General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 711: Migratory thrombophlebitis is associated with all of the following except?

A. Prostate (Correct Answer)
B. Lung
C. Gastrointestinal tract
D. Pancreas

Explanation: **Explanation:** **Migratory Thrombophlebitis**, also known as **Trousseau Sign of Malignancy**, is a paraneoplastic syndrome characterized by recurrent episodes of venous thrombosis that appear in different locations over time [1]. **Why Prostate is the correct answer:** The underlying pathophysiology involves the release of **procoagulants** (like tissue factor and mucins) from tumor cells, which activate the coagulation cascade [1]. While many visceral malignancies trigger this, **Prostate cancer** is classically associated with a different hematological complication: **Disseminated Intravascular Coagulation (DIC)** or primary fibrinolysis, rather than migratory thrombophlebitis. Therefore, it is the "except" in this list. **Analysis of other options:** * **Pancreas:** This is the **most common** association [2]. Carcinoma of the body and tail of the pancreas is the classic cause of Trousseau syndrome due to the high production of procoagulant mucins. * **Lung & Gastrointestinal Tract:** Both are frequently associated with migratory thrombophlebitis. Adenocarcinomas of the lung, stomach, and colon are well-documented triggers for this paraneoplastic phenomenon. **High-Yield Clinical Pearls for NEET-PG:** 1. **Trousseau Sign (Malignancy):** Do not confuse this with the Trousseau sign of **hypocalcemia** (carpal spasm with BP cuff inflation). 2. **Mechanism:** Tumor-derived **mucins** interact with selectins, and **tissue factor** expression leads to thrombin generation. 3. **Treatment:** Heparin (LMWH) is generally preferred over warfarin in cancer-associated thrombosis because the procoagulant stimulus is continuous. 4. **Key Association:** Always rule out occult visceral malignancy (especially Pancreas) when a patient presents with unexplained migratory superficial thrombophlebitis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 522-523. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 407-408.

Question 712: Verrucous carcinoma is:

A. Extremely well differentiated squamous cell carcinoma (Correct Answer)
B. Poorly differentiated squamous cell carcinoma
C. Adenosquamous carcinoma
D. Adenocarcinoma

Explanation: **Explanation:** **Verrucous carcinoma (VC)** is a distinct, low-grade variant of **squamous cell carcinoma (SCC)**. It is characterized by its unique growth pattern and high degree of cellular maturity. **1. Why Option A is Correct:** Verrucous carcinoma is defined as an **extremely well-differentiated** malignancy. Histologically, it consists of heavily keratinized, mature squamous epithelium arranged in "church-spire" keratosis. Unlike typical SCC, it lacks significant cellular atypia, pleomorphism, or high mitotic activity. It grows in a slow, locally aggressive, "pushing" fashion rather than an infiltrative one, and it rarely metastasizes. **2. Why the other options are incorrect:** * **Option B:** Poorly differentiated SCC shows high-grade nuclear atypia, frequent mitoses, and loss of intercellular bridges—features entirely absent in the highly organized structure of VC [1]. * **Option C & D:** Verrucous carcinoma is purely of squamous origin. Adenosquamous carcinoma and Adenocarcinoma involve glandular differentiation (mucin production or gland formation), which is not a feature of VC. **High-Yield Clinical Pearls for NEET-PG:** * **Common Sites:** Oral cavity (Ackerman’s tumor), glans penis (Buschke-Löwenstein tumor) [2], and the sole of the foot (Epithelioma cuniculatum). * **Etiology:** Strongly associated with **HPV types 6 and 11** and smokeless tobacco (snuff) [2]. * **Key Histological Feature:** "Pushing borders" (bulbous rete pegs) rather than irregular invasion. * **Management Note:** Radiotherapy is generally avoided as it may trigger **anaplastic transformation** into a highly aggressive SCC. Surgical excision is the treatment of choice [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 644-645. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 974-975.

Question 713: Klinefelter syndrome is associated with all, except:

A. Delayed puberty
B. Male phenotype
C. Azoospermia
D. Barr body absent (Correct Answer)

Explanation: **Explanation:** **Klinefelter Syndrome (47, XXY)** is the most common cause of male hypogonadism and occurs due to meiotic non-disjunction of sex chromosomes [1]. **Why "Barr body absent" is the correct (except) answer:** A Barr body represents an inactivated X chromosome. According to the Lyon hypothesis, the number of Barr bodies is equal to **(Total number of X chromosomes - 1)**. Since Klinefelter patients have two X chromosomes (XXY), they possess **one Barr body** (2-1=1). Therefore, stating that the Barr body is absent is incorrect. **Analysis of Incorrect Options:** * **Male phenotype:** Despite the extra X chromosome, the presence of the **Y chromosome** (specifically the SRY gene) ensures the development of male external genitalia and a male phenotype [2]. * **Delayed puberty:** Patients typically present with primary testicular failure. Low testosterone levels lead to delayed or incomplete puberty, characterized by a eunuchoid body habitus (long legs, narrow shoulders) and decreased secondary sexual characteristics [1]. * **Azoospermia:** Atrophy of the seminiferous tubules and replacement by hyaline fibrosis leads to a lack of sperm production (azoospermia), making infertility a hallmark of this condition [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Karyotype:** Most commonly 47, XXY. * **Hormonal Profile:** ↑ FSH, ↑ LH, ↓ Testosterone, ↑ Estradiol (leading to **gynecomastia** [3]). * **Key Risks:** Increased risk of **Male Breast Cancer**, Extragonadal Germ Cell Tumors (Mediastinal), and Autoimmune diseases (SLE). * **Histology:** Characterized by **Leydig cell hyperplasia** (clumping) and hyalinization of tubules. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 174-175. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, p. 151. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, p. 1054. [4] 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. 94-95.

Question 714: Alpha-1 antitrypsin deficiency is associated with which of the following?

A. Cirrhosis
B. Neonatal hepatitis
C. Pulmonary emphysema
D. All of the above (Correct Answer)

Explanation: **Explanation:** Alpha-1 Antitrypsin (AAT) deficiency is an autosomal codominant disorder characterized by low serum levels of AAT, a protease inhibitor [1]. The pathogenesis involves a single amino acid substitution (PiZ mutation), which causes the AAT protein to misfold and aggregate within the endoplasmic reticulum of hepatocytes [3]. **Why "All of the above" is correct:** 1. **Pulmonary Emphysema:** AAT normally inhibits **neutrophil elastase** [2]. In its absence, elastase unchecked destroys the alveolar walls, leading to **panacinar emphysema**, typically involving the lower lobes [4]. 2. **Neonatal Hepatitis:** The accumulation of misfolded AAT proteins is toxic to hepatocytes. In infants, this manifests as neonatal cholestasis or hepatitis [1]. 3. **Cirrhosis:** Persistent accumulation of these protein aggregates leads to chronic liver injury, eventually progressing to cirrhosis and increasing the risk of Hepatocellular Carcinoma (HCC) [3]. **Clinical Pearls for NEET-PG:** * **Histology:** The hallmark finding is **PAS-positive, diastase-resistant pink globules** within the cytoplasm of periportal hepatocytes. * **Genetics:** The normal phenotype is **PiMM**. The most clinically significant deficient phenotype is **PiZZ** [2]. * **Smoking:** Smoking significantly accelerates the onset of emphysema in AAT-deficient patients by inactivating the remaining trace amounts of AAT [2]. * **Diagnosis:** Initial screening is via serum AAT levels; gold standard is phenotyping/genotyping. **Summary:** Since AAT deficiency affects both the lungs (due to lack of circulating protein) and the liver (due to toxic gain-of-function of the misfolded protein), it is associated with all the conditions listed [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 856-858. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 683-684. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, p. 858. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 683.

Question 715: Which of the following is a peroxisomal free radical scavenger?

A. Superoxide dismutase
B. Glutathione peroxidase
C. Catalase (Correct Answer)
D. Selenium

Explanation: ### Explanation **Correct Answer: C. Catalase** **Mechanism and Localization:** Free radical scavenging is a critical cellular defense mechanism against oxidative stress. **Catalase** is a specialized antioxidant enzyme primarily localized within **peroxisomes** [1]. Its primary function is to decompose hydrogen peroxide ($H_2O_2$) into water and molecular oxygen ($2H_2O_2 \rightarrow 2H_2O + O_2$) [1], [2]. This reaction is vital because it prevents the accumulation of $H_2O_2$, which could otherwise react with ferrous iron (Fenton reaction) to produce the highly toxic hydroxyl radical ($\cdot OH$) [1]. **Analysis of Incorrect Options:** * **A. Superoxide dismutase (SOD):** SOD converts superoxide ($O_2^{\cdot-}$) into $H_2O_2$ [2]. It exists in two main forms: Manganese-SOD (found in **mitochondria**) and Copper-Zinc-SOD (found in the **cytosol**) [1]. It is not the primary peroxisomal scavenger. * **B. Glutathione peroxidase:** This enzyme also neutralizes $H_2O_2$ and lipid peroxides, but it is primarily located in the **cytosol and mitochondria** [1]. It requires reduced glutathione (GSH) as a cofactor. * **C. Selenium:** Selenium is not an enzyme itself but an essential **trace element** that acts as a cofactor for the enzyme glutathione peroxidase. **High-Yield Clinical Pearls for NEET-PG:** * **Fenton Reaction:** $Fe^{2+} + H_2O_2 \rightarrow Fe^{3+} + \cdot OH + OH^-$ [1]. This is the most dangerous reaction in free radical pathology. * **Peroxisome Function:** Apart from scavenging $H_2O_2$, peroxisomes are involved in the **beta-oxidation of Very Long Chain Fatty Acids (VLCFA)**. * **Zellweger Syndrome:** A rare congenital disorder characterized by the absence of functional peroxisomes, leading to the accumulation of VLCFA and neurological impairment. * **Glutathione (GSH):** The ratio of reduced to oxidized glutathione (GSH/GSSG) is a key indicator of a cell's capacity to detoxify reactive oxygen species. **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. 59. [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. 100-101.

Question 716: A white infarct is typically due to which of the following?

A. Hemorrhage
B. Infection
C. Venous thrombosis
D. Arterial occlusion (Correct Answer)

Explanation: **Explanation:** Infarction refers to an area of ischemic necrosis caused by the occlusion of either the arterial supply or the venous drainage. Infarcts are classified based on their color into **White (Anemic)** and **Red (Hemorrhagic)** [1]. **Why Arterial Occlusion is Correct:** White infarcts occur due to **arterial occlusion** in **solid organs** with **end-arterial circulation** (e.g., heart, spleen, and kidney) [1]. Because these organs are solid and have a single blood supply, the density of the tissue limits the seepage of blood from adjoining capillary beds into the necrotic area, resulting in a pale, sharply defined, wedge-shaped area of necrosis [1]. **Analysis of Incorrect Options:** * **Hemorrhage:** This is a consequence of vascular rupture, not the primary mechanism of a white infarct. * **Infection:** While an infarct can become infected (septic infarct), infection is not the primary cause of the "white" appearance. * **Venous Thrombosis:** This typically leads to **Red (Hemorrhagic) infarcts** [1]. When venous drainage is blocked, blood stagnates and engorges the tissue, leading to a dark/red appearance (e.g., testicular torsion or ovarian torsion) [2]. **High-Yield NEET-PG Pearls:** * **White Infarct Locations:** Heart (Myocardium), Spleen, and Kidney [1]. * **Red Infarct Locations:** Occur in loose tissues (Lungs), tissues with dual blood supply (Lungs, Small Intestine), or following reperfusion [1]. * **Morphology:** Most infarcts are wedge-shaped, with the apex pointing toward the occluded vessel [1], [3]. * **Histology:** The dominant histologic characteristic of infarction is **coagulative necrosis** (except in the brain, which undergoes liquefactive necrosis) [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 140-142. [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. 143-144. [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 717: Increased proliferation of cells is called:

A. Hypertrophy
B. Atrophy
C. Hyperplasia (Correct Answer)
D. Metaplasia

Explanation: **Explanation:** The correct answer is **Hyperplasia**. This is a cellular adaptation characterized by an **increase in the number of cells** in an organ or tissue, resulting from the proliferation of differentiated cells and replacement by tissue stem cells [1]. It occurs in cell populations capable of replication (e.g., epithelium, bone marrow). **Analysis of Options:** * **Hypertrophy (A):** This refers to an **increase in the size of cells**, leading to an increase in the size of the organ [1]. It occurs in cells with limited capacity to divide, such as cardiac and skeletal muscle. * **Atrophy (B):** This is the **reduction in the size and number of cells**, leading to a decrease in the size of an organ or tissue. It is often caused by decreased workload, loss of innervation, or diminished blood supply. * **Metaplasia (D):** This is a reversible change in which one **differentiated cell type** (epithelial or mesenchymal) is replaced by another cell type. A classic example is Squamous Metaplasia in the airways of smokers. **High-Yield Clinical Pearls for NEET-PG:** * **Physiological Hyperplasia:** Examples include the proliferation of female breast glandular epithelium at puberty and pregnancy (hormonal) [1] or liver regeneration after partial resection (compensatory) [2]. * **Pathological Hyperplasia:** Usually caused by excessive hormonal or growth factor stimulation (e.g., Endometrial hyperplasia, Benign Prostatic Hyperplasia) [1]. * **Key Distinction:** Hyperplasia is a controlled process; if the stimulus (e.g., hormone) is removed, the hyperplasia disappears. This distinguishes it from **neoplasia**, where growth is autonomous. * **Combined Adaptation:** Hypertrophy and hyperplasia often occur together, such as in the **gravid uterus** (estrogen-induced) [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. 85-88. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 112-113.

Question 718: Which of the following cytokines are involved in the resolution of inflammation?

A. TNF-alpha, IL-1, and CRP
B. TNF-beta, IL-6, and CRP
C. TNF-alpha, IL-10, and IL-1 receptor antagonist (Correct Answer)
D. TNF-gamma

Explanation: **Explanation:** The resolution of inflammation is an active process coordinated by specific anti-inflammatory cytokines and mediators that "switch off" the inflammatory response to prevent tissue damage and promote healing. **Why Option C is Correct:** The resolution phase involves the suppression of pro-inflammatory signals. * **IL-10:** Known as the "prototypical anti-inflammatory cytokine," it inhibits the production of IL-12 and reduces MHC II expression on macrophages. * **IL-1 Receptor Antagonist (IL-1ra):** This is a naturally occurring protein that competitively binds to IL-1 receptors, blocking the potent pro-inflammatory effects of IL-1. * **TGF-beta (often grouped with TNF-alpha in this context):** While the option lists TNF-alpha (usually pro-inflammatory), in the context of resolution, it is often a distractor or refers to the complex feedback loops where certain TNF superfamily members or TGF-beta promote fibrosis and repair [3]. *Note: In many standard texts, TGF-beta and IL-10 are the primary anti-inflammatory duo.* **Why Other Options are Incorrect:** * **Option A & B:** **TNF-alpha, IL-1, and IL-6** are the "classic" pro-inflammatory cytokines responsible for the acute phase response, fever, and leukocyte recruitment [2]. **CRP (C-Reactive Protein)** is an acute-phase reactant, not a cytokine, and serves as a marker of active inflammation [2]. * **Option D:** **IFN-gamma** (often mislabeled as TNF-gamma) is a potent activator of macrophages (M1 pathway) and is central to chronic inflammation and granuloma formation, not resolution. **High-Yield Clinical Pearls for NEET-PG:** * **M2 Macrophages:** These are the "alternatively activated" macrophages responsible for resolution and repair, stimulated by **IL-4 and IL-13** [1]. * **Lipoxins & Resolvins:** These are lipid mediators (derived from arachidonic acid and omega-3 fatty acids) that actively signal the termination of inflammation. * **TGF-beta:** The most important cytokine for synthesis of extracellular matrix and scar formation (fibrosis) [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 115. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 111. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 115-116.

Question 719: Which stain is NOT used for lipids?

A. Oil red
B. Congo red (Correct Answer)
C. Sudan III
D. Sudan black

Explanation: **Explanation:** The correct answer is **Congo red** because it is the gold-standard stain for **Amyloid**, not lipids. 1. **Why Congo red is the correct answer:** Congo red is a specific stain used to identify amyloid fibrils. Under ordinary light, it stains amyloid pink-red [1]. However, its diagnostic hallmark is seen under **polarized microscopy**, where amyloid exhibits a characteristic **apple-green birefringence** [1, 2]. It has no affinity for lipid molecules. 2. **Why the other options are incorrect:** * **Oil Red O:** This is a lysochrome (fat-soluble) dye used specifically to demonstrate neutral triglycerides and lipids in frozen sections. It imparts a bright red color to fat droplets. * **Sudan III & Sudan Black B:** These are the most common stains for lipids. Sudan III stains lipids orange-red, while Sudan Black B is the most sensitive of the Sudan dyes, staining neutral fats black. Sudan Black is also used in hematopathology to differentiate AML (positive) from ALL (negative). **NEET-PG High-Yield Pearls:** * **Processing Requirement:** To stain lipids, tissues must be processed as **frozen sections**. Conventional paraffin embedding involves alcohols and xylol, which dissolve lipids, leaving behind empty vacuoles (clear spaces). * **Other Lipid Stains:** Osmium tetroxide (stains fat black and is used for electron microscopy). * **Amyloid Stains:** Apart from Congo red, other stains include Thioflavin T/S (fluorescent) and Crystal violet (metachromatic). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 268-269. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 580-581.

Question 720: A 24-year-old female presents with severe pain during menses (dysmenorrhea). To treat her symptoms, you advise her to take indomethacin in the hopes that it will reduce her pain by interfering with the production of which substance?

A. Bradykinin
B. Histamine
C. Phospholipase A2
D. Prostaglandin F2 (Correct Answer)

Explanation: **Explanation:** The correct answer is **Prostaglandin F2 (PGF2α)**. **1. Why Prostaglandin F2 is Correct:** Primary dysmenorrhea is caused by the release of excessive prostaglandins (specifically **PGF2α** and PGE2) from the secretory endometrium during menstruation. These prostaglandins cause potent **myometrial contractions**, leading to uterine ischemia and nerve sensitization, which manifest as crampy pelvic pain [1]. **Indomethacin** is a Non-Steroidal Anti-Inflammatory Drug (NSAID) that acts as a non-selective inhibitor of the **Cyclooxygenase (COX)** enzymes. By inhibiting COX, it prevents the conversion of arachidonic acid into prostaglandins, thereby reducing uterine hyperactivity and relieving pain [1]. **2. Why Incorrect Options are Wrong:** * **A. Bradykinin:** While bradykinin is a potent mediator of pain and vasodilation in acute inflammation, it is not the primary driver of menstrual uterine contractions [3]. * **B. Histamine:** Released primarily by mast cells, histamine mediates vasodilation and increased vascular permeability in immediate hypersensitivity (Type I) reactions, not the mechanical pain of dysmenorrhea [2]. * **C. Phospholipase A2:** This enzyme is responsible for releasing arachidonic acid from membrane phospholipids [1]. While inhibiting it would reduce prostaglandins, **Indomethacin acts downstream** of this enzyme (at the COX level). Steroids, not NSAIDs, inhibit Phospholipase A2 via lipocortin/annexin A1. **3. NEET-PG High-Yield Pearls:** * **Drug of Choice:** NSAIDs (like Mefenamic acid or Ibuprofen) are the first-line medical treatment for primary dysmenorrhea. * **Aspirin Sensitivity:** In some patients, inhibiting the COX pathway shifts arachidonic acid metabolism toward the **Lipoxygenase (LOX) pathway**, increasing leukotrienes and potentially triggering "Aspirin-Exacerbated Respiratory Disease" (Asthma + Nasal polyps). * **PGF2α Analogue:** Carboprost (a PGF2α analogue) is used clinically to treat Postpartum Hemorrhage (PPH) because of its potent uterine-contracting properties. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 95-96. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 94-95. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 100-101.

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