Inflammation and Repair Practice Questions

Q: First mediator of inflammation to be released is

Histamine. ***Histamine*** - Histamine is the **first mediator of inflammation released** by mast cells and basophils during an allergic or inflammatory response [1][3]. - It promotes **vasodilation** and increased vascular permeability, leading to typical symptoms of inflammation [1][2]. *PAF* - Platelet-activating factor (PAF) is released later in the inflammatory process and is primarily involved in **amplifying** the response rather than initiating it. - It plays a role in **platelet aggregation** and acting on vascular smooth muscle but is not the first released mediator. *Nitric oxide* - Nitric oxide is produced by endothelial cells and plays a role in **vascular relaxation and inflammation**, but it is not among the first mediators released. - It is involved in more **regulatory functions** in the inflammatory response rather than the initial trigger. *IL-1* - Interleukin-1 (IL-1) is a cytokine that is important for the **inflammatory response**, but it is produced after the initial release of mediators like histamine [2]. - It is primarily secreted by **activated macrophages** and contributes to the **amplification** of the immune response [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 84-85. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-94.

Q: Chemotaxis is mediated by-

Leukotriene B4 and C5a. ***Leukotriene B4 and C5a*** - Both **Leukotriene B4** [2] and **C5a** [1] are potent **chemoattractants** that guide the migration of neutrophils and other immune cells to sites of inflammation. - They are crucial in amplifying the **immune response**, particularly during acute inflammatory reactions. *Histamine* - Primarily involved in **vasodilation** and increased **vascular permeability**, rather than mediating chemotaxis. - Does not specifically attract immune cells to sites of injury or infection like leukotrienes do. *Bradykinin* - Mainly functions in **pain sensation** and promoting **vascular permeability**, not as a direct chemotactic agent. - It influences inflammation but does not effectively recruit immune cells to tissues. *Leukotriene C4 and C3a* - **Leukotriene C4** is involved in bronchoconstriction, while **C3a** [1] has roles in the complement system but is less potent than C5a in chemotaxis. - These mediators have different primary roles in inflammation, lacking the specificity of B4 and C5a for leukocyte attraction. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 99-100. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 95-96.

Q: Which of the following is derived from fibroblast cells?

Collagen. ***Collagen*** - Collagen is a structural protein that is predominantly produced by **fibroblast cells** in the extracellular matrix [1][2]. - It provides tensile strength and structural support to various tissues, playing a crucial role in wound healing and tissue repair [2]. *TGF-13* - Transforming Growth Factor-beta 1 (TGF-β1) is primarily produced by **immune cells** and is involved in cell growth and differentiation, not primarily by fibroblasts. - It plays a role in **fibrosis** and inflammation, but is not directly synthesized by fibroblast cells themselves. *MMP2* - Matrix Metalloproteinase-2 (MMP-2) is produced by various cell types, including **endothelial and epithelial cells**, but not predominantly by fibroblasts. - It is involved in the degradation of **extracellular matrix** components rather than being a product of fibroblast synthesis. *Angiopoietin* - Angiopoietin is primarily secreted by **endothelial cells** and plays a significant role in blood vessel formation and maturation. - It is not derived from fibroblast cells and is unrelated to their primary function of producing the extracellular matrix. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 31-32. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 34-35.

Q: Interleukin responsible for Pyrexia is:

IL1. ***IL1*** - **Interleukin-1 (IL-1)** is a primary **endogenous pyrogen**, directly acting on the thermoregulatory center in the hypothalamus to induce fever. - It stimulates the production of **prostaglandin E2 (PGE2)**, which then alters the hypothalamic set point, leading to increased body temperature. *IL3* - **Interleukin-3 (IL-3)** is a **hematopoietic growth factor** that primarily stimulates the proliferation and differentiation of hematopoietic stem cells. - Its main role is in the development of various blood cell lineages, not directly in inducing fever. *IL4* - **Interleukin-4 (IL-4)** is a key cytokine in **allergic reactions** and **Th2 immune responses**, promoting B cell activation and IgE production. - It does not directly cause pyrexia; its primary functions are related to humoral immunity and immune regulation. *IL8* - **Interleukin-8 (IL-8)**, also known as **CXCL8**, is a potent **chemotactic factor** for neutrophils and other immune cells. - Its main function is to recruit inflammatory cells to sites of infection or injury, not to induce fever directly.

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

P-selectin. ***P- selectin*** - P-selectin is a **cell adhesion molecule** crucial for the **rolling** of leukocytes on endothelial cells during the inflammatory response [1]. - It is expressed on activated endothelial cells and binds to **sialylated carbohydrates** on leukocytes, facilitating their transient adhesion [1]. *IL-8* - IL-8 is a **chemokine** that primarily acts as a chemotactic factor for neutrophils rather than mediating rolling on endothelium. - While it attracts leukocytes to sites of inflammation, it does not play a role in the initial contact or rolling process. *ICAM-1* - ICAM-1 is an **intercellular adhesion molecule** that facilitates **firm adhesion** rather than rolling of leukocytes. - It primarily interacts with **integrins** on leukocytes to stabilize their adhesion after rolling has occurred. *(3, integrin* - Integrins play a significant role in **firm adhesion** and not the rolling phase, interacting with receptors like ICAM-1. - The binding of integrins to their ligands occurs after leukocytes have initially rolled on the endothelium. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 87.

Q: What is the maximum tensile strength of a healed wound compared to the original tissue?

70-80% of original strength. ***70-80% of original strength*** - A healed wound, even under optimal conditions, can only achieve a maximum of **70-80%** of the tensile strength of the original **uninjured tissue** [1]. - This is because the repair process involves the formation of **fibrous scar tissue** which differs structurally from the original tissue, particularly in the organization and type of collagen fibers. *100% of original strength* - This option is incorrect because healed wounds, even completely mature ones, rarely regain the **full strength** of the original tissue [1]. - The replacement of damaged tissue with **scar tissue** inherently limits perfect functional and structural restoration. *50% of original strength* - While tensile strength gradually increases during wound healing, it typically exceeds **50%** as the wound matures. - This value is often seen in the **early stages** of healing but not as the maximum achievable strength. *None of the options* - This option is incorrect because **70-80% of original strength** is a well-established range for the maximum tensile strength of a healed wound. - This range reflects the physiological limitations of **scar tissue remodeling** and collagen deposition. **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 is not an acute phase reactant?

Endothelin. ***Endothelin*** - Endothelin is a **vasoconstrictive peptide** primarily involved in regulating **blood vessel tone** and blood pressure. - While it plays a role in processes like inflammation and tissue repair, it is not synthesized or regulated in the same rapid, systemic manner as a classic acute phase reactant. *C-reactive protein* - **C-reactive protein (CRP)** is a rapidly responding acute phase reactant produced by the liver in response to **inflammation**, infection, and tissue injury. - Its levels can rise dramatically within hours of an inflammatory stimulus and are used as a marker for disease activity. *Haptoglobin* - **Haptoglobin** is an acute phase reactant that binds to free **hemoglobin** released from red blood cells during hemolysis, preventing oxidative damage. - Its levels typically increase during acute inflammation or infection, although it can also decrease with severe hemolysis. *Fibrinogen* - **Fibrinogen** is a critical acute phase protein involved in the **coagulation cascade** and wound healing. - Its concentration increases significantly during acute inflammation, contributing to the elevated **erythrocyte sedimentation rate (ESR)**.

Q: Which of the following statements about interleukin-1 is false?

IL-1 inhibits IL-2 production by T-cells.. ***IL-1 inhibits IL-2 production by T-cells*** - This statement is false because **IL-1** actually **enhances the production of IL-2** by T-cells, which is crucial for T-cell proliferation and immune response. - **IL-1 acts synergistically with IL-6 and TNF-α** to promote inflammation and immune cell activation, where IL-2 plays a key role. *The primary source of IL-1 is the monocyte-macrophage system* - This statement is true; **monocytes and macrophages** are the main producers of **IL-1α and IL-1β** upon activation by various stimuli. - Other cells, such as neutrophils, dendritic cells, and endothelial cells, can also produce IL-1, but monocytes and macrophages are the predominant source. *IL-1 is an endogenous pyrogen* - This statement is true; **IL-1** is a potent **endogenous pyrogen** that acts on the hypothalamus to induce fever, a hallmark of the acute phase response. - It triggers prostaglandin synthesis in the hypothalamus, leading to an elevation in the body's thermoregulatory set point. *IL-1 promotes acute phase protein synthesis in the liver* - This statement is true; **IL-1** is a key mediator that stimulates **hepatocytes** to produce **acute phase proteins**, such as C-reactive protein and serum amyloid A. - This hepatic response is part of the innate immune system's effort to control infection and inflammation.

Q: Which of the following statements is NOT true regarding transforming growth factor-beta (TGF-beta)?

Activation of macrophages. ***Activation of macrophages*** - Transforming growth factor (TGF) **does not activate macrophages**; rather, it can have an immunosuppressive effect on their activity. - The primary role of TGF is in **regulating inflammation** and promoting tissue repair, which does not include direct activation of macrophages. *Proliferation of endothelial cells* - TGF is known to stimulate the **proliferation of endothelial cells**, contributing to new blood vessel formation (angiogenesis). However, TGF-β can also suppress endothelial proliferation and migration while enhancing ECM protein production [1]. - It plays a significant role in **vascular remodeling** during wound healing and tissue regeneration. *Proliferation for fibroblast* - TGF is a key mediator in **fibroblast proliferation**, promoting production of extracellular matrix components [2]. - This process is essential for tissue healing and fibrosis, contrary to the statement in the question. *Chemotaxis of fibroblasts* - TGF facilitates **chemotaxis of fibroblasts**, guiding them to sites of injury for tissue repair [2]. - This chemotactic property is significant in **fibrosis** and tissue remodeling processes. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 115-116. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 117-119.

Q: Macrophages are converted to epithelioid cells by which cytokine?

IFN-γ. ***IFN-γ: A cytokine involved in classical macrophage activation*** - **Interferon-gamma (IFN-γ)** is a key cytokine produced by activated T cells and NK cells that plays a crucial role in activating macrophages and converting them into **epithelioid cells** [1]. - This conversion is essential for the formation of **granulomas**, a hallmark of chronic inflammatory responses, particularly in infections like tuberculosis [1]. *TNF-α: A cytokine involved in granuloma maintenance* - **Tumor Necrosis Factor-alpha (TNF-α)** is vital for the **formation and maintenance** of granulomas, but it is not directly responsible for the initial conversion of macrophages to epithelioid cells. - While TNF-α helps to **organize and contain** the infection within the granuloma, IFN-γ drives the phenotypic change of macrophages. *TGF-β: A cytokine involved in tissue remodeling* - **Transforming Growth Factor-beta (TGF-β)** is predominantly involved in **tissue repair, fibrosis, and immune regulation**, promoting extracellular matrix production. - It does not primarily induce the differentiation of macrophages into epithelioid cells; rather, it often plays a role in the later stages of granuloma development, contributing to **fibrotic encapsulation** [1]. *IL-4: A cytokine involved in alternative macrophage activation* - **Interleukin-4 (IL-4)** is a characteristic cytokine that drives **alternative macrophage activation (M2 pathway)**, leading to roles in allergic responses and tissue repair [1]. - The M2 phenotype is distinct from the classically activated (M1) phenotype associated with epithelioid cell formation, which is driven by IFN-γ. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109.

Question 1

First mediator of inflammation to be released is

Accepted Answer

Histamine

Answer

Nitric oxide

Answer

PAF

Answer

IL-1

Question 2

Chemotaxis is mediated by-

Accepted Answer

Leukotriene B4 and C5a

Answer

Histamine

Answer

Leukotriene C4 and C3a

Answer

Bradykinin

Question 3

Which of the following is derived from fibroblast cells?

Accepted Answer

Collagen

Answer

MMP2

Answer

Angiopoietin

Answer

TGF-β

Question 4

Interleukin responsible for Pyrexia is:

Accepted Answer

IL1

Answer

IL4

Answer

IL3

Answer

IL8

Question 5

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

Accepted Answer

P-selectin

Answer

ICAM-1

Answer

Integrin

Answer

IL-8

Question 6

What is the maximum tensile strength of a healed wound compared to the original tissue?

Accepted Answer

70-80% of original strength

Answer

100% of original strength

Answer

50% of original strength

Answer

None of the options

Question 7

Which of the following is not an acute phase reactant?

Accepted Answer

Endothelin

Answer

C-reactive protein

Answer

Haptoglobin

Answer

Fibrinogen

Question 8

Which of the following statements about interleukin-1 is false?

Accepted Answer

IL-1 inhibits IL-2 production by T-cells.

Answer

IL-1 is an endogenous pyrogen.

Answer

The primary source of IL-1 is the monocyte-macrophage system.

Answer

IL-1 promotes acute phase protein synthesis in the liver.

Question 9

Which of the following statements is NOT true regarding transforming growth factor-beta (TGF-beta)?

Accepted Answer

Activation of macrophages

Answer

Proliferation of fibroblasts

Answer

Inhibition of T-cell proliferation

Answer

Chemotaxis of fibroblasts

Question 10

Macrophages are converted to epithelioid cells by which cytokine?

Accepted Answer

IFN-γ

Answer

TNF-α

Answer

TGF-β

Answer

IL-4

Inflammation and Repair — MCQs

Inflammation and Repair — MCQs

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