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pharmacology 2 > glucocorticoids > Flashcards

glucocorticoids Flashcards

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1
Q

corticotrophins make

A

ACTH

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2
Q

lactotrophs make

A

prolactin PRL

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3
Q

somatotropin make

A

GH

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4
Q

tyrotrophs make

A

TSH

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5
Q

gonadotrophhs make

A

FSH/LH

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6
Q

HPA axis

A

regulates synthesis and secretion of adrenal corticosteroids
hypothalamus releases CRF in a pulsatile manner
CRF acts on corticotrophins in the anterior lobe pituitary making it release ACTH
ACTH
- acts on adrenal glands to stimulate glucocorticoids
- has a trophic effects on the adrenal cortex (atrophy of the adrenal cortex without sufficient ACTH)
- negative feedback effect on the hypothalamus

glucocorticoids have a negative feedback loop to the HT and downstream effects on the body

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7
Q

3 effects of ACTH

A
  • acts on adrenal glands to stimulate glucocorticoids
  • has a trophic effects on the adrenal cortex (atrophy of the adrenal cortex without sufficient ACTH)
  • negative feedback effect on the hypothalamus
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8
Q

THE HPA axis is responsible for

A

regulating synthesis and secretion og adrenal corticosteroids

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9
Q

what does the hypothalamus do in the HPA axis

A

releases CRF in a pulsatile manner

CRF stimulated anterior lobe pituitary to produce ACTH

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10
Q

3 zones adrenal cortex

A
  1. zona glomerulosa
  2. zona fasciculata
  3. zona reticularis
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11
Q

zona glomerulosa makes

A

mineralocorticoids

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12
Q

zona fascicula makes

A

glucocorticoids

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13
Q

zona reticularis makes

A

sex hormones

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14
Q

glucocorticoids

A

cortisol/hydrocortisone - main ones
corticosterone
secreted in a circadian/diural rhythm - peak at 9am and troph at midnight

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15
Q

mineralocorticoids

A

aldosterone

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16
Q

adrenal steroidogenesis

A

synthesised from cholesterol
side chain cleavage (this is the rate limiting step)
AACTH (GC) and angiotensin 2 (MC) positively regulate conversion of cholesterol to pregnenolone
cortex zone - expression of spefici steroidogenic enzymes, required for synthesis of aldosterone of GCs or sex hormones

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16
Q

adrenal steroidogenesis

A

synthesised from cholesterol
side chain cleavage (this is the rate limiting step)
AACTH (GC) and angiotensin 2 (MC) positively regulate conversion of cholesterol to pregnenolone
cortex zone - expression of spefici steroidogenic enzymes, required for synthesis of aldosterone of GCs or sex hormones

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17
Q

cortex zone -

A

cortex zone - expression of spefici steroidogenic enzymes, required for synthesis of aldosterone of GCs or sex hormones

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18
Q

ACTH and angiotensin 2

A

increase conversion of cholesterol to pregnenolone

increases side chain cleavage

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19
Q

aminoglutethimide

A

reduced side chain cleavage

stops production of steroids

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20
Q

aaldosterone synthesis is increased by

A

angiotensin 2

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21
Q

metabolic effects of glucocorticoids

A
  • CHO metabolism
  • protein catabolism
  • adipose tissue distribution

antiinflammatory/immunosuppressive effects endogenously

resistance to stress

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22
Q

metabolic effects of mineralocorticoids

A

water and electrolyte homeostasis

  • Na retention
  • H2O retention
  • K excretion
  • H excretion

all in order to maintain blood pressure

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23
Q

glucocorticoids are bound to

A

cortisol binding globulins CBG
when they reach the plasma membrane they can cross without needing a receptor
glucocorticoid receptor is in the cytoplasm (not the plasma membrane) (GR) binds hydrocortisone and dimerises and translocates to the nucleus
binds GREs (glucocorticoid response elements) to alter transcription of target genes

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24
glucocorticoid receptor
ligand activated transcription factor | ligand is hydrocortisol
24
glucocorticoid receptor
ligand activated transcription factor | ligand is hydrocortisone
25
when glucocorticoid receptor Is bound
it dimerises and binds glucocorticoid response elements which alter transcription of target genes
26
glucocorticoids receptor is located in
the cytoplasm, not plasma membrane
27
transcriptional activation by glucocorticoid receptor
most glucocorticoid metabolic effects represses pro inflammatory genes transcriptional tethering - tether partner transcription factors to alter gene transcription
28
GR and MR
highly homologous receptors aldosterone is specific for MR does not activate GR) cortisol binds both, binds MR with equal affinity as aldosterone cortisol circulates at much higher levels than aldosterone
29
why do MR expressing tissues response to aldosterone and not cortisol
because they express 11beta hydroxysteroid dehydrogenase converts cortisol to cortisone cortisone is inactive and doesn't activate MR
29
why do MR expressing tissues response to aldosterone and not cortisol
because they express 11beta hydroxysteroid dehydrogenase converts cortisol to cortisone cortisone is inactive and doesn't activate MR
30
Addison's disease
primary adrenal insufficiency usually autoimmune in origin in western societies causing bilateral destruction of the adrenal cortex in third world countries it is more likely to be infection (mostly TB) diagnosis effects mineralocorticoid producing, glucocorticoids producing and sex hormone producing layers (all three layers)
31
clinical presentation of Addisons disease
- fatigue and weakness nausea and vomiting, diarrhoea, salt craving hypoglycaemia and low blood pressure hyperpigmentation due to increase ACTH - GC deficiency affects CHO metabolism causing decrease in glucose (hypoglycaemia) - MC deficiency affects blood pressure, low blood pressure, hyponatraemic, hyperkalaemic - impaired stress tolerance (addisonian/adrenal crisis)
32
secondary deficiency of corticosteroids causes
- usually exogenous steroid use - HPA axis suppression due to low ACTH - hypopituitarism - postpartum pituitary necrosis - Sheehan's syndrome
32
deficiencies in Addison's disease
GC deficiency affects CHO metabolism causing decrease in glucose (hypoglycaemia) - MC deficiency affects blood pressure, low blood pressure, hyponatraemic, hyperkalaemic - addisonian/adrenal crisis (impaired stress tolerance)
33
secondary deficiency of corticosteroids
MC secretion is preserved Na/K balance is normal ACTH levels are low/normal - no hyperpigmentation rapid ACTH test will differentiate from primary disease
34
adrenal crisis in 1st and 2nd degree
endocrine emergency precipitated by any stress that increases adrenal demands treated with IV/IM hydrocortisone/cortisol
35
glucocorticoid excess causes
Cushing's syndrome, which can be caused by - cuchings disease increase in ACTH produced by a corticotrophin adenoma in the pituitary - increase in ACTH from ectopic source - increase in GCs from adrenal adenoma/carcinoma - increase in GCs from prescribed GCs = iatrogenic
36
effects of glucocorticoids
CHO metabolism - hyperglycaemia, T2DM protein - catabolism, protein breakdown, thin skin, purple stretch marks, fragile blood vessels causing bruising, fractures from osteoporosis, fat - redistribution, face, back and abdomen anti inflammatory/immunosuppression - infections CNS - mood changes, cognitive impairment, psychosis
37
common signs of sucking's syndrome
catabolic - thin skin and striae, bruising, muscle wasting (thin arms and legs) fat redistribution - moon faces, buffalo hump, abdomen
38
clinical uses of GCs and MCs as replacement therapies
physiological doses - replacement therapy adrenocortical insufficiency - IV replacement in ED once stabilised, replaced with physiological levels hydrocortisone to replicate diurnal rhythm (double dose in the morning) fludrocortisone once daily (synthetic MC) in cases of stress - surgery, infection, major trauma - double hydrocortisone dose
39
clinical uses of GC as anti-inflammatory
supra physiological doses - GCs only
40
anti inflammatory action of GC
inhibit inflammation - early during - heat, pain and swelling - late - during wound healing and repair target all types of inflammation - infections, chemical stimuli, physical stimuli - inappropriate immune responses - hypersensitivity and autoimmune disease prophylactically used to prevent allograft rejection neoplasia - combination chemotherapy and cerebral oedema
41
effects of GCs
- anti inflammatory/immunosupressive | - metabolic effects - CHO metabolism, protein catabolism, adipose tissue distribution
42
to isolate anti inflammatory effects of GCs
keep anti inflammatory effects but avoid metabolic effects some synthetic corticosteroids have increased effect on GR and reduced effect on MR some last longer bioavailability altered to they can be topically administered cannot completely seperate anti inflammatory from metabolic effects
43
hydrocortisone
equally effective on GC more effective on MC but inactivated short half life, short duration of action
44
prednisolone
oral glucocorticoid in wide use clinically 4x more potent than hydrocortisone lower affinity for MC intermediate half life
45
triamcinolone
topical relative GC receptor potency 5x as potent doesn't activate MC receptor intermediate half life
46
dexamethosone
far more potent on GC receptor doesn't activate MC long half life
47
fludrocortisone
most potent on MC | intermediate half life
48
pharmacokinetics of GC
oral, IM, IV, inhaled, topical, intra-articular, rectal where possible use locally due to side effects good oral availability
49
GC injectables
succinate/PO4 esters rapidly absorbed Solu-medrone validate/acetate esters slowly absorbed Depo-medrone topical/local - huge variety but all have systemic effects
50
distribution, metabolism and excretion of GCs
lipid soluble - need to be carried by a carrier protein (some albumin) rapidly distributed to cells through blood stream plasma half life is short, biological half is long sulphated and glucuronated in the liver and excreted into the bile and urine
51
iatrogenic Cushing's syndrome
common side effect of systemic GCs universal with high dose, long term GC use patients looks cushingoid
52
if children are given GC
growth suppression if >6 months
53
suppression of HPA axis in GC use
adrenal atrophy may occur abrupt withdrawal causes addisionian crisis must slowly withdraw high dose steroids
54
minimising risk of GC use
- use GC sparing agents - Lowest effectje dose for the shortest time time dose effectively - give in the morning - alternative days with double dose
55
steroid card/bracelet
all patients on steroids should be wearing a bracelet carrying steroid card
56
topical GC
vast range available | applicable for psoriasis, excess, dermatitis, allergic conjunctivitis
57
inhaled GC
used for asthma and allergic rhinitis | metered dose inhalers e.g. fluticasone
58
intra-lesional GC
long acting depot injection | intra/peri articular in RA for bursitis, tenditis etc
59
rectal GC
hydrocortisone ointment/suppositories, prednisolone enema/suppositories inflammatory bowel disease (UC, chrons)
60
GC with vaccines and attenuated live virus immunisation interaction
failure to develop immunity | systemic infection for live virus vaccines
61
insulin and oral hypoglycaemia agents with GC interaction
hyperglycaemia
62
antacids and GC interaction
Impaired GC absorption
63
carbamazepine, phenytoin, barbiturates with GC interaction
GC metabolism induction may occur | dose may need to be increased
64
digoxin and GC interaction
can cause arrhythmias if there is hypokalaemia

pharmacology 2 (19 decks)

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