NEET-PG 2013 - Internal Medicine Practice Questions

Q: Response to iron therapy in iron deficiency anemia is denoted by?

Reticulocytosis. 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.

Q: Which of the following is NOT a feature of Peutz-Jeghers syndrome?

Autosomal recessive inheritance. ***High risk of malignancy*** - Peutz-Jeghers syndrome is primarily associated with **benign hamartomatous polyps**, not a **high risk of malignancy**, which distinguishes it from other syndromes. - Although patients may develop cancers [1], the syndrome itself does not inherently denote a high malignancy risk like other syndromes such as familial adenomatous polyposis. *Autosomal dominant* - This syndrome is indeed **autosomal dominant**, caused by mutations in the STK11 gene. - Families with this condition typically show **vertical transmission**, characteristic of autosomal dominant inheritance. *Hamartomatous polyp* - Individuals with Peutz-Jeghers syndrome develop **hamartomatous polyps**, which are a hallmark feature of the condition [1]. - These polyps can occur in the gastrointestinal tract and are benign lesions rather than adenomatous type seen in other syndromes [1]. *Mucocutaneous pigmentation* - Mucocutaneous pigmentation, such as **freckling around the lips and buccal mucosa**, is a key clinical feature of Peutz-Jeghers syndrome. - This pigmentation usually appears in childhood and is often a distinguishing sign of the syndrome.

Q: What is the primary condition associated with positive anti-dsDNA antibodies?

SLE. ***SLE*** - **Anti-dsDNA antibodies** are a highly specific marker for **Systemic Lupus Erythematosus (SLE)** and are included in its diagnostic criteria [1]. - The levels of **anti-dsDNA antibodies** can also correlate with disease activity, particularly in cases of **lupus nephritis** [1]. *RA* - **Rheumatoid Arthritis (RA)** is primarily associated with **rheumatoid factor (RF)** and **anti-citrullinated protein antibodies (ACPA)** or **anti-CCP antibodies**. - While ANA (antinuclear antibodies) can be positive in RA, **anti-dsDNA antibodies** are not a characteristic serological marker [1]. *Scleroderma* - **Scleroderma**, or systemic sclerosis, is characterized by specific antibodies such as **anti-Scl-70 (topoisomerase I)**, **anti-centromere antibodies**, and **anti-RNA polymerase III antibodies**, depending on the subtype. - **Anti-dsDNA antibodies** are not typically found in scleroderma and do not play a role in its diagnosis [1]. *PAN* - **Polyarteritis Nodosa (PAN)** is a **necrotizing vasculitis** of medium-sized arteries and is not associated with **anti-dsDNA antibodies**. - PAN is generally considered an **ANCA-negative vasculitis**, and its diagnosis relies more on clinical features, angiography, and biopsy findings.

Q: What is the complete classic triad of findings that defines Young's syndrome?

Azoospermia, bronchiectasis, and chronic sinusitis. ***Azoospermia, bronchiectasis, and chronic sinusitis*** - Young's syndrome is characterized by the triad of **azoospermia** (due to obstructive epididymal dysfunction), **bronchiectasis**, and **chronic sinusitis** [1]. - This syndrome primarily affects **middle-aged men** and is often mistaken for cystic fibrosis due to similar respiratory symptoms. *Azoospermia, asthma, and chronic rhinitis* - This option incorrectly lists **asthma** and **chronic rhinitis** instead of bronchiectasis and chronic sinusitis. - While respiratory symptoms are part of Young's syndrome, specifically **bronchiectasis** and **sinusitis** are key [1]. *Oligospermia, bronchiectasis, and chronic sinusitis* - This option is incorrect because Young's syndrome is defined by **azoospermia** (complete absence of sperm), not just **oligospermia** (low sperm count). - The obstructive nature of the epididymal dysfunction in Young's syndrome leads to a complete lack of sperm. *Azoospermia, chronic bronchitis, and nasal polyps* - This option incorrectly identifies **chronic bronchitis** and **nasal polyps** as part of the classic triad. - The correct respiratory components are **bronchiectasis** and **chronic sinusitis**, which signify persistent inflammation and structural lung changes rather than simply bronchitis.

Q: Which of the following statements about hypercalcemia in sarcoidosis is false?

Parathormone level is increased. ***Parathormone level is increased*** - In **sarcoidosis-associated hypercalcemia**, the parathormone (PTH) level is typically **low or suppressed**. [1] - This is because the hypercalcemia is due to **extra-renal 1-$\alpha$ hydroxylation** of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D (calcitriol) by macrophages in granulomas, not primary hyperparathyroidism. [1] *PTHrP level is increased* - This statement is **false** for sarcoidosis. Elevated **parathyroid hormone-related peptide (PTHrP)** is a common cause of hypercalcemia in **malignancy**, particularly squamous cell carcinomas, but not in sarcoidosis. - Hypercalcemia in sarcoidosis is **PTH-independent** and not mediated by PTHrP. [1] *Oral steroids are useful* - This statement is **true**. **Corticosteroids** (like oral prednisone) are effective in treating hypercalcemia in sarcoidosis. - They work by **inhibiting the activity of 1-$\alpha$ hydroxylase** in alveolar macrophages and reducing intestinal calcium absorption. *Calcitriol level is increased* - This statement is **true**. In sarcoidosis, activated **macrophages within granulomas** aberrantly express **1-$\alpha$ hydroxylase**. [1] - This leads to the **extra-renal synthesis of calcitriol** (1,25-dihydroxyvitamin D), which increases intestinal calcium absorption and bone resorption, causing hypercalcemia. [1]

Q: Which antibodies in a mother with SLE are responsible for congenital heart disease in the child?

Anti-Ro & Anti-La. ***Anti-Ro & Anti-La*** - These antibodies are actively transported across the **placenta** and can target fetal cardiac tissue, leading to **congenital heart block** [2]. - They are classically associated with **neonatal lupus erythematosus**, which includes congenital heart block and transient skin lesions [1], [2]. *Anti-histone* - **Anti-histone antibodies** are primarily associated with **drug-induced lupus erythematosus**, rather than congenital heart defects. - While present in some SLE patients, they do not have a direct causal link to fetal cardiac abnormalities. *Anti-ds DNA* - **Anti-dsDNA antibodies** are highly specific for **systemic lupus erythematosus (SLE)** and are associated with disease activity, especially **lupus nephritis** [1]. - They are not directly implicated in causing congenital heart disease in the offspring. *Anti-centromere* - **Anti-centromere antibodies** are characteristic of **CREST syndrome**, a limited form of systemic sclerosis. - They are not found in SLE and thus have no role in SLE-related congenital heart disease.

Q: In a patient presenting with symptoms of drug-induced lupus erythematosus, which antibody is most commonly found?

Anti-histone antibody. ***Anti-histone antibody*** - **Anti-histone antibodies** are present in approximately 90-95% of patients with **drug-induced lupus erythematosus**. - Their presence, especially with a history of exposure to an inducing drug such as **hydralazine** or **procainamide**, strongly suggests this diagnosis. *Anti-Ro* - **Anti-Ro antibodies** are more commonly associated with **Sjogren's syndrome** and **neonatal lupus**, rather than drug-induced lupus [1]. - While they can be present in systemic lupus erythematosus, they are not the hallmark antibody for the drug-induced form. *Ds-DNA* - **Anti-double-stranded DNA (anti-dsDNA) antibodies** are highly specific for **systemic lupus erythematosus (SLE)** and often correlate with disease activity, particularly **lupus nephritis**. - They are typically **negative** or present in very low titers in drug-induced lupus erythematosus. *Anti-Sm* - **Anti-Smith (anti-Sm) antibodies** are highly specific for **systemic lupus erythematosus (SLE)** and are considered a diagnostic marker for the disease [1]. - They are rarely found in patients with drug-induced lupus erythematosus.

Q: Which of the following statements about Alport's syndrome is incorrect?

Autosomal dominant. ***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.

Q: Which of the following statements about HIV associated nephropathy (HIVAN) is incorrect?

HIVAN is associated with shrunken kidneys.. ***Shrunken kidneys*** - In HIV-associated nephropathy, kidneys typically appear **enlarged** due to hyperplasia of podocytes and other glomerular changes. - **Shrunken kidneys** are not a characteristic feature, making this statement incorrect. *Develops when CD4<200* - HIV-associated nephropathy often arises when CD4 counts drop **below 200 cells/mm³**, indicating severe immunosuppression. - This is a common threshold for the occurrence of opportunistic infections and kidney issues in HIV patients. *15% cases show mesengial proliferation* - **Mesangial proliferation** can occur in about **15% to 30%** of cases of HIV-associated nephropathy, which aligns with the typical histological findings. - Incorrect assumptions might stem from misunderstanding the varying morphologies associated with HIV nephropathy. *Proteinuria* - **Proteinuria** is a common clinical feature of HIV-associated nephropathy, with the condition often presenting with significant protein loss in the urine. - The nephropathy especially results in **nephrotic syndrome**, characterized by high levels of proteinuria.

Q: Chronic atrophy of adrenal gland will result in which hormone deficiency ?

Cortisol. ***Cortisol*** - **Chronic atrophy of the adrenal gland**, often seen in conditions like **Addison's disease** [1], primarily leads to a deficiency of **glucocorticoids**, the main one being cortisol [2]. - **Cortisol** is produced in the **zona fasciculata** of the adrenal cortex, which is highly susceptible to damage in atrophic conditions [2]. *Aldosterone* - While aldosterone is produced in the adrenal cortex (**zona glomerulosa**), its deficiency is more characteristic of primary adrenal insufficiency affecting the entire cortex, not necessarily solely from 'chronic atrophy' which can have varied pathophysiology [2]. - In some autoimmune forms of adrenal atrophy (Addison's disease), **aldosterone deficiency** can occur, but **cortisol deficiency** is a more universal and defining feature [1][3]. *Dehydroepiandrosterone (DHEA)* - **DHEA** is an adrenal androgen produced in the **zona reticularis** of the adrenal cortex [2]. Its deficiency is also common in adrenal atrophy. - However, **cortisol deficiency** generally has more immediate and life-threatening clinical consequences compared to DHEA deficiency. *Epinephrine* - Epinephrine is produced by the **adrenal medulla**, which is distinct from the adrenal cortex where atrophy typically occurs in conditions causing hormone deficiencies. - Therefore, **adrenal gland atrophy** primarily affecting the cortex would not lead to **epinephrine deficiency** as the medulla usually remains functional.

Question 1

Response to iron therapy in iron deficiency anemia is denoted by?

Accepted Answer

Reticulocytosis

Answer

Increase in hemoglobin

Answer

Restoration of enzymes

Answer

Increase in iron binding capacity

Question 2

Which of the following is NOT a feature of Peutz-Jeghers syndrome?

Accepted Answer

Autosomal recessive inheritance

Answer

Mucocutaneous pigmentation

Answer

Autosomal dominant

Answer

Hamartomatous polyp

Question 3

What is the primary condition associated with positive anti-dsDNA antibodies?

Accepted Answer

SLE

Answer

RA

Answer

Scleroderma

Answer

PAN

Question 4

What is the complete classic triad of findings that defines Young's syndrome?

Accepted Answer

Azoospermia, bronchiectasis, and chronic sinusitis

Answer

Oligospermia, bronchiectasis, and chronic sinusitis

Answer

Azoospermia, asthma, and chronic rhinitis

Answer

Azoospermia, chronic bronchitis, and nasal polyps

Question 5

Which of the following statements about hypercalcemia in sarcoidosis is false?

Accepted Answer

Parathormone level is increased

Answer

PTHrP level is increased

Answer

Oral steroids are useful

Answer

Calcitriol level is increased

Question 6

Which antibodies in a mother with SLE are responsible for congenital heart disease in the child?

Accepted Answer

Anti-Ro & Anti-La

Answer

Anti-ds DNA

Answer

Anti-centromere

Answer

Anti-histone

Question 7

In a patient presenting with symptoms of drug-induced lupus erythematosus, which antibody is most commonly found?

Accepted Answer

Anti-histone antibody

Answer

Ds-DNA

Answer

Anti-Sm

Answer

Anti-Ro

Question 8

Which of the following statements about Alport's syndrome is incorrect?

Accepted Answer

Autosomal dominant

Answer

Nerve deafness

Answer

Glomerulonephritis

Answer

X-linked

Question 9

Which of the following statements about HIV associated nephropathy (HIVAN) is incorrect?

Accepted Answer

HIVAN is associated with shrunken kidneys.

Answer

HIVAN is characterized by proteinuria.

Answer

HIVAN typically develops when CD4 count is less than 200.

Answer

About 15% of cases show mesangial proliferation.

Question 10

Chronic atrophy of adrenal gland will result in which hormone deficiency ?

Accepted Answer

Cortisol

Answer

Aldosterone

Answer

Dehydroepiandrosterone (DHEA)

Answer

Epinephrine

NEET-PG 2013 — Internal Medicine