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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
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1. information processing (verbal speed, i.e.)
2. working memory |
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age at which brain functions and capabilities decline rapidly
|
>70
|
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the most consistent cognitive change in aging
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slowing of responses
|
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when do seniors have more difficulty remembering names and objects?
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when they are not in a familiar routine
|
|
seniors do poorly on memory tasks that involve these 3 things
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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
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1. cardiogenic shock
2. HTN 3. cardiac arrest 4. heart failure |
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how do cardiac conditions cause delirium?
|
lack of cerebral perfusion
|
|
the 2 most prevalent metabolic disturbances causing delirium
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1. hypoNa
2. hypoglycemia |
|
3 CNS causes of delirium
|
1. stroke
2. seizure 3. vasculitis |
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possible cause of delirium in cancer patients
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paraneoplastic phenomenia such as limbic encephalitis
|
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common malnutrition causing delirium in alcoholic pts
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vitamin B1 deficiency
|
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most common way that infx affect the nervous system
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indirectly by toxins
|
|
common presenting sx of elderly pts w/ generalized sepsis
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altered mental status often precedes fever or leukocytosis
|
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6 common risk factors of delirium due to infection
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1. UTI
2. low serum albumin 3. proteinuria 4. fever 5. hypothermia 6. azotemia |
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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
|
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3 sx of phencyclidine overdose
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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...
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permanent brain damage
|
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action at these receptors can cause manifestations of sedative or alcohol overdoses
|
GABA receptors
|
|
2 sx of sedative overdose
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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
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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
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sundowning
|
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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 |
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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
|
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apathetic but not severely depressed, dramatic personality changes, emotionally incontinent (cannot inhibit emotional expression)
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frontal lobe disorder
|
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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
|
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2 most common psychiatric sx in pts w/ adult hypothyroidism
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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
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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
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when might you use a benzo for a panic disorder pt?
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a pt who requires drug therapy and who has failed on antidepressants
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these can be produced by emotional trauma accompanying certain experiences
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phobias
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intense, irrational fear or aversion to a particular object or situation
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specific phobia
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4 common phobias
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1. insects
2. injections 3. heights 4. elevators |
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a fear that one will act in an embarrassing or humiliating manner
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social phobia (speaking, eating, or performing in public)
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tx of choice for phobic disorders
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psychotherapy
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2 drug classes that can be used to tx phobic disorders
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benzos
BB - reduces autonomic hyperarousal and tremor |
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characterized by persistent worry + sx of hyperarousal
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generalized anxiety disorder
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this disorder has a high rate of comorbidity w/ MDD
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generalized anxiety disorder
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can GAD ever occur in the absence of major life events?
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yes
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is a person w/ GAD more likely to present to a GP or a psychiatrist?
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GP
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6 psychiatric disorders w/ obsessive thinking, apprehension, persistent fear, and worry that can be confused with GAD
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1. OCD
2. panic disorder 3. somatoform disorder 4. psychotic disorders paranoid subtypes 5. eating disorders 6. personality disorders |
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for which disorder does insurance coverage tend to discriminate, causing pts to not get appropriate tx?
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GAD
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what are the indications for tx of GAD w/ benzos?
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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
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when do you see physiologic dependence of benzos?
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when they are given continuously for >3 months
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daytime sedation, ataxia, accident proneness, and memory problems are adverse effects of these drugs when given as tx for GAD
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benzos
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what is buspirone and what can it be used for?
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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
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how long must you give buspirone before you start to see it mitigate anxiety?
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at least 3 weeks
|
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these drugs have been found extremely beneficial in GAD
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TCAs (imipramine) and HCAs (venlafaxine)
* these also have a delayed therapeutic effect like buspirone |
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SSRIs have not been tested adequately for the tx of this
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GAD
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