General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 281: The increase in size of individual cells is referred to as:

A. Hypertrophy (Correct Answer)
B. Hyperplasia
C. Hypodontia
D. Differentiation

Explanation: **Explanation:** **Correct Answer: A. Hypertrophy** Hypertrophy is defined as an **increase in the size of cells** [1], which consequently leads to an increase in the size of the organ [2]. This occurs due to the increased synthesis of structural proteins and organelles within the cell [2]. It is the primary adaptive response in cells that have a limited capacity to divide (permanent cells), such as cardiac and skeletal muscle. **Analysis of Incorrect Options:** * **B. Hyperplasia:** This refers to an increase in the **number of cells** in an organ or tissue [1]. While hyperplasia and hypertrophy often occur together (e.g., the pregnant uterus), they are distinct cellular processes [2]. * **C. Hypodontia:** This is a clinical term referring to a developmental condition where one or more teeth are congenitally missing. It is unrelated to cellular adaptation. * **D. Differentiation:** This is the process by which a cell becomes specialized in structure and function (e.g., a stem cell becoming a mature erythrocyte). **High-Yield Clinical Pearls for NEET-PG:** 1. **Pure Hypertrophy:** Occurs in **Permanent Cells** (Cardiac muscle). For example, Left Ventricular Hypertrophy (LVH) due to hypertension. 2. **Physiological Hypertrophy:** Examples include the enlargement of skeletal muscle in bodybuilders or the massive growth of the uterus during pregnancy [2]. 3. **Mechanism:** Triggered by mechanical sensors (stretch), growth factors (IGF-1), and vasoactive agents (α-adrenergic agonists, Endothelin-1) [2]. 4. **Key Distinction:** Hypertrophy = Size; Hyperplasia = Number [1]. If the question mentions "increase in organ size due to cell proliferation," the answer is Hyperplasia. **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. 45-46.

Question 282: What is the most important change that occurs in irreversible cell injury?

A. Decreased basophilia
B. Pyknosis
C. Accumulation of myelin figures
D. Membrane damage (Correct Answer)

Explanation: ### Explanation The transition from reversible to irreversible cell injury is defined by two critical phenomena: the inability to reverse mitochondrial dysfunction and **profound disturbances in membrane function** [1]. **1. Why Membrane Damage is the Correct Answer:** Membrane damage is considered the "point of no return." Damage to various membranes leads to fatal consequences [1]: * **Plasma membrane damage:** Leads to the loss of osmotic balance and the leakage of vital cellular contents and enzymes into the extracellular space [1]. * **Lysosomal membrane damage:** Results in the leakage of acid hydrolases (RNases, DNases, proteases) into the cytoplasm, leading to enzymatic digestion of the cell (autolysis) [1]. * **Mitochondrial membrane damage:** Results in the opening of the mitochondrial permeability transition pore, leading to the failure of ATP generation and the release of pro-apoptotic proteins [1]. **2. Analysis of Incorrect Options:** * **A. Decreased basophilia:** This is a feature of necrosis (due to loss of RNA) but is a secondary descriptive change rather than the primary mechanism of irreversibility. * **B. Pyknosis:** This refers to nuclear shrinkage and increased basophilia. While it is a hallmark of irreversible injury, nuclear changes occur *after* significant membrane and biochemical damage has already taken place. * **C. Accumulation of myelin figures:** These are whorled phospholipid masses derived from damaged cell membranes. They are seen in **both** reversible and irreversible injury, though they are more prominent in the latter [1]. **3. NEET-PG High-Yield Pearls:** * **Earliest change in reversible injury:** Generalized swelling of the cell and its organelles (Hydropic change) [1]. * **Hallmark of Irreversibility:** Severe mitochondrial swelling, large amorphous densities in the mitochondrial matrix, and extensive plasma membrane damage [1]. * **Clinical Correlation:** The leakage of intracellular enzymes across damaged membranes is the basis for blood tests used to detect tissue-specific injury (e.g., Troponins in MI, ALT/AST in hepatitis) [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. 49-62.

Question 283: What is the number of Barr bodies typically seen in the somatic cells of an individual with Klinefelter syndrome?

A. 0
B. 1 (Correct Answer)
C. 2
D. 3

Explanation: **Explanation:** The number of Barr bodies in a somatic cell is determined by the formula: **Number of Barr bodies = (Total number of X chromosomes) – 1.** This phenomenon is based on the **Lyon Hypothesis**, which states that in individuals with more than one X chromosome, all but one are randomly inactivated during early embryonic development to ensure dosage compensation [1]. 1. **Why Option B is Correct:** Individuals with **Klinefelter syndrome** typically have a **47, XXY** karyotype. Applying the formula (2 X chromosomes – 1), we find that one X chromosome remains active while the other undergoes condensation into heterochromatin, forming **one Barr body**. This is usually visible at the periphery of the nucleus or as a "drumstick" in polymorphonuclear leukocytes (neutrophils). 2. **Why Other Options are Incorrect:** * **Option A (0):** Seen in normal males (46, XY) or females with Turner syndrome (45, XO), as they possess only one X chromosome [1]. * **Option C (2):** Seen in individuals with a 48, XXXY karyotype or "Super-female" (47, XXX) syndrome. * **Option D (3):** Seen in rare cases of 49, XXXXY or 48, XXXX karyotypes. **High-Yield Clinical Pearls for NEET-PG:** * **Barr Body Identification:** Best visualized in the buccal smear (squamous epithelial cells) or as a **drumstick** in neutrophils. * **Klinefelter Syndrome Features:** Small firm testes, gynecomastia, infertility (azoospermia), increased stature (long legs), and elevated FSH/LH levels with low testosterone. * **Most Common Karyotype:** 47, XXY is the most frequent; however, mosaicism (e.g., 46, XY/47, XXY) can occur. * **Rule of Thumb:** The number of Barr bodies is always one less than the total number of X chromosomes, regardless of the presence of a Y chromosome. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 173-174.

Question 284: AE type of amyloid is seen in which of the following conditions?

A. Medullary carcinoma thyroid (Correct Answer)
B. Primary amyloidosis
C. Multiple myeloma
D. Familial amyloidosis

Explanation: **Explanation:** Amyloidosis is characterized by the extracellular deposition of misfolded proteins [2]. The classification of amyloid depends on the precursor protein involved. **Correct Answer: A. Medullary Carcinoma Thyroid** The **AE (Amyloid Endocrine)** type refers to amyloid derived from polypeptide hormones. In Medullary Carcinoma of the Thyroid (MCT), the tumor cells (parafollicular C-cells) secrete excessive **Calcitonin** [1]. This hormone undergoes misfolding and deposits within the tumor stroma as amyloid. On histology, this appears as an acellular, eosinophilic material that shows apple-green birefringence under polarized light with Congo red stain. **Analysis of Incorrect Options:** * **B & C. Primary Amyloidosis and Multiple Myeloma:** Both are associated with **AL (Amyloid Light chain)** type [3]. This is derived from immunoglobulin light chains (usually lambda) produced by neoplastic plasma cells [3]. * **D. Familial Amyloidosis:** This is most commonly associated with **ATTR (Amyloid Transthyretin)** type, specifically a mutated form of the transthyretin protein [3]. (Note: Familial Mediterranean Fever is associated with **AA** type). **High-Yield Clinical Pearls for NEET-PG:** * **AA Amyloid:** Seen in chronic inflammatory conditions (Rheumatoid Arthritis, Osteomyelitis, TB). Precursor: Serum Amyloid-Associated protein. * **Aβ2-microglobulin:** Seen in patients on long-term **hemodialysis**. * **Aβ Amyloid:** Found in the cerebral plaques of **Alzheimer’s disease**. * **Stain of choice:** Congo Red (produces apple-green birefringence). * **Gold standard for diagnosis:** Abdominal fat pad biopsy or rectal biopsy. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1102-1103. [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.

Question 285: Which of the following is NOT an action of bradykinin?

A. Vasodilation
B. Bronchodilation (Correct Answer)
C. Increased vascular permeability
D. Pain

Explanation: **Explanation:** Bradykinin is a potent inflammatory mediator belonging to the kinin system, derived from high-molecular-weight kininogen (HMWK) through the action of the enzyme kallikrein. **Why Bronchodilation is the Correct Answer:** Bradykinin is a potent **bronchoconstrictor**, not a bronchodilator [1]. It acts on the smooth muscles of the bronchial tree, leading to airway narrowing. This effect is particularly significant in patients with asthma or hyper-reactive airways. **Analysis of Incorrect Options:** * **Vasodilation (Option A):** Bradykinin is one of the most powerful endogenous vasodilators [1]. It stimulates the release of nitric oxide (NO) and prostacyclin from endothelial cells, leading to the relaxation of vascular smooth muscle and a decrease in blood pressure. * **Increased Vascular Permeability (Option B):** Similar to histamine, bradykinin causes contraction of endothelial cells in post-capillary venules, creating gaps that allow fluid and proteins to leak into the extravascular space (edema) [1]. * **Pain (Option D):** Bradykinin is a key mediator of the pain response [1]. It sensitizes nociceptors (pain receptors) and directly stimulates them, contributing to the "dolor" (pain) aspect of acute inflammation. **High-Yield Clinical Pearls for NEET-PG:** * **ACE Inhibitors Connection:** Angiotensin-Converting Enzyme (ACE) is responsible for the degradation of bradykinin. Therefore, ACE inhibitors lead to increased bradykinin levels, which is the underlying cause of the common side effects: **dry cough** and **angioedema**. * **C1 Esterase Inhibitor Deficiency:** This leads to Hereditary Angioedema due to the overproduction of bradykinin. * **Comparison:** While bradykinin causes vasodilation of systemic vessels, it causes **constriction** of non-vascular smooth muscle (bronchi and GI tract) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 100-101.

Question 286: Which of the following cells secretes histamine?

A. Eosinophil
B. Basophil (Correct Answer)
C. Neutrophil
D. Monocyte

Explanation: **Explanation:** **Basophils** (along with tissue mast cells) are the primary sources of **histamine** in the body [1]. Histamine is a vasoactive amine stored in the large, coarse, purple-black granules of basophils. Upon activation—typically via IgE cross-linking during Type I Hypersensitivity reactions—these cells undergo degranulation, releasing histamine to cause vasodilation and increased vascular permeability [1], [3]. **Analysis of Incorrect Options:** * **Eosinophils (A):** These cells are primarily involved in parasitic infections and allergic responses [2]. Instead of secreting histamine, they contain **Histaminase**, an enzyme that degrades histamine to help limit the inflammatory response. * **Neutrophils (C):** These are the "first responders" of acute inflammation. Their granules contain myeloperoxidase (MPO), lysozyme, and alkaline phosphatase, but they do not secrete histamine [2]. * **Monocytes (D):** These are mononuclear phagocytes that circulate in the blood. They secrete cytokines (like IL-1 and TNF) and transform into macrophages in tissues, but they are not a source of histamine [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Mast Cells vs. Basophils:** While both secrete histamine, mast cells reside in tissues (skin, GI tract), whereas basophils circulate in the blood [1]. * **Basophilia:** An increase in basophil count is a classic marker for **Myeloproliferative Disorders**, specifically **Chronic Myeloid Leukemia (CML)**. * **Histamine Receptors:** H1 receptors mediate allergic symptoms (bronchoconstriction, permeability), while H2 receptors stimulate gastric acid secretion. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 210-211. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 210. [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. 187-188.

Question 287: On sectioning of an organ at the time of autopsy, a focal, wedge-shaped firm area is seen accompanied by extensive hemorrhage, with a red appearance. The lesion has a base on the surface of the organ. What is the most likely diagnosis?

A. Lung with pulmonary thromboembolism (Correct Answer)
B. Heart with coronary thrombosis
C. Liver with hypovolemic shock
D. Kidney with septic embolus

Explanation: ### Explanation The clinical description provided—a **focal, wedge-shaped, firm, red (hemorrhagic) lesion** with its base on the organ surface—is the classic macroscopic appearance of a **Red Infarct** (Hemorrhagic Infarct) [1]. **1. Why Option A is Correct:** Red infarcts typically occur in organs with a **dual blood supply** or loose parenchyma [1]. The lung receives blood from both the pulmonary and bronchial arteries [2]. When a pulmonary artery branch is obstructed (e.g., by thromboembolism), the bronchial circulation continues to pump blood into the necrotic area. However, because the tissue is loose and the venous drainage is often compromised, blood extravasates into the alveolar spaces, giving the infarct its characteristic red, hemorrhagic appearance [1], [2]. The "wedge shape" reflects the territory supplied by the occluded branching vessel, with the apex pointing toward the occlusion and the base at the pleura [3]. **2. Why the Other Options are Incorrect:** * **B. Heart (Coronary Thrombosis):** The heart is a solid organ with end-arterial circulation. Infarcts here are typically **White Infarcts** (Anemic Infarcts) because there is no secondary blood supply to bleed into the necrotic zone [1]. * **C. Liver (Hypovolemic Shock):** Shock usually causes diffuse centrilobular necrosis (Nutmeg liver appearance) rather than a focal, wedge-shaped infarct. The liver is also resistant to infarction due to its dual supply (Portal vein and Hepatic artery). * **D. Kidney (Septic Embolus):** While a septic embolus can cause an infarct, renal infarcts are typically **White Infarcts** (solid organ, end-arterial supply) [1]. They appear pale and are often surrounded by a thin rim of hyperemia, but they are not primarily hemorrhagic. Underwood's notes the classic triangular (conical) shape of kidney infarcts [3]. **3. NEET-PG Clinical Pearls:** * **White Infarcts (Anemic):** Occur in solid organs with single/end-arterial supply (Heart, Spleen, Kidney) [1]. * **Red Infarcts (Hemorrhagic):** Occur in organs with dual blood supply (Lungs, Small Intestine), loose tissues, or following venous occlusion and reperfusion [1]. * **Morphology:** All infarcts (except the brain) undergo **Coagulative Necrosis**. Brain infarcts undergo **Liquefactive Necrosis** [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 140. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 137-138. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 148-149.

Question 288: A patient develops tachypnea, dyspnea, and tachycardia on day 3 following a femur fracture, progressing to delirium and coma. What is the most likely diagnosis?

A. Acute respiratory distress syndrome
B. Deep vein thrombosis
C. Fat embolism (Correct Answer)
D. Infarction

Explanation: **Explanation:** The clinical presentation of a **femur fracture** followed by a "latent period" of 24–72 hours (Day 3) and the triad of respiratory distress (tachypnea/dyspnea), neurological symptoms (delirium/coma), and a petechial rash (though not mentioned here, it is pathognomonic) is classic for **Fat Embolism Syndrome (FES)**. [1] **Why Fat Embolism is correct:** Following a long bone fracture, marrow fat or lipids are released into the ruptured marrow sinusoids. [1] These fat globules cause mechanical obstruction in the pulmonary and systemic microvasculature. Additionally, the release of free fatty acids causes direct biochemical injury to the endothelium, leading to the rapid onset of respiratory and neurological symptoms. **Why other options are incorrect:** * **Deep Vein Thrombosis (DVT):** While DVT can lead to pulmonary embolism, it typically presents later (usually after a week of immobilization) and primarily causes respiratory symptoms without the immediate neurological "delirium" seen in FES. [2] * **Acute Respiratory Distress Syndrome (ARDS):** While FES can progress to ARDS, ARDS is a clinical state of respiratory failure rather than the primary diagnosis in the context of a fresh fracture. * **Infarction:** This is a general term for tissue death due to lack of blood supply. While emboli cause infarction, it is not a specific diagnosis for this clinical scenario. **NEET-PG High-Yield Pearls:** * **Classic Triad:** 1. Respiratory distress, 2. Neurological symptoms, 3. Petechial rash (found in conjunctiva, axilla, and neck). * **Gurd’s Criteria:** Used for diagnosing FES. * **Pathology:** "Oil Red O" stain can be used to demonstrate fat globules in the lung or sputum. * **Timeline:** Symptoms typically appear **24–72 hours** post-injury. [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. 146-147. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 705.

Question 289: Minute 1 to 2mm hemorrhages are known as what?

A. Petechiae (Correct Answer)
B. Purpura
C. Ecchymosis
D. Bruises

Explanation: **Explanation:** The correct answer is **Petechiae**. This question tests the morphological classification of hemorrhages into skin and mucous membranes based on size and underlying etiology. **1. Why Petechiae is correct:** Petechiae are minute, pinpoint hemorrhages measuring **1 to 2 mm** in diameter [1]. They occur due to the rupture of capillaries or venules [2]. Pathophysiologically, they are most commonly associated with **platelet disorders** (thrombocytopenia or platelet dysfunction) [1], increased intravascular pressure, or clotting factor deficiencies. **2. Why the other options are incorrect:** * **Purpura (B):** These are slightly larger hemorrhages measuring **3 to 5 mm** [1]. They can be caused by the same factors as petechiae, but are also frequently seen in conditions involving vascular inflammation (vasculitis) or increased vascular fragility (e.g., Vitamin C deficiency) [3]. * **Ecchymosis (C):** These are larger subcutaneous hematomas, typically greater than **1 to 2 cm** (often referred to as "bruises"). They involve a larger area of tissue and undergo a characteristic color change (blue-red to blue-green to golden-yellow) as hemoglobin is degraded into bilirubin and hemosiderin. * **Bruises (D):** This is a lay term for ecchymosis, usually resulting from trauma. **High-Yield Clinical Pearls for NEET-PG:** * **Size Hierarchy:** Petechiae (<2mm) → Purpura (3-5mm) → Ecchymosis (>1-2cm). * **Palpability:** "Palpable purpura" is a classic sign of **Leukocytoclastic Vasculitis** (Henoch-Schönlein purpura). * **Vitamin C Deficiency (Scurvy):** Characterized by "perifollicular hemorrhages" (petechiae around hair follicles). * **Differentiation:** Unlike inflammatory erythema, these hemorrhagic spots **do not blanch** under pressure (diascopy test). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 132. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 620-621. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 664-665.

Question 290: On which chromosome is the ABO blood group gene located?

A. Chromosome 1
B. Chromosome 3
C. Chromosome 6
D. Chromosome 9 (Correct Answer)

Explanation: The ABO blood group system is determined by a single gene locus, the **ABO gene**, which is located on the **long arm of Chromosome 9 (9q34.2)**. [1] This gene encodes glycosyltransferases that catalyze the addition of specific sugar residues to the H substance (a precursor carbohydrate chain). * The **A allele** encodes N-acetylgalactosaminyltransferase. [1] * The **B allele** encodes galactosyltransferase. [1] * The **O allele** is a "null" allele resulting from a frameshift mutation, leading to an inactive enzyme and leaving the H substance unmodified. **Analysis of Incorrect Options:** * **Chromosome 1:** This is the location of the **Rh (Rhesus) blood group system** (specifically the RHD and RHCE genes). [1] This is a common point of confusion for students. * **Chromosome 3:** While it carries many genes, it is not associated with major blood group systems. * **Chromosome 6:** This is the location of the **Major Histocompatibility Complex (MHC)**, which encodes **HLA antigens**. [2] These are crucial for tissue typing and organ transplantation but are distinct from the ABO system. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** ABO blood groups follow **codominant inheritance** (A and B are codominant, while O is recessive). * **H Antigen:** The gene for the H substance (FUT1) is located on **Chromosome 19**. * **Bombay Phenotype:** Occurs when an individual lacks the H gene (hh), meaning they cannot produce A or B antigens even if they possess the ABO genes on Chromosome 9. * **Universal Donor/Recipient:** O-negative is the universal donor (packed RBCs); AB-positive is the universal recipient. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 627-628. [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. 179-180.

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Genetic Disorders

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