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Intro to Toxicology
Pharm-II
| Question | Answer |
|---|---|
| A poisonous substance produced by a living organism or by products that must be excreated before reaching dangerous levels in the blood stream | toxin |
| A constellation of physical findings that support the clinical dx of poisoning | toxidrome |
| Are all toxidromes cut and ddry | no many have a very confusing picture |
| Two parts of the NS | ANS: SNS and PNS, and Somatic Nervous system |
| Two NMTs for PNS and SnS | PSN: Ach at preganclionic and ganglionic synpse, Ach and post ganglionic too SNS: Ach and NE |
| What are signs of a ↑ and ↓ PNS toxidrome | ↑: Cholinergic, ↓: Anticolingergic |
| What are signs for ↑ and ↓ SNS toxidromess | ↑: Sympathomiemetic ↓ Opiate/sedative |
| Name the 3 types of receptors cholinergics effect | Muscarinic, Nicotinic and central effects |
| What are the muscarinic and nicotinic S/S | DUMBBELS AND MTWHF |
| Why can chonlinergic effects be confusing | have both miosis and mydrasis, and brady, and tachy, can have agination and coma |
| Name 4 cholinergic agents | organophosphates (pestacides+ Carbamates (Physotigmine), mushrooms, nerve agents (sarin) |
| What cholinergic agent is very powerful and can cause dealth | sarin |
| What is the defining symptom of a anti-cholinergic toxidrome | hot but can’t sweat |
| Name some neumonics to remember anti-cholinergics | hot, blind, dry, red, mad, bloated from Uriniary retention |
| Other sxs of anti-cholinergic | tachy, HTN, fasiculations, sz, ileus |
| Atropine, scopolamine | anti-cholinergics |
| Benadryl | anti-histamines |
| Haldol | anti-psychotics |
| Compazine/Phenergan | anti-emetics |
| SSRIs and TCAs | antidepressants |
| Plants that have anti-cholinergic effects | jimson weed, deadly nightshade |
| Problem with the plant effects | they last a loooonnnngggg time |
| S/S of ↓ SNS | miosis, brady, HOTN, ↓ LOC and coma, ↓ RR and effort, Hypotonia, reflexia, ↓ bowel sounds (Everything DOWN) |
| What are examples of opiates/sedatives | morphine, oxycodone, methadone, barbituates, benzodiazepines, ethanol |
| Defining symptoms for SNS and ↑ PNS | hot and SWEATY |
| S/S of ↑ SNS | hyperthermia, HTN, tachy, mydriasis, Uriniary retention, psychosis, Sz diaphoresis, Hyperactive bowel sounds |
| SNS stimulants | cocaine, amphetamine, MDMA, PCP, epi, psuedoepi, thophallin, caffeine, withdraws (alcohol benzos) |
| Serotonin syndrome | changes in both SNS and PNS |
| How do we classify serotonin syndrome | 1-2 sxs from each pathway |
| 3 pathways in SS | cognitive/behavioral, NMT, ANS |
| Why does serotonin syndrome usually occur | OD on more than one agent |
| 4 causes to SS | Drings inhibit seratoninc breakdown, prevent synaptic reuptake, agonize serotonin receoptors, ↑ serotonin release |
| Drugs that inhibit serotonin breakdown | MAOIS, linezolid: abx |
| Drugs that prevent synaptic reuptake of serotonin | SSRIS, cocain, dextromethorphan, TCAs, trazodone, venlafzxine, st. johns, wort, tramadol |
| Drugs that agonize serotoninc receptors | LSD, buspirone |
| Drugs that ↑ serotonin release | lithium, amphetamines, MDMA |
| How long does it take for SS to occur | minutes to hours |
| Tx of a poisoned [pt | BLS, ALS, PALS, ABCs, |
| Labs to order with poisoned pt | blood, chem 7 coags, LFTs, CPK, serum osmolaryt, abg UA, serum levels of salicylate, and APAP |
| When do we decide drug levels | will it help my tx? |
| Drugs to tx cholinergic OD | atropine and pralidoxime |
| MOA of atropine | dry out resp. secretions, competitive inhibition of ACH at active sites |
| MOA of pralidoxime | breaks covalent bond w/ active site on ACH-ase, commonly indicated for organophophate poisioning, |
| Tx for anti-cholinergic OD | diazepam, and manage anxiety/agitation, Sz? Hyperthermia |
| Dangerous AE’s | sz and hyperthermia |
| Txx of opiates/sedative OD | narcan or naloxone |
| How does narcan work | competitive inhibition |
| If od on opiates and sedatives and they are cancer patients or post-surg what do we do | may not want to reverse at all, just monitor and maintain airway |
| What is another agent to tx opiate/sedative OD | flumazenile: competitive reversal? |
| Severe complication w/ flumazenil w/ chronic users | may induce sz’s and those who use therapeutically. |
| Tx of sympathomimetic OD | diazepam and cooling, antipyretics |
| What is an actual antidote to a serotonin syndrome like OD | cyproheptadine |
| MOA of cyproheptadine | anti-hisamine, blocks serotonin, apetite stimulant |
| Management with this drug | szs and hyperthermia |
| 3 types of GI decontamination | Activated charcoal, gastric lavage, whole bowel irrigation |
| MC GI decontam | Activated charcoil |
| What is activated charcoal not useful fore | Iron, lead, lithium, alcohol, corossives, hydrocarbons |
| CI for activated charcoal | high risk for aspiration or w/ impaired gastric motility/ilius |
| Fxns of sorbitol | pulls fluid into gut, DON”T use in elderly or dehydrated, or children, or alone as tx (HYDRATE) |
| What is a gastric lavage and use | 2-4L+ into stomach NS and pumped back out, (effective w/I 1st hour) not as common |
| Risks of gastric lavage | hypothermia, electrolyte imbalance, mechanical damage to esophagus, aspiration, laryngospasms |
| CI for gastric lavage | if at anytime the pt’s airway might become compromised, hydrocarbans and corrosives (usually intubated w/ large tube) |
| What is used for whole bowel irrigation | polyethylene glycol |
| Indications for WBI | OD on extended release medications or those drugs that don’t bind charcoal |
| CI for WBI | GI bleed, ilius, obstruction, perforation |
| What happens w/ acetainphen tox | liver failure w/ hypoglycemia, jaundice, R upper quadrant pain, coagulopathy, can lead to DIC coma dealth |
| How does liver failure occur | nl metabolisms produces a little bit of NAPQI, excess produces too much, causes tox and necrosis |
| What drug measurement do we want to get to know tx | 4hr level of drugs of APAP level |
| NAC | N-acytyl cystine |
| How do we know if our pt needs NAC | chart: hours compared to blood level |
| Dosage for NAC | q 4 hrs, 17 doses dilueted w/ juice (tastes awful) |
| Two types of anticholinesterase insecticides OD | carbamate (more revisable coavalent bond w/ Ach-ase) and Organophosphate (bond becomes reversible over time) |
| Initial management of an organophosphate OD | decontaminate the pt and your self |
| Antidotes to anti-ach | atropine, pralidoxime (2-PAM) |
| What happens when don’t give enough 2-PAM early on | major pitfall in tx of oraganophoshate OD |
| Probs w/ CCB OD | vasodilation, ↓ cardiac contractility, ↓ conduction velocity |
| Other effects of CCB | impair insulin release→hyperglycemia, impaired cellular metabolism especially in cardiac metab |
| Tx CCB OD | ABCs, supportive, tx HOTN/brady w/ NS, dopamine, epi, atropine |
| What should we consider w/ CCB OD | GI decon |
| Tx w/ persistent HOTN | IV calcium choloride , may have to give insulin +dextrose |
| How does glucagon help CCB OD | ↑ cardiac fxn and help w/ HOTH and brady |
| Initial iron tox signs | N/V/D GIIIII!!!! Followed by abscente of sxs for 6-48hrs |
| Later signs of iron tox | maybe continued GI, ↓ perfusion, UO, severe tox, hepatic injury, coagulopathy, hypoglycemia, acidosis, cards shock, sz, coma, ARDS |
| Complication of iron tox | GI tissue necrosis |
| Why can sepsis happens w/ iron tox | breakdown barrier in GI tract |
| Tx iron tox | WBI? But need IV deferoxamine ASAP |
| When should we give defroxamine | s/s iron tox, or no s/s but iron concentration >500mcg/dL |
| What is defroxamine | chelation agent, makes a complex that is dialzable |
| AE’s of this | turns urine red/orange, continue to give it past the nl of urine |
| Effects of TCA tox | inhibition of fast Na+ channels: ↓ MC depolarization, QRS widening, AV block, Vtach, ↓ MC contractility, HOTN d/t block of alpha receptors, show anticholinergic effects |
| Severe complications w/ TCA tox | can lead to coma/dealth in 1-6hrs |
| Tx of TCA OD | bicarb bicarb, bicarb |
| How do we think about tx of poisended pt | ABCs, support, BLS, ALS< PALS, then toxidrome? Antidote? |
Created by:
becker15
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