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Physiology > Lecture 13: Adrenal gland > Flashcards

Lecture 13: Adrenal gland Flashcards

1
Q

Where are the adrenal glands located in relation to kidneys

A

Dorsal-medial to kidneys

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2
Q

What is blood supply and venous drainage of adrenal gland

A

Suprarenal arteries and veins

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3
Q

What is the direction of adrenal gland perfusion

A

Blood moves through sinusoidal system through cortex first then medulla

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4
Q

What hormone does zona glomerulosa secrete and what is the target

A

Hormone= mineralocorticoids (ex: aldosterone)

Target: kidney

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5
Q

What hormones does the zona reticularis secrete and what is the target

A

Hormone= androgens (DHEA)

Target= male and female sex organs

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6
Q

What hormones does the zona fasciculata secrete and what is the target

A

Hormone= glucocorticoids (cortisol)

Target: liver (glucogenesis)

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7
Q

What hormones does the adrenal medulla produce and what is the target

A

Hormones= catecholamines (NE and E)

Target: liver, muscles, heart

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8
Q

All cells in cortex have lipid droplets, mitochondria and smooth ER why?

A

Lipid droplets- source of cholesterol
Mitochondria: first step in steroid synthesis from cholesterol —> pregnenolone

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9
Q

What regulates cholesterol—> pregnenolone

A

HPA Axis: ACTH

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10
Q

What regulates pregnenolone—> Mineralocorticoids

A

RAAS and ACTH

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11
Q

What regulates pregnenolone—> glucocorticoids and androgens

A

HPA: ACTH

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12
Q

What regulates the adrenal medulla: SNS or PNS

A

Autonomic control of the SNS

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13
Q

What enzyme differentiates adrenal corticosteroids from progesterone

A

C-21

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14
Q

What enzyme differentiates cortisol from aldosterone

A

C-17

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15
Q

Zona glomerulus synthesizes aldosterone and lacks which enzyme that is necessary for cortisol and androgen synthesis

A

17-alpha hydroxylase

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16
Q

Due to absence of 17-alpha hydroxylase in zona glomerulus, pregnenolone can only be converted to progesterone by ___

A

3B-HSD

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17
Q

What 3 mechanisms result in aldosterone synthesis

A
  1. RAAS (decrease BP or ECF)
  2. Plasma K+ (increase K+, increase aldosterone, increase K+ excretion from kidney)
  3. ACTH via HPA axis- weak effect
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18
Q

What receptor does aldosterone bind

A

Mineralocorticoid receptor

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19
Q

Aldosterone binds MR and activates what gene targets

A

Apical ENaC (increase Na+ reabsorption in CD)
Basolateral Na+/K+ ATPase

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20
Q

Which solutes are absorbed and secreted during aldosterone activation

A

Na+ reabsorbed, K+ secreted, H+ excreted

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21
Q

How does aldosterone affect BP

A

Increase BP by increasing Na+ and H20 reabsorption

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22
Q

What is Conn’s Syndrome: Primary hyperaldosteronism usually caused by

A

Aldosterone secreting tumor

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23
Q

What are the physiological effects of Conn’s syndrome: primary hyperaldosteronism

A

Hypernatremia, fluid retention, hypertension, hypokalemia, metabolic alkalosis, low renin

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24
Q

What are some common symptoms of Conn’s syndrome: primary hyperaldosteronism

A

PU/PD, hypertension, fatigue, headache, visual disturbances, neuropathy

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25
Q

What are some symptoms of feline primary hyperaldosteronism

A

Hypertension, vision loss, muscle weakness, plantigrade posture

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26
Q

Zona fasciculata synthesizes cortisol, what enzyme is needed to cortisol synthesis

A

17-alpha hydroxylase

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27
Q

If 17-alpha hydroxylase is blocked can life be sustained?

A

Yes, corticosterone is a glucocorticoid produced in aldosterone synthesis and can be used a a replacement

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28
Q

What hormone requires binding proteins in order to be transported

A

Steroids

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29
Q

Are bound or free hormones available to signal

A

Free hormones

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30
Q

Where are receptors for glucocorticoid and mineralocorticoids located

A

Cytoplasm- steroid hormones are non-polar and lipophilic therefore they can readily diffuse across cell membrane

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31
Q

What receptors are ligand inducible transcription factors that activate transcription of specific genes

A

MR’s and GR’s

32
Q

MR’s and GR’s have a shared homology in their ligand binding and DNA binding domains, what is the problem?

A

Plasma cortisol is 100-1000x higher than aldosterone, therefore cortisol binds MR with high affinity

33
Q

How is selectivity of aldosterone for MR’s achieved

A

Tissues targeted by aldosterone contain enzyme 11B-hydroxysteroid dehydrogenase II (11B-HSD2) which converts cortisol to cortisone- inactive form so can’t bind MR’s

34
Q

A decrease in 11B-HSD2 would lead to …..

A

Decreased conversion of cortisol to cortisone and increased aldosterone like effects—> including Na+ retention

35
Q

Zona reticularis is responsible for synthesizing androgens, what enzymes are needed

A

17, 20 lyslase promotes converted to DHEA and androstenedione

36
Q

Zona reticularis lacks which enzyme that permits synthesis of aldosterone

A

21B- hydroxylase

37
Q

What plasma binding protein does aldosterone bind to

A

Albumin

38
Q

What plasma binding protein does cortisol bind to

A

Transcortin

39
Q

What plasma binding protein does DHEA bind to

A

Albumin

40
Q

What are the primary hormones released by the adrenal medulla

A

NE and E

41
Q

What are chromaffin cells

A

Cells in the medulla- modified neuronal tissue that release NE and E into the blood

42
Q

Where does catecholamine synthesis occur

A

Chromaffin cells

43
Q

What is the order of catecholamine synthesis to NE

A
  1. L tyrosine—> tyrosine hydroxylase
  2. L-DOPA—> L-aromatic amino acid decarboxylase
  3. Dopamine—-> dopamine B hydroxylase
  4. L-noradrenaline (NE)
44
Q

What is the order of catecholamine synthesis to Epi

A
  1. L tyrosine—> tyrosine hydroxylase
  2. L-DOPA—> L-aromatic amino acid decarboxylase
  3. Dopamine—-> dopamine B hydroxylase
  4. L-noradrenaline (NE)—> PNMT (cortisol)
  5. L-adrenaline (epi)
45
Q

What converts NE to E

A

PNMT

46
Q

What hormone activates synthesis of PNMT

A

Cortisol

47
Q

What are the effects of catecholamines

A

Regulate homeostasis of cardiac and vascular tone, fight or flight response

48
Q

How does catecholamine secretion impact the vascular system

A

Increase cardiac contractility, increased heart rate, increased BP, increased arteriolar vasoconstriction

49
Q

How does catecholamine impact the mobilization of fuel in times of shock

A

Increased glucogenolysis, inhibition of glycogen synthesis, increased gluconeogenesis, inhibited insulin secretion, increased glucagon secretion, increased lipolysis

50
Q

What is the goal of catecholamines in mobilizing fuel in times of shock

A

Promote glucose production for use by the brain

51
Q

How does epinephrine impact alpha 1 receptors

A

Causes arterial smooth muscle contraction

52
Q

How does epinephrine impact alpha-2 receptors

A

Inhibit- synaptic nerve endings and smooth muscle contraction

53
Q

How do catecholamines impact B1 receptors

A

Affects heart activity- increased HR

54
Q

How does epinephrine impact B2 receptors

A

Inhibits- smooth muscle relaxation and metabolism

55
Q

What enzyme degrades NE

A

Monoamine oxidase (neuronal cytoplasm)

56
Q

What enzyme degrades Epi

A

Catechol-0-methyltransferase (interstitial fluid of synapse, heart, liver kidney)

57
Q

What is the byproduct of MAO and COMT

A

Vanillylmandelic acid

58
Q

Vanillylmandelic acid serves as a measure of ___ activity

A

SNS

59
Q

What is a pheochromocytoma

A

Catecholamine secreting tumor

60
Q

What are some symptoms of pheochromocytomas

A

Hypertension, rapid pulse, chest pain, excessive sweating, headache, hyperglycemia, fatigue

61
Q

What are some common presentations of cushings

A

Central obesity, collagen fiber weakness, urinary free cortisol, glucose increase, suppressed immunity, hypercortisolism, hypertension, hyperglycemia, hypercholesterolemia, latrogenic, neoplasms, glucose intolerance, growth retardation, PU/PD, alopecia, muscle weakness

62
Q

What are 2 possible causes of Cushing’s

A

Endogenous- overproduction of cortisol
Exogenous- taking medicines containing glucocorticoids, such as hydrocortisone

63
Q

What are some common endogenous causes of cushings

A

Pituitary tumors (70%)
Adrenal tumors (15%)
Other (15%)

64
Q

In dogs cortisol interferes with ___ binding resulting in incomplete central DI

A

ADH binding

65
Q

What are some canine specific serum abnormalities that co-occur with Cushing’s

A

Elevated SAP, elevated ALT, hypercholesterolemia, hyperglycemia, decreased BUN

66
Q

Why is cholesterol and glucose elevated in serum of patients with Cushing’s?

A

Elevated glucose result of increased cortisol which main function is to increase gluconeogenesis in liver

Elevated cholesterol: ACTH transfer cholesterol to mitochondria in steroid synthesis

67
Q

How is a urine cortisol: creatinine ration useful in diagnosing cushings

A

Elevated distinguishes between healthy and dogs with hyperadrenocorticism

*prone to false +

68
Q

How does an ACTH stim test help diagnose cushings

A

Measure cortisol response- useful for confirming iatrogenic hyperadrenocorticism

69
Q

What receptor does Dexamethasone have high affinity for

A

Glu receptors

70
Q

What does a low dose dexamethasone test determine

A

Presence of Cushing’s (DOES NOT DETERMINE WHICH TYPE)

71
Q

How does a low does dexamethasone suppression test work and what could potential results indicate

A

Give low dose dex, then measure cortisol at 4-8hrs

Reduction or no change in cortisol: adequate HPA axis

Elevated cortisol: allows for diagnosis of cushings

72
Q

How can you distinguish between cushing’s disease and cushing’s syndrome

A

High dose dexamethasone suppression

73
Q

How does a high dose dexamethasone suppression test work (testing ACTH)

A

Works on principle that autonomous ACTH hypersecretion by pituitary can be suppressed by supraphysiological concentrations of steroid

Reduced/no ACTH: supports diagnosis of pituitary origin

unchanged ACTH: adrenal or ectopic tumor

74
Q

How does a high dose dexamethasone suppression test work (testing CORT)

A

Reduced CORT: supports pituitary origin

75
Q

Why does dexamethasone suppression not suppress cortisol concentrations as a result of adrenal tumors and which form of Cushing’s involves adrenal gland

A

Adrenal tumors have maximally suppressed ACTH production via
normal feedback mechanism.

Cushing’s syndrome- primary adrenal hyperplasia. Producing high levels cortisol without influence from ACTH which is why high dose dex test doesn’t decrease levels in Cushing’s syndrome

76
Q

How does the reduction in ACTH or CORT following HDDS test indicate pituitary origin

A

dex can provide negative feedback onto pituitary and reduce ACTH and CORT is cushing’s disease which is from overactive pitutiary. Cushing’s syndrome is a result of primary adrenal hyperplasia releasing high levels of CORT independent of ACTH stimualtion, so adrenal origion won’t respond

Physiology (10 decks)

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