MRCOG Part 1 · Pathology · Cellular Response to Disease

Inflammation and Healing: MRCOG Part 1 questions and key facts

Inflammation and tissue repair represent fundamental pathological processes evaluated in the MRCOG Part 1 examination. Acute inflammation involves immediate vascular alterations mediated prominently by histamine, which drives increased post-capillary venule permeability, plasma leakage, and tissue oedema. Chronic inflammation is recognised histologically by plasma cells in chronic endometritis and non-caseating granulomas in conditions such as sarcoidosis. Tissue repair progresses through coordinated inflammatory, proliferative and remodelling phases. During healing, fibroblast-derived myofibroblasts mediate active wound contraction, whilst provisional type III collagen is systematically replaced by organised, cross-linked type I collagen. The examination frequently pairs specific cell types and chemical mediators directly with their clinical settings, including histamine with early vascular permeability, stromal plasma cells with chronic endometritis, and myofibroblasts with active wound contraction.

The Uterio bank has 7 questions on this topic. 2 arebelow in full; the syllabus detail is in the Pathology study guide.

How the exam tests Inflammation and Healing

  • Distinguishing chemical mediators of acute vascular permeability, focusing on histamine actions on H1 receptors and post-capillary venules.
  • Identifying histological hallmarks of chronic inflammation, particularly stromal plasma cells in chronic endometritis and non-caseating granulomas in sarcoidosis.
  • Wound remodelling: type III collagen replaced by type I, and tensile strength reaching about 80% of normal by 12 weeks.
  • Cellular drivers of wound healing, specifically the role of alpha-smooth muscle actin-positive myofibroblasts in wound contraction.

High-yield facts

  1. Histamine released from mast cells binds endothelial H1 receptors to cause arteriolar vasodilation and increased post-capillary venule permeability, driving early oedema.
  2. Kinins increase permeability and pain, prostaglandins cause vasodilation, pain, and fever, whilst cytokines such as TNF and IL-1 act over hours rather than minutes.
  3. Serotonin is a preformed vasoactive mediator stored primarily in platelets and enterochromaffin cells that increases vascular permeability.
  4. Healing tissue achieves approximately 80% of original tensile strength by about 12 weeks following injury.
  5. Healed tissue rarely, if ever, regains 100% of its original baseline tensile strength.
  6. During wound remodelling, provisional type III collagen is gradually replaced by stronger, more organised, and cross-linked type I collagen.
  7. Plasma cells within the endometrial stroma are the defining histological feature required for the diagnosis of chronic endometritis.
  8. Neutrophils signify acute endometritis, whereas macrophages are found in both acute and chronic inflammatory states.
  9. Myofibroblasts differentiate from fibroblasts driven by TGF-beta and express alpha-smooth muscle actin to generate contractile forces for wound closure.
  10. Sarcoidosis is characteristically defined by the histological presence of non-caseating granulomas comprising epithelioid macrophages and lymphocytes.

Common pitfalls

  • Assuming a healed wound regains full original strength; tensile strength reaches only about 80% by 12 weeks and rarely, if ever, returns to 100%.
  • Mistaking macrophages or neutrophils for the diagnostic cell of chronic endometritis, which is defined by identifying stromal plasma cells.
  • Confusing fibroblasts with myofibroblasts, which specifically express alpha-smooth muscle actin to pull wound margins together.
  • Assuming serotonin is the primary vascular permeability mediator; histamine is the principal vasoactive amine driving early acute inflammatory oedema.

Practice questions: Inflammation and Healing

Single best answer, exactly as the exam asks. Commit to an option before opening the explanation.

Question 1

Pathology

During the initial stages of acute inflammation, vascular changes occur leading to oedema. Which chemical mediator, primarily released from mast cells and platelets, plays a key role in increasing vascular permeability?

  1. ASerotonin
  2. BHistamine
  3. CProstaglandins
  4. DCytokines
  5. EKinins
Show answer and explanation

Correct answer: B. Histamine

Key takeaway

In the initial phase of acute inflammation, histamine released from mast cells is the principal mediator causing increased vascular permeability and subsequent oedema formation.

Histamine is a key vasoactive amine stored in the granules of mast cells, basophils, and platelets. Upon encountering an inflammatory trigger (e.g., injury, infection, immune reaction), these cells rapidly release histamine. Histamine binds to H1 receptors on endothelial cells, causing arteriolar vasodilation and, critically, increasing the permeability of post-capillary venules. This increased permeability allows plasma fluid and proteins to leak into the interstitial tissue, resulting in oedema – a cardinal sign of acute inflammation.

Serotonin (5-hydroxytryptamine) is another preformed vasoactive mediator found mainly in platelets (in humans) and enterochromaffin cells. While it has actions similar to histamine (increasing vascular permeability), its role in human inflammation is generally considered less significant than histamine's. Prostaglandins are lipid mediators synthesised de novo during inflammation; they contribute to vasodilation, pain, and fever but generally act later than the initial histamine release. Cytokines (like TNF and IL-1) are proteins produced by various cells that orchestrate broader inflammatory responses, including endothelial activation and leucocyte recruitment, typically over hours rather than minutes. Kinins (e.g., bradykinin) are peptides produced via enzymatic cascades in plasma; they increase vascular permeability, cause vasodilation, and induce pain, contributing to oedema but acting alongside other mediators.

Question 2

Pathology

Following tissue injury and repair, approximately what percentage of its original tensile strength does collagen in a healing wound typically achieve by the 12th week?

  1. A80%
  2. B20%
  3. C50%
  4. D100%
  5. E10%
Show answer and explanation

Correct answer: A. 80%

Key takeaway

Wound tensile strength increases progressively during the remodelling phase due to collagen maturation and cross-linking, typically reaching approximately 80% of the original tissue strength by 12 weeks.

The process of wound healing involves several overlapping phases: inflammation, proliferation, and remodelling. During the remodelling phase, which begins after a few weeks and can last for months or even years, the wound undergoes significant changes. Type III collagen, initially laid down during the proliferative phase, is gradually replaced by stronger Type I collagen. This collagen becomes more organised and cross-linked, steadily increasing the tensile strength of the healed tissue. By the 12th week (approximately 3 months), the wound typically achieves around 80% of the original tissue's tensile strength. It is important to note that healed tissue rarely, if ever, regains 100% of its original strength.

The other options represent incorrect timelines for achieving this level of strength. At earlier stages, such as a few weeks post-injury, the tensile strength is much lower, corresponding to the 10%, 20%, or 50% marks, reflecting the less organised and weaker collagen present. Achieving 100% strength is generally not considered physiologically possible for healed scar tissue compared to intact original tissue.

5 more inflammation and healing questions in the bank

Every question carries a full explanation and a key takeaway like the ones above. Pay once for 1, 3, 6 or 12 months; no subscription.

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What the syllabus covers under inflammation and healing

  • Acute Inflammation
  • Chronic Inflammation
  • Wound Healing

Read the full section in the Pathology guide, or check the next exam dates.