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143 Cards in this Set
- Front
- Back
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What are the most pronounced changes of an aging brain
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information processing- verbal speed and working memory is slowed
decreased brain functioning after age 70 (cannot remember names of objects) characterized by slow responses |
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occurrence of delirium
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50% of surgical pts postop
80% of terminal pts will experience delirium pts with dementia unrecognized UTI Delirium predicts cognitive decline |
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four general conditions that can lead to delirium
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1. systemic disease secondarily affecting the brain
2. 1* intracranial disease 3. exogenous toxic agents 4. withdrawal from substances of abuse |
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systemic disease
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any systemic disease can cause delirium
1. poor cerebral blood flow 2. failure of cerebral metabolism 3. cardiac conditions causing a dec in cerebral perfusion 4. hyponatremia 5. hypoglycemia 6. CNS causes 7. Paraneoplastic phenomena 8. b1 deficiency in alcoholics 9. fever |
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primary intracranial disease
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brain lesion
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exogenous toxic agents
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1. substance abuse
-stimulants cause agitated paranoid sate -LSD -SSRIs- serotonin syndrome (delirium is a prominent feature) NMDA- if taken with phencyclidine -GABA- similar to alcohol overdose symptoms -Anticholinergics -Digoxin, meperidine, lidocaine, and mexiletine |
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what pathway do stimulants work through? LSD?
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stimulants- dopamine/catecholamine pathways
LSD- serotonin receptors |
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treatment to stimulant OD
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haloperidol (dopamine-blocking agent)
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physistigmine
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reverses anticholinergic delirium
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naloxone
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reverses narcotic induced delirium
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clinical findings of delirium
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pt may be apathetic - don't assume cognitive status
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signs and symptoms of delirium
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fluctuating course and symptoms keep changing
-mental status varies watch for sundowning |
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sundowning
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daytime drowsiness and nighttime insomnia with confusion
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lab finds of delirium
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vital signs- abnormal
CBC, sed rate, electrolytes, BUN, glucose, LFTs, tox screen may all be abnormal |
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other causes for mental status changes
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subarachnoid hemorrhage
subdural hematoma right-hemisphere stroke |
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EEG of delirium pt
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shows generalized slowing
mild delirium will show posterior rhythms present throughout the brain |
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differential dx of delirium
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delirium is acute (dementia is longstanding)
tremor, asterixis, and restlessness are common symptoms can be mistaken for psychosis but delirium will show cognitive dysfunction which is less common in psychotic disorders |
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pseudodelirium
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psychiatric illness that causes symptoms of delirium
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treatment of delirium
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finding the underlying cause of the problem
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treatment resistance problems
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mechanical restraints (increase morbidity which is bad)
chemical sedation- more effective and less dangerous= haloperidol |
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side effects of haloperidol
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torsades and QT prolongation
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sitter
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a useful alternative for agitated delirious pts
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treatment for delirium with anxiety
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benzos and haloperidol
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preferred benzos
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lorazepam, oxazepame, and midazolam
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pain management for delirious pts
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opiates- morphine
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meperidine
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associated with hallucinations and should NOT be given if pt is delirious
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3 general causes of delirium
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-medical condition
-intoxication -withdrawal |
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dopamine + delirium theory
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suggests that dopamine is in excess to acetylcholine if pt is delirious
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NMDA withdrawal seizures
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NMDA is upregulated by ethanol and if overly stimulated it can lead to brain damage and seizures
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Delirium tremens
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caused when GABA receptors are insufficiently stimulated due to withdrawal from benzos or alcohol
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symptoms of anticholinergic deliriuim
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agitation, papillary dilation, dry skin, urinary retention, and memory impairment
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3 drugs that can cause confusion
1 Drug that causes both confusion and hallucinations |
1. digoxin
2. lidocaine 3. mexiletine 1. meperidine = contraindicated in delirium |
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Dementia
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characterized by the slow evolution of multiple cognitive deficits leading to memory impairment and personality disturbance
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Brain structures + dementia
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brain structures are destroyed bc of degenerative disease, vascular disease, infection, inflammation, tumors, hydrocephalus, or traumatic brain injury
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CT vs MRI for dementia pt
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CT gives less than MRI
-both are important in excluding focal lesions or other conditions such as hydrocephalus |
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AD type dementia
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memory problems dominate but mood, cognition, and behavior are affected
-may see temper outbursts and personality changes |
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AD dementia characteristics
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beta amyloid plaques
-neurons and synapses are reduced esp in the basal nucleus of meynert -acetylcholine-cholinergic containing neurons are reduced -neurofibrillary tangles contain TAU protein -disconnections in the hippocampus (memory center) |
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tau proteins
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abnormally phosphorylated protein that causes neurofibrillary tangles
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basal nucleus of Meynert
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a location in the brain where acetylcholine-cholinergic-containing neurons are reduced
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Genetics of AD
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Chromosome 1
Chromosome 14 Chromosome 19 Chromosome 21 |
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Presenilin 1
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associated with Chromosome 14 and causes the increased production of amyloid
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Presenilin 2
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assocated with Chromosome 1 and causes the increased production of amyloid
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down syndrome
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pts with down syndrome are more likely to develop histological features of AD
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ApoE E4
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associated with late-onset familial sporadic forms of AD
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MRI results of AD
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decreased brain volume but increased CSF volume
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Possible early detection of AD
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hippocampal sclerosis
hippocampal atrophy |
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benign senile forgetfulness
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pt presents with similar symptoms as AD but pts forget unimportant details and have trouble remembering recent information
-AD pts forget events randomly and have difficulty with recent and remote memory |
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treatment of AD
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improve cholinergic activity by using acetylcholine precursors and choline esterase inhibitors
-donepezil -rivastigmine |
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NSAIDs role in dementia
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may reduce incidence of dementia but has not been proven in AD
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vascular dementia
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caused by many factors such as
-volume of lesion -number of cerebral injuries -location of cerebral injury |
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risk factors for vascular dementia
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HTN
DM age male sex smoking (same as for a stroke) |
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multi-infarct dementia
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advances in a stepwise fashion
-the deep middle cerebral artery (supplied by the lenticulostriate branches) is most likely to be effected -bilateral infarcts are very common |
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dementia due to right hemisphere lesion
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pt is unable to understand the nuances of affect
-denial of illness, hemi-inattention, and constructional apraxia |
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dementia due to a left hemisphere lesion
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language impairment, Broca's aphasia
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Broca's aphasia
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nonfluent speech, impaired writing, defective naming and hemiparesis
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frontal lobe pts
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differentiate from depression bc frontal lobe pts are apathetic but not deeply depressed
-will have more severe personality -"emotionally incontinent" |
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major depressive disorder
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2-3x more common in adolescent and adult females
-prepubital boys and girls are affected equally |
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life events theory for major depressive disorder
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there is usually a predisposing factors
-life events can precede the onset of depression but only in a small # of cases does major depression actually occur |
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neurotransmitter theory of major depressive disorder
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major depression could be caused by a neurotransmitter deficiency
-antidepressants increase postsynaptic signaling of serotonin, NE, or both by inhibiting their re-uptake |
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neuroendocrine theory
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emotional trauma may precede the onset of depression, hyperthryroidism, and Cushing
-unclear if the endocrine changes are precipitants or secondary affects |
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Cortisol secretion
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half of pts with major depression have HYPERsecretion of cortisol
-cortisol levels return to normal when depression is cured |
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3 common effects of thyroid hormone
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1. pts with hypothyroidism may have depression and cognitive decline
2. T3 accelerates therapeutic effects of antidepressants 3. TRH induces an increased sense of wellbeing and relaxation in both nl subjects and psychiatric pts |
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major depressive episode
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characterized by depressed mood and loss of interest or pleasure
-must predominate for 2 weeks -cause significant distress or impairment socially, occupationally, or in other areas of functioning |
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depressed mood
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-most characteristic symptom of major depression
Feelings: sad, low, empty, hopeless observations: changes in posture or speech, facies, dress -anhedonia, change in appetite, change in sleep, change in body activity, loss of energy, feelings of worthlessness and guilt, slowing of thought and inability to make decisions |
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pseudodementia
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seen in severe forms of major depressive disorder esp in old people
-confused for early signs of dementia |
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masked depression
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pts who do not report a depressed mood
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anhedonia
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inability to enjoy usual activity (universal to depressed pts)
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initial insomnia
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common when pt has comorbid anxiety with depression
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hypersomnia
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common in atypical depression and SAD
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suicidal ideation
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risk of suicide throughout a depressive episode is highest immediately AFTER the start of tx and during the 6-9 month period of abatement of symptoms
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seasonal affective disorder
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depressive symptoms that begin in the fall or winter and remit in spring
treatment- light therapy and SSRIs |
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diagnosing depression
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pts complain to PCP of somatic issues "I can't sleep" or "I have no energy"
-medications produce symptoms of depression so check all prescriptions |
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bereavement
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not a mental disorder even though it produces symptoms of depression
-antidepressants are justified when behavioral symptoms are prolonged or if pt has continued functional impairment |
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general tx for depression
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must treat florid symptoms acutely
must continue therapy to prevent relapse (atleast 6 months after therapeutic index has been reached) |
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maintenance therapy indications for major depression
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if pt is over 40 had 2 more episodes of depression
if the 1st episode occurred after age 50 if pt has hx of 3 or more depressive episodes -slow tapering can be started 5 years after initation of tx if pt is asymptomatic |
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reasons for medication failure in dperessed pts
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-dose and serum level is inadequate
-duration of tx -side effects -noncompliance |
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alternative treatment for depression
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ECT
combination of TCA with MAOI Lithium T3 sleep deprivation psychostimulants |
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combination of TCA and MAOI
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combining 2 drugs such as imipramine (TCA) and phenelzine (MAOI) may result in very serious side effects ie hypertensive reactions
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Methods to trigger response from antidepressant
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-T3, Lithium, and sleep deprvation are the most important ways to trigger a response
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risk of relapse of depression
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25% relapse within the first 6 months
esp if they discontinued antidepressant meds **there is a decreased risk of relapse if pt maintains antidepressant medication for 6 months |
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side effects of MAOIs
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(similar to adrenergic or muscarinic/cholinergic antagonism)
-development of acute HTN crisis -metabolism of AA tyramine is blocked -pounding HA -medical emergency if pt has flushing and blood vessel distention |
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phentolamine
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an adrenergic antagonist
-used to treat side effects of MAOIs |
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MAOIs drug interactions
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-pseudophedrine (sympathomimetic)
-SSRIs + MAOIs = central serotonin syndrome --> leading to confusion restlessness, diaphoresis, tremor, diarrhea, and hyperrelexia |
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central serotonin syndrome
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results from interaction from MAOI and SSRI but it is usually mild in nature and resolves iwthin 24 hours after discontinuation
-do NOT start an MAOI within 2 weeks of most SSRIs |
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TCA side effects
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result from their binding to serotonin, NE, and histamine and muscarinic sites
-can induce AV conduction delays -contraindicated in pts with 1st and 2nd degree AV block |
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SSRIs side effects and function
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- selectively block the uptake of serotonin
-cause nausea, anxiety, anorexia, and sexual dysfunction *note sexual dysfunction can be persistent but can me managed when the dose is lowered or drug is switched to bupropion or nefazodone |
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drug and dietary restrictions while taking an MAOI
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food: all cheese, sauerkraut, fermented or aged foods, fermented alcohol
drugs: amphetamines, decongestants, TCAs |
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ECT
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alternative therapy for major depression (80-90% of treatments)
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when is ECT used for major depression
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1* when treatment is urgently needed, hx of better response, and strong pt preference
2* when pt responded poorly to alternative tx, pt deteroirated rapidly, and if response is need urgently **there are NO contraindications and may be used for the elderly and pregnant |
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side effects of ECT
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death (1 in 10,000 or 0.01% to 1 in 1000 or 0.1%)
cognitive changes (usually temporary) postictal confusion leading to postictal sedation with midazolam interictal confusion memory impairment (retrograde and anterograde) cardiovascular- transient arrhythmias |
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treatment of ECT
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6-12 treatments total
-3x a week for 6-12 months -may use multiple monitored ECT - induction of many seizures to decrease the treatment course -25% of pts relapse within the first 6 months |
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prognosis of major depressive disorder
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the average number of life time episode is 5
-psychosocial stressors can cause the first 2 depressive episodes but following stressors have less influence -the number of past episodes can serve as a predictor for the future -major depressive disorder may be preceded by dysthymic disorder |
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dysthymic disorder
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"lies on the border between the normal and pathological"
-symptoms are less intensity than major depression -AKA subsyndromal mood disorder |
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dysthymic disorder occurrence
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most commonly occurring mood disorder bc of its protracted course
-affects women more than men |
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dysthymic disorder differential
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distinguish between major depression bc there are less vegitative symptoms - less loss of appetite, less loss of libido, less insomnia
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tx of dysthymic
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antidepressants: TCAs, MAOIs, and SSRIs
- start with SSRIs if pts don't response move to nortriptyline or desiparmine |
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psychotherapeutic interventions for dysthymic
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use if social and occupational functioning are impaired
use the interpersonal psychotherapy and cognitive behavioral therapy |
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interpersonal psychotherapy
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develops more effective strategies for dealing with social and interpersonal relations (dual goal)
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cognitive behavioral therapy
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based on assertion that depression is associated with negative thought patterns, cogntive errors, and faulty information processing
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dysthymic disorder as a risk factor
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it is a risk factor for developing major depression
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bipolar I disorder
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consists of episodes of mania and depression
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bipolar II disorder
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episodes of hypomania and depression
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risk factors for bipolar disorder
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female
family fx upper class |
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risk factors for those WITH bipolar disorder
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recurrent manic or depressive episodes as a person ages
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distribution of bipolar disorder
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equal distribution between males and females but females are more likely to have serious bipolar disorder esp rapid-cycling bipolar disorder
-- there is no clear association between life events and manic or hypomanic episode |
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Genetics and bipolar
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there is genetic evidence for bipolar disorder
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symptoms of bipolar I
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rare to be monopolar
hallmark or mania: persistently elevated, expansive or irritable mood somatic features: when depressed pts sleep too much when manic- sleep little to not at all ** must control the insomia to treat acute manic episode behavioral- speech cognitive- racing thoughts risk of suicide- oh yea huge risk |
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role of lithium in bipolar I disorder
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reduces the risk of suicide attempts and good for the tx of acute manic episodes and maintenance therapy which should be used for 6-12 months
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hypomanic symptoms
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similar to mania (elevated mood, insomnia, racing thoughts, loud rapid speech, psychotic features, and risk of suicide) but do not reach the same level of intensity or social impairment
-vocational function usually remains normal |
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bipolar II disorder
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has a hypomanic state with depression
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rapid-cycling bipolar disorder
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pts experience 4 or more affective episodes in a year
-may have clinical or subclinical hypothyroidism which predisposes pt to a more rapidly cycling course |
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lap findings for bipolar disorder
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none
-HPT axis should a blunted TSH response to TRH -hypothyroidism is very common dx wiht bipolar disorder |
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differential dx for bipolar
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must differentiate between schizophrenia, schizoaffective disorder, ADHD, and borderline histrionic personality disorder and mania
-substance abuse is very common |
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treatment of bipolar
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acute manic episodes- lithium, divalproex, valproic acid
delusional syms and agitation- haloperidol maintenance- lithium, valproic acid, and carbamazepine combination therapy can lead to optimal stabilization |
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drugs to be avoided with bipolar
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TCAs, alcohol, steroids, and stimulants because they are mood destabalizers
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2 main indications of lithium
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acute or hypomanic episodes
prevention of mania and depression *watch for breakthrough depression *explain to pt that bipolar disease is chronic and to watch for the warning signs |
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lithium combination THERAPY
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lithium + SSRIs or buproprion
lithium + benzos or antipsychotics for acute phase mania |
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management of breakthrough depression in bipolar disorder
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inc lithium dose
maximize thyroid function add an SSRI sleep deprivation ECT |
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side effects of lithium
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inc thirst, fine tremor (beta blocker to treat), polyuria, memory problems, V/D muscle weakness, seizures, coma, death, sick sinus syndrome
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carbamazepine
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can be used to treat bipolar disorder
side effcts - rash leading to discontinuation -acute liver damage -jaundice -blood dyscrasias -granulocytopenia and agranulocytosis |
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valproic acid
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used for acute management of mania
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cyclothalamic disorder
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pts alternate between extreme dysthymia (gloomy and depressed) and hyperthymia (cheerful and uninhibited)
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symptoms of cyclothalamic disorder
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moody, impulsive, erratic, and volatile but do not meet the criteria for bipolar disorder bc it is less severe and shorter duration
-changes in mood are abrupt (within hours) -controversial dx |
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anxiety disorder
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a heightened arousal leading to tension, tachycardia, tachypnea, tremor, and apprehension
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normal fear
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emotional reaction to threats and cause an emotional response that is related to the actual danger
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anxiety symptoms
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occur without obvious danger or when the response to the threat is excessive
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panic attack
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a misperception of suffocation -- a false suffocation response
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panic disorder
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recurring spontaneous unexpected anxiety attacks with rapid onset and short duration
-pts fear they are experiencing a MI or stroke |
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symptoms of panic attack
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severe within 10 mins but can peak within a few seconds
-SOB, tachypnea, tachycardia, chest discomfort should diminish after 30 mins |
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agoraphobia
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excess phobic avoidance
develop safe people and safe places |
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treatment of panic disorder
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behavioral or cognitive behavioral therapy
DRUGS: low dose benzos MAOIs (phenelzine) SSRIs |
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phobia
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- an intense irrational fear or aversion to a particular object or situation other than a social situation
emotional trauma accompanying experiences ie riding in a car, speaking in public |
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social phobia
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fear that they will act in an embarrassing or humiliating manner
-speaking in public, eating in public, using public restrooms, and performing in public |
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treatment of phobia
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psychotherapy
drugs -benzos, beta blockers |
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GAD
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associated with high rates depression and may occur without a change in major life events
-chronic disorder |
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teratment
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usually not taken seriously by physicians or insurance companies
Benzos reduce symptoms but are not curative and should be reduced as soon as pt returns to normal functioning - watch for dependence - prescription refills should be monitored closely buspirone TCAs (imipramine and venlafaxine) SSRIs |
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side effects of benzos
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ataxia, daytime sedation, accident proneness, and memory problems
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Buspirone
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used as an alternative treatment for GAD bc it has no motor, memory, or concentration impairments with NO abuse potenital
bad part: takes 3 weeks to work on anxiety |
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axis 1
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mental illness itself
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axis 2
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personality disorder and mental retardation
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axis 3
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physical illness
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axis 4
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life stressors
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axis 5
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global assessment of function
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