The Hong Kong College of Anaesthesiologists

Intermediate Fellowship Examination

July- August 2001

Examiners’ Report

General
Question 2
Question 3

Question 4
Question 5

Question 6
Question 7

Question 8

Question 9

Question 10
Question 11
Question 12

Physiology
Written Section
Q1. Discuss the use of alveolar to arterial gradient in oxygen tension in the assessment of a patient with
hypoxaemia.

Alveolar-Arterial O2 gradient = PAO2 – PaO2

Alveolar Gas Equation
PaCO2
PAO2 = [(Pb - PH20) x FiO2] — ---------
R

Pb=Barometric pressure; 760 mmHg

o
PH20=Saturated vapour pressure of H2O at 37 C; 47 mmHg
R=resp quotient, 0.8
Normal A - a PO2 = 10-20 mm Hg

Cause of Hypoxemia A-a gradient

Hypoventilation normal
Low FiO2 normal
Diffusion impairment increased
V/Q mismatch increased
Right-to-Left (intracardiac) shunt increased

Other factors that increase Aa gradient (assuming shunt unchanged)

1. increase FiO2, esp for large shunt >20%
2. low cardiac output
3. low Hb

Comments
Five candidates passed this question. To pass the question, the candidate should give the Alveolar Gas Equation,
the normal A-a gradient, and the A-a gradient in various causes of hypoxaemia. The common omissions included
not writing the Alveolar Gas Equation, and not using the A-a gradient to identify the possible causes of
hypoxaemia. Few candidates appreciated factors that increased A-a gradient apart from shunting.

Q2. Describe physiological adaptation to high altitude.

1. Hyperventilation – blood gases

2. Change in ventilation over ensuing month
(i.e. increase with bicarbonate excretion then decrease with longer term adaptation)
3. Polycythema
4. Increased blood volume
5. Improvement in gas exchange:
- blood volume
- hypoxic varoconstriction
- pulmonary hypertension
6. Hb dissociation curve – effects of low PCO2 and 2-3DPG

Comments
Thirteen candidates passed this question. Most candidates knew the facts, but failed to organise the points
effectively, resulting in omissions. Candidates were in general weaker in describing the haemodynamic
adaptations.

Q3. Describe the structure of a liver lobule. List six functions carried out by the liver.
Liver lobules:
functional units of the liver
each approx 2 mm in diameter
bile duct, portal vein and hepatic artery at periphery; hepatic vein at centre
blood flows through sinuses centripetally, bile flow through cannaliculi centrifugally
hepatocytes organized in plates around thin-walled blood vessels called sinusoids sinusoids are lined with
epithelial cells and special phagocytes called Kupffer's cells
hepatocyte layer surrounding each sinusoid is only 1 to 2 hepatocytes thick

Liver Functions:
- glycogen storage;
- bile acid metabolism and fat absorption;
- gluconeogenesis
- urea synthesis;
- albumin synthesis;
- drug metabolism;
- bile pigment formation/bilirubin metabolism;
- clotting factors;
- etc.

Comments
Thirteen candidates passed this question. Candidates performed fairly well in this question. In general, the answers
on liver functions were better than those on structure of the liver lobule.

Q4. List the measurements that are available to help you assess “nutritional status”?

1. Body weight
2. Body mass index
3. Lean body mass/body fat
4. Skinfold measurements
5. Mid upper arm circumference
6. Plasma proteins:
- albumin
- transferrin
- pre albumin
7. Immunology:
- lymphocyte counts
- skin hypersensitivity
8. Muscle strength:
- dynamometry
- respiratory function tests

Comments
Four candidates passed this question. Candidates’ overall knowledge in the subject was poor. Most managed to put
down only a few of the measurements listed above. Very few candidates listed muscle mass and strength as a
measurement of nutritional status.

Q5. Compare a unit of freshly collected whole blood with a unit of banked packed red blood cells which is five
week old.

Fresh WB Banked PRBC

o
Temperature ambient 4C
Platelet activity normal <5%
Clotting factors activity normal minimal
Plasma Na+ Normal or slightly increased Around 120 mEq/L
Plasma K+ normal 25-30 mEq/L
pH 7.5 <7
2,3-DPG activity normal <1 mcM/ml
% survival red cells 100 70
Hematocrit Around 40% >60%
Free haemoglobin minimal >200 mg/dL

Comments
Eleven candidates passed this question. This was a straightforward question. Better candidates tabulated the points.
Poor candidates failed to comment on the differences in platelet and clotting factors activities. Common
misconceptions included temperature and the calcium concentration of the fresh whole blood.

Q6 Explain the causes of sampling errors when a blood sample is collected from an arterial cannula for arterial
blood gases measurement.

Def. Sampling Errors

any difference between the true value and the estimated value of a measurement derived from a sample
because of incorrect selection or handling of the sample

Causes of sampling errors

1. Residual fluid from dead space
inadequate volume
withdrawn too quickly: non-Newtonian fluid
2. Heparin is the recommended anticoagulant. EDTA, citrates, and oxalates alter the pH.
3. Glass syringes should be used if possible because CO2 and O2 don't dissolve into the wall of a glass syringe.
4. Air bubbles in blood sample
PaO2 will increase and the PaCO2 will decrease, as O2 is about 105 mm Hg and CO2 is negligible in the
bubble in room air
5. Samples must be stored in an iced slurry
Blood contains living RBC and WBC and cooling will reduce their metabolism.
6. Analyze samples as soon as possible but when properly stored, several hours will result in little change in the
blood gas measurements.

Comments
Six candidates passed this question. Very few candidates provided a definition for sampling error. Most candidates
knew heparin was the recommended anticoagulant, but few knew it was adjusted to pH around 7. Poor candidates
listed the points with inadequate explanations, such as the effects of air bubbles and ongoing cellular metabolism
during storage and transport. One candidate mis-read the question and explained the use of arterial cannula for
arterial pressure measurement.

Q7. Describe the cardiovascular adjustments that occur when an individual exercises for an hour on a treadmill
at 70% of his maximum capacity (i.e. moderately severe exercise).

Initial sympathetic activation.

Increase in cardiac output:
starts before onset of exercise.
marked ↑rate; ↑SV, ↑contractility
HR (/min) SV (ml) CO (L/min)
Rest 70 70 5
Max Exercise 180 120 22
Cardiac output maintained by increase in venous return:
muscle pump;
negative intrathoracic pressure.
Initial constriction of blood supply to skin and gut.
↓SVR due to vasodilation in muscles and skin.
SBP moderate rise, DBP unchanged or ↓
Eventual fluid depletion leads to decrease in blood volume and progressive rise in heart rate.

Comments
Eleven candidates passed this question. Candidates’ knowledge in the topic was patchy in general. Significant
omissions included initial sympathetic activation before onset of exercise, mechanisms for increased venous return,
and the relative increase in heart rate and stroke volume during exercise.

Q8. Outline the cardiovascular changes during normal aging.

Vascular: arteries and veins:

General loss of elastin and damage to collagen, resulting in generalized loss of elasticity and increase in
stiffness through the CVS
Stiffness of arteries lead to loss of arterial compliance, systolic hypertension and roughly 0.5% per year
increase in SVR
Stiffness of veins lead to lowering of venous compliance, more marked hypotension with blood loss
Heart:
Stiffness of heart lead to reduced ventricular compliance, increased ventricular end diastolic pressure,
impaired ventricular filling and therefore decrease in stroke volume and cardiac output, increased importance
of atrial contraction in ventricular filling
Ventricular hypertrophy is common due to death of myocytes and common occurrence of HT. With
ventricular hypertrophy, there is prolongation of ventricular contraction leading to impairment of ventricular
relaxation and filling (diastolic dysfunction)
Autonomic:
Gradual decrease in vagal activity, but similar resting heart rate
Progressive increase in basal sympathetic activity, greater sympathetic response (catecholamine output) to
autonomic stress such as change of posture
Reduced -receptor agonist responsiveness
Response to hypotension: tachycardia, increased contractility and vasoconstriction all reduced.

Comments
Four candidates passed this question. To pass this question, candidates should include some description on the
vasuclar, cardiac, and autonomic changes in the cardiovascular system. A few candidates spent time describing the
changes of diseases instead of normal aging. Most candidates had mis-conception about the autonomic changes,
stating wrongly that there were increase in vagal and decrease in sympathetic activities. Very few candidates
appreciated reduced -receptor responsiveness in aging.

Q9. What is primary hyperalgesia? Explain the mechanism by which primary hyperalgesia develops.

Primary hyperalgesia is the rapid occurrence of an area of hyperalgesia around a site of cutaneous injury.
Hyperalgesia means an exaggerated response to a painful (noxious) stimulus.

Primary hyperalgesia develops as a result of nociceptor sensitization. Nociceptors are sensitized mainly by local
mediators released as a result of cell injury. Both A-delta and C pathways can become sensitized. Mechanical
injury will predominantly sensitize mechano-nociceptors and thermal injury thermo-nociceptors. However,
mechanical injury can also sensitize thermo-nociceptors to a lesser extent and vice versa. These mediators include
potassium, bradykinin, 5-HT, eicosanoids and substance P. The area of sensitization spreads by diffusion of the
released mediators as well as by axon-axonal reflexes with antidromic impulse conduction. Loss of central
inhibition may be a possible alternate mechanism.

Comments
Nine candidates passed this question. To pass this question, candidates should provide a definition for primary
hyperalgesia and explained nociceptor sensitization by the mediators. Many candidates confused hyperalgesia with
allodynia. Some candidates wrongly regarded primary hyperalgesia as a phenomenon of chronic pain. Many
candidates discussed secondary hyperalgesia and “wind-up”, which were irrelevant. Very few candidates
mentioned the antidromic pathway.

Q10. Classify hypersensitivity reactions. Briefly compare and contrast the different types and give examples.

Hypersensitivity Type I Type II Type III Type IV

Reactions
Synonym Anaphylaxis Cytotoxic Immune Complex Cell mediated
(Immediate) (Antibody mediated (Delayed)
depedndent)
Onset Seconds to minutes Hours to a day Hours to days 2-3 days
Specific immune IgE IgG, IgM IgG, IgM Cytotoxic T cells
Chemical mediators Mast cells/basophils Complements Complements Cytokines
granules: histamine,
PG
Immune Accumulation of Phagocytosis and Accumulation of Lymphocytes and
pathophysiology neutrophils, lysis of target cells neutrophils and macrophages,
eosinophils. macrophages. granulomas
Smooth muscle Release of lytic
contraction lysosomal enzymes
Clinical examples Anaphylaxis, Transfusion Serum sickness Tuberculosis,
Allergic rhinitis, reaction, SLE, contact dermatitis,
Bronchial asthma Hyperacute organ Acute chronic organ
rejection, glomerulonephritis rejection
myasth gravis

Comments
Eleven candidates passed this question. To pass this question, candidates should provide a correct classification
(Gell and Coombs 1968), onset time frame, immune mediators and the clinical examples. Some candidates
described five, and others three hypersensitivity reactions. Many candidates were not clear about the type of
immunoglobulins involved and the role of complements. In particular, many candidates confused Type II and III
reactions.

Q11. Give a brief description of plasma proteins and their functions.

Plasma proteins- structurally and functionally diverse. Conc 60-80 g/dl.

1. Albumin:
most abundant (40g/dl), syn in liver, T1/2 20 days.
Metabolised in liver, kidney, gut.
Main role: transport, colloid osmotic pressure.
2. 1 globulins.
1-Antitrypsin: serine protease inhib produced by liver. Inactivates trypsin, chymotrypsin, activated plasmin
and other proteases.
1- lipoproteins: lipid transport.
1-acid glycoprotein: acute phase protein; physio role unknown. Binds drugs.
3. 2 globulins
2 macroglobulin: inhibits proteases from infectious organisms.
Prothrombin: clotting factor synthesized by liver.
Haptoglobulin: binds free haemoglobin, transport to liver.
Caeruloplasmin: produced by liver, transports copper, also an oxidase enzyme and free radical scavenger.
4. - globulins.
Transferrin: trasnports iron.
Haemopexin: binds haem, releases to RES.
5. Fibrinogen:
produced by liver, important in coagulation.
6. -globulins:
Immunoglobulins produced by plasma cells.

Functions of plasma proteins:

Transport : albumin, lipoproteins, transferrin, TBG, transcortin.
Coagulation.
Enzymes: plasma cholinesterase, acute phase proteins.
Oncotic pressure.
Buffering action.

Comments
Thirteen candidates passed this question. Many candidates gave an incomplete list of plasma protein, mentioning
only albumin and globulin without subtypes and examples. Likewise, many had an incomplete list of their
functions. Candidates scored extra marks for stating the plasma concentrations of proteins and albumin, instead of
just mentioning that albumin > 80% plasma proteins. Some candidates confused osmotic and oncotic pressures.
Some wasted time in writing a long account of oncotic pressure. Few mentioned complements. The role of albumin
in pharmacokinetics is not relevant. Haemoglobin is not a plasma protein.

Q12. What is sinus arrhythmia? Outline the pathways involved in this phenomenon.

Sinus arrhythmia is the rhythmic variation in heart rate in normal individuals occurring at the frequency of normal
breathing. There is increase in HR during inspiration and decrease in HR during expiration
Possible mechanisms: Sympathetic activity increases during inspiration and vagal activity diminishes during
inspiration. The variation in HR is mainly due to variation in vagal activity. The reflexes involved may include
(1) Bainbridge reflex as a result of increase venous return during inspiration
(2) change in lung volume, thus activating stretch receptors in lung and cause reflex changes in vagal discharge
(3) central reflexes: “crosstalk” between the respiratory centre and the cardiac autonomic centre in the medulla
(4) increase in LV filling during expiration and cause reflex decrease in HR via baroreceptor reflex

Comments
Six candidates passed this question. Many candidates did not know what sinus arrhythmia was, and confused it
with VT and atrial flutter. Increased automaticity and re-entry are pathologic mechanisms resulting in arrhythmias
such as SVT and VT. A large number of candidates wrote irrelevant answers describing pathological rhythms. The
examiners wondered whether this was a hazard of candidates reading only past papers and revision handouts, and
not reading the examination question.

Oral Section

The following topics were covered in the oral section.

Measurement of ventilation in a patient on a ventilator

Principle of end-tidal CO2 measurement
Relationship between end-tidal and mixed venous CO2
Change in PaO2 with age
What is meant by afterload
Action potential of nerves- compound action potentials, types of nerve fibres, c fibres
Draw a spirogram- closing volume
Define dead space
Valsalva manouvre- explain, factors modifying
Detailed structure of skeletal muscle
Pyloric obstruction in an adult- acid-base changes, determining hydrogen ion loss from pH changes, buffering
Why can the PaCO2 be high in patients with emphysema/chronic obstructive pulmonary disease Measurement
of alveolar O2 levels
Ventilation/perfusion mismatch
Assessment of energy requirements- measurement of oxygen consumption, BMR
Methods available for measuring BP, factors affecting accuracy, damping
Renal blood flow- counter current multiplier system
Factors affecting myocardial O2 supply and consumption
Body water content
Measurement of plasma volume
How is the cell membrane potential generated, why is there a potential difference, distribution of ions
Breathlessness- why is it easier to breathe sitting up

Physiology Viva Questions

Measurement of ventilation in a patient on a ventilator
Principle of end-tidal CO2 measurement
Relationship between end-tidal and mixed venous CO2
Change in PaO2 with age
Draw a spirogram- closing volume
Define dead space
Why can the PaCO2 be high in patients with emphysema/chronic obstructive pulmonary disease
Measurement of alveolar O2 levels
Ventilation/perfusion mismatch
Breathlessness- why is it easier to breathe sitting up
What is meant by afterload
Valsalva manouvre- explain, factors modifying
Factors affecting myocardial O2 supply and consumption
Methods available for measuring BP, factors affecting accuracy, damping
Renal blood flow- counter current multiplier system
Action potential of nerves- compound action potentials, types of nerve fibres, c fibres
Detailed structure of skeletal muscle
Pyloric obstruction in an adult- acid-base changes, determining hydrogen ion loss from pH changes, buffering
Assessment of energy requirements- measurement of oxygen consumption, BMR
Body water content
Measurement of plasma volume
How is the cell membrane potential generated, why is there a potential difference, distribution of ions