Inflammation and Repair Practice Questions

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.

Q: Rolling of leucocytes on endothelial cells is mediated by which of the following proteins?

Selectins. **Selectins** - **Selectins** mediate the initial, weak and transient adhesion of **leukocytes** to the **endothelial cells** lining blood vessels [1]. - This interaction slows down the leukocytes, causing them to **roll** along the vascular endothelium as a prerequisite for **extravasation** [1]. *Integrins* - **Integrins** are responsible for the **firm adhesion** of leukocytes to endothelial cells, but not the rolling [1]. - They bind to **ICAM-1 (intercellular adhesion molecule-1)** on endothelial cells, leading to stable arrest of the leukocyte [1]. *PECAM-1* - **PECAM-1 (Platelet Endothelial Cell Adhesion Molecule-1)** plays a role in **diapedesis** or **transmigration**, the movement of leukocytes *through* the endothelial cell junctions [1]. - It facilitates the passage of the leukocyte by interacting with PECAM-1 on the endothelial cells, but does not mediate rolling [1]. *Transferrin* - **Transferrin** is an iron-binding protein found in blood plasma that regulates free **iron levels** in the body. - It is crucial for **iron transport** and metabolic processes but has no direct role in leukocyte adhesion or rolling on endothelial cells. **References:** [1] 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 substances is a growth factor that is capable of inducing all the steps necessary for angiogenesis?

Basic fibroblast growth factor. ***Basic fibroblast growth factor*** - **Basic fibroblast growth factor (bFGF or FGF2)** is a potent inducer of **angiogenesis**, promoting endothelial cell proliferation, migration, and tube formation. - It plays a crucial role in **wound healing** and **tumor growth** by stimulating the development of new blood vessels. *TGF-α* - **TGF-alpha** primarily acts as a **mitogen** for epithelial cells and fibroblasts, promoting cell growth and differentiation. - While it can indirectly influence angiogenesis, it does not directly induce all steps of the process like bFGF. *PDGF* - **Platelet-derived growth factor (PDGF)** is a mitogen for **fibroblasts, smooth muscle cells, and glial cells**, involved in wound healing and tissue remodeling. - Its primary role in angiogenesis is thought to be in the **stabilization of new vessels** by recruiting pericytes and smooth muscle cells, rather than initiating new vessel formation. *EGF* - **Epidermal growth factor (EGF)** primarily stimulates the **proliferation and differentiation of epidermal and epithelial cells**. - While it contributes to tissue repair and cell growth, its direct role in inducing all stages of angiogenesis is less prominent compared to bFGF.

Q: Oxygen dependent killing is done through

NADPH oxidase. ***NADPH oxidase*** - **NADPH oxidase** is the enzyme responsible for the **respiratory burst**, producing **superoxide radicals (O2-)** which are crucial for oxygen-dependent killing by phagocytes. - This enzyme converts **molecular oxygen** into highly reactive **superoxide** by reducing NADP+ using NADPH. *Superoxide dismutase* - **Superoxide dismutase (SOD)** neutralizes **superoxide radicals** by converting them into hydrogen peroxide, acting as an antioxidant defense mechanism, rather than a killing mechanism. - While it deals with reactive oxygen species, its role is to protect the cell from oxidative damage, not to generate products for microbial killing. *Glutathione peroxidase* - **Glutathione peroxidase** is an antioxidant enzyme that reduces **hydrogen peroxide** and organic hydroperoxides to water using **reduced glutathione**, thus protecting cells from oxidative stress. - It does not directly produce reactive oxygen species for microbial killing but rather detoxifies them. *Catalase* - **Catalase** converts **hydrogen peroxide** into water and oxygen, functioning to protect cells from the damaging effects of hydrogen peroxide. - Like superoxide dismutase and glutathione peroxidase, its primary role is protective against reactive oxygen species, not in generating them for pathogen eradication.

Q: C-C beta chemokines include

Eotaxin. ***Eotaxin*** - **Eotaxin** (CCL11, CCL24, CCL26) is a key **C-C chemokine** that primarily attracts **eosinophils** to sites of allergic inflammation. - C-C chemokines are characterized by having two adjacent cysteine residues (CC) near the N-terminus. *IL-8* - **IL-8** (CXCL8) is a **C-X-C chemokine**, meaning it has an amino acid residue separating the first two cysteines (CXC motif). - Its primary role is to act as a potent **neutrophil chemoattractant** and activator. *Fractalkine* - **Fractalkine** (CX3CL1) is a unique chemokine belonging to the **C-X3-C chemokine** family, characterized by three amino acids separating the first two cysteines (CX3C motif). - It exists as both a **soluble chemokine** and a **membrane-bound molecule** involved in cell adhesion and leukocyte trafficking. *Lymphotactin* - **Lymphotactin** (XCL1) is a member of the **C chemokine (or XC chemokine)** family, distinguished by having only one cysteine residue at the N-terminus. - It is primarily involved in the chemotaxis of **T cells** and **NK cells**.

Q: A 45-year old patient presented with fever, night sweats and weight loss. On X-ray, a mass was seen in apical lobe. On histopathology, caseous necrosis was present. What is the name of underlying process?

Granulomatous inflammation (Type IV hypersensitivity). ***Granulomatous inflammation (Type IV hypersensitivity)*** - The presence of **caseous necrosis** on histopathology, combined with symptoms like fever, night sweats, and weight loss, and an apical lung mass, is highly characteristic of **tuberculosis** [1]. - Tuberculosis is a classic example of a **type IV hypersensitivity reaction** involving **epithelioid macrophages** (modified macrophages), **lymphocytes**, and **Langhans giant cells** forming **granulomas** with central **caseous necrosis** [2], [3]. - This represents **granulomatous inflammation**, which is the hallmark histopathological finding in tuberculosis [1]. *Decreased supply of growth factor* - This typically leads to **atrophy** or **apoptosis**, which are distinct from the inflammatory and necrotic process described. - It does not explain the characteristic histological finding of **caseous necrosis** or the systemic symptoms. *Acute decrease in blood supply* - An acute decrease in blood supply (ischemia or infarction) would lead to **coagulative necrosis** in most tissues, not the **caseous necrosis** seen in this presentation. - While infarction can cause tissue death, the specific histological and clinical picture points away from simple ischemia. *Enzymatic degeneration* - **Enzymatic degeneration**, particularly from pancreatic enzymes, is typical of **fat necrosis** (e.g., in acute pancreatitis), where fat cells are broken down. - This process does not produce the characteristic **caseous necrosis** and granulomatous inflammation seen in the patient's lung. **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. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, p. 360.

Q: Tensile strength of a wound becomes normal after:

Never. ***Never*** - A healed wound, even after complete maturation, only achieves about **80% of the original tissue's tensile strength** - The process of scar formation involves the realignment of collagen fibers and increased cross-linking, but it can **never perfectly replicate** the pre-injury tissue architecture and strength - This is a fundamental principle of wound healing - scar tissue is structurally different from normal tissue *6 months* - By 6 months, a wound's tensile strength has typically reached its **maximum potential** of approximately 80%, but this is still less than 100% of the original tissue's strength - This period marks the end of the significant remodeling phase, where collagen fibers are reorganized and strengthened *4 months* - At 4 months, the wound is still undergoing substantial **remodeling and strengthening**, achieving approximately 70-80% of eventual tensile strength - While considerable strength is gained by this time, further improvements continue for several more months *6 weeks* - At 6 weeks, the wound has achieved about **50-70% of its eventual tensile strength** - This stage is characterized by increased collagen deposition and cross-linking, making the wound clinically strong, but it is far from its maximum or normal strength

Question 1

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 2

What is the mechanism of secondary healing?

Accepted Answer

Granulation tissue

Answer

Neovascularization

Answer

Scab formation

Answer

Granuloma formation

Question 3

Rolling of leucocytes on endothelial cells is mediated by which of the following proteins?

Accepted Answer

Selectins

Answer

Integrins

Answer

Transferrin

Answer

PECAM-1

Question 4

Characteristic of acute inflammation is

Accepted Answer

Vasodilation and increase permeability

Answer

Vasoconstriction

Answer

Platelet aggregation

Answer

Infiltration by neutrophils

Question 5

Which of the following substances is a growth factor that is capable of inducing all the steps necessary for angiogenesis?

Accepted Answer

Basic fibroblast growth factor

Answer

TGF -a

Answer

PDGF

Answer

EGF

Question 6

Oxygen dependent killing is done through

Accepted Answer

NADPH oxidase

Answer

Superoxide dismutase

Answer

Glutathione peroxidase

Answer

Catalase

Question 7

C-C beta chemokines include

Accepted Answer

Eotaxin

Answer

IL-8

Answer

Fractalkine

Answer

Lymphotactin

Question 8

A 45-year old patient presented with fever, night sweats and weight loss. On X-ray, a mass was seen in apical lobe. On histopathology, caseous necrosis was present. What is the name of underlying process?

Accepted Answer

Granulomatous inflammation (Type IV hypersensitivity)

Answer

Decreased supply of growth factor

Answer

Acute decrease in blood supply

Answer

Enzymatic degeneration

Question 9

Tensile strength of a wound becomes normal after:

Accepted Answer

Never

Answer

6 months

Answer

4 months

Answer

6 weeks

Question 10

A 45 year old patient presents with history of fever, night sweats and weight loss. On X-ray, a mass in apical lobe of lung is seen. On histopathology, it was found to have caseous necrosis. What is the likely underlying process involved -

Accepted Answer

Hypersensitivity reaction with modified macrophages, lymphocytes and giant cells

Answer

Acute decrease in blood supply

Answer

Decreased supply of growth factors

Answer

Enzymatic degeneration

Inflammation and Repair — MCQs

Inflammation and Repair — MCQs

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