L4 - adrenal cortex, glucocorticoids Flashcards

1
Q

what are adrenal cortx hormones

A

corticosteroids, androgens

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2
Q

what are adrenal cortx hormones

A

corticosteroids, androgens

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3
Q

types of corticosteroids

A

glucocorticoids, mineralcorticiouds

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4
Q

what are adrenal cortex hormones dervived from

A

cholostral, synthesised from acetyl CoA or taken from circulation

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5
Q

what enzymes used to synthesise corticosteroids

A

P450 cytochrome enzymes

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6
Q

three zona of adrenak cortex

A

glomerulusa, fasciculata and reticularis

- each zona produce diff hormones

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7
Q

what bond is important in the cholestral structure and why

A

C20-22, cos this bond will be metabolised into other metabolites and hormones

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8
Q

how to start any adrenal steriodogenesis from cholestral

A

cholestral taken up by mitochondria through StaR step

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9
Q

where is Star located in the mitochondria

A

its membrane

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10
Q

what happens to cholestral once it is in matrix

A

becomes pregnenolone

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11
Q

struture of star protein

A

has cholestral transfer protein

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12
Q

what molecules promotes and suppress star protein ( regulation of star )

A

ACTH, LH for promotion

Alcohol for supression

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13
Q

what enzymes catalsyses the conversion from cholestral to pregn

A

P450scc

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14
Q

reactions involving P450scc

A

scc in the name means side cleavge

  • first - 2 hydrolxylase reactions
  • second - cleavage of the bond
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15
Q

what does P450scc need for function

A

electrons from a donor molecule

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16
Q

what are the two proteins that work with P450scc in a complex

A

adrenodoxin reductase and adrenodoxin

17
Q

what molecule induces the gene expression in this P450scc complex

A

ACTH

18
Q

how many C in glucocorticoids (glucort)

A

21

19
Q

eg of glucort

A

cortisol and corticosterone (inactive form of cortisol)

20
Q

cortisol function

A

hormone for stress

21
Q

how is cortisol transported in the blood and why

A

cortisol is lilophilic so its hard for it to travel in blood effeciently
- 90% bound to plasma protein like transcortin and albumin

22
Q

pathway of producing cortisol and what axis is this

A

hypoth release releasing factor (CRH)> anteroir pituitary release ACTH> adrenal coretx > cortisol made
- HPA axis

23
Q

how to generate ACTH

A

cleaved from prohormone of POMC

24
Q

mechanism of action of glucort

A

as glucort receptors

25
Q

actions of glucort , -metabolism using carbohydrates

A
  • glucose level increases through gluneogenesis

- stops glucose entry in tissues

26
Q

actions of glucort , metabolsim of proteins

A

in muslces, protein broken down so muslce wastage

27
Q

action of glucorts in liver

A

increases AA uptake for protein synthesis and gluconeogenesis

28
Q

action of glucort, metabolsim of fat

A

FA mobilised for gluneogensis in adipose tissues

-redistribution of fat around face, abdominal area

29
Q

action of glucort in electro lyte balance

A

when there is large amount of glucort- there are mineralcort activity

30
Q

action of glucort in bones

A

decreases absorption of calcium and increaces excretion

31
Q

action of glucort in cns

A

mood

cognition

32
Q

action of glucort in IS

A

decreases levels of lymphocytes (weak IS) and increases neutrophils, RBC and platelets

33
Q

therapeutic action of glucort

A

reduces inflamm bu reducing leukocyte action

- reduced allergies by decreasing histamine synthesis

34
Q

what happens if there’s excess glucort

A

leads to cushings syndrome

  • makes a tumour in pituitary
  • adernal adenoma
  • ACTH prodcuted too much since it doesn’t respond to neg feedback
35
Q

treatment for cushings syndrome

A

surgery, radiotherapy, drugs (11 hydroxylase inhibitor - doesn’t make cortisol)

36
Q

primary and secondary disorder associated with decreased adrenal function

A

primary - autoimmune like addisons disease

-seco-pituitary disease so decreases ACTH

37
Q

symptoms of addisions disease

A

fatigue, weight loss, ion imbalance

38
Q

treatment in addison disease

A

cortisol replacement therapy