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. III Q1 (p.2)3.7Drug binding gp120 blocks attachmentAnswer E (attachment); gp41, not gp120, performs fusion.Practise in 3.7 knowledge check
- Ch. III Q2 (p.3)3.3Poststreptococcal GN: immune-complex depositionCh. 2 (acute inflammation).Practise in 3.3 knowledge check; case sorter; Almost Twins
- Ch. III Q3 (p.4)3.3Caseating granuloma: delayed T cell–mediated reactionCh. 1 caseous necrosis; Ch. 2 granuloma.Practise in 3.3 knowledge check
- Ch. III Q4 (p.5)3.5Systemic sclerosis: anti-Scl-70Practise in 3.5 knowledge check
- Ch. III Q5 (p.6)3.3Immune-complex GN in an SLE-like case with 'humps'Also 3.5 (SLE).Stem reuses Q2's PSGN wording ('subepithelial humps') but adds SLE features; both readings give immune-complex deposition.Practise in Chapter review
- Ch. III Q6 (p.7)3.5SLE: anti-dsDNAPractise in 3.5 knowledge check
- Ch. III Q7 (p.8)3.2PPD: class II HLA presents antigen to CD4 Th1 cellsAlso 3.3 (type IV).Practise in 3.2 knowledge check; case sorter
- Ch. III Q8 (p.9)3.7ACE-inhibitor angioedema: bradykininCh. 2 (mediators).Practise in 3.7 knowledge check; One Fact Changes
- Ch. III Q9 (p.10)3.5Scleroderma: smooth-muscle atrophy of the lower esophagusOption A says 'lower half'; the smooth-muscle segment is the lower two-thirds. The slide's 'lamina propria' mechanism is corrected to the muscularis propria.Practise in 3.5 knowledge check
- Ch. III Q10 (p.11)3.5SLE: anti-Smith; false-positive VDRLCh. 4 (antiphospholipid thrombosis).Practise in 3.5 knowledge check
- Ch. III Q11 (p.12)3.3Rheumatoid arthritis taught as an immune-complex reactionAlso 3.5.The sore throat 7 weeks earlier points toward rheumatic fever (type II), but the joint pattern and nodules describe RA, listed as type III (L3 p.23). Answer C.Practise in Chapter review
- Ch. III Q12 (p.13)3.7Hereditary angioedema: C1 esterase inhibitor deficiencyOption D reads 'Deficient C1 esterase'; the deficient protein is C1 esterase inhibitor.Practise in 3.7 knowledge check; Almost Twins
- Midterm sim. Q16 (p.6)3.3Poison ivy: delayed-type hypersensitivityPractise in 3.3 knowledge check; case sorter
- Midterm sim. Q17 (p.6–7)3.3p-ANCA necrotizing vasculitis: ANCA vs immune complexOption (B) missing and no key supplied. Expected answer is E (immune complex, PAN as taught on L3 p.23–24), but p-ANCA indicates pauci-immune, ANCA-driven neutrophil activation. The practice item adds IF and complement findings so the mechanism is decidable.Practise in 3.3 knowledge check; One Fact Changes
- Midterm sim. Q18 (p.7)3.3Graves disease: stimulating antireceptor antibodyOption (B) missing. 'Cytopathic autoantibodies' (A) is the only type II choice printed but misdescribes Graves; the antibody stimulates the receptor.Practise in 3.3 knowledge check (with the case image)
- Midterm sim. Q19 (p.8)3.3Skin-prick test is IgE-mediatedAlso 3.2 (Ig classes).Practise in Chapter review
- Midterm sim. Q20 (p.8)3.3ABO transfusion reaction: antibody-mediated complement fixationAlso 3.4 (ABO matching).Practise in 3.3 knowledge check; case sorter
- L3 p.53.1NLR inflammasome → caspase-1 → IL-1β/IL-18Practise in 3.1 knowledge check
- L3 p.4 (diagram)3.1Active/passive, natural/artificial immunityPractise in 3.1 knowledge check
- L3 p.9 (diagram), p.343.1Positive and negative selection; AIREPractise in 3.1 knowledge check
- L3 p.73.1Immune privilegePractise in 3.1 knowledge check
- L3 p.12–14 (diagrams)3.2MHC I (TAP) vs MHC II (invariant chain, CLIP)Practise in 3.2 knowledge check
- L3 p.8, 113.2CD40–CD40L and class-switch cytokinesPractise in 3.2 knowledge check
- L3 p.21 (diagram)3.2Immunoglobulin classesPractise in 3.2 knowledge check (image)
- L3 p.18–19 (photos)3.3Atopic signs; skin-prick and specific-IgE testingPractise in 3.3 topic
- L3 p.223.3Direct vs indirect Coombs; anti-DPractise in Chapter review
- L3 p.24–253.3Serum sickness vs Arthus reactionPractise in Case sorter (penicillin, skin-test cases)
- L3 p.30–31 (micrographs)3.4Hyperacute, acute cellular and chronic rejectionPractise in 3.4 knowledge check (image)
- L3 p.323.4GVHD and graft-versus-tumorPractise in 3.4 knowledge check
- L3 p.343.5Tolerance: FOXP3/IPEX, AIREPractise in 3.5 knowledge check; The Missing Arrow
- L3 p.35 (IF patterns)3.5ANA patterns: centromerePractise in 3.5 knowledge check (image)
- L3 p.37, 393.5Antiphospholipid antibodies: prolonged PTT, false-positive VDRL, thrombosisCh. 4 (thrombosis).Practise in 3.5 knowledge check
- L3 p.40–43 (photos, renal micrograph)3.5Systemic sclerosis: vascular injury to fibrosisPractise in 3.5 topic
- L3 p.44–46 (tables)3.6Primary immunodeficienciesCh. 5 (22q11), Ch. 7 (ATM).Practise in 3.6 knowledge checks; Almost Twins
- L3 p.513.7HIV stages and testsPractise in 3.7 knowledge check
- L3 p.52 (photos)3.7AIDS-defining infections and tumorsPractise in 3.7 knowledge check (image)
- L3 p.543.7C2, C6–C9 deficiency; hereditary angioedemaPractise in 3.7 knowledge check
- AL-MED centerpiece3.3Target → effector → type, then one clue changes (9 cases)Practise in Hypersensitivity case sorter
- AL-MED practice3.4Acute antibody-mediated rejection and C4dNot in the lecture; added from standard references.Practise in 3.4 knowledge check
- AL-MED topic3.7DAF/CD59 loss in PNH; C3 deficiencyNot in the lecture; supporting context.Practise in 3.7 topic
- AL-MED practice (syllabus week 3)3.7Chronic inflammation → SAA → AA amyloidCh. 1 (amyloid, L1 p.46–48).Practise in 3.7 knowledge check; chapter review
- AL-MED bridge3.6LAD, CGD, Chédiak–Higashi by step that failsCh. 2 (L2 p.14, 19, 21–22).Practise in 3.6 topic
Source page map
Which lecture pages feed each section. Page numbers are PDF pages of the supplied files.
- 3.1Hematopoiesis, innate vs adaptive, TLR/NLR/inflammasome, noncellular innate immunityL3 p.2–6
- 3.1Immune privilegeL3 p.7
- 3.1Active/passive, natural/artificial immunity (diagram)L3 p.4
- 3.1V(D)J, thymic selection, memoryL3 p.3, 9
- 3.2MHC, HLA chromosome 6, class III, MHC I/II pathwaysL3 p.12–14
- 3.2Two signals, CD40–CD40L, class switchingL3 p.8, 11
- 3.2T-cell differentiation, Th subsets, CD8 functionsL3 p.9–10
- 3.2Immunoglobulin structuresL3 p.21
- 3.3Hypersensitivity overview (ABCD)L3 p.15
- 3.3Type I: mechanism, late phase, clinical signs, testsL3 p.16–19
- 3.3Type II mechanisms, receptor antibodies, Coombs testsL3 p.20–22
- 3.3Type III, serum sickness, ArthusL3 p.23–25
- 3.3Simulation Q16–20 (hypersensitivity)Midterm sim. p.6–8
- 3.3Type IV, contact dermatitis, PPDL3 p.26–27
- 3.4Graft types, requirements for graft viabilityL3 p.28–29
- 3.4Rejection types and micrographsL3 p.30–31
- 3.4Graft-versus-host reactionL3 p.32
- 3.5Mechanisms of autoimmunity, toleranceL3 p.33–34
- 3.5Autoantibodies, SLE mechanism, clinical findings, labs, lupus IFL3 p.35–39
- 3.5Systemic sclerosis and CRESTL3 p.40–43
- 3.6Congenital immunodeficiency tablesL3 p.44–46
- 3.6LAD, Chédiak–Higashi, CGD (bridge)L2 p.14, 19, 21–22
- 3.7HIV structure, pathogenesis, life cycleL3 p.47–50
- 3.7HIV stages, tests, AIDS-defining conditionsL3 p.51–52
- 3.7Complement disorders, hereditary angioedemaL3 p.54–55
- 3.7Amyloid (syllabus week 3; not in L3)L1 p.46–48
- 3.2–3.7Chapter III cases Q1–Q12Ch. III cases p.2–13
Sources and notes
Sources
- L3Lesson 3 Immunopathology.pdf (55 pages)
- Ch. III casesCases chapter III.pdf (14 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)
- L2Lesson 2 Inflammation.pdf — Inflammation and tissue repair (52 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
- Late-phase reaction. Source: Mast cells synthesize prostaglandins, leukotrienes and PAF de novo 6–24 h after re-exposure. Taught here: Lipid mediators are made within minutes and belong to the immediate reaction; the late phase (about 2–24 h) is mainly recruited eosinophils, neutrophils and Th2 cells. L3 p.16–17, 19
- Skin-prick test. Source: Scratch (prick) test has the best overall sensitivity. Taught here: Intradermal testing is more sensitive; prick testing is preferred first because it is safer and more specific. RAST has largely been replaced by specific-IgE immunoassays. L3 p.19
- HDN and ITP in type II. Source: Listed under IgM-mediated complement lysis. Taught here: HDN is maternal IgG (only IgG crosses the placenta); ITP is IgG-coated platelets removed by splenic macrophages. ABO transfusion reactions are the IgM–complement example. L3 p.20
- Contact dermatitis timing. Source: Inflammatory response usually within hours of re-exposure. Taught here: Elicitation is delayed, typically 24–72 h; patch tests are read at 48–72 h. L3 p.27
- Antibody component of acute rejection. Source: Recipient preexisting alloreactive antibodies. Taught here: Preformed high-titer antibodies cause hyperacute rejection; acute antibody-mediated rejection is usually from donor-specific antibodies formed after transplantation, marked by C4d. L3 p.30
- Chronic rejection vessels. Source: Atherosclerosis of vascular endothelium. Taught here: Graft arteriosclerosis: concentric intimal smooth-muscle proliferation and fibrosis, not lipid plaques. L3 p.30
- Anti-RNP. Source: Anti-RNP antibodies in systemic sclerosis (most common). Taught here: High-titer anti-U1 RNP is the marker of mixed connective tissue disease and also occurs in SLE. L3 p.35
- Esophagus in systemic sclerosis. Source: LES dysfunction because of collagen deposition in lamina propria. Taught here: Atrophy and fibrosis of the smooth muscle of the muscularis propria in the lower esophagus; Case III Q9 option A ('lower half') is the closest wording. L3 p.41Ch. III cases p.10
- HIV protease. Source: Viral protease uncoats the virus. Taught here: Protease cleaves Gag and Gag-Pol after budding (maturation); protease inhibitors act there, as the lecture's life-cycle diagram shows. L3 p.49–50
- CXCR4. Source: CXCR4 mutation = fulminant HIV. Taught here: Emergence of CXCR4-using (X4) viral strains predicts faster CD4 decline; the protective host variant is CCR5Δ32. L3 p.49
- HIV testing. Source: ELISA screening; Western blot and nucleic-acid confirmation. Taught here: 4th-generation antigen/antibody immunoassay, then HIV-1/2 differentiation assay and nucleic-acid testing; Western blot is no longer recommended. L3 p.51
- Simulation Q17. Source: p-ANCA small-artery fibrinoid necrosis; option (B) missing; no key. Taught here: Expected answer E (immune complex, PAN as taught), but p-ANCA indicates pauci-immune ANCA-driven neutrophil activation (Robbins groups it with antibody-mediated disease). Distinguish by IF (granular vs pauci-immune) and complement (low vs normal). Midterm sim. p.6–7L3 p.23–24
- Simulation Q18. Source: Option (B) missing; printed choices include 'cytopathic autoantibodies'. Taught here: Graves IgG stimulates the TSH receptor without destroying cells; the missing option was probably the intended answer. Midterm sim. p.7
- Case III Q5. Source: SLE-like features with PSGN wording ('subepithelial humps'). Taught here: Either reading gives immune-complex deposition; lupus deposits are usually subendothelial (class IV) or subepithelial without humps (class V). Ch. III cases p.6
- Case III Q11. Source: Throat infection 7 weeks earlier added to an RA stem. Taught here: Joint pattern and nodules describe RA (type III in the lecture; T cells also contribute); rheumatic fever arthritis is migratory, large-joint and follows pharyngitis by 2–4 weeks. Ch. III cases p.12L3 p.20, 23
- Case III Q12. Source: Option D: 'Deficient C1 esterase'. Taught here: The deficient protein is C1 esterase inhibitor (L3 p.54). Ch. III cases p.13
Brief in the sources, expanded here as supporting context
- Antiphospholipid syndrome has no dedicated slide (antibodies on p.39, strokes and miscarriage on p.37); the in-vitro/in-vivo paradox is added from standard references.
- Complement: the lecture covers HAE, C2 and C6–C9 (p.54). C3, C5, DAF/CD59 and PNH are supporting context.
- Acute antibody-mediated rejection (C4d), crossmatch technique, direct vs indirect allorecognition and GVL beyond one line are added from standard references.
- Amyloidosis is in the week-3 syllabus but not in L3; 3.7 follows L1 p.46–48 and bridges to Chapter 1.
- Phagocyte defects (LAD, CGD, Chédiak–Higashi) are taught in L2; 3.6 summarizes and links to Chapter 2.
- Immunoglobulin functions are shown only as structures (p.21) and switch cytokines (p.8); the function table is added.
- Inflammasome and pyroptosis in HIV, FMF and AA amyloid, checkpoint-inhibitor autoimmunity and ALPS are added links.
- HIV opportunistic infections by CD4 count extend the lecture's stage thresholds (p.51) with standard cut-offs (<100, <50).
- No images accompany the Chapter III cases; image checks use L3 micrographs and the two simulation images.