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Physiology > Endo - Adrenal > Flashcards

Endo - Adrenal Flashcards

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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

Study These Flashcards
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)

Study These Flashcards
A

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

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