Over the Counter Prescriptions Flashcards
Popular human and vet drugs
Ibuprofen, aspirin, naproxen, carprofen
Tx pain, inflamm., and fever
Highly protein bound drug interactions
NSAID toxicities
GI (low doses)
Renal (middle doses)
Neurologic (higher doses)
Hepatic
Coagulopathy
How do NSAIDs work?
Direct inhibition of COX
Blocks PGs and thromboxane
COX 1 and COX2
COX 2 selective: less suppression of COX 1 (species specific)
Non-specific COX inhibition- inhibits both
Enterohepatic circulation
GI effects associated with NSAID toxicity
Ulcerogenic effects
Suppresses PG synthesis (GI mucosal defense)
Topical irritant (ion trapping)
Renal side effects associated with NSAID toxicity
Volume depletion (disrupt electrolytes)
Vasoconstriction, ↓ blood flow to glomerulus
Hematologic side effects associated with NSAID toxicity
Inhibit activity in platelets → platelet aggregation
Hepatopathy side effects associated with NSAID toxicity
Formation of reactive metabolites that cause the hepatocellular injury
Activation of apoptosis
Disruption of organelle function
Weeks, months, years
CS of NSAID toxicity (most to least common)
Vomiting, depression/ stupor, diarrhea, anorexia, ataxia/ incoordination, blood stool and PU/PD
NSAID toxicity diagnostics
Minimum database (norm norm anemia, ↓ TP, ↑ BUN and creat)
Confirmatory test: ibuprofen levels
Endoscopy
NSAID toxicity tx
Initial management <2hr after ingestion- emesis, AC, cathartic, IV crystalloids
Restore mucosal defense mechanisms (GI protectants)
Differentials of NSAID toxicity
Hemmoraghic gastroenteritis
Addison’s dz
GI FB
IBD
Neoplasia
Hepatic failure
Acetaminophen
Analgesic/ antipyretic
Cats more susceptible
Toxic dose: 600 mg/kg for dogs, 50-100 mg/kg for cats
Mechanisms of toxicity of acetaminophen
Metabolized in the liver by glucuronidation → sulfation → cytochrome P450 →releasing toxic component NAPQI
Gluthathione
Necessary for cellular protection against oxidative injury
Becomes depleted with ↑ NAPQI
How does glutathione depletion look in a dog and cat
Dog: liver most affected
Cats: RBCs have oxidative damage
CS of acetaminophen in dogs
Hepatocellular injury and necrosis (vomit, lethargy, trembling, chemosis, anorexia)
Methemoglobinemia
Facial/ paw edema
Glutathione depletion consequences
More susceptible to oxidative damage (loss of mitochondrial function, ATP depletion and cell necrosis)
CS of acetaminophen in cats
Cyanosis*
Methemoglobinemia*
Hepatoxicosis
Edema of face and paws
Dx for acetaminophen toxicity
Minimum database (↑ ALT and TBR)
Confirmatory testing (acetaminophen concentration in plasma, serum and urine)
Tx for acetaminophen toxicity
Stopping additional absorption (AC)
Providing supportive care
N-acetylcysteine (counteracts toxicity)
SAMe, ascorbic acid and cimetidine
N-acetylcysteine
Antidote for acetaminophen toxicity
Glutathione pre-cursor: helps build up glut stores
Prevent hepatic necrosis
Convert methb to hb
Vitmain D3
Human supplements
Used for tx psoriasis in humans
MOA for vitamin D3
Maintains Ca homeostasis
↑ Ca absorbed from GI (↑ plasma Ca)
Works with dist. tubules to help with Ca absorption
Mobilize Ca from bones
Differentials for hypercalcemia
Hyperparathyroidism
Addisons
Renal dz
Vitamin D
Idiopathic
Osteolytic regions
Neoplasia
Spurious
Presenting complaint for Vit D3
History of ingestion
V/D, lethargy (12-24 hr post ingestion)
+/- arrhythmia and seizures
Diagnostics for VD3 toxicity
Minimum database
Urinalysis, rads/ US
Calcium/ phosphorus product
Tx for VD3 toxicity
Prevent absorption (AC)
Promote calciuresis (fluids)
Inhibits release of Ca and P from bone (bisphosphonates, mimidrenate)
Phosphate binders
Cocaine
Schedule 2 drug, natural alkaloid, lipophilic
Erythroxylon coca
Used for local topical anesthetic and determine cause of miotic pupil
Forms of cocaine
Hydrochloride salt (dissolved in water)
Free base (pure, HCl)
Mechanism of toxicity for cocaine
Strong CNS stimulant (sympathomimetic effects)
Blocks reuptake of norepinephrine and serotonin
CS of cocaine
Hyperactivity, ataxia, mydriasis, vomiting, hypersalivation, tremors, tachycardia
Diagnostics of cocaine
Chemistry (electrolytes)
Blood gas
HR, body temp
Cocaine levels (serum, plasma and stomach contents)
Tx of cocaine toxicity
Decontamination (gastric lavage)- don’t induce vomit (↑ aspiration)
Stabile neuro and cardiac systems
Maintain acid base balance (balance bicarb)
Differentials of cocaine
Pseudoephedrine (cold meds)
Caffeine, Chocolate
Permethrin
Organophosphates
Marijuana
Delta 9 tetrahydrocannibinol (THC)- psychoactive effects
Wide range of safety
Animal exposures of marijuana
Ingestion of owners supply
Second hand smoke
Marijuana butter
MOA of marijuana
Oral absorption → effects in 30-60 min → lipid soluble → enterohepatic circulation
CB1 receptors
Brain in animals: memory, perception, movement control
THC most reactive
CB2
Mostly in periphery (throughout body)
Analgesic effect, ↓ inflammation
CS of marijuana toxicity
Depression, ataxia, incoordination, incontinence
Tremors, mydriasis, hypothermia, weakness, bradycardia
Minimum database for marijuana toxicity
Body temp and cardiac rate and rhythm
Confirmatory: stomach contents and urine
Tx of marijuana toxicity
Emesis if acute, lipid emulsion
Symptomatic/ supportive: monitor temp, fluids
Recovery: 24-72 hr
