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Flashcards in Endo - Adrenal Deck (55):
1

long term stress response (glucocorticoids)

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

2

adrenal zones (+hormones)

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

3

making E/NE

tyrosine --> dopa --> dopamine --> NE --> E
cortisol needed to make E from NE

4

E:NE release

4x more E
more important for beta 2 receptors

5

embryonic origin of adrenal gland

cortex (mesoderm)
medulla (neuroectoderm)

6

adrenal gland innervation

cortex (nearly none)
medulla (SNS)

7

making aldosterone

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

8

making cortisol

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

9

making androgens

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

10

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

ZG doesn't have 17-alpha hydroxylase

11

things that stimulate cortisol

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

12

things that inhibit cortisol

↑ cortisol levels
Opioids
Somatostatin

13

ACTH effects on adrenal gland

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

14

POMC

preproopiomelanocortin is precursor for ACTH
when ACTH is metabolized it makes MSH

15

cortisol release type

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

16

cortisol diurnal pattern

ACTH + cortisol peak before waking
lowest before sleep

17

what determines circadian rhythm

suprachiasmatic nucleus

18

things that alter suprachiasmatic nucleus

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

19

cortisol and stress

stress overrides negative feedback
enhance activity of CRH-ACTH system

20

cortisol transport

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

21

cortisol inactivation

takes place in liver
inactivates and conjugates w/ glucuronide or sulfate to up solubility for kidneys

22

cortisol half life

70 min

23

cortisol mech

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

cortisol effects (time)

lag period - need to synth new protein
last a long time - slow protein turnover

25

cortisol actions (broad)

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

26

cortisol actions (metabolism)

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

cortisol w/ protein and fat

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

cortisol and muscles

basal levels of cortisol needed for normal contractility
excess --> atrophy

29

cortisol and bones

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

30

cortisol and CV

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

31

cortisol and kidney

up GFR
inhibit ADH
none --> dehydration (?)

32

cortisol and CNS

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

33

cortisol and fetus

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

34

cortisol and immune

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

35

Cushing's syndrome

hypersecretion of cortisol
ACTH dependent or independent

36

ACTH dependent hypersecretion causes

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

37

ACTH independent hypersecretion causes

adrenal tumor
iatrogenic - give GCCs for arthritis, allergies, transplants

38

Cushing's syndrome Sx

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

39

cushing's syndrome Dx

1. high cortisol in plasma, urine, saliva -- unreliable
2. 24 hr urine cortisol -- screening
3. dexamethasone suppression test

40

Cushing's Dx using DEX (broad)

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

Cushing's Dx using DEX (steps + results)

1. 2 mg overnight
2. 8 mg overnight

42

Cushing's Dx using DEX (results)

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

cortisol hyposecretion types

primary adrenal insufficiency (Addison's)
secondary adrenal insufficiency

44

Addison's mech

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

45

Addison's Sx

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

46

secondary adrenal insufficiency mech

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

secondary adrenal insufficiency Sx

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

48

adrenal insufficiency Dx

cosyntropin stimulation test
rapid: screening
prolonged: differential

49

cosyntropin stimulation test

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

high cortisol, high ACTH

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

51

high cortisol, low ACTH

adrenal tumor

52

low cortisol, high ACTH

primary adrenal insufficiency (Addison's)

53

low cortisol, low ACTH

secondary adrenal insufficiency

54

congenital adrenal hyperplasia mechanism

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

55

congenital adrenal hyperplasia Sx

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