Drug Addiction Flashcards

1
Q

There are two types of synapses:
Electrical and Chemical synapses. Most synapses in our CNS are chemical synapses. What is the advantage of chemical synapses?

A.  Synaptic gap is small
B.  Faster transmission
C.  Slower transmission
D.  Amplification of signal
E.  Synaptic gap is large
A

D. Amplification of signal

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2
Q

How do Tricyclics (TCAs) work? What do they treat?

A
  • treat depression
  • block reuptake of Norepinephrine and Serotonin
  • TCAs not really used anymore because they raise BP and are addictive
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3
Q

Both TCAs and SSRIs are effective in treating depression. Between Imipramine (TCA / a tricyclic) and Fluoxetine (a SSRI),
which drug has more side effects?
Example: on systemic blood pressure

A. Fluoxetine / Prozac ( SSRI )

B. Imipramine / Tofranil ( Tricyclic )

A

B. Imipramine / Tofranil ( Tricyclic )

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4
Q

SSRIs, compared to tricyclic antidepressants, which of the following is NOT true?

SSRIs are:

A.  safer in overdose
B.  less addictive
C.  more selective to serotonin
D.  more effective
E.  have fewer side effects
A

D. more effective

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5
Q

How do cells respond to excess neurotransmitter in the short and long term?

A

Short term:

  1. Desensitize receptors (shown above)
  2. Hide (internalize) receptors in the cytoplasm.
  3. Degrade receptors

Long term:
4. Decrease the number of receptors (by altering gene expression)

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6
Q

What are the comon narcotics?

A
  • opium
  • morphine
  • codeine
  • heroin
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7
Q

What are the common abused stimulants?

A
  • cocaine
  • amphetamine
  • methamphetamine (speed)
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8
Q

How does chronic consumption of alcohol affect Cl channels in the CNS? and on glutamate channels?

A
  • alcohol increased Cl flux acutely
  • chronic consumption will decrease the # of Cl channels
  • chronic intake will also increase the # of glutamate channels
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9
Q

Where is the reward center in the brain? What neurotransmitter does it use?

A
  • Nucleus Accumbens
  • Dopamine
  • (VTA projects to NuAcc, termed mesolymbic system)
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10
Q

What is cocaine’s mechanism of action?

A
  • prevents reuptake of dopamine in VTA neurons projecting to the NuAcc
  • postsynaptic neuron downregulates DA receptors
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11
Q

What is Meth’s mechanism of action?

A

-enters VTA nerve terminals at NuAcc and increases the release of dopamine

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12
Q

What are Delirium Tremens?

A

-seizures caused by alcohol withdrawal

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13
Q

All cells, including neurons, adapt to the presence of
excess neurotransmitters.

Which of the following is NOT a response to excess
neurotransmitter?

A.  Desensitization of receptors
B.  Hide / internalize receptors
C.  Decrease the number of receptors
D.  Degrade the receptors
E.  Increase the number of receptors
A

E. Increase the number of receptors

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14
Q

What is used to treat heroin addiction?

A

Methadone

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15
Q

Why is Diazepam used in patients who are recovering from alcohol addiction?

A

-to prevent seizures (Delerium Tremens)

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16
Q

What drugs will causes pin point pupils?

A
  • Organophosphates/Insectisides

- Morphine, heroin, codeine

17
Q

What drugs will cause dilated pupils?

A
  • Meth
  • Cocaine
  • MDMA
18
Q

What is the treatment for alcoholism?

A
  • Disulfiram

- Diazepam

19
Q

What is the treatment for smoking cessation?

A
  • nicotine transdermal patch

- Varenicline/Chantix

20
Q

What are two opioid antagonists used to treat opioid addiction?

A

Naloxone

Naltrexone

21
Q

What is a opioid partial agonist used to treat opioid addiction?

A

-Buprenorphine

22
Q

What is an opioid agonist with a long half life used to treat opioid addiction?

A

-Methadone

23
Q
Which one of the following pituitary hormones may be 
increased in patients prescribed metoclopramide (Reglan) for gastrointestinal hypomotility?

A. ACTH
B. FSH
C. Prolactin
D. TSH
E. Growth hormone
A

C. Prolactin

24
Q

How do opioids affect dopamine release from VTA?

A
  • Endorphin neurons inhibit presynaptic (to the VTA) GABA neurons
  • More opioids means more inhibition on presynaptic neurons, removing GABA inhibition on VTA neurons
  • This leads to more VTA dopamine release on NuAcc