substance abuse pharmacology Flashcards
(97 cards)
1
Q
substance misuse
A
consumption of a substance for purposes different from what is medically recommended
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
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
4
Q
addiction
A
psychological compulsion towards a substance
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
6
Q
individual factors contributing to abuse/dependence
A
- genetics
- poor impulse control
- anxiety and depression
- other neuropsychiatric comorbidities
7
Q
3 ways comorbid conditions can be tied to substance abuse
A
- self medication with the substance to relieve syptoms of the mental illness
- causal effects of substance use may increase mental illness
- risk factors for mental illness and substance abuse may overlap
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
9
Q
role of ventral tegmental area
A
release dopamine at amygdala, prefrontal cortex, and nucleus accumbens
10
Q
amygdala governs
A
avoidance and fear
11
Q
prefrontal cortex governs
A
decision making and behavioral control
12
Q
nucleus accumbens governs
A
reward and salience
13
Q
the response to environmental stimuli is ultimately governed by
A
dopaminergic systems
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
15
Q
what system is involved in habit formation
A
dopaminergic mesolimibic system
16
Q
the perception of natural reward comes from
A
phasic release of dopamine in the nucleus accumbens
-tolerance can develop
17
Q
role of the amygdala
A
processing of fear and information related to danger and other emotional responses
18
Q
cravings originated from what part of the brain
A
amygdala
19
Q
drug seeking behavior is driven by
A
nucleus accumbens
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
21
Q
tolerance
A
time dependent reduction in responsiveness to the same dose of a substance
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
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
24
Q
how long must a person be off a substance to reduce risk of relapse
A
about 7 years
25
stages of dependence
1. binge/intoxication
2. withdrawal/negative effects
3. preoccupation (no money, arrest, overdose)
4. abstinence/treatment
5. relapse
26
non-specific mechanisms of action of ethanol
- enhances membrane fluidity
| - inhibits numerous proteins and enzymes
27
specific mechanisms of action of ethanol
- enhances GABA-A receptor function
- inhibits NMDA receptors
- activates 5-HT3 receptors (stimulates vomiting)
- may inhibit GABA-B receptors
28
who is at greatest risk of alcoholism
anxious and depressed patients
29
absorption of ethanol
rapidly absorbed from small intestine and colon
- maximal blood concentration in 30-90 minutes
- absorbed through lungs and skin
30
distribution of ethanol
- distributed uniformly in tissues and body fluids
| - readily crosses placenta and BBB
31
metabolism of ethanol
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
32
elimination of ethanol is not
concentration dependent and is thus zero order
33
alcohol concentration associated with respiratory depression and death
>400 mg/dl
34
treatment of acute alcohol intoxication
- gastric lavage
- endotracheal intubation
- rebalance of electrolytes
- infusion of thiamine THEN glucose (to avoid making acidosis worse)
35
neuropsychiatric effects of chronic alcohol consumption
Wernike's encephalopathy and korsakoff syndrome
36
GI effects of chronic alcohol
- anemia
- esophageal cancer
- vitamin and protein deficiency
- cirrhosis
- acute pancreatitis
37
symptoms of alcohol withdrawal
- motor agitation
- anxiety
- insomnia
- reduction of seizure threshold
- delirium tremens (delirium, agitation)
38
treatment options for seizures in alcohol withdrawal
long acting benzos like chlordizepoxide and diazepam
39
thiamine deficiency leads to
- accumulation of pyruvic acid and acidosis
| - impairment of krebs cycle and reduced ATP synthesis
40
cause of beriberi
thiamine deficiency
41
dry beriberi
neurological signs and symptoms
42
wet beriberi
CV signs and symptoms
43
wernicke-korsakoff syndrome is caused by
thiamine deficiency in alcoholism
44
wernicke's encephalopathy symptoms
- confusion
- cerebellar ataxia
- ophthalmoplegia
45
korsakoff syndrome symptoms
- psychosis
- loss of short term memory
- rhythmical to-and-fro motion of eyeballs
46
disulfiram MoA
blocks aldehyde dehydrogenase
| aversive therapy, makes patient have all the negative symptoms
47
drugs to use in alcoholism
disulfiram
naltrexone
acamprosate
48
acamprosate MoA
- GABA-A activator and NMDA blocker
| - substitution effect
49
avoid acamprosate in who
those with renal impairment
50
avoid naltrexone in who
opiate dependent patients
51
when to use ethanol as an antidote
for methanol or ethylene poisoning
52
methanol gets converted into
formic acid which is highly toxic
53
properties of inhalants
very similar to alcohol
54
activation of opioid receptors causes
- increase in K efflux
| - decrease in Ca influx
55
rate at which opioids undergo tolerance
very rapidly
56
central effects of opioids
- sedation
- respiratory depression
- antitussive
- N/V
- epileptogenesis
- temperature regulation
- miosis
- motor tone
57
mechanism of opioid respiratory depression
- depressed rhythm generation
| - desensitization of brainstem chemoreceptors which normally respond to increasing PCO2
58
neuroendocrine effects of opioids
- decrease in adrenal hormones
- decrease in gonadal hormones
- increase in prolactin
* these do not undergo tolerance*
59
CV effects of opioids
- peripheral vasodilation and orthostatic hypotension
- histamine release
- reduces cardiac work and oxygen consumption
60
acute administration of opioids can induce what CV effects
arrhythmias and hypovolemic shock
61
opioid effects that undergo tolerance
- euphoria
- analgesia and sedation
- respiratory depression
62
signs of opioid withdrawal
- diaphoresis
- rhinorrhea
- lacrimation
- insomnia
- diarrhea
63
triad of symptoms associated with opoid overdose
coma
pinpoint pupils
depressed respiration
64
treatment of opioid overdose
- ventilatory support
| - IV naloxone
65
mechanism of cocaine
blocks dopamine transporter which causes more dopamine to be available in nucleus accumbens
66
symptoms of cocaine withdrawal
- depression
- fatigue
- vivid and disturbing dreams
- sleep disturbances
- irritability
- increased appetite and weight gain
- cravings for a long time
67
effects of methamphetamine
- high blood pressure
- chest pain
- rapid heart rate
- heart attack
- grinding teeth
68
bath salts
- cathinone
- methcathinone
- mephedrone
- MDPV
69
methylenedioxymethamphetamine (MDMA) characteristics
- amphetamine derivative with greater action on serotonin transporter
- causes relaxed euphoric state with no hallucinations
70
caffeine MoA
A2A adenosine receptor antagonist which makes the body think there is lots of ATP, increasing activity of neurons and other cells
71
main receptor involved in nicotine dependence
alpha-4-beta-2
72
nicotine MoA
mimics effects of acetylcholine and directly activates dopamine cells
73
withdrawal symptoms of nicotine
irritability
restlessness
increased appetite
decreased heart rate
74
lethal dose of nicotine
50-60 mg
75
signs of nicotine overdose
- paralysis and coma
| - arrhythmia and respiratory failure
76
treatment of nicotine poisoning
- activated charcoal and GI evacuation
- IV benzo for seizure management
- respiratory support
77
pharmacological therapy for nicotine dependence
- bupropion-DA and NE reuptake inhibitor
- varenicline - partial nicotinic agonist
- clonidine - counters autonomic effects
78
adverse effects of partial nicotinic receptor agonist
insomnia
headache
nausea
79
hallucinogens dependence and withdrawal risk
very low
80
mechanisms of hallucinogens
- stimulation of 5-HT2a/2c receptors (LSD)
- NMDA antagonist (phencyclidine aka PCP)
- muscarinic antagonist (scopoloamine)
- selective kappa opioid activation (salvinorin)
81
hallucinogen that doesn't cause memory loss of the event
salvinorin
82
effects of phencyclidine
- schizophrenia-like manifestations
- violent behavior
- increased HR
- increased BP and temp
- decreased pain sensation
- risk of suicide
83
psychoactive ingredient of cannabis
THC
84
THC MoA
partial agonist of cannabinoid CB1 and CB2 receptors
85
CB1 receptors control
```
memory
thought processing
perception
movement
*all impaired by THC*
```
86
CB2 receptors are found where
immune cells
| *THC is anti-inflammatory*
87
endocannabinoids
anandamide
| 2-arachydonoyl-glycerol (2-AG)
88
endocannabinoids MoA
reduce GABA and glutamate release through retrograde activation of presynaptic CB1 receptors
89
main retrograde system for homeostatic control in CNS
depolarization-induced suppression of inhibition/excitation (for GABA/glutamate)
90
synthesis of endocannabinoids
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
cannabidiol MoA
FAAH inhibitor which prevents anandamide from being degraded and increases anandamide levels
92
the reason cannabis does not lead to habit formation and physical dependence
the suppression of GABA and glutamate in the VTA has opposite effects on dopamine release
93
behavioral effects of cannabis
- short term memory impairment
- altered preception
- increased appetite
94
other effects of cannabis
- hypothermia
- reduction of N/V
- reduction of pain
95
cognitive and psychosocial effects of cannabis with substantial evidence
- learning, memory and attention impairment after acute use
| - development of schizophrenia
96
cognitive and psychosocial effects of cannabis with limited evidence
- impaired academic achievement
- impaired social functioning
- learning, memory and attention deficits (after sustained abstinence)
97
potential uses for cannabis
- chronic pain
- anti emetics
- MS spasticity
- short term sleep disturbances
- decreasing weight loss with HIV/AIDS
