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I3 Exam 1 > Anti-inflammatory steroids - Ceryak > Flashcards

Anti-inflammatory steroids - Ceryak Flashcards

1
Q

Where are adrenal corticosteroids synthesized

A

adrenal cortex

  • cortisol
  • aldosterone
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2
Q

Are glucocorticoids inflammatory?

A

no they are anti-inflammatory

- cortisol

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3
Q

What do mineralocorticoids affect?

A

water, electrolyte balance

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4
Q

What is the largest zone of the adrenal cortex?

A

zona fasciulata

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5
Q

Which zone of the adrenal cortex is cortisol synthesized in

A

zona fascicolata

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6
Q

What stimulates cortisol synthesis

A

ACTH

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7
Q

Which zone is the aldosterone synthesized in?

A

zona glomerulosa

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8
Q

What stimulates aldosterone synthesis

A

angiotensin II and K+

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9
Q

What are the steps of HPA axis

A
  • stress stimulus
  • NT are released and activate the hypothalamus to release releasing hormones
  • releasing hormones act on the ant. pit.
  • ant. pit. releases ACTH
  • ACTH acts on the adrenal cortex
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10
Q

Where is ACTH released from

A

anterior pituitary

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11
Q

Where is CRH released

A

hypothalamic neurons

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12
Q

What are cortisol levels at 8 am

A

16 micrograms/100 ml

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13
Q

What are cortisol levels at 4 am?

A

4 micrograms/100 ml

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14
Q

What happens when ACTH binds to its receptor in the adrenal cortex

A

adenylyl cyclase is activated

- increased cAMP leads to increased PKA

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15
Q

What does PKA phosphorylate in the adrenal cortex?

A

phosphorylates cholesterol ester hydrolase (CEH) which increases its activity

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16
Q

What does cholesterol ester hydrolase (CEH) activation lead to

A

free cholesterol is formed to serve as a substrate for corticosteroid synthesis

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17
Q

What is cholesterol converted to to form cortisol

A

pregnelone

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18
Q

Where is cholesterol converted to pregnelone

A

mitochondria

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19
Q

What is the effect of ACTH on cholesterol?

A

ACTH frees up cholesterol as a substrate for corticosteroid synthesis

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20
Q

Where do glucocorticoids bind their receptor?

A

cytosol

- can freely pass the plasma membrane

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21
Q

What happens when glucocorticoids bind their receptor

A

the steroid-receptor dimerized complex is translocated into the nucleus

  • inside the nucleus it binds to a GRE on the regulatory portion of the gene
  • affect protein synthesis
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22
Q

Transrepression by glucocorticoid

A

directly interact with and alter the function of other transcription factors, such as NF-Kb in the nucleus of cells

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23
Q

What is a glucocorticoid response element

A

a specific nucleotide sequence that is recognized by the receptor complex

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24
Q

What is the effect of glucocorticoids on the liver

A

increased synthesis of glucose, glycogen deposition

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25
Q

What is the effect of glucocorticoids on skeletal muscles

A

increased protein breakdown and inhibit protein synthesis

26
Q

What is the effect of glucocorticoids on fatty acids

A

increased free fatty acids, permissive for lipolytic signals (epinephrine, growth hormone)

27
Q

What do you see at high levels of glucocorticoids

A

muscle wasting, redistribution of body fat (back of neck and face)

28
Q

What is the effect of glucocorticoids of on the CV system

A
  • hypertension with prolong high levels
29
Q

What is the effect of glucocorticoids on calcium homeostasis

A

decreased renal absorption, decreased Ca/ Mg/ PO4 absorption in the GI

30
Q

What is the effect of glucocorticoids on collagen and bone deposition

A

inhibit collagen synthesis and bone deposition = osteoporosis in adults
- slows bone growth in children

31
Q

What is the effect of glucocorticoids on CNS

A

modulate perception and mood and behavior

32
Q

What does aldosterone bind to

A

renal cortical collecting duct mineralocorticoid receptor

- translocates into the nucleus and binds to the GRE and functions as a transcription factor

33
Q

What does aldosterone do to the cell?

A

increased Na transporter on the lumen of the cell
- pump more Na+ into extracellular space
- uptake of potassium and export of sodium
= increase in H2) and volume = hypertension

34
Q

What do mineralocorticoid target tissues express

A

11-beta hydroxysteroid dehydrogenase type 2

- inactivates cortisol to cortisone to prevent excessive stimulation of the mineralocorticoid receptor

35
Q

Why can eating large amount of licorice lead to hypertesnion

A

cortisol can’t be deactivated

  • cortisol binding MR which leads to extracellular fluid volume
  • licorice inhibits enzyme so cortisol can act like aldosterone and induce hypertension
36
Q

What happens to the eNac and Na/k+ transporters with aldosterone?

A

both are upregulated

  • allowing more Na+ to be reabsorbed and more water
  • increases blood volume
37
Q

Do clinically used corticosteroid bind the same receptors?

A

yes

38
Q

What are glucocorticoids primarily used for

A

anti-inflammatory and immunosuppressive actions

39
Q

fludrocortisone

A

potent GC and MC activity

40
Q

What is dexamethasone used for

A

diagnose various causes of hypercorticism

41
Q

Where are corticosteroids metabolized and excreted?

A

liver metabolism and urine excretion

42
Q

Is dexamethasone more potent than hydrocortisone?

A

yes, 30x more potent in terms of anti-inflammatory

43
Q

Is fludrocortisone more potent than hydrocortisone?

A

yes 250x in the salt retaining properties

44
Q

Which drug is the mineralocorticoid of choice for mineralocorticoid replacement therapy

A

fludrocortisone

45
Q

What do pro-inflammatory cytokines act on in the HPA axis?

A

hypothalamus to induce CRH release

  • ant. pit. to release ACTH
  • circulating cortisol also has direct effects on immune suppression
46
Q

How do glucocorticoids decrease production of prostaglandin and leukotriene?

A

inhibition of phospholipase A2 and decreased synthesis of COX2

47
Q

Which proteins transcription is activated in the presence of glucocorticoids

A

anti-inflammatory proteins:
IL-10
annexin A1
IxB

48
Q

Which proteins are suppressed in the presence of glucocorticoids

A 
IL-1, IL-2, IL-6, IL-8
VEGF
COX-2
prostaglandins
TNF
IFN-gamma
49
Q

What happens to COX2 and TNF alpha in the presence of glucocorticoids

A

transcriptionally repressed

50
Q

What is the role of TNF

A

inflammation induction

- activates immune cell

51
Q

What happens with COX 2 in the presence of glucocorticoids

A
  • decreased COX 2

- decreased prostaglandin

52
Q

What happens to annexin A1 (lipocortin 1) production in the presence of glucocorticoids

A
  • decreasd lipocortin 1
    decreased arachidonic acid
  • decreased prostaglandin
53
Q

What does annexin A1 lipocortin inhibit

A

phospholipase A2

- AA can’t be cleaved so downstream mediators aren’t formed

54
Q

How can you tell if something wrong is coming from the HPA axis in the dexamethasone suppression test

A
  • ACTH and CRH production will be supressed
55
Q

How can you tell if something is an ectopic tumor that is producing ACTH in the dexamethasone suppression test

A
  • not going to be suppressed by dexamethasone
56
Q

At what time point do glucocorticoids start to have a negative effect

A

greater than 2 weeks

57
Q

What causes AE of glucocorticoids

A
  • cessation of therapy - abrupt withdrawal

- continued use for supraphysiological doses for inflammation (mimic Cushing syndrome)

58
Q

What can cause acute adrenal insufficiency

A

suppression of the HPA by prolonged therapy with high doses of glucocorticoids

59
Q

How to recover from taking glucocorticoids

A

slowly tapering the dose

60
Q

What are the drug induced Cushing’s syndrome symptoms

A

altered fat deposition, muscle weakness and atrophy, striae (protein in dermis is being degraded), bruising, acne

61
Q

What are the metabolic effects of Cushing’s

A

fluid/electrolyte imbalance

  • hypertesion
  • hyperglycemia due to increased gluconeongesis
  • growth suppression
  • osteoporosis
  • decreased wound healing
  • suppression of immune system

I3 Exam 1 (12 decks)

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