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Toxicology > Toxicology - Exam 2 Material > Flashcards

Toxicology - Exam 2 Material Flashcards

1
Q

Regarding copper toxicity, what are the hisotlogical lesions that youre gonna see?

A
  • Tubular nephrosis, acute , multifocal, severe with hemoglobin casts

Gastroenteritis

**Hepatocellular necoris, acute, ** multifocal severe

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2
Q

Regarding copper toxicity,

  • what are some different sources for food animals?
  • Which animals are affected?
A

1) dietary imbalance
2) A) Sheep (this spp is most sensitive) and note that the exposure is CHRONIC B) THIS IS AN AUTOSOMAL RECESSIVE DISEASE IN DOGS –> COPPER STORAGE DISEASE
3)

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3
Q

What is the mechanism of action for copper toxicity?

A
  • oral –> chronic exposure but abrupt onset
  • Excess copper stored in the liver; note that Cu-Mo-S are excreted in the bile; and lysosomes (function to ???)
  • Liver has high storage capacity/reach capacity + stress

Cu released –> hepatocellular necrosis –> serum Cu –> hemolysis (most the time)

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4
Q

Discuss the clinical pathology for copper toxxicity

A
  • Liver enzymes –> elevated GGT and AST
  • Anemia due to hemolysis
  • Hemoglobinemia/uria, hyperbilrubinemia/uria
  • Methemoglobinemia (brown blood)
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5
Q

Regarding copper toxicity, discuss treatment/prevention

A

Prognosis: guarded - poor for lcinically affected animals (both small animals and large animals)

Treatment + prevention: enhance copper excretion (FA):
- **Mo-S source: enhances feceal, urinary, biliary excretion/slows down absorpption and enhancs excretion
- Chelators –> Decrease body burden

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6
Q

Discuss copper storage disease (chronic active hepatitis) for canines and treatment for it

A

Chronic accumulation!
- Not excessive in diet
- Autosomal reccessive –> seen in Bedlington terrier breed and sometimes in West Highland white terriers

Chronic bouts of intermittent hepatti

Treatment –> Penicillamine (chelator that reduces body burden and zinc acetate (reduces absorption long term); treatment is usually long tterm

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7
Q

Regarding cyanobacteria, discuss the basics of it

A
  • Targets the liver and CNS
  • Criteria about charcteristics where these algal blooms are found –> 1) ubiqitoud 2) stagnant-slow moving 3) decreased oxygen, 4) increased nutrients (phosphates, nitrates and sulfates), 5) quiet weather 6) warmish water - Temperature and pH (?????) 7)high light intensity
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8
Q

Discuss the mechanims of action for cyanobacteria

A

All species suscpetible

Microcystin/nodularin/cylindrospermopsin - specific to the liver
- Massive necrosis with hemoorhage
- Cylindrospermopsin - renal necrosis
- cylindrospermopsin also affects the kidneys

Shock –> DIC –> Death

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9
Q

Discuss clinical isgns associated with cyanobacteria

A

Clinical signs are liver specific
- elevated ALT, bile acids, bulirubinemia/uria and prolonged PT-PTT
- low albumin, low protein, low BUn, cholesterol
- Potential renal changes

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10
Q

Discuss the basics of anticoagulant rodenticide toxicity

A
  • All species are sueceptible except for cats, carts are pretty resistant to it.
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11
Q

What is the mechanims of action for Anticoagulant rodenticide toxicity

A
  • Vitamin K is an essential cofactor in actiavtion of clotting factors II, VII, IX, X. When rhis occurs, ‘active’ vitam,in K –> inactive vitamin K epoxide
  • **Vitamin K epoxide reductase
  • Rodenticdes inhibit enzyme –> prevents recycling ‘active’ vitammin K**
  • Loss of clotting factors, therefore we are likely going to see prolonged clotting times
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12
Q

Regarding anticoagulant rodenticide toxicity, what are the clinical signs?

A
  • Onset: 2-3-5 days; clotting prolongation occurs erlier but after 36-48 hours, we start seeing a delay when 65-80% of factors are lost)

Treatment is dependent upon: hemorrhage site, speed, and volume. HEMORRHAGE CAN OCCUR ANYWHERE

  • 70% BLEEDING INTO THE LUNG, THORAX, AND MEDIASTINUM
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13
Q

Discuss diagnosis criteria for anticoagulant rodenticide toxicity

A
  • History of use/exposure: Assume long acting
  • Clinical pathology, clinical signs: site, volume, speed of hemorrhage

DO NOT RULE OUT IF OATIENT IS NOT ANEMIC … prolonagtion of clotting times occurs before anemia is seen

Reememebr, it is important to differentiate between 1) loss vs 2) hemolysis vs 3) lack of production

DO NOT LIST MALABSORPTION AS AN ANSWER ON THE EXAM

For clotting pannel, expect prolonged PT and PTT

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14
Q

Discuss the treatmnent for antiocoagulant rodenticide toxicity

A

1) do the math!!!! if the dose is NOT TOXIC, send the animal home
2) Toxic dose: establish baseline clotting panel

**A) Decontaminate **
B) Plasma/blood transfusions if needed
C) Vitamin K1

Think about decontamination several hours post ingestion, then most likely you are gonna wanna administer Vitamin K1. If you have a patient that vomits after you administered activated charcoal, then you MUST ADMINISTER THE FIRST DOSE SUB-Q. Treat for 4 weeks too. After 4 weeks therapy, you must wait 36 - 48 hours before checking the clotting times to see if they’re still clapped or not.

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15
Q

Regarding NSAIDs, what is a prostaglandin?

A

A prostaglanding is a lipid derived chemical messemnger mostly acting in a paracrine fashion which means they act on the site where they are released

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16
Q

What are the actions of NSAIDs?

A
  • NOte that these actions result from the inhibition of prostalglkandinng synthesis

1) Anty-inflkammatory (COX-2)
2) Antip-pyretic (COX-3) –> this means that it functiona to reduce fever
3) Analgesia (COX-2)
4) Gastric ulceration (COX-1)
5) Reduced renal blood flow
6) May interefere with parturition
7) Inhibition of platelet aggregatuon
8) COX2 and the heart
9)

17
Q

With regards to the actions of NSAIDs and specifically, the action of NSAIDs that inhibit platelet aggregatuion

1) Why is aspirin significant?
2) Why is warfarin significant?
3) Acetominaphen –? why is it significant?

A

1) Aspirin has an irreversible action
2) Warfarin –> warfaroin has the potential for drug interactions; warfarin also acts as an anticoagulant which is signifiant because warfarin also competes with many NSAIDs for binding to plasma proteinS

18
Q

With regards to cantharidin toxicity, what species is most susepctible to this? Next, discuss its mechanism of action

A

Cantharidin is a toxin that comes from beetles; the most suspectible species to this toxin is horses then cows.

Mechanims of action:
- lipid solubvle/highly irritating –> penetrates and causes acantholysis
- - readily absorbed, the majority of it is excreted in the the urine uchnaged
- Hypocalcemia/hypomagnesemia

19
Q

Regarding canthariding toxicity, discuss the clinical pathology that is expcted

Next, discuss the gross and histologic lesions

A

Clinical pathology:
- decreased Calcium and decreased magnesium and an inflammatory leukogram

1Gross lesions: **Congestion, inflammation, hemorrhage GIT + renal system*

Histologic lesions: Gastroenteritis, nephritis, cystitis, myocardial necoris

mnost importantly –> look for the vesiculation of the nonglandular portion of the gastric mucosa

20
Q

Discuss the toic of dryer sheets and cationdtergents along with treatnment:

A
  • Cationic detergents **toxicity related to concentration + pH (<3 or > 11): GIT inflammation and necrosis: caustic/corrosive
  • Treatment: options include: treat the patient (sympotmatic)
  • Most important GI protectants are: analgesics, anti inflammatoryies, PEG tube, endoscopy, antibiotics, other symptomatic care
21
Q

Discuss the topic of cationdetergents

A

Includes fabric softeners, germicides, sanitizers, dryer sheets, pot-pourris –> quarternary ammonium compounds with groups attached

  • Highly to extremly toxic –> corrosoive effect of concentration
  • Solutions > 1% can be corrosive
  • Oral ingestopn –> salivation, vomiting, muscle weakness and fasiculations, CNS + respiratory depression, fever, seizures, colllapse, coma

Treatment:
- milk, water, or egg whites
- follow with AC + cathartic
- esophagoscopy
- Maintain fluid and electrolyte balance
-

22
Q

Discuss the topic of acetominaphen

Discuss the topic of acetomenaphen and over exposure (what happens to the methabolic pathways):

A
  • **analgesic, antipyretic ** - some anti inflammatory (inidicatioons that it does inhibit cyclooxygenase-COX2)

Toxicity:
- Cats –> extremely sensitive (ferrets are also sensitive)

DE TOX PATHWAYS **(GLUCOURONIDATION/SULFATION-MORE SATURABLE IN CATS) ** BECOME OVERLOADED –> more acetominaphen to reactive intermediate (RI) –> glutathione supply is depleted –> **RI ** responsible for hepatic necoris and red blood cell lysis/methemoglobin

23
Q

Discuss the clinical siogns associated with cats ingesting acetomenaphen and the clinical pathology that should be exopected

A
  • Delay in onset
  • CATS: primary target is RBC (increased dose, more likely to see liver)/ secondary target is liver/ third most important target is kidney/hypoxia)
  • **Methemoglobin, ** , heinz bodies, **hemolysis, **, hemoglobinuria/emia
  • Liver necorsis leads to: salivation, vomiting, aabdominal pain, anorexia
  • Brown blood/mucous membranes can be white or cyanotic or muddy or icteric
  • Facial paw edmema
24
Q

Discuss acetomenaphen ingestion in cats and the expected clinical signs and clinical pathology

A
  • Delay in onset
  • DOGS: primary target is liver, secondary target is RBC, third most important target is kidney (hypoxia)
  • Liver necrosis –> disease, failure: anorexia, vomiting, depression-lethargy, abdominal pain –> icterus, weight loss (elevated liver enzymes-bile acids and decreased protein, clotting pronlems, etc)
  • **RBC ** –> **milder methemoglobinemia, hemolysis ** leading to hypoxemia, hypoxia: weakness, letargy, cyanosis, tachypnea,
  • Death due to hypoxia and/or liver failure
  • Facial paw edema
  • **Blood is brown/mucuous membranes can be white or cyanotic or muddy or icteric **
25
Q

Regarding acetimineophen ingestion in animals, discuss the treatment protocol

A
  • decontaminate: if asymptimatic, then AC Cathartic VS if sym,potmatic, then often too late/risks v benefits + factors
  • N-acecytylcysteine:: sulfhydryl donor (precurosr for gluathione)/binds toxin/dececreases methemoglobin formation
  • Supportive care: liver protectants include Denamrin (SAMe and silybin)
26
Q

Discuss Paraquat toxicity

A

Paraquat: herbicide (dessicant, very popular)
- all animals susuceptible:
Oral exposure: acute
- Acumulates in the lung –> long half life
- Most is excreted unchanged in the urine
- MECHANISM OF ACTION: Production of free radicals –> substrate is oxygen –> membrane destruction –> leads to cell death

27
Q

What are the clinicalsigns of paraquat toxicity

A

Acute:
- **GIT ** –> initial; vomiting, lethargy, abdominal pain, anorexia, ulcers
- Pulmonary –> initial; inflammatiopn, necoris, edema, hemorahhge

Chronic:
-** Pulmonary chnages continue but its now fibrotic
- Renal: same as GIT**

Actually there are 2 phases, chronic and acute. So there is an acute phase and a chronic phase, but overall it is an ACUTE exposure. Acute presents with GI signs and pulmonary signs. In the chronic phase, if they survive, they present with pulmonary signs and perhaps renal signs. As the oaraquat goes to the lung, it causes a tremendous amount of inflammation, necrosis, hemorrhage, and edema. Odds are that most patients will not survive acute phase but if they do and enter the chronic phase, there is noticeable worsening of the respiratory changes but as it is excreted out of the kidney, you will see the renal necrosis. So then you will see the fibrosis stage and you can also see those nonspecific signs of renal disease and the pathological signs/chnages of renal disease. These include azotemia, BUN, casts in urine, white cells, etc. . Yada yada

28
Q

Discuss the lesions assoiated with paraquat toxicity

A

Gross:
- Acute: Hemorrhage, necrosis, edema, heavy lung/GIT inflammation, necoris,s edemaa, ulcers,
- Chronic: + fibrosis in the long

Microscopic:
- Acute: hemoorahge, edema, necoris - lung, GIT
- Chronic: + interstitial lung fibroplasia/renal necoris, others –> cardiac, hepatic, adrenal

29
Q

zregarding paraquat toxicity, discuss treatment and prognosis

A

Depends on cliniical presentation + stage:
- Decontaminate (AS): emesis, AC, cathartic
- **Antiemetics ** (stop vomiting before giving AC), analgesics
- GI protectants: sucralfate, proton pump inhibitors, H2-antagonists
- Iv fluids

Prognosis: Not good

30
Q

Discuss Slaframine (mycotoxin) –> Slobbering

A
  • Fungus that likes to grow on clobers; alfalfa, legumes
  • Toxin: Slaframine–> potent salivary gland antagonist
  • Grazing/hay –> compound is very stble
  • Affects all ANIMALS THAT GRAZE/EAT HAY
  • Exessive salivation

Treatment:
- feed source
- salivation
- Remove access to feed

31
Q

Discuss AVcute nitrate poisoning

A
  • Extremely common
  • Ruminants only: all species suscepotible to preformed nitrite (not comon to find nitrite source)
  • Poisonings: ingestion of nitrate accumulating forage (concentrate)

Classic history: cows that may have being fed OAT HAY

Risk factors: plant:
- fertilization

Risk factors: Ruminants:
-**High consumption rate
lack of adaptation
Older cows
Pecking order **

32
Q

What are some nitrate accumulators?

A
  • Chenopodium
  • Oat hay
  • Sorghum
33
Q

Discuss the mechanism of actionof nitrate poisoning

A
  • The reason we see this in ruminants is because in ruminants, nitrate gets into the rumen and the rumen microflora convert it to ammonia (or convert it to NO2, Nitrite, but then this nitrite eventually gets converted into ammonia so that all is well according to Talcock) but in really overdose situations, the nitrate bugs cannot convert enough into nitrite and ammonia. So nitrite will convert hemoglobin (hemoglobin iron in the ferret state which can carry oxygen) into methemoglobin (methemoglobin in the ferric state which cannot cry oxygen) which causes the blood to turn brown.
34
Q

Discuss the clincial signs of nitrate posioning

Discuss diagnosis criteria for it as well

Discuss treatment for it as well

A

MetHgb: 20 - 50 %
- lethargy
- dyspnea
- salivation
MetHbg: > 70%
- death (recumbency)
- dead animals otherwise look fine

  • Source: feed
  • only other main differential in ruminants: Chlorate

Treatment: Methylene blue??? and also avoid stress

35
Q

Discuss phenoxy herbidcide toxicity

  • Discuss clinical signs
A
  • All annimals suspectible: K9 - most sensitive –> Canines have poor ability to tubular secrete organic acids
  • Rapid absoriton fomr the GI Tract –> excreted primarily unchnaged via urine
  • Abrupt onset: GIT + neuromuscular
    - low exposure –> SELF LIMIITNG; GONE IN 24 HOURS
    - high exposure –> ataxia, **Myotonia **
36
Q

Discuss the diagnostic cirteria for phenoxy herbicide toxicity

A
  • history of use
  • Clinical signs: GIT + neuromuscular
  • Electromyogram: myotonia - dogs

Treatment:
- IF AYMSYMPTOMATIC –> The big D
- If SYMPTOMATIC, 1)anti emetic; AC, cathartic, gastric lavage are best options; also, Diuresis

Prognosis: Excellent

37
Q

Consider Mustard (NOt for hotdogs but the plant) and discuss the problems expected with this

A
  • anemia
  • atypical bovine emphysema and edema (fog fever)
  • bloat; GI upset
  • Polioencephalomalacia
  • Goiter
  • Nitrate
  • -
38
Q
A

Toxicology (11 decks)

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