Endocrine hypertension and hypoglycemia Flashcards Preview

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

What is the most common symptom of hypertension

A

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

2
Q

Hypokalemia

A

Cramps, EKG changes, etc…

3
Q

What are the three major endocrine causes of hypertension

A
  • Cushing’s syndrome (excess cortisol)
  • Pheocromocytoma (excess catecholamines)
  • Hyperaldosteronism
4
Q

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

A

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

5
Q

What will a pt with pheocromocytoma often present with

A

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

6
Q

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

A

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
Q

Why would you measure aldosterone and renin levels simultaneously?

A

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
Q

What are the four leading causes of Endocrine hypertension

A

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

9
Q

Pheochromocytoma

A

catecholamine producing tumor of chromaffin cells that typically produces hypertension

10
Q

What is the rule of tens in pheochromocytoma

A

10% are malignant and 10% are extra-adrenal

11
Q

Pheochromocytoma can be familial

A
  • auto dominant
  • Multiple endocrine neoplasia
    - hyperparathyroidism and medullary thyroid carcinoma
12
Q

Hypoglycemia is frequent in who?

A

Diabetics

13
Q

What numbers = HTN

A

systolic over 140, diastolic over 90

14
Q

Low Renin HTN pts respond better to what types of medications

A

Diuretics and Calcium channel blockers

15
Q

High Renin pts respond better to?

A

ACEi

16
Q

What is the major source of Epinephrine in the plasma?

A

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

17
Q

Norepinephrine is less of a hormone and more of a neurotransmitter

A

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

18
Q

MEN 2A

A

Pheochromocytoma, hyperparathyroidism, medullary carcinoma

19
Q

MEN 2B

A

Pheo, multiple mucosal, medullary carcinoma

20
Q

How do you remember the MENs

A

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
Q

Pheochromocytoma is a tumor of what types of cells

A

chromaffin

22
Q

Clinical signs of Pheo

A

headache, tachycardia, sweating, episodic htn

23
Q

Metabolic features of pheochromocytoma

A

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
Q

Diagnosis of pheochromocytoma

A

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

25
Q

90% of pheochromocytomas are located where

A

Adrenal medulla

26
Q

99% of pheochromocytomas are where?

A

in the abdomen

27
Q

In summary, pheo dx is done by:

A

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

28
Q

Mineralocorticoid receptors are activated by what?

A

Aldosterone AND cortisol (weakly)

29
Q

Why does cortisol activate mineralocorticoid receptors only weakly?

A

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

30
Q

Mineralocorticoid excess causes what two pathologic conditions

A

Hypertension- Due to high intravascular plasma volume

Hypokalemic Alkalosis

31
Q

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

A

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

32
Q

Mechanism of Aldosterone secretion:

A

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
Q

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

A

it increases BP directly in this way

34
Q

Primary hyperaldosteronism=

A

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

35
Q

Secondary hyperaldosteronism

A

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

36
Q

What is used to diagnose primary hyperaldosteronism

A

aldosterone: renin ratio

37
Q

Hypertension and spontaneous hypokalemia means you should suspect

A

Primary hyperaldosteronism

38
Q

Aldosterone:Renin over 30

A

suspect primary hyperaldosteronism

39
Q

Aldo : Renin over 50

A

Definitely primary hyperaldo

40
Q

Glucocorticoid excess =

A

Cushings

41
Q

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

A

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