Distal renal tubular acidosis is associated with:
What is the preferred test for confirming H. pylori eradication?
Anomic aphasia is due to defect in
Which of the following is a characteristic feature of myasthenia gravis?
All the following are true about multiple myeloma except for which of the following?
The most classical symptom of VIPOMA is:
Which of the following is a characteristic feature of primary Sjogren's syndrome?
What is the first symptom of leprosy?
Migraine is due to
In which condition is paradoxical splitting of the second heart sound observed?
NEET-PG 2012 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 81: Distal renal tubular acidosis is associated with:
- A. Hypocitraturia
- B. Oxalate stones
- C. Calcium stones (Correct Answer)
- D. Uric acid stones
Explanation: ***Calcium stones*** - Distal renal tubular acidosis (Type 1 RTA) causes metabolic acidosis due to impaired distal tubular **hydrogen ion secretion**. - This leads to **increased urinary calcium excretion** (hypercalciuria) and decreased urinary citrate, creating an environment favorable for the formation of **calcium phosphate renal stones**. *Oxalate stones* - While oxalate is a component of some calcium stones (calcium oxalate), **primary hyperoxaluria** or dietary excess of oxalate are the main causes, not directly distal RTA. - Distal RTA specifically promotes **calcium phosphate stone formation** due to pH changes and hypercalciuria. *Hypocitraturia* - **Hypocitraturia** is indeed a feature of distal RTA as the kidney attempts to excrete acid by reabsorbing citrate, making the urine less inhibitory to stone formation. - However, the most direct and common clinically observed consequence in stone formation is the development of **calcium stones**, as hypocitraturia combined with hypercalciuria facilitates their formation. *Uric acid stones* - **Uric acid stones** typically form in persistently **acidic urine** and are associated with conditions like gout or myeloproliferative disorders. - While distal RTA results in systemic acidosis, the urine pH in distal RTA is typically **alkaline or inappropriately neutral**, which does not favor uric acid stone formation.
Question 82: What is the preferred test for confirming H. pylori eradication?
- A. Urease breath test (Correct Answer)
- B. Culture
- C. Serological test
- D. Biopsy urease test
Explanation: ***Urease breath test*** - The **urea breath test** is highly sensitive and specific for detecting active *H. pylori* infection and its eradication by measuring radioactive or non-radioactive labeled carbon dioxide released from metabolizing urea. - It is a non-invasive test preferred after treatment to confirm eradication, as it directly detects bacterial urease activity. *Culture* - **Culture** requires an invasive endoscopic biopsy, is expensive, and takes several days to yield results; therefore, it is not the preferred method for routine eradication confirmation. - While it offers the advantage of **antibiotic susceptibility testing**, its invasiveness and turnaround time make it less practical for post-treatment assessment. *Serological test* - **Serological tests** (blood tests for antibodies) remain positive for **H. pylori antibodies** for extended periods even after successful eradication, rendering them unsuitable for confirming eradication. - These tests primarily indicate past exposure rather than current, active infection. *Biopsy urease test* - A **biopsy urease test** involves an invasive endoscopy to obtain a tissue sample, which is then tested for urease activity. - Although useful for initial diagnosis, its invasiveness makes it less preferred for confirming eradication compared to the non-invasive breath test.
Question 83: Anomic aphasia is due to defect in
- A. Left inferior parietal lobe
- B. Left temporal lobe
- C. Temporal occipital lobe (Correct Answer)
- D. Cerebellum
Explanation: ***Temporal occipital lobe*** - Anomic aphasia, characterized by difficulty recalling **words or names (anomia)**, is most commonly associated with lesions in the **left temporo-occipital region**. - This area is crucial for **semantic processing** and word retrieval. *Left inferior parietal lobe* - Damage to the left inferior parietal lobe is more commonly associated with **conduction aphasia**, characterized by impaired repetition despite fluent speech and good comprehension. - It is also involved in aspects of **reading (alexia)** and **writing (agraphia)**. *Left temporal lobe* - While portions of the left temporal lobe (especially Wernicke's area) are critical for language comprehension, damage primarily to this area typically results in **Wernicke's aphasia**, where speech is fluent but meaningless, and comprehension is severely impaired. - Anomia can be a feature of Wernicke's aphasia, but the primary deficit is comprehension. *Cerebellum* - The cerebellum plays a significant role in **motor control**, balance, and coordination, but it is not directly involved in the **generation or comprehension of language** in the same way as cortical areas. - Damage to the cerebellum might lead to **dysarthria** (speech motor difficulties), but not typical aphasia.
Question 84: Which of the following is a characteristic feature of myasthenia gravis?
- A. Decreased levels of myosin in muscle fibers
- B. Absence of troponin C in muscle fibers
- C. Increased transmission at the myoneural junction
- D. Presence of antibodies against acetylcholine receptors (Correct Answer)
Explanation: ***Presence of antibodies against acetylcholine receptors*** - **Myasthenia gravis** is an **autoimmune disorder** characterized by the production of **antibodies against acetylcholine receptors** at the neuromuscular junction [1]. - These antibodies block, alter, or destroy the acetylcholine receptors, leading to impaired nerve-to-muscle communication and **muscle weakness** [2]. *Decreased levels of myosin in muscle fibers* - Myosin is a **motor protein** crucial for muscle contraction, and its decreased levels are not a primary feature of myasthenia gravis, but rather other **myopathies** or muscle wasting conditions. - The disease mechanism in myasthenia gravis is primarily at the **neuromuscular junction**, not within the muscle fibers themselves. *Absence of troponin C in muscle fibers* - **Troponin C** is a component of the troponin complex essential for **calcium-mediated muscle contraction**, found inside muscle fibers. - Its absence would lead to severe and widespread muscle dysfunction, unlike the specific and fluctuating weakness seen in **myasthenia gravis**. *Increased transmission at the myoneural junction* - Myasthenia gravis is characterized by **decreased** or **impaired transmission** at the myoneural (neuromuscular) junction due to the destruction or blockade of acetylcholine receptors [2]. - Increased transmission would lead to **muscle hyperactivity** or spasms, which is contrary to the **fatigable weakness** observed in myasthenia gravis.
Question 85: All the following are true about multiple myeloma except for which of the following?
- A. Hypercalcemia
- B. Presence of Bence-Jones proteins in urine
- C. Osteolytic bone disease
- D. Chromosomal translocation t(8;14), commonly seen in Burkitt's lymphoma (Correct Answer)
Explanation: ***t(8-14) translocation*** - The **t(8;14) translocation** is not typically associated with multiple myeloma; rather, it is commonly seen in **Burkitt lymphoma** [2]. - Multiple myeloma is primarily linked with chromosomal abnormalities such as **deletions** and **translocations involving different chromosomes**. *Osteolytic bone disease* - A hallmark feature of multiple myeloma, **osteolytic lesions** result from increased osteoclastic activity and are often seen in the skull, spine, and ribs [1]. - Patients frequently present with **bone pain** due to these lesions, which are characteristic of the disease [1]. *Light chain proliferation* - In multiple myeloma, a significant feature is the overproduction of **monoclonal light chains** [1]. - This leads to **light chain disease** or **renal impairment**, further supporting the diagnosis [1]. *Bence-Jones proteins in urine* - The presence of **Bence-Jones proteins**, which are free light chains, is a classic finding in multiple myeloma [1]. - They are often detected in the **urine** and can be used to monitor disease progression or response to treatment [1].
Question 86: The most classical symptom of VIPOMA is:
- A. Gall stones
- B. Secretory diarrhea (Correct Answer)
- C. Steatorrhea
- D. Flushing
Explanation: The original text cannot be accurately enriched with the provided references to because none of the source materials directly address the pathophysiology or clinical presentation of VIPoma. The available references focus on general gastroenteropancreatic neuroendocrine tumors (NETs) , radiation-induced intestinal damage , arsenic poisoning , gastrointestinal bleeding , and the physiology of taste , but they do not provide the specific confirmation needed for the 'classical symptom' of VIPoma (secretory diarrhea).
Question 87: Which of the following is a characteristic feature of primary Sjogren's syndrome?
- A. Can occur in children
- B. Increased complement C4 is associated with thymoma
- C. Can be associated with rheumatoid arthritis
- D. Enlargement of salivary glands (Correct Answer)
Explanation: ***Enlargement of salivary glands*** - **Sjögren's syndrome** is characterized by chronic inflammation of **exocrine glands**, leading to swelling and dysfunction, most notably in the **parotid** and **submandibular glands**. - This glandular enlargement often presents as recurrent or persistent **bilateral swelling** of the major salivary glands. *Can occur in children* - While possible, Sjögren's syndrome is predominantly a disease of **adults**, with incidence peaking in individuals between **40 and 60 years old**. - **Juvenile Sjögren's syndrome** is rare and typically presents with more variable symptoms, making it less of a characteristic feature of the primary disease in the general population. *Increased complement C4 is associated with thymoma* - **Increased complement C4** levels are generally not associated with Sjögren's syndrome; instead, **hypocomplementemia** (low C4) can be seen in some patients, indicating immune complex activity. - **Thymoma** is primarily linked to **myasthenia gravis** and other paraneoplastic syndromes, not a direct or characteristic association with Sjögren's syndrome or C4 levels in this context. *Can be associated with rheumatoid arthritis* - Sjögren's syndrome can be classified as **primary** (occurring alone) or **secondary** (occurring in conjunction with another autoimmune disease). - Its association with **rheumatoid arthritis** defines **secondary Sjögren's syndrome**, meaning it's not a characteristic feature of the *primary* form of the disease itself.
Question 88: What is the first symptom of leprosy?
- A. Decreased vibration & position sense
- B. Decreased pain (Correct Answer)
- C. Decreased temperature
- D. Decreased light touch
Explanation: Decreased pain - Leprosy primarily targets Schwann cells in peripheral nerves, leading to sensory loss [1]. - The sensation of pain is typically affected earliest, often presenting as areas of numbness [1]. Decreased vibration & position sense - These sensations are typically carried by larger myelinated fibers, which tend to be affected later in the disease progression of leprosy. - While eventually involved, they are not usually the first symptom of sensory loss. Decreased temperature - Temperature sensation is also an early modality affected in leprosy, as it's carried by small, unmyelinated or thinly myelinated fibers [1]. - However, pain is often cited as the very first sensory loss, even preceding temperature changes in some cases. Decreased light touch - Light touch sensation is generally an early loss, similar to pain and temperature, due to damage to nerve fibers in the skin. - But, when distinguishing the absolute first symptom, pain perception often shows impairment even before light touch in affected areas.
Question 89: Migraine is due to
- A. Cortical spreading depression (Correct Answer)
- B. Dilatation of cranial blood vessels
- C. Constriction of cranial blood vessels
- D. Inflammation of the meninges
Explanation: ***Cortical spreading depression*** - The current understanding is that **cortical spreading depression (CSD)** is the initiating event in migraine with aura, characterized by a wave of neuronal and glial depolarization that spreads across the cerebral cortex, leading to a temporary shutdown of neuronal activity [1]. - CSD is thought to activate the **trigeminal nerve**, subsequently causing the release of inflammatory neuropeptides and contributing to the pain phase [1]. *Dilatation of cranial blood vessels* - While **vasodilation of intracranial and extracranial blood vessels** does occur during the headache phase of migraine, it is now considered a *consequence* of the initial neurological events rather than the primary cause [1]. - This vasodilation contributes to the throbbing sensation of migraine pain but does not explain the aura or the initiation of the attack. *Constriction of cranial blood vessels* - **Vasoconstriction** was previously thought to be the cause of the migraine aura, but this theory has largely been disproven. - While some temporary constriction may precede CSD, it is not the primary mechanism behind the migraine attack. *Inflammation of the meninges* - While **neurogenic inflammation** of the meninges, involving the release of inflammatory mediators like **calcitonin gene-related peptide (CGRP)**, does play a role in sensitizing the trigeminal system and contributing to migraine pain, it is a downstream effect. - It is not the initial trigger for a migraine attack but rather part of the pain pathway activated by events like CSD.
Question 90: In which condition is paradoxical splitting of the second heart sound observed?
- A. Right Bundle Branch Block (RBBB)
- B. Left Bundle Branch Block (LBBB) (Correct Answer)
- C. Ventricular Septal Defect (VSD)
- D. Atrial Septal Defect (ASD)
Explanation: ***Left Bundle Branch Block (LBBB)*** - In LBBB, the **left ventricle** depolarizes and contracts *after* the right ventricle, causing the **aortic valve (A2)** to close *after* the **pulmonic valve (P2)** [1]. - During inspiration, right ventricular ejection time is prolonged, which further delays P2. However, in LBBB, A2 is already delayed, and the inspiratory delay of P2 can bring P2 closer to A2, or even cause them to merge, making the splitting *less wide* or *disappear* on inspiration, which is paradoxical. *Right Bundle Branch Block (RBBB)* - RBBB causes a **delay in right ventricular depolarization**, leading to a **delayed P2** (pulmonic valve closure). - This typically results in **wide and fixed splitting of S2**, where the splitting persists during expiration and widens further with inspiration, which is not paradoxical. *Ventricular Septal Defect (VSD)* - A VSD can cause a **loud holosystolic murmur** and may lead to increased pulmonary blood flow. - While it can affect the timing of heart sounds, it does not typically cause paradoxical splitting of S2. *Atrial Septal Defect (ASD)* - An ASD causes a **left-to-right shunt**, leading to chronic volume overload of the right ventricle and increased pulmonary blood flow. - This often results in a **widely fixed splitting of S2**, where the split between A2 and P2 is constant regardless of respiration, which is different from paradoxical splitting.