Which of the following is true regarding carcinoid tumor?
In which condition is Tau protein primarily implicated?
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?
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?
Which type of artery is most commonly involved in PAN?
Which of the following is not a feature of Poststreptococcal Glomerulonephritis (PSGN)?
Major contribution to cachexia with advanced cancer?
What is the immediate emergency treatment for carbon monoxide (CO) poisoning?
NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 21: 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 22: 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 23: 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 24: 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].
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: Which type of artery is most commonly involved in PAN?
- A. Muscular (Correct Answer)
- B. Capillaries
- C. Elastic
- D. Arterioles
Explanation: ***Muscular*** - **Polyarteritis nodosa (PAN)** predominantly affects **medium to small-sized muscular arteries**, leading to inflammation, necrosis, and microaneurysms [1]. - This involvement often causes **organ ischemia** and symptoms related to the affected organs, such as the kidneys, gastrointestinal tract, and skin [1]. *Elastic* - **Elastic arteries**, such as the aorta and its major branches, are typically spared in PAN due to their larger size and distinct histological structure. - Diseases like **Takayasu arteritis** or **Giant cell arteritis** are more commonly associated with vasculitis affecting large elastic arteries. *Arterioles* - While arterioles can be affected in various forms of vasculitis, they are not the primary target in classic PAN. - Involvement of arterioles is more characteristic of **microscopic polyangiitis** or **Churg-Strauss syndrome** [2]. *Capillaries* - **Capillaries** are the smallest blood vessels, and their involvement is rare in PAN. - Conditions like **Henoch-Schönlein purpura** or some drug-induced vasculitides more typically affect capillaries, often resulting in palpable purpura [2].
Question 28: 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 29: Major contribution to cachexia with advanced cancer?
- A. Tumor-necrosis-factor (TNF) (Correct Answer)
- B. Histamine
- C. Interferon
- D. Clathrin
Explanation: ***Tumor-necrosis-factor (TNF)*** - **Tumor necrosis factor (TNF-α)** is a prominent cytokine involved in the pathogenesis of cancer cachexia, leading to muscle wasting and weight loss [1]. - It induces inflammation, increases **catabolism**, and reduces anabolism, contributing significantly to the metabolic dysfunction seen in cancer patients [1]. *Histamine* - **Histamine** is primarily known for its role in allergic reactions and inflammatory responses, but it is not a major direct driver of cachexia. - While it can be released in various inflammatory conditions, its direct contribution to the severe muscle wasting and metabolic changes of cachexia is limited compared to other cytokines. *Interferon* - **Interferons (IFNs)** are cytokines typically associated with antiviral responses and immune modulation, which can have diverse effects on metabolism. - While some interferons can indirectly contribute to systemic inflammation and fatigue, they are not considered a primary or major direct mediator of muscle catabolism and fat loss characteristic of cancer cachexia. *Clathrin* - **Clathrin** is a protein involved in the formation of clathrin-coated vesicles, essential for **endocytosis** and intracellular trafficking. - It has no direct role in the systemic metabolic dysregulation or muscle wasting associated with cancer cachexia.
Question 30: What is the immediate emergency treatment for carbon monoxide (CO) poisoning?
- A. 5% CO2 inhalation
- B. 10% CO2 inhalation
- C. High flow O2 (Correct Answer)
- D. Nitroglycerine
Explanation: ***High flow O2*** - **High-flow oxygen** is the immediate emergency treatment for CO poisoning because it helps to displace CO from **hemoglobin**, thereby increasing oxygen delivery to tissues [1], [2]. - CO has a much **higher affinity** for hemoglobin than oxygen, so administering high concentrations of oxygen helps to reverse this binding and accelerate CO elimination [2]. *5% CO2 inhalation* - Administering **CO2** would worsen the patient's condition as it can cause **respiratory acidosis** and increase cerebral blood flow, potentially exacerbating CO toxicity. - CO2 inhalation would not effectively displace **carbon monoxide** from hemoglobin. *10% CO2 inhalation* - Similar to 5% CO2, **10% CO2 inhalation** would be detrimental, leading to significant **acidosis** and further compromising respiratory function. - This treatment does not address the primary issue of **carbon monoxide** binding to **hemoglobin** [2]. *Nitroglycerine* - **Nitroglycerine** is a vasodilator primarily used for conditions like **angina** or **heart failure**; it has no role in treating CO poisoning. - It would not help in displacing **carbon monoxide** or improving tissue oxygenation.