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(HGC) ACNP804 Exam 1 > Hypertension: Harrison's & Saseen > Flashcards

Hypertension: Harrison's & Saseen Flashcards

1
Q

Most contemporary guidelines endorse what kind of blood pressure goals for most patients?

A

< 140/90

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2
Q

Most contemporary guidelines endorse what kind of blood pressure goals for patients with diabetes or chronic kidney disease?

A

< 130/80

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3
Q

Some controversy exists about certain groups of patients & blood pressure goals? What patient groups?

A

Patients with CAD, vascular disease (stroke, PAD), & those with a 10 year risk of CAD

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4
Q

What should the clinician’s first consideration be in selecting anti-hypertensive drug therapy?

A

Is there a compelling indication for a SPECIFIC drug therapy?

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5
Q

What are some comorbidities that create compelling indications for specific anti-hypertensive drugs?

A 
#Diabetes
#Chronic kidney disease
#Coronary artery disease
#Left ventricular dysfunction
#Previous ischemic stroke
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6
Q

First line regimen for patients with DIABETES?

Add-on therapy?

A

1st line: ACE-inhibitor or ARB

Add-on: Thiazide, then beta-blocker &/or CCB

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7
Q

First line regimen for patients with CHRONIC KIDNEY DISEASE:

A

ACE-inhibitor or ARB

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8
Q

First line regimen for patients with CORONARY ARTERY DISEASE?
Add-on therapy?

A

1st line: beta-blocker & ACE-inhibitor or ARB

Add-on: Aldosterone antagonist, CCB, and/or thiazide diuretic

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9
Q

First line regimen for patients with LEFT VENTRICULAR DYSFUNCTION?
Add-on therapy?

A

1st line: Diuretic, ACE-inhibitor or ARB, & Beta-blocker

Add-on: Aldosterone antagonist &/or hydralazine with isosorbide dinitrate

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10
Q

First line regimen for patients with PREVIOUS ISCHEMIC STROKE:

A 
#ACE-inhibitor
with or without
#Thiazide diuretic
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11
Q

True or false: most diabetics with hypertension can be controlled on a single drug.

A

False. Most require 2-3 drugs to attain control.

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12
Q

Why are ACE or ARBs recommended as 1st line therapy for diabetics with hypertension?

A

Both have been proven to reduce the risk of CV events & kidney disease progression in diabetic patients.

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13
Q

Why are calcium-channel blockers particularly useful in diabetics with hypertension?

A

They do not affect glycemic control.

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14
Q

How does estimated glomerular filtration rate affect the selection of diuretic in a hypertensive diabetic patient?

A

eGFR > 30: thiazide diuretic

eGFR < 30: loop diuretic

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15
Q

What is the thiazide diuretic used in clinical trials regarding hypertensive diabetic patients?

A

Chlorthalidone

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16
Q

Beta-blockers are considered 3rd or 4th line add-on for diabetic patients with hypertension. Why?

A

Risk of hyperglycemia with beta-blocker therapy

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17
Q

True or false: all beta-blockers carry the same risk for hyperglycemia in diabetic patients.

A

False: in the GEMINI trial, carvedilol had no significant effect on glucose, but metoprolol did.

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18
Q

How does the clinician identify CKD in a hypertensive patient for the purposes of drug therapy?

A

CKD in Stage 3 or higher:

1) eGFR < 60 (serum creatinine > 1.3 in women or 1.5 in men)
2) Albuminuria > 300 mg/day

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19
Q

Diuretics can serve 2 purposes in the hypertensive CKD patient. What are they?

A

1) BP control

2) volume regulation

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20
Q

When should the clinician choose a thiazide diuretic for a CKD patient? A loop diuretic?

A

Thiazide: eGFR > 30
Loop: eGFR < 30, or patient in volume overload/edema

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21
Q

Why are beta-blockers the cornerstone of anti-hypertension therapy in patients with CAD?

A 
Proven long term benefits: reduces risk of death by more than 20%. Effects: 
#reduces stimulation of myocardium
#balances myocardium oxygen supply vs. demand
#treats ischemic symptoms
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22
Q

How does an ACE or ARB benefit the hypertensive CAD patient?

A

Preventing adverse cardiac remodeling

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23
Q

In addition to the first line of beta-blocker & ACE/ARB, how can a CCB benefit a hypertensive CAD patient?

A

Treat ischemic symptoms

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24
Q

When should the clinician select a dihydropyridine CCB vs. a non-dihydropyridine CCB?

A

If added to beta-blocker, select the DIHYDROPYRIDINE CCB (to avoid excessive bradycardia). If beta-blocker is contraindicated, select the NON-DIHYDROPYRIDINE CCB, because of ability to lower heart rate & reduce myocardial oxygen demand (i.e. what the beta-blocker WOULD be doing if they could take it).

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25
Q

In addition to lower BP, diuretic therapy has what other purpose in the patient with hypertension & LV dysfunction?

A

Treating or preventing fluid overload

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26
Q

Use of beta-blockers in addition to ACE/ARB for patients with LV dysfunction has an additional benefit. What is it?

A

Increased ejection fraction

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27
Q

What rule should the clinician remember when starting beta-blocker therapy on a hypertensive patient with LV dysfunction?

A

Start low, go slow!

[Start at a low dose & titrate up to a target dose.]

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28
Q

For African-American patients in particular, what 3rd or 4th line therapy has been shown to reduce CV events in hypertensive patients with LV dysfunction?

A

Hydralazine in combo with isosorbide dinitrate

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29
Q

History of a CVA, especially ischemic, is a compelling indication for use of…

A

a diuretic!

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30
Q

Certain drug combinations have been shown in trials to reduce risk of recurrent stroke, MI, & CV events in patients with prior stroke. What are they?

A 
#Diuretics alone 
#Diuretics in combination with ACE-inhibitors
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31
Q

True or false: ARB therapy has been shown to reduce risk of recurrent stroke in hypertensive patients.

A

False. It has not been shown to reduce CVA risk either as first or second line therapy.

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32
Q

How do ACE-inhibitors work?

A

By inhibiting ACE, resulting in decreased angiotensin II. This causes decreased vasoconstriction, decreased aldosterone secretion, & sodium/water retention.

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33
Q

How do ARBs work?

A

Blockade of angiotensin II type 1 receptor. Decreases the effects of angiotensin II, causing decreased vasoconstriction, decreased aldosterone secretion, & sodium/water retention.

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34
Q

How do CCBs: Dihydropyridines work?

A

Blocking cellular calcium entry through L-type channel. Results in reduced total peripheral resistance through arterial vasodilation.

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35
Q

How do CCBs: Non-dihydropyridines work?

A

Blocking cellular calcium entry through L-type channel. Results in reduced total peripheral resistance through arterial vasodilation. ADDITIONALLY: decreased myocardial contractility results in negative inotropic effect, blocked AV nodal conduction results in decreased HR.

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36
Q

How do thiazide diuretics work?

A 
#Short term: natriuresis, resulting in reductions in cardiac output & decreased blood volume
#Longer term: decreased peripheral vascular resistance
37
Q

How do beta-blockers work?

A

Blockade of beta-1 receptors. Results in reduced cardiac output & reduced HR. Inhibit renin release, decreases adrenergic CNS effects, reduces catecholamine release/response.

38
Q

How do aldosterone antagonists work?

A

Blockade of aldosterone receptors. Decreased vasoconstriction & decreased sodium/water retention.

39
Q

Volume loss (intentional or unintentional) while on ACE-inhibitor therapy may result in…

A

…major decreases in BP and deterioration in renal function to the point of acute renal failure.

40
Q

ACE-inhibitors as monotherapy may not be as effective in what type of hypertension? This can be overcome by…

A

Salt-sensitive, low-renin forms of hypertension (as often found in African-American, diabetic, and elderly hypertensive patients). This can be overcome by administering in higher-than-usual doses.

41
Q

What is a very distinct adverse effect of ACE-inhibitors? Will switching to a different ACEI help?

A

A dry cough. Switching to another ACEI does not seem to help, as it is a class effect.

42
Q

If a patient develops angioedema on an ACE-inhibitor, should they ever take one again?

A

That would be a NOPE! You’re gonna have to go with an ARB on that one.

43
Q

ACE-inhibitor use during pregnancy?

A

NEVER. NOPE. DO NOT.

44
Q

ARBs use during pregnancy?

A

NOPE. DON’T EVEN TRY IT.

45
Q

True or false: ARBs also cause “The Cough.”

A

False. Also, patients who have angioedema on an ACE can use ARB without that effect.

46
Q

What are the 2 classes of CCBs?

A 
#Dihydropyridines
#Non-dihydropyridines
47
Q

Other uses for dihydropyridine CCBs?

A 
#Cyclosporine-induced hypertension
#Raynaud phenomenon
48
Q

Other uses for non-dihydropyridine CCBs?

A 
#Atrial fibrillation
#Migraine headache prevention
49
Q

What is an advantage of 2nd-generation dihydropyridines?

A

They are highly selective for vasculature, so they avoid the affects on cardiac contractility that 1st-generation ones had.

50
Q

Side effects common to ALL CCBs:

A 
#GERD
#Constipation (almost ALWAYS happens with verapamil)
51
Q

Side effects of dihydropyridine CCBs:

A 
#Flushing
#Headache
#Peripheral Edema
52
Q

What can be done to avoid the peripheral edema side effect of dihydropyridines?

A 
#reduce the dihydropyridine dose
#add an ACE or ARB
#encourage pt to elevate lower extremities
53
Q

Non-dihydropyridines are contraindicated in what group?

A

Patients with LV dysfunction. Can cause CHF exacerbation!

54
Q

What are the 2 CCBs that inhibit the CYP450 3A4 system?

A

Verapamil & diltiazem

55
Q

CCBs are more effective than ACE/ARB in what group?

A

African-Americans & those with low-renin, salt-sensitive HTN

56
Q

True or false: the BP reducing effects of thiazide diuretics are mainly due to decreased circulating volume.

A

False. They are due to the short-term, long-term, & chronic effects of the diuretic on the body.

57
Q

What are the short-term effects of thiazide diuretics? How long are we talking?

A

First 2-4 weeks: reductions in BP are related to decreases in cardiac output & plasma volume. There’s also an increase in plasma renin activity & a transient increase in peripheral vascular resistance.

58
Q

What are the long-term effects of thiazide diuretics? How long are we talking?

A

After 4 weeks: cardiac output & plasma volume return to normal levels, but BP stays low because of persistent DECREASE in peripheral vascular resistance.

59
Q

What are the chronic effects of thiazide diuretics? How long are we talking?

A

Persistent reduction in total peripheral resistance

60
Q

Four subclasses of beta-blockers

A 
#Cardioselective beta-blockers
#Non-selective beta-blockers
#Beta-blockers with intrinsic sympathomimetic activity
#Mixed alpha-/beta-blockers
61
Q

Why should patients be taught never to abruptly discontinue their beta-blocker?

A

Rebound hypertension time!

62
Q

What side effect might you get if you combine verapamil or diltiazem with a beta-blocker?

A

Sharp reduction in heart rate and risk of heart block! Fancy!

63
Q

True or false: the newest guidelines consider beta-blockers first line therapy for uncomplicated hypertension?

A

False! That’s old school thinking. Newer information tells us that beta-blockers should not supplant ACEs/ARBs.

64
Q

What are the 2 clinically available aldosterone antagonists?

A 
#spironolactone
#eplerenone
65
Q

What are potential side effects of spironolactone?

A 
#painful gynecomastia (in men)
#erectile dysfunction
#menstrual irregularities
66
Q

Can spironolactone-induced gynecomastia be reversed?

A

Yes but it takes a while

67
Q

What effect might aldosterone antagonists have on potassium levels?

A

Hyperkalemia can be a problem! Mostly it happens when AAs are given to people with CKD or in combination with ACE/ARBs (which are known to increase serum potassium).

68
Q

Two special groups for whom hydralazine (an arterial vasodilator) is recommended:

A 
#pregnant women
#African-American patients with CHF (in combo with isosorbide dinitrate!)
69
Q

The most widely used alpha-agonist?

A

Clonidine! Congratulations!

70
Q

Methyldopa is used almost exclusively for…

A

…gestational hypertension or management of chronic hypertension in pregnant patients. It has a very long history of safety! (It ain’t broke we we ain’t trying to fix it.)

71
Q

What is an advantage of fixed-dose combination drugs?

A

Decreasing the number of pills increases adherence to therapy.

72
Q

What’s a positive Osler sign?

A

Inflating the cuff above systolic BP, but finding the brachial or radial artery is still palpable. A component of pseudohypertension.

73
Q

What is “essential” hypertension, aka “idiopathic” or “primary” hypertension?

A

HTN without a clear etiology

74
Q

What is “secondary” hypertension?

A

HTN with an apparent reason for the BP elevation

75
Q

What might cause secondary hypertension with wide pulse pressure?

A 
#Decreased vascular compliance (arteriosclerosis)
#Increased cardiac output (aortic regurg, thyrotoxicosis, hyperkinetic heart syndrome, fever, AV fistula, patent ductus)
76
Q

What might cause secondary hypertension with both systolic & diastolic increases?

A 
#Renal: parenchymal disease, cysts, tumors, obstructive uropathy
#Renovascular: arteriosclerosis, fibromuscular dysplasia
#Adrenal: Primary aldosteronism, Cushing's, 17 alpha-hydroxylase or 11 beta-hydroxylase deficiencies, pheochromocytoma
#Aortic coarctation
#Obstructive sleep apnea
#Pre-eclampsia, eclampsia
#Neurogenic: psychogenic, diencephalic syndrome, familial dysautonomia, polyneuritis, acute increased ICP, acute spinal cord section
#Endocrine: Hypothyroid, hyperthyroid, hypercalcemia, acromegaly
#Meds: Estrogens, adrenal steroids, decongestants, appetite suppressants, cyclosporine, TCAs, MAOIs, erythropoetin, NSAIDs, cocaine

AND A PARTRIDGE IN A PEAR TREE. GEEZ.

77
Q

What is the etiology of essential hypertension?

A

We don’t freakin’ know, honestly.

Tends to be familial & likely is consequence of interaction between environment & genetic factors.

78
Q

What are the major “end organs” damaged by hypertension?

A 
#Heart
#Brain
#Kidneys
#Peripheral arteries
79
Q

How does chronic hypertension damage the heart?

A 
**Heart disease is the most common cause of death in hypertensive patients**
#Left ventricular hypertrophy
#CHF
#CAD
#Cardiac arrythmias
80
Q

How does chronic hypertension damage the brain?

A 
#CVA (high BP is highest risk factor for CVA)
#HTN is associated with impaired cognition with aging
#Malignant hypertension: hypertensive encephalopathy
81
Q

How does chronic hypertension damage the kidneys?

A 
#Both a target organ AND a potential cause
#Loss of autoregulation leads to renal injury & CKD
82
Q

How does chronic hypertension damage the peripheral arteries?

A

Peripheral arterial disease (intermittent claudication)

83
Q

Non-pharmacological HTN Management

A 
#Weight reduction (BMI < 25 kg/m2)
#Dietary salt reduction ( < 6 g NaCl daily)
#DASH diet (rich in fruits/veggies, low fat dairy with reduced saturated & total fat)
#Moderation of ETOH consumption (≤ 2 drinks daily for men, ≤ 1 for women)
#Physical activity
84
Q

Hypertensive Urgency

A 
#Situation in which BP must be controlled within a few hours
#Asymptomatic HTN ≥ 220/125
#Patient with optic disc edema, target organ damage/complications, dangerous perioperative HTN
85
Q

Hypertensive Emergency

A 
#Situations in which BP must be controlled within 1 hour to avoid morbidity or death
#Generally DBP ≥ 130
#Hypertensive encephalopathy or nephropathy
#Other emergencies: intracranial hemmorhage, MI, aortic dissection, pulmonary edema, preeclampsia/eclampsia, malignant HTN
86
Q

Examples of thiazide diuretics

A 
#chlorthalidone
#hydrochlorothiazide
#indapamide
#metolazone
87
Q

Examples of loop diuretics

A 
#furosemide
#bumetanide
88
Q

Examples of potassium sparing diuretics

A 
#amiloride
#spironolactone
#triamterene

(HGC) ACNP804 Exam 1 (6 decks)

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