Exam 3: Drugs for Hypertension and Vascular Tone Flashcards Preview

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Flashcards in Exam 3: Drugs for Hypertension and Vascular Tone Deck (137):
1

HTN tx threshold without DM/renal disease:

140/90

2

HTN tx threshold with DM/renal disease:

130/80

3

First-line tx for HTN:

Thiazide diuretic (without "compelling indication")

4

Best drugs for HTN in pts with heart failure:

Thiazide + β-blocker or ACEI

5

Best drugs for HTN in pts with MI:

β-blocker

6

Best drugs for HTN in pts with high CVD risk:

Thiazide, β-blocker, ACEI, CCB

7

Best drugs for HTN in pts with DM:

Thiazide + ACEI

8

Best drugs for HTN in pts with CKD:

ACEI or ARB

9

Best drugs for HTN in pts with recurrent strokes:

Thiazide + ACEI

10

Best drugs for HTN in pts with isolated systolic HTN:

Thiazide + CCB

11

Define hypertensive urgency:

DBP > 120 with evidence of end organ *damage*

12

Tx for hypertensive urgency:

↓ DBP to 100-105 within 24 hours with clonidine

13

Define hypertensive crisis:

DBP > 120 with evidence of end organ *failure*

14

Tx for hypertensive crisis:

↓ DBP to 100-105 asap using NTG, NTP, labetalol, fenoldapam

15

Effects of angiotensin II:

Vasoconstriction (arterial)
Na+ retention
Thirst/ADH secretion
Aldosterone secretion

16

Effect of aldosterone:

↑ Na+ reabsorption

17

ACEIs are 2nd-line therapy for pts with:

HTN
CHF
Mitral regurg

18

ACEIs are more effective in pts with:

DM

19

ACEIs delay the progression of:

Renal disease

20

AT-1 and AT-2 receptors are:

GPCRs
AT-1 effects > AT-2 effects

21

AT-1 receptor effects:

Vasoconstriction, esp. in glomerular afferent arterioles
↑ norepi release
Proximal tubule reabsorption of Na+
Aldosterone secretion

22

MoA of ACEIs:

Block conversion of angiotensin I to II via interaction with zinc ion

Works on ACE in endothelium

23

Clinical effects of ACEIs:

↓ arterial pressure
↓ cardiac load

24

Indications for ACEIs:

HTN
Cardiac failure
Post-MI
Diabetic neuropathy
CRI

25

Pre-op hold for ACEIs:

One full day pre-op

26

S/E of ACEIs:

Intra-op hypotension**
Granulocytopenia
Angioedema*
Proteinuria
Cough*
Hyperkalemia

27

Contraindications for ACEIs:

Renal artery stenosis

28

Cough/angioedema from ACEIs related to:

Bradykinin

29

Dosage of captopril:

12.5-25mg q8h

30

Onset and half-time of captopril:

Onset: 15 min
E1/2t: 2 hrs

31

Advantages of captopril:

Does not interfere with SNS outflow d/t short E1/2t

32

S/E of captopril:

Rash
Loss of taste
Antagonized by NSAIDs
Hyperkalemia
Angioedema

33

Enalapril vs. captopril:

Enalapril is IV; does not cause rash/renal insufficiency due to lacking sulfhydryl group

34

Elimination of lisinopril:

Administered in active form; excreted unchanged by kidney

35

Onset and duration of effect of enalapril/lisinopril/ramipril:

Enalapril/lisinopril: onset 60-120min, effect 18-30hrs

Ramipril: onset 30-60min, effect 24-60hrs

36

MoA for ARBs:

Competitive binding to AT1 receptors to inhibit action of angiotensin II

37

S/E of ARBs:

Similar to ACEIs but less cough, no bradykinin accumulation

38

Contraindications for ARBs:

Renal artery stenosis
Pregnancy

39

Naming of ARBs:

-sartan

40

Drug class of hydralazine:

Phthalazine derivative

41

MoA of hydralazine:

Activates guanylate cyclase causing vasodilation (primarily arterial)

42

Dosage of hydralazine:

2.5 - 10mg IV

43

Peak, duration and half-time of hydralazine:

Onset: 10-20 minutes
Duration: 6 hr
E1/2t: 3 hrs

44

Elimination of hydralazine:

Extensive first-pass effect
IV: 15% excreted unchanged

45

S/E of hydralazine:

Reflex tachycardia
Tolerance/tachyphylaxis
Na+/H2O retention
Angina w/ EKG changes
Drug-induced lupus-like syndrome

46

Clinical use of hydralazine:

In combination with β-blocker and diuretic to limit SNS activation

47

MoA of minoxidil:

Directly relaxes arteriolar smooth muscle via influx of potassium --> hyperpolarization

48

Indications for minoxidil:

Severe HTN due to renovascular disease, renal failure, transplant rejection

49

Clinical use of minoxidil:

Combined with β-blocker and diuretic

50

PK of minoxidil:

90% oral absorption
Peak: 1 hr
E1/2t: 4 hrs
10% of drug excreted unchanged by kidneys

51

S/E of minoxidil:

↑ HR
↑ renin, norepi
Na+/H2O retention
Pulmonary HTN
Pericardial effusion/tamponade

52

EKG changes with minoxidil:

Flat/inverted T wave
Increased voltage of QRS

53

Indications for peripheral vasodilators:

Facilitate forward flow in AR, MR, HF
Controlled hypotension in OR
Treat hypertensive crisis

54

MoA of sodium nitroprusside:

Interacts with oxyhemoglobin to release NO and cyanide

55

Metabolism of sodium nitroprusside:

Transfer of electron from iron in oxyhemoglobin to SNP yields metHgb + unstable SNP radical with 5 cyanide ions

One cyanide reacts with metHgb to form nontoxic product

Remainder metabolized by liver/kidney to thiocyanate

56

Cyanide toxicity occurs above this rate of sodium nitroprusside:

2 mcg/kg/min over long periods

57

Cyanide toxicity from SNP correlates to:

Lactate levels

58

Tx of cyanide toxicity from sodium nitroprusside:

D/c the SNP infusion
100% O2
Sodium bicarb
Sodium thiosulfate 150 mg/kg over 15 min

59

Tx of severe cyanide toxicity:

Sodium nitrate 5 mg/kg (converts Hgb to metHgb which binds with cyanide)

60

S/s of thiocyanate toxicity:

N/V
Tinnitus
Fatigue
Hyperreflexia
Confusion
Psychosis
Miosis
Seizure
Coma

61

Dosage of sodium nitroprusside:

.3 - 10 mcg/kg/min IV

62

Max dose of sodium nitroprusside:

10 minute infusion

63

Onset/DOA of sodium nitroprusside:

Immediate onset
Short DOA

64

Clinical considerations for use of sodium nitroprusside:

Continues IV dosing
Use A-line!!

65

CV effects of sodium nitroprusside:

Direct venous and arterial dilation
↑ HR from baroreceptor reflex
Intracoronary steal in areas of MI damage!

66

CNS effects of sodium nitroprusside:

↑ CBF
↑ ICP

67

Pulmonary effects of sodium nitroprusside:

Attenuation/blunting of hypoxic vasoconstriction

68

Hemologic effects of sodium nitroprusside:

Increase in GMP inhibits platelet aggregation

69

Clinical uses for sodium nitroprusside:

Controlled hypotension
HTN crisis
Cardiac disease

70

Controlled hypotension dosing of sodium nitroprusside:

0.3 - 0.5mcg/kg/min

71

HTN crisis dosing of sodium nitroprusside:

1-2 mcg/kg IV bolus

72

MoA of nitroglycerin:

Vasodilation via generation of NO (glutathione pathway)

73

Tx of methemoglobinemia:

Methylene blue 1-2mg/kg IV over 5 min

74

Half-time of nitroglycerin:

1.5 minutes

75

CV effects of nitroglycerin:

Venodilation
↓ ventricular EDP
↓ CO
Minimal change in HR
↑ in coronary blood flow to ischemic areas!

76

Tolerance to nitroglycerin is seen after:

24 continuous hours of tx

77

CNS effects of nitroglycerin:

↑ ICP
Headache

78

Pulmonary effects of nitroglycerin:

↓ PVR
Bronchial dilation
Inhibition of pulmonary hypoxic vasoconstriction

79

Coagulation effects of nitroglycerin:

Inhibition of plt aggregation

80

GI effects of nitroglycerin:

Relaxation of GI smooth muscle

81

Benefits of nitroglycerin for angina:

↓ venous return to heart, thus ↓ ventricular EDP

↓ myocardial O2 reqs

82

Benefits of nitroglycerin for cardiac failure:

↓ preload
Relieves pulm edema
Limits MI damage

83

Controlled hypotension dosing and contraindication for nitroglycerin:

4-5 mcg/kg/min IV

Not recommended in cranial surgery pre-dura opening

84

Sphincter of Oddi dosing of nitroglycerin:

200 mcg (1ml) IV bolus

85

PK of isosorbid:

Good oral absorption
Oral DOA: 6 hrs
Sublingual DOA: 2 hrs

86

S/E of isosorbid:

Orthostatic hypotension

87

Active metabolite of isosorbid:

isosorbid-5-mononitrate

88

MoA of trimethaphan:

Ganglionic blocker and peripheral vasodilator

Blocks ANS and venodilates

89

Onset of trimethaphan:

Rapid

90

Dose of trimethaphan:

10-200 mcg/kg/min IV

91

Clinical effects of trimethaphan:

↓ BP, CO, SVR

92

Increased HR from trimethaphan due to:

PSNS blockade, NOT reflex

93

S/E of trimethaphan:

Mydriasis, ↓ GI activity, urinary retention (anticholinergic)

94

Phosphodiesterase inhibitors work by:

Inhibition of breakdown of intracellular cAMP/cGMP, causing vascular smooth muscle relaxation and inotropy

95

Avoid concurrent use of phosphodiesterase inhibitors and:

Nitrates

96

Indications for phosphodiesterase inhibitors:

Heart failure

97

Examples of CCBs:

Verapamil
Diltiazem
Nifedipine

98

MoA of CCBs:

Bind to receptor on voltage-gated Ca2+ channels maintaining them in closed/inactive state

99

CCBs that work on the AV node:

Phenyl-alkyl-amines
Benzothiazepines

100

CCBs that work on the arterial beds:

1,4-dihydropyridines

101

Importance of L-type Ca2+ channel:

Determines vascular tone and cardiac contractility

102

Clinical effects of CCBs:

↓ contractility, HR, SA node activity, conduction across AV node

↓ SVR/BP (due to vascular smooth muscle relaxation)

103

S/E of CCBs:

Cancer
Prolonged bleeding
Cardiac issues
Constipation

104

Inhalational agents + CCBs =

Myocardial depression/vasodilation

105

NMBs + CCBs =

Potentiation of the NMBs

106

Verapamil + β-blockers =

Myocardial depression

107

Verapamil + LA =

Increased risk of LA toxicity

108

Verapamil + dantrolene =

Hyperkalemia and potential cardiac collapse

109

Digoxin + CCBs =

Decreased clearance of digoxin

110

H2 blockers + CCBs =

Potentially increased plasma levels of CCBs due to altered hepatic enzyme activity

111

Tx of CCB toxicity:

IV administration of calcium or dopamine

112

Vascular indications for CCBs:

Systemic HTN
Pulmonary HTN
Cerebral arterial spasm
Raynaud's
Migraine

113

Non-vascular indications for CCBs:

Bronchial asthma
Esophageal spasms
Dysmenorrhea
Premature labor

114

Structure of verapamil:

Levoisomer specific for slow Ca2+ channel

115

Site of action of verapamil:

AV node

116

Clinical effects of verapamil:

Depresses AV node
Negative chronotropic effect on SA node
Negative inotropic effect on myocardium
Vasodilation of coronary and systemic arteries

117

Indications for verapamil:

SVT
Vasospastic angina
HTN
Hypertrophic cardiomyopathy
Maternal/fetal tachydysrhythmias
Premature labor

118

PK of verapamil:

Highly protein bound
Extensive first pass effect
Peak: 30-45 minute (oral) 15 min (IV)
E1/2t: 6-12 hrs

119

Site of action for nifedipine:

Peripheral arterioles

120

Verapamil vs. nifedipine:

Nifedipine has greater coronary/peripheral vasodilator effect

121

SA/AV node effects of nifedipine:

Little to no effect

122

Indications for nifedipine:

Angina

123

PK of nifedipine:

90% protein bound
Hepatic metabolism
Excreted in urine
Effect: 20 min (oral)
Peak: 60-90 min (oral)
E1/2t: 3-7 hrs

124

S/E of nifedipine:

Vertigo
Headache
Flushing
Hypotension
Parasthesias
Muscle weakness
Renal dysfunction

125

Abrupt d/c of nifedipine can cause:

Coronary vasospasm

126

Class of drug of diltiazem:

Benzothiazepine derivative

127

Site of action of diltiazem:

AV node

128

Potency of diltiazem:

Between verapamil and nifedipine

129

Clinical uses of diltiazem:

Same as verapamil

130

Dosage of diltiazem:

0.25 - 0.35 mg/kg over 2 min; can repeat in 15 min

IV infusion: 10 mg/hr

131

PK of diltiazem:

70-80% protein bound
Excreted in bile and urine
Onset: 15 min (oral)
Peak: 30 min
E1/2t: 4-6 hrs

132

Indications for centrally acting agents:

HTN
Sedation
↓ anesthesia reqs
Improve peri-op hemodynamics
Analgesia

133

MoA of clonidine:

BP ↓ from ↓ HR, SVR

134

Abrupt cessation of clonidine causes:

Rebound HTN

135

S/E of clonidine:

Bradycardia
Sedation
Xerostomia
Impaired concentration
Nightmares
Depression
Vertigo
EPS
Lactation (men)

136

PK of clonidine:

50/50 hepatic metabolism, renal excretion

137

Withdrawal syndrome from clonidine:

Occurs with doses > 1.2mg/day
18 hrs after acute D/D
Lasts 24-72 hrs
Tx: rectal/transdermal clonidine