Pain and substance exam 2 Flashcards
(133 cards)
1
Q
What is alcohol poisoning
A
large amounts drank fast
not w/ sustained drinking of moderate amounts of alcohol
2
Q
What does alcohol affect in the brain
A
endogenous opiates and NT
-GABA, glutamine, dopamine
3
Q
Alcohol impact on cardiac, GI, cancer, immune system, and neurologic
A
cardiac: HTN, CAD, stroke, cardiomyopathy*, arrhythmia
GI: liver disease, pancreatitis
cancer: breast, oral/eso, liver, colon
immune system: increased risk of infection
neurologic: dementia, learning issues, depression, anxiety
4
Q
CAGE questionnaire
A
C: felt need to cut down
A: people annoyed you by criticizing your drinking
G: felt guilty about your drinking
E: drank first thing in morning (eye opener)
positive response to at least 2 questions suggests abuse
5
Q
What is AUDIT
A
10 question screening for alcohol dependence, use problems, and amount of alcohol consumption in adults
6
Q
Initial signs and symptoms of alcohol withdrawal
A
intoxicated, slurred speech and ataxia, sedated or unconscious, nystagmus
7
Q
As blood alcohol levels decrease what symptoms are present
A
tachycardia, diaphoresis, HTN, N/V, tremors, hallucinations
SEIZURES and delirium tremens (24-48 hr)
8
Q
Stage 1 alcohol withdrawal timeline
A
8 hours
anxiety, insomnia, nausea, ab pain
9
Q
Stage 2 alcohol withdrawal timeline
A
1-3 days
high BP, increased body temp
10
Q
Stage 3 alcohol withdrawal timeline
A
1 wk
hallucinations, fever, seizures, agitation
11
Q
_______ should be used for up to 1 wk following alcohol cessation
A
CIWA-Ar
12
Q
Lab tests for alcohol
A
BAC (100 mg/dl = 0.1%)
CBC (assess anemia)
CMP
tox screen
13
Q
What is the clinical institute withdrawal assessment for alcohol (CIWA-Ar)
A
indicated severity of w/drawal sx from 0-67
high score = worse withdrawal sx
<10 sggests mild withdrawal and do not need therapy
14
Q
Goals of alcohol withdrawal treatment
A
prevent or treat acute sx and med or psychiatric conditions
long term abstinence after detox
enter med or alcohol dependent tx program
15
Q
Non pharm for alcohol withdrawal
A
during acute w/drawal non pharm is not recommended
can be life-threatening
16
Q
What drug is considered the standard of care for acute alcohol withdrawal
A
BZD (long acting preferred)
17
Q
What BZD with active metabolites that are >100 hours and needs self tapering
A
Chlordiazepoxide (librium)
18
Q
What BZDs are used for alcohol withdrawal
A
Chlordiazepoxide, Diazepam, Lorazepam, Oxazepam
19
Q
You avoid the use of what two BZD in patients with ESRD or AKI
A
Diazepam, Lorazepam
20
Q
Lipophilicity of BZD for alcohol withdrawal
A
Chlordiazepoxide, Lorazepam, Oxazepam: less
Diazepam: highly
21
Q
What are the BZD regimen options
A
front loading therapy
symptom triggered therapy
fixed dose therapy
22
Q
What is the BZD front loading therapy
A
high dose BZD repeated q1-2hr until pt sedated
risks: excessive sedation, respiratory depression, delirium
may be considered w/ h/o severe alcohol withdrawal (seizures, DTs)
can be combined with sx/triggered therapy
23
Q
What is the BZD symptom triggered therapy
A
only admin when CIWA-Ar is 8 or more
standard of care of treating alcohol w/drawal in the inpt setting (minimizes risk over sedation)
increase frequency from q2h to q1-2h when score >10
24
Q
What is the BZD fixed dose therapy
A
fixed dose and then tapered
may need breakthrough med
risk includes excessive sedation or respiratory depression
25
Supportive care for alcohol withdrawal: fluids
for N/V/D, increased temp or agitation
IV NS, LR, or D5W
26
Supportive care for alcohol withdrawal: electrolyte imbalance
from poor nutrition from alcohol abuse
K, Mg*, PO4 need replacement
27
Supportive care for alcohol withdrawal: glucose abnormalities
may occur due to interference with hepatic gluconeogenesis (leads to hypoglycemia)
monitor blood glucose in inpt and admin rescue meds
28
Other medications for supportive care
Thiamine (Vit B1): ppx (wernicke encephalopathy)
Folate: multivitamin recommended
Banana Bag: IV fluids with multivitamin and/or folic acid and/or thiamine and/or magnesium
29
Other medication therapy for alcohol withdrawal
Alpha 2 agonists: clonidine, dexmedetomidine
Beta-Blockers: atenolol, propranolol
Antipsychotics: haloperidol, atypicals
Barbiturates: phenobarbital*, carbamazepine, VPA, gabapentin
30
Severe alcohol withdrawal treatment
no need for antiepiletic med unless progress to status epilepticus
increase BZD dose
other: phenobarbital*, propofol, dexmedetomidine
pt transferred to ICU and require intubation
31
What is delirum tremens
severe form of alcohol withdrawal involving sudden and severe mental or nervous system changes
32
AUD treatment (maintenance phase)
psychosocial interventions (motivational enhancement therpay)
family therapy
CBT
12-step program
rehabilitation program
33
Combination of psychosocial intervention and pharmacologic therapies are beneficial to what
reduce frequency and risk of binge drinking
34
Disulfiram (antabuse) for AUD
used as a deterrent
reactions occur if taken w/in 12-24 hr of consuming alcohol
abstinence is critical when using this therapy
duration of therapy is indefinite
35
Monitoring and ADE of disulfiram (antabuse)
-cause acetaldehyde accumulation, leading to throbbing headache, N/V, chest pain, confusion, hypotension
facial flushing, liver enzymes
used cautiously in liver disease
36
Naltrexone (vivitrol) for AUD
used to reduce cravings
will not cause alcohol withdrawal, can cause opioid withdrawal
duration of therapy indefinite
37
When can you not use Naltrexone (vivitrol) for AUD
in acute hepatitis or severe hepatic failure
not be used if pt is on opioids
38
Acamprostate for AUD
used to reduce cravings (modulates glutamate)
therapy should be started when pt is abstinence after alcohol withdrawal
duration of therapy indefinite
monitoring: GI (diarrhea), renal, pt reporting craving
39
When to dose reduce Acamprostate for AUD
no hepatic metabolism
reduce to 333 mg TID for 30-50 mL/min
CI with ≤30 mL/min
40
Other therapies in AUD maintenance treatment
anticonvulsants
antidepressants
41
Recommendations for naltrexone or acamprosate for moderate-severe AUD if:
pt has goal of reducing alcohol consumption or acheiving abstienence
prefers pharm therapy or have not responded to non pharm therapy
pt has no CI to therapies
42
Recommendations for moderate-severe AUD if:
pt has goal of achieving abstinence (not just reducing consumption)**
perferes disulfiram or not respond to naltrexone or acamprosate
pt understands risk of alcohol consumption while taking
no CI to disulfiram
43
Recommendations for topiramate or gabapentin in moderate-severe AUD if:
pt has a goal of reducing alcohol consumption or achieving abstinence
prefers therapies or are intolerant to or have not responded to naltrexone and acamprosate
pt has no CI to therapies
44
Recommendations against AUD treatment
antidepressant unless there is a disorder an antidepressant is indicated for
use of acamprosate in renal impairment
use of acamprosate for 1st line therapy in mild-mod renal impairment
use of naltrexone in acute hepatitis or hepatic failure
use of naltrexone with concomitant opioids
45
Proof
a measure of a beverage's alcohol content
twice the percentage of alcohol by wt
90 proof = 45% alcohol
45
Temperance societies
promoted abstinence from distilled products then later promoted total abstinence
46
What causes faster or slower absorption of alcohol
slower: food or water in stomach
faster: presence of carbonated beverages
most absorbed in small intestine
47
Where is alcohol metabolized
liver
48
When alcohol is present, metabolism of other drugs is what
slower
49
Behavioral effects of alcohol
euphoria, reduce anxiety, reduce inhibitions
sexual behavior, blackouts, crime and violence
50
Physiological effects of alcohol
dilation of blood vessels
diuretic effect
hormonal effects
51
Fetal alcohol syndrome
facial and developmental abnormalities associated with mother's alcohol use during pregnancy
52
Diagnostic criteria for fetal alcohol syndrome
growth reduction before/and or after birth
pattern of abnormal features of face and head
evidence of CNS abnormality
53
Disease model (AUD)
alcohol dependence is the primary disease and not the result of another underlying cause
54
Contraindications of oxazepam
myasthenia gravis, COPD, hepatic disease
55
Chlordiazepoxide contraindications
myasthenia gravis, ataxia, hypoventilation, glaucoma, hepatic disease, severe sleep apnea
56
Disulfiram MOA
inhibits alcohol dehydrogenase, leads to many of the side effects associated with a hangover
second line tx for AUD
57
Disulfiram considerations
abstain from alcohol for at least 12 hours before admin
58
Disulfiram ADE
headache, metallic or garlic taste in mouth, liver toxic, neurotoxic
59
Disulfiram DDI
APAP, theophylline, caffeine
60
Acaprosate MOA
normalizes basal GABA concentrations
blocks glutamate increase during alcohol withdrawal
NMDA receptor antagonist
61
Acamprosate CI
kidney impairment
62
Acamprosate ADE
allergic rxn, abnormal heart rhythms, BP change, insomnia, impotence
63
Adverse health effects of smoking
lung cancer, CV disease, COPD (emphysema)
increased risk: young, many cigs, long time
64
Smoking during pregnancy increases the risk of what
miscarriage
low birth weight
sudden infant death syndrome (SIDS)
65
What is the lethal dose of a cig
60 mg
66
Nicotine MOA
mimics acetylcholine
first stimulates and then blocks ACh receptor sites
cause the release of adrenaline
67
Low level nicotine poisoning sx
nausea, dizziness, general weakness
68
CNS and circulatory effects of nicotine
increase HR, BP, oxygen needed to heart, platelet aggregation, electrical activity of cortex
decreased oxygen carrying ability of blood
69
What is the primary reinforcing substance in tabacco
nicotine
70
Bupropion MOA
NDRI and nicotine acetylcholine receptor antagonist
71
Bupropion DDI
CYP2B6 inhibitors and inducers
CUP2D6 inducers
72
Vareniciine MOA
partial nicotinic acetylcholine agonist (a4b2)
73
Varenicline ADE
night terrors, thoughts of suicide, exacerbation of underlying psychiatric conditions
74
Pathophysiology of nicotine
ACh receptor agonist
CNS and PNS stimulation and depression
75
Cig smoking or low doses of nicotine causes what
increased alertness and cognitive functioning
leads to pleasure and relaxation
76
Complaints of nicotine withdrawal
cravings, difficulty concentrating, frustration, irritability, impatience, hostility, insomnia, restlessness
77
What is hedonic dysregulation
malaise or inability to experience pleasure
78
What are the 5 A's of tobacco cessation
Ask, Assess, Advice, Assist, Arrange
79
What NRTs are not OTCs
inhaler and nasal spray
80
How long are NRT products approved for
8-12 weeks
81
NRT: patch
>10 cigs: 21 mg/day
<10 cigs: 14 mg/day
Duration 10 wks
first day of patch = quit day
highest adherence for NRT
82
NRT: Gum
1st cig ≤30 min: 4 mg
1st cig >30 min: 2 mg
max 24 pieces a day
ADE: pyrosis, nausea, hiccups
gum is chewed and parked
83
NRT: lozenge
1st cig ≤30 min: 4 mg
1st cig >30 min: 2 mg
max 20 pieces a day
ADE: nausea
84
NRT: inhaler
continuously puffing for 20 min prn
pt must stop smoking before use
3 months duration with 6-12 wk taper
do not eat 15 min before and after use
85
NRT nasal spray:
1 spray 1-2 times/hr
max 10 sprays/hr (80 sprays/day)
highest peak nicotine
3 month duration
86
Harms associated with e-cigs
EVALI (lung injury)
related to Vit E acetate
pt should not go back to cig after use
87
For bupropion smoking cessation should occur in the _____ week of therapy
2nd
start bupropion prior to smoking cessation
duration 6 months to 1 yr
stop after 12 wks if pt stops smoking
88
Bupropion BBW
suicidal thoughts, depression, psychosis
89
If pt is on bupropion and there is no progress at wk 7 what should you do
can disc med and use an alternate therapy or consider combo
90
Varenicline has a higher efficacy monotherapy for everything except for what
patch
91
Varenicline MOA
partial nicotinic acetylcholine receptor agonist
92
Varenicline duration of therapy
pt quit smoking 1 wk after starting med
up to 12 wks until quit date
93
Varenicline ADE
insomnia (vivid dreams, nightmares)
94
Varenicline warnings and precautions
suicidal thoughts, depression, psychosis
increased seizure risk
95
Cannabinoids MOA
partial agonist at CB1, agonist at CB2
can act as antagonist for both
96
Cannabinoids interactions
reduce THC clearance
97
Cannabinoids side effects
high doses reduce sedating effects of THC
-tiredness, diarrhea, change in appetite
98
delta 9 THC
partial agonist at CB1
primary psychoactive agent in cannabis
99
Cannabis preparations
hashish (most potent)
sinsemilla (2nd most potent)
100
Anandamide MOA
mediated by CB1 receptors in CNS and CB2 receptors in the periphery
101
Where are CB1 receptors found
found mainly in brain
high density: basal ganglia, hippocampus, cerebral cortex, nucleus accumbens
102
Where are CB2 receptors found
outside the brain in immune cells
potential role of cannabinoids in modulation of immune system
103
Physiological effects of marijuana
Increase HR
reddening of eyes
dryness of mouth and throat
pulmonary: breathing, impairment of pulmonary function
104
Behavioral effects of marijuana
self admin
subjective effects: euphoria, mellowness, hunger
food intake
verbal behavior: talking decreases along, non verbal interaction increase
105
Acute cognitive effects of marijuana infrequent users
slower thinking, impaired short-term memory, inhibitory control, loss of sustained concentration, visuospatial processing
106
Acute cognitive effects of marijuana frequent users
slowed cognitive procession, may be tolerant to effects
107
What is dronabinol used for
schedule III
antiemetic
may help with withdrawal symptoms
108
dronabinol MOA
CB1 and CB2 activation
109
What are the 4 subgroups that cannabinoid psychological effects are classified in
affective: euphoria, easy laugh
sensory: increased perception of one's own body
somatic: feeling body floating or sinking in bed
cognitive: disorientation of time, memory lapses, difficulty concentrating
110
dronabinol DDI
sleeping pills, narcotics, muscle relaxers, anxiolytics, anti-depressants, seizure meds
111
dronabinol CI
psychosis, allergic to sesame oil, BP
112
Epidolex
treatment of seizure disorders
113
Nabilone MOA
decrease signals to brain that trigger nausea and vomiting
114
Treatment for CUD
no current pharmacotherapies approved by FDA
115
behavioral and psychosocial treatment for CUD
CBT, MET, CM
116
Cannabis intoxication diagnostic criteria
at least 2 within 2 hours of use
-conjunctival inj, increased appetite, dry mouth, tachycardia
117
Cannabid w/drawal criteria
3 of the following within 1 wk after cessation
-irritability, anxiety, sleep difficulty, wt loss, restlessness, depressed mood
at least 1 with discomfort: ab pain, tremors, sweating, fever, chills, headahce
118
CBT and MET for CUD
decrease number of days of use
reduce number of joints used
improve severity of CUS
increase abstinence rates (only CBT)
effects are synergistic
119
What drugs improve withdrawal symptoms of CUD
dronabinol and nabilone
120
What drug helps decrease cannabis use and improvement of withdrawal symptoms
gabapentin
121
dronabinol FDA indications
anorexia in pt with AIDS
chemotherapy induced nausea and vomiting
122
dronabinol clinical effect for CUD
reduce withdrawal sx, reduce craving, improve sleep, low abuse potential
123
What is the schedule class for marinol and syndros
marinol: CIII
syndros: CII
124
Dosing of donabinol
target 30-120 mg/day
125
Dronabinol warnings and precautions
CV: BP change, syncope, tachycardia
CNS: depression, mania, schizophrenia
GI: n/v, ab pain
Seizures
126
What is the disulfiram rxn of dronabinol
oral solution only
metronidazole or disulfiram
disc 14 or more days before initation
cannot admin these meds until 7 days after disc dronabinol
127
When should dronabinol be taken
30 min prior to a meal or on an empty stomach
128
What is cannabinoid hyperemesis syndrome (CHS)
cyclical vomiting in habitual marijuana users
typically used cannabis for years, daily users
129
Clinical Presentation of CHS
taking long hot baths or showers to manage sx
severe n/v
vomiting recurs in a cyclic pattern over months
resolution of sx after stopping cannabis use
130
Pathophysiology of CHS
may be related to n/v pathway
cannabinoids act on GI system and may alter hormones
131
Treatment of CHS
cessation of cannabis use (1-4 days)
hot showers
supportive care: IV fluids, correction of electrolyte deficiencies, antiemetics (IV ondansetron)
132
Second line emerging therapy for CHS
haloperidol (D2 receptors act on n/v pathway, may be involved with CB1 signaling pathway)
topical capsaicin: interact with TRVP1/2
