What is the first cellular response observed after a sharp nerve cut?
Which of the following is a type of small vessel vasculitis?
Which type of white blood cell plays a primary role in cardiac remodeling and chronic inflammation in heart failure?
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
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 31: What is the first cellular response observed after a sharp nerve cut?
- A. Chromatolysis (Correct Answer)
- B. Polymorphic arrangement
- C. Increased protein synthesis
- D. Macrophage activation
Explanation: ***Chromatolysis*** - **Chromatolysis** is the dissolution of the Nissl bodies (rough endoplasmic reticulum) in the neuron cell body following axonal injury, which is the **first observable cellular response** [1]. - This process is a preparatory step for neuronal regeneration, indicating the cell's attempt to repair the damaged axon [1]. *Polymorphic arrangement* - This term is not typically used to describe an immediate cellular response to a nerve cut; it might refer to diverse cell shapes or arrangements in different contexts but is not a recognized initial post-injury event. - The neuron's immediate response involves changes within the cell body, not a re-arrangement of its cellular structure with other cells. *Increased protein synthesis* - While increased protein synthesis does occur during neuronal repair and regeneration, it is a consequence of chromatolysis and part of a later, more sustained response, not the very first visible cellular change [1]. - **Chromatolysis precedes** and facilitates the subsequent increase in protein synthesis necessary for axonal regrowth [1]. *Macrophage activation* - **Macrophage activation** is a crucial part of the inflammatory response and debris clearance following nerve injury, but it is not the *first cellular response* of the neuron itself [2]. - Macrophages migrate to the site of injury hours to days after the initial insult, whereas chromatolysis begins within the neuron's cell body much earlier [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1254-1256. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 697-698.
Question 32: Which of the following is a type of small vessel vasculitis?
- A. Classical PAN
- B. Giant cell arteritis
- C. Granulomatosis with polyangiitis (GPA) (Correct Answer)
- D. None of the options
Explanation: ***Granulomatosis with polyangiitis (GPA)*** - GPA is a prototypic **ANCA-associated small vessel vasculitis** characterized by necrotizing granulomas and vasculitis [1], [2]. - It commonly involves the **upper and lower respiratory tracts** and the **kidneys** with necrotizing granulomatous inflammation [1], [2]. - Classified as small vessel vasculitis according to the **Chapel Hill Consensus Conference** classification. *Classical PAN* - This refers to **Polyarteritis Nodosa (PAN)**, which is a **medium-sized vessel vasculitis**. - PAN is characterized by multifocal inflammatory and necrotizing lesions of medium-sized muscular arteries, **not small vessels**. *Giant cell arteritis* - **Giant cell arteritis (GCA)** is a **large vessel vasculitis** that primarily affects the aorta and its major branches, particularly the temporal artery [3]. - Symptoms include headache, jaw claudication, and visual disturbances, reflecting the involvement of larger blood vessels [3]. *None of the options* - This option is incorrect because Granulomatosis with polyangiitis (GPA) is a clear example of a small vessel vasculitis. - There is a correct answer among the provided choices. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 519-520. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 536-537. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 515-516.
Question 33: Which type of white blood cell plays a primary role in cardiac remodeling and chronic inflammation in heart failure?
- A. Eosinophils
- B. Macrophages (Correct Answer)
- C. T cells
- D. B cells
Explanation: ***Macrophages*** - **Macrophages** are increasingly recognized for their critical role in the pathogenesis and progression of **heart failure**, contributing to **cardiac remodeling**, chronic inflammation, and fibrosis - They infiltrate failing myocardium and play dual roles: promoting both **inflammation** and **tissue repair** - Their activation state (M1 vs M2 phenotypes) can significantly influence cardiac function and prognosis in heart failure patients - They secrete **cytokines**, **growth factors**, and **matrix metalloproteinases** that contribute to ventricular remodeling *Eosinophils* - **Eosinophils** are primarily involved in **allergic reactions** and defense against **parasitic infections** - While they can contribute to inflammation in specific cardiac conditions (e.g., **eosinophilic myocarditis**, **Loeffler endocarditis**), they are not primarily associated with the general pathophysiology of chronic heart failure *T cells* - **T cells** are central to **adaptive immunity**, including cell-mediated responses and modulation of immune reactions - Though T cells play a role in inflammatory processes in certain forms of heart disease, particularly **viral myocarditis**, they are not the predominant immune cell driving chronic cardiac remodeling in heart failure *B cells* - **B cells** are responsible for producing **antibodies** and are key players in humoral immunity - While B cells can contribute to autoimmune forms of heart disease and certain inflammatory processes, they are not typically the primary immune cell associated with the progression of chronic heart failure
Question 34: 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 35: 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 36: 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 37: 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 38: 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 39: 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 40: 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.