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Toxicology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

DAMNIT

A
  • Degenerative, Developmental, Dementia
  • Anomalous, Anatomic, Allergic, Autoimmune
  • Metabolic, Mechanical
  • Neoplastic, nutritional
  • Inflammatory, infectious, immune medated, idiopathic, Ischemic
  • Toxic, Trauma
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2
Q

5 Steps to Emergency Stabilization

A
  • Assess & Maintain Adequate Respiration
  • Assess & Maintain Adequate Cardiovascular Function
  • Control CNS Stimulation
  • Control CNS / Respiratory Depression
  • Control Temp
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3
Q

How to Assess & Maintain Adequate Respiration

A

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

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4
Q

How to Assess & Maintain Cardiovascular Function

A 
4 Step Fluid Resuscitation Plan
•	Hypotension / Hypertension
•	Acid base / Electrolyte / Elemental disturbances
•	Cardiac disturbances (ECG)
•	Reassess
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5
Q

How to Control CNS Stimulation

A

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

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6
Q

How to Control CNS & Respiratory Depression & Temperature Change

A

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

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7
Q

6 Goals in a Toxicology Case

A 
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
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8
Q

Normal TPR for Dogs

A

Temperature:
• 99.5-102.5

heart rate/pulse:
• 60-120 bpm

Respiratory rate:
• 10-30 rpm

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9
Q

Dangerous pH’s

A

< 3

> 11

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10
Q

Normal TPR for Cats

A

Temperature:
• 100-102.5

Resting heart rate/pulse:
• 110-130 bpm

Respiratory rate:
• 20-30 rpm

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11
Q

Safety Factor for Toxicity

A

o for animals that toxicity was not studied

o Reduce LD50 by 10 for toxic dose

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12
Q

Topical Decontamination

A

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

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13
Q

Ocular & Inhalation Decontamination

A

Ocular Exposure
o Flush for 15-20 mins
o Monitor for symptoms

Inhalation Exposure
o Remove animal from environment

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14
Q

Options to decontaminate oral exposure

A

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

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15
Q

Situations not to give an emetic in

A
  • 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
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16
Q

Choices of Emetics for Dogs

A
  • Apomorphine hydrochloride
  • Ropinirole ophthalmic solution
  • Hydrogen peroxide 3%

Do not use
o Syrup of ipecac
o Salt

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17
Q

Apomorphine hydrochloride

A 
o	Triggers dopaminergic receptors
o	IV
o	Immediate & short duration
o	Only give 1 dose
o	Side Effects: persistent Vs & nausea, resp & CNS depression
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18
Q

Ropinirole ophthalmic solution

A

o Triggers dopaminergic receptors
o Can give 2nd dose 20 mins later
o Side Effects: prolonged Vs & nausea, tachycardia

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19
Q

Hydrogen peroxide 3% as Emetic

A

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

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20
Q

How to get cats to vomit

A 
o	Xylazine IM
o	Dexmedetomadine IM
o	Hydromorphone SQ
o	Onset: 2-20 mins
o	Side effects: sedation
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21
Q

Gastric Lavage

A
  • 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
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22
Q

Enemas & Whole Bowel Irrigation

A

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

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23
Q

Surgical Endoscopy

A
  • Foreign bodies
  • Persistent material
  • Consider stability of patient, cost, etc
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24
Q

Activated Charcoal

A
  • 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)
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25
Q

Basics of Cathartics

A
  • 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)
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26
Q

Side Effects of Cathartics

A
  • Volume depletion
  • Hypotension
  • Electrolyte imbalances (saline cathartics)
  • Diarrhea
  • Renal
  • CNS depression
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27
Q

Cholestyramine

A
  • 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
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28
Q

Intravenous lipid therapy/emulsion/rescue

A
  • efficacy not well documented. Lots of case reports
  • no controlled studies
  • Last resort
  • May enhance lipid-soluble toxin absorption from GIT
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29
Q

Facilitate Removal After Absorption by Altering Metabolism

A

o Ethylene glycol (Pase 1 & 2)
o treat w/ ethanol or fomepazole
o inhibitors of alcohol dehydrogenase

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30
Q

Facilitate Removal After Absorption by Enhancing Excretion Rate

A

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
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31
Q

Facilitate Removal After Absorption by Direct Removal

A

o Chelation therapy

o hemodialysis

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32
Q

Cotton Plant

A
  • Cotton plant – Gossypium
  • Is very good protein, nutrient, fat, fiber, & energy
  • Protein = 26-40%
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33
Q

Gossypol Basics & Toxicity

A

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

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34
Q

Gossypol; Animals Affected & Mechanism of Action

A

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\

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35
Q

Gossypol; Clinical Signs & Lesions

A 
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
36
Q

Gossypol Diagnosis

A
  • Access to cottonseed
  • Heart failure
  • Analyses of free gossypol in diet
  • Tissue testing
37
Q

Gossypol Treatment

A

Acute
o Decontaminate

Chronic
o Remove source or dilute
o Treat for heart failure
o Supplement w/ vitamins, iron, protein

38
Q

3 Ice Melts & Toxic Effects

A

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

39
Q

Basics of Ionophores;most common drugs

A
  • 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
40
Q

Reasons for Ionophore Toxicosis

A

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

41
Q

Ionophores Mechanism of Action; part effected in each species

A

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

42
Q

Ionophore Toxicosis Clinical Signs Initially & Later (specific drugs)

A

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

43
Q

Ionophore Toxicosis Clin Path

A 
o	Non-specific or non-consistent
o	Increase bilirubin 
o	Increase CK, LDH 
o	Increase troponin 
o	Myoglobinemia/uria (not common)
44
Q

Ionophore Toxicosis Lesions & Diagnosis

A 
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)
45
Q

Ionophore Toxicosis Treatment & Prognosis for Asymptomatic & Symptomatic Patients

A

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

46
Q

Basics of Macadamia Nuts

A
  • unknown toxic principal, mechanism, or system affected
  • only nut is toxic
  • one kernel weighs 2.5-5g
  • excellent prognosis
  • recovery in 24-48hrs
47
Q

Macadamia Nuts Toxic Dose & Treatment

A

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
48
Q

Grapes Toxicosis basics; potential toxins

A
  • 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)
49
Q

Grape Toxicosis Clinical Signs, Pathology, & Lesions

A 
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

50
Q

Grape Toxicosis Treatment for Asymptomatic & Symptomatic Animals

A

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
51
Q

Basics of Vitamin D Toxicosis & What forms an animal may get ahold of

A
  • 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

52
Q

Mechanism of Action for Cholecalciferol & Vit D Meds

A 
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

53
Q

Clinical Signs Due to Vit D Toxicosis

A

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

54
Q

Clinical Pathology of Vit D Toxicosis

A

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

55
Q

Gross & Microscopic Lesions of Vit D Toxicosis

A

Gross
• Mineralized tissue (kidney, lung, arteries)
• Often not apparent

Microscopic
• Mineralization / degeneration & necrosis
• Hypertrophy & hyperplasia of parfollicular cells of thyroid

56
Q

Six Parts of a Signalment

A
  • species,
  • breed,
  • age,
  • sex,
  • weight,
  • reproductive status
57
Q

Normal TPR Horse

A

Temp
• 99 to 100.5

Pulse
• 28-40

Resp
• 8-16

58
Q

Normal TPR Cow

A

Temp
• 100-102.5

Pulse
• 40-80

Resp
• 10-30

59
Q

How to Assess Hydration Status

A

Base
• Packed Cell Volume, Total Protein

Other
• BUN, Creatinine
• Lactate, Glucose
• USG, Urine Output, BW

60
Q

Essential Equipment for Necropsy

A 
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
61
Q

Gastric Lavage Technique

A
  • 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
62
Q

How many lbs in Kg

A

1kg = 2.2lb

63
Q

PPM or Parts per Million

A

PPM = mg/kg = 1 mg/L

64
Q

gallon to quarts to pints to cups

A

1 gallon = 4 quarts = 8 pints = 16 cups

65
Q

Cups to oz

A

1 cup = 8 ounces

66
Q

tsp & tbsp to ml

A

1 tsp = 5 mL

1 tbsp = 15 mL

67
Q

oz to g or ml

A

1 ounce = 28 g or 29 ml

68
Q

tons to lbs

A

1 ton = 2000 pounds

69
Q

liters to quarts

A

1 liter = 1 quart;

70
Q

GOSHDARNIT

A 
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
71
Q

Vit D Toxicosis Diagnosis

A

o History
o Hypercalcemia and/or hyperphosphatemia
o Hypercalcemic panel!

72
Q

Vit D Toxicosis Treatment

A

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

73
Q

Types of Ethylene Glycol & Crystals Produced

A
  • Antifreeze
  • Propylene glycol
  • Methanol
  • Diethylene glycol
  • Calcium oxylate monohydrate crystals
74
Q

Basics of Ethylene Glycol Toxicity & Pharmacodynamics

A

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)

75
Q

Effects of Ethylene Glycol & it’s Metabolites

A

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

76
Q

Chemical Path of Ethylene Glycol Metabolism

A

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

77
Q

Clinical Signs of Ethylene Glycol Tocicity

A 
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

78
Q

Clinical Pathology & Lesions of Ethylene Glycol Tocicity

A 
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

79
Q

PEACE PAIN

A 
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)
80
Q

Diagnosis of Ethylene Glycol Toxicity

A

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!

81
Q

Treatment for Ethylene Glycol Toxicity

A

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

82
Q

Why treat Ethylene Glycol Toxicity w/ Ethanol or Fomepazole

A 
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 


83
Q

Propylene Glycol Basics, clinical signs, toxic dose, treatment

A

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 


84
Q

Diethylene glycol, Methanol, & Ethanol

A

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

85
Q

Issue w/ fermented dough & Symptoms

A

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

86
Q

fermented dough risks & treatment

A

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 


Toxicology (6 decks)

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