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VETM 443 Clin Pharm Tox > Pain and Opioids > Flashcards

Pain and Opioids Flashcards

1
Q

what is pain

A

an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage

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2
Q

what is nociception

A

neural process of encoding noxious stimuli

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3
Q

how can pain be measured

A

pain threshold or pain tolerance level

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4
Q

which fibres are involved in nociception of skin, fascia, bone (sharp, localized pain)

A

A fibers. C are the muscle and viscera ones

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5
Q

which fibres are involved in nociception of muscle, viscera pain (dull, diffuse)

A

C fibers (A fibres are skin, fascia, and bone pain)

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6
Q

at is the primary excitatory NT involved in nociception

A

glutamate

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7
Q

_________ is increased sensitivity to noxious stimuli, while _______ is when normally non-noxious stimuli become capable of eliciting a pain response

A

hyperalgesia, allodynia

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8
Q

inflammatory mediators such as prostaglandins and leukotrienes perform what 2 functions

A

activate silent nociceptors and nociceptor sensitization

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9
Q

what is spinal facilitation of pain or wind up

A

high frequency APs train second order neurons to respond more vigorously to subsequent stimulation (increase glutamate and other NTs, activate inactive NMDA receptors, influx of Ca, up regulate post-synaptic membrane)

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10
Q

what is pre-emptive analgesia

A
  • Pain leads to increased sensitivity (increased nociceptor sensitivity, activation of “silent” nociceptors, wind‐up/spinal facilitation of pain, neuroplasticity): therefore we use PRE‐ EMPTIVE ANALGESIA - easier to control pain before nociceptive stimulus happens
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11
Q

are general anesthetics generally analgesics

A

generally not. need to provide both

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12
Q

_____ has a conscious component, while ______ does not

A

pain, nociception

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13
Q

what do descending inhibitory pathways do

A

Decrease neurotransmitter release from primary afferents and reduce excitability of secondary neurons

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14
Q

give 3 physiological pain inhibition mechanisms

A

endogenous opioid agonists, up regulation of peripheral opioid receptors at site of injury, migration of opioid-producing leukocytes to site of injury

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15
Q

give 4 sites of analgesia

A

block nociception at peripheral nociceptors prevent transmission to sp cord, prevent transmission to brain, enhance descending inhibitory pathways

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16
Q

most effective way to prevent and treat pain is to _____, this is referred to as balanced pain management

A

affect all of the different levels

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17
Q

three types of opioid receptors are

A

mu, kappa, delta

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18
Q

opioid receptors are GPCRs. how can they lead to reduced NT release?

A

inhibition of calcium channels in presyn neurons

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19
Q

opioid receptors are GPCRs. how can they lead to hyper polarization?

A

increased potassium outflow in postmen neurons

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20
Q

how do opioid receptors inhibit calcium inflow in primary afferent neurons

A

Inhibits calcium inflow into presynaptic neuron through direct binding to calcium channels, and through cAMP‐ modulated mechanisms, reducing NT release

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21
Q

opioid receptors enhance K+ outflow from postsynaptic neurons in spinal cord. enhanced K+ outflow leads to what

A

hyperbole of postmen neurons

22
Q

give 6 effects of mu receptor

A

analgesia, respiratory depression, sedation/excitement (dose and species dependent), decrease in GI motility and secretions, euphoria, and nausea/vomiting

23
Q

give 3 effects of kappa receptor

A

analgesia, sedation, decreased GI motility (the mu receptor does these as well)

24
Q

I’ve effect of delta receptor

A

analgesia (kappa and mu do this too)

25
Q

drugs that interact with opioid receptors can be thought of in 4 ways, give em to me

A

full agonists (maximal effect), partial agonists (same effect as full agonists, but effects plateau), agonist-antagonists (vary effects depending on receptor and dose), antagonists (competitive antagonists)

26
Q

all of the opioid drugs act on which receptor

A

mu receptor. some on kappa and delta as well

27
Q

when given in combination with sedatives or anesthetics, what effect do opioids have

A

additive/synergistic sedative and analgesia effects

28
Q

give at least 3 clinically important adverse effects of opioids

A

respiratory depression (centrally mediated decrease in response to increased PCO2)
vomiting (chemoreceptor trigger zone and dopamine effects)
constipation/ileus
severe pruritus
histamine release
hyperthermia in cats
CNS excitation/dysphoria/seizures

29
Q

why is morphine not recommended for animals with CHF

A

variable effects on coronary blood flow

30
Q

PK of opioids: tell. me about half-life and duration of action

A

short half life, 0.5-2 hours, and duration of action also short and depends on dose/pain, 2-4 hours

31
Q

local use of opioids: opioid receptor expression is upregulated locally by what

A

inflammatory cytokines

32
Q

this gold standard opioid is a mu agonist, kappa partial agonist, is safe effective and cheap, less effective in cats than dogs, and not routinely used in horses due to CNS effects

A

morphine

33
Q

this opioid is a morphine derivative, mu agonist, emetic, less histamine response than morphine, oral bioavailability probably very low, short half-life

A

hydromorphone

34
Q

this opioid is a mu agonist, NMDA antagonist, NE and serotonin reuptake inhibitor, may be more effective for chronic pain than other mu agonists, causes fewer CNS effects and less vomiting than other mu agonists, especially in cats

A

methadone

35
Q

this synthetic mu agonist is more lipophilic than morphine and more potent, given IV or transdermally, wide safety margin in dogs, generally fewer adverse effects that with other opioids, common drug of abuse

A

fentanyl

36
Q

this is a partial mu agonist and a kappa agonist opioid, has a ceiling on analgesic and respiratory effects, transmucosal absorption, less CNS effects in cats, high affinity for mu receptor (potency) but lower efficacy

A

buprenorphine

37
Q

drug is a kappa agonist, mu antagonist or partial agonist, effective analgesic for mild/moderate pain, may reduce effects of mu agonists, prominent sedative effects, antiemetic and antitussive, occasionally used to reverse mu agonists but not in cats, commonly used in combination with sedatives

A

butorphanol

38
Q

centrally acting multimodal analgesic; active metabolite is a mu agonist, current recommendation is do not use as sole analgesic in dogs, but many be useful as adjunctive analgesic but be mindful of potential for treatment failure

A

tramadol

39
Q

reversal of opioids is performed by what kind of agonist or antagonist

A

competitive opioid receptor antagonist

40
Q

this competitive antagonist of all opioid receptors, especially mu, is also a GABA antagonist and can indue seizures. generally given at small doses to reverse respiratory depression

A

naloxone

41
Q

of fentanyl, buprenorphine, and heroin, which can induce total apnea at lowest dose

A

fentanyl

42
Q

what 3 things to base opioid decision making on in small animals

A

severity of pain, route of admin, and ok in cats

43
Q

what kind of drugs are drugs of abuse

A

opioids

44
Q

sedative effects of alpha 2 agonists are caused by decreased what release

A

norepinephrine release from brainstem neurons via negative feedback mechanisms

45
Q

how do descending inhibitory pathways work

A

decrease NT release form primary afferents and reduce excitability of secondary neurons

46
Q

all the alpha 2 receptors agonists currently used in vet med also have

A

alpha 1 activation. usually causes excitation and increased motor activity

47
Q

this drug is a short-acting general anaesthetic, common for flied procedures, and is an analgesic due to NMDA receptor antagonist and analgesic at subanesthetic doses, is useful in geriatric patients due to excellent safety profile

A

ketamine

48
Q

ketamine antagonizes ____ receptors and acts as a ____ analgesic

A

NMDA; central

49
Q

lidocaine, bupivacaine, and mepivacaine are all

A

local anesthetics, they block Na channels and stop AP conduction in nerve fibres

50
Q

By decreasing or abolishing the transient increase in permeability of excited cell membranes to sodium ions, local anesthetics basically stop what

A

nerve conduction

51
Q

adverse effects of local anesthetics are related to what

A

Na channel blockade

VETM 443 Clin Pharm Tox (18 decks)

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