Sample questions – CERTIFYING EXAMINATION Cardiology

A. MC- Questions:

  1. All of the following drugs are used for their negative dromotropic action on the  AV-node,  EXCEPT:

A).       Digoxin  
B).       Mexiletin  
C).       Propranolol  

D).       Diltiazem  
E).       Atenolol

  Correct answer : B) Mexiletin

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  2.         Mitral valvular endocardiosis represents an important group of acquired canine cardiac disorders.

            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:

  Essay Questions

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.

  A. Pathophysiologic mechanisms of action: 

        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          

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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

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  Example: Graphic

  Short axis view of a 3-year old male domestic shorthair. The cat was presented for dyspnea

              All of the following statements are correct, EXCEPT :

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

 

  Kodachrome slide example

 

 

Further information about ECVIM-CA can be obtained from:

The President of the ECVIM-CA :
Dr. Claudia Reusch,
Clinic for Small Animal Internal Medicine, 
Universitiy of Zuerich
Winterthurerstr. 260
CH-8057 Zuerich, Switzerland
Tel: (41)-1-6358301  
Fax: (41)-1-6358930
E-mail: creusch@vetclinics.unizh.ch
The Secretary of the ECVIM-CA :
Dr. Ian Ramsey,
Dept. Clinical Veterinary Studies
University
of Glasgow
Bearsden G61 1QH
U.K.
Tel: (44)-141-3305700 Fax:(44)-141-9427215
E-Mail: I.Ramsey@vet.gla.ac.uk
Administrative Assistant:
Mrs. Sharon Green
Avenue du Guéret 1
B – 1300 Limal
Tel: + 32 (0)10 400 603
Fax: + 32 (0)10 400 703

E-Mail: secretariat@ecvim-ca.org