Inflammation and Repair Practice Questions

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.

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: Which of the following cell types is classified as a labile cell?

Surface epithelium. ***Surface epithelium*** - Surface epithelium is classified as **labile tissue**, meaning it undergoes constant regeneration due to its high turnover rate [1]. - Cells in this tissue are typically found in areas that experience frequent damage or abrasion, such as the skin and lining of the intestines. *Cardiac cell* - Cardiac cells are considered **permanent cells**, as they do not undergo significant regeneration after injury or damage. - Damage to cardiac cells typically leads to **fibrosis** rather than repair of the original tissue. *Liver parenchymal cell* - Liver parenchymal cells are categorized as **stable cells**, which can regenerate but do so under specific circumstances, such as injury. - They have a slower turnover rate compared to labile cells and do not constantly renew under normal conditions. *Vascular endothelial cells* - Vascular endothelial cells are considered **stable cells** as well, typically maintaining a stable population but capable of regeneration following injury. - They do not have the same rapid turnover and regeneration capability as labile cells do, especially under normal physiological conditions. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 113-115.

Q: Which mediators are involved in the resolution of inflammation?

Resolvins, protectins, and lipoxins. ***Resolvins, protectins, and lipoxins*** - These are **specialized pro-resolving mediators (SPMs)** derived from omega-3 and omega-6 polyunsaturated fatty acids that actively promote the resolution phase of inflammation. - **Lipoxins** (from arachidonic acid) inhibit neutrophil chemotaxis and promote macrophage-mediated clearance of apoptotic cells. - **Resolvins** (from EPA and DHA) actively terminate inflammatory signals, reduce neutrophil infiltration, and enhance bacterial clearance. - **Protectins** promote resolution by limiting neutrophil recruitment and enhancing clearance of inflammatory debris. - These mediators represent the **endogenous "stop signals"** that actively resolve inflammation rather than simply suppressing it. *IL-10, IL-1 receptor antagonist, and TGF-β* - While these have **anti-inflammatory** effects, they are not classified as primary resolution mediators. - **IL-10** inhibits pro-inflammatory cytokine synthesis and suppresses immune responses (immunosuppressive rather than pro-resolving). - **IL-1 receptor antagonist (IL-1Ra)** blocks IL-1 signaling, preventing inflammation amplification. - **TGF-β** promotes tissue repair and has immunosuppressive functions. - These are **anti-inflammatory mediators** that prevent or dampen inflammation, distinct from specialized pro-resolving mediators that actively orchestrate the resolution process. *TNF-alpha, IL-1, and CRP* - **TNF-alpha** and **IL-1** are classic **pro-inflammatory cytokines** that initiate and amplify inflammation. - **CRP (C-reactive protein)** is an acute-phase reactant and biomarker of inflammation, not a mediator of resolution. *Interferon-gamma and IL-12* - **IFN-γ** and **IL-12** promote **Th1 immune responses** and cellular immunity. - These are pro-inflammatory mediators involved in host defense against intracellular pathogens, not resolution of inflammation.

Q: Which of the following does not belong to the family of selectins?

A selectin. ***A selectin*** - ***A selectin*** is not a recognized member of the selectin family, which includes other specific types. - The known selectins are **E-selectin**, **L-selectin**, and **P-selectin**, demonstrating a distinct classification [1]. *E selectin* - E selectin is a specific type of selectin expressed on **endothelial cells** activated by cytokines [1]. - It plays a crucial role in **leukocyte adhesion** during inflammation, distinguishing it as part of the selectin family [1]. *L selectin* - L selectin is involved in the **homing** of leukocytes to lymph nodes and forms part of the selectin family [1]. - Responsible for the initial tethering and rolling of leukocytes on **venular endothelium** [1]. *P selectin* - P selectin is found on platelets and endothelial cells and is critical in the **aggregation** of platelets and leukocytes. - It is also an established member of the selectin family, involved in **inflammatory responses** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 87.

Q: Maximum collagen deposition in wound healing is seen at -

End of third week. ***End of third week*** - By the end of the **third week**, the proliferative phase of wound healing is well underway, characterized by significant **collagen deposition**. [1] - At this stage, **Type III collagen** is initially laid down, which is later replaced by stronger **Type I collagen**, contributing to increasing wound strength. *End of first week* - The first week primarily involves the **inflammatory phase** and the initial stages of **proliferation**, with minimal new collagen deposition. [2] - While some **fibroblasts** are present, the amount of collagen synthesized is still relatively low. *End of second week* - Collagen synthesis is ongoing during the second week, but the **peak deposition rate** and overall amount of collagen accumulated are typically not as high as at the end of the third week. - The wound is gaining strength, but further increase in collagen content and remodeling is yet to occur. *End of 2 months* - By 2 months, the wound is in the **remodeling phase**, where the total collagen content might be substantial but the *rate of new collagen synthesis* has slowed down. - At this stage, there is a balance between **collagen synthesis** and **degradation**, and the collagen fibers are being reorganized and cross-linked to further improve tensile strength. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 117-119. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 115.

Q: Which of the following vasoactive amines is primarily involved in inflammation?

Histamine. ***Histamine*** - Released by **mast cells and basophils** [1], histamine plays a crucial role in the inflammatory response, causing **vasodilation** [1] and increased vascular permeability [1]. - It is a key mediator in allergic reactions and contributes to symptoms like **reddening** and **swelling** at the site of inflammation. *All* - This option incorrectly implies that **all listed substances** are vasoactive amines involved in inflammation, which is not true. - Only **histamine** is primarily related to the inflammation process among the options given [1]. *Angiotensin* - Angiotensin primarily affects **blood pressure regulation** and fluid balance, not directly involved in inflammation like histamine. - It works through the **renin-angiotensin system**, primarily altering vascular tone rather than mediating inflammatory responses. *Renin* - Renin is an enzyme that activates the **renin-angiotensin system** but does not act as a vasoactive amine in inflammation [1]. - Its role is primarily in **blood pressure regulation** and fluid homeostasis, rather than direct involvement in the inflammatory process. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 84-85, 93-94, 101. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 94-95.

Q: Fever occurs due to which of the following mechanisms?

IL-1. ***IL1*** - Interleukin-1 (IL-1) is a **proinflammatory cytokine** that plays a key role in the immune response and is a primary mediator of fever [1]. - It stimulates the **hypothalamus** to increase body temperature set-point, thus inducing fever. *Enkephalin* - Enkephalins are **opioid peptides** involved in pain modulation, not in the fever response. - They primarily act in the **central nervous system** and do not directly influence thermoregulation. *Endorphin* - Endorphins, like enkephalins, are also **opioid peptides** related to pain relief and mood regulation, with no significant role in fever induction. - Their main function is to provide **analgesic** effects rather than influencing body temperature. *Histamine* - Histamine is predominantly involved in **allergic responses** and inflammation but is not a direct mediator of fever. - It causes **vasodilation** and increases vascular permeability, but does not raise the body temperature set-point like IL-1 does. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 110-111.

Question 1

Which of the following statements about wound healing is false?

Accepted Answer

Hematomas promote wound healing

Answer

Inhibited by diabetes mellitus (DM)

Answer

Inhibited by foreign body

Answer

Inhibited by infection

Question 2

Macrophages are converted to epithelioid cells by which cytokine?

Accepted Answer

IFN-γ

Answer

TNF-α

Answer

TGF-β

Answer

IL-4

Question 3

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 4

Which of the following cell types is classified as a labile cell?

Accepted Answer

Surface epithelium

Answer

Liver parenchymal cells

Answer

Vascular smooth muscle cells

Answer

Neurons

Question 5

What is the sequence of events in acute inflammation?

Accepted Answer

Transient vasoconstriction - Vasodilatation - Increased permeability - Stasis

Answer

Transient vasoconstriction - Stasis - Vasodilatation - Increased permeability

Answer

Transient vasoconstriction - Vasodilatation - Stasis - Increased permeability

Answer

Vasodilatation - Stasis - Transient vasoconstriction - Increased permeability

Question 6

Which mediators are involved in the resolution of inflammation?

Accepted Answer

Resolvins, protectins, and lipoxins

Answer

TNF Alfa, IL-1, and CRP

Answer

IL-10, IL-1 receptor antagonist, and TGF-β

Answer

Interferon-gamma and IL-12

Question 7

Which of the following does not belong to the family of selectins?

Accepted Answer

A selectin

Answer

P selectin

Answer

L selectin

Answer

E selectin

Question 8

Maximum collagen deposition in wound healing is seen at -

Accepted Answer

End of third week

Answer

End of first week

Answer

End of 2 months

Answer

End of second week

Question 9

Which of the following vasoactive amines is primarily involved in inflammation?

Accepted Answer

Histamine

Answer

Epinephrine

Answer

Norepinephrine

Answer

Serotonin

Question 10

Fever occurs due to which of the following mechanisms?

Accepted Answer

IL-1

Answer

Endorphin

Answer

Enkephalin

Answer

Histamine

Inflammation and Repair — MCQs

Inflammation and Repair — MCQs

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