Psych exam 1 Flashcards
1
Q
What is the mental status exam (AMSIT)
A
documents patient’s CURRENT thinking, feeling, and behavior
2
Q
AMSIT: A (general appearance, behavior, speech
A
demographics, physique, hair, clothes, cleanliness
inc or dec psychomotor activity, distractibility sterotypy
mutism, preservation, echolalia, neologisms
3
Q
AMSIT: M (mood and affect)
A
position on 7 pt depression elation continuum
range, intensity, stability, appropriateness
4
Q
AMSIT: S (sensorium)
A
orientation to time and place
memory
calculating ability
5
Q
AMSIT: I (intellectual function)
A
level of current function: above ave, ave, below ave
general knowledge
use of vocab
6
Q
AMSIT: T (thought)
A
Form tangentiality, circumstantiality, loose associations, flight of ideas
Content: delusions, hallucinations, ideas of referance
Judgement
Abstract ability
Insight
7
Q
What is the purpose of the psychiatric rating scale
A
obj way of measuring sub data (thoughts, feelings, perceptions)
screen or diagnose disorders
evaluate adverse effects
8
Q
What is a pink slip
A
application for emergency admission
9
Q
Who can fill out a pink slip
A
psychiatrist, clinical psychologist, physician, health/police/parole officer, sheriff, CNP in psychiatry
10
Q
How does someone fill out a pink slip
A
person must be taken inconspicuously
person must be treated with consideration and respect
person can make phone calls to attorney
obtain counsel to evaluate person’s mental condition
11
Q
How long are people admitted from a pink slip
A
examined w/in 24 hr of arrival
not mentally ill needs to be released asap
if mentally ill, person may be detained for not more than 3 court days following exam day
12
Q
At the end of the 3 day pink slip period what happens
A
admit the person as a voluntary pt or file and affidavit w/ court for mentall ill person or discharge pt
13
Q
Civil vs criminal competency
A
civil: able to make reasonable decisions
criminal: able to testify or stand trial
14
Q
What is guardianship
A
legal process used to protect individuals who are unable to care for themself
15
Q
What is malingering
A
intentional production of false or exaggerated physical or psychological problems
goal is receiving a specific benefit
16
Q
What is borderline
A
ongoing pattern of varying moods, self-image, and behavior
impulsive actions and problems in relationships, experience intense episodes of anger, depression and anxiety, view things in extreme
17
Q
Onset of schizophrenia
A
late adolescence to early adulthood, earlier in males
18
Q
What is schizophrenia
A
complex syndrome of disorganized and bizarre thought, delusions, hallucinations, inappropriate affect, and impaired psychosocial functioning
19
Q
What medications precipitate psychosis
A
anticholinergics
dopamine/dopamine agonists
stimulants
steroids
cannabids
cocaine
lsd
20
Q
What are the 4 dopamine hypothesis of schizophrenia
A
mesolimbic pathway (+ symptoms)
mesocortical pathway (- symptoms)
nigrostriatal pathway (extra-pyramidal side effects)
tuberoinfundibular pathway (hyperprolactinaemia)
21
Q
For schizophrenia DSM-V one of the sx must be what
A
2 or more for significant portion of time in 1 month:
delusions, hallucinations, disorganized speech
(could also have disorganized or catatonic behavior, negative symptoms)
22
Q
For schizophrenia DSM-V continuous signs of the disturbance persist for at least __ months
A
6
23
Q
schizophrenia phases of disorder
A
prodromal, active, residual
(pt experience periods of remission)
24
Q
schizophrenia acute episode
A
lost reality, disconnected thought process, hallucinations, delusions
uncooperativeness, hostility, poor hygiene, disrupted sleep and appetite
25
Positive symptoms of schizophrenia (most improved with antipsychotics)
suspiciousness, delusions, hallucinations, conceptual disorganization, ideas of reference, illusions, loose associations, agitation
26
Negative symptoms of schizophrenia (associated with poor psychosocial function)
blunted, alogia (no speech), anhedonia (no pleasure), poor grooming, poor judgement, lack of abstract thinking, social w/drawal
27
Cognitive symptoms of schizophrenia (related w/ poor psychosocial function)
impaired attention, working memory, executive function, problem solving, and difficulty reading social cures
28
Affective symptoms of schizophrenia
guilt, anxiety, tension, irritability, worry
29
Aggressive/hostile symptoms of schizophrenia
overall hostility, verbal/physical abuse or assault, self-injurious behaviors, arson/property damage
social and occupational dysfunction
30
How to treat schizophrenia
pt compliance
meds
psychotherapy
31
Antipsychotic drugs strongly block postsynaptic ___ receptors in the CNS
D2
32
Drugs that increase dopaminergic activity either aggravate schizophrenia or produce what
psychosis
33
NMDA receptor antagonist causes symptoms similar to those of schizophrenia however __________ acts also as a potent D2 receptor partial agonist
phencyclidine
34
5-HT2 receptors modulate __________ neurotransmission
glutamate
35
What is the target for schizophrenia drugs
mescortical/mesolimbic pathways
36
The nigrostraiatal and tuberoinfundibular pathways causes what reaction
extrapyramidal side effects
37
Typical antipsychotics alleviate positive symptoms while atypicals alleviate what
positive and negative
(they block D2 and 5-HT2A)
38
Typical antipsychotics MOA
blockade of postsynaptic D2 receptors
-causes mesolimbic and mesocortical pathways to relieve some behavioral manifestations
-basal ganglia underlies the motor side effects
-tuberoinfundibular pathway increases prolactin secretion
39
Typical antipsychotics may also block what receptors
muscarinic, alpa 1 adrenergic, histamine, 5-HT2 receptors
40
extrapyramidal side effects and treatment for drug induced parkinsonism
antimuscarinic antiparkinsonian agents, lower dose of antipsychotic agent
41
extrapyramidal side effects and treatment for akathisia
antimuscarinic antiparkinsonian agents, lower dose of antipsychotic agent
42
extrapyramidal side effects and treatment for acute dystonia
spasma of muscles
antiparkinsonian agents
43
Thiothixene MOA
similar to phenothiazines, higher dopamine blocking potency, parkinsonian effects and prolactin elevation
44
Loxapine MOA
little anticholinergic effect, claimed no weight gain
45
Haloperidol MOA
more potent than phenothiazines; also used to treat Huntington's disease and Tourettes syndrome
46
What happens when overdose with aliphatic and piperidine phenothiazines
CNS excitation followed by depression, coma
47
Overdose with piperazine phenothiazines, thioxanthenes, butyrophenones causes what
CNS excitation or depression
Acute dystonic reactions
48
Treatment for overdosing for neuroleptics
support vital signs
treat arrhythmias
gastric lavage
treat hypotension by volume expansion or alpha adrenergics
49
Molindone MOA
low affinity for D2 receptors than more antipsychotics agents and relatively low affinity for D1 receptors
50
Pimozide MOA
antagonist of D2, D3, and D4 receptor and the 5-HT7 receptor
51
Clozapine MOA
D4 antagonist, not very potent at D1 or D2, strong anticholinergic, 5-HT2A antagonist, anti-H1
52
Risperidone MOA
antagonist at D2 and 5-HT2 receptors, affinity for D2 similar to haloperidol
53
Quetiapine MOA
antagonist at D2 and 5-HT2 receptors, potent actions at alpha adrenergic receptors
54
Ziprasidone MOA
antagonist at D2 and 5-HT2 receptor, modest SSRI-like
55
Olanzapine MOA
antagonist at D1, D2, and D4 receptors, may also block 5-HT2C, 5-HT3, and alpha 1 and H1
-may improve depression in psychotic depression
-approved for bipolar
56
Aripiprazole MOA
partical agonist at D2 receptors, 5-HT2A antagonist and partial agonist at 5-HT1A receptors, mild anticholinergic actions
57
Cariprazine MOA
partial agonist at D2 receptors, partial agonist at 5-HT1A receptors and antagonist activity at 5-HT2A receptors
58
General therapeutic goals for schizophrenia
management of acute psychotic episode within 7 days
stabil: 6-12 wk
maintenance: 1 yr, have drug for up to 5 yr
59
First gen antiphyschotics MOA
primarily block dopamine (D2) receptors, minimal serotonin (5-HT2A) receptor blockade
60
First gen antiphyschotics pathways
mesolimbic pathway good
mesocortical pathway bad
nigrostriatal pathway bad -> EPS
tuberoinfundibular pathway bad -> increase prolactin
61
What are the 4 EPS side effects
acute dystonic reaction
pseudoparkinsonism
akathisia
tardive dyskinesia
62
acute dystonic reaction potential reactions
oculogyric crisis
pharyngeal/laryngeal spasm
torticollis/retrocollis
glossospasm
opisthotonus
(considered medical emergency)
63
What is dystonia
bizarre involuntary tonic contractions of skeletal muscles appears within 24-96 hours
64
acute dystonic management
potent anticholinergics (NO PO)
Diphenhydramine 50 mg IM
Benztropine 2 mg IM
(cont oral for 1 wk)
65
pseudoparkinsonism signs and symptoms
tremor
rigidity
akinesia/bradykinesia
shuffling gait
(appears within 3 months)
66
pseudoparkinsonism management
decrease antipsychotic dose
change to atypical antipyschotic
Benztropine
Trihexyphenidyl
Amantadine
67
Akathisia (restlessness) signs
may be reason for noncompliance
can not sit still
68
Akathisia management
change to atypical antipsychotic
bezno
Propranolol
69
Tardive Dyskinesia signs and symptoms
long term exposure of drug
involuntary movements of face, lips, jaw, limbs
70
Tardive Dyskinesia management
commonly irreversible
use AIMS q6months
disc anticholinergic
Valbenazine
Deuterabenazine
71
NMS signs and symptoms
hyperthermia
extremem muscle rigidity
mental status change
autonomic disturbances
(can lead to rhabdo)
72
NMS management
disc antipsychotic
supportive care
Dantrolene IV
Bromocriptine
BZD
(restart antipsychotic after at least 2 wks)
(avoid high potency drugs and depots)
73
Other ADE of first gen antipsychotics
derm: allergic rxn, photosensitivity, long-term skin changes
hyperprolactinemia
QTc prolongation: thioridazine, haloperidol
M1, H1, alpha 1: anticholinergics, sedation, wt gain
74
Second gen antipsychotics MOA
potent serotonin (5-HT2A) antagonism, moderate to high dopamine (D2) antagonism
75
Second gen antipsychotics pathways
mesolimbic pathway good
mesocortical pathway good
nigrostriatal pathway good -> decrease EPS
tuberoinfundibular pathway bad -> decrease prolactin
76
Second gen antipsychotics weight gain
highest with clozapine, olanzapine
low risk aripirazole,brex, carip, lura, zipra
may not plateau
metformin may help
77
Second gen antipsychotics lipid changes
triglycerides increased
metabolic syndrome
highest risk with clozapine, olanzapine, quetiapine
78
Second gen antipsychotics DM
way more common in schizophrenia
w/in 6 months of tx in most
mild insulin resistance to DKA
79
Monitoring at baseline for antipsychotics
personal/ family history
BMI
waist circumference
BP
fasting blood glucose
fasting lipid profile
80
Monitoring at 12 wk for antipsychotics
BMI
BP
fasting plasma glucose
fasting lipid profile
81
Monitoring annually for antipsychotics
personal/family history
waist circumference
BP
fasting plasma glucose
fasting lipid profile
82
QT prolongation with antipsychotics
Prolonged
men: >450
women: >470
83
Other ADE of 2nd gen antipsychotics
EPS, increased prolactin, anticholinergic effects, orthostatic hypotension, sedation, seizures, hematologic, derm
84
Drug interactions for antipsychotics
caution with QTc prolonging agents
smoking increase plasma levels
drugs that lower seizure threshold
synergistic sedation/respiratory depression
85
Important to note with lurasidone
must take with >350 calories
86
Important to note with quetiapine
Hypnotic: 50 mg
Antidepressant: 300 mg
Antipsychotic: 600 mg
87
What antipsychotic has digital health tracking
aripiprazole
88
Cobenfy
works on muscarinic receptors
89
What is treatment resistant schizophrenia
clozapine DOC (failed two antipsychotic trials)
FDA approved for suicidal behavior
90
Clozapine dosing
risk of orthostatic hypotension
12.5-25 mg qd or BID (in hosptial)
if missed >48 hours start lowest dose in hospital
91
Clozapine BBW
neutopenia/agranulocytosis
myocarditis and cardiomyopathy
seizures
92
Clozapine side effects
constipation, increased wt, hypersalivation
93
Clozapine monitoring
ANC >1500 to start tx if under <1000 stop
due to risk of neutropenia
94
ANC calculation
total WBC * (% neutrophils + % bands)/100
95
When to check ANC on Clozapine
at start
weekly for first 6 months
q2w btw 6-12 months
q4w after 12 months
96
What classifies as normal, mild, moderate, and severe neutropenia
normal: cont
1500
mild: increase monitoring
1000
moderate: interrupt
500
severe: disc (do not rechallenge)
97
What is benign ethnic neutropenia
ANC is lower than normal
in African Americans, Middle Eastern, non-caucasian
can start Clozapine if ANC >1000
if drop under <500 do not rechallenge
98
If patient on Clozapine gets myocarditis or cardiomyopathy what should you do
this happens in first 8 wk of therapy with peak at 3 wks of exposure
can be fatal, do not rechallenge
99
Clozapine DDI
CYP1A2
smoking
avoid with carbamazepine, chemo
avoid with meds that lower seizure threshold
respiratory depression with BZD
avoid with QTc prolongation drugs
100
What are the B52 drugs
diphenhydramine
haloperidol
lorazepam
DO NOT GIVE WITH BZD
used when acute agitation when verbal redirection and de-escalation are not successful
101
What to give in acute psychosis
haloperidol +/- diphrnhydramine + lorazepam
or ziprasisone IM or olanzapine IM
102
What are the NTs in depression
Serotonin, NE, Peptides, Growth Factors
(people make too much cortisol everyday, CRF)
103
The elevation of NE and serotonin levels may lead to what
change in mRNA
neurogenesis (neuronal stem cells proliferate)
104
What does brain-derived neurotrophic factor (BDNF) do
regulates neuronal differentiation and survival, synaptic signaling
activate TrkB receptor
antidepressants increase BDNF levels
105
TCA MOA
NE and serotonin reuptake inhibition
(antidepressants will block the transporters)
106
Amitriptyline MOA
5-HT and NE reuptake inhibition
block alpha 1 adrenergic and H1 receptors
107
Clomipramine MOA
5-HT and NE reuptake inhibition
anticholinergic activity
108
Desipramine MOA
NE reuptake inhibition
anticholinergic block of alpha 1 adrenergic and H1 receptors
109
Imipramine MOA
5-HT and NE reuptake inhibition
anticholinergic blockade of alpha 1 and H1 receptors
110
Nortriptyline MOA
5-HT and NE reuptake inhibition
block alpha 1 and H1 receptors
111
Side effect of central anti-histamine
sedation, weight gain
112
Side effect of anticholinergics
dry mouth, constipation, cycloplegia
113
Side effect of increase 5-HT and NE
increase appetite
114
Side effect of peripheral alpha 1 blockade
sedation, postural hypotension
115
Phenelzine and Tranylcypromine MOA
irreverisble or long acting inhibitors of MAO and are non selective (inhibit MAO-A and MAO-B)
116
Phenelzine and Tranylcypromine side effect
covalent bonding requires a 3-4 wk drug washout
117
SSRIs are used for what
anxiety disorders, bulimia, smoking withdrawal, OCD
(only prozac for depression)
118
MOA of SSRIs
block 5-HTT
desensitize 5-HT1A receptors
desensitize 5-HT1B receptors
119
Effects of stress and antidepressants on BDNF expression
increase cortisol, inhibits BDNF
SSRIs increase 5-HT and increase BDNF
120
Specific issues with depression
suicidality (SSRIs are better than TCA)
pregnancy (do not use paxil)
SSRI disc syndrome (mainly paxil least with fluoxetine)
121
Serotonin syndrome
confusion, agitation, hypomania
sweating, HTN, hyperthermia, nausea, diarrhea
tremor, rigidity, hyperreflexia, restlessness, myoclonus
DO not combine with TCA or MAO
122
Trazodone MOA
block central alpha 1, H1 and 5-HT2A receptors
123
Nefazodone MOA
like SSRIs action and 5-HT2 blockade
(serotonin antagonist and reuptake inhibitor SARI)
OFF market
124
Bupropion MOA
dopamine reuptake inhibitor
for ADHS and smoking cessation
125
Venlafaxine/Desvenlafaxine MOA
5-HT and NE reuptake inhibition
for depression, anxiety, panic disorder, OCD
126
Duloxetine MOA
5-HT and NE reuptake inhibition
for anxiety, diabetic neuropathy, chronic pain
127
Mirtazapine MOA
5-HT2 and 5-HT3 blockade
central alpha 2 adrenergic blockade, H1 antagonist, anticholinergic
128
St Johns Wort
ineffective in severe depression
129
Onset of depression
males peak >55 yo
feamales peak 35-45
130
What is depression
one or more major depressive episodes without a h/o mania or hypomania
131
Pathophysiology of depression
monoamine: depression caused by decreased brain levels of serotonin, dopamine, and NE
dysregulation: failure of homeostatic NT system regulation contributes or causes depressive symptoms
132
Clinical presentation and diagnosis of depression
5 or more symptoms present for 2 wks (SIG EP SAC)
sleep, interest, guilt
energy, psychomotor
suicide, appetite, concentration
133
Common presenting somatic complaints of depression
headache, malaise, vague ab or joint pain, disturbed sleep, sex or relationship problems, chronic fatigue
134
Response, Remission, Recovery, Relapse, Recurrence of depression
Response: 50% reduction in sx
Remission: absence of sx (back at baseline)
Recovery: no sx/relapse after remission
Relapse: return of sx w/in 6 months of remission
Recurrence: separate episode of depression (longer than 9-12 months)
135
Acute phase of depression
6-12 wk
induce remission
return to baseline level of functioning
reduce likelihood of relapse and recurrence
136
Continuation phase of depression
4-9 months
goal to eliminate residual sx or prevent relapse
137
Maintenance phase of depression
at least 12 months
goal to prevent recurrence
maintenance therapy: 3 or more episodes after recovering
138
What happens in the first 3 wks of depression tx
wk 1: improved sleep/appetite, decreased anxiety
wk 2: increased activity and libido, improved self-care
wk 3: improved mood, less helplessness, decreased suicidal thoughts
139
When should you follow up after starting depression meds
call in 7 days
meet in office at 2 weeks
140
The combination of what 2 things have the best results for patients
psychotherapy and medications
141
ECT
more effective than medications
controlled seizure
indicated when risk outweigh the benefits, h/o resistant depression, pt preference
needs anesthetics, neuromuscular blocking agents, and anticholinergics
142
CI of ECT
none (cautious of)
CHF, recent stroke, elevated intracranial pressure, aneurysms, signs of hemodynamic instability
143
VNS (vagal nerve stimulation)
for chronic depression lasting more than 2 yrs
depression not responding to 4 antidepressants +/- ECT
144
TMS (transcutaneous magnetic stimulation)
sends short magnetic field pulses to the prefrontal cortex
145
First line tx for depression
antidepressants first-line for mod-severe episode
acceptable first line: SSRI, SNRI, bupropion, mirtazapine
other: TCA, serotonin modulators, MAOI
146
Warnings and precautions with depression meds
handouts needed for all antidepressants, stimulants, some antipsychotics, hypnotics
need info on: prevent ADE, help decision-making regarding ADE, ensure adherence to directions
147
Box warnings on antidepressants
increase suicidal thoughts
no increased risk in adults over 24
decreased over age of 65
148
What is the best depression rating scale
HAM-D (gold standard)
<7 normal, 8-13 mild, 14-18 moderate, 19-22 severe, >23 very severe)
149
_____ are considered the first-line antidepressants due to their relative safety in overdose and tolerability
SSRIs
(approved for depression and some anxiety disorders)
150
Mechanism of SSRIs
inhibit the reuptake of serotonin increasing serotonin activity in the brain. Little to no effect on other neurotransmitters
151
ADE of SSRIs
headahce, akathisia, tremor, n/v/d (only lasts 1-2 wks)
dose-dependent: nausea, anxiety, fatigue, sex dysfunction
152
What happens during sertraline withdrawal
suicidal thoughts increase
irritability
nausea or vomiting
dizziness
nightmares
headaches
tingling sensations on the skin
153
Serotonin syndrome is assocaited with what antidepressants
any that increase serotonergic NT
could be fatal
154
Serotonin syndrome (shivers)
shivering
hyperflexia
increased temp
vital signs instability
encephalopathy
restlessness
sweating
155
How to treat mild then moderate to severe serotonin syndrome (resolves in 1-2 days)
mild: drug w/drawal (lorazepam for agitation)
mod-sev: block serotonin action (cyproheptadine, chlorpromazine)
Propranolol 1-3 mg IV q5m up to 0.1 mg/kg
156
Serotonin Syndrome: onset, course, neuromuscular findings, reflexes, pupils
onset: abrupt
course: rapid resolving
neuromuscular findings: myoclonus and tremor
reflexes: increased
pupils: mydriasis
(DDI or overdose)
157
Neuroleptic Malignant Syndrome: onset, course, neuromuscular findings, reflexes, pupils
onset: gradual
course: prolonged
neuromuscular findings: rigidity
reflexes: decreased
pupils: normal
(idiosyncratic, dopamine antagonists)
158
Which SSRIs cause QT prolongation
citalopram
escitalopram
159
Which SSRI is the most activating and which is the most sedating
activating (take in AM): fluoxetine
sedating (take in PM): paroxetine
160
Which SSRI is preferred in patients with cardiac risk
sertraline
161
SNRI MOA
inhibit the reuptake of BOTH 5-HT and NE increasing their activity in the brain
162
Duloxetine ADE
urinary difficulty/hesitancy
hepatotoxicity
163
Venlafaxine ADE
dose related increase in diastolic BP
>300: 13%
164
What is duloxetine CI in for CrCl and what is it also approved for
<30 ml/min
GAD, diabetic neuropathy, fibromyalgia, chronic musculoskeletal pain
165
Why do TCAs have a reduced use in depression practice
risk of overdose and availability of equally effective meds with fewer side effects
166
TCA MOA
inhibit reuptake of 5-HT and NE, also block H1, M1, and alpha 1 receptors
167
TCA ADE
dose related anticholinergic effects
cardiotoxicity with overdose
168
What TCAs have less side effects tertiary or secondary
secondary (desipramine and nortriptyline)
169
What is the most activating antidepressant
bupropion (ER preferred, doses must be 8 hours apart)
CI in eating disorders (bulimia, anorexia)
170
Bupropion MOA
inhibit reuptake of NE and dopamine
(no serotonergic effect)
171
Bupropion ADE
dose related seizures (CI in those pts)
minimal sex dysfunction
anxiety, wt loss, insomnia
172
Mirtazapine MOA
pre-synaptic alpha 2 adrenergic antagonist (increase release of NE and 5-HT)
173
Mirtazapine ADE
somnolence, dry mouth, increased appetite, wt gain
stimulates appetite in older pts (inc wt loss)
good for sleep promoting
174
Serotonin modulators MOA
exhibit mixed serotonergic effects
175
Serotonin modulators ADE
sedation (trazodone), dizziness, orthostatic hypotension, dry mouth, priapism
176
MAO-I MOA
inhibit enzyme monoamine oxidase which is responsible for breakdown of NE, DA< and 5-HT
177
MAO-I ADE
hypotension, sedation, insomnia, wt gain, sex dysfunction
178
MAO-I DDI
hypertensive crisis
serotonin syndrome
hypotension and sedation
must have 14 day wash out (5 wks for fluoxetine)
179
MAO-I drug food interaction
MAO-I + Tyramine = HTN crisis
No: aged cheddar, blue, swiss cheese, smoked foods_
180
What 3 drugs are potent CYP2D6 inhibitors
fluoxetine, paroxetine, bupropion
181
Alternative pharmacotherapy options
st. johns wart (mild depression)
omega-3 fatty acids
182
What agents added to antidepressants are augmentation therapies
antipsychotics
mood stabilizers
(aripiprazole, quetiapine)
183
Esketamine indication and MOA
treatment-resistant depression as monotherapy or in conjunction with oral antidepressant
NMDA receptor antagonist
184
Peds treatment for depression
fluoxetine preferred in pt under 18 yo
sx: boredom, anxiety, somatic complaints, impulsivity)
185
How are ped pt different than adults in their response to antidepressants
activation (increased energy)
more sensitive to withdrawal
indiction of mania (may develop bipolar)
186
Agent to use in pregnancy depression
cardiac defects, pulmonary HTN with paroxetine
all agents are relatively safe
187
What is the risk of untreated depression in pregnancy
poor prenatal care, wt gain, affects child development, increased risk of post-partum depression
188
What drug is used to treat post-partum depression
brexanolone
