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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
Q

How does cortisol affect proteins in your body?

A

cortisol promotes degradation and increased delivery of hepatic gluconeogenic precursors

26
Q

How does cortisol affect your lipids?

A

cortisol promotes lipolysis and increased delivery of FFA and glycerol

27
Q

How does cortisol affect carbohydrates?

A

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
Q

Peak cortisol secretion occurs during what time of the day typically?

A

early in the morning between hours 6 - 8 of sleep

29
Q

Why does excessive secretion of ACTH cause darkening of the skin?

A

due to melanocyte-stimulating hormone (a-MSH) sequence within the ACTH molecule, and the B-MSH activity of B-lipoprotein

30
Q

What are the effects of aldosterone on the kidney?

A
  • 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
Q

Where is the main sensory input to measure the volume of blood in the body?

A

in the modified smooth muscle cells of the JGA on afferent arteriole

32
Q

What do the macula densa cells sense?

A

salt delivery to distal tubule and communicate with JG cells

33
Q

Where is angiotensinogen produced?

A

in the liver

34
Q

What is Cushing syndrome?

A

is hypercortisolism regardless of origin

35
Q

What is Cushing disease?

A

hypercortiosolism due to an adenoma of the anterior pituitary microadenoma)

36
Q

What is the first step in establishing the presence of hypercortisolism?

A
  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
Q

What is the 1-mg overnight dexamethasone suppression test used for?

Also are there situations where you can get false positives?

A

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
Q

What is the purpose of high-dose dexamethasone test?

A

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
Q

Decipher the results of ACTH stimulation test used to determine adrenal insufficiency.

A

cortisol increases after ACTH: normal
No change in cortisol level: adrenal insufficiency

40
Q

What is the purpose of performing an ACTH stimulation test?

A

to diagnose adrenal insufficiency

to diagnose atrophied adrenal non-responsive

41
Q

What do we measure after a 24 hour urine cortisol establishes presence of hypercortisolism to determine etiology of hypercortisolism?

A

ACTH

42
Q

How do we decipher a test if a person has hypercortisolism when we then measure ACTH?

A

ACTH low = adrenal source of cortisol overproduction
ACTH normal or high = pituitary or ectopic source (secondary condition)

43
Q

How was metayrapone used to test adrenal enzyme deficiency?

A

simulates 11 β-hydroxylase deficiency (precursor to make cortisol)

Normal = ACTH goes up

Pituitary insuffiency = ACTH fails to rise

44
Q

What is primary hypercortisolism?

A

when there is an adrenal source

45
Q

What is secondary hypercortisolism?

A

pituitary vs ectopic

46
Q

What are the characteristic of Cushing syndrome? (Name 5)

A
  • 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
Q

Other names for hypocortisolism?

A

primary hypocortisolism (in primary adrenal insufficiency, Addison’s disease)

48
Q

Clinical features of hypocortisolism?

A

weakness, fatigue, anorexia, weight loss, hypotension, hyponatremia, hypoglycemia, increases in ACTH result in hyperpigmentation of skin and mucous membranes

49
Q

What is the most common cause of secondary hypocortisolism?

A

(secondary adrenal insufficiency) is caused most commonly due to sudden withdrawal of exogenous glucocorticoid therapy

Kaplan Physio: Endocrine (9 decks)

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