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Microbial Pharmacology > NSAIDS treatment of Gout > Flashcards

NSAIDS treatment of Gout Flashcards

1
Q

What are the classic signs of inflammation?

A

Redness(rubor), swelling(tumor), Heat(calor), Pain(dolor)

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2
Q

What are the first reactions upon initiation of inflammation?

A

Vasodilation, leaky BVs
kinins(bradykinin), neuropeptides(SubstanceP), vasoactive amines(histamine, 5HT)
Arachadonic acid metabolites (Prostaglandin
Thromboxanes, Prostacyclin), and cytokines(TNF-alpha) Oxy FR, and proteases.

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3
Q

What are the actions of NSAIDS?

A

Anagesia, AntiPyretic, Antiinflammatory, Primary target is COX-1 and COX-2

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4
Q

Is acetaminophen and NSAID?

A

no

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5
Q

What are the main two prostzglandins involved in infalmmation?

A

PGE2 and PGI2

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6
Q

What is the function of the COX enzymes?

A

Convert Arachadonic Acid into Prostaglandins.

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7
Q

What is the unique function of COX-1?

A

Continually Expressed, widely distributed. Housekeeping functions. Protects Stomach lining from gastric acid.

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8
Q

What is the unique function of COX-2?

A

Inducible, production of inflammatory molecules. Renal perfusion
Vascular Endothelium: Prostacyclin(PGI2)

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9
Q

What are the different types of NSAIDS?

A

Non-Selective:Acetacylic Acid(aspirin), Ibuprofen, Indomethacin
Selctive for COX-2: Celecoxib

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10
Q

What are rhe clinical uses of NSAIDS?

A

Pain, Fever, Inflammation, Antithrombotic, Misc uses.

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11
Q

What can Aspirin be hydrolysed to?

A

Salicylic acid

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12
Q

What are the low dose effects of aspirin?

A

Analgesia, antipyretic

HL 3-5 hrs

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13
Q

What are the high dose effects of aspirin?

A

Anti inflammatory

HL > 12hrs

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14
Q

What form is aspirin in the Plasma?

A

Bound to Albumin

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15
Q

How is Salicylic acid excreted in urine?

A

Conjugated with glucuronic acid.

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16
Q

What are the pharmacologic Considerations of Aspirin?

A

Acetylation and inhibition of COX are irreversible.

17
Q

How does Aspirin decrease inflammation?

A

Inhb. of COX2 and PG

Inhb. Inflammatory cell migration.

18
Q

How does Aspirin decrease fever?

A

Blocks Prostaglandins to CNS to reset temp control. Dilates superficial BVs

19
Q

How does Aspirin prevent coagulation?

A

Inhibits Thromboxane synthesis

20
Q

What are the adverse effects of Aspirin?

A 
GI tract upset (COX-1)
GI irritation (decrease PG E2 and PGI2)
Platelet inhibition
Hepatic and Renal Tox. (decreases kidney function)
Hypersensitivity
Tinnitus
Reyes Syndrome: Encephalopathy
21
Q

What is the primary treatment for gout?

A

Indomethacin

22
Q

What is the benefit of using COX-2 selective inhibitors?

A

Similar benefits with less GI symptoms (higher risk for Cardiac events)

23
Q

What are the contraindications for COX-2 selective inhibitors

A

Underlying Cardiac disease

24
Q

What are the theraputic actions of Acetaminophen?

A

Pain and fever reducer

No antiinflammatory efects

25
Q

What is the main drawback to acetaminophen?

A

Acute toxicity is very dangerous! Acute Liver failure ==> Transplant!

26
Q

What is the MOA of Capscacin?

A

activates vanilloid receptors ==> Release of Substance P

27
Q

What are the drug reactions of NSAIDS?

A

Displacement of protein binding, diuretic, anticoagulants, GI effects

28
Q

What chemical builds up in Gout?

A

Monosodium urate.

29
Q

What is the treatment course for gout?

A

Terminate acute gouty attack
Control of pain and inflammation,
Prevent future attack
Low purine foods and limit alcohol

30
Q

What is the use of Colchicine?

A

Reduces pain and inflammation in Gout. Inhibits leukocyte migrationand phagocytosis

31
Q

What are adverse effects of Colchicine?

A

Diarrhea

32
Q

What is used for Gout Prophylaxis?

A 
Xanthine Oxidase inhibitors(Allopurinol, Febuxostat)
Uricosuric Drugs (Probenecid or sulfinpyrazone)

Microbial Pharmacology (13 decks)

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