Inflammation and Repair — MCQs

A 45-year-old man comes to the physician because of a productive cough and dyspnea. He has smoked one pack of cigarettes daily for 15 years. His temperature is 38.8°C (102°F). Physical examination shows decreased breath sounds and dullness on percussion above the right lower lobe. An x-ray of the chest shows a right lower lobe density and a small amount of fluid in the right pleural space. The patient's symptoms improve with antibiotic treatment, but he develops right-sided chest pain one week later. Pulmonary examination shows new scratchy, high-pitched breath sounds on auscultation of the right lobe. Histologic examination of a pleural biopsy specimen is most likely to show which of the following findings?

Q379

What is the mechanism of secondary healing?

Q380

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

Inflammation and Repair Indian Medical PG Practice Questions and MCQs

Question 371: Hypertrophic scar is characterized by the following, except

A. it involves the flexor surface
B. it outgrows the wound area (Correct Answer)
C. it is non-familial
D. it is not related to the race

Explanation: ***it outgrows the wound area*** - This statement is characteristic of a **keloid scar**, not a hypertrophic scar. Keloids are distinguished by their growth beyond the original wound margins [1]. - **Hypertrophic scars**, on the other hand, remain confined within the boundaries of the original injury, though they may be raised and erythematous [1]. *it involves the flexor surface* - While hypertrophic scars can occur on any body surface, they are commonly found on areas of **high tension**, such as the **flexor surfaces** of joints (e.g., knee, elbow) or the chest and shoulders. - This involvement is due to constant movement stretching the healing skin, which can stimulate excessive collagen production. *it is non-familial* - Hypertrophic scars are generally **not associated with a strong genetic predisposition** or familial inheritance patterns. - Their development is primarily linked to factors like wound tension, infection, and individual healing responses rather than inherited tendencies. *it is not related to the race* - The incidence of hypertrophic scars does **not show a significant racial predilection**, unlike keloid scars, which are more common in individuals with darker skin types. - Hypertrophic scars can affect individuals from all racial backgrounds. **References:** [1] Kumar v, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 119-121.

Question 372: Which of the following factors is labelled as cytokine in the pathogenesis of Systemic Inflammatory Response Syndrome (SIRS)?

A. Leukotrienes
B. Nitric oxide
C. Complements
D. Tumor necrosis factor (Correct Answer)

Explanation: ***Tumor necrosis factor*** - **Tumor necrosis factor (TNF-α)** is a prominent pro-inflammatory cytokine and a key mediator in the pathogenesis of **Systemic Inflammatory Response Syndrome (SIRS)** [1]. - It plays a crucial role in initiating and amplifying the inflammatory cascade, leading to systemic effects like fever, increased vascular permeability, and tissue damage [1]. *Leukotrienes* - **Leukotrienes** are lipid mediators derived from arachidonic acid, involved in inflammation and allergic reactions [1]. - They are not classified as **cytokines**, which are protein signaling molecules [1]. *Nitric oxide* - **Nitric oxide (NO)** is a gaseous signaling molecule with various physiological roles, including vasodilation and neurotransmission. - While it contributes to the pathophysiology of SIRS, particularly in regulating vascular tone, it is not a **cytokine**. *Complements* - **Complements** are a system of plasma proteins that are part of the innate immune response, helping to clear pathogens [1]. - They participate in inflammation but are distinct from **cytokines**, which are regulatory proteins [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-101.

Question 373: A 20 year old female was operated for perforation peritonitis and after closing the rectus sheath her abdominal wound was left open to heal with proliferative granulation tissue which contracted and epithelialized to form a scar. This patient had undergone healing by:

A. Delayed primary intention
B. Secondary intention (Correct Answer)
C. Primary intention
D. Tertiary intention

Explanation: ***Secondary intention*** - **Secondary intention healing** occurs when a wound is left open to heal from the bottom up, characterized by a large tissue deficit, **formation of granulation tissue**, wound contraction, and epithelialization [1, 2]. - This method is used in cases of infection, excessive tissue loss, or when there's a high risk of contamination, allowing the wound to heal naturally without surgical closure [1]. *Delayed primary intention* - This involves leaving a wound open for a few days to decrease the risk of infection or swelling, then **surgically closing it** once the risk is minimized. - The patient's wound was left open to heal by **granulation and epithelization**, not for eventual surgical closure. *Primary intention* - **Primary intention healing** occurs when wound edges are approximated, usually by sutures, staples, or adhesive, resulting in minimal tissue loss and a fine scar [1]. - This was not the case here as the wound was left open due to risks associated with perforation peritonitis. *Tertiary Intention* - **Tertiary intention** or delayed primary closure is where a wound is initially treated as secondary intention, but then closed surgically at a later date, typically 3-5 days after initial wound care. - The prompt specifies the wound was left open to heal by **granulation tissue** which then contracted and epithelized, without mention of later surgical closure. **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. 105-107. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 119.

Question 374: What is the correct order of the normal phases of wound healing?

A. Haemostatic phase → Inflammatory phase → Proliferative phase → Remodelling phase (Correct Answer)
B. Proliferative phase → Haemostatic phase → Inflammatory phase → Remodelling phase
C. Remodelling phase → Proliferative phase → Destructive phase → Inflammatory phase
D. Destructive phase → Proliferative phase → Remodelling phase → Inflammatory phase

Explanation: ***Haemostatic phase → Inflammatory phase → Proliferative phase → Remodelling phase*** - This sequence accurately describes the well-established biological progression of **wound healing**, starting with immediate injury response and leading to tissue maturation [1], [2]. - Each phase builds upon the previous one, ensuring proper clot formation, immune response, tissue repair, and final strengthening of the wound [1], [2]. *Proliferative phase → Haemostatic phase → Inflammatory phase → Remodelling phase* - This order is incorrect because the **proliferative phase** occurs much later than the initial haemostatic and inflammatory responses [1]. - **Haemostasis** must occur first to stop bleeding before subsequent healing processes can begin effectively [2]. *Remodelling phase → Proliferative phase → Destructive phase → Inflammatory phase* - This option is incorrect as the **remodelling phase** is the final stage of wound healing, not the initial one [1]. - The term "**destructive phase**" is not a standard physiological phase in normal wound healing. *Destructive phase → Proliferative phase → Remodelling phase → Inflammatory phase* - This sequence is incorrect because, similar to the previous option, "**destructive phase**" is not a recognized normal phase of wound healing. - The **inflammatory phase** occurs early in the process, not as the final stage [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 117-119. [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. 105-108.

Question 375: What mechanism explains the pathogenesis of Jarisch-Herxheimer reaction in patients treated for syphilis?

A. Massive release of treponemal endotoxins
B. Inflammatory response to rapid spirochete lysis (Correct Answer)
C. Autoimmune reaction triggered by treatment
D. Allergic reaction to penicillin

Explanation: The Jarisch-Herxheimer reaction (JHR) is primarily caused by the rapid destruction of a large number of spirochetes, leading to the release of lipoproteins and other antigenic substances. This release triggers an acute systemic inflammatory response, manifesting as fever, chills, headache, and myalgias. While bacteria do release toxins, Treponema pallidum, the causative agent of syphilis, is a spirochete and does not produce classical endotoxins (which are typically associated with gram-negative bacteria) [1]. The inflammatory mediators are released from the host in response to the rapid breakdown of the spirochetes themselves, not pre-formed endotoxins. JHR is an acute reaction that occurs shortly after the initiation of antibiotic therapy and resolves spontaneously, which is not characteristic of a prolonged autoimmune disease. There is no evidence to suggest that the body produces antibodies against its own tissues as a result of syphilis treatment in JHR. An allergic reaction to penicillin would typically present with hives, pruritus, bronchospasm, or anaphylaxis, and would persist with repeated doses of the drug. The Jarisch-Herxheimer reaction is distinct from an allergic reaction; it is a predictable inflammatory response to spirochete killing and can occur even with non-penicillin therapies for syphilis. **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. 63-64.

Question 376: A male patient is not responding to oxygen therapy and has been diagnosed with ARDS (Acute Respiratory Distress Syndrome). What is the role of IL-8 in ARDS?

A. Endothelial cell activation
B. Recruitment of neutrophils (Correct Answer)
C. Macrophage activation
D. Promote surfactant production

Explanation: Recruitment of neutrophils - **Interleukin-8 (IL-8)**, also known as **CXCL8**, is a powerful **chemotactic cytokine** that primarily attracts and activates neutrophils [3]. - In **ARDS**, this recruitment leads to an influx of neutrophils into the pulmonary interstitium and alveolar spaces, contributing to inflammation and lung injury [1]. *Endothelial cell activation* - While other **cytokines** and inflammatory mediators can activate **endothelial cells** in ARDS [2], IL-8's primary role is not direct endothelial activation but rather **neutrophil chemotaxis** [3]. - **Endothelial cell activation** leads to increased vascular permeability and leukocyte adherence, which is often a consequence of overall inflammation, not solely IL-8 [4]. *Macrophage activation* - **Macrophages** are activated by various stimuli and other **cytokines**, such as **TNF-alpha** and **IFN-gamma**, as part of the inflammatory response. - While macrophages produce IL-8, its main function is not to activate macrophages themselves but to attract **neutrophils**. *Promote surfactant production* - **Surfactant production** is primarily regulated by **Type II pneumocytes** and is often impaired in ARDS due to damage to these cells [1]. - IL-8 is a **pro-inflammatory cytokine** and plays no direct role in promoting surfactant synthesis; in fact, its inflammatory effects can indirectly worsen surfactant dysfunction. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 681. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 679. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 87-89. [4] 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.

Question 377: Arrange the following cellular events of inflammation in the correct sequence: 1. Rolling 2. Cytokine-mediated integrin activation 3. Adhesion 4. Migration

A. 1,2,3,4 (Correct Answer)
B. 3,4,1,2
C. 2,1,4,3
D. 4,1,2,3

Explanation: ***1,2,3,4*** - The correct sequence of cellular events for leukocyte recruitment during inflammation begins with **rolling** [1], followed by **cytokine-mediated integrin activation** [2], then firm **adhesion** to the endothelium [1], and finally **migration** (diapedesis) into the tissues [3]. - This step-by-step process ensures effective targeting of leukocytes to the site of injury or infection [1]. *3,4,1,2* - This sequence is incorrect as **adhesion** cannot occur before **rolling**, and **migration** is the final step after adhesion, not an early one. - **Cytokine-mediated integrin activation** must precede firm adhesion [1]. *2,1,4,3* - This order is incorrect because **rolling** (1) is the initial interaction that allows leukocytes to slow down on the endothelium [2], and it occurs before **cytokine-mediated integrin activation** (2) which strengthens the binding. - **Migration** (4) is also misplaced as it should be the last step after firm adhesion (3). *4,1,2,3* - This sequence is incorrect as **migration** (4) is the last step in the process, not the first. - **Rolling** (1) initiates the process by transiently interacting with endothelial cells, followed by activation and adhesion. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 87. [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.

Question 378: A 45-year-old man comes to the physician because of a productive cough and dyspnea. He has smoked one pack of cigarettes daily for 15 years. His temperature is 38.8°C (102°F). Physical examination shows decreased breath sounds and dullness on percussion above the right lower lobe. An x-ray of the chest shows a right lower lobe density and a small amount of fluid in the right pleural space. The patient's symptoms improve with antibiotic treatment, but he develops right-sided chest pain one week later. Pulmonary examination shows new scratchy, high-pitched breath sounds on auscultation of the right lobe. Histologic examination of a pleural biopsy specimen is most likely to show which of the following findings?

A. Dense bacterial infiltrate
B. Epithelioid infiltrate with central necrosis
C. Red blood cell infiltrate
D. Fibrin-rich infiltrate (Correct Answer)

Explanation: ***Fibrin-rich infiltrate*** - The patient's initial presentation is consistent with **bacterial pneumonia** and subsequent pleural effusion [2]. The development of new **scratchy, high-pitched breath sounds** and chest pain after initial improvement with antibiotics, along with effusion, strongly suggests the development of **pleurisy** or **pleural fibrosis** a common complication of pneumonia [1]. - **Pleurisy** involves inflammation of the pleura, leading to **fibrin deposition** on the pleural surfaces, which causes the characteristic friction rub (scratchy breath sounds) and chest pain [1]. A pleural biopsy would thus show a fibrin-rich infiltrate [2]. *Dense bacterial infiltrate* - While bacteria are the initial cause of pneumonia, a **pleural biopsy** in this context, after antibiotic treatment has been started and pleurisy has developed, would not primarily show a dense bacterial infiltrate in the pleural space itself. - Bacteria are typically located within the lung parenchyma in pneumonia, and while they can seed the pleura, the predominant finding in active pleurisy would be inflammatory cells and fibrin rather than a dense bacterial mass, which would be more indicative of active empyema. *Epithelioid infiltrate with central necrosis* - This description is classic for a **granulomatous inflammation** with caseous necrosis, highly suggestive of **tuberculosis**. - The patient's symptoms are more acute and resolve with broad-spectrum antibiotics, which would be atypical for tuberculosis, and there are no other features like night sweats or weight loss to suggest it. *Red blood cell infiltrate* - A red blood cell infiltrate would indicate **hemorrhage** into the pleural space (hemothorax). While trauma or malignancy can cause hemothorax. - There is no history of trauma or features suggestive of malignancy, and the friction rub is more indicative of inflammation and fibrin deposition than hemorrhage. **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. 194-195. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 317-318.

Question 379: What is the mechanism of secondary healing?

A. Neovascularization
B. Scab formation
C. Granuloma formation
D. Granulation tissue (Correct Answer)

Explanation: ***Granulation tissue*** - **Secondary intention healing** involves the formation of abundant **granulation tissue** to fill the tissue defect [1]. - Granulation tissue consists of new **capillaries**, **fibroblasts**, and inflammatory cells, which lay the groundwork for wound closure [2]. *Neovascularization* - **Neovascularization** is the specific process of forming new blood vessels within the wound, which is a component of granulation tissue formation, but not the overall healing mechanism [2]. - While essential for delivering nutrients and oxygen, it's a sub-process rather than the primary mechanism for secondary healing itself. *Scab formation* - **Scab formation** is an initial protective mechanism, primarily associated with superficial wounds and not the intrinsic mechanism of tissue repair and closure in secondary healing. - A scab primarily protects the underlying wound from infection and desiccation while healing occurs beneath it. *Granuloma formation* - **Granuloma formation** is a specific type of chronic inflammatory response characterized by collections of macrophages, often seen in persistent infections or foreign body reactions, not typical secondary wound healing [2]. - It indicates a **cell-mediated immune response** to a non-degradable stimulus, aiming to wall off the offending agent. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 117-119. [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. 105-107.

Question 380: Rolling of leucocytes on endothelial cells is mediated by which of the following proteins?

A. Integrins
B. Transferrin
C. PECAM-1
D. Selectins (Correct Answer)

Explanation: **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.

Practice by Chapter

Acute Inflammation: Vascular Events

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Acute Inflammation: Cellular Events

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Chemical Mediators of Inflammation

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Chronic Inflammation

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Granulomatous Inflammation

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Systemic Effects of Inflammation

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Wound Healing

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Tissue Regeneration

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Fibrosis and Repair

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Resolution of Inflammation

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