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endocrine - adrenal gland Flashcards

0
Q

Complex of N/NE with ATP, Ca and proteins inside the granules.

A

Chromogranins

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1
Q

Synthesis of epinephrine

A
  1. Transport of tyrosine into chromaffin cells cytoplasm
  2. Hydroxylation of tyrosine into DOPA
  3. DOPA to dopamine
  4. Transport of dopamine into chromaffin granules (secretory vesicles)
  5. Dopa to norepi within chromaffin granules as chromogranins
  6. Norepi diffuses out of granule thru facilitated diffusion
  7. Methylation of norepi to epi
  8. Transport of epi back into granules
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2
Q

Reduces osmotic burden of storing individual molecule of epi with chromaffin granules

A

Chromogranins

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3
Q

Important in biogenesis on secretory vesicles and organization of components within vesicles

A

Chromogranins

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4
Q

Secretion of noepi and epi is regulated by

A

Descending sympa signals in response to stress.
Hypothalamus and brain stem send a chemical signal as ACTH to bind to nicotinic receptor in chromaffin cells which increases acty of tyrosine hydroxylase and B-hydroxylase in which stimulates exocytosis of granules

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5
Q

Mechanism of action of catecholamine

A

Exerted thru adrenergic receptor

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6
Q

Tissue distribution and potency agonist:

a1 receptor

A

Adrenergic post synaptic nerve terminals

Norepi=epi

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7
Q

Tissue distribution and potency agonist:

a2 receptor

A

Adrenergic pre synaptic terminals

Norepi=epi

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8
Q

Tissue distribution and potency agonist:

B1 receptor

A

Heart

Epi=norepi

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9
Q

Tissue distribution and potency agonist:

B2 receptor

A

Liver

Epi>norepi

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10
Q

Tissue distribution and potency agonist:

B3 receptor

A

Adipose tissue

Norepi>epi

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11
Q

2 primary degradation enzymes of catecholamine

A
  1. Monoamine oxidase MAO

2. Catechol-O-methyltransferae COMT

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12
Q

Degradation enzyme of catecholamine that predominates in neuronal mitochondria

A

MAO

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13
Q

Degradation enzyme of catecholamine that predominates as methylation of Norepi/epi in non-neuronal tissue

A

COMT

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14
Q

Degradation enzyme of catecholamine that is predominant

A

COMT

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15
Q

Metabolism of catecholamine

A

Draw!

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16
Q

Chromaffin cell tumor that produce, store, metabolize and secrete catecholamine (in excess).
Causing irregular secretion of epi and norepi leading to attacks of raised bp, palpitations, and headache.

A

Pheochromocytoma

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17
Q

Pheochromocytoma is majorly bilateral/ unilateral?

A

90% unilateral and sporadic

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18
Q

Clinical features of pheochromocytoma

A 
Sweating 
Hypertension
Headaches
Anxiety/fear
Forceful heartbeat with or without tachycardia 
Flushing
Fatigue 
Tremors
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19
Q

In pheochromocytoma, hypertension is mainly due to

A

Increased peripheral resistance

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20
Q

In pheochromocytoma, lability of Bp is caused by

A

Episodic catecholamine release
Impaired Symphathetic reflex
Unrecognized chronic volume expansion

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21
Q

Biochemical diagnosis of pheochromocytoma

A

Catecholamine excess

Urinary fractionated metaphrenine or plasma free metaphrenine will predict size and location of tumor

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22
Q

How is blood collection done in diagnosis of pheochromocytoma?

A

Supine for 20min
Overnight fast
No nicotine, alcohol within 12hrs
Avoid acetaminophen, TCA and phrnoxybenzamine

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23
Q

Imaging of choice for pheochromocytoma

A

CT scan

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24
Q

Imaging of choice in pheochromocytoma preferred for extra adrenal, pregnant, children and those allergic to contrast.

A

MRI

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25
Q

Imaging of choice in pheochromocytoma if there is metastasis, previous operation or for familial, multiple pheochromocytoma

A

MIBG - 1st choice, gets into cell but not metabolized in cell
PET scan - metabolized further in cell

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26
Q

Largest and most Steroidogenic zone in adrenal Cortex

A

Zona fasciculata

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27
Q

Rate-limiting enzyme in Steroidogenesis

A

Cyp11A1

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28
Q

1st reaction in Steroidogenic pathway

A

Free cholesterol transported in inner mitochondria thru STAR protein, and converted into pregnenolone by CYP11A1

29
Q

Reaction 2 in modification of FC to cortisol

A

Pregnenolone to progesterone by 3B-HSD or

Pregnenolone to 17-OH-pregnenolone by CYP17 (hydroxylase func)

30
Q

Reaction 3 in modification of FC to cortisol

A

Progesterone to 17-OH-progesterone by cyp17(hydroxylase) or

17-OH-pregnenolone (^5) to 17-OH-progesterone(^4) by 3B-HSD

31
Q

Reaction 4 in modification of FC to cortisol

A

17-OH-progesterone to 11-deoxycortisol by CYP21B

32
Q

Reaction 5 in modification of FC to cortisol

A

11- deoxycortisol to cortisol by cyp11B1

33
Q

Reaction 4 in modification of FC to corticosterone

A

17-Oh-progesterone to 11-deoxycorticosterone by cyp21B

34
Q

Reaction5 in modification of FC to corticosterone

A

11-deoxycorticosterone to corticosterone by cyp11B1

35
Q

Mechanism of cortisol

A

Glucocorticoid receptor

36
Q

In the absence of cortisol, GR stays I. Cytoplasm bound to molecular chaperone such as

A

Heat-shock protein 90

Cyclophilin

37
Q

Regulation of cortisol production

A

Thru Hypothalmus-ant. Pituitary-adrenal axis

38
Q

ACTH binds to what receptor in zona fasciculata

A

Melanocortin-2 receptor

39
Q

Acute effect of ACTH

A
  1. Rapid transport of cholesterol to OMM
  2. Increase STAR protein gene expression
  3. Resulting to increase pregnenolone activity
40
Q

Chronic effect of ACTH

A
  1. Increase transportation of genes encoding Steroidogenic enzyme and coenzyme
  2. Increase LDL and HDL receptor
41
Q

Cortisol serves as negative feedback thru

A
  1. Inhibition of pomc gen expression at corticotropes.

2. Inhibition of pro-CRH gene expression at hypothalamus

42
Q

Metabolic action of cortisol in response to stress

A

Increase cortisol
Decrease insulin/glucagon ratio
Increase epi and norepi from sympathoadrenal output

43
Q

Metabolic action of chronically elevated cortisol in healthy individuals

A

Increase cortisol
Increase insulin/glucagon ratio
Decrease epi and norepi

44
Q

Zona reticularis begins to appear after birth at..

A

5 year old

45
Q

Adrenal androgens (DHEAS) appear in circulation at

A

6 year old

46
Q

Steroidogenic pathway in zona reticularis

A

Pregnenolone to 17-OH-pregnenolone (CYP17) to DHEA (CYP17 -lyase) to DHEAS (SULT2A1) or
DHEA to aldrostenedione (3B-HSD)

47
Q

DHEAS/DHEA: has high affinity binding to albumin

A

DHEAS

48
Q

DHEAS/DHEA: low affinity binding to protein

A

DHEA

49
Q

Zona glomerulosa is primarily regulated by

A

RAS
Extracellular K
ANP

50
Q

Zona glomerulosa is secondarily regulated by

A

ACTH

51
Q

Unique features of zona glomerulosa

A
  1. Absence of cyp17

2. Presence of cyp11b2 (aldosterone synthase)

52
Q

Steroidogenic pathways in zona glomerulosa

A

Pregnenolone to progesterone (3B-HSD) to 11-doc (cyp21b) to corticosterone to 18-OH-corticosterone to aldosterone (cyp11B2)

53
Q

Zona glomerulosa has low affinity binding to transport proteins

A

True

54
Q

Zona glomerulosa almost all inactivated by

A

Liver (conjugated to glucoronide)

55
Q

Mechanism of action of zona glomerulosa

A

Intracellular mineralocorticoid receptor

56
Q

Presence of this enzyme converts cortisol to cortisone (inactivates)

A

11B-HSD2

57
Q

Cortisone is converted back to cortisol in liver, skin and other tissues by

A

11B-HSD1

58
Q

Physiologic action of aldosterone in kidney

A

Increase NA reabsorption

Increase K and H secretion

59
Q

Results from continuous administration of aldosterone in 2-3days

A

Aldosterone escape

60
Q

Regulation of aldosterone secretion

A

RAAS

61
Q

Renin is produced by

A

Juxta glomerular cell

62
Q

Renin is release in response to

A

Low bp

Low Na delivery to macula densa

63
Q

Stimulators of aldosterone

A

Angiotensin II = increase STAR and cyp11b2 (potent vasoconstrictor)
Extracellular K
Acute elevated ACTH

64
Q

Inhibitors of aldosterone

A

ANP (directly inhibits aldosterone production / indirectly inhibits renin release)
Chronic elevated ACTH

65
Q

What happens when there is Hypervolemia

A

Hypervolemia means high Na level, this will inhibit the renin release which will lower aldosterone secretion resulting back to normovolemia

66
Q

Primary hyperaldosteronism

Usually due to aldosterone- secreting tumor

A

Conn’s syndrome

67
Q

Conn’s disease results in

A 
K depletion 
Na retention 
Ms weakness
Hypertension
Polyuria
68
Q

Increase ACTH due to any enzyme block decreasing cortisol synthesis.
May cause masculinization of female fetus or incomplete masculinization of male fetus

A

Congenital adrenal hyperplasia

69
Q

Congenital adrenal hyperplasia usually due to

A

Cyp21

Med Prep (52 decks)

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