HTN Flashcards

1
Q

HTN definition

A

Systolic BP above 140 and/or diastolic above 90 based on 3 measurements separated in time. Can be primary or secondary.

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2
Q

Primary hypertension (Essential)

A

HTN with no identifiable cause. This is 95% of cases of HTN.

Risk factors include a family history of HTN or heart disease, a high sodium diet, smoking, obesity, ethnicity (blacks more than whites), and advanced age.

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3
Q

History and PE for primary HTN

A

HTN is asymptomatic until complications develop

Patients should be evaluated for end-organ damage to the brain (stroke, dementia), eye (cotton-wool exudates, hemorrhage), heart (LVH), and kidney (proteinuria, chronic kidney disease). Renal bruits may signify renal artery stenosis as the cause of the HTN

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4
Q

Diagnosis of Primary HTN

A

Obtain a UA, BUN/Cr, CBC, and lytes to assess extent of end-organ damage and possible secondary causes

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5
Q

Treatment of primary HTN

A

1) Rule out secondary causes of HTN, particularly in patients with new-onset HTN at extremes of age
2) Begin with lifestyle mods. Weight loss is the single most effective lifestyle mod.
3) BP goal in otherwise healthy patients is less than 140/90. Goal in diabetics or patients with renal disease with proteinuria is less than 130/80
4) Diuretics, ACEIs, B-blockers have been shown to decrease mortality in uncomplicated HTN. They are first line unless a comorbid condition requires another med
5) Periodically test for end-organ complications, including renal complications (BUN, Cr, urine protein-to-creatinine) and cardiac complications (ECG evidence of hypertrophy)

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6
Q

Causes of secondary HTN

A

CHAPS

Cushing's syndrome
Hyperaldosteronism (Conn's)
Aortic coarctation
Pheochromocytoma
Stenosis of renal arteries
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7
Q

Primary renal disease

A

Cause of secondary HTN

1) Often unilateral renal parenchymal disease
2) Treat with ACEIs, which slow the progression of renal disease

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8
Q

Renal artery stenosis

A

Causes secondary HTN

1) Especially common in patient less than 25 and greater than 50 with recent onset HTN. Etiologies include fibromuscular dysplasia (younger patients) and atherosclerosis (older)
2) Diagnose with MRA or renal artery doppler. May be treated with angioplasty or stenting. Consider ACEIs in unilateral disease. In bilateral disease, ACEIs can accelerate kidney failure by preferentially vasodilating the efferent aterioles. Open surgery is second option if angio is not effective or doable.

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9
Q

OCP use

A

Can cause secondary HTN

1) Common in women over 35, obese women, and those with long-standing use.
2) Discontinue OCPs (effect may be delayed)

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10
Q

Pheochromocytoma

A

Can cause secondary HTN

1) An adrenal gland tumor that secretes epinephrine and norepinephrine, leading to episodic headaches, sweating, and tachycardia.
2) Diagnose with urinary metanephrines and catecholamine levels or plasma metanephrine. Surgical removal of tumor after treatment with both alpha and beta blockers

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11
Q

Conn’s Syndrome (hyperaldosteronism)

A

1) Most often secondary to an aldosterone-producing adrenal adenoma. Causes triad of HTN, unexplained hypoK and metabolic alkalosis.
2) Metabolic workup with plasma aldosterone and renin level. Increased aldosterone and decreased renin levels suggest primary hyperaldosteronism. Surgical removal of tumor.

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12
Q

Cushing’s Syndrome

A

another cause of secondary HTN

1) Due to ACTH-producing pituitary tumor, an ectopic ACTH secreting tumor or cortisol secretion by an adrenal adenoma/carcinoma. Also due to exogenous steroid exposure.
2) Surgical removal of tumor; removal of exogenous steroids

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13
Q

Coarctation of the aorta

A

Another cause of secondary HTN

Treat with surgery

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14
Q

Treating HTN in uncomplicated patient

A

DBAc (diuretics, B, ACE)

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15
Q

Treating HTN in CHF

A

DBAcAr + aldosterone antagonists

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16
Q

Treating HTN in Diabetes

A

DBAcArC (C is CCB)

17
Q

Treating HTN post MI

A

BAcAr + aldosterone antagonists

18
Q

Treating HTN in CKD

A

AcAr

19
Q

Treating HTN in BPH

A

D + alpha blockers

20
Q

Treating HTN in isolated systolic HTN

A

DAcArC (dihydropyridines - amlodipine, nicardipine, nifedipine, nimodipine)

21
Q

Hypertensive crises

A

A spectrum of clinical presentations in which elevated blood pressures lead to end-organ damage

22
Q

History and physical for hypertensive crises

A

Present with end organ damage revealed by renal disease, chest pain (ischemia or MI), back pain (aortic dissection) or changes in mental status (hypertensive encephalopathy)

23
Q

Diagnosis of hypertensive crisis

A

1) Hypertensive urgency - high BP with mild to moderate symptoms (HA, CP) without end-organ damage
2) Hypertensive emergency - high BP with signs or symptoms of impending end organ damage like acute kidney injury, intracranial hemorrhage, papilledema, or ECG changes suggestive of ischemia or pulmonary edema
3) Malignant HTN - diagnosed on the basis of progressive renal failure and/or encephalopathy with papilledema

24
Q

Treatment of hypertensive crisis

A

1) Urgency - can be treated with oral antihypertensives (B-blockers, clonidine, ACEIs) with goal of gradually lowering BP over 24-48h
2) Emergency - treat with IV meds (lebatalol, nitroprusside, nicardipine) with goal of lowering mean arterial pressure by no more than 25% over first 2 hours to prevent cerebral hypoperfusion or coronary insufficiency

25
Q

Diuretics

A

Thiazide, loop, K sparing

1) Mech: Reduced extracellular volume and thereby reduce vascular resistance
2) Side effects: HypoK (not with K sparing), hyperglycemia, hyperlipidemia, hyperuricemia, azotemia

26
Q

B-blockers

A

1) Mech: Reduce cardiac contractility and renin release

2) Side effects: Bronchospasm (in severe active asthma), bradycardia, CHF exacerbation, impotence, fatigue, depression

27
Q

ACEIs

A

1) Mech: Block aldosterone formation, reducing peripheral resistance and salt/water retention
2) Side effects: Cough, rashes, leukopenia, hyperK

28
Q

ARBs

A

Losartan, Valsartan, Irbesartan

1) Mech: Block aldosterone effects, reducing peripheral resistance and salt/water retention
2) Side effects: Rashes, leukopenia, hyperK (no cough)

29
Q

CCBs

A

Dihydro (nifediine, felodipine, amlodipine) and non-dihydro (dilt and verapamil)

1) Mech: Lowers smooth muscle tone and causes vasodilation; may also reduce cardiac output
2) Side effects: Dihydro - HA, flushing, peripheral edema. Nondihydro - lower contractility

30
Q

Vasodilators

A

Hydralazine, minoxidil

1) Mech: Lower peripheral resistance by dilating arteries/arterioles
2) Side effects: Hydralazine - HA, lupus-like syndrome. Minoxidil - orthostasis, hirsutism

31
Q

Alpha 1 blockers

A

Prazosin, terazosin, phenoxybenzamine

1) Mech: Cause vasodilation by blocking actions of norepinephrine on vascular smooth muscle
2) side effect: orthostatic hypotension

32
Q

Centrally acting adrenergic agents

A

Methyldopa, clonidine

1) Mech: Inhibit the sympathetic nervous system via central alpha 2 adrenergic receptors
2) Side effects: Somnolence, orthostatic hypotension, impotence, rebound HTN