Exam 5 lecture 7 Flashcards

1
Q

describe current trends in stimulant overdose deaths

A

All increasing.

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2
Q

What parts of the brain are activated by stimulants

A

VTA and Nucc Acc (emotion, fear, reward, planning, memory, learning)

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3
Q

Nicotine MOA

A

Acts on acetylcholinergic receptor by causing inflow of Na and outflow of K, causing action potential.

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4
Q

What determines how many molecules of Ach bind to receptor

A

Heterogenity of subunits

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5
Q

why does nicotine bind to Ach receptor?

A

Nictotine is structurally similar to Ach

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6
Q

What are the structural similarities and differences of nicotine and acetylcholine

A

Both have charged amine groups and hydrogen bond acceptor groups

Nicotine is membrane penetrable at physiological PH (weak base)

Nicotine is also not degraded by by acetylcholinesterase

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7
Q

What effect does nicotine not being degraded by acetylcholinesterase have

A

longer duration of action of nicotine (more potent)

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8
Q

Rank addictive probability, cocaine, nicotinem heroine

A

Nicotine
heroin
cocain

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9
Q

Drug therapy used to treat nicotine dependence

A

partial agonist (varenicline)

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10
Q

What are things to know about partial agonist drugs used for quitting nicotine

A

Highly addictive. Partial agonists increase quit rate

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11
Q

Why is pseudoephedrine BTC

A

Can be converted to Meth fairly easily

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12
Q

What are some commonly abused psychostimulants

A

MDMA
Meth
Ritalin
cocaine

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13
Q

What is Fenethyline? Use?

A

Amphetamine + theophylline

Wide spread use in arabian peninsula
ADHD

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14
Q

MOA of cocaine

A

antagonist of amine transprters
DAT SERT NERT

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15
Q

Rank the receptors cocaine will have most effect on

A

Dat>SERT>NERT

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16
Q

MOA of methamphetamines/bathsalts

A

Competitive reuptake
Block DA reuptake

Push out DA from vesicle and induces reverse transport

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17
Q

What are the clinical effects of methamohetamine abuse

A

neurologic- delirium, tremor
psych-anxiety, panaroia, delusions, hallucinations
ENT- profuse dental decay
cardiovascular- tachycardia, hypertension, vasospasms
skin- diaphoresis

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18
Q

describe what is seen in brain scan of meth abuser

A

DA receptor in normal brain has high concentration.

Meth abusers will have a down regulation of dopamine receptors. Receptor downregulation believed to mediate withdrawal sx

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19
Q

is dopamine downregulation evidence of a broken brain

A

No, recovery of of DA receptors shows ability to return to homeostasis

20
Q

Do addictive drugs increase brain dopamine

A

decrease in C-raclopride binding reflect increase synaptic ventral striatal dopamine levels.

21
Q

Can low dose psychostimulants increase productivity?

A

This off label use is not well supported by research and can progress to stimulant use disorder

22
Q

What is sympathomimetic toxidrome? symptoms? EXAM

A

MATHS
M-Mydriasis
A- agitation, arrhythmia, angina
T- tachycardia
H-Hypertension, Hyperthermia
S- Seizure, sweating

23
Q

Management of sympathomimetic toxidrome

A
  1. treat agitation, HTN and seizures with BZDs
  2. Avoid pure BB due to unopposed alpha antagonism
24
Q

What are things to know about sympathomimetic syndrome

A

HTN usually responds to sedation
hyperthermia denotes poor prognosis

25
Differentiate between Hemp and marijuana
Legal to federally grow and distribute hemp Illegal for marijuana Hemp contains- 0.3% of less THC Marijuana contains 15-20% Cannabis is schedule I substance
26
Difference of delta 8 and 9
Delta 9 and delta 8 only differ in placement of double bond. Delta 8 only has 25% of the psychoactive activity of Delta 9
27
What is more potent, synthetic or natural marijuana
Synthetic
28
why is hemp grown
Textile, agroculture etc
29
Acute cannabis intoxication effects
Perceptual- Temporal slowing, auditory, visual or depersonalization Physical- tachycardia, hypotension, dry mouth, increased appetite Affective- Euphoria, Anxiety, disinhibition, emotional lability Cognitive- suspicious or paranoid ideation, impaired judgement, impaired rxn time
30
What is the endocannaboid system? What is it comprised of? exam
RECEPTORS- CB1 and CB2 LIGANDS- Anandemide and 2 AG TRANSPORTER- EMT endocannabinoid membrane transporter ENZYMES- Fatty acid amide hydrolase, monoglycerol lipase
31
What do endocannabinoids and phytocannabinoids do?
They are RETROGRADE REGULATORS of neurotransmission inhibiting release of GABA and glutamine
32
What is the difference between THC and CB1R?
THC is a partial agonist at CV1R where as synthetic cannabinoids are full agonists.
33
What expression is higher in brain? CB1 or CB2?
CB1 expression is higher than CB2 in brain.
34
Where dies CB2 exist?
Glia
35
Do people get respiratory depression when exposed to large doses of THC? Why?
No, low levels of receptors exist in brainstem
36
What expression is seen as higher in periphery? CB1 or CB2
CB2 is seen to be higher in periphery than CB1
37
Where is CB2 found in periphery? CB1?
CB2- lymphocytes (B cells, T cells) CB1- Liver (upregulated in liver fibrosis)
38
What are some FDA approved Cannabinoid drugs? What are they used for?
Marinol- synthetic delta 9 THC in sesame oil, schedule III, counter loss of appetite Nabilone- THC mimetic, schedule II, anti emetic and chronic pain
39
What are some challenges with medical marijuana use?
Lack of quality control Absence of adequately designed studies for assessing efficacy and ADR Growing influence of tobacco and alcohol companies in industry
40
How has percentage concentration of CBD and THC changed over time?
Marked increase
41
Is cannabis use associated with mental health disorders?
- extremely difficult to prove and controversial -growing evidence for association with several disorders, cause and effect not established.
42
Risk factors and pathways to psychosis with cannabis use
Age of onset and potency appear to be key determinants
43
What are the diagnostic criteria of cannabinoid hyperemesis syndrome
cycling vomit/nausea presentation after prolonged excessive use of cannabis Relief by sustained cessation
44
Treatment of cannabinoid hyperemesis
Cannabis cessation BZDs Haloperidol Capscasin cream on abdomen
45
MOA of capscasin in cannabinoid hyperemesis syndrome
1. substance P activates NK1R to induce vomiting 2. Activation of TRPV-1 by heat or capscasin leads to depletion of substance P 3. Chronic cannabis use causes desensitization and downregulation of TRPV1
46