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122 Cards in this Set
- Front
- Back
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What is an example of an airway injury?
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Caustic ingestions
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A = AIRWAY
What are examples of situations when there is an inability to protect the airway? |
When someone has taken 1. Sedative hypnotics, 2. Opioids, 3. Anticonvulsants
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B = Breathing
What drug might have been taken when breathing is too slow, too fast or when wheezing is occurring? |
Too slow = Opioids
Too fast = Aspirin, Salicylate hydrocarbons Wheezing = Organophosphates/Pesticides |
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C = Circulation
Low blood pressure examples? CCB, BB, D High blood pressure examples? S, C, M |
Low blood pressure examples = Calcium channel blockers, beta blockers, digoxin
High blood pressure examples = Strokes, Cocaine, Methamphetamine |
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D = Disability, Dstick
Altered Mental Status examples? Low Blood Sugar examples? |
Altered Mental Status = Sleepy, comatose, Agitated as seen with PCP, Hallucinating which can be seen with benadryl. These can be measured on the glasgow coma scale.
Dstick is a bedside dextrose check for low blood sugar. Low blood sugar can be a reason for altered mental status, causes can also be oral hypoglycemics, sulfonylurias and insulin overdose |
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E = Exposure
What should be done to reduce exposure? |
Take off the patient's clothes, look in the pockets for drug bottles and needles. Look for other injuries.
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What is associated with the anticholinergic toxidrome?
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Hot as a hare, mad as a hatter, blind as a bat, dry as a bone, and red as a beet.
1. Febrile, warm to touch 2. Agitated delirium, hallucinations 3. Mydriasis, very dilated pupils 4. Dry skin and mucous membranes (can't sweat) 5. Flushed |
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What are examples of drugs that cause the anticholinergic toxidrome?
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Diphenhydramine, Tricyclic Antidepressants, Atropine, Jimson Weed
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What are the signs for the cholinergic toxidrome?
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D - Diarrhea
U - Urination M - Miosis = small pupils B - Bronchorrhea B - Bronchospasm E - Emesis L - Lacrimation S - Salivation |
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What are examples of drugs that will cause cholinergic toxidrome?
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Nerve gases, organophosphates, alzheimer's meds = cholinesterase inhibitors.
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The opioid toxidrome is characterized by what?
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CNS depression, respiratory depression, miosis = small pupils, bradycardia, hypothermia
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What are examples of drugs that cause the opioid toxidrome?
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morphine, methadone, heroin, and suboxone.
NOTE: Suboxone is a pretty pill that tastes nice and causes opioidtoxicity, kids are attracted to it. |
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What is a hallmark of the opioid toxidrome?
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Respiratory depression.
NOTE: Opioid deaths are a huge problem in Massachusetts |
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Sedative hypnotic toxidrome is characterized by?
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CNS depression, Respiratory depression, midsize or small pupils, bradycardia
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What are examples of substances that cause sedative hypnotic toxidrome?
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Benzodiazepines, barbiturates, alcohols.
NOTE: Benzodiazepines usually won't kill you, but benzos in combination with ETOH etc. cause death. |
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Sympathomimetic Toxidrome is characterized by?
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Agitated, mydriasis = large pupils, hyperthermia, hypertension, tachycardia, diaphoresis, normal to increased bowel sounds.
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What are examples of substances that cause sympathomimetic toxidrome?
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Cocaine, amphetamines, pseudophedrine, also seen in kids who abuse ADHD medications
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Seratonin syndrome is characterized by what?
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A triad of autonomic instability, hypertension, and tachycardia. Mental status changes = agitation to coma, neuromuscular hyperactivity: clonus and hyperreflexia, lower extremity much greater than uper extremity.
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What would possibly cause seratonin syndrome?
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Exposure to pre-serotenergic meds: SSRIs, MAOI, Lithium, Linezolid = ABX, Tramadol, Meperidine etc.
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How do you differentiate between the anticholinergic toxidrome and the sympathomimetic toxidrome? In regards to skin exam and bowel sounds?
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SKIN EXAM
Anticholinergic = Dry and flushed Sympathomimetic = Diaphoretic BOWEL SOUNDS Anticholinergic = Decreased Sympathomimetic = Normal |
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TCA Types
CANDID |
Clomipramine
Amitriptyline Nortriptyline Doxepin Imipramine Desipramine |
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Less common TCA types, most likely seen in other countries
DPTL |
Dothiepan
Protriptyline Trimipramine Lofepramine |
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TCA combination meds:
LT |
Limbitrol: Amitriptyline and chordiazepoxide
Triavil, Etrafon: Amitryptiline and perphenazine |
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What drugs will cause a false positive TCA screen? Quiet Car Cycle Anti Phenos = Thio chlor per trime
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Cyclobenzaprine
Carbamazepine Quetiapine Antihistamines = diphenhydramine, cyproheptadine Phenothiazines = Thioridazine, chlorpromazine, perphenazine, trimeprazine NOTE: Benadryl has two rings, but can cause a false + TCA screen. |
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TCA Pharmacokinetics:
Demethylation (active metabolites) I to D A to N Hydroxylation (CYP 2D6) D to 2-H N to 10-H Drug/Drug CYP1A2 - Cim Cip CYP2C19 - Keto CYP2D6 - Cim |
Demethylation:
Imipramine to desipramine Amitriptyline to nortriptyline Hydroxylation: Desipramine to 2-hydroxydesipramine Nortripytyline to 10-hydroxynortyriptyline Drug/Drug = CYP1A2 - cimetidine, cipro CYP2C19 - Ketoconazole CYP2D6 - Cimetidine |
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What is the Mnemonic for TCA?
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T = Tremor
C = Cardiovascular A = Anticholinergic |
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What are drugs that can cause QRS widening, ie. differential diagnosis = antiarrhythmics.
Class 1A = Pro, Dis, Qui Class 1C = Flec, En, Pro, Mor |
Class 1A = Procainamide, Disopyramide, Quinidine
Class 1C = Flecainide, Encainide, Propafenone, Moricizine |
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Drugs that cause QRS widening, ie. non antiarrhythmics.
Car, Coc, Chlor, Anti thio meso, Di Di Pro Beta |
Carbamazepine
Cocaine Chloroquine Antipsychotics (thioridazine/mesoridazine) Digoxin Diphenhydramine Propoxyphene Beta-Blockers |
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What are non-drug causes of QRS widening?
Hyper cardiac cardio, cardiac hypo |
hyperkalemia
cardiac ischemia cardiomyopathy cardiac conduction system disease hypothermia (J wave) <33 degrees celsius |
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MAOIs
Par Pro Phen, Sel Tran, Bro Fur Is, Moc Nial |
Pargyline
Phenelzine Procarbazine Selegiline Tranylcypromine Brofaromine Furazolidone Isocarboxazide Moclobemide Nialamide |
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Which MAOIs are reversible and don't cause as much toxicity?
Phen Bro Moc |
Phenelzine
Brofaromine Moclobemide |
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MAOIs are used to treat what?
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Depression, vascular headache, narcolepsy, panic disorders, OCD, PTSD, and Phobias
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What is a clinical presentation of mild MAOI intoxication?
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Anxiety, flushing/headache, tremors/myoclonus/shivering, tachycardia, tachypnea
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What is a clinical presentation of severe MAOI intoxication?
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Hypertensive crisis which can lead to intercranial hemorrhage, delirium, and hyperthermia. NOTE: Must get BP down!!!
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MAOI TX:
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ABC's
D = Decontamination - Gastric lavage, and activated charcoal HTN: Catecholamine mediated - phentolamine: alpha adrenergic blocker, labetolol: nonselective a/b blocker, nitroprusside: vascular smooth muscle. Agitation - benzodiazepines Rhabdomyolysis - IVF +/- bicarb, urine output Hyperthermia - cool exam room, tepid water/sponging/fanning, ice water gastric/colonic lavage, sedation, paralysis |
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SSRIs
Flu Flu Par Sert Cit Escit |
Fluoxetine, Fluvoxamine, Paroxetine, Sertraline, Citalopram, Escitalopram
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SRIs
Nef Traz Ven Dul |
Nefazodone S, A
Trazadone S, A Venlafaxine S, N, D Duloxetine S, N |
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What are the four potential mechanisms that lead to seratonin syndrome?
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No breakdown: MAOIs
Increased Release: MDMA Percursor/Agonist: Li, LSD, Tryptophan, Buspirone Block Reuptake: SRIs, TCAs, Opiates, Cocaine |
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Differential diagnosis for Seratonin Syndrome?
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Malignant Hyperthermia
Neuroleptic Malignant Syndrome Withdrawal: EtOH/Sedative Hypnotics Heatstroke Thryotoxicosis Meningitis/encephalitis |
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How does Neuromuscular Malignant Syndrome differ from Seratonin Syndrome?
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Dopamine, Chronic (days), "Iron Pipe"
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SRI treatment
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ABC's
D = Decontamination - Activated Charcoal Agitation - Benzodiazepine Rhabdomyolysis - IVF Hyperthermia |
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What are the Seratonin, 5HT-2A antagonist?
Cyp Methyl |
Cyproheptadine and Methylsergide
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What is the main problem with Bupropion overdose?
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Seizures, and will give a false + amphetamine screen
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What are the main toxicities of Mirtazapine?
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Sedation which leads to coma
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Salicylates cross the blood brain barrier slowly unless?
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there is a condition of acidosis
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RANGE OF TOXICITY, SALICYLATES:
Therapeutic Serum Levels? Home Treatment-Accidental? Mild? Moderate? Severe? |
Therapeutic Serum Levels = 10-30
Home Tx-Accidental = 150 Mild = 150-300 Moderate = 300-500 Severe = >500 |
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What are the mild/moderate symptoms of salicylate toxicity?
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Tinnitus, letheragy, N/V, respiratory alkalosis, tachypnea/hyperpnea, metabolic acidosis, fever, fluid and electrolyte abnormalities
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what are the severe symptoms of salicylate toxicity?
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Hypotension, coma, seizures, encephalopathy, pulmonary edema, acidemia, coagulopathy, cerebral edema, and dysrhythmias
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This develops within 3-4 hours of significant salicylate ingestion. Due to increased production of pyruvic and lactic acid, increased lipid metabolism, inhibition of aminotransferases.
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Anion gap metabolic acidosis
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Tx of accidental ingestions of salicylate?
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150-200 mg/kg may be managed at home with dilution and observation
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Greater than 200 mg/kg of salicylates are Tx how?
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Referred to ED for AC and salicylate levels. Levels are obtained every two hours until you get two levels that are less than 30 mg/kg. Peak levels may be delayed by six hours or more with tablets, and 12 hours or more with enteric coated preparations.
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What do you do if salicylate levels start to rise again later after Tx has already been given?
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Re-administer AC, could be due to a Bezoar or because of coated extended release tablets.
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Apart from giving AC and measuring salicylate levels, what are other options of Tx?
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Lavage may be used if performed soon after ingestion, Repeat AC with very large ingestions if bezoar is present, consider whole bowel irrigation in conjunction with repeat AC in large overdoses with enteric coated formulas, correct acid base, fluid and electrolyte distrubances. Balance hypotnoic saline solutions with dextrose and K along with sodium bicarb. Urine alkalinization
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When do you use hemodialysis in salicylate toxicity?
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When a patient has acute levels >80-90 or chronic levels over 50. Also, when there is refractory acidosis, severe CNS symptoms ie. seizure and coma, pulmonary edema, renal failure, and when a patient continues to deteriorate despite appropriate therapy.
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This is produced by the mixed function CYP450 enzymes, it is normally rapidly detoxified by glutathione in the liver cells. IN overdose, production fo the metabolite overwhelms the glutathione supply and this reactions with the hepatic ells causing cell death.
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NAPQI - Acetaminophen metabolite
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What are the factors that affect hepatotoxicity of acetamenophen?
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Decreased glutothionine stores caused by malnutrition and anorexia. This can also be seen in people who abuse alcohol. Often times they are malnourished because they receive the bulk of their carbohydrates from EtOH. Inducers of CYP1A2 and 2E1 include ethanol, carbamazepine, phenytoin and INH = Isoniazid
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What are the toxic doses of acetamenophen in children and adults?
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Acute ingestions of 150-200 mg/kg in children, or 7.5g in adults. Chronic toxicity has been seen with ingestion of high therapeutic doses 4-6g/day in high risk patients. Toxicity has been seen with children taking 60-150 mg/kg/d for 6-8 days
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How many phases are associated with acetamenophen toxicity?
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4
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What is phase 1 of acetamenophen toxicity?
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Phase 1: 0.5-24hours - Anorexia, N/V, frequent (early), malaise. Transaminases may be elevated but essentially a normal or asymptomatic appearance.
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What is a sign in phase 1 that you have hepatotoxicity?
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If you have vomiting within 8-10 hours of ingestion than this is a sign of hepatotoxicity.
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What is phase 2 of acetamenophen toxicity?
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Phase 2: 24-72 hours - Anorexia, N/V may resolve, Renal function compromise, abdominal pain, transaminases continue to rise - in patients who recover they may peak between 48-72 hours, and may be as high as 50,000 Iu/L - AST/ALT elevation over 1000 Iu/L commonly seen within 24-72 hours after overdose, with changes in PTT and bilirubin
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What is phase 3 of acetamenophen toxicity?
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Phase 3: 72-96 hours - Sequelae of hepatic necrosis, renal failure, jaundice, hepatic encephalopathy, coagulation defects. Centrilobular necrosis (where NAPQI is generated). Periportal sparing seen on biopsy. Death due to multiorgan failure.
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What is phase 4 of acetamenophen toxicity?
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Phase 4: 4-14 days - Surviving patients show complete resolution of hepatic dysfunction.
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How is acetaminophen Tx carried out?
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put levels measured over 4 hours on the Rumack nonogram to measure what Tx. is necessary. If less than 3-4 hours since exposure give AC, if extended release and over 3-4 hours than give AC, otherwise you use NAC either the 72, 48 or 21 hour protocol.
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What are the four very important insecticides?
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Organophosphates, Carbamates, Organochlorines, and Pyrethrins
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Organophosphates Group 1?
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Posphorylchlorines, X = Quartenary Nitrogen, used as weapons of war, MOA stimulates cholinergic receptors, acts as cholinesterase inhibitors
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Organophosphates Group 2?
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Fluorophosphates, X = Fluorine, example Sarin gas.
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Organophosphats Group 3?
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Cyanide or Halogen, except fluorine, cyanophosphates: Tabun
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Organophosphates Group 4?
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Largest group, majority are dimethoxy or diethoxy, mostly insecticides: Malathion and Parathion
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What are the symptoms of muscarinic toxicity?
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Not Ion mediated, but G-protein mediated.
DUMBBELS |
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What are the symptoms of nicotinic toxicity?
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Na channel mediated.
MCPHT Muscle Fasciculations, Cramps/weakness, Paralysis, High Blood Pressure, Tachycardia |
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Organophosphate Tx.
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ABC's
Bronchorrea or excess oral secretions oxygenate and use atropine. Atropine only works at muscarinic sites. Also, intubate, using a nondepolarizing NM blocker. Circulation - IV fluids >2L or more due to diarrhea. Tx Seizures, gastric emptying if toxin ingested. Give antidote. |
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What is the antidote for organophosphate poisoning?
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Atropine and 2-Pam
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What are a few temporizing measures you can use to help in organophosphate toxicity?
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Give pt. diphenhydramine for antimuscarinic effects. Give glycopyrrolate to help lessen CNS penetration.
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Where does pralidoxime has its most significant effects?
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Nicotinic sites, it causes an improvement in muscle strength. It also works very well at muscarinic sites. Has a bigger Vd and T1/2 in sick patients.
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What are fast rates of pralidoxime administration associated with?
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Cardiac arrest.
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What are two things that can happen as delayed effects from organophosphates?
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Intermediate syndrome - Weakness after initial improvement (1-4 days), Bulbar, respiratory and proximal muscle weakness which resolves in 2-3 weeks. This may be due to inadequate pralidoxime presence.
OPIDN - Organophosphate induced delayed neuropathy - Occurs 1-3 weeks out, Parasthesias then distal flaccidity, agent-specific, Possible Inhibition of neuronal target esterase |
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This is a derivative of Physostigma venenosum Balfour?
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Carbamates - Calabar bean alkaloid
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What is the MOA for Carbamates?
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Bind to serine residue on AChE, same effects as organophosphates, carbamate-AChE bond, not as strong, hydrolysis/decarbamylation occur more readily, AChE reactivated in 2-4 hours, no aging like organophosphates
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Carbamates have the same symptoms as organophosphats except?
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Altered mental status, and depression of RBC cholinesterase is not as long. Symptoms usually resolve within 24-48 hours and the plasma elimination T1/2 is 1-2 hours.
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Tx for carbamates
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ABC, Atropine, Pralidoxime
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Organochlorines 4 categories?
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Hexachlorocyclohexane (Lindane)
DDT Cyclodienes Mirex and Chlordecone |
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Which Organochlorines are well absorbed via the skin?
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Lindane and cyclodienes
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Organochlorines are primarily metabolized CYP 450, most of them act as?
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Inducers.
They are lipophilic and bioaccumulation is dependant on rate of metabolism. Biliary excretion and enterohepatic circulation occur. |
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What is the MOA of DDT?
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Delays closing of Na channels and prevents opening of K channels. This leads to repeated action potentials, temors, and exaggerated startle reflexes.
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Which organochlorine, when under chronic exposure, a patient will experience neurotoxicity, tremors/startle response, Kepone Shakes, reproductive toxicity?
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Chlordecone
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Which organochlorine has been shown to be estrogenic with a possible link to breast cancer, as well as a cause of aplastic anemia and leukemia
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DDT
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How do you diagnose organochlorines?
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History is most important
Chlorinated hydrocarbons are radiopaque Gas Chromatography for confirmation, no correlation derived for levels and effect. |
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Tx for organochlorines?
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Decontamination: Soap and Water
Protection for caretakers Protect Airway Intentional Ingestion: NG evacuation Charcoal Cholestyramine - interupts enterohepatic circulation. Seizures Due to GABA inhibition - Benzos - GABA agonist. Barbiturates can be used but there is a greater risk of respiratory depression. Treat hyperthermia and rhabdomyolysis. |
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Pyrethrins are? Pyrethroids are? What are these derivatives of and what is the MOA?
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Pyrethrins are natural extracts and Pyrethroids are synthetic extracts. They are derivatives of the chyrsanthemum flower. They are lipophilic but rapidly metabolized. Their MOA is Na channel blockade.
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Pyrethrins/Pyrethroid Tx.
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Decontamination of Skin
Activated Charcoal Treat Allergic RXN Benzos for seizures or neurologic Sx, follow with phenytoin A-tocopheryl (Vit. E) useful for parasthesias |
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Rodenticides are?
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ANTU, Ba Carbonate, Cyanide, Strychnine, and Vacor
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Strychnine MOA
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Antagonism of glycine in spinal cord. Glycine is an inhibitory neurotransmitter. So, muscle spasm, opishotonos, risus sardonicus, Seizures occur.
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What differentiates Strychnine toxicity from tetanus?
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The mental status change is more profound
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What is the LD in humans, and the T 1/2 of strychnine?
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LD in humans = 1-2mg/kg (50-100mg) and the T 1/2 = 10-16 hours, undergoes hepatic metabolism
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What is the Tx for strychnine toxicity?
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Restore inhibition - pt. in dark room, minimal stimuli, benzos, barbiturates, paralysis and intubation. Use a non-depolarizing agent to intubate.
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This rodenticide has been off the market since 1979, less than 10 exposures yearly, it is an analogue of niacinamide that interrupts ox phos and intermediary metabolism.
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Vacor
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What is a specific problem with Vacor
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Destroys pancreatic B cells which leads to Insulin Dependent Diabetes Mellitus. Also, orthostasis, autonomic and peripheral neuropathy
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How do you Tx. Vacor toxicity?
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Niacinamide and insulin for hyperglycemia
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Superwarfarins cause what?
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Elevation of PT/INR, Bleeding. block vitamin K 2-3 epoxide reductase leading to the inactivation of clotting factors and vitamin K.
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What are the most effective ingestions of superwarfarin?
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Large single ingestions or multiple small ingestions.
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Tx. of Superwarfarin toxicity?
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ACCP guidelines for elevated INR
Vitamin K FFP Fresh Frozen Plasma -Replaces clotting factors, risks of blood products, only for bleeding or high risk of bleed. |
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What are the big five CYP 450's
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1A2
2D6 2E1 3A4 2C19 |
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CYP1A2 accounts for approximately 15% of drug metabolism.
Substrates? HINT T.C.A. TCA C Inducers? CP Barbacue Smoke Inhibitors? GECC |
Substrates: Theophylline, Caffeine, Acetaminophen, TCAs, Coumadin
Inducers: Charbroiled Food, Tobacco Smoke, Carbamazepine and Phenobarbital Inhibitors: Grapefruit Juice, Erythromycin, Ciprofloxacin, and Clarithromycin |
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What is the most extreme example of the serotonin syndrome?
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an MAO inhibitor with meperidine or dextromethorphan.
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What is a metabolic seratonin precursor?
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L-Tryptophan
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What is a drug that inhibits seratonin metabolism?
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MAOI
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What are drugs that increase seratonin release?
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Amphetamines, lithium, MDMA
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What drugs inhibit seratonin reuptake?
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Cocaine, dextromethorphan, meperidine, SSRIs, TCAs, Trazadone, Venlafaxine
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What drugs act as serotonin receptor agonist?
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buspirone, LSD-Lysergic Acid
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What drug acts as a dopamine agonist?
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L-Dopa
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CYP2D6
Substrates? CDSE Inducers? Inhibitors? CSA |
Substrates: Codeine, Dextromethorphan, SSRIs (particularly paroxetine) and Ecstasy
Inducers: None Known Inhibitors: Cimetidine, SSRIs, amphetimine class agents including ecstasy |
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CYP2D6 possesses marked heterogeneity (10 fold difference in activity) this is responsible for the lack of what in select patients?
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Codeine analgesia
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CYP2E1
Substrates: AE Inducers: ICE Inhibitors: D |
CYP2E1
Substrates: Acetaminophen, Ethanol Inducers: Isoniazid, Carbamazepine, Ethanol Inhibitors: Disulfram |
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What can increase the risk of APAP hepatotoxicity?
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INH, CBZ (tegretol) and ethanol
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What are the special instructions that should be given to anyone discharged who is taking APAP?
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Never "around the clock" or "until fever breaks"
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Which CYP accounts for the largest fraction of CYP activity?
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CYP3A4
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CYP3A4
Substrates: CCATSS Inducers: CDGPPNR Inhibitors: KIMPCG |
CYP3A4
Substrates: Amiodarone, Carbemazepine, Cisapride, Sildenafil, Steroid hormones, Theophylline Inducers: Carbamazepine, Dexamethasone, Griseofulvin, Phenobarbital, Phenytoin, Non-nucleoside reverse transcriptase inhibitors (nevirapine), Rifampin Inhibitors: Cimetidine, grapefruit juice, Itraconazole, Ketoconazole, Macrolides, Protease inhibitors |
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CYP2C19 metabolizes a large portion of what?
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Pyschotropic agents
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CYP2C19
Substrates: TCAs, CD Inducers: R Inhibitors: FF |
CYP2C19
Substrates: TCAs, Citalopram, Diazepam Inducers: Rifampin Inhibitors: Fluoxetine and Fluvoxamine |
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Drugs that cause prolonged QT syndrome/Torsades
PCCEHQVTTACP |
Phenothiazines, Cisapride, Clarithromycin, Erythromycin, Haloperidol, Quetiapine, Venlafaxine, Tricyclics, Terfenadine, Astemizole, Citalopram, Procainamide
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With antidepressants, the medical history should span how many weeks?
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Six
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