Psych

Front 1

changes in the brain due to addiction

Back 1

tolerance, sensitization(cravings), dependence, withdrawal

Mesolimbic DA: VTA to NA

Front 2

too much vs too little
DA
5HT
NE
ACh

Back 2

DA: XS -- Schizophrenia, Neuroleptic malignant syndrome, Addiction (mesolimbic)
DA: deficit -- Parkinson's, EPS, ADHD?

5HT: XS --
5HT: deficit -- depression

NE/Ach deficit - ADHD??

Front 3

what does the addicted rat want to inject where?

Back 3

DA/Amphetamine/Cocaine into NA

opiates into VTA (disinhibition causes DA release in the NA)

DA as final common pathway

Ethanol, Nicotine, Cannabis cause increased DA into the NAcc

Front 4

relapse triggers

Back 4

low dose drug exposure(priming)
drug associated cues
Stress

Front 5

cross priming

Back 5

person addicted to cocaine should not start with alcohol because that will cause them to relapse with the cocaine

Front 6

alcoholism stats

Back 6

50% have comorbidity
women: anxiety and mood DO
men: substances, conduct DO, antisocial PD

Bipolar and secondary alcoholism

25-55% of alcoholics develop a secondary depression

alcoholism = depression as suicide risk!

Front 7

questions for alcohol addiction

Back 7

CAGE

Cut down?
Annoyed?
Guilty?
Eye opener?

Front 8

NT affects of Alcohol

Back 8

potentiates GABAa
inhibits NMDA
5HT3 R potentiation
mu opioid receptor alcohol promotes agonist binding

mesolimbic DA Ssystem - reinforcing

Front 9

GABA binding

Back 9

Alcohol
Benzodiazepines
Barbituates

all help with seizures - withdrawal from these substances causes seizures

Front 10

management of alcohol intoxication

Back 10

nutritional support
IV thiamine
then alcohol

Front 11

amnestic disorders that are alcohol induced

Back 11

Wernicke's encephalopathy
-thiamine deficiency
-abrupt onset of encephalopathy
-truncal ataxia
-opthalmoplegia

Korsakoff's psychosis - chronic
-severe anterograde amnesia
-confabulation
-thalamic nuclei and mamallary bodies
frontal lobes

Front 12

Alcohol withdrawal

Back 12

autonomic hyperactivity (increased HR, BP, RR, T, sweat)

anxiety

Insomnia
Psychomotor agitation
N/V
tremor

rare: auditory, visual, tactile hallusc/illsn, grand mal seizure

peak at 3 days (lasts 7-10)

Front 13

delirium tremes

Back 13

1/3 of pt with seizures go on to develop DT's with more medically compromised populations

confusion
disorientation
fluctuating/clouded consciousness
perceptual disturbance
mortality 1-2@ (emboli, arrhythmias, metabolic disturbances, ifxn, hyperkalemia, hyperpyrexia, dehydration

Front 14

management of Alcohol withdrawa;

Back 14

Benzodiazepines (silver bulled to Alco withdrawal) Lorazepan

...

Front 15

after detox - now treat the addiction

Back 15

denial is major defense mechanism
family help with intervention - might occur over time.

Front 16

first step in AA

Back 16

we admit that we are powerless over alcohol and that our lives have become unmanageable (to overcome the denial)

Front 17

two approaches with alcoholics

Back 17

1) make sure the depression/bipolar are treated
2) Naltrexone(opioid antagonist), Acamprosate, Disulfram

Front 18

naltrexone

Back 18

opioid antagonist
reduces craving
easier to say no

Front 19

acamprosate

Back 19

GABA ergic -
reduces cravings
easier to say no

Front 20

whats better than treatment with either naltrexone or acamprosate??

Back 20

treatment with both!

Front 21

disulfiram

Back 21

alcohol sensitizing agent
inhibits Alcohol dehydrogenase
buildup of acetaldehyde
--> disulfiram - ethanol reaction

complication - quite ill if they do binge on alcohol

bad: doesn't help with cravings

some patients take all three togehteR:
naltrexone, acaprosate, disulfiram

Front 22

alcohol physical sx

Back 22

increased MCV (vit 12 deficiency)
B1 - thyamine deficiency

Front 23

opioid - opiates

Back 23

opiates: opium and naturally occurring derived drugs = morphine and codeine

opioid: synthetic, different chemically, but acting at the same receptors: hydrocodone (vicodin)

all euphorogenic
capacity to reinforce
avoidance of averse feelings will reinforce (withdrawal is so bad)

Front 24

opioid intoxication

Back 24

sedation

euphoric, constricted pupils- the PS is activated - patients are relaxed, slurred speech

Front 25

opioid withdrawal

Back 25

agitated, anxious, DIALATED PUPIL, dysphoric mood +

flu-like: nausea, vomiting, muscle aches, diarhea lacrimation, insomina

Front 26

OD opiate

Back 26

reverse the opium intoxication: opium antagonism via:

NALOXONE (20 min half life - very short)

Front 27

opioid detoxification

Back 27

methadone (mu receptor agonist)
clonidine is an antihypertnesive used to make the withdrawal more barable

Buprenorpine - partial agonist on mu

Front 28

opioid dependence

Back 28

after detoxification - now treat the addiction
maintenance therapy:
mu replacement:
methadone (also detox agent)
LAAM
buprenorphine (parital ago - can't die from the OD of this)

naltrexone (reduce cravings - helps that heroin doesn't give them the high anymore)

Front 29

careful with ??? after OD heroin

Back 29

naloxone will wear off fast - 20min - don't let the OP pt go - we should treat them - prognosis is bad for the long term -

Front 30

benzodiazepines with half life differences

Back 30

help with sleep, anxiety, panic, anti-seizure,

the lower the half-life, the more dangerous for addiction - ex: Xanax is most addicting, then valium (diazepam)

also: they cause dependence and abuse, paradoxical agitation, disinhibition,

Front 31

prescription sleep

Back 31

Benzodiazepine-like:
Zolpidem (Ambien)
Zaleplon (Sonata)
Eszopiclone (Lunesta)

Front 32

when do we do maintenance treatment?

Back 32

if the condition has progressed to for example severe heroin addiction, the patient should be kept on maintenance treatment - however, if the patient is not that addicted, we want to get them clean of the substances - and not use the maintenance = just more mu ago: methadone/buprenorphine

Front 33

cannabis intoxication

Back 33

>4000 years old
gateway

hashish - resin

intoxication:
dry mouth, tachycardia, red eyes, appetite changes

Front 34

cannabis withdrawal

Back 34

mild flu-like:
irritable, tremor, diaphoresis, nausea, appetite changes, sleep disturbance,

similar to opioid withdrawal in animal studies with synthetic cannabinoid antagonist

Front 35

cannabis chronic abuse sx

Back 35

cognitive difficulties
impaired motor function
depression
paranoia
psychosis
feminization
amotivational syndrome

Front 36

cocaine speed of reactions with different modes of acqusition

Back 36

intranasal: 2-3min
injection dissolved cocaine (IV): 15-30s
smoking "crack" cocaine ": 6-8s

crack: It is a freebase form of cocaine that can be made using baking soda (sodium bicarbonate) or sodium hydroxide,[1] in a process to convert cocaine hydrochloride (powder cocaine) into methylbenzoylecgonine (freebase cocaine).

Front 37

cocaine mechanism of euphoria

Back 37

increased DA/NE/5HT
simulant essentially !
inhibition of reuptale
mesolimbic DA system

Front 38

pupils with cocaine

Back 38

DIALATED (vs opiates)

Front 39

treatment for cocaine dependence

Back 39

12 step, behavioral

wellbutrin?
cocaine vaccine! !

Front 40

personality =

Back 40

character+temperament

Front 41

devoted becomes what pathologically?

Back 41

dependent

Front 42

self confident pathologically?

Back 42

narcisstic

Front 43

vigilant pathologically

Back 43

paranoid

Front 44

mercurial (loves relationships, energetic, shows how they feel, creative, explorative, skilled at distracting from reality when it's painful)

Back 44

borderline

Front 45

adventerous pathological

Back 45

antisocial

Front 46

aggressive pathological

Back 46

sadistic

Front 47

serious pathologicallt

Back 47

depressed

Front 48

conscientious pathological

Back 48

obsessive compulsive

Front 49

dramatic pathological

Back 49

histrionic

Front 50

solitary pathological

Back 50

schizoid

Front 51

sensitive pathologically

Back 51

avoidant

Front 52

leisurely style pathologically

Back 52

passive-aggressive

Front 53

borderline and treatment

Back 53

they get more anti-depressants than MDD! hard to control -

Front 54

treatment of PD

Back 54

1) heterogenous group, treatment not "one fits all"
2) tx plan should address axis II plus co-morbid Axis I conditions
3) both psychohterapy and pharmacotherapy should always be considered
4) motivation for tx varies greatly among PD
5) Cluster A are very mistrustful
6) Cluster B can
seek tx (BPD, HPD)
deny the need for tx (ASPD, NPD)
be untreatable (ASPD)
7) cluster c will seek tx,
8) have to be flexible

Front 55

schizotypal

Back 55

common markers with schizophrenia
and they have + sx

Front 56

schizotypal

Back 56

hallucinations,
once a week was enough
very violent scary dreams
derealization feelings
anxiety overwhelmed
spending sprees- impulsivity
self-destructive
chaotic mental states
after 4 yrs he realized that medication might work - TCA and then MOA - carbamate
she had to be on meds

Front 57

stimulant danger

Back 57

cerebrovascular vascoconstriction

Front 58

what outdoes food and even sex with respect to DA stimulation?

Back 58

Amphetamines!! ! and also cocaine and even nicotine and morphine(slower onset)

Front 59

DA inactivation? and then cocaine?

Back 59

reuptake


binds to the reuptake inhibitor!! (amino acid transporter- 2 states of helix springs - actin like)

Front 60

in nl state of DA vs stimulators

Back 60

with chronic use of amphetamines -- the DA transporter is upregulated;
the receptors on post symaptic are also downregualted because they have been bombarded with DA for so long

Also MAO - bkdn DA - the metabolate forms 6hydroxine

overactive neurons are killed

too much knowledge can give you seizure/stroke!

Front 61

brain scans of PD vs Cocaine/Amphetamine addicts

Back 61

due to cytotoxicity of the metabolite of MAO with too much DA - the striatum looks equally affected

the D2 receptors are degenerated

Front 62

life just sux

Back 62

they need a supercharge od DA to stimulate the reward sx

Front 63

3 ways to diminish DA In the synapse

Back 63

transporter is upregulated, cells that make the DA are killed, receptor function is reduced - don't recover even after 4month abstinence

Front 64

learn

Back 64

glutamate to learn, GABA to stay seated

Front 65

D2 receptor

Back 65

decreases correlated with decreases in orbitofrontal and cingulate brain metablism in stimulant abusers

frontal ctx needed for getting in / staying in med school

Front 66

stimulant abusers perfusion

Back 66

adherent platlets, vasoconstriction
occipital brain perfusion defect
occipital bad perfusion - made last as with fontal ctx

blood supply serves the other areas well

Front 67

depending on the stickyness of your platelets

Back 67

right insula (reptitive)
cingulate (decision)
temporal (auditory)
occipital


)calcarine cortex


2nd
dorsal stream
frontal eye fields

Front 68

cocaine abusers and the sad videotape

Back 68

they are not emotionally affected, - they are only activated by people takinf cocaine - cocaine clues

they are inhibiting themselves not to go and steel...
automatic - there is no real thinking involved - they see it they act

Front 69

GABA and cocaine

Back 69

GABA deficit after chronic cocaine
cortical CBF reflects mostly GABA inter-neuronal activity

GABA activity reduced during visual activaton to usual cues like sadness compared to normals

cocaine cues lead to over- arousal in users but are irrelevant to normals, so little visual cortex activity in normals.


they don't understant complex emotional events that they are seeing
cocaine abusers can not decide quickly

stimulat abusers--> DA deficiency like PD
vasoconsticaion - corical
affective sensory stimuli

Front 70

beta endorphine and naltrexone

Back 70

block the feedback - presynaptic blockade

post synaptic are also blocked by the naltrexone - but there are many more receptors in the presyatpticl cell

the b-endorphins don't rise with sb with no addiciton

Front 71

naltrexone works best if

Back 71

you're worse off

Front 72

genetic responsitivity to naltrexone

Back 72

G-protein coupling is intense

naltrexone works much better with sons of alcoholics

Front 73

prone to alcohlism

Back 73

low lvs of beta-endorphines


of you give them ONE drink - they get a very big charge out if it

Front 74

mu opiate receptor knockout

Back 74

don't like alcohol

Front 75

the farthery you go north there is

Back 75

more and more this polymorphism

high genetic risk of alcoholism

Front 76

polymorphism with altitude

Back 76

the beta endorphine helps you withstand pain

3 fold greater affinity with beta-endorphines

they have low levels of beta- endorphine bc they have a sensitive receptor
then when they are stimulated they have a 3x increase of halliness

Front 77

nicotine drugs

Back 77

Nicotine patch, gum, lozenge, inhaler, spray
Bupropion
Varenicline: Partial nicotinic receptor agonist

Front 78

personality disorders A-C

Back 78

A: schizoid, schizotypal, paranoid
B: nihilistic, histrionic, borderline, antisocial
C: avoidant, dependent, OCPD

Front 79

treatments for stage fright

Back 79

beta blockers - -olols

Front 80

treatment for hypochondriac

Back 80

imipramine, fluoxetine, paroxetine

Front 81

only SSRI approved for only OCD

Back 81

furoxetine

Front 82

drug for GAD

Back 82

SSRI / SNRI / TCA

or

transient: Benzodiazepines


specifically:
fluoxetine, paroxetine, escitalopram, citalopram, sertraline

Front 83

difficulr DD-ineractions antidepresant

Back 83

nefazodone 3A4 enzyme

Front 84

buproprion

Back 84

seizure counterindicated, not for anxiety disorders

no serotonin activity
no sexual side effects

Front 85

antipsychotics

Back 85

typical: D2 antagonism: haldoperidol (high potency - you don't need alot, so there is little Ach SE) vs Clopromazine(trazodone) which is low potency (less risk of Neuroleptic malicnancy disorder, and less EPS)


Atypical - shorter D2, 5HT2 compoent:
Quetiapine, Olazepine (wieght gain)
Clozapine (weight gain)
Abilify - aripirazole
Ziprasidone (no weight gain)
Risperidone (peds, dose dependent - can become typical AP)
perospirone
Paliperidone

Front 86

varenicline

Back 86

as the dose increases, slowly produce a blocker - they won't feel good

must start with slow dose -

CHANTIX

partial BLOCKER at the NA

Front 87

selegiline

Back 87

MOA-I inside tabacco smoke!!

so, when you stop smoking - thy get sad - and to replace the smoke antidepressant - we use segiline

Front 88

SERT

Back 88

ss prone to depression after repeated stress

Front 89

NE and DA in the prefrontal cortex

Back 89

attnetion and positive moor goal directed behavior

Front 90

2D6 inhbition

Back 90

some SSRI block this - and this one might be needed for the breakdown by this ezye - and the other drug will go up to toxic lvl 3A4 inhibition is worse