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Kaplan Physio: Endocrine > Adrenal Cortex > Flashcards

Adrenal Cortex Flashcards

1
Q

What are 2 substances that can stimulate aldosterone secretion?

A

Ang II and/or K+

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2
Q

What is the starting point in the synthesis of all adrenal steroids?

A

cholesterol

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3
Q

What is the source of cholesterol in the body mainly from?

A

from LDL in the blood

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4
Q

What is the rate limiting step for all steroid hormone synthesis?

A

cholesterol being transported into the mitochondria by StAR (steroidogenic acute regulatory protein)

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5
Q

Cholesterol, once in the mitochondria, is converted to pregnenolone via what enzyme?

A

SCC also called desmolase

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6
Q

DHEA stands for what?

A

dehydroepiandrosterone

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7
Q

Glucocorticoid produced by the adrenal cortex?

A

cortisol

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8
Q

Mineralicorticoid produced by the adrenal cortex?

A

aldosterone

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9
Q

What are the pertinent enzymes required for cortisol synthesis?

A

17 α-OH, 21 β-OH, 11 β-OH

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10
Q

Beyond SCC, what is the pertinent enzyme required for adrenal androgen synthesis?

A

17 α-OH

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11
Q

What are adrenal androgens conjugated with in the adrenal cortex that makes them more water soluble?

A

conjugated with sulfate

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12
Q

Cortisol has negative feedback on what hormones secreted from the hypothalamic pituitary axis?

A

negative feedback on CRH from hypothalamus and ACTH from anterior pituitary.

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13
Q

Where in the adrenal cortex is aldosterone synthesized?

A

zona glomerulosa

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14
Q

Where in the adrenal cortex is cortisol synthesized ?

A

zona fasiculata

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15
Q

Where in the adrenal cortex are androgens synthesized?

A

Zona reticularis

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16
Q

In contrast to cortisol, what major enzyme does aldosterone not require for synthesis?

A

17 α-OH

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17
Q

What is a weak mineralocorticoid that is synthesized and secreted mostly from the zona fasiculata that is very important when discussing congenital adrenal hyperplasia?

A

11-deoxycorticosterone

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18
Q

What is an important compound to test for and used for infant screening because alterations may indicate possible enzyme deficiencies in the adrenal cortex?

A

intermediate 17 hydroxyprogesterone which is a precursor for cortisol

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19
Q

What are the stress hormones?

A

cortisol
GH
glucagon
epinephrine

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20
Q

Major action of GH in stress response?

A

mobilizes fatty acids by increasing lipolysis in adipose tissue

21
Q

Major action of glucagon in the stress response?

A

mobilizes glucose by increasing liver glycogenolysis

22
Q

What is the major action of cortisol in the stress response?

A

mobilizes fat, protein, carbs

23
Q

What is the major action of epinephrine in the stress response?

A

mobilizes glucose via glycogenolysis and fat via lipolysis

24
Q

A deficiency in stress hormones may lead to hyperglycemia or hypoglycemia?

A

hypoglycemia

25
How does cortisol affect proteins in your body?
cortisol promotes degradation and increased delivery of hepatic gluconeogenic precursors
26
How does cortisol affect your lipids?
cortisol promotes lipolysis and increased delivery of FFA and glycerol
27
How does cortisol affect carbohydrates?
cortisol raises blood glucose, making more glucose available for nervous tissue 2 mechanisms involved * cortisol counteracts insulin's action in most tissue * cortisol increases hepatic output of glucose by regulating enzymes involved in gluconeogenesis, particularly phosphoenolypyurvate carboxykinase (PEPCK)
28
Peak cortisol secretion occurs during what time of the day typically?
early in the morning between hours 6 - 8 of sleep
29
Why does excessive secretion of ACTH cause darkening of the skin?
due to melanocyte-stimulating hormone (a-MSH) sequence within the ACTH molecule, and the B-MSH activity of B-lipoprotein
30
What are the effects of aldosterone on the kidney?
* promotes the activity of Na/K -ATPase - dependent pump that moves Na+ into the renal ECF in exchange for K+ * enhances epithelial Na+ channels (ENaC) in the luminal membrane of principal cells; net effect is to increase Na+ reabsorption, which in turn increase water reabsorption * Stimulates H+ secretion by intercalated cells; thus, excess aldosterone causes alkalosis, while insufficient aldosterone causes acidosis
31
Where is the main sensory input to measure the volume of blood in the body?
in the modified smooth muscle cells of the JGA on afferent arteriole
32
What do the macula densa cells sense?
salt delivery to distal tubule and communicate with JG cells
33
Where is angiotensinogen produced?
in the liver
34
What is Cushing syndrome?
is hypercortisolism regardless of origin
35
What is Cushing disease?
hypercortiosolism due to an adenoma of the anterior pituitary microadenoma)
36
What is the first step in establishing the presence of hypercortisolism?
1. 24 hour urine free cortisol or 1 mg overnight dexamethasone suppression test (a single random cortisol level should not be used to diagnose hypercortisolism
37
What is the 1-mg overnight dexamethasone suppression test used for? | Also are there situations where you can get false positives?
tests for the presence of Cushing syndrome, regardless of the cause - cortisol decreases: normal - cortisol does not decrease: hypercortisolism - false-positives from depression or alcoholism
38
What is the purpose of high-dose dexamethasone test?
used to differentiate pituitary adenoma from ectopic ACTH secretion and adrenal tumors cortisol decreases: pituitary source cortisol does not decrease: ectopic ACTH, adrenal tumor
39
Decipher the results of ACTH stimulation test used to determine adrenal insufficiency.
cortisol increases after ACTH: normal No change in cortisol level: adrenal insufficiency
40
What is the purpose of performing an ACTH stimulation test?
to diagnose adrenal insufficiency to diagnose atrophied adrenal non-responsive
41
What do we measure after a 24 hour urine cortisol establishes presence of hypercortisolism to determine etiology of hypercortisolism?
ACTH
42
How do we decipher a test if a person has hypercortisolism when we then measure ACTH?
ACTH low = adrenal source of cortisol overproduction ACTH normal or high = pituitary or ectopic source (secondary condition)
43
How was metayrapone used to test adrenal enzyme deficiency?
simulates 11 β-hydroxylase deficiency (precursor to make cortisol) Normal = ACTH goes up Pituitary insuffiency = ACTH fails to rise
44
What is primary hypercortisolism?
when there is an adrenal source
45
What is secondary hypercortisolism?
pituitary vs ectopic
46
What are the characteristic of Cushing syndrome? (Name 5)
* obesity because of hyperphagia, classically central affecting mainly the face neck, trunk, and abdomen: "moon facies" and "buffalo hump" * protein depletion as a result of excessive protein catabolism * inhibition of inflammatory response and poor wound healing * hyperglycemia leads to hyperinsulinemia and insulin resistance * hyperlipidemia * bone breakdown and osteoporosis * thinning of the skin with wide purple striae located around abdomen * increased adrenal androgens, when present in women, can result in acne, mild hirsutism, and amenorrhea. In men decreased libido and impotence * mineralocorticoid effects of high level of glucocorticoid and deoxycorticosterone lead to salt and water retention ( hypertension), potassium depletion, and a hypokalemic alkalosis. * increase thirst and polyruia ( anxiety, depression, and other emotional disorders may be present
47
Other names for hypocortisolism?
primary hypocortisolism (in primary adrenal insufficiency, Addison's disease)
48
Clinical features of hypocortisolism?
weakness, fatigue, anorexia, weight loss, hypotension, hyponatremia, hypoglycemia, increases in ACTH result in hyperpigmentation of skin and mucous membranes
49
What is the most common cause of secondary hypocortisolism?
(secondary adrenal insufficiency) is caused most commonly due to sudden withdrawal of exogenous glucocorticoid therapy

Kaplan Physio: Endocrine (9 decks)

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