Endocrine hypertension and hypoglycemia Flashcards Preview

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Flashcards in Endocrine hypertension and hypoglycemia Deck (41):
1

What is the most common symptom of hypertension

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

2

Hypokalemia

Cramps, EKG changes, etc...

3

What are the three major endocrine causes of hypertension

- Cushing's syndrome (excess cortisol)
- Pheocromocytoma (excess catecholamines)
- Hyperaldosteronism

4

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

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

5

What will a pt with pheocromocytoma often present with

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

6

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.

7

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.

8

What are the four leading causes of Endocrine hypertension

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

9

Pheochromocytoma

catecholamine producing tumor of chromaffin cells that typically produces hypertension

10

What is the rule of tens in pheochromocytoma

10% are malignant and 10% are extra-adrenal

11

Pheochromocytoma can be familial

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

12

Hypoglycemia is frequent in who?

Diabetics

13

What numbers = HTN

systolic over 140, diastolic over 90

14

Low Renin HTN pts respond better to what types of medications

Diuretics and Calcium channel blockers

15

High Renin pts respond better to?

ACEi

16

What is the major source of Epinephrine in the plasma?

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

17

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

18

MEN 2A

Pheochromocytoma, hyperparathyroidism, medullary carcinoma

19

MEN 2B

Pheo, multiple mucosal, medullary carcinoma

20

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

21

Pheochromocytoma is a tumor of what types of cells

chromaffin

22

Clinical signs of Pheo

headache, tachycardia, sweating, episodic htn

23

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).

24

Diagnosis of pheochromocytoma

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

25

90% of pheochromocytomas are located where

Adrenal medulla

26

99% of pheochromocytomas are where?

in the abdomen

27

In summary, pheo dx is done by:

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

28

Mineralocorticoid receptors are activated by what?

Aldosterone AND cortisol (weakly)

29

Why does cortisol activate mineralocorticoid receptors only weakly?

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

30

Mineralocorticoid excess causes what two pathologic conditions

Hypertension- Due to high intravascular plasma volume

Hypokalemic Alkalosis

31

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.

32

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

33

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

it increases BP directly in this way

34

Primary hyperaldosteronism=

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

35

Secondary hyperaldosteronism

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

36

What is used to diagnose primary hyperaldosteronism

aldosterone: renin ratio

37

Hypertension and spontaneous hypokalemia means you should suspect

Primary hyperaldosteronism

38

Aldosterone:Renin over 30

suspect primary hyperaldosteronism

39

Aldo : Renin over 50

Definitely primary hyperaldo

40

Glucocorticoid excess =

Cushings

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

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