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Physiology > Endo - Adrenal > Flashcards

Endo - Adrenal Flashcards

1
Q

long term stress response (glucocorticoids)

A
  1. protein/fat converted to glucose or broken down for energy
  2. increased blood glucose
  3. suppress immune
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2
Q

adrenal zones (+hormones)

A 
zona glomerulosa (aldosterone)
zona fasciculata (cortisol + androgens)
zona reticularis (cortisol + androgens)
medulla (E/NE)
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3
Q

making E/NE

A

tyrosine –> dopa –> dopamine –> NE –> E

cortisol needed to make E from NE

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4
Q

E:NE release

A

4x more E

more important for beta 2 receptors

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5
Q

embryonic origin of adrenal gland

A

cortex (mesoderm)

medulla (neuroectoderm)

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6
Q

adrenal gland innervation

A

cortex (nearly none)

medulla (SNS)

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7
Q

making aldosterone

A

rate limiting step: Ang II stimulates cholesterol desmolase (chl to pregnenolone)
pregnenolone –> progesterone
–> deoxycorticosterone (#2 most potent natural MCC)
–> corticosterone
–> aldosterone

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8
Q

making cortisol

A

rate limiting step: ACTH stimulates cholesterol desmolase (chl to pregnenolone)
pregnenolone / progesterone
+ 17 alphahydroxylase
–> –> cortisol

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9
Q

making androgens

A

rate limiting step: ACTH stimulates cholesterol desmolase (chl to pregnenolone)
pregnenolone / progesterone
+ 17 alphahydroxylase
–> –> androgens

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10
Q

why is only aldosterone made in ZG? (not cortisol or androgens)

A

ZG doesn’t have 17-alpha hydroxylase

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11
Q

things that stimulate cortisol

A 
ACTH
↓ cortisol levels
Stress
ADH
Serotonin
Sleep-wake transition
α-agonists, β-antagonist
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12
Q

things that inhibit cortisol

A

↑ cortisol levels
Opioids
Somatostatin

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13
Q

ACTH effects on adrenal gland

A

stim production of cortisol, adrenal androgens and aldosterone (slightly)
only cortisol feeds back
adrenal gland hyperplasia (via IGF-1)

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14
Q

POMC

A

preproopiomelanocortin is precursor for ACTH

when ACTH is metabolized it makes MSH

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15
Q

cortisol release type

A

pulsatile
constant in amt released, changes in freq
summation for larger pulses

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16
Q

cortisol diurnal pattern

A

ACTH + cortisol peak before waking

lowest before sleep

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17
Q

what determines circadian rhythm

A

suprachiasmatic nucleus

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18
Q

things that alter suprachiasmatic nucleus

A 
chronic GCCs (blunt morning peak)
lack of natural light during day, artificial light at night
variable work schedule*
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19
Q

cortisol and stress

A

stress overrides negative feedback

enhance activity of CRH-ACTH system

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20
Q

cortisol transport

A

bound in blood
corticosteroid-binding globulin (CBG, transcortin) - 75%
albumin - 15-20%
unbound 5%

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21
Q

cortisol inactivation

A

takes place in liver

inactivates and conjugates w/ glucuronide or sulfate to up solubility for kidneys

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22
Q

cortisol half life

A

70 min

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23
Q

cortisol mech

A
  1. unbind from transport protein
  2. enter cell
  3. bind to receptor complex (includes HSPs - heat shock proteins)
  4. HSPs released
  5. receptor binds to DNA
  6. regulates gene expression
24
Q

cortisol effects (time)

A

lag period - need to synth new protein

last a long time - slow protein turnover

25
Q

cortisol actions (broad)

A

stim gneo in response to low blood sugar
increase protein/lipid breakdown (makes gneo substrates)
anti-inflammatory
suppress immune response

26
Q

cortisol actions (metabolism)

A

up gneo
up protein/lipid breakdown
inhibits insulin-stimulated gluc uptake by muscle/adipose (like GH)
blocks suppressive effects pf insulin on hepatic glucose output
———–> provide brain w/ glucose

27
Q

cortisol w/ protein and fat

A

direct lipolytic effect is small
permissive for lipolytic action of catecholamines
stim appetite
stim lipogenesis in certain spots (face/trunk)
increase protein breakdown up decrease AA utilization everywhere but liver (down protein synth)

28
Q

cortisol and muscles

A

basal levels of cortisol needed for normal contractility

excess –> atrophy

29
Q

cortisol and bones

A 
decrease bone formation*:
- down vit D synth
- inhibit making osteoblasts
- up apoptosis of osteoblasts/cytes
increase bone reabsorption 
- make cytokines --> activate osteoclasts
30
Q

cortisol and CV

A

basal levels needed for normal BP (permits vessels to respond to adrenergic.angiotensin)
excess –>. hypertension

31
Q

cortisol and kidney

A

up GFR
inhibit ADH
none –> dehydration (?)

32
Q

cortisol and CNS

A

receptors: hippocampus, reticular activating substance, autonomic nuclei
affects learning, emotions
excess: insomnia, euphoria or depression

33
Q

cortisol and fetus

A

stim synth of surfactant
stim maturation of GI enzymes
+ help fetal CNS, retina, skin

34
Q

cortisol and immune

A

inhibit inflammatory (asthma)
prevents rejection of transplant
vulnerable to infection

35
Q

Cushing’s syndrome

A

hypersecretion of cortisol

ACTH dependent or independent

36
Q

ACTH dependent hypersecretion causes

A

pituitary microadenoma (Cushing’s disease - 80%)
ACTH secreting ectopic tumor (20%)
CRH secreting ectopic tumor (rare)

37
Q

ACTH independent hypersecretion causes

A

adrenal tumor

iatrogenic - give GCCs for arthritis, allergies, transplants

38
Q

Cushing’s syndrome Sx

A 
truncal obesity
moon face
hypertension
skin atrophy
diabetes
gonadal dysfxn
muscle weakness
hirsuitism, acne
mood changes
osteoporosis
39
Q

cushing’s syndrome Dx

A
  1. high cortisol in plasma, urine, saliva – unreliable
  2. 24 hr urine cortisol – screening
  3. dexamethasone suppression test
40
Q

Cushing’s Dx using DEX (broad)

A

DEX suppression test
25x higher affinity for cortisol receptors than cortisol
See if cortisol levels drop when DEX is given as a result of negative feedback

41
Q

Cushing’s Dx using DEX (steps + results)

A
  1. 2 mg overnight

2. 8 mg overnight

42
Q

Cushing’s Dx using DEX (results)

A

after 2 mg –> normal people cortisol will drop a lot (neg feeddback
after 8 mg –> Cushing’s disease will drop 50% (tumor only inhibited by high levels)
after 8 mg –> adrenal tumors won’t drop (no feedback)

43
Q

cortisol hyposecretion types

A

primary adrenal insufficiency (Addison’s)

secondary adrenal insufficiency

44
Q

Addison’s mech

A

autoimmune destruction of adrenal cortex –>
deficiencies in cortisol, aldosterone and adrenal androgens
excess ACTH from lack of feedback

45
Q

Addison’s Sx

A 
hyperpigmentation (esp @ elbows, knuckles - from excess ACTH --> excess MSH)
weakness
depression
weight loss
hypotension
46
Q

secondary adrenal insufficiency mech

A

lack of ACTH from drugs or tumors/infections of pituitary gland
deficiency of cortisol but not aldosterone
sluggish response to ACTH due to atrophy

47
Q

secondary adrenal insufficiency Sx

A

like Addison’s (but w/o hyperpigmentation)
mild orthostatic hypotension
poor response to stress

48
Q

adrenal insufficiency Dx

A

cosyntropin stimulation test

rapid: screening
prolonged: differential

49
Q

cosyntropin stimulation test

A

cosyntropin is synthetic ACTH

normal: cortisol goes up
primary: cortisol never goes up
secondary: cortisol starts to go up after a long time (sluggish)

50
Q

high cortisol, high ACTH

A

cushing’s disease (pit tumor) or ectopic ACTH tumor

51
Q

high cortisol, low ACTH

A

adrenal tumor

52
Q

low cortisol, high ACTH

A

primary adrenal insufficiency (Addison’s)

53
Q

low cortisol, low ACTH

A

secondary adrenal insufficiency

54
Q

congenital adrenal hyperplasia mechanism

A

21-hydroxylase deficiency –>
no cortisol or aldosterone made
–> up ACTH (no neg feedback)
–> up androgen production

55
Q

congenital adrenal hyperplasia Sx

A

females: virilized females (masculinized genitals and behavior)
males: precocious puberty

Physiology (22 decks)

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