Weekly Pathology Exam - May 1, 2026 (Section A: MCQs)

35 clinical MCQs in Weekly Exam: Pathology. Which blood type is considered the universal donor for red blood cells?

Questions, Answers & Explanations

  1. Q1. Which blood type is considered the universal donor for red blood cells?

    Answer: Type O

    Explanation: Type O red blood cells lack A and B antigens, and Type O Rh-negative (O-) red blood cells also lack the Rh antigen, making them compatible with recipients of all blood types in emergencies when specific crossmatching is not feasible, particularly for red blood cells.

  2. Q2. Which blood type is considered the universal recipient for red blood cells?

    Answer: Type AB

    Explanation: Individuals with Type AB blood have both A and B antigens on their red blood cells and therefore do not produce anti-A or anti-B antibodies. This allows them to receive red blood cells from Type A, Type B, Type AB, and Type O donors without an immediate ABO incompatibility reaction.

  3. Q3. What is the main function of plasma in blood transfusions?

    Answer: To provide clotting factors and proteins

    Explanation: Plasma, particularly fresh frozen plasma (FFP), is transfused to replace clotting factors in patients with coagulopathies or significant bleeding, as well as to provide other essential plasma proteins.

  4. Q4. Which of the following is a contraindication for blood transfusion?

    Answer: Fluid overload without signs of severe anemia

    Explanation: Fluid overload is a relative contraindication, especially if the patient is not severely anemic or actively bleeding, as a transfusion would exacerbate the condition. The other options represent common indications for transfusion.

  5. Q5. The term 'crossmatch' in blood transfusion refers to:

    Answer: Mixing recipient's serum with donor's red blood cells to check for agglutination

    Explanation: Crossmatching involves mixing the recipient's serum with donor red blood cells to detect any antibodies in the recipient's plasma that would react with antigens on the donor red blood cells, ensuring compatibility beyond ABO/Rh typing and antibody screening.

  6. Q6. Which of the following is a possible complication of blood transfusion?

    Answer: Hypocalcemia

    Explanation: Citrate, an anticoagulant used in blood products, can chelate calcium, potentially leading to hypocalcemia, especially with rapid or large volume transfusions.

  7. Q7. Which antigen is present on the surface of red blood cells in Type B blood?

    Answer: B antigen

    Explanation: Type B blood is characterized by the presence of B antigens on the surface of red blood cells and anti-A antibodies in the plasma.

  8. Q8. What is the most important factor in determining blood compatibility between a donor and recipient?

    Answer: ABO and Rh blood type matching

    Explanation: ABO and Rh blood group matching are critical to prevent immediate and severe hemolytic transfusion reactions caused by pre-existing antibodies in the recipient.

  9. Q9. Which of the following is the primary concern in transfusing Rh-negative blood to an Rh-positive patient?

    Answer: It is generally safe and causes no significant issue.

    Explanation: Transfusing Rh-negative blood to an Rh-positive patient is generally safe because the Rh-positive recipient does not have anti-Rh antibodies and will not react to the absence of the Rh antigen. The primary concern is Rh-positive blood to an Rh-negative patient, which can cause alloimmunization.

  10. Q10. What is the role of the Rh factor in blood transfusion?

    Answer: It is a major antigen that can cause hemolytic reactions if mismatched.

    Explanation: The Rh factor (D antigen) is a significant antigen after ABO, and mismatching (e.g., Rh-positive blood to an Rh-negative recipient who has been previously sensitized) can lead to severe hemolytic transfusion reactions.

  11. Q11. Which of the following components is typically transfused for patients with low platelet counts?

    Answer: Platelets

    Explanation: Platelet transfusions are administered to patients with thrombocytopenia (low platelet counts) or dysfunctional platelets to prevent or treat bleeding.

  12. Q12. Which of the following should be monitored during a blood transfusion to detect possible complications?

    Answer: Patient's temperature, heart rate, blood pressure, and respiratory rate

    Explanation: Vital signs (temperature, heart rate, blood pressure, respiratory rate) are crucial to monitor during a transfusion as sudden changes can indicate a transfusion reaction, such as fever, tachycardia, hypotension, or dyspnea.

  13. Q13. What is the normal pH range of human blood?

    Answer: 7.35-7.45

    Explanation: The human body maintains a very narrow and tightly regulated blood pH range of 7.35 to 7.45 to ensure optimal enzyme function and metabolic processes.

  14. Q14. A patient with chronic obstructive pulmonary disease (COPD) has ABG results showing pH 7.28, PaCO2 58 mmHg, and HCO3- 26 mEq/L. What is the primary acid-base disorder?

    Answer: Respiratory acidosis

    Explanation: The pH of 7.28 indicates acidosis. The elevated PaCO2 (normal 35-45 mmHg) indicates respiratory involvement. The HCO3- of 26 mEq/L (normal 22-26 mEq/L) is in the normal range, indicating that the primary problem is respiratory and there is some, but not full, metabolic compensation. This points to an acute or partially compensated respiratory acidosis.

  15. Q15. Which buffer system is the PRIMARY extracellular buffer system in the body?

    Answer: Bicarbonate-carbonic acid buffer system

    Explanation: The bicarbonate-carbonic acid buffer system is the most important extracellular buffer, linking directly to the respiratory system (CO2 excretion) and renal system (HCO3- reabsorption/excretion).

  16. Q16. A diabetic patient presents with rapid, deep breathing (Kussmaul respirations). Which acid-base disorder is this compensatory mechanism addressing?

    Answer: Metabolic acidosis

    Explanation: Kussmaul respirations are a compensatory mechanism (hyperventilation) to blow off CO2 and reduce carbonic acid, thereby increasing pH, in response to metabolic acidosis, commonly seen in diabetic ketoacidosis.

  17. Q17. What is the normal range for arterial PaCO2?

    Answer: 35-45 mmHg

    Explanation: The normal arterial partial pressure of carbon dioxide (PaCO2) is 35-45 mmHg, reflecting the efficiency of alveolar ventilation in removing CO2.

  18. Q18. A patient with severe vomiting develops metabolic alkalosis. Which mechanism explains this?

    Answer: Loss of gastric acid (HCl)

    Explanation: Severe vomiting leads to the loss of hydrogen chloride (HCl) from the stomach. This loss of acid causes an increase in serum bicarbonate levels, resulting in metabolic alkalosis.

  19. Q19. What is the normal range for serum bicarbonate (HCO3-)?

    Answer: 22-26 mEq/L

    Explanation: The normal serum bicarbonate concentration is 22-26 mEq/L, playing a crucial role in the bicarbonate buffer system.

  20. Q20. Which enzyme in renal tubular cells catalyzes the reaction between CO2 and water to form carbonic acid?

    Answer: Carbonic anhydrase

    Explanation: Carbonic anhydrase rapidly catalyzes the reversible reaction of carbon dioxide and water to form carbonic acid (H2CO3), which then dissociates into H+ and HCO3-. This is vital for acid-base balance in the kidneys.

  21. Q21. A patient has ABG results: pH 7.50, PaCO2 30 mmHg, HCO3- 23 mEq/L. What is the diagnosis?

    Answer: Respiratory alkalosis

    Explanation: The pH of 7.50 indicates alkalosis. The low PaCO2 (normal 35-45 mmHg) indicates respiratory involvement, as blowing off CO2 reduces acidity. The HCO3- of 23 mEq/L (normal 22-26 mEq/L) is within the normal range, indicating that the primary problem is respiratory and there is no significant metabolic compensation, pointing to acute respiratory alkalosis.

  22. Q22. What is the formula for calculating anion gap?

    Answer: Na+ - (Cl- + HCO3-)

    Explanation: The anion gap is calculated as [Na+] - ([Cl-] + [HCO3-]). It represents the concentration of unmeasured anions in the plasma, such as phosphates, sulfates, and organic acids.

  23. Q23. Which condition is characterized by an increased anion gap metabolic acidosis?

    Answer: Diabetic ketoacidosis

    Explanation: Diabetic ketoacidosis (DKA) is a classic cause of increased anion gap metabolic acidosis due to the accumulation of ketone bodies (beta-hydroxybutyrate, acetoacetate), which are unmeasured anions.

  24. Q24. A patient at high altitude develops dizziness and tingling in the extremities. Which acid-base disorder is most likely?

    Answer: Respiratory alkalosis

    Explanation: At high altitudes, the decreased partial pressure of oxygen (hypoxia) stimulates hyperventilation. This leads to excessive expulsion of CO2, causing a decrease in PaCO2 and an increase in pH, resulting in respiratory alkalosis. Dizziness and tingling (paresthesias) are common symptoms.

  25. Q25. A patient with von Hippel-Lindau (VHL) syndrome develops multiple tumors. Which molecular mechanism BEST explains the increased angiogenesis in these tumors?

    Answer: Stabilization of HIF-1alpha leading to increased VEGF production

    Explanation: The VHL gene product normally functions as a ubiquitin ligase component, targeting hypoxia-inducible factor 1-alpha (HIF-1alpha) for degradation. In VHL syndrome, a mutated VHL gene leads to stabilized HIF-1alpha, even under normoxic conditions, which then upregulates pro-angiogenic factors like VEGF, promoting tumor angiogenesis.

  26. Q26. A tumor reaches 1.8 mm in diameter but fails to grow further for several years. Which statement BEST explains this phenomenon?

    Answer: The tumor has outgrown its blood supply and failed to induce angiogenesis.

    Explanation: Tumors cannot grow beyond 1-2 mm in diameter without developing their own blood supply through angiogenesis. If angiogenesis fails, the tumor becomes dormant due to lack of oxygen and nutrients.

  27. Q27. During tumor angiogenesis, MMP-9 performs multiple functions. Which combination of activities is CORRECT?

    Answer: Degrades basement membrane and activates VEGF.

    Explanation: Matrix metalloproteinase-9 (MMP-9) plays a crucial role in angiogenesis by degrading components of the extracellular matrix (like the basement membrane), which allows endothelial cells to migrate and form new vessels. It can also release matrix-bound growth factors, including certain forms of VEGF, making them bioavailable.

  28. Q28. A researcher studies newly formed tumor vessels and compares them to normal capillaries. Which characteristic would MOST likely be observed in tumor vasculature?

    Answer: Leakiness and abnormal pericyte coverage

    Explanation: Tumor vasculature is typically disorganized, tortuous, and highly permeable (leaky) due to defective endothelial cell junctions and incomplete or absent pericyte coverage. This leads to inefficient and erratic blood flow.

  29. Q29. Normal p53 plays a role in preventing angiogenesis. Which mechanism explains this anti-angiogenic effect?

    Answer: Upregulating inhibitors of angiogenesis, such as thrombospondin-1 (TSP-1), and inhibiting HIF-1alpha activity

    Explanation: Wild-type p53 can suppress angiogenesis by several mechanisms, including upregulating expression of anti-angiogenic factors like thrombospondin-1 (TSP-1) and inhibiting the activity or expression of pro-angiogenic factors like HIF-1alpha and VEGF.

  30. Q30. Three angiogenesis inhibitors—angiostatin, endostatin, and vasculostatin—share what common characteristic?

    Answer: They are all fragments of extracellular matrix proteins.

    Explanation: Angiostatin is a fragment of plasminogen, endostatin is a fragment of collagen XVIII, and vasculostatin is a fragment of collagen IV. They are all endogenous inhibitors of angiogenesis derived from larger matrix proteins.

  31. Q31. Newly formed endothelial cells in tumor vessels contribute to tumor growth through which mechanism BEYOND providing nutrients?

    Answer: Secreting growth factors that directly stimulate tumor cell proliferation

    Explanation: Beyond simply supplying oxygen and nutrients, tumor endothelial cells can actively secrete various growth factors (e.g., PDGF, FGF, IGF) and cytokines that directly stimulate the proliferation, survival, and migration of nearby tumor cells, thus creating a pro-tumorigenic microenvironment.

  32. Q32. A metastatic tumor cell must successfully complete multiple steps to establish a distant metastasis. At which stage do MOST tumor cells fail?

    Answer: Colonization and growth at the secondary site

    Explanation: While many cells fail at various steps, the vast majority of circulating tumor cells fail to successfully colonize and grow into a macroscopic secondary tumor at a distant site. This step is highly inefficient and represents a major bottleneck in the metastatic cascade.

  33. Q33. Loss of E-cadherin function promotes metastasis through which TWO mechanisms?

    Answer: Decreased cell-cell adhesion and increased cell motility.

    Explanation: E-cadherin is a critical cell-cell adhesion molecule. Loss of its function (e.g., through mutation or downregulation) leads to reduced cell-cell adhesion, allowing tumor cells to detach from the primary tumor, and increases their motility and invasiveness, key steps in metastasis.

  34. Q34. A breast cancer sample shows high expression of CXCR4 and CCR7 chemokine receptors. To which organs is this tumor MOST likely to metastasize?

    Answer: Bone marrow and lymph nodes

    Explanation: CXCR4 and CCR7 are chemokine receptors that bind to specific ligands highly expressed in particular organs. CXCR4 ligands (like CXCL12) are abundant in bone marrow and lung, while CCR7 ligands (like CCL19/CCL21) are high in lymph nodes. This often guides tumor cells to these specific metastatic sites (the 'seed and soil' hypothesis).

  35. Q35. During ECM invasion, tumor cells must complete four sequential steps. Which is the FIRST step?

    Answer: Attachment of tumor cells to ECM components.

    Explanation: The first step in ECM invasion is the detachment of tumor cells from each other (often via loss of E-cadherin) and their attachment to components of the extracellular matrix, such as laminin and fibronectin, which serves as a foothold for subsequent degradation and migration.

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