Practice 5 structured short- and long-answer medical questions on Weekly Pathology Exam - May 15, 2026 (Sections B & C). Review model answers for exam revision.
Answer: Mallory-Denk hyaline bodies are eosinophilic, intracytoplasmic inclusions found primarily in hepatocytes. Morphologically, they are irregular to amorphous, glassy in appearance, and stain intensely with eosin. They are often found in zones of hepatocellular injury. Their significance lies in their association with chronic liver diseases, particularly alcoholic liver disease, but also non-alcoholic steatohepatitis (NASH), Wilson's disease, and alpha-1-antitrypsin deficiency. Their presence indicates hepatocellular stress and can correlate with the severity of liver injury and prognosis.
Answer: Apoptosis is programmed cell death, a highly regulated process involving the activation of specific enzymes (caspases) that lead to cell shrinkage, chromatin condensation, and formation of apoptotic bodies, which are then phagocytosed by adjacent cells. Necrosis is accidental cell death resulting from acute injury, characterized by cell swelling, membrane lysis, leakage of cellular contents, and an inflammatory response. Two key distinguishing features are: 1. Apoptosis is an active, energy-dependent process involving specific molecular pathways, whereas necrosis is a passive process driven by external injury. 2. Apoptosis leads to intact apoptotic bodies that are cleared without inflammation, while necrosis causes cell lysis and triggers a significant inflammatory reaction.
Answer: Metaplasia is a reversible change in which one adult cell type is replaced by another adult cell type. It is typically an adaptive response to chronic irritation or stress. Example: Squamous metaplasia in the bronchial epithelium of a smoker, where ciliated columnar epithelium is replaced by stratified squamous epithelium. Dysplasia refers to a precancerous condition in which there is a loss of normal cellular arrangement and differentiation, characterized by cellular atypia (variation in size, shape, and nuclear morphology). It is often a precursor to invasive carcinoma. Example: Cervical dysplasia (CIN), which can progress to cervical squamous cell carcinoma.
Answer: Amyloidosis is a condition characterized by the extracellular deposition of misfolded proteins, known as amyloid fibrils, in various tissues and organs. These deposits are typically insoluble, beta-pleated sheet structures that can lead to organ dysfunction. The three main types of amyloid deposits based on their composition are: 1. AL amyloid (light chain amyloid): derived from immunoglobulin light chains, commonly seen in multiple myeloma and other plasma cell dyscrasias. 2. AA amyloid (serum amyloid A protein): a reactive amyloid associated with chronic inflammatory conditions. 3. ATTR amyloid (transthyretin amyloid): can be hereditary or acquired, affecting the heart and nerves.
Answer: Gross Examination: The liver may be enlarged or shrunken with a nodular surface. HCC can present as a single large mass, multiple nodules, or a diffuse infiltrative growth pattern. The tumor may appear variegated, with areas of necrosis, hemorrhage, and fibrosis. Invasion into the portal vein or hepatic veins may be evident. Microscopic Examination: Histologically, HCC is characterized by malignant hepatocytes arranged in various architectural patterns, including trabecular, solid, pseudoglandular, and sarcomatous. Key features of malignancy include: 1. Cellular atypia: Variation in cell size and shape (pleomorphism), enlarged and hyperchromatic nuclei, prominent nucleoli, and increased nuclear-to-cytoplasmic ratio. 2. Architectural disarray: Loss of normal hepatic lobular architecture, with thick trabeculae of tumor cells, sinusoids compressed or absent, and increased mitotic activity (often atypical mitoses). 3. Invasion: Evidence of vascular invasion (intravascular tumor cells within portal or hepatic veins) is a critical diagnostic and prognostic feature. Direct invasion of surrounding liver parenchyma is also present. 4. Alpha-fetoprotein (AFP): While not a morphological feature on biopsy, elevated AFP levels are a strong serological marker that correlates with HCC and often with the tumor burden. In the context of chronic hepatitis B infection, pathogenesis of HCC involves: 1. Chronic inflammation and fibrosis: Persistent HBV infection leads to chronic inflammation, hepatocyte injury, regeneration, and eventually fibrosis and cirrhosis. Cirrhosis is a major risk factor for HCC. 2. Viral integration: HBV DNA can integrate into the host hepatocyte genome. This integration can disrupt tumor suppressor genes (e.g., p53, p16) and activate oncogenes (e.g., Wnt pathway), promoting uncontrolled cell proliferation. 3. Genetic mutations: Accumulation of genetic mutations in hepatocytes due to chronic inflammation, oxidative stress, and viral integration contributes to malignant transformation. 4. Immune evasion: HBV can interfere with the host immune response, allowing infected cells to survive and proliferate. 5. Regenerative nodules: Repeated cycles of injury and regeneration in a cirrhotic liver can lead to the development of dysplastic nodules, which are precursors to HCC.