General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 521: Hemolytic disease of the newborn is an example of which type of hypersensitivity reaction?

A. Type III hypersensitivity
B. Type II hypersensitivity (Correct Answer)
C. Arthus reaction
D. Type IV hypersensitivity

Explanation: **Explanation:** **Type II Hypersensitivity (Antibody-Mediated Cytotoxicity)** is the correct answer [1]. In Hemolytic Disease of the Newborn (HDN), such as Rh incompatibility, maternal IgG antibodies cross the placenta and bind to specific antigens on the surface of fetal Red Blood Cells (RBCs) [2]. This leads to RBC destruction via two Type II mechanisms: **Opsonization** (leading to phagocytosis by splenic macrophages) and **Complement-mediated lysis** [1]. Since the reaction involves antibodies (IgG/IgM) directed against fixed cell-surface antigens, it is a classic Type II reaction [1]. **Analysis of Incorrect Options:** * **Type III Hypersensitivity:** This involves the deposition of **circulating antigen-antibody (immune) complexes** in tissues (e.g., SLE, Post-streptococcal glomerulonephritis). It does not involve antibodies targeting specific cell-surface antigens. * **Arthus Reaction:** This is a localized form of **Type III hypersensitivity** characterized by tissue necrosis following the injection of an antigen into a previously sensitized individual (e.g., certain vaccinations). * **Type IV Hypersensitivity:** This is **T-cell mediated (delayed)** and does not involve antibodies. Examples include the Mantoux test, contact dermatitis, and granuloma formation. **NEET-PG High-Yield Pearls:** * **Mnemonic for Hypersensitivity (ACID):** **A**naphylactic (I), **C**ytotoxic (II), **I**mmune-Complex (III), **D**elayed (IV). * **Antibody involved in HDN:** Only **IgG** can cross the placenta; IgM (seen in ABO incompatibility) usually does not, making Rh incompatibility clinically more severe [2], [3]. * **Other Type II Examples:** Myasthenia Gravis, Graves' disease, Goodpasture syndrome, and Rheumatic fever [1]. * **Direct Coombs Test:** Used to detect these antibodies already bound to the baby's RBCs [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 214. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 469-470. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 603-604, 627-628.

Question 522: In diseases, cell death of growth hormone cells occurs by which mechanism?

A. Aging
B. Apoptosis (Correct Answer)
C. Necrosis
D. All of the above

Explanation: **Explanation:** The correct answer is **Apoptosis**. **Why Apoptosis is correct:** Apoptosis, or programmed cell death, is the primary mechanism for the physiological and pathological elimination of specific cell populations [1]. In the context of the anterior pituitary, the loss of growth hormone-producing cells (somatotrophs) occurs via apoptosis. This is often triggered by the withdrawal of trophic support (Growth Hormone Releasing Hormone) or specific pathological insults [1],[3]. Unlike necrosis, apoptosis allows for the removal of cells without inciting an inflammatory response, maintaining the structural integrity of the surrounding gland [2]. **Why other options are incorrect:** * **Aging:** While aging involves a gradual decline in cellular function (senescence), it is a process rather than the specific *mechanism* of cell death [2]. The actual death of cells during the aging process of an organ is typically executed via apoptosis. * **Necrosis:** This is an accidental, uncontrolled form of cell death resulting from severe acute injury (e.g., ischemia or toxins) [2]. It is characterized by cell swelling, membrane rupture, and inflammation. While it can occur in the pituitary (e.g., Sheehan syndrome), it is not the standard mechanism for the specific loss of growth hormone cells in chronic disease states. **High-Yield Facts for NEET-PG:** * **Councilman bodies** in viral hepatitis and **Psammoma bodies** (in some instances) are classic examples of apoptotic processes. * **Caspases** are the executioner enzymes of apoptosis [4]. * **Mnemonic:** Apoptosis is "neat" (no inflammation), whereas Necrosis is "messy" (pro-inflammatory). * In the endocrine system, the regression of the lactotrophic population after weaning is another classic example of physiological apoptosis [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, p. 45. [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. 80-81. [4] 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.

Question 523: Myotonic dystrophy is due to which genetic abnormality?

A. Expansion in a coding region
B. CAG trinucleotide repeat mutation
C. CTG trinucleotide repeat mutation (Correct Answer)
D. Mutation involving chromosome 15

Explanation: **Explanation:** **Myotonic Dystrophy (Type 1)** is an autosomal dominant disorder [3] and the most common form of adult-onset muscular dystrophy. It is caused by a **trinucleotide repeat expansion (CTG)** [3] in the 3' untranslated region (UTR) [2] of the **DMPK gene** [3] located on chromosome 19 [3]. This is a classic example of a "non-coding region" expansion, where the toxic mRNA interferes with RNA-binding proteins, leading to multisystem dysfunction. **Analysis of Options:** * **Option C (Correct):** The specific repeat in Myotonic Dystrophy Type 1 is **CTG** [3]. A key feature is **anticipation**, where the disease becomes more severe and occurs earlier in successive generations due to the expansion of these repeats during gametogenesis [1]. * **Option A:** Incorrect. While some repeat disorders occur in coding regions (like Huntington’s), Myotonic Dystrophy occurs in the **3' non-coding region** [2]. * **Option B:** Incorrect. **CAG** repeats are characteristic of Polyglutamine diseases, most notably **Huntington’s Disease** and Spinocerebellar Ataxias [2]. * **Option D:** Incorrect. Chromosome 15 mutations are associated with Prader-Willi and Angelman syndromes (imprinting disorders), not Myotonic Dystrophy (Chromosome 19) [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Triad:** Muscle weakness/wasting, **Myotonia** (delayed relaxation, e.g., inability to release a handshake), and multisystem involvement [3]. * **Associated Features:** Frontal balding, cataracts, gonadal atrophy, and cardiac conduction defects. * **Diagnosis:** Genetic testing (PCR/Southern Blot) is the gold standard. * **Mnemonic:** **C**ataracts, **T**oupee (balding), **G**onadal atrophy (**CTG**). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, p. 177. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 177-179. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 732-733.

Question 524: Which of the following diseases is transmitted as an X-linked inheritance?

A. Phenylketonuria
B. Alport syndrome (Correct Answer)
C. Myotonic dystrophy
D. Spinal muscular atrophy

Explanation: **Explanation:** **Alport Syndrome (Correct Answer):** Alport syndrome is a genetic disorder characterized by defects in **Type IV Collagen** (the "basement membrane collagen"). It typically presents with the clinical triad of **hereditary nephritis (hematuria/ESRD), sensorineural deafness, and ocular anomalies** (e.g., anterior lenticonus) [1]. In approximately **80% of cases**, it is inherited in an **X-linked dominant** pattern due to mutations in the *COL4A5* gene [1]. This makes it the most common hereditary glomerular disease with X-linked transmission. **Analysis of Incorrect Options:** * **Phenylketonuria (PKU):** This is a classic **Autosomal Recessive** metabolic disorder caused by a deficiency of the enzyme phenylalanine hydroxylase [3]. * **Myotonic Dystrophy:** This is an **Autosomal Dominant** condition. It is notable for being a trinucleotide repeat disorder (CTG repeat) and exhibiting the phenomenon of "anticipation." * **Spinal Muscular Atrophy (SMA):** This is an **Autosomal Recessive** neuromuscular disease caused by a mutation in the *SMN1* gene on chromosome 5. **High-Yield Clinical Pearls for NEET-PG:** * **Alport Syndrome Mnemonic:** "Can't see (lenticonus), can't pee (nephritis), can't hear a buzzing bee (deafness)." * **Electron Microscopy (EM) Finding:** Characteristic **"Basket-weave appearance"** due to irregular thinning and thickening of the Glomerular Basement Membrane (GBM). * **Inheritance Patterns:** Most metabolic enzyme deficiencies are Autosomal Recessive, while structural protein defects are often Autosomal Dominant. Alport syndrome is a high-yield exception to remember as X-linked [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 929-930. [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 525: Enzymatic degradation of chromatin by endonucleases is referred to as:

A. Karyolysis (Correct Answer)
B. Pyknosis
C. Karyorrhexis
D. None of the above

Explanation: ### Explanation The hallmark of irreversible cell injury and cell death is nuclear change [1]. These changes occur in a sequential or distinct manner depending on the type of necrosis. **Why Karyolysis is Correct:** **Karyolysis** refers to the fading of the basophilia of chromatin. This process is driven by the **enzymatic degradation of DNA by endonucleases** (specifically DNase) released from lysosomes. As the DNA is hydrolyzed, the nucleus loses its staining intensity and eventually disappears completely within 1 to 2 days. **Analysis of Incorrect Options:** * **B. Pyknosis:** This is characterized by **nuclear shrinkage** and increased basophilia. The DNA condenses into a solid, shrunken, dark mass. It is the first stage of nuclear morphology changes in cell death [1]. * **C. Karyorrhexis:** This follows pyknosis. The pyknotic nucleus undergoes **fragmentation** (rupture of the nuclear membrane), breaking into multiple small, dense "nuclear dust" particles [1]. **High-Yield NEET-PG Pearls:** * **Sequence of Nuclear Changes:** Pyknosis (Condensation) → Karyorrhexis (Fragmentation) → Karyolysis (Dissolution). * **Apoptosis vs. Necrosis:** While karyolysis is a classic feature of **necrosis**, the characteristic nuclear change in **apoptosis** is internucleosomal DNA fragmentation (forming a "ladder" pattern on electrophoresis), but the nucleus typically fragments into membrane-bound apoptotic bodies without complete enzymatic dissolution (karyolysis) in the same manner. * **Basophilia:** Loss of basophilia in karyolysis is due to the loss of DNA, which is the acidic component that binds basic dyes like Hematoxylin. **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. 53.

Question 526: Russell bodies are typically seen in which of the following cell types?

A. Lymphocytes
B. Neutrophils
C. Macrophages
D. Plasma cells (Correct Answer)

Explanation: **Explanation:** **Russell bodies** represent a classic example of **intracellular protein accumulation**. They are eosinophilic, large, homogeneous immunoglobulin inclusions found within the **Plasma cells**. 1. **Why Plasma cells are correct:** Plasma cells are specialized B-lineage cells dedicated to the synthesis of antibodies (immunoglobulins) [1]. When there is an excessive production of immunoglobulins or a defect in their transport/secretion, the proteins accumulate within the cisternae of the **Rough Endoplasmic Reticulum (RER)**. This distends the RER, forming rounded, eosinophilic "Russell bodies." This is a hallmark of chronic inflammation and certain plasma cell dyscrasias like Multiple Myeloma [2]. 2. **Why other options are incorrect:** * **Lymphocytes:** While plasma cells are derived from B-lymphocytes, the mature lymphocyte itself does not have the extensive RER machinery required to produce the volume of protein necessary to form Russell bodies. * **Neutrophils:** These cells are characterized by primary and secondary granules (lysosomes) containing enzymes like myeloperoxidase, not immunoglobulin accumulations. * **Macrophages:** These cells typically show accumulations of phagocytosed material (e.g., carbon, lipids, or hemosiderin) rather than endogenous immunoglobulin inclusions. **High-Yield NEET-PG Pearls:** * **Russell Bodies:** Intracellular (cytoplasmic) immunoglobulin inclusions in plasma cells. * **Dutcher Bodies:** Intranuclear immunoglobulin inclusions (actually cytoplasmic invaginations into the nucleus), typically seen in **Waldenström Macroglobulinemia** [3]. * **Mott Cells:** A plasma cell containing multiple Russell bodies, giving it a "grape-like" or "berry-like" appearance. * **Staining:** Russell bodies are PAS (Periodic Acid-Schiff) positive. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 266-267. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 607-608. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 606-607.

Question 527: Which of the following conditions does not exhibit an X-linked pattern of inheritance?

A. Duchenne muscular dystrophy
B. Emery-Dreifuss muscular dystrophy
C. Myotonic dystrophy (Correct Answer)
D. Becker muscular dystrophy

Explanation: **Explanation:** The correct answer is **Myotonic Dystrophy** because it follows an **Autosomal Dominant** pattern of inheritance, unlike the other options which are X-linked [1], [2]. **1. Why Myotonic Dystrophy is the correct answer:** Myotonic Dystrophy (specifically Type 1) is caused by an unstable expansion of **CTG trinucleotide repeats** in the *DMPK* gene located on **Chromosome 19** [1]. Because it is autosomal dominant, it affects males and females equally and often exhibits **anticipation** (increasing severity in successive generations). Clinically, it is characterized by "myotonia" (delayed muscle relaxation, such as difficulty releasing a handshake), cataracts, and endocrine dysfunction [2]. **2. Why the other options are incorrect:** * **Duchenne Muscular Dystrophy (DMD):** This is the most common and severe form of muscular dystrophy. It follows an **X-linked recessive** pattern due to a complete absence of the dystrophin protein [2]. * **Becker Muscular Dystrophy (BMD):** Also follows an **X-linked recessive** pattern. It is a milder version of DMD where dystrophin is truncated or decreased in quantity rather than absent [2]. * **Emery-Dreifuss Muscular Dystrophy (EDMD):** While there are autosomal forms, the most classic and common form is **X-linked**, caused by mutations in the *STA* gene encoding the protein **emerin**. **High-Yield Clinical Pearls for NEET-PG:** * **Gower’s Sign:** Classically seen in DMD due to proximal muscle weakness. * **Trinucleotide Repeat Disorders:** Remember the mnemonic **"My Tonia has CTG"** (Cataracts, Toupee/Balding, Gonadal atrophy). * **X-linked Recessive Mnemonic:** "Tailor's **D**og **B**arks **H**oudly" (**D**uchenne, **B**ecker, **H**emophilia, **H**unter Syndrome, **G**6PD deficiency). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 732-733. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1245-1246.

Question 528: Pinpoint hemorrhages of less than 1 cm in diameter are known as?

A. Petechiae (Correct Answer)
B. Ecchymoses
C. Purpura
D. Pustules

Explanation: **Explanation:** The question assesses the classification of hemorrhages into the skin, mucous membranes, or serosal surfaces based on size and morphology. **1. Why Petechiae is correct:** **Petechiae** are minute, pinpoint hemorrhages, typically **1 to 2 mm** in diameter (always <3 mm) [1]. They occur due to the rupture of capillaries or venules. Pathophysiologically, they are most commonly associated with **low platelet counts (thrombocytopenia)** [1], [2], defective platelet function, or increased intravascular pressure [2]. **2. Why other options are incorrect:** * **Purpura (Option C):** These are slightly larger hemorrhages measuring between **3 mm to 1 cm (or 0.3 to 1 cm)** [1]. They can be caused by the same factors as petechiae, as well as trauma or vascular inflammation (vasculitis). * **Ecchymoses (Option B):** These are larger subcutaneous hematomas, typically **greater than 1 to 2 cm**, commonly referred to as "bruises." They involve more extensive extravasation of blood into the subcutaneous tissue. * **Pustules (Option D):** This is a dermatological term for a small, elevated, circumscribed lesion of the skin that is filled with **pus** (neutrophils and debris), not blood. **High-Yield Clinical Pearls for NEET-PG:** * **Sequence of Color Change in Ecchymoses:** Hemoglobin (red-blue) → Bilirubin (blue-green) → Hemosiderin (golden-brown). This is a classic forensic and pathology favorite. * **Palpable Purpura:** A hallmark sign of **Leukocytoclastic Vasculitis** (Henoch-Schönlein Purpura). * **Vitamin C Deficiency (Scurvy):** Often presents with **perifollicular petechiae** due to defective collagen synthesis in vessel walls. * **Size Hierarchy:** Petechiae (<3mm) < Purpura (3mm–1cm) < Ecchymoses (>1cm). **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.

Question 529: Autopsy of the spleen of a patient with portal hypertension shows Gamna-Gandy bodies. These bodies are characterized by the presence of hemosiderin and which of the following?

A. Sodium ions (Na+)
B. Calcium ions (Ca++) (Correct Answer)
C. Magnesium ions (Mg++)
D. Calcium (Ca)

Explanation: **Explanation:** **Gamna-Gandy bodies** (also known as Siderofibrotic nodules) are a classic histopathological finding in the spleen, most commonly associated with **portal hypertension** and congestive splenomegaly. **1. Why the Correct Answer is Right:** The underlying mechanism involves chronic passive congestion of the spleen, leading to focal hemorrhages within the splenic parenchyma. As the red blood cells break down, hemoglobin is converted into **hemosiderin** [1]. Over time, these areas undergo fibrous scarring. These nodules become encrusted with mineral deposits, specifically **Calcium ions (Ca++)** and iron (hemosiderin). Under a microscope, they appear as yellow-brown, firm, "tobacco-fleck" nodules consisting of fibrous tissue, elastic fibers, and mineralized deposits. **2. Analysis of Incorrect Options:** * **Option A (Sodium ions):** Sodium is an extracellular cation involved in fluid balance but does not play a role in the mineralization or "petrification" of necrotic or fibrotic tissue. * **Option C (Magnesium ions):** While magnesium is found in bone, it is not a primary constituent of Gamna-Gandy bodies. * **Option D (Calcium):** While technically similar to B, in medical pathology, we refer to the deposition of **Calcium ions (Ca++)** within the tissue matrix during the process of dystrophic calcification [2]. Option B is the more precise biochemical representation. **3. Clinical Pearls & High-Yield Facts for NEET-PG:** * **Common Associations:** Portal hypertension (most common), Sickle Cell Anemia, and Hemochromatosis. * **Appearance:** On MRI (Gradient Echo sequences), Gamna-Gandy bodies appear as "signal voids" due to the paramagnetic effect of iron. * **Staining:** They stain positive with **Prussian Blue** (for iron) and **Von Kossa** (for calcium). * **Pathological Process:** This is an example of **dystrophic calcification** (calcification occurring in damaged/necrotic tissue despite normal serum calcium levels) [2]. **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. 75-76. [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. 134-135.

Question 530: Respiratory burst is due to which enzyme?

A. NADPH oxidase (Correct Answer)
B. Catalase
C. SOD
D. Glutathione peroxidase

Explanation: **Explanation:** **Respiratory burst** (or oxidative burst) is the rapid release of reactive oxygen species (ROS) from phagocytes (neutrophils and macrophages) to destroy engulfed pathogens. 1. **Why NADPH Oxidase is correct:** The process is initiated by the enzyme **NADPH oxidase** (located in the phagosomal membrane) [1]. It catalyzes the conversion of molecular oxygen ($O_2$) into **superoxide radicals** ($O_2^{\bullet-}$), using NADPH as an electron donor [1]. This is the "rate-limiting step" of the respiratory burst. Superoxide is then converted to hydrogen peroxide ($H_2O_2$), which, in the presence of Myeloperoxidase (MPO), forms the highly bactericidal Hypochlorous acid ($HOCl$ or bleach). 2. **Why other options are incorrect:** * **Catalase:** This enzyme breaks down $H_2O_2$ into water and oxygen [1]. It is a protective mechanism used by bacteria (like *S. aureus*) to neutralize the host's oxidative burst. * **SOD (Superoxide Dismutase):** This enzyme converts superoxide radicals into $H_2O_2$ [1]. While part of the pathway, it is considered an antioxidant defense rather than the enzyme that *triggers* the burst. * **Glutathione Peroxidase:** This is an intracellular antioxidant enzyme that neutralizes $H_2O_2$ to protect the cell from oxidative damage; it does not initiate the respiratory burst [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Chronic Granulomatous Disease (CGD):** Caused by a genetic deficiency in **NADPH oxidase**. Patients suffer from recurrent infections with **Catalase-positive** organisms (e.g., *S. aureus, Aspergillus, Serratia*). * **Diagnostic Tests for CGD:** Nitroblue Tetrazolium (NBT) dye test (remains colorless/negative) or the more modern **Dihydrorhodamine (DHR) flow cytometry** (decreased fluorescence). * **MPO Deficiency:** Most common defect of phagocytosis, but usually asymptomatic because the respiratory burst (NADPH oxidase step) remains intact. **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. 59-60.

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Hemodynamic Disorders

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Genetic Disorders

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