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Physiology Exam 2 Endocrine (Shelby) > Adrenal - cortex stuff! > Flashcards

Adrenal - cortex stuff! Flashcards

1
Q

What does corticotrophin releasing hormone (CRH) do?

A

stimulates corticotrophs to release ACTH

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2
Q

decrease in which hormone causes the symptoms of decreased pubic and axillary hair and decreased libido in females?

A

decreased androgens

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3
Q

When is the greatest secretory activity of cortisol?

A

MORNING

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4
Q

21 b-hydroxylase deficiency effect on ACTH?

A

ACTH levels are HIGH (due to no cortisol)

high ACTH = trophic effect on adrenal gland (GROWTH OF GLAND)

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5
Q

What is the only thing that inhibits corticotrophin releasing hormone (CRH)

A

cortisol

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6
Q

17a-hydroxylase deficiency

(hyper/hypo)tension
(hyper/hypo)kalemia
metabolic (alkalosis/acidosis)

A

hypertension
hypokalemia
metabolic alkalosis

(same as conn syndrome except there is LESS aldosterone… effects from increased 11-DOC and corticosterone)

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7
Q

Conn syndrome is caused by:

A

an aldosterone-secreting tumor

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8
Q

Why is skin pigmentation normal with secondary and tertiary adrenocortical insufficiency but hyperpigmented in primary adrenocortical insufficiency (Addisons)

A

2/3: normal because ACTH is not over secreted from pituitary (hypothalamus and pituitary are the problems)

primary: hyperpigment because ACTH is over secreted from pituitary due to low cortisol from the adrenal gland which is the problem

(a-MSH is the reason for pigmentation which is a derivative of ACTH)

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9
Q

Why are renin levels low in Conn syndrome?

A

Due to the hypertension caused by aldosterone.

Only aldosterone is increased due to the tumor

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10
Q

Why does the adrenal gland enlarge with 21 b-hydroxylase deficiency

A

trophic effect on adrenal gland from high levels of ACTH (due to lack of cortisol)

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11
Q

What layers of the cortex contain desmolase

A

all layers

zona glomerulosa
zona fasiculata
zona reticularis

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12
Q

decrease in which hormone causes the symptoms of hypoglycemia, weight loss, and muscle weakness in Addison’s disease?

A

decreased cortisol

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13
Q

What is the LEAST important secretagogue for aldosterone synthesis?

A

ACTH

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14
Q

21 b-hydroxylase deficiency leads to:

(hyper/hypo)natremia
(hyper/hypo)glycemia

A

hyponatremia (no aldosterone!)

hypoglycemia (no cortisol!)

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15
Q

What causes hyperpigmentation of skin on elbows, knees, nipples, and scars in Addison’s disease?

A

increased ACTH —> increased a-MSH fragment

increased ACTH caused by low cortisol because only cortisol is the inhibitor of CRH —> which keeps ACTH stimulated

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16
Q

cortisol (and androgens) levels in the blood reflect a ______ and _______ release of ACTH

A

circadian and pulsatile release of ACTH

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17
Q

What are androgens responsible for in women?

A
  1. axillary hair
  2. pubic hair
  3. libido
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18
Q

What are the results of a 21 b-hydroxylase deficiency in utero?

A 
masculinization of female
penis-like clitoris
scrotum-like labia
deep voice
increased muscle mass
amenorrhea
hirsutism
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19
Q

cortisol effects on bone:

A

decrease calcium absorption —> decrease plasma calcium —> mobilizes calcium from bone —> inhibits bone formation —> bone loss

(no calcium taken up from GI or kidneys, so the bones release calcium to make up for the decrease in plasma calcium which causes the bones to be deficient and cannot form new bone cells)

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20
Q

decrease in which hormone causes the symptoms of hyperkalemia, hypotension, metabolic acidosis, and salt craving in Addison’s disease?

A

decreased aldosterone

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21
Q

Which part of the adrenal gland responds to SHORT term stress?

A

medulla

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22
Q

Why are adrenal androgens referred to as 17-ketosteroids?

A

because they have a ketone at C17

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23
Q

cortisol effect on:

protein:
lipids:
glucose uptake:

A

protein CATABOLISM (synthesis is decreased)
lipoLYSIS (provides glycerol)
decreased glucose uptake by tissue (more in blood)

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24
Q

What does aldosterone bind to to stimulate sodium and water reabsorption? and potassium and H+ secretion?

A

intracellular mineralcorticoid receptor (MR1)

which binds to a mineralcorticoid responsive element (MRE)

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25
Q

How is secretion of ACTH enhanced during periods of stress?

A

increased AMPLITUDE of CRH burst

NOT frequency

26
Q

cortisol action on the cardiovascular system:

2

A
  1. with catecholamines regulates blood pressure

2. up-regulates a-1 receptor responsiveness

27
Q

What is the SECOND most important secretagogue for aldosterone synthesis?

A

increase is plasma K+ concentration

NOT ACTH!

28
Q

What is secondary adrenocortical insufficiency?

A

failure of corticoptrophs to adequately secrete ACTH

pituitary problem

29
Q

The overall metabolic effect of cortisol is to increase _________ by enhancing _________

A

blood glucose

gluconeogenesis

30
Q

cortisol has what effect on insulin sensitivity? Why?

A

decreased sensitivity to glucose

goal is to have increased BLOOD glucose, insulin would decrease blood glucose by putting it in the cell

31
Q

Cushing’s syndrome

cortisol levels =
ACTH levels =

A

Cushing’s syndrome

cortisol levels = HIGH
ACTH levels = LOW

32
Q

17a-hydroxylase deficiency

aldosterone =
cortisol =
androgens =

A 
aldosterone = decreased
cortisol = none
androgens = none
33
Q

cortisol effect on connective tissue and muscle

A

inhibits fibroblast proliferation
inhibits collagen formation
skin thins
impaired connective tissue support of capillaries
increased proteolysis in muscle —> weakness

34
Q

What are 2 other terms for newborn females with androgenital syndrome from 21 b-hydroxylase deficiency

A

female pseudohermaphrodite

contra-sexual development

35
Q

21 b-hydroxylase deficiency would cause an increase in __________ and a decrease in ___________

A

increased androgens

decreased cortisol and aldosterone

36
Q

What three things does ACTH do in the adrenal gland

A
  1. growth of adrenal gland
  2. transfers cholesterol into mitochondria
  3. activates desmolase to convert cholesterol to pregnenolone
37
Q

What is the most important secretagogue for aldosterone synthesis?

A

angiotensin 2 — RAAS system

NOT ACTH!

38
Q

Free cholesterol is transferred to the mitochondria, and then to the innter mitochondrial membrane by:

A

steroidgenic acute regulatory protein (StaR)

39
Q

Conn syndrome effect on:

Sodium
Water
Potassium
H+

A

Sodium - reabsorption = HYPERnatremia
Water - retention = HYPERtension
Potassium - secretion = HYPOkalemia
H+ - secretion = metabolic ALKALosis

40
Q

What stimulates aldosterone? (two things)

A
  1. decrease in BP

2. decrease in ECF volume

41
Q

What is tertiary adrenocortical insufficiency?

A

insufficient CRH

hypothalamus problem

42
Q

Why is androgen synthesis in the adrenal cortex not as important for males as females

A

major source of male androgens is from the testes

43
Q

Which part of the adrenal gland responds to PROLONGED stress?

A

cortex

44
Q

Which adrenocortical hormones are decreased in Addison’s disease?

A

cortisol
aldosterone
androgens

because there is autoimmune destruction of the adrenal gland

45
Q

Where is cholesterol derived from? (3 places)

What is the MAIN source?

A
  1. LDL particles from diet (MAIN)
  2. hydrolysis of cholesterol esters from vesicles
  3. de novo synthesis from acetyl CoA
46
Q

How can you detect 21 b-hydroxylase deficiency in a lab test?

A

presence of 17-ketosteroids in the urine

47
Q

too much cortisol = muscle weakness, how?

not enough cortisol = muscle weakness, how?

A

too much = proteolysis in muscle

not enough = due to hypoglycemia

48
Q

Cushing’s syndrome =

Cushing’s disease =

A

Cushing’s syndrome = adrenal hyperplasia
Cushing’s disease = overactive pituitary or ACTH secreting cells in lung

both = too much cortisol and too much androgens

49
Q

What 3 types of steroids are produced by the adrenal gland?

A
  1. glucocorticoids
  2. mineralcorticoids
  3. androgens
50
Q

How does cortisol inhibits ACTH release?

A

INDIRECTLY! NOT DIRECTLY! NEED TO KNOW!!!!!

cortisol inhibits CRH —> decreased CRH = decreased ACTH

51
Q

Cushing’s disease/syndrome

symptoms:

A 
hyperglycemia
proteolysis
thin skin --- "striae" 
muscle wasting
central obesity
moon face
buffalo hump
hypertension
virilization

YOU KNOW THESE ALREADY

52
Q

cortisol effect on immune system

A

synthesis of lipocortin —> inhibits phospholipase 2 —> inhibits release of prostaglandins and leukotrienes

inhibits IL-2 —> inhibits release of histamine and serotonin

53
Q

How big is the adrenal gland? (length and weight)

A

length = 3-5 cm

weight 1.5-2.5 grams

54
Q

What is the large gene that ACTH is derived from?

A

POMC

proopiomelanocortin

55
Q

Why are aldosterone levels NORMAL in secondary and tertiary adrenocortical insufficiency but NOT in primary adrenocortical insufficiency (Addisons)

A

2/3 : normal because aldosterone is stimulated by RAAS and adrenal gland is not the problem

primary: low because adrenal gland is the problem and not making the aldosterone

56
Q

What stimulates corticotrophs to release ACTH

A

corticotrophin releasing hormone (CRH)

57
Q

Where are AT2 receptors and potassium channels found in the adrenal cortex?

A

zona glomerulosa

58
Q

Why is aldosterone decreased in 17a-hydroxylase deficiency

A

all progesterone is converted into 11-deoxycorticosterone (because cortisol and androgens cannot be made)

11-deoxycorticosterone builds up, and so does corticosterone, both of which act as mineral corticoids which produce HYPERTENSION

aldosterone inhibited during hypertension because RENIN is inhibited and RAAS system is the MOST IMPORTANT SECRETAGOGUE FOR ALDOSTERONE

59
Q

aldosterone effect on:

Sodium
Water
Potassium
H+

A

Sodium - reabsorption = HYPERnatremia
Water - retention = HYPERtension
Potassium - secretion = HYPOkalemia
H+ - secretion = metabolic ALKALosis

60
Q

Cushing’s disease

cortisol levels =
ACTH levels =

A

Cushing’s disease

cortisol levels = HIGH
ACTH levels = HIGH

61
Q

Which arteries supplies the adrenal gland?

A

suprarenal arteries (superior, middle, and inferior)

Physiology Exam 2 Endocrine (Shelby) (11 decks)

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