Endocrine Hypertension

Question 1

When should you screen for secondary causes of HTN?

Answer 1

Severe or resistant HTN (3+ agents, including a diuretic)
Acute rise
Proven onset before puberty
Age less than 30 with no fam history/obesity
Features suggestive of a secondary cause

Question 2

Causes of secondary HTN

Answer 2

Renovascular disease
Primary renal disease
Sleep apnea syndrome
Coarctation of the aorta
Meds (OCPs, NSAIDs, stimulants, antidepressants)
Endocrine causes

Question 3

Endocrine causes of HTN

Answer 3

Adrenal: pheochromocytoma, primary aldosteronism, Cushing’s, etc
Thyroid: hypo (diastolic), hyper (systolic)
Apparent mineralocorticoid excess
Pituitary dependent (acromegaly, Cushing)

Question 4

When should you suspect renovascular disease?

Answer 4

When there is an acute elevation in serum creatinine of at least 30% after administration of ACEI or ARB

Question 5

2 main causes of primary aldosterism

Answer 5

Bilateral idiopathic hyperplasia (60%)

Aldosterone-producing adenoma (35%)

Question 6

Clinical features of primary aldosteronism

Answer 6

HTN (severe)
Hypokalemia and alkalosis
Symptoms of K depletion (fatigue, weakness, muscle cramps, polydipsia/polyuria, paresthesias, headaches, palpitations)

Question 7

3 steps to diagnose primary aldosteronism

Answer 7

1. Case-detection tests (aldosterone to renin ratio)
2. Confirmatory testing (oral Na loading test, IV saline infusion test)
3. Subtype studies (adrenal CT, adrenal venous sampling, genetic testing)

Question 8

Aldosterone to renin ratio

Answer 8

Can help you differentiate among different causes of hypertension and hypokalemia
All meds can be continued except mineralocorticoid receptor antagonists
If aldosterone is high and renin is low, that points to primary aldosteronism

Question 9

Oral sodium loading test

Answer 9

High Na diet for 3 days (goal intake of 5000 mg)
On the third day, a 24 hour urine specimen is collected for measurement of aldosterone, Na, and creatinine
If aldosterone is high, that is consistent with autonomous aldosterone secretion
Similar to what is done with IV saline infusion

Question 10

3 subtype studies for primary aldosteronism

Answer 10

Adrenal CT
Adrenal venous sampling
Genetic testing

Question 11

Treatment for primary aldosteronism

Answer 11

Surgery (unilateral laparoscopic adrenalectomy - may not be a certain cure but BP will improve and hypokalemia is 100% cured)
Pharmacologic: salt restriction, spironolactone, eplerenone

Question 12

Pheochromocytoma vs paraganglioma

Answer 12

Both are tumors of chromaffin cells that secrete catecholamines
Just depends where they are
Pheo: adrenal
Para: extra-adrenal

Question 13

5 clinical features of a pheochromocytoma (and what is the most important)

Answer 13

Pressure
Pain (headache)*
Perspiration*
Palpitation*
Pallor
Paroxysms are technically the 6th P

Question 14

Paroxysms

Answer 14

"Spells" in pheo
10-60 min duration
Daily to monthly
Spontaneous
Precipitating factors: diagnostic procedures, drugs, strenuous exercise, micturition (in a bladder paraganglioma)

Question 15

How can you get hypotension with a pheo?

Answer 15

Orthostatic/paroxysmal hypotension
From ECF volume contraction
Loss of postural reflexes due to prolonged catecholamine stimulation
Tumor release of adrenomedullin (can cause vasodilation)

Question 16

Signs and symptoms of a Pheo

Answer 16

Nausea and vomiting
Abdo pain
Severe constipation
Chest pains (anxiety, angina/MI with normal coronaries)
CHF
Cardiac dysrhythmia and conduction defects
Hypercalcemia
Mild glucose intolerance
Lipolysis

Question 17

4 tests to diagnose pheo

Answer 17

Urinary metanephrines
Urinary catecholamines
Plasma nephrines
Plasma catecholamines
Both urine tests are better than plasma metanephrines

Question 18

2 types of drugs that alter catabolism metabolism

Answer 18

Amphetamines

Tricyclics

Question 19

Chromogranin A

Answer 19

Specific diagnostic test in the DDx of pheochromocytoma
Good sensitivity, poor specificity
If its negative its helpful, not so much if its positive

Question 20

Clonidine suppression test

Answer 20

Distinguishes between pheo and false positive increases in plasma catecholamines and metanephrines
Clonidine is a centrally active alpha 2-adrenergic receptor agonist that normally suppresses the release of catecholamines from neurons but does not affect the catecholamine secretion from a pheo
Plasma cat will decrease in primary HTN, not with pheo

Question 21

What is the imaging modality of choice in pheo?

Answer 21

CT

Question 22

When should genetic testing be considered

Answer 22

Paraganglioma
Bilateral adrenal pheochromocytoma
Unilateral adrenal pheo and a fam history of pheo or para
Unilateral adrenal pheo onset at a young age
Clinical findings suggestive of any familial pheo syndromes

Question 23

3 main findings in Von Hippel-Lindau disease

Answer 23

Pheochromocytomas
CNS hemangioblastoma
Retinal Hemangiomas

Question 24

3 P causes of multiple endocrine neoplasia (MEN)

Answer 24

Parathyroid (primary hyperpara)
Anterior pituitary tumors (prolactinoma, GH secreting, ACTH secreting, etc)
Pancreatic islet tumors (gastrinoma, insulinoma, etc)

Question 25

Treatment of pheo

Answer 25

Surgery (adrenalectomy)

Make sure BP is stabilized before

Question 26

Why do you need to give alpha blockers before beta blockers before treating pheo?

Answer 26

Giving beta blockers first would cause vasoconstriction

Patients can get a hypertensive crisis