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Question 1
Correct
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A 32-year-old patient with a known history of asthma presents with a worsening of his asthma symptoms. He typically uses a salbutamol inhaler, beclomethasone inhaler, and theophylline. However, his theophylline levels are currently below the therapeutic range. It seems that a newly prescribed medication may be causing a decrease in his theophylline levels.
Which of the following drugs is most likely causing this interaction?Your Answer: Phenytoin
Explanation:Theophylline, a medication commonly used to treat respiratory conditions, can be affected by certain drugs, either increasing or decreasing its plasma concentration and half-life. Drugs that can increase the plasma concentration of theophylline include calcium channel blockers like verapamil, cimetidine, fluconazole, macrolides such as erythromycin, methotrexate, and quinolones like ciprofloxacin. On the other hand, drugs like carbamazepine, phenobarbitol, phenytoin (and fosphenytoin), rifampicin, and St. John’s wort can decrease the plasma concentration of theophylline. It is important to be aware of these interactions when prescribing or taking theophylline to ensure its effectiveness and avoid potential side effects.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 2
Incorrect
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A 22-year-old arrives at the emergency department after ingesting a combination of pills following a heated dispute with their partner. The patient reports consuming approximately 30 tablets of various types, which were obtained from their partner's grandparents. However, the patient is unaware of the specific names of the tablets. You contemplate administering activated charcoal. What accurately describes the mechanism of action of activated charcoal?
Your Answer: Forms ionic bonds with poisons
Correct Answer: Absorbs poisons onto its surface by weak electrostatic forces
Explanation:Activated charcoal prevents the absorption of poisons by absorbing them onto its surface through weak electrostatic forces.
Further Reading:
Poisoning in the emergency department is often caused by accidental or intentional overdose of prescribed drugs. Supportive treatment is the primary approach for managing most poisonings. This includes ensuring a clear airway, proper ventilation, maintaining normal fluid levels, temperature, and blood sugar levels, correcting any abnormal blood chemistry, controlling seizures, and assessing and treating any injuries.
In addition to supportive treatment, clinicians may need to consider strategies for decontamination, elimination, and administration of antidotes. Decontamination involves removing poisons from the skin or gastrointestinal tract. This can be done through rinsing the skin or using methods such as activated charcoal, gastric lavage, induced emesis, or whole bowel irrigation. However, induced emesis is no longer commonly used, while gastric lavage and whole bowel irrigation are rarely used.
Elimination methods include urinary alkalinization, hemodialysis, and hemoperfusion. These techniques help remove toxins from the body.
Activated charcoal is a commonly used method for decontamination. It works by binding toxins in the gastrointestinal tract, preventing their absorption. It is most effective if given within one hour of ingestion. However, it is contraindicated in patients with an insecure airway due to the risk of aspiration. Activated charcoal can be used for many drugs, but it is ineffective for certain poisonings, including pesticides (organophosphates), hydrocarbons, strong acids and alkalis, alcohols (ethanol, methanol, ethylene glycol), iron, lithium, and solvents.
Antidotes are specific treatments for poisoning caused by certain drugs or toxins. For example, cyanide poisoning can be treated with dicobalt edetate, hydroxocobalamin, or sodium nitrite and sodium thiosulphate. Benzodiazepine poisoning can be treated with flumazanil, while opiate poisoning can be treated with naloxone. Other examples include protamine for heparin poisoning, vitamin K or fresh frozen plasma for warfarin poisoning, fomepizole or ethanol for methanol poisoning, and methylene blue for methemoglobinemia caused by benzocaine or nitrates.
There are many other antidotes available for different types of poisoning, and resources such as TOXBASE and the National Poisons Information Service (NPIS) can provide valuable advice on managing poisonings.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 3
Incorrect
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A 21 year old female arrives at the emergency department and admits to ingesting 56 aspirin tablets around 90 minutes ago. She consumed the tablets impulsively following a breakup with her partner but now regrets her decision. She denies experiencing any symptoms. At what point would you initially measure salicylate levels?
Your Answer: 1 hour post ingestion
Correct Answer: 4 hours post ingestion
Explanation:For asymptomatic patients, it is recommended to measure salicylate levels 4 hours after ingestion. However, if the patient is experiencing symptoms, the initial levels should be taken 2 hours after ingestion. In this case, the levels should be monitored every 2-3 hours until a decrease is observed.
Further Reading:
Salicylate poisoning, particularly from aspirin overdose, is a common cause of poisoning in the UK. One important concept to understand is that salicylate overdose leads to a combination of respiratory alkalosis and metabolic acidosis. Initially, the overdose stimulates the respiratory center, leading to hyperventilation and respiratory alkalosis. However, as the effects of salicylate on lactic acid production, breakdown into acidic metabolites, and acute renal injury occur, it can result in high anion gap metabolic acidosis.
The clinical features of salicylate poisoning include hyperventilation, tinnitus, lethargy, sweating, pyrexia (fever), nausea/vomiting, hyperglycemia and hypoglycemia, seizures, and coma.
When investigating salicylate poisoning, it is important to measure salicylate levels in the blood. The sample should be taken at least 2 hours after ingestion for symptomatic patients or 4 hours for asymptomatic patients. The measurement should be repeated every 2-3 hours until the levels start to decrease. Other investigations include arterial blood gas analysis, electrolyte levels (U&Es), complete blood count (FBC), coagulation studies (raised INR/PTR), urinary pH, and blood glucose levels.
To manage salicylate poisoning, an ABC approach should be followed to ensure a patent airway and adequate ventilation. Activated charcoal can be administered if the patient presents within 1 hour of ingestion. Oral or intravenous fluids should be given to optimize intravascular volume. Hypokalemia and hypoglycemia should be corrected. Urinary alkalinization with intravenous sodium bicarbonate can enhance the elimination of aspirin in the urine. In severe cases, hemodialysis may be necessary.
Urinary alkalinization involves targeting a urinary pH of 7.5-8.5 and checking it hourly. It is important to monitor for hypokalemia as alkalinization can cause potassium to shift from plasma into cells. Potassium levels should be checked every 1-2 hours.
In cases where the salicylate concentration is high (above 500 mg/L in adults or 350 mg/L in children), sodium bicarbonate can be administered intravenously. Hemodialysis is the treatment of choice for severe poisoning and may be indicated in cases of high salicylate levels, resistant metabolic acidosis, acute kidney injury, pulmonary edema, seizures and coma.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 4
Incorrect
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A 35-year-old patient with a history of schizophrenia comes in with side effects from a medication that he recently began taking for this condition. Upon examination, you observe that he is experiencing severe muscular rigidity, a decreased level of consciousness, and a body temperature of 40ºC.
Which of the following medications is most likely causing these symptoms?Your Answer: Citalopram
Correct Answer: Chlorpromazine
Explanation:First-generation antipsychotics, also known as conventional or typical antipsychotics, are potent blockers of dopamine D2 receptors. However, these drugs also have varying effects on other receptors such as serotonin type 2 (5-HT2), alpha1, histaminic, and muscarinic receptors.
One of the major drawbacks of first-generation antipsychotics is their high incidence of extrapyramidal side effects. These include rigidity, bradykinesia, dystonias, tremor, akathisia, and tardive dyskinesia. Additionally, there is a rare but life-threatening reaction called neuroleptic malignant syndrome (NMS) that can occur with these medications. NMS is characterized by fever, muscle rigidity, altered mental status, and autonomic dysfunction. It typically occurs shortly after starting or increasing the dose of a neuroleptic medication.
In contrast, second-generation antipsychotics, also known as novel or atypical antipsychotics, have a lower risk of extrapyramidal side effects and NMS compared to their first-generation counterparts. However, they are associated with higher rates of metabolic effects and weight gain.
It is important to differentiate serotonin syndrome from NMS as they share similar features. Serotonin syndrome is most commonly caused by serotonin-specific reuptake inhibitors.
Here are some commonly encountered examples of first- and second-generation antipsychotics:
First-generation:
– Chlopromazine
– Haloperidol
– Fluphenazine
– TrifluoperazineSecond-generation:
– Clozapine
– Olanzapine
– Quetiapine
– Risperidone
– Aripiprazole -
This question is part of the following fields:
- Pharmacology & Poisoning
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Question 5
Correct
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A 45 year old woman is brought into the emergency department after intentionally overdosing on a significant amount of amitriptyline following the end of a relationship. You order an ECG. What ECG changes are commonly seen in cases of amitriptyline overdose?
Your Answer: Prolongation of QRS
Explanation:TCA toxicity can be identified through specific changes seen on an electrocardiogram (ECG). Sinus tachycardia, which is a faster than normal heart rate, and widening of the QRS complex are key features of TCA toxicity. These ECG changes occur due to the blocking of sodium channels and muscarinic receptors (M1) by the medication. In the case of an amitriptyline overdose, additional ECG changes may include prolongation of the QT interval, an R/S ratio greater than 0.7 in lead aVR, and the presence of ventricular arrhythmias such as torsades de pointes. The severity of the QRS prolongation on the ECG is associated with the likelihood of adverse events. A QRS duration greater than 100 ms is predictive of seizures, while a QRS duration greater than 160 ms is predictive of ventricular arrhythmias like ventricular tachycardia or torsades de pointes.
Further Reading:
Tricyclic antidepressant (TCA) overdose is a common occurrence in emergency departments, with drugs like amitriptyline and dosulepin being particularly dangerous. TCAs work by inhibiting the reuptake of norepinephrine and serotonin in the central nervous system. In cases of toxicity, TCAs block various receptors, including alpha-adrenergic, histaminic, muscarinic, and serotonin receptors. This can lead to symptoms such as hypotension, altered mental state, signs of anticholinergic toxicity, and serotonin receptor effects.
TCAs primarily cause cardiac toxicity by blocking sodium and potassium channels. This can result in a slowing of the action potential, prolongation of the QRS complex, and bradycardia. However, the blockade of muscarinic receptors also leads to tachycardia in TCA overdose. QT prolongation and Torsades de Pointes can occur due to potassium channel blockade. TCAs can also have a toxic effect on the myocardium, causing decreased cardiac contractility and hypotension.
Early symptoms of TCA overdose are related to their anticholinergic properties and may include dry mouth, pyrexia, dilated pupils, agitation, sinus tachycardia, blurred vision, flushed skin, tremor, and confusion. Severe poisoning can lead to arrhythmias, seizures, metabolic acidosis, and coma. ECG changes commonly seen in TCA overdose include sinus tachycardia, widening of the QRS complex, prolongation of the QT interval, and an R/S ratio >0.7 in lead aVR.
Management of TCA overdose involves ensuring a patent airway, administering activated charcoal if ingestion occurred within 1 hour and the airway is intact, and considering gastric lavage for life-threatening cases within 1 hour of ingestion. Serial ECGs and blood gas analysis are important for monitoring. Intravenous fluids and correction of hypoxia are the first-line therapies. IV sodium bicarbonate is used to treat haemodynamic instability caused by TCA overdose, and benzodiazepines are the treatment of choice for seizure control. Other treatments that may be considered include glucagon, magnesium sulfate, and intravenous lipid emulsion.
There are certain things to avoid in TCA overdose, such as anti-arrhythmics like quinidine and flecainide, as they can prolonged depolarization. Amiodarone should
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 6
Correct
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A 45-year-old man comes in feeling extremely sick with nausea and vomiting. He is suddenly disoriented and claims that everything appears to be yellow. A blood test shows that his potassium level is 6.8 mmol/l.
Which of the following medications is most likely causing his symptoms?Your Answer: Digoxin
Explanation:Digoxin is a medication used to treat atrial fibrillation and flutter, as well as congestive cardiac failure. It belongs to a class of drugs called cardiac glycosides. Its mechanism of action involves inhibiting the Na/K ATPase in cardiac myocytes, which leads to an increase in intracellular sodium concentration. This, in turn, indirectly increases the availability of intracellular calcium through Na/Ca exchange.
The rise in intracellular calcium levels caused by digoxin results in a positive inotropic effect, meaning it strengthens the force of heart contractions, and a negative chronotropic effect, meaning it slows down the heart rate.
Therapeutic plasma levels of digoxin typically range between 1.0-1.5 nmol/l. However, higher concentrations may be necessary, and the specific value can vary between different laboratories. It is important to note that the risk of toxicity significantly increases when digoxin levels exceed 2 nmol/l.
Signs and symptoms of digoxin toxicity include nausea, vomiting, diarrhea, abdominal pain, confusion, tachyarrhythmias or bradyarrhythmias, xanthopsia (yellow-green vision), and hyperkalemia (an early sign of significant toxicity).
Several factors can potentially contribute to digoxin toxicity. These include being elderly, having renal failure, experiencing myocardial ischemia, having hypokalemia, hypomagnesemia, hypercalcemia, hypernatremia, acidosis, or hypothyroidism.
Additionally, there are several drugs that can increase the risk of digoxin toxicity. These include spironolactone, amiodarone, quinidine, verapamil, diltiazem, and drugs that cause hypokalemia, such as thiazide and loop diuretics.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 7
Incorrect
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A 65-year-old man develops corneal microdeposits as a side effect of prolonged amiodarone usage.
What proportion of individuals taking amiodarone for more than six months will experience corneal microdeposits?Your Answer: Less than 10%
Correct Answer: Greater than 90%
Explanation:Corneal microdeposits are found in almost all individuals (over 90%) who have been taking amiodarone for more than six months, particularly at doses higher than 400 mg/day. These deposits generally do not cause any symptoms, although approximately 10% of patients may experience a perception of a ‘bluish halo’ around objects they see.
Amiodarone can also have other effects on the eye, but these are much less common, occurring in only 1-2% of patients. These effects include optic neuropathy, nonarteritic anterior ischemic optic neuropathy (N-AION), optic disc swelling, and visual field defects.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 8
Correct
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A 68 year old patient with dementia is brought into the emergency department by a caregiver due to a suspected accidental overdose. The caregiver reports finding several of the patient's medication bottles with multiple tablets missing. An ECG is conducted and reveals a prolonged QT interval. The caregiver presents you with the medication containers. Which of the following medications is the most probable culprit for the prolonged QT interval?
Your Answer: Citalopram
Explanation:Antipsychotics and antidepressants are drugs that are known to cause QT prolongation, which is a potentially dangerous heart rhythm abnormality. Similarly, SSRIs and other antidepressants are also associated with QT prolongation. On the other hand, beta-blockers like bisoprolol are used to shorten the QT interval and are considered as a treatment option for long QT syndrome. However, it’s important to note that sotalol, although classified as a beta blocker, acts differently by blocking potassium channels. This unique mechanism of action makes sotalol a class III anti-arrhythmic agent and may result in QT interval prolongation.
Further Reading:
Long QT syndrome (LQTS) is a condition characterized by a prolonged QT interval on an electrocardiogram (ECG), which represents abnormal repolarization of the heart. LQTS can be either acquired or congenital. Congenital LQTS is typically caused by gene abnormalities that affect ion channels responsible for potassium or sodium flow in the heart. There are 15 identified genes associated with congenital LQTS, with three genes accounting for the majority of cases. Acquired LQTS can be caused by various factors such as certain medications, electrolyte imbalances, hypothermia, hypothyroidism, and bradycardia from other causes.
The normal QTc values, which represent the corrected QT interval for heart rate, are typically less than 450 ms for men and less than 460ms for women. Prolonged QTc intervals are considered to be greater than these values. It is important to be aware of drugs that can cause QT prolongation, as this can lead to potentially fatal arrhythmias. Some commonly used drugs that can cause QT prolongation include antimicrobials, antiarrhythmics, antipsychotics, antidepressants, antiemetics, and others.
Management of long QT syndrome involves addressing any underlying causes and using beta blockers. In some cases, an implantable cardiac defibrillator (ICD) may be recommended for patients who have experienced recurrent arrhythmic syncope, documented torsades de pointes, previous ventricular tachyarrhythmias or torsades de pointes, previous cardiac arrest, or persistent syncope. Permanent pacing may be used in patients with bradycardia or atrioventricular nodal block and prolonged QT. Mexiletine is a treatment option for those with LQT3. Cervicothoracic sympathetic denervation may be considered in patients with recurrent syncope despite beta-blockade or in those who are not ideal candidates for an ICD. The specific treatment options for LQTS depend on the type and severity of the condition.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 9
Incorrect
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A 62-year-old woman comes in with a gout flare-up after starting a new antihypertensive medication prescribed by her doctor. Which of the following antihypertensives is the LEAST likely to be the cause?
Your Answer: Atenolol
Correct Answer: Losartan
Explanation:Thiazide diuretics, like bendroflumethiazide and hydrochlorothiazide, have the potential to raise levels of uric acid in the blood, which can worsen gout symptoms in individuals who are susceptible to the condition.
Other medications, such as diuretics, beta-blockers, ACE inhibitors, and non-losartan ARBs, are also linked to an increased risk of gout.
On the other hand, calcium-channel blockers like amlodipine and verapamil, as well as losartan, have been found to lower uric acid levels and are associated with a reduced risk of gout.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 10
Correct
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A child presents with a severe acute asthma attack. After a poor response to the initial salbutamol nebulizer, you administer another nebulizer that also contains ipratropium bromide.
What is the most common side effect experienced with ipratropium bromide?Your Answer: Dry mouth
Explanation:Ipratropium bromide commonly leads to dry mouth as a side effect. Additionally, it may result in constipation, cough, sudden bronchospasm, headache, nausea, and palpitations. In patients with prostatic hyperplasia and bladder outflow obstruction, it can cause urinary retention. Furthermore, susceptible individuals may experience acute closed-angle glaucoma as a result of using this medication.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 11
Incorrect
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You are suturing a young patient with a significant laceration. While performing the procedure, the patient begins to express discomfort. You observe that the patient seems restless and their muscles are experiencing spasms. You suspect that the patient is displaying symptoms of local anesthetic toxicity. Apart from following standard ALS protocols, what intravenous medication can be administered in case of a cardiac arrest?
Your Answer: Calcium gluconate
Correct Answer: Intralipid
Explanation:Intralipid is a lipid emulsion that is commonly used as a source of nutrition in parenteral nutrition. However, it has also been found to be effective in treating local anesthetic toxicity. When administered intravenously, Intralipid acts as a lipid sink, meaning it can bind to the local anesthetic agent and remove it from the affected tissues, thereby reversing the toxic effects.
In cases of cardiac arrest related to local anesthetic toxicity, Intralipid can be administered as a bolus followed by an infusion. The recommended dose is typically 1.5 mL/kg bolus over 1 minute, followed by an infusion of 0.25 mL/kg/minute for 10 minutes. This can be repeated if necessary.
It is important to note that while Intralipid has shown promising results in treating local anesthetic toxicity, it should not replace standard ALS protocols. Basic life support (BLS) measures, such as cardiopulmonary resuscitation (CPR), should still be initiated immediately, and advanced cardiac life support (ACLS) protocols should be followed.
Further Reading:
Local anaesthetics, such as lidocaine, bupivacaine, and prilocaine, are commonly used in the emergency department for topical or local infiltration to establish a field block. Lidocaine is often the first choice for field block prior to central line insertion. These anaesthetics work by blocking sodium channels, preventing the propagation of action potentials.
However, local anaesthetics can enter the systemic circulation and cause toxic side effects if administered in high doses. Clinicians must be aware of the signs and symptoms of local anaesthetic systemic toxicity (LAST) and know how to respond. Early signs of LAST include numbness around the mouth or tongue, metallic taste, dizziness, visual and auditory disturbances, disorientation, and drowsiness. If not addressed, LAST can progress to more severe symptoms such as seizures, coma, respiratory depression, and cardiovascular dysfunction.
The management of LAST is largely supportive. Immediate steps include stopping the administration of local anaesthetic, calling for help, providing 100% oxygen and securing the airway, establishing IV access, and controlling seizures with benzodiazepines or other medications. Cardiovascular status should be continuously assessed, and conventional therapies may be used to treat hypotension or arrhythmias. Intravenous lipid emulsion (intralipid) may also be considered as a treatment option.
If the patient goes into cardiac arrest, CPR should be initiated following ALS arrest algorithms, but lidocaine should not be used as an anti-arrhythmic therapy. Prolonged resuscitation may be necessary, and intravenous lipid emulsion should be administered. After the acute episode, the patient should be transferred to a clinical area with appropriate equipment and staff for further monitoring and care.
It is important to report cases of local anaesthetic toxicity to the appropriate authorities, such as the National Patient Safety Agency in the UK or the Irish Medicines Board in the Republic of Ireland. Additionally, regular clinical review should be conducted to exclude pancreatitis, as intravenous lipid emulsion can interfere with amylase or lipase assays.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 12
Correct
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A 3-year-old toddler is brought to the Emergency Department after ingesting a few of his mother's ibuprofen tablets 30 minutes ago. The child is currently showing no symptoms and is stable. The attending physician recommends giving a dose of activated charcoal. The child weighs 15 kg.
What is the appropriate dosage of activated charcoal to administer in this case?Your Answer: 20 g orally
Explanation:Activated charcoal is a commonly utilized substance for decontamination in cases of poisoning. Its main function is to attract and bind molecules of the ingested toxin onto its surface.
Activated charcoal is a chemically inert form of carbon. It is a fine black powder that has no odor or taste. This powder is created by subjecting carbonaceous matter to high heat, a process known as pyrolysis, and then concentrating it with a solution of zinc chloride. Through this process, the activated charcoal develops a complex network of pores, providing it with a large surface area of approximately 3,000 m2/g. This extensive surface area allows it to effectively hinder the absorption of the harmful toxin by up to 50%.
The typical dosage for adults is 50 grams, while children are usually given 1 gram per kilogram of body weight. Activated charcoal can be administered orally or through a nasogastric tube. It is crucial to administer it within one hour of ingestion, and if necessary, a second dose may be repeated after one hour.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 13
Incorrect
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A 35-year-old woman comes in with a worsening of her asthma symptoms. She has been experiencing heart palpitations and decided to self-medicate with one of her sister's heart medications. Shortly after taking the medication, her asthma symptoms worsened.
Which of the following medications is most likely to have caused her asthma exacerbation?Your Answer: Bisoprolol
Correct Answer: Propranolol
Explanation:Non-selective beta-blockers, like propranolol, can cause severe bronchospasm in individuals with asthma, particularly when taken in high doses. The current guidelines from the British Thoracic Society (BTS) recommend avoiding the use of beta-blockers in asthma patients. However, there is some evidence suggesting that the long-term use of cardioselective beta-blockers does not appear to trigger asthma attacks in individuals with mild or moderate asthma.
Beta-blockers play a crucial role in the treatment of patients who have a history of previous myocardial infarction or systolic dysfunction. In individuals with asthma and one of these diagnoses, it is unlikely that the potential benefits of beta-blockers outweigh the risks of worsening asthma symptoms.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 14
Incorrect
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A 15 year old girl is brought to the emergency department by her parents and reveals that she ingested 36 paracetamol tablets 6 hours ago. What is the most accurate explanation for how an overdose of paracetamol leads to liver damage?
Your Answer: Paracetamol free radical metabolites damage hepatocytes via oxidation
Correct Answer: N-acetyl-p-benzoquinone imine binds to and denatures hepatocytes
Explanation:Liver damage occurs as a result of an overdose of paracetamol due to the formation of a toxic metabolite called N-acetyl-p-benzoquinone imine (NAPQI). When the normal pathways for metabolizing paracetamol are overwhelmed, NAPQI is produced. This toxic metabolite depletes the protective glutathione in the liver, which is usually responsible for neutralizing harmful substances. As a result, there is an insufficient amount of glutathione available to conjugate the excess NAPQI. Consequently, NAPQI binds to hepatocytes, causing their denaturation and ultimately leading to cell death.
Further Reading:
Paracetamol poisoning occurs when the liver is unable to metabolize paracetamol properly, leading to the production of a toxic metabolite called N-acetyl-p-benzoquinone imine (NAPQI). Normally, NAPQI is conjugated by glutathione into a non-toxic form. However, during an overdose, the liver’s conjugation systems become overwhelmed, resulting in increased production of NAPQI and depletion of glutathione stores. This leads to the formation of covalent bonds between NAPQI and cell proteins, causing cell death in the liver and kidneys.
Symptoms of paracetamol poisoning may not appear for the first 24 hours or may include abdominal symptoms such as nausea and vomiting. After 24 hours, hepatic necrosis may develop, leading to elevated liver enzymes, right upper quadrant pain, and jaundice. Other complications can include encephalopathy, oliguria, hypoglycemia, renal failure, and lactic acidosis.
The management of paracetamol overdose depends on the timing and amount of ingestion. Activated charcoal may be given if the patient presents within 1 hour of ingesting a significant amount of paracetamol. N-acetylcysteine (NAC) is used to increase hepatic glutathione production and is given to patients who meet specific criteria. Blood tests are taken to assess paracetamol levels, liver function, and other parameters. Referral to a medical or liver unit may be necessary, and psychiatric follow-up should be considered for deliberate overdoses.
In cases of staggered ingestion, all patients should be treated with NAC without delay. Blood tests are also taken, and if certain criteria are met, NAC can be discontinued. Adverse reactions to NAC are common and may include anaphylactoid reactions, rash, hypotension, and nausea. Treatment for adverse reactions involves medications such as chlorpheniramine and salbutamol, and the infusion may be stopped if necessary.
The prognosis for paracetamol poisoning can be poor, especially in cases of severe liver injury. Fulminant liver failure may occur, and liver transplant may be necessary. Poor prognostic indicators include low arterial pH, prolonged prothrombin time, high plasma creatinine, and hepatic encephalopathy.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 15
Incorrect
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You refer a patient with a history of recurrent supraventricular arrhythmias to the cardiology on-call team. While discussing the patient with the cardiology registrar on the phone, she explains that she is currently busy, but suggests that you start verapamil now and that she will review the patient as soon as she can. You review the patient's medication chart to determine if this is an appropriate course of action.
Which of the following drugs should not be co-prescribed with verapamil?Your Answer: Warfarin
Correct Answer: Bisoprolol
Explanation:Verapamil is a type of calcium-channel blocker that is commonly used to treat irregular heart rhythms and chest pain. It is important to note that verapamil should not be taken at the same time as beta-blockers like atenolol and bisoprolol. This is because when these medications are combined, they can have a negative impact on the heart’s ability to contract and the heart rate, leading to a significant drop in blood pressure, slow heart rate, impaired conduction between the upper and lower chambers of the heart, heart failure (due to decreased ability of the heart to pump effectively), and even a pause in the heart’s normal rhythm. For more information, you can refer to the section on verapamil interactions in the British National Formulary (BNF).
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 16
Incorrect
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A 45 year old comes to the emergency department with swelling of the lips and tongue that developed slowly over the past 3 hours. There is no accompanying rash. The patient denies consuming anything unusual and has no known allergies. The patient recently began taking multiple new medications after experiencing a heart attack one month ago. You suspect that the patient is experiencing non-allergic drug induced angioedema. What is the most probable cause of the patient's symptoms?
Your Answer: Aspirin
Correct Answer: Ramipril
Explanation:The most frequent cause of non-allergic drug induced angioedema is ACE inhibitors. Symptoms usually appear several days to weeks after beginning the medication. It is important to note that penicillin and NSAIDs are the primary drug culprits for angioedema, but they trigger it through an IgE mediated allergic mechanism, resulting in both angioedema and urticaria. The onset of symptoms in these cases typically occurs within minutes to hours after exposure.
Further Reading:
Angioedema and urticaria are related conditions that involve swelling in different layers of tissue. Angioedema refers to swelling in the deeper layers of tissue, such as the lips and eyelids, while urticaria, also known as hives, refers to swelling in the epidermal skin layers, resulting in raised red areas of skin with itching. These conditions often coexist and may have a common underlying cause.
Angioedema can be classified into allergic and non-allergic types. Allergic angioedema is the most common type and is usually triggered by an allergic reaction, such as to certain medications like penicillins and NSAIDs. Non-allergic angioedema has multiple subtypes and can be caused by factors such as certain medications, including ACE inhibitors, or underlying conditions like hereditary angioedema (HAE) or acquired angioedema.
HAE is an autosomal dominant disease characterized by a deficiency of C1 esterase inhibitor. It typically presents in childhood and can be inherited or acquired as a result of certain disorders like lymphoma or systemic lupus erythematosus. Acquired angioedema may have similar clinical features to HAE but is caused by acquired deficiencies of C1 esterase inhibitor due to autoimmune or lymphoproliferative disorders.
The management of urticaria and allergic angioedema focuses on ensuring the airway remains open and addressing any identifiable triggers. In mild cases without airway compromise, patients may be advised that symptoms will resolve without treatment. Non-sedating antihistamines can be used for up to 6 weeks to relieve symptoms. Severe cases of urticaria may require systemic corticosteroids in addition to antihistamines. In moderate to severe attacks of allergic angioedema, intramuscular epinephrine may be considered.
The management of HAE involves treating the underlying deficiency of C1 esterase inhibitor. This can be done through the administration of C1 esterase inhibitor, bradykinin receptor antagonists, or fresh frozen plasma transfusion, which contains C1 inhibitor.
In summary, angioedema and urticaria are related conditions involving swelling in different layers of tissue. They can coexist and may have a common underlying cause. Management involves addressing triggers, using antihistamines, and in severe cases, systemic corticosteroids or other specific treatments for HAE.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 17
Incorrect
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A 35-year-old individual goes to the emergency room feeling sick for the past 48 hours after moving into a new apartment. Earlier today, a boiler technician came to conduct the gas safety inspection for the landlord and advised the patient to go to the A&E department due to high carbon monoxide levels and a faulty boiler. You suspect the presence of carbon monoxide poisoning. What is the primary symptom typically associated with carbon monoxide poisoning?
Your Answer: Peripheral paraesthesia
Correct Answer: Headache
Explanation:The primary symptom typically associated with carbon monoxide poisoning is a headache.
Carbon monoxide (CO) is a dangerous gas that is produced by the combustion of hydrocarbon fuels and can be found in certain chemicals. It is colorless and odorless, making it difficult to detect. In England and Wales, there are approximately 60 deaths each year due to accidental CO poisoning.
When inhaled, carbon monoxide binds to haemoglobin in the blood, forming carboxyhaemoglobin (COHb). It has a higher affinity for haemoglobin than oxygen, causing a left-shift in the oxygen dissociation curve and resulting in tissue hypoxia. This means that even though there may be a normal level of oxygen in the blood, it is less readily released to the tissues.
The clinical features of carbon monoxide toxicity can vary depending on the severity of the poisoning. Mild or chronic poisoning may present with symptoms such as headache, nausea, vomiting, vertigo, confusion, and weakness. More severe poisoning can lead to intoxication, personality changes, breathlessness, pink skin and mucosae, hyperpyrexia, arrhythmias, seizures, blurred vision or blindness, deafness, extrapyramidal features, coma, or even death.
To help diagnose domestic carbon monoxide poisoning, there are four key questions that can be asked using the COMA acronym. These questions include asking about co-habitees and co-occupants in the house, whether symptoms improve outside of the house, the maintenance of boilers and cooking appliances, and the presence of a functioning CO alarm.
Typical carboxyhaemoglobin levels can vary depending on whether the individual is a smoker or non-smoker. Non-smokers typically have levels below 3%, while smokers may have levels below 10%. Symptomatic individuals usually have levels between 10-30%, and severe toxicity is indicated by levels above 30%.
When managing carbon monoxide poisoning, the first step is to administer 100% oxygen. Hyperbaric oxygen therapy may be considered for individuals with a COHb concentration of over 20% and additional risk factors such as loss of consciousness, neurological signs, myocardial ischemia or arrhythmia, or pregnancy. Other management strategies may include fluid resuscitation, sodium bicarbonate for metabolic acidosis, and mannitol for cerebral edema.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 18
Incorrect
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A 22-year-old woman is brought in by ambulance. She has a decreased level of consciousness and is challenging to awaken. She has a history of anxiety and depression and was discovered at home next to an empty bottle of diazepam tablets.
Which acid-base disorder would you anticipate being caused by a substantial benzodiazepine overdose?Your Answer: Respiratory alkalosis
Correct Answer: Respiratory acidosis
Explanation:Common causes for different acid-base disorders.
Respiratory alkalosis can be caused by hyperventilation, such as during periods of anxiety. It can also be a result of conditions like pulmonary embolism, CNS disorders (such as stroke or encephalitis), altitude, pregnancy, or the early stages of aspirin overdose.
Respiratory acidosis is often associated with chronic obstructive pulmonary disease (COPD) or life-threatening asthma. It can also occur due to pulmonary edema, sedative drug overdose (such as opiates or benzodiazepines), neuromuscular disease, obesity, or other respiratory conditions.
Metabolic alkalosis can be caused by vomiting, potassium depletion (often due to diuretic usage), Cushing’s syndrome, or Conn’s syndrome.
Metabolic acidosis with a raised anion gap can occur due to lactic acidosis (such as in cases of hypoxemia, shock, sepsis, or infarction) or ketoacidosis (such as in diabetes, starvation, or alcohol excess). It can also be a result of renal failure or poisoning (such as in late stages of aspirin overdose, methanol or ethylene glycol ingestion).
Metabolic acidosis with a normal anion gap can be caused by conditions like renal tubular acidosis, diarrhea, ammonium chloride ingestion, or adrenal insufficiency.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 19
Incorrect
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A 25-year-old man presents having ingested an overdose of an unknown substance. He is drowsy and slurring his speech. His vital signs are as follows: heart rate 116 beats per minute, blood pressure 91/57 mmHg, oxygen saturation 96% on room air. Glasgow Coma Scale score is 11 out of 15. The results of his arterial blood gas (ABG) on room air are as follows:
pH: 7.24
pO2: 9.4 kPa
PCO2: 3.3 kPa
HCO3-: 22 mmol/l
Na+: 143 mmol/l
Cl–: 99 mmol/l
Lactate: 5 IU/l
Which SINGLE statement regarding this patient is true?Your Answer: She is likely to have a type B lactic acidosis
Correct Answer: Her anion gap is elevated
Explanation:Arterial blood gas (ABG) interpretation is essential for evaluating a patient’s respiratory gas exchange and acid-base balance. The normal values on an ABG may slightly vary between analyzers, but generally, they fall within the following ranges:
pH: 7.35 – 7.45
pO2: 10 – 14 kPa
PCO2: 4.5 – 6 kPa
HCO3-: 22 – 26 mmol/l
Base excess: -2 – 2 mmol/lIn this particular case, the patient’s history indicates an overdose. However, there is no immediate need for intubation as her Glasgow Coma Scale (GCS) score is 11/15, and she can speak, albeit with slurred speech, indicating that she can maintain her own airway.
The relevant ABG findings are as follows:
– Mild hypoxia
– Decreased pH (acidaemia)
– Low PCO2
– Normal bicarbonate
– Elevated lactateThe anion gap is a measure of the concentration of unmeasured anions in the plasma. It is calculated by subtracting the primary measured cations from the primary measured anions in the serum. The reference range for anion gap varies depending on the methodology used, but it is typically between 8 to 16 mmol/L.
In this case, the patient’s anion gap can be calculated using the formula:
Anion gap = [Na+] – [Cl-] – [HCO3-]
Using the given values:
Anion gap = [143] – [99] – [22]
Anion gap = 22Therefore, it is evident that she has a raised anion gap metabolic acidosis. It is likely a type A lactic acidosis resulting from tissue hypoxia and hypoperfusion. Some potential causes of type A and type B lactic acidosis include:
Type A lactic acidosis:
– Shock (including septic shock)
– Left ventricular failure
– Severe anemia
– Asphyxia
– Cardiac arrest
– Carbon monoxide poisoning
– Respiratory failure
– Severe asthma and COPD
– Regional hypoperfusionType B lactic acidosis:
– Renal failure
– Liver failure
– Sepsis (non-hypoxic sepsis)
– Thiamine deficiency
– Al -
This question is part of the following fields:
- Pharmacology & Poisoning
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Question 20
Incorrect
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A 32-year-old woman is admitted to the department after ingesting an excessive amount of tricyclic antidepressants (TCAs) four hours ago.
Which of the following ECG findings is most frequently observed in cases of TCA overdose?Your Answer: Prolongation of the QT interval
Correct Answer: Sinus tachycardia
Explanation:The most commonly observed change in the electrocardiogram (ECG) during a tricyclic antidepressant (TCA) overdose is sinus tachycardia. Additionally, other ECG changes that can be seen in TCA overdose include prolongation of the PR interval, broadening of the QRS complex, prolongation of the QT interval, and the occurrence of ventricular arrhythmias in cases of severe toxicity. The cardiotoxic effects of TCAs are caused by the blocking of sodium channels, which leads to broadening of the QRS complex, and the blocking of potassium channels, which results in prolongation of the QT interval. The severity of the QRS broadening is associated with adverse events: a QRS duration greater than 100 ms is predictive of seizures, while a QRS duration greater than 160 ms is predictive of ventricular arrhythmias.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 21
Incorrect
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A 67 year old individual experiences muscle rigidity and fever after being intubated. Your supervisor instructs you to administer dantrolene. What is the mechanism of action of dantrolene?
Your Answer: Binds to troponin head of actin filament
Correct Answer: Inhibits calcium efflux from the sarcoplasmic reticulum
Explanation:Dantrolene works by blocking the release of calcium ions from the sarcoplasmic reticulum in skeletal muscle cells. This reduces the amount of calcium available to bind to troponin on actin filaments, which in turn decreases the muscle’s ability to contract and reduces energy usage.
Further Reading:
Malignant hyperthermia is a rare and life-threatening syndrome that can be triggered by certain medications in individuals who are genetically susceptible. The most common triggers are suxamethonium and inhalational anaesthetic agents. The syndrome is caused by the release of stored calcium ions from skeletal muscle cells, leading to uncontrolled muscle contraction and excessive heat production. This results in symptoms such as high fever, sweating, flushed skin, rapid heartbeat, and muscle rigidity. It can also lead to complications such as acute kidney injury, rhabdomyolysis, and metabolic acidosis. Treatment involves discontinuing the trigger medication, administering dantrolene to inhibit calcium release and promote muscle relaxation, and managing any associated complications such as hyperkalemia and acidosis. Referral to a malignant hyperthermia center for further investigation is also recommended.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 22
Correct
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A 35-year-old woman is given chloramphenicol for an infection while she is pregnant. As a result of this treatment, the newborn develops a deformity.
Which of the following deformities is most likely to occur as a result of using this medication during pregnancy?Your Answer: Grey baby syndrome
Explanation:Grey baby syndrome is a rare but serious side effect that can occur in neonates, especially premature babies, as a result of the build-up of the antibiotic chloramphenicol. This condition is characterized by several symptoms, including ashen grey skin color, poor feeding, vomiting, cyanosis, hypotension, hypothermia, hypotonia, cardiovascular collapse, abdominal distension, and respiratory difficulties.
During pregnancy, there are several drugs that can have adverse effects on the developing fetus. ACE inhibitors, such as ramipril, if given in the second and third trimesters, can lead to hypoperfusion, renal failure, and the oligohydramnios sequence. Aminoglycosides, like gentamicin, can cause ototoxicity and deafness. High doses of aspirin can result in first-trimester abortions, delayed onset labor, premature closure of the fetal ductus arteriosus, and fetal kernicterus. However, low doses of aspirin (e.g., 75 mg) do not pose significant risks.
Benzodiazepines, such as diazepam, when administered late in pregnancy, can cause respiratory depression and a neonatal withdrawal syndrome. Calcium-channel blockers, if given in the first trimester, may lead to phalangeal abnormalities, while their use in the second and third trimesters can result in fetal growth retardation. Carbamazepine can cause hemorrhagic disease of the newborn and neural tube defects.
Chloramphenicol, as mentioned earlier, can cause grey baby syndrome. Corticosteroids, if given in the first trimester, may cause orofacial clefts. Danazol, if administered in the first trimester, can cause masculinization of the female fetuses genitals. Pregnant women should avoid handling crushed or broken tablets of finasteride, as it can be absorbed through the skin and affect male sex organ development.
Haloperidol, if given in the first trimester, may cause limb malformations, while its use in the third trimester increases the risk of extrapyramidal symptoms in the neonate. Heparin can lead to maternal bleeding and thrombocytopenia. Isoniazid can cause maternal liver damage and neuropathy and seizures in the neonate. Isotretinoin carries a high risk of teratogenicity, including multiple congenital malformations, spontaneous abortion, and intellectual disability.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 23
Incorrect
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A 25-year-old woman with a previous history of depression is admitted to the emergency department following an overdose of amitriptyline tablets. The patient displays notable signs of toxicity, prompting the administration of intravenous sodium bicarbonate. What is the objective of this treatment?
Your Answer: Urinary pH 7.0-8.0
Correct Answer: Serum pH 7.45 to 7.55
Explanation:Sodium bicarbonate is used to treat severe TCA toxicity by reducing the risk of seizures and arrhythmia. The goal is to increase the serum pH to a range of 7.45 to 7.55 through alkalinisation.
Further Reading:
Tricyclic antidepressant (TCA) overdose is a common occurrence in emergency departments, with drugs like amitriptyline and dosulepin being particularly dangerous. TCAs work by inhibiting the reuptake of norepinephrine and serotonin in the central nervous system. In cases of toxicity, TCAs block various receptors, including alpha-adrenergic, histaminic, muscarinic, and serotonin receptors. This can lead to symptoms such as hypotension, altered mental state, signs of anticholinergic toxicity, and serotonin receptor effects.
TCAs primarily cause cardiac toxicity by blocking sodium and potassium channels. This can result in a slowing of the action potential, prolongation of the QRS complex, and bradycardia. However, the blockade of muscarinic receptors also leads to tachycardia in TCA overdose. QT prolongation and Torsades de Pointes can occur due to potassium channel blockade. TCAs can also have a toxic effect on the myocardium, causing decreased cardiac contractility and hypotension.
Early symptoms of TCA overdose are related to their anticholinergic properties and may include dry mouth, pyrexia, dilated pupils, agitation, sinus tachycardia, blurred vision, flushed skin, tremor, and confusion. Severe poisoning can lead to arrhythmias, seizures, metabolic acidosis, and coma. ECG changes commonly seen in TCA overdose include sinus tachycardia, widening of the QRS complex, prolongation of the QT interval, and an R/S ratio >0.7 in lead aVR.
Management of TCA overdose involves ensuring a patent airway, administering activated charcoal if ingestion occurred within 1 hour and the airway is intact, and considering gastric lavage for life-threatening cases within 1 hour of ingestion. Serial ECGs and blood gas analysis are important for monitoring. Intravenous fluids and correction of hypoxia are the first-line therapies. IV sodium bicarbonate is used to treat haemodynamic instability caused by TCA overdose, and benzodiazepines are the treatment of choice for seizure control. Other treatments that may be considered include glucagon, magnesium sulfate, and intravenous lipid emulsion.
There are certain things to avoid in TCA overdose, such as anti-arrhythmics like quinidine and flecainide, as they can prolonged depolarization.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 24
Incorrect
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A 72-year-old woman has been referred to the Emergency Department by her primary care physician after a review of her digoxin prescription. Her physician reports that her current digoxin levels are elevated.
At what digoxin level is toxicity typically observed?Your Answer: 0.5 nmol/L
Correct Answer: 2 nmol/L
Explanation:Digoxin is a medication used to manage heart failure and atrial fibrillation. It works by inhibiting the Na+/K+ ATPase in the myocardium, which slows down the ventricular response and has a positive effect on the heart’s contraction. Although less commonly used nowadays, digoxin still plays a role in certain cases.
One advantage of digoxin is its long half-life, allowing for once-daily maintenance doses. However, it is important to monitor the dosage to ensure it is correct and to watch out for factors that may lead to toxicity, such as renal dysfunction and hypokalemia. Once a steady state has been achieved, regular monitoring of plasma digoxin concentrations is not necessary unless there are concerns.
In atrial fibrillation, the effectiveness of digoxin treatment is best assessed by monitoring the ventricular rate. The target range for plasma digoxin concentration is 1.0-1.5 nmol/L, although higher levels of up to 2 nmol/L may be needed in some cases. It is important to note that the plasma concentration alone cannot reliably indicate toxicity, but levels above 2 nmol/L significantly increase the risk. To manage hypokalemia, which can increase the risk of digoxin toxicity, a potassium-sparing diuretic or potassium supplementation may be prescribed.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 25
Correct
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A 52-year-old woman with a history of hypertension has ingested an excessive amount of atenolol tablets.
Which of the following antidotes is appropriate for treating beta-blocker overdose?Your Answer: Insulin
Explanation:There are various specific remedies available for different types of poisons and overdoses. The following list provides an outline of some of these antidotes:
Poison: Benzodiazepines
Antidote: FlumazenilPoison: Beta-blockers
Antidotes: Atropine, Glucagon, InsulinPoison: Carbon monoxide
Antidote: OxygenPoison: Cyanide
Antidotes: Hydroxocobalamin, Sodium nitrite, Sodium thiosulphatePoison: Ethylene glycol
Antidotes: Ethanol, FomepizolePoison: Heparin
Antidote: Protamine sulphatePoison: Iron salts
Antidote: DesferrioxaminePoison: Isoniazid
Antidote: PyridoxinePoison: Methanol
Antidotes: Ethanol, FomepizolePoison: Opioids
Antidote: NaloxonePoison: Organophosphates
Antidotes: Atropine, PralidoximePoison: Paracetamol
Antidotes: Acetylcysteine, MethioninePoison: Sulphonylureas
Antidotes: Glucose, OctreotidePoison: Thallium
Antidote: Prussian bluePoison: Warfarin
Antidote: Vitamin K, Fresh frozen plasma (FFP)By utilizing these specific antidotes, medical professionals can effectively counteract the harmful effects of various poisons and overdoses.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 26
Incorrect
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A 32-year-old woman is given a medication for a medical ailment during the first trimester of her pregnancy. As a result, the newborn experiences nasal hypoplasia, bone stippling, and bilateral optic atrophy.
Which of the listed drugs is the probable culprit for these abnormalities?Your Answer: Chloramphenicol
Correct Answer: Warfarin
Explanation:During the first trimester of pregnancy, the use of warfarin can lead to a condition known as fetal warfarin syndrome. This condition is characterized by nasal hypoplasia, bone stippling, bilateral optic atrophy, and intellectual disability in the baby. However, if warfarin is taken during the second or third trimester, it can cause optic atrophy, cataracts, microcephaly, microphthalmia, intellectual disability, and both fetal and maternal hemorrhage.
There are several other drugs that can have adverse effects during pregnancy. For example, ACE inhibitors like ramipril can cause hypoperfusion, renal failure, and the oligohydramnios sequence if taken during the second and third trimesters. Aminoglycosides such as gentamicin can lead to ototoxicity and deafness in the baby. High doses of aspirin can result in first trimester abortions, delayed onset labor, premature closure of the fetal ductus arteriosus, and fetal kernicterus. However, low doses of aspirin (e.g. 75 mg) do not pose significant risks.
Benzodiazepines like diazepam, when taken late in pregnancy, can cause respiratory depression and a neonatal withdrawal syndrome. Calcium-channel blockers, if taken during the first trimester, can cause phalangeal abnormalities, while their use in the second and third trimesters can lead to fetal growth retardation. Carbamazepine can result in hemorrhagic disease of the newborn and neural tube defects. Chloramphenicol can cause gray baby syndrome. Corticosteroids, if taken during the first trimester, may cause orofacial clefts.
Danazol, if taken during the first trimester, can cause masculinization of the female fetuses genitals. Finasteride should not be handled by pregnant women as crushed or broken tablets can be absorbed through the skin and affect male sex organ development. Haloperidol, if taken during the first trimester, may cause limb malformations, while its use in the third trimester increases the risk of extrapyramidal symptoms in the newborn.
Heparin can lead to maternal bleeding and thrombocytopenia. Isoniazid can cause maternal liver damage and neuropathy and seizures in the baby. Isotretinoin carries a high risk of teratogenicity, including multiple congenital malformations and spontaneous abortion.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 27
Correct
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A 35-year-old woman is given a medication during the advanced stages of pregnancy. As a result, the newborn experiences respiratory depression and develops a neonatal withdrawal syndrome.
Which of the following medications is the most probable cause of these abnormalities?Your Answer: Diazepam
Explanation:During the later stages of pregnancy, the use of diazepam has been linked to respiratory depression in newborns and a withdrawal syndrome. There are several drugs that can have adverse effects during pregnancy, and the list below outlines the most commonly encountered ones.
ACE inhibitors, such as ramipril, can cause hypoperfusion, renal failure, and the oligohydramnios sequence if given in the second and third trimesters. Aminoglycosides, like gentamicin, can lead to ototoxicity and deafness. High doses of aspirin can result in first-trimester abortions, delayed onset labor, premature closure of the fetal ductus arteriosus, and fetal kernicterus. However, low doses (e.g., 75 mg) do not pose significant risks.
Benzodiazepines, including diazepam, can cause respiratory depression and a neonatal withdrawal syndrome when administered late in pregnancy. Calcium-channel blockers can cause phalangeal abnormalities if given in the first trimester and fetal growth retardation if given in the second and third trimesters. Carbamazepine can lead to hemorrhagic disease of the newborn and neural tube defects.
Chloramphenicol is associated with grey baby syndrome. Corticosteroids, if given in the first trimester, may cause orofacial clefts. Danazol, when administered in the first trimester, can cause masculinization of the female fetuses genitals. Pregnant women should avoid handling crushed or broken tablets of finasteride as it can affect male sex organ development.
Haloperidol, if given in the first trimester, may cause limb malformations. In the third trimester, there is an increased risk of extrapyramidal symptoms in the neonate. Heparin can lead to maternal bleeding and thrombocytopenia. Isoniazid can cause maternal liver damage and neuropathy and seizures in the neonate. Isotretinoin carries a high risk of teratogenicity, including multiple congenital malformations, spontaneous abortion, and intellectual disability.
Lithium, if given in the first trimester, poses a risk of fetal cardiac malformations. In the second and third trimesters, it can result in hypotonia, lethargy, feeding problems, hypothyroidism, goiter, and nephrogenic diabetes insipidus in the neonate.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 28
Incorrect
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A 40-year-old man is brought to the Emergency Department by his wife after taking an overdose of one of his prescribed medications. He is agitated, confused, and experiencing visual hallucinations. His heart rate is currently 115 bpm, and his pupils are dilated. Obtaining a history from him is challenging as he is mumbling. Further questioning reveals that he has ingested an anticholinergic drug.
What is the most suitable initial treatment for this patient?Your Answer: Intralipid
Correct Answer: Diazepam
Explanation:Patients who present with an anticholinergic toxidrome can be difficult to manage due to the agitation and disruptive behavior that is typically present. It is important to provide meticulous supportive care to address the behavioral effects of delirium and prevent complications such as dehydration, injury, and pulmonary aspiration. Often, one-to-one nursing is necessary.
The management approach for these patients is as follows:
1. Resuscitate using a standard ABC approach.
2. Administer sedation for behavioral control. Benzodiazepines, such as IV diazepam in 5 mg-10 mg increments, are the first-line therapy. The goal is to achieve a patient who is sleepy but easily roused. It is important to avoid over-sedating the patient as this can increase the risk of aspiration.
3. Prescribe intravenous fluids as patients are typically unable to eat and drink, and may be dehydrated upon presentation.
4. Insert a urinary catheter as urinary retention is often present and needs to be managed.
5. Consider physostigmine as the specific antidote for anticholinergic delirium in carefully selected cases. Physostigmine acts as a reversible acetylcholinesterase inhibitor, temporarily blocking the breakdown of acetylcholine. This enhances its effects at muscarinic and nicotinic receptors, thereby reversing the effects of the anticholinergic agents.Physostigmine is indicated in the following situations:
1. Severe anticholinergic delirium that does not respond to benzodiazepine sedation.
2. Poisoning with a pure anticholinergic agent, such as atropine.The dosage and administration of physostigmine are as follows:
1. Administer in a monitored setting with appropriate staff and resources to manage adverse effects.
2. Perform a 12-lead ECG before administration to rule out bradycardia, AV block, or broadening of the QRS.
3. Administer IV physostigmine 0.5-1 mg as a slow push over 5 minutes. Repeat every 10 minutes up to a maximum of 4 mg.
4. The clinical end-point of therapy is the resolution of delirium.
5. Delirium may reoccur in 1-4 hours as the effects of physostigmine wear off. In such cases, the dose may be cautiously repeated. -
This question is part of the following fields:
- Pharmacology & Poisoning
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Question 29
Incorrect
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A 65-year-old patient comes in after a chronic overdose of digoxin. She complains of nausea, extreme fatigue, and overall feeling unwell.
What is the indication for using DigiFab in this patient?Your Answer: Heart rate of 40 bpm
Correct Answer: Significant gastrointestinal symptoms
Explanation:Digoxin-specific antibody (DigiFab) is an antidote used to counteract digoxin overdose. It is a purified and sterile preparation of digoxin-immune ovine Fab immunoglobulin fragments. These fragments are derived from healthy sheep that have been immunized with a digoxin derivative called digoxin-dicarboxymethoxylamine (DDMA). DDMA is a digoxin analogue that contains the essential cyclopentanoperhydrophenanthrene: lactone ring moiety coupled to keyhole limpet hemocyanin (KLH).
DigiFab has a higher affinity for digoxin compared to the affinity of digoxin for its sodium pump receptor, which is believed to be the receptor responsible for its therapeutic and toxic effects. When administered to a patient who has overdosed on digoxin, DigiFab binds to digoxin molecules, reducing the levels of free digoxin in the body. This shift in equilibrium away from binding to the receptors helps to reduce the cardiotoxic effects of digoxin. The Fab-digoxin complexes are then eliminated from the body through the kidney and reticuloendothelial system.
The indications for using DigiFab in cases of acute and chronic digoxin toxicity are summarized below:
Acute digoxin toxicity:
– Cardiac arrest
– Life-threatening arrhythmia
– Potassium level >5 mmol/l
– Ingestion of >10 mg of digoxin (in adults)
– Ingestion of >4 mg of digoxin (in children)
– Digoxin level >12 ng/mlChronic digoxin toxicity:
– Cardiac arrest
– Life-threatening arrhythmia
– Significant gastrointestinal symptoms
– Symptoms of digoxin toxicity in the presence of renal failure -
This question is part of the following fields:
- Pharmacology & Poisoning
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Question 30
Incorrect
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A 25-year-old man is brought to the Emergency Department by his friend following taking an overdose of one of his prescribed medications. He is agitated, confused and is experiencing visual hallucinations. His heart rate is currently 110 bpm, and his pupils are dilated. It is difficult to obtain a history from him as he is mumbling. You also note that he appears flushed and his skin is warm to the touch.
Which of the following drugs is most likely to be responsible?Your Answer: Atenolol
Correct Answer: Chlorpromazine
Explanation:This patient exhibits clinical features that are consistent with the ingestion of a drug that blocks the action of the neurotransmitter acetylcholine in the central and peripheral nervous system. There are several anticholinergic drugs commonly used in clinical practice. Some examples include antihistamines like promethazine and diphenhydramine, typical and atypical antipsychotics such as haloperidol and quetiapine, anticonvulsants like carbamazepine, antidepressants like tricyclic antidepressants, and antispasmodics like hyoscine butylbromide. Other sources of anticholinergic effects can come from plants like datura species and certain mushrooms.
When someone ingests an anticholinergic drug, they may experience a toxidrome, which is characterized by an agitated delirium and various signs of acetylcholine receptor blockade in both the central and peripheral nervous system. The central inhibition leads to an agitated delirium, which is marked by fluctuating mental status, confusion, restlessness, visual hallucinations, picking at objects in the air, mumbling, slurred speech, disruptive behavior, tremor, myoclonus, and in rare cases, coma and seizures. The peripheral inhibition can cause dilated pupils, sinus tachycardia, dry mouth, hot and flushed skin, increased body temperature, urinary retention, and ileus.
In summary, the ingestion of an anticholinergic drug can result in a toxidrome characterized by an agitated delirium and various signs of central and peripheral acetylcholine receptor blockade. It is important to be aware of the potential effects of these drugs and to recognize the clinical features associated with their ingestion.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 31
Correct
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A 32-year-old male patient arrives at the Emergency Department after ingesting an overdose 45 minutes ago. He is currently showing no symptoms and is stable in terms of blood flow. The attending physician recommends administering a dose of activated charcoal.
Which of the following substances or toxins is activated charcoal effective in decontaminating?Your Answer: Aspirin
Explanation:Activated charcoal is a commonly used substance for decontamination in cases of poisoning. Its main function is to adsorb the molecules of the ingested toxin onto its surface.
Activated charcoal is a chemically inert form of carbon. It is a fine black powder that has no odor or taste. It is produced by subjecting carbonaceous matter to high heat, a process known as pyrolysis, and then treating it with a zinc chloride solution to increase its concentration. This process creates a network of pores within the charcoal, giving it a large absorptive area of approximately 3,000 m2/g. This allows it to effectively inhibit the absorption of toxins by up to 50%.
The usual dose of activated charcoal is 50 grams for adults and 1 gram per kilogram of body weight for children. It can be administered orally or through a nasogastric tube. It is important to administer it within one hour of ingestion, and it may be repeated after one hour if necessary.
However, there are certain situations where activated charcoal should not be used. These include cases where the patient is unconscious or in a coma, as there is a risk of aspiration. It should also be avoided if seizures are imminent, as there is a risk of aspiration. Additionally, if there is reduced gastrointestinal motility, activated charcoal should not be used to prevent the risk of obstruction.
Activated charcoal is effective in treating overdose with certain drugs and toxins, such as aspirin, paracetamol, barbiturates, tricyclic antidepressants, digoxin, amphetamines, morphine, cocaine, and phenothiazines. However, it is ineffective in cases of overdose with iron, lithium, boric acid, cyanide, ethanol, ethylene glycol, methanol, malathion, DDT, carbamate, hydrocarbon, strong acids, or alkalis.
There are potential adverse effects associated with the use of activated charcoal. These include nausea and vomiting, diarrhea, constipation, bezoar formation (a mass of undigested material that can cause blockages), bowel obstruction, pulmonary aspiration (inhalation of charcoal into the lungs), and impaired absorption of oral medications or antidotes.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 32
Incorrect
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A 32-year-old man with a known history of asthma presents with a headache, vomiting, and dizziness. His heart rate is elevated at 116 bpm. He currently takes a salbutamol inhaler and theophylline for his asthma. He had visited the Emergency Department a few days earlier and was prescribed an antibiotic.
Which antibiotic was most likely prescribed to this patient?Your Answer: Co-amoxiclav
Correct Answer: Erythromycin
Explanation:Theophylline is a medication used to treat severe asthma. It is a bronchodilator that comes in modified-release forms, which can maintain therapeutic levels in the blood for 12 hours. Theophylline works by inhibiting phosphodiesterase and blocking the breakdown of cyclic AMP. It also competes with adenosine on A1 and A2 receptors.
Achieving the right dose of theophylline can be challenging because there is a narrow range between therapeutic and toxic levels. The half-life of theophylline can be influenced by various factors, further complicating dosage adjustments. It is recommended to aim for serum levels of 10-20 mg/l six to eight hours after the last dose.
Unlike many other medications, the specific brand of theophylline can significantly impact its effects. Therefore, it is important to prescribe theophylline by both its brand name and generic name.
Several factors can increase the half-life of theophylline, including heart failure, cirrhosis, viral infections, and certain drugs. Conversely, smoking, heavy drinking, and certain medications can decrease the half-life of theophylline.
There are several drugs that can either increase or decrease the plasma concentration of theophylline. Calcium channel blockers, cimetidine, fluconazole, macrolides, methotrexate, and quinolones can increase the concentration. On the other hand, carbamazepine, phenobarbitol, phenytoin, rifampicin, and St. John’s wort can decrease the concentration.
The clinical symptoms of theophylline toxicity are more closely associated with acute overdose rather than chronic overexposure. Common symptoms include headache, dizziness, nausea, vomiting, abdominal pain, rapid heartbeat, dysrhythmias, seizures, mild metabolic acidosis, low potassium, low magnesium, low phosphates, abnormal calcium levels, and high blood sugar.
Seizures are more prevalent in acute overdose cases, while chronic overdose typically presents with minimal gastrointestinal symptoms. Cardiac dysrhythmias are more common in chronic overdose situations compared to acute overdose.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 33
Correct
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A 35 year old male is brought into the emergency department after ingesting 150 paracetamol tablets in a impulsive suicide attempt. The patient is now worried about the potential liver failure and other possible injuries associated with paracetamol overdose. What other organs or systems are at risk of injury in cases of paracetamol overdose?
Your Answer: Renal tubule
Explanation:When someone takes too much paracetamol, it can harm their liver cells and the tubules in their kidneys. This is because paracetamol produces a harmful substance called NAPQI, which is normally combined with glutathione. However, when there is too much NAPQI, it can cause damage and death to liver and kidney cells.
Further Reading:
Paracetamol poisoning occurs when the liver is unable to metabolize paracetamol properly, leading to the production of a toxic metabolite called N-acetyl-p-benzoquinone imine (NAPQI). Normally, NAPQI is conjugated by glutathione into a non-toxic form. However, during an overdose, the liver’s conjugation systems become overwhelmed, resulting in increased production of NAPQI and depletion of glutathione stores. This leads to the formation of covalent bonds between NAPQI and cell proteins, causing cell death in the liver and kidneys.
Symptoms of paracetamol poisoning may not appear for the first 24 hours or may include abdominal symptoms such as nausea and vomiting. After 24 hours, hepatic necrosis may develop, leading to elevated liver enzymes, right upper quadrant pain, and jaundice. Other complications can include encephalopathy, oliguria, hypoglycemia, renal failure, and lactic acidosis.
The management of paracetamol overdose depends on the timing and amount of ingestion. Activated charcoal may be given if the patient presents within 1 hour of ingesting a significant amount of paracetamol. N-acetylcysteine (NAC) is used to increase hepatic glutathione production and is given to patients who meet specific criteria. Blood tests are taken to assess paracetamol levels, liver function, and other parameters. Referral to a medical or liver unit may be necessary, and psychiatric follow-up should be considered for deliberate overdoses.
In cases of staggered ingestion, all patients should be treated with NAC without delay. Blood tests are also taken, and if certain criteria are met, NAC can be discontinued. Adverse reactions to NAC are common and may include anaphylactoid reactions, rash, hypotension, and nausea. Treatment for adverse reactions involves medications such as chlorpheniramine and salbutamol, and the infusion may be stopped if necessary.
The prognosis for paracetamol poisoning can be poor, especially in cases of severe liver injury. Fulminant liver failure may occur, and liver transplant may be necessary. Poor prognostic indicators include low arterial pH, prolonged prothrombin time, high plasma creatinine, and hepatic encephalopathy.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 34
Incorrect
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A 68-year-old man complains of chest pain and difficulty breathing. He was recently prescribed bendroflumethiazide.
What is the most frequently observed side effect of bendroflumethiazide?Your Answer: Hyperkalaemia
Correct Answer: Impaired glucose tolerance
Explanation:Common side effects of bendroflumethiazide include postural hypotension, electrolyte disturbance (such as hypokalaemia, hyponatraemia, and hypercalcaemia), impaired glucose tolerance, gout, impotence, and fatigue. Rare side effects of bendroflumethiazide include thrombocytopenia, agranulocytosis, photosensitive rash, pancreatitis, and renal failure.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 35
Incorrect
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A 32-year-old man is brought in to the department, having taken an overdose of his tricyclic antidepressants 4 hours earlier.
Which of the following is LEAST likely to be seen on the ECG of a patient that has taken a tricyclic antidepressant overdose?Your Answer: Ventricular arrhythmias
Correct Answer: Shortening of the PR interval
Explanation:The cardiotoxic effects of TCAs occur when they block sodium channels, leading to broadening of the QRS complex, and potassium channels, resulting in prolongation of the QT interval. The severity of adverse events is directly related to the degree of QRS broadening. If the QRS complex is greater than 100 ms, it is likely that seizures may occur. If the QRS complex exceeds 160 ms, ventricular arrhythmias may be predicted. In cases of TCA overdose, certain changes can be observed on an ECG. These include sinus tachycardia, which is very common, prolongation of the PR interval, broadening of the QRS complex, prolongation of the QT interval, and in severe cases, ventricular arrhythmias.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 36
Incorrect
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A 60-year-old man has accidentally consumed an excessive amount of amitriptyline tablets and is currently experiencing toxic side effects.
Which of the following mechanisms is NOT involved in mediating these toxic effects?Your Answer: Blockade of noradrenaline reuptake at the preganglionic synapse
Correct Answer: Opening of potassium channels
Explanation:Tricyclic antidepressant (TCA) overdose is a significant problem in cases of drug overdose and is one of the most common causes of fatal drug poisoning. Any overdose of amitriptyline that exceeds 10 mg/kg has the potential to be life-threatening. If the overdose surpasses 30 mg/kg, it will lead to severe toxicity, cardiotoxicity, and coma.
The toxic effects of TCAs are caused by various pharmacological actions. These include anticholinergic effects, direct blocking of alpha-adrenergic receptors, inhibition of noradrenaline reuptake at the preganglionic synapse, blockade of sodium channels, and blockade of potassium channels.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 37
Correct
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You conduct a medication review on a 68-year-old man with a history of angina. He is currently prescribed 10 mg bisoprolol once daily and GTN spray as needed. However, he continues to experience symptoms.
Which ONE medication should be avoided in this patient?Your Answer: Verapamil
Explanation:Beta-blockers, like bisoprolol, and verapamil have a strong negative effect on the force of ventricular contraction. When these medications are taken together, they can significantly reduce ventricular contraction and lead to a slow heart rate, known as bradycardia. Additionally, the risk of developing AV block is increased. In certain situations, this combination can result in severe low blood pressure or even a complete absence of heart rhythm, known as asystole. Therefore, it is important to avoid using these medications together to prevent these potentially dangerous effects.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 38
Correct
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A 60-year-old patient with type II diabetes mellitus has ingested an excessive amount of gliclazide.
What are the possible antidotes that can be administered in cases of sulphonylurea poisoning?Your Answer: Octreotide
Explanation:There are various specific remedies available for different types of poisons and overdoses. The following list provides an outline of some of these antidotes:
Poison: Benzodiazepines
Antidote: FlumazenilPoison: Beta-blockers
Antidotes: Atropine, Glucagon, InsulinPoison: Carbon monoxide
Antidote: OxygenPoison: Cyanide
Antidotes: Hydroxocobalamin, Sodium nitrite, Sodium thiosulphatePoison: Ethylene glycol
Antidotes: Ethanol, FomepizolePoison: Heparin
Antidote: Protamine sulphatePoison: Iron salts
Antidote: DesferrioxaminePoison: Isoniazid
Antidote: PyridoxinePoison: Methanol
Antidotes: Ethanol, FomepizolePoison: Opioids
Antidote: NaloxonePoison: Organophosphates
Antidotes: Atropine, PralidoximePoison: Paracetamol
Antidotes: Acetylcysteine, MethioninePoison: Sulphonylureas
Antidotes: Glucose, OctreotidePoison: Thallium
Antidote: Prussian bluePoison: Warfarin
Antidote: Vitamin K, Fresh frozen plasma (FFP)By utilizing these specific antidotes, medical professionals can effectively counteract the harmful effects of various poisons and overdoses.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 39
Incorrect
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A 45-year-old woman is brought in by ambulance. She has ingested a significant amount of aspirin.
What type of acid-base imbalance would you anticipate to be present during the initial phases of an aspirin overdose?Your Answer: Metabolic alkalosis
Correct Answer: Respiratory alkalosis
Explanation:An overdose of aspirin often leads to a combination of respiratory alkalosis and metabolic acidosis. Initially, the stimulation of the respiratory center causes hyperventilation and results in respiratory alkalosis. However, as the overdose progresses, the direct acidic effects of aspirin cause an increase in the anion gap and metabolic acidosis.
Here is a summary of common causes for different acid-base disorders:
Respiratory alkalosis can be caused by hyperventilation due to factors such as anxiety, pulmonary embolism, CNS disorders (such as stroke or encephalitis), altitude, pregnancy, and the early stages of aspirin overdose.
Respiratory acidosis can occur in individuals with chronic obstructive pulmonary disease (COPD), life-threatening asthma, pulmonary edema, sedative drug overdose (such as opioids or benzodiazepines), neuromuscular diseases, and obesity.
Metabolic alkalosis can be caused by vomiting, potassium depletion (often due to diuretic usage), Cushing’s syndrome, and Conn’s syndrome.
Metabolic acidosis with a raised anion gap can result from conditions such as lactic acidosis (caused by factors like hypoxemia, shock, sepsis, or tissue infarction), ketoacidosis (associated with diabetes, starvation, or excessive alcohol consumption), renal failure, and poisoning (including the late stages of aspirin overdose, methanol or ethylene glycol ingestion).
Metabolic acidosis with a normal anion gap can be seen in renal tubular acidosis, diarrhea, ammonium chloride ingestion, and adrenal insufficiency.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 40
Incorrect
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A 42-year-old man is brought into the emergency department with suspected methanol poisoning. You collect a blood gas sample. What acid-base disturbance is commonly associated with methanol poisoning?
Your Answer: Low anion gap acidosis
Correct Answer: Raised anion gap acidosis
Explanation:Methanol poisoning is linked to an increase in anion gap acidosis.
Further Reading:
Arterial blood gases (ABG) are an important diagnostic tool used to assess a patient’s acid-base status and respiratory function. When obtaining an ABG sample, it is crucial to prioritize safety measures to minimize the risk of infection and harm to the patient. This includes performing hand hygiene before and after the procedure, wearing gloves and protective equipment, disinfecting the puncture site with alcohol, using safety needles when available, and properly disposing of equipment in sharps bins and contaminated waste bins.
To reduce the risk of harm to the patient, it is important to test for collateral circulation using the modified Allen test for radial artery puncture. Additionally, it is essential to inquire about any occlusive vascular conditions or anticoagulation therapy that may affect the procedure. The puncture site should be checked for signs of infection, injury, or previous surgery. After the test, pressure should be applied to the puncture site or the patient should be advised to apply pressure for at least 5 minutes to prevent bleeding.
Interpreting ABG results requires a systematic approach. The core set of results obtained from a blood gas analyser includes the partial pressures of oxygen and carbon dioxide, pH, bicarbonate concentration, and base excess. These values are used to assess the patient’s acid-base status.
The pH value indicates whether the patient is in acidosis, alkalosis, or within the normal range. A pH less than 7.35 indicates acidosis, while a pH greater than 7.45 indicates alkalosis.
The respiratory system is assessed by looking at the partial pressure of carbon dioxide (pCO2). An elevated pCO2 contributes to acidosis, while a low pCO2 contributes to alkalosis.
The metabolic aspect is assessed by looking at the bicarbonate (HCO3-) level and the base excess. A high bicarbonate concentration and base excess indicate alkalosis, while a low bicarbonate concentration and base excess indicate acidosis.
Analyzing the pCO2 and base excess values can help determine the primary disturbance and whether compensation is occurring. For example, a respiratory acidosis (elevated pCO2) may be accompanied by metabolic alkalosis (elevated base excess) as a compensatory response.
The anion gap is another important parameter that can help determine the cause of acidosis. It is calculated by subtracting the sum of chloride and bicarbonate from the sum of sodium and potassium.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 41
Incorrect
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You assess a 62-year-old woman who is currently receiving treatment with a DMARD for severe psoriatic arthropathy. She has been experiencing increasing difficulty breathing during physical activity for the past few months. During the examination, you detect fine bibasal crepitations. You order a chest X-ray, which reveals signs of pulmonary fibrosis.
What is the SINGLE medication she is most likely taking?Your Answer: Chloroquine
Correct Answer: Methotrexate
Explanation:There is a significant link between methotrexate and the development of pulmonary fibrosis. While there have been instances of pulmonary fibrosis occurring as a result of infliximab, this particular side effect is more commonly associated with methotrexate use.
Methotrexate can also cause other side effects such as nausea and vomiting, abdominal pain, gastrointestinal bleeding, dizziness, stomatitis, hepatotoxicity, neutropenia, and pneumonitis.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 42
Incorrect
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A 14 year old boy is brought into the emergency department after being bitten on the leg while playing in the woods near his neighborhood. The patient claims that the bite was from a snake that he saw quickly disappear into the bushes after biting him. You present the patient with pictures of native snake species in the area, and the patient identifies the common Eastern garter snake as the culprit. Which of the following statements is accurate regarding the treatment of bites from this particular snake species?
Your Answer: All patients should receive antivenom as soon as possible after the snake species has been identified
Correct Answer: The affected limb should immobilised in a sling
Explanation:The key components of first aid for snake bites in the UK involve immobilizing the patient and the affected limb, as well as administering paracetamol for pain relief. When it comes to venomous snake bites, it is important to immobilize the limb using a splint or sling, but not to use a tourniquet or pressure bandage for adder bites. In certain areas, such as NSW, Australia, where venomous snakes can cause rapidly progressing and life-threatening paralysis, pressure bandage immobilization is recommended. However, this is not the case in the UK. Anti-venom is not always necessary for adder bites, and its administration should be based on a thorough assessment of the patient’s condition and the presence of appropriate indications. Paracetamol is the preferred choice for pain relief in UK snake bites, as aspirin and ibuprofen can worsen bleeding tendencies that may result from adder bites. Similarly, heparin should be avoided for the same reason.
Further Reading:
Snake bites in the UK are primarily caused by the adder, which is the only venomous snake species native to the country. While most adder bites result in minor symptoms such as pain, swelling, and inflammation, there have been cases of life-threatening illness and fatalities. Additionally, there are instances where venomous snakes that are kept legally or illegally also cause bites in the UK.
Adder bites typically occur from early spring to late autumn, with the hand being the most common site of the bite. Symptoms can be local or systemic, with local symptoms including sharp pain, tingling or numbness, and swelling that spreads proximally. Systemic symptoms may include spreading pain, tenderness, inflammation, regional lymph node enlargement, and bruising. In severe cases, anaphylaxis can occur, leading to symptoms such as nausea, vomiting, abdominal pain, diarrhea, and shock.
It is important for clinicians to be aware of the potential complications and complications associated with adder bites. These can include acute renal failure, pulmonary and cerebral edema, acute gastric dilatation, paralytic ileus, acute pancreatitis, and coma and seizures. Anaphylaxis symptoms can appear within minutes or be delayed for hours, and hypotension is a critical sign to monitor.
Initial investigations for adder bites include blood tests, ECG, and vital sign monitoring. Further investigations such as chest X-ray may be necessary based on clinical signs. Blood tests may reveal abnormalities such as leukocytosis, raised hematocrit, anemia, thrombocytopenia, and abnormal clotting profile. ECG changes may include tachyarrhythmias, bradyarrhythmias, atrial fibrillation, and ST segment changes.
First aid measures at the scene include immobilizing the patient and the bitten limb, avoiding aspirin and ibuprofen, and cleaning the wound site in the hospital. Tetanus prophylaxis should be considered. In cases of anaphylaxis, prompt administration of IM adrenaline is necessary. In the hospital, rapid assessment and appropriate resuscitation with intravenous fluids are required.
Antivenom may be indicated in cases of hypotension, systemic envenoming, ECG abnormalities, peripheral neutrophil leucocytosis, elevated serum creatine kinase or metabolic acidosis, and extensive or rapidly spreading local swelling. Zagreb antivenom is commonly used in the UK, with an initial dose of 8 mL.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 43
Incorrect
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A 35 year old male is brought into the emergency department after being found disoriented and lethargic by a family member. The family member informs you that the patient has a history of depression and that there were multiple empty bottles of aspirin at the patient's residence. Initial tests are conducted, including a salicylate level. Upon reviewing the salicylate result, you commence the urinary alkalinisation protocol. What is the desired treatment range?
Your Answer: Urinary pH is 7.35-7.45
Correct Answer: Urinary pH is 7.5-8.5
Explanation:Urinary alkalinisation aims to achieve a urinary pH of 7.5-8.5. This process helps enhance the elimination of salicylates. It is important to regularly monitor urinary pH, ideally on an hourly basis.
Further Reading:
Salicylate poisoning, particularly from aspirin overdose, is a common cause of poisoning in the UK. One important concept to understand is that salicylate overdose leads to a combination of respiratory alkalosis and metabolic acidosis. Initially, the overdose stimulates the respiratory center, leading to hyperventilation and respiratory alkalosis. However, as the effects of salicylate on lactic acid production, breakdown into acidic metabolites, and acute renal injury occur, it can result in high anion gap metabolic acidosis.
The clinical features of salicylate poisoning include hyperventilation, tinnitus, lethargy, sweating, pyrexia (fever), nausea/vomiting, hyperglycemia and hypoglycemia, seizures, and coma.
When investigating salicylate poisoning, it is important to measure salicylate levels in the blood. The sample should be taken at least 2 hours after ingestion for symptomatic patients or 4 hours for asymptomatic patients. The measurement should be repeated every 2-3 hours until the levels start to decrease. Other investigations include arterial blood gas analysis, electrolyte levels (U&Es), complete blood count (FBC), coagulation studies (raised INR/PTR), urinary pH, and blood glucose levels.
To manage salicylate poisoning, an ABC approach should be followed to ensure a patent airway and adequate ventilation. Activated charcoal can be administered if the patient presents within 1 hour of ingestion. Oral or intravenous fluids should be given to optimize intravascular volume. Hypokalemia and hypoglycemia should be corrected. Urinary alkalinization with intravenous sodium bicarbonate can enhance the elimination of aspirin in the urine. In severe cases, hemodialysis may be necessary.
Urinary alkalinization involves targeting a urinary pH of 7.5-8.5 and checking it hourly. It is important to monitor for hypokalemia as alkalinization can cause potassium to shift from plasma into cells. Potassium levels should be checked every 1-2 hours.
In cases where the salicylate concentration is high (above 500 mg/L in adults or 350 mg/L in children), sodium bicarbonate can be administered intravenously. Hemodialysis is the treatment of choice for severe poisoning and may be indicated in cases of high salicylate levels, resistant metabolic acidosis, acute kidney injury, pulmonary edema, seizures and coma.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 44
Incorrect
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A 28 year old woman comes to the emergency department after being bitten on the foot by a snake when she accidentally stepped on it. She explains that the incident occurred while she was walking in a forest. The patient presents a photograph of the snake she took with her phone, and you recognize it as a common European adder (vipera berus). You contemplate administering Zagreb antivenom. What is the most frequently observed complication associated with administering antivenom for adder bites?
Your Answer: Supraventricular tachycardia
Correct Answer: Early anaphylactoid reactions
Explanation:To ensure prompt response in case of an adverse reaction, it is important to have adrenaline, antihistamine, and steroid readily available when administering Zagreb antivenom.
Further Reading:
Snake bites in the UK are primarily caused by the adder, which is the only venomous snake species native to the country. While most adder bites result in minor symptoms such as pain, swelling, and inflammation, there have been cases of life-threatening illness and fatalities. Additionally, there are instances where venomous snakes that are kept legally or illegally also cause bites in the UK.
Adder bites typically occur from early spring to late autumn, with the hand being the most common site of the bite. Symptoms can be local or systemic, with local symptoms including sharp pain, tingling or numbness, and swelling that spreads proximally. Systemic symptoms may include spreading pain, tenderness, inflammation, regional lymph node enlargement, and bruising. In severe cases, anaphylaxis can occur, leading to symptoms such as nausea, vomiting, abdominal pain, diarrhea, and shock.
It is important for clinicians to be aware of the potential complications and complications associated with adder bites. These can include acute renal failure, pulmonary and cerebral edema, acute gastric dilatation, paralytic ileus, acute pancreatitis, and coma and seizures. Anaphylaxis symptoms can appear within minutes or be delayed for hours, and hypotension is a critical sign to monitor.
Initial investigations for adder bites include blood tests, ECG, and vital sign monitoring. Further investigations such as chest X-ray may be necessary based on clinical signs. Blood tests may reveal abnormalities such as leukocytosis, raised hematocrit, anemia, thrombocytopenia, and abnormal clotting profile. ECG changes may include tachyarrhythmias, bradyarrhythmias, atrial fibrillation, and ST segment changes.
First aid measures at the scene include immobilizing the patient and the bitten limb, avoiding aspirin and ibuprofen, and cleaning the wound site in the hospital. Tetanus prophylaxis should be considered. In cases of anaphylaxis, prompt administration of IM adrenaline is necessary. In the hospital, rapid assessment and appropriate resuscitation with intravenous fluids are required.
Antivenom may be indicated in cases of hypotension, systemic envenoming, ECG abnormalities, peripheral neutrophil leucocytosis, elevated serum creatine kinase or metabolic acidosis, and extensive or rapidly spreading local swelling. Zagreb antivenom is commonly used in the UK, with an initial dose of 8 mL.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 45
Correct
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A 72-year-old woman with a history of hypertension and kidney disease is prescribed a new diuretic medication. Upon reviewing her blood test results, you observe the presence of hyperkalemia.
Which of the following diuretics is most likely to be the cause?Your Answer: Spironolactone
Explanation:Spironolactone is a medication used to treat conditions such as congestive cardiac failure, hypertension, hepatic cirrhosis with ascites and edema, and Conn’s syndrome. It functions as a competitive aldosterone receptor antagonist, primarily working in the distal convoluted tubule. In this area, it hinders the reabsorption of sodium ions and enhances the reabsorption of potassium ions. Spironolactone is commonly known as a potassium-sparing diuretic.
The main side effect of spironolactone is hyperkalemia, particularly when renal impairment is present. In severe cases, hyperkalemia can be life-threatening. Additionally, there is a notable occurrence of gastrointestinal disturbances, with nausea and vomiting being the most common. Women may experience menstrual disturbances, while men may develop gynecomastia, both of which are attributed to the antiandrogenic effects of spironolactone.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 46
Correct
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A 42-year-old male patient with epilepsy complains of feeling down. You observe that he has rough facial features, gum hypertrophy, and noticeable facial acne. Additionally, he exhibits an unsteady gait while walking.
Which ONE anti-epileptic medication is most likely causing his symptoms?Your Answer: Phenytoin
Explanation:Phenytoin is a potent anti-epileptic drug that is no longer recommended as the initial treatment for generalized or partial epilepsy due to its toxic effects. Users often experience common symptoms such as ataxia, nystagmus, diplopia, tremor, and dysarthria. Additionally, other side effects may include depression, decreased cognitive abilities, coarse facial features, acne, gum enlargement, polyneuropathy, and blood disorders.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 47
Correct
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A 32-year-old man is given a medication for a medical ailment during the 2nd-trimester of his partner's pregnancy. As a result, the newborn experiences cataracts, optic atrophy, and microphthalmia.
Which of the following medications is the most probable culprit for these abnormalities?Your Answer: Warfarin
Explanation:During the first trimester of pregnancy, the use of warfarin can lead to a condition known as fetal warfarin syndrome. This condition is characterized by nasal hypoplasia, bone stippling, bilateral optic atrophy, and intellectual disability in the baby. However, if warfarin is taken during the second or third trimester, it can cause optic atrophy, cataracts, microcephaly, microphthalmia, intellectual disability, and both fetal and maternal hemorrhage.
There are several other drugs that can have adverse effects during pregnancy. For example, ACE inhibitors like ramipril can cause hypoperfusion, renal failure, and the oligohydramnios sequence if taken during the second and third trimesters. Aminoglycosides such as gentamicin can lead to ototoxicity and deafness in the baby. High doses of aspirin can result in first trimester abortions, delayed onset labor, premature closure of the fetal ductus arteriosus, and fetal kernicterus. However, low doses of aspirin (e.g. 75 mg) do not pose significant risks.
Benzodiazepines like diazepam, when taken late in pregnancy, can cause respiratory depression and a neonatal withdrawal syndrome. Calcium-channel blockers, if taken during the first trimester, can cause phalangeal abnormalities, while their use in the second and third trimesters can lead to fetal growth retardation. Carbamazepine can result in hemorrhagic disease of the newborn and neural tube defects. Chloramphenicol can cause gray baby syndrome. Corticosteroids, if taken during the first trimester, may cause orofacial clefts.
Danazol, if taken during the first trimester, can cause masculinization of the female fetuses genitals. Finasteride should not be handled by pregnant women as crushed or broken tablets can be absorbed through the skin and affect male sex organ development. Haloperidol, if taken during the first trimester, may cause limb malformations, while its use in the third trimester increases the risk of extrapyramidal symptoms in the newborn.
Heparin can lead to maternal bleeding and thrombocytopenia. Isoniazid can cause maternal liver damage and neuropathy and seizures in the baby. Isotretinoin carries a high risk of teratogenicity, including multiple congenital malformations and spontaneous abortion.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 48
Incorrect
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You are caring for a hypoxic patient in the resuscitation bay. One of the potential diagnoses is methaemoglobinaemia. If the diagnosis of methaemoglobinaemia is confirmed, which of the following treatments would be the most appropriate to administer?
Your Answer: Prussian Blue
Correct Answer: Methylene blue
Explanation:If IV methylene blue is obtained, it is typically used to treat a specific cause. However, if there is no response to methylene blue, alternative treatments such as hyperbaric oxygen or exchange transfusion may be considered. In cases where the cause is NADH-methaemoglobinaemia reductase deficiency, ascorbic acid can be used as a potential treatment.
Further Reading:
Methaemoglobinaemia is a condition where haemoglobin is oxidised from Fe2+ to Fe3+. This process is normally regulated by NADH methaemoglobin reductase, which transfers electrons from NADH to methaemoglobin, converting it back to haemoglobin. In healthy individuals, methaemoglobin levels are typically less than 1% of total haemoglobin. However, an increase in methaemoglobin can lead to tissue hypoxia as Fe3+ cannot bind oxygen effectively.
Methaemoglobinaemia can be congenital or acquired. Congenital causes include haemoglobin chain variants (HbM, HbH) and NADH methaemoglobin reductase deficiency. Acquired causes can be due to exposure to certain drugs or chemicals, such as sulphonamides, local anaesthetics (especially prilocaine), nitrates, chloroquine, dapsone, primaquine, and phenytoin. Aniline dyes are also known to cause methaemoglobinaemia.
Clinical features of methaemoglobinaemia include slate grey cyanosis (blue to grey skin coloration), chocolate blood or chocolate cyanosis (brown color of blood), dyspnoea, low SpO2 on pulse oximetry (which often does not improve with supplemental oxygen), and normal PaO2 on arterial blood gas (ABG) but low SaO2. Patients may tolerate hypoxia better than expected. Severe cases can present with acidosis, arrhythmias, seizures, and coma.
Diagnosis of methaemoglobinaemia is made by directly measuring the level of methaemoglobin using a co-oximeter, which is present in most modern blood gas analysers. Other investigations, such as a full blood count (FBC), electrocardiogram (ECG), chest X-ray (CXR), and beta-human chorionic gonadotropin (bHCG) levels (in pregnancy), may be done to assess the extent of the condition and rule out other contributing factors.
Active treatment is required if the methaemoglobin level is above 30% or if it is below 30% but the patient is symptomatic or shows evidence of tissue hypoxia. Treatment involves maintaining the airway and delivering high-flow oxygen, removing the causative agents, treating toxidromes and consider giving IV dextrose 5%.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 49
Incorrect
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A 45-year-old with a history of bipolar disorder is brought into the emergency department after intentionally taking an excessive amount of lithium. What acid-base disturbances would you anticipate in a patient who has overdosed on lithium?
Your Answer: Normal ion gap acidosis
Correct Answer: Low anion gap acidosis
Explanation:Excessive intake of lithium is linked to the development of low anion gap acidosis. In cases of lithium overdose, a common outcome is the occurrence of low anion gap acidosis.
Further Reading:
Arterial blood gases (ABG) are an important diagnostic tool used to assess a patient’s acid-base status and respiratory function. When obtaining an ABG sample, it is crucial to prioritize safety measures to minimize the risk of infection and harm to the patient. This includes performing hand hygiene before and after the procedure, wearing gloves and protective equipment, disinfecting the puncture site with alcohol, using safety needles when available, and properly disposing of equipment in sharps bins and contaminated waste bins.
To reduce the risk of harm to the patient, it is important to test for co-lateral circulation using the modified Allen test for radial artery puncture. Additionally, it is essential to inquire about any occlusive vascular conditions or anticoagulation therapy that may affect the procedure. The puncture site should be checked for signs of infection, injury, or previous surgery. After the test, pressure should be applied to the puncture site or the patient should be advised to apply pressure for at least 5 minutes to prevent bleeding.
Interpreting ABG results requires a systematic approach. The core set of results obtained from a blood gas analyser includes the partial pressures of oxygen and carbon dioxide, pH, bicarbonate concentration, and base excess. These values are used to assess the patient’s acid-base status.
The pH value indicates whether the patient is in acidosis, alkalosis, or within the normal range. A pH less than 7.35 indicates acidosis, while a pH greater than 7.45 indicates alkalosis.
The respiratory system is assessed by looking at the partial pressure of carbon dioxide (pCO2). An elevated pCO2 contributes to acidosis, while a low pCO2 contributes to alkalosis.
The metabolic aspect is assessed by looking at the bicarbonate (HCO3-) level and the base excess. A high bicarbonate concentration and base excess indicate alkalosis, while a low bicarbonate concentration and base excess indicate acidosis.
Analyzing the pCO2 and base excess values can help determine the primary disturbance and whether compensation is occurring. For example, a respiratory acidosis (elevated pCO2) may be accompanied by metabolic alkalosis (elevated base excess) as a compensatory response.
The anion gap is another important parameter that can help determine the cause of acidosis. It is calculated by subtracting the sum of chloride and bicarbonate from the sum of sodium and potassium.
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This question is part of the following fields:
- Pharmacology & Poisoning
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Question 50
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A 35-year-old woman is being evaluated after a benzodiazepine overdose. As part of her treatment, she is given a dose of flumazenil.
Which SINGLE statement about flumazenil is NOT true?Your Answer: The maximum dose is 10 mg per hour
Explanation:Flumazenil is a specific antagonist for benzodiazepines that can be beneficial in certain situations. It acts quickly, taking less than 1 minute to take effect, but its effects are short-lived and only last for less than 1 hour. The recommended dosage is 200 μg every 1-2 minutes, with a maximum dose of 3mg per hour.
It is important to avoid using Flumazenil if the patient is dependent on benzodiazepines or is taking tricyclic antidepressants. This is because it can trigger a withdrawal syndrome in these individuals, potentially leading to seizures or cardiac arrest.
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This question is part of the following fields:
- Pharmacology & Poisoning
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