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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

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2
Q

Pharmacokinetic properties affecting addictive liability

A

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

Half life: Short > Long

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3
Q

Cocaine - Mechanism

A

Inhibits dopamine reuptake by blocking DAT
Also blocks SERT and NET

Relative risk of addiction = 5

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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

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5
Q

Nicotine - Mechanism

A

Agonist at nicotinic receptor

Relative risk of addiction = 4

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6
Q

MDMA - Mechanism

A

Phenylethylamine class of hallucinogens

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

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7
Q

Hallucinogens - Mechanism

A

5HT2A receptor partial agonist

Relative risk of addiction = 1

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8
Q

Dissociative Anesthetics - Agents & Mechanism

A

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

PCP
Ketamine
Dextromethorphan

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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”)

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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

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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

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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

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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

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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

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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

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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

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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

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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

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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
Inhalants
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
Anticholinergic agents
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
Absorption & Distribution of EtOH
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
Major pathway of EtOH metabolism
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
What underlies the alcohol flushing reaction?
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
Antabuse - Mechanism
Inhibits aldehyde dehydrogenase; results in 5-10X increase in acetaldehyde levels causing headache, nausea, vomiting, orthostatic hypotension, and convulsions
31
Minor pathway of EtOH metabolism
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
What is the role of NAD/NADH in alcohol metabolism and metabolic disruptions associated with EtOH abuse?
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
Metabolic consequences of NADH accumulation in chronic EtOH abuse
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
Acute CNS effects of EtOH
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
Sleep effects of EtOH
Suppression of Stage IV and REM sleep Rebound REM upon withdrawal increases likelihood of nightmares
36
Hepatic effects of EtOH
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
GI effects of EtOH
GI irritation, gastric ulceration, gastritis, pancreatitis, decreased absorption of AAs, thiamine, and B12
38
Cardiovascular effects of EtOH
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
Renal effects of EtOH
Inhibits ADH causing diuresis
40
Wernicke's encephalopathy
Thiamine (B1) deficiency Presents with classic triad of opthalmoplegia, nystagmus, and ataxia
41
Chronic CNS effects of EtOH
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
Alcohol withdrawal - Presentation & Treatment
Agitation, tremor, insomnia, anorexia, disorientation, seizures Treated with benzodiazepines (lorazepam), a2 adrenergic agonists (Clonidine)
43
Fetal Alcohol Syndrome
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
Alcohol DDIs
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
Treatment of acute EtOH intoxication
Respiratory support IV fluids Glucose + Thiamine Electrolytes (K+ and Mg2+)
46
Acamprosate
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)

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