Integrative Physiology Indian Medical PG Practice Questions and MCQs
Practice Indian Medical PG questions for Integrative Physiology. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Integrative Physiology Indian Medical PG Question 1: Which of the following statements about adiponectin is incorrect?
- A. Secreted by adipose tissue
- B. Increases FFA oxidation
- C. Lowers glucose
- D. Positive Correlation with BMI (Correct Answer)
Integrative Physiology Explanation: ***Positive Correlation with BMI (INCORRECT STATEMENT)***
- Adiponectin levels are **inversely correlated with BMI**, NOT positively correlated; as BMI increases, adiponectin levels generally decrease.
- This inverse relationship is significant because lower adiponectin levels are associated with increased insulin resistance and **metabolic syndrome**.
- This statement is **false**, making it the correct answer to this question.
*Secreted by adipose tissue (Correct statement)*
- Adiponectin is a **hormone primarily secreted by adipocytes** (fat cells).
- It plays a crucial role in regulating glucose and lipid metabolism, and its secretion is altered in conditions like obesity.
- This statement is **true**.
*Lowers glucose (Correct statement)*
- Adiponectin **enhances insulin sensitivity** in peripheral tissues like skeletal muscle and liver, leading to increased glucose uptake and utilization.
- This action helps to **lower blood glucose levels** and improve glycemic control.
- This statement is **true**.
*Increases FFA oxidation (Correct statement)*
- Adiponectin **promotes fatty acid oxidation** in muscle and liver, reducing intracellular lipid accumulation.
- By increasing fatty acid burning, it helps to **decrease circulating free fatty acid (FFA) levels**, which can contribute to insulin resistance if elevated.
- This statement is **true**.
Integrative Physiology Indian Medical PG Question 2: Mr. Murali has 126 mg/dl of fasting plasma glucose. His venous plasma glucose 2h after ingestion of 75g oral glucose load is 149 mg/dl. This patient comes under which stage of WHO diagnostic criteria of diabetes & intermediate hyperglycemia?
- A. Decreased glucose resistance
- B. IFG - Impaired fasting glucose
- C. Diagnosis of diabetes (Correct Answer)
- D. Impaired glucose tolerance
Integrative Physiology Explanation: **Diagnosis of diabetes**
- The **fasting plasma glucose (FPG)** of 126 mg/dL meets the WHO criterion for **diabetes**, which is FPG ≥ 126 mg/dL [1].
- Although the 2-hour post-glucose load (149 mg/dL) falls within the **impaired glucose tolerance (IGT)** range (140-199 mg/dL), the elevated fasting glucose alone is sufficient for a diabetes diagnosis according to WHO guidelines.
*Decreased glucose resistance*
- This term is not a standard diagnostic category recognized by the WHO for glucose metabolism disorders.
- Glucose resistance is more commonly associated with conditions like **insulin resistance** rather than a specific diagnostic stage [1].
*IFG - Impaired fasting glucose*
- **Impaired fasting glucose (IFG)** is defined by a fasting plasma glucose level between 100 mg/dL and 125 mg/dL.
- Mr. Murali's fasting glucose of 126 mg/dL is higher than the upper limit for IFG [1].
*Impaired glucose tolerance*
- **Impaired glucose tolerance (IGT)** is defined by a 2-hour post-glucose load plasma glucose level between 140 mg/dL and 199 mg/dL.
- While Mr. Murali's 2-hour reading of 149 mg/dL falls within this range, the elevated fasting glucose level takes precedence for the overall diagnosis [1].
Integrative Physiology Indian Medical PG Question 3: Which of the following statements best describes the mechanism of action of insulin on target cells?
- A. Insulin binds to a receptor on the outer surface of the plasma membrane, activating adenylate cyclase through the Gs protein.
- B. Insulin binds to a cytoplasmic receptor and is transferred as a hormone receptor complex to the nucleus to modulate gene expression.
- C. Insulin enters the cell and causes the release of calcium ions from intracellular stores.
- D. Insulin binds to a transmembrane receptor on the outer surface of the plasma membrane, activating the tyrosine kinase in the cytosolic domain of the receptor. (Correct Answer)
Integrative Physiology Explanation: ***Insulin binds to a transmembrane receptor on the outer surface of the plasma membrane, activating the tyrosine kinase in the cytosolic domain of the receptor.***
- **Insulin** is a **peptide hormone** and cannot freely pass through the lipid bilayer, thus it binds to a **transmembrane receptor** on the cell surface.
- This binding leads to the activation of the receptor's intrinsic **tyrosine kinase activity** in the intracellular domain, initiating a signaling cascade.
*Insulin binds to a cytoplasmic receptor and is transferred as a hormone receptor complex to the nucleus to modulate gene expression.*
- This mechanism describes the action of **steroid hormones**, which are lipid-soluble and can cross the cell membrane, binding to **intracellular receptors**.
- **Insulin** acts via a **cell surface receptor** and its downstream effects are mediated through signal transduction pathways, not direct nuclear translocation.
*Insulin binds to a receptor on the outer surface of the plasma membrane, activating adenylate cyclase through the Gs protein.*
- This mechanism is characteristic of **G-protein coupled receptors (GPCRs)**, which activate or inhibit enzymes like adenylate cyclase via G-proteins to produce second messengers like cyclic AMP.
- The **insulin receptor** is a **receptor tyrosine kinase**, not a GPCR, and does not directly activate adenylate cyclase via Gs protein.
*Insulin enters the cell and causes the release of calcium ions from intracellular stores.*
- While some hormones and neurotransmitters can trigger the release of intracellular **calcium ions**, this is typically mediated by specific pathways (e.g., GPCRs linked to phospholipase C).
- **Insulin** does not directly enter target cells to cause calcium release; its actions are primarily mediated through receptor tyrosine kinase signaling pathways.
Integrative Physiology Indian Medical PG Question 4: Metabolic changes seen in starvation include all of the following except?
- A. Ketogenesis
- B. Protein degradation
- C. Increased gluconeogenesis
- D. Increased glycolysis (Correct Answer)
Integrative Physiology Explanation: ***Increased glycolysis***
- In starvation, the body's primary goal is to conserve **glucose** for essential organs like the brain, as glucose supply is limited. Therefore, glycolysis, the breakdown of glucose, is *decreased*, not increased.
- The body shifts to using alternative fuels such as **fatty acids** and **ketone bodies** to spare glucose.
*Increased gluconeogenesis*
- **Gluconeogenesis**, the synthesis of glucose from non-carbohydrate precursors like amino acids and glycerol, is *increased* during starvation to maintain blood glucose levels.
- This process is crucial for providing glucose to tissues that primarily rely on it, such as the brain and red blood cells.
*Ketogenesis*
- **Ketogenesis**, the production of ketone bodies from fatty acids, is significantly *increased* during prolonged starvation.
- **Ketone bodies** become a major energy source for the brain and other tissues when glucose is scarce, helping to spare muscle protein.
*Protein degradation*
- **Protein degradation** (proteolysis) is *increased* during starvation, especially in the initial phases, to provide amino acids for gluconeogenesis.
- Muscle protein is a primary source of these amino acids, contributing to muscle wasting observed in prolonged starvation.
Integrative Physiology Indian Medical PG Question 5: Match the following drugs in Column A with their contraindications in Column B.
| Column A | Column B |
| :-- | :-- |
| 1. Morphine | 1. QT prolongation |
| 2. Amiodarone | 2. Thromboembolism |
| 3. Vigabatrin | 3. Pregnancy |
| 4. Estrogen preparations | 4. Head injury |
- A. A-1, B-3, C-2, D-4
- B. A-4, B-1, C-3, D-2 (Correct Answer)
- C. A-3, B-2, C-4, D-1
- D. A-2, B-4, C-1, D-3
Integrative Physiology Explanation: ***A-4, B-1, C-3, D-2***
- **Morphine** is contraindicated in **head injury** as it can increase intracranial pressure and mask neurological symptoms.
- **Amiodarone** is contraindicated in patients with **QT prolongation** due to its risk of inducing more severe arrhythmias like Torsades de Pointes.
- **Vigabatrin** is contraindicated during **pregnancy** due to its potential for teratogenicity and adverse effects on fetal development.
- **Estrogen preparations** are contraindicated in patients with a history of **thromboembolism** due to their increased risk of blood clot formation.
*A-1, B-3, C-2, D-4*
- This option incorrectly matches **Morphine** with QT prolongation and **Estrogen preparations** with head injury, which are not their primary contraindications.
- It also incorrectly links **Vigabatrin** with thromboembolism and **Amiodarone** with pregnancy.
*A-3, B-2, C-4, D-1*
- This choice incorrectly associates **Morphine** with pregnancy and **Vigabatrin** with head injury, which are not the most critical or direct contraindications.
- It also misaligns **Amiodarone** with thromboembolism and **Estrogen preparations** with QT prolongation.
*A-2, B-4, C-1, D-3*
- This option incorrectly matches **Morphine** with thromboembolism and **Amiodarone** with head injury, which are not their most significant contraindications.
- It also incorrectly links **Vigabatrin** with QT prolongation and **Estrogen preparations** with pregnancy.
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