Clinical applications in autonomic disorders US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Clinical applications in autonomic disorders. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Clinical applications in autonomic disorders US Medical PG Question 1: Which receptor type mediates the slow phase of synaptic transmission in autonomic ganglia?
- A. Muscarinic (M3)
- B. Muscarinic (M2)
- C. Muscarinic (M1) (Correct Answer)
- D. Nicotinic (N2)
Clinical applications in autonomic disorders Explanation: ***Muscarinic (M1)***
- **M1 receptors** are **Gq-protein coupled receptors** that activate phospholipase C, leading to increased intracellular calcium and diacylglycerol, which mediates the slow excitatory postsynaptic potential in autonomic ganglia.
- This activation results in a **slow depolarization** that prolongs the excitability of ganglionic neurons after the initial fast synaptic transmission.
*Muscarinic (M3)*
- **M3 receptors** are primarily found on **smooth muscle**, glands, and endothelium, mediating contraction, secretion, and vasodilation, respectively.
- While also **Gq-protein coupled**, their role in autonomic ganglia is not the main mediator of the slow phase of synaptic transmission.
*Muscarinic (M2)*
- **M2 receptors** are **Gi-protein coupled receptors** mainly found in the heart, mediating decreased heart rate and contractility.
- In autonomic ganglia, M2 receptors could have a modulatory role, but they are not responsible for the slow excitatory phase of synaptic transmission.
*Nicotinic (N2)*
- **Nicotinic N2 receptors** (also known as **NN or neuronal nicotinic receptors**) mediate the **fast excitatory postsynaptic potential** (EPSP) in autonomic ganglia by opening ion channels.
- This leads to rapid depolarization and action potential generation, which is distinct from the **slower, prolonged phase** of transmission.
Clinical applications in autonomic disorders US Medical PG Question 2: A 24-year-old G1P0 presents to her obstetrician at 26 weeks’ gestation complaining of worsening headaches and blurry vision. Her past medical history is notable for hypertension and diabetes mellitus. Her temperature is 98.6°F (37°C), blood pressure is 160/95 mmHg, pulse is 100/min, and respirations are 18/min. On physical exam, she is tender to palpation in her abdomen and has mild edema in her extremities. A urine dipstick demonstrates 3+ protein. The patient is immediately started on IV magnesium sulfate, diazepam, and a medication that affects both a- and ß-adrenergic receptors. Which of the following medications is most consistent with this mechanism of action?
- A. Pindolol
- B. Labetalol (Correct Answer)
- C. Esmolol
- D. Propranolol
- E. Metoprolol
Clinical applications in autonomic disorders Explanation: ***Labetalol***
- **Labetalol** is an **alpha-beta blocker** that is commonly used to treat **hypertensive emergencies** in pregnancy, such as **severe preeclampsia**.
- It works by blocking both **alpha-1 adrenergic receptors** (causing vasodilation) and **beta-1/2 adrenergic receptors** (reducing heart rate and contractility).
*Pindolol*
- **Pindolol** is a **beta-blocker** with **intrinsic sympathomimetic activity (ISA)**, meaning it partially stimulates beta receptors while blocking the effects of norepinephrine.
- It primarily affects beta-adrenergic receptors and does not significantly block alpha-adrenergic receptors.
*Esmolol*
- **Esmolol** is a **short-acting, cardioselective beta-1 blocker** primarily used for acute management of **tachycardia** and **hypertension** in critical care settings.
- It does not have significant alpha-adrenergic blocking activity.
*Propranolol*
- **Propranolol** is a **non-selective beta-blocker** that blocks both beta-1 and beta-2 adrenergic receptors.
- It does not have alpha-adrenergic blocking activity.
*Metoprolol*
- **Metoprolol** is a **selective beta-1 blocker** (cardioselective) mainly used for **hypertension**, **angina**, and **heart failure**.
- It primarily affects beta-1 adrenergic receptors and does not have significant alpha-adrenergic blocking activity.
Clinical applications in autonomic disorders US Medical PG Question 3: A 43-year-old man is brought to the emergency department 45 minutes after his wife found him on the floor sweating profusely. On arrival, he is lethargic and unable to provide a history. He vomited multiple times on the way to the hospital. His temperature is 37.3°C (99.1°F), pulse is 55/min, respirations are 22/min, and blood pressure is 98/65 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 80%. Examination shows profuse diaphoresis and excessive salivation. He withdraws his extremities sluggishly to pain. The pupils are constricted and reactive. Scattered expiratory wheezing and rhonchi are heard throughout both lung fields. Cardiac examination shows no abnormalities. There are fine fasciculations in the lower extremities bilaterally. Muscle strength is reduced and deep tendon reflexes are 1+ bilaterally. His clothes are soaked with urine and feces. Which of the following is the mechanism of action of the most appropriate initial pharmacotherapy?
- A. Non-selective α-adrenergic antagonism
- B. Competitive antagonism of mACh receptors (Correct Answer)
- C. Alkaloid emesis-induction
- D. Enteral binding
- E. Urine alkalization
Clinical applications in autonomic disorders Explanation: ***Competitive antagonism of mACh receptors***
- The patient's symptoms, including **profuse sweating, salivation, constricted pupils, wheezing, bradycardia, hypotension, fasciculations**, and incontinence, are classic signs of **cholinergic crisis** due to **organophosphate poisoning**.
- **Atropine**, a competitive antagonist of muscarinic acetylcholine (mACh) receptors, is the primary initial pharmacotherapy for organophosphate poisoning, counteracting the excessive parasympathetic stimulation.
*Non-selective α-adrenergic antagonism*
- This mechanism would typically be used to treat conditions involving **excessive alpha-adrenergic activity**, such as a pheochromocytoma or severe hypertension.
- It would **worsen the hypotension** already present in this patient and does not address the underlying cholinergic overstimulation.
*Alkaloid emesis-induction*
- While vomiting occurred, inducing further emesis with an alkaloid is **contraindicated** in cases of organophosphate poisoning due to the risk of **aspiration pneumonitis** and the patient's altered mental status.
- Furthermore, modern management of poisoning rarely recommends routine emesis induction.
*Enteral binding*
- **Activated charcoal** acts by enteral binding to prevent absorption of toxins from the gastrointestinal tract.
- While it may be considered in some poisonings, the rapid onset of severe symptoms and the potential for aspiration in a lethargic patient makes **airway protection** and **antidote administration** the immediate priorities.
*Urine alkalization*
- Urine alkalization is a technique used to enhance the renal excretion of certain acidic drugs by increasing their ionization in the urine, preventing reabsorption.
- It is **not relevant** for the initial management of organophosphate poisoning, which primarily requires anticholinergic agents and cholinesterase reactivators.
Clinical applications in autonomic disorders US Medical PG Question 4: An investigator is studying a local anesthetic that causes increased sympathetic activity. When given intravenously, it causes euphoria and pupillary dilation. Which of the following is the most likely effect of this drug at the synaptic cleft?
- A. Increased release of norepinephrine
- B. Decreased reuptake of norepinephrine (Correct Answer)
- C. Decreased release of acetylcholine
- D. Increased release of serotonin
- E. Decreased breakdown of norepinephrine
Clinical applications in autonomic disorders Explanation: ***Decreased reuptake of norepinephrine***
- This drug causes **euphoria** and **pupillary dilation**, which are classic signs of increased **sympathetic nervous system** activity and **CNS stimulation**, consistent with enhanced **noradrenergic transmission**.
- Decreasing the **reuptake of norepinephrine** would increase its concentration in the **synaptic cleft**, leading to more prolonged activation of **alpha and beta adrenergic receptors**.
*Increased release of norepinephrine*
- While increased release would also elevate **norepinephrine** in the **synaptic cleft**, reuptake inhibition is a more common mechanism for drugs producing similar effects like **cocaine** and **amphetamine-like stimulants**.
- Without specific information, **reuptake inhibition** aligns better with the broad activation of **adrenergic receptors** and central effects described.
*Decreased release of acetylcholine*
- This would primarily affect **cholinergic systems**, and while some interactions exist, it does not directly explain the intense **adrenergic activation**, **euphoria**, and **pupillary dilation** observed.
- **Acetylcholine** primarily mediates **parasympathetic responses** and **skeletal muscle contraction**, not the sympathetic effects seen here.
*Increased release of serotonin*
- Increased **serotonin** release is associated with hallucinogenic effects and mood modulation, but it does not directly lead to the pronounced **pupillary dilation** and widespread **alpha/beta adrenergic receptor activation** described.
- The drug explicitly affects **adrenergic receptors**, making an effect on **norepinephrine** more direct.
*Decreased breakdown of norepinephrine*
- This mechanism, typically involving **MAO inhibitors**, would increase **norepinephrine** levels but is described as activating both **alpha and beta adrenergic receptors**, which points more towards a direct increase in synaptic availability rather than metabolic inhibition.
- While it prolongs the action of **norepinephrine**, the primary mechanism described for such a general stimulant often involves **reuptake inhibition** or **enhanced release**.
Clinical applications in autonomic disorders US Medical PG Question 5: A 30-year-old woman is undergoing work up for progressive weakness. She reports that at the end of the work day, her "eyelids droop" and her "eyes cross," but in the morning she feels "ok." She reports that her legs feel heavy when she climbs the stairs of her house to go to sleep at night. As part of her work up, the physician has her hold her gaze toward the ceiling, and after a minute, her lids become ptotic. She is given an IV medication and her symptoms resolve, but return 10 minutes later. Which of the following medications was used in the diagnostic test performed for this patient?
- A. Neostigmine
- B. Pyridostigmine
- C. Physostigmine
- D. Edrophonium (Correct Answer)
- E. Echothiophate
Clinical applications in autonomic disorders Explanation: ***Edrophonium***
* The clinical picture strongly suggests **myasthenia gravis**, characterized by fluctuating muscle weakness that worsens with activity and improves with rest, exemplified by the patient's symptoms at the end of the day.
* **Edrophonium** is an **ultrashort-acting acetylcholinesterase inhibitor** used in the **Tensilon test** to diagnose myasthenia gravis. Its rapid onset and brief duration of action (symptoms resolve briefly then return) match the scenario described.
*Neostigmine*
* While **neostigmine** is an acetylcholinesterase inhibitor, it has a **longer duration of action** compared to edrophonium and is typically used for the *treatment* of myasthenia gravis, not primarily for the rapid diagnostic test.
* It is also used to reverse the effects of non-depolarizing neuromuscular blockers.
*Pyridostigmine*
* **Pyridostigmine** is a commonly used, **intermediate-acting acetylcholinesterase inhibitor** used for the *chronic management* of myasthenia gravis due to its longer duration (3-6 hours).
* It would not produce the rapid, transient improvement and return of symptoms seen in the diagnostic test described.
*Physostigmine*
* **Physostigmine** is an acetylcholinesterase inhibitor that can cross the **blood-brain barrier** and is primarily used to treat central anticholinergic toxicity.
* It is not used for the diagnosis of myasthenia gravis due to its central effects and different clinical indications.
*Echothiophate*
* **Echothiophate** is an **irreversible acetylcholinesterase inhibitor** used topically for glaucoma.
* Its irreversible nature and long duration of action make it unsuitable for a diagnostic test like the one described, as the effects would not resolve quickly.
Clinical applications in autonomic disorders US Medical PG Question 6: A 33-year-old man comes to the emergency department because of a dry mouth and blurred vision for the past 30 minutes. Prior to this, he was on a road trip and started to feel nauseous, dizzy, and fatigued, so his friend gave him a drug that had helped in the past. Physical examination shows dry mucous membranes and dilated pupils. The remainder of the examination shows no abnormalities. Administration of which of the following drugs is most likely to cause a similar adverse reaction in this patient?
- A. Loratadine
- B. Phenylephrine
- C. Oxycodone
- D. Oxybutynin (Correct Answer)
- E. Pilocarpine
Clinical applications in autonomic disorders Explanation: ***Oxybutynin***
- Oxybutynin is an **anticholinergic** drug primarily used to treat overactive bladder.
- Its adverse effects, such as **dry mouth** (xerostomia), blurred vision (due to cycloplegia and mydriasis), nausea, dizziness, and fatigue, are directly related to its **muscarinic receptor blockade**.
*Loratadine*
- Loratadine is a **second-generation antihistamine** that is largely non-sedating and has minimal anticholinergic effects.
- While it can cause dry mouth in rare cases, it is much less likely to cause the constellation of severe anticholinergic symptoms seen here, especially **blurred vision due to mydriasis**.
*Phenylephrine*
- Phenylephrine is an **alpha-1 adrenergic agonist** used as a decongestant or to increase blood pressure.
- Its primary effects are vasoconstriction; it does not typically cause dry mouth, blurred vision, or the other anticholinergic symptoms described.
*Oxycodone*
- Oxycodone is an **opioid analgesic** that primarily acts on mu-opioid receptors.
- Common side effects include constipation, nausea, sedation, and respiratory depression, but not dry mouth or blurred vision as a prominent anticholinergic effect.
*Pilocarpine*
- Pilocarpine is a **muscarinic agonist** used to treat dry mouth or glaucoma.
- It would cause symptoms directly opposite to those observed, such as increased salivation and miosis, rather than dry mouth and dilated pupils.
Clinical applications in autonomic disorders US Medical PG Question 7: You have been asked to deliver a lecture to medical students about the effects of various body hormones and neurotransmitters on the metabolism of glucose. Which of the following statements best describes the effects of sympathetic stimulation on glucose metabolism?
- A. Norepinephrine causes increased glucose absorption within the intestines.
- B. Without epinephrine, insulin cannot act on the liver.
- C. Peripheral tissues require epinephrine to take up glucose.
- D. Epinephrine increases liver glycogenolysis. (Correct Answer)
- E. Sympathetic stimulation to alpha receptors of the pancreas increases insulin release.
Clinical applications in autonomic disorders Explanation: ***Epinephrine increases liver glycogenolysis.***
- **Epinephrine**, released during sympathetic stimulation, primarily acts to increase **glucose availability** for immediate energy.
- It achieves this by stimulating **glycogenolysis** (breakdown of glycogen into glucose) in the liver via **beta-adrenergic receptors**.
*Norepinephrine causes increased glucose absorption within the intestines.*
- **Norepinephrine** primarily causes **vasoconstriction** and can *decrease* **intestinal motility** and nutrient absorption due to shunting blood away from the digestive tract during stress.
- Glucose absorption is mainly regulated by digestive enzymes and transport proteins, not directly increased by norepinephrine.
*Without epinephrine, insulin cannot act on the liver.*
- **Insulin** acts on the liver independent of epinephrine to promote **glucose uptake**, **glycogenesis**, and **lipid synthesis**.
- Epinephrine and insulin have **antagonistic effects** on liver glucose metabolism; epinephrine increases glucose output, while insulin decreases it.
*Peripheral tissues require epinephrine to take up glucose.*
- **Insulin** is the primary hormone required for **glucose uptake** by most peripheral tissues, especially **muscle** and **adipose tissue**, via **GLUT4 transporters**.
- Epinephrine generally *reduces* glucose uptake by peripheral tissues to preserve glucose for the brain during stress.
*Sympathetic stimulation to alpha receptors of the pancreas increases insulin release.*
- Sympathetic stimulation, primarily acting through **alpha-2 adrenergic receptors** on pancreatic beta cells, actually **inhibits** **insulin secretion**.
- This inhibition helps to increase blood glucose levels by reducing insulin's glucose-lowering effects.
Clinical applications in autonomic disorders US Medical PG Question 8: A 19-year-old woman is brought to the emergency room by her mother. She found her daughter pale, cold to the touch, and collapsed next to her bed earlier this morning. The patient has no previous medical or psychiatric history, but the mother does report that her daughter has not had her periods for the last 3 months. In the emergency department, the patient is alert and oriented. Her vitals include: blood pressure 80/60 mm Hg supine, heart rate 55/min. On physical examination, the patient appears pale and emaciated. A urine pregnancy test is negative. She is suspected of having an eating disorder. Which of the following treatment options would be contraindicated in this patient?
- A. Olanzapine
- B. Bupropion (Correct Answer)
- C. Cognitive-behavioral therapy
- D. Selective serotonin reuptake inhibitors
- E. High caloric food
Clinical applications in autonomic disorders Explanation: ***Bupropion***
- **Bupropion** is contraindicated in patients with **anorexia nervosa** or **bulimia nervosa** due to the increased risk of **seizures**.
- Patients with eating disorders often have electrolyte imbalances and metabolic derangements, which further lower the seizure threshold.
*Olanzapine*
- **Olanzapine**, an atypical antipsychotic, can be used in patients with anorexia nervosa to help with **weight gain** and reduce rigid thinking patterns.
- It is particularly useful when significant **anxiety** or **psychotic features** are present, which can exacerbate the eating disorder.
*Cognitive-behavioral therapy*
- **Cognitive-behavioral therapy (CBT)** is a cornerstone of treatment for eating disorders, including anorexia nervosa.
- It helps patients identify and change distorted thoughts and behaviors related to food, weight, and body image.
*Selective serotonin reuptake inhibitors*
- **SSRIs** may be used in anorexia nervosa, primarily after **weight restoration**, to address co-occurring **depression** or **anxiety disorders**.
- They are generally not effective for acute weight gain but can prevent relapse and treat underlying mood disturbances.
*High caloric food*
- Providing **high-caloric food** and nutritional rehabilitation is essential in managing anorexia nervosa to reverse the state of **malnutrition**.
- This must be done carefully to avoid **refeeding syndrome**, a potentially fatal shift in fluid and electrolytes that can occur with rapid refeeding.
Clinical applications in autonomic disorders US Medical PG Question 9: A 57-year-old man is brought to the emergency department by his son for odd behavior. The patient and his son had planned to go on a hike today. On the drive up to the mountain, the patient began acting strangely which prompted the patient's son to bring him in. The patient has a past medical history of constipation, seasonal allergies, alcohol abuse, and IV drug abuse. His current medications include diphenhydramine, metoprolol, and disulfiram. The patient's son states he has been with the patient all morning and has only seen him take his over the counter medications and eat breakfast. His temperature is 102.0°F (38.9°C), blood pressure is 147/102 mmHg, pulse is 110/min, and oxygen saturation is 98% on room air. The patient appears uncomfortable. Physical exam is notable for tachycardia. The patient's skin appears dry, red, and flushed, and he is confused and not responding to questions appropriately. Which of the following is the best treatment for this patient's condition?
- A. Naloxone
- B. IV fluids, thiamine, and dextrose
- C. Physostigmine (Correct Answer)
- D. Atropine
- E. Neostigmine
Clinical applications in autonomic disorders Explanation: ***Physostigmine***
- The patient's symptoms (fever, tachycardia, hypertension, dry flushed skin, confusion, and agitation) are classic for **anticholinergic toxicity**, likely caused by **diphenhydramine**.
- **Physostigmine** is a reversible **acetylcholinesterase inhibitor** that crosses the blood-brain barrier, effectively counteracting both peripheral and central anticholinergic effects.
*Naloxone*
- **Naloxone** is used to reverse **opioid overdose**, which typically presents with **respiratory depression** and miosis, not seen here.
- While the patient has a history of IV drug abuse, the clinical picture does not align with opioid intoxication.
*IV fluids, thiamine, and dextrose*
- This combination is standard empirical treatment for altered mental status in patients with suspected **alcohol abuse** or **nutritional deficiencies**.
- While the patient has a history of alcohol abuse, his primary presentation points more specifically to anticholinergic toxicity.
*Atropine*
- **Atropine** is an **anticholinergic agent**; administering it would worsen the patient's already present anticholinergic toxicity.
- It is used to treat cholinergic crises, such as organophosphate poisoning, by blocking acetylcholine receptors.
*Neostigmine*
- **Neostigmine** is an **acetylcholinesterase inhibitor** but does **not cross the blood-brain barrier**, meaning it would only address peripheral cholinergic effects and not the patient's central nervous system symptoms like confusion.
- It is often used for myasthenia gravis or reversal of neuromuscular blockade.
Clinical applications in autonomic disorders US Medical PG Question 10: A 3-year-old girl swallowed a handful of pills after her grandmother dropped the bottle on the ground this afternoon. She presents to the ER in a very drowsy but agitated state. She is clutching her abdomen, as if in pain, her skin is dry and flushed, and she does not know her name or where she is. Her pupils are dilated. Her grandmother reports that she has not urinated in several hours. The grandmother's medical history is significant for allergic rhinitis and osteoarthritis, both of which are treated with over the counter medications. What is the appropriate treatment for this child?
- A. N-acetylcysteine
- B. Naloxone
- C. Physostigmine (Correct Answer)
- D. Deferoxamine
- E. Atropine
Clinical applications in autonomic disorders Explanation: ***Physostigmine*** is the correct answer.
- The patient's presentation with **dry, flushed skin**, **dilated pupils**, agitation, drowsiness, abdominal pain, and urinary retention is highly suggestive of **anticholinergic toxicity**.
- **Physostigmine** is a **cholinesterase inhibitor** that increases acetylcholine levels, directly reversing the effects of anticholinergic poisoning.
*N-acetylcysteine*
- **N-acetylcysteine** is the specific antidote for **acetaminophen overdose**, which is not indicated by the patient's symptoms.
- The symptoms described do not match the typical presentation of acetaminophen toxicity (e.g., hepatic damage).
*Naloxone*
- **Naloxone** is used to reverse **opioid overdose**, which typically presents with respiratory depression and miosis (pinpoint pupils), contrary to this patient's dilated pupils and lack of respiratory compromise.
- The clinical picture does not suggest opioid intoxication.
*Deferoxamine*
- **Deferoxamine** is a chelating agent used to treat **iron overdose**, which can cause gastrointestinal symptoms but does not typically present with the anticholinergic signs seen here.
- There are no indications of iron toxicity in the patient's history or symptoms.
*Atropine*
- **Atropine** is an **anticholinergic agent** itself and would worsen the patient's symptoms by further blocking acetylcholine receptors.
- It is used to treat cholinergic crises, not overdose of anticholinergic drugs.
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