Toxo Final Durgs MOA and or toxin 2

wilsbach's version from 2016-04-28 20:28

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Question Answer
*most time sensitive tox?Ethylene glycol
flush eyes directionmedial to lateral
CI gastric evacCaustic agents, Petroleum based product (Abolishes gag reflex), Neuro patients (No airway protection), Recent abdominal surgery, Cardio unstable patients
H2O2 MOA?peripheral irritation of gastric mucosa--> emesis
ipecac syrup MOAalkaloids central(CRTZ) and peripheral(irritation) emesis induction
emetic of choice for dogsapomorphine hydrochloride
apomorphine MOA/reversalcentrally act on CRTZ (iv or conjunctival admin) ... might cause sedation and stuff but can reverse with naloxone
emetic of choice in cats?alpha 2 agonist ie xylazine
MOA xylazine/reversalcentrally acting emetic, reverse with yohimbine if you see Bradycardia, arrhythmias, muscle tremors
polyethylene glycol used forit is osmotically balanced for whole bowel irrigation
measure tubes going into stomach to what rib?13th
big risk with gastric lavageaspiration pneumonia
activated charcoal doesnt work on?xylitol, alcohols, acids or bases
Saccharides (sorbitol) used for?CATHARTICS-- metabolized to fructose, works osmotically, might risk dehydration and inc Na conc in body
magnesium sodium citrate used for?CATHARTIC: (Studies show sorbitol acts quicker than saline)
how many times to admin catharticsONLY ONCE
hemodialysis is particularly helpful for... (2)ethylene glycol and acetominophen
why would you inject soya bean oil into a pt?IV lipid therapy-- do for lipophilic drug tox (avermectin, LAs, beta blockers, antidepressants, Ca++ channel blockers)
K1 dependant clotting factors need K1 activates their pro-forms (2,7,9,10)
2 first gen anticoagswarfarin and Diphacinone.
2 second gen anticoagsBrodifacoum, Bromadiolone (two bros)
why we care if first vs second gen anticoagsecond gen lasts WAY LONGER (when in doubt tx 3-4kwk)
how long for anticoag to show up2-3d
dog comes in coughing. what should you suspectanticoag tox. can bleed into dorsal tracheal membrane (pulm parynchymal hge too)
which coag test most prolonged, why?2,7,9,10 affected, and external path only has 7, which is affected, so super prolonged PT
PIVKA looks at?"Accumulation of inactivated vit K dependent factor pre-cursors" aka: no K1 to activate precursors, look for built up precursors
DO NOT GIVE K1.... DO GIVE K1....DONT IV- can cause anaphylaxis. DO give with fatty meal (ADEK vitamins) need fat to be absorbed. takes 2-3 days to work, support in meantime!! also means when stopped, need to watch in 2-3 days to make sure didnt need more
what does fernandez say the MOA of bromethalin is?Neurotoxic, interferes with cell membrane pumps. Ion pump dysfunction --> cell swelling, death! (werner's says uncouples oxidative phosphorylation--> dec ATP in brain)
smells like fish?zinc phosphide (gopher bait)
MOA zinc phosphide?when zinc phosphide hits acidic pH of stomach(gastric pH must be between 1-3), it starts to produce phosphine gas. induces death via anoxia. asphyxiate on a cellular level.
want to know what toxin killed them....what do?Rapidly freeze stomach contents
GDV might be caused by...zinc phosphide (forming phosphine gas in the stomach)
tx zinc phosphide with?ANTACIDS-- activated by acidic pH of stomach, so raise pH
metaldehyde MOA?readily crosses the BBB--> decreases in GABA levels--> excitation (hyperexcitable)--> disinhibition of neuronal excitation (so spongebob gabas a lot and is hyper and has a pet snail) (snails are METAL)
LD 50 of EG between species?CATS WAY MORE SENSITIVE THAN DOGS (so sensitive that kits dont even detect their toxic beginning threshold)
MOA of EGMetabolized by liver (ALCOHOL DEHYDROGENASE) into toxic intermediates: glycoaldehyde, glycolic acid* (most toxic!!), glyoxylic acid--> make toxic compounds
stages of EG tox(1) STAGE ONE: NEURO SIGNS (golden period-- when antidote works best) 30 min to 12 hr (up to half a day) (2) STAGE TWO: RESP SIGNS. and cardio, severe metabolic acidosis. 12-24hr after ingestion (half a day to a day) (3) STAGE 3: FINALLY, KIDNEY SIGNS. 24-72hr after ingestion (day to 3 days)
UA with EG will look likeCalcium oxalate monohydrate or dihydrate crystals
fomepizoleThis is 4-mp-- tx for EG tox
2 tx for EG(1) fomepizole- inhibits alcohol dehydrogenase (2) ethanol- COMPETES for alcohol dehydrogenase
grapes cause?renal failure- toxin unknown, not dose dependant
which is worse- OP or carbamatesOP (irreversible, longer lasting)
OPs perm bind by...12-24 hr (you have half a day bro)
atropine test for whatOP tox-- OP works on nicotinic, muscarinic, and CNS. atropine only works on muscarinic- so if you give atropine and they only get a little better but not all the way, you know its OP
tx for OP toxATROPINE for muscarinic, 2PAM (Pralidoxime) for nicotinic
whos sensitive to pyrethroids?cats
MOA pyrethrinskeeps voltage gated Na channels open (neuro signs ensure)
Methocarbamol?mm relaxor, good to give with pyrethrin tox (#1 is dermal decontamination tho)
when do you see amanita signs?half a day with no symptoms, then SEVERE GI signs, 12-24hr you have fulminant liver fail
xylitol tox MOA(1) HYPOGLYCEMIA: xylitol stims pancreas to excessively release insulin-->Weakness, disorientation, tremors, seizures. (2) Hepatic necrosis: unknown MOA, seen with higher doses 8-12hr post ingestion.
methylxanthine MOATHIS IS CHOCOLATE. Fernandez says: ↑iCa2+, catecholamine release. Werners says: ANTAGONIZES adenosine receptor (which is a calming receptor)--> EXCITEMENT. also inc intracellular Ca++ (inc NT release and inc contractility of the heart) <--explains what fernandez said
most toxic methylxanthine is...theobromine
how does the dose of methylxanthine matter?(first, bakers choco>milk obv) mild is hyperactive and GI, moderate cardiac (inc bp inc hr), severe is neuro signs
MOA of cyanobacteria?Microcystins (hepatotoxins) & anatoxins (anatoxin –a and anatoxin-as), powerful neurotoxins*****
Microcystins?hepatotoxin from cyanobact (signs in 30min)
anatoxinsneurotoxin from cyanobact (ana is a song that lights up my brain but it's pretty
most dangerous snake of the ones we learnedrattlers (pitvipers)
which is worse: adult or juv snake bitejuvenile- cant control how much venom to release
2 most common problems caused by snake venom?COAGULOPATHY, thrombocytopenia
what might you see on a snakebite blood smear?echinocytes
elytes affected by snake bite?hypoK hypoMg
way to know if bite is progressingsharpie that shit
snake bite swelling is like...non-pitting edema, hard and thick, ecchymotic hge
do vs donts for snake bite first aidDO NOT DO: Ice area, incision suction, tourniquet (not proven to work, might cause more harm than good.) DO: Keep the patient calm, Lower bite sight below level of heart, Emergency care ASAP
prob with antiveninsBIOLOGICS= ANAPHYLAXIS RISK equine less expensive than ovine one
plasma for snake bite?not appropriate- all it does is temporarily give some clotting factors- but does not neutralize toxin or stop 1* process, and inc risk of anaphylactic reaction. So if theyre bleeding, just give more antivenom!! This is what neutralizes the toxin.
venom vx?might lessen clinical course, not for all venom types tho
drug NOT to give with snake biteNSAIDs-- theyre bleeding enough
dogs or cats snake bite worse?cats worse
BW spider webs Spin funnel-shaped webs in dry, dimly lit secluded places, especially corners. Web often looks like cobwebs, disorganized, “messy”
latrodectusBW spider
most suseptible to latrodectus?CATS, horses, gpigs (dogs not as much)
toxin/MOA of bw spiderAlpha-latrotoxin, potent mammalian neurotoxin (no local toxins so often cant find bite)
snake most tox when? BW spider most tox when?snake: warm weather. spider: fall