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PT2 Psyche 1-6 > substance abuse pharmacology > Flashcards

substance abuse pharmacology Flashcards

1
Q

substance misuse

A

consumption of a substance for purposes different from what is medically recommended

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2
Q

substance abuse

A

maladaptive pattern of substance use leading to clinical impairment or distress, characterized by at least one of:

  • failure to fulfill major role obligations
  • recurrent use in situations which it is physically hazardous
  • substance-related legal problems
  • use despite problems caused or exacerbated by the substance
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3
Q

substance dependence

A

maladaptive pattern of substance use leading to clinical impairment or distress, characterized by at least three of:

  • tolerance
  • compulsive use
  • impaired control/relapse
  • craving
  • socio-occupational dysfunction
  • persistent use despite psychophysical harm
  • withdrawal
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4
Q

addiction

A

psychological compulsion towards a substance

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5
Q

environmental factors contributing to abuse/dependence

A
  • low socioeconomic status
  • early physical or sexual abuse
  • social deprivation
  • witnessing violence
  • peer pressure
  • cultural norms
  • drug availability
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6
Q

individual factors contributing to abuse/dependence

A
  • genetics
  • poor impulse control
  • anxiety and depression
  • other neuropsychiatric comorbidities
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7
Q

3 ways comorbid conditions can be tied to substance abuse

A
  1. self medication with the substance to relieve syptoms of the mental illness
  2. causal effects of substance use may increase mental illness
  3. risk factors for mental illness and substance abuse may overlap
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8
Q

how to diagnose comorbid mental disorders with substance abuse

A

patient must be abstinent for 2-3 weeks before mental disorder symptoms can be evaluated

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9
Q

role of ventral tegmental area

A

release dopamine at amygdala, prefrontal cortex, and nucleus accumbens

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10
Q

amygdala governs

A

avoidance and fear

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11
Q

prefrontal cortex governs

A

decision making and behavioral control

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12
Q

nucleus accumbens governs

A

reward and salience

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13
Q

the response to environmental stimuli is ultimately governed by

A

dopaminergic systems

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14
Q

how does habit formation occur

A

natural stimuli needed for the survival of the organism and species are coupled with rewarding responses which when repeatedly activated lead to repetition of behavior

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15
Q

what system is involved in habit formation

A

dopaminergic mesolimibic system

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16
Q

the perception of natural reward comes from

A

phasic release of dopamine in the nucleus accumbens

-tolerance can develop

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17
Q

role of the amygdala

A

processing of fear and information related to danger and other emotional responses

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18
Q

cravings originated from what part of the brain

A

amygdala

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19
Q

drug seeking behavior is driven by

A

nucleus accumbens

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20
Q

hypofunction of prefrontal cortex facilitates rewarding response by

A
  • poor impulse control and problems in decision making

- facilitating activation of amygdala and nucleus accumbens

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21
Q

tolerance

A

time dependent reduction in responsiveness to the same dose of a substance

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22
Q

release of corticotrophin releasing hormone/factor causes

A
  • activation of stress response
  • increase of heart rate and blood pressure
  • activation of amygdala and cravings
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23
Q

2 types of triggers for cravings

A
  • cues linked to specific locations/times controlled by hippocampus
  • stress triggers release of CRF and norepinephrine leading to amygdala activation
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24
Q

how long must a person be off a substance to reduce risk of relapse

A

about 7 years

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25
Q

stages of dependence

A
  1. binge/intoxication
  2. withdrawal/negative effects
  3. preoccupation (no money, arrest, overdose)
  4. abstinence/treatment
  5. relapse
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26
Q

non-specific mechanisms of action of ethanol

A
  • enhances membrane fluidity

- inhibits numerous proteins and enzymes

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27
Q

specific mechanisms of action of ethanol

A
  • enhances GABA-A receptor function
  • inhibits NMDA receptors
  • activates 5-HT3 receptors (stimulates vomiting)
  • may inhibit GABA-B receptors
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28
Q

who is at greatest risk of alcoholism

A

anxious and depressed patients

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29
Q

absorption of ethanol

A

rapidly absorbed from small intestine and colon

  • maximal blood concentration in 30-90 minutes
  • absorbed through lungs and skin
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30
Q

distribution of ethanol

A
  • distributed uniformly in tissues and body fluids

- readily crosses placenta and BBB

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31
Q

metabolism of ethanol

A

mostly done by alcohol dehydrogenase which converts ethanol into acetaldehyde, which is where the headache, hypotension, and N/V come from
acetaldehyde is metabolized by aldehyde dehydrogenase

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32
Q

elimination of ethanol is not

A

concentration dependent and is thus zero order

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33
Q

alcohol concentration associated with respiratory depression and death

A

> 400 mg/dl

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34
Q

treatment of acute alcohol intoxication

A
  • gastric lavage
  • endotracheal intubation
  • rebalance of electrolytes
  • infusion of thiamine THEN glucose (to avoid making acidosis worse)
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35
Q

neuropsychiatric effects of chronic alcohol consumption

A

Wernike’s encephalopathy and korsakoff syndrome

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36
Q

GI effects of chronic alcohol

A
  • anemia
  • esophageal cancer
  • vitamin and protein deficiency
  • cirrhosis
  • acute pancreatitis
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37
Q

symptoms of alcohol withdrawal

A
  • motor agitation
  • anxiety
  • insomnia
  • reduction of seizure threshold
  • delirium tremens (delirium, agitation)
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38
Q

treatment options for seizures in alcohol withdrawal

A

long acting benzos like chlordizepoxide and diazepam

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39
Q

thiamine deficiency leads to

A
  • accumulation of pyruvic acid and acidosis

- impairment of krebs cycle and reduced ATP synthesis

40
Q

cause of beriberi

A

thiamine deficiency

41
Q

dry beriberi

A

neurological signs and symptoms

42
Q

wet beriberi

A

CV signs and symptoms

43
Q

wernicke-korsakoff syndrome is caused by

A

thiamine deficiency in alcoholism

44
Q

wernicke’s encephalopathy symptoms

A
  • confusion
  • cerebellar ataxia
  • ophthalmoplegia
45
Q

korsakoff syndrome symptoms

A
  • psychosis
  • loss of short term memory
  • rhythmical to-and-fro motion of eyeballs
46
Q

disulfiram MoA

A

blocks aldehyde dehydrogenase

aversive therapy, makes patient have all the negative symptoms

47
Q

drugs to use in alcoholism

A

disulfiram
naltrexone
acamprosate

48
Q

acamprosate MoA

A
  • GABA-A activator and NMDA blocker

- substitution effect

49
Q

avoid acamprosate in who

A

those with renal impairment

50
Q

avoid naltrexone in who

A

opiate dependent patients

51
Q

when to use ethanol as an antidote

A

for methanol or ethylene poisoning

52
Q

methanol gets converted into

A

formic acid which is highly toxic

53
Q

properties of inhalants

A

very similar to alcohol

54
Q

activation of opioid receptors causes

A
  • increase in K efflux

- decrease in Ca influx

55
Q

rate at which opioids undergo tolerance

A

very rapidly

56
Q

central effects of opioids

A
  • sedation
  • respiratory depression
  • antitussive
  • N/V
  • epileptogenesis
  • temperature regulation
  • miosis
  • motor tone
57
Q

mechanism of opioid respiratory depression

A
  • depressed rhythm generation

- desensitization of brainstem chemoreceptors which normally respond to increasing PCO2

58
Q

neuroendocrine effects of opioids

A
  • decrease in adrenal hormones
  • decrease in gonadal hormones
  • increase in prolactin
  • these do not undergo tolerance*
59
Q

CV effects of opioids

A
  • peripheral vasodilation and orthostatic hypotension
  • histamine release
  • reduces cardiac work and oxygen consumption
60
Q

acute administration of opioids can induce what CV effects

A

arrhythmias and hypovolemic shock

61
Q

opioid effects that undergo tolerance

A
  • euphoria
  • analgesia and sedation
  • respiratory depression
62
Q

signs of opioid withdrawal

A
  • diaphoresis
  • rhinorrhea
  • lacrimation
  • insomnia
  • diarrhea
63
Q

triad of symptoms associated with opoid overdose

A

coma
pinpoint pupils
depressed respiration

64
Q

treatment of opioid overdose

A
  • ventilatory support

- IV naloxone

65
Q

mechanism of cocaine

A

blocks dopamine transporter which causes more dopamine to be available in nucleus accumbens

66
Q

symptoms of cocaine withdrawal

A
  • depression
  • fatigue
  • vivid and disturbing dreams
  • sleep disturbances
  • irritability
  • increased appetite and weight gain
  • cravings for a long time
67
Q

effects of methamphetamine

A
  • high blood pressure
  • chest pain
  • rapid heart rate
  • heart attack
  • grinding teeth
68
Q

bath salts

A
  • cathinone
  • methcathinone
  • mephedrone
  • MDPV
69
Q

methylenedioxymethamphetamine (MDMA) characteristics

A
  • amphetamine derivative with greater action on serotonin transporter
  • causes relaxed euphoric state with no hallucinations
70
Q

caffeine MoA

A

A2A adenosine receptor antagonist which makes the body think there is lots of ATP, increasing activity of neurons and other cells

71
Q

main receptor involved in nicotine dependence

A

alpha-4-beta-2

72
Q

nicotine MoA

A

mimics effects of acetylcholine and directly activates dopamine cells

73
Q

withdrawal symptoms of nicotine

A

irritability
restlessness
increased appetite
decreased heart rate

74
Q

lethal dose of nicotine

A

50-60 mg

75
Q

signs of nicotine overdose

A
  • paralysis and coma

- arrhythmia and respiratory failure

76
Q

treatment of nicotine poisoning

A
  • activated charcoal and GI evacuation
  • IV benzo for seizure management
  • respiratory support
77
Q

pharmacological therapy for nicotine dependence

A
  • bupropion-DA and NE reuptake inhibitor
  • varenicline - partial nicotinic agonist
  • clonidine - counters autonomic effects
78
Q

adverse effects of partial nicotinic receptor agonist

A

insomnia
headache
nausea

79
Q

hallucinogens dependence and withdrawal risk

A

very low

80
Q

mechanisms of hallucinogens

A
  • stimulation of 5-HT2a/2c receptors (LSD)
  • NMDA antagonist (phencyclidine aka PCP)
  • muscarinic antagonist (scopoloamine)
  • selective kappa opioid activation (salvinorin)
81
Q

hallucinogen that doesn’t cause memory loss of the event

A

salvinorin

82
Q

effects of phencyclidine

A
  • schizophrenia-like manifestations
  • violent behavior
  • increased HR
  • increased BP and temp
  • decreased pain sensation
  • risk of suicide
83
Q

psychoactive ingredient of cannabis

A

THC

84
Q

THC MoA

A

partial agonist of cannabinoid CB1 and CB2 receptors

85
Q

CB1 receptors control

A 
memory
thought processing
perception
movement
*all impaired by THC*
86
Q

CB2 receptors are found where

A

immune cells

THC is anti-inflammatory

87
Q

endocannabinoids

A

anandamide

2-arachydonoyl-glycerol (2-AG)

88
Q

endocannabinoids MoA

A

reduce GABA and glutamate release through retrograde activation of presynaptic CB1 receptors

89
Q

main retrograde system for homeostatic control in CNS

A

depolarization-induced suppression of inhibition/excitation (for GABA/glutamate)

90
Q

synthesis of endocannabinoids

A

stimulation of postsynaptic neurons causes the synthesis of anandamide and 2-AG; typically after CB1 and CB2 receptors are activated the endocannabinoids undergo reuptake in both terminals and are degraded

91
Q

cannabidiol MoA

A

FAAH inhibitor which prevents anandamide from being degraded and increases anandamide levels

92
Q

the reason cannabis does not lead to habit formation and physical dependence

A

the suppression of GABA and glutamate in the VTA has opposite effects on dopamine release

93
Q

behavioral effects of cannabis

A
  • short term memory impairment
  • altered preception
  • increased appetite
94
Q

other effects of cannabis

A
  • hypothermia
  • reduction of N/V
  • reduction of pain
95
Q

cognitive and psychosocial effects of cannabis with substantial evidence

A
  • learning, memory and attention impairment after acute use

- development of schizophrenia

96
Q

cognitive and psychosocial effects of cannabis with limited evidence

A
  • impaired academic achievement
  • impaired social functioning
  • learning, memory and attention deficits (after sustained abstinence)
97
Q

potential uses for cannabis

A
  • chronic pain
  • anti emetics
  • MS spasticity
  • short term sleep disturbances
  • decreasing weight loss with HIV/AIDS

PT2 Psyche 1-6 (6 decks)

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