Endocrine hypertension and hypoglycemia Flashcards
What is the most common symptom of hypertension
Asymptomatic…by the time headache and pulmonary edema come around you are usually already in trouble
Hypokalemia
Cramps, EKG changes, etc…
What are the three major endocrine causes of hypertension
- Cushing’s syndrome (excess cortisol)
- Pheocromocytoma (excess catecholamines)
- Hyperaldosteronism
What is the first thing you’ll notice in a pt with Cushing’s syndrome
Obesity (moon face, edema, etc..) KNOW!!!
What will a pt with pheocromocytoma often present with
headaches, pounding heart rate, excessive sweating, etc.. KNOW!!!
How might you test to make sure that something is disobeying physiological regulation in regards to aldosterone release
Infuse saline and see if Aldosterone levels are still high. Remember, the RAAS (renin-angiotensin-aldosterone system) has one main function, that is to retain sodium. If you give Saline (containing sodium) and the aldosterone doesn’t drop, you’ve got a problem.
Why would you measure aldosterone and renin levels simultaneously?
Renin drives aldosterone secretion. If renin is high, the increased aldosterone levels are explained (this is called secondary hyperaldosteronism). If Renin is low, you know it is a primary aldosterone problem.
What are the four leading causes of Endocrine hypertension
Aldosterone-producing Adenoma
Bilateral Adrenal Hyperplasia
Glucocorticoid suppresible aldosteronism
Adrenal Carcinoma
Pheochromocytoma
catecholamine producing tumor of chromaffin cells that typically produces hypertension
What is the rule of tens in pheochromocytoma
10% are malignant and 10% are extra-adrenal
Pheochromocytoma can be familial
- auto dominant
- Multiple endocrine neoplasia
- hyperparathyroidism and medullary thyroid carcinoma
Hypoglycemia is frequent in who?
Diabetics
What numbers = HTN
systolic over 140, diastolic over 90
Low Renin HTN pts respond better to what types of medications
Diuretics and Calcium channel blockers
High Renin pts respond better to?
ACEi
What is the major source of Epinephrine in the plasma?
Adrenal Medulla….this makes E a hormone in the traditional sense
Norepinephrine is less of a hormone and more of a neurotransmitter
Most of the Norepinephrine is gone once it is released from the sympathetic axon terminals
MEN 2A
Pheochromocytoma, hyperparathyroidism, medullary carcinoma
MEN 2B
Pheo, multiple mucosal, medullary carcinoma
How do you remember the MENs
Both MEN 2A and 2B include pheochromocytoma and medullary carcinoma of the thyroid.
2A includes hyperpArAthyroidism (2 A’s in para)
2B mucosal neuroma
Pheochromocytoma is a tumor of what types of cells
chromaffin
Clinical signs of Pheo
headache, tachycardia, sweating, episodic htn
Metabolic features of pheochromocytoma
Hypercatabolism and hyperglycemia (due to high level of catecholamines which, as we know, depress insulin secretion and encourage glucagon secretion and glucose production in liver).
Diagnosis of pheochromocytoma
Increased serum metanephrines and 24 hour urine metanephrines or catecholamines (either one will work)
90% of pheochromocytomas are located where
Adrenal medulla
99% of pheochromocytomas are where?
in the abdomen
In summary, pheo dx is done by:
sugestive clinical evidence, plasma/urine catecholamines, localization by CT or MRI
Mineralocorticoid receptors are activated by what?
Aldosterone AND cortisol (weakly)
Why does cortisol activate mineralocorticoid receptors only weakly?
It is converted to cortison in the kidneys by 11Beta hydroxysteroid dehydrogenase
Mineralocorticoid excess causes what two pathologic conditions
Hypertension- Due to high intravascular plasma volume
Hypokalemic Alkalosis
What things that you would expect to happen with aldosterone excess do NOT happen?
Hypernatremia and edema…hypernatremia is pretty well controlled by ADH and thirst.
Mechanism of Aldosterone secretion:
Renin (from JGA) —> Ang 1 —> converted to Ang 2 by ACE in endothelial cells—> Ang 2 stimulates aldosterone secretion which increases plasma sodium, increases ECF, which is sensed by JGA and renin production stops
ANG 2 is also a potent vasoconstrictor!!!! KNOW
it increases BP directly in this way
Primary hyperaldosteronism=
usually an adrenal adenoma. Renin will be low because negative feedback will be intact
Secondary hyperaldosteronism
Increased renin secretion due to volume loss or some condition where congestive heart failure
What is used to diagnose primary hyperaldosteronism
aldosterone: renin ratio
Hypertension and spontaneous hypokalemia means you should suspect
Primary hyperaldosteronism
Aldosterone:Renin over 30
suspect primary hyperaldosteronism
Aldo : Renin over 50
Definitely primary hyperaldo
Glucocorticoid excess =
Cushings
Most of cushings can be explained by the known actions of cortisol. When you are trying to think of the actions of cortisol, think about cushings
You get trunkal obesity due to stimulation of appetite
Muscle weakness and connective tissue weakness doe to catabolic effects
Bone mass decreases
