Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Nervous System IV > Pharmacology of Reward & Addiction > Flashcards

Pharmacology of Reward & Addiction Flashcards

1
Q

Rapidity of onset of drug action by MOA

A

Inhalation > IV > Insufflation > Oral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pharmacokinetic properties affecting addictive liability

A

Rapidity of onset of action: Inhalation > IV > Insufflation > Oral

Half life: Short > Long

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Cocaine - Mechanism

A

Inhibits dopamine reuptake by blocking DAT
Also blocks SERT and NET

Relative risk of addiction = 5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Methamphetamine - Mechanism

A

Inhibits dopamine reuptake and increases DA release by reversing DAT
Also blocks SERT and NET

Relative risk of addiction = 5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Nicotine - Mechanism

A

Agonist at nicotinic receptor

Relative risk of addiction = 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

MDMA - Mechanism

A

Phenylethylamine class of hallucinogens

Blocks and reverses SERT causing decreased 5HT re-uptake as well as 5HT release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Hallucinogens - Mechanism

A

5HT2A receptor partial agonist

Relative risk of addiction = 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Dissociative Anesthetics - Agents & Mechanism

A

NMDA receptor antagonists; also block reuptake of DA and 5HT

PCP
Ketamine
Dextromethorphan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Opioid mechanism & Reinforcing effects

A

Agonist at endogenous mu opioid receptors
Release of histamine

Cause euphoria, analgesia, sedation, anxiety reduction, and warm flushing of the skin (“rush”)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Opioid tolerance

A

High levels of tolerance develop to euphoria, respiratory depression, analgesia, sedation, and nausea

Little tolerance develops to constipation or pupillary constriction

Withdrawal symptoms develop after 1-2 weeks of daily use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Treatment for opiate withdrawal

A

Clonidine (alpha-2 agonist) alleviates symptoms of sympathetic overactivity (nausea/vomiting, cramps, sweating, tachycardia)

Methadone / Buprenorphine via cross-tolerance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Mechanism of CNS Depressants

A

All classes act to facilitate GABA activity at Cl- receptors

Barbituates and EtOH also decrease glutamate activity at higher doses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

CNS Depressant Overdose - Presentation & Treatment

A

Confusion, emotional lability, depressed reflexes, respiratory depression, hypotension, coma, death

Treatment:
Benzos: Flumazenil (specific receptor antagonist)
Alcohol: Thiamine + glucose + electrolytes
All: Cardiopulmonary support, IV fluids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

CNS depressant withdrawal syndrome

A

Rebound hyperexcitability of the CNS including insomnia, anxiety, sweating, nausea/vomiting, grand mal seizures, fever, delirium, psychosis, death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

CNS stimulant toxicity - Presentation and Treatment

A

PNS sympathetic overactivity: tachycardia, hypertension, hyperthermia, sweating, psychomotor agitation, angina, MI, arrhythmias, stroke, paranoid psychosis

Treatment: Diazepam for seizures, vasodilatos (Phentolamine) to reduce BP, Haloperidol for overt psychosis
Supportive: Cardiopulmonary support, control of fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

CNS Stimulants - Tolerance and Withdrawal

A

Tolerance develops to anorexia, euphoria, and hyperthermia; supersensitivity may develop to psychomotor effects and paranoia

Withdrawal is mild and includes fatigue, depression; if severe, may be treated with TCADs/Buproprion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Nicotine toxicity

A

60mg = fatal dose

Toxicity presents as nausea/vomiting, abdominal pain, salivation, diarrhea, headache, hypotension, irregular pulse, convulsions, and death by respiratory failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Nicotine - Tolerance and withdrawal

A

Tolerance develops to euphoric effects and nausea

Withdrawal characterized by irritability, depressed mood, difficulty concentrating, restlessness, increased appetite/weight gain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Nicotine replacement therapy

A

Peak nicotine blood levels are lower than with smoking, so withdrawal symptoms are suppressed without production of the same euphoric effects

20% abstinence rate at 12 months

20
Q

Zyban

A

i.e. Buproprion XR

Current treatment of choice for nicotine addiction when combined with NRT

21
Q

Chantix

A

Aka Varenicline

Partial agonist at nicotine receptors; eases withdrawal symptoms and blocks euphoric CNS effects of smoking when users continue to smoke

22
Q

Indoleamines

A

Class of hallucinogenic drugs which act as 5HT2A partial agonists, causing altered perception

LSD
DMT
Psilocybin

23
Q

MDMA Toxicity and Treatment

A

Anxiety, dissociation, depersonalization, paranoid, confusion, palpitations, hypertension, hyperthermia, convulsions

Treatment:
Benzodiazepines for severe anxiety/panic
Antipsychotics for hallucinations

24
Q

PCP Toxicity & Treatment

A

Delirium, tachypnea, hypertension, tachycardia, hyperthermia, muscle rigidity (rhabdomyolysis), coma, seizures, death from cardiopulmonary failure

Also presents with belligerence, agitation, violence, and psychosis

Treatment: Phentolamine or hyralazine for hypertension, Diazepam for convulsions, antipsychotics for hallucinations

25
Q

Inhalants

A

All classes are lipid-soluble organic compounds, i.e. glues and adhesives, aerosols, cleaning solutions, paint thinners, fuels

Mechanism: CNS depression causing euphoria, giddiness, light headedness, and disinhibition

26
Q

Anticholinergic agents

A

i.e. Benzotropine, Scopolamine, Atropine, Datura

Block mAChRs - can cause mood elevation, hallucination, deliriu

Acute toxicity - Disorientation/delirium, memory impairment, dry mouth, unreactive pupils

Treatment: Physostigmine (AChEI)

27
Q

Absorption & Distribution of EtOH

A

Rapid absorption; presence of food in GI tract slows absorption by delaying passage to small intestine, where absorption is greatest

Distributes into total body water with greatest equilibration in well-vascularized organs; less distribution to fat than water, so women develop more highly concentrated BAC than men

28
Q

Major pathway of EtOH metabolism

A

EtOH is converted to acetaldehyde by alcohol dehydrogenase; acetaldehyde is converted to acetic acid by acetaldehyde dehydrogenase

0 order kinetics - metabolism occurs at a constant rate of 7-10 g/hour corresponding to a BAC reduction of 0.02/hour

29
Q

What underlies the alcohol flushing reaction?

A

Some Asian sub-populations have high rates of mutations in the high affinity form of acetaldehyde dehydrogenase; this causes excess accumulation of acetaldehyde, which is responsible for the flushing reaction

30
Q

Antabuse - Mechanism

A

Inhibits aldehyde dehydrogenase; results in 5-10X increase in acetaldehyde levels causing headache, nausea, vomiting, orthostatic hypotension, and convulsions

31
Q

Minor pathway of EtOH metabolism

A

Accounts for 10-25% of ethanol metabolism at higher BACs

Ethanol is converted to acetaldehyde by CYP450-2EI (mixed function oxidase); acetaldehyde is converted to acetic acid by aldehyde oxidase

Induction of this pathway by ethanol increases metabolism of acetaminophen to hepatotoxic metabolites

32
Q

What is the role of NAD/NADH in alcohol metabolism and metabolic disruptions associated with EtOH abuse?

A

Alcohol dehydrogenase requires NAD as a cofactor in the metabolism of EtOH to acetaldehyde, generating NADH; NADH must be re-oxidized to NAD for the pathway to continue but can accumulate in chronic EtOH abuse

33
Q

Metabolic consequences of NADH accumulation in chronic EtOH abuse

A

Hypoglycemia - via decreased gluconeogenesis
Lactic acidosis

Convulsions - via increased Mg2+ excretion

Fatty liver - via increased fatty acid synthesis and decreased fat breakdown

Gout - via decreased uric acid excretion

34
Q

Acute CNS effects of EtOH

A

Potentiation of GABA pathways and inhibition of glutamate NMDA pathways

Depression of inhibitory cortical neurons is seen first, resulting in a stimulatory phase prior to CNS depression

35
Q

Sleep effects of EtOH

A

Suppression of Stage IV and REM sleep

Rebound REM upon withdrawal increases likelihood of nightmares

36
Q

Hepatic effects of EtOH

A

Initial reversible damage by increased fatty acid deposition causing fatty liver disease and alcoholic hepatitis

Eventual cell death and replacement by collagen causing irreversible cirrhosis (20% of chronic alcoholics); decreased synthesis of clotting proteins increases bleeding time, enlargement of the liver leads to portal hypertension, decreased venous return, ascites, and esophageal varices

37
Q

GI effects of EtOH

A

GI irritation, gastric ulceration, gastritis, pancreatitis, decreased absorption of AAs, thiamine, and B12

38
Q

Cardiovascular effects of EtOH

A

1-2 drinks/day may be cardioprotective via increased HDL and decreased platelet adhesiveness

Chronic alcohol use causes:
Vasodilation (blocks vasoconstrictor response to cold) and myocardial damage

39
Q

Renal effects of EtOH

A

Inhibits ADH causing diuresis

40
Q

Wernicke’s encephalopathy

A

Thiamine (B1) deficiency

Presents with classic triad of opthalmoplegia, nystagmus, and ataxia

41
Q

Chronic CNS effects of EtOH

A

Korsakoff’s psychosis - Due to Thiamine (B1) deficiency; presents as disorientation, amnesia, confabulations

Cerebral atrophy - frontal lobe degeneration with irreversible personality changes and dementia

Cerebellar atrophy - irreversible ataxia

42
Q

Alcohol withdrawal - Presentation & Treatment

A

Agitation, tremor, insomnia, anorexia, disorientation, seizures

Treated with benzodiazepines (lorazepam), a2 adrenergic agonists (Clonidine)

43
Q

Fetal Alcohol Syndrome

A

Pre/postnatal growth retardation + altered morphogenesis + intellectual disability

1st trimester use - risk of morphogenic abnormality
2nd trimester use - risk of spontaneous abortion
3rd trimester use - risk of decreased fetal growth

44
Q

Alcohol DDIs

A

In a non-dependent alcoholic with normal liver function, alcohol induces CYP2E1 causing faster metabolism; can precipitate acetaminophen toxicity

Acute synergistic effects with CNS dependents; chronically, cross-tolerance can develop

Aspirin - GI bleeding

Metronidazole - Antabuse-like reaction

45
Q

Treatment of acute EtOH intoxication

A

Respiratory support
IV fluids
Glucose + Thiamine
Electrolytes (K+ and Mg2+)

46
Q

Acamprosate

A

Weak NMDA receptor antagonist - may mediate glutamate hyperexcitability during alcohol withdrawal

Reduction in alcohol craving and relapse rates in conjunction with psychotherapy

Nervous System IV (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions