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Board Review > Hypertension > Flashcards

Hypertension Flashcards

1
Q

Diuril

A

Chlorthiazide

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2
Q

Thalitone

A

Chlorthalidone

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3
Q

Microzide (capsule), Oretic, Esidrix

A

Hydrochlorothiazide

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4
Q

Lozol

A

Indapamide

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5
Q

Zaroxolyn

A

Metolazone

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6
Q

Bumex

A

Bumetanide

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7
Q

Demadex

A

Torsemide

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8
Q

Edecrin

A

Etharcrynic Acid

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9
Q

Midamor

A

Amiloride (potassium sparing diuretic)

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10
Q

Dyrenium

A

Triamterene

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11
Q

Maxzide, Dyazide

A

Triamterine + HCTZ

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12
Q

Aldactone

A

Spironolactone

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13
Q

Inspra

A

Eplerenone

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14
Q

Avapro

A

Irbesartan

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15
Q

Benicar

A

Olmesartan

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16
Q

Micardis

A

Telmisartan

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17
Q

Tevetan

A

Eprosartan (ARB)

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18
Q

Edarbi

A

Azilsartan

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19
Q

Univasc

A

Moexipril

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20
Q

Aceon

A

Perindopril

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21
Q

Mavic

A

Trandalopril

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22
Q

Sectral

A

Acebutolol

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23
Q

Tenormin

A

Atenolol

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24
Q

Zebeta

A

Bisoprolol

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25
Q

Bystolic

A

Nebivolol

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26
Q

Cartrol

A

Carteolol

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27
Q

Corgard

A

Nadolol

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28
Q

Visken

A

Pindolol

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29
Q

Blocadren

A

Timolol

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30
Q

Trandate, Normodyne

A

Labetolol

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31
Q

Sular

A

Nisoldipine

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32
Q

DynaCirc CR

A

Isradipine CR

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33
Q

Cardene SR

A

Nicardipine ER

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34
Q

Cleviprex

A

Clevidipine

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35
Q

Duraclon Inj

A

Clonidine

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36
Q

Wytensin

A

Guanabenz (Centrally acting alpha agonist)

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37
Q

Tenex

A

Guafancine

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38
Q

Aldomet

A

Methyldopa

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39
Q

Minipress

A

Prazosin (Alpha blocker)

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40
Q

Hytrin

A

Terazosin

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41
Q

Cardura

A

Doxazosin

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42
Q

Lotrel

A

Amlodipine + Benazapril

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43
Q

Lexxel

A

Enalapril + Felodipine

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44
Q

Tarka

A

Trandalopril + Verapamil

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45
Q

Twynsta

A

Amlodipine + Telmisartan

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46
Q

Exforge

A

Amlodipine + Valsartan

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47
Q

Azor

A

Amlodipine + Olmesartan

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48
Q

Tekamlo

A

Aliskiren + Amlodipine

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49
Q

Tekturna HCT

A

Aliskiren + HCTZ

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50
Q

Amturnide

A

Aliskiren + Amlodipine + HCTZ

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51
Q

Valtruna

A

Aliskiren + Valsartan

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52
Q

Lotensin HCT

A

Benazepril + HCTZ

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53
Q

Capozide

A

Captopril + HCTZ

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54
Q

Vaseretic

A

Enalopril +HCTZ

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55
Q

Prinzide, Zestoretic

A

Lisinopril + HCTZ

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56
Q

Uniretic

A

Moexpril + HCTZ

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57
Q

Accuretic

A

Quinapril + HCTZ

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58
Q

Monopril HCT

A

Fosinopril + HCTZ

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59
Q

Atacand HCT

A

Candesartan + HCTZ

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60
Q

Tevetan HCT

A

Eprosartan + HCTZ

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61
Q

Avalide

A

Irbesartan + HCTZ

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62
Q

Hyzaar

A

Losartan + HCTZ

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63
Q

Micardis HCT

A

Telmisartan + HCTZ

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64
Q

Diovan HCT

A

Valsartan + HCTZ

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65
Q

Benicar HCT

A

Olmesartan + HCTZ

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66
Q

Tenoretic

A

Atenolol + Chlorthalidone

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67
Q

Ziac

A

Bisoprolol + HCTZ

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68
Q

Inderide

A

Propranolol + HCTZ

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69
Q

Lopressor HCT

A

Metoprolol + HCTZ

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70
Q

Corzide

A

Nadolol + Bendroflumethiazide

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71
Q

Timolide

A

Timolol + HCTZ

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72
Q

Aldoril

A

Methyldopa + HCTZ

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73
Q

Diupres

A

Reserpine + Chlorthiazide

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74
Q

Hydropres

A

resperine + HCTZ

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75
Q

Aplresazide

A

Hydralazine + HCTZ

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76
Q

Exforge HCT

A

Amlodipine, Valsartan and HCTZ

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77
Q

Tribenzor

A

Amlodipine, olmesartan and HCTZ

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78
Q

what are sysmptoms of very high blood pressure?

A

head ahce ,throbbing, fatcige and SOB

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79
Q

What are the 5 classes of standard antihypertensive drugs?

A
  1. diuretics, 2. _-adrenoceptor antagonists (_-blockers) 3. Ca-channel blockers 4. inhibitors of angiotensin (ACE-inhibitors/AT1-blockers) 5. _-adrenergic blockers
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80
Q

what are the centrally acting antihypertensive drugs?

A
  1. clonidine, 2. methyldopa 3. reserpine
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81
Q

what are the vasodilators?

A
  1. nitrates, 2. nitroprusside 3. dihydralazine
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82
Q

what is a normal SBP?

A

<120 mmHg

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83
Q

what is a prehypertension SBP?

A

120-139 mmHg

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84
Q

what is a stage 1 hypertension SBP?

A

140-159 mmHg

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85
Q

what is a stage 2 hypertension SBP?

A

>160 mmHg

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86
Q

what is a normal DBP?

A

<80mmHg

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87
Q

what is a prehypertension DBP?

A

80-89

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88
Q

what is a stage 1 hypertension DBP?

A

90-99

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89
Q

what is a stage 2 hypertension DBP?

A

>100

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90
Q

what drugs are indicated for prehypertension without compelling indication?

A

no antihypertensive drug indicated

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91
Q

what is the initial drug therapy for stage 1 hypertension without compelling indication?

A

Thiazide diuretics for most.May consider ACEI, ARB, BB, CCB, or combination.

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92
Q

what is the initial drug therapy for stage 2 hypertension without compelling indication?

A

2 drug combination for most: usually thiazide diuretic and ACEI or ARB or BB or CCB

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93
Q

what is the initial drug therapy for prehypertensive and stage 1 hypertensive patients with compelling indications?

A

drugs for the compelling indications

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94
Q

What is the initial drug therapy for stage 2 hypertensive patients with compelling indications?

A
  1. drugs for the compelling indications 2. other antihypertensive drugs (diuretics, ACEI, BB, CCB) as needed.
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95
Q

What is the relative risk of stroke in hypertensive vs. normotensive patients?

A

7-fold

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96
Q

what is the relative risk of CAD in hyptertensive vs. normotensive patients?

A

2-3 fold

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97
Q

what is the relative risk of heart failure in hypertensive vs. normotensive patients?

A

2-3 fold

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98
Q

what is the relative risk of peripheral vascular disease in hypertensive vs. normotensive patients?

A

2-3 fold

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99
Q

what kind of compound is clonidine?

A

_2-sympathomimetic drug, 2nd choice in treatment of hypertension, with interesting off label uses

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100
Q

what are the relevant pharmacokinetics of clonidine? How excreted, half life

A

p.o.; i.v.; transdermal patch:t1/2 = 8-12h mainly renal excretion

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101
Q

what are the relevant pharmacodynamics of clonidine?

A
  1. centrally mediated hypotensive effects: a. reduction of cardiac output b. relaxation of capacitance vessels c. reduction of peripheral resistance 2. renal blood flow maintained 3. initial hypertensive episode may occur 4. various CNS effects 5. pronounced rebound effect after
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102
Q

what are the adverse effects of clonidine?

A

high doses/predisposition:1. symptomatic bradycardia 2. AV-block 3. functional cardiac failure 4. dry mouth 5. drowsiness 6. sedation 7. constipation 8. mental depression

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103
Q

What is the primary use of clonidine?

A

second line treatment of hypertension

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104
Q

what are the other (empirical) clinical uses of clonidine?

A
  1. symptomatic treatment of withdrawal syndromes (heroin, alcohol, benzodiazepenes) 2. prevention / treatment of alcoholic delirium 3. postmenopausal syndrome 4. refractory diarrhea (short bowel syndrome) 5. adjunct in analgo-sedation (dexmedetomidine)
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105
Q

What type of compound is methyldopa?

A

centrally acting antihypertensive drug

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106
Q

is methyldopa safe for use in pregnancy?

A

yes

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107
Q

what are the relevant pharmacokinetics of methyldopa?

A

p.o.:t1/2= 4-6h, up to 24h including active metabolites

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108
Q

what are the adverse effects of methyldopa?

A

centrally mediated hypotensive effects quite comparable, but not identical to clonidine

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109
Q

what are the important prototypical _1-blockers and their half lives?

A
  1. prazosin (3-4h) 2. terazosin (12h) 3. doxazosin (22h)
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110
Q

what are the relevant pharmacokinetics of the _1-blockers?

A

po or iv

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111
Q

what are the relevant pharmacodynamics of _1-blockers?

A
  1. blockade of _1-receptors in arterioles/venules 2. NO effect on pre-synaptic _2-receptors 3. NO effect on inhibitory feedback for NE release
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112
Q

what are the adverse effects of _1-blockers?

A
  1. first dose phenomenon 2. orthostatic hypotension 3. dizziness 4. palpitations 5. headache 6. tests for ANA may turn positive 7. reflex tachycardia
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113
Q

what are the first choice diuretics in the treatment of hypertension?

A

thiazides like HCTZ

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114
Q

what are the second choice diuretics in the treatment of hypertension?

A

K+ sparing diuretics:amiloride, triamterene spironolactone

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115
Q

what is the choice diuretic for treatment of hypertension in patients with GFR < 30ml/min or refractory hypertension?

A
  1. loop diuretic like furosemide2. thiazide type metolazone
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116
Q

what are the rules for routine use of thiazides?

A
  1. low dose thiazide, may already work at sub-diuretic doses within 2-4 weeks; to be taken in the morning2. if hypokalemia is a problem, combine with K+ sparing diuretic but watch for hyperkalemia with this combination 3. keeping the patient “on dry weight” may be a good thing, BUT, dehydration may cause mental confusion, may aggravate COPD, or peripheral arterial occlusive disease 4. important adverse effects: hypokalemia, impaired glucose tolerance, hyperlipidemia
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117
Q

what are the relevant pharmacokinetics of metolazone?

A
  1. oral bioavailability 65% 2. t1/2 = 8-10h 3. duration of action 12-24 h
118
Q

what are the pharmacodynamic of metolazone similar to?

A

thiazide diuretics like HCTZ

119
Q

what is the difference in the pharmacodynamics of metolazone vs. HCTZ?

A

also effective at GFR <30ml/min

120
Q

what are the uses of metolazone?

A
  1. hypertension (low dose 1.25 - 2.5 - 5mg) also used in combination treatment 2. edema (10-20 mg) 3. can replace other thiazides in combination treatment of furosemide resistance
121
Q

what are the _-adrenoceptor antagonists and their respective selectivities?

A
  1. propanolol (_1 + _2, non selective) 2. atenolol (_1 > _2) 3. metoprolol (_1 > _2) 4. pindolol (partial agonist, ISA) 5. labetalol (4 isomers, _-blocker & _ blocker, _2-agonist) 6. carvedilol (2 isomers, _-blocker, _-blocker) 7. esmolol (_1 > _2, short acting, emergency med)
122
Q

what is the specificity of propanolol?

A

_1 and _2, non-selective

123
Q

what is the specificity of atenolol?

A

_1 > _2

124
Q

what is the specificity of metoprolol?

A

_1 > _2

125
Q

what is the specificity of pindolol?

A

partial agonist, ISA

126
Q

what is ISA?

A

intrinsic sympathomimetic activity

127
Q

what is the specificity of labetalol?

A

4 isomers, _&_-blocker, _2-agonist

128
Q

what is the specificity of carvedilol?

A

2 isomers, _-blocker, _-blocker

129
Q

what is the specificity of esmolol?

A

_1 > _2, short acting, emergency med

130
Q

when does one NEVER prescribe _blockers and why?

A

never use beta-blockers in asthma or COPD because _1-selectivity is relative

131
Q

when are unselective _blockers contraindicated?

A
  1. pregnancy 2. Diabetes Mellitus
132
Q

in what condition is the use of _-blockers tricky?

A

CHF

133
Q

what are some of the many conventional contraindications of _-blockers?

A
  1. asthma 2. COPD 3. PAD 4. SA or AV-node abnormalities
134
Q

what effect do _blockers have on LDL?

A

increase

135
Q

what effect do _blockers have on HDL?

A

decrease

136
Q

what effect do _ blockers have on triglycerides?

A

strong increase

137
Q

what effect do _1blockers have on LDL?

A

decrease

138
Q

what effect do _1-blockers have on HDL?

A

strong increase

139
Q

what effect do alpha 1 blockers have on triglycerides?

A

null

140
Q

how do _1 blockers affect insulin sensitivity?

A

they do not affect insulin sensitivity

141
Q

what changes in cardiac output do _1blockers produce?

A

minimal changes in cardiac output

142
Q

do _1 blockers cause cold extremity syndrome?

A

they do not

143
Q

do _-blockers cause orthostatic hypotension?

A

they do not

144
Q

what are the prototypical calcium channel blockers?

A
  1. verapamil 2. diltiazem 3. nifepidine (and dihydropyridines)
145
Q

what are the relevant pharmacokinetics of calcium channel blockers?

A

p.o.; i.v.: highly bound by serum proteins, hepatic metabolism, renal excretion

146
Q

how are calcium channel blockers eliminated?

A
  1. metabolized in liver 2. excreted by kidney
147
Q

what are the relevant pharmacodynamics of calcium channel blockers?

A
  1. block L-type calcium channels –>cardiodepressant effects 2. arteriolar vasodilation
148
Q

what are the adverse effects of dihydropyridines?

A

due to excessive vasodilation: 1. dizziness 2. headache 3. flushing 4. digital dysaesthesia 5. nausea 6. peripheral edema 7. constipation 8. reflex tachycardia

149
Q

what are the adverse effects of verapamil and diltiazem?

A
  1. bradycardia 2. slow SA and AV conduction 3. increase digoxin levels in the blood
150
Q

how do short acting calcium channel blockers affect risk of myocardial infarction?

A

the use of short acting Ca channel blockers nifedipine, diltiazem, and verapamil was associated with an increased risk of myocardial infarction

151
Q

what is the onset and duration of verapamil, nifedipine, and diltiazem?

A

fast onset short acting

152
Q

what are the 1st generation Ca channel blockers?

A

verapamil SR nifedipine GITS

153
Q

what are the second generation calcium channel blockers?

A
  1. amlodipine 2. felodipine 3. nisoldipine 4. isradipine
154
Q

what are the second generation ca channel blockers which are long acting?

A
  1. amlodipine 2. felodipine 3. nisoldipine
155
Q

what are the slow onset second generation ca channel blockers?

A
  1. amlodipine 2. felodipine
156
Q

What are the 2 types of inhibitors of angiotensin?

A
  1. ACE- inhibitors 2. AT1- Blockers
157
Q

What are the prototypical ACE Inhibitors?

A
  1. captopril 2. enalapril 3. enalaprilat 4. lisinopril 5. benazepril 6. fosinopril 7. moexipril 8. quinapril 9. ramipril
158
Q

what are the ACE inhibitors used for?

A

all used to treat hypertension some also labelled for use in CHF

159
Q

what are the prototypical AT1-blockers?

A
  1. losartan2. valsartan
160
Q

what is losartan used for?

A

labelled for hypertension and CHF

161
Q

what is valsartan used for?

A

hypertension

162
Q

what are the relevant pharmacokinetics of captopril?

A

po: renal elimination

163
Q

what are the relevant pharmacodynamics of captopril?

A

Angiotensin II antagonism: - decrease vasoconstriction - decrease norepinephrine release - decrease aldosterone secretion - Vasodilation Bradykinin related: - no reflex tachycardia - no significant change in cardiac output - no water and sodium retention - some reduction of sympathetic tone

164
Q

how is captopril eliminated?

A

renal elimination

165
Q

what are the effects of captopril on the vasculature?

A

vasodilation, decrease vasoconstriction

166
Q

what are the effects of captopril on the sympathetic nervous system?

A

decrease NE releasesome reduction of sympathetic tone

167
Q

what is the effect of captopril on aldosterone secretion?

A

decrease aldosterone secretion

168
Q

is reflex tachycardia associated with captopril?

A

no

169
Q

is a significant change in cardiac output associated with captopril?

A

no

170
Q

is sodium/water retention associated with captopril?

A

no

171
Q

what are the adverse effects of captopril?

A
  1. hypotension2. dry cough, bronchospasm 3. skin rashes, angioneurotic edema 4. neutropenia, leukopenia 5. taste perversion 6. hyperkalemia 7. proteinuria
172
Q

what conditions are contraindications of captopril?

A
  1. renal artery stenosis 2. renal failure 3. history of angioedema (asthma, COPD) 4. pregnancy (oligohydramnion)
173
Q

what are the signs of captopril toxicity?

A

hypotension without marked tachycardia

174
Q

what are the unwanted interactions associated with captopril?

A
  1. NSAIDs reduce antihypertensive response by inhibition of the bradykinin pathway2. K+ sparing diuretics aggravate hyperkalemia 3. hypersensitivity reactions to other drugs may be aggravated 4. increased plasma levels of digoxin, lithium
175
Q

what are the wanted interactions associated with captopril?

A

K+ wasting diuretics yield over-additive antihypertensive effect

176
Q

elalapril is the prodrug of what?

A

enalaprilat

177
Q

how is enalapril converted into enalaprilat?

A

intrahepatic conversion

178
Q

what are the relevant pharmacokinetics of enalapril?

A

po:tmax=3-4h t1/2=11h renal elimination start with 2-5mg/d up to a maximum 40 mg/d

179
Q

what are the relevant pharmacokinetics of enalaprilat?

A

iv: use in hypertensive emergencies

180
Q

what is the tmax of enalapril?

A

3-4 h

181
Q

what is the t1/2 of enalapril?

A

11h

182
Q

how is enalapril eliminated?

A

renal elimination

183
Q

how is enalapril dosed?

A

start with 2.5-5 mg and increase up to 40mg/d

184
Q

when is enalaprilat used?

A

iv in hypertensive emergencies

185
Q

how do the pharmacodynamics and adverse effects of enalapril compare to captopril?

A

enalapril is: more potent slower onset/longer duration of action compound contains no sulfhydryl group (no taste perversion)

186
Q

what proportion of ACE inhibitors are prodrugs?

A

most are prodrugs

187
Q

what makes fosinopril and moexipril different than all other ACE inhibitors?

A

fosinopril and moexipril are eliminated by the liver and all others are eliminated by the kidneys

188
Q

do ACE inhibitors have variable influence on tissue specific AG subsystems?

A

this remains to be verified

189
Q

what are the indications for ACE inhibitors?

A
  1. hypertension 2. CHF 3. Myocardial Infarction 4. Progressive renal disease (DM nephropathy)
190
Q

what type of drug is losartan?

A

Angiotensin II receptor subtype 1 blocker (AT1 blocker)

191
Q

what are the relevant pharmacokinetics of losartan?

A

po: bioavailability=33% t1/2= 2h active metabolite t1/2= 6-9h hepatic elimination usual dose 50-100 mg/d

192
Q

what are the relevant pharmacodynamics of losartan?

A

Like ACE inhibitors: - decrease vasoconstriction - decrease NE release decrease aldosterone secretion Unlike ACE inhibitors: no effect on bradykinin

193
Q

what are the adverse effects of losartan?

A

Like ACE inhibitors except for bradykinin related AE: no cough - no angioedema

194
Q

what conditions are contraindicated in the use of losartan?

A
  1. renal artery stenosis2. renal failure 3. pregnancy
195
Q

What is the first step in the guidelines for treatment for hypertension?

A
  1. Single drug therapy- THIAZIDE or _BLOCKER… or Ca channel blocker or ACEI or Alpha Blocker
196
Q

what is the second step in the guidelines for the treatment for hypertension?

A
  1. Combination Therapy- a. combine a thiazide with a _blocker/CaChannel blocker/ACEI (or _1 blocker) b. combine Ca channel blocker with a _blocker/ACEI
197
Q

what is the third step in the guidelines for treatment of hypertension?

A
  1. Triple therapy between drugs listed above (thiazide/_b/CaCB/ACEI/_B)or add furosemide or add clonidine
198
Q

Which antihypertensives are contraindicated in COPD, Asthma?

A

_ Blockers ACE inhibitors

199
Q

which antihypertensives are contraindicated in Bradycardia?

A

clonidine _ blockers Verapamil/Diltiazem

200
Q

which antihypertensives are contraindicated in Diabetes Mellitus?

A

ThiazidesUNSELECTIVE _ Blockers

201
Q

which antihypertensives are contraindicated in Gout?

A

thiazides

202
Q

which antihypertensives are contraindicated in CAD?

A

hydralazinePrazosin Minoxidil

203
Q

which antihypertensives are contraindicated in peripheral artery occlusive disease?

A

_ blockers

204
Q

which antihypertensives are contraindicated in CHF?

A

Ca++ antagonists HIGH DOSE _Blockers

205
Q

which antihypertensives are contraindicated in Renal Failure?

A

Amiloride Triamterene Spirololactone ACE Inhibitors

206
Q

why are _ Blockers contraindicated in COPD/Asthma?

A

Induction of bronchospasm

207
Q

why are ACE Inhibitors contraindicated in COPD/Asthma?

A

induction of cough, Use AT1 blocker

208
Q

why are clonidine, _Blockers, Verapamil/Diltiazem contraindicated in Bradycardia?

A

aggravation, risk of Adams-Stokes syndrome

209
Q

why are thiazides contraindicated in DM?

A

reduce glucose tolerance

210
Q

why are unselective _ Blockers contraindicated in DM?

A

blunt symptoms of hypoglycemia

211
Q

why are thiazides contraindicated in Gout?

A

reduced excretion of uric acid

212
Q

why are hydralazine, prazosin, and minoxidil contraindicated in CAD?

A

provocation of angina pectoris (reflectory tachycardia)

213
Q

why are _ Blockers contraindicated in peripheral artery occlusive disease?

A

aggravation/manifestation

214
Q

why are Ca++ antagonists and high dose _ Blockers contraindicated in CHF?

A

negative inotropic

215
Q

why are amiloride, triamterene and spironolactone contraindicated in renal failure?

A

may cause hyperkalemia

216
Q

why are ACE inhibitors contraindicated in Renal failure?

A

plasma concentration increases–> side effect

217
Q

what are the positive criteria for the selection of Diuretics for Tx of hypertension?

A

old age black race CHF chronic renal failure (loop diuretics)

218
Q

what are the positive criteria for the selection of _ blockers in the Tx of hypertension?

A

youth white race post-MI migraine senile tremor atrial fibrillation PSVT

219
Q

what are the positive criteria for selection of long acting Ca channel blockers in the Tx of hypertension?

A

old age black race migraine

220
Q

what are the positive selection criteria for the selection of ACE inhibitors in the Tx og hypertension?

A

youth white Diabetes Mellitus Type I w/ nephropathy impotence from other drugs NOT IN PREGNANCY

221
Q

what are the positive criteria for selection of AT1-blockers in the Tx of hypertension?

A

conditions for which ACEI are indicated, but can’t be used due to hypersensitivity or cough

222
Q

what are the positive criteria for selection of _ blockers in the Tx of hypertension?

A

prostatism DM dyslipidemia

223
Q

What are the favorable combinations of antihypertensives?

A
  1. Thiazide + ACEI 2. Dihydropyridine + _ Blocker 3. K wasting diuretic + K sparing diuretic
224
Q

why is Thiazide + ACEI a favorable combination?

A

more effective and reduction of adverse effects

225
Q

why is dihydropyridine + _blocker a favorable combination?

A

more effective

226
Q

why is a K wasting + a K sparing diuretic a favorable combination?

A

reduction of adverse effects

227
Q

what factors contribute to cardiac output?

A

HR

228
Q

what does the PSNS do to HR?

A

decreases it

229
Q

what does the SNS do to HR?

A

increases it

230
Q

what do catecholamines do to HR?

A

increases HR

231
Q

what factors contribute to blood pressure?

A

Cardiac output and systemic vascular resistance

232
Q

what factors contribute to SVR?

A

direct innervation circulating regulators local regulators

233
Q

what is the effect of _1Adrenergic receptors on SVR?

A

increases it by direct innervation

234
Q

how do catecholamines affect systemic vascular resistance?

A

increase it

235
Q

how does ATII affect SVR?

A

increases it

236
Q

what is the effect of NO on SVR?

A

decreases it

237
Q

what is the effect of prostacyclin on SVR?

A

decreases it

238
Q

what is the effect of endothelin on SVR?

A

increases it

239
Q

how does ATII affect SVR as a local regulator?

A

increases it

240
Q

what is the effect of O2 on SVR?

A

increases it

241
Q

what is the effect of H+ on SVR?

A

decreases it

242
Q

what is the effect of adenosine on SVR?

A

decreases it

243
Q

which drugs affect BP by affecting CO by affecting HR?

A

_B CCB

244
Q

which drugs affect BP by affecting CO by affecting SV by affecting contractility?

A

_B CCB

245
Q

which drugs affect BP by affecting CO by affecting SV by affecting Preload by affecting venous tone?

A

_1B sodium nitroprusside ACE inhibitors AT1 Antagonist

246
Q

which drugs affect BP by affecting CO by affecting SV by affecting Preload by affecting Intravascular volume by affecting Na+/H2O retention?

A

Diuretics ACE inhibitors AT1 Antagonists

247
Q

which drugs affect BP by directly affecting SVR?

A

CCB Direct Arterial Vasodilators

248
Q

which drugs affect BP by affecting SVR by affecting direct innervation?

A

_1B Central _2 agonists

249
Q

which drugs affect BP by affecting SVR by affecting circulating regulators?

A

_1 B central _2 agonists ACE inhibitors AT1 antagonists

250
Q

which drugs affect BP by affecting SVR by affecting local regulators?

A

endothelin antagonistssodium nitroprusside ACE inhibitors AT1 antagonists

251
Q

what is a hypertensive emergency?

A

clinical situation that requires immediate BP- reduction to prevent or limit target organ damage

252
Q

what is hypertensive urgency?

A

any situations in which BP should be lowered within a few hours

253
Q

what is the general strategy for treating hypertensive emergency?

A

intensive care monitoring pareneral drugs

254
Q

what is the general strategy for treating hypertensive urgency?

A

oral therapy

255
Q

what is the goal for BP reduction in crisis?

A

generally no immediate reduction of BP to ‘normal’ levels

256
Q

the endothelium modulates vascular resistance through what?

A

endocrine or paracrine release of vasoactive molecules such as NO and PGI2

257
Q

in a hypertensive emergency, endothelial control of vascular tone may be overwhelmed, leading to what?

A
  1. end-organ hyperperfusion 2. arteriolar fibrinoid necrosis 3. increased endothelial permeability with perivascular edema
258
Q

loss of endothelial fibrinolytic activity coupled with activation of coagulation and platelets promotes what?

A

DIC

259
Q

what are the causes of hypertensive emergencies?

A
  1. essential hypertension2. renal parenchymal disease 3. renovascular disease 4. pregnancy 5. endocrine 6. drugs 7. drug withdrawal 8. central nervous disorders 9. autonomic hyperreactivity
260
Q

what is the term for hypertensive emergency associated with pregnancy?

A

eclampsia

261
Q

what endocrine disorders can cause hypertensive emergency?

A

pheochromocytomacushings renin-producing tumors

262
Q

which drugs can cause hypertensive emergencies?

A

cocainecrack sympathomimetics amphetamines CsA MAO-I+Tyramine

263
Q

withdrawal of which drugs can cause hypertensive emergency?

A

clonidine nifedipine

264
Q

which central nervous disorders can cause hypertensive emergencies?

A

injury stroke tumor

265
Q

what are the important History items to cover in hypertensive crisis?

A
  1. severity/duration of pre-existing hypertension, details of therapy
266
Q

what are the important Symptoms to cover in hypertensive crisis?

A
  1. CP (MI, aortic dissection) 2. back pain (aortic dissection) 3. dyspnea (CHF, pulmonary edema) 4. neurology, seizures, altered consciousness (hypertensive encephalopathy)
267
Q

what are the 5 key parts of an initial assessment of hypertensive crisis?

A
  1. BP2. Fundoscopic exam 3. CV 4. Neuro 5. Lab
268
Q

what should be considered about BP taken in hypertensive emergency?

A

take supine and standing take on both arms

269
Q

what should be considered in fundoscopic exam during hypertensive emergency?

A

new hemorrhages exudates papilledema

270
Q

what should be considered in CV assessment during hypertensive emergency?

A

evidence of CHF

271
Q

what should be considered in a neuro exam during hypertensive crisis?

A

consciousness vision visual fields meningeal irritation focal signs

272
Q

what labs should be checked during assessment of hypertensiv crisis?

A

urea electrolytes creatinine CBC (hemolysis, schistiocytes) ECG CXR UA plasma renin/aldo

273
Q

what are the consensus recommendations for Tx of hypertensive crisis?

A
  1. admit ICU, IV drugs 2. arterial BP measure line 3. therapy: a. lower BP =100-110 mmHg c. further reduction of BP within days
274
Q

which hypertensive crisis drug is toxic in pts with renal impairment?

A

sodium nitroprusside

275
Q

what is the onset of sodium nitroprusside?

A

immediate

276
Q

what is the onset of labetalol?

A

5-10 min

277
Q

what is the onset of hydralazine?

A

10 min

278
Q

what is the onset of fenoldopam?

A

5-10 min

279
Q

what is the onset of enalaprilat?

A

15 min

280
Q

what is the onset of nicardipine?

A

5-10 min

281
Q

what is the onset of phentolamine?

A

1-2 min

282
Q

what is the duration of sodium nitroprusside?

A

1-2 min

283
Q

what is the duration of labetalol?

A

2-6 h

284
Q

what is the duration of hydralazine?

A

2-6 h

285
Q

what is the duration of nicardipine?

A

2-4h

286
Q

what is the duration of phentolamine?

A

3-5 min

287
Q

what are the adverse effects of sodium nitroprusside?

A

hypotension nausea vomiting cyanate toxicity

288
Q

what are the adverse effects of labetalol?

A

nausea vomiting heart block bronchospasm

289
Q

what are the adverse effects of hydralazine?

A

reflex tachycardia

290
Q

what are the adverse effects of enalaprilat?

A

hypotension renal failure

291
Q

what are the adverse effects of nicardipine?

A

reflex tachycardia flushing

292
Q

what are the adverse effects of phentolamine?

A

reflex tachycardia

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