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Physiology 2 > Exam 3: Adrenal Gland > Flashcards

Exam 3: Adrenal Gland Flashcards

1
Q

What are the two classes of hormones secreted by the adrenal gland?

A

Steroids (glucocorticoids, mineralicoids) and catecholamines (epinephrine and norepinephrine)

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2
Q

Synthesis of cortisol and adrenal androgens are under the control of what?

A

ACTH

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3
Q

What is the precursor for all adrenocortical steroids?

A

Cholesterol

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4
Q

What is the rate limiting step in steroid hormone synthesis?

A

The conversion of cholesterol or pregnenolone by desmolase

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5
Q

Cholesterol needs to be in the mitochondria for steroid hormone synthesis. Free cholesterol is transferred to the mitochondria and then to the inner mitrochondrial membrane via what protein?

A

Steroidogenic Acute regulatory protein (STaR)

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6
Q

Pregnenolone in the zona glomerulosa is converted to what hormone?

A

Aldosterone

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7
Q

Pregnenolone in the Zona fasciculata is converted to what hormone?

A

Cortisol

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8
Q

Pregnenolone in the Zona reticularis is converted to what hormone?

A

Androstenedione

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9
Q

What enzyme converts pregnenolone to Progesterone?

A

3B-Hydroxysteroid dehydrogenase

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10
Q

What enzyme converts progesterone to 11- deoxycorticosterone?

A

21B-hydroxylase

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11
Q

What enzyme converts 11-deoxycorticosterone to corticosterone?

A

11B-hydroxylase

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12
Q

What enzyme converts s corticosterone to aldosterone?

A

Aldosterone synthase

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13
Q

What stimulates desmolase to convert cholesterol to pregnenolone?

A

ACTH

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14
Q

ACTH promotes the secretion of cortisol as well as what other hormone?

A

Aldosterone

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15
Q

When is aldosterone released?

A

When there is a decrease in BP and/or decrease in ECF volume

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16
Q

What is Conns syndrome?

A

Primary hyperaldosteronism, caused by aldosterone secreting tumor

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17
Q

What are the classic features of Conn syndrome?

A
  • Increased Na reabsorption (hypernatremia, fluid retention, and HTN)
  • Increased K secretion (Hypokalemia)
  • Increased H secretion (alkalosis)
  • low renin levels
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18
Q

What happens when there is a 17alpha- hydroxylase deficiency?

A

Glucocorticoids and androgens are produces very little, so steroid hormone intermediates are building up. Aldosterone levels are also low because of symptoms of corticosterone excess and HTN inhibits renin release and therefore, aldosterone release

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19
Q

What enzyme converts pregnenolone to 17-hydroxypregnenolone?

A

17alpha-hydroxylase

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20
Q

What enzyme converts progesterone to 17-hydroxyprogesterone?

A

17alpha hydroxylase

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21
Q

What enzyme converts 17-hydroxyprogesterone to 11-deoxycortisol?

A

21B-hydroxylase

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22
Q

What enzyme converts 11-deoxycortisol to cortisol?

A

11B-hydroxylase

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23
Q

Why cant the zona glomerulosa convert cholesterol to cortisol or andreostenedione?

A

It lacks 17alpha-hydroxylase

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24
Q

What stimulates corticotrophs to release ACTH?

A

CRH

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25
Q

What does ACTH do?

A
  • Stimulates adrenal gland growth

- transfers cholesterol into the mitochondria and activates cholesterol desmolase

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26
Q

What does cortisol do to the HPA axis?

A
  • Directly inhibits CRH

- inhibits the action of CRH on corticotrophs, decreasing ACTH release

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27
Q

When is cortisol secretory activity the greatest?

A

During the morning, and drops throughout the day and evening.

28
Q

What happens to ACTH in periods of stress?

A

ACTH secretion is enhanced and is the result of increased amplitude of CRH burst, rather than frequency

29
Q

What is the overall metabolic effect of cortisol?

A

To increase blood glucose by enhancing gluconeogenesis

30
Q

Other than gluconeogenesis, what other two pathways does cortisol enhance?

A
  • Protein catabolism, providing amino acids.

- Lipolysis, providing glycerol

31
Q

What are the cardiovascular actions of cortisol?

A
  • maintenance of normal blood pressure

- permissive for alpha 1 receptor responsiveness

32
Q

What are the effects of cortisol on the bone?

A
  • decreases intestinal and renal calcium absorption, decreasing plasma Ca
  • Mobilizes Ca from the bone and inhibits bone formation
  • Excessive use of glucocorticoids or chronically high plasma levels of cortisol will result in bone loss
33
Q

What are the effects of cortisol on the connective tissue and muscle?

A
  • Inhibits fibroblast proliferation and collagen formation
  • in high amounts of cortisol the skin things and connective tissue support of capillaries is increased
  • increased proteolysis in muscle leading to weakness
34
Q

What are the anti-inflammatory and and immune effects of cortisol?

A
  • Induces synthesis of lipocortin, which inhibits Phospholipase 2, preventing the release of PGs and leukotrienes
  • Inhibits production of IL-2. Inhibits release of histamine and serotonin
35
Q

Cortisol is able to bind to Mineralocorticoid (aldosterone) receptors with high affinity. Why doesn’t this actually happen?

A

1) cortisol circulates bound to albumin and cortisol binding globulin, allowing only a small fraction of free hormone to cross cells membrane
2) aldosterone target cells possess 11B-hydroxysteroid dehydrogenase (11B-HSD) type II, which converts cortisol to its inactive form, which has less affinity to the MR.
3) Aldosterone dissociates from the MR 5 times more slowly than cortisol

36
Q

MR and GR as classified as Type I and II. Where are type I receptors and what are they more specific to?

A

Type I receptors are predominantly in the kidney and specific to aldosterone

37
Q

What does HSD type I do?

A

Converts cortisone to cortisol

38
Q

What does HSD type II do?

A

Converts cortisol to cortisone

39
Q

Where is 11B-HSD1 found abundantly and why?

A

11B-HSD1 is abundant in adipose tissue. Cortisol produces insulin resistance, and 11B-HSD1 produces excess cortisol, thus promoting insulin resistance in adipose tissue

40
Q

Where is HSD2 found commonly?

A

In classic aldosterone target tissues (Kidney)to exclude cortisol from nonselective MR induces actions.

41
Q

What is Addison’s disease also known as?

A

Primary adrenocorticol insuffiency

42
Q

What happens in Addison’s disease?

A

There is decreased synthesis in all adrenocortical hormones, as a result of autoimmune destruction of the gland

43
Q

What are the classic signs and symptoms of Addison’s disease?

A
  • Loss of cortisol (hypoglycemia during stress, weight loss, and muscle weakness)
  • Loss of aldosterone (hyperkalemia, hypotension, and metabolic acidosis)
  • Loss of androgens
44
Q

Why can hyperpigmentation of skin on elbows, knees, and nipples occur in Primary adrenocortical insuffiency?

A

-ATCH is increased due to decreased adrenal hormone, and ACTH contains Melanocytes stimulating hormone (MSH) fragment

45
Q

What is ACTH derived from?

A

Proopiomelanocortin (POMC)

46
Q

What happens in secondary adrenocortical insufficiency?

A

Failure of corticotrophs to adequately secrete ACTH

47
Q

What happens in tertiary adrenocortical insufficiency?

A

Insufficient CRH

48
Q

What is the different between Cushing syndrome (primary adrenal hyperplasia) and cushings disease (overactive anterior pituitary)?

A

ACTH is low in Cushing syndrome and high in Cushing disease

49
Q

What are the symptoms of Cushing’s syndrome/disease?

A

-Hyperglycemia, increased proteolysis, thin skin, easy bruising, central obesity, moon face, buffalo hump, and hypertension

50
Q

What enzyme converts 17-hydroxypregnenolone to dehydroepiandrosterone (DHEA)?

A

17,20-lyase

51
Q

What enzyme converts 17-hydroxyprogesterone to androstenedione?

A

17,20 lyase

52
Q

What enzyme converts dehydroepiandrosterone (DHEA) to androstenedione?

A

3B-hydroxysteroid dehydrogenase

53
Q

What is the most common hydroxylase deficiency?

A

21B-hydroxylase

54
Q

What happens in 21B hydroxylase deficiency?

A

No conversion to glucocorticoids or mineralocorticoids, resulting in sodium loss and hypoglycemia.

  • Steroid intermediates build up and are converted to androgens, leading to androgenital syndrome
  • ACTH is high and tropic effect is seen
55
Q

What happens in androgenital syndrome?

A
  • Hypersecretion of adrenal androgens (increased DHEA and androstenedione), resulting in masculinization in females
  • Deepening of voice, increased muscle mass, amenorrhea and hirsutism, and clitoral enlargement
56
Q

Where does catecholamines synthesis occur in the adrenal gland?

A

The adrenal medulla

57
Q

Where does synthesis of catecholamines occur within the medulla?

A

Chromaffin cells from tyrosine

58
Q

What is the rate limiting step in catecholamine synthesis?

A

Conversion of tyrosine to DOPA via Tyrosine hydroxylase

59
Q

How does cortisol help in catecholamine synthesis?

A

Activates the last step of synthesis (from NE to epi) by activating PNMT

60
Q

What effects does Epi have in times of stress?

A
  • Increased glycogenolysis
  • inhibition of glycogen synthesis
  • increased gluconeogenesis
  • inhibited insulin secretion
  • increased glucagon secretion
  • increased lipolysis

*** it does these things to sustain glucose production for use by the CNS

61
Q

What are the cardiovascular effects of Epi?

A
  • Increase contracility, HR, and conduction
  • increased BP
  • Increase arteriolar vasoconstriction
62
Q

What are the two enzymes that degrade catecholamines?

A

-Monoamine oxidase (MAO) and catechol-0-methytransferase (COMT)

63
Q

What is the predominant mechanism for degrading NE?

64
Q

What is the predominant mechanism for degrading Epi?

65
Q

Where does MAO work?

A

Neuronal cytoplasm

66
Q

Where does COMT work?

A

Heart, liver, and kidney

67
Q

What is pheochromocytoma?

A

-Catecholamine secreting tumor

Physiology 2 (13 decks)

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