Pharma 1

Question 2

What is the source of arachidonic acid in the body?

Answer 2

It is released from membrane phospholipids by the phospholipase A2 enzyme.

Question 3

How are prostaglandins derived from arachidonic acid?

Answer 3

They are derived by the action of the cyclooxygenase (COX) enzyme.

Question 4

How many isoforms does the cyclooxygenase (COX) enzyme have?

Answer 4

COX has 3 isoforms: COX-1( physiological , constitutive ) , COX-2 ( pathologic , inducible ) , and COX-3.

Question 5

What is the primary role of COX-1?

Answer 5

COX-1 is constitutive and involved in the synthesis of protective prostaglandins.

Question 6

What physiological functions are COX-1 prostaglandins responsible for?

Answer 6

They protect the stomach from HCl, regulate renal blood flow (RBF), and regulate platelet aggregation.

Question 7

What characterizes COX-2 compared to COX-1?

Answer 7

COX-2 is inducible and is involved in the synthesis of undesirable prostaglandins related to inflammation and bronchoconstriction.

Question 8

What is the primary function of COX-3?

Answer 8

COX-3 is found only in the brain and may be involved in the synthesis of prostaglandins related to fever and pain.

Question 9

Give a hint about eicosanoids synthesize

Answer 9

phospholipids => arachidonic acid => 2 pathways :Arachidonic acid with cox => prostaglandin & thromboxane A2 Arachidonic acid with lox => leukotriene

Question 10

Name the types of inhibitors mentioned for eicosanoid synthesis.

Answer 10

Corticosteroids => inhibit PLA2NSAIDs => inhibit coxleukotriene inhibitors.

Question 11

Classify the non-steroidal anti-inflammatory drugs (NSAIDs).

Answer 11

They are classified into non-selective COX inhibitors and selective COX-2 inhibitors.

Question 12

What are non-selective COX inhibitors?

Answer 12

Drugs that inhibit both COX-1 and COX-2.

Question 13

what are the examples of non selective COX inhibitors ?

Answer 13

salicylic acid derivatives => aspirin acetic acid derivatives => indomethacin , diclofenac propionic acid derivatives => ibuprofen , ketoprofen

Question 14

Give example about selective cox 2 inhibitors ?

Answer 14

celecoxib

Question 15

What is the pharmacokinetic property of acetyl-salicylic acid regarding absorption?

Answer 15

Absorption => oral => complete & rapid absorption Most absorption from stomach => Pka => 3.5

Question 16

How is the distribution of acetyl-salicylic acid characterized?

Answer 16

Widely distributed to all tissues including the CNS.Plasma ptn binding is high ( warfarin bleeding )

Question 17

What type of enzymes are responsible for the metabolism of acetyl-salicylic acid?

Answer 17

Metabolism occurs by hepatic microsomal enzymes.

Question 18

How can the excretion of acetyl-salicylic acid be increased?

Answer 18

Excretion is increased by alkalinization of urine (pH 8) (By NaHCO3 ) => ionization of aspirin

Question 19

What characterizes the mechanism of action of acetyl-salicylic acid?

Answer 19

It involves non-selective irreversible inhibition of COX, leading to inhibition of both PGs and TXs synthesis.

Question 20

How do other NSAIDs differ from acetyl-salicylic acid in terms of COX inhibition?

Answer 20

Other NSAIDs produce reversible inhibition.

Question 21

Enumerate pharmacologic effects of acetyl-salicylic acid

Answer 21

analgesic antipyretic Anti-inflammatory, anti-immunological and anti-rheumatic effects GIT Hepatic hematologic renal resp

Question 22

what pain is affected by aspirin ?

Answer 22

mild to moderate pain (not severe pain).

Question 23

How is aspirin effect on heat ?

Answer 23

Aspirin is antipyretic but not hypothermic agent i.e. it can
lower elevated body temp. but not normal body temp.

Question 24

what is the GIT effect of aspirin

Answer 24

2 types of ulcer : Acute gastric ulcer => ingestion of large dose , pathogenesis => trapping of aspirin ions due 2 PKA chronic gastric ulcer => chronic ingestion of therapeutic dose , pathogenesis is due 2 chronic inhibition of synthesis protective prostaglandin => PGE1,PGE2,PGI2

Question 25

what is the hepatic effect of salicylates ?

Answer 25

mild hepatic injury : dose dependent , reversible asymptomatic,=> mild increase in serum transamines =>SGOT&SGPTsevere hepatic injury : Reye's syndrome, occur in children below 12 when aspirin is taken to control fever of viral infections ( chicken pox , influenza) ,,, associated with encephalopathy & etiology is unknown

Question 26

what is the hematologic effect of aspirin ?

Answer 26

Antiplatelet action: Aspirin in low dose (75-150mg) inhibit platelet aggregation => Irreversible inhibition of COX enzyme → decrease TXA2 → decrease platelet aggregation.Anticoagulant action : Aspirin in high doses (> 6 gm /day) inhibits hepatic synthesis of vit K dependent coagulation factors (treated by vit K).

Question 27

why taking aspirin in low dose affectable 2 stroke patients while it's not recommended 2 increase dose ?

Answer 27

Vascular endothelium produces PGI2 (prostacyclin) that produces VD and inhibition of platelet aggregation. Platelets produce TXA2 that causes VC and increase platelet aggregation.In high doses (> 300 mg), aspirin inhibits both vascular PGI2 and platelet TXA2.In small doses (75-150 mg), aspirin inhibits only platelet TXA2 → selective antiplatelet action.

Question 28

what is the renal effect of aspirin ?

Answer 28

Analgesic nephropathy: Aspirin produce chronic renal ischemia due to decrease synthesis of renal PGE2 and PGI22. Salt & water retention: Due to ↓ RBF & ↑ aldosterone

Question 29

what is the respiratory effect of aspirin ?

Answer 29

Aspirin induced asthma

Question 30

what is the therapeutic use of salycelate ?

Answer 30

analgesic→ Dose: 300 - 900 mg t.d.s orallyantipyretic→ don't use routinely → fever is protective mechanism → dose 300 - 900 mg t.d.s orallyanti-inflammatory → rheumatic fever, rheumatoid arthritis, osteoarthritisanti-thrombotic → ischemic heart disease, deep vein thrombosis, AF → Dose: 75 - 150 mg once /day orally.

Question 31

what is the S.E of aspirin ?

Answer 31

GIT → acute & choronic gastric ulcers hepatic → reyes synderome in 12> children , mild reversible hepatic injury in adultskidney → analgesic nephropathy , salt & water retention blood → ↑ bleeding tendency hypersensitivity → aspirin asthma in patients with asthma due 2 accumulation of LTs

Question 32

What are the precautions and contraindications for aspirin use?

Answer 32

1. GIT disorders: peptic ulcer and gastritis. 2. Hemorrhagic disorders: hemophilia, thrombocytopenia, etc. 3. Chronic renal diseases: aspirin may aggravate renal failure. 4. Chronic liver diseases: patients may have bleeding tendency. 5. Severe hypertension: risk of fatal bleeding. 6. Pregnancy: long-term therapy may delay labor. 7. Before surgery: must stop at least 7 days prior. 8. Children

Question 33

How do non-selective COX inhibitors differ from selective COX-2 inhibitors in their mechanism of action?

Answer 33

Non-selective COX inhibitors inhibit both COX-1 (constitutive) and COX-2 (inducible) enzymes, while selective COX-2 inhibitors primarily inhibit the COX-2 enzyme.

Question 34

What pharmacological effects do both non-selective COX inhibitors and selective COX-2 inhibitors share?

Answer 34

Both classes have equal anti-inflammatory, analgesic, and antipyretic effects.

Question 35

What are the side effects associated with gastric and renal function for non-selective COX inhibitors compared to selective COX-2 inhibitors?

Answer 35

Gastric side effects: Frequent for non-selective COX inhibitors, less frequent for selective COX-2 inhibitors. Renal side effects: Frequent for both.

Question 36

What is the side effect of thrombotic reactions in non-selective COX inhibitors compared to selective COX-2 inhibitors?

Answer 36

Non-selective COX inhibitors decrease thrombotic reactions due to decreased platelet aggregation, while selective COX-2 inhibitors increase it due to increased platelet aggregation.

Question 37

compare () non selective cox & cox 2 inhibitor due 2 S.E of hypersensitivity

Answer 37

frequent in non selective cox & less frequent in selective cox 2 inhibitor

Question 38

What is the mechanism of action of acetaminophen (Paracetamol)?

Answer 38

selective COX III inhibitor that inhibits prostaglandin synthesis in the brain only, resulting in analgesic and antipyretic actions without anti-inflammatory action.little or No effects on the CVS, GIT, respiratory or platelet functions

Question 39

What are the therapeutic uses of acetaminophen (Paracetamol)?

Answer 39

used when aspirin is contraindicated, such as in patients with peptic ulcer or hemophiliaadministered during pregnancy with greater safety than aspirin.

Question 40

What are the adverse effects of acetaminophen (Paracetamol) ?

Answer 40

therapeutic dose → skin rash and drug fever as allergic reactions, hemolytic anemia in patients with G-6-PD deficiency, and long term use may lead to renal failure. toxic dose → dose-dependent hepatotoxicity, leading to hepatic necrosis.

Question 41

what is the mnemonic of contraindications of aspirin ?

Answer 41

GIT , BLOOD , LIVER , KIDNEY واحدة حامل عندها عيال جابولها الضغط وتعمل عملية