Cardiovascular pathology

Question 1

23264 – Monckeberg’s sclerosis is
1: an example of dystrophic calcification
2: typically associated with a raised serum calcium level
3: a common accompaniment of Buerger’s disease
4: commonly seen in young adults

Answer 1

TFFF
Robbins 6th ed. CHAPTER: 2; 13 PAGE: 43; 498; 523b

Question 2

22769 – Monckeberg’s arterial sclerosis
1: affects largely the muscular arteries
2: predisposes towards thrombosis
3: is characterised by medial calcification
4: is a frequent cause of peripheral ischaemia

Answer 2

TFTF
Robbins 6th ed. Chapter: 12 Page: 498

Question 3

27186 – S: The distribution of atherosclerotic lesions along the course of the great vessels could be explained by arterial wall stress because R: humans adopt an erect posture, increasing the pressure in the distal arteries by gravity.

Answer 3

S is true, R is true and a valid explanation of S
The distribution of atherosclerotic lesions is quite striking: they increase progressively from the thoracic aorta to the iliac and femoro-popliteal systems. This seems to reflect two properties of the
blood pressure. Firstly, because of the erect posture, pressure increases from above down, being some 30 mmHg higher at the level of the inguinal ligaments than at the heart, due to gravity. Systemic hypertension is a major risk factor for atherosclerosis. Secondly, the vibrational components of the pressure, that is the pulse wave, increase in the more distal arteries. This is due to dispersive properties where different frequencies propagate at different speeds so that the arterial pulse waveform acquires an exaggerated dicrotic notch and oscillations during diastole in the distal vessels. Although there is much remaining to be learned about the pathogenesis of atherosclerosis, current theories include a role for endothelial injury promoted by wall stress. Hence, the statement and reason are arguably true and related as cause and effect.

Question 4

15789 – According to current understanding, the third of the following stages to occur in the development of atherosclerosis is
A. synthesis and secretion of extracellular matrix
B. platelet and monocyte synthesis and release of cytokine ‘growth factors’
C. smooth muscle cell migration into the intima
D. atrophy and degeneration of medial muscle and elastica
E. matrix vesicles initiate dystrophic calcification

Answer 4

A
First the ‘growth factors’ (after the endothelial injury and the platelet and monocyte attachment), then the migration of ‘smooth muscle cells’ (these are, in fact, ‘myofibroblasts’) recruited from uncommitted ‘reserve cells’ in the media, then the making and depositing of connective tissue component of the atheroma.

Question 5

180 – S: Symptoms of left ventricular failure may have rapid onset while right ventricular failure occurs gradually because R: infarction of right ventricular myocardium is uncommon

Answer 5

S is true, R is true but not a valid explanation of S
Pure right ventricular lesions are indeed uncommon, however the rate of onset of symptoms in cardiac failure is related to the mobility of fluid volumes rather than the rate of onset of ischaemic damage to the myocardium. The capacity of the pulmonary system is only a few hundred millilitres, so that in the event of sudden left ventricular dysfunction, significant volume overload of the pulmonary system occurs rapidly with blood flowing in from the systemic circuit and right ventricle. However, peripheral oedema involves many litres of fluid (often five to ten litres before gross oedema is apparent), which can only be accumulated slowly by dietary intake and renal fluid retention. Thus, it is impossible to suddenly develop peripheral oedema and venous overload. Therefore, the assertion is correct, but the reason given, though it is a true statement in itself, is not a valid reason for the assertion.

Question 6

22469 – Pressure-volume vascular overload is the major reason for the oedema caused by
1: adult respiratory distress syndrome
2: serum sickness
3: acute anaphylaxis
4: congestive (dilated) cardiomyopathy

Answer 6

FFFT
Robbins 4th ed. Chapter:3 Pages: 87-89, 118 5 176, 180

Question 7

15826 – Pressure-volume overload is the pathogenesis of oedema occurring in
1: local anaphylaxis
2: adult respiratory distress syndrome
3: lymphoedema
4: acute left heart failure

Answer 7

FFTT
The oedema of left heart failure is due to pressure-volume overload, as is (in a somewhat different way), lymphoedema. Local anaphylaxis is a histamine release phenomenon. ARDS is due primarily to
endothelial and pneumocyte injury.

Question 8

15815 – The major pathogenetic mechanism causing ‘nutmeg liver’ in congestive cardiac failure is
A. cardiogenic hepatomegaly
B. pressure atrophy of hepatocytes
C. reduced arterial oxygen saturation
D. hepatic hypoperfusion
E. intestinal vasopressor polypeptide

Answer 8

D
The pathogenesis is that the centrilobular cells get the last remnants of oxygen in the blood which has already supplied the gut and then the periportal cells; all of this in a pathophysiological situation of profound global hypoperfusion due to the cardiac problem.

Question 9

27228 – Right ventricular failure is most likely to be a long-term sequel of which cardiac pathology?
A. Aortic stenosis
B. Aortic incompetence
C. Mitral stenosis
D. Atrial fibrillation
E. Stenosis of the left main coronary artery

Answer 9

C
The right ventricle may fail secondary to pressure overload transmitted back from a failing left ventricle. This mechanism is prominent in mitral stenosis, where the left atrial pressure may be elevated twenty or more mmHg, thus effectively doubling right ventricular workload. Such great elevations in left atrial pressure are less common in aortic valve disease or ischaemia, and would only be seen in patients with severely decompensated failure and a grossly dilated left ventricle.

Question 10

27198 – In a patient with rapidly progressing congestive cardiac failure, myocardial biopsy shows round cell infiltrates and tissue oedema. This would be consistent with
A. a healing infarct
B. alcoholic cardiomyopathy
C. acute thiamine deficiency
D. viral myocarditis
E. dilated cardiomyopathy

Answer 10

D
Oedema with round cell infiltrates indicates an acute inflammatory process with an active immunological challenge in progress, as seen in viral myocarditis (D correct). The necrosis of infarction provokes a prominent neutrophil infiltration and the debris of dead myocytes is conspicuous. Thiamine deficiency is seen in starving alcoholics and extreme dieters: the lesion is biochemical, since thiamine forms a cofactor for enzymes in energy metabolism of glucose, and patients develop acute left ventricular failure which is promptly reversed by thiamine injection. Dilated cardiomyopathy, seen as an idiopathic state, or as a late sequel of viral myocarditis, or in chronically debilitated alcoholics, shows a biopsy picture of extensive fibrosis, rather than an active inflammatory process.

Question 11

7162 – Stenoses in coronary atherosclerosis
A. in the left coronary are typically more diffuse than lesions than in the right
B. in the anterior interventricular artery (left anterior descending) are usually distal
C. in the circumflex artery are usually distal
D. involve a worse prognosis for two-vessel disease than for untreated left main disease
E. usually spare the right posterior descending artery

Answer 11

E
Patterns of coronary disease have very characteristic distributions. In the left coronary system, the stenoses are usually short and lesions of the (left) anterior interventricular and circumflex are usually proximal. Lesions on the right are more diffuse and distal, but usually spare the (right) posterior descending artery (E correct). Prognosis of untreated lesions worsens progressively with one, two or three arteries involved, but left main coronary artery disease is comparable to three-artery disease (worse than two).

Question 12

14872 – The most specific serum indicator of acute myocardial infarction is
A. troponin T
B. the BB isoenzyme of creatinine phosphokinase
C. the MM isoenzyme of creatine phosphokinase
D. the MB isoenzyme of creatine phosphokinase
E. lactic dehydrogenase

Answer 12

Troponin T
Refer to Robbins, 6th Ed, Ch 13, page 561

Question 13

12560 – A large cardia infarct, three days old, may show all of the following EXCEPT
A. coagulative necrosis
B. peripheral inflammatory reaction
C. thrombus formation on the endocardial surface
D. red cells among the dead muscle fibres
E. perivascular accumulation of lymphocytes

Answer 13

E
A large cardiac infarct three days old will show coagulative necrosis (A false). This typically excites an acute inflammatory reaction at its margins (B false), and may provoke the formation of a thrombus on
the endocardial surface (C false). Cardiac infarcts typically show seepage of red cells among the muscle fibres (D false).
Perivascular accumulation of lymphocytes is not a feature of the reaction to infarcts (E true).

Question 14

27174 – S: Non-Q wave infarction is associated with a lower risk of reinfarction because R: the partial thickness lesion involves less muscle necrosis.

Answer 14

S is false and R is true
Although most infarcts are predominantly subendocardial when examined pathologically, the pattern with Q waves does reflect more complete transmural extension of the lesion. However, the viable muscle in the territory of the affected vessel in non-Q infarction remains at risk of re-infarction, and so the risk is greater, not less, with non-Q patterns. Thus, the statement is incorrect, and the reason is a correct statement but not a valid explanation.(D correct)

Question 15

27132 – With respect to myocardial ischaemia
A. acute unstable angina is usually precipitated by increased oxygen demand
B. angina pectoris is typically due to plaque disruption and platelet deposition
C. painless myocardial ischaemic episodes precipitated by emotional stress in patients with documented coronary occlusive lesions, are a recognised entity with similar prognostic implications to classical angina
D. angina in the absence of angiographically normal coronary vessels is moderately common
E. ‘syndrome X’ only occurs in patients with demonstrated single vessel lesions

Answer 15

C
A and B are reversed - it is the acute coronary syndromes of myocardial infarction and unstable (crescendo) angina which are due to thrombosis, while classical angina is precipitated by increased myocardial workload in the presence of fixed reductions in calibre of major vessels. Not all ischaemia is painful - the mechanisms are poorly understood, but the prognostic implications are similar to symptomatic ischaemia: statement C is correct. Options D and E are inverted. Angina is rare in the absence of occlusive lesions: when it occurs it is known as ‘syndrome X’ and believed to be due to
lesions in the microvasculature.

Question 16

27138 – Sudden cardiac death is commonly
A. due to pump failure
B. due to asystole
C. due to a ventricular tachyarrhythmia
D. prevented by class I antiarrhythmics
E. due to supraventricular tachycardia

Answer 16

C
Although any type of interference with the electrical or mechanical functions of the heart may lead to sudden death, in fact the overwhelmingly commonest cause is ventricular fibrillation - option C. Asystole may follow interruption to the conducting system below the AV node with occlusion of the left circumflex artery, but is less common than tachyarrhythmia. Cardiogenic shock is fortunately uncommon. When due to loss of a large zone of myocardium, its poor prognosis is not improved by early thrombolytic intervention. Antiarrhythmics are useful in treating arrhythmias, but disappointing
when used prophylactically. Class Ic agents actually increase post-infarct mortality, emphasising the arrhythmogenic potential of antiarrhythmic drugs.

Question 17

14946 – S: The size of hypertrophied cardiac muscle fibres cannot exceed a
certain maximum because R: the phenotype of the myocytes is altered and
the process is limited by apoptosis

Answer 17

S is true, R is true and a valid explanation of S
Refer to Robbins, 6th Ed, Ch 2, page 35

Question 18

12686 – S: If a patient with mitral stenosis has a pulmonary embolus, infarction is especially likely to occur because R: the bronchial arterial supply is reduced in mitral stenosis

Answer 18

S is true, R is true and a valid explanation of S
Blockage of a pulmonary artery does not usually cause infarction in healthy subjects, because the bronchial arterial supply provides well-aerated blood. In mitral stenosis the bronchial arterial supply is reduced (R true), and blockage of a pulmonary artery is likely to lead to infarction.

Question 19

22119 – Common predisposing causes of aortic dissection include
1: idiopathic cystic medionecrosis
2: syphilitic aortitis
3: systemic hypertension
4: atherosclerosis

Answer 19

TFTF
Robbins 5th ed. Page: 499-502.

Question 20

16005 – New blood vessel formation (angiogenesis) is a feature of
1: chronic inflammation
2: metastatic spread of cancer
3: tuberculous granuloma formation
4: pulmonary silicosis

Answer 20

TTFF
Chronic inflammation is a continuing attempted healing which never completes itself unless/until the damaging agent is removed. Continuous granulating scar formation is characteristic of this process - ie. angiogenesis. Likewise, metastatic cancer foci can not establish a separate existence without establishing a microvasculature for supply of nutrients, including oxygen. Tubercles and silicotic nodules are generally described as ‘avascular’ - this may or may not be absolutely true but overt granulation tissue formation with angiogenesis is not a feature of either.

Question 21

27077 – S: Provocation by exercise and relief by rest are characteristic of limb pain due to arterial insufficiency because R: exercise requires an increased blood flow to meet the metabolic needs of working muscle.

Answer 21

S is true, R is true and a valid explanation of S
Resting skeletal muscle has very low requirements for blood flow: as little as 1% of the values seen in maximal exercise. Pain of arterial insufficiency is provoked by exercise, since the flow restriction of the stenosis results in diminished flow and pressure at the working muscles. This is the critical diagnostic feature of intermittent claudication thus statement and response are true and linked (A correct). Other causes of lower limb pain, such as osteoarthritis, will not have the pattern of predictable onset with exercise and relief within a short period of rest. An arterial bruit at the site (and distal to) the stenosis, may not always be apparent at rest, but can appear during exercise as flow is increased due to the functional hyperaemia in working muscle, and flow velocity in the stenosis crosses the threshold for turbulence. Rest pain in arterial insufficiency is an extremely grave symptom, and in the light of the minimal nutritional requirements of resting muscle and connective tissues of the lower limb, indicates a profoundly reduced ability of the vasculature to supply blood flow.

Question 22

27089 – Incompetence of the venous valve of the long saphenous trunk at the saphenofemoral junction, with competent leg and ankle perforators, is most likely to be associated with
A. oedema
B. pigmentation
C. cutaneous ulceration
D. simple varicose veins
E. none of the above features

Answer 22

D
The presence of an incompetent saphenofemoral valve alone leads to varices in the long saphenous system. Since the ankle perforating vein valves are competent, the pressure in the superficial veins will fall on walking; and these patients tend not to develop the severe signs of venous hypertension (oedema, pigmentation, trophic changes, ulcers) seen in those suffering from incompetent valves in the ankle perforators. Typically, they suffer simple varicose veins (option D). The degree of pathology correlates better with the measured venous pressure during exercise and standing, than with the clinical assessment of venous valves.

Question 23

12692 – S: Thrombosis arising in the pelvic veins is the commonest cause of fatal pulmonary embolism because R: thrombosis is more frequent in the
pelvic veins than in calf veins

Answer 23

both S and R and false
Fatal pulmonary embolism is usually due to impaction of a large embolus in the main pulmonary artery and its branches, or in the right ventricle. An embolus of this size commonly arises in the leg veins. Thrombi occur in both the pelvic and the leg veins. In fatal pulmonary embolism, the size of the embolus is the point at issue.

Question 24

27102 – Deep venous thrombosis is more common in patients with a history of any of the following except
A. malignancy
B. oral contraceptive usage
C. surgery, especially abdominal, pelvic or hip, or immobilisation
D. obesity, old age, or past history
E. anaemia

Answer 24

E
Deep venous thrombosis can occur in any clinical setting, and pulmonary embolism is the commonest potentially preventable cause of death after major surgery. There is an impressive list of known risk factors, all connected more-or-less plausibly to either hypercoagulability or venous stasis. Among common conditions, anaemia is one of the few not conspicuously associated with DVT (E True). Polycythaemia, as a cause of elevated blood viscosity, is a known association with DVT.

Question 25

27120 – Acute superficial thrombophlebitis is commonly associated with all except
A. pain, induration, heat and tenderness along the involved vein
B. oedema of the limb
C. trauma
D. neighbouring bacterial infection
E. venous cannulation

Answer 25

B
Thrombophlebitis of superficial veins is often caused by trauma, cannulation, or a nearby infection. Its clinical signs are obvious. The process tends to remain localised to a single vein system: therefore, venous hypertension of the limb with oedema does not usually occur (option B).

Question 26

27095 – Lymphoedema occurs when lymphatic vessels fail to remove from the interstitial space
A. salt
B. water
C. protein
D. cells
E. none of the above components

Answer 26

C
The question does not ask what lymphatics remove, but rather, which of the things that they normally remove is the cause of oedema when lymphatic function is absent. Interstitial fluid pressure depends on the equilibrium of Starling forces: the hydrostatic pressure in the capillary pushing fluid out, and the osmotic pressure of plasma proteins pulling fluid back into the capillary. Capillaries are generally fully permeable to salt, water and small molecules, but nearly completely impermeable to proteins like albumin. The ‘nearly’ is the catch. Lymphatics remove a small amount of interstitial fluid, including the protein that leaks slowly through capillaries. In the absence of lymphatic function, that protein accumulates, abolishing the colloid osmotic pressure gradient from blood to interstitial fluid which normally pulls fluid back into the capillary. The result is oedema - lymphoedema. Thus, option C is the required answer.