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P. pharm > Schizophrenia Spectrum & Other Psychotic Disorders- A&P > Flashcards

Schizophrenia Spectrum & Other Psychotic Disorders- A&P Flashcards

1
Q

What neurotransmitter systems are associated w/ all forms of psychosis

A

dopamine
serotonin
glutamate

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2
Q

psychosis

A

A syndrome (mix of sx) associated w/ many psych disorders but isn’t a specific disorder itself

At minimum hallmark sx= delusions and hallucinations (positive sx)

set of sx in which person’s mental capacity, affective response, and capacity to recognize reality, communicate and realate to others is impaired

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3
Q

delusions

A

fixed beliefs (often bizzare) that have an inadequate rational basis and cant be changed by rational arguments or evidence in the contrary

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4
Q

hallucinations

A

perceptual experiences of any sensory modality- esp. auditory= that occur without real external stimulus yet are vivid and clear just like normal perceptions but not under voluntary control

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5
Q

“other” sx of psychosis

A

disorganized speech or behavior, gross distortions of reality testing (perceptional distortions and motor disturbances)
neg sx= diminished emotional expression and decreased motivation

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6
Q

3 categories of psychosis

A

paranoid
disorganized/excited
depressive

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7
Q

perceptual distortions

A

being distressed by hallucinatory voices, hearing voices that accuse blame or threaten punishment, seeing visions, reporting hallucinations of touch taste or odor, or reporting that familiar things and people have changed

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8
Q

motor disturbances

A

peculiar, rigid postures, overt signs of tension, inappropriate grins/giggles, peculiar repetitive gestures, talking muttering or mumbling to oneself, or glancing around as if hearing voices

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9
Q

paranoid psychosis

A

paranoid projections, hostile belligerence, and grandiose expansiveness

often in schizophrenia and drug-induced

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10
Q

paranoid projection

A

preoccupation with delusional beliefs, believing that people are talking about oneself, believing one is being persecuted or being conspired against, and believing people or external forces control ones actions

ex: Parkinson’s disease psychosis common paranoid delusions= belief that one’s spouse is being unfaithful or that spouse or loved ones are stealing from them

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11
Q

hostile belligerence

A

verbal expression of feelings of hostility, expressing attitude of disdain, manifesting a hostile sullen attitude, manifesting irritability and grouchiness, tending to blame others for problems, expressing feelings of resentment, complaining and finding fault, as well as expressing suspicion of people

seen in schizophrenia and drug-induced psychosis

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12
Q

grandiose expansiveness

A

exhibiting an attitude of superiority, hearing voices that praise and extol, believing one has unusual powers or is a well know personality, or that one has a divine mission

schizophrenia and manic psychosis

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13
Q

disorganized/excited psychosis

A

conceptual disorganization, disorientation, and excitement

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14
Q

conceptual disorganization

A

giving answers that are irrelevant or incoherent, drifting off the subject, using neologisms, or repeating certain words/phrases

seen in any psychotic disorder

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15
Q

disorientation

A

not knowing where one is, the season of the year, the calendar year, or one’s own age and is common in psychoses associated with dementias and drug-induced

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16
Q

excitement

A

expressing feelings without restraint, manifesting speech that is hurried, exhibiting an elevated mood, an attitude of superiority, dramatizing oneself or ones sx, manifesting loud and boisterous speech, exhibiting overactivity or restlessness, excess of speech

mania or schizophrenia

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17
Q

depressive psychosis

A

psychomotor retardation, apathy, anxious self punishment and blame

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18
Q

psychomotor retardation and apathy

A

slowed speech, indifference to ones future, fixed facial expression, slowed movements, deficiencies in recent memory, manifesting blocking in speech, apathy toward oneself or ones problems, slovenly appearance, low or whispered speech, failure to answer questions

hard to distinguish from neg sx

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19
Q

anxious self punishment and blame

A

tendency to blame or condemn oneself, anxiety about specific matters, apprehensiveness regarding vague future events, attitude of self deprecation, manifesting depressed mood, expressing feelings of guilt and remorse, preoccupation with suicidal thoughts, unwanted ideas and specific fears, feeling unworthy or sinful, seen often in psychotic depression

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20
Q

3 major hypotheses of psychosis & their neurotransmitter

A

dopamine (DA)= hyperactive dopamine at D2 receptors in the mesolimbic pathway.

glutamate= NMDA receptor hypofunction

serotonin= 5HT2A receptor hyperfunction in the cortex

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21
Q

dopamine theory of psychosis main characteristics

A

mechanism= dopamine D2 agonist
hallucinations= auditory
freq. delusions= paranoid
no insightfulness

psychostimulants (cocaine, amphetamine)

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22
Q

glutamate/NMDA theory of psychosis main characteristics

A

mechanism= NMDA antagonist
hallucinations= visual
freq. delusions= paranoid
no insightfulness

dissociative anesthetics (PCP, ketamine)

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23
Q

serotonin theory of psychosis main characteristics

A

mechanism= serotonin 5HT2A agonist (lesser extent 5HT2c)
hallucinations= visual
freq. delusions= mystical
yes insightfulness

psychedelics (LSD, psilocybin)

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24
Q

two groups of dopamine receptors

A

D1-like receptors= excitatory and positively linked to adenylate cyclase. Includes both D1 and D5 receptors

D2-like receptors= inhibitory and negatively linked to adenylate cyclase. Includes D2, D3, D4

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25
Q

is dopamine excitatory or inhibitory

A

either or; depends on which DA receptor subtype it binds

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26
Q

what dopamine receptors can be located presynaptically and what does this mean

A

D2 and D3
due to inhibitory actions, can act as auto-receptors aka gatekeepers (a receptor that regulates, via positive or negative feedback processes, the synthesis and/or release of its own physiological ligand) to inhibit further DA release

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27
Q

where in the brain are there very minimal D2/D3 auto-receptors and what does this mean

A

prefrontal cortex
(mesocortical DA neurons arising from ventral tegmental area (VTA) in brainstem project to prefrontal)

without D2/D3 autoreceptors, DA release is not shit off by this mechanism and is thus freer to diffuse away from the synapse where released. Also have few/any DATs on presynaptic nerve terminals in prefrontal cortex allowing larger diffusion radius of DA away from presynaptic terminals

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28
Q

what postsynaptic receptor is predominant in prefrontal cortex & why is this good

A

D1
least sensitive to DA & requires higher concentration of DA to be present to be activated

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29
Q

5 classic dopamine pathways in brain

A
  1. tuberoinfundibular (hypothalamus to anterior pituitary)
  2. thalamic
  3. nigrostriatal (brainstem substantia nigra via axons terminating in the striatum)
  4. ** mesocortical (DA hypotheses psychosis; cell bodies in CTA to prefrontal cortex)
  5. ** mesolimbic (DA hypotheses psychosis; DA in VTA of brainstem to ventral striatum in limbic system)
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30
Q

Function of neurons in tuberoinfundibular DA pathway

A

hypothalamus to anterior pituitary
usually tonically active and inhibit prolactin release

postpartum= decreased activity > increased prolactin to increase lactation

lesions or drugs can disrupt= decreased activity > increased prolactin. SE: galactorrhea (breast enlargement), amenorrhea, sexual dysfunction

pathway maybe preserved in untreated schizophrenia

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31
Q

Function of neurons in thalamic DA pathway

A

under investigation
may be involved in sleep and arousal mechanisms by gating info passing through the thalamus to the cortex and other brain areas

no evidence of abnormal functioning in schizophrenia

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32
Q

Function of neurons in nigrostriatal DA pathway

A

brainstem substantia nigra via axons terminating in the striatum
part of extrapyramidal nervous system, control motor movements via connection to thalamus and CSTC loops

Normally BLOCKS motor movements but DA inhibits this action at D2 receptors and says “don’t stop” or “go more”

dopamine stimulates motor movements in both direct/indirect pathways

no evidence of abnormal function in schizophrenia but deficiencies of DA in these pathways cause movement disorders like Parkinson’s & can also cause akathisia (restlessness) & dystonia.
*Same disorders can be replicated w/ drugs that block D2DA receptors in this pathway= EPS. Chronic blockade can lead to tardive dyskinesia
hyperactivity of DA can cause hyperkinetic movement disorders like chorea, dyskinesias and tics (Huntington’s, Tourette syndrome)

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33
Q

Function of neurons in mesolimbic DA pathway

A

DA in VTA of brainstem to ventral striatum in limbic system

involved in motivation, pleasure, reward (ALL reward/reinforcement) including normal rewards (good food, orgasm), rewards too high (drug-induced), or too low

Too much DA= positive sx psychosis, drug-induced high of substance abuse
Too little DA= anhedonia, apathy, lack of energy (neg sx schizophrenia, unipolar and bipolar depression)

hyperDA in schizophrenia mesostriatal rather than purely mesolimbic because VTA-substantia nigra complex is integrative hub

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34
Q

Function of neurons in mesocortical DA pathway

A

cell bodies in CTA to prefrontal cortex
dorsolateral prefrontal cortex= cognition and executive functions
ventromedial= emotions and affect

still debate but belief= cognitive and some neg. sx schizophrenia may be due to deficit of DA in mesocortical projections to dorsolateral prefrontal cortex & affective and other neg sx d/t deficit of DA activity in mesocortical projections to ventromedial prefrontal cortex

underactivity/improper functioning= consequence of neurodevelopmental abnormalities in N-methyl-D-aspartate (NMDA) glutamate system

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35
Q

glutamate hypothesis of psychosis and schizophrenia

A

NMDA subtype of glutamate receptor is hypofunctional at critical synapses at specific site: certain GABA interneurons in prefrontal cortex
can lead to DA hyperactivity= psychosis

d/t neurodevelopmental abnormalities in schizophrenia, neurodegenerative in Alzheimer/dementia, and NMDA receptor blocking actions of drugs like dissociative anesthetics ketamine & PCP

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36
Q

glutamate

A

major excitatory neurotransmitter (& amino acid= primary use) in CNS, “master switch” of brain since can turn on/excite all CNS neurons

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37
Q

important glutamate pathways

A
  1. cortico-brainstem
  2. cortico-striatal
  3. hippocampal-striatal (theories link to schizophrenia)
  4. thalamo-cortical
  5. cortico-thalamic
  6. cortico-cortical (direct)
  7. cortico-cortical (indirect)
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38
Q

serotonin theory of psychosis

A

hyperactivity/imbalance of serotonin (5HT) activity, particularly at serotonin 5HT2A receptors can result in psychosis

disruption of 5HT functioning leading to positive sx psychosis can be hypothetically d/t neurodevelopmental abnormalities in schizophrenia, neurodegeneration in parkinson’s Alzheimer and other dementia, and drugs like LSD, mescaline, psilocybin

psychoses r/t serotonin= more visual hallucinations

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39
Q

serotonin vs dopamine hallucination

A

serotonin= visual
dopamine= auditory

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40
Q

what kind of neurotransmitter is serotonin

A

monoamine neurotransmitter (dopamine & norepinephrine as well) which regulates a brain network that is one of the most targeted by psychotropic meds

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41
Q

what enzyme does the synthesis of 5HT start with

A

tryptophan

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42
Q

difference between DA and 5HT and their transporters DAT & SERT

A

not all dopamine neurons contain DATs but all serotonin neurons contain SERTs

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43
Q

serotonin receptors vs those on dopamine and norepinephrine

A

dopamine & norepinephrine neurons have same receptors at both ends (axon terminals & dendrites, soma) while in serotonin neuron, axon-terminal receptors are different from somatodendritic receptors

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44
Q

presynaptic 5HT1A receptors

A

negative feedback receptors/inhibitory
detect serotonin released from dendrites which causes slowing of neuronal impulse flow through neuron and reduction of serotonin release from axon terminal

downstream effect can be excitatory

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45
Q

presynaptic 5HT2B receptors

A

feed forward receptors
activate serotonin neuron to cause more impulse flow and increased serotonin release from presynaptic nerve terminals

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46
Q

presynaptic 5HT1B/D receptors

A

aka terminal autoreceptor
negative feedback autoreceptors to detect presence of 5HT; causes blockade of 5HT release

serotonin inhibits release of dopamine, norepinephrine, histamine, and acetylcholine at 5HT1B receptors

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47
Q

postsynaptic serotonin regulation of other neurotransmitters

A

each neurotransmitter controls its own synthesis/release as well as actions of others via postsynaptic actions and networks of brain circuits

they act synaptically and trans-synaptically

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48
Q

does serotonin excite or inhibit

A

either or; depends upon the serotonin receptor subtype where it’s interacting and whether the postsynaptic neuron itself releases glutamate (excitatory) or GABA (inhibitory)

norepinephrine, dopamine, histamine, and acetylcholine can also receive direct input from serotonin or indirect through glutamate or GABA

*drugs acting on serotonin also have downstream effect on all other neurotransmitters

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49
Q

5HT2a receptors

A

excitatory but can be excitatory or inhibitory depending on where in brain

5HT2a antagonists= tx psychosis & mood disorders
agonists= hallucinogens

50
Q

5HT2c receptors

A

excitatory neurons on GABA interneurons that generally inhibit release of downstream neurotransmitters

5HT2x agonists= tx obesity
antagonists= tx psychosis/mood disorders

51
Q

5HT3 receptors

A

in brainstem chemoreceptor trigger zone outside of blood-brain barrier known for role in centrally mediated n/v

at other locations (especially prefrontal cortex) located on GABA interneuron= excitatory on GABA & therefore inhibit wherever GABA interneurons go like 5HT2c receptors

*inhibit acetylcholine & norepinephrine at cortical level

5HT3 antagonists enhance release of acetylcholine & norepinephrine. Reduces glutamate which in turn regulates serotonin (will decrease when normally excites d/t feedback loop)

52
Q

5HT6 receptors

A

postsynaptic, key regulators of release of acetylcholine release and control of cognitive processes

blocking improves learning/memory

53
Q

5HT7 receptors

A

postsynaptic, excitatory, localized on inhibitory GABA interneurons

inhibit release of downstream neurotransmitters especially glutamate at cortical level
regulate serotonin release at level of brainstem raphe

5HT7 antagonists= tx psychosis & mood

54
Q

serotonin & dopamine in parkinsons

A

loss dopamine nerve terminals in motor striatum of niagrostriatal pathway= motor sx

loss of serotonin nerve terminals in prefrontal and visual cortex= up-regulation and too many 5HT2A receptors in cortex > imbalance in excitatory action on glutamate > psychosis

5HT2a antagonists block psychosis in parkinsons

55
Q

serotonin in dementia

A

accumulation of plaques, tangles, & Lewy bodies, damage from strokes, knocks out cortical neurons > lack of inhibition of glutamate neurons; if GABA can’t counter= psychosis

selective 5HT2a antagonist decrease psychosis in dementia

56
Q

link between psychosis hypotheses of serotonin hyperfunction at 5HT2a receptors and dopamine hypothesis

A

excessive 5HT2a stimulation at glutamatergic pyramidal neurons leads to dopamine hyperactivity & NMDA hypofunction > psychosis

57
Q

length of time of sx to = schizophrenia

A

disturbance that lasts 6 months or more including at least 1 month of positive sx (delusions, hallucinations, disorganized speech, grossly disorganized/catatonic behavior) or neg sx

58
Q

negative sx schizophrenia

A
  1. alogia- dysfunction in communication; restrictions in fluency/productivity of thought/speech
  2. affective blunting/flattening- restrictions in range/intensity of emotional expression
  3. asociality- reduced social drive/interaction
  4. anhedonia- reduced ability to experience pleasure
  5. avolition- reduced desire, motivation, or persistence; restrictions in initiation of goal-directed behavior

*more but these are the 5 classic types
can be before dx and neg sx can persist between psychotic episodes

59
Q

prodromal neg sx schizophrenia

A

neg sx can be subsyndromal occurring before onset of full syndrome of schizophrenia, Important to detect/monitor over time in high-risk pt so tx can start at first sign psychosis

60
Q

neg sx schizophrenia based solely on observation

A

reduced speech, poor grooming, limited eye contact, reduced emotional responsiveness, reduced interest, reduced social drive

61
Q

what other (non diagnostic) sx of schizophrenia are there besides neg/pos sx

A

cognitive, affective, and aggressive sx

62
Q

cognitive sx schizophrenia

A

impaired attention/information processing, manifesting as difficulties w/ verbal fluency, problems with serial learning, and impairment in vigilance for executive functioning

begin before onset first psychotic illness, manifest as lower IQ scored. Worsen during prodrome before full blown psychosis & progressively worsens throughout disease

*no short term memory disturbance; issues with executive functioning

63
Q

affective sx schizophrenia

A

depressed mood, anxious, guilt, tension, irritability, worry
difficult to distinguish from neg sx and from comorbid mood/anxiety disorder

need to be treated; if not relieve dby drugs for positive sx psychosis, consider drugs to tx anxiety/depression to tx sx AND prevent suicide; will not be effective if sx are true negative sx

64
Q

aggressive sx schizophrenia

A

ivert hostility, assaultiveness, physical abuse, violence, verbally abusive behaviors, sexually acting out, self injurious, arson/property damage

different from agitation because intentional harm

not common but more common than general population; stigma; more likely to experience violence against them

65
Q

categories of violence in institutionalized schizophrenia pt pg. 148

A

impulsive (most common in institutions; precipitated by provocation as response to stress associated w/ neg emotions anger/fear)
predatory/organized (planned behavior; result of frustration/response to threat; common in psychopathic or antisocial personalities; associated w/ criminogenic more than psychotic sx)
psychotic (least common in institutions; positive sx psychosis)

66
Q

genetics & schizophrenia

A

genes don’t = mental illness but do code for proteins and epigenetic regulators
Genes must conspire amongst themselves and environmental stressors to = mental illness

*genes= risk not cause per se

67
Q

environmental stressors for schizophrenia

A

cannabis, emotionally traumatic experiences, sleep deprivation, being a migrant, etc.
environment puts load on neural circuits where risk genes expressed and cause circuits to malfunction under pressure. Same stressors can cause normal genes to malfunction > neuroplasticity and synaptogenesis

only half of all identical twins of pts w/ schizophrenia also have it

68
Q

epigenetics

A

the study of how your behaviors and environment can cause changes that affect the way your genes work

normal genes can= mental illness if expressed when should be silenced or vice versa

69
Q

neurodevelopment & schizophrenia

A

a bunch of neurons are made out of stem cells at conception but only a minority selected for inclusion in developing brain; abnormalities can occur w/ neuronal selection process leading to neurodevelopmental disorders
New neurons cont. to form, differentiation and myelination, synaptogenesis cont. throughout life & any disruption= neurodevelopmental illness

schizophrenia= neurodevelopmental process of synaptogensis/brain restructuring gone awry

70
Q

What’s theory as to why schizophrenia manifests in adolescence

A

brain restructuring occur throughout life but most active during late childhood/adolescence (aka competitive elimination)
only 1/2 to 2/3 synapses from childhood left for adulthood

so elimination of compensatory critical synapses or formation of abnormal “weak” synapses could cause inefficient info processing in its circuit causing sx schizophrenia

71
Q

neurodegeneration in schizophrenia

A

progressive downhill course
strengthening/weakening of synapses continues to occur throughout lifetime based off what’s used or not. “Use it or lose it”
abnormal synaptogenesis prevents normal synapses from functioning even if using and/or the wrong synapses are used/strengthened in schizophrenia

loss of brain tissue with recurrent episodes of psychosis

72
Q

disorders where psychosis is defining feature

A

schizophrenia
substance/medication induced psychotic disorders
schizophreniform disorder
delusional disorder
brief psychotic disorder
shared psychotic disorder
psychotic disorder due to another medical condition
childhood psychotic disorder

73
Q

disorders where psychosis is associated feature (not defining)

A

mania
depression
cognitive disorders
Alzheimer/other dementia
Parkinson’s

74
Q

are sx of schizophrenia unique to schizophrenia

A

NO
several other illnesses can share same 5 sx dimensions

75
Q

what is thought to lead to parkison’s disease psychosis (PDS)

A

accumulation of Lewy bodies in cerebral cortex and in serotonin cell bodies in midbrain raphe

76
Q

why is it important to distinguish agitation from psychosis in dementia

A

can be difficult but neuronal pathways are different and so are treatments

77
Q

neurolepsis

A

extreme slowness, absence of motor movements in animals; human counterpart= drugs that cause secondary neg sx: psychomotor slowing, emotional quieting, affective indifference

caused by blocking D2 receptors

78
Q

what causes secondary neg sx

A

targeting dopamine D2 receptors in mesolimbic/mesostriatal and mesocortical pathways

79
Q

what dopamine pathway causes hyperprolactemia w/ D2 antagonists

A

D2 receptors in the tuberoinfundibular dopamine D2 receptors

which causes gynecomastia, galactorrhea, amenorrhea therefore infertility, rapid demineralization of bones, sexual dysfunction, weight gain

80
Q

what dopamine pathway causes motor side effets w/ D2 antagonists

A

targeting nigrostriatal dopamine D2 receptors
same pathway that degenerates in Parkinson’s

acute: drug induced parkinsonism (DIP)- tremor, muscular ridigity, bradykinesia, akinesia
EPS is old-fashioned/imprecise term for motor SE bc different sx= diff presentation/tx

chronic: tardive dyskinesia

81
Q

tx drug-induced parkinsonism (DIP)

A

anticholinergics by blocking muscarinic cholinergic receptors, exploiting normal balance between dopamine and acetylcholine in striatum because dopamine neurons in nigrostriatal motor pathway make postsynaptic connections on cholinergic interneurons

anticholinergics block downstream release of acetylcholine

82
Q

what causes DIP with D2 antagonists

A

dopamine normally blocks acetylcholine from postsynaptic nigrostriatal cholinergic neurons but D2 blockers cause acetylcholine release > excitation postsynaptic muscarinic cholinergic receptors on GABAergic neurons > movements/sx DIP

83
Q

considerations for anticholinergics to treat DIP

A

peripheral and central SE
many drugs for psychosis also have anticholinergic SEs

concern for cognitive functioning and paralytic ileus

seek alternatives like drugs for psychosis w/o antichol. properties

84
Q

alternative to anticholinergic for DIP

A

amantadine
can also help w/ TD and levodopa-induced dyskinesias

85
Q

drug-induced acute dystonia

A

d2 blockers esp w/o serotonergic/anticholinergic properties

intermittent spasmodic or sustained involuntary contraction of muscles in face neck trunk pelvis extremities eyes

need IM anticholinergic

chronic late-onset can lead to TD & require diff tx

86
Q

akathisia

A

syndrome of motor restlessness often seen with D2 blockers

subjective (inner restlessness, mental unease, dysphoria) objective (restless movements mostly lower-limb- pacing, rocking when stnading)

sometimes drug-induced sometimes d/t psychiatric disorder

tx with beta adrenergic blockers or BZOs; serotonin 2A antagonists also

87
Q

neuroleptic malignant syndrome

A

rare fatal complication D2 blocker
extreme muscle rigidity, high fevers, coma, death

medical emergency > STOP d2 blocker > muscle relaxer (dantrolene or dopamine agonsists) intensive medical tx

88
Q

conventional D2 antagonists (first generation antipsychotics)

A

not first line, use if don’t respond to newer drugs for psychosis

89
Q

*agitation

A

psychiatric emergency
For agitated patients not willing or able to take oral medications, IM medications such as Olanzepine
and Haldol can be used

90
Q

*when to use IM antipsychotics like olanzapine or haldol

A

For agitated patients not willing or able to take oral medications, IM medications such as Olanzepine
and Haldol can be used

91
Q

*what should be administered with IM first generation antipsychotic like Haldol

A

IM haloperidol should be administered with benztropine or diphenhydramine to reduce the risk of severe EPS or dystonia.

severely agitated patients, we suggest using a benzodiazepine in combination with the antipsychotic
(e.g. Haldol + Lorazepam + Cogentin.

92
Q

*what pathway do first generation antipsychotics block dopamine

A

Mesocortical

93
Q

*main SE second generation antipsychotics

A

Can cause EPS but at a lower risk
* ↓ incidence of Tardive dyskinesia
* Metabolic side effects : Weight gain, HLD,
hyperglycemia, Diabetes, HTN, Cardiac and
respiratory S/E
* Some Antihistaminic, antiadrenergic and
antimuscarinic effects
* Elevated Liver function tests (LFTs)- check yearly
* QTC Prolongation

94
Q

*time it take second generation antipsychotics to work

A

6-8 weeks

95
Q

*main SE of typical antipsychotics

A
  1. High antiadrenergic, anticholinergic and antihistaminic s/e (e.g. sedation, weight gain)
  2. Elevated liver enzymes, jaundice
  3. Seizures – all antipsychotics lower the seizure threshold
  4. Orthostatic hypotension
  5. QTC prolongation – obtain baseline EKG
  6. Sexual dysfunction
  7. Rashes, photosensitivity
  8. Elevated liver enzymes, EPS (Akathisia, dystonia, Parkinsonism)
  9. **Hyperprolactinemia (decreased libido, galactorrhea, gynecomastia, impotence, amenorrhea)
  10. Tardive dyskinesia
  11. Neuroleptic Malignant Syndrome (FALTERED)
96
Q

*most effective tx akathisia (psychomotor restlessness)

A

β-adrenergic receptor antagonists (beta-blockers)

97
Q

*should you co-order meds with antipsychotics to prevent EPS? Why/why no?

A

Do not co-prescribe drugs in efforts to prevent EPS. Associated w/ high anticholinergic side effects

If necessary, anticholinergics should be prescribed at the lowest dose possible.

98
Q

*3 types EPS, sx, duration

A

Acute Dystonia, Akathisia, & Pseudo-Parkinsonism

99
Q

*Acute dystonia sx/tx/when develops

A
  • Sudden onset
  • Fixed/Sustained painful
    contraction of the neck muscles
    (torticollis), tongue, eyes
    (oculogyric crisis)
  • Can be life threatening if it affects
    airway

Txt: Cogentin, Artane, Benadryl,
Benzos- Ativan
* Lower dose if possible

Hours to days

100
Q

*Akathisia sx/tx/when develops

A
  • Internal and external restlessness
  • Subjective anxiety, restlessness,
    inability to remain still
  • Constant need to pace or walk

Txt: Drug of choice= Beta blocker
(Propranolol), Benzos (Klonopin,
Ativan)
* Lower dose if possible

Days to months

101
Q

*pseudo-parkinsonism sx/tx/when develops

A

Bradykinesia(shuffled gait),
masklike face, cogwheel rigidity,
pill-rolling tremor

  • Txt: Cogentin, Artane, Benadryl,
    Symmetrel (Amantadine)
  • Lower dose if possible

Days to months

102
Q

*How many D2 receptors need to be blocked to cause EPS

A

Antipsychotics must occupy more than 80% of D2 receptors to cause EPS

103
Q

*Clozapine(Clozaril)/Fazaclo (ODT)

A

Used to treat refractory schizophrenia(i.e., treatment
resistant)
- *****Only antipsychotic shown to decrease SI risk
-Less likely to cause TD
- Weight gain is most prominent
-More anticholinergic s/e- tachycardia, constipation etc.
- **Hypersalivation (sialorrhea) occurs in 30-80%
- Agranulocytosis( highest first 3 months of treatment)=
Monitor WBC and Absolute neutrophil count (ANC)
-D/C med if ANC is <1.5 (1500)
-ANC

Off label use
- Treatment resistant bipolar disorder
- Dementia
- Parkinson’s related psychosis or agitation

Common adverse effects
- HTN
- Hypotension
- Tachycardia
- Dislipidemia
- Weight gain
- Constipation
- Sialorrhea
- Drowsiness/sedation

104
Q

*Only antipsychotic shown to decrease SI risk

A

Clozapine(Clozaril)*

105
Q

*Management of Sialorrhea

A
  • Chew sugarless gum
  • Place towel over pillow especially if nocturnal sialorrhea is a
    problem
  • Med: Glycopyrrolate (Robinul) -fewer Anticholinergic side
    effects)
  • Benztropine, Artane etc.
106
Q

*What med for parkinson-related psychosis

A

Pimavanserin =Nuplazid =Used in Parkinson’s related psychosis (newer med)

first-in-class atypical antipsychotic that does not induce clinically significant antagonism of dopaminergic, adrenergic, histaminergic, or muscarinic receptors.

107
Q

*considerations for metabolic syndrome r/t antipsychotics

A

H1 receptor antagonism is associated with sedation and weight gain

❖Weight gain – Metformin can be used to reduce or prevent
❖Hyperlipidemia
❖Hyperglycemia
*** > Monitor Baseline and ongoing(i.e. 3 months etc.)
* Weight
* Waist circumference
* BP
* HbA1c
* Fasting lipids
NOTE: For patients established on antipsychotic medications, yearly labs should be considered.

see page 15 of study guide for table w/ monitoring freq. for metabolic syndrome with olanzapine, quetiapine, & clozapine

108
Q

*Characteristics of metabolic syndrome

A
  • Abdominal obesity
  • Elevated triglycerides
  • Low HDL levels
  • BP higher than 135/85 mm Hg
109
Q

Alogia, Anhedonia, Avolition and cognitive symptoms =

A

negative sx

110
Q

Delusions, hallucinations, hostility, grandiosity = ___

A

positive sx

111
Q

This class is associated with fewer neurological side effects and effective
for both positive and negative symptoms

A

second generation antipsychotics

112
Q

This class is effective for only positive symptoms and can in fact worsen
negative symptoms due to decrease DA in the Mesocortical pathway

A

first generation antipsychotics

113
Q

Associated with metabolic side effects =

A

atypical/second generation

114
Q

What are the metabolic side effects associated with Atypical
antipsychotics

A

hyperglycemia, weight gain, risk metabolic syndrome, elevated triglycerides

115
Q

Includes medications such as Haloperidol, Chlorpromazine, Fluphenazine, Perphenazine=

A

first generation antipsychotics

116
Q

Medications for acute agitation or psychosis=

A

BZO

117
Q

FGA reduce dopamine transmission by blocking _______________ receptors.

A

D2

118
Q

SGA block both ______________ and ________________ receptors

A

D2 & 5HT2a

119
Q

H1 blockade leads to symptoms of __________________ and __________

A

?

120
Q

Safest and best tolerated anticonvulsant for patients taking clozapine
who experience dose related seizures =_

A

?

121
Q

Less incidence of antiadrenergic, anticholinergic and antihistaminic side
effects but greater EPS =__________________________________________

A

P. pharm (8 decks)

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