Inhalants (pt.3), Pain management/analgesia, Opioids Flashcards Preview

Anesthesia > Inhalants (pt.3), Pain management/analgesia, Opioids > Flashcards

Flashcards in Inhalants (pt.3), Pain management/analgesia, Opioids Deck (40)
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1
Q

Name 3 potential theories of how inhalant anesthetics works (the receptors they may act on)

A

1) GABA
2) two-pore K
3) glycine

2
Q

What is MAC?

A

the concentration of vapor in the lungs that is needed to prevent movement in 50% of subjects in response to surgical pain stimulus

3
Q

Mac is an index of?

A

potency

4
Q

Why is MAC hard to translate from research to clinical setting? (3)

A

1) use only inhalants (don’t account for pre-meds or injectables)
2) use only healthy animals
3) MAC varies by each patient

5
Q

Give the MAC for:

1) ISO
2) SEVO

A

1) 1.3–1.6

2) 2.3–2.6

6
Q

Two things that increase MAC?

A

hyperthermia

CNS stimulants

7
Q

4 things that decrease MAC?

A

pregnancy

hypothermia

extremes of age (young and old)

Other anesthetic agents (pre-med or injectable)

8
Q

Name 7 things that DO NOT change MAC

A
duration of anesthesia
gender
anticholinergics (atropine)
pH
PaCO2
PaO2
BP
9
Q

Name the beneficial side effects of inhalants as dose increases (4)

A

1) unconsciousness
2) muscle relaxation
3) loss of nociceptive response
4) loss of sympathetic response

10
Q

Two effects of anesthetics on:

1) CV system
2) respiratory system

A

CV system:

1) decreases CO (myocardial depression)
2) decreases systemic vascular resistance (vasodilation)

Respiratory:

1) decreases minute ventilation (shallow breaths)
2) decreased response to increased CO2

11
Q

Are inhalants metabolized by the body?

A

NO

12
Q

Neural process of encoding noxious stimuli

A

Nociception

13
Q

Name the 5 stages of pain pathway

A

1) transduction (detection and conversion to AP)
2) transmission (AP to spinal cord)
3) modulation (amplified or suppressed)
4) projection (sent to brain)
5) perception

14
Q

Which area of the brain is involved with perception of pain?

A

Cortex (thalamus encodes meaning to the pain)

15
Q

Concerning A-delta fibers, describe:

1) myelination status
2) size of receptive field
3) type of pain transmitted

A

1) lightly myelinated
2) small receptive field
3) rapidly transmits sharp, localized, transient pain

16
Q

Concerning C- fibers, describe:

1) myelination status
2) size of receptive field
3) type of pain transmitted

A

1) unmyelinated
2) large receptive field
3) slowly transmit generalized, burning, throbbing, and persistent pain

17
Q

Which neurons are involved with:

1) acute, high-intensity stimuli (incisional)
2) tissue injury and inflammation
3) injury to peripheral sensory nerves (neuropathic)

A

1) A-delta (also C fibers)
2) C fibers
3) A-beta; also C fibers

18
Q

Pain due to a stimulus which does not normally provoke pain

A

allodynia

19
Q

Two substypes of neuropathic pain; define neuropathic pain

A

central
peripheral

pain caused by injury to or dysfunction of somatosensory nerves

20
Q

What are 4 signs of neuropathic pain?

A

hyperalgesia
allodynia
chronicity
Failure of traditional analgesics

21
Q

Glutamate receptors (AMPA & NMDA) in:

1) physiologic state
2) neuropathic state

A

1) AMPA–active
NMDA–inactive

2) AMPA–sensitized
NMDA–active

22
Q

What 4 categories are used in the AAHA to assess pain?

A

1) loss of normal behavior
2) expression of abnormal behavior
3) reaction to touch
4) physiologic parameters

23
Q

3 classes of drugs that can be used to treat peri-operative incisional pain?

A

Opioids
Alpha-2 agonists
Local/regional anesthetics

24
Q

What type of pain can lidocaine be used for?

A

peripheral neuropathic pain (blocks the bad Na channels)

25
Q

Name 2 drugs used for central neuropathic pain and their MOAs

A

1) Ketamine–>NMDA receptor antagonist

2) Gabapentin (Ca channel blocker)

26
Q

Drugs that are naturally derived from opium

A

Opiate

27
Q

Which is a broader term:

Opioid or opiate?

A

opioid (includes naturals AND synthetics)

28
Q

Name the two clinically relevant opioid receptors and where they exist in highest concentration

A

1) Mu (MOP)–highest in dorsal horn (lower in brain)

2) Kappa (KOP)–highest in brain (sedation); lower in dorsal horn

29
Q

Which step in the pain transmission pathway do opioids effect and where?

A

modulation @ dorsal horn & midbrain (descending inhibitory tracts)

30
Q

Differentiate:

1) potency
2) efficacy

A

1) AMOUNT of substance needed to achieve desired affect

2) ABILITY of substance to achieve a desired affect

31
Q

Three clinical effects of mu agonist?

A

analgesia
mild sedation
excitement (depending on spp. and dose)

32
Q

Which mu agonist is associated with histamine release?

A

Morphine

33
Q

Rank the mu agonists (5) by increasing potency

A

Morphine=methadone
Hydromorphone
Fentanyl
Remifentanil

Fentanyl & Remi are equal in potency

this is also the order of longest to shortest duration of action AND longest to shortest time to onset

34
Q

Why does remifentanil have such a short duration of action?

A

it’s brokendown by tissue esterases

35
Q

Describe butorphanol’s interactions at the mu and kappa receptors & it’s clinical effects

A

Mu–antagonist (inhibits full mu agonists)

Kappa–agonist

causes sedation & mild analgesia

36
Q

Naloxone is a ?

A

opioid ANTAGONIST

37
Q

3 causes of peripheral neuropathic pain

A

1) sensitization of peripheral nociceptors
2) direct nerve injury
3) alteration in Na channels (lower threshold or spontaneous activation)

38
Q

Opioids stimulate receptors in which 2 areas to cause sedative effects

A

Midbrain

forebrain

39
Q

13 side effects of opioids

A

1) decreased ventilation
2) apnea after bolus
3) vomiting
4) reset body temp
5) panting (dogs)
6) cough suppression
7) immunosuppression
8) decreased HR
9) histamine release
10) delayed gastric emptying
11) alterations in peristalsis
12) defecation
13) miosis/mydriasis

40
Q

Buprenorphine is a _____

A

partial agonist (ceiling effect & reduces effects of full Mu agonists)