core conditions - 2 Flashcards

Question 1

Q

Definition of old age psych?

who to always ask about with patients with dementia?

Answer

A

anyone referred to mental health services who is over 65 years

always ask about CARERS and how they’re doing
- for every pt with dementia there is almost always at least one carer

Question 2

Q

CAUSES OF COGNITIVE IMPAIRMENT? 6

Answer

A

dementia
delerium
organic brain disease (eg CVA, encephalitis)
psychoactive substance misuse
psychosis
depression

Question 3

Q

Types of dementia:

common? 5
rarer? 3

Answer

A

COMMON

alzheimers
vascular
mixed alzheimers + vascular
lewy-body
fronto-temporal

RARE

parkinson’s-disease dementia
HIV dementia
huntington’s dementia

Question 4

Q

ICD-10 definition of dementia? (incl timescale)

Answer

A

Syndrome due to disease of the brain

progressive neurodegenerative condition

Consciousness not clouded

Disturbance of multiple higher cortical functions:

Memory & learning = Registration, storage and retrieval of new information
language
orientation
abstract thinking
problem solving
attention and concentration
Judgement and thinking,
Processing of information,
Emotional control,
Social behaviour or motivation.

Can affect reason and communication skills - Difficulty attending to more than one stimulus at a time

Diagnosis = must impair ADLs, usually >6 months.

—> Dementia is NEVER part of ‘normal aging’.

Question 5

Q

What are the 5 ‘A’s of dementia?

ie the 5 main groups of features / symptoms

Answer

A

1) aMNESIA

2) aPHASIA
an impairment of language, affecting the production or comprehension of speech and the ability to read or write

3) aGNOSIA
inability to interpret sensations and hence to recognize things, typically as a result of brain damage. eg “visual agnosia”

4) aPRAXIA
loss of the ability to execute or carry out skilled movements and gestures, despite having the desire and the physical ability to perform them

5) aSSOCIATED behaviours – Behavioural and psychological symptoms of dementia.

Question 6

Q

THREE types of assessment of cognition?

what are each used for?

what 2 things must you always ensure a patient has before assessing cognition?

Answer

A

INFORMAL ASSESSMENT
Crude description of cognitive function based on your history taking (e.g. “orientated to time, place and person”)

FORMAL SCREENING TEST
Tests with high sensitivity used to screen whether further investigation / referral is warranted (e.g. AMTS)

FORMAL DIAGNOSTIC TEST
Tests with high specificity used as tools for diagnosis (e.g. MoCA / ACE-III)

make sure pt has:

1) glasses
2) hearing aids

Question 7

Q

ASSESSMENT OF SUSPECTED DEMENTIA:

where normally referred to?
two histories to take? 2
bedside test to do? 1
bloods to do? 7
imaging? 1

Answer

A

referred to MEMORY CLINIC

histories:

from pt
collateral

cognitive test (eg ACE-3)

BLOODS:

FBC
U+E
LFT
folate
ferritin
B12
TFTs

(also cholesterol + lipids if suspect vascular?)

Imaging = norm CT (but can use MRI if need more detail or younger person)

Question 8

Q

Differentials for dementia in older people to rule out? 8

incl acronym

Answer

A

DEMENTIA (=acronym)

D = Drugs / Delirium
E = Emotions (ie depression)
M = Metabolic disorders
E = Eye + Ear impairment
N = Nutritional disorders
T = Tumours, Toxins, Trauma
I = Infection
A = Alcohol, Arteriosclerosis

nb around 25% of over 65yo have depression

Question 9

Q

BEHAVIOURAL + PSYCHOLOGICAL SYMPTOMS of DEMENTIA (BPSD):
- what dementias found in?

BEHAVIOURAL symptoms:

communication / towards others? 4
other emotional? 4
physical? 3

PSYCHOLOGICAL symptoms

mood? 2
psychotic symptoms? 2
other? 2

Answer

A

BPSDs are found in all types of dementia

BEHAVIOURAL

1) COMMUINCATION (/towards others)
- apathy
- repetitive questions / behaviour
- disinhibition / culturally inapprpriate behaviour
- swearing + aggression (incl physical)

2) OTHER EMOTIONAL
- agitation
- restlessness
- crying
- screaming

3) PHYSICAL
- Wandering
- Pacing
- Hoarding

PSYCHOLOGICAL

1) MOOD
- anxiety
- depression

2) PSYCHOTIC SYMPTOMS
- delusions
- hallucinations

3) OTHER
- misidentification
- insomnia

Question 10

Q

ASSESSMENT OF BPSD:

what charts to use? how work?
what treatable causes to look for? 6 (incl acronym)
exam to do?
hx to do?

Answer

A

Behavioural ABC charts

A = Antecedent
- What happened BEFORE the behaviour?

B = Behaviour
What was the BEHAVIOUR?

C = Consequence
What was the CONSEQUENCE?

look for causes = PINCH ME

P – Pain
IN – Infection
C – Constipation
H – Hydration
M – Medication
E – Environmental

mental state exam
collateral hx (and pt hx)

Question 11

Q

Management of BPSD:

1st line?
2nd line?
3rd line?

Answer

A

1st line = TREAT THE CAUSE

‘pinch me’ causes
refer to medics if necessary

2nd line = ENVIRNOMENTAL MODIFICATION

and practical management
eg education for family / staff

3rd line = MEDICATION

use as last resort
only RISPERIDONE is licensed for management of agitation
use lowest possible dose for shortest possible time
if alzheimers, Acetylcholinesterase inhibitors (e.g. Donepezil) can be useful

avoid A/Ps if possible as increased risk of:

parkinsonism
falls
stroke
cardiovascular event
death

Question 12

Q

ALZHEIMERS:

epidemiology?
static risk factors? 3
modifiable / acquired risk factors? 6 (2 medical, 4 social)

Answer

A

most common cause of dementia in ANY age group (about 50% - vascular is 20%)

STATIC RISKS

advancing age
trisomy 21
mutations of amyloid precursor protein (apoprotein E4)

MODIFIABLE /ACQUIRED

previous head injury
hypothyroidism
smoking
alcohol
obesity
social isolation

Question 13

Q

ALZHEIMERS:

- describe THREE main pathophysiological features?

Answer

A

1) Widespread CEREBRAL ATROPHY – esp. medial temporal lobe = cortex and hippocampus

2) AMYLOID PLAQUES + NEUROFIBRILLARY TANGLES (caused by aggregation of tau protein)
- Accumulation of these = reduction in transmission of information and eventual brain cell death.

3) DEFICIT of ACETYLCHOLINE -> Loss of neurons and synapses

Question 14

Q

ALZHEIMERS:

- normal presentation and course of illness?

Answer

A

–> Usually presents with MEMORY LOSS, with evidence of varying changes in:
planning
reasoning
speech
orientation
Steady, gradual decline is common in AD with faster deterioration following delirium or physical illness
memory impairment is usually the most prominent feature

Question 15

Q

ALZHEIMERS MANAGEMENT:

bio? 3 (in which order)
psych? 3
social? 3

Answer

A

BIO

1) treat reversible causes (eg thyroid, depression)
2) acetylcholinesterase inhibitors (eg DONEPEZIL)
3) NMDA receptor antagnoist (eg MEMANTINE)

nb Both acetylcholinesterase inhibitors and NMDA receptor antagonists work by increasing levels of acetylcholine

They don’t reverse the decline but can slow the rate of progression
also used to help with associated BPSDs

PSYCH

emotional support
cognitive stimulation / rehabilitation
treat co-morbid conditions (eg CBT for anxiety)

SOCIAL

carer support
occupational therapy
social care interventions

nb the psych + social is same for all dementias - is only the bio that changes depending on diagnosis

Question 16

Q

Factors associated with poorer prognosis in alzheimers? 7

Answer

A

Greater severity at presentation
Male
onset <65
Parietal lobe damage
Severe focal deficits
Prominent behavioural problems
Depression

Question 17

Q

VASCULAR DEMENTIA

cause?
presentation?
pattern of progression?
risk factors? 9

Answer

A

2nd most common cause of dementia over 65 years

Dementia due to infarction of the brain due to vascular disease.

Infarcts are usually small but cumulative in effect.

Deterioration is step wise, not continuous
onset more acute (often following stroke)
often motor/sensory deficits in VD (depends where the ‘mini-strokes’ are)
emotional + affective changes common

have vascular risk factors

Risk Factors:

PMHx of Cardiovascular disease
Smoking
Diabetes
HTN
Hyperlipidaemia
Polycythaemia
Coagulopathies, Sickle cell anaemia
Valvular disease
Rare familial onset in 40s.

Question 18

Q

VASCULAR DEMENTIA

bio management? 3
bio option if mixed diagnosis? 1
psych management? 3
social management? 3

Answer

A

BIO

LIFESTYLE changes (smoking cessation, exercise)
consider daily ASPIRIN / anticoagulants
consider meds to MODIFY RISK FACTORS (ie manage HTN, ^cholesterol + DM)
NMDA antagonists (eg memantine) can be used if there’s a mixed diagnosis (nb actyl-cholinesterase inhibitors are not used in VD)

PSYCH

emotional support
cognitive stimulation / rehabilitation
treat co-morbid conditions (eg CBT for anxiety)

SOCIAL

carer support
occupational therapy
social care interventions

nb the psych + social is same for all dementias - is only the bio that changes depending on diagnosis

Question 19

Q

FRONTOTEMPORAL DEMENTIA

norm age of onset?
typical presentation and progression?
three main features?

Answer

A

—> Uncommon but possibly under diagnosed.

45-64 years at presentation

higher proportion of those with dementia under 65 have FTD (AD still most common)
FHx components in 15%

Frontal and Temporal lobes = associated with personality, behaviour and language

Insidious onset and gradual progression

Memory and visuospatial ability spared

Presentation:

1) BEHAVIOUR-VARIANT
- changes in personality, behaviour, interpersonal and executive skills
- Early emotional blunting + apathy
- Early loss of insight

2) PROGRESSIVE NON-FLUENT APHASIA (PNFA)
- loss of language skills (ability to produce or understand language)

3) SEMANTIC DEMENTIA
- loss of semantic memory (knowledge)

Question 20

Q

FRONTOTEMPORAL DEMENTIA

investigations used for diagnosis? 2
bio management options? 1
what med NOT to use? 1
psych management? 3
social management? 3

Answer

A

FRONTAL LOBE TESTS (they do poorly)

MRI

younger pts so higher level of accuracy
shows fronto-temporal atrophy

BIO
- some evidence for use of SSRIs in improving disinhibition

DO NOT use acetylcholinesterase inhibitors

emphasis on psychosocial!

PSYCH

emotional support
cognitive stimulation / rehabilitation
treat co-morbid conditions (eg CBT for anxiety)

SOCIAL

carer support
occupational therapy
social care interventions

nb the psych + social is same for all dementias - is only the bio that changes depending on diagnosis

Question 21

Q

LEWY-BODY DEMENTIA

three core features?
additional features? 3

Answer

A

CORE FEATURES

1) FLUCTUATING presentation (cognition, attention + alertness)
2) spontaneous motor features of PARKINSONISM (up to 70%)
3) VISUAL HALLUCINATIONS (about 2/3rds)

OTHER FEATURES

frequent falls
nighttime agitation
depression (50%)

nb also a lot more sensitive to A/Ps (ie neuroleptic sensitivity) and so more likely to have EPSEs and neuroleptic malignant syndrome if given them

Question 22

Q

Pathophysiology of lewy-body dementia?

age of onset?
gender split?

Answer

A

Protein deposits develop in nerve cells (Neocortical Lewy body plaques)

Lewy Bodies are ‘alpha-synuclein cytoplasmic inclusions’ in the substantia Nigra, paralimbic and neocortical areas

onset 50-85 years
- F>M

Question 23

Q

How to differentiate dementia in Parkinson’s (DPD) vs Lewy Body (LBD)?

Answer

A

For DPD there must have been PD symptoms for at least a year before cognitive symptoms

If cognitive symptoms and Parkinson’s features start within a year of each other (either being present first) then it’s LBD

Question 24

Q

two types of imaging to do for lewy-body dementia + findings?

Answer

A

CT Head – shows generalised atrophy

SPECT - reduced striatal uptake of ligand for presynaptic dopamine transporter site.

Question 25

Q

MANAGEMENT of LEWY-BODY dementia:

BIO balance between?
other BIO option? 1
psych? 3
social? 3

Answer

A

fine balance between PARKINSONSIM and PSYCHOSIS

A/Ps increase parkinsonsim
L-Dopa increase psychosis

^so both could be used symptomatically
- but notoriously difficult to treat

Acetyl Cholinesterase Inhibitors can help e.g. RIVASTIGMINE

emphasis on psychosocial

PSYCH

emotional support
cognitive stimulation / rehabilitation
treat co-morbid conditions (eg CBT for anxiety)

SOCIAL

carer support
occupational therapy
social care interventions

nb the psych + social is same for all dementias - is only the bio that changes depending on diagnosis

Question 26

Q

In PMHx of pt with suspected dementia, what medical conditions should you specifically ask about that might impact memory? 8

(or be risk factors for some dementias)

Answer

A

MI
stroke / TIA
HTN
diabetes
thyroid disease
epilepsy
past traumatic head injury
mental health problems (particularly depression)

Question 27

Q

Aside from social services, what other services can you recommend for people with dementia?

Answer

A

Meals on wheels
Respite care
Day centers
Sitting services
Financial assessment
Home assessment

Question 28

Q

Two signs of increasing severity of BPSD / dementia which often lead to hospital admission

Answer

A

MIRROR SIGN
- pt start talking to themselves in the mirror

SUNDOWNING
- pt becomes aggresive around tea time (4-5:30), often settles as evening progresses

Question 29

Q

DELIRIUM

what is it?
describe the main different features? 7

incl diff types? 2

Answer

A

ACUTE CONFUSIONAL STATE

1) acute CONFUSION
- or acute-on-chronic
- important to know a baseline (get collateral)

2) impaired CONSCIOUSNESS
- may be transient, fluctuating GCS/AVPU
- reduced awareness of environment

3) impaired COGNITION
- impairment in short-term memory and attention
- assess with AMTS
- almost always disorientated to time + place

4) PERCEPTUAL disturbance
- eg hallucinations, norm visual or misinterpretation
- may ave thought disorder

5) MOOD disturbance
- eg agitation or aggression
- emotional lability

6) SLEEP-WAKE cycle disturbance
7) PSYCHOMOTOR abnormalities

course often FLUCTUATES throughout the day! - worse at night!

TYPES

hyperactive
hypoactive (often undiagnosed)

Question 30

Q

which pts are vulnerable to delirium:

age? 2
reason for being in hospital? 2
comorbidities? 3
iatrogenic? 1

Answer

A

AGE

elderly (20-30%)
very young

REASON IN HOSP

post-op pts
burns victims

COMORBIDITIES

dementia
blind or deaf
alcohol dependence

IATROGENIC
- many medications increase risk

basically anything that reduces your cognitive ‘reserves’

Question 31

Q

common groups of causes of delirium? 6

give examples of each

Answer

A

INFECTIONS
= UTI
= chest infection
= wound abscess / cellulitis
- meningitis / encephalitis
- endocarditis

INTRA-CRANIAL
= stroke / TIA / bleed
= traumatic head injury
- raised ICP (incl tumour)

METABOLIC
= electrolyte disturbances (esp low sodium + low calcium)
= liver failure / hepatic encephalopathy
= uraemia / kidney failure
- anaemia
- heart failure
- hypothermia

ENDOCRINE
= hypoglycaemia
= thyroid (hypo/hyper)
- pituatory disease
- parathyroid
- adrenal (cushings/addisons)
- porphyria

MEDICATIONS / SUBSTANCES
= alcohol intoxication / withdrawal (wernickes - thiamine)
= illegal/psychoactive drugs
= carbon monoxide posioning
(see other flashcard for prescribed drugs that can cause/worsen)

OTHER

terminal medical condition
severe asthma (or other lung/heart problems)

nb may be a combination of things

Question 32

Q

Which classes of medication increase risk of delirium:

psych / neuroactive? 6
cardiovascular? 4
pain / inflammation? 3
other? 5

three biggest culprits out of this list? 3

independent risk factor relating to medication?

Answer

A

nb this excludes illegal / non prescribed (eg alcohol, carbon monoxide, legal highs etc)

PSYCH / NEUROACTVE
= benzos (use + withdrawal)
- antipsychotics
- lithium
- anticonvulsants
- antiparkinsonian
- antidepressants (esp TCAs)

CARDIOVASCULAR

antihypertensives
diuretics
digoxin
betablockers

PAIN / INFLAM
= opioids
- NSAIDs
- steroids

OTHER
= anticholinergics (incl TCAs)
- insulin
- salicylates
- ketamine (used in anaesthetics)
- old/sedating antihistamines

POLYPHARMACY = independent risk factor (ie regardless of which meds on, if on a lot then increased risk)

nb many drugs have an anti-cholinergic effect so be careful when prescribing

Question 33

Q

DELIRIUM:

what to establish in history? 3
exams to do? 2
what to do before do any investigations? 1
investigations to consider? (5 bedside, 2 bloods, 2 imaging)

Answer

A

establish timeline (Qs to identify cause)
recent interventions
baseline cognition (from collateral)
full physical (to look for signs of infection etc)
MSE

REVIEW DRUG CHART (before do any investigations)

MSU (urine dip useless in elderly)
urine drug screen (if suspect)
blood glucose
blood gas
ECG (can show metabolic signs)
bloods (norm ones +/- bone profile + cultures)
drug levels (eg if on digoxin/lithium etc)
CXR (if any chest signs)
CT head (if any neurology)

Question 34

Q

DELIRIUM:

management? 3
what additional nursing measures can help manage? 7

Answer

A

treat underlying cause
manage other comorbidities
consider stopping any meds that may be contributing (eg benzos)
Nurse him in a SIDE ROOM (with fam member if poss)
Ensure GLASSES and HEARING AIDS are within reach and are working
KEEP pt ORIENTATED to time place and person (give him a clock and talk to him regularly)
COMMUNICATE clearly and frequently
Avoid INFECTION or CONSTIPATION
Control PAIN
ensure HYDRATION + NUTRITION

nb DOLS sometimes appropriate

Question 35

Q

prognosis of delirium?

Answer

A

Gradual reduction of symptoms with effective treatment of cause

Symptom resolution may be much slower in elderly

Often patchy amnesia following recovery

High mortality

May be marker for subsequent development of dementia

Question 36

Q

definition of organic mental disorders?

- priority of management?

Answer

A

Psychological or behavioral abnormalities associated with a dysfunction of the brain. History and physical examination or laboratory tests demonstrate the presence of a specific organic factor judged to be etiologically related to the abnormal mental state and loss of previously acquired functional abilities

nb delirium and dementias are examples, as are space occupying lesions, drug-induced psychosis etc

MANAGEMENT:

1) treat underlying cause
2) treat symptoms (eg antipsychotics)

Question 37

Q

Specific Qs to ask about a person’s substance use? (ie in addition to norm full psych hx)

Answer

A

1) WHICH drugs used (ask about each one directly: alcohol, cannabis, heroin, benzo, prescription etc)
2) AMOUNT and FREQUENCY used - bags, cost, ask if they think it’s strong or weak
3) ROUTE of use (IV, snort, smoke)

4) DURATION
- of most recent episode
- also when start intially
- try and establish a timeline

5) when LAST USED and how much
6) WHO do they use with?
7) WHY do they use
8) how FUNDING use
9) any TREATMENT or periods of REMISSION? - what happened?
10) any evidence of DEPENDENCE? (see other flashcard)

also in PMHx ask about any physical complications: groin abscess, endocarditis, BBV

and do very thorough risk assessment!!! - and FORENSIC HX

Question 38

Q

What specific things to assess in risk assessment of someone with substance misuse? 7

Answer

A

overdose
medical complications
psychosis from cocaine/cannabis
DSH/suicide
financial overspending
risk to others (violence, neglect to dependents)
risk from others (relationships, drug dealers)

Question 39

Q

What groups of things looking for in physical exam of patients with substance misuse?

Answer

A

signs of acute INTOXICATION / WITHDRAWAL
COMPLICATIONS (DVT, cellulitis, groin abscess, femoral aneurysm, liver disease)
COMORBIDITIES (liver disease, COPD, BBV)
signs of SELF-NEGLECT / malnutrition

Question 40

Q

baseline investigations for someone presenting with substance misuse:

bedside? 2
bloods? 4

Answer

A

URINE DRUG SCREEN (even if they admit, they may miss some out)
ECG (esp for cocaine but, eg need one before start methadone as can lengthen QTc)

BLOODS

FBC
U+E
LFT
BBV screen

(blood cultures if symptomatic)

nb if head injury, have lower threshold for CT scan as alcohol etc increases risk of bleeds

Question 41

Q

ICD-10 diagnosis of substance dependence:

physical? 3
psychological? 2
social? 2
time period!

additional feature commonly seen (but not needed for diagnosis)? 1

Answer

A

PHYSICAL

experience WITHDRAWAL symptoms if don’t use
use of substance RELIEVES withdrawal symptoms
TOLERANCE (need to escalate dose in order to achieve same effect)

PSYCH

CRAVING: intense desire to use
DIFFICULTY CONTROLLING onset, termination + amount used

SOCIAL

SALIENCE (neglecting alternate forms of leisure or pleasure in life)
persistent use despite clear evidence of HARM (physical, psych and social)

need AT LEAST 3 features in past 12 months!

NARROWING of REPERTOIRE of substance use is also commonly seen but not essential for diagnosis

nb there is a broader, less-severe condition of ‘harmful use of substances’ which covers majority of problem drinking and drug use = ‘a pattern of psychactive substance use causing damage to health - physical +/or psychological’

Question 42

Q

6 stages of change model?

- what type of management of substance misue at eah stage?

Answer

A

STAGES OF CHANGE MODEL

1) PRE-CONTEMPLATION
- no intention on changing behaviour
= HARM REDUCTION techniques (incl education about risks + how to reduce)

2) CONTEMPLATION
- aware a problem exists but with no commitment to action
= use MOTIVATIONAL INTERVIEWING

3) PREPERATION
- intent on taking action to address the problem
= use MI and get on TREATMENT and SUPPORT

4) ACTION
- active modification of behaviour
= TREATMENT and SUPPORT

5) MAINTENANCE
- sustaine change, new behaviours replaces old
= continued SUPPORT + may still be on TREATMENT

6) RELAPSE
- fall back into previous pattern of behaviour
= SUPPORT + MI

people do relapse frequently - but never give up on them!! - every time may be the time they quit for good!

upward spiral - learn from each relapse

Question 43

Q

HARM REDUCTION:

action/advice to prevent deaths? 5
action/advice to prevent BBV transmission? 4
places to refer to? 3

Answer

A

PREVENT DEATHS

not injecting or injecting more safely (teach safe injecting techniques - eg anatomy of groin)
not using drugs alone
call an ambulance if necessary
dispense naloxone pens
education on reducing amount taken after intervals where tolerance is lost (eg after release from prison)

PREVENT BBV

not sharing needles - needle exchange programmes
safer sex (condoms)
give Heb A + B vaccine
BBV screening, incl hep C

REFER WHEN APPROPRIATE

specialist drug services
voluntary sector services
infectious disease services

Question 44

Q

Treatment approaches in substance misuse disorder:
- BIO options for ALCOHOL? 4

(psych + social on another flashcard)

Answer

A

BIO for ALCOHOL

1) chlordiazapoxide (acute detox)
2) thiamine (prevent wernicke’s)
3) ACAMPROSATE (reduces cravings + pleasurable effect)
4) DISULFARIM (makes you throw up, used less)

nb can also use naltrexone (see bio management of opioids flashcard) with alcohol

ALSO treat any other comrbidities - eg depression

Question 45

Q

Treatment approaches in substance misuse disorder:
- BIO options for OPIOIDS? 3

(psych + social on another flashcard)

Answer

A

METHADONE
- easier to start in hospital OR use if do need to use opioids in addition

BUPRENORPHINE

starting to be used more frequently
partially agonist, at high quantities have a blockade effect - so if they try to use heropin on top of it then don’t get a high
but people have to be withdrawal in order to start

NALTREXONE

opioid blocker
so can use so they don’t get high when they take opioids
can also use with alcohol

^nb different to naloxone!!!

ALSO treat any other comrbidities - eg depression

Question 46

Q

Treatment options in substance misuse:

psych? 3
social? 3

(bio on another flashcard)

Answer

A

PSYCH

motivational interviewing
CBT
group therapy

SOCIAL

12 steps programme
alcoholics / narcotics anonymous
rehab programme

also sort out finances, employment, housing etc

Question 47

Q

Main classes of antidepressants? 5

give examples of each

Answer

A

SSRIs

sertraline (good for co-morbid anxiety - norm 1st line)
fluoxetine (long half life so good if poor compliance, only one for <18yo)
citalopram (can lengthen QTc)
paroxetine (discontinuation problems)

SNRIs

duloXetine
venlafaXine

TCAs

amitryptilline
clomIPRAMINE
imIPRAMINE

NaSSA
- mirtazapine

MAOIs

Phenelzine
Isocarboxazid
Moclobemide

“mirtazapine, like NASA, can send people to sleep”

Question 48

Q

SSRIs

examples? 4
mechanism of action?

Answer

A

SERTRALINE (good for co-morbid anxiety - norm 1st line)
FLUOXETINE (long half life so good if poor compliance, only one for <18yo)
CITALOPRAM (can lengthen QTc)
PAROXETINE (discontinuation problems)

inhibit SEROTONIN reuptake -> increase in conc

Question 49

Q

SSRIs

examples? 4
clinical indications? 3

Answer

A

SERTRALINE (good for co-morbid anxiety - norm 1st line)
FLUOXETINE (long half life so good if poor compliance, only one for <18yo)
CITALOPRAM (can lengthen QTc)
PAROXETINE (discontinuation problems)

1) 1st line for moderate-severe DEPRESSION (mild depression, if psych therapies insufficient)
2) ANXIETY disorders (GAD, OCD, PTSD)
3) BULIMIA NERVOSA (fluoxetine only)

Question 50

Q

SSRIs

examples? 4
common side effects?
rare but serious side effects?
safe in pregnancy?

Answer

A

SERTRALINE (good for co-morbid anxiety - norm 1st line)
FLUOXETINE (long half life so good if poor compliance, only one for <18yo)
CITALOPRAM (can lengthen QTc)
PAROXETINE (discontinuation problems)

COMMON

agitation / anxiety
sexual dysfunction

= nausea
= diarrhoea

headaches
dizziness
insomnia

RARE

hyponatraemia (esp in elderly)
platelet dysfunction (GI bleeds - PPI in elderly)
initital increase in suicide risk (first 1-4months) - esp in <30yo

also warn about discontinuation syndrome with abrupt withdrawal

PREGNANCY
1st trimester = risk of cardiac abnormalities
3rd Trimester = perinatal problems e.g. RDS, irritability, feeding problems.
RISK/BENEFIT - AVOID if POSS

Question 51

Q

symptoms of discontinuation syndrome of acute withdrawal from SSRIs + SNRIs? 6

Answer

A

dizziness
headaches
gait instability
diarrhoea
abdo pain
fatigue

Question 52

Q

SNRIs

examples? 2
mechanism of action?

Answer

A

duloXetine (good if comorbid pain or incontinence)
venlafaXine

inhibit reuptake or serotonin AND noradrenaline

Question 53

Q

SNRIs

examples? 2
clinical indications?

Answer

A

duloXetine (good if comorbid pain or incontinence)
venlafaXine

1) 2nd line MAJOR DEPRESSION, when ssris are ineffective/not tolerated

2) GAD
- venlafaxine only

3) MENOPAUSAL symptoms
- venlafaxine only

Question 54

Q

SNRIs

examples? 2
common side effects? 8
rare but serious? 4
monitoring required? 1

Answer

A

duloXetine (good if comorbid pain or incontinence)
venlafaXine

COMMON

= nausea
- constipation

dizziness
sedation
insomnia

= dry mouth
- headache

sexual dysfunction

RARE

can increase BP
QTc prolongation -> arrythmias
suicidal ideation
hyponatraemia (esp elderly)

nb tend to get more side effects with SNRIs than with SSRIs (as targetting >1 receptor)

MONITORING
- monitor BP in pts on high doses

Question 55

Q

TRICYCLIC ANTIDEPRESSANTS

examples?
mechanism of action?

Answer

A

amitryptilline
clomIPRAMINE
imIPRAMINE

INHIBIT REUPTAKE of sertraline and noradrenaline.

also BLOCK several other neurotransmitter receptors e.g muscarinic, alpha1 and H1.

Question 56

Q

TRICYCLIC ANTIDEPRESSANTS

examples?
clinical indications? 4

Answer

A

amitryptilline
clomIPRAMINE
imIPRAMINE

1) 2nd line moderate-severe DEPRESSION
2) neuropathic PAIN (not licensed)
3) prophylaxis of tension/migraine HEADACHES (low dose amitryptilline)

4) OCD
- clomipramine only

Question 57

Q

TRICYCLIC ANTIDEPRESSANTS
- examples?

SIDE EFFECTS:

anticholinergic?
histamine + A1/2?
cardiac? 2
other? 2
monitoring required? 1
who to avoid prescribing for? 1

Answer

A

amitryptilline
clomIPRAMINE
imIPRAMINE

ANTICHOLINERGIC

blurred vision
dry mouth
constipation
urinary retention

HISTAMINE + A1/2

sedation
postural hypotension

CARDIAC

tachycardia
arrythmias + ECG changes

OTHER

weight gain
excessive sweating (esp at night)

nb can worsen glaucoma

monitoring = ECG

avoid prescribing if high chance of OD - AS VERY DANGEROUS!!!

Question 58

Q

Symptoms / signs of TCA overdose:

CNS? 2
CARDIOVASCULAR? 3
ANTICHOLINERGIC? 6
ECG findings?
management? 2

Answer

A

CNS

sedation + coma (tend to precede cardiotoxicity)
seizures

CARDIOVASCULAR

sinus TACHY (anti-cholin)
HYPOtension (mild hypertesion initially)
broad complex tachy-dysrhythmias -> broad complex brady pre-arrest

ANTICHOLIBNERGIC

agitation / restlessness / delirium
dry, warm flushed skin
mydriasis (pupil dilation)
myoclonic jerks
urinary retention
ileus

ECG

normal initially
TACHY (brady is pre-terminal)
widening QRS
dysrhythmias
also RBBB

MANAGEMENT

supportive (incl activated charcoal if early)
SODIUM BICARB

(nb don’t get too hung up on learn specifc - know cardiac + neuro effects + management)

Question 59

Q

NaSSA

examples? 1
mechanism of action?

Answer

A

mirtazepine = only one used

Potent agonist at several serotonin receptor subtypes, competitive agonist of H1 α1 and α2

Question 60

Q

NaSSA

examples? 1
clinical indications?

Answer

A

mirtazepine = only one used

1) DEPRESSION
2) ANXIETY (incl OCD)

Question 61

Q

NaSSA

examples? 1
common side effects? 5
rare side effects? 4

Answer

A

mirtazepine = only one used

COMMON

= drowsiness
= increased appetite + weight

dry mouth
headaches
constipation

RARE

hyponatraemia (although rarer than in other anti-Ds)
pancreatitis
agitation
suicidal ideation

used for people with insomnia / appetite loss to help!

“mirtazapine, like NASA, can send people to sleep”

Question 62

Q

MAOIs

examples? 3
mechanism of action?
indications? 2
side effects? (5 mild, 1 serious)

Answer

A

Phenelzine
Isocarboxazid
Moclobemide

RARELY USED now dt dietary restrictions!

Inactivate enzymes (monoamine oxidase) that oxidise noradrenaline, serotonin, dopamine, tyramine and other amines.

1) refractory depression
2) refractory anxiety

MILD SEs

dry mouth
postural hypotension
headaches
confusion
constipation

SERIOUS SE = HYPERTENSIVE CRISIS

food containing tyramine causes accumulation of tyramine which cannot be broken down -> hypertensive crisis
Avoid all cheeses, red wine, beer, smoked fish, Marmite, liver, salami, pepperoni amongst others. - Also interact with local anaesthetics, some opiates, cocaine

Question 63

Q

SEROTONIN SYNDROME:

aside from anti-depressants, what other substances can lead to? 3
symptoms? 9
management? 2

Answer

A

combo of ANTI-DEPRESSANTS, plus:

st john’s wart
ecstasy (aka MDMA)
cocaine

SYMPTOMS - rapid onset!

restlessness
fever + diaphoresis
tremor
myoclonus
increased reflexes
mydriasis (dilation of pupils)
confusion
fits
arrythmias

MANAGEMENT

stop anti-depressants
supportive (incl intubation if necessary)

nb most mild + better within 24hrs

Question 64

Q

How to differentiate between serotonin syndrome + neuroleptic malignant syndrome:

causative agents?
speed of onset?
neuromuscular findings?
reflexes?
pupils?

Answer

A

CAUSES

combo of serotonin agents (incl cocaine, ecstasy) in serotonin syndrome
A/Ps in NMS

ONSET + COURSE

SS = abrupt (6 hours of taking) + quick to resolbe
NMS = gradual onset + prolonged recovery

NEUROMUSCULAR

SS = myoclonus + tremour
NMS = diffuse rigidity (w CK risk)

REFLEXES

SS = increased
NMS = decreased

PUPILS

SS = dilated
NMS = normal

Answer 65

A

Both are dopamine D2-receptor blockers

but also act on histamine + serotonin receptors (varies with drug)
FGAs (typical) are non-selective
SGAs (atypical) are more selective

MESOCORTICAL pathway
= cognition + executive function
- low levels cause negative symptoms (A/Ps may worsen these)

MESOLIMBIC pathway
= motivation, emotion, reward
- high levels cause positive symptoms (A/Ps work here!)

NIGROSTRIATAL pathway
= stimulation of movement
- (A/Ps can cause EPSEs here)

TUBERINFUNDIBULAR pathway
= DA functions as prolactin inhibitory hormone (PIH)
- (A/Ps can cause high prolactin levels)

Answer 66

A

ORAL (1st line - least restrictive)
IM (fast-acting, eg for quick sedation)
DEPO* 1-3months (long acting IM, for poor compliance - need oral until stable plasma levels)

FGA

haloperidOL*
fluphenaZINE*
flupentixOL*
zuclopenthixOL*
chlorpromaZINE
pimoZIDE

SGA
- olanzaPINE*
- risperiDONE*
- quetiaPINE
- aripipraZOLE
= clozaPINE

= available as depo

“FGA are OLd and still reading ZINEs”

“SGA are what people PINE over now”

Answer 67

A

INDICATIONS

1) acute psychosis
2) schizophrenia

3) schizoaffective disorder
4) mania

5) sedation
6) anti-emetic (eg haloperidol for palliative care)

1) sedation = within hours
2) SEs = hours-days
3) anti-psychotic = days-weeks

FGA

haloperidOL*
fluphenaZINE*
flupentixOL*
zuclopenthixOL*
chlorpromaZINE
pimoZIDE

SGA
- olanzaPINE*
- risperiDONE*
- quetiaPINE
- aripipraZOLE
= clozaPINE

= available as depo

“FGA are OLd and still reading ZINEs”

“SGA are what people PINE over now”

Answer 68

A

FGA ONLY

increased prolactin
galactorrhoea + amenorrhoea
EPSEs

BOTH

long QTc
lower seizure threshold
sedation
anti-cholinergic SEs
apathy
weight gain

SGA ONLY
- metabolic syndrome (olanzapine / clozapine)

(olanzapine not used in pts w diabetes or obesity)

CLOZAPINE

constipation (kills more than agranulocytosis)
neutropenia (4%)
agranulcytosis (1%)
myocarditis
reduced seizure threshold

RARE, BUT SERIOUS
= neuroleptic malignant syndrome

nb can also get postural hypotension + impotence in men!

ANOTHER WAY OF CATEGORISING SE’s:

ANTI-DOPAMINERGIC

EPSEs
Raised prolactin (galactorrhoea and amenorrhoea in women. Sexual dysfunction, osteoporosis)

ANTI-ADRENERGIC

Sedation
Postural hypotension
Inability to ejaculate

ANTI-CHOLINERGIC

Dry mouth
Constipation
Blurred vision

ANTI-HISTAMINIC

Sedation
Weight gain

OTHER

Cardiac conduction defects– prolongation of QT interval, rarely Torsades de Pointes and sudden death
Diabetes and metabolic syndrome – weight gain, raised triglycerides, raised fasting glucose.

RARE – Neuroleptic malignant syndrome.

Answer 69

A

ADAPT

Acute Dystonia
Akasthesia
Parkinsonism
Tardive dyskinesia

increasing time of onset as you go down list (days - years)

ACUTE DYSTONIA
= torticolis (spasms)
= grimacing
= oculogyric crisis
- acute onset
=== anti-cholinergics (eg procyclidine)

AKASTHESIA
= feeling of physical restlessness
=== procyclidine, propranolol, benzos, dose change

PARKINSONISM
= expressionless face, rigidity, tremor
=== anti-cholinergics (eg procyclidine)

TARDIVE DYSKINESIA
- aka choreoathetoid movements
= involuntary chewing, sucking, grimacing, eye blinking
- onset a few years after start medication
=== dose reduce or change drug, hard to treat (anti-cholinergics make it worse)

Answer 70

A

blurred vision
dry mouth
constipation
urinary retention

Answer 71

A

RARE SE of A/Ps

norm after first starting A/Ps but can be insidious onset a few months after initiation / dose change

MEDICAL EMERGENCY

variable BP
tachycardia
high fever
sweating
altered mental state
rigid muscles / hypertonicity

BLOODS

raised CK
raised WCC

MANAGEMENT

stop offending agent
supportive treatment (may need ITU)

mortality = 10%

Answer 72

A

‘atypical atypical’

better efficacy than other A/Ps

can only use if:

TWO A/Ps tried for at least 6 weeks
at least one being a SGA
agranulocytosis (1%)
leucopenia (5%)
constipation -> paralytic ileus (kills most)
myocarditis
reduced seizure threshold

registered with national monitoring service
- FBC weekly initially, then fortnightly, then monthly

also loads of obs + ECG when titrating up

if stop for >48 hours then have to retitrate dose up again

Answer 73

A

drugs affecting DOPAMINE

L-dopa (will cancel out effect)
metoclopramide (will increase EPSEs)

drugs affecting CPY450 PATHWAY
- esp antiepileptics + abx (eg clarithromycin)

drugs that PROLONG QTc

Answer 74

A

Large studies have found the efficacy of all antipsychotics to be equal (except Clozapine), so choose based on other factors

TO TAKE INTO ACCOUNT

prev A/P tried
age, gender
co-morbidities
preference wrt formulation
pt views
carer views

norm start an ORAL SGA at lowest effective dose

try for 2-3 weeks

if SE or poor response, change
if some effect, continue for 4 wks

compliance is really important - risk of relapse if stop in first 6 months is huge! (concordance is 25-75% day 10 post-discharge)

offer healthy eating + physical exercise programme to reduce risk of metabolic syndrome

continue for 1-2 years, monitor + stop gradually (if multiple relapses. then may be life-long)

Answer 75

A

OBS

BP
HR

BEDSIDE

BMI
ECG

BLOODS

FBC
U+E
LFT
TFT
Prolactin
HbA1c
Lipids

basically do the same for monitoring??? not sure of frequency though… *** - think most stuff is annually and when dose change etc

FBC weekly then less frequently for CLOZAPINE

Answer 76

A

lithium
sodium valproate
carbamazepine
lamotrigine

can use A/Ps too if psychotic symptoms / severe mania

nb can use anti-depressants for bipolar to augment but rarely used as can trigger mania

other indications

1) schizoaffective disorder
2) severe unipolar depression
3) prevention of aggression in pts with learning disability

(also obvs anti-epileptics can be used for seizures etc too!)

Answer 77

A

LITHIUM

reduces excitatory neurotransmitters (ie dopamine + glutamate)
increases inhibitory neurotransmitters (ie GABA)

SODIUM VALPROATE

inhibits neuronal Na+ channels + increases GABA
reduces neuronal excitability -> reduces electrical ‘kindling’ in the temporal lobe + limbic system

CARBAMAZEPINE
- inhibit neuronal Na+ channels -> stabilises resting membrane potential -> reduces electrical ‘kindling’ in the temporal lobe + limbic system

LAMOTRIGINE
- inhibit neuronal Na+ channels -> stabilises resting membrane potential -> reduces electrical ‘kindling’ in the temporal lobe + limbic system

Answer 78

A

EARLY

dry mouth
metallic taste
polydipsia
polyuria
FINE tremor
nausea / GI upset
fatigue / drowsiness

LATE

neuro effects (ataxia, dysarthria)
nephrogenic diabetes insipidus (monitor kidneys)
hypothyroidism - 20% (TFTs)
hypercalcaemia (Ca2+)
arrythmias (ECG)
weight gain (BMI)

^monitor these every 6 months - a year

monitor lithium levels a week after initiation + dose changes - once steady state - monitor every 3 month (level taken 12 hours post dose)

is also teratogenic - epstein’s anomaly more common (although not as much as valproate)

Answer 79

A

SODIUM VALPROATE

GI upset
neuro effects (tremor, ataxia, behavioural disturbances
weight gain (monitor BMI)
thrombocytopenia (monitor FBCs)
transient increase in liver enzymes (monitor LFTs)

= very teratogenic!!!

CARBAMAZEPINE

GI upset
Neuro effects (dizziness and ataxia)
Hypersensitivity → rash
Oedema
Hyponatraemia (U+Es)

LAMOTRIGINE

GI upset
Neuro effects (tremor, dizziness, insomnia, aggression)
Dry mouth
Skin rash → SJS (rare)

“all mood stabilisers have GI upset + some form of neuro effects”

Answer 80

A

diuretics
NSAIDs
ACEi
ARBs
metronidazole

can all INCREASE lithium levels

(nb other interactions too)
- basically anything that affects renal excretion -> build up of lithium

be aware of CYP450 drugs with anti-epileptics as may induce, inhibit +/or be affected by this! - ie they interact with a lot of meds!!!

Answer 81

A

therapeutic = 0.5-1

toxicity >1.5 (but treat symptoms)

EARLY

blurred vision
dysarthria (slurred speech)
COARSE tremor
ataxia
anorexia
nausea + vomiting
diarrhoea

LATE

hyper-reflexia
confusion / delirium
renal failure
convulsions
coma -> death

nb fine tremor is normal SE of lithium, coarse tremor is a sign of toxicity!!

Answer 82

A

therapeutic = 0.5-1

toxicity >1.5 (but treat symptoms)

COMMON CAUSES

UTI
renal failure
dehydration
drugs (NSAIDs, diuretics)

(basically anything that reduces renal functioning can cause!)

MANAGEMENT

stop lithium
treat cause (eg abx for UTI)
fluids
dialysis (if bad)

Answer 83

A

BEDSIDE

BMI
ECG

BLOODS

U+E
lithium levels
TFTs
Ca2+

do every 3 months??

nb must stay on the same drug BRAND of lithium - concentrations vary between brands

Answer 84

A

dangerous in OD = lithium

(although tbh all are but lithium has a very narrow therapeutic range)

best for depressive phase of BPD = lamotrigine

avoided in WCBA = sodium valproate

Answer 85

A

Benzodiazepines facilitate and binding of neurotransmitter GABA to the GABAA receptor, resulting in sedative, hypnotic (sleep-inducing), anxiolytic (anti-anxiety) and anticonvulsive effects

oral
sublingual
rectally
IM
IV

SHORT ACTING
= half life < 10hrs
- midazolam
- loprazolam
- lorazepam
- lormetazepam
- temazepam

LONG ACTING
= half life > 15hrs
- diazepam
- chlordiazepoxide
- nitrazepam
- flurazepam
- alprazolam
- clobazam

(don’t bother learning all these drug names)

Answer 86

A

1) SEIZURES + status epilepticus
= buccal midazolam, IV lorazapam

2) ALCOHOL WITHDRAWAL
= chlordiazepoxide

3) sedation for INTERVENTIONS
= midazolam

4) sedation for AGITATION / aggression
= lorazepam

5) severe, disabling or distressing ANXIETY
= diazepam

6) severe, disabling or distressing INSOMNIA
= temazepam

only use short term (2-4 wks) as tolerance and addiction common

generally use short-acting for insomnia and long-acting for anxiety

Answer 87

A

COMMON

drowsiness / sedation
unsteadiness (^falls in elderly)
confusion / memory problems
muscle weakness
slurred speech
paradoxical increase in aggression (5-10%)

SERIOUS

dependence (-> withdrawal)
resp depresison in OD (-> coma + death)

Answer 88

A

elderly (^risk falls, confusion etc)
respiratory impairment
neuromuscular disease
liver failure (may precipitate hepatic impairment)

Answer 89

A

FLUMAZENIL

= BZD receptor antagonist, for acute toxicity.

Answer 90

A

Withdrawal syndrome

anxiety
insomnia
tremor
nausea
perceptual disturbances

^very similar to alcohol withdrawal

Occurs within 2-3/7 of stopping short-acting, or 7/7 long-acting BZD.

Short-acting BZDs more likely to be associated with dependence and withdrawal.

MANAGEMENT

switch to diazepam (long-acting) and then taper
additional psych / social support too!

Answer 91

A

other sedating drugs
opioids
alcohol
CYP450 (inhibitors may increase effects)

all increase risks of sedation, resp depression etc

Answer 92

A

zopiclone
zolpidem
zaleplon

act at, or close to, the BZD receptor site

oral route

Answer 93

A

INSOMNIA (short-term use only)

zopiclone
zolpidem
zaleplon

Answer 94

A

bitter aftertaste / dry mouth
residual drowsiness the next day

biggest risk = tolerance + rebound insomnia on withdrawal

interact with other sedatives (incl alcohol) to increase effect

nb risk in eldery of confusion + falls

Answer 95

A

OLD / 1ST GEN ANTI-HISTAMINES

diphenhydramine
doxylamine

MIRTAZEPINE
- esp for depression w insomnia

MELATONIN
- aka circadin

nb, aside from mirtazepine, these should all be used short term as build tolerance

nb also opioids may help with insomnia but should not be used purely for this indication

Answer 96

A

mild insomnia (use sleep hygiene instead)
energy drinks / excess caffeine (counteract activity, reduce these)
over 65s (risk excessive sedation, falls + confusion)
excessive alcohol use (both CNS depressors)
severe hepatic impairment (as can increase accumulation dt lowered metabolism)

Answer 97

A

Inhibits acetylcholine breakdown – increased cholinergic neurotransmission

Both muscarinic and nicotinic
In the brain cholinergic NT increases.

Other:

Stimulates smooth muscle of bowel
Relaxes sphincter of bladder and bowel
Constrict pupils
Increases secretions e.g. sweat, saliva, bronchial

think of it as doing the opposite to an anti-cholinergic drug (like a TCA)

oral route

Donepezil
Galantamine
Rivastigmine

Answer 98

A

Donepezil
Galantamine
Rivastigmine

1) mild-moderate ALZHEIMERS (incl mixed alzheimers-vascular)
2) LEWY BODY dementia (Rivastigmine only)

don’t use for fronto-temporal demnetia - makes worse!

nb also used for:

myasthenia gravis
relief of post-op urinary retention

Answer 99

A

Donepezil
Galantamine
Rivastigmine

basically the OPPOSITE of anti-cholinergic side effects!

nausea
vomiting
abdo cramps
diarrhoea
bradycardia
muscle cramps
hypersalivation
excess sweating
insomnia

monitor pulse

Answer 100

A

Memantine

increase levels of acetylcholine

oral route

Answer 101

A

Memantanine

1) moderate-severe ALZHEIMERS

(use after acetylcholinesterase inhibitors failed / stopped working)

Answer 102

A

Memantanine

dizziness
sedation
constipation

Answer 103

A

OPEN Qs

could you tell me about your usual drinking habits?

could you take me through a typical day of drinking for you?

when did you first start drinking? what did you drink then?

how have things changed since you first started drinking?

SPECIFIC Qs

time of first drink of the day?
any days off?
alone or socially?
efforts to control?

Answer 104

A

fine intention tremour (also tongue - harder to feign!)
high HR
high BP
GI upset
nausea / vomiting
diaphoresis
headache (incl photosensitivity)
anxiety / agitation
loss of orientation
hallucinations (norm visual)

COMPLICATIONS

delirium tremens
seizures
wernicke’s encephalopathy

(see my ED notes for time scales of these**)

Answer 105

A

chlordiazepoxide (reducing or PRN dosing)
thiamine
fluids

refer to drug + alcohol services in community!

Answer 106

A

weed, maijuana, herb, hash, grass, ganja, dope, bud, puff, pot

(legal class B)

smoke w tobacco
vape
ingest

Binds to cannabinoid receptor CB1. Indirectly increases dopamine release. Lipid soluble so stays in body for weeks - useful for drug testing!

THC – psychoactive component

CBD – non-psychoactive, thought to reduce negative psychological experiences

nb ‘skunk’ = higher THC content and lower CBD content

nb CBD thought to be beneficial for pain, epilepsy and others, although not sufficient evidence. CBD recently recognised as a medicine in the UK, but not licensed.

Answer 107

A

ACUTE PSYCH

relaxation
euphoria
altered perceptions (could be illusions or hallucinations)
short-term memory loss
irritability
paranoia
drowsy

ACUTE PHYSICAL

increased HR
increased appetite
dry mouth
dry eyes
bloodshot eyes

Answer 108

A

all risks of smoking tobacco
low motivation
depression
anxiety
psychosis / schizophrenia (5x baseline risk)

Answer 109

A

nb although rarer than most other drugs - 10-20% of people who use every day develop a physical dependence on cannabis (more likely if start using when younger age)

anxiety / irritability
insomnia
loss of appetite
abdo pains
nausea
sweating
chills
depression / anxiety / modd swings
loss of concentration

physical symptoms within first 48hrs, subside by a week then psych symptoms increase from 7-14 days and can last for weeks

Answer 110

A

MDMA, MD, mandy, molly, pills, crystal

(legal class A)

swallowed
‘dabbing’ onto gums

Blocks serotonin reuptake, increasing serotonin in the synapse (so is like a super-SSRI), also has a lesser effect on increasing dopamine and noradrenaline

Answer 111

A

ACUTE PSYCH

euphoria
empathy towards others
increased energy
reduced tiredness
altered sensual experiences (eg music, anxiety, panic attacks, confusion)

ACUTE PHYSICAL

high HR
high BP
dry mouth (so they drink)
hyperthermia
dilation of pupils
loss of appetite
tightening / repetitive movement of jaw (bruxism/’gurning’)

Answer 112

A

lethargic
increased need for sleep
low mood
anxiety

Answer 113

A

pills (unaware of dose or what cut with = danger of overdose / poisoning)
water intoxication / hyponatraemia
memory problems
depression
anxiety

Answer 114

A

speed, whizz, billy, sulph, base

(legal class B, A if injected)

snort
dab
swallowed (‘bomb)
injected

binds to transporter proteins for monoamines such as dopamine, noradrenaline, serotonin and taken up into neurons. Once inside, disrupts the storage of monoamines in synaptic vesicles. More neurotransmitters in neuron. Then, by unknown mechanism, makes transporters run in reverse, leading to increased release of monoamines, esp. dopamine and noradrenaline. May also inhibit reuptake and inhibit monamine oxidase.

Answer 115

A

ACUTE PSYCH

alert / wide awake
excited / chatty
increased focus / concentration
panicked
agitated / aggressive
delusions + hallucinations

ACUTE PHYSICAL

high HR
high BP
high temp
high RR
arrythmias
insomnia
LOW appetite (opposite to cannabis)

(almost manic symptoms without the psychosis and flight of ideas)

COME DOWN

lethargic
low mood

Answer 116

A

dependency
pscyhosis
depression
anxiety

OTHER USES

treatment for ADHD
‘study drug’

Answer 117

A

cravings
anhedonia
depression
anxiety
increased need for sleep
increased appetite

Answer 118

A

yaba, christine, tina, meth, ice, glass, crystal meth, crank

(legal class B, A if injected)

Chemically very similar to amphetamines. However, extra methyl group means crosses blood brain barrier more readily as it is highly lipophillic, therefore more of it reaches brain, it reaches it faster, and it stays for longer as it resists breakdown from MAO more

swallowed
snorted
smoked
injected

Answer 119

A

highly addictive!
affect on cognition
risk of MI

all the risks of amphetamine, but more so

Answer 120

A

blow, coke, crack, charlie, white, wash, toot, flake, stones, sniff, snow, rocks, percy, pebbles, freebase, ching, change, C

snort
smoke (crack)
inject

Mainly unknown. Thought to be inhibition of monoamine reuptake and blocking monoamine transporters. Dopamine, noradrenaline and serotonin. Dopamine thought to be most important in causing the desired effects as well as dependency

Answer 121

A

ACUTE PSYCH

elated mood
increased confidence
feelings of having great mental capacities
increased energy

HIGHER DOSES:

anxiety / panic
hallucinations

PHYSICAL

high HR
sweating
dry mouth
loss of appetite
vasoconstriction
dilated pupils

COME DOWN

low mood
poor concentration
runny nose
tremours

Answer 122

A

RISKS

stroke
MI / arrest
bowel gangrene
ENT complications (epistaxis, chronic rhinorrhoea, septum damage)

(also dependence)

nb if a young person comes in with chest pain, always ask about cocaine use!

EFFECT OF EVERYDAY USE

restlessness / hyperactivity
‘wired’ + paranoid
insomnia -> exhaustion
nausea
weight loss

Answer 123

A

tired, exhausted + unable to sleep
extreme emotional + physical distress
anorexia
sweating

Answer 124

A

benzos, downers, valium, vallies, roofies, rohypnol, jellies

(legal class C)

swallowed
injected

binds to GABA receptor and increases effect of GABA (more chloride ions in post-synaptic neuron, hyperpolarises, less excitable)

Answer 125

A

ACUTE PSYCH

sedation
reduction in anxiety

ACUTE PHYSICAL

reduced RR
reduced HR
reduced temp

Answer 126

A

addiction

- overdose

Answer 127

A

decreased concentrations
depression
anxiety / panic attacks
tremours
headaches
seizures
nausea
vomiting

Answer 128

A

smack, skag, horse, brown, gear

legal class A

smoked
snorted
injected

crosses blood brain barrier and is converted to morphine, whereby it binds to mu-opioid receptors - reduces excitability of neurons, reduces GABA (an inhibitory neurotransmitter, therefore increased dopamine- high)

Answer 129

A

PSYCH

happy / euphoric
relaxed
sleepy

PHYSICAL

reduced RR
reduced HR
low temp
constricted pupils

Answer 130

A

HR + BP

opioid DOWN
sympathomimetics UP
sedatives DOWN

RR

opioid DOWN
sympathomimetics UP
sedatives DOWN

TEMP

opioid DOWN
sympathomimetics UP
sedatives DOWN

PUPILS

opioid SMALL
sympathomimetics LARGE
sedatives NO CHANGE

BOWEL SOUNDS

opioid REDUCED
sympathomimetics LOUD
sedatives REDUCED

DIAPHORESIS

opioid LESS
sympathomimetics YES
sedatives LESS

SYMPATHOMIMETICS

cocaine
amphetamines & meth

SEDATIVE / HYPNOTICS

benzos + barbs
Z drugs
antihistamines

Answer 131

A

offence to SUPPLY (or OFFER to suppy) any PSYCHOACTIVE substance, regardless of its potential for harm

possession is not an offense - but production + supply is!

psychoactive substance
= any substance which is capable of producing a psychoactive effect in a person who consumes it (+ is not an exempted substance)

EXEMPTIONS

caffeine
alcohol
nictoine
nutmeg
poppers

nb this acts includes nitrous oxide

Answer 132

A

METHADONE

once a day, take supervised in pharmacy
liquid, tablet, injection
long half life (24+hr, may reduce to 8hrs in pregnancy)

BUPRENORPHINE

semi-synthetic opioid
agonist / antagonist opioid receptor modulator
norm sub-lingual tablet

NALTREXONE

long acting opiate antagonist
oral, depot, implant
blocks euphoric effects, little effct on cravings
also used in alcohol dependency (better evidence base)

LOFEXIDINE

alpha2-adrenergic receptor agonist
used to relieve withdrawal symptoms, particularly those caused by noradrenaline
can be used in conjunction with naltrexone for detox

Answer 133

A

B complex vitamins (B-l (thiamin), vitamin B-3 (niacin))
AND folacin (folic acid)

B vitamins to prevent wernickes encephalopathy + sub-acute degeneration of cord

check for loads of others, incl Vit D, norm electrolytes etc - do full blood panel

Answer 134

A

COMPLEMENTARY
= therapies used alongside treatments offered by your doctor
- yoga
- meditation
- acupuncture
- massage

ALTERNATIVE
= approaches which are generally meant to replace the treatments offered by your doctor
- traditional chinese medicine
- ayurvedic medicine
- St John's Wart

Answer 135

A

DON’T WANT treatment from dr (eg psych meds or talking therapies)
ALREADY TRIED treatment from dr + didn’t work or had unacceptable side effects
on WAITING LIST for treatment but need help now
want more options for treatment IN ADDITION to treatment from dr

Answer 136

A

1) they are not evidence-based (except maybe accupuncture) and so may not produce desired benefit
2) alternative medications may INTERACT with prescribed meds
3) also may not be what they say on packet, market is UNREGULATED

Answer 137

A

never recommend directly BUT if they ask you, say:

As with all medicines and therapies, different things work for different people, and it’s not easy to predict which therapy you would find most useful or effective.

Most of the evidence for complementary and alternative therapies is based on traditional use rather than modern scientific studies. This means it’s really difficult to know whether they are an effective treatment for mental health problems.

However, many people do say they find them helpful in managing or relieving the symptoms they experience.

BUT be careful as many medications can cause harm 1) dt INTERACTIONS (also pregnancy) and 2) dt lack of REGULATION - so talk to dr first

But no harm at all to trying complementary methods (acupuncture, massage etc)

‘complementary + alternative therapies’ leaflet produced by MIND

Answer 138

A

1) LEAST RESTRICTIVE OPTION and maximising independence
2) EMPOWERMENT and INVOLVEMENT (of pts and family)
3) Respect and DIGNITY
4) PURPOSE and effectiveness (clear therapeutic aim to admission)
5) EFFICIENCY + EQUITY.

Answer 139

A

Informal = admitted to hospital voluntarily (must have capacity to consent to admission

formal / detained = pt admitted under MHA (aka sectioned)

Answer 140

A

1) must be suffering from MENTAL DISORDER (any disorder or disability of mind), of a nature or degree which warrants detention in hospital

AND

2) must be at RISK to own health +/or own safety +/or risk to others

AND

3) must be UNWILLING to be admitted voluntarily OR LACK the CAPACITY to make this decision

so always assess capacity - because even if they agree to admission, they may lack the capacity to make that decision - and so may have to section even if they appear to want to go voluntarily

Answer 141

A

A diagnosis of learning disability isn’t sufficient for detention in its own right

Their presentation must be associated with abnormally aggressive or seriously irresponsible conduct in order to detain

Answer 142

A

A specific relative of the pt who is organised through a hierarchy system
- Not the same as next of kin

They can apply for a section
Ability to request a pt to be discharged from the section
Can apply for a review of the section
Duty to inform this relative when the pt is detained

Answer 143

A

2 = ASSESSMENT

up to 28 days
2 doctors + 1 AHMP (MH assessment)

3 = TREATMENT

up to 6 months (initially)
2 doctors + 1 AHMP (MH assessment)

5(2) = DOCTORS HOLDING

up to 72 hours
fully registered DR (FY2 +)

5(4) = NURSES HOLDING

up to 6 hours
mental health nurse

Answer 144

A

135 - POLICE POWERS
= warrant to search + remove pt from PRIVATE property + take to a 'place of safety' for assessment
= requires a magistrate warrant
- duration n/a
- not renewed
- triggers 136

136 - POLICE POWERS
= allows police to remove pt from PUBLIC area to ‘place of safety’ for assessment
- up to 24hrs
- not renewed (can be extended by 12 hrs)
- triggers MHA assessment (for section 2/3)

nb don’t need warrant for 136

BOTH

police
no right to treat
no right to appeal

Answer 145

A

2 = admission for ASSESSMENT

up to 28 days
can’t renew
2 doctors + 1 AHMP (MH assessment)
can treat
can appeal (within 1st 14 days)

ENDS:

revoked
detain under section 3 (need another assessment)

Answer 146

A

3 = admission for TREATMENT

up to 6 months (initially)
can be renewed for another 6m and then annually
2 doctors + 1 AHMP (MH assessment)
can treat
can appeal (twice in first 6m then annually)

ENDS:

revoked
renewed

Answer 147

A

5(2) = DOCTORS HOLDING powers

up to 72 hours
can’t be renewed
fully registered DR (FY2 +)
must be INPATIENT (not A&E)
can’t treat (but can under MCA if lack capacity!!)
can’t appeal

END:

triggers MHA assessment
(or just revoke)

Answer 148

A

5(4) = NURSES HOLDING

up to 6 hours
mental health nurse
up to 6 hours
can’t be renewed
mental health nurse
must be INPATIENT (not A&E)
can’t treat (but can under MCA if lack capacity!!)
can’t appeal

END:

triggers 5(2) assessment by FY2+
(or just revoke)

Answer 149

A

can treat under:

section 2 (assessment)
section 3 (treatment)

can treat:

1) the CAUSE of the mental disorder:
- causes of delirium
- acute intoxication

2) the MENTAL DISORDER
- anti-depressants, anti-psychotics
- includes ECT

3) DIRECT CONSEQUENCES of mental disorder:
- self-neglect
- overdose (eg parvolex)
- self-injury
- feeding in ED (incl NG tubes)

If need to treat:
A) under a section which doesn’t cover treatment
OR
B) a physical health condition unrelated to MH condition

then ASSESS CAPACITY and treat under MCA (if lack)

Answer 150

A

aka CTO

allows treatment for MH condition in community (instead of hospital)

legal order for supervised community treatment, with specific criteria (eg attend appts, let nurses give A/Ps depo)

can be recalled to hospital if criteria not met (don’t have to do any)

initially for 6 months, renewed for further 6m then annually (basically section 3)

can only be used under section 3!

go on section 3 first then it’s converted into a CTO

Answer 151

A

1) WHY detaining
- Eg ”Mr smith is 46 yo gentleman who is suffering from auditory hallucinations which are telling him to go and jump of a bridge. He has a prior diagnosis of paranoid schizophrenia and appears to be suffering a relapse of symptoms”
2) WHO the RISK is to
- eg “Mr smith is at risk to himself if he listens to the auditory hallucinations and jumps of a bridge, he is also unlikely to consent to treatment as he lacks insight and also lacks capacity to make that decision”
3) brief CAPACITY assessment OR that they are REFUSING treatment
4) that you have considered a LESS RESTRICTIVE option
- “eg I have considered allowing mr smith to remain as an informal patient, but it is likely that he would leave the ward and prove a risk to himself”
5) POTENTIAL BENEFITS of detainment
- eg for assessment and diagnosis, to get to therapeutic dose of A/Ps etc

Answer 152

A

1) A person is ASSUMED to have capacity (thumb)
2) YOU have taken all practicable steps must be taken to ENABLE DECISION MAKING. (index)
3) People are able to make UNWISE decisions (middle)
4) Any actions or decisions made on behalf of a person who lacks capacity must be in that person’s BEST INTERESTS (ring)
5) Decisions made on behalf of someone lacking capacity must be LEAST RESTRICTIVE (little)

Answer 153

A

DIAGNOSTIC TEST
- at the time of the decision the person has an impairment of, or disturbance in functioning of, the mind or brain (incl learning disability etc)?

if no, person has capacity!

if yes:

FUNCTIONAL TEST
- is pt able to:

1) UNDERSTAND the info relevant to the decision
2) RETAIN this info
3) WEIGH UP information as part of making the decision
4) COMMUNICATE their decision

Info relevant to decision = eg what procedure involves, risks, intended benefits

length of retention depends on decision (eg endoscopy retain for several hours-days, what want for dinner - only need to do for secs/mins)

Ability to weigh up information may be impaired in an overdose due to depression because of underlying suicidal ideations - so can say they lack capacity to refuse treatment for OD - so can give the treatment against their will

Communication doesn’t have to be verbal - can be written or shake head etc

Answer 154

A

Decision specific.

Time specific

say: pt doesn’t have capacity for this procedure at this time - NOT the person doesn’t have capacity

capacity should be assessed by the person who will be then making the decision, if they do lack capacity

over 16 years
(under 16 is gillick competence)

Answer 155

A

ADVANCED DIRECTIVE

(advanced decision and living will are outdated terms for same thing)
Allows REFUSAL of specific treatments under the law
must be SPECIFIC - specific scenario and specifically what you are refusing
Valid for ECT under MHA
Need to have capacity when made
Needs to be witnessed
Always check if someone has one
In an emergency - provide treatment and then consider options later once see directive

ADVANCED STATEMENT

Again, written down when pt has capacity
GENERAL statement which GUIDES Drs if need to make DECISIONS in best interests of pts
eg: wishes, feelings, values, beliefs
Not legally binding, but should be used in ‘best interest’ decisions

Answer 156

A

1) HEALTH + welfare
2) property + FINANCES

one individual can be both
- or each position can be shared

pt asigns before they lose capacity

“who would you want to make decisions for you once you’ve lost the capacity to make them for yourselves?”
can do on gov.uk website
encourage pts with early dementia to do

As a physician, can apply for the courts to displace these powers if you disagree with decisions

nb Must EXPLICITLY state that you give them the right to refuse life-sustaining treatment

Answer 157

A

Best interests are PERSONAL - so need to gather as much info as possible to make a best guess as to what that person would have wanted before they lacked capacity

Can talk to:

Patient (even if they lack capacity)
Relatives and carers - what would they have accepted/refused
Medical knowledge - to know what options are available - find least restrictive option
Can appoint an IMCA to find out this info and act as an advocate for the pt

Answer 158

A

independent mental capacity advocate

people who lack capacity and do not have family or friends to consult

consult if:
A) decision involves ‘serious medical treatment’
B) decision involves a hospital stay of >28 days or care home stay of >8 weeks

Answer 159

A

ACID TEST

1) Are they under continuous supervision and control? (continuous doesn’t need to mean 24/7)
2) Are they not free to leave?

if answer yes to both: then you are depriving the pt of their liberty and should have a DOLS in place

restriction is in best interest and MHA wouldn’t be more appropriate (eg LD or short term delirium)

pt LACKS CAPACITY

is in a hospital OR care home (only valid in one location)

DoLS give NO RIGHT to treatment.
- If treatment’s required then we must assess capacity and if they lack capacity provide treatment in their best interests

Soon to be replaced by Liberty Protection Safeguards (LPS)

two types

1) emergency DOLS
- 7 days
- just a form

2) standard DOLS
- up to a year
- needs a DOLS assessment

DOLS assessment
- best interest assessor AND mental health assessor

Challenging a DOLS

request a review
appeal to the court of protection

nb 18 years or over

Answer 160

A

TO SELF

self-neglect (incl wandering)
physical health (incl not taking meds)
self-harm / suicide
financial risk (if manic/psychotic)
sexual risk

TO OTHERS

physical harm to others
reckless driving
neglecting children or dependent adults
financial exploitation
arson (esp w LD)

FROM OTHERS

financial exploitation
violence from others
domestic violence
expolitation (esp LD + elderly)

nb any self-harm in older people is taken a lot more seriously (as more likely to be attempted suicide and not just ‘cry for help’)

Answer 161

A

TO SELF

any thoughts of harming self?
if you did get these thoughts, what would you do?
able to look after yourself?
any financial worries?

TO OTHERS

anyone out to get you? what would you do if you faced that person in the street?
any thoughts of protecting yourself or harming others?
any dependents? children?

FROM OTHERS

do you feel safe at home?
who has control of your finances?

Answer 162

A

LIKELIHOOD

plans?
means? (eg access to gun)

IMMEDIACY
- planned a date? as soon as they leave?

IMPACT
- something potentially lethal? or superficial arm cutting?

Answer 163

A

FIXED

hx of self-harm / suicide attempts?
hx of substance misuse
past trauma
Fhx of suicide
age (<20 or >45)
gender (male)

DYNAMIC

bereavement
relationship breakdown
loss of job
current financial stress
current substance misuse
current mental health deterioration

Answer 164

A

S = Sex (male)
A = Age (<20 or >45)
D = Depression

P = Previous suicide attempts
E = Excessive drug use / Ethanol
R = Rational thinking loss (eg psychosis)
S = Seperated (or no Spouse)
O = Organised plan
N = No social support / isolated
S = Sickness (chronic illness)

Answer 165

A

PSYCHOTIC phenomena
HOPELESSNESS for future
sense of ENTRAPMENT
well-formed PLANS
PAIN or chronic medical illness
lack of SOCIAL support (or perception of)

for child/adolescent: PARENTAL psychotic OR suicidal behaviour

Answer 166

A

BEFORE

PLANNED or impulsive? (planned worse)
how did you get the MEANS? (just in house or stockpilling?)
leave a NOTE?

DURING

WHERE? (private place worse)
make steps to AVOID BEING FOUND (locking door, forest, not texting people)
under influence of ALCOHOL?
METHOD? (violent bad, also high no pills)

AFTER

did you SEEK HELP? (bad if did)
do you REGRET it now?

Answer 167

A

1) verbal de-escalation
2) medication

lorazepam (1-2mg PO/IV/IM)
Antipsychotic IM

norm use lorazepam (esp if think under infuence of drugs, if known psychotic disorder then use A/Ps)

be careful w lorazepam if high on opioids or alcohol or if risk of resp depression (eg COPD)

Procyclidine for EPSEs!

Answer 168

A

An abnormal, extreme and persistent variation from the normal (statistical) range of one or more personality attributes (traits), causing the individual and/or family and/or society to suffer

can only be diagnosed aged after 18 years

childhood trauma
violence
attachment issues
ADHD
behavioural issues

aetiology: Interaction between genetic predisposition and invalidating environment Ie bad early experience

Answer 169

A

CLUSTER A: ODD / ECCENTRIC

paranoid
schizoid
schizotypical (ideas of reference)

CLUSTER B: DRAMATIC / IMPULSIVE

antisocial (dissocial)
emotionally unstable (borderline)
histrionic
narcissistic

CLUSTER C: ANXIOUS / FEARFUL

anxious (avoidant)
dependent
anankastic (obsessive-compulsive)

Answer 170

A

Help individual find lifestyle that suits them, minimising negative effects
Consistency of care
Education of insight – to prevent shifting of blame over other
Psychological treatment – DBT for cluster B (?and others)

nb also Medication for comorbid conditions

SSRIs
Anti-psychotics.

Answer 171

A

1) IQ under 70
2) loss adaptive social functioning
3) onset before age of 18

mild, moderate, severe + profound (based on level of IQ, don’t learn the cut offs)

—> Does NOT include impairment developed >18 years, people with ABI after 18, people with complex medical conditions affecting intellectual abilities that develop >18 year e.g. Huntington’s, Alzheimer’s.

nb Many people with learning disabilities prefer the term ‘learning difficulty’.

However, in UK education services, ‘learning difficulty’ also includes people who have ‘specific learning difficulties’ (e.g., dyslexia), but who do not have a significant impairment in intelligence.
intellectual disability (USA) = learning disability (UK)

About 2% of population have at least a mild learning disability

Answer 172

A

most common cause = unknown

down’s syndrome
Fragile X (X-linked inheritance, excess CCG repeats)
prader-willi
tuberous sclerosis
di-george (associated w psychosis)
maternal drug or alcohol use (foetal alcohol syndrome / spectrum disorder)

PERINATAL

oxygen deprivation during birth
injury secondary to birth complications (eg bleed)
difficulties resulting from premature birth

AFTER BIRTH

illnesses (eg meningitis)
head injuries
environmental conditions

also a lot of people have multiple causes of the above

Answer 173

A

cerebral palsy (more likely to have a learning disability)
autism
epilepsy (30% of people w epilepsy have an LD)
mental health condition (25-40% people with LD will have MH problems)

nb also dementia more common - esp alzheimers in down’s

Answer 174

A

BIO

Medical management as appropriate - but lower doses and be aware of comorbidities (Response to medication may take longer or there may be increased sensitivity to side-effects)
ALWAYS check thyroid in downs

PSYCHO

may not be able to engage with psychological therapies
Standard assessment tools for dementia in the general population may not be appropriate. (Be aware of changes in behaviour as an early indicator of dementia)

SOCIAL

really important - MDT approach
Support with complex social functions – finances, parents, carers
Education support in mainstream schools
Sheltered accommodation/ residential care

don’t worry tooo much about remembering this stuff off by heart

Answer 175

A

challenging behaviour = Any kind of behaviour which causes a problem to the patient or any other people around them

behaviour is influenced by:

BIO

Mental Illness. Epilepsy. Pain. Hunger.
Lesch Nhyan Syndrome (self injury).
Prader Willi (overeating)

PSYCHO
- Fear. Learned responses. Belief.

SOCIAL

Limited space. Noise.
Others demands.Boredom

MANAGEMENT:

use ABC charts to work out what causing behaviour
avoid triggers
use positive reinforcement

Brainscape's Knowledge GenomeTM

core conditions - 2 Flashcards

Brainscape's Knowledge Genome^TM