Over the Counter Prescriptions Flashcards by Trenni Jefferson

Popular human and vet drugs

Ibuprofen, aspirin, naproxen, carprofen
Tx pain, inflamm., and fever
Highly protein bound drug interactions

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NSAID toxicities

GI (low doses)
Renal (middle doses)
Neurologic (higher doses)
Hepatic
Coagulopathy

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How do NSAIDs work?

Direct inhibition of COX
Blocks PGs and thromboxane

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COX 1 and COX2

COX 2 selective: less suppression of COX 1 (species specific)
Non-specific COX inhibition- inhibits both
Enterohepatic circulation

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GI effects associated with NSAID toxicity

Ulcerogenic effects
Suppresses PG synthesis (GI mucosal defense)
Topical irritant (ion trapping)

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Renal side effects associated with NSAID toxicity

Volume depletion (disrupt electrolytes)
Vasoconstriction, ↓ blood flow to glomerulus

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Hematologic side effects associated with NSAID toxicity

Inhibit activity in platelets → platelet aggregation

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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

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CS of NSAID toxicity (most to least common)

Vomiting, depression/ stupor, diarrhea, anorexia, ataxia/ incoordination, blood stool and PU/PD

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NSAID toxicity diagnostics

Minimum database (norm norm anemia, ↓ TP, ↑ BUN and creat)
Confirmatory test: ibuprofen levels
Endoscopy

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NSAID toxicity tx

Initial management <2hr after ingestion- emesis, AC, cathartic, IV crystalloids
Restore mucosal defense mechanisms (GI protectants)

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Differentials of NSAID toxicity

Hemmoraghic gastroenteritis
Addison’s dz
GI FB
IBD
Neoplasia
Hepatic failure

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Acetaminophen

Analgesic/ antipyretic
Cats more susceptible
Toxic dose: 600 mg/kg for dogs, 50-100 mg/kg for cats

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Mechanisms of toxicity of acetaminophen

Metabolized in the liver by glucuronidation → sulfation → cytochrome P450 →releasing toxic component NAPQI

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Gluthathione

Necessary for cellular protection against oxidative injury
Becomes depleted with ↑ NAPQI

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How does glutathione depletion look in a dog and cat

Dog: liver most affected
Cats: RBCs have oxidative damage

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CS of acetaminophen in dogs

Hepatocellular injury and necrosis (vomit, lethargy, trembling, chemosis, anorexia)
Methemoglobinemia
Facial/ paw edema

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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