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Pharmacology III > Block I: HTN > Flashcards

Block I: HTN Flashcards

1
Q

How is BP determined?

A

CO X PR

where CO= HR xSV

where SV= EDV-ESV

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2
Q

[] is resistance/friction that arterioles have against the flow of blood

A

peripheral resistance

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3
Q

what can increase PR?

A
  1. vasoconstriction

2. athersclerosis

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4
Q

what can decrease PR?

A

vasodilation

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5
Q

vasoconstriction has [] affect on PR and [] effect on BP

A

increases PR, increases BP

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6
Q

vasodilation has [] affect on PR and [] effect on BP

A

decrease, decrease

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7
Q

atherosclerosis has [] affect on PR and [] affect on BP

A

increase, increase

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8
Q

[] is the amount of blood that is pumped out of the heart per minute

A

cardiac output (normal 5L in avg. adult)

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9
Q

how is CO determined?

A

HR X SV

SV=EDV-ESV

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10
Q

what 4 factors affect HR

A
  1. autonomic innervation
  2. hormones
  3. fitness level
  4. age
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11
Q

what factors affect stroke volume

A
  1. heart size
  2. fitness level
  3. gender
  4. contractility
  5. duration contraction
  6. pre-load (EDV)
  7. afterlaod resistance (ESV)
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12
Q

[] is the volume of blood in ventricles at end of diastole

A

EDV

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13
Q

[] is resistance left than the ventricle must overcome to circulate blood

A

ESV

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14
Q

stimulation of [] will cause all factors of BP to rise

A

SNS

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15
Q

SNS stimulation of BP will cause all factors to []

A

rise

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16
Q

what causes SNS stimulation on heart

A
  1. stress
  2. exercise
  3. pheochromocytoma
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17
Q

[] is failure of heart to adequately pump enough blood to meet body’s needs

A

chronic HF

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18
Q

what are some compensatory mechanisms of heart failure?

A
  1. hypertrophy of cardiac muscle & chamber size
  2. neurohumoral reflex (activate SNS)
  3. kidneys & RAAS
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19
Q

describe the goal of hypertrophy to compensate during HF

A

an attempt to increase stroke volume

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20
Q

describe the goal of neuralhumoral reflexes in HF

A

activate sympathetic nervous system

alpha 1 -> vasoconstrict
beta 1 -> increase HR and force myocardial contraction

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21
Q

what happens when SNS activates alpha-1 receptors

A

vasoconstriction

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22
Q

what happens when SNS stimulates beta-1 receptors

A

increase HR and force myocardial contraction

positive inotropic and choriotropic respectively

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23
Q

describe the role of kidneys in HF

A

will activate RAAS –> vasoconstriction and release aldosterone –> increase Na and water retention

increase BP and blood volume

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24
Q

what needs to be reduced to control heart failure?

A

cardiac work load

  1. HR
  2. SV (EDV-ESV)
  3. PR
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25
Q

what drugs interfere with RAAS?

A
  1. ACEI
  2. ARBS
  3. Renin inhibitors
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26
Q

what drug class do the “prils” belong to?

A

ACEI

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27
Q

what is the moa of the “prils”

A

ACEI (angiotensin converting enzyme inhibitor)

block angiotensin 1 from being converted to angiotensin 2
-thereby decreasing vasoconstriction and aldosterone release (inhib. Na and water retention)

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28
Q

what are some indications for ACEI?

A
  1. HTN
  2. HF
  3. post MI
    (also CKD)
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29
Q

what suffix belongs to ARBs?

A

“artans”

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30
Q

what is the MOA of the “artan” drugs

A

angiotensin receptor blocker

block angiotensin 2 from binding target cell and exerting effect

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31
Q

indications ARB

A
  1. HTN
  2. HF
  3. post MI
    (helpful in CKD)
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32
Q

describe some AE affects of ACEI/ARB

A
  1. cough (due to bradykinin)

2. angioedema (more common in black individuals)

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33
Q

ACEI [>/

A

ACEI

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34
Q

what are some drugs that affect the SNS to help with HTN

A
  1. centrally acting sympatholytic
  2. neuronal blockers
  3. alpha blockers
  4. beta blockers
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35
Q

what is the role of alpha-1 receptors when stimulated by SNS

A

contraction of smooth muscle via NE

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36
Q

what is the role of beta-1 receptors when stimulated by SNS

A

cardiac stimulation via NE (increase force & rate contraction)

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37
Q

[] is the name of a centrally acting symatholytic

A

Clonidine

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38
Q

what is the MOA clonidine

A

centrally acting sympatholytic

acts on vasomotor centers of medulla oblongata & stimulates inhibitory receptors to reduce activity of sympathetic nerves that control HR and CO (thereby decreasing BP)

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39
Q

what are some other uses for clonidine?

A

centrally acting sympatholytic

  1. AHDH off label
  2. drug WD
  3. menopausal flushing
  4. diarrhea
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40
Q

Guanthidine is a []

A

neuronal blocker

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41
Q

what drug is a neuronal blocker?

A

Guanthidine

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42
Q

what drug is a centrally acting sympatholytic?

A

conidine

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43
Q

MOA Guanthidine

A

Neuronal blockers

causes significant inhibition of sympathetic activity

reserved for HTN that doesn’t respond to other drugs

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44
Q

what type of drugs are the ‘zosins’

A

alpha blockers

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45
Q

what suffix belongs to alpha blockers

A

zosins

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46
Q

what is the moa of alpha-1 blockers

A

normally alpha-1

  • produces contraction and vasoconstriction when stimulated by NE
  • increases PR
  • increases BP

blockers reverse these effects

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47
Q

where are alpha-1 receptors located

A

smooth muscle of arteries, veins, sphincters & urinary tract

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48
Q

where are alpha-2 receptors located

what is their role?

A

adrenergic nerve endings, activated NE and EPI

negative feedback mechanism, regulates release of additional NE

  • inhibits ACH release
  • inhibits insulin release
  • would want to agonize to treat HTN
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49
Q

what is the MOA of the zosins

A

alpha-1 blocker

block alpha-1 stimulation from NE, thereby blocking vasoconstriction and reducing PR

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50
Q

what drug class do the “olols” belong to

A

beta blockers

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51
Q

beta [] receptors are the predominant heart receptors

A

1

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52
Q

what is the role of beta-1 receptors

A

predominant heart

  • increase myocardial contractility
  • increase HR
  • increase renin release
  • cause tachycardia

*antagonize to treat heart issues

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53
Q

what is the role of beta-2 receptors

A

primarily in lung

  • cause bronchodilation
  • vasodilation (decreased PR)
  • relaxed uterine smooth muscle

*caution use non selective BB in asthmatic and COPD patients

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54
Q

where are beta-2 receptors most predominately

A

smooth muscle and tissue

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55
Q

MOA ‘olols’

A

beta blockers

-inhibit sustained NE activation from SNS (inhibit cardiac stimlation)

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56
Q

indication beta blockers

A
  1. chronic heart failure (carvedilol, b-olol, metoprolol succ)
  2. reduced LV systolic function (L sided heart failure)
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57
Q

AE BB

A
  1. exacerbate symptoms in acute decompensated HF
  2. WD symptoms (ischemic)
  3. may affect glucose levels and mask effect hypoglycemia
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58
Q

orthostatic hypotension is a risk in [] drug

A

alpha inhibitor

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59
Q

[] should NOT be used in decompenstated HF

A

BB

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60
Q

[] can mask the symptoms of hypoglycemia

A

BB

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61
Q

[] may cause ischemic WD symptoms

A

BB

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62
Q

what is a relative contraiction in BB

A

COPD/Asthma in non-selective BBs

-if b-2 stimulation is blocked it may cause bronchoconstriction

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63
Q

hydralazine is [] type of drug

A

arterial vasodilation

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64
Q

minoxidil is [] drug

A

arterial vasodilator

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65
Q

MOA hydralazine

A

decrease sympathetic done, cause vasodilation

ARTERIAL

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66
Q

MOA minoxidil

A

decrease sympathetic tone, cause vasodilation

ARTERIAL

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67
Q

what kind of drug is nitroglycerin

A

vasodilator of veins and arteries

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68
Q

what kind of drug is nitroprusside

A

venous & arterial dilator

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69
Q

[] are often used on comnimation with diuretics and BB due to fluid retention and reflex tachycardia

A

vasodilators (hydralazine, minoxidil, nitroglycerin, nitroprusside)

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70
Q

[] is indicated FOR acute decompensated HF

A

vasodilators (hydralazine, minoxodil, nitroglycerin, nitroprusside)

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71
Q

[] is NOT indicated for decompensated HF

A

BB

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72
Q

[] is indicated for

  1. HTN
  2. post mi
  3. decompnensated HF
A

vasodilators

hydralazine, minoxodil, nitroglycerin, nitroprusside

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73
Q

MOA CCB

A

bind to long acting calcium channels to block influx of calcium in cardiac smooth muscle

  • block depolarization
  • block AP
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74
Q

nifedipine, amlodipine, and nicardipine belong to [] class

A

dihydropyridine CCBs

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75
Q

MOA of the dipines

A

dihydropyridine CCB

arterial dilation, decreased HR, decreased AV conduction & decreased myocardial contractility

due to blocking of long acting calcium channels

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76
Q

indications for dipine drugs

A
  1. HTN
  2. CAD
  3. angina
  4. cardiac arrythmias (diff from nonDHP)
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77
Q

what is the drug class verapamil

A

non DHP CCB

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78
Q

what is the drug class of diltiazem

A

non DHP CCB

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79
Q

what is the caution of non DHP

A

bradycardia

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80
Q

what is the MOA diltiazem

A

non DHP CCB

atrial dilation

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81
Q

what is the MOA verapamil

A

non DHP CCB

eterial dilation

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82
Q

indiations for non DHP CCB

A
  1. HTN
  2. CAD
  3. angina

(DHPs inddicatied for arrythmias, but non DHPs NOT indicated)

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83
Q

AE of CCB (CV)

A
  1. hypotension
  2. palpitations
  3. bradycardia
  4. peripheral edema
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84
Q

GI AE CCB

A

constipation

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85
Q

how can diuretics be helpful in treating HTN

A

increase excretion of water and salt from body (reverse effects adolosterone)

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86
Q

indications diuretcis

A
  1. edema
  2. HTN
  3. HF
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87
Q

[] is the most common cause of cardiovascular disease

A

HTN

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88
Q

stimulation of alpha-1 receptors leads to []

A

vasoconstrictoin (antagonize to treat HTN)

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89
Q

stimulation alpha-2 receptors leads to []

A

inhibit NE release (block sympathetic stimulation and vasoconstriction)

  • negative feedback mechanism
  • would want to agonize to treat HTN
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90
Q

beta-1 receptor activation leads to []

A

increased HR and contractility, increased renin

want to antagonize for HTN

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91
Q

beta-2 receptors activation leads to []

A

smooth muscle relaxation, can cause bronchodilation

blocking Beta-2 can lead to bronchoconstrction, caution COPD and asthma

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92
Q

[] is the most influential contributor to homeostatic regulation of BP

A

RAAS

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93
Q

effects of RAAS

A
  1. regulate NA (aldosterone causes Na and water retentaion, K wasting)
  2. blood volume (increases due to aldosterone)
  3. SNS activity & vascular tone (increase BP HR CO)
94
Q

how is RAAS stimulated?

A
  1. decreases perfusion kidneys
  2. decreased Na and Cl delivered to distal tubule
    (activate need to alsodterone to absorb NA)
  3. direct stimulation beta-1 receptors (release renin)
95
Q

what receptors release renin?

96
Q

what are 2nd causes HTN

A
  1. renovascualr dx
  2. pheochromocytoma
  3. primary aldosteronism
  4. cushing’s
  5. coarctation of aorta
  6. sleep apnea
  7. head injury
  8. brain tumor
97
Q

medications to cause HTN

A
  1. corticosteroids
  2. NSAIDS
  3. Na/water retention SE
  4. estrogen
98
Q

what are ways SNS Can be activated, what effect does this have on BP

A

can cause HTN

  1. amphetamines
  2. sympathomimetic agents
  3. antidepressants (SNRI< Trycyclics
99
Q

st. john’s wort can [] BP

100
Q

alcohol can [] BP

101
Q

according to ACC/AHA guidelines, what is HTN

102
Q

according to JNCP guidelines what is HTN

103
Q

what is ACC/AHA stage 1 HTN

A

130-39/80-89

104
Q

what is ACC/AHA Stage 2 HTN

A

> /= 140/90

105
Q

what is the BP threshold for everyone EXCEPT a 1o year ASCVD risk < 10% and stable ischemic heart disease

A

> /=130/80

106
Q

what is the BP threshold for a patient a ASCVD risk of < 10%

A

> /= 140/90

107
Q

what is a BP threshold of a patient with stable ischemic heart disease

A

> /= 140/90

108
Q

normal BP patients should be followed up how requently

109
Q

patients with hx HTN but are at goal/nonpharm

how frequently should they fu

A

1-6 months

110
Q

medication change, when to see pt back?

111
Q

1 Kg weight reduction can result in [] BP change

A

1 mmHG for every 1 KG

112
Q

general counseling points DASH

A

increase fruits, veggies, whole grains, low fat

-decrease saturated adn total fat

113
Q

what is Na intake goal for HTN pt

A

< 1500 mg/day

aim for at least 1,00 mg/day reduction

114
Q

what ion should increased dietarily to help with HTN

A

K+

aim for 3,500-5,000 mg/d

115
Q

what drug class blocks aldosterone release, vasoconstriction, and Na retention (ultimately lowering BP)

A

prils, ACEI

116
Q

name some AE ACEI

A
  1. hypotension (in volume depleted pts. i.e. diuretic, HF, renal impairment)
  2. cough, dry persistent
    (more prevalent AA) due ot bradykinin
  3. angioedema (due to bradykinin)
117
Q

[] is an emergency adverse effect of ACEI and is []x more fatal in AA

A

angioedema, can happen with ARB too

5x

118
Q

[] is asymmetric swelling of face, mouth, and upper airway

could be in absence of urticaria or itching

A

angioedema

ACEI > ARB

119
Q

what electrolyte disturbance may occur wiht ACEI/ARB

A

increased K+, due to block in aldosterone

120
Q

ACEI/ARBS contraindicated in []

A

pregnancy

  • oligohydraminos
  • hypotension
  • renal failure
  • death

renal artery stenosis (BRAS) wont be enough perfusion of glomerulus with artery stenosis and dilation efferent arteriole

121
Q

how might ACEI/ARB affect the kidney

A

block constriction of efferent arteriole, less pressure in glomerulus

decreased GFR, increase Scr

122
Q

what should be monitored while one ACEI/ARB

A

SCr

if increases >30% there is too much strain on kidney

123
Q

what kind of dose adjustment is assoc with ACEI/ARB

A

50% decrease if on diuretics, elderly or with renal impairment

124
Q

[] have been shown to decrease progression of renal disease and are great for CKD

A

ACEI/ARB

but caution with AKI

125
Q

what drugs can be benificial in in HFeEF

126
Q

can you combine and combo if ACEI, ARB, or renin inhibitor

127
Q

how would you monitor a patient on ACEI/ARB

A
  1. BMP ( K+, SCr) specificially

2. BP

128
Q

ARBS have {higher/lower] rates of cough and angioedema in comparison to ACEI

129
Q

can you give an ARB To a pregnant patient

A

no

  • oligohydramnios
  • hypotension
  • renal failure
  • death
130
Q

if a patient has a cough on an ACEI, what shoul you do next

A

switch to an ARB

131
Q

how do you monitor an ARB

A
  1. BMP (K+, Scr)

2. BP

132
Q

what is the primary action of the dipine drugs

A

DHP CCB

-primarily DILATE blood vessels

133
Q

AE dipine drugs

A

DHP CCB

  • peripheral edema (may not be relieved by diuretics because it is not a fluid retention issue)
  • HA
  • dizziness
  • flushing
  • reflex tachycardia (more likely IR)
134
Q

caution with dipine drugs

A

DHP CCB

  • unstable angina
  • CYP 3A4 interactions
  • -simvastatin should not excess 20 mg/day
135
Q

how do you monitory a DHP CCB

136
Q

name non DHP CCB

A
  1. diltiazem

2. verapamil

137
Q

caution non DHP CCB

A

bradycardia

138
Q

AE NON DHP CCB

A
  1. Constipation
  2. gingival hyperplasia
  3. bradycardia
  4. avoid in hf pt.
139
Q

how would you monitor non DHP CCB

140
Q

a patient has a HR of 56 BPM, what meds should they avoid?

A

verapamil, diltiazem, BB “ olols”

141
Q

interactions with non DHP?

A

CYP3A4 interactions

-no more than 10 g simvastatin

142
Q

chlorthalidone is what type of drug

A

thiazide diuretic

143
Q

HCTHZ is what kindof ddrug

A

Thiazide diuretic

144
Q

MOA chlorthalidone

A

thiazide diuretic

act on early distal tubule to block reabsorption of Na, Cl, water
 (HCTZ too)
-excretion  K + increased
-decrease, K, Na, Mg
-increase uric acid, glucose, Ca2+
145
Q

what drug may increase uric acid

A

diuretics, thiazides ecp.

146
Q

what drug may increase glucose

A

thiazide diuretic

147
Q

what may render HCTZ ineffective

A

CrCl < 30 (kidneys need to be perfused for thiazide to exert effect)

148
Q

what drug may cause photosensitivity

A

thiazide diuretics

149
Q

chlorthalidone has a [higer/lower] half life than HCTZ

A

higher, more likley to reduce CV symptoms

ACC/AHA rec. over HCTZ

150
Q

how would you monitor a patient on a thiazide diuretic

A
  1. BMP (Na, K Scr, glucose)

2. BP

151
Q

fursomide belongs wo what class

A

loop diuretic

152
Q

torsemide belongs to what class

A

loop diuretic

153
Q

[] diuretics are preferred if there is concomitant renal dysfunction

A

loop (furosemide, torsemide)

154
Q

triamterene/HCTZ is a [] diuretic

A

K sparring

155
Q

aldosterone blocker is a [] diuretic

A

K sparring

156
Q

epleredone is a [] diuretic

157
Q

Spironolactone is a [] diuretic

158
Q

what diuretic is thought to have the weakest diuresis

A

K SPARRING

159
Q

what diuretic can be used to offset thiazide induce K+ loss

A

K sparring

  • spironolactone
  • triamterene/HCTZ
  • aldosterone blocker
  • elperedone
160
Q

what caution should be made with spironolactone/aldosterone blocker/triamterene/HCTZ/elperedone and ACEI/ARB

A

hyperkalemia,

using K sparing with ACEI/ARB (that already blocks aldosterone and spares K) may lead to too much K

161
Q

is atenolol selective

162
Q

is betaxolol selective

163
Q

is bisoprolol selective

164
Q

is metorpolol selective

A

yes, succ. and tart

165
Q

is nadolol selective

166
Q

is propranolol selective

167
Q

is timolol selective

168
Q

is carvedilol selective

A

NO (also with alpha-1 activity)

169
Q

is labetalol selective

A

NO (also alpha-1 activity(

170
Q

what kind of drug is pindolol

A

BB with intrinsic sympathomimetic

171
Q

MOA BB

A

stop angiotensin II from binding target cells in heart

  • decreased contractility
  • decreased cardiac output
172
Q

Caustion non selective bb

A

COPD, asthma, may cause bronchonstriction by blocking B2 (bronchodilate when bound to NE)

173
Q

what drugs should not be mixed for fear bradycardia

A

non DHP CCB (verapamil, diltiazem), BB

174
Q

name the selective BB

A

beta-1 selective

ABBA MEN

Atenolol
Betaxolol
Bisoprolol
Acebutolol
Metoprolol
Esmolol
Nevivolol
175
Q

what drug can cause hypoglycemia, how is this mechanism

A

BB,
epi acts via beta-adrenergic receptors

will increase glucose, but BB will block this action and cause hypoglycemia WIHTOUT warning signs
(only hypoglycemia symptom that will occur is sweating)

176
Q

what are some AE of BB

A
  1. decreased exercise tolerace
  2. exacerbation decomensated HF
  3. bronchospasm
  4. mask hypoglycemia
  5. depression
  6. fatigue
  7. sexual dysfunction
177
Q

cuation with stopping BB

A

rebound HTN

178
Q

what are teh more 1st line HTN drugs

A
  1. ACEI/ARB
  2. CCB
  3. diuretic
179
Q

how would you moitor a BB patient

180
Q

What class does clonidine belong to?

A

Alpha-2 agonist

181
Q

what class does methyldopa belong to?

A

Alpha-2 agonist

182
Q

what is the MOA of clonidine

A

alpha-2 agonist

block CNS stimulation to BLOCK increase in vasopressin and sympathetic discharge. (SNS speeds up HR, alpga-2 agonsit will block and constriction)

  • decrease peripheral resistance to decrease BP
  • VASODILATE

**Remember alpha-2 is the inhibiting factor so you want to AGONIZE it

183
Q

what is the MOA of methyldopa

A

alpha-2 agonist

block CNS stimulation to BLOCK increase in vasopressin and sympathetic discharge. (SNS speeds up HR, alpga-2 agonsit will block and constriction)

  • decrease peripheral resistance to decrease BP
  • VASODILATE

**Remember alpha 2 is the inhibiting factor, so you want to AGONIZE it

184
Q

What kinds of cautions should you educate your patients on before you give them an alpha 2 agonist

A
  1. AVOID with cradycardia or drugs that can cause it ( BB, non DHP)
  2. rebound HTN with aprubt d/c (like BB)
  3. may cause orthostatic hypertension
185
Q

what 2 patient groups are important to keep in mind with alpha-2 agonists

A
  1. elderly (orthostatic hypotension)

2. pregnancy (methyldopa PREFFERED)

186
Q

what drug can be used a patch once weekly to treat HTN?

A

clonidine, alpha-2 agonist

187
Q

what HTN drug is preferred in pregnancy

A

methyldopa

188
Q

How would you monitor a patient on an alpha-2 agonist

189
Q

what kind of drug is Aliskiren

A

a renin inhibitor

190
Q

MOA Aliskiren

A

inhibit renin release from kidney, block entire RAAS system

directly block the conversion of angiotensin to angiotensin 1

191
Q

what 3 drug groups are contraindicated in pregnancy

A
  1. ACEI
  2. ARB
  3. renin inhibitor
192
Q

what 3 drug groups should NOT be combined

A
  1. ACEI
  2. ARB
  3. renin inhibitor
193
Q

what are some AE of aliskiren

A
  1. angioedema
  2. hyperkalemia
  3. elevated SCr
  4. decreased GFR
  5. hypotenson
194
Q

What cautions must you consider when Rxing Aliskiren

A
  1. pregnancy (cont!)
  2. BRAS
  3. angioedema
195
Q

how would you monitor a patient on aliskiren

A
  1. BP

2. BMP (K+, SCr)

196
Q

Doxazosin is a [] drug

A

Alpha-1 blocker

remember alpha-1 STIMULATES heart muscle, want to block this

197
Q

MOA Doxazosin

A

alpha-1 blocker

vasodilate veins/arteries by inhibiting alpha-1 receptors (when stimulated to vasoconstrict)

198
Q

AE doxazosin

A
  1. orthostatic hypotenstion (esp. after 1st dose and elderly)
  2. priapaism
199
Q

according to beer’s criteria [] is NOT Recommended for routine use in HTN due to risk of orthostatic hypotension

200
Q

what needs monitored for a patient on doxazosin

201
Q

[] is NOT recommended fo rinital monothereapy due to increased risk CV events

202
Q

hydralazine belongs to what group

A

direct vasodilator

203
Q

minoxodil belongs to what group

A

direct vasodilator

204
Q

MOA minoxidil

A

direact vasodilation, relexation or arteriolar smooth musle (LITTLE EFFECT ON VEINS)

205
Q

MOA hydralazine

A

direct vasodilation, relaxation of arteriolar smooth muscle (LITTLE EFFECT ON VEINS)

206
Q

AE direct vasodilators

A

reflex tachycardia

edema

hypertrichosis

lupus-like syndrome

HF (retention water and salt)

ischemic heart disease

207
Q

[] can cause lupus-like syndrome

A

minoxodil, direct vasodilator

208
Q

[] can cause hypertrichosis

A

direct vasodilaotr (minoxodil and hydralazine)

209
Q

[] should be given with a diuretic to minimize fluid gain

A

direct vasodilator, hydralazine or minoxodil

210
Q

[] should be given with a BB to prevent tachycardia and increase myocardial workload

A

direct vasodilator, hydralazine minoxodil

211
Q

what is preffered inital therapy for HTN

A

Ccb
Acei/ARB
Thiazide

CAT
*just never combine ACEI/ARB

212
Q

what can be given to treat ischemic heart disease?

A

BB +/- ACEI/ARB

+/- CCB if goal not met

213
Q

what should be avoided in ischemic heart diseae

A

atenolol (use any other BB)

214
Q

What can be used to treat HFrEF?

A

BB +/- ACEI/ARB

215
Q

what BB are prefered to treat HFrEF?

A
  1. bisoprolol
  2. carvedilol
  3. metoprolol suc.
216
Q

what should be avoided in treatment of HFrEF?

A

NON-DHP, CCB

217
Q

what is first like for HFpEF

A

diuretics

remember hfPef, diuretics make you P

218
Q

what treatments are best for CKD

A

ACIE (pref) ARB if cannot tolerate ACEI

219
Q

for acute intracerebral hemorrhage or acute ischemic stroke, what is important to know when treating these pts.

A

dont lower NP to quicly

220
Q

what should be done for secondary stroke prevention?

A
  1. wait to start HTN thereapt
  2. no HX HTN, start only when BP greater than 140/90
  3. select therapy based on comorbidities
    - thiazide, ACEI/ARB
221
Q

in DM all [] med are appropriate

A

first line (ACEI.ARB, CCB, Thiazide)

222
Q

Describe how treatment should be done in AA patients

A
  1. use CCB or thiazide first
  2. Use ACEI/ARB or BB IFFFFFFF HFrEF or CKD
    (these are greater than risk AE with BB or ACEI/ARB)
223
Q

what are 3 preferred drugs in pregnancy

A
  1. Nifedipine ER
  2. Labetalol
  3. Methyldopa
224
Q

How should you treat HTN with airway issues like asthma, COPD

A
  1. avoid non-selective BB
  2. use ABBA MEN selective BB
  3. sympathomimetic agents may raise BB
225
Q

how to treat HTN pts. with gout

A
  1. avoid thiazides (other diuretics may be okay)
226
Q

define orthostatic hypotension

A

a decrease in SBP of > 20 mmHG

decreased in DBP of > 10 mmHG

when changing from supine to standing

227
Q

what drugs put a patient at risk for orthostatic hypotension

A
  1. clonidine
  2. alpha blockers
  3. sometimes ACEI, ARB, diuretics

most common in vasodilators

start low and titrate up*

228
Q

describe a hypertensive crisis

A

SBP > 180 mmHG

DBP > 120 mmHG

229
Q

when do hypertensive crises require hospitalization and IV antihypertensives

A

if end-organ damage is present

reduce SBP < 140 mmHG in first hr

SBP < 120 mmHG with IV meds

dont correct too quick, should take hours

230
Q

name evidences of end organ damage in hypertensive crisis

A
  1. encephalopathy
  2. acute MI
  3. untable angina
  4. strokes
  5. AKI
  6. aortic anneurysm
231
Q

if hypertensive crisis present with no end organ damage, what is protocol

A

reinstiture or intensify PO antihypertensives, arrange f/u

Pharmacology III (6 decks)

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