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Psychiatry > Substance-related disorders > Flashcards

Substance-related disorders Flashcards

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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
Korsakoff syndrome | - features?
retrograde/anterograde amnesia with compensatory confabulation
26
What is confabulation?
unconsciously making up answers when memory has failed
27
Cocaine MoA
blocks dopamine reuptake from synaptic cleft, causing a stimulant effect as well as behavioral reinforcement "reward"
28
How can cocaine OD cause death and why? 4
cocaine has severe vasoconstrictive effects : ``` cardiac arrhythmias/chest pain cardiomyopathies MI stroke TIAs seizures (status epilpeticus) respiratory depression tactile hallucinations ```
29
What type of hallucinations do cocaine cause?
tactile hallucinations
30
Cocaine intoxication effects
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 ```
31
treatment of cocaine mild-moderate intoxication? severe?
mild-moderate agitation/anxiety: benzos | severe agitation/psychosis: antipsychotics (haloperidol)
32
why is it that cocaine is often accompanied by other substance use d/o (ie opiates, OH)?
because these are often used to temper the irritability and hyper-vigilance that can follow cocaine intoxication and withdrawal
33
cocaine withdrawal effects
CRASH (post-intoxication depression) - malaise, fatigue, - hypersomnolence - depression - hunger - constricted PUPILS - vivid dreams - psychomotor ∆s - dysphoric - suicidal
34
how long does it take for cocaine withdrawal symptoms to resolve? how long does it take to clear from the body?
within 18 hours clears within 3 days
35
Classic Amphetamines MoA Designer Amphetamines MoA clinical use for both
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
classic amphetamines?
dextroamphetamine methylphenidate methamphetamine
37
designer amphetamines?
MDMA (Ecstasy) | MDEA (Eve)
38
signs of amphetamine abuse
``` dilated pupils INCREASED libido perspiration respiratory depression chest pain ```
39
chronic amphetamine use can result in these 2 things
Acne Accelerated tooth decay ("meth mouth") - due to decreased saliva production in conjunction with increased cravings for sugar
40
signs of amphetamine intoxication
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
signs of amphetamine withdrawal
prolonged depression/dysphoria fatigue /increased need for sleep psychomotor slowing INCREASED appetite
42
3 signs of amphetamine overdose
hyperthermia dehydration rhabdomyolysis (renal failure)
43
Phencyclidine (PCP) MoA
antagonizes NMDA receptors + activates dopaminergic neurons
44
Ketamine is similar to what other drug? what kind of effects does it produce?
PCP, but less potent produces tachycardia, tachypnea, hallucinations, amnesia
45
What is the PCP triad of intoxication? (earliest signs)
early signs: nystagmus, muscle rigidity, numbness
46
Other signs of PCP intoxication
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
Lab signs of PCP intoxication
elevated creatine phosphokinase + AST
48
treatment for PCP intoxication
benzodizepines (lorazepam) - agitation, anxiety, muscle spasms, seizures antipsychotics (haloperidol) - severe agitation or psychotic sx
49
PCP withdrawal effects
flashbacks
50
what do cocaine and PCP intoxication both have in common
tactile + visual hallucinations
51
what is the problem with using typical antipsychotics in PCP intoxication? 4
increased risk of PCP-induced hyperthermia, dystonia, anti-cholinergic reactions, and decreased seizure threshold -> use atypicals instead
52
2 sedative hypnotics that are commonly abused | what is their MoA and common clinical use?
benzodiazepines (BDZ) - increase frequency of Cl channel opening -> anxiety d/o barbiturates - increase duration of Cl channel opening -> epilepsy, anesthesia effects
53
intoxication with sedative-hypnotics (benzos and barbiturates) can result in these sx
drowsiness, confusion, impaired judgement nystagmus, slurred speech, incoordination, ataxia mood lability hypotension, RESPIRATORY DEPRESSION coma, death confused, wobbly, low vitals
54
what can exacerbate sedative-hypnotics?
when EtOH or opioids are used in conjunction, as these can result in synergistic effects on the symptoms
55
treatment for barbiturate OD
NaHCO3 - alkalinizes urine to promote renal excretion
56
treatment for benzodiazepine OD | precautionary warnings associated with this treatment
flumazenil - short acting BDZ antagonist; can precipitate seizures when treating OD
57
what is so concerning about sedative-hypnotics withdrawal?
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
treatment for sedative-hypnotics OD/withdrawal in general?
Benzodiazepine TAPER +/- carbamazepine/valproic acid taper for seizure prophylaxis
59
common opioid in cough syrup?
dextromethorphan
60
opioid MoA
stimulates opiate receptors (µ, k, ∂) -> analgesia, sedation, dependence effects on dopaminergic system -> addiction, reward
61
serotonin syndrome can result if these recreational drugs are combined with antidepressants amphetamines opioids
amphetamines + SSRI opioids + meperidine OR MAOi
62
opioid intoxication sx
``` N, V drowsiness, sedation decreased pain perception decreased GI motility -> constpation pupil constriction seizures respiratory depression -> coma, death ```
63
treatment in opioid OD
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
opioid withdrawal sx
``` lacrimation, rhinorrhea, sweating dilated pupils yawning piloerection (goosebumps) altered vitals: fever, HTN, tachycardia N, V, abd cramps arthralgia, myalgia cravings ```
65
treatment in opioid dependence 3
methadone buprenorphine naltrexone
66
methadone MoA | ADR
long-acting opioid-R agonist ADR: QT prolongation *best for opioid-dependent pregnant women*
67
buprenorphine MoA | ADR
partial opioid-R agonist present in SUBOXONE (buprenorphine + naloxone)
68
what is naloxone? where can it be found? what is the purpose of adding this to buprenorphine?
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
how can you quickly tell if someone has opioid overdose?
give IV naloxone - rapid recovery of consciousness is consistent with opioid OD
70
T/F hallucinogens (LSD) do not cause physical dependence or withdrawal
TRUE
71
sx of hallucinogens (LSD) intoxication
``` perceptual changes (illusions, hallucinations, distorted body image, synesthesia) dilated pupils palpitations, tachycardia HTN hyperthermia tremors incoordination ```
72
sx of hallucinogens (LSD) withdrawal
flashbacks later in life
73
sx of marijuana intoxication
``` *euphoria* conjunctival injection dry mouth, increased appetite mild tachycardia, anxiety perceptual disturbances impaired motor coordination ```
74
sx of marijuana withdrawal
``` irritability, anxiety insomnia, restlessness strange dreams depression HA, sweating N, cravings decreased appetite ```
75
caffeine MoA
adenosine antagonist, which results in increased cAMP + stimulant effect via dopaminergic system
76
3 Rx that is used for treatment of nicotine dependence
1) varenicline (chantix) 2) bupropion (zyban) 3) nicotine replacement therapy (transdermal patch, gum)
77
varenicline (chantix) - MoA and clinical use
partial agonist of nAChR (nicotinic cholinergic receptor) -> prevents withdrawal sx
78
bupropion (zyban) - MoA and clinical use
antidepressant | partial agonist at nAChR + inhibitor of Dopamine uptake -> reduces withdrawal sx

Psychiatry (12 decks)

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