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Sample questions – CERTIFYING EXAMINATION Cardiology
A. MC- Questions: A). Digoxin ______________________________________________________________
All of the following statements are correct, EXCEPT : A)
Males are affected more often than females. B)
Murmur intensity cannot be used to estimate the severity of mitral
regurgitation. C)
Fractional shortening is a reliable index to estimate myocardial function
in these patients. D)
Tearing of the left atrium with tamponade is an extremely rare
complication. E)
Diuretics and ACE‑inhibitors are the corner stones of the therapy
in most symptomatic patients. Correct answer:
C) Fractional shortening is not related to the myocardial performance B. Essay Question: Angiotensin
Converting Enzyme Inhibitors (ACEI) represent a novel therapy for congestive
heart failure. Describe the
pathophysiologic mechanism by which they act and discuss potential adverse
clinical effects based upon the physiologic derangements caused by these agents.
Heart failure diminishes cardiac output that results in reduced renal
afferent arterial pressure, and the compensatory mechanism, increased
sympathetic traffic. Sodium
delivery to the renal afferent arteriole is reduced.
These three stimuli cause renin release from the renal JGA which
initiates activation of the renin‑angiotensin‑aldosterone system in
HF. Renin
cleaves angiotensin I (an inactive prohormone) from angiotensinogen. Angio I. is
then converted to angiotensin II (AII) in the lungs by angiotensin converting
enzyme (ACE). AII is a very potent vasoconstrictor, the effects of which
increase arterioloar tone, vascular impedance to LV ejection, and thus, increase
cardiac afterload and (subsequently) decrease stroke volume. Cardiac output =
the product of HR x SV (stroke volume is effected by preload, afterload,
contractility). AII stimulates
adrenal cortical release of aldosterone which enhances renal sodium retention
and thus, water retention. Blood pressure and fluid volume are increased.
Both are further augmented by AII‑mediated vasoconstriction and
increased ADH release. AII may also
enhance vasoconstriction by degrading vasodilitory bradykinin and decreasing
vasodilatory prostaglandin synthesis. Eventually,
the effects of RAAS produce detrimental increases in vascular preload (leading
to congestion), increased afterload (decreasing cardiac output), exacerbating or
leading to CHF. B.
Adverse Effects:
If GFR is decreased by poor cardiac output,
is further decreased by overzealous volume reduction (diuresis) and possibly,
volume contraction from low sodium diets, GFR will worsen.
ACEI drugs, by blocking the vasoconstrictive effects of AII on the
efferent renal arteriole, postglomerular arteriolar resistance is reduced and
causes GFR to plummet.The GFR is dependent on high efferent arteriolar tone
which, if blocked by ACEI's, resultes in functional renal insufficiency.
ACEI's blunt the RAAS from increasing circulating sodium, and subsequent
volume repletion, by blocking secretion of aldosterone from AII stimulous.
Loop diuretics may hasten sodium loss. ACEI may cause anorexia, vomiting
or diarrhea which further worsen volume depletion.
Hypotension is a potential side effect.
Hyperkalemia is a potential serious side effect of some ACEI drugs
because they interfere with ability of the kidney to excrete K+ (by blunting
release of aldosterone). This is
more likely to occur if hyponatremia is present, K++ supplements are used or K+
sparing diuretics are administered.
Few publications about the effective role of Bradikinine-effect
prolongation, as well as the modification of the endotheline dysfunction induced
by chronic volume overload in dog have been published, but they certainly play a
major role in the efficacy of ACE inhibitors Topic:
Physiology Category:
Cardiology
_____________________________________________________________________ Example:
Graphic:
Lead
II ECG tracing recorded from a 5-year old Great Dane. The dog was in heart
failure.
All of the following statements are correct, EXCEPT : A)
The rapid heart rate is due to high catecholamines concentrations,
enhancing the conduction of the AV-node B)
This arrhythmia is common in dogs with DCM C)
This arrhythmia decreased late diastolic ventricular filling D)
Primary therapeutic goal will be to reduce heart rate E)
This arrhythmia is common in Cardiomyopathic Doberman Pinscher, and is a
risk of sudden death
A)
These myocardial changes are common in cats B)
These disease has probably a genetic predisposition C)
The primary cause of these myocardial changes may be myocardits D)
Histologic lesions should include myocardial cell degeneration and focal
endocardial fibrosis. E)
These cat may easily develop pleural effusion |
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Further information about ECVIM-CA can be obtained from:
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