Term
| What is the target of prostacyclin? |
|
Definition
Endothelium
Platelets
Kidney
Brains |
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Term
| What is the target of thromboxane-A2 |
|
Definition
Platelets
Vascular smooth-muscle cells
Macrophages
Kidney |
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Term
| What is the target of prostagladin D2 |
|
Definition
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Term
| What is the target of prostaglandin E2 |
|
Definition
Brain
Kidney
Vascular smooth muscle cells
Platelets |
|
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Term
| What is the target of prostaglandin F2 |
|
Definition
Uterus
Airways
Vascular smooth muscle cells
Eyes |
|
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Term
Cox-1
Where is it
How is it activated |
|
Definition
- Location: Most tissues
- Activated: Costituitively active
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|
|
Term
Cox-2
Where is it
How is it activated |
|
Definition
- Location: Specific tissues
- Activated: Activated by cytokines + other inflammatory mediators
|
|
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Term
| MOA of Aspirin vs other NSAIDs |
|
Definition
Aspirin:
- Aspirin covalently/irreversibly inhibits Cox-1 and Cox-2
- Recovery is mediated by the formation of more COX by tissues
- Platelets cannot make new COX, so it is irreversible at the platelet level
Other NSAIDs:
- These produce REVERSIBLE inhibition of Cox
|
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Term
Celecoxib
Benefits
Use
Contraindications |
|
Definition
- Benefits is that it leaves COX-1 unaffected and that is going to: 1) Lower GI ulcers (but unproven) 2) Does NOT impact platelets and bleeding time
- Approved for: 1) Dysmenorrhea 2) Osteoarthritis 3) Rheumatoid arthritis 4) Acute post-operative pain
- Contraindicated in aspirin allergy + 3rd trimester pregnancy
|
|
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Term
| "Class effect" of both selective and non-selective NSAIDs |
|
Definition
| Increased risk of serious CV-events |
|
|
Term
| GI effects of PGI2 and PGE2 and PGF2 |
|
Definition
- PG-E2: Vasodilation to increase blood flow through stomach mucosa to help acid clearance. Also decreases gastric acid secretion
- PG-I2: Increases bicarbonate + mucus secretions
- PG-F2: Increases bicarbonate + mucus secretions
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