-47) * 0.21 – 40/0.8 " = 150 – 50 = 100 " PAO2 = 100 = 100/760 of FAO2 = 13%

o So O2 in FRC = 2100 * 0.13 = 276 ml. • What if you're breathing 100% oxygen



o FAO2 = 663/760 = 87% o So FRC store = 1830mls

• How do u measure FRC (West P. 15) o Single breath nitrogen test (washout)

" Single breath 100% O2 to washout N2/CO2 in ana DS. " Then expire through mouthpiece/pneumatochograph/sampling

N2 analyser " 2 curves:

" N2% over time (from this N2% vs volume obtained) " N2% v volume. " A. DS to midpoint of transition. (TV) " Extension = CC measure: where expire to RV), will see

higher N2%; as at this point of closure of basal segment, N2 from apex, which is less diluted by O2 100%.

o Helium dilution test (wash in) " Breath known quantity of helium ([He]1 * V1) " After equilibrium, [He]2 measured " V1 * [He]1 = (V1+FRC) * [He]2

o Body plythsmography – try to avoid explaining this. " = double application of Boyle’s Law and solving the equation

for the single unknown FRC.

NB:

- body plethys also for AWR/FRC - He for FRC - N2 for ana DS (ie Fowler’s), FRC, CC.

• What factors change FRC

Big 5 as per KB111

o Weight; dec with obesity o Height; inc with height o Position; inc with erect than supine; prone vs supine. o Disease; inc with dec lung recoil (emphysema); dec with fibrosis

" Upward pressure by abdo content, obesity, pregnancy, bowel distension

" Reduced alveolar volume: atelectasis, consolidation, oedema. o Muscle relaxation; dec with paralysis; anaesthesia (independent of

relaxant) " Special = Pregnancy, neonate (lower absolute FRC), age (no

change) • Why does it reduce with anaes. What about pain

o With pain: " Reduce both FRC/VC, 2nd incisional pain and reflex

dysfunction of diaphragm. " Epidural analgesia doesn’t influence rate of recovery of lung

function, nor prevention of atelectasis/pneumonia? From 1991 Can JA.



o Anaesthesia reduce as …….. relax diaphragm / intercostal

4. Tell me about pituitary gland

- An important organ involved in many endocrine functions. - Ant (pars tuberalis, intermedius, distalis = site of production)/ Post

• Where are they from embryonically o Ant pit develops from an outgrowth of the roof of the mouth aka

Rathke’s pouch. (ie oral ectoderm) o Post pit aka neurohypophysis = from downward evagination of the

brain. (ie neuroectoderm) • Whats the pouch of ant pituitary called

o Pouch of Rathke? • What does their diff origin mean.

o Different hormonal release mechanism: " Ant: by neurohormones at median eminence!diffuse to

primary plexus!travel down large portal veins in stalk!2nd cap plexus in ant pit ! diffuse to ant pit and cause action.

" The magnocellular neurosecretory cells (in hypothalamus) project axons down the infundibulum to terminals in the posterior pituitary ! neurohormone released directly into circulation.

• What's portal circulation mean o Generally = any part of the systemic circulation in which blood

draining from the capillary bed of one structure flows through a larger vessel(s) to supply the capillary bed of another structure before returning to the heart;

• What hormones are produced in pituitary o Post: secrete ADH and oxytocin. Humans have arginie vasopressin,

pigs have lysine. These produced in supraoptic nucleus and paraventricular nucleus of hypothaloamus ! via nerve axons in vesicles to post pit.

o Ant: GH/prolactin, FSH/LH/TSH, ACTH. (produced in ant lobe of ant pit).

• Tell me about thyroid hormones o Highly PPB-TBG mainly. (>99%) o T1/2: 3 = 1 day, 4 = 1 week. o Activity: T3 3~5x more active than T4. o ~1:10, T3 vs T4. o Synthesis: Iodine (food) àconverted to iodide and absorbed upper

SIàthyroid follicular cells uptakeàiodide converted to iodineàiodine+tyrosineàmono-iodotyrosine (MIT)

o TP (thyroid peroxidise): catalyse organification: MIT, DIT, T4 (thyroxine) or T3 (tri-iodothyronine). Thyroglobulin store in follicular cell.

• What are their systemic effects " Action: Intracellular receptor!gene regulation up or down.



" BMR : Metabolism – some catabolic effect CHO/Fat, but normally anabolic protein. If high, catabolic protein.

" CNS-brain develop, sexual fxn. –ve feedback to TRH/TSH. Tight control of level. T3/T4.

" Bone Growth. " CVS: Permissive action on catecholamines, and also direct

chrono/ino. If level too high, may cause AF. " Res: inc RR 2nd up BMR.

• What controls their secretion o TRH +ve effect o Somatostatin –ve effect o Negative feedback by hormone to ant pit and to hypothalamus, and by

TSH to hypothalamus. • Tell me about ACTH

o CRH, ADH +ve release (subject to stress and diurnal rhythm) o Somatostatin?, glucocorticoid negative feedback on CRH and ACTH. o Action:

" Cortisol release from zona fasciculate. " Prevents atrophy of adrenal cortex

1. What blood tests can be used to estimate renal function

• Measured by measuring GFR: by Cr level; 24 hr CrCl, Inulin Cl.

• Which of urea and creatinine is better o Cr; as filtered, not absorbed, small secretion only. o Urea, reabsorbed. 50-60% reabsorbed.

• What are the problems with using urea to estimate renal function o Reabsorbed, altered by ADH secretion, in turn altered by volume

status and indirectly osmolality. • what are the problems with using creatinine to estimate renal function

o muscle bulk (male/female) o level vary with protein intake o GFR overestimated as Cr secreted. o Insensitive: GFR ½ before abnormal Cr level seen.

• Can you draw a graph of plasma creatinine vs GFR - what does its shape indicate

o • What is clearance

o repeat • How can clearance be used to estimate GFR

o If filtered, and no reabosrption or secretion, then Cl = GFR. o modified version of Fick principle (Renal clearance formula) o GFR = UV / P

• What is eGFR and how is it different from GFR o Estimate; different as it’s a surrogate measure.

• How is eGFR calculated



o (MDRD formula) Modification of Diet in Renal Disease; uses estimation from creatinine clearance adjusted for age, weight, gender

o Or Cockcroft Gault formula. " Cockcroft-Gault CrCl = (140-age) * Wt* (0.85 if female) / (72

* Cr) o Cystatin C has a low MW, and it is GFR filtered. Serum cystatin C

may be more precise than creatinine levels. o Cystatin C levels are less dependent on age, sex, race and muscle mass

compared to creatinine.

2. Resting Membrane potential - questions as listed above

3. Can you write down the alveolar gas equation

- yes

• What would happen if we dropped you out of a helicopter at the top of Mt Everest

o We fall due to gravity o Low atmospheric pressure at altitude, so get hypoxaemia

• How would this change the alveolar gas concentrations o PAO2 calculated. o PACO2 mimics PaCO2.

• What about this part (examiner pointed at PaCO2/R part of the equation), would this change

o No • What is the ideal alveolar gas equation

o

4. What is Starlings law of the heart

- describes the relationship between EDV and SV:↑myocardial stretch at end diastole → ↑SV, within a limit.

- Achieved by ↑velocity of ventricular muscle contraction. - Optimised sarcomere ~2 µm; beyond this, greater stretch → ↓

force of contraction - Ie. x = stretch; y = force

• Can you represent this graphically o yes

• What clinical parameters can be alternative labels for the x and y axis o (i.e. LVEDV and SV)

• What would the curve look like with sympathetic nervous system activation • What would the curve look like in heart failure



•

April 2008 Physiology

Altitude

• What happens if you rapidly ascend to the top of Mount Everest? • Why do these changes occur? • What occurs over the next few days? (triphasic response, in Nunn) • What happens over the next month? (3 mechanisms: increased uptake,

increased delivery, more efficient utilisation) • Why do aeroplanes fly at particular altitudes? What is the cabin pressure?

How does this affect oxygen saturation? Is it a problem?

(with regard to cabin pressure, it's about 0.7-0.8 atmospheres. cheaper airlines run at lower pressures as it means there's a reduction in the amount of air that must be moved-about 100 tons!)

Venous admixture

• Define it. • When might it occur (endobronchial intubation, atelectasis, pneumonia,

pneumothorax) • What are the physiological causes of venous admixture? (bronchial and

coronary circulation)



• What is the PO2 in the coronary sinus? WHat colour is the blood? (black) • How do you quantify shunt (Shunt equation). How do you measure the

variables?

Reaction to injury

• "What happens if I cut my hand?" (3 possible avenues: pain pathways/stress response, bleeding, withdrawal reflexes)

• Went down the stress response pathway....sympathetic response, fluid retention, cortisol.

• What does the other hand do?

April 2009 Valsalva Maneouvre

• Describe it (MAP and HR changes), what is happening in each phase? • Square wave, and autonomic dysfunction • Valsalva Ratio

SI Units

• What are they? • Base Units?

o Kelvin – temp; thermodynamic equilibrium of water at its triple point o Mass o Length o Duration o Luminosity o Current o Mole

• What is Current? What is Ohm's law? • What is a volt? • What is Impedance? Why is it important clinically?

o Impedance to outflow of blood from LV o used in diathermy to isolate pt from diathermy box

• Other vague questions about the voltage at a power point and what it meant!



Pulse Oximetry

• What is it? What does it involve? - LED's and sensor • Beer-Lambert Laws, which is which? Wavelengths of light, Hb species • errors and assumptions • What do different R values mean?

Oxygen Cascade

• Draw the cascade. Stopped at each point • How do I get 159mmhg for dry air? • Alveolar ventilation, and Alveolar gas equation. What does the pCO2/R

mean? Different R values? Correction factor? • Venous admixture - define, what is it made up of? (True shunt, pathological

shunt, VQ scatter) • When does shunting occur physiologically?

o (ie, position, pregnancy, ageing with CC>FRC) • How does VQ scatter change with ageing?



o More shunt/VQ scatter, as CC approaches FRC erect at age 65. Tendency for atelectasis and dec inc V/Q ratio (scatter).

Overall, examiners very friendly.. despite much blathering they helped me through it!

Other people got - Hepatic Blood flow, Ultrasound, Capnography, pain pathways

Cardiac and Haemorrhage

• What is normal circulating blood volume for 70kg man. • How do you know this? • What physiological responses would there be if there was an instantaneous

1500mL blood loss? • What are the sensors / effectors • What are high and low pressure baroreceptors

Sleep

What is sleep?

• Necessary, reversible state of reduced level of consciousness. Easily roused by sensory stimuli.

• Rem v non rem • 4 -6 cycles; 90min/cycle.

What are the physiological changes associated with sleep?

• Heart / lung / brain / GI / metabolic endocrine / muscle (6) • REM: dream, EEG / variable HR, BP / dec tone, MV, resp derive, FRC /

marked dec muscle tone • Non-REM: EEG / dec HR, BP / dec tone, MV, resp drive but not as much as

REM / dec muscle tone • Common: inc cortisol, ADH, dec MR / inc gut motility.

What EEG changes do you see with sleep?

• REM: beta, alpha. • 1 theta, 2 theta + (sleep spindle, K complex), 3 delta + theta, 4 delta • What are the names of the different waves and complexes you see in

EEGs

How does sleep differ from general anaesthesia?

Drug induced state of: reversible LOC, amnesia, +/- analgesia, paralysis, ANS suppress.; not necessary for life, not rousable unless drug is turned removed from the system.



How can you monitor levels of consciousness?

Clinical vs EEG monitor

How does BIS work?

EEG processing then compare with in-built algorithm, an score is assigned from 0-100. BIS 40-60 indicates GA suitable for surgery.

• Burst suppression (looks at incidence of burst suppression) • Power analysis (looks at ratio of beta wave) • BIS analysis

Fourier analysis: complex waveform broken down into sine waves and epochs of waves analysed re: frequency/amplitude.

Problems:

• agent dependent • poor PPV and NPV for awareness • inter-individual variation. • Not fully validated in paeds.

Others eg.: Auditory Evoked potentials: response of brainstem/mid brain/cortex to acoustic stimulus of the auditory nerve.

Entropy: describes order of chaotic wave pattern of EEG.

PhysiologyVIVA’sApril2013 April 2009 - · PDF fileBy Ku, Shanmuganathan, Hollingworth...

Documents

Transcript of PhysiologyVIVA’sApril2013 April 2009 - · PDF fileBy Ku, Shanmuganathan, Hollingworth...