Biochemistry
1 questionsMost abundant source of fuel in starvation -
NEET-PG 2015 - Biochemistry NEET-PG Practice Questions and MCQs
Question 511: Most abundant source of fuel in starvation -
- A. Liver glycogen
- B. Muscle glycogen
- C. Adipose tissue (Correct Answer)
- D. Blood glucose
Explanation: ***Adipose tissue*** - **Adipose tissue** stores **triglycerides**, which are hydrolyzed into fatty acids and glycerol to serve as the body's primary energy source during prolonged starvation. - The energy reserve in adipose tissue is significantly larger than glycogen stores, providing **sustained fuel** for days or weeks. *Liver glycogen* - **Liver glycogen** is a readily available source of glucose but is rapidly depleted within **12-24 hours** during starvation. - Its primary role is to maintain **blood glucose levels** for glucose-dependent tissues like the brain. *Muscle glycogen* - **Muscle glycogen** is used primarily for **muscle contraction** and cannot be directly released into the bloodstream to maintain blood glucose levels. - While it's a significant energy reserve for working muscles, it does not contribute to systemic fuel needs during starvation. *Blood glucose* - **Blood glucose** is the immediate circulating fuel, but it is tightly regulated and its levels decrease during starvation as glycogen stores are depleted. - It is not an abundant stored source of fuel but rather a transport form of energy.
Pharmacology
9 questionsWhich of the following is a PGE1 analogue used in medical treatments?
Which of the following is a long-acting beta-2 agonist?
Which triptan is available in nasal spray form?
Acetaminophen [Paracetamol] induced liver toxicity is due to which metabolite?
Which of the following drugs is commonly used as a rescue medication for acute asthma attacks?
Maximum effect of bronchodilatation in asthma is caused by -
What is an atypical side effect of montelukast?
Which of the following statements about oral iron preparations is correct?
Which of the following statements best describes the underlying mechanism of heparin-induced thrombocytopenia?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 511: Which of the following is a PGE1 analogue used in medical treatments?
- A. Carboprost
- B. Alprostadil (Correct Answer)
- C. Epoprostenol
- D. Dinoprostone
Explanation: ***Alprostadil*** - **Alprostadil** is a synthetic **prostaglandin E1 (PGE1)** analogue. - It is used in neonates to maintain the **patency of the patent ductus arteriosus** and in adults for the treatment of **erectile dysfunction**. *Carboprost* - **Carboprost** is a synthetic analogue of **prostaglandin F2 alpha (PGF2α)**. - It is primarily used to manage **postpartum hemorrhage** due to its potent uterotonic effects. *Epoprostenol* - **Epoprostenol** is a synthetic analogue of **prostacyclin (PGI2)**. - It is known for its potent **vasodilatory** and **antiplatelet** properties, making it useful in treating **pulmonary arterial hypertension**. *Dinoprostone* - **Dinoprostone** is a synthetic form of **prostaglandin E2 (PGE2)**. - It is used to **induce labor** or **cervical ripening** due to its role in uterine contractions and cervical dilation.
Question 512: Which of the following is a long-acting beta-2 agonist?
- A. Isoprenaline
- B. Ephedrine
- C. Salbutamol
- D. Formoterol (Correct Answer)
Explanation: ***Formoterol*** - **Formoterol** is a **long-acting beta-2 agonist (LABA)** commonly used in the treatment of asthma and COPD. - It provides **bronchodilation** for up to 12 hours due to its high lipophilicity, allowing it to remain in the cell membrane and continuously activate beta-2 receptors. *Isoprenaline (non-selective adrenergic agonist)* - **Isoprenaline** is a **non-selective beta-adrenergic agonist**, meaning it activates both beta-1 and beta-2 receptors. - It is **short-acting** and primarily used as a vasodilator or to stimulate heart rate, not as a long-acting bronchodilator. *Ephedrine (non-selective adrenergic agonist)* - **Ephedrine** is a **mixed-acting sympathomimetic amine** that increases the release of norepinephrine and directly stimulates alpha and beta receptors. - It has a short duration of action and is primarily used as a decongestant or bronchodilator in emergency situations, not as a long-acting agent. *Salbutamol (short-acting beta-2 agonist)* - **Salbutamol** is a **short-acting beta-2 agonist (SABA)**, providing rapid onset but a short duration of action (typically 4-6 hours). - It is used for **relieving acute bronchospasm** and is not considered a long-acting medication for maintenance therapy.
Question 513: Which triptan is available in nasal spray form?
- A. Sumatriptan (Correct Answer)
- B. Rizatriptan
- C. Naratriptan
- D. Frovatriptan
Explanation: ***Sumatriptan*** - **Sumatriptan** is available in multiple formulations, including **oral, subcutaneous injection, and nasal spray**, making it versatile for migraine treatment [1], [2]. - The nasal spray formulation allows for **faster absorption** and onset of action, which can be beneficial for patients with nausea or vomiting during migraine attacks [1]. *Rizatriptan* - **Rizatriptan** is primarily available in **oral tablet** and **orally disintegrating tablet** (ODT) forms [2]. - It does not have a commonly available nasal spray formulation for migraine treatment [2]. *Naratriptan* - **Naratriptan** is available as an **oral tablet** and is known for its **longer half-life** and generally milder side effect profile compared to sumatriptan [2]. - It is not available in a nasal spray formulation [2]. *Frovatriptan* - **Frovatriptan** is available exclusively as an **oral tablet** and is notable for having the **longest half-life** among triptans, making it useful for preventing recurring migraines [2]. - There is no nasal spray formulation for frovatriptan [2].
Question 514: Acetaminophen [Paracetamol] induced liver toxicity is due to which metabolite?
- A. Co-Q
- B. Cytochrome 'C'
- C. NAPQI (Correct Answer)
- D. N-acetylcysteine
Explanation: ***NAPQI*** - **N-acetyl-p-benzoquinone imine (NAPQI)** is a highly reactive and toxic metabolite produced during acetaminophen metabolism, especially in overdose situations [1, 3]. - When glutathione stores are depleted due to excessive NAPQI formation, this metabolite covalently binds to hepatic macromolecules, causing **hepatocellular damage and necrosis** [1, 3].*N-acetylcysteine* - **N-acetylcysteine (NAC)** is the antidote for acetaminophen overdose, not the toxic metabolite itself [2, 3]. - NAC works by replenishing hepatic **glutathione stores**, which helps detoxify NAPQI and prevent liver injury [2, 3].*Co-Q* - **Coenzyme Q10 (CoQ10)** is an endogenous antioxidant and electron carrier in the mitochondrial respiratory chain. - It is not a metabolite of acetaminophen and plays no direct role in acetaminophen-induced liver toxicity.*Cytochrome 'C'* - **Cytochrome c** is a protein involved in the electron transport chain in mitochondria and plays a critical role in apoptosis. - While cellular damage from NAPQI can eventually lead to cytochrome c release and apoptosis, cytochrome c itself is not a metabolite of acetaminophen or the direct cause of toxicity.
Question 515: Which of the following drugs is commonly used as a rescue medication for acute asthma attacks?
- A. Salbutamol (Correct Answer)
- B. Theophylline
- C. Terbutaline
- D. Budesonide
Explanation: ***Salbutamol*** - **Salbutamol** (albuterol) is a **short-acting beta-2 agonist (SABA)** that rapidly relaxes bronchial smooth muscle. - Its quick onset of action makes it ideal for immediate relief of **bronchoconstriction** during an acute asthma attack. - It is the **most commonly used** and **first-line rescue medication** for acute asthma worldwide. *Terbutaline* - **Terbutaline** is also a **short-acting beta-2 agonist (SABA)** similar to salbutamol and can be used as a rescue medication. - While it has comparable bronchodilator effects, **salbutamol is more commonly used** as the preferred rescue inhaler in clinical practice. - Both are SABAs, but salbutamol has become the standard first-choice rescue medication globally. *Theophylline* - **Theophylline** is a **methylxanthine** that acts as a bronchodilator but has a **narrow therapeutic index** and slower onset of action. - It is used as a **maintenance therapy** for chronic asthma and not as a rescue drug for acute exacerbations. *Budesonide* - **Budesonide** is an **inhaled corticosteroid (ICS)** used as a **long-term controller medication** to reduce airway inflammation. - It has a slow onset of action and is *not* effective for immediate relief during an acute asthma attack.
Question 516: Maximum effect of bronchodilatation in asthma is caused by -
- A. Beta 2-Agonist (Correct Answer)
- B. Corticosteroids
- C. Theophylline
- D. Anticholinergic
Explanation: ***Beta 2-Agonist*** - **Beta-2 agonists** directly relax bronchial smooth muscle by stimulating beta-2 adrenergic receptors, leading to significant and rapid bronchodilation. - This direct action on airway muscle relaxation makes them the most potent and fastest-acting bronchodilators for acute asthma symptoms. *Corticosteroids* - **Corticosteroids** reduce airway inflammation and hypersensitivity over time but do not provide immediate or maximal bronchodilation. - Their primary role is in long-term control of asthma, preventing exacerbations rather than acutely reversing bronchospasm. *Theophylline* - **Theophylline** is a methylxanthine that causes modest bronchodilation by inhibiting phosphodiesterase and blocking adenosine receptors. - It has a narrow therapeutic index, numerous side effects, and is less effective than beta-2 agonists for bronchodilation. *Anticholinergic* - **Anticholinergics** (e.g., ipratropium) block muscarinic receptors, preventing acetylcholine-induced bronchoconstriction. - They provide bronchodilation but are generally less potent and have a slower onset of action compared to beta-2 agonists in asthma.
Question 517: 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 518: Which of the following statements about oral iron preparations is correct?
- A. Most commonly used preparation is ferrous gluconate
- B. Ferrous fumarate is most efficient
- C. Ferric preparations are more effective
- D. Different preparations have different bioavailability (Correct Answer)
Explanation: ***Different preparations have different bioavailability*** - The **bioavailability** of oral iron preparations varies depending on the specific salt used, its formulation, and the presence of absorption enhancers or inhibitors. - This difference in absorption impacts the required dose and efficacy in treating **iron deficiency anemia**. *Most commonly used preparation is ferrous gluconate* - **Ferrous sulfate** is the most commonly prescribed and cost-effective oral iron preparation due to its high iron content and good bioavailability. - While ferrous gluconate is used, its iron content is lower than ferrous sulfate, making it less frequently the primary choice. *Ferrous fumarate is most efficient* - While **ferrous fumarate** has a high elemental iron content, its efficiency doesn't necessarily surpass that of ferrous sulfate or other preparations when considering factors like bioavailability and side effect profile. - **Ferrous sulfate** is often considered efficient due to its balance of elemental iron content, bioavailability, and cost-effectiveness. *Ferric preparations are more effective* - **Ferrous (Fe2+)** iron is generally better absorbed than **ferric (Fe3+)** iron, as ferric iron needs to be reduced to its ferrous form before absorption. - Unless specifically formulated for enhanced absorption (e.g., ferric maltol), ferric preparations are typically *less* effective for initial iron repletion.
Question 519: Which of the following statements best describes the underlying mechanism of heparin-induced thrombocytopenia?
- A. Low molecular weight heparin can also cause heparin-induced thrombocytopenia.
- B. Vitamin K is not an antidote for heparin-induced thrombocytopenia.
- C. Heparin-induced thrombocytopenia can occur after several days of heparin therapy.
- D. Antibodies are formed against heparin-platelet factor 4 complexes. (Correct Answer)
Explanation: **_Antibodies are formed against platelet factor 4._** - The underlying mechanism of **heparin-induced thrombocytopenia (HIT)** involves the formation of antibodies against complexes of **heparin and platelet factor 4 (PF4)** [2]. - These antibodies bind to the **heparin-PF4 complexes** on the surface of platelets, leading to platelet activation, aggregation, and consumption, which results in thrombocytopenia and a prothrombotic state [2]. *Low molecular weight heparin can also cause heparin-induced thrombocytopenia.* - While **low molecular weight heparin (LMWH)** has a lower incidence of causing HIT compared to unfractionated heparin, it can still trigger the condition [1], [2]. - This is because LMWH, like unfractionated heparin, can form complexes with PF4, leading to the same immune response in susceptible individuals [2]. *Vitamin K is not an antidote for heparin-induced thrombocytopenia.* - **Vitamin K** is the antidote for warfarin overdose, which works by reversing its anticoagulant effects [3]. - It has no role as an antidote for HIT because HIT is an **immune-mediated reaction** involving platelet activation, not a direct anticoagulant effect that can be reversed by Vitamin K [2]. *Heparin-induced thrombocytopenia can occur after several days of heparin therapy.* - HIT typically manifests after **5 to 10 days of heparin exposure**, as it takes time for the immune system to produce antibodies against the heparin-PF4 complexes [2]. - However, in patients with prior exposure to heparin, HIT can occur much sooner, even within **24 hours**, due to pre-existing antibodies.