Exam 2 Flashcards
DAMNIT
- Degenerative, Developmental, Dementia
- Anomalous, Anatomic, Allergic, Autoimmune
- Metabolic, Mechanical
- Neoplastic, nutritional
- Inflammatory, infectious, immune medated, idiopathic, Ischemic
- Toxic, Trauma
5 Steps to Emergency Stabilization
- Assess & Maintain Adequate Respiration
- Assess & Maintain Adequate Cardiovascular Function
- Control CNS Stimulation
- Control CNS / Respiratory Depression
- Control Temp
How to Assess & Maintain Adequate Respiration
Resp. rate, depth, pattern, noises
Place patent airway
• endotracheal tube or tracheotomy
Adequate ventilation complications
• Ventilatory failure of patient
• Hypoxia due to interference w/ O2 absorption
• Bronchospasm or bronchoconstriction
Prevent Aspiration
• use cuffed endotracheal tube
How to Assess & Maintain Cardiovascular Function
4 Step Fluid Resuscitation Plan • Hypotension / Hypertension • Acid base / Electrolyte / Elemental disturbances • Cardiac disturbances (ECG) • Reassess
How to Control CNS Stimulation
o Control or minimize tremors & seizures
o Can be life threatening
o Use anticonvulsants, sedatives, or anesthetics
o Diazepam or Midazolam – first choice, tremors & seizures
o Methocarbamol – multiple routes, good for tremors, used for Pyrethrin toxicity
o Acepromazine – good to lower BP & control hyperactivity, monitor HR & BP
How to Control CNS & Respiratory Depression & Temperature Change
Control CNS / Respiratory Depression
o Naloxone – reverse opioid overdose (Can give orally)
o Atipamezole - reverse Alpha 2
Control Temp
o Correct cause of temp change first
o SLOWLY cool patients to 102.5-103.5
6 Goals in a Toxicology Case
o Emergency Stabilization / Life Support o Plan of Attack (Working Dagnosis) o Decontamination o Symptomatic & supportive care o Facilitate removal after absorption o Client education
Normal TPR for Dogs
Temperature:
• 99.5-102.5
heart rate/pulse:
• 60-120 bpm
Respiratory rate:
• 10-30 rpm
Dangerous pH’s
< 3
> 11
Normal TPR for Cats
Temperature:
• 100-102.5
Resting heart rate/pulse:
• 110-130 bpm
Respiratory rate:
• 20-30 rpm
Safety Factor for Toxicity
o for animals that toxicity was not studied
o Reduce LD50 by 10 for toxic dose
Topical Decontamination
Dry
• Brush, vacuum, shave THEN bathe
Liquid H2O Soluble
• Bathe w/ warm H2O & mild detergent
Fat Soluble
• Use “hand-degreaser” -> bathe w/ mild detergent -> rinse
Ocular & Inhalation Decontamination
Ocular Exposure
o Flush for 15-20 mins
o Monitor for symptoms
Inhalation Exposure
o Remove animal from environment
Options to decontaminate oral exposure
Dilution
• Dilutie w/ milk, water, or egg whites
• Flush rostrally
Emetics
• Emetic -> after ~45 mins give an anti-emetic or pro-kinetic -> give activated charcoal
• Don’t use on rodents, rabbits, horses, ruminants
Situations not to give an emetic in
- Corrosive agents
- Hydrocarbons-volatile
- Symptomatic or soon to be
- Already vomited or GI empty
- Brachycephalic breeds
- Medical conditions: megaesophagus, laryngeal paralysis, risk of aspiration pneumonia, recent surgery
- Toxicant/drug has anti-emetic properties
Choices of Emetics for Dogs
- Apomorphine hydrochloride
- Ropinirole ophthalmic solution
- Hydrogen peroxide 3%
Do not use
o Syrup of ipecac
o Salt
Apomorphine hydrochloride
o Triggers dopaminergic receptors o IV o Immediate & short duration o Only give 1 dose o Side Effects: persistent Vs & nausea, resp & CNS depression
Ropinirole ophthalmic solution
o Triggers dopaminergic receptors
o Can give 2nd dose 20 mins later
o Side Effects: prolonged Vs & nausea, tachycardia
Hydrogen peroxide 3% as Emetic
o At home use not clinic
o Don’t use in cats (necrosuppurative hemorrhagic gastritis)
o Onset 5-15 mins
o Duration: 30-45mins
o 1mL/lb
o Stimulates gastric mucosal sensory receptors -> vomiting center
o Side Effects: Ds, prolonged Vs, lethargy
o Can cause esophagitis & hemorrhagic gastroenteritis
How to get cats to vomit
o Xylazine IM o Dexmedetomadine IM o Hydromorphone SQ o Onset: 2-20 mins o Side effects: sedation
Gastric Lavage
- Orogastric tube -> oral fluids -> aspiration of content
- Instill fluids & THEN before tube removal, instill activated charcoal
- Use when emetics are unproductive or contraindicated
- Only material same or less than diameter of tube will come out
Enemas & Whole Bowel Irrigation
Enemas
• Remove toxin from distal GI
• Not common or useful in many tox cases
• Avoid hypertonic sodium phosphate enemas
Whole Bowel Irrigation
• Clean the entire bowel
• Not common
• Takes a long time & sedation
Surgical Endoscopy
- Foreign bodies
- Persistent material
- Consider stability of patient, cost, etc
Activated Charcoal
- Binds non-specifically & prevents absorption
- 1g/Kg
- Combine w/ cathartic
- Can give multiple doses
- Rapid admin = V so administer over 1-2hrs
- Patient should be well hydrated
- Can cause hypernatremia, hypermagnesemia, hyperosmolality
- Don’t combine w/ oral drugs (inhibit absorbtion of med)
Basics of Cathartics
- give w/ 1st dose of activated charcoal
- accelerate the expulsion from the GIT
- osmotic induced fluid retention
- fluid volume causes stimulation of GI motility
- make sure patient is well hydrated
- saccharide (sorbitol)
- saline cathartics (bad choice)
Side Effects of Cathartics
- Volume depletion
- Hypotension
- Electrolyte imbalances (saline cathartics)
- Diarrhea
- Renal
- CNS depression
Cholestyramine
- binds weak acidic compounds
- binds to bile acids in intestine and forms an insoluble complex excreted in feces used for compounds that undergo enterohepatic recirculation or are trapped in bile
- use unflavored, no xylitol
Intravenous lipid therapy/emulsion/rescue
- efficacy not well documented. Lots of case reports
- no controlled studies
- Last resort
- May enhance lipid-soluble toxin absorption from GIT
Facilitate Removal After Absorption by Altering Metabolism
o Ethylene glycol (Pase 1 & 2)
o treat w/ ethanol or fomepazole
o inhibitors of alcohol dehydrogenase
Facilitate Removal After Absorption by Enhancing Excretion Rate
Diuresis
• Works on toxin in plasma, non-protein bound, non-lipohilic
Ion trapping in urine • Usually don’t use • Can cause worse acid/base disturbance • Acidify w/ ammonium chloride • Alkanize w/ sodium bicarbonate
Facilitate Removal After Absorption by Direct Removal
o Chelation therapy
o hemodialysis
Cotton Plant
- Cotton plant – Gossypium
- Is very good protein, nutrient, fat, fiber, & energy
- Protein = 26-40%
Gossypol Basics & Toxicity
o Most abundant pigment in cottonseeds roots & stems
o Different strains vary
Toxicity
• “historical”
• cardiac toxin
• free unprocessed seed – potentially toxic
• processed - not toxic
• acute toxicosis – rare
• more likely to be due to accumulation / chronic
Gossypol; Animals Affected & Mechanism of Action
Animals Affected
• Immature ruminants
• Monogastrics
• Mature ruminants are pretty resistant
Mechanism of Action
• Lipid soluble
• In bile & feces as gossypol-iron complex
• Disruption of intra & extracellular K+ -> decrease K -> impair cardiac function\
Gossypol; Clinical Signs & Lesions
Clinical Signs • Abrupt appearance • Sudden death • Heart failure • Drop in production • Anemia • Effusion, edema • Decrease male & female fertility
Lesions • Icterus – liver & hemolysis • Anemia • Hemoglobinemia/uria • Abomasitis
Gossypol Diagnosis
- Access to cottonseed
- Heart failure
- Analyses of free gossypol in diet
- Tissue testing
Gossypol Treatment
Acute
o Decontaminate
Chronic
o Remove source or dilute
o Treat for heart failure
o Supplement w/ vitamins, iron, protein
3 Ice Melts & Toxic Effects
Potassium chloride
o Increase K ->
o Weakness & cardiac issues
Magnesium Chloride
o Increase Mg ->
o Hypotension, cardiac issues, weakness, neuromuscular issues, low Phosphorous
Sodium Chloride
o Increase Na ->
o Tremors, PU/PD, seizures, vomiting
Basics of Ionophores;most common drugs
- Can be found in food additives
- Most commonly Monensin or Lasalocid
- Affects cows, sheep, poultry, goats, swine
- Used to alter microflora, increase feed efficiency, decrease lactic acidosis, & as a coccidiostat
Reasons for Ionophore Toxicosis
o Access to ionophores by non-target/susceptible species like horse, dog (acute)
o Mixing / math errors (acute; subacute: few days)
o Almost always history of recent feed change, 12-72 hrs
o macrolide antibiotics can make toxicosis 4 fold
Ionophores Mechanism of Action; part effected in each species
o Lipid soluble – limited but rapid absorption
o Metabolized by liver -> bile -> feces
o Small amounts go systemically – POTENT
o no long- term sequestration in tissues
o Cardiac muscle: cow, horse, poultry, camelids
o Skeletal muscle: swine, sheep, dog, cat, poultry, camelids
o Punches hole that allows Na+ & Ca++ in & K+ out, -> decrease oxidative phosphorylation -> myofiber necrosis
Ionophore Toxicosis Clinical Signs Initially & Later (specific drugs)
Initial
• GIT (12-72 hr)
• Partial to complete feed aversion/anorexia within 24 hrs
• diarrhea
• Weakness, ataxia, depression occurs up to days or later
Later
• Heart: drop dead / left and right heart failure
• Paresis / paralysis
• dyspnea, respiratory failure
• Salinomycin & Lasalocid affect nervous system depression
Ionophore Toxicosis Clin Path
o Non-specific or non-consistent o Increase bilirubin o Increase CK, LDH o Increase troponin o Myoglobinemia/uria (not common)
Ionophore Toxicosis Lesions & Diagnosis
Lesions o None or subtle o L/R heart failure o Pale streaking of skeletal muscle o Acute tubular necrosis of kidney o Centrolobular necrosis (liver) o Axonal degeneration of nerves/spinal cord
Diagnosis o Recent feed change o Appropriate signs o Feed analysis o Tissue samples (specifically heart in horses)
Ionophore Toxicosis Treatment & Prognosis for Asymptomatic & Symptomatic Patients
o Remove source
Asymptomatic: • Decontaminate: • SA: emesis, AC+ cathartic, gastric lavage, Vit E + Se, IV lipid rescue • LA: mineral oil and AC, Vit E + Se • Monitor daily for 5-7 days at least
Symptomatic:
• treat symptoms
• most likely to die if heart failure
• more likely to survive if only muscle damage
Basics of Macadamia Nuts
- unknown toxic principal, mechanism, or system affected
- only nut is toxic
- one kernel weighs 2.5-5g
- excellent prognosis
- recovery in 24-48hrs
Macadamia Nuts Toxic Dose & Treatment
Toxic Dose
o Unsure
o Go by the rule 1 nut/kg of BW
Treatment o Decontamination thru Emesis AC and cathartic? o Monitor temp and hydration o Monitor for pancreatitis o Methocarbamol if tremors o Bulk diet to encourage motility
Grapes Toxicosis basics; potential toxins
- All grape types & seeds toxic
- Cooked/processed is controversial
- Jelly or wine not toxic
- Affects DOGS, cats, ferrets
- Any dose is toxic
- Causes renal dz
- Variable whether dog will succumb or not
- potential toxin = tartaric acid & potassium bitartrate (also in cream of tarter & tamarinds)
Grape Toxicosis Clinical Signs, Pathology, & Lesions
Clinical Signs o Non-specific o w/in 16-24hrs of ingestion o Vomit w/in 2hrs -> most likely develop renal dz if not treated o Diarrhea o Anorexia, lethargy, abdominal pain
Pathology o Azotemia o Hyper-electrolytes o Polyuria first then anuria (if there is pee there is hope!) o No crystals
Lesions
o Proximal tubule degeneration & necrosis
Grape Toxicosis Treatment for Asymptomatic & Symptomatic Animals
Asymptomatic
• Decontaminate w/ emesis, AC, & cathartic
• Fluid therapy
• Diurese to enhance renal excretion & GFR
• Monitor
• Prognosis is great if caught early!
Symptomatic • Fluid therapy • Phosphate binders • Monitor • Dialysis or transplant • Many will recover over time but expensive
Basics of Vitamin D Toxicosis & What forms an animal may get ahold of
- Toxic to small animals
- Can affect large animals but not common
- Young animals more susceptible
- Need to know exact name/form due to different T1/2, onset of action
Cholecalciferol (Vit D3) rodenticide
o D-con
o Could have anti-coagulant or not
Human meds
o Calcitrol
o Dovonex
o Vitamin supplements
Feed/math mixing errors
Mechanism of Action for Cholecalciferol & Vit D Meds
Mechanism of Action Cholecalciferol o Deposits in fat tissue -> o Can stay in fat for ~2mo -> o Absorbed in small intestine -> o Liver -> o Kidney o Can take 12hrs - 5 days to see toxicosis o Dose dependent
Mechanism of Action Vit D meds
o Onset < 3-6hrs
o Dose dependent
Clinical Signs Due to Vit D Toxicosis
Acute & persistently elevated Ca & P
• Due to increased Ca & P absorption from GI
• Increased osteoclastic activity in bone
• Increased Ca reabsorption by distal renal tubules
First signs (due to increased Ca) • GI, Nervous system, Anorexia, increased urination
Later (due to mineralization)
• Increased GI & Nervous system issues
• Dyspnea, exercise intolerance
• Renal issues, abdominal pain, PU/PD
Clinical Pathology of Vit D Toxicosis
o Occur before symptoms
o Hypercalcemia
o Hyperphosphatemia
o Ca x P > 60-70 mg/dl
Later
• Azotemia, acidosis, hyperkalemia
• Hyposthenuria, proteinuria, casts, glucouria
• Medullary washout, nephrogenic diabete insipidus
Gross & Microscopic Lesions of Vit D Toxicosis
Gross
• Mineralized tissue (kidney, lung, arteries)
• Often not apparent
Microscopic
• Mineralization / degeneration & necrosis
• Hypertrophy & hyperplasia of parfollicular cells of thyroid
Six Parts of a Signalment
- species,
- breed,
- age,
- sex,
- weight,
- reproductive status
Normal TPR Horse
Temp
• 99 to 100.5
Pulse
• 28-40
Resp
• 8-16
Normal TPR Cow
Temp
• 100-102.5
Pulse
• 40-80
Resp
• 10-30
How to Assess Hydration Status
Base
• Packed Cell Volume, Total Protein
Other
• BUN, Creatinine
• Lactate, Glucose
• USG, Urine Output, BW
Essential Equipment for Necropsy
o gloves o sharp knife, and equipment to keep it sharp (stone/steel) o tissue forceps and scissors o saw (or hatchet, ax or cleaver) o shears o fixative and containers o sterile syringes, needles, whirl packs o pen o camera
Gastric Lavage Technique
- tube length = tip of nose to 9th intercostal space
- place speculum to prevent chewing on tube ->
- insert tube w/ head in normal position ->
- lower head ->
- instill fluid & AC at 5-10ml/kg
- allow fluid to flow out or suction out
- repeat 8-10 times
How many lbs in Kg
1kg = 2.2lb
PPM or Parts per Million
PPM = mg/kg = 1 mg/L
gallon to quarts to pints to cups
1 gallon = 4 quarts = 8 pints = 16 cups
Cups to oz
1 cup = 8 ounces
tsp & tbsp to ml
1 tsp = 5 mL
1 tbsp = 15 mL
oz to g or ml
1 ounce = 28 g or 29 ml
tons to lbs
1 ton = 2000 pounds
liters to quarts
1 liter = 1 quart;
GOSHDARNIT
Causes of hypercalcemia o Granulomatous o Osteolytic o Spurious o Humoral hypercalcemia of malignancy, Hyperparathyroidism, Hyperthyroidism o Vitamin D toxicity o Addison’s disease (hypoadrenocorticism o Renal failure o Neoplasia, Nutritional o Idiopathic o Tumor
Vit D Toxicosis Diagnosis
o History
o Hypercalcemia and/or hyperphosphatemia
o Hypercalcemic panel!
Vit D Toxicosis Treatment
Asymptomatic (normal Ca & P)
• Decontaminate: emetic, AC, cathartic
• May use cholestyramine instead of AC
• Monitor Ca, P, BUN, Cr, USG, PCV, TP every 12-24hrs for 4d
Symptomatic
• Lower Ca and/or P w/ Bisphosphonates (can take 2-4d)
• Fluid therapy 2-3x maintenance w/ physiologic saline, plasmalyte, or Norm R
• Prednisone/Prednisolone to promote calciuresis
• Low Ca/P diet
• GI protectant (sulcralfate) in necessary
• Oral P binders (aluminum hydroxide)
• Monitor every 3-6hrs until patient seems normal
Types of Ethylene Glycol & Crystals Produced
- Antifreeze
- Propylene glycol
- Methanol
- Diethylene glycol
- Calcium oxylate monohydrate crystals
Basics of Ethylene Glycol Toxicity & Pharmacodynamics
Toxicity
o All species susceptible
o Difficult to diagnose
o Need to intervene in cats w/in 3hrs dogs in 6-8hrs
Pharmacodynamics
o Rapid absorption (1-4hrs) -> decontamination difficult
o T ½ = 2-10hrs
o Metabolites are bad
o All gone in 16-24hrs
o >50% EG excreted in urine unchanged (osmotic diuretic)
Effects of Ethylene Glycol & it’s Metabolites
Ethylene glycol, glycoaldehyde, glycolic acid
• CNS depression -> coma -> death
Metabolites (glycolic acid)
• Severe metabolic acidosis
All Metabolites
• Cytotoxic to renal tubular cells
Calcium oxalate monohydrate crystals
• mechanical obstruction
Chemical Path of Ethylene Glycol Metabolism
o Ethylene glycol ->
o Rate limiting step ->
o Glycoaldehyde (more toxic & short T ½) ->
o Glycolic acid (long T ½)
o Rate limiting step ->
o Glyoxylic acid (most toxic & short T1/2) ->
o Benzoic acid, oxalic acid, formic acid ->
o Hippuric acid, calcium oxalate monohydrate
Clinical Signs of Ethylene Glycol Tocicity
Stage 1 • 1-3 (or 12) hours • CNS depression • V, lethargy, ataxia, PU/PD • Uncommonly death
Stage 2 • 6-12hrs • Metabolic acidosis • Worsen/lessen CNS depression • Tachypnea • PU/PD
Stage 3
• 6-24hrs or longer
• Oliguria/anuria
• Renal dz/failure
Clinical Pathology & Lesions of Ethylene Glycol Tocicity
Clin Path o Not specific but consistent o Most happen btwn 6-8hrs o Monitor CBC/UA every 3hrs for 9hrs o Increase osmolality o Increase anion gap o Metabolic aciocis o Crystalluria o Azotemia o Hyperkalemia o Hyperphosphotemia o Isosthenuria
Lesions
o Proximal tubule degeneration & necrosis
PEACE PAIN
o Reasons for Hypocalcemia o Phosphate enema o Eclampsia o Albumin is low o Chronic renal disease o Ethylene glycol toxicity o Parathyroid deficiency o Acute pancreatitis o Intestinal malabsorption o Nutritional (deficiency in vitamin D)
Diagnosis of Ethylene Glycol Toxicity
o Exposure history
o CBC, chem, UA, acid-base panel
Chemical analysis kit
• Often false (+) & (-)
• Use in 1st 12hrs
• Only shows exposure
o Put substance in freezer to see if it freezes
o CNS depression!
Treatment for Ethylene Glycol Toxicity
o Maybe decontaminate if VERY early exposure
Fluid therapy
• Diurese
• Help dehydration
• Support kidneys
o Monitor Chem, UA, electrolytes every 3-9hrs for 12-24hrs then daily for 3d
o Check for hypocalcemia every 4-6hrs for 24hrs
o Give ethanol or fomepazole
o Correct acidosis
o Correct Ca
o Get them to eat
Why treat Ethylene Glycol Toxicity w/ Ethanol or Fomepazole
o No metabolism of EG -> o excreted unchanged in the urine –> o no toxic metabolites o Don’t use if in stage 3/when EG no longer around o Do not combine
Ethanol
• competitive inhibitor of ADH
• Cheap / effective
• Few Side effects
fomepazole
• direct inhibitor of ADH
• More expensive
• More effective / fewer side effects
Propylene Glycol Basics, clinical signs, toxic dose, treatment
o “safer” antifreeze
o Fatalities rare!
o False positive on EG kit
Clinical Signs • CNS depression • Ataxia, incoordination, vomiting, PU/PD • Acidosis (metabolized to lactate) • Hyperosmolality • No kidney problem! • Heinz body anemia in cats (some dogs)
Toxic dose:
• 3-4× EG
Treatment
• hemodialysis if severe
Diethylene glycol, Methanol, & Ethanol
Diethylene Glycol
o No crystals
o Rare toxicosis in vet med
Methanol
o Only stage 1 & 2
o No renal component
o Treat w/ fluids & correct symptoms
Ethanol
o Only stage 1 & 2
o No renal component
o Treat w/ fluids & correct symptoms
Issue w/ fermented dough & Symptoms
o Yeast creates ethanol & CO2
o Can cause alchohol poisoning
Symptoms
• vomiting ataxia, incoordination, CNS depression, urinary incontinence, hypothermia,
• looks like stage 1 of EG
fermented dough risks & treatment
Risks
• Ethanol depression
• Bloat
Treatment
• Fast absorption -> decontamination not really a thing
• Cold water lavage with stomach tube – ice chips
• sometimes you might need to surgically remove
• Monitor for hypothermia
• Prevent aspiration – maintain airway –
ventilation
• IV fluids – maintenance, dilution, diuresis
