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67 Cards in this Set

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Examples of pyschotic disordes
delusions
hallucinations
disorganized thought/speech
bizarre behavior
catatonic motor behavior
Notes of delusions- psychosis
erroneous beliefs held in the absence of concrete evidence

Delusions of persecution
Delusions of reference - certain gestures, comments, or mass media are aimed specifically at the person
Delusions of granduer
bizarre delusion - someone is putting/removing thoughts from the person's head, they are being controlled by someone else
Notes on hallucinations- psychosis
imagined sensory perceptions in any sensory modality

generally not aware that they are not real
Notes on disorganized thought and speech - psychosis
lots of jumping around
irrelevant answers to questions
may be so bad that they are totally intelligible -- word salad
notes on bizarre behavior - pyschosis
odd gestures/facial expressions
strange postures
bizarre clothing
odd laughing
catatonic motor behavior- psychosis
unusual motor behavior
decreased reactivty to enviro (catatonic stupor)
bizarre postures (catatonic posturing)
excessive movement (catatonic excitement)
Schizoprhenia - positive symptoms
excess/distortion of normal function

AKA "psychotic symptoms"

Usual cause of referral for TRT
Schizoprhenia - negative symptoms
reduction of function

blunted affect, poor eye contact, monotone

poverty of speech (alogia)

loss of drive/energy - avolition

Not as noticeable, but very debilitating
Schizoprhenia - cognitive symptoms
persistent decrease in IQ

impaired attention
imparied (ST) memory
impaired executive function - form/carry out plans
Schizoprhenia - other features
ahedonia - reduced ability to experience pleasure
dysphoria - unpleasant internal sensations
sleep disturbances - change night and day
Lack of insight - dont recognize the disease
suicide
substance-related disorders
Course of Schizophrenia
prodromal phase --> active phase

prodromal = low level +, -, and cognitive
-may not be obvious

onset can be gradual but often is "psychotic break" -- lots of positive symptoms

can have remissions and exacerbations or chronic level

can have stable level or progressively worse
Biological basis of schizophrenia
physical or biochemical defect

interaction of genetics and enviro
Neurodevelopmental/neurodegenerative hypothesis
Neurodevelopmental - enviro inult occurs in utero/early life --> no symptoms until adulthood after brain remodels and 'unmasks' it

Modified recently to include progressive damage- continuous/sporadic neurodegeneration
Iriginal Dopamine hypothesis of schizophrenia
oldest theory

orginally:
EXCESS DA in certain pathways

Evidence: (a) AP drugs are DA receptor antagonists (b) drugs that up DA activity produce + symptoms

mesolimbic pathway is affected: VTA, nucleus accumbens, amygdala, other subcortical limbic structures

also affects meocortical
Modified DA hypothesis of schizophrenia - what we use
EXCESS DA in meolimbic = positive symptoms

LESS DA in mesocortical = neg, cognitive symptoms
glutamate hypothesis of symptoms
Newer

symptoms due to deficiency of glutaminergic tranmission in some CNS pathways

glutamate NMDA antagonists produce almost +, -, and cognitive effects

also modulates DA pathways, so this may be the cause of the other theories
Convetions AP's
chlorpromazine
haloperidol
Atypical AP's
clozapine
risperidone
olanzapine
quetiapine
ziprasidone
aripiprazole
chemical structures of APs
phenothiazines
butyrophenones
Low potency AP's
chlorpromazine
clozapine
high potency AP's
haloperidol
resperidone

potency does not mean effectiveness
pharmacological charactersistics of conventional AP's
Antipsychotics activity
-improve + symptoms
-no effect on neg, cog

variable onset:
2-3 wks, or 1-7 days

NEver have tolerance
mech of action for AP action
block post-syn D2 receptors in mesolimbic

need to block 65% of receptors
explanation of delayed onset
depolarization block of neurons
What are the effects of blocking DA in:
Neotriatum/nigrostriatal
hypothalamus
limbic nuclei/mesolimbic
pre-frontal cortex/meoscortical
Neotriatum/nigrostriatal - Block = motor SE
hypothalamus - block = endocrine Se's
limbic nuclei/mesolimbic - block = improve symptoms
pre-frontal cortex/meoscortical - block = neg, cognitive symptoms
Acute effect of D2 Block
antagonists = more effect on autoreceptors so more firing --> no net decrease in transmission
chronic effect of D2 block
persistent depolarization = depolarization block

adds to post-syn DA blockade
pharmacological activity - sedative effect
drowsiness

from H1 and alpha-1 block, also muscarinic

NOT related to AP effects
-tolerance to sedation, not AP
-sedation starts w/ dose 1, AP later
pharmacological activity - anti-agitation
reduced aggressive, agitated, hyperactive behavior

old term = rapid tranquilization --> used to stop person when in physical restraints

rapid onset

Mech of Action:
don't really know
-sedative?
-D2 block?
pharmacological activity -
anti-emetic activity
blocks D2 receptors in CTZ
-not good at stopping vomitting from other causes

possibly affects muscarinic and H1 effects (vestibular effects)
factors influencing the vomitting center
cerebral cortex/limbic system = see something gross
chemoreceptor trigger zone = blood flow monitor
vestibular apparatus = motion sickness
visceral afferent nerves = from the gut
pharmacological activity -
Extrapyramidal effects
disorders of movement
-from blocked D2 in striatum

positively correlated with AP potency
pharmacological activity -
block of muscarinic, alpha-1, and H1 receptors
NEG correlation w/ potency

mainly source of SEs BUT
-Muscarinic and H1 may help with anti-emetics
-M1 may protect against EPS
pharmacological activity -
5HT blocking activity
mainly 5HT2

Adverse - wt. gain
Therapeutic - up AP, down EPS
pharmacological activity -
lowering sz threshold
mech of action = unknown

NEG correlation with potency
pharmacological activity -
thermoregulatory effects
poikilthermia - inability to regulate body temp from enviro

NEG correlated with potency

due to PNS block of alpha-1 and muscarinic, CNS thermoregulatory
pharmacological activity -
enhanced prolactin
INHIBIT the tuberoinfundibular DA pathway that STOPS prolactin release
-D2 block in anterior pituitary

immediate effect after 1 dose

POS correlation with potency
pharmacological activity -
Abuse/dependence
No PSYCH
No strong physical

discontinuation effect can occur
-transient hypnotic
-don't DC too quickly
Kinetics of APs
1st pass = poor F

irregular ss per person

long t1/2 --> QD dosing after tolerance to SEs

t1/2 is longer in brain than in bood
Side Effects of APs
Cognitive/behavioral effects
CV effects
Hypo/Hyperthermia
Anticholinergic
Endocrine effects
Metabolic effects
Sexual dysfunction
Seizures
EPS
Neuroleptic malignant syndrome
Acute poisoning
Drug interactions
Side Effects of APs:
Cognitive/Behavioral
Sedation
-sometimes desired effects
-moderate tolerance develops
-additive effects with other drugs
- common with low potency

Dysphoria
AKA neuroleptic-induced deficit syndrome
-down conc, emotional responsiveness, response to enviro, motivation, thinking speed, movement speed
-common
-hard to differentiate from neg/cognitive fx of disease
-cause unknown

confusion/disorientation
-more common in old people
Side Effects of APs:
CV effects
Postural Hypotension
-common, but tolerates
-alpha-block (PNS)= vasodilation, plus baroreceptor (CNS) fx

Prolonged QT interval
-worst = thiaridazine
-use caution with pts with CVD
Side Effects of APs:
Hypo/Hyperthermia
most susceptible in kids/elderly
Side Effects of APs:
Anticholinergic effects
common, but tolerate
sucky, but not dangerous

mydriasis, dry eyes, blurry vision
constipation
xerostomia
urinary problems
anhidrosis
Side Effects of APs:
Endocrine effects
mostly from up prolactin

man-boobs, man-lactation
down sperm production, up body hair

menstrual irregularities, down bone density

up risk of breast cancer --> basic effect of increased prolactin
Side Effects of APs:
Metabolic syndrome
components= wt gain, glucose intolerance, insulin resistance, hyperlipidemia

body wt gain may be main cause

NEG correlation with potency

common, major cause of non-adherence

possible causes -
*H1 block = up appetite, down activity
*5HT2C block = up appetite
*hyperprolactinemia= up fat deposition
Side Effects of APs:
sexual dysfunction
common in both sexes
from hyperprolactinemia, alpha-block, D2 block in pleasure pathway

Symptoms:
down libido, erectile dysfunction, retrograde ejaculation
Side Effects of APs:
Seizures
decreased sz threshold -->TC sz results

dose dependent

Not likely at normal doses
Side Effects of APs - EPS:
Acute: (1h post-dose)
-dystonias
-akathisia
-pseudoparkinsonism

Delayed: (60-90day post dose)
-tardive dyskinesia
Side Effects of APs - EPS:
Dystonias
breif or prolonged contractions

POS correlation with potency, dose

NEG correlation with age - highest in teens

TRT= effective:
muscarinic antagonist, spontaneously stop
-benztropine
-triheyphenidyl
-diphenhydramine
Side Effects of APs - EPS:
Akathisia
uncontrollable restlessness, inner tension

No age influence

POS correlation with potency, dose

best TRT is propanolol

often persistant
Side Effects of APs - EPS:
pseudoparkinsonism
core symptoms:
-bradykinesia
-rigidity
-tremor

POS correlation with potency, dose, and age

TRT:
muscarinic blockers
amantidine
Side Effects of APs - EPS:
Tardive Dyskinesia
involunatary movements

Onset: 3mo to years

5% per year

NOT correlated with potency, but may be correlated with lifetime D2 block

No TRT:
Switch to atypical APs
Side Effects of APs - EPS:
Neurobiological EPS
subcortical system --> modulates cortical system

thought to be based on ACh/DA balance
- too little DA action= parkinson, akathisia, dystonia
- too much DA action = Tardive dyskinseia
Side Effects of APs - EPS:
basis of Tardive dyskinesia
1. development of DA supersensitivity in NEOSTRIATUM

2. Down GABAnergic inhibition
Side Effects of APs -
Neuroleptic malignant syndrome
agruably EPS

Symptoms:
hyperthermia, muslce rigidity, EPS, change in consciousness, major fluctuations in BP/HR

POS correlation with potency

TRT:
dantrolene
bromocriptine
DC AP, support vital fcns
Side Effects of APs -
acute poisoning
low acute toxicity
-hard but possible for suicide

Symptoms:
coma, resp arrest, cardiac arrhthmias, SZ
clinical applications of AP's
psychoses
manic states
depression
N&V
Tourettes syndrome
Clinical Applications of AP's:
psychoses
All types

All equally effectively, but different potency

very effective on + symptoms, not good on neg/cognitive
High relapse, even with good compliance

Wide Variation in dose due to potency
-Megadose= stupid, only up SE's

Non-adherence likely:
confusion, SEs, lack insight into disease, paranoia

20% won't relapse if they stop taking it
-no way to predict
Clinical Applications of AP's:
N&V
prochlorperazine (COMPAZINE) for IP
droperidol (INAPSINE) for OP

useful for CTZ mediated, not as good for GI disturbance, cancer, motion sickness
Clinical Applications of AP's:
Tourette's syndrome
common = haloperidol
Atypical AP's
clozapine
risperidone
olanzapine
quetiapine
ziprasidone
aripiprazole
Clozapine
low incidence of EPS
Clozapine Potential Mech's of action
1. high M-block
-rebalance ACh vs. DA, but doesn't account for Tardive Dyskinesia block or mechanism for other atypicals

2. selective action on mesolimbic vs. nigrostriatal
No nigrostriatal DA block for ALL atypicals

3. low D2 affinity
clozapine has lower affinity than than conventionals --> need higher conc in in nigrostriatum for effect and lower conc in mesolimbic --> lower affinity means not enough get blocked in NS

Doesn't explain ALL atypicals

4. hihg 5HT2A/D2 block
all atypicals except aripiprazole block more 5HT2A than D2, main competitor to D2 hypothesis
Clozapine other comments
little effect on prolactin

agranulocytosis

hypersalivation
seizures
wt gain/metabolic syndrom
shared characteristics
5HT2A/D2 blocking ratio

low EPS/Tardive dyskinesia

probably effective against some neg symptoms

possibly effective against cog effects

no agranulocytosis

minimal prolactin elevation except risperidone

metabolic syndrome

similar to conventional agents
aripiprazole
D2 PARTIAL agonist
5HT1A agonist