Endocrine hypertension Flashcards
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
____ is a catecholamine producing tumor of chromaffin cells that typically produced HTN.
pheochromocytoma
What percent of pheochromocytomas are malignant? extra-adrenal?
10;10
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
How is pheochromocytoma treated pre-op, intra-op, and post-op?
pre: alpha, beta blockade; fluids
Intraop: IV, fluids
Postop: fluids pressors
What are 3 general conventional risk factors for hypoglycemia?
inadequate caloric consumption, increased insulin sensitivity, impaired glucose production
Neurogenic symptoms of hypoglycemia
sweating, palpitation, tremulousness, hunger, nervousness
Neuroglycopenic symptoms?
impaired concentration, tiredness, dizziness, tingling, blurred vision
Severe neuroglycopenia
seizure coma
4 major components of syndrome of hypoglycemia associated autonomic failure
- recent antecedent hypoglycemia
- hypoglycemia unawareness (impaired symptomatic responses)
- Defective glucose counter-regulation (impaired hormonal responses)
- Recurrent episodes of hypoglycemia
How common is secondary HTN?
less than 5% of all HTN
Describe degradation of catecholamines
By MOA and COMT–> VMA, normetanephrine, metanephrine (can be measured in urine and serum)
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
Epineprhine is synthesized where? Ne?
E: adrenal medulla
Ne: nerves
4 reasons why pheochromocytoma is important to diagnosis
- curable
- risk for lethal HTN paroxysm
- Some are malignant (10%)
- Clue to presence of familial syndrome
Clinical presentation of pheochromocytoma
Episodic sweating, palpitation, headache, tachycardia, anxiety
Metabolic features of pheochromocytoma
signs of hypercatabolism and hyperglycemia
Hematologic features of pheochromocytoma
Orthostatic hypotension, elevated hct, erythrocytosis,
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
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
Imaging of pheochromocytoma tumor
MRI, CT, scintigraphy
Tx of pheochromocytoma
Resection, pre-op control with alpha blockers is a must.
Actions of mineralcorticoids
stimulate distal renal tubules to reabsorb sodium, excrete K and H
Expand ECF, increase BP, lower plasma K, increase pH
The mineralcorticoid receptor is activated by ____.
Aldosterone and cortisol
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.
Why don’t you get hypernatremia and edema with mineralcorticoid excess?
regulation by ADH and ANP
Regulators of aldosterone
ECF volume, angII (renin can be stimulated by sympathetics), hyperkalemia, NOT ACTH
When is the ratio of plasma aldosterone to renin useful?
Diagnose primary hyperaldosteronism. Aldosterone will be high renin will be low.
Etiology of primary hyperaldosteronism
2/3 of cases are due to aldosterone secreting adenoma, <2 cm, others are bilateral adrenal hyperplasia
Clinical findings in primary hyperaldosteronism
hypertension, hypokalemia (muscle weakness, cramps, polyuria) total body Na increased, but NOT hypernatremia
DDx for primary hyperaldosteronism
incidental adrenal nodules are common, thiazide use
Tx for primary hyperaldosteronism
resection, spironolactone
Is there edema with hyper-aldosteronism?
Nope.Compensatory mechanisms
Primary aldosteronism is most commonly due to a benign adenoma in the ______.#
zone glomerulosa
An aldosterone-to-renin ratio of ______ is diagnostic of hyperaldosteronism. #
> 20-30
How can a Na suppression test diagnose hyperaldosteronism?#
Na-load pt and measure aldosterone. Should go down.
Clinical presentation of Cushing
central obesity, moon facies, buffalo hump, HTN, glucose intolerance, purple striae,
Glucocorticoids stimulate hepatic synthesis of ____
angiotensinogen
