Biochemistry
4 questionsMost abundant source of fuel in starvation -
Most important carbohydrate store for maintaining blood glucose homeostasis -
Which of the following statements about the enzymes involved in the conversion of glucose to glucose-6-phosphate in glycolysis is true?
Enzyme deficient in Hers disease -
NEET-PG 2015 - Biochemistry NEET-PG Practice Questions and MCQs
Question 501: 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.
Question 502: Most important carbohydrate store for maintaining blood glucose homeostasis -
- A. Blood glucose
- B. Glycogen in adipose tissue
- C. Hepatic glycogen (Correct Answer)
- D. None of the options
Explanation: ***Hepatic glycogen*** - The liver contains **100-120g of glycogen**, which is the most crucial carbohydrate store for **maintaining blood glucose homeostasis**. - **Hepatic glycogen** can be mobilized and released as glucose into the bloodstream to supply all body tissues, especially during fasting. - Although muscle glycogen is quantitatively larger (~400-500g), it cannot contribute to blood glucose as muscle lacks glucose-6-phosphatase. - The liver's unique ability to release free glucose makes hepatic glycogen the **most metabolically important** carbohydrate store. *Blood glucose* - **Blood glucose** (~5g total in circulation) represents carbohydrates available for immediate energy, not a storage form. - This is far too small to be considered a major carbohydrate reserve. *Glycogen in adipose tissue* - **Adipose tissue** primarily stores **fat (triglycerides)**, with negligible glycogen content. - Adipose tissue plays virtually no role in carbohydrate storage. *None of the options* - This is incorrect because **hepatic glycogen** is indeed the most important carbohydrate store for glucose homeostasis.
Question 503: Which of the following statements about the enzymes involved in the conversion of glucose to glucose-6-phosphate in glycolysis is true?
- A. Glucokinase is induced by insulin. (Correct Answer)
- B. Hexokinase is specific for glucose.
- C. Glucokinase is inhibited by glucose-6-phosphate.
- D. Hexokinase has a high Km for glucose.
Explanation: ***Glucokinase is induced by insulin.*** - **Insulin** promotes glucose uptake and utilization in the liver and pancreatic beta cells, where glucokinase is primarily expressed. - Induction of **glucokinase** by insulin ensures that glucose is efficiently phosphorylated and trapped within hepatocytes when blood glucose levels are high. - This is a key mechanism for postprandial glucose homeostasis. *Incorrect: Hexokinase is specific for glucose.* - **Hexokinase** is NOT specific for glucose; it can phosphorylate various hexoses including **fructose**, **mannose**, and **galactose**. - Its broad substrate specificity distinguishes it from glucokinase, which has greater specificity for glucose. *Incorrect: Glucokinase is inhibited by glucose-6-phosphate.* - Unlike **hexokinase**, which is subject to product inhibition by glucose-6-phosphate, **glucokinase is NOT inhibited** by its product. - This lack of feedback inhibition allows glucokinase to continue phosphorylating glucose even when glucose-6-phosphate levels are elevated, which is appropriate for its role as a glucose sensor in liver and pancreatic beta cells. *Incorrect: Hexokinase has a high Km for glucose.* - **Hexokinase** has a **low Km** (~0.1 mM) for glucose, meaning it has high affinity and is saturated at normal blood glucose levels. - In contrast, **glucokinase** has a high Km (~10 mM), allowing it to respond proportionally to changes in blood glucose concentration.
Question 504: Enzyme deficient in Hers disease -
- A. Muscle phosphorylase
- B. Liver phosphorylase (Correct Answer)
- C. Acid maltase
- D. Debranching enzyme
Explanation: ***Liver phosphorylase*** - Hers disease, also known as Glycogen Storage Disease Type VI, is specifically caused by a deficiency of **liver phosphorylase**. - This enzyme is crucial for the breakdown of **glycogen in the liver**, leading to an inability to release glucose into the bloodstream during fasting. *Muscle phosphorylase* - Deficiency of **muscle phosphorylase** (myophosphorylase) causes **McArdle disease** (Glycogen Storage Disease Type V), which primarily affects muscle energy. - Patients typically present with exercise intolerance, muscle pain, and cramps, not the hepatic symptoms seen in Hers disease. *Acid maltase* - Deficiency of **acid maltase** (also known as alpha-glucosidase) is responsible for **Pompe disease** (Glycogen Storage Disease Type II), a lysosomal storage disorder. - This enzyme deficiency leads to glycogen accumulation in lysosomes in various tissues, including muscle, liver, and heart, causing muscle weakness and cardiomyopathy. *Debranching enzyme* - A deficiency in the **debranching enzyme** (amylo-1,6-glucosidase) causes **Cori disease** or **Forbes disease** (Glycogen Storage Disease Type III). - This results in the accumulation of abnormally structured glycogen with short outer branches in the liver, muscle, and heart.
Internal Medicine
1 questionsWhat is the primary effect of beta blockers in the management of thyroid storm?
NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 501: What is the primary effect of beta blockers in the management of thyroid storm?
- A. Increases metabolism of thyroxine
- B. Blocks thyroxine receptors
- C. Decreases synthesis of thyroxine
- D. Provides rapid relief of symptoms (Correct Answer)
Explanation: Detailed management of thyrotoxic crisis (thyroid storm) is a medical emergency where patients should be given propranolol, either oral or intravenous, to manage life-threatening symptoms [1]. ***Provides rapid relief of symptoms*** - Beta blockers primarily address the **adrenergic manifestations** of thyroid storm, such as **tachycardia**, **tremors**, anxiety, and palpitations [1]. - By blocking **beta-adrenergic receptors**, they provide rapid symptomatic relief and reduce cardiovascular stress, without affecting hormone levels [2]. Thyroid hormones normally increase the expression of genes for beta-adrenergic receptors and G-proteins, leading to increased heart rate and force of contraction [2]. *Increases metabolism of thyroxine* - Beta blockers do not increase the **metabolism** or breakdown of thyroxine; their action is primarily on the **peripheral effects** of thyroid hormones. - While some beta blockers like **propranolol** can inhibit the peripheral conversion of T4 to T3, this is a secondary effect and not their primary role in providing rapid symptomatic relief [1]. *Blocks thyroxine receptors* - Beta blockers do not block **thyroxine receptors**; thyroid hormones exert their effects by binding to intracellular receptors, not adrenergic receptors [2]. - Their action is on the **adrenergic system**, which is overstimulated by the high levels of thyroid hormones. *Decreases synthesis of thyroxine* - Beta blockers do not directly decrease the **synthesis of thyroxine** by the thyroid gland. - That action is performed by **antithyroid drugs** like methimazole and propylthiouracil, which inhibit hormone production [1].
Pharmacology
5 questionsWhich of the following drugs is not used in the treatment of akathisia?
Where is the benzodiazepine binding site located on GABA receptors?
Which of the following is an aromatase inhibitor?
Which antithyroid drug is preferred during the first trimester of pregnancy due to relatively lower placental transfer?
Which of the following oral antidiabetic drugs is an insulin secretagogue?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 501: Which of the following drugs is not used in the treatment of akathisia?
- A. Benzodiazepine
- B. Propranolol
- C. Trihexyphenidyl
- D. Haloperidol (Correct Answer)
Explanation: ***Haloperidol*** - **Haloperidol** is a typical antipsychotic drug known to **cause** or worsen **akathisia**, rather than treat it. - Akathisia is an extrapyramidal symptom, and **first-generation antipsychotics** like haloperidol are frequent culprits due to their strong **D2 receptor blockade**. *Benzodiazepine* - **Benzodiazepines** like lorazepam or clonazepam are often used to treat akathisia due to their **sedative** and **anxiolytic** properties. - They act by enhancing **GABAergic transmission**, which can help calm the motor restlessness associated with akathisia. *Propranolol* - **Propranolol**, a **beta-blocker**, is a first-line treatment for akathisia, particularly effective for its objective motor symptoms. - It works by reducing **adrenergic activity**, which is thought to contribute to the motor restlessness. *Trihexyphenidyl* - **Trihexyphenidyl** is an **anticholinergic** agent primarily used to treat **parkinsonian-like extrapyramidal symptoms** (e.g., dystonia, pseudoparkinsonism). - While sometimes used for generalized EPS, it is **less effective** for the specific motor restlessness of akathisia compared to beta-blockers or benzodiazepines.
Question 502: Where is the benzodiazepine binding site located on GABA receptors?
- A. β-subunit
- B. δ-subunit
- C. γ-subunit (Correct Answer)
- D. α-subunit
Explanation: ***γ-subunit*** - The **benzodiazepine binding site** is located at the interface between the **α and γ subunits** of the GABA-A receptor, with the **γ-subunit (especially γ2) being essential** for benzodiazepine sensitivity. - The presence of the **γ2 subunit** is **mandatory** for benzodiazepine binding - receptors lacking this subunit are **insensitive to benzodiazepines**. - Benzodiazepines bind to this site and act as **positive allosteric modulators**, increasing the frequency of **chloride channel opening** in response to GABA. - This is the **standard answer** for NEET-PG and medical PG examinations in India. *α-subunit* - The **α-subunit** contributes to forming the benzodiazepine binding pocket at the α-γ interface. - Different **α-subunit isoforms** (α1, α2, α3, α5) determine the pharmacological profile and tissue distribution of benzodiazepine effects. - However, the **α-subunit alone** cannot bind benzodiazepines without the γ-subunit. *β-subunit* - The **β-subunit** contains the primary binding site for **GABA** itself. - It does not participate in benzodiazepine binding but is crucial for the receptor's overall function and GABAergic signaling. *δ-subunit* - The **δ-subunit** replaces the γ-subunit in certain GABA-A receptor subtypes that mediate **tonic inhibition**. - Receptors containing **δ-subunits** are **insensitive to benzodiazepines** but sensitive to neurosteroids and certain general anesthetics. - This is a key distinguishing feature between phasic (γ-containing) and tonic (δ-containing) GABA-A receptors.
Question 503: Which of the following is an aromatase inhibitor?
- A. Letrozole (Correct Answer)
- B. Tamoxifen
- C. Danazol
- D. Taxane
Explanation: ***Letrozole*** - **Letrozole** is a commonly used **aromatase inhibitor**, which works by blocking the enzyme **aromatase** that converts androgens into estrogens [1]. - This reduction in estrogen levels is crucial in treating **hormone-sensitive breast cancers** [1]. *Tamoxifen* - **Tamoxifen** is a **selective estrogen receptor modulator (SERM)**, not an aromatase inhibitor [2]. - It acts by blocking estrogen receptors in breast tissue while potentially stimulating them in other tissues like bone and uterus [2]. *Danazol* - **Danazol** is a synthetic androgen that suppresses the hypothalamic-pituitary-gonadal axis, leading to **decreased estrogen production**. - It works by inhibiting gonadotropin release and directly inhibiting ovarian steroidogenesis, rather than blocking the aromatase enzyme directly. *Taxane* - **Taxanes** are a class of **chemotherapy drugs** that interfere with cell division by stabilizing microtubules. - They are used to treat various cancers, including breast cancer, but do not act as aromatase inhibitors.
Question 504: Which antithyroid drug is preferred during the first trimester of pregnancy due to relatively lower placental transfer?
- A. Carbimazole
- B. Propylthiouracil (Correct Answer)
- C. Both
- D. None of the options
Explanation: ***Propylthiouracil*** - **Propylthiouracil (PTU)** is the preferred antithyroid drug during the **first trimester** of pregnancy because it crosses the placenta less readily than methimazole/carbimazole. - While it still crosses the placenta, its lower placental transfer and association with fewer fetal anomalies in early pregnancy make it a safer initial choice, especially to minimize the risk of **fetal embryopathy** associated with methimazole. *Carbimazole* - **Carbimazole** (which is metabolized to methimazole) can cross the placenta more easily than PTU and has been associated with **fetal anomalies**, particularly in the first trimester. - Its use is generally avoided during the first trimester due to concerns about congenital malformations such as **aplasia cutis** and **esophageal atresia**. *Both* - While both drugs can cross the placenta to some extent, their safety profiles and recommended use during pregnancy differ significantly. - Carbimazole (methimazole) has a higher risk of teratogenicity in the first trimester compared to PTU. *None of the options* - This option is incorrect because propylthiouracil is indeed known to cross the placenta and is commonly used in pregnancy, especially during the first trimester. - The choice of antithyroid drug is a critical consideration in managing hyperthyroidism in pregnancy.
Question 505: Which of the following oral antidiabetic drugs is an insulin secretagogue?
- A. Metformin
- B. Pioglitazone
- C. Nateglinide (Correct Answer)
- D. Acarbose
Explanation: **Nateglinide** - **Nateglinide** is a **meglitinide**, which is a type of **insulin secretagogue**. - It stimulates **insulin release** from pancreatic beta cells by blocking ATP-sensitive potassium channels. *Metformin* - **Metformin** is a **biguanide** that primarily works by **decreasing hepatic glucose production** and increasing insulin sensitivity in peripheral tissues. - It does not directly stimulate insulin secretion. *Pioglitazone* - **Pioglitazone** is a **thiazolidinedione** (TZD) that improves insulin sensitivity by activating **PPAR-gamma receptors**. - It does not directly affect insulin secretion but rather enhances the body's response to existing insulin. *Acarbose* - **Acarbose** is an **alpha-glucosidase inhibitor** that delays the digestion and absorption of carbohydrates in the small intestine. - This reduces postprandial glucose excursions and does not directly stimulate insulin secretion.