Practice 5 structured short- and long-answer medical questions on Weekly Pathology Exam - October 9, 2026 (Sections B & C). Review model answers for exam rev...
Answer: Hyperplasia is an increase in the number of cells in an organ or tissue, leading to an increase in size. Example: Endometrial hyperplasia in response to unopposed estrogen. Hypertrophy is an increase in the size of individual cells, leading to an increase in the size of the organ or tissue. Example: Cardiac hypertrophy in a patient with long-standing hypertension. Both processes are adaptive responses to increased functional demand or hormonal stimulation. Key distinction: Hyperplasia involves cell division, hypertrophy involves cell enlargement.
Answer: Benign neoplasms typically exhibit well-defined borders, are encapsulated, and show minimal cellular pleomorphism (variation in cell size and shape) and nuclear atypia (abnormal nuclear morphology). Mitotic figures are rare and normal. Malignant neoplasms, conversely, often have irregular borders, invade surrounding tissues, and display significant cellular pleomorphism and nuclear atypia. Mitotic figures are common, often atypical, and may be absent in well-differentiated tumors. Differentiated features are typically retained in benign tumors, while malignant tumors show loss of differentiation (anaplasia).
Answer: Atherosclerosis is a chronic inflammatory disease characterized by the buildup of atherosclerotic plaques in the arteries. The pathogenesis begins with endothelial dysfunction, often due to risk factors like hyperlipidemia, hypertension, or smoking. This leads to increased permeability of the endothelium, allowing LDL cholesterol to enter the arterial wall and undergo oxidation. Oxidized LDL triggers an inflammatory response, recruiting macrophages which engulf lipids to form foam cells. Smooth muscle cells proliferate and migrate to the plaque, contributing to its growth. Fibrous cap formation and calcification further characterize the plaque. Key risk factors include: hyperlipidemia (especially elevated LDL cholesterol), hypertension, smoking, diabetes mellitus, obesity, family history, and age.
Answer: Necrosis is an unprogrammed form of cell death resulting from irreversible injury, characterized by cell swelling, membrane rupture, and leakage of cellular contents, triggering an inflammatory response. Morphological features include eosinophilia of cytoplasm and nuclear pyknosis, karyorrhexis, and karyolysis. Apoptosis, conversely, is an programmed, energy-dependent process of cell suicide, characterized by cell shrinkage, chromatin condensation, nuclear fragmentation, and formation of apoptotic bodies, without inducing inflammation. It is mediated by caspases. Morphologically, cells become smaller, the nucleus condenses (pyknosis), and the cell fragments into membrane-bound vesicles (apoptotic bodies).
Answer: Inflammation is a protective response by the body to injury or infection. It can be broadly categorized into acute and chronic inflammation. **Acute Inflammation:** This is a rapid, short-lived response to harmful stimuli like pathogens or tissue damage. It aims to eliminate the initial cause of cell injury, clear out necrotic cells and tissues, and initiate tissue repair. * **Vascular Events:** * **Vasodilation:** Mediated by histamine and nitric oxide, leading to increased blood flow to the injured area, causing redness (rubor) and heat (calor). * **Increased Vascular Permeability:** Post-capillary venules become leaky due to endothelial cell contraction (histamine, bradykinin) or junctions widening. This allows plasma proteins (like antibodies and complement) and leukocytes to escape into the extravascular space, causing edema (tumor) and pain (dolor). * **Stasis:** As blood flow slows, leukocytes marginate along the vessel walls. * **Cellular Events:** * **Leukocyte (Neutrophil) Recruitment:** Mediated by adhesion molecules (selectins, integrins) expressed on endothelium and leukocytes. * **Margination and Rolling:** Leukocytes slow down and attach loosely to the endothelium. * **Adhesion:** Firm attachment of leukocytes to endothelium. * **Diapedesis/Transmigration:** Leukocytes squeeze through the gaps between endothelial cells into the tissue. * **Chemotaxis:** Leukocytes migrate towards the site of injury along a chemical gradient (chemokines, complement fragments). * **Phagocytosis:** Leukocytes engulf and destroy microorganisms and cellular debris. Neutrophils are the primary responders in acute inflammation. * **Key Mediators of Acute Inflammation:** Histamine, kinins (bradykinin), prostaglandins, leukotrienes, complement system components, cytokines (TNF-α, IL-1). * **Clinical Scenario for Acute Inflammation:** Appendicitis. The initial insult (e.g., obstruction) triggers a rapid inflammatory response characterized by neutrophil infiltration, vasodilation, edema, and pain, leading to the typical symptoms of appendicitis. **Chronic Inflammation:** This is a prolonged response that occurs when the acute inflammatory response is insufficient to eliminate the stimulus, or when the stimulus is persistent. It is characterized by the simultaneous occurrence of active inflammation, tissue destruction, and attempts at repair. * **Cellular Players:** * **Mononuclear Cells:** Macrophages are the central cells, derived from monocytes. They are involved in phagocytosis, antigen presentation, and cytokine production. * **Lymphocytes:** T cells and B cells play crucial roles in specific immune responses and antibody production. * **Plasma Cells:** Differentiated B cells that produce antibodies. * **Fibroblasts:** Involved in tissue repair and fibrosis. * **Epithelioid Cells and Giant Cells:** Formed from activated macrophages, characteristic of granulomatous inflammation. * **Key Mediators of Chronic Inflammation:** Cytokines (TNF-α, IL-1, IL-6, IL-12, IFN-γ), chemokines, growth factors (TGF-β). * **Distinguishing Features of Chronic Inflammation:** * **Infiltration with mononuclear cells:** Macrophages, lymphocytes, plasma cells. * **Tissue destruction:** Mediated by enzymes released from inflammatory cells. * **Attempts at healing:** Angiogenesis (new blood vessel formation) and fibrosis (scarring). * **Clinical Scenario for Chronic Inflammation:** Rheumatoid Arthritis. This autoimmune disease involves persistent inflammation of the synovial joints. The chronic inflammation is characterized by infiltration of mononuclear cells (lymphocytes, macrophages), leading to synovial proliferation, cartilage destruction, and joint deformity over time. It is driven by cytokines and T-cell activation.