Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

SAM- Tox > Rodenticide > Flashcards

Rodenticide Flashcards

1
Q

Cholecalciferol: Forms & Sources

A

FORMS
o Plant derived: Ergocalciferol (D2)
o Animal derived: Cholecalciferol (D3)

SOURCES:

  • Ingestion of rodenticides
  • Human medicine ingestion ( psoriasis cream)
  • Pet food (Blue buffalo 2010)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Cholcalciferol: Toxic dose (acute vs chronic)

A

Acute ingestion: Exposure to rat/mouse bait in the backyard.
Chronic ingestion: Kitty that licks psoriasis cream off the owners arm.

o Toxic lethal dose depends on the biochemical form
o Vitamin D3 is 10 times more potent than D2

o Single oral lethal dose ~ 13 mg/kg
0.1 mg/kg mild GI signs
> 0.5 mg/kg hypercalcemia, renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Cholecalciferol: What predispositions make dog more succeptible?

A

Primary renal failure, Addisons ( animals prone to hypercalcemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Cholecalciferol: Mechanism of Toxicity

A

Vitamin D absorbed/ingested-> LIVER( 25hydroxyvitaminD)-> KIDNEY (1,25-di-hydroxyvitamin D)-> Vitamin D receptors in SI, Colin, & Lungs activated

GUT - Calcium & Phosphorus absorption increase
Kindneys- Calcium renal absorption increases ( increase Phosphorous too)
BONE-If you have low calcium floating around in the body, the Vit D is going to help increase resorption of calcium from the bone, so that you can increase that calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Hypercalcemia Differentials

A 
HARD IONS
o	H: 
	Hypercalcemia of malignancy (lymphoma, multiple myeloma, adenocarcinoma of anal glands) 
	Hyperparathyroidism 
o	A: 
	Addison’s disease, aluminum tox
o	R: 
	Renal failure – throws off Ca:P ratio 
o	D:
	Vitamin D tox – vitamin D is needed to absorb Ca. too much vit D = too much Ca absorbed 
o	I: 
	Iatrogenic, Idiopathic 
o	O: 
	Osteolytic disease like HOD (hypertrophic osteodystrophy)  
o	N:
	Neoplasia (osteosarcoma), metastatic bone disease such as mets from a mammary tumor 
o	S: 
	Spurious
o	Hypercalcemia of malignancy
o	Hypoadrenocrticism
o	Chronic kidney disease
o	Primary hyperparathyroidism
o	Osteolytic bone disease
o	Ingestion of Vitamin D ointments (psoriasis cream)
o	Granulomatous disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Cholecalciferol Toxicity early signs (12-36 hrs)

A
  • Depression, weakness, anorexia
    Thennnn
    • Vomiting, polyuria/polydipsia, constipation, dehydration – bc we have CS of renal disease
    • Dark Feces ( GI ulceration)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Cholecalciferol : Later Clinical signs

A

• Acute kidney injury, oliguria/anuria
-Calcification of the renal tubules
• ECG changes
-Shortened QT, prolonged PR intervals
• Hematemesis/melena
-Grave prognosis , GI Mineralization and ulceration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Cholecalciferol: What should be monitored in Minimum database?

A 
o	Monitor total calcium
   - 15-18mg/dL (Normal 9.5-11.5)
o      ionized calcium
      -calcium/phosphorus product that is greater than 60 - 70  -mineralization
o       phosphorus
o        BUN
 o      Creatinine
 o     UA
        - Isosthenuria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cholecalciferol : Treatment in acute ingestion

A

o Acute ingestion (<6 hours)

  • Induce emesis
  • Activated charcoal
  • Monitor calcium at baseline and q 24-48 hours for 5-7 days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cholecalciferol: What does Supportive care look like for this toxicity

A

IV fluids - NaCl
- high levels of fluids to correct dehydration, volume expansion, and the sodium will induce calciuresis

Phosphate binders
- if animal is eating, used to bind phosphorus before its absorbed into the system

antiemetic therapy
- animals vomit a lot want to decrease electrolyte disturbances

Antacids
- in case there are Gi ulcers due to mineralization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cholecalciferol: What does Supportive care look like for this toxicity ( 2)

A

Glucocorticoids
- decrease calcium absorption from bones & GI. After HARDIONS ruled out. No tumors,

Furosemide
- animal must be well hydrated first

Biphostphonate ( Pamidronate)

  • Alendronate: cats use this for Primary Hypercalcemia
  • Inhibits osteoclastic bone resorption
  • Reduces calcium concentration within 48 hours
  • Given as Iv infusion, must have IV fluid bolouses too, because can be Nephrotoxic

Salmon Calcitonin

  • Inhibits osteoclast activity reducing resorption of calcium from bones
  • Risk of anaphylaxis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Bromethalin: What is it? What systems does in affect?

A
  • Used in Rat, gopher… etc poisoning

- neurotoxic ( w/ no antidote)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Bromethalin Toxic dose

A

Cats are more sensitive

  • LD50 ~0.5 mg/kg in cats
  • 5 mg/kg in dogs

o Clinical signs are seen at much lower doses

  • Cats ~ 0.2 mg/kg
  • Dogs ~1 mg/kg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Bromethalin Toxokinetics : What part of the body is it distributed to most?

A

Gi tract absorption
- Peak plasma levels 4 hrs

Liver metabolization
- desmethylbromethalin is the toxic metabolite

Throughout body - Highest in Body fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Bromthalin : Clinical signs of the primary target of the drug. Acute vs Delayed onset

A

Primary target:CNS
- Depression, abnormal behavior, ataxia, tremors, seizures

Dose dependent clinical signs
ACUTE >LD50 2-24 hrs post injection
 •	Severe muscle tremors
•	Hyperthermia
•	Seizures
•	Hyperesthesia
Delayed onset neurological signs 
Days- 2 weeks, less toxic dose
•	Hind limb ataxia/paresis
•	Patellar hyperreflexia
•	Mild to severe CNS depression
•	Seizure---- Coma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Bromethalin: Minimum Database information

A 
CBC/CHEM
EEG
- 	Not pathognomonic for  Bromethalin toxicity
-	Seizure foci 
-	Cerebral edema and hypoxia
17
Q

Bromethalin Antemortem and postmortem Confirmatory tests

A

o Antemortem:
Exposure history
Appropriate clinical signs

o Postmortem:
Diffuse vacuolization of white matter
Bromethelin residues in the fat, liver, kidney and brain tissue

18
Q

Bromethalin: No antidote so how do we treat?

A
  1. Reduce GI absorption
    - Emesis within 1 hour- Only to alert, neurologically normal animals
    - Activated Charcoal - Repeat every 4-6 hours for at least 2-3 days

2a. Provide Symptomatic and supportive Care
- Mannitol, hypertonic saline
- Keep head elevated 30°
- No jugular venipuncture

2b. Control Seizures
- Phenobarbital
- Keppra
- Midazolam/diazepam/lorazepam PRN or CRI

19
Q

Anticoagulant Rodenticides: What is the source of these rodenticides

A

1st Gen: Warfarin Based, rats becae resistant
2nd Gen: More toxic: brodifacoum, difenacoum, bromadiolone, indandione
- Last longer than the previous, problem with exposure to animals and
children

20
Q

Anticoagulant Mechnaism of Toxicity

A
  1. Secondary intoxication- uncommon ( cat eats a mouse thats eaten the toxin)
  2. coagulopathy -mVitamin K depletion clotting factors effected include:
    • 7 , 2, 9, 10
      • 7 has the shortest half-life so the prothrombin time is first prolonged
21
Q

Anticoagulant Rodenticide : Clinical signs seen?

A

lag period between exposure and clinical signs shown
- 3-5 days

Depletion of coagulation factors
- 7 ( halflife 6.2 hrs) , 9, 10, 2

Presenting complaint:
- Lethargy, anorexia, dyspnea, hemoptysis, lameness

Physical Exam :
may bleed from anywhere ( often the lungs- 50% of the time)
-     hematomesis, epistaxis, dyspnea
May bleed into joints
-     lameness 
Bleed in GI
-     Bloody Diarrhea, Vomitting blood
22
Q

Anticoagulant Rodenticide: What are the results of some of the minimum database tests?

A

Blood samples before treatment

CBC (depending on the progression of the disease)
- Thrombocytopenia, Mild anemia
Serum Chemistry
Coagulation Panel
- Aptt & Pt prolonged
Prothrombin Time
- Extrinsic pathway measurement ( including factor VII)
- Prolonged first 48 hrs, prolonged before APTT
Blood Typing, cross match
- May need to do blood transfusion
Imaging
- Rads( dtr source of bleeding) , Abdominal Ultrasound
confirmatory Testing
- Gas chromatography ( takes a couple days, useful in legal cases

23
Q

Anticoagulant Rodenticide: Treatment for acute ingestion ( Within 1st Few hrs )

A

o Induce emesis
- For acute ingestion we’re going to induce vomiting, decontaminate, check PT 48 hrs later, if prolonged start in Vit K, if not prolonged (which is more likely) carry on, is normal.

o Decontaminate with activated charcoal

24
Q

Anticoagulant Rodenticide: Treatment for acute ingestion ( Within 1st Few hrs ) But we find that after 48 hrs the Pt is prolonged

A

• Oral Vitamin K (phytonadione)
- 2.5 mg/kg orally every 12 hours
- 4 weeks
• Recheck PT 48 hours after last dose of vitamin K, If still prolonged
- Continue for additional 1-2 weeks

25
Q

Anticoagulant Rodenticide: Treatment of chronic exposure

A

Post-ingestion >4-12 hour
• Administer activated charcoal
• Check PT in 36-48 hours

Post-ingestion > 12 hour (no active bleeding) •	PT at 48 and 72 hours if Vitamin K1 not started o	If 72 hour PT normal, no further treatment o	If abnormal, administer Vitamin K1
26
Q

Anticoagulant Rodenticide: Treatment if patient is bleeding

A 
Correct coagulopathy
•	Clotting factors
o	Fresh frozen Plasma
o	Fresh whole blood
o	Give til clotting factors are normal
Provide Vitamin K1: •	DO NOT give IV - anaphylaxis •	Best given with food

Supportive care •	Oxygen •	Blood products •	Fluids

o Recheck PT:
36-48 hours after last dose of Vitamin K
• If normal, stop therapy
• If prolonged, extend another week
o Prognosis depends on the site and severity of hemorrhage

27
Q

Zinc Phosphide: How si this used and what systems are effected?

A
  • Gopher and Mole control
  • Gi clinicial signs
    - Zinc phosphide + stomach acid = phosphine gas release = vomiting (hemorrhagic)
    - Disrupts Cellular Respiration
    - Gas can be poisonous to staff

1 tablespoon in a 10kg dog can be significant

28
Q

Zinc Phosphide : Clinical signs and onset of clinical signs

A

onset: 15 min- 4 hrs

Signs : Vomiting (+/- blood), lethargy, depression, dullness, weakness, seizure, convulsion, death.

29
Q

Zinc Phosphide : What diagnostics should we run and what may we discover from them?

A

o EKG – usually not too many abnormal findings – nonspecific tachyarrhythmias
o BP – may see some evidence of circulatory failure
o Chest rads – pulmonary edema ***
o CBC, Chem, UA – unremarkable
o Coagulation profile
o Histopathology and toxicology
 For tox screen you can freeze the gastric contents and analyze it for zinc phosphide
o Silver nitrate paper- phosphine binds to the paper causes a color change

30
Q

Zinc Phosphide

A

Asymptomatic Patient : autodecontamination
- theyre already throwing up getting rid of toxin

Symptomatic Patient: Stbilize, mantain BP,& Temp
- dont really want to decontaminate with emesis because of the exposure to others

31
Q

Zinch Phosphide: How do we protect the staff from this posionous gas that the animal can give off

A

release delay of gas

  • open ventilation
  • increase gastric pH to 4
    - Magnesium hydroxide & Aluminum Hydroxide
  • mineral/ vegetable oil
32
Q

Zinc Phosphide

A 
Oxygen supplementation
	Benzodiazepines?
	Add magnesium??
	N-acetyl cysteine
•	is a glutathione precursor and so it can replenish glutathione levels which sometimes are decreased in these animals as well
	Acid reducers
	Liver protectants
	The other thing would be analgesics, a lot of times these animals are super painful in their abdomen so this can be another thing that we can use.

SAM- Tox (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions