Term
| What are the uses for NSAIDs? |
|
Definition
| -antipyretic, anti-inflmmatory, and analgesic |
|
|
Term
| What are the homeostatic mechanisms in the CV system are affected by NSAIDs? |
|
Definition
| -PGI1 vasodilator and anti-thrombotic agent |
|
|
Term
| Which homeostatic mechanisms in the GI system are affected by NSAIDs? |
|
Definition
| -affect pdn of mucus and bicarb, mucosal blood flow, surface hydrophobicity, epi proliferation adn migration |
|
|
Term
| Which homeostatic mechanisms in the kidney system that are affected by NSAIDs? |
|
Definition
| -affect renal blood flow, diuretic and natriretic effects, GFR |
|
|
Term
| Which homeostatic mechanisms in the CNS that are affected by NSAIDs? |
|
Definition
| -fever, nociceptive processing |
|
|
Term
| Are COX-1 or COX-2 naturally-occurring? |
|
Definition
|
|
Term
| What does COX-1 do in the body? |
|
Definition
-generates protective prostaglandins in the stomach, intestine, and kidney
-generates thromboxane which mediates platelet aggregation |
|
|
Term
| What does COX-2 do in the body? |
|
Definition
-generates pro-inflammatory prostaglandins
-generates protective renal prostaglandins and for the healing of gastric ulcers |
|
|
Term
| What are the three major groups of NSAIDs? |
|
Definition
0classical nonselective agents
-newer COX-2 preferential drugs
-even newer COX-2 selective coxibs |
|
|
Term
| What are the GI effects of COX? |
|
Definition
-inh of COX-1 = local systemic effects
-dec mucosal blood flow & neutrophil adherence to vascular endothelium
-rapidly absorbed via oral administration
-2-4h peak concentration
-Stomach: influenced by pH of stomach and upper GI
-SI: if NSAID is excreted in the bile, proximal SI is exposed to high concentrations of the drugs
-LI: permeability changes in both the SI and LI can lead to diarrhea |
|
|
Term
| Explain how COX-1 and COX-2 are necessary for renal function? |
|
Definition
-COX-1 is concentrated in vascular smooth muscle and collecting ducts
-COX-2 concentrated in macular densa, cortical thick ascending limb, and medullar interstitial cells |
|
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Term
|
Definition
|
|
Term
| Describe the metabolism of NSAIDs? |
|
Definition
-only unbound drug is active
-metabolized in liver
-excreted in urine, eliminated in bile |
|
|
Term
| What are the clinical signs of NSAID toxicity? |
|
Definition
-GI bleed
-acute renal failure
-minimum database: CBC + biochem profile + UA + abdominal rads/US + crossmatch |
|
|
Term
| What are is the treatment plan for NSAID toxicity? |
|
Definition
-eliminate toxin
-limit absorption
-promote excretion
-prevent reabsorption |
|
|
Term
| How do you treat NSAID toxicity? |
|
Definition
-emesis + AC
-GI protectants
-symtehtic prostaglandins: Misoprostal
-IV fluids
-anti-emetics
-blood products
-pain meds
-surgery with endoscope first
-IV lipid emulsion therapy |
|
|
Term
| How does lipid emulsion therapy work? |
|
Definition
| -toxic agent is sequestered inlipid compartment within the IV space and then eliminated |
|
|
Term
| What is cholestyramine? How does it treat NSAID toxicity? |
|
Definition
-anion exchange resin: binds with bile acids in the intestine preventing their reabsorption
-stops enterohepatic recirculation |
|
|
Term
|
Definition
| -acute gastritis after ingestion of gabage that has infectious agents, toxins, or dietary components that cause inflammation, overwhelming the gastric mucosal barrier |
|
|
Term
| What are the clinical signs of garbage gut? |
|
Definition
-severe cases: dehydration + fever + painful + hematemesis
-can lead to pancreatitis, GI ulceration, systemic inflammation |
|
|
Term
| Which diagnostics do we run for garbage gut? |
|
Definition
| -minimum database + abdominal rads |
|
|
Term
| How do we treat garbage gut? |
|
Definition
-dietary rest
-GI protectants
-anti-emetics
-fluid therapy if indicated |
|
|
Term
| Who is at risk for tremorgenic mycotoxins? |
|
Definition
|
|
Term
| Which foods are commonly infected with tremorgenic mycotoxins? |
|
Definition
| -moldy dairy products, walnut/peanuts, stored grains, compost garbage, refrigerated foods, and spaghetti |
|
|
Term
| What is the most common toxin of tremorgenic mycotoxins? |
|
Definition
|
|
Term
| What are the clinical signs of tremorgenic mycotoxins? |
|
Definition
-muscle tremors
-ataxia
-convulsions
-GI upset |
|
|
Term
| How do we treat tremorgenic mycotoxins? |
|
Definition
-AC
-cathartics
-methocarbamol for tremors
-diazepam if seizing
-GI protectants
-fluid therapy: if indicated |
|
|
Term
| In which species do we commonly see gorilla glue toxicity? |
|
Definition
|
|
Term
| What is the genus of onions? |
|
Definition
|
|
Term
| What is the MOA of onion toxicity? |
|
Definition
|
|
Term
| What is the TP of onions? |
|
Definition
|
|
Term
| Is onion toxicity more common in dogs or cats? |
|
Definition
| -dogs are more common but cats are less sensitivity |
|
|
Term
| Which dog breeds are most commonly affected by onion toxicosis? |
|
Definition
|
|
Term
| What are the clinical signs of onion toxicosis? |
|
Definition
-GI signs
-Heinz body anemia: pale mm + icterus +weakness + rapid breathing/HR + diarrhea + staggering + collapse |
|
|
Term
| HOw do you treat onion toxicosis? |
|
Definition
-emesis + AC
-IV fluids
-whole blood transfusion
-supplemental O2
-supportive care |
|
|
Term
| What is the most common source of pennies? |
|
Definition
|
|
Term
| Describe the metabolism of zinc in the body. |
|
Definition
-bound to albumin and macroglobulins
-transported liver, distributed to pancreas, kidney, and spleen
-excreted in feces |
|
|
Term
| What are the clinical signs of zinc toxicity? |
|
Definition
| -pale mucous membranes + jaundice + vomiting |
|
|
Term
| What do we see on clin path of zinc toxicity? |
|
Definition
-regenrative anemia
-neutrophilic leukocytosis
-hemoglobinemia
-gemoglobinuria
-bilirubinemia
-inc BUN, creatinine, proteinuria
-inc amylase, lipase, hepatic enzymes
-serum Zn levels > 5 ppm
-hemolysis and Heinz bodies |
|
|
Term
| HOw do we treat Zinc toxicosis? |
|
Definition
-remove source: Zn levels will return to normal in 48h
-Treat anemia: O2 therapy, nRBCs transfusion, O2 carrying fluids
-treat chock and dehydration
-treat renal failure if indicated
-may progress to DIC
-chelation therapy not indicated if you remove source: CaEDTA, Penicillamine
-H2 Receptor blockers: antacids |
|
|
Term
| What is the MOA of anticoagulant rodenticide? |
|
Definition
-inhibits K1 epoxide reductase
-interferes with clotting factors 2, 7, 9, and 10 |
|
|
Term
| True or False: Ingestion of intoxicated rodents affects animals that eat them. |
|
Definition
|
|
Term
| In In which cases are anticoagulant rodenticide toxicity expected to be worse? |
|
Definition
-hepatic/renal compromise
-GI malabsorption syndrome
-pediatrics
-geriatrics
-low BCS
-patients on highly protein-bound drugs
-in utero
-neonates |
|
|
Term
| What are the clinical signs of anticoagulent rodenticide toxicity? |
|
Definition
-dyspnea
-lethargy
-pallor
-epistaxis
-vomiting
-etc
-BLEEDING IS INTRACAVITAL
-Cats: otic hemorrhage |
|
|
Term
| What diagnostic test for anticoagulant rodenticide toxicity? |
|
Definition
-Proteins INduced by Vitamin K Absences
-detects a buildup of nonfunctional clotting factor precursors
-abnormal result within 12 hours
-PT, PTT, and ACT |
|
|
Term
| Which pathways are affected by PT, PTT, and ACT? In which time frame will each elongate with anticoagulant toxicity? |
|
Definition
-PT: extrinsic & common pathways (inc w/in 8h)
-PTT: intrinsic & common pathway (inc w/in 72h)
-ACT: intrinsic & common pathway (inc w/in 72h) |
|
|
Term
| What do we see on CBC with anticoagulant rodenticide toxicity? |
|
Definition
| -anemia and thrombocytopenia |
|
|
Term
| What do we soon on rads of anticoagulant rodenticide toxicity? |
|
Definition
| -pleural/peicardial/abdominal effusion |
|
|
Term
| What do we see on necropsy with anticoagulant rodenticide toxicity? |
|
Definition
-flaccid heart
-hepatic centrilobular necrosis
-myocardial hemorrhage
-pulmonary hematoma |
|
|
Term
| How do we treat anticoagulant rodenticide toxicty? |
|
Definition
-ingestion w/in 4-6h: induce vomiting, AC
-ingestion beyond 6h: Vitamin K1 |
|
|
Term
| How long do we treat anticoagulant rodenticide toxicity with Warfarin? What about Bromadionlone? What if it is unknown? |
|
Definition
-Warfarin: 14 dyas
-Bromadiolone: 21 days
-Unknown/Brodifacoum: 30 days |
|
|
Term
| Which drugs should we avoid with anticoagulant rodenticide toxicity? |
|
Definition
-furosemide
-sulfonamides
-coricosteroids
-NSAids
-chloramphenicol
-metronidazole |
|
|
Term
| What is the most common form of acetaminophen? |
|
Definition
|
|
Term
| Which species is especially sensitive to acetaminophen? |
|
Definition
|
|
Term
| Describe the metabolism of acetaminophen in the body? |
|
Definition
-rapidly and almost completely absorbed from GIT
-peak plasma levels 10-60 mins
-two major conjugation pathways are used to metabolize APAP
-renally excreted
-hepatoxicity
-the feline |
|
|
Term
| What are the clinical signs of acetaminophen toxicity in cats? |
|
Definition
-methemoglobinemia
-cyanosis, dark mucous membranes, dyspnea, pigmenturia, and edema of the front paws, and face, hyperbilirubinuria
-inc liver enzymes at 2-3days |
|
|
Term
| What are the clinical signs of acetaminophen toxicity in dogs? |
|
Definition
-GI signs: nausea, vomiting, depression, and anorexia
-inc ALT
-dec albumin and urea
0inc bilirubin in 24h |
|
|
Term
| What is the principal mainifestation of acetaminophen toxicity in SA? |
|
Definition
|
|
Term
| What is the toxic dose of acetiminophen in cats? In dogs? |
|
Definition
-Feline toxic dose: 60 mg/kg
-Canine toxic dose: 200 mg/kg |
|
|
Term
| How do we treat acetiminophen toxicity in small animals? |
|
Definition
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