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TIN > WK 4- ANTI-INFLAMMATORY DRUGS > Flashcards

WK 4- ANTI-INFLAMMATORY DRUGS Flashcards

1
Q

What are the 2 subclasses of NSAIDS

A

Non-Selective and COX-2 selective

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2
Q

What drug is an example of a Non-Selective NSAID

A

Ibuprofen

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3
Q

What drug is an example of COX-2 Selective NSAID

A

Celecoxib

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4
Q

What is the MOA of NSAIDS

A

-inhibit COX enzymes→ inhibit production of prostaglandins and thromboxanes → stop formation of local mediators of pain, fever and inflammation

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5
Q

What is the function of COX-1

A

-constitutive, expressed in most tissues, has a housekeeping role such as tissue homeostasis, production of prostaglandins that are gastric cytoprotective, cause platelet aggregation

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6
Q

What is the function of COX-2

A

-inducible during inflammation and is activated by cytokines (IL-1, TNF), causes production of prostaglandins

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7
Q

What are the adverse effects of non-selective NSAIDs

A

GI: Dyspepsia, nausea and GI damage due to suppression of gastroprotective PG, risk of haemorrhage (as antiplatelet)

  • Cardio: increased risk of MI, stoke and hypertension
  • Renal: reversible renal insufficiency in individuals with compromised renal function, compensatory PGE2-mediated vasodilatation is inhibited, Analgesic-associated nephropathy (decrease renal blood flow and GFR)
  • Resp: bronchospasm in aspirin-sensitive asthmatics
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8
Q

What are the adverse effects of Selective COX-2 inhibitors

A

GI: increased risk of serious GI adverse events
Cardio: MI and stroke

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9
Q

Why is COX-2 selective inhibitors contraindicated in patients with CV history

A

-thromboxane A2 is formed in platelets through COX-1→ TXA2 causes vasoconstriction and increased platelet aggregation→ PG12 normally offsets this by causing vasodilation and restraining platelet activation→ COX-2 inhibits block production of PG12 and PGE2 but doesn’t inhibit TXA2→ causes hypertension, thrombosis and increased

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10
Q

What is the MOA of Corticosteroids/Glucocorticoids

A

-cross membrane and binds to intracellular glucocorticoid receptors and initiates transcriptional regulation of expression of genes involved in metabolic and inflammatory responses

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11
Q

What are the effects of inflammatory mediators cause by corticosteroids

A
  • decrease in transcription for cell adhesion factors and cytokines
  • decrease in activation of T helper cells
  • reduced proliferation of T cells
  • decrease in fibroblast function (decrease healing and repair)
  • decreased activity of osteoblasts
  • decreased expression of COX-2
  • decrease in IgG production
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12
Q

What is the indication for NSAID use

A

symptomatic relief from fever, minor pain, inflammation

-acute inflammatory conditions and chronic joint disease eg osteoarthritis, rheumatoid arthritis

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13
Q

What is the indication for corticosteroid use

A

anti-inflammatory and immunosuppressant effects also used for replacement therapy in adrenal insufficiency- used in asthma, dermatitis, chrons disease, UC, RA

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14
Q

What are the adverse effects of corticosteroid use

A

Immune: decreased response to infection or injury / risk of opportunistic infection eg peptic ulceration, oral thrush
Ortho: osteoporosis and increased risk of fractures -alterations in calcium and phosphate metabolism -reduce osteoblast and increase osteoclast activity
Endo: hyperglycaemia -decreased glucose uptake / increased gluconeogenesis, muscle wasting and weakness, growth retardation in children, iatrogenic cushings syndrome
-CNS: euphoria, depression, psychosis
-Renal: sudden withdrawal after prolonged therapy may result in acute adrenal insufficiency via suppression of HPA axis

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15
Q

What are the 4 classes used as anti-rheumatic drugs

A
  1. 5aminosalicylates 2. TNF-alpha antagonist 3. Cytokine modulators 4. DMARDS (disease modifying antirheumatic drugs)
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16
Q

What is the MOA of sulfasalazine (5aminosalicylates)

A

Form a complex between sulfonainide and salycylate that scavenges toxic oxygen metabolites and blocks damage caused by ROS metabolites (produced by neutrophils)

17
Q

What are the adverse effects of sulfasalazine (5aminosal..)

A

malaise, headache , GI disturbances

18
Q

What is the MOA of TNF alpha antagonist (lol)

A

Bind to and block the action of TNF-alpha and stop it contributing to inflammation (stop chemotaxis and recruitment of other immune cells)

19
Q

What are the adverse effects of TNF-alpha antagonists

A

immunosuppression, lymphoproliferative disorders, malignancies, infections, AutoAb

20
Q

What patients should be reviewed before giving TNF-alpha antag (precautioned)

A

Demyelinating disorders, heart failure, serious infections

21
Q

What is the MOA of rituximab (cytokine modulator)

A

chimeric anti-CD20 molecule that binds to CD20 molecules on B cells and causes destruction and lysis of the cell–> both unhealthy and healthy
-healthy cells will grow back

22
Q

What is the MOA of abatacept (cytokine modulator)

A

Binds to B7 on APC and stop it binding to CD28 on T cell–> prevents costimulation of T cell, leaving it anergic and unable to secrete cytokines that cause inflammation

23
Q

What adverse effects occur from cytokine modulators

A

infection, weakness, infusion related reactions

24
Q

What is the mechanism of action of methotrexate in RA

A

Prevents the breakdown of purine (by inhibiting AICAR transforylase)-> causes build up of adenosine (anti-inflam)–> also cause increase of Fas expression (CD95), stop IL-1 binding, stop intracellular adhesion molecules/activation of T cells/B cells

25
Q

What are the adverse effects of methotrexate

A

decreased folate, hepato and neurotoxicity, blood dyscarias-> highly toxic and only given once a week

26
Q

What is colchine and its MOA and indication

A

Used in treatment of gout-> stops neutrophil migration, chemotaxis, adhesion and phagocytosis so inhibits release of glycoprotein that is produced during phagocytosis of urate crystals (stops them being phagocytosed)

27
Q

What is gout

A

is a metabolic disease caused by increased plasma urate concentration-> causes the formation of crystals in synovial tissues of joints-> painful intermittent attacks of acute arthritis and inflammation-> inflammation activates kinins, complements and plasma systems-> causes local accumulation of neutrophils that release toxic oxygen metabolites and cell lysis (colchine inhibits neutrophil migration)

28
Q

What is the MOA of integrin antagonist (vedolizumab)

A

used to treat moderate to severe chrons disease when not response to other treatment-> uses IgG1 Ab against A4:B7 integrin present on the surface of T lymphocytes (especially those activated in the gut)-> inhibits adhesion of T cells to MADCAM1 in the GIT-> stops GI inflammation

29
Q

What is the MOA of leukotriene receptor antagonist (eg. montelukast)

A

Leukotriene cysLT1 (receptor) antagonist blocks action of leukotriene D4 and secondary ligands and LTC4/LTE4 in lungs and bronchioles-> reduces bronchoconstriction and inflammation

30
Q

What are leukotriene receptor antagonists used in

A

asthma, allergic rhinits, exercise induced bronchoconstriction

31
Q

What is osteoarthritis

A

degenerative joint disease that is progressive and non inflamm–> occurs in diarthrodal joints (weight bearing) and causes progressive loss of cartilage and formation of thick subcondral bone in the joint space-> causes pain, weakness, joint stiffness, joint deformities

32
Q

What is an example of a non-pharmaceutical treatment in RA

A

-omega 3 fatty acids–> effective in RA, converted to resolvins (anti-inflamm)

TIN (14 decks)

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