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m2 > corticosteroids > Flashcards

corticosteroids Flashcards

1
Q

what are corticosteroids used as a treatment for?

A

treatments for inflammatory and autoimmune diseases

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2
Q

what drug mimics cortisol?

A

synthetic prednisone

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3
Q

at what time of day are our cortisol levels highest?

A

morning

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4
Q

what does too high/too low levels of cortisol cause?

A

immune activity to go down

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5
Q

what processes does cortisol play a role in?

A 
o	Fluid loss – ADH
o	Infection – immune reaction
o	Tissue damage – inflammation
o	Metabolic disturbance – insulin
o	Neural disturbance – neurochemical
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6
Q

what are the main side effects of corticosteroids?

A
  • Glycosuria
  • Hypertension
  • Glaucoma
  • Osteoperosis
  • Juvenile growth retardation
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7
Q

what are other side effects of corticosteroids?

A

oedema, weight gain, myopathy, hyperlipidaemia, thrombosis, GI bleeding, peptic ulcers, pancreatitis etc

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8
Q

what is cushings syndrome?

A

excess cortisol in the body

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9
Q

what are the main effects of cushings syndrome?

A

upper body obesity with thin arms and legs; red, round face; high blood sugar; high blood pressure; vertigo; blurry vision; acne; female balding; water retention etc

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10
Q

what does a lack of cortisol in the body cause?

A

Addisons disease

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11
Q

what 2 main cells are involved in osteoperosis?

A

osteoclasts

osteoblasts

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12
Q

what effect do corticosteroids have on osteoblasts and osteoclasts?

A

Corticosteroids decrease osteoblast function and increase osteoclast function

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13
Q

what causes avascular necrosis?

A

Due to loss of blood vessels going to that part of the bone

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14
Q

what organs and metabolic pathways do glucocorticoids have an effect on?

A 
immune system
cardiovasculatue
carbohydrate metabolism
kidney
skeletal system
CNS
lipid metabolism
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15
Q

where is the human glucocorticoid receptor?

A

found in the cytoplasm and nucleus of most body cells

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16
Q

what are the two main forms of the glucocorticoid receptor?

A

o Alpha – binds steroid (777aa)

o Beta – doesn’t bind steroid (742aa)

17
Q

what type of receptor is the glucocorticoid receptor?

A

dominant negative repressor

18
Q

how and why does high levels of GCR affect the steroid action?

A

When there’s lots of the beta form of the receptor it blocks the potential sites of binding DNA so it’s harder for the steroids to have their effect

19
Q

what form of the GCR is high in steroid resistant rheumatoid arthritis?

A

B form

20
Q

what are the 2 activities of GCR activities?

A

genomic

non-genomic

21
Q

what are the genomic actions of GCR?

A

o Transactivation of gene transcription by direct interaction with DNA
o Transrepression by interaction with other proteins in cytoplasm or nucleus

22
Q

what are the non-genomic actions of GCR?

A

o Interaction of GC with cytoplasmic GR
o Interaction of GC with plasma membrane GR
o Interaction of GC with membranes

23
Q

explain the mechanism of glucocorticoid action

A
  • Steroid is lipophilic – can get through plasma membranes
  • Binds with the glucocorticoid receptor
  • Goes to the nucleus and bind DNA to have their effects
  • Transactivational effects are what cause the side effects
24
Q

explain the normal action of TNF-a

A
  • TNF-a activates cells - pro-inflammatory molecule
  • TNF binds to its receptor - activates transcription factors NFkB, STTA, CREB and AP1
  • This complex moves to the nucleus - has pro-inflammatory effects here
25
Q

explain the GR trans-repressive action

A

if you have corticosteroids, they bind to receptor/transcription factor complex
• Heat shock proteins dissociates
• Receptor dimerises and cross-couples with transcription factors like NFkB
• NFkB can’t have its proper effect on transcription of genes  wipes out transcriptional effects of TNFa

26
Q

what are the 3 main non-genomic effects of glucocorticoid?

A

membrane GR
cytosolic GR signalling
intercalation in membrane

27
Q

why do we need membrane GR?

A

to sample medium around the cell and signal to the inside of the cell when steroid is coming

28
Q

what is the effect of glucocorticoid being intercalated in membranes? how can this be used clinically?

A

Steroid can link in with the membrane cholesterol and make the membrane more sticky and less fluid so membrane receptors can’t interact – cell function drops off.
o Useful in traumatic brain injury to protect the brain

m2 (24 decks)

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