6 Endocrinology: Adrenal Hormones Flashcards

1
Q

The 5 general functions of cortisol are? (global card)

A
  • Mobilize/make glucose (plus stop using & store glucose)
  • Mobilize amino acids and send them all to the liver
  • Mobilize Fatty Acid (FA) stores
  • Suppress immunity/inflammation
  • Mature the CNS, retina, skin, lungs
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2
Q

What a simple way to remember catecholamine (from adrenal medulla) effects? (global card)

A

They are like thyroid hormone, but:

  • No CNS effects
  • Spares protein
  • Short-acting
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3
Q

The 3 zones of cortex G-F-R release what hormones?

A

aldosterone, glucocorticoids, androgens

[deeper you go, sweeter it gets]

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4
Q

Which: cortex, or medulla? Is a modified sympathetic ganglion (lacking a post-ganglionic axon)

A

Medulla

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5
Q

Adrenal Medulla releases what?

A

catecholamines (norepi, epi) in response to sympathetic stimulation

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6
Q

Blood flow which direction in the adrenal glands? why does this matter?

A
  • cortex->medulla

- One-two punch of hormones, and cortisol causes norepinephrin to become epinephrine.

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7
Q

So, what ARE the effects of catecholamines? (global card) (think of sympathetics)

A
  • Up cardiac output, ventilation
  • Mobilize fats
  • Mobilize/make glucose but…
  • Send all glucose to the brain
  • Dilate pupils
  • Decrease digestion
  • Up muscle tension, neuromuscular transmission
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8
Q

The 4 catecholamine receptors are alpha 1 & 2, beta 1 & 2. Which catecholamine does not act on all 4?

A

Norepi (Doesn’t do beta 2’s)

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9
Q

What are catecholamines made from?

A

tyrosine

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10
Q

What is the steps by which catecholamines are made?

A
tyrosine->
L-Dopa->
Dopamine->
Norepi->
Epi
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11
Q

Which step of catecholamine synthesis is not regulated by ACTH, but by cortisol?

A

Norepi->Epi

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12
Q

Pheocromocytoma is a tumor where? Are symptoms continuous or sporadic?

A
  • Adrenal medulla (chromaffin tissue)

- Sporadic

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13
Q

Pg. 6 has a figure showing cholesterol synthesis into steroids, tons of steps so easier to see in a graphic.

A

Now I’ll ask you 2 questions about it…

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14
Q

What receptor brings cholesterol into cells?

A

LDL receptor (also Acetyl CoA can be made into cholesterol)

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15
Q

What enzyme converts cholesterol into pregnenalone once StAR protein brings it into the mitochondria?

A

desmolase

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16
Q

As steroids, How are cortisol and aldosterone circulated?

A

Either bound or free

[cortisol w/ transcortin or albumin, aldosterone w/ plasma proteins]

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17
Q

What organ inactivates steroids?

A

liver!!!!!!!!!!!!!

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18
Q

What does aldosterone do? What would happen if you had too much/too little?

A
  • Na reabsorb, K secrete
  • Exactly what you would expect, EXCEPT in hyper-aldosterone, “escape” increases GFR and allows fluids and Na to leave body
19
Q

As a steroid, where is aldosterone’s receptor located?

A

cytoplasm

20
Q

As a steroid, what happens once aldosterone binds receptor?

A

disassociate hsp90, heads into nucleus, becomes a transcription factor

21
Q

11 beta hydroxysteroid dehydrogenase Type 2 does what?

A

Degrades cortisol so it doesn’t bind aldosterone’s receptor and mimic aldosterone’s effect (licorice & stevia inhibit this enzyme, causing up blood pressure….)

22
Q

What organs do the following: Secretes angiotensinogen? Secretes renin? Converts angiotensin 1? produces aldosterone?

A
  • liver
  • kidney
  • lungs
  • adrenal cortex
23
Q

In order of importance, what causes aldosterone secretion?

A

-Up K+
-Renin system
-Down Na+
-ACTH
[ANP prevents secretion]

24
Q

How does cortisol cause anti-inflammation? (global card)

A
  • stabilize lysosomes
  • decrease capillary permeability
  • decrease WBC migration and phagocytosis
  • decrease cellular glucose usage
  • drops immune cell proliferation/Ab production
  • inhibit NF-KappaB
25
Q

What does cortisol do to vascular system?

A

maintains normal B.P.

26
Q

What does cortisol do to kidneys?

A

Up GFR, more dilute urine

27
Q

What does cortisol do to CNS?

A

modulate mood and sleep

28
Q

What does cortisol do to lungs?

A

make surfactant

29
Q

What does cortisol do to skin?

A

thins it

30
Q

What turns on cortisol and ACTH?

A

stress, and mornings

31
Q

Of the 3 short, ultra-short, and long-loop feedback, cortisol has which?

A

short, long

32
Q

ACTH (stimulates cortisol release) comes from what pro-peptide? Why does this matter?

A
  • POMC

- Because ACTH contains MSH in its sequence, increasing skin pigmentation

33
Q

What is the rate-limiting step in steroid synthesis? What does ACTH do to this step?

A
  • desmolase

- Activates it via cAMP

34
Q

Combined cortisol/aldosterone deficiency is called what? What are the effects?

A
  • Addison’s
  • stress, skin darkening, hyperkalemia (heart block, vomiting, muscle weakness), decreased extracellular fluid volume, hypoglycemia
35
Q

T/F Addison’s disease comes on quickly?

A

F

36
Q

In hypersecretion of aldosterone, what happens to plasma renin concentration?

A

decreases (Diagnostic indicator! due to feedback inhibition)

37
Q

Cushing’s disease is what?

A

adenoma causing cortisol secretion (responds to dexamethasone)

38
Q

Cushing’s syndrome is what?

A

Other causes for cortisol over-secretion (WON’T respond to dexamethasone feedback inhibition)

[dexamethasone mimics cortisol]

39
Q

What are the effects on the body of Cushing’s? (global card)

A
  • up blood glucose
  • Down immunity
  • Thin skin
  • Muscle weakness, bone weakness
  • Hypertension (recall aldosterone, cortisol use same receptor…)
  • Fat goes to chest/abdomen (buffalo hump!)
40
Q

How would I treat Cushing’s?

A

remove or irradiate the pituitary or adrenal gland. (or use drugs that inhibit steroids)

41
Q

In congenital adrenal hyperplasia, what is the mechanism?

A

-Broken enzyme stops cortisol & aldosterone synthesis->removes feedback inhibition->Tons of ACTH makes the adrenal gland huge.

[U.S. screens babies for this, it is autosomal recessive]

42
Q

What body problems result from congenital adrenal hyperplasia?

A

salt-wasting, tons of androgens are made due to ACTH over-secretion

43
Q

What is adrenogenital syndrome?

A

hairy woman, or penis growth to full-size occurs as a 4-year-old (due to DHEA)