MOA: eliminate or dec availability of adrenal steroids except aldosterone related to the insecticide DDT; cytotoxic Use: hyperadrenocorticism (Cushing's) or steroid-secreting tumors

Capstone - Ex 3 Flashcards by Sarah Huntington

How does inflammation cause pain? (peripheral)

Activates TRP channels

- PGs, bradykinin, cytokines, lipids

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How is pain increased (centrally)?

Increased Abs through pain pathways to brain

- e.g. “wind up”

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NSAIDs and Analgesia

MOA: dec PG synthesis and dec TRP activation

- COX inhibition

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Local anesthetics and Analgesia

MOA: block APs

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Ketamine and Analgesia

MOA: glutamate antagonist

- NMDA antagonist

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Opioids and Analgesia

MOA: work at many synaptic sites (e.g. mu and kappa agonists)

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A2 agonists and Analgesia

MOA: work postsynaptically on non-adrenergic neurons

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Two classes of endogenous steroids produced in adrenal cortex - Corticosteroids

Cortisol (glucocorticoid)
- zona fasciculata
Aldosterone (mineralocorticoid)
- zona glomerulosa

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Glucocorticoid Summary

production of inflammatory mediators
dec PGs via phospholipase A inhibition
WBC migration and fxn is suppressed
Cell-mediated immunity is suppressed

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NSAIDs

MOA: inhibit COX

- dec PG synthesis

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Hydrocortisone (cortisol)

MOA: dec PGs via Phospholipase A inhibition

Use: topically for pruritus and inflammation assoc’d with allergy

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Fludrocortisone

MOA: dec PGs via Phospholipase A inhibition

Use: systemically for cortisol and aldosterone replacement during adrenal insufficiency

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Prednisone & methylprednisolone

MOA: dec PGs via Phospholipase A inhibition

Use: systemically for LONG-term management of allergy, chronic inflammation, and immunosuppression

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Prednisone vs prednisolone

Prednisone:
- Pro drug that is metabolized to prednisolone

(Methyl)prednisolone:

cats/horses have less conversion from prodrug to this
hepatic failure has less conversion

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Dexamethasone

MOA: dec PGs via Phospholipase A inhibition

Use: systemically for immediate relief of hypersensitivity and septic shock, long-term control of allergy, and immunosuppression

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How can the adverse effects of long-term GC use be reduced?

Alternate-day therapy

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Mitotane

MOA: eliminate or dec availability of adrenal steroids except aldosterone

related to the insecticide DDT; cytotoxic

Use: hyperadrenocorticism (Cushing’s) or steroid-secreting tumors

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How do NSAIDs effect pain and inflammation?

MOA: inhibit PG synthesis via blocking COX

Pain: PGs inc intensity and duration of firing from nociceptors - blocking them exerts analgesic effect

Inflammation: PGs dilate small arterioles which enhance edematous actions of histamine and bradykinin - blocking them exerts anti-edematous effect

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What is the most-commonly reported adverse effect following NSAD therapy?

GI issues!!

Renal and hepatic toxicities are reported with much lower frequency

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Species-specific activity and COX Selectivity

Cannot extrapolate between species!

E.g. Carprofen is COX2 selective in dogs, COX1 selective in horses, and may be more non-selective in horses

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Which COX-selective drugs have less GI effects?

COX-2

Aspirin, ibuprofen are COX1 selective, which is why they have worse effects in dogs!

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NSAIDs and Cats

Which are good?

Most are cleared via glucuronidation in the liver (cats aren’t good at this)

Meloxicam and piroxicam are better! metabolized by oxidation

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What are the primary reasons NSAIDs are used in animals?

anti-inflammatory

Anti-pyretic

Analgesic

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At what point in the nociceptive pathways do NSAIDs exert their predominant effect?

Nociceptors at TRP channels

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What are the risks of NSAiDs and GC use concurrently

GI ulcers

What organ system is of most concern when giving an NSAID to adult cat

Kidney (esp with ahminoglycosides, ACEi, Beta-blockers, diuretics)

What are the pros and cons of using aspiring for chronic pain in the dog?

Pro: inexpensive, effective, easy to use Con: GI, tolerance, blood thinning

Why do NSAIDs fail to control pain in some patients?

- pain not due to PGs (inflammation) - pain is too strong/intense - tolerance - individual variation

What can you give with NSAID to enhance post-op analgesia?

opioids

Why do we choose NSAIDs over GC for post-op pain control?

NSAIDs don't suppress immune function and fewer side effects

How do NSAIDs work?

Block COX and dec PGs

Why do we use opioids in animals?

Analgesia for severe pain and sedation

Why are clinically available opioids scheduled (controlled) by the DEA?

Misuse and abuse by humans

How common is opioid addiction in vet patients?

not common

General anesthesia vs Analgesia

GA: - amnesia (loss of consciousness) - analgesia (loss of pain) - immobilization (mm relaxation) Analgesia: - loss of sensitivity pain

Tolerance and efficacy?

Higher tolerance, lower efficacy

Can pts develop tolerance to resp depressants or constipation effects of opioids?

Resp depression: patients develop tolerance quickly Constipation: dogs tolerate well, other spp not so much

Can animals become dependent on opioids?

Yes, physically - their body no longer regulates nociceptive signals

How do we avoid withdrawal in patients?

Taper dose

MOA of endogenous/exogenous opioids - Nociceptive signals

MOA: Mu or kappa agonist --> opiates bind and hyperpolarize the membrane --> dec NT release

Why is the affinity of an opiod to the opiate receptor important to know?

affinity relates to DOA

Which opioid is difficult to reverse due to high binding affinity?

Buprenorphine - a partial mu agonist, binds with high affinity

Is butorphanol (potency = 5 ) more or less effective than morphine for the treatment of severe, acute pain in the dog? why?

Butorphanol - kappa agonist and mu antagonist Butorphanol is less effective because its not a mu agonist (like morphine) - only a partial agonist - short DOA

Resp depression effects of butorphanol vs fentanyl

Butorphanol: ceiling effect Fentanyl: lose dose - no effect; high dose - profound effect

opioids and GI motility in horses

DEC GI stasis!

How do high doses of hydromorphone affect body temperature in cats?

Cats = hyperthermia other spp = hypothermia

MOA for analgesia with tramadol

Weak mu agonist, 5HT and NE reuptake inhibitor

How could you treat opioid-induced excitement in a dog?

Naloxone or sedative

Common way clients administer buprenorphine to cats

trans mucosal

Why is fentanyl administered as an IV infusion or a transdermal patch?

short DOA

What are some consequences of morphine-induced histamine release?

- vasodilation (hypotension) - bronchoconstriction - pruritus, sweating

Are opioids used to treat pain in animals with a hx of seizures?

Yes, not contraindicated in therapeutic doses Seizures only seen with OD's

Whats the predominant CV effect of hydromorphone in the dog?

Bradycardia

How would you characterize the sedative effects of opioids?

Drowsiness/sleepiness without amnesia (only in ill or old animals)

Which opioid is likely to induce vomiting in the dog and the cat?

morphine *see vomiting with pre-meds

How can you completely reverse the effects of hydromorphone or butorphanol? what about buprenorphine?

Naloxone! You cannot completely reverse bup - time and naltrexone can be attempted

What is the rationale for giving buprenorphine and meloxicam to a cat following dental sx?

Pain relief for 6-8 hours post-op with opioid NSAID to reduce inflammation and pain

MOA of Diazepam

Benzodiazepines - enhance GABA inhibition

Is diazepam effective in young, healthy animals?

NO! its better used in old or ill animals

Why is diazepam combined with ketamine and xylazine to induce anesthesia in the horse?

muscle relaxation, anticonvulsant, sedation

Diazepam vs midazolam

Midazolam is water soluble and shorter acting

Flumazenil

Benzodiazepine antagonist - give it to reverse sedation/fear/anxiety/not waking up fast enough

Primary use of ACE

tranquilizer (anxiolytic)

Can you reverse Ace?

NO!!!

effects of Ace on CV

Depresses CV - vasodilation/hypotension = reflex tachycardia

How can you enhance sedative effects of ace in a dog or cat/

give opioids or alpha 2

Can you give ace in patients with hx of seizures?

Yes, hasn't been proven to induce seizures BUT you can't reverse ace so there is that risk

Alpha2 agonists MOA of analgesic and sedative effects

They inhibit excitatory NT release

Alpha 2 agonist effects on CV system?

BIG drop in CO, vasoconstriction/hypertension, reflex bradycardia

Alpha 2 agonist effects on resp system

Mild resp depression, increases CO2 threshold

Adv and dis-advantages of giving atropine with alpha2 agonists

Adv: counteracts bradycardia/hypotension DA: doesn't inc CO - not advised to give anticholinergic with alpha2

How do you reverse dexmedetomidine?

yohimbine or atipamezole

what are the potential adverse effects of atipamezole?

profound hypotension, reflex tachycardia, excitement/pain