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Endocrine > The Adrenal Gland- Functions and Diseases > Flashcards

The Adrenal Gland- Functions and Diseases Flashcards

1
Q

the adrenal medulla is of _____ origin

A

ectodermal

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2
Q

the adrenal cortex is of _____ origin

A

epidermal (mesoderm)

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3
Q

what does the adrenal cortex secrete

A

aldosterone
cortisol
androgens

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4
Q

what does the adrenal medulla secrete

A

catecholeamines

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5
Q

what is the main secretory product of the zona glomerulosa

A

mineralocorticoid (aldosterone)

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6
Q

what is the main secretory product of the zona fasciculata

A

glucocorticoids (cortisol)

androgens

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7
Q

what is the main secretory product of the zona reticularis

A

glucocorticoids (cortisol)

androgens

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8
Q

what is the main product of adrenal medulla

A

catechole. norep and epin

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9
Q

this protein is involved in the rate limiting step in production of steroid hormones by transporting cholesterol into the mitochondria

A

StAR

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10
Q

____ converts cholesterol into ___ (first enzyme)

A

desmolase, pregnenolone

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11
Q

what enzymes are in the aldosterone arm

A

21 B hydroxylase

11 B hydroxylase

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12
Q

what enzyme is in all 3 arms: aldosterone, cortisol, androgens

A

3B hydroxysteroid dehydrogenase

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13
Q

what enzymes are in the cortisol arm

A

21 B hydroxylase
11B hydroxylase
17 a hydroxylase

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14
Q

what enzymes are in the androgen arm

A

17 a hydroxylase

17,20 lyase

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15
Q

a loss of the 21 B hydroxylase enzyme will lead to what?

A

pregnenolone sent to make androgens, no negative feedack for sex hormones

  • virulization of fetus
  • lose cortisol
  • hyponatremia and hypovolemia (no aldost)
  • congenital adrenal hyperplasia (95% of cases)
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16
Q

17a hydroxylase deficiency

A
  • pregnenolone is directed towards mineralocorticoid synthesis
  • lose secondary sex characteristics
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17
Q

ACTH is derived from post-translational processing of ____

A

POMC

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18
Q

POMC is broken down into ___ and ___ one of which increases __

A

ACTH and a-MSH

-a-MSH increases melanin synthesis

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19
Q

cortisol has a negative feedback on what

and what kind of feedback loop is this (long or short)

A 
hypothalamus (-) CRH
Anterior pituitary (-) ACTH

-long loop negative feedback

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20
Q

when is cortisol released the most?

A

in the morning and is around 20 mircrograms/dl

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21
Q

what can exogenous administration of cortisol due to certain cells

A

may shut down ACTH production and adrenal cells that produce cortisol atrophy

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22
Q

what does exogenous cortisol do to CRH,ACTH,Cortisol

A

decreases all of them

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23
Q

cushings syndrome is what and has what effects on CRH, ACTH, and cortisol

A

SYNDROME: tumor of the adrenal gland, unregulated secretion of cortisol

-decreases CRH and ACTH

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24
Q

cushings disease is what and has what effects on CRH, ACTH, and cortisol

A

DISEASE: tumor of the anterior pituitary

  • increased ACTH, and cortisol
  • decreased CRH
  • ACTH has trophic effect on adrenal gland too
25
Q

addison’s disease and cortisol and what is primary vs secondary

A

causes hypocortisolism

  • primary is autoimmune attack of adrenal gland
  • secondary is from chronic exogenous glucocorticoid treatment
26
Q

cushings syndrome symptoms

A

buffalo hump on back of neck
moon face
excess weight gain in abdomen
dark red or purple stretch marks

27
Q

angiotensin ___ can constrict blood vessels to increase BP

A

II

28
Q

what is the direct effect of aldosterone secretion

A

ACTH

29
Q

what is the secondary stimulation of aldosterone secretion

A

angiotensin II

30
Q

steps in action of aldosterone in renal sodium resab

A

1) aldosterone from blood enters P cell of distal nephron and binds aldosterone receptor
2) hormone-receptor complex goes to nuclues and txn occurs for mRNA
3) translation of mRNA to make epithelial sodium channels and potassium channels
- potassium out
- sodium in
4) alters the activity of the Na+/K+ ATPase at the basolateral end to pump out sodium and bring in more K+

31
Q

conn’s syndrome

A

primary hypealdosteronism, adenoma in the adrenal cortex

32
Q

secondary hyperaldosteronism

A

excessive renin secretion by the juxtaglomerular cells in the kidney

33
Q

hypoaldosteronism causes (3)

A

destruction of the adrenal cortex
defects in aldosterone synthesis
inadequate stimulation of aldosterone secretion

34
Q

what cells of the adrenal medulla produce catecholeamines

A

chromaffin cells

35
Q

adrenal medulla produces primarly ___ and small amounts of __

A

epinephrine (80%)

norepinephrine (20%)

36
Q

synthesis of catecholamines

A

tyrosine–>DOPA–>Dopamine–>norep–>epin

37
Q

what enzyme converts norepinephrine to epin and what stimulates this

A

PNMT and cortisol stimulates this

38
Q

___ stimulates the synthesis of DOPA

A

ACTH

39
Q

steps of norep and epin synthesis and locations

A

1) tyrosine to DOPA to Dopamine in the cytosol
2) Dopamine enters chromaffin granule through VMAT-1
3) Dopamine Beta hydroxylase converts to NE in granule
4) NE leaves granule through VMAT1 and is converted to epin by PNMT in cytosol
5) epin back into granule through VMAT1 and stored in complex

40
Q

the storage complex in the chromaffin granule contains what

A

ATP, Ca2+, NE, Epi, inside a chromogranin

41
Q

what is the RL step in NE and E synthesis

A

hydroxylation of tyrosine by tyrosine hydroxylase to produce DOPA

Tyrosine —tyrosine hydroxylase—> DOPA

42
Q

what are chromogranins and what can they be used to mark

A

complexes that decrease osmotic burden of storing individual molecules of E within chromaffin granules
-can be marker of sympathetic paraganglion-derived tumors (paragangliomas)

43
Q

what can be measured to determine total catecholamine production

A

VMA

44
Q

epinephrine is degraded by _____ (enzyme) and turned into ___

A

COMT, metanephrine

45
Q

norepinephrine is degraded by ____ (enzyme) and turns to ___

A

COMT, normetanephrine

46
Q

normetanephrine and metanephrine are converted to ___ by what enzyme

A

VMA by MAO

47
Q

which receptors respond better to NE than E

A

a1,a2 and B3

48
Q

which receptors respond equal to NE and E

A

B1

49
Q

which receptors respond better to E than E

A

B2

50
Q

what are the 3 main symptoms of pheochromocytoma

A

headaches, sweating, palpitations

51
Q

what is a pehochromocytoma

A

tumor of chromaffin tissue

52
Q

short term stress stimulates adrenal medulla via what

A

preganlionic sympathetic fibers (catechole released)

53
Q

prolonged stress response from what

A

ACTH from AP

54
Q

17a hydroxylase deficiency leads to what presentation

A

male: ambiguous genitalia, undescended testes
female: lacks secondary sexual development

55
Q

21 hydroxylase deficiency presentation

A

presents in infancy as salt wasting (hypotension),
hypoglycemia
childhood has precociouis puberty
XX: virulization

**most common CAH

56
Q

11 B hydroxylase defeciency effect on BP

A

decreases aldosterone but increaess 11-deoxycorticosterone which increases blood pressure

57
Q

11 B hydroxylase deficiency presentation

A

XX: virilization

58
Q

what is common presentation with all congenital adrenal hyperplasias

A

enlargement of both adrenal glands due to increaseased ACTH stimulation in response to low cortisol

Endocrine (14 decks)

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