Shrinking Lung Syndrome is seen in:
What is the mode of inheritance for the most common form of hypophosphatemic rickets?
Most common route of infection in pasteurella cellulitis -
Most common complication of diphtheria is -
Eschar is seen in all the Rickettsial diseases except:
What is the causative agent of trench fever?
What is the significance of the absence of Vi-antibody in a patient with typhoid fever?
Which of the following statements regarding Pertussis is INCORRECT?
What is the primary cause of Common Variable Immunodeficiency (CVID)?
ABO non- secretors are more prone to ?
NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 31: 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 32: 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 33: 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.
Question 34: 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 35: 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 36: 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 37: What is the significance of the absence of Vi-antibody in a patient with typhoid fever?
- A. Indicates a poor prognosis
- B. Indicates a favorable prognosis (Correct Answer)
- C. No impact on prognosis
- D. Suggests a negative response to treatment
Explanation: ***Indicates a favorable prognosis*** - The **Vi (Virulence) antigen** is a **polysaccharide capsule** that helps *Salmonella typhi* evade the immune system and is associated with **virulence** and **carrier state development**. - **Absence of Vi-antibody** indicates infection with a **less virulent strain**, successful **immune clearance**, and **lower likelihood** of developing a chronic carrier state. *Indicates a poor prognosis* - The **absence of Vi-antibody** is actually associated with **better outcomes**, not worse prognosis. - **Poor prognosis** in typhoid fever is typically related to complications like **intestinal perforation** or **septic shock**, not Vi-antibody status [1]. *No impact on prognosis* - **Vi-antibody status** is a **recognized prognostic marker** in typhoid fever and does have clinical significance. - The **presence of Vi-antibodies** may indicate **persistent infection** or **carrier state development**, making it a relevant prognostic indicator. *Suggests a negative response to treatment* - **Absence of Vi-antibody** typically indicates **successful treatment response** and **effective clearance** of the organism. - **Negative treatment response** would be evidenced by **persistent fever**, **positive cultures**, or **clinical deterioration** despite appropriate antibiotic therapy.
Question 38: Which of the following statements regarding Pertussis is INCORRECT?
- A. The drug of choice is Erythromycin.
- B. Cerebellar ataxia is a known complication. (Correct Answer)
- C. Some infections may be subclinical.
- D. The most infective stage is the catarrhal stage.
Explanation: ***Cerebellar ataxia is a known complication.*** - **Cerebellar ataxia** is not a typical or known complication of pertussis. Complications usually involve the respiratory, neurological (e.g., seizures, encephalopathy due to hypoxia), and nutritional systems due to severe coughing. - While neurological complications can occur, **ataxia** specifically is not frequently sighted in the context of pertussis. *Some infections may be subclinical.* - Some individuals, especially those partially immunized or older, can experience **subclinical or atypical infections** with pertussis, often presenting as a mild cough. - This characteristic makes it difficult to control the spread of the disease as infected individuals may not be recognized. *The most infective stage is the catarrhal stage.* - The **catarrhal stage**, characterized by non-specific cold-like symptoms, is the most contagious phase because bacterial shedding is highest. - During this stage, symptoms are mild and often indistinguishable from a common cold, leading to widespread transmission before diagnosis. *The drug of choice is Erythromycin.* - **Erythromycin**, or other macrolides like azithromycin or clarithromycin, are the drugs of choice for treating pertussis. - These antibiotics are most effective when administered early in the **catarrhal stage** to reduce disease severity and prevent transmission.
Question 39: 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 40: 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.