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76 Cards in this Set

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most drugs of abuse do what/where?
increase dopamine in the nucleus accubens
Addiction (def)
compulsively using a drug despite negative social, medical, and economic effects
Heroin (effects)
Heroin stimulates the mu opiod receptors. It is highly lipid soluble and passes through the blood brain barrier easily. It breaks down into morphine
opioid withdrawal symptoms
Short term (5 to 10 days)- insomnia, drug craving, nausea/vomiting, hypertension, dysphoria

Long Term- cylical weight increase, drug craving, anxiety, insomnia.
Treatment options for Opioid withdrawal.
Agonist- methadone (simply replaces with another addictive drug.

Suppresion of autonomic hyperactivity- uses clonidine, an a2 receptor agonist.

Antagonist plus General Anestesia- quick w/d symptoms, rapid onset...but shortens w/d period
Rationalle and Difficulties of Agonist approach to Opioid relapse prevention
Rationalle- maintain a constant activation of target sites by keeping blood concentration at a steady ammount. Leads to cross tolerance, but avoids rapid on/off activation of reward mediator.

Difficulties- reward may not underlie all drug consumption, can lead to addiction, may need to take it for a lifetime, and stopage can bring on w/d symptoms
Rationalle and Difficulties with Antagonist approach to Opiod relapse prevention
Rationalle- tries to eliminate a drugs rewarding effects by blocking their targets

Difficulties- can produce w/d like symptoms, taking more drugs can overcome antagonist, many drug's targets serve important physiological functions, reward doesn't always underlie consumption.
Why is antagonist approach difficult with alcohol?
B/c alcohol works through many different types of receptors.....ie opioid, GABA, glutamate.
W/d symptoms of alcohol
hypertehermia, insomnia, anxiety, convulsions, and in some cases delirium tremens, which is an acute psychosis

--can take a week and can be fatal
Treatment of alcohol abuse
use a long acting sedative

---Benzodiazepine should be tapered off slowly in order to prevent emergence of w/d symps. (benzo is only abused by people already addicted to something else)
Aversion Therapy (rationalle and difficulties) for alcohol abuse
Use Disulfiram, which leads to a buildup of acetaldehye....causes a negative reaction whenever you drink (vomiting, headache, etc..)

Difficulties- compliance among alcoholics.
Antagonist approach to alcohol w/d treatment
Naltrexone- an opiod receptor antagonist, blocks the reward associated with alcohol.

NOTE: both this and disulfiram affect the liver and shouldn't be used together or in a chronic liver disease pt.
Anticraving treatment for alcohol.
Use alcamporsate, a glutamate receptor antagonist
Anticraving rationalle and difficulties
Rationalle- during prolonged drug consumption, the desire for taking the drug switches from reward (want) to craving (Need)....result of physiological changes due to repeated taking of the drug

Difficulties- must identify the plasticity that occured and effectively block or mask it.
Tobacco mechanism of action
stimulates the central nicotinic receptors and may inhibit monoamine oxidase.
Agonist/antagonist/anticraving approach to treating tobacco
Agonist- Use nicotine replacement therapy (most discont. within 2 weeks)

Antagonist- Along with nicotine replacement, use an antagonist. may reduce the side effects of each compound.

Anticraving- Bupropion- inhibits the uptake of monoamines....reduces nicotine cravings and may prevent relapse.
Symptoms of schizo
hallucinations, early onset, compounded by stress, progresses , resistance to treatment, high suicide rate, emotionally withdrawal, difficult to diagnose
Positive/Negative/Cognitive Affects of Schizo
Pos- distortion of perception, distorted thoughts, disorganized speaking.

Neg- diminished fluency of speech or thought, affective blunting, reduced motivation, anhedonia(diminished capacity to derive enjoyment), social w/d

cognitive deficits-problems with memory, learning, attention
Criteria for Schizo
Must have a prolonged duration, symps. must not be due to mood disorders, and mustn't be the result substance abuse.
How does schizo develop?
Birth- slight emotional and motor impairments
Child- cognitive impairments (memory, attention) and neg. symptoms may begin

Acute pahse- first psychotic episode-confusing changes in behavior.
Episodic psychoses- pts. often expiereince periods of partial and full remission.
Prognosis of schizo depends on?
Severity of negative symptoms and cognitive deficits, as drugs can't fix them.......some go into partial or full remission, others have rapid cognitive decline
What causes schizo?
Environmental factors-viral infection, etc....

Genetic factors

Developmental factors- evidence of change in brain structure and function
Dopamine Hypothesis
Increased dopamine activity undelies schizo symptoms.

antipsychotic agents block DA receptors.

treatment efficacy is associated with a reduction in HVA (dopamine metabolite)

Increase in dopamine can be seen in schizos

individuals with a less effective COMT form are at a high risk for schizo
problems with dopamine hypothesis
dopamine antagonists don't treat all symptoms of schizo

theraputic efficacy doesn't emerge immediately.
gluamate hypothesis
blocking the NMDA receptor can exazerbate or produce schizo

schizos show a decrease in glutamate in the cerebrospinal fluid and also have elevated levels of NMDA antagonists (NAAG).
what are the two types of antipsychotic agents and what do they work on?
typical- block D2 like receptors
ex. haldol---commonly used, potent..fewer side effects
atypical- block seratonin 2A receptors.
Typical adverse effects
autonomic-
muscarinic- dry mouth, constipation, uniary retention
alphanoradrenergic- impotence, orthostatic hypertension

removes dopamines inhibition of prolactin, results in false pregnancies and altered libido

can also result in neuroleptic Malignant syndrome, a sudden life threatening disorder causing rigidity, stupor, and autonomic instability.
Typical drug extrapyrimidal motor sideeffects
parkinsons like syndrome, akathisisa(constant pain and discomfort....need to move), acute dystonia(muscle spasm in the face, back and neck......due to dopamine receptor blockage), tardive dyskinesia- abnrmal spasms or muscle movement...potentially irrecersible.
Typical adverse effects
autonomic-
muscarinic- dry mouth, constipation, uniary retention
alphanoradrenergic- impotence, orthostatic hypertension

removes dopamines inhibition of prolactin, results in false pregnancies and altered libido

can also result in neuroleptic Malignant syndrome, a sudden life threatening disorder causing rigidity, stupor, and autonomic instability.
Atypical Adverse effects
dry mouth, constipation, unirary retention

weight gain, higher cholesterol,

Clozapine has those plus agranulocytosis, a decr. in white blood cells.......need to have weekly blood counts.
Drug Interactions of typical and atypical
barbituates, alcohol, benzos, opiod analgensics, and antihistimanes cause CNS depression.

Anticholiergics cause toxicity and hallucinations

Erythromycin, clarithromycin inhibit antipsychotic mechanisms
Obstacles to treating schizo
patients and families don't believe they have it, stigma, disorganized thinking may inhibit compliance, sever side effects, substance abuse.
what does chronic drug treatment of schizo do and when should it be stopped?
It decreses the intensity and frequency of psychotic episodes and should be ceased 2-5 years into remission
antipsychotic agent uses.
Treat psychoses do to schozo affective, shizopreniform disorders, brief psychotic events, and psychotic effects from other disorders.

Treat several movement disorders, incl. huntingtons

an antiemetic following the stimulation of the cemoreceptor trigger zone of the medulla.
Advantages of Atypical vs typical
Typical- costs much less and lacks clozapine side effects

atypical- lacks haloperidal's 'side effects and treats both pos and neg. symptoms.
When should you use clozapine?
treatment resistant schizo, high agression and suicide risk, prominent neg/cogn deficits, previous neuroleptic malignant syndro, parkinsons.
what are some future treatments of schizo?
increase NMDA receptor functions and increase group2/3 metabotropic glutamate receptor function.
explain what happens in Parkinsons, Alzheimers, and Huntingtons diseaase
Park- loss of dopamine in the substantia nigra

Alzheimers- destruction of the hippocampus and neocortex region of the brain

Huntingtons- pathological changes observed in the neostriatum
Genetic vs. other factors

What are Park/Hunt/Alz
Hunt is all genetic, but park and alz are a mixture
What are some environmental causes of Alz?
Elevated levels of mercury, aluminum, and BMAA's (especially prevelant in guam
What are some environmental causes of Park?
MPTP-leads to the prevelance of MPP and enters through monoamine transporters
Some oxidative signs of Parkinson's
drop in glutathione in the substantia nigra (1st diagnostic test)
-dopamine metabolism leads to peroxide
-high iron levels in substantia negra
oxidative sign of Alzheimers?
brain shows signs of damage due to free radical generation
What are the key features of Parkinsons?
bradykinesia- slowness of initiating and executing movement
muscular rigidity
termor-resting, usually ceases during voluntary movement
stooped posture and instability
cognitive deficits
explain how dopamine affects the basal ganglia and movement
dopamine shuts ff the indirect pathway, thus you dn't get get its inhibition of movement.

Indirect is a d2 like receptor, direct is a d1 like receptor. Explains why parkinsons, which is a loss of dopamine, causes inability to execute movement.
why don't you use dopamine in the treatment of parkinsons?
b/c it can't cross the blood brain barrier
explain levadopa's purpose
a parkinsons treatment requiring decarboxilization for the production of dpamine. Only about 3 percent of it actually gets through BBB. Also, you usually receive a COMT inhibitor so that it doesn't change before going into BBB
what is carbidopa?
It aids in LDopa getting across BBB and decreases peripheral side effects of ldopa....thus people can take drug longer
comment on LDopa's clinical efficacy?
1/3 respond well, 1/3 respond ok, 1/3 don't respond at all. There are intense side effects.....and it doesn't slow the disease, just treats symptoms....thus use it in moderate stage.
peripheral side effects of LDopa?
anorexia, nausea, and vomiting

cardiac arrythmias.
central side effects of LDopa
depression, anxiety, insomnia, hallucinations, euphoria


dyskinesia (sudden uncontrollable movements

abrupt cessation can lead to w/d symptoms

wearing off syndrome- reduction of efficacy...emergence of symptoms at end of cycle

on off syndrome- complete lack of efficacy/efficacy
What are some interactions of ldopa?
MAO A or non specific MAO inhibitors.......not MAO B inhibiters which elevate dopamine.......can result in a hypertensive crisis

antidepressants, vitanmin B6 (encourages peripheral metabolsim of ldopa)
what are some contraindications of ldopa?
Psychosis, glaucoma, active peptic ulcer, melanoma.
what are some alternative treatments for parkinsons?
Dopamine agonists-stimulate d2 receptors, less efficacy then ldopa, can produce psychosis, often used with ldopa

MAO inhibiters- selective inhibiter, increases the efficay of Ldopa

COMT inhibiters- incr. in the ammt of LDOPA reaching brain....reduces wearing off syndrome.

Muscarinic antagonists- can be used to treat mild parkinsons, very short lived effects, treats dyskinesia and bradykinesia

Amantadine- antiviral that blocks NMDA Receptors, very shortlived effects, diminishes bradykinesia, rigidity, an tremors.
what are some surgical interventions for parkinsons.
high freq. stimulation of thalamus and subthalamus reduces tremors

stimulation of globulus pallidus reduces dyskinesia.
Symptoms and treatment of huntingtons?
bried jerk like movement of the extremities, face, personality changes, cognitive deficits.

Dopamine antagnists--rarely used except when symptoms lead to falling.

antidepressants, antipsychotics.
Treatment of Alzheimers?
Involve the augmenting of cholinergic function of the brain (nerons of this part are lost).

Inhibits Acetylcholinesterase
What are the two classes of depression and what are they?
Major Depression- the symptoms of depression impede an individuals ability to function and are in excess relatively to a life event. Is the most common psychotic disorder

Bipolar- a cycling between mania and dpression.
Amine hypothesis to depression
the inhibition of monoamine neurotransmission causes depression, and the inhibition of 5-HT and norepinephrine inhibitors causes a relapse of depression following the depletion of the substances.
Problems with the Amine theory of depression
not everyone with inhibited 5-HT receptors and norepi receptors experiences depression.
conclusions about amine hypothesis of depression
inhibition of monoamines isn't the only cause of depression, but may be a mediating factor in the treatment
Prolonged administration to antidepression causes
changes in the number of andronergic and seratonin receptors

a decr. in the secondary messanger activity

a change the function of glucocorticoid receptors
Mecahnisms and examples of the 4 types of antidepressents
tricyclics- all inhibit norepi, some block seratonin......others (like imipramine) block norandrenergic, muscarinic, and histamine receptors.


SSRI- most commonly used, block seratonin, zoloft, paxil

MAO inhibiters- inhibit the metabolism of MA's.....MAoa- metabolizes dopa and seratonin MAOb- focuses on dopamine
ex. phen lzine

Atypical- many different effects bupropion, blocks dopa, nor, and ser
What are some clinical uses for antidepressants other than the obvious?
CHronic pain, eating disorders, anxiety disorders
Adverse effects of tricylics
postural hypotension, anxiety, memory impairment, blurred vision, weight gain, sedation...OD of it can lead to coma, respirtory depression, seiqueres, delirium, and cardiac issues
Adverse effects of MAO inhibiters
high risk of postural hypotension, insomnia, weight gains..........OD can lead to hallucinations, convulsions, and agitation.
adverse effects of taking SSRI's
most safe drug, nausea, vomiting, insomnia, sexual dysfunction
side effects of taking buproprin
GI issues, epileptic seizures
drug interatcions of MAO inhibiters
antidepressants- can cause seratonin syndrome....characterized by seizures, coma, hyperthermia.

Indirect acting sypathomimetrics- can increase tyramine levels, which vasoconstricts. (cold medicines)
how d you treat resistant depression?
increase dose, increase duration, switch compounds, electroshock therapy
some characteristics of mania
insomnia, loss of inhibition, impaired judgement, inability to speak, paranoia and hyperactivity
Which drugs exazerbate/lessen mania?
exz- dopamine and norepi
make better-catecholamine
What does lithium do and what are some precautions?
lithium can even out mood swings. You can treat flare ups while using as an ongoing treatment.

---effects may take awhile to happen....other drugs may need to be used concurrently

----overdone can result in nausea, convulsions, coma, and death.
what do antipsychotic and benzo agents do for biploarism?
can treat sever manic symptoms until lithium takes effect
what effect do antidepressents have on bipolarism?
used during the depression portion of it......but when given in the absence of lithium can switch to the manic phase (SSRI's don't do this as much)
Valproic acid's affects on bipolarism
actually as effective in controling non rapid cycling bipolarism as lithium and more effective in rapid cycling. But, can cause liver dysfuntion