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Pharm2: Module 2 > Antihypertensives part 1 > Flashcards

Antihypertensives part 1 Flashcards

1
Q

what is arterial blood pressure directly proportional to

A

Cardiac output and peripheral vascular resistance

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2
Q

what controls cardiac output and peripheral vascular resistance

A

Baroreflexes and Renin-Angiotensin-Aldosterone System (RAAS)

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3
Q

What are the types of Hypertension

A

Primary/essential HTN
Malignant HTN
Resistant HTN
Pulmonary HTN
Pseudo-HTN
White Coat/Office HTN
Isolated Systolic HTN

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4
Q

What is the BP for Stage 2 hypertension

A

140 or higher OR / 90 or higher

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5
Q

what is the BP for Stage 3 hypertension

A

Higher than 180 AND / OR / higher than 120

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6
Q

what are the end-stage complications of uncontrolled HTN

A

Heart Disease
Heart Failure
Stroke
Chronic Kidney Disease

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7
Q

What are the antihypertensive drug categories

A

Diuretic agents
ACE inhibitors
ARBs
Calcium Channel Blockers
Beta-adrenergic Blockers
Alpha-adrenergic Blockers

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8
Q

What are the categories of Diuretics

A

Distal Tubule Diuretics (Thiazides)
Loop Diuretics
Potassium Sparing Diuretics
Carbonic Anhydrase inhibitors
Osmotic Diuretics

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9
Q

What are Thiazides/distal tubule diuretics

A

Hydrochlorothiazide
Chlorthalidone
Metolazone
Indapamide

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10
Q

What is the MOA for Thiazides

A

Blocks reabsorption of Na+ and Cl- in the early segment of the distal convoluted tubule -> increase water retention -> increase urine
*most commonly used

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11
Q

What is the site of action for thiazides

A

*Distal tubule, proximal tubule

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12
Q

What is Hydrochlorothiazide

A

Thiazide diuretic
prototypical drug
ideal starting agent for HTN, chronic edema or idiopathic hypercalciuria
Can also treat CaOx stones and Meniere’s disease

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13
Q

What is the pharmacokinetics of Hydrochlorothiazide

A

oral - onset 2 hours
absorbed rapidly and eliminated unchanged

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14
Q

What are the AE/SE of hydrochlorothiazide

A

Increased toxicity of digitalis or lithium

hypokalemia, hyperuricemia, hyperglycemia, hypotension, hyponatremia, hypercalcemia

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15
Q

When is hydrochlorothiazide contraindicated?

A

in Gout

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16
Q

What drug combinations can cause hypokalemia with hydrochlorothiazide

A

if given with corticosteroids or ACTH

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17
Q

What is the outcome of combining HCTZ with alcohol, barbituates or narcotics

A

orthostatic hypotension

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18
Q

What is Chlorthalidone

A

thiazide - like diuretic
used for HTN, HF, hypercalciuria, diabetes

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19
Q

What are the pharmacokinetics of chlorthalidone

A

oral or IV (IV is rare)
long half-life, low bioavailability
excreted in urine unchanged

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20
Q

What are the SE/AE of Chlorthalidone

A

hyponatremia
hypochloremia
hypotension
hypokalemia

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21
Q

What is Metolazone

A

Thiazide-like diuretic
usually added to a loop diuretic in the tx of edema in HF
10x more potent than HCTZ
*Safe in renal insuff

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22
Q

what are the pharmacokinetics of Metolazone

A

oral admin
excreted in the urine unchanged

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23
Q

What are the SE/AE of Metolazone

A

hyponatremia
hypochloremia
hypotension
hypokalemia

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24
Q

What is Indapamide

A

Thiazide-like diuretic
HTN and Decompensated HF
Not commonly used

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25
Q

What is the pharmacokinetics of Indapamide

A

oral admin
Hepatic Metabolism, excreted in urine and bile

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26
Q

What are the AE/SE of Indapamide

A

hyponatremia
hypochloremia
hypotension
hypokalemia

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27
Q

What are the loop diuretics

A

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

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28
Q

What is the MOA for loop diuretics

A

blocks reabsorption of sodium and chloride in the thick segment of the ascending loop of Henle - prevents passive reabsorption of water

Inhibit chloride reabsorption

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29
Q

What is the site of action for loop diuretics

A

Loop of Henle

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30
Q

What are the primary side effects of loop diuretics

A

Hyponatremia
dehydration
hypotension
hypokalemia
hyperglycemia
dose-dependent ototoxicity
-Caution in pts w sulfa allergy

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31
Q

What are the drug interactions with Furosemide (lasix)

A

Digoxin
K+ sparing diuretics
Lithium
Antihypertensive agents
NSAIDs

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32
Q

What is Furosemide (lasix)

A

Loop-diuretic - Most common
good when needing to move large volumes of fluid
- HF, decompression cirrhosis, acute pulmonary edema
Hypercalcemia
especially useful in severe renal impairment
*thiazide can be added if needed

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33
Q

What are the pharmacokinetics of Furosemide (Lasix)

A

Oral admin
Diuresis begins 60 minutes after admin and lasts 8 hours
hepatic metabolism - renal excretion

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34
Q

What inhibits the effects of furosemide

A

probenecid and indomethacin

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35
Q

what types of drugs have increased toxicity with furosemide

A

ototoxic and nephrotoxic drugs and lithium

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36
Q

What is Bumetanide

A

Loop-diuretic - most potent
used for edema caused by heart failure, chronic renal disease and cirrhosis
hypercalcemia

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37
Q

what is the pharmacokinetics of Bumetanide

A

Oral admin
onset: 30-60 minutes
Duration: 4-6 hours

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38
Q

what can large doses of Bumetanide cause

A

severe myalgias

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39
Q

What is not an AE/SE of Bumetanide

A

no Ototoxicity reported

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40
Q

What are the drug interactions with Bumetanide

A

Digoxin
K+ sparing diuretics
lithium
antihypertensive agents
NSAIDs

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41
Q

What is Torsemide

A

Loop diuretic
used for Edema caused by HF, chronic renal disease and cirrhosis
HTN
Hypercalcemia

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42
Q

What are the pharmacokinetics of Torsemide

A

Oral admin
onset: within 60 minutes
Duration: 6-8 hours

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43
Q

What are SE/AE of Torsemide

A

Headache and dizziness

Hyponatremia
hypochloremia
Dehydration
Hypotension
Hypokalemia
Hypoglycemia
dose-dependent ototoxicity

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44
Q

what are the drug interactions with Torsemide

A

Digoxin
K+ sparing diuretics
Lithium
Antihypertensive agents
NSAIDs

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45
Q

What are K+ Sparing diuretics

A

Amiloride (Midamore)
Spironolactone(aldactone)
Trimterene (Dyrenium)
Eplerenone (Inspra)

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46
Q

what is the MOA for K+ sparing diuretics

A

blocks the action of aldosterone in the distal nephron -> retention of K+ and increase the excretion of Na+
Also blocks androgen receptors-> blocks androgen synthesis

(inhibits potassium secretion and influence sodium excretion- reduced K+ loss in urine)

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47
Q

what is the site of action for K+ sparing diuretics

A

Distal Tubule

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48
Q

What are the primary side effects of K+ sparing diuretics

A

Hyperkalemia
Anuria(trimterene-rare)

49
Q

what is spironolactone

A

aldosterone antagonist, K+ sparing
used for HTN, edema in HF, ascites, cirrhosis, nephrotic syndrome, hyperaldosteronism, ache

most commonly used with a thiazide/loop diuretic to counteract K+ wasting effects

50
Q

What is the pharmacokinetics of Spironolactone

A

Oral admin
Effects are delayed, can take up to 48 hours

51
Q

What are the AE/SE of spironolactone

A

hyperkalemia, Endocrine effects (gynecomastia)

52
Q

What are the interaction with Spironolactone

A

with drugs that raise K+ levels, increase risk for digitalis toxicity

53
Q

What are other conditions that can be treated with Spironolactone

A

anti-androgen effects can treat chronically oily skin, acne, hirsutism

54
Q

Is spironolactone safe during pregnancy

A

NO

55
Q

What is Eplerenone

A

aldosterone antagonist, K+ sparing
used to treat edema in HF, resistant HTN and hyperaldosteronism

56
Q

What are the pharmacokinetics for Eplerenone

A

Oral admin
Metabolized by CYP

57
Q

What are the AE/SE for Eplerenone

A

Hyperkalemia
Less risk for gynecomastia than spironolactone

58
Q

What is Amiloride

A

non-aldosterone antagonists, K+ sparing
3rd or 4th line to tx HTN/HF
may correct metabolic alkalosis caused by other diuretics

59
Q

What is the pharmacokinetics of Amiloride

A

oral admin
more rapid onset than spironolactone

60
Q

What are the SE/AE of amiloride

A

Hyperkalemia
Nausea
Vomitting
leg cramps
dizziness
diabetics may develop glucose intolerance

61
Q

What is Triamterene

A

non-aldoserone antagonists, K+ sparing
HTN/Edema
produces mild diuresis
can be used alone or in combo (thiazide diuretic to treat HTN)

62
Q

What are the pharmacokinetics of Triamterene

A

Oral admin
initial resposne develops within hours

63
Q

what are the SE/AE of triamterene

A

May turn urine blue
causes crystalluria and cast formation and decreased renal blood flow - caution with renal disease
Hyperkalemia, N/V, leg cramps, dizziness

64
Q

what are Carbonic Anhydrase inibitors

A

Acetazolamide (diamox)

65
Q

What is the MOA for Acetazolamide

A

inhibits carbonic anhydrase in the proximal rental tubule -> promoting renal excretion of Na+, K+, bicarboate and water

66
Q

what is the site of action for Acetazolamide

A

Proximal tubule

67
Q

What are the pharamacokinetics of Acetazolamide

A

oral or IV admin
Eliminated renally

68
Q

What are the AE/SE of Acetazolamide

A

metabolic acidosis
renal stones
hyperammonemia in cirrhotic pts
conta in pts with sulfa allergy

69
Q

What is contraindicated with the use of Acetazolamide

A

Sulfa allergy

70
Q

What is Acetazolamide used for

A

cardiac anhydrase inhibitor
chronic open-angle glaucoma and prophylaxis of altitude sickness

71
Q

What are osmotic diuretics

A

Mannitol (resectisol)

72
Q

What is Mannitol

A

osmotic diuretic
maintains urine flow following acute toxic ingestion of substrates capable of producing acute renal failure
reduction of intracranial pressure
glaucoma treatment

73
Q

What is the MOA for Mannitol

A

increase concentration of filtrates in the kidney and blocks reabsorption of water

74
Q

what is the site of actio for Mannitol

A

glomerulus/proximal convoluted tubule

75
Q

what is the pharmacokinetics of Mannitol

A

IV admin
Onset: 30-60 minutes
Duration: 6-8 hours

76
Q

what are the SE/AE of Mannitol

A

HA
Nausea
Dizziness
Polydipsia
Dehydration
Confusion
Chest pain

77
Q

Is mannitol safe in pregnancy

A

YES

78
Q

What is hypercacemia

A

when there is too much calcium within the blood
normal serum calcium levels is ~8-10.5mg/dL

79
Q

What are symptoms of severe hypercalcemia that require treatment

A

Neuomuscular effects: impaired concerntation, confusion, fatigue and muscle weakness
GI effects: nausea, abd pain, anorexia, constipation
Renal effects: polydipsia and polyuria resulting from nephrogenic diabetes insipidus and nephrolithiasis resulting from hypercalcemia
Cardiovascular effects: HTN, vascular calcification, shorted QT interval

80
Q

What is the safest and most effective treatment of hypercalcemic crisis

A

saline rehydration
furosemide (lasix) diuresis

81
Q

What should NOT be used to treat hypercalcemia

A

Thriazide Diuretics
they can exacerbate hypercalemia by increasing tubular calcium resoprtion

82
Q

What is nephrogenic diabetes insipidus

A

body makes enough vasopressin but your kidneys don’t respond to the hormone as they should.
As a result, too much fluid gets flushed out in your urine. Causes include: some medicines, especially those used to treat bipolar disorder link

83
Q

how is nephrogenic diabetes insipidus diagnosed

A

based on uring and blood tests

84
Q

what are the symptoms of nephrogenic diabetes insipidus

A

polyuria and plolydipsia (risk of dehyrdration)

85
Q

What is the treatment of nephrogenic diabetes insipidus

A

directed towards individuals symptoms
ensure proper fluid intake and reduce urine output

HCTZ (inhibits amount of salt absobed by kidneys and reduces water loss)

86
Q

What are renin-angiotensin-aldosterone system (RAAS) agents

A

Common:
ACE inhibitors (ACEi)
Angiotensin receptor blocker (ARBs)
Aldosterone antagonists

Less common:
Renin inhibitor
Endothelin Anatgonist

87
Q

What are ACE inhibitors

A

Enalapril
Captopril
Lisinopril

88
Q

What is suppressed with ACE inhibitors

A

suppressed synthesis of angiotensin II
suppressed aldosterone, resulting in natriuresis
Decreased peripheral vascular resistance

89
Q

What are ACE inhibitors the first line treatment of

A

HTN in pts with high coronary disease risk, diabetes, stroke, heart failure, myocardial infarction or chronic kidney disease

preferred in pts with diabetic nephropathy b/c glucose levels are not affected and drugs are renoprotective

90
Q

What is the MOA for ACE inhibitors

A

inhibits ACE -> reduces levels of angiotensin II -> suppresses aldosterone excretion -> decreases peripheral resistance AND increases sodium and water excretion

91
Q

What is enalapril

A

RAAS - ACE inhibitor
used for treatment of HTN with pts w/ increased CAD risk, DM, stroke, MI, HF, CKD
preferred in pts with diabetic nephropathy

92
Q

what are the pharmacokinetics of Enalapril (Prinivil)

A

oral (prodrug- undergoes hepatic metabolism), IV admin
dose adjust in kidney disease

93
Q

What are the AE/SE of ACE inhibitors

A

First dose hypotension, cough, hyperkalemia, renal failure, angioedema, neutropenia

94
Q

What are the interactions and contraindications for ACE inhibitors

A

Contra in pregnancy
Interactions w diuretics, antihypertensives, drugs that raise K+ levels, lithium, NSAIDs

95
Q

What is Captopril (Capoten)

A

RAAS- ACE inhibitor
Tx of HTN in pts w incr CAD risk, DM, stroke, MI, HF, CKD
-Preferred in pts w diabetic nephropathy

-Not common 1st line agent

96
Q

What is a unlikely SE/AE of captopril

A

infrequently causes agranulocytosis or neutropenia

97
Q

What are the pharmacokinetics of Captopril

A

oral admin, 2-3 times per day
dose adjust in kidney disease

DOES NOT undergo hepatic conversion to active metabolites

98
Q

What is Lisinopril

A

RAAS- ACE inhibitor
used to treat HTN and HF
Preferred in pts w diabetic nephropathy, can cause some lowering of blood sugars

99
Q

What are the pharmacokinetics of ACE inhibitors

A

oral admin - once daily
dose adjust in kidney disease
DOES NOT undergo hepatic conversion to active metabolites

100
Q

What are Angiotensin Receptor Blockers (ARB)

A

Losartan
Valsartan
Candesartan
Olmesartan

101
Q

What is the MOA of ARB medications

A

Blocks angiotensin II receptors in blood vessels, adrenals and other tissues -> dilation of arterioles and veins

102
Q

What is Losartan (Cozaar)

A

RAAS - ARB
used to treat:
HTN
stroke prevention
Diabetic nephropathy
reduces serum uric acid levels

103
Q

What are the pharmacokinetics of Losartan

A

oral, once daily dosing
extensive first-pass hepatic metabolism (converstion to active metabolite)

104
Q

Are ARB medications safe in pregnancy

A

NO

105
Q

What are the AE/SE of ARB medications

A

Angioedema and renal failure
Drug interactions: additive effect w antihypertensive drugs

106
Q

What is Valsartain

A

1st IRB approved for HF
HTN

107
Q

What are the pharmacokinetics of Valsartan

A

oral admin, TWICE daily dosing

108
Q

What is Candesartain

A

RAAS- ARB
used to treat HTN and HF
once daily dosing
inactive metabolites

109
Q

What is Olmesartan

A

RAAS-ARB
used to treat HTN
once daily dosing
inactive metabolites
significant mean blood pressure reduction

110
Q

What are Renin Inhibitors

A

Aliskiren
inhibits renin, acting early in the RAAS

111
Q

what is the MOA for Aliskiren

A

binds tightly with renin and thereby inhibits the cleavage of angiotensinogen into angiotensin I
can influence entire RAAS

112
Q

What are the pharmacokinetics of Alikiren

A

oral admin - metabolized by CPY3A4
bioavailability low, doing wiht high fat meal makes it lower
half-life 24 hours

113
Q

what are the AE/SE of Aliskiren

A

diarrhea, cough, angioedema
Contraindicated in pregnancy

114
Q

What are Endothelin Antagonists

A

Ambrisentan
Bosentan

115
Q

What is the MOA for Ambrisentan

A

selectively blocks type A endothelin receptors

116
Q

What is the MOA for Bosentan

A

Nonselectively blocks endothelin receptors

117
Q

What are the uses for ambrisentan

A

treatment of pulmonary arterial hypertension (PAH)
improve exercise ability, delay clinical worsening of PAH
can be used in combo with tadalafil

118
Q

What are the SE/AE of Ambrisentan

A

edema, nasal congestion, palpitations, abdominal pain, constipation

Pharm2: Module 2 (4 decks)

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