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Pharmacology 2 > 7.7 psychotic drugs > Flashcards

7.7 psychotic drugs Flashcards

1
Q

Psychoses (major and obvious)

A

are disorders in which pateints exhibits fals beliefs (delusions) and false perceptions (ahllucinations). There is detachment from reality

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2
Q

Affective disorders

A

emotional distrubances in which the mood is excessively low (depression) or high (mania), may be bipolar (manic depressive) with cyclically alternating manic depressive phases or unipolar (mania or depression) with waxing and waning course

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3
Q

Neuroses (not detached from reality)

A

less severe, unlike psychoses, ability to comprehend reality is not lost, though pt may undergo extreme suffereing, anxiety, phobic states (panic disorder), obsessive compulsive disorders, reactive depression, post raumatic stress disorder, hysterical conversion, personality disorders

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4
Q

psychotropic or psychoactive drugs

A

durgs which affect mental processes eg cognition or affect

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5
Q

classes of psychotropic drugs

A

antipsychotics, antianxiety, antidepressants, antimanic, psychotomimetic

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6
Q

antipsychotics

A

(neuroleptics or major tranquilizers) –useful in all types of psychoses, particulary schizophrenia

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7
Q

antianxiety

A

(anxiolytic-sedative, minor tranquilizer) used for anxiety and phobic states

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8
Q

antidepressants

A

used for minor as well as major depressive illness, phobic states, obsessive compulsive behavior and certain anxiety disorders

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9
Q

antimanic (mood stabilizers)

A

used to control mania and break into cyclic affective disorders

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10
Q

Drugs for affective disorders

A

antidepressants and antimaniac drugs are sometimes collectively referred as drugs for affective disorders

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11
Q

Psychotomimetic (psychedelic, hallucinogens)

A

seldom used in therapy, however produces psychosis ike states, majority are drugs of abuse

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12
Q

Schizophrenia

A

a debilitating psychosis characterized by delusion, hallucinations (often in the form of voices, auditory) and thinking or speech disturbances, affects 1% of the world population, heredofamilial, prenatal abnormal cerebrum (MRI) and neurotransmitters,

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13
Q

Schizophrenia biochemical nature

A

biochemical abnormality, possibly an overactivty of the mesolimbic, mesocortical dopaminergic neurons, inc in D2 receptors in Nucleus Accumbens - PET (Dopamine hypothesis) –> positive symptoms

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14
Q

dopamine hypothesis

A

functional excess of cerebral dopamine leads to schizophrneia

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15
Q

drugs that block dopamine receptors or deplete monoamines (reserpine)

A

ameliorate schizophrenic systems (+ve)

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16
Q

drugs that activate dopamine receptors or release amines (amphetamines)

A

exacerbate symptoms or cause psychoses

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17
Q

Antipsychotic effects is related to

A

antidopaminergic drug potency drug potency (IC50–dose required to block 50% of receptors)

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18
Q

Dopamine hypothesis of schizophrenia

A

incomplete (explains positive symptoms, antipsychotic drugs are only partially effective for most and ineffective for some pts –indicates dopamine physicology not completely responsible for the pathogenesis of Schizophrenia, involvement of (glutamate) NMDA, cholinergic 5HT receptors likely

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19
Q

Positive symptoms of schizophrenia

A

disorer of Perception and inferences delusions, hallucinations, thought disorder

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20
Q

delusions

A

fixed false beliefs (invulnerable to logical contradictory evidcnes) “flat earth society”

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21
Q

Hallucinations

A

auditory “running commentary voices” and others

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22
Q

thought disorder

A

thougth insertion, thougth broadcast, illogicla decisions

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23
Q

Negative symptoms

A

abnormal relationships, expressions or speech –affective flattening, alogia, anhedonia, apathy

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24
Q

Affective flattening

A

lack of or inappropriate emotional expression

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25
Q

Alogia

A

absence of words

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26
Q

Anhedonia

A

inability to derive pleasure from any activity

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27
Q

Apathy

A

withdrawal from the social contact

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28
Q

Cognitive dysfucntions in schizophrenia

A

impaired attention, impaired working memory, impaired executive function

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29
Q

Dopamine agonists cause

A

psychosis ex. Amphetamines, levodopa, ampmorphine

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30
Q

Dopamine antagonists have

A

antipsychotic actions

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31
Q

Serotonin abnormality in schizophrenia

A

dec in 5H2/5H1A receptors in prefrontal cortex of pts

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32
Q

glutamatergic dysfunction in schizophrenia

A

a deficiency of glutamatergic activity – decrease hipocampal NMDA (glutamate) receptors

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33
Q

Dopamine paths

A

slide 20, 21–take pictures

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34
Q

Dopamine paths in the brain - mesolimbic

A

dopamine travels from the midbrain tegmental area to the nucleus acumbens. Increased activity in this pathway may cause delusions, ahllucinations, and other so-called positive symptoms and cognitive symptoms of schizophrenia

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35
Q

Dopamine paths in the brain - mesocortical

A

decreased activity in pathway that goes from the midbrain to the prefrontal lobe cortex may caue apathy, withdrawal, lack of motivation and pleasure, and other so-called negative symptoms of schizophrenia, mesocortical dysfunction also disinhibits mesolimbic pathway

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36
Q

slide 24

A

take a picure

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37
Q

what accounts for negative symptoms of schizophrenia

A

dec mesocortical dopaminergic account for the negative symptoms

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38
Q

what accounts for the positive symptoms of schizophrenia

A

increased meoslimbic dopamine neurotransmission results in positive and cognitive symptoms

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39
Q

Dopamine paths in the brain - nigrostriatal

A

the pathway from substantia nigra to striatum, involved in the coordination of the body movements, inhibition of this pathways (DA antagonsits) results in extra pyramidal side effects of anti-psychotics

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40
Q

DA agonists my cause

A

dyskinesias

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41
Q

Dopamine paths in the brain - tuberoinfundibular

A

it is from hypthalamus to pituitary and inhibits prolactin secretion – block of this pathways results in increase prolactin secretion

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42
Q

increased prolactin secretion form DA antagonists results in

A

gynecomastia, infertility, amenorrhea

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43
Q

Dopamine paths in the brain - medullary0periventricular

A

consists of neurons in the motor nucleus of the vagus, may be involved in eating behaviour

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44
Q

Dopamine paths in the brain - incertohypothalamic

A

forms connections from the medial zona incerta to the hypothalamus and amygdala, regulate sexual behaviour

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45
Q

nigrostriatal origin

A

substantia nigra

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46
Q

nigrostriatal innervation

A

caudate nuc, putamen

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47
Q

nigrostiratal fn

A

extra pyramidal motor control

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48
Q

mesolimbic origin

A

midbrain ventral tegmentum

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49
Q

mesolimbic innervation

A

limbic system

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50
Q

mesolimbic fn

A

arousal memory motivation

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51
Q

mesocortical origin

A

MVT

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52
Q

mesocortical innervation

A

frontal and prefrontal cortex

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53
Q

mesocortical fn

A

cognition communication

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54
Q

tuberoinfundibular origin

A

hypothalamus

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55
Q

tuberoinfundibular innervation

A

pituitary

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56
Q

tuberoinfundibular fn

A

regulates prolactin secretion

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57
Q

Dopamine receptors

A

5 types D1 to D5, Fall in 2 categories D1like, D2 like

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58
Q

D1 like receptors

A

Gs - inc cAMP

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59
Q

D2 like

A

Gi - dec cAMP —these ones are what we are worried about in schizophrenia

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60
Q

D2a

A

nigrostriatal

61
Q

D2c

A

mesolimbic

62
Q

classes of neuroleptic drugs

A

typical conventional first generation, atypical second generation

63
Q

typical first generation antipsychotics

A

phenothiazines, butyrophenes, thiotixines

64
Q

phenothiazines

A

chlorpromazine, fluphenazine, thioridazine

65
Q

butyrophenones

A

haloperidol

66
Q

thiotixines

A

thiotixine

67
Q

atypical second generation antipsychotics

A

Dopamine/serotonin blockers, Dopamine partial agonists

68
Q

Dopamine/Serotonin blockers

A

Clozapine, Olanzapine, Risperidone, Asenapine, Quetiapine, Ziprasidone, Iloperidone, Paliperidone

69
Q

Dopamine partial agonists

A

Aripriprazole

70
Q

Mechanism of action – dopamine receptor blocking activity in the brain

A

all antipsychotic drugs (primarily first generation) block dopamine receptors in the brain and the periphery, antipsychotic drugs bind to dopamine receptors in varying degrees

71
Q

Mechanism of action –serotonin receptor blocking activity in the brain

A

atypical antispychotics (second generation) exhibit their action primaryly through inhibition of serotonin receptors 5HT2

72
Q

Mechanism of action – Other

A

also block cholinergic (muscarinic), adrenergic (alpha) and histaminergic (H1) receptors

73
Q

Mechanism of action

A

dopamine receptor blockers, serotonin receptors blcokers, others

74
Q

Typical first generation work by

A

primarily block the D2 receptor in the mesolimbic pathways, decrease the dopaminergic transmission in the mesolimbic pathways to nucleus accumbens, alleviates positive symptoms, more extrapyramidal features (due to binding of D2 receptors in nigrostriatal pathway as well)

75
Q

Atypical second generation work by

A

block the 5HT2 preferentially and D2 receptrs faster dissociation from D2R, increase the release of dopamine in mesocortical pathways to prefrontal lobe, inc 5HT1A receptors –> alleviates negative symptoms more than typical, less extrapyramidal adverse effects (dec D2)

76
Q

Atypical in nigrostriatal path

A

increased dopamine release counteracts the extrapyramidal side effects caused by D2 receptor block

77
Q

therapuetic effects

A

take several weeks to develop

78
Q

most of these drugs show

A

little correlation btw plasma levels and therapeutic action (not good for TDM -therapeutic drug monitoring)

79
Q

Actions of Antipsychotics

A

Antipsychotic actions, extrapyramidal effects, Antiemetic effects, antimuscuranic effects, CNS effects, CVS effects, other effects

80
Q

antipsychotic actions

A

atypical agens such as clozapine-like drugs, ameliorate the negative symptoms, all altipsychotics have a calming effect and reduce spontaneous physical movement (neurolepsis),

81
Q

Extrapyramidal effects

A

dystonias, parkinson-like symptoms (pseudoparkinsonism; reversible), akathisia (motor restlessness), and tardive dyskinesia (involuntary movements of the tongue, lips, neck, trunk, and limbs) occur with chronic treatment, blocking of dopamine receptors in the nigrostriatal pathway CAUSE of these symptoms, atypical antipsychotics exhibit low incidence of these symptoms (bc in the nigrostriatal pathway, increased dopamine release counteracts the extrapyramidal side effects caused by D2 receptor blockade)

82
Q

Antiemetic effects

A

excpet tioridazine and aripiprazole, moste of the antipsychotics have antiemetic effects, they block D2 receptors of the CTZ (floor of the 4th ventricle) of medulla, atypical antipsychotics are not effective antiemetics

83
Q

antimuscarinic effects

A

some of the antipsychotics (particularly thioridazine, chlorpromazine, clozapine) produce antimuscarinic effects, cause blurring of vision, dryness of mouth, inhibition of GI and urinary muscles–leading to constipation and urinary retention

84
Q

CNS effects

A

hyperprotactinemia, poikilothermic effect

85
Q

hyperprolactinemia

A

inc the secretion of prolactin (by blocking D2 receptors in pituitary), atypical antipsychotics are less likely to produce prolactin elevations

86
Q

Poikilothermic effect

A

on the bodytemperatur (body tem varies with environment) bc DA blocage affects temperature regulation areas

87
Q

CVS effects

A

orthostatic hypotension (alpha 1 antagonist), relex tachycardia, inc QTc , ventricular arrhythmia, both typical and atypical agents show does dependent inc of torsade de pointes VT and sudden cardiac death

88
Q

Other effects

A

H1 antagonists–increases appetite and produces sedation (chlorpormazine, clozapine, olanzapine, quetiapine)

89
Q

Chlorpromazine on CNS

A

motor activity is decreased, sleep pattern is set normal (however not used as sedative-hypnotics), emesis is blocked, improve cognitive abilities, no impairment of intellectual functions, decrease the seizure threshold, inc the secretion of the prolactin, poikiolothermic effect on body temperature (body temp varies with environment), minimal respiratory depression compared to barbiturates

90
Q

Chlorpromazine as D2 antagonists

A

aleeviation of positive s/s and presence of extrapyramidal s/s

91
Q

chlorpromazine as an alpha 1 antagonist

A

hypotension

92
Q

chlorpromazine as an H1 antagonist

A

increased appetite and produce sedation

93
Q

Chlorpromazine anticholinergic action

A

urinary retention, dry mouth

94
Q

chlorpormazine on CVS

A

hypotension, QT interval prolongation and ventricular arrhythmia

95
Q

Thioridazine

A

pharmacological properties similar to Chlorpromazine

96
Q

compared to chlorpromazine, thioridazine produces

A

greater antimuscarinic effects (probably the reason to cause fewer extrapyramidal side effects)

97
Q

high doses of thioridazine may cause

A

pigmentary retinopayt (retinitis pigmentosa) and cardiac arrhythmia, and sexual dysfunction –retrograde ejaculation

98
Q

Fluphenazine and Trifluoperazine

A

potent pehnothiazines, produce fewer autonomic side effects but more EP side effects than do low-potency penothiazines

99
Q

Haloperidol

A

highly potent, properties similar to fluphenazine and may cause significant EPS

100
Q

EPS sypmptms

A

fluphenazine=haloperidol>CPZ>thioridaine

101
Q

Sedative

A

CPZ=Thio>Fluphenazine= Haloperidol

102
Q

Hypotension (alpha blockade)

A

CPZ=Thio>Fluphenazine= Haloperidol

103
Q

antimuscarinic effects

A

Thio>CPZ>Fluphenazine= Haloperidol (opposite to EPS)

104
Q

sturcture of typical antipschotics

A

lipophillic, orally effectve

105
Q

good drugs for noncompliant pts

A

haloperidol and fluphenazine are available as IM long acting (depot) preparations (2-4 weeks), hence rapid initiation of treatment and maintenance is possible in noncompliant pts –>administerd by a deep Z-track IM method

106
Q

tolerance to antipsychotics

A

tolerance to the sedative and hyptensive action but not for antipsychotic and extra pyramidal effects. No physical dependence.

107
Q

Adverse effects of typical antispychotics

A

extrapyramidal symptoms, CNS, ANS, endocrine, weight gain, neuroleptic malignant syndrome, Retinopathy

108
Q

Acute EPS

A

Acute muscular dystonia, Akinesia, Pseudo-parkinsonism, Akathisea

109
Q

acute muscular dystonia

A

4hrs (irregular spasms of the facial, neck and trunk muscles torticollis, locked jaw, jerky movements, trouble speaking

110
Q

akinesia

A

4 days – can’t initiate movements

111
Q

pseudo-parkinsonism

A

1-4 weeks – rigiditiy, tremor, hypokinesia, mask like face, shuffling gait, pillrolling

112
Q

akathisia

A

4 weeks – restlessness, irresistible compulsion to be in motion

113
Q

Chronic EPS

A

tardive dyskinesia –4 monts to years – facial and limb movements choreathetosis (tics) like chewing, putting, puffing of cheeks, lip licking, tongue protrusion, chroeoathetoid-like movemens, caused by supersensitivity of dopamine receptros due to chronic blockade (months or years) of dopamine receptors in caudate, putamen); Tarditive dyskinesia is induced by all antipsychotics (except clozapine and more seen with Haloperidol) and is often irreversible

114
Q

Management of EPS

A

lower the dose of typical andtipsychotics and swithc over to atypical ones, antimuscarinic drugs like benztropine or dipehnhydramine, TD is irreversible

115
Q

Adverse CNS effects of typicals

A

sedation (central H1 block), mental confusion (central muscarinic blck), aggravation of seizures in epileptics

116
Q

Adverse ANS effects of typicals

A

alpha blocker – postural hypotension, reflex tachycardia, anticholinergic – dry mouth, constipation, urinary retention, blurred vision

117
Q

Adverse endocrine effects of typicals

A

amenorrhea – galactorrhea, infertility, impotence (due to hyperprolactinemia) D2 blockade, in male – decreased libido, gynecomastia, inhibition of ejactulation/retrograde ejaculation, in female –Amenorrhea–galactorrhea, infertility

118
Q

Adverse weight gain of typicals

A

5HT2 block and H1 block

119
Q

Neuroleptic malignant syndrome is most common with

A

haloperidol

120
Q

neuroleptic malignant syndrome

A

lifethreatening extreme muslce rigidity, fever, autonomic dysfunction (tachycardia, diaphoresis, and urinary and fecal incontinence), altered level of consciousness, myoglobinemia, associated with 20% mortality rate, occurs due to excessive rapid blockade of psotsynaptic dopamine receptors

121
Q

Treatment of Neuroleptic malignant syndrome

A

immediately stop offending antipsychotic drug and start bromocriptine/Pergolide (dopamine receptor agonist)/ Amantadien/Dantrolene and Diazepam, along with symptomatic management

122
Q

Retinopathy of typicals

A

retinal diposits

123
Q

Cardiotoxicity with typicals

A

torsades–“quinidine-like” effects,

124
Q

retinopathy and cardiotoxicity is especially seen with

A

thioridazine at high dose

125
Q

clozapine

A

potent 5HT2 blocker, weak D2 blcoking, most effective antipsychotic agent (superior over other antipsychotics), reduce both positive and negative symptoms (but more negative symptoms)

126
Q

Limitation of Clozapine

A

agranulocytosis (requires weekly WBC monitoring) and Seizures (even in non-epileptics)

127
Q

Clozapine and EPS

A

lower incidence of EPS and no tardive dyskinesia

128
Q

Clozapine effects

A

inc salivation (wet pillow syndrome, bed wetting and other autonomic side effects like weight gain, orthostatic hypotension, hyperglycemia (diabetes)

129
Q

Clozapine and prolactin

A

does not cause a rise in prolactin level

130
Q

Clozapine is reserved for

A

drug resistant shizophrnia due to its side-effect profile

131
Q

Olanzapine vs Clozapine

A

similar in that it causes minimal EPS BUT does NOT cause agranulocytosis, fewer autonomc side effects (due to less blcokade of histamine, muscarinic and alpha adrenergic receptors), less incidence of seizures compared to clozapine

132
Q

most common adverse effects of olanzapine

A

sedation and weight gaint (more than clozapine) and can cause hyperglycemia (diabetes)

133
Q

Olanzapine vs Haloperidol

A

as effective as haloperidol in alleviating the positive symptoms of schizophrenia and is superior to haloperidol in alleviating the negative symptoms

134
Q

Risperidone

A

blocks 5HT2 receptors and improves negative symptoms primarily, pharmacologically similar to olanzapine, nowadays used as first line antipsychotics drugs, not as effective as clozapine in treatment-resistant cases but does not carry a resk of blood dyscrasias (agranulocytosis) and has a low incidence of EPS (dose-dependent)

135
Q

Risperidone vs. Olanzapine

A

causes less sedation, but more EPS than Olanzapine

136
Q

Risperidone on QT

A

prolongs the QT interval and may predispose pts to cardiac arrhythmias (including torsades de pointes)

137
Q

Aripiprazole

A

blocks 5HT2 receptors, partial agonists of D2 receptors, hence less chance of tardive dyskinesia, also has little risk of weight gain or prolactin increase but amy increase anxiety, nausea, and insomnia as a result of its partial agonist properties, low potential for EPS, not good for severe psychosis due to its partial agonistic effects

138
Q

Quetiapine

A

distinct in having a weak D2 effect, also 5HT2 antagonsit effect, also potent alpha1 and histamine blocker

139
Q

Quetiapine causes

A

sedation, dizziness, drymouth and weight gain and hyperglycemia (diabetes), cataract formation (although mentioned in drug’s package, not seen during clinical trials), Excellent EPS profile

140
Q

Ziprasidone

A

seldom causes minimal weight gain and is unlikely to increase prolactin, but may cause QT prolongation and somnolence, low potential for EPS, C/I–history of cardiac arrhythmias

141
Q

Parenteral (IM) atypical antipsychotics

A

Aripiprazole, ziprasidone, Long acting – olanzapine, paliperidone, resperidone

142
Q

chart on slide

A

77

143
Q

antipsychotics on schizophrnia

A

antipsychotics – the mainstay of treatmetn, many pts show little response and virtually none show a complete response

144
Q

use of antipsychotics

A

nausea and vomiting (drug induced or radiation induced) , EXCEPT Thioridazine and Aripiprazole

145
Q

use of antipsychotics on tourette syndrome

A

vocal and motor tics —pimozide, haloperidol, fluphenazine/risperidone, olanzapine, ziprasidone

146
Q

Use of antipsychotics on neuroleptanalgesia

A

droperidol

147
Q

for hiccups

A

cholpromazine

148
Q

for behavior and irritability secondary to autism

A

risperidone

Pharmacology 2 (12 decks)

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