What is the most common cause of lung abscess in comatose patients?
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:
What is the primary cause of Common Variable Immunodeficiency (CVID)?
ABO non- secretors are more prone to ?
Buboes form is which stage of LGV?
What is the PRIMARY evidence-based intervention for preventing catheter-associated urinary tract infections (CAUTIs)?
Which condition is not associated with complement deficiency?
Wide pulse pressure is seen in all except which of the following?
NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 41: What is the most common cause of lung abscess in comatose patients?
- A. Staph aureus
- B. Oral anaerobes (Correct Answer)
- C. Klebsiella
- D. Tuberculosis
Explanation: Oral anaerobes - **Comatose patients** are at high risk for **aspiration** of oropharyngeal flora, which predominantly consists of anaerobic bacteria. [1] - Aspiration of these organisms, especially in compromised lung tissue, frequently leads to **necrotizing pneumonia** and subsequent abscess formation. [1] *Staph aureus* - While *Staphylococcus aureus* can cause lung abscesses, particularly in the context of **hematogenous spread** (e.g., endocarditis) or nosocomial infections, it is not the most common cause in *comatose patients* who typically aspirate oral flora. [2] - *S. aureus* lung abscesses are often associated with multiple, smaller lesions rather than a single, large abscess from aspiration. *Klebsiella* - *Klebsiella pneumoniae* can cause severe, **rapidly progressive pneumonia** that may lead to abscess formation, especially in individuals with **alcoholism** or **diabetes**. - However, it is less common than oral anaerobes as the primary cause of abscess in the general population of comatose patients, whose main risk factor is aspiration of normal oral flora. [1] *Tuberculosis* - **Mycobacterium tuberculosis** can cause cavitary lung lesions, but these are typically chronic and result from primary or reactivated tuberculosis disease, not acute aspiration. [3] - Lung abscesses caused by tuberculosis are histologically distinct from pyogenic abscesses and are characterized by **granulomatous inflammation** and caseous necrosis.
Question 42: 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 43: 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 44: 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 45: What is the primary cause of Common Variable Immunodeficiency (CVID)?
- A. Defective B cell function
- B. Absent B cells
- C. Reduced number of B cells
- D. Defective B cell differentiation (Correct Answer)
Explanation: ***Defective B cell differentiation*** - CVID is characterized primarily by a failure of **B cells** to differentiate into **plasma cells**, which are responsible for producing antibodies [1]. - This defective differentiation leads to **hypogammaglobulinemia**, or low levels of immunoglobulins [1]. *Absent B cells* - Complete absence of B cells is characteristic of severe combined immunodeficiency (SCID) or X-linked agammaglobulinemia (XLA), not CVID [1]. - In CVID, B cells are typically present, but they are dysfunctional. *Reduced number of B cells* - While some patients with CVID may have reduced B cell numbers, this is not the primary or defining defect. - The key issue is the inability of existing B cells to mature and produce antibodies effectively. *Defective B cell function* - While B cell function is indeed defective in CVID, the root cause of this malfunction is specifically the **failure of differentiation** into mature plasma cells. - The B cells are unable to perform their primary function of antibody production due to this arrest in their development.
Question 46: ABO non- secretors are more prone to ?
- A. Increased risk of infections (Correct Answer)
- B. Autoimmune diseases
- C. Cardiovascular diseases
- D. Cancer
Explanation: Increased risk of infections - Non-secretors of ABO antigens exhibit an increased susceptibility to a variety of infections, particularly bacterial and viral pathogens. - This is thought to be due to the absence of ABO antigens in secretions, which typically act as decoy receptors to prevent pathogen adhesion to host cells. Autoimmune diseases - While some associations between ABO blood groups and autoimmune diseases exist, non-secretor status is not consistently linked to a higher overall risk of autoimmune conditions. Cardiovascular diseases - ABO blood groups have been associated with cardiovascular risk, with non-O blood types generally having a slightly higher risk of certain cardiovascular events. - However, secretor status (the ability to secrete ABO antigens into bodily fluids) itself is not a prominent independent risk factor for cardiovascular diseases. Cancer - There are some documented associations between specific ABO blood types and certain types of cancer (e.g., non-O blood types with pancreatic cancer), but this is distinct from secretor status. - Being an ABO non-secretor is not a primary, broadly recognized risk factor for developing cancer.
Question 47: Buboes form is which stage of LGV?
- A. Secondary (Correct Answer)
- B. Tertiary
- C. Latent
- D. Primary
Explanation: ***Secondary*** - Buboes, which are swollen, painful lymph nodes, are a hallmark of the **secondary stage** of **Lymphogranuloma Venereum (LGV)** [1]. - This stage typically develops weeks after the initial infection, following the unnoticed or transient primary lesion. *Primary* - The primary stage of LGV is characterized by a **small, painless papule or ulcer** at the site of inoculation, which often goes unnoticed. - **Buboes are not formed** during this initial, often asymptomatic, phase. *Tertiary* - The tertiary stage of LGV involves **chronic inflammation** and **tissue destruction**, leading to complications like **genital elephantiasis**, rectal strictures, and fistulas. - While there is chronic lymphedema, the acute, painful buboes are characteristic of the secondary stage, not this late, destructive phase. *Latent* - The concept of a latent stage is not typically used to describe the progression of LGV in the same way as other infections like syphilis. - LGV progresses through distinct symptomatic primary, secondary, and potentially tertiary stages without a prolonged asymptomatic latency period between symptom presentations.
Question 48: What is the PRIMARY evidence-based intervention for preventing catheter-associated urinary tract infections (CAUTIs)?
- A. Use of face mask during catheter insertion
- B. Prophylactic antibiotics are effective
- C. Early catheter removal when clinically appropriate
- D. Closed drainage technique to minimize bacterial entry (Correct Answer)
Explanation: ***Closed drainage technique to minimize bacterial entry*** - Maintaining a **closed drainage system** prevents the entry of bacteria into the urinary tract, which is a primary cause of CAUTIs. - This technique involves ensuring the connection between the catheter and the drainage bag remains sealed at all times, minimizing **environmental contamination**. *Prophylactic antibiotics are effective* - **Prophylactic antibiotics** are generally not recommended for routine CAUTI prevention due to concerns about **antibiotic resistance** and limited evidence of effectiveness [1]. - Their use is typically reserved for specific high-risk procedures or patient populations. *Use of face mask during catheter insertion* - While maintaining **asepsis** during catheter insertion is crucial, the use of a face mask specifically addresses **respiratory droplet transmission**, which is not the primary route of bacterial entry into the urinary system during catheterization. - **Sterile gloves** and a **sterile field** are more directly relevant for preventing contamination during insertion [1]. *Early catheter removal when clinically appropriate* - While **early catheter removal** is a critical strategy for CAUTI prevention by reducing dwell time, the question asks for the *primary* evidence-based intervention [1]. A **closed drainage system** directly addresses the mechanism of bacterial entry while the catheter is in place. - Reducing catheter duration minimizes risk, but the closed system ensures safety during the necessary period of catheterization.
Question 49: Which condition is not associated with complement deficiency?
- A. SLE
- B. PNH
- C. Membranous nephritis (Correct Answer)
- D. Hereditary angioedema
Explanation: Membranous nephritis - Membranous nephritis is associated with immune complex deposition rather than complement deficiencies. [1] - The disease is characterized by thickening of the glomerular basement membrane without significant complement involvement. [1] PNH - Paroxysmal nocturnal hemoglobinuria (PNH) is due to a defect in the GPI-anchor leading to complement-mediated hemolysis. - Complement activation plays a critical role in the destruction of red blood cells in this condition. Hereditary angioedema - Hereditary angioedema is caused by deficiencies in C1 inhibitor, leading to uncontrolled activation of complement. - This results in edema episodes, directly linked to complement pathway dysregulation. SLE - Systemic lupus erythematosus (SLE) involves complement consumption due to autoantibody formation against nuclear antigens. - The disease often presents with hypocomplementemia, indicating complement system involvement.
Question 50: Wide pulse pressure is seen in all except which of the following?
- A. Aortic Regurgitation
- B. PDA
- C. A.V. malformation
- D. Aortic stenosis (Correct Answer)
Explanation: **Aortic stenosis** - In **aortic stenosis**, there is a fixed obstruction to left ventricular outflow, leading to a compensatory increase in systolic pressure to overcome the stenotic valve [2]. - The **reduced stroke volume** and impaired flow through the rigid valve cause a lower pulse pressure, often resulting in a **narrow pulse pressure**. *PDA (Patent Ductus Arteriosus)* - In **PDA**, blood flows from the aorta to the pulmonary artery during systole and diastole, causing a decrease in diastolic pressure. - This creates a **run-off phenomenon**, leading to a **wide pulse pressure** due to high systolic and low diastolic pressures. *Aortic Regurgitation* - **Aortic regurgitation** involves blood flowing back into the left ventricle during diastole, causing a rapid fall in diastolic pressure [1]. - The increased stroke volume from the left ventricle leads to a high systolic pressure, resulting in a **wide pulse pressure** [1]. *A.V. malformation (Arteriovenous Malformation)* - An **AV malformation** creates a shunt where arterial blood flows directly into the venous system, bypassing the capillary bed. - This leads to a **decrease in peripheral resistance** and an increased cardiac output, causing a higher systolic pressure and a lower diastolic pressure, thereby producing a **wide pulse pressure**.