A 32-year-old woman is found unconscious on the office floor just before lunch by her colleagues. She had previously instructed them on the location of an emergency kit in case this ever happened so they are able to successfully inject her with the substance inside. Her past medical history is significant for type 1 diabetes for which she takes long acting insulin as well as periprandial rapid acting insulin injections. She has previously been found unconscious once before when she forgot to eat breakfast. The substance inside the emergency kit most likely has which of the following properties.
Q922
Following gastric surgery, a 45-year-old woman complains of severe nausea and vomiting on the 2nd postoperative day. On physical examination, her vitals are stable and examination of the abdomen reveals no significant abnormality. The patient is already receiving a maximum dosage of ondansetron. Metoclopramide is given, and she experiences significant relief from nausea and vomiting. Which of the following best explains the mechanism of action of this drug?
Q923
A 23-year-old man is brought to the emergency department by ambulance following a motor vehicle accident. He was pinned between 2 cars for several hours. The patient has a history of asthma. He uses an albuterol inhaler intermittently. The patient was not the driver, and admits to having a few beers at a party prior to the accident. His vitals in the ambulance are stable. Upon presentation to the emergency department, the patient is immediately brought to the operating room for evaluation and surgical intervention. It is determined that the patient’s right leg has a Gustilo IIIC injury in the mid-shaft of the tibia with a severely comminuted fracture. The patient’s left leg suffered a similar injury but with damage to the peroneal nerve. The anesthesiologist begins to induce anesthesia. Which of the following agents would be contraindicated in this patient?
Q924
An otherwise healthy 76-year-old man is brought to the physician because of poor sleep for the past several years. Every night he has been sleeping less and taking longer to fall asleep. During the day, he feels tired and has low energy and difficulty concentrating. Sleep hygiene and relaxation techniques have failed to improve his sleep. He would like to start a short-term pharmacological therapy trial but does not want a drug that makes him drowsy during the day. Which of the following is the most appropriate pharmacotherapy for this patient?
Q925
A 57-year-old man is brought to the emergency department for worsening pain and swelling of his left ankle for the past 2 hours. The pain is severe and awakened him from sleep. He has hypertension and hyperlipidemia. Current medications include hydrochlorothiazide and pravastatin. His temperature is 37.8°C (100.1°F), pulse is 105/min, and blood pressure is 148/96 mm Hg. Examination shows exquisite tenderness, erythema, and edema of the left ankle; active and passive range of motion is limited by pain. Arthrocentesis of the ankle joint yields cloudy fluid with a leukocyte count of 19,500/mm3 (80% segmented neutrophils). Gram stain is negative. A photomicrograph of the joint fluid aspirate under polarized light is shown. Which of the following is the most appropriate pharmacotherapy?
Q926
A 23-year-old woman with asthma is brought to the emergency department because of shortness of breath and wheezing for 20 minutes. She is unable to speak more than a few words at a time. Her pulse is 116/min and respirations are 28/min. Pulse oximetry on room air shows an oxygen saturation of 92%. Examination of the lungs shows decreased breath sounds and scattered end-expiratory wheezing over all lung fields. Treatment with high-dose continuous inhaled albuterol is begun. This patient is at increased risk for which of the following adverse effects?
Q927
A 57-year-old man presents to the emergency department with shortness of breath. He was eating dinner with his family during the holidays and felt very short of breath, thus prompting him to come in. The patient has a past medical history of diabetes, hypertension, 2 myocardial infarctions, and obesity. Physical exam is notable for bilateral pulmonary crackles and a jugular venous distension. Chest radiography reveals an enlarged cardiac silhouette and blunting of the costophrenic angles. The patient is started on a medication for his acute symptoms. Two hours later, he states his symptoms have vastly improved and repeat chest radiography is notable for an enlarged cardiac silhouette. Which of the following is a property of the medication most likely given?
Q928
A 30-year-old woman presents to her physician for her annual checkup. She has diabetes mellitus, type 1 and takes insulin regularly. She reports no incidents of elevated or low blood sugar and that she is feeling energetic and ready to face the morning every day. Her vital signs and physical are normal. On the way home from her checkup she stops by the pharmacy and picks up her prescription of insulin. Later that night she takes a dose. What is the signaling mechanism associated with this medication?
Q929
A 54-year-old man comes to the physician for a follow-up examination. One week ago, he was treated in the emergency department for chest pain, palpitations, and dyspnea. As part of his regimen, he was started on a medication that irreversibly inhibits the synthesis of thromboxane A2 and prostaglandins. Which of the following is the most likely adverse effect of this medication?
Q930
An investigator is studying brachial artery reactivity in women with suspected coronary heart disease. The brachial artery diameter is measured via ultrasound before and after intra-arterial injection of acetylcholine. An increase of 7% in the vascular diameter is noted. The release of which of the following is most likely responsible for the observed effect?
Autonomic/CV Drugs US Medical PG Practice Questions and MCQs
Question 921: A 32-year-old woman is found unconscious on the office floor just before lunch by her colleagues. She had previously instructed them on the location of an emergency kit in case this ever happened so they are able to successfully inject her with the substance inside. Her past medical history is significant for type 1 diabetes for which she takes long acting insulin as well as periprandial rapid acting insulin injections. She has previously been found unconscious once before when she forgot to eat breakfast. The substance inside the emergency kit most likely has which of the following properties.
A. Promotes glucose release from skeletal muscles
B. Promotes glycogen breakdown in the liver (Correct Answer)
C. Promotes glycogen formation in the liver
D. Promotes glucose uptake in muscles
E. Inhibits activity of pancreatic alpha and beta cells
Explanation: ***Promotes glycogen breakdown in the liver***
- The woman is experiencing **hypoglycemia** due to her type 1 diabetes and missed meal, leading to unconsciousness. The emergency kit contains **glucagon**, which counteracts hypoglycemia.
- **Glucagon** primarily acts on the liver to increase blood glucose levels by promoting **glycogenolysis** (breakdown of glycogen stores into glucose), which provides rapid glucose release within minutes.
- Glucagon also stimulates **gluconeogenesis** (synthesis of new glucose from non-carbohydrate sources), though this is a slower process that takes hours and is less important for acute hypoglycemia treatment.
*Promotes glucose release from skeletal muscles*
- While skeletal muscles store glycogen, they lack the enzyme **glucose-6-phosphatase**, so they cannot directly release glucose into the bloodstream.
- Muscle glycogen is used only for the muscle's own energy needs, not for systemic glucose regulation.
*Promotes glycogen formation in the liver*
- **Glycogen formation** (glycogenesis) is stimulated by **insulin**, which lowers blood glucose levels.
- This action would worsen hypoglycemia, making it inappropriate treatment for an unconscious diabetic patient.
*Promotes glucose uptake in muscles*
- **Insulin** is the primary hormone that promotes **glucose uptake** into muscle cells, thereby lowering blood glucose.
- Administering a substance that promotes glucose uptake would exacerbate hypoglycemia.
*Inhibits activity of pancreatic alpha and beta cells*
- Inhibiting **alpha cells** would reduce glucagon secretion, which is counterproductive in hypoglycemia as glucagon raises blood glucose.
- Inhibiting **beta cells** would reduce insulin secretion; while this might prevent further insulin release, the primary need in acute hypoglycemia is to rapidly increase blood glucose through glycogenolysis.
Question 922: Following gastric surgery, a 45-year-old woman complains of severe nausea and vomiting on the 2nd postoperative day. On physical examination, her vitals are stable and examination of the abdomen reveals no significant abnormality. The patient is already receiving a maximum dosage of ondansetron. Metoclopramide is given, and she experiences significant relief from nausea and vomiting. Which of the following best explains the mechanism of action of this drug?
A. Inhibition of dopamine receptors in the area postrema (Correct Answer)
B. Decreased esophageal peristaltic amplitude
C. Stimulation of motilin receptors in gastrointestinal smooth muscle
D. Enhancement of small intestinal and colonic motility by dopamine antagonism
E. Inhibition of serotonin receptors on the nucleus tractus solitarius
Explanation: ***Inhibition of dopamine receptors in the area postrema***
- **Metoclopramide** primarily acts as a **dopamine D2 receptor antagonist**, particularly in the **chemoreceptor trigger zone (CTZ)** located in the **area postrema**, which is outside the blood-brain barrier.
- By blocking dopamine receptors in the CTZ, metoclopramide effectively reduces the signaling that triggers **nausea and vomiting**, providing relief from postoperative emesis.
*Decreased esophageal peristaltic amplitude*
- **Metoclopramide** is known to **increase**, not decrease, esophageal peristaltic amplitude and lower esophageal sphincter pressure.
- This action is part of its **prokinetic effect**, which helps in the movement of food down the esophagus.
*Stimulation of motilin receptors in gastrointestinal smooth muscle*
- While **motilin** is a hormone that stimulates gastrointestinal motility, **metoclopramide** does not act by stimulating motilin receptors.
- Metoclopramide's prokinetic effects are primarily mediated by **dopamine antagonism** and enhancement of **acetylcholine release**.
*Enhancement of small intestinal and colonic motility by dopamine antagonism*
- **Metoclopramide** does enhance **small intestinal motility** through **dopamine antagonism**, but its effect on **colonic motility** is less pronounced and not its primary mode of action.
- Its main prokinetic benefit is seen in the upper gastrointestinal tract, promoting gastric emptying and small bowel transit.
*Inhibition of serotonin receptors on the nucleus tractus solitarius*
- **Metoclopramide** is also a **5-HT3 receptor antagonist** and a **5-HT4 receptor agonist**, but its primary antiemetic effect is attributed to **dopamine D2 receptor antagonism** in the CTZ.
- The **nucleus tractus solitarius** is involved in integrating visceral sensory information, but direct inhibition of serotonin receptors there is not the primary mechanism of its antiemetic action, unlike drugs like **ondansetron** which are potent 5-HT3 antagonists.
Question 923: A 23-year-old man is brought to the emergency department by ambulance following a motor vehicle accident. He was pinned between 2 cars for several hours. The patient has a history of asthma. He uses an albuterol inhaler intermittently. The patient was not the driver, and admits to having a few beers at a party prior to the accident. His vitals in the ambulance are stable. Upon presentation to the emergency department, the patient is immediately brought to the operating room for evaluation and surgical intervention. It is determined that the patient’s right leg has a Gustilo IIIC injury in the mid-shaft of the tibia with a severely comminuted fracture. The patient’s left leg suffered a similar injury but with damage to the peroneal nerve. The anesthesiologist begins to induce anesthesia. Which of the following agents would be contraindicated in this patient?
A. Halothane
B. Propofol
C. Etomidate
D. Succinylcholine (Correct Answer)
E. Neostigmine
Explanation: ***Succinylcholine***
- Given the history of the patient being pinned between two cars for several hours, there is a significant risk of **rhabdomyolysis** and subsequent hyperkalemia.
- **Succinylcholine**, a depolarizing neuromuscular blocker, can cause a sudden and significant release of potassium from muscle cells, leading to **life-threatening hyperkalemia** in patients with rhabdomyolysis or crush injuries.
*Halothane*
- While **halothane** has been associated with **malignant hyperthermia**, the patient's history does not directly suggest an increased risk for this condition here.
- It also has a bronchodilating effect, which could be beneficial for a patient with a history of **asthma**.
*Propofol*
- **Propofol** is a commonly used intravenous anesthetic for induction and maintenance, providing rapid onset and recovery.
- There are generally no specific contraindications for propofol in a patient with a crush injury or asthma.
*Etomidate*
- **Etomidate** is an intravenous anesthetic agent known for its **cardiovascular stability**, making it a good choice for hemodynamically unstable patients.
- It can cause adrenal suppression, but this is usually a concern with prolonged infusions, not a single induction dose.
*Neostigmine*
- **Neostigmine** is an acetylcholinesterase inhibitor used to reverse the effects of non-depolarizing neuromuscular blockers.
- It is not an induction agent and would not be used at the beginning of anesthesia induction.
Question 924: An otherwise healthy 76-year-old man is brought to the physician because of poor sleep for the past several years. Every night he has been sleeping less and taking longer to fall asleep. During the day, he feels tired and has low energy and difficulty concentrating. Sleep hygiene and relaxation techniques have failed to improve his sleep. He would like to start a short-term pharmacological therapy trial but does not want a drug that makes him drowsy during the day. Which of the following is the most appropriate pharmacotherapy for this patient?
A. Zaleplon (Correct Answer)
B. Temazepam
C. Flurazepam
D. Diphenhydramine
E. Suvorexant
Explanation: ***Zaleplon***
- Zaleplon is a **non-benzodiazepine hypnotic** with a very short half-life (1 hour), which makes it ideal for patients who have trouble falling asleep and want to avoid next-day drowsiness.
- Its rapid elimination minimizes residual hypnotic effects and cognitive impairment the following day, making it suitable for a short-term trial in elderly patients concerned about daytime sedation.
*Temazepam*
- Temazepam is an intermediate-acting **benzodiazepine hypnotic** with a half-life of 10-20 hours, which could lead to next-day drowsiness, especially in elderly patients.
- While it helps with sleep maintenance, its longer duration of action makes it less suitable for someone specifically avoiding daytime sedation.
*Flurazepam*
- Flurazepam is a **long-acting benzodiazepine hypnotic** with a half-life of 47-100 hours (due to active metabolites), making it highly likely to cause significant next-day drowsiness and a risk of accumulation in elderly individuals.
- Its prolonged action is counter to the patient's desire to avoid daytime sedation and is generally avoided in older adults due to increased fall risk and cognitive impairment.
*Diphenhydramine*
- Diphenhydramine is an **antihistamine** with significant anticholinergic side effects and a long half-life, which commonly causes next-day sedation, cognitive impairment, and confusion, particularly in the elderly.
- Due to these adverse effects, it is not recommended as a primary treatment for insomnia in older adults, especially given the patient's concern about daytime drowsiness.
*Suvorexant*
- Suvorexant is an **orexin receptor antagonist** with a half-life of approximately 12 hours, which commonly causes next-day drowsiness and cognitive impairment.
- While it is effective for insomnia, its longer duration of action compared to zaleplon makes it less ideal for patients specifically concerned about avoiding daytime sedation, particularly in elderly individuals who may be more sensitive to these effects.
Question 925: A 57-year-old man is brought to the emergency department for worsening pain and swelling of his left ankle for the past 2 hours. The pain is severe and awakened him from sleep. He has hypertension and hyperlipidemia. Current medications include hydrochlorothiazide and pravastatin. His temperature is 37.8°C (100.1°F), pulse is 105/min, and blood pressure is 148/96 mm Hg. Examination shows exquisite tenderness, erythema, and edema of the left ankle; active and passive range of motion is limited by pain. Arthrocentesis of the ankle joint yields cloudy fluid with a leukocyte count of 19,500/mm3 (80% segmented neutrophils). Gram stain is negative. A photomicrograph of the joint fluid aspirate under polarized light is shown. Which of the following is the most appropriate pharmacotherapy?
A. Ketorolac and aspirin
B. Triamcinolone and probenecid
C. Colchicine (Correct Answer)
D. Probenecid
E. Colchicine and allopurinol
Explanation: ***Colchicine***
- This patient presents with **acute gout**: sudden onset severe monoarticular arthritis (left ankle), awakened from sleep, with **negatively birefringent needle-shaped crystals** on joint fluid analysis under polarized light
- **Colchicine** is appropriate first-line therapy for acute gout flares by inhibiting neutrophil migration and microtubule polymerization, thereby reducing inflammation
- The patient is on **hydrochlorothiazide**, a known precipitant of gout attacks through increased uric acid retention
*Ketorolac and aspirin*
- While **ketorolac** (NSAID) could be effective for acute gout, **aspirin should be avoided** as low-dose aspirin can paradoxically increase uric acid levels and potentially worsen the attack
- This combination is inappropriate due to the aspirin component
*Triamcinolone and probenecid*
- **Triamcinolone** (corticosteroid) is an appropriate alternative for acute gout in patients with NSAID or colchicine contraindications
- However, **probenecid** (uricosuric agent) is **contraindicated during acute flares** as it can mobilize uric acid stores and worsen inflammation
- Probenecid is used only for chronic gout management, not acute treatment
*Probenecid*
- **Probenecid** is a uricosuric agent that increases renal uric acid excretion for **long-term management of hyperuricemia**
- It should **never be initiated during an acute gout attack** as it can precipitate or prolong the flare
- Used for chronic prevention, not acute treatment
*Colchicine and allopurinol*
- While **colchicine** is appropriate for acute gout, adding **allopurinol** is inappropriate
- **Allopurinol** (xanthine oxidase inhibitor) reduces uric acid production and is used for **chronic gout prevention**
- **Allopurinol should not be initiated during an acute flare** as it can worsen or prolong the attack
- If already on allopurinol chronically, it should be continued, but never started acutely
Question 926: A 23-year-old woman with asthma is brought to the emergency department because of shortness of breath and wheezing for 20 minutes. She is unable to speak more than a few words at a time. Her pulse is 116/min and respirations are 28/min. Pulse oximetry on room air shows an oxygen saturation of 92%. Examination of the lungs shows decreased breath sounds and scattered end-expiratory wheezing over all lung fields. Treatment with high-dose continuous inhaled albuterol is begun. This patient is at increased risk for which of the following adverse effects?
A. Miosis
B. Hypokalemia (Correct Answer)
C. Sedation
D. Hypoglycemia
E. Urinary frequency
Explanation: ***Hypokalemia***
- **High-dose continuous albuterol** (a beta-2 adrenergic agonist) stimulates the **Na+/K+-ATPase pump**, leading to an intracellular shift of potassium.
- This can result in a significant drop in serum potassium levels, especially with systemic absorption or prolonged use, which is a common adverse effect in acute asthma exacerbations.
*Miosis*
- **Miosis**, or pupil constriction, is typically caused by parasympathetic agonists or opioid use, or anticholinergic effects of some drugs.
- Albuterol is a **sympathomimetic** agent that would more likely cause mydriasis (pupil dilation) due to its adrenergic effects, not miosis.
*Sedation*
- **Sedation** is not a common adverse effect of albuterol; in fact, patients may experience **nervousness** or **tremor** due to its stimulant properties.
- Sedation is more commonly associated with central nervous system depressants or antihistamines.
*Hypoglycemia*
- Albuterol, a beta-2 agonist, can cause **hyperglycemia** by stimulating glycogenolysis and gluconeogenesis, not hypoglycemia.
- Hypoglycemia is typically seen with insulin overdose, oral hypoglycemic agents, or certain endocrine disorders.
*Urinary frequency*
- **Urinary frequency** is not a direct or common adverse effect of albuterol.
- It could be a symptom of other conditions like diabetes, urinary tract infections, or diuretic use, but not albuterol.
Question 927: A 57-year-old man presents to the emergency department with shortness of breath. He was eating dinner with his family during the holidays and felt very short of breath, thus prompting him to come in. The patient has a past medical history of diabetes, hypertension, 2 myocardial infarctions, and obesity. Physical exam is notable for bilateral pulmonary crackles and a jugular venous distension. Chest radiography reveals an enlarged cardiac silhouette and blunting of the costophrenic angles. The patient is started on a medication for his acute symptoms. Two hours later, he states his symptoms have vastly improved and repeat chest radiography is notable for an enlarged cardiac silhouette. Which of the following is a property of the medication most likely given?
A. Increases cardiac contractility and decreases afterload
B. Chronic use leads to long-term nephrogenic adaptations (Correct Answer)
C. Increases cardiac contractility and afterload
D. Can lead to respiratory depression
E. Causes venodilation and a decrease in preload
Explanation: ***Chronic use leads to long-term nephrogenic adaptations***
- The patient's presentation with acute shortness of breath, crackles, JVD, enlarged cardiac silhouette, and blunting of costophrenic angles is classic for **acute decompensated heart failure** with **pulmonary edema**. The prompt improvement of symptoms and resolution of pulmonary edema suggests a **loop diuretic** like **furosemide** was administered.
- **Chronic use of loop diuretics** can lead to long-term **nephrogenic adaptations**, such as hypertrophy of the distal nephron and increased counter-regulatory hormone production (renin-angiotensin-aldosterone system), which can contribute to diuretic resistance over time.
*Increases cardiac contractility and decreases afterload*
- Medications that increase cardiac contractility (positive inotropes) and decrease afterload (vasodilators) are sometimes used in heart failure, but they are not the primary treatment for **acute pulmonary edema** leading to rapid resolution of fluid overload.
- While improved contractility might benefit cardiac output, the immediate goal in pulmonary edema is **volume reduction** and **preload reduction**.
*Increases cardiac contractility and afterload*
- Medications that increase both cardiac contractility and afterload (e.g., some vasopressors) would be detrimental in this setting, as increased afterload would further burden the failing heart and worsen pulmonary congestion.
- This combination is not used to treat acute decompensated heart failure with pulmonary edema.
*Can lead to respiratory depression*
- **Opioids** like morphine can cause respiratory depression and are sometimes used in acute heart failure to reduce preload and anxiety, but they are not the primary cause of the rapid resolution of pulmonary edema and would not be considered the "most likely" medication in this scenario without other indicators.
- While they might provide some symptomatic relief, the *main* intervention for pulmonary edema here points to diuresis.
*Causes venodilation and a decrease in preload*
- **Nitroglycerin** causes venodilation and a decrease in preload, which is beneficial in acute heart failure. However, while it helps alleviate pulmonary congestion via preload reduction, the rapid and significant improvement in pulmonary edema (as suggested by "blunting of costophrenic angles" being mentioned in the initial presentation and the overall improvement in symptoms) points more strongly to the potent fluid removal action of a loop diuretic.
- Though nitroglycerin is often used in combination with diuretics in acute heart failure, a diuretic is the most effective single agent for rapidly addressing the **fluid overload** evident in pulmonary edema.
Question 928: A 30-year-old woman presents to her physician for her annual checkup. She has diabetes mellitus, type 1 and takes insulin regularly. She reports no incidents of elevated or low blood sugar and that she is feeling energetic and ready to face the morning every day. Her vital signs and physical are normal. On the way home from her checkup she stops by the pharmacy and picks up her prescription of insulin. Later that night she takes a dose. What is the signaling mechanism associated with this medication?
A. Increased concentration intracellular cAMP
B. Increased permeability of the cell membrane to negatively charged molecules
C. Activation of tyrosine kinase (Correct Answer)
D. Rapid and direct upregulation of enzyme transcription
E. Increased permeability of the cell membrane to positively charged molecules
Explanation: ***Activation of tyrosine kinase***
- **Insulin** primarily binds to the **insulin receptor**, which is a **receptor tyrosine kinase**.
- Upon insulin binding, the intrinsic tyrosine kinase activity of the receptor is activated, leading to **autophosphorylation** and phosphorylation of downstream signaling proteins like **IRS-1**.
*Increased concentration intracellular cAMP*
- This mechanism is characteristic of signaling pathways involving **G protein-coupled receptors** that activate adenylyl cyclase, such as those for **glucagon** or **catecholamines**.
- Insulin does not primarily signal through **cAMP** as a second messenger.
*Increased permeability of the cell membrane to negatively charged molecules*
- Changes in membrane permeability to negatively charged molecules are usually associated with **GABAergic** or **glycinergic neurotransmission**, leading to inhibitory postsynaptic potentials.
- This is not a primary mechanism for **insulin signaling**.
*Rapid and direct upregulation of enzyme transcription*
- While insulin does influence gene expression over longer periods, its immediate effects involve **protein phosphorylation** and translocation, not direct, rapid transcriptional changes at the moment of receptor binding.
- Steroid hormones typically mediate more direct transcriptional regulation.
*Increased permeability of the cell membrane to positively charged molecules*
- This mechanism is characteristic of **ligand-gated ion channels** that allow influx of ions like **Na+** or **Ca2+**, important in neuronal excitation or muscle contraction.
- Insulin signaling primarily involves **kinase cascades** and not direct changes in membrane permeability to positive ions.
Question 929: A 54-year-old man comes to the physician for a follow-up examination. One week ago, he was treated in the emergency department for chest pain, palpitations, and dyspnea. As part of his regimen, he was started on a medication that irreversibly inhibits the synthesis of thromboxane A2 and prostaglandins. Which of the following is the most likely adverse effect of this medication?
A. Tinnitus
B. Gout attack
C. Chronic rhinosinusitis
D. Acute interstitial nephritis
E. Gastrointestinal hemorrhage (Correct Answer)
Explanation: ***Gastrointestinal hemorrhage***
- The medication described, which **irreversibly inhibits thromboxane A2 and prostaglandins**, is **aspirin**. Aspirin's inhibition of **prostaglandin synthesis** in the stomach reduces the protective mucous barrier, leading to an increased risk of **gastric ulcers** and **hemorrhage**.
- **Thromboxane A2 inhibition** by aspirin also impairs platelet aggregation, thereby increasing the risk of bleeding, including **gastrointestinal hemorrhage**.
- This is the **most common serious adverse effect** of chronic aspirin therapy, occurring in approximately 2-4% of patients on long-term low-dose aspirin for cardiovascular prophylaxis.
*Tinnitus*
- **Tinnitus** is a known adverse effect of **salicylate toxicity**, which usually occurs with higher doses of aspirin (>3-4 g/day). While possible, it's **uncommon with standard prophylactic doses** (81-325 mg/day) used for cardiovascular events.
- The question describes a regimen for a cardiac patient, implying a therapeutic dose rather than an overdose scenario.
*Gout attack*
- Aspirin's effect on **uric acid excretion** is dose-dependent: low doses (<1-2 g/day) can **decrease uric acid excretion**, potentially precipitating a gout attack, while high doses increase excretion.
- However, this effect is **less common** than GI complications, and aspirin is generally avoided in patients with known gout due to this complex effect and the availability of safer alternatives.
*Chronic rhinosinusitis*
- **Chronic rhinosinusitis** is not a direct adverse effect of aspirin. However, **aspirin-exacerbated respiratory disease (AERD)**, a condition involving asthma, nasal polyps, and chronic rhinosinusitis, can be triggered by aspirin in susceptible individuals.
- This is a **rare, specific syndrome** affecting approximately 7% of adults with asthma, not a general adverse effect for all patients on aspirin.
*Acute interstitial nephritis*
- **Acute interstitial nephritis** is more commonly associated with **non-steroidal anti-inflammatory drugs (NSAIDs)**, which also inhibit prostaglandin synthesis, but their effect on cyclooxygenase (COX) enzymes is typically reversible, unlike aspirin.
- While NSAIDs can cause AIN by acting as haptens and triggering an immune response, aspirin is **less frequently implicated** in this specific renal pathology compared to other NSAIDs.
Question 930: An investigator is studying brachial artery reactivity in women with suspected coronary heart disease. The brachial artery diameter is measured via ultrasound before and after intra-arterial injection of acetylcholine. An increase of 7% in the vascular diameter is noted. The release of which of the following is most likely responsible for the observed effect?
A. Norepinephrine from the adrenal medulla
B. Endothelin from the peripheral vasculature
C. Serotonin from neuroendocrine cells
D. Atrial natriuretic peptide from atrial myocytes
E. Nitric oxide from endothelial cells (Correct Answer)
Explanation: ***Nitric oxide from endothelial cells***
- **Acetylcholine** stimulates endothelial cells to release **nitric oxide (NO)**, a potent vasodilator, leading to an increase in vascular diameter. This is the basis of **endothelium-dependent vasodilation**.
- The measurement of brachial artery reactivity involves assessing the ability of blood vessels to dilate in response to various stimuli, which is largely mediated by **NO**.
*Norepinephrine from the adrenal medulla*
- **Norepinephrine** is primarily a vasoconstrictor, acting on alpha-adrenergic receptors to cause **smooth muscle contraction** and a decrease in vascular diameter.
- It is released in response to stress and sympathetic nervous system activation, leading to systemic effects rather than localized vasodilation from acetylcholine.
*Endothelin from the peripheral vasculature*
- **Endothelin** is a powerful **vasoconstrictor** produced by endothelial cells, playing a role in maintaining vascular tone and blood pressure.
- Its action would lead to a decrease, not an increase, in vascular diameter, which is contrary to the observed effect in this scenario.
*Serotonin from neuroendocrine cells*
- **Serotonin (5-HT)** can have both vasoconstrictive and vasodilatory effects depending on the receptor type and vascular bed, but it is not the primary mediator of **acetylcholine-induced vasodilation**.
- Neuroendocrine cells release serotonin as a neurotransmitter and hormone, but its role in brachial artery reactivity to acetylcholine is not dominant.
*Atrial natriuretic peptide from atrial myocytes*
- **Atrial natriuretic peptide (ANP)** is a hormone released by atrial myocytes in response to atrial stretch, primarily promoting vasodilation and increased sodium and water excretion to **lower blood pressure**.
- While it causes vasodilation, it is not directly stimulated by acetylcholine in the context of brachial artery reactivity testing.