Inflammation and Repair Practice Questions

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: 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 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: 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.

Q: Increased vascular permeability in acute inflammation is due to what?

Histamine. ***Histamine*** - Histamine is a key **mediator** released during acute inflammation that causes **increased vascular permeability** by inducing **contraction of endothelial cells** [1][2]. - Its release contributes to the hallmark signs of inflammation, including **swelling** and **redness** [2]. *IL 2* - IL 2 primarily functions as a **growth factor** for T cells, not directly influencing vascular permeability in acute inflammation. - It is more involved in the **adaptive immune response** rather than in the acute phase of inflammation. *TGF beta* - TGF beta is primarily involved in **fibrosis** and **tissue repair** and does not play a direct role in increasing vascular permeability during acute phases. - It acts more as an **anti-inflammatory** cytokine rather than a pro-inflammatory mediator. *FGF* - Fibroblast growth factor (FGF) is mainly involved in **angiogenesis** and wound healing rather than direct modulation of vascular permeability during acute inflammation. - It does not contribute to **edema formation** associated with acute inflammatory responses. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 187-188. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101.

Q: Increased permeability in acute inflammation is due to all except?

Lytic enzymes. ***Lytic enzymes*** - **Lytic enzymes** play a role in the breakdown of tissue and are not primarily responsible for increased vascular permeability in acute inflammation [2]. - They are more involved in tissue destruction rather than facilitating permeability changes [2]. *Cytokines* - **Cytokines** are crucial mediators in the inflammatory response and increase vascular permeability by affecting endothelial function. - They promote the expression of adhesion molecules and induce other inflammatory mediators, contributing to permeability. *Endothelial injury* - **Endothelial injury** directly contributes to increased permeability by damaging the endothelial barrier, allowing fluid and proteins to leak into tissues. - It often occurs due to various insults, such as infections, toxins, and mechanical stress during inflammation. *Cell contraction* - **Cell contraction** refers to the retraction of endothelial cells, which leads to increased gaps in the endothelium and enhances permeability [1]. - This mechanism is induced by inflammatory mediators like histamine and contributes significantly to acute inflammation [1,2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 187-189. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101.

Question 1

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 2

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 3

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 4

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 5

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 6

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 7

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

Accepted Answer

Histamine

Answer

Epinephrine

Answer

Norepinephrine

Answer

Serotonin

Question 8

Fever occurs due to which of the following mechanisms?

Accepted Answer

IL-1

Answer

Endorphin

Answer

Enkephalin

Answer

Histamine

Question 9

Increased vascular permeability in acute inflammation is due to what?

Accepted Answer

Histamine

Answer

IL-2

Answer

TGF-β

Answer

FGF-2

Question 10

Increased permeability in acute inflammation is due to all except?

Accepted Answer

Lytic enzymes

Answer

Cytokines

Answer

Endothelial cell contraction

Answer

Endothelial injury

Inflammation and Repair — MCQs

Inflammation and Repair — MCQs

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