M4 study guide Flashcards

1
Q

What receptors do opioid analgesics affect?

A

MU + Kappa

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2
Q

What are the effects of of activation of MU receptors?

A

Pure agonists produce analgesia, respiratory depression, sedation, physical dependence, slowed GI motility

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3
Q

How do opioid analgesics affect receptors?

A

acts primarily by activating MU receptors, also producing a weak activation of Kappa receptors

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4
Q

Best practices r/t use of topical anesthetics

A

minimize the amount being absorbed to avoid toxicity can be done by 1. apply the smallest amt 2. avoid application to large surface areas 3. avoid applications to broken or irritated skin 4. avoid strenuous exercise, wrapping the site, heating the site-all of which can accelerate absorption through increasing skin temp

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5
Q

Name some topical anesthetics

A

Lidocaine, tetracaine, cocaine

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6
Q

What are topical anesthetics used for?

A

Used to relieve pain, itching, and soreness of various causes including; infections, thermal/sunburns, diaper rash, wounds bruises, insect bites, plant poisoning

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7
Q

Complications r/t topical anesthetics?

A

Can be absorbed and produce serious life threatening effects. Cardiac toxicity can result in bradycardia, heart block, or cardiac arrest. CNS toxicity can result in respiratory depression, seizures, coma

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8
Q

Risk for toxicity increases w/ amount absorbed, determined primarily by:

A
  1. Amount applied 2. Skin condition 3. Skin temp
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9
Q

What is the reward circuit?

A

A system that normally serves to reinforce behaviors essential for survival

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10
Q

What is the major neurotransmitter released on the reward circuit?

A

Dopamine

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11
Q

Neurotransmitter effects on the reward circuit in those with SUD

A

Drugs can activate the circuit and cause dopamine release (may be 2-10x as much as what normally is released)
When the system is activated this causes a tendency to repeat behavior, w/ repeated action over time the system under goes synaptic remodeling, thereby consolidating changes in brain function

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12
Q

What occurs if the brain is put into excessive amounts of activation of the reward circuit in someone with SUD

A

The brain will 1. produce less domapine 2. reduce the number of dopamine receptors

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13
Q

What are the effects of alcohol on the CNS

A

depression of CNS and activation of reward circuit

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14
Q

What 3 receptors/neurotransmitters are involved w/ alcohol and CNS

A

GABA-inhibitory neurotransmitter-alcohol binds to GABA causing CNS depression
Glutamate receptors-alcohol binds to glutamate receptors it blocks excitation and reduces CNS activity
5-HT3 receptors-rewarding effects of alcohol. Triggers the reward circuit

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15
Q

All 3 of these promote release of dopamine

A

GABA, 5-HT3 receptors, Glutamate receptors

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16
Q

How are migraines treated

A

Treatment is based on severity and functional improvement.
Abortive therapy + Preventative therapy

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17
Q

Mild migraine

A

NSAID e.g aspirin, naproxen

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18
Q

Moderate Migraine

A

DHE or Ergotamine (ergot alkoloid), NSAID combo products

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19
Q

Severe Migraine

A

Metoclopramide, Triptans-Imitrex (First line drug tx migraines), NSAIDS (ketoralac), Ergotamine or DHE

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20
Q

How often should you use abortive meds for migraines

A

no more than 1-2 times a week

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21
Q

Antiemetics and Migraine therapy

A

important adjuncts to help treat migraines

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22
Q

Non specific analgesics

A

Abortive therapy
NSAIDS + NSAID combos e.g aspirin
Opioid analgesics

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23
Q

Migraine specific drugs

A

Serotonin receptor agonists (triptans)
Ergots

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24
Q

Prophylaxis meds for migraines

A

Beta blockers-first line drug (propanolol used most often)
AEDs-Divalproex and Topiramate have the stongest efficacy
Tricyclic anti-depressants
Estrogens
CGRP receptor antagonists

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25
Q

Vasoconstrictors and local anesthetics

A

Vasoconstrictors (epinephrine) decrease local blood flow + delays systemic absorption of an anesthetic

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26
Q

What 2 benefits does delaying absorption of local anesthetics have

A

Prolongs anesthesia and reduces risk of toxicity

27
Q

Opioid agonists

A

Activates MU and Kappa receptors
e.g. morphine, codeine, meperidine
Produces analgesia, euphoria, sedation, resp depression, physical dependence, and constipation

28
Q

Opioid antagonist

A

Antagonist at MU and Kappa receptors
e.g. Naloxone
Reversal of respiratory depression and CNS depression caused by overdose of opioid agonist

29
Q

Methyllnatrexone

A

used to treat constipation induced by opioids
Is a opioid antagonist

30
Q

Migraine pain

A

Moderate-severe lasting up to 3 days

31
Q

Migraine character

A

Throbbing, unilateral or biltaeral

32
Q

Migraine prodrome

A

Aura: visual field cut, flashing lights, zig zags

33
Q

Migraine Associated symptoms

A

N/V, photophobia, phonophobia

34
Q

Migraine precipitating factors

A

Anxiety, stress, fatigue, menstruation, ETOH, tyramine containing foods

35
Q

Migraine epidemiology

A

More severe/common in women + famillial hx

36
Q

Migraine aggravating factors

A

Physical activity

37
Q

Agonist-Antagonist

A

When administered alone they produce analgesia, if given to a patient taking a pure agonist, these drugs can antagonize analgesia cause by the pure agonsist

38
Q

Pentazocine, nalbuphine, butorphenol

A

Agonist-antagonist drugs
antagonist at MU + agonist at Kappa

39
Q

Buprenorphine

A

Partial agonist
Partial agonist at MU + partial agonist/ weak antagonist at Kappa

40
Q

Tolerance

A

Results from regular drug use, can be defined as a state in which a particular dose elicits a smaller response that it did with initial use
As tolerance increases, higher and higher doses are needed to elicit desired effects

41
Q

Cross Tolerance

A

Tolerance from one drug confers tolerance to another
generally develops among drugs within the same class

42
Q

Withdrawal syndrome

A

constellation of s/s that occurs in physically dependent individuals when they discontinue drug use

43
Q

Physical Dependence

A

Defined as a state in which an abstinence syndrome will occur if drug is discontinued
Takes place as a result of prolonged drug exposure

44
Q

Psychological dependence

A

An intense subjective need for a particular psychoactive drug

45
Q

Cross-dependence

A

Ability of one drug to support physical dependence on another drug. Generally exists among drugs in the same pharmacologic family

46
Q

How is SUD defined

A

A cluster of cognitive, behavioral, and physiological symptoms with continued use despite significant substance related problems
Dependence is not required but may be present
All dependent people do not have SUD
SUD is not equivalent to addiction

47
Q

Preferred therapies for patients with chronic pain

A

Non pharmacologic therapy and nonopioid therapy should be used to treat chronic pain before starting opioid therapy
Current recommendations suggest initiating therapy with IR medications first
Use of nonopioid adjuvant meds should be continued to maximize pain control

48
Q

Naloxone when given to someone who is physically dependent on opioids

A

Naloxone will precipitate an immediate withdrawal reaction
an excessive dose can transport a patient from a state of poisoning to a state of acute withdrawal

49
Q

Naloxone

A

Opioid antagonist, used to reverse effects of opioid overdose

50
Q

How should naloxone be administered?

A

Series of small doses rather than one large dose

51
Q

Side effects/ adverse effects of opioids including morphine

A

Constipation
Respiratory depression-can occur 90 mins after PO ingestion
urinary retention-encourage pt to void Q4
tolerance and dependence-happens w/ continued use
Sedation
Euphoria
Orthostatic hypotension
Emesis-promotes n/v; pt may need antiemetics

52
Q

Practice considerations when prescribing opioid drugs to patients with non cancer related pain

A

Opioids only after non opioids have failed
1 prescriber 1 pharmacy
discuss benefits/risks
Good documentation

53
Q

3 principles of Treatment of headache

A
  1. abort or prevent headache
  2. patient responses vary
  3. some HA drugs can cause dependence
54
Q

Schedule 1 drugs

A

high potential for abuse, no approved medical use in US, therefore not prescribed e.g. cocaine, heroin

55
Q

Schedule 2 drugs

A

Must be typed of filled in ink or indelible pencil and signed by the prescriber, or electonically
Oral prescriptions only in emergencies, must obtain written within 72 hours
cannot be refilled
cant write multiple prescriptions on the same day for the same patient and the same drug

56
Q

Schedule 3 drugs

A

Oral, written, or electronic prescriptions; if authorized by the prescriber these medications can be refilled up to 5 time; refills must be made within 6 months of the original order
If additional meds are needed beyond the amt. provided for in original prescription a new prescription must be written

57
Q

Schedule 4 drugs

A

Same as schedule 3 drugs

58
Q

Schedule 5 drugs

A

Same rules as schedule 3 and 4
Can be dispensed by a pharmacist if certain criteria are met.
The amt. dispensed is limited
Recipient is at least 18 years old
The pharmacist writes and initials a record indicating the date,name, amt. of drug, and the name and address of the recipient
State and local laws do not prohibit dispensing schedule 5 drugs w/out prescription

59
Q

What is Fentanyl

A

Opioid agonist, 100x more potent than morphine
can be given transdermal, parenteral, transmucosal, intranasal
Schedule 2 drug
Adverse Rx: respiratory depression, sedation, constipation, urinary retention, nausea

60
Q

Drug-drug interaction involving CYP system in patients receiving Fentanyl

A

Fentanyl is metabolized by CYP3A4, therefore fentanyl can be increased by CYP3A4 inhibitors (Ketoconazole and Ritonavir) these patients should be monitored closely for signs of respiratory depression and other signs of toxicity

61
Q

Nicotine replacement therapy (NRT)

A

Nicotine gum
Nicotine lozenge
Nicotine patch
Nicotine inhaler
Nicotine nasal spray

62
Q

Nicotine Free products

A

Sustained release bupropion
Varenicline (Chantix)

63
Q

Varenicline (Chantix)

A

taken to decrease nicotine cravings and suppress symptoms of withdrawal