Which of the following conditions can lead to pulmonary infarction?
What do Döhle bodies represent in neutrophils?
In which organ are corpora amylacea typically observed in a pathological context?
What color is emitted by FITC after absorbing blue light?
Which of the following does not belong to the family of selectins?
Which of the following is not typically seen in Disseminated Intravascular Coagulation (DIC)?
Li–Fraumeni syndrome is associated with mutations in which of the following genes?
What type of anaemia is primarily associated with leukaemia?
Maximum collagen deposition in wound healing is seen at -
What laboratory findings are associated with common variable hypogammaglobulinemia?
NEET-PG 2012 - Pathology NEET-PG Practice Questions and MCQs
Question 11: Which of the following conditions can lead to pulmonary infarction?
- A. Saddle embolus at bifurcation
- B. Arterioles being blocked
- C. None of the above.
- D. Blockage of 2nd and 3rd generation end arteries (Correct Answer)
Explanation: ***None*** - Indicates that all the listed options do indeed contribute to **pulmonary infarction**. - **Pulmonary infarction** typically occurs due to vascular obstruction; thus, this choice signifies all other options are related. [1] *Saddle embolus at bifurcation* - A **saddle embolus** can cause significant blockage at the **pulmonary artery bifurcation**, leading to acute pulmonary infarction. [2] - This type of embolism can severely reduce blood supply to both lungs, directly contributing to infarction. [3] *Arterioles are blocked* - Obstruction of **small arterioles** can lead to localized ischemia and subsequent infarction in the pulmonary region. [1] - This phenomenon is consistent with the pathophysiology of pulmonary infarction, hence it is a contributing factor. *Blockage of 2nd and 3rd gen end arteries* - Infarction can occur if there is blockage of the **2nd and 3rd generation of pulmonary arteries**, leading to compromised blood flow. [1] - These smaller branches play a critical role in perfusing lung tissue, and their blockage can result in pulmonary infarction. [4] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 137-138. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 323-324. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 140. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 705-706.
Question 12: What do Döhle bodies represent in neutrophils?
- A. Presence of dilated endoplasmic reticulum in neutrophils (Correct Answer)
- B. Increased mitochondria in neutrophils
- C. Golgi apparatus proliferation in neutrophils
- D. Lysosomal activity in neutrophils
Explanation: ***Presence of dilated endoplasmic reticulum in neutrophils*** - **Döhle bodies** are inclusions found in the cytoplasm of neutrophils, classic hallmarks of **severe infection** or inflammatory conditions. - They represent remnants of dilated **rough endoplasmic reticulum**, which appears as pale-blue, irregular aggregates on stained blood smears. *Increased mitochondria in neutrophils* - An increase in mitochondria is not a characteristic feature associated with Döhle bodies. - While mitochondria are essential for cellular energy production, their proliferation does not form visible inclusions known as Döhle bodies. *Golgi apparatus proliferation in neutrophils* - Proliferation of the Golgi apparatus is not typically observed as a Döhle body. - The Golgi apparatus is involved in protein modification and packaging, but its changes do not manifest as these specific inclusions. *Lysosomal activity in neutrophils* - Lysosomal activity involves the breakdown of cellular debris and pathogens and is not directly related to the formation of Döhle bodies. - Although lysosomes are abundant in neutrophils, their activity does not result in the presence of Döhle bodies.
Question 13: In which organ are corpora amylacea typically observed in a pathological context?
- A. Thymus
- B. Lymph node
- C. Spleen
- D. Prostate (Correct Answer)
Explanation: ***Prostate*** - **Corpora amylacea**, also known as prostatic concretions, are common, benign findings in the prostate gland, especially with increasing age. - They are composed of glycoproteins and often found within the **acini and ducts of the prostate**. *Thymus* - The thymus is known for **Hassall's corpuscles**, which are epithelial reticular cells arranged concentrically, playing a role in T-cell selection. - **Corpora amylacea** are not typically found in the normal thymus. *Lymph node* - Lymph nodes are characterized by their lymphoid follicles, germinal centers, and medullary cords. - While they can have various inclusions or changes in disease states, **corpora amylacea** are not a typical pathological finding in lymph nodes. *Spleen* - The spleen is primarily involved in filtering blood and immune responses, with distinct red and white pulp regions. - **Corpora amylacea** are not associated with the normal or pathological histology of the spleen.
Question 14: What color is emitted by FITC after absorbing blue light?
- A. Yellow-green (Correct Answer)
- B. Orange-red
- C. Apple-green
- D. Golden-brown
Explanation: ***Yellow-green*** - Fluorescein isothiocyanate (FITC) is a common fluorochrome used in **fluorescence microscopy** and flow cytometry. - Upon excitation by blue light (typically around 495 nm), FITC emits light in the **yellow-green spectrum**, specifically around 521 nm. - This is the **spectroscopically accurate** description of FITC's emission peak. *Orange-red* - **Orange-red emission** is characteristic of fluorochromes like **phycoerythrin (PE)** or **Texas Red**, not FITC. - These fluorochromes have different **excitation and emission maxima** compared to FITC. *Apple-green* - While FITC fluorescence is sometimes clinically described as **"apple-green"** (especially in immunofluorescence), this is a **subjective visual description** rather than a precise spectral term. - The more **spectroscopically accurate** description is **yellow-green**, which reflects FITC's specific emission peak at 521 nm. - "Apple-green" typically suggests a purer green without the yellow component. *Golden-brown* - **Golden-brown** is not a typical emission color for fluorochromes like FITC. - This color is generally associated with **pigments** or stained tissues (e.g., lipofuscin, hemosiderin), not fluorescent probes.
Question 15: Which of the following does not belong to the family of selectins?
- A. P selectin
- B. L selectin
- C. A selectin (Correct Answer)
- D. E selectin
Explanation: ***A selectin*** - ***A selectin*** is not a recognized member of the selectin family, which includes other specific types. - The known selectins are **E-selectin**, **L-selectin**, and **P-selectin**, demonstrating a distinct classification [1]. *E selectin* - E selectin is a specific type of selectin expressed on **endothelial cells** activated by cytokines [1]. - It plays a crucial role in **leukocyte adhesion** during inflammation, distinguishing it as part of the selectin family [1]. *L selectin* - L selectin is involved in the **homing** of leukocytes to lymph nodes and forms part of the selectin family [1]. - Responsible for the initial tethering and rolling of leukocytes on **venular endothelium** [1]. *P selectin* - P selectin is found on platelets and endothelial cells and is critical in the **aggregation** of platelets and leukocytes. - It is also an established member of the selectin family, involved in **inflammatory responses** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 87.
Question 16: Which of the following is not typically seen in Disseminated Intravascular Coagulation (DIC)?
- A. Thrombocytopenia
- B. PT elevation
- C. Fibrinogen decreased
- D. Normal aPTT (Correct Answer)
Explanation: ***Normal APTT*** - In Disseminated Intravascular Coagulation (**DIC**), **APTT** is typically **prolonged** due to consumption of clotting factors [1]. - The presence of normal APTT indicates that coagulation pathways are not significantly affected, which is contrary to what is seen in DIC. *Fibrinogen decreased* - **Decreased fibrinogen levels** are common in DIC, reflecting its consumption during the coagulation process [1]. - This depletion is linked to the increased clotting and is a hallmark of DIC, making this statement false in the context of the question. *Thrombocytopenia* - **Thrombocytopenia** occurs in DIC as platelets are consumed during the formation of microclots [1]. - A significant drop in platelet count is a key feature of DIC, therefore this statement does not align with the "except" clause. *PT elevation* - Prothrombin Time (**PT**) is usually **elevated** in DIC due to the consumption of clotting factors [1]. - This reflects the ongoing activation of the coagulation cascade, supporting the exclusion in the question context. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 625-626.
Question 17: Li–Fraumeni syndrome is associated with mutations in which of the following genes?
- A. Gene RB1
- B. Gene BRCA1
- C. Gene P21
- D. Gene TP53 (Correct Answer)
Explanation: ***Gene TP53*** - Li-Fraumeni syndrome is a rare, inherited cancer susceptibility syndrome associated with germline mutations in the **TP53 tumor suppressor gene**. - The **TP53 gene** encodes the p53 protein, which plays a critical role in cell cycle arrest, DNA repair, and initiation of apoptosis in response to cellular stress, thus preventing tumor formation. *Gene P21* - The **p21 gene** (CDKN1A) is a cyclin-dependent kinase inhibitor that acts downstream of p53, mediating p53-induced cell cycle arrest. - While p21 is involved in the p53 pathway, mutations in p21 itself are not the primary cause of Li-Fraumeni syndrome. *Gene RB1* - The **RB1 gene** encodes the retinoblastoma protein, a tumor suppressor involved in cell cycle regulation, particularly in controlling passage from G1 to S phase. - Mutations in **RB1** are primarily associated with hereditary retinoblastoma and osteosarcoma, not Li-Fraumeni syndrome. *Gene BRCA1* - The **BRCA1 gene** is a tumor suppressor gene involved in DNA repair, especially homologous recombination. - Germline mutations in **BRCA1** are strongly associated with hereditary breast and ovarian cancer syndrome, not Li-Fraumeni syndrome.
Question 18: What type of anaemia is primarily associated with leukaemia?
- A. Aplastic anaemia
- B. Iron deficiency anaemia
- C. Megaloblastic anaemia
- D. Myelophthisic anaemia (Correct Answer)
Explanation: ***Myelophthisic anaemia*** - This condition arises from the **displacement of normal hematopoietic tissue** in the bone marrow by abnormal cells, like those seen in leukaemia, leading to **extramedullary hematopoiesis**. - Marrow infiltration causes **pancytopenia** and often results in the presence of **immature granulocytes** and **nucleated red blood cells** in the peripheral blood (leukoerythroblastosis). *Iron deficiency anaemia* - This type of anaemia is caused by insufficient iron for **hemoglobin synthesis**, often due to chronic blood loss or inadequate dietary intake. - While leukaemia patients can develop iron deficiency due to bleeding, it is not the **primary type of anaemia** directly resulting from the marrow infiltration by leukaemic cells. *Megaloblastic anaemia* - Characterized by the production of abnormally large, immature red blood cells, primarily due to **vitamin B12** or **folate deficiency**. - There is no direct causal link between leukaemia and the development of megaloblastic anaemia as a **primary haemato-pathological mechanism**. *Aplastic anaemia* - Characterized by **pancytopenia** due to bone marrow failure with hypocellular marrow, not marrow infiltration. - While both leukaemia and aplastic anaemia can present with cytopenias, aplastic anaemia shows a **hypocellular marrow** whereas leukaemia shows a **hypercellular marrow** with infiltration by malignant cells.
Question 19: Maximum collagen deposition in wound healing is seen at -
- A. End of third week (Correct Answer)
- B. End of first week
- C. End of 2 months
- D. End of second week
Explanation: ***End of third week*** - By the end of the **third week**, the proliferative phase of wound healing is well underway, characterized by significant **collagen deposition**. [1] - At this stage, **Type III collagen** is initially laid down, which is later replaced by stronger **Type I collagen**, contributing to increasing wound strength. *End of first week* - The first week primarily involves the **inflammatory phase** and the initial stages of **proliferation**, with minimal new collagen deposition. [2] - While some **fibroblasts** are present, the amount of collagen synthesized is still relatively low. *End of second week* - Collagen synthesis is ongoing during the second week, but the **peak deposition rate** and overall amount of collagen accumulated are typically not as high as at the end of the third week. - The wound is gaining strength, but further increase in collagen content and remodeling is yet to occur. *End of 2 months* - By 2 months, the wound is in the **remodeling phase**, where the total collagen content might be substantial but the *rate of new collagen synthesis* has slowed down. - At this stage, there is a balance between **collagen synthesis** and **degradation**, and the collagen fibers are being reorganized and cross-linked to further improve tensile strength. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 117-119. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 115.
Question 20: What laboratory findings are associated with common variable hypogammaglobulinemia?
- A. Low serum immunoglobulin levels (Correct Answer)
- B. Decreased B cell count
- C. Increased B cell count
- D. Neutropenia
Explanation: ***Low serum immunoglobulin levels*** - **Common variable hypogammaglobulinemia (CVID)** is characterized by significantly **low levels of IgG, IgA, and/or IgM** due to impaired B cell differentiation into plasma cells. - This deficiency in antibodies is the hallmark of the disorder, explaining the increased susceptibility to infections. *Decreased B cell count* - While CVID involves impaired B cell function, the **B cell counts** in the peripheral blood are typically **normal** or sometimes even elevated [1]. - The problem lies in their inability to differentiate and produce adequate antibodies, not in their numerical presence [1]. *Increased B cell count* - An increased B cell count is not a characteristic finding in CVID; peripheral B cell numbers are usually normal [1]. - If B cell counts are significantly increased, other conditions such as certain **lymphoproliferative disorders** should be considered. *Neutropenia* - **Neutropenia** (low neutrophil count) is not a primary diagnostic feature of CVID, although it can occur in some patients with autoimmune complications. - The defining laboratory finding is the **deficiency of immunoglobulins**, leading to recurrent infections. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 249-250.