A 54-year-old woman comes to the emergency department because of sharp chest pain and shortness of breath for 1 day. Her temperature is 37.8°C (100°F), pulse is 110/min, respirations are 30/min, and blood pressure is 86/70 mm Hg. CT angiography of the chest shows a large embolus at the right pulmonary artery. Pharmacotherapy with a tissue plasminogen activator is administered. Six hours later, she develops right-sided weakness and slurred speech. Laboratory studies show elevated prothrombin and partial thromboplastin times and normal bleeding time. A CT scan of the head shows a large, left-sided intracranial hemorrhage. Administration of which of the following is most appropriate to reverse this patient's acquired coagulopathy?
Q562
A 6-year-old boy is presented to a pediatric clinic by his mother with complaints of fever, malaise, and cough for the past 2 days. He frequently complains of a sore throat and has difficulty eating solid foods. The mother mentions that, initially, the boy’s fever was low-grade and intermittent but later became high grade and continuous. The boy was born at 39 weeks gestation via spontaneous vaginal delivery. He is up to date on all vaccines and is meeting all developmental milestones. The past medical history is noncontributory. The boy takes a multivitamin every day. The mother reports that he does well in school and is helpful around the house. The boy’s vital signs include blood pressure 110/65 mm Hg, heart rate 110/min, respiratory rate 32/min, and temperature 38.3°C (101.0°F). On physical examination, the boy appears uncomfortable and has difficulty breathing. His heart is mildly tachycardic with a regular rhythm and his lungs are clear to auscultation bilaterally. Oropharyngeal examination shows that his palatine tonsils are covered with pus and that there is erythema of the surrounding mucosa. Which of the following mediators is responsible for this patient’s elevated temperature?
Q563
A 55-year-old man presents after an episode of severe left ankle pain. The pain has resolved, but he decided to come in for evaluation as he has had pain like this before. He says he has experienced similar episodes of intense pain in the same ankle and his left knee in the past, which he associates with eating copious amounts of fatty food during parties. On one occasion the pain was so excruciating, he went to the emergency room, where an arthrocentesis was performed, revealing needle-shaped negatively birefringent crystals and a high neutrophil count in the synovial fluid. His past medical history is relevant for essential hypertension which is managed with hydrochlorothiazide 20 mg/day. His vital signs are stable, and his body temperature is 36.5°C (97.7°F). Physical examination shows a minimally tender left ankle with full range of motion. Which of the following is the most appropriate long-term treatment in this patient?
Q564
A 42-year-old woman comes to her primary care physician because of an irritating sensation in her nose. She noticed recently that there seems to be a lump in her nose. Her past medical history is significant for pain that seems to migrate around her body and is refractory to treatment. She has intermittently been taking a medication for the pain and recently increased the dose of the drug. Which of the following processes was most likely responsible for development of this patient's complaint?
Q565
A 35-year-old man who works in a shipyard presents with a sharp pain in his left big toe for the past 5 hours. He says he has had this kind of pain before a few days ago after an evening of heavy drinking with his friends. He says he took acetaminophen and ibuprofen for the pain as before but, unlike the last time, it hasn't helped. The patient denies any recent history of trauma or fever. No significant past medical history and no other current medications. Family history is significant for his mother who has type 2 diabetes mellitus and his father who has hypertension. The patient reports regular drinking and the occasional binge on the weekends but denies any smoking history or recreational drug use. The vital signs include pulse 86/min, respiratory rate 14/min, and blood pressure 130/80 mm Hg. On physical examination, the patient is slightly overweight and in obvious distress. The 1st metatarsophalangeal joint of the left foot is erythematous, severely tender to touch, and swollen. No obvious deformity is seen. The remainder of the examination is unremarkable. Joint arthrocentesis of the 1st left metatarsophalangeal joint reveals sodium urate crystals. Which of the following drugs would be the next best therapeutic step in this patient?
Q566
A 60-year-old homeless man presents to the emergency department with an altered mental status. He is not answering questions. His past medical history is unknown. A venous blood gas is drawn demonstrating the following.
Venous blood gas
pH: 7.2
PaO2: 80 mmHg
PaCO2: 80 mmHg
HCO3-: 24 mEq/L
Which of the following is the most likely etiology of this patient's presentation?
Q567
A 38-year-old male is admitted to the hospital after a motor vehicle accident in which he sustained a right diaphyseal femur fracture. His medical history is significant for untreated hypertension. He reports smoking 1 pack of cigarettes per day and drinking 1 liter of bourbon daily. On hospital day 1, he undergoes open reduction internal fixation of his fracture with a femoral intramedullary nail. At what time after the patient's last drink is he at greatest risk for suffering from life-threatening effects of alcohol withdrawal?
Q568
A 23-year-old woman is brought to the emergency department by her friend because of strange behavior. Two hours ago, she was at a night club where she got involved in a fight with the bartender. Her friend says that she was smoking a cigarette before she became irritable and combative. She repeatedly asked “Why are you pouring blood in my drink?” before hitting the bartender. She has no history of psychiatric illness. Her temperature is 38°C (100.4°F), pulse is 100/min, respirations are 19/min, and blood pressure is 158/95 mm Hg. Examination shows muscle rigidity. She has a reduced degree of facial expression. She has no recollection of her confrontation with the bartender. Which of the following is the most likely primary mechanism responsible for this patient's symptoms?
Q569
A 16-year-old girl is brought to the physician because of generalized fatigue and an inability to concentrate in school for the past 4 months. During this period, she has had excessive daytime sleepiness. While going to sleep, she sees cartoon characters playing in her room. She wakes up once or twice every night. While awakening, she feels stiff and cannot move for a couple of minutes. She goes to sleep by 9 pm every night and wakes up at 7 am. She takes two to three 15-minute naps during the day and wakes up feeling refreshed. During the past week while listening to a friend tell a joke, she had an episode in which her head tilted and jaw dropped for a few seconds; it resolved spontaneously. Her father has schizoaffective disorder and her parents are divorced. Vital signs are within normal limits. Physical examination is unremarkable. Which of the following is the most appropriate initial pharmacotherapy?
Q570
A 24-year-old man is brought to the emergency department because of violent jerky movements of his arms and legs that began 30 minutes ago. His father reports that the patient has a history of epilepsy. He is not responsive. Physical examination shows alternating tonic jerks and clonic episodes. There is blood in the mouth. Administration of intravenous lorazepam is begun. In addition, treatment with a second drug is started that alters the flow of sodium ions across neuronal membranes. The second agent administered was most likely which of the following drugs?
Autonomic/CV Drugs US Medical PG Practice Questions and MCQs
Question 561: A 54-year-old woman comes to the emergency department because of sharp chest pain and shortness of breath for 1 day. Her temperature is 37.8°C (100°F), pulse is 110/min, respirations are 30/min, and blood pressure is 86/70 mm Hg. CT angiography of the chest shows a large embolus at the right pulmonary artery. Pharmacotherapy with a tissue plasminogen activator is administered. Six hours later, she develops right-sided weakness and slurred speech. Laboratory studies show elevated prothrombin and partial thromboplastin times and normal bleeding time. A CT scan of the head shows a large, left-sided intracranial hemorrhage. Administration of which of the following is most appropriate to reverse this patient's acquired coagulopathy?
A. Vitamin K
B. Desmopressin
C. Aminocaproic acid (Correct Answer)
D. Protamine sulfate
E. Plasmin
Explanation: ***Aminocaproic acid***
- Aminocaproic acid is an **antifibrinolytic** agent that inhibits the activation of plasminogen to plasmin and directly inhibits plasmin, thereby stopping fibrinolysis.
- It is the most appropriate drug to reverse the effects of **tissue plasminogen activator (tPA)**, which caused the intracranial hemorrhage, by blocking the breakdown of clots.
*Vitamin K*
- Vitamin K is essential for the synthesis of **coagulation factors II, VII, IX, and X** and proteins C and S.
- It would be used to reverse the effects of **warfarin**, a vitamin K antagonist, which is not the cause of coagulopathy here.
*Desmopressin*
- Desmopressin (DDAVP) promotes the release of **von Willebrand factor** and factor VIII from endothelial cells, improving platelet aggregation and adhesion.
- It is primarily used to treat **von Willebrand disease** and mild hemophilia A or to reverse the antiplatelet effects of certain drugs like aspirin.
*Protamine sulfate*
- Protamine sulfate is used to reverse the anticoagulant effects of **heparin** by forming a stable ion pair.
- The patient's coagulopathy is due to tPA, not heparin, so protamine sulfate would not be effective.
*Plasmin*
- Plasmin is an enzyme that **breaks down fibrin clots**, leading to fibrinolysis.
- Administering plasmin would exacerbate the patient's bleeding tendency and intracranial hemorrhage, as the issue is excessive fibrinolysis caused by tPA.
Question 562: A 6-year-old boy is presented to a pediatric clinic by his mother with complaints of fever, malaise, and cough for the past 2 days. He frequently complains of a sore throat and has difficulty eating solid foods. The mother mentions that, initially, the boy’s fever was low-grade and intermittent but later became high grade and continuous. The boy was born at 39 weeks gestation via spontaneous vaginal delivery. He is up to date on all vaccines and is meeting all developmental milestones. The past medical history is noncontributory. The boy takes a multivitamin every day. The mother reports that he does well in school and is helpful around the house. The boy’s vital signs include blood pressure 110/65 mm Hg, heart rate 110/min, respiratory rate 32/min, and temperature 38.3°C (101.0°F). On physical examination, the boy appears uncomfortable and has difficulty breathing. His heart is mildly tachycardic with a regular rhythm and his lungs are clear to auscultation bilaterally. Oropharyngeal examination shows that his palatine tonsils are covered with pus and that there is erythema of the surrounding mucosa. Which of the following mediators is responsible for this patient’s elevated temperature?
A. Leukotriene D4
B. Prostaglandin F2
C. Prostaglandin E2 (Correct Answer)
D. Thromboxane A2
E. Prostaglandin I2
Explanation: ***Prostaglandin E2***
- **Prostaglandin E2 (PGE2)** is a key mediator of fever, acting directly on the **hypothalamus** to reset the body's thermoregulatory set point.
- In response to infection and inflammation, immune cells release **pyrogens** (like IL-1, TNF-alpha), which stimulate PGE2 synthesis in the brain, leading to increased body temperature.
*Leukotriene D4*
- **Leukotriene D4 (LTD4)** is a potent mediator of **bronchoconstriction** and increased **vascular permeability**, particularly in allergic reactions and asthma.
- While it plays a role in inflammation, it does not directly cause fever by altering the hypothalamic set point.
*Prostaglandin F2*
- **Prostaglandin F2 (PGF2)** has various physiological roles, including **uterine contraction** and **bronchoconstriction**, and is important for reproductive functions.
- It is not primarily involved in mediating the febrile response to infection.
*Thromboxane A2*
- **Thromboxane A2 (TXA2)** is predominantly involved in **platelet aggregation** and **vasoconstriction**, playing a crucial role in hemostasis and thrombosis.
- While it is a product of the arachidonic acid pathway, it does not directly contribute to fever.
*Prostaglandin I2*
- **Prostaglandin I2 (PGI2)**, also known as **prostacyclin**, is a potent **vasodilator** and inhibitor of **platelet aggregation**, protecting the vascular endothelium.
- It typically counteracts the effects of TXA2 and is not a mediator of fever.
Question 563: A 55-year-old man presents after an episode of severe left ankle pain. The pain has resolved, but he decided to come in for evaluation as he has had pain like this before. He says he has experienced similar episodes of intense pain in the same ankle and his left knee in the past, which he associates with eating copious amounts of fatty food during parties. On one occasion the pain was so excruciating, he went to the emergency room, where an arthrocentesis was performed, revealing needle-shaped negatively birefringent crystals and a high neutrophil count in the synovial fluid. His past medical history is relevant for essential hypertension which is managed with hydrochlorothiazide 20 mg/day. His vital signs are stable, and his body temperature is 36.5°C (97.7°F). Physical examination shows a minimally tender left ankle with full range of motion. Which of the following is the most appropriate long-term treatment in this patient?
A. Colchicine
B. Intra-articular steroid injection
C. Nonsteroidal antiinflammatory drugs (NSAIDs)
D. Xanthine oxidase inhibitor (Correct Answer)
E. Uricosuric drug
Explanation: ***Xanthine oxidase inhibitor***
- The patient's presentation with recurrent episodes of severe joint pain, association with fatty foods, and the finding of **negatively birefringent, needle-shaped crystals** in synovial fluid are classic for **gout**. Xanthine oxidase inhibitors like **allopurinol** or **febuxostat** are the most appropriate **long-term treatment** to reduce uric acid production and prevent future attacks.
- His use of **hydrochlorothiazide**, a thiazide diuretic, further increases the risk of gout by increasing renal uric acid reabsorption, reinforcing the need for urate-lowering therapy.
*Colchicine*
- **Colchicine** is primarily used for the **acute treatment** or **prophylaxis of gout flares** during the initiation of urate-lowering therapy. It does not lower serum uric acid levels.
- While effective in managing acute symptoms, it is not a long-term solution for preventing gout attacks in a patient with recurrent flares and confirmed crystal deposition.
*Intra-articular steroid injection*
- **Intra-articular steroid injections** can effectively treat **acute gout flares**, especially when systemic NSAIDs or colchicine are contraindicated or ineffective.
- However, this is an acute treatment for symptom relief and does not address the underlying **hyperuricemia** or prevent future episodes, making it unsuitable as a long-term strategy for recurrent gout.
*Nonsteroidal antiinflammatory drugs (NSAIDs)*
- **NSAIDs** are effective in treating the **acute inflammation and pain** of a gout flare. The patient's current pain has resolved, so NSAIDs are not indicated at this time.
- Similar to colchicine, NSAIDs treat the symptoms of an acute attack but do not lower uric acid levels or prevent future episodes.
*Uricosuric drug*
- **Uricosuric drugs** (e.g., probenecid) increase the excretion of uric acid via the kidneys. They are indicated for patients who **underexcrete uric acid** and have good renal function.
- These drugs are contraindicated in patients with **renal impairment** or a history of **uric acid kidney stones**. Without knowing the patient's 24-hour uric acid excretion or renal function in detail, and considering his hypertension and potential renal impact of diuretics, a xanthine oxidase inhibitor is generally preferred as first-line long-term therapy.
Question 564: A 42-year-old woman comes to her primary care physician because of an irritating sensation in her nose. She noticed recently that there seems to be a lump in her nose. Her past medical history is significant for pain that seems to migrate around her body and is refractory to treatment. She has intermittently been taking a medication for the pain and recently increased the dose of the drug. Which of the following processes was most likely responsible for development of this patient's complaint?
A. Decreased lipoxygenase pathway activity
B. Increased mucous viscosity
C. Increased lipoxygenase pathway activity (Correct Answer)
D. Decreased prostaglandin activity
E. Increased allergic reaction in mucosa
Explanation: ***Increased lipoxygenase pathway activity***
- This patient likely has **aspirin-exacerbated respiratory disease (AERD)**, characterized by a triad of **asthma, aspirin sensitivity, and chronic rhinosinusitis with nasal polyposis**. The history of "pain that seems to migrate around her body and is refractory to treatment" suggests a chronic pain condition, for which she is taking a medication that exacerbates her nasal symptoms. This medication is likely a **NSAID**.
- **NSAIDs** inhibit **cyclooxygenase (COX) enzymes**, shunting arachidonic acid metabolism towards the **lipoxygenase pathway**. This leads to an overproduction of **leukotrienes**, which are potent bronchoconstrictors and promoters of inflammation and nasal polyp formation.
*Decreased lipoxygenase pathway activity*
- A decrease in lipoxygenase pathway activity would generally lead to **reduced leukotriene production**, which would typically *alleviate* symptoms like nasal irritation and polyp formation, not cause them.
- This scenario would likely improve rather than worsen respiratory and allergic symptoms, making it inconsistent with the patient's presentation.
*Increased mucous viscosity*
- While increased mucous viscosity can contribute to nasal congestion and discomfort, it is a **symptom or consequence** of underlying inflammation, not the primary pathophysiological cause in AERD.
- It does not explain the specific link to aspirin/NSAID use and the formation of **nasal polyps**.
*Decreased prostaglandin activity*
- **Decreased prostaglandin activity** is caused by **NSAID inhibition of COX enzymes**. While this is a crucial step in AERD, it is the *consequence* (shunting to lipoxygenase pathway) rather than the direct cause of the nasal polyps.
- The direct cause of the patient's nasal obstruction and pain from the ASA is the **overproduction of leukotrienes**, not merely the absence of prostaglandins.
*Increased allergic reaction in mucosa*
- While AERD involves mast cell activation and eosinophilic inflammation, it is not primarily an **IgE-mediated allergic reaction** in the classical sense.
- The trigger is **pharmacological (NSAIDs)**, not an environmental allergen, and the underlying mechanism is an imbalance in arachidonic acid metabolism rather than a specific antigen-antibody interaction.
Question 565: A 35-year-old man who works in a shipyard presents with a sharp pain in his left big toe for the past 5 hours. He says he has had this kind of pain before a few days ago after an evening of heavy drinking with his friends. He says he took acetaminophen and ibuprofen for the pain as before but, unlike the last time, it hasn't helped. The patient denies any recent history of trauma or fever. No significant past medical history and no other current medications. Family history is significant for his mother who has type 2 diabetes mellitus and his father who has hypertension. The patient reports regular drinking and the occasional binge on the weekends but denies any smoking history or recreational drug use. The vital signs include pulse 86/min, respiratory rate 14/min, and blood pressure 130/80 mm Hg. On physical examination, the patient is slightly overweight and in obvious distress. The 1st metatarsophalangeal joint of the left foot is erythematous, severely tender to touch, and swollen. No obvious deformity is seen. The remainder of the examination is unremarkable. Joint arthrocentesis of the 1st left metatarsophalangeal joint reveals sodium urate crystals. Which of the following drugs would be the next best therapeutic step in this patient?
A. Probenecid
B. Allopurinol
C. Naproxen (Correct Answer)
D. Aspirin
E. Morphine
Explanation: ***Naproxen***
- This patient is experiencing an acute **gout flare**, characterized by sudden onset of severe pain, erythema, and swelling in the first metatarsophalangeal joint (podagra), confirmed by **sodium urate crystals** in joint fluid.
- **NSAIDs** like naproxen are first-line treatment for acute gout attacks to reduce inflammation and pain, especially since acetaminophen and ibuprofen have been ineffective, and the patient has no contraindications.
*Probenecid*
- **Probenecid** is a **uricosuric agent** used for **long-term management of gout** by increasing uric acid excretion.
- It is **not indicated for acute flares** as it does not provide immediate pain relief and can sometimes worsen an acute attack by mobilizing uric acid.
*Allopurinol*
- **Allopurinol** is a **xanthine oxidase inhibitor** used for **long-term prevention of gout flares** by reducing uric acid production.
- Starting allopurinol during an acute flare can sometimes **exacerbate the attack** by causing rapid shifts in uric acid levels; it should typically be initiated after the acute flare has resolved.
*Aspirin*
- **Aspirin** can have **variable effects on uric acid levels** depending on the dose; low doses tend to reduce uric acid excretion and can precipitate gout, while high doses are uricosuric but are not typically used for gout treatment.
- It is generally **not recommended for acute gout flares** due to its inconsistent effect on uric acid and the availability of more effective anti-inflammatory agents.
*Morphine*
- **Morphine** is a strong opioid analgesic used for severe pain, but it does **not address the underlying inflammation** of an acute gout flare.
- While it could alleviate pain, the primary treatment strategy should target inflammation with NSAIDs, colchicine, or corticosteroids before considering opioids, especially given the side effect profile of opioids.
Question 566: A 60-year-old homeless man presents to the emergency department with an altered mental status. He is not answering questions. His past medical history is unknown. A venous blood gas is drawn demonstrating the following.
Venous blood gas
pH: 7.2
PaO2: 80 mmHg
PaCO2: 80 mmHg
HCO3-: 24 mEq/L
Which of the following is the most likely etiology of this patient's presentation?
A. Heroin overdose (Correct Answer)
B. COPD
C. Ethylene glycol intoxication
D. Aspirin overdose
E. Diabetic ketoacidosis
Explanation: ***Heroin overdose***
- The patient exhibits severe **respiratory depression** (high PaCO2 of 80 mmHg and altered mental status) leading to **respiratory acidosis** (pH 7.2) which is characteristic of opiate overdose.
- The **normal bicarbonate (HCO3-) of 24 mEq/L** suggests an acute, uncompensated respiratory acidosis, consistent with an acute overdose event.
*COPD*
- While patients with COPD can have high PaCO2, they typically develop **chronic respiratory acidosis** and would have a **compensated metabolic alkalosis** with elevated bicarbonate levels.
- The **normal bicarbonate** in this patient points away from a chronic respiratory condition.
*Ethylene glycol intoxication*
- Ethylene glycol intoxication causes a **high anion gap metabolic acidosis**, which would present with a **low bicarbonate level**.
- This patient's bicarbonate is normal, ruling out this etiology.
*Aspirin overdose*
- Aspirin overdose commonly causes a **mixed acid-base disturbance**, initially a **respiratory alkalosis** (due to central nervous system stimulation) and subsequently a **metabolic acidosis**.
- The patient's presentation of prominent respiratory acidosis and a normal bicarbonate level is inconsistent with aspirin overdose.
*Diabetic ketoacidosis*
- Diabetic ketoacidosis is characterized by a **high anion gap metabolic acidosis** with significantly **reduced bicarbonate levels**.
- The patient's normal bicarbonate level effectively rules out diabetic ketoacidosis.
Question 567: A 38-year-old male is admitted to the hospital after a motor vehicle accident in which he sustained a right diaphyseal femur fracture. His medical history is significant for untreated hypertension. He reports smoking 1 pack of cigarettes per day and drinking 1 liter of bourbon daily. On hospital day 1, he undergoes open reduction internal fixation of his fracture with a femoral intramedullary nail. At what time after the patient's last drink is he at greatest risk for suffering from life-threatening effects of alcohol withdrawal?
A. 24-48 hours
B. 1 week
C. Less than 24 hours
D. 48-72 hours (Correct Answer)
E. 5-6 days
Explanation: ***48-72 hours***
- The most severe and life-threatening symptoms of alcohol withdrawal, such as **delirium tremens (DTs)**, typically manifest within **48 to 72 hours** after the last drink.
- This period is characterized by **autonomic hyperactivity**, profound confusion, hallucinations, and seizures.
*24-48 hours*
- This period may see the onset of more severe withdrawal symptoms like **hallucinations** (alcoholic hallucinosis) and **generalized tonic-clonic seizures**.
- While serious, these symptoms are generally less life-threatening than the full-blown delirium tremens that follows.
*1 week*
- By one week, if left untreated, patients would likely already have experienced the peak severity of withdrawal.
- While some mild symptoms might persist or resolve, the highest risk for acute, life-threatening events has usually passed.
*Less than 24 hours*
- Within this early timeframe, symptoms are usually milder, including **tremors, anxiety, nausea, vomiting, and insomnia**.
- These are considered "minor withdrawal symptoms" and are not typically life-threatening.
*5-6 days*
- By 5-6 days, patients who are going to develop **delirium tremens** would generally have already experienced its onset.
- The peak of severe withdrawal symptoms is usually within the 48-72 hour window, and by day 5-6, symptoms might be resolving or the patient would be in a critical state with established DTs.
Question 568: A 23-year-old woman is brought to the emergency department by her friend because of strange behavior. Two hours ago, she was at a night club where she got involved in a fight with the bartender. Her friend says that she was smoking a cigarette before she became irritable and combative. She repeatedly asked “Why are you pouring blood in my drink?” before hitting the bartender. She has no history of psychiatric illness. Her temperature is 38°C (100.4°F), pulse is 100/min, respirations are 19/min, and blood pressure is 158/95 mm Hg. Examination shows muscle rigidity. She has a reduced degree of facial expression. She has no recollection of her confrontation with the bartender. Which of the following is the most likely primary mechanism responsible for this patient's symptoms?
A. Stimulation of cannabinoid receptors
B. Inhibition of NMDA receptors (Correct Answer)
C. Inhibition of norepinephrine, serotonin, and dopamine reuptake
D. Stimulation of 5HT2A and dopamine D2 receptors
E. Inhibition of dopamine D2 receptors
Explanation: ***Inhibition of NMDA receptors***
- The patient's symptoms, including **combativeness**, **erratic behavior**, **delusions** ("Why are you pouring blood in my drink?"), **hypertension**, **tachycardia**, and **muscle rigidity**, are characteristic of **PCP intoxication**.
- **Phencyclidine (PCP)** acts primarily as an **NMDA receptor antagonist**, blocking calcium channels and leading to these neurotoxic effects.
*Stimulation of cannabinoid receptors*
- **Cannabis intoxication** typically involves **euphoria**, distorted perception, impaired memory, and increased appetite, which are not the primary features described here.
- While agitation can occur, the severe combativeness, delusions, and specific vital sign changes point away from cannabinoid receptor stimulation as the primary mechanism for this presentation.
*Inhibition of norepinephrine, serotonin, and dopamine reuptake*
- This mechanism is characteristic of stimulants like **cocaine** or **amphetamines**. While these drugs can cause agitation, paranoia, hypertension, and tachycardia, they typically do not cause the prominent **muscle rigidity** and **delusional thought** content as described.
- The "smoking a cigarette" context might suggest stimulants, but the overall clinical picture is more consistent with PCP.
*Stimulation of 5HT2A and dopamine D2 receptors*
- Stimulation of **5HT2A receptors** is associated with **hallucinogens** like LSD, causing perceptual distortions and altered consciousness, but typically not the intense combativeness, muscle rigidity, and specific delusions seen here.
- While **dopamine D2 receptor stimulation** can contribute to psychosis, it's not the primary mechanism that brings together all the described symptoms in this acute, severe presentation.
*Inhibition of dopamine D2 receptors*
- **Dopamine D2 receptor inhibition** is the mechanism of action for antipsychotic medications and generally leads to a reduction in psychotic symptoms, not the intense agitation, combativeness, and psychotic features observed in this patient.
- Such inhibition can lead to extrapyramidal symptoms, but not the acute, substance-induced presentation described.
Question 569: A 16-year-old girl is brought to the physician because of generalized fatigue and an inability to concentrate in school for the past 4 months. During this period, she has had excessive daytime sleepiness. While going to sleep, she sees cartoon characters playing in her room. She wakes up once or twice every night. While awakening, she feels stiff and cannot move for a couple of minutes. She goes to sleep by 9 pm every night and wakes up at 7 am. She takes two to three 15-minute naps during the day and wakes up feeling refreshed. During the past week while listening to a friend tell a joke, she had an episode in which her head tilted and jaw dropped for a few seconds; it resolved spontaneously. Her father has schizoaffective disorder and her parents are divorced. Vital signs are within normal limits. Physical examination is unremarkable. Which of the following is the most appropriate initial pharmacotherapy?
A. Modafinil (Correct Answer)
B. Venlafaxine
C. Risperidone
D. Oral contraceptive pill
E. Citalopram
Explanation: ***Modafinil***
- This patient's symptoms (excessive daytime sleepiness, hypnagogic hallucinations, sleep paralysis, cataplexy, and refreshing naps) are highly suggestive of **narcolepsy**.
- **Modafinil** is a wake-promoting agent and is a first-line treatment for excessive daytime sleepiness in narcolepsy.
*Venlafaxine*
- **Venlafaxine** is a serotonin-norepinephrine reuptake inhibitor (SNRI) that can be used to treat cataplexy in narcolepsy by suppressing REM sleep.
- While cataplexy is present, the primary and most debilitating symptom is excessive daytime sleepiness, for which modafinil is the initial choice.
*Risperidone*
- **Risperidone** is an antipsychotic medication, primarily used to treat schizophrenia and bipolar disorder.
- Although the patient experiences hypnagogic hallucinations, these are part of narcolepsy symptoms and not indicative of a primary psychotic disorder warranting antipsychotic treatment.
*Oral contraceptive pill*
- An **oral contraceptive pill** is used for contraception or managing hormonal-related conditions such as irregular menstruation, acne, or polycystic ovary syndrome.
- There is no indication in the patient's presentation that would warrant treatment with oral contraceptives.
*Citalopram*
- **Citalopram** is a selective serotonin reuptake inhibitor (SSRI) and is typically used to treat depression or anxiety disorders.
- While sometimes used off-label for cataplexy in narcolepsy due to its REM-suppressing effects, it is not the initial treatment for the primary symptom of excessive daytime sleepiness.
Question 570: A 24-year-old man is brought to the emergency department because of violent jerky movements of his arms and legs that began 30 minutes ago. His father reports that the patient has a history of epilepsy. He is not responsive. Physical examination shows alternating tonic jerks and clonic episodes. There is blood in the mouth. Administration of intravenous lorazepam is begun. In addition, treatment with a second drug is started that alters the flow of sodium ions across neuronal membranes. The second agent administered was most likely which of the following drugs?
A. Lamotrigine
B. Phenobarbital
C. Topiramate
D. Carbamazepine
E. Fosphenytoin (Correct Answer)
Explanation: ***Fosphenytoin***
- This patient is experiencing **status epilepticus** as evidenced by prolonged tonic-clonic seizures. **Lorazepam** is the first-line short-acting benzodiazepine for acute seizure termination, but a second, longer-acting antiepileptic drug is needed for maintenance.
- **Fosphenytoin** is a prodrug of **phenytoin** that can be administered intravenously; **phenytoin** works by blocking **voltage-sensitive sodium channels**, thereby altering the flow of sodium ions and stabilizing neuronal membranes.
*Lamotrigine*
- While **lamotrigine** does block voltage-gated sodium channels, it is primarily used for **partial seizures** and **generalized tonic-clonic seizures** as a maintenance therapy, not typically as an acute treatment for status epilepticus.
- It requires **slow titration** due to the risk of severe skin reactions (e.g., Stevens-Johnson syndrome), making it unsuitable for immediate use in status epilepticus.
*Phenobarbital*
- **Phenobarbital** is an antiepileptic drug that enhances **GABAergic neurotransmission**, leading to neuronal hyperpolarization and reduced excitability. It is a very effective and older anticonvulsant.
- Although it can be used for status epilepticus, it acts primarily on GABA receptors, not directly on **sodium ion channels** as described in the question.
*Topiramate*
- **Topiramate** has multiple mechanisms of action, including blocking voltage-gated sodium channels and enhancing GABA activity, but it is typically used as a **maintenance therapy** for various seizure types.
- It is not a first-line agent for acute management of **status epilepticus** and its primary mechanism mentioned isn't restricted to sodium channel modulation as explicitly as phenytoin.
*Carbamazepine*
- **Carbamazepine** is a sodium channel blocker, similar to phenytoin, and is effective for **partial** and **tonic-clonic seizures**.
- However, it is primarily an **oral medication** and its slow absorption makes it inappropriate for acute intravenous treatment of status epilepticus.