Master Pathology
for PMDC NLE Step 1
Access 50+ high-yield questions tailored for the 2026 syllabus. Includes AI-powered explanations and performance tracking.
Core Concepts
Pathology is the study of disease: its etiology, pathogenesis, morphological changes, and clinical manifestations.
- Cell Injury & Adaptation:
- Reversible: Cellular swelling, fatty change.
- Irreversible (Necrosis): Coagulative, Liquefactive, Caseous, Fat, Fibrinoid, Gangrenous. Apoptosis (programmed cell death, no inflammation).
- Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia, Dysplasia.
- Inflammation & Repair:
- Acute: Neutrophils, vascular changes (vasodilation, permeability). Mediators: Histamine, Prostaglandins, Leukotrienes.
- Chronic: Macrophages, lymphocytes, plasma cells. Granulomatous inflammation (epithelioid macrophages, giant cells).
- Repair: Regeneration vs. Fibrosis/Scar (granulation tissue). Key factor: TGF-β.
- Hemodynamics:
- Edema: Increased hydrostatic P, decreased oncotic P, lymphatic obstruction.
- Thrombosis: Virchow's Triad (endothelial injury, stasis, hypercoagulability).
- Embolism: Thromboembolism (PE), Fat, Air, Amniotic fluid.
- Infarction: Ischemic necrosis. Red (venous occlusion) vs. White (arterial occlusion).
- Shock: Cardiogenic, Hypovolemic, Septic, Anaphylactic, Neurogenic.
- Neoplasia:
- Benign vs. Malignant: Differentiation, growth, invasion, metastasis.
- Carcinogenesis: Oncogenes (gain-of-function, e.g., RAS), Tumor Suppressor Genes (loss-of-function, e.g., P53, RB).
- Metastasis: Lymphatic, Hematogenous, Seeding.
- Grading (differentiation) vs. Staging (TNM, extent of spread).
- Immunopathology & Genetics:
- Hypersensitivity: Type I (IgE), II (Abs to cell), III (Immune Complex), IV (T-cell mediated).
- Autoimmunity: Loss of self-tolerance.
- Immunodeficiency: Primary (congenital) vs. Secondary (acquired, e.g., HIV).
- Genetic Disorders: Mendelian, Chromosomal, Multifactorial.
Clinical Presentation
Pathological processes manifest variably based on type, severity, and organ system. Common signs/symptoms include:
- Inflammation/Infection: Fever, pain, redness, swelling, organ dysfunction.
- Neoplasia: Masses, weight loss, fatigue, paraneoplastic syndromes.
- Ischemia/Infarction: Acute pain, organ failure.
- Genetic Disorders: Developmental anomalies, systemic dysfunctions.
- Immunological Disorders: Allergic reactions, autoimmune flare-ups, recurrent infections.
- General: Fatigue, weakness, unexplained weight changes.
Diagnosis (Gold Standard)
Histopathological Examination of tissue biopsies/resections is the gold standard for many diseases (e.g., neoplasia, inflammatory).
- Process: Gross & microscopic examination (H&E stain).
- Ancillary Studies:
- Immunohistochemistry (IHC): Detects specific antigens.
- Molecular Diagnostics: PCR, FISH, gene sequencing for mutations.
- Cytopathology: Examination of exfoliated cells (e.g., Pap smear).
Other tools (imaging, labs) support diagnosis; histopathology confirms.
Management (First Line)
Management is disease-specific, but general principles for pathological processes include:
- Eradicating/Removing Cause: Antibiotics (infections), surgery/chemo/radiation (tumors), foreign body removal.
- Controlling Immune/Inflammatory Responses: NSAIDs, corticosteroids, immunosuppressants.
- Restoring Hemodynamic Balance: Fluid resuscitation (shock), anticoagulation (thrombosis).
- Supportive Care: Pain management, nutritional support, organ support.
- Genetic Counseling/Symptomatic Treatment: For incurable genetic disorders.
Exam Red Flags
- Necrosis vs. Apoptosis: Necrosis (pathological, cell swelling, inflammation) vs. Apoptosis (programmed, cell shrinkage, no inflammation).
- Granulomatous Inflammation: Epithelioid macrophages, giant cells; key causes: TB, Fungi, Sarcoidosis.
- Virchow's Triad for Thrombosis: Endothelial injury is the most critical component.
- Metaplasia vs. Dysplasia: Metaplasia (reversible cell type change, e.g., Barrett's esophagus). Dysplasia (disordered growth, pre-neoplastic).
- Oncogenes vs. Tumor Suppressor Genes: Oncogenes (gain-of-function, e.g., RAS) promote growth. Tumor Suppressor Genes (loss-of-function, e.g., P53) inhibit growth.
- Hypersensitivity Types: Master their mechanisms & classic examples:
- Type I (IgE, anaphylaxis).
- Type II (Abs to cell surface, AI hemolytic anemia).
- Type III (Immune complexes, SLE, post-strep GN).
- Type IV (T-cell mediated, contact dermatitis, TB test).
- TNM Staging (prognosis based on extent of spread) vs. Grading (differentiation of tumor cells).
- Hallmarks of Cancer: Sustained proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis.
Sample Practice Questions
A 45-year-old man sustains a deep laceration to his forearm while working. After initial wound care, he returns for follow-up a week later. On examination, the wound is actively healing and appears red, granular, and slightly raised. A biopsy is taken from the healing tissue. Which of the following is the predominant histological feature expected in the biopsy of this healing wound at this stage?
A 68-year-old man, 3 days post-total hip replacement surgery, suddenly experiences acute shortness of breath, pleuritic chest pain, and becomes hypotensive. His oxygen saturation drops to 85% on room air. ECG shows sinus tachycardia with right axis deviation. Physical examination reveals distended neck veins. What is the most likely pathological event that occurred in this patient?
A 45-year-old male undergoes a routine colonoscopy, which reveals hundreds of adenomatous polyps throughout his colon. His medical history includes a strong family history of early-onset colon cancer, with his father and paternal uncle diagnosed in their 40s. Genetic testing is performed and identifies a germline mutation. Which of the following genes is most likely affected in this patient?
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