Inflammation and Tissue Repair - MCQs

## SECTION 1: RECOGNITION AND INITIATION OF INFLAMMATION **1.** A 45-year-old man develops a wound infection. The tissue macrophages recognize the bacteria through pattern recognition receptors. Which of the following best describes the mechanism by which Toll-like receptors (TLRs) contribute to the inflammatory response? a) They directly phagocytose bacteria and present antigens to T cellsb) They recognize pathogen-associated molecular patterns and trigger production of inflammatory mediatorsc) They form pores in bacterial cell walls leading to osmotic lysisd) They bind to antibodies coating bacteria to enhance complement activatione) They release histamine from preformed granules upon bacterial contact **Answer: b) They recognize pathogen-associated molecular patterns and trigger production of inflammatory mediators** **Explanation:** TLRs are pattern recognition receptors expressed on sentinel cells like macrophages, dendritic cells, and epithelial cells. They recognize conserved microbial structures (PAMPs) in different cellular compartments - plasma membrane for extracellular microbes, endosomes for ingested microbes, and cytosol for intracellular microbes. Upon engagement, TLRs trigger signaling pathways that lead to production of inflammatory mediators including cytokines, adhesion molecules, and chemokines. They don't directly phagocytose (that's the role of phagocytic receptors), don't form membrane pores (that's complement's membrane attack complex), don't bind antibodies (that's Fc receptors), and don't release histamine (that's mast cells). **2.** A research study examines cellular responses to tissue necrosis from various causes including ischemia, trauma, and chemical injury. Which sensor mechanism is responsible for detecting damaged cells regardless of the cause of injury? a) Mannose-binding lectin recognizing microbial sugarsb) TLR-4 detecting lipopolysaccharidec) NOD-like receptors detecting uric acid and ATPd) Complement C3b opsonizing cellular debrise) Scavenger receptors binding oxidized LDL **Answer: c) NOD-like receptors detecting uric acid and ATP** **Explanation:** NOD-like receptors (NLRs) are cytosolic receptors that recognize diverse molecules released from damaged cells, making them the universal sensors of cell damage. These include uric acid (DNA breakdown product), ATP (from damaged mitochondria), reduced intracellular K+ (from membrane injury), and cytoplasmic DNA. NLRs activate the inflammasome, which produces IL-1, triggering inflammation. The other options are more specific: mannose-binding lectin and TLR-4 recognize microbes specifically, C3b is a complement product that assists in phagocytosis, and scavenger receptors primarily handle modified lipoproteins. Only NLRs detect damage from ANY cause - ischemia, trauma, or toxins. **3.** During an inflammatory response to bacterial infection, which sequence correctly describes the temporal pattern of leukocyte infiltration? a) Lymphocytes → neutrophils → monocytes → plasma cellsb) Eosinophils → basophils → neutrophils → macrophagesc) Neutrophils (6-24h) → monocytes (24-48h) → lymphocytes (later stages)d) Monocytes → neutrophils → eosinophils → mast cellse) Mast cells → neutrophils → lymphocytes → monocytes **Answer: c) Neutrophils (6-24h) → monocytes (24-48h) → lymphocytes (later stages)** **Explanation:** The typical sequence in acute inflammation shows neutrophils predominating in the first 6-24 hours, then being replaced by monocytes at 24-48 hours. Neutrophils arrive first because they're more numerous in blood, respond faster to chemokines, and attach more firmly to early adhesion molecules like P-selectin and E-selectin. Neutrophils are short-lived in tissues (undergo apoptosis within days), while monocytes survive longer and may proliferate, becoming the dominant population in prolonged reactions. Lymphocytes typically appear in later stages or in chronic inflammation. Eosinophils are seen mainly in allergic reactions and parasitic infections, not typical bacterial infections. **4.** A patient with hereditary angioedema experiences recurrent episodes of severe swelling. This condition results from deficiency of C1 inhibitor. Which of the following best explains the pathophysiology? a) Uncontrolled activation of the membrane attack complex causes cell lysisb) Excessive C3a and C5a production leads to mast cell degranulation and increased vascular permeabilityc) Deficient opsonization results in persistent bacterial infections triggering inflammationd) Impaired phagocytosis allows accumulation of immune complexese) Loss of selectin-mediated leukocyte rolling causes defective neutrophil recruitment **Answer: b) Excessive C3a and C5a production leads to mast cell degranulation and increased vascular permeability** **Explanation:** C1 inhibitor (C1 INH) is a key regulatory protein that blocks activation of C1, the first protein of the classical complement pathway. Without it, there's uncontrol