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Endo/Repro Block1 > Adrenal Phys [TRH] > Flashcards

Adrenal Phys [TRH] Flashcards

1
Q

What are the 3 zones of the adrenal cortex and what does each synthesize?

A
  1. Zona Glomerulosa [outermost]
    • synthesizes: mineralcorticoid; aldosterone
  2. Zona Fasciculata [middle]
    • synth= glucocorticoids, cortisol
  3. Zona Reticularis [innermost]
    • ​synthesizes: androgens; DHEA & androstenedione,

***the 3 zones make up 90% of the adrenal gland [medulla = 10%]

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2
Q

What is the adrenal medulla derived from?

What is its “structure” & what does it secrete?

A
  • derived from neural crest
  • it can be thought of as a modified sympathetic ganglion that secretes catecholamines directly into circulation
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3
Q

Corticotropin Releasing H/Factor [CRH]

  • where is it made?
  • what promotes its release?
A
  • short t1/2 [9 mins]
  • synthesized in the hypothalamus
  • ant pit corticotrophs have CRFR1 receptor
    • GPCR
  • proinflammatory cytokines & chronic stress promote release of CRF
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4
Q

When is ectopic produxn of ACTH possible?

A

in cancer

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5
Q

What is the enzyme required for cholesterol conversion to pregenelone?

What is it a rate limiting step for?

A

side-chain cleavage enzyme [CYP11A=P450scc]

**made in adrenal cortex

rate limiting in: adrenal steroid synthesis

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6
Q

What R does predominantly ACTH bind?

-where is it?

A

MC2-R: melanocortin 2 receptor

  • located 1’ in adrenal cortex
    • also in skin melanocytes
    • adipocytes –> where it medi8s stress induced lipolysis via ACTH release
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7
Q

Where is MC1-R 1’ located?

  • what does it bind?
  • what does ^^ACTH levels do?
A
  • MC1-R is the 1’ MCR in the skin [regulates pigmentation]
    • high affinity binding for most MSH isoforms
    • ACTH @ high levels will also bind MC1-R
      • chronically high ACTH levels can induce skin & gum hyperpigmentation
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8
Q

What does excess POMC cause?

A
  • ^^MSH & ^^ACTH levels
    • –> both can stimul8 hyperpigmentation
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9
Q

MC3-R, where is it located?

Where is MC4-R is it located?

What do MC3 & 4 R’s regulate?

A

MC3-R: in the brain

  • knockouts for MC3-R are obese

MC4-R: in CNS [esp. hypothalamus], placenta, & GIT

  • 1’ MCR for food intake regulation
  • inactivating mutations of MC4-R cause obesity in mice & ppl

**Both MC3&4 R’s in CNS regulate food intake but MC3R also regulates energy homeostasis

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10
Q

Where is MC5R located? What does it do?

A

MC5R: expressed in adrenals, skin, stomach, lung & spleen

-involved in sebum prodxn

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11
Q

What are the 3 types of adrenocorticoids?

A

“adrenal cortical steroids”

  • glucocorticoids
  • mineralocorticoids
  • sex steroids, mostly androgens
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12
Q

glucocorticoids…

bind?

do?

are recognized when?

A
  • recognized: early to cause an ^^glu in circulation levels
    • CORTISOL: mobilizes AA’s 4m proteins for hepatic GNeo
      • cortisol is 1’ active glucocorticoid
      • deficiency = hypoglycemia
  • bind glucocorticoid R’s [GR]
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13
Q

mineralcorticoids…

are?

do?

bind?

A
  • ALDOSTERONE is main example
    • little activity as a glucoC
  • promote salt & H20 retention in the kidney
  • bind to mineralocorticoid R’s [MR]
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14
Q

Sex steroids, mostly androgens…

are?

bind?

do?

A
  • DHEA [dehydroepiandrosterone], androstenedione, some testosterone
  • bind androgen R’s [AR]
  • minor role in estrogen synthesis
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15
Q

How does cortisol circulate?

A

10% circulates as free cortisol

90% bound:

  • -60% CBG [aka transcortin]
  • -30% w/ albumin
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16
Q

What increases & decreases CBG?

A

^^^CBG = esrtogens & pregnancy

decreased CBG = ^^^cortisol & liver cirrhosis

17
Q

What happens after a glucocorticoid [usually cortisol] binds a R?

A
  • R’s are usually cytoplasmic
  • Bound H R moves to nucleus –> forms homodimer
  • Homodimer acts as transcription factor –> bind to genes w/ glucocorticoid response elements [GRE]
    • recruits transcription co-factors
    • then inti8s transcription or inhibits it
18
Q

what is the aldosterone receptor?

A

NR3C2

nuclear R subfamily 3, grpC, member 2

19
Q

Where are Mineralocorticoid R’s [MR’s] found?

what does it bind?

A
  • kidney, colon, sweat glands, heart, hippocampus, brown adipose
  • binds: equal affinity for aldosterone & cortisol
    • but in some tissues, cortisol will bind and become inactive–/.thus not “working” on mR’s
20
Q

4 steps of glucocorticoid metabolism

A
  1. intracellular active glucocorticoid –> inactive
    • via 11 beta hydroxylase type 2 [in K, colon, placenta, fetus, & salivary gland]
  2. inactive steroid cannot activate MC2R
  3. inactive steroids converted to active
    • via 11 beta hydroxylase type 1 [in liver, adipose, lung, vascular tissue, CNS, & mac’s]
  4. tissue location of 11BhT1 & 2 defines net result of metabolism

**many synthetic glucoC’s [prednisolone/cortisone etc] are 11-ketosteroids that must be reduced to get biologically active

21
Q

Where does most of glucoC metabolism occur?

A
  • most happens in the liver
    • conjugated cortisol/-sone are soluble & excreted by K’s
    • use these to measure adrenal steroid prodxn w/ 24hrU
  • other conversion enzymes are in the K, colon, & salivary gl.
22
Q

which is an active steroid, cortisol or cortisone?

A

CORTISOL!!!

  • in mineralC-responsive tissues [K for ex], convert cortisol to inactive cortisone
23
Q

how do glucoC’s affect metabolism?

A

by increasing plasma glucose!!

24
Q

What are the effects of aldosterone?

aka what does it do?

A
  • stimulates K retention of Na+ & h20
  • stimulates Na+ & h20 reabsorption in the colon, salivary glands & sweat glands
  • enhances K excretion of K+
  • hypersecretion of aldosterone–> HTN
25
Q

what type of regulation is used in the glucoC endocrine axis?

A

negative feedback regulation

26
Q

what are all steroids synthesized from?

What enzymes are involved in steroid synthesis?

A
27
Q

Describe the pattern of adrenal steriod synthesis…

what are the 3 main enzymes we should know?

A
28
Q

What deficits are caused by the following enzyme deficiencies:

  • 17a-hydroxylase
  • 21-hydroxylase
  • 11B-hydroxylase
A
29
Q

describe the role of ACTH & aldosterone on blood P?

A
30
Q

Describe 1’ hypersecretion of cortisol?

Describe 2 types of 2’ hypersecretion of cortisol?

A
31
Q

What are 2 types of hyposecretion of cortisol?

A
32
Q

What is Cushing’s disease?

  • MCC?
  • Sx’s/signs [2 diff manifestations]
A

Cushings: excess ACTH secretion

  • MCC= pituitary adenoma
  • Sx’s/signs:
    • ^^ACTH & ^^cortisol
    • +/- aldosterone

Cushings: iatrogenic or 1’ adrenal tumor

  • Sx/signs: ^^cortisol but decreased ACTH
33
Q

Addison Disease

1’ vs. 2’

MCC Sx’s

A

1’ Addison’s: usually immune mediated destrxn of adrenal cortex OR congenital adrenal dysgenesis/H insufficiency

  • decreased cortisol & aldo
  • compensatory ^^POMC–> ^^ACTH & ^^MSH

2’ Addisons: iatrogenic after sudden w/drawal of exogemous glucoC [exo cortisol = decreased endo ACTH]

MCC Sx’s: fatigue, weak, anorexia, loss of appetite, D, hyperpigmentation [due to ^^POMc & ACTH & MSH]

Endo/Repro Block1 (11 decks)

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