قناة سنة ثانية بشري (دفعة 53)

5. Role of Aspirin in Inhibiting Clot Formation • TXA₂ and prostacyclin are made from membrane phospholipids • Aspirin inhibits COX enzyme (Cyclo-oxygenase) • COX inhibition → ↓ TXA₂ → ↓ platelet aggregation • Platelets cannot synthesize new COX (no nucleus) → Effect lasts 10 days (platelet lifespan) • Long-term aspirin → ↑ bleeding time and ↓ clot formation

4. Thrombopoiesis • Platelet production from megakaryocytes • Stimulated by Thrombopoietin (TPO) • Platelets have no nucleus → formed by cytoplasmic fragmentation • Life span = 10 days

3. Functions of Platelets A. Hemostasis 1. Vasoconstriction via: • Serotonin • Thromboxane A₂ (TXA₂) 2. Formation of Platelet Plug • Adhesion → Aggregation → Temporary seal 3. Produce Factor XIII → stabilizes clot 4. Clot retraction • Through Thrombin + Ca²⁺ • Uses thrombosthenin, actin, myosin • Makes clot smaller & stronger 5. Release PDGF → promotes repair of damaged vessel B. Blood Coagulation 1. Platelet Factor 3 (PF3) • Accelerates thrombin formation 2. Platelet Factor 4 (PF4) • Neutralizes heparin (a natural anticoagulant)

2. Platelet Structure A. Platelet Membrane Glycoproteins • Gp Ia → Adhesion • Gp Ib → Receptor for von Willebrand factor (vWF) • Gp IIb/IIIa → Receptor for fibrinogen → platelet aggregation Membrane phospholipids • Contain Platelet Factor 3 (PF3) • Needed for synthesis of prostaglandins and Thromboxane A₂ (TXA₂) B. Platelet Cytoplasm 1. Delta (Dense) Granules • Contain: Ca²⁺, ATP, ADP 2. Alpha Granules • Platelet Factor 4 (PF4) • Platelet-Derived Growth Factor (PDGF) • Platelet Activation Factor (PAF) • Factor VIII • Factor XIII (Fibrin-stabilizing factor) • vWF 3. Dense Tubular System • Synthesis of: • Prostaglandins • TXA₂ • Serotonin

1. Structure & Basic Facts • Very small, colorless, non-nucleated cells. • Produced from megakaryocytes in bone marrow. • Count: 150,000–400,000 / mm³ • Life span: ~10 days • Destroyed by macrophages in the spleen • Irregular shape → helps adhesion to damaged tissue. • Production regulated by Thrombopoietin (TPO) from: • Kidneys • Liver

3 . Platelets : ⬇️⬇️⬇️⬇️

هي شويه وانزلو ال wbc وال plt .

هذا شيت ال blood group كمل ي شبااب مازال عندنا حاجات بسيطه في الكورس ♥️.

Erythroblastosis Fetalis (Hemolytic Disease of the Newborn) Cause • Rh− mother + Rh+ fetus. • At 1st delivery → fetal Rh+ blood enters mother → mother forms anti-Rh antibodies. • In 2nd pregnancy → antibodies cross placenta → fetal RBC destruction. Manifestations • Severe anemia • Hydrops fetalis (severe edema, heart failure) • Jaundice → bilirubin → brain damage (Kernicterus) Prevention • Give Anti-D antibody (Rh immunoglobulin) at 28–30 weeks of pregnancy. Treatment 1. Exchange transfusion • Replace baby’s blood with Rh- blood (~400 mL over 2 hours). • Removes Rh+ cells, antibodies, and reduces bilirubin. 2. Phototherapy • UV light breaks down bilirubin.

Hemolytic Transfusion Reaction • Happens when recipient antibodies attack donor RBC antigens. • Causes RBC clumping → blocked vessels → hemolysis → shock. Consequences • RBC agglutination • Hemolytic jaundice • Severe hypotension • Oliguria → acute renal failure Dangerous complications • Allergic reactions • Transmission of infections (e.g., hepatitis, HIV)