Term
| What are the top 3 types of poisonings that make up 50% of cases? |
|
Definition
Lead (cattle)
Copper (sheep)
Ethylene Glycol - Antifreeze in cats and dogs |
|
|
Term
| What is the most common species brought the ISU Emergency room for poisoning? |
|
Definition
|
|
Term
| How would you define a TOXIN? |
|
Definition
A poison that originates from biological processes
-biotoxin
-zootoxins (snakes, insects, etc)
-mycotoxins (fungal)
-PLants (phyotoxin) |
|
|
Term
| What is the difference between the terms Toxicosis and Toxicity ? |
|
Definition
Toxicosis refers to the disease state of being poisoned
Toxicity refers to the AMOUNT of toxicant that will cause adverse effects |
|
|
Term
|
Definition
| No Observed Adverse Effect Level |
|
|
Term
|
Definition
|
|
Term
| What is the minimum lethal dose? |
|
Definition
| This is the minimum amount that will begin to cause changes that could be lethal. |
|
|
Term
| How do you calculate Chronicity factor? |
|
Definition
Acute LD50
____________
90 Day LD50
this measures cumulative toxicity or continued organ damage |
|
|
Term
Which rodenticide has a longer plasma half life?
A) Diphacinone
B) Warfarin
C) Brodifacoum |
|
Definition
Answer: C) brodifacoum has half life of 6 days
Warfarin has the shortest half life - maxing out at only 14 hours |
|
|
Term
| How long after ingestion of anticoagulant rodenticide would clinical coagulopathies be seen? |
|
Definition
3-6 days after ingestion
but can be seen as soon as 36 hours after ingestion
THIS IS DOSAGE DEPENDENT and it is delayed because the preformed clotting factors must be used up first |
|
|
Term
| What are the clinical signs associated with warfarin poisoning? |
|
Definition
Anticoagulant - so hemorrhage and blood loss signs like
Weakness, anemia, dsypnea, epistaxis, melena, lameness, ataxia, CNS signs from subdural bleeding |
|
|
Term
| With anticoauglant rodenticide poisoning, which clotting factor will first be affected? |
|
Definition
Prothrombin time
(2-3 days post exposure) |
|
|
Term
| What is the antidote for Anticoagulant poisoning? |
|
Definition
Vitamin K1
use this if anemia is not severe
if severe - increase the PCV and clotting factors right away - transfusion
(vitmamin K takes 6 hours to start having effects ) |
|
|
Term
| Why should you avoid using Vitamin K3 to treat anticoagulant poisoning in horses? |
|
Definition
|
|
Term
What is the term used to signify where half of a group of animals in a toxicology study has died?
A. ED50
B. LD50 (definition)
C. Therapeutic Index
D. Standard Safety Margin
E. None of the above |
|
Definition
Answer: B) LD50
(lethal dose of 50%) |
|
|
Term
| In toxicology, what does HNTD refer to? |
|
Definition
| Highest Non-Toxic Dose - this is the largest dose not resulting in clinical or pathological chemical-induced alterations |
|
|
Term
| What is the equation for determining the therapeutic index of a substance? |
|
Definition
Therapeutic index = LD50/ED50
(lethal dose of 50% / effective dose of 50%) |
|
|
Term
| How do you measure the Standard Safety Margin (SSM)? How does this differ from the therapeutic index? |
|
Definition
SSM = LD1 / ED50.
This is a more conservative and clinically relevant estimate than the therapeutic index. |
|
|
Term
You add 1 lb of drug to a ton of feed.
What is the fractional percentage of drug in the feed?
What is the ppm? |
|
Definition
1 ton = 2000 lbs
Fractional percentage: 1 lb/2000 lbs X 100 = 0.05%
PPM: mg/kg = 0.05% X 10,000 = 500ppm |
|
|
Term
When working up a possible toxicosis, lab tests reveal azotemia. Which of the following could now be eliminated from your possible toxin list?
A) Antifreeze
B) Arsenic
C) Cadmium
D) Lead |
|
Definition
Answer: D) Lead
lead would show basophilic stippling, whereas the others listed would cause lab result to show azotemia. |
|
|
Term
| When working up a possible toxicosis, lab tests reveal hypocalcemia. Which toxins are associated with this? |
|
Definition
| Antifreeze, oxalate plant poisoning |
|
|
Term
| Which toxins might cause hemolysis? |
|
Definition
Garlic
Onion
Red Maple
Copper
Zinc
Phenothiazine
Anthelminitics |
|
|
Term
| Which toxins may cause coagulopathies? |
|
Definition
Moldy sweet clover
anticoagulant rodenticides
prolonged toxic liver disease |
|
|
Term
| Which toxins are associated with causing crystalluria? |
|
Definition
Antifreeze
oxalate plants |
|
|
Term
| Which toxins are associated with aplastic anemia? |
|
Definition
Phenylbutazone
chloramphenicol
gasoline
petroleum solvents
trichothecene mycotoxins |
|
|
Term
| Which toxins are associated with causing an increase in AST, ALT, LDH? |
|
Definition
Afalatoxin
fumonisins
pyrrolizidine alkaloids
cocklebur
lantana
moldy alfalfa
blue green algae
amanita mushrooms |
|
|
Term
| Which toxins are associated with causing basophilic stippling of RBCs? |
|
Definition
Lead poisoning
(inconsistent with equines) |
|
|
Term
| What is the MOA of Anticoagulant Rodenticides? |
|
Definition
Inhibit the recycling of vitamin K from epoxide to reduced form
- reduced form is the active form needed for coagulation cascade
- factor VII (early) and Factor IX (late) affected
*blocks vitamin K epoxide reductase*
delayed effect from depletion of clotting factors = clinical coagulopathy 3-6 days post ingestion |
|
|
Term
| With an anticoagulant rodenticide posioning, which will decrease first: PT or PTT? |
|
Definition
PT drops first
PTT drops later |
|
|
Term
| When is clinical coagulopathy seen seen after ingestion of anticoagulant rodenticide? |
|
Definition
as short as 36 hours, but about 3-6 days
***DOSE DEPENDENT*** |
|
|
Term
Which is more toxic (has a lower LD50)?
A) Warfarin
B) Brodifacoum
C) Bromadiolone
D) Diphacinone |
|
Definition
Answer: B) BRODIFACOUM
LD50 = 0.22-4 mg/kg !!! |
|
|
Term
| At what ingested dose of anticoagulant rodenticides should therapy be started? |
|
Definition
ie. Brodifacoum
When the ingested dose is 1/4 the LD10.
LD10 of Brodifacoum = 0.20 mg/kg |
|
|
Term
| What are some risk factors that will increase the toxic effects of anticoauglant rodenticides? |
|
Definition
age: very old/young
Concurrent liver disease
moldy sweet clover in horse/ruminants
Protein replacing dugs (phenylbutazone, sulfonamides, corticosteroids, aspirin) |
|
|
Term
| What are the clinical signs seen with Anticoagulant rodenticide toxicity? |
|
Definition
Hemorrhage/blood loss
-anemia
-weakness
-dyspnea
-epistaxis
-melena
-lamness
-ataxia
-occasional CNS signs from subdural bleeding
-hemothorax
-placental hemorrhage> abortion
-acute death |
|
|
Term
| How would you diagnose a toxicity from anticoagulant rodenticides? |
|
Definition
-hemorrhagic syndrome noted
-prolonged clotting time
-increased PT (2-3d post exposure)
-Activated PTT (3-5d post exposure)
-PIVKA (thrombotest)
-detection of active ingredient in liver, blood, bait
-liver: sample of choice in dead animals
-blood: sample of choice in live animals |
|
|
Term
| What is the preferred sample to collect in live animals suspected in anticoagulant rodenticide toxicosis? |
|
Definition
BLOOD (whole blood)
- check PT, PTT, PIVKA, detection of active ingredient |
|
|
Term
| What is the preferred sample to collect on necropsy from a suspected case of anticoagulant rodenticide toxicosis ? |
|
Definition
LIVER
- detection of active ingredient, PIVKA, PT, PTT |
|
|
Term
| You have an animal presented with clinical signs of anticoagulant rodeniticide poisoning. What are your differential diagnoses? |
|
Definition
Idiopathic coagulopathy
Autoimmune thrombocytopenia
DIC
Hereditary (Von Wildbrand's Disease)
Liver disease (decreased clotting factor synthesis) |
|
|
Term
| What is the treatment for Anticoagulant rodenticide toxicity? |
|
Definition
Supportive therapy
Vitamin K1 (orally w/fatty food, or IV)
blood/plasma transfusion |
|
|
Term
| Why is there minimal shyness acquired towards cholecalciferol baits? |
|
Definition
| There is a delayed toxicosis in rodents of 2-3 days after ingestion |
|
|
Term
| Besides Cholecalciferol bait packs, what are some other potential sources of Vitamin D3 toxicosis? |
|
Definition
| D3 feed additives, vitamin supplements, calcipotriene skin antipsoriasis cream |
|
|
Term
| What is amount of Cholecalciferol in vitamin D3? |
|
Definition
1 IU D3 = 0.025 ug Cholecalciferol
1ug D3 = 40 IU D3
1ppm D3 = 40 IU |
|
|
Term
| When supplementing vitamin D, what is the difference between using D2 and D3? |
|
Definition
D3 is 10X more potent than D2 for Calcium uptake.
this can cause errors in supplementation |
|
|
Term
| How is Vitamin D3 metabolized in the body? |
|
Definition
absorbed rapidly in the Small Intestines
-> plasma to liver and kidney
LIVER: metabolized to 25-hydroxy D3 (cp450 dependent)
KIDNEY: converts to toxic 1,25 dihydroxy (this is the rate limiting step that delays action) --- here is where it would cause its toxic effects, by causing the kidneys to increase plasma Ca levels
>>> primarily excreted in the bile to feces |
|
|
Term
| What is the daily requirement of Vitamin D3 for Dogs? |
|
Definition
|
|
Term
| What is the toxicity of Cholecalciferol to dogs? |
|
Definition
1-3 mg/kg toxic (2.6 mg/kg bait)
10-20 mg/kg single dose dose = lethal |
|
|
Term
| Which will cause toxicosis at lower doses: cholecalciferol or Calcipitriol? |
|
Definition
Calcipitriol
toxicity = 50 ug/kg
Cholecalciferol toxicity = 1-3 mg/kg |
|
|
Term
Generally speaking, which animal would be more susceptible to the toxic effects of chlolrcalciferol?
A) Cat
B) Puppy
C) Adult Dog |
|
Definition
Answer: A) Cats are most susceptible
then puppies
and lastly dogs
(cats are just smarter and tend not to eat tubes of anti-psoriasis cream...) |
|
|
Term
| What is the MOA of Cholecalciferol? |
|
Definition
converted to 1, 25 hidydroxyvitamin D in kidneys
~~Increased serum Ca levels:
- increase Ca(and P) absorption in gut
- PTH (osteoclast bone resorption)
- renal retention of Ca via distal tubule resorption
>>>>>results in hypercalcemia, hyperphosphatemia, renal tubular damage/necrosis, soft tissue mineralization |
|
|
Term
| Based on the pathophysiologic effects of the substance, how do toxic levels of Vitamin D3 effect the body? |
|
Definition
Converted to toxic metabolite in the kidney (1, 25 dihydroxyD3)
- increases Ca and P absorption in gut
- Increases PTH (bone resrption )
- renal retention of Ca in distal tubules
===== increased serum calcium
this causes:
>hypercalcemia, hyperphosphatemia (reduces cAMP, dec ADH -> diuresis)
>renal damage/necrosis-> azotemia
>Soft tissue mineralization (esp renal tubules and arterioles) |
|
|
Term
Which clinical sign would be least likely in Vitamin D3 toxicosis?
A) Hypertension
B) PU/PD
C) Azotemia
D) Seizures
E) Weakness |
|
Definition
Answer: D) Seizures
Neurologic signs are least likely with vitamin D toxicosis |
|
|
Term
| What are the clinical signs associated with Vitamin D3 toxicosis? |
|
Definition
INCREASED SERUM CALCIUM
Renal changes (necrosis and mineralization)
- azotemia
- PU/PD
Bradycardia
depression
anorexia
vomiting (initially)
hypertension
muscle weakness |
|
|
Term
| On necropsy, what are some lesions that would be found in association with cholecaliferol? |
|
Definition
Renal
- tubular necorsis
- mineralization
- red-gray cortex
Aortic plaques
Arterial & cardiac mineralizations
thyroid hypertrophy/hyperplasia
mineralizations of lung, stomach, intestine |
|
|
Term
You run some testing on a dog. What levels of the following would support a diagnosis of cholecalciferol toxicosis:
Serum Ca?
Serum Phosphorus?
BUN?
Creatinine?
USG? |
|
Definition
Serum Ca = ELEVATED
Serum phosphorus = elevated
BUN = Elevated
Creatinine = elevated
USG = decreased (hyposthenuric) |
|
|
Term
| What would diagnose a Vitamin D3 toxicosis ? |
|
Definition
Inc Serum Ca
Inc Serum Phosphorus
Bradycardia
USG @ 1.002-1.004
Increased BUN and Creatinine
Increased 25 dihydroxyl D3 (metabolite)
serum iPTH suppressed
mineralization lesions
kidney tissue calcium level increased |
|
|
Term
| What are some possible differentials for Vitamin D3 toxicosis? |
|
Definition
Hypercalcemia of malignancy
Chronic renal failure
primary hyperparathyroidism
feline idiopathic hypercalcemia |
|
|
Term
| How would you treat a dog that can ingested Cholecalciferol in a potentially toxic dose? |
|
Definition
- induce vomiting if soon after ingestion
(continue for 2 days to prevent enterohepatic cycling)
- saline diuresis (2-3X maintenance)
- furosemide 5 mg/kg IV, then 2.5mg/kg BID-TID PO |
|
|
Term
| How would you treat a dog that can ingested Cholecalciferol in a potentially toxic dose? |
|
Definition
- induce vomiting if soon after ingestion
(continue for 2 days to prevent enterohepatic cycling)
- saline diuresis (2-3X maintenance)
- furosemide 5 mg/kg IV, then 2.5mg/kg BID-TID PO |
|
|
Term
| How would you treat a dog that can ingested Cholecalciferol in a potentially toxic dose? |
|
Definition
- induce vomiting if soon after ingestion
(continue for 2 days to prevent enterohepatic cycling)
- saline diuresis (2-3X maintenance)
- furosemide 5 mg/kg IV, then 2.5mg/kg BID-TID PO
- prednisone 2-3mg/kg Sid-BID PO
- Calcitonin 4-6 IU/kg SQ
- Biphosphonates IV saline infusion 2 mg/kg for 2 hours
- Ca restrictio, antiemetics,GI protectants |
|
|
Term
| What is the purpose of giving prednisone to treat Vitamin D3 toxicosis? |
|
Definition
Blocks osteoclast activation
decrease GI and renal uptake of calcium |
|
|
Term
| What properties of Zn Phosphide makes the biggest difference between how a dog and a rat react to it? |
|
Definition
STRONG EMETIC
dogs can vomit
rats cannot
- thus this can be protective to dogs upon ingestion. |
|
|
Term
| What is the MOA of Zinc phosphide? |
|
Definition
hydrolyzed in stomach: into phosphine gas and Zn2+
PH3 = blocks cytochrome oxidase and membrane ion transport (myocardium)
Zn = strong emetic (dogs will vomit, but rats cannot) |
|
|
Term
| What increases the toxicity of Zinc Phosphide? |
|
Definition
more toxic when consumed with food!
this stimulates gastric acids, which will hydrolyze the bait causing rxn.
LD50 in dogs empty stomach= 300mg/kg VS
LD50 in dogs with food = 40 mg/kg |
|
|
Term
What is the LD50 for Zinc Phosphide in dogs?
Sheep?
Birds?
Fish? |
|
Definition
Dogs (empty stomach) = 300mg/kg
Sheep = 60 mg/kg
Dogs (with food) = 40 mg/kg
Birds = 7-10 mg/kg
Fish = 0.5 mg/L |
|
|
Term
| What are the clinical signs associated with Zinc Phosphide toxicosis? |
|
Definition
VARIABLE - difficult to DX
- vomiting
- anorexia
- lethargy
- rapid deep respirations
- abdominal pain
- ataxia, weakness
- seizures, running, hyperesthesia |
|
|
Term
| How do you diagnose Zinc Phosphide toxicosis? |
|
Definition
DIFFICULT - variable and non specific signs
- HX of exposure
- dead fish/garlic odor
- zn phosphide in stomach content
Necropsy
- hepatic fatty change, myocardial and renal tubular damage, lung edema
**collect tissue samples, freeze and seal = very volatile |
|
|
Term
| What special precautions should be taken when collecting samples for suspected Zinc Phosphide toxiciosis? |
|
Definition
The toxin is VOLATILE!
this means that when collecting tissue samples: freeze and seal them right away |
|
|
Term
| How do you treat Zinc Phosphide toxicosis? |
|
Definition
- activated charcoal
- cathartics
- antacids
- - combat acidosis, hypocalcemia, liver damage
- B vitamins, glucose (for liver damage)
- Demulcents (GI irritant protectors)
- PREVENTION |
|
|
Term
| How are chlorinated hydrocarbons excreted from the body? |
|
Definition
They are not:
instead BIOMAGNIFICATION occurs and the compound accumulates in the body |
|
|
Term
| What is the MOA of chlorinated hydrocarbons? |
|
Definition
They are Diphenyl aliphatics: which means they interfere with Na floe in the nerve membranes.
This lowers the threshold for anther action potential |
|
|
Term
| What are the clinical signs associated with Chlorinated hydrocarbon toxicosis? |
|
Definition
HYPERSENSITIVITY
belligerent behavior
muscle tremors
tonoclonic convulsions |
|
|
Term
| Which species are most sensitive to pyrethrins? |
|
Definition
Cats are most sensitive
fish are too
safe to most other animals
birds are relatively resistant to them |
|
|
Term
Which of is more stable:
Pyrethrins or Pyrethroids? |
|
Definition
| Pyrethroids are more stable, they are synthetic |
|
|
Term
| What is the MOA of Type 1 pyrethroids? |
|
Definition
-slows opening of neural sodium channels
-lowers firing threshold of nerve
= stimulation and excitement, muscle tremors |
|
|
Term
| What is the MOA of type 2 pyrethroids? |
|
Definition
- depolarization of membranes
- inhibitory (GABA)
= weakness and paralysis |
|
|
Term
| Which type of pyrethroid would more likely cause paralysis: 1 or 2? |
|
Definition
Type 2 -
depolarization and GABA inhibition = weakness and paralysis
where type 1 causes excitation and tremors |
|
|
Term
| Which type of pyrethroid would more likely cause muscle tremors: 1 or 2? |
|
Definition
Type 1
- lowers threshold of nerve firing causing excitation and tremors
type 2 inhibits GABA and causes depolarization which results in weakness/paralysis |
|
|
Term
How long do clinical signs of pyrethrin/ pyrethroid toxicity take to show?
How long for them to resolve? |
|
Definition
Onset: often less than an hour
Recovery: 24-72 hours |
|
|
Term
| What are the clinical signs associated with pyrethrin/pyrethroid toxicosis? |
|
Definition
type1: tremors, seizures, hyperexcitibility
Type2: weakness, salivation abnormal posturing, paralysis |
|
|
Term
| How would you diagnose pyrethrin/pyrethroid toxicosis? |
|
Definition
There is NO definitive test:
mostly based on hx of exposure,
increased PMN and dec glucose. |
|
|
Term
| How would you treaat pyrethrin/pyrethroid toxicosis? |
|
Definition
- discontinue exposure
- bathe animal
- methocarbamol (dec tremors)
- supportive care
- seizure control
= good prognosis |
|
|
Term
| Which animals are most sensitivie to organophosphate and carbamate toxicosis? |
|
Definition
CATS
Poultry
dogs
all animals susceptible |
|
|
Term
| Where do organophosphates and carbamates distribute in the body? |
|
Definition
Rapidly absorbed orally, dermally, inhalant
> goes to plasma > liver > CNS > excreted in urine |
|
|
Term
| How are organophosphates and carbamates metabolized? |
|
Definition
They are metabolized by mixed function oxidases (MFO system)
- deactivated by hydrolysis
- excreted in urine
- ** increased toxicity with phenothiazines |
|
|
Term
| Phenothiazines increase the toxicity of what compounds? |
|
Definition
| Organophophates and carbamates |
|
|
Term
| What is the MOA of organophosphates and carbamates? |
|
Definition
Inhibit AChE at cholinergic synapse
- continuous stimulation and accumulation of ACh
-- parasympatetic stimulation |
|
|
Term
| What are the clinical signs associated with organophosphate or carbamate toxicosis? |
|
Definition
Acutely onset parasympathetic stimulation:
emesis
excessive salivation, lacrimation, urination, defication, bronchoconstriction, miosis, bradycardia
Nicotinic effects:
- tremors, stiffness, paralysis>> death from respiratory failure |
|
|
Term
| How do you diagnose oraganophosphate or carbamate toxicosis? |
|
Definition
Measure cholinesterase activity in blood or brain
- chemical analysis of rumen/stomach content, hair, or suspected contaminated source |
|
|
Term
| What precautions must be taken when collecting samples for diagnosis of organophosphate toxicosis? |
|
Definition
| you must refrigerate the sample |
|
|
Term
| What are the available treatments for organophosphate or carbamate toxicosis? |
|
Definition
-atropine sulfate (only use 2-3 times)
-2PAM (not for carbamates), give immediately
- glycopyrrolate (anticholinergic but doesnt penetrate CNS)
-oral activated charcoal |
|
|
Term
| What is the MOA of Amitraz in causing toxicosis? |
|
Definition
Acts as Alpha 2 adrenergic agonist
= GI stasis, bradycardia, CNS depression, increased blood glucose, sedation |
|
|
Term
| What are the clinical signs associated with amitraz toxicosis ? |
|
Definition
2-4 hour onset of:
sedation
CNS depression
ataxia, mydriasis
hypothermia
bradycardia
hypotension
vocal spasm
muscular weakness
vocal spasm
micturition (urination) |
|
|
Term
| Which animals are more at risk for amitraz toxicosis? |
|
Definition
CATS
old and debilitated animals
diabetic animals |
|
|
Term
| How do you diagnose Amitraz as a source of toxicosis? |
|
Definition
Hx of exposure
clinical signs (CNS depression, etc)
hypergylcemia
chemical detection in excretions, blood, skin.
>only confirms exposure, be sure to rule out all other causes of clinical signs |
|
|
Term
| What treatments are available for amitraz toxicosis? |
|
Definition
Remove source
- bathe
- emetics, gastric lavage, activated charcoal
Yohimbine (to reverse bradycardia)- use in horses
Atipamizole (reverse bradcardia, has fewer side effects) |
|
|
Term
| How is nicotine absorbed and distributed through the body? |
|
Definition
oral absorption
- ionized in acid medium in stomach (because it is an alkaloid)
- absorption slow |
|
|
Term
| What is the MOA of Nicotine in causing toxicsis? |
|
Definition
| Mimics action of ACh at cholinergic synapse |
|
|
Term
| How does the ingested dose of nicotine affect the clinical outcome of toxicosis? |
|
Definition
Small doses = stimulation
large doses = paralysis |
|
|
Term
| What are the clinical signs associated with nicotine toxicosis in cats and dogs? |
|
Definition
initially stimulation and excitement
excessive salivation
emesis, diarrhea
rapid respiration
muscle tremors
- progresses to muscle weakness and paralysis
shallow rapid resp > collapse, coma
Quick death from respiratory paralysis |
|
|
Term
| What treatments are available for nicotine toxicosis? |
|
Definition
**acidify urine to increase ion trapping
atropine
activated charcoal
Respiratory support |
|
|
Term
| What drugs would be contra-indicated in treatment of nicotine toxicosis? |
|
Definition
Antacids -
promotes absorption in stomach |
|
|
Term
| What would increase the toxicity of pyrethrin? |
|
Definition
|
|
Term
| How is rotenone metabolized in the body? |
|
Definition
Activated in the liver to a toxic metabolite - -
demethylate to detoxify |
|
|
Term
| What is the MOA of Rotenone? |
|
Definition
| Complexes with NADH to inhibit electron transport |
|
|
Term
| What are the clinical signs associated with rotenone toxicosis? |
|
Definition
| vomiting, lethary, dyspnea, tremors, hypoglycemia |
|
|
Term
| What treatments are available for rotenone toxicosis? |
|
Definition
Diazepam
Dextrose IV (to treat hypoglycemia)
-- good prognosis |
|
|
Term
| What is the MOA of Imidicloprid? |
|
Definition
| blocks post-synaptic nictinic ACh receptors in insects |
|
|
Term
| What are the clinical signs of imidicloprid toxicosis? |
|
Definition
This is very safe -
only issue is that it may cause hair loss at site of application |
|
|
Term
| What is the MOA of fipronil ? |
|
Definition
GABA inhibitor
frontline baby ! |
|
|
Term
Where does paraquat distribute in the body?
How is it excreted? |
|
Definition
limited absorption
- concentrates in pulmonary tissue
-excreted in urine unmetabolized |
|
|
Term
| How does Paraquat cause damage when ingested? |
|
Definition
concentrates in pulmonary tissue -
- selective uptake by alveolar cells
- free radical formation
- oxidizes oxygen to superoxide
- then returned to original compound
= damages pulmonary tissue |
|
|
Term
What are the clinical signs associated with acute paraquat toxicosis?
Chronic? |
|
Definition
Acute:
vomit, diarrhea, ataxia
> renal failure, hepatocellular necrosis
> pulmonary edema, resp distress
Chronic:
pulmonary fibrosis
****irreversible lesions after 8 days** |
|
|
Term
| How would paraquat toxicosis appear pathologically during necropsy? |
|
Definition
LUNGS:
-atelectasis, hemorrhage, emphysema
- type 1 alveolar cell necrosis
Renal tubular necrosis |
|
|
Term
| How would you diagnose paraquat toxicosis? |
|
Definition
Can be detected in urine for 2-3 days post exposure
- can also be detected in stomach contents |
|
|
Term
| How would you treat paraquat oxicosis? |
|
Definition
**if clinical signs present = poor prognosis
- detox with activated charcoal, cathartics
- BENTONITE adsorbent
- fluids and diuresis
- acetylcystine/superoxide dismutase (biochemical antagonists)
- supportive care |
|
|
Term
| What is the antidote for phenoxy fatty acid toxicosis? |
|
Definition
| NO specific antidote available |
|
|
Term
| Which species are most commonly presented for lead poisoning? |
|
Definition
|
|
Term
| How is lead absorbed in the body? |
|
Definition
requires ionization = absorbed better in acidic environment
--- usually poorly absorbed
from gut > liver, lungs, kidney > bone
can cross BBB in young
can cross placeta
EXCRETED: feces and less so urine |
|
|
Term
| What is the primary MOA in lead toxicosis? |
|
Definition
Binds to Sulfhydryl groups
- affects Heme synthesis
- alters GABA transmission |
|
|
Term
| What is the MOA in copper induced toxicosis? |
|
Definition
Excessive Cu storage in lysosomes
stress causes release of Cu from lysosomes in LIVER
>>>> Cu in blood = hemolysis and hepatocellular necrosis |
|
|
Term
| Which breeds of dogs are associated with copper storing abnormalities? |
|
Definition
Bedlington
Skye
West highland terrier
doberman |
|
|
Term
| Which species is most affected by Zinc toxicosis? |
|
Definition
Dog
then cats, ferrets, birds, zoo animals
(not really a problem in large animals) |
|
|
Term
| What are the 3 forms of arsenic? |
|
Definition
Elemental
Organic
Inorganic
**form is major factor in toxicity |
|
|
Term
| Where does arsenic distribute in the body? |
|
Definition
Initial accumulation in the liver:
>slowly distributes to spleen, lung
>later accumulated in keratinized tissues
- crosses BBB and Placenta
Excreted: trivalent form in feces, pentavalent form in urine |
|
|
Term
| Which form of arsenic is most toxic? |
|
Definition
| Trivalent inorganic form is 5-10X more toxic than pentavalent form |
|
|
Term
| What is the MOA of inorganic arsenic toxicosis? |
|
Definition
Binds with sulfhydryl enzymes
- blocks cellular respiration
- competes with phosphate
- uncouples oxidative phosphorlyation
acts on high resp tissue like gut epithelium and capillaries |
|
|
Term
| What is the MOA in Iron Toxicosis? |
|
Definition
increased serum fe
> free radical damage to cellular membranes
> increased vascular permeability
>>>>hemorrhage, vascular dilation, shock, acidosis, death
hepatic fe = mitochondrial damage> liver damage |
|
|
Term
| What are the 3 forms of mercury? |
|
Definition
Elemental
inorganic
organomercurial |
|
|
Term
| What tissues are most affected by Fluoride? |
|
Definition
Mineralized tissues:
bone and teeth |
|
|
Term
How is mercury absorbed in the body?
How is it excreted? |
|
Definition
Poor GI absorption
VAPORS are absorbed best
Excretion: through kidneys in urine, and exhaled from lungs
Organics: cross BBB and Placenta |
|
|
Term
| What is the MOA of Mercury toxicosis? |
|
Definition
Targets Kidney and CNS
- binds sulfhydryl groups
---inhibits enzymes and protein synthesis
-------mitchondrial inhibition from alpha-lipoic acid |
|
|
Term
| If basophilic stippling is noted on a blood smear, what would your top differential be? |
|
Definition
LEAD TOXICOSIS
...Know it !
also Zinc toxicosis |
|
|
Term
| With lead toxicosis, what would you see on clin path diagnostics? |
|
Definition
increased nRBC
BASOPHILIC Stippling
anemia |
|
|
Term
| How would you diagnose a lead toxicosis? |
|
Definition
History
lead in whole blood, kidney, liver
Basophilic stippling on blood smear
Radiographs
Ca-EDTA mobilization test |
|
|
Term
| How would you treat Lead toxicosis? |
|
Definition
CHELATION THERAPY
CaEDTA, D-penicillamine, succimer
-remove source
-decontaminate GI tract
oral MgSO4 as laxative and insoluble PbS complex formation |
|
|
Term
What clinical signs would be seen in acute Copper toxicosis?
Chronic? |
|
Definition
Acute: liver damage, diarrhea,
Chronic:
-accumulation- weeks to months
-acute hemolytic crisis (Cu released from stores as triggered by stress event) |
|
|
Term
| What pathologic lesions would be seen on a sheep with copper toxicosis? |
|
Definition
Icterus
yellow friable liver
dark red serum, urine
black kidneys |
|
|
Term
| What are the clinical signs associated with copper toxicosis? |
|
Definition
depression, anorexia, weakness
hemoglobnuria
icterus |
|
|
Term
| How would you diagnose copper toxicosis? |
|
Definition
Liver biopsy - cu containing
- also can be found in kidneys, serum and feed (source) |
|
|
Term
| How would you treat an animal with copper toxicosis? |
|
Definition
-CHELATE WITH D-Penicillamine (increases excretion)
- sodium molybdate and ground gypsum
- eliminate source
- supportive care |
|
|
Term
| What clinical sign would be seen in a DOG with copper storage toxicosis? |
|
Definition
young adult dogs
- chronic hepatopathy
- ACUTE ICTERUS & liver dz
- PU/PD, coagulopathy, lethargy, weakness, anorexia |
|
|
Term
| How is Zinc absorbed and how does it distribute in the body? |
|
Definition
Absorption: inhibited by Ca, Cd, Cu and Phytic acid
-- interferes with absorption/utilization of Fe & Cu
Distribution: 2/3 loosely bound to protein, rest tightly bound (in serum) |
|
|
Term
| What are the clinical signs associated with Zinc toxicosis? |
|
Definition
Early: Vomiting and anorexia
Late: depression, Diarrhea, weakness, pale MM, Icterus
Clin path: basophilic stippling, high nRBC, polychromasia, > regenerative anemia, inc ALP, bilirubin, hemoglobinuria, hematuria |
|
|
Term
| How would you diagnose a case of Zinc Toxicosis? |
|
Definition
-Abdominal radiographs (often it is from ingestion of a coin/ metal object)
- hemorrhagic gastritis
-proximal renal tubular necrosis |
|
|
Term
| How would you treat a zinc toxicosis? |
|
Definition
Remove source (coin or metal object)
- symptomatic supportive care
- Chelators (D-penicillamine or CaEDTA)
- H2 receptor blockers |
|
|
Term
| What are the clinical signs associated with Arsenic toxicosis? |
|
Definition
Acute/subacute onset
Inorganic form causes:
- GI TRACT UPSET
- - vomiting
- - intense abdominal pain
-diarrhea, fluid loss
>acute death
> weakness, staggering |
|
|
Term
| How would you diagnose arsenic toxicosis? |
|
Definition
URINE testing (eliminated quickly)
- blood NOT good as diagnostic source
- can accumulate in hair, liver, kidney
Lesions: GI hemorrhage, edema, renal tubular degeneration |
|
|
Term
| How would you treat arsenic toxicosis? |
|
Definition
BAL - Dimercaprol
- best if used before onset of clinical signs
- REHYDRATE
- poor prognosis
Thoctic acid or succimer can also be used |
|
|
Term
| What are the clinical signs of Iron toxicosis, as they progress through stages? |
|
Definition
1-6 hrs > corrosive effect, vomiting, diarrhea, GI hemorrhge
6-12 hrs> apparent remission
12-24 hrs > severe lethargy, GI signs, metabolic acidosis, liver necrosis, coagulopathy, CV collapse, shock
Weeks later> GI scarring and stricture |
|
|
Term
| What is the most common way dogs incur iron toxicosis? |
|
Definition
Ingestion of human iron supplements
(pills can be found on radiograph) |
|
|
Term
| How can you diagnose Iron toxicosis? |
|
Definition
Radiographs (of ingested iron pills)
increased serum iron
- can exceed total iron binding capacity = toxicosis |
|
|
Term
| How would you treat an animal with iron toxicosis? |
|
Definition
CHELATE with DEFEROXAMINE
(until serum fe is below Total iron binding capacity = days)
GI protectants
Electrolytes
NO CHARCOAL - doesnt work |
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