A 38-year-old man presents with sudden onset abdominal pain and undergoes an emergent laparoscopic appendectomy. The procedure is performed quickly, without any complications, and the patient is transferred to the post-operative care unit. A little while later, the patient complains of seeing people in his room and hearing voices talking to him. The patient has no prior medical or psychiatric history and does not take any regular medications. What is the mechanism of action of the anesthetic most likely responsible for this patient’s symptoms?
Q112
A 38-year-old woman comes to the physician because of a 3-week history of involuntary movements of her extremities. One year ago, she was fired from her position as an elementary school teacher because she had stopped preparing lessons and was frequently absent without notice. She now lives with her mother. She appears emaciated and malodorous. Examination shows rapid, nonrepetitive jerks of her limbs and face that frequently end with the patient covering her face and yawning. She has an unsteady gait. Genetic testing shows a mutation on chromosome 4. This patient's condition is most likely associated with increased levels of which of the following substances?
Q113
An 18-year-old man is known to be allergic to peanuts, and he mistakenly eats biscuits containing some traces of peanuts. Within 15 minutes, he develops generalized redness of the skin and urticaria, associated with shortness of breath and diffuse wheezing. His blood pressure is 80/55 mm Hg and heart rate is 124/min. He is given intramuscular epinephrine and transported emergently to the local hospital. This patient’s presentation is an example of which of the following hypersensitivity reactions?
Q114
A 23-year-old woman presents to the emergency department with acute onset of shortness of breath, wheezing, and chest tightness. This is her 4th visit for these symptoms in the last 5 years. She tells you she recently ran out of her normal "controller" medication. Concerned for an asthma exacerbation, you begin therapy with a short-acting beta2-agonist. What is the expected cellular response to your therapy?
Q115
A 23-year-old male is brought by police officers from a social gathering due to combative behavior and altered mental status. The police say that phencyclidine was found on the premises. The patient is alone, and acquiring an accurate history proves difficult. However, you do learn that the patient is having visual hallucinations. Vital signs show a blood pressure of 155/95 mmHg, pulse is 103/min, respirations is 20/min, oxygen saturation of 99%. Airway, breathing, and circulation are intact. The patient appears violent, and is trying to remove his clothes. Multiple hospital staff are needed to restrain the patient in bed. A finger-stick glucose show 93 mg/dL. The team is unable to place an IV, and thus intramuscular midazolam is administered to achieve sedation; however, he is still agitated. What is the mechanism of action of the best alternative sedative drug for this patient?
Q116
A 36-year-old man is brought to the emergency department because of facial spasm and an inability to speak for 2 hours. He has had no loss of consciousness or rhythmic movements. He has a history of schizophrenia and was recently put on clozapine for resistant symptoms. He appears to be aware of his surroundings. At the hospital, his blood pressure is 135/85 mm Hg, the pulse is 86/min, the respirations are 16/min, and the temperature is 36.7°C (98.1°F). Physical examination shows the superior deviation of both eyes to the right side, trismus, and spasm of the neck muscles with a deviation of the head to the left. He follows directions without hesitation. The remainder of the physical examination shows no abnormalities. The most appropriate next step is to administer which of the following?
Q117
A 71-year-old man arrives to the emergency room appearing cyanotic and having weak, shallow respirations. He is brought in by his home care nurse, who reports that the patient has a history of myasthenia gravis and frequent urinary tract infections. The patient was in his normal state of health until 5 days ago when he developed a urinary tract infection. He was prescribed gentamicin with improvement of his urinary symptoms. This morning, while trying to eat breakfast, he began complaining of poor grip strength and progressive difficulty breathing. The patient’s medications include pyridostigmine and aspirin, both of which his nurse reports he takes every day as prescribed. The patient’s temperature is 99°F (37.2°C), blood pressure is 128/78 mmHg, pulse is 92/min, and respirations are 28/min with an oxygen saturation of 86% O2 on room air. Upon physical exam, the patient is noted to have gray-blue skin, hypophonia, weak upper extremities, and normal leg strength. An arterial blood gas is drawn with results as shown below:
PO2: 55 mmHg
PCO2: 60 mmHg
pH: 7.30
The patient is intubated. Which of the following is the next best step in management?
Q118
A 20-year-old female presents to your clinic for evaluation. She complains of months of daily rhinorrhea, which she describes as watery and clear, as well as nasal congestion bilaterally. In addition, she reports frequent watery and itchy eyes, as well as daily sneezing. Her temperature is 100.1 deg F (37.8 deg C), blood pressure is 120/70 mmHg, pulse is 70/min, and respirations are 15/min. On exam, you note edematous, boggy turbinates with watery rhinorrhea. Which of the following is a treatment for the patient's condition?
Q119
An 18-year-old female is brought to the emergency department by her boyfriend. She is screaming uncontrollably. Eventually, she states that she is afraid that "death is near" but cannot give a rational reason for this thought. She reports both seeing colors "coming out of other people's mouths" and "hearing" these colors. The patient's boyfriend experienced similar sensory symptoms a few hours ago; he explains they were trying to have a "spiritual experience." Physical exam is significant for mydriasis, hypertension, hyperthermia, piloerection, tachycardia, and sweating. Upon which of the following receptors does the most likely drug she ingested act?
Q120
A 29-year-old man is outside his home doing yard work when a bee stings him in the right arm. Within 10 minutes, he reports breathlessness and multiple, circular, pruritic rashes over his right arm. He drives to his family physician’s office for evaluation. His past medical history is significant for hypertension and he takes lisinopril. Known allergies include latex, Hymenoptera, and aspirin. His blood pressure is 118/68 mm Hg; heart rate is 104/min and regular; respiratory rate is 22/min; temperature is 37.7°C (99.8°F). There is non-pitting edema but erythema with raised wheels are present in the region of the right arm. Auscultation of the lungs reveals mild wheezing at the lung bases. Which of the following is the best course of action in the management of this patient?
Cholinergic/Adrenergic drugs US Medical PG Practice Questions and MCQs
Question 111: A 38-year-old man presents with sudden onset abdominal pain and undergoes an emergent laparoscopic appendectomy. The procedure is performed quickly, without any complications, and the patient is transferred to the post-operative care unit. A little while later, the patient complains of seeing people in his room and hearing voices talking to him. The patient has no prior medical or psychiatric history and does not take any regular medications. What is the mechanism of action of the anesthetic most likely responsible for this patient’s symptoms?
A. Stimulation of μ-opioid receptors
B. N-methyl-D-aspartate receptor antagonism (Correct Answer)
C. Increased duration of GABA-gated chloride channel opening
D. Blocking the fast voltage-gated Na+ channels
E. Increased frequency of GABA-gated chloride channel opening
Explanation: ***N-methyl-D-aspartate receptor antagonism***
- The patient's symptoms of **hallucinations** and **auditory phenomena** post-anesthesia are characteristic of **emergence delirium**, often associated with **ketamine**.
- Ketamine acts primarily as an **NMDA receptor antagonist**, which can lead to dissociative anesthesia and psychomimetic effects upon emergence.
*Stimulation of μ-opioid receptors*
- Opioids primarily cause **analgesia**, respiratory depression, and sedation by stimulating **μ-opioid receptors**.
- While opioids can cause some central nervous system effects like confusion or nightmares, the severe **hallucinations** described are not typical for this mechanism.
*Increased duration of GABA-gated chloride channel opening*
- This mechanism describes the action of **benzodiazepines** which potentiate GABAergic neurotransmission by increasing the **frequency** of chloride channel opening, while **barbiturates** increase the **duration**.
- These drugs typically cause **sedation** and **anxiolysis**, not acute psychosis or vivid hallucinations upon emergence.
*Blocking the fast voltage-gated Na+ channels*
- This is the primary mechanism of action for **local anesthetics** and certain **antiarrhythmic drugs**, leading to inhibition of nerve impulse conduction.
- While some systemic toxicity can occur with local anesthetics, it typically manifests as **seizures** or cardiovascular collapse, not dissociative emergence phenomena.
*Increased frequency of GABA-gated chloride channel opening*
- This is the mechanism of action for **benzodiazepines**, which enhance GABA's inhibitory effects by increasing the **frequency** of chloride channel opening.
- Similar to increased duration of opening, this leads to **sedation** and anxiolysis, not the vivid hallucinations seen in this patient.
Question 112: A 38-year-old woman comes to the physician because of a 3-week history of involuntary movements of her extremities. One year ago, she was fired from her position as an elementary school teacher because she had stopped preparing lessons and was frequently absent without notice. She now lives with her mother. She appears emaciated and malodorous. Examination shows rapid, nonrepetitive jerks of her limbs and face that frequently end with the patient covering her face and yawning. She has an unsteady gait. Genetic testing shows a mutation on chromosome 4. This patient's condition is most likely associated with increased levels of which of the following substances?
A. Gamma-aminobutyric acid
B. N-acetyl aspartate
C. Glutamate (Correct Answer)
D. Dopamine
E. Acetylcholine
Explanation: ***Glutamate***
- **Huntington's disease** is characterized by **chorea, psychiatric symptoms, and cognitive decline**, caused by CAG repeat expansion on chromosome 4 producing abnormal huntingtin protein.
- The mutant huntingtin protein leads to **glutamate excitotoxicity** through multiple mechanisms: impaired glutamate reuptake, enhanced NMDA receptor sensitivity, and mitochondrial dysfunction.
- **Increased glutamatergic activity and extracellular glutamate levels** contribute to progressive neuronal death, particularly of GABAergic medium spiny neurons in the striatum.
- This glutamate-mediated excitotoxicity is the primary mechanism driving neurodegeneration in Huntington's disease.
*Gamma-aminobutyric acid (GABA)*
- GABAergic neurons in the striatum are preferentially lost in Huntington's disease, resulting in **decreased GABA levels**, not increased.
- The loss of GABAergic inhibition contributes to **disinhibition of motor pathways** and the characteristic choreiform movements.
*N-acetyl aspartate (NAA)*
- NAA is a neuronal marker that is **decreased** in neurodegenerative diseases like Huntington's, reflecting **neuronal loss and dysfunction**.
- Reduced NAA is seen on MR spectroscopy but does not cause the motor symptoms.
*Dopamine*
- While there is **relative dopamine hyperactivity** in the striatum due to loss of GABAergic inhibition, dopamine levels themselves are not necessarily increased.
- Dopamine-depleting agents (e.g., **tetrabenazine, deutetrabenazine**) are used therapeutically to reduce chorea by decreasing dopaminergic transmission.
*Acetylcholine*
- Acetylcholine levels are **not primarily elevated** in Huntington's disease pathophysiology.
- Cholinergic function may be affected in advanced disease contributing to cognitive symptoms, but this is not the primary mechanism of chorea.
Question 113: An 18-year-old man is known to be allergic to peanuts, and he mistakenly eats biscuits containing some traces of peanuts. Within 15 minutes, he develops generalized redness of the skin and urticaria, associated with shortness of breath and diffuse wheezing. His blood pressure is 80/55 mm Hg and heart rate is 124/min. He is given intramuscular epinephrine and transported emergently to the local hospital. This patient’s presentation is an example of which of the following hypersensitivity reactions?
A. Delayed hypersensitivity
B. Immediate hypersensitivity (Correct Answer)
C. Type II hypersensitivity
D. Contact dermatitis
E. Serum sickness
Explanation: ***Immediate hypersensitivity***
- The rapid onset (within 15 minutes) of symptoms like **generalized redness**, **urticaria**, **shortness of breath**, **wheezing**, and **hypotension** after exposure to peanuts is characteristic of an **anaphylactic reaction**, which is a severe form of immediate (Type I) hypersensitivity.
- This reaction involves **IgE-mediated mast cell and basophil degranulation**, leading to the rapid release of histamine and other inflammatory mediators.
*Delayed hypersensitivity*
- This type of hypersensitivity, also known as **Type IV hypersensitivity**, typically manifests 24 to 72 hours after antigen exposure.
- It is mediated by **T-cells** and macrophages, not antibodies, and is commonly seen in reactions like **tuberculin skin tests** or contact dermatitis.
*Type II hypersensitivity*
- This reaction involves **antibody-mediated cytotoxicity**, where antibodies (IgG or IgM) bind to antigens on cell surfaces, leading to cell destruction.
- Examples include **hemolytic transfusion reactions** and **autoimmune hemolytic anemia**, which do not match the presented symptoms.
*Contact dermatitis*
- This is a form of **Type IV hypersensitivity** that results from direct contact of the skin with an allergen, leading to a localized rash.
- It presents with **localized skin inflammation** and typically has a delayed onset, usually days after exposure, unlike the rapid systemic reaction described.
*Serum sickness*
- This is a **Type III hypersensitivity reaction** characterized by the formation of **immune complexes** that deposit in tissues, causing symptoms like fever, rash, and arthralgia.
- It typically occurs days to weeks after exposure to certain drugs or foreign proteins, which does not align with the immediate, severe systemic symptoms.
Question 114: A 23-year-old woman presents to the emergency department with acute onset of shortness of breath, wheezing, and chest tightness. This is her 4th visit for these symptoms in the last 5 years. She tells you she recently ran out of her normal "controller" medication. Concerned for an asthma exacerbation, you begin therapy with a short-acting beta2-agonist. What is the expected cellular response to your therapy?
A. Gs protein coupled receptor activates adenylyl cyclase and increases intracellular cAMP (Correct Answer)
B. Gq protein coupled receptor activates phospholipase C and increases intracellular calcium
C. Gq protein coupled receptor activates adenylyl cyclase and increases intracellular cAMP
D. Gs protein coupled receptor activates phospholipase C and increases intracellular calcium
E. Gi protein coupled receptor inhibits adenylyl cyclase and decreases cAMP
Explanation: ***Gs protein coupled receptor activates adenylyl cyclase and increases intracellular cAMP***
- **Short-acting beta2-agonists (SABAs)** like **albuterol** bind to **beta2-adrenergic receptors** on airway smooth muscle cells, which are **Gs protein-coupled receptors**.
- Activation of **Gs protein** stimulates **adenylyl cyclase**, leading to an increase in intracellular **cyclic AMP (cAMP)**, which triggers downstream relaxation of bronchial smooth muscle.
*Gq protein coupled receptor activates phospholipase C and increases intracellular calcium*
- **Gq protein-coupled receptors** are typically associated with **alpha1-adrenergic receptors** or **muscarinic M1/M3 receptors**, which, when activated, cause **bronchoconstriction** not bronchodilation.
- Activation of **Gq protein** leads to activation of **phospholipase C**, which generates **IP3** and **DAG**, ultimately increasing intracellular **calcium** and promoting contraction.
*Gq protein coupled receptor activates adenylyl cyclase and increases intracellular cAMP*
- This option incorrectly pairs **Gq protein** with the activation of **adenylyl cyclase** and an increase in **cAMP**.
- **Gq protein** signaling primarily involves the **phospholipase C pathway** and **calcium** mobilization, not direct adenylyl cyclase activation.
*Gs protein coupled receptor activates phospholipase C and increases intracellular calcium*
- This option incorrectly pairs **Gs protein** with the activation of **phospholipase C** and an increase in intracellular **calcium**.
- **Gs protein** is specifically coupled to the **adenylyl cyclase/cAMP pathway**, while **phospholipase C** and **calcium** are associated with **Gq protein** signaling.
*Gi protein coupled receptor inhibits adenylyl cyclase and decreases cAMP*
- **Gi protein-coupled receptors** inhibit **adenylyl cyclase** and decrease intracellular **cAMP**, which would lead to **bronchoconstriction**, not bronchodilation.
- This mechanism is associated with **M2 muscarinic receptors** on presynaptic terminals, which regulate acetylcholine release, or alpha2-adrenergic receptors, which are not the primary target for bronchodilation in asthma exacerbations.
Question 115: A 23-year-old male is brought by police officers from a social gathering due to combative behavior and altered mental status. The police say that phencyclidine was found on the premises. The patient is alone, and acquiring an accurate history proves difficult. However, you do learn that the patient is having visual hallucinations. Vital signs show a blood pressure of 155/95 mmHg, pulse is 103/min, respirations is 20/min, oxygen saturation of 99%. Airway, breathing, and circulation are intact. The patient appears violent, and is trying to remove his clothes. Multiple hospital staff are needed to restrain the patient in bed. A finger-stick glucose show 93 mg/dL. The team is unable to place an IV, and thus intramuscular midazolam is administered to achieve sedation; however, he is still agitated. What is the mechanism of action of the best alternative sedative drug for this patient?
A. Mu-opioid receptor partial agonist
B. Competitive opioid receptor antagonist
C. Alpha-2 and H1 receptor antagonist
D. Increases duration of chloride channel opening of GABA-A receptors
E. Antagonist of D2 receptors (Correct Answer)
Explanation: ***Antagonist of D2 receptors***
- The patient is likely suffering from **phencyclidine (PCP) intoxication**, characterized by **agitation**, **combative behavior**, **altered mental status**, **hypertension**, **tachycardia**, and **visual hallucinations**.
- **Haloperidol**, a potent **D2 dopamine receptor antagonist**, is often the preferred second-line treatment for agitation in PCP intoxication when benzodiazepines are insufficient, as it effectively reduces the psychotic and agitated state.
*Mu-opioid receptor partial agonist*
- This mechanism describes drugs like **buprenorphine**. While used for opioid addiction, it is not an appropriate sedative for acute PCP intoxication.
- Using an opioid agonist or partial agonist in a combative, agitated patient with unclear history could worsen respiratory depression or complicate the clinical picture.
*Competitive opioid receptor antagonist*
- This describes **naloxone**, used to reverse opioid overdose. It would not be helpful for PCP intoxication, as PCP acts via different receptor systems (NMDA antagonism, dopamine reuptake inhibition).
- Administering naloxone in this scenario would have no therapeutic benefit for the patient's agitation and psychosis.
*Alpha-2 and H1 receptor antagonist*
- This describes the mechanism of drugs like **mirtazapine** (primarily antidepressant) or **clonidine** (alpha-2 agonist, not antagonist, used for sedation/hypertension but less effective for acute psychotic agitation).
- While some antipsychotics have H1 antagonism, this specific combination is not the primary mechanism of the most effective conventional antipsychotics used for severe agitation.
*Increases duration of chloride channel opening of GABA-A receptors*
- This mechanism describes **barbiturates**. While some barbiturates can cause sedation, they are generally not preferred as first-line agents in this situation due to a higher risk of respiratory depression and a narrow therapeutic index compared to benzodiazepines or antipsychotics.
- The initial intramuscular midazolam (a benzodiazepine) works by increasing the *frequency* of chloride channel opening, not duration, making this option incorrect for the *best alternative*.
Question 116: A 36-year-old man is brought to the emergency department because of facial spasm and an inability to speak for 2 hours. He has had no loss of consciousness or rhythmic movements. He has a history of schizophrenia and was recently put on clozapine for resistant symptoms. He appears to be aware of his surroundings. At the hospital, his blood pressure is 135/85 mm Hg, the pulse is 86/min, the respirations are 16/min, and the temperature is 36.7°C (98.1°F). Physical examination shows the superior deviation of both eyes to the right side, trismus, and spasm of the neck muscles with a deviation of the head to the left. He follows directions without hesitation. The remainder of the physical examination shows no abnormalities. The most appropriate next step is to administer which of the following?
A. Labetalol
B. Diphenhydramine (Correct Answer)
C. Flumazenil
D. Calcium gluconate
E. Morphine
Explanation: ***Diphenhydramine***
- The patient's symptoms (facial spasm, inability to speak, ocular deviation, trismus, neck muscle spasm) are characteristic of **acute dystonia**, a **drug-induced extrapyramidal symptom (EPS)**.
- While **clozapine** has a **low risk of EPS** compared to typical antipsychotics due to its weak D2 receptor binding, acute dystonia can still rarely occur, particularly when initiating therapy.
- **Anticholinergic medications** like diphenhydramine (an antihistamine with anticholinergic properties) or benztropine are the **first-line treatment** for acute dystonia, quickly relieving symptoms by restoring the **dopamine-acetylcholine balance** in the basal ganglia.
- Symptoms typically resolve within **15-30 minutes** of parenteral administration.
*Labetalol*
- Labetalol is a **beta-blocker** used to treat **hypertensive emergencies** or **tachycardia**.
- The patient's blood pressure (135/85 mm Hg) and pulse (86/min) are within normal range, and there is no indication for antihypertensive therapy.
*Flumazenil*
- Flumazenil is a **benzodiazepine receptor antagonist** used to reverse **benzodiazepine overdose**.
- The patient's symptoms are not consistent with benzodiazepine toxicity (which would present with sedation, respiratory depression, or altered consciousness), and there is no mention of benzodiazepine use.
*Calcium gluconate*
- Calcium gluconate is used to treat **hypocalcemia**, stabilize cardiac membranes in **hyperkalemia**, or reverse **calcium channel blocker toxicity**.
- There is no clinical or laboratory evidence of electrolyte imbalance or calcium channel blocker exposure.
*Morphine*
- Morphine is an **opioid analgesic** used for **severe pain management**.
- The patient's primary complaint is involuntary muscle spasms and dystonia, not pain, and opioids are not indicated for the treatment of acute dystonia.
Question 117: A 71-year-old man arrives to the emergency room appearing cyanotic and having weak, shallow respirations. He is brought in by his home care nurse, who reports that the patient has a history of myasthenia gravis and frequent urinary tract infections. The patient was in his normal state of health until 5 days ago when he developed a urinary tract infection. He was prescribed gentamicin with improvement of his urinary symptoms. This morning, while trying to eat breakfast, he began complaining of poor grip strength and progressive difficulty breathing. The patient’s medications include pyridostigmine and aspirin, both of which his nurse reports he takes every day as prescribed. The patient’s temperature is 99°F (37.2°C), blood pressure is 128/78 mmHg, pulse is 92/min, and respirations are 28/min with an oxygen saturation of 86% O2 on room air. Upon physical exam, the patient is noted to have gray-blue skin, hypophonia, weak upper extremities, and normal leg strength. An arterial blood gas is drawn with results as shown below:
PO2: 55 mmHg
PCO2: 60 mmHg
pH: 7.30
The patient is intubated. Which of the following is the next best step in management?
A. Plasmapheresis (Correct Answer)
B. Thymectomy
C. Neostigmine
D. Edrophonium
E. Atropine
Explanation: ***Plasmapheresis***
- The patient is experiencing a **myasthenic crisis**, characterized by **respiratory failure** and worsening muscle weakness, likely precipitated by the **gentamicin** (an aminoglycoside known to exacerbate myasthenia gravis).
- **Plasmapheresis** or **intravenous immunoglobulin (IVIG)** are the first-line treatments for myasthenic crisis to rapidly remove circulating autoantibodies and improve neuromuscular transmission.
*Thymectomy*
- **Thymectomy** is considered for patients with **thymoma** or generalized myasthenia gravis, but it is an elective surgical procedure and not an acute management for a myasthenic crisis.
- While it can induce remission or improve symptoms in the long term, it is not the immediate next step for a patient in respiratory distress.
*Neostigmine*
- **Neostigmine** is a **cholinesterase inhibitor** used for symptomatic treatment of myasthenia gravis, but administering additional cholinesterase inhibitors during a myasthenic crisis can paradoxically worsen weakness if it is a **cholinergic crisis** (though less likely here given the history and precipitating factor).
- The patient is already on **pyridostigmine**, and increasing cholinergic agents can lead to an accumulation of acetylcholine, causing **desensitization of receptors** and further paradoxically worsening weakness.
*Edrophonium*
- **Edrophonium** is a **short-acting cholinesterase inhibitor** used in the **Tensilon test** to differentiate between myasthenic crisis and cholinergic crisis.
- It is a diagnostic tool and not a definitive treatment for a severe myasthenic crisis requiring intubation.
*Atropine*
- **Atropine** is an **anticholinergic agent** used to counteract muscarinic side effects of cholinesterase inhibitors, such as bradycardia or excessive secretions, especially if a cholinergic crisis is suspected.
- It does not address the underlying autoimmune attack on neuromuscular junctions and is not a primary treatment for the weakness in a myasthenic crisis.
Question 118: A 20-year-old female presents to your clinic for evaluation. She complains of months of daily rhinorrhea, which she describes as watery and clear, as well as nasal congestion bilaterally. In addition, she reports frequent watery and itchy eyes, as well as daily sneezing. Her temperature is 100.1 deg F (37.8 deg C), blood pressure is 120/70 mmHg, pulse is 70/min, and respirations are 15/min. On exam, you note edematous, boggy turbinates with watery rhinorrhea. Which of the following is a treatment for the patient's condition?
A. Intravenous vancomycin
B. Intravenous penicillin
C. Oral acetaminophen
D. Intranasal fluticasone (Correct Answer)
E. Oral amoxicillin
Explanation: ***Intranasal fluticasone***
- The patient's symptoms of **watery rhinorrhea**, bilateral **nasal congestion**, **itchy eyes**, and **sneezing** are classic for **allergic rhinitis**.
- **Intranasal corticosteroids** such as fluticasone are highly effective first-line treatments for managing the inflammation and symptoms of allergic rhinitis.
*Intravenous vancomycin*
- **Vancomycin** is an **antibiotic** used to treat serious bacterial infections, particularly those caused by **methicillin-resistant Staphylococcus aureus (MRSA)**.
- The patient's symptoms are characteristic of an allergic reaction, not a bacterial infection, and thus antibiotics are inappropriate.
*Intravenous penicillin*
- **Penicillin** is an **antibiotic** used to treat a wide range of bacterial infections.
- Given the symptoms of allergy, there is no indication for antibiotic therapy.
*Oral acetaminophen*
- **Acetaminophen** is an **analgesic** and **antipyretic** used to relieve pain and fever.
- While the patient has a mild fever (100.1 deg F), her primary symptoms are allergic, not indicative of pain or a severe febrile illness requiring this medication as a primary treatment for her *condition*.
*Oral amoxicillin*
- **Amoxicillin** is a broad-spectrum **antibiotic** commonly used for bacterial infections.
- Its use is not indicated here as the patient's presentation aligns with allergic rhinitis, not a bacterial infection.
Question 119: An 18-year-old female is brought to the emergency department by her boyfriend. She is screaming uncontrollably. Eventually, she states that she is afraid that "death is near" but cannot give a rational reason for this thought. She reports both seeing colors "coming out of other people's mouths" and "hearing" these colors. The patient's boyfriend experienced similar sensory symptoms a few hours ago; he explains they were trying to have a "spiritual experience." Physical exam is significant for mydriasis, hypertension, hyperthermia, piloerection, tachycardia, and sweating. Upon which of the following receptors does the most likely drug she ingested act?
A. 5-hydroxytryptamine (Correct Answer)
B. Cannabinoid
C. NMDA
D. Mu opioid
E. GABA
Explanation: ***5-hydroxytryptamine***
- The patient's symptoms, including **hallucinations** (seeing and hearing colors), **delusions** ("death is near"), and **autonomic hyperactivity** (mydriasis, hypertension, tachycardia, hyperthermia, sweating), are classic for **serotonergic hallucinogen** intoxication.
- Classic serotonergic hallucinogens like **LSD** (lysergic acid diethylamide) and psilocybin act primarily as partial agonists at the **5-HT2A serotonin receptors** in the brain.
*Cannabinoid*
- While cannabinoids (e.g., from cannabis) can cause altered perception and tachycardia, they typically do not produce the same level of **pronounced hallucinations**, **delusions**, or the full spectrum of **autonomic hyperactivity** seen here.
- Cannabinoids primarily act on **cannabinoid receptors (CB1 and CB2)**, not 5-HT receptors.
*NMDA*
- **NMDA receptor antagonists** (e.g., phencyclidine [PCP], ketamine) can cause hallucinations and agitation, but their classic presentation often includes **nystagmus**, **dissociative anesthetic effects**, and severe **aggression**, which are not centrally highlighted in this case.
- These drugs block the N-methyl-D-aspartate (NMDA) receptor, a glutamate receptor.
*Mu opioid*
- **Mu opioid receptor agonists** (e.g., heroin, morphine) cause central nervous system depression, miosis (pinpoint pupils), respiratory depression, and euphoria.
- The patient's presentation with **mydriasis**, **agitation**, and **autonomic overactivity** is the opposite of opioid intoxication.
*GABA*
- **GABA-A receptor agonists** (e.g., benzodiazepines, barbiturates) are central nervous system depressants that cause sedation, anxiolysis, and muscle relaxation.
- The patient's symptoms of extreme **agitation**, **hallucinations**, and **autonomic arousal** are inconsistent with GABAergic drug effects.
Question 120: A 29-year-old man is outside his home doing yard work when a bee stings him in the right arm. Within 10 minutes, he reports breathlessness and multiple, circular, pruritic rashes over his right arm. He drives to his family physician’s office for evaluation. His past medical history is significant for hypertension and he takes lisinopril. Known allergies include latex, Hymenoptera, and aspirin. His blood pressure is 118/68 mm Hg; heart rate is 104/min and regular; respiratory rate is 22/min; temperature is 37.7°C (99.8°F). There is non-pitting edema but erythema with raised wheels are present in the region of the right arm. Auscultation of the lungs reveals mild wheezing at the lung bases. Which of the following is the best course of action in the management of this patient?
A. Go to the emergency department
B. Methylprednisolone and go to the emergency department
C. Diphenhydramine and go to the emergency department
D. Epinephrine and go to the emergency department (Correct Answer)
E. Albuterol and go to the emergency department
Explanation: ***Epinephrine and go to the emergency department***
- This patient is experiencing **anaphylaxis**, indicated by breathlessness, generalized urticaria, and a known bee sting allergy, which requires immediate treatment with **epinephrine**.
- **Epinephrine** is the first-line and most critical treatment for anaphylaxis as it reverses bronchoconstriction, stabilizes mast cells, and increases blood pressure. After administering epinephrine, prompt transfer to the **emergency department** is essential for monitoring and further management.
*Go to the emergency department*
- While going to the emergency department is necessary, it is not sufficient as the **initial and most critical treatment (epinephrine)** is missing.
- Delaying the administration of epinephrine for anaphylaxis can lead to rapid deterioration and life-threatening complications.
*Methylprednisolone and go to the emergency department*
- **Methylprednisolone (corticosteroids)** can help prevent biphasic anaphylaxis and reduce inflammation but are **not a first-line treatment for acute anaphylaxis** and do not provide immediate relief from bronchospasm or hypotension.
- The immediate priority is addressing the acute symptoms with epinephrine, followed by transport to the emergency department, where corticosteroids may be administered.
*Diphenhydramine and go to the emergency department*
- **Diphenhydramine (an antihistamine)** can help alleviate mild cutaneous symptoms like pruritus and urticaria, but it **does not treat the life-threatening respiratory or cardiovascular symptoms** of anaphylaxis.
- It should not be used as the sole or primary treatment for anaphylaxis, especially in the presence of breathlessness.
*Albuterol and go to the emergency department*
- **Albuterol (a bronchodilator)** can help relieve bronchospasm and breathlessness, but it **does not address other critical aspects of anaphylaxis** such as vasodilation or mast cell stabilization.
- While useful as an adjunct, it is not a substitute for epinephrine in the management of systemic anaphylaxis.
