In RDS in a child, which cells are found defective?
Microscopic examination of the reperfused myocardium is likely to have which of the following findings?
Loss of foot processes seen on electron microscopy of renal biopsy is a classical feature in which of the following?
Large, irregular and friable vegetations are seen in?
Which of the following is a cause of Hirschsprung disease in a patient?
Why is citrate phosphate dextrose (CPD) better than acid citrate dextrose (ACD) for storage of blood?
A middle-aged female presented with a 4cm mass in the upper outer quadrant of the breast. Biopsy showed densely packed cells within large extracellular spaces. Which of the following is the most likely diagnosis of this patient?
NEET-PG 2020 - Pathology NEET-PG Practice Questions and MCQs
Question 11: In RDS in a child, which cells are found defective?
- A. Bronchial epithelium
- B. Type 2 pneumocytes (Correct Answer)
- C. Type 1 pneumocytes
- D. Clara cells
Explanation: ***Type 2 pneumocytes*** - **Type 2 pneumocytes** are responsible for producing **surfactant**, which reduces surface tension in the alveoli and prevents their collapse [2], [3]. - In **Respiratory Distress Syndrome (RDS)**, especially in premature infants, these cells are immature or insufficient, leading to **surfactant deficiency** [1]. - This is the **primary cellular defect** in RDS, making it the correct answer [2]. *Bronchial epithelium* - The **bronchial epithelium** primarily lines the conducting airways and is involved in mucociliary clearance, not surfactant production. - Defects in this epithelium are associated with conditions like **bronchitis** or **asthma**, not the primary pathogenesis of RDS. *Type 1 pneumocytes* - **Type 1 pneumocytes** are thin, flat cells that form the majority of the alveolar surface (95%) and are crucial for gas exchange. - While they are affected by the damage in RDS, their primary defect is not the cause of the disease; the underlying problem is **surfactant deficiency** from Type 2 pneumocytes [2]. *Clara cells* - **Clara cells** (now called club cells) are non-ciliated secretory cells found in the bronchioles that produce Clara cell secretory protein (CCSP). - They play a role in detoxification and immune modulation but are **not responsible for surfactant production** or the pathogenesis of RDS. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 465-466. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 313-314. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, p. 466.
Question 12: Microscopic examination of the reperfused myocardium is likely to have which of the following findings?
- A. Neutrophilic infiltration
- B. Contraction band necrosis (Correct Answer)
- C. Cardiac myocyte swelling
- D. Waviness of fibers
Explanation: ***Contraction band necrosis*** - This lesion is characteristic of **reperfusion injury**, resulting from the reintroduction of **calcium** into ischemic cells, causing hypercontraction of sarcomeres [1]. - The bands represent irreversibly contracted sarcomeres and are a hallmark of cell death in the setting of restored blood flow [1]. *Neutrophilic infiltration* - While present in myocardial infarction, **neutrophilic infiltration** primarily begins hours after injury and is part of the inflammatory response to necrotic tissue, not a specific marker of reperfusion itself [2]. - It's a general feature of **acute inflammation** and necrosis but doesn't specifically distinguish reperfused myocardium from non-reperfused ischemic injury in the acute phase [2]. *Waviness of fibres* - **Waviness of fibers** is an early microscopic change in **ischemic myocardium**; it's due to the stretching of dead or dying muscle fibers adjacent to healthy, contracting fibers [2]. - This finding is typically seen within the first few hours of ischemia, before significant reperfusion injury is evident. *Cardiac myocyte swelling* - **Cardiac myocyte swelling** (cellular edema) is an early and non-specific sign of **ischemic injury** due to the failure of ion pumps, leading to intracellular accumulation of water [2]. - While present in ischemia, it's not a unique characteristic of reperfusion injury; reperfusion leads to more specific changes like contraction band necrosis [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 554-556. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 552.
Question 13: Loss of foot processes seen on electron microscopy of renal biopsy is a classical feature in which of the following?
- A. Minimal change disease (Correct Answer)
- B. Membranous nephropathy
- C. Rapidly progressive glomerulonephritis
- D. IgA nephropathy
Explanation: ***Minimal change disease*** - **Loss of foot processes** (podocyte effacement) is the hallmark ultrastructural finding in **minimal change disease** on electron microscopy [1]. - This effacement of podocyte foot processes leads to increased permeability of the **glomerular filtration barrier** to albumin, causing **nephrotic syndrome** [1], [2]. *IgA nephropathy* - Characterized by **IgA immune complex deposition** in the **mesangium** on immunofluorescence. - Electron microscopy typically shows **mesangial immune deposits**, not primarily foot process effacement. *Membranous nephropathy* - Identified by the presence of **subepithelial immune deposits** and **thickening of the glomerular basement membrane** (GBM) [3]. - On electron microscopy, these deposits are visible, often with overlying **spikes** of GBM material separating them. *Rapidly progressive glomerulonephritis* - Defined by the rapid loss of renal function and the presence of **crescents** in more than 50% of glomeruli on light microscopy [2]. - While there may be secondary podocyte changes due to severe inflammation, **foot process effacement** is not its primary diagnostic feature. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 927-928. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 527-528. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 532-533.
Question 14: Large, irregular and friable vegetations are seen in?
- A. Infective endocarditis (Correct Answer)
- B. Rheumatic heart disease
- C. Non-bacterial thrombotic endocarditis (NBTE)
- D. Libman-sacks endocarditis
Explanation: ***Infective endocarditis*** - **Large, irregular, and friable vegetations** are characteristic of infective endocarditis, formed by a mesh of **platelets, fibrin, microorganisms**, and inflammatory cells [1]. - These vegetations can lead to serious complications such as **embolization** and destruction of heart valves [2]. *Rheumatic heart disease* - Characterized by **small, warty vegetations** that are typically located on the lines of closure of the heart valves, not large and friable [1]. - These vegetations are sterile and result from inflammation and fibrin deposition, usually not involving active microbial infection. *Non-bacterial thrombotic endocarditis (NBTE)* - Features **small, sterile vegetations** composed of fibrin and platelets, often found on previously undamaged valves [1]. - These vegetations are typically **firm** and non-inflammatory, distinct from the friable and infected vegetations of infective endocarditis. *Libman-sacks endocarditis* - Manifests as **sterile, verrucous vegetations** that can occur on either side of the valve leaflets (aortic or mitral) in patients with **systemic lupus erythematosus (SLE)** [1]. - While they can be large, they are usually not described as friable in the same manner as infective endocarditis and are sterile. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 568. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 295-296.
Question 15: Which of the following is a cause of Hirschsprung disease in a patient?
- A. Failure of involution of vitelline duct
- B. Failure of migration of neural crest cells (Correct Answer)
- C. Excessive peristalsis of the affected part of the gut
- D. Obstruction secondary to an infectious agent
Explanation: ***Failure of migration of neural crest cells*** - Hirschsprung disease is characterized by the absence of **ganglion cells** (Auerbach and Meissner plexuses) in the distal colon [1]. - This aganglionosis results from the failure of **neural crest cells** to migrate completely from the esophagus to the anus during embryonic development [1]. *Failure of involution of vitelline duct* - This condition is associated with **Meckel's diverticulum**, which is a remnant of the vitelline duct, not Hirschsprung disease. - **Meckel's diverticulum** can cause symptoms like GI bleeding or obstruction, but it does not involve aganglionosis of the colon. *Excessive peristalsis of the affected part of the gut* - Hirschsprung disease is characterized by a **lack of peristalsis** in the aganglionic segment, leading to functional obstruction [1]. - The healthy, proximal colon may show increased peristalsis in an attempt to overcome the obstruction, but the affected segment itself is aperistaltic. *Obstruction secondary to an infectious agent* - Obstruction due to an infectious agent is typically related to **inflammatory processes** or strictures caused by infections (e.g., severe colitis). - This mechanism of obstruction does not involve the **developmental anomaly** of missing ganglion cells, which is central to Hirschsprung disease. **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. 94-95.
Question 16: Why is citrate phosphate dextrose (CPD) better than acid citrate dextrose (ACD) for storage of blood?
- A. Maintains pH stability during storage
- B. Contains phosphate and dextrose (Correct Answer)
- C. Prevents hemolysis in stored blood
- D. Reduces metabolic activity in stored blood
Explanation: ***Contains phosphate and dextrose*** - CPD contains **phosphate**, which acts as a buffer and helps maintain crucial 2,3-bisphosphoglycerate (2,3-BPG) levels in red blood cells, improving oxygen delivery capacity. - The presence of **dextrose** provides a substrate for glycolysis, which is essential for ATP production and red blood cell viability during storage. - This combination allows CPD to extend blood storage life to approximately **35 days** compared to ACD's **21 days**. *Maintains pH stability during storage* - Both ACD and CPD help maintain pH stability due to their **citrate** content, which acts as an anticoagulant and buffer. - However, CPD's phosphate component offers superior buffering capacity, but pH maintenance alone is not the primary distinguishing advantage. - This is a shared characteristic of both solutions, not the key reason CPD is preferred. *Prevents hemolysis in stored blood* - Both CPD and ACD prevent hemolysis by chelating **calcium**, which prevents coagulation and maintains red blood cell integrity. - While both solutions successfully prevent hemolysis, this is not the distinguishing feature that makes CPD superior. - The primary advantage of CPD lies in its better support of red blood cell metabolism and viability through phosphate and dextrose. *Reduces metabolic activity in stored blood* - This is **incorrect** - the purpose of anticoagulant solutions is to preserve blood components, not to reduce metabolic activity. - The dextrose in CPD is provided precisely to **fuel essential metabolic activity** (glycolysis) to sustain red blood cells during storage. - While refrigeration at 1-6°C slows metabolism, CPD actively supports rather than reduces the metabolic processes necessary for RBC survival.
Question 17: A middle-aged female presented with a 4cm mass in the upper outer quadrant of the breast. Biopsy showed densely packed cells within large extracellular spaces. Which of the following is the most likely diagnosis of this patient?
- A. Tubular carcinoma of breast
- B. Medullary carcinoma of breast
- C. Colloid carcinoma of breast (Correct Answer)
- D. Papillary carcinoma of breast
Explanation: ***Colloid carcinoma of breast*** - This type of carcinoma is characterized by **malignant cells floating in abundant extracellular mucin (colloid)**, which aligns with the description "densely packed cells within large extracellular spaces." - It often presents as a **well-circumscribed mass** and has a generally **good prognosis**. *Tubular carcinoma of breast* - Characterized by **well-differentiated tubules** with open lumens and a single layer of epithelial cells. - It does not typically feature large extracellular spaces filled with mucin. *Medullary carcinoma of breast* - This typically presents as a **soft, fleshy tumor** with syncytial sheets of large anaplastic cells and a prominent lymphoid infiltrate [1]. - It does not involve significant extracellular mucin or large extracellular spaces. *Papillary carcinoma of breast* - This carcinoma is defined by **papillary growth patterns** with fibrovascular cores lined by epithelial cells. - While it can be associated with cystic spaces, these are not typically described as "large extracellular spaces" filled with mucinous material. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 455-456.