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Pharm > Antihypertensives & Diuretics > Flashcards

Antihypertensives & Diuretics Flashcards

1
Q

BP =

A

CO x SVR

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2
Q

List the factors that contribute to blood pressure:

A
  • contraction of heart ventricles
  • SVR
  • elasticity of arterial wall
  • blood volume
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3
Q

Secondary causes of HTN:

A
  • CKD
  • Cushing’s
  • Untreated OSA
  • Obesity
  • Pheochromocytoma
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4
Q

Drugs that can cause HTN:

A
  • Na+ and H2O retention
  • steroids
  • NSAIDs
  • sympathomimetics
  • MAOIs
  • acute withdrawal from Clonidine
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5
Q

Where are baroreceptors located and where do they form the vagus nerve?

A
  • located in carotid sinus (off the ICA just above split from common carotid)
  • located in aortic arch (where they join up to form the vagus nerve)
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6
Q

Describe the cascade of events when BP drops:

A
  • baroreceptors send signals to adrenal medulla
  • catecholamines released
  • sympathetic activity increased/activate A & B receptors
  • B1: increase HR and SV –> increase CO and BP
  • A1: vasoconstriction
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7
Q

Sympatholytics =

A

adrenergic antagonists

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8
Q

Describe the actions of sympatholytics:

A
  • inhibit activity of SNS (mediated by Epi and NE)
  • bind to adrenergic receptors of smooth muscle - vasodilation and decreased SVR
  • alpha-blockers and beta-blockers
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9
Q

MOA of Phenoxybenzamine:

A
  • irreversible
  • non-competitive
  • non-selective adrenergic antagonist
  • changes shape of receptor so it cannot bind to catecholamines
  • takes 24 hours to synthesize new receptors
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10
Q

What condition is Phenoxybenzamine used to treat? When should it be started?

A
  • Pheochromocytoma
  • started 7-10 days before operation d/t slow onset
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11
Q

SE of Phenoxybenzamine:

A
  • HTN
  • tachycardia
  • arrhythmias
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12
Q

MOA of Phentolamine:

A
  • reversible
  • competitive adrenergic antagonist
  • lasts 4 hours (fast)
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13
Q

What conditions is Phentolamine used to treat?

A
  • Pheochromocytoma
  • Extravasation of an A-receptor agonist (NE)
  • ED
  • HTN crisis
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14
Q

Non-selective adrenergic antagonists block A1 receptors (good), but also A2. What happens when A2 receptors are blocked?

A
  • NE acts on A2 receptors to inhibit its own release
  • blocking A2 causes an increase in NE
  • NE can stimulate B1 receptors
  • HTN and tachycardia
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15
Q

MOA of selective A1 antagonists:

A
  • selectively and reversibly block A1 receptors in vascular smooth muscle
  • reduced PVR & BP
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16
Q

SE of A1 antagonists:

A

hypotension
tachycardia
(baroreceptor reflex)

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17
Q

Name the selective A1 antagonists:

A

“-osin”
Prazosin
Terazosin
Doxazosin
Alfuzosin
Silodosin
Tamsulosin

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18
Q

Alfuzosin/Silodosin/Tamsulosin used to treat:
Side effects:

A
  • treat: enlarged prostate
  • SE = orthostatic hypotension, HA, nasal congestion
    (reflex tachycardia less likely)
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19
Q

Name a selective A2 antagonist:
What is it used for?

A

Yohimbine

  • dietary supps for ED
  • reverse sedation in vet med
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20
Q

Where are B1 receptors located and what does stimulation of them do?

A
  • heart: increase HR and contractility
  • kidney: stimulate juxtaglomerular cells to release renin
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21
Q

Where are B2 receptors located and what does simulation of them do?

A
  • smooth muscle
  • lungs: bronchodilation
  • GI: decreases motility
  • eye: maintains shape
  • liver: promotes glucagon release
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22
Q

Describe the first generation BB MOA and effects:

A
  • non-selective
  • mostly act on B1 receptors in heart
  • decrease HR, delay AV node conduction, reduce contractility
  • decrease CO and O2 demand of the heart
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23
Q

What are the first gen BB?

A

Propranolol
Pindolol
Nodolol
Timolol
Sotalol

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24
Q

Which BB is lipid soluble? What is it used for?

A
  • Propranolol
  • can penetrate the CNS and is used for migraine prophylaxis
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25
Q

What BB is used to treat glaucoma?

A
  • Timolol
  • when applied topically, decreases intraocular pressure
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26
Q

First gen/non-selective BB should be avoided in which patient populations?

A

COPD & asthma d/t chance for bronchoconstriction

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27
Q

What makes 2nd gen BB different?

A
  • selective for B1 receptors
  • more suitable for chronic lung patients
  • “cardio-selective” BB
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28
Q

List the 2nd gen BB:

A

Atenolol
Acebutolol
Bisoprolol
Esmolol
Metoprolol

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29
Q

What makes 3rd gen BB different?

A
  • includes both non-selective & selective BB
  • non-selective: block both B1, B2 and A1
  • produce peripheral vasodilation
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30
Q

Carvedilol and Labetalol fall under which generation of BB?

A

3rd gen
non-selective/selective BB

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31
Q

What effect do 3rd gen BB have on the kidneys?

A
  • inhibit B1 receptors on kidneys
  • suppress renin release
  • suppress formation of angiotensin II
  • suppress secretion of aldosterone
  • cause decrease in SVR & BP
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32
Q

What is the 3rd gen selective BB? What does it do?

A
  • Nebivolol
  • produces vasodilation by introducing NO from endothelial cells to relax smooth muscle
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33
Q

Two BB have intrinsic sympathomimetic activity. What are they and how does this occur?

A
  • Pindolol & Acebutolol
  • block but also weakly stimulate B1 and B2 receptors
  • diminished effect on HR and CO
  • nice for pts with preexisting heart block/bradycardia
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34
Q

Which BB depends on kidneys as primary route of elimination?

A

Atenolol

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35
Q

Which BB is metabolized by RBC esterase?

A

Esmolol

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36
Q

SE of BB:

A
  • bradycardia
  • hypotension
  • fatigue
  • cold hands and feet
  • dry mouth/skin/eyes
  • HA
  • GI upset
  • diarrhea or constipation
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37
Q

MOA of CCB:

A

work on voltage-gated ion channels to block inward movement of Ca2+ across myocardial and vascular smooth muscle to cause arterial vasodilation

38
Q

Effects of CCB:

A
  • decrease myocardial contractility
  • decrease myocardial O2 requirements
  • decrease arteriole tone and SCR
  • decrease LV stress
  • reduce or block impulse generation in the SA node & conduction in the AV node
39
Q

Clinical uses of CCB:

A
  • HTN
  • SVT
  • prevent cerebral vasospasm
  • decrease CP
40
Q

MOA of dihydropyridines:

A
  • selectively inhibit L-type Ca2+ channels in vascular smooth muscle
  • cause vasodilation & decreased SVR
41
Q

List the dihydropyridines:

A

Nifedipine
Nicardipine
Nimodipine
Clevidipine

42
Q

Nifedipine is used for…

A
  • tx of angina
  • no direct depression of SA or AV node
  • SE: flushing, vertigo, HA
43
Q

Nicardipine is used for…

A
  • tx of angina and HTN
  • no direct depression of SA or AV node
44
Q

Which drug has the greatest vasodilating effect of all CCB?

A

Nicardipine

45
Q

Which CCB crosses the BBB?

A

Nimodipine

46
Q

How is Clevidipine metabolized?

A

plasma esterase
(elimination half-time = 1 min)

47
Q

What 3 drugs is Clevidipine incompatible with?

A

Hydromorphone
Epi
Milrinone

48
Q

MOA of nondihydropyridines:

A
  • non-selective inhibitors of L-type Ca2+ channels
49
Q

Name the 2 dihydropyridines:

A

Diltiazem
Verapamil

50
Q

SE of nondihydropyridines:

A

excessive bradycardia
cardiac conduction abnormalities

51
Q

Which nondihydropyridine is more effective at decreasing contractility?

A

Verapamil > Diltiazem

52
Q

SE of nondihydropyridines:

A
  • hypotension
  • bradycardia
  • AV block
  • HA
  • abdominal discomfort
  • peripheral edema
53
Q

MOA and effects of ACE inhibitors:

A
  • inhibit conversion of angiotensin I to angiotensin II in the lungs
  • cause relaxation of BV, decrease in blood volume, decrease BP, and decrease heart O2 demand
54
Q

Brief overview of the RAAS:

A
  • renin released from juxtaglomerular cells of afferent arteriole
  • renin converts angiotensinogen to angiotensin I
  • angiotensin I is converted to angiotensin II by angio converting enzymes in the lung
  • angio II promotes vasoconstriction and aldosterone release
55
Q

Which ACE inhibitor should not be used in renal patients?

A

Captopril
(all ACE inhibitors are eliminated by kidneys)

56
Q

What is important to note about Lisinopril?

A

limit salt substitutes or K+ supps d/t r/f hyperkalemia

57
Q

SE of ACE inhibitors:

A
  • hypotension
  • COUGH
  • hyperkalemia
  • HA/dizziness
  • renal impairment
58
Q

ACE inhibitors are contraindicated in which patient populations?

A
  • renal artery stenosis
  • insulin-dependent DM
  • hyperkalemia
  • pregnancy
59
Q

MOA of ARBs:

A

interfere with binding of ATII with its receptor –> inhibition of ATII mediated vasoconstriction by inhibiting aldosterone

60
Q

Important SE of Losartan:

A
  • hyperkalemia (d/t increasing aldosterone)
  • increases lithium reabsorption by kidneys
61
Q

What are the centrally acting adrenergic drugs?

A

Clonidine
Methyldopa

62
Q

MOA of centrally acting adrenergic drugs:

A

selective stimulate pre-synaptic A2 receptors –> provide negative feedback to reduce catecholamine production/release

63
Q

What is Clonidine used to treat?

A
  • HTN
  • ADHD
  • anxiety
  • ETOH withdrawal
64
Q

Why should you not abruptly stop Clonidine?

A

withdrawal after long term use can be associated with HTN crisis d/t increased sympathetic activity

65
Q

Methyldopa needs WHAT to be effective?

A

converted to its active metabolite (methylnorepinephrine)

66
Q

What is the site of action of carbonic anhydrase inhibitors?

A

proximal tubule

67
Q

MOA of carbonic anhydrase inhbitors:

A
  • block sodium bicarbonate reabsorption
  • cause sodium bicarb diuresis
68
Q

SE of carbonic anhydrase inhibitors:

A
  • hyperchloremic metabolic acidosis
  • renal stones
  • renal K+ wasting
69
Q

Clinical indications for carbonic anhydrase inhibitor use:

A
  • urinary alkalization
  • metabolic alkalosis
  • glaucoma
70
Q

Clinical indications for osmotic diuresis use:

A
  • increase urine volume
  • reduce ICP or IOP
71
Q

Classification and effects of Mannitol:

A
  • osmotic diuretic
  • extracts water from intracellular compartment
72
Q

SE of Mannitol:

A
  • CHF complications
  • pulmonary edema
  • HA
  • N/V
  • dehydration
  • hypernatremia
73
Q

Where do osmotic diuretics work in the kidney?

A

proximal tubule and descending loop of Henle

74
Q

Loop diuretic site of action:

A

ascending loop of Henle

75
Q

Loop diuretic MOA:

A

selectively inhibits Na+, K+, and Cl- reabsorption through competition for the Cl- binding site

76
Q

Clinical indications for loop diuretic use:

A
  • pulmonary edema/edema in general
  • acute hypercalcemia
  • enhance K+ excretion in renal failure
77
Q

Toxicity effects of loop diuretics:

A
  • hypokalemic metabolic alkalosis
  • ototoxicity
  • hyperuricemia
78
Q

What drug class is Bumtanide?

A

loop diuretic
(40x more potent than Lasix)

79
Q

MOA of thiazide diuretics:

A
  • inhibit reabsorption of Na+ and Cl- from distal tubule
  • enhance Ca2+ reabsorption in distal convoluted tubule
80
Q

Site of action of thiazide diuretics:

A

distal tubule and distal convoluted tubule

81
Q

Clinical indications for thiazide diuretics:

A
  • HTN
  • CHF
  • nephrolithiasis
  • nephrogenic diabetes insipidus
82
Q

Adverse effects of thiazide diuretics:

A

*hyponatremia
- hypokalemia metabolic alkalosis
- impaired carb tolerance (hyperglycemia, hyperlipidemia)

83
Q

Contraindications to thiazide diuretic use:

A
  • hepatic cirrhosis
  • borderline renal failure
  • CHF
84
Q

Thiazide diuretics share cross sensitivity with which drug class?

A

sulfonamides

85
Q

2 examples of thiazide diuretics:

A
  • hydrocholorothiazide
  • cholorothiazide
86
Q

Where is the only site in the nephron that membrane water permeability can be regulated?

A

collecting tubule
*site of mineral corticoid effects

87
Q

Site of action of K+ sparing diuretics:

A

cortical collecting tubule and late distal tubule

88
Q

MOA of K+ sparing diuretics:

A
  • antagonize effects of aldosterone
  • reduce Na+ in collecting ducts and tubules
89
Q

Which class of diuretics is used for mineral corticoid management?

A

K+ sparing

90
Q

Toxicity risks of K+ sparing diuretics:

A
  • hyperkalemia
  • hyperchloremic metabolic acidosis
  • acute renal failure
  • kidney stones
91
Q

Describe Spirinolactone:

A

(K+ sparing diuretic)
synthetic steroid that acts as a single diuresis for ascites & liver failure

Pharm (19 decks)

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