Inflammation and Repair — MCQs

A 28-year-old woman cuts her hand while dicing vegetables in the kitchen. The wound is cleaned and sutured. Five days later, the site of injury contains an abundance of chronic inflammatory cells that actively secrete interleukin-1, tumor necrosis factor-a, interferon- a, numerous arachidonic acid derivatives, and various enzymes. What are these cells?

Inflammation and Repair Indian Medical PG Practice Questions and MCQs

Question 61: Endothelial ligands VCAM and ICAM are involved in which process?

A. Phagocytosis
B. Adhesion (Correct Answer)
C. Chemotaxis
D. Leukocyte activation

Explanation: **Explanation:** The correct answer is **Adhesion**. This process is a critical step in the leukocyte extravasation cascade, where leukocytes bind firmly to the vascular endothelium before migrating into the extravascular space [1]. **1. Why Adhesion is Correct:** Adhesion is mediated by the interaction between **Integrins** on the leukocyte surface and **Immunoglobulin superfamily ligands** on the endothelial cells [1]. * **ICAM-1** (Intercellular Adhesion Molecule-1) binds to the integrins **LFA-1** and **MAC-1**. * **VCAM-1** (Vascular Cell Adhesion Molecule-1) binds to the integrin **VLA-4** [1]. These interactions are triggered by cytokines (TNF and IL-1), which upregulate the expression of these ligands on the endothelium, converting "rolling" into "firm adhesion" [1]. **2. Why Other Options are Incorrect:** * **Phagocytosis:** This is the process of engulfing and destroying pathogens (involving opsonins like C3b and IgG), occurring *after* the leukocyte has reached the site of injury. * **Chemotaxis:** This refers to the unidirectional movement of leukocytes toward a chemical gradient (e.g., C5a, LTB4, IL-8). It occurs after transmigration [2]. * **Leukocyte Activation:** This involves the metabolic "priming" of the cell to produce ROS or degranulate, triggered by various receptors, but it is not the primary function of ICAM/VCAM. **High-Yield Clinical Pearls for NEET-PG:** * **Rolling** is mediated by **Selectins** (E, P, and L-selectins) [1]. * **Transmigration (Diapedesis)** is mediated by **PECAM-1 (CD31)** [2]. * **Leukocyte Adhesion Deficiency (LAD) Type 1** is caused by a defect in the **CD18** subunit of integrins, leading to impaired firm adhesion, delayed umbilical cord separation, and recurrent bacterial infections without pus formation [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 86-87. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 87-89.

Question 62: Chemotaxis is the main function of which molecule?

A. C5a (Correct Answer)
B. ICAM1
C. P-selectin
D. IL-5

Explanation: **Explanation:** **Correct Answer: A. C5a** Chemotaxis is the process by which leukocytes move toward a site of injury along a chemical gradient [3]. **C5a** (a fragment of the complement system) is one of the most potent endogenous chemoattractants [1]. It acts by binding to G-protein coupled receptors on neutrophils, monocytes, and eosinophils, triggering actin polymerization and directional locomotion. **Analysis of Incorrect Options:** * **B. ICAM-1 (Intercellular Adhesion Molecule-1):** This is an immunoglobulin superfamily molecule expressed on endothelial cells. Its primary function is **adhesion** (specifically, the firm attachment of leukocytes via integrins), not chemotaxis. * **C. P-selectin:** This molecule is stored in Weibel-Palade bodies and is responsible for the initial **rolling** phase of leukocyte extravasation by binding to Sialyl-Lewis X ligands. * **D. IL-5:** While a cytokine, its primary role is the **activation and recruitment of eosinophils**, particularly in allergic inflammation and parasitic infections. It is not the "main" generalized chemotactic agent compared to C5a. **NEET-PG High-Yield Pearls:** * **Major Chemoattractants:** Remember the mnemonic **"B-L-T-C"**: **B**acterial products (N-formylmethionine), **L**eukotriene B4 (LTB4), **T**umor Necrosis Factor/Interleukins (specifically **IL-8**), and **C**omplement C5a. * **C3a and C5a** are also known as **Anaphylatoxins** because they cause mast cell degranulation, leading to increased vascular permeability [2]. * Exogenous chemoattractants are usually bacterial lipids or peptides. **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. 163-164. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 99-100. [3] 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. 190-191.

Question 63: How does a keloid differ from a hypertrophic scar?

A. Decreased fibroblast proliferation
B. Increased fibroblast proliferation
C. Growth beyond the original wound margins (Correct Answer)
D. Excessive fibrous tissue deposition

Explanation: ### Explanation The fundamental distinction between a **keloid** and a **hypertrophic scar** lies in the extent of tissue growth relative to the initial injury site. Both conditions result from an aberration in the healing process characterized by excessive collagen deposition [1]. **Why Option C is Correct:** A **keloid** is defined by its ability to grow **beyond the boundaries of the original wound** and invade surrounding healthy tissue [2]. It rarely regresses spontaneously and often recurs after excision. In contrast, a **hypertrophic scar** remains **confined to the borders** of the original wound and frequently undergoes partial regression over time. **Analysis of Incorrect Options:** * **Options A & B:** Both keloids and hypertrophic scars involve **increased fibroblast proliferation** and activity [1]. Therefore, "decreased proliferation" (A) is incorrect for both, and "increased proliferation" (B) is a similarity, not a differentiating factor. * **Option D:** Excessive fibrous tissue (collagen) deposition is the **pathophysiological hallmark of both** conditions [2]. While keloids have a more disorganized arrangement of thick "keloidal" (Type I and III) collagen bundles, the mere presence of excessive tissue does not distinguish between the two. --- ### NEET-PG High-Yield Pearls * **Collagen Type:** Keloids have thick, disorganized **Type I and III collagen** bundles; hypertrophic scars have more organized, parallel collagen fibers. * **Predilection:** Keloids are more common in individuals with darker skin pigmentation and typically affect the earlobes, shoulders, and sternum [1]. * **Genetic Association:** Keloids often have a genetic predisposition (TGF-̢ overexpression), whereas hypertrophic scars are usually triggered by local factors like wound tension or infection. * **Treatment Note:** Surgical excision alone of a keloid often leads to recurrence; it usually requires adjuvant therapy (e.g., intralesional steroids). **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. 106-107. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 121.

Question 64: All the following organs are likely to undergo coagulative necrosis except?

A. Spleen
B. Heart
C. Kidney
D. Brain (Correct Answer)

Explanation: ### Explanation **Correct Option: D (Brain)** **Underlying Concept:** Coagulative necrosis is the most common pattern of necrosis, typically caused by ischemia (hypoxia) in solid organs. In this process, injury denatures not only structural proteins but also enzymes, which blocks the proteolysis of the dead cells. As a result, the basic cell outline and tissue architecture are preserved for several days, giving it a firm texture. The **Brain** is the notable exception to this rule [1]. Ischemic injury to the central nervous system (CNS) results in **Liquefactive Necrosis** [1]. Because the brain is rich in lipids and lytic enzymes (and lacks a strong internal protein framework), the dead tissue is rapidly digested into a liquid viscous mass, eventually forming a cyst or cavity [3]. **Analysis of Incorrect Options:** * **A, B, and C (Spleen, Heart, Kidney):** These are all solid organs. Ischemia leading to infarction in these organs results in **Coagulative Necrosis**. For example, a Myocardial Infarction (Heart) or a wedge-shaped splenic/renal infarct are classic examples where the cellular "tombstones" (preserved outlines without nuclei) are visible under a microscope [3]. **NEET-PG High-Yield Pearls:** * **Coagulative Necrosis:** Characteristic of all solid organ infarcts **EXCEPT** the brain [3]. * **Liquefactive Necrosis:** Seen in Brain infarcts and **abscesses** (due to bacterial/fungal infections where inflammatory cells release enzymes) [1]. * **Caseous Necrosis:** "Cheese-like" appearance; characteristic of **Tuberculosis** (granulomatous inflammation). * **Fat Necrosis:** Seen in **Acute Pancreatitis** (enzymatic) and breast trauma (non-enzymatic) [2]. Look for "saponification" or chalky white deposits. * **Fibrinoid Necrosis:** Seen in immune-mediated vascular damage (e.g., Polyarteritis Nodosa, Malignant Hypertension). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1268-1269. [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. 149-150. [3] 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. 148-149.

Question 65: An itching wound suggests a:

A. Hypersensitivity reaction (Correct Answer)
B. Infection
C. Contraction
D. Separation

Explanation: **Explanation:** The sensation of itching (pruritus) in a wound is primarily mediated by the release of chemical mediators, most notably **histamine**, from mast cells [1]. This process is a hallmark of a **Type I Hypersensitivity reaction** [2]. When a wound is exposed to allergens (such as topical medications, sutures, or dressings), IgE-mediated mast cell degranulation occurs, leading to itching, redness, and edema [2], [3]. While mild itching can occur during the late stages of normal wound healing due to collagen cross-linking and mechanical stretching, a clinically significant "itching wound" in a pathology context points toward an exaggerated immune response or hypersensitivity [1]. **Analysis of Incorrect Options:** * **Infection:** Typically presents with the classic signs of inflammation (*rubor, calor, tumor, dolor*) and purulent discharge. The predominant sensation is pain (dolor) rather than itching. * **Contraction:** This is a physiological part of the proliferative phase of healing mediated by **myofibroblasts**. While it can cause a "tightening" sensation, it does not characteristically cause pruritus. * **Separation (Dehiscence):** This is a mechanical failure of the wound (often due to increased abdominal pressure or poor suturing). It presents as a structural breakdown, not an itching sensation. **NEET-PG High-Yield Pearls:** * **Mediator of Itch:** Histamine is the primary mediator, acting on H1 receptors on free nerve endings (C-fibers) [1]. * **Wound Contraction:** Mediated by **myofibroblasts**; occurs significantly in healing by secondary intention. * **Granulation Tissue:** Composed of new thin-walled capillaries (angiogenesis), proliferating fibroblasts, and edema. It is NOT the same as a granuloma. * **Keloid vs. Hypertrophic Scar:** Keloids extend beyond the boundaries of the original wound and contain thick **Type I and III collagen** bundles (disorganized), whereas hypertrophic scars stay within the boundaries. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 646-647. [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. 171-172. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 210-211.

Question 66: Wound strength reaches approximately 70% after how much time?

A. 1 week
B. 1 month
C. 3 months (Correct Answer)
D. 6 months

Explanation: **Explanation:** The tensile strength of a healing wound is a function of collagen deposition and remodeling. This process follows a specific chronological pattern: * **Correct Answer (C):** By the end of **3 months**, wound strength reaches approximately **70% to 80%** of the strength of unwounded skin [1]. This is the plateau phase where the rate of strength gain slows down significantly. It is important to note that a scar rarely, if ever, regains 100% of the original tissue strength [1]. **Analysis of Incorrect Options:** * **Option A (1 week):** At the end of the first week (when sutures are typically removed), the wound strength is only about **10%** [1]. This is why wound dehiscence is a risk if excessive tension is applied early. * **Option B (1 month):** Strength increases rapidly over the next few weeks due to collagen cross-linking and the shift from Type III to Type I collagen, but it has not yet reached the 70% threshold [1]. * **Option D (6 months):** While remodeling continues for up to a year, the specific milestone of 70-80% strength is traditionally associated with the 3-month mark in standard pathology texts (Robbins) [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Collagen Switch:** In early wound healing (granulation tissue), **Type III collagen** predominates. During maturation/remodeling, it is replaced by **Type I collagen**, which provides greater tensile strength [1]. * **Vitamin C & Copper:** These are essential cofactors for collagen cross-linking (prolyl hydroxylase and lysyl oxidase, respectively). Deficiency leads to poor wound healing. * **The 10% Rule:** Remember that at 1 week, strength is 10% [1]. This is a frequent "distractor" in exams. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 119-121.

Question 67: Which of the following statements regarding coagulative necrosis is false?

A. It is the most common type of necrosis.
B. Ischemia can lead to coagulative necrosis.
C. Affected tissue appears as a 'tombstone'.
D. Affected tissue has a cheese-like appearance. (Correct Answer)

Explanation: **Explanation:** **Why Option D is the correct answer (False statement):** A "cheese-like" (friable, yellow-white) appearance is the hallmark of **Caseous necrosis**, not coagulative necrosis [1]. Caseous necrosis is typically seen in granulomatous inflammation, most notably in Tuberculosis [1]. In contrast, coagulative necrosis results in firm, opaque, and pale tissue. **Analysis of other options:** * **Option A (Most common type):** This is a true statement. Coagulative necrosis is the most frequent pattern of cell death encountered in clinical practice. * **Option B (Ischemia):** This is true. Ischemia (loss of blood supply) is the primary cause of coagulative necrosis in all solid organs except the brain (where ischemia leads to liquefactive necrosis). * **Option C (Tombstone appearance):** This is a classic histological description. In coagulative necrosis, the cell's structural framework is preserved for several days despite the loss of the nucleus. The cells appear as "ghostly" outlines or "tombstones" because the denaturation of proteins prevents immediate proteolysis. **NEET-PG High-Yield Pearls:** 1. **Mechanism:** The primary mechanism is the **denaturation of structural proteins and enzymes**, which blocks proteolysis (autolysis). 2. **Microscopy:** Characterized by increased eosinophilia (due to loss of cytoplasmic RNA) and nuclear changes (pyknosis → karyorrhexis → karyolysis). 3. **Exception Rule:** Ischemia in the **Brain** leads to **Liquefactive necrosis**, not coagulative. 4. **Clinical Example:** Myocardial Infarction (MI) is the most common clinical example of coagulative necrosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, p. 55.

Question 68: All of the following processes show features of acute inflammation except?

A. Apoptosis (Correct Answer)
B. Pyroptosis
C. Necroptosis
D. Necrosis

Explanation: **Explanation:** The fundamental distinction between different types of cell death lies in their ability to trigger an inflammatory response. **1. Why Apoptosis is the Correct Answer:** Apoptosis is a form of **programmed cell death** [1] that is characterized by the activation of caspases, leading to DNA fragmentation and the formation of **apoptotic bodies**. Crucially, the plasma membrane remains intact, preventing the leakage of intracellular contents. These apoptotic bodies express "eat-me" signals (like phosphatidylserine) that recruit macrophages for phagocytosis without the release of pro-inflammatory cytokines [1]. Therefore, apoptosis is traditionally considered **immunologically silent** and does not show features of acute inflammation [1]. **2. Why the other options are incorrect:** * **Necrosis:** This is accidental, uncontrolled cell death. It involves the loss of membrane integrity, leading to the leakage of cellular contents (DAMPs) into the extracellular space, which directly triggers an **acute inflammatory response**. * **Pyroptosis:** This is a form of programmed cell death specifically associated with the **inflammasome** and **Caspase-1**. It results in the release of highly pro-inflammatory cytokines like **IL-1β and IL-18**, inherently causing inflammation. * **Necroptosis:** Often called "programmed necrosis," it follows a signaling pathway (RIPK1/RIPK3) that results in membrane rupture similar to necrosis, thereby inducing inflammation [1]. **Clinical Pearls for NEET-PG:** * **Inflammasome:** A multi-protein complex that recognizes PAMPs/DAMPs and is the key driver of **Pyroptosis**. * **Caspases:** Apoptosis uses Caspase 3, 8, and 9 [1]; Pyroptosis uses **Caspase 1, 4, and 5**. * **High-Yield Fact:** While apoptosis is generally non-inflammatory, "Secondary Necrosis" can occur in vitro if apoptotic cells are not cleared, eventually leading to inflammation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 63-71.

Question 69: What is the term for leukocyte migration through the capillary wall?

A. Rolling
B. Diapedesis (Correct Answer)
C. Migration
D. Pavementing

Explanation: **Explanation:** The correct answer is **Diapedesis** (also known as **Transmigration**). This is the process by which leukocytes squeeze through the intercellular junctions of the vascular endothelium to enter the extravascular space [1], [2]. **Why Diapedesis is correct:** After leukocytes adhere firmly to the endothelial surface, they migrate primarily through the systemic venules and pulmonary capillaries. This process is mediated by adhesion molecules, most notably **PECAM-1 (CD31)**, which is expressed on both the leukocytes and the endothelial cell junctions [1]. Once through the endothelium, leukocytes secrete collagenases to pierce the vascular basement membrane [1]. **Analysis of Incorrect Options:** * **A. Rolling:** This is the initial, transient attachment of leukocytes to the endothelium [3]. It is mediated by the **Selectin** family (L-selectin on leukocytes; E and P-selectin on endothelium) [3]. * **C. Migration:** This is a general term. Specifically, the movement of leukocytes *within* the tissue toward a chemical gradient is called **Chemotaxis** [1]. * **D. Pavementing:** This refers to the stage of **firm adhesion** where the leukocyte surface becomes flattened against the endothelial lining, resembling "pavement" stones [3]. This step is mediated by **Integrins** (e.g., LFA-1, VLA-4) on leukocytes and **Ligands** (e.g., ICAM-1, VCAM-1) on the endothelium [3]. **NEET-PG High-Yield Pearls:** * **Sequence of events:** Margination → Rolling → Adhesion/Pavementing → Diapedesis → Chemotaxis [2]. * **LAD-1 (Leukocyte Adhesion Deficiency Type 1):** Caused by a defect in the **CD18** subunit of integrins, leading to impaired firm adhesion and recurrent infections without pus formation [1]. * **LAD-2:** Caused by a defect in **Sialyl-Lewis X** (ligand for selectins), leading to impaired rolling. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 87-89. [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, p. 87.

Question 70: A 28-year-old woman cuts her hand while dicing vegetables in the kitchen. The wound is cleaned and sutured. Five days later, the site of injury contains an abundance of chronic inflammatory cells that actively secrete interleukin-1, tumor necrosis factor-a, interferon- a, numerous arachidonic acid derivatives, and various enzymes. What are these cells?

A. B lymphocytes
B. Macrophages (Correct Answer)
C. Plasma cells
D. Smooth muscle cells

Explanation: ### Explanation The correct answer is **Macrophages (Option B)**. **Why Macrophages are correct:** In the timeline of wound healing, by day 5, the initial acute inflammatory response (dominated by neutrophils) has transitioned to a chronic inflammatory phase and the formation of granulation tissue [1]. Macrophages are the "master orchestrators" of this stage. They are derived from circulating monocytes and are responsible for: 1. **Cytokine Secretion:** They are the primary source of **IL-1 and TNF-α**, which regulate the inflammatory response [1], [2]. 2. **Growth Factors:** They secrete PDGF, TGF-β, and FGF to stimulate fibroblasts and angiogenesis [1]. 3. **Interferons & Arachidonic Acid:** They produce IFN-α and various prostaglandins/leukotrienes. 4. **Debridement:** They secrete proteases and collagenases to clean the wound site [1]. **Why the other options are incorrect:** * **A. B lymphocytes:** While present in chronic inflammation, their primary role is recognizing antigens and differentiating into plasma cells; they do not secrete the broad array of enzymes and cytokines (like TNF-α) described. * **C. Plasma cells:** These are terminally differentiated B cells dedicated solely to **antibody (immunoglobulin) production**. They do not secrete arachidonic acid derivatives or TNF-α. * **D. Smooth muscle cells:** In wound healing, specialized "myofibroblasts" (derived from fibroblasts) are responsible for wound contraction, but they do not function as secretory inflammatory cells. **NEET-PG High-Yield Pearls:** * **Timeline of Wound Healing:** Neutrophils (0–24 hrs) → Macrophages (2–3 days; peak at day 5) → Fibroblasts/Granulation tissue (3–5 days) → Collagen remodeling (weeks to months) [1]. * **Macrophage Activation:** **M1 pathway** (Classical) is pro-inflammatory (induced by IFN-γ); **M2 pathway** (Alternative) is for tissue repair and fibrosis (induced by IL-4, IL-13) [2]. * **Key Cytokine:** **TGF-β** is the most important cytokine for synthesis and deposition of connective tissue proteins (fibrosis) [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] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 105-106.

Practice by Chapter

Acute Inflammation: Vascular Events

Practice Questions

Acute Inflammation: Cellular Events

Practice Questions

Chemical Mediators of Inflammation

Practice Questions

Chronic Inflammation

Practice Questions

Granulomatous Inflammation

Practice Questions

Systemic Effects of Inflammation

Practice Questions

Wound Healing

Practice Questions

Tissue Regeneration

Practice Questions

Fibrosis and Repair

Practice Questions

Resolution of Inflammation

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free