Endocrine hypertension

Question 1

What 3 endocrine conditions are really associated with HTN? What are some others?

Answer 1

Pheochromocytoma, mineralcorticoid excess, glucocorticoid excess

Acromegaly, DM, obesity, congenital adrenal hyperplasia, estrogen-induced HTN, pregnancy induced HTN, renin secreting tumors, hypothyroidism, hyperthyroidism, liddle syndome

Question 2

____ is a catecholamine producing tumor of chromaffin cells that typically produced HTN.

Answer 2

pheochromocytoma

Question 3

What percent of pheochromocytomas are malignant? extra-adrenal?

Answer 3

10;10

Question 4

Describe familial syndrome assosiated with pheochromocytoma?

Answer 4

usually AD, MEN 2A (hyperparathyroidism and medullary thyroid carcinoma), multiple endocrine neoplasia (type 2B; multiple mucosal neuromas and medullary thyroid carcinoma), familial pheochromocytoma without associated disorder

Question 5

How is pheochromocytoma treated pre-op, intra-op, and post-op?

Answer 5

pre: alpha, beta blockade; fluids
Intraop: IV, fluids
Postop: fluids pressors

Question 6

What are 3 general conventional risk factors for hypoglycemia?

Answer 6

inadequate caloric consumption, increased insulin sensitivity, impaired glucose production

Question 7

Neurogenic symptoms of hypoglycemia

Answer 7

sweating, palpitation, tremulousness, hunger, nervousness

Question 8

Neuroglycopenic symptoms?

Answer 8

impaired concentration, tiredness, dizziness, tingling, blurred vision

Question 9

Severe neuroglycopenia

Answer 9

seizure coma

Question 10

4 major components of syndrome of hypoglycemia associated autonomic failure

Answer 10

1. recent antecedent hypoglycemia
2. hypoglycemia unawareness (impaired symptomatic responses)
3. Defective glucose counter-regulation (impaired hormonal responses)
4. Recurrent episodes of hypoglycemia

Question 11

How common is secondary HTN?

Answer 11

less than 5% of all HTN

Question 12

Describe degradation of catecholamines

Answer 12

By MOA and COMT–> VMA, normetanephrine, metanephrine (can be measured in urine and serum)

Question 13

What is the difference in hemodynamic response to E and to NE?

Answer 13

E: increased systolic, but not anything else
NE: increased systolic, diasoltic, and reflex restraint of increase of HR

Question 14

Epineprhine is synthesized where? Ne?

Answer 14

E: adrenal medulla
Ne: nerves

Question 15

4 reasons why pheochromocytoma is important to diagnosis

Answer 15

1. curable
2. risk for lethal HTN paroxysm
3. Some are malignant (10%)
4. Clue to presence of familial syndrome

Question 16

Clinical presentation of pheochromocytoma

Answer 16

Episodic sweating, palpitation, headache, tachycardia, anxiety

Question 17

Metabolic features of pheochromocytoma

Answer 17

signs of hypercatabolism and hyperglycemia

Question 18

Hematologic features of pheochromocytoma

Answer 18

Orthostatic hypotension, elevated hct, erythrocytosis,

Question 19

How is the presence of pheochromocytoma diagnosed?

Answer 19

24 hr urine: E, NE or metanephrines
Plasma NE and E
Drug free state (give clonidine if you have to) and basal state

Question 20

Location of pheochromocytome tumor

Answer 20

90% are adrenal, 99% in abdomen, rest are in mediastinum

Multiple in 10% of sporadic pheos, but bilateral adrenomedullary disease is the rule in familial pheo

Question 21

Imaging of pheochromocytoma tumor

Answer 21

MRI, CT, scintigraphy

Question 22

Tx of pheochromocytoma

Answer 22

Resection, pre-op control with alpha blockers is a must.

Question 23

Actions of mineralcorticoids

Answer 23

stimulate distal renal tubules to reabsorb sodium, excrete K and H
Expand ECF, increase BP, lower plasma K, increase pH

Question 24

The mineralcorticoid receptor is activated by ____.

Answer 24

Aldosterone and cortisol

Question 25

What does 11B hydroxysteroid dehydrogenase do? What happens if this enzyme is inactivated or overcome?

Answer 25

Inactivates cortisol to keep it from activating the MR.

MC effects including hypertension and hypokalemia.

Question 26

Why don’t you get hypernatremia and edema with mineralcorticoid excess?

Answer 26

regulation by ADH and ANP

Question 27

Regulators of aldosterone

Answer 27

ECF volume, angII (renin can be stimulated by sympathetics), hyperkalemia, NOT ACTH

Question 28

When is the ratio of plasma aldosterone to renin useful?

Answer 28

Diagnose primary hyperaldosteronism. Aldosterone will be high renin will be low.

Question 29

Etiology of primary hyperaldosteronism

Answer 29

2/3 of cases are due to aldosterone secreting adenoma, <2 cm, others are bilateral adrenal hyperplasia

Question 30

Clinical findings in primary hyperaldosteronism

Answer 30

hypertension, hypokalemia (muscle weakness, cramps, polyuria) total body Na increased, but NOT hypernatremia

Question 31

DDx for primary hyperaldosteronism

Answer 31

incidental adrenal nodules are common, thiazide use

Question 32

Tx for primary hyperaldosteronism

Answer 32

resection, spironolactone

Question 33

Is there edema with hyper-aldosteronism?

Answer 33

Nope.Compensatory mechanisms

Question 34

Primary aldosteronism is most commonly due to a benign adenoma in the ______.#

Answer 34

zone glomerulosa

Question 35

An aldosterone-to-renin ratio of ______ is diagnostic of hyperaldosteronism. #

Answer 35

> 20-30

Question 36

How can a Na suppression test diagnose hyperaldosteronism?#

Answer 36

Na-load pt and measure aldosterone. Should go down.

Question 37

Clinical presentation of Cushing

Answer 37

central obesity, moon facies, buffalo hump, HTN, glucose intolerance, purple striae,

Question 38

Glucocorticoids stimulate hepatic synthesis of ____

Answer 38

angiotensinogen