Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Psychiatry > Revision > Flashcards

Revision Flashcards

1
Q

what is the difference between mania and hypomania

A

can generally function in hypomania

in mania cant usually function properly, can get psychotic symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

when does depression become treatment resistant

A

after 2 adequate trails of antidepressants with no response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how does ECT work

A

causes release of neurotransmitters - serotonin, dopamine, noradrenaline (why in can improve symptoms of parkinsons)

also causes growth in pathway between amygalada and prefrontal cortex (pathway involved in anxiety)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the drug of choice for generalised anxiety

A

SSRIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

is tremor a side effect of lithium

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is formulation

A

how the patient gor ill considering genetics, psychological factors, precipitating factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are predisposing factors

A

genetics, early childhood, medical conditions, FMHx, things that happened in life before the illness started

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are precipitating factors

A

what caused the illness to start (stressor or other events that are related to the current symptoms- trauma, how you coped during change, personality development)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are perpetuating factors

A

any conditions in the patient, family, community or larger system that exacerbate rather than solve the problem (relationship conflict, lack of education, financial stress, lack of employment)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what PD is DSH common in

A

emotionally unstable, bordline subtype

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

a MMSE below what suggests a cognitive problems

A

<24

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what does MMSE test for

A

cognitive function (confusion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what SE should you be cautious of with fluoxetine in young people

A

increased suicidal thoughts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is clozapine and when is it used

A

an atypical antipsychotic- should only be given for treatment resistant schizophrenia after 2 antipsychotics have been tried (haloperidol, Prochlorperazine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are the side effets of clozapine

A

Can cause agranulocytosis (lower white blood cells to a level where they cant fight infection), need to be monitored with regular FBCs. Can cause weight gain, diabetes, drowsiness, dizziness, hypersalivation, myocarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the opposite of psychomotor retardation

A

psychomotor agitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the inheritance of huntingtons

A

autosomal dominant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are the psychiatric symptoms of huntingtons disease

A 
depression 
compulsions 
suicidality 
aggression 
blunted affect (lack of affect/ no reactivity)
psychosis 
anxiety
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the cognitive symptoms of huntingons disease

A

decline in executive function
short and long term memory deficits
dementia- progressive decline in global cognition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is included in executive function

A

planning, abstract thinking, cognitive flexibility, being able to use rules, initiation of actions, social communication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are the motor symptoms of huntingtons disease

A 
choreiform movements 
rigidity 
writhing movements 
gait disturbance 
problems chewing/ swallowing/ speaking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is the genetics of huntingtons

A

CAG repeat encoding polyglutamine
genetic anticipation
toxic effect of glutamine on neuronal cells
40 repeats = 100% penetrance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

is genetic anticipation worse via female or male transmission

A

CAG repeats multiply by more during male transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is dementia

A

progressive decline in global cognitive function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is implicit memory

A

eg carrying out tasks that are well practised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what inheritance of alzheimers

A

multifactoral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what suggests a familial form of dementia

A

more relatives affected
relatives affected at earlier age
unusual or atypical features

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is the lifetime risk of dementia

A

10%

25% if first degree relative affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what percentage of UK population have BPAD

A

1%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is the inheritance of BPAD

A

multifactorial

higher in monozygotic twins than in dizygotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what delusions are common in psychotic depression

A

that you/ your organs are rotten

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what drug is the primary treatment for schizophrenia

A

atypical antipsychotics- risperidone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

when are atypical antipsychotics not used

A

lack of response, obesity/ FNHx of obesity - causes metabolic syndrome, parkinsons, heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is the primary mechanism of antipsychotics

A

block dopamine receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what are the two types of antipsychotic

A

typical and atypical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what symptoms are typical antipsychotics more likely to cause

A

extrapyramidal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what atypical antipsychotics are most likely to cause metabolic syndrome

A

olanzapine, risperidone, quetiapine, aripiprazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what atypical antipsychotic should you use if you are worried about metabolic syndrome

A

aripiprazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what is the treatment for schizophrenia

A

atypical antipsycotic, try two if first one has no effect

clozapine after trial of first if still no effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what is clozapined used for

A

3rd line for treatment resistant schizophrenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what do you need to monitor in clozapine

A

blood tests for agranulocytosis
cradiac function
bowel paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what is the pharmacological treatment for acute agitation in psychosis

A

benzodiazepine (-epams)

then typical antipsychotic (haloperidol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

name two typical antipsychotics

A

haloperidol

chlorpromazine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what are depot antipsychotics

A

IM injection with extended release- helps in compliance issues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what is the treatment or OCD

A

CBT, exposure therapy, SSRI (setraline), 3rd line= tricylic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what is the mechanism of action of benzodiazepines

A

GABA agonist (main inhbitory neurotransmitter)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what are the risks of benzos

A

tolerance and addiction - dont get tolerance for SEs (resp depression, loose gag reflex - aspiration)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what are the withdrawal symptoms from benodiazepines

A

irritability, insomnia, dizziness, panic, nausea, sweating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

which benzodiazepine has the ‘best’ half life

A

lorazepam- 12-20 hours, good for taking once a day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what are the treatments for GAD

A

1st line for GAD= CBT

2nd= SSRI (sertraline)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what is the treatment for panic disorder

A

exposure therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what can be done to reduce the risk of dependence of benzodiazepines

A

foe acute treatment only (1-2 weeks), slowly reduce dose

53
Q

are the negative/ positive symptoms of schizophrenia harder to treat

A

negative harder

54
Q

do people with psychosis have insight

A

generally no- can be restricted

55
Q

is hallucinations with insight psychosis

A

no

56
Q

what can you get command hallucinations in

A

depressive psychosis (2nd person, in context of mood)
mania with psychosis (grandiosity, irritability, flamboyant, elated mood)
schizophrenia (ideas of reference, 3rd person hallucinations, can go against mood that day)

57
Q

what conditions do you get visual hallucinations in

A

organic problems- delirium, injury, intoxication, trauma, autoimmune conditions

(very uncommon in schizophrenia)

58
Q

which conditions are tactile hallucinations more common in

A

organic conditions (injury, infection, trauma, intoxication)

59
Q

give a example of a pseudohallucination

A

hearing a voice originating from within your own head (a thought)

60
Q

what are the three first rank symptoms of schizophrenia

A

thought disorder
delusions of control/ passivity
3rd person auditory hallucinations

61
Q

what are the positive symptoms of schizophrenia

A

delusions of reference, thought disorders (insertion, broadcasting, withdrawal, echo), delusions that are persistently held, neologisms, misuse of vocabulary

62
Q

what are the negative symptoms of schizophrenia

A

apathy, blunting of affect, poverty of speech/ thought, catatonia (waxy flexibility, posturing, may echo your speech, may not eat/ speak, can become agitated very quickly)

63
Q

where is brocas area

A

posterior inferior frontal gyrus

64
Q

where is wernickes area

A

superior temporal gyrus

65
Q

what is wernickes dysphagia

A

receptive, fluent aphasia

speech comprehension is poor but actual speech fine, confabulation

66
Q

what type of dysphagia when brocas area damaged

A

expressive, non fluent dysphagia

understands but cant speak fluently

67
Q

what is brodmanns area 4

A

primary motor cortex

68
Q

what are the types of memory

A

short term- recall for seconds/ minutes without rehearsal

long term: episodic (things that happened), facts

69
Q

what part of brain puts memories from short term into long term

A

hippocampus

70
Q

where are long term memories stores

A

via permanent changes throughout cortex within individual neurones

71
Q

what is dementia

A

global decline in cognitive function, progressive, irreversible

72
Q

where is brain does alzheimers affect first

A

medial temporal lobe - nucleus basalis of meynert

73
Q

what is agnosia

A

difficulty in comprehending sensory information- (visual agnosia cant recognise objects)

74
Q

what is the most common cause of dementia

A

alzheimers

75
Q

what is prospagnosia

A

difficulty in recognising faces

76
Q

what is the pathology of alzheimers

A 
amyloid plaques (insoluble folded proteins) formed outwith cells 
Tau proteins are hyper-phosphorylation and create tangles
77
Q

what does the nucleus basalis of meynert do

A

attention/ arousal

78
Q

what does the medial septal nucleus do

A

learning and memory

79
Q

what happens to cholinergic projections in dementia

A

acetylcholine is very important for memory- gets reduces due to other changes in brain

80
Q

what drug is used to treat dementia

A

acetylcholinesterase inhibitors - boost cholinergic transmission:

  • slows progression
  • doesnt affect underlying disease process

(reduces uptake of acetylcholine so more in synapse)

81
Q

name three acetylcholinesterase inhibitors

A

donepezil
galatamine
rivastigmine

82
Q

what is memantine

A

NMDA receptor agonist

licensed to treat alzheimers

83
Q

what does NMDA respond to

A

glutamate (excitatory NT)

84
Q

what is seen on imaging in vascular dementia

A

mild white matter hyperintensities

periventricular then spread through white matter

85
Q

step wise cognitive decline= ?

A

vascular dementia

86
Q

what is the pathology of lewy body dementia

A

clumps of alpha synuclein around the brain
loss of dopamine producing neurones in the substantia nigra - causes parkinsonism
neuronal changes in the nucleus of basalis of meynert

87
Q

what is the treatment for lewy body dementia

A

cholinesterase inhibitors- rivastigmine

88
Q

what are the features of lewy body dementia

A 
visual spatial problems early
fluctuating cognition and consciousness 
visual hallucination 
autonomic dysfunction - hypotension 
REM sleep behaviour disorder
89
Q 
name the dementia:
55-65 age of onset 
loss of neurones 
gliosis
abnormal proteins in neurones 
atrophy in temporal and frontal lobes
A

frontotemporal

90
Q

what are the symptoms of frontotemporal dementia

A 
behavioural and personality changes 
progressive non fluent aphasia 
semantic dementia (language)
lack of interest in other people 
disinhibition
91
Q

what are the symptoms of wernickes encephalopathy

A

ophthalmoplegia
ataxia
confusion

visual and hearing impairment
reduced conscious level 
hypothermia 
lactic acidosis 
circulatory changes
92
Q

what causes wernickes encephalopathy

A

thiamine deficiency (thiamine needed for glucose metabolism- when deficient get mitochondrial injury and cell death)

  • alcoholism
  • malnutrition
  • hyperemesis graviderum
93
Q

what is used to treat thiamine deficiency

A

pabrinex

94
Q

atropy of mamillary bodies due to thiamine deficiency= ?

A

korsakofs syndrome

95
Q

what are features of korsakoffs

A

anterograde amnesia (cant form new memories)
confabulation
telescoping of events (think things happened more recently than then actually did)

96
Q

what are the types of alcohol relates brain damage

A 
wernickes 
korsakoffs
myelin sheath degredation 
neuroinflammation 
fall -/ subdural haematoma
97
Q

does the mental state exam include information form a 3rd party

A

no only from patient themselves

other info recorded in collateral history

98
Q

what is the bets predictor for suicide

A

hopelessness

99
Q

what conditions can you get loss of interest in food

A 
disordered eating (NOT AN or BN)
depression
100
Q

in younger people what weight meets criteria for ICD-10 for anorexia nervosa

A

weight to height of less than 85%

adults use BMI

101
Q

what is the difference between a learning difficulty and disability

A

difficulty= involves only one area of cognition

disability- affects global cognitive function and ability to learn

102
Q

what are the learning disability IQ parameters

A 
70-120 normal 
50-69 mild 
35-49 moderate
20-34 severe 
<20 profound
103
Q

what are non epileptic attack disorders highly associated with

A

childhood sexual abuse

104
Q

are patients conscious during non epileptic attack disorders

A

no, will have amnesia and are not aware what happened

105
Q

how are non epileptic attack disorders differnt from epileptic seziures

A

NEAD are functional disorders

tend to last longer, remain continent, lack injuries associated with epileptic attacks

106
Q

what is illness belief

A

functional conditions arise as patients view that a physical illness is more acceptable than a mental illness

107
Q

what does a deficit of vit B1 cause

A

wernickes encephalopathy

108
Q

what is the difference between lewey body and frontotemporal dementia

A

lewey body is a type of FTD

109
Q

what causes all FTD, lewey body and alzeheimers

A

overproduction and tangle of TAU protein which blocks transmiassion in brain
FTD and lewey body is in frontotemporal lobes
Alzheimers is in hippocampus

110
Q

what happens to cortisol in depression

A

is raised, loose negative feedback control, will fail to be suppressed by dexamethasone, increased expression in urine

111
Q

what does chronically raised cortisol in depression result in

A

reduced brain volume

112
Q

what is first line Tx for depression

A

SSRI

113
Q

what is the first line x for OCD

A

SSRI

psychotherapy also useful

114
Q

what is mild depression always treated with

A

CBT alone

115
Q

what is (almost) pathognomonic of schizphrenia

A

formal thought disorders

116
Q

is paranoid delusions of reference always caused by schizophrenia

A

no- is a psychotic symptom

117
Q

what is the first line treatment for schizophrenia

A

atypical antipsychotic

  • ripseridone (first line for most psychotic disorders)
  • olanzapine (risk of metabolic syndrome)
  • clozapine (only for treatment resistant)
118
Q

what is an obsession

A

a type of thought that is invasive, irrational (patient knows it doesnt make sense but can help thinking about it), is difficult to get rid of, is ego dystonic

119
Q

what is a mental compulsion

A

a thought which forces a patient to do an act to make it go away

120
Q

how long is a standard course of ECT

A

6-12 sessions

121
Q

what is mixed affective state

A

presentation of BPAD- when episodes of mania/ hypomania and depression are not discrete and can mix
eg someone with mania/ hypomania develops symptoms of low mood or preoccupation with physical health

122
Q

what are the features of PSTD

A

flashbacks, avoidance of where it happened, bad dreams, low mood
needs to have symptoms for at least 6 months to allow acute stress reaction and adjustment disorders (1-2 weeks) to resolve

123
Q

what is adult with incapacity act good for

A

emergency detainment- quicker than mental health act, don’t need psychiatrist, can treat

124
Q

can you treat under the mental health act

A

only under short term detention

125
Q

how long does an emergency detention last (MHA)

A

3 days

126
Q

how long does a short term detention last (MHA)

A

28 days (four weeks)

127
Q

how long does a compulsive treatment order last

A

6 months

128
Q

what is the treatment for emotionally unstable personality disorder

A

DBT

lasts 6-12 months

Psychiatry (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions