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

Anti-inflammatory steroids - Ceryak Flashcards

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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
What is the effect of glucocorticoids on skeletal muscles
increased protein breakdown and inhibit protein synthesis
26
What is the effect of glucocorticoids on fatty acids
increased free fatty acids, permissive for lipolytic signals (epinephrine, growth hormone)
27
What do you see at high levels of glucocorticoids
muscle wasting, redistribution of body fat (back of neck and face)
28
What is the effect of glucocorticoids of on the CV system
- hypertension with prolong high levels
29
What is the effect of glucocorticoids on calcium homeostasis
decreased renal absorption, decreased Ca/ Mg/ PO4 absorption in the GI
30
What is the effect of glucocorticoids on collagen and bone deposition
inhibit collagen synthesis and bone deposition = osteoporosis in adults - slows bone growth in children
31
What is the effect of glucocorticoids on CNS
modulate perception and mood and behavior
32
What does aldosterone bind to
renal cortical collecting duct mineralocorticoid receptor | - translocates into the nucleus and binds to the GRE and functions as a transcription factor
33
What does aldosterone do to the cell?
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
What do mineralocorticoid target tissues express
11-beta hydroxysteroid dehydrogenase type 2 | - inactivates cortisol to cortisone to prevent excessive stimulation of the mineralocorticoid receptor
35
Why can eating large amount of licorice lead to hypertesnion
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
What happens to the eNac and Na/k+ transporters with aldosterone?
both are upregulated - allowing more Na+ to be reabsorbed and more water - increases blood volume
37
Do clinically used corticosteroid bind the same receptors?
yes
38
What are glucocorticoids primarily used for
anti-inflammatory and immunosuppressive actions
39
fludrocortisone
potent GC and MC activity
40
What is dexamethasone used for
diagnose various causes of hypercorticism
41
Where are corticosteroids metabolized and excreted?
liver metabolism and urine excretion
42
Is dexamethasone more potent than hydrocortisone?
yes, 30x more potent in terms of anti-inflammatory
43
Is fludrocortisone more potent than hydrocortisone?
yes 250x in the salt retaining properties
44
Which drug is the mineralocorticoid of choice for mineralocorticoid replacement therapy
fludrocortisone
45
What do pro-inflammatory cytokines act on in the HPA axis?
hypothalamus to induce CRH release - ant. pit. to release ACTH - circulating cortisol also has direct effects on immune suppression
46
How do glucocorticoids decrease production of prostaglandin and leukotriene?
inhibition of phospholipase A2 and decreased synthesis of COX2
47
Which proteins transcription is activated in the presence of glucocorticoids
anti-inflammatory proteins: IL-10 annexin A1 IxB
48
Which proteins are suppressed in the presence of glucocorticoids
``` IL-1, IL-2, IL-6, IL-8 VEGF COX-2 prostaglandins TNF IFN-gamma ```
49
What happens to COX2 and TNF alpha in the presence of glucocorticoids
transcriptionally repressed
50
What is the role of TNF
inflammation induction | - activates immune cell
51
What happens with COX 2 in the presence of glucocorticoids
- decreased COX 2 | - decreased prostaglandin
52
What happens to annexin A1 (lipocortin 1) production in the presence of glucocorticoids
- decreasd lipocortin 1 decreased arachidonic acid - decreased prostaglandin
53
What does annexin A1 lipocortin inhibit
phospholipase A2 | - AA can't be cleaved so downstream mediators aren't formed
54
How can you tell if something wrong is coming from the HPA axis in the dexamethasone suppression test
- ACTH and CRH production will be supressed
55
How can you tell if something is an ectopic tumor that is producing ACTH in the dexamethasone suppression test
- not going to be suppressed by dexamethasone
56
At what time point do glucocorticoids start to have a negative effect
greater than 2 weeks
57
What causes AE of glucocorticoids
- cessation of therapy - abrupt withdrawal | - continued use for supraphysiological doses for inflammation (mimic Cushing syndrome)
58
What can cause acute adrenal insufficiency
suppression of the HPA by prolonged therapy with high doses of glucocorticoids
59
How to recover from taking glucocorticoids
slowly tapering the dose
60
What are the drug induced Cushing's syndrome symptoms
altered fat deposition, muscle weakness and atrophy, striae (protein in dermis is being degraded), bruising, acne
61
What are the metabolic effects of Cushing's
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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