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Pharm - Cardiovascular > Drugs for Essential Hypertension > Flashcards

Drugs for Essential Hypertension Flashcards

1
Q

High normal or prehypertension pressures begin at?

A

120/80 and up

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2
Q

stage 1 hypertension pressures begin at

A

140/90 and up

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3
Q

stage 2 hypertension pressures begin at?

A

160/100 and up

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4
Q

hypertensive urgency when BP is? specifics?

A
  • 180/120 a nd up
  • NO associated acute end organ damage of CNS, cardiovascular, or kidneys
  • lower BP over hours to days as close monitored outpatient
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5
Q

hypertensive emergency when BP is? specifics?

A
  • just markedly elevated BPs
  • PRESENCE of acute end organ damage due due acute rise in BP
  • need immediate thereapy to reduce BP within min to hours
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6
Q

RHTN risk factors?

A 
older age
obesity
diabetes
obstructive sleep apnea
high salt diet
African american
female
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7
Q

RHTN definition:

A

BP that is not controlled despite use of 3 or more antihypertensive drugs (one must be diuretic) taken at optimal doses

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8
Q

Pseudo-RHTN definition

A

uncontrolled BP due to white coat effect, poor adherence to meds, or incorrect BP measurement techniques

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9
Q

Primary HTN etiology:

A

idiopathic or genetic basis

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10
Q

Secondary HTN etiology:

A

1) Common:
a) renal parenchymal disease
b) obstructive sleep apnea
c) renal artery stenosis
d) primary aldosteronism
2) Uncommon:
a) pheochromocytoma
b) cushing syndrome
c) hyperparathyroidism
d) coarctation of the aorta

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11
Q

blood pressure goal for HTN patient?

A

less than 140/90

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12
Q

BP goal for pt with diabetes or chronic kidney disease?

A

less than 130/80

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13
Q

super general MOA for antihypertensive agents?

A

MAP = CO x TPR
CO = HR x SV
ALL hypertensives work to reduce one of the above components - may have additinoal CNS effects

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14
Q

hypertensive crisis definition?

A

encompases both HTN emergencies and urgencies = has to do with how quickly the BP went up

may happen with tyramine or amphetamine or cocaine use

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15
Q

Treatment of HTN is based on what methodolgy?

A

Reduce risk of CV event to reduce CV morbidity and mortality – NOT JUST TREATING THE BP NUMBERS

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16
Q

Lifestyle mods for HTN treatment:

A

reduce weight

  • adopt dash diet
  • lower sodium intake
  • physical activity
  • moderation of EtOH consumption
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17
Q

Hypertension treatment algorithm - No compelling indication options?

A

1) single drug:
a) ACEI
b) ARB
c) CCB
d) thaizide

OR

2) Two drugs:
a) ACEI OR ARB with CCB
b) ACEI OR ARB with thiazide
c) CCB with thiazide

Aldosterone add on if RHTN

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18
Q

Hypertension treatment algorithm - Diabetes plan

A

1) First line: ACEI or ARB

2) Add on: Thiazide then Beta blocker and/or CCB

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19
Q

Hypertension treatment algorithm - chronic kidney disease plan:

A

First line: ACEI or ARB

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20
Q

Hypertension treatment algorithm - coronary artery disease plan

A

1) First line: beta blocker(or alternative is CCB) & ACEI or ARB
2) Add on: aldosterone antagonist, CCB, and/or thiazide

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21
Q

Hypertension treatment algorithm - left ventricular dysfunction plan

A

1) First line:
a) diuretic (THIAZIDE)
b) ACEI or ARB and beta blocker
2) Add on: aldosterone

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22
Q

Hypertension treatment algorithm - Previous ischemic stroke plan:

A

First line: ACEI with or without thiazide

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23
Q

stimuli for Juxtaglomerular cells to inc or dec renin release:

A 
INC:
1) inc catecholamines
2) decrease serum K
DEC:
1) inc serum K
2) inc tubular Na effect at the macula densa
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24
Q

Angiotensin II and II effects:

A

1) inc aldosterone synthesis and secretion
2) increase vasoconstriction
3) increase release of vasopressin
4) inc release of adrenal catecholamines
5) inc central sympathetic outflow

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25
Q

Renin-Angiotensin-Aldosterone system quick breakdown:

A

-JG cells secrete renin
-Renin converts: angiotensinogen to angiotensin1
-ACE in lungs converts angio1 to angio 2 and 3
-Angio 2 and 3 stim aldosterone release
=renal Na retention = save water = inc blood pressure bc more water

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26
Q

Angiotensin-converting enzyme inhibitors for HTN

-Drugs?

A

captpril
lisinopril
fosinopril

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27
Q

Angiotensin-converting enzyme inhibitors for HTN

-3 broad groups:

A
  • sulfydryl - structurally similar to captopril
  • dicarboxyl - structurally related to enalapril (lisinopril)
  • phosphorus - structurally related to fosinopril
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28
Q

captopril and lisinopril vs fosinopril kinetics?

A

capro and lisin are active molecules while fosino needs to be converted to its diacid form

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29
Q

Angiotensin-converting enzyme inhibitors - MOA?

A
  • inhibiting ACE =
    1) decreased production of angiotensin2 = decreased vasoconstriction, decreased aldosterone secretion and sodium and water retention
    2) decreased breakdown of bradykinin (normally causes vasoconstriction!) and other vasoactive peptides, which results in vasodilation and allergic responses
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30
Q

First line or add on therapy for uncomplicated HTN - which drug type?

A

ACEI or ARB

  • equal effectiveness
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31
Q

First line for HTN with diabetes - drug? Why?

A
  • ACEI -special advantange in the treatment of patients with diabetes, slowing the development and progression of diabetic glomerulopathy
  • ARB
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32
Q

First line for HTN with CKD- drug? why?

A
  • ACEI -slow progression of CKD such as glomerulosclerosis

- ARB

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33
Q

First line for HTN with CAD, LV dysfuntion, and ischemic stroke- drug? why?

A

-ACEI- given immediately post MI period shown to improve ventricular function and reduce morbidity and mortality

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34
Q

ACEI and diuretic drug combo?

A

GOOD combo! enhanced efficacy of the diuretics bc ACEI stop the rise in aldosterone in response to Na loss = aldosterone cant stop loss of Na —-> this means that even samll doses of diuretics may substantially improve the antihypertensive efficacy of ACEI

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35
Q

ACEI - Clinical Pharmacology

A

1) ACEI cleared by the kidneys–> reduce dose in kidney failure
2) Fos and spirapril cleared equally by liver and kidney
3) elevated plasma renin = hyperresponsiveness to ACEI –> reduce dose in patients with high plasma renin levels (HF, Na depleted)

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36
Q

ACEI- contraindications:

A

DO NOT USE IN:

  • **1) PREGNANCY - fetal adverse side effects
    2) bilateral renal artery stenosis - ACEI do not help glomerular filtration rate - could reduce filtration fraction and GFR
    3) Hx of angioedema - rare but potentially fatal adverse effect of ACEI
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37
Q

ACEI - potentially favorable situations:

A

1) low normal potassium
* **2) pre-diabetes
3) albuminuria

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38
Q

ACEI - potentailly unfavorable situations:

A

1) high-normal K
* **2) hyperkalemia
* **3) volume depletion

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39
Q

ACEI - adverse effects:

A

1) hypotension (first dose, Na depleted, CHF, multi HTN Rx)
2) coughing 5-20%
3) angioedema
4) inc plasma K
5) acute renal failure
6) fetopathic potential
7) skin rash

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40
Q

***If patient is coughing with ACEI which drug should you try?

A

***ARB

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41
Q

ACEI - good for which age and race? worse for which age and race?

A
  • good for young and middle aged whites

- not good for older african americans

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42
Q

Angiotensin Receptor blockers

  • Drugs:
  • What do they do?
A
  • losartan
  • candesartan
  • irbesartan
  • valsartan
  • telmisartan
  • olmesartan
  • eprosartan

-Block AT1AngII receptor

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43
Q

Safer ACEIs for people with CKD?

A

fosinopril and spirapril

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44
Q

AT1AngII receptor located in what tissues?

A

brain
kidney
adrenal glomerulosa cells

  • RESPONSIBLE FOR MOST OF CARDIOVASCULAR EFFECTS
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45
Q

AT2AngII receptor located in what tissues?

A

adrenal medulla
kidney
CNS

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46
Q

ARB - MOA/Resulting change for blockage of AT1AngII receptor:

A

-decreased AngII effects = decreased vasoconstriction, decreased aldosterone secretion, and Na and water retention

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47
Q

Which angII induced effects are blcked?

A

1) contraction of vascular smooth muscle
2) thirst
3) vasopressin release
4) aldosterone secretion
5) release of adrenal catecholamines
6) enhancement of noradrenergic neurotransmission
7) increases in sympathetic tone
8) changes in renal function
9) cellular hypertrophy and hyperplasia - long term!

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48
Q

First line therapy for ONLY CAD and LV dysfunciton?

A

ARB!

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49
Q

If patient is intolerant to ACEI use which drug?

A

ARB!

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50
Q

Avoid ARB use in which patients?

A
  • pregnant

- bilateral renal artery stenosis

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51
Q

ARB use with potentially favorable situations?

A
  • low potassium

- pre-diabetics

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52
Q

ARB use with potentially unfavorable situations:

A

high normal K
hyperkalemia
-volume depletion

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53
Q

Non and Dihydropyridine Calcium channel blockers for essential HTN: DRUGS?

A

DHP -THESE DRUGS MORE EFFECTIVE IN VASCULATURE:

  • nifedipine
  • amlodipine
  • felodipine
  • NDHP - THESE MORE IN THE HEART:
  • verpamil; diltiazem
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54
Q

CCB - MOA?

A

1) MOA:
a) depress SA nodal automaticity and AV nodal conduction
b) decrease ventricular contractility
c) similiar to Class II, primary effects on nodal phase 0 depolarization (Ca channels)
2) Ca Channel Blockers (CCBs) interfere with entry of Ca into cells through voltage dependent L and T type calcium channels - diminish the degree to which Ca can enter
3) No CCB bind to all pores- therefore blockade by CCB is incomplete
4) major sites of action:
a) vascular smooth muscle cells
b) cardiac myoctes
c) SA and AV nodal cells

55
Q

First line therapy for ONLY diabetes and or CAD?

A

CCB - DHP! - nifedipine, amlodipine, felodipine

56
Q

Avoid CCB - DHP use when?

A

-left ventricular dysfuntion - ALL except amlodipine and felodipine

57
Q

CCB - DHP potentially favorably situations?

A
  • reynaud syndrome
  • **-elderly patients with isolated systolic hypertension
  • cyclosporine-induced hypertension
58
Q

CCB - DHP potentially unfavorable situations?

A
  • peripheral edema

* ** -high normal heart rate or tachycardia

59
Q

CCB - NDHP -

Drugs?

A

veramapil and diltaiazem

class IV antihypertensive

60
Q

CCB - NDHP MOA:

A

Class IV (FOR VERAPAMILonly? maybe?)

1) “slow” inward Ca channels in nodal tissue are primarily affected
2) decreased SA automaticity = decreased HR
3) decreased conduction = increased PR interval
4) cardiac depression (dec ventricular contractility and dec HR)
5) no effect on ventricular Na conduction - ineffective on ventricular arrhythmia

61
Q

NDHP CCBs relationship to CAD?

A

CCBs are an alternative to Beta blockers - prolongation of PR interval bc slowed rate of conduction trhoguh AV node – myocardial O2 consumption down

62
Q

Avoid NDHP- CCB use when?

A
  • second or third degree heart block– drug slows down conduction so if there is a block then conduction already sucks
  • **-left ventricular dysfunction
63
Q

NDHP situations with potentially favorable events:

A

reynauds syndrome

  • *migrane headaches
  • *arrhythmias
  • *high normal heart rate or tachycardia
64
Q

NDHP situations with potentially unfavorable effects:

A

peripheral edema

**low normal heart rate

65
Q

NDHP - Drugs?

adverse effects?

A
  • verapamil diltazem
  • headache, plushing diziness ankle edema
  • constipation
  • exacerbate CHF
  • hypotension
  • AV hear block in combo with beta blockers
66
Q

Thiazide diuretics -

MOA for hypertension

A

MOA:

  • inh Na transport predominantly in the distal collecting ducts by blocking the Na/Cl co transporter (NCC - DIF FROM THICK ASCENDING BC K IS NOT TRANSPORTED HERE)
  • some has CAI inhibitory activity
  • increase Ca reabsorption
  • vasodilation- weaker effect that NKCC inhibitors
67
Q

First line HTN with left ventricular dysfunction and/or ischemic stroke use?

A

Thiazide diuretics

68
Q

Thiazides are an add on therapy for which mobidities?

A

CAD, diabetes, and can be added for ischemic stroke disease (but ischemic stroke is ACEI with or without thiazide if you can hopefully recall that…)

69
Q

Avoid thiazide use when:

A

1) prior allergic rxn to sulfa drugs
2) gout
3) hyponatremia
4) hypokalemia
5) pre diabetes

70
Q

Thiazide potentially favorable situations:

A
  • osteoporosis or at increased risk of osteoporosis

- hgih normal K

71
Q

Thiazide potentially unfavorable situations :

A
  • gout
  • pre diabetes-elevated fasting glucose
  • low normal K
72
Q

Beta adrenergic antagonists for HTN

  • DRUGS?
  • REview mechanism
A

-Propanolol, metoprolol pindolol
labetalol
ANTAGONISTS=
HEART: -hits the Beta 1 = dec inotropy and chronotropy, decreased myocardial O2 use; dec renin release
Respiratory: hits B2 = block = increased airway resisitance
EYE: dec aqueous humor production and dec intraoccular pressure
METABOLISM: inh lipolysis; dec glucagon release; inc VLDL; dec HDL

73
Q

Beta adrenergic antagonists for HTN - adverse effects:

A
  • fatigue
  • worse periph vascular disease
  • worse bronchospasms
  • dec sexual func
  • inc incidene of diabetes
  • mask hypoglycemia symptoms
74
Q

Beta adrenergic antagonists for HTN - first line therapy for complicated?

A

CAD and left ventricular dysfunction

75
Q

propanolol selectivity:

A

NON selective

76
Q

metoprolol selectivity?

A

cardio selective

77
Q

pindolol selectivty?

A

ISA - -intrinsic sympathomimetic activity (ISA)

78
Q

labetolol selectivity:

A

mixed alpha and beta

79
Q

Beta adrenergic antagonists for HTN - situations with potentially favorable effects:

A
  • migrane headache
  • tacharrythmia
  • high-normal heart rate or tachycardia
  • hyperthyroidism
  • essential tremor
  • preoperative hypertenison
80
Q

aldosterone antagonisms for HTN – DRUGS:

A

spironolactone and eplerenone

81
Q

aldosterone antagonisms for HTN - MOA:

A

1) diuretic effect: competitively inh the binding of aldosterone to MRs (Aldosterone antagonists) = *less Na uptake & less K excretion
2) additional effects:
a) spironolactone increases probability of survival of heart falure with standard therapy to 45-65%
b) prevent L ventricular remodeling and fibrosis: latter major mech that leads to dev and progression of HF.
c) prevention of sudden cardiac death: by promoting K and Mg loss while inc the incidence of ventric arrhythmia-reduces cardiac fibrosis, inproves HR variability, reduce QT dispersion and reduce early morning rise in HR in pt with HF -less hypokalemia= less sudden death
d) hemodynamic effects: antihypertensive properties - BP reduction also slows the progression LV remodeling and incidence of cardiovascl events
3) Vascular effects:
a) decreased vascular NADPH oxidase activity
b) reduced generation of reactive oxygen species
c) reversal of endthelial dysfunction - spironolactone inc NO bioactivity = improves vasodilator dysfunction and slows thrombotic response to injury

82
Q

aldosterone antagonisms for HTN - roles?

A

-mostly as add on therapy for resistant HTN, CAD or left ventricular dysfunction

83
Q

aldosterone antagonisms for HTN - situation with potentially favorable effects:

A
  • low normal potassium

- CKD - early stage more helpful than late/end

84
Q

aldosterone antagonisms for HTN - situation with potentially unfavorable effects:

A

High-normal K

85
Q

very good effect to prevent cardiac remodeling in HF or long time HTN

A

aldosterone antagonists

86
Q

other agents for treatment of HTN (NOT REDUCE RISK OF CV EVENT):

A
  • alpha blockers
  • artieral vasodil
  • central alpha 2
  • direct renin inh
  • rauwolfia alkaloids
87
Q

other agents for HTN - alpha1

-drugs? MOA?

A
  • prazosin, doxazosin, terazosin
  • selective antagonist at vascular smooth muscle a1 receptors
  • a1»»»»a2
88
Q

other agents for HTN - alpha1 blockers

-adverse effects:

A
  • mild tolerance development to antihypertensive effect
  • mild reflex tachycardia
  • sexual dysfunction
89
Q

other agents for HTN - central alpha2 agonists

  • which drugs?
  • MOA?
A
  • clonidine & alpha-methyldopa

- activate central alpha 2 receptors = dec central sympathetic out flow(=decreased release of NE) = dec BP

90
Q

Most commonly prescribed antihypertensive?

A

cetnral alpha2 agonists
-alpha methyldopa
clonidine

91
Q

whcih central alpha2 agonist can be used transdermal/patch? good for?

A
  • clonidine

- good for: liable HTN; hospitalized pts who cannot take orally; pt who are prone to early morning surges in BP

92
Q

Role of alpha-methyldopa?

Which category?

A
  • alpha2 agonist - central!

- exclusively used in gestational hypertension and in the management of chronic hypertension in pregnancy bc its safe

93
Q

alpha methyldopa - MOA?

-adverse effects?

A
  • stimulatescentral alpha 2 = decreased NE release

- adverse: fewer anticholinergic side effects; hepatotox; direct combs test

94
Q

Hydralazine

  • what kind of drug?
  • MOA?
A
  • arterial vasodilator - act directly on the vessel!
  • IP3 induced Ca release from smooth muscle SR –> dec contraction
  • opens Ca activated K channels in smoo`th muscle (hyperpolarization) = relaxation
  • relaxes arterioles/no effect on veins
95
Q

Hydralazine-

  • drug type?
  • adverse effects:
A
  • arterial vasodilator
  • drug induced lupus with long term use
  • compensatory tachycardia and Na retention when used for chronic hypertension hydralazine should be used in combo with diuretic and beta blocker or NDHP to fix these effects
96
Q

Minoxidil

  • what kind of drug?
  • MOA?
A
  • arterial vasodilator
  • MOA: K_ATP channel opener: activates ATP dependent K channels –> relaxes arteriolar VSMCs (vascular smooth msucle cells)- no effect on veins
  • does not inh Ca release from sarcoplasmic reticulum
97
Q

Minoxidil- CV effects?

A
  • decrease BP
  • increase blood flow to the heart, Skin, skeletal muscles, GI and CNS
  • inc CO
  • inc RBF
98
Q

WHcih drug is used only for severe refractory hypertension?

A

**minoxidil - used in combo with B-blockers or diuretics

99
Q

minoxidil - adverse effects:

A
  • fluid and salt retention
  • *-reflex increase in myocardial contractility
  • hypertrichosis
100
Q

Na nitroprusside-

used for what? how administered?

A

-IV agent used in hypertensive emergencies and the rapid management of CHF

101
Q

Sodium Nitroprusside MOA:

A

donates NO hich activate soluble guanylyl cyclase, leading to cGMP mediated Ca sequestration in vascular smooth msucle resutls in:

a) very potent vasodilator with rapid onset and short duration of action (1-10 min)
* *b) decreases both afterload and preload (venodilation)

102
Q

sodium nitroprusside - Adverse effect:

A
  • methemoglobinemia
  • cyanide poisoning
  • cell death due to inh of cellular respiration
103
Q

Direct renin inhibitor-

Drug? MOA?

A
  • only drug is aliskiren

- MOA: binds directlymt the catalytic site of renin = cant cleave angiotensinogen to generate angI = lower BP

104
Q

Direct renin inh is most efficacious to lower BP wehn?

A

used with a thiazide, ACEI ARB or CCB

105
Q

Direct renin inh-

adverse effects

A
  • can cause **hyperkalemia in pt with CKD and diabetes or those receiving a K sparing diuretic, ARBs
  • can cause acute kidney failure in pt with severe bilat renal artery stenosis
  • *-NEVER USE IN PREGNANCY
  • half dose for pateitns with risk for orthostatic HTN
106
Q

Rauwolfia Alkaloids DRUG?

A

reserpine -

107
Q

Rauwolfia Alkaloids - DRUG? MOA?

A
  • reserpine
  • blocks transport of NE into storage granules
  • depletes NE from sympathetic nerve endings –> dec sympathetic tone ; dec PVR = dec BP
  • depletes chatecholamines in brain and myocardium = sedation, depression and dec cardiac output
108
Q

Most effective use of rauwolfia alkaloids?

A
  • (reserpine)
  • use in combo with thaizide to mitigate related Na and H2O retention
  • not usually used for HTN
109
Q

Reserpine - side effects:

A
  • sedation
  • deperssion
  • dec CO
  • orthostatic hTN
  • dec symp = inc parasym results in nasal stuffiness, inc gastric acid secretion, diarrhea, bradycardia
  • use low doses to minimize side effects
110
Q

most common cause of resistant HTN (not responding to treatment)?

A

inadequate dosing of diuretics

111
Q

Mineralocorticoid used to treat resistant HTN? this drug is usually used with which other drug(s)?

A
  • spironolactone

- used with a RAS blocker aka (ACEI or ARB)

112
Q

amiloride

  • MOA?
  • adverse effect/
A
  • directly blocks epithelial Na channel (ENaC)

- increases in serum K and creatinine

113
Q

**selective renal artery catheterization- What does it do? used to treat what?

A
  • low power radiofreq treatment along renal arteries to de-nervate both kidneys
  • reduce BP in patients with Resitant HTN (RHTN)
114
Q

Baroreflex activation therapy

  • review baroreceptor mech
  • how does this therapy work?
A
  • inc baro firing = dec symp and inc parasym tone = dec peripheral vascular resistance, heart rate, SV, and BP
  • electrical stimulation with implantable device
115
Q

HTN & PREGO - ADV/DISADV:

labetalol

A
  • **adv: safe -prefered over beta blcokers (bc alpha blockade helps uteroplacental blood flow)
    disadv: short duration and bid or tid dosing
116
Q

HTN & PREGO - ADV/DISADV:

Methyldopa

A

***Adv: saFE

Disav: short duration and bid or tid dosing

117
Q

HTN & PREGO - ADV/DISADV:

long-acting nifedipine

A

adv: safe

118
Q

HTN & PREGO - ADV/DISADV:

hydralazine

A
  • ***disadv: inc risk of maternal hypotension and placental abruption when used acutely
  • **adv: extensive clinical experience
119
Q

HTN & PREGO - ADV/DISADV:

metoprolol

A

adv: once day dosing for long acting
disadv: not a lot of data

120
Q

HTN & PREGO - ADV/DISADV:

diuretics

A

-Generally avoided- may impair pregancy associated expansion in plasma volume

121
Q

HTN & PREGO - ADV/DISADV:

atenolol

A

-Generally avoided- may impair fetal growth

122
Q

HTN & PREGO - ADV/DISADV:

nitroprusside

A

-Generally avoided- risk of fetal cyanide pisoning if used for more than 4hrs

123
Q

HTN & PREGO - ADV/DISADV:

ACEI

A

-contraindicated-mutliple fetal anomalie

124
Q

HTN & PREGO - ADV/DISADV:

ARBs

A

-contraindicated-mutliple fetal anomalie

125
Q

oarl use only for severe refractory HTN?

A

minoxidil

126
Q

CAn use in patient with MI?

A

sodium nitroprusside - dec both afterload and preload

127
Q

preferred diuretic for RHTN?

A

clorthalidone - more potent, longer duration, gerater BP reduction than hydrchlorothiazide

128
Q

drug to give that helps reverse CV remodeling?

A

spironolactone

129
Q

drugs that improve remodeling of the heart:

A

ACEI
ARB
Spironolactone

130
Q

Drugs that decrease PRELOAD? AFTERLOAD? BOTH? MOA?

A

Might be a good thing to look up…

AFTERLOAD:
-minoxidine-K_ATP channels open = smooth muscle relax
-hydralazine - IP3 release of Ca –> Ca dependend K channels open = hyperpolarization and relaxation
-DHPs
BOTH:
-sodium nitroprusside - donates NO –> activates sol GC –> Ca sequestration = relax smooth muscle bc no calcium = vasodilation of both arteries and veins

131
Q

hypertensive emergency give?

A

sodium nitroprussion IV

132
Q

Never use in pregnancy:

OK for pregnancy?

A

ACEI
ARB
direct renin

OK=alpha methyldopa, hydralazine

133
Q

drug induced lupus with use?

A

hydralazine

procainamide

Pharm - Cardiovascular (6 decks)

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