Which of the following is NOT a criterion for the diagnosis of Primary Hyperaldosteronism?
Most common cause of Addison's Disease in India is:
Female with blood sugar of 600 mg% and sodium of 110 mEq. Insulin was given, what will happen to serum sodium levels ?
What condition is characterized by hypertension and hypokalemia?
What is the recommended postprandial capillary glucose level (in mg/dl) for adequate diabetes control?
What is the most common form of leptospirosis?
What is the causative agent of trench fever?
Eschar is seen in all the Rickettsial diseases except:
Most common complication of diphtheria is -
Most common route of infection in pasteurella cellulitis -
NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 61: Which of the following is NOT a criterion for the diagnosis of Primary Hyperaldosteronism?
- A. Diastolic Hypertension without edema
- B. Low Plasma Renin Activity
- C. Hyperkalemia (Correct Answer)
- D. Hyperaldosteronism which is not suppressed by volume expansion
Explanation: Primary hyperaldosteronism is typically characterized by **hypokalemia** due to excessive aldosterone-mediated potassium excretion in the urine, not hyperkalemia [1]. Hyperkalemia would suggest other conditions, such as **adrenal insufficiency** or kidney disease, rather than primary hyperaldosteronism [2]. *Diastolic Hypertension without edema* - **Diastolic hypertension** is a common presentation of primary hyperaldosteronism due to increased **sodium and water retention**, leading to expanded extracellular volume. - The absence of significant edema is also common, as the body often develops an **"escape phenomenon"** where natriuresis occurs despite high aldosterone, preventing overt fluid overload [3]. *Low Plasma Renin Activity* - In primary hyperaldosteronism, the high aldosterone levels **suppress renin secretion** through negative feedback mechanisms. - Therefore, a **low plasma renin activity** (PRA) or plasma renin concentration (PRC) is a key diagnostic feature [4]. *Hyperaldosteronism which is not suppressed by volume expansion* - Normally, volume expansion would suppress aldosterone secretion. However, in primary hyperaldosteronism, aldosterone production is **autonomous** and remains elevated even after volume expansion. - This lack of suppression is a critical diagnostic criterion, often assessed through various **confirmatory tests** like saline infusion or oral sodium loading.
Question 62: Most common cause of Addison's Disease in India is:
- A. Autoimmune
- B. HIV
- C. Tuberculosis (Correct Answer)
- D. Malignancy
Explanation: ***Tuberculosis*** - In India, **tuberculosis** is the most common cause of **Addison's disease** due to the high prevalence of TB infections. - Adrenal involvement in TB can lead to gradual destruction of the adrenal cortex, resulting in **adrenal insufficiency**. *Autoimmune* - **Autoimmune adrenalitis** is the leading cause of Addison's disease in developed Western countries. - It involves the destruction of adrenal cortical cells by the body's own immune system, often associated with other autoimmune conditions. *Malignancy* - **Malignancy**, particularly metastatic cancer to the adrenals, can cause adrenal insufficiency but is a less common primary cause of Addison's disease overall. - While possible, it is not the most prevalent cause in India compared to infectious etiologies. *HIV* - **HIV infection** can lead to adrenal dysfunction, but it's typically through opportunistic infections like CMV, cryptococcosis, or direct HIV effects, rather than being the direct cause of widespread adrenal destruction. - It increases the risk of adrenal insufficiency but is not the most common etiology in India for Addison's disease.
Question 63: Female with blood sugar of 600 mg% and sodium of 110 mEq. Insulin was given, what will happen to serum sodium levels ?
- A. Sodium levels may appear to increase (Correct Answer)
- B. Sodium levels decrease
- C. Sodium levels remain unchanged
- D. Relative sodium deficiency may occur
Explanation: ***Sodium levels may appear to increase*** - The patient's initial presentation with severe hyperglycemia (600 mg%) and hyponatremia (110 mEq/L) suggests **hyperglycemia-induced pseudohyponatremia**. - **Insulin administration** will lower blood glucose, causing water to shift back into the cells from the extracellular space, thereby correcting the dilutional effect and leading to an **apparent increase in serum sodium levels**. *Sodium levels decrease* - This is incorrect because the hyponatremia in this scenario is largely **dilutional** due to hyperglycemia. - As glucose levels decrease with insulin, the osmotic drive for water movement out of cells diminishes, leading to **normalization**, not further decrease, of sodium concentration. *Sodium levels remain unchanged* - This is incorrect because the underlying cause of the initial low sodium is dilution from high glucose. - Once **hyperglycemia is treated**, the osmotic gradient changes, and water shifts, directly impacting and changing the serum sodium concentration. *Relative sodium deficiency may occur* - This option is incorrect because the initial hyponatremia is not primarily due to an absolute lack of sodium in the body but rather a **dilutional effect** caused by the osmotic pull of glucose. - As hyperglycemia resolves, the extracellular fluid becomes less diluted, and the measured sodium concentration will **rise**, not indicate a deficiency.
Question 64: What condition is characterized by hypertension and hypokalemia?
- A. Gitelman's Syndrome
- B. Liddle's Syndrome (Correct Answer)
- C. Bartter Syndrome
- D. All of the options
Explanation: ***Liddle's Syndrome*** - This syndrome is characterized by **overactivity of the epithelial sodium channel (ENaC)** in the collecting ducts, leading to increased sodium reabsorption and potassium excretion. [1] - The resulting **sodium retention causes hypertension**, while the **potassium excretion leads to hypokalemia**. *Gitelman's Syndrome* - This is an **autosomal recessive kidney disorder** causing a defect in the **thiazide-sensitive NaCl cotransporter** in the distal convoluted tubule. - It presents with **hypokalemia and hypomagnesemia**, but typically with **normal or low blood pressure**, not hypertension. *Bartter Syndrome* - This is a group of **autosomal recessive salt-wasting tubulopathies** affecting the **Na-K-2Cl cotransporter** in the thick ascending limb of the loop of Henle. - It leads to **hypokalemia, metabolic alkalosis, and normal or low blood pressure**, similar to chronic loop diuretic use. *All of the options* - While all mentioned conditions involve **hypokalemia**, only **Liddle's Syndrome** is consistently associated with **hypertension**. - **Gitelman's and Bartter syndromes** typically present with **normal or low blood pressure**.
Question 65: What is the recommended postprandial capillary glucose level (in mg/dl) for adequate diabetes control?
- A. < 180 mg/dl (Correct Answer)
- B. < 200 mg/dl
- C. < 100 mg/dl
- D. < 140 mg/dl
Explanation: ***< 180 mg/dl*** - This is the **recommended target** for postprandial (1-2 hours after a meal) capillary glucose levels in most non-pregnant adults with diabetes to achieve **adequate glycemic control** [1], [2]. - Maintaining levels below 180 mg/dl helps to minimize the risk of **long-term microvascular and macrovascular complications**. *< 100 mg/dl* - While this is an ideal fasting glucose level, it is generally **too low for postprandial glucose**, and attempting to maintain such levels might increase the risk of **hypoglycemia** in many patients with diabetes [1]. - This target is more appropriate for **fasting or pre-meal glucose** goals. *< 140 mg/dl* - This is a **more stringent target** that may be appropriate for some individuals with diabetes, particularly those who are carefully managed and at low risk of hypoglycemia. - However, for the general population with diabetes, **< 180 mg/dl is the more commonly accepted and achievable goal** for postprandial readings [2]. *< 200 mg/dl* - A postprandial glucose level of < 200 mg/dl is considered **good control** in some contexts, but it's often a **less strict target** than < 180 mg/dl for optimal long-term management. - While better than uncontrolled high levels, consistently approaching 200 mg/dl may still contribute to **increased risk of complications** over time compared to tighter control.
Question 66: What is the most common form of leptospirosis?
- A. Icteric form
- B. Hepatorenal form
- C. Anicteric form (Correct Answer)
- D. Weil's disease
Explanation: ***Anicteric form*** - The **anicteric form** accounts for about 90% of all leptospirosis cases, presenting with milder, flu-like symptoms without jaundice. - Patients typically experience **fever, headache, myalgia**, and conjunctival suffusion during the initial septicemic phase [1], followed by an immune phase that can involve meningitis or uveitis [1]. *Icteric form* - The **icteric form** (Weil's disease) is a severe manifestation, characterized by jaundice, renal failure, and hemorrhage, occurring in a minority of cases (5-10%). - Although more severe and often life-threatening, it is **less common** than the anicteric presentation [1]. *Hepatorenal form* - This term describes the severe complications of leptospirosis, including **liver and kidney dysfunction**, specifically associated with Weil's disease. - While a critical aspect of severe leptospirosis, it is a description of the organ involvement rather than a distinct common form of the disease. *Weil's disease* - **Weil's disease** is the most severe and potentially fatal form of leptospirosis, characterized by **jaundice, renal failure, hemorrhage, and myocarditis**. - It is a severe subset of the icteric form, making it a very serious but **uncommon variant** of the overall disease.
Question 67: What is the causative agent of trench fever?
- A. Q-fever
- B. Boutonneuse fever
- C. Indian tick typhus
- D. Bartonella quintana (Correct Answer)
Explanation: ***Bartonella quintana*** - **Trench fever** is a **rickettsial-like illness** primarily transmitted by the human body louse. - The causative agent is the bacterium **Bartonella quintana**, which causes recurrent fever, headache, and body pains. *Q-fever* - Q-fever is caused by the bacterium **Coxiella burnetii** and is typically transmitted through airborne exposure to contaminated aerosols from infected animals. - It presents with fever, headache, and atypical pneumonia, and is not associated with human body lice. *Boutonneuse fever* - This fever is caused by **Rickettsia conorii**, transmitted by the **brown dog tick**. - Characterized by a **maculopapular rash** and an **eschar (tache noire)** at the site of the tick bite. *Indian tick typhus* - This is a form of spotted fever group rickettsiosis caused by **Rickettsia conorii subspecies indica**, transmitted by ticks [1]. - It presents with fever, rash, and an eschar, similar to boutonneuse fever, but is specified for the Indian subcontinent [1].
Question 68: Eschar is seen in all the Rickettsial diseases except:
- A. Scrub typhus
- B. Rickettsial pox
- C. Indian tick typhus
- D. Endemic typhus (Correct Answer)
Explanation: ***Endemic typhus*** - **Endemic typhus**, caused by *Rickettsia typhi*, is transmitted by **fleas** and typically presents without an eschar. - The disease is characterized by fever, headache, and a maculopapular rash, but the **inoculation site lesion (eschar) is rare or absent**. *Scrub typhus* - **Scrub typhus**, caused by *Orientia tsutsugamushi*, is known for causing a prominent **eschar** [1] at the site of the **chigger mite bite**. - This **painless black scab** is a classic diagnostic feature of the disease [1]. *Rickettsial pox* - **Rickettsial pox**, caused by *Rickettsia akari*, almost invariably presents with an **eschar**, often referred to as an **inoculation lesion**. - This lesion appears as a papule that vesiculates and then forms a scab, indicating the site of the **mite bite**. *Indian tick typhus* - **Indian tick typhus** (part of the **spotted fever group rickettsioses**), caused by *Rickettsia conorii*, frequently presents with a characteristic **eschar** at the site of the **tick bite**. - This eschar, known as a **tache noire**, is a valuable diagnostic clue in affected patients.
Question 69: Most common complication of diphtheria is -
- A. Myocarditis (Correct Answer)
- B. Pneumonia
- C. Meningitis
- D. Endocarditis
Explanation: ***Myocarditis*** - Diphtheria toxin can directly damage myocardial cells, leading to inflammation and dysfunction of the heart muscle, making **myocarditis** the most common and serious complication. - This can result in **heart failure**, arrhythmias, and even death, highlighting its significance in diphtheria. *Pneumonia* - While respiratory complications can occur in diphtheria, **pneumonia** is not the most common or life-threatening complication associated with the diphtheria toxin itself. - Secondary bacterial infections might lead to pneumonia, but it is not a direct toxic effect like myocarditis. *Meningitis* - **Meningitis**, an inflammation of the membranes surrounding the brain and spinal cord, is an extremely rare complication of diphtheria. - Diphtheria primarily affects the upper respiratory tract and heart [1], with neurological complications typically manifesting as neuropathies rather than meningitis. *Endocarditis* - Although diphtheria can cause cardiac complications, **endocarditis** (inflammation of the heart's inner lining, including the valves) is not a common complication. - Myocarditis, due to the direct toxic effect on heart muscle, is far more prevalent than endocarditis in diphtheria.
Question 70: Most common route of infection in pasteurella cellulitis -
- A. Animal bites or scratches (Correct Answer)
- B. Aerosols or dust
- C. Contaminated tissue
- D. Human to human
Explanation: ***Animal bites or scratches*** - *Pasteurella multocida* is a common commensal bacterium in the oral flora of **cats and dogs**. - **Animal bites or scratches** are the primary mode of transmission for *Pasteurella* infections, particularly cellulitis, due to direct inoculation. *Aerosols or dust* - Transmission via **aerosols or dust** is rare for *Pasteurella* infections, which typically require direct contact or inoculation. - While other bacteria can spread this way, *Pasteurella* cellulitis is not commonly acquired through airborne routes. *Contaminated tissue* - While possible in some contexts, **contaminated tissue** is not the most common route of infection for *Pasteurella* cellulitis. - Direct inoculation from an **animal's oral flora** is far more frequent than contact with contaminated environmental tissues. *Human to human* - *Pasteurella* infections are generally **not transmissible from human to human**. - The organism is primarily associated with animals and their bites or scratches.