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Psyc 475 > Lecture 27-29 > Flashcards

Lecture 27-29 Flashcards

1
Q

Acute pain

A

Biologically useful

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2
Q

Chronic pain (4)

purpose + time + type

A
  • no purpose
  • Longer than 3 months
  • Noiciceptive (tissue damage)
  • Neuropathic (dysfunction of the nervous system)
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3
Q

Fentanyl (2)

solubility + potency/affinity

A
  • highly lipid soluble
  • More potent then morphine, heroine and oxycontin/High affinity (50-100 times more potent then morphine) because more soluble
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4
Q

Fentanyl overdose is treated with:

A

Naloxone: competitive inhibitor for opiod receptors

can knock off opiod from receptor and also takes uo receptor spot

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5
Q

Opiod receptors (3):

type + binding of mu + classes

A
  • all are G-protein coupled, inhibitory
  • Binding of a ligant to mu receptor activates potassium channels, inhibits calcium channels and camp
  • 5 classes: (Mu, Kappa, Delta, noiciception receptor and zeta receptor)
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6
Q

Fentanyl

agonist/antagonist?

A
  • MOP (mu) receptor agonist
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7
Q

Carfentanyl (3)

agonist/antagonist + affinity/potency + used as

A
  • MOP receptor agonist
  • Very high affinity (10K times more potent than morphine)
  • Used as an IV anesthetic for large animals
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8
Q

Pharmacological effects of opiods (3):

pain + euphoria + respiration /relieve?

A
  • Reduction of pain without loss of conciousness
  • Increase VTA cell firing as opioids bind to mu-opioid receptors which are densely expressed on GABAergic neurons in the VTA. Activation of mu-opioid receptors inhibits GABA release by hyperpolarizing GABAergic neurons. GABA loses inhibitory response on DA neurons leading to euphoria.
  • Depression of respiration (opiod antagonist in medulla relieves this)
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9
Q

Gastrointestinal symptoms with opiods (3)

relief of + by (2)

A
  • relief of diarrhea
  • increases intestinal tone
  • decreases motility for absorption
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10
Q

loperamide/imodium (3)

What + treats +BBB

A
  • opiod receptor agonist
  • helps relieve diarrhea
  • Cannnot pass through BBB
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11
Q

P-glycoprotein (2)

what it does + what it is

A
  • Gatekeeper at the blood brain barrier
  • Permits entry of loperamide and is an ATP dependent membrane pump
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12
Q

Opiod metabolism (2)

enzyme + abnormality

A
  • Primary metabolized by CYP 2D6 and CYP 3A4
  • up to 30% of patients have abnormalities in these enzymes. Rapid metabolizers = pain comes back quick. Inactive or absent enzymes = opiod built up in blood
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13
Q

Tolerance and dependence of opiods (2)

A
  • Receptor fail to initiate signal after long term binding
  • Desensitized receptors uncouple from the G-protein and receptors are internalized and returned to the membrane to be resensitized to opiod binding

Constitutive receptor trafficking

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14
Q

Morphine (5)

administered + effective as an + GI + solubility +metabolized in

A
  • administered via injection, inhalation, orally, rectally
  • Effective as an epidural as there are opiod receptors in the spinal cord
  • Slow absorption profile through the GI tract
  • more water soluble then lipid, cross BBB slowly
  • Metabolized in liver
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15
Q

Codeine

A
  • is a prodrug and must be metabolized by CYP 2D6 by the body and turned into morphine
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16
Q

Heroin (3)

Produced from + potency + clinic use

A
  • produced from morphine
  • three times more potent than morphine bc more lipid soluble and reach BBB faster
  • No clinical use outside the UK
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17
Q

Cocaine routes of administration includes ——–. There is rapid brain entry and high abuse potential and repeated exposure causes ——

A
  • inhalation, smoking, IV, injection
  • long lasting homeostatic changes in brain related to addiction
18
Q

Cocaine pharmacokinectics:

Absorption sites (3) + brain pentration + placental barrier

A
  • Absorbed from all sites of application
    Mucous memranes: poor absorptio due to vasoconstriction, 20-30% of drug is absorbed (most sent to liver)
  • Lungs
  • Stomach
  • Penetrates brain rapidly
  • freely crosses the placental barrier, levels similar to mother
19
Q

Cocaine metabolism (2)

enzyme + metabolite/urine

A
  • metabolized by butyrylcholinesterase
  • Major metabolite is benzoylecgonine (BE) and is detected in urin for up to 48 hrs and longer in chronic users (2 weeks)
20
Q

Cocaine and alcohol (3)

produce + what it does (2)

A
  • Produces brand new metabolite cocaethylene which is more toxic and longer lasting
  • It blocks DAT (DA transporter) = euphoria
  • potent ca2+ channel blocker in heart = cardiovascular risk
21
Q

Cocaine mechanism of action (2)

monoamine + na+

A
  • Blockade of monoamine reuptake (DA,NE,5–HT)
  • Na+ channel blockade (local anethetic)
22
Q

Cocaine effect on synaptic dopamine

A
  • Agonist because it stimulates DA release
  • It is not an antagonist since that blocks synaptic transmission and cocaine doesnt do this
23
Q

Wildtype VS D1 knockout mice conclusion

A

behaviour activation via cocaine requires D1 receptor if D1 is gone, cocaine increase DA release bit DA has nowhere to bind

24
Q

Freeze and Rush

A
25
Q

Cocaine and low and high dose symptomns

A

Low: affects the sympathetic NS (increase heart rate, BP brondhodilation, pupil dilation, increase body temp)

High: agitation, impulsiveness, anxiety, extreme energy, hostile, formication (ants)

26
Q

Continued high dose of cocaine can result in

A

psychosis

27
Q

Coke run

A

repeated cycles of cocaine use

28
Q

Cocaine chronic usage induce (3):

A
  • aortic stiffening
  • Increase in ventricular thickness
  • High BP
29
Q

Amphetamine therapeutic uses (4)

A
  • Narcolepsy
  • ADHD
  • Supporessionof appetite
  • anti-obesity
30
Q

Cocaine vs Amphetamine (5)

A
  • All lipid soluble
  • Well absorbed
  • Amphetamine has a longer duration of effect (12 hours) while cocaine has 30-60 min.
  • Cocaine is less potent
  • Cocaine acts as a local anesthetic
31
Q

Amphetamine mechanism of action (4)

A

Modifies the action of DA similar to cocaine
1. induces release of DA from presynaptic neuron
2. Interacts with DA vesicles, releases free DA in nerve terminal
3. Blocks reuptake, transport free DA out of the nerve terminal
4. At high doese, binds to MAO (monoamine oxidase) preventing degradation of DA in nerve terminal. Also induces release of NE and inhibits reuptake.

32
Q

Low doses of amphetamine

A
  • similar to cocaine, increase body alertness
  • increase BP, heart rate, performance enhancer
33
Q

Moderate dose of Amphetamine sympt:

A
  • stimulation of respiration
  • Tremors
  • Greater increase in motor activiry
  • increase in anxiety disorders
34
Q

Chronic high doses of amphetamine

A
  • anorexia
  • repetitive acts
  • aggressive outburst
35
Q

Methamphetamine can be easily synthesized from —— and can be vaporurized and smoked once cystalized.

A

pseudoephedrine

36
Q

Smoking methamphetamine can cause near immediate absorption and approximately 60% is metabolized by the —-. The primary metabolite produced is —— and excreted through the kidneys (40% excreted unchanged).

A
  • liver
  • amphetamine
37
Q

Structural abnormalities in brains of people who use mathamphetamine exoeriment (4):

what we see general + neuronal loss + Hippo + addicated ppl suffer from

A
  • all chronic users and we sae a reduction of grey matter (cell body and neuron) and an increase in white matter (inflammation)
  • Neuronal loss replaced by glial scars
  • Loss of grey matter in hippocampus (correlates with word recall performance)
  • addicted people suffers from depression, anxiety and concentration difficulties
38
Q

Methylphenidate (Ritalin) (3)

mechanism + effects + treatment for

A
  • Activates catecholamine transmission by blocking DAT and NET increasing extracellular levels of Da and NE
  • Effects include increased arousal, alertness, ability to concentrate; elevated mood, low to medium doses have positive effect on cognitive function
  • Treat ADHD
39
Q

ADHD by DSM5 (3)

3 categories

A
  1. Predominantly inattentive type (girls) attention
  2. Predominantly hyperactive-impulse type (boys)
  3. Combined subtype
40
Q

Synthesic cathinones Emax experiment

A

Psyc 475 (10 decks)

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