Quiz for Week 15 - Questions

Question 1. Sketch the anatomy of the coronary vessels.

Question 2. Which ECG leads are best placed to record changes when the lesion is on
the (a) diaphragmatic aspect of the heart, (b) antero-septal region? Which arteries are
involved?

Question 3. Indicate the time relationships of the arterial pressure wave to the heart
sounds, ECG, and left ventricular pressure.

Question 4. Identify the serum lipoproteins and their role in atherosclerosis.

Question 5. Identify, and briefly comment on the functions of, the cells involved in
atheroma formation.

Question 6. An obese 45-year-old man who smokes 20 cigarrettes a day is referred to the
lipid clinic. Investigations found the following blood plasma results:

BP 160/100
Fasting glucose 7.5mM (3.27.0mM)
Triglycerides 3.5 mM (<2mM)
Total cholesterol 8.0 mM (<5.5mM)
HDL 0.85mM (0.92.2mM)

a) How do you rate this mans cardiovascular risk? Explain your answer.
b) What lifestyle changes would you recommend to improve his health?
c) Does he have an abnormality of carbohydrate metabolism?

Question 7. Identify the differences between apoptosis and necrosis.

Question 8. How do tPA and streptokinase work?

Question 9. How do nitrates like glyceryl trinitrate work?

Question 10. Name the 2 major classes of cholesterol-lowering drugs and describe the
mechanism of action of each.

Question11. Identify steps in problem-solving when counselling in the post-infarct
situation.



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DONT TURN THE PAGE UNTIL YOU HAVE WORKED ON THESE QUESTIONS IN
MONDAYS PBL TUTORIAL, OR ATTEMPTED WRITTEN ANSWERS YOURSELF.
Quiz for Week 15 Answer Guides


Question 1. Sketch the anatomy of the coronary vessels.

Answer should indicate the origin of the coronary arteries above the aortic valve cusps, and the
territory of the major vessels and branches. The venous drainage should be identified. Some
anomalous drainage going into the left atrium instead of the right contributes to the normal right to
left shunt.


Question 2. Which ECG leads are best placed to record changes when the lesion is on
the (a) diaphragmatic aspect of the heart, (b) antero-septal region? Which arteries are
involved?

(a) II, III and aVF;
(b) precordial leads, esp V2 V5; arteries follow on from Question 1


Question 3. Indicate the time relationships of the arterial pressure wave to the heart
sounds, ECG, and left ventricular pressure.

This is a good diagram to draw as it encapsulates most of the critical ideas about the cardiac cycle:
it is in every physiology book though the wave shapes tend to be artistic rather than realistic.


Question 4. Identify the serum lipoproteins and briefly describe their role in
atherosclerosis.

LDL has the highest cholesterol content and transports lipids to the periphery; CVS risks
increase with levels.
VLDL contains triglyceride; risks increase with levels.
HDL is involved in cholesterol transport out of the tissues back to the liver; increased levels
reduce risk.
Total cholesterol risk increases sharply above about 5.2 mmol/l. Oxidised cholesterol
increases with age and disturbs the feedback control loops so that total cholesterol rises
progressively from infancy onwards.


Question 5. Identify, and briefly comment on the functions of, the cells involved in
atheroma formation.

Endothelial cells: platelet aggregation/thrombus formation, LDL uptake.
Platelets: form thrombus.
Smooth muscle cells: take up LDL forming foam cells.
Macrophages: oxidize LDL and take up lipids.
Neutrophils: phagocytosis, secrete proteases and inflammatory mediators causing ongoing
damage.


Question 6. An obese 45-year-old man who smokes 20 cigarrettes a day is referred to the
lipid clinic. Investigations found the following blood plasma results:

BP 160/100
Fasting glucose 7.5mM (3.27.0mM)
Triglycerides 3.5 mM (<2mM)
Total cholesterol 8.0 mM (<5.5mM)
HDL 0.85mM (0.92.2mM)

a) How do you rate this mans cardiovascular risk? Explain your answer.
b) What lifestyle changes would you recommend to improve his health?
c) Does he have an abnormality of carbohydrate metabolism?

a) His cardiovascular risk is high on account of his moderately elevated total cholesterol, low HDL,
smoking, hypertension and possibly diabetes.
b) Weight reduction, low cholesterol diet, smoking cessation and regular mild exercise.
c) This level of fasting glucose is consistent with diabetes mellitus. It needs to be confirmed
because diagnosis cannot be made on the basis of one measurement.


Question 7. Identify the differences between apoptosis and necrosis.

Apoptosis is programmed cell death, involving activation of a sequence of genes; it is ordered and
results in a compacted, dehydrated cell with fragmented chromatin, which is disposed of neatly by
phagocytosis by surrounding cells.

Necrosis results from injuries such as ischaemia and occurs when cells cannot maintain basic
homeostasis: - such as maintaining ion gradients for osmoregulation (volume regulation) and
electrical polarization of the membrane, keeping out calcium, maintaining the pool of glutathione to
prevent oxidative damage, etc. It results in inflammation, cellular infiltration, and the repair phase
will produce scar tissue.


Question 8. How do tPA and streptokinase work? What are the advantages and
disadvantages of each?

Streptokinase is an enzyme which acts by binding to plasminogen. The streptokinase-plasminogen
complex then activates other plasminogen molecules by converting them to the active proteolytic
enzyme, plasmin, which cleaves fibrin. Because it is derived from beta-haemolytic streptococci, it is
cheap but its effectiveness can be reduced in patients who have developed antibodies to it through
previous strep infections.

tPA acts by a different mechanism from the endogenous tissue plasminogen activator. It specifically
activates only the plasminogen that is within blood clots, thus minimising haemorrhage from general
plasminogen activation. However, it is much more expensive than streptokinase.


Question 9. How do nitrates like glyceryl trinitrate work?

Nitrovasodilators reduce total peripheral resistance, reducing arterial blood pressure (afterload),
dilating the large veins, reducing venous return (preload) and therefore reducing cardiac workload
in two ways. They are NOT coronary vasodilators. They donate oxides of nitrogen including nitric
oxide, which is biologically active in minute concentrations. NO is normally produced by vascular
endothelial cells and acts as a vasodilator by activation of guanylate cyclase, producing cyclic GMP,
which triggers a cascade of phosphorylation reactions leading to relaxation of vascular smooth
muscle.


Question 10. Name the 2 major classes of cholesterol-lowering drugs and describe the
mechanism of action of each.

i) Statins: Examples are simvastatin and lovastatin.
These act by inhibiting HMG-CoA reductase, the rate-limiting enzyme in the hepatic
synthesis of cholesterol. In the face of decreased cholesterol levels, the liver up-
regulates its LDL receptors, thereby pulling in LDL-cholesterol from the periphery for use
in bile acid synthesis.

ii) Anion exchange resins: Examples are cholestyramine and colestipol.
These act by binding irreversibly to bile salts, thus interfering with the enterohepatic
circulation of bile salts between the gut and the liver and removing them from the body.
Since bile salts are required for the emulsification and absorption of dietary fats, there is
a resultant increase in hepatic LDL receptors which again result in an increased rate of
removal of cholesterol from the blood for conversion to bile salts.


Question 11. Identify steps in problem-solving when counselling in the post-infarct
situation.

Problem clarification;
Goal setting;
Examine possible solutions and their impact on the patient;
Develop action plan agreed with the patient.