In evaluation of a case of immotile nasal cilia, which of the following investigations should prove useful?
Which of the following conditions does not typically cause subconjunctival hemorrhages?
Anisocoria in Horner's syndrome is due to
Macular sparing is associated with lesions in:
Which of the following is the common cause of respiratory failure type 2 ?
Aspirin sensitive asthma is associated with:
Which of the following is seen in sarcoidosis
Central bronchiectasis is seen with
Post-tubercular bronchiectasis is most commonly seen with
In a patient with COPD, what is the best management option?
NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 81: In evaluation of a case of immotile nasal cilia, which of the following investigations should prove useful?
- A. Rhinogram
- B. Sweat sodium levels
- C. Nitric oxide test (Correct Answer)
- D. Xray nasal and paranasal sinuses
Explanation: Nitric oxide test - A low nasal nitric oxide (nNO) concentration is a key diagnostic criterion for Primary Ciliary Dyskinesia (PCD), a genetic disorder characterized by immotile or dyskinetic cilia [1]. - Nasal NO is significantly reduced in PCD patients due to impaired ciliary function, making this test highly useful for screening. *Rhinogram* - A rhinogram is a radiographic imaging technique primarily used to visualize the nasal cavity and paranasal sinuses, often to detect structural abnormalities or foreign bodies. - It does not directly assess ciliary function or provide information about ciliary motility. *Sweat sodium levels* - Elevated sweat chloride or sodium levels are the diagnostic hallmark of cystic fibrosis, a genetic condition primarily affecting mucus production. - While cystic fibrosis can cause respiratory symptoms, it does not directly lead to immotile nasal cilia in the same manner as PCD. *Xray nasal and paranasal sinuses* - An X-ray of the nasal and paranasal sinuses can reveal structural issues, such as sinus opacification or polyps, which may accompany ciliary dysfunction. - However, it does not provide direct information about the motility or structural integrity of the cilia themselves.
Question 82: Which of the following conditions does not typically cause subconjunctival hemorrhages?
- A. Whooping cough
- B. Scurvy
- C. Pellagra (Correct Answer)
- D. Purpura
Explanation: ***Pellagra*** - Pellagra is a **nutritional deficiency disease** caused by a lack of **niacin (vitamin B3)**, characterized by symptoms affecting the **skin, gastrointestinal tract, and nervous system** (dermatitis, diarrhea, dementia, and death if untreated) [1]. - It does **not typically cause subconjunctival hemorrhages** as it primarily affects other organ systems and isn't associated with vascular fragility in the conjunctiva like the other conditions listed [2]. *Whooping cough* - **Violent coughing paroxysms** in whooping cough (pertussis) can significantly increase **venous pressure in the head and neck**. - This elevated pressure can rupture small conjunctival blood vessels, leading to **subconjunctival hemorrhages**. *Scurvy* - Scurvy is caused by **vitamin C deficiency**, which is essential for collagen synthesis and maintaining **blood vessel integrity**. - Lack of vitamin C leads to **fragile capillaries**, making patients prone to bleeding, including **subconjunctival hemorrhages**. *Purpura* - Purpura refers to **purple-colored spots on the skin caused by bleeding underneath the skin**. It is a general term for various conditions characterized by **small vessel bleeding**. - These conditions often involve **vascular fragility or platelet abnormalities**, making individuals susceptible to bleeding in different sites, including the conjunctiva, resulting in **subconjunctival hemorrhages**.
Question 83: Anisocoria in Horner's syndrome is due to
- A. Disruption of the oculosympathetic pathway (Correct Answer)
- B. Disruption of the oculoparasympathetic pathway
- C. Disruption of the oculomotor nerve
- D. Disruption of the abducens nerve
Explanation: ***Disruption of the oculosympathetic pathway*** - Horner's syndrome results from a lesion interrupting the **oculosympathetic pathway**, leading to classic symptoms of **miosis**, **ptosis**, and **anhidrosis** [1]. - The **miosis** (constricted pupil) specifically arises from the unopposed action of the **parasympathetic innervation** to the pupil dilatory muscles when sympathetic innervation is disrupted. *Disruption of the oculoparasympathetic pathway* - Disruption of the oculoparasympathetic pathway would result in **mydriasis** (dilated pupil), not miosis as seen in Horner's syndrome [2]. - This pathway is responsible for stimulating the **pupillary constrictor muscles**, and its disruption would lead to an inability to constrict the pupil [3]. *Disruption of the oculomotor nerve* - The **oculomotor nerve** (CN III) carries parasympathetic fibers to the eye, and its disruption typically causes a **fixed and dilated pupil** due to unopposed sympathetic action [3]. - Oculomotor nerve palsy also presents with **ptosis** and **down-and-out deviation** of the eye, which are not characteristic of isolated Horner's syndrome [1], [4]. *Disruption of the abducens nerve* - The **abducens nerve** (CN VI) solely innervates the **lateral rectus muscle**, responsible for abducting the eye. - Disruption of the abducens nerve causes **diplopia** and an inability to abduct the affected eye, with no direct impact on pupil size.
Question 84: Macular sparing is associated with lesions in:
- A. Lesions in the optic nerve
- B. Lesions in the lateral geniculate body
- C. Lesions in the occipital cortex (Correct Answer)
- D. Lesions in the optic chiasma
Explanation: ***Lesions in the occipital cortex*** - **Macular sparing** occurs when the central visual field (macula) is preserved despite damage to the occipital cortex, often due to its dual blood supply from the **middle cerebral artery** and the **posterior cerebral artery**. [2] - This phenomenon typically results from a **vascular lesion** in the occipital lobe, leading to a **homonymous hemianopia** with a distinct sparing of the foveal region. [2], [3] *Lesions in the optic nerve* - Lesions in the optic nerve cause **monocular vision loss** or central scotomas, rather than the homonymous visual field defects associated with macular sparing. [2] - Damage here affects the visual pathway **before** the optic chiasm, impacting the entire visual input from one eye. [2] *Lesions in the lateral geniculate body* - Lesions in the **lateral geniculate body (LGB)** produce **contralateral homonymous hemianopia** or quadrantanopia, but typically **do not exhibit macular sparing** as consistently as cortical lesions. - The LGB processes visual information from both eyes before relaying it to the visual cortex. [1] *Lesions in the optic chiasma* - Lesions in the **optic chiasma** classically cause **bitemporal hemianopia**, affecting the temporal visual fields of both eyes. [2] - This type of visual field defect is distinct from the homonymous defects seen with macular sparing, as it results from damage to the **crossing nasal fibers**. [2]
Question 85: Which of the following is the common cause of respiratory failure type 2 ?
- A. Chronic bronchitis exacerbation (Correct Answer)
- B. Acute attack asthma
- C. ARDS
- D. Pneumonia
Explanation: ***Chronic bronchitis exacerbation*** - **Chronic bronchitis** is a common cause of **Type 2 respiratory failure**, characterized by **hypercapnia** (elevated CO2) due to impaired alveolar ventilation [1]. - An exacerbation worsens **airflow obstruction** and leads to increased work of breathing and CO2 retention [1]. *Acute attack asthma* - While severe asthma can cause respiratory failure, it typically presents initially as **Type 1 (hypoxemic)**, with severe bronchospasm and V/Q mismatch [2]. - **Hypercapnia** in asthma is a sign of **severe, impending respiratory collapse** rather than the primary cause of respiratory failure. *ARDS* - **Acute Respiratory Distress Syndrome (ARDS)** is a classic cause of **Type 1 (hypoxemic) respiratory failure**, characterized by widespread inflammation and fluid accumulation in the lungs [2]. - ARDS primarily involves impaired oxygenation rather than CO2 elimination issues, unless it progresses to severe stages with significant muscle fatigue. *Pneumonia* - **Pneumonia** predominantly causes **Type 1 (hypoxemic) respiratory failure** due to consolidation and V/Q mismatch in affected lung areas, leading to impaired oxygen diffusion [2]. - While severe, widespread pneumonia can eventually lead to ventilatory failure, its initial and primary impact is on oxygenation.
Question 86: Aspirin sensitive asthma is associated with:
- A. Extrinsic asthma
- B. Associated with nasal polyp (Correct Answer)
- C. Obesity
- D. Usually associated with urticaria
Explanation: **Associated with nasal polyp** - **Aspirin-exacerbated respiratory disease (AERD)**, also known as aspirin-sensitive asthma, is characterized by a triad of **asthma**, **rhinosinusitis with nasal polyposis**, and respiratory reactions to **aspirin** and other NSAIDs [1]. - The presence of **nasal polyps** is a key clinical feature differentiating AERD from other forms of asthma [1]. *Obesity* - While **obesity** can exacerbate asthma severity, it is not specifically associated with the pathogenesis or diagnosis of **aspirin-sensitive asthma**. - It is a general risk factor for various health issues, including more severe asthma, but lacks specificity for AERD. *Extrinsic asthma* - **Extrinsic asthma** (allergic asthma) is typically triggered by environmental allergens and involves an **IgE-mediated response** [2]. - AERD is considered a **non-allergic** or **intrinsic asthma** phenotype, as it is not triggered by traditional allergens but by pharmacologic agents [1]. *Usually associated with urticaria* - **Urticaria** (hives) can be a feature of aspirin and NSAID sensitivity, particularly in some forms of **NSAID-induced urticaria/angioedema**. - However, the classic respiratory reactions of **aspirin-sensitive asthma** (bronchospasm, rhinitis) are distinct from urticarial reactions and typically do not present with primary urticaria.
Question 87: Which of the following is seen in sarcoidosis
- A. Decreased calcium levels in the blood (Hypocalcemia)
- B. Increased phosphate levels in the blood (Hyperphosphatemia)
- C. Increased calcium levels in the blood (Hypercalcemia) (Correct Answer)
- D. Decreased phosphate levels in the blood (Hypophosphatemia)
Explanation: ***Increased calcium levels in the blood (Hypercalcemia)*** - In sarcoidosis, activated macrophages in granulomas produce **1-alpha hydroxylase**, which converts **25-hydroxyvitamin D to 1,25-dihydroxyvitamin D (calcitriol)** [1]. - This increased calcitriol leads to enhanced intestinal **calcium absorption** and occasional bone resorption, resulting in **hypercalcemia** [1]. *Decreased calcium levels in the blood (Hypocalcemia)* - **Hypocalcemia** is not characteristic of sarcoidosis; the disease typically involves dysregulated vitamin D metabolism causing elevated, not decreased, calcium [1]. - Conditions like **hypoparathyroidism** or **vitamin D deficiency** (unrelated to the sarcoidosis pathogenesis) would cause hypocalcemia. *Increased phosphate levels in the blood (Hyperphosphatemia)* - **Hyperphosphatemia** is not a feature of sarcoidosis. Calcium and phosphate levels often have an inverse relationship, so with hypercalcemia, phosphate levels tend to be normal or slightly decreased due to suppression of parathyroid hormone. - Hyperphosphatemia is more commonly associated with **renal failure** or certain **endocrine disorders**. *Decreased phosphate levels in the blood (Hypophosphatemia)* - While **hypophosphatemia** can occur in conditions with high vitamin D activity (as increased active vitamin D can promote renal phosphate excretion), it is not the primary or most notable electrolyte disturbance specifically linked to sarcoidosis. - **Hypercalcemia** is the more consistently observed electrolyte abnormality in sarcoidosis related to ectopic vitamin D production [1].
Question 88: Central bronchiectasis is seen with
- A. Cystic fibrosis (Correct Answer)
- B. Tuberculosis
- C. Bronchogenic carcinoma
- D. Cystic Adenomatoid Malformation (CAM)
Explanation: ***Cystic fibrosis*** - **Cystic Fibrosis (CF)** is a genetic disorder commonly associated with **central bronchiectasis**, particularly affecting the upper lobes and central airways. - The abnormal mucus production in CF leads to chronic infection, inflammation, and eventual **dilation of the bronchi**, prominent in the central regions. *Bronchogenic carcinoma* - **Bronchogenic carcinoma** can cause **post-obstructive bronchiectasis** distal to the tumor due to airway obstruction and reduced clearance. - However, the bronchiectasis tends to be **localized** to the segment supplied by the obstructed bronchus, rather than being diffusely central. *Tuberculosis* - **Tuberculosis (TB)** can lead to bronchiectasis, often affecting the **upper lobes** and causing localized airway damage. - While TB can cause changes in the bronchi, it is typically linked with **focal or segmental bronchiectasis** resulting from inflammatory destruction, not diffuse central bronchiectasis like CF. *Cystic Adenomatoid Malformation (CAM)* - **Cystic Adenomatoid Malformation (CAM)** is a **congenital lung lesion** with abnormal airway development, but it does not primarily involve bronchiectasis. - CAM is characterized by **cystic structures** or abnormal lung tissue, not the permanent dilation of the bronchi seen in typical bronchiectasis.
Question 89: Post-tubercular bronchiectasis is most commonly seen with
- A. Pertussis
- B. Cystic fibrosis
- C. Kartagener syndrome
- D. Tuberculosis (Correct Answer)
Explanation: ***Tuberculosis*** - **Tuberculosis (TB)**, particularly childhood TB, is a leading cause of post-infectious bronchiectasis, especially in regions with high TB prevalence [1]. - The inflammatory and destructive processes associated with TB infection in the lungs can lead to irreversible dilation and damage of the bronchi [1]. *Pertussis* - While **pertussis** can cause severe respiratory inflammation and chronic cough, it is a less common cause of widespread, irreversible bronchiectasis compared to tuberculosis [1]. - The damage caused by pertussis is typically more acute and less likely to lead to long-term structural changes like those seen in post-tubercular bronchiectasis. *Cystic fibrosis* - **Cystic fibrosis** is a genetic disorder that causes thick, sticky mucus to build up in the lungs, leading to chronic infections and bronchiectasis [1]. - However, post-tubercular bronchiectasis refers specifically to bronchiectasis developing *after* a tuberculosis infection, not as a primary genetic condition. *Kartagener syndrome* - **Kartagener syndrome** is a genetic disorder characterized by defects in ciliary function, leading to impaired mucociliary clearance and recurrent respiratory infections, which can result in bronchiectasis [1]. - Similar to cystic fibrosis, this is a primary genetic cause of bronchiectasis, distinct from bronchiectasis occurring as a sequela of tuberculosis.
Question 90: In a patient with COPD, what is the best management option?
- A. Quit smoking (Correct Answer)
- B. Bronchodilators
- C. Low flow oxygen
- D. Mucolytics
Explanation: ***Quit smoking*** - **Smoking cessation** is the single most effective intervention for slowing the progression of **COPD** and improving lung function [1]. - It reduces exacerbation rates and improves overall mortality, making it the cornerstone of management [1]. *Bronchodilators* - **Bronchodilators** (e.g., beta-agonists, anticholinergics) are crucial for symptomatic relief by opening airways, but they do not alter the disease progression [1]. - While essential for managing symptoms, they are not the "best" in terms of modifying the disease course. *Low flow oxygen* - **Oxygen therapy** is indicated for patients with **severe hypoxemia** (PaO2 < 55 mmHg or SaO2 < 88%) to improve survival and quality of life [2]. - It is a supportive treatment for advanced disease and does not prevent or slow the progression of COPD itself. *Mucolytics* - **Mucolytics** may be used in some patients with COPD and chronic productive cough to reduce sputum viscosity and improve clearance. - Their benefit is primarily symptomatic, and they do not have a significant impact on disease progression or mortality.