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Flashcards in Drugs Deck (40)
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1
Q

examples of opioids

A

morphine, fentanyl, codeine, butorphanol, noxalone

2
Q

opioid pure agonists (mu1 and mu2)

want Mu1, Mu2 is side effects

A

morphine- bronchoconstriction
fentanyl- strong
codiene- mild

3
Q

opioid mixed agonist/antagonist

A

butorphanol- agonist kappa, ant mu

4
Q

opioid antagonist

A

noxalone- reverse

5
Q

opioid MOA at opioid receptor

A

ascending pathway
dec Ca at pre synaptic causing dec transmitter release
increase K/Cl causing hyperpolarization and inhibition of AP

6
Q

opioid MOA in the CNS

A

descending pathway

increase GABA inhibition (?) causing stimulation of inhibitory neurons

7
Q

opioid side effects

A

resp depression from dec sensitivity to pCO2
hypotension/bradycardia at high doses
histamine release
vomiting

8
Q

alpha adrenergic agonists indications

A

dose dependent sedation
analgesia- SHORTER THAN SEDATION
muscle relaxation
minor painful procedures

9
Q

MOA of alpha adrenergic agonists

A

phase 1- inc NA release (pre) and inc vascular contraction (post) (inc BP)-> bradycardia
Phase 2- dulling of sympathetic drive and hypotension-> PROFOUND bradycardia

10
Q

targets of alpha adrenergic agonists

A

sedation- locus cerelus
cardiovascular regulating center in brainstem
analgesia- dorsal horn, thalamus, sympathetic neurons

11
Q

contraindications of alpha adrenergic agonists

A

pregnancy
heart, kidney, liver disease
shock

12
Q

examples of alpha adrenergic agonists (and antagonists)

A

xylazine (yohimbine)

medetomidine (atipomezole)

13
Q

Phenothiazines indications

A

preanesthetic and calming

NO ANALGESIA

14
Q

phenothiazine MOA

A

block dopamine receptors
peripheral alpha adrenoceptor blockage
inhibit adenosine uptake
block emesis at CTZ

15
Q

pharmacological effects of phenothiazine

A
blocks alpha-> dilate BV-> hypotension-> increase HR
dec PCV because splenic sequestration
anti-emesis
catalepsy
sedation
16
Q

Contraindications of phenothiazine

A

not for shock or debilitated (because it leads to hypotension)
not in colic or epileptic patients

17
Q

examples of phenothiazines

A

acepromazine

prochlorpromazine

18
Q

Benzodiazapine MOA and common name

A

allosteric effect of GABA receptor-> enhancing GABA binding-> release of Cl-> increase in inhibitory binding

valium

19
Q

benzodiazapine pharmocological effects

A

skeletal muscle relaxation
minimal cardio effects
anti- anxiety

20
Q

benzodiazapine indication

A
tranquilizer
sedation
behavior modification
stops seizures
appetite stimulation for cats
21
Q

what are the sedatives

A

alpha 2 adrenergic agonists (analgesia)
phenothiazines (NO ANALGESIA)
benzodiazapine (NO ANALGESIA)

22
Q

inhaled anesthetic agents

A

nitrous oxide, halothane (sensitizes heart to Adr-> arrythmias), sevofluorane (2 fast 2 furious)

isofluorane- very soluble, <1% metabolized, very common

23
Q

stages of analgesia

A
  1. amnesia, euphoria
  2. excitation, delerium- want to skip (quick induction and recovery)
  3. surgical plane, regular resp, decrease eye movement
  4. death- too far- resp cardio decrease
24
Q

injectable anesthetic

A

barbituates
dissociative (ketamine)
propofol
steroid (alfaxone)

25
Q

barbituate types and what they are indicated for

A

NO ANALGESIA
thio- ultrashort acting, rapid induction, short procedures, IV only
oxy- short acting, euthanasia (pentobarbitol sodium)

26
Q

Barbituate MOA

A

inc Cl channel opening duration-> inc GABA-> hyperpolarization-> dec target cell excitation

27
Q

CNS effects of barbituates

A

dec cerebral blood flow and O2 consumption

depressive on medullary control center- dec resp and baroreflex

28
Q

cardio effects of barbituates

A

inc HR, dec SV

bolus admin-> vasodilation and hypotension

29
Q

how are barbituates cleared

A
redistribution
THIO
-skinny animals- slow recovery
-fat animals- hangover effect
OXY
- termination requires metab by liver (cytochrome p450)
30
Q

contraindications of barbituates

A

skinny or fat animals

hepatic injury

31
Q

Dissociative ketamine

A

use with benzos
great analgesic
no muscle relaxant
not fully unconscious

32
Q

MOA of dissociative ketamine

A

antagonist- glutamate, NMDA and muscarinic Ach receptor- dec CNS excitation
agonist- opioid receptor

33
Q

dissociative ketamine CNS effects

A

cataleptic state- thalamus not communicating with cortex
inc cerebral blood flow (not for head trauma)
inc cerebral pressure- hallucinations/emergence rxn

34
Q

dissociative ketamine cardi/resp effect

A

inc sympathetic-> inc HR, RR, O2 consumption, BP

35
Q

propofol

A

short half life, rapid recovery,

for induction and short procedures

36
Q

mechanism of propofol

A

GABA mimetic

rapid metabolism

37
Q

Steroid (alfaxone)

A

best but expensive
modulates GABA transmission
half life of 5 mins so repeated injection without accumulation
needs soluble vehicle- IM or IV (CD)

38
Q

local anesthetics

A

lignocaine

39
Q

lignocaine MOA

A

block Na channels (use dependent)- no AP

small unmyelinated fibers (like pain fibers) easily blocked

40
Q

lignocaine ester versus amide linked

A

ester
- tissue plasma, quickly metabolized
amide linked
- metab in liver slowly, but most commonly used