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Toxicology > Toxicology - Exam 1 > Flashcards

Toxicology - Exam 1 Flashcards

1
Q

What is included in a patients signalment?

A

Age
Weight
Breed
Sex
Reproductive status

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2
Q

List TPRs for Canine

A

Temp: 99.5 - 102.5
HR: 60 - 120
RR: 10 - 30

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3
Q

List the TPRs for Feline

A

Temp: 100 - 102.5
HR: 110 - 130
RR: 20 - 30

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4
Q

List the TPRs for Bovine

A

Temp: 100 - 102.5
HR: 40 - 80
RR: 10 - 30

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5
Q

List the TPRs for Equine

A

Temp: 99 - 100.5
HR: 28 - 40
RR: 8 - 16

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6
Q

How much hydrogen peroxide is needed to induce vomitting?

A

1 ml/lb of hydrogen peroxide to induce vomitting

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7
Q

Whats the DAMNIT scheme

A
  • D –> degenerative, developmemntal
  • Anatomic, anomaly, allergic, auto immune
  • Metabolism, mechanica
  • Neoplastic, nutriutional
  • Infectious, inflammatory, immune mediated,m idiopathic, and ischemic
  • Toxic, trauma, tumor
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8
Q

What subjective parameters can be used to assess hydration status of a patient?

A

1) condition of mucuous membranes (dry, tacky, moist)
2) Skin tenting
3) Condition of the eyes (sunken, tearing)

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9
Q

What objective parameters can be used to assess the hydration status of a patient?

A

1) PCV
2) TP
3) BUN
4) Creatinine
5) Lactate
6) Glucose
7) USG
8) Urine output
9) Body weight

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10
Q

What are 8 essential items that you need to have in order to do an effective nceorpsy?

A

Personal protective garmants: –> 1) Gloves, coveralls, boots
Instruments: –> 2) sharp knife, knife sharpener, 3) forceps, scissors, 4) saw (hatchet, ax)
**Miscellaneous: ** –> 5) fixative & containers, syringes, swabs, 6) whirl-pak bags 7) marking pen 8) camera (cell phone)

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11
Q

What are the major target organs of monensin in cattle and what gross lesions will you see from this toxin?

A

Heart is the primary target, 7 days post exposure:
- Heart changes (enlarged, flabby, white streaks or spots)
- Effusions (thoracic, pericardial, abdominal)
- Edemnatous tissues
- Pulmonary edema
- Potentially hepatic necrosis (appear as pale, tan areas)

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12
Q

What are the main goals with regards to emergency stabilization/life support?

A

1) assess and maintain adequate respiration
2) Assess and maintain adequate cardiovascular function
3) Control CNS simulation
4) Control CNS/Respiratory depression
5) Control temperature (hypothermia or hyperthermia)

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13
Q

How can you get a cat to vomit?

A
  • dexmedetomidine / xylazine, hydromorphone and brimonidine can be affectivealternatives
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14
Q

What ius activated charcoal used for?

A

Activated charcoal is used in all animals and it binds nonspecifically and prevents absoprption (binds food and binds medications)

Activated charcoal + sorbitol (saccharide cathartic) = induces emesis

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15
Q

What is a cathartic (what does it function to do?)? Name a cathartic

A

Goal: accelerate the expulsion from the GIT (osmotic induced fluid retention –> fluid volume causes stimulation of GI motility

Note that the patient should be well hydrated if you choose to use a cathartic

Name of a cathartic: Saccharide (sorbitol)

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16
Q

For corrosive agents, whats the difference betwen acidic and alkaline corrosvies?

A
  • **Alkaline corrosives ** –> pH > 11
  • Acidic corrosives –> pH < 3
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17
Q

What are the dufferent parts of a confirmed toxological diagnosis?

A

1) Signalment, Hx, circumstances of exposure
2) Clinical signs
3) Specific evidience of pathophysiologic derangement - clinical tests
4) Gross and Histo lesions: ultimate dx = necropsy
5) Detection of toxicant in animal tissues or enviornment
6)

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18
Q

What are the different (6) goals of an acutely poisioned patient?

A

1) emergency stabilizationb/life support
2) Cardiovascular
3) Control CNS simulation
4) Control CNS/Respiratory Depression
5) Control temperatures

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19
Q

With regards to actuely poisoned patients, discuss the tiopic of Emgerncy stvabbilization/life support

A

Assess respiration –> respiratory rate, depth, patterns, noises
**1) Patent airway –> protect the airway
2) Adequate ventilation –> complications: ** –> ventilatory failure, bronchospams/constriction, hypoxia
Prevent aspiration

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20
Q

With regards to actuely poisoned patients, discuss the tiopic of Cardiov

A

Assess and maintain HR, and BP, mucous membranes, CRT, skin turgor
Assess hydration status
Objective parameters: 1) PCV
2) TP
3) BUN
4) Creatinine
5) Lactate
6) Glucose
7) USG
8) Urine output
9) Body weight

Subjective parameters: 1) mucous membranes 2) skiin tenting

Hypotensdion
Hypertension
Acid base/electro imbalance
Anion Gap
Cardiac disturbances

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21
Q

With regards to actuely poisoned patients, discuss the tiopic of Control CNS stimulation

A
  • tremors/.seizures –> life threatening
  • Diazepam –> anxiolytic and sedative –> good for seizures and tremors
  • Midazolam –> good for seizues and tremors
  • Phenobarbitol –> good for seizures
  • Levetireacetam –> good for seizures
  • Methocarbamol –> multiple routes, muslce relaxer, sedative –> good for tremors
  • ## Acepromazine
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22
Q

With regards to Control CNS/Respiratory depression, what drug is used for this?

A

Naloxone (reverse opiod)

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23
Q

With regards to dog consumption of mothballs (contaiing napthalene) that cause neorlogic signs (mostly seizures), 1) what drug is used to induce emesis? 2) Next, what is an effective anti emmetic that can be used with dogs?

A

1) Apomorphine
2) Maropitant/metaclopramide, ondansetron, dolesetron

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24
Q

With regards to dog consumption of mothballs (contaiing napthalene) that cause neorlogic signs (mostly seizures), a dog is eventually given activated charcoal and sorbitol. So describe what these two drugs are and how they work?

A

1) Activated charcoal is an osmotically actiavted substance which will nonpecifically bind to ‘potential toxins’ in the GIT and prevent them from being asbsorbed. Sorbitol is an omsitically active sacchride cathartic that causes an opsmotically induced fluid rentetnion in the GIT that causes stimulation of GI motility and enhance the fecal excretion of AC-toxin substance
2)

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25
Q

With regards to small breed dogs that can experience discomfort and have some msucle tremors post administration of actiavted charcoal and sorbitol treatment, what is the specific electrolyte disturbabnce associated with these neurologic signs? also what is the specific fluid therapy treatment that should be used to correct the undelrying electrolytre abnormnality discussed above?

A

Hypernatremia

Fluid therapy to correct the underlying dehydration/fluid shift

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26
Q

What is the agrument for why one would want to pursue the gold standard treatment of DDM?

Also discuss what would be the gold standard treatment plan for tgis patient?

A

We dont know what the toxic principle is and we dont know a true toxic dose. **Not all dogs exposed to raisins will succumb to renal disease, ** and **it has been estimated that < 10 - 40% of exposed dogs will ** - we just dont know which dogs will respond. There is evidence to suggest that dogs that vomit within 2 hours of exposure have a higher incidnece of succumbing to renal disease . To be on the safe side, the recomendation would be to intiate decontaimation procedures followed by Iv fluids diuresis.

–> Induce emesis, enti emetic, activated charcoal/sorbitol slurry,, 2x maintenace fluid therapy for 48 hours, monitor BUN-Cr-USG-PCV-TP

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27
Q

With regards to a feline case of onion tocity where a cat ingest a lot of onion soup, what drug should be used to induce emesis (list he most effective anti emetic that can be used in a cat). Also state which drug can be used to reverse the effects of the intial drug given

A

Dexmedetomidine –> Atipamezaole

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28
Q

What is monesin and why would it be given to cattle?

A

Moensin is a feed additive used in cattle to increase feed efficiency and rate of gain, act as a coccidiostat/will also decrease the incidience of lactic acidosis, bloat, fog fever

29
Q

With regards to an acute moensin inbtoxification with cattle (for the histological lesions)

A
  • Pulmonary edema, hydrothorax, hydroperotinoeum
  • Centrilobular necrosis, acute, severe
  • ## Monophasic degeneration and necrosis: acute, severe, heart: acute, mild, pelvic limb, skeletal muscle, tongue and diaphragm
30
Q

What is the toci principe associated with cottonseed ingestion in cattle?

A

Gossypol

31
Q

Regarding gossypol, why are calves particularly sensitive to the toxin found in unprocessed cottonseed, compared to adult cows?

A

Pre ruminant calves do not have the large rumen that contains solule protrin that can bind the free gossypol (toxic form) and make it unavailable for absorption

32
Q

What are two other types of antifreeze that are often consumed by dogs besides ethylene glycol?

A

Propylene glycol
Methanol

33
Q

Discuss the idea of ethylen glycol kit test and why one might recomend that you should a serum chemistry panel and a urinalysis

A

False postives are pretty common with these test kits, partioculary because you know that this patient is receiving mosit dog food. Plus you should not rely totally on the kit by itself - it should be considered a screening tool, and you would like to have some supprtive documentation that differentiates between EG and PG/methanol. All three will cause hyperosmolality, acidosis, but only EG will cause the crystals.

34
Q

With regards to ethylene glycol intoxidfication, what are the electrolyte abnormnalities that you will see? Nexrt, name the specific crystal that you would expect to see in the urine sediment? Next, discuss the different (cheap vs expensive inibitors) inhibitors that you can use for treatment.

A
  • Increased osmolaiity
  • Elevated anion gap
  • Metabolic acidosis
  • Isosthenuria
  • ## Normocalcemia

Calcium oxolate, monohydrate.

The competitive inhibitor is ethanol while the direct inhibitor (more expensive) is **fomepazole (4-MP) ** of the enzyme alcohol dehydrogenase

35
Q

With regards to ingestion of cholecalciferol rodenticide, what are two consistent changes that you would expect to see on the serum chemistry panel? Also indicate which one chnages first. Also, name of the group of drugs that you will be using to treat this patient with

A

Hypercalcemia and hyperphosphatemia (this one chnages first)

Bisphosphonates (pamidronate disodium)

36
Q

Discuss what cholestyramine is and why it might be used in place of activated charcoal

A

Cholestyramine binds weak acidic compounds and bile acids –> so it will trap vitamin D in the bile because vitamin D undergoes enterohepatic recirculatoon and gets excreted into the bile. This allows for vitamin D to get excreted out of the body via the feces.

37
Q

With regards to grape ingestioon via a dog, indicate 1) the proposed toxin and what fruit this proposed toxin is found in along wiht the coking opowder it is found in. 2) What eye drops can be used to induce vomiting?
3) What drug will be used to reverse the intiial drug given?

A

1) Tartaric acid which is found in tamarind (fruit) or the cooking powder knonw as cream of tartar
2) Ropinrole (Clevor)
3) Metoclomramide (but NOTE that this drug does NOT work effectively on CATS)

38
Q

With regards to grape ingestioon via a dog, indicate what the intial IV fluid therapy rate and how long should it be given? Then state why administering fluids will be effective for a trearment

A

1) An initial IV fluid therapy rate at a rate of 2-2.5-3X maintenance for a minimum of 48 hours

2) This will A) Enhance renal excretion of the water soluvble compoound B) Enhance GFR to decrease tubular contact time and prevent any reabsorption that might occur

39
Q

Regarding a feline that ingested a large amount of Vitamin D3 (cholecalciferol) in a capsule, indicarte 1) The most effective emetic 2) what can be used to reverse the initial drug 3) once the kitty was BAR, it was given the most effective anti-emetic in cats 4) Now, a decision must be made to either decontaminate with repeated doses of actibvated charcoal (3 times within 24 hours; first dose with sorbitol) or oral cholestyramine (3 times daily, for 4 days), so which one will you pick?

A

1) Dexmedetomidine
2) Atipamezole or Antisedan
3) Maropitant (NK receptor)

4) Best option is cholestyramine, mixed with something palatble –> cholecalciferol and its metabolites (lipophilic) need to be bound to bile acids for enterohepatic recirculation to occur and cholestryamine will bind this bilke-salts complex and enhance fecal excretion

40
Q

Regarding a feline that ingested a large amount of Vitamin D3 (cholecalciferol) in a capsule, indicate, 1) list three mechanisms for why the calcium and phosphorus values in this cate will increase as a result of this toxicity 2) what are some resopinsible treatments for this cat athis time?

A

1) enhanced calcium and phosphorus absorption from the gastrointestinal tract
2) enhanced osteolytic activity in bones, releasing calcioum and phosphorous into circulation
3) Increased calcium reabsorption by the distal renal tubules

2) - bisphosphonates
- Low Ca/P diet
- Presnisolone
- Aluminum hydroxide gel

41
Q

Regarding a dog that consumed 1.2 to 1 tsp of sourdough starter off the kitchen counter, 1) what are the two major concerns with pets when they ingest raw fermenting bread dough. 2) In situations where large exposures have occured and it is deemed necessary to perform a gastric lavage, what shoyld be kept in mind that is true regarding the gastric lavage?

A

1) patient should be in sternal or right lateral recumbency and sedated with a cuffed endotracheal tube in place
2) The length of the tube should extend from the tip of the nose to the xiphoid process or the 9th intercostal space
3) Fluids can be administered and retrieved either by gravity or light suction

42
Q

Regarding ethylene glycol toxicity in a dog, when the diagbnosis has not yet beebn made and the results to the ethylene glycol test come back as ‘weak positive’, why would this test be considered a screening test only and should only be interpereted, if possible, with compatible clinical signs and clinicopathological data

A

There is a risk of false negatives (run too early or too late in the process) or **false positives (which are also possible)

43
Q

Regarding ethylene glycol toxicity in a dog, 1) what clinical pathological chnages would you expect to see? 2) if this exposure to ethylene glycol was considered to be toxic, what type of crystal woukd you expect to see in the urine?

A

1) Elevated osmolarity, elevated anion gap, HYPOCALCEMIA, isosthenuria, metabolic acidosis, hyperphosphatemia (resulting from the phosphate rust removers)/no metabolic acidosis occurs and also no azotemia should be present at this time WITH THIS SPECIFIC CASE OF EG TOXICITY
2) CALCIUM OXOILATE MONOHYDRATE
3)

44
Q

Regarding ethylene glycol toxicity in a dog, discuss the thought process behind treating the canine with fomepizole (4-mthypyrazole) when there was no clnical pathologic chnages consistent with EG exposure and no crystals. Do you agree with this treatment choose, why or why not?

A

Main thing here is think about the pros and cons to treatment:
- Supporting treatment with either fomepizole or ethanol are:
- a history of no potential exposure and some compatible clnical signs

               VERSUS
  • NOT SUPPORTING TREATMENT:
    • Absolutely no appropriate clinical pathologic changes an no crystals which all should be present at thid time
    • You should continue monitoring CBC/serum chemistry panel and UA up until 12 hours and you should consider whether you are pro or con: risk of developing renal disease is a bad outcome that comes with a high mortality rate
45
Q

Regardiong ethylene glycol toxicity in a dog and treatment, one could use ethanol to treat the patinet instead of fomepizole …. therefore, describe specifically how each of these drugs work in treatment of EG intoxicated patients

A
  • Ethanol is a comnpetitive inhibitor and fomepizole is a direct inhibitor of alcohol dehydrogenase activity (first rate limiting step) so less EG gets metabolzied to its toxic metabolites and more gets excreted unchanged in urine.
46
Q

Regarding a clinet case where they belive that there dog was posioned by the dog food that the dog consumed, discuss the 5 step process that you will need to discuss with the client to determine if there is a clear cause and effect between the fog eating the dog food and gtetting ill

A
  • First address the intial statemnt that there is no test for toxicities and that everything is toxic in the right dose and there is no test on the planet that can test for evruthing and there is no way you can test for evrything
  • Next, there is so many diseases in toxicology and outside of toxicology that present very similarly so you must approach this in a logical manner
  • Next, ask why there is a concern about toxins and gain as much history as possible
  • Next, reccomend a full physical exmaniation (or full necropsy) to create a reasonable list for the DAMN-IT scheme.
  • Then, determine what diagnostic procedures are necessary to pursure the differentials
  • ANy potential necropsy finding can hopefully prov ide some leads, where it is the absence or presence of changes
  • write down the list of differentials
  • collect as many samples as possible for toxicity sampling if your investigation leads down this road –> whether it be biological or environmental
47
Q

Random exam questions
- Name that drug that cna be given to dogs via IV that ois >90% effective to induce vomiting
- ame the mmemonic ofr hypercalcemia in the dog GOSH DARN IT shceme and indicate what the A can stand for?
- When you give single or multiplke doses of actibated charcoal to a smalll breed dog or cat, you must monitor the hydration staus opf your patient for a minimum of four hours because you can potenitally se tremors or CNS signs due to this specific electrolyte abnormality
- List a minimum of eight objective parameters that youy can use to asssess the hydration status of a patient

A
  • Apomorphine
  • Addison’s disease (hypoadrenocorticism)
  • Hypernatremia
  • Objective parameters to asserss hydration status are:
    1) PCV
    2) TP
    3) BUN
    4) Cr
    5) Lactate
    6) Glucose
    7) USG
    8) Urine output
    9) BW
48
Q

Regarding a dog that has ingested grapes and is experieincing toxicity from it, what are the two treatment options for inducing emesis and how do they induce emesis?

A
  • Emetic: apomorphine (IV)
  • Emetic: ropinirole (opthalmic drops) or Clevor

Both of these drugs induce emesis by: stimulate dopaminergic receptioors of the chemoreceptor trigger zone which sends information to the viomiting center

49
Q

After a dog has ingested grape and is undergoing grape toxicity, it has been given an emetic to induce emesis. Now that emesis was successful, what are: 1) some anti-emetics that can be given prior to giving activated charcoal with sorbitol. 2) Next, describe why it might be necessary to do these two decontamination procedures (since emesis was successful) and 3) describe exactly why the AC and sorbitol decontaimanbtion procedures work

A

1) maropitant or odensetron or metoclopramide
2) WHY: Vomiting rarely evactuates 100% of the GI contents; dont know exactly when exposure occurred so materiak can be durther donw in the GIT
3) - How AC works –> Non specifically binds them to a alrge number of large,non polar, nonprotein bound, lipophilic compounds to prevent them from ebinf abosrbed by allowinfg them to be excreted through the feces
4) How sorbitol works –>** A saccahride acthartic that causes an osmotically induced fluid retention, and this fluid reteniton in the GIT stimulates GI motility, enhanhcing excretiuon of the toxin out through the feces**
5)

50
Q

After a dog has ingested grape and is undergoing grape toxicity, the next step is to intiiate IV fluid therapy, at 2-3 times the maintenance, for 1) ______ and then discharge at 2) ______ once fluids jave tapered off and everything looks normal on your chemistry panel and UA. Therefore, 3) provide two reasons why diruesis is recomended
.Finally 4) prior to intiating aggresive fluid therapy, you would want to assess the cradiovascular system. So what criteria would you monitor to assess the CV system?

A

1) 48 hours
2) 72 hours
3) A) enhance renal excretion of the toxins B) enhance glomerular filtration ratem therby decreasing tubular contact with the toxins and not allowing reabsorption to occur
4) 1) Heart rate 2) BLood pressure-central venous pressure 3) pulse rate (quality and rythm) 4) ECG 5) Capillary refill time 6) color and moistness of mucous membranes 7) skin tenting

51
Q

Regarding a cat that ingested a lot of beef jerky that was covered in onion and garlic pwoder, what is the most effective emetic in cats? ALso, how does this emetic works (whats its mehcnaims of action).

Next, once emesis was successful in the cat, the cat began to exhibit sedation, so what drug can be administered to reverse the signs of sedation? Next, once this cat was given oral cactivated charcoal and sorbitol and also placed on 2x mainatenace fluid therapy for four hours because there was a concern of this cat dveloping what electrolyte abnormality?

A

Dexmedetomidine:

stimulation of alpha 2 andrenergic recpetors of ther chemorecpetor trigger zone ——–> emetic center

Atipamezole –> this revrses the signs of sedation

Hypernatremia

52
Q

What is the specific type of enema that should never be used in small animal,s especially dogs and cats?

A

hypertonic sodium phosphate

52
Q

Regarding a suspected case of Bovine viral diahhrea in a herd of calves, if you are going to perform a necropsy, why is it essential to sample from 3 different dead calves when collecting tissue samples?

A

1) To look for similarities in gross and histologic changes
2) You want to necropsy animals that are representaive of the sitiuation anf problem.
– If you justr necropsyt one animal, then this animal could have died from something completely unrelated to the current situation.
3) If it is an opportunity to collect lots of samples that are in goood condition, partiocularly if some naimals have started to decompose

52
Q

Regarding a case of calves that are suspected of having bovine viral diahhrea, the post mortem chnages were described as having severe edema in the lungs and associated tissues. Based on the histologic chnages, cardiotioxins rose to the top of the differential diagnosis list- particularly gossypol and ionophores. 1) Therefore, name the feed that would have top be present in the diet for gossypoil to be a reasonable differential diagnostic 2) Describe why calves are more suspectioble to acute gossypol toxicosis as conmpoared to adult cows

A

1) Cottonseed
2) Calvbes do not have fully funcitoning rumens and not enough soluble proteins to bind to the toxic ‘free form’ of gossypol

53
Q

Regarding a case of calves that are suspected of having bovine viral diahhrea, the post mortem chnages were described as having severe edema in the lungs and associated tissues. Based on the histologic chnages, cardiotioxins rose to the top of the differential diagnosis list- particularly gossypol and ionophores. 1) letss say that the feed aversion and diahhhrea are consistent with ionophores, describe how ionophores can cause diahhrea 2) list two reasons why ionophores might be present in that ‘grain/mineral mix’

A

1) Ionophores alter the microflroa of the GIT, which sets up a situation for diahhrea to occur
2) Increase feed efficiencyt and wiefght of gain + coccidiostat (best answrs for calves)

54
Q

Regarding inonophore intoxiofcation in claves, what are the expected histological chnages that you will see?
what are two different physiological mechnaisms that cause gossypol to induce anemia?

-

A
  • pulmonary edema, severe, acute, diffuse
  • hepatorcellular degeneration and necoris, mild to moderate, centrilobular, acute
  • 1) an increase in RBC fragility that kleads to hemolysis; 2) free gossypol binds iron that leads to microcytic hypochromic anemia
55
Q

A female dog ingets some leatonin, which is significant because melaotning contains XYLITOL. 1) Name the safest method to induce emesis for a dog at home? 2) describe specifically why a GI protectant like omeprazole or pantoprazole would be recomended once the patient arrives at the clinic

A

1) 3% hydrogen peroxide
2) esophagitis and hemorrhagic gastroenteritis have been reported post hydrogen peroxide use

56
Q

A clinet shows up becuase her cat ingested one Vitamin D capsule one hour ago. The first question you should have is, is this cholecaliciferol, 25-hydroxycholecaleciferol, or 1,25-dihydroxycholecaliciferol. Name three reasons why it is important to ask this question?

Next, discuss what the deconbtaimnation procedure should be for this patient

What are you going to expect to find on the serum chemistry panel after intial exposure to the drug.

A

1) all of these compounds have different toxic doses (affects the math)
2) All of these compounds have different half lives (which affects how long you guys will be treating the patient
3) all of these compounds have different times to onset of clinical signs (affects whetehr or not this is an emergency

cholestyramine, three ties daily for 4 days

anorexia, hypercalcemia, hyperphosphatemia, polyuria

57
Q

A clinet shows up becuase her cat ingested one Vitamin D capsule one hour ago. The first question you should have is, is this cholecaliciferol, 25-hydroxycholecaleciferol, or 1,25-dihydroxycholecaliciferol.

When considering treatment for this patient, describe what are the two most important things to do that fits the following criteria: 1) IV fluid therapy, 2-3x miantenance –> name the best fluid to use . 2) A category of drugs that orimarily affects the bone and has a peak affect in 72 hours

A

1) physiologic saline, plasmalyte, Nomr-R
2) Bisphosphonates

58
Q

Regarding the topic of ice melts, discuss the absics

A
  • includes sodium chlorid,e magnesium chloride, and potassium chloride
  • oral and GI signs –> dermal irritatin can occur
  • **electrolyte imbalances with large ingestion
  • also includes calcium chloride, calcium carbonate, and and calcium magnesium acetate
  • potental for **severe irritation and ulcers with large ingestion

Treatment:
- induce emesis; NO AC
- monirotr electrolytes,
- for calcium products, use GI protectants (sulcralfate) and antibiotics as neeeded

59
Q

Discuss ethylne glycol

A

Antifreeze products that include –> propylene glycol, methanol and diethylene glycol

For diagnosing thias, you need a good history becaude without it, clinical signs are hard to ddetetc

in cats, 3 hours but in dogs, 6-8 hours

60
Q

Discuss the mechanism of action for ethylene glycol toxicity

A
  • first 3 cause CNS depressionn
  • Metabolites cause **metabolic acidosis, and electrolyte abnormalities and the metabolites cause cytotoxicity
  • oxalatae cyrtsals that cause mechanical obstruction and cytotoxicity
  • Acute oxalate nephrosis
    -Crystals in the URINE indicate exposure, notnecessarily renal damage yet
61
Q

Discuss the clinical signs for ethylene glycol toxicity and specifically discuss why PU/PD occurs

A

vary –> dose, time of presentation

Stage 11-3 (-12?) hours –> CNS depression
- vomitng, lethargic, abdominal discomfort, ataxic, **PU/PD –> this occurs because 1) 50% of EG is excreted unchanged in the urine and i acts as an osmotic diuretic and its pulling fluid out resulting in a compensatory polydipsia. 2) When EG is metabolized and the metaboliuted float around inn the blood stream, they function to cause a hyperosmality.

stage 2 –> occurs within 6-8 hours
- metabolic acidosis, tachypnea, stiill PU?PD

Stage 3 –> 6-12 hours, up to 12-24 hours or longer
- **oliguric/anuric renal disease **/failure

62
Q

Discuss what you expect to see for clin path on the CBC?Chem panel with regards to a case of ethylene glycol toxicity

A
  • increased osmolality, increased anioin gap and metabolic acidosis –> all of these signs appear early on (soon after the time of onset)
  • look for hypocalcemia
  • crystalluira –> this does not always equate with renal disease, just evidence of exposure
  • oliguric/anuric renal disease —> stage 3
  • calcium oxalate monohydrate crystals are what you will see i think
63
Q

Since you need to calculate the anioon gap on the exam, what is the equation for it

A

Anion gap (AG) = [Na+] + [K+] - ([Cl-] + HCO3])

64
Q

Whats the pneumonic for Hypocalcemia?

A

PEACE PAIN is the pneumonic for hypocalcemia
- Phosphat enema
- Eclampsia (onset of seizures)
- Albumin is low
- Ethylene glycol toxicity
- Parathyroid deficiency
- ACute pancreatitis
- Intestinal malabsoprtion
- Nutrional (deficiency of vitamin D)
-

65
Q

Discuss the gross and histolopgic lesions for ethylene glycol toxicity

A

Gross –> nonspecific
Microscopic –> proximal tubule degeneration and necorsis + birefringent calcium oxalate crystals

66
Q

Discuss treatment for ethylene glycol toxicity

A
  • **Ethanol ** –> competitive inibitor of alcohol dehydrogenase
  • 4-methylpyrazole, AKA fomepizole –> direct inhibitor of alcohol dehydrogenase
  • correct acidosis
  • **correct Ca
  • Get them to eat

Prognosis = stage 1 and stage 2 are guarded; stage 3 is expensive, quality of life, and cannot predict full recovery

  • differentials of acute renal disease: lily (cats), NSAIDs, ethylene glycol, paraquat, aminoglycosides antibiotics, leptosporosiscream of tartar, and vitamin D
67
Q

Discuss the “others” in regards to EG toxicity

A
  • **Diethylene glycol: ** - stage 1, 2, 3 - no crystals because metabolized to 2-OH-ethoxyacetic acid
  • diethylene glycol includes solvent, antifreeze, and brake fluid

methanol –> stage 1 and stage - NO renal component
- methanol includes antifreeze
- Treatment includes: **fluids, ethanol/fomepizole, supportive/sympotmatic care, particularly for acidosis/ hemodialysis

Toxicology (11 decks)

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