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Physio II > Adrenal Gland > Flashcards

Adrenal Gland Flashcards

1
Q

Glucocorticoids, mineral corticoids, and catecholamines are released from what gland?

A

Adrenal gland

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2
Q

Blow flood from suprarenal arteries creates a sinusoid system in the adrenal medullae, this help modulate what?

A

Enzyme activity

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3
Q

What are the 3 layers of the adrenal cortex?

A
  1. Z. glomerulosa (outer most)
  2. Z. fasciculata
  3. Z. reticularis (inner most)

“Go Find Rex, Make Good Sex”

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4
Q

T or F: All steroids share the same first step (cholesterol converted to prenenolone via desmolase)?

A

True

Mobilization of cholesterol (via ATII receptor, K+ channels) → free cholesterol travels to mitochondria → inner mitochondrial membrane (via STaR) → converted to pregnenolone via desmolase (this is the rate limiting step and dependent on STaR)

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5
Q

What are the rate limiting enzymes in the conversion of cholesterol to pregnenolone?

A

Desmolase, dependent on STaR

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6
Q

The Z. glomerulosa produces what hormones?

A

mineralcorticoid: Aldosterone

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7
Q

T or F: Aldosterone provide negative feedback on CRH & ACTH

A

FALSE

Cortisol is the only corticoid that provides negative feedback on CRH & ACTH

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8
Q

The Z. glomerulosa lack what enzyme forcing pregnenolone to only be converted to progesterone => aldosterone?

A

Lacks 17𝛂-hydroxylase

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9
Q

MR type 1 receptors are greatest in what organ?

A

Kidney

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10
Q

What hormones stimulates ACTH to produce aldosterone?

A

ATII (RAAS)

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11
Q

What layer of the adrenal cortex lacks 17,20-lyase (prevents production of androstenedione) and lacks aldosterone synthase (prevents production of aldosterone)?

A

Z. fasciculata

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12
Q

T or F: GR Type II receptors are located in all cells?

A

True

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13
Q

The cortisol-cortisone shunt includes what two enzymes?

A

11B-HSD1 (activates: cortisone to cortisol)
11B-HSD2 (inactivates: cortisol to cortisone)

Liver cortisol → kidney where inactivated by 11B-HSD2, cortisone can’t bind to MR → cortisone travels back to liver → activated by 11B-HSD1 → binds to GR receptors

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14
Q

What hormones lead to the production of cortisol?

A

GnRH → CRH → ACTH → Cortisol (glucocorticoid)

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15
Q

T or F: Cortisol provide negative feedback to GnRH, CRH, and ACTH

A

TRUE

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16
Q

What corticoids produce a long term response to stress?

A

Mineralocorticoids (aldosterone) and glucocorticoids (cortisol)

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17
Q

What enzyme does Z. reticularis lack preventing production of aldosterone and cortisol?

A

21𝛽 Hydroxylase

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18
Q

What hormone class does Z. reticularis produce?

A

Androgens (androtenedione)

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19
Q

Do angrogens have feed back on CRH and ACTH?

A

No

Cortisol is the only hormone that has negative feedback on CRH and ACTH

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20
Q

The following are a result of a deficiency of what enzyme?

  1. No conversion of: progesterone → 11-deoxycorticosterone OR 17-hydroxyprogesterone → 11 deoxycortisol
  2. Cortex does NOT produce glucocorticoids or mineralocorticoids → sodium loss and hypoglycemia
  3. Steroid intermediates build up → converted to androgens → Adrenogenital syndrome & ↑ 17-ketosteroids in urine
  4. ↑ ACTH (b/c lack of neg feedback from cortisol) → tropic effects
A

21𝛽 Hydroxylase Deficiency

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21
Q

Plasma levels of Cortisol and what other hormone are reflect pulsatile and circadian release of ACTH?

A

Cortisol and Androtenidione (Androgens)

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22
Q

Androstenedione are a major source of androgens for females, these produce what effect in the female? (2)

A

secondary sex charactristics and libido

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23
Q

Does catecholamine synthesis take place in the adrenal cortex or medulla?

A

Medulla (specifically chromaffin cells)

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24
Q

What is the rate limiting step in catecholamine synthesis?

A

Tyrosine conversion to DOPA via tyrosine hydroxylase

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25
Q

Tyrosine conversion to dopamine takes place in the cytosol or granules?

A

Cytosol

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26
Q

Dopamine conversion to NE takes place in the cytosol or granules?

A

Granules

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27
Q

NE conversion to E takes place in the cytosol or granules?

A

Cytosol

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28
Q

What enzyme is responsible for conversion of NE to E?

A

phenylethanolamine-N-methyltransferase

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29
Q

Where is Epi store in the body?

A

Granules

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30
Q

Activation of tyronsine hydroxylase is a result of acute or chromic stimulation of catecholamine synthesis?

A

Acute

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31
Q

Increased expression and concetration of tyronsine hydroxylase is a result of acute or chromic stimulation of catecholamine synthesis?

A

Chronic

32
Q

T or F: Catecholamine secretion result in a rapid and short lived response (t1/2 = ~ 2min) ?

A

True.

Response to “fight or flight”, hypotension, shock, HF, hypoglycemia

33
Q

Increased HR, ↑ glycogenolysis, gluconeogenesis, glucagon secretion and lipolysis are the effects of what hormone?

A

Epinephrine

34
Q

What enzyme monitors NE > Epi degradation and secretion?

A

MOA (neural cytoplasm)

35
Q

What enzyme monitors Epi > NE degradation and secretion?

A

Catechol-0-methyltransferase (COMT) (heart, liver, kidney)

36
Q

T or F: Plasma levels of cortisol are greater than plasma levels of aldosterone?

A

TRUE

37
Q

Mineralocorticoid receptors (MR) and glucocorticoid receptors (GR) are structurally similar. Does aldosterone or cortisol bind with higher affinity?

A

Cortisol

38
Q

Under healthy conditions will cortisol bind to MR receptors?

A

No

39
Q

What 3 mechanisms prevent cortisol from binding to MR receptors under health conditions?

A
  1. Cortisol bound to albumin & cortisol-binding globulin (only small % of free hormone crosses cell membrane)
  2. Aldosterone converts cortisol to cortisone (↓ cortisol affinity to MR)
  3. Aldosterone dissociates from MR more slowly than cortisol
40
Q

Over expression of 11B-HSD1 in adipose tissues will lead to over time?

A

Production of excess cortisol → insulin resistance/ features of metabolic syndrome

41
Q

During what time of the day are cortisol/ATCH levels highest?

A

Morning

Levels rise during sleep/ peak in AM & drop throughout the day (reflects circadian release of ACTH)

42
Q

Does stress increased the burst amplitude of CRH or the duration of CRH release?

A

Burst amplitude→ ↑ ACTH → ↑ Cortisol

43
Q

What is the primary action of cortisol

A

↑ blood glucose

44
Q

What hormone do the following describe?

↑ glycogenolysis (early stages of fasting)
↑ glycogenesis (late-stage fasting)
↑ gluconeogenesis
↑ glucose sparing

↓ glucose uptake in tissues other than brain

A

Cortisol

45
Q

Epinephrine will increase or decrease insulin secretion via 𝛂-adrenergic stimulation of 𝛃-cells

A

Decrease insulin secretion

46
Q

Generally, does epinephrine favor release or storage of energy stores

A

Release (during short term stress)

47
Q

Generally, does Cortisol favor release or storage of energy stores?

A

Release (during long term stress)

48
Q

↑ protein catabolism, ↑ lipolysis lead to enhanced what?

A

Gluconeogenesis

49
Q

What hormone maintains BP by maintain a-1 responsiveness to catecholamines?

A

Cortisol

50
Q

What hormone inhibits bone formation, decreases bone density, and leads to muscles wasting/weakness?

A

Cortisol

51
Q

What hormone thins skin, impair collagen formation an decreases connective tissue support in capillaries?

A

Cortisol

52
Q

What corticoid is stimulated by ↓ BP/ ECF volume

A

Aldosterone

53
Q

ATII > ↑ plasma K+ > ACTH will increase the secretion of what hormone?

A

Aldosterone

54
Q

Aldosterone binds to MR or GR stimulating Na reabsorption & K secretion?

A

MR

55
Q

What is the net effect of Aldosterone on ECF?

A

Expansion of ECF volume

56
Q

Conn’s syndrome is due to increased or decreased levels of aldosterone?

A

Increased

  • Aldosterone secreting tumor
  • hypernatremia, fluid retention, hypokalemia, metabolic alkalosis, HTN = ↓ renin
57
Q

Will a 17a-hydroxylase deficiency result in increased or decreased levels of aldosterone?

A

Decreased

  • ↑ corticosterones, but HTN = ↓ renin SO No ATII → ↓ aldosterone
  • hypokalemia, metabolic alkalosis
58
Q

Cushing’s syndrome is due to high or low levels of cortisol?

A

HIGH

↑ active cortisol binds to aldosterone receptors (MR) → aldosterone-like effects

59
Q

What enzyme is down regulated in Cushing’s syndrome?

A

11B-HSD2 → ↑ active cortisol binds to aldosterone receptors (MR) → aldosterone-like effects

60
Q

Primary adrenocortical insufficiency leads to what disease?

A

Addison’s Disease: autoimmune destruction of the adrenal cortex → ↓ synthesis of all adrenocortical hormones

61
Q

Low levels of what hormone will produce hypoglycemia during stress, weight loss, muscle weakness

A

Cortisol

62
Q

Low levels of what hormone will produce hyperkalemia, hypotension, metabolic acidosis, salt craving

A

Aldosterone

63
Q

Low levels of what hormone will produce ↓ 2˚ sex characteristic in postpuberty females, ↓ libido

A

Androgrens

64
Q

Will ACTH secretion by increased or decreased in Addison’s disease?

A

Increased due to lack of negative feedback from cortisol

65
Q

High levels of what hormone will produce hyperpigmentation of elbows, knees, nipples, scars (𝛂-MSH fragment)

A

ACTH

66
Q

With secondary (failure of corticotrophs to adequately secrete ACTH) and Tertiary (insufficient CRH) adrenocortical insufficiency levels of what two hormones will be low? What hormone will have normal levels?

A
  • Cortisol and androgen deficiency

- Normal aldosterone

67
Q

Will you have hyperpigmentation w/ secondary and Tertiary adrenocortical insufficiency?

A

No

68
Q

Moon face, buffalo hump, central obesity, thin skin/striate and muscle wasting are sx of what mineralcorticoid disease?

A

Cushing’s

Excess glucocorticoids and androgens

69
Q

Primary adrenal hyperplasia decreased ACTH levels, this leads to what syndrome?

A

Cushing’s syndrome

70
Q

An overactive pituitary increased ACTH levels this leads to what disease?

A

Cushing’s

71
Q

What are the effects of F being expose to ↑ DHEA and androstenedione in utero (adrenogenital syndrome)?

A

Masculinization of female (female pseudohermaphrodite): penis like clitoris, scrotum like vagina, ovaries present, primary amenorrhea

72
Q

What are the effects of F having ↑ DHEA and androstenedione as an adult (Adrenogenital syndrome)?

A

Adult females develop male traits = deepening of voice, ↑ muscle mass, amenorrhea and hirsutism, clitoral enlargement and acne

73
Q

A pheochromocytoma (catecholamine secreting tumor) will lead to hyper or hypo function of the adrenal medulla?

A

Hyperfunction –> HTN, ↑ HR, chest pain, excessive sweating, HA, hyperglycemia, fatigue

(Adrenomedullary Dysfunction)

74
Q

Following an adrenalectomy, a pt will have hyper or hypo function of the adrenal medulla

A

HYPO –> no overt clinical difficulties

Adrenomedullary Dysfunction

75
Q

Cushing’s syndrome (hypercortisolism) is associated with mutated secretion of what hormone?

A

growth hormone

Physio II (14 decks)

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