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208 Cards in this Set

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2 aspects of cognitive performance that show the most profound changes with aging
1. information processing (verbal speed, i.e.)
2. working memory
age at which brain functions and capabilities decline rapidly
>70
the most consistent cognitive change in aging
slowing of responses
when do seniors have more difficulty remembering names and objects?
when they are not in a familiar routine
seniors do poorly on memory tasks that involve these 3 things
1. unfamiliar material
2. free recall
3. speed
4 major groups of conditions causing delirium (although it is usually caused by multiple factors)
1. systemic disease affecting the brain
2. primary intracranial disease
3. exogenous toxic agents
4. withdrawal from substances of abuse
when any type of systemic disease causes delirium, it's due to a failure of one of these 2 things
1. failure of cerebral perfusion
2. failure of cerebral metabolism
4 cardiac conditions that may cause delirium
1. cardiogenic shock
2. HTN
3. cardiac arrest
4. heart failure
how do cardiac conditions cause delirium?
lack of cerebral perfusion
the 2 most prevalent metabolic disturbances causing delirium
1. hypoNa
2. hypoglycemia
3 CNS causes of delirium
1. stroke
2. seizure
3. vasculitis
possible cause of delirium in cancer patients
paraneoplastic phenomenia such as limbic encephalitis
common malnutrition causing delirium in alcoholic pts
vitamin B1 deficiency
most common way that infx affect the nervous system
indirectly by toxins
common presenting sx of elderly pts w/ generalized sepsis
altered mental status often precedes fever or leukocytosis
6 common risk factors of delirium due to infection
1. UTI
2. low serum albumin
3. proteinuria
4. fever
5. hypothermia
6. azotemia
does delirium always present the same way clinically regardless of the systemic disease causing it?
yes, pretty much
which neurotransmitters do stimulants act through?
dopamine and catecholamine pathways
most common presentation of stimulant overdoses
agitated paranoid state
also present w/ confusion, psychomotor agitation, and violence
how does haloperidol tx delirium?
it is a dopa-blocking agent that gets rid of excess dopamine relative to Ach
what receptors does LSD attach to?
serotonin receptors
people taking SSRIs can develop serotonin syndrome. what is a common prominent feature?
delirium
3 sx of phencyclidine overdose
1. assaultive behavior
2. agitation
3. diminished responsiveness to pain
which receptors do phencyclidine affect?
NMDA receptors
ethanol-induced upregulation of these receptors may underlie withdrawal seizures
NMDA receptors
stimulation of NMDA receptors can lead to...
permanent brain damage
action at these receptors can cause manifestations of sedative or alcohol overdoses
GABA receptors
2 sx of sedative overdose
1. slurred speech
2. incoordination
this occurs when there is insufficient stimulation of GABA receptors from withdrawal from benzos or alcohol
delirium tremens
5 sx of anticholinergic delirium
1. agitation
2. pupil dilation
3. dry skin
4. urinary retention
5. memory impairment
meperidine
narcotic likely to cause confusion and hallucinations
4 common agents that can cause delirium
1. digoxin
2. lidocaine
3. antiarrhythmic agents
4. mexiletine
the following drugs reverse delirium due to which drugs:
physostigmine
naloxone
flumazenil
physostigmine - anticholinergics
naloxone - narcotics
fumazenil - benzos
what % of post-op patients become delirious
what % of terminal pts become delirious before they die
50%
80%
does delirium predict future cognitive decline?
yes
neuro disorder in which there is a fluctuating course, w/ sx ever-changing and the mental status varying, w/ deficits appearing suddenly and disappearing quickly
delirium
daytime drowsiness and nighttime insomnia and confusion; often the first presentation of delirium
sundowning
8 tests you should get to try to find the cause of delirium + 2 extra tests you may get
1. CBC
2. ESR
3. BMP
4. LFTs
5. UA
6. Tox screen
7. CXR
8. EKG

1. CT (structural damage)
2. LP (intrathecal infx)
what are delirious person's vitals like?
often abnormal
3 kinds of structural damage that may cause early mental status changes
1. SAH
2. SDH
3. right-hemisphere stroke
when might an EEG be used to evaluate delirium? what might you see? in mild? in severe?
after all other studies are unrevealing
usually see slowing of typical pattern
mild --> dominant posterior rhythm slowing
severe --> theta and delta waves present throughout
are tremor, asterixis, and restlessness more common in delirium or dementia? how about dysphasia or apraxia?
delirium
dementia
are signs of cognitive dysfunction more common in delirium or psychotic disorders? what's the difference in the EEG?
delirium
EEG is normal in psychoses
psychiatric illness causing sx of delirium
pseudodelirium
which psychiatric condition is often associated w/ delirium, esp. in elderly patients?
depression, b/c pts get dehydrated and malnourished
what is the main goal in tx of delirium?
find the underlying cause
delirious pts have increased circulating catecholamines, which causes increases in these 3 vitals
HR, BP, RR
are mechanical restraints better or worse for a patient?
worse
DOC for delirium in the critically ill adult
haloperidol (a neuroleptic) given IV
2 possible cardiac complications of haloperidol
1. long QT
2. Torsades
1. lorazepam
2. oxazepam
3. midazolam
3 benzos used in the tx of delirium
adverse effect of barbituates being used as sedatives in delirium pts
depresses resp and cardiovascular systems
what are suggested for managing pain in delirious pts
opiates w/ short half-lives, especially morphine
why is meperidine contraindicated in pain management of delirious pts?
it causes hallucinations
what must be checked before and during sedative or opiate tx of delirium?
creatinine clearance and LFTs
malnourished pts may have reduced plasma binding
in life-threatening delirium who should you consult w/ regarding dosing of sedatives/opiates?
anesthesia
characterized by slow evolution of multiple cognitive deficits, some degree of memory impairment, and personality disturbance
dementia
7 things commonly seen on autopsy of dementia pts
1. degenerative disease
2. vascular disease
3. infection
4. inflammation
5. tumors
6. hydrocephalus
7. traumatic brain injury
which imaging modality is much more useful in distinguishing conditions like vascular dementias or normal pressure hydrocephalus?
MRI
4 aspects that Alzheimer's affects
1. memory problems
2. cognition
3. mood
4. behavior (temper outbursts, screaming, agitation, severe personality changes)
what 3 things are seen at the microscopic level in the dx of Alzheimer's
1. amyloid plaques (from beta-amyloid protein)
2. number of neurons and synapses is reduced, especially Ach-colinergic-containing neurons in the basal nucleus of Meynert
3. neurofibrillary tangles containing abnormally phosphorylatied protein called tau (causes defective construction of microtubules and neurofilaments)
one of the earliest areas of the brain to be disconnected in Alzheimer's
what is seen on MRI of this area?
the hippocampus, which is why memory disorder is an early manifestation
can see hippocampal sclerosis or atrophy
which 4 chromosomes have been implicated in Alzheimer's disease
1. chromosome 21 (many Down syndrome pts get it)
2. chromosome 14 (early-onset disease - presenilin 1: increased production of amyloid)
3. chromsome 1 (presenilin 2 - increased production of amyloid)
4. chromosome 19 (ApoE E4 allele)
what 2 things are seen on MRI in Alzheimer's pts
1. reduced brain volume
2. higher CSF volume
condition in which pts forget unimportant details and recent information only
benign senile forgetfulness
(Alzheimer's pts will forget events randomly and both recent and remoted memory)
tx of Alzheimer's is focused on improving _________ by administering _________ and _________
cholinergic activity
Ach precursors or Ach-esterase inhibitors
donepezil
rivastigmine
2nd-generation cholinesterase inhibitors
(donepezil is more specific for CNS Ach-esterase)
these common drugs are found to slow the development of Alzheimer's
NSAIDs
what kills Alzheimer's pts?
comorbidities such as pneumonia
the prognosis of this disease is universally fatal
Huntington's disease
3 factors that lead to cerebrovascular disease producing vascular dementia
1. volume of lesion
2. number of cerebral injuries
3. location of cerebral injuries (cortical vs. subcortical)
5 risk factors for vascular dementia (same as those for strokes)
1. HTN
2. smoking
3. DM
4. advanced age
5. male sex
this kind of dementia advances in a stepwise fashion
multi-infarct dementia
most likely area to be affected in multi-infarct dementia
middle cerebral artery territory supplied by the lenticulostriate branches
bilateral infarcts are common
expression and understanding of affect: right or left hemisphere functions?
right hemisphere
unable to understand nuances of affect --> which part of the brain has damage?
denial of illness, hemi-attention, constructional apraxia --> which part of the brain has damage?
1. right temperoparietal
2. right parietal
language impairment complicates the dx of affective disorder in lesions of this part of the brain
left hemisphere
nonfluent speech, impaired writing, defective naming, hemiparesis
Broca's aphasia
apathetic but not severely depressed, dramatic personality changes, emotionally incontinent (cannot inhibit emotional expression)
frontal lobe disorder
there is strong argument for a predisposition to depression. why?
crucial life events have been found to precede the onset of depresion, but only in a small number of cases of depression
how so all antidepressants work?
what does this tell us about what causes depression?
inhibit the reuptake of neurotransmitters from the synpatic cleft, increasing the concentration of them at postsynaptic receptor sites
depression is caused by a neurotransmitter deficiency
emotional trauma can preced the onset of these 2 kinds of disorders
1. depression
2. endocrine disorders (hyperthyroidism, Cushing's)
which 2 endocrine systems are most extensively studied in psych?
HPA axis and HPT axis
about 1/2 of pts w/ major depressive disorder have hypersecretion of this, which goes down after depression is cured
cortisol
2 most common psychiatric sx in pts w/ adult hypothyroidism
1. depression
2. cognitive decline
a small dose of this will accelerate the therapeutic effect of several antidepressants in women
T3 (triiodothyronine)
administration of this may induce an increased well-being and relaxation in normal subjects as well as psychiatric disease, esp. depression
TRH
3 categories of depression
1. depressive sx (not sufficiently severe to warrant clinical dx or intervention)
2. bipolar (one or more episodes of mania)
3. non-bipolar disorder
is major depressive disorder in adolescent and adult females more or less common than in adolescent and adult males? how about prepubertal children?
2-3x more common in females
children are affected equally
depressed mood or loss of interest for at least 2 weeks that causes impairment of social and occupational functioning
major depressive disorder
most characteristic sx of MDD
depressed mood - sad, low, empty, hopeless, gloomy, etc.
changes in posture, speech, facies, dress, and grooming
MDD in which the patient does not report depressed mood
masked depression
inability to enjoy usual activities
anhedonia
what % of pts have a reduction in appetite during depression?
is it more or less common than increase in appetite?
70% have reduction
more common than increase in appetite
most common sleep disturbance in depression
what % of pts have sleep disturbances?
what kind of insomnia is common in those w/ comorbid anxiety?
insomnia (initial, middle, late)
80%
initial insomnia
what sleep disturbance is common in atypical depression and seasonal affective disorder?
hypersomnia
significant loss of energy
anergia
severe form of depression in which there is slowing of thought and performance, although accuracy is retained (commonly confused with early signs of dementia in elderly)
psuedodementia
when is risk of suicide highest in a depressive episode?
immediately after initiation of tx and during the 6-9 month period following symptomatic recovery
when does SAD occur usually?
begins in fall or winter and ends in spring
tx for SAD
ligh therapy
SSRIs
most common way for depressed pt to present
to a GP rather than a psychiatrist w/ a physical complaint (I can't sleep, I have no energy, etc.)
is bereavement a mental disorder?
no, even though it has sx characteristic of MDD
when might you give a person w/ bereavement antidepressants?
1. behavioral sx are prolonged
2. continued functional impairment
4 principles of tx for depression
1. be aware of cycling course of the disease
2. acute tx for florid sx
3. continuation tx to prevent early relapse
4. maintenance tx to make relapse less likely
are antidepressants helpful in young pts?
are they helpful in elderly pts?
young - controversial
elderly - very helpful; remember to have reduced doses due to reductions in hepatic clearance and protein binding
explain initial tx of depression
antidepressants started at low dose and increased for 7-10 days; continued for at least 6 months for continuation therapy
3 reasons for continuing maintenance therapy of depression for extended periods (even years)
1. age >40 w/ 2 or more episodes
2. first episode at age >50
3. h/o 3+ episodes
when might you stop antidepressant medication?
slow-tapering after at least 5 years of tx if the pt is asymptomatic
side effects of these drugs include those associated with adrenergic or muscarinic/cholinergic antagonism: blocked tyramine metabolism --> acute HTN crisis: pounding headaches, flushing, blood vessel distension
MAOIs
slow IV administration of alpha-adrenergic antagonist phentolamine is used to tx...
acute HTN crisis caused by MAOIs
MAOIs can interfere w/ the metabolism of these drugs
sympathomimetic amines: pseudoephedrine and pheylpropanolamine (decongestants)
coadministration of MAOIs w/ these drugs causes confusion, restlessness, diaphoresis, tremor, diarrhea, hyperreflexia
SSRIs
this is called central serotonin syndrome (usually mild and resolves w/in 24 hours of d/c on drugs)
how long should you wait to put a pt on an MAOI after taking them off an SSRI or TCA
2 weeks
coadministration of MAOIs w/ these drugs causes delirium and HTN
TCAs
side effects of TCAs occur b/c of...
binding to specific (NE or serotonin) or nonspecific (histamine, muscarinic) sites
2 food and 2 drugs that very dangerous to ingest while on MAOIs
cheese and sauerkraut
amphetamines and decongestants
2 food and 1 drug that are moderately dangerous when ingested w/ MAOIs
fermented/aged foods and alcohols
TCAs
side effects of TCAs
heart arrhthymias:AV conduction blocks
relative contraindication to TCAs
absolute contraindication to TCAs
1st degree block
2nd degree block
bupropion or nefazodone
drugs that can be given in place of SSRIs if pt has a lot of side effects
4 side effects of SSRIs
1. nausea
2. anorexia
3. anxiety
4. sexual dysfunction
why do antidepressants have a lot of drug interactions? name one drug
they are highly protein bound, so they can be displaced or displace other drugs that are similar
warfarin
% of depression pts who respond well to antidepressants
4 reasons for tx failure
60-70%
1. inadequate dose
2. inadequate duration (min. 6 weeks)
3. prominent side effects
4. noncompliance
3 augmentation strategies to change the effects of TCAs on pts w/ tx failure
2 others that may help in limited way
if none of these work, can try:
last option:
1. lithium carbonate
2. thyroid hormone (T3)
3. sleep deprivation (effects are immediate after 1 night of wakefulness)

1. amphetamines
2. methylphenidate

TCA+MAOI combo therapy

ECT
imipramine + phenelzine

side effects?
TCA+MAOI combo therapy used as augmentation strategy for depressed pts

hypertensive reactions
what is ECT most commonly used for?
depression
3 reasons to use ECT as a primary tx
2 reasons to use ECT as a secondary tx
1. urgent need (psych or medical) for a rapid response
2. pt hx of better response w/ ECT
3. strong pt preference

1. pt responded poorly to other tx
2. pt deteriorated and a response is needed urgently
can you use ECT in pregnancy and in elderly pts?
yes
can ECT cause brain damage?
no, but transient cognitive changes do occur
4 adverse effects of ECT
1. postictal confusion for minutes to hours
2. interictal confusion (uncommon)
3. memory impairment (retrograde and antegrade amnesia, but not usually cumulative)
4. transient arrhythmias (b/c SNS and PNS are stimulated sequentially)
what drug can you use for postictal sedation after ECT?
what drug can be used to diminish cardiac complication risk in ECT?
a benzo (midazolam)
oxygen
how many treatments are included in a typical ECT course
how often are they given?
how long should ECT be continued after remission?
what is the lifetime max # of tx?
6-12 treatments
3x/week
6-12 months
no maximum
treatment for depression in which multiple seizures are induced (2-10) during a signle tx
MMECT (multiple monitored ECT)
this plays a large role in the selection of a particular form of psychotherapy
pt preference
this disorder may preccede depression
dysthymic disorder
average number of lifetime episodes of depression
in which episodes are psychosocial stressors more important in triggering?
5
the 1st 2 episodes
% of pts that relapse w/in 1st 6 months of remission of depression
25%, usually due to d/c of antidepressant
disorder in which there are chronic, less severe depressive sx that can persist for >2 years; sx are lower intensity than those of MDD; "lies on the border of normal and pathological"
dysthymic disorder
aka subsyndromal mood disorder
the protracted course of this disorder makes it the most commonly encountered form of mood disorder
dysthymic disorder
is dysthymic disorder more common in men or women?
women
are vegetative sx such as insomnia, loss of appetite or libido, wt loss more common in MDD or dysthymic disorder?
MDD
which drugs should be used for initial tx of dysthymic disorder? why?
if there is no response, what should be prescribed?
what else can be used?
SSRIs b/c they have less side effects
imipramine and desipramine (TCAs)
interpersonal psychotherapy and cognitive-behavioral therapy (goal is to develop effective strategies for dealing w/ social and interpersonal relations)
based on the assertion that depression is associated w/ negative thought patterns, cognitive errors, and faulty information processing
cognitive-behavioral therapy
having this disorder is a risk factor for developing MDD
dysthymic disorder
disorder consisting of episodes of mania cycling w/ depressive episodes
bipolar I disorder
disorder consisting of episodes of hypomania cycling w/ depressive episodes
bipolar II disorder
is there a clear association b/w life events and the onset of manic or hypomanic episodes?
no
3 risk factors for bipolar disorder
1. being female
2. FH of bipolar
3. upper socioeconomic class
what occurs as a bipolar pt gets older in regards to episodes?
increasing risk of recurrent manic or depressive episodes as they age
is bipolar more common in men or women?
M=F, but more females have more serious disease, esp. rapid-cycling bipolar
is there a genetic component in bipolar disorder?
yes
persistently elevated, expansive, or irritable mood; euphoric, cheerful mood w/ indiscriminate enthusiasm and optimism and the quickly becoming irritable
hallmark of manic episode
difficult to tx manic episode of bipolar I if you can't control...
associated insomnia
speeding speech full of puns, jokes, and irrelevancies --> loud, intrusive, rapid, difficult to follow
bipolar I disorder
racing thoughts and flight of ideas, buying sprees, sexual indiscretions, unwise business investments; psychotic features like paranoia, delusions, hallucinations
bipolar I disorder
giving this drug for bipolar I disorder dramatically decreases risk of suicide
lithium maintenance tx
how are hypomanic sx different from manic sx?
1. sx are less severe
2. social impairment is low or absent - seldom that it compromises pt's capacity to function vocationally
3. rarely presents w/ psychotic sx
how many episodes does a pt have to have in order for it to be considered rapid-cycling bipolar disorder?
4 or more affective episodes per year
the development of this disorder predisposes bipolar patients to rapid-cycling
clinical or subclinical hypothyroidism (this is very common in pts w/ bipolar disorder, in which there is a blunted TSH response to TRH)
lab findings of bipolar disorder
there are none
4 ddx for bipolar disorder
1. schizophrenia or schizoaffective disorder (psychotic features)
2. ADHD (hyperactivity, impulsivity, and poor judgment)
3. borderline or histrionic personality disorders (impulsivity and paranoid ideations)
4. substance abuse (common concomitant with bipolar disease)
4.
best tx for depressive episodes of bipolar disease
best tx for manic episodes of bipolar disorder
best tx for delusional sx and agitation
depressive - SSRIs or bupropion (less likely that TCAs to trigger the switch to mania or hypomania)
manic - lithium, valproic acid, or carbamazepime (use combo of these drugs)
delusions/agitation - antipsychotics like haloperidol or benzos like clonazepam
what nonpharmacologic measure should be taken for bipolar disease
optimizing sleep/controlling insomnia
eliminate mood destabilizers (TCAs, steroids, alcohol, stimulants)
2 indications for lithium:
1. management of acute manic/hypomanic episodes (usually used in combo with a benzo or neuroleptic)
2. prevention of further episodes of both mania and depression
how long should the pt be kept on lithium after the resolution of an acute manic episode
6-12 months
do pts seek tx in early hypomanic states? why or why not?
no, b/c the state is generally perceived as pleasant
4 steps to take if there is a "break through" depressive episode while on lithium for bipolar disease
1. increase lithium dose
2. maximize thyroid function
3. add an SSRI (DOC) or bupropion or MAOI
4. consider sleep deprivation or ECT for severe depression (substantial improvement; useful for those who don't respond to meds)
kinetics and dynamics of lithium
well-tolerated by most pts
narrow therapeutic window
close association b/w plasma levels and toxicity
2 benign side effects of lithium
7 serious side effects of lithium
how do you manage side effects?
what should be done to minimize cardiac risk?
1. fine tremor
2. thirst/polyuria

1. N/V/D
2. coarse tremor (tx w/ BB)
3. muscle weakness
4. memory problems
5. seizures
6. coma
7. sudden death (probably cardiac origin - sick sinus syndrome)

reduce dosage

routine monitoring of EKG and pulse
3 common side effects of carbamazepine
1. rash - need to d/c the drug
2. liver damage, increased enzymes, frank jaundice
3. blood dyscrasias - granulocytopenia, agranulocytosis
is valproic acid better for treating acute manic episodes or long-term maintenance?
acute manic episodes
disorder characterized by alternation b/w dysthymia (gloomy and depressed) and hyperthymia (cheerful and uninhibited)
cyclothymia
moody, impulsive, erratic, and volatile, but not the full syndromal criteria for bipolar
cyclothymia
is there an association b/w cyclothymic disorder and the other mood disorders or type B personality disorders?
controversial
periods of depression alternating w/ periods of hypomania that are less severe or shorter than in bipolar 1 disorder; irregular and aburpt changes in mood, sometimes w/in hours of each other
cyclothymia
characterized by heightened arousal and apprehension manifested by physical sx of tension, tachycardia, tachypnea, tremors that occur w/o obvious threat or when the response to threat is excessive
anxiety
these may be a result of a misperception of suffocation (false suffocation response); may have strong sensitivty to and misinterpretation of physical sensations
panic attacks/panic disorder
recurring, spontaneous, unexpected anxiety attacks w/ rapid onset and short duration; likely to fear they are experiencing a heart attack or stroke
panic disorder
5 common sx of panic disorder
how many have to be present to meet the dx criteria?
when do the sx reach max severity? when do they usually go away?
1. SOB
2. tachypnea
3. tachycardia
4. tremor
5. chest discomfort

4 must be present
within 10 minutes (sometimes w/in a few seconds)
they are usually gone w/in 30 min
do pts w/ panic attacks usually seek help?
yes
extensive phobic avoidance
agoraphobia
can panic disorder occur w/o agoraphobia?
yes
do panic attacks just happen randomly, or do particular situations usually trigger them?
particular situations stimulate the panic, and the pts will begin to avoid those situations or settings; the attacks don't happen as often in "safe places" or w/ "safe people"
tx of choice for panic disorder
behavioral or cognitive-behavioral therapy
low-dose benzos
TCAs, esp. imipramine
MAOIs, esp. phenelzine
SSRIs esp. paroxetine and fluoxetine
drugs that can be used to tx panic disorder
this drug is used to tx panic disorder b/c it reduces the frequency and intensity of panic attacks and has antianxiety and antiphobic effects; however, it has side effects and safety problems such as acute HTN reactions w/ diet high in tyramine
phenelzine (MAOI)
these drugs have supplanted other antidepressants and benzos in the tx of panic disorder
SSRIs, esp. paroxetine or fluoxetine
when might you use a benzo for a panic disorder pt?
a pt who requires drug therapy and who has failed on antidepressants
these can be produced by emotional trauma accompanying certain experiences
phobias
intense, irrational fear or aversion to a particular object or situation
specific phobia
4 common phobias
1. insects
2. injections
3. heights
4. elevators
a fear that one will act in an embarrassing or humiliating manner
social phobia (speaking, eating, or performing in public)
tx of choice for phobic disorders
psychotherapy
2 drug classes that can be used to tx phobic disorders
benzos
BB - reduces autonomic hyperarousal and tremor
characterized by persistent worry + sx of hyperarousal
generalized anxiety disorder
this disorder has a high rate of comorbidity w/ MDD
generalized anxiety disorder
can GAD ever occur in the absence of major life events?
yes
is a person w/ GAD more likely to present to a GP or a psychiatrist?
GP
6 psychiatric disorders w/ obsessive thinking, apprehension, persistent fear, and worry that can be confused with GAD
1. OCD
2. panic disorder
3. somatoform disorder
4. psychotic disorders paranoid subtypes
5. eating disorders
6. personality disorders
for which disorder does insurance coverage tend to discriminate, causing pts to not get appropriate tx?
GAD
what are the indications for tx of GAD w/ benzos?
as adjunctive therapy to psychotherapy; they are not curative and should not be used alone; used to reduce sx; they should be d/c after a few weeks
when do you see physiologic dependence of benzos?
when they are given continuously for >3 months
daytime sedation, ataxia, accident proneness, and memory problems are adverse effects of these drugs when given as tx for GAD
benzos
what is buspirone and what can it be used for?
anxiolytic used as an alternative to benzos in the tx of GAD b/c it does not cause motor, memory, or concentration impairments and it has no abuse potential, dependency, or withdrawal
how long must you give buspirone before you start to see it mitigate anxiety?
at least 3 weeks
these drugs have been found extremely beneficial in GAD
TCAs (imipramine) and HCAs (venlafaxine)
* these also have a delayed therapeutic effect like buspirone
SSRIs have not been tested adequately for the tx of this
GAD