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Pharm Exam I > Antihypertensives Day I > Flashcards

Antihypertensives Day I Flashcards

1
Q

lifetime risk for HTN

A

90%

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2
Q

HTN is a risk factor for what diseases

A

heart dz
stroke
heart failure
renal dz

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3
Q

examples of how HTN develops:

A

sex, stress, genetics, sympathetic stimulation, CO, renal sodium retention, GI - obesity, alcohol, micronutrients, insulin, aldosterone, age

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4
Q

risk factors for HTN

A

smoking, BMI >30, physical inactivity, dyslipidemia, DM, renal dysfunction, men >55 women >65, family hx of premature CV dz

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5
Q

ages of men vs women for risk factors of HTN

A

men >55 women >65

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6
Q

BMI of what increases risk of HTN

A

> /=30

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7
Q

2 types of HTN

A

essential & secondary

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8
Q

what is essential HTN

A

natural process causing HTN - 90% of cases

usually a hereditary component

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9
Q

what is secondary HTN

A

caused by other disease state: chronic kidney dz, renovascular dz, cocaine, tumor, natural supplements

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10
Q

what is systolic BP

A

number that represents the cardiac contraction

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11
Q

what is diastolic BP

A

number that represents nadir (lowest point) aka filling of heart

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12
Q

what is cardiac output

A

amount of blood pumped out by ventricles (represents SBP)

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13
Q

what is TPR

A

total peripheral resistance

sum of peripheral resistance in peripheral vasculature (represents DBP)

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14
Q

equation for BP

A

BP = CO x TPR

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15
Q

2 major mechanisms of pathogenesis of HTN

A
  1. increase in peripheral resistance

2. increased CO

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16
Q

how is increased peripheral resistance a mechanism of pathogenesis of HTN

A

functional vascular constriction/structural vascular hypertrophy
-over activity of sympathtetic nervous system (NOR, EPI) & genetic components

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17
Q

how is increased cardiac output a mechanism of pathgenesis for HTN

A
  1. increased preload - increased fluid, excess sodium intake, renal sodium retention
  2. venous constriction - excess RAAs stimulation, sympathetic nervous system overactivity
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18
Q

majority of pts will require how many meds to control HTN

A

at least two

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19
Q

life style modifications for HTN

A

stop smoking, weight loss, DASH diet, dietary sodium reduction, increased physical activity, limit alcohol (1/female, 2/male)

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20
Q

what is the most effective life style modification to lower HTN

A

weight loss - pts wont change everything at once so pick this major one to focus on and give small goals at a time

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21
Q

firstline options for HTN (4)

A
  1. thiazides
  2. CCB’s
  3. ACE-I
  4. ARBs
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22
Q

which of the first line choices for HTN is best?

A

none, all of the four classes are equally efficacious

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23
Q

which of the first line drugs are not the best choice for blacks

A

ACE-I and ARBs - response is completely different than other races

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24
Q

patients with HTN that also have DM or renal dz first line choices

A

ACE-I or ARBs –> even in blacks

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25
Q

can ACE-I and ARBs be used together

A

NO - increases renal failure

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26
Q

if pt has a cardiac hx and HTN what else can you use

A

beta blocker

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27
Q

3 options for treatment approach to HTN

A
  1. 1 drug - max out dose before adding next drug
    (used if pt absolutely does not want to be on more than one drug)
  2. 1 drug then add 2nd drug prior to maxing out doses, then 3rd
    (used most - bc most pts need 2 drugs to fix HTN, so start asap with 2)
  3. start 2 drugs only if SBP >160 and DBP is >100 - max out doses then 3rd drug
    (for exam purposes only - in real life, still would start only one at a time in case of rxn you know which drug is causing it)
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28
Q

3 examples of thiazide diuretics

A

HCTZ, chlorthalidone, metolzaone

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29
Q

MOA of thiazide diuretics

A

inhibit sodium reabsorption in the distal tubule

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30
Q

which thiazide diuretic is the most potent

A

metolzaone - rarely used except for lasix resistance, only one dose needed

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31
Q

where do thiazide diuretics work in the kidney

A

DCT

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32
Q

typical dose of thiazide diuretics

A

25mg most efficacious
can start at 12.5 but doesn’t do much
50mg - increases side effects with little increase in efficacy

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33
Q

ADE of thiazide diuretics

A

orthostatic hypotension (minimal in comparison)
electrolyte abnormalities
photosensitivity
increase in urination

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34
Q

what electrolyte abnormalities come with thiazide diuretics

A

decrease: K, Na
increase: Ca, uric acid, glucose (minimal)

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35
Q

precautions (not CI’s of thiazide diuretics)

A
  1. caution in sulfa allergies (contraindication if anaphylaxis otherwise, monitor)
  2. ineffective in pts with severe renal dz CrCl
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36
Q

examples of ACE inhibitors

A

benazepril, captopril, enalapril, fosinopril, lisinopril (main one used)

= the ‘prils

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37
Q

MOA of ACE inhibitors (3)

A

inhibits ACE to block production of AT II
inhibits breakdown of bradykinin (vasodilator)
dilates the efferent arteriole of kidney - positive effect - good for renal or DM pts

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38
Q

benefits of ACE-I on bradykinin (1)

disadvantages of ACE-I on bradykinin

A

benefit: lowers BP
disadvantage: inflammatory mediator = increase inflammation = cough

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39
Q

place in therapy for ACE inhibitors

A

a first line drug for HTN
first line option in CKD
used in CHF

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40
Q

dose of ACE-I

A

often 1/day sometimes twice/day esp in CHF

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41
Q

what labs to monitor with ACE-I

A

serum K+ and sCr w/i 4 weeks of initiation or dose increase

-normal to see a benign increase in creatinine - kidney getting used to drug (should only be

42
Q

what is angioedema

A

swelling of face lips eyes throat = life threatening = can’t use ACE-I ever again, questionable to use ARBs due to potential for crossreactivity

43
Q

ACE-I and salt substitutes

A

cannot take salt substitutes bc will increase K+ even more (salt substitutes use K instead of Na)

44
Q

ADE of ACE-I

A
  1. cough - up to 20% ( a good amount of pts) due to bradykinin incr
  2. angioedema - rare
  3. hyperkalemia - esp with CKD or DM
  4. other: neutropenia, agranulocytosis, proteinuria, glomerulonephritis, acute renal failure
45
Q

CI’s of ACE-I

A
  1. pregnancy
  2. previous angioedema
  3. bilateral renal artery stenosis - renal toxicity
46
Q

DI’s of ACE-I

A
  1. K+ supplements
  2. K+ sparing diuretics
  3. NSAIDS - can incr BP on its own by constricting prostaglandins in afferent arteriole of kindey - if 1/mo OK, but not if 800mg 3x/day
47
Q

dosing of ACE-I

A

most 1/day - can be dose more than 1/day to incr efficacy

except captopril which is 2-3/day

48
Q

which ACE-I is a prodrug and of what

A

enalapril is a prodrug of enalaprilat

49
Q

which ACE-I is only one available in IV form

A

enalapril

50
Q

most commonly used ACE-I and dosing

A

lisonpril - 10-40mg daily

51
Q

which ACE-I decreases absorption if taken with food

A

captopril

52
Q

least used ACE-I and why

A

captopril - multiple dosing/day and cant take with food

53
Q

what does ARB stand for

A

angiotensin II receptor blockers

54
Q

examples of ARBs

A

irbesartan, losartan, olmesartan, valsartan

= ‘sartans

55
Q

which ARB can cause chronic diarrhea

A

olmesartan

56
Q

MOA of ARBs

A

inhibits angiotensin II at its receptor sites
(AT II is made but blocked)
does not inhibit bradykinin

57
Q

ARBs place in therapy

A

one of first line drugs in HTN
first line option for CKD
used in CHF

58
Q

dose of ARBs

A

once daily

59
Q

labs to monitor with ARBs

A

potassium

60
Q

ADE of ARBs

A

hypotension, orthostatic hypotension, angioedema, hyperkalemia, dizziness

61
Q

CIs of ARBs

A
  1. pregnancy
  2. caution in renal artery stenosis (ACE-I’s is absolute CI)
  3. technically can be used if angioedema present with ACE-I but can be cross reactive so better to just pick something else
62
Q

DIs of ARBs

A

K+ supplements
K+ sparing diuretics
NSAIDS

63
Q

what is the only drug in the renin inhibitor class

A

aliskiren

64
Q

MOA of Aliskiren

A

first oral agent that directly inhibits renin

65
Q

role in treatment for aliskiren

A

unclear with HTN bc new drug

66
Q

downside of aliskiren

A

increased SEs and decreased efficacy

67
Q

ADRs of aliskiren

A

ADRs are similar to ACE-I and similar to ARBs = don’t use together

68
Q

is aliskiren used as monotherapy or combo therapy

A

either

69
Q

CCBs

A

calcium channel blockers

70
Q

2 categories of calcium channel blockers

A
  1. non dihydropyridines

2. dihydropyridines

71
Q

examples of nondihydropyridines

A 
verapamil
diltiazem (has lots of formulations that cannot be interchangeable)
72
Q

examples of dihydropyridines

A

amlodipine (most used)
nifedipine (2nd most)
felodipine
isradipine

73
Q

role of calcium channels in the body

A
  • when channels are opened: causes calcium influx into smooth muscle (cardiac and peripheral vasculature)
  • results in activation of intracellular calcium with ultimately leads to muscle contraction (activates myosin and actin)
74
Q

MOA of CCBs

A

inhibits calcium influx into cells to prevent muscle contraction
inhibition at cardiac smooth muscle (decreases ionotropy & chronotropy)
inhibition at vascular smooth muscle - vasodilation

75
Q

MOA of dihydropyridines

A

inhibits calcium influx into vascular smooth muscle - not the heart = peripheral vasodilation = pooling in feet and legs = edema

**may be used in CHF bc doesn’t work on the heart

76
Q

non dihydropyridines MOA

A

inhibits calcium influx into cardiac smooth muscle

  • decrease rate and force of contraction
  • can’t be used in CHF
77
Q

CCB place in therapy

A

first line option for HTN

78
Q

other uses of CCBs

A
  1. diltiazem and verapamil - supraventricular tachycardia, atrial fibrillation
  2. verapamil - migraine prophylaxis
79
Q

ADE of all CCB

A

hypotension

80
Q

ADR of non dihydropyridines

A
  1. constipation **
  2. bradycardia
  3. exacerbation of CHF
  4. heart block
  5. gingival hyperplasia
81
Q

ADEs of dihydropyridines

A
  1. peripheral edema - worst with nifedipine - dose effect (incr with dose)
  2. reflex tachycardia
  3. flushing
  4. H/A
82
Q

DI with verapamil -

A

metabolized by C P450 3A4 and also inhibits

83
Q

dihydropyridines are useful for pts with

A

isolated increased SBP

84
Q

Clevidipine I (IV only) is CI in

A

soy or egg allergy

85
Q

1 in how many adults have HTN

A

1 in 3 adults

86
Q

example of loop diuretics

A

furosemide (lasix)
bumetanide
torsemide
**not first line for HTN, just other types of diuretics

87
Q

how do thiazide diuretics and loop diuretics help HTN

A

these do not lower blood pressure

they are good at fluid removal (which indirectly helps lower BP)

88
Q

MOA of loop diuretics

A
  1. inhibits active transport of NA Cl and K in thick ascending lim of loop of Henle causing excretion of these ions
  2. collecting duct excretes more water in response
89
Q

place in therapy for loop diuretics

A
  1. CHF
  2. Edema
  3. HTN - not commonly used for
90
Q

ADE of loop diuretics

A
  1. electrolytes abnormalities
  2. dehydration (peeing too much)
  3. ototoxicity (if combined with other ototoxic drug - aminoglycocides = bad)
  4. increase SCr (if pt is dehydrated, decr dose)
91
Q

what electrolyte abnormalities do loop diuretics cause

A

decr: K, Na, Ca, Mg
incr: uric acid (gout pts)

92
Q

dose of furosemide (lasix)

A

usually 1/day but can be 2/day

if 2/day: every 6 hours (laSIX) both doses before 4 pm (9a & 3p) so that by bedtime, peeing slows

93
Q

precautions with loop diuretics

A

gout pts
sulfa allergic pts
nephrotoxicity

94
Q

2 types of potassium sparing diuretics

A
  1. aldosterone receptor blockers (NOT ARBs)

2. Potassium Sparing Drugs

95
Q

examples of aldosterone receptor blockers

A
  1. spironolactone

2. eplerenone

96
Q

MOA of aldosterone receptor blockers

A

competes with aldosterone prevents sodium reabsorption and potassium excretion (dependent on presence of aldosterone)

97
Q

examples of potassium sparing drugs

A

triamterene

amiloride

98
Q

moa of potassium sparing drugs

A

block sodium reabsorption and potassium excretion, effect independent of aldosterone***

99
Q

where do K sparing diuretics work

A

collecting duct

100
Q

K+ sparing diuretics place in therapy

A 
HTN: in combo with thiazide (not usually monotherapy) not first line
Spironolactone - class IV heart failure (also III) - mortality benefit
101
Q

ADE of K+ spring diuretics

-specifically spironolactone

A

Hyperkalemia (caution in renal failure pts)

spironolactone - gynecomastia, menstrual irregularites

102
Q

use of eplerenone

A

eplerenone - more selective thus less side effects but not used much because most of the research data is with spironolactone

Pharm Exam I (3 decks)

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