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Pharm Flashcards

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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
Labetalol ratio of beta:alpha
3:1 beta to alpha antagonism
26
Carvedilol ratio of beta:alpha
1:1
27
Labetalol clinical usage
-HTN urgencies/emergencies
28
Carvedilol clinical usage
- 2nd line for chronic HTN (inferior to ACEI/ARB/CCB) | - HTN urgency
29
Labetalol MOA
-inhibits alpha 1, beta 2 (vasodilation) beta 1 (little effect on HR and CO)
30
Labetalol adverse effects
Bronchospasm, can prolong or enhance hypoglycemia, HF, orthostatic hypotension, sexual dysfunction
31
Where are alpha 1 receptors?
Arterial smooth muscle, venous smooth muscle, trigone, prostatic smooth muscle
32
Zosin MOA
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)
33
End result of alpha-1 antagonists
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
34
Zosin clinical usages
-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)
35
Zosin adverse effects
Orthostatic hypotension (severe with syncope> "first dose" effect; little with long-term) >> take @ bed - Reflex tachy - Headache, weakness, dizziness - Edema (Na and H2O retention)
36
Phenoxybenzamine and phentolamine use
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)
37
Phenoxybenzamine and phentolamine adverse effects
- Orthostatic hypotension - Nasal stuffiness - Tachy (arrhythmias) - inhibited ejaculation - fatigue - sedation - nausea
38
Cardiac Glycosides
Digoxin
39
Digoxin MOA
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
40
Digoxin Clinical Usage
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
41
Digoxin Adverse effects
``` 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 ```
42
Digibind
digoxin antidote fab fragment of digoxin specific antibody Use in life threatening cases of digoxin toxicity
43
Vasodilator Drugs
Isosorbide Dinitrate | Hydralazine
44
Isosorbide Dinitrate MOA
venous dilator -> reduces preload | stimulates intracellular cGMP, relaxes arterial and venous smooth muscle
45
Hydralazine MOA
arterial dilator -> reduce afterload | Help increase forward CO
46
Isosorbide Dinitrate & Hydralazine Clinical Usage
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
Ivabradine MOA
reduces cardiac rate through blockade of the If current
48
Ivabradine Clinical Usage
``` 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
Ivabradine Adverse Effects
Bradycardia HTN Afib
50
Ivabradine Contraindications
acute decompensated HF BP< 90/50 AV block or bradycardia severe hepatic impairment
51
Sacubitril/Valsartan MOA
Sacubitril -> inhibits neprilysin (enzymes that degrades natriuretic peptides) Valsartan -> ARB Oral administration
52
Sacubitril/Valsartan Clinical Usage
``` HF NYHA class II-IV , Stage C and reduced ejection fraction ```
53
Sacubitril/Valsartan Adverse Effects
Hypotension | Hyperkalemia
54
Sacubitril/Valsartan Contraindications
Pregnancy - BBW
55
Positive Inotropic
Dobutamine Dopamine Inamrinone Milrinone
56
Acute Decompensation (vasodilators)
Nitroglycerin Nitroprusside Nesiritide
57
Dobutamine MOA
activates B1 receptors with some effect on B2 and a1 Increases SV & CO Modest decrease in TPR
58
Dopamine MOA
activates B and a receptors Low dose -> vasodilation of renal and mesenteric artery beds High dose -> positive inotropic Higher dose -> vasoconstriction of arteries
59
Milrinone and Inamrinone MOA
increase cAMP -> increase force of contraction in heart, increase velocity of relaxation, vasodilation
60
Positive inotropic drug Clinical Usage
IV infusion - severe refractory HF Alleviate symptoms Stage D NOT TO BE USED IN LONG-TERM treatment
61
Pharmacologic agents for ADHF
Stage C - loop diuretics (volume overload) & nitroglycerin, nitroprusside, or nesiritide (vasodilators) Stage D - dobutamine/dopamine or phosphodiesterase inhibitors - milrinone or inamrinone (inotropic agents)
62
Nitroglycerin MOA
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
Nitroglycerin Contraindication
Inferior ST-elevated MI
64
Nesiritide MOA
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
Nesiritide Adverse Effects
Renal Damage Hypotension Headache
66
Vasodilator Clinical Usage | Nitroglycerin, Nesiritide, Nitroprusside
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
ACE Inhibitors
Captopril Enalapril Lisinopril
68
ARBs
Losartan | Valsartan
69
Selective beta-1 blockers
Metoprolol Bisoprolol Atenolol
70
Nonselective beta-blockers
Propranolol
71
Beta blocker that blocks beta 1 and 2 and alpha 1
Carvedilol
72
Loop diuretics
Furosemide Bumetanide Ethacrynic acid
73
Thiazide diuretics
Hydrochlorothiazide | Chlorthalidone
74
K-sparing diuretics
Spironolactone Eplerenone Amiloride Triamterene
75
CCBs
Amlodipine Dilitiazem Verapamil
76
Loop diuretics MOA
Blocks NKCC2 in thick ascending limb (competes Cl-) | Lasts 4-6 hours; after 6 excretion falls d/t volume depletion
77
Loop diuretics clinical usage
- 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
Loop diuretics adverse effects
- Fluid and electrolyte loss - hypokalemic metabolic alkalosis - ototoxicity - hyperuricemia - hypomagnesemia - allergic rxn (except ethacrynic acid)
79
Thiazides MOA
Blocks NCC channel in DCT at Cl- site > enhances calcium reabsorption > induces vasodilation
80
Thiazides clinical usage
- 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
Thiazides adverse effects
- Hypokalemic metabolic alkalosis - Hyperuricemia - hyponatremia - hyperglycemia - hyperlipidemia - hypersensitivity rxn - hypercalcemia
82
Spironolactone and eplerenone MOA
competitive antagonist at aldosterone receptor
83
Amiloride and triamterene MOA
Blocks ENaC channel directly
84
K sparing diuretics clinical usage
- 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
K sparing diuretics adverse effects
Hyperkalemia Tumorigenic - S Gynecomastia - S
86
ACEI MOA
Inhibits conversion of AngI to AngII; | Inhibits inactivation of bradykinin
87
ACEI Clinical Usage
- 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
ACEI adverse effects
- hypotension > usually with 1st tx - functional renal insufficiency - hyperkalemia - cough and angioedema
89
ARBs MOA
AT1 receptor antagonists
90
ARBs clinical usage
Use when ACEI is effective but causes cough
91
ARBs adverse effects
-renal insufficiency, hypotension, hyperkalemia, angioedma
92
Aliskiren MOA
Inhibit renin
93
Aliskiren clinical usage
hypertension
94
Amlodipine MOA
Decrease TPR (vasodilator) less cardiac depressant effect d/t reflex tachy
95
Non-dihydropyridines MOA
- Direct effect on SA node | - Decrease contractility> decreased CO
96
Dihydrophyridine clinical usage
1st line HTN, CV | Nimodipine > subarachnoid hemorrhage
97
Nondihydropyridine clinical usage
Can be given in rate control in pt with a fib or control of angina
98
Dihydropyridine adverse effects
Reflex tachy
99
Nondihydropyridine adverse effects
Diminish cardiac contractility and slow cardiac conduction, exacerbate HF or pulmonary edema
100
CCB adverse effects
constipation (V), flushing, headache, dizziness, peripheral edema
101
metoprolol MOA
blocks beta1 receptor > decrease HR; decrease renin> decrease contractility; decrease TPR > decrease CO
102
atenolol MOA
ISA > mild peripheral vasodilation w/o reducing CO (partial agonist)
103
BB clinical usage
- HTN with COMPELLING INDICATION - Hyperthyroidism - asymptomatic LV systolic dysfunction (stage B), hx of MI, reduced EF
104
BB adverse effects
- 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
BB contraindications
ADHF, symptomatic bradycardia or heart block w/o pacemaker, hx of asthma, symptomatic hypotension, fluid overload
106
Aldosterone antagonist clinical usage
- 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

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