Biochemistry
1 questionsWhich of the following is a positive acute phase protein that enhances the acute phase response?
NEET-PG 2015 - Biochemistry NEET-PG Practice Questions and MCQs
Question 361: Which of the following is a positive acute phase protein that enhances the acute phase response?
- A. Fibrinogen (Correct Answer)
- B. Transferrin
- C. Albumin
- D. Prealbumin
Explanation: ***Fibrinogen*** - **Fibrinogen** is a key **positive acute phase protein** whose concentration increases significantly during inflammation - Its elevation contributes to the acute phase response by promoting **blood clotting** and influencing **erythrocyte sedimentation rate (ESR)** - Along with C-reactive protein (CRP), haptoglobin, and serum amyloid A, fibrinogen is among the major positive acute phase reactants *Transferrin* - **Transferrin** is a **negative acute phase protein**, meaning its concentration decreases during inflammation - This reduction is part of the body's iron-sequestration strategy to limit iron availability for invading pathogens - The decrease in transferrin helps restrict bacterial growth by reducing available iron *Albumin* - **Albumin** is a prominent **negative acute phase protein**, with its concentration decreasing during acute inflammation due to redistribution and reduced synthesis - It plays a vital role in maintaining **oncotic pressure** and transporting various substances - Its decline reflects the severity of inflammation and is used as a marker of the acute phase response *Prealbumin* - **Prealbumin** (also known as transthyretin) is a **negative acute phase protein** and a sensitive marker of nutritional status - Its rapid decline during inflammation makes it a useful indicator, as its synthesis is quickly reduced - It has a short half-life (2-3 days), making it more sensitive to acute changes than albumin
Dermatology
1 questionsHLA-Cw6 is associated with
NEET-PG 2015 - Dermatology NEET-PG Practice Questions and MCQs
Question 361: 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
3 questionsExtremities are warm in which type of shock
In which condition is Serum Amyloid Associated (SAA) protein most commonly found?
Shrinking Lung Syndrome is seen in:
NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 361: 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**.
Question 362: 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 363: 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].
Microbiology
1 questionsInterleukin 2 is produced by
NEET-PG 2015 - Microbiology NEET-PG Practice Questions and MCQs
Question 361: Interleukin 2 is produced by
- A. T helper cells 1 (Correct Answer)
- B. T helper cells 2
- C. Natural killer cells
- D. Basophils
Explanation: ***T helper cells 1*** - **T helper 1 (Th1) cells** are a primary source of **interleukin-2 (IL-2)**, which is crucial for the proliferation and survival of T cells. - IL-2 acts as a **T-cell growth factor**, promoting the expansion of activated T cells, including cytotoxic T lymphocytes. *T helper cells 2* - **T helper 2 (Th2) cells** primarily produce cytokines like **IL-4, IL-5, IL-6, IL-10, and IL-13**, which are involved in humoral immunity and allergic responses. - While Th2 cells are important for immune responses, they are not major producers of IL-2. *Natural killer cells* - **Natural killer (NK) cells** are part of the innate immune system and produce cytokines such as **interferon-gamma (IFN-$\gamma$)** and **tumor necrosis factor-alpha (TNF-$\alpha$)**. - They are not a significant source of IL-2, which is primarily a T-cell derived growth factor. *Basophils* - **Basophils** are granulocytes involved in allergic reactions and anti-parasitic immunity, producing mediators like **histamine** and cytokines such as **IL-4** and **IL-13**. - Basophils do not produce IL-2; their role is distinct in the immune response compared to T cells.
Pharmacology
3 questionsWhat is an atypical side effect of montelukast?
Ximelagatran is used as ?
Which antitubercular drug makes the patient non-infective the earliest?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 361: What is an atypical side effect of montelukast?
- A. Goodpasture syndrome
- B. Membranous glomerulonephritis
- C. Bronchial asthma
- D. Churg-Strauss syndrome (Correct Answer)
Explanation: ***Churg-Strauss syndrome*** - The apparent development of **Churg-Strauss syndrome** (eosinophilic granulomatosis with polyangiitis) has been reported in patients treated with montelukast, although it is believed to be related more to the unmasking of the disease rather than a direct drug effect. - This typically occurs when **corticosteroids** are tapered or withdrawn as montelukast takes over, revealing the underlying vasculitis. *Goodpasture syndrome* - **Goodpasture syndrome** is an autoimmune disease causing rapidly progressive glomerulonephritis and pulmonary hemorrhage, characterized by anti-glomerular basement membrane (GBM) antibodies. - There is no established association between montelukast use and the development of Goodpasture syndrome. *Membranous glomerulonephritis* - **Membranous glomerulonephritis** is a common cause of nephrotic syndrome, characterized by immune complex deposition on the glomerular basement membrane. - This condition is not typically linked to the use of montelukast. *Bronchial asthma* - **Bronchial asthma** is the condition montelukast is used to treat, acting as a leukotriene receptor antagonist to reduce inflammation and bronchoconstriction. - It is a primary indication for the drug, not a side effect.
Question 362: Ximelagatran is used as ?
- A. Anticoagulant (Correct Answer)
- B. Fibrinolytic
- C. Platelet inhibitor
- D. Clot buster
Explanation: ***Anticoagulant*** - Ximelagatran is a **direct thrombin inhibitor**, meaning it directly blocks the action of thrombin, a key enzyme in the coagulation cascade. - By inhibiting thrombin, it prevents the formation of **fibrin clots**, thus acting as an anticoagulant. *Platelet inhibitor* - **Platelet inhibitors** prevent platelets from clumping together to form a clot, often by targeting pathways like ADP receptors or COX-1 enzyme. - Examples include **aspirin** and **clopidogrel**, which have different mechanisms of action than Ximelagatran. *Clot buster* - **Clot busters** are also known as thrombolytic agents, which actively dissolve existing blood clots. - They work by activating **plasminogen** to produce plasmin, an enzyme that breaks down fibrin. *Fibrinolytic* - **Fibrinolytics** are a class of drugs that enhance **fibrinolysis**, the natural process of breaking down blood clots. - **Thrombolytics** are a subset of fibrinolytic drugs used therapeutically to dissolve clots.
Question 363: Which antitubercular drug makes the patient non-infective the earliest?
- A. Ethambutol
- B. Pyrazinamide
- C. Isoniazid (INH) (Correct Answer)
- D. Rifampin
Explanation: ***Isoniazid (INH)*** - **Isoniazid** renders TB patients **non-infectious the fastest**, typically within **2-3 days** of starting treatment - It has the most **rapid bactericidal effect** against actively multiplying extracellular **Mycobacterium tuberculosis**, which are the primary organisms responsible for transmission - INH works by inhibiting **mycolic acid synthesis**, disrupting the bacterial cell wall of rapidly dividing bacilli - This makes it the most critical drug for **early infection control** and reducing community transmission *Rifampin* - While **rifampin** is highly bactericidal and has excellent sterilizing activity, it takes **slightly longer** than INH to render patients non-infectious - Rifampin is particularly effective against **semi-dormant organisms** and intracellular bacilli - It is the most important drug for **preventing relapse** and shortening treatment duration, but INH acts faster in reducing infectivity *Ethambutol* - **Ethambutol** is primarily **bacteriostatic**, inhibiting arabinosyl transferase and interfering with cell wall synthesis - Its main role is to **prevent emergence of drug resistance** rather than rapidly reducing bacterial load - Has minimal impact on early infectivity reduction *Pyrazinamide* - **Pyrazinamide** is most effective against **semi-dormant bacilli** within macrophages and in acidic environments - Its **sterilizing activity** helps shorten overall treatment duration but does not contribute significantly to rapid reduction in infectivity - Works slowly and is not bactericidal against actively multiplying extracellular organisms
Physiology
1 questionsInterleukin responsible for Pyrexia is:
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 361: Interleukin responsible for Pyrexia is:
- A. IL1 (Correct Answer)
- B. IL4
- C. IL3
- D. IL8
Explanation: ***IL1*** - **Interleukin-1 (IL-1)** is a primary **endogenous pyrogen**, directly acting on the thermoregulatory center in the hypothalamus to induce fever. - It stimulates the production of **prostaglandin E2 (PGE2)**, which then alters the hypothalamic set point, leading to increased body temperature. *IL3* - **Interleukin-3 (IL-3)** is a **hematopoietic growth factor** that primarily stimulates the proliferation and differentiation of hematopoietic stem cells. - Its main role is in the development of various blood cell lineages, not directly in inducing fever. *IL4* - **Interleukin-4 (IL-4)** is a key cytokine in **allergic reactions** and **Th2 immune responses**, promoting B cell activation and IgE production. - It does not directly cause pyrexia; its primary functions are related to humoral immunity and immune regulation. *IL8* - **Interleukin-8 (IL-8)**, also known as **CXCL8**, is a potent **chemotactic factor** for neutrophils and other immune cells. - Its main function is to recruit inflammatory cells to sites of infection or injury, not to induce fever directly.