Dermatology
1 questionsHLA-Cw6 is associated with
NEET-PG 2015 - Dermatology NEET-PG Practice Questions and MCQs
Question 201: HLA-Cw6 is associated with
- A. Behcet's disease
- B. Pemphigus vulgaris
- C. Psoriasis vulgaris (Correct Answer)
- D. Myasthenia gravis
Explanation: ***Psoriasis vulgaris*** - **HLA-Cw6** is the **strongest genetic risk factor** associated with an increased susceptibility to psoriasis vulgaris, particularly early-onset forms. - Its presence is linked to a more severe and widespread presentation of the disease. *Myasthenia gravis* - This autoimmune disorder is primarily associated with **HLA-DR3** and **HLA-B8**, and autoantibodies against the acetylcholine receptor. - While other HLA alleles may be involved, **HLA-Cw6** is not a primary or strong genetic association for myasthenia gravis. *Behcet's disease* - **HLA-B51** is the most significant genetic association with Behcet's disease, particularly in populations of Middle Eastern and East Asian descent. - Symptoms include **recurrent oral and genital ulcers**, **uveitis**, and skin lesions. *Pemphigus vulgaris* - This autoimmune blistering disease is strongly associated with **HLA-DR4** and **HLA-DRw6**, especially in individuals of Jewish descent. - It involves autoantibodies targeting **desmoglein 1 and 3**, leading to acantholysis within the epidermis.
Internal Medicine
5 questionsIn which non-neoplastic condition is CEA commonly elevated?
Shrinking Lung Syndrome is seen in:
Which of the following findings is diagnostic of iron deficiency anemia?
In which condition is Serum Amyloid Associated (SAA) protein most commonly found?
Extremities are warm in which type of shock
NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 201: In which non-neoplastic condition is CEA commonly elevated?
- A. Pancreatitis
- B. Inflammatory bowel disease (Correct Answer)
- C. Hemolytic anemia
- D. Liver disease
Explanation: ***Inflammatory bowel disease*** - **Carcinoembryonic antigen (CEA)** levels can be elevated in conditions involving active inflammation and rapid cell turnover within the gastrointestinal tract, such as **inflammatory bowel disease (IBD)** [1]. - While CEA is primarily a tumor marker, its elevation in IBD reflects the extensive mucosal inflammation and repair processes, rather than malignancy. *Hemolytic anemia* - **Hemolytic anemia** involves the destruction of red blood cells and does not typically lead to elevated CEA levels. - Elevated CEA is associated with certain epithelial conditions, not primary hematologic disorders. *Pancreatitis* - While **pancreatitis** can cause elevated levels of other markers like amylase and lipase, it is not consistently associated with elevated CEA. - CEA elevation in pancreatic conditions usually points towards a **pancreatic malignancy**. *Liver disease* - **Liver disease**, particularly severe inflammation or cirrhosis, can sometimes cause a mild elevation in CEA due to impaired clearance or increased production in damaged tissue. - However, levels are typically not as high or consistently elevated as in IBD, and significant elevation often prompts investigation for **primary hepatic or metastatic malignancy**.
Question 202: 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 203: Which of the following findings is diagnostic of iron deficiency anemia?
- A. Increased TIBC, decreased serum ferritin (Correct Answer)
- B. Decreased TIBC, decreased serum ferritin
- C. Increased TIBC, increased serum ferritin
- D. Decreased TIBC, increased serum ferritin
Explanation: ***Increased TIBC, decreased serum ferritin*** - **Iron deficiency anemia** is characterized by depleted iron stores, leading to a **decreased serum ferritin** level, which is the most sensitive and specific marker for iron deficiency [4]. - In response to low iron stores, the body upregulates iron absorption and transport mechanisms, resulting in an **increased Total Iron Binding Capacity (TIBC)**, as there are more transferrin molecules available to bind iron [1]. *Decreased TIBC, decreased serum ferritin* - While a **decreased serum ferritin** is consistent with iron deficiency, a **decreased TIBC** is more indicative of **anemia of chronic disease** [1], where the body sequesters iron, leading to reduced iron availability for binding. - In **anemia of chronic disease**, both ferritin (an acute phase reactant) and TIBC can be reduced due to the inflammatory state [1], [2]. *Increased TIBC, increased serum ferritin* - An **increased TIBC** is seen in iron deficiency, but an **increased serum ferritin** indicates adequate or even **overloaded iron stores**, which contradicts the diagnosis of iron deficiency anemia. - High ferritin levels can be seen in conditions like **hemochromatosis** (iron overload) or **inflammation**, where ferritin acts as an acute phase reactant [5]. *Decreased TIBC, increased serum ferritin* - This combination is typical of **anemia of chronic disease**, where inflammation causes **increased serum ferritin** (as an acute phase reactant) and a **decreased TIBC** due to reduced production of transferrin [1]. - In this type of anemia, iron is often trapped within macrophages, making it unavailable for erythropoiesis despite seemingly normal or elevated stores [3].
Question 204: In which condition is Serum Amyloid Associated (SAA) protein most commonly found?
- A. Alzheimer's disease
- B. Malignant hypertension
- C. Chronic inflammatory states (Correct Answer)
- D. Chronic renal failure
- E. Acute myocardial infarction
Explanation: ***Chronic inflammatory states*** [1][2] - Serum amyloid-associated protein is elevated in response to **chronic inflammation**, such as in rheumatic diseases and infections [1][2]. - It serves as a **biomarker** indicating systemic inflammation and is part of the **acute-phase response** [1]. *Chronic renal failure* - While renal failure can lead to amyloidosis, it is not a direct cause of serum amyloid-associated protein elevation. - **Renal impairment** is more associated with a decrease in clearance rather than production of amyloid proteins. *Alzheimer's disease* - Although amyloid plaques are a hallmark of Alzheimer's, they are related to **A-beta peptide**, not serum amyloid-associated protein. - Alzheimer's pathology primarily involves **neurodegeneration** rather than inflammatory response. *Malignant hypertension* - Malignant hypertension primarily affects the **vascular system** and does not directly involve the production of serum amyloid-associated protein. - It is characterized by end-organ damage, rather than a state of chronic inflammation. *Chronic inflammatory conditions like RA, TB & leprosy, osteomyelitis, ankylosing spondylitis, IBD, bronchiectasis, some tumors* [1][2] - While these conditions can be associated with systemic inflammation, they are too specific and do not comprehensively encompass the broader concept of **chronic inflammatory states**. - This option fails to highlight that serum amyloid-associated protein is a marker for **various chronic inflammatory states** beyond just those listed [1].
Question 205: Extremities are warm in which type of shock
- A. Hypovolemic shock
- B. Neurogenic shock (Correct Answer)
- C. Anaphylactic shock
- D. Cardiogenic shock
Explanation: ***Neurogenic shock*** - This type of shock is caused by a loss of **sympathetic tone**, leading to widespread **vasodilation** and a relative hypovolemia, resulting in warm, flushed extremities. - The decreased systemic vascular resistance causes **blood pooling** in the periphery rather than being shunted to vital organs, contributing to the warm skin. *Hypovolemic shock* - Characterized by **decreased blood volume**, leading to activation of the sympathetic nervous system and **vasoconstriction** to shunt blood to vital organs. - This results in **cold, clammy extremities** due to reduced peripheral perfusion. *Anaphylactic shock* - An acute, life-threatening hypersensitivity reaction involving massive release of inflammatory mediators, causing widespread **vasodilation** and increased vascular permeability. - While it can cause flushing and warmth initially due to vasodilation, it often leads to significant fluid shifts and can present with both warm and then cool, clammy skin as shock progresses. *Cardiogenic shock* - Caused by **severe cardiac pump failure**, leading to decreased cardiac output and poor tissue perfusion. - The body's compensatory mechanisms, including sympathetic activation, cause **peripheral vasoconstriction**, leading to **cold, clammy extremities**.
Microbiology
1 questionsThe process by which antigen-specific B lymphocytes are selected and activated to proliferate and produce antibodies is called:
NEET-PG 2015 - Microbiology NEET-PG Practice Questions and MCQs
Question 201: The process by which antigen-specific B lymphocytes are selected and activated to proliferate and produce antibodies is called:
- A. Clonal selection (Correct Answer)
- B. Class switching
- C. Group switching
- D. Hybridisation
Explanation: ***Clonal selection*** - **Clonal selection** is the fundamental process by which an antigen-specific B lymphocyte is **selected** when its B cell receptor (BCR) recognizes and binds to a matching antigen. - This binding triggers the B cell to become **activated**, **proliferate** (undergo clonal expansion), and **differentiate** into plasma cells that produce antibodies specific to that antigen. - This process is the cornerstone of **adaptive immunity**, ensuring that only B cells with receptors matching the encountered antigen are stimulated to respond. *Class switching* - **Class switching** (isotype switching) occurs AFTER clonal selection and activation. - It allows already-activated B cells to change the **antibody class** they produce (from IgM to IgG, IgA, or IgE) while maintaining the **same antigen specificity**. - This process modifies effector functions but does NOT involve the initial selection and activation of antigen-specific B cells. *Group switching* - This is not a recognized term in immunology. - It does not describe any standard process of B cell activation or antibody production. *Hybridisation* - **Hybridization** refers to the formation of double-stranded nucleic acids from complementary strands or the creation of hybrid cells (e.g., hybridomas for monoclonal antibody production). - It is not the physiological process by which B lymphocytes are selected and activated in response to antigen exposure.
Pathology
1 questionsWhich of the following is NOT seen in polycythemia vera?
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 201: Which of the following is NOT seen in polycythemia vera?
- A. Increased erythropoietin (Correct Answer)
- B. Intrinsic abnormality of hematopoietic precursors
- C. Erythropoietin independent growth of red cell progenitors
- D. Most common cause of primary polycythemia
Explanation: ***Increased erythropoietin*** - In polycythemia vera, patients usually exhibit **low erythropoietin levels** due to feedback inhibition from increased red blood cell mass. - The condition is driven by a **myeloproliferative disorder** [2], not by increased erythropoietin stimulation. *Most common cause of polycythemia* - This option is incorrect because polycythemia vera is specifically a type of **primary polycythemia** [1], rather than the most common cause, which is often **secondary causes** such as hypoxia or abnormal erythropoietin production. - Other causes including chronic lung disease or renal tumors are more prevalent sources of increased red blood cell production. *Intrinsic abnormality of hematopoietic precursors* - While polycythemia vera indeed involves an **abnormality in hematopoietic stem cells** [1], it is not the only mechanism leading to polycythemia; many cases have secondary causes. - Hence, this option misrepresents the specific and more accurate characterization of polycythemia vera. *Erythropoietin independent growth of red cell progenitors* - Polycythemia vera is associated with **erythropoietin-independent** proliferation of hematopoietic cells [2], which is characteristic of the condition due to mutations in **JAK2** [2,3]. - This accurately reflects a significant feature of the disease, aligning closely with the pathophysiology. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 663-664. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 614-615. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 626-627.
Pharmacology
2 questionsWhich of the following statements about glucocorticoids is true?
Which of the following agents requires the MOST caution when combined with spironolactone due to increased risk of hyperkalemia:
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 201: Which of the following statements about glucocorticoids is true?
- A. Glucocorticoids directly activate T-helper cells.
- B. Glucocorticoids have no effect on immune cells.
- C. Glucocorticoids downregulate MHC class II expression. (Correct Answer)
- D. Glucocorticoids enhance the activity of cytotoxic T cells.
Explanation: ***Glucocorticoids downregulate MHC class II expression.*** - Glucocorticoids exert **immunosuppressive effects** by reducing the expression of **MHC class II molecules** on antigen-presenting cells. - This downregulation impairs the ability of antigen-presenting cells to activate **CD4+ T-helper cells**, thereby suppressing adaptive immune responses. *Glucocorticoids directly activate T-helper cells.* - Glucocorticoids do not directly activate T-helper cells; rather, they have an **inhibitory effect** on T-cell function and proliferation. - They tend to promote **T-cell apoptosis** and reduce cytokine production, thus dampening T-helper cell responses. *Glucocorticoids have no effect on immune cells.* - This statement is incorrect as glucocorticoids have profound and widespread **immunosuppressive and anti-inflammatory effects** on various immune cells. - They influence the function, proliferation, and survival of **lymphocytes, macrophages, and granulocytes**. *Glucocorticoids enhance the activity of cytotoxic T cells.* - Glucocorticoids generally **suppress immune responses**, including the activity of **cytotoxic T cells (CTLs)**, rather than enhancing it. - They tend to inhibit the production of **interleukins** necessary for CTL activation and proliferation.
Question 202: Which of the following agents requires the MOST caution when combined with spironolactone due to increased risk of hyperkalemia:
- A. ACE inhibitors (Correct Answer)
- B. Beta-blockers
- C. Amlodipine
- D. Chlorothiazide
Explanation: ***ACE inhibitors*** - Spironolactone is a **potassium-sparing diuretic** that increases potassium levels by blocking aldosterone's effects in the collecting duct [1]. - **ACE inhibitors** also decrease aldosterone production [2], leading to reduced potassium excretion and a significant risk of **severe hyperkalemia** when combined with spironolactone [1, 2].*Beta-blockers* - While beta-blockers can cause a slight increase in plasma potassium by inhibiting cellular potassium uptake, this effect is generally modest and does not pose a major hyperkalemia risk when co-administered with spironolactone. - Their primary interaction concerns blood pressure and heart rate, not direct potassium handling.*Amlodipine* - Amlodipine is a **calcium channel blocker** that primarily causes vasodilation and does not significantly alter potassium balance. - Therefore, it does not substantially increase the risk of hyperkalemia when used concurrently with spironolactone.*Chlorothiazide* - Chlorothiazide is a **thiazide diuretic** that promotes potassium excretion, leading to a risk of hypokalemia. - When combined with spironolactone, a potassium-sparing diuretic, these agents can **partially offset each other's effects** on potassium balance, potentially reducing the risk of hyperkalemia compared to ACE inhibitors.