Drugs Of Abuse Flashcards

1
Q

Is a CNS depressant
Like volatile anesthetics, it causes a measurable increase in fluidity of lipid membranes
-very small, lipophilic molecule

A

Alcohol/ ethanol

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2
Q

What is the mechanism of action of alcohol?

A
  1. Activates GIRK by binding to a pocket here
  2. Enhancing GABA-mediated inhibition via GABA -A receptor
  3. Potentiates Glycine receptor-induced inhibition
  4. Inhibiting NMDA receptor function
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3
Q

What drug causes Fatty liver and liver failure and cirrhosis ?

A

Ethanol

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4
Q
It is a drug that causes the following: 
A. Slurred speech 
B. Motor incoordination
C. Increased confidence 
D. Euphoria 
E. *impaired foetal development in pregnant women* 

Long term effect —>
Neurological degeneration—>
Dementia and peripheral neuropathy ( in heavy drinkers)

A

Ethanol

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5
Q

A drug that increase fatty acid release from adipose tissue and impaired fatty acid oxidation

A

Ethanol/ alcohol

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6
Q

What treats alcohol/ ethanol toxicity?

A
  1. Disulfiram
  2. Naltrexone
  3. Acamprostate
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7
Q

It is a drug that inhibit AC
Open K channels
Close Ca channels
Thus —> inhibitionof synaptic transmission

A

Narcotics

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8
Q

What are examples of Narcotics?

A

Heroin
Fentanyl
Oxycodone

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9
Q

What is an example of CNS depressant?

A

Ethanol

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10
Q

What are examples of psychomotor stimulants?

A
  1. Methylxanthines
  2. Nicotine
  3. Cocaine
  4. Amphetamines
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11
Q

Psycho mimetic agents example?

A

Cannabinoids

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12
Q

How can we divide the CNS stimulants?

A
  1. Psychomotor stimulants

2. Psycho mimetic drugs

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13
Q

Causes excitement and euphoria

Decrease fatigue and increase motor activity

A
Psychomotor stimulants 
Examples: 
Methylxanthines 
Nicotine
Cocaine 
Amphetamines
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14
Q

Is a drug examples of it :
Tea
Cocoa
Caffiene

Effect on smooth muscle, CNS, kidney ( effect on bronchial smooth muscle)—> asthma treatment

A

Methylxanthines

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15
Q

What is the mechanism of action of Methylxanthines ?

A

Inhibit phosphodiesteraes which normally hydrolyse CAMP
So—> high CAMP

Some also purine A2 receptor antagonist —> smooth muscle relaxant effects

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16
Q

A drug should be avoided in peptic ulcer patients

A

Caffeine

17
Q

A drug that has the following effects ?

  1. Decrease fatigue
  2. Increase mental alertness ( stimulates the cortex)
  3. Positive inotropic/ chronotropic actions
  4. Diuretics
  5. Avoided in peptic ulcer patient
A

Caffeine

18
Q

What are side effects of caffeine?

A

Insomnia / anxiety/ agitation ( moderate dose)
Emesisis / convulsion
Cardic arrythmias

19
Q

If a pregnant female drinks more than 3 cups of instant coffe / day —> miscarriage risk

A

Caffeine

20
Q

Withdrawal of caffeine

A

Lethargy
Irritability
Headache

21
Q

Is a drug that its mechanism of action?
Directly coupled to ion channels —> once nicotine binds —> channel opens —> allowing entry of cations Na and Ca
Cations further activate voltage -dependent calcium channels —> further calcium entry —> mediate fast excitatory synaptic transmission at NMJ / autonomic ganglia and many sites in the CNS

A

Nicotine

22
Q

What happens if we use too much nicotine?

A

Desensitization : chronic nicotine admin —> increase in no. Of nACHR

23
Q

It is a drug which its poisoning is ( biphasic) starts with stimulatory effect ( tachycardia and high BP etc) followed by depressor effects ( central respiratory paralysis, bradycardia, severe hypotension)

A

Nicotine

24
Q

What is the mechanism of action of cocaine?

A

It has a direct action and indirect action

  1. Direct action —> blockade of DA re-uptake and that of NA and 5-HT
    Into pre-synaptic terminals from which these transmitters are released by blocking their respective transporters —> elevating synaptic concentration
  2. Indirect —> opioidergic , glutamatergic and GABAergic system
  3. Local anaesthetic effect —> Na channel block
25
Q

What are the actions of cocaine ?

A

Increase in mental awareness, euphoria , hallucinations, delusion and paranoia( from stimulation of the cortex and brainstem)

Produces the adrenergic fight and flight syndrome :
Tachycardia / hypertension/ pupillary dialtion/ peripheral vasoconstriction

Side effect?
Appetite suppression

26
Q

It is a drug that
Promote release of NA from central adrenergic receptor into synaptic cleft

At DA neuron,
Amph bind to DA re-uptake transporter —> reverse action —> transport free dopamine into synaptic cleft

Amph is taken up into cell —> DA release into synapse
Amph diffuses into vesicle —> DA release into nerve terminal —> increased DA at synaptic cleft

A

Amphetamines

27
Q

What is the action of amphetamines ?

A

Stimulates the entire cerebeospinal axis , cortex, brainstem, and medulla

Increased alertness, 
decreased fatigue 
Decreased appetite 
Insomnia 
Convulsions
Indirect stimulation of the sympathetic system
28
Q

What are side effects of amphetamines?

A
Insomnia 
Panic states 
Amphetamines psychosis ( resembles acute schizophrenic attack, with chronic use ) 
Palpitations, cardiac arrhythmia 
Suicidal tendencies 
Irritability
29
Q

What are examples of paychomimetic drugs ?

A

They are also known as hallucinogens

They produce several changes in thought patterns and mood
The individual using them is incapable of normal decision making

Primary action is inducing altered states that resemble dreams

30
Q

What are examples of psycho-mimetic drugs ?

A

Tetrahydrocannabinol
Phencyclidine
LSD

31
Q

Cannabinoids and cannabis mechanism of action?

A

They have 2 receptors:
CB1 —> brain
CB2 —> CB2 periphery
Both are G protein coupled receptors

CB1: MOA when activated
Mechanism of action complex
CB1 receptors can coupled to different G proteins and different prefernces as to which signaling pathway is activated

It has been shown to inhibit AC
Activate K conductance
Inhibit Ca conductance —> inhibition if synaptic transmission possibly ( direct and indirect action)
Part of what happens after CB-1

32
Q

It is a weak partial agonist at CB1 and CB2 receptors —>
increased appetite
Decreased pain
Change in mood

A

THC

33
Q

It is a negative allosteric modulator on CB1 ( on site functionally distinct from agonist/ antagonist binding site )

Effects on CB2
Effects on 5HT1a/2a/3a and TRPV1 vanilloid receptors ( amongst other direct and indirect effects which are not required at this level)

A

Cannabidiol CBD

34
Q

Anti-emetic drug

A

Nabilone

35
Q

Anti-epileptic drug approved for intractable childhood seizures

A

Cannabidiol

36
Q

What are the effects of cannabis ?

A

Euphoria
Relaxation
Sharpened sensory awarness
Learning , memory and motor performance impaired
Reduction in the IOP ( used in glaucoma)
Increased appetite ( the munchies)

Could be used as
Analgesia
Anti-emetic action

37
Q

Cannabis better than opiates how?

A

Less likely to cause dependence
No respiratory or cardiovascular effects in overdose , just drowsiness and confusion, thus relatively safer than opiates and ethanol
However, if does cause hallucinations and psychosis and there have been incidents where people have killed because they werent in their full mental awareness because of the paychosis that happens

38
Q

What is LSD?

A

It is very potent , hallucinations, and delusions may lead to violence
Also, may have flash back hallucinations long after the drug was taken
May lead to psychopathological changes

In susceptible patients?
LSD and phencyclidine —> shizophrenic attacks

39
Q

What is the mechanism of action of LSD?

A

LSD affects large number of GPCRs, including all DA and NA receptors and others
LSD binds to most 5HT receptor subtypes except for 5HT3 and 5HT4