NEET-PG 2015 - Pathology Practice Questions

Q: Characteristic feature of IgA nephropathy?

Serum complement level is normal. ***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.

Q: What is the first cellular response observed after a sharp nerve cut?

Chromatolysis. ***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.

Q: Which chromosomal translocation is associated with follicular thyroid carcinoma?

PAX8 - PPARγ. ***PAX8 - PPARγ*** - The **PAX8-PPARγ fusion oncogene** is a well-established molecular marker directly associated with **follicular thyroid carcinoma (FTC)**. - This translocation leads to the expression of a fusion protein that contributes to **thyroid cell proliferation** and **tumorigenesis**. *ALK - NPM1* - The **ALK-NPM1 fusion** is primarily observed in some types of **anaplastic large cell lymphoma**, not thyroid cancers. - This translocation typically results in an **activated anaplastic lymphoma kinase (ALK)**, driving lymphoproliferation. *ETV6 - NTRK3* - The **ETV6-NTRK3 rearrangement** is characteristic of **secretory carcinoma** (formerly mammary analogue secretory carcinoma), often affecting salivary glands, and is not a common finding in thyroid malignancies. - This fusion leads to the activation of the **NTRK3 receptor tyrosine kinase**, involved in cell growth and survival. *RET - PTC1* - The **RET-PTC1 rearrangement (RET/papillary thyroid carcinoma 1)** is specifically associated with **papillary thyroid carcinoma (PTC)**, which is histologically distinct from follicular thyroid carcinoma. - This fusion activates the **RET proto-oncogene**, promoting cell proliferation and survival in papillary thyroid cancer.

Q: What does ristocetin testing indicate in von Willebrand disease?

Decreased agglutination. ***Decreased agglutination*** - In von Willebrand disease, **ristocetin induces less agglutination** due to a deficiency or dysfunction of von Willebrand factor. - This results in **impaired platelet adhesion** [1], crucial for effective hemostasis. *Increased agglutination* - Would suggest an increased platelet interaction, which is **not characteristic of von Willebrand disease**. - It can occur in conditions with enhanced von Willebrand factor, unlike in this case. *No agglutination* - Suggests complete lack of platelet interaction, which is **not typical** in von Willebrand disease. - There is often some level of interaction, albeit reduced, not a total absence of agglutination. *Normal agglutination* - Indicates no abnormalities, which **contradicts the known pathology** of von Willebrand disease. - Patients typically demonstrate decreased levels of agglutination, not normal findings in this test.

Q: Which of the following is a type of small vessel vasculitis?

Granulomatosis with polyangiitis (GPA). ***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.

Q: Carcinoma originating from glands is called?

Adenocarcinoma. ***Adenocarcinoma*** - Carcinoma that arises from **glandular epithelium** is specifically classified as adenocarcinoma [1]. - It often presents in organs like the **breast**, **prostate**, and **gastrointestinal tract** [4,5]. *Fibrosarcoma* - This is a **malignant tumor** derived from **fibrous connective tissue**, not glands. - Typically occurs in **soft tissues**, and is distinct from epithelial tumors like adenocarcinoma. *Squamous cell carcinoma* - Originates from **squamous epithelial cells** and primarily affects areas such as the **skin** and **mucous membranes** [2]. - It is not associated with glandular structures, differing markedly from adenocarcinoma. *Basal cell carcinoma* - Arises from **basal cells** in the **epidermis** (skin), not from glandular tissue. - It is the most common type of skin cancer and is largely not relevant to glandular origin. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 335-336. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 336-337. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 777-778. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 348-349.

Q: Which of the following findings is diagnostic of iron deficiency anemia?

Increased TIBC, decreased serum ferritin. ***Increased TIBC, decreased serum ferritin*** - **Iron deficiency anemia** is characterized by depleted iron stores, leading to a **decreased serum ferritin** level, which is the most sensitive and specific marker for iron deficiency [4]. - In response to low iron stores, the body upregulates iron absorption and transport mechanisms, resulting in an **increased Total Iron Binding Capacity (TIBC)**, as there are more transferrin molecules available to bind iron [1]. *Decreased TIBC, decreased serum ferritin* - While a **decreased serum ferritin** is consistent with iron deficiency, a **decreased TIBC** is more indicative of **anemia of chronic disease** [1], where the body sequesters iron, leading to reduced iron availability for binding. - In **anemia of chronic disease**, both ferritin (an acute phase reactant) and TIBC can be reduced due to the inflammatory state [1], [2]. *Increased TIBC, increased serum ferritin* - An **increased TIBC** is seen in iron deficiency, but an **increased serum ferritin** indicates adequate or even **overloaded iron stores**, which contradicts the diagnosis of iron deficiency anemia. - High ferritin levels can be seen in conditions like **hemochromatosis** (iron overload) or **inflammation**, where ferritin acts as an acute phase reactant [5]. *Decreased TIBC, increased serum ferritin* - This combination is typical of **anemia of chronic disease**, where inflammation causes **increased serum ferritin** (as an acute phase reactant) and a **decreased TIBC** due to reduced production of transferrin [1]. - In this type of anemia, iron is often trapped within macrophages, making it unavailable for erythropoiesis despite seemingly normal or elevated stores [3].

Q: Which genetic condition is considered the most lethal due to monosomy?

Autosomal monosomy. ***Autosomal monosomy*** - **Autosomal monosomy** is the most lethal form of monosomy because it involves the loss of an entire autosome, leading to a severe imbalance in gene dosage. [1] - The human body cannot typically survive with the loss of a whole autosome, resulting in early embryonic or fetal demise. [1] *Chromosomal monosomy* - This is a broader term that includes both **autosomal monosomy** and **sex chromosome monosomy**. - While many forms of chromosomal monosomy are lethal, **sex chromosome monosomy (e.g., Turner syndrome)** is survivable, making the general term "chromosomal monosomy" less specific for the *most lethal* condition. [1] *Autosomal trisomy* - **Autosomal trisomy** involves an extra copy of an autosome (e.g., Trisomy 21 for Down syndrome), which, while causing significant health issues, is generally less lethal than the complete loss of an autosome. [1] - Many individuals with autosomal trisomies can survive to birth and beyond, unlike most cases of autosomal monosomy. [1] *Chromosomal trisomy* - This refers to having an extra copy of any chromosome, including **autosomes** and **sex chromosomes**. - While conditions like **Trisomy 13 (Patau syndrome)** and **Trisomy 18 (Edwards syndrome)** are highly lethal, the presence of *extra* genetic material is typically less universally lethal than the *absence* of an entire autosome. [1] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 168-169.

Q: What does Ghon's focus indicate in the context of tuberculosis?

Primary complex. ***Primary complex*** - A **Ghon's focus** is the initial parenchymal lesion (typically subpleural) that develops during primary tuberculosis infection [1]. - The Ghon's focus, together with an enlarged regional lymph node (usually hilar or mediastinal), forms the **Ghon's complex** or **Primary complex** [2]. - When this complex undergoes calcification and healing, it is called a **Ranke complex**, which indicates past healed primary TB. *Post primary tuberculosis* - Also known as **reactivation tuberculosis** or **secondary tuberculosis**, this typically occurs years after the primary infection, usually in the apices of the lungs [2]. - It represents reactivation of dormant bacilli, not the initial primary infection lesion. - Characterized by cavitary lesions and often more severe pulmonary symptoms. *Miliary tuberculosis* - This is a form of progressive, widespread tuberculosis characterized by the presence of **tiny, millet-seed sized lesions** disseminated throughout the body via hematogenous spread [3]. - It indicates a severe and life-threatening form of TB resulting from massive lymphohematogenous dissemination. - Not related to the localized primary complex. *Tuberculous lymphadenitis* - This refers to **tuberculous infection of lymph nodes**, most commonly in the cervical region (scrofula). - While lymph node involvement is part of the primary complex, Ghon's focus specifically refers to the **parenchymal lung lesion**, not the lymph node component alone [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 379-380. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 319-320. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 320-321.

Question 1

Characteristic feature of IgA nephropathy?

Accepted Answer

Serum complement level is normal

Answer

More common in old age

Answer

It is a type of membranoproliferative GN

Answer

Gross hematuria presents after 10 days

Question 2

What is the first cellular response observed after a sharp nerve cut?

Accepted Answer

Chromatolysis

Answer

Polymorphic arrangement

Answer

Increased protein synthesis

Answer

Macrophage activation

Question 3

Which chromosomal translocation is associated with follicular thyroid carcinoma?

Accepted Answer

PAX8 - PPARγ

Answer

ALK - NPM1

Answer

ETV6 - NTRK3

Answer

RET - PTC1

Question 4

What does ristocetin testing indicate in von Willebrand disease?

Accepted Answer

Decreased agglutination

Answer

Normal agglutination

Answer

Increased agglutination

Answer

No agglutination

Question 5

Which of the following is a type of small vessel vasculitis?

Accepted Answer

Granulomatosis with polyangiitis (GPA)

Answer

Classical PAN

Answer

Giant cell arteritis

Answer

None of the options

Question 6

Carcinoma originating from glands is called?

Accepted Answer

Adenocarcinoma

Answer

Basal cell carcinoma

Answer

Squamous cell carcinoma

Answer

Fibrosarcoma

Question 7

Which of the following findings is diagnostic of iron deficiency anemia?

Accepted Answer

Increased TIBC, decreased serum ferritin

Answer

Decreased TIBC, decreased serum ferritin

Answer

Increased TIBC, increased serum ferritin

Answer

Decreased TIBC, increased serum ferritin

Question 8

Which genetic condition is considered the most lethal due to monosomy?

Accepted Answer

Autosomal monosomy

Answer

Chromosomal monosomy

Answer

Autosomal trisomy

Answer

Chromosomal trisomy

Question 9

What does Ghon's focus indicate in the context of tuberculosis?

Accepted Answer

Primary complex

Answer

Post primary tuberculosis

Answer

Miliary tuberculosis

Answer

Tuberculous lymphadenitis

Question 10

Which of the following is not considered an example of excess tissue growth?

Accepted Answer

Granulation tissue

Answer

Neoplasia

Answer

Hyperplasia

Answer

Fibrosis

NEET-PG 2015 — Pathology