Endocrine hypertension Flashcards Preview

Endocrinology > Endocrine hypertension > Flashcards

Flashcards in Endocrine hypertension Deck (38):
1

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

Pheochromocytoma, mineralcorticoid excess, glucocorticoid excess

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

2

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

pheochromocytoma

3

What percent of pheochromocytomas are malignant? extra-adrenal?

10;10

4

Describe familial syndrome assosiated with pheochromocytoma?

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

5

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

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

6

What are 3 general conventional risk factors for hypoglycemia?

inadequate caloric consumption, increased insulin sensitivity, impaired glucose production

7

Neurogenic symptoms of hypoglycemia

sweating, palpitation, tremulousness, hunger, nervousness

8

Neuroglycopenic symptoms?

impaired concentration, tiredness, dizziness, tingling, blurred vision

9

Severe neuroglycopenia

seizure coma

10

4 major components of syndrome of hypoglycemia associated autonomic failure

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

11

How common is secondary HTN?

less than 5% of all HTN

12

Describe degradation of catecholamines

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

13

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

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

14

Epineprhine is synthesized where? Ne?

E: adrenal medulla
Ne: nerves

15

4 reasons why pheochromocytoma is important to diagnosis

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

16

Clinical presentation of pheochromocytoma

Episodic sweating, palpitation, headache, tachycardia, anxiety

17

Metabolic features of pheochromocytoma

signs of hypercatabolism and hyperglycemia

18

Hematologic features of pheochromocytoma

Orthostatic hypotension, elevated hct, erythrocytosis,

19

How is the presence of pheochromocytoma diagnosed?

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

20

Location of pheochromocytome tumor

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

21

Imaging of pheochromocytoma tumor

MRI, CT, scintigraphy

22

Tx of pheochromocytoma

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

23

Actions of mineralcorticoids

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

24

The mineralcorticoid receptor is activated by ____.

Aldosterone and cortisol

25

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

Inactivates cortisol to keep it from activating the MR.

MC effects including hypertension and hypokalemia.

26

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

regulation by ADH and ANP

27

Regulators of aldosterone

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

28

When is the ratio of plasma aldosterone to renin useful?

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

29

Etiology of primary hyperaldosteronism

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

30

Clinical findings in primary hyperaldosteronism

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

31

DDx for primary hyperaldosteronism

incidental adrenal nodules are common, thiazide use

32

Tx for primary hyperaldosteronism

resection, spironolactone

33

Is there edema with hyper-aldosteronism?

Nope.Compensatory mechanisms

34

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

zone glomerulosa

35

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

>20-30

36

How can a Na suppression test diagnose hyperaldosteronism?#

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

37

Clinical presentation of Cushing

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

38

Glucocorticoids stimulate hepatic synthesis of ____

angiotensinogen