What the supplied questions test

Sources

• L1L1 Cell injury.pdf — Cell injury. Cell adaptation. Cell death (lecture slides, 59 pages)Primary source for Lesson 1 content, diagrams and questions 1–10. Page numbers refer to this file.
• SyllabusSyllabus 1 (1).pdf — Pathology course syllabus (2 pages)Defines the midterm scope (Chapters 1–7); Chapter 1 is Lesson 1.
• Midterm sim.Cases for simulation of midterm examination on pathology.pdf (16 pages)Q1–Q6 test Chapter 1 directly (pp. 1–2); Q7 (p. 3) crosses over from Chapter 2.
• Ch. II casesCASES CHAPTER II.pdf (20 pages)Q8 (brain infarct at 1 week, p. 9), Q10 (myocardial infarct at 2 days, p. 11) and Q17 (cervical dysplasia, p. 18) cross over into Chapter 1.
• Ref.Standard references used to verify mechanismsRobbins & Kumar Basic Pathology (cell injury, ischemia, apoptosis, amyloidosis); West's Respiratory Physiology (gas exchange, V/Q, shunt); standard toxicology texts (CO, cyanide, methemoglobinemia).

Course PDFs are not served by this site. Page numbers refer to the supplied files so you can verify claims. Images labelled “Lecture image” are cropped from those files; “Teaching schematic” marks original drawings.

Source notes: where the sources differ or are ambiguous

• Glycolysis and oxygen. Source: “O₂ is crucial for ATP synthesis both in glycolysis and oxidative phosphorylation.” Taught here: Glycolysis makes ATP without using oxygen; oxygen is required only at complex IV for oxidative phosphorylation. Hypoxia shifts cells toward glycolysis because it still works. L1 p.9
• Hypoventilation. Source: lists “respiratory acidosis = retention of CO₂” as a cause of hypoxemia. Taught here: Hypoventilation is the cause: a higher alveolar PCO₂ lowers alveolar PO₂. Respiratory acidosis is the accompanying acid–base finding. L1 p.10
• Atelectasis. Source: grouped with “ventilation problems” among V/Q defects. Taught here: Collapsed alveoli that are still perfused act as a shunt (V/Q ≈ 0), so supplemental oxygen helps little. Partly ventilated (low V/Q) units respond well to oxygen. L1 p.10
• Pulmonary embolism. Source: “perfusion defect… increase in pathologic dead space.” Taught here: Dead space wastes ventilation but does not by itself lower PaO₂. Hypoxemia in PE comes mainly from blood diverted to the remaining lung (low V/Q regions) and shunting. L1 p.10
• Cyanide. Source: “O₂ cannot diffuse into tissue”; bitter almond breath called pathognomonic. Taught here: Oxygen is delivered but cannot be used by cytochrome oxidase, so extraction falls and venous blood stays oxygen-rich. The almond odor is a classic but unreliable clue that many people cannot smell. L1 p.15
• Carbon monoxide colour. Source: cherry-red skin, blood and brain. Taught here: A classic association that is usually postmortem and often absent in living patients; diagnosis relies on carboxyhemoglobin by co-oximetry. L1 p.13
• Glutathione roles. Source: “Glutathione peroxidase neutralizes H₂O₂, hydroxyl, and NAPQI”; NAC “donates cystine”. Taught here: Glutathione peroxidase reduces H₂O₂ and lipid peroxides using GSH. NAPQI is conjugated to GSH (spontaneously and by glutathione S-transferase). No enzyme removes hydroxyl radical; it is prevented by clearing H₂O₂ and binding iron. N-acetylcysteine supplies cysteine for GSH synthesis. L1 p.22
• Amylin. Source: “Amylin (derived from insulin)”. Taught here: Amylin (islet amyloid polypeptide) is co-secreted with insulin by β cells; it is a separate peptide, not a fragment of insulin. L1 p.47
• Vulnerable renal regions. Source: “Renal cortex and medulla”. Taught here: Most vulnerable: the straight segment of the proximal tubule (S3) in the outer medulla and the medullary thick ascending limb, where oxygen tension is low and transport work is high. L1 p.16
• Physiologic free radicals. Source: attributed to cytochrome c during oxidative phosphorylation. Taught here: Electrons leak mainly at complexes I and III and partially reduce oxygen to superoxide. L1 p.20