bs Flashcards

1
Q

insomnia

A
  • dyssomnia is problem with timing, quality, or amount of sleep
  • parasomnia is behavior of sleep, so restless legs, snoring etc
  • diagnosis:
  • difficulty intiating or maintaining sleep, early morning waking without able to go back
  • impairs your life
  • at least 3 NIGHTS A WEEK FOR A MONTH
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2
Q

insomnia etiology

A
  • endogenous: excess excitatory NT at night (NE, serotonin, dopamine, histamine)
  • deficiency of inhibitory GABA, melatonin, adenosine
  • exogenous: use of stimulants of CNS like caffeine, withdrawl of sedatives like alcohol, barbituates, and benzodiazapenes, or medical condition like chronicpain
  • psychiatric: mental disorder, depression, bipolar like manics cant fall asleep, anxiety and PTSD
  • anxiety leads to insomnia
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3
Q

insomnia management

A
  1. diagnose, and educate
  2. behaviorla conseling, sleep hysgeine and stimulus control
  3. therapy: sleep restriction, cognitive (talking through sleep and imagery), and ehavioral (sleep log)
  4. pharmacotherapy: OTC melatonin, antihistamines -> Rx antihistamines melatonin 1+2 -> mild habit forming benz receptor agonists or orexin antagonist -> benzodiazapenes or off label drugs
    - determine youre patient before giving habit forming drugs, and if they have something like apnea, dont give them a sedative
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4
Q

schizophrenia

A
  • divergence bw behavior and thought content
  • deterioration in mental status and behavior
  • gene and environment interaction
  • 1% disease

-psychosis is hallmark symptom
presents as 1. hallucination-alteration in sensory perception 2. delusions/abnormalities in thought content 3. abnormalities in thought organization and process- not linear thoughts, ex is my car rubber moon cheese

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5
Q

definitions for schizo

A

hallucination: sensory perception without an external stimuli
delusions: fixed false beliefs w/o basis- delusion of persecution is most common
thought blocking: abrupt halt in train of speech/thinking. can be bc of halluxinations
circumstantiality: when responding to a question, gives alot of info not necessary, but answers question
tangentiality: starting a logical response but then moving further and further away
loose associations: loss of meaning bw thoughts and words

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6
Q

characteristics of schizo

A
  • one episode of psychosis (hallucination/delusion/abnormality of thought process
  • persistent disturbance of thoughts/behavior/apperance/speech/emotionaffect
  • impaired social occupational functioning

different from delirium or substance abuse bc there is no clouding of consciousness bc schizo is alert and oriented and attention and memory intact when not psychotic

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7
Q

DSM 5 for schizo

A

A. 2 characteristics for at least one month

  • delusions
  • halluciations
  • disorganized catatonic behavior )neurological immobility)
  • negative symptoms (flat affect, alogia, avoliton-no drive)
  • disorganized speech

B. social/ occupation effect

C. duration: must persist for 6 months, so one month symptoms from A, with prodrome period

D. schizoaffective and mood disorder exclusion: cant be another illness

E. substance/medical exclusion- cant be other drugs

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8
Q

Key Symptoms

A
positive
-additional to expeceted
-delusions
-hallucinations
-agitation
talkative
-thought disorder
** responds well to most to traditional and atypical antipsychotics

negative

  • missing expected behavior
  • lack of motivation
  • social withdrawl
  • flat affect
  • cognitive disturbance
  • bad grooming and speech
    • sometimes, responds with atypicals

atypical antipsychotics block D2 receptor of domapine, and 5HT2a of seratonin

the traditonals only blocked D2 dopamine receptors

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9
Q

Course has three phases

A
phase 1: prodrome before first psychotic break
-avoiding social activities
quiet, passive, irritable
-interest in religion
-physical complaints
-anxiety and depression

phase 2: psychotic/active with loss of touch with reality
-poitive symptoms of delusions, hallucinations, agitation, talkative

phase 3: residual is the period between psychotic episodes. youre in touch with reality but not behaving normally
-negative symptoms, weird thinking, etc

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10
Q

etiology and other factors of schizo

A
  • occurs earlier in men than women, avg age in men is 15-25 avg age in women is 25-35
  • women respond better to antipsychotic mefs, but they have a greater risk for tardive dyskinesia
  • —- cumulative days of D2 receptor dopamine blockade can lead to permanent movement disorders of choreic movements
  • viral infections in preganancy can cause schizo
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11
Q

neurological abnormalities in schizo

A
  • abnormal frontal lobe, decreased use of glucose in prefrontal cortex
  • lateral ventricles and third ventricles enlarge
  • loss of assymetry between cerebral hemispheres- normal is asymetrical. in schizo you become symmetrical
  • density of brain changes, volume of hippocampus, amygdala, and parahippocampal gyrus go down
  • EEG sleep study shows less alpha waves, increased theta and delta waves and epiletpiform activity of EEG
  • weird eye movements
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12
Q

neurotransmitter abnormalities

A
  • dopamine hypothesis
  • excessive DA in mesolimbic tract. stimulant drugs, amphetamines, and cocaine can cause psychotic symptoms by amplifying this tract
  • negative symptoms are causes by DECREASED activity in mesocortical tract
  • elevated homovanillic acid is a metabolite of DA is increased and seen in pts with schizo
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13
Q

Neurotransmitter abnormalities

A
  • seratonin hyperactivity
  • hallucinogens like LSD increase seratonin and cause hallucinations and delusions, so possibly hyperactive seratonin is causing schizo
  • can be treated with the newer second class atypical antipsychotics bc they have anti seratonin 5HT receptor activty
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14
Q

NT abnormalities

A
  • glutamate hypothesis
  • glutamate is the major excitatory NT in CNS
  • expereimtnally seen that an antagonist of NMDA glutamante receptor will cause psychosis and an agonist will relieve symptoms
  • theory is NMDA recepter hypoactivity theory
  • mutated NMDA receptors are underactive
  • they sit on GABA interneurons bw a cortical GLU pyramidal neuron and its secondary neuron. so, with NMDAR defect, you get a loss of inhibition and allow excessive firing and increased firing in the VTA which leads to dopamine release and extra DA into limbic system causing psychosis

normal is GLU-GABA-GLU-DA

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15
Q

other disorders causing psychosis

A
  • psychotic disorder caused by general medical condition: B12, folate, temporal lobe epilepsy, cortico steroid induced
  • manic phase of bipolar disorder
  • substance induced: cocaine, crystal meth, ritalin slash any stimulants, ketamine, PCP, LSD, bath salts

other psychotic disorders

  • brief psychotic disorder is 1-29 days of schizophrenia symptoms
  • schizophrenifrm disorder is 1-6 months of symptoms
  • schizoaffective is schizo+mania or depression
  • delusional disorder is delusons but no other sympotms
  • spared psychotic disorder is one person is delusional and another person shares the delusion
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16
Q

management

A
  • effective antipsychotics block the D@ receptor in mesoLIMBIC pathway of DA
  • can be a lifelong treatment. this doesnt lower DA availability but it blocks neurons from firing excessively even in face of high DA concetration
  • typicals: first genration high and low ptency antipsychotics. high potency drugs are better at binding and sticking to D2 receptors and can cause more side effects in the nigrostriatal (movement) and tuberoinfundibular (high prolactin)
  • atypicals: clock DA and 5HT seratonin receptors. are FIRST LINE agents bc of fewer neuro side effects like parkinsonism and TD. can cause more metblic side effects though. long acting injectable also available

psycotherapy manageent

  • long term support for family and patients
  • compliance with drug regimen
  • types of psychtherapy is cogitive behavioral to improve meso cortcal, family theeapy, and perr therapy
17
Q

prognosis schizo

A
  • suicide common
  • downhill course for most ppl, but cans tabilize later
  • good prognosis for ppl with family support and women,
18
Q

adhd

A
  • adhd has to start before age 12 and has to be apparent in multiple settings
  • called a neurodevelopmental disorder
  • 4 types:
  • adhd combined: cant focus, inattentive, and hyperactive
  • adhd inattentive: just inattentive
  • adhd hyperactve/impulsive: you can focus but youre impulsive. this is uncommon
  • other

DSM5 says need 6 INATTENTIVE symptoms for 6 months

  • mistakes bc of poor attention to detail
  • cant sustain attention
  • doesnt listen
  • doesnt follow through
  • does not organize
  • avoids tasks
  • loses things
  • is distracted
  • is forgetful

6 HYPERACTIE/IMPULSIVE symptoms which change as you age bc of peer pressure

  • fidgets
  • leaves seat
  • climbs and rubs
  • not quiet/talks alot/blurts out
  • cant wait turn
  • interupts
19
Q

course of adhd

A
  • apparent at young age when the age appropriate norms for waiting and paying attention and delayed gratification arent met
  • milder cases wont be noticed until later in life when youre demands are greater
  • inattentiveness will persist longer than hyperactivity and impulsivity
20
Q

ADHD genetics

A
  • 76% is heritable
  • ch 16
  • genes linked to ADHD include dopaminergic, noradrenergic, serotoninergic, and then neurotransmission and neuronal plasticity with snap25, etc. has to do with vesicles not being able to be released. reminder that adhd is a disease of low stimulation by dopamine, ne, and seratonin and this has to do with neuronal firing and hypo or hyperactivity
21
Q

firing and tone matter

A
  • so low dopamine tone means major depressive disorder, the negative effects of schizo in mesocortical pathway.
  • high dopamine firing means hypervigilant and psychosis
  • ADHD is also abnormal pruning of neurons. idea is that ADHD brain is developing 2 years slower than regular brain
  • adhd had anterior circuits but the anterior circuits don’t fire bc of bad genes and bad circuitry. anterior cingulate are hypoactive
22
Q

firiing

A

decreased NE and DA in the prefrontal cortex

-

23
Q

differential diagnosis and associated conditions

A

you have to rule out things before you say its ADHD

  • autism
  • learning diasbility
  • substance use
  • personailty
  • bipolar

-ANXIETY is number one cooccuring illness with ADHD

24
Q

medical management

A

stimulants
-promote DA and NE activity increase but they all carry risk for addiction. can stunt growth like half an inch.

nonstimulants
-are NE reuptake inhibitors but they have less efficacy. can be sedating and can lower BP

psychotherapy
-behavioral cogntive for self control, parent training, relaxation, education support,

25
Q

ADHD pharm for preschoolers

A
  • first behavior bc dont want to medicate a three year old
  • then amphetamines bc youre not worried about them dealing or selling. amphetamines take your pump and reverse it. however they have effects on heart rate and stuff
  • then methyphenidate
26
Q

adhd pharm in children

A

-slow release methylphenidate
-slow release amphetamine
-immediate release stimulant
then clinidene ER which is an alpha 2 agonist for NE so it has bp lowering capabilities

27
Q

adhd pharm in adults

A

give adults non addictve first

  • NE things, like cloninde alpha 2 agoinst
  • then slow release amphetamine
  • then slow reease mph
  • them immediate release stimulant
28
Q

nonstimulants vs stimulants

A
  • atomoxetine are NE reuptake inhibitors. increases ne and not habit forming
  • clondine and guanficine: agonize the alpha 2 receptor. this decreases adhd by lowering bp bc it acts on a2 autoreceptors lowering bp. . in the frontal cortex though, these receptors are located on glutamate pyramidal neurons heteroreceptors and they improve the signal to noise ratio. helps the frontal cortex bc fc is responsible for prioritizing, response inhibition, and vigilance

methyphenidate works by being a NE and dopamine reuptake inhibitor

ampetamines increase nt like dopamine in the brain.

29
Q

bipolar

A

dysthymia is chronic low level depression and cyclothymia is chronic low level mania

  • major depression affects alot of the general population
  • psychomotor retardation is depression causing the patient to feel and act slowed down
30
Q

dsm for mania

A

1.distinct, abnormal, elevated, expansive mood for 7 days minimum

  1. at least 3 of the follow symptoms for at least 2 weeks
    - increased self esteem
    - grandiosity,
    - less sleep
    - increased speech
    - racing thoughts
    - distractibility
    - increased activity and energy
    - increased dangerous impulsivity

these must cause distress and dysfunction in your life

31
Q

hypomania is like a milder mania

A
  • instead of being present for 7 days, hypmania is present for 4 days
  • same symptoms as mania (distractable, talkatve, racing thoughts, hyperactive, impulsive, gradiose, and hyposomnic)
  • the symptoms cause a change in function and personality that people aroudn you notice but not severe enough to cause marked impariments
32
Q

major depressive eposide

A

pervasive sad, down, irritable mood for 2 weeks, causing distress and dysfunction

33
Q

Bipolar 1

A

MANIA + MDE

-need to have manic episode at least, could be mixed and then need to have a major depressive episode

34
Q

Bipolar 2

A

HYPOMANIA + MDE

35
Q

cyclothymia

A

minor depression with hypomania. stcuk btween dysthymia and hypomania. once your cross into mania or depression no longer cyclothymic

36
Q

more info

A
  • will spend more time depressed than mianic
  • depressed phase is more disabling but manic is more catastrophic
  • wont remember your manic episodes
  • avg patient spends 6 months euthymic
37
Q

etiology and occurance

schizo is opposite of depression

schizo is low receptor, high nt

depression is high receptor low nt

A

bio factors

  • increased monoamine neurotransmitters like da, sr, and ne
  • or the monoamine receptor deficeny theory, saying not alot of receptors so the normal amt of nt get released, but it keeps hitting the receptors
  • genetics
  • kindinling- too much neurotransmission in limbic pathway
38
Q

drugs

A
  • DO NOT USE ANTIDEPRESSANTS. this will increase NT and this would make mania worse.
  • instead, give SSRI, so less seratonin
  • in you ave to give an antideprssant, give a mood stabilizer first

-antipsychotics which are used in schizo which lock the dopamine and seratinin receptor might be good in mania of bipolar. uniquely suited to treat both sides of bipolarity

-mmod stabilizers aka antimanic agents
if psychotherapy doesnt work.
-lithium. will provide Ca++ membrane stability and promotes neuronal health and protective factors. hurts kidneys and thyroid
-divalproex increases gaba activty and tone
-carbamazepine-blocks Na+ channels and promotes neuronal health
-atypical antipsychotics block d2 receptor and increase neuronal health