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TPX Neuro, Psych, & Sub abuse > Week 1: Alcoholism, Sub Abuse, Epilepsy > Flashcards

Week 1: Alcoholism, Sub Abuse, Epilepsy Flashcards

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1
Q

Alcoholism

A

A chronic disease that when active results in compulsive, out of control use of alcohol with negative consequences

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2
Q

DSM 5 Criteria for Alcohol Use Disorder

A
  1. More than once wanted to cut down or stop drinking, or tried to , but couldn’t
  2. spent a lot of time drinking? or being sick or getting over other after affects?
  3. wanted a drink so badly you couldn’t think of anything else?
  4. found that drinking or being sick from drinking often interfered with taking care of home family, or caused job or school troubles

5.continued to drink even though it was causing troubles with your family and friends

  1. given up or cut back on activities that were important to you or pleasurable in order to drink
  2. more than once gotten into situations whole or after drinking that increased your chances of injury

8.continued to drink even though it was making you feel depressed or anxious or adding to another health problem, or having had a memory black out

  1. had to drink much more than you once did to get the effect you want

10.foun d that when the effects of alcohol were wearing off, you had withdrawal symptoms

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3
Q

DSM5 Alcohol Use Disorder Severity Criteria

a. considered AUD if..
b. Mild:
c: Moderate:
d. Severe

A

a. the presence of at least 2 of symptom criteria indicated AUD

b. mild: presence of 2-3 symptoms

c. Moderate: the presence of 4-5 symptoms

d. Severe: presence of 6 or more symptoms

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4
Q

Type I Alcoholism

A

develops gradually over the life span
*equally prevalent in men and women.
*less severe in health consequences

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5
Q

Type II alcoholism

A

an early on set

more prevalent in men and more severe in its health consequences0

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6
Q

Lab tests that are helpful in Alcoholism dx

A

MCV (mean corpucle volume) elevation

high levels of liver transaminases (AST, ALT

high levels of uric acid, triglycerides

ethyl glucuronide or ethyl sulfate

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7
Q

effects of etoh @ diff BAC

A

legal limit: 0.08%
0.13-0.15: gross motor impairment and lack of physical control. blurred vision and major loss of balance. euphoria reduced and dysphoria beginning to appear

0.16-0.20%- dysphoria: NV, sloppy drunk

0.25% needs assistance walk, total mental confusion. dysphoria w. some mental confusion

0.30: loss of conciousness

> /=0.40: onse of coma, possible death

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8
Q

Pharmacodynamics of Alcohol

A

Alcohol is a cns DEPRESSENT
*Acute: Stimulates GABA(inhibitory neurotransmitter )system
CHRONICALLY: downregulation of inhibitory receptors, so abrupt withdrawal causes less effective inhibitory neaurotransmitters.

*Acute: inhibits NMDA Glutamate (stimulatory) neurotransmitter system
chronically: upregulates stimuatory neurotransmitters so abrupt withdrawal causes more effective stimulation

*activates opioid peptide system: reinforces craving and rewarding effects: contributes to addiction
*also increase dopamine release which is a reqrding system as well

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9
Q

Basic etoh PK

A

lipid soluble

zero order metabolis(capacity limited)

Absorption:
25% absoprbed in sotmach
75% from small intestine
lipid and protein delay absorption
*can be effected by

Distribution:
Vd=approx total body water
decreasing Vd from men->-women->to obese

Metabolism: Zero order metabolism via alcohol dehydrogenase

ETOH->acetylaldehyde->Acetyl coA–>co2+7ckal/gram+H2O

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10
Q

gender pk differences of ETOH

A

MEN: MORE WATER, MORE VD

WOMEN: LESS WATER, AND less efficient prehepatic alcohol dehydrogenase

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11
Q

Organ system effected by chronic excessive alcohol use

A

cns:
*Addiction
*Wernicke-Korsakoff Syndrome
*Cortical atrophy/dementia

hepatic/Pancreatic:
*Steatosis, or fatty liver
alcohol hepatitis
cirrhosis
pancreatitis

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12
Q

wernicke-Korsakoff syndrome

Wernicke encephalopathy

cause:
SS:
action:

A

SS: confusion
loss of musce coordination ataxia
Leg tremor
vision changes
nystagmus
dyplopia
eyelid drooping

Acute neurologic condition that occurs due to severe actue deficieny of thiamine. due to poor oral intake

action: admin thiamine to anyone suspected of having etoh withdrawal. do not give glucose before thiamine b/c glucose can aexhaust thiamine supply and worsen confusion

REVERSIBLE

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13
Q

wernicke-Korsakoff syndrome

Korsakoff syndrome

cause:
SS:

A

SS: antregrade amnesia
severe loss of memory
confabulation
hallucinations

results from long standing wernickers

IRREVERSIBLE

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14
Q

Alcohol withdrawal

whendoes-it-occur

howserioous-is-it

how-to-prevent

A

very serious med complication. lif threatening

can occur in ppl drinking excessively from weeks to months

NEVER TELL PTS with hx alcohol abuse to simply stop

management can be outpt but often require in pt withdrawal management

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15
Q

Patho of Alcohol Withdrawal

A

Chronic stimulation of GABA inhibitory rceptors downregulate effective gaba receptors, so abrupt withdrawal prevents proper inhibition

chronic INHIBITION OF NMDA stimulatory receptors upregulates stimulatory receptors. causing more effective stimulatory receptors during abrupt etoh withdrawal

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16
Q

alcohol withdrawal presentation

A

minor withdrawal 5-10 hrs
*autonimic hyperactivity, tremulousness, hyperhydrosis, tachycardia, htn, GI upset, anxiety, insomina, and vivid dreams

Major withdrawal: (12-72 hrs)
*hallucinations (usually sensory, not auditory or visual)
seizures

Delerium tremons (medical emergency)-48-96 hours
*dirordered conciousness (auditory and visual hallucinations)
*Life threatening state
*hallucinations
*disorienatation
*tachycardia
*HTN
Low grade fever
agitation
diaphoresis
*elevated cardiac indices
*hyperventilation and respiratory alkalosis
*sensorium clouding

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17
Q

Delerium Tremens

who is mortality risk greater for

A

eldery

concamitant copd

cor ebody temp>104

co existing liver dx

death usually due to arrhythmia or seocndary complications (pnemonia, heart failure

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18
Q

Management/ Prophylaxis of ETOH withdrawal

A

thiamine 50-100 mg daily

0.45 NS and D5W (D5W only after thiamine administration)

Multivitamins

standing orders for
*clonidine
benzos

*note some institutions may use CIWA-Ar Scale (Clinical institute withdrawal assessment of alcohol scale

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19
Q

Management of etoh wihdrawal

monitoring

A

monitor p q4-8hrs by means if ciwa-aR SCAle until score is <8-10 for 24hrs

pts with ciwa-ar <8-10, nonpharmacologic mintoring is cceptable

pts with ciwa-ar 8-15: benefit from medicationthis ruding risk of complications

ciwa-AR ACORE>15: MAJOR RISK OF COMPLICATIONS

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20
Q

System triggered treatment regimen of etoh withdrawal

A

administer one of the following qh whn ciwa-ar score > 8-10

*diazepam 10-20 mg
*Lorazepam 2-4 mg

not usually used unless closs personal monitoring

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21
Q

fixed schedule regimen for etoh withdrawal

A

Diazepam 10 mg q6hr for 4 doses, then 5 mg q6hr for 8 doses

Lorazepam 2 mg q6 hr for 4 doses then 1 mg qhr for 8 doses

other benzos may be used at equiv doses.

not short acting benzos because they dont last as long

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22
Q

maintenance of etoh sobriety

A

group support (AA)

Disulfuram

NAltrexone

Acamprosate

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23
Q

Disulfuram

moA

dosing

AE

A

moa: inhibits aldehyde dehydrogenous enzyme in alcohol metab pthway. Increases levels of acetaldehyde, which can cause unwanted side effects such as N&V, anxiety, agitation. serves as negative reinforcement

dosing: inital 500 mg once daily for 1-2 weeks
maintenance: 250-500mg once daily. MDD:500 mg.
duratio of therapy is to contirnue until pt is fully recoeverd socially and a basis for permanent self control. maintenance therapy may be needed for months or years

AE: drowsiness, headache, faitgue, psychosis
rash, metallic or garlic-like aftertatse, impotence, hepatitis, hepatic failure, peripheral neuritis and neuropathy, optic enuritis

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24
Q

disulfuram considerations

A

not selective for etoh. many other substanes have aledyhe dehydrogenase in pathway and can exacerbate the negative symptoms of disulfuram
*ABX->nitromidazoles. e.g metonidazole
*first gen sulfonylureas (tolbutamide)
several cephalosporins (cefoperazone and cefotetan
*antifungals (Griseofulvin)

do not adminster until the pt has been abstinant from etoh for atleast 12 hours

disease concerns: use in caution w. pts with..
diabetes
hepatic impairment
hypothyroidism
nephritis
seizure disorder hx

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25
Q

Naltrexone
moA

dosing

AE–

A

moA: competative antagonist at opiate receptor sites

dosing: IM 380 mg once every 4 weeks
oral: 50 mg daily

AE

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26
Q

Naltrexone considerationsfor-etoh-maintenance

A

should pt need opioid analgesics, it will not be effective

choose alternative analgesics.

daily oral and monthly im dosing available

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27
Q

Acamprosate

moa:

dosing:

AR:–

A

moa: sTRucturally similar to GABA. increases gaba inhibitory and decreases glutamate within system.

dosing: 666 mg 3 x day

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28
Q

Acamprosate considerations

A

3x a day dosing. 666 mg
dose adjustment for low body weight

treatment should be initiated as soon as possible following the period of alcohol withdraway, when pt has achieved abstinance

renal adjustments:
Crcl 30-50: 333 mg 3xday
<30: contraindicated

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29
Q

addiction:

A

primary chronic, neurobiological disease, with genetic , psychocial and environmental factors influencing its develoment and manifestation

5C;s:
*chornicity,
*impaired control over drug abuse,
*compulsive use,
*continued use despite harm,
*craving

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30
Q

drug abuse

A

maladaptive pattern of subatance use chaacterized by repeated adverse consequences related to the repeated use of substance

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31
Q

sensitization

A

increased response to a drug with repeated use. shifts curve to the left.

takes same or less drug to get effects

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32
Q

tolerance

A

state of adaption i which exposure to a drug inuces changed that result in diminution of one or more of the drugs over time

2 types:
metabollic: liver enzymes
cellular: receptor downregulation

can be also
acute:
protracted

cross tolerance: tolerance to one drug leads to tolerance in another drug

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33
Q

physical ependence

A

pt needs the drug to function normally and to avoid withdrawal

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34
Q

physiological depenence

A

body adapts to presence of drug. needs drug on board to maintain homestasis

specific withdrawal symptoms can be produced by abrupt cessation, rapid dose reductoin, decreasing blood level of a drug and/ or administration

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35
Q

define-withdrawal symptoms

A

behviors displayed by a user when drug use ends

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36
Q

repeated self adminstration

A

mesolmbic dopamine system. abused drugs all tend to activate this system

3 stages:
pleasure: huge dopaminergic release

associative learning through classical conditioning: cues or context of abuse substance can induce dopiminergic release

incentive silenced by craving,

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37
Q

evaluating risk factors for substance use disorders

A

dysfunctional childhood, abuse

ADHD, school problems, conduct disorder

early onset of substance use (esp. before age of 14)

personal history of substance use disorder

genetic predisposition

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38
Q

Toxicology testing for substnces

testingroute
detection-time
pro
con

A

hair: 7days-3 months

pro: long observation period

cons: few labs, need 150 strands.

urine: gold standars
pro: reasonable detection limits
can or need to normalize creatinine

cons: pts. can falsify. need teo be temp stabilied

blood:

con: short tection time
somewhat inasive

pro: can use if cant get urine or solive. can observe

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39
Q

Interpreting qualitative Immunoassays for substance detection

A
  1. synthetic opioids(methadone, fentanyl) do not produce a positive test for opiates

2.some opiates (oxycodone, buprenorphine) typically do not produce a positive test for opiates

3.some benzos (clonazepam) may not produce a positive test for benzos

4.some otc meds (pseudoephedrine) may notproduce a positive test for amphetamines

5.environmental exposure to marijuana will not produce a positive test

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40
Q

interprating urine toxicology results

A

drugs w. short half lives (methamphetamine, lorazepam, cocaine, heroin) will cause the urine toxicology test to be positive for only a few days fter last use

drugs w. long halflives (e.g buprenorphine, cannabinoids, diazepam, methadone) may cause the urine test to be positive for several days-weeks after last use

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41
Q

how to normalize creatinine

A

Creatinine-normalized drug level
= [urine drug level]/[urine Cr] x100

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42
Q

General substance abuse treatment consideratoins

A

pharmacotherapy

Outpt vs inpt addiction treatment

counseling

groups: Narcotics anonym./Alcoholic Anon.

Identifying comorbid conditions

Lab: nutritional exams, LFT,thyroid, CBC, metabolic panel, HIV, Hep C

psychiatric dx: other substances, ptsd, SUBSTANCE ABUSE PSYCHIATRIC DISORDERS, ANTISOCIAL AND BORderline personality disorder,, bipolar, SzPh, depression, anxiety

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43
Q

Depressants

class:Benzos

examples:

moa:

SS effects:

SS withdrawal

A

class: Benxodiazepam: sedative hypnotics

usually end in -PAM (lorezepam)

moa: potentiate GABA inhibitory receptos within cns

SS effects:
*decrease bp
*MEMORY IMPAIRMENT
*confusion
*anterograde amnesia
*gi effects
*urinary retention
slurred speach
poor coordinationrespirstory depression

SS withdrawal
*anxiety
*insomnia
*muscle tention
*irritability
*SEIZURES
*hallucinations
*nightmares
*LIFE THREATENING

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44
Q

Benzo Overdose General Treatment

A

*mainly supportive

*rarely use FLumazenil
moa: competitive antagonist of GABA benzo receptor
dose: 0.2mg/min up to 3mg max

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45
Q

Flumazenil Treatment considerations

A

effects occur in 1-3 min

CI in bezo dependant pts. or pts. w. hx of seizures

AE: SS of withdrawal +N&V

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46
Q

Benzo withdrawal treatment (for pt who needs to get off)

A

Taper benzo depending on dose and duration

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47
Q

Depressants

class: BArbiturates

examples:

moa:

SS effects:

SS withdrawal

A

ex: end in -barbital

moa: potentiate GABA inhibitory receptos within cns (same as ETOH and benzos

SS effects:
*decrease bp
*MEMORY IMPAIRMENT
*confusion
*anterograde amnesia
*gi effects
*urinary retention
slurred speach
poor coordinationrespirstory depression

SS withdrawal
*anxiety
*insomnia
*muscle tention
*irritability
*SEIZURES
*hallucinations
*nightmares
*LIFE THREATENING

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48
Q

Barbiturate general overdose treatment

A

supportive

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49
Q

Barbiturate withdrawal tratment (for pt that needs to get off)

A

taper
change to longer acting barb (phenobarb)

if using barb for anticonvulsive therapy, substitute anticonvulsant

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50
Q

Depressants

class: Gamma-hydroxybutyrate (GHB)

examples:

moa:

SS effects:

SS withdrawal:

SS toxicity

A

Depressants

class: GHB

examples:

moa: derived from GABA. has inhibitory effects in cns. . short half life

SS effects:
*amnesia
*hypotonia
*often use as date rape drug

SS withdrawal:
*agitation
*mental status changes
*elevated bp. hr
*tachycardia

SS toxicity:
*coma
*seizures
*respiratory depression
*vomiting

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51
Q

GHB general overdose treatment

A

supportive
vent
O2
fluids
thiamine

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52
Q

Depressants

class: opiatesDepressants

moa:

SS effects:

SS withdrawal:

A

Depressants

class: opiates

examples: fentanyl, hydrocodone, codeine, ec.

moa: bing to opiate receptors in cns, causing inhibition of ascending pain pathways, altering response to pain produces generalized cns depression.

SS effects:
euphoria
dysphoria
apathy
motor retardation
sedation
slurred speech
attention impairment
miosis
constipation

SS withdrawal:
not fatal(but delerious)
lacrimation
rhinnorhea
mydriasis
piloerection
diaphoresis
diarrhea
yawning
fever
insomnia
muscle ache

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53
Q

General Opioid overdose treatment

A

Supportive

Naloxone
moa: pure opioid antagonist, competes and displaces narcotics@opioid receptor sites

dose: naloxone 0.4-2 mg iv/im/sq Q2-3 MIN
SPRAY: 2 or 4 mg (contents of 1 nasal spray)as a single dose in one nostril. may repeat q 2-3 min until help arrives

54
Q

naloxone consideration

A

used for opioid overdose

rapid onset

nasal spray availble

use if unconcious or respirtory depressed

multiple-uses-may-be-needed-every-two-to-three-min

55
Q

genral list of opiod withdraal therapies

A

methadone

LAAM

Buprenorphine

clonidine

Lofexidine (lucemyra)

56
Q

Methadone

moa:

indications (as far as substance abuse)

PK:

metabolism

dosing:

A

moa: opiate that binds to opiate receptors, causing inhibition pain pathways , altering perception of resoonse to pain, generalized cns depression

indications (as far as substance abuse):
opioid use disorder withdrawal opioid use disorder maintenance

PK: long t 1/2

metaboism: major cyp3A4

major AE: qt prolongation

dosing: differ for withdrawal and detox

57
Q

Methadone considerations for use in opioid withdrawal

A

dosing: 20-80 mg, taper 5-10 mg daily.

decreases tolerance , so pt has risk of overdose if pt relapses due to using pretolerance amount

58
Q

goals of methadone maintenance therapy for opioid use disorder

A

goals:
1) supress symptoms of withdrawal
2)extinguish opiate craving
3) block the reinforcing effects of illicit opiates

59
Q

Methadone considerations for use in opioid use disroder maintenance

A

START LOW AND GO SLOW

(induction. half of each days dose remains in body and is added to next days dose so levels increase w.o dose increase

initial dose no greater than 30-40mg in day 1

peak levels should be no more than twice the trough

SS can be effective indicators of stages:

relef withdrawal
reach tolerace
establish adequate maintenance dose

standard-of-care-for-maintenance-trtmt-in-pregnant-women

60
Q

Methadone maintenance program

A

pt must report qday and take dose in witnessed manner

must complete physical exam and labs within 14 dys of initiating methadone maintenance program

can evntually qualify to take their methadone home only after demonstrating…
capable of andling and taking unsupervised
abstinence from unauthorized substances
regular atendance
stable homeand social environments
methadone can be safely stored

61
Q

Buprenorphine

moa:

indications (as far as substance abuse)

PK:–

metabolism

dosing:

A

moa: exerts its analgesic effects via high affinity binding to mu opiate recptor. partial opiate agonists

indications (as far as substance abuse)

PK:–

metabolism; cyp3a4

dosing: general: 4mg-32mg/day
many different formulations

62
Q

Buprenorphine considerations for use in opioid use disorder withdrawal

A

MUST BE IN OPIATE WITHDRAWAL ALREADY BEFORE USE

(due to strong opiate reeptor affintiy. will bump off opiates from receptor and precipitate withdrawal)

limited opiod effects due to partial agonism, but also continues to block other opioids from attatching to receptor

63
Q

Buprenorphine considerations for use in opioid maintenance

A

induction phase: find minimum dose pt d/c or drastically reduced opioid use

stabilization: marked by pt experiencing no withdrawl effects

maintenance: may be indefinite, psychosocial services

64
Q

unlikely candidates for buprenorphine maintenance therapy

A

overall, is the pt willing and able to safely possess a controlled substace and use it properly.

comorbid depenence on other cns depressants should NOT neesarily proclude someone from buprenorphine maintenance therapy

65
Q

Buprenorphine formulations

formulation:
dosage form:
drugs included in formulations

A

1)Subutex
ONLY buprenorphine
SL tablet
dose:2 or 8 mg

2)suboxone= buprenorphine/naloxone at higher doses b/c lower bioavailability

SL tablets or film

3)Zubsolv= buprenorphine/naloxone at lower doses(higher bioavailability) (lower dose reduces abuse potential if misused )

SL tablets

4)Bunavail
buprenorphine/ naloxone (at even lower doses)
buccal films

5)sublocade
bupenorphine ONLY
SQ injection

66
Q

dose conversions from suboxone to Zubsolv

A

suboxone Zusolv

8mg/2mg 5.7/1.4 mg
2mg/0.5 mg 1.4 mg/0.36 mg

overall: 8 mg suboxone=5.7 mg Zubsolv

67
Q

dose conversion of subaxone to buvanail

A

approximately 2:1
suboxone Buvanail

4mg/1mg 2.1mg/0.3mg
8mg/
12mg/

68
Q

Sublocade treatment considerations

A

Long acting buprenorphine formulation for patients on 8mg or more of buprenorphine

LAI (SQ)

benefits:reduce diversion and abuse.
good option for noncompliant pts-do not need to take a sl tab or film q day

once a month injection

BBW: if adminstered IV, will form solid mass. also do not admin IM.

69
Q

Sublocade treatment considerations

A

Long acting buprenorphine formulation for patients on 8mg or more of buprenorphine containing product for atleast 7 days

LAI (SQ)-rotate injection. will form small lump that will last 7 days. dont rub

benefits:reduce diversion and abuse.
good option for noncompliant pts-do not need to take a sl tab or film q day

once a month injection

BBW: if adminstered IV, will form solid mass. also do not admin IM.

REMS treatment

70
Q

Conversion from buprenorpine to Sublocade

A

8 mg buprenorphine=300 mg SQ q month for 2 months, then 100 mg q mo therafter

71
Q

Clonidine

moa:

indication:

AE:

metabolism

dosing:

A

moa: stimaulates alpha-2 receptors, acitvating inhibitory neorins, reducing sympathetic outflow from the cns (which negated withdrawal’s sympathetic stimulation )

INDICATION:opioid withdrawal

AE: orthostatic hypotension, bradycardia, hypotension, insonia, dizziness, drowsiness, (basically parasympathetic activation)

metabolism

dosing:

72
Q

Lucimera

moa:

indication:

AE:

A

SAME AS CLONIDINE,

moa: stimaulates alpha-2 receptors, acitvating inhibitory neorins, reducing sympathetic outflow from the cns (which negated withdrawal’s sympathetic stimulation )

indication: single indication for opioid withdrawal

AE: orthostatic hypotension, bradycardia, hypotension, insonia, dizziness, drowsiness, (basically parasympathetic activation)

73
Q

Other symptom anagement for opioid withdrawal

A

pain management
*NSAIDS, APA, muscle relants, neuropathic agents

N$V management: with *N:metoclopramide, ondansetron
*diarrhea: antidiarrheals

anxiety: insomnia medications, muscle relaxants, hydroxyzine

74
Q

Naltrexone for opioid maintenance

moa:

indication:

AE:

A

moa: attenuates or blocks reversible subjective affects of iv administered opioids by binding to opioid receptor

indication: maintenance

AE: GI upset for oral, injectio site reaction for IM

75
Q

naltrexone for opioid use disorder maintenance considerations

A

must be opiate free for atleast 7-10 days. if given when not opiate free, may induce withdrawal symptoms

BBW: acute hepatits,

IM naltrexone preffered in opioid maintenance over oral naltrexone
(dose 380 mg IM q 4 weeks

76
Q

Vivitrol (Naltrexone XR)

A

IM

77
Q

why is repeated doses of naloxone (narcan) sometimes needed, especially if pt is overdosed on opioids such as fentanyl, or carfentanyl.

A

fentanyl has higher binding affintiy and longer half life than naloxone, so once nalaxone dissipates, fentanyl will rebind to opioid receptors.

readministration is needed until help arrives and pt can be transferred to a hospital

78
Q

Non opiate pain management

A

APAP
Nsaids- ibuprofen or keterolac

neuropathic pain: TCA, gabapentin/pregablin

79
Q

Depressants

class: Dextromethrophan (DXM)

examples:

moa:

SS effects:

SS withdrawal

A

moa: inhibits NMDA(stimulatory) receptors

SS effects:
heightened sense of perceptual awareness
altered time perception
visual hallucinations
lethargy
ataxia
slurred speech
sweating
hypertension

abuse can cause death, brain damage, seizure, loss of conciousness, and irregular heartbeat

80
Q

Stimulants

class: Cocaine

examples:

moa:

SS effects:

SS withdrawal

A

class:
examples:

moa: NE and DE reuptake inhibitor

metabolites: ecgonine methyl ester
benzoylecgonine
cocaethyline only in presense of alcohol
SS effects:
euphoria
loquacity
mydriasis
change in bp, tachycardia
sweat chills
n&V
decreased fatigue
paranoia
aggression
motor agitation

Toxicity: cardiacarrest
nasal septum ulceration

SS withdrawal
depression
fatigue
nightmares
sleep disturbance
increased appetite
bradyarrthmyias
tremor

81
Q

geenral cocaine overdose treatment

A

supportive
if needed..
lorazepam (benzos)
haldol
antiarrythmiac agents prn cardiac complications

82
Q

Stimulants

class: Amphetamine

examples:

moa:

SS effects:

SS withdrawal

A

Stimulants

class:

examples:

moa: block reuptake of DA and NE, increase release of DA and NE, MAOi

SS effects:
decreased fatigue
alert awake
increased activity
hyperthermia
irritability
meth mouth
tremor
confusion
convulsions

SS withdrawal
fatigue
depression
cognitive impairment

LABS: fires, explosions

83
Q

amphetime over dose treatment

A

suppportive

haldol

lorazepam

84
Q

Stimulants

class: Ecstasy MDMA

examples:

moa:

SS effects:

SS withdrawal

A

Stimulants

class:

examples:

moa: unknown

SS effects:
EMPATHY
RELAXATION
rave
euphoria
anxiety
decreased inhibition
paranoia
touch
hyperthermia
increase HR and BP

SS withdrawal

85
Q

Stimulants

class: PCP aka angel dusty

examples:

moa:

SS effects:

SS withdrawal

A

Stimulants

class: Cocaine

examples:

moa: DA, 5HT, NE reuptake inhibitor

SS effects:
euphoria, dellusion
hostility
hallucinatoins
emotion lability

SS withdrawal

86
Q

Stimulants

class: Ketamine

examples:

moa:

SS effects:

SS withdrawal

A

Stimulants

class: Ketamine

examples:

moa: PRODUCES CATALEPTIC STATE IN WIHCH PT IS DISSOCIATED FROM SURROUNDING ENVIRONMENT BY DIRECT ACTION OF THE LIMBIC SYSTEM

SS effects:
increased bp, hr
hallucinations
vivid dreams
delerium
resp. depression

SS withdrawal

87
Q

Hallucinogenics

class: LSD

examples:

moa:

SS effects:

SS withdrawal

A

class:

examples:

moa: stimulate presynaptic 5HT1a and 1b and post synaptic 5HT2

SS effects:
mydriasis
increased temp bp hr
sweating
losso f apetite
dry mouth
tremor
hallucinations
sensory crossover (smell colors)

SS withdrawal

88
Q

LSD overdose treatment

A

supportive
lorazepam (for ttrmt of psychosis)
haldol (agitation)

89
Q

Marijuana

examples:

moa:

SS effects:

SS withdrawal

A

moa: cannabinoid receptors, release dopamine. primary psycoactive molecule is delta 9-THC

SS effects:
euphoria
disinhibition
blood shot eyes
euphoria
hunger
thirst
dry mouth
tachycardia
fear, distrust, panis
decreased coordination
amennorhea

SS withdrawal

90
Q

inhalants

moa:

SS effects:

SS withdrawal

A

“huffing” glues, butane, gasolane, aerosols

moa: rapidlt absorbed via cappilaries in the lungs. penetrate BB

effects:
nausea
headache
deprived o2 in brain
arrythmias
suffocation
brain damage
decreased bp
lossof coordination

91
Q

combo drugs of abuse

A

cocaine+etoh>cocathylene

Q-ball=quetiapne+cocaine

Speedball= heroine+cocaine

stimulant +depressent are very dangerous

92
Q

Krokodil

A

derived fromcodeine

contains solvents like gasoline and lighter fluid

can cause ulcers skin necrosis and infection

overdose: slow shallow breathing (its an opiate)
small pupils
slurred speech

93
Q

bath salts

A

synthetic stimulants

belong to phenyethylamine

amphetamine like stimulatory effects: euphoria, energy, alert

intoxication: cambativenedd, hallucinations, agitation, paranoia, confusion , hallucinatoins

overdose: tachycardia, htn, agitated delerium, diaphoresis, mydriasis, hyperthermia

most common cause of death: arrhythmias, hyperthermia, intracerbral hemmorhae
treatment: iv benzos, fluid resuscitation

94
Q

synthetic cannabinoids

A

much mor epotent than THC from natully occuring marjuana

95
Q

Kratom

A

ree native to africa and asia

13x more potent than morphine

stimilants at low doses

opiate effects at higher doses

can results in addiction and dependence.
can experience withdrawal

can result in psychosis and death

96
Q

SEizures

A

uncontrolled electrical activity in the brain, which may produce a physical convulsion, minor physical signs, thought disturbances, or a combo of these symptos

97
Q

epilepsy

A

condition characterized by a relatively long term distubance of brain sturctures and / or function hat produces an increased suceptibility to seizures

atleast 2 seizures unattriuted to some other disease processes

98
Q

new onset seizures in ages >50 are atributed to

A

tumor
bleed
infection
fibrosis secondary to a stroke 6-12 mo. earlier
generally dont hve good prognosis

99
Q

Nonepileptic seizer-causes

A

usualyl causd by ..
extreme metabolic disruption,local effects of brian tumor

infection

withdraal form sedarive/hypnotic drugs including ETOH

RENAL FAILURE

HYPOXIC ENCEPHALOpathy(near drowning if they survive)

febrile convulsions

100
Q

epileptic seiazures

A

disorder of brain where there are a cluster of cells (eleptogenic foci) that begin to fire at an abnormal rate

typically epileptics reccurent seizures have relatively predictable pattern

101
Q

seizure classification

A

single seizure (non EPILEPTIC)

A. determine if cause is due to
metabolic
toxic
hemodynamic
psychogenic

if another one occurs and non attributed to other causes, pt is considered an
EPILEPTIC

seizures further classified to
A) generalized seizures
b)partial seizures

102
Q

partial sezires

A

begin at discrete and relatively limited focus

pattern depends on function of area stimulated

smple partial seizure: uncomplicated, affects only limited aspects of neural function
motor or sensory symptoms (ex pt smells an awful smell )
conciousness and memory undisturbed

complex partial seizures:
alteration of conciousness follows initial siple seizure. may be aware and alert. may exhiit automatisms, purposeless and automatic behaviors(lip smacking, suching, fumbling with clothing, etc.

103
Q

geenralized seizures

A

involves entire cerebellum

  1. absence seizures (petit mal)
    minor impairment of short duration
    A. blank stare or other facial expression
    B. after 2-10 seconds resumes pre-seizure activity
    C. disruption in intentional behavior

may include lip smacking, puting, eyeblinking
can occur 100s of times/day

a. tonic clonic sezire (grand mal)
maximal seizure response of brain in which brain systems can be recruited

some ppl have prodrome -depression, irribitality, apathy or malaise, or euphoria
1-2 myoclonic jerks

3 phases:
a: tonic (10-20 seconds)
brief muscle flexing, pronounced extension, bladder empty,breathing stops.

b.clonic: 1/2-2min
muscle relaxation
violent spasms of contraction and relaxation(strongets muscles dominate)
resperiations resume but innefective

terminal phase:
limp and quiet with normal breathing
may be follwed by several hours of deep sleep
or may become conciousness with no recollection of seizure

104
Q

geenralized seizures

A

involves entire cerebellum

absene seizures (petit mal)
minor impairment of short duration

blank stare or other facial expression

after 2-10 seconds resumes pre-seizure activity

disruption in intentional behavior

may include lip smacking, puting, eyeblinking
can occur 100s of times/day

a. tonic clonic sezire (grand mal)
maximal seizure response of brain in which brain systems can be recruited

some ppl have prodrome -depression, irribitality, apathy or malaise, or euphoria
1-2 myoclonic jerks

3 phases:
a: tonic (10-20 seconds)
brief muscle flexing, pronounced extension, bladder empty,breathing stops.

b.clonic: 1/2-2min
muscle relaxation
violent spasms of contraction and relaxation(strongets muscles dominate)
resperiations resume but innefective

terminal phase:
limp and quiet with normal breathing
may be follwed by several hours of deep sleep
or may become conciousness with no recollection of seizure

status epilepticus (medical emergency

105
Q

management of epilepsy

A
  1. accurate dx for proper mangement

notes: choice of therapy does not depent on seizure type

goal therapy is to reduce the number of seizures to lowest frequency possible with manageble side effcts.. not to completely stop seizures

106
Q

first aide for seizures

A

A. generalized tonic-clonic seizures

  1. record time of seizure onset

stay with pt until seizure ends

have someone call 911

prevent person from hurting him or her self. place something under the head, loosen ight clothing, and clear area of sharp or hard objects

do not force any objects into pts. mouth

so not restrain pt

turn parient on side to allow saliva to drain from mouth

stay w.patient until seizure ends naturally

do not pour liquids into pts mouth or offer any food, drink or medicatoin until fully awake

give artifical respiration if pt does not resume breathing after seizure

provide area for pt to rest until fully awakened, accompanied by responsile adult

be reassuring and supportiv when conciousness returns

107
Q

medical emergency for seizures

A

greater than 10min

difficulty in rousing at 20 min intervals

complaints of difficulty with vision

vomiting

persistent headache after rest period

uncociousness with failure to respond

unequal size pupils or excessively dilated

108
Q

polytherapy considerations for epilepsy

A

for refractory pts.

risk factors: inadequate response o 1st AED prescribed

109
Q

pharmacist pt in a seizure hx

A

when was your first seizure

how often do you have seizures

when was your most recent seizures

what did u do, eat, or take the day of your most recent seizure

what anticonvulsant medications have u used in the past

what medications are u currently taking

medication specific questions regarding toxicity

determine relevant counseling oints for this pt and thir specific meications

be sure pt understands the goal of therapy

gengo rule of life#14, your pt, your decision, your responsibility

110
Q

AED and oral contraceptives

A

many Anti epileptic Drugs are enzyme inducing

phenobarbital, phenytoin, primidone, and carbamezapine increase clearance of estrogen, reducing OC effectiveness

management:
counsel pt on use of additional forms of contraceptive

might want to discuss w. neurologst to switch to non enzyme inducing AED if possible

do not recommend increasing estrogen dose. increases risk of stroke

111
Q

Pregnancy and epilepsy

A

STRESS that..
*seizures are deletarious to fetus/mother
*care should be provided by an experienced clinican
*clinican should be establish prior to conception

diet should ocntain folate, aong w. folate supplementation

discuss withdrawal of aed WITH obgyn/ neurologist

use AED if necessary at the lowest dose

avoid valproic acid and carbamezapine . if not avoidabl use lower dvided doses
avoid lamatrogene
avoid vpa+cbz+pb polytherapy

if phenobarbital is used be alert for neonatal withdrawal

112
Q

AED and breast feeding

A

no reason not to have woman breast feeding (baby has already been exposed to this drug in mom at possible higher concentrations)

113
Q

which AED cause neural tube dfects

A

carbamezapine

valproic acid

114
Q

Levetracetam (Keppra)

moa:

AE

Dose:

advantages–

disadvantages–

A

moa: non competitive antagonist at AMPA glutamate receptor

AE: generally well tolerated, weight gain. enhances cns depressants

Dose: immediate release: initial 500 mg twice daily

115
Q

Leveteracetam considerations

A

renal adjustments

Crcl-thirty-tofifty-:twofifty-sevenfifty-BID

Crcl

116
Q

Oxcarbamazepine

moa:

PK:

AE

Dose:

advantages

disadvantages–

monitoring

A

moa:

PK:

AE: most commin in children (somnelance and headaches. N&V)
rash
27% cross reactivity with tegretol

Dose:five-mg/kg/day,w-weekly-increments-of-same
target-thirty-fifty-mg/kg/day
BID

advantages: lower potential for drug interactions

disadvantages

lab monitoring:
sodium
hepatic
doesnt need routine hematologic

117
Q

Lamotrigine

moa:

PK:

AE

Dose:

advantages

disadvantages

A

moa:

PK:

AE

Dose:Start 0.5 mg/kg/day (divided bid) x 2weeks, then then 1 mg/kg/day x 2 weeks, then increase in 1 mg/kg/ day q 2 weeks until respond
MAXFOURHUNDRED

advantages: broad spectrum of activity
low teratogenic potential
non sedative

disadvantages
rash: STEVEN-JOHNSON esp w. rapid titrtion or coadmin with vpa

TITRATE SLOW

118
Q

Gabapentin

moa:

PK:

AE

Dose:

advantages

disadvantages

A

moa:

PK: higher the dose, the lower the precentage absorbed

AE: occasional somnelance, dizziness, ataxia, weight gain at high doses
may have potential for abuse

Dose:

advantages: low incidence of neurotoxic side effects

useful for comorbid neuropathis pain and or mood stabilization

disadvantages:
TID dosing
not considered very potent
complex absorption, leads for need of rapid dose increase

119
Q

phenytoin

moa:

PK:

AE

Dose:

advantages

disadvantages

A

moa:

PK: terrible aquoes absorption.

no dorse proportionality

easy to reach toxicity (concentration dependent and independent)

AE:
concentration dependent: nystagmust, double invision, blurred vision, incoordination, drowsiness, dizziness (look like ETOH intoxication)

idio sycratic : aplastic anemia, granlucytopenia, hepatotoxicty, rash, steven johnson

chronic: hum hypertrophy, acne hirsutism, peripheral neuopathy, chrnic cerebellum damage, osteoporosis, fetl vitamin k depletion

Dose:

advantages

disadvantages

120
Q

Fosphenytoin

moa:

PK:

AE

Dose:

advantages

disadvantages

A

moa:

PK:

AE

Dose:

advantages:PHOSPHORYLATED-FENYTOIN-FOR-IV-ADMIN

disadvantages

121
Q

Valproic Acid

moa:

PK:

AE

Dose:

advantages

disadvantages

A

moa:

PK:first order pk

AE: GI, elevated LFT, neural tube defect in children when used in pregnancy
CI in hepativ dysfunction and heavy drinkers or hepatic cirrhosis

Dose:

advantages

disadvantages:NEURAL-TUBE-DEFECTS

122
Q

valproic acid-CONSIDERATIONS

A

cleaning agent for floor .

GI
drug interactions
gi dosing decrease
pt instuctions
dont break chew tablet or capsule

123
Q

carbamezapine moa:

PK:

AE

Dose:

advantages

disadvantages

A

moa:

PK:

AE: dizziness, drowsiness, hyponatremia, water intoxication

Dose:

advantages

disadvantages

124
Q

carbamezapine considerations

A

autoinduction: usually fo r2 cycles

hyponatremia

can cause aplastic anemia(fatal) and transient leukopenia.d/c only if ANC goes below <1500 and decrease platlet count and red bloodcell count

monitor:baseline cbc and platelet
monitor serum levels due to autoinduction

125
Q

Patho of seizures

A

Shift in balance between inhibitory neurotransmitter (GABA) and excitatory neurotransmitter (Glutamate) transmission,

Increase glutamate activity-> causes increase in action potentials from irritable focus area
*cause by increased depolarization due to influx of positive ions such as Na+ and Ca+.

decrease in GABA-> causes inhibition of hyper polarization that is supposed to decrease action potential-> thus potentiating an action potential to occur n
Also there can be an increase in GABA reuptake
Can also be an increase in GABA breakdown

126
Q

Mechanisms of Inhibiting Glutamate activity
(And drug examples to inhibit them)

A

A. MOA: inhibit sodium channels. Prevents depolarization of neuron, and prevents the release of glutamate ( an excitatory amino acid)

Carbamazepine
Oxcarbezapine
Phenytoin
Fosphenytoin
Lamotrigine
Topiramate
Valproate
Lacosamide

B. MOA: calcium channel blockade
MOA: block calcium channels in neuron. Prevents fusion of vesicle to neuron cell membrane, that releases the excitatory NT glutamate

Ex: Ethosuximide

C. MOA: prevent Vesicle fusion to cell membrane to prevent glutamate release

Ex: Levetiracetam (keppra)

D. MOA: prevent glutamate from binding to neuron via NMDA RECEPTOR to create an action potential

Ex: Ketamine

127
Q

Mechanisms of increasing GABA activity

A
128
Q

Mechanisms of increasing GABA activity for seizures

A
  1. Stimulate GABA A receptors to increase frequency of cl channel opening, in order for cl to flow in and hyperpolarize the cell, causing a decrease in action potentials

Ex: benzodiazepines

  1. Bind to GABA A RECEPTORS, increases duration of colorize channel openings
    Ex: phenobarbital,
    Propofol
    Topirmate ( has glutamate inhibition activity AND increasing gaba activity )

BEN LIKES IT MORE FREQUENT, BARB LIKES IT LONGER

  1. Inhibits GABA REUPTAKE BY INHIBITING reuptake receptor.
    Ex: TIAGABINE( not generally used. Used when inadequate response to first line therapy)
  2. Prevent breakdown of GABA by inhibiting enzyme that breaKS DOWN GABA once taken back up
    Ex: VIGABETRON
    Valproate (decreases glutamate activity AND increases GABA activity )
129
Q

First line Specific agents for types of seizures

NOTE: this is what I learned from YouTube. Not class

A

Focal : carbamezapjme
Oxcarbezapine

Generalized (absence): ethosuxemide

Generalized( myoclonic): valproate, levetiracetam

Generalized (tonic clinic): valproate, levetiracetam, phenobarbital

Status Epilepticus:
1st step. Benzodiazepines
2nd step. Ppx. Prevents further seizures
A. Fosphenytoim
B. Valproate
C. Levetiracetam
D.lacosamide

Step 3: if pt is still having seizures, propofol, ketamine

Last line if pt still has seizures: phenobarbital

130
Q

AED AE

A

Cardiac/resp. Depression
1. Benzos
2. Barbiturates
3. Propofol

Steven Johnson syndrome
1. Lacosamide
2. Carbamezapine
3. Ethosuximide

Hepatotoxicity
1. Valproate
2. Carbamezapine

CYP450 interactions
CYP INDUCERS:
1. Barbiturates
2. Phenytoin
3. Carbamezapine
NOTE: CAN DECREASE EFFICACY IF ESTROGEN. COUNSEL PTS ON COC TO USE BACKUP CONTRACEPTION

CYP450 INHIBITORS: Valproate

Teratogenic
1. Valproate: neural tube defects
2. Phenytoin, fosphenytoin-fetal hydrantoin
3. Carbamezapine: cleft palate

131
Q

Specific ADR FOR AED

A

Valproate: pancreatitis

Carbamezapine: SIADH

PHENYTOIN/phosphenytoin: gingival hyperplasia

Topiramate: metabolic acidosis. Kidney stones

TPX Neuro, Psych, & Sub abuse (7 decks)

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