Exam 3 Flashcards
(93 cards)
1
Q
Copper
A
- Essential trace element
- Some areas in PNW are deficient
- Commonly employed feed additive
2
Q
Dietary Imbalance & Copper
A
o Cu to Mo (Molybdenum) ratio out of whack (too little Mo & too much Cu)
o Should be 6pt Cu to 1pt Mo
o Molybdenum & sulfur slow absorption of Cu & enhance excretion in bile
o Often comes from feeding sheep feed mineral mixes made for cow, pig, pultry
3
Q
Sources of Copper Toxicity in Small Animals
A
Ingestion of coins
o Very very slow absorption into liver
o Recurring bouts of hepatitis
o usually no hepatocellular necrosis
If pre-existing liver issues, Cu can’t get excreted
4
Q
Animal Effected by Cu Toxicity
A
Most sensitive:
o Sheep > pre-ruminant calves, goats, llamas, alpacas
Not common
o Young, small, companion animals-exotics
5
Q
2 Classifications of Cu Toxicity
A
Primary
• Too much copper not enough Mo
• Group animal
Secondary
• Pre existing liver issue
• 1 animal
6
Q
Cu Toxicity Mechanism of Action
A
o Chronic oral exposure o Absorption dependent on form o Excess Cu stored in liver & lysosomes o Cu excreted in bile o Cu/Mo/S excreted in urine o Liver reaches storage capacity + stress -> hepatocellular necrosis -> elevated serum Cu -> hemolysis
7
Q
Clinical Signs of Cu Toxicity
A
Clinical Signs o Abrupt onset o Weakness o Abdominal pain o Dysphagia o Teeth grinding o Lethargy o Icterus o Red/brown urine o Production loss
8
Q
Clinical Pathology & Histopathology of Cu Toxicity
A
Clin Path o Increased GGT & AST o Anemia o Hemoglobinemia/uria o Hyperbilirubinemia/uria o methemoglobinemia
Histopath
o Hepatic necrosis of varying patterns
o Pigment in hepatocytes & kupffer cells
o Acute renal tubule degeneration & necrosis
o Hemoglobin casts in urine due to hypoxia & hemolysis
o no lesions = NO Cu toxicity
9
Q
Diagnosis of Cu Toxicity
A
o Look for GI, liver, hemolysis, & kidney signs
o Check liver enzymes,
o biopsy of liver & kidney for histo**
o NO serum Cu
10
Q
Treatment for Cu Toxicity
A
o Guarded/poor prognosis
o Fluids, blood transfusion
o Liver protectants; SAMe, milk thistle, n-acetylcysteine
o Enhance Cu excretion by increasing Mo & S
o Zinc, iron, selenium
o Chelators to decrease burden; D-penicillamine, tetrathiomolybdate
o NO AC
11
Q
Copper Storage Dz; Baiscs, Diagnosis, Treatment
A
o Chronic accumulation
o Not excessive in diet
o Autosomal recessive – Bedlington terrier & West Highland white terriers
o Others affected - Dobermans, Skyeterriers, Labradors, mixed, lots others
o Chronic bouts of intermittent hepatitis
Diagnosis
• Antemortem liver biopsy & histology
Treatment
• Penicillamine (chelator–reduces body burden)
• zinc acetate (reduces absorption long term)
• trientine
• tetrathiomolybdate
12
Q
Mycotoxin
A
o Produced by fungi/mold
o When mold grows it produces toxin
o Not all moldy feed contains mycotoxins, not all feed w/ mycotoxins are moldy and/or toxic
13
Q
Aflatoxin Basics & Mechanism
A
o Aspergillus
o B1 & M1
o Found in corn, cottonseed, grain
o Affects cows, swine, poultry, pets
Mechanism • Acute or chronic HEPATOTOXIC • Immunosuppressive • Nephrotoxic • Mutagenic • Carcinogenic
14
Q
Aflatoxin Acute & Chronic Clinical Signs
A
Acute • LIVER • Vomiting • Lethargy • Anorexia • Weakness / abdominal pain • Icterus • Petechiation • Ascites
Chronic • Not common • Drop body weight • Unthriftiness • Drop in production • Poor fertility • Increase incidence of disease • 2° photosensitization
15
Q
Aflatoxin Clinical Pathology & Diagnosis
A
Clinical Pathology • LIVER • Increased ALT, AST • Increased bile acids • Hyperbilirubinemia/uria • Decreased cholesterol, albumin, protein C • Increased PT, PTT • Isosthenuria
Diagnosis
• Analyze liver, kidney, lung for aflatoxin (difficult)
• Chromatography of feed
• Need representative sample of feed
16
Q
Aflatoxin Treatment
A
• Guarded prognosis
Small Animal
• Liver protectants; SAMe, milk thistle, N-acetylcysteine
• Ursodiol, steroids, transfusion, etc
Large Animal
• Not cost effective to treat
• Use aluminosilicates binders on feed to get rid of contamination
17
Q
Cyanobacteria Basics & Toxicity
A
- Blue-green algae
- Target liver & CNS
- Mostly in freshwater w/ decreased O2 & increased Phosphorous, nitrates, sulfates
Toxicity o All species susceptible o Microcystin, nodularin, cylindrospermopsin cause necrosis & hemorrhage of liver o Cylindrospermopsin also affects kidney o Results in DIC
18
Q
Cyanobacteria Clinical Signs & Pathology
A
Clinical Signs o LIVER o Acute onset (1-4hrs) o V & D & Abdominal pain o Weakness o Anorexia o Petechiation o Edema o DIC
Clinical Pathology
o Increased ALT, bile acids, bilirubenemia/uria
o Prolonged PT & PTT
o Low albumin, protein, BUN, cholesterol
19
Q
Cyanobacteria Lesions & Diagnosis
A
Lesions
o Enlarged & necrotic live
Diagnosis o Exposure to stagnant water o Liver signs o ID of algae o Toxin analysis of water
20
Q
Cyanobacteria Treatment
A
Asymptomatic
• Decontaminate if very early
• Cholestyramine
Symptomatic • Corticosteroids • Fuids • Transfusion • Liver protectants, SAMe, milk thistle, n-acetylcysteine • Cholestyramine
21
Q
Iron Toxicosis Basics
A
- Poisoning uncommon
- Soluble or ferris iron most important
- Different amounts of elemental iron
- Different bioavailability
- Estimate: 5-15% ingested gets absorbed
- Well documented toxic doses of elemental iron
22
Q
Sources of Iron
A
o Iron, vitamin/mineral supplements o Fertilizers o Blood meal o Moss repellants o Molluscicide o Body-hand-feet warmers o Desiccant packs o Birth control pills o Foreign bodies
23
Q
Mechansims of Action of Iron Toxicity
A
o Oral
o Absorbed by intestinal cells
o Cells damaged and sloughed off
OR if acute overwhelm of Fe ->
o Fe goes systemically o No efficient way to excrete Fe o Transferrin circulates Fe o Stored as Ferritin or hemosiderin o Systemically affects LIVER, vascular, cardiac
24
Q
Clinical Signs of Iron Toxicity
A
o Acute
o No V in 8-12hrs = OK!
o V, D, lethargy, anorexia, abdominal pain
After apparent recovery from initial GI signs
• @ 12-96hrs
• GI signs re-appear
• petechiation, ecchymosis, effusions, tachypnea, shock
25
Gross & Histo Lesions of Iron Toxicity
Gross
• Inflammation, hemorrhage, necrosis of GI & liver
Histo
• Inflammation, necrosis, hemorrhage
26
Diagnosis of Iron Toxicity
```
o Exposure history
o GI + liver + maybe heart
o Radiographs reveal radiopaque tablets
o Total serum Fe
o Total Fe binding capacity (slow results)
o Post-mortem liver biopsy
```
27
Treatment of Iron Toxicity
```
Decontaminate if appropriate!
• emesis,
• lavage with Mg-Al hydroxide or sodium bicarbonate
• cathartic,
• whole bowel irrigation?
• bulk cathartic
• NO activated charcoal
```
GI protectants
• sucralfate, H2-antagonists, proton pump inhibitors
IV fluids
• Very important
liver protectants
• Denamarin – SAMe and silybin, n-acetylcysteine, ursodiol
Chelation
• deferoxamine (others)
• for high exposures
• binds Fe & excretes in urine
Monitor continuously
• signs and/or serum iron levels!
28
Desiccants; Basics, Sources, Treatment
* often contain iron carbonate
* non-activated ones more of a risk for iron
* Activated = iron oxide
* Low toxicity -> mild GI upset
* Make sure they pass
* Make them drink lots of water
* Some have iron (50-70%) = discoloration to urine
Sources
o shoe boxes, lamps, medications, electronic equipment, foods
Treatment
o emesis if appropriate, magnesium hydroxide, bulk cathartic
o Can monitor movement with radiographs if have iron
o Rare - chelation for iron if high enough exposure
29
Hand/Feet Warmers; Basics & Treatment
* Iron carbonate but iron oxide when activated
* GI upset
* Rarely enough for liver, heart, vascular
* Non-activated are more risk
* Heat may be a problem
```
Treatment
o Emesis
o Milk of magnesia (Mg hydroxide)
o Bulk cathartic (Metamucil
o Monitor movement on radiograph
```
30
Birth Control Basics
* Estrogens, progesterones, placebos, maybe iron
* <1mg/kg of estrogen is OK
* >10mg/kg progesterone = sedation & lethargy
* HIGH progesterone -> recumbancy & seizures
* Iron -> GI upset & discolored urine
31
Xylitol; Basics, Uses, Sources
* 5 carbon sugar alcohol
* Affects dogs (maybe birds)
* Hypoglycemia & liver dz
```
Uses
o Sugar sub
o Anticariogenic
o Antimicrobial
o Low glycemic index
o Cooling
o Moisturizing
o Prevents fermentation & molding
```
Sources
o Gum
o Toothpaste
32
Xylitol Toxicity Calculations
o 0.3 g xylitol / piece, if xylitol is not the first sugar alcohol
o 1.0 g xylitol / piece, if xylitol is the first sugar alcohol
o not consistent
o call company for actual conc
33
Xylitol Mechanism of Action & Symptoms
o Xylitol liquid absorbed rapidly –>
o metabolized by liver to glucose, glycogen, lactate
o depending on form can have delayed absorption
Symptoms
• Nonspecific
• diarrhea, gas (true for all sugars)
34
Xylitol Clinical Pathology
Initially
• Increased & Hypoglycemia
• Decrease K & P
• Can last from few hours to few days
```
Later (9-12hrs)
• LIVER
• Elevated liver enzymes
• Hyperbilirubinemia
• Elevated bile acids
• Prolonged clotting times
• Hypocholesterolemia
• Hypoalbuminemia
```
35
Lesions from Xylitol
Gross
• Hemorrhages
• Enlarged liver
Histo
• Hepatic necrosis
36
Diagnosis of Xylitol Toxicity
o Exposure history
o Hypoglycemia, hypokalemia
o Hepatic dz
o Causes false (+) on ethylene glycol kit
37
Treatment for Xylitol Toxicity
Asymptomatic
• Decontaminate: emesis (careful) / lavage, cathartic (AC not effective)
• monitor blood glucose for 12-48 hours - every 2-4-6 hours,
• provide oral or IV dextrose supplements
• patient should be *euglycemic for minimum 6 hours without supplementation before discharge
• Should consider liver protectants for all exposed patients!
Symptomatic or exposures > 100-500 mg/kg
• Hypoglycemia phase - Dextrose: for 12-48 hour, monitor K & P
• Hepatic phase – liver protectants 2-4weeks
• Continuous monitoring of liver enzymes up to 72 hours
• recheck at 1, 2 and 4 weeks
38
Zinc, Aluminum, or Magnesium Phosphide Basics
* rodenticide, insecticide, grain fumigant
* all animals susceptible
* ingesting bait or treated feed or inhaling fumes
* inhale phosphine gas -> pulmonary edema, cardiac failure, liver failure
39
Zinc, Aluminum, or Magnesium Phosphide Mechanism of Action
o Contact with water + acidic environment of stomach = phosphine gas
o Phosphide and phosphine gas are severe irritants –> inflammation and necrosis
Metabolic poison
• block cytochrome C oxidase ->
• blocks electron transfer and oxidative phosphorylation ->
• no ATP production and an energy crisis in cells ->
• increase in cell membrane/vascular permeability ->
• CV collapse, failure of all organs
40
Zinc, Aluminum, or Magnesium Phosphide Clinical Signs
o Acute onset & fast progression (15 min – 4 hrs)
GI
• Severe pain w/ distension, anorexia, salivation, diarrhea, vomiting
• better prognosis
CNS:
• malaise, ataxia, tremors, seizures, altered behavior
• poorer prognosis
Respiratory:
• labored breathing, increased RR, coughing, sneezing, pulmonary edema
• poorer prognosis
Cardiovascular:
• Increased HR, arrhythmias, hypovolemic shock
• poorer prognosis
Acutedeath, especially in horses and birds
GI, heart, lung, liver, kidney
41
Zinc, Aluminum, or Magnesium Phosphide Diagnosis
o History of baiting
o Clinical signs : multiple organs & rapid progression
o Odor of gas: ‘*rotten fish’ ‘acetylene’, ‘garlic’ (get out if smell this or ammonia!!!)
o congestion/necrosis lung, kidney, liver, heart, GIT;
o Confirm: phosphine gas of stomach contents and source material (airtight & frozen)
42
Zinc, Aluminum, or Magnesium Phosphide Treatment
Asymptomatic
• Decontaminate
```
Symptomatic
• Anti-emetics
• control the diarrhea
• IV fluids
• corticosteroids,
• analgesics,
• antibiotics,
• GI protectants
• Lavage 5% sodium bicarbonate, antacids (in theory)
```
43
Arsenic Basics
* Organic is rare & attacks peripheral nervous system
* Inorganic more common & attacks GI & systemic
* Trivalent more toxic than pentavalant
* No toxicosis from cribbing
* Toxicosis form environment contaminated with ash
44
Sources of Arsenic
o Herbicide (NV: Pb-As),
o old *rodenticide
o Wood preservative
o
Ant baits - uncommon
45
Clinical Signs of Arsenic Toxicity
o abrupt onset;
o oral – acute, peracute, subacute
o rarely chronic in animals,
o “chronic poor doing”.
o Abdominal pain
o Ataxia, weakness, lethargy
o Salivation, vomiting/regurgitation, diarrhea
o severe fluid loss and shock / death (abrupt in cattle – case)
o “Happy pig/poultry syndrome” (organic form)
46
Diagnosis of Arsenic Toxicity
Antemortem:
• blood, urine (short half-life)
Postmortem:
• liver, kidney (hair chronic)
• rumenitis
• submucosal edema
47
Treatment of Arsenic Toxicity
```
o fluids!!!!
o succimer (chelator for chronic exposure)
```
48
Vomitoxin Basics
* Deoxynivalenol–DON–vomitoxin
* production animal problem
* Grain WHEAT & less commonly grass,hay
* All species susceptible
* Swine most sensitive
* dogs (contaminated feed)
* rarely fatal
49
Vomitoxin Clinical Signs
acute
• feed refusal, drop in weight,
• vomiting-regurgitation, diarrhea
chronic
• some feed refusal,
• diminished immune responses,
• poor production with respect to weight loss
50
Vomitoxin Diagnosis & Treatment
Diagnosis
o Feed source
o Recent feed change
o Test representative smaple of feed for vomitoxin
Treatment
o Remove source
51
Meat Package Padding
* Silica gel, cellulose, polygel
* Non-toxic
* GI upset
* Can cause obstruction due to moisture absorption
* Keep animal well hydrated
52
Phenoxy Herbicides Basics
* 2,4-D
* N, P, K
* All animals susceptible but dogs most
* Can be exposed due to properly applied and not dry or access to puddles
* Short half-life except in dogs
* Rarely fatal, excellent prognosis
53
Phenoxy Herbicides Clinical Signs
o Rapid absorption from GIT
o excreted primarily via urine unchanged!
o Abrupt onset: GIT + neuromuscular
Low exposures:
• Anorexia, vomiting- regurgitation, diarrhea
• self-limiting; gone in 24 hrs
High exposures
• GIT, ataxia, *myotonia
54
Phenoxy Herbicides Diagnosis & Treatment
```
Diagnosis
o GI & neuromuscular symptoms
o History of use
o Myotonia!
o Chemical in urine or serum
```
Treatment
o Asymptomatic - Decontaminate
o Symptomatic - Diuresis for 48 hrs
55
Batteries & Magnets Basics
Dry cell batteries
o Acid or *alkaline
o Can leak
Lithium disc/button batteries
o No corrosives
• Both damage mucosal lining!!!
Magnet:
o no GI signs, make sure they pass:
o one is OK, two or more problematic!!!!!!
56
Batteries & Magnets Treatment
not damaged battery
• emesis
• no need for GI protectants
damaged battery
• use GI protectants
• dilution
lithium / button battery
• emesis
• use GI protectants
o Want to see them pass in *36 hours
o No AC
```
GI protectants:
o demulcents,
o sucralfate,
o H2-antagonists,
o proton pump inhibitors,
o misoprostol
```
57
Basics of NSAIDs & Toxicity
* Ibuprofen, naproxen, carprofen
* Dogs more often than cats
* Large animal usually chronic
Toxicity
o Inappropriate use, accidental consumption, malicious
o Different products have different half-lives, protein-binding, enterohepatic recirculation, excretory pathways, some lipophilic,
o Toxic’ doses hard to find
o DO THE MATH
o Cats: up to 8-10x more sensitive (if not a dose listed in chart)
58
Mechanism of Action for NSAIDs
o Rapidly absorbed
Major:
• inhibition of cyclooxygenase (PG synthetase) activity ->
• lack of PGI2, PGE2 ->
• gastric ulceration and renal necrosis
Minor:
• inhibits platelet cyclooxygenase -> decreased platelet aggregation
• CNS effects – opioid receptors
• immune mediated attack against an altered protein in liver of dogs
59
Clinical Signs of NSAID Toxicity
```
o acute
o GI upset: 4-6 hrs, or less
o GI ulceration: 12 hrs – 4 days
o Renal: 12 hrs – 5 days
o Depression – lethargy (93%)
o anorexia, vomiting ( blood),
o abdominal pain, diarrhea,
o ataxia
o less common: tachypnea & PUPD
```
60
Lesions of NSAID Toxicity
```
o Asymptomatic - none
o hemoconcentration,
o GIT (vomiting, diarrhea, ulcers),
o kidney / liver
o hemorrhage, inflammation, ulceration, erosion of GIT
o renal papillary necrosis;
o hepatic necrosis
```
61
Treatment of NSAID Toxicity
o Prognosis GREAT if treat EARLY + AGGRESSIVELY
o Most will present asymptomatic!
o CBC, chem, UA for baseline
Decontaminate:
• emesis, repeated AC, cathartic, gastric lavage
Diuresis
• 2-3x maintenance fluids for min of 48hrs
• enhance excretion
• increase GFR & decrease touch time
H2 antagonists
• 2-3 days
• Reduce gastric excretion
Proton pump inhibitor
• 7-10 days
• Omeprazole
• Reduce gastric acid
Misoprostol
• PG analogue
• 3, 5, or 7 days
• enhances mucosal defense
o monitor BUN, Cr, USG, PCV, TP, liver enzymes
o liver protectants
o naloxone for neuro signs
o IV lipid therapy
62
Basics of Cough Drops
o Menthol + sugar
o GI distress
o Hypoglycemia & liver dz if xylitol present
o Wide margin of safety for menthol
o Menthol can affect kidneys, lungs, heart, CNS
63
Cantharidin (Blister Beetle) Toxicity Basics
```
o MANY species
o Risky ones in OK & TX
o Beetles found in alfalfa
o Used maliciously
o Human medicine
o A few to hundreds of beetles required to cause toxicities
o Equine, bovine
```
64
Cantharidin (Blister Beetle) Mechanism of Action
o Lipid soluble
o highly irritating – penetrates and causes acantholysis
o protein phosphatase inhibitor
o Readily absorbed & majority excreted unchanged in urine
o Hypocalcemia & hypomagnesemia
65
Cantharidin (Blister Beetle) Clinical Signs
```
o Abrupt onset:
o Severe GIT distress: restlessness, irritability, sweating, pawing, grunting, trembling
o Increased RR + HR
o diarrhea, gastric reflux
o frequent-straining urination
o Up to 20% have CNS: head pressing, disorientation, seizures, lethargy
o Rare Myocardial signs
o Shock, death
```
66
Cantharidin (Blister Beetle) Clinical Pathology & Lesions
o Hypocalcemia & hypomagnesimia
o Congestion, inflammation, hemorrhage in GI (maybe renal)
o Gastroenteritits, nephritis, cystitis,
o maybe myocardial necrosis
o Look for vesiculation of nonglandular stomach
67
Cantharidin (Blister Beetle) Diagnosis
o Ingestion of alfalfa
o GI, renal, maybe myocardial & CNS signs
o ID of beetle
o Urine chemical analysis
68
Cantharidin (Blister Beetle) Treatment
```
o Remove source
o Enhance renal excretion w/ diuresis
o Enhance fecal excretion w/ AC
o Correct dehydration
o Correct Ca & Mg
o Manage pain
o 50% survival w/ aggressive treatment
```
69
Dryer Sheets Toxicity
Fresh
o Cationic detergents
o GI inflammation & necrosis
Used
o Foreign body or pass
Treatment
o GI protectants
o anti-inflammatories
o endoscopic removal
70
Cationic Detergents Basics
o fabric softeners, germicides, sanitizers, dryer sheets, potpourris
o quarternary ammonium compounds with groups attached: benzalkonium chloride, alkyl dimethyl 3,4-dichlorobenzene
o Highly to extremely toxic
o corrosive effect of concentration & pH
o systemic effect of dose
o Solutions > 1% can be corrosive
71
Cationic Detergents Clinical Signs
o salivation, vomiting,
o muscle weakness and fasciculations,
o CNS + respiratory depression, fever, seizures, collapse, coma
o Corrosive lesions of paws
o swelling, ulceration, sloughing of GI mucosa
72
Cationic Detergents Treatment
o milk, water, or egg whites
o follow with AC + cathartic
o esophagoscopy
o maintain fluid and electrolyte balance
o analgesics
o prophylactic antibiotics
o GI protectants
o percutaneous endoscopic gastrotomy (PEG) tube placement (adequate caloric intake)
o wash paws and hair
o monitor for hyperthermia and inflammation
73
Acetominophen Toxicity Bascis
o Dogs & cats
o Cats extremely sensitive: DO NOT USE – any type of exposure should be considered a risk (ferrets also sensitive)
o Male cats more sensitive than females to succumbing to liver disease
o Rapidly absorbed,
o metabolized by mixed function oxidase (MFO),
o relatively short half-lives
74
Normal Therapeutic Use of Acetominophen
o small amount oxidized to reactive intermediate -> scavenged by glutathione -> urine
DOG:
• 75% conjugated with glucuronic acid;
• 20% sulfates
• rest unchanged & excreted in bile & urine
CAT
• no use therapeutically:
• 90% sulfates; 5% cysteine; 1% glucuronic acid
• excreted in bile, urine
75
Over Exposures to Acetominophen
o De-tox pathways overloaded ->
o more acetaminophen to convert to reactive intermediate ->
o glutathione supply is depleted ->
o reactive intermediate responsible for hepatic necrosis and red blood cell lysis / methemoglobin
o “Para-aminophenol” is also responsible for methemoglobin formation and hemolysis
76
Clinical Signs of Acetominophen Toxicity in Cats & Dogs
```
Cats
• Delayed onset
• RBCs then liver then kidney
• Methemoglobinemia, Heinz bodies, hemolysis
• Hypoxemia, hypoxia
• Weakness, lethargy, tachypnea, cyanosis
• Liver necrosis
• Facial & paw edema
```
```
Dogs
• Delayed onset
• Liver then RBCs then kidney
• Liver necrosis
• anorexia, vomiting, depression-lethargy, abdominal pain, icterus, weight loss
• Methemoglobinemia, hemolysis
• Hypoxemia, hypoxia
• Death due to hypoxia or liver failure
• Facial & paw edema
```
77
Acetominophen Toxicity Diagnosis
```
o Exposure history,
Clinical signs, Clinical pathology
o Liver, RBC maybe kidney
o Rule out other cuses for symptoms
o hepatic necrosis, icterus,
o renal nephrosis
o evidence of hemolysis
o chemical analysis of serum
```
78
Acetominophen Toxicity treatment
o Do the math
Asymptomatic
• Decontaminate: emetics, AC, cathartic; gastric lavage-AC-
Symptomatic
• Often too late to decontaminate
• N-acetylcysteine: binds toxin -> decrease methgb formation
• Ascorbic acid (Vit C)
• fluids, oxygen, blood transfusions, oxyglobin / plasma, vitamin K1, glucose, liver protectants Denamarin (SAMe and silybin)
• Monitor: liver enzymes, CBC, Chem panel, UA, RBC count
Prognosis
• Depends on dose & damage
79
Wood Glue
o Polyurethanes
o Contact w/ moisture -> expands, foams, hardens
```
Treatment
o No emesis
o No fluids or food by mouth
o Radiographs
o surgery
```
80
Acute Nitrate Poisoning
```
o VERY common
o Ruminants only
o Ingestion of nitrate accumulating forage
o Chenopodium, oat hay, sorghum
o Nitrate most in lower stem of plant
```
81
Risk Factors for Nitrate Poisoning
```
o Fertilizer
o Harsh weather
o Soil/environment
o High consumption
o Lack of adaptation
o Old cow
o Winter/spring months
```
82
Mechanism of Action of Nitrate Poisoning
o NO3 -> NO2 -> NH3 in rumen ->
o NO2 binds w/ hemoglobin in blood ->
o MetHgb(Fe3+) ->
o MetHgb reductase becomes overwhelmed
83
Clinical Signs of Nitrate Poisoning
```
o BROWN BLOOD
o Lethargy
o Dyspnea
o Salivation
o Ataxia, tremors, recumbency
o Pale/cyanotic mucous membranes
o Death
```
84
Diagnosis, Treatment, & Prevention of Nitrate Poisoning
Diagnosis
o Abrupt onset of clinical signs
o Abortions
o Chemical analysis of representative feed
o Test eyeball post mortem
o Serum/plasma test only if showing symptoms
Treatment
o Methylene blue
o Avoid stress
Prevention
o Test feed
85
Basics of Zinc
o US pennies minted 83’ forward, Zn sulfate footbaths
o Not common
o Acute problem
o Small dogs & birds
o Zn leaches very quickly due to stomach acid
o Excreted in urine, faces(bile), pancreas
86
Zinc Toxicity
o Hours to days
o Overwhelmed excretory pathway -> GI symptoms
o Oxidative damage to RBCs -> acute hemolytic crisis
87
Zinc Toxicity Clinical Signs
```
o Acute onset GI
o Vomiting, diarrhea, lethargy, anorexia, abdominal pain
o Anemia & pale mucous membranes
o Renal hypoxia & Zn induced nephrosis
o Increased liver enzymes
o Increased pancreatic enzymes
o Angioedema
o DIC (rare)
```
88
Zinc Toxicity Lesions
GI
• Inflammation & necrosis
Kidney
• Tubular nephrosis with hemoglobin casts
Liver
• Hepatic inflammation + necrosis / pigment
Pancreas
• Inflammation, necrosis / fibrosis
89
Zinc Toxicity Diagnosis & Treatment
```
Diagnosis
o History of exposure
o Radiographs
o Only corroded coins are issue
o Serum analysis
o Postmortem lesions on liver, kidney, pancreas
```
```
Treatment
o Remove source
o Diurese
o Blood transfusion
o O2
o analgesic & anti-emetic
o GI protectant sucralfate, H2-antagonist and proton pump inhibitor
o Monitor PCV
o Maybe chelation therapy
```
90
3 Types of mercury & risks
Elemental mercury
o Ok
o Bulk w/ bread or pumpkin
o Radiographs to ensure passes
Inorganic Mercury
o Bad
o Severe GI damage & multisystemic issues
Organic Mercury
o Bad
o Nervous system issues
91
Basics & Mech of Action of Anticoagulant Rodenticides
o All animals effected
o Usually dogs & wildlife
o Different T 1/2s & toxic doses depending on product
o Secondary poisoning uncommon except in GREAT mousers & wild raptors
Mech of Action
o Vit K epoxide reductase inactivates Vit K ->
o Clotting factors II, VII, IX, X not activated ->
o Delay in seeing prolonged clotting times
92
Clinical Signs & Diagnosis of Anticoagulant Rodenticides
```
Clinical Signs
o Onset in 2-3 days
o Clotting prolongation at 12-16-48 hours
o Hemorrhage
o lethargy, anorexia,
o dyspnea, abnormal lung sounds
o epistaxis, hemoptysis:
o most common bleeding into the lungs, thorax, mediastinum
```
```
Diagnosis
o History of use
o Hemorrhage
o Anemia
o Clotting panel (PT, PTT, ACT)
o Radiograph
o Give plasma & tap hemorrhage
o Chemical analysis of blood & liver
```
93
Treatment of Anticoagulant Rodenticides
o Do the math
o Non-toxic dose = send home
Non-bleeding & toxic dose
• Decontaminate even several hours post exposure
• Give Vit K for 4 weeks
• After 24-36hrs check PT & PTT
```
bleeding & toxic dose
• plasma & maybe blood transfusion
• Give Vit K for 4 weeks
• After 24-36hrs check PT & PTT
• Restrict exercise
• Give O2
• antibiotics
```
