Inflammation
Bronchiectasis is permanent, abnormal dilatation of the bronchi with chronic inflammation and infection, leading to a clinical syndrome of chronic productive cough, recurrent chest infections and sometimes haemoptysis.
What our notes say
- Bronchiectasis is permanent, abnormal dilatation of the bronchi with chronic inflammation and infection, leading to a clinical syndrome of chronic productive cough, recurrent chest infections and sometimes haemoptysis. (Bronchiectasis)
- Interstitial lung diseases (ILD), or diffuse parenchymal lung diseases, are a heterogeneous group of more than 200 disorders that cause inflammation and/or fibrosis of the lung interstitium (alveolar walls and the tissue around airways and vessels). (Interstitial Lung Diseases)
- Surgery: timing is early (within days) for a clean surgical injury, or after about 3 months once the inflammation and oedema have settled. (Junior Clerkship in Reproductive Health (MBOG 4200): end of year examination, 4 )
- Ferritin is the best blood test of iron stores, and a normal CRP means it is not falsely raised by inflammation. (Internal Medicine End of Semester CAT (MBChB 4): haematology and renal, 30 MCQs )
- Increased capillary permeability or inflammation (infection, cancer) → exudate. (Pleural Effusion)
- Airway inflammation (eosinophils, mast cells, Th2 lymphocytes, IgE) after exposure to a trigger. (Asthma)
Study material on Inflammation
- General Pathology Revision: Cell Injury, Inflammation & Adaptation (MBPA 3500 Paper 1)
- Breast Inflammation: Mastitis, Periductal Mastitis & Duct Ectasia
- Cat. Pathology: Acute Inflammation, Mediators & Pulmonary Embolism
- Pathology of Acute Skin Inflammation: Urticaria & Eczema
- Pathology Mechanisms: Inflammation, PE, & Impaired Healing
- Medical MCQs: Chemical Pathology & Haematology Exam Review
- General Pathology I
- general Pathology Q&A
- Lung Pathology — Must-Know
- Liver Histology & Physiology
- Inflammation and Tissue Repair - MCQs
- General Pathology
- Dr. Irungu Sent SEM 2
- Weekly Pathology Exam - October 9, 2026 (Sections B & C)
- General Pathology Continuous Assessment July 2021
- Weekly Pathology Exam - April 10, 2026 (Section A: MCQs)
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Practice questions on Inflammation
During acute inflammation, what causes the conversion of a "marginating pool" of neutrophils to become available in circulation?
- Increased production of selectins on endothelium
- Accelerated release from bone marrow due to cytokines like TNF and IL-1
- Enhanced expression of integrins in high-affinity state
- Production of colony-stimulating factors increasing marrow proliferation
- Reduced apoptosis of circulating neutrophils
Answer: B. The question addresses the immediate increase in circulating neutrophils (leukocytosis) that occurs early in inflammation. This happens because cytokines like TNF and IL-1 cause accelerated release of granulocytes from bone marrow storage pools, including both mature and immature neutrophils (causing a "left shift"). This is a rapid response utilizing already-produced cells. CSF production increases marrow proliferat
In examining a tissue biopsy showing chronic inflammation, which finding would most strongly suggest immune-mediated rather than infectious etiology?
- Presence of neutrophils in tissue
- Organized lymphoid follicles with germinal centers (tertiary lymphoid organs)
- Granulation tissue with new blood vessels
- Abundant eosinophils
- Fibrin deposition in extravascular space
Answer: B. Tertiary lymphoid organs - organized lymphoid follicles resembling lymph nodes - form in chronically inflamed tissues particularly in autoimmune diseases like rheumatoid arthritis (synovium) and Hashimoto thyroiditis (thyroid). Their formation suggests persistent immune activation against self or environmental antigens rather than microbes. Neutrophils are typical of acute bacterial infections. Granulation tissue is
Which mechanism accounts for the immediate transient phase of increased vascular permeability in acute inflammation?
- Direct endothelial injury and cell necrosis
- Leukocyte-dependent endothelial injury
- Histamine-induced endothelial cell contraction creating interendothelial gaps
- VEGF-stimulated angiogenesis
- New blood vessel formation with immature endothelium
Answer: C. The immediate transient response (within seconds to minutes, lasting 15-30 minutes) is caused by histamine and other vasoactive mediators inducing endothelial cell contraction in venules, creating gaps between cells. This is the FIRST and fastest mechanism. Direct endothelial injury causes immediate but sustained leakage (hours to days) - not transient. Leukocyte-dependent injury comes later after cells are recruited
During acute inflammation, complement activation produces several bioactive fragments. Which function is specifically performed by C3b?
- Stimulating histamine release from mast cells
- Chemotaxis of neutrophils and monocytes
- Opsonization of microbes for phagocytosis
- Formation of membrane attack complex
- Activation of the kinin system
Answer: C. Each complement fragment has specific roles. C3b covalently attaches to microbial surfaces and acts as an opsonin - it's recognized by complement receptors on phagocytes (neutrophils and macrophages), promoting phagocytosis. C3a and C5a are anaphylatoxins that stimulate mast cell histamine release and cause increased permeability. C5a (not C3b) is the main chemotactic fragment for leukocytes. C5b initiates formation
A research study examines endothelial changes during inflammation. Which molecule is most important for converting rolling neutrophils to firmly adherent cells?
- E-selectin binding to sialyl-Lewis X
- P-selectin engaging PSGL-1
- Chemokines activating integrins to high-affinity state
- PECAM-1 homotypic interactions
- L-selectin binding to GlyCAM-1
Answer: C. The progression from rolling to firm adhesion requires integrin activation. Chemokines (produced at injury sites and displayed on endothelial proteoglycans) bind to rolling leukocytes and trigger inside-out signaling that converts integrins (LFA-1, MAC-1, VLA-4) from low to high affinity states. These high-affinity integrins then bind firmly to endothelial ligands (ICAM-1, VCAM-1), arresting the cells. E-selectin and
What distinguishes serous from fibrinous inflammation?
- Serous inflammation contains more neutrophils
- Fibrinous inflammation involves larger molecules leaking due to greater vascular permeability
- Serous inflammation always occurs in body cavities
- Fibrinous inflammation is always caused by bacterial infections
- Serous inflammation represents chronic while fibrinous is acute
Answer: B. The key difference is the SIZE of molecules that leak and the degree of vascular permeability. Serous inflammation has mild permeability increase allowing cell-poor fluid (like plasma ultrafiltrate) to escape - seen in blisters or mild peritoneal irritation. Fibrinous inflammation has GREATER permeability allowing large molecules like fibrinogen to escape and form fibrin deposits - characteristic of inflammation in p