Enviromental/Toxocology Flashcards

1
Q

What is the MOA of Fenoldapam

A

Selective dopamine -1 receptor (DA-1) agnoist

Induces vasodilation and selectively increases renal cortical and outer medullary blood flow and GFR

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2
Q

JVIM 2018 Fenoldapam for the prevention of AKI with heat stroke

A

No difference in AKI in heatstroke with or without fenoldapam

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3
Q

JVECC 2017 What hemostatic abnormalities were found in naturally occurring heatstroke

A

No difference in any parameters at presentation
Non survivors: prolonged PT @ 12 hrs, decreased TPCA @ 12 hrs, Increased PTT @ 12/24 hrs; Lower fibrinogen at 24 hrs
Mortality 40%

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4
Q

Define heatstroke in dogs

A

Rectal temp > 105.8F
Leads to endothelial injury neutrophilic infiltration, widespread cellular apoptosis, microthrombi and hemorrhagic diathesis

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5
Q

JVIM 2019 AMiodarone and itraconazole for treatment of trypanosomiasis in dogs

A

Improved survival with treatment for 12 months

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6
Q

JVIM 2019 What is the MOA for amiodarone and itraconazole for the treatment of trypanosomiasis in dogs

A

Antifungals: T.crui and fungi share similar pathways for biosytnethsis of sterols
Amiodarone disrupts the calcium homeostasis in T. Cruzi; blocks critical protease cruzipain and inhibits production of sterols

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7
Q

JVECC 2017 What were the main toxicity of topical flurbiprofen exposure in a cat

A

AKI, anemia, and gastroduodenal peforation

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8
Q

JVECC 2017 what treatment was used for oleander toxicity in dogs

A

Digoxin specific antibiody fragments (digifab)

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9
Q

What is the MOA for oleandar toxicity

A

Structually similar to digitalis.

Inhibits the Na/K atapse by inducing a conformational change

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10
Q

Which toxins are likely to be removed by TPE

A

Low Vd and highly protien bound likely to be removed with TPE

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11
Q

JVECC 2017 (2 articles) and JVIM 2019 Which NSAIDS have been reported to be used with TPE

A

Meloxicam, Ibuprofen, naproxen, dericoxib

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12
Q

JVECC 2017 What signs are anticipated with Inocybe mushroom ingestion and why

A

SLUDD- most common vomiting

Mainly parasympathetic effects as acts on muscarine

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13
Q

JVAMA 2017 What is isoniazid and how does it work

A

Anitmycobacterial useful for tuberculosis
Results in pyridoxin depletion
Poorly protien bound with small v/d

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14
Q

JAVMA 2017 What incrased survivial in dogs with isoniazid toxicity

A

Increased body weight and IV administration of pyridoxine (dose 1:1)
Decreased survival with increase dose and seizures

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15
Q

JVECC 2017 What is single pass lipid dialysis

A

Using 5% lipid in diaslyte used for highly lipohilic toxins such as ivermectin and baclofen
Can use same mechanism with albumin for highly protien bound

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16
Q

JVECC 2017 what is the MOA of ivermectin toxicosis

A

Binding results in GABA gated chloride channels in the CNS, leading to membrane hyperpolarization and blockade of neural impulses.

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17
Q

What is the MOA of loperimide

A

Lipid soluble pure Mu opiod agonist. Dosenth have analgesic or sedative effects because P-glycoprotie mediated efluxx prevents its accumulation in CNS

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18
Q

What is the treatment for loperimide toxicity and which patients may have issues

A

ABCB1 mutation

Naloxone, time, interlipids

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19
Q

What are adverse effects of intralipids

A

Lipemia, triglycerides, Pancreatitis, if extravasation- pain @ infusion site,
People- anaphylaxis

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20
Q

JVECC 2018 What were the signs of metformin toxicity in a dog

A

Severe hypoglycemia and hyperlactemia

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21
Q

Which toxins are best removed via hemodialysis

A

Low molecular weight, low Vd, low protein binding

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22
Q

Which toxin characteristics benifit from hemoperfusion in addition to hemodialysis

A

Larger size > 1500 Daltons, and increased protein binding

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23
Q

JVECC 2018 Which extracorpeal toxin removal method would you use for cyclosporine and why

A

HD + HP; due to high Vd and MW of 1200 Da

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24
Q

What is the MOA of Minoxidil

A

ATP sensitive potassium channel opener with potent vasodilatory effects

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25
Q

JAVMA 2018 What is th treatment for minoxidil

A

with mostly alpha adrengic agonists and avoid Beta to not increase cardiac O2 demands

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26
Q

What is the MOA of ionophores

A

Influx of Na and CA leads to intracellular Ca overload

Respiratory failure

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27
Q

JVECC 2018 Which extracorpeal toxin removal method would you use for methotrexate toxicity

A

HD + charcoal HP

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28
Q

JVECC 2018 What are teh side effects of rapid administration of undiluted levetiractam

A

Tachycardia, hypergycemia, hypotension

Improved with Epinephrine

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29
Q

JVECC 2019 Which extracorpeal toxin removal method was used for cannabinoid toxicity despite what characteristics of THC

A

HD + HP
Shown effective for THC in people as it causes withdrawals
THC is lipophilic and highly protein bound

30
Q

What is the MOA of organophsophate toxicosis

A

Inhibits acetylcholinesterase by binding to esteric site.. Leads to build up of ACh in synaptic cleft

31
Q

What signs/acronyms due you see with acute muscarinic

A

SLUDD: Salivation, lacrimation, urination, diarrhea, dyspnea
DUMBELs: Dyspnea/diarrhea, urination, miosis, bradycardia, emesis, lacrimation, salivation

32
Q

What is the response to a test dose of 0.02 mg/kg of atropine that rules out organophate toxicity

A

mydrasis and tachycardia

33
Q

What is the treatment for organophosphate toxcitity

A

2PAM: pralidoxime chloride
Reverse initial ionic binding of organophosphates to AChE
Must be given in timely fashion, but may still see improvements at 72-96 hrs

34
Q

JVECC What is the mechanism and signs of chlorfenapyr

A

insecticide that uncoupler of phosphorylation

Peracute fever, neuro signs, GI signs

35
Q

JVECC 2019 Activated charcoal with sorbital showed what changes in electrolytes with water restriction

A

Increase in Na, K, CL and lactate, calculated osmolality
Significant weight loss.
Hyper Na attributed to dehydration

36
Q

JAVMA 2019 What is the MOA and signs anticipated with duloxetine toxicity in dogs

A

Seritonin and nor-epinephrine reuptake inhibitor

Trembling, lethargy vomiting, mydrasis…. seritonin syndrome

37
Q

JVECC 2019 What are the signs with barium nitrate toxicity

A

flacid pralsyis with fasiculations

Acidemia and severe hypokalemia

38
Q

JVECC 2019 What dose of mannitol and what were the signs that were noted with toxicity

A

6 g/kg over 24 hrs:
AKI with hypertonic hyponatremia with renal tubular dysnfuction
High osmol gap as mannitol is an unmeasured osmol

39
Q

JVECC 2019 what type of toxicity was noted with cheese tree root and where

A

Australia

ALF

40
Q

JVIM in evaluation of TPE for NSAID toxicities what was noted to increase length of hospitalization

A

Decreased PCV at presentation

41
Q

JVECC 2019 What is the MOA of eastern coral snake envenimation and what was the outcome with MV

A

Good outcome 7/8 survived 58 hrs MV regardless of antivenom
Alpha neurotoxins that competively block post synaptic nicotinic acetycholine receptor site
See diffuse LMN weakness–> paralysis –> Death from Resp failure

42
Q

JVECC 2019 Define serum sickness and what was it noted with

A

antivenom
Type III hypersensitivity reaction that is delayed generally 1 week (1 day to months)
Fevere, puritis, ecchymosis, uticaria, arthralgia

43
Q

What are the proposed MOA of ILE

A

Improved mycoardial performance: Free fatty acids to myocardium as preferred substrate; FFA stimulate voltage gated calcium channels
Lipid sink: Log P > 1.0 pulls toxins from CNS and heart back to plasma

44
Q

What dose is recommended for ILE

A

Not to exceed 10 ml/kg/day of 20 %

1.5 ml/kg IV bolus folled by a .25-0.5 ml/kg/min fur 30-60 minutes

45
Q

What properties are needed for toxin removal with hemodialysis

A

< 500 Daltons, moderate to large Vd, minimal protein bidning

Ex: EG, Enrfoloxacin, barbituates

46
Q

What properties are needed for toxin removal with hemoperfusion

A

Charcoal needs to have high affinitinity and moderate to large volume of distribution
Size and protein binding do not affect

47
Q

What toxins work well with HD/HP

A

NSAIDs, phenobarb, cafiene, theobromine, and vincristine

48
Q

what properties are needed for toxin removal with aphresis (TPE

A

small volume of distribution
Efficacy unaffected by protein binding or size
amanited, Vincristine, NSAIDs

49
Q

What type of kidney damage is caused by grape/raisins/currants

A

severe renal tubular degeneration, protein/cellular debris obstruction of the tubules

50
Q

What type of kidney injury is caused by lily toxicant

A

Proximal tubular epithelial necrosis edema, tubule obstruction
pancreatitis is also observed

51
Q

What is the MOA of anticoagulant rodenticides

A

inhibit physiologic vit K recycling inhibiting vitamin K epoxide reductase in the liver
Protein C decreased earliest clinical indicator

52
Q

What is the MOA of neurotoxic rodenticide

A

Bromethalin- neurotoxin that uncouples oxidative phsophorylation, decreasing ATP production
Undergoes enterhepatic circulation

53
Q

What is the MOA of cholecalciferol rodenticides

A

Cholecaciferal convered to calcitriol in the kidney

Results in increase Ca and Phos absorption from Gut, bone and kidneys

54
Q

What calcium phosphorus ration = mineraliztion

A

> 60 mg/dl

55
Q

What is the treatment for cholecalciferol rodenticides

A

cholestyramine 0.3-1 gram/kg PO q 8 hrs

56
Q

What is the pathophys of heat stroke

A

Initially have increased CO due to peripheral vasodilation and decreased SVR
Peripheral and splanchnic blood pooling and dehydration lead to hypovolemia
Leads to decreased CO and failure of heat loss mechanisms of radiation and convection and increased temperature

57
Q

What are serious complications of Heat stroke

A

Rhabdomyolysis, AKI, ARDS and DIC

58
Q

What are risk factors for Heat stroke

A

Prior occurance; obesity, Breed (golden, lab, brachycephalic), Body weight > 15 kg; Increased environmental temp/humidity; lack of acclimation/fitness

59
Q

What is the heat shock response

A

Rapid molecular cytoprotective mechanism that involves production of heat shock proteins (HSP 72)
increase in HSP 72 improves cytoprotection

60
Q

What bloodwork abnormalities have been previously associated with increased mortality in heat stroke

A

Nucleated RBCs > 18/ 100 wbcs
Increased ALP & GGT
Hypoglycemia

61
Q

What is the MOA of Bufo toad toxicity

A
biogenic amines (epi/norepi) cause hallucinogenic or CNS signs
Steroid derivatives- digitalis like toxin
62
Q

What is ethylene glycol’s metabolism

A

EG –> + Alcohol dehydrogenase –> Glycoaldehyded (CNS Signs) –> + aldehyde dehydrogenase –> glycolic acid (metabolic acidosis, increased anion gap and AKI) —> gllyoxilic acid —> oxalic acid (AKI), Glycen, and alpha hydroxy beta ketoadipate

63
Q

Which of ethylen glycol’s metabolites cause injury

A

Glycoaldehyde CNS signs
Glycolic acid: Metabolic acidosis, increased anion gap, and AKI
Oxalic acid: AKI

64
Q

How quickly do you see changes in osmol gap and anion gap in EG toxicity

A

osmol gap 1 hr

anion gap 3 hrs

65
Q

In EG toxicity what might a POC lactate be high

A

Increased lactate is really the metabolite glycolate

lactate level is normal

66
Q

What is the gold standard diagnostic for ethylen glycol

A

Gas chromatography

67
Q

What are tests in hospital that can be run to test for Ethylene glycol

A

Woods lap for dye in some products of urine, mouth, and paws. Only in urine for ~6 hrs
Kacey EG test strip for plasma: Lower limit is 20 mg/dl which is lethal dose for cats. Fals postiives with alcohol for blood draw, and propylene glycol
React eG: bust be read within certain time frame, and high false positive
Slide for some chem machines: does not cross react with propylene glycol

68
Q

What are the treatments for ethylene glycol

A

4MP (fomepizole)- inhibits alcohol dehydrogenase

ethanol- competiviely binds alcohol dehydrogenase

69
Q

What are the negative side effects of the ethylene glycol treatments

A

4MP: CNS depression, anaphylaxis with second dose
Ethanol: Worsening ataxia/neuro signs, polyuria–> dehydration

70
Q

What properties of Ethylene glycol make it suitable for HD

A

Low molecular weight and low protein binding of EG and metabolites, good throughout course