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Pharmacology > Inflammation (L19) > Flashcards

Inflammation (L19) Flashcards

1
Q

what is the purpose of inflammation?

A

restrict
• damage limitation
• stop pathogen movement

remove
• destroy invading pathogens
• clear damaged tissue

repair
• tissue regeneration
• healing/scarring

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2
Q

signs of inflammation

A
  • erythema (redness)
  • swelling
  • heat
  • pain

all leads to a loss of function

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3
Q

what are the 2 inflammatory responses?

A

innate immune response

adaptive immune response

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4
Q

innate immune response

A

rapid response at injury site

destruction of pathogens and phagocytosis

no memory component

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5
Q

adaptive immune response

A

specific response that can be remembered

triggered by innate activation

involves APCs, T cells and B cells

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6
Q

local inflammatory response

A

macrophages express receptors for many microbial constituents

bacteria trigger macrophages (through LPS) receptors to release cytokines and chemokine

vasodilation and increased vascular permeability causes redness, heat and swelling

inflammatory cells migrate to tissue, releasing inflammatory mediators that cause pain

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7
Q

stages of the innate inflammatory response

A

signalling is always there

inflammatory cell accumulation starts just after the microvascular event (6 hours)

you then get the systemic effects - makes you feel tired, pain and headaches

takes about 4 days before you see any healing

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8
Q

what cells are involved in local inflammation?

A

mast cells

macrophages

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9
Q

what do mast cells do?

A

important for clearing inflammation

communication hubs of the immune response

release granules containing histamine and active agents

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10
Q

what do macrophages do?

A

phagocytosis and activation of bactericidal mechanisms

antigen presentation

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11
Q

what does a tissue injury lead to the release of?

A

vasoactive mediators

chemotactic factors

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12
Q

what do vasoactive mediators cause?

A
  • dilation of arterioles
  • construction of venules
  • increased vascular permeability

this leads to oedema

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13
Q

what do chemotactic factors cause?

A

the recruitment/stimulation of inflammatory cells

this leads to either chronic or acute inflammation

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14
Q

how do we resolve a tissue injury?

A

body wants to pull the 2 healthy edges together
• by clotting and fibrin

we don’t want fibrin there long term - has no activity

once wound is closed we want to replace fibrin with healthy tissue - complete restoration = no scarring

if fibrin is replaced with collagen there is scarring

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15
Q

what are eicosanoids?

A

structures that are 20 carbons in size

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16
Q

what is arachidonic acid?

A

an eicosanoid

the precursor for most inflammatory molecules

made from phospholipids by phospholipase A2 (a platelet activating factor)

17
Q

what are the 3 classes of inflammatory molecules?

A

prostaglandins

thromboxanes

leukotrienes

they are all eicosanoids

18
Q

prostaglandins

A

cycle-oxygenase converts arachidonic acid into PGH2 (an intermediate plastglastin)

PGH2 then gets converted into 2 compounds by cyclic endoperoxidases

19
Q

what are the 2 compounds produced from PGH2 by cyclic endoperoxidases?

A

PGI2 (prostacyclin) - vasodilator, hyperalgesic, stops platelet aggregation

TXA2 (thromboxane) - thrombotic, vasoconstrictor, looks more like a box

20
Q

leukotrienes

A

chemical mediators produced by white blood cells containing 3 conjugated double bonds between carbon atoms

they all come from arachidonic acid

12-lipoxygenase makes most of the compounds

5-lipoxygenase is the better target for drug action as it is further upstream so makes more products

21
Q

what action could a drug perform to reduce inflammation?

A
  • interfere with immune cell response
  • block the pain signals (analgesic)
  • prevent blood vessels becoming leaky
  • stop cell infiltration to damaged tissue
  • reduce body temp (antipyretic)
  • prevent response from happening at all (immunosuppression)
22
Q

what are anti-inflammatory drugs?

A

drugs used to combat pain and inflammation

23
Q

what are the 4 categories of anti-inflammatory drugs?

A

antihistamines - antagonists of the histamine receptors

NSAIDS - non-steroidal anti-inflammatory drugs

glucocorticoids - steroidal anti-inflammatory drugs

immunosuppressants - reduction of immune cell activation or response

24
Q

examples of NSAIDs

A

paracetamol

ibuprofen

aspirin

celecoxib

25
Q

pros and cons of paracetamol

A

pro
• analgesic and antipyretic activity

con
• no anti-inflammatory action
• liver damage on overdose

26
Q

pros and cons of ibuprofen

A

pro
• short term analgesic
• anti-inflammatory activity

con
• gastric irritation
• increased risk of ulceration
• category D drug for pregnancy > 30 weeks

27
Q

pros and cons of aspirin

A

pro
• acetylates COX
• irreversible inhibitor
• anti-platelet activity

con
• increases risk of GI bleeding
• irritation

28
Q

pros and cons of celecoxib

A

pro
• specific COX-2 inhibitor
• fewer side effects

con
• increased risk of stroke and heart attack
• category D drug for pregnancy > 30 weeks

29
Q

where do most NSAIDs act?

A

on COX enzymes

30
Q

what are the 2 COX enzymes

A

COX-1

COX-2

31
Q

COX-1

A
  • housekeeper
  • regulates stomach acid
  • performs many functions
  • expressed widely

unwanted responses thought to be exerted mainly through COX-1 isoform inhibition

32
Q

COX-2

A
  • induced upon inflammatory cell activation
  • expressed in kidney and heart

anti-inflammatory, analgesic and antipyretic activity of NSAIDs thought to be exerted manning by COX-2 isoform inhibition

33
Q

steroidal anti-inflammatories (glucocorticoids)

A

can either by immunosuppressant or anti-inflammatory

34
Q

what happens when glucocorticoids are administered?

A

1) enters cells
2) binds to glucocorticoid receptor (GR)
3) GR moves to nucleus and binds to regulatory sites on DNA
4) gene transcription modified
5) enzyme production changes

35
Q

glucocorticoid effects

A

increase tyrosine aminotransferases - immunosuppressive

increase lipocortin - inhibits eicosanoid generation

decrease NFkB regulated genes - including COX

decrease AP1 regulated genes - would healing, collagen, vitamin D and C metabolism

36
Q

adverse effects of glucocorticoids

A

cushings syndrome - build up of cortisol with long term high dose corticosteroids use
• moonfaced
• purple strice
• buffalo hump

Pharmacology (24 decks)

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