What the supplied questions test

Sources

• L4Lesson 4 Water, electrolyte, acid–base and hemodynamic disorders.pdf (50 pages)
• Midterm sim.Cases for simulation of midterm examination on pathology.pdf (16 pages)Mixed midterm simulation, questions numbered as in the file.
• Ch. IV casesChapter IV case filenot suppliedNo standalone Chapter IV case file was supplied. Chapter 4 practice uses the midterm simulation, lecture questions and original variants.
• SyllabusSyllabus 1 (1).pdf — Pathology course syllabus (2 pages)Defines the midterm scope (Chapters 1–7).
• L1L1 Cell injury.pdf — Cell injury. Cell adaptation. Cell death (59 pages)
• Ref.Standard references used to verify mechanismsRobbins & Kumar Basic Pathology; Abbas Cellular and Molecular Immunology; Guyton & Hall Medical Physiology; standard toxicology texts.

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

• Osmolality formula. Source: 2(Na⁺ + K⁺) + glucose/18 + BUN/2.8. Taught here: 2 × Na⁺ + glucose/18 + BUN/2.8: doubling sodium already counts its anions; potassium adds little. L4 p.3
• Naming of hypo- and hypernatremias. Source: “Hypertonic loss of Na⁺” (a hyponatremia); “hypotonic loss of Na⁺” (a hypernatremia). Taught here: The adjective describes the fluid lost relative to plasma; explained in 4.2. L4 p.9, 13
• Hyperglycemic water shift. Source: Water shift “much greater than with hypernatremia”. Taught here: The shift follows the rise in effective osmolality; glucose and sodium are equally effective per osmole. L4 p.16
• DI terminology and urine values. Source: “Nephrotic DI”, “PDI”; UOsm < 500; > 800 after desmopressin in central DI. Taught here: Nephrogenic DI. Urine usually < 300 mOsm/kg in complete DI; after desmopressin, judge the size of the rise (> 50%), since medullary washout can keep the absolute value below 800. L4 p.17–18
• SIADH threshold. Source: “Serum Na⁺ < 120 mEq/L is diagnostic of SIADH.” Taught here: No sodium cut-off defines SIADH: hypotonic hyponatremia, urine osmolality > 100, urine Na⁺ > 20–30, euvolemia, normal thyroid and adrenal function, no diuretics. L4 p.19
• Hypokalemic rhabdomyolysis. Source: Insulin inhibition → less glycogen → ATP lack. Taught here: Mainly loss of K⁺-mediated vasodilation in exercising muscle (ischemia); reduced insulin and glycogen contribute. L4 p.20
• Acid–base cut-offs and wording. Source: PaCO₂ > 40 = respiratory acidosis; HCO₃⁻ < 24 = metabolic acidosis; compensation called “metabolic alkalosis” or “respiratory alkalosis”. Taught here: 40 and 24 are midpoints for formulas; disorders are named from values outside 35–45 and 22–26. Compensation is a secondary change, not a primary disorder. L4 p.23–29
• Kussmaul breathing and warm skin. Source: Listed under normal-gap acidosis. Taught here: Features of any metabolic acidosis; Kussmaul breathing is classic in DKA, a high-gap acidosis. L4 p.28
• Diuretics and urine chloride. Source: Loop/thiazide diuretics listed as chloride-responsive. Taught here: Saline-responsive, but urine Cl⁻ is high while the diuretic acts and low after it wears off. L4 p.29
• Mixed-disorder heading. Source: Chronic bronchitis + loop diuretic listed under “metabolic acidosis + respiratory alkalosis”. Taught here: That example is a respiratory acidosis with a metabolic alkalosis. L4 p.30
• Starling balance. Source: Normally plasma oncotic pressure exceeds hydrostatic pressure, so fluid stays in vessels. Taught here: Some fluid filters continuously and lymphatics return it; edema appears when filtration outruns lymph flow. L4 p.32
• Paradoxical embolism route. Source: Through an ASD or VSD. Taught here: Most often through a patent foramen ovale. L4 p.37
• Systemic embolism sources. Source: “embolization from aaa an mca” (garbled). Taught here: Aortic aneurysms and ulcerated aortic plaques. L4 p.38
• Decompression sickness. Source: “atelectasis (collapse of small airways)”. Taught here: Atelectasis is collapse of alveoli. L4 p.41
• Reticulocyte timing after hemorrhage. Source: Reticulocytosis begins in 5–7 days. Taught here: Becomes evident over several days and peaks about a week after the bleed. L4 p.43
• Cardiac marker timing. Source: CK-MB rises after 6–12 h, peaks 16–24 h; troponin rises at 4 h, peaks at 24 h. Taught here: Troponin rises ~3–4 h, peaks ~24–48 h, stays up 7–14 days; CK-MB rises ~4–6 h, peaks ~24 h, normal by 48–72 h. L4 p.45
• SvO₂ in septic shock. Source: “MVO₂ is decreased. Tissues are unable to extract O₂…” Taught here: Poor extraction leaves venous blood oxygen-rich: SvO₂ normal or high in warm septic shock, falling only when cardiac output fails. L4 p.47
• Septic LVEDP. Source: Decreased “due to decreased compliance”. Taught here: Preload falls because venodilation and capillary leak reduce venous return. L4 p.47
• Obstructive shock list. Source: Includes restrictive cardiomyopathy. Taught here: Usually grouped with cardiogenic shock; constrictive pericarditis and tamponade are obstructive (tamponade raises PCWP). L4 p.49
• Simulation Q31 bicarbonates. Source: Serum HCO₃⁻ 8 in the stem; the answer gas (D) has HCO₃⁻ 14. Taught here: Serum value for the anion gap and delta–delta; the gas's own value for Winters. A 6 mEq/L gap between methods is unrealistic; the answer is unaffected. Midterm sim. p.12–13
• Simulation ABG tables. Source: Q32 C: pH 7.52 with PaCO₂ 27/HCO₃⁻ 19; Q33 A: pH 7.51 with 50/42; Q34 F printed 7.32 (7.34 in Q31/Q33). Taught here: Henderson–Hasselbalch gives 7.47, 7.55 and 7.34. The items test direction; answers C, A and F stand. Midterm sim. p.13–14