An 18-year-old boy presents to the clinic with shortness of breath and fever for the last 2 days. He also has a cough for the same duration. He is asthmatic and uses inhaled albuterol for symptom relief when required. He used albuterol today 3 times at 10-minute intervals but has not had relief of his symptoms. On physical examination, his temperature is 38.3°C (101.0°F), pulse is 130/min, blood pressure is 116/80 mm Hg, and respirations are 28/min. Auscultation of the chest reveals bilateral crackles. Considering that he has already taken inhaled albuterol and has tachycardia, the physician nebulizes him with inhaled ipratropium bromide, which significantly improves his symptoms. Which of the following is the mechanism of action of this drug?
Q52
A 59-year-old man comes to the physician because of a 1-year history of increased urinary frequency, weak urinary stream, and occasional straining to void urine. Rectal examination shows a large, nontender prostate without asymmetry or nodularity. His serum creatinine, prostate-specific antigen, and urinalysis are all within the reference range. A diagnosis of benign prostatic hyperplasia is made, and treatment with tamsulosin is begun. Which of the following changes in intracellular messaging is most likely to occur in response to this drug?
Q53
A 16-year-old college student presents to the emergency department with a 3-day history of fever, muscle rigidity, and confusion. He was started on a new medication for schizophrenia 2 months ago. There is no history of sore throat, burning micturition, or loose motions. At the hospital, his temperature is 38.6°C (101.5°F); the blood pressure is 108/62 mm Hg; the pulse is 120/min, and the respiratory rate is 16/min. His urine is cola-colored. On physical examination, he is sweating profusely. Treatment is started with antipyretics and intravenous hydration. Which of the following is most likely responsible for this patient's condition?
Q54
A 56-year-old man presents with constipation and trouble urinating for the past day. He says that he tried drinking a lot of water but that did not help. He also says that he has been tired all the time recently. Past medical history is significant for schizophrenia, diagnosed 3 months ago, and being managed on chlorpromazine. Current medications also include sildenafil. The vital signs include blood pressure 80/45 mm Hg, respiratory rate 23/min, heart rate 86/min and temperature 38.7°C (101.7°F). On physical examination, the patient appears agitated and confused. Which of the following medications is the most likely cause of this patient's presentation?
Q55
A 55-year-old man is brought to the emergency department 3 hours after ingesting approximately 30 tablets of an unknown drug in an apparent suicide attempt. His temperature is 36.5°C (97.7°F), pulse is 40/min, respiratory rate is 19/min, and blood pressure is 85/50 mm Hg. Examination shows cold, clammy extremities. Scattered expiratory wheezing is heard throughout both lung fields. His fingerstick blood glucose concentration is 62 mg/dL. ECG shows prolonged PR intervals and narrow QRS complexes. Intravenous fluid resuscitation and atropine do not improve his symptoms. Administration of which of the following drugs is most appropriate next step in management of this patient?
Q56
A 59-year-old male presents to his primary care physician complaining of a tremor. He developed a tremor in his left hand approximately three months ago. It appears to be worse at rest and diminishes if he points to something or uses the hand to hold an object. His past medical history is notable for emphysema and myasthenia gravis. He has a 40 pack-year smoking history. Physical examination reveals slowed movements. The patient takes several seconds to rise from his chair for a gait analysis which reveals a shuffling gait. The physician decides to start the patient on a medication that prevents the degradation of a neurotransmitter. This medication is also indicated for use in which of the following conditions?
Q57
Pancreatic islets were isolated from a healthy, non-diabetic donor to perform an experiment to look at insulin secretion inhibition. Compounds would be added to separate wells containing the islets bathed in a high glucose solution for one hour. After one hour, the supernatant would be collected, and the insulin content would be measured with an enzyme-linked immunosorbent assay (ELISA). Which of the following compounds would result in the least insulin secretion when added to the islets?
Q58
A 29-year-old female visits her gynecologist because of an inability to conceive with her husband. Past medical history reveals that she has been amenorrheic for several months, and she complains of frequent white nipple discharge. Urine tests for beta-HCG are negative. A receptor agonist for which of the following would be most likely to treat her condition:
Q59
A 35-year-old woman comes to the physician because of blurred vision for the past 2 months. During this period, she has also had difficulty chewing and swallowing. She reports that her symptoms worsen throughout the day and improve with rest. There is no personal or family history of serious illness. The patient works as a teacher and has had a great deal of stress lately. She does not smoke and drinks a glass of wine occasionally. She takes no medications. Her temperature is 37°C (98.6°F), pulse is 68/min, and blood pressure is 130/80 mm Hg. Physical examination shows bilateral ptosis and mask-like facies. Muscle strength is decreased in both lower extremities. The anti–acetylcholine receptor (AChR) antibody test is positive. Electromyography shows a decremental response following repetitive nerve stimulation. Which of the following is the most appropriate next step in the management of this patient?
Q60
A 30-year-old man is brought to the emergency department by his brother for the evaluation of progressive confusion over the past 6 hours. The patient is lethargic and unable to answer questions. His brother states that there is no personal or family history of serious illness. His temperature is 37°C (98.6°F), pulse is 110/min, and blood pressure 135/80 mm Hg. Physical examination shows warm, dry skin and dry mucous membranes. The pupils are dilated. The abdomen is distended and bowel sounds are hypoactive. Laboratory studies are within normal limits. An ECG shows no abnormalities. Intoxication with which of the following substances is the most likely cause of this patient's symptoms?
Cholinergic/Adrenergic drugs US Medical PG Practice Questions and MCQs
Question 51: An 18-year-old boy presents to the clinic with shortness of breath and fever for the last 2 days. He also has a cough for the same duration. He is asthmatic and uses inhaled albuterol for symptom relief when required. He used albuterol today 3 times at 10-minute intervals but has not had relief of his symptoms. On physical examination, his temperature is 38.3°C (101.0°F), pulse is 130/min, blood pressure is 116/80 mm Hg, and respirations are 28/min. Auscultation of the chest reveals bilateral crackles. Considering that he has already taken inhaled albuterol and has tachycardia, the physician nebulizes him with inhaled ipratropium bromide, which significantly improves his symptoms. Which of the following is the mechanism of action of this drug?
A. Inhibition of vagally-mediated contraction of bronchial smooth muscles (Correct Answer)
B. Inhibition of degranulation of mast cells
C. Inhibition of phosphodiesterase-4, leading to prevention of release of cytokines and chemokines
D. Inhibition of adenosine receptors in the respiratory tract
E. Stimulation of β2-adrenergic receptors in bronchial smooth muscle
Explanation: ***Inhibition of vagally-mediated contraction of bronchial smooth muscles***
- Ipratropium bromide is a **short-acting muscarinic antagonist (SAMA)** that blocks M3 muscarinic receptors on bronchial smooth muscle
- This action **inhibits acetylcholine's effect**, leading to bronchodilation by preventing vagally-mediated bronchoconstriction
- Particularly useful as an **adjunct to β2-agonists** in acute asthma exacerbations and COPD
*Inhibition of degranulation of mast cells*
- This is the mechanism of action of **mast cell stabilizers** like cromolyn sodium and nedocromil
- These drugs are used for **asthma prophylaxis**, not acute symptom relief
- They prevent the release of inflammatory mediators like histamine from mast cells
*Inhibition of phosphodiesterase-4, leading to prevention of release of cytokines and chemokines*
- This is the mechanism of action of **phosphodiesterase-4 (PDE4) inhibitors** such as roflumilast
- Primarily used in **severe COPD** to reduce inflammation
- PDE4 inhibition increases intracellular cAMP, which has anti-inflammatory effects
*Inhibition of adenosine receptors in the respiratory tract*
- This is the mechanism of action of **methylxanthines** like theophylline and aminophylline
- Blocking adenosine receptors provides bronchodilation and reduces inflammation
- Now considered **second-line therapy** due to narrow therapeutic index
*Stimulation of β2-adrenergic receptors in bronchial smooth muscle*
- This is the mechanism of action of **β2-agonists** like albuterol (already used by this patient)
- Not the mechanism of ipratropium, which is an **anticholinergic** agent
- The patient had already received albuterol without adequate relief, prompting the addition of ipratropium
Question 52: A 59-year-old man comes to the physician because of a 1-year history of increased urinary frequency, weak urinary stream, and occasional straining to void urine. Rectal examination shows a large, nontender prostate without asymmetry or nodularity. His serum creatinine, prostate-specific antigen, and urinalysis are all within the reference range. A diagnosis of benign prostatic hyperplasia is made, and treatment with tamsulosin is begun. Which of the following changes in intracellular messaging is most likely to occur in response to this drug?
A. Decreased activity of phospholipase C (Correct Answer)
B. Increased activity of protein kinase C
C. Increased production of diacylglycerol
D. Decreased activity of protein kinase A
E. Increased activity of adenylyl cyclase
Explanation: ***Decreased activity of phospholipase C***
- **Tamsulosin** is an **alpha-1 adrenergic receptor antagonist** that works by blocking alpha-1 receptors on the smooth muscle of the prostate and bladder neck, causing relaxation.
- Alpha-1 receptor activation normally utilizes the **Gq protein pathway**, which leads to the activation of phospholipase C, thus blocking these receptors decreases phospholipase C activity.
*Increased activity of protein kinase C*
- **Protein kinase C** is activated by **diacylglycerol (DAG)** and intracellular calcium, both of which are products of the phospholipase C pathway.
- Since tamsulosin decreases phospholipase C activity, it would subsequently lead to a *decrease*, not an increase, in protein kinase C activity.
*Increased production of diacylglycerol*
- **Diacylglycerol (DAG)** is a secondary messenger produced by the action of **phospholipase C** on **phosphatidylinositol bisphosphate (PIP2)**.
- As tamsulosin inhibits the alpha-1 receptor and thus phospholipase C activity, it would *decrease* the production of DAG.
*Decreased activity of protein kinase A*
- **Protein kinase A (PKA)** is typically activated by **cyclic AMP (cAMP)**, which is produced by **adenylyl cyclase**.
- The alpha-1 receptor pathway (affected by tamsulosin) primarily involves phospholipase C, not adenylyl cyclase or protein kinase A.
*Increased activity of adenylyl cyclase*
- **Adenylyl cyclase** is responsible for converting **ATP to cAMP**, which is part of the Gs protein signaling pathway (beta-adrenergic receptors) or Gi protein pathway (alpha-2 adrenergic receptors).
- Tamsulosin specifically targets **alpha-1 adrenergic receptors** which are coupled to **Gq proteins**, not Gs or Gi proteins; therefore, it does not directly affect adenylyl cyclase activity.
Question 53: A 16-year-old college student presents to the emergency department with a 3-day history of fever, muscle rigidity, and confusion. He was started on a new medication for schizophrenia 2 months ago. There is no history of sore throat, burning micturition, or loose motions. At the hospital, his temperature is 38.6°C (101.5°F); the blood pressure is 108/62 mm Hg; the pulse is 120/min, and the respiratory rate is 16/min. His urine is cola-colored. On physical examination, he is sweating profusely. Treatment is started with antipyretics and intravenous hydration. Which of the following is most likely responsible for this patient's condition?
A. Diazepam
B. Phenytoin
C. Levodopa
D. Amantadine
E. Chlorpromazine (Correct Answer)
Explanation: ***Chlorpromazine***
- The patient's symptoms of **fever**, **muscle rigidity**, and **confusion**, combined with a history of starting an antipsychotic medication (**Chlorpromazine**), are highly indicative of **neuroleptic malignant syndrome (NMS)**.
- **Chlorpromazine** is a typical antipsychotic known to block dopamine receptors, which can lead to NMS. The **cola-colored urine** suggests **rhabdomyolysis**, a common complication of severe muscle rigidity in NMS.
*Diazepam*
- **Diazepam** is a benzodiazepine used to treat anxiety, seizures, and muscle spasms, and does not typically cause NMS.
- Its mechanism of action involves enhancing GABAergic neurotransmission, which is distinct from the dopaminergic blockade associated with NMS.
*Phenytoin*
- **Phenytoin** is an anticonvulsant medication that can cause a variety of side effects, but NMS is not one of them.
- Common side effects include **gingival hyperplasia**, **ataxia**, and **nystagmus**.
*Levodopa*
- **Levodopa** is primarily used to treat Parkinson's disease by increasing dopamine levels in the brain.
- While abrupt withdrawal of **Levodopa** can sometimes precipitate NMS-like symptoms in Parkinson's patients due to inadequate dopamine, starting it does not cause NMS, and it is not typically used for schizophrenia.
*Amantadine*
- **Amantadine** is an antiviral drug also used to treat Parkinson's disease; it is not an antipsychotic.
- It primarily acts as a dopamine agonist and NMDA receptor antagonist, and its use is not associated with causing NMS.
Question 54: A 56-year-old man presents with constipation and trouble urinating for the past day. He says that he tried drinking a lot of water but that did not help. He also says that he has been tired all the time recently. Past medical history is significant for schizophrenia, diagnosed 3 months ago, and being managed on chlorpromazine. Current medications also include sildenafil. The vital signs include blood pressure 80/45 mm Hg, respiratory rate 23/min, heart rate 86/min and temperature 38.7°C (101.7°F). On physical examination, the patient appears agitated and confused. Which of the following medications is the most likely cause of this patient's presentation?
A. Chlorpromazine (Correct Answer)
B. Ziprasidone
C. Haloperidol
D. Aripiprazole
E. Lithium
Explanation: ***Chlorpromazine***
- The patient's presentation with **constipation**, **trouble urinating**, **fever**, **tachycardia**, **hypotension**, **agitation**, and **confusion** is highly suggestive of **anticholinergic toxicity**.
- **Chlorpromazine**, a low-potency first-generation antipsychotic, has significant **anticholinergic side effects** due to its potent blockade of muscarinic receptors, making it the most likely cause.
*Ziprasidone*
- Ziprasidone is a **second-generation antipsychotic** known for a lower propensity for anticholinergic side effects compared to first-generation agents like chlorpromazine.
- While it can cause side effects, severe anticholinergic toxicity is less common and less pronounced with ziprasidone.
*Haloperidol*
- Haloperidol is a **high-potency first-generation antipsychotic** with relatively weak anticholinergic properties compared to chlorpromazine.
- It is more commonly associated with **extrapyramidal symptoms** rather than the severe anticholinergic syndrome described.
*Aripiprazole*
- Aripiprazole is a **second-generation antipsychotic** with **dopamine partial agonist** properties and very low anticholinergic activity.
- It would be an unlikely cause of the profound anticholinergic toxicity observed in this patient.
*Lithium*
- Lithium is a **mood stabilizer** used in bipolar disorder and does not possess significant anticholinergic properties.
- Lithium toxicity typically presents with **tremor**, **nausea**, **vomiting**, **diarrhea**, and **neurological symptoms** like ataxia, rather than the specific constellation of anticholinergic symptoms seen here.
Question 55: A 55-year-old man is brought to the emergency department 3 hours after ingesting approximately 30 tablets of an unknown drug in an apparent suicide attempt. His temperature is 36.5°C (97.7°F), pulse is 40/min, respiratory rate is 19/min, and blood pressure is 85/50 mm Hg. Examination shows cold, clammy extremities. Scattered expiratory wheezing is heard throughout both lung fields. His fingerstick blood glucose concentration is 62 mg/dL. ECG shows prolonged PR intervals and narrow QRS complexes. Intravenous fluid resuscitation and atropine do not improve his symptoms. Administration of which of the following drugs is most appropriate next step in management of this patient?
A. Activated charcoal
B. Sodium bicarbonate
C. Naloxone
D. Glucagon (Correct Answer)
E. Pralidoxime
Explanation: ***Glucagon***
- This patient presents with **bradycardia**, **hypotension**, **hypoglycemia**, **bronchospasm** (expiratory wheezing), and **prolonged PR intervals** after ingesting an unknown drug. These symptoms are classic for **beta-blocker overdose**.
- **Glucagon** is indicated in severe beta-blocker overdose when conventional therapies like atropine and IV fluids are ineffective, as it increases cAMP independent of the beta-adrenergic receptor.
*Activated charcoal*
- While generally useful for recent ingestions to prevent absorption, its utility significantly decreases **3 hours post-ingestion**, especially as the drug may have already been absorbed.
- Furthermore, this patient is exhibiting **severe clinical toxicity**, requiring specific antidotal treatment rather than just decontamination.
*Sodium bicarbonate*
- **Sodium bicarbonate** is primarily used in cases of **tricyclic antidepressant (TCA) overdose** to treat QRS widening and metabolic acidosis.
- It is not indicated for beta-blocker overdose, as the ECG shows prolonged PR intervals with narrow QRS complexes, not QRS widening.
*Naloxone*
- **Naloxone** is the antidote for **opioid overdose**, characterized by respiratory depression, miosis, and sedation.
- This patient's symptoms (bradycardia, hypotension, bronchospasm, prolonged PR interval) are not consistent with opioid toxicity.
*Pralidoxime*
- **Pralidoxime** is an antidote for **organophosphate poisoning**, acting as a cholinesterase reactivator.
- Organophosphate poisoning presents with cholinergic symptoms (e.g., salivation, lacrimation, urination, defecation, bronchospasm, miosis), but also tachycardia, not the profound bradycardia seen here.
Question 56: A 59-year-old male presents to his primary care physician complaining of a tremor. He developed a tremor in his left hand approximately three months ago. It appears to be worse at rest and diminishes if he points to something or uses the hand to hold an object. His past medical history is notable for emphysema and myasthenia gravis. He has a 40 pack-year smoking history. Physical examination reveals slowed movements. The patient takes several seconds to rise from his chair for a gait analysis which reveals a shuffling gait. The physician decides to start the patient on a medication that prevents the degradation of a neurotransmitter. This medication is also indicated for use in which of the following conditions?
A. Hyperprolactinemia
B. Seasonal allergies
C. Influenza
D. Major depressive disorder (Correct Answer)
E. Restless leg syndrome
Explanation: ***Major depressive disorder***
- The patient's symptoms (resting tremor worse at rest, bradykinesia, shuffling gait) are classic for **Parkinson's disease**, caused by dopamine deficiency in the substantia nigra
- The medication that **prevents neurotransmitter degradation** refers to **MAO-B inhibitors** (e.g., selegiline, rasagiline), which inhibit monoamine oxidase type B, preventing the breakdown of dopamine
- **MAO inhibitors** as a class prevent the degradation of monoamine neurotransmitters (dopamine, norepinephrine, serotonin)
- **Non-selective MAO inhibitors** (phenelzine, tranylcypromine) and **MAO-A inhibitors** (moclobemide) are used to treat **major depressive disorder**, particularly treatment-resistant depression
- Both MAO-B inhibitors (for Parkinson's) and MAO-A inhibitors (for depression) work by preventing enzymatic degradation of neurotransmitters
*Hyperprolactinemia*
- Treated with **dopamine agonists** (bromocriptine, cabergoline) that directly stimulate dopamine D2 receptors to suppress prolactin secretion
- These are not degradation inhibitors but receptor agonists
*Seasonal allergies*
- Treated with antihistamines, nasal corticosteroids, or leukotriene inhibitors
- No role for medications that prevent neurotransmitter degradation
*Influenza*
- Treated with antiviral medications (oseltamivir, zanamivir) that inhibit neuraminidase
- Note: While oseltamivir inhibits viral neuraminidase (an enzyme), this is unrelated to neurotransmitter degradation in the CNS
*Restless leg syndrome*
- Primarily treated with **dopamine agonists** (pramipexole, ropinirole) that stimulate dopamine receptors
- While dopamine is involved, the mechanism is receptor stimulation, not prevention of degradation
Question 57: Pancreatic islets were isolated from a healthy, non-diabetic donor to perform an experiment to look at insulin secretion inhibition. Compounds would be added to separate wells containing the islets bathed in a high glucose solution for one hour. After one hour, the supernatant would be collected, and the insulin content would be measured with an enzyme-linked immunosorbent assay (ELISA). Which of the following compounds would result in the least insulin secretion when added to the islets?
A. Isoproterenol
B. Dobutamine
C. Glyburide
D. Tolbutamide
E. Clonidine (Correct Answer)
Explanation: ***Clonidine***
- Clonidine is an **alpha-2 adrenergic agonist**, which acts to inhibit insulin secretion from pancreatic beta cells. Alpha-2 receptors, when activated, reduce intracellular cAMP levels, thereby **suppressing insulin release**.
- In a high glucose environment, this inhibitory action of clonidine would result in the **least insulin secretion** compared to other listed compounds which either stimulate insulin secretion or have less direct inhibitory effects.
*Isoproterenol*
- Isoproterenol is a **non-selective beta-adrenergic agonist** (β1 and β2). Activation of beta-adrenergic receptors on pancreatic beta cells generally **stimulates insulin secretion** by increasing intracellular cAMP.
- Therefore, adding isoproterenol would lead to **increased insulin release**, not decreased.
*Dobutamine*
- Dobutamine is primarily a **beta-1 adrenergic agonist**, though it has some beta-2 effects. Beta-1 activation on pancreatic cells is not the primary mechanism associated with insulin regulation.
- While it may have some minor impact, its main action is on cardiac contractility and it is **not known to significantly inhibit insulin secretion** from beta cells.
*Glyburide*
- Glyburide is a **sulfonylurea drug** that works by binding to the SUR1 subunit of the **ATP-sensitive potassium (KATP) channel** on pancreatic beta cells, thereby closing it.
- This closure leads to **depolarization of the cell membrane**, calcium influx, and ultimately **increased insulin secretion**.
*Tolbutamide*
- Tolbutamide is another **sulfonylurea drug**, similar to glyburide, that acts by binding to and blocking the **ATP-sensitive potassium (KATP) channels** on pancreatic beta cells.
- This mechanism leads to beta cell depolarization, **calcium entry**, and **stimulation of insulin release**.
Question 58: A 29-year-old female visits her gynecologist because of an inability to conceive with her husband. Past medical history reveals that she has been amenorrheic for several months, and she complains of frequent white nipple discharge. Urine tests for beta-HCG are negative. A receptor agonist for which of the following would be most likely to treat her condition:
A. Dopamine (Correct Answer)
B. Somatostatin
C. Insulin
D. Vasopressin
E. Serotonin
Explanation: ***Dopamine***
- The patient's symptoms of **amenorrhea**, difficulty conceiving, and **galactorrhea** (white nipple discharge) in a non-pregnant state are classic for **hyperprolactinemia**.
- **Dopamine agonists** like cabergoline or bromocriptine are the first-line treatment as dopamine inhibits prolactin release from the anterior pituitary.
*Somatostatin*
- **Somatostatin** inhibits the release of various hormones, including **growth hormone** and **TSH**, but does not directly or primarily regulate prolactin in a therapeutic context for hyperprolactinemia.
- While somatostatin analogs can be used for neuroendocrine tumors that secrete other hormones, they are **not the treatment of choice** for simple hyperprolactinemia.
*Insulin*
- **Insulin** is a hormone involved in **glucose metabolism** and has no direct role in the regulation of prolactin or the treatment of hyperprolactinemia.
- Its primary therapeutic use is in the management of **diabetes mellitus**.
*Vasopressin*
- **Vasopressin** (ADH) regulates **water reabsorption** in the kidneys and affects blood pressure.
- It is **not involved** in the regulation of prolactin secretion or the management of galactorrhea/amenorrhea.
*Serotonin*
- **Serotonin** typically has a **stimulatory effect** on prolactin release, meaning agonists would worsen hyperprolactinemia, whereas antagonists might decrease it.
- Therefore, a receptor agonist for serotonin would be **contraindicated** and not a treatment for this condition.
Question 59: A 35-year-old woman comes to the physician because of blurred vision for the past 2 months. During this period, she has also had difficulty chewing and swallowing. She reports that her symptoms worsen throughout the day and improve with rest. There is no personal or family history of serious illness. The patient works as a teacher and has had a great deal of stress lately. She does not smoke and drinks a glass of wine occasionally. She takes no medications. Her temperature is 37°C (98.6°F), pulse is 68/min, and blood pressure is 130/80 mm Hg. Physical examination shows bilateral ptosis and mask-like facies. Muscle strength is decreased in both lower extremities. The anti–acetylcholine receptor (AChR) antibody test is positive. Electromyography shows a decremental response following repetitive nerve stimulation. Which of the following is the most appropriate next step in the management of this patient?
A. Serum ACTH and CRH levels
B. Plasmapheresis
C. Anti-VGCC antibody level
D. Physostigmine therapy
E. CT scan of the chest (Correct Answer)
Explanation: ***CT scan of the chest***
- The patient has symptoms suggestive of **myasthenia gravis**, including **ptosis**, **diplopia** (blurred vision), **dysphagia**, and **fatigue that worsens with activity and improves with rest**. The positive **anti-acetylcholine receptor (AChR) antibody** test and **decremental response on EMG** confirm the diagnosis. A computed tomography (CT) scan of the chest is crucial to evaluate for a **thymoma**, which is present in 10-15% of patients with myasthenia gravis and can be surgically resected, potentially leading to symptom improvement or remission.
- Approximately 85% of myasthenia gravis patients have detectable **AChR antibodies**, making this test highly specific for the condition. The presence of these antibodies, along with the characteristic clinical picture and electromyography findings, establishes the diagnosis of myasthenia gravis. Thymectomy is often considered in patients with generalized myasthenia gravis, even in the absence of a thymoma, due to potential therapeutic benefits.
*Serum ACTH and CRH levels*
- This test is primarily used to investigate conditions related to the **hypothalamic-pituitary-adrenal axis**, such as **Cushing's disease** or **Addison's disease**.
- There are no symptoms presented that would suggest altered ACTH or CRH levels, making this an inappropriate diagnostic step for the current patient's presentation.
*Plasmapheresis*
- **Plasmapheresis** is a treatment for **acute severe myasthenia gravis** or **myasthenic crisis**, involving the removal of plasma to eliminate circulating antibodies.
- While it is a treatment for myasthenia gravis, it is not the *next step* in initial workup after diagnosis for a stable patient as described; the priority is to investigate underlying causes like thymoma.
*Anti-VGCC antibody level*
- **Anti-voltage-gated calcium channel (VGCC) antibodies** are characteristic of **Lambert-Eaton Myasthenic Syndrome (LEMS)**, often associated with **small cell lung cancer**.
- The patient's symptoms (e.g., ptosis, worsening with activity) and the positive **AChR antibodies** are classic for myasthenia gravis, not LEMS, making this test unnecessary.
*Physostigmine therapy*
- **Physostigmine** is an **acetylcholinesterase inhibitor** that reverses anticholinergic effects and can be used in some contexts, but it's not a primary treatment for myasthenia gravis.
- The standard pharmacotherapy for myasthenia gravis includes other anticholinesterase inhibitors like **pyridostigmine**, or immunomodulatory agents. This is a treatment, not a diagnostic step in the workup.
Question 60: A 30-year-old man is brought to the emergency department by his brother for the evaluation of progressive confusion over the past 6 hours. The patient is lethargic and unable to answer questions. His brother states that there is no personal or family history of serious illness. His temperature is 37°C (98.6°F), pulse is 110/min, and blood pressure 135/80 mm Hg. Physical examination shows warm, dry skin and dry mucous membranes. The pupils are dilated. The abdomen is distended and bowel sounds are hypoactive. Laboratory studies are within normal limits. An ECG shows no abnormalities. Intoxication with which of the following substances is the most likely cause of this patient's symptoms?
A. Cannabis
B. Amphetamine
C. Opioid
D. Carbon monoxide
E. Antihistamine (Correct Answer)
Explanation: ***Antihistamine***
- The patient's symptoms, including **dilated pupils**, confusion, lethargy, dry skin and mucous membranes, distended abdomen, and hypoactive bowel sounds, are consistent with an **anticholinergic toxidrome**. This pattern is often seen with antihistamine overdose due to their anticholinergic properties.
- The elevated pulse despite normal blood pressure and temperature also aligns with anticholinergic effects.
*Cannabis*
- Cannabis intoxication typically causes **conjunctival injection**, xerostomia, increased appetite, and impaired coordination.
- While it can cause lethargy, it does not explain the dilated pupils, dry mucous membranes, or hypoactive bowel sounds.
*Amphetamine*
- Amphetamine intoxication usually presents with **tachycardia**, hypertension, agitation, paranoia, and diaphoresis, not dry skin or hypoactive bowel sounds.
- Though pupils are typically dilated, the overall clinical picture points away from amphetamine overdose.
*Opioid*
- Opioid overdose is characterized by **respiratory depression**, **miosis (pinpoint pupils)**, and altered mental status, which contradict the dilated pupils and normal respiratory effort (implied by normal oxygenation and stable vital signs) in this case.
- While it can cause lethargy and hypoactive bowel sounds, other key features are missing or are opposite.
*Carbon monoxide*
- Carbon monoxide poisoning classically presents with **headache**, nausea, vomiting, confusion, and sometimes the classic "**cherry-red skin**" (though this is rare and late).
- It does not cause dilated pupils, dry mucous membranes, or hypoactive bowel sounds as seen in this patient.
