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Anti-inflammatory Drugs

D. CLASS

M.A

ACTION

SE

NOTE

Non-steroidal

-All mediated through inhibition of COX activity and PG production

-Anti-inflammatory -Analgesic -Antipyretic

-GI disturbances: N+V, gastric erosions, ulceration, haemorrhage, perforation -Skin reactions: mild rashes, photosensitivity -Renal disease - -Peripheral oedema/hypertension

- Aspirin= Largely superceded as an anti-inflammatory agent by other NSAIDs/coxibs

Anti-inflammatory

Drugs (NSAIDs)

 

aspirin

-

prevent action of IL1 on

-Anti platelet effect (COX-1 effect)

PLA2

-asymptomatic Liver abnormalities

usually, normalise when drug is stopped

 

-Reye’s syndrome (in children, with aspirin) -bone marrow toxicity -Bronchospasm in “aspirin sensitive” asthmatics -CNS effects : headaches, dizziness, confusion, seizures, drowsiness (NB indomethacin) -Salicycism: Tinnitus, dizziness, nausea, vomiting -Can be fatal in overdose

-Drug interactions

Warfarin

- inhibition of warfarin catabolism

- haemorrhage due anti-platelet effects and GI mucosal damage

- aspirin also displaces warfarin from plasma proteins

Betablockers, ACE inhibitors, diuretics loss of hypotensive +/- diuretic effect Increased levels of lithium, methotrexate and phenytoin increasing the risk of toxic effects Spironolactone, ACE inhibitorshyperkalaemia NB ibuprofen can interfere with the anti-platelet effect of aspirin (Binds to COX-1 instead of aspirin, but is reversible and shorter acting)

COX-2 specific

Selectively inhibit cox2

inflammation responce

-Oedema -hypertension -Cardiovascular Risk Myocardial infarction, stroke with prolonged usage even in patients without known vascular disease Inhibition of COX-2 derived PGI2, but ongoing production of TXA2 via COX-1 -Best avoided in patients with vascular dz

-Equivalent anti-inflammatory effects to non-selective NSAIDs BUT -Less risk of GI damage

inhibitors

(-Celecoxib)

-Nimesulide COX-2 preferentialLESS GI DAMAGE

D.CLASS

M.A

ACTION

SE

NOTE

Paracetamol

-Binds to COX-3

-analgesic and antipyretic effects = Equivalent to aspirin

 

-plasma half-life 1 to 4 hr -metabolised in the liver and excreted in the urine

(acetaminophen)

- allergic skin reactions

 

- GI disturbance

 

- low anti-inflammatory properties

- analgesic nephropathy (long-term)

-In acute overdose, risk of dose-dependent, *hepatic necrosis Renal tubular necrosis, hypoglycemic coma and thrombocytopenia Due to Saturation of conjugating enzymesDepletion of glutathione Accumulation of toxic metabolite N-acetyl-p- benzoquinone

Early symptoms: nausea, vomiting, diaphoresis and general malaise Treatment:

-Gastric lavage/activated charcoal -N-acetylcysteine (increases liver glutathione formation), should be administered as early as possible, preferably within 16 hours

Licofelone

-

AA analogue –

-Symptomatic improvement in OA comparable with NSAIDs -possible role in preventing joint damage in OA

-May be safer than NSAIDs esp. from a GI viewpoint

 

competitive dual inhibitor of COX and 5LO Inhibits production of PGs and LTs

D. CLASS

M.A

ACTION

USES

SE

ADMI

NOTE

 

-Is complexCombine with cytosolic glucocorticoid receptor (GRentry to nucleus

Anti- inflammatory action

-

inflammatory conditions :RA, gout,

Effective but side-effects limit long term use

-oral

Osteoporosis Prevention during steroid treatment

Corticosteroids

generally

asthma, inflammatory bowel diseaseAct more rapidly and potent

-IV

-Reduced capillary permeability

-

Side-effects limit use as

-IM

 

-

migration/ activation of circulating

anti-inflammatory agents than NSAIDs -Maintenance therapy in many inflammatory conditions also e.g. RA

replacement therapy, e.g. malignancies

-

maintenance therapy -Cushingoid facies -truncal obesity, myopathy

-Skin disorders, bruising -hirsuitism -dysphoria -hypertension -hyperglycaemia = Glucose intolerance,affect on carhydrates metabolism -acne .-Peptic ulcer disease prevented by Proton pump inhibitor -Cataract formation -Infection -Mental disturbance -HPA axis suppression

-intrasynovial

-Weight-bearing exercise -Calcium, -Vitamin D (Calcichew -Bisphosphonates e.g. risedronate, alendronate 1/52

 

leucocytes BUT IN NEUTROPHILS

Binds transcription factors AP-1 and NF-kB. support tight structure of chromatin by inhibiting histone deacetylation.

basophils, eosinophils and monocytes but increase in neutrophils lymphocytes

-

-

(T>B; CD4+>CD8+)

   
 

all \ neutrophil

This prevents transcription factors from binding to and efffecting expression of their gene target. Inhibits transcription of COX 2 and inflammatory cytokines (interleukins and TNFa)+ -Reduced expression of adhesion molecules

Induces Lipocortin-1 inhibits Phospholipase A2 Reduced synthesis of prostaglandins and leukotrienes

Irreversible osteoporosis, osteonecrosis

-