stuff 🩷

👑 A patient receives an ABO-incompatible blood transfusion and within minutes develops fever, lower back pain, hemoglobinuria, and intravascular clotting. Laboratory studies demonstrate extensive intravascular hemolysis. 🔹Which of the following sequences BEST explains the pathogenesis of this reaction? 🔹A) Preformed IgG binds donor RBCs → Fc-mediated ADCC → perforin/granzyme release → hemolysis 🔹B) Preformed IgM binds donor RBC antigens → classical complement activation → MAC formation and C3b deposition → intravascular hemolysis 🔹C) Anti-RBC antibodies form circulating immune complexes → vascular deposition → neutrophil-mediated vasculitis 🔹D) Sensitized T lymphocytes recognize donor RBC antigens → cytokine release → macrophage activation → RBC destruction

👑 A 24-year-old Rh-negative woman delivers her first Rh-positive child. Two years later, during her second pregnancy with another Rh-positive fetus, laboratory testing reveals high titers of anti-Rh antibodies. The fetus subsequently develops severe hemolytic anemia. 🔹Which ONE of the following statements is CORRECT? 🔹A) Disease occurs because maternal IgM crosses the placenta and activates complement. 🔹B) Rhogam is used to neutralize bilirubin released from fetal RBCs. 🔹C) The first pregnancy primarily acts as the sensitization phase. 🔹D) The disease represents antibody-dependent cellular dysfunction.

👑 Which of the following findings would most strongly support complement-mediated Type II hypersensitivity rather than ADCC? 🔹A) Fc receptor engagement 🔹B) Release of perforin 🔹C) Generation of C3b 🔹D) Release of TNF

👑 A patient develops muscle weakness due to antibodies directed against acetylcholine receptors. Which of the following best describes the mechanism? 🔹A) MAC-mediated lysis of muscle fibers 🔹B) Antibody-mediated cellular dysfunction 🔹C) Immune complex deposition 🔹D) Delayed T-cell mediated injury

👑 Type II Hypersensitivity Pearl #1 🔹Not every Type II hypersensitivity destroys cells. 🔹Myasthenia gravis = antibody BLOCKS receptor. 🔹Graves disease = antibody STIMULATES receptor. 👑 Type II Hypersensitivity Pearl #2 🔹In transfusion reactions, hemoglobin doesn’t just disappear after RBC destruction. 🔹Free hemoglobin has 2 fates: 🔹→ Hemoglobinuria (passes into urine) 🔹→ Bilirubin formation (can become toxic) 👑 Type II Hypersensitivity Pearl #3 🔹The dangerous Rh+ pregnancy is usually NOT the first one. 🔹1st pregnancy = sensitization. 🔹2nd Rh+ pregnancy = memory response. 🔹The fetus is attacked by maternal IgG crossing the placenta.

Mode of killing NK >ADCC Mode of killing Cytotoxic t cell CD8+ >hit&run

نراكم غدا صلوا و ناموا و الي بعدكم ممبلشين شدوها هال3 ايام مظل شي و نخلص بالتوفيق يارب 😀

راجعوها

🔰Opsonization … C3b 🔰edema …C2a 🔰anaphylatoxins … C5a , C3a 🔰chemotactic for neutrophils … C5a 🔰chemotactic for macrophages … IL8 🔰eosinophilia …IL5 🔰basophilia , mucus secretion in RT … IL3 🔰cachexia… TNF-alpha 🔰induction of acute phase protein from the liver… IL1 ,IL6 , TNF-alpha.

👑 A researcher creates a genetically modified IgE molecule that retains normal FcεRI binding but completely loses its Fab region. After mast-cell sensitization, the subject is exposed to allergen. 🔹What happens? 🔹A) Immediate severe anaphylaxis 🔹B) Normal degranulation 🔹C) No degranulation 🔹D) Increased complement activation

سؤال فلسفي اذا رادوا يصعبوها :)

👑 A patient receives an IV radiographic contrast agent and immediately develops hypotension, bronchospasm, and urticaria. Laboratory testing later shows no evidence of allergen-specific IgE. Which mechanism best explains the reaction? 🔹A) Type II hypersensitivity 🔹B) Immune-complex deposition 🔹C) Direct mast-cell mediator release 🔹D) Complement fixation by IgE

الي غلطتوا راجعوا هذي