Endocrine hypertension and hypoglycemia

Question 1

What is the most common symptom of hypertension

Answer 1

Asymptomatic…by the time headache and pulmonary edema come around you are usually already in trouble

Question 2

Hypokalemia

Answer 2

Cramps, EKG changes, etc…

Question 3

What are the three major endocrine causes of hypertension

Answer 3

• Cushing’s syndrome (excess cortisol)
• Pheocromocytoma (excess catecholamines)
• Hyperaldosteronism

Question 4

What is the first thing you’ll notice in a pt with Cushing’s syndrome

Answer 4

Obesity (moon face, edema, etc..) KNOW!!!

Question 5

What will a pt with pheocromocytoma often present with

Answer 5

headaches, pounding heart rate, excessive sweating, etc.. KNOW!!!

Question 6

How might you test to make sure that something is disobeying physiological regulation in regards to aldosterone release

Answer 6

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.

Question 7

Why would you measure aldosterone and renin levels simultaneously?

Answer 7

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.

Question 8

What are the four leading causes of Endocrine hypertension

Answer 8

Aldosterone-producing Adenoma
Bilateral Adrenal Hyperplasia
Glucocorticoid suppresible aldosteronism
Adrenal Carcinoma

Question 9

Pheochromocytoma

Answer 9

catecholamine producing tumor of chromaffin cells that typically produces hypertension

Question 10

What is the rule of tens in pheochromocytoma

Answer 10

10% are malignant and 10% are extra-adrenal

Question 11

Pheochromocytoma can be familial

Answer 11

• auto dominant
• Multiple endocrine neoplasia
  - hyperparathyroidism and medullary thyroid carcinoma

Question 12

Hypoglycemia is frequent in who?

Answer 12

Diabetics

Question 13

What numbers = HTN

Answer 13

systolic over 140, diastolic over 90

Question 14

Low Renin HTN pts respond better to what types of medications

Answer 14

Diuretics and Calcium channel blockers

Question 15

High Renin pts respond better to?

Answer 15

ACEi

Question 16

What is the major source of Epinephrine in the plasma?

Answer 16

Adrenal Medulla….this makes E a hormone in the traditional sense

Question 17

Norepinephrine is less of a hormone and more of a neurotransmitter

Answer 17

Most of the Norepinephrine is gone once it is released from the sympathetic axon terminals

Question 18

MEN 2A

Answer 18

Pheochromocytoma, hyperparathyroidism, medullary carcinoma

Question 19

MEN 2B

Answer 19

Pheo, multiple mucosal, medullary carcinoma

Question 20

How do you remember the MENs

Answer 20

Both MEN 2A and 2B include pheochromocytoma and medullary carcinoma of the thyroid.
2A includes hyperpArAthyroidism (2 A’s in para)
2B mucosal neuroma

Question 21

Pheochromocytoma is a tumor of what types of cells

Answer 21

chromaffin

Question 22

Clinical signs of Pheo

Answer 22

headache, tachycardia, sweating, episodic htn

Question 23

Metabolic features of pheochromocytoma

Answer 23

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).

Question 24

Diagnosis of pheochromocytoma

Answer 24

Increased serum metanephrines and 24 hour urine metanephrines or catecholamines (either one will work)

Question 25

90% of pheochromocytomas are located where

Answer 25

Adrenal medulla

Question 26

99% of pheochromocytomas are where?

Answer 26

in the abdomen

Question 27

In summary, pheo dx is done by:

Answer 27

sugestive clinical evidence, plasma/urine catecholamines, localization by CT or MRI

Question 28

Mineralocorticoid receptors are activated by what?

Answer 28

Aldosterone AND cortisol (weakly)

Question 29

Why does cortisol activate mineralocorticoid receptors only weakly?

Answer 29

It is converted to cortison in the kidneys by 11Beta hydroxysteroid dehydrogenase

Question 30

Mineralocorticoid excess causes what two pathologic conditions

Answer 30

Hypertension- Due to high intravascular plasma volume Hypokalemic Alkalosis

Question 31

What things that you would expect to happen with aldosterone excess do NOT happen?

Answer 31

Hypernatremia and edema...hypernatremia is pretty well controlled by ADH and thirst.

Question 32

Mechanism of Aldosterone secretion:

Answer 32

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

Question 33

ANG 2 is also a potent vasoconstrictor!!!! KNOW

Answer 33

it increases BP directly in this way

Question 34

Primary hyperaldosteronism=

Answer 34

usually an adrenal adenoma. Renin will be low because negative feedback will be intact

Question 35

Secondary hyperaldosteronism

Answer 35

Increased renin secretion due to volume loss or some condition where congestive heart failure

Question 36

What is used to diagnose primary hyperaldosteronism

Answer 36

aldosterone: renin ratio

Question 37

Hypertension and spontaneous hypokalemia means you should suspect

Answer 37

Primary hyperaldosteronism

Question 38

Aldosterone:Renin over 30

Answer 38

suspect primary hyperaldosteronism

Question 39

Aldo : Renin over 50

Answer 39

Definitely primary hyperaldo

Question 40

Glucocorticoid excess =

Answer 40

Cushings

Question 41

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

Answer 41

You get trunkal obesity due to stimulation of appetite Muscle weakness and connective tissue weakness doe to catabolic effects Bone mass decreases