NSAIDS & PCM

Question 1

What is inflammation?

Answer 1

• Reaction of tissue & microcirculation to pathogenic insult
• Complex biological respond to harmful stimuli
• Protective attempt & initiate healing process

Question 2

Sign of inflammation?

Answer 2

Redness - vasodilate (WBC attack foreign body)
Heat - thermoregulatory (Brain) (Protect us)
Swelling - increase vascular permeability
Pain - sensitization nociceptor (Pain -> increase tissue pressure)

Question 3

General Mechanism of inflammation?

Answer 3

Tissue injury -> chemical process (Phospholipase A2) -> Arachidonic acid -> Cyclooxygenase (COX) = enzyme form imp mediator call eicosanoid (prostaglandins, prostacyclin & thromboxane) -> COX 1 & COX2

COX 1 - prostacycin, thromboxanes, prostagladin -> stimulate normal body function
-Responsible synthesis protective prostagladin

COX 2 (Keluar inflamme untuk menyerang) - Synthesis Prostagladins (inflammatory reaction) -> Pain/fever
-COX 2 synthesis PGs responsible for pain & inflammation.

COX 3 - Degree Nurse do not need to know yet

Question 4

Mechanism of inflammation?

Answer 4

Inflammatory response produce symptoms ->

Blood cell release inflammatory mediator ->

Mediator
(increase blood flow, capillary permeability, allow large molecule across cell wall)
(Histamine-vasodilate, cytokines - control inflamatory process, prostaglandin - inflammatory reaction) ->

Chemotaxis ( Neutrophil destroy pathogen) ->

Phaoctosis (Neutrophil digest bacteria) ->

Tissue begin repair -> Fiboblast promote growth & granulate tissue capilllary buds (angiogenesis, new blood vessel form) -> Supply nutrient & Collagen secrete -> Calcium deposite

Question 5

Mediator of inflammatory response?

Answer 5

Histamine - causedilate & increase permeability capillaries

PGs (PGE2) -Promote vasodilation -> pain/fever PG12 - ⬆️ vascular permeability -> enhance pain -> produce bradykinin

Plasma proteases (Bradykinin) -> vasoactive protein -> induce vasodilation -> induce pain

Leukotrienes - increase vascular permeability

Thromboxane A2 - fam of lipid ( eicosanoids) -> platelet aggregate -> smooth muscle contract -> enhance func inflammatory cell

Question 6

NSAIDs used for?

Answer 6

• Reduce inflame

- inhibit COX enzyme & PG synthesis

Question 7

2 type of anti-inflammatory drugs?

Answer 7

• Steroidal anti-inflammatory (Cortisone, hydrocortisone)

- NSAIDs (PCM, Aspirin)

Question 8

Newer drugs COX-2 specific safer?

Answer 8

Yes

Question 9

Non-opioids analegesic?

Answer 9

NSAIDs

PCM

Question 10

Classification of NSAIDs?

Answer 10

• Non selectve COX inhibator - tradisional (Aspirin, Diclofenac,ibu, naproxen, mefenamic acid)
• Selective COX 2 inhibator (Celecoxib, Etoricoxib)
  MOA: exhbit peripheral & cetral effects, antiinflamme + analgesic effect)
• Analgesic antipyratic w poor antiinflammatory action
  (PCM)
• Preferential COX-2 inhibators
  (Meloxicam)

Question 11

Which drug is the most important NSAIDs? (Non selective COX inhibator)

Answer 11

Aspirin

Question 12

Aspirin is?

Answer 12

• Potent anti inflammatory drug
• Mild analgesic & antipyretic
• Prevent platelet aggregation

Question 13

how prostaglandin affect kidney?

Answer 13

Prostaglandins (PGs) with best-defined renal functions are PGE2 and prostacyclin (PGI2). These vasodilatory PGs increase renal blood flow and glomerular filtration rate under conditions associated with decreased actual or effective circulating volume, resulting in greater tubular flow and secretion of potassium.

Question 14

Why GIT adverse effect (Aspirin)?

Answer 14

PGs in GIT = cytoprotective

• inhibit acid secretion
• secretion mucus
• Inhibit PGs remove protection

Question 15

MOA PCM?

Answer 15

Inhibit PGs production @CNS (central COX enzyme)

Question 16

Contraindication PCM?

Answer 16

• G6PD!!!! will die
• low kideney/liver func
• Alcohol dependance

Question 17

PCM overdose?

Answer 17

-give methionine & Fluimucil -boost level glutathione in liver