All of the following statements about Giant cell arteritis are true except?
What change is seen in the vessels during the initial stage of Raynaud's phenomenon?
Starry sky appearance is seen in which of the following?
What occurs during the stage of Grey hepatization?
Oncocytic carcinoma arises from -
What do Döhle bodies represent in neutrophils?
A mutation in the transthyretin (TTR) protein causes which of the following types of amyloidosis?
Cystic medial necrosis is seen in?
What is the most important prognostic factor of Wilms tumour?
Which condition is characterized by spongiform degeneration of the cerebral cortex?
NEET-PG 2012 - Pathology NEET-PG Practice Questions and MCQs
Question 21: All of the following statements about Giant cell arteritis are true except?
- A. Involves large to small sized arteries (Correct Answer)
- B. Granulomatous inflammation
- C. Segmental nature of the involvement
- D. Can involve the aorta and its major branches
Explanation: ***Involves large to small sized arteries*** - Giant cell arteritis (GCA) predominantly affects **medium to large-sized arteries**, most commonly the branches of the **carotid artery**, such as the temporal arteries [1]. - While it can affect various arteries, it does not typically involve **small-sized arteries**, such as arterioles, directly as a primary site of inflammation. *Granulomatous inflammation* - GCA is characterized histologically by **granulomatous inflammation** within the arterial wall, which includes multinucleated **giant cells** and lymphocytes [2]. - This specific inflammatory pattern is a hallmark feature used in the diagnosis of GCA upon biopsy [2]. *Segmental nature of the involvement* - The arterial inflammation in GCA is often **segmental**, meaning that affected arteries may have inflamed and non-inflamed sections alternating along their length [2]. - This segmental involvement often necessitates **longer biopsies** (e.g., 2-3 cm for temporal artery biopsy) to increase the diagnostic yield. *Can involve the aorta and its major branches* - GCA can indeed affect the **aorta** (aortitis) and its major branches, leading to complications like **aneurysms** or **dissections**. - Involvement of these larger vessels can manifest as symptoms such as **claudication** in the limbs or asymptomatic aneurysms detectable on imaging [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 688-689. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 516-517.
Question 22: What change is seen in the vessels during the initial stage of Raynaud's phenomenon?
- A. No pathological changes (functional vasospasm only) (Correct Answer)
- B. Thrombosis
- C. Fibrinoid necrosis
- D. Hyaline sclerosis
Explanation: ***No pathological changes (functional vasospasm only)*** - Raynaud's phenomenon, particularly **primary Raynaud's** (Raynaud's disease), is characterized by **functional vasospasm** of arterioles, especially in fingers and toes, in response to cold or stress [1]. - In its initial stages, there are no structural changes or pathological alterations within the vessel walls; the vasoconstriction is entirely **functional** [1]. *Thrombosis* - **Thrombosis** involves the formation of a blood clot within a vessel, obstructing blood flow. - While severe Raynaud's can, in rare cases, lead to digital ischemia and microthrombosis, it is **not the primary or initial change** seen in typical Raynaud's phenomenon. *Fibrinoid necrosis* - **Fibrinoid necrosis** is a type of vascular damage associated with severe autoimmune diseases or malignant hypertension, where fibrin and plasma proteins deposit in the vessel wall. - This is a **structural, irreversible change** and is not characteristic of the initial, functional vasospasm seen in Raynaud's phenomenon. *Hyaline sclerosis* - **Hyaline sclerosis** is a change in small arteries and arterioles, often seen in benign essential hypertension or as part of the aging process, where the vessel wall thickens and becomes hyaline (glassy) due to plasma protein leakage and fibrosis. - This represents a **chronic structural change** and is not the acute, intermittent, functional vasoconstriction defining the initial stage of Raynaud's. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 520-522.
Question 23: Starry sky appearance is seen in which of the following?
- A. Burkitt's Lymphoma (Correct Answer)
- B. Diffuse Large B Cell Lymphoma
- C. Anaplastic Large Cell Lymphoma (ALCL)
- D. Follicular Lymphoma
Explanation: ***Burkitts lymphoma*** - The **starry sky appearance** is a characteristic histopathological finding due to interspersed macrophages containing **phagocytosed apoptotic cells** and necrotic debris in Burkitt's lymphoma [1]. - It is associated with **MYC gene translocation** and presents typically in children or young adults, commonly affecting the **jaw or abdomen**. *CIL* - CIL (chronic inflammatory leukocytosis) does not exhibit a **starry sky appearance**; it typically reflects a reactive process without specific histological features. - The histology is more characterized by **increased white blood cell counts** rather than tissue architecture alterations seen in lymphomas. *Diffuse large B cell lymphoma* - While this lymphoma can show **varied morphology**, it does not have a **starry sky appearance** as a defining feature, rather presenting with **large atypical B-cells**. - The histological appearance is generally of a **diffuse infiltrate**, which lacks the classic starry sky histology. *ALCL* - Anaplastic large cell lymphoma (ALCL) is characterized by **large, pleomorphic cells** but does not show a starry sky appearance. - The histological pattern primarily focuses on **large anaplastic lymphoid cells** rather than the scattered macrophages seen in Burkitt's lymphoma. **References:** [1] 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, p. 606.
Question 24: What occurs during the stage of Grey hepatization?
- A. Accumulation of fibrin (Correct Answer)
- B. Red blood cells fill the alveoli
- C. White blood cells fill the alveoli
- D. Bacteria fill the alveoli
Explanation: ***Accumulation of fibrin*** - Grey hepatization is characterized by the **presence of fibrinous exudate** in the alveoli, indicating significant lung pathology, usually in cases of pneumonia [1,2]. - This stage follows red hepatization and reflects the **progression of inflammation** within the lung tissue [1,2]. *RBC's fill the alveoli* - This occurs during the **red hepatization** stage, where RBCs invade alveoli, not grey hepatization [1,2]. - **Grey hepatization** is marked by **fibrinous deposits** instead of erythrocytes [1,2]. *Organisms fill the alveoli* - While organisms, such as bacteria, can be present, they are more characteristic of the **initial infection phase** rather than grey hepatization [1]. - This stage reflects more on the **inflammatory response** than the presence of pathogens. *WBC's fill the alveoli* - The infiltration of **WBCs (like neutrophils)** represents an earlier inflammatory process, usually preceding grey hepatization [1,2]. - In grey hepatization, the focus is on the **accumulation of fibrin**, not directly on WBC infiltration [1,2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 711-712. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 317-318.
Question 25: Oncocytic carcinoma arises from -
- A. Perivascular region
- B. Renal glomerulus
- C. Loop of Henle
- D. Collecting duct (intercalated cells) (Correct Answer)
Explanation: ***Collecting duct*** - Oncocytic carcinoma primarily originates from the **collecting ducts** of the kidney, where oncocytes are characteristically found [1]. - It is associated with specific **morphological features**, including abundant eosinophilic cytoplasm. *Loop of henle* - This part of the nephron primarily functions in **concentration of urine** and is not a common site for oncocytic tumors. - Tumors arising here typically do not exhibit **oncocytic features** and are more often linked to different renal cell types. *Glomerulus* - The glomerulus is involved in **filtration of blood** and lacks oncocytic differentiation. - Oncocytic carcinoma does not arise from glomerular structures, as it features distinct cellular characteristics. *Perivascular* - This term refers to the tissue surrounding blood vessels and is not a site for oncocytic carcinoma development. - Such tumors would not align with the histological features or origins typically seen in oncocytic carcinoma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 959.
Question 26: 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 27: A mutation in the transthyretin (TTR) protein causes which of the following types of amyloidosis?
- A. Familial Mediterranean fever
- B. Dialysis associated amyloidosis
- C. Prion protein associated amyloidosis
- D. Familial amyloidotic polyneuropathy (Correct Answer)
Explanation: ***Familial amyloidotic polyneuropathy*** - This condition is specifically caused by **mutations in the transthyretin (TTR) protein**, leading to amyloid deposition primarily in nerves [1]. - It presents with **peripheral neuropathy**, including sensory and autonomic symptoms, which align with TTR mutations [1]. *Familial Mediterranean fever* - This is an autoinflammatory disorder caused by mutations in the **MEFV gene**, unrelated to transthyretin. - It is characterized by recurrent **fever, abdominal pain**, and **serositis**, not amyloidosis caused by TTR. *Prion protein associated amyloidosis* - Relates to prion diseases like **Creutzfeldt-Jakob disease**, caused by abnormal **prion proteins** rather than TTR [1]. - Symptoms are usually **neurodegenerative** in nature, not linked to familial amyloidogenic processes. *Dialysis associated amyloidosis* - This form of amyloidosis is due to the accumulation of **beta-2 microglobulin**, not mutations in TTR [1]. - Commonly presents with **joint pain** and carpal tunnel syndrome associated with long-term dialysis [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 266.
Question 28: Cystic medial necrosis is seen in?
- A. Marfan syndrome (Correct Answer)
- B. Friedreich's ataxia
- C. Down syndrome
- D. Kawasaki disease
Explanation: ***Marfans syndrome*** - Cystic medial necrosis is a prominent feature of Marfan syndrome, leading to **aortic dilation** and increased risk of dissection [1] [2]. - It is associated with **connective tissue abnormalities**, specifically affecting elastic fibers in the aorta [2]. *Kawasaki disease* - Primarily affects children, leading to **vasculitis** of medium-sized arteries, especially the coronary arteries. - Does not characteristically cause **cystic medial necrosis** in the aorta. *Friedrichs ataxia Pattern* - An autosomal recessive disorder characterized by degeneration of spinal cord and peripheral nerves, not related to cystic medial necrosis. - Presents with **ataxia**, **scoliosis**, and **diabetes**, lacking cardiovascular changes associated with cystic medial necrosis. *Downs syndrome* - A genetic condition resulting from **trisomy 21**, associated with various congenital anomalies but not specifically with cystic medial necrosis. - Includes features like **heart defects** but does not involve the aortic changes seen in Marfan syndrome. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 511-512. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 153-154.
Question 29: What is the most important prognostic factor of Wilms tumour?
- A. Mutation of WT1 gene
- B. Histopathology (Correct Answer)
- C. Ploidy of cells
- D. Age < 1 yr
Explanation: ***Histopathology*** - The presence of **anaplastic histology**, particularly diffuse anaplasia, is the most significant adverse prognostic factor in Wilms tumor. - Tumors with favorable histology (triphasic, blastemal, stromal, or epithelial predominant) have an excellent prognosis, while those with anaplastic features have significantly worse outcomes [1]. *Ploidy of cells* - While **aneuploidy** (specifically, **hyperdiploidy**) has been associated with improved prognosis in some childhood cancers, its role as an independent prognostic factor in Wilms tumor is less significant than histology [2]. - It is not the most important factor in determining the overall outcome. *Age < 1 yr* - **Younger age** (typically less than 1 year) at diagnosis is generally associated with a **more favorable prognosis** in Wilms tumor. - This is because these tumors are often smaller, less aggressive, and more likely to have favorable histology. *Mutation of WT1 gene* - **WT1 gene mutations** are implicated in the development of Wilms tumor, particularly in syndromes like WAGR (Wilms tumor, aniridia, genitourinary anomalies, intellectual disability). - While critical for pathogenesis, the mere presence of a WT1 mutation is **not the primary determinant** of prognosis compared to tumor histology. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 488-490. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 486-487.
Question 30: Which condition is characterized by spongiform degeneration of the cerebral cortex?
- A. Creutzfeldt-Jakob disease (Correct Answer)
- B. Subacute sclerosing panencephalitis
- C. Fatal familial insomnia
- D. Cerebral toxoplasmosis
Explanation: ***Creutzfeldt-Jakob disease*** - This is a **prion disease** characterized by rapid cognitive decline, myoclonus, and distinctive EEG changes, with **spongiform degeneration of the cerebral cortex** as the hallmark neuropathological feature [1]. - The spongiform changes are due to intracellular vacuoles within neurons and astrocytes, giving the brain tissue a **spongy appearance** [2]. - CJD shows **widespread cortical involvement**, making it the classic answer for cortical spongiform degeneration [2]. *Subacute sclerosing panencephalitis* - This condition is a rare, **chronic, progressive encephalitis** caused by persistent measles virus infection. - It is characterized by widespread **demyelination, gliosis, and intranuclear inclusion bodies**, but not spongiform degeneration. *Fatal familial insomnia* - This is another **prion disease** that also exhibits spongiform degeneration, but the key difference is **anatomical distribution** [2]. - FFI primarily affects the **thalamus** (a subcortical structure) and causes severe insomnia, dysautonomia, and motor signs [2]. - While spongiform changes occur in FFI, they are most prominent in the **thalamus rather than the cerebral cortex**, making CJD the better answer for cortical spongiform degeneration [2]. *Cerebral toxoplasmosis* - This is an **opportunistic infection of the brain** caused by **_Toxoplasma gondii_**, primarily seen in immunocompromised individuals. - It typically results in the formation of **abscesses or ring-enhancing lesions**, rather than spongiform degeneration. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 712-713. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1284-1286.