Inflammation and Repair Practice Questions

Q: The maximum tensile strength that a wound can reach after healing is complete, in comparison to normal skin, is

60%–80%. ***60%–80%*** - A fully healed wound, after complete maturation (typically **3 months**), achieves approximately **70–80%** of the **tensile strength** of normal unwounded skin [1]. - This is the **maximum tensile strength** that can be attained despite ongoing **collagen remodeling** and cross-linking [1]. - The strength never reaches 100% because scar tissue has a different collagen architecture compared to normal tissue, with **Type I collagen** replacing the original dermis but in a less organized pattern. *50%–60%* - This range underestimates the final tensile strength achieved by completely healed wounds. - At approximately **6 weeks**, wounds may be at this strength level, but further maturation increases strength to 70–80% [1]. *20%–30%* - This represents the tensile strength at an **early stage** of wound healing (around 3 weeks). - By the time healing is **complete**, the tensile strength is substantially higher than this range. *30%–50%* - This range also underestimates the maximum tensile strength of fully healed wounds. - While this may represent intermediate stages of healing, the final mature scar achieves greater strength approaching 70–80%. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 119-121.

Q: Langhans' giant cells are characteristically seen in

peritoneal tuberculosis. ***Peritoneal tuberculosis*** - **Langhans' giant cells** are a characteristic histological feature of **granulomatous inflammation**, particularly seen in **tuberculosis** [1], [2]. - They are formed by the fusion of epithelioid histiocytes and are a hallmark of **mycobacterial infections**, including peritoneal tuberculosis [2]. - While not pathognomonic, their presence in the appropriate clinical context strongly suggests tuberculosis [1]. *Typhoid Peyer's patch* - **Typhoid fever** causes **macrophage infiltration** with **necrosis** and **ulceration** in Peyer's patches. - The inflammatory response is mononuclear but does **not** form **epithelioid granulomas** or Langhans' giant cells. - Histology shows mononuclear cell infiltration and typhoid nodules, not granulomatous inflammation. *Tuberculoma* - A **tuberculoma** is a localized form of tuberculosis and **also contains Langhans' giant cells** within its granulomatous structure [1]. - However, peritoneal tuberculosis represents a broader clinical entity where identification of these cells in peritoneal tissue/fluid is diagnostically significant. - Both are forms of TB, but the question context favors the systemic/cavity involvement over a localized mass lesion. *Lymphoma* - **Lymphoma** shows malignant proliferation of lymphoid cells with effacement of normal architecture. - It does **not** show **granulomatous inflammation** or Langhans' giant cells. - Histology reveals sheets of atypical lymphoid cells, not epithelioid granulomas. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 383-384. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109.

Q: Hypertrophic scar is characterized by the following, except

it outgrows the wound area. ***it outgrows the wound area*** - This statement is characteristic of a **keloid scar**, not a hypertrophic scar. Keloids are distinguished by their growth beyond the original wound margins [1]. - **Hypertrophic scars**, on the other hand, remain confined within the boundaries of the original injury, though they may be raised and erythematous [1]. *it involves the flexor surface* - While hypertrophic scars can occur on any body surface, they are commonly found on areas of **high tension**, such as the **flexor surfaces** of joints (e.g., knee, elbow) or the chest and shoulders. - This involvement is due to constant movement stretching the healing skin, which can stimulate excessive collagen production. *it is non-familial* - Hypertrophic scars are generally **not associated with a strong genetic predisposition** or familial inheritance patterns. - Their development is primarily linked to factors like wound tension, infection, and individual healing responses rather than inherited tendencies. *it is not related to the race* - The incidence of hypertrophic scars does **not show a significant racial predilection**, unlike keloid scars, which are more common in individuals with darker skin types. - Hypertrophic scars can affect individuals from all racial backgrounds. **References:** [1] Kumar v, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 119-121.

Q: Which of the following factors is labelled as cytokine in the pathogenesis of Systemic Inflammatory Response Syndrome (SIRS)?

Tumor necrosis factor. ***Tumor necrosis factor*** - **Tumor necrosis factor (TNF-α)** is a prominent pro-inflammatory cytokine and a key mediator in the pathogenesis of **Systemic Inflammatory Response Syndrome (SIRS)** [1]. - It plays a crucial role in initiating and amplifying the inflammatory cascade, leading to systemic effects like fever, increased vascular permeability, and tissue damage [1]. *Leukotrienes* - **Leukotrienes** are lipid mediators derived from arachidonic acid, involved in inflammation and allergic reactions [1]. - They are not classified as **cytokines**, which are protein signaling molecules [1]. *Nitric oxide* - **Nitric oxide (NO)** is a gaseous signaling molecule with various physiological roles, including vasodilation and neurotransmission. - While it contributes to the pathophysiology of SIRS, particularly in regulating vascular tone, it is not a **cytokine**. *Complements* - **Complements** are a system of plasma proteins that are part of the innate immune response, helping to clear pathogens [1]. - They participate in inflammation but are distinct from **cytokines**, which are regulatory proteins [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-101.

Q: Arrange the following cellular events of inflammation in the correct sequence: 1. Rolling 2. Cytokine-mediated integrin activation 3. Adhesion 4. Migration

1,2,3,4. ***1,2,3,4*** - The correct sequence of cellular events for leukocyte recruitment during inflammation begins with **rolling** [1], followed by **cytokine-mediated integrin activation** [2], then firm **adhesion** to the endothelium [1], and finally **migration** (diapedesis) into the tissues [3]. - This step-by-step process ensures effective targeting of leukocytes to the site of injury or infection [1]. *3,4,1,2* - This sequence is incorrect as **adhesion** cannot occur before **rolling**, and **migration** is the final step after adhesion, not an early one. - **Cytokine-mediated integrin activation** must precede firm adhesion [1]. *2,1,4,3* - This order is incorrect because **rolling** (1) is the initial interaction that allows leukocytes to slow down on the endothelium [2], and it occurs before **cytokine-mediated integrin activation** (2) which strengthens the binding. - **Migration** (4) is also misplaced as it should be the last step after firm adhesion (3). *4,1,2,3* - This sequence is incorrect as **migration** (4) is the last step in the process, not the first. - **Rolling** (1) initiates the process by transiently interacting with endothelial cells, followed by activation and adhesion. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 87. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Migration in the tissues toward a chemotactic stimulus, pp. 86-87. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 87-89.

Q: Which of the following cytokines plays the most crucial role in mediating the inflammatory response and tissue damage in gonococcal arthritis?

IL-1β. ***IL-1β*** - **IL-1β** is the most crucial cytokine mediating inflammatory response and tissue damage specifically in **gonococcal arthritis** - Neisseria gonorrhoeae infection triggers potent **IL-1β production** through complement activation and bacterial lipooligosaccharide (LOS) [1] - IL-1β drives the production of **matrix metalloproteinases (MMPs)** and other degradative enzymes, leading to **cartilage and bone destruction** - It amplifies the inflammatory cascade by inducing other pro-inflammatory cytokines and chemokines [1] - Experimental models show that **IL-1β blockade significantly reduces joint damage** in gonococcal infections *IL-8* - **IL-8** (CXCL8) is a critical **neutrophil chemokine** that causes the characteristic massive neutrophil infiltration in gonococcal arthritis [1] - While essential for leukocyte recruitment and the purulent synovial fluid seen in this condition, it is primarily a **chemotactic mediator** rather than the main driver of tissue destruction [1] *IL-6* - **IL-6** is a pro-inflammatory cytokine involved in the **acute phase response** and systemic inflammatory features [1] - It contributes to fever, synovitis, and B-cell responses during infection - However, its role in directly mediating joint tissue damage in gonococcal arthritis is **secondary** to IL-1β *TNF-α* - **TNF-α** is a potent pro-inflammatory cytokine important in many forms of arthritis, particularly **rheumatoid arthritis** and chronic inflammatory conditions [1] - While it does contribute to inflammation in septic arthritis, in **gonococcal arthritis specifically**, the cytokine profile is **dominated by IL-1β and IL-8** - The pathophysiology of gonococcal infection differs from other bacterial arthritides where TNF-α may play a more central role **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 97-99.

Question 1

The maximum tensile strength that a wound can reach after healing is complete, in comparison to normal skin, is

Accepted Answer

60%–80%

Answer

30%–50%

Answer

20%–30%

Answer

50%–60%

Question 2

Langhans' giant cells are characteristically seen in

Accepted Answer

peritoneal tuberculosis

Answer

typhoid Peyer's patch

Answer

tuberculoma

Answer

lymphoma

Question 3

Hypertrophic scar is characterized by the following, except

Accepted Answer

it outgrows the wound area

Answer

it involves the flexor surface

Answer

it is non-familial

Answer

it is not related to the race

Question 4

Which of the following factors is labelled as cytokine in the pathogenesis of Systemic Inflammatory Response Syndrome (SIRS)?

Accepted Answer

Tumor necrosis factor

Answer

Leukotrienes

Answer

Nitric oxide

Answer

Complements

Question 5

A 20 year old female was operated for perforation peritonitis and after closing the rectus sheath her abdominal wound was left open to heal with proliferative granulation tissue which contracted and epithelialized to form a scar. This patient had undergone healing by:

Accepted Answer

Secondary intention

Answer

Delayed primary intention

Answer

Primary intention

Answer

Tertiary intention

Question 6

Which one of the following factors is NOT involved in the pathogenesis of Systemic inflammatory response syndrome (SIRS)?

Accepted Answer

Microvascular occlusion

Answer

Free radical production

Answer

Increased cytokine production

Answer

Abnormal nitric oxide synthesis

Question 7

What is the correct order of the normal phases of wound healing?

Accepted Answer

Haemostatic phase → Inflammatory phase → Proliferative phase → Remodelling phase

Answer

Proliferative phase → Haemostatic phase → Inflammatory phase → Remodelling phase

Answer

Remodelling phase → Proliferative phase → Destructive phase → Inflammatory phase

Answer

Destructive phase → Proliferative phase → Remodelling phase → Inflammatory phase

Question 8

Arrange the following cellular events of inflammation in the correct sequence:

1. Rolling
2. Cytokine-mediated integrin activation
3. Adhesion
4. Migration

Accepted Answer

1,2,3,4

Answer

3,4,1,2

Answer

2,1,4,3

Answer

4,1,2,3

Question 9

Which of the following cytokines plays the most crucial role in mediating the inflammatory response and tissue damage in gonococcal arthritis?

Accepted Answer

IL-1β

Answer

TNF-α

Answer

IL-8

Answer

IL-6

Question 10

What is the mechanism of secondary healing?

Accepted Answer

Granulation tissue

Answer

Neovascularization

Answer

Scab formation

Answer

Granuloma formation

Inflammation and Repair — MCQs

Inflammation and Repair — MCQs

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