CE L3 Therapy rationale Flashcards

1
Q

Where are endogenous corticoids released from?

A

Adrenal cortex

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2
Q

Mineralocorticoids affect ……

A

water and electrolyte balance

via aldosterone

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3
Q

e.g. of glucocorticoids (2)

A

hydrocortisone and corticosterone

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4
Q

Glucocorticoids affect …….. (2)

A
  • Carbohydrate and protein metabolism

- Anti-inflammatory and immunosuppressive effects

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5
Q

Deficiency of corticoids results in ….

A

Addison’s disease

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6
Q

Excessive GC results in ….

A

Cushings syndrome

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7
Q

Excessive MC results in ….

A

Conns sydrome

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8
Q

Where is cortisol released from?

A

Adrenal glands

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9
Q

What causes increase in cortisol release? (2)

via what route?

A
Stress and proinflammatory cytokines
cause hypothalamus to release CRH
causes pituitary to release ACTH
causes adrenals to release cortisol
(-ve signalling back to pituitary and hypothalamus)
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10
Q

What does CRH stand for?

Where does it signal from/to?

A

Corticotropin releasing hormone

signals from pituitary to hypothalamus

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11
Q

What does ACTH stand for?

Where does it signal from/to?

A

Adrenocorticotropic hormone

signals from the pituitary to the adrenal glands

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12
Q

Corticoids act on early or late inflammatory response?

A

Both

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13
Q

Actions of corticoids (3)

A

decreased extravasation
inhibit cell activation
decreased production of inflammatory mediators

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14
Q

GC binds to receptors located where?

A

cytoplasmic receptors

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15
Q

GC-receptor complex goes to ….. and acts as….

A

nucleus

acts as a transcription factor

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16
Q

Transcription factor binds to …. to activate/repress genes?

A

reponse element

17
Q

GC may repress or activate genes?

A

Both

18
Q

GC can interact/inhibit binding of other transcription factors such as ….

A

AP1 and NFKB

19
Q

metabolic s/e

A

osteoporosis

diabetogenic + increased appetite

20
Q

mineralocorticoid s/e

A

oedema, CV events

due to Na/H20 retention

21
Q

GC s/e

A

immunosuppression - infections

supresses HPA axis through feedback

22
Q

The two proinflammatory cytokines involved in proliferation?

Which is also involved in apoptosis?

A

TNF and IL1

TNF also involved in apoptosis through activation of NFkB

23
Q

When are TNF and IL1 released inappropriately and what happens?

A

during inflammation

tissue destruction and organ damage

24
Q

What cells produce TNF and IL1

A

macrophages and monocytes

25
Q

How many forms of IL1 are there?

Where are they synthesised?

A

2 (alpha and beta)

In the microtubules

26
Q

Where is IL1 beta found

A

mostly circulating

27
Q

where is IL1 alpha found

A

cytosolic or membrane bound

28
Q

What enzyme is involved in IL1 synthesis

A
Caspase 1 (also known as IL1 converting enzyme)
(ICE inhibitors are anti inflammatory)
29
Q

the release of IL1 is facilitated by (2)

A

ATP and P2X7

30
Q

Effects of IL1

A

Fever
Synth of COX2 and iNOS
Increased expression of VCAM and RANKL
Bone erosion

31
Q

C5a increases …. RNA

A

IL1

32
Q

release of IL1 is increased in macrophages/monocytes that are stimulated by….

A

IFNg

33
Q

CD40L activates ……. in EC and SM cells

A

ICE

34
Q

IL receptors are part of which superfamily?

A

Ig

35
Q

Type I IL1 receptors are found on ………… cells

Type II IL1 receptors are found on …………. cells

A

most cells
B cells - decoy receptors
(both exist as soluble receptors)

36
Q

Type I IL1 receptors have a signalling domain similar to ……….. which leads to activation of ………….. (3)……….

A

Toll like receptors

Activation of IRAK, NFKb and AP1