General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 791: Pyogenic infection and brain infarction are associated with which type of necrosis?

A. Coagulative necrosis
B. Liquefaction necrosis (Correct Answer)
C. Caseous necrosis
D. Fat necrosis

Explanation: **Explanation:** **Liquefactive necrosis** is the correct answer because it is characterized by the transformation of the tissue into a liquid, viscous mass. This occurs due to the complete digestion of dead cells by hydrolytic enzymes. 1. **Why it is correct:** * **Pyogenic Infections:** In bacterial or fungal infections, inflammatory cells (specifically neutrophils) release potent lysosomal enzymes that digest the tissue, resulting in the formation of pus [2]. * **Brain Infarction:** Unlike other solid organs, the brain lacks a strong connective tissue framework and is rich in lipids and lysosomal enzymes. Ischemic injury in the CNS triggers rapid enzymatic digestion, leading to liquefaction rather than structural preservation [1]. 2. **Why other options are incorrect:** * **Coagulative Necrosis:** This is the most common pattern in most solid organs (heart, kidney, spleen) following ischemia. The tissue architecture is preserved for a few days because proteins and enzymes are denatured simultaneously. * **Caseous Necrosis:** Characteristic of Tuberculosis. It presents as a "cheese-like" friable white appearance, combining features of both coagulative and liquefactive necrosis within a granuloma. * **Fat Necrosis:** Seen in acute pancreatitis (enzymatic) or breast trauma (non-enzymatic), where activated lipases release fatty acids that combine with calcium (saponification). **High-Yield Clinical Pearls for NEET-PG:** * **Exception Rule:** Ischemia in all solid organs leads to coagulative necrosis **EXCEPT** the brain (Liquefactive) [1]. * **Wet Gangrene:** This is essentially coagulative necrosis with a superimposed liquefactive action of bacteria. * **Microscopic Hallmark:** In liquefactive necrosis, the tissue shows a complete loss of cellular outlines and architecture, replaced by cellular debris and inflammatory exudate [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1268-1269. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 192-193.

Question 792: Apoptosis is:

A. Single cell programmed cell death (Correct Answer)
B. Intracytoplasmic accumulation of toxic substances
C. A type of degenerative cellular change
D. Neoplastic change in the cell

Explanation: **Explanation:** **Apoptosis** is defined as a pathway of cell death that is induced by a tightly regulated intracellular program [1]. It is often referred to as **"programmed cell death"** because the cell activates enzymes (caspases) that degrade its own nuclear DNA and cytoplasmic proteins [1]. 1. **Why Option A is correct:** Unlike necrosis, which involves large groups of cells and an inflammatory response, apoptosis typically involves **single cells** or small clusters [1]. The cell membrane remains intact, but the cell shrinks and breaks into "apoptotic bodies," which are then phagocytosed without triggering inflammation [1]. 2. **Why the other options are incorrect:** * **Option B:** Intracytoplasmic accumulation (e.g., fatty change, amyloid, or glycogen) refers to intracellular accumulations, which are signs of metabolic derangement or reversible injury, not a programmed death pathway. * **Option C:** Degenerative changes (like hydropic swelling) are usually reversible stages of cell injury. While apoptosis is a form of cell death, it is a distinct, active molecular process rather than a passive "degeneration." * **Option D:** Neoplasia refers to uncontrolled, autonomous cell proliferation (cancer). In fact, a *failure* or inhibition of apoptosis is a hallmark of neoplastic transformation [3]. **High-Yield NEET-PG Pearls:** * **Morphological Hallmark:** Chromatin condensation (pyknosis) is the most characteristic feature [1]. * **Key Enzymes:** **Caspases** (Cysteine aspartate-specific proteases) [1]. * *Initiator caspases:* 8, 9, 10 [1]. * *Executioner caspases:* 3, 6, 7 [1]. * **Mitochondrial (Intrinsic) Pathway:** Regulated by the **Bcl-2 family** [2]. Pro-apoptotic (Bax, Bak) vs. Anti-apoptotic (Bcl-2, Bcl-xL) [2]. * **DNA Pattern:** Characterized by **internucleosomal cleavage** of DNA, which appears as a "step-ladder pattern" on gel electrophoresis [1]. **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. 63-64. [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. 64-65. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 310.

Question 793: Which of the following is an X-linked recessive disorder?

A. Marfan Syndrome
B. Phenylketonuria
C. Neurofibromatosis
D. Duchenne muscular dystrophy (Correct Answer)

Explanation: **Explanation:** **Duchenne Muscular Dystrophy (DMD)** is the correct answer because it is a classic example of an **X-linked recessive (XLR)** disorder [2]. It is caused by a mutation in the *DMD* gene located on the X chromosome (Xp21), which encodes the protein **dystrophin** [1]. Since males have only one X chromosome, a single mutated copy leads to the disease, whereas females are typically asymptomatic carriers [2]. **Analysis of Incorrect Options:** * **Marfan Syndrome:** This is an **Autosomal Dominant (AD)** disorder caused by a mutation in the *FBN1* gene on chromosome 15, leading to defective fibrillin-1. * **Phenylketonuria (PKU):** This is an **Autosomal Recessive (AR)** metabolic disorder caused by a deficiency of the enzyme phenylalanine hydroxylase [3]. * **Neurofibromatosis (Type 1 and 2):** Both types are **Autosomal Dominant (AD)**. NF1 involves the *NF1* gene on chromosome 17, and NF2 involves the *merlin* gene on chromosome 22. **NEET-PG High-Yield Pearls:** * **DMD Clinical Signs:** Look for **Gower’s sign** (using hands to "climb up" the legs to stand) and **pseudohypertrophy of calves** (fatty replacement of muscle) [1]. * **Diagnosis:** The gold standard is genetic testing; however, **Creatine Kinase (CK)** levels are massively elevated from birth. * **Mnemonic for XLR Disorders:** "**O**bliged **F**amily **H**istory **M**akes **G**enerations **K**now **C**ertain **D**iseases" (**O**cular albinism, **F**abry, **H**emophilia, **M**enkes, **G**6PD, **K**unter-Hunter, **C**hronic Granulomatous Disease, **D**uchenne/Becker MD). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1244-1245. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, p. 151. [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.

Question 794: Which of the following is a pro-inflammatory cytokine?

A. IL-1 (Correct Answer)
B. IL-10
C. IL-4
D. IL-13

Explanation: ### Explanation **Correct Option: A (IL-1)** Interleukin-1 (IL-1) is a classic **pro-inflammatory cytokine** primarily produced by activated macrophages [3]. It plays a central role in the acute inflammatory response by inducing the expression of adhesion molecules on endothelial cells, stimulating the production of other cytokines (like IL-6), and acting as an endogenous pyrogen to induce **fever** via the hypothalamus [1]. Along with TNF-̑, IL-1 is responsible for the systemic effects of inflammation (Acute Phase Response) [1]. **Analysis of Incorrect Options:** * **B. IL-10:** This is a potent **anti-inflammatory cytokine**. It inhibits the synthesis of pro-inflammatory cytokines (TNF, IL-12) and reduces the expression of MHC Class II molecules on macrophages, thereby "turning off" the immune response. * **C. IL-4:** This cytokine is primarily involved in the **Th2 response**. It promotes B-cell differentiation into IgE-producing plasma cells and is a key mediator of alternative macrophage activation (M2), which is involved in tissue repair rather than acute inflammation [3]. * **D. IL-13:** Similar to IL-4, IL-13 is an anti-inflammatory/regulatory cytokine that promotes the **M2 macrophage phenotype** and plays a role in allergic inflammation and fibrosis, rather than the initiation of the acute pro-inflammatory cascade [3]. **NEET-PG High-Yield Pearls:** * **Major Pro-inflammatory Cytokines:** TNF-̑, IL-1, IL-6, and Chemokines (e.g., IL-8) [2]. * **Major Anti-inflammatory Cytokines:** IL-10 and TGF-̒ (The "Peacekeepers"). * **Endogenous Pyrogens:** IL-1 and TNF-̑ (increase prostaglandin synthesis in the hypothalamus) [1]. * **Acute Phase Reactants:** IL-6 is the primary stimulator for the liver to produce CRP and Fibrinogen [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 111. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 97-99. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 105-106.

Question 795: Which of the following is a disorder associated with the calcium channel ryanodine receptor?

A. Malignant hyperthermia (Correct Answer)
B. Duchene Muscular Dystrophy
C. Tibial muscular dystrophy
D. Limb girdle muscle dystrophy

Explanation: **Explanation:** **Malignant Hyperthermia (MH)** is the correct answer because it is directly caused by mutations in the **RYR1 gene**, which encodes the **Ryanodine Receptor**. This receptor is a calcium release channel located on the sarcoplasmic reticulum of skeletal muscle. In genetically susceptible individuals, exposure to volatile anesthetics (e.g., halothane) or depolarizing muscle relaxants (e.g., succinylcholine) triggers the uncontrolled release of calcium. This leads to sustained muscle contraction, hypermetabolism, excessive heat production (hyperthermia), and rhabdomyolysis. **Analysis of Incorrect Options:** * **Duchenne Muscular Dystrophy (B):** Caused by a mutation in the *DMD* gene leading to a complete absence of **dystrophin**, a protein that links the cytoskeleton to the extracellular matrix [1]. * **Tibial Muscular Dystrophy (C):** Associated with mutations in the **titin** gene (*TTN*), which affects the structural integrity of the sarcomere. * **Limb Girdle Muscular Dystrophy (D):** A heterogeneous group of disorders most commonly caused by mutations in **sarcoglycans** or **dysferlin**, rather than calcium channels [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Malignant Hyperthermia is typically **Autosomal Dominant**. * **Antidote:** The drug of choice for treatment is **Dantrolene**, which acts by binding to the RYR1 receptor and inhibiting calcium release. * **Associated Condition:** Mutations in the RYR1 receptor are also the most common cause of **Central Core Disease**, a congenital myopathy. * **Early Sign:** The earliest clinical sign of MH is often an increase in **end-tidal CO2** (ETCO2) and masseter muscle rigidity. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1244-1245. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, p. 1244.

Question 796: An infarct is most frequently characterized by what type of necrosis?

A. Fatty
B. Caseous
C. Gangrenous
D. Coagulative (Correct Answer)

Explanation: **Explanation:** **Coagulative necrosis** is the hallmark of cell death caused by ischemia (hypoxia) in all solid organs of the body, except the brain [1]. When an **infarct** occurs, the sudden loss of blood supply leads to the denaturation of structural proteins and enzymes [1]. This process blocks proteolysis, allowing the dead cells to maintain their basic tissue architecture and "tombstone" outline for several days until leukocytes arrive to digest the debris. **Analysis of Incorrect Options:** * **Fatty Necrosis:** This is specific to areas of fat destruction, typically seen in acute pancreatitis (enzymatic) or breast trauma (non-enzymatic) [2]. It is characterized by "saponification" (calcium soap formation) [2]. * **Caseous Necrosis:** This "cheese-like" necrosis is characteristic of granulomatous inflammation, most notably **Tuberculosis** [2]. The tissue architecture is completely obliterated, unlike in coagulative necrosis. * **Gangrenous Necrosis:** This is not a distinct pattern of cell death but a clinical term. It usually refers to coagulative necrosis of a limb (dry gangrene) or coagulative necrosis modified by bacterial liquefaction (wet gangrene). **High-Yield Clinical Pearls for NEET-PG:** * **The Exception:** Ischemic cell death in the **Central Nervous System (Brain)** results in **Liquefactive necrosis**, not coagulative, due to the high lipid content and lack of supportive stroma. * **Microscopic Appearance:** In coagulative necrosis, cells become acidophilic (increased eosinophilia/pinkness) and lose their nuclei (pyknosis, karyorrhexis, and karyolysis) [3]. * **Heart:** Myocardial infarction is the most common clinical example of coagulative necrosis [3]. **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. 53-55. [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, p. 55. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 552.

Question 797: Fibrinoid necrosis is seen in all the following except?

A. Malignant hypertension
B. Acute rheumatic fever
C. Polyarteritis (Correct Answer)
D. Polyarteritis nodosa

Explanation: **Explanation:** **Fibrinoid necrosis** is a specialized form of cell death characterized by the deposition of immune complexes and plasma proteins (like fibrin) into the walls of blood vessels. On H&E staining, it appears as a bright pink, circumferential, "smudged" area. **1. Why "Polyarteritis" is the correct answer:** The term **"Polyarteritis"** is a vague, non-specific term. In medical pathology, the specific condition associated with fibrinoid necrosis is **Polyarteritis Nodosa (PAN)** [1]. While it may seem like a semantic nuance, NEET-PG often tests precision in nomenclature. In the context of this question, "Polyarteritis" serves as the distractor because it does not represent a specific clinical entity compared to the established pathological processes listed in the other options. **2. Analysis of Incorrect Options:** * **Malignant Hypertension:** Extreme elevation in blood pressure causes mechanical stress that forces plasma proteins into the vessel wall, leading to classic fibrinoid necrosis of the arterioles (hyperplastic arteriolosclerosis). * **Acute Rheumatic Fever:** This condition features fibrinoid necrosis within the **Aschoff bodies** (specifically in the collagenous stroma of the heart). * **Polyarteritis Nodosa (PAN):** This is the prototypical systemic necrotizing vasculitis [3]. It involves transmural fibrinoid necrosis of medium and small-sized arteries [1]. **3. Clinical Pearls for NEET-PG:** * **Key Association:** Fibrinoid necrosis is primarily seen in **Type III Hypersensitivity** reactions (Immune-complex mediated). * **Common Sites:** PAN (vessels), Malignant HTN (vessels), Rheumatic nodules/Aschoff bodies (heart), and Rheumatoid arthritis (nodules) [2]. * **Visual Cue:** Look for the word **"Smudgy Eosinophilic"** appearance in clinical vignettes. * **Exception:** It is generally *not* seen in venous pathology; it is an arterial/stomal process. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 517-519. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 520-521. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 278-279.

Question 798: Striae of Retzius are prominent in which of the following zones of enamel caries?

A. Translucent zone.
B. Dark zone.
C. Body of the lesion. (Correct Answer)
D. Surface zone.

Explanation: **Explanation:** Enamel caries is a dynamic process characterized by subsurface demineralization [1]. When viewed under a polarizing microscope using longitudinal sections, four distinct zones are identified based on the degree of mineral loss (porosity). **Why "Body of the Lesion" is correct:** The **Body of the lesion** is the largest portion of incipient enamel caries, located between the dark zone and the surface zone. It represents the area of maximum demineralization (pore volume of 5% to 25%). Due to this significant loss of mineral content, the underlying histological structures, specifically the **Striae of Retzius** (incremental growth lines of enamel), become exceptionally prominent and clearly observable. **Analysis of Incorrect Options:** * **Translucent Zone:** This is the advancing front of the lesion. It is the first observable change with only 1% porosity. The Striae of Retzius are not yet enhanced here. * **Dark Zone:** Located just superficial to the translucent zone, it has a porosity of 2-4%. While more demineralized than the translucent zone, it does not show the marked structural prominence seen in the body. * **Surface Zone:** This zone remains relatively intact and radio-opaque (porosity <1%) due to remineralization from fluoride and salivary ions. Because it is highly mineralized, internal structures like the Striae of Retzius are masked. **High-Yield NEET-PG Pearls:** * **Porosity Sequence:** Translucent (1%) → Dark (2-4%) → Body (5-25%) → Surface (<1%). * **The Dark Zone** is considered a "zone of repair" or remineralization. * **Striae of Retzius** are analogous to the rings in a tree trunk, representing the incremental pattern of enamel formation. * In the **Body of the lesion**, the striae appear enhanced due to the preferential dissolution of the mineral phase along these incremental lines. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 734-735.

Question 799: In a chronic smoker, bronchi showed stratified squamous cells with underlying glands. What type of change is this?

A. Metaplasia (Correct Answer)
B. Anaplasia
C. Dysplasia
D. Neoplasia

Explanation: **Explanation:** The correct answer is **Metaplasia** [1]. **Why Metaplasia is correct:** Metaplasia is a reversible change in which one differentiated cell type (epithelial or mesenchymal) is replaced by another differentiated cell type [1]. In chronic smokers, the normal **ciliated columnar epithelium** of the bronchi is replaced by **stratified squamous epithelium** [3]. This occurs because squamous cells are more rugged and better able to survive the chronic irritation and chemical stress caused by cigarette smoke [1]. However, this protective mechanism comes at a cost: the loss of mucus secretion and ciliary action, which are vital for respiratory defense [1]. **Why other options are incorrect:** * **Anaplasia:** Refers to a lack of differentiation. It is a hallmark of malignancy where cells lose their structural and functional characteristics, appearing primitive or "embryonic." * **Dysplasia:** Characterized by disordered growth and maturation of an epithelium [2]. While metaplasia can progress to dysplasia if the stimulus persists, the description of organized stratified squamous cells indicates a completed metaplastic transition [2]. * **Neoplasia:** Refers to "new growth" (a tumor) that is autonomous and persists even after the stimulus is removed. **High-Yield Clinical Pearls for NEET-PG:** * **Most common type:** Squamous metaplasia (as seen in the bronchus, cervix, and bladder) [3]. * **Barrett’s Esophagus:** A classic example of **columnar metaplasia**, where squamous epithelium changes to columnar (intestinal) epithelium due to acid reflux [4]. * **Reversibility:** Metaplasia is reversible if the irritant (e.g., smoking) is removed. * **Mechanism:** It does not result from a change in the phenotype of an already differentiated cell; rather, it is a **reprogramming of tissue stem cells**. * **Vitamin A deficiency:** Can induce squamous metaplasia in the respiratory tract and eyes (Xerophthalmia). **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. 49. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 723. [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. 91-92. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 348-349.

Question 800: Fine-needle aspiration cytology (FNAC) is contraindicated in which of the following conditions?

A. Disseminated malignancy
B. Bleeding disorders (Correct Answer)
C. Lymph node malignancy
D. Liver disorders

Explanation: **Explanation:** **Why Bleeding Disorders is the Correct Answer:** Fine-needle aspiration cytology (FNAC) is a minimally invasive procedure, but it still involves the mechanical trauma of a needle passing through vascular tissues. In patients with **bleeding disorders** (e.g., hemophilia, severe thrombocytopenia, or those on anticoagulants), the primary risk is the inability to achieve hemostasis at the puncture site [1]. This can lead to significant complications such as uncontrolled local hemorrhage, hematoma formation, or internal bleeding if a deep organ is sampled [2]. Therefore, a deranged coagulation profile is a relative or absolute contraindication depending on the site and urgency. **Analysis of Incorrect Options:** * **A & C (Disseminated/Lymph Node Malignancy):** FNAC is actually a **primary diagnostic tool** for these conditions. It is used to confirm metastasis in disseminated disease and to differentiate between reactive hyperplasia, lymphoma, or metastatic carcinoma in lymph nodes. * **D (Liver Disorders):** General liver disorders (like hepatitis or fatty liver) are not contraindications. However, if the liver disorder results in **coagulopathy** (low prothrombin levels), it is the bleeding risk, not the liver disease itself, that poses the contraindication [1]. **High-Yield Facts for NEET-PG:** * **Absolute Contraindication:** Lack of patient cooperation and uncorrectable bleeding diathesis. * **Specific Site Contraindications:** FNAC is generally avoided in **Phaeochromocytoma** (risk of hypertensive crisis) and **Hydatid cyst** (risk of anaphylactic shock due to fluid leakage). * **Complications:** The most common complication of FNAC is a local hematoma [1]. * **Needle Gauge:** Typically, 22–25 gauge needles are used for FNAC to minimize trauma. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 621-622. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 624-625.

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Genetic Disorders

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