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Case-based MCQ

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🧠 Case-based MCQ 🔸 #MCQ_77 🔤🔤🔤🔤🔤🔤🔤🔤🔤🔤🔤🔤🔤 This patient has likely overdosed on imipramine, a tricyclic antidepressant (TCA).  Because of the inhibitory effects of TCAs on multiple receptor types, overdose can cause a variety of symptoms, including CNS toxicity (eg, unconsciousness, seizures), anticholinergic toxicity (eg, hyperthermia, dilated pupils, intestinal ileus, flushed skin), hypotension, and cardiac toxicity. Cardiac toxicity is caused by TCA inhibition of fast sodium channels in the His-Purkinje system and myocardium.  This decreases conduction velocity, increases the duration of repolarization, and prolongs absolute refractory periods.  QRS prolongation and ventricular arrhythmias (eg, ventricular tachycardia, ventricular fibrillation) may result. A QRS interval >100 msec or ventricular arrhythmia in the setting of TCA overdose is an indication for sodium bicarbonate therapy.  Sodium bicarbonate likely improves cardiac toxicity through the following mechanisms: Increasing serum pH makes the TCA less pharmacologically active, decreasing its avidity for sodium channels. Increasing extracellular sodium concentration raises the electrochemical gradient across cardiac cell membranes, decreasing the impact of the TCA-induced sodium channel blockade. Sodium bicarbonate infusion also improves TCA-induced hypotension, which is caused by alpha-1 adrenergic receptor antagonism in combination with cardiac toxicity, and is the leading cause of mortality in TCA overdose. Sodium bicarbonate is an adjunctive therapy for treating severe hyperkalemia (or rapidly increasing serum potassium) associated with ECG changes (eg, peaked T waves, short QT interval, increased QRS interval).  However, TCA overdose is not associated with severe hyperkalemia. TCA overdose causes hyperthermia via its anticholinergic effect (ie, muscarinic receptor inhibition) on sweat glands, which decreases sweating and heat dissipation.  This anticholinergic effect is typically unaltered by sodium bicarbonate administration. Sodium bicarbonate administration may increase serum sodium levels; however, this medication is administered to treat cardiac toxicity rather than hyponatremia, which is not typically associated with TCA overdose.  In addition, 3% saline, rather than sodium bicarbonate, is the preferred medication for treating severe hyponatremia. Respiratory depression is not directly caused by TCA overdose but can occur indirectly because of CNS depression (ie, antihistamine effects) or complications of seizure activity.  Sodium bicarbonate is unlikely to improve these indirect causes of respiratory depression. Tricyclic antidepressant (TCA) overdose can cause CNS toxicity, anticholinergic findings, hypotension, and cardiac toxicity.  Cardiac toxicity is due to the inhibition of fast sodium channels and may result in QRS prolongation and ventricular arrhythmia.  Sodium bicarbonate can improve both cardiac toxicity and TCA-induced hypotension.

🧠 Case-based MCQ 🔸 #MCQ_77 🔤🔤🔤🔤🔤🔤🔤🔤🔤🔤🔤🔤🔤 A 55-year-old woman is brought to the emergency department after being found unconscious in her apartment.  En route to the hospital, the patient had a seizure and was urgently intubated for airway protection.  Medical history is significant for treatment-resistant major depression, hypertension, and hyperlipidemia.  The patient takes imipramine, atorvastatin, and lisinopril.  Temperature is 38.2 C, blood pressure is 90/50 mm Hg, pulse is 120/min, and respirations are 14/min.  Oxygen saturation is 98% on 40% fraction of inspired oxygen.  Examination shows bilateral dilated pupils that are minimally reactive to light.  The skin appears flushed.  Cardiopulmonary examination reveals clear lungs and normal heart sounds.  The abdomen is slightly distended with decreased bowel sounds.  Muscle tone and reflexes are normal.  Sodium bicarbonate therapy is administered.  Sodium bicarbonate is indicated in this patient primarily to treat which of the following? A. Cardiac toxicity B. Hyperkalemia C. Hyperthermia D. Hyponatremia E. Respiratory depression

🧠 Case-based MCQ 🔸 #MCQ_77 🔤🔤🔤🔤🔤🔤🔤🔤🔤🔤🔤🔤🔤 Correct Answer Is E Caustic ingestion Clinical features Chemical burn or liquefaction necrosis resulting in: Laryngeal damage: hoarseness, stridor Esophageal damage: dysphagia, odynophagia Gastric damage: epigastric pain, bleeding Management Secure airway, breathing, circulation Decontamination: remove contaminated clothing & visible chemicals; irrigate exposed skin Chest x-ray if respiratory symptoms Endoscopy within 24 hr Complications Upper airway compromise Perforation Strictures/stenosis (2-3 weeks) Ulcers Cancer This patient who ingested sodium hydroxide (a strongly caustic alkaline solution) now has pain, dysphagia, and erythema of the oropharynx, which is concerning for caustic esophageal injury.  This injury can be caused by ingestion of: acidic substances, which cause coagulation necrosis (eg, protein denaturation) that results in an eschar, thereby preventing further acid penetration and injury. alkaline substances (eg, many cleaning supplies), which cause liquefactive necrosis (eg, cell membrane dissolution) that often leads to deeper penetration of tissues and therefore more severe injuries. Mucosal injury results from contact with the caustic substance (rather than from systemic absorption); therefore, patients often have immediate oropharyngeal, retrosternal, or epigastric pain as well as dysphagia and hypersalivation (eg, drooling).  Vomiting and hematemesis may also occur.  Patients should initially undergo assessment and stabilization of the airway, breathing, and circulation.  Serial chest and abdominal x-rays should be obtained to identify any signs of perforation, such as pneumomediastinum, pleural effusions, or subdiaphragmatic air (none of which are seen in this patient).  An upper gastrointestinal x-ray study with water-soluble contrast should be performed in patients with suspected perforation. The severity of esophageal injury cannot be predicted by either clinical symptoms or the extent of oral injury seen on physical examination.  Therefore, in the absence of perforation or severe respiratory distress, endoscopic evaluation within the first 24 hours is recommended to assess the severity of esophageal damage. Activated charcoal can decrease the systemic absorption of poisons; however, caustic ingestions cause immediate local damage on contact with the esophagus.  In addition, charcoal would obstruct the view during endoscopy. Inducing vomiting with ipecac is not appropriate because it would reexpose the esophagus to the caustic agent and potentially cause further injury. Corticosteroid therapy has been hypothesized to reduce the risk of late complications (eg, stricture) but has not been shown to be effective.  In addition, it may increase the risk of secondary infections. Because esophageal damage occurs instantaneously, neutralizing agents are not effective.  In addition, acid-base reactions are exothermic and could cause further injury. Caustic alkali ingestion causes immediate esophageal injury with liquefactive necrosis.  In stable patients with no evidence of perforation, endoscopy should be performed within the first 24 hours to assess the severity of the injury and guide further management

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A 40-year-old man is brought to the emergency department due to retrosternal and epigastric pain after ingesting an unknown amount of sodium hydroxide–based drain cleaner 45 minutes ago.  He has a history of major depressive disorder and a prior suicide attempt.  The patient has difficulty swallowing his saliva and is drooling.  Temperature is 36.8 C, blood pressure is 120/70 mm Hg, pulse is 110/min, and respirations are 20/min.  Examination shows oropharyngeal erythema and mild edema.  The lungs are clear to auscultation.  Abdominal examination shows tenderness at the epigastrium without rebound or guarding.  Chest x-ray reveals no abnormalities.  Intravenous normal saline infusion is initiated.  Which of the following is the most appropriate next step in management of this patient? A. Activated charcoal in water B. Gastric decontamination with ipecac C. Intravenous methylprednisolone D. Neutralization of alkali with dilute acetic acid solution E. Upper gastrointestinal endoscopy

🧠 Case-based MCQ 🔸 #MCQ_76 🔤🔤🔤🔤🔤🔤🔤🔤🔤🔤🔤🔤🔤 Correct Answer Is C Subarachnoid hemorrhage (SAH) usually results from rupture of a saccular aneurysm and classically presents with a sudden-onset, severe headache, often called a thunderclap headache.  The location of the headache can be highly variable, but it is commonly accompanied by vomiting and photophobia, and some patients may experience a brief loss of consciousness.  Neck pain (or stiffness) and low-grade fever are also common due to blood-induced meningeal irritation. SAH is associated with high morbidity and mortality, and recognition is complicated by a wide range of clinical presentations.  Although nearly 20% of patients die before reaching the hospital, approximately 40% present in a normal state of alertness without any neurologic deficit.  Noncontrast CT scan of the brain is the initial diagnostic step of choice as it has high sensitivity for detecting blood pooling in the basal cisterns or sulci of the subarachnoid space. If CT scan is unremarkable and there is still reasonable suspicion for SAH, lumbar puncture is performed to evaluate for red blood cells or xanthochromia.  Xanthochromia is a pink or yellow tint of the cerebral spinal fluid (CSF) caused by hemoglobin degradation products (eg, bilirubin) that appear as soon as 2 hours following a subarachnoid bleed and persist in the CSF for weeks. Administration of 100% oxygen is appropriate therapy for a cluster headache, which presents as a unilateral, severe headache that is usually accompanied by signs of parasympathetic hyperactivity (eg, ptosis, miosis, nasal congestion) on the ipsilateral side. Cervical spine x-ray is appropriate to evaluate for fracture following cervical spine trauma, but it is not indicated for spontaneous onset of severe headache. Meningitis can present with fever, neck stiffness, and headache.  However, the dramatic onset and rapidly progressive severity of symptoms in this patient should raise strong suspicion for SAH, and given the high mortality associated with unrecognized SAH, a CT scan—which is less invasive and can generally be performed more rapidly than lumbar puncture—is the best next step.  If the CT scan is negative, lumbar puncture, which would evaluate for both xanthochromia (from SAH) and signs of meningitis, should be considered.  Meningitis patients often have high-grade fever and chills and appear ill. Sumatriptan can be helpful for migraine headaches.  Migraines are often accompanied by nausea and photophobia, but they also typically have a prodrome and are not associated with fever. Subarachnoid hemorrhage typically presents with a sudden-onset, severe headache that may be accompanied by vomiting, neck stiffness, fever, and loss of consciousness.  CT scan of the brain is the best initial diagnostic step.

🧠 Case-based MCQ 🔸 #MCQ_76 🔤🔤🔤🔤🔤🔤🔤🔤🔤🔤🔤🔤🔤 A 42-year-old woman is brought to the emergency department due to severe headache.  Three hours ago, the patient suddenly began experiencing bilateral headache, which rapidly worsened in severity.  She also has had neck pain and an episode of vomiting.  The patient has had no prior headaches, and medical history is significant for hypertension.  Temperature is 38.2 C , blood pressure is 154/92 mm Hg, and pulse is 102/min.  Oxygen saturation is 98% on room air.  On physical examination, the patient appears in obvious discomfort and keeps her eyes closed.  She follows simple instructions, and there is no focal weakness or numbness.  Funduscopy shows no papilledema.  There is increased resistance to passive neck flexion, and it also elicits pain.  Which of the following is the best next step in management of this patient? A. 100% oxygen inhalation B. Cervical spine x-ray C. CT scan of the brain D. Lumbar puncture E. Sumatriptan injection

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Correct Answer Is A As the presentation is within the eight hours, the next best step is obtaining a blood sample for serum paracetamol level + ALT and starting N-acetyl cysteine (NAC) immediately. Since it is unlikely that Joan’s serum paracetamol level & ALT is available within 8 hours and that Joan had symptoms of toxicity (RUQ pain or tenderness, nausea, vomiting) hence she should be commenced on NAC immediately. The decision to continue or cease NAC is then based on the paracetamol concentration. NAC can be safely stopped if the paracetamol level is within the safe range and continued if it is in the toxic range. Management for paracetamol poisoning is summarized as below:   ALT = alanine aminotransferase. * Cooperative adult patients who have potentially ingested ≥ 10 g or ≥ 200 mg/kg (whichever is less). For paracetamol ingestions ≥ 30 g, activated charcoal should be offered until 4 hours after ingestion. † Baseline ALT measurement. ‡ If paracetamol concentration will not be available until ≥ 8 hours after ingestion, commence acetylcysteine while awaiting paracetamol concentration. § For acetylcysteine dosage, see Box 7. ¶ Patients should be advised that if they develop abdominal pain, nausea or vomiting, further assessment is required.

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Joan is 60-year old woman who is suffering migraine. The pain has been crushing and disabling despite medical therapy with maximum dose of paracetamol. Seven hours ago in a desperate attempt she took 20 500mg paracetamol tablets to make the pain go away. She is now in the emergency department of the tertiary hospital you work in with complaints of right upper quadrant abdominal pain, nausea, and vomiting. She weighs 65 kilograms. Which one of the following is the next best step in management? A. Give her intravenous N-acetyl cysteine infusion immediately B. No treatment required C. Do immediate gastric lavage and give her activated charcoal D. Check liver function tests & serum paracetamol level prior to decision making on giving N-acetyl cysteine E. Refer the patient to toxicology registrar

Repost from Medical Mnemonics
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A is correct, Now You say why?