Anti-inflammatories (year 2) Flashcards

1
Q

name the drugs that can be used as anti-inflammtories

A
NSAIDs
glucocorticoids
anticytokines
immunosuppressants
antihistamine
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2
Q

what is the mode of action of NSAIDs?

A

inhibit COX enzyme

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3
Q

what does the COX enzyme do?

A

forms prostanoids from arachidonic acid

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4
Q

what does the prostanoid group contain?

A

prostaglandins and thromboxanes

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5
Q

what three effects do NSAIDs have?

A

anti-inflammatory
analgesic
antipyretic

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6
Q

what prostaglandin do NSAIDs reduce that reduces inflammation?

A

prostaglandin E2 and prostacyclin

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7
Q

what does a decrease in prostaglandin E2 and prostacyclin causes?

A

reduced vasodilation and oedema

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8
Q

how does a decrease in prostaglandins result in analgesia?

A

decrease in sensitisation of nociceptive nerve endings to inflammatory mediators

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9
Q

why do NSAIDs have a lot of adverse effects?

A

prostaglandins are important in normal homeostatic function

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10
Q

what are some of the normal functions prostaglandins?

A

gastric protection - mucus production and proton pump inhibitor
platelet aggregation
renal blood flow autoregulation

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11
Q

which of the COX enzymes is a constitutive enzyme and which is an induced enzyme?

A

constitutive - 1

induced - 2

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12
Q

what is a constitutive enzyme?

A

one found in most tissues with a role in homeostasis

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13
Q

which COX is mainly responsible for the mediators of inflammation?

A

COX-2

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14
Q

inhibition of which COX enzyme are most of the side effects of NSAIDs due to?

A

1

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15
Q

describe the absorption of NSAIDs

A

weak acids that are readily absorbed from the GI tract

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16
Q

how are NSAIDs transported in blood?

A

bound to albumin

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17
Q

why is the fact NSAIDs are distributed bound to albumin important?

A

changes in protein alters the transport and efficacy of the drug
if given with another drug that is bound to albumin then they compete

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18
Q

how are NSAIDs eliminated from the body?

A

hepatic phase I and II metabolism

excreted in urine/faeces

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19
Q

what species should NSAIDs be given sparingly and why?

A

cats - insufficient cytochrome P450 and glucoronidation conjugation

20
Q

what species should you not give paracetamol?

A

cats

21
Q

when might NSAIDs be used?

A

infectious disease
pain
osteoarthritis

22
Q

what is the main side effects of reduced prostaglandins?

A

GI ulceration and erosion leading to gastric bleeding

23
Q

other than GI ulceration what are other side effects of NSAIDs?

A

vomiting, diarrhoea, renal toxicity, hepatotoxicity, CNS depression, circulatory disturbance

24
Q

when should NSAIDs not be used?

A

with other NSAIDs or glucocorticoids
pregnancy
with renal, liver or cardiac impairment

25
Q

what are some examples of NSAIDs?

A

phenylbutazone, meloxicam, firocoxib, paracetamol, aspirin,

26
Q

what are the advantages of phenylbutazone?

A

long duration of action (intense protein binding)

cheap

27
Q

what animals is phenylbutazone not licensed in?

A

food producing animals

28
Q

what is the therapeutic use of meloxicam?

A

acute/chronic pain and inflammation

29
Q

which COX enzyme does meloxicam preferentially bind to?

A

2 - meaning less side effects

30
Q

where does paracetamol act in the body?

A

specific effect in CNS so has poor local inflammatory action - don’t get peripheral adverse effects

31
Q

what animals is paracetamol licensed in?

A

pigs and dogs

32
Q

where is paracetamol metabolised?

A

liver - highly toxic to cats

33
Q

which COX enzyme does aspirin inhibit?

A

1 - significant side effects

34
Q

aspirin inhibits platelet aggregation, what does this mean it can be used as?

A

an anti clotting agent

35
Q

what effects do glucocorticoids have on neutrophils?

A

reduce extravasation and activation

36
Q

what effects do glucocorticoids have on fibroblasts?

A

reduce the function so reduce collagen production and hence reduce wound healing

37
Q

what chemical mediators do glucocorticoids reduce the production of?

A

prostanoids, cytokines, IgG, complement components, nitric oxide

38
Q

what chemical mediators do glucocorticoids increase the synthesis of?

A

anti-inflammatory mediators such as IL1

39
Q

what do large doses of glucocorticoids for extended periods of time cause?

A

iatrogenic cushings

40
Q

what are the adverse effects of glucocorticoids?

A

GI ulceration, decrease wound healing, myopathy, osteoporosis, oedema, thrombosis, abortion, diabetes, laminitis

41
Q

what are cytokines?

A

soluble protein or polypeptides released from a cell

42
Q

cytokines are important in the control of what system?

A

immune

43
Q

what are the 4 main classes of cytokines?

A

chemokine
interferons
interleukins
colony stimulating factors

44
Q

what is colchicine?

A

an anti fibrotic drug

45
Q

what is colchicine used for?

A

treat liver fibrosis