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Heart 2 > Pharm > Flashcards

Pharm Flashcards

1
Q

Centrally acting alpha-2 agonists and route

A

Clonidine (oral), methyldopa (oral, IV)

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2
Q

Direct vasodilators and route

A

Hydralazine (oral, IM, IV), minoxidil (oral), fenoldopam (IV), nitroprusside (IV)

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3
Q

a and B antagonists

A

Labetalol (oral/IV), carvedilol (oral)

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4
Q

Selective a1 antagonists

A

prazosin, terazosin, doxazosin (all oral)

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5
Q

non-selective a antagonists

A

phenoxybenzamine (oral), phentolamine (IM/IV)

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6
Q

Clonidine MOA

A

Stimulates a2 receptors in CNS →↓ symathetic outflow (vasomotor center, baroreceptor control is retained)→↓TPR (a1 on arteries) and ↓ HR, CO (B1 on
heart) decrease seen mostly with clonidine

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7
Q

Methyldopa MOA

A
  • Lipid soluble agent→ access the CNS (activate a2 receptors→ reduce sympathetic outflow from vasopressor centers in the brainstem
  • Stimulation of central a2 receptors result in the reciprocal increase in vagal tone and bradycardia
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8
Q

Clonidine clinical usage

A
  • 2nd line for chronic HTN

- HTN urgencies

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9
Q

Clonidine adverse effects

A

*Sedation/ depression (transdermal route- less
sedation)
*Abrupt withdrawal (hypertensive crisis,
rebound hypertension, symptoms of sympathetic
over- activity)
*Sexual Dysfunction

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10
Q

Methyldopa clinical usage

A

*Primarily used for hypertension during
pregnancy (Chronic HTN→ HTN that antedates pregnancy, present before the 20th week of pregnancy, or persists longer than 12 weeks
postpartum; Gestational HTN→ after 20 weeks of gestation in the absence of proteinuria)

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11
Q

Methyldopa adverse effects

A
  • Sedation, depression, nightmares, vertigo

* Longterm → (+) Coombs test (discontinuation reverses)

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12
Q

Hydralazine MOA

A

Vasodilation of Artery → ↓TPR → ↓BP → Activates SNS and ↑Renin which leads to Reflex Tachycardia and Salt & Water Retention → ↑BP and CO (combine
with BB and Loop diuretic to prevent reflex
tachycardia and fluid retention)

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13
Q

Minoxidil MOA

A

Vasodilation of Artery (through activation of K+ channels on smooth m > resting potential > limits contraction) → ↓TPR → ↓BP → Activates SNS and ↑Renin which leads to Reflex Tachycardia and Salt & Water Retention → ↑BP and CO (combine
with BB and Loop diuretic to prevent reflex
tachycardia and fluid retention)

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14
Q

Hydralazine clinical usage

A

*Hypertensive urgencies/emergencies;
*Response less predictable than other IV
agents (good agents for pregnant women)
*COMBO with minoxidil = chronic tx for more severe HTN (2nd line)

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15
Q

Minoxidil clinical usage

A

*Reserve for hypertension patients who do
not respond adequately to maximum
therapeutic doses of a diuretic and 2 other
antihypertensive agents
*COMBO with hydralazine = chronic tx for more severe HTN (2nd line)

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16
Q

Hydralazine and Minoxidil adverse effects

A

*Excessive vasodilation and hypotension (tachycardia,

Na & H20 retention, flushing, palpitations, dizziness, angina, headache)

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17
Q

Hydralazine adverse effects

A

Slow acetylators: lupus-like syndrome (fever, arthralgia, skin rash)

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18
Q

Minoxidil adverse effects

A
  • Hypertrichosis

* PERICARDIAL EFFUSION

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19
Q

Fenoldopam MOA

A

Activates post-synaptic dopamine D1 receptors > decrease TPR and increase renal blood flow

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20
Q

Fenoldopam clinical usage

A

HTN emergencies

  • short-term tx up to 48 hours
  • beneficial in pt with renal insufficiency d/t increased renal blood flow, diuresis, natriuresis
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21
Q

Fenoldopam adverse effects

A
  • Hypotension
  • Reflex tachy
  • flushing
  • headache
  • increased intraocular pressure
  • hypokalemia
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22
Q

Nitroprusside MOA

A

NO > activate guanylyl cyclase > increase cGMP > activates calcium sensitive K channels > arterial and venous dilation > decreased TPR and decreased venous return (little/no effect on CO)

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23
Q

Nitroprusside clinical use

A

-HTN emergencies (titrate BP)
-controlled hypotension during surgery
-acute decompensated HF
(IV infusion with rapid onset and very short DOA)

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24
Q

Nitroprusside adverse effects

A
  • CYANIDE TOXICITY (rapid metabolization liberates cyanide, renal failure can increase toxicity)
  • HYPOTENSION (headache, dizziness, palpitations)
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25
Q

Labetalol ratio of beta:alpha

A

3:1 beta to alpha antagonism

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26
Q

Carvedilol ratio of beta:alpha

A

1:1

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27
Q

Labetalol clinical usage

A

-HTN urgencies/emergencies

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28
Q

Carvedilol clinical usage

A
  • 2nd line for chronic HTN (inferior to ACEI/ARB/CCB)

- HTN urgency

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29
Q

Labetalol MOA

A

-inhibits alpha 1, beta 2 (vasodilation) beta 1 (little effect on HR and CO)

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30
Q

Labetalol adverse effects

A

Bronchospasm, can prolong or enhance hypoglycemia, HF, orthostatic hypotension, sexual dysfunction

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31
Q

Where are alpha 1 receptors?

A

Arterial smooth muscle, venous smooth muscle, trigone, prostatic smooth muscle

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32
Q

Zosin MOA

A

Blocks alpha 1 on arteries > vasodilation > decrease TPR, reflex tachy, reflex H2O and Na retention > decrease BP, increase CO
and veins > venodilation > decrease venous return > decreased CO (long-term little/no change in HR/CO)

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33
Q

End result of alpha-1 antagonists

A

With chronic use, any short-term effects on HR, CO, and plasma renin activity return to pretreatment levels
-reduction in BP achieved via vasodilation induced decrease in TPR

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34
Q

Zosin clinical usages

A

-BPH (increase urine flow)
-Raynaud’s (CCBs first line)
-2nd line for chronic HTN (good for pt with BPH)
(increased risk of HF compared to thiazides)

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35
Q

Zosin adverse effects

A

Orthostatic hypotension (severe with syncope> “first dose” effect; little with long-term)&raquo_space; take @ bed

  • Reflex tachy
  • Headache, weakness, dizziness
  • Edema (Na and H2O retention)
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36
Q

Phenoxybenzamine and phentolamine use

A

Pheochromocytoma (blocks alpha 1 receptors from catecholamine-producing tumor)
-Phentolamine can also be used in HTN urgencies/emergencies > limited use in severe HTN d/t alpha 2 inhibition)

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37
Q

Phenoxybenzamine and phentolamine adverse effects

A
  • Orthostatic hypotension
  • Nasal stuffiness
  • Tachy (arrhythmias)
  • inhibited ejaculation
  • fatigue
  • sedation
  • nausea
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38
Q

Cardiac Glycosides

A

Digoxin

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39
Q

Digoxin MOA

A

Blocks Na/K ATPase -> increases cytoplasmic levels of Na and decreases drive of Na/Ca exchanger -> high levels of Ca in cytoplasm -> more Ca absorbed into SR via SERCA2 -> allows for more Ca in SR and stronger contraction

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40
Q

Digoxin Clinical Usage

A

used with diuretics, ACEI, and BB
Useful in A-fib
Stage C & D HF patients when ACEI and BB fail to control symptoms
NOT FOR ACUTE DECOMPENSATED HF
Improves clinical symptoms and quality of life but DOES NOT improve survival

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41
Q

Digoxin Adverse effects

A 
sinus bradycardia
AV block
Increased sympathetic tone, tachycardia
Ca overload
Hypokalemia and hypercalcemia increase the action/toxicity of digoxin
Narrow TI
Cardiac arrhythmias
Anorexia, diarrhea, N/V
Dizziness, confusion
Blurred vision
Green & yellow halos around objects
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42
Q

Digibind

A

digoxin antidote
fab fragment of digoxin specific antibody
Use in life threatening cases of digoxin toxicity

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43
Q

Vasodilator Drugs

A

Isosorbide Dinitrate

Hydralazine

44
Q

Isosorbide Dinitrate MOA

A

venous dilator -> reduces preload

stimulates intracellular cGMP, relaxes arterial and venous smooth muscle

45
Q

Hydralazine MOA

A

arterial dilator -> reduce afterload

Help increase forward CO

46
Q

Isosorbide Dinitrate & Hydralazine Clinical Usage

A

Recommended to use together
Patients who cannot use ACEI or ARB
Stage C HF
Persistently symptomatic blacks that are already on optimal therapy with a diuretic, ACEI, BB

47
Q

Ivabradine MOA

A

reduces cardiac rate through blockade of the If current

48
Q

Ivabradine Clinical Usage

A 
NYHA class II to III, Stage C
EF< 35%, HR > 70
On maximally tolerated doses of B or who are contraindicated to use a BB
49
Q

Ivabradine Adverse Effects

A

Bradycardia
HTN
Afib

50
Q

Ivabradine Contraindications

A

acute decompensated HF
BP< 90/50
AV block or bradycardia
severe hepatic impairment

51
Q

Sacubitril/Valsartan MOA

A

Sacubitril -> inhibits neprilysin (enzymes that degrades natriuretic peptides)
Valsartan -> ARB
Oral administration

52
Q

Sacubitril/Valsartan Clinical Usage

A 
HF
NYHA class II-IV , Stage C and reduced ejection fraction
53
Q

Sacubitril/Valsartan Adverse Effects

A

Hypotension

Hyperkalemia

54
Q

Sacubitril/Valsartan Contraindications

A

Pregnancy - BBW

55
Q

Positive Inotropic

A

Dobutamine
Dopamine
Inamrinone
Milrinone

56
Q

Acute Decompensation (vasodilators)

A

Nitroglycerin
Nitroprusside
Nesiritide

57
Q

Dobutamine MOA

A

activates B1 receptors with some effect on B2 and a1
Increases SV & CO
Modest decrease in TPR

58
Q

Dopamine MOA

A

activates B and a receptors
Low dose -> vasodilation of renal and mesenteric artery beds
High dose -> positive inotropic
Higher dose -> vasoconstriction of arteries

59
Q

Milrinone and Inamrinone MOA

A

increase cAMP -> increase force of contraction in heart, increase velocity of relaxation, vasodilation

60
Q

Positive inotropic drug Clinical Usage

A

IV infusion - severe refractory HF
Alleviate symptoms
Stage D
NOT TO BE USED IN LONG-TERM treatment

61
Q

Pharmacologic agents for ADHF

A

Stage C - loop diuretics (volume overload) & nitroglycerin, nitroprusside, or nesiritide (vasodilators)
Stage D - dobutamine/dopamine or phosphodiesterase inhibitors - milrinone or inamrinone (inotropic agents)

62
Q

Nitroglycerin MOA

A

Forms free radical NO
Activates guanylyl cyclase -> increased cGMP levels -> dephosphorylation of myosin light chains -> smooth muscle relaxation
Prominent effect in veins & decreases preload

63
Q

Nitroglycerin Contraindication

A

Inferior ST-elevated MI

64
Q

Nesiritide MOA

A

recombinant human BNP
binds to guanylyl cyclase and increases cGMP levels in smooth muscle -> dilates arteries and veins
In kidneys causes natriuresis
Induces diuresis

65
Q

Nesiritide Adverse Effects

A

Renal Damage
Hypotension
Headache

66
Q

Vasodilator Clinical Usage

Nitroglycerin, Nesiritide, Nitroprusside

A

IV for acutely decompensated HF
Added to diuretics for pt with severe symptomatic fluid overload but NOT Stage D
Nitroglycerin - relief on angina
Control of HTN complicating HF

67
Q

ACE Inhibitors

A

Captopril
Enalapril
Lisinopril

68
Q

ARBs

A

Losartan

Valsartan

69
Q

Selective beta-1 blockers

A

Metoprolol
Bisoprolol
Atenolol

70
Q

Nonselective beta-blockers

A

Propranolol

71
Q

Beta blocker that blocks beta 1 and 2 and alpha 1

A

Carvedilol

72
Q

Loop diuretics

A

Furosemide
Bumetanide
Ethacrynic acid

73
Q

Thiazide diuretics

A

Hydrochlorothiazide

Chlorthalidone

74
Q

K-sparing diuretics

A

Spironolactone
Eplerenone
Amiloride
Triamterene

75
Q

CCBs

A

Amlodipine
Dilitiazem
Verapamil

76
Q

Loop diuretics MOA

A

Blocks NKCC2 in thick ascending limb (competes Cl-)

Lasts 4-6 hours; after 6 excretion falls d/t volume depletion

77
Q

Loop diuretics clinical usage

A
  • DOC for acute circumstances
  • Edema > resulting from cardiac, renal, or vascular disease that reduce blood flow to kidney
  • HF (prevent or treat fluid retention for stage C and D - most commonly used)
  • Interstitial or pulmonary edema
  • For severe HTN and/or pt with reduced renal fxn
78
Q

Loop diuretics adverse effects

A
  • Fluid and electrolyte loss
  • hypokalemic metabolic alkalosis
  • ototoxicity
  • hyperuricemia
  • hypomagnesemia
  • allergic rxn (except ethacrynic acid)
79
Q

Thiazides MOA

A

Blocks NCC channel in DCT at Cl- site > enhances calcium reabsorption > induces vasodilation

80
Q

Thiazides clinical usage

A
  • HTN first line (low dose > high dose just adds diuretic effect with little effect on BP)
  • HF in combo with furosemide (if needed) for stages C and D
81
Q

Thiazides adverse effects

A
  • Hypokalemic metabolic alkalosis
  • Hyperuricemia
  • hyponatremia
  • hyperglycemia
  • hyperlipidemia
  • hypersensitivity rxn
  • hypercalcemia
82
Q

Spironolactone and eplerenone MOA

A

competitive antagonist at aldosterone receptor

83
Q

Amiloride and triamterene MOA

A

Blocks ENaC channel directly

84
Q

K sparing diuretics clinical usage

A
  • Mineralocorticoid excess or hyperaldosteronism
  • Hypokalemia caused by other diuretics
  • Select pt who have LVEF of 35% or less and are already on ACEI and BB and stage C, NYHA class II-IV
  • recommended for pt w/ moderate-severe symptoms of HF (monitor renal fxn and K)
85
Q

K sparing diuretics adverse effects

A

Hyperkalemia
Tumorigenic - S
Gynecomastia - S

86
Q

ACEI MOA

A

Inhibits conversion of AngI to AngII;

Inhibits inactivation of bradykinin

87
Q

ACEI Clinical Usage

A
  • First line HTN, CVD, CKD
  • Used with diuretics to block RAAS - prevent destruction of bradykinin
  • HF (stage A, pt at risk of artherosclerotic vascular disease, DM, or HTN and associated CV factors)
  • HF - asymptomatic LV systolic dysfunction (stage B, hx of MI, reduced EF)
88
Q

ACEI adverse effects

A
  • hypotension > usually with 1st tx
  • functional renal insufficiency
  • hyperkalemia
  • cough and angioedema
89
Q

ARBs MOA

A

AT1 receptor antagonists

90
Q

ARBs clinical usage

A

Use when ACEI is effective but causes cough

91
Q

ARBs adverse effects

A

-renal insufficiency, hypotension, hyperkalemia, angioedma

92
Q

Aliskiren MOA

A

Inhibit renin

93
Q

Aliskiren clinical usage

A

hypertension

94
Q

Amlodipine MOA

A

Decrease TPR (vasodilator) less cardiac depressant effect d/t reflex tachy

95
Q

Non-dihydropyridines MOA

A
  • Direct effect on SA node

- Decrease contractility> decreased CO

96
Q

Dihydrophyridine clinical usage

A

1st line HTN, CV

Nimodipine > subarachnoid hemorrhage

97
Q

Nondihydropyridine clinical usage

A

Can be given in rate control in pt with a fib or control of angina

98
Q

Dihydropyridine adverse effects

A

Reflex tachy

99
Q

Nondihydropyridine adverse effects

A

Diminish cardiac contractility and slow cardiac conduction, exacerbate HF or pulmonary edema

100
Q

CCB adverse effects

A

constipation (V), flushing, headache, dizziness, peripheral edema

101
Q

metoprolol MOA

A

blocks beta1 receptor > decrease HR; decrease renin> decrease contractility; decrease TPR > decrease CO

102
Q

atenolol MOA

A

ISA > mild peripheral vasodilation w/o reducing CO (partial agonist)

103
Q

BB clinical usage

A
  • HTN with COMPELLING INDICATION
  • Hyperthyroidism
  • asymptomatic LV systolic dysfunction (stage B), hx of MI, reduced EF
104
Q

BB adverse effects

A
  • Heart - exercise fatigue, bradycardia, AV conduction abnormalities
  • Increased airway resistance
  • CNS - depression, fatigue, sexual dysfunction
  • BB withdrawal - accelerated angina, MI, sudden death
  • Lipid metabolism - increased TGs, decrease HDL
  • Glucose intolerance - inhibit glycogenolysis in liver, masks hypoglycemia, inhibit insulin secretion
  • Exacerbation of PVD - unopposed vasoconstriction from blocking B2 activity > primarily non-selective beta antagonist
  • Worsening HF
105
Q

BB contraindications

A

ADHF, symptomatic bradycardia or heart block w/o pacemaker, hx of asthma, symptomatic hypotension, fluid overload

106
Q

Aldosterone antagonist clinical usage

A
  • LVEF 35% or less and are already on ACEI and BB and stage C, NYHA II-IV
  • recommended for pt w/ moderate-severe symptoms of HF
  • monitor renal function and K

Heart 2 (5 decks)

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