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APRN A. Pharm- Test 2 > Week 5 > Flashcards

Week 5 Flashcards

1
Q

what drugs are alpha 2 agonist- central acting

A

Clondine and Methyldopa

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2
Q

What class is clondine

A

Alpha 2 Agonist- Central Acting

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3
Q

What class is methyldopa

A

Alpha 2 Agonist- Central Acting

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4
Q

Route of Clonidine

A

Po/ transdermal patch

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5
Q

route of methyldopa

A

PO

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6
Q

mechanism of action of alpha 2 agonist (clonidine and methyldopa)

A

Activates Alpha2 receptors in medulla of the brain → decreases sympathetic tone (HR / BP)

decreases sympathetic outflow to heart, kidneys and blood vessels

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7
Q

uses for clondine

A

HTN (2nd or 3rd line), ADHD, opioid withdrawal and tourettes

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8
Q

uses of methyldopa

A

FIRST LINE for pregnant moms

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9
Q

contraindication to clonidine

A

MI, renal function impairment, bradycardia, sinus node dysfunction

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10
Q

contraindication to methyldopa

A

MI, hepatic disease, MAOI use

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11
Q

side effects of clonidine

A

cognitive impairment, depression

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12
Q

is clonidine and methyldopa monotherapy

A

NO

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13
Q

labs to check for clonidine and methyldopa

A

liver and kidney function, can cause rebound HTN if stopped abruptly

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14
Q

DDI of methyldopa and clonidine

A

NO BETA BLOCKERs, MAOIs and TCAs

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15
Q

which drugs are selective alpha 1 adrenergic antagonists

A

doxazosin, prazosin, terazosin

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16
Q

what class is doxazosin

A

selective alpha 1 adrenergic antagonists (original sin)

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17
Q

what class is prazosin

A
  • BOLDED* selective alpha 1 adrenergic antagonists
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18
Q

what class is terazosin

A

selective alpha 1 adrenergic antagonists

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19
Q

how do selective alpha 1 adrenergic antagonists work? (prazosin)

A

block postsynaptic alpha1 receptors in vascular smooth muscle and smooth muscle in bladder, neck, and prostate.

Decrease in arterial and venous vasoconstriction

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20
Q

what are Selective Alpha 1 Adrenergic Antagonists used for?

A

HTN and BPH

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21
Q

what is prazosin used for?

A

HTN but NOT BPH, also PTSD

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22
Q

side effects of Selective Alpha 1 Adrenergic Antagonists (prazosin)

A

Syncope
Reflective tachycardia
Orthostatic hypotension
Intraoperative floppy iris syndrome (during cataract surgery)
Parasympathetic symptoms

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23
Q

how is prazosin metabolized?

A

in the liver, but does not cause reflex tachycardia

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24
Q

how to stop taking Selective Alpha 1 Adrenergic Antagonists like prazosin?

A

DO NOT STOP ABRUPTLY

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25
Q

what drugs are nonselective beta blockers

A

PROPANOLOL and nadolol

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26
Q

what does it mean to be a nonselective beta blocker?

A

blocks both beta 1 and 2

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27
Q

what class is propanolol?

A

nonselective beta blocker

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28
Q

what drugs are selective beta blockers?

A

metoprolol and atenolol

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29
Q

how do beta blockers work?

A

B1 blocks receptors at SA node decrease HR & contractility—
slows conduction at AV junction.

B1 blocker: reduces renin release in RAS, lowers BP: Less angiotensin II.

B2 Blocker: inhibits bronchodilation receptors in lungs— causes bronchoconstriction.

Angina: Decrease myocardial o2 demand

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30
Q

what is propanolol used for

A

Angina
HTN: Not first line
Post MI prophy for arrhythmia
Migraine (not acute- needs wean on & Off)
(+Angina w. Hypertrophic subaortic stenosis)

Acts on thyroid prevents conversion of t4-t3

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31
Q

contraindications of propanool

A

AV BLOCK
Peripheral vascular disease

1st gen Caution CHF
Asthma or other resp conditions

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32
Q

difference between metoprolol and propanolol

A

propanolol is nonselective (blocks B1 and B2), metoprolol works more on B1

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33
Q

uses for metoprolol

A

Angina
HTN: Not first line
Post MI prophy for arrhythmia

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34
Q

contraindications of metoprolol

A

AV BLOCK

Asthma: can be considered

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35
Q

side effects of beta blockers

A

Most common:

CV: Brady & Hypotension (Watch for fatigue, drowsiness, weakness), orthostatic.

Caution: DM, Masks symptoms of hypoglycemia & hyperthyroidism

-Abrupt w/d can cause:
thyroid storm, Severe angina, MI, Ventricular arrhythmia,

-CNS: anx, dep, drowsy, nightmare, AMS

-GI: motility ( Anorexia, N/V/D, Constipation,

-Decreased libido= nonadherence to med.

ALL BB WEAN ON & OFF

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36
Q

lab considerations with all betablockers

A

watch all renal and liver labs

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37
Q

what is considered a 3rd generation beta blocker?

A

CARVEDILOL, labetalol

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38
Q

how do 3rd generation betablockers differ from other generations?

A

Selective alpha1 and nonselective beta blockers. Decrease BP and PVR by increasing vasodilation, decreasing myocardial oxygen demand, and CO.

Alpha 1 blockage is predominant (less likely to cause brady or decrease CO and decrease the reflex vasoconstriction).

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39
Q

common uses of carvedilol

A

HTN
Reduce progression of heart failure
Ventricular dysfunction s/p MI
Off-label: cirrhosis, gastroesophageal varices, a-fib, and Nstemi

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40
Q

side effects of 3rd generation betablockers

A

Hypotension, bradycardia, bronchospasm & hypoglycemia (In DM due to masking sx)

It pt has peripheral vascular disease → may cause aggravation of arterial insufficiency.

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41
Q

contraindication of labetalol?

A

bronchospastic disease

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42
Q

considerations of 3rd gen beta blockers (cardivilol and labetalol)

A

Do not stop abruptly in CAD pts → angina exacerbation, MI, v-fib / v-tach.

Caution with bronchospastic disease (but can give)

Less likely for orthostatic hypotension and exercise-induced reflex tachycardia

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43
Q

when is 3rd gen beta blockers preferred?

A

preferred for HTN in pts with severely damaged hearts d/t sympathetic drive

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44
Q

what drugs are ACEIs

A

end in PRIL

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45
Q

what class is lisinopril?

A

ACEI

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46
Q

how do ACEIs work?

A

Angiotensin-converting enzyme (ACE) inhibitors prevent the enzyme ACE from converting angiotensin I into angiotensin II. Angiotensin II is a vasoconstrictor that can cause high blood pressure by narrowing blood vessels and releasing hormones that raise blood pressure. Captopril has the shortest half-life.

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47
Q

common use for lisinopril?

A

HTN, post MI, heart failure

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48
Q

contraindications of ACEIs

A

Bilateral renal artery stenosis, angioedema, pregnancy, hyperkalemia

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49
Q

common side effects of ACEIs

A

Hypotension, dizziness, fatigue, DRY HACKING COUGH, HYPERkalemia

some may cause photosensitivity, rash and neutropenia in high doses

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50
Q

who are ACEIs drug of choice for?

A

younger, white, diabetes, HF and MF

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51
Q

cautions and CIs for ACEIs

A

ANGIOEDEMA** no ACEs to be used again (higher risk in Asian and black populations), prevents remodeling post MI,

adverse reaction usually w/i first few doses

caution with hypovolemia, hyponatremic and hepatic impairment

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52
Q

drug interactions of ACEIs

A

NSAIDs, OTC drugs (cold remedies), lithium , antihypertensives, nitrates, alcohol, phenothiazines

53
Q

what drugs are ARBs (angiotensin receptor blockers?

A

end in SARTAN (losartan), candesartin, olmesartan, telmisaratan, valsartan

54
Q

how do ARBS work?

A

Angiotensin II receptor blockers (ARBs) work by binding to and inhibiting the angiotensin II type 1 receptor (AT1). This inhibits the renin-angiotensin system, which can cause arteriolar contraction and sodium retention

55
Q

what is lorsartan used for?

A

HTN, stroke reduction, diabetic nephropathy

56
Q

caution and contraindications of losartan?

A

Bilateral renal artery stenosis, angioedema, pregnancy, hyperkalemia

57
Q

side effects of losartan

A

Hypotension, dizziness, fatigue, photosensitivity, HYPERkalemia

58
Q

DDI of losartan and ARBs

A

LOWERS INHIBITORS OF CYP450, Antacids, allopurinol, capsaicin, probenecid, rifampin, fluconazole, indomethacin, digoxin, cimetidine, phenobarbital, diuretics

59
Q

why do people switch from ACEI to ARB

A

less likely to be coughing

60
Q

what drug class is digoxin?

A

cardiac glycoside

61
Q

how does digoxin work

A

Inhibit sodium pump
Na and Ca build up in cell
Positive inotropy
High VD in skeletal muscle

62
Q

how is digoxin used?

A

Rate control AFTER BB is ineffective afib/svt
HFrEF < 40% (not first line)

63
Q

contraindications of digoxin

A

Contraindicated in AV block & ventricular arrhythmias (uncontrolled)

64
Q

side effects of digoxin

A

Low therapeutic index
Toxicity, low GFR
Lab levels and patient presentation

“Green halo and yellow vision”

65
Q

how is digoxin metabolized?

A

kidney

66
Q

drug interactions of digoxin

A

MANY- food slows absorption, (amiodarone, dilt, quindine), electrolyte abn, albumin bound

67
Q

What drug is a class 1A anti-arrhythmic

A

dispyramide

68
Q

what is disopyramide used for

A

VT, reduced LVEF

69
Q

what drug is a class 1 B anti-arrhythmic

A

mexilente

70
Q

what is mexilente used for

A

exercise induced VT

71
Q

what drugs are class 1C anti-arrhythmic

A

flecainide and propafenone

72
Q

what are flecainide and propafenone used for?

A

anti-arrhythmic for ppl who dont respond to less toxic drugs, AF/VT and VF

73
Q

what drug is a class 2 anti-arrhythmic

A

propanolol (also beta blocker)

74
Q

what is propanolol used for in the sense of anti-arrhythmic

A

SVT

75
Q

what drugs are class 3 anti-arrhythmic

A

amiodarone, dronedarone and sotalol

76
Q

what is amiodarone used for

A

SVT and VT

77
Q

what is dronedarone used for

A

AF (not long term)

78
Q

what’s sotalol used for

A

beta blocker also used for VT

79
Q

what drugs are class 4 anti-arrhythmic

A

diltiazem and verapamil (also CCB)

80
Q

what are dilt and verapamil used for in sense of anti-arrhythmic

A

rate control, reentry SVT and AF

81
Q

what class is hydralazine

A

acts on NO2

82
Q

what drug acts on NO2

A

hydralazine

83
Q

what drug is a K channel stimulator

A

minoxidil

84
Q

what class is minoxidil

A

K channel stimulator

85
Q

how does hydralazine and minoxidil work?

A

Peripheral vasodilator: direct dilation of arteriolar smooth muscle decreased PVR

Do not dilate Coronaries

Do not relax venous smooth muscle

86
Q

used for hydralazine and minoxidil

A

HTN (not first line) and PVD

87
Q

contraindications of hydralazine and minoxidil

A

caution of CVD, PAH, does not dilate coronary arteries

88
Q

side effects of minoxidil and hydralazine

A

Decreased peripheral and pulmonary vascular resistance

Tachycardia + increased contractility

Water retention
HA
tachyphylaxis

Does not cause orthostatics and ED like most other antihypertensives.

89
Q

which drugs are dihydropyridine CCBs?

A

nifedipine, amlodipine, felodipine

90
Q

how do CCBs work?

A

binding to and blocking the L-type calcium channels in the heart, vascular smooth muscle, and pancreas, preventing calcium from entering the cells.

Calcium is necessary for the muscular linings of blood vessels to contract, and for the heart’s muscle to contract

91
Q

what drugs are non-dihydropyridine CCBs?

A

verapamil and diltiazem

92
Q

what is nifedipine used for

A

Angina, HTN, Raynaud’s

93
Q

what is verapamil used for?

A

HTN, angina and a. Fib rate control, SVT, migraine prophy, antiarrhythmic!

93
Q

what is amlodipine used for

A

HTN, angina

94
Q

what is diltiazem used for?

A

Angina, HTN, esophageal spasm, Antiarrhythmic!

95
Q

what are contraindications of dihyrdopyridine CCBs?

A

(nifidepine, amlodipine)- cause peripheral edema, reflex tachycardia

96
Q

what are contraindications of non-dihydropyridine CCBs?

A

(verapamil and diltiazem)- Avoided in HF, can worsen bradycardia, no WPW syndrome patients

97
Q

side effects of dihydropyridine CCBs

A

Reduction in BP causes dizziness, headache, hypotension, syncope, GI symptoms, hyperglycemia, photosensitivity

98
Q

side effects of non-dihydropyridine (Verapamil)

A

Constipation, Bradycardia, Heart Block

99
Q

side effects of non-dihydropyridine

A

Photosensitivity, Bradycardia, Heart Block

100
Q

what drugs are thiazide diuretics?

A

hydrocholorthiazide, chlorothalidone and metolazone

101
Q

drug interactions of most CCBs

A

CYP3A4 involved in metabolism: GRAPEFRUIT JUICE, additive effect with other hypertensives, watch NSAIDs

102
Q

what class is hydrochlorothiazide?

A

thiazide diuretics

103
Q

what is the mechanism of action of thiazide?

A

Distal renal tubule to inhibit sodium reabsorption (longer lasting and cause less brisk diuresis)

Decreases plasma volume, and CO. (though effects return to baseline, Peripheral vascular resistance remains ([mechanism unknown]).

104
Q

What is hydrochlorothiazide used for?

A

HF, HTN (first line)

105
Q

contraindications of hydrocholorthiazide?

A

hypokalemia, gout/renal calculi and hyperuricemia

106
Q

side effects of hydrochlorothiazide?

A

Electrolyte imbalance, photosensitivity, hypotension, severe hyponatremia, hyperglycemia, GI upset, tinnitus/hearing loss

107
Q

DDI with hydrochlorothiazide

A

drugs that decrease BP, avoid using with ACEi and ARB

108
Q

what drugs are loop diuretics?

A

furosemide and bumetanide

109
Q

how do loop diuretics work?

A

Inhibit Na reabsorption in ascending loop of henle
(short acting and cause large natriuresis)

Decreases plasma volume, and CO. (though effects return to baseline, Peripheral vascular resistance remains ([mechanism unknown]).

110
Q

what is lasix and bumex used for

A

HF and HTN

111
Q

side effects of lasix/bumex

A

Electrolyte imbalance, photosensitivity, hypotension, severe hyponatremia, hyperglycemia, GI upset, tinnitus/hearing loss

112
Q

what drugs are potassium sparing diuretics?

A

spironolactone and amiloride

113
Q

how does spironolactone work?

A

Inhibit excretion of potassium distally

Decreases plasma volume, and CO. (though effects return to baseline, Peripheral vascular resistance remains ([mechanism unknown]).

114
Q

what are all diuretics used for (context of this week)

A

HF, HTN

115
Q

c/i of spironolactone

A

hyperkalemia

116
Q

side effects of spironolactone

A

Gynecomastia (50%)
Electrolyte imbalance (HYPERk)
In pts with gout → hyperuricemia
Hypotension

Occasional GI upset (take meal)

Tinnitus/ hearing loss

117
Q

which drugs cause hyperkalemia

A

ACEi, ARB, renin inhibitors

118
Q

what drug may cause lower extremity edema and constipation

A

amlodipine

119
Q

which beta blocker is known to reduce mortality and HF

A

carvedilol

120
Q

what is most accurate about the mechanism of furosemide when being used to induced diuresis in a patient with edema or fluid overload

A

Antagonizes Na+/K+/2Cl- transporter, which then blocks about 20 to 30% of sodium reabsorption by the nephron

121
Q

what MOA applies to digoxin

A

Inhibits the sodium potassium ATP pump in the cardiac myocyte leading to an increase in the force of contraction

122
Q

Which anti-rhythmic agents should generally be avoided in heart failure because of their inability to prevent cardiac remodeling

A

diltiazem

123
Q

Which ECG abnormalities is most likely to occur in with the use of amiodarone or sotalol, especially in patients with hypokalemia

A

QT prolongation

124
Q

which diuretic agents typically do not need potassium supplementation

A

aldosterone inhibitors

125
Q

when should diuretics be taken?

A

upon awakening

126
Q

how does chronic use of BB treat HTN

A

Reducing peripheral vascular resistance

127
Q

What dermatological issue is linked to amiodarone?

A

Progressive change of skin tone toward a blue spectrum wtf

128
Q

consequences of rapid BB withdrawal

A

angina and coronary artery disease

APRN A. Pharm- Test 2 (3 decks)

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