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Pharmacology > Block 2: Renin-Angiotensin and CCBs > Flashcards

Block 2: Renin-Angiotensin and CCBs Flashcards

0
Q

specialized epithelial cells found in distal tubule are called?

A

macula densa

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1
Q

what cells contain renin granules?

A

juxtaglomerular cells

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2
Q

what is renin?

A

an acid protease that cleaves angiotensinogen into angiotensin I

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3
Q

what drug inhibits renin?

A

aliskiren

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4
Q

what does ACE do?

A

converts angiotensin I (inactive) to angiotensin II (active)

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5
Q

ACE inhibitors (3)

A

captopril, enalapril, lisinopril

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6
Q

what are the effects of aldosterone on the kidney and where in the kidney does it act?

A

enhances sodium reabsorption and potassium excretion, principal cells of distal tubule and collecting duct

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7
Q

what is the purpose of renin release?

A

to retain salt and water in your body

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8
Q

does stimulation of sympathetic nervous system cause renin release to increase or decrease, and through what receptors does this occur?

A

increase, beta1 adrenergic receptors

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9
Q

how do beta blockers affect renin release, and what are the 2 examples?

A

they reduce sympathetic nerve activity and therefore reduce renin release. metoprolol and propranolol

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10
Q

what is the effect of AT1 receptor antagonists and ACE inhibitors on renin release?

A

they stimulate renin release

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11
Q

how do AT1 receptor antagonists and ACE inhibitors stimulate renin release?

A

angiotensin II causes feedback inhibition of renin by acting directly on juxtaglomerular cells. these drugs block this feedback inhibition

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12
Q

what second messenger molecule is important in angiotensin II actions?

A

calcium

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13
Q

effects of angiotensin II via AT1 receptors (5)

A

vasoconstriction, vascular proliferation, aldosterone secretion, cardiac myocyte proliferation, increased sympathetic tone

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14
Q

what are the effects of aldosterone on the heart? (2)

A

cardiac fibrosis and left ventricular hypertrophy

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15
Q

what angiotensin receptor is responsible for hypertension?

A

AT1

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16
Q

angiotensin II: preload vs afterload

A

increases afterload

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17
Q

angiotensin II role in CHF (5)

A

vasoconstrictor, activates sympathetic nervous system, arrhythmogenic, promotes hypertrophy and apoptosis, releases aldosterone

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18
Q

role of aldosterone in CHF (3)

A

promotes sodium and water retention, cardiac fibrosis, left ventricular hypertrophy

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19
Q

what are 4 important common properties of inhibitors of renin-angiotensin system?

A

decrease BP with no change in heart rate, contraindicated in pregnancy, improve renal function in diabetic patients, do not interfere with regulation of glucose metabolism, and can cause hypotension

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20
Q

losartan: mechanism, therapeutic use

A

AT1 receptor antagonist, prevents angiotensin II from binding AT1 receptors –> decreased aldosterone secretion, vasodilation, decreased sympathetic activation
use: hypertension

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21
Q

what is important to remember when prescribing losartan?

A

takes 4-8 weeks to see maximal BP lowering effects

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22
Q

what drugs enhance the action of losartan?

A

diuretics

23
Q

what kinds of drugs improve survival in CHF patients? (3)

A

ACE inhibitors, ARBs (losartan), and mineralocorticoid antagonists

24
Q

ACE inhibitors: mechanisms

A
  1. blocks conversion of angiotensin I to angiotensin II, decreasing aldosterone, causing vasodilation, and decreasing BP
  2. blocks bradykinin degradation. bradykinin causes vasodilation by activating B2 receptors
25
Q

how does bradykinin cause vasodilation?

A

by activating B2 receptors and causing an increase in NO and prostaglandins

26
Q

do ACE inhibitors cause hyper- or hypokalemia and how?

A

hyperkalemia, by lowering aldosterone

27
Q

aliskiren: mechanism, therapeutic use, what types of drugs enhance its action?

A

inhibits renin, hypertension

diuretic, ACE inhibitor, or angiotensin antagonist

28
Q

mineralocorticoid antagonists: therapeutic uses

A

used with thiazide or loop diuretic to treat hypertension or edema

29
Q

name the two dihydropyridine CCBs

A

nifedipine and amlodipine

30
Q

what kind of calcium channels do CCBs block?

A

L-type calcium channels

31
Q

why don’t CCBs affect skeletal muscle tone?

A

they don’t affect the release of intracellular calcium that mediates skeletal muscle contraction

32
Q

what integral part of cardiac cells do calcium channels take part in?

A

the upstroke of the AP in the SA and AV nodes depends on calcium channels and is required for contraction of atrial and ventricular muscle cells

33
Q

what is the role of calcium channels in vascular smooth muscle cells?

A

depolarization –> calcium influx –> contraction

34
Q

which 2 CCBs act preferentially on cardiac cells?

A

verapamil and diltiazem

35
Q

which 2 CCBs act preferentially on arterial smooth muscle cells?

A

the dihydropyridines (nifedipine, amlodipine)

36
Q

why are dihydropyridines more vascular smooth muscle-specific?

A

the binding sites for these drugs are on the outside surface of the channel protein and therefore binding is more dependent on membrane voltage. the more depolarized/positive the membrane is, the more these drugs will bind. because vascular smooth muscle cells are more depolarized, these drugs preferentially bind there to induce vasodilation

37
Q

dihydropyridines: arteries or veins? preload or afterload?

A

preferentially block calcium channels in arteries and have little effect on veins. thus, these drugs significantly reduce afterload but not preload

38
Q

CCB effects on bronchioles

A

cause bronchodilation, and are therefore safe to use in asthmatic patients

39
Q

CCBs for angina (3)

A

diltiazem, dihydropyridines (amlodipine and nifedipine)

40
Q

why is diltiazem good for angina?

A

it decreases SA node firing rate and reduces afterload by causing peripheral vasodilation

41
Q

why is diltiazem good for preventing or ameliorating ischemia?

A

it dilates coronary arteries, permitting increased blood flow to myocardium

42
Q

why are dihydropyridines good for angina?

A

as coronary vasodilators they reduce myocardial oxygen demand and arterial pressure

43
Q

which CCBs cause coronary vasodilation?

A

all of them

44
Q

which CCBs cause peripheral vasodilation?

A

dihydropyridines (amlodipine, nifedipine)

45
Q

which CCBs cause decrease in heart rate?

A

non-dihydropyridines (verapamil and diltiazem)

46
Q

what CCBs are used for supraventricular arrhythmias?

A

diltiazem or verapamil (non-dihydropyridines)

47
Q

why are diltiazem and verapamil good for supraventricular arrhythmias?

A

they reduce firing rate of SA nodde and reduce conduction through the AV node

48
Q

CCBs used for supraventricular tachycardia

A

diltiazem and verapamil

49
Q

CCBs: preload vs. afterload

A

all CCBs decrease afterload

50
Q

which CCBs are used for hypertension?

A

nifedipine and amlodipine (dihydropyridines)

51
Q

why are the dihydropyridines good for hypertension?

A

they are potent vasodilators

52
Q

what should you worry about when prescribing dihydropyridines for hypertension and how can you prevent this from happening?

A

reduced BP can cause reflex tachycardia. beta blockers like propranolol are often administered to prevent this

53
Q

dihydropyridines are contraindicated in patients with what?

A

tachyarrhythmias

54
Q

which CCB has a half-life of 30-50 hours and is the only one that can be taken once a day?

A

amlodipine

55
Q

which CCBs can worsen CHF symptoms and why?

A

verapamil and diltiazem, negative inotropic effects

56
Q

which CCBs can worsen AV block? why?

A

diltiazem and verapamil because they dampen AV node conduction

Pharmacology (6 decks)

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