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Pharma 7: Drugs Of Abuse Flashcards

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1
Q

What is in common with all dependence producing drugs

A

The activation of the mesolimbic dopaminergic neurons and increasing DA release from the nucleus accumbens

i. stimulate firing of A10 cells
ii. amphetamine, cocaine—> release DA or prevent its uptake

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2
Q

The mesolimbic dopaminergic pathway

A

REWARD PATHWAY

From ventral midbrain (A10 group) to the nucleus accumbens and limbic regions via the medial forebrain bundle

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3
Q

The effect of removing D2 receptors in transgenic mice

A

REMOVED THE REWARD SYSTEM
Ie administered morphine without reward without affecting dopamines effects

!they still experienced withdrawal—> D2 responsible for reward NOT withdrawal effects

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4
Q

Other mediators involved in DA mesolimbic pathway

A

5-HT
Glu
GABA

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5
Q

Habituation

A

When the drug is administered repeatedly, after it is stopped the patient experiences aversive effects

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6
Q

The effect of chronic administration of opioids and cocaine

A

Increase the activity of adenyl cyclase in regions like nucleus accumbens

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7
Q

The drugs of abuse on a neurochemical level

A

Opioids, cocaine—>increase AC—>compensates for the acute inhibitory effect of Drugs of Abuse on cAMP—>rebound increase of cAMP after the drug is terminated—>increase cAMP-dependent protein kinases—>increase excitability of cells

Explain tolerance and dependence

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8
Q

Narcotics

A

Morphine
Heroin
Fentanyl
Oxycodone

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9
Q

CNS depressants

A 
Ethanol
Barbiturates
Anesthetics
Solvents
Glutethimide
Methaqualone
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10
Q

Anxiolytic drugs

A

BZDs

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11
Q

Psychomotor stimulants

A

Methylxanthines including caffine
Nicotine
Cocaine
Amphetamine

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12
Q

Psychomimetic agents

A

Cannabinoids
LSD
Mescaline
Phencyclidine

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13
Q

Entactogens

A

Empathy, love emotional MDMA

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14
Q

ETHANOL/alcohol

MOA

A

Cns depressant (small, lipophilic)

Similar to volatile anesthetics—> causes increase in fluidity of lipid membranes

May act through specific membrane ion channels and receptors

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15
Q

Ethanol

Effects

A

Slurred speech, motor in coordination, increased self confidence and euphoria

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16
Q

Ethanol teratogenic

A

Impaired fetal development

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17
Q

Ethanol effect on liver

A

Stress—>sympathetic discharge—> causes increase release of fatty acids from liver

Combines with ethanol imposing metabolic load—>impaired fatty acid oxidation be

!fatty liver—> cirrhosis and liver failure

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18
Q

Drugs used to treat tolerance and dependence on ethanol

A

Disulfiram
Naltrexone
Acamprosate

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19
Q

Narcotics MOA

A

Inhibit AC
OPEN K CHANNELS
Close Ca channels

All together—> inhibit synaptic transmission

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20
Q

Currently, there is an epidemic of

A

Fentanyl overdose

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21
Q

Categories of CNS STIMULANTS

A
  1. Psychomotor stimulants

2. Psychomimetic drugs

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22
Q

Psychomotor stimulants

A
  1. Methylxanthines—> theophylline (tea), theobromine (cocoa) and caffeine (coffee, tea, cocoa)
  2. Nicotine
  3. Cocaine
  4. Amphetamines
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23
Q

Methylxanthies

Administration

A

Orally

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24
Q

Methylxanthines can be used to treat

A

Asthma

Effects on smooth muscles, cns, kidney and bronchial sm

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25
Methylxanthines MOA
Inhibit PDE therefore no hydrolozation of cAMP—> increase cAMP concentration Some act as PURINE A2 RECEPTOR ANTAGONISTS—> smooth muscle relaxant
26
Caffeine actions
Decrease fatigue Increase mental alertness due to stimulation of cortex Positive inotropic and chronotropic effects Diuretic
27
Caffeine CAUTION
Avoid in pt with peptic ulcer Pregnancy—> no more than 3 cups of instant coffee/day Any more would increase risk of miscarriage
28
Caffeine side effects
Insomnia, anxiety, agitation if moderate dose Emesis and convulsions in high dose Arrhythmias in lethal dose
29
Nicotine Adminsitration
Inhalation
30
Dependence and tolerance with nicotine
Increased activity of the mesolimbic DA pathway
31
Nature of nicotinic Ach receptors
Ligand gated channels
32
Nicotine MOA
Acts on nAchR which is directly coupled to ion channel—> channel opens—> allows entry of Na, Ca—> entrance of Ca further opens voltage dependent Ca channels—> more Ca entry This works to cause fast excitatory synaptic transmission at NMJ, autonomic ganglia
33
Desensitization and Nicotine
Chronic nicotine administering—> increase number of nAchR
34
Actions of nicotine
Improve attention and learning time Reduces anxiety and tension
35
Nicotine poisoning
Biphasic nature Ie starts with stimulatory effects like tachycardia and HTN that are followed by depressor effects like central resp paralysis, bradycardia and severe hypotension
36
Nicotine Side effects
1. Irritability 2. Tremors 3. Intestinal cramps 4. Diarrhea 5. Increased heart rate 6. Htn
37
Symptoms of nicotine withdrawal
``` Irritability Anxiety Restlessness Difficulty concentrating Headaches Insomnia ```
38
Cocaine Administration
Chewing Snorting IV
39
Cocaine MOA
A-direct action: Differential reuptake blockade of NA, 5-HT and ”DA” ie monoamine blockade into presynaptic terminal—> elevate synaptic concentrations Reuptake block is accomplished by blocking their transporters B-indirect action: Acts indirectly on opioidergic, glutaminergic, GABAnergic
40
Cocaine as local anesthetic
Na channel block
41
Cocaine Effects
1. Increased mental awareness 2. Euphoria 3. Hallucinations 4. Delusions 5. Paranoia (stimulation of cortex and brainstem) 6. Adrenergic f/f syndrome—> tachy, htn, pupillary dilation, peipheral vasoconstriction
42
Cocaine Side effects
``` Anxiety Mental depression Appetite suppression Seizures Fatal cardiac arrythmias ```
43
Cocaine withdrawal symptoms
Physical and emotional depression +agitation
44
Amphetamines Administration
Iv, smoking, orally
45
Amphetamines MOA
1. Promotes release of NA from central adrenergic receptors into synaptic cleft 2. At DA neuron: increases DA at cleft i. Bind to DA reuptake transporter—> reverse action—> transport of free Da into cleft ii. Amphetamine taken up into cell—> DA released into synapse iii. Amph diffuses into vesicle—> Da released into nerve terminal
46
Amphetamines Effects
1. Stimulate cerebrospinal axis ie cortex branstem 2. Increased alertness 3. Decrease fatigue 4. Depress apetite 5. Insomnia 6. At high dose—> convulsions 7. Indirect sns stimulation
47
Amphetamines Side effects
Insomnia Panic states Amphetamine psychosis—> similar to schizophrenia attack when taken chronically Palpitations Cardiac arrhythmia Suicidal tendencies Irritability
48
Psychomimetic drugs/hallucinogens Primary action
Induce altered states that resemble dreams—> changed thought patterns—> cant make decisions
49
Psychomimetic drugs
Tetrahydrocannabinol Phencylidine LSD Mescaline Psilocybin Cause sensory changes, hallucinations and delusions (similar to acute schizophrenia)
50
Tetrahydrocannabinol (THC)
Main active substance of cannabis *cannabis, morphine—> metabolically active metabolites
51
Cannabinoids action
Depressant and psychotomimetic actions Alters mood, cognition
52
Cannabinoids Administration
IV | Smoking
53
Cannabinoids structure
Highly lipid soluble
54
Anandamide
AA’ | ENDOGENOUS LIGAND FOR CB1
55
Cannabinoids receptors
CB1 (brain; hippocampus, cerebellum sn and mesolimbic system) and CB2 (periphery; mainly lymphoid) G protein coupled receptors CB1–> inhibit AC....activate K conductance,,decrease Ca—> inhibit synaptic transmission
56
Analgesics?
Cb1 and ch1-paf
57
Cannabinoids effects
``` Euphoria Relaxation Sharpened sensory awareness Impaired memory, learning, motor Reduces IOP—> used in glaucoma Increases appetite ``` Analgesic, antiemetic—> NABILONE
58
Cannabinoids vs opiates, nicotine, alcohol
Less likely to cause dependence No resp, cv effects if OD (only drowsiness, confusion)there4 safer
59
Cannabinoids Side effects
Long term psych effects—> schizophrenia, apathy, under achievement Low doses—> sensory distortion, hallucinations—
60
LSD
Potent hallucinations and delusions—> violence "Flashback hallucinations" long after drug was taken—>psychopathalogic changes If susceptible—> lsd and phencyclidine—> schizophrenic attacks

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