Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology > Lecture 8 - Opioids > Flashcards

Lecture 8 - Opioids Flashcards

1
Q

Describe the analgesic pain ladder:

Step 1 - Mild

A

non-narcotics
1st choice = ASA
Alternatives = acetaminophen or NSAID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the analgesic pain ladder:

Step 2 - Mild to Moderate

A

non-narcotics + weak narcotics
1st choice = ASA + codeien
Alternatives = codeine or Acetaminophen + codeine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the analgesic pain ladder:

Step 3 - Moderate to Severe

A

moderate strength narcotics
1st choice = codeine or morphine
Alternatives = oxycodone, levorphanol, anileridine, oxymorphone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the analgesic pain ladder:

Step 4 - Severe

A

strong narcotics
1st choice = morphine
Alternatives = methadone, hydromorphone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

List 3 endogenous opioids

A
  • endorphines
  • enkaphalins
  • dynorphins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe endorphins

A
  • from pituitary and hypothalamus
  • polypeptides
  • from poropiomelanocortin and prodynorphin
  • potent analgesics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe enkephalins

A
  • from proenkephalin and prodynorphin
  • pentapeptide ligands
  • involved in modulated pain response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe dynorphins

A
  • from proenkephalin B
  • polypeptides
  • physiological role not yet understood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Are opioids direct neurotransmitters?

A

No - they just make the neuron more likely to fire - but are not directly neurotransmitters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the 3 Mechanisms of action?

A

1 - hyper polarization of nerves by opening K+/Ca2+ channels in 1st (receptor to medulla) and 2nd order neurons (medulla to thalamus)

2 - inhibition of ascending pathways in the CNS

3 - excitation of descending adrenergic and seratonergic pathways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What can opioids be used for?

A
  • pain control
  • sedation and anxiolysis
  • can be used before anesthesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the #1 cause of opioid death?

A

depression of respiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

List the 7 pharmacological effects of opioids

A

1 - inhibition of pain and pain perception
2 - sedation and anxiolysis
-drowsiness and lethargy
-cognitive impairment
-relaxation inhibition of pain
3 - depression of respiration (main cause of death from opioid overdose)
4 - cough suppression (opioids suppress the cough centre in the brain)
5 - reduction of intestinal motility (codeine used to treat diarrhea)
6 - pupillary constriction (KEY SYMPTOM OF OVERDOSE)
7 - nausea and vomiting (first stimulated, then inhibited)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

_____ are used for pain, diarrhea, coughing, panic breathing (COPD)

A

opioids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What 3 things do we dose opioids by ?

A

by the mouth
by the clock
by the ladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Briefly explain the WHO pain ladder (slide 8)

A

0-3: mild pain

  • acetaminophen
  • NSAIDs
  • maybe caffeine

4-6: moderate pain
-codeine (mild opioid)

7-10: severe pain
-morphine (strong opioid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

If you are increasing to a stronger or different pain med, do you discontinue the original medication?

A

no
never
not in a million years

  • *never stop the lower pain control!
  • pain meds work by different mechanisms so you always want to keep the pain controlled and don’t want to take away any form of pain management
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

By the mouth:

-Oral dosing is ___ effective than IV

A

less

*because of first pass metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe 3 points of by the mouth

A

1 - oral dosing has longer term effect requiring less frequent doses
2 - oral dosing avoids the highs and thus is less addictive
3 - oral dosing is safer in terms of overdose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe 3 points of by the clock

A

1 - uses less drug. It takes more drug to bring pain down than it does to maintain a person pain-free (maintain dosing)
2 - avoids the euphoria associated with release of pain, so less addictive potential
3 - avoids the development of chronic pain syndrome (from pain pathway rewirling)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the #1 problem with dosing by the clock?

A

Pt does not want to comply because they do not feel pain and do not want to become addicted

*have to explain to pt that by dosing by the clock, you are actually reducing risk of addiction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe points of by the ladder

A

1 - it assures that the safest and least potent drug required for any specific case is used
2 - avoids addictive potential because opioids (and strong opioids) are not used until required

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

_____ - weakest commonly used opioid and has the least addiction risk

A

codeine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

codeine has ___% of potency of morphine

A

10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Potency of codeine is so ___, it is has it’s own special step on the pain ladder (possibly now shared with tramadol)

A

low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is codeine used for?

A

pain
diarrhea
coughing
inhibit breathing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

_____ = unique weak opioid agonist

A

tramadol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the main downside to tramadol?

A

expensive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Unlike other opioids, tramadol has two complementary mechanisms: describe them

A

1 - like other opioids, activates the micro-opioid receptor

2 - weak inhibitor of norepinephrine and serotonin reuptake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Tramadol has ____ potential for addiction and shows greater pain control

A

less

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Oral dose of morphine has relatively ___ availability

A

poor (approx 20-30%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

onset of oral morphine?

A

15-60 mins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

duration of action of oral morphine?

A

3-6 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

IV morphine is ____ as potent as oral morphine

A

twice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

duration of action for IV morphine?

A

almost immediate to 2 hours (high population variability)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Is oxycodone more potent than morphine?

A

yes up to 2X more potent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Oral bioavailability of oxycodone?

A

80% (remember that morphine has 20-30% oral bioavailability)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Oxycodone has a slightly ____ half-life than morphine

A

greater

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

You give oxycodone at ___ the dose of morphine for the equivalent effect

A

half

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

slow release form of oxycodone = ?

A

OxyContin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Oxycodone + tylenol = ?

A

Percocet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Oral hydromorphone onset = ?

A

15-30 mins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

IV hydromorphone duration of action ?

A

3-4 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Peak effect of hydromorphone = ?

A

30-60 mins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Is hydromorphone stronger than morphine = ?

A

yes - 5X as potent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Where is hydromorphone used?

A

surgical settings for moderate to severe pain (cancer, bone trauma, burns, etc.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Fentanyl is highly ______

A

lipophilic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Fentanyl is very _____

A

potent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Fentanyl comes as what dosage forms?

A

transdermal (patch)
sublingual
intravenous (rarely)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Fentanyl has ___ times the analgesic potency of morphine

A

80

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Fentanyl has ___ times the analgesic potency of hydromorphone

A

10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

latency of sublingual fentanyl?

A

7-12 mins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

duration of sublingual fentanyl?

A

1-2 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is sublingual fentanyl used for?

A

acute but temporary pain (fast onset, short duration) such as debriding wounds and breakthrough pain in palliative care

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

latency of transdermal fentanyl ?

A

12-17 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

duration of transdermal fentanyl ?

A

72-96 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is transdermal pain used for?

A

used in more severe pain (cancer, palliative care)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Sufentanyl is __x more potent than fentanyl

A

10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Naltrexone is an oral opioid ____

A

INHIBITOR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Naltrexone is a ??

A

reverse agonist (kind of considered an antagonist)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

latency of naltrexone ?

A

15-30 mins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

duration of naltrexone ?

A

24-72 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

peak of naltrexone ?

A

6-12 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

How does naltrexone work?

A

reverses the psychotomimetic effects of opiate agonists, reverses hypotension and cardiovascular instability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

naltrexone is not highly effective in treating ??

A

opioid addiction

mainly due to compliance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

naltrexone is effective to some extent in treating ??

A

alcohol addiction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Naloxone (Narcan) is a ?

A

potent opioid antagonist

68
Q

Naloxone (Narcan) has a strucure almost identical to ?

A

oxymorphone

69
Q

Naloxone (Narcan) very quickly blocks ?

A

opioid binding

70
Q

When is Naloxone (Narcan) used?

A

in emergency situations such as respiratory depression in clinical situations or heroin overdose

71
Q

Naloxone (Narcan) has a ____ half life

A

short

72
Q

Naloxone (Narcan) blocks all major effects of _____

A

opioids (including pain control)

73
Q

Describe methadone’s half life

A

very long but variable

  • up to 5 days
  • but effective for only 6-12 hours
74
Q

Is methadone more potent than morphine?

A

yes - at least 10X more potent

75
Q

Although methadone is less addictive, it is a greater risk for ?

A

accidental overdose

76
Q

Can any pharmacist dispense methadone?

A

not everyone - it requires special training and licensure

77
Q

What is methadone primarily used for?

A

narcotic maintenance

-so like weening addicts off of narcotics/opioids

78
Q

Dosing schedule is based on ??

A

time, not pain!

by the clock!

79
Q

What is the rule for switching opioids?

A

30% rule

if you switch to a new opioid - you calculate the dose that would be equivalent and then use 30% less

80
Q

Why do you use the 30% rule?

A

because for some unknown reason when you start a new drug, it can be more effective than when you have continued use of a drug

*this is done to prevent overdose

81
Q

Why would you ever rotate opioids?

A

to improve analgesia

82
Q

When would you discontinue therapy?

A
  • when there is intolerable or unacceptable side-effects (myoclonus-neurotoxic effect, respiratory depression, level of conscience) with little or no evidence of analgesia
  • high doses of opioids without analgesia
  • there is evidence of addiction
  • there is no evidence of any effort to increase function in the face of reasonable analgesia
83
Q

Define tolerance

A

reduced potency of analgesic effects of opioids following repeated administration

84
Q

What is the negative consequence with tolerance?

A

increased doses are necessary to produce pain relief - this increases risk of dependence and addiction

85
Q

Define physical dependence

A

normal response to chronic opioid administration

86
Q

List signs of dependence that would be evident with opioid withdrawl

A 
yawning
sweating
tremor
fever
increased HR
insomnia
muscle/abdominal cramps
dilated pupils
87
Q

How do you avoid dependence?

A

decrease dose by 20-30% per day

88
Q

_____ = psychological dependece

A

addiction

89
Q

Define addiction

A

a pattern of drug use characterized by a … craving for opioids … manifest .. [by] compulsive drug-seeking behaviour leading to .. overwhelming involvement in use and procurement of the drugs

90
Q

List 3 ways to deal with tolerance

A
  • prevent dose escalation
  • use a medication holiday following slow withdrawal
  • plan for this at the beginning of treatment
91
Q

List some other effects of opioids on the body

A
  • causes vomiting by stimulating the chemoreceptor trigger zone in the brainstem - then depresses vomiting
  • pinpoint pupils - no tolerance
  • vasodilation - flushing of skin and decrease in blood pressure
  • methadone causes sweating
  • constipation
  • decreases sex hormones in males and females - decreases libido and fertility
92
Q

Pain works by 3 different pathways: describe them

A

1 - descending inhibitory pathways (NE, seretonin, enkephalins)

  • TCAs
  • SSRIs
  • SNRIs
  • alpha adrenergic agents
  • opioids
  • tramadol

2 - peripheral sensitization (Na+)

3 - central sensitization
(Ca2+, NMDA)

93
Q

What works on pain in the descending inhibitory pathways?

A

NE and S are pain mediators - inhibit pain signals from reaching the higher levels of brain

-part of the modulatory system in the spinal cord and brain

94
Q

Drug classes that work on the descending inhibitory pathways for pain?

A

1 - antidepressants

  • TCAs
  • SSRIs
  • SNRIs

2 - alpha 2 adrenergic agonists

3-opioids (esp tramadol)

95
Q

How do TCAs work on descending inhibitory pathways?

A
  • increases serotonin and/or NE in the synapse by inhibiting reuptake
  • takes 1-3 weeks for pain control so used for chronic pain
  • may have anticholinergic effects (dry mouth, dry eyes, etc.)
  • more effective for conditions like diabetic neuropathy than other anti-depressants
96
Q

Examples of TCAs

A

nortriptyline

amitryptyline

97
Q

What is the 1st line treatment for neuropathic pain?

A

nortriptyline

98
Q

How do SSRIs work on descending inhibitory pathways?

A

-specific inhibitor of Serotonin reuptake

99
Q

Side effects of SSRIs

A
  • suicide
  • impaired platelet aggregation
  • CNS depression
  • QT prolongation
  • serotonin syndrome
  • SIADH/hyponatremia
  • sexual dysfunction
100
Q

examples of SSRIs

A

paroxetine (paxil)
fluoxetine (prozac)
sertraline (zoloft)

101
Q

How do SNRIs work on descending inhibitory pathways?

A
  • serotonin and norepinephrine reuptake inhibitors

- also weakly inhibits dopamine reuptake

102
Q

side effects of SNRIs??

A
  • suicide
  • impaired platelet aggregation
  • CNS depression
  • hypercholesterolemia
  • hypertension
  • serotonin syndrome
  • sexual dysfunction
  • SIADH/ hyponatremia
  • QT prolongation
103
Q

example of SNRI

A

venlafaxine

104
Q

What is venlafaxine used for?

A

neuropathic pain

DM neuropathy

105
Q

onset of venlafaxine ?

A

1-2 weeks

max 6

106
Q

common adverse effects of venlafaxine?

A

nausea
dizziness
drowsiness

107
Q

How do alpha 2 adrenergic agonists work on descending inhibitory pathways?

A
  • stimulate alpha-adrenoreceptors in brainstem - activating inhibitory neuron thus reducing sympathetic outflow of CNS
  • prevents pain signal transmission
108
Q

examples of alpha adrenergic agonists?

A
  • clonidine (Catapres)

- tizanidine (Zanaflex)

109
Q

What is clonidine used for?

A

neuropathic pain that is not responding to other treatment

110
Q

Unlabeled uses of clonidine?

A
  • heroin or nicotine withdrawal
  • dysmenorrhea
  • menopausal vasomotor symptoms
  • migraine prophylaxis
111
Q

routes available for clonidine?

A

epidural infusion
oral
transdermal

112
Q

side effects of clonidine

A

bradycardia

CNS and respiratory depression

hypotension

113
Q

Tizanidine is used to treat?

A
  • tension type headache
  • back pain
  • neuropathic pain
  • myosfascial pains
114
Q

Is tizaidine better than clonidine?

A

Yes

  • less side effects
  • less likely to cause hypotension
  • better tolerated than clonidine
115
Q

Peripheral sensitization - caused by?

A

sodium channels on nerves

-neuropathic pain triggered by spontaneous peripheral nerve activity mediated by sodium channels

116
Q

Causes of pain through peripheral sensitization ?

A

-local tissue injury
-ischemia
etc

releasing inflammatory factors thereby increasing Na channels leading to excitability of the nerve

117
Q

Medication classes which dampen the peripheral sensitization include?

A
  • carbamazepine
  • TCAs
  • Topiramate
  • Lidocaine
118
Q

How does carbamazepine (Tegretol) work on peripheral sensitization?

A
  • anticonvulsant
  • limits influx of Na+ ions across the cell membrane
  • trigeminal or glossopharyngeal neuralgia and neuropathic pain
119
Q

How does Topiramate (Topamax) work on peripheral sensitization?

A
  • anticonvulsant

- limits influx of sodium ions across the cell membrane, antagonizes glutamate receptors

120
Q

Adverse effects of Topiramate?

A
  • dizziness
  • ataxia
  • somnolence (strong desire for sleep)
  • psychomotor slowing
  • parasthesia
  • weight loss
121
Q

What do you need to monitor for topiramate?

A

electrolytes

kidney function

122
Q

How does lidocaine work on peripheral sensitization?

A

-topical application reduces discharge of small afferent nerve fibres by blocking voltage gated Na channels (decreases membrane permeability)

123
Q

Lidocaine comes as?

A

gel

transdermal patch

124
Q

What is lidocaine used for?

A

post-herpetic neuralgia or

peripheral neuropathic or other aetiologies

125
Q

Side effects of lidocaine?

A

arrythmias
seizures
coma
respiratory depression or death

with patch:

  • application site erythema
  • swelling
  • burning
  • discomfort
126
Q

Describe central sensitization-1?

A

calcium channels

  • occurs in the dorsal horn of the spinal cord
  • release of excitatory neurotransmitters (incl. glutamate and substance P)
  • increased calcium transport causes spontaneous impulses (APs) - pain message sent to brain
127
Q

What types of medication decrease Ca channel activity?

A

GBP - gabapentin

PreGab - pregabalin

128
Q

Describe central sensitization-2?

A

NMDA receptor

  • occurs in the dorsal horn of the spinal cord
  • release of excitatory neurotransmitters (including glutamate and substance P)
129
Q

What medications work on central sensitization 2 ?

A

medications that are NMDA antagonists (decrease nerve impulse)

  • ketamine
  • dextromethorphan
  • methadone
130
Q

How does Ketamine (Kelatar) work on central sensitization?

A

NMDA receptor antagonist

  • decreases central sensitization and modulation by lowering the threshold for nerve transduction and reduces the effects of substance P
  • also targets the opioid receptor, Na and K channels to reduce pain (dissociative agent)
131
Q

common adverse rxn of ketamine ?

A

local skin rxns

132
Q

Describe how dextromethorphan (Robitussin) works on central sensitization ?

A

low affinity uncompetitive NMDA antagonist - high doses needed (45-400 mg/day)

  • also binds opioid receptors
  • short half life (2-4 hours)
133
Q

side effects of dextromethorphan (Robitussin)

A

serotonin syndrome (if in combination with other antidepressants)

  • rash
  • nausea/vomiting
  • drowsiness/sedation
  • constipation/diarrhea
  • confusion
  • nervousness
  • closed eye hallucinations
134
Q

Describe how methadone works on central sensitization

A
  • mu and delta opioid agonist
  • also blocks NMDA receptor
  • inhibits reuptake of NE
  • crossing BBB rapidly
  • lipophilic so distributes in muscle and fat
  • high bioavailability
135
Q

side effects of methadone?

A
  • CNS & respiratory depression
  • QT prolongation
  • constipation
  • nausea and vomiting
  • dizziness and disorientation
136
Q

What is gout?

A

caused by accumulation of uric acid crystals in joints

137
Q

What is gout associated with?

A

ingesting red meat, cheese, wine (large intakes of purines)

138
Q

gout a.k.a. ?

A

rich man’s disease

139
Q

Uric acid production pathway

A

purine nucleotides (dietary and cellular)

inosinic acid

hypoxanthine
(xanthine oxidase)
xanthine
(xanthine oxidase)
uric acid
140
Q

Drug therapy of gout?

A
  • cholchicine
  • allopurinol
  • probenecid
  • NSAIDs (indomethacin)
141
Q

Describe colchicine

A
  • weak anti-inflammatory agent
  • not analgesic or antipyretic
  • impairs PMN motility and chemotaxis and thus inflammatory response to urate crystals
  • dose to toxicity - nausea, vomiting, diarrhea, abdominal cramping, may cause death
  • no effect on plasma or urinary uric acid
  • may be considered for low dose continuous prophylactic therapy
  • decreases motility of immune cells
  • doesn’t affect underlying disease
  • just reduces inflammation
142
Q

Describe allopurinol

A
  • xanthine oxidase inhibitor
  • reduces urate formation
  • active metabolite (oxypurinol/alloxanthine)
  • risk of hypoxanthine stones
143
Q

What is allopurinol used for?

A

-for prophylaxis when acute gouty attacks happen frequently

144
Q

Caution with alloupurinol?

A

fluid intake

acute attack of gout

145
Q

adverse events with allopurinol

A 
allergic rxns
bone marrow
suppression
liver toxicity
renal toxicity
146
Q

Describe NSAIDs (indomethacin)

A
  • most common type of drug given for all kinds of arthritis
  • drug of choice for gouty arthritis
  • less toxic than colchicine with short term use
  • not uricosuric
  • affords symptomatic relief
  • GI side effects with indomethacin
147
Q

How do NSAIDs (indomethacin) work?

A

decreases inflammation

helps with uric acid formation a little bit

148
Q

How does Probenecid work?

A
  • uricosuric: inhibits reabsorption of uric acid (decreases amount of uric acid in the blood)
  • half-life dose dependent
  • highly protein bound
  • inhibits excretion of other acidic drugs
  • caution: renal urate stones (fluid intake)
149
Q

Define: local anesthetic

A
  • an agent that interrupts pain impulses in a specific region of the body without a loss of patient consciousness
  • normally, the process is completely reversible - the agent doe snot produce any residual effect on the nerve fibre
150
Q

end in “caine” = ?

A

sodium channel blocker

  • decrease nerve sensitization
  • decrease pain
151
Q

Where are local anesthetics used?

A

to render a specific portion of the body insensitive to pain

152
Q

How do local anesthetics work?

A

interfere with nerve impulse transmission to specific areas of the body

153
Q

Do you lose consciousness with local anesthetics?

A

noooooope

154
Q

Describe topical anesthetics

A
  • applied directly to skin or mucous membranes

- creams, solutions, ointments, gels, ophthalmic drops, lozenges, suppositories

155
Q

Describe parenteral anesthetics

A

injected into the CNS by various spinal injection techniques

156
Q

Describe surface anesthesia

A
  • this type of anesthesia is accomplished by the application of a local anesthetic to skin or mucous membranes
  • surface anesthesia is used to relieve itching, burning, and surface pain (ex minor sunburns)
157
Q

Describe nerve block anesthesia

A
  • local anesthetic is injected around a nerve that leads to the operative site
  • usually more concentrated forms of local anesthetic solutions are used for this type of anesthesia
158
Q

Describe peridural anesthesia

A

this type of anesthesia is accomplished by injecting a local anesthetic into the peridural space (one of the coverings of the spinal cord)

159
Q

Describe spinal anesthesia

A

the local anesthetic is injected into the subarachnoid space of the spinal cord

160
Q

List the 5 types of local anesthesia

A
  • epidural
  • infiltration
  • nerve block
  • spinal
  • topical
161
Q

Describe the drug effects of local anesthesia

A
  • first, autonomic activity is lost
  • then pain and other sensory functions are lost
  • motor activity is the last to be lost
  • as local agents wear off, they do so in reverse order (motor, sensory, then autonomic activity are restored)
162
Q

Indications of local anesthetics ?

A
  • surfical, dental, and diagnostic procedures
  • treatment of certain types of pain:
  • infiltration anesthesia
  • nerve bock anesthesia
163
Q

Indication for infiltration anesthesia

A
  • minor surgical and dental procedures
    • injection of the anesthetic solution intradermally, subcutaneously, or submucosally across the path of nerves supplying the target area
    • may be given in a circular pattern around the operative area
164
Q

Indication for nerve block anesthesia

A
  • surgical, dental and diagnostic procedures
    • also used for therapeutic management of pain
    • the anesthetic agent is injected directly into or around the nerve trunks or nerve ganglia that supply the area to be numbed
165
Q

adverse side effects of local anesthetics ?

A

-usually limited

adverse effects result if:

  • inadvertent intravascular injection occurs
  • excessive dose or rate of injection is given
  • slow metabolic breakdown
  • injection into a highly vascular tissue

Pharmacology (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions