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p3 year :) > epilepsy, AUD, sub abuse > Flashcards

epilepsy, AUD, sub abuse Flashcards

1
Q

what are the four main AED MOAs?

A

1) prolong Na channel INactivation
2) inhibit Ca channels
3) increase GABA Cl efflux
4) glutamate antagonist

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2
Q

which AEDs prolong Na channel inactiavtion?

A
  • valproate
  • carbamazepine
  • phenytoin
  • lamotrigine
  • topiramate
  • zonisamide
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3
Q

which AEDs inihbit Ca influx?

A
  • valproate
  • ethosuximide
  • trimethadione
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4
Q

which AEDs increase GABA Cl efflux?

A
  • valproate
  • barbituates (phenobarbital)
  • benzodiazepines
  • gabapentin
  • vigabatrin – has GABA in it
  • tiagabine – kind of has GABA in it
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5
Q

which AEDs are glutamate antagonists?

A
  • levetiracetam
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6
Q

phenytoin MoA

A
  • block Na and Ca influx –> prevent AP –> dec seizure activity
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7
Q

phenytoin common uses

A

not common, if used will be in severely diabled pt in an institution

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8
Q

phenytoin dose

A

200-400 mg/day

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9
Q

phenytoin dose-related AE

A
  • GI upset
  • sedation
  • HA
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10
Q

phenytoin non-dose related AE

A

-**hyperplasia of gingival (gum overgrowth)
- hirsutism
- fetal malformations

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11
Q

phenytoin metabolism

A
  • induces liver enzymes (dec concentration of other drugs)
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12
Q

carbamazepine MoA

A

prevent Na influx –> dec AP –> dec seizure activity

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13
Q

carbamazepine metabolism

A
  • MOST POTENT INDUCER OF HEPATIC METABOLISM OF ANY DRUG –> dec concentration of other drugs
    -    auto-induction (induces its own metabolism) –> therefore, will titrate up to a therpeutic concentraton (check concentration, this is the goal now for the pt), then drug concentration will dec, need to increase the dose 2-3 times –> finally reach stable dose
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14
Q

carbamazepine dose

A

200-800 mg/day
BID as SR product

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15
Q

carbamazepine AE

A
  • *hyponatraemia (low Na), water intoxication
  • congenital malformations for fetus
  • GI
  • drowsy
  • HA
  • rash (hypersensitivity)
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16
Q

carbamazepine in pregnancy

A

can cause two different conditions:
1) fetal aplastic anemia (RBC)
2) mild leukopenia (WBC)

therefore…
do baseline CBC –> check CBC in 6 weeks –> will see a dec in WBC which is normal and will rebound, if a dec in other cells types (like RBC) STOP immediately –> aplastic anemia –> check CBC in 1 month –> WBC should be back to normal, if not STOP immediately

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17
Q

sodium valproate vs valproic acid

A

valproic acid: poor solubility –> GI problems

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18
Q

valproate MoA

A

1) increase GABA (Cl efflux)
2) prevent Na influx
3) prevent Ca influx

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19
Q

valproate metabolism

A

inhibitor –> increases concentration of carbamazepine, phenytoin, topiramate, phenobarbital

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20
Q

valproate AE

A
  • increase appetite
  • weight gain
  • hepatotoxicity
  • **neural tube defects (spina bifida)
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21
Q

valproate in pregnancy

A

CONTRAINDICATED
- bc of spina bifida NTD
- need to change med before pregnancy !!!!!

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22
Q

first generation AED

A

less tolerable, less effective:
- valproate
- carbamazepine
- phenytoin

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23
Q

second generation AED

A

more tolerable, more effective, generally lack DDI, expensive, limited clinical experience:
- lamotrigine
- oxcarbazepine
- topiramate
- zonisamide
- levetiracetam
- vigabatrin
- gabapentin
- tiagabine

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24
Q

vigabatrin MoA

A

inhibits GABA metabolism –> inc GABA –> dec AP –> dec seizure activity

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25
Q

vigabatrin place in therpay

A

NOT 1st line bc of side effects

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26
Q

vigabatrin AE

A
  • visual field defects
  • psychosis, depression –> happens overtime/slow decline
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27
Q

vigabatrin CI

A

any history of phycosis –> hard to Dx what is from drug

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28
Q

gabapentin MoA

A

(structural analog of GABA) –> inc GABA

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29
Q

gabapentin CI

A

predisposition to substance abuse

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30
Q

gabapentin metabolism

A

NOT an inducer/inhibitor

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31
Q

gabapentin AE

A
  • somnolence (sleepy)
  • dizzy
  • fatigue
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32
Q

gabapentin place in therapy

A

ONLY AN ADJUNCT TO THERAPY, not monotherapy!!

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33
Q

lamotrigine MoA

A

prolong Na channel inactivation (prevent Na influx) –> dec AP –> dec seizure activity

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34
Q

lamotrigine AE

A

-**SJS RASH
- dizzy/vertigo
- somnolence (sleepy) –> can reduce with slow titration
- influenza-like

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35
Q

lamotrigine metabolism

A

NOT an inducer/inhibitor

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36
Q

lamotrigine SJS

A

usually develops short term after treatment
- always ask pt if they have a rash

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37
Q

lamotrigine initiation

A

NEED to titrate long and slow or will not be tolerated!!!

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38
Q

lamotrigine CI

A

too high risk seizure where a long slow titration cannot occur

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39
Q

topiramate MoA

A

prevent Na influx –> dec AP –> dec seizure activity

also inc GABA

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40
Q

other use of topiramate

A

migraine prophylaxis

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41
Q

topiramate initiation

A

slowly titrated over 3 weeks (not as slow as lamotrigine) –> if dose too high, will cause intoxication

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42
Q

topiramate AE

A
  • **tip of the tongue syndrome: hard to find words –> DO NOT INCREASE DOSE anymore once this occurs
  • **BILATERAL parasthesia (tingling/pricking in extremities) –> stroke would be unilateral
  • **dehydration –> retinal issue in ONE EYE (inc pressure, one eyed glaucoma), AND, kidney stones –> are preventable
  • psychological or cognitive dysfunction
  • weight loss
  • urolithiasis (kidney stones in urinary system)
  • teratogenicity (in animals not humans)
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43
Q

oxcarbazepine MoA

A

prevent Na influx –> dec AP –> dec seizure activity

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44
Q

oxcarbazepine AE

A

similar to carbazepine
- less likely to cause rash

if change carb to oxcar, pt will probably react the same to it

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45
Q

what is Keppra?

A

levetiracetam

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46
Q

levetiracetam MoA

A

antagonist at the AMPA glutamate receptor –> prevent ENT –> dec AP –> dec seizure activity

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47
Q

levetiracetam benefits

A

very effective, very well tolerated, very common

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48
Q

levetiracetam metabolism

A

renally cleared!! –> the only AED that is –> therefore need renal dosing!

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49
Q

levetiracetam dose

A

IR: 500mg BID –> inc to max dose of 1.5g BID (makes sense that IR is BID)

ER: 1g qd –> inc to max 3 g qd

**renal dosing!! –> dec max IR to 750mg or 500mg

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50
Q

levetiracetam AE

A
  • enhance CNS depressants
  • weight gain
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51
Q

tiagabine MoA

A

inhibit GABA uptake –> inc GABA –> inc inhibition –> dec AP –> dec seizure activity

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52
Q

tiagabine AE

A
  • sedation
  • mild memory impairment
  • abdominal pain
  • abnormal physical weakness/lack of energy (asthenia)
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53
Q

zonisamide MoA

A

prevent Na influx –> dec AP –> dec seizure activity

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54
Q

zonisamide AE

A
  • drowsy
  • HA
  • N/V
  • loss of appetite
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55
Q

when to change AEDs in patient seeking pregnancy

A

6-12 months before pregnant –> most common time to have seizures is when changing drugs

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56
Q

AEDs CI in pregnancy

A
  • phenytoin
  • valproate
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57
Q

AEDs recommended in pregnancy

A
  • phenobarbital
  • lamotrigine
  • oxcarbazapine
  • ethosuximide
  • (topiramate)

oxcarb better than carb!!

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58
Q

which AEDs cause contraceptive failure

A
  • phenytoin
  • **carbamazepine
  • oxcarbazepine
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59
Q

2 big concerns about sharing needles

A

1) abcesses: skin popping
2) xylazine: **severe necrotic skin ulcerations –> not always at injection site

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60
Q

classes of substance abuse drugs

A

1) alcohol
2) tobacco
3) stimulants
4) depressants
5) hallucinogens
6) marijuana
7) inhalants
8) misc

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61
Q

types of depressants

A

1) sedative-hypnotics
2) GHB
3) opiates
4) DXM

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62
Q

types of sedative-hypnotics

A

1) benzos
2) barbiturates

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63
Q

benzodiazepine MoA

A

increase GABA inhibition –> therefore inc inhibition –> therefore depressant

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64
Q

benzo metabolism

A

by liver –> inactive and active metabolites

***active metabolites INCREASE effect –> caution elderly

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65
Q

benzo half life

A

long half life, accumulation of drug

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66
Q

benzo tolerance

A

rapid tolerance with chronic dosing

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67
Q

benzo AEs

A
  • dec BP
  • drowsy
  • GI upset
  • urinary retention
  • anterograde amnesia (don’t remember drug administration)
  • respiratory and CNS depression
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68
Q

benzo withdrawl

A
  • **anxiety
  • **insomnia
  • muscle tension
  • irritable
  • depression
  • paranoia
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69
Q

benzo OD treatment

A

1) supportive
2) flumazenil

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70
Q

flumazenil MoA

A

competitive inhibition of benxo receptor on GABA –> inhibits the inhibition of GABA –> increases stimulation to prevent the over-depressant effect

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71
Q

flumazenil dose

A

0.2 mg/min –> 3 mg max

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72
Q

flumazenil CI

A
  • TCA use (-triplylines)
  • benzo dependent

**withdrawal seizures

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73
Q

in general, OD treatments will cause what side effects?

A

the withdrawal side effects of the drug of abuse

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74
Q

benzo withdrawl treatment

A

1) taper down

**convert to 1 long-acting benzo –> taper down from there

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75
Q

what are roofies

A

flunitrazepam –> benzo

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76
Q

barbiturate MoA

A

depressant –> inc GABA inhibition

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77
Q

barbiturate effects/AEs

A

intoxication similar to alcohol, similar benzo effects too
- disinhition
- mood
- unsteady gait
- slur speech
- poor judgement
- amnesia

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78
Q

barbiturate OD treatment

A

suportive

79
Q

barbiturate withdrawal treatment

A

taper barb down –> change to one long acting barb
**add an anticonvulsant if at high risk of withdrawal seizures

80
Q

barbiturate withdrawal s/s

A
  • anxiety
  • postural hypotension
  • **seizures
  • insomia
81
Q

long acting benzo

A

diazepam

82
Q

long acting barb

A

phenobarbital

83
Q

gamma-hydroxybutyrate (GHB) (Xyrem) MoA

A

derived from GABA –> inc GABA and GHB receptor inhibition –> depressant

  • CIII Xyrem used for narcolepsy
84
Q

GHB PK

A
  • fast half life, fast time to peak, no active metabolites –> therefore quick and hard to catch on toxicology –> hence date rape drug
85
Q

GHB effects

A
  • **amnesia
  • hypotonia (weak muscle tone)
86
Q

GHB toxic effects

A
  • coma
  • seizure
  • repiratory depression
87
Q

GHB withdrawal effects

A
  • agitations
  • mental status change
  • inc BP
  • inc HR
88
Q

GHB OD therapy

A

supportive –> fluids, vent, O2
maybe thiamine

89
Q

common opioid lacing concerns

A

1) cocaine is laced with fentanyl
2) heroin is laced with xylazine

90
Q

xylazine MoA

A

central alpha 2 -adrenergic agonist –> dec NE and DA release –> depressant

allows for longer highs from other drugs

91
Q

xylazine withdrawal effects

A
  • agitation
  • severe enxiety
92
Q

xylazine OD effects

A
  • coma
  • cardiac failure
  • respiratory depression/arrest
  • disfiguring skin ulcers
  • infections –> gangrene –> limb amputation
    *ulcers can develop away from injection site
93
Q

what is not effective for xylazine OD?

A
  • Narcan or naloxone –> bc not an opioid
  • animal reversal OD agents –> not sure if safe/effective in humans
94
Q

xylazine elimination

A

rapid!!! (short half life)
- not show up on tox reports anyways – need special detection

95
Q

xylazine OD treatment

A

supportive

**consider that this may be present if pt is not responding to Narcan

96
Q

xylazine withdrawl treatment

A

clonidine –>acts the same as xylazine, will dec the inc in NE from withdrawl of drug that is causing agitation

97
Q

opioid MoA

A

bind opioid receptors in CNS –> inhibit ascending pain pathways –> general CNS depressant

98
Q

opiate drugs

A
  • heroin
  • morphine
  • codeine
  • hydrocodone
  • hydromorhphone
  • fentanyl
  • oxycodone
  • tramadol
  • tapentadol
  • meperidine
99
Q

opioid effects

A
  • euphoria
  • sedation
  • *constipation
  • slur speech
  • miosis (pinpoint pupils)
100
Q

opioid withdrawal s/s

A
  • lacrimation (tears)
  • mydriasis (large pupils)
  • insomnia
  • **restless leg syndrome
  • physical pain
  • insomnia
101
Q

opioid overdose treatment

A

1) naloxone (Narcan)
2) supportive

102
Q

naloxone MoA

A

pure opioid antagonist –> displaces narcotic at receptor

103
Q

naloxone dose

A

0.4-2 mg IV/IM/SQ q2-3min
OR
2mg or 4 mg IN as a single dose in one nostril, alternate nostrils q2-3 min until assistance comes

*administer if unconcscious and respiratory depression

104
Q

opioid withdrawal treatment categories

A

1) withdrawal/detox
2) maintenance
3) abstinence

105
Q

opioid withdrawal options

A
  • methadone
  • LAAM
  • buprenorphine
  • clonidine
  • lofexidine
106
Q

opioid withdrawal maintenance options

A
  • methadone
  • LAAM
  • buprenorphine
107
Q

opioid withdrawal abstinence options

A
  • naltrexone
108
Q

methadone MoA

A

full opioid agonist
** want to gradually titrate up and therefore stop use of street drugs –> converting patient fully to this

109
Q

methadone metabolism

A

substrate and inihibitor of P450!!! –> many DDIs!!!!

110
Q

methadone and pregnancy

A

induce hepatic enzymes during pregnancy to dec half life –> may need to inc dose

111
Q

methadone AE

A

QT prolongation

112
Q

methdone dosing

A

withdrawal/detox:
20-80mg, taper down by 5-10mg/day
*huge risk if taper off –> dec tolerance –> if go back on street heroin at same dose as before –> life threatening!!

113
Q

three goals of methadone maintenance

A

1) suppress s/s of opioid withdrawal
2) extinguish opioid craving
3) stop reinforcing effective of illicit opioids by increasing opioid tolerance –> street drugs have less of an effect now

114
Q

methadone maintenance dosing

A

initial: 30-40mg day 1 –> induction phase will keep half the dose until the next day, therefore concentration will inc without dose increasing –> MDD about 100mg/day

115
Q

how to titrate methadone maintenance dose

A

use s/s withdrawal
- relieve withdrawal
- reach tolerance
- stop craving
- get to adequate dose
- perserve thee effects!

116
Q

what needs to be done within 14 days of starting methadone maintenance therapy?

A

labs and physical exam!!

117
Q

how do methadone maintenance pts get dose?

A

everyday supervised dose administration

start going everyday –> after 90 days can go twice a week –> after 2 years can go once a month

need to prove compliance, safe storage, etc…

118
Q

buprenorphine MoA

A

partial opioid agonist

good bc –> has a higher affinity than most full agonists so it kicks them off –> also has weak opioid activity to prevent/relieve withdrawal symptoms — ohhhhhhhh

counsel to take when feel withdrawal, not when take other opioid

119
Q

buprenorphine in preg

A

induces metabolism –> dec concentration

120
Q

buprenorphine metabolites

A

active with longer half life –> norbuprenorphine

121
Q

buprenorphine detox

A

induction, dose reduction
*transition opioid until go opioid free

122
Q

buprenorphine maintenance steps

A

1: induction – find minimum dose where no craving, no opioid use, no AEs, no withdrawal
2: stabilization at that dose
3: maintenance of that dose indefinitiely

123
Q

good candidiates for buprenorphine

A
  • addicted not just dependent
  • no CIs
  • interested
  • expect compliance
  • willing to follow safety protocol
124
Q

bad candidiates for buprenorphine

A
  • dependence on other CNS depressant as well
  • untreated psych
  • multiple relapses
  • poor response
  • complec medical
125
Q

major diffence between methadone and buprenorphine

A

methadone: more follow up
buprenorphine: more accessible

126
Q

buprenorphine dosing

A

SAME for detox and maintenance

general:
buprenorphine 4mg-32mg/day
can do qd or bid (?)

127
Q

buprenorphine options

A

Subutex
Probuphine
Sublocade

128
Q

buprenorphine/naloxone options

A

Suboxone
Zubsolv
Bunavail

129
Q

which bup products are tablets?

A

Subutex
Suboxone – SL tab or film
Zubsolv

130
Q

which bup products are films

A

Suboxone – SL film
Bunavail –> buccal film

131
Q

which bup products is an implant

A

Probuphine

132
Q

which bup product is SQ

A

Sublocade

133
Q

why is there naloxone in bup?

A

prevent abuse – people injecting the bup into their veins

oral bup: poor bioavaliabillity
parental bup: high bioavliability

134
Q

how do the bioavaliability of the bup/nalox products compare?

A

Zubsolv and Bunavail have higher F than Suboxone –> therefore less Bup is needed for some concentration –> less abuse potential

135
Q

what is a low creatinine indicative of?

A

very dilute urine (drank water)

136
Q

what is a low drug level indicative of

A

missed dose –> may have diverted it!

137
Q

what bup products are first line

A

bup/nalox

138
Q

sublocade benefits

A
  • injectable –> reduce diversion, increase compliance
139
Q

sublocade dose

A

300mg SQ qmonth x2 months –> 100mg SQ qmonth —> if withdrawal, inc to 300mg SQ qmonth

140
Q

what is special about sublocade?

A

1) BBW: harm/death if IV – forms clump
2) REMS required

141
Q

sublocade indication

A

maintenance treatment of opioid dependence
AFTER
adjusted to 8-24mg of transmucosal bup product x7 days

142
Q

sublocade counseling

A

do not rub injection site

143
Q

clonidine MoA

A

stimulate alpha 2 adrenergic receptors –> dec sympathetic –> dec NE –> prevent fight/fight withdrawal

**works against xylazine bc have same MoA

144
Q

clonidine AEs

A
  • drowsy
  • dizzy
  • dry mouth
  • HA
  • abdominal pain
145
Q

lofexdine MoA

A

stimlate alpha 2 adrenergic receptors –> same as clonidine

146
Q

lofexidine AEs

A
  • orthostatic hypotension
  • insomnia
  • dizzy
  • dry mouth
  • drowsy
147
Q

naltrexone MoA

A

competitive complete opioid antagonist

148
Q

naltrexone dose

A

25mg po qd x1week, then 50 mg qd
OR
380mg IM qmonth

149
Q

naltrexone requirement

A

MUST BE OPIOID FREE 7-10 DAYS
- if not, will cause withdrawal
- IM needs tox negative

150
Q

naltrexone BBW

A

acute hepatitis
hepatocellular injury

151
Q

which drugs do you need to be opioid free for 7-10 days for?

A

naltrexone po
naltrexone IM
Vivitrol (naltrexone XR) (po or IM)

152
Q

naltrexone AE

A

GI upset

153
Q

dextromethorphan MoA

A

inhibit NMDA receptor –> dec stimulation –> depressant

154
Q

DXM effects

A

-hallucinations
- slur speech
- HTN
- lethargy
- altered time perception

155
Q

stimulants

A
  • cocaine
  • amphetamine
  • methamphetamine
  • PCP
  • ketamine
156
Q

cocaine MoA

A

inhibit NE and DA reuptake –> inc NE and DA –> hence stimulant

snort, inject, smoke, gum
HCl vs crack form

157
Q

cocaine effects

A
  • *nasal septum ulceration
  • *kindling – hallucinations, psychosis –> the more you use, the more potential for these
  • mydriasis
  • aggression
  • sweats
  • N/V
158
Q

cocaine withdrawal

A
  • depression
  • fatigue
  • nightmares
  • sleep disturbance
  • tremor
159
Q

cocaine metabolites

A

inactive

160
Q

bromocriptine MoA

A

dopamine agonist

hence why maybe cocaine withdrawal bc same MoA as cocaine

161
Q

amphetamine MoA

A

block DA and NE reuptake + inc DA and NE release + inhibit monoamine oxidase –> stimulant

162
Q

amphetamine effects

A
  • *meth mouth –> DONT GET IF RX AMOUNTS ahhhhh
  • alert
  • dec fatigure
  • irritable
  • insomnia
  • confused
  • anxiety
163
Q

amphetamine withdrawal

A
  • fatigue
  • depression
  • cog impairment

if cooking at home –> fires, explosions

164
Q

what is ecstatsy MDMA

A

derivative of amphetamine, destroys serotonin producing neurons

165
Q

ecstasy MDMA

A
  • empathy
  • suppress need to eat, drink, sleep
  • amphetamine ones
166
Q

PCP MoA

A

DA, 5HT, NE reuptake inhibitor –> stimulant

167
Q

PCP effects

A

euphoria, delusion, hallucination

low doses: sedation, slur speech, paresthesia

high doses: inc HR, inc BP, muscle rigidity, coma, seizure

168
Q

ketamine MoA

A

anesthetic, cataleptic (muscle rigidity), release catecolamines (E, NE) to maintain BP and HR –> stimulant

169
Q

ketamine effects

A
  • inc BP
  • inc HR
  • hallucinate
  • delirium
  • vivid dreams
  • seizures
  • cardiac arrest
170
Q

hallucinogens

A

-LSD
-psilocybin
-mescaline

171
Q

LSD MoA

A

stimulate pre and post synaptic serptonin –> inc serotonin –> hallucinate

172
Q

LSD effects

A
  • mydriasis
  • inc temp, bp, hr
  • dry mouth
  • dizzy
  • flashbacks
173
Q

marijiana MoA

A

cannabinoid receptors, release dopamine

174
Q

marijiana effects

A
  • euphoria
  • disinhibition
  • impaired cognition –> short term, memory, skills
  • bronchioles relax and enlarge
  • hunger
  • thrist
175
Q

marijuana metabolites

A

lots of metabolites

176
Q

inhalants MoA

A

huff glues, solvents, gas, etc… –> rapidly absorbed by lungs –> penetrate BBB

177
Q

inhalant effects

A
  • Nausea
  • HA
  • brain low O2
  • brain damage
  • suffocation
  • impaired pulmonary function
178
Q

combo drugs

A

more prone to OD because don’t appreciate the toxicitity of each individually

179
Q

misc drugs

A
  • krokodil
  • bath salts
  • synthetic marijuana
  • kratom
180
Q

krokodil MoA

A

from codeine, potent short acting opioid –> therefore depressant
**impure and contaminated

181
Q

krokodil effects

A

SQ –> local tissue damage, ulcers, skin necorisis, infection

182
Q

krokodil OD effects

A
  • slow shallow breathing
  • small pupils
  • slur speech
183
Q

bath salts MoA

A

synthetic stimulants

184
Q

bath salt effects

A

amphetamine like stimulatory effects

185
Q

bath salts OD effects

A
  • tachycardia
  • HTN
  • hyperthermia –> most common cause of death
186
Q

bath salts OD treatment

A
  • IV benzos
  • fluids
    -sedation
187
Q

synthetic cannabinoids MoA

A

much more potent receptor agonists that marijuana

188
Q

synthetic cannabinoid effects

A

more pronounced effect than marijuana bc synthetic

189
Q

kratom MoA

A

stimulate aplha 2 adrenergic, block serotonin, opioid

190
Q

kratom effects

A

stimulant at low doses
depressant at high doses

191
Q

pregnancy risks for patients

A
  • test infant hair
  • HIV risk
192
Q

pregnancy opioid use disorder recommendations

A

1st: methadone
2nd: Subutex > Suboxone

193
Q
A

p3 year :) (5 decks)

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