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PA3.1-4,PA4.1 | Inflammation & Healing — Graded Quiz
Graded
12 questions · Untimed · 2 attempts
Click any question card to reveal the correct answer.
A 32-year-old woman presents with a 3-day history of swelling, redness, and warmth over her right forearm following an insect sting. On biopsy, the dermis shows a dense neutrophilic infiltrate with focal tissue liquefaction. She is given ibuprofen for pain. Which pair of inflammatory mediators is MOST directly inhibited by this drug, and what is the net clinical effect of inhibiting both?
A
Histamine and bradykinin; reduced vascular permeability and pain by blocking H1 receptors and B2 receptors
B
Prostaglandin E2 and thromboxane A2; reduced fever, pain, and platelet aggregation by inhibiting COX-1 and COX-2
✓
C
Leukotriene B4 and C4; reduced neutrophil chemotaxis and bronchoconstriction by inhibiting 5-lipoxygenase
D
TNF-α and IL-6; reduced systemic acute-phase response by blocking cytokine release from activated macrophages
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A 6-year-old boy has had recurrent life-threatening bacterial infections (Staphylococcus, Pseudomonas) since infancy, requiring multiple hospitalisations. Neutrophil count is normal. The NBT (nitroblue tetrazolium) test shows no colour change (fails to turn blue). Genetic testing reveals a mutation in the CYBB gene encoding gp91phox. Which SPECIFIC step in neutrophil killing is defective, and what is the downstream consequence?
A
Opsonisation — the mutation prevents IgG Fc receptor expression, so bacteria are not opsonised and phagocytosis is severely impaired
B
NADPH oxidase assembly — gp91phox is the catalytic subunit of the oxidase; its absence prevents superoxide generation in the phagosome, abolishing the oxidative burst
✓
C
Degranulation — the mutation prevents azurophilic granule fusion with the phagosome, so myeloperoxidase is not delivered to kill bacteria
D
Neutrophil rolling — CD18 (integrin) is absent, preventing firm adhesion and emigration to infection sites
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A 52-year-old man with known HIV infection (CD4 count 85 cells/μL, uncontrolled) develops a slowly enlarging indurated ulcer on his right cheek. Biopsy shows a focal aggregate of plump macrophages with abundant pale pink cytoplasm (epithelioid histiocytes) arranged in a tight cluster, surrounded by a lymphocytic cuff and rare giant cells. Ziehl-Neelsen stain is negative. Fungal silver stain reveals round yeast forms within macrophages. The MOST important host immune mechanism that would normally contain this infection is:
A
Neutrophilic oxidative burst generating HOCl to kill the fungus in early phagosomes
B
IFN-γ produced by Th1 cells activating macrophages to kill the intracellular fungus and sustain granuloma formation
✓
C
Natural killer cells releasing perforin/granzyme B to directly lyse macrophages harbouring the fungus
D
IL-4 and IL-13 driving M2 macrophage polarisation to sequester fungal organisms in fibrous granulomas
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A 28-year-old woman undergoes appendicectomy for acute appendicitis. Histology of the appendix shows transmural neutrophilic infiltration, fibrinous exudate on the serosa, and areas of mucosal ulceration. One week later, she presents with a fever spike to 39°C and rigors. Blood cultures grow E. coli. CT abdomen shows a well-defined 4 cm rim-enhancing collection in the right iliac fossa. Which morphological pattern of acute inflammation does the CT collection MOST likely represent?
A
Serous inflammation — watery exudate with low protein content pooling in the right iliac fossa after peritoneal irritation
B
Suppurative (purulent) inflammation — an abscess consisting of a central zone of pus (dead neutrophils, liquefied tissue) surrounded by a pyogenic membrane
✓
C
Fibrinous inflammation — fibrin polymerised from high-molecular-weight exudate, forming an organised collection that rim-enhances on CT
D
Pseudomembranous inflammation — a false membrane of fibrin and necrotic debris overlying the peritoneal surface, creating the CT rim
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A 60-year-old man with a long history of smoking and COPD presents with a 6-week history of productive cough, low-grade fever, and 5 kg weight loss. Sputum cultures are repeatedly negative on standard media. Bronchoscopic biopsy shows epithelioid histiocyte clusters with Langhans giant cells and central caseous necrosis. Ziehl-Neelsen stain shows acid-fast bacilli. The patient is started on RIPE therapy. Three months later he develops rheumatoid arthritis and his rheumatologist proposes adding etanercept (anti-TNF-α). Why is this combination potentially dangerous?
A
Etanercept increases the risk of rifampicin hepatotoxicity by inducing CYP3A4, leading to toxic metabolite accumulation
B
TNF-α is required to maintain granuloma integrity by sustaining macrophage activation; blocking it causes granuloma dissolution and reactivation of contained TB bacilli
✓
C
Anti-TNF therapy causes neutropenia by suppressing G-CSF secretion, leaving the patient unable to mount a new neutrophilic response to TB
D
Etanercept activates regulatory T cells that suppress IFN-γ production, converting M1 macrophages to M2 phenotype in existing granulomas
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A 46-year-old woman with stage IV ovarian carcinoma and malignant ascites presents to oncology clinic. Her ascites fluid is sent to the lab. Results: protein 45 g/L, LDH 520 U/L (serum LDH 180 U/L), specific gravity 1.022, cytology shows malignant cells. Which mechanism PRIMARILY drives the formation of this type of ascites, and how does it differ from the mechanism in a patient with hepatic cirrhosis?
A
Malignancy: increased capillary hydrostatic pressure from portal hypertension. Cirrhosis: decreased plasma oncotic pressure from hypoalbuminaemia
B
Malignancy: exudate from increased capillary permeability due to tumour-mediated VEGF release and direct peritoneal invasion. Cirrhosis: transudate from increased hydrostatic pressure plus decreased oncotic pressure
✓
C
Malignancy: lymphatic obstruction by peritoneal metastases blocking thoracic duct drainage. Cirrhosis: inflammatory mediators causing exudative ascites
D
Both malignancy and cirrhosis produce exudates via the same mechanism of peritoneal inflammation; the difference lies only in the causal agent
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A 35-year-old HIV-positive man (CD4 count 210/μL) presents with 3 months of cough, low-grade fever, and 8 kg weight loss. CXR shows bilateral hilar lymphadenopathy and patchy infiltrates. Bronchoscopic biopsy shows non-caseating epithelioid granulomas. BAL and serology exclude TB, MAI, and fungal infection. He is started on anti-retroviral therapy. Six weeks later his symptoms worsen paradoxically, CD4 rises to 290/μL, and repeat biopsy shows larger, more florid granulomas with Langhans giant cells. The MOST likely explanation for this clinical paradox is:
A
Drug resistance — ART selected for resistant mycobacteria that now proliferate unchecked
B
Immune reconstitution inflammatory syndrome (IRIS) — recovery of Th1 CD4 cells generates a florid granulomatous response against a pre-existing antigen that was previously contained silently
✓
C
ART-induced hypersensitivity — a type IV delayed hypersensitivity reaction to ART metabolites accumulating in macrophages
D
Sarcoidosis — granulomatous inflammation is triggered by ART-induced immune dysregulation causing polyclonal B-cell activation
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A 55-year-old man with a BMI of 38 undergoes elective right total knee arthroplasty. His post-operative course is uneventful for 5 days. On day 6, the surgeon notices that only a thin film of granulation tissue has formed in the wound bed, despite adequate surgical apposition and no signs of infection. Laboratory results: HbA1c 9.8%, albumin 28 g/L, Hb 9.2 g/dL. Which factor is MOST directly responsible for impaired granulation tissue formation in this patient?
A
Anaemia (Hb 9.2 g/dL) — oxygen deficiency prevents HIF-1α-mediated VEGF upregulation needed for angiogenesis in granulation tissue
B
Hyperglycaemia (HbA1c 9.8%) — advanced glycation end-products cross-link collagen in granulation tissue and impair macrophage-to-M2 transition needed for fibroblast activation
C
Hypoalbuminaemia (albumin 28 g/L) combined with hyperglycaemia — reduced collagen substrate (glycine, proline) and impaired growth factor signalling from protein deficiency, compounded by diabetic macrophage dysfunction impairing VEGF and TGF-β delivery to the wound
D
Hyperglycaemia (HbA1c 9.8%) — diabetic microangiopathy and impaired macrophage function reduce VEGF and TGF-β delivery to the wound bed, inhibiting fibroblast recruitment and neovascularisation
✓
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A histopathology slide from a surgical excision specimen shows a zone with: (1) central structureless eosinophilic material, (2) surrounding plump macrophages with abundant pink cytoplasm (epithelioid histiocytes), (3) occasional multinucleated giant cells with nuclei arranged peripherally in a horseshoe pattern, and (4) an outer rim of lymphocytes. Ziehl-Neelsen stain: positive. Which cell type in zone (3) is shown, and what is the functional significance of the horseshoe nuclear arrangement?
A
Foreign-body giant cells — nuclei scattered centrally because phagocytosis of a large non-degradable particle requires nuclear clustering for maximal lysosomal enzyme deployment
B
Langhans giant cells — nuclei arrange peripherally in a horseshoe because multiple macrophages fuse by cytoplasmic coalescence; the peripheral arrangement reflects the original cell membrane positions before fusion
✓
C
Reed-Sternberg cells — the binucleate 'owl-eye' appearance indicates lymphomatous transformation of granuloma macrophages in TB-complicated lymphoma
D
Touton giant cells — peripheral nuclei wreath around central eosinophilic material indicating xanthomatous change, pathognomonic of fat necrosis
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A 29-year-old woman undergoes lumpectomy for a 1.8 cm grade 2 infiltrating ductal carcinoma. The wound is sutured primarily. On day 3, histology of an incidental biopsy from the wound margin shows: fibroblasts actively synthesising collagen, thin-walled new capillaries in a loose connective tissue matrix, and scattered macrophages without neutrophils. What is the MOST accurate description of the healing stage and the rate-limiting growth factor for the vascular component?
A
Day 1–2 inflammatory phase; TGF-β is the rate-limiting cytokine for neutrophil-to-monocyte transition
B
Day 3–5 proliferative phase (granulation tissue formation); VEGF is the rate-limiting growth factor for neovascularisation, acting on endothelial cell receptors to stimulate sprouting angiogenesis
✓
C
Day 7–10 remodelling phase; PDGF is the rate-limiting factor for myofibroblast differentiation driving collagen crosslinking
D
Day 3–5 proliferative phase; EGF is the rate-limiting growth factor that stimulates fibroblast migration and collagen deposition
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A 58-year-old man is admitted with severe community-acquired pneumonia requiring ICU care. Over 48 hours he develops high fever (39.5°C), tachycardia (HR 118), leukocytosis (WBC 22,000/μL with 85% neutrophils), and C-reactive protein of 285 mg/L. His serum iron is 5 μmol/L, ferritin is 1,200 μg/L, and fibrinogen is 8.2 g/L. Which BEST explains the combination of low serum iron and high ferritin in this patient?
A
Haemolytic anaemia — the pneumonia organism lyses red cells, releasing intracellular ferritin and consuming transferrin-bound iron
B
Acute-phase response — IL-6 upregulates hepcidin synthesis, which internalises ferroportin in macrophages, trapping stored iron intracellularly and reducing serum iron; IL-1 and IL-6 also upregulate ferritin synthesis directly
✓
C
Protein deficiency — low albumin reduces iron-binding capacity so iron is sequestered in liver ferritin to prevent free-radical generation
D
Renal retention — acute inflammatory glomerular injury reduces urinary iron excretion, diverting iron into hepatic ferritin stores
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An 18-year-old man develops a raised, itchy, firm, reddish-brown scar on his sternum 6 months after an open-heart surgery incision. The scar has grown well BEYOND the original wound margins. Biopsy shows exuberant deposition of thick collagen bundles in haphazard orientation, with markedly increased fibroblasts. Which aberration of wound healing does this represent, and how does it differ from a hypertrophic scar?
A
Hypertrophic scar — excess collagen deposition confined within the wound boundaries; regresses spontaneously over 6–12 months; same risk in all ethnic groups
B
Keloid — excess collagen deposition BEYOND the wound margins due to persistent fibroblast activation; does NOT regress spontaneously; higher incidence in individuals with dark skin pigmentation
✓
C
Desmoid tumour — clonal proliferation of myofibroblasts penetrating beyond the wound; a locally aggressive neoplasm requiring surgical excision
D
Hypertrophic scar evolving into a keloid — both are the same pathological entity at different time points and are histologically indistinguishable
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