Tricyclic antidepressants and selective serotonin reuptake inhibitors are two classes of antidepressants that can cause toxicity when taken in overdose amounts. Tricyclic antidepressants cause toxicity through sodium channel blockade in the heart which can lead to cardiac issues. Selective serotonin reuptake inhibitors most commonly cause serotonin syndrome when taken in combination with other serotonergic drugs due to excessive serotonin in the brain and body. Both types of overdoses require supportive care focused on symptoms, with activated charcoal and sodium bicarbonate used for tricyclic overdoses and cooling measures for serotonin syndrome.
Tricyclic antidepressants have been used since the 1950s and include compounds with three rings. They are the largest group of drugs used to treat depression. Overdoses can be life-threatening due to their rapid absorption and effects on the central nervous system, cardiovascular system, and respiratory system. Treatment for overdoses involves stabilizing the patient, reducing drug absorption, increasing elimination, treating seizures and arrhythmias, and observing the patient for at least 6 hours if symptoms resolve before discharge.
Paracetamol is a commonly used analgesic and antipyretic that is well absorbed orally. At normal doses, it is metabolized through conjugation pathways and excreted in urine. However, in overdose the conjugation pathways become saturated and it is metabolized through the toxic NAPQI pathway. This can lead to glutathione depletion and liver injury. N-acetylcysteine is the antidote and works best if given within 10 hours of overdose to replenish glutathione levels before liver damage occurs. Symptoms of overdose include nausea, vomiting and liver damage signs like jaundice and coagulopathy.
1) Paracetamol is metabolized in the liver and can cause toxicity in high doses by depleting glutathione levels, allowing the reactive metabolite NAPQI to damage cells.
2) For paracetamol overdose, N-acetylcysteine should be administered within 8-10 hours as an antidote to replenish glutathione levels. The treatment involves intravenous administration over 21 hours.
3) Management also involves monitoring liver function tests and providing supportive care. Liver transplantation may be considered for severe liver failure due to paracetamol poisoning.
This document discusses depression, mania, and various antidepressant medications. It covers the symptoms of depression and mania. It then discusses various classes of antidepressants including SSRIs, SNRIs, TCAs, MAOIs, and atypical antidepressants. For each class, it describes the mechanisms of action, therapeutic uses, adverse effects, and examples of medications within the class.
This document provides an overview of antidepressant drugs. It discusses the criteria for major depression and epidemiology. It then covers the pharmacology of different classes of antidepressants including SSRIs, SNRIs, serotonin receptor antagonists, bupropion, and MAOIs. For each class, it discusses mechanisms of action, pharmacokinetics, uses, adverse effects, and drug interactions.
Opioid overdose is a leading cause of death worldwide, killing an estimated 69,000 people per year. Opioids depress the respiratory drive, leading to apnea, reduced breathing rate, hypoxemia, cerebral hypoxia, and cardiac arrest. Prolonged cerebral hypoxia from impaired breathing is the main mechanism of brain injury and death in opioid overdoses. Naloxone is an opioid antagonist that can reverse the effects of opioid overdose when administered promptly through various routes such as IV, IM, SC, or intranasally. It displaces opioids from receptors and restores normal breathing without abuse potential.
Benzodiazepines are commonly prescribed sedative-hypnotic agents that were introduced in 1960. They are used for conditions like anxiety, insomnia, alcohol withdrawal, and seizures by enhancing the effects of the inhibitory neurotransmitter GABA. While generally safe, benzodiazepines can cause side effects with prolonged use or overdose like dependence, withdrawal symptoms, and respiratory depression. The effects of different benzodiazepines vary based on their ability to cross the blood-brain barrier and metabolism, with short-acting agents having faster onsets but shorter durations of action.
Tricyclic antidepressants have been used since the 1950s and include compounds with three rings. They are the largest group of drugs used to treat depression. Overdoses can be life-threatening due to their rapid absorption and effects on the central nervous system, cardiovascular system, and respiratory system. Treatment for overdoses involves stabilizing the patient, reducing drug absorption, increasing elimination, treating seizures and arrhythmias, and observing the patient for at least 6 hours if symptoms resolve before discharge.
Paracetamol is a commonly used analgesic and antipyretic that is well absorbed orally. At normal doses, it is metabolized through conjugation pathways and excreted in urine. However, in overdose the conjugation pathways become saturated and it is metabolized through the toxic NAPQI pathway. This can lead to glutathione depletion and liver injury. N-acetylcysteine is the antidote and works best if given within 10 hours of overdose to replenish glutathione levels before liver damage occurs. Symptoms of overdose include nausea, vomiting and liver damage signs like jaundice and coagulopathy.
1) Paracetamol is metabolized in the liver and can cause toxicity in high doses by depleting glutathione levels, allowing the reactive metabolite NAPQI to damage cells.
2) For paracetamol overdose, N-acetylcysteine should be administered within 8-10 hours as an antidote to replenish glutathione levels. The treatment involves intravenous administration over 21 hours.
3) Management also involves monitoring liver function tests and providing supportive care. Liver transplantation may be considered for severe liver failure due to paracetamol poisoning.
This document discusses depression, mania, and various antidepressant medications. It covers the symptoms of depression and mania. It then discusses various classes of antidepressants including SSRIs, SNRIs, TCAs, MAOIs, and atypical antidepressants. For each class, it describes the mechanisms of action, therapeutic uses, adverse effects, and examples of medications within the class.
This document provides an overview of antidepressant drugs. It discusses the criteria for major depression and epidemiology. It then covers the pharmacology of different classes of antidepressants including SSRIs, SNRIs, serotonin receptor antagonists, bupropion, and MAOIs. For each class, it discusses mechanisms of action, pharmacokinetics, uses, adverse effects, and drug interactions.
Opioid overdose is a leading cause of death worldwide, killing an estimated 69,000 people per year. Opioids depress the respiratory drive, leading to apnea, reduced breathing rate, hypoxemia, cerebral hypoxia, and cardiac arrest. Prolonged cerebral hypoxia from impaired breathing is the main mechanism of brain injury and death in opioid overdoses. Naloxone is an opioid antagonist that can reverse the effects of opioid overdose when administered promptly through various routes such as IV, IM, SC, or intranasally. It displaces opioids from receptors and restores normal breathing without abuse potential.
Benzodiazepines are commonly prescribed sedative-hypnotic agents that were introduced in 1960. They are used for conditions like anxiety, insomnia, alcohol withdrawal, and seizures by enhancing the effects of the inhibitory neurotransmitter GABA. While generally safe, benzodiazepines can cause side effects with prolonged use or overdose like dependence, withdrawal symptoms, and respiratory depression. The effects of different benzodiazepines vary based on their ability to cross the blood-brain barrier and metabolism, with short-acting agents having faster onsets but shorter durations of action.
1. Opioid overdose can occur from both prescription and illicit opioid use. Common opioids involved include morphine, heroin, fentanyl, oxycodone, and hydrocodone.
2. Symptoms of opioid overdose include respiratory depression, sedation, small pupils, nausea, vomiting, and decreased heart rate. Naloxone is used as an antidote to reverse the effects of opioid overdose.
3. Treatment of opioid overdose focuses on supporting breathing, administering naloxone, monitoring for complications, and managing withdrawal symptoms which can include restlessness, nausea, and drug craving. Prevention strategies aim to reduce opioid misuse and increase access to treatment.
Management of Opioid Analgesic OverdoseSun Yai-Cheng
This document summarizes the management of opioid analgesic overdoses. It notes that opioid overdoses can have life-threatening effects on multiple organ systems. The duration of action varies between opioid formulations and an overdose can prolong intoxication. Prescriptions for opioid analgesics in the US increased 700% from 1997-2007. Opioid overdoses lead to over 27,500 health care facility admissions in 2010. Clinical signs of overdose include respiratory depression, apnea, miosis, and stupor. Naloxone is the antidote and works by reversing opioid receptor activity but has a shorter duration than many opioids. Higher and repeated naloxone doses may be needed for long-acting opioids like
This document provides an overview of stroke, including its definition, types, risk factors, pathophysiology, clinical presentation, diagnosis, treatment both initially and long-term, and management considerations. The two main types of stroke are ischemic (87%) and hemorrhagic (13%). Risk factors include modifiable factors like hypertension and non-modifiable factors like age. Treatment involves stabilizing the patient, diagnosing with imaging, treating the cause, preventing complications, and long-term prevention with medications like aspirin, statins, and anticoagulants depending on the cause of stroke.
Depression is a mental illness characterized by changes in mood and loss of interest. It has several potential causes like abuse, loss, isolation, stress, or unemployment. There are different types of depression including unipolar, reactive, endogenous, and bipolar. Antidepressants work by increasing neurotransmitters like serotonin, norepinephrine, and dopamine in the brain. Common antidepressants include SSRIs, SNRIs, TCAs, and MAO inhibitors. SSRIs are now the first-line treatment due to their safer side effect profile compared to older TCAs.
This document discusses antipsychotic and mood stabilizing drugs. It begins by classifying antipsychotics such as phenothiazines, butyrophenones, and atypical antipsychotics. It then describes the mechanism of action, uses, and adverse effects of typical antipsychotics like chlorpromazine and haloperidol. Atypical antipsychotics like clozapine and risperidone are also discussed. The document also covers mood stabilizers lithium and sodium valproate, focusing on lithium's mechanism and use in treating mania and bipolar disorder. Management of schizophrenia, mania, and bipolar disorder is described.
Selective serotonin reuptake inhibitors (SSRIs) are a class of antidepressants that work by inhibiting the reuptake of serotonin. SSRIs include fluoxetine, sertraline, paroxetine, fluvoxamine, citalopram, and escitalopram. They are highly selective for serotonin reuptake compared to other neurotransmitters. While SSRIs share the common mechanism of inhibiting serotonin reuptake, they differ in their pharmacokinetic properties such as half-life, metabolic pathways, and drug interaction potential. Adverse effects of SSRIs include nausea, sexual dysfunction, headaches, and weight changes.
Benzodiazepines are a class of psychoactive drugs whose core structure is a fusion of benzene and diazepine rings. The first benzodiazepine, chlordiazepoxide, was discovered in 1955. In 1977, benzodiazepines were the most prescribed medications globally. They are commonly used as minor tranquilizers to treat anxiety, insomnia, seizures, and alcohol withdrawal. While generally safe, benzodiazepines can cause sedation, dependency, respiratory depression, and cognitive impairment in elderly patients with long-term use.
General principles involved in management of poisoning- by rxvichu!!RxVichuZ
Hellow friends!!! I am back....with my 13th ppt!!
This ppt is regarding TOXICOLOGY,which happens to be my 1st....and i am happy to release the same on INDEPENDENCE DAY!!
Wishing a very happy and blissful Independence Day to all....i release my toxicology ppt regarding GENERAL PRINCIPLES IN POISONING MANAGEMENT.....
Since its my 1st attempt in Toxicology, i would love to hear ur reviews, and comments....so that i can improve in upcoming editions......
Keep reading...thanks for ur support!!!
With love and regards,
Vishnu.R.Nair (rxvichu-alwz4uh!!)
:) :)
Pharmacological management of heart failureNaser Tadvi
Heart failure is caused by decreased cardiac output and increased sympathetic discharge. Drugs used to treat heart failure include diuretics to reduce preload, ACE inhibitors to reduce afterload, beta blockers to attenuate sympathetic activation, and digitalis for its inotropic effects. Newer drugs target vasodilation and myosin activation to further increase cardiac efficiency while reducing energy demands. Combination therapy following an assessment of cardiac function and volume status provides the best approach for management of heart failure.
Salicylate poisoning can occur from ingesting derivatives of salicylic acid like aspirin. It causes metabolic disturbances as salicylates uncouple oxidative phosphorylation, increasing oxygen consumption and heat production. This can lead to hyperventilation, tachycardia, fever, hypoglycemia and metabolic acidosis. Treatment involves gastric decontamination, fluid resuscitation, urinary alkalinization and hemodialysis in severe cases to enhance renal excretion of the toxin. Prognosis is generally good with acute ingestion but worse with chronic use due to increased risks of mortality and morbidity.
Gut decontamination or methods of poison removal in clinical toxicology Soujanya Pharm.D
Gastrointestinal decontamination refers to removing toxins from the gastrointestinal tract. Methods include inducing vomiting, gastric lavage, cathartics, activated charcoal, and whole bowel irrigation. Inducing vomiting with ipecac or apomorphine is only recommended for alert patients within 4-6 hours of ingestion. Gastric lavage may be considered for life-threatening ingestions within 1-2 hours but has risks. Cathartics like sorbitol and magnesium can help purge the bowels. Activated charcoal binds toxins and is most effective within 1 hour. Whole bowel irrigation with solutions like PEG-ELS may help for late presentations over 4 hours after ingestion. These methods aim to reduce toxin
- Seizures arise from abnormal neuronal firing in the brain. Antiepileptic drugs work by inhibiting neuronal firing through various mechanisms like enhancing GABA inhibition, blocking sodium channels, or reducing calcium influx.
- Common antiepileptic drugs include carbamazepine, lamotrigine, phenytoin, topiramate, valproate, ethosuximide, levetiracetam, and gabapentin. They act on targets like GABA, sodium channels, calcium channels, and glutamate receptors.
- Choosing an antiepileptic drug depends on seizure type, epilepsy syndrome, side effect profile, interactions, and cost. While drugs control seizures for many
The document discusses opioid poisoning from substances derived from the opium poppy plant like morphine and codeine. It notes that opioids work by stimulating receptors in the central nervous system, causing sedation and respiratory depression which can lead to respiratory failure and death. Symptoms of acute opioid poisoning range from euphoria to vomiting and lethargy while chronic use can cause depression, weight loss, and social withdrawal. Treatment focuses on maintaining breathing and circulation along with the antidote naloxone to reverse effects while also providing supportive care and counseling.
Please find the power point on Management of antipsychotic overdose. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Organophosphate poisoning occurs when organophosphate compounds such as insecticides and nerve agents inhibit the enzyme acetylcholinesterase. Symptoms range from mild effects like blurred vision and excess saliva to severe effects like respiratory failure and death. Treatment involves atropine to block acetylcholine effects and pralidoxime or obidoxime to reactivate acetylcholinesterase. Nursing care focuses on maintaining airway, breathing, circulation and preventing infection while the toxic substances are metabolized and excreted from the body. Organophosphate poisoning is a significant global health problem causing millions of hospitalizations annually.
Phenytoin is an anti-seizure medication that works by blocking voltage-gated sodium channels in neurons. It has nonlinear pharmacokinetics and a narrow therapeutic index. Common side effects include gingival hyperplasia and nystagmus. Serious potential side effects include bone marrow suppression, low blood pressure, and Stevens-Johnson syndrome. It must be carefully monitored due to risks of toxicity at high doses.
This document provides information on anti-epileptic drugs (AEDs) including their mechanisms of action, uses, and side effects. It discusses the classification, treatment, and management of epilepsy and seizures. Some key points include:
- AEDs work by enhancing GABA inhibition, blocking sodium channels, or inhibiting calcium currents to suppress neuronal firing and seizures.
- Common AEDs include phenytoin, carbamazepine, valproic acid, lamotrigine, levetiracetam, and topiramate.
- AEDs are used to treat generalized tonic-clonic, absence, myoclonic and partial seizures. Some are also used for neuropathic
Tricyclic antidepressants (TCAs) have been used in drug therapy since the 1950s and were a major cause of mortality from poisoning until 1993. TCAs remain widely prescribed for depression and other indications. TCA overdose can cause life-threatening toxicity due to anticholinergic effects, cardiac sodium channel blockade, and alpha-1 adrenergic receptor blockade. Clinical manifestations include sinus tachycardia, hypotension, seizures, QT prolongation, and changes in mental status. Treatment involves supportive care, sodium bicarbonate for acidosis, benzodiazepines for seizures, and lipid emulsion or inotropes for refractory hypotension.
This document provides an overview of antidepressant toxicity, including tricyclic antidepressant (TCA), selective serotonin reuptake inhibitor (SSRI), and monoamine oxidase inhibitor (MAOI) toxicity. It discusses the clinical presentation, mechanisms, risk assessment, and management of toxicity for each class. TCA toxicity can cause cardiac conduction delays, arrhythmias and hypotension. SSRI overdoses rarely cause toxicity on their own but serotonin syndrome can occur with combinations. MAOI toxicity results from interactions causing increased monoamine levels and produces adrenergic effects like hypertension. Management involves supportive care, sodium bicarbonate for TCA cardiac issues, benzodiazepines for seizures/agitation, and cy
1. Opioid overdose can occur from both prescription and illicit opioid use. Common opioids involved include morphine, heroin, fentanyl, oxycodone, and hydrocodone.
2. Symptoms of opioid overdose include respiratory depression, sedation, small pupils, nausea, vomiting, and decreased heart rate. Naloxone is used as an antidote to reverse the effects of opioid overdose.
3. Treatment of opioid overdose focuses on supporting breathing, administering naloxone, monitoring for complications, and managing withdrawal symptoms which can include restlessness, nausea, and drug craving. Prevention strategies aim to reduce opioid misuse and increase access to treatment.
Management of Opioid Analgesic OverdoseSun Yai-Cheng
This document summarizes the management of opioid analgesic overdoses. It notes that opioid overdoses can have life-threatening effects on multiple organ systems. The duration of action varies between opioid formulations and an overdose can prolong intoxication. Prescriptions for opioid analgesics in the US increased 700% from 1997-2007. Opioid overdoses lead to over 27,500 health care facility admissions in 2010. Clinical signs of overdose include respiratory depression, apnea, miosis, and stupor. Naloxone is the antidote and works by reversing opioid receptor activity but has a shorter duration than many opioids. Higher and repeated naloxone doses may be needed for long-acting opioids like
This document provides an overview of stroke, including its definition, types, risk factors, pathophysiology, clinical presentation, diagnosis, treatment both initially and long-term, and management considerations. The two main types of stroke are ischemic (87%) and hemorrhagic (13%). Risk factors include modifiable factors like hypertension and non-modifiable factors like age. Treatment involves stabilizing the patient, diagnosing with imaging, treating the cause, preventing complications, and long-term prevention with medications like aspirin, statins, and anticoagulants depending on the cause of stroke.
Depression is a mental illness characterized by changes in mood and loss of interest. It has several potential causes like abuse, loss, isolation, stress, or unemployment. There are different types of depression including unipolar, reactive, endogenous, and bipolar. Antidepressants work by increasing neurotransmitters like serotonin, norepinephrine, and dopamine in the brain. Common antidepressants include SSRIs, SNRIs, TCAs, and MAO inhibitors. SSRIs are now the first-line treatment due to their safer side effect profile compared to older TCAs.
This document discusses antipsychotic and mood stabilizing drugs. It begins by classifying antipsychotics such as phenothiazines, butyrophenones, and atypical antipsychotics. It then describes the mechanism of action, uses, and adverse effects of typical antipsychotics like chlorpromazine and haloperidol. Atypical antipsychotics like clozapine and risperidone are also discussed. The document also covers mood stabilizers lithium and sodium valproate, focusing on lithium's mechanism and use in treating mania and bipolar disorder. Management of schizophrenia, mania, and bipolar disorder is described.
Selective serotonin reuptake inhibitors (SSRIs) are a class of antidepressants that work by inhibiting the reuptake of serotonin. SSRIs include fluoxetine, sertraline, paroxetine, fluvoxamine, citalopram, and escitalopram. They are highly selective for serotonin reuptake compared to other neurotransmitters. While SSRIs share the common mechanism of inhibiting serotonin reuptake, they differ in their pharmacokinetic properties such as half-life, metabolic pathways, and drug interaction potential. Adverse effects of SSRIs include nausea, sexual dysfunction, headaches, and weight changes.
Benzodiazepines are a class of psychoactive drugs whose core structure is a fusion of benzene and diazepine rings. The first benzodiazepine, chlordiazepoxide, was discovered in 1955. In 1977, benzodiazepines were the most prescribed medications globally. They are commonly used as minor tranquilizers to treat anxiety, insomnia, seizures, and alcohol withdrawal. While generally safe, benzodiazepines can cause sedation, dependency, respiratory depression, and cognitive impairment in elderly patients with long-term use.
General principles involved in management of poisoning- by rxvichu!!RxVichuZ
Hellow friends!!! I am back....with my 13th ppt!!
This ppt is regarding TOXICOLOGY,which happens to be my 1st....and i am happy to release the same on INDEPENDENCE DAY!!
Wishing a very happy and blissful Independence Day to all....i release my toxicology ppt regarding GENERAL PRINCIPLES IN POISONING MANAGEMENT.....
Since its my 1st attempt in Toxicology, i would love to hear ur reviews, and comments....so that i can improve in upcoming editions......
Keep reading...thanks for ur support!!!
With love and regards,
Vishnu.R.Nair (rxvichu-alwz4uh!!)
:) :)
Pharmacological management of heart failureNaser Tadvi
Heart failure is caused by decreased cardiac output and increased sympathetic discharge. Drugs used to treat heart failure include diuretics to reduce preload, ACE inhibitors to reduce afterload, beta blockers to attenuate sympathetic activation, and digitalis for its inotropic effects. Newer drugs target vasodilation and myosin activation to further increase cardiac efficiency while reducing energy demands. Combination therapy following an assessment of cardiac function and volume status provides the best approach for management of heart failure.
Salicylate poisoning can occur from ingesting derivatives of salicylic acid like aspirin. It causes metabolic disturbances as salicylates uncouple oxidative phosphorylation, increasing oxygen consumption and heat production. This can lead to hyperventilation, tachycardia, fever, hypoglycemia and metabolic acidosis. Treatment involves gastric decontamination, fluid resuscitation, urinary alkalinization and hemodialysis in severe cases to enhance renal excretion of the toxin. Prognosis is generally good with acute ingestion but worse with chronic use due to increased risks of mortality and morbidity.
Gut decontamination or methods of poison removal in clinical toxicology Soujanya Pharm.D
Gastrointestinal decontamination refers to removing toxins from the gastrointestinal tract. Methods include inducing vomiting, gastric lavage, cathartics, activated charcoal, and whole bowel irrigation. Inducing vomiting with ipecac or apomorphine is only recommended for alert patients within 4-6 hours of ingestion. Gastric lavage may be considered for life-threatening ingestions within 1-2 hours but has risks. Cathartics like sorbitol and magnesium can help purge the bowels. Activated charcoal binds toxins and is most effective within 1 hour. Whole bowel irrigation with solutions like PEG-ELS may help for late presentations over 4 hours after ingestion. These methods aim to reduce toxin
- Seizures arise from abnormal neuronal firing in the brain. Antiepileptic drugs work by inhibiting neuronal firing through various mechanisms like enhancing GABA inhibition, blocking sodium channels, or reducing calcium influx.
- Common antiepileptic drugs include carbamazepine, lamotrigine, phenytoin, topiramate, valproate, ethosuximide, levetiracetam, and gabapentin. They act on targets like GABA, sodium channels, calcium channels, and glutamate receptors.
- Choosing an antiepileptic drug depends on seizure type, epilepsy syndrome, side effect profile, interactions, and cost. While drugs control seizures for many
The document discusses opioid poisoning from substances derived from the opium poppy plant like morphine and codeine. It notes that opioids work by stimulating receptors in the central nervous system, causing sedation and respiratory depression which can lead to respiratory failure and death. Symptoms of acute opioid poisoning range from euphoria to vomiting and lethargy while chronic use can cause depression, weight loss, and social withdrawal. Treatment focuses on maintaining breathing and circulation along with the antidote naloxone to reverse effects while also providing supportive care and counseling.
Please find the power point on Management of antipsychotic overdose. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Organophosphate poisoning occurs when organophosphate compounds such as insecticides and nerve agents inhibit the enzyme acetylcholinesterase. Symptoms range from mild effects like blurred vision and excess saliva to severe effects like respiratory failure and death. Treatment involves atropine to block acetylcholine effects and pralidoxime or obidoxime to reactivate acetylcholinesterase. Nursing care focuses on maintaining airway, breathing, circulation and preventing infection while the toxic substances are metabolized and excreted from the body. Organophosphate poisoning is a significant global health problem causing millions of hospitalizations annually.
Phenytoin is an anti-seizure medication that works by blocking voltage-gated sodium channels in neurons. It has nonlinear pharmacokinetics and a narrow therapeutic index. Common side effects include gingival hyperplasia and nystagmus. Serious potential side effects include bone marrow suppression, low blood pressure, and Stevens-Johnson syndrome. It must be carefully monitored due to risks of toxicity at high doses.
This document provides information on anti-epileptic drugs (AEDs) including their mechanisms of action, uses, and side effects. It discusses the classification, treatment, and management of epilepsy and seizures. Some key points include:
- AEDs work by enhancing GABA inhibition, blocking sodium channels, or inhibiting calcium currents to suppress neuronal firing and seizures.
- Common AEDs include phenytoin, carbamazepine, valproic acid, lamotrigine, levetiracetam, and topiramate.
- AEDs are used to treat generalized tonic-clonic, absence, myoclonic and partial seizures. Some are also used for neuropathic
Tricyclic antidepressants (TCAs) have been used in drug therapy since the 1950s and were a major cause of mortality from poisoning until 1993. TCAs remain widely prescribed for depression and other indications. TCA overdose can cause life-threatening toxicity due to anticholinergic effects, cardiac sodium channel blockade, and alpha-1 adrenergic receptor blockade. Clinical manifestations include sinus tachycardia, hypotension, seizures, QT prolongation, and changes in mental status. Treatment involves supportive care, sodium bicarbonate for acidosis, benzodiazepines for seizures, and lipid emulsion or inotropes for refractory hypotension.
This document provides an overview of antidepressant toxicity, including tricyclic antidepressant (TCA), selective serotonin reuptake inhibitor (SSRI), and monoamine oxidase inhibitor (MAOI) toxicity. It discusses the clinical presentation, mechanisms, risk assessment, and management of toxicity for each class. TCA toxicity can cause cardiac conduction delays, arrhythmias and hypotension. SSRI overdoses rarely cause toxicity on their own but serotonin syndrome can occur with combinations. MAOI toxicity results from interactions causing increased monoamine levels and produces adrenergic effects like hypertension. Management involves supportive care, sodium bicarbonate for TCA cardiac issues, benzodiazepines for seizures/agitation, and cy
Life threatening side effects of PsychotropicsDr Wasim
This document summarizes several life-threatening side effects of psychotropic medications, focusing on antipsychotics. It discusses QT prolongation which can lead to fatal arrhythmias. It also discusses diabetic ketoacidosis, drug-induced SIADH which can cause hyponatremia, increased risk of pneumonia, and serious hematological and cardiovascular side effects of clozapine including agranulocytosis, thromboembolism, myocarditis, and cardiomyopathy. Monitoring and management of these side effects is important for patient safety.
NSTE-ACS (Non-ST-elevation acute coronary syndromes) describes conditions like unstable angina and NSTEMI characterized by reduced blood flow without persistent ST elevation. It is usually caused by partially occlusive thrombi forming on atherosclerotic plaques or arterial walls. Diagnosis involves chest pain symptoms and elevated cardiac biomarkers. Treatment focuses on anti-ischemic drugs, antithrombotic therapies, risk factor modification, and sometimes revascularization. Prinzmetal's variant angina involves coronary artery spasms causing transient chest pain and ST elevation.
Digitalis toxicity is caused by the cardiac glycoside digoxin, which is commonly used to treat heart conditions but has a narrow therapeutic window. Digoxin toxicity can cause various cardiac arrhythmias by inhibiting the sodium-potassium pump in cardiac cells. Management of digoxin toxicity involves supportive care, treating arrhythmias, correcting electrolyte abnormalities, and administering digoxin antibody fragments for severe cases. Symptoms and signs of digoxin toxicity can affect the heart, gastrointestinal system, central nervous system, and vision.
This document summarizes various classes of antihypertensive drugs including their mechanisms of action, pharmacokinetics, adverse effects and uses. It discusses diuretics, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, beta blockers, alpha blockers, beta+alpha blockers and central sympatholytics. Key drugs discussed include captopril, losartan, verapamil, propranolol, prazosin, carvedilol and clonidine. The document provides classifications of hypertension and details the pharmacology of several individual antihypertensive drugs.
This document summarizes information about skeletal muscle relaxants. It discusses that these drugs are used to treat skeletal muscle spasticity and can act centrally or peripherally. Peripherally acting muscle relaxants are further divided into neuromuscular blocking agents and directly acting agents. Neuromuscular blocking agents are classified as depolarizing or non-depolarizing based on their mechanism of action at the neuromuscular junction. The key depolarizing agent discussed is succinylcholine and the key non-depolarizing agents discussed are tubocurarine and pancuronium. Dantrolene is highlighted as a directly acting agent that works by interfering with calcium release from muscle stores. Adverse
This document discusses angina pectoris, also known as stable angina. It defines angina as chest pain or discomfort that occurs due to decreased blood flow to the heart muscle. It then describes the different types of angina and their causes. The main causes are atherosclerosis, coronary artery spasm, traumatic injury, and embolic events which can all restrict blood flow to the heart. The document outlines the goals of treatment which are to prevent heart attacks and death while reducing angina symptoms. It then discusses the various pharmacological treatments used including nitrates, beta blockers, calcium channel blockers, antiplatelet agents, ACE inhibitors, and ranolazine. Non-pharmacological options like percutaneous coronary
1) Chemotherapeutic agents can cause toxicities affecting the heart, lungs, kidneys, liver, and bone marrow. Careful preoperative assessment is important, and certain agents increase risks during anesthesia.
2) Patients receiving chemotherapy like bleomycin are at high risk for pulmonary complications and require conservative fluid management. Those with prior anthracycline treatment are also at risk of cardiac issues.
3) Neuraxial techniques may be preferable for some cancer surgeries as they decrease the stress response compared to general anesthesia, which has been linked to increased metastasis in animal studies. Regional approaches can lower opioid requirements as well.
Muscarinic receptors bind to acetylcholine and have 5 subtypes that are found in various tissues. Antimuscarinic drugs block these receptors' activity. There are over a dozen antimuscarinic drugs that are used for various conditions by blocking effects of acetylcholine in the CNS, eyes, lungs, gut, and bladder. They work by competitively binding muscarinic receptors. Toxic effects include dry mouth, constipation, blurred vision, urinary retention, fever, and in overdose, delirium, arrhythmias, and seizures. The drugs must be used cautiously in infants, the elderly, and those with glaucoma or prostate issues.
Anaesthetic emergencies and procedures in veterinary practicesIVRI
This document discusses various anesthetic emergencies and procedures. It covers topics like cardiovascular emergencies, hemorrhage, cardiac arrest, allergic reactions, and cardiopulmonary resuscitation. For cardiac arrest, it recommends following the ABCD protocol of securing the airway, providing breathing support, performing cardiac compressions, and administering epinephrine and other drugs. It describes performing external chest compressions initially, but notes internal cardiac massage is more effective for resuscitation after 2 minutes if there is no response.
Presentation deals with thorough understanding of management of toxicities and poisoning and measures and care to be taken of the patient. Useful for Clinical Pharmacologist, Chemical Biologists, Undergraduate and Postgraduate Students of Pharmacy and Pharmacology
This document discusses various rheumatologic emergencies that require prompt treatment to prevent serious complications or death. It defines emergencies as situations that immediately endanger life or organ function. True emergencies have mortality rates around 50% even with timely intervention. Examples of rheumatologic emergencies discussed include septic arthritis, Atlantoaxial dislocation, acute upper airway obstruction in RA, acute transverse myelitis and cerebrovascular accident in SLE, alveolar hemorrhage and pulmonary renal syndrome in vasculitis, scleroderma renal crisis, respiratory muscle weakness in inflammatory myopathies, and catastrophic antiphospholipid syndrome. The document provides details on symptoms, diagnostic evaluation, and treatment approaches for each of
This document provides an overview of stroke, including:
- Stroke is defined as rapid neurological deficit caused by focal brain infarction or hemorrhage.
- Risk factors include hypertension, atrial fibrillation, diabetes, hyperlipidemia, and smoking.
- Strokes are either ischemic (85%) due to thrombosis or embolism, or hemorrhagic (15%) due to bleeding.
- Clinical features depend on the location of brain injury but may include weakness, speech problems, visual issues, and headache.
- Investigations include brain imaging (CT or MRI), blood tests, and cardiac workup to determine the cause.
- Treatment involves supportive care, thrombolysis
This document discusses various drugs used to treat angina pectoris, which is chest pain due to myocardial ischemia. It describes several classes of antianginal drugs that work by either increasing oxygen supply to the heart or decreasing oxygen demand. These include organic nitrates like glyceryl trinitrate, beta-blockers, calcium channel blockers, and ACE inhibitors. The document provides details on the mechanisms and sites of action of these drug classes as well as their adverse effects. Alternative treatment methods for ischemic heart disease like rotational atherectomy are also mentioned.
9. NSAIDS.pptxNSAIDS inhibit the enzyme cyclooxygenase (COX) types 1 and 2, w...samiyamohammed284
Renal
Renally produced prostaglandins (PGE2 and PGI2) are essential
in maintaining adequate renal perfusion when the level of circulating vasoconstrictors Platelets
Impaired platelet function (reduced aggregation).
as a result of decreased thromboxane A2 (TXA2) production.
TXA2 is present in large amounts in activated platelets and acts locally as a chemo-attractant for other platelets, leads to the formation of a platelet plug and induces localized vasoconstric
This document provides information on coronary artery disease and myocardial infarction. It discusses the causes, risk factors, clinical presentations, diagnostic tests, and treatments for angina and myocardial infarction. The major goals of care for a client experiencing a myocardial infarction are to initiate prompt care and minimize damage to the heart muscle.
Pharmacology of neuromuscular_blocking_drugs_and_anticholinesterases_totw_026...ermidebas
This document provides an overview of neuromuscular blocking drugs (NMBDs) and anticholinesterases. It discusses how NMBDs are classified as depolarizing or non-depolarizing. Suxamethonium is the only depolarizing drug and causes rapid onset of paralysis. Non-depolarizing drugs like atracurium and cisatracurium are competitive antagonists that bind nicotinic receptors. Anticholinesterases like neostigmine reverse non-depolarizing blockade by inhibiting acetylcholinesterase. The document outlines properties, indications, administration and side effects of various NMBDs and anticholinesterases.
This document discusses several key facts about heart disease:
- Living with others can lower heart attack risk by reducing stress and depression. Many heart attacks occur on Monday mornings when stress hormones spike in the morning. Sexual activity rarely causes heart issues due to its short duration.
It then provides information on coronary artery disease including non-modifiable risk factors like age and family history, and modifiable factors like smoking, obesity, and high cholesterol. Care and management of coronary artery disease includes lifestyle changes, medications like statins, and possible surgical interventions.
It concludes with sections on angina pectoris including types, symptoms, and drug treatments like nitroglycerin. Diagnostic tests and the nursing management of
The document discusses different types of shock including their causes, pathogenesis, and management. It defines shock as an imbalance between oxygen supply and demand resulting in organ dysfunction. The main types are distributive, cardiogenic, obstructive, and hypovolemic shock. Septic shock is discussed in depth including its pathogenesis involving an inflammatory response to infection, diagnostic criteria using SOFA and qSOFA scores, and elements of care including resuscitation, infection control, and supportive therapies. Cardiogenic shock is defined as a low cardiac output state resulting from various cardiac causes such as myocardial infarction. Hypovolemic shock reduces cardiac output through a decrease in preload from losses such as hemorrhage.
Antiarrhythmic drugs work by altering the conduction of electrical signals in the heart and changing the refractory periods of cardiac cells. They are classified into four classes based on their effects. Class IA drugs like quinidine and procainamide work by slowing the rise of the action potential upstroke, decreasing conduction velocity, and prolonging the refractory period. They have moderate potassium channel blocking effects. Class IA drugs are used for supraventricular arrhythmias and ventricular tachycardia but can cause toxicity like heart block or dangerous arrhythmias.
The document discusses the biological basis of cardiac repair after myocardial infarction. It notes that massive cardiomyocyte loss due to infarction overwhelms the heart's limited regenerative capacity, resulting in scar formation. Necrotic cells trigger an intense inflammatory response through danger signals and toll-like receptor signaling that recruits leukocytes. As inflammation subsides, fibroblasts proliferate and deposit collagen, maintaining ventricular integrity. Dysregulated inflammation, impaired resolution, or excessive fibrosis can cause adverse remodeling and heart failure. Modulating the inflammatory and reparative response may prevent post-infarction heart failure.
This document discusses angina pectoris, including its causes, types, and treatment strategies. It begins by defining angina pectoris as chest pain or discomfort caused by coronary heart disease when the heart muscle does not receive enough blood, usually due to narrowed or blocked arteries. It then describes the three main types of angina - classic, unstable, and variant - and their distinguishing features. The remainder of the document focuses on drug therapies for angina, explaining how organic nitrates, beta-blockers, and calcium channel blockers work to reduce oxygen demand or increase supply to relieve anginal symptoms. It provides details on the mechanisms and effects of these major drug classes and notes some of their potential side effects.
Ototoxicity refers to damage to the auditory or vestibular system caused by drugs or chemicals. Many known ototoxins cause cellular damage through generation of reactive oxygen species rather than direct action. The inner ear has limited regenerative ability, so ototoxic injury often leads to permanent hearing or balance problems. Exposure to industrial solvents and heavy metals can also cause ototoxicity. Noise exposure may increase the risk of ototoxicity by lowering the levels of chemicals needed to cause harm. Various antioxidants have shown potential to protect against ototoxicity in animal studies.
Chlorine gas is a pulmonary irritant that causes acute damage to the upper and lower respiratory tract. It has been used as a chemical weapon and is still involved in some attacks. Exposure to chlorine gas leads to inflammation of the airways and lungs and can cause pulmonary edema. Symptoms range from irritation to death depending on concentration. Treatment involves oxygen, fluids, bronchodilators, and corticosteroids. Prolonged effects are possible but most recover without long-term issues.
This document discusses the autonomic nervous system. It describes how the autonomic nervous system is divided into the sympathetic and parasympathetic nervous systems. The sympathetic nervous system is responsible for the "fight or flight" response and increases heart rate and blood pressure. Its neurotransmitters are epinephrine and norepinephrine. The parasympathetic nervous system is responsible for "rest and digest" functions and decreases heart rate and increases digestion. Its main neurotransmitter is acetylcholine. The document outlines the receptors, effects, and roles of the sympathetic and parasympathetic nervous systems on various organs.
1. Warfarin toxicity is caused by overdose or drug interactions that inhibit vitamin K recycling, preventing production of clotting factors. Bleeding is the main risk.
2. Treatment involves stopping warfarin, administering vitamin K1 to restore clotting factors, and plasma or PCC to rapidly reverse coagulopathy based on INR.
3. Superwarfarins require weeks of vitamin K1 due to their long half-lives. Activated charcoal may be given for recent ingestions. Monitoring INR guides further treatment.
This document discusses the mechanisms of action and pharmacological properties of nonopioid analgesics, including acetaminophen and nonsteroidal anti-inflammatory drugs (NSAIDs). It explains that these drugs inhibit the cyclooxygenase (COX) enzymes involved in prostaglandin synthesis, thereby reducing pain and inflammation. The document outlines the pathways involved in prostaglandin synthesis from arachidonic acid. It also describes the therapeutic effects and potential gastrointestinal, renal, platelet, and allergy-related side effects that can result from COX inhibition.
Chlorine gas is a pulmonary irritant that causes acute damage to the upper and lower respiratory tract. It has been used as a chemical weapon and is still involved in some attacks. Exposure to chlorine gas leads to inflammation of the airways and lungs and can cause pulmonary edema. Symptoms range from irritation to death depending on concentration. Treatment involves oxygen, fluids, bronchodilators, and corticosteroids. High risk patients may require hospitalization for monitoring due to risk of respiratory failure.
This document discusses adrenergic antagonists (sympatholytics) which inhibit the sympathetic nervous system by blocking adrenergic receptors or neurons. It describes various types of adrenergic blocking drugs that are selective for α and β receptors. Non-selective α-blockers like phenoxybenzamine cause irreversible blockade while phentolamine is competitive. Selective α1-blockers lower blood pressure with minimal effects on cardiac output. Orthostatic hypotension is a common side effect of α-blockers due to inhibition of venous vasoconstriction.
Toxicity of hydrocarbons can affect many organs but most commonly the lungs due to aspiration. Hydrocarbons are a diverse group of organic compounds including gasoline, oils, and solvents. Their physical properties like viscosity and volatility determine toxicity risk. Inhalation can cause pneumonitis while ingestion risks aspiration pneumonia. Symptoms include respiratory, CNS, cardiac, and GI issues. Treatment is supportive with monitoring for pulmonary or cardiac complications.
Drugs taken during pregnancy can directly harm the fetus, alter placental function, or induce preterm labor. Most drugs transfer through the placenta and reach levels in the fetus of 50-100% of maternal levels. Factors like timing and dose of exposure determine if a drug causes birth defects. While some drugs are known teratogens, effects of most are unclear due to challenges studying drugs in pregnancy. Careful risk/benefit analysis of medication needs during pregnancy is required.
This document discusses antidepressant drugs and their mechanisms of action. It begins by describing how antidepressants work by altering neurotransmitter systems like serotonin and norepinephrine in the brain. Several classes of antidepressants are then discussed, including MAOIs, TCAs, SSRIs, SNRIs, and NDRIs. Each works differently but generally aims to increase neurotransmitter activity in the brain. The document examines specific drugs in each class, their history, mechanisms, and common side effects. Mood disorders like depression and bipolar disorder are also briefly overviewed.
Lithium intoxication can cause mild symptoms like weakness and nausea or more severe symptoms like delirium, coma, and organ damage. Long term effects are also possible and include neurological issues like cerebellar dysfunction. Diagnosis involves checking the patient's history, measuring lithium levels in their blood, and conducting tests like ECG and bloodwork. Treatment focuses on hydration, electrolyte balance, gastric lavage, diuretics, and hemodialysis for moderate to severe cases to reduce lithium levels in the blood. Special care must be taken with fluid management in patients at risk for lithium-induced diabetes insipidus. Hemodialysis is the primary treatment for severe lithium toxicity due to lith
This document discusses emetics, which induce vomiting, and antiemetics, which prevent vomiting. It describes the physiology of vomiting including the vomiting center and chemoreceptor trigger zone in the brain. It explains the mechanisms and sites of action of various classes of antiemetic drugs including antihistamines, 5-HT3 receptor antagonists, dopamine antagonists, cannabinoids, glucocorticoids, and others. It provides details on specific antiemetic drugs like metoclopramide, ondansetron, dexamethasone, and their indications, mechanisms, pharmacokinetics and adverse effects.
Antifungal drugs work by targeting differences between fungal and human cell membranes and metabolism. Azoles like fluconazole inhibit ergosterol synthesis while polyenes like amphotericin B bind to ergosterol in the fungal cell membrane. Topical antifungals like nystatin and tolnaftate treat superficial infections while systemic drugs like fluconazole and itraconazole treat deep infections. Common adverse effects include nausea, liver toxicity, and drug interactions. The choice of antifungal depends on the infecting organism, infection severity, and route of administration needed.
Constipation is defined as infrequent and difficult bowel movements. It affects 2-27% of the population and has many potential causes. Treatment options include non-drug approaches like diet and exercise changes as well as various drug approaches using laxatives. There are several classes of laxatives including bulk-forming, emollient, hyperosmotic, saline, and stimulant laxatives. All laxative use requires monitoring for side effects and electrolyte disturbances.
This document provides an overview of Alzheimer's disease including its causes, symptoms, stages, diagnosis, and treatment approaches. It discusses how Alzheimer's is characterized by plaques and tangles in the brain made up of beta-amyloid and tau proteins. Current treatment aims to improve cognitive function and behaviors through cholinesterase inhibitors and memantine, though none can stop or reverse the disease. Non-pharmacological interventions like education, communication, and stimulation therapies may provide additional support.
Organophosphorous compounds work by inhibiting acetylcholinesterase, leading to overstimulation of muscarinic and nicotinic receptors. Signs and symptoms include muscarinic effects like excessive sweating, urination, and salivation ("DUMBELS") and nicotinic effects like muscle weakness. Treatment involves atropine to reverse muscarinic effects, pralidoxime to reactivate acetylcholinesterase within 48 hours, benzodiazepines for seizures, and supportive care like ventilation and fluid management. Measuring red blood cell acetylcholinesterase levels can help confirm exposure.
Drugs taken during pregnancy can affect the fetus in several ways. They may act directly on the fetus, altering the placenta's function, or causing uterine contractions. Factors like dose, timing and pharmacokinetics influence fetal effects, which range from no impact to death. While many drugs are relatively safe, careful risk-benefit assessment is needed due to variable and sometimes unknown risks. Precautions like using the lowest effective dose can help minimize harm to the developing fetus or newborn.
- Video recording of this lecture in English language: https://youtu.be/Pt1nA32sdHQ
- Video recording of this lecture in Arabic language: https://youtu.be/uFdc9F0rlP0
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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Kosmoderma Academy, a leading institution in the field of dermatology and aesthetics, offers comprehensive courses in cosmetology and trichology. Our specialized courses on PRP (Hair), DR+Growth Factor, GFC, and Qr678 are designed to equip practitioners with advanced skills and knowledge to excel in hair restoration and growth treatments.
Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
The UK is currently facing a Adhd Medication Shortage Uk, which has left many patients and their families grappling with uncertainty and frustration. ADHD, or Attention Deficit Hyperactivity Disorder, is a chronic condition that requires consistent medication to manage effectively. This shortage has highlighted the critical role these medications play in the daily lives of those affected by ADHD. Contact : +1 (747) 209 – 3649 E-mail : sales@trinexpharmacy.com
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
The skin is the largest organ and its health plays a vital role among the other sense organs. The skin concerns like acne breakout, psoriasis, or anything similar along the lines, finding a qualified and experienced dermatologist becomes paramount.
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
2. Tricyclic antidepressants
► Tricyclic antidepressants (TCAs) were one of the
most important causes of mortality resulting
from poisoning until 1993 and still continue to be a
major cause of death from self-poisoning.
► Although selective serotonin reuptake inhibitors
(SSRIs) have overtaken them to become first-line
therapy for depression, TCAs remain widely
prescribed for depression and an increasing
number of other indications including anxiety
disorders, attention deficit disorder, pediatric
enuresis, and chronic pain syndromes.
3. Pharmacokinetics
► They are highly protein bound
► have a large volume of distribution
► a long half life of elimination that generally exceeds 24
hours and in the case of amitriptyline is 31 to 46 hours.
► The ingestion of large quantities of tricyclics in self
poisoning causes altered pharmacokinetics.
► Gastrointestinal absorption may be delayed because of
inhibition of gastric emptying
► significant enterohepatic recirculation prolongs the final
elimination.
► The amount of unbound tricyclic may also increase if the
overdose causes respiratory depression resulting in an
acidosis, which reduces protein binding.
4. pathophysiology
The toxic effects of tricyclics are caused by
four main pharmacological properties:
►Inhibition of norepinephrine and seretonin
reuptake at nerve terminals.
►Direct α adrenergic block.
►A membrane stabilising or quinidine-like
effect on the myocardium; sodium channel
blocking.
►Anticholinergic action.
5.
6. ► The cardiovascular toxicity, which is the most common
cause of morbidity and mortality from TCAs, is related to
their sodium channel blockade and α-adrenergic blockade.
► TCAs bind to and inhibit the movement of sodium ions into
the fast sodium channel thereby slowing phase O
depolarization in the His-Purkinje system and ventricular
myocytes. This results in slowed cardiac conduction by
slowing the propagation of ventricular depolarization which
is manifested as a prolonged QRS on the ECG.
► Specifically, TCAs inhibit outward potassium current by
blocking potassium channels in phase 3, which ultimately
results in prolongation of the QT interval.
7.
8.
9.
10. ► Sinus tachycardia is the most common cardiac
disturbance seen following TCA overdose.
Competitive blockade at muscarinic receptors
plays a primarily role
► although norepinephrine reuptake inhibition also
contributes to the tachycardia and
hypertension.
► prolonged blockade can cause depletion of
norepinephrine from the presynaptic nerve terminal,
and inhibition of α1-adrenergic receptors which
results in the subsequent development of
refractory hypotension and bradycardia in cases
of serious overdose.
11. ►This hypotension can be exacerbated by
hypoxia, acidosis, and volume-depletion.
► Neurologic effects of TCAs, including
agitation and delirium, primarily result
from CNS blockade of muscarinic receptors.
►by impairing sweating heat dissipation is
reduced and this can result in a fever,
especially if seizures occur.
12. Clinical manifestations
►Clinical symptoms of antidepressant toxicity
often progress rapidly and
unpredictably, and, many times, patients
present asymptomatically or minimally
symptomatic and progress to life-
threatening cardiovascular and neurologic
toxicity within an hour.
13. NERVOUS SYSTEM
► Early manifestations include altered mental status,
delirium, psychotic behavior, and agitation,
and hallucinations. These symptoms can later
proceed rapidly to coma.
► Drowsiness, slurred speech, sedation (H1 block)
► Seizures are usually generalized and often occur
within 1-2 hours of ingestion.
► Seizures occurs in 4% of patients with overdose
and in 14% of fatal cases
15. ►Tricyclic antidepressant toxicity can be
caused by either an acute ingestion or a
chronic ingestion.
►Toxicity secondary to chronic ingestions
usually presents with symptomatology that
is an exaggeration of the usual side effects
of tricyclics.
16. TREATMENT
►ECG is the most important for diagnosis and
follow up.
►activated charcoal may reduce the
absorption of tricyclics and the benefits of
both single and multiple doses have been
described.
►
17. ►Dysrhythmias
- Sodium bicarbonate is the first-line therapy
if TCA ingestion is known or strongly
suspected (life saving)…………… why?
►Procainamide, quinidine, β-blockers, and
calcium channel blockers are
contraindicated.
►Lidocaine may show beneficial activity.
18. ►Hypotension
- Hypotension is treated with sodium
bicarbonate and intravenous fluids.
- Vasopressors are recommended for
refractory hypotension; best
norepinephnrine.
►Seizures
- Benzodiazepines
- Hemodialysis is not effective why?
19. Intravenous lipid emulsion (ILE) infusion
► The use of ILE as a potential treatment for drugs
in overdose arose from an extension of its use in
treating bupivacaine-induced cardiotoxicity.
► The discovery of the potential benefit of ILE as a
therapy for local anesthetic toxicity occurred from
a chance observation of a patient with a carnitine
deficiency who was undergoing anesthesia.
► The patient seemed to be particularly susceptible
to bupivacaine-induced arrhythmias.
20. ►An effort to link carnitine deficiency to the
underlying mechanism of bupivacaine
cardiotoxicity resulted in the discovery that
preloading with lipid seemed to be
cardioprotective, attenuating the adverse
hemodynamic effects of bupivacaine.
►
21. ► 1) In the “lipid sink” hypothesis, the infused lipid
acts as a pharmacokinetic drug compartment into
which lipid-soluble “sink” and are rendered
inactive.
► 2) Augmentation of cardiac energy supplies
through provision of excess substrate may
overcome the blockade of fatty acid transport into
cardiac mitochondria.
► (3) Direct activation of voltage-gated cardiac
calcium channels may increase cytosolic calcium
levels and improve cardiac performance.
22. SSRIs toxicity
► Selective serotonin reuptake inhibitors (SSRIs),
widely prescribed medications for the treatment of
depression, obsessive-compulsive disorder,
anorexia nervosa, panic disorder, anxiety, and
social phobia.
► have a high therapeutic to toxicity ratio.
► However, although they are associated with less
toxicity than tricyclic antidepressants, they are
often involved in co-ingestions that can precipitate
the potentially lethal serotonin syndrome (SS).
► fluoxetine (Prozac), sertraline, paroxetine,
citalopram, escitalopram, and fluvoxamine
23. ►SS represents a group of signs and
symptoms that manifest in the
neuromuscular, autonomic nervous, and
gastrointestinal systems, in which
concentrations of serotonin receptors are
the highest.
►Less frequently, SS can be precipitated by
an overdose of a single SSRI.
24. ► SS is often caused by combinations of SSRIs with
other proserotonergic agents, including the
following:
► Monoamine oxidase inhibitors (MAOIs)
► TCAs
► Trazodone (Desyrel)
► Serotonin-norepinephrine reuptake inhibitors
(SNRIs) Venlafaxine and duloxetine
► Norepinephrine-dopamine reuptake inhibitors
► Lithium
► Opioids
► Amphetamines and cocaine
25. pharmacokinetics
►SSRIs are metabolized in the liver by
cytochrome P-450
► They are highly bound to plasma proteins
and have a large volume of distribution.
Peak plasma levels are reached in 2-8
hours.
►Half life variable but about 22 hours. A
notable exception is fluoxetine
(Prozac) and its active metabolite,
norfluoxetine, which have half-lives of
2-4 days and 8-9 days, respectively.
26. Signs and symptoms
►serotonergic projections to the thalamus
and cortex result in effects on sleep-wake
cycles, mood, thermoregulation, appetite,
pain perception, and sexual function.
►Excess 5-HT in these pathways causes
1. mental status changes, confusion,
2. agitation, ataxia
3. Fever
4. Toxicity of descending pathways to the
brainstem and medulla results in
hyperreflexia, myoclonus, and tremor.
27. ►Autonomic nervous system effects include
diaphoresis, mydriasis, hypertension,
tachycardia, hyperthermia, piloerection, and
muscular rigidity.
►Cardiovascular effects most commonly
include sinus tachycardia, flushing,
hypertension, and in rare cases,
hypotension.
►Dose-dependent QT prolongation has been
reported with citalopram (Celexa).
28. ►Due to the high levels of serotonin in gastric
and intestinal mucosal enterochromaffin
cells, the most common minor adverse
effects of SSRI therapy are gastrointestinal;
eg, abdominal cramping, nausea, and
diarrhea.
►SSRIs have also been shown to moderately
increase the risk of upper gastrointestinal
bleeding.
30. ►Most cases fully resolve without residual
deficits if supportive care has been
provided.
►The prognosis is generally favorable.
►Most fatalities occur within the first 26
hours.
►Patients who remain asymptomatic for 6-8
hours after ingestion are unlikely to require
further treatment.
31. Patient education
►educated about symptoms of serotonin
toxicity and SS.
►Patients should be counseled about
potential interactions among any
medications they take—including over-the-
counter medications (particularly
dextromethorphan-containing cold
remedies), illicit drugs (especially
amphetamines, cocaine, and mescaline),
and herbal dietary supplements (eg, St.
John's wort, ginseng)—that might affect the
patient's tissue concentrations of serotonin.
32. ►A minimum of 2 weeks should elapse
between termination of an SSRI or MAOI
and initiation of a new one.
►Drugs with a longer half-life (ie, fluoxetine)
require up to 5 weeks of wash out.
►Elderly patients and those taking liver Mixed
Function Oxidases inhibitors may require an
extended wash-out period as well.
33. Managment
►ABCD
►Treat hyperthermia with cooling blankets,
fans, ice packs, and IV fluids. Antipyretics
are not indicated.
► Administer activated charcoal if a
potentially lethal amount or combination of
proserotonergic agents has been ingested
and if the presentation is within 1-2 hours.
►Treat neuromuscular abnormalities with
benzodiazepines.
34. ►Severely ill patients can be treated
pharmacologically with 5HT antagonists,
such as cyproheptadine.
►It is available only in oral form, which can
be crushed and infused via nasogastric
tube.
►Caution should be exercised in hyperthermic
patients, because cyproheptadine has
anticholinergic properties and theoretically
can worsen hyperthermia.
35. ► Autonomic instability requires treatment with
short-acting agents that are amenable to titration,
such as nitroprusside and esmolol.
► Treat rahabdomyolysis with aggressive hydration,
and alkalinize urine with sodium bicarbonate for
renal protection.
► Symptomatic patients with
citalopram/escitalopram overdose may require
admission to a monitored bed for 24 hours
because of the risk of delayed toxicity, which can
cause prolonged QT interval and consequent
cardiac dysrhythmias (eg, torsades de pointes).
36. Toxicity of MAOIs
►Two categories of MAOs exist: MAO-A and
MAO-B.
►The widely prescribed MAOIs are rather
unique in the fact that they bind irreversibly
(moclobemide is an exception, since it is a
reversible inhibitor) at their sites of action,
are eliminated from circulation by such
binding
►Additionally, MAOs are located in many
tissues, including the gut wall.
37. ►MAOIs absorbed through the
gastrointestinal tract bind significantly to
MAO in the gut mucosa and liver producing
significant first pass effect.
►MAO in the gut mucosa essentially breaks
down potentially toxic dietary monoamines,
such as tyramine, and "prevent" their
absorption.
►The inhibition of gut MAO by these
medications coupled with ingestion of
substances containing tyramine may
produce significant toxicity.
38. Tyramine-containing foods
► Aged cheeses
►Aged, pickled, or smoked meats (eg, salami)
or fish
►Yeast extracts
►Beer
►Red wine more than white wine
►Avocado
►Ginseng
39. ►Recently, a transdermal preparation of a
"selective" MAO-B drug, selegiline, has
appeared on the market, which by-passing
the first pass effect of gut and hepatic MAOI
effects, appears to produce antidepressant
effects with significantly reduced risk for
dietary-induced toxicity
40. MAOI poisoning is classified into
the following 3 subtypes:
►Actual poisoning from an overdose is
uncommon
►Drug-food interaction is so-called tyramine
reaction or cheese reaction. It is usually
rapid in onset, occurring within 17-90
minutes after ingestion. Most symptoms
resolve in 6 hours. Fatalities have been
reported due to complications from
hypertensive emergencies.
►Drug-drug interaction
41. Symptoms are that of increased
catecholamines activity
►hypertension, tachycardia, tremors,
seizures, and hyperthermia.
42. Managment
►Decontamination because of the potential
for severe toxicity and lack of antidotes, an
aggressive decontamination is very
important.
►Consider gastric lavage, particularly in
patients with recent ingestion (within an
hour).
►Administer charcoal: Secure unprotected
airway prior to lavage and charcoal
administration if needed.
►Hemodialysis is less effective
43. ►Fluid therapy is of paramount importance.
Patients may be significantly dehydrated
from hyperthermia.
►Hyperthermia:
►Tachycardia:
►Hypertension:
►Seizures:
44. Case
► A 10-kg, 20-month-old girl presented to the
emergency department of a district general
hospital 1 hour after ingesting her grandmother’s
medication, including 45 mg/kg dosulepin.
► At presentation, the patient was noted to be
drowsy but responsive to voice and had obvious
nystagmus.
► She subsequently developed a tonic-clonic seizure
and, despite rectal and intravenous administration
of diazepam, her seizures persisted.
► Thiopentone (5 mg/kg) was administered and
resulted in seizure termination.
45. ► Suxamethonium (2 mg/kg) was used to facilitate
tracheal intubation.
► A nasogastric tube was passed, gastric lavage was
attempted, and activated charcoal (1 mg/kg) was
administered.
► Electrocardiography showed narrow-complex
tachycardia with a rate of 130 beats per minute,
and the patient’s blood pressure was 80/40 mm
Hg.
► The patient’s QRS complexes began to broaden
progressively despite the administration of a
sodium bicarbonate infusion (8.4%; 10 mL diluted
in 500 mL of saline solution, initiated at 30 mL/
hour),
46. ►The patient developed ventricular
tachycardia with a rate of 180 beats per
minute, although her systolic blood pressure
was maintained at 80 mm Hg.
►In the presence of ongoing deterioration, an
intravenous lipid emulsion (ILE) was
administered.
►A bolus dose of 10 mL of ILE (1 mL/kg) was
administered.
47. ► followed by an infusion of 150 mL/hour (0.25
mL/kg per minute).
► Within minutes after administration of the ILE, the
patient’s QRS complexes began to narrow.
► Her heart rate continued to increase; when it was
200 beats per minute, her blood pressure
decreased to 60/30 mm Hg.
► A synchronized directcurrent shock of 50 J was
delivered, and narrow-complex sinus tachycardia
(150 beats per minute) was immediately restored
which was associated with return of the baseline
blood pressure
48. ► The ILE infusion was continued for 1 hour after
the bolus, to ensure extension of the infusion
period into the expected peak plasma
concentration period (which occurs 3 hours after
ingestion of dothiepin).
► The patient was transferred to the PICU and
remained in stable condition with narrow QRS
complexes and adequate blood pressure. She was
sedated, given ventilation, and monitored
overnight.
► The following day, she was extubated successfully
and had no additional neurologic or
cardiovascular complications.