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?
Radiotherapy induced radiation pneumonitis is mediated by all of the following cytokines and factors except -
What is the first cellular response observed after a sharp nerve cut?
Which histological type of lung cancer is most commonly associated with metastasis?
Most common type of renal carcinoma is:
Characteristic feature of IgA nephropathy?
IgA nephropathy is not associated with which of the following?
What is the primary process involved in Wallerian degeneration?
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 11: 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 12: 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 13: 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 14: Radiotherapy induced radiation pneumonitis is mediated by all of the following cytokines and factors except -
- A. PAF (Correct Answer)
- B. NF-kB
- C. TNF-α
- D. TGF-β
Explanation: ***PAF*** - **Platelet-activating factor (PAF)** is primarily involved in **anaphylaxis**, **asthma**, and **allergic responses**, mediating inflammation through platelet aggregation and smooth muscle contraction. - While it has pro-inflammatory effects, it is **not a primary mediator** of the specific inflammatory cascade seen in radiotherapy-induced radiation pneumonitis. *TNF-α* - **Tumor Necrosis Factor-alpha (TNF-α)** is a crucial **pro-inflammatory cytokine** that plays a significant role in the initial acute phase of radiation pneumonitis. - It induces **cytotoxicity**, **apoptosis**, and the production of other inflammatory mediators, contributing to lung tissue damage. *TGF-β* - **Transforming Growth Factor-beta (TGF-β)** is a key cytokine involved in the **fibrotic phase** of radiation pneumonitis. - It promotes **fibroblast proliferation**, collagen synthesis, and extracellular matrix deposition, leading to lung scarring. *NF-kB* - **Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-kB)** is a master **transcription factor** that regulates the expression of numerous genes involved in inflammation and immune responses. - Radiation exposure **activates NF-kB**, leading to the transcription of various pro-inflammatory cytokines, including TNF-α, which contribute to radiation pneumonitis.
Question 15: 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 16: Which histological type of lung cancer is most commonly associated with metastasis?
- A. Small cell carcinoma (Correct Answer)
- B. Squamous cell carcinoma
- C. Adenocarcinoma
- D. Large cell carcinoma
Explanation: ***Squamous cell CA*** - Known for its **aggressive nature** and propensity to metastasize, particularly in later stages. - Typically arises in the **central part of the lungs**, often associated with smoking and leads to local invasion and distant spread. *Alveolar-carcinoma* - Rarely found and tends to be **less aggressive** compared to squamous cell carcinoma. - Usually has a more localized effect without the same potential for widespread metastasis. *Small cell carcinoma* - Although it is **highly metastatic**, it is less common than squamous cell carcinoma in terms of overall lung cancer incidence. - Characterized by its rapid growth and early metastasis [1], but mostly associated with a specific subtype of lung cancer cases. *Adenocarcinoma* - Generally presents as a **peripheral lung lesion** and has **less propensity for early metastasis** compared to squamous cell carcinoma. - More common in non-smokers and tends to have a less aggressive metastatic pattern. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 337-338.
Question 17: Most common type of renal carcinoma is:
- A. Clear cell type (Correct Answer)
- B. Chromophobe type
- C. Papillary type
- D. Collecting duct type
Explanation: ***Clear cell type*** - The **clear cell type** is the most common subtype of renal carcinoma, constituting about **70-80%** of cases [3]. - It is typically associated with **von Hippel-Lindau syndrome** and presents with clear or "foamy" cells due to lipid accumulation [3]. *Chromophobe type* - This type comprises about **5-10%** of renal cell carcinomas and usually has a better prognosis [1]. - Characterized by **pale cells with distinct cell borders** and lacks the common features of clear cell carcinoma [1]. *Tubular type* - The tubular variant is less common and does not represent a major subtype of renal cell carcinoma. - It is often confused with other variants but lacks the distinct characteristics of the clear cell type. *Papillary type* - The papillary type accounts for about **10-15%** of renal carcinomas and is characterized by papillary structures [2]. - This type generally has a distinct chromosomal mutation profile compared to the clear cell type [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 959. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 958-959. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 959-961.
Question 18: Characteristic feature of IgA nephropathy?
- A. More common in old age
- B. It is a type of membranoproliferative GN
- C. Gross hematuria presents after 10 days
- D. Serum complement level is normal (Correct Answer)
Explanation: ***Serum complement level is normal*** - In **IgA nephropathy**, serum complement levels remain **normal** as this condition is not associated with complement consumption [1]. - This distinguishes it from other glomerulonephritides like **membranoproliferative GN**, where complement levels may be decreased. *Gross hematuria presents after 10 days* - Gross hematuria in IgA nephropathy often occurs **upon infection** or triggers, but not strictly after a set duration like 10 days [1]. - Typically, hematuria is seen with **episodic** flares rather than presenting consistently after a specific time frame. *More common in old age* - IgA nephropathy is actually more common in **young adults**, particularly males, rather than the elderly. - It is not characterized by age but rather often presents in **teenage years to early adulthood**. *It is a type of membranoproliferative GN* - IgA nephropathy is a **separate entity** and is predominantly characterized by the deposition of IgA in the mesangial regions [1], not classified under membranoproliferative GN. - This condition has distinct **pathological features** and immunological characteristics, differentiating it from membranoproliferative forms. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 928-929.
Question 19: IgA nephropathy is not associated with which of the following?
- A. Focal mesangial proliferation
- B. Gross hematuria concurrent with upper respiratory infection
- C. Immunofluorescence deposits contain IgA and IgG
- D. Decreased complement level (Correct Answer)
Explanation: ***Decreased complement level*** - IgA nephropathy is typically associated with **normal serum complement levels** (C3 and C4), which is an important distinguishing feature. - Unlike post-streptococcal glomerulonephritis or lupus nephritis where complement levels are **low/decreased**, IgA nephropathy does not cause systemic complement consumption. - While complement activation does occur locally in the glomerulus (via lectin and alternative pathways), it does not lead to a decrease in serum complement levels. *Focal mesangial proliferation* - This is a **common histological finding** in IgA nephropathy, reflecting the proliferative response to IgA deposition in the mesangium. - The mesangial cells proliferate in an attempt to clear the immune deposits. *Gross hematuria concurrent with upper respiratory infection* - This is a **classic clinical presentation** of IgA nephropathy, often referred to as **synpharyngitic hematuria**. - The episode of gross hematuria typically occurs **within 1-2 days** of the onset of an upper respiratory tract infection, distinguishing it from post-streptococcal glomerulonephritis where hematuria appears 1-3 weeks later. *Immunofluorescence deposits contain IgA and IgG* - The defining feature of IgA nephropathy on immunofluorescence is the **predominant deposition of IgA**, often accompanied by C3. - While IgA is the primary immunoglobulin, **IgG and IgM can also be present** in variable amounts, but IgA must be the dominant or co-dominant immunoglobulin for the diagnosis.
Question 20: What is the primary process involved in Wallerian degeneration?
- A. Nerve degeneration (Correct Answer)
- B. Muscle degeneration
- C. Nerve regeneration
- D. Muscle regeneration
Explanation: ***Nerve degeneration*** - **Wallerian degeneration** specifically refers to the process of **axon degeneration** that occurs distal to the site of injury when a nerve fiber is severed [2]. - This process involves the breakdown of the **axon** and its myelin sheath, leading to loss of function [1]. *Muscle degeneration* - While prolonged nerve degeneration can lead to muscle **atrophy** due to denervation, **muscle degeneration itself** is not the primary process of Wallerian degeneration. - Wallerian degeneration focuses on the **nerve itself**, not the target tissue. *Nerve regeneration* - **Nerve regeneration** is the process where damaged nerves attempt to regrow and re-establish connections [2]. - This is a subsequent, and not always successful, event that can occur *after* Wallerian degeneration has cleared the debris [1]. *Muscle regeneration* - **Muscle regeneration** refers to the repair and regrowth of damaged muscle tissue, typically involving satellite cells. - It is unrelated to Wallerian degeneration, which is a process affecting the **nerve**. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 697-698. [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. 109-110.