Case and source map
What the supplied questions test
Every case and lecture question that belongs to this chapter, the concept it tests, and the place in the chapter where you practise it. Lecture coverage, case coverage and original practice are labelled separately.
Case map
- Ch. II Q1 (p.2)2.2LAD I: no neutrophil adherence or extravasation (omphalitis, necrosis without pus, WBC 37,000)Ch. 3 immunodeficiency.The stem omits delayed cord separation; recurrent omphalitis stands in for it.Practise in 2.2 knowledge check
- Ch. II Q2 (p.3)2.1Pain of appendicitis: prostaglandin and bradykininPractise in 2.1 knowledge check
- Ch. II Q3 (p.4)2.6Secondary TB: giant cells around caseation (with chest radiograph)Ch. 1 caseous necrosis.Practise in 2.6 knowledge check (image)
- Ch. II Q4 (p.5)2.7Day-5 laceration: granulation tissueMacrophages (option C) are still present at day 5, but their influx peaks at days 2–3; granulation tissue is the best answer.Practise in 2.7 knowledge check
- Ch. II Q5 (p.6)2.3Neutrophil clearance of pneumococci through H₂O₂ (→ HOCl)HOCl is the end product, but H₂O₂ is the only microbicidal option offered.Practise in 2.3 knowledge check
- Ch. II Q6 (p.7)2.6Sarcoidosis: cell-mediated response to an antigen (skin biopsy)Ch. 3 hypersensitivity (type IV).Erythema nodosum itself is a septal panniculitis without granulomas; the biopsy shown represents cutaneous sarcoid plaques.Practise in 2.6 knowledge check (image)
- Ch. II Q7 (p.8)2.3Abnormal DHR test → NADPH oxidase (CGD)Ch. 3 immunodeficiency.Practise in 2.3 knowledge check and the recruitment lab
- Ch. II Q8 (p.9)2.1Brain infarct one week later: microgliaCh. 1 liquefactive necrosis.Also practised in Chapter 1 (/learn/cell-injury/chapter-review#q-r-brain-cells), which extends the case to three weeks.Practise in Chapter review
- Ch. II Q9 (p.10)2.7Zinc deficiency after small-bowel resections; zinc in wound healingCh. 6 trace elements (/learn/environmental-nutritional/trace-elements).Practise in 2.7 knowledge check
- Ch. II Q10 (p.11)2.1Myocardium 2 days after infarction: loss of nuclei and neutrophilsCh. 1 coagulative necrosis.Also practised in Chapter 1 (/learn/cell-injury/chapter-review#q-r-mi-cells, three days).Practise in 2.1 knowledge check
- Ch. II Q11 (p.12)2.5Diverticular abscess: lysosomal enzymesCh. 1 liquefactive necrosis.Practise in 2.5 knowledge check
- Ch. II Q12 (p.13)2.6Hypersensitivity pneumonitis granuloma: IFN-γ and IL-12 (lung biopsy)Ch. 3 hypersensitivity.Practise in 2.6 knowledge check (image)
- Ch. II Q13 (p.14)2.2Neutrophil elastase; neutrophils recruited by LTB₄The young age and lower-zone emphysema suggest α₁-antitrypsin deficiency; the question asks only which chemoattractant recruited the neutrophils.Practise in 2.2 knowledge check
- Ch. II Q14 (p.15)2.1Edema around an abscess: separation of endothelial junctionsCh. 4 edema.Practise in 2.1 knowledge check
- Ch. II Q15 (p.16)2.7Day-5 sutured wound: angiogenesis and type III collagenPractise in 2.7 knowledge check
- Ch. II Q16 (p.17)2.7Hypertrophic cesarean scar: TGF-βPractise in 2.7 knowledge check
- Ch. II Q17 (p.18)2.6Cervical dysplasia (same stem as Midterm sim. Q6)Ch. 7 dysplasia and invasion (/learn/neoplasia/dysplasia-invasion); also Ch. 1 review (/learn/cell-injury/chapter-review#q-r-cin).The stem calls dysplasia an “adaptation to chronic injury”; dysplasia is disordered growth, not an adaptation.Practise in Chapter review
- Ch. II Q18 (p.19)2.7Burn contracture: myofibroblastsPractise in 2.7 knowledge check
- Midterm sim. Q7 (p.3)2.1Myocardium 24 h after a fatal infarct: neutrophilsCh. 1 necrosis.The Word version reads “expires hours later”; the PDF says 24 hours. Neutrophils need about 12–24 h to arrive.Practise in Chapter review
- Midterm sim. Q8 (p.3)2.1Early swelling after a puncture: increased permeabilityCh. 4 edema.Practise in 2.1 knowledge check
- Midterm sim. Q9 (pp.3–4)2.6Plasma cells and lymphoid follicles (IUD): chronic endometritisPractise in 2.6 knowledge check (image)
- Midterm sim. Q10 (p.4)2.2Initial tethering: selectinsPractise in 2.2 knowledge check
- Midterm sim. Q11 (p.4)2.4Bronchoconstriction and vasoconstriction: leukotrienesCh. 3 type I hypersensitivity.Practise in 2.4 knowledge check
- Midterm sim. Q12 (p.4)2.3Hypochlorous acid made by myeloperoxidasePractise in 2.3 knowledge check
- Midterm sim. Q13 (pp.4–5)2.6Multinucleated giant cell: IFN-γ and IL-12 (image)Ch. 3 HIV.In advanced AIDS granulomas are often poorly formed; the answer (IFN-γ, IL-12) is unaffected.Practise in 2.6 knowledge check (image)
- Midterm sim. Q14 (p.5)2.4Ceruloplasmin, fibrinogen, α₂-macroglobulin, SAA, CRP: acute-phase proteinsCh. 3 SLE.Ceruloplasmin and α₂-macroglobulin are not on the lecture's APR list (L2 p.29); α₂-macroglobulin rises only modestly in humans.Practise in 2.4 knowledge check
- Midterm sim. Q15 (pp.5–6)2.7Granulation tissue: fibroblasts and endothelial cells (image)Practise in 2.7 knowledge check (image)
- L2 cardinal signs (pp.3–4)2.1Five cardinal signs and their mechanismsPractise in 2.1 Five cardinal signs
- L2 vascular events (pp.5, 7)2.1Vasoconstriction → dilation → venular permeability → edemaPractise in The Missing Arrow (vascular chain)
- L2 neutrophil pools (p.9)2.2Circulating vs marginating pool (micrographs)Practise in 2.2 knowledge check (image)
- L2 neutrophil arrival (p.10)2.2Margination, rolling, adhesion, PECAM-1, transmigration, chemotaxisPractise in 2.2 Rolling and tight adhesion
- L2 leukocyte adhesion deficiencies (p.14)2.2LAD I and LAD IIThe slide defines LAD-2 as an endothelial selectin deficiency; it is a fucosylation defect of the leukocyte ligand (sialyl-Lewis X).Practise in Recruitment and killing lab
- L2 “What does opsonin mean?” (p.18)2.3Opsonins: IgG, C3b, CRPPractise in 2.3 Recognition and opsonins
- L2 respiratory burst (p.20)2.3NADPH oxidase → superoxide → H₂O₂ → MPO → HOClThe slide labels HOCl as a radical (HOCl•); it is an oxidant, not a free radical.Practise in The Missing Arrow (burst chain)
- L2 NBT test (p.25)2.3NBT and DHR testing in CGDPractise in 2.3 knowledge check (image)
- L2 arachidonic acid pathways (p.26)2.4COX and LOX products and drug targetsPractise in 2.4 knowledge check
- L2 mediator and cytokine tables (pp.27–29)2.4Mediators, cytokines IL-1 to IL-12, acute-phase reactantsThe table attributes IgE class switching to IL-5; IgE switching is IL-4 (and IL-13).Practise in 2.4 Cytokines
- L2 ESR (p.31)2.4Fibrinogen, rouleaux and the ESR (smear)Plasma proteins reduce the red cells' negative surface charge; they are not positively charged.Practise in 2.4 knowledge check (image)
- L2 patterns of acute inflammation (pp.32–38)2.5Serous, fibrinous, purulent, pseudomembranous, ulcerativePractise in 2.5 knowledge check (image)
- L2 termination and consequences (p.39)2.5Lipoxins; resolution, scar, abscess, fistula, chronic inflammationPractise in 2.5 knowledge check
- L2 granuloma morphology and formation (pp.42–46)2.6Epithelioid cells, giant cells, IL-12/IFN-γ/TNF, caseating vs non-caseatingThe slide describes giant cells as fusion of nuclei; macrophages fuse as whole cells and the nuclei stay separate.Practise in Almost Twins and The Missing Arrow
- L2 regeneration and granulation tissue (pp.47–49)2.7Granulation tissue and angiogenesis (micrograph)The slide calls recruitment of marrow endothelial precursors angiogenesis; that is vasculogenesis.Practise in 2.7 knowledge check (image)
- L2 healing by intention (p.50)2.7Primary, secondary and tertiary intentionPractise in One Fact Changes (sutured or left open)
- L2 abnormalities in repair (p.52)2.7Keloid vs hypertrophic scar (photographs)Practise in Almost Twins (scars)
- Recruitment and killing lab2.3LAD I, LAD II, Chédiak–Higashi, CGD and MPO deficiency by failed step, blood and tissuePractise in Interactive lab
- Original variant2.2Glucocorticoid demargination; impaired healingPractise in 2.2 knowledge check and chapter review
- Original variant2.3Chédiak–Higashi syndrome (smear)Practise in 2.3 knowledge check (image) and chapter review
- Original variant2.3Recruitment defect vs killing defectPractise in Chapter review
- Original variant2.3MPO deficiency: no HOCl, CandidaPractise in Chapter review
- Original variant2.4CRP vs ESR kineticsPractise in 2.4 knowledge check
- Original variant2.4Fever: IL-1/TNF → hypothalamic PGE₂Practise in Chapter review
- Original variant2.4Hepcidin and anemia of chronic diseasePractise in Chapter review
- Original variant2.4Serum amyloid A → AA amyloidosisCh. 1 amyloid.Practise in Chapter review
- Original variant2.5Pseudomembranous colitis (endoscopy)Practise in 2.5 knowledge check (image)
- Original variant2.5Colovesical fistula after diverticulitisPractise in 2.5 knowledge check
- Original variant2.5Cellulitis vs abscessPractise in Chapter review
- Original variant2.5Lobar pneumonia resolves on an intact frameworkPractise in Chapter review
- Original variant2.5Fibrinous pericarditis organizing into scarPractise in Chapter review
- Original variant2.1Parapneumonic exudate (Light criteria)Ch. 4 edema.Practise in Chapter review
- Original variant2.6Anti-TNF therapy and TB reactivationCh. 3 hypersensitivity.Practise in 2.6 knowledge check
- Original variant2.7Granulation tissue vs granulomaPractise in Chapter review and Almost Twins
- Original variant2.7Impaired healing in diabetesPractise in Chapter review
Source page map
Which lecture pages feed each section. Page numbers are PDF pages of the supplied files.
- 2.1Definition; acute vs chronic; neutrophilsL2 p.2, 6, 8
- 2.1Five cardinal signs and their mediatorsL2 p.3–4
- 2.1Vascular sequenceL2 p.5, 7
- 2.1Pain mediators, infarct cells, endothelial gaps (Q2, Q8, Q10, Q14)Ch. II cases p.3, 9, 11, 15
- 2.2Margination; circulating vs marginating poolsL2 p.9, 11
- 2.2Neutrophil arrival; rolling; adhesion; ICAM/VCAM; catecholamines and corticosteroidsL2 p.10, 12–13
- 2.2Leukocyte adhesion deficienciesL2 p.14
- 2.2Transmigration (PECAM-1); chemotaxisL2 p.15–16
- 2.3Phagocytosis; opsoninsL2 p.17–18
- 2.3Chédiak–Higashi syndromeL2 p.19
- 2.3Respiratory burstL2 p.20
- 2.3Chronic granulomatous disease; catalase-positive organisms; NBT and DHRL2 p.21–25
- 2.4Cyclooxygenase and lipoxygenase pathwaysL2 p.26
- 2.4Mediator table; cytokines; histamine, NO; acute-phase reactantsL2 p.27–29
- 2.4CRP and ESRL2 p.30–31
- 2.5Purulent inflammation; cellulitisL2 p.32–34
- 2.5Fibrinous, serous, pseudomembranous, ulcerative patternsL2 p.35–38
- 2.5Termination and outcomes; lipoxinsL2 p.39
- 2.6Chronic inflammation; causes; cellsL2 p.40–41
- 2.6Granuloma morphology and formation; infliximabL2 p.42–43
- 2.6Caseating vs non-caseating granulomasL2 p.44–46
- 2.7Regeneration; granulation tissue; angiogenesis growth factorsL2 p.47–49
- 2.7Healing by primary, secondary and tertiary intentionL2 p.50
- 2.7Factors that impair wound healing; collagen synthesisL2 p.51
- 2.7Keloid vs hypertrophic scarL2 p.52
- 2.1–2.7Chapter II case questions Q1–Q18Ch. II cases p.2–19
- 2.1–2.7Midterm simulation Q7–Q15Midterm sim. p.3–6
- 2.1–2.7Week 2 scope: vascular events, recruitment, mediators, chronic inflammation, repairSyllabus p.1
Sources and notes
Sources
- L2Lesson 2 Inflammation.pdf — Inflammation and tissue repair (52 pages)
- Ch. II casesCASES CHAPTER II.pdf (20 pages)
- Midterm sim.Cases for simulation of midterm examination on pathology.pdf (16 pages)Mixed midterm simulation, questions numbered as in the file.
- L1L1 Cell injury.pdf — Cell injury. Cell adaptation. Cell death (59 pages)
- SyllabusSyllabus 1 (1).pdf — Pathology course syllabus (2 pages)Defines the midterm scope (Chapters 1–7).
- 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
- LAD II. Source: “LAD-2 is a deficiency of an EC selectin that normally binds neutrophils”; clinical list (delayed cord separation, gingivitis, neutrophilia) given for both types. Taught here: LAD II is a fucosylation defect (GDP-fucose transporter): the leukocyte selectin ligand sialyl-Lewis X is missing; endothelial selectins are normal. Delayed cord separation is the LAD I clue; LAD II brings the Bombay phenotype, intellectual disability and short stature. L2 p.14
- Endothelial integrins. Source: “venular EC expression of integrin adhesion molecules”. Taught here: Endothelium expresses integrin ligands (ICAM-1, VCAM-1); the integrins (LFA-1 = CD11a/CD18, Mac-1 = CD11b/CD18, VLA-4) are on leukocytes and are activated by chemokines. L2 p.13
- CGD and hypochlorous acid. Source: “HOCl• (bleach)”; CGD neutrophils “will use bacterial HOCl”. Taught here: HOCl is an oxidant, not a free radical. CGD neutrophils can use H₂O₂ made by catalase-negative bacteria, which their own myeloperoxidase converts to HOCl; catalase-positive organisms destroy that H₂O₂. L2 p.20–21
- IL-5. Source: IL-5 “enhances class type switching to IgE”. Taught here: IgE class switching is driven by IL-4 (and IL-13). IL-5 drives eosinophil production and activation and supports B-cell growth and IgA. L2 p.28
- Angiogenesis and vasculogenesis. Source: Vessels “de novo from EC precursors recruited from the bone marrow (i.e., angiogenesis)”. Taught here: Sprouting from pre-existing vessels is angiogenesis; building vessels from marrow-derived endothelial precursors is vasculogenesis. Both contribute to repair. L2 p.48
- Giant cells. Source: “fusion of the nuclei of epithelioid cells into one giant cell”. Taught here: Whole macrophages fuse their cytoplasm; the nuclei remain separate, which is why the cell is multinucleated. L2 p.42
- ESR mechanism. Source: Plasma proteins (fibrinogen, immunoglobulins) “have a positive charge”. Taught here: Fibrinogen and immunoglobulins are large, asymmetric proteins that reduce the red cells' negative surface (zeta) potential and bridge them into rouleaux; they are not positively charged at blood pH. L2 p.31
- Dysplasia as an adaptation. Source: Ch. II Q17 (= Sim Q6): “Which of the following adaptations to chronic injury…” with dysplasia as the answer. Taught here: Dysplasia is disordered growth with atypia, a possible precursor of carcinoma, not a true adaptation. Ch. II cases p.18
- Timing in Sim Q7. Source: The Word version says the patient “expires hours later”; the PDF says 24 hours. Taught here: Neutrophils need about 12–24 hours to appear in an infarct; the PDF wording supports the keyed concept (neutrophils). Midterm sim. p.3
- Acute-phase list in Sim Q14. Source: Ceruloplasmin and α₂-macroglobulin listed as acute-phase markers; neither is on the lecture's APR table. Taught here: Both are positive acute-phase proteins; α₂-macroglobulin rises only modestly in humans. The answer (acute-phase proteins) is unaffected. Midterm sim. p.5L2 p.29
Brief in the sources, expanded here as supporting context
- No answer key was supplied for the Chapter II cases or the simulation; every answer was derived and checked (audit: docs/pathology-audit/chapter-2.md).
- Triggers and sentinel cells (PAMPs, DAMPs, inflammasome) expand the lecture's one-line definition; they explain sterile inflammation in an infarct.
- Infarct cell timelines (Ch. II Q8, Q10; Sim Q7) are not in L2; they are taught from L1 and Robbins in 2.1.
- Exudate vs transudate criteria (specific gravity, Light criteria) are added; L2 shows only the word “exudate” on its arrival diagram.
- LAD II, Chédiak–Higashi clinical features and MPO deficiency appear in L2 only as pictures or an enzyme label; details come from Robbins and Abbas.
- Collateral injury by granule enzymes and the route to an abscess expand the lecture's purulent-inflammation slide.
- Ceruloplasmin and α₂-macroglobulin come from Sim Q14, not from the lecture's acute-phase table.
- Resolvins, protectins and efferocytosis expand the single lipoxin bullet on the termination slide; fistula is defined (the slide lists it without explanation).
- Macrophage M1/M2 activation, the tuberculin test and IL-12/IFN-γ receptor defects are supporting context for the granuloma loop.
- Wound-healing time course, tensile strength, collagen III → I, re-epithelialization and contracture are added from Robbins; L2 gives granulation tissue, growth factors, intention and impairing factors.
- Cervical dysplasia (Ch. II Q17) is taught in Chapters 1 and 7; Chapter 2 practises it once in the review.