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Psychiatry > Substance-related disorders > Flashcards

Substance-related disorders Flashcards

1
Q

∆ btwn substance-induced mood symptoms vs primary mood symptoms?

A

substance-induced mood symptoms - improve during abstinence

primary mood symptoms - persist

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2
Q

DSM criteria of ABUSE

A

pattern of substance use that leads to IMPAIRMENT OR DISTRESS for at least 1 year

  • failure to fulfill obligations
  • use in dangerous situations (driving)
  • legal problems
  • social/interpersonal problems related to use
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3
Q

DSM criteria of DEPENDENCE

A

pattern of substance use that leads to IMPAIRMENT OR DISTRESS for at least 1 year
- TOLERANCE
- WITHDRAWAL effects
- using more than originally intended with persistent desire or unsuccessful efforts to cut down
- significant time in getting, using, or recovering from substance
- decrease social, occupational, or recreational activities
continued use despite subsequent or psychological problem

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4
Q

definition of withdrawal

A

development of substance-specific symptoms due to abrupt cessation of use that has been heavy and prolonged

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5
Q

definition of tolerance

A

need for increasing amounts of substance to achieve the desired effect (or diminished effect if using the same amount of the substance)

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6
Q

MoA of alcohol (what R does it act on) and its net effects

A

activates GABA-R and serotonin-R in the CNS
inhibits glutamate R and VG Ca channels

net: depressant

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7
Q

how does alcohol affect body’s pH and the anion gap?

what other substances cause the same effects?

A

metabolic acidosis + increased AG

methanol
ethylene glycol

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8
Q

What should you always give an alcoholic and why?

A

Thiamine - prevents/treat Wernicke’s encephalopathy

Folate

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9
Q

treatment of immediate alcohol withdrawal (anxious, diaphoretic, and tachycardic) and justification

What should you give in a patient whose liver function is compromised?

A

benzodiazepine taper (chlordiazepoxide/Librium, diazepam, lorazepam) to minimize risk of ASH: arrhythmias, seizures, HTN

Lorazepam = Liver Low

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10
Q

what do you worry about in chronic alcoholics?

A

withdrawal - potentially lethal due to compensatory hyperactivity (ASH = arrhythmias, seizures, HTN)

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11
Q

when do signs of OH withdrawal first manifest?

A

6-24 hours

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12
Q

when do generalized tonic-clonic seizures of OH withdrawal manifest?

A

6-48 hours, with peak around 13-24 hrs

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13
Q

signs of OH wtihdrawal

A

Tremors, irritability, GI ∆s
diphoresis, HTN, tachycarida, FEVER, disorientation
tonic clonic seizures, DTs, hallucinations

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14
Q

What is delirium tremens/DT?
When does it begin?
Signs?
Treatment? 2

A

48-72 hours

delirium, tremors, visual hallucinations, autonomic instability

Dilantin (phenytoin) and benzodiazepines (chlordiazepoxide/Librium, diazepam, lorazepam)
Thiamine, folic acid, and multivitamin (banana bag)

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15
Q

how can you tell someone is an alcoholic based on their LFTs?

A

AST:ALT ratio is > 2:1

elevated GGT

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16
Q

how can you tell someone is an alcoholic based MCV?

A

macrocytosis

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17
Q

4 Rx to treat alcohol dependence

A

1) disulfiram (antabuse) - blocks aldehyde dehydrogenase
2) naltrexone (revia, IM-vivitrol)
3) acamprosate (campral)
4) Topiramate (Topomax)

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18
Q

disulfiram (antabuse) MoA

A

blocks aldehyde DH and causes an adverse rxn to the alcohol (flushing, HA, N/V, palpitations, SOB)

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19
Q

naltrexone (revia, IM-vivitrol) MoA

A

blocks opioid receptors, thereby blocking dopaminergic (reward) pathways and reduces desire/craving and the high associated with OH use

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20
Q

what happens if you give thiamine before glucose to a patient with altered mental status from OH abuse?

A

prevents Wernicke’s Korsakoff’s syndrome from occurring

If glucose was given before thiamine, it will exacerbate the rate of cell death and worsen the condition

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21
Q

Acamprosate (campral) MoA

when is it started?
who can it be used in? not used in?

A

GABA-like mimetic that inhibits glutamatergic system

started in patients with liver disease
contraindicated in patients with severe renal disease

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22
Q

Topiramate (Topomax) MoA

A

anticonvulsant that can reduce alcohol cravings; potentiates GABA and inhibits glutamate receptors

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23
Q

2 long-term complications of OH abuse

A 
Wernicke's encephalopathy (ACUTE)
Korsakoff syndrome (CHRONIC)
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24
Q

Wernicke’s encephalopathy

  • features?
  • cause?
  • how to reverse?
A

broad-based/stumbling ataxia, confusion, nystagmus, gaze palsies

B1 deficiency

reverse with thiamine followed by glucose

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25
Q

Korsakoff syndrome

- features?

A

retrograde/anterograde amnesia with compensatory confabulation

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26
Q

What is confabulation?

A

unconsciously making up answers when memory has failed

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27
Q

Cocaine MoA

A

blocks dopamine reuptake from synaptic cleft, causing a stimulant effect as well as behavioral reinforcement “reward”

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28
Q

How can cocaine OD cause death and why? 4

A

cocaine has severe vasoconstrictive effects :

cardiac arrhythmias/chest pain
cardiomyopathies
MI
stroke
TIAs
seizures (status epilpeticus)
respiratory depression
tactile hallucinations
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29
Q

What type of hallucinations do cocaine cause?

A

tactile hallucinations

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30
Q

Cocaine intoxication effects

A

cocaine is an indirect sympathomimentic, therefore intoxication mimics the flight/fight response:

euphoria
heightened self-esteem
autonomic instability (tachycardia, HTN)
DILATED pupils
weight loss
psychomotor ∆s
chills
sweating
nausea
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31
Q

treatment of cocaine mild-moderate intoxication? severe?

A

mild-moderate agitation/anxiety: benzos

severe agitation/psychosis: antipsychotics (haloperidol)

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32
Q

why is it that cocaine is often accompanied by other substance use d/o (ie opiates, OH)?

A

because these are often used to temper the irritability and hyper-vigilance that can follow cocaine intoxication and withdrawal

33
Q

cocaine withdrawal effects

A

CRASH (post-intoxication depression)

  • malaise, fatigue,
  • hypersomnolence
  • depression
  • hunger
  • constricted PUPILS
  • vivid dreams
  • psychomotor ∆s
  • dysphoric
  • suicidal
34
Q

how long does it take for cocaine withdrawal symptoms to resolve? how long does it take to clear from the body?

A

within 18 hours

clears within 3 days

35
Q

Classic Amphetamines MoA
Designer Amphetamines MoA

clinical use for both

A

Classic: blocks reuptake/facilitates release of DA and NE –> stimulant
Clinical use: ADHD, narcolepsy, depressive d/o

Designer: release DA, NE, 5HT
Use: dance clubs, raves

36
Q

classic amphetamines?

A

dextroamphetamine
methylphenidate
methamphetamine

37
Q

designer amphetamines?

A

MDMA (Ecstasy)

MDEA (Eve)

38
Q

signs of amphetamine abuse

A 
dilated pupils
INCREASED libido
perspiration 
respiratory depression
chest pain
39
Q

chronic amphetamine use can result in these 2 things

A

Acne
Accelerated tooth decay (“meth mouth”) - due to decreased saliva production in conjunction with increased cravings for sugar

40
Q

signs of amphetamine intoxication

A

similar to that of cocaine intoxication:

  • tachycardia, arrhythmias
  • HTN
  • pupil DILATION
  • diaphoresis
  • chills
  • N/V
  • CP
  • respiratory depression
  • muscle weakness/dystonia/dyskinesia
  • weight loss due to decreased appetite
  • confusion
  • seizures/coma
41
Q

signs of amphetamine withdrawal

A

prolonged depression/dysphoria
fatigue /increased need for sleep
psychomotor slowing
INCREASED appetite

42
Q

3 signs of amphetamine overdose

A

hyperthermia
dehydration
rhabdomyolysis (renal failure)

43
Q

Phencyclidine (PCP) MoA

A

antagonizes NMDA receptors + activates dopaminergic neurons

44
Q

Ketamine is similar to what other drug? what kind of effects does it produce?

A

PCP, but less potent

produces tachycardia, tachypnea, hallucinations, amnesia

45
Q

What is the PCP triad of intoxication? (earliest signs)

A

early signs: nystagmus, muscle rigidity, numbness

46
Q

Other signs of PCP intoxication

A

early signs: nystagmus, muscle rigidity, numbness

agitation, impaired judgement, assaultiveness, high tolerance to pain, ataxia, depersonalization, tactile and visual hallucinations, synesthesia, impaired speech, HTN, tachycardia

47
Q

Lab signs of PCP intoxication

A

elevated creatine phosphokinase + AST

48
Q

treatment for PCP intoxication

A

benzodizepines (lorazepam) - agitation, anxiety, muscle spasms, seizures

antipsychotics (haloperidol) - severe agitation or psychotic sx

49
Q

PCP withdrawal effects

A

flashbacks

50
Q

what do cocaine and PCP intoxication both have in common

A

tactile + visual hallucinations

51
Q

what is the problem with using typical antipsychotics in PCP intoxication? 4

A

increased risk of PCP-induced hyperthermia, dystonia, anti-cholinergic reactions, and decreased seizure threshold

-> use atypicals instead

52
Q

2 sedative hypnotics that are commonly abused

what is their MoA and common clinical use?

A

benzodiazepines (BDZ) - increase frequency of Cl channel opening
-> anxiety d/o

barbiturates - increase duration of Cl channel opening
-> epilepsy, anesthesia effects

53
Q

intoxication with sedative-hypnotics (benzos and barbiturates) can result in these sx

A

drowsiness, confusion, impaired judgement
nystagmus, slurred speech, incoordination, ataxia
mood lability
hypotension, RESPIRATORY DEPRESSION
coma, death

confused, wobbly, low vitals

54
Q

what can exacerbate sedative-hypnotics?

A

when EtOH or opioids are used in conjunction, as these can result in synergistic effects on the symptoms

55
Q

treatment for barbiturate OD

A

NaHCO3 - alkalinizes urine to promote renal excretion

56
Q

treatment for benzodiazepine OD

precautionary warnings associated with this treatment

A

flumazenil - short acting BDZ antagonist; can precipitate seizures when treating OD

57
Q

what is so concerning about sedative-hypnotics withdrawal?

A

tonic clonic seizures may result; life threatening (in general, withdrawal from sedating drugs is life-threatening due to compensatory hyperactivity, while withdrawal from stimulants is not)

58
Q

treatment for sedative-hypnotics OD/withdrawal in general?

A

Benzodiazepine TAPER +/- carbamazepine/valproic acid taper for seizure prophylaxis

59
Q

common opioid in cough syrup?

A

dextromethorphan

60
Q

opioid MoA

A

stimulates opiate receptors (µ, k, ∂) -> analgesia, sedation, dependence

effects on dopaminergic system -> addiction, reward

61
Q

serotonin syndrome can result if these recreational drugs are combined with antidepressants

amphetamines
opioids

A

amphetamines + SSRI

opioids + meperidine OR MAOi

62
Q

opioid intoxication sx

A 
N, V
drowsiness, sedation
decreased pain perception
decreased GI motility -> constpation
pupil constriction
seizures
respiratory depression -> coma, death
63
Q

treatment in opioid OD

A

1) naloxone or naltrexone (opioid antagonist) - can precipitate severe withdrawal
2) clonidine - treatment of moderate withdrawal sx
3) NSAIDs - muscle pain/cramps
4) diclyclomine - abdominal cramps

64
Q

opioid withdrawal sx

A 
lacrimation, rhinorrhea, sweating
dilated pupils
yawning
piloerection (goosebumps)
altered vitals: fever, HTN, tachycardia
N, V, abd cramps
arthralgia, myalgia
cravings
65
Q

treatment in opioid dependence 3

A

methadone
buprenorphine
naltrexone

66
Q

methadone MoA

ADR

A

long-acting opioid-R agonist
ADR: QT prolongation
best for opioid-dependent pregnant women

67
Q

buprenorphine MoA

ADR

A

partial opioid-R agonist

present in SUBOXONE (buprenorphine + naloxone)

68
Q

what is naloxone? where can it be found? what is the purpose of adding this to buprenorphine?

A

competitive µ receptor antagonist – rapidly blocks the effects of other opioids (heroin, cocaine) and produces rapid onset of withdrawal symptoms

Naloxone is not active when taken PO, so withdrawal symptoms occur only if injected (lower abuse potential)!

found in suboxone (buprenorphine + naloxone)

69
Q

how can you quickly tell if someone has opioid overdose?

A

give IV naloxone - rapid recovery of consciousness is consistent with opioid OD

70
Q

T/F hallucinogens (LSD) do not cause physical dependence or withdrawal

A

TRUE

71
Q

sx of hallucinogens (LSD) intoxication

A 
perceptual changes (illusions, hallucinations, distorted body image, synesthesia)
dilated pupils
palpitations, tachycardia
HTN
hyperthermia
tremors
incoordination
72
Q

sx of hallucinogens (LSD) withdrawal

A

flashbacks later in life

73
Q

sx of marijuana intoxication

A 
*euphoria*
conjunctival injection
dry mouth, increased appetite
mild tachycardia, anxiety
perceptual disturbances
impaired motor coordination
74
Q

sx of marijuana withdrawal

A 
irritability, anxiety
insomnia, restlessness
strange dreams
depression
HA, sweating
N, cravings
decreased appetite
75
Q

caffeine MoA

A

adenosine antagonist, which results in increased cAMP + stimulant effect via dopaminergic system

76
Q

3 Rx that is used for treatment of nicotine dependence

A

1) varenicline (chantix)
2) bupropion (zyban)
3) nicotine replacement therapy (transdermal patch, gum)

77
Q

varenicline (chantix) - MoA and clinical use

A

partial agonist of nAChR (nicotinic cholinergic receptor) -> prevents withdrawal sx

78
Q

bupropion (zyban) - MoA and clinical use

A

antidepressant

partial agonist at nAChR + inhibitor of Dopamine uptake -> reduces withdrawal sx

Psychiatry (12 decks)

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