General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 861: What is the function of micro-RNA?

A. Encodes proteins
B. Modulates the translation of target mRNAs into their corresponding proteins (Correct Answer)
C. Regulation of gene expression
D. mRNA splicing

Explanation: **Explanation:** Micro-RNAs (miRNAs) are small, non-coding, single-stranded RNA molecules (approximately 22 nucleotides long) that function primarily in the **post-transcriptional regulation of gene expression** [2]. The correct answer is **B** because miRNAs function by binding to complementary sequences on target messenger RNAs (mRNAs). This binding typically leads to **translational repression** or mRNA degradation, thereby modulating the amount of protein produced [3]. This process is mediated by the RNA-induced silencing complex (RISC) [3]. **Analysis of Options:** * **A (Encodes proteins):** Incorrect. miRNAs are non-coding RNAs; they do not serve as templates for protein synthesis [2]. * **C (Regulation of gene expression):** While technically true in a broad sense, Option B is the **more specific and accurate** functional description required for competitive exams. miRNAs regulate expression specifically at the post-transcriptional level (translation) [2]. * **D (mRNA splicing):** Incorrect. Splicing is primarily performed by small nuclear RNAs (snRNAs) within the spliceosome. **High-Yield Clinical Pearls for NEET-PG:** * **OncomiRs:** miRNAs that contribute to cancer development by downregulating tumor suppressor genes (e.g., miRNA-21) or acting as tumor suppressors themselves (e.g., miRNA-15, miRNA-16) [1]. * **siRNA vs. miRNA:** While both inhibit gene expression, siRNAs are typically exogenous (synthetic) and require perfect base-pairing, whereas miRNAs are endogenous and can function with imperfect pairing. * **Dicer Enzyme:** The ribonuclease that processes pre-miRNA into mature miRNA in the cytoplasm [3]. **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. 230-231. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 16-17. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 17-18.

Question 862: Duchenne muscular dystrophy is inherited as which of the following patterns?

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

Explanation: **Explanation:** **Duchenne Muscular Dystrophy (DMD)** is a severe, progressive neuromuscular disorder caused by a mutation in the **DMD gene** located on the short arm of the **X chromosome (Xp21)**. 1. **Why X-linked Recessive is correct:** The DMD gene is the largest known human gene. Because it is located on the X chromosome, the disease primarily affects males (XY), who have only one copy of the X chromosome [1]. Females (XX) are typically asymptomatic carriers unless they have skewed X-inactivation. The mutation leads to a complete absence of **dystrophin**, a protein essential for maintaining the structural integrity of the muscle cell membrane (sarcolemma) by linking the cytoskeleton to the extracellular matrix [2]. 2. **Why other options are incorrect:** * **Autosomal Recessive/Dominant:** These would imply the gene is located on non-sex chromosomes (1-22). While some Limb-Girdle Muscular Dystrophies follow these patterns, DMD is strictly sex-linked. * **X-linked Dominant:** In this pattern, both males and females would be equally and severely affected in every generation. In DMD, females are generally protected by their second healthy X chromosome. **High-Yield Clinical Pearls for NEET-PG:** * **Gower’s Sign:** Use of hands to "climb up" the legs to stand, due to proximal muscle weakness. * **Pseudohypertrophy:** The calves appear large but are actually composed of fibrofatty tissue, not muscle. * **Becker Muscular Dystrophy (BMD):** Also X-linked recessive, but involves *truncated* (functional) dystrophin, leading to a milder clinical course [2]. * **Diagnosis:** Elevated Serum Creatine Kinase (CK) levels are seen from birth; Muscle biopsy shows variation in fiber size and replacement by fat/fibrosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, p. 151. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1244-1245.

Question 863: Mikulicz's disease is classified as which of the following?

A. An inflammatory disease
B. A neoplastic disease
C. An autoimmune disease (Correct Answer)
D. A viral infection

Explanation: **Explanation:** **Mikulicz’s disease** is a chronic condition characterized by the symmetrical enlargement of the lacrimal and salivary glands. It is now recognized as a part of the spectrum of **IgG4-related diseases (IgG4-RD)**. 1. **Why the correct answer is right (C):** Mikulicz’s disease is classified as an **autoimmune disease** because it involves an immune-mediated fibro-inflammatory process. Histologically, it is characterized by dense lymphoplasmacytic infiltration (predominantly IgG4+ plasma cells) and "storiform" fibrosis [1]. It was historically confused with Sjögren’s syndrome, but it is distinct as it lacks the typical anti-SSA/SSB antibodies and shows a dramatic response to glucocorticoids [1]. 2. **Why the incorrect options are wrong:** * **A (Inflammatory):** While inflammation is present, "inflammatory disease" is a broad category. In the context of NEET-PG, the specific underlying mechanism is autoimmune/IgG4-related. * **B (Neoplastic):** Although the glandular swelling may mimic a tumor (pseudotumor), it is a benign reactive process, not a malignancy. * **D (Viral):** There is no evidence of a viral etiology (like Mumps or HIV) causing the specific histopathological features of Mikulicz’s disease. **High-Yield Clinical Pearls for NEET-PG:** * **IgG4-Related Disease:** Mikulicz’s disease is the prototype. Other manifestations include Riedel’s thyroiditis, Autoimmune Pancreatitis (Type 1), and Retroperitoneal fibrosis. * **Triad of Mikulicz:** Symmetrical involvement of lacrimal, parotid, and submandibular glands. * **Key Histology:** "Storiform" (cartwheel-like) fibrosis and obliterative phlebitis. * **Mikulicz Syndrome vs. Disease:** *Disease* is primary/idiopathic (IgG4-RD); *Syndrome* refers to glandular enlargement secondary to other diseases like Sarcoidosis, Leukemia, or Lymphoma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 235-236.

Question 864: What is the most specific immunohistochemical marker to rule out invasive ductal carcinoma?

A. Ki-67
B. p63 (Correct Answer)
C. Desmin
D. HER2/neu

Explanation: **Explanation:** The fundamental histological distinction between **in situ** carcinoma (like DCIS) and **invasive ductal carcinoma (IDC)** of the breast is the presence or absence of a **myoepithelial cell layer**. In invasive carcinoma, the tumor cells breach the basement membrane [2], [3] and the protective myoepithelial layer is lost. **Why p63 is the correct answer:** p63 is a nuclear immunohistochemical marker that specifically stains **myoepithelial cells**. In a normal breast duct or in DCIS, p63 will show continuous or focal nuclear staining around the epithelial clusters. In **invasive ductal carcinoma**, the myoepithelial layer is entirely absent. Therefore, a positive p63 stain outlining a nest of cells effectively **rules out** invasion at that site. **Analysis of Incorrect Options:** * **Ki-67 (Option A):** This is a proliferation marker used to assess the growth fraction of a tumor. While it helps in grading and molecular subtyping (Luminal A vs. B), it cannot distinguish between in situ and invasive lesions. * **Desmin (Option B):** This is a marker for muscle differentiation (smooth and skeletal). While it may stain stromal myofibroblasts, it is not a specific marker for the myoepithelial layer in breast pathology. * **HER2/neu (Option D):** This is a growth factor receptor used to determine prognosis and eligibility for targeted therapy (Trastuzumab). It is expressed on the membrane of the malignant epithelial cells themselves [1], not the myoepithelial layer. **NEET-PG High-Yield Pearls:** * **Other Myoepithelial Markers:** Apart from p63 (nuclear), other markers include **SMA** (Smooth Muscle Actin), **Calponin**, and **SMMHC** (Smooth Muscle Myosin Heavy Chain). * **p63** is considered highly specific because, unlike SMA, it does not cross-react with stromal fibroblasts or vascular smooth muscle. * **E-cadherin** is the marker used to differentiate between **Ductal** (Positive) and **Lobular** (Negative/Loss of expression) carcinoma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1061-1062. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1060-1061. [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. 209-210.

Question 865: Steroid hormones exert their effects by binding to which of the following?

A. Cell surface receptors
B. G proteins
C. Transcription factors (Correct Answer)
D. Cyclic adenosine monophosphate (AMP)

Explanation: **Explanation:** **Mechanism of Action:** Steroid hormones (e.g., estrogen, progesterone, cortisol, aldosterone) are **lipophilic** (lipid-soluble) molecules derived from cholesterol. Due to their chemical nature, they easily diffuse across the lipid bilayer of the plasma membrane. Once inside the cell, they bind to specific **intracellular receptors** located in the cytoplasm or nucleus [1]. The hormone-receptor complex then translocates to the nucleus (if not already there) and binds directly to specific DNA sequences called Hormone Response Elements (HREs). In this capacity, the hormone-receptor complex acts as a **ligand-activated transcription factor**, modulating the transcription of specific genes into mRNA, which ultimately leads to new protein synthesis. **Analysis of Incorrect Options:** * **A. Cell surface receptors:** These are used by hydrophilic (water-soluble) hormones like peptide hormones (e.g., Insulin, Glucagon) and catecholamines, which cannot cross the cell membrane. * **B. G proteins:** These are membrane-associated proteins that act as molecular switches for G-protein coupled receptors (GPCRs). They trigger secondary messenger cascades rather than direct gene transcription. * **C. Cyclic AMP:** This is a **second messenger** used by many peptide hormones (e.g., ACTH, ADH via V2 receptors). Steroid hormones do not require second messengers as they act directly on the genome. **High-Yield Clinical Pearls for NEET-PG:** * **Speed of Action:** Because steroid hormones require gene transcription and protein synthesis, their effects have a **slow onset** (hours to days) but are **long-lasting**. * **Exceptions:** While most steroids bind in the cytoplasm, **Thyroid hormones (T3/T4)**—though not steroids—also use this mechanism but bind to receptors already fixed on the chromatin in the nucleus. * **Vitamin D and Retinoic Acid** also belong to this superfamily of nuclear receptors [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Central Nervous System Synapse, pp. 446-447.

Question 866: A stellate granuloma is seen in which condition?

A. Crohn's disease
B. Hodgkin's disease
C. Cat scratch disease (Correct Answer)
D. Berylliosis

Explanation: ### Explanation **Correct Answer: C. Cat scratch disease** **Reasoning:** A **stellate granuloma** is a specialized form of granulomatous inflammation characterized by a central area of necrotic debris (often containing neutrophils/microabscesses) surrounded by palisading epithelioid histiocytes and fibroblasts. This "star-shaped" (stellate) appearance is a hallmark of **Cat Scratch Disease**, caused by *Bartonella henselae*. In the lymph nodes, these lesions progress from lymphoid hyperplasia to the formation of these characteristic suppurative granulomas. **Analysis of Incorrect Options:** * **A. Crohn’s Disease:** Characterized by **non-caseating granulomas** (found in about 40-60% of cases) throughout the transmural layers of the bowel wall [1]. They are not stellate. * **B. Hodgkin’s Disease:** While granulomas can occasionally be seen in the stroma of Hodgkin lymphoma (especially the Mixed Cellularity subtype), the diagnostic feature is the **Reed-Sternberg (RS) cell**. * **C. Berylliosis:** This occupational lung disease presents with **non-caseating granulomas** that are histologically indistinguishable from Sarcoidosis (often containing Schaumann and Asteroid bodies) [2]. **NEET-PG High-Yield Pearls:** * **Differential Diagnosis for Stellate Granulomas:** 1. Cat Scratch Disease (Most common) 2. Lymphogranuloma Venereum (LGV) 3. Tularemia 4. Fungal infections (e.g., Sporotrichosis) * **Cat Scratch Disease Key Fact:** It typically presents as painful regional lymphadenopathy (usually axillary or cervical) following a cat scratch or bite. * **Warthin-Starry Stain:** This silver stain is used to visualize the causative organism, *Bartonella henselae*. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 365-366. [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. 198-200.

Question 867: Which of the following is an opsonin?

A. C3a
B. C3b (Correct Answer)
C. C4a
D. C5a

Explanation: **Explanation:** **Opsonization** is the process by which specific molecules (opsonins) coat a pathogen, marking it for recognition and destruction by phagocytes (neutrophils and macrophages) [1]. Phagocytes possess specific receptors for these opsonins, which facilitates firm attachment and subsequent engulfment [1]. **Why C3b is the correct answer:** **C3b** is the most potent and primary opsonin of the complement system [2]. When the complement cascade is activated (via classical, alternative, or lectin pathways), C3 is cleaved into C3a and C3b [3]. C3b binds covalently to the surface of microbes [3]. Phagocytes express **CR1 (Complement Receptor 1)**, which binds to C3b, significantly enhancing the efficiency of phagocytosis [1], [4]. **Analysis of Incorrect Options:** * **C3a, C4a, and C5a:** These are collectively known as **Anaphylatoxins** [3]. They do not act as opsonins. Instead, they trigger mast cell degranulation (releasing histamine), increase vascular permeability, and induce vasodilation [3]. * **C5a** is also a potent **chemotactic agent**, responsible for recruiting neutrophils to the site of inflammation [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Major Opsonins:** The two most important opsonins in the body are **C3b** (complement) and **IgG** (specifically the Fc portion of IgG) [1]. * **Other Opsonins:** Collectins, Fibronectin, and C-reactive protein (CRP) can also act as minor opsonins. * **iC3b:** An inactive form of C3b that also functions as an opsonin. * **Deficiency:** Patients with C3 deficiency are highly susceptible to recurrent infections with pyogenic bacteria due to impaired opsonization. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 89-91. [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. 162-163. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 99-100. [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. 163-164.

Question 868: Which of the following genetic aberrations is not a causative mechanism in cases of Prader-Willi syndrome?

A. Gene deletions
B. Defective genomic imprinting
C. Single nucleotide polymorphisms (SNPs) (Correct Answer)
D. Uniparental disomy

Explanation: Prader-Willi Syndrome (PWS) is a classic example of **genomic imprinting**, where the expression of a gene depends on whether it is inherited from the mother or the father [1]. PWS occurs due to the **loss of function of the paternal allele** on the long arm of chromosome 15 (15q11-q13) [1]. **Why Option C is correct:** **Single Nucleotide Polymorphisms (SNPs)** are variations at a single base pair level that occur commonly throughout the genome. While they contribute to genetic diversity and disease susceptibility, they are **not** a recognized causative mechanism for PWS. PWS is caused by large-scale structural or epigenetic changes, not single-base substitutions. **Why the other options are incorrect:** * **Gene Deletions (Option A):** This is the most common cause (~65-75%). It involves a microdeletion of the paternal 15q11-q13 region [1]. * **Uniparental Disomy (Option D):** Occurs in ~20-30% of cases. The individual inherits two copies of chromosome 15 from the mother (maternal UPD) and none from the father, leading to a lack of active paternal genes [1]. * **Defective Genomic Imprinting (Option B):** Occurs in ~1-3% of cases. Here, the paternal chromosome is present but carries a maternal imprinting pattern (epigenetic defect), rendering the paternal genes inactive [1]. **High-Yield Clinical Pearls for NEET-PG:** * **PWS Phenotype:** Infantile hypotonia, hyperphagia (leading to morbid obesity), hypogonadism, small hands/feet, and mental retardation. * **Angelman Syndrome (The "Happy Puppet"):** The "sister" condition caused by the loss of the **maternal** allele on the same locus (15q11-q13) [2]. * **Diagnostic Gold Standard:** DNA Methylation analysis (detects all three mechanisms) [1]. * **Mnemonic:** **P**rader-Willi = **P**aternal deletion; **A**ngelman = **M**aternal deletion (**PAM**). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 182-183. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 181-182.

Question 869: Most commonly, in which organ are amyloid deposits seen?

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

Explanation: **Explanation:** **1. Why Kidney is the Correct Answer:** The **kidney** is the most common and clinically significant organ involved in systemic amyloidosis (both AL and AA types). Amyloid deposits typically occur in the glomeruli (mesangium and capillary walls), leading to basement membrane thickening and increased permeability [3]. This manifests clinically as **nephrotic syndrome** (massive proteinuria), which eventually progresses to chronic kidney disease. Renal failure is the leading cause of death in systemic amyloidosis. **2. Analysis of Incorrect Options:** * **Spleen:** While frequently involved, it is usually asymptomatic [3]. It presents in two patterns: *Sago spleen* (deposits in splenic follicles) and *Lardaceous spleen* (deposits in splenic sinuses/red pulp). * **Liver:** Often involved in systemic amyloidosis, leading to hepatomegaly [3]. Deposits occur first in the **Space of Disse** and then progress to compress hepatic cords, but liver failure is rare compared to renal failure [1]. * **Heart:** Primarily involved in AL amyloidosis and Senile Systemic Amyloidosis (Transthyretin) [3]. It leads to **restrictive cardiomyopathy** and arrhythmias, but it is less frequently involved than the kidney in overall systemic cases. **3. High-Yield Clinical Pearls for NEET-PG:** * **Staining:** Amyloid shows **Apple-green birefringence** under polarized light when stained with **Congo Red** [1]. * **Most common site for biopsy:** Rectal biopsy or Abdominal fat pad aspiration (less invasive). * **Most common organ involved:** Kidney [3]. * **Most common cause of death:** Renal failure (overall), though Cardiac amyloidosis has the worst prognosis. * **Physical Exam:** Look for "Macroglossia" (enlarged tongue), a characteristic sign of AL amyloidosis [2]. **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. 269-270. [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. 136-140.

Question 870: Loss of heterozygosity is associated with which of the following conditions?

A. Acute myeloid leukemia
B. Acute lymphoblastic leukemia
C. Retinoblastoma (Correct Answer)
D. Acute promyelocytic leukemia

Explanation: **Explanation:** **Loss of Heterozygosity (LOH)** is a critical genetic event in the development of cancer, particularly involving **Tumor Suppressor Genes (TSGs)**. According to **Knudson’s Two-Hit Hypothesis**, both alleles of a TSG must be inactivated to trigger oncogenesis [3]. In hereditary cases, an individual inherits one defective allele (germline mutation) but remains phenotypically normal because the second allele is functional (heterozygous state). LOH occurs when the remaining functional allele is lost through deletion, mitotic recombination, or gene conversion, leading to the expression of the disease [2]. **Why Retinoblastoma is correct:** Retinoblastoma is the classic model for LOH [1]. It involves the **RB1 gene** on chromosome **13q14**. In the familial form, the first "hit" is inherited, and the second "hit" (LOH) occurs somatically in the retinal cells [1]. This results in the loss of the "brake" on the cell cycle (E2F inhibition), leading to uncontrolled proliferation [4]. **Why other options are incorrect:** * **AML, ALL, and APL:** These are primarily driven by **gain-of-function mutations** in proto-oncogenes or **balanced chromosomal translocations** (e.g., t(15;17) in APL) that create fusion proteins (PML-RARA). While deletions can occur, LOH is not the hallmark mechanism for these leukemias as it is for Retinoblastoma. **High-Yield Clinical Pearls for NEET-PG:** * **RB1 Gene:** Located on **13q14**; it regulates the **G1-S checkpoint**. * **Two-Hit Hypothesis:** Applies to RB, APC (Familial Adenousand Polyposis), and VHL genes. * **Clinical Sign:** The most common presenting sign of Retinoblastoma is **Leukocoria** (white pupillary reflex). * **Secondary Tumors:** Patients with germline RB1 mutations have a high risk of developing **Osteosarcoma** later in life. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 300. [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. 227-228. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 298-300. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 300-301.

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