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Patient > Adrenal glands and Corticosteroids as drug targets > Flashcards

Adrenal glands and Corticosteroids as drug targets Flashcards

1
Q

what is cortisol?

A

a glucocorticoid

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2
Q

effect of cortisol?

A

raises blood sugar, protein/ fat metabolism

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3
Q

what is aldosterone?

A

mineralocorticoid

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4
Q

effect of aldosterone?

A

increases serum Na, raises BP

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5
Q

what are the effects of androgen precursors?

A

maturation and development

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6
Q

where are the adrenal glands?

A

sit on top of the kidneys

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7
Q

what happens if you lose an adrenal gland?

A

if you lose one the other ups its game

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8
Q

3 parts of the adrenal gland? and functions?

A

outer capsule- where the blood vessels land and deviate
adrenal cortex- produces steroids
adrenal medulla- cathecholamine prosecution

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9
Q

is the adrenal cortex electrically active?

A

no

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10
Q

is the adrenal medulla electrically active?

A

yes

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11
Q

3 regions of the adrenal cortex?

A

zona glomrulosa- closest to the capsule
zona fasiculata
zona reticularis

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12
Q

which zones produce the corticosteroids?

A

zona glomerulosa- aldosteron

zona fasiculata- cortisol

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13
Q

what does the zone reticularis produce?

A

produces adrenal androgens

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14
Q

what are adrenal androgens the primary precursors for?

A

testosterone

oestrogen

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15
Q

in steridogenesis within the adrenal cortex, are the steroids synthesised and stored?

A

no, synthesised on demand from cholesterol

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16
Q

what is the rate limiting step of sterroidogenesis?

A

cholesterol–> pregnenolone

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17
Q

what is the basic steroid backbone?

A

17 carbon resides

4 ring

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18
Q

what stimulates the conversion of cholesterol to pregnenolone?

A

ACTH stimulates the induction of pregnenolone synthase

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19
Q

physiological actions of adrenal steroids: glucocorticoids?

A

metabolic effects- glucose like effects
anti-inflammatory
immunosuppressive

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20
Q

physiological actions of adrenal steroids:

mineralcorticoids

A

water and electrolyte balance- associated with Na conservation and raising of extracellular volume to fight low BP

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21
Q

physiological actions of adrenal steroids:

adrenal androgens

A

maturation and development- key precursors for oestrogen and testosterone

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22
Q

what is transcortin?

A

corticosteroid binding globulin

binds 90% of cortisol and 60% of aldosterone

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23
Q

does transporting bind synthetic steroids?

A

no

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24
Q

what does albumin bind?

A

synthetic and natural steroids

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25
Q

what are the actions of steroids?

A

changes in transcription and translation

altering the synthesis of specific proteins

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26
Q

why can this alteration of proteins by steroids take a while?

A

have to change protein turnover and get into the DNA- roughly 20-30 minutes

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27
Q

can aldosterone have quick effects on protein synthesis? why?

A

yes due to receptors on the cell surface

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28
Q

explain to steps to cortisol release when you get an emotional response?

A

emotional response (stress/ excitement etc) activates the hypothalamus
hypothalamus releases CRH which stimulates the release of ACTH from the pituitary
this then enters the circulation and reaches the adrenal cortex where it stimulates pregnenolone synthase
the synthesis of cortisol then begins.

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29
Q

does cortisol release from an emotional response experience negative feedback?

A

yes- switches of ACTH production and CRH production

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30
Q

effects of cortisol in an emotional response?

A 
Promoting lipolysis 
Promoting gluconeogenesis 
Protein catabolism 
Sensitizing blood vessels 
Reducing inflammation
31
Q

do mineralcorticoid have wide tissue distribution?

A

no- limited

32
Q

effect of mineral corticoids?

A

causes NA uptake, leading to fluid resorption and K loss

33
Q

what can act as a competitive inhibitor of mineralocorticoid receptors

A

spironolactone

34
Q

what does spironolactone treat?

A

hypertension

diuretic

35
Q

what happens when aldosterone is released?

A

it increases BP by increasing salt retention
when bp falls, renin converts angiotensin 1——> antiotension 2
a2 causes constriction and raises BP

36
Q

what does Angiotensin 2 cause?

A

vasoconstriction and raises BP

37
Q

short acting synthetic steroids?

A

hydrocortisone

fludrocortisone

38
Q

how long is the half life of hydrocortisone and fludrocortisone?

A

short acting

t1/2 is 8-12 hours

39
Q

intermediate acting synthetic steroids examples?

A

prednisolone

40
Q

how long is the half life of prednisolone?

A

12-36 hours

intermediate

41
Q

long acting synthetic steroids examples?

A

dexamethasone and betamethasone

42
Q

how long is the half life of dexamethasone and betamethasone

A

36-72 hours

long acting

43
Q

what does chemical modification of steroids influence?

A

the selectivity

44
Q

examples of steroids which have GC and MC activity?

A

prednisolone

45
Q

examples of steroids with pure GC activity?

A

dexamethasone, betamethasone, beclomethasone

46
Q

examples of steroids with pure MC?

A

fludrocortisone

47
Q

TF: it is easy to remove the anti-inflammatory responses in synthetic steroids?

A

false

48
Q

THERE IS AN IMPORTANT STRUCTURE OF STEROID AND THEIR ACTIVITY IN THIS LECTURE YOU NEED TO LEARN!

A

LEARN

49
Q

what is an example of a hypo function of steroids?

A

Addisons disease

50
Q

what is the Addisons mnemonic?

A 
A: appetite loss and weight loss
D: discolouration of the skin 
D: Dehydration 
I: increased thirst 
S: salt, soy sauce and liquorice cravings 
O: oligomenorrhoea: irregular periods 
N: no energy 
S: sore muscles
51
Q

what is the adrenal crisis in Addisons disease?

A

profound fatigue
dehydration
vascular collapse
renal shutdown

52
Q

Addisons: adrenal crisis:
_____ serum NA
_____ serum K

A

decreased

increased

53
Q

treatment of addisons?

A

hydrocortison (GC) with or without fludrocortisone (MC)

54
Q

why does the treatment of Addisons by hydrocortison with or without fludrocortisone have limited side effects?

A

mimics natural plasma levels

55
Q

what is an example of hyper function?

A

congenital adrenal hyperplasia- overproduction

56
Q

what happens in untreated congenital adrenal hyperplasia?

A

androgens are over produced and the other hormones aren’t as there’s no cortisol made, they cant switch off as cortisol is what causes negative feedback.
there is a drive from the CRH and ACTH but no switching off by cortisol

57
Q

what is treatment for congential adrenal hyperplasia?

A

exogenous cortisol

58
Q

how does exogenous cortisol treat CAH?

A

replaces lost cortisol that’s not made

brings back endocrine/ physiological control by switching negative feedback on

59
Q

why can steroids be used as an anti-inflammative/ immunosuppressant?

A

reduce mediators of inflammation and immune responses including:
cytokines, PGs, NO, IgG

60
Q

applications for steroids when used for their anti-inflammative/ immunosuppressant effect?

A 
asthma
eczema 
arthiritis 
psoriasis 
allergies 
itching
61
Q

steroid agents used for anti-inflammative/ immunosuppressant

A

hydrocortisone, prednisolone, beclomethasone, dexamethasone, budesonide, etc

62
Q

what are the inappropriate metabolic influences of excessive glucocorticoid administration/ use?

A

drug induced Cushing syndrome

oesteoperosis

63
Q

do you get an increased risk of infection with GC?

A

yes- powerful anti-inflams

64
Q

side effects of inhaled GCs?

A

thrush- growth of opportunistic Candida albicans

65
Q

how can thrush be reduced when using inhaled GCs?

A

using spacer of rinsing the mouth after use

66
Q

symptoms of Cushing syndrome?

A 
increased abdominal and face fat 
lipolysis 
red round moon face 
hypertension/ glycaemia 
vertigo 
blurry vision
acne 
female balding 
water retention 
menstural irregulatities 
thin skin 
poor wound healing 
osteoporosis 
muscle wasting 
purple striae 
depression
67
Q

what is a treatment of hyper function of steroids?

A

inhibition of steroid synthesis:
aminoglutethimide
selective inhibition: metyrapone

68
Q

mechanism of action of aminoglutethimide?

A

inhibits enzymes in the pathway

reduces steroidal output from adrenal cortex

69
Q

aminoglutethimide is used to treat?

A

Cushings- hyper activation disorder
postmenopausal breast cancer
prostate cancer

70
Q

metyrapone mechanism of action?

A

selective inhibitor
inhibits 11b-hydroxylase
reduces GC and MC synthesis

71
Q

what does metyrapone treat?

A

bushings

hyperaldosteronism

72
Q

side effects pf metyrapone?

A

hirsutism in women due to excessive androgens

73
Q

how can metyrapone test anterior pituitary function?

A

decreased GC will also decrease negative feedback drive and increase levels of ACTH

IF YOU MEASURE THE acth levels whilst giving this drug you can see if an individual has an issue with the pituitary gland

if you fail to get the negative feedback mechanism it would indicate there’s tumour in the pituitary

74
Q

how can tetracosatide/ synacthen be used to test for adrenal insufficiency?

A

they are ACTH mimetic

stimulates synthesis and release of adrenal hormones

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