General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 411: Which of the following conditions is associated with PAS-positive macrophages?

A. Whipple's disease (Correct Answer)
B. Tropical sprue
C. Celiac disease
D. Crohn's disease

Explanation: **Explanation:** The correct answer is **Whipple’s disease**. This condition is caused by the gram-positive actinomycete **Tropheryma whipplei**. The hallmark pathological finding is the infiltration of the small intestinal lamina propria by bulky, foamy **macrophages** [1]. These macrophages contain "sickle-shaped" inclusions which are actually partially digested bacterial cell walls. These remnants are rich in glycoproteins, making them strongly **PAS (Periodic Acid-Schiff) positive** and **diastase-resistant**. **Why other options are incorrect:** * **Tropical sprue:** Characterized by total/subtotal villous atrophy and crypt hyperplasia. While it involves chronic inflammation, it does not feature PAS-positive macrophage infiltration. * **Celiac disease:** An immune-mediated enteropathy triggered by gluten. Histology shows increased intraepithelial lymphocytes (IELs), villous atrophy, and crypt hyperplasia, but lacks the specific macrophage inclusions seen in Whipple’s. * **Crohn’s disease:** A type of Inflammatory Bowel Disease (IBD) characterized by transmural inflammation and **non-caseating granulomas** [2]. It does not typically present with PAS-positive macrophages. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Triad:** Malabsorption (diarrhea/weight loss), migratory polyarthritis, and lymphadenopathy [1]. * **Electron Microscopy:** Shows the characteristic "bacillary organisms" (T. whipplei). * **Differential Diagnosis:** *Mycobacterium avium-intracellulare* (MAI) infection in HIV patients also shows PAS-positive macrophages; however, MAI is **Acid-Fast Bacilli (AFB) positive**, whereas Whipple’s is **AFB negative** [1]. * **Treatment:** Long-term antibiotics (usually Ceftriaxone followed by Trimethoprim-sulfamethoxazole). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 798-799. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 365-366.

Question 412: Iron in tissues is stained with which of the following stains?

A. Sudan O
B. Prussian Blue (Correct Answer)
C. PAS
D. None of the above

Explanation: **Explanation:** **Prussian Blue (Perls' Stain)** is the correct answer because it is the gold-standard histochemical stain used to detect **ferric iron (Fe³⁺)** in tissues [1]. The underlying chemical principle involves the reaction of ferric iron with potassium ferrocyanide in an acidic medium, resulting in the formation of a bright blue pigment called ferric ferrocyanide (Prussian Blue). This stain is primarily used to visualize iron stored in the form of **hemosiderin** within macrophages (siderophages) or parenchymal cells [1]. **Analysis of Incorrect Options:** * **Sudan O (Sudan III/IV):** These are lipid-soluble dyes used to stain **neutral fats (lipids)** and triglycerides. They are commonly used on frozen sections to diagnose fat embolism or steatosis. * **PAS (Periodic Acid-Schiff):** This stain detects **glycogen** and mucopolysaccharides. It is widely used to visualize basement membranes, fungal walls, and glycogen storage diseases. **Clinical Pearls for NEET-PG:** * **Hemochromatosis vs. Hemosiderosis:** Prussian Blue is essential for grading iron overload in the liver and heart [1]. * **Sideroblastic Anemia:** This stain identifies "Ringed Sideroblasts" in the bone marrow (iron-laden mitochondria surrounding the nucleus). * **Heart Failure Cells:** In chronic passive congestion of the lungs, Prussian Blue identifies hemosiderin-laden macrophages in the alveoli. * **Note:** It does **not** stain iron in hemoglobin or ferritin directly; it specifically targets the insoluble hemosiderin. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 854-855.

Question 413: Cat eye syndrome is associated with which chromosomal abnormality?

A. Trisomy 21
B. Trisomy 18
C. Trisomy 13
D. Trisomy 22 (Correct Answer)

Explanation: **Explanation:** **Cat Eye Syndrome (Schmid-Fraccaro Syndrome)** is a rare chromosomal disorder caused by the presence of an extra chromosome, specifically a **partial tetrasomy of chromosome 22**. This occurs due to a small supernumerary marker chromosome (sSMC) derived from the duplication of the short arm (p) and a small part of the long arm (q) of chromosome 22. Because this results in four copies of this specific genetic material instead of the usual two, it is functionally categorized under abnormalities of **Chromosome 22**. **Analysis of Options:** * **Trisomy 22 (Correct):** While Cat Eye Syndrome is technically a partial tetrasomy, in the context of standard competitive exams like NEET-PG, it is associated with chromosome 22. Full Trisomy 22 is usually lethal in utero [1], but mosaicism or partial duplications (like Cat Eye Syndrome) are clinically viable. * **Trisomy 21 (Incorrect):** This is **Down Syndrome**, characterized by flat facial profiles, simian crease, and mental retardation [2]. * **Trisomy 18 (Incorrect):** This is **Edwards Syndrome**, characterized by rocker-bottom feet, clenched fists with overlapping fingers, and micrognathia [2]. * **Trisomy 13 (Incorrect):** This is **Patau Syndrome**, characterized by midline defects like cleft lip/palate, holoprosencephaly, and polydactyly [2]. **Clinical Pearls for NEET-PG:** * **The "Cat Eye" appearance:** Refers to **Coloboma of the iris** (a vertical gap in the iris), though this is only present in about 50% of cases. * **Classic Triad:** Iris coloboma, Anal atresia (with fistula), and Preauricular pits/tags. * **Other features:** Congenital heart defects and renal malformations. * **Cytogenetics:** Look for the marker chromosome **inv dup(22)(q11)**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 168-169. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 171-172.

Question 414: Free radical injury includes all except?

A. Damaged cell membranes
B. Loss of enzymatic activity
C. Single strand break of DNA
D. Vacuolar degeneration (Correct Answer)

Explanation: **Explanation:** Free radicals are highly reactive chemical species with a single unpaired electron in an outer orbit. They cause cell injury via three primary mechanisms: lipid peroxidation of membranes, oxidative modification of proteins, and DNA damage [2]. **Why Vacuolar Degeneration is the correct answer:** **Vacuolar degeneration** (also known as hydropic change) is a hallmark of **reversible cell injury** caused by a failure of energy-dependent ion pumps (like the Na+/K+ ATPase) in the plasma membrane [1]. This leads to an influx of water and sodium into the cell, causing the cytoplasm to appear "vacuolated." While free radicals can eventually lead to cell death, vacuolar degeneration is specifically the morphological expression of **acute swelling** due to ATP depletion, not a direct mechanism of oxidative stress [1]. **Analysis of Incorrect Options:** * **A. Damaged cell membranes:** Free radicals (specifically ROS) attack the double bonds of polyunsaturated fatty acids in membrane lipids, a process called **lipid peroxidation**, leading to extensive membrane damage [2]. * **B. Loss of enzymatic activity:** Free radicals cause the **oxidation of amino acid side chains** and the formation of protein-protein cross-links (e.g., disulfide bonds) [2]. This results in the unfolding or degradation of critical structural proteins and enzymes. * **C. Single strand break of DNA:** Free radicals react with thymine in nuclear and mitochondrial DNA, causing **single-strand breaks** [2]. This is a major mechanism behind cell aging and malignant transformation [4]. **Clinical Pearls for NEET-PG:** * **Fenton Reaction:** $Fe^{2+} + H_2O_2 \rightarrow Fe^{3+} + OH^\bullet + OH^-$ (The most important reaction generating the highly reactive hydroxyl radical) [3]. * **Antioxidant Enzymes:** Remember the "Big Three": **Superoxide Dismutase (SOD)** (converts $O_2^\bullet$ to $H_2O_2$), **Catalase** (decomposes $H_2O_2$), and **Glutathione Peroxidase** [2], [3]. * **Morphological hallmark of irreversible injury:** Severe mitochondrial swelling and large amorphous densities in the mitochondrial matrix. **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. 49-50. [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, p. 59. [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. 102-103.

Question 415: The action of putrefactive bacteria on necrotic tissue results in what?

A. Infarction
B. Embolism
C. Gangrene (Correct Answer)
D. Coagulation

Explanation: **Explanation:** **Gangrene** is defined as a form of necrosis (usually coagulative) that is modified by the secondary action of **putrefactive bacteria** [1]. When tissue undergoes necrosis due to a loss of blood supply, it becomes a substrate for saprophytic bacteria (like *Clostridia* species). these bacteria digest the dead tissue, leading to the characteristic foul smell and black discoloration (due to iron sulfide formation from decomposed hemoglobin). **Why other options are incorrect:** * **Infarction:** This is the process of tissue death (necrosis) resulting specifically from an acute obstruction of the blood supply (ischemia) [1]. While infarction often precedes gangrene, it refers to the death itself, not the subsequent bacterial decomposition. * **Embolism:** This refers to a detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin. It is a *cause* of ischemia/infarction, not a result of bacterial action on dead tissue. * **Coagulation (Coagulative Necrosis):** This is the most common pattern of cell death where the architecture of dead tissues is preserved for a few days. It is the underlying process in most gangrene cases, but "gangrene" is the specific term used once putrefaction is added to the clinical picture. **High-Yield Clinical Pearls for NEET-PG:** * **Dry Gangrene:** Primarily coagulative necrosis; limited bacterial action; common in distal limbs (e.g., Buerger’s disease, Diabetes) [1]. * **Wet Gangrene:** Predominantly liquefactive necrosis due to significant bacterial superinfection; occurs in moist tissues like the bowel, lung, or mouth (Noma) [1]. * **Gas Gangrene:** A specific type of wet gangrene caused by *Clostridium perfringens*, characterized by gas bubbles (crepitus) in the tissues [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, 143-144.

Question 416: A ring chromosome is a result of which chromosomal abnormality?

A. Deletion (Correct Answer)
B. Inversion
C. Duplication
D. Translocation

Explanation: **Explanation:** A **ring chromosome** is a structural chromosomal abnormality that occurs when a chromosome undergoes **terminal deletions** at both the short (p) and long (q) arms. Following the loss of these distal segments, the remaining "sticky" ends of the central portion fuse together to form a ring shape. Because the formation of a ring chromosome necessitates the loss of genetic material from the telomeric regions, it is fundamentally a result of **deletion**. **Analysis of Options:** * **A. Deletion (Correct):** As described, the breakage of both ends of a chromosome followed by fusion is the mechanism. The resulting loss of genetic material often leads to clinical phenotypes (e.g., Ring 20 syndrome). * **B. Inversion:** This involves a single chromosome undergoing two breaks, with the intervening segment rotating 180° and reinserting. There is no loss of genetic material (balanced). * **C. Duplication:** This refers to the presence of an extra copy of a segment of a chromosome. * **D. Translocation:** This involves the exchange of segments between non-homologous chromosomes (e.g., Robertsonian or Reciprocal translocations). **High-Yield NEET-PG Pearls:** * **Karyotype Notation:** A ring chromosome is denoted by the symbol **'r'** (e.g., 46,XX,r(15)). * **Clinical Significance:** Ring chromosomes are often unstable during mitosis, leading to mosaicism [2]. * **Common Example:** **Ring 14 syndrome** (characterized by seizures and intellectual disability) and **Ring X** (a variant of Turner Syndrome) [1]. * **Telomeres:** Normally, telomeres prevent end-to-end fusion; ring formation only occurs when telomeres are lost via deletion. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 175-177. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 168-169.

Question 417: NK cells express which of the following markers?

A. CD 15, CD 55
B. CD16, CD56 (Correct Answer)
C. CD 16, CD 57
D. CD21, CD 66

Explanation: **Explanation:** Natural Killer (NK) cells are a subset of innate lymphoid cells that play a critical role in the surveillance and destruction of virally infected cells and tumor cells [1]. They do not express T-cell receptors (CD3) [4] or B-cell receptors (surface Ig) [3], making their specific surface markers high-yield for exams. **Why Option B is correct:** * **CD16 (FcγRIII):** This is a low-affinity receptor for the Fc portion of IgG. It allows NK cells to bind to antibody-coated target cells, mediating **Antibody-Dependent Cellular Cytotoxicity (ADCC)**. * **CD56 (NCAM):** This is the prototypical marker used to identify NK cells in clinical practice (Flow Cytometry). While its exact functional role in NK cells is less clear, it is essential for identification. **Analysis of Incorrect Options:** * **Option A:** **CD15** is a marker for Reed-Sternberg cells (Hodgkin Lymphoma) and granulocytes [2]. **CD55** (DAF) is a complement regulatory protein; its deficiency is seen in Paroxysmal Nocturnal Hemoglobinuria (PNH). * **Option C:** While **CD57** can be expressed on mature NK cells, it is not as definitive or universally used as the combination of CD16 and CD56. * **Option D:** **CD21** (CR2) is the receptor for the C3d complement fragment and the **Epstein-Barr Virus (EBV)**, found on B-cells [3]. **CD66** is a marker for granulocytes. **High-Yield Clinical Pearls for NEET-PG:** * **NK Cell Lineage:** They are derived from the Common Lymphoid Progenitor (CLP) but function as part of the **innate immune system**. * **Mechanism of Action:** They kill via **Perforins** (create pores) and **Granzymes** (induce apoptosis). * **The "Missing Self" Hypothesis:** NK cells are activated when they encounter cells lacking **MHC Class I** molecules (which are often downregulated by viruses and tumors to evade T-cells) [1]. * **Cytokine Production:** NK cells are a major source of **IFN-γ**, which activates macrophages [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 200-201. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 596-598. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 199-200. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 198-199.

Question 418: What is the mode of inheritance for Huntington's chorea?

A. Autosomal dominant (Correct Answer)
B. Autosomal recessive
C. X-linked recessive
D. X-linked dominant

Explanation: **Explanation:** **Huntington’s Disease (HD)** is a neurodegenerative disorder characterized by the mode of **Autosomal Dominant** inheritance [2]. It is caused by an unstable expansion of **CAG trinucleotide repeats** in the *HTT* gene located on **Chromosome 4p** [1]. Because it is autosomal dominant, an affected individual has a 50% chance of passing the gene to each offspring, and the disease typically manifests in every generation. * **Why Option A is correct:** HD follows the "Vertical Transmission" pattern typical of autosomal dominant traits. A key feature is **Anticipation**, where the disease manifests earlier and more severely in successive generations, particularly when inherited from the father (paternal transmission). * **Why Options B, C, and D are wrong:** * **Autosomal Recessive** conditions (e.g., Cystic Fibrosis, Wilson’s disease) usually require two copies of the mutated gene and often skip generations. * **X-linked** conditions (e.g., Hemophilia, Alport syndrome) show a sex-linked inheritance pattern where males are predominantly affected (recessive) or there is no male-to-male transmission (dominant). HD affects both sexes equally and shows direct male-to-male transmission. **High-Yield Clinical Pearls for NEET-PG:** * **Trinucleotide Repeat:** CAG (C-A-G: **C**audate **A**trophy **G**ene) [1]. * **Pathology:** Marked atrophy of the **Caudate Nucleus** and Putamen (Striatum), leading to "boxcar ventricles" on imaging [3]. * **Neurotransmitters:** Characterized by a **decrease in GABA and Acetylcholine**, and an increase in Dopamine. * **Clinical Triad:** Chorea (involuntary movements), Dementia, and Psychiatric disturbances (depression/aggression). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 177-179. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 148-150. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1299-1300.

Question 419: What is the chromosomal karyotype in Patau syndrome?

A. 47XX,+21
B. 46XX/47XX,+18
C. 45XX,der(14;21)
D. 47XX,+13 (Correct Answer)

Explanation: **Explanation:** **Patau Syndrome** is a chromosomal disorder caused by **Trisomy 13** [1]. In a normal human karyotype, there are 46 chromosomes (23 pairs). In Patau syndrome, there is an extra copy of chromosome 13, resulting in a total of 47 chromosomes. The correct karyotype for a female with this condition is **47,XX,+13** [1]. **Analysis of Options:** * **Option A (47,XX,+21):** This represents Trisomy 21, which is **Down Syndrome**, the most common autosomal trisomy [1]. * **Option B (46,XX/47,XX,+18):** This represents a **mosaicism** for Trisomy 18 (**Edwards Syndrome**) [1]. While Edwards syndrome is Trisomy 18, the question asks specifically for Patau syndrome. * **Option C (45,XX,der(14;21)):** This describes a **Robertsonian Translocation** involving chromosomes 14 and 21. This individual is a balanced carrier and is phenotypically normal but at high risk of having children with Down Syndrome [1]. **High-Yield Clinical Pearls for NEET-PG:** To differentiate the three major trisomies, remember the "Ages of Trisomy": 1. **Trisomy 13 (Patau):** Think "P" for **P**uberty (age 13). Key features: **P**olydactyly, **P**unched-out scalp lesions (Aplasia cutis), **P**alate (Cleft lip/palate), and Holoprosencephaly. 2. **Trisomy 18 (Edwards):** Think "E" for **E**lection (age 18). Key features: **E**minent occiput, **E**lfin ears, Rocker-bottom feet, and Clenched fists (overlapping fingers). 3. **Trisomy 21 (Down):** Think "D" for **D**rinking (age 21). Key features: Simian crease, Brushfield spots, and early-onset Alzheimer’s. *Note: Patau syndrome has the worst prognosis among the three, with most infants not surviving past the first year of life.* [1] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 171-172.

Question 420: Which disease has autosomal recessive inheritance?

A. Cystic fibrosis (Correct Answer)
B. Hydrocephalus
C. Duchene muscular dystrophy
D. Vitamin D resistant rickets

Explanation: **Explanation:** The correct answer is **Cystic Fibrosis (A)**. **Cystic Fibrosis (CF)** is one of the most common **autosomal recessive (AR)** disorders, particularly in Caucasian populations [2]. It is caused by a mutation in the **CFTR gene** located on **chromosome 7q** [1], [4]. In AR inheritance, an individual must inherit two copies of the mutated gene (one from each parent) to manifest the disease. The pathophysiology involves defective chloride ion transport, leading to abnormally thick secretions in the lungs, pancreas, and reproductive tract [1], [2]. **Analysis of Incorrect Options:** * **Hydrocephalus (B):** This is a clinical sign (excess CSF) rather than a single genetic disease. While it can be part of genetic syndromes, the most common inherited form (Aqueductal stenosis) is typically **X-linked recessive**. * **Duchenne Muscular Dystrophy (C):** This is a classic **X-linked recessive** disorder caused by a mutation in the *Dystrophin* gene. It primarily affects males, while females are typically asymptomatic carriers. * **Vitamin D Resistant Rickets (D):** Also known as Hereditary Hypophosphatemic Rickets, this is a rare example of **X-linked dominant** inheritance. **High-Yield NEET-PG Pearls:** * **Mnemonic for AR disorders:** "ABCDE-S"—**A**lbinism, **B**enign Prostatic Hyperplasia (not genetic, but used for flow), **C**ystic Fibrosis/CAH [1], **D**eafness (sensorineural), **E**nzyme deficiencies (most inborn errors of metabolism like PKU [3], Galactosemia, and Lysosomal storage diseases are AR [1]). * **Exception:** Most enzyme deficiencies are AR, **EXCEPT** Hunter Syndrome and G6PD deficiency, which are X-linked recessive. * **CF Diagnosis:** The gold standard is the **Sweat Chloride Test** (Chloride >60 mEq/L). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 150-151. [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. 120-122. [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. 119-120. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, p. 476.

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