Antacids and Mucosal Protectants Indian Medical PG Practice Questions and MCQs
Practice Indian Medical PG questions for Antacids and Mucosal Protectants. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Antacids and Mucosal Protectants Indian Medical PG Question 1: All of the following are adverse effects of thalidomide except:
- A. Constipation
- B. Myocarditis (Correct Answer)
- C. Peripheral neuropathy
- D. Sedation
Antacids and Mucosal Protectants Explanation: ***Myocarditis***
- **Myocarditis** is not an established adverse effect of thalidomide in standard pharmacology references.
- While thalidomide can cause cardiovascular effects such as **bradycardia** and **thromboembolic events**, direct myocardial inflammation is not a recognized complication.
- This is the correct answer as it is NOT an adverse effect of thalidomide.
*Constipation*
- **Constipation** is a very common gastrointestinal side effect of thalidomide due to its **anticholinergic-like effects**.
- Patients often require proactive management with laxatives to mitigate this side effect.
*Peripheral neuropathy*
- **Peripheral neuropathy** is the most significant and dose-limiting adverse effect of thalidomide, often presenting as **sensory deficits** in a stocking-glove distribution.
- It can be **irreversible** and may necessitate discontinuation of the drug.
- This is a major concern requiring regular monitoring during treatment.
*Sedation*
- **Sedation** and **drowsiness** are common adverse effects of thalidomide due to its **central nervous system depressant properties**.
- This effect often leads to administration before bedtime to minimize impact on daily activities.
Antacids and Mucosal Protectants Indian Medical PG Question 2: Identify the correct match, regarding the drug and its adverse effect.
- A. Aliskiren - hypokalemia
- B. Hydralazine - heart failure
- C. Atenolol - hemolytic anemia
- D. Verapamil - constipation (Correct Answer)
Antacids and Mucosal Protectants Explanation: ***Verapamil - Constipation***
- **Verapamil**, a **non-dihydropyridine calcium channel blocker**, frequently causes constipation due to its effect on smooth muscle in the gastrointestinal tract, leading to **decreased intestinal motility**.
- This adverse effect is common and often dose-dependent, making it a significant consideration in patient management.
*Aliskiren - hypokalemia*
- **Aliskiren**, a **direct renin inhibitor**, can cause **hyperkalemia** by reducing angiotensin II levels, which normally stimulate aldosterone secretion.
- It does not typically cause hypokalemia; rather, potassium-sparing effects are often observed.
*Hydralazine - heart failure*
- **Hydralazine** is a **vasodilator** used to treat hypertension and **heart failure** with reduced ejection fraction by reducing afterload.
- It does not cause heart failure; instead, it is often prescribed to improve cardiac function in patients with heart failure.
*Atenolol - hemolytic anemia*
- **Atenolol** is a **beta-blocker** primarily used for hypertension, angina, and arrhythmias.
- **Hemolytic anemia** is a rare adverse effect associated with certain drugs, but it is not a known or common side effect of atenolol.
Antacids and Mucosal Protectants Indian Medical PG Question 3: Constipation is a possible side effect of drugs taken by the oral route. Which of the following medications is least likely to cause constipation?
- A. promethazine
- B. loperamide
- C. docusate (Correct Answer)
- D. diphenhydramine
Antacids and Mucosal Protectants Explanation: ***docusate***
- **Docusate** is a **stool softener** and is actually used to prevent and treat constipation, making it the least likely to cause it.
- It works by increasing the amount of water and fat the stool absorbs, making it easier to pass.
*promethazine*
- **Promethazine** is an antihistamine with **anticholinergic properties** that can slow down gut motility.
- Reduced gastrointestinal motility is a common side effect of drugs with anticholinergic effects, leading to **constipation**.
*loperamide*
- **Loperamide** is an **opioid receptor agonist** that works by slowing down gut contractions.
- It is specifically used as an **antidiarrheal medication**, and constipation is a well-known side effect of its action.
*diphenhydramine*
- **Diphenhydramine** is an antihistamine with significant **anticholinergic effects**.
- Its anticholinergic action reduces intestinal motility and secretions, frequently causing **constipation**.
Antacids and Mucosal Protectants Indian Medical PG Question 4: Antacid drug that typically causes diarrhea.
- A. Sodium bicarbonate
- B. Magnesium hydroxide (Correct Answer)
- C. Calcium carbonate
- D. Aluminium hydroxide
Antacids and Mucosal Protectants Explanation: ***Magnesium hydroxide***
- **Magnesium-containing antacids** commonly cause **diarrhea** due to their osmotic laxative effect, drawing water into the intestines.
- The magnesium ions are poorly absorbed and act as an **osmotic agent** in the gut lumen.
*Sodium bicarbonate*
- **Sodium bicarbonate** can cause **systemic alkalosis** due to absorption of bicarbonate ions, especially with high doses or impaired renal function.
- It does not typically cause diarrhea; instead, the CO2 produced from its reaction with stomach acid can cause **belching** and gastric distension.
*Calcium carbonate*
- **Calcium carbonate** is more frequently associated with **constipation** due to calcium's ability to slow intestinal motility.
- Excessive use can lead to **hypercalcemia** and milk-alkali syndrome.
*Aluminium hydroxide*
- **Aluminium-containing antacids** are notorious for causing **constipation** by slowing gut motility.
- Long-term use can also lead to **hypophosphatemia** as aluminum binds to phosphate in the GI tract.
Antacids and Mucosal Protectants Indian Medical PG Question 5: Excess of calcium intake leads to?
- A. Cardiomyopathy
- B. Osteomalacia
- C. Osteoporosis
- D. Milk alkali syndrome (Correct Answer)
Antacids and Mucosal Protectants Explanation: ***Milk alkali syndrome***
- **Milk-alkali syndrome** is caused by excessive intake of calcium (especially in the form of calcium carbonate) and absorbable alkali, leading to **hypercalcemia**, metabolic alkalosis, and acute kidney injury.
- The combination of abnormally high calcium intake, often from supplements, and the use of antacids or milk, drives this condition.
*Cardiomyopathy*
- **Cardiomyopathy** refers to diseases of the heart muscle that make it harder for the heart to pump blood, and it is not directly caused by excess calcium intake.
- While severe hypercalcemia can affect cardiac function, it typically causes arrhythmias or altered contractility, not a primary **cardiomyopathy**.
*Osteomalacia*
- **Osteomalacia** is a softening of the bones, typically due to **vitamin D deficiency** or impaired metabolism, leading to inadequate mineralization of new bone matrix.
- This condition is caused by insufficient calcium and phosphate for normal bone formation, not by an **excess of calcium intake**.
*Osteoporosis*
- **Osteoporosis** is a disease where bones become weak and brittle due to **loss of bone mass** and microarchitectural deterioration. [1]
- Chronic excess calcium intake does not cause osteoporosis; in fact, adequate calcium intake is crucial for **bone health** and preventing osteoporosis. [1]
Antacids and Mucosal Protectants Indian Medical PG Question 6: A patient is on phenytoin for a seizure disorder. He was prescribed sucralfate 4 times a day for peptic ulcers. What should be the minimum duration of time between consumption of these drugs?
- A. 90 minutes
- B. 60 minutes
- C. 120 minutes (Correct Answer)
- D. 30 minutes
Antacids and Mucosal Protectants Explanation: **_120 minutes_**
- **Sucralfate** forms a protective barrier in the stomach and can **adsorb other medications**, significantly reducing their absorption.
- A minimum separation of **2 hours (120 minutes)** is recommended between sucralfate and other oral medications to prevent drug interactions.
*90 minutes*
- While a longer interval is beneficial, **90 minutes** may not be sufficient to completely avoid the significant reduction in **phenytoin absorption** caused by sucralfate.
- Given the narrow therapeutic index of phenytoin, a more conservative approach with a longer separation is preferred.
*60 minutes*
- A **60-minute interval** is generally considered too short to prevent the **adsorption of phenytoin** by sucralfate.
- This short duration increases the risk of **subtherapeutic phenytoin levels** and potential seizure recurrence.
*30 minutes*
- A **30-minute interval** is entirely inadequate and would almost certainly lead to a significant **reduction in phenytoin absorption**.
- This would place the patient at high risk of **seizure recurrence** due to insufficient drug levels.
Antacids and Mucosal Protectants Indian Medical PG Question 7: The immunoglobulins that can be transported across the placenta include:
- A. IgA only
- B. Neither IgG nor IgA
- C. IgG only (Correct Answer)
- D. Both IgG and IgA
Antacids and Mucosal Protectants Explanation: ***IgG only***
- **IgG** is the only class of immunoglobulin that can actively be transported across the **placental barrier** from mother to fetus, providing passive immunity.
- This transport is mediated by specialized receptors (FcRn) on placental cells, ensuring the fetus receives protection against pathogens.
*IgA only*
- **IgA** is primarily found in **mucosal secretions** (e.g., breast milk, tears, saliva) and plays a crucial role in mucosal immunity.
- It does not significantly cross the placenta and therefore does not contribute to fetal immunity in utero.
*Neither IgG nor IgA*
- This statement is incorrect because **IgG** is well-established as being transported across the placenta.
- Such an absence of maternal antibodies would leave the fetus highly vulnerable to infections during development and early life.
*Both IgG and IgA*
- While **IgG** readily crosses the placenta, **IgA** does not, making this option incorrect.
- The primary route for IgA transfer to the infant is through **breast milk** after birth, providing crucial immunity for the newborn's gastrointestinal tract.
Antacids and Mucosal Protectants Indian Medical PG Question 8: In the context of bilateral renal artery stenosis, which antihypertensive drug is considered contraindicated?
- A. Beta-blockers
- B. Calcium channel blockers
- C. ACE inhibitors (Correct Answer)
- D. Diuretics
Antacids and Mucosal Protectants Explanation: ***ACE inhibitors***
- In bilateral renal artery stenosis, ACE inhibitors can precipitate **acute kidney injury** by severely reducing **glomerular filtration pressure**, as both kidneys rely on **angiotensin II** for maintaining this pressure [1].
- They inhibit the production of **angiotensin II**, leading to **efferent arteriolar dilation** and a drop in glomerular hydrostatic pressure, which is critical for filtration in stenosed kidneys [2].
*Beta-blockers*
- Beta-blockers are generally considered safe and effective in treating hypertension associated with renal artery stenosis, as they do not directly interfere with **renal autoregulation** in the same critical way as ACE inhibitors.
- They lower blood pressure by reducing **cardiac output** and inhibiting renin release but do not acutely compromise **glomerular filtration** in the presence of stenosis.
*Calcium channel blockers*
- Calcium channel blockers are safe to use in bilateral renal artery stenosis and are often effective in controlling blood pressure.
- They dilate **afferent arterioles**, which can actually help maintain or improve **glomerular filtration rate** by increasing blood flow to the glomerulus.
*Diuretics*
- Diuretics can be used cautiously in renal artery stenosis to manage blood pressure and fluid overload.
- However, aggressive diuresis can lead to intravascular volume depletion, which might exacerbate **renal hypoperfusion** in already stenosed kidneys.
Antacids and Mucosal Protectants Indian Medical PG Question 9: Adverse effects of phenytoin include the following EXCEPT:
- A. Ataxia
- B. Hirsutism
- C. Hypercalcemia (Correct Answer)
- D. Lymphadenopathy
Antacids and Mucosal Protectants Explanation: ***Hypercalcemia***
- Phenytoin can actually lead to **hypocalcemia** due to its effect on vitamin D metabolism, increasing its degradation and leading to osteomalacia or rickets [1].
- Therefore, **hypercalcemia** is not an expected adverse effect of phenytoin use.
*Lymphadenopathy*
- **Generalized lymphadenopathy** is a known, though less common, adverse effect of phenytoin, sometimes mimicking lymphoma.
- It's part of a broader hypersensitivity reaction that can occur with the drug.
*Ataxia*
- **Ataxia** is a common dose-dependent adverse effect of phenytoin, especially at higher therapeutic or toxic levels [1], [2].
- It manifests as impaired coordination and balance due to cerebellar dysfunction [1].
*Hirsutism*
- **Hirsutism**, or excessive hair growth, is a well-known chronic side effect of phenytoin [1].
- This effect is more aesthetically concerning than medically dangerous and is particularly common in young women [1].
Antacids and Mucosal Protectants Indian Medical PG Question 10: How do thiazides cause hypercalcemia?
- A. Decreased calcium excretion (Correct Answer)
- B. Increased parathyroid hormone secretion
- C. Decreased calcitonin secretion
- D. Increased calcium absorption
Antacids and Mucosal Protectants Explanation: ***Decreased calcium excretion***
- Thiazides inhibit the **Na-Cl co-transporter** in the **distal convoluted tubule**, leading to increased reabsorption of calcium [1], [2].
- This increased reabsorption of calcium is mediated by a low intracellular sodium concentration, which enhances the activity of the **Na+/Ca2+ exchanger** on the basolateral membrane [1].
*Increased parathyroid hormone secretion*
- Thiazides **do not directly stimulate** parathyroid hormone (PTH) secretion; instead, they *decrease* calcium excretion, which would typically *lower* PTH levels through negative feedback.
- Elevated PTH would lead to increased bone resorption and kidney calcium reabsorption, but this is not the **primary mechanism** for thiazide-induced hypercalcemia [2].
*Decreased calcitonin secretion*
- **Calcitonin** is a hormone that *lowers* blood calcium levels, and its decrease would theoretically contribute to hypercalcemia.
- However, thiazides have **no direct effect** on calcitonin secretion, making this an unlikely primary mechanism.
*Increased calcium absorption*
- While increased calcium absorption from the gut can contribute to hypercalcemia, thiazides do **not directly increase intestinal calcium absorption**.
- Their primary action for influencing calcium levels is within the **kidney**, specifically on reabsorption, not absorption from the GI tract [1], [2].
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