Pharmacology

Front 1

most drugs of abuse do what/where?

Back 1

increase dopamine in the nucleus accubens

Front 2

Addiction (def)

Back 2

compulsively using a drug despite negative social, medical, and economic effects

Front 3

Heroin (effects)

Back 3

Heroin stimulates the mu opiod receptors. It is highly lipid soluble and passes through the blood brain barrier easily. It breaks down into morphine

Front 4

opioid withdrawal symptoms

Back 4

Short term (5 to 10 days)- insomnia, drug craving, nausea/vomiting, hypertension, dysphoria

Long Term- cylical weight increase, drug craving, anxiety, insomnia.

Front 5

Treatment options for Opioid withdrawal.

Back 5

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

Front 6

Rationalle and Difficulties of Agonist approach to Opioid relapse prevention

Back 6

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

Front 7

Rationalle and Difficulties with Antagonist approach to Opiod relapse prevention

Back 7

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.

Front 8

Why is antagonist approach difficult with alcohol?

Back 8

B/c alcohol works through many different types of receptors.....ie opioid, GABA, glutamate.

Front 9

W/d symptoms of alcohol

Back 9

hypertehermia, insomnia, anxiety, convulsions, and in some cases delirium tremens, which is an acute psychosis

--can take a week and can be fatal

Front 10

Treatment of alcohol abuse

Back 10

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)

Front 11

Aversion Therapy (rationalle and difficulties) for alcohol abuse

Back 11

Use Disulfiram, which leads to a buildup of acetaldehye....causes a negative reaction whenever you drink (vomiting, headache, etc..)

Difficulties- compliance among alcoholics.

Front 12

Antagonist approach to alcohol w/d treatment

Back 12

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.

Front 13

Anticraving treatment for alcohol.

Back 13

Use alcamporsate, a glutamate receptor antagonist

Front 14

Anticraving rationalle and difficulties

Back 14

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.

Front 15

Tobacco mechanism of action

Back 15

stimulates the central nicotinic receptors and may inhibit monoamine oxidase.

Front 16

Agonist/antagonist/anticraving approach to treating tobacco

Back 16

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.

Front 17

Symptoms of schizo

Back 17

hallucinations, early onset, compounded by stress, progresses , resistance to treatment, high suicide rate, emotionally withdrawal, difficult to diagnose

Front 18

Positive/Negative/Cognitive Affects of Schizo

Back 18

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

Front 19

Criteria for Schizo

Back 19

Must have a prolonged duration, symps. must not be due to mood disorders, and mustn't be the result substance abuse.

Front 20

How does schizo develop?

Back 20

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.

Front 21

Prognosis of schizo depends on?

Back 21

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

Front 22

What causes schizo?

Back 22

Environmental factors-viral infection, etc....

Genetic factors

Developmental factors- evidence of change in brain structure and function

Front 23

Dopamine Hypothesis

Back 23

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

Front 24

problems with dopamine hypothesis

Back 24

dopamine antagonists don't treat all symptoms of schizo

theraputic efficacy doesn't emerge immediately.

Front 25

gluamate hypothesis

Back 25

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).

Front 26

what are the two types of antipsychotic agents and what do they work on?

Back 26

typical- block D2 like receptors
ex. haldol---commonly used, potent..fewer side effects
atypical- block seratonin 2A receptors.

Front 27

Typical adverse effects

Back 27

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.

Front 28

Typical drug extrapyrimidal motor sideeffects

Back 28

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.

Front 29

Typical adverse effects

Back 29

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.

Front 30

Atypical Adverse effects

Back 30

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.

Front 31

Drug Interactions of typical and atypical

Back 31

barbituates, alcohol, benzos, opiod analgensics, and antihistimanes cause CNS depression.

Anticholiergics cause toxicity and hallucinations

Erythromycin, clarithromycin inhibit antipsychotic mechanisms

Front 32

Obstacles to treating schizo

Back 32

patients and families don't believe they have it, stigma, disorganized thinking may inhibit compliance, sever side effects, substance abuse.

Front 33

what does chronic drug treatment of schizo do and when should it be stopped?

Back 33

It decreses the intensity and frequency of psychotic episodes and should be ceased 2-5 years into remission

Front 34

antipsychotic agent uses.

Back 34

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.

Front 35

Advantages of Atypical vs typical

Back 35

Typical- costs much less and lacks clozapine side effects

atypical- lacks haloperidal's 'side effects and treats both pos and neg. symptoms.

Front 36

When should you use clozapine?

Back 36

treatment resistant schizo, high agression and suicide risk, prominent neg/cogn deficits, previous neuroleptic malignant syndro, parkinsons.

Front 37

what are some future treatments of schizo?

Back 37

increase NMDA receptor functions and increase group2/3 metabotropic glutamate receptor function.

Front 38

explain what happens in Parkinsons, Alzheimers, and Huntingtons diseaase

Back 38

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

Front 39

Genetic vs. other factors

What are Park/Hunt/Alz

Back 39

Hunt is all genetic, but park and alz are a mixture

Front 40

What are some environmental causes of Alz?

Back 40

Elevated levels of mercury, aluminum, and BMAA's (especially prevelant in guam

Front 41

What are some environmental causes of Park?

Back 41

MPTP-leads to the prevelance of MPP and enters through monoamine transporters

Front 42

Some oxidative signs of Parkinson's

Back 42

drop in glutathione in the substantia nigra (1st diagnostic test)
-dopamine metabolism leads to peroxide
-high iron levels in substantia negra

Front 43

oxidative sign of Alzheimers?

Back 43

brain shows signs of damage due to free radical generation

Front 44

What are the key features of Parkinsons?

Back 44

bradykinesia- slowness of initiating and executing movement
muscular rigidity
termor-resting, usually ceases during voluntary movement
stooped posture and instability
cognitive deficits

Front 45

explain how dopamine affects the basal ganglia and movement

Back 45

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.

Front 46

why don't you use dopamine in the treatment of parkinsons?

Back 46

b/c it can't cross the blood brain barrier

Front 47

explain levadopa's purpose

Back 47

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

Front 48

what is carbidopa?

Back 48

It aids in LDopa getting across BBB and decreases peripheral side effects of ldopa....thus people can take drug longer

Front 49

comment on LDopa's clinical efficacy?

Back 49

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.

Front 50

peripheral side effects of LDopa?

Back 50

anorexia, nausea, and vomiting

cardiac arrythmias.

Front 51

central side effects of LDopa

Back 51

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

Front 52

What are some interactions of ldopa?

Back 52

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)

Front 53

what are some contraindications of ldopa?

Back 53

Psychosis, glaucoma, active peptic ulcer, melanoma.

Front 54

what are some alternative treatments for parkinsons?

Back 54

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.

Front 55

what are some surgical interventions for parkinsons.

Back 55

high freq. stimulation of thalamus and subthalamus reduces tremors

stimulation of globulus pallidus reduces dyskinesia.

Front 56

Symptoms and treatment of huntingtons?

Back 56

bried jerk like movement of the extremities, face, personality changes, cognitive deficits.

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

antidepressants, antipsychotics.

Front 57

Treatment of Alzheimers?

Back 57

Involve the augmenting of cholinergic function of the brain (nerons of this part are lost).

Inhibits Acetylcholinesterase

Front 58

What are the two classes of depression and what are they?

Back 58

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.

Front 59

Amine hypothesis to depression

Back 59

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.

Front 60

Problems with the Amine theory of depression

Back 60

not everyone with inhibited 5-HT receptors and norepi receptors experiences depression.

Front 61

conclusions about amine hypothesis of depression

Back 61

inhibition of monoamines isn't the only cause of depression, but may be a mediating factor in the treatment

Front 62

Prolonged administration to antidepression causes

Back 62

changes in the number of andronergic and seratonin receptors

a decr. in the secondary messanger activity

a change the function of glucocorticoid receptors

Front 63

Mecahnisms and examples of the 4 types of antidepressents

Back 63

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

Front 64

What are some clinical uses for antidepressants other than the obvious?

Back 64

CHronic pain, eating disorders, anxiety disorders

Front 65

Adverse effects of tricylics

Back 65

postural hypotension, anxiety, memory impairment, blurred vision, weight gain, sedation...OD of it can lead to coma, respirtory depression, seiqueres, delirium, and cardiac issues

Front 66

Adverse effects of MAO inhibiters

Back 66

high risk of postural hypotension, insomnia, weight gains..........OD can lead to hallucinations, convulsions, and agitation.

Front 67

adverse effects of taking SSRI's

Back 67

most safe drug, nausea, vomiting, insomnia, sexual dysfunction

Front 68

side effects of taking buproprin

Back 68

GI issues, epileptic seizures

Front 69

drug interatcions of MAO inhibiters

Back 69

antidepressants- can cause seratonin syndrome....characterized by seizures, coma, hyperthermia.

Indirect acting sypathomimetrics- can increase tyramine levels, which vasoconstricts. (cold medicines)

Front 70

how d you treat resistant depression?

Back 70

increase dose, increase duration, switch compounds, electroshock therapy

Front 71

some characteristics of mania

Back 71

insomnia, loss of inhibition, impaired judgement, inability to speak, paranoia and hyperactivity

Front 72

Which drugs exazerbate/lessen mania?

Back 72

exz- dopamine and norepi
make better-catecholamine

Front 73

What does lithium do and what are some precautions?

Back 73

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.

Front 74

what do antipsychotic and benzo agents do for biploarism?

Back 74

can treat sever manic symptoms until lithium takes effect

Front 75

what effect do antidepressents have on bipolarism?

Back 75

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)

Front 76

Valproic acid's affects on bipolarism

Back 76

actually as effective in controling non rapid cycling bipolarism as lithium and more effective in rapid cycling. But, can cause liver dysfuntion