Weekly Pathology Exam - March 13, 2026 (Section A: MCQs)

77 clinical MCQs in Weekly Exam: Pathology. A 51-year-old man has a blood pressure of 150/95 mm Hg. If his hypertension remains untrea

Questions, Answers & Explanations

  1. Q1. A 51-year-old man has a blood pressure of 150/95 mm Hg. If his hypertension remains untreated for years, which of the following cellular alterations would most likely be seen in his myocardium?

    Answer: Hypertrophy

    Explanation: Cardiac muscle cells are permanent cells and cannot divide; therefore, they respond to increased workload (stress) by increasing in size (hypertrophy) rather than number.

  2. Q2. A 38-year-old woman experienced severe abdominal pain with hypotension and shock. The mesentery shows focal, chalky white deposits. Which of the following events has most likely occurred?

    Answer: Fat necrosis

    Explanation: Chalky white deposits in the mesentery are characteristic of fat necrosis, often seen in acute pancreatitis where released lipases break down triglycerides into fatty acids that complex with calcium (saponification).

  3. Q3. In an experiment, cells are subjected to radiant energy (x-rays) resulting in hydrolysis of water. Which of the following cellular enzymes protects the cells from this type of injury?

    Answer: Glutathione peroxidase

    Explanation: Radiant energy creates free radicals via radiolysis of water. Glutathione peroxidase is an antioxidant enzyme that neutralizes free radicals like hydrogen peroxide.

  4. Q4. A 68-year-old woman suddenly lost consciousness. Two months later, a head CT scan showed a large cystic area in the left parietal lobe. Which pathologic process has occurred?

    Answer: Liquefactive necrosis

    Explanation: Liquefactive necrosis is the characteristic pattern of cell death in the central nervous system following ischemic injury, eventually resulting in a cystic space.

  5. Q5. Which of the following cells is most likely to have the highest telomerase activity?

    Answer: Germ cells

    Explanation: Telomerase is active in germ cells and stem cells to maintain telomere length, allowing for sustained cellular proliferation; it is absent in most somatic cells.

  6. Q6. A 23-year-old woman experiences onset of menstrual bleeding. Which process occurs in the endometrium just before the onset of bleeding?

    Answer: Apoptosis

    Explanation: Normal menstruation is triggered by the withdrawal of progesterone, leading to programmed cell death (apoptosis) of the endometrial lining.

  7. Q7. During pregnancy, which process in the breast allowed a woman to breastfeed her infant for a year?

    Answer: Hyperplasia and hypertrophy of glandular epithelium

    Explanation: Hormonal stimulation during pregnancy leads to both an increase in the number (hyperplasia) and size (hypertrophy) of the breast glandular cells to prepare for lactation.

  8. Q8. The uterus of a woman increases from 7 x 4 x 3 cm to 34 x 18 x 12 cm during pregnancy. Which cellular process contributed most to this increase?

    Answer: Myometrial hypertrophy

    Explanation: The massive enlargement of the uterus during pregnancy is primarily due to the hypertrophy of smooth muscle cells (myometrium).

  9. Q9. A ΔF508 mutation in CFTR results in a misfolded protein. In which cellular location is this protein retained/degraded?

    Answer: Endoplasmic reticulum

    Explanation: In the most common CFTR mutation (ΔF508), the misfolded protein is recognized by the quality control machinery of the Endoplasmic Reticulum and degraded before reaching the cell surface.

  10. Q10. What is the normal pH range of human blood?

    Answer: 7.35 - 7.45

    Explanation: The physiological pH of arterial blood is strictly maintained between 7.35 and 7.45.

  11. Q11. A COPD patient has pH 7.28, PaCO2 58 mmHg, and HCO3- 26 mEq/L. What is the primary acid-base disorder?

    Answer: Respiratory Acidosis

    Explanation: A low pH (<7.35) indicates acidosis, and a high PaCO2 ( 45 mmHg) indicates a respiratory cause.

  12. Q12. Which buffer system is the PRIMARY extracellular buffer system in the body?

    Answer: Bicarbonate buffer

    Explanation: The Bicarbonate-Carbonic acid system is the most significant ECF buffer due to its high concentration and the ability of the lungs/kidneys to regulate it.

  13. Q13. Which acid-base disorder is addressed by Kussmaul respirations in a diabetic patient?

    Answer: Metabolic Acidosis

    Explanation: Kussmaul breathing (deep, rapid) is a compensatory response to metabolic acidosis (DKA) to wash out CO2 and raise pH.

  14. Q14. What is the normal range for arterial PaCO2?

    Answer: 35 - 45 mmHg

    Explanation: The normal partial pressure of arterial carbon dioxide (PaCO2) is 35–45 mmHg.

  15. Q15. A patient with severe vomiting develops metabolic alkalosis. Which mechanism explains this?

    Answer: Loss of gastric HCL

    Explanation: Vomiting causes the loss of hydrochloric acid from the stomach, leading to an increase in blood bicarbonate levels (metabolic alkalosis).

  16. Q16. What is the normal range for serum bicarbonate (HCO3-)?

    Answer: 22 - 28 mEq/L

    Explanation: The standard range for serum bicarbonate is 22 to 28 mEq/L (sometimes cited as 21-27 depending on the lab).

  17. Q17. Which enzyme in renal tubular cells catalyzes the reaction between CO2 and water?

    Answer: Carbonic anhydrase

    Explanation: Carbonic anhydrase (CA) is essential for the rapid conversion of CO2 and water into carbonic acid, facilitating H+ secretion and HCO3- reabsorption.

  18. Q18. ABG results: pH 7.50, PaCO2 30 mmHg, HCO3- 23 mEq/L. What is the diagnosis?

    Answer: Respiratory Alkalosis

    Explanation: High pH ( 7.45) indicates alkalosis; low PaCO2 (<35 mmHg) indicates the cause is respiratory.

  19. Q19. What is the formula for calculating anion gap?

    Answer: Na - (Cl + HCO3)

    Explanation: The Anion Gap = Sodium - (Chloride + Bicarbonate). It identifies unmeasured anions in metabolic acidosis.

  20. Q20. Which condition is characterized by an increased anion gap metabolic acidosis?

    Answer: Diabetic Ketoacidosis

    Explanation: DKA causes accumulation of ketoacids (unmeasured anions), such as beta-hydroxybutyrate, which increases the anion gap.

  21. Q21. A patient at high altitude develops dizziness and tingling. Which acid-base disorder is most likely?

    Answer: Respiratory Alkalosis

    Explanation: Lower oxygen levels at altitude cause hyperventilation, which lowers PaCO2 and leads to respiratory alkalosis.

  22. Q22. According to Knudson's hypothesis, what distinguishes familial retinoblastoma from sporadic cases?

    Answer: Familial cases inherit one 'hit' and require only one somatic mutation

    Explanation: Knudson's two-hit hypothesis states that in familial cases, one mutated RB allele is inherited (first hit), so only one somatic mutation (second hit) is needed for tumor development.

  23. Q23. Which event would MOST effectively prevent E2F-mediated transcription of S-phase genes?

    Answer: Hypophosphorylated RB binding to E2F

    Explanation: Active (hypophosphorylated) RB binds to the E2F transcription factor, sequestering it and preventing the transition to S-phase.

  24. Q24. A tumor shows constitutive activation of growth signaling. Which mechanism is LEAST likely responsible?

    Answer: Up-regulation of p16

    Explanation: p16 is a CDK inhibitor (tumor suppressor). Up-regulation would inhibit growth signaling, whereas the other options promote it.

  25. Q25. In CML, the BCR-ABL fusion protein drives malignancy primarily by:

    Answer: Constitutive tyrosine kinase activity

    Explanation: The translocation t(9;22) creates the BCR-ABL fusion gene, which encodes a protein with permanent tyrosine kinase activity that drives cell proliferation.

  26. Q26. Tumor cells continue dividing despite contact with neighboring cells. Which protein's function is most likely compromised?

    Answer: E-cadherin (NF2/Merlin pathway)

    Explanation: Contact inhibition is mediated by E-cadherin and the NF2 gene product (Merlin). Loss of this signaling allows cells to pile up and continue dividing.

  27. Q27. Why must BOTH copies of a tumor suppressor gene be lost for tumor development, unlike oncogenes?

    Answer: One functional tumor suppressor allele is usually sufficient for control

    Explanation: Tumor suppressor genes (like RB) generally follow a recessive pattern at the cellular level; as long as one allele is functional, it can regulate the cell cycle.

  28. Q28. Which statement BEST explains why p53 is called the 'guardian of the genome'?

    Answer: It induces cell cycle arrest, DNA repair, or apoptosis in response to damage

    Explanation: p53 acts as a transcription factor that monitors DNA integrity; it triggers arrest for repair or apoptosis if damage is irreparable.

  29. Q29. In late-stage tumors, TGF-β signaling often promotes metastasis. This occurs because:

    Answer: Downstream growth-inhibitory signals are lost but EMT pathways remain

    Explanation: While TGF-β is normally growth-inhibitory, many cancers lose the inhibitory components of the pathway but use the signaling to drive Epithelial-Mesenchymal Transition (EMT).

  30. Q30. A patient with Li-Fraumeni syndrome has an inherited defect involving:

    Answer: TP53

    Explanation: Li-Fraumeni syndrome is characterized by an inherited germline mutation in the TP53 gene, leading to various early-onset cancers.

  31. Q31. During mitosis, which cyclin-CDK complex is responsible for nuclear membrane breakdown?

    Answer: Cyclin B / CDK1

    Explanation: Cyclin B / CDK1 (also known as Mitosis-Promoting Factor) triggers the transition from G2 to M phase and the breakdown of the nuclear envelope.

  32. Q32. Which scenario would MOST likely result in failed DNA damage repair followed by apoptosis?

    Answer: Normal p53 and massive double-strand breaks

    Explanation: If DNA damage is too severe, normal p53 directs the cell toward apoptosis via BAX/BAK activation.

  33. Q33. A tumor shows loss of APC function. What is the immediate downstream effect?

    Answer: Accumulation of β-catenin in the nucleus

    Explanation: APC normally marks β-catenin for degradation. When APC is lost, β-catenin accumulates and moves to the nucleus to promote growth-gene transcription.

  34. Q34. In VHL syndrome, which molecular mechanism explains increased angiogenesis?

    Answer: Stabilization of HIF-1α leading to VEGF production

    Explanation: VHL protein normally facilitates degradation of HIF-1α. Loss of VHL allows HIF-1α to accumulate, even in normoxia, driving the expression of VEGF.

  35. Q35. A tumor fails to grow beyond 1.8 mm. Which explains this phenomenon?

    Answer: Lack of angiogenesis (angiogenic switch not yet occurred)

    Explanation: Without the recruitment of blood vessels (angiogenesis), tumors cannot grow beyond 1-2 mm because they rely on simple diffusion for oxygen and nutrients.

  36. Q36. During tumor angiogenesis, MMP-9 performs which function?

    Answer: Degrades ECM and releases sequestered VEGF

    Explanation: Matrix Metalloproteinase-9 (MMP-9) degrades the ECM, physically clearing a path for vessels and releasing bound angiogenic factors like VEGF.

  37. Q37. Which characteristic is MOST likely observed in tumor vasculature compared to normal capillaries?

    Answer: Leaky and tortuous vessels

    Explanation: Tumor vessels are notoriously disorganized, tortuous, and leaky due to sustained, imbalanced production of pro-angiogenic factors.

  38. Q38. How does normal p53 exert an anti-angiogenic effect?

    Answer: Both A and B

    Explanation: p53 inhibits angiogenesis both by upregulating inhibitors like thrombospondin-1 and by repressing the expression of VEGF.

  39. Q39. Angiostatin, endostatin, and vasculostatin share what common characteristic?

    Answer: They are fragments of larger proteins (like plasminogen or collagen)

    Explanation: These are naturally occurring angiogenesis inhibitors derived from the proteolytic cleavage of precursors (e.g., Angiostatin from Plasminogen).

  40. Q40. Newly formed endothelial cells in tumor vessels contribute to tumor growth by:

    Answer: Secreting PDGF and IGF

    Explanation: Endothelial cells provide paracrine growth factors like PDGF and Insulin-like Growth Factors (IGFs) that directly stimulate the growth of adjacent tumor cells.

  41. Q41. At which stage of the metastatic cascade do MOST tumor cells fail?

    Answer: Survival in the circulation

    Explanation: Metastasis is an inefficient process; most cells are destroyed in the circulation by shear stress or immune cells (NK cells) before they can extravasate.

  42. Q42. Loss of E-cadherin function promotes metastasis by:

    Answer: Reducing cell-cell adhesion and releasing β-catenin signaling

    Explanation: E-cadherin loss allows cells to detach from each other (losing cohesiveness) and can release β-catenin, triggering growth-promoting gene expression.

  43. Q43. A breast cancer sample shows high expression of CXCR4 and CCR7. To which organs is this tumor MOST likely to metastasize?

    Answer: Lymph nodes and Lungs (where ligands CXCL12 and CCL21 are expressed)

    Explanation: Many tumors express chemokine receptors that guide them to specific 'homing' sites where the corresponding chemokines are secreted.

  44. Q44. Which is the FIRST step of ECM invasion by tumor cells?

    Answer: Loosening of cell-cell junctions

    Explanation: The order is: 1. Loosening of cell-cell junctions, 2. Degradation of ECM, 3. Attachment, 4. Migration. (Note: Loosening/detachment is often considered the initiating event of the process).

  45. Q45. Cleavage of collagen IV and laminin by MMPs serves what purpose beyond degradation?

    Answer: Creates cryptic sites that promote cell migration

    Explanation: MMPs can reveal 'cryptic' binding sites on cleaved ECM proteins that bind to integrin receptors on tumor cells and stimulate migration.

  46. Q46. Which lipoprotein transports dietary triglycerides from the intestines to tissues?

    Answer: Chylomicrons

    Explanation: Chylomicrons are formed in the intestinal mucosa to transport dietary (exogenous) lipids into the circulation.

  47. Q47. What is the primary function of HDL cholesterol?

    Answer: Reverse cholesterol transport (from tissues to liver)

    Explanation: HDL is considered 'good' cholesterol because it picks up cholesterol from peripheral tissues and returns it to the liver.

  48. Q48. Which enzyme breaks down triglycerides in adipose tissue during lipolysis?

    Answer: Hormone-Sensitive Lipase

    Explanation: Hormone-sensitive lipase (HSL) mobilizes fatty acids from stored adipose tissue triglycerides.

  49. Q49. What happens to VLDL as it loses triglycerides to the tissues?

    Answer: It transforms into IDL and then LDL

    Explanation: The removal of triglycerides from VLDL by lipoprotein lipase results in the formation of Intermediate Density Lipoprotein (IDL) and eventually LDL.

  50. Q50. Which hormone promotes lipogenesis and inhibits lipolysis?

    Answer: Insulin

    Explanation: Insulin is an anabolic hormone that promotes the storage of fat (lipogenesis) and inhibits the breakdown of fat (lipolysis).

  51. Q51. What is the genetic defect in familial hypercholesterolemia (Type IIa)?

    Answer: Deficiency of LDL receptors

    Explanation: Familial hypercholesterolemia is caused by mutations in the LDL receptor gene, leading to high levels of circulating LDL.

  52. Q52. Which clinical sign consists of yellowish nodules on the Achilles tendon?

    Answer: Tendinous xanthoma

    Explanation: Tendinous xanthomas are lipid deposits found in tendons, very commonly the Achilles tendon, in patients with severe hypercholesterolemia.

  53. Q53. What condition can severe hypertriglyceridemia (e.g. 1000 mg/dL) lead to?

    Answer: Acute Pancreatitis

    Explanation: Extremely high triglyceride levels are a well-known risk factor for developing acute pancreatitis.

  54. Q54. What is lipemia retinalis?

    Answer: Milky appearance of retinal vessels in high TG levels

    Explanation: Lipemia retinalis occurs when triglyceride levels exceed 2000 mg/dL, causing retinal vessels to appear white or milky.

  55. Q55. Which statin is commonly used to lower LDL cholesterol?

    Answer: Atorvastatin

    Explanation: Statins (HMG-CoA reductase inhibitors) like atorvastatin are the first-line treatment for lowering LDL.

  56. Q56. What is the primary metabolic pathway for fatty acid breakdown in mitochondria?

    Answer: Beta-oxidation

    Explanation: Beta-oxidation is the process by which fatty acids are broken down into acetyl-CoA units to enter the TCA cycle.

  57. Q57. Which apolipoprotein defect is responsible for familial dysbetalipoproteinemia (Type III)?

    Answer: ApoE

    Explanation: Type III Hyperlipoproteinemia results from inheritance of the ApoE2 isoform, which has low affinity for LDL and Remnant receptors.

  58. Q58. The primary difference between Quality Control (QC) and Quality Assurance (QA) is:

    Answer: QC is a part of QA

    Explanation: QA is an all-encompassing system (pre-analytical, analytical, post-analytical), while QC refers specifically to the monitoring of the analytical process.

  59. Q59. Which chart is most commonly used in Internal Quality Control?

    Answer: Levey-Jennings chart

    Explanation: Levey-Jennings charts are used to plot QC values over time to identify shifts, trends, and random errors.

  60. Q60. In the pre-analytical phase, which factor is MOST critical?

    Answer: Proper patient identification and sample labeling

    Explanation: Most laboratory errors occur in the pre-analytical phase, frequently involving misidentification or improper specimen collection.

  61. Q61. Positive controls in quality control are used to:

    Answer: Ensure the reagents are working and the assay can detect the analyte

    Explanation: Positive controls contain a known amount of analyte and are used to confirm that the assay is performing correctly.

  62. Q62. Which statistical rules are commonly applied to control chart data?

    Answer: Westgard rules

    Explanation: Westgard rules are a set of multi-rule criteria used to determine if an analytical run is 'in control' or should be rejected.

  63. Q63. External Quality Assessment (EQA) primarily serves to:

    Answer: Compare laboratory performance with other labs (inter-laboratory accuracy)

    Explanation: EQA (Proficiency Testing) involves an external agency sending 'blind' samples to multiple labs to compare their results and ensure standardization.

  64. Q64. The analytical phase of quality control primarily focuses on:

    Answer: The actual testing process (reagents, equipment, calibration)

    Explanation: The analytical phase encompasses all activities involved in the actual measurement of the analyte.

  65. Q65. Certified Reference Materials (CRMs) are primarily used for:

    Answer: Standardizing/Calibrating instruments

    Explanation: CRMs have a highly accurate, certified value and are used to calibrate assays to ensure accuracy (traceability).

  66. Q66. Which phase of quality control is responsible for the highest percentage of laboratory errors?

    Answer: Pre-analytical phase

    Explanation: Statistics consistently show that roughly 60-70% of lab errors occur before the sample even reaches the analyzer.

  67. Q67. All are granulomatous diseases EXCEPT:

    Answer: Staphylococcal abscess

    Explanation: A Staphylococcal abscess is a localized collection of pus (suppurative/purulent inflammation), not a granulomatous response.

  68. Q68. The following are chemical mediators of chronic inflammation EXCEPT:

    Answer: Histamine

    Explanation: Histamine is a major mediator of acute inflammation (vasodilation and increased permeability), while the others are involved in chronic signaling.

  69. Q69. The most important cell in chronic inflammation is:

    Answer: Macrophage

    Explanation: Macrophages are the hallmark cells of chronic inflammation, responsible for phagocytosis and cytokine secretion.

  70. Q70. The following are functions of cellular adaptations EXCEPT:

    Answer: Promoting carcinogenesis

    Explanation: Cellular adaptations (atrophy, hypertrophy, etc.) are intended to preserve cell viability; while some (like metaplasia) increase the risk of cancer, it is not their function.

  71. Q71. A tuberculous granuloma is comprised of:

    Answer: Central caseous necrosis, epithelioid cells, and Langhans giant cells

    Explanation: The classic TB granuloma is a 'caseating granuloma' featuring central necrosis surrounded by activated macrophages (epithelioid cells) and giant cells.

  72. Q72. Events surrounding chronic inflammation include all EXCEPT:

    Answer: Transient vasoconstriction

    Explanation: Transient vasoconstriction is an immediate, very brief response in acute inflammation; chronic inflammation is characterized by destruction and repair (fibrosis).

  73. Q73. White blood cells attach to endothelial cells in the inflammatory process using surface receptors called:

    Answer: Selectins and Integrins

    Explanation: Rolling is mediated by selectins, and firm adhesion is mediated by integrins on the leukocyte surface interacting with ligands on the endothelium.

  74. Q74. A white blood cell that is involved in the acute inflammatory response is:

    Answer: Neutrophil

    Explanation: Neutrophils are the primary 'first responders' and hallmark cells of acute inflammation.

  75. Q75. In the process of phagocytosis, the oxidative arm produces the following EXCEPT:

    Answer: Glutathione

    Explanation: Glutathione is an antioxidant used to neutralize reactive oxygen species; superoxide, H2O2, and hypochlorite are the actual 'weapons' (oxidants).

  76. Q76. Wound healing involves all the processes outlined below EXCEPT:

    Answer: Metaplasia

    Explanation: The three phases of wound healing are inflammation, proliferation, and maturation/remodeling. Metaplasia is a cellular adaptation, not a step in normal healing.

  77. Q77. Wound healing is affected by all of the following EXCEPT:

    Answer: Hair color

    Explanation: Factors affecting wound healing include local factors (infection, blood supply) and systemic factors (nutrition, steroids, diabetes), but not genetic traits like hair color.

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