Pharmacology - Nsaid+Gout+Innate Inflammation

Front 1

What is an Acute inflammatory reaction?

Back 1

local event in response to a disease carrying organism: immunological specific reaction and an innate reaction.

Front 2

What are the vascular events of an innate acute inflammatory response?

Back 2

Vasodilation, increased permeability of post capillary venules, and extrusion of fluid

Front 3

what are the cells involved in an innate acute inflammatory response?

Back 3

1) white blood cells: neutrophils, monocytes, lymphocytes, natural killer cells 2) tissue cells: vascular endothelium, mast cells, macrophages

Front 4

Give three examples of chemical mediators derived from the cells of an innate acute inflammatory response?

Back 4

cytokines, histamines, neuropeptides

Front 5

Give two examples of Eicosanoids

Back 5

Prostanoids, and leukotrienes

Front 6

Whats the difference between COX-1 and COX-2?

Back 6

COX-1 is present in most cells and involved in tissue homeostasis and COX-2 induced in activated inflammatory cells

Front 7

What are the precursors of Eicosanoids?

Back 7

Phospholipids

Front 8

What are the actions of Bardykinin?

Back 8

1) vasodilation (mediated by NO and PGI2) 2) increase vascular permeability 3) stimulate pain nerve endings (potentiated by PGs)

Front 9

What cells release histamine?

Back 9

Mast cells

Front 10

What acts on Mast cells to cause the release of histamine?

Back 10

complement (C3a) or in t1 hypersensitivity an antigen antibody reaction on the cell surface.

Front 11

What are the actions of NO?

Back 11

dilate blood vessels, increase vascular permeability, and stimulate PG release

Front 12

What enzyme form NO?

Back 12

NO synthase

Front 13

Give 4 examples of cytokines in an innate acute inflammatory response?

Back 13

interleukins (IL-2), chemokines (attract and activate mobile inflammatory cells), colony stimulating factors, growth factors.

Front 14

What are the 4 broad types of anti inflammatory drugs?

Back 14

glococorticoids, non-steroidal anti inflammatory drugs, anti-rheumatoid drugs, drugs for gout.

Front 15

How do NSAID anti inflammatory action work?

Back 15

reduce vasodilation and thus permeability that is a result of COX-2 vasodilation.

Front 16

give on strong anti-inflammatory NSAID, one median and one weak.

Back 16

Naproxen, Ibuprofen, paracetamol

Front 17

Explain the mechanism for the analgesic action of NSAID?

Back 17

Decreases the production of PG which sensitise nerve endings to inflammatory mediators to pain producing mediators, eg bradykinin)

Front 18

Explain the mechanism for the antipyretic action of NSAID?

Back 18

Prevent the formation of E-type PG (stimulated byIL-1) in the hypothalamus which would cause fever

Front 19

What kind of cox inhibitor is aspirin?

Back 19

Irreversible

Front 20

Explain the unwanted actions of NSAID on the gut?

Back 20

Mainly due to COX-1 inhibition: GI-disterbences-prevent PG formation which leads to protective mechanisms (mucus+bicarbonate) Misoprostol a PG agonist can help.

Front 21

Other than GI disturbances what are the unwanted effects of NSAID?

Back 21

Skin reaction, Adverse renal effects as PG promotes blood flow therefore natriuresis, Bone marrow depression, and liver disorders. Reyer's syndrome, bronchospasm in asthmatics

Front 22

Which NSAID is NOT used for gout?

Back 22

ibuprofen

Front 23

Give 3 (not NSAIDs) drugs that are used for gout?

Back 23

Allopurinol - decreases uric acid synth' long term treatment. Colchicine - inhibits migration of neutrophils to joint. Probenecid - increase uric acid excretion from proximal tubule

Front 24

Which NSAID could be given for chronic pain?

Back 24

Piroxicam

Front 25

Which NSAID could be give for non-inflamatory pain?

Back 25

paracetamol

Front 26

Which NSAID could be give for short term analgesia?

Back 26

Ibuprofen

Front 27

Explain the result and treatment of an aspirin overdose.

Back 27

It's an acid base disturbances (uncoupled oxidative phosphorylation & hyperventilation due to stimulation of respiratory centres). Treat – leave if OD not high or forced alkaline diuresis to ↑ elimination – run blood over charcoal.

Front 28

Explain the result and treatment of an paracetamol overdose.

Back 28

metabolised in liver to N-acetyl-p-benzoquinone.imine – toxic to liver cells (free radical), unless conjugated to glutathione. Liver damage if ↓ glutathione. Treat – if early enough, use N-acetyl cystein to ↑ glutathione synthesis – buffer toxic free radical. If too long, liver damage to excessive and very ↓ glutathione, Px will die