NEET-PG 2021 Practice Questions

Q: A patient presents with generalized and easy fatigability. He reports weakness while working in a factory with exposure to benzene. Which of the following conditions should be suspected in this patient?

Leukemia. ***Leukemia*** - **Benzene exposure** is a well-established risk factor for developing **leukemia**, particularly acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS). - **Generalized fatigue** and **easy fatigability** are common symptoms of leukemia, resulting from anemia, bone marrow infiltration, and systemic effects of the disease. - Benzene is classified as a **Group 1 carcinogen** by IARC with strong evidence for leukemogenesis. *Aplastic Anemia* - While benzene exposure can cause **aplastic anemia** (bone marrow failure), this condition typically presents with **pancytopenia** and more severe symptoms including bleeding and infections. - However, given the occupational exposure and symptoms, **leukemia** remains the primary concern as it is more commonly associated with chronic benzene exposure. - Aplastic anemia from benzene is less common than benzene-induced leukemia. *Hepatocellular Carcinoma* - While benzene exposure can be **hepatotoxic**, it is not primarily associated with an increased risk of **Hepatocellular Carcinoma**. - Risk factors for hepatocellular carcinoma include **chronic viral hepatitis** (HBV, HCV) and **alcoholism**. *Carcinoma Gall Bladder* - There is **no significant association** between benzene exposure and the development of **gallbladder cancer**. - Risk factors for gallbladder cancer include **gallstones**, porcelain gallbladder, and chronic inflammation. *Urinary Bladder Cancer* - **Aromatic amines** and **anilines** (often found in dye, rubber, and chemical industries) are established causes of bladder cancer, not typically benzene itself. - While benzene is a carcinogen, **bladder cancer** is not considered a primary or strong association with its exposure.

Q: All are increased in IDA except

Transferrin saturation. ***Transferrin saturation*** - In **iron deficiency anemia (IDA)**, there is insufficient iron to saturate transferrin, leading to a **decreased** transferrin saturation. This is the exception among the given options. - Transferrin saturation is calculated as (serum iron / TIBC) x 100, and both **serum iron** and its percentage saturation are low in IDA. *TIBC* - **Total iron-binding capacity (TIBC)** is typically **increased** in IDA as the liver produces more transferrin in an attempt to capture more iron [1]. - This elevated TIBC reflects the body's compensatory mechanism to maximize available iron uptake. *Soluble transferrin receptor* - **Soluble transferrin receptor (sTfR)** levels are **elevated** in IDA because iron-deficient erythroblasts upregulate the production of transferrin receptors on their surface as they try to scavenge more iron. - The elevated sTfR is a sensitive and specific marker for **iron deficiency**, particularly useful in differentiating IDA from anemia of chronic disease [1]. *Erythropoietin* - **Erythropoietin (EPO)** levels are **increased** in IDA due to the kidney's response to the decreased oxygen-carrying capacity of the blood (anemia) [1]. - EPO stimulates the bone marrow to produce more red blood cells, which exacerbates the demand for iron, often leading to further iron depletion if iron stores are low.

Q: Which of the following is considered a poor prognostic marker in multiple myeloma (MM)?

B2 microglobulins. ***B2 microglobulins*** - Elevated levels of **B2 microglobulin** are a significant indicator of increased tumor burden and are used in the **International Staging System (ISS)** for multiple myeloma, correlating with shorter survival [1]. - This protein is present on the surface of most nucleated cells and its accumulation reflects **renal impairment** or increased cell turnover. *Serum Creatinine* - While elevated **serum creatinine** can indicate **renal insufficiency**, a common complication in MM, it is not a direct measure of tumor burden or aggression in the same way as B2 microglobulin [1]. - **Renal failure** can be a poor prognostic factor in MM, but creatinine itself is a marker of organ damage rather than disease progression or malignancy. *Hypercalcemia* - **Hypercalcemia** is a common complication in MM due to increased **bone resorption**, but it is generally manageable and not considered a primary prognostic marker for disease aggressiveness itself. - While severe hypercalcemia can contribute to overall morbidity, its presence doesn't directly stage the disease or predict survival as significantly as B2 microglobulin. *Telomerase* - **Telomerase** is an enzyme involved in maintaining telomere length and is often overexpressed in various cancers, including MM, allowing cells to proliferate indefinitely. - While it plays a role in the **pathogenesis** of MM, its utility as a prognostic marker in routine clinical practice is not as established or as widely used as B2 microglobulin.

Q: An 18-year-old male presents to the OPD with gum bleeding, fever, low total leukocyte count (TLC), and low platelet count. General examination is unremarkable. Further investigations reveal a low reticulocyte count, absent megakaryocytes, and no immature cells in the bone marrow. What is the most likely diagnosis?

Aplastic anemia. ***Aplastic anemia*** - This condition is characterized by **pancytopenia** (low TLC and platelet count, implied low red blood cell count by low reticulocyte count) due to **bone marrow failure**. - The absence of **megakaryocytes** and other immature cells in the bone marrow confirms the **hypocellularity** typical of aplastic anemia. *Immune Thrombocytopenic Purpura (ITP)* - While ITP presents with **low platelet count** and potential gum bleeding [1], the bone marrow typically shows **normal or increased megakaryocytes**. - ITP does not explain the **low total leukocyte count** or low reticulocyte count seen in this patient [1]. *Myelodysplastic Syndrome (MDS)* - MDS involves **ineffective hematopoiesis** and can present with cytopenias, but the bone marrow is usually **hypercellular or normocellular** with dysplastic changes. - The absence of immature cells and overall hypoplasia does not fit the typical picture of MDS. *Acute Myeloid Leukemia (AML)* - AML is characterized by an overproduction of **immature myeloid cells (blasts)** [3], which are conspicuously absent in this patient's bone marrow description. - While AML can cause pancytopenia, the presence of **immature cells** in the bone marrow is its hallmark [3]. Gum hypertrophy is also a common clinical sign in AML [2].

Q: A chronic alcoholic patient presents with increasing abdominal girth. A liver biopsy reveals reddish inclusions within the hepatocytes. What are these inclusions composed of?

Intermediate filaments. ***Intermediate filaments*** - In chronic alcoholic patients, reddish inclusions within hepatocytes are characteristic of **Mallory bodies** (also known as alcoholic hyaline) [1]. - Mallory bodies are aggregates of **intermediate filaments**, specifically **cytokeratin filaments**, that have been damaged. *Hemosiderin* - **Hemosiderin** is an iron-storage complex and appears as **golden-brown granules** within cells [1]. - While iron overload can occur in alcoholic liver disease, hemosiderin is not the primary component of the reddish inclusions described as Mallory bodies. *Triglycerides* - **Triglycerides** accumulate in hepatocytes in **fatty liver disease** (steatosis), which is common in alcoholics [1]. - These appear as clear lipid vacuoles rather than reddish inclusions. *Glycogen* - **Glycogen** is a branched polysaccharide of glucose, found in the cytoplasm, and appears as clear vacuoles or small, periodic acid-Schiff (PAS)-positive granules. - Hepatic glycogen accumulation is not described as reddish inclusions in the context of alcoholic liver disease. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 388-390.

Q: A woman on Pap smear shows disorganized growth of cells with hyperchromatic nuclei. Which phenomenon is occurring here?

Dysplasia. ***Dysplasia*** - **Dysplasia** refers to disordered growth and maturation of cells, often characterized by **cellular pleomorphism**, **loss of architectural orientation**, **nuclear hyperchromatism**, and increased mitotic activity [1]. - In a Pap smear, these features are indicative of **precancerous changes** in the cervical epithelium, requiring further investigation [2]. *Metaplasia* - **Metaplasia** is the reversible replacement of one differentiated cell type with another, often in response to chronic irritation [2]. - While it can be a precursor to dysplasia, metaplasia itself involves mature, well-differentiated cells, not the **disorganized growth** and **hyperchromatic nuclei** described. *Hypertrophy* - **Hypertrophy** is an increase in the size of cells, leading to an increase in the size of the organ. - This process involves mature cells and does not include the characteristic **disorganized growth** or nuclear abnormalities seen in the question. *Carcinoma* - **Carcinoma** is a malignant tumor derived from epithelial cells, characterized by uncontrolled growth and invasion. - While the described changes could progress to carcinoma, the term carcinoma implies **frank malignancy** with invasive potential, whereas dysplasia refers to **precancerous changes** (CIN I, II, III) [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1007-1010. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Female Genital Tract Disease, pp. 467-468.

Q: HNPCC has defect in which

Mismatch repair gene. ***Mismatch repair gene*** - **HNPCC (hereditary non-polyposis colorectal cancer)**, also known as Lynch syndrome, is caused by inherited mutations in genes responsible for **DNA mismatch repair** [1]. - These genes, such as **MLH1, MSH2, MSH6, and PMS2**, normally correct errors that occur during DNA replication, preventing the accumulation of mutations. *Base pair excision* - **Base excision repair** is a distinct DNA repair pathway that primarily fixes small base lesions, such as damaged or modified bases. - This mechanism is not primarily implicated in the development of HNPCC. *Point mutation* - A **point mutation** refers to a single nucleotide change in a DNA sequence, which can be the *result* of a defective repair mechanism but is not the defect itself. - While mismatch repair defects lead to an increased rate of point mutations, the underlying *defect* in HNPCC is in the repair system, not in the mutation type. *Nucleotide excision* - **Nucleotide excision repair** is a major pathway for removing bulky, helix-distorting DNA lesions, such as those caused by UV radiation. - Defects in this pathway are associated with conditions like **xeroderma pigmentosum**, not HNPCC. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 817.

Q: In a patient with general fatigue, normal TLC/ DLC, and superficial discrete lymphadenopathy, with lymph node biopsy showing effaced architecture, atypical cells with indented nuclei and prominent nucleoli, positive for CD10 and BCL-2, which of the following is the most likely diagnosis?

Follicular Lymphoma. ***Follicular Lymphoma*** - The description of **atypical cells with indented nuclei** (cleaved cells) and **prominent nucleoli**, along with **CD10** and **BCL-2 positivity**, are classic features of follicular lymphoma [1], [2]. - **Effaced architecture** of the lymph node, and **superficial discrete lymphadenopathy** in an adult, further support this diagnosis [1]. *Mycosis Fungoides* - This is a **cutaneous T-cell lymphoma** characterized by skin lesions (patches, plaques, tumors) and rarely involves lymph nodes in the early stages. - It would show **CD3+ T-cells** on immunophenotyping, not CD10+ B-cells. *Burkitt's Lymphoma* - Characterized by rapidly growing tumors and a **"starry sky"** histological pattern with numerous macrophages [3]. - While it is CD10 positive, it would typically be **BCL-2 negative** due to the specific translocation involved (t(8;14) c-MYC/IgH). *Hodgkin Lymphoma* - Defined by the presence of **Reed-Sternberg cells** (large, multinucleated cells with prominent nucleoli, often described as "owl's eye" appearance). - These cells are typically **CD15+ and CD30+**, and BCL-2 expression is less specific and CD10 is not characteristic. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 561-562. [2] 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. 602-604. [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, p. 606.

Q: A child accidentally ingested a fruit from a tree while playing. After the ingestion, he presented with symptoms of restlessness, painful swallowing, photophobia, dry skin, urinary retention, and elevated body temperature. What is the most likely cause of poisoning, and what is the appropriate antidote for it?

Datura poisoning & Physostigmine. ***Datura poisoning & Physostigmine*** - The symptoms of **restlessness, painful swallowing, photophobia, dry skin, urinary retention, and elevated body temperature** are classic signs of **anticholinergic toxicity**, which is characteristic of **Datura poisoning**. - **Physostigmine** is an **acetylcholinesterase inhibitor** that increases acetylcholine levels, effectively reversing the anticholinergic effects of Datura. *Yellow Oleander poisoning & Atropine* - **Yellow Oleander poisoning** primarily causes **cardiac effects** (e.g., bradycardia, arrhythmias) due to cardiac glycosides, not the anticholinergic symptoms described. - **Atropine** is an **anticholinergic agent** and would worsen the symptoms of Datura poisoning rather than being an antidote for it. *Datura poisoning & Pralidoxime* - While **Datura poisoning** is correct given the symptoms, **Pralidoxime** is an antidote for **organophosphate poisoning**, acting as a cholinesterase reactivator, and has no efficacy in anticholinergic toxicity. *Organophosphate poisoning & Pralidoxime* - **Organophosphate poisoning** presents with **cholinergic symptoms** (e.g., salivation, lacrimation, urination, defecation, GI upset, emesis, miosis, bronchospasm, bradycardia), which are opposite to the anticholinergic signs seen here. - Although **Pralidoxime** is a correct antidote for organophosphate poisoning, the clinical picture does not support this diagnosis. *Mushroom (Amanita) poisoning & Atropine* - **Certain mushroom poisonings** (e.g., muscarine-containing mushrooms like *Inocybe* and *Clitocybe* species) cause **cholinergic symptoms** (salivation, sweating, miosis, bradycardia), not anticholinergic symptoms. - While **Atropine** would be the correct antidote for muscarinic mushroom poisoning, the clinical presentation here shows anticholinergic toxicity, not cholinergic excess.

Q: What is the mechanism of action of Tocilizumab?

Inhibits binding of IL-6 to its receptor IL-6R. ***Inhibits binding of IL-6 to its receptor IL-6R*** - **Tocilizumab** is a **monoclonal antibody** that specifically targets the **interleukin-6 (IL-6) receptor**. - By blocking IL-6 from binding to its receptor, Tocilizumab **inhibits IL-6 mediated signaling**, thereby reducing inflammation and immune responses. *TNF Alpha inhibition* - **TNF-alpha inhibitors** (e.g., adalimumab, infliximab) target **tumor necrosis factor-alpha**, a different pro-inflammatory cytokine. - While both TNF-alpha and IL-6 are involved in inflammatory diseases, their signaling pathways and therapeutic targets are distinct. *IL-18 inhibition* - **IL-18** is another pro-inflammatory cytokine, but Tocilizumab does **not directly target** or inhibit its activity. - Drugs that target IL-18 or its pathways are distinct from those targeting IL-6. *IL-17 inhibition* - **IL-17 inhibitors** (e.g., secukinumab, ixekizumab) are biologics that target **interleukin-17**, particularly useful in psoriasis and ankylosing spondylitis. - Tocilizumab's mechanism is specific to **IL-6**, not IL-17. *Inhibits binding of IL-1* - **Interleukin-1 (IL-1)** is a key mediator of inflammation, but specific **IL-1 inhibitors** (e.g., anakinra, canakinumab) act by blocking IL-1 or its receptor. - Tocilizumab's mechanism is specific to the **IL-6 cytokine-receptor interaction**, not IL-1.

Question 1

A patient presents with generalized and easy fatigability. He reports weakness while working in a factory with exposure to benzene. Which of the following conditions should be suspected in this patient?

Accepted Answer

Leukemia

Answer

Hepatocellular Carcinoma

Answer

Carcinoma Gall Bladder

Answer

Urinary Bladder Cancer

Answer

Aplastic Anemia

Question 2

All are increased in IDA except

Accepted Answer

Transferrin saturation

Answer

TIBC

Answer

Soluble transferrin receptor

Answer

Erythropoietin

Question 3

Which of the following is considered a poor prognostic marker in multiple myeloma (MM)?

Accepted Answer

B2 microglobulins

Answer

Serum Creatinine

Answer

Hypercalcemia

Answer

Telomerase

Question 4

An 18-year-old male presents to the OPD with gum bleeding, fever, low total leukocyte count (TLC), and low platelet count. General examination is unremarkable. Further investigations reveal a low reticulocyte count, absent megakaryocytes, and no immature cells in the bone marrow. What is the most likely diagnosis?

Accepted Answer

Aplastic anemia

Answer

Immune Thrombocytopenic Purpura (ITP)

Answer

Myelodysplastic Syndrome (MDS)

Answer

Acute Myeloid Leukemia (AML)

Question 5

A chronic alcoholic patient presents with increasing abdominal girth. A liver biopsy reveals reddish inclusions within the hepatocytes. What are these inclusions composed of?

Accepted Answer

Intermediate filaments

Answer

Hemosiderin

Answer

Triglycerides

Answer

Glycogen

Question 6

A woman on Pap smear shows disorganized growth of cells with hyperchromatic nuclei. Which phenomenon is occurring here?

Accepted Answer

Dysplasia

Answer

Metaplasia

Answer

Hypertrophy

Answer

Carcinoma

Question 7

HNPCC has defect in which

Accepted Answer

Mismatch repair gene

Answer

Base excision repair

Answer

Point mutation

Answer

Nucleotide excision repair

Question 8

In a patient with general fatigue, normal TLC/ DLC, and superficial discrete lymphadenopathy, with lymph node biopsy showing effaced architecture, atypical cells with indented nuclei and prominent nucleoli, positive for CD10 and BCL-2, which of the following is the most likely diagnosis?

Accepted Answer

Follicular Lymphoma

Answer

Mycosis Fungoides

Answer

Burkitt's Lymphoma

Answer

Hodgkin Lymphoma

Question 9

A child accidentally ingested a fruit from a tree while playing. After the ingestion, he presented with symptoms of restlessness, painful swallowing, photophobia, dry skin, urinary retention, and elevated body temperature. What is the most likely cause of poisoning, and what is the appropriate antidote for it?

Accepted Answer

Datura poisoning & Physostigmine

Answer

Yellow Oleander poisoning & Atropine

Answer

Datura poisoning & Pralidoxime

Answer

Organophosphate poisoning & Pralidoxime

Answer

Mushroom (Amanita) poisoning & Atropine

Question 10

What is the mechanism of action of Tocilizumab?

Accepted Answer

Inhibits binding of IL-6 to its receptor IL-6R

Answer

TNF Alpha inhibition

Answer

IL-18 inhibition

Answer

Inhibits binding of IL-1

Answer

IL-17 inhibition

NEET-PG 2021

Internal Medicine

Pathology

Pharmacology