Free FMGE Pathology questions

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Cellular swelling results from failure of energy-dependent ion pumps and is an early reversible manifestation of injury. Severe membrane and nuclear damage generally indicates irreversible injury.

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Ischemic infarction in most solid organs produces coagulative necrosis. The brain is an important exception, where ischemia typically causes liquefactive necrosis.

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Ischemic destruction in the central nervous system classically results in liquefactive necrosis. Enzymatic digestion ultimately produces a fluid-filled cavity.

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Caspases are cysteine proteases central to the initiation and execution of apoptosis. Their activation produces controlled dismantling of cellular components.

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Neutrophils are the predominant cells during the early stages of most acute bacterial inflammatory reactions. Monocytes/macrophages become more prominent later.

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Epithelioid cells are activated macrophages with abundant eosinophilic cytoplasm. Their aggregation is a defining feature of granulomatous inflammation.

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Early wound repair involves type III collagen deposition. Remodeling later increases stronger type I collagen.

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Virchow triad consists of endothelial injury, abnormal blood flow, and hypercoagulability. These factors promote pathological thrombus formation.

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Most pulmonary thromboemboli arise from deep venous thromboses, particularly proximal lower-extremity veins. Emboli travel through the right heart to the pulmonary arterial circulation.

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p53 can induce cell-cycle arrest following DNA damage, allowing repair or triggering apoptosis if injury is irreparable. Loss of p53 therefore facilitates survival of genetically abnormal cells.

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Metastatic potential is a defining characteristic of malignancy. Size and growth rate alone cannot reliably distinguish benign from malignant tumors.

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Amyloid deposits bind Congo red and exhibit characteristic apple-green birefringence under polarized light. This is a classic diagnostic pathological finding.

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Iron stores are depleted in iron deficiency, causing low serum ferritin. The liver increases transferrin production, producing an increased total iron-binding capacity.

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Folate and vitamin B12 deficiency impair DNA synthesis, producing nuclear-cytoplasmic asynchrony. Macro-ovalocytes and hypersegmented neutrophils are characteristic findings.

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CML is associated with the Philadelphia chromosome, resulting from t(9;22). This produces the BCR-ABL fusion tyrosine kinase.

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Acute promyelocytic leukemia is associated with t(15;17), producing the PML-RARA fusion. It has an important association with DIC.

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Classical Hodgkin lymphoma Reed-Sternberg cells characteristically express CD15 and CD30. Their immunophenotype helps separate classical Hodgkin lymphoma from several mimics.

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Minimal change disease is a common cause of nephrotic syndrome in children. Its classic ultrastructural feature is diffuse effacement of podocyte foot processes.

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ERBB2 encodes the HER2 receptor tyrosine kinase. Amplification or overexpression defines a therapeutically important molecular subset of breast carcinoma.

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Papillary thyroid carcinoma classically shows nuclear clearing, grooves, and intranuclear pseudoinclusions. Psammoma bodies may also be present.