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
MOA of moldy foods
mycotoxins: PenetremA and roquefortine produced by Penicillium Sp.
Inhibition of calcium regulated potassium channels → alters release of neurotransmitters (glutamate, aspartic acid, GABA) in both peripheral and central synapses
inhibits inhibitory glycine, reduces gaba
clinical signs of mycotoxin exposure
- GI : vomiting, diarrhea, hypersalivation
- CV: tachycardia
- NS: generalized muscle tremors, ataxia, weakness, hyperesthesia, agitation, stiff gaits, seizures ,stupor to coma
treatment for mycotoxin exposure
Asymptomatic: emesis + charcoal
Symptomatic: control muscle tremors, treat hyperthermia, supportive care
– Methocarbamol- muscle relaxant
– +/- Benzodiazepam: midazolam or diazepam
– Seizure control if ”true seizures”
– Active cooling measures if rectal temperature >105
– Anti-emetics
– IV fluids for cardiovascular support
penny ingestion causes
zinc toxicity → hemolytic anemia
clinical signs of penny ingestion
Clinical signs: vomiting, pigmenturia, lethargy inappetence,
diarrhea
Physical Exam Findings:
* Pale mm’s
* Tachycardia
* Heart murmur
* Icterus (50%)
how to treat penny ingestion
xray and remove penny
check zinc levels
pRBC transfusions if needed
supportive care
chelation NOT done
breakdown of ethylene glycol
glycolic acid → metabolic acidosis
calcium oxolate → renal tubular necrosis and hypocalcemia
clinical signs of ethylene glycol ingestion
1-12 hours
* Gastric irritation and increased plasma osmolality:nausea, vomiting, mental dullness, ataxia, PU/PD, hypothermia.
12-24 hours post ingestion
* Metabolic acidosis, increased RR, tachyarrhythmias, hypocalcemia
24-72 hours post ingestion (earlier in cats)
* Oliguric or anuric renal failure
how to diagnosis early signs of ethylene glycol ingestion
- elevated osmolar gap
- ↑↑ high anion gap metabolic acidosis (↑ glycolic acid)
- urinalysis: calcium oxalate crystals, isosthenuria, hematuria, proteinuria, glucosuria, casts, white blood cells
- Woods Lamp: examine mouth, paws or urine to look for fluorescence
- Kacey EG test strips
diagnosis of late ethyelene glycol ingestion
- Azotemia: Increased BUN and Creatinine
- Hyperphosphatemia
- Hyperkalemia
- US findings:
– Large, bright kidneys
treatment for ethylene glycol
- vomiting not recommended
- prevent conversion of EG to toxic metabolites and enhancing excretion: Fomepizole or ethanol within 8 hrs before kidney damage: inhibits alcohol dehydrogenase
- hemodialysis
- Once renal damage has occurred – supportive care (IV fluids, anti-emetics), hemodialysis: poor prognosis
2 y.o. FS Pug is presented for lethargy and pigmenturia
Mm’s pale, HR: 120, strong femoral pulses
Rectal temperature is 101
Urine has a ‘red tinge’
PCV: 20%,TP 8.0 g/dL
what did they eat?
zinc/penny
