Heart failure cells are seen in -
Obliterative endarteritis in vasa vasorum is seen in -
Concentric hypertrophy of left ventricle is seen in -
Which of the following statements is true regarding the Duffy Fy(a-b-) blood group?
What is a distinguishing feature of reticulocytes?
Osmotic fragility test is commonly used for which of the following conditions?
Shelf life of platelets in a blood bank is
Which antigen is tested in routine Rh typing?
Which of the following is NOT seen in polycythemia vera?
What is the Rose Waaler test used for?
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 51: Heart failure cells are seen in -
- A. Pulmonary edema (Correct Answer)
- B. Pulmonary infarction
- C. Pulmonary abscess
- D. Pulmonary tuberculosis
Explanation: ***Pulmonary edema*** - Heart failure cells, or **hemosiderin-laden macrophages**, are typically found in the lungs during pulmonary edema due to left-sided heart failure [1]. - This condition leads to **increased pulmonary capillary pressure**, causing leakage of red blood cells into the alveoli, which macrophages then phagocytose [1]. *Pulmonary abscess* - Characterized by a **localized collection of pus** within the lung, typically due to infection, rather than heart failure. - Does not typically involve **hemosiderin-laden macrophages** indicative of chronic pulmonary congestion. *Pulmonary infarction* - Causes **tissue death** due to obstruction of blood flow, leading to necrosis rather than heart failure cells. - Typically presents with **infarcted lung tissue**, showing a different pathological process than seen in heart failure. *PulmonaryTB* - Primarily caused by **Mycobacterium tuberculosis**, leading to cavitary lesions and granulomatous inflammation, not heart failure cells. - The presence of **caseating granulomas** is characterized but does not indicate chronic pulmonary congestion. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 536-538.
Question 52: Obliterative endarteritis in vasa vasorum is seen in -
- A. Essential Hypertension
- B. Tertiary Syphilis (Correct Answer)
- C. Systemic Lupus Erythematosus
- D. Pulmonary Tuberculosis
Explanation: ***Tertiary Syphilis*** - **Obliterative endarteritis** of the **vasa vasorum** is a hallmark pathological finding in tertiary syphilis, particularly affecting the **aorta**. - This inflammation and occlusion of the small blood vessels supplying the aorta lead to **ischemic injury** of the aortic wall, causing **aneurysms** and **aortic regurgitation**. *Essential Hypertension* - While hypertension can lead to vascular changes like **arteriolosclerosis** and **hyperplastic arteriolosclerosis**, it does not typically involve obliterative endarteritis of the vasa vasorum. - The vascular damage in essential hypertension is more generalized to smaller arteries and arterioles, not specifically the vasa vasorum. *Systemic Lupus Erythematosus* - SLE is an **autoimmune disease** that can cause **vasculitis**, but the specific pattern of obliterative endarteritis of the vasa vasorum is not characteristic. - Vascular involvement in SLE is diverse, ranging from small vessel vasculitis to accelerated atherosclerosis, but distinct from syphilitic changes. *Pulmonary Tuberculosis* - Tuberculosis is primarily an **infectious granulomatous disease** affecting the lungs and other organs; it does not typically cause obliterative endarteritis of the vasa vasorum. - Although it can cause vascular complications like **aneurysms** (e.g., Rasmussen's aneurysm) due to erosion, the underlying mechanism is not the same as syphilitic changes.
Question 53: Concentric hypertrophy of left ventricle is seen in -
- A. Congenital aortic stenosis due to bicuspid aortic valve (Correct Answer)
- B. Mitral Stenosis
- C. Aortic Regurgitation
- D. Hypertrophic Obstructive Cardiomyopathy
Explanation: ***Congenital aortic stenosis due to bicuspid aortic valve*** - **Aortic stenosis** creates a **pressure overload** on the left ventricle, leading to a compensatory increase in myocardial wall thickness without significant chamber dilation, which is the classic example of **concentric hypertrophy** [1]. - A **bicuspid aortic valve** is a common congenital anomaly that causes aortic stenosis and thus concentric left ventricular hypertrophy [2]. - This represents **acquired concentric hypertrophy** due to hemodynamic stress. *Mitral Stenosis* - **Mitral stenosis** primarily causes a pressure overload on the **left atrium**, leading to left atrial enlargement [3]. - While it can indirectly affect the left ventricle, it typically does not cause **concentric left ventricular hypertrophy** itself. *Aortic Regurgitation* - **Aortic regurgitation** leads to a **volume overload** on the left ventricle as blood flows back into the ventricle during diastole. - This typically results in **eccentric hypertrophy**, where both the ventricular wall thickness and chamber size increase significantly (dilated ventricle with increased mass) [1]. *Hypertrophic Obstructive Cardiomyopathy* - **Hypertrophic obstructive cardiomyopathy (HOCM)** is a **primary genetic myocardial disease** characterized by **asymmetric septal hypertrophy** rather than uniform concentric hypertrophy. - While HOCM involves significant myocardial hypertrophy, it represents a distinct pathophysiologic entity with **asymmetric distribution** (predominantly septal), not the classic concentric pattern seen with pressure overload states. - The hypertrophy in HOCM is **intrinsic (genetic)** rather than **adaptive (hemodynamic)** like in aortic stenosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 536. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 562-563. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 533-534.
Question 54: Which of the following statements is true regarding the Duffy Fy(a-b-) blood group?
- A. lacks H- antigen
- B. lacks A-antigen
- C. All of the options
- D. lacks Fy(b) antigen (Correct Answer)
Explanation: ***lacks Fy(b) antigen*** - The **Duffy Fy(a-b-)** phenotype indicates absence of both Fy<sup>a</sup> and Fy<sup>b</sup> antigens on red blood cells. - Since the phenotype is **Fy(a-b-)**, it definitively lacks the **Fy<sup>b</sup> antigen** (indicated by the "b-" notation). - This phenotype is common in people of **African descent** and confers natural **resistance to Plasmodium vivax malaria**, as these antigens serve as receptors for the parasite to enter RBCs. *lacks H- antigen* - The **H antigen** belongs to the **H/h blood group system** and is a precursor to A and B antigens in the ABO system. - The absence of H antigen (Bombay phenotype - Oh) is completely **unrelated to the Duffy blood group system**. - Duffy antigens are on the **DARC (Duffy Antigen Receptor for Chemokines)** protein, distinct from the H antigen. *lacks A-antigen* - The **A antigen** is part of the **ABO blood group system** and defines blood types A and AB. - The Duffy blood group system is **genetically and structurally independent** from the ABO system. - Having Fy(a-b-) phenotype does not affect A antigen expression. *All of the options* - This is incorrect because the Duffy Fy(a-b-) phenotype **specifically refers only to the absence of Duffy antigens** (Fy<sup>a</sup> and Fy<sup>b</sup>). - It has **no relationship** with A, B, or H antigens, which belong to different blood group systems controlled by different genes on different chromosomes.
Question 55: What is a distinguishing feature of reticulocytes?
- A. Slightly larger in size than RBCs
- B. Presence of residual RNA and ribosomes (Correct Answer)
- C. Mature in bone marrow
- D. Constitute approximately 1% of the red cells
Explanation: ***Presence of residual RNA and ribosomes*** - This is the **defining and most distinguishing feature** of reticulocytes that differentiates them from mature red blood cells. - Reticulocytes contain residual **ribosomal RNA** and other organelles that are lost when they mature into erythrocytes. - This residual RNA forms a **reticular (network-like) pattern** when stained with supravital stains like **new methylene blue** or **brilliant cresyl blue**, which is the basis for their name and identification. - The presence of RNA allows for **reticulocyte counting**, an important marker of bone marrow erythropoietic activity. *Slightly larger in size than RBCs* - While reticulocytes may be slightly larger (polychromatophilic appearance), size variation is **not specific** and overlaps significantly with mature RBCs. - Size is not a reliable distinguishing feature and is not used for identification or counting. *Mature in bone marrow* - Reticulocytes are **released from the bone marrow** as immature red cells and complete their maturation in the **peripheral circulation** over 24-48 hours. - They do not fully mature in the bone marrow; their presence in peripheral blood is normal. *Constitute approximately 1% of the red cells* - Normal reticulocyte count is **0.5-2%** (or approximately 1%) of total red blood cells in healthy adults. - This is a **population characteristic** indicating normal erythropoietic activity, not a distinguishing cellular feature.
Question 56: Osmotic fragility test is commonly used for which of the following conditions?
- A. Megaloblastic anemia
- B. Aplastic anemia
- C. Hereditary spherocytosis (Correct Answer)
- D. Iron deficiency anemia
Explanation: ***Hereditary spherocytosis*** - The **osmotic fragility test** helps in diagnosing hereditary spherocytosis, where **spherical red blood cells** are more prone to hemolysis in hypotonic solutions [1][2]. - This condition is characterized by **spherocytes** (abnormally shaped RBCs) leading to increased osmotic fragility [1][3]. *Megaloblastic anemia* - Megaloblastic anemia is primarily associated with **deficiencies in B12 or folate**, affecting the size and maturation of red blood cells, not their osmotic fragility. - The diagnosis focuses on **serum vitamin levels** and **bone marrow examination** rather than osmotic fragility. *Iron deficiency anemia* - Iron deficiency anemia features **microcytic** and **hypochromic RBCs**, and its diagnosis relies on **iron studies**, not osmotic fragility tests. - The osmotic fragility test does not reveal significant changes in red blood cells for this condition. *Aplastic anemia* - Aplastic anemia involves **pancytopenia** due to bone marrow failure and does not typically show altered osmotic fragility. - The diagnosis is confirmed through **bone marrow biopsy**, not by assessing osmotic fragility. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 597-598. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 640-641. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 638.
Question 57: Shelf life of platelets in a blood bank is
- A. 5 days (Correct Answer)
- B. 7 days
- C. 10 days
- D. 21 days
Explanation: **5 days** - Platelets stored at **room temperature (20-24°C)** have a limited shelf life due to the risk of bacterial contamination and metabolic changes. - This short storage period ensures the **viability and function** of platelets for transfusion. *7 days* - A 7-day shelf life was initially proposed but was not widely adopted due to concerns about increased **bacterial growth** and the practical challenges of extended storage at room temperature. - The risk of **bacterial sepsis** significantly increases with longer room temperature storage. *10 days* - This duration is beyond the currently accepted shelf life for platelets, leading to an unacceptably high risk of **bacterial contamination** and reduced therapeutic efficacy. - Storing platelets for 10 days would likely result in an increased incidence of **transfusion-associated sepsis**. *21 days* - A shelf life of 21 days is typical for **red blood cells** when stored at 1-6°C with specific anticoagulants, but it is far too long for platelets. - Platelets stored for this duration at room temperature would be significantly **non-viable** and pose a severe risk of bacterial infection.
Question 58: Which antigen is tested in routine Rh typing?
- A. C antigen
- B. D antigen (Correct Answer)
- C. A antigen
- D. B antigen
Explanation: ***D antigen*** - Routine Rh typing specifically tests for the **D antigen**, which determines the Rh status of an individual as Rh-positive or Rh-negative [1]. - The presence of the **D antigen** is crucial for blood transfusions and pregnancy management [1]. *A antigen* - The **A antigen** is tested in the context of the ABO blood group system, not specifically for Rh typing. - It does not provide information regarding the Rh factor which is critical in blood compatibility. *C antigen* - Similar to the **A antigen**, the **C antigen** is part of the broader Rh system but is not routinely assessed in standard Rh typing. - Its testing is typically reserved for specific clinical scenarios involving Rh incompatibility. *B antigen* - The **B antigen** pertains to the ABO blood group and does not relate to the Rh factor or routine Rh typing. - Rh typing is solely focused on the **presence of the D antigen** to determine the Rh status. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 627-628.
Question 59: Which of the following is NOT seen in polycythemia vera?
- A. Increased erythropoietin (Correct Answer)
- B. Intrinsic abnormality of hematopoietic precursors
- C. Erythropoietin independent growth of red cell progenitors
- D. Most common cause of primary polycythemia
Explanation: ***Increased erythropoietin*** - In polycythemia vera, patients usually exhibit **low erythropoietin levels** due to feedback inhibition from increased red blood cell mass. - The condition is driven by a **myeloproliferative disorder** [2], not by increased erythropoietin stimulation. *Most common cause of polycythemia* - This option is incorrect because polycythemia vera is specifically a type of **primary polycythemia** [1], rather than the most common cause, which is often **secondary causes** such as hypoxia or abnormal erythropoietin production. - Other causes including chronic lung disease or renal tumors are more prevalent sources of increased red blood cell production. *Intrinsic abnormality of hematopoietic precursors* - While polycythemia vera indeed involves an **abnormality in hematopoietic stem cells** [1], it is not the only mechanism leading to polycythemia; many cases have secondary causes. - Hence, this option misrepresents the specific and more accurate characterization of polycythemia vera. *Erythropoietin independent growth of red cell progenitors* - Polycythemia vera is associated with **erythropoietin-independent** proliferation of hematopoietic cells [2], which is characteristic of the condition due to mutations in **JAK2** [2,3]. - This accurately reflects a significant feature of the disease, aligning closely with the pathophysiology. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 663-664. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 614-615. [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. 626-627.
Question 60: What is the Rose Waaler test used for?
- A. Ring precipitation
- B. Precipitation in gel
- C. Complement fixation test
- D. Passive hemagglutination test (Correct Answer)
Explanation: ***Passive hemagglutination test*** - The **Rose Waaler test** is a historical **rheumatoid factor (RF)** detection method based on **passive hemagglutination**. - It uses sheep red blood cells coated with a subagglutinating dose of rabbit anti-sheep red blood cell antibody to detect RF in patient serum. *Complement fixation test* - This assay detects the presence of **antibody** or **antigen** by observing whether **complement** is consumed in an antigen-antibody reaction. - The Rose Waaler test does not involve the measurement of complement consumption. *Precipitation in gel* - This technique, such as **immunodiffusion**, involves the formation of a visible **precipitate** when soluble antigens and antibodies diffuse through a gel matrix and meet at optimal concentrations. - The Rose Waaler test relies on agglutination of red blood cells, not precipitation in gel. *Ring precipitation* - A **ring precipitation test** involves layering an antigen solution over an antibody solution, creating an antigen-antibody complex visible as a **precipitate ring** at the interface of the two solutions. - This method is distinct from the Rose Waaler test which uses red blood cell agglutination.