What does the measurement of Glomerular Filtration Rate (GFR) help determine in kidney function?
Diabetic foot is associated with following type of gangrene -
Extremities are warm in which type of shock
In which condition is Serum Amyloid Associated (SAA) protein most commonly found?
Shrinking Lung Syndrome is seen in:
What is the mode of inheritance for the most common form of hypophosphatemic rickets?
In which non-neoplastic condition is CEA commonly elevated?
Major contribution to cachexia with advanced cancer?
Which type of artery is most commonly involved in PAN?
Which of the following statements about sickle cell disease is true?
NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 11: What does the measurement of Glomerular Filtration Rate (GFR) help determine in kidney function?
- A. Heart rate
- B. Recovery from shock
- C. Stage of kidney disease (Correct Answer)
- D. Blood volume
Explanation: Stage of kidney disease - A low GFR indicates impaired kidney function, helping to classify the severity and stage of chronic kidney disease (CKD) [1]. - Monitoring GFR over time is crucial for assessing disease progression and guiding treatment strategies [1]. *Heart rate* - Heart rate is a measure of cardiac function and is not directly assessed by GFR. - Kidney function can indirectly affect heart rate over time (e.g., in advanced kidney disease with fluid overload), but GFR itself doesn't measure it. *Recovery from shock* - While kidney function is important during shock, GFR primarily measures the kidney's filtration capacity at a given moment. - Recovery from shock involves many physiological parameters beyond just kidney filtration, such as blood pressure and organ perfusion. *Blood volume* - Blood volume is regulated by many mechanisms, including hormonal systems (e.g., renin-angiotensin-aldosterone system) and fluid intake/excretion. - Although kidneys play a role in fluid balance, GFR specifically measures the rate of filtration of blood plasma, not the overall blood volume [1].
Question 12: Diabetic foot is associated with following type of gangrene -
- A. Dry gangrene
- B. Wet gangrene (Correct Answer)
- C. Gas gangrene
- D. Fournier's gangrene
Explanation: ***Wet gangrene*** - Diabetic foot commonly leads to **ischemia** and **infection** [1], resulting in wet gangrene characterized by moist, necrotic tissue. - This type of gangrene is associated with **rapid progression** and can result in systemic toxicity, making prompt treatment essential. *Fournier's gangrene* - This type of gangrene specifically affects the **perineal** region and is not directly associated with diabetic foot. - It usually arises from infections related to **perineal trauma** or surgical procedures. *Gas gangrene* - Caused by **Clostridium** species and typically follows a traumatic injury or surgical procedure, not specifically related to diabetes. - Presents with **crepitus** and rapid systemic symptoms, different from the chronic nature of diabetic ulcers. *Dry gangrene* - Associated with **chronic ischemia** and necrosis, it occurs in conditions like peripheral arterial disease, not primarily with infections seen in diabetic foot [1]. - It usually develops gradually without the sudden onset of symptoms characteristic of wet gangrene.
Question 13: 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 14: In which condition is Serum Amyloid Associated (SAA) protein most commonly found?
- A. Alzheimer's disease
- B. Malignant hypertension
- C. Chronic inflammatory states (Correct Answer)
- D. Chronic renal failure
- E. Acute myocardial infarction
Explanation: ***Chronic inflammatory states*** [1][2] - Serum amyloid-associated protein is elevated in response to **chronic inflammation**, such as in rheumatic diseases and infections [1][2]. - It serves as a **biomarker** indicating systemic inflammation and is part of the **acute-phase response** [1]. *Chronic renal failure* - While renal failure can lead to amyloidosis, it is not a direct cause of serum amyloid-associated protein elevation. - **Renal impairment** is more associated with a decrease in clearance rather than production of amyloid proteins. *Alzheimer's disease* - Although amyloid plaques are a hallmark of Alzheimer's, they are related to **A-beta peptide**, not serum amyloid-associated protein. - Alzheimer's pathology primarily involves **neurodegeneration** rather than inflammatory response. *Malignant hypertension* - Malignant hypertension primarily affects the **vascular system** and does not directly involve the production of serum amyloid-associated protein. - It is characterized by end-organ damage, rather than a state of chronic inflammation. *Chronic inflammatory conditions like RA, TB & leprosy, osteomyelitis, ankylosing spondylitis, IBD, bronchiectasis, some tumors* [1][2] - While these conditions can be associated with systemic inflammation, they are too specific and do not comprehensively encompass the broader concept of **chronic inflammatory states**. - This option fails to highlight that serum amyloid-associated protein is a marker for **various chronic inflammatory states** beyond just those listed [1].
Question 15: 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 16: What is the mode of inheritance for the most common form of hypophosphatemic rickets?
- A. Autosomal Recessive (AR)
- B. Autosomal Dominant (AD)
- C. X-Linked Recessive (XR)
- D. X-Linked Dominant (XD) (Correct Answer)
Explanation: ***X-Linked Dominant (XD)*** - The most common form of hypophosphatemic rickets is **X-linked hypophosphatemic rickets (XLH)**, which is inherited in an X-linked dominant pattern. - This condition is caused by mutations in the **PHEX gene** on the X chromosome, leading to impaired phosphate reabsorption in the kidneys. *Autosomal Recessive (AR)* - While some rare forms of hypophosphatemic rickets exist with **autosomal recessive** inheritance, they are not the most common. - These forms typically involve mutations in genes affecting phosphate transport or vitamin D metabolism, distinct from the primary defect in XLH. *Autosomal Dominant (AD)* - There are also rare **autosomal dominant** forms of hypophosphatemic rickets, such as hereditary hypophosphatemic rickets with hypercalciuria (HHRH) or autosomal dominant hypophosphatemic rickets (ADHR). - However, these are less common than the X-linked dominant form (XLH). *X-Linked Recessive (XR)* - **X-linked recessive** inheritance typically affects males more severely and exclusively, with carrier females usually unaffected or mildly affected. - In X-linked dominant conditions like XLH, both males and females are affected, though females may exhibit variable expressivity.
Question 17: In which non-neoplastic condition is CEA commonly elevated?
- A. Pancreatitis
- B. Inflammatory bowel disease (Correct Answer)
- C. Hemolytic anemia
- D. Liver disease
Explanation: ***Inflammatory bowel disease*** - **Carcinoembryonic antigen (CEA)** levels can be elevated in conditions involving active inflammation and rapid cell turnover within the gastrointestinal tract, such as **inflammatory bowel disease (IBD)** [1]. - While CEA is primarily a tumor marker, its elevation in IBD reflects the extensive mucosal inflammation and repair processes, rather than malignancy. *Hemolytic anemia* - **Hemolytic anemia** involves the destruction of red blood cells and does not typically lead to elevated CEA levels. - Elevated CEA is associated with certain epithelial conditions, not primary hematologic disorders. *Pancreatitis* - While **pancreatitis** can cause elevated levels of other markers like amylase and lipase, it is not consistently associated with elevated CEA. - CEA elevation in pancreatic conditions usually points towards a **pancreatic malignancy**. *Liver disease* - **Liver disease**, particularly severe inflammation or cirrhosis, can sometimes cause a mild elevation in CEA due to impaired clearance or increased production in damaged tissue. - However, levels are typically not as high or consistently elevated as in IBD, and significant elevation often prompts investigation for **primary hepatic or metastatic malignancy**.
Question 18: 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 19: 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 20: Which of the following statements about sickle cell disease is true?
- A. Sickling is completely reversible with oxygenation, making it clinically insignificant.
- B. Sickling leads to a significant increase in overall MCHC levels in the blood.
- C. Fetal hemoglobin inhibits sickling. (Correct Answer)
- D. Sickling occurs exclusively in the homozygous state and never in the heterozygous state.
Explanation: ***Sickling is reversible with oxygenation*** - When oxygen tension is restored, hemoglobin S can re-hydrate and revert to its normal shape, reducing sickling. - This reversible process is essential for managing episodes of vaso-occlusive crisis in sickle cell disease. *Fetal hemoglobin facilitates Sickling* - Fetal hemoglobin (HbF) actually inhibits sickling by stabilizing the erythrocyte shape and reducing the proportion of hemoglobin S [1]. - Individuals with higher levels of HbF experience fewer sickling-related complications [1]. *Sickling occurs both in heterozygous and homozygous state* - Sickling primarily occurs in the homozygous state (HbSS); heterozygotes (HbAS) usually do not experience significant sickling effects [1]. - Heterozygous individuals may have a selective advantage against malaria, but they are not prone to sickle cell crises. *Sickling Leads to decreased MCHC* - Sickling does not directly lead to decreased mean corpuscular hemoglobin concentration (MCHC); MCHC is typically normal in sickle cell patients. - In fact, sickle cell disease often results in hemolysis and can lead to increased MCHC in some cases.