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326 Cards in this Set
- Front
- Back
Tobacco is the only source of
|
Nicotine
|
|
Tobacco Plant Latin name
|
Nicotiana tabacum
|
|
___________ leaves are dried and cured depending on the intended use
|
Tobacco
|
|
The only source of nicotine?
|
Tobacco
|
|
Nicotiana tabacum
|
Tobacco plant
|
|
Tobacco leaves are __________ and ___________ depending on the intended use
|
dried and cured
|
|
Is Nicotine sold as a drug?
|
No
|
|
Why isn't nicotine sold as a drug?
|
Politics and economics
|
|
Is Nicotine regulated by the government?
|
No
|
|
The Supreme court ruled that the FDA cannot regulate tobacco products until given
|
authority by congress (2000)
|
|
Nicotine administration
|
Smoking
Chewing Dipping Trans-dermal patch Chewing gum Nasal spray |
|
Nicotine absorption
|
absorbed in the lungs
distributes rapidly through the body and then to the brain |
|
Nicotine stays in the brain for
|
30 minutes
|
|
After leaving the brain, nicotine
|
concentrates in the kidneys, liver, salivary glands and stomach
|
|
Nicotine is excreted _________ by the kidneys and _________ by the liver
|
unchanged
metabolized |
|
Does nicotine pass the blood/brain and placental barriers?
|
Yes
|
|
Where is nicotine found in the body?
|
Sweat, Saliva, and breast milk
|
|
How many people have a genetic defect to metabolize nicotine
|
16-25%
|
|
What defect are some non-smokers likely to have
|
Genetic defect to metabolize nicotine
|
|
Nicotine stimulates and then blocks _____________ receptors as dose ___________
|
nicotinic cholinergenic
increases |
|
Nicotine ___________ and then __________ nicotinic cholinergic receptors as dose ______________
|
stimulates
blocks Increases |
|
Nicotine effects the _____ and the _______
|
PNS
CNS |
|
Nicotine elevates levels of what neurotransmitters?
|
catecholamines
|
|
Nicotine stimulates ________ in the reward pathway
|
dopamine
|
|
Nicotine stimulates dopamine in the __________ pathway.
|
reward
|
|
Nicotine - muscle tremors
|
Stimulates receptors in the neuromuscular junction
|
|
Nicotine decreases some __________ movements
|
reflexive
|
|
Nicotine increases ______ and _____ and __________ vessels in the skin
|
HR
BP constricts |
|
Nicotine constricts vessels in the ___________
|
skin
|
|
Nicotine - wrinkles and aging
|
reduces skin temp
|
|
Nicotine stimulates __________ but decreases _________ to them causing ___________ risk
|
Bowels
bloodflow herniation |
|
Effects of tobacco on the CNS:
CNS arousal |
Release of adrenalin (epinephrine)
|
|
Effects of tobacco on the CNS:
Respiration |
Increases
|
|
Effects of tobacco on the CNS:
Brain stem emesis center |
Stimulates
|
|
Effects of tobacco on the CNS:
Cells in the ____ connecting to ___ contain a subtype of __________ receptors |
VTA
NA nicotinic |
|
Effects of tobacco on the CNS:
Stimulates cells in the _______ Excessive release of ____________ in the ______ |
VTA
dopamine NA |
|
Effects of nicotine on the CNS:
effects the ___________ neurotransmitter system |
serotonergic
|
|
Smokers in a PET scan show increased activation of _____ while they experience the "pleasure" of smoking
|
NA
|
|
Smokers in a PET scan show (increased/decreased) activation of _____ while they experience the "pleasure" of smoking
|
Increased
NA |
|
Although nicotine generates brain activation, smokers report feeling _______.
|
relaxed
|
|
Although nicotine generates brain ________, smokers report feeling relaxed
|
activation
|
|
Long term smokers have _____levels of psychological well-being as compared to non-smokers
|
lower
|
|
bad mood worsens when a person stops smoking but improves within ________.
|
3-4 weeks
|
|
Nicotine enhances
|
performance
|
|
In what way does nicotine enhance performance?
|
faster information processing and motor reactions
|
|
Nicotine, like caffeine - parabolic function
|
too much - performance goes down
|
|
performance and nicotine withdrawal
|
performance deteriorates
|
|
irritability
weight gain sleep disturbances drowsiness |
Nicotine withdrawal
|
|
why drowsiness during nicotine withdrawal
|
increase in brain activity in areas associated with sleep
|
|
Nicotine - 3 theories
|
Nicotine bolus theory
Psychological tool theory Withdrawal avoidance theory |
|
Nicotine bolus theory
|
immediate high of the puff
|
|
Nicotine - psychological tool theory
|
Manually controlling nicotine in blood - can control performance effects
|
|
Withdrawal avoidance theory
|
avoid withdrawal
|
|
Smokers also use
|
caffeine and alcohol
|
|
Smokers are more likely to be
|
rebellious
|
|
Smokers are more likely to do these things
|
change jobs
divorce crash cars |
|
What do smokers do more of and less of
|
more - sex
less - academics |
|
When do people start smoking?
|
teenagers
|
|
Cancer of the hypopharynx
|
smoking and drinking combo
|
|
Prenatal smoking
|
increase stillbirth and newborn illness
|
|
Smoking causes
|
lung cancer, emphysema, bladder and mouth cancer
|
|
Nicotine treatment - drug
|
buproprion - Wellbutrin
|
|
What is important to quit smoking
|
friend and family support
|
|
How to quit smoking
|
Nicotine replacement - patch, gum and nasal sprays
|
|
Cannabis plant - name
|
Cannabis sativa
|
|
Cannabis plant - How many types?
|
Some think 3 different
Others different subtypes of the same species |
|
2 phenotypes of cannabis
|
hemp
main intoxicant (highest concentration) |
|
Cannabis - active ingredient
|
Delta-9 tetrahydrocannabinol
THC |
|
Have cannaboid drugs been artificially made? Why?
|
yes
Medical applications |
|
THC is found where in the plant
|
all parts
|
|
Marijuana - name
|
Spanish word for cheap tobacco
|
|
Marijuana - how made
|
dried leaves and flowers of the cannabis plant
|
|
How potent is dried marijuana
|
low
|
|
Ganja, bhang
|
India
Bhang like MJ Ganga is 3 x's more potent |
|
Ganja - Jamaica
|
whole plant
|
|
Hashish - what is it?
|
resin from the flowering tops of cannabis plant
|
|
Hashish - potency
|
10x's more potent than MJ
|
|
Hashish - refined
|
potent hash oil or red oil
|
|
Over the past 50 years - MJ potency Why?
|
increased 50%
Crossbreeding |
|
Cannabis history where did people start using?
|
central Asia
|
|
When cannabis spread across the globe
|
in the second century BCE
|
|
Who spread cannabis across the globe
|
Scythians
|
|
Cannabis is from what language
|
Scythian
|
|
How long has cannabis been described in China
|
6000 years
|
|
How was cannabis used, historically
|
as a medicine
|
|
Why was cannabis used as an intoxicant?
|
Potency got stronger
|
|
Who brought cannabis to the US
|
Mexican laborers in the early 20 century
|
|
THC administered
|
smoking
|
|
After inhalation effects of THC begin in
|
30-60 minutes
|
|
How long do the effects of THC last
|
1 hour or so
|
|
Blood THC levels peak in
|
15 minutes
|
|
If THC is eaten, _________ reduces the potency
|
digestion
|
|
What increases absorption of THC and what does not
|
Deep inhalation
holding in lungs |
|
Why are cannabinoids readily distributed around the body
|
high lipid solubility
|
|
where do canabinoids concentrate in the body
|
kidneys and bile of the liver
|
|
how much THC enters the brain
|
1%
|
|
THC metabolizes in both the
|
lungs but most in the liver
|
|
Delta-9 THC is converted in the liver to a _________ potent form that crosses the _______ easily
|
more
blood-brain |
|
Excretion of THC - how fast and how long
|
Slow
lasts for 30 days after a single use |
|
When were THC receptors discovered? What was discovered later?
|
1980's
2 ID'd later |
|
What are the 2 THC receptors called?
|
CB1
CB2 |
|
CB1 is focal generally in
|
CNS
|
|
CB1 is focal specifically in
|
cortex
hippocampus cerebellum basal ganglia hypothalamus brainstem spinal cord |
|
CB2 is generally found in
|
PNS
|
|
Do other CB receptors exists?
|
Scientists think so
|
|
Endogenous cannabinoid
|
anandamide
|
|
MDMA classified as a _________ with mild ________ properties
|
stimulant
hallucinogenic |
|
MDMA enhances cellular concentrations of
|
serotonin
dopamine |
|
All _________-type subsances share common effects and problems related to their use
|
amphetamine
|
|
All amphetamine-type substances share common _______ and ______ related to their use
|
effects
problems |
|
Ecstasy -Forms
|
tablets
capsules powder liquid |
|
Ecstasy - routes of administration
|
oral
smoked anal vagina IV |
|
Ecstasy - anal/vaginal
|
shelved
shafted |
|
Ecstasy - dose mgs
|
75-150 mg in one good quality tablet
|
|
Ecstasy - How many tablets?
|
1-2 more can be taken if desired effect not reached
|
|
How old are Party Drugs user?
|
Young - mid teens or early to mid-20s
|
|
Party drugs - who uses? Male or female?
|
young males
|
|
Party drugs demographics
|
well-educated, employed or studying
|
|
Party Drugs - arrests
|
little contact with police, social authorities or treatment agencies
|
|
Party Drugs - what are they
|
Ecstasy
Alcohol Ketamine GHB |
|
Party Drugs - patterns
|
25% weekly
60% bingeing w/in 6 mos 52% favorite |
|
Party drugs users - poly drug use
|
common 6-7 drugs used in last 60 mos
|
|
What other drugs are used with party drugs?
|
Depressants - alcohol, benzodiazepines
Stimulants - hallucinogens, Ketamine, GHB |
|
MDMA - history when?
|
1912
|
|
MDMA history who?
|
Anton Kollisch
|
|
MDMA history why?
|
to stop bleeding
|
|
Merck held patent for MDMA so it wasn't used for
|
65 years
|
|
_______ was an intermediate compound in the synthesis of methylhydrastinine. Merck was not interested in the properties
|
MDMA
|
|
Methylenedioxymethamphetamine
|
MDMA
|
|
MDMA - 2004
|
second most common drug used by "first timers"
|
|
MDMA legal until
|
1985
|
|
MDMA prescribed for
|
OCD
|
|
MDMA is illegal now?
|
Yes
|
|
Ecstasy stimulates
|
serotonin
|
|
Tight muscles
dilated pupils, visual distortions Sudden nausea Strong pulse, increase temp Confusion |
The Ecstasy Experience:
Coming up |
|
Happy
Relaxed Heightened senses Energy, confident talkative decreased urine output increased thirst |
The Ecstasy Experience -
Plateau |
|
Physical exhaustion
Flat effect depressed tired anxious irritable |
The Ecstasy Experience -
Coming down |
|
Comedown more intense if poly drug user
|
The Ecstasy Experience -
Poly drug user |
|
The Ecstasy Experience -
timeline |
Coming up 0-4 hours
Plateau - 4 hours Coming down - 4-8 hours |
|
Hyperthermia
Dehydration Overhydration Safety issues OD |
Problems associated with MDMA
Immediate |
|
Fluid retention/Renal failure
Agitation confused mental state psychosis tachycardia hypertension hyperthermia nausia muscle rigidity |
Ecstasy - OD
|
|
Ecstasy Dependence
|
Low likelihood
|
|
Ecstasy-Tolerance _______ effects and enjoyment
|
reduces
|
|
Tolerance causes reduced effects as lifetime use increases
|
The Ecstasy Experience -
Loss of magic |
|
LSD
|
Lysergic Acid diethylamide
|
|
LSD is similar to
|
serotonin
|
|
LSD is ___________ and __________-like
|
indoleamine
chatecholamine |
|
psilocybin
Lysergic acid amide bufotenine |
Indoleamine-like drugs
|
|
Chatecholamine-like drugs
|
Peyote
mecaline |
|
LSD History - year
|
1943
|
|
LSD - became popular in the
|
60's
|
|
LSD associated with who?
|
Timothy Leary
|
|
LSD - true hallucinogen in ____ doses, in _______ doses get a high
|
high
low |
|
LSD - dose
|
0-300 micrograms
|
|
LSD - administration
|
Gelatin tabs
Sugar cubes microdots |
|
LSD - lowest dose
|
Blotting paper
|
|
How long to feel the effects of LSD
|
30-90 mins
|
|
LSD - how much reaches brain
|
1%
|
|
LSD - half life
|
110 minutes
|
|
LSD - metabolism
|
in the liver
excreted in feces |
|
Monoamines
Catecholamines |
Epinephrine
Nor-Epinephrine Dopamine Serotonin - not a chatecholamine |
|
Psychomotor stimulants
|
Amphetamines
Ephedrine Cocaine Cathinone |
|
Psychomotor stimulant effect on the nervous system
|
Stimulate neuronal transmission at synapses
|
|
Which synapses do psychomotor drugs stimulate
|
Ones that use epinephrine, nor-epinephrine, dopamine and serotonin
|
|
What are the monoamines and which is not a catecholamine?
|
Epinephrine
Nor-Epinephrine Dopamine Serotonin - not a catecholamine |
|
Amphetamines are created in the ______
|
Lab
|
|
Amphetamine can be synthesized from ________ and ________ to make__________
|
Ephedrine
Pseudoephedrine crystal meth |
|
Ephedrine and pseudo ephedrine to make crystal meth can come from where?
|
Sudafed
|
|
Which of the psychomotor stimulants is naturally occurring
|
Ephedrine -
Cocaine Cathinone |
|
Cocaine and cathinone are from ___________
|
Eastern Africa
Southern Arabia |
|
Cocaine history - Who used it, how did they use it and where were they
|
Chewed by indian tribes in South America
|
|
Cocaine history - where found and when?
|
Peruvian burial sites back to 2500 BCE
|
|
Is coca-cola still made from coca leaves?
|
yes with the cocaine component removed
|
|
Ma Huang
|
Ephedrine
|
|
Ephedrine was first used in _________ and called ____________ for 5000 years
|
Ma huang in china for 5000 years
|
|
Ephedrine became so popular in the late 1800's and early 1900's that ____________.
|
Scientists searched for a synthetic
|
|
When was amphetamine synthesized?
When did people start using it? |
1910
1927 |
|
Methamphetamine History - when did AMA allow and for what?
|
1937
Narcolepsy and depression |
|
Methamphetamine History - what was it used for in 1943?
|
Diet pills
|
|
Natural stimulant from Khat leaves
|
Cathinone
|
|
Cathinone
|
Natural stimulant from Khat leaves
|
|
Cathinone is chemically similar to what other drugs
|
ephedrine and amphetamines
|
|
Cathinone induces what neurotransmitter release?
|
dopamine
|
|
Cathinone has been used where and for how long?
|
Eastern and central Africa and Arabian peninsula since recorded history
|
|
How is cathenone administered?
|
Chew leaves or make tea
|
|
Why aren't amphetamine and cocaine eaten?
|
they are weak bases
|
|
Can amphetamine and cocaine be absorbed in the digestive system?
How are they better administered? |
Yes
Injected, sniffed, smoked or inhaled |
|
Cocaine and amphetamines are ________ distributed through the body
|
Easily
|
|
Amphetamines and cocaine are metabolized by _________ and excreted in ___________
|
Liver
Urine |
|
Which has a shorter half-life, Cocaine or amphetamine
|
Cocaine
|
|
Increase activity in MA synapses by stimulating leaking of transmitter, thus increasing the amount of transmitter released and by blocking reuptake of the transmitter by post-synaptic cell
|
Amphetamines and cathinone
|
|
Blocks uptake of the transmitter
|
Cocaine
|
|
Closely related to the meso-limbic dopamine system which governs reinforcement/reward
|
Monoamine (MA) systems in the brain
|
|
Basal ganglia regulates
|
Body movement
|
|
Body movement is regulated in the
|
Basal ganglia
|
|
Meso-limbic dopamine system (reinforcement and reward)
Basal ganglia Release of Dopamine in the NA |
Which areas of the brain are associated with psychomotor stimulants?
|
|
Release of dopamine in the NA possibly initiates
|
addictive effects
|
|
Psychomotor drugs in the body
CNS or PNS? What are the effects? |
PNS
Increase HR and BP Dilate blood vessels and air passages in lungs |
|
Psychomotor drugs were first used for
|
Asthma
|
|
Amphetamine causes ____________.
|
insomnia
|
|
Psychomotor drug on behavior
|
Improve mood at first but then depression
|
|
Stereotypic behavior
|
the senseless repetition of a meaningless act
|
|
When taken continuously, psychomotor drugs cause________, _________, and ________
|
Stereotypic behavior, psychosis and paranoia
|
|
In low doses amphetamine and cocaine can _____________ performance and eliminates ________ associated with cognitive or perceptual tasks or athletic activity
|
improve
fatigue |
|
Amphetamines can cause _________ in animals trained under the influence
|
dissociation
|
|
What is dissociation
|
when you can recall what you've learned under the influence of a drug
|
|
Cocaine tolerance - Acute
|
every 20-30 mins for 10-12 hours
|
|
Coke out
|
Acute cocaine tolerance where the drug no longer becomes effective at improving mood
|
|
How long does a coke out last?
|
24 hours
|
|
Cocaine meth - chronic tolerance
How long appetite effects on BP and HR Lethal dose |
after 2 weeks
appetite comes back a little effects decrease goes up |
|
Amphetamine and cocaine withdrawal is characterized by
|
intense depression
|
|
fMRI and PET scans show changes in ____________ activation up to a _______ after a person stops using cocaine and amphetamine
|
frontal cortex
year |
|
What are the patterns of cocaine and amphetamine use and do we see it in animals too?
|
Yes
intense use with little eating or sleeping followed by a period of abstinence and recovery followed by another run |
|
Two most addictive and reinforcing drugs
|
Amphetamine and cocaine
|
|
Liver damage
Inflammation and ulceration of mucous membranes in nasal passages Money loss |
Harmful effects of Cocaine
|
|
Hallucinations, paranoia, cravings, antisocial behavior, concentration/attention problems, blurred vision, weight loss
|
Bad effects of Cocaine while in a run
|
|
restlessness, excessive talking, confusion, dizziness, tremors
|
Harmful effects of amphetamine - short term
|
|
paranoid psychotic behavior
|
Harmful effects of amphetamine - long term
|
|
Paranoid psychotic behavior associated with amphetamine use is probably due to
|
lack of sleep and food
|
|
Amphetamine - After 4 uses there is damage to what neurons
|
dopaminergenic
|
|
Treatment for psychomotor drugs
|
Detox using valium for acute withdrawal
|
|
Treatment for psychomotor drugs - What is the best treatment for psychomotor drugs?
|
inpatient
|
|
Serotonin agonist in the CNS
Locus Coeruleus Cortex |
LSD in the brain
|
|
What is a serotonin agonist?
|
mimics serotonin
|
|
Part of the brain most effected by LSD
|
Locus coeruleus
neocortex |
|
Locus coeruleus is part of the ____________ pathway
|
fear/reward
|
|
What is believed to be the source of hallucinations with LSD?
|
Cortical alteration
|
|
Colorful visions
Mystical feelings Strong emotions Love and empathy |
LSD
|
|
Impairs reaction time
inattentiveness Improves some motor tasks |
Behavior on LSD
|
|
LSD Tolerance
|
2-3 days - the drug stops working for about a week
|
|
LSD withdrawal
|
no known symptoms but flashbacks
|
|
Ecstasy what is it and what is it's main ingredient?
|
combined properties of chatecholamine-like drugs and amphetamine
MDMA |
|
Enhances social intimacy
Induces self-insight and empathy to others |
Ecstasy
|
|
Ecstasy -
How taken How long until absorbed half-life |
orally
2 hours 8 hours |
|
enhances the release of and then blocks the reuptake of catecholamines, mostly serotonin
|
Ecstasy - in brain
|
|
deplete serotonin
causes depression, sleep disorders and anxiety |
Ecstasy - heavy use
|
|
loss of temperature regulation
dehydration heat-stroke |
Ecstasy - heavy dose
|
|
Dissociative anesthetics
|
Ketamine and PCP
|
|
Ketamine or PCP administration
|
snorted, injected or taken orally
|
|
Ketamine or PCP - how long until you feel it?
|
minutes
|
|
block NMDA receptors in the cortex
|
Ketamine or PCP - in brain
|
|
Ketamine or PCP - what do they induce?
|
numbness, analgesia and relation
memory loss |
|
GHB is a ___________ of GABA
|
metabolite
|
|
GHB is a metabolite of _________
|
GABA
|
|
GHB - outlawed in
|
1990
|
|
GHB - does it have medical uses?
|
yes
|
|
GHB -
How taken effects begin peak |
orally
15-30 min 25-45 min |
|
GHB -
low dose High dose |
relaxation and sleep
un-arousable sleep and coma |
|
Has it's own receptor in the CNS and modifies activities of several NT's
|
GHB - receptors and NT's
|
|
GHB -
Acts like causes other name is it self-administered by non-humans |
Anesthetic
Alcohol-like intoxication with amnesia Date rape drug no |
|
bloodshot eyes
droopy eyelids dry mouth munchies HR increase Fluctuations BP and BT |
THC
|
|
THC - sleep
small dose large dose |
increase drowsiness
interferes with sleep |
|
THC - helpful effects
|
Glaucoma - reduces pressure
anti-emetic - chemo Spasticity - MC Pain, weight, appetite loss - cancer, AIDS |
|
THC - can it cause Hallulcinations?
|
yes in high doses
|
|
THC -
short-term memory driving tolerance |
can't store new information
interfere's drive slow yes for all effects |
|
THC withdrawal - when
what happens |
after frequent high dose use
Hot flashes, runny nose, loose stool and sweating |
|
THC harmful effects
large doses long term use |
Paranoia or anxiety in large doses
cannabis dementia |
|
Cannabis dementia
|
memory loss
similar brain volume reduction as seen with alcoholics |
|
THC - Reproductive
|
lower testosterone
prevent egg implantation |
|
THC prenatal exposure
|
can cause hyperactivity, cognitive behavioral disorders observed at pre-school ages
|
|
THC increases lung cancer risk when combined with
|
cigarette smoking
|
|
THC increases lung cancer risk when combined with
|
cigarette smoking
|
|
Methylxanthines
|
Caffeine
Theophylline Theobromine |
|
Methylxanthines -
How taken Absorbed where peak levels in how long |
orally
some in stomach but most in intestines 30-60 mins |
|
Methylxanthines - Do they cross the blood brain and placental barrier?
Are they in breast milk? |
yes, yes
|
|
How much caffeine is excreted, unchanged in the urine?
|
2%
|
|
Caffeine metabolism is slowed by and sped up by
|
alcohol
smoking and broccoli |
|
Caffeine metabolism in women
|
varies based on monthly cycle hormone levels
|
|
Caffeine metabolism
Where How long Half life |
liver
slowly eliminated 3.5 hours |
|
block receptors of the inhibitory neuromodulator adenosine resulting in over stimulatoin
|
Caffeine in the brain
|
|
What does a neuromodulator do
|
controls the action of several neurotransmitter systems
|
|
What is the general effect of adenosine
|
slow neuron firing
|
|
Caffeine releases what NT's
|
Epinephrine and other chatecholamines
|
|
Does caffeine improve performance?
|
yes
|
|
Caffeine 100-200 mgs IV
Higher dose |
similar feelings as cocaine
unpleasant sensations |
|
Caffeine
tolerance WD |
Tolerance with repeated use
Can be severe peaks in 20-48 hours and can last a week |
|
Is it possible to meet the requirements of substance abuse for caffeine?
|
yes
|
|
Caffeine average use how much and what drink
|
200+ mg daily
Coffee first and soda next |
|
Problems with caffeine use
reproductive prenatal heart disease and cancer |
high levels can alter chromosomes
Reduced blood flow to fetus lowering birth weight - 4+ cups increase SIDS High caffeine intake |
|
Caffeine effects on brain
|
unknown
|
|
Caffeinism
|
looks like anxiety neurosis
|
|
MAOI - name
|
Monoamine oxidase inhibitor
|
|
MAOI - drugs
|
Naridil, Parnate, Ludiomil
|
|
TCA - name
|
Tricyclic antidepressents
|
|
TCA - drugs
|
Tofranil, Elavil, Norpramin, Aventyl, Adapin, Remeron
|
|
First generation antidepressants
|
MAOI
TCA |
|
Second generation antidepressants
|
SSRI
SNRI DARI |
|
SSRI - name
|
Selective serotonin reuptake inhibitors
|
|
SNRI- name
|
Selective norepiniphrine reuptake
|
|
DARI - name
|
Dopamine reuptake
|
|
SNRI - drugs
|
Manerex, Asendin, Desyrel
|
|
DARI - drugs
|
Wellbutrin, zyban
|
|
Depression definition
|
affective or mood disorder
|
|
is depression associated with schizophrenia?
|
maybe
|
|
Common cold of mental illness
|
depression
|
|
What percentage of people in the US are suffering from a mood disorder in a given 6 mo period and how many in their lives?
|
3%
6% |
|
Depression
Gender more likely what % seek help How many work absences cyclic with mania gender difference |
women 2 times
20% 172 million/ day bipolar no gender difference |
|
Antidepressants -
admin peak blood level How long before effect |
orally
4 hours 2 weeks |
|
Which AD are metabolized slower than second generation AD's
|
Tricyclics
|
|
Most currently used AD drugs effect ________ in some way
|
Serotonin
|
|
MAOI's block destruction of
|
some toxins in food
Tyramine - pickled herring and cheese |
|
Depression - bio causes
|
Monoamine theory
Serotonin |
|
Monoamine theory of depression
|
Depression disrupts or is the result of disruption of the monoamine system resulting in lower level of MA neurotransmitters at the synapse
|
|
Serotonin theory of depression
|
Decreased activity in the serotonin system causes depression or leads to vulnerability to depression
|
|
TCA/SSRI
Max blood concentration |
1-3
4-8 |
|
AD first pass metabolism
|
much of the first dose is destroyed by the digestive system
|
|
What inhibits first pass metabolism of AD's and what is the effect
|
Alcohol - bigger dose of AD than expected
|
|
AD's in system
barrier cross concentrate in half life |
blood brain and placental (breast milk)
Lungs, kidneys, liver and brain up to 75 days |
|
Because of the half life of AD's what is it important to do
|
wean off of them
|
|
SSRI and kids
|
Work in children but side effects and effects on brain development are not known
|
|
TCA's in NS
|
block activity in the parasympathetic NS
|
|
dry mouth, constipation, dizziness, irregular HB, blurred vision, ringing in ears, uring retention, excessive sweating, and tremors
|
TCA blocking activity in the parasympathetic NS results in
|
|
SSRI effects in the body
|
nausea, headache, nervousness, insomnia
|
|
Serotonin syndrome
Cause |
Acute increase in serotonin
|
|
disorientation, agitation, confusion, fever, shivering, diarrhea
|
Serotonin syndrome
effects |
|
Serotonin syndrome happens when
|
doubling up different SSRI's or combining with psychomotor stimulants
|
|
TCA - sleep
|
Sleepiness
Crazy nightmares |
|
Wellbutrin - sleep
Other AD's sleep |
Increases REM
Decreases REM - improves depression |
|
Prozac - cosmetic psychopharmacology
|
1990 said prozac could fix your personality
|
|
Some suggest that effects become less potent in a few months but not conclusive
Negative side effects lessen within a few weeks except for tiredness |
AD - Tolerance
|
|
AD - Withdrawal
How TCA SSRI |
Should be weaned off
Restlessness, anxiety, chills, compulsive body movements Dizziness, insomnia, anxiety, nausea, quick onset severe depression/anger, irritability |
|
AD - harmful effects
reproduction teratogenic miscarriage |
affect ejaculation
no known but some new data says yes 2x's as likely to miscarry |
|
AD - Harmful effects
voilence and suicide |
Some reports but studies don't show this. may be due to 3rd variables
|
|
if combined with other drugs serotonin syndrome can lead to respiratory, circulatory and kidney failure
but none with SSRI's alone |
SSRI - Overdose
|
|
3rd most common cause of drug related death
Heart failure small ED-LD difference |
TCA - Overdose
|
|
combining alcohol and heroin or methadone can cause death
|
AD overdose
|