14
sinus rhythm of the heart due to disease or injury induced
damage to the impulse conducting systems. They also result
from the development of ectopic pacemakers or abnormal
pacemaker rhythms. Drugs such as lidocaine are used to
normalize these rhythms. Lidocaine, a local anesthetic,
depresses cardiac excitability, answer (b). The refractory period
of cardiac muscle is increased, thus slowing the heart down. All
of the other alternatives given would exacerbate the arrhythmia.
16. When digitalis is used in atrial fibrillation, the therapeutic objective is
to
a. Abolish cardiac decompensation
b. Inhibit vagal impulses to the heart
c. Decrease the rate of A-V conduction
d. Increase the rate of cardiac repolarization
e. Produce a decrease in the rate of atrial contraction
(c)
Antiangina Drugs
17. Nitroglycerin dilates the coronary arteries in angina pectoris by
a. Decreasing the heart rate reflexly
b. Increasing the metabolic work of the myocardium
c. Direct action on smooth muscle in the vessel walls
d. Increasing the effective refractory period in the atrium
e. Blocking beta-adrenergic receptors
(c)
18. Propranolol is of value in treating angina pectoris because it
a. Has a direct action on vascular smooth muscle
b. Blocks autoregulatory mechanisms in the heart
c. Inhibits oxygen metabolism in cardiac cells
d. Provides relief within seconds of an acute anginal attack
e. Prevents chronotropic responses to endogenous epinephrine
emotions and exercise
(e)
ACE Inhibitors
19. Administration of angiotensin results in
a.
Anti-inflammatory effects
b.
Antihistaminic effects
c.
Increased blood pressure
d.
Increased heart rate
e.
A sedative effect
(c)
20. The primary antihypertensive effect of captopril (Capoten) is due to
accumulation of
a.
Serotonin
b.
Angiotensin I
c.
Angiotensin III
d.
Bradykinin metabolites
(b) Captopril is an angiotension-converting enzyme inhibitor that
blocks the activation of angiotension I to angiotension II. The
decreased blood concentration of angiotension II reduces blood
pressure, because angiotension II is a potent vasoconstrictor.
Thus (c) is wrong, accumulation of angiotension I is the usual
effect. Captopril also maintains lowered BP by elevating
bradykinin (which has potent vasodilatory action) in the blood by
blocking its metabolism. Thus (d) is wrong, bradykinin
metabolites do not accumulate.
21. Administration of angiotensin results in
a.
A sedative effect
b.
Increased heart rate
c.
Increased blood pressure
d.
Antihistaminic effects
e.
Anti-inflammatory effects
(c) I guess because more angiotensin II would be formed, and
that is a potent vasoconstrictor
Mechanism of Action
Diuretics
22. Which of the following is NOT characteristic of the thiazide diuretics?
a.
Increase renal excretion of sodium and chloride
b.
Increase renal excretion of potassium
c.
Increase the toxicity of digitalis
d.
Exacerbate existing diabetes
e.
Cause hypokalemia
f.
Cause hypoglycemia
(f) first off, how can you have an option (f)?! (a) is how diuretics
lower BP, (b) is why they can cause hypokalemia, which is
conveniently option (e), and hypokalemia can potentiate digitalis
induced arrythmias option(c). Theyy apparently can also cause
hyperglycemia, which would relate to option (d). How the heck
are you supposed to remember all of this?
23. The most useful diuretic drugs act by
a.
Increasing the glomerular filtration rate
b.
Decreasing the renal reabsorption of sodium
c.
Decreasing the renal excretion of chloride
d.
Increasing the renal reabsorption of potassium
e.
Increasing the secretion of antidiuretic hormone
(b) people with high BP are always told to reduce salt intake,
since high sodium levels cause fluid retention which can
increase BP, so ipso facto, reducing renal reabsorption of
sodium makes BP go down
24. Which of the following drugs act by inhibiting renal reabsorption of
sodium?
a.
Urea
b.
Chlorothiazide
c.
Theophylline
d.
digitalis glycosides
e.
Procainamide
(b) same question as above, just reversed.
Cardiac Glycosides
25. Digoxin exerts its positive inotropic effect by
a. Activation of adenylcyclase
b. Inhibition of phosphodiesterase
c. An agonist effect of beta-receptors
Generated by Foxit PDF Creator © Foxit Software
http://www.foxitsoftware.com For evaluation only.
