Secondary HTN Flashcards

1
Q

when should you consider secondary hypertension?

A

Age less than 30 or above 50 with new hypertension

Dramatic increase in BP with abrupt onset

Difficult to control - patient is on 3+ medications (severe/resistant HTN)

no risk factors or family history

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2
Q

what are the classic ideologies of secondary hypertension? (alphabet soup)

A

Aldosterone, Apnea (sleep)
Bruits, Baby
Coarctation, Calcium, Cushing’s, Catecholamines, Creatinine
Drugs
Endocrine (thyroid)

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3
Q

What is the most common cause of secondary hypertension?

A

end stage renal disease - presents in over 80% of patients with ESRD

More severe if there is glomerular diseases vs interstitial diseases, or with polycystic kidney disease

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4
Q

How can renal artery stenosis cause secondary hypertension?

A

Stenosis of one/both renal arteries (usually atherosclerotic lesions), most common in older males

Kidneys sense less fluid, activate RAAS system —> increased plasma, fluid, secondary hypertension

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5
Q

Pt is a 68yo M presenting with onset of severe HTN and deterioration of kidney function within one week of starting an ACE inhibitor. Pt doesn’t have risk factors or family history of HTN. What should you be thinking?

A

renovascular HTN - correctable cause of severe/malignant secondary HTN

Stenosis of one/both renal arteries (usually atherosclerotic lesions), most common in older males

giving an ACE/ARB (dilates efferent arteriole) in this context reduces glomerular pressure (since there is stenosis of afferent arteriole) —> deterioration of kidney function

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6
Q

how does fibromuscular dysplasia typically present?

A

Angiopathy of medium sized arteries, predominately affects young females

Can affect different vascular beds, most often renal arteries —> renovascular disease, secondary HTN

Causes focal irregular thickening in the blood vessels and medial/intimal hyperplasia and fibrosis —> luminal stenosis

“string of beads” appearance

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7
Q

what are the classical physical exam signs of aortic coarctation, a possible cause of secondary hypertension?

A

systolic hypertension in the upper extremities + reduced systolic blood pressure in the lower extremities

Radial artery to femoral pulse delay

secondary HTN due to RAAS activation (decreased renal perfusion)

should be excluded in all new cases of unexplained HTN!!

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8
Q

hypokalemic hypertension with a high aldosterone to PRA ratio is suggestive of what?

A

mineralocorticoid excess / primary aldosteronism

hypokalemia may present as paresthesias or muscle weakness, metabolic alkalosis

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9
Q

what is the most sensitive versus most specific diagnostic testing for pheochromocytoma?

A

Neural crest cell origin - tumor of adrenal medulla or extra-adrenal para-ganglionic tissue —> secretion of epinephrine, norepinephrine or dopamine

Presents with palpitations, pain (headache), perspiration

Most sensitive – plasma free metanephrines
Most specific – 24 hour urine total metanephrines

[DO NOT BIOPSY - can cause life-threatening release of catecholamines!!!]

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10
Q

All cases of pheochromocytoma should be treated with surgery. In preparation, alpha-blockade MUST be given (for 10-14 days) before beta-blockade to control HR. Explain why.

A

alpha blockade must be started first to avoid hypertensive crisis!

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