MLT GlobeBasic Pathology: Inflammation – page 4
134 Basic Pathology MCQs on Inflammation with answers and explanations.
Which finding is NOT one of the classical local cardinal signs of inflammation?
The cardinal signs are redness, heat, swelling, pain (Celsus) and loss of function (added later). Pallor reflects reduced blood flow, the opposite of inflammatory hyperaemia.
Which neutrophil granule enzyme degrades extracellular elastin and bacterial proteins and can damage tissue when released?
Neutrophil elastase, a serine protease, destroys microbes and extracellular matrix; unopposed activity (e.g. alpha-1 antitrypsin deficiency) injures lung tissue. The other enzymes have no bactericidal role.
A few hours after a puncture wound, a child's thumb is red and swollen. The swelling at this stage results mainly from:
In acute inflammation, mediators such as histamine contract endothelial cells, letting protein-rich exudate leak into tissue. Arteriolar constriction is only a brief initial event and would not cause swelling.
A pus-draining tract runs from a deep abscess to open on the skin surface but ends blindly inside. This lesion is a:
A sinus is a blind-ended tract opening onto an epithelial surface. A fistula is an abnormal channel linking two epithelial surfaces or hollow organs.
In acute inflammation, a brief arteriolar vasoconstriction is followed next by which vascular change?
The sequence is transient vasoconstriction, vasodilation, increased permeability, stasis, then margination and emigration of leukocytes.
Which cytokines mainly mediate systemic effects of inflammation such as fever and the acute-phase response?
IL-1, TNF and IL-6 act on the hypothalamus and liver to cause fever and acute-phase proteins. C5a and LTB4 are chemotactic; cysteinyl leukotrienes cause bronchospasm.
Granulomas most commonly form in response to:
Granulomas form when macrophages cannot eliminate an agent, e.g. mycobacteria or foreign material, leading to T-cell–driven macrophage activation.
Which combination best characterizes chronic non-specific inflammation histologically?
Chronic inflammation shows mononuclear infiltrates (lymphocytes, plasma cells, macrophages), tissue destruction and repair by fibrosis and angiogenesis.
Cytosolic sensors react to molecules released or altered by damaged host cells (DAMPs). Which of the following is NOT a damage-associated molecular pattern?
ATP, uric acid, released DNA and a fall in intracellular K+ signal host cell damage. Lipopolysaccharide is a microbial product, i.e. a pathogen-associated molecular pattern (PAMP).
Uric acid crystals released from dead cells are sensed by a multiprotein complex that activates caspase-1 and IL-1 beta. Where is this sensor located?
The inflammasome is a cytosolic complex (NLR family) that detects DAMPs such as uric acid and ATP, activating caspase-1 to cleave pro-IL-1 beta.
Toll-like receptors detect microbial products at which cellular sites?
TLRs are transmembrane receptors on the cell surface (e.g., TLR4 for LPS) and in endosomes (e.g., TLR3, 7, 9 for nucleic acids), so they sense both extracellular and ingested microbes.
Which of the following is a microbial molecule that is recognized by receptors, rather than being a receptor itself?
PAMPs and DAMPs are ligands. TLRs, NOD-like receptors and C-type lectin receptors are the cellular receptors that recognize them.
Once the offending agent is removed, acute inflammation normally subsides. Which of the following does NOT help terminate the response?
Inflammation stops because mediators degrade quickly, neutrophils die within hours to days, and anti-inflammatory signals are produced. Increased adhesion molecules would sustain leukocyte recruitment.
The arterial intimal plaque of which disease is a chronic inflammatory lesion rich in macrophages and lymphocytes?
Atherosclerosis is a chronic inflammatory response of the arterial wall: lipid-laden macrophages (foam cells) and T lymphocytes dominate the plaque. The other conditions are acute, neutrophil-rich.
Which complement pathway is triggered directly by microbial surface polysaccharides and endotoxin without the need for antibody?
The alternative pathway is activated by microbial surface molecules and complex polysaccharides in the absence of antibody. The classical pathway requires antigen-antibody complexes.
Escape of protein-rich fluid into tissues, producing edema, is regarded as the hallmark of acute inflammation. Which vascular change causes it?
Increased permeability of venules lets plasma proteins escape as an exudate, the hallmark of acute inflammation. Transient vasoconstriction precedes vasodilation and does not cause exudation.
Which disease can show acute inflammatory episodes superimposed on a chronic course, with repeated attacks triggered by allergens?
Asthma features chronic airway inflammation with recurring acute exacerbations. Septic shock and ARDS are acute; pulmonary fibrosis is chronic and progressive.
Firm adhesion of leukocytes to endothelium depends on integrins. Where are these molecules expressed?
Integrins (e.g., LFA-1) are leukocyte surface proteins that bind endothelial ligands such as ICAM-1 and VCAM-1. Selectins mediate earlier rolling.
Which enzyme is characteristic of neutrophil azurophilic (primary) granules?
Myeloperoxidase is stored in azurophilic granules. Alkaline phosphatase and collagenase are in specific (secondary) granules; lysozyme occurs in both.
The complement fragments C3a and C5a increase vascular permeability indirectly. Which mediator do they cause mast cells to release?
C3a and C5a (anaphylatoxins) trigger mast cell degranulation, releasing histamine — an example of one mediator stimulating the release of another.