A 7-year-old boy is brought to the physician by his mother because of a 2-week history of intermittent shortness of breath and a dry cough that is worse at night. He had an upper respiratory tract infection 3 weeks ago. Lungs are clear to auscultation. Spirometry shows normal forced vital capacity and peak expiratory flow rate. The physician administers a drug, after which repeat spirometry shows a reduced peak expiratory flow rate. Which of the following drugs was most likely administered?
Q712
A 27-year-old woman presents to the clinic with a runny nose and productive cough for the past two weeks. She also complains of headaches and lethargy. She was started on sertraline after she was diagnosed with major depressive disorder 2 months ago and had the dosage periodically increased to achieve symptom control. She is afraid of starting any other medication because of possible side-effects or life-threatening drug interactions. What advice is most accurate regarding possible complications to her current pharmacotherapy?
Q713
A 28-year-old woman presents with severe diarrhea and abdominal pain. She says she has had 10 watery stools since the previous morning and is experiencing severe cramping in her abdomen. She reports similar past episodes of diarrhea with excruciating abdominal pain and mentions that she has taken diphenoxylate and atropine before which had helped her diarrhea and pain but resulted in severe constipation for a week. Which of the following receptors does diphenoxylate activate to cause the effects mentioned by this patient?
Q714
A 28-year-old man presents to his primary care physician because he has been experiencing constipation for the last 6 days. He says that the constipation started 1 day after he started taking an over the counter medication for sinus congestion and a chronic cough. He has no other findings associated with the constipation. His past medical history is significant for seasonal allergies but he is not currently taking any other medications besides the one he reported. Which of the following drugs was most likely responsible for this patient's symptoms?
Q715
A 30-year-old man presents with a 1-month history of frequent intermittent headaches. He says the headaches typically occur between 3–4 times/day, mostly at night, each lasting minutes to 1–2 hours. He describes the pain as severe, stabbing, unilateral, and localized to the left periorbital region. He says he frequently notes increased tear production and conjunctival injection in the left eye and rhinorrhea during these headaches. He mentions that he had a similar 3-week episode of these same, frequent intermittent headaches 3 months ago which stopped completely until 1 month ago. He denies any seizures, loss of consciousness, nausea, vomiting, photophobia, or phonophobia. His past medical history is significant for stable angina secondary to coronary artery disease diagnosed on a stress echocardiogram 1 year ago. He reports occasional alcohol use, which he says precipitates the headaches, but denies any smoking or recreational drug use. The patient is afebrile, and his vital signs are within normal limits. A physical examination is unremarkable. A noncontrast computed tomography (CT) scan of the head is normal. Which of the following is the best abortive treatment for this patient?
Q716
A 55-year-old obese woman is referred to the cardiology clinic for progressive dyspnea. She has had no recent travel or sick contacts. Besides a multivitamin, she has only tried online weight-loss medications for the past five years, including fenfluramine-phentermine. An echocardiogram reveals a dilated right ventricle with systolic pressure of 60 mmHg as well as both tricuspid and pulmonary regurgitation. A right heart catheterization shows a mean pulmonary artery pressure of 40 mmHg. What disease process is most analogous to this patient's presentation?
Q717
A 21-year-old woman with type 1 diabetes mellitus suddenly develops tremors, cold sweats, and confusion while on a backpacking trip with friends. She is only oriented to person and is unable to follow commands. Her fingerstick blood glucose concentration is 28 mg/dL. Her friend administers an intramuscular injection with a substance that reverses her symptoms. Which of the following is the most likely mechanism of action of this drug?
Q718
A 17-year-old boy was brought to the emergency department because of palpitations and lightheadedness that began 16 hours ago. He admitted to binge drinking the night before. He was sedated and electrically cardioverted. An ECG that was recorded following cardioversion is shown. After regaining consciousness, he was admitted for observation. Serum concentration of creatinine and electrolytes were measured to be within the reference range. Twelve hours after cardioversion, the patient complains again of palpitations. He does not have lightheadedness or chest pain. His temperature is 37.1°C (98.8°F), pulse is 220/min, respirations are 20/min, and blood pressure is 112/84 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 98%. Physical examination shows no abnormalities. A newly recorded ECG shows a shortened PR interval, and wide, monomorphic QRS complexes with a regular rhythm. Which of the following is the most appropriate next best step in management?
Q719
A 49-year-old man with alcohol use disorder is brought to the emergency department immediately after two episodes of coffee-ground emesis. His pulse is 116/min and blood pressure is 92/54 mm Hg. Physical examination shows a distended abdomen with shifting dullness. Skin examination shows jaundice, erythematous palms, and dilated veins in the anterior abdominal wall. After fluid resuscitation, he is given a drug that decreases portal venous pressure. The drug works by inhibiting the secretion of splanchnic vasodilatory hormones as well as blocking glucagon and insulin release. This drug is a synthetic analog of a substance normally produced in which of the following cells?
Q720
A 24-year-old man presents to his family practitioner for routine follow-up of asthma. He is currently on albuterol, corticosteroids, and salmeterol, all via inhalation. The patient is compliant with his medications, but he still complains of episodic shortness of breath and wheezing. The peak expiratory flow (PEF) has improved since the last visit, but it is still less than the ideal predicted values based on age, gender, and height. Montelukast is added to his treatment regimen. What is the mechanism of action of this drug?
Autonomic/CV Drugs US Medical PG Practice Questions and MCQs
Question 711: A 7-year-old boy is brought to the physician by his mother because of a 2-week history of intermittent shortness of breath and a dry cough that is worse at night. He had an upper respiratory tract infection 3 weeks ago. Lungs are clear to auscultation. Spirometry shows normal forced vital capacity and peak expiratory flow rate. The physician administers a drug, after which repeat spirometry shows a reduced peak expiratory flow rate. Which of the following drugs was most likely administered?
A. Ipratropium bromide
B. Epinephrine
C. Methacholine (Correct Answer)
D. Methoxyflurane
E. Atenolol
Explanation: ***Methacholine***
- The patient's symptoms (intermittent shortness of breath, dry cough worse at night, history of URI) are suggestive of **asthma**. A methacholine challenge test is used to diagnose **asthma** when baseline spirometry is normal.
- **Methacholine** is a **muscarinic agonist** that causes **bronchoconstriction** in hyperreactive airways, leading to a decrease in lung function parameters like **peak expiratory flow rate** in asthmatic patients.
*Ipratropium bromide*
- **Ipratropium bromide** is an **anticholinergic bronchodilator** that would cause **bronchodilation**, leading to an increase in peak expiratory flow rate, not a decrease.
- It works by blocking muscarinic receptors in the airways, preventing acetylcholine-induced bronchoconstriction.
*Epinephrine*
- **Epinephrine** is a **sympathomimetic** drug that acts on both alpha and beta-adrenergic receptors, causing significant **bronchodilation** by stimulating beta-2 receptors in the airways.
- This would result in an **increase** in peak expiratory flow rate, not a reduction.
*Methoxyflurane*
- **Methoxyflurane** is a volatile halogenated anesthetic and is not used in the diagnosis or management of asthma.
- It primarily affects the central nervous system and can cause kidney toxicity.
*Atenolol*
- **Atenolol** is a **beta-1 selective blocker** used primarily for cardiovascular conditions like hypertension and angina.
- While non-selective beta-blockers can cause bronchoconstriction in asthmatics by blocking beta-2 receptors, atenolol's beta-1 selectivity makes this less likely, and it is **not used as a diagnostic bronchoprovocation agent** for asthma.
- **Methacholine challenge** is the standard diagnostic test for airway hyperreactivity.
Question 712: A 27-year-old woman presents to the clinic with a runny nose and productive cough for the past two weeks. She also complains of headaches and lethargy. She was started on sertraline after she was diagnosed with major depressive disorder 2 months ago and had the dosage periodically increased to achieve symptom control. She is afraid of starting any other medication because of possible side-effects or life-threatening drug interactions. What advice is most accurate regarding possible complications to her current pharmacotherapy?
A. Treat life-threatening complication with gradual drug withdrawal.
B. Migraine medication can trigger a life-threatening complication. (Correct Answer)
C. Over-the-counter (OTC) medications are safe for her to use.
D. Sertraline cannot be used concurrently with neuroleptics
E. Monoamine-oxidase-inhibitors are safe for concurrent use.
Explanation: ***Migraine medication can trigger a life-threatening complication.***
- Certain **migraine medications**, particularly **triptans** (e.g., sumatriptan), significantly increase the risk of **serotonin syndrome** when co-administered with **SSRIs** like sertraline due to additive serotonergic effects.
- **Serotonin syndrome** is a potentially life-threatening condition characterized by mental status changes, autonomic instability, and neuromuscular hyperactivity.
*Treat life-threatening complication with gradual drug withdrawal.*
- Treating a **life-threatening complication** often requires immediate medical intervention and possibly abrupt cessation of the offending drug, rather than gradual withdrawal, especially in cases like severe **serotonin syndrome**.
- Gradual withdrawal is typically for avoiding **discontinuation syndrome** (withdrawal symptoms) when ceasing SSRIs, not for managing acute, severe adverse drug reactions.
*Over-the-counter (OTC) medications are safe for her to use.*
- No, many **OTC medications** can interact with sertraline, such as **NSAIDs** (increased bleeding risk), or **cold/flu remedies** containing **dextromethorphan** or **pseudoephedrine** (potential for serotonin syndrome or increased BP).
- Patients on sertraline should always consult their physician before taking any OTC medications due to potential **drug interactions**.
*Sertraline cannot be used concurrently with neuroleptics*
- While interactions can occur, sertraline (an SSRI) can be and often is used concurrently with **neuroleptics** (antipsychotics) to manage comorbid conditions like psychosis or severe mood disorders, sometimes to augment antidepressant effects.
- The combination requires careful monitoring for side effects, but it is not an absolute contraindication like with MAOIs or some triptans.
*Monoamine-oxidase-inhibitors are safe for concurrent use.*
- This statement is incorrect; **Monoamine Oxidase Inhibitors (MAOIs)**, such as phenelzine or selegiline, are **absolutely contraindicated** with SSRIs like sertraline.
- Concurrent use of MAOIs and SSRIs can precipitate severe and potentially fatal **serotonin syndrome** due to excessive serotonin levels.
Question 713: A 28-year-old woman presents with severe diarrhea and abdominal pain. She says she has had 10 watery stools since the previous morning and is experiencing severe cramping in her abdomen. She reports similar past episodes of diarrhea with excruciating abdominal pain and mentions that she has taken diphenoxylate and atropine before which had helped her diarrhea and pain but resulted in severe constipation for a week. Which of the following receptors does diphenoxylate activate to cause the effects mentioned by this patient?
A. 5-HT3 receptor
B. NK1 receptor
C. D2 receptor
D. µ receptor (Correct Answer)
E. H2 receptor
Explanation: ***µ receptor***
- Diphenoxylate is an **opioid agonist** that primarily acts on the **µ-opioid receptors** in the GI tract.
- Activation of these receptors **inhibits GI motility**, increases fluid absorption, and reduces intestinal secretions, leading to its antidiarrheal effects and a common side effect of constipation.
*5-HT3 receptor*
- The 5-HT3 receptor is a **serotonin receptor** involved in the **vomiting reflex** and visceral pain sensation.
- Antagonists like ondansetron block this receptor to treat nausea and vomiting, not diarrhea.
*NK1 receptor*
- The NK1 receptor (Neurokinin 1 receptor) binds **substance P** and is primarily involved in mediating **nausea, vomiting**, and pain.
- Antagonists like aprepitant are used to prevent chemotherapy-induced nausea and vomiting.
*D2 receptor*
- The D2 receptor is a **dopamine receptor** involved in motor control, reward, and **nausea/vomiting**.
- Antagonists like metoclopramide block this receptor, leading to prokinetic effects and antiemesis, but are not the primary target for diphenoxylate.
*H2 receptor*
- H2 receptors are **histamine receptors** found in the **gastric parietal cells** and are responsible for stimulating gastric acid secretion.
- Antagonists like famotidine are used to reduce stomach acid and treat conditions like GERD and ulcers.
Question 714: A 28-year-old man presents to his primary care physician because he has been experiencing constipation for the last 6 days. He says that the constipation started 1 day after he started taking an over the counter medication for sinus congestion and a chronic cough. He has no other findings associated with the constipation. His past medical history is significant for seasonal allergies but he is not currently taking any other medications besides the one he reported. Which of the following drugs was most likely responsible for this patient's symptoms?
A. Guaifenesin
B. Dextromethorphan
C. Loratadine
D. N-acetylcysteine
E. Diphenhydramine (Correct Answer)
Explanation: ***Diphenhydramine***
- Diphenhydramine is a **first-generation antihistamine** with significant **anticholinergic effects**, which commonly include constipation due to reduced gastrointestinal motility.
- The patient's presentation of constipation after starting an over-the-counter medication for sinus congestion and cough strongly suggests a drug with antimuscarinic properties.
*Guaifenesin*
- Guaifenesin is an **expectorant** that helps thin mucus, making it easier to clear from the airways.
- It does not typically cause constipation; its common side effects are usually mild, such as nausea or dizziness.
*Dextromethorphan*
- Dextromethorphan is a **cough suppressant** that acts on the cough center in the medulla.
- While it can cause some gastrointestinal upset or drowsiness, constipation is not a common side effect.
*Loratadine*
- Loratadine is a **second-generation antihistamine** that is less sedating and has minimal anticholinergic effects compared to first-generation antihistamines.
- Therefore, it is unlikely to cause constipation.
*N-acetylcysteine*
- N-acetylcysteine is a **mucolytic agent** that breaks down disulfide bonds in mucus, used to help clear thick secretions.
- It is not associated with constipation as a side effect and is sometimes used as a treatment for acetaminophen overdose.
Question 715: A 30-year-old man presents with a 1-month history of frequent intermittent headaches. He says the headaches typically occur between 3–4 times/day, mostly at night, each lasting minutes to 1–2 hours. He describes the pain as severe, stabbing, unilateral, and localized to the left periorbital region. He says he frequently notes increased tear production and conjunctival injection in the left eye and rhinorrhea during these headaches. He mentions that he had a similar 3-week episode of these same, frequent intermittent headaches 3 months ago which stopped completely until 1 month ago. He denies any seizures, loss of consciousness, nausea, vomiting, photophobia, or phonophobia. His past medical history is significant for stable angina secondary to coronary artery disease diagnosed on a stress echocardiogram 1 year ago. He reports occasional alcohol use, which he says precipitates the headaches, but denies any smoking or recreational drug use. The patient is afebrile, and his vital signs are within normal limits. A physical examination is unremarkable. A noncontrast computed tomography (CT) scan of the head is normal. Which of the following is the best abortive treatment for this patient?
A. Intranasal lidocaine
B. Hydrocodone
C. Sumatriptan
D. High-flow 100% oxygen (Correct Answer)
E. Dihydroergotamine
Explanation: ***High-flow 100% oxygen***
- This patient presents with classic symptoms of **cluster headaches**: frequent, severe, unilateral periorbital pain along with **autonomic symptoms** (tearing, conjunctival injection, rhinorrhea), episodic pattern, and alcohol as a trigger.
- **High-flow 100% oxygen** via a non-rebreather mask is a highly effective and generally safe abortive treatment for cluster headaches.
*Intranasal lidocaine*
- While intranasal lidocaine can be used as an abortive treatment for cluster headaches, its efficacy is generally **lower** compared to high-flow oxygen or triptans.
- It might be considered for patients who cannot tolerate or respond to first-line treatments, but it is not the **best** initial abortive option.
*Hydrocodone*
- **Opioids like hydrocodone** are generally **contraindicated** for the treatment of cluster headaches due to their limited efficacy in acute attacks and significant risk of dependence, abuse, and medication overuse headache.
- Cluster headaches are characterized by short, severe attacks that require rapid-acting specific treatments, which opioids do not provide.
*Sumatriptan*
- **Sumatriptan** (specifically subcutaneous sumatriptan) is another **first-line abortive treatment** for cluster headaches and works rapidly and effectively.
- However, this patient has a history of **stable angina secondary to coronary artery disease**. Triptans are **contraindicated** in patients with ischemic heart disease due to their vasoconstrictive properties, which can exacerbate myocardial ischemia.
*Dihydroergotamine*
- **Dihydroergotamine** is an ergot derivative that can be effective for acute migraine and, to some extent, cluster headaches, acting as a vasoconstrictor.
- Similar to triptans, **dihydroergotamine is contraindicated** in patients with coronary artery disease or other cardiovascular conditions due to the risk of vasoconstriction and potential for cardiac events.
Question 716: A 55-year-old obese woman is referred to the cardiology clinic for progressive dyspnea. She has had no recent travel or sick contacts. Besides a multivitamin, she has only tried online weight-loss medications for the past five years, including fenfluramine-phentermine. An echocardiogram reveals a dilated right ventricle with systolic pressure of 60 mmHg as well as both tricuspid and pulmonary regurgitation. A right heart catheterization shows a mean pulmonary artery pressure of 40 mmHg. What disease process is most analogous to this patient's presentation?
A. Chronic obstructive pulmonary disease
B. Subacute endocarditis
C. Chronic thromboembolic disease
D. Left heart failure
E. Carcinoid syndrome (Correct Answer)
Explanation: ***Carcinoid syndrome***
- Carcinoid syndrome is well-known to cause **pulmonary hypertension** and **right-sided valvular heart disease**, particularly **tricuspid and pulmonary regurgitation**, which is analogous to the patient's presentation following fenfluramine-phentermine use.
- Both fenfluramine-phentermine and carcinoid syndrome cause valvular disease through **serotonin-mediated mechanisms**. Fenfluramine increases serotonin release and blocks reuptake, leading to **endocardial fibrosis** and valvular damage that mimics carcinoid heart disease.
- The right-sided predominance occurs because the lungs metabolize serotonin, protecting the left heart.
*Chronic obstructive pulmonary disease*
- While **COPD** can lead to pulmonary hypertension and right heart failure (**cor pulmonale**), there is no mention of a smoking history or respiratory symptoms like chronic cough or wheezing that are typical of COPD.
- The patient's primary risk factor is obesity and prior medication use, not factors directly implicating COPD.
*Subacute endocarditis*
- **Subacute endocarditis** typically involves bacterial infection of heart valves, presenting with fever, malaise, and new murmurs, which are not described in this patient's presentation.
- While it can cause valvular disease, it doesn't typically cause primary pulmonary hypertension or isolated right-sided disease in this manner.
*Chronic thromboembolic disease*
- **Chronic thromboembolic pulmonary hypertension (CTEPH)** results from organized blood clots in the pulmonary arteries, leading to right ventricular strain and pulmonary hypertension.
- There is no mention of prior **pulmonary emboli** or other risk factors for chronic thromboembolism in the patient's history.
*Left heart failure*
- **Left heart failure** can cause **pulmonary hypertension** due to backward pressure from the left side of the heart, but the echocardiogram specifically highlights isolated right ventricle dilation and right-sided valvular issues.
- While the patient has dyspnea, there are no findings suggestive of primary left ventricular dysfunction, such as reduced ejection fraction or left atrial enlargement.
Question 717: A 21-year-old woman with type 1 diabetes mellitus suddenly develops tremors, cold sweats, and confusion while on a backpacking trip with friends. She is only oriented to person and is unable to follow commands. Her fingerstick blood glucose concentration is 28 mg/dL. Her friend administers an intramuscular injection with a substance that reverses her symptoms. Which of the following is the most likely mechanism of action of this drug?
A. Activation of glucokinase
B. Inhibition of glucose-6-phosphatase
C. Inhibition of glycogen phosphorylase
D. Activation of adenylyl cyclase (Correct Answer)
E. Inhibition of α-glucosidase
Explanation: ***Activation of adenylyl cyclase***
- The patient is experiencing **hypoglycemia** (blood glucose 28 mg/dL) with severe symptoms (confusion, unable to follow commands), indicating a need for rapid glucose elevation. The drug administered is likely **glucagon**.
- **Glucagon** primarily acts on hepatic cells by binding to G-protein coupled receptors, leading to the activation of **adenylyl cyclase**. This increases intracellular **cAMP**, which then activates protein kinase A, ultimately leading to increased **glycogenolysis** and **gluconeogenesis** to raise blood glucose.
*Activation of glucokinase*
- **Glucokinase** is an enzyme involved in the **phosphorylation of glucose** to glucose-6-phosphate, primarily in the liver and pancreatic beta cells. Its activation would promote glucose utilization and storage, thereby **lowering blood glucose**, which is contrary to the desired effect in hypoglycemia.
- This enzyme is crucial for sensing glucose levels and initiating insulin secretion or glucose storage, not for rapid glucose elevation during hypoglycemia.
*Inhibition of glucose-6-phosphatase*
- **Glucose-6-phosphatase** is a key enzyme in the final step of both **gluconeogenesis** and **glycogenolysis**, converting glucose-6-phosphate to free glucose in the liver. Inhibition of this enzyme would **prevent glucose release** into the bloodstream and worsen hypoglycemia.
- This enzyme's activity is crucial for maintaining blood glucose homeostasis, especially during fasting, by allowing the liver to export glucose.
*Inhibition of glycogen phosphorylase*
- **Glycogen phosphorylase** is the enzyme responsible for initiating **glycogenolysis**, the breakdown of glycogen into glucose-1-phosphate. Inhibition of this enzyme would **prevent the breakdown of glycogen**, thereby hindering the body's ability to release stored glucose and exacerbating hypoglycemia.
- Glucagon, in contrast, *activates* glycogen phosphorylase to increase glucose output.
*Inhibition of α-glucosidase*
- **α-glucosidase inhibitors** (e.g., acarbose, miglitol) are oral hypoglycemic drugs that **slow down the digestion and absorption of carbohydrates** in the small intestine.
- These drugs are used to **lower postprandial blood glucose** in type 2 diabetes and would worsen hypoglycemia if given to this patient, not reverse it.
Question 718: A 17-year-old boy was brought to the emergency department because of palpitations and lightheadedness that began 16 hours ago. He admitted to binge drinking the night before. He was sedated and electrically cardioverted. An ECG that was recorded following cardioversion is shown. After regaining consciousness, he was admitted for observation. Serum concentration of creatinine and electrolytes were measured to be within the reference range. Twelve hours after cardioversion, the patient complains again of palpitations. He does not have lightheadedness or chest pain. His temperature is 37.1°C (98.8°F), pulse is 220/min, respirations are 20/min, and blood pressure is 112/84 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 98%. Physical examination shows no abnormalities. A newly recorded ECG shows a shortened PR interval, and wide, monomorphic QRS complexes with a regular rhythm. Which of the following is the most appropriate next best step in management?
A. Administer procainamide (Correct Answer)
B. Administer verapamil
C. Administer adenosine
D. Administer atenolol
E. Administer magnesium sulfate
Explanation: ***Administer procainamide***
- The patient's ECG findings of a **shortened PR interval** and **wide, monomorphic QRS complexes** with a regular rhythm, along with a history of recurrent palpitations after binge drinking, are highly suggestive of **Wolff-Parkinson-White (WPW) syndrome** with an **AV reentrant tachycardia (AVRT)**.
- In stable patients with **wide-complex tachycardia** due to WPW, **procainamide** is the drug of choice because it **blocks the accessory pathway**, slowing conduction and potentially terminating the arrhythmia.
*Administer verapamil*
- **Verapamil**, a calcium channel blocker, **slows conduction through the AV node**. In WPW syndrome, blocking the AV node can paradoxically increase conduction down the **accessory pathway**, potentially leading to ventricular fibrillation, especially if the patient is in atrial fibrillation.
- It is **contraindicated** in wide-complex tachycardias with suspected accessory pathways.
*Administer adenosine*
- **Adenosine** primarily acts by **blocking the AV node**. Similar to verapamil, in the presence of an **accessory pathway**, blocking the AV node can divert more impulses down the accessory pathway, potentially accelerating the ventricular rate and leading to a more dangerous arrhythmia like **ventricular fibrillation**.
- While adenosine is a first-line treatment for **narrow-complex SVT**, it is generally **contraindicated** in wide-complex tachycardias of unknown origin or suspected WPW.
*Administer atenolol*
- **Atenolol**, a beta-blocker, also **slows conduction through the AV node**. Like verapamil and adenosine, its use in WPW syndrome with a wide complex tachycardia can be **dangerous** by potentially increasing conduction down the accessory pathway.
- Beta-blockers are generally **contraindicated** in WPW in this context due to the risk of precipitating ventricular fibrillation.
*Administer magnesium sulfate*
- **Magnesium sulfate** is primarily used for torsades de pointes and is not indicated for the management of wide-complex tachycardia associated with WPW syndrome.
- It plays a role in managing certain electrolyte imbalances and some arrhythmias like **polymorphic ventricular tachycardia**, but not the specific type of reentrant tachycardia seen here.
Question 719: A 49-year-old man with alcohol use disorder is brought to the emergency department immediately after two episodes of coffee-ground emesis. His pulse is 116/min and blood pressure is 92/54 mm Hg. Physical examination shows a distended abdomen with shifting dullness. Skin examination shows jaundice, erythematous palms, and dilated veins in the anterior abdominal wall. After fluid resuscitation, he is given a drug that decreases portal venous pressure. The drug works by inhibiting the secretion of splanchnic vasodilatory hormones as well as blocking glucagon and insulin release. This drug is a synthetic analog of a substance normally produced in which of the following cells?
A. G cells
B. D cells (Correct Answer)
C. K cells
D. S cells
E. I cells
Explanation: ***D cells***
- The patient's presentation with **coffee-ground emesis**, **hypotension**, and signs of **chronic liver disease** (jaundice, erythematous palms, dilated abdominal veins, ascites) suggests **gastrointestinal bleeding** due to **portal hypertension**, likely from **esophageal varices**.
- The drug described, which reduces portal venous pressure by inhibiting splanchnic vasodilatory hormones and blocking glucagon/insulin release, is **octreotide**. Octreotide is a synthetic analog of **somatostatin**, which is primarily produced by **D cells** in the pancreatic islets and gastrointestinal mucosa.
*G cells*
- **G cells** primarily secrete **gastrin**, which stimulates gastric acid secretion.
- Gastrin does not directly inhibit splanchnic vasodilatory hormones or affect portal venous pressure in this manner.
*K cells*
- **K cells** secrete **gastric inhibitory polypeptide (GIP)**, a hormone that stimulates insulin release and inhibits gastric acid secretion.
- GIP is not involved in reducing portal hypertension or inhibiting splanchnic vasodilatory hormones.
*S cells*
- **S cells** secrete **secretin**, which stimulates bicarbonate secretion from the pancreas and liver.
- Secretin's primary action is not to decrease portal venous pressure or inhibit splanchnic vasodilatory hormones.
*I cells*
- **I cells** secrete **cholecystokinin (CCK)**, which stimulates gallbladder contraction and pancreatic enzyme release.
- CCK does not play a role in managing portal hypertension or inhibiting splanchnic vasodilatory hormones.
Question 720: A 24-year-old man presents to his family practitioner for routine follow-up of asthma. He is currently on albuterol, corticosteroids, and salmeterol, all via inhalation. The patient is compliant with his medications, but he still complains of episodic shortness of breath and wheezing. The peak expiratory flow (PEF) has improved since the last visit, but it is still less than the ideal predicted values based on age, gender, and height. Montelukast is added to his treatment regimen. What is the mechanism of action of this drug?
A. Montelukast inhibits the release of inflammatory substances from mast cells.
B. Montelukast activates adrenergic receptors on the bronchial smooth muscles.
C. Montelukast inhibits lipoxygenase, thus decreasing the production of inflammatory leukotrienes.
D. Montelukast binds to IgE.
E. Montelukast blocks receptors of some arachidonic acid metabolites. (Correct Answer)
Explanation: ***Montelukast blocks receptors of some arachidonic acid metabolites.***
- Montelukast is a **leukotriene receptor antagonist** that specifically blocks the **cysteinyl leukotriene 1 (CysLT1) receptor**.
- By blocking these receptors, montelukast prevents the inflammatory effects primarily mediated by **leukotrienes C4, D4, and E4**, which are metabolites of arachidonic acid and potent bronchoconstrictors and promoters of inflammation in asthma.
*Montelukast inhibits the release of inflammatory substances from mast cells.*
- This mechanism describes **mast cell stabilizers** like **cromolyn sodium** or **nedocromil**, which prevent the degranulation of mast cells and the subsequent release of inflammatory mediators.
- Montelukast does not directly prevent the release of these substances; rather, it blocks the receptors for some of them.
*Montelukast activates adrenergic receptors on the bronchial smooth muscles.*
- The activation of **adrenergic receptors** (specifically **beta-2 adrenergic receptors**) on bronchial smooth muscles by drugs like **albuterol** and **salmeterol** leads to bronchodilation.
- Montelukast is not an adrenergic agonist; it targets leukotriene pathways.
*Montelukast inhibits lipoxygenase, thus decreasing the production of inflammatory leukotrienes.*
- This mechanism describes **5-lipoxygenase inhibitors**, such as **zileuton**, which prevent the synthesis of leukotrienes from arachidonic acid.
- Montelukast does not inhibit lipoxygenase; instead, it blocks the receptors where leukotrienes would normally bind.
*Montelukast binds to IgE.*
- This mechanism describes **omalizumab**, a **monoclonal antibody** that binds to circulating **IgE antibodies**, preventing them from binding to mast cells and basophils.
- Omalizumab thereby reduces the allergic response; montelukast works on a different pathway.
