Inflammation and Repair Practice Questions

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: Which of the following is not classified as a chemokine?

IL-1. ***Histamine*** - Histamine is a **biogenic amine** involved in local immune responses, not classified as a chemokine [1]. - It functions primarily in **vasodilation** and **increased vascular permeability**, contrasting with chemokine roles. *IL-1* - IL-1 is a **cytokine** that plays a role in inflammatory responses but is not a chemokine [1]. - It primarily acts as a mediator for **fever** and **acute inflammation**. *IL-8* - IL-8 is a **chemokine** specifically known for attracting **neutrophils** to sites of inflammation [1]. - It plays a crucial role in **immune response** and is classified within the CXC chemokine family. *Eotaxin* - Eotaxin is a specific **chemokine** that primarily attracts **eosinophils** to sites of inflammation, especially in allergic reactions. - It is involved in the pathogenesis of **asthma** and other eosinophil-associated conditions. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-94.

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.

Q: First cell to migrate into a wound due to chemotaxis to start the process of wound healing is -

Neutrophil. ***Neutrophil*** - Neutrophils are the **first responders** in the wound healing process, rapidly migrating to the site due to **chemotactic signals** [1,2]. - Their primary role includes **phagocytosing pathogens** and debris, facilitating the subsequent healing phases. *Lymphocyte* - Lymphocytes typically arrive later in the healing process and are mainly involved in **immune response** rather than initial wound healing. - They play a significant role in **adaptive immunity** but do not participate in the **early inflammatory phase**. *Platelet* - While platelets aggregate at the wound site and are crucial for **clot formation**, they do not migrate into the wound through chemotaxis like neutrophils [1]. - Their primary function is to initiate the **hemostatic response** rather than directly phagocytosing debris. *Macrophage* - Macrophages are important for **later stages** of wound healing, clearing debris and coordinating tissue repair, but they arrive after neutrophils. - They are involved in the **remodeling phase** and are not the first cells to respond to the wound. **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. 188-189. [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: The primary vasoactive mediator present in mast cells is

Histamine. ***Histamine*** - **Histamine** is a primary **vasoactive amine** stored in the granules of **mast cells** and **basophils**. - Upon mast cell activation, histamine is rapidly released, causing **vasodilatation**, increased **vascular permeability**, and **bronchoconstriction**; it is a key mediator in immediate hypersensitivity reactions. *Heparin* - **Heparin** is an **anticoagulant proteoglycan** found in mast cell granules, but it is not considered the primary vasoactive mediator. - Its main function is to prevent **blood clotting**, which is distinct from the immediate allergic responses mediated by histamine. *Tryptase* - **Tryptase** is a **neutral protease** found almost exclusively in human **mast cells** and is released upon their activation. - While it is a valuable marker for mast cell activation and plays a role in tissue remodeling, it is an **enzyme** rather than a primary vasoactive mediator like histamine. *Chymase* - **Chymase** is another **neutral protease** stored in **mast cell granules**, similar to tryptase. - It participates in **extracellular matrix degradation** and **angiotensin conversion** but is not the main mediator responsible for the immediate vascular and smooth muscle effects seen in allergic reactions.

Q: All of the following are mediators of acute inflammation, except which one?

Angiotensin. ***Angiotensin*** - Angiotensin is primarily involved in **blood pressure regulation** and **fluid balance**, not in mediating acute inflammation [1]. - It does not participate in the **vascular or cellular responses** characteristic of acute inflammatory processes. *Prostaglandin E2* - Prostaglandin E2 is a key **mediator of inflammation** [1][2], promoting vasodilation and increasing **vascular permeability** [3]. - It contributes to pain and fever during the **inflammatory response** [1]. *Kallikrein* - Kallikrein plays a significant role in activating the **bradykinin** system, which enhances vascular permeability during inflammation. - It is involved in the **kallikrein-kinin system**, thus participating actively in acute inflammatory processes. *C 3a* - C 3a is a fragment of the complement system involved in the **anaphylatoxin** response, promoting inflammation [4]. - It contributes to **chemotaxis** [1] and enhances vascular permeability [4], making it a mediator in acute inflammation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-94. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 95-96. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 99-100.

Q: The principal cell in a granuloma is

Histiocyte. ***Histiocyte*** - Histiocytes are the principal **macrophages** in a granuloma, playing a key role in the **immune response** [1][2]. - They are responsible for phagocytosis and the formation of **epithelioid cells**, which are typical of granulomatous inflammation [1]. *Giant cell* - While giant cells are present in granulomas, they are formed from the **fusion of macrophages** and are not the principal cell type [1]. - Their presence signifies a chronic inflammatory response but does not define the granuloma itself. *Langhans* - Langhans giant cells are a specific type of giant cell that may be found in granulomas, particularly in conditions like **tuberculosis** [1]. - They are characterized by a **multi-nucleated** appearance but are not the principal cell in granuloma formation [1]. *Lymphocyte* - Lymphocytes are part of the **adaptive immune response** and may be present in granulomas, but they are not the main cell type [1][3]. - Their role is more of a supportive function, typically acting later in the inflammatory response rather than in granuloma formation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109. [2] 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. 198-200. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 360-362.

Q: Elaboration of which of the following mediators will be most beneficial in preventing further ischemic injury to the cerebral cortex?

Nitric oxide. ***Nitric oxide*** - Increased production of **nitric oxide** leads to **vasodilation**, improving blood flow to ischemic areas and potentially preventing further neuronal damage. - As a **vasodilator**, nitric oxide can help restore oxygen and nutrient supply to the cerebral cortex affected by ischemia. *Bradykinin (involved in vasodilation and vascular permeability)* - While bradykinin causes **vasodilation**, it also significantly increases **vascular permeability**, which can lead to **cerebral edema** in the context of ischemic injury, worsening patient outcomes. - The increased vascular permeability associated with Bradykinin causes **fluid leakage** into the brain tissue, potentially increasing intracranial pressure and exacerbating secondary injury. *Leukotriene E4 (involved in inflammatory responses)* - **Leukotriene E4** is a potent mediator of **inflammation** and **vasoconstriction**, which would further restrict blood flow and worsen ischemic injury rather than prevent it. - Its pro-inflammatory actions contribute to the **secondary injury cascade** following ischemia, exacerbating tissue damage. *Platelet-activating factor (contributes to inflammation and thrombosis)* - **Platelet-activating factor (PAF)** promotes **platelet aggregation** and **inflammation**, leading to further thrombosis and exacerbating vascular occlusion, thereby worsening ischemia. - Its role in **thrombosis** would directly counteract efforts to restore blood flow to the ischemic cerebral cortex.

Q: Wound strength is 70% after how many weeks?

12 weeks. ***3 months*** - Wound strength typically reaches **70%** of its maximum after approximately **3 months** post-surgery or injury [1]. - After this period, collagen formation and remodeling lead to significant strength improvement in the healing tissue [1]. *6 months* - By **6 months**, wound strength may exceed **70%**, but **70%** is achieved around **3 months**. - This option suggests a longer timeframe than necessary for initial strength recovery. *1 week* - At **1 week**, wound strength is quite low, usually around **10%** [1], with ongoing processes of healing and inflammation. - Insufficient time has elapsed for substantial collagen synthesis or remodeling, making this option inaccurate. *1 month* - While some improvement occurs by **1 month**, wound strength is still below **70%** at this stage, often around **30-50%** [1]. - Wound healing progresses significantly in the subsequent weeks, emphasizing the need for a longer recovery period to achieve 70% strength [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 119-121.

Q: In acute inflammation, due to the contraction of the endothelial cell cytoskeleton, which of the following occurs?

Early transient increase in permeability. ***Early transient increase in permeability*** - During acute inflammation, the **contraction of the endothelial cell cytoskeleton** leads to a rapid and temporary increase in vascular permeability [1]. - This process allows for the **exudation of fluid and plasma proteins** [1][2], contributing to the inflammatory response. *Early permanent increase in permeability* - Permanent changes in permeability do not occur early; they typically result from **severe injury** or prolonged inflammation. - Early events in inflammation are characterized by a **transient** rather than a permanent change [1]. *Delayed permanent increase in permeability* - Delayed permeability increases occur later in the inflammatory process due to **endothelial cell injury**, not the initial contraction. - This concept relates to more chronic inflammatory processes rather than **acute inflammation**. *Delayed transient increase in permeability* - Delayed transient increases are not typical and **can lead to confusion** regarding cellular responses in acute vs. chronic inflammation. - This oes not accurately represent the **initial response** during acute inflammation. **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, pp. 84-85.

Question 1

Increased vascular permeability in acute inflammation is due to what?

Accepted Answer

Histamine

Answer

IL-2

Answer

TGF-β

Answer

FGF-2

Question 2

Which of the following is not classified as a chemokine?

Accepted Answer

IL-1

Answer

IL-8

Answer

Eotaxin

Answer

MCP-1

Question 3

Increased permeability in acute inflammation is due to all except?

Accepted Answer

Lytic enzymes

Answer

Cytokines

Answer

Endothelial cell contraction

Answer

Endothelial injury

Question 4

First cell to migrate into a wound due to chemotaxis to start the process of wound healing is -

Accepted Answer

Neutrophil

Answer

Lymphocyte

Answer

Macrophage

Answer

Platelet

Question 5

The primary vasoactive mediator present in mast cells is

Accepted Answer

Histamine

Answer

Tryptase

Answer

Heparin

Answer

Chymase

Question 6

All of the following are mediators of acute inflammation, except which one?

Accepted Answer

Angiotensin

Answer

Kallikrein

Answer

Prostaglandin E2

Answer

C3a

Question 7

The principal cell in a granuloma is

Accepted Answer

Histiocyte

Answer

Lymphocyte

Answer

Giant cell

Answer

Langerhans

Question 8

Elaboration of which of the following mediators will be most beneficial in preventing further ischemic injury to the cerebral cortex?

Accepted Answer

Nitric oxide

Answer

Bradykinin

Answer

Leukotriene E4

Answer

Platelet-activating factor

Question 9

Wound strength is 70% after how many weeks?

Accepted Answer

12 weeks

Answer

1 week

Answer

4 weeks

Answer

24 weeks

Question 10

In acute inflammation, due to the contraction of the endothelial cell cytoskeleton, which of the following occurs?

Accepted Answer

Early transient increase in permeability

Answer

Early permanent increase in permeability

Answer

Delayed permanent increase in permeability

Answer

Delayed transient increase in permeability

Inflammation and Repair — MCQs

Inflammation and Repair — MCQs

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