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PHYSIOLOGY II > Lecture 13: Adrenal Gland > Flashcards

Lecture 13: Adrenal Gland Flashcards

1
Q

CUSHING’S presentations

A
  • C- central obesity, collagen fiber weakness
  • U - urinary free cortisol and glucose increase
  • S - striae, suppressed immunity
  • H - hypercortisolism, hypertension, hyperglycemia, hypercholesterolemia
  • I - iatrogenic
  • N - neoplasms
  • G - glucose intolerance, growth retardation
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2
Q

endogenous vs exogenous causes of cushings syndrome

A

ENDOGENOUS overproduction of cortisol
EXOGENOUS taking medicines containing glucocorticoids like hydrocortisone

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3
Q

the zona glomerulosa produces ….

A

mineralocorticocoides which target the kidney

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4
Q

the zona fasciulata produces..

A

glucocorticoids which target the liver

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5
Q

the zona reticularis produces..

A

androgens which target M+F sex organs

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6
Q

the medulla of the adrenals produces..

A

catecholamines which target liver, muscle, heart

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7
Q

why do all cells within the adrenal gland cortex have lipid droplets, mitochondria, and smooth ER

A

b/c the hormones are released as they are produced - there is no storage mechanism for steroid hormones anywhere in the body

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8
Q

what is the major catecholamine produced by the central portion of the adrenal medulla

A

epinephrine

norenipenphrine

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9
Q

conversion of cholesterol into pregnenolone is regulated by what

A

HPA axis: ACTH

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10
Q

conversion of pregnenolone into mineralocorticoids like aldosterone is regulated by what

A

the renin-angiotensin system and ACTH

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11
Q

conversion of pregnenolone into glucocorticoids and or androgens is regulated by what

A

HPA axis: ACTH

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12
Q

what is the medulla of the adrenal cortex regulated by

A

autonomic control of the sympathetic NS

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13
Q

_______hydroxylase activity differentiates adrenal corticoids from progesterone

A

C-21

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14
Q

_____ Hydroxylase differentiates cortisol from aldosterone

A

C-17

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15
Q

The zona glomerulosa lacks _____ hydroxylase, the enzyme necessary for cortisol and androgen synthesis

A

17-α hydroxylase
so pregnenolone can only be converted to progesterone by 3β-HSD

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16
Q

the zona glomerulosa does NOT synthesize ______ or ______

A

glucocorticoids or androgens

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17
Q

what stimuli activate the RAAS cascade

A
  • decreases in bp
  • decrease in ECF volume
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18
Q

K+ increases _______ which increases _____ excretion in the kidney

A

aldosterone, K

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19
Q

when Aldosterone binds mineralocorticoid receptor, it activates what target genes

A
  • Apical ENaC (recovery of Na)
  • basolateral Na/K ATPase
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20
Q

what is the main regulator of the aldosterone pathway

A

Angiotensin II

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21
Q

effects of aldosterone on solute transport

A
  • Na+ reabsorption
  • K+ secretion
  • increase in extracellular fluid
  • BP increases
  • H+ excretion sitmulated
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22
Q

what is Conn’s Syndrome

pretty rare

A

primary hyperaldosteronism
usually caused by aldosterone secreting tumor

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23
Q

what are the physiological effects of Conn’s syndrome

A
  • Increased Na resorption: hypernatremia, fluid retention, hypertension
  • increased K+ secretion: hypokalemia
  • increased H+ secretion: metabolic alkalosis
  • RAAS inhibited: low renin
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24
Q

symptoms of Conn’s Syndrome

A
  • polydipsia
  • hypertension
  • fatigue
  • frequent urination
  • heachae
  • visual disturbances
  • neuropathy
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25
Q

zona _____ has all the enzymes needed for cortisol synthesis, including 17-α hydroxylase

A

fasciculata

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26
Q

steroid transport requires ______

b

A

binding proteins
* corticosteroid binidng globulin or transcortin bind 75% of cortisol
* 15% bound to albumin
* 10% free

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27
Q

albumin carries ____% of aldosterone and ___% is found w/ transcortin, leaving 40% free

A

50%
10%

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28
Q

steroid transport requires binding proteins however it is the ______ hormone that is available to signal

A

Free

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29
Q

there is no _____ of steroids in the endocrine glands, they are released as they are synthesized

A

storage

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30
Q

the rate at which a hormone is _______ is the primary driver of its levels in blood

A

secreted
but can also be influenced by the rate at which hormones are broken down or the rate at which they are excreted in the kidneys

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31
Q

Glucocorticoid and mineralocorticoid receptors are ______

A

cytoplasmic

32
Q

Mineralocorticoid receptors (MRs) and Glucocorticoid receptors (GR) have a shared homology in their lignand and DNA binding domians… what problem does this cause

A
  • plasma CORT concentration is 100-1000x higher than that of aldosterone
  • CORT binds MR w/ high affinity

How can selectivity of aldosterone for MRs be achieved??

33
Q

How can selectivity between MRs and GRs be achieved?

A

in tissues targeted by aldosterone, the activity of 11β-hydroxysteroid dehydrogenase II (11β-HSD2)** converts cortisol into cortisone, **a form that does NOT activate the MRs b/c it is inactive

34
Q

what would a decrease in 11β-HSD2 lead to

A

decreased conversion of CORT to cortisone and increased aldosterone like effects

CORT binds to MR w high affinity and produces aldosterone like effects including Na+ retention

35
Q

in males, androgens come from the _____ and in females, the major source of androgens is _____

A

males - testes
females - cortex

36
Q

zona reticularis has ___,___ lyslase which is necessary for DHEA and androstenedione

A

17,20 lyslase

37
Q

17,20 lysase promotes conversion of pregnenolone to _____ and ______

A

DHEA and Androstenedione

38
Q

Zona reticularis lacks ____ which limits aldoesterone synthesis

A

21β-hydroxylase

39
Q

steroid synthesis requires the presence of catalytic enzymes, thus adrenal steroid synthesis, like gonadal steroid synthesis, is _______

A

regional

40
Q

plasma binding protein for DHEA

A

Albumin

41
Q

plasma binding protein for cortisol

A

transcortin

42
Q

plasma binding protein for aldosterone

A

albumin

43
Q

what is the receptor for aldosterone

A

Mineralocorticoid Receptor (MR)

44
Q

what is the receptor for cortisol

A

Glucocorticoid receptor (GR)

45
Q

what is the receptor for DHEA

A

Androgen receptor (AR)

46
Q

component of the autonomic NS, innervated by sympathetic fibers

A

Adrena medulla

47
Q

primary hormones of the adrenal medulla

A

Norepinephrine (NE) and epinephrine (E)

48
Q

the sympathetic NS innervates the adrena medulla w/ a ______ fiber that releases _______

A

preganglionic fiber that releases acetylcholine

49
Q

______ cells in the adrenal medulla are modified neuronal tissue

A

Chromaffin

50
Q

what do Chromaffin cells do

A

release NE and E into the blood

51
Q

where does catecholamine synthesis occur

A

in chromaffin cells from tyrosine

enzyme dependent

52
Q

what are the norepinephrine producing enzymes in catecholamine synthesis

A
  • Tyrosine Hydroxylase (TH)
  • L-aromatic amino acid decarboxylase (AADD)
  • Dopamine β hydroxylase (DBH)
53
Q

what is the epinephrine producing enzyme in catecholamine synthesis

A

Phenylethanolamine-N-methyltransferase (PNMT)

54
Q

chromaffin cells are specialized to store catecholamines for release when sitmulated by…

A

the sympathetic NS

55
Q

what hormone activates the last step of catecholamine synthesis

A

cortisol

56
Q

Chromaffin cells that express ______ can convert NE to E

A

Phenylethanolamine-N-methyltransferase (PNMT)

80% E to 20% NE ratio

57
Q

dopamine causes a negative feedback on ____ activity

A

tyrosine

58
Q

what are the physiological effects of catecholamine

A
  • effects are RAPID and short lived (half life 2 min)
  • increases cardiac contractility, HR, BP, arteriolar vasoconstriction
  • bronchiolar dilation
  • pupillary dilation
  • decreases GI function
  • increases alertness and brain activity
  • mobilizes fuel in times of shock
59
Q

what is the goal of catecholamine in mobilizing fuel when stimulated for fight or flight

A

promote glucose production for use by the brain

60
Q

what things cause an increased secretion of catecholamine

A
  • fight or flight response
  • hypotension
  • shock
  • heart failure
  • hypoglycemia
61
Q

NE effects on α1 and α2 receptors

A

α1: arteriolar smooth muscle contraction
α2: sympathetic nerve endings and sm contraction

62
Q

NE effects on β1 and β2 receptors

A

β1: affects heart activity
β2: sm relaxation and metabolism

63
Q

what are the 2 main enzymes for E and NE degradation

A
  • monoamine oxidase (MAO)
  • catechol-O-methyltransferase (COMT)
64
Q

primary degradation enzyme for NE

A

MAO in neuronal cytoplasm

65
Q

primary degradation enzyme for E

A

COMT in interstitial fluid of synapse, heart, liver, kidney

66
Q

what is the metabolic byproduct of catecholamine degradation

A

Vanillylmandelic acid (VMA)
excreted in urine and can serve as a measure of SNS activity

67
Q

what is the metabolic byproduct of catecholamine degradation that can be used to measure SNS activity

A

Vanillylmandelic acid (VMA)

68
Q

term for adrenomedullary hyperfunction

A

Pheochromocytoma
- catecholamine secreting tumor
- >20x more secretion than normal

69
Q

symptoms of adrenomedullary hyperfunction(Pheochromocytoma)

A
  • hypertension, rapid pulse, chest pain
  • excessive sweating
  • headache, fatigue
  • hyperglycemia
70
Q

endogenous causes of cushing’s syndrome…

A
  • pituitary tumor = cushing’s disease (70% of cases)
  • adrenal tumor (15% of cases)
  • other or unknown causes
71
Q

breeds in which Cushing’s disease is common

A
  • poodles (esp. miniature)
  • dachshunds
  • boxers
  • boston terriors
  • yorkies
  • saffordshire terriers
72
Q

canine specific serum abnormalities that co-occur w/ Cushing’s

A
  • elevated alkaline phosphatase (SAP)
  • elevated alanine transaminase (ATL)
  • hypercholesterolemia
  • hyperglycermia
  • decreased BUN
73
Q

explain the (-) feedback loop b/w CORT and ACTH

A
  • low blood CORT stimulates pituitary gland to produce ACTH
  • ACTH stimulates adrenals to produce CORT
  • once blood CORT levels return to normal, ACTH production slows to prevent an excess in CORT
74
Q

what would an elevated urine cortisol: creatnine ratio indicate

A

hyperadrenocorticism

75
Q

low dose dexamethasone suppression test

A

give low dose dexmethasone suppression test, then measure CORT levels 4-8 hours after
a reduction in CORT below a certain level or no change, would suggest HPA axis working normally

if cort levels increase, >50% from baseline, cushings

76
Q

what is dexmethasone

A

Dex is a synthetic corticosteroid w/ high affinity for Glucose receptors

77
Q

high dose dexamthasone test

A

tests for negative feedback

a high dose of dex followed by reduced ACTHsupports diagnosis of pituitary origin

if ACTH is unchanged suggests an adrenal or ectopic tumor

can also measure CORT
High dose dex followed by low CORT = pituitary origin

PHYSIOLOGY II (17 decks)

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