Hypertension Kaakeh Exam 3 Flashcards

1
Q

True or false: Low sodium intake and high potassium intake are both risk factors for developing HTN.

A

False–its the other way around. High sodium, low potassium intake.

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2
Q

Which gender has a higher prevalence of HTN 45yo?

A

Male 45

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3
Q

Name other risk factors for developing HTN.

A

Elderly age, AA ethnicity, obesity, excess alcohol intake, genetic predisposition.

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4
Q

What technique must be used to diagnose HTN?

A

Two readings at least 5 minutes apart, sitting in chair, confirmed in contralateral arm.

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5
Q

What BP measurement techniques may help to evaluate “white coat” HTN?

A

Ambulatory BP monitoring and self-monitoring

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6
Q

What stage of hypertension does 135/94 fall into?

A

Stage 1 because of diastolic BP

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7
Q

An increase of 20/10mmHg ____ the risk of CVD over 115/75.

A

doubles

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8
Q

What is the number needed to treat to prevent 1 death by lowering BP was 10mmHG over 10 years?

A

11

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9
Q

Humoral, neuronal, vascular endothelial, electrolyte regulation defect, and peripheral autoregulation defect are all theories regarding the cause of _____ HTN.

A

Primary

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10
Q

Name causes of secondary HTN.

A

Sleep apnea, CKD, renal artery stenosis, chronic steroid therapy, cushing’s syndrome, primary aldosteronism, pheochromocytoma, coarctation of the aorta, thyroid disease, parathyroid disease, food, drugs.

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11
Q

What OTC drugs can elevate BP?

A

NSAIDs, pseudoephedrine, ephedrine, high sodium meds, licorice, cocaine, ketamine, caffeine, nicotine, ecstasy, smokeless tobacco, some herbals.

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12
Q

What Rx drugs can elevate BP?

A

NSAIDs, corticosteroids, estrogens, OCs, sympathomimetics, erythropoietin, ketoocnazole, others!

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13
Q

Patinet KJ has HTN that is still uncontrolled even with three medications and you discovered that she is hypokalemic. She also has a father with HTN diagnosed at 35. What should KJ be tested for?

A

Primary aldosteronism.

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14
Q

How is primary aldosteronism treated?

A

Pretreatment for 3-4 weeks with spironolactone 100mg-400mg PO once daily, then surgical removal of adrenal tumor.

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15
Q

Which is usually harder to pick up on–HTN secondary to hyperthyroidism or hypothyroidism?

A

HTN secondary to hypothyroidism–HTN secondary to hyperthyroidism usually shows obvious signs of thyrotoxicosis. Hypothyroidism mechanism mediated by local control failure as basal metabolism falls–vasoconstriction.

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16
Q

What drug class primarily affects SV?

A

Diuretics

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17
Q

What drug classes primarily affect HR?

A

Beta blockers, non-DHP CCBs

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18
Q

What drug classes primarily affect peripheral resistance?

A

ACEIs, ARBs, hydralazine, sympatholytics.

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19
Q

How do you calculate MAP?

A

1/3(SBP) + 2/3(DBP) – especially important in ICU/CCU, septic shock, head injury, AAA

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20
Q

What are the five target organs that can be hurt by elevated BP?

A

Heart (CHD, CHF, LVH), brain (hemorrhage, TIA), eye (retinopathy, AV nicking), kidney (renal failure, CKD, proteinuria), blood vessels (PVD, AAA)

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21
Q

Why should we care about prehypertension?

A

Because prehypertension alone raises the risk of stroke by about 50%. Also may lead to HTN.

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22
Q

Which guideline was more aggressive–JNC7 or JNC8?

A

JNC 7

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23
Q

When should you consider a 2-drug combination, according to JNC7? According to JNC8?

A

JNC7: when patient is in stage 2 HTN
JNC8: same or SBP >20mmHg above and DBP >10mmHg above

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24
Q

What was the drug class of choice in JNC7?

A

Thiazide diuretics

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25
Q

What are the preferred drug classes in CKD? (JNC7)

A

ACEI/ARBs

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26
Q

What are the preferred drug classes in heart failure? (JNC7)

A

Thiazides, BBs, ACE/ARB, aldosterone antagonist

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27
Q

What are the preferred drug classes post-MI? (JNC7)

A

BB, ACEI, aldosterone antagonist

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28
Q

What are the preferred drug classes in recurrent stroke prevention? (JNC7)

A

Thiazides, ACEIs

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29
Q

What are the preferred drug classes in diabetes? (JNC7)

A

ACEI/ARB, maybe CCB

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30
Q

Which blood pressure is more important in predicting CVD risk according to JNC7?

A

Systolic

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31
Q

Which HTN guideline had a more stringent selection process for clinical trials included and graded recommendations?

A

JNC8

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32
Q

Which HTN guideline included lifestyle modifications and compelling indications?

A

JNC7

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33
Q

Which HTN guideline addressed racial, CKD, and diabetic subgroups?

A

JNC8

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34
Q

Which HTN guideline addressed secondary HTN and resistant HTN?

A

JNC7

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35
Q

Which HTN guideline has a higher treatment goal for patients > or = 60 years old? What is that goal?

A

JNC8;

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36
Q

What is the blood pressure goal in all other patients except those >/= 60 years old without comorbidities?

A
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37
Q

What are the four first-line drug classes according to JNC8?

A

Thiazide diuretics, ACEIs, ARBs, CCBs

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38
Q

What initial treatment should be used in the black population?

A

Thiazide diuretics or CCBs (if no DM/CKD)

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39
Q

What drug classes are recommended with CKD, regardless of race of DM status?

A

ACEI or ARB

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40
Q

What drug classes are recommended with DM, regardless of race or CKD status?

A

ACEI or ARB

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41
Q

Why might chlorthalidone be used over HCTZ?

A

More potent, longer half-life, shown to reduced morbidity/mortality in literature. However, might be more expensive.

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42
Q

According to JNC8, when should BP be assessed after initial treatment?

A

1 month after–can either increase dose or add 2nd

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43
Q

What first line therapies should not be used together?

A

ACEIs and ARBs

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44
Q

When should you consider other second-line classes of drugs?

A

If goal not met with 3 medications, or if contraindication to a class.

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45
Q

There are five main targets of non-pharmacologic therapy: weight reduction, DASH diet, dietary sodium reduction, aerobic physical activity, and moderation of alcohol consumption. Which of these can have the greatest impact on blood pressure?

A

Weight reduction – 5-20mmHg/10kg lost

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46
Q

What is the recommendation for alcohol limitation in men? women?

A

Men: 2 or less drinks per day
Women: 1 or less drinks per day

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47
Q

What is the goal for aerobic physical activity?

A

30 minutes per day, most days of the week

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48
Q

What foods are emphasized on the DASH diet? Which are limited?

A

Increase vegetables, fruits, fat-free or low-fat dairy, whole grains, fish, poultry, beans, seeds, nuts, veggie oil
Decrease sodium, sweets, sugary beverages, red meats

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49
Q

What is the sodium intake recommendation for most patients?

A
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50
Q

What is the sodium intake recommendation for patients over 51 years old, with HTN, with DM, with CKD, or black descent?

A
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51
Q

What first line HTN therapy may be beneficial in osteoporosis?

A

Thiazide diuretics

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52
Q

What are some negative effects of thiazides?

A

DM, gout, renal insufficiency, hyponatremia, effect on lipids

53
Q

When should thiazides be dosed?

A

In morning to avoid initial noctural diuresis.

54
Q

At what CrCl are loops more effective?

A
55
Q

What is an appropriate initial dose of chlorthalidone? Max dose?

A

Initial: 12.5 mg/day
MAX: 100 mg/day (clinical max closer to 25-50)

56
Q

Why should addition of another agent be considered when increasing a thiazide dose?

A

Dose response curve plateaus–not necessarily more efficaceous.

57
Q

What are potential adverse effects of thiazides?

A

Hypokalemia, hypomagnesemia, hypercalcemia, hyperuricemia, hyperglycemia, hyperlipidemia, sexual dysfunction. Lithium toxicity.
CI: sulfa allergy, anuria

58
Q

What is the name of the primary clinical trial that showed reduction in fatal CHD, nonfatal MI, HF, and stroke with thiazides?

A

ALLHAT – basis of thiazide recommendation in JNC7

59
Q

What loop diuretic is not contraindicated in sulfa allergy? Why is it not preferred?

A

Ethacrynic acid; higher incidence ototoxicity

60
Q

Which of the workhorse diuretics does not come to equilibrium and lose its diuretic effect after a few weeks?

A

Loop diuretics

61
Q

What is an appropriate initial dose of furosemide? Max?

A

Initial: 20mg in 1-2 doses
MAX: 80mg in 1-2 doses

62
Q

What is the initial dose of torsemide? Max?

A

Initial: 2.5mg/day
MAX: 10mg/day

63
Q

What is the initial dose of bumetanide? Max?

A

Initial: 0.5mg in 1-2 doses
MAX: 2mg in 1-2 doses

64
Q

What is the initial dose of ethacrynic acid? Max?

A

Initial: 50mg in 1-2 doses
MAX: 200mg BID

65
Q

What are adverse effects of loop diuretics?

A

Hypokalemia, hypomagnesiemia, hypocalcemia, ototoxocity, hyperuricemia, sulfa allergy.

66
Q

Why are potassium-sparing diuretics generally reserved for diuretic-induced hypokalemia patients?

A

Because they are weak diuretics and only really used in combination for hypokalemia benefit.

67
Q

How is amiloride dosed initially? Max?

A

Initial: 5mg/day
MAX: 20mg/day

68
Q

How is triamterene dosed as monotherapy? In combination? Max?

A

Monotherapy initial: 100mg in 1-2 doses
Combination initial: 37.5mg, 1-2 times a day
MAX: 300mg/day

69
Q

What are adverse effects of potassium sparing diuretics?

A

Hyperkalemia (esp in combo with ACEI/ARB/K supplements). Avoid in CKD/DM patients.

70
Q

How is spironolactone dosed initially? Max?

A

Initial: 12.5mg/day
MAX: 50mg/day in 1-2 divided doses

71
Q

How is eplerenone dosed initially? Max?

A

Initial: 50mg/day
MAX: 50mg BID

72
Q

In what patients is eplerenone contraindicated?

A

Patients with T2DM and proteinuria, CrCl

73
Q

What are adverse effects of aldosterone antagonists?

A

Hyperkalemia (esp with ACEI/ARB/K+ supp), avoid in CKD/DM, gynecomastic with spironolactone.

74
Q

What is a common cause of diuretic resistance?

A

NSAID coadministration

75
Q

What are common drug interactions with diuretics?

A

Digitalis, lithium, ACE/ARB (with K sparing), corticosteroids, NSAIDs, etc.

76
Q

What should patients starting diuretic therapy be educated on?

A

Encourage lifestyle modifications, check BP frequently, take in AM to avoid nocturia, monitor BS if relevant

77
Q

What are monitoring parameters for diuretics?

A

BP, BUN/SCr, serum electrolytes, cholesterol/TGs, skin rash, uric acid if gout.

78
Q

What are the pharmacodynamic effects of ACEI/ARBs?

A

Vasodilation, reduced PVR, reduced BP, no change HR, no change CO, minimal diuresis.

79
Q

What angiotensin inhibitor class is best post-MI and in LVD?

A

ACEIs

80
Q

What angiotensin inhibitor class is best in CHF?

A

ARBs

81
Q

What conditions are contraindications for ACEI/ARB therapy?

A

Pregnancy, nursing, hx angioedema, bilateral renal artery stenosis, pre-existing severe kidney dysfunction, hyperkalemia.

82
Q

Why must a physical exam be conducted before initiation of ACEI/ARB therapy?

A

Need to look for renal artery stenosis. First bruits look for, then imaging.

83
Q

What are the compelling indications for ACEI use?

A

CKD patients, left ventricular hypertrophy

84
Q

What are adverse reactions from ACEIs?

A

Cough (dry, usually b/c increase bradykinin), angioedema, hyperkalemia, neutropenia, agranulocytosis, proteinuria, glomerulonephritis, acute renal failure, loss of taste.

85
Q

When should K and SCr be monitored after initiation or dose increase?

A

Within 4 weeks

86
Q

What are adverse effects of angiotensin receptor blockers?

A

Orthostatic hypotension, renal insufficiency, hyperkalemia, less cough than ACEIs

87
Q

What patients may benefit from a 50% initial dose?

A

Patients at high hypotension risk–patients taking diuretic, volume depleted patients, and elderly

88
Q

What patients are at highest risk for acute kidney failure with an ACEI/ARB?

A

Patients with severe bilateral renal artery stenosis or severe stenosis in artery to solitary kidney.

89
Q

What unique SE does aliskiren have compared to ACEI/ARBs? How is it dosed?

A

Diarrhea; 150mg-300mg PO daily

90
Q

What are the monitoring parameters for angiotensin inhibitors?

A

SCr, BP, serum K, angioedema, dizziness, cough

91
Q

What should patients be educated on with angiotensin inhibitors?

A

Educate on HTN, compliance, BP measurement, K rich food, pregnancy precautions, ADRs (angioedema especially)

92
Q

When are non-DHP CCBs contraindicated?

A

Preexisting bradycardia, conduction defects, HF due to systolic dysfunction

93
Q

What CCBs can be used for arrhythmias?

A

non-DHPs

94
Q

What effect do DHP CCBs have on heart rate?

A

Reflex tachycardia, but no direct effect.

95
Q

When are DHP CCBs contraindicated?

A

Heart block

96
Q

What are ADEs from DHP CCBs?

A

Reflex sympathetic discharge, tachycardia, dizziness, HA, flushing, peripheral edema, gingival hyperplasia.

97
Q

What are some special situations that make CCBs preferred?

A

Raynaud’s syndrome, older patients with isolated systolic HTN, potent vasodilators.

98
Q

What situations are diltiazem and verapamil effective in? What different ADRs do they have?

A

Supraventricular tachyarrhythmias. SE: bradycardia, HA, dizziness, AV block, systolic HF, constipation.

99
Q

How are diltiazem ER and verapamil ER dosed?

A

Initial: 120mg/day PO for both
MAX: 360mg/day for diltiazem
480mg/day for verapamil

100
Q

What drug class should not be used with non-DHP CCBs because of effect on heart rate?

A

Beta-blockers

101
Q

What are the monitoring parameters for CCBs?

A

BP, HR (non-DHP), peripheral edema (DHP), constipation (non-DHP)

102
Q

What should patients starting CCB therapy be educated about?

A

Frequent BP monitoring, lab testing (?), edema, constipation prevention

103
Q

What compelling indication would lead you to use a beta blocker?

A

Angina, post-MI, reduced mortality HF, arrhythmias, migraine, thyrotoxicosis, perioperative HTN

104
Q

What are ADEs for beta blockers?

A

Bronchospasm, bradycardia, mask hypoglycemia, impaired peripheral circulation, fatigue, decreased exercise tolerance, depression, withdrawal–dont stop suddenly. Caution asthma/COPD, renal insufficiency, DM, HF exacerbation, 2nd or 3rd degree heart block.

105
Q

What agents are reserved for last-line therapy in patients with special indications or difficult to control BP?

A

Hydralazine, minoxidil

106
Q

What are ADEs for hydralazine?

A

Drug-induced rash, SLE, fluid retention, reflex tachycardia, palpitations, chest pain, GI, HA, hepatotoxicity

107
Q

How is hydralazine dosed initially? Max?

A

Initial: 10mg PO QID (target 25-100mg/day PO)
MAX: 300mg/day PO divided

IV: 10-50mg IV q30min prn

108
Q

How is minoxidil dosed?

A

2.5-80mg daily in 1-2 divided doses

109
Q

What are the side effects of minoxidil?

A

Hypertrichosis/hirsutism, fluid retention, all others that hydralazine has without SLE. Black box warning pericarditis/tamponade, exacerbate angina, should be given with diuretic and beta blocker.

110
Q

When should the direct vasodilators not be used? Used with caution?

A

CI: dissecting aortic aneurysm
Caution: CVA (permissive HTN), renal impairment, CAD, liver disease, SLE (hydralazine)

111
Q

What antihypertensive is preferred in pregnancy? How is it dosed? Second line therapies?

A

Methyldopa (Aldomet)
Initial: 250mg PO BID-TID (usual target 250mg BID)
MAX: 3g/day

IV: 250-100mg q6-8h (MAX 1g IV 16h)

Second line: beta blockers and vasodilators

112
Q

At what frequency should HTN be followed up after goal reached?

A

q3-6mos

113
Q

What agents are recommended in AA patients?

A

Thiazides and CCBS (B blockers next?)

114
Q

What patients are at high risk of fall due to postural hypotension? How should their BP be monitored?

A

Elderly patients; monitor in upright position

115
Q

What cognitive disorder does BP control halt progression of?

A

Dementia

116
Q

What medicine puts women at higher risk of HTN?

A

OCs

117
Q

In what conditions is permissive hypertension okay?

A

Stroke and MI, especially if patient at high risk

118
Q

Define hypertensive urgency. What should be addressed first?

A

Mark BP elevation (>180/120) and NO TOD.

Look for drugs, pain, anxiety, cocaine, withdrawal 1st.

119
Q

How is hypertensive urgency treated? What is the goal?

A

Hospitalization not required, can be treated with short acting oral therapy (avoid SL and IM) like clonidine, labetalol, captopril.
Goal: decrease BP to “normal” within 24-48 hours to avoid TOD (stroke)

120
Q

Define hypertensive emergency.

A

Marked BP elevation (>180/120) AND TOD (includes encephalopathy, MI, unstable angina, pulmonary edema, eclampsia, stroke, head trauma, life-threatening arterial bleeding, aortic dissection, diminished renal clearance).

121
Q

How do you treat hypertensive emergency? What is your goal?

A

Treat with parenteral antihypertensive therapy to decrease MAP ~25% within 2 hours. If stable, continue to decrease BP over 2-6 hours. May take days! Do NOT want to lead to hyperperfusion.

122
Q

What drugs are helpful in pheocromocytoma?

A

A-1 blockers to counteract catecholamine surge.

123
Q

What are the active ingredients in Tribenzor?

A

Olmesartan, amlodipine, and HCTZ (PO once daily)

124
Q

What are the active ingredients in Exforge HCT?

A

Valsartan, amlodipine, HCTZ (PO once daily)

125
Q

What are the active ingredients in Amturnide?

A

Aliskiren, amlodipine, HCTZ (PO once daily)

126
Q

What are pros and cons for combination products?

A

May decrease pill burden by decreasing pills and simplifying dosing regimen. However, higher cost.

127
Q

What situation is resistant HTN?

A

Uncontrolled BP even after 3 medications at maximally tolerated doses. Must rule out nonadherence, secondary causes, salt intake, etc.

128
Q

What are possible causes of resistant HTN?

A

Improper BP measurement, excess sodium intake, medication (inadequate doses or interactions with OTCs), excess alcohol intake, secondary causes.