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KC Cardio Module-1 > In depth HTN pharm > Flashcards

In depth HTN pharm Flashcards

1
Q

Thiazide Diuretics- 4

A

Hydrochlorothiazide/HCTZ (Hydrodiuril)
Chlorthalidone (Diuril)
Indapamide (Lozol)
Metolazone (Zaroxolyn)

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2
Q

Thiazide AE’s:

A
  • Electrolyte abnormalities: hyponatremia, hypokalemia, hypomagnesemia, hypercalcemia, contraction alkalosis
  • Gout, hyperuricemia
  • Hyperglycemia, worsening DM
  • Hypovolemia (overdiuresis)
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3
Q

Thiazide Dosing?

A

AM dosing

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4
Q

Thiazide MOA:

A

increasing renal excretion of sodium and may have some vasodilator effects

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5
Q

Diuretics are most effective when combined with:

A

ACEI or ARBs, may be used with CCBs

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6
Q

Clinical outcome benefits (reduction of strokes and major cardiovascular events) have been best established with:

A

chlorthalidone, indapamide, and to a lesser extent with hydrochlorothiazide

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7
Q

clinicians should avoid prescribing thiazides first line in:

A

diabetics

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8
Q

newly started on a thiazide or a thiazide like diuretic or if prescribed a dosage increase should have this lab:

A

electrolyte panel checked within 10-14 days of initiation to evaluate for:
Hypokalemia and Hyponatremia

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9
Q

Benefits of using Clorthalidone:

A

CV events were significantly less common and SBP and LDL cholesterol levels were lower

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10
Q

Loop Diuretics- 3

A

Furosemide (Lasix)
Bumetanide (Bumex)
Torsemide (Demadex)

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11
Q

Loop dosing?

A

AM or afternoon dosing

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12
Q

Loop AE’s:

A

Hyponatremia, hypokalemia, hypomagnesemia, hypocalcemia, hyperuricemia, hyperglycemia, overdiuresis

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13
Q

Higher Loop Doses for:

A

for pts with severely decreased glomerular filtration rate, if the patient is accustomed to med or heart failure

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14
Q

Potassium-Sparing Diuretics- 2

A
  • Triamterene (combo w/ HCTZ is Dyazide or Maxzide)

- Spironalactone (Aldactone)

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15
Q

Potassium-Sparing Diuretics dosing?

A

AM or afternoon dosing

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16
Q

Potassium-Sparing Diuretics AE’s:

A
  • Hyperkalemia especially in combination with an ACE inhibitor, ARB or potassium supplements
  • Avoid in patients with CKD or diabetes
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17
Q

Potassium-Sparing Diuretics often used in conjunction with _______ and increases risk for __________

A

thiazide; hyperkalemia

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18
Q

Aldosterone Antagonists- 2

A

Eplerenone (Inspra)

Spironolactone (Aldactone)

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19
Q

Aldosterone Antagonists AE’s:

A
  • Hyperkalemia especially in combination with ACE I, ARB or potassium supplements
  • Avoid in CKD or DM patients
  • Gynecomastia and impotence (spironolactone > eplerenone)
  • Due to risk of hyperkalemia, eplerenone used cautiously in CrCl < 50 mL/min & T2DM & proteinuria
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20
Q

Angiotensin Converting Enzyme (ACE) inhibitors- 5

A 
Quinapril (Accupril)
Ramipril (Altace)
Benazepril (Lotensin)
Enalapril (Vasotec)*
Lisinopril (Prinivil, Zestril)
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21
Q

ACE-inhibitors tx of choice in patients with:

A

hypertension, chronic kidney disease, and proteinuria

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22
Q

ACE-inhibitors reduce Morbidity and mortality in:

A

HF, recent MI

- Halt or may regress remodeling in LVH

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23
Q

ACE-inhibitors MOA:

A
  • blocking conversion of ang I to ang II (a potent vasoconstrictor) & block activation of RAAS
  • Also inhibits the breakdown of bradykinin, a potent vasodilator
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24
Q

ACE-inhibitors require monitoring:

A

serum K+ & Cr within 2 weeks of initiation or dose increase. Must be stopped if hyperkalemia or increasing serum creatinine

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25
Q

ACE-inhibitors AE’s:

A 
Dry cough: may occur at any time 
20-25% of pts and due to increased bradykinin, more common in women, AA, Asians
Angioedema: more common in blacks
Hyperkalemia: particularly in CKD or DM
C/I in pregnancy
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26
Q

ARB’s- 6

A 
Losartan (Cozaar)		
Candesarten (Atacand)
Valsartan (Diovan)		
Olmesartan (Benicar)	
Telmisartan (Micardis)     
Irbesartan (Avapro)
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27
Q

ACE-I and ARBS are most effective in:

A

whites and Asians and less effective in blacks

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28
Q

ARB’s MOA:

A

stop the vasoconstricting effect of angiotensin II by blocking it’s receptor

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29
Q

ARB’s preferred over ACE’s when:

A

IF insurance coverage available because they cause less cough and have a lower risk of angioedema

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30
Q

ARB’s C/I:

A
  • pregnancy, and need to monitor renal status and potassium when initiating
  • contraindicated with h/o ACEI associated angioedema
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31
Q

ACE/ARB’s used together:

A

Combination therapy reduces proteinuria more than monotherapy but worsens major renal outcomes

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32
Q

Direct Renin Inhibitor- 1

A

Aliskiren (Tekturna)

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33
Q

DRI MOA:

A

Inhibits conversion of angiotensinogen to angiotensin I

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34
Q

DRI efficacy demonstrated in combination with:

A

amlodipine, HCTZ, but not for use with ACEI/ARB

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35
Q

DRI AE’s:

A
  • orthostatic hypotension, hyperkalemia

- Does not block bradykinin breakdown; less cough than ACE Inhibitors

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36
Q

CCB MOA:

A

Inhibit influx of Ca2+ across cardiac and smooth muscle cell membranes resulting in coronary and peripheral vasodilation

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37
Q

DHP MOA:

A

block calcium channels in the vasculature

38
Q

Non-DHP MOA:

A

block cardiac calcium channels primarily

39
Q

DHP-3

A

Amlodipine (Norvasc)
Felodipine (Plendil)
Nifedipine (Procardia, Adalat)

40
Q

Non-DHP-2

A

Diltiazem (Cardizem, Tiazac)

Verapamil ( Calan)

41
Q

DHP MOA:

A

Potent arteriolar vasodilators with no effect on AV nodal conduction

42
Q

non-DHP MOA:

A

Decrease HR by blocking the SA and AV nodes, used to slow Av nodal conduction may treat supraventricular tachyarrhythmias

43
Q

DHP AE’s:

A
  • baroreceptor-mediated reflex tachycardia due to potent vasodilating effects (avoid SA forms)
  • worsens peripheral edema (bc increases vascular permeability; less common w/ DRI adm.)
  • flushing, lightheadedness, dizziness, and HA in 10- 20%
44
Q

non-DHP AE’s:

A
  • bradycardia
  • AV block
  • systolic HF (may cause or worsen edema)
  • concurrent use with BB
45
Q

Verapamil and to a lesser degree diltiazem known to:

A

decrease cardiac contractility and heart rate; should not be used with a BB or in bradyarrhythmias (SSS, 2nd/3rd AVB)

46
Q

SA CCB’s known to:

A

worsen HF and should not be used in patients with decompensation
(Long-acting are safe)

47
Q

Verapamil alone known to cause:

A

constipation

48
Q

CCB overdose:

A
  • seen in pts ingesting 5-10x the standard dose
  • cardiac depression and bradycardia
  • clear mentation, but neuro status can decline rapidly
  • EKG: prolonged PR interval and bradyarrythmias
  • hyperglycemia (inhibition of calcium release)
  • remainder of lytes normal; check tox screen
49
Q

CCB overdose and tx

A
  • IVF resuscitation and atropine for bradycardia
  • GI decontamination (AC)
  • admin. of IV calcium
  • glucagon
  • pressors (norepi)
  • high dose insulin therapy
50
Q

β1 receptors located and stimulation effects?

A
  • heart and kidney

- increases HR, contractility, and renin release

51
Q

β2 receptors located and stimulation effects?

A
  • lungs, liver, pancreas, arteriolar smooth muscle
  • bronchodilation and vasodilation
  • mediate insulin secretion and glycogenolysis
52
Q

BB MOA:

A

block cardiac beta 1 receptors reducing responsiveness to sympathetic activity and may also target beta 2 receptors in the lungs if they are non-cardioselective or if given at high doses

53
Q

BB used cautiously w/:

A

asthma or chronic obstructive pulmonary disease (COPD), regardless of beta-selectivity profile

54
Q

BB not recommended 1st line in tx for:

A

HTN except in the case of a compelling cardiac indication; post-MI, or heart failure (symptomatic or asymptomatic LV dysfxn)

55
Q

BB least effective in this ethnicity:

56
Q

BB have a ADR w/ and are not recommended in what population?

A
  • glucose metabolism, especially when combined with a diuretic
  • block awareness of hypoglycemia
  • not recommended in diabetics (unless compelling indication)
57
Q

Main AE’s w/ BB:

A
  • reduced sexual function, fatigue, and reduced exercise tolerance
  • may also precipitate heart block or bradyarrhythmias
58
Q

Cardioselective BB: 4

A

Bisoprolol (Zebeta)
Metoprolol succinate (Toprol XL)
Metoprolol tartate (Lopressor)
Atenolol (Tenormin)

59
Q

Non-selective: 2

A

Nadolol (Corgard)

Propranolol (Inderal)

60
Q

Non-selective MOA BB:

A

Inhibit β1 and β2 receptors at all doses

61
Q

Cardioselective BB safer in ___________ and more helpful to gain control of ____________

A
  • PAD, DM and COPD

- tachyarrhythmias (atrial fib or sinus tachycardia)

62
Q

Beta blockers must be started:

A
  • started low dose and dose titrated cautiously in LV dysfunction and HFrEF due to their myocardial depressive effects
  • should not be abruptly discontinued if possible, since this may cause rebound HTN, worsening angina or MI. If able, slowly wean dose down over 1-2 weeks
63
Q

BB are NOT recommended in pts:

64
Q

Mixed- 2

A

Carvedilol (Coreg)

Labetolol (Trandate)

65
Q

Mixed AE’s associated w/ more:

A

orthostatic hypotension (lowers standing BP more than supine BP)

66
Q

Mixed MOA:

A

Block β receptors (decrease HR) and α1 receptors (peripheral vasodilation)

67
Q

Mixed reduces mortality in pts w/:

A

systolic HF treated with diuretic and ACE inhibitor

68
Q

Carvedilol (Coreg) MC used in and specifics:

A

BP lowering in patients with HF or DM

- less effect on glucose metabolism

69
Q

Labetolol (Trandate) MC used:

A
  • Oral/IV BP lowering

- Used in pregnancy

70
Q

alpha-1 blockers- 3

A

Prazosin (Minipress)
Terazosin (Hytrin)
Doxazosin (Cardura)

71
Q

alpha-1 blockers MOA:

A
  • blockade of alpha-1 causes peripheral vasodilation and BP lowering
  • blocks alpha-1 receptors on the prostate, allowing for easier urine flow
72
Q

alpha-1 blockers AE’s:

A
  • Orthostatic hypotension
  • 1st dose phenomenon: transient dizziness, faintness, palpitations, syncope within 1 to 3 hours of 1st dose
  • Edema, may give with a diuretic, but monitor for orthostasis
73
Q

alpha-1 blockers caution w/:

A

elderly (greater tendency for orthostasis)

74
Q

alpha-1 blockers dosed at:

75
Q

Central alpha-2 agonists: 2

A

Clonidine (Catapres)

Methyldopa (Aldomet)

76
Q

Central alpha-2 agonists MOA:

A
  • Stimulate α2-adrenergic receptors in the brain: reduces sympathetic outflow from the CNS and increases vagal tone (decrease HR and vasculature tone)
  • Peripheral stimulation of presynaptic α2-receptors: may further reduce sympathetic tone
  • Decreases epinephrine and sympathetic tone
77
Q

one of the safest drugs to use in pregnant HTN:

A

methyldopa (aldomet)

78
Q

this drug directly counteracts the sxs of etoh withdrawal

A

clonidine (catapres)

79
Q

Clonidine dosage benefits and target populations:

A
  • given by patch once weekly (pts w/ compliance issues)
  • safe in renal failure and frequently used in ESRD pts with severe/refractory HTN
  • alcohol withdrawal
80
Q

Central alpha-2 agonists AE’s:

A
  • Sodium/water retention leading to edema
  • Orthostatic hypotension
  • Dizziness
  • Clonidine: rebound HTN and anticholinergic SE (dry mouth, constipation, flushing)
81
Q

Direct Arterial Vasodilators: 2

A

hydralazine (aspresoline)

minoxidil

82
Q

Direct Arterial Vasodilators AE’s:

A
  • Edema (may use with diuretic (loop) in order to minimize)
  • Angina (caution w/ CAD)
  • Reflex tachycardia (may use with BB)
  • Hydralazine is known to cause drug induced lupus
  • Excessive hair growth with minoxidil
83
Q

Direct Arterial Vasodilators MOA:

A

Direct arterial smooth muscle relaxation causes antihypertensive effect (with little/no venous vasodilation)

84
Q

Minoxidil often used for:

A

renal failure pts. w/ difficult HTN

85
Q

Hydralazine often used for:

A

used IV to control BP (HR neutral), combo w/ HF and CKD patients (safe w/ renal failure)

86
Q

Non-selective BB Uses:

A

HTN- migraine prophylaxis, essential tremor, portal HTN, thyrotoxicosis

87
Q

If stopped abruptly, clonidine can lead to:

A

Hypertensive urgency or emergency

87
Q

TZD’s should not be used in:

A

Age>80; hyponatremia; SSRI; gout; urinary incontinence

88
Q

Alpha-1 blockers Uses:

A

Comorbid BPH and HTN

89
Q

Mixed alpha/beta blockers reduce mortality in pts w/:

A

Systolic HF treated w/ diuretic and ACE-I

90
Q

Cardiospecific BB concern with high doses?

A

Loss of B1 selectivity (ask pt about COPD/asthma)

KC Cardio Module-1 (7 decks)

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