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Foundations- Pharmacology > NSAIDs and Corticosteroids > Flashcards

NSAIDs and Corticosteroids Flashcards

1
Q

describe NSAIDs (5)

A
  1. non-steroidal anit-inflammatory drugs
  2. mainstay in treatment of pain (significant manifestation of inflammation) that is most effective when given pre-emptively
  3. anti-pyretic, anti-endotoxemic, and anti-neoplastic
  4. produce anti-inflam analgesic effects by inhibiting cyclooxygenase (COX), which is the enzyme that metabolizes arachidonic acid to prostaglandins, which along with leukotrienes are key factors in production of peripheral senstion
  5. used to treat mild-moderate inflammatory pain and visceral pain
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2
Q

what are some good homeostatic things that prostaglandins do in the body? (2) what can PG inhibition lead to?

A
  1. produce protective gastric barrier to intralumenal acidity, sustain normal gastric secretions, and maintain normal gut motility
  2. regulate renal blood flow and maintain normal renal tubular function

inhibiting PGs can lead to altered GI motility, GI ulceration, renal or liver toxicity, impairment of jejunal epithelial restitution, and has the potential to delay clotting

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3
Q

how do leukotrienes work?

A

mediate inflammation via inflammatory cell recruitment and activation

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4
Q

what is the mechanism of action of NSAIDs? (5)

A
  1. inhibit the biosynthesis of prostaglandins by preventing arachidonic acid from binding to the COX enzyme active site
  2. arachidonic acid is formed through the actions of the enzyme phospholipase on cellular membrane lipids in response to tissue damage OR release of inflammatory mediators and interacts with 2 enzymes: lipoxygenase (LOX) and cyclooxygenase (COX)
  3. regulation of the COX enzyme is the main MOA of NSAIDs; COX has multiple isoforms (COX-1, COX-2 (inducible with tissue damage and inflammation), and maybe even COX-3)
  4. the anti-nociceptive effects occur both peripherally and centrally
    -penetrate tissues to have a local effect
    -the central effects are at both spinal and supraspinal levels with contributions from COX-1 and COX-2; the central effect may account for the overall wellbeing and improved appetite seen
  5. all NSAIDs are weakly acidic and over 90% are bound to albumin, which influences their distribution and drug-drug interaction potential
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5
Q

describe classification of NSAIDs

A
  1. based on their COX-1 versus COX-2 suppression profile;
  2. expressed as the ratio derived from the concentration needed to inhibit 50% of COX-1 over 50% of COX-2;
  3. the greater the ratio above 1, the more specific the NSAID is for COX-2
  4. have COX-1 selective, COX-2 preferential, COX-2 selective, and COX-2 specific classes
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6
Q

describe the adverse effects and contraindications of NSAIDs in the GI tract (6)

A
  1. because COX-1 and COX-2 are necessary for proper function, maintenance, and repair or GI mucosa,
  2. and because COX-1 related prostaglandins help regulate mucosal blood flow, secretion of buffers and mucous, and turnover of epithelial cells,
  3. and because COX-2 plays a role in mucosal production and repair
  4. THE GI TRACT IS BY FAR THE MOST COMMON SITE OF NSAID TOXICITY
  5. the more selective a drug is for COX-2, the more likely it is to cause GI ulceration and prevent healing or pre-existing lesions
  6. NSAIDs should be used with caution in dehydrated, debilitated, very young, or very old animals
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7
Q

describe the adverse effects and contraindications of NSAIDs in the kidneys

A
  1. because prostaglandins regulate renal blood flow and glomerular filtration, especially during periods of hypotension (anesthesia anyone?)
  2. and because BOTH COX-1 and COX-2 enzymes are required to maintain adequate renal perfusion
  3. and because renal prostaglandins work in concert with catecholamines to autoregulate renal blood flow and maintain renal perfusion
  4. AND because during conditions of stress, prostaglandins are upregulated in the kidneys to maintain adequate renal blood flow
  5. NSAID suppression of renal prostaglandin can disrupt autoregulation and result in renal ischemia, can lead to acute renal papillary renal necrosis
  6. cats may be uniquely sensitive to NSAID toxicity because the possess approx 1/2 the number of nephrons at birth compared to most species
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8
Q

describe the adverse effects and contraindications of NSAIDs in the liver (3)

A
  1. NSAIDs have been implicated in hepatocellular damage and hepatic failure in several species
  2. NSAIDs are metabolized in the liver and excessive dosing can lead to hepatotoxicity
  3. specifically excessive dosing of phenylbutazone can produce hepatotoxicity in horses
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9
Q

talk about NSAIDs and cats (3)

A
  1. cats have trouble metabolizing NSAIDs that are reliant on the glucuronidation pathway because they lack glucuronyl transferase!
  2. good NSAIDs to use: meloxicam, piroxicam, robenacoxib: metabolized via oxidation
  3. don’t chronically use meloxicam (one injection every year or so due to systemic NSAID effects) and only prescribe robenacoxib for 3 days at a time
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10
Q

discuss NSAIDs and platelets (5)

A
  1. COX-1 enzyme produces thromboxane, which is necessary for proper platelet function
  2. NSAIDs that strongly suppress COS-1 can have significant effects on platelets and clot formation
  3. aspirin specifically can inhibit aggregation and is used therapeutically for this purpose
  4. ketofen has been shown clinically to affect hemostasis; AVOID IN CASES WHERE SURGICAL BLEEDING DIFFICULT TO CONTROL

5, coxib-type NSAIDs do no affect platelet function- yay!

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10
Q

what are 9 general contraindications of NSAIDs?

A
  1. acute renal insufficiency
  2. hepatic insufficiency
  3. dehydration
  4. hypotension (esp under anesthesia)
  5. conditions associated with low effective circulating volume (CHF, ascites)
  6. coagulopathies
  7. evidence of gastric ulceration
  8. shock/hemorrhage
  9. patients with spinal injury
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11
Q

give 4 specific conditions in which NSAID use is contraindicated

A
  1. asthma: aspirin can exacerbate
  2. not during pregnancy; may lead to cessation of labor, premature DA closing, or disrupt fetal circulation
  3. avoid in breeding females: COX-2 induction is necessary for ovulation and embryo implantation
  4. avoid in lactating mothers
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12
Q

describe clinical use of NSAIDs

A
  1. most commonly used class of analgesics to reduce effects of primary disease such as acute and chronic pain, inflammation, fever, endotoxemia, and hypercoagulability, and some neoplastic processes
  2. should be reserved for patients without renal, GI, or hepatic dysfunction (but give horses with colic banamine!)
  3. should be avoided in immature animals without mature organs (<6 weeks)
  4. can affect the adverse effects of anesthetic agents affecting cardiac output, blood pressure, and tissue perfusion, so avoid pre-op NSAID use
  5. during NSAID therapy, all patients should be monitored for hematochezia or melena, vomiting, increased water consumption, and nonspecific changes in demeanor
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13
Q

describe acetaminophen (3)

A
  1. used in dogs for analgesia; can be used in combo with opioids
  2. is not technically approved for use in animals and DO NOT EVER EVER GIVE TO A CAT!! (glucuronidation lack), can result in hepatic necrosis
  3. other adverse effects in dogs and cats: methemoglobinemia and heinz body formation
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14
Q

describe aspirin (4)

A
  1. mainly COX-1 inhibitor, irreversible so duration of effect is related to COX enzyme turnover rate (unique; other NSAIDs work via competition with AA for binding sites so effects are related to concentration and disposition maybe FYI)
  2. related to chondodestruction, irreversible platelet dysfunction, and GI bleeding and ulceration
  3. effective anti-platelet therapy in horses!
  4. antipyretic and lower RI infections in cattle
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15
Q

describe carprofen/rimadyl (4)

A
  1. the only NSAID licensed in the US for dogs; oral and injectable (good for post-op)
  2. more potent than aspirin or phenylbutazone for treatment of pain and inflammation and safer than older NSAIDs with low antithromboxane activity
  3. in healthy cats, can use a single dose without causing GI or renal lesions
  4. effective for treating visceral pain in horses
16
Q

describe deracoxib/deramaxx (3)

A
  1. one of the first coxib-type NSAIDs approve for vet use in US as oral formulation for control of postop and osteoarthritis pain in dogs
  2. effective for decreasing lameness and pain associated with synovitis
  3. but has been associated with GI perforation so recommended only on label use and NEVER in combo with corticosteroids or other NSAIDs
17
Q

describe meloxicam (3)

A
  1. this plus onsior are the only approved injectable NSAIDs for cats in the US
  2. plus an oral formulation just for dogs
  3. repeated use in cats associated with acute renal failure and death so only give one dose at a time, but longterm oral is okay in dogs
18
Q

describe ketoprofen (3)

A
  1. COX-1 selective effective in dogs for orthopedic pain
  2. only licensed for horse injection; potent anti-inflam effects, accumulates in inflam exudates and inflamed joints
  3. increased incidence of adverse effects including prolonged bleeding times and gastric lesions
19
Q

describe diclofenac/surpass (2)

A
  1. topical 1% liposomal cream approved for use in horses
  2. works locally on area applied to only (lower frequency and severity of toxicity)
20
Q

describe dipyrone (3)

A
  1. thought to work similar to acetaminophen, but is hella old
  2. best as an antipyretic and used in bacteremic neonatal foals
  3. CANNOT enter human food chain!!
21
Q

describe etodolac (2)

A
  1. old, less common
  2. used for orthopedics in dogs but fucks up GI tract
22
Q

describe dirocoxib/previcox (3)

A
  1. the only coxib-type NSAID for horses
  2. the most COX-1 sparing NSAID for dogs; approved for OA
  3. comparable to phenylbutazone in horses
23
Q

describe flunixin meglumine (banamine) (6)

A
  1. moderately effective for soft tissue and ortho pain and optho pain
  2. systemic use in dogs results in gastric ulceration, perforation, and peritonitis, as well as increased plasma ALT activity and creatinine and renal failure
  3. one of the more commonly used NSAIDs in horses, can give oral, IV, IM
  4. effective for treating OA pain and comparable to phenylbutazone for treatment of navicular syndrome
  5. give prior to colic SX to decrease inflammation
  6. the only NSAID labeled for use in cattle for treatment of pyrexia for resp tract disease, mastitis, and endotoxemia
24
Q

describe phenylbutazone (8)

A
  1. licensed for dogs but not as safe as other NSAIDs
  2. adverse effects include GI ulceration, gastro-esophageal intussuception, pancytopenia, nonregen anemia, and thrombocytopenia
  3. NOT REC FOR CATS: bone marrow suppression, GI, renal, and hepatic injury
  4. MOST COMMON NSAID in horses
  5. want to give IV to avoid tissue necrosis and sloughing
  6. prolonged half-life in horses and repeat dosing extends efficacy (pre-purchase and competition complications), but high (70%) bioavailability with oral admin
  7. repeat use in horses bad for GI, kidneys, clotting, oral ulcers, bone healing, colon
  8. ILLEGAL to use in cattle because health hazards to humans!de
25
Q

describe proxicam (2)

A
  1. not approved for vet use; not a great analgesic
  2. has only been used in dogs and cats as part of multi modal neoplasia treatments
26
Q

describe robenacoxib/onsior

A

1, a highly COX-2 selective coxib-type NSAID licensed for dogs and cats; injectable and oral (high bioavailability after oral admin)

  1. oral admin has no toxic effects in cats
  2. give for a maximum of 3 days
  3. DONT give with other NSAIDs or corticosteroids BUT can be combined with opioids for enhanced analgesia
  4. undergoes liver metabolism, COX-1 sparing
27
Q

describe tepoxalin (3)

A
  1. oral wafer, take home; inhibits COX-2, COX-2, and LOX synth
  2. may be more effective than carporfen or meloxicam for uveitis in dogs
  3. few adverse effects observed
28
Q

describe ketorolac tromethamine

A
  1. opthalmic NSAID with systemic absorption so can have GI lesions
29
Q

describe EP2 antagonists/piprants/galliprant (3)

A
  1. prostaglandin E2 serves important homeostatic functions and also regulates pain and inflammation specifically via EP4 receptor
  2. piprants/EP4 antagonists help regulate
  3. grapirant/galliprant is approved orally for control of pain and inflam from OA
30
Q

describe corticosteroids (2)

A
  1. a class of steroid hormones produced in the adrenal cortex involved in the stress response, immune regulation, carb and protein metabolism, electrolyte balance, and inflam modulation
  2. the main endogenous corticosteroid is cortisol, this is the standard that we use to measure the potency of our synthetic cortocosteroids
31
Q

give MOA of corticosteroids and do you use with NSAIDS?

A
  1. decrease inflammation to exert analgesic effect by inhibiting phospholipase A2, which prevents membrane phospholipid from entering the AA pathway, thereby inhibiting COX and LOX production
  2. act synergistically with NSAIDs to increase incidence of GI effects so DONT use together!
32
Q

describe clinical use of steroids (3)

A
  1. can administer almost any route with almost 100% biovailability orally
  2. use targeted therapy to reduce risk of adverse events (deposit corticosteroids directly at site of inflam or pain
  3. commonly use intraarticular injection in horses with OA
33
Q

list 9 adverse effects of steroids and what this means for out clinical use

A
  1. impaired wound healing
  2. thinning of skin and CT
  3. iatrogenic Cushing’s
  4. increased IOP and glaucoma
  5. gastritis
  6. intestinal ulceration and bleeding
  7. fluid retention and hypertension
  8. decreased bone mineralization and osteonecrosis
  9. increased blood glucose and dysregulation of diabetes mellitus

good for short term use but not long term

Foundations- Pharmacology (4 decks)

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