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Week 27: Adrenal Dysfunction > Endocrine Hypertension > Flashcards

Flashcards in Endocrine Hypertension Deck (26)
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1

When should you screen for secondary causes of HTN?

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

2

Causes of secondary HTN

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

3

Endocrine causes of HTN

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

4

When should you suspect renovascular disease?

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

5

2 main causes of primary aldosterism

Bilateral idiopathic hyperplasia (60%)
Aldosterone-producing adenoma (35%)

6

Clinical features of primary aldosteronism

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

7

3 steps to diagnose primary aldosteronism

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)

8

Aldosterone to renin ratio

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

9

Oral sodium loading test

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

10

3 subtype studies for primary aldosteronism

Adrenal CT
Adrenal venous sampling
Genetic testing

11

Treatment for primary aldosteronism

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

12

Pheochromocytoma vs paraganglioma

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

13

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

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

14

Paroxysms

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

15

How can you get hypotension with a pheo?

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

16

Signs and symptoms of a Pheo

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

17

4 tests to diagnose pheo

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

18

2 types of drugs that alter catabolism metabolism

Amphetamines
Tricyclics

19

Chromogranin A

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

20

Clonidine suppression test

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

21

What is the imaging modality of choice in pheo?

CT

22

When should genetic testing be considered

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

23

3 main findings in Von Hippel-Lindau disease

Pheochromocytomas
CNS hemangioblastoma
Retinal Hemangiomas

24

3 P causes of multiple endocrine neoplasia (MEN)

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

25

Treatment of pheo

Surgery (adrenalectomy)
Make sure BP is stabilized before

26

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

Giving beta blockers first would cause vasoconstriction
Patients can get a hypertensive crisis