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Pharmacology > 2.3 Stimulant Drugs > Flashcards

2.3 Stimulant Drugs Flashcards

1
Q

Stimulant drugs

A
  • increased activity of the brain

- amphetamines, cocaine, nicotine, and caffeine

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2
Q

Amphetamines

A
  • drugs of widespread abuse
  • uses restricted to certain medical conditions
  • amphetamine, dextroamphetamine, and methamphetamine
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3
Q

To amphetamine related compounds

A
  • methylphenidate (Ritalin) used to treat attention deficit hyperactivity disorder
  • MDMA (ecstasy) derived from methamphetamine
  • fosters feeling of intimacy and empathy improving intellectual capacities
  • it is neurotoxic causing the neuronal damage and death
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4
Q

Chemistry of amphetamines

A
  • structurally similar to the neurotransmitters norepinephrine and dopamine
  • can be synthesized readily, this has resulted in the illicit manufacturing of the substances especially methamphetamine
  • Purity of these illicit substances is viable may contain side products of the chemical reaction, unreacted chemicals, and cutting edge agents
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5
Q

pharmacology of amphetamines

A
  • increase excitation by increasing the amount of dopamine or Norepinephrine in the synaptic cleft
  • Amphetamines are substrates for the dopamine transporter which which is the transport of that clears dopamine out of the synaptic cleft after neurotransmission
  • Amphetamines compete with dopamine for the dopamine transporter and the result is the amphetamines end up in the presynaptic nerve
  • What’s the nerve amphetamines block the visicular monoamine transporter which is the transporter responsible for bringing dopamine into vesicles to be packaged for released when the next nerve impulse arrives
  • Since dopamine is blocked from being packaged into vesicles, there’s a large increase in in concentration of free dopamine in the neuron
  • This large concentration of dopamine in the neuron forces the dopamine to travel through the dopamine transporter in the reverse direction meaning back out into the synaptic cleft
  • The result is an increase of dopamine in the synaptic cleft and hence an increase in CNS excitation
  • The same mechanism of action applies for norepinephrine just with norepinephrine specific transporters
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6
Q

Mechanism of action of ecstasy

A
  • similar to the amphetamines, but has a preferential effect on the serotonin containing neurons, and causes a release of serotonin.
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7
Q

CNS effects of amphetamines

A
  • A decreased threshold for transmitting sensory input to the cerebral cortex, leading to excitation
  • A feeling of euphoria and reward
  • temperature regulation and feeding centre modifications, leading to appetite suppression
  • an increase in aggressive behaviour and mood swings
    -common amphetamines vary in the magnitude of the CNS affect
    methamphetamine> dextroamphetamine> amphetamine
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8
Q

CNS excitation

A
  • Can cause overstimulation, restlessness, dizziness, mild confusion, tremor, and in rare instances, panic and psychosis, especially with high doses
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9
Q

Effects of amphetamines in non-CNS tissues - short term use

A
  • heart attack, heart pain, changes in blood pressure, or fainting
  • cardiovascular collapse
  • increased respiratory rate
  • overdose may result in a seizure, high fever, or stroke
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10
Q

Effects of long term amphetamine use

A
  • chronic sleeping problems
  • Poor appetite
  • anxiety, repetitive behavior, psychosis, aggressive behaviour
  • elevated blood pressure and abnormal cardiac rhythm
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11
Q

Concurrent drug use

A
  • other drugs maybe saw concurrently with amphetamines (benzodiazepines, opioids) in an attempt to antagonize various toxic affects of the amphetamines
  • this can lead to additional problems
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12
Q

Therapeutic uses of amphetamines

A
  1. Narcolepsy - Chronic sleep disorder
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13
Q

Therapeutic uses of amphetamines

A
  1. ADHD - this disorder consists of disruptive behaviour and decreased attention/concentration spans.
    - Drug therapy increases classroom attention/concentration and can improve scholastic performance
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14
Q

Treatment for these disorders

A

-methylphenidate (Ritalin) Is the drug of choice for both of these disorders due to the decrease incidence of both cardiovascular and appetite suppressing affects, compared to amphetamine

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15
Q

Amphetamine abuse potential and dependence

A
  • Produce euphoria and are effective CNS stimulants for these reasons, they are widely abused
  • Amphetamines are most commonly taken orally, injected, or smoked
  • occasionally they are sniffed or snorted
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16
Q

Abuse potential of. Amphetamines

A
  • they abuse liability extremely high as they produce a powerful euphoria
  • water soluble saline forms of the drug allow for large doses that are readily injectable, resulting in a rapid and intense response
  • Do you know parent harmfulness of the amphetamines due to their long-term toxicities like cardiovascular effects and drug induced psychoses
  • this does not appear to be a deterrent to abusers and substantial health risk also occur due to users lifestyle (contaminated needles, poor nutrition)
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17
Q

Tolerance of amphetamines

A
  • tolerance develops to the euphoria and mood elevating affects the anoretic effects, the cardiovascular and respiratory stimulatory effect, and the lethal effects of the drugs
  • tolerance does not develop to the therapeutic affects or drug induced psychosis
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18
Q

Dependence on Amphetamines

A

-cessation of use results in mood depression that may be profound, prolonged sleep, huge appetite, lack of energy, and fatigue

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19
Q

Addiction of amphetamines

A
  • Usually self administered to produce euphoria and an Arubt awakening sensation “rush”
  • effects act as rewards and users will crave the drugs effects so intensely that if it is not available they will experience panic
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20
Q

Cocaine

A
  • local anaesthetic in the CNS stimulant
  • narcotic
  • more cocaine more cna stimulant
  • inhibits the active reuptake of primarily dopamine and serotonin into the presynaptic nerve terminal
  • Increases the concentration of these transmitters in the synaptic cleft, and intern increases the activation of the post synaptic receptors
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21
Q

Effects of cocaine on the CNS

A
  • similar to amphetamine and it’s a cute effects and it’s patterns of toxicity
  • cocaine has a shorter duration of action usually less than an hour, compared to 12 with amphetamines
  • lower incidence of complications associated with intravenous use, as cocaine is usually sniffed or smoked
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22
Q

Cocaine therapeutic uses

A
  • local anaesthetic for the mouth and throat
  • Rarely used, as better local anaesthetics have been developed that have chemical structure similar, but do not have the dependence liability
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23
Q

Origins of cocaine

A

-alkaloid found in the leaves of the Coco bush indigenous to Bolivia Columbia and Peru

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24
Q

Long-term effects of cocaine

A
  • toxic psychosis, including paranoia
  • hallucinations or sensations of insects crawling under the skin
  • impaired sexual function
  • permanent brain damage and impairment of neuronal function may occur
  • High blood pressure and irregular heart rhythm
  • changes to the nasal Mucosa, as the drug is sniffed
25
Q

Abuse potential of cocaine

A
  • One of the highest abuse liabilities due to powerful euphoria, which can be reached rapidly by injecting the drug, or smoke in the freebase
  • inherent harmfulness involves the fact that users will experience physical and psychological effects do not appear to cheer the abuser
26
Q

Tolerance to cocaine

A
  • tolerance develops to the mood elevating affect, not to the drug induced psychotic affect
  • does not develop as readily to the Hallucinatory and behavioural effects of cocaine as compared to the amphetamines
27
Q

Dependence of cocaine

A

-Withdrawal symptoms are very similar to those associated with dependence on amphetamines

28
Q

Addiction to cocaine

A
  • can occur

- Behavioural effects of cocaine usually are pleasurable and rewarding this reinforces repeated drug use

29
Q

Nicotine

A

-naturally occurring substance found in tobacco, and is the ingredient in tobacco responsible for smoking dependence

30
Q

Nicotine absorption

A
  • existing smoke in small particles, when inhaled, these droplets are rapidly absorbed
  • it is also absorbed from the gastrointestinal tract, oral Mucosa, and across the skin
  • smokers can control the dose of nicotine absorbed by the Depth of inhalation, and by the frequency of smoking
31
Q

Nicotine distribution

A

-Distributed throughout the body, and rapidly gains access to the brain

32
Q

Nicotine metabolism

A

-Nicotine is rapidly metabolized in the liver

33
Q

Nicotine excretion

A

-Tablets are excreted in the urine half life of nicotine in the body is about two hours

34
Q

Nicotine mechanism of action

A
  • stimulates nicotinic receptors at synopsis, similar to acetylcholine
  • activation of nicotinic receptors increases psychomotor activity, cognitive function, attention, and memory
  • large doses nicotine can cause agitation, tremors, and seizures
  • Effects in the CNS are mediated, at least in part, nicotinic receptors mediated release of the CNS neurotransmitters dopamine and serotonin
35
Q

Therapeutic uses of nicotine

A
  • only use is in smoking cessation programs, or nicotine is administered in the form of a chewing gum, transdermal patches, or buccal spray
  • attempts to maintain the blood nicotine levels and satisfy a craving for a cigarette, allowing for the tapering off of the nicotine dose
36
Q

Short term use effects of smoking

A
  • in non-smoker, view paths may result in dizziness, headache, nausea, vomiting and abnormal cramps
  • disappear in a chronic user
  • regular use, nicotine produces mild euphoria, enhanced arousal, increased ability to concentrate, and a sense of relaxation
  • May cause a small increase in heart rate and blood pressure and may suppress appetite
37
Q

Long term use effects of smoking

A
  • tobacco smoke contains nicotine, carbon monoxide, carcinogenic aromatic hydrocarbons, tours, and many other products of combustion
  • Long term respiratory and carcinogenic effects of smoking are related to these products of combustion, and not to nicotine
38
Q

Cardiovascular disease and smoking

A
  • caused by nicotine and carbon monoxide
  • carbon monoxide reduces the capacity of the red blood cells to carry oxygen
  • Both increase the plaques in the vessel and blood clots
  • 5 to 19 fold increase risk of death due to cardiac causes then the non-smoker
39
Q

Lung disease in smoking

A
  • what type of lung disease is a smoker syndrome, characterized by difficulty in breathing, wheezing, chest pain, congested lungs, and increased lung infections
  • increased risk of emphysema and other forms of chronic obstructive lung disease
40
Q

Cancer risk with smoking

A

-increase the risk of cancer of the lungs, the oral cavity in the throat, the bladder, and the uterus

41
Q

Second hand smoke

A
  • increased risk of cardiovascular disease and cancer

- in children, increases risk of bronchitis, ammonia, asthma, and sudden infant death syndrome

42
Q

Smoking and pregnancy

A
  • adverse effects on the developing foetus
  • 2 to3 fold increase in the incidence of the foetus being small or being born preterm
  • maternal exposure to secondhand smoke also increases the chance of a low birth weight neonate
  • The mechanism for this adverse effect on the foetus appears to be due to the decreased oxygen delivery to the foetus
43
Q

Nicotine abuse potential

A
  • powerful reinforcer that has a high degree of abuse liability
  • addicting substance
  • attempts at cessation often fail due to the high craving
  • Usually involve counselling and pharmacological support like nicotine replacement programs
44
Q

Nicotine tolerance

A
  • tolerance to nicotine does not appear to occur to any great extent
  • most smokers will smoke to keep nicotine blood levels at a certain range
  • The number of cigarettes smoked each day is the number needed to keep the nicotine at this level
45
Q

Nicotine dependence

A
  • Irritability, restlessness, anxiety, insomnia, fatigue, and inability to concentrate
  • upon waking in the morning smoker is in a state of nicotine withdrawal
46
Q

Nicotine addiction

A

-Addiction does occur and manifest as an extreme urge to smoke

47
Q

Caffeine

A
  • predominantly affects the CNS and the cardiovascular system
  • taken orally, caffeine is rapidly and completely absorbed
  • Blood levels are significant after 30 minutes and they peak two hours after ingestion
  • distributed to all parts of the body and freely crosses into the brain and placenta
  • Half life varies among individuals from 2 1/2 hours to 10
  • genetics determine the rate at which we metabolize and excrete caffeine, their rapid metabolizer’s and slow metabolizer, explains why at dinner keeps some awake but not others
48
Q

Mechanism of action

A
  • 100 to 250 mg increases mental performance and motor activity, and decreases drowsiness and fatigue
  • in the brain, activation of receptors, adenosine receptors stimulate GABAergic Neurons that done inhibit dopamine release
  • exerted by competitively blocking adenosine receptors in the brain
  • when blocked, the neurons are released from the adenosine inhibition, causing an increase in the dopamine release
  • Overall effect is stimulation of the CNS
49
Q

Short term effects of caffeine on the CNS

A
  • can produce mild mood elevation and reduce fatigue
  • small increase in performance may exist, not been proved
  • flow of thought maybe clear and more rapid
  • when taken by abstainers, caffeine produces nervousness and can interfere with sleep
  • High doses produce irritability, nervousness, rambling flow of thoughts and speech, and psycho motor agitation
50
Q

Short term effects of caffeine on the cardiovascular

A
  • produces constriction of cerebral blood vessels (useful during a headache), peripheral blood flows increased, and cardiac muscle is stimulated so heart rate is increased
  • High doses rapid and irregular heartbeat
51
Q

Short term effects of caffeine on respiration

A
  • mild stimulation of the respiratory rate and relaxation of bronchial smooth muscle occurs
  • caffeine is used to stimulate breathing in preterm newborns as it helps their immature brains and lungs remember to breathe
52
Q

Short term effects of caffeine lethal dose

A

-A lethal dose of caffeine exists, And is equal to about 10 g of caffeine

53
Q

Long term effects of caffeine

A

-lead to restlessness, nervousness, insomnia, increased urinary output, gastric upset, and rambling speech and thought

54
Q

Caffeine and smoking

A
  • nicotine increases the metabolism of caffeine so smokers the duration of action of caffeine is shortened, as metabolized and cleared from the body faster
  • when a person quits, metabolism returns to normal, caffeine will be active in the body longer than individuals used to
  • When someone quits, decrease their caffeine intake to compensate for the increased length of time caffeine will be in their body
55
Q

Caffeine and pregnancy

A
  • caffeine is not associated with foetal abnormalities
  • large doses, increase the risk of stillbirth from 4/1000 to 12/1000, slightly decreased foetal growth rate, and slightly increases the chance of miscarriage
  • Modest doses has no effect on the fetus
  • metabolism of caffeine is Lauren pregnant women, extending the duration of action of caffeine (2x longer trimester 2, 3x in 3)
56
Q

Abuse potential for caffeine

A
  • abuse liability is low
  • acts as a mild reinforcer
  • hi experience from caffeine is mild in intensity
  • inherent harmfulness very low
  • Low to modest intake does not appear to be associated with adverse events
57
Q

Tolerance of caffeine

A

-Torrance does develop to caffeine in some individuals

58
Q

Dependence to caffeine

A

-abrupt cessation if caffeine intake will result in headache, fatigue, and drowsiness I

59
Q

Addiction to caffeine

A
  • mild addiction can occur

Pharmacology (11 decks)

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