Inflammation and Repair — MCQs
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A 60-year-old male patient complains of discoloration of his right leg. He is a known case of diabetes mellitus. Physical examination reveals blackish discoloration of the right leg with a dry and shrunken appearance. Which of the following most appropriately describes the condition of this patient?
Which of the following is an inhibitor of inflammation?
The process by which red blood cells move out of vessels through widened inter endothelial junction is referred to as:
All of the following are characteristic of exudates EXCEPT:
Which of the following is an endogenous chemoattractant?
Which of the following is NOT a labile cell?
Neovascularization is maximum on which day?
Which of the following causes the maximum effect in myocardial reperfusion injury?
In chronic granulomatous inflammation, which of the following processes is most likely to predominate?
Which chemical mediators are known to cause fever?
Inflammation and Repair Indian Medical PG Practice Questions and MCQs
Question 201: A 60-year-old male patient complains of discoloration of his right leg. He is a known case of diabetes mellitus. Physical examination reveals blackish discoloration of the right leg with a dry and shrunken appearance. Which of the following most appropriately describes the condition of this patient?
- A. Wet gangrene
- B. Dry gangrene (Correct Answer)
- C. Psoriasis
- D. Pemphigus
Explanation: ### Explanation **Correct Option: B. Dry gangrene** The patient is presenting with classic features of **Dry Gangrene**, a form of coagulative necrosis. In diabetic patients, peripheral vascular disease (atherosclerosis) leads to chronic ischemia [1]. The characteristic "blackish discoloration" is due to the liberation of hemoglobin and the formation of iron sulfide by the action of hydrogen sulfide. The "dry and shrunken" appearance occurs because the blood supply is cut off slowly, allowing for tissue dehydration. A key feature of dry gangrene is a clear **line of demarcation** between the gangrenous part and the healthy tissue [1]. **Why other options are incorrect:** * **A. Wet gangrene:** This occurs in naturally moist tissues (e.g., bowel, mouth) or when dry gangrene becomes superinfected with bacteria (e.g., *Proteus*, *Staphylococci*) [1]. It is characterized by swelling, a foul smell, and a lack of a clear line of demarcation. It carries a higher risk of septicemia. * **C. Psoriasis:** An autoimmune skin disorder characterized by well-demarcated erythematous plaques with silvery scales, typically on extensor surfaces. It does not cause tissue necrosis or blackening. * **D. Pemphigus:** A group of bullous (blistering) autoimmune diseases affecting the skin and mucous membranes, characterized by acantholysis (loss of intercellular connections). **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** Dry gangrene = Coagulative necrosis; Wet gangrene = Liquefactive necrosis (due to bacterial enzymes). * **Gas Gangrene:** Caused by *Clostridium perfringens*; characterized by crepitus due to gas bubbles in the tissue [1]. * **Diabetes Link:** Diabetics are prone to both types; dry gangrene due to macrovascular disease and wet gangrene (diabetic foot) due to poor wound healing and secondary infection [1]. **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. 103-104.
Question 202: Which of the following is an inhibitor of inflammation?
- A. Histamine
- B. Lipoxin (Correct Answer)
- C. Leukotriene
- D. None of the above
Explanation: The correct answer is **Lipoxin**. **Why Lipoxin is the correct answer:** Inflammation is a tightly regulated process that includes "stop signals" to prevent tissue damage. **Lipoxins (LXA4 and LXB4)** are endogenous anti-inflammatory mediators derived from arachidonic acid via the lipoxygenase pathway. Unlike pro-inflammatory leukotrienes, lipoxins are produced through **platelet-leukocyte interactions** (transcellular biosynthesis). Their primary functions include: * Inhibiting neutrophil chemotaxis and adhesion to endothelium [1]. * Stimulating the recruitment of non-phlogistic (non-inflammatory) monocytes. * Promoting the clearance of apoptotic cells (efferocytosis) by macrophages, thereby signaling the **resolution phase** of inflammation. **Why the other options are incorrect:** * **Histamine:** A vasoactive amine released by mast cells [1]. It is a potent **pro-inflammatory** mediator responsible for vasodilation and increased vascular permeability during the immediate phase of acute inflammation [1]. * **Leukotrienes (LTB4, LTC4, LTD4, LTE4):** These are **pro-inflammatory** metabolites of arachidonic acid [1]. LTB4 is a powerful chemoattractant for neutrophils, while the cysteinyl leukotrienes (C4, D4, E4) cause bronchospasm and increased vascular permeability [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 95-101.
Question 203: The process by which red blood cells move out of vessels through widened inter endothelial junction is referred to as:
- A. Pavementing
- B. Diapedesis (Correct Answer)
- C. Rouleaux formation
- D. Chemotaxis migration
Explanation: ### Explanation **Correct Answer: B. Diapedesis** **Mechanism:** During the vascular phase of acute inflammation, chemical mediators (like histamine and bradykinin) cause endothelial cell contraction, leading to **widened inter-endothelial junctions** [5]. While leukocytes actively migrate through these gaps (transmigration), **Red Blood Cells (RBCs)** are passively pushed out of the vessel into the extravascular space due to increased hydrostatic pressure [1]. This passive movement of RBCs through the vessel wall is specifically termed **Diapedesis** [1]. --- ### Analysis of Incorrect Options: * **A. Pavementing:** This refers to the stage of leukocyte extravasation where neutrophils line up and adhere horizontally along the vascular endothelium after the process of rolling [3]. It involves adhesion molecules like ICAM-1 and VCAM-1 [4]. * **C. Rouleaux formation:** This is a hematological phenomenon where RBCs stack like coins. It occurs due to increased plasma proteins (like fibrinogen or globulins) which decrease the zeta potential of RBCs. It is a marker of inflammation (increased ESR) but not a mechanism of movement across vessels. * **D. Chemotaxis migration:** This is the process by which inflammatory cells (leukocytes) move toward a site of injury following a chemical gradient (e.g., C5a, LTB4, IL-8) [2]. RBCs do not exhibit chemotaxis as they lack the necessary receptors and motility. --- ### High-Yield Clinical Pearls for NEET-PG: 1. **Leukocyte Extravasation Sequence:** Margination → Rolling (Selectins) → Adhesion/Pavementing (Integrins) → Transmigration/Diapedesis (PECAM-1/CD31) → Chemotaxis [2]. 2. **Diapedesis vs. Transmigration:** While both occur at the same site (inter-endothelial junctions), "Transmigration" usually refers to the active movement of WBCs, whereas "Diapedesis" is the classic term for the passive escape of RBCs [1]. 3. **Most common site of Diapedesis:** Post-capillary venules (due to the highest density of receptors and thinnest walls). 4. **Key Chemotactic Agents:** C5a, LTB4, IL-8, and Bacterial products (N-formyl methionine). **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. Inflammation and Repair, pp. 87-89. [3] 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. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 87. [5] 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.
Question 204: All of the following are characteristic of exudates EXCEPT:
- A. Predominantly polymorphonuclear cells
- B. Protein content less than 1 gm/dL (Correct Answer)
- C. Specific gravity greater than 1.015
- D. Turbid appearance of the fluid
Explanation: ### Explanation The fundamental distinction in fluid accumulation is between **Exudate** (inflammatory) and **Transudate** (non-inflammatory). **Why Option B is the Correct Answer:** Exudates are formed due to increased vascular permeability, allowing large molecules like proteins and cells to escape into the interstitial space [1]. Therefore, an exudate is characterized by a **high protein content (typically >3 g/dL)**. A protein content of less than 1 g/dL (or <3 g/dL) is a hallmark of a **transudate**, which results from imbalances in hydrostatic or osmotic pressure without changes in vessel wall permeability [1]. **Analysis of Incorrect Options:** * **Option A (Predominantly polymorphonuclear cells):** In acute inflammation, exudates are rich in leukocytes, particularly neutrophils (polymorphs), as they migrate toward the site of injury [2]. * **Option C (Specific gravity >1.015):** Due to the high concentration of proteins and cellular debris, exudates have a high specific gravity (usually >1.020). Transudates have a low specific gravity (<1.012). * **Option D (Turbid appearance):** Because exudates contain high levels of protein, white blood cells, and sometimes bacteria or lipids, the fluid appears cloudy or turbid [2]. Transudates are typically clear or straw-colored. **NEET-PG High-Yield Pearls:** 1. **Light’s Criteria:** Used clinically to differentiate pleural fluid. An exudate meets at least one of these: * Pleural fluid protein/Serum protein ratio >0.5 * Pleural fluid LDH/Serum LDH ratio >0.6 * Pleural fluid LDH > 2/3rd the upper limit of normal serum LDH. 2. **Mechanism:** Exudate = Inflammation (Increased permeability); Transudate = Systemic factors (e.g., Heart failure, Cirrhosis, Nephrotic syndrome) [1]. 3. **Fibrinogen:** Exudates often contain fibrinogen, which can lead to spontaneous clotting of the fluid sample. **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. 186-188. [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. 192-193.
Question 205: Which of the following is an endogenous chemoattractant?
- A. C5a (Correct Answer)
- B. Bacterial products
- C. Lipopolysaccharide A
- D. C8
Explanation: **Explanation:** Chemotaxis is the process by which leukocytes move toward a site of injury along a chemical gradient [1]. Chemoattractants are categorized into two groups: **Endogenous** (produced by the host body) and **Exogenous** (derived from the external environment) [1]. **Why C5a is Correct:** **C5a** is a potent **endogenous** chemoattractant [1][2]. It is a byproduct of the complement cascade (specifically the alternative and classical pathways). Along with attracting neutrophils, eosinophils, and monocytes, it acts as an anaphylatoxin, triggering mast cell degranulation [1][2]. Other major endogenous mediators include **Leukotriene B4 (LTB4)**, **Interleukin-8 (IL-8)**, and **Soluble gas (Nitric Oxide)**. **Analysis of Incorrect Options:** * **B. Bacterial products:** These are **exogenous** chemoattractants [1]. The most common examples are peptides containing **N-formylmethionine** termini, which are unique to bacteria and recognized by host cells [1]. * **C. Lipopolysaccharide (LPS):** Also known as endotoxin, LPS is a component of the outer membrane of Gram-negative bacteria. It is an **exogenous** agent that triggers a massive immune response but is not synthesized by the host. * **D. C8:** While C8 is a component of the complement system, its primary role is the formation of the **Membrane Attack Complex (MAC)** (C5b-C9) to induce cell lysis [2]. It does not possess chemotactic properties. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Endogenous Chemoattractants:** **"B85"** → LTB**4**, IL-**8**, C**5**a. * **IL-8** is the most specific chemoattractant for **neutrophils**. * **Eotaxin** is the specific chemoattractant for **eosinophils**. * Chemoattractants bind to **G-protein coupled receptors (GPCRs)** on the leukocyte surface, leading to cytoskeletal rearrangement via actin polymerization [1]. **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. 87-100.
Question 206: Which of the following is NOT a labile cell?
- A. Bone marrow
- B. Epidermal cells
- C. Small intestine mucosa
- D. Hepatocytes (Correct Answer)
Explanation: ### Explanation The classification of cells based on their proliferative capacity is a fundamental concept in pathology, categorized into **Labile**, **Stable**, and **Permanent** cells. **Why Hepatocytes are the correct answer:** Hepatocytes are **Stable (Quiescent) cells** [1], [2]. These cells are normally in the **G0 phase** of the cell cycle and have a low baseline level of replication [3]. However, they retain the capacity to rapidly enter the cell cycle (G1 phase) in response to injury or loss of tissue mass (e.g., partial hepatectomy) [1], [2]. This regenerative capacity is a classic example of stable cell behavior. **Why the other options are incorrect:** Options A, B, and C are all examples of **Labile (Continuously Dividing) cells** [1]. These cells are constantly being lost and replaced by maturation from stem cells and by proliferation of mature cells. They do not enter G0 but instead follow a continuous cycle from one mitosis to the next. * **Bone marrow (A):** Hematopoietic stem cells continuously produce blood cells [1], [5]. * **Epidermal cells (B):** The stratified squamous epithelium of the skin undergoes constant desquamation and replacement [1], [4]. * **Small intestine mucosa (C):** Surface epithelia of the GI tract are rapidly turned over every few days [1], [3]. **High-Yield NEET-PG Pearls:** * **Permanent Cells:** These cells have left the cell cycle and cannot undergo division in postnatal life. Examples include **Neurons, Cardiac myocytes, and Skeletal muscle cells**. Injury to these tissues results in scarring (fibrosis), not regeneration. * **Cell Cycle Control:** Labile cells never enter G0; Stable cells are in G0 but can be recruited; Permanent cells are terminally differentiated in G0 [3]. * **Stem Cells:** The regenerative capacity of labile cells is dependent on the preservation of the underlying stem cell population and the integrity of the basement membrane/extracellular matrix [1], [5]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 112-113. [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. 108-109. [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. 79-80. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 38-39. [5] 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. 104-105.
Question 207: Neovascularization is maximum on which day?
- A. 3rd day
- B. 5th day (Correct Answer)
- C. 7th day
- D. 10th day
Explanation: ### Explanation The process of wound healing by primary intention follows a predictable chronological sequence. **Neovascularization (angiogenesis)**, the formation of new blood vessels from pre-existing ones, is a hallmark of the proliferative phase of wound healing [1]. **Why 5th Day is Correct:** By the **5th day**, granulation tissue formation reaches its peak. At this stage, the incision space is filled with loose connective tissue, and neovascularization is at its **maximum intensity**, giving the wound its characteristic pink/red appearance [1]. Concurrently, collagen fibrils become more abundant and begin to bridge the incision. **Analysis of Incorrect Options:** * **3rd Day:** By day 3, neutrophils have largely been replaced by macrophages. Granulation tissue begins to invade the incision space, but the vascular network is still developing and has not yet reached its peak density [1]. * **7th Day:** By the end of the first week, the acute inflammatory response subsides. While collagen continues to accumulate, the vascularity begins to decrease as the wound enters the remodeling phase. * **10th Day:** By this stage, the proliferative phase is winding down. Fibroblasts continue to proliferate, but the "blanching" process begins as increased collagen deposition compresses the newly formed vessels, leading to decreased vascularity. **NEET-PG High-Yield Pearls:** * **Day 1:** Neutrophils appear at the margins; blood clot forms. * **Day 3:** Macrophages predominate; granulation tissue starts forming [1]. * **Day 5:** **Peak neovascularization** and maximum granulation tissue [1]. * **Week 2:** Continued collagen accumulation and fibroblast proliferation; "blanching" begins. * **Month 1:** Scar consists of connective tissue devoid of inflammation, covered by intact epidermis. * **Tensile Strength:** At the end of 1 week, it is ~10% of unwounded skin; it reaches ~70-80% by 3 months but rarely recovers 100% of original strength. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 115-119.
Question 208: Which of the following causes the maximum effect in myocardial reperfusion injury?
- A. Neutrophil
- B. Monocytes
- C. Eosinophils
- D. Free radicals (Correct Answer)
Explanation: ### Explanation **Correct Answer: D. Free Radicals** **Pathophysiology of Reperfusion Injury:** Myocardial reperfusion injury occurs when blood flow is restored to ischemic tissue. Paradoxically, the restoration of oxygen triggers a massive "burst" of **Reactive Oxygen Species (ROS)** or free radicals (such as superoxide, hydrogen peroxide, and hydroxyl radicals) [1]. The primary mechanisms include: 1. **Mitochondrial Dysfunction:** Damaged mitochondria undergo incomplete reduction of oxygen, leaking free radicals [1]. 2. **Enzymatic Action:** Ischemia increases xanthine oxidase activity, which generates superoxide upon reoxygenation. 3. **Calcium Overload:** Reperfusion leads to an influx of calcium, which further promotes ROS production and opens the mitochondrial permeability transition pore (mPTP), leading to cell death [1], [3]. **Analysis of Incorrect Options:** * **A. Neutrophils:** While neutrophils do contribute to reperfusion injury by releasing proteases and causing microvascular obstruction ("no-reflow" phenomenon), their recruitment is a secondary response. The immediate, maximum damage is initiated by the rapid generation of free radicals. * **B. Monocytes:** These cells arrive much later in the inflammatory cascade (usually after 24–48 hours) to clear debris and initiate repair. They do not play a primary role in the acute phase of reperfusion injury. * **C. Eosinophils:** These are primarily involved in Type I hypersensitivity reactions and parasitic infections; they have no significant role in myocardial reperfusion injury. **High-Yield NEET-PG Pearls:** * **The "Oxygen Paradox":** Reintroducing oxygen to ischemic tissue can cause more lethal injury than the ischemia itself. * **Morphological Hallmark:** Reperfusion injury is often characterized by **Contraction Band Necrosis** (hypercontraction of myofibrils due to calcium influx) [3]. * **Antioxidants:** Substances like Superoxide Dismutase (SOD), Catalase, and Glutathione Peroxidase act as scavengers to neutralize these free radicals [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. 102-103. [2] 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. 59-60. [3] 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. 57-61.
Question 209: In chronic granulomatous inflammation, which of the following processes is most likely to predominate?
- A. Exudation
- B. Congestion
- C. Transudation
- D. Proliferation (Correct Answer)
Explanation: **Explanation:** In pathology, inflammation is broadly categorized into acute and chronic types based on the duration and the nature of the cellular response. **Why Proliferation is Correct:** Chronic granulomatous inflammation is characterized by a prolonged response to persistent irritants (e.g., *Mycobacterium tuberculosis*, silica, or sarcoidosis) [1]. The hallmark of this process is **proliferation** [3]. This involves the multiplication and accumulation of: 1. **Modified Macrophages:** These transform into **epithelioid cells**, which may fuse to form multinucleated giant cells (e.g., Langhans giant cells) [2]. 2. **Fibroblasts:** Leading to fibrosis as the body attempts to wall off the offending agent [2]. 3. **Vascular elements:** Through angiogenesis. Unlike acute inflammation, which is "exudative," chronic inflammation is "productive" or "proliferative." **Why Other Options are Incorrect:** * **A. Exudation:** This is the hallmark of **acute inflammation**. It involves the escape of protein-rich fluid and cells (neutrophils) into the extravascular space due to increased vascular permeability. * **B. Congestion:** This refers to the dilation of small blood vessels (hyperemia), which is an **early vascular event** in acute inflammation, leading to redness (rubor) and heat (calor). * **C. Transudation:** This involves fluid leakage with low protein content, typically due to systemic hydrostatic or osmotic pressure imbalances (e.g., heart failure), rather than an inflammatory process. **High-Yield NEET-PG Pearls:** * **Definition of a Granuloma:** A focal collection of epithelioid macrophages surrounded by a collar of lymphocytes and plasma cells [2]. * **Epithelioid Cells:** These are the diagnostic feature of a granuloma; they have pale pink granular cytoplasm and "slipper-shaped" nuclei [2]. * **Key Mediator:** **IFN-γ** (Interferon-gamma), secreted by TH1 cells, is the most important cytokine for activating macrophages into epithelioid cells [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. 198-200. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109. [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. 197-199.
Question 210: Which chemical mediators are known to cause fever?
- A. Interleukin-1 (IL-1)
- B. Tumor Necrosis Factor (TNF)
- C. Prostaglandins
- D. All of the above (Correct Answer)
Explanation: **Explanation:** Fever (pyrexia) is a systemic manifestation of inflammation regulated by the hypothalamus [1]. The process is driven by **pyrogens**, which can be exogenous (e.g., bacterial LPS) or endogenous (cytokines). 1. **IL-1 and TNF (Options A & B):** These are the primary **endogenous pyrogens** [1]. When macrophages and other immune cells are activated, they release IL-1 and TNF into the circulation. These cytokines travel to the hypothalamus, specifically the *organum vasculosum of the lamina terminalis* (OVLT). 2. **Prostaglandins (Option C):** IL-1 and TNF stimulate the enzyme **Cyclooxygenase (COX)**, which converts arachidonic acid into **Prostaglandin E2 (PGE2)**. PGE2 acts on the thermoregulatory center of the anterior hypothalamus to "reset" the body’s temperature set-point to a higher level, resulting in fever [1]. **Why "All of the above" is correct:** The pathway follows a cascade: **IL-1/TNF → COX activation → PGE2 production → Fever.** Since all three mediators are essential components of this thermoregulatory shift, they are all correctly identified as mediators of fever [1]. **High-Yield NEET-PG Pearls:** * **PGE2** is the specific prostaglandin most directly responsible for raising the hypothalamic set-point [1]. * **Mechanism of Antipyretics:** NSAIDs (like Aspirin or Paracetamol) reduce fever by inhibiting the COX enzyme, thereby blocking the synthesis of PGE2. * **Other Systemic Effects:** Besides fever, IL-1 and TNF also stimulate the liver to produce **Acute Phase Reactants** (e.g., CRP, Fibrinogen, Serum Amyloid A). * **IL-6** is another major cytokine involved in the systemic inflammatory response and induction of fever. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101.
Practice by Chapter
Acute Inflammation: Vascular Events
Practice Questions
Acute Inflammation: Cellular Events
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Chemical Mediators of Inflammation
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Chronic Inflammation
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Granulomatous Inflammation
Practice Questions
Systemic Effects of Inflammation
Practice Questions
Wound Healing
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Tissue Regeneration
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Fibrosis and Repair
Practice Questions
Resolution of Inflammation
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