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Questions and Answers
What is the primary receptor that cardio-selective beta blockers bind to in cardiac tissue?
What is the primary receptor that cardio-selective beta blockers bind to in cardiac tissue?
What is a potential risk factor for toxicity when taking beta blockers?
What is a potential risk factor for toxicity when taking beta blockers?
What is a common clinical feature of beta blocker toxicity?
What is a common clinical feature of beta blocker toxicity?
What is a characteristic of non-selective beta blockers?
What is a characteristic of non-selective beta blockers?
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What is the term for the Na+ channel blocking effects of some beta blockers?
What is the term for the Na+ channel blocking effects of some beta blockers?
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What is the timeframe for the onset of toxicity with non-sustained release beta blockers?
What is the timeframe for the onset of toxicity with non-sustained release beta blockers?
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What is the timeframe for the onset of toxicity with sustained release beta blockers?
What is the timeframe for the onset of toxicity with sustained release beta blockers?
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What is a characteristic of some beta blockers, also known as 'intrinsic sympathomimetic activity'?
What is a characteristic of some beta blockers, also known as 'intrinsic sympathomimetic activity'?
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What is the therapeutic range of theophylline concentrations?
What is the therapeutic range of theophylline concentrations?
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What is the suggested treatment for Theophylline-Related Agitation and Anxiety?
What is the suggested treatment for Theophylline-Related Agitation and Anxiety?
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What complication can occur due to theophylline toxicity?
What complication can occur due to theophylline toxicity?
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What is the purpose of measuring plasma theophylline concentrations?
What is the purpose of measuring plasma theophylline concentrations?
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What is the reason to avoid haloperidol in treating Theophylline-Related Agitation and Anxiety?
What is the reason to avoid haloperidol in treating Theophylline-Related Agitation and Anxiety?
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Why should charcoal haemoperfusion be considered for patients with Theophylline toxicity?
Why should charcoal haemoperfusion be considered for patients with Theophylline toxicity?
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What is the recommended interval for repeating measurements of plasma theophylline concentrations in severe poisoning?
What is the recommended interval for repeating measurements of plasma theophylline concentrations in severe poisoning?
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What is the alternative to charcoal haemoperfusion if it is not available?
What is the alternative to charcoal haemoperfusion if it is not available?
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What is the apparent half-life of theophylline in cases of overdose?
What is the apparent half-life of theophylline in cases of overdose?
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What is a common cardiac effect of theophylline toxicity?
What is a common cardiac effect of theophylline toxicity?
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What is the suggested dose of Diazepam for treating convulsions in adults?
What is the suggested dose of Diazepam for treating convulsions in adults?
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Why should potassium replacement be done cautiously in Theophylline toxicity?
Why should potassium replacement be done cautiously in Theophylline toxicity?
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What is the purpose of the grading system for acute theophylline toxicity?
What is the purpose of the grading system for acute theophylline toxicity?
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What is the suggested dose of Lorazepam for treating convulsions in adults?
What is the suggested dose of Lorazepam for treating convulsions in adults?
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What is the initial management step in patients with acute theophylline toxicity?
What is the initial management step in patients with acute theophylline toxicity?
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What is the case report that has been successful in enhancing theophylline elimination after overdose?
What is the case report that has been successful in enhancing theophylline elimination after overdose?
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What type of agents are streptokinase and urokinase?
What type of agents are streptokinase and urokinase?
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What is the half-life of factor VII?
What is the half-life of factor VII?
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What is the purpose of monitoring prothrombin time?
What is the purpose of monitoring prothrombin time?
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What is the effect of enzyme inhibitors of hepatic microsomal enzymes on bleeding risk?
What is the effect of enzyme inhibitors of hepatic microsomal enzymes on bleeding risk?
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What is the impact of genetic variability on warfarin dosing?
What is the impact of genetic variability on warfarin dosing?
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What is the difference in potency between S-warfarin and R-warfarin?
What is the difference in potency between S-warfarin and R-warfarin?
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What is the half-life of racemic warfarin?
What is the half-life of racemic warfarin?
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What is the reversal agent for warfarin?
What is the reversal agent for warfarin?
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What is the characteristic of long-acting anticoagulants?
What is the characteristic of long-acting anticoagulants?
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What is the minimum dose of vitamin K to be given to a child?
What is the minimum dose of vitamin K to be given to a child?
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What is the management for warfarin excess in patients not normally on warfarin?
What is the management for warfarin excess in patients not normally on warfarin?
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Why should vitamin K be delayed after activated charcoal use?
Why should vitamin K be delayed after activated charcoal use?
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What is unfractionated heparin dosed in?
What is unfractionated heparin dosed in?
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What is the effect of repeat dosing of unfractionated heparin?
What is the effect of repeat dosing of unfractionated heparin?
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What is the purpose of monitoring APTT?
What is the purpose of monitoring APTT?
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What is the difference between unfractionated heparin and low-molecular-weight heparins (LMWHs)?
What is the difference between unfractionated heparin and low-molecular-weight heparins (LMWHs)?
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What is the management of prolonged APTT without bleeding?
What is the management of prolonged APTT without bleeding?
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What happens to intravenous heparins?
What happens to intravenous heparins?
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Study Notes
Theophylline Toxicity
- Acute theophylline toxicity can cause dilated pupils, hallucinations, and convulsions.
- Factors that inhibit CYP activity can alter theophylline clearance, leading to prolonged elimination after overdose.
- Complications of theophylline toxicity include rhabdomyolysis, cardiac arrhythmias, and ventricular tachycardia or fibrillation.
Therapeutic Range and Toxicity Assessment
- Therapeutic range of theophylline concentrations: 10-20 mg/L (55-110 micromol/L).
- Acute toxic effects correlate well with serum theophylline concentrations.
- Plasma theophylline concentrations should be measured urgently in patients with clinical features of toxicity.
- Repeat measurements every 2-4 hours in severe poisoning (>60 mg/L).
Management of Theophylline Toxicity
- Ensure a clear airway and adequate ventilation and oxygenation.
- Monitor oxygen saturation, especially in patients with underlying respiratory disease.
- Vitamin K can be used as a reversal agent in warfarin overdose.
Warfarin Toxicity
- Warfarin toxicity can cause bleeding, which is the most important clinical effect of anticoagulant excess.
- Risk factors for warfarin toxicity include elderly individuals, patients with underlying clotting abnormalities, and patients with liver disease.
- Genetic variability can affect warfarin dosing, and genetic factors may assist in preventing therapeutic over-anticoagulation.
- Warfarin consists of R- and S-warfarin isomers, with S-warfarin being up to five times more potent than R-warfarin.
Reversal Agent and Management of Warfarin Excess
- Vitamin K can competitively reactivate vitamin K epoxide-reductase to overcome warfarin's action.
- Speed of recovery depends on vitamin K dose and clotting factor re-synthesis rates.
- Phenindione is an alternative vitamin K antagonist to warfarin, but it is more likely to cause adverse reactions.
Long-Acting Anticoagulants
- Difenacoum and brodifacoum are long-acting anticoagulants that are more potent than warfarin.
- They have a very long duration of action, requiring prolonged therapy and monitoring over several months.
Beta-Blocker Toxicity
- Beta-blockers can cause competitive antagonism at the beta-adrenergic receptor.
- Clinical effects may vary due to functional crossover between receptor subtypes.
- Highly beta1 selective agents (e.g., bisoprolol, atenolol) have less affinity to beta2 receptor in respiratory tissue.
- Non-selective agents (e.g., propranolol) have Na+ channel blocking effects sometimes termed 'quinidine-like effects' or 'membrane stabilizing activity'.
- Partial agonist activity at adrenoceptors can lead to 'intrinsic sympathomimetic activity' (ISA).
Management of Beta-Blocker Toxicity
- Cardiovascular features of toxicity include bradycardia, hypotension, and heart block.
- Treatment involves supportive care, including management of bradycardia and hypotension according to standard ALS algorithms.
- Consider charcoal haemoperfusion or haemodialysis for severe toxicity.
Heparin and Low-Molecular-Weight Heparins
- Unfractionated heparin is a complex mixture of different molecular weights, not a single molecule.
- Heparin breakdown products are smaller heparin-like molecules and are also active anticoagulants.
- Low-molecular-weight heparins (LMWHs) avoid the problem of variable activity and have more activity against factor X and less against activated factor II.
- LMWHs are normally prescribed as a weight-related dose, adjusted for renal function.
- Monitoring of heparin effect is done using the activated partial thromboplastin time (APTT).
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