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z S1: Module > HTN-1 > Flashcards

HTN-1 Flashcards

1
Q

Normal BP

A

<120/80 mmHg

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2
Q

Elevated BP

A

120-129 mmHg / ≤ 80 mmHG

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3
Q

Stage 1 Hypertension BP

A

≥ 130 mmHg systolic
OR
≥ 80 mmHf diastolic

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4
Q

Stage 2 Hypertension BP

A

≥ 140 mmHg systolic
OR
≥ 90 mmHg diastolic

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5
Q

Hypertensive Urgency / Emergency BP

A

≥ 180 mmHg systolic
OR
≥ 120 mmHg diastolic

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6
Q

What are the hypertension risk factors

A

Age
FH
Smoking
Obesity
Metabolic Syndrome
High alcohol intake
Diabetes
High sodium intake
Dyslipidemia

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7
Q

What are the two major processes that regulate BP

A

-baroreceptors and the sympathetic nervous system
-renin-angiotensin aldosterone system

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8
Q

Pathophysiology of decreased BP on alpha and beta receptors

A

decrease BP
decrease signal to brain
increase sympathetic nervous system
increase catecholamines

alpha increase peripheral resistance
beta effects heart

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9
Q

Pathophysiology of decreased BP in blood volume

A

decrease BP
decrease signal to kidneys
renin -> angio -> angio II vasoconstrictor
aldosterone increases sodium and water

results in higher blood volume

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10
Q

What are the secondary causes of hypertension

A

renal disease
Cushing’s disease
pheochromocytoma
pregnancy
sleep apnea
contraceptives
sympathomimetics
NSAIDs
steroids
SSRIs/SNRIs
cocaine
nicotine
amphetamines
licorice

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11
Q

What is the primary goal of treating hypertension

A

reduce morbidity and mortality by decreasing the risk of target organ damage

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12
Q

What are the best practices for checking BP

A

sit for 5 minutes
no caffeine
arm placement
correct cuff size
check both arms
feet flat on floor
not talking
clothing removed from where cuff placed

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13
Q

Higher CVD risk = more important to have a ______ goal and assure we get there ________

A

tighter
quickly

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14
Q

What is the CV risk for stage 1 hypertension and ASCVD or 10 year CVD risk ≥ 10%

A

high CV risk

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15
Q

What is the CV risk for stage 1 hypertension and no ASCVD and 10-year CVD risk < 10%

A

Low CV risk

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16
Q

What are the ASCVD risks

A

ACS (acute coronary syndrome) CAD (coronary artery syndrome)
PAD (peripheral artery disease)
TIA (transient ischemic attack)
Stroke
MI (myocardial infarction)
Angina (stable or unstable)
CABG or PCI/stent (coronary/arterial revascularization)

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17
Q

What calculation can you use for a patient between the ages of 40-79 to estimate risk of CV event in the next 10 years

A

American College of Cardiology Risk Calculator

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18
Q

If a patient is less than 40 and has 2 or more risk factors included in calculation (smoking, african american, HLD, DM) they are considered what kind of CV risk

A

High CV risk

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19
Q

If a patient has an elevated BP (120-129/<80) what is their recommendations

A

Start with nonpharmacologic therapy, reassess BP in 3-6 months

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20
Q

If a patient has stage 1 hypertension and a high CV risk what is their recommendation

A

-Start with nonpharmacologic and pharmacologic therapy
-Reassess BP in 1 month
-If at goal reassess 3-6 months
-Not at goal reassess for adherence and intensification of therapy

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21
Q

If a patient has stage 1 hypertension and a low CV risk what is their recommendation

A

-Start with nonpharmacologic therapy
-Reassess BP in 3-6 months
-Not at goal consider pharmacologic therapy

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22
Q

If a patient has stage 2 hypertension what is their recommendation

A

-Start with nonpharmacologic and pharmacologic therapy
-Reassess BP in 1 month
-At goal reassess 3-6 months
-Not at goal asses for adherence and consider intensification of therapy

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23
Q

Food considerations for improving BP

A

Na+ restriction
High-fiber and natural foods
Limit high saturated fats
Low-fat dairy products

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24
Q

Lifestyle consideration for improving BP

A

Exercise
Aerobic activity
Dynamic resistance
Isometric resistance
Moderate alcohol
Smoking cessation

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25
Q

cardiac output times peripheral resistance equals

A

blood pressure

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26
Q

What two things effect cardiac output

A

cardiac (heart rate, heart contraction)
volume control (renal renin-angiotension, aldosterone)

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27
Q

What two things effect peripheral resistance

A

sympathetic control (vasoconstrictor, vasodilator)
humoral (catecholamines, prostagandins)

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28
Q

What part of the renal system is not permeable to water

A

distal convoluted tubule

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29
Q

What part of the renal system is not permeable to salt

A

thin descending tubule

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30
Q

Where are thiazide agents located

A

distal convoluted tubule

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31
Q

Where are loop diuretics located

A

thick ascending tubule

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32
Q

Where are potassium sparing agents located

A

collecting tubule

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33
Q

What are diuretics mechanism of action

A

decreases extracellular volume, enhancing sodium excretion in the urine, leading to a decrease in cardiac output

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34
Q

What is the most frequent used class of antihypertensive agents in the US

A

thiazide diuretics

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35
Q

Results of thiazide diuretics

A

high K+ secretion causing hypokalemic because K+ is not reabsorbed

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36
Q

What drug class do these belong to:
hydrochlorothiazide (hydrodiuril)
chlorthalidone (hygroton)
Indapamide
Metolazone

A

thiazide diuretics

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37
Q

What is the GFR goal of kidneys

A

<30 ml/min

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38
Q

ACE and ARBs will ________ diuretic induced loss of K+

A

counteract

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39
Q

Hydrochlorothiazide primary and secondary site

A

primary: kidney
secondary: vascular smooth muscle cells

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40
Q

What drug class do these belong to:
furosemide (lasix)
bumetanide (bumex)
ethacrynic acid (edecrin)
torsemide (demadex)

A

Loop diuretic
(block Na/K/Cl

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41
Q

What diuretics is the highest capacity especially if renal function is not normal and has the highest capacity Na/Cl/K pump

A

loop diuretics (twice a day medications for hypertension, heart failure, and ascites)

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42
Q

Loop diuretics increase the urinary secretion of what ions

A

na
cl
ca
mg
K+

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43
Q

What drug class do these belong to:
amiloride (midamor)
triamterene (dyrenium)

A

potassium sparing channel blockers

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44
Q

What drug class do these belong to:
spironolactone (aldactone)
eplerenone (inspra)

A

potassium sparing receptor blockers

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45
Q

What class of diuretic can you not use with ACE and ARBs

A

potassium sparing

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46
Q

What is the function of potassium sparing channel blockers

A

block pore of the epithelial sodium channel
(decrease volume, hyperkalemic)

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47
Q

What is the function of potassium sparing receptor blockers

A

steroid hormone produced by adrenal gland
regulate Na+, K+, and acid/base balance in blood

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48
Q

Potassium sparing diuretics ________ transepithelial _____ transport

A

enhances
NaCl

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49
Q

ACE inhibition

A

-BP is decreased due to decrease in blood volume, peripheral resistance and cardiac load
-inhibit vasoconstriction and release of aldosterone which inhibits the retention of sodium and water

50
Q

What does ACE inhibition do to bradykinin

A

increases it

51
Q

What do all ACE inhibitors end in

A

“-pril”

52
Q

What do ACE-I treat

A

chronic renal disease
aldosterone (they tend to enhance the efficacy of diuretic drugs)
young middle-aged Caucasians

53
Q

Adverse effects of ACE-I

A

-rise in serum K+
-caution with K+-sparing diuretics, K+ supplements, NSAIDs, beta-blockers
-bradykinin: dry cough, angioedema
-dysgeusia
-contradicted with pregnancy

54
Q

ARBs do not inhibit ACE-mediated degradation of ___________

A

bradykinin

55
Q

What do all AT1 receptor blockers end in

A

“-sartan”

56
Q

What do AT1 and AT2 do

A

AT1: vascular, myocardial tissue, kidney, brain, and adrenal glomerulosa cells
AT2: adrenal medulla, kidney, CNS

57
Q

What are the three steps of AT1 receptor activation

A

Altered Peripheral Resistance (direct vasoconstriction, enhance sympathetic discharge)

Altered Renal Function (increase Na+ reabsorption in the proximal tubule and distal tubule)

Altered Cardiac Function (relax smooth muscle to promote vasodilation, increase salt and water secretion, reduce plasma volume decreasing cellular hypertrophy)

58
Q

AT1 receptor blockers treatment

A

high angiotenstion II: volume depketion, renovascular hypertension, cardiac function, cirrhosis
no bradykinin
not effective in old, blacks, low-renin patients

59
Q

Adverse effects of AT1 receptors

A

insignificant rise in serum K+ (hyperkalemia)
contraindicated in pregnancy

60
Q

Aliskiren hemifuramate (tekturna)

A

-inhibits the catalytic activity of renin producing Ang1, Ang2, aldosterone which decreases BP
-systolic and diastolyic
-monotherapy and combo therapy
-contraindicated in pregnancy

61
Q

When do you start two medicines for hypertension

A

> 30 mmHg above systolic or >20 mmHg diastolic
African American: >20mmHg above systolic or >10mmHG diastolic

62
Q

What numbers of BP is a hypertension emergency

A

> 180 systolic or >120 diastolic

63
Q

What medicine to use for systolic heart failure (SHF/CHF)

A

ACE and beta blocker

64
Q

What medicine to use for post-MI

A

ACE-I and beta blocker

65
Q

What medicine to use for diabetes with albuminuria

A

ACE-I or ARB

66
Q

What medicine to use for CKD with albuminuria

A

ACE-I or ARB

67
Q

What medicine to use for stroke

A

ACE-I or ARB

68
Q

If there are no compelling indications for hypertension what are the trifecta of choices to use

A

thiazide diuretics (-pine)
ACE-I and ARBs
Calcium Channel Blockers

69
Q

If patients are over 60 or black what is the recommended medication class to use

A

thiazide or calcium channel blocker
(beta blocker NOT recommended)

70
Q

What do alpha blockers cause

A

orthostatic hypotension
(important to titrate slow and start low)

71
Q

Central alpha 2 agonists

A

Only for resistant hypertension or hypertensive emergency
ADRs don’t go away (adverse drug reaction)
Avoid in HF
Alcohol dependence
ADHD ER formulation
Methyldopa used in pregnancy

72
Q

Vasodilators

A

Resistant HTN (systolic)
Use with diuretic to decrease fluid retention

73
Q

Moderate dose of 2 or more medications are _____ effective than high doses of one medication

A

more

74
Q

Thiazides and CCBs cause ____ excretion and vasodilation

A

Na+

75
Q

ACE-I and ARBs improve ____-induced edema by causing venule dilations

A

CCB (calcium channel blocker)

76
Q

ACE and ARBs may improve ___________ from thiazides

A

hypokalemia

77
Q

When should a follow-up be after starting/changing therapy

A

2-4 weeks

78
Q

When should a follow-up be if BP is stable and controlled

A

3-6 months

79
Q

Diuretics increase the excretion of electrolytes and water from the body ______ affecting protein, vitamin, glucose, or amino acid reabsorption

A

without

80
Q

Diuretics are used to treat _____ and hypertension

A

edema

81
Q

What is the primary target organ of diuretics where they interfere with reabsorption of ions

A

kindey

82
Q

What are osmotics site of action and mechanism of action

A

Site: proximal tubule
mechanism: osmotic effects decrease sodium and water reabsorption

83
Q

What are carbonic anhydrase inhibitors site of action and mechanism of action

A

site: proximal convoluted tubule
mechanism: inhibition of renal carbonic anhydrase decreases sodium bicarbonate reabsorption

84
Q

What are thiazides site of action and mechanism of action

A

site: thick ascending loop and distal tubule
mechanism: inhibit na/cl symporter

85
Q

What are loop or high ceiling site of action and mechanism of action

A

site: thick ascending limb
mechanism: inhibit na/k/cl transport system

86
Q

What are potassium-sparing site of action and mechanism of action

A

site: distal tubule and collecting duct
mechanism: inhibit sodium and water reabsorption by competitive inhibition of aldosterone or blockage of sodium channels

87
Q

What are osmotics MOA

A

decrease na and h2o reabsorption

88
Q

Osmotics are ______ polar and have a ______ molecular weight

A

highly
low

89
Q

Are osmotics secreted as charged or uncharged parent drugs

A

uncharged

90
Q

Carbonic anhydrase inhibitors MOA

A

inhibit carbonic anhydrase which decreases H+ exchange for Na+ ion in the kidney. Lose Na, HCO3, and H2O

91
Q

Carbonic anhydrase inhibitors treat what

A

glaucoma and acidify urine (result in metabolic acidiosis)

92
Q

Sulfonamides are ______ and are common with all CAIs

A

acidic

93
Q

Methyls improve ________

A

lipophilicity

94
Q

Secondary aliphatic amines _______ water solubility

A

increase

95
Q

An ionizable amino group cause ______ water solubility

A

higher

96
Q

MOA of thiazides

A

compete for Cl- binding of Na/Cl symport which inhibits reabsorption of Na and Cl ions -> hyponatremia, hypokalemia, hypomagnesia

97
Q

In thiazides what group is important at position 6

A

EWG

98
Q

In thiazides what is present at position 3 and 4

A

double bond to make them more active

99
Q

In thiazides what is at position 3 to increase a longer duration of action

A

alkyls to increase lipid solubility

100
Q

What is the duration of action of loops or high ceiling diuretics

A

short duration of action to cause excretions of ions

101
Q

What is the only loop without sulfur

A

ethacrynic

102
Q

MOA of loops

A

Inhibit Na/K/Cl symporter, may alter warfarin, ototoxicity with ethacrynic acid

103
Q

Potassium Sparing side effects

A

do not use with ACE-I or ARBs
sexual side effects due to nonselective binding receptors

104
Q

What is present at position 9 or 11 in potassium sparing

A

epoxide

105
Q

What is replaced at position 7 in potassium sparing diuretics

A

thioester with ester

106
Q

What is present at position 17 in potassium-sparing diuretics

A

gamma lactone ring

107
Q

What is MOA of potassium-sparing diuretics

A

bind to negatively charged regions of Na channel (weak bases)

108
Q

What do ACE-I’s cut

A

dipeptides

109
Q

ACE needs zinc in order to do what

A

bind by ionic bond with amines then zinc helps dipeptide cleavage, hydrogen bond between substrate and ACE

110
Q

ACE-I have _____ bioavailability and undergo phase 1 metabolism by ________

A

low
esterases

111
Q

What ring minics the C-terminal in ACE-I

A

N-ring

112
Q

Large hydrophobic rings ______ potency

A

increase

113
Q

___________ group is best for zinc binding in ACE-I because they shorten duration of action

A

sulfhydryl

114
Q

Esterification produces orally bioavailable prodrugs in ACE-I because zinc binding to which two groups is optimal

A

carboxylate
phosphinate

115
Q

ACE-I are usually acidic excepts for which two drugs because they contain amines

A

captopril
fosinopril

116
Q

In ARBs esters need to be _______ in order to produce a free acid

A

hydrolyzed

117
Q

ARBs need an _______ group

A

acidic and it has to be ortho

118
Q

The tetrazole ring in ARBs need to be ______

A

ionized

119
Q

Incomplete absorption in ARBs results in _____ lipid solubility and _____ bioavailability because the drug is unchanged

A

low
low

120
Q

Renin Inhibitors MOA

A

enzyme secreted by kidneys to decrease glomerular filtration rate resulting in low BP

121
Q

What functional group do you want in renin inhibitors to mimic their sites

A

isopropyl

z S1: Module (8 decks)

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