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Physiology II > Adrenal Gland > Flashcards

Adrenal Gland Flashcards

1
Q

Which adrenal gland is larger?

A

Left

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2
Q

What vessel crosses the adrenal gland?

A

Phrenicoabdominal trunk

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3
Q

What is the cortex?

A

Pale yellowish outer part

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4
Q

What is the adrenal medulla?

A

Dark brown inner part

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5
Q

Which part of the adrenal gland can regenerate following injury?

A

Adrenal cortex. The medulla is of neural origin so it does not regenerate

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6
Q

Where is the Zona glomerulosa?

A

Superficial part of cortex

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7
Q

What does the Zona glomerulosa make?

A

Mineralocorticoids

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8
Q

What does the Zona fasciculata produce?

A

Glucocorticoids

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9
Q

What does the zona reticularis produce?

A

Sex hormones

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10
Q

Which parts of the cortex are responsive to ACTH

A

Zona fasciculata and reticularis

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11
Q

What happens to the cortex if there is a loss of ACTH?

A

Cortex gets thinner

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12
Q

What is general adaptation syndrome?

A

Non-specific response to injury or stress. Causing enlargement of the adrenal gland. ZG is not affected

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13
Q

What hormones are derived from cholesterol?

A

Adrenocortical hormones (C21)

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14
Q

What is the source of cholesterol?

A
  • Synthesis in adrenal cortex

- Plasma LDL cholesterol

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15
Q

Where is the OH in mineralcorticoids?

A

C11

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16
Q

Where is the OH groups in glucocorticoids?

A

C11, C17

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17
Q

What are the carrier proteins for glucocorticoids?

A
  • Transcortin (75%)
  • Albumin(15)
  • Free (10%)
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18
Q

What are the carrier proteins for mineralcorticoids?

A
  • Albumin (50%)
  • Transcortin (10%)
  • Free (40%)
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19
Q

What could effect carrier protein levels?

A

Liver damage

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20
Q

What synthesizes carrier proteins?

A

Liver

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21
Q

What is the adrenarche?

A

Region of the zona reticularis that changes during puberty in some animals

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22
Q

Where are the recognition methyl groups in corticoids?

A

19,18,21

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23
Q

What does corticotropin do in the adrenal gland?

A

Activates the pathway of the metabolism of cholesterol to either mineral or glucocorticoid depending on the cell it is going through

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24
Q

What are two location of the cellular location of enzymes in the cholesterol pathway?

A
  • Mitochondria

- SER

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25
Q

Which adrenal hormone has a higher concentration in the blood?

A

Cortisol (10fold higher)

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26
Q

What is the half-life of cortisol?

A

60min

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27
Q

What is the half-life of aldosterone?

A

20min

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28
Q

The total glucocorticoid in the blood depends on what?

A
  • Secretion rate
  • Metabolism
  • Amt of carrier protein
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29
Q

What metabolizes steroids?

A

Reduction to water soluble by glucuronides in the liver and then excreted in the urine

30
Q

What is the most potent mineralcorticoid?

A

Aldosterone

31
Q

How do you prevent overstimulation of aldosterone receptor by cortisol?

A

11-B-hydroxysteroid dehydrogenase converts cortisol to inactive cortisone

32
Q

What are the physiological actions of aldosterone?

A
  • Incr Na reabsorption
  • Incr angiotensin II production
  • Decr. potassiom by renal excretion
  • Conservation of water
33
Q

What is the behavioral actions of aldosterone?

A

With Angiotensin II drives salt-seeking behavior

34
Q

How do you regulate aldosterone?

A
  • Plasma potassium will stimulate aldosterone
  • Angiotensin Ii stimulates it
  • Poorly regulated by ACTH
  • Suppressed by atrial natriuretic facto
  • High Na and low K decrease aldosterone
35
Q

What is the angiotensin cascade?

A

Renin is released from the kidney due to hypotension. This combined with angiotensinogen from the liver converted to AGT I. AGT 1 to AGT II by ACE. This no goes to the adrenal gland and promotes aldosterone secretion

36
Q

Where in the kidneys does aldosterone and AGTII act?

A
  • Distal tubule

- Collecting duct

37
Q

What are the effects of aldosterone in the kidney?

A
  • Na and water get reabsorbed

- K is excreted

38
Q

What is the most important glucocorticoid?

A

Cortisol

39
Q

What are the effects of Cortisol?

A
  1. Stimulate gluconeogenesis
    - incr blood glucose
    - Anti insulin effect
  2. Protein and fat catabolism
  3. Redistribution of body fat
  4. Water and electrolyte distribution
  5. Trace mineral distribution
  6. Blocks inflammatory response
  7. Suppresses immune system
40
Q

What are the effects of stimulating protein and fat catabolism?

A
  • Negative nitrogen balance, urinary loss of nitrogen

- Mobilize metabolism of fatty acid

41
Q

Where is fat redistributed if over exposed to cortisol?

A

Moved from the extremities and SQ abdominal sites to pelvis, neck, thorax, liver, and omentum

42
Q

What are clinically important uses of glucocorticoids?

A
  • Block inflammatory responses

- Suppress immune system

43
Q

What is the rate limiting step in cortisol regulation?

A

ACTH increases cholesterol and you get pregnenolone conversion

44
Q

What regulates release of ACTH?

A
  • Vasopressin
  • CRH
  • Sleep
  • Stress
  • Diurnal rhythm
45
Q

What other hormones does glucocorticoid have permissive effects on?

A
  • Glucagon in the liver

- Catecholamines

46
Q

How can you test function of adrenocortical function?

A
  1. Plasma cortisol
  2. ACTH response test
  3. Dexamethasone suppression test
47
Q

How do you perform a dexamethasone suppression test?

A

Dex is a synthetic glucocorticoid and when administered and doesn’t interfere with plasma cortisol. Should see a decrease in cortisol because of the negative feedback

48
Q

How to differentiate hyper aldosteronism and hyperadrenocorticism?

A

Should see an increase in Ang II if it is hyperaldosteronism

49
Q

What is the classic triad for dogs with hyperadrenocorticism?

A
  1. PD/PU
  2. Pendulous abdomen
    - hepatomegaly
    - abdominal weakness
  3. Bilateral alopecia
50
Q

What is the hallmark sign of hyperadrenocorticism in cats?

A

Thin skin

51
Q

What is the hallmark of horses with hyperadrenocorticism?

A
  • Long hair coat out of season
  • Laminitis
  • Weight loss
  • PD
  • Muscle wasting
52
Q

What are the effects of cushing’s on the liver?

A
  • Fat deposited on abdominal viscera
  • Fatty liver disease
  • High activity of 11-beta HSD type 1 in liver and visceral fat. Allows for inhanced inflammation of abdominal viscera
  • increases fibrosis and hepatic cancer risks
53
Q

What is the effects of cushing’s on bone?

A
  • Decrease osteoblast
  • Increase osteoclasts
  • Bone metabolism on resorption
  • apoptosis of mature osteoblasts and osteocytes
  • delayed maturation
  • Less GI calcium absorption
  • increases PPAR gamma 2
  • Suppress BMP2
  • decrease growth hormone effect
54
Q

How does Mitotane help manage hyperadrenocorticism?

A

Kills rapidly dividing cells to suppress cancer.

-will produce necrosis of the zona fasciculata and reticularis

55
Q

How does trilostane help HAC?

A

Inhibits 3 beta hydroxysteroid dehydrogenase

56
Q

How does ketoconazole help HAC?

A

Blocks synthesis of cortisol

57
Q

How does L-deprenyl help HAC?

A

Inhibit dopamine degradation so more dopamine to inhibit glucocorticoid release

58
Q

What can cause hypoadrenocorticism?

A
  1. Lymphatic infiltration of adrenal cortex
  2. Secondary to mitotane treatment
  3. Autoimmune destruction of adrenal cortex
  4. Secondary lack of CRH or ACTH
59
Q

What are some signs of hypoadrenocorticism (Addison’s like syndrome)?

A
  • Hyperkalemia (arrhytmias)
  • Hyponatremia
  • Muscle atrophy, depression weight loss
  • Brady cardia and widened QRS complex
  • Hypotension
60
Q

How is the adrenal medulla oriented?

A

Deep in adrenal with an extensive of vascular system that flows from the cortex to the medulla.

61
Q

What does the Adrenal medulla produce?

A

Catecholamines

  • Epinephrine
  • Norepinephrine
62
Q

What innervates the adrenal medulla?

A

Preganglionic sympathetic fibers. Splanchnic nerve (T12, T13, L1)

63
Q

How are catecholamines produced?

A

Tyrosine is key precursor. Epinephrine can only be made in chromaffin cells

64
Q

How are catecholamines stored?

A

Cytoplasmic granules

65
Q

How is epinephrine carried?

A

Free (50%)

Albumin (50%)

66
Q

What can modulate release of catecholamines?

A

Glucocorticoids that flow in and causes disinhibition

67
Q

What can inhibit synthesis of catecholamines?

A
  • NE

- EPI

68
Q

What is the rate limiting step of the synthesis of catecholamines?

A

Hydroxylation of tyrosine

69
Q

What mediates the actions of catecholamines?

A
  • alpha- and beta-adrenergic receptors
  • alpha receptors (vasoconstriction)
  • beta receptors (Increase HR, vasodilation by Epi)
70
Q

What is part of the regulation of release of catecholamines?

A
  • Sympathetic preganglionic neurons (Ach)
  • Cortisol
  • Stress or hypoglycemia

Physiology II (50 decks)

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