Which of the following is not an obstructive lung disease?
Which of the following statements about Gilbert syndrome is false?
What is the most common location of gastrinoma?
Which of the following statements about Alport's syndrome is incorrect?
Anemia with reticulocytosis is seen in -
Thalassemia gives protection against ?
Response to iron therapy in iron deficiency anemia is denoted by?
Primary hypercholesterolemia is:
Which of the following is NOT a symptom of mild dehydration?
If a claw hand develops in a patient with Leprosy, what is the classification of the deformity?
NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 31: Which of the following is not an obstructive lung disease?
- A. Emphysema
- B. Interstitial fibrosis (Correct Answer)
- C. Asthma
- D. Bronchitis
Explanation: ***Interstitial fibrosis*** - **Interstitial fibrosis** is a **restrictive lung disease**, characterized by **reduced lung elasticity** and lung volumes, rather than airway obstruction [1]. - In this condition, the **lung tissue becomes scarred and stiff**, making it difficult to expand fully during inspiration [1]. *Emphysema* - **Emphysema** is a classic **obstructive lung disease** caused by the destruction of the **alveolar walls**, leading to enlarged air spaces and loss of elastic recoil [3]. - This destruction results in **airflow limitation**, particularly during exhalation, as airways collapse prematurely. *Asthma* - **Asthma** is an **obstructive lung disease** characterized by **reversible airway inflammation**, bronchoconstriction, and increased mucus production [2]. - These factors lead to **episodic airflow obstruction**, making it difficult to breathe, especially during exacerbations [2]. *Bronchitis* - **Bronchitis**, particularly **chronic bronchitis**, is an **obstructive lung disease** defined by chronic inflammation of the bronchi. - This inflammation causes **mucus hypersecretion** and narrowing of the airways, leading to persistent cough and airflow limitation.
Question 32: Which of the following statements about Gilbert syndrome is false?
- A. Normal liver histology
- B. Autosomal dominant
- C. Elevated bilirubin levels are present
- D. Causes cirrhosis (Correct Answer)
Explanation: ***Causes cirrhosis*** - **Gilbert syndrome** is a benign condition characterized by intermittent unconjugated hyperbilirubinemia and does **not lead to cirrhosis** [1]. - Cirrhosis is a severe form of **liver scarring** resulting from chronic damage, which is not a feature of Gilbert syndrome. *Normal liver histology* - The liver structure and function in individuals with Gilbert syndrome are typically **normal**, distinguishing it from other liver disorders [2]. - Histological examination of liver biopsies usually reveals no abnormalities, reflecting the **benign nature** of the condition. *Autosomal dominant* - Gilbert syndrome is inherited in an **autosomal recessive** pattern, not autosomal dominant [2]. - It results from a reduction in the activity of the **UGT1A1 enzyme**, which is responsible for bilirubin conjugation [1], [2]. *Elevated bilirubin levels are present* - Individuals with Gilbert syndrome experience **intermittent unconjugated hyperbilirubinemia**, meaning their indirect bilirubin levels are elevated [3]. - This elevation is usually mild and can be exacerbated by stress, fasting, or illness, but it is typically **harmless** [1], [2].
Question 33: What is the most common location of gastrinoma?
- A. Pancreas
- B. Duodenum (Correct Answer)
- C. Jejunum
- D. Gall bladder
Explanation: ***Duodenum*** - The **duodenum** is the most common site for gastrinomas, accounting for over **half of all cases**, particularly in sporadic gastrinoma and Zollinger-Ellison syndrome. - These tumors are often **small** and **multiple** in the duodenum, making them challenging to locate. *Pancreas* - Pancreatic gastrinomas are also common, representing approximately **25-40% of cases**, but are less frequent than duodenal gastrinomas. - Pancreatic gastrinomas tend to be **larger** and more amenable to surgical resection when compared to duodenal gastrinomas. *Jejunum* - Gastrinomas found in the jejunum are **rare**, accounting for only a small percentage of cases. - The small intestine distal to the duodenum is an **uncommon site** for primary gastrinoma formation. *Gall bladder* - The **gallbladder** is not a typical location for gastrinoma development. - Gastrinomas are neuroendocrine tumors that arise from **gastrin-producing cells**, which are not found in the gallbladder.
Question 34: Which of the following statements about Alport's syndrome is incorrect?
- A. Nerve deafness
- B. Glomerulonephritis
- C. Autosomal dominant (Correct Answer)
- D. X-linked
Explanation: ***Autosomal dominant*** - While there are rare autosomal dominant forms, the most common and classic presentation of **Alport's syndrome is X-linked recessive**, affecting males more severely. - This statement is incorrect because it implies that autosomal dominant inheritance is the primary or typical mode, which is not true for the majority of cases. *Nerve deafness* - **Sensorineural hearing loss**, particularly for high frequencies, is a common and characteristic extra-renal manifestation of Alport's syndrome. - This symptom typically progresses with age and is a key diagnostic feature. *Glomerulonephritis* - **Progressive glomerulonephritis** is the hallmark renal feature of Alport's syndrome, leading to hematuria, proteinuria, and eventually end-stage renal disease. - It is caused by mutations in collagen type IV genes, which disrupt the integrity of the glomerular basement membrane. *X-linked* - The majority of Alport's syndrome cases (about 85%) are **X-linked recessive**, caused by mutations in the *COL4A5* gene located on the X chromosome. - This explains why males are more severely affected and typically present with earlier onset and more rapid progression of renal disease.
Question 35: Anemia with reticulocytosis is seen in -
- A. Hemolysis (Correct Answer)
- B. Iron deficiency anemia
- C. Vitamin B12 deficiency
- D. Aplastic anemia
Explanation: ***Hemolysis*** - Reticulocytosis indicates a compensatory response to anemia, often occurring in hemolytic processes where the **bone marrow increases red blood cell production** in response to red blood cell destruction. - Conditions like **sickle cell disease** or **autoimmune hemolytic anemia** lead to hemolysis, further confirming increased reticulocyte count. *Iron deficiency anemia* - Typically presents with a **low reticulocyte count** as the bone marrow does not have sufficient iron to produce new red blood cells. - This condition is characterized by **microcytic, hypochromic** red blood cells due to inadequate iron stores. *Vitamin B12 deficiency* - Often results in a **macrocytic anemia** with a variable reticulocyte count; however, reticulocytosis is generally not seen initially. - This deficiency affects DNA synthesis, leading to ineffective erythropoiesis and the presence of **megaloblastic changes**. *Aplastic anemia* - Characterized by a **decrease in all types of blood cells** (pancytopenia) and typically has a **low reticulocyte count** due to bone marrow failure. - There is insufficient production of red blood cells, hence **reticulocytosis is not observed**.
Question 36: Thalassemia gives protection against ?
- A. Protection against filaria
- B. Protection against kala-azar
- C. Protection against leptospirosis
- D. Protection against malaria (Correct Answer)
Explanation: Protection against malaria - Individuals with thalassemia, particularly thalassemia trait, have some degree of protection against severe forms of malaria, specifically Plasmodium falciparum [1]. - The altered red blood cell structure and reduced hemoglobin content in thalassemia make the red blood cells less hospitable for the parasites, hindering their replication and survival [1]. Protection against filaria - Filaria is caused by parasitic worms (nematodes) transmitted by mosquitoes, leading to lymphatic filariasis (elephantiasis) or onchocerciasis (river blindness). - Thalassemia's primary impact is on red blood cell health and oxygen transport, offering no known protective effect against nematode infections or their associated pathology. Protection against kala-azar - Kala-azar (visceral leishmaniasis) is caused by Leishmania parasites transmitted by sandflies, primarily affecting the reticuloendothelial system (spleen, liver, bone marrow). - There is no established scientific evidence indicating that thalassemia provides protection against Leishmania infections or their clinical manifestations. Protection against leptospirosis - Leptospirosis is a bacterial infection caused by Leptospira bacteria, typically acquired through contact with contaminated water or animal urine. - Thalassemia is a genetic blood disorder; its physiological effects are unrelated to the mechanisms of infection or immunity against bacterial pathogens like Leptospira.
Question 37: Response to iron therapy in iron deficiency anemia is denoted by?
- A. Increase in hemoglobin
- B. Reticulocytosis (Correct Answer)
- C. Restoration of enzymes
- D. Increase in iron binding capacity
Explanation: Reticulocytosis - Reticulocytosis is one of the earliest signs of a positive response to iron therapy in iron deficiency anemia, occurring within 5-10 days. - It signifies that the bone marrow is effectively producing new red blood cells after iron supplementation. Restoration of enzymes - While iron is a crucial component of many enzymes (e.g., catalase, cytochrome oxidase), its restoration takes time and is not the primary immediate indicator of therapeutic response. - Clinical improvement and other hematological parameters precede the full restoration of enzyme function. Increase in hemoglobin - An increase in hemoglobin is a definitive sign of successful treatment, but it occurs later than reticulocytosis, typically visible after several weeks to months of therapy. - Hemoglobin levels rise as the new, iron-sufficient red blood cells fully mature and replace the older, iron-deficient ones. Increase in iron binding capacity - In iron deficiency anemia, total iron-binding capacity (TIBC) is typically increased due to more transferrin being available to bind iron [1]. - Successful iron therapy would lead to a decrease in TIBC as transferrin sites become saturated with iron, not an increase.
Question 38: Primary hypercholesterolemia is:
- A. Type I
- B. Type IIb
- C. Type IIa (Correct Answer)
- D. Type III
Explanation: ***Type Ha*** - **Primary hypercholesterolemia** specifically refers to **Familial Hypercholesterolemia**, which is classified as Type Ha due to a genetic defect affecting LDL receptor activity [1]. - It typically presents with **high cholesterol levels** and an increased risk of premature cardiovascular disease [1]. *Type I* - Type I hyperlipoproteinemia is associated with **chylomicronemia**, leading to elevated triglycerides rather than cholesterol. - Symptoms include **pancreatitis** and eruptive xanthomas, not primarily high cholesterol levels. *Type III* - Type III hyperlipoproteinemia is known as **Dysbetalipoproteinemia**, associated with **increased IDL** and can cause elevated cholesterol, but is not classified as primary hypercholesterolemia. - It typically presents with **tuberous xanthomas** and is linked to **apolipoprotein E deficiency**. *Type IIb* - Type IIb hyperlipoproteinemia involves **elevation of LDL and VLDL**, but it is not classified as primary hypercholesterolemia; it is a mixed dyslipidemia. - This type usually features **increased cholesterol** and **triglycerides**, distinguishing it from the familial form classified as Type Ha.
Question 39: Which of the following is NOT a symptom of mild dehydration?
- A. Thirst
- B. Restlessness
- C. Dry tongue
- D. Normal BP (Correct Answer)
Explanation: ***Normal BP*** - In **mild dehydration**, the body's compensatory mechanisms, such as increased heart rate and vasoconstriction, typically manage to maintain a **normal blood pressure**. [1] - A significant drop in **blood pressure** (hypotension) is usually indicative of **moderate to severe dehydration**, where these compensatory mechanisms begin to fail. [2] *Thirst* - **Thirst** is one of the **earliest and most reliable** indicators of dehydration, as the body signals a need for fluid intake. [3] - It arises in response to increased plasma osmolality and decreased blood volume, both occurring even in **mild dehydration**. [3] *Restlessness* - **Restlessness** can be an early sign of discomfort and altered mental status associated with **mild dehydration**, particularly in infants and young children. - As the body struggles to maintain fluid balance, individuals may experience irritability and general unease. *Dry tongue* - A **dry tongue** and **dry sticky mucous membranes** are common signs of mild to moderate dehydration. - This symptom results from reduced salivary production due to decreased fluid volume in the body.
Question 40: If a claw hand develops in a patient with Leprosy, what is the classification of the deformity?
- A. Grade 0
- B. Grade I
- C. Grade II (Correct Answer)
- D. Grade III
Explanation: A **claw hand** deformity, characterized by hyperextension of the metacarpophalangeal joints and flexion of the interphalangeal joints, indicates a significant and **visible disability** but the affected part is still functional to a limited degree. In the context of leprosy, this observable and permanent deformity falls under **Grade II** on the WHO disability grading scale, signifying a clear and established disability. This grade indicates **no disability** or deformity related to leprosy. A patient with a claw hand has an obvious physical deformity and functional impairment, thus not fitting this classification. This grade refers to a **detectable impairment** but **no visible deformity**. A claw hand is a clearly visible deformity, making Grade I an inappropriate classification. While Grades are typically 0, I, and II in the WHO disability grading for leprosy, some classifications might refer to severe, non-functional deformities as higher grades. However, Grade II adequately captures **visible and significant deformities** like a claw hand, and a Grade III is not a standard or commonly used classification for a claw hand in leprosy in the WHO system.