Test 4: 51-52 Flashcards
—- Produce hydroxide ions upon contact with water and are
proton acceptors
alkalids
clinical signs of acid or alkalid
Ocular: corneal ulcers
Dermal: pain, ulceration
Oral: pain, vocalization, dysphagia, ptyalism (salivation), vomiting, abdominal pain, ulcerations
Inhalation (less common): dyspnea, edema, inflammation
how to treat acid or alkalid exposure
dilute
supportive care: IV fluids, pain meds
gastroprotection: sulcralfate, proton pump inhibitors, H2 blockers
avoid oral drugs when possible
do not neutralize or vomit
what is the toxic ingredient in chocolate
methylxanthines (i.e caffeine and
theobromine)
why is chocolate bad
methylxanthines (i.e caffeine and theobromine)
Increased contractility of cardiac and skeletal muscle,CNS stimulant via:
- inhibition of phosphodiesterases and adenosine leading to increased cAMP → increases in intracellular calcium
- Direct stimulation of release of catecholamines (epinephrine and norepinephrine) from the adrenal medulla
how is chocolate metabolized
caffeine: rapid absorption in 30-60 mins
Theobromine: delayed absorption up to 10 hrs
excretion: primarily biliary, undergoes enterohepatic recirculation
– ~10% excreted unchanged in the urine
– May be reabsorbed across the bladder wall
clinical signs of chocolate ingestion
- GI: nausea, vomiting/regurgitation, diarrhea
- CV: tachycardia, HTN, VPCs, other tachyarrythmias, bradycardia (rare)
- Nervous: hyperexcitability, hyperthermia, ataxia, seizures
- Muscular: muscle tremors
- Renal:PU/PD, urinary incontinence
- Respiratory: tachypnea, respiratory failure (very high doses)
- Hypokalemia
treatment for acute witnessed ingestion of chocolate
Decontaminate!
* Emesis: within 6 hours of chocolate ingestion as long as no contra-indications (within 1-2 hours for caffeine only ingestions)
* Multi-dose activated charcoal (1-2 g/kg PO with or without a cathartic) and then every 6-8 hours without a cathartic for 24-48 hours for severe, life threatening ingestions
* Single dose AC is fine for patients with smaller, less severe ingestions
* Walk frequently (or urinary catheterization) to decrease bladder re-absorption
treatment for clinical chocolate ingestion
- Control hyperactivity : Acepromazine or benzodiazepam
- For seizures: benzodiazepam +/- phenobarbital or keppra
- Evaluate ECG and BP: If (HR > 180)
* If sinus tachy or HTN: beta blocker (propranolol versus esmolol)
* If Vtach: lidocaine - IV fluids for cardiovascular support and promote diuresis
- Antiemetics: cerenia or ondansetron
- Walk frequently or urinary catheterization
why grapes bad
Causes renal failure due to acute tubular necrosis in susceptible DOGS
* More likely idiosyncratic > dose related
* More than 50% of dogs will have no clinical signs
MOA: UNKNOWN!
* Maybe a mycotoxin, pesticides, or components of the fruit that cannot be metabolized?
* suspect potassium bitarate or tartaric acid
clinical signs of grapes
GI: vomiting, diarrhea, abdominal pain, anorexia
Renal: oligo or anuric renal failure, elevations in BUN, creatinine, potassium
Hepatobiliary: mild elevations in liver enzymes (typically ALT)
Endocrine/Metabolic: hypercalcemia, hyperphosphatemia, metabolic acidosis
Neuromuscular: weakness and ataxia
Treatment for acute grape exposure
- Decontamination!
- Emesis induction up to 6 hours of exposure
- Unknown whether activated charcoal is helpful → typically administer single dose
- IV fluid diuresis (ideal) versus SQ fluids daily for 48-72 hours for renal support
- Monitor renal values daily
Prognosis is guarded (poor to grave) for animals with ARF
* May require hemodialysis if oligo- or anuric
effects of xylitol ingestion
cause massive release of insluin Hypoglycemia
Acute hepatic necrosis may develop in some dogs
clinical signs of xylitol
Vomiting
Nervous system signs from hypoglycemia: behavior changes, weakness, ataxia, tremors, seizures
delayed Hepatic necrosis may lead to exacerbation of hypoglycemia, diarrhea, depression, icterus, melena
Petechiations/Ecchymosis with acute hepatic failure (may bleed from venipuncture sites)
treatment for acute xylitol ingestion
- Check BG every 4-6 hrs: give dextrose bolus and start IV fluids with dextrose
- Decontamination – emesis only for asymptomatic patients
- Feed small frequent meals
- Consider Denamarin or SAMe for large ingestions or other liver protectants
- Monitor liver enzymes every 24 hours for 3 days
- If acute hepatic failure – supportive care,vitamin K, FFP, etc
breakdown of ethylene glycol
glycolic acid → metabolic acidosis
calcium oxolate → renal tubular necrosis and hypocalcemia
