Pharm Flashcards
What drug class is used to treat Raynauds disease?
Dihydropyridines (Ca2+ channel blockers) that work to decrease BP by decreasing CA2+ influx into vascular smooth muscle and therefore decrease systemic vascular resistance
Nifedipine, amlodipine, Felodipine
T/F: ABPs and ACE-I are safe to use in pregancy?
False, they are teratogenic
Minoxidil and hydrlazine are what class of drugs? Important side effects?
They are direct vasodilators that relax smooth muscle of peripheral arterioles causing vasodilation
Minoxidil (rogaine)
Side effects include reflex tacchycardia which is why they are given with B-blockers
Drug-induced postural (orthostatic) hypotension is usually due to venous pooling or excessive diuresis and inadequate blood volume. Venous pooling is normally prevented by _______ in vascular smooth muscle; thus, orthostatic hypotension is caused or exacerbated by ______
α-receptor activation
α1 blockers such as Terazosin, Doxazosin
MOA: Blocks post-synaptic α1-adrenergic receptor antagonist on vascular smooth muscle
A significant number of patients started on ACE inhibitor therapy for hypertension are intolerant and must be switched to a different class of drug. What is the most common manifestation of this intolerance? (A) Angioedema (B) Glaucoma (C) Headache (D) Incessant cough (E) Ventricular arrhythmias
Chronic, intolerable cough is an important adverse effect of captopril and other ACE inhibitors. It may be reduced or prevented by prior administration of aspirin
ACE-I:
(“-pril” suffix)
Captopril, lisinopril, benozapril, quinapril, ramipril, enalapril
Do ACE-I and ARBs cause hyper or hypokalemia?
Other side effects?
Aliskiren (direct renin inhibitor) and other inhibitors of the renin-angiotensin-aldosterone system (ACE-I and ARB) may cause hyperkalemia, not hypokalemia.
ACE-I cause dry cough
ARBs do NOT cause cough
Both cause angioedema
Verapamil and Diltiazem are what class of drugs and may cause what side effects?
Verapamil and Diltiazem are Ca2+ channel blockers (non-dihydropyramidines) and fcn as negative ionotropes
they often causes constipation, probably by blocking L-type calcium channels in the colon.
Also: Leg edema, bradycardia, AV nodal blockade, hypotension, worsening heart failure
T/F: Beta blockers do not cause orthostatic hypotension.
True
T/F: alpha-1 blockers do not cause orthostatic hypotension.
False, alpha-1 blockers such as Terazosin, Doxazosin, or clonidine can cause orthostatic hypotension
To decrease HR, would a beta blocker or alpha blocker work?
Beta blocker
How do Beta blockers decrease BP?
Decrease HR
Decrease SV
Decrease CO (due to neg chronotropic and inotropic effects)
Decreases renin (therefore decreases aldo retention of H20 in nephron…inhibiting water retention)
How do beta blockers help in patients with HTN?
B blockers to reduce CO (neg inotropic and chronotropic) and reduce renin secretion by blocking B receptors on JGA cells
How do beta blockers help in patients with angina pectoris?
↓ O2 consumption by ↓ heart rate and contractility
Why should Non-selective ß1 and ß2 antagonists (propanolol) should be avoided in patients with asthma and COPD?
Because of the risk of bronchoconstriction caused by ß2 blockade.
_______ is a potassium sparking diuretic that blocks aldosterone receptors in distal nephron. It also has anti-androgenic effects that can lead to gynecomastia
Spironolactone
What class of drugs are useful in controlling HTN in a patient with diabetic neuropathy, heart failure, and hyperuricemia?
ACE-inhibitors have been shown to slow the progression of renal disease, which is why they are the most preferred antihypertensive medication in diabetic patients.
Beta-blockers (B1) are not recommended in patients with diabetes since it can block the normal signs and symptoms of hypoglycemia
T/F: Thaizides and loop diuretics can cause gout?
True
Gout is characterized by hyperuricema and pain and inflammation.
T/F: Loop diuretics, thiazides and B-blockers like metropolol can cause dyslipidemia?
True.
In the presence of an agonist, which receptor would cause increase in preload? (alpha 1, alpha 2, beta 1, or beta 2)?
alpha 1 agonist will constrict veins, causing increase in venous return and thus increase in preload
In the presence of an agonist, which receptor would cause increase renin release? (alpha 1, alpha 2, beta 1, or beta 2)?
B1
In the presence of an agonist, which receptor would cause increase in conduction velocity? (alpha 1, alpha 2, beta 1, or beta 2)?
B1 via AV node (positive dromotropy)
In the presence of an agonist, which receptor would cause increase in HR? (alpha 1, alpha 2, beta 1, or beta 2)?
B1 (positive chronotropy)
In the presence of an agonist, which receptor would cause increase contractile force? (alpha 1, alpha 2, beta 1, or beta 2)?
B1 causes increase in force of contraction (positive inotropy), conduction velocity, and increase in CO and O2 consumption
In the presence of an agonist, which receptor would cause decrease in renin? (alpha 1, alpha 2, beta 1, or beta 2)?
alpha1