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MSII Unit 4 > Pharm > Flashcards

Pharm Flashcards

1
Q

What drug class is used to treat Raynauds disease?

A

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

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2
Q

T/F: ABPs and ACE-I are safe to use in pregancy?

A

False, they are teratogenic

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3
Q

Minoxidil and hydrlazine are what class of drugs? Important side effects?

A

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

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4
Q

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 ______

A

α-receptor activation
α1 blockers such as Terazosin, Doxazosin
MOA: Blocks post-synaptic α1-adrenergic receptor antagonist on vascular smooth muscle

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5
Q 
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
A

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

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6
Q

Do ACE-I and ARBs cause hyper or hypokalemia?

Other side effects?

A

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

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7
Q

Verapamil and Diltiazem are what class of drugs and may cause what side effects?

A

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

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8
Q

T/F: Beta blockers do not cause orthostatic hypotension.

A

True

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9
Q

T/F: alpha-1 blockers do not cause orthostatic hypotension.

A

False, alpha-1 blockers such as Terazosin, Doxazosin, or clonidine can cause orthostatic hypotension

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10
Q

To decrease HR, would a beta blocker or alpha blocker work?

A

Beta blocker

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11
Q

How do Beta blockers decrease BP?

A

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)

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12
Q

How do beta blockers help in patients with HTN?

A

B blockers to reduce CO (neg inotropic and chronotropic) and reduce renin secretion by blocking B receptors on JGA cells

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13
Q

How do beta blockers help in patients with angina pectoris?

A

↓ O2 consumption by ↓ heart rate and contractility

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14
Q

Why should Non-selective ß1 and ß2 antagonists (propanolol) should be avoided in patients with asthma and COPD?

A

Because of the risk of bronchoconstriction caused by ß2 blockade.

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15
Q

_______ is a potassium sparking diuretic that blocks aldosterone receptors in distal nephron. It also has anti-androgenic effects that can lead to gynecomastia

A

Spironolactone

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16
Q

What class of drugs are useful in controlling HTN in a patient with diabetic neuropathy, heart failure, and hyperuricemia?

A

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

17
Q

T/F: Thaizides and loop diuretics can cause gout?

A

True

Gout is characterized by hyperuricema and pain and inflammation.

18
Q

T/F: Loop diuretics, thiazides and B-blockers like metropolol can cause dyslipidemia?

A

True.

19
Q

In the presence of an agonist, which receptor would cause increase in preload? (alpha 1, alpha 2, beta 1, or beta 2)?

A

alpha 1 agonist will constrict veins, causing increase in venous return and thus increase in preload

20
Q

In the presence of an agonist, which receptor would cause increase renin release? (alpha 1, alpha 2, beta 1, or beta 2)?

A

B1

21
Q

In the presence of an agonist, which receptor would cause increase in conduction velocity? (alpha 1, alpha 2, beta 1, or beta 2)?

A

B1 via AV node (positive dromotropy)

22
Q

In the presence of an agonist, which receptor would cause increase in HR? (alpha 1, alpha 2, beta 1, or beta 2)?

A

B1 (positive chronotropy)

23
Q

In the presence of an agonist, which receptor would cause increase contractile force? (alpha 1, alpha 2, beta 1, or beta 2)?

A

B1 causes increase in force of contraction (positive inotropy), conduction velocity, and increase in CO and O2 consumption

24
Q

In the presence of an agonist, which receptor would cause decrease in renin? (alpha 1, alpha 2, beta 1, or beta 2)?

A

alpha1

25
Q

In the presence of an agonist, which receptor would cause increase in afterload? (alpha 1, alpha 2, beta 1, or beta 2)?

A

Alpha 1 agonism will contract arterioles (skin, viscera) causing an increase in TPR and therefore an increase in diastolic pressure and thus an increase in afterload

26
Q

In the presence of an agonist, which receptor would cause bronchiolar dilation? (alpha 1, alpha 2, beta 1, or beta 2)?

A

B2 agonism will cause increase in bronchiolar dilation, which is useful for patients with COPD or asthma. This is why non-selective B-blockers (propranolol) should be avoided when treating a patient with COPD/Asthma for HTN, since it may worsen respiratory symptoms.

27
Q

T/F: In a patient with CHF symptoms in need of a HTN medication, verapimil (Ca2+ channel blocker) is a good option?

A

False
Verapamil is a L-type Ca2+ channel blocker that has been associated with an accelerated progression of CHF because of its strong negative inotropic effects (decreased contractile force)

28
Q

Aspirin, clopidogrel, prasugrel, ticagrelor, and ticlopidine all have anti-_____ effects

A

Anti-platelet

29
Q 
Which antiplatelet medication functions by selectively and irreversibly inhibiting ADP binding to P2Y12 (blocks ADP-dependent activiation of glycoprotein IIb/IIIa)?
Aspirin
Clopidogrel
Ticlopidine
Cilostazol
Dipyradimole
A

Clopidogrel
Thienopyridine antiplatelet agent
Great antithrombotic; standard of care w/ stent
Side effect is bleeding, but not as severe as with prasugrel

30
Q 
Which antiplatelet medication functions by Irreversibly binds P2Y12 receptor (G protein-coupled chemoreceptor for ADP) but has a massive risk of bleeding
Aspirin
Clopidogrel
Prasugrel
Cilostazol
Dipyradimole
A

Prasugrel
Reduce thrombotic events in those w/percutaneous coronary intervention (e.g., stent)
Drug is limited to patients under 75 in age, greater than 60 Kg in weight, and no history of stroke or TIA.

31
Q 
Which antiplatelet medication functions by reversibly blocking ADP receptors and is a great antitrhombotic but requires bid dosing?
Clopidogrel
Ticagrelor
Prasugrel
Cilostazol
Dipyradimole
A

Ticagrelor

32
Q 
Which angina drug is used for treatment for claudication with peripheral vascular disease by Inhibits platelet aggregation via increasing cAMP levels
Clopidogrel
Ticagrelor
Prasugrel
Cilostazol
Dipyradimole
A

Cilostazol

contraindicated in heart failure

33
Q 
Which angina drug causes Increases platelet intracellular cAMP (inhibits phosphodiesterase 5, activates adenylate cyclase, inhibits uptake of adenosine from vascular endothelium and RBCs)...used to decrease peripheral vascular disease and in stress test of heart?
Clopidogrel
Ticagrelor
Prasugrel
Cilostazol
Dipyradimole
A

Dipyradimole
Pyrimido-pyrimidine antiplatelet agent

Use is limited in CAD because it vasodilates coronary arteries which can enhance exercise induced ischemia
Is used in cerebral artery disease

34
Q

How to beta blockers help treat MI/angina/ischemia?

A

Bind to beta receptors and block effects of Epi and NE, which means that catecholamines cant bind to the myocardium and you don’t get increase in HR or contractility and therefore decrease myocardial O2 demand.

Main point is that you are decreasing O2 demand by heart with these drugs therefore in conditions where thre are issues with O2 demand (blockage of vessels) these help minimize the effect

35
Q

Most beta-blockers used in CAD are beta1 or beta2 selective?

A

Most beta-blockers used in CAD are beta-1 selective

By decreasing contractility and heart rate, myocardial oxygen demand is decreased

36
Q

What are some of the contraindications for B blocker use?

A

Severe bradycardia (B blockers slow HR and this would compound this)
High degree AV block (will worsen AV block)
Unstable LV failure
Asthma/COPD

Other side effects: they make you fatigued, lethargic, decrease exercise tolerance, impotence

37
Q

What role does ACE inhibitors play in vasoconstriction/dilatation?

A

Angiotensin II is responsible for vasoconstriction (elevated bradykinin levels, which is a vasodilator)

Angiotensin II also stimulates the release of ADH/vasopressin that causes an increase in h2o reabsorption…blocking this (ACE-I) will cause less reabsorption and more water loss in urine…decreasing BP

MSII Unit 4 (8 decks)

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