Endo - Control Of Blood Pressure

Front 1

Where does most of the body's NE come from?

Back 1

Almost all the body's NE comes from sympathetic nerve fibers

Front 2

Where does most of the body's EPI come from?

Back 2

Almost all the body's EPI comes from the Adrenal Medulla

Front 3

What is the rate limiting step in the synthesis of catecholamines?

Back 3

Tyrosine Hydroxylase. This enzyme is an important drug target as well.

Front 4

Why is the adrenal portal system critical?

Back 4

The presence of glucocorticoids are required to synthesis catecholamines!

Front 5

What are the two catechol receptors important to the endo course?

Back 5

Alpha-1 and Beta-1 adrenergic receptors.

Front 6

Can a pheochromocytoma by diagnosed by a serum EPI level?

Back 6

No - pheochromocytoma tumors often produce only medium-high levels of h'mone.

Front 7

What urine metabolite can be used to detect a pheochromocytoma?

Back 7

VMA will often "spill" into the urine with large pheochromocytoma.

Front 8

May imaging studies be used to screen for pheochromocytoma?

Back 8

No, only to localize them once discovered clinically or through lab tests.

Front 9

The drug Metyrosine is...

Back 9

Metyrosine inhibits tyrosine hydroxylase (initial, rate-limiting step). Used to treat pheochromocytoma.

Front 10

What is the function of Renin in the RAA axis?

Back 10

Renin initiates the RAA axis cascade

Front 11

What are the four regulators of renin release?

Back 11

* Sympathetic/adrenergic activity
* Decreased renal perfusion pressure
* Low Na+ in the urinary lumen
* Low serum K+

Front 12

What cells in the kidney make renin?

Back 12

The Juxtaglomerular cells, or JG cells.

Front 13

What are the two ways Angiotensin-II increases blood pressure?

Back 13

Directly, it causes vasoconstriction. Indirectly, it stimulates the release of aldosterone from the adrenal cortex.

Front 14

What are the two types of hyperaldosteronism?

Back 14

Primary: low renin, nearly always pathology in the adrenal cortex.
Secondary: high renin due to renal circulation problems, etc.

Front 15

List a differential dx for secondary hyperaldosteronism.

Back 15

Hemorrhage, renal stenosis, cardiac failure and dehydration.

Front 16

What factors regulate ADH release?

Back 16

* Serum osmolarity
* Intravascular volume
* Blood pressure
* Neural input from the hypothalamus
* temperature, medications, etc.

Front 17

What are the S/Sx of Diabetes Insipidus?

Back 17

* Copious, dilute urine.
* No glucoseuria or other osmotic diuresis
* No hypokalemia
* No hypercalcemia
* No diuretics

Front 18

How is central vs nephrogenic DI diagnosed?

Back 18

Central DI will have low ADH levels, nephrogenic DI has high ADH levels.

Front 19

What is the treatment for Diabetes Insipidus?

Back 19

* Water!
* for Central DI: exogenous ADH
* for Nephrogenic: treat causes, or exogenous ADH

Front 20

What are the two causes of high serum sodium concentrations?

Back 20

1) Too little water
2) Too much ADH

Front 21

What recently-developed plasma test is used to detect pheochromocytomas?

Back 21

Virtually all pheochromocytomas continuously secrete excessive metanephrines due to the tumor's own catabolism of catecholamines. Metanephrines may be detected in the blood.

Front 22

What two tests are most commonly used to diagnose pheochromocytomas?

Back 22

Plasma free metanephrines and 24-hour collection of urine catecholamines.

Front 23

What three endocrine systems help regulate blood pressure?

Back 23

1) SANS/Catecholamines
2) Renin-Angiotensin-Aldosterone
3) Post. Pit/ADH

Front 24

What hormonal mechanism exists to help REDUCE blood pressure in a hypertensive state?

Back 24

Atrial natriuretic factors will increase sodium excretion when blood pressure or blood volume runs high.

Front 25

What hepatic enzyme metabolizes circulating catecholamines? What intermediates are produced?

Back 25

1) Hepatic enzyme: Catechol-O-methyltransferase (COMT)
2) Metanephrine and Normetanephrine are the intermediates produced

Front 26

What effect does high serum K+ have on renin release? On aldosterone secretion?

Back 26

* High serum K+ inhibits renin release by the JG cells.
* High serum K+ promotes aldosterone release by the adrenal medulla.

Front 27

What change in sensitivity protects a hypotensive, hypokalemic patient against further potassium loss?

Back 27

Hypotension will normally lead to increased Angiotensin II via R.A.A. axis activation. But low serum potassium will desensitize the Z. glomerulosa cells to Angiotensin II, protecting against additional K loss.

Front 28

What is the usual cause of increased renin secretion?

Back 28

Decreased renal blood flow is the usual cause of high renin secretion.

Front 29

What causes primary hyperaldosterone secretion?

Back 29

Primary Hyperaldosterone secretion is an autonomous secretion of aldosterone by the adrenal glands. 1/2 are due to adrenal adenoma, and 1/2 are due to adrenal hyperplasia.

Front 30

When should primary hyperaldosterone secretion be suspected?

Back 30

Early-onset hypertension is suspect for hyperadosterone secretion.

Front 31

What are the most common causes of SIADH?

Back 31

1) Lung tumors (bronchiogenic carcinoma)
2) Pneumonia
3) CNS pathology
4) Medications (SSRIs, Vincristine, nicotine, narcotics, etc.)

Front 32

Hyponatremia usually means...
Hypernatremia usually means...

Back 32

Hyponatremia usually means too much water, but NOT too little salt.
Hypernatremia usually means to little water, but NOT too much salt.

Front 33

What two conditions confound the diagnosis of SIADH?

Back 33

SIADH may not be diagnosed in the presence of unchecked hypothyroidism or hypoadrenalism.