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B4W3 > PHARMACOLOGY OF ANTI-INFLAMMATORIES AND IMMUNE SUPPRESSION > Flashcards

PHARMACOLOGY OF ANTI-INFLAMMATORIES AND IMMUNE SUPPRESSION Flashcards

1
Q

what is acute inflammation?

A

an acute response to an irritant that occurs quickly but is resolved

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2
Q

what is chronic inflammation?

A

an illness persisting for a long time or constantly recurring

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3
Q

what is a metabolite?

A

a substance essential to the metabolism of a particular organism or metabolic process

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4
Q

what are the 6 stages of acute inflammation?

A

increased blood flow, accumulation of tissue fluid, migration of leukocytes, increased core temperature, pain and suppuration

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5
Q

how is blood flow increased in inflammation? why?

A

serotonin and histamine are released from damaged cells which causes arterioles supplying the damaged area and capillaries to dilate
it provides more oxygen and nutrients for the increased cellular activity

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6
Q

how is tissue fluid formation increased in acute inflammation?

A

increased capillary permeability and elevated bp due to increased blood flow. also the leaky capillary walls mean plasma proteins can escape into tissues and increase the osmotic pressure of tissue fluid which draws more fluid out of the blood

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7
Q

how can tissue oedema be harmful and beneficial?

A

harmful- swelling around respiratory passages

beneficial- swelling around inflamed joints limits movement which encourages healing

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8
Q

describe the migration of neutrophils in acute inflammation?

A

loss of fluid from the blood thickens it, slowing blood flow and allowing the WBCs to adhere to the vessel wall. they then squeeze between endothelial cells and enter tissues via diapedesis.

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9
Q

what are the benefits of increased temperature in acute inflammation?`

A

inhibits growth and division of microbes and promotes the activity of phagocytes.

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10
Q

why does body temperature rise in acute inflammation?

A

when interleukin is released from macrophages and granulocytes in response to microbial toxins or immune compexes

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11
Q

why does pain sometimes arise in acute inflammation? why is it useful?

A

when local swellings compress sensory nerve endings

it encourages protection of the damaged site so can indirectly promote healing

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12
Q

what is suppuration?

A

the formation of pus which is dead phagocytes, dead cells, fibrin, inflammatory exudate, living and dead microbes

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13
Q

what is an abscess?

A

a localised collection of pus in tissues

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14
Q

when do we see the development of chronic inflammation?

A

when acute inflammation does not result in resolution because the area infected is not readily accessible to body defences.

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15
Q

how is chronic inflammation different to acute inflammation?

A

chronic has similar processes but they last a longer time, there is more tissue damage, the main inflammatory cells are lymphocytes, fibroblasts are activated to lead to fibrosis, granulomas may form

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16
Q

what are granulomas?

A

small areas of inflammation with collections of defensive cells

17
Q

describe the cycloxygenase pathway?

A

membrane phospholipids can be broken down into arachidonic acid by phospholipase A2. arachidonic acid can be metabolised by COX enzymes to form prostaglandins, prostacyclins and thromboxanes

18
Q

describe the lipoxygenase pathway?

A

membrane phospholipids are broken down into arachidonic acid by phospholipase A2. arachidonic acid can then be metabolised by lipoxygenase into leukotrienes and lipoxins

19
Q

what are the differences between COX 1 and COX 2?

A

COX 1 is always on and has functions in homeostasis, GI tract, renal tract, platelet function and macrophage differentiation
COX 2 is inducible and has inflammatory functions

20
Q

what does prostacyclin do?

A

it inhibits platelet activation and is an effective vasodilator

21
Q

what are some NSAID examples?

A 
aspirin
indomethacin
paracetamol
ibuprofen
diclofenac
22
Q

what effects do NSAIDs have?

A

antipyretic, anti-inflammatory and analgesic

23
Q

what are some adverse side effects of NSAIDs?

A

abdominal discomfort, ulcerations in stomach and duodenum, myocardial infarction, heart burn, vomiting, ringing in the ear, wheezing, rash

24
Q

which isoform of COX does aspirin target?

A

COX 1 and COX 2

25
Q

what are differences between ibuprofen and aspirin?

A

made from different acids, ibuprofen binds reversibly and aspirin binds irreversibly, ibuprofen has less adverse side effects

26
Q

describe aspirins mechanism of action?

A

aspirin binds to serine position 529 in the COX enzyme so arachidonic acid cannot bind. because aspirin binds irreversibly, to restore COX enzyme function, new COX enzymes need t be formed.

27
Q

describe the effects of aspirin on platelets?

A

inhibition of COX prevents formation of thromboxane which is required for platelet activation. platelets cannot produce new COX due to no nucleus so the effects of aspirin are permanent for platelet life

28
Q

describe the effects of aspirin on endothelial cells?

A

COX 1 and COX 2 being inhibited prevents the formation of prostacyclin which is important for vasodilation. endothelial cells can produce new COX enzyme so it can re-establish its activity

29
Q

what if we take aspirin and ibuprofen?

A

ibuprofen would bind to serine 529 instead of aspirin so this would mean the anti-platelet effects that aspirin has wouldn’t happen

30
Q

what are coxibs? why where they made?

A

a new drug that is specific to COX-2 isoform

it ensures we get the inflammatory response and prevents inhibition of COX 1

31
Q

give an example of a coxib?

A

celecoxib

32
Q

what are NO-NSAIDs?

A

nitric oxide donating NSAIDs. they have gastro-protective effects and increased anti-inflammatory activity

33
Q

where are glucocorticoids synthesised from?

A

cholesterol

34
Q

how can glucocorticoids be administered?

A

cream, inhalers tablets

35
Q

describe the mechanism of glucocorticoids?

A

as it is lipid based, it can diffuse through the cell wall an bind to a receptor within the cytoplasm which loses its Hsp90 protein. the complex of the receptor and steered then moves to the nucleus where it will cause activation or inhibition of gene expression of inflammatory mediators

36
Q

what are risks of taking oral glucocorticoids?

A

local immunosuprresion and increased risk of infection. it can also cause dysphonia

37
Q

what effects can glucocorticoids have on the cardiovascular system?

A

hypertension, cardiac hypertrophy and elevated risks of cardiac events

38
Q

what are 2 examples of glucocorticoids?1

A

prednisolone and dexamethasone

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