Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
112 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
Describe the basic structures of a synapse
|
strength of nerve impulse in presynaptic neuron affects how much NT is released. NTs are in vesicles. Synaptic gap between pre and post synaptic neurons. Reuptake ports on presyn and receptor sites on postsyn.
|
|
|
|
What are the steps in synaptic transmission
|
Synthesis of NT; trnasport and storage in vesicle; NT is released; NT binds at receptor site; Enzymes in gap breakdown the NT and/or the NT is reuptaken into the presyn.
|
|
|
|
What is an agonist ?
|
mimics the NT or augments its effects in some way
|
|
|
|
What is an antagonist ?
|
blocks NT from entering the receptor site; prevents its action
|
|
|
|
define stereospecific
|
physical shapes match
|
|
|
|
Does a NT fit only one receptor site?
|
no, NT often like a "master key" that opens many different sites.
|
|
|
|
name 7 NTs
|
Ach; DA; NE; 5HT; GABA (Gamma-Amino-Butyric Acid); Glu (glutamate); opiods (endorphins & enkephalins)
|
|
|
|
What are Ach's behavioral roles?
|
Memory (concentration and cognition); parasympathetic nervous system. REST and DIGEST
|
|
|
|
What are Ach's SE's?
|
If Ach is LOW: dry mouth, blurred vision, urinary retention, confused states, memory impairment; constipation. Decreased parasympathetic NS response.
|
|
|
|
Many Alzheimer's Disease drugs increase/decrease Ach. What other common substance acts in this way as well?
|
INCREASE -- they are agonists. Nicotine is also an Ach agonist.
|
|
|
|
What are the parts of the CNS?
|
brain and spinal cord
|
|
|
|
What are the parts of the PNS (peripheral nervous system)?
|
ANS (autonomic nervous system)(stimulates to action the involuntary organs such as the heart, smooth muscles and glands) and SNS (somatic nervous system)(voluntary action of skeletal muscles and carries information from sensory organzs to the CNS)
|
|
|
|
how is the ANS further divided, and what are the roles of each part?
|
Sympathetic NS (fight or flight)(arousal, increase heart rate, respiration, pupil dilation; inhibit digestion; constrict arteries) and Parasympathetic NS (rest and digest; decreased heart rate, respiration; pupil constriction; GI system more active; relax arteries)
|
|
|
|
Where does Ach work in the brain?
|
cortex (affects cognition); thalamus (relays impulses from sensory nerves); septal-hippocampus (memory); parasympathetic NS (gut, heart)
|
|
|
|
What are the behavioral roles of DA?
|
Mesolimbic DA reward pathway; regulate hormones; initiate smooth movements
|
|
|
|
What classes of drugs affect DA?
|
Stimulants (amphetamines)/cocaine/wellbutrin are agonists; adverse effects include psychosis and anxiety and mania. Typical antipsychotics block DA; adverser effects include apathy, emotional blunting, eps effects
|
|
|
|
What are eps effects?
|
too little DA: Parkinsonian-like symptoms (hand tremor, slow movements, mask-like face, cogwheel rigidity - "thorazine shuffle"; dystonia; inner restlessness; tardive dyskinesia (movemetn d/o - lip smacking).
|
|
|
|
What are the 4 DA pathways?
|
mesolimbic (from midbrain to limbic system [nucleus accumbens, hippocampus & amygdala]: rewards, memory); nigrostriatal (from nigra to striatum: movement SE's); mesocortical (from midbrain to cortex: ability to focus, executive f/x; tuberoinfundibular (from hypothalamus to pituitary: hormonal side effects)
|
|
|
|
What are the behavioral roles of NE?
|
Focus is on SNS; Increase arousal level of eyes, heart & lungs; decrease GI activity
|
|
|
|
What diseases are associated with NE issues?
|
Anxiety D/Os and hypervigilance f/x of PTSD (too much NE)
|
|
|
|
What are adverse and positive effects of increased NE load?
|
Some antidepressants activate NE: can cause sympathomimetics (i.e., mimic SNS arousal)(increase heart rate, blood pressure, sweating, tremors, jitteriness, and anxiety); Cause risk of heart attack and stroke. Pos f/x are antidepressant and increased alertness
|
|
|
|
Where does NE work?
|
Diffuse throughout brain and body; causes arousal in SNS; comes from "blue place" locus ceruleus in the brain stem
|
|
|
|
What is behavior role of 5HT?
|
Mood regulation, sleep and appetite, descending (i.e., down spinal cord) pain pathways
|
|
|
|
What are the 5HT systems; where does it work?
|
From Raphe nuclei (cells on midline of brain stem) to entire cortex
|
|
|
|
What is behavioral role of GABA?
|
It is an inhibitory NT; it lets negative ions in the postsyn neuron (which makes it less likely to fire)
|
|
|
|
What diseases are associated with GABA?
|
anxiety, siezures/epilepsy (if have low GABA)
|
|
|
|
What drugs affect GABA and how?
|
Antianxiety drugs (e.g., Xanax), alcohol and barbituates all increase GABA (which increases physiological inhibition). GABA is pharmacologically and behaviorally a downer.
|
|
|
|
What are the GABA systems? Where is it?
|
there is Lots of GABA in lots of places in the brain.
|
|
|
|
What is the behavioral role of Glu?
|
It is a major excitatory NT (postsynaptic cells are more likely to fire).
|
|
|
|
What diseases are associates with GLU?
|
schizophrenia (low or blocked glutamate)
|
|
|
|
What drugs are associated with GLU?
|
new one for Alzheimer's disease.
|
|
|
|
Where is GLU found
|
throughout the brain
|
|
|
|
What are the behavioral roles of the opiods, and name 2 classes of opiods.
|
Endorphins and enkephalins are both endogenous opiods. They are analgesics, increase euphoria and decrease GI motility
|
|
|
|
What diseases are associated with opiods?
|
pain syndromes
|
|
|
|
What treatments are associated with opiods?
|
acupuncture; nalaxone is an opiod blocker; pain mgmt (morphine most effective); addiction drugs are all agonists: heroin, oxycontin, fentanyl (patch often), vicodin, demerol
|
|
|
|
name different routes of administration of meds and info about each one.
|
Oral- slower deliv; levels can be variable; can swallow a pill?. Inhalation- fast deliv, mostly for abused drugs & asthma. Injection- infection poss; fast; precise measurement. IV, IM (usu done in emerg, antidotes to chem warfare, epi-pens), SC (subcutaneous-shallow (old Tb tst). Intranasal- snort cocaine. Transdermal- long term deliv (pain meds, BC, nicotine).
|
|
|
|
what kinds of cells cross the blood-brain barrier?
|
1. Fat - lipid soluble 2. Short - small molecules 3. single - not attached to a big protein in the blood 4. No direction - no pos or neg charge. Think George in "Seinfeld"
|
|
|
|
significance of blood brain barrier
|
Psychoactive substances must cross b-b b to get to neurons; there are 3 steps. Capillaries in the brain have no pores, just "tight junctions" to protect the nerve cells. Glial cells wrap the capillaries (lipid-type cells). Nerve cell membranes are also lipid-type.
|
|
|
|
What are the factors that affect individual variability to different medications?
|
SAGE: Size (+ sensitive if smaller). Age (+ sens if older because of decreased metabolic rate, i.e., 80+). Gender (relative % of fat to water - female more sens.). Experience (+ sens if less exposure - liver & brain do not "know" how to process it). Also Ethnicity - enzyme profile varies.
|
|
|
|
What is the dose response curve
|
% of Ss responding by level of dose required to get an effect (i.e., efficacy).
|
|
|
|
Significance of dose response curve
|
Most drugs in a class don't vary much by efficacy for a GROUP (usu. about 70% of group will respond). New drugs often have lower DR curve (i.e., need smaller dose for efficacy - so are more potent).
|
|
|
|
Define Elimination Half Life
|
Time for plasma level of drug to reduce by 50%. Slow absorption of drug usually means slow elimination of drug (e.g., Prozac)
|
|
|
|
How does half life relate to time for a drug to reach efficacy?
|
Achieving a steady state plateau (drug in = drug out) takes about 4 half lives. Prozac has long half life, so takes longer to work.
|
|
|
|
Why and how does the effect of a drug terminate?
|
1. Biotransformation (liver either synthesizes it - binds it to something else in a conjugation or uses non-synthetic action such as hydrolysis to break it down/divide it. 2. Excretion (kidney f/x). NINETY % of psychoactive drugs are excreted in urine.
|
|
|
|
Why are there genetic and ethnic differences in BIOLOGICAL response to pharmacotherapy?
|
Genetic polymorphism (liver enzyme systems differ - esp the CYP enzyme systems)
|
|
|
|
Define physical dependence
|
Need the drug to function normally; this is defined by the presence of withdrawal
|
|
|
|
define withdrawal
|
"discontinuation syndrome" or onset of a physiological and behavioral symptoms when a drug is discontinued
|
|
|
|
How does DSM define substance abuse
|
pattern of use leading to significant impairment or distress demonstrated by one of the following: a. impairment of fx in one area as result of use; b. hazardous behavior from use; c. legal problems form use; d. continued use despite significant problems
|
|
|
|
how does DSM define substance dependence
|
more severe than abuse. Tolerance (need more 4 same effect) & withdrawal are typical but NOT req. Use larger amts over time; can't cut down; ++time spent to obtain or recover from use; activities ignored/avoided; unable to quit despite consequ. Specifier w/ or w/o phys dependence
|
|
|
|
What is Monoamine hypothesis of depression?
|
just an explanation of what is different about a depressed brain; does not look at WHY the state came to be. "Depression involves a funcitonal deficit of NE and/or 5HT." [DA is also a monoamine, but she and most others don't think it is involved.]
|
|
|
|
What is the evidence for the monoamine hypothesis?
|
1. Depleting monoamine vesicles can induce depression. 2. Increasing 5ht and/or NE treats depression. 3. Low 5HT in violent suicide attempters.
|
|
|
|
Discuss evidence of low 5HT and violent suicide.
|
Asbergcompared Ss who had attempted suicide w/depressed non-suicidal controls and nondepressed controls. Looked at levels of 5HT metabolite in spinal fluid. Violent suicide attempters (hanging or drowning) had very low levels vs. non-violent suicide attempts (pills).
|
|
|
|
What are the origins or biological depressions?
|
1. medical illness 2. female hormone fluctuation 3. medications and substance abuse. 4. Endogenous biological depressions (probably involves a genetic vulnerability and stress -- this is the diathesis-stress model)
|
|
|
|
What are the most important medical illnesses are associated with or cause depression?
|
chronic pain is associated w/dep. Chronic fatigue syndrome is assoc w/dep. Hypothyroid cases depression. Parkinson's disease casus depression. There are many others; these are most important.
|
|
|
|
What factors associated with female sex hormone fluctuations are linked to depression? Why is this significant?
|
1. birth control pills 2. post partum depression 3. premenstrual dysphoric disorder 4. menopause Significance: changes in hormones may be part of the reason for higher rates of depression in women.
|
|
|
|
What drugs can cause or trigger depression?
|
alcohol; stimulant withdrawal (e.g., cocaine); antianxiety drugs; antihypertensives; birth control pills; corticosteroids (can also trigger bipolar sx) and hormones
|
|
|
|
What are the 5 main antidepressant medication classes, and some examples of each kind?
|
1. Tricyclics (TCAs) - Tofranil, Elavil. 2. Selective Serotonis Reuptake Inhibitors (SSRIs) - Prozac, Paxil, Zoloft, etc. 3. Monoamine Oxidase Inhibitors (MAOIs) - Nardil 4. Third Generation - atypical action or also work on NE 5. Herbs - St. John's Wort
|
|
|
|
What are the SE's of Tricyclics?
|
1. Anticholinergic effects 2. orthostatic hypotension (stand up and black out) 3. Tachycardia (fast heart rate)
|
|
|
|
What are SE's of SSRIs?
|
1. nausea 2. anxiety (usu S/T), which can involve insomnia 3. GI upset 4. sweating 5. headache 6. restlessness 7. sexual dysfunction
|
|
|
|
What class of drugs are all antiobsesisonal
|
SSRIs
|
|
|
|
What are half life differences between Paxil, Zoloft and Prozac
|
Paxil - 1 day; fast in,abrupt withdrawal. Zoloft - 2 days. Prozac 7 to 10 days; slower in , gradual withdrawal.
|
|
|
|
Does Prozac change one's personality re: suicidality and aggression?
|
Researchers differ; hard to get objective data. Studies may just reflect outliers
|
|
|
|
SSRIs and adolescent suicide
|
FDA added black box warning and resulting decrease of # of prescriptions written was correlated with incrase in suicides. SO: should watch closely for suicidality in adolescents who are NEWLY on SSRIs, who start to activate, but don’' yet believe that change is permanent.
|
|
|
|
Are there sexual SE's related to SSRIs?
|
yes. Originally very underestimated (claimed 18% but now it's more like 49%)
|
|
|
|
How do you treat the sexual SE's from SSRIs?
|
1. Switch to a med w/lower rates of sexual SE's such as Wellbutrin or Serzone or Remeron. 2. Take an "antidote" in addition to the SSRI such as Buspar or Ritalin
|
|
|
|
What are SXs of SSRI overdose?
|
Need a LOT to OD. Sxs are: nervousness, myclonus (twitching), dizziness, tachycardia (rapid heart beat), hallucinations, fever, fainting
|
|
|
|
Why are MAOIs less prescribed than other antidepressants?
|
Because of tyramine reaction. Body can't break down tyramines in food (aged cheese, red wine, etc.). Elevated risk of heart attack or stroke because of elevated blood pressure
|
|
|
|
Why psychotherapy AND meds?
|
1. may need to address affect 2. studies show increased efficacy 3. no side FX to therapy 4. Meds don't know WHY things are better
|
|
|
|
When should a ct consider medication?
|
1. look at risks vs. benefits 2. how severe is the problem. 3. risk of suicidality and/or danger to others. 4. what has been the response to psychotherapy? 5. How chronic is the illness?
|
|
|
|
What meds can you use to tx anxiety?
|
SSRIs; BZs; atypical anxiolytics (i.e., busprirone); non-BZ hypnotics (Lunesta, Rozerem); other anxiolytics (TCAs, antihistimines like Benadryl, NE Blockade)
|
there are 5
|
|
|
Which NT is most clearly associated with anxiety?
|
GABA
|
|
|
|
What happens when GABA binds at the postsynaptic receptor?
|
Allows Cl- into the neuron, so makes it less likely to fire
|
|
|
|
What else might bind at a GABA site?
|
Barbituates, BZx and steroids
|
there are 3
|
|
|
What effect does a BZ have on a GABA recpetor?
|
It is an agonist, and potentiates GABA: it opens the Cl- channel more. This has a down/chill effect
|
|
|
|
Why prescribe BZs?
|
Anxiety dxs (Panic attacks, insomnia) & medical reasons (pre-op, for certain procedures such as MRI, muscle relaxant needed, or angina, ulcers, asthma, & vertigo)
|
2 categories w/examples
|
|
|
What happens with taking increasing doses of CNS depressants (sedative-hypnotics or alcohol)?
|
Frontal lobe activity is repressed (so have decreasing exec fx) which leads to increased disinhibition. . Go from alert/normal to anxiety relief to disinhibition to sedation to sleep to general anesthesia to coma/shock to death
|
|
|
|
What are adverse effects of BZs?
|
Visual motor impairment -so watch out driving (i.e., dizziness, psychomotor retardation, incoordination, staggering); confusion; amnesia
|
3 general categories
|
|
|
What interacts dangerously w/BZs, why are they dangerous, what happens?
|
1. anxiolytics (BZs) and CNS depressants (alcohol/barbituates/hypnotics). 2. They have synergistic effects, not just additive effects (geometric progression not arithmatic). 3. can lead to respiratory depression which causes death
|
|
|
|
What happens with BZ withdrawal and why does this happen? How deal with this?
|
1. Do become physically addicted to BZs as well as psychologically addicted. 2. mild-moderate withdrawal Sxs are anxiety, restlessness, insomnia, nightmares; severe withdrawal Sxs are seizures, high fever, psychosis. 3. taper off
|
|
|
|
What are nonBZs given for anxiety?
|
Buspar; Inderal (beta blocker - blocks sympathetic NS and decreases NE); Catapres (often given to kids); Benadryl and other antihistimines
|
4
|
|
|
Advantages and disadvantages of Buspar?
|
1. less drowsiness; does not impair psychomotor or cognition; low abuse potential; not synergistic w/alcohol. 2. less effective for some people; slower onset of effects
|
|
|
|
What might be comorbid with GAD and what is consequence for medication?
|
anxiety, depression so often try SSRIs first
|
|
|
|
If only have GAD, or if have GAD and substance abuse, what would you prescribe
|
buspirone
|
|
|
|
What is first choice med for panic d/o
|
SSRI (panic d/o is associated with drastic reduction of 5HT receptors)
|
|
|
|
What med if have panic d/o and depression
|
SSRI
|
|
|
|
What med if need immediate relief from panic d/o, and have a hx of mania
|
high potency BZ like Klonopin
|
|
|
|
Two general rules for clients prescribed BZs re: adherence?
|
start low and go slow; stay on at least 6 months
|
|
|
|
What meds are prescribed for social phobia?
|
beta blocker (i.e., Inderal); BZ such as Klonopin; SSRIs that are more sedative; TCA like Anafranil which is anti-obsessional
|
4
|
|
|
What meds for OCD
|
SSRIs alone or in combo (BZ or trazodone or Ambien or Anafranil [TCA]) a. if anxious add Buspar b. If depressed add Lithium. C. if delusional/tics, add antipsychotic
|
|
|
|
How medicate PTSD?
|
FEW random clinical trials. Is somewhat effective to TREAT SYMPTOMS. Use SSRI (Zoloft is actually approved by FDA for this or Prozac), MAOI (for hyperarousal), BZ for anxiety, TCA.
|
|
|
|
Incidence of comorbidity with anxiety d/os? Which ones?
|
30 - 60% !! Depression or substance abuse
|
|
|
|
what kinds of drugs can induce mania?
|
antidepressants (all kinds), anxiolytics (both when goin on and off, all kinds), stimulants (cocaine, ritalin, etc.), endocrine meds (corticosteroids, androgens, thyroid), other (l Dopa, anything that increases DA)
|
5 categories
|
|
|
How do you medicate for bipolar?
|
use a mood stabilizer (monotherapy w/lithium, Depakote or Tegretol, tho now less common) or a ms w/a newer anticonvulsant, or a cocktail drug like Symbyax. VERY complicated med algorithms
|
|
|
|
If have good dx of bipolar, how decide on meds?
|
individual symptoms, hx of response to meds, SE's that ct will tolerate, med conditions such as liver issues, cost, convenience (access to meds, frequency of dose & how that affects adherence)
|
|
|
|
What are negatives of LI use?
|
in past, were fatalities and toxicity issues. Less research because is not patentable. Now do have decent research on dosage, so fewer complications, bec using lower doses. REQUIRES blood monitoring (med workup before start). Narrow therapeutic index (range of safe dose)
|
|
|
|
What is Li efficacy?
|
60 - 80% of bipolar I cts improve. NOT as good for rapid cyclers
|
|
|
|
What are most common Li SE's?
|
Reduced affective range. Thirst (20%). Excessive urination (60%). Weight gain (20%). Fine tremor in hand (50%). Fatigue. Metalic taste in mouth.
|
7
|
|
|
What are most disturbing Li SE's?
|
(limited affective range). Weight gain. Cognitive f/x (feel fuzzy, reduced concentration). Excessive urination. Nausea. Fatigue
|
6
|
|
|
Discuss Li toxicity
|
narrow therapeutic index. Signs incl nausea/vomiting, confusion, drowsiness, slurred speech, muscle twitching, irregular heart geat, blurred vision. Dose by weight so contrain if wt fluctuates. Might dec thyroid. may hange kidney fx (Li elim only thru kidney - no liver metabol)
|
|
|
|
What kind of med workup is needed for Li med?
|
weight. Thyroid fx. Kidney fx. CBC (need white blood count). Consider EKG for heart disease. Check for pregnancy.
|
|
|
|
What patient education is needed re: mood stabilizers for bipolar?
|
meds are required, but you don't become addicted (as in need eyeglasses). Bipolar is a recurrent illness. Need to stay aware of early signs of recurrent episode. Go over risks and benefits of individual med. Be aware of drug interactions. Stay alert for toxic reactions.
|
|
|
|
Why do clients have difficulty adhering to bipolar meds?
|
miss the highs. Fear dependence on the drug. Possible decreased productivity and creativity because not experiencing the highs.
|
|
|
|
What is Depakote for? What is its efficacy? How does it work?
|
anticonvulsant mood stabilizer - increasingly popular to try first (vs. lithium). Efficacy is comparable to Li. It is a GABA agonist
|
|
|
|
What are advantages of Depakote?
|
onset is faster than Li (2 - 5 days). Therapeutic index is wider. Fewer SE's in general. Less need for medical workup and monitoring. Fewer drug interactions.
|
|
|
|
What are common SE's of Depakote?
|
sedation, nausea, diarrhea, hair loss, weight gain
|
|
|
|
What are rare SE's of Depakote?
|
Liver issues (hepatotoxicity). Death -- only if given w/other meds - no fatalities from Depakote alone
|
|
|
|
What are SE's of Tegretol (carbamazepine)? Efficacy?
|
supposed to have same efficacy as Depakote, but is less prescribed because most MDs don't feel it works as well. SE's: RASH, DOUBLE vision, sedation, nausea, dizziness, ataxia (disturbed movement) - walk as if drunk.
|
|
|
|
compare onset of response to bipolar meds
|
lithium 7 to 10 days. Tegretol (carbamazepine) 7 to 14 days. Depakote (valproate) ** 2 to 5 days
|
|
|
|
What mood stabilizers can you use in pregnancy?
|
None are very good. LI is ok after 1st trimester (causes cardiac malformations then). Tegretol causes digital malformations, neural tube defects, spina bifida. Valproate causes neural tube defects, craniofacial malformations and spina bifida
|
|
|
|
What are SE's of Symbyax vs. placebo?
|
More of each of these: weight gain, increased appetite, asthenia (abnormal sensations), peripheral edema, tremor, diarrhea
|
|
|
|
What are SE's of Lamictal (lamotrigine)?
|
BIG one is skin rash (can be life threatening). Headache, dizziness, nausea/vomiting, double vision, sedation & abnormal dreams, tremor
|
|
|
|
What are APA tx guidelines for bipolar?
|
1. Eva dx 2. Eval safety of ct and others 3. Estab tx alliance 4. Monitor tx response 5. Provide educ to ct and family 6. Promote tx adherence 7. Promote awareness of STRESSORS 8. Work re ct re: RELAPSE signs 9. Eval & manage FUNCTIONAL impairments
|
|
