Which antibody is primarily associated with warm autoimmune hemolytic anemia (AIHA)?
Which of the following findings is diagnostic of iron deficiency anemia?
What does ristocetin testing indicate in von Willebrand disease?
Which of the following does not predispose to leukemia?
Which subtype of Acute Myeloid Leukemia (AML) is associated with the best prognosis?
Which of the following is not a feature of Poststreptococcal Glomerulonephritis (PSGN)?
In which condition is Tau protein primarily implicated?
Which of the following is true regarding carcinoid tumor?
Which type of thyroid cancer is associated with primary hyperparathyroidism and phaeochromocytoma?
What is the primary effect of beta blockers in the management of thyroid storm?
NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 21: Which antibody is primarily associated with warm autoimmune hemolytic anemia (AIHA)?
- A. IgE
- B. IgM
- C. IgG (Correct Answer)
- D. IgD
Explanation: ***IgG*** - **Warm autoimmune hemolytic anemia (AIHA)** is primarily associated with **IgG antibodies**, which mediate hemolysis at body temperature [1]. - IgG antibodies typically bind to red blood cells and lead to their destruction by the **reticuloendothelial system** [1]. *IgM* - Often involved in **cold agglutinin disease**, not warm AIHA, as it primarily reacts at lower temperatures [2]. - Usually results in **hemolysis** in peripheral areas, like the extremities, rather than at normal body temperature [2]. *IgD* - Known primarily as a marker on **B cells**, it plays a minimal role in hemolytic anemia and is not involved in antibody-mediated hemolysis. - Lack of significant **serological presence** in autoimmune hemolytic processes makes it an unlikely candidate. *IgE* - Primarily associated with **allergic reactions** and parasitic infections rather than autoimmune hemolytic conditions [2]. - Does not typically participate in **hemolysis** or bind to red blood cells in AIHA.
Question 22: Which of the following findings is diagnostic of iron deficiency anemia?
- A. Increased TIBC, decreased serum ferritin (Correct Answer)
- B. Decreased TIBC, decreased serum ferritin
- C. Increased TIBC, increased serum ferritin
- D. Decreased TIBC, increased serum ferritin
Explanation: ***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].
Question 23: What does ristocetin testing indicate in von Willebrand disease?
- A. Normal agglutination
- B. Increased agglutination
- C. No agglutination
- D. Decreased agglutination (Correct Answer)
Explanation: ***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.
Question 24: Which of the following does not predispose to leukemia?
- A. Smoking
- B. Chemical exposure
- C. Alcohol (Correct Answer)
- D. Genetic disorder
Explanation: ***Alcohol*** - Alcohol consumption does not have a well-established association with an increased risk of leukemia compared to other factors. - While excessive alcohol can impact overall health, it is not considered a primary risk factor for developing leukemia. *Chemical exposure* - Certain chemicals, such as **benzene** and **formaldehyde**, are known to be **leukemogenic** and can increase the risk of leukemia. [1] - Occupational exposure to these chemicals has been linked to **acute myeloid leukemia (AML)** and other types of leukemia. [1] *Smoking* - Smoking has been clearly associated with an increased risk of **acute myeloid leukemia (AML)** and other hematologic malignancies. [1] - The toxins in tobacco smoke can cause **DNA damage**, contributing to the development of leukemia. *Genetic disorder* - Certain genetic disorders, like **Down syndrome** and **Fanconi anemia**, are associated with an increased risk of leukemia. - Individuals with these genetic predispositions have a higher likelihood of developing various forms of leukemia.
Question 25: Which subtype of Acute Myeloid Leukemia (AML) is associated with the best prognosis?
- A. Acute myelo monocytic leukemia.
- B. Acute monocytic leukemia.
- C. Erythro leukemia
- D. Acute promyeloblastic leukemia (M3) (Correct Answer)
Explanation: ***Acute promyeloblastic leukemia (M.3)*** [1] - **Best prognosis** in acute myeloid leukemia (AML) is associated with acute promyeloblastic leukemia due to its responsiveness to **all-trans retinoic acid (ATRA)** treatment. [1] - This type often presents with a **prominent coagulopathy**, but successful treatment can lead to **long-term remission**. *Acute monocytic leukemia* - Generally associated with **poor prognosis** and is characterized by a high white blood cell count and organ infiltration. - It lacks the favorable features seen in acute promyeloblastic leukemia, such as effective treatment outcomes. *Erythroleukemia* - Known for having a **poor prognosis** due to its aggressive nature and frequent association with complex chromosomal abnormalities. [1] - Treatment responses are often suboptimal compared to that of acute promyeloblastic leukemia. *Acute myelomonocytic leukemia* - Typically has an **intermediate prognosis** [1] and presents with a mixture of myeloid and monocytic features. - It does not have the same treatment responsiveness and favorable outcomes as seen in acute promyeloblastic leukemia.
Question 26: Which of the following is not a feature of Poststreptococcal Glomerulonephritis (PSGN)?
- A. HTN
- B. Increased urea
- C. Increased creatinine
- D. Normal C3 level (Correct Answer)
Explanation: ***Normal C3 level*** - In Post-streptococcal glomerulonephritis (PSGN), **C3 levels are typically decreased** due to complement consumption during the inflammatory process. [1] - A **normal C3 level** would not be consistent with PSGN, as it suggests no significant complement activation. *Increased urea* - Increased urea can occur due to **impaired renal function**, which is common in PSGN due to glomerular inflammation. [1] - It's a typical finding reflecting the kidneys' inability to excrete waste products properly. *HTN* - Hypertension is frequently associated with PSGN due to **volume overload** and activation of the renin-angiotensin system. [1] [2] - It is a common clinical feature that results from increased fluid retention. *Increased creatinine* - Increased creatinine levels indicate **renal impairment**, which is characteristic of PSGN as kidney function is affected during this condition. [1] - This finding highlights the reduction in glomerular filtration rate (GFR), typical in glomerulonephritis. [2]
Question 27: In which condition is Tau protein primarily implicated?
- A. Lewy body dementia
- B. Picks disease (Correct Answer)
- C. Amyloidosis
- D. Alzheimer's disease
Explanation: Pick's disease - Pick's disease is a **frontotemporal dementia** characterized by aggregates of **hyperphosphorylated tau protein** within neurons, forming **Pick bodies**. - These tau inclusions lead to neuronal degeneration, particularly in the **frontal and temporal lobes**, causing distinct behavioral and language deficits. *Alzheimer's disease* - While **tau protein** is implicated in Alzheimer's disease through the formation of **neurofibrillary tangles**, the primary protein is **beta-amyloid**, which forms plaques [1]. - Alzheimer's disease typically presents with **memory loss** as the predominant initial symptom, unlike Pick's disease [1]. *Lewy body dementia* - Lewy body dementia is primarily characterized by the aggregation of **alpha-synuclein protein** into Lewy bodies within neurons. - While tau pathology can sometimes co-exist, it is not the **primary diagnostic hallmark** of this condition. *Amyloidosis* - Amyloidosis refers to a group of diseases characterized by the abnormal extracellular deposition of **insoluble fibrillar proteins** called amyloids. - The amyloid protein can be derived from various precursors, such as **amyloid light chains** or **serum amyloid A**, which is distinct from tau.
Question 28: Which of the following is true regarding carcinoid tumor?
- A. Associated with serotonin production
- B. Potentially malignant tumor
- C. Neuroendocrine tumor (Correct Answer)
- D. Most common site is lung
Explanation: ### Most common site is lung - Carcinoid tumors are more commonly found in the **gastrointestinal tract**, specifically the appendix and ileum, rather than the lungs [1]. - This statement is false as they can occur in the lungs but are not the most common site overall. ### Potentially malignant tumor - Carcinoid tumors can be classified as **malignant,** especially if they show aggressive behavior or metastasis. - Many carcinoid tumors, particularly those in the gastrointestinal tract, can be **non-functional** and less aggressive [1]. ### Neuroendocrine tumor - Carcinoid tumors are indeed a type of **neuroendocrine tumor**, arising from **neuroendocrine cells**. - This classification emphasizes their origin and potential for secretion of hormones like **serotonin**. ### Associated with serotonin production - Many carcinoid tumors produce **serotonin**, leading to symptoms like **carcinoid syndrome** when they metastasize, particularly to the liver [1]. - This statement is true, indicating their involvement in neuroendocrine secretions.
Question 29: Which type of thyroid cancer is associated with primary hyperparathyroidism and phaeochromocytoma?
- A. Medullary carcinoma of the thyroid (Correct Answer)
- B. Papillary carcinoma of the thyroid
- C. Anaplastic carcinoma of the thyroid
- D. Follicular carcinoma of the thyroid
Explanation: ***Medullary carcinoma of the thyroid*** - Associated with **multiple endocrine neoplasia (MEN) syndrome type 2**, which includes primary hyperparathyroidism and phaeochromocytoma [1]. - Medullary carcinoma arises from **C cells** (parafollicular cells) and is linked with **elevated calcitonin** levels. *Papillary carcinoma of the thyroid* - The most common type of thyroid cancer, but **not associated** with MEN syndromes. - Typically presents as a solitary **nodule** and is linked with **radiation exposure** rather than endocrine syndromes. *Anaplastic carcinoma of the thyroid* - A highly aggressive and undifferentiated form of thyroid cancer, often associated with **poor prognosis**. - Usually arises in older adults and does not have associations with **hyperparathyroidism** or phaeochromocytoma. *Follicular carcinoma of the thyroid* - Characterized by **thyroid follicle formation** and can be associated with **iodine deficiency**, but not with MEN syndromes. - It usually presents as a **solitary thyroid nodule** and lacks connection with **primary hyperparathyroidism**.
Question 30: What is the primary effect of beta blockers in the management of thyroid storm?
- A. Increases metabolism of thyroxine
- B. Blocks thyroxine receptors
- C. Decreases synthesis of thyroxine
- D. Provides rapid relief of symptoms (Correct Answer)
Explanation: Detailed management of thyrotoxic crisis (thyroid storm) is a medical emergency where patients should be given propranolol, either oral or intravenous, to manage life-threatening symptoms [1]. ***Provides rapid relief of symptoms*** - Beta blockers primarily address the **adrenergic manifestations** of thyroid storm, such as **tachycardia**, **tremors**, anxiety, and palpitations [1]. - By blocking **beta-adrenergic receptors**, they provide rapid symptomatic relief and reduce cardiovascular stress, without affecting hormone levels [2]. Thyroid hormones normally increase the expression of genes for beta-adrenergic receptors and G-proteins, leading to increased heart rate and force of contraction [2]. *Increases metabolism of thyroxine* - Beta blockers do not increase the **metabolism** or breakdown of thyroxine; their action is primarily on the **peripheral effects** of thyroid hormones. - While some beta blockers like **propranolol** can inhibit the peripheral conversion of T4 to T3, this is a secondary effect and not their primary role in providing rapid symptomatic relief [1]. *Blocks thyroxine receptors* - Beta blockers do not block **thyroxine receptors**; thyroid hormones exert their effects by binding to intracellular receptors, not adrenergic receptors [2]. - Their action is on the **adrenergic system**, which is overstimulated by the high levels of thyroid hormones. *Decreases synthesis of thyroxine* - Beta blockers do not directly decrease the **synthesis of thyroxine** by the thyroid gland. - That action is performed by **antithyroid drugs** like methimazole and propylthiouracil, which inhibit hormone production [1].