ECC2- SA Toxins Drugs

• inhibit COX-2 and/or 1 (non-selective COX inhibitors cause more adverse effects because COX-1 has protective properties)
• prostaglandins produced by COX-1 important for maintenance of gastric mucosal barrier, renal perfusion, and platelet function
• prostaglandins produced by COX-2 responsible for inflammatory response, tissue injury, and nociception

• [dose dependent starting with GI and so on]
• GI: vomiting, diarrhea, melena, loss of appetite, abdominal pain, hematemesis, peritonitis (if very severe ulceration and perforation)
• Renal: isosthenuria, azotemia, urine casts, PU/PD, oliguria/ anuria, dehydration, lethargy, GI signs, glucosuria
• Neurologic: seizures, ataxia, altered mentation
• Hepatic: [idiosyncratic] lethargy, anorexia, vomiting, icterus, elevated liver enzymes and bili
• Coagulation: hyper- or hypo-coaguable

loss of prostaglandin--> decreased protective gastric mucus and bicarb, loss of maintenance of mucosal blood flow, increased gastric acid secretion

• loss of basal vasodilation that is mediated by prostaglandins--> ischemic injury of the kidney
• especially profound when dehydrated patients ingest NSAIDs

NSAIDs are primarily metabolized by liver

• block COX--> reduce the production of thromboxane (platelet activator)--> hypocoaguable--> bleeding disorders
• OR lack of prostacyclin (platelet inhibitor) production (another end product of arachadonic acid pathway)--> hypercoaguable--> thromboembolic dz

• Decontamination: emesis, activated charcoal
• IVF therapy
• GI protectants: PPI or H2 blocker, anti-emetics, sucralfate
• +/- misoprostol: if in acute phase, can give synthetic PG analogue; many bad side effects

• baseline renal panel and liver enzymes
• monitor urine sediment for casts (isosthenuria is not sensitive because you are diuresing the animal with fluids)

• metabolites are the toxic component (not acetominophen itself)- N-acetyl-para-benzoquinoneimine (NAPQI)
• NAPQI generated from cytochrome P-450 pathway--> causes disruption of protein function and cell membrane damage--> generation of reactive oxygen species--> subsequent hepatocellular damage
• PAP is another metabolite--> causes methemoglobinemia, heinz bodies, and hemolytic anemia

• feline hemoglobin has more reactive sulfa-hydroxyl groups--> methemoglobinemia manifests first and liver damage only develops those who survive the acute insult\
• dogs show hepatic damage first

• brown MMs
• edema of face an paws
• hypothermia
• anorexia
• depression
• weakness
• coma
• elevated liver enzymes, icterus

• emesis, activated charcoal
• N-acetylcysteine (replenishes glutathione stores and prevents further accumulation of NAPQI)
• hepatic protectants- SAMe
• IVF therapy

sympathomimetic alkaloids--> release of endogenous catecholamines--> impairing catecholamine metabolism and also increase serotonin levels in the CNS

• hypertension [alpha stimulation]
• tachycardia [beta stimulation], sometimes reflex bradycardia from hypertension
• arrhythmias
• ataxia
• mydriasis
• hyperthermia/ heat stroke
• tremors
• seizures
• hypotension with CV collapse

• emesis, activated charcoal
• cyproheptadine (treats CNS signs by addressing excess serotonin)
• IVF therapy
• acidification of urine (increases excretion) with ascorbic acid
• phenothiazine drugs for sedation (no benzos...worsen dysphoria)
• methocarbamol for muscle tremors
• +/- anti-seizure meds
• minimize stimulation- dark quiet room

• THC is psychoactive constituent
• cannaboid receptors (CB1 and CB2)- CB1 are in CNS and CB2 are in periphery--> CB2 are primarily responsible for clinical signs of toxicity

• dogs are hyperesponsive to sound and fast movement, but dull/ glazed over when not being stimulated
• mental depression/ coma if severe
• dribbling urine
• vomiting
• bradycardia (usually)

• emesis if ingested (difficult because THC has anti-nausea properties)
• activated charcoal (extensive enterohepatic- repeated dosing)
• IVF therapy
• if very severe, intralipid therapy (THC is lipid soluble)

theobromine and caffeine= methylxanthines--> antagonism of phosphodiesterase--> increase in cAMP--> increase in catecholamines

• hyperexcitability
• tremors
• tachycardia +/- arrhythmias
• hypertension
• seizures
• vomiting
• rarely hypotension/ brady
• pancreatitis

• emesis, activated charcoal (enterohepatic- repeat dosing)
• +/- beta blockade
• IVF therapy
• +/- sedation is super excitable
• frequent walks for urination or catheter- methylxanthines will be reabsorbed through bladder mucosa if not urinated out fast enough

• unknown- end result is renal damage
• VERY dependent on patient- some are very sensitive, some can eat grapes all the time and not be effected

• PU/PD
• oliguria/ anuria
• azotemia
• isosthenuris
• dehydration
• vomiting
• diarrhea
• anorexia, lethargy

• emesis
• IVF therapy
• manage AKI

• stimulates profound insulin release but is not actually used as an energy source--> result in profound hypoglycemia
• hepatic failure ay also occur

• weakness
• ataxia
• seizures
• if liver damage, icterus, bleeding disorders, vomiting, diarrhea

• emesis
• dextrose for hypoglycemia
• liver protectants- denamarin

• [allium genus]
• sulfoxide and disulfide compounds cause oxidative damage to red blood cells--> heinz bodies and eccentrocytes, methemoglobinemia, hemolysis

• anemia/ palloe
• weakness
• tachycardia, tachypnea
• hemoglobinuria
• vomiting
• diarrhea

• emesis, charcoal
• IVF therapy (to minimize renal injury from hemoglobinuria)
• antioxidants- ascorbic acid, vit E, N-acetylcysteine