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!Small Animal Medicine > Over the Counter Prescriptions > Flashcards

Over the Counter Prescriptions Flashcards

1
Q

Popular human and vet drugs

A

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

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2
Q

NSAID toxicities

A

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

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3
Q

How do NSAIDs work?

A

Direct inhibition of COX
Blocks PGs and thromboxane

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4
Q

COX 1 and COX2

A

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

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5
Q

GI effects associated with NSAID toxicity

A

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

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6
Q

Renal side effects associated with NSAID toxicity

A

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

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7
Q

Hematologic side effects associated with NSAID toxicity

A

Inhibit activity in platelets → platelet aggregation

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8
Q

Hepatopathy side effects associated with NSAID toxicity

A

Formation of reactive metabolites that cause the hepatocellular injury
Activation of apoptosis
Disruption of organelle function
Weeks, months, years

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9
Q

CS of NSAID toxicity (most to least common)

A

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

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10
Q

NSAID toxicity diagnostics

A

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

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11
Q

NSAID toxicity tx

A

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

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12
Q

Differentials of NSAID toxicity

A

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

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13
Q

Acetaminophen

A

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

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14
Q

Mechanisms of toxicity of acetaminophen

A

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

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15
Q

Gluthathione

A

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

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16
Q

How does glutathione depletion look in a dog and cat

A

Dog: liver most affected
Cats: RBCs have oxidative damage

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17
Q

CS of acetaminophen in dogs

A

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

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18
Q

Glutathione depletion consequences

A

More susceptible to oxidative damage (loss of mitochondrial function, ATP depletion and cell necrosis)

19
Q

CS of acetaminophen in cats

A

Cyanosis*
Methemoglobinemia*
Hepatoxicosis
Edema of face and paws

20
Q

Dx for acetaminophen toxicity

A

Minimum database (↑ ALT and TBR)
Confirmatory testing (acetaminophen concentration in plasma, serum and urine)

21
Q

Tx for acetaminophen toxicity

A

Stopping additional absorption (AC)
Providing supportive care
N-acetylcysteine (counteracts toxicity)
SAMe, ascorbic acid and cimetidine

22
Q

N-acetylcysteine

A

Antidote for acetaminophen toxicity
Glutathione pre-cursor: helps build up glut stores
Prevent hepatic necrosis
Convert methb to hb

23
Q

Vitmain D3

A

Human supplements
Used for tx psoriasis in humans

24
Q

MOA for vitamin D3

A

Maintains Ca homeostasis
↑ Ca absorbed from GI (↑ plasma Ca)
Works with dist. tubules to help with Ca absorption
Mobilize Ca from bones

25
Q

Differentials for hypercalcemia

A

Hyperparathyroidism
Addisons
Renal dz
Vitamin D
Idiopathic
Osteolytic regions
Neoplasia
Spurious

26
Q

Presenting complaint for Vit D3

A

History of ingestion
V/D, lethargy (12-24 hr post ingestion)
+/- arrhythmia and seizures

27
Q

Diagnostics for VD3 toxicity

A

Minimum database
Urinalysis, rads/ US
Calcium/ phosphorus product

28
Q

Tx for VD3 toxicity

A

Prevent absorption (AC)
Promote calciuresis (fluids)
Inhibits release of Ca and P from bone (bisphosphonates, mimidrenate)
Phosphate binders

29
Q

Cocaine

A

Schedule 2 drug, natural alkaloid, lipophilic
Erythroxylon coca
Used for local topical anesthetic and determine cause of miotic pupil

30
Q

Forms of cocaine

A

Hydrochloride salt (dissolved in water)
Free base (pure, HCl)

31
Q

Mechanism of toxicity for cocaine

A

Strong CNS stimulant (sympathomimetic effects)
Blocks reuptake of norepinephrine and serotonin

32
Q

CS of cocaine

A

Hyperactivity, ataxia, mydriasis, vomiting, hypersalivation, tremors, tachycardia

33
Q

Diagnostics of cocaine

A

Chemistry (electrolytes)
Blood gas
HR, body temp
Cocaine levels (serum, plasma and stomach contents)

34
Q

Tx of cocaine toxicity

A

Decontamination (gastric lavage)- don’t induce vomit (↑ aspiration)
Stabile neuro and cardiac systems
Maintain acid base balance (balance bicarb)

35
Q

Differentials of cocaine

A

Pseudoephedrine (cold meds)
Caffeine, Chocolate
Permethrin
Organophosphates

36
Q

Marijuana

A

Delta 9 tetrahydrocannibinol (THC)- psychoactive effects
Wide range of safety

37
Q

Animal exposures of marijuana

A

Ingestion of owners supply
Second hand smoke
Marijuana butter

38
Q

MOA of marijuana

A

Oral absorption → effects in 30-60 min → lipid soluble → enterohepatic circulation

39
Q

CB1 receptors

A

Brain in animals: memory, perception, movement control
THC most reactive

40
Q

CB2

A

Mostly in periphery (throughout body)
Analgesic effect, ↓ inflammation

41
Q

CS of marijuana toxicity

A

Depression, ataxia, incoordination, incontinence
Tremors, mydriasis, hypothermia, weakness, bradycardia

42
Q

Minimum database for marijuana toxicity

A

Body temp and cardiac rate and rhythm
Confirmatory: stomach contents and urine

43
Q

Tx of marijuana toxicity

A

Emesis if acute, lipid emulsion
Symptomatic/ supportive: monitor temp, fluids
Recovery: 24-72 hr

!Small Animal Medicine (32 decks)

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