In which condition is Tau protein primarily implicated?
Which of the following is true regarding carcinoid tumor?
Which of the following does not predispose to leukemia?
Shrinking Lung Syndrome is seen in:
Which of the following is a cause of post-transplantation hypertension? I. Rejection II. Cyclosporine nephrotoxicity III. Renal transplant artery stenosis (RTAS) IV. Recurrent disease in the allograft. Select the correct option.
Which of the following statements is false regarding the declaration of brain stem death in a hospital?
What does ristocetin testing indicate in von Willebrand disease?
Extremities are warm in which type of shock
Which antibody is primarily associated with warm autoimmune hemolytic anemia (AIHA)?
Which of the following findings is diagnostic of iron deficiency anemia?
NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 21: 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 22: 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 23: 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 24: Shrinking Lung Syndrome is seen in:
- A. SLE (Correct Answer)
- B. Rheumatoid Arthritis
- C. Scleroderma
- D. Sarcoidosis
Explanation: ***SLE*** - **Shrinking lung syndrome (SLS)** is a rare but recognized pulmonary manifestation of **systemic lupus erythematosus (SLE)** [1]. - It is characterized by **dyspnea**, **pleuritic chest pain**, and elevated diaphragms with reduced lung volumes, often without significant interstitial lung disease [1]. *Rheumatoid Arthritis* - While **rheumatoid arthritis** can cause various lung manifestations like **interstitial lung disease (ILD)**, pleural effusions, and rheumatoid nodules, **shrinking lung syndrome** is not typically associated with it [2]. - Lung disease in RA often involves **pulmonary fibrosis** or bronchiolitis, differing from the restrictive physiology of SLS. *Scleroderma* - **Scleroderma (Systemic Sclerosis)** commonly affects the lungs, primarily leading to **interstitial lung disease (ILD)** and **pulmonary hypertension** [1]. - **Shrinking lung syndrome**, with its characteristic restrictive pattern and elevated diaphragms, is not a typical presentation of lung involvement in scleroderma. *Sarcoidosis* - **Sarcoidosis** is characterized by the formation of **non-caseating granulomas**, primarily affecting the lungs and lymph nodes. - Lung involvement in sarcoidosis typically presents as **interstitial lung disease** or nodular infiltrates, not the distinct features of **shrinking lung syndrome** [3].
Question 25: Which of the following is a cause of post-transplantation hypertension? I. Rejection II. Cyclosporine nephrotoxicity III. Renal transplant artery stenosis (RTAS) IV. Recurrent disease in the allograft. Select the correct option.
- A. None of the above are correct causes.
- B. I, II, and IV are correct causes.
- C. I and III are correct causes.
- D. All of the options are correct causes of post-transplantation hypertension. (Correct Answer)
Explanation: ***All of the options are correct causes of post-transplantation hypertension.*** - Post-transplantation hypertension often has a multifactorial etiology, with **rejection**, **cyclosporine nephrotoxicity**, **renal transplant artery stenosis (RTAS)**, and **recurrent disease in the allograft** all being significant contributors. - Each of these conditions can lead to mechanisms that elevate blood pressure, such as **renal ischemia**, activation of the **renin-angiotensin system**, and inflammatory responses affecting renal function. *I, II, and IV are correct causes.* - This option is incorrect because it excludes **renal transplant artery stenosis (RTAS)** (III), which is a well-established cause of secondary hypertension in transplant recipients due to reduced blood flow to the allograft. - **RTAS** activates the renin-angiotensin-aldosterone system (RAAS), leading to **vasoconstriction** and **sodium retention**, contributing to hypertension. *I and III are correct causes.* - This option is incorrect as it omits other crucial causes like **cyclosporine nephrotoxicity** (II) and **recurrent disease in the allograft** (IV), both of which are documented contributors to post-transplantation hypertension. - **Cyclosporine nephrotoxicity** causes afferent arteriolar vasoconstriction and glomerulosclerosis, directly increasing blood pressure. *None of the above are correct causes.* - This option is incorrect because **rejection**, **cyclosporine nephrotoxicity**, **renal transplant artery stenosis (RTAS)**, and **recurrent disease in the allograft** are all recognized and significant causes of post-transplantation hypertension. - Each condition has distinct pathological mechanisms that contribute to **elevated blood pressure** in transplant recipients.
Question 26: Which of the following statements is false regarding the declaration of brain stem death in a hospital?
- A. Presence of neurologist is not required
- B. Drug overdose should be ruled out
- C. All of the above (Correct Answer)
- D. Patient must be in coma
Explanation: ***All of the above*** - This option indicates that all the preceding statements are false. Let's analyze why each individual statement is indeed false in the context of brain stem death declaration [1]. - This implies there is a misunderstanding regarding each aspect of brain stem death criteria, which often requires specific conditions like a neurologist's involvement (though not always strictly mandatory in all protocols), ruling out drug overdose, and the patient being in a coma. *Presence of neurologist is not required* - This statement is false because while it's not universally mandated that a neurologist be one of the two certifying doctors, one of them must be a **senior physician (consultant)** and both must be experienced in brain stem death diagnosis. - In many settings, especially for complex cases or where local protocols specify, a neurologist or neurosurgeon's involvement is highly recommended or required to confirm brain stem death. *Drug overdose should be ruled out* - This statement is false because the absence of drugs that could **mimic brain stem death (e.g., sedatives, muscle relaxants)** is a crucial precondition for testing [3]. - It is essential to ensure that the patient's neurological state is not confounded by reversible causes like drug intoxication before proceeding with brain stem death tests [3]. *Patient must be in coma* - This statement is false because while a patient declared brain stem dead will indeed be in a coma, the criteria for **brain stem death** specifically focus on the irreversible cessation of brainstem function [1], not merely a comatose state [2]. - A coma is a precondition for assessing brain stem death, but the declaration itself requires specific tests demonstrating the absence of **brainstem reflexes** [4] and **apnea** [3], confirming the permanent loss of brainstem activity.
Question 27: 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 28: Extremities are warm in which type of shock
- A. Hypovolemic shock
- B. Neurogenic shock (Correct Answer)
- C. Anaphylactic shock
- D. Cardiogenic shock
Explanation: ***Neurogenic shock*** - This type of shock is caused by a loss of **sympathetic tone**, leading to widespread **vasodilation** and a relative hypovolemia, resulting in warm, flushed extremities. - The decreased systemic vascular resistance causes **blood pooling** in the periphery rather than being shunted to vital organs, contributing to the warm skin. *Hypovolemic shock* - Characterized by **decreased blood volume**, leading to activation of the sympathetic nervous system and **vasoconstriction** to shunt blood to vital organs. - This results in **cold, clammy extremities** due to reduced peripheral perfusion. *Anaphylactic shock* - An acute, life-threatening hypersensitivity reaction involving massive release of inflammatory mediators, causing widespread **vasodilation** and increased vascular permeability. - While it can cause flushing and warmth initially due to vasodilation, it often leads to significant fluid shifts and can present with both warm and then cool, clammy skin as shock progresses. *Cardiogenic shock* - Caused by **severe cardiac pump failure**, leading to decreased cardiac output and poor tissue perfusion. - The body's compensatory mechanisms, including sympathetic activation, cause **peripheral vasoconstriction**, leading to **cold, clammy extremities**.
Question 29: 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 30: 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].