Exam 3 Flashcards
Copper
- Essential trace element
- Some areas in PNW are deficient
- Commonly employed feed additive
Dietary Imbalance & Copper
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
Sources of Copper Toxicity in Small Animals
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
Animal Effected by Cu Toxicity
Most sensitive:
o Sheep > pre-ruminant calves, goats, llamas, alpacas
Not common
o Young, small, companion animals-exotics
2 Classifications of Cu Toxicity
Primary
• Too much copper not enough Mo
• Group animal
Secondary
• Pre existing liver issue
• 1 animal
Cu Toxicity Mechanism of Action
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
Clinical Signs of Cu Toxicity
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
Clinical Pathology & Histopathology of Cu Toxicity
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
Diagnosis of Cu Toxicity
o Look for GI, liver, hemolysis, & kidney signs
o Check liver enzymes,
o biopsy of liver & kidney for histo**
o NO serum Cu
Treatment for Cu Toxicity
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
Copper Storage Dz; Baiscs, Diagnosis, Treatment
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
Mycotoxin
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
Aflatoxin Basics & Mechanism
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
Aflatoxin Acute & Chronic Clinical Signs
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
Aflatoxin Clinical Pathology & Diagnosis
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
Aflatoxin Treatment
• 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
Cyanobacteria Basics & Toxicity
- 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
Cyanobacteria Clinical Signs & Pathology
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
Cyanobacteria Lesions & Diagnosis
Lesions
o Enlarged & necrotic live
Diagnosis o Exposure to stagnant water o Liver signs o ID of algae o Toxin analysis of water
Cyanobacteria Treatment
Asymptomatic
• Decontaminate if very early
• Cholestyramine
Symptomatic • Corticosteroids • Fuids • Transfusion • Liver protectants, SAMe, milk thistle, n-acetylcysteine • Cholestyramine
Iron Toxicosis Basics
- 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
Sources of Iron
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
Mechansims of Action of Iron Toxicity
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
Clinical Signs of Iron Toxicity
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
Gross & Histo Lesions of Iron Toxicity
Gross
• Inflammation, hemorrhage, necrosis of GI & liver
Histo
• Inflammation, necrosis, hemorrhage
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
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!
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
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
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
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
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
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)
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
Lesions from Xylitol
Gross
• Hemorrhages
• Enlarged liver
Histo
• Hepatic necrosis
Diagnosis of Xylitol Toxicity
o Exposure history
o Hypoglycemia, hypokalemia
o Hepatic dz
o Causes false (+) on ethylene glycol kit
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
