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Therapeutics > Exam 5 lecture 7 > Flashcards

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
Q

Differentiate between Hemp and marijuana

A

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
Q

Difference of delta 8 and 9

A

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
Q

What is more potent, synthetic or natural marijuana

A

Synthetic

28
Q

why is hemp grown

A

Textile, agroculture etc

29
Q

Acute cannabis intoxication effects

A

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
Q

What is the endocannaboid system? What is it comprised of? exam

A

RECEPTORS- CB1 and CB2
LIGANDS- Anandemide and 2 AG
TRANSPORTER- EMT endocannabinoid membrane transporter
ENZYMES- Fatty acid amide hydrolase, monoglycerol lipase

31
Q

What do endocannabinoids and phytocannabinoids do?

A

They are RETROGRADE REGULATORS of neurotransmission inhibiting release of GABA and glutamine

32
Q

What is the difference between THC and CB1R?

A

THC is a partial agonist at CV1R where as synthetic cannabinoids are full agonists.

33
Q

What expression is higher in brain? CB1 or CB2?

A

CB1 expression is higher than CB2 in brain.

34
Q

Where dies CB2 exist?

A

Glia

35
Q

Do people get respiratory depression when exposed to large doses of THC? Why?

A

No, low levels of receptors exist in brainstem

36
Q

What expression is seen as higher in periphery? CB1 or CB2

A

CB2 is seen to be higher in periphery than CB1

37
Q

Where is CB2 found in periphery? CB1?

A

CB2- lymphocytes (B cells, T cells)
CB1- Liver (upregulated in liver fibrosis)

38
Q

What are some FDA approved Cannabinoid drugs? What are they used for?

A

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
Q

What are some challenges with medical marijuana use?

A

Lack of quality control
Absence of adequately designed studies for assessing efficacy and ADR
Growing influence of tobacco and alcohol companies in industry

40
Q

How has percentage concentration of CBD and THC changed over time?

A

Marked increase

41
Q

Is cannabis use associated with mental health disorders?

A
  • extremely difficult to prove and controversial
    -growing evidence for association with several disorders, cause and effect not established.
42
Q

Risk factors and pathways to psychosis with cannabis use

A

Age of onset and potency appear to be key determinants

43
Q

What are the diagnostic criteria of cannabinoid hyperemesis syndrome

A

cycling vomit/nausea
presentation after prolonged excessive use of cannabis
Relief by sustained cessation

44
Q

Treatment of cannabinoid hyperemesis

A

Cannabis cessation
BZDs
Haloperidol
Capscasin cream on abdomen

45
Q

MOA of capscasin in cannabinoid hyperemesis syndrome

A
  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
Q
A

Therapeutics (38 decks)

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