Toxicology Exam 2 - Old Exam Questions Flashcards
Regarding nitrate posioning in cattle, discuss the mechnaims of action that leads to death
- Discuss the histologic lesions that you would expect to see
What is the best organ to use for necorpsy post mortem to confirm anatkytically thats it nitrite intoxification
- NItrate (NO3) overhwelms the normal metabolims to ammonia: both **No3 and its conversion to nitrite (NO2) which is 10x more toxic than nitrate, will convert hemoglobiin to methemoglobin. ** The methemoglobin reduyctase enzyme is overhwlemed and the animal dies due to tissue hypoxia
Expected histologic lesions: NO specific lesions - just nonspecific fidnings
eyeball
When considering zinc or coppper intoxidfication, name three physiologic watys (mechanisms) that anemia can occur and which evidence would support the different mechanisms for it
1) loss (hemorrhage)
2) Destruction (hemolysis)
3) Decreased prodution
Evidence to support hemolysis: elevated bilirubin, icteric serum
Evidence that does support hemmorhage: no visible signs of hemorahage, TP is not low
Evidence that does not support decreased production: refgenerative repsonse, reticulocytes, other cell lines present
Which type of coin is specifically invovled in zinc intoxification?
- ## US pennies minted after 1982
Consider a cat that has supposedly overdosed on mmelixicam. 1) Meloxicam is an NSAID - so name the enzyme that it inhibits 2) Discuss the two major treatment options at this time and and how they are targeted toward prevenitng two major problmes from occuring
3) This cat was given activated cgarcoal with sorbitol every 8 hours for 24 hours, followed by the anti emetic every 24 hours known as _____ which works best in cats.
4) Name some reasonable treatments options for this cat
5) Name the gold standard treatment for patients like this kitty that have LARGE exposure dosages and are asymptomatic:
6) Name the drug that can be used to reverse CNS depression
1) Enzyme: Prostaglandin synthesis or cycloxygenase
2) Two major potential concerns: gastric ulceration and renal papilary necorissi
3) Maropitant
4) A) IV plasmalyte, two times maintenance for 48 hours B) Pantoprazole C) Misoprotol D) Sucralfate
5) Therapeutic plasma exhcnage
6) Naloxone
Discuss the mechanism of action for zinc phosphide
- Zinc phosphide, when it comes into contact with the water and the acidic environment of the stomach (low pH), it releaes phosphine gas. the risj to you is inhalation, which causes significant pulmonary edema and inflamation that can lead to death
Discuss the expected clin [ath finding that come with xylitol toxicity in dogs
- Hypoglycemia, hypokalemia, hypophosphatemi
Consider a horse with phenylbuazone intoxification. 1) Describe the toxic effects of phenylbutazone (especially when considering an acute exposure)
- This is a cyloxygenase inibitor, which subsequelty iniibits downstream prostaglanding synthesis (PGE, PGI). At toxic levels, his means a decrease in protective prostaglandins of the GI tract as well as decreased pkatelet aggregation. If left untreated, I would expect to see gastric mucosal ulcerationb, GI upset, and platelet inhibiton (increased clottin/bleeeding)
Cinsider iron toxicity
- clinical signs and linical pathologic chnages seen in its toxicities are related to both the GI tract and the red blood cell, and death is due to hypoxia ssociated with hemolysis
- ## Radiograpohs can be helpful to track the iron source as it moves through the GI tract and deferoxamine is the chelator of choice if the serum iron concentartions exceed 3-4 PPM
Most reports of alfatoxin involve dogs eating commercially processed dog food. Name the most common specific food substrate in the dog food that can commonly be contaminated with alfatoxin
Why can it often be hard to detetc alfatoxin in the feed, even. when it has been detected in the miulk of exposed cattle?
2) there are often hotspots of alfatoxin in the feed, meaning the toxin (mold) is not evenly distributed throughout the feed sample. To idenitfy the toxiun, a representatie sample (a large/from different areas =) of the feed must be tested.
When consideirng dogs that havebeen exposed to phenoxy herbicid eotoxicities, it causes a specific neuromsucular conditon called what? ALso, explain why dogs are uniquely sensitive to these herbicide toxicities and its toxic effects
1) Myotonia
2) Dogs are sensitive to this because they are “NOT talented at the aer of renal tubular secretion”
3)
Name the specific trichothecene mycotoxin that can cause feed refusal and and vomiting in swine?
Also name the grain that it is most likely to be found in
1) Fusarium Spp
2) Wheat
When you say copper, I say ________
2) Name the most common source of excess coppper for sheep that can lead to chronic copper intoxifications
Name the two tissues that you absolutely must submit for toxicology testing to analytically ocnfimr a coppee toxicosis
4) name the expected histopathologic chnages that you would expect to see in this animal?
5) Once you exmianed that the remaing sheep are still at risk, you should supplement the diet with what two elements and how does this treatment work?
1) sheep
2) Diet that is not intended for sheep (diet formulated for Cows with higher Cu levels)
3) Liver and kidney
4) Tubular necoris with heme pigment, acute, multifocal, severe, kidney and also Splenic enlargemnt, hemosidiosis, spleen and also centrilobular hepatic necoris with cholesatsis, acute, multifocal, liver
5) Molybdenum and Sulfur. Mo-Su-Cu form a complex so excess Cu can be excreted in bile
Name the three physiologic processes that can lead to anemia?
- Loss (hemorrhage)
- Destruction (lysis)
- No production
Consider a dog that has ingested a 2nd gneration rodenticide with diphacinone present at a concentration of 0.005%.
Explain the mechanism of action behind diphacinone and explain why there is a delay betwen ingestion and the onset of clinical signs?
- It inhibits the **enzyme vitamin K epoxide reductase ** which is th enzyme repsoinsible for converting the inactive Vitamin K epoxide (thats gets formed when clotting factors 2, 7, 9, and 10 get actoivated) * to the recycled active vitamin K. It takes time to deplete the stores of vitamin K and it also takes times to depete the stores of clotting factors and this is why there is a delay
Supooswe you have a kitty that eats an acetimenophen tablet.
1) What are you gon a use to induce emesis win this cat?
2) What two specific chnages are you gonna look for on the CBC/Chem panel with a case of acetimenophen toxicosis like this?
3) Ultimately, what is gonna be the secondary target organ for this toxicity?
4) List the two major detoxification pathways of acetomenophen in dogs and cats and inidcate which one i used in cats
4) Finally, describe how N-acetylcysteine works for acetomenophen intoxications?
1) Dexmedetomidine
2) Hemolysis (anemia) & Methemoglobinemia
3) Liver
4) Glucouronidation and sulfation
5) N-acetylcysteine can enter the cell and serve as a precursor for gluathion, which is the compound that binds, the active metaboliye and allows it to be excreted without harming the RBc and the liver
