General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 121: Which of the following is NOT a cause of edema?

A. Increased hydrostatic pressure
B. Decreased colloid osmotic pressure
C. Lymphatic obstruction
D. Decreased intravascular pressure (Correct Answer)

Explanation: **Explanation:** The formation of edema is governed by **Starling’s Law**, which describes the movement of fluid between the intravascular and interstitial compartments. Edema occurs when there is an imbalance in these forces, leading to excess fluid accumulation in the interstitium [1] [5]. **Why "Decreased intravascular pressure" is the correct answer:** Intravascular pressure (specifically hydrostatic pressure) is the force that pushes fluid out of the capillaries. If this pressure **decreases**, less fluid is pushed into the tissue spaces. Therefore, decreased intravascular pressure would actually prevent edema rather than cause it. **Analysis of other options:** * **A. Increased hydrostatic pressure:** This is a primary cause of edema. When venous return is impaired (e.g., Congestive Heart Failure or Deep Vein Thrombosis), the rising pressure forces fluid out into the tissues [1]. * **B. Decreased colloid osmotic pressure:** Plasma proteins (mainly albumin) exert oncotic pressure that "pulls" fluid back into the vessels [2]. Conditions like Nephrotic syndrome (protein loss) or Cirrhosis (decreased synthesis) lead to low albumin, causing fluid to leak out [1] [2]. * **C. Lymphatic obstruction:** Lymphatics normally drain the small amount of fluid that remains in the interstitium. Obstruction (e.g., Filariasis or post-surgical scarring) leads to **lymphedema** [3] [4]. **NEET-PG High-Yield Pearls:** 1. **Albumin** is the most important protein for maintaining plasma oncotic pressure [2]. 2. **Renal Edema** (Nephrotic syndrome) typically presents first as **periorbital edema** (loose connective tissue). 3. **Cardiac Edema** (Right heart failure) is typically **dependent edema** (pitting edema of the ankles) [1]. 4. **Sodium and Water retention** (e.g., in Renal failure) increases both hydrostatic pressure and dilutes oncotic pressure, acting as a double mechanism for edema [3] [5]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 124. [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. 126-127. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 124-126. [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. 125-126. [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. 124-125.

Question 122: CD-95 is a marker of which of the following?

A. Death receptor (Correct Answer)
B. MHC complex
C. T helper cells
D. NK cells

Explanation: **Explanation:** **CD95**, also known as **Fas receptor**, is a critical cell surface marker that belongs to the Tumor Necrosis Factor Receptor (TNFR) superfamily [1]. It is the primary mediator of the **Extrinsic Pathway of Apoptosis** [1]. 1. **Why Option A is Correct:** When the Fas receptor (CD95) binds to its specific ligand, **FasL (CD95L)**, it undergoes trimerization [1]. This leads to the recruitment of the adapter protein **FADD** (Fas-associated death domain), forming the **DISC** (Death-Inducing Signaling Complex) [1]. This complex activates **Caspase-8** (or Caspase-10), which directly triggers the executioner caspases, leading to programmed cell death [1]. Thus, CD95 is a classic "Death Receptor." 2. **Why Other Options are Incorrect:** * **MHC Complex:** MHC molecules (HLA) are involved in antigen presentation, not direct apoptosis signaling. * **T helper cells:** The primary marker for T-helper cells is **CD4**. While activated T-cells may express FasL, CD95 itself is the receptor found on target cells. * **NK cells:** The characteristic markers for NK cells are **CD16** and **CD56**. **High-Yield Clinical Pearls for NEET-PG:** * **ALPS (Autoimmune Lymphoproliferative Syndrome):** Caused by mutations in the Fas receptor (CD95), Fas ligand, or Caspase-8/10. It presents with lymphadenopathy, splenomegaly, and autoimmunity due to the failure of self-reactive lymphocytes to undergo apoptosis. * **Caspase Cascade:** Remember that the Extrinsic pathway (CD95) uses **Caspase-8**, while the Intrinsic (Mitochondrial) pathway uses **Caspase-9** [1]. * **FLIP:** A protein that inhibits apoptosis by blocking the activation of Caspase-8. **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. 64-67.

Question 123: What is Trisomy 21?

A. Down's syndrome (Correct Answer)
B. Turner syndrome
C. Klinefelter syndrome
D. Edward syndrome

Explanation: **Explanation:** **Trisomy 21** refers to the presence of an extra copy of chromosome 21, resulting in a total of 47 chromosomes [1]. This is the genetic basis for **Down’s syndrome**, the most common chromosomal disorder and a frequent cause of intellectual disability [1]. In 95% of cases, it occurs due to **meiotic non-disjunction**, which is strongly associated with advanced maternal age. **Analysis of Options:** * **Option A (Correct):** Down’s syndrome is synonymous with Trisomy 21 [1]. * **Option B (Incorrect):** **Turner syndrome** is a monosomy (45, XO), characterized by the absence of one X chromosome in females. * **Option C (Incorrect):** **Klinefelter syndrome** involves an extra X chromosome in males (47, XXY). * **Option D (Incorrect):** **Edward syndrome** is caused by **Trisomy 18** [1]. (Mnemonic: "E" for Edward and Eighteen). **High-Yield Clinical Pearls for NEET-PG:** * **Cytogenetics:** 95% are due to non-disjunction; 4% due to **Robertsonian translocation** (usually involving chromosome 14 or 22); 1% due to mosaicism [1]. * **Clinical Features:** Simian crease, Brushfield spots (iris), epicanthal folds, and macroglossia [1]. * **Cardiac Associations:** Endocardial cushion defects (ASD/VSD) are the most common. * **Gastrointestinal:** Duodenal atresia ("Double bubble" sign) and Hirschsprung disease. * **Future Risks:** Increased risk of **Acute Leukemia** (ALL and AML-M7) and early-onset **Alzheimer’s disease** (due to the APP gene on chromosome 21). * **Screening:** Low Alpha-fetoprotein (AFP) and high hCG/Inhibin-A in maternal quadruple screening. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 168-172.

Question 124: What substance is deposited in Bronze diabetes?

A. Bronze
B. Copper
C. Iron (Correct Answer)
D. Carbon

Explanation: **Explanation:** **Bronze Diabetes** is the classic clinical triad of skin hyperpigmentation, diabetes mellitus, and cirrhosis, occurring as a complication of **Hereditary Hemochromatosis** [1]. **Why Iron is the correct answer:** The underlying pathology is a systemic overload of **Iron** [1]. In hereditary hemochromatosis (most commonly due to a mutation in the *HFE* gene), there is excessive intestinal absorption of iron [2]. This excess iron is deposited in various organs as **hemosiderin** [1]. * **Skin:** Iron deposition, combined with increased melanin production, gives the skin a metallic "bronze" appearance [1]. * **Pancreas:** Iron deposition in the Islets of Langerhans causes selective damage to beta cells, leading to secondary diabetes mellitus [1]. * **Liver:** Chronic deposition leads to micronodular cirrhosis [1]. **Why other options are incorrect:** * **Bronze:** This is a clinical description of the skin color, not a substance deposited in the body. * **Copper:** Excessive copper deposition is characteristic of **Wilson’s Disease**, which typically presents with Kayser-Fleischer rings and basal ganglia involvement, not "bronze" skin [3]. * **Carbon:** Deposition of carbon (coal dust) in the lungs is known as **Anthracosis**, commonly seen in smokers and urban dwellers. **High-Yield NEET-PG Pearls:** 1. **Gene Mutation:** Most common is **C282Y** on the *HFE* gene (Chromosome 6). 2. **Stain of Choice:** **Prussian Blue** (Perl’s stain) is used to visualize iron/hemosiderin [1]. 3. **Early Sign:** The most common early symptom is often joint pain (arthropathy) or fatigue. 4. **Cardiac Involvement:** Can lead to restrictive or dilated cardiomyopathy. 5. **Treatment:** Therapeutic phlebotomy is the gold standard [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 854-855. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, p. 854. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 855-856.

Question 125: What is the total number of chromosomes typically found in an individual with Turner syndrome?

A. 45 (Correct Answer)
B. 47
C. 46
D. 42

Explanation: **Explanation:** **Turner Syndrome** is a common chromosomal abnormality characterized by **monosomy of the X chromosome** [2]. In a typical individual, there are 46 chromosomes (44 autosomes and 2 sex chromosomes) [3]. In Turner syndrome, one sex chromosome is missing, resulting in a **45,X** karyotype [2]. This occurs most frequently due to non-disjunction during paternal meiosis. * **Option A (45): Correct.** The individual has 44 autosomes and only one X chromosome (45,X0) [2]. This loss of genetic material from the short arm of the X chromosome leads to the characteristic clinical features [1]. * **Option B (47): Incorrect.** This represents **trisomy** [4]. Examples include Klinefelter syndrome (47,XXY), Down syndrome (Trisomy 21), or Patau syndrome (Trisomy 13) [4]. * **Option C (46): Incorrect.** This is the **euploid** (normal) number of chromosomes in humans (46,XX or 46,XY) [3]. * **Option D (42): Incorrect.** This number does not correspond to any recognized viable human chromosomal syndrome. **High-Yield Clinical Pearls for NEET-PG:** 1. **Most common cause of primary amenorrhea:** Turner syndrome is a leading genetic cause. 2. **Clinical Features:** Short stature (due to *SHOX* gene deletion) [1], webbed neck (cystic hygroma), widely spaced nipples (shield chest), and streak ovaries (accelerated oocyte loss). 3. **Cardiac Associations:** Bicuspid aortic valve (most common) and Coarctation of the aorta. 4. **Renal Association:** Horseshoe kidney. 5. **Karyotype Variations:** While 45,X is the most common (50%), mosaicism (e.g., 45,X/46,XX) also occurs and may present with a milder phenotype. **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. 173-174. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 167-168. [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. 92-93.

Question 126: Development of the female breast at puberty is an example of:

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

Explanation: **Explanation:** The development of the female breast at puberty is a classic example of **physiological adaptation** driven by hormonal stimulation (primarily estrogen and progesterone). **Why Option C is Correct:** Breast enlargement during puberty involves two simultaneous cellular processes: 1. **Hyperplasia:** An increase in the *number* of cells within the glandular epithelium (捕ducts and lobules). 2. **Hypertrophy:** An increase in the *size* of existing cells, particularly within the connective tissue and stromal components [1]. In organs composed of cells capable of division (like the breast or uterus), hypertrophy and hyperplasia almost always occur together in response to trophic signals [2]. **Analysis of Incorrect Options:** * **A. Hypertrophy:** While hypertrophy does occur, selecting this alone is incomplete. Pure hypertrophy typically occurs in "permanent" cells that cannot divide, such as skeletal muscle (weightlifting) or cardiac muscle (hypertension). * **B. Hyperplasia:** While glandular proliferation is a hallmark of breast development, it does not account for the total increase in tissue mass and stromal volume. * **D. Atrophy:** This refers to a decrease in cell size and number, leading to reduced organ size (e.g., breast tissue post-menopause). **High-Yield Clinical Pearls for NEET-PG:** * **Uterus during pregnancy:** Like the pubertal breast, it undergoes both **hypertrophy and hyperplasia** [1]. * **Pure Hypertrophy:** Occurs in the **Heart** (Left Ventricular Hypertrophy). * **Pure Hyperplasia:** Can be physiological (compensatory hyperplasia after partial hepatectomy) or pathological (Endometrial hyperplasia due to excess estrogen). * **Key Concept:** If a cell can divide, it will undergo both; if it cannot divide, it only undergoes hypertrophy [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. 85-87. [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. 46-47.

Question 127: Apoptosis is regulated by which gene?

A. p53 (Correct Answer)
B. BRAC
C. N-myc
D. RB

Explanation: **Explanation:** **Correct Answer: A. p53** The **p53 gene**, often called the "Guardian of the Genome," is the primary regulator of apoptosis in response to DNA damage [1]. When DNA damage is irreparable, p53 triggers apoptosis by upregulating pro-apoptotic proteins like **BAX and BAK** (which create pores in the mitochondrial membrane) and inducing the release of Cytochrome C [1], [3]. This activates the intrinsic (mitochondrial) pathway of apoptosis. If the damage is repairable, p53 arrests the cell cycle in the G1 phase via p21 to allow for repair [2]. **Analysis of Incorrect Options:** * **B. BRCA:** These are DNA repair genes (BRCA1/2). Mutations are primarily associated with hereditary breast and ovarian cancer syndromes, but they do not directly "regulate" the apoptotic signaling cascade like p53. * **C. N-myc:** This is a proto-oncogene [3]. Amplification of N-myc is a classic marker for **Neuroblastoma** and leads to uncontrolled cell proliferation rather than the regulation of programmed cell death. * **D. RB (Retinoblastoma gene):** Known as the "Governor of the Genome," RB regulates the **G1 to S phase transition** of the cell cycle by binding to the E2F transcription factor [4]. While it controls the cell cycle, it is not the primary regulator of apoptosis. **High-Yield Clinical Pearls for NEET-PG:** * **Li-Fraumeni Syndrome:** A germline mutation in p53 leading to multiple early-onset cancers (Sarcoma, Breast, Leukemia, Adrenal). * **Bcl-2:** An anti-apoptotic protein (the "survival" gene) often overexpressed in Follicular Lymphoma due to t(14;18) [3]. * **Caspases:** The executioners of apoptosis. Caspase 8 is for the extrinsic pathway; Caspase 9 is for the intrinsic pathway; **Caspase 3** is the common executioner. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 303-304. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 302-303. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 310. [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. 227-228.

Question 128: According to WHO classification, which class of membranous glomerulonephritis is typically seen in Systemic Lupus Erythematosus (SLE)?

A. Class II
B. Class III
C. Class IV
D. Class V (Correct Answer)

Explanation: **Explanation:** The classification of Lupus Nephritis (LN) is based on the International Society of Nephrology/Renal Pathology Society (ISN/RPS) system, which is the standard adopted by the WHO. **Why Class V is correct:** **Class V Lupus Nephritis** is specifically defined as **Membranous Lupus Nephritis** [1]. It is characterized by global or segmental subepithelial immune complex deposits (containing IgG and complement) and diffuse thickening of the glomerular basement membrane. Clinically, patients typically present with **nephrotic-range proteinuria**, similar to primary membranous glomerulopathy [1]. **Analysis of Incorrect Options:** * **Class II (Mesangial Proliferative LN):** Characterized by purely mesangial hypercellularity and matrix expansion with mesangial immune deposits. It usually presents with mild hematuria or proteinuria. * **Class III (Focal LN):** Involves less than 50% of the total glomeruli [2]. It shows active or inactive focal, segmental, or global endocapillary or extracapillary lesions [2]. * **Class IV (Diffuse LN):** The **most common and most severe form** [2]. It involves more than 50% of the glomeruli. It is characterized by "wire-loop" lesions (subendothelial deposits) and carries the worst prognosis if untreated [2]. **High-Yield NEET-PG Pearls:** * **Most Common Class:** Class IV (Diffuse Proliferative) [2]. * **Most Severe/Worst Prognosis:** Class IV [2]. * **Wire-loop lesions:** Characteristic of Class IV (due to massive subendothelial deposits) [2]. * **Full House Effect:** Immunofluorescence in SLE typically shows "Full House" positivity (IgG, IgA, IgM, C3, and C1q) [1]. * **Class VI:** Represents Advanced Sclerotic LN (>90% globally sclerosed glomeruli), representing the end-stage of the disease. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 532-533. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 230-232.

Question 129: Type 1 Dentinogenesis imperfecta is caused by mutation in which gene?

A. DMP-1 gene
B. BSP-1 gene
C. DSPP gene (Correct Answer)
D. SPP1 gene

Explanation: **Dentinogenesis Imperfecta (DI)** is a genetic disorder of tooth development characterized by translucent, discolored teeth and weakened dentin. **Why the correct answer is right:** The **DSPP gene** (Dentin Sialophosphoprotein) encodes two major non-collagenous proteins: Dentin Sialoprotein (DSP) and Dentin Phosphoprotein (DPP). These are critical for the mineralization of the dentin matrix. Mutations in the DSPP gene lead to defective dentin formation. According to the revised classification, **DI Type II and Type III** are caused by DSPP mutations. *Note on Classification:* Historically, DI Type I was associated with Osteogenesis Imperfecta (COL1A1/COL1A2 mutations). However, in modern dental pathology (Shields classification), isolated DI is primarily linked to **DSPP gene** mutations on chromosome 4q22.1. **Why the incorrect options are wrong:** * **DMP-1 (Dentin Matrix Acidic Phosphoprotein 1):** While involved in odontoblast differentiation, mutations here typically cause Autosomal Recessive Hypophosphatemic Rickets, not classic DI. * **BSP-1 (Bone Sialoprotein 1):** Also known as Osteopontin, it is involved in bone remodeling but is not the primary gene mutated in DI. * **SPP1 (Secreted Phosphoprotein 1):** This is the gene symbol for Osteopontin; it plays a role in bone matrix but not the structural pathogenesis of DI. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Appearance:** Teeth appear "opalescent" (blue-grey or amber-brown). * **Radiological Hallmark:** Bulbous crowns with constricted necks and **obliteration of pulp chambers/root canals**. * **Shields Classification:** * **Type I:** Associated with Osteogenesis Imperfecta (Blue sclera). [1] * **Type II:** Most common; isolated DI (DSPP mutation). * **Type III:** "Brandywine type"; features "shell teeth" with large pulp chambers. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1186-1188.

Question 130: Amyloid is stained by which of the following stains?

A. PAS
B. Congo red (Correct Answer)
C. H & E
D. Methenamine silver

Explanation: **Explanation:** Amyloid is a pathological proteinaceous substance deposited between cells in various tissues [1]. The gold standard for identifying amyloid is the **Congo red stain** [1]. **1. Why Congo Red is Correct:** Under ordinary light, Congo red stains amyloid a characteristic **pink or red** color [1]. However, its most diagnostic feature is observed under **polarized light**, where amyloid displays a pathognomonic **apple-green birefringence** [1]. This occurs because the dye molecules align perfectly with the cross-beta-pleated sheet configuration of the amyloid fibrils [1]. **2. Why Other Options are Incorrect:** * **PAS (Periodic Acid-Schiff):** Primarily used to highlight carbohydrates, glycogen, and basement membranes. While amyloid is a glycoprotein and may show weak PAS positivity, it is not a specific or diagnostic stain [2]. * **H & E (Hematoxylin and Eosin):** On standard H&E, amyloid appears as an amorphous, eosinophilic (pink), extracellular hyaline material [1]. It is indistinguishable from other hyaline deposits, making H&E insufficient for a definitive diagnosis. * **Methenamine Silver (GMS):** This is typically used to visualize fungi, basement membranes (in renal pathology), and certain bacteria (like *Pneumocystis*). It does not specifically stain amyloid. **3. High-Yield Clinical Pearls for NEET-PG:** * **Other Stains:** Thioflavin T and S (Fluorescent stains) are highly sensitive but less specific than Congo red. Crystal Violet and Methyl Violet show **metachromasia** (staining amyloid rose-red). * **Most Common Type:** Globally, AL (Amyloid Light chain) is the most common systemic form [3]. * **Precursor Proteins:** AL is derived from plasma cells (Immunoglobulin light chains); AA is derived from SAA (associated with chronic inflammation) [1]. * **Diagnosis:** Abdominal fat pad aspiration or rectal biopsy are common screening procedures for systemic amyloidosis. **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. Diseases of the Immune System, pp. 264-266. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 266-267.

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