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Year 5 - Fatty > Psych > Flashcards

Psych Flashcards

1
Q

What are the 3 main symptoms of depression?

A

Low mood, Anergia and Anhedonia

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2
Q

What are the 3 types of eating disorders

A

Anorexia Nervosa - 0.6%
Bulimia Nervosa - 1%
Binge Eating Disorder - 2.8%

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3
Q

What is the age of onset for AN and BN?

A

AN - 16-22, all social classes

BN - >22y/o

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4
Q

What is eating disorders co-morbid with?

A

Substance misuse, depression and OCD

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5
Q

What is the heritability of AN?

A

58%

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6
Q

Whats the aetiology of BN?

A

5-HT dysregulation

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7
Q

What is a squad test? (ED)

A

tests for proximal myopathy

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8
Q

What is seen on an ECG for bulimia?

A

Long QT and bradycardia

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9
Q

What determines immediate admission for high risk eating disorder patients?

A 
Low BMI <13
WL <1kg/week
Septic looking signs (<34.5,BP<80/50, cold peripheries, thrombocytopenia/purpuric rash)
HR <40bpm + long QT 
Suicide risk
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10
Q

ICD10 diagnostic criteria for AN:

A
  • BMI <17.5 (or weight less than 15% expected weight)
  • deliberate weight loss
  • fear of fat/distorted body image
    (should have no endocrine dysfunction)
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11
Q

How do you calculate BMI

A

weight (KG)/ height (M)^2

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12
Q

What is atypical anorexia nervosa?

A

Young boys that are losing weight to get a six pack but are currently at a healthy weight

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13
Q

What is the weight of BN and AN?

A

AN - underweight

BN - normal weight (BMI > 17.5)

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14
Q

Can there be binging and purging in AN?

A

Yes

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15
Q

3 diagnostic criteria for Bulimia:

A

1) Binging or persistent preoccupation with eating and/or irresistible craving for food
2) Purging behaviours (diuretics, excessive exercise, laxatives, insulin therapy, vomiting)
3) Psychotherapy (feeling loss of control, morbid dread of fatness)

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16
Q

Signs and symptoms of Bulimia:

A
  • Less severe but similar to anorexia

- Amenorrhoea despite normal weight

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17
Q

What is binge eating disorder?

A

Most common eating disorder but no purging pathology

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18
Q

Differential for Bulimia:

A

upper GI disorder, personality disorder, depressive disorder, obesity

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19
Q

Management for bulimia? (mild)

A
  • Screen for immediate admission otherwise manage in the community
  • Guided self-help, recommend BEAT charity, monitor for 12 weeks
  • Routine referral to CEDS if failure to respond
    FEATURES: infrequent binging and purging (<2 weeks)
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20
Q

Management for bulimia? (moderate)

A
  • Screen for immediate admission otherwise manage in the community
  • Guided self-help, recommend BEAT charity, monitor for 8 weeks
  • Routine referral to CEDS if failure to respond
    FEATURES: frequent binging and purging (> 2 weeks), some medical consequences such as chest pain
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21
Q

Management for bulimia? (severe)

A
  • Screen for immediate admission otherwise manage in the community
  • Urgent referral to CEDS (community eating disorder service)
    FEATURES: daily purging, significant electrolyte imbalance, comorbidity
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22
Q

Prognosis of Bulimia?

A

After 10 years, 70% recover and 1% die. Better than AN.

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23
Q

What are bad prognostic indicatiors of bulimia?

A
  • Very low weight
  • Severe binging/purging
  • Co-morbid depression
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24
Q

Biochemical changes of bulimia?

A

Hypokalaemia (vomitting)

Hypercalcaemia

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25
Q

Management of bulimia presentation at GP?

A
  • Treat medical condition (dental review regularly for acid wear on teeth)
  • Treat co-morbid psychiatric illness (depression, OCD, substance misuse)
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26
Q

Medication treatment of moderate-severe bulimia?

A

SSRIs (high dose 60mg fluoxetine) –> reduce binging and purging and helps impulses

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27
Q

Plan for children and adults (therapy) in bulimia.

A

Children: 1st line - family therapy
Adults: 1st line - Guided self-help programmed; 2nd line - CBT-ED

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28
Q

Investigations for Bulimia?

A

Check electrolytes and ECG changes.

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29
Q

What is refeeding syndrome?

A
  • Seen in eating disorder patients
  • Characterised by electrolyte imbalance (principally low serum phosphate, potassium, and magnesium) caused by their sudden intracellular movement due to the switch from fat to carbohydrate metabolism and associated increased secretion of insulin
  • Defined mainly by low phosphate
  • Low K (arrythmias) > Low PO4 (hypophosphatemic HF) > Low Mg
  • Signs: fatigue, weakness, confusion, high BP, seizures, arrhythmia, heart failure
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30
Q

Risk factors for Anorexia?

A

OCD
Childhood feeding difficulties
Family history

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31
Q

Signs and symptoms of anorexia?

A

Secondary to malnutrition (restricting subtype) and binge-purging

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32
Q

Can binging, purging and vomiting also be anorexia?

A

Yes if they are underweight. Normal weight is bulimia.

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33
Q

What are differential diagnosis of anorexia?

A
  • Medical causes of weight loss (e.g. hyperthyroidism, malignancy, gastrointestinal disease, Addison’s disease, chronic infection, inflammatory conditions, and AIDS)
  • Depression
  • BN
  • Psychosis (self-starvation might occur if food is believed to be poisoned)
  • Eating disorder not otherwise specified
  • Body dysmorphic disorder (BDD is a condition characterised by body image distortion (e.g.belief that the nose is misshapen. Deliberate weight loss in BDD would be unusual)
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34
Q

Is there ever watchful waiting for eating disorders?

A

No

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35
Q

Immediate admission for eating disorder:

A

Urgent medical treatment is needed in high-risk patients with nutritional decompensation. Markers of this include:
• BMI <13
• weight loss >1kg/week
• purpuric rash
• cold peripheries
• core body temperature <34.5°C
• hypotension (systolic <80mmHg, diastolic <50mmHg)
• bradycardia (<40bpm) with prolonged QT interval on ECG

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36
Q

Management of anorexia (mild):

A

-Monitor/advice/support for 8 weeks
-Beat charity support
FEATURES: BMI>17, no additional co-morbidity
- Routine referral fo CEDS if failure to respond

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37
Q

Management of anorexia (moderate):

A
  • Routine referral to CEDS

FEATURES: BMI 15-17, no evidence of system failure

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38
Q

Management of anorexia (severe):

A
  • Urgent referral to CEDS (community eating disorder service)
    FEATURES: BMI<15, rapid weight loss, evidence in system failure
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39
Q

Management of anorexia for GP presentation?

A
  • Engage and educate (stop laxatives/diuretic use as it does not reduce calorie intake)
  • Signpost support (beat charity, MIND, NHS)
  • Treat co-morbid psychiatric illness (depression, OCD, substance misuse)
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40
Q

What is the eating disorder questionnaire?

A

SCOFF questionnaire

  • Do you make yourself Sick (induce vomiting) because you feel uncomfortably full?
  • Do you worry that you have lost Control over how much you eat?
  • Have you recently lost more than One stone (14 lb [6.4 kg]) in a three-month period?
  • Do you think you are too Fat, even though others say you are too thin?
  • Would you say that Food dominates your life?

One point for every yes answer; a score 2 indicates a likely case of anorexia nervosa or bulimia
nervosa (sensitivity: 100 percent; specificity: 87.5 percent).

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41
Q

Plan for anorexic patients at GP?

A
  • Nutrition and weight restoration (set target weight + make eating plan to gain 0.5-1kg/week)
  • CBT-ED, MANTRA or SSCM (or family therapy if less than 18 years)
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42
Q

Endocrine dysfunction in anorexia:

A

The hypothalamic–pituitary–gonadal axis is affected, causing amenorrhoea in women and impotence in men. Libido is lost in both sexes. If AN begins before puberty, menarche and breast development are delayed or arrested.

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43
Q

Prognosis of anorexia:

A

After 10 years, 50% recover, 10% die and 40% ongoing problems

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44
Q

Bad prognostic factors for anorexia:

A
  • Very low weight
  • Later onset
  • Bulimic features
  • Longer illness duration
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45
Q

Complications of anorexia:

A
  • Infertility
  • Early death
  • Osteoporosis
  • Cardia arrhythmias and failure
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46
Q

Children management of anorexia

A

1st line: Family therapy

2nd line: ED-CBT

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47
Q

When and what medication therapy for anorexia

A

When: If physical symptoms such as rapid weight loss and BMI<13.5
What: Fluoxetine (especially if there are preoccupations with food)

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48
Q

Indications for family therapy for eating disorders

A
  • Short history of illness

- Young onset (less than 19)

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49
Q

Indications of interpersonal therapy for ED:

A
  • Longer history of illness

- Onset older (later-onset disease)

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50
Q

2nd line treatment of anorexia

A
  • All if 1st line is unacceptable
  • Eating-disorder-focussed Focal Psychodynamic Therapy (FPT)
  • Adolescent-focussed psychotherapy (AFP)
  • Motivational interviewing
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51
Q

1st Line treatment of anorexia

A

Offer any of these:

1) CBT-ED - 40 weekly sessions (address low self-esteem, perfectionism and control issues)
2) Maudsley Anorexia Nervosa Treatment in Adults (MANTRA) - 20 weekly sessions (focus on what the cause of anorexia is)
3) Specialist Supportive Clinical Management (SSCM) - 20 weekly sessions led by practitioner (explore problems of anorexia, educate on nutrition and eating habits, explore a future beyond anorexia)

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52
Q

Investigations of anorexia

A
  1. Height, weight, and BMI.
  2. Squat test: Ask the patient to squat down and rise to standing without using their arms (difficult with proximal myopathy).
  3. Essential blood tests
    • ESR, TFTs—exclude most organic causes of weightloss, e.g. hyperthyroidism. ESR is normal or low in anorexia.
    • FBC, U&E, phosphate, albumin, LFT, creatininekinase, glucose—evaluate nutritional state and risk.
  4. ECG: Bradycardia, arrhythmias, and a prolongedQT interval.
  5. Other tests as indicated, e.g. DEXA scans (low bonedensity).
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53
Q

What are the different type of psychotherapies for eating disorders?

A

Psychotherapies
• Motivational interviewing is an important approach when trying to engage ambivalent patients who lack insight into their disorder—or hold positive views of their illness
• Family therapy—rather than simply focusing on the patient, this involves the whole family. Patients with a short history of early onset anorexia (onset before 19 years) show greatest response.
• Interpersonal therapy aims at improving social functioning and interpersonal skills. This is better for patients with later onset or longer duration of illness.
• Cognitive behavioural therapy—addresses control, low self-esteem, and perfectionism

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54
Q

What are the conditions of inpatient anorexia treatment

A
  • BMI <13 or extremely rapid weight loss
  • serious physical complications
  • high suicide risk
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55
Q

The 3 Ps of personality disorder

A
  • Pervasive: occurs in all/most areas of life
  • Persistent: evident in adolescence and continues through adulthood
  • Pathological: cause distress to self or others, impairs function
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56
Q

What is Cluster A personality disorder

A
  • Odd or eccentric
    “Weird”
  • Paranoid, schizoid, schizotypal
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57
Q

What is Cluster B personality disorder

A
  • Dramatic, erratic or emotional
    “Wild”
  • Dissocial, borderline (EUPD), histrionic, narcissistic
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58
Q

What is Cluster C personality disorder

A
  • Anxious and fearful
    “Worried”
  • Anankastic, anxious-avoidant, dependant
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59
Q

What is the ICD-10 definition of personality disorder:

A
  • A set of consistent thoughts, feelings and behaviours shown across in time in a variety of settings which may lead to suffering of the individual or others “exaggerated personality traits”
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60
Q

ICD 10 Personality disorder criteria

A

R- relationships affected (pathological)
E - enduring (persistent)
P - Pervasive
O - Onset in childhood/adolescence (Persistent)
R - Results in distress (Pathological)
T - Trouble in occupational/social performance (Pathological)

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61
Q

OCEAN personality factors (not required by ICD-10)

A 
O - openess to imagination
C - Conscientiousness 
E - Extraversion
A - Agreeableness
N - Neuroticism
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62
Q

Aetiology and epidemiology of personality disorder

A

M > F in cluster A, anankastic, dissocial types
F > M in histrionic, emotionally unstable types
Around 10% of the population and 2% have EUPD

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63
Q

What neurotransmitter is low in personality clutster B types

A

Low 5-HT/seretonin levels.

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64
Q

What is a schizotypal personality?

A
  • There are some positive schizophrenia symptoms
  • Eccentric thoughts and ideas (main difference between this and schizoid)
  • Paranoid or bizarre ideas
  • Social withdrawal
  • Cold/inappropriate affect
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65
Q

What is a schizoid personality?

A
  • Negative schizophrenia symptoms
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66
Q

Paranoid personality disorder symptoms

A 
S- Sensitive
U- Unforgiving
S- Suspicious
P- Posessive and jealous personality disorder
E- Excessive self-importance
C- Conspiracy theories
T- Tenacious sense of rights 
Differentials: Schizophrenia, delusional disorder
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67
Q

Schizoid personality disorder symptoms

A

A- Anhedonic
L- Limited emotional range
L- Little sexual interest
A- Apparent indifference to praise/criticism
L- Lack close relationships
O- One player activities
N- Normal social conventions ignored
E- Excessive fantasy world
Differentials: Depression, autism spectrum, psychosis, phobia
JUST NEGATIVE SYMPTOMS AND SIGNS OF SCHIZOPHRENIA

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68
Q

Histrionic personality disorder symptoms

A 
A - Attention seeking
C - Concerned with appearance
T - Theatrical
O - Open to suggestion 
R - Racy and suggestive
S - Shallow affect
Differentials: BAPD 1/2, substance
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69
Q

EUPD symptoms

A

A - Affective instability
E - Explosive behaviour
I - Impulsive (inc self harm)
O - Outburts of anger
U - Unable to plan/consider consequences
Differentials: affective disorder, psychosis

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70
Q

Dissocial personality symptoms

A

F - Forms, but cannot maintain relations
I - Irresponsible
G - Guiltless
H - Heartless
T - Temper easily lost
S - Someones else’s fault
Differentials: Substance misuse, psychosis, manic

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71
Q

2 types of EUPD

A
  • Borderline (disturbance in self-thoughts)

- Impulsive (mainly impulsivity)

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72
Q

Anankastic personality disorder symptoms

A 
D -  Doubtful
E - Excessive detail 
T - Tasks not completed
A - Adheres to rules
I - Inflexible 
L - Likes own way
E - Excludes pleasure and relationships
D - Dominated by intrusive thoughts 
Differentials: OCD, autism spectrum
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73
Q

Anxious/avoidant personality disorder

A

A - Avoids social contact
F - Fear rejection/criticism
R - Restrictive lifestyle
A - Apprehensiveness
I - Inferiority
D - Does not get involved unless sure of acceptance
Differentials: phobia, autism, schizophrenia, depression

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74
Q

Dependant personality disorder

A 
S - Subordinate
U - Undemanding
F - Fears abandonment
F - Feels helpless when alone
E - Encourages others to make decisions
R - Reassurance needed
Differentials: Cognitive impairment, anxiety disorder
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75
Q

What is splitting?

A

An immature response where a person cannot reconcile the good and bad in someone and only views people as all good or all bad
(often cannot maintain relationships)

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76
Q

What is dissociation?

A

An immature ego defence where one assumes a different identity with a situation

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77
Q

What is sublimation?

A

A mature ego defence where one takes an unacceptable personality trait and uses it to drive a respectable work that does not conflict with their ego/values (eg youth with anger issues signs up to a boxing academy)

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78
Q

What is reaction formation?

A

An immature ego defence where one suppresses unacceptable emotions and replaces them with their exact opposite (eg a man with homoerotic desires becomes a champion of anti-homo policy)

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79
Q

What is regression?

A

Revert to an immature behaviour in a stressful situation (bang desk in frustration)

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80
Q

What is identification?

A

Someone models the behaviour of someone else (eg an older brother playing with a dead younger brothers toys)

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81
Q

What is displacement?

A

Defence mechanism when someone takes out their emotions on a neutral person (not likely to respond to them)

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82
Q

What is projection?

A

A person assumes an innocent/neutral character is responsible or as guilty as the patient, for the patient’s actions

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83
Q

Investigations for personality disorder?

A
  • Collateral history
  • Check for REPORT criteria
  • List personality traits and match to cluster criteria (> 3 and REPORT required)
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84
Q

Management of personality disorder?

A

1st Line: Crisis plan (contact numbers, sedative antihistamies)
Biopsychosocial approach:
Meds: Antipsychotics, Antidepressants, Anticonvulsants

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85
Q

What medication reduces impulsivity and aggression in Cluster B?

A

Antipsychotics

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86
Q

What medication reduces impulsivity and anxiety in Cluster B/C?

A

Antidepressants (SSRIs)

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87
Q

What medication is useful for labile (quickly changing) affect in Cluster B?

A

Anticonvulsants (Lithium)

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88
Q

What type of CBT is 1st line in antisocial PD?

A

Group based CBT

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89
Q

What is DBT?

A
  • Dialectical behaviour therapy (subtype of CBT)

- 1st line of Emotionally unstable PD

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90
Q

What is the indication of DBT?

A
  • Focuses on factors contributing to emotional instability
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91
Q

What 2 factors does DBT aim to introduce?

A

Validation: emotions are acceptable
Dialectics: Showing you things in life are rarely black or white, helping be more open

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92
Q

What is CAT?

A
  • Similar to CBT
  • Cognitive analytics therapy
  • Focuses on specific issues to describe, understand their origins, and develop methods to change ideas surrounding the specific problems
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93
Q

What is metallisation? And what is it used for?

A

For emotionally unstable PD

  • Integrative psychotherapy; bringing together aspects of psychodynamic, CBT and systemic approaches
  • Teaches you how to think about thinking
  • This can help you understand other people’s viewpoints as you can examine their thinking
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94
Q

What is a Type A personality?

A
  • Impatient, aggressive, competitive people, thought to be at higher risk of heart disease
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95
Q

What is PD associated with? (Fx history)

A

Personality disorder is associated with a family history of personality disorder, as well as a history of depression and alcohol dependency

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96
Q

What childhood temperament is associated with PD?

A

Children with ‘difficult’ temperaments have greater problems coping as adults, possibly because they find it harder to develop supportive relationships, and are more distressed by negative events. Early attachment difficulties are also associated with personality disorder

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97
Q

Childhood experience and PD?

A

Personality disorder is associated with insecure attachment and traumatic, neglectful, or chaotic upbringing.Many people experience traumatic childhoods, and it is not understood why most are resilient, whilst others develop a personality disorder or another mental illness(e.g. depression, eating disorders, or schizophrenia).

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98
Q

What is acting out?

A

Impulses are expressed through actions, without conscious awareness of the underlying emotion (e.g. Phoebe’s self-harm rather than sadness)

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99
Q

What is fantasising?

A

Using imagination to escape from the painfulness of reality (e.g. Masson’s daydreams prevent him from feeling lonely).

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100
Q

What is the neurotransmitter theory of PD?

A

There is evidence of lower serotonin levels in dissocial personality disorder. Serotonin has been implicated in regulation of impulsivity and aggression

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101
Q

EUPD (borderline) symptoms

A

S - Self-image unclear
C -Chronic empty feelings
A -Abandonment fears
R - Relationships are intense and unstable
S - Suicides and self harm
Differentials: adjustment disorder, depression, psychosis (patients occasionally experience fleeting psychotic features)

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102
Q

EUPD (impulsivity) symptoms

A

L - Lacks impulse control
O - Outbursts or threats of violence
S - Sensitivity to being thwarted or criticized
E - Emotional instability
I - Inability to plan ahead
T - Thoughtless of consequences
Differentials: Adult ADHD, affective disorder, adjustment disorder

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103
Q

What is the definition of substance misuse?

A

A pattern of substance use causing physical, mental, social and occupational dysfunction

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104
Q

What is acute intoxication?

A

A transient state of emotional and behavioural change after psychoactive substance use: dose dependant and time limited

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105
Q

What 3 things does physical withdrawal only occur from?

A
  1. Alcohol
  2. Opiates
  3. Benzodiazepines
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106
Q

What is harmful use?

A

A pattern of use likely to cause physical or psychological damage.

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107
Q

What is dependancy?

A

A cluster of physiological, behavioural and cognitive symptoms in which the use of a substance takes a much higher priority than other behaviours that once had a greater value (ICD-10)

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108
Q

What is withdrawal?

A

A transient state occurring while readjusting to lower levels of a drug in the body.

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109
Q

What is psychotic disorder?

A

Psychotic symptoms occurring during or immediately after PS use, characterised by vivd hallucinations, abnormal affect, psychomotor disturbances, persecutory delusions and delusions of reference.

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110
Q

What is amnesic disorder?

A

Memory and other cognitive impairments cause by substance use (ie. Wernickes)

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111
Q

What is residual and late onset psychotic disorders?

A

Where effects on behaviour, affect or cognition lasting beyond the period during which direct PS effect might be expected.

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112
Q

What is the definition of impairment?

A

Any loss of abnormality of psychological, physiological or anatomical structure of function.

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113
Q

What is the definition of disability?

A

Any restriction or lack of ability (from impairment) to perform an activity considered normal

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114
Q

What is the definition of handicap?

A

A disadvantage for a given individual that limits or prevents the fulfilment of a role that is normal

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115
Q

What is the definition of a learning disability?

A
  • IQ of less than 70
  • Impaired social/adaptive functioning
  • Onset in childhood
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116
Q

What are the levels of intellectual disability?

A

Mild - IQ 50-70
Moderate - IQ 35-50
Severe - IQ 20-35
Profound - IQ < 20

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117
Q

What are the indicators of LD?

A

LD register
LD school
Difficulty reading and writing
Special Education Needs Assessment

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118
Q

What is the signs and symptoms of children with LD?

A

Milestone delay
Difficulty managing schoolwork
Poor sleep-wake cycle

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119
Q

What is the signs and symptoms of adolescents with LD?

A

Difficulty with peers
Inappropriate sexual behaviours
Difficulty transitioning

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120
Q

What is the signs and symptoms of adults with LD?

A

Difficult day-to-day functioning

Needs extra support

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121
Q

What are the investigations for LD?

A
  • Intellectual impairment: WAIS III (Wechsler Adult Intelligence Scale)
  • Verbal IQ + Performance IQ = Full scale IQ
- Adaptive and social functioning: 
ABAS II (Adaptive behaviour assessment system)
Clinical Interview (leave plenty of time) - establish presence in childhood
Physical examinations (sight and hearing)
School reports
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122
Q

What is the management of LD?

A
  • Biopsychosocial MDT (psychiatrist, OT, SALT, specialist nurse, educational support, social support)

General help:

  • Choice board
  • Scheduling board
  • Self-help board
  • Communication aids

Medications: Start slow, go slow (treat co-morbid medical and psychiatric problems)
- Melatonin - helps with poor sleep cycles

Psychosocial interventions:

  • CBT
  • Family therapy
  • Psychodynamic therapy
  • Art therapy

Challenging behaviours: (identify/remove cause –> behavioural analysis –> antipsychotics)
- Risperidone - short-term use, last line if no cause can be found

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123
Q

What are the complications of LD?

A
  • Patients with LD have a higher prevalence of psychological symptoms than general population
  • Can be difficulty diagnosing other psychological conditions due to language difficulties and atypical presentations
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124
Q

Is LD more prevalent in males than females?

A

Males

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125
Q

What is the clinical presentation of LD?

A 
Learning disability usually presents in childhood, but may be missed if mild. Abilities can be delayed, reduced ,or absent in:
• language
• schooling
• motor ability
• independent living
• employment
• social ability

Behavioural difficulties may arise, secondary to a combination of communication problems, psychiatric or physical illness, epilepsy, or suboptimal support for individual needs. ‘Behavioural phenotypes’ are commonly recognized behaviours in particular syndromes, e.g. self-harm in Lesch-Nyhan syndrome.

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126
Q

What are the symptoms of a mild LD disorder?

A
  • Language is usually reasonably good, although its development may be delayed.
  • Problems may go undiagnosed, although individuals struggle through school or may be labelled with behavioural problems.
  • With appropriate support, many people live and work independently.
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127
Q

What are the symptoms or a moderate LD?

A
  • Language and cognitive abilities are less developed.
  • Reduced self-care abilities and limited motor skills may necessitate support.
  • May need long-term accomodation with their family or in a staff-supported group home.
  • Simple practical work should be achievable in supported settings.
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128
Q

What are the symptoms or a severe LD?

A
  • Marked impairment of motor function.
  • Little/no speech during early childhood (some may develop during school years).
  • Simple tasks can be performed with assistance.
  • Likely to require their family home or 24-hour-staffed home.
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129
Q

What are the symptoms or a profound LD?

A
  • Severely limited language, communication, self-care, and mobility.
  • Significant associated medical problems.
  • Usually require higher levels of support.
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130
Q

What is diagnostic overshadowing?

A

Diagnostic overshadowing describes the tendency to attribute everything to the learning disability itself. Changes in behaviour, mental state, or ability are dismissed, despite usually indicating physical or mental illness in people without a learning disability.

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131
Q

What are differential diagnosis for LD?

A
  1. Autistic spectrum disorders: people with Asperger’s syndrome (autism with normal intelligence) may have significant social deficits, communication difficulties, and difficulties in living independently
  2. Epilepsy may cause transient cognitive impairment. Very frequent uncontrolled seizures can mimic persistent cognitive impairment.
  3. Adult brain injury or progressive neurological conditions: learning disabilities are neurodevelopmental disorders, occurring while the brain is still developing. If the patient presents late, it is important to decide whether or not impaired intellect was present before any adult illness.
  4. Psychiatric: severe and enduring mental illness such as schizophrenia can lead to chronic cognitive impairment, reduced social functioning, and associated speech disorders—mimicking a learning disability. Exclude intellectual impairment prior to the onset of psychiatric symptoms.
  5. Educational disadvantage/neglect: lacking the opportunity to learn must be distinguished from a learning disability
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132
Q

What are the investigations you can carry out for LD?

A
  1. IQ testing
  2. Functional assessment of skills, strengths and weakness
  3. Detailed developmental history from parents
  4. FBC, U&E, LFT, TFT, bone profile—to exclude reversible disturbances.
  5. Additional blood tests for known LD causes
  6. Investigations for associated physical illnesses, e.g.EEG for epilepsy
  7. Genetic testing if appropriate
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133
Q

Treatment steps for LD?

A
  1. Prevention
    - Education
    - Improved antenatal/perinatal care
    - Genetic counselling
    - Early detection and treatment of reversible causes
  2. Treat physical comorbidity
  3. Treat psychiatric comorbidity
  4. Educational support
  5. Psychological therapy
  6. Other support
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134
Q

What is a medically unexplained symptom?

A

A physical complaint without evidence of underlying organic cause

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135
Q

What is a medically unexplained symptom by ICD 10?

A

Partial or complete loss of the normal integration between memories of the past, awareness of identity and immediate sensations and control of bodily movements.

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136
Q

What is dissociative disorder?

A

Disorders of physical functions under voluntary control and loss of sensation

  • dissociation is a process of ‘separating off’ certain memories from normal consciousness
  • in contrast to conversion disorder involves psychiatric symptoms e.g. Amnesia, fugue, stupor
  • dissociative identity disorder (DID) is the new term for multiple personality disorder as is the most severe form of dissociative disorder
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137
Q

What is conversion disorder?

A

An internal conflict which is converted into physical manifestations

  • typically involves loss of motor or sensory function
  • the patient doesn’t consciously feign the symptoms (factitious disorder) or seek material gain (malingering)
  • patients may be indifferent to their apparent disorder - la belle indifference - although this has not been backed up by some studies
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138
Q

What is somatisation disorder?

A

Disorders involving pain or autonomically-controlled sensations

  • multiple physical SYMPTOMS present for at least 2 years
  • patient refuses to accept reassurance or negative test results
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139
Q

Subtypes of dissociative disorder are?

A
  • Dissociative amnesia: Loss of memory (too great to be explained by ordinary forgetfulness)
  • Dissociative fugue: Dissociative amnesia + purposeful travel beyond everyday range (“Travel far and wide”)
  • Dissociative stupor: Lack of voluntary movement/normal responses to external stimuli. Evidence of stress from recent events
  • Trance and possession disorder: Temporary loss of personal identity and full sense of awareness of surroundings
  • Dissociative motor disorders: Loss of ability to move whole/part of limbs. Close resemblance to ataxia, apraxia, akinesia, aphonia, dysarthria, dyskinesia and seizures.
  • Dissociative convulsions: Mimic epileptic seizures (tongue biting, bruising from falls and incontinence is rare). Consciousness maintained or replace by a state of stupor or trance
  • Dissociative anaesthesia: Areas of anaesthesia do not follow normal dermatomal distribution. May be accompanied by paresthesia.
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140
Q

Risk factors of dissociative disorders:

A
  • Traumatic events
  • Intolerable problems
  • Disturbed relationships
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141
Q

Signs and symptoms of dissociative disorder:

A

Onset = acute, specific, dramatic, following sudden stress of conflict
Presentation:
- Paralysis
- Aphonia (cannot speak)
- Blindness
- Seizures
- Multiple personalities
- Stupor
- Fugue (loss of memory and wonder away from home)
- Psychogenic amnesia (loss of all memories, including own identity)

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142
Q

Investigations of dissociative disorder:

A

1st: Exclude organic cause
- raised prolactin after real seizure
- normal prolactin after dissociative convulsion
2nd: Identify and treat any co-morbid depression

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143
Q

Management of dissociative disorder:

A
  • 75% of people have self-limiting spontaneous recovery
  • Supportive therapy:
    Encourage return to normal activity
    Avoid reinforcing behaviour (providing a wheelchair for dissociative stupor/motor disorder)
    Address physical stressors rather than focus on physical manifestations
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144
Q

What is somatisation? ICD-10 definition

A
  • Multiple, recurrent and frequently changing physical symptoms of > 2 years.
  • Have complicated history of contact with medical care –> many negative investigations carried out
  • Symptoms may be referred to any part or system of the body
  • The disorder is chronic and fluctuating –> disruption of social, interpersonal and family behaviour
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145
Q

Is somatisation more common in men or women?

A

10:1 Female to male

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146
Q

Subtypes of somatisation:

A
  • Undifferentiated somatoform disorder: Multiple varying and persistent complaints of <2 years
  • Hypochondrial disorder: Persistent preoccupation with idea of having a serious/progressive physical disorders. Normal sensations interpreted as abnormal or distressing. Co-morbid anxiety and/or depression common. Patient maintains their belief depite being told otherwise (overvalued idea) - Often cancer, pre-occupation with a single problem
  • Somatoform autonomic dysfunction: Symptoms presented as if due to physical disorder of system/organ largely or completely under control of the ANS. Objective autonomic arousal (palpitations, sweating, flushing, tremor). Subjective non-specific (fleeting aches/pains, burning sensation, bloating)
  • Persistent somatoform pain disorder: Persistent, severe and distressing pain (not otherwise explained). Evidence of emotional conflict of psychological problems
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147
Q

Signs and symptoms of somatisation:

A
  • Multiple recurrent and frequently changing physical symptoms
  • History of interactions with medical professionals without outcomes
  • Social and occupational impacts
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148
Q

Investigations of somatisation:

A
  • Full history and MSE (with physical examination)
  • Exclude organic cause (eg stroke)
  • Exclude co-morbid conditions (eg. with HADS for potential depression)
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149
Q

Management of somatisation disorder:

A

Make sure continuity of care - see by the same doctor each time
1st: Explain and reassure
2nd: CBT
Also treat co-morbid conditions (eg depression)

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150
Q

Definition of somatisation?

A

This is the unconscious expression of psychological distress through physical symptoms ,e.g. rather than anger, a patient experiences abdominal pain

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151
Q

Management of MUS?

A
  1. Assessment - history and examination
  2. Explain and reassure - Use the Reattribution Model:
    • Ensure they feel understood.
    • Broaden the agenda from a physical cause to a physical and psychological explanation.
    • Make the link between symptoms and psycho-logical factors.
  3. Avoid over-investigation, unnecessary specialist referral or medications
  4. Emotional support
  5. Encourage normal function
  6. Antidepressants - even without depression symptoms
  7. Treat co-morbid conditions
  8. CBT
  9. Graded exercise - helpful in some conditions eg fibromyalgia and CFS
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152
Q

Prognosis of MUS?

A

Shorter duration of MUS and milder symptoms are linked to better prognosis.

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153
Q

What is the definition of conduct disorder?

A

Repetitive and persistent pattern of antisocial behaviour with violates basic rights of others that are not in line with age appropriate social norms

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154
Q

Who does conduct disorder affect?

A

Childhood and adolescence

Less than 18 years old

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155
Q

What is the aetiology of conduct disorder?

A
  • Unknown: parental (violence, failure to set rules)

- Child: (low IQ, CNS impairment)

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156
Q

Prevalence of conduct disorder?

A

5-10 y/o: 7% boys and 3% girls

11-16 y/o: 8% boys and 5% girls

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157
Q

Risk factors for conduct disorder

A
  • Low socioeconomic status
  • Deprived living
  • Children in the care system
  • ADHD
  • Substance misuse
  • Male
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158
Q

Signs and symptoms of conduct disorder:

A

Repetitive and persistent pattern of dissocial, aggressive or defiant conduct:
- Excessive levels of fighting or bullying
- Cruelty to other people or animals
- Severe destructiveness of property
-Fire-setting
More severe than ordinary mischief or adolescent rebelliousness

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159
Q

Investigations of conduct disorder:

A
  • Reports from parents/teachers

- Developmental assessment

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160
Q

Management of conduct disorder:

A

1st: Parent management training programmes (Triple-P or Webster-Stratton)
- Needs strong parental cooperation and motivation
- If weak outcome due to lack of parental engagement, move to 2nd line
2nd: Child individual or group interventions focussed on problem solving and anger management
- Often, affected children do not have the motivation to engage with these well

Remedial educational teaching (for missed school)
Alternative peer activities

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161
Q

Prognosis of conduct disorder:

A 
- 50% develop antisocial personality disorder
Poorer prognosis:
- Early onset
- Family criminal record
- Low IQ
- Low socio-economic status 
- Co-morbidities
- Poor parenting
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162
Q

Types of conduct disorder:

A
  • Oppositional-defiant disorder: (characterised by angry, defiant behaviour to authority)
  • Unsocialised CD (significant abnormality with relationships with other children)
  • Socialised CD (generally well-integrated into a peer group)
  • CD confined to family context
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163
Q

What is delusional disorder? ICD-10

A

Persistent/life-long delusions with few/no hallucinations
- <3 months is temporary
- >3 permanent
Cannot include:
- Clear auditory hallucinations
- Schizophrenia symptoms (delusions of control, blunting of affect)
- Evidence of organic/brain disease
NOTE: the presence of an occasional or transitory auditory hallucinations does NOT rule out this diagnosis

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164
Q

Aetiology of delusional disorder?

A
  • Old age
  • Low socioeconomic status
  • Immigration
  • Substance abuse
  • Social Isolation
  • Premorbid personality disorder
  • Family history
  • Group delusions
  • Sensory Impairment
  • Head injury
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165
Q

Is acute or insidious onset better prognosis of delusional disorder?

A

Acute onset is better prognosis

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166
Q

Biological reasons for delusional disorder?

A
  • Excess dopamine and ACh activity
  • Neurological lesions to the temporal lobe, limbic system, Basal ganglia
  • Cortical damage (persecutory delusions)
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167
Q

Pyschosocial reasons for delusional disorder?

A
  • Freud (delusions serve defensive functions)
  • Distrust, suspicion, jealousy, low self-esteem
  • Social isolation, seeing own defects in others
  • Rumination over meaning and motivation
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168
Q

Signs and symptoms of delusional disorder?

A
  • A
  • S
  • E
  • P (hallucinations and delusions): Non-bizzare delusions, rarely hallucinations
  • T (forms, content possession): Process un-impaired, content preoccupied, single theme of thoughts
  • I: Impaired (delusions affect thought and behaviour)
  • C: Intact
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169
Q

What is erotomaniac thought?

A

AKA De Clerembault syndrome

Excessive sexual desire, often believe a VIP in love with them

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170
Q

What is othello syndrome?

A

Believe partner is unfaithful

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171
Q

What is fregoli syndrome?

A

> 2 people are same person changing disguises to deceive

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172
Q

What is Folle a deux?

A

Shared delusions/hallucinations between people

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173
Q

What is factitious disorder?

A

Consciously pretending to have a medical illness.

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174
Q

Investigations for delusional disorder?

A
  • Full history and collateral history
  • MSE
  • Exclude organic causes
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175
Q

Differentials for delusional disorder?

A
  • Substance induced
  • Dementia + delirium
  • Hypochondriasis
  • Mood disorder with delusions
  • Body dysmorphia
  • Paranoid personality disorder
  • Schizophrenia
  • OCD
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176
Q

Management of delusional disorder:

A
  • Consider admissions if high risk to self or others
    Biological
  • Antipsychotics (poor evidence)
  • SSRI (cover other potential missed differentials)
  • BDZ (for anxiety)

Psychological:

  • Individual CBT
  • Pyschoeducation

Social:

  • Social skills training
  • Pyschoeducation
  • Family therapy
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177
Q

What is the definition of acute stress reaction? ICD-10

A

A transient disorder that develops in an individual without an other apparent mental disorder in response to exceptional physical and mental stress and that usually subsides within hours or days
- does not tend to persist greater than 1 month
- DSM-V says symptoms must last greater than 3 days
- If they last longer than 1 month, consider PTSD
Onset of symptoms within minutes

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178
Q

How does ASD differ from PTSD?

A
  • PTSD is diagnosed based on symptoms in clusters, not in totality
  • PTSD has a dissociative sub-type, however, in ASD, depersonalisation and derealisation are symptoms
  • PTSD includes non-fear based symptoms (risky behaviour) but ASD does not
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179
Q

Aetiology of ASD?

A
  • Physical or sexual assault
  • Death
  • War
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180
Q

Signs and symptoms of ASD?

A

Key features:

  • Initial state of daze (may manifest as stupor)
  • Constriction of consciousness field
  • Narrowing attention
  • Attention to comprehend stimuli; disorientation

Other symptoms:

  • Autonomic signs of panic (fight of flight): occurs in minutes and disappear in hours/days
  • Tachycardia
  • Sweating
  • Hyperactive
  • Tachypnoea
  • Hypertension
  • Partial or complete amnesia may be present
  • Depersonalisation
  • Derealisation
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181
Q

Investigations of ASD?

A
  • Full history and collateral history
  • MSE if indicated
  • Needs to be a clear history between stressor and reaction
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182
Q

Management of ASD?

A
  • Support and reassurance

- BDZ for short-term distress

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183
Q

Complications and prognosis of ASD?

A
  • May progress to PTSD

- If formal, immediate, psychological ‘debriefing’ is undertaken, future PTSD risk increased

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184
Q

What is the definition of adjustment disorder? ICD-10

A

States of subjective distress and emotional disturbance, usually interfering with social functioning and performance, arising in the period of adaptation to a significant life change or stressful life event

  • Beginning within 1 month of the stressful event
  • Not lasting longer than 6 months

Prolonged abnormal response to stress starting within 1 month of stressful event, not lasting over 6 months

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185
Q

Aetiology and risk factors of adjustment disorder?

A
  • Maladaptive psychological response to stressful life events - divorce, unemployment
  • Any age of onset
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186
Q

Signs and symptoms of adjustment disorder?

A

CONSIDER AN ASSOCIATED CONDUCT DISORDER (ESP IN ADOLESCENCE)

  • Depressed mood
  • Anxiety and worry
  • Feeling of inability to cope
  • Disability in the performance of daily routine

Symptoms of anxiety or depression without biological symptoms to depression. Should not be sufficient severity/prominent in its own right to justify more specific diagnosis

Persons reaction deemed greater than expected for the situation, but not as severe to diagnose anxiety or depression

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187
Q

What is normal grief reaction?

A
  • recognisable sequence of stages that can last up to 2 years
    eg. shock –> anger –> guilt –> searching –> sadness –> acceptance
  • vivid dreams of dead person being alive, pseudohallucinations
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188
Q

What is abnormal/prolonged grief reaction?

A
  • Delayed onset, greater intensity of symptoms or prolongation of the reaction, preoccupation with negative thoughts, suicidal ideations, hallucinatory experiences
  • More likely when relationship with deceased was problematic or there was a sudden death
  • Distinguish from depression:
    Sadness and symptoms are focused around the person that was lost
    In depression, the symptoms are more free-floating and not focussed on anything in particular
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189
Q

Investigations of adjustment disorder?

A
  • Full history and collateral history

- MSE if needed

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190
Q

Management of adjustment disorder/grief reaction?

A
  • Support, reassurance and problem-solving usually all that are recovered

Adjustment disorder:

  • Biological –> antidepressants, antianxiolytics/hypnotics
  • Psychosocial –> supportive counselling

Grief reaction:

  • Biological –> antidepressants
  • Psychosocial –> supportive counselling
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191
Q

Prognosis of adjustment disorder?

A
  • Short-term interruption to life

- Symptoms usually improve after resolution of cause

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192
Q

Definition of PTSD? ICD-10

A

Arises as a delayed onset or protracted response to a stressful event or situation of an exceptionally threatening or catastrophic nature, which is likely to cause pervasive distress in almost everyone

  • Must last > 1 month
  • Often begins within 6 months of trauma (often within the 1st month of the trauma)
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193
Q

Aetiology of PTSD?

A

6.8% lifetime prevalence

F>M

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194
Q

Risk factors of PTSD?

A
  • FHx
  • Female
  • Traumatic events
  • Neurotic personality type
  • Neuroanatomy
  • Genetics
  • Low social class
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195
Q

Biological reasons for PTSD?

A
  • Genetics: Some predisposition

- Neuroanatomical: Hyperactive amygdala (emotional processing), atrophied hippocampus (memory storage)

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196
Q

Psychosocial reasons for PTSD?

A
  • Traumatic events: 10% extreme trauma sufferers
  • Neurotic traits
  • Family history of psychiatric problems
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197
Q

Signs and symptoms of PTSD?

A

(1) Re-experiencing: intrusive memories (flashbacks, nightmares, repetitive images, physical sensations)
(2) Avoidance of triggers: (activities and situations reminiscent of the trauma)
(3) Hyperarousal: (hyper-vigilance, enhanced starttle reflex, insomnia, irritability, cannot relax)

Other:

  • mental health problems: depression, anxiety, phobias
  • self-harming or destructive behaviour: drug or alcohol misuse
  • Physical symptoms: headaches, dizziness, chest pain, stomach aches
  • Anhedonia/emotional numbing
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198
Q

Prognosis of PTSD?

A
  • Majority recover

- Some suffer for many years leading to an enduring personality change

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199
Q

Investigations for PTSD?

A
  • Full history

- Trauma screening questionnaire (10 questions, measure re-experiencing and arousal symptoms)

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200
Q

Management of PTSD?

A

Begin by classifying the level of functional impairment as mild, moderate and severe

MILD: symptoms < 4 weeks –> watchful waiting + treat co-morbid conditions

CBT with trauma focus: offer to all patients with moderate-severe PTSD, presenting > 1 month

Eye movement desensitisation and reprocessing (EDMR): offer if moderate-severe PTSD, >3 months after non-combat relayed event
(patient recalls experience in as much detail as possible in a state of relaxation, whist their eyes are fixed on the therapists finger as it moves from side to side –> aids memory processing)

201
Q

What is trauma focused CBT?

A
  • Combination of exposure therapy and trauma-focused therapy
  • Computerised or face-to-face
    NB: immediate post-trauma formal debriefing actually increases risk of PTSD
202
Q

Pharmacological management of PTSD?

A

Not currently recommended
1st line: SSRI (setraline) or SNRI (venlafaxine)
2nd line: atypical antipsychotics

203
Q

What is re-experiencing in PTSD?

A
  • Flashbacks: vividly reliving the trauma, feeling as though it is ‘happening all over again’.
  • Nightmares.
  • Intrusive memories: being unable to keep the mind clear of memories of what happened.
204
Q

What is avoidance in PTSD?

A

Avoiding reminders of the event (these often trigger flashbacks and increased anxiety). People often try to avoiding thinking about the trauma

205
Q

What is hyperarousal in PTSD?

A
  • Persistent inability to relax.
  • Hypervigilance: the patient feels as though they are always on ‘red alert’.
  • Enhanced startle reflex (exaggerated reaction to the unexpected).
  • Insomnia.
  • Poor concentration.
  • Irritability.
206
Q

What are differentials of PTSD?

A
  • Depression
  • Anxiety
  • Adjustment disorder
207
Q

Autism key factors?

A
  • presentation at 2-4 years old
  • most have decreased IQ
  • Boys 75% > girls 25%
208
Q

Risk factors for autism?

A
  • Siblings with ASD
  • parental psychotic/affective disorder
  • Birth CNS defect
  • prematurity (<35 weeks gestation age)
  • sodium valproate
  • LD
  • chromosomal disorder (Downs)
  • genetics disorder (fragile x syndrome)
  • ADHD
209
Q

Medical condition association of autism?

A
  • Fragile X syndrome
  • Tuberous sclerosis
  • Neurofibromatosis
  • Di-george
  • Rett’s syndrome
  • Mitochondrial disorders
  • Downs
  • Prader-willi/Anglemans syndrome
  • Epilepsy
210
Q

How common is autism?

A

1.4 per 1000

211
Q

What is asperger syndrome?

A
  • Distinguished by no delay in language/cognitive development
  • 0.3 per 1000
  • psychosis in adult life
  • marked clumsiness
212
Q

What is Rett syndrome?

A
  • Medical disorder
  • X linked
  • MECP 2 gene
  • Affects girls more than boy
  • <0.2 per 1000
  • Develop normally till 2 years
  • sudden deterioration + less social interaction + struggle to feed
  • Symptoms include impairments in language and coordination and repetitive movements. Those affected often have slower growth, difficulty walking, and a smaller head size.
213
Q

How common is childhood disintegrative disorder (CDD)?

A
  • <0.2 per 1000
  • Childhood disintegrative disorder (CDD), also known as Heller’s syndrome and disintegrative psychosis, is a rare condition characterised by late onset of developmental delays—or severe and sudden reversals—in language, social function, and motor skills.
214
Q

What is pervasive developmental disorder not otherwise specified?

A
  • 4.5 per 1000

- Most common type of autism

215
Q

ICD-10 criteria for Autism SD Part A?

A

(A) Abnormal or impaired development evident <3 years old

  • receptive or expressive language
  • development of selective social attachments or of reciprocal social interaction
  • functional or symbolic play
216
Q

ICD-10 criteria for Autism SD Part B?

A

(B) A total of >6 symptoms from 1,2,3 with >2 from 1 and >1 from each of 2 and 3:

(1) Qualitative impairment in social interaction:
- Failure to adequately use eye to eye gaze
- Failure to develop peer relationships
- Lack of socio-emotional reciprocity
- Lack of spontaneous seeking to share enjoyment, interest etc with other people

(2) Qualitative abnormalities in communication
- delay in or total lack of development of spoken languages (no attempt to compensate)
- relative failure to initiation or sustain conversation
- stereotyped and repetitive use of language or idiosyncratic use of words or phrases
- lack of varied spontaneous make believe play

(3) Restricted repetitive and stereotyped pattern of behaviour, interest and activities
- Preoccupation with stereotyped and restricted patterns of interest
- apparently compulsive adherence to specific routines or rituals
- repetitive motor mannerisms involving hand, finger flapping and whole body movements
- preoccupation with non-functional elements of play materials (such as their odour)

217
Q

ICD-10 criteria for Autism SD Part C?

A

The clinical picture is not better described by other medical disorders.

218
Q

What is the early diagnostic trio for Autism SD?

A

Deficits in evident when <3 years old:

  • verbal and non-verbal communication
  • reciprocal social interaction
  • restrictive or repetitive behaviours/interest
219
Q

What is the hallmark for Autism SD?

A
  • Immediate/delayed (>2 year old) echolalia
  • immediate non-communicative repetition of words or phrases - the child is simply repeating exactly what was heard without synthesising the intrinsic language
220
Q

Investigations for Autism SD?

A
  • hearing, speech and language assessment
  • cognitive assessment (eg WICS, WPPSI)
  • Autism diagnosis assessment (GOLD STANDARD):
  • -> ADI-R: autism diagnostic inventory - revised
  • -> ADOS: Autism diagnostic observatory schedule
  • Childhood autism rating scale (CARS)
221
Q

Management of autism?

A
  • MDT/patient-centred care is key as this is a spectrum. Everyone is different
222
Q

Who is part of the Autism SD MDT?

A
  • paediatrician
  • child
  • adolescent psychiatrist
  • educational or clinical psychologist
  • SALT
  • OT
  • specialist health visitor/social worker
  • specialist nurse
223
Q

What is the 1st line management for Autism SD?

A
  • Psychosocial play-based intervention
  • increase attention, engagement (play specialist) and reciprocal communication (SALT)
  • increase carers and teachers understanding of patients communication/interaction pattern (EarlyBird <4; EarlyBirdPlus (4-8))
  • Include techniques to expand the child’s communication, interactive play and social routines
224
Q

What is applied behaviour analysis for Autism SD?

A
  • From behavioural nurses

- Focuses on improving specific behaviours as well as adaptive learning skills

225
Q

What should you offer family/carers of children with Autism SD?

A
  • Offer an assessment of the family/carer needs
  • Plan for the future including transition for the child
  • Plan for extra support (educational, social)
226
Q

When to transition Autism SD to adult services?

A
  • When they are 16 and older
  • Care plan approach system
  • Involve the young person and offer a social care assessment at age 18
227
Q

What is the 1st line for Autism SD challenging behaviour?

A
  • Psychosocial assessment (anticipate and reduce factors increasing risk of behaviour)
  • Reduce impairment in communication (consider visual aids)
  • co-existing physical disorders (otitis media)
  • co-exsisting mental health problems (ADHD,GAD)
  • physical environment (lighting, noise)
  • reduce unintentional reinforcement or behaviour that reinforces
228
Q

What is the 2nd line for Autism SD challenging behaviour?

A
  • Pharmacological - used if behaviour making psychosocial training ineffective:
  • Antipsychotic medication (review at 3-4 weeks; stop at 6 weeks if no clinical indication)
  • Melatonin for sleep difficulties
  • Methyphenidate (Ratilin) for attention difficulties
  • SSRIs for obsessional behaviours
229
Q

Symptoms and signs of Autism SD?

A
  1. Reciprocal social interaction: Autistic children are not interested in people; they appear aloof, tend to play alone, and lack the ability to ‘read’ emotional states in others. Attachments are impoverished, with-out mutuality or warmth; these children do not turn to parents for comfort. Eye contact may be odd, either avoidant or ‘looking through’ you.
  2. Communication abnormalities: Expressive speech and comprehension are delayed or minimal. Ideas are taken literally (concrete thinking). Gestures are usually absent (e.g. pointing, waving goodbye). Later, speech may consist of monologues, interminable questions, or echolalia (repeating what has been said), but there is no exchange. Classically ‘I’ and ‘me’ are confused with ‘you’, ‘he’, and ‘she’ (pronominal reversal)
  3. Restricted behaviours and routine: Autism is characterised by repetitive, stereotyped behaviours and restricted interests—rather than imaginative play. Even small changes in routine (e.g. the wrong spoon) can result in intense tantrums.
230
Q

Differential diagnosis for Autism SD?

A
  1. Deafness causes poor language acquisition.
  2. Asperger’s syndrome
  3. Specific language disorder: delayed speech but normal IQ and social ability.
  4. Learning disability: IQ problems but relatively intact social skills.
  5. Rare disorders, e.g. childhood schizophrenia, Rett’ss syndrome.
  6. Neglect can lead to language delay and poor socialization—reversible unless severe
231
Q

Investigations for Autism SD?

A
  1. Hearing tests.
  2. Speech and language assessment.
  3. Neuropsychological testing—assess IQ and confirm diagnosis.
232
Q

Management of Autism SD?

A
  1. Support and advice for families, e.g. the National Autistic Society.
  2. Behaviour therapy —reinforce positive behaviours
  3. Speech and language therapy.
  4. Special education.
  5. Treat comorbid problems (e.g. epilepsy).
  6. Antipsychotics or mood stabilizers are occasionally used for extreme aggression or hyperactivity.
233
Q

Prognosis of Autism SD?

A

Only 1–2% of adults gain full independence, with most needing lifelong support and care. Good prognostic indicators are an IQ over 70 and acquisition of some useful language

234
Q

What is aspergers?

A
  • An autistic spectrum disorder.
  • Male:female = 8:1.
  • Poor social skills and restricted interests.
  • Normal language and IQ.
  • Tendency to literal interpretation of language and difficulty in reading social cues.
  • Management: advice, support, routine, social skills training.
  • Prognosis is much better than for autism.
235
Q

What is Tic disorder?

A

Tics are repetitive, involuntary, and purposeless movements or vocal utterances. They are categorised as simple(e.g. blinking, throat-clearing) or complex (e.g. self-hitting, swearing). Transient simple tics affect 10% of children, and are three times more common in boys.There is often a family history of problems and obsessive–compulsive disorder is commonly comorbid. Stress or stimulant medications usually worsen tics. They recede when the sufferer is concentrating on something else.Tics can be voluntarily suppressed at the cost of internal tension, which is relieved by their expression. Reassurance and stress management are effective treatments but clonidine (adrenergic agonist) or haloperidol(antipsychotic) are also useful.

236
Q

What is ADHD?

A

A type of hyperkinetic disorder (HKD) defined as persistent and severe impairment of psychological development

237
Q

What is ICD-10 criteria for ADHD?

A

Impaired attention and overactivity:

  • Impaired attention –> lack of persistent task involvement and quick moving on from incomplete tasks
  • Overactivity –> characterised by restlessness, talkativeness, noisiness and fidgeting
  • Impulsivity

Present prior to 6 years of age, and of long duration (6 months)

Impairment present in 2 or more settings (home, classroom, clinic)

Exclude organic causes

238
Q

Aetiology of ADHD?

A
  • Dysfunction of brain neurone circuitry that rely on dopamine as a NT which control self-monitoring/regulation
  • 3:1 boys vs girls
  • prevalence 2.5% (double of ASD)
239
Q

Risk factors of ADHD?

A
  • Family history
  • prematurity
  • LBW
  • FAS
  • conduct/mood disorder
  • ASD
  • LD
240
Q

Investigations for ADHD?

A
  • Assess social/educational impact in context of age
  • Rating scales –> cannot provide a diagnosis :
    Conners comprehensive behaviour rating scale (age 6-18)
    Strengths and difficulties questionnaire
241
Q

Management of ADHD?

A

MDT focussed

242
Q

Who is in the ADHD management?

A
  • Paediatrician
  • Psychiatrist
  • ADHD SNs
  • Mental health and learning disability trust
  • CAMHS
  • parent groups
  • social care workers
  • social/college and school nurses
243
Q

Prognosis of ADHD?

A

Manifestation of ADHD will change as child gets older:

  • hyperactivity tends to becomes less of a problem
  • inattention becomes more pronounced as the task they face become more complex

Outcome:

  • some may grow out of it
  • 90% get conduct disorder if untreated
  • 15% have ADHD as an adult
244
Q

Dietary advice for ADHD?

A
  • not particularly evidence based
  • importance of balance diet and regular exercise
  • explore foods that seem to influence behaviour (recommend keeping a food diary)
  • dietician referral if relationship with certain foods is observed in the dairy
245
Q

Monitoring medication in ADHD?

A

▪ Baseline height, weight, HR, BPand ECG
▪ Monitor:
• Response with symptom rating scales (e.g. Conner’s)
• Development of tics after taking stimulant medication
• Sexual dysfunction, seizures, sleep disturbance and worsening behaviour
▪ Measure weight (BMI for adults) every 3 months (<10yo) or 6months (>10yo)
▪Measure height , HR and BP every 6 months (may suppress appetite and cause growth impairment)
• Include plotting on a growth chart
• If interruptions to growth → referral and a planned break to allow catch-up growth

246
Q

1st line treatment for ADHD?

A

1st line in all cases if there is a negative impact on child’s/young person’s development of family life:
▪ Consider period of watchful waiting for up to 10weeks (self-help, simple behavioural management)
▪ Group-based ADHD-focused support for parents
▪ Refer to specialist if severe symptoms of >10w

247
Q

Treatment of ADHD for children younger than 5 years after a 10 week watch and wait?

A

▪ 1st line: offer ADHD-focused group parent-training programme to parents and carers
• 10-16 meetings in a group of 10-12 participants
• Education on ADHD, parenting strategies, environmental changes
▪ 2nd line: specialist service referral

248
Q

Treatment of ADHD for children greater than 5 years after a 10w watch and wait?

A

▪ 1st line: offer ADHD-focused group parent-training programme to parents and carers
• 10-16 meetings in a group of 10-12 participants
• Education on ADHD, parenting strategies, environmental changes

▪ 2nd line: specialist service referral and medications if ADHD persists:
• 1st line (6 weeks) = methylphenidate → trial for 6 weeks
o Pharmacokinetics: CNS stimulant (DA, NA reuptake inhibitor)
o SEs: abdominal pain, nausea, dyspepsia
• 2nd line (monitor SEs) = lisdexamphetamine → 3rd line if side effects
• 3rd line = dexamphetamine
• 4th line = atomoxetine (NARI) or guanfacine

• Side effects:

  • Loss of appetite
  • Palpitations
  • Mood changes
  • Tics

▪ 3rd line: CBT if problems in social skills, self-control, active listening, dealing with
expressing feelings

▪ Other medications:
• Clonidine → sleep disturbance, rages or tics
• Antipsychotics→aggression and irritability

249
Q

Symptoms of ADHD?

A
  • Hyperactivity
    Children are boisterous with excessive energy. They seem constantly on the move: running, jumping, climb-ing, unable to sit still for any length of time without fidgeting, squirming, or wandering about. They are usually noisy and garrulous.

-Inattention
Children are distractible and unable to concentrate, flitting chaotically between activities and leaving tasks unfinished.

-Associated features.
These children are impulsive and reckless, rarely stopping to consider the consequences of their actions. This can result in risky behaviour, e.g. poor road safety. They tend to be clumsy and accident prone, and may be dis-obedient, although often through impulsivity rather than deliberate naughtiness. Additionally, they are socially disinhibited, paying little attention to normal social conventions; they interrupt others and find it hard to wait their turn. Learning disability and conduct disorder are associated.

250
Q

Differentials for ADHD?

A
  1. Depression/anxiety—both can cause agitation.
  2. Mania (extremely rare in childhood).
  3. Conduct disorder
251
Q

Management of ADHD?

A
  1. Family: education on ADHD; advice on parenting and boundaries.
  2. Behavioural management
  3. Support for teachers: appropriate schooling placement.
  4. Family therapy.
  5. Stimulant medication (e.g. methylphenidate, dexamphetamine). This increases monoamine pathway activity, improving concentration and allowing learning and maturation. Adverse effects include appetite suppression and insomnia. ‘Drug holidays’ (weekends and school holidays) limit growth retardation to 1cm. Stimulant medications are not addictive in ADHD
252
Q

What is conduct disorder?

A

Behaviour is persistently antisocial, not merely ‘rebellious’,e.g. bullying, stealing, fighting, fire-setting, truancy, and cruelty to animals or people. In socialized CD the child has a peer group (often sharing in the antisocial behaviour). Children with unsocialized CD are rejected by other children, which often makes them more isolated and hostile.

253
Q

Differential diagnosis of Conduct disorder?

A
  1. Oppositional defiant disorder: a milder form of CD, occurring in children under 10, with provocative, angry, and disobedient behaviour towards adults. No extreme antisocial behaviour is present.
  2. ADHD
  3. Depression: some children present with antisocial behaviour.
254
Q

Management of conduct disorder?

A
  1. Family education: the family members need to understand CD and recognize that they may reinforce problems.
  2. Parent management training: teaches parents to reward good behaviour and deal constructively with negative behaviours.
  3. Family therapy: the family meets with a skilled therapist to discuss current problems. They are helped to cooperate in problem solving.
  4. Educational support.
  5. Anger management for the child.
  6. Treat comorbid problems, e.g. ADHD.
255
Q

Prognosis of conduct disoder?

A

50% develop substance misuse disorder or dissocial personality disorder as adults.

256
Q

What is the definition of panic disorder?

A
  • recurrent attacks of severe anxiety, which is not restricted to any particular situation or set of circumstances and are therefore unpredictable
  • several within a month
  • relatively fine with minimal anxiety in between episodes
  • Panic disorder should not be a main diagnosis if a depressive disorder exists at the time attacks start
257
Q

What is another name of panic disorder?

A

Episodic paroxysmal anxiety

258
Q

What are the signs and symptoms of panic disorder?

A
  • described as 100% anxiety with accompanying physical symptoms
  • sudden onset, occur out of the blue, lasts less then 30 mins
  • alarming thoughts (i am going to die) provoke further panic until reassurance or engagement in ‘safety behaviour’ occurs (call ambulance, take aspirin)
  • palpitations
  • chest tightness
  • choking sensation
  • pins and needles
  • depersonalisation
  • shaking
  • dizziness/faints
  • sweating
259
Q

Management of panic disorder?

A
  • Education, reassurance and self-help

Step 1: low intensity psychological intervention

  • self help (individual, non-guided) 6 weeks
  • self help (individual, guided) 6 weeks with weekly therapist appointment

Step 2: high-intensity psychological intervention with or without medication
1st line: CBT and SSRI (citalopram)
2nd line: after 12 weeks change class to TCA (imipramine) or add BDZ (not exceeding 2-4 weeks)
Psychodynamic psychotherapy

Step 3: refer to psychiatry

260
Q

Prognosis of panic disorder:

A

65% achieve complete remission

10-20% continue to have significant symptoms

261
Q

What is the ICD-10 definition of specific phobia?

A

Phobias restricted to highly specific situation such as proximity to slugs or snails

262
Q

Signs or symptoms of specific phobias?

A
  • Contact can evoke panic
  • May have a family history of this phobia
  • most phobias lead to tachycardia, but blood or injury phobia cause an initial tachycardia followed y vasovagal bradycardia and hypotension –> may cause nausea and fainting
263
Q

Management of specific phobia?

A
  • Education, reassurance and self help
  • Exposure response prevention (ERP): exposing someone to maximal fear until the fear becomes extinct - all at once
  • Relaxation therapy and breathing techniques
  • Short-term BDZ for certain specific phobias (never long term)
264
Q

What is ICD definition of social phobias?

A
  • Fear scrutiny by other people leading to avoidance of social situation
  • Associations: low self esteem and fear of criticism
  • Male and female equally affected
265
Q

Differentials of social phobia?

A
  • Shyness
  • Agoraphobia - need to escape more important
  • Anxious personality disorder - lifelong
  • ASD/Aspergers - awkward when relaxed
  • Schizo - delusions/paranoia
266
Q

Signs and symptoms of social phobia?

A
  • Complaints of blushing, hand tremor, nausea or urinary urgency in social situations (explore situations)
  • Self-medicate with alcohol or drugs (to desentise)
  • Panic attacks

NB. Will tolerate anonymous crowds, unlike agoraphobics, but smaller groups may spike anxiety

267
Q

Management of social phobia?

A
  • Education, reassurance and self-help
  • Exposure response prevention (ERP)
  • CBT
  • SSRIs
268
Q

What do specific phobias not respond well to?

A

They do not respond well to antidepressants. Most people just tend to avoid the situation.

269
Q

What is the seriousness of a phobia related to?

A

Related to the level of disability.

270
Q

Which phobias have the biggest impact on life?

A

Social phobias and agoraphobia

271
Q

What is the ICD-10 definition of agoraphobia?

A
  • A fairly well defined cluster of phobias embracing fears of leaving home, entering shops, crowds and public places, or travelling alone in trains, buses or planes
272
Q

What is agoraphobia classified with?

A

With or without a panic disorder

273
Q

What is uniting fear?

A

Inability to escape to safe place –> overwhelming urge to return home to safety

274
Q

What are problem situations of agoraphobia?

A 
travelling 
queueing 
supermarkets
crowds
parks
275
Q

Do all agoraphobics have anxiety?

A

Some may have little anxiety as they can avoid specific triggers well.

276
Q

What is the age of onset of agoraphobia?

A

20-35 year olds

Gradual or precipitated by a panic attack

277
Q

What are the signs and symptoms of agoraphobia?

A
  • Panic attacks

- Avoidance of phobic situations with or without isolation behaviour

278
Q

What are associated features of agoraphobia?

A
  • Depressive/obsessional symptoms

- Social phobias

279
Q

Management of agoraphobia?

A
  • Education, reassurance and self-help
  • Exposure response prevention (ERP)

Therapy: Desensitisation approach

(1) : patient identifies goal and constructs hierarchy of feared situations
(2) patient tackles hierarchy from least to most frightening
(3) aim to stay in situation until anxiety subsidised –> challenges existing thoughts

CBT: reduce patient’s expectation of threat, and behaviours that maintain threat-related beliefs

  • explore the actual likelihood and impact of the anticipated catastrophe
  • test the feared situation and their belief in a catastrophic outcome using behavioural experiments
  • improves self confidence of the patient
280
Q

What is the DSM-V definition of generalised anxiety disorder?

A
  • At least 6 months of excessive, difficult to control worry about everyday issues, that is disproportionate to any inherent risk, and causes distress or impairment - worry not due to mental disorder, substance abuse or other conditions.
281
Q

What is the duration of GAD?

A

at least 6 months

282
Q

What are the symptoms of GAD?

A

At least 3 of the following most of the time:

  • restlessness/nervousness
  • irritability
  • being easily fatigued
  • muscle tension
  • poor concentration
  • sleep disturbance
283
Q

Risk factors of GAD?

A
  • Divorced
  • Lone parents
  • Living alone
  • 35-54 y/o
284
Q

Protective factors of GAD?

A
  • 16-24
  • married
  • cohabiting
285
Q

Key features of GAD?

A

Defining feature: free floating anxiety, no specific threat, >6 months

Symptoms: psychological and physical

Coping mechanisms: avoidance, alcohol, drugs and depression

286
Q

Investigations of GAD?

A
  • GAD-7 questionnaire (5=mild, 10=moderate and 15=severe)
  • Becks anxiety inventory
  • Hospital anxiety and depression scale (HADS)
287
Q

Management of GAD?

A

Based on assessed severity and a stepwise approach:

Step 1: written information on GAD + active monitoring + regular exercise

Step 2: Low intensity psychological interventions
psychological intervention
- self help (individual, non-guided) 6 weeks
- self help (individual, guided) 6 weeks with weekly therapist appointment
- psychoeducational groups, 6 weeks and less than 12 per groups

Step 3:
(a) high intensity psychological interventions
CBT: 12-15 weeks, 16-20 hours a week
- testing the predictions of worry with behavioural experiments
- looking further into errors of thinking
Applied relaxation: 12-15 weeks

(b) medications stepwise:
Step 1: SSRI (NICE=setraline; only SSRI licensed=paroxetine)
- weekly follow up due to increased risk of suicidal thinking/self harm initially
Step 2: different SSRI after 8 weeks of step 1
Step 3: SSRI –> SNRI (venlafaxine)
- weekly follow up due to increased risk of suicidal thinking/self harm initially
Step 4: Pregabalin (antiepileptic)
Step 5: quetiapine (atypical antipsychotic)

Adjunct: propanolol (physical symptoms) –> never give BDZ to people with anxiety

288
Q

What is the aetiology of stress reaction disorders?

A

Genetics - unknown genes
Neurochemical - dysregulated serotonin, NA, GABA
Early experiences/life events - threatening events
Behavioural/cognitive theories - conditioning, negative reinforcement, cognitive theory (worrying NATs repeated), attachment theory (insecure as a child –> anxiety

289
Q

Signs and symptoms of stress reaction disorders?

A

Autonomic arousal

Psychological - worries, insomnia, night terrors
Motor - restlessness
Neuromuscular - tremor, tension headache
Gastro - dry mouth, nausea, flatulence
Cardio - palpitations
Resp - tight chest, dysponoea
Genitourinary - urinary frequency, erectile dysfunction

290
Q

Investigations of stress reaction disorder?

A

History and physical exam - focus on social and occupational history to gauge effect on QoL

S - symptoms of anxiety 
E - episodic or continuous
D - drink and drugs
A - avoidance and escape
T - timing anf triggers
E - effect on life 
D - depression

Collateral history

291
Q

What are the rating scales of stress reaction disorder?

A
  • Becks anxiety inventory

- Hospital anxiety and depression scale (HADS)

292
Q

Management of stress reaction disorder?

A
  • Education, reassurance and self-help: all anxiety disorders
  • Exposure therapy: phobias
  • CBT: GAD, phobias, panic disorder, OCD
  • SSRIs: GAD, phobia, panic disorder, OCD
293
Q

What does SSRIs initially cause?

A

Starting or suddenly stopping SSRIs cause anxiety symptoms for a short while

294
Q

What is the ICD-10 definition of OCD?

A

Recurrent obsessional thoughts or compulsive acts

  • obsessional thoughts and/or compulsive acts, present on most days for >2 consecutive weeks
  • must be a source of stress plus/minus interfere with ADLS
295
Q

What are obsessions?

A

Involuntary thoughts, images, impulses which are:

  • self-recognised as a product of own mind
  • > 1 thought or act resisted unsuccessfully
  • thoughts of carrying out the act are not pleasureable
  • thoughts must be unpleasantly repetitive
  • themed commonly (contamination, aggression, infection, sex, religion)
  • egodystonic (themes/ideas against that which the personal associates with their ego)
296
Q

What are compulsions

A

Repetitive mental operations or physical acts:

  • Compelled to perform in response to own obsessions or irrationally defined rules
  • Performed to reduce anxiety through irrational belief they will prevent a dreaded event
297
Q

Differential diagnosis for OCD?

A

Obsessions and compulsions:

  • Body dysmorphic disorder (appearance peroccupation)
  • Anankastic personality disorder (lifelong personality - rigid, orderliness, hygienic)

Mainly obsessions:

  • depressive disorder (Beck’s -ve triad, 50% OCD co-morbid)
  • Other anxiety disorders
  • Hypochondrial disease
  • Schizo

Mainly compulsions:
- Habit and impulse control disease

298
Q

How to differentiate depression from OCD?

A

If symptoms develop together, prioritise what developed first
If unknown, depression priority

299
Q

Aetiology of OCD?

A

1% M>F
70% <25 yo

Biological:

  • Genetics: relatives = 3x increased risk
  • Neurological: Basal ganglia implicated and affected by Sydenham’s chorea, encephalitis lethergica and tourette’s syndrome
  • Infection: streptococcal; throat –> anti-BG ABs

Psychosocial:
- Personality: 25% have premorbid anankastic personality (rigid, orderliness)

300
Q

Signs and symptoms of OCD/

A
  • Obsessional thoughts
  • Compulsions (rituals repeated over and over):
    = tension/discomfort ofter neutralised by compulsion (these are not inherently enjoyable)
    = find out how many times a day
    = find out how many times a day they get these and how often they do it for
  • Anxiety (which gets worse then longer they ignore the compulsion)
301
Q

Investigations for OCD?

A

Bloods: FBC, TSH
Rating scale: Yale-Brown OCD scale
OCD screening questions:
- Do you wash and clean a lot?
- Do you check the time a lot?
- Is there any thought that keeps bothering you that you would like to get rid of?
- Do your daily activities take a long time to finish?
- Are you concerned about putting things in a special order or are you very upset by a mess?
- Do these problems trouble you?

302
Q

Prognosis of OCD?

A
  • 25% significantly improve
  • 50% have moderate improvement
  • 25% have chronic or worsening symptoms
  • Co-morbid depression is common (50%)
303
Q

4 phases of cognitive therapy for OCD?

A
  • Relabel
  • Reattribute
  • Refocus
  • Revalue
304
Q

Management of OCD for mild functional impairment?

A

CBT with ERP (exposure and response prevention)

Background: CBT aims to prevent compulsive behaviour as a tool to reduce obsessions allowing the tolerated anxiety to be habituated and eventually, extinguished

Therapy: ERP=gradual/graded approach

(1) Pt supported to (ie) touch something dirty and, instead of immediately washing hands, is supported and talks the experience through with the therapist
(2) pt constructs hierarchy of feared situations and works through them

305
Q

Management of OCD for moderate functional impairment?

A
  • Intensive CBT with ERP
  • SSRI (continue for 12 months after remission)
  • Depression –> 20mg
  • Anxiety –> 40mg
  • OCD, BM –> 60 or 80 g

Fluoxetine > setraline

After 12 weeks of SSRI: TCA (Clomipramine) or alternative SSRI

306
Q

Management of OCD for severe functional impairment?

A

Referral

307
Q

What is substance abuse?

A

A pattern of substance use causing physical, mental, social or occupational dysfunction

308
Q

How does ICD-10 define subtance abuse?

A

(1) the substance

(2) the type of disorder

309
Q

What is acute intoxication?

A

Transient state of emotional & behavioural change after psychoactive substance (PS) use

  • Dose dependent
  • Time limited
310
Q

What is harmful use?

A

a pattern of use likely to cause physical or psychological damage

311
Q

What is dependancy?

A

a cluster of physiological, behavioural and cognitive symptoms in which the use of a substance takes on a much higher priority than other behaviours that once had a greater value (ICD-10)

312
Q

What is withdrawal?

A

transient state occurring while re-adjusting to lower levels of a drug in the body

313
Q

What is a psychotic disorder?

A

psychotic symptoms occurring during or immediately after PS use, characterised by vivid hallucinations, abnormal affect, psychomotor disturbances, persecutory delusions and delusions of reference

314
Q

What is amnesic disorder?

A

memory and other cognitive impairments caused by substance use (i.e. Wernicke’s)

315
Q

What is residual and late onset psychotic disorders?

A

where effects on behaviour, affect, personality or cognition lasting beyond the period during which direct PS effect might be expected

316
Q

M:F ratio in alcohol and substance misuse disorders?

A

Alcohol: 2:1

Substance misuse: 4:1

317
Q

Substance history components?

A
  1. Current use:
    a. T (Type)
    b. R (Route)
    c. A (Amount)
    d. P (Pattern)
  2. Current use:
    a. Dependency
    b. Effect on life
  3. Past use
  4. Future use
318
Q

What are the dependance theories?

A
  • Classical conditioning – association (i.e. seeing a needle –> craving heroin)
  • Operant conditioning – rewarding behaviours are repeated (i.e. drug provide pleasure) and behaviours that relieve unpleasant experiences are repeated
  • Social learning theory – we copy behaviour of others (i.e. Vietnam Heroin use)
  • Activation of dopaminergic reward centres:
    •Block DA re-uptake – cocaine, amphetamines
    •Increase DA and other NTs – alcohol, opiates
  • Blunted reward system deficiency
319
Q

What is the ICD-10 definition of BPAD?

A

> /= 2 episodes, 1 must be manic associates (hypomania, mania, mixed and the other depressive) AND

  • mania lasts around 4 m
  • depression lasts about 6m

Complete recovery between episodes

320
Q

What are the signs and symptoms of BPAD?

A

Mania is more associated with irritability than elevated mood

Appearance and behaviour - excitable, irritable, distracted, inappropriate clothing
Speech - pressured –> mutism (in extreme cases)
Emotion (mood and affect) - increased self-esteem, grandiose, labile mood, insomnia, loss of inhibition, increased appetite
Perception (hallucinations and delusions) - grandiose delusions, paranoia, catatonic stupour
Thought (form, content, possession) - flight of ideas, racing thought, over-optimism, suicidal ideas, 1st rank symptoms
Insight - minimal –> reckless behaviour
Cognition - Nil impact

Decreased need for sleep and food
Increased libido

321
Q

What is mania?

A

A distinct period of abnormally and persistently elevated, expansive or irritable mood with > 3 characteristics of mania, lasting at least 7 days

  • impact occupational/social functioning +/- psychosis
  • 1st rank symptoms are not likely to persist past the acute episode
322
Q

What is hypomania?

A

> 3 characteristic symptoms of mania lasting >/= 4 days

  • no impact on occupational/social functioning
  • no psychosis or delusions
  • slightly less exaggerated mania symptoms
323
Q

What is mixed mania?

A
  • Mixture of rapid alternation (within a few hours) of manic/hypomania and depressive symptoms
324
Q

What is Type 1 BPAD?

A

Manic episodes interspersed with depressive episodes

325
Q

What is Type 2 BPAD?

A

Recurrent depressive episodes with less prominent hypomanic episodes

326
Q

What is rapid cycling BPAD?

A

> /= 4 episodes a year cycling between mania and depression (responds well to sodium valproate)

327
Q

What is the aetiology and risk factors of BPAD?

A
  • Genetic - 1st degree relative to 7x increase risk
  • Anatomical - decreased grey matter mass in emotional regulation areas, increased ventral limbic area activity
  • Transmitters - Increased NA, DA, serotonin trigger mania
  • Stressful life events
328
Q

What are the differential diagnosis of BPAD?

A

Organic - drugs, dementia, frontal lobe disease, delirium, cerebral HIV, Myoxedema Madness

  • Schizo/schizoaffective disorder
  • Puerperal disorders
  • Cyclothymia (persistent mild mood instability - never sufficiently severe to BPAD/depression)
329
Q

What is the management for BPAD?

A

Refer to specialist care for diagnosis (urgent or non-urgent) as cannot be diagnosed in primary care:

Referral options:

  • symptoms of hypomania –> routine referral to CMHT
  • symptoms of mania or severe depression –> urgent referral to CMHT / admission to psych ward
330
Q

What is the management of acute BPAD?

A

Acute mania or hypomania management:

  • gradually taper off and stop inducing medications (eg. SSRI)
  • Monitor fluid/food intake
  • Sedation may be required (clozepam, lorazepam)
  • ECT only if mania is not responsive to treatment

If not on treatment aim to stabilise them before starting lithium:

  • 1st line: antipsychotic (olanzapine > haloperidol, quetiapine, risperidone)
  • 2nd line: different antipsychotic (switch to different antipsychotic from list above)
  • 3rd line: add lithium or sodium valproate (lithium is not as effective acutely and you might need higher doses and risk toxicity)

If on treatment:

  • Optimise medication / stop antidepressants
  • Check compliance
  • Check lithium levels –> add atypical
  • Short term sedative (benzos)
331
Q

What is the long term management of BPAD?

A

4 weeks after the acute episode:

  • 1st: Lithium alone (monitor lithium toxicity and may take 5 weeks to titre correctly)
  • Lithium not effective: Lithium + Valproate (Valproate no monitoring)
  • Lithium poorly tolerated –> Valproate alone or Olanzapine alone
332
Q

What is the SEs of Vaproate?

A
  • Hair loss
  • Weight gain
  • Nausea
333
Q

What is the SEs of Valproate?

A
  • Hair loss
  • Weight gain
  • Nausea
334
Q

What is the management of BPAD with co-existence depression?

A

You cannot use antidepressants by themselves as they may cause a switch to mania. To reduce the risk, only give antidepressants with mood stabilisers or antipsychotics:
1st line: Fluoxetine and olanzepine
2nd line: Quetiapine alone
3rd line: Olanzapine or Lamotrigine ALONE

If presenting in a manic episode on any antidepressants –> taper and stop them

335
Q

What is the psychological therapy for BPAD?

A

Indications and purpose:

  • May improve compliance with medications long term
  • Offered after the acute manic event has resolves

CBT: test excessively positive thoughts and gain a sense of perspective

  • identify relapse indicators
  • Create relapse prevention strategies (developing routine, ensuring good-quality sleep, promoting a healthy lifestyle, avoiding excessive stimulation/stress, addressing substance misuse, ensuring drug compliance)
  • Pyschodynamic psychotherapy
336
Q

What are the social interventions for BPAD?

A

Can aid return to education and/or work

- Family support and therapy

337
Q

What is the prognosis for BPAD?

A
  • Manic episodes begin abruptly and are often shorter than depressive episodes
  • Recovery is usually complete between episodes
  • Remissions become shorter with are and depressions become more frequent
  • 15% with BPAD will commit suicide (lithium reduces this to same levels as general population)
338
Q

What is unipolar affective disorder and bipolar affective disorder?

A
  • Recurrent episodes of depression

- Recurrent episodes of mania and depression

339
Q

What are the core signs and symptoms of depression?

A
  • low mood
  • anhedonia
  • anergia
340
Q

What are adjunct symptoms of depression and when do you ask them?

A

Ask when core symptoms >/= 1 present for most days, most of the time, for at least 2 weeks

F - Fatigue (anergia)
I - Insomnia/early waking
C - Poor concentration
A - Increased or decreased appetite/weight
S - Suicidal thoughts or acts
A - Agitation or slowing of movements
G - Guilt or self -blame
341
Q

What medications might cause depression?

A
  • Steroids
  • COCP
  • Beta-blockers
  • Statins
  • Ranitidine
  • Retinoids (isotretinoin)
  • HIV meds
342
Q

What is the sub-threshold/dysthymia severity of depression?

A

Between 2 and 5 symptoms

For at least 2 years

343
Q

What is the mild severity of depression?

A

Around 5 or more symptoms

Mild functional impairment

344
Q

What is the moderate severity of depression?

A

Around 5 or more symptoms

Mild through to severe functional impairment

345
Q

What is the severe severity of depression?

A

Most symptoms

Severe functional impairments and can have psychotic symptoms

346
Q

What are the subtypes of depression?

A
  1. Seasonal affective disorder - episodes of depression, recur annually at the same time with remission in between
  2. Atypical depression - somatic symptoms (weight gain, hypersomnia)
  3. Anxiety-induced insomnia - increased sleep + eating = increased mood
  4. Agitated depression - psychomotor agitation instead of retardation
  5. Depressive stupor - psychomotor retardation so bad that they grind to a halt
347
Q

What monoamines are involved in depression?

A

NA - mood and energy
5-HT - sleep, appetite, memory, mood
DA - psychomotor activity, reward

348
Q

What is the aetiology of depression?

A

Very common, 16.8%

Females 2x more common than males

349
Q

What investigations are useful for diagnosing depression?

A
  • Full history (check for mood elevation)
  • Collateral history
  • Physical exam
  • MSE
  • Bloods: FBC (anaemia), LFTs (hypothyroid), glucose/HBA1C (diabetes)
  • Rating scale: PHQ9, HADS, BID-II (adults) or CDI (children) - EPDS (pregnancy)
350
Q

What are the differentials for depression?

A
  1. Physical - hyperthyroid, head injury, quiet delirium
  2. Adjustment disorder - mild affective symptoms following life events –> do not reach the severity of depression
  3. Bereavement - normal grief for <6months (look for numbness, pining, depression and recovery)
  4. BPAD, schizoaffective disorder, schizo - previous mania or psychotic episodes
  5. Substances withdrawal
  6. Postnatal depression/puerperal illness
  7. Dementia - depression may mimic dementia, but dementia can start with affective disorders. (global memory loss in severe depression can cause pseudodementia and has a quicker onset, short-term memory loss in alzheimers)
351
Q

What is the management of depression in children and young people for mild depression?

A

Treated in primary care:
1st line:
- Watchful waiting (for 2 weeks, and follow-up)
- Self help (mind.org, youngminds.org)
- Lifestyle advice (ie. sleep hygiene, diet, exercise)

2nd line:
- CBT (digital or group)

Needs no net (2-3m) –> referral to CAMHS

352
Q

What is the management of depression in children and young people for moderate to severe depression?

A

Treated in CAMHS:

5-11 years: psychological intervention:

  • family-based IPT (interpersonal therapy) or
  • Family therapy OR
  • Individual CBT

12-18 years: psychological intervention
- Individual CBT

Needs not met –> family therapy, IPT-A (adolescents), psychodynamic psychotherapy

353
Q

What is the management of depression in children and young people for depression unresponsive to treatment?

A

Treated in CAMHS:

- Intensive psychological therapy

354
Q

What is the management of depression in adults?

A

CHECK SUICIDE RISK:

  • suicidal act or intent
  • risk factors: young male, occupation (doctor, vet), live alone, mental illness, unmarried

Step 1:

  • Indications: initial suspected depression, subthreshold symptoms
  • watchful waiting with follow up in 2 weeks
  • Education - sleep hygiene, self help, information, support (MIND UK, depression UK)

Step 2:

  • Indications: presistant subtreshold symptoms, mild depression
  • Low intensity psychological interventions:
    1. Group CBT
    2. Computerised CBT (online material supported by trained practitioners to review progress, over 9-12 weeks including follow up)
    3. Guided self-help (written materials supported by trained practitioner to review progress, 6-8 sessions over 9-12 weeks including follow-up)
    4. Structured group (delivered in groups with support from a trained practitioner, 3 sessions per weeks over 10-14 weeks)
    5. Medications only if:
  • history of moderate to severe depression
  • sub-threshold depressive symptoms lasting >2 years
  • mild depression complicating care of chronic physical health problems

Step 3:

  • Indications: presistant subtreshold symptoms refractory to step 2, moderate depression
  • High-intensity psychosocial interventions:
    1. Individual CBT - 16-20 sessions over 3-4months (talking therapy based on idea that thoughts, mood and behaviour intertwined)
    2. Interpersonal therapy / IPT - 16-20 sessions over 3-4months and IPT > CBT if due to death (identifies how interactions with others are affecting the patients mood and ways of improving these interactions)

Medications: (and regular review every 2 weeks for 3 months or every week if suicidal)

Step 4:

  • Indications: severe depression, risk to life, neglect
  • High intensity psychosocial interventions
  • Medications –> ECT if necessary
355
Q

What is the management of a suicidal patient with depression?

A

Urgent referral to crisis team

356
Q

What are the 1st line medications for depression?

A

SSRI (setraline, citalopram, fluoxetine, paroxetine)

  • Setraline: stepped increase from 50mg to 200mg (50mg increase every 2 weeks, over 6 weeks)
  • 2 trails of SSRIs before moving to 2nd line
357
Q

What are the 2nd line medications for depression?

A

Taper down SSRI, switch to SNRI (venlafaxine, duloxetine)

  • Venlafaxine: stepped increase from 37.5mg BD –> 75mg BD –> 75mg morning / 150mg evening
  • SNRI pharmacology does not switch from SSRI effect to SNRI effect until reach max dose
358
Q

What are the 3rd line medications for depression?

A

Treatment resistance = augment treatment with

  • Antipsychotic (ie quetiapine 150-300mg)
  • Lithium (blood level of 0.4-0.8)
  • Other antidepressant (eg. mirtazapine or mianserin)
359
Q

What are the 4th line medications for depression?

A

ECT

360
Q

What are the common side effects of Mirtazapine?

A
  • Weight gain

- Increase sleep

361
Q

What are the common side effects of Setraline?

A
  • Smallest side effect profile

- For those with co-morbid conditions like IHD

362
Q

What is the indication for Fluoxetine?

A

Children

363
Q

What is the indication for Paroxetine?

A

Major depressive episode

364
Q

What is catch-up phenomena in depression?

A

Recover from depressive, treatment is subsequently stopped, and that person falls back into depression leads to a worse depression state than before

365
Q

What is seretonin syndrome?

A
  • Large seretonin increase in the body
  • Cause by SSRI or SNRI
  • increased mood change
  • restlessness
  • difficulty sleeping
  • unsteadiness
  • sweating
  • gastrointestinal symptoms: pain, cramping, diarrhoea, vomiting
  • paraesthesia
366
Q

What is psychotic depression

A

A severe form of depression with delusions and hallucinations

Cotard syndrome - a set of nihilistic delusions where the patient believes they are dead, and their body parts are rotting

367
Q

What is the difference of delusions in depression and schizophrenia?

A

“He wants to kill me with an axe” –> ask why

Psychotic depression = “the world is better off without me”

Schizo = “I have no idea, I got a message”

368
Q

Which is the best antidepressant to use in pregnant women?

A

None is specifically liscenced to be use in pregnancy but:

Paroxetine may have mild risk:
1st trimester = congenital heart defects
3rd trimester = persistant pulmonary hypertension

369
Q

How to deal with mild or moderate depression in pregnancy?

A

Encourage to taper down anti-depressants and switch to:

  • Mild: Facilitated self help
  • Moderate: CBT
370
Q

How to deal with severe depression in pregnancy?

A

Continue antidepressant or switch to a drug with lower risk of adverse effects

371
Q

What is delusional disorder?

A

Delusional disorder = persistent/life long delusions with few/no hallucinations
- <3 months = temporary; >/= 3 months = persistent

Cannot include:

  • clear auditory hallucinations
  • schizo symptoms (delusions of control, blunting of affect)
  • evidence of organic/bran/ disease

NOTE: occasional or transitory auditory hallucinations does NOT rule out the diagnosis

372
Q

What is the aetiology and risk factor of delusional disorder?

A
  • Old age
  • Social isolation
  • Group delusions
  • Low socioeconomic status
  • Immigration
  • Substance abuse
  • Permorbid personality disorder
  • FHx
  • Sensory impairment
  • Head injury
373
Q

What factor shows a better prognosis for delusional disorder?

A
  • Acute has a better diagnosis

- insidious has a worse diagnosis

374
Q

What are the biological reasons for delusional disorder?

A

Excess DA and ACh activity

  • Neurological lesions to the temporal lpobe, limbic system, BG
  • Cortical damage (persecutory delusions)
375
Q

What are the psychosocial reasons for delusional disorder?

A
  • Freud (delusions serve defensive functions)
  • Distrust, suspicion, jealousy, low self-esteem
  • Social isolation, seeing own defects in others
  • Rumination over meaning and motivation
376
Q

What is the MSE for delusional disorders?

A

A - Nil
S - Nil
E - Nil
P - Non-bizarre delusions, rarely hallucinations
T - Process unimpaired, content preoccupied, single theme of thoughts
I - Impaired (delusions affect thought and behaviour)
C - Intact

377
Q

What are the different forms or delusions?

A
  • Erotomaniac (excess sexual desire, often believe a VIP in love with them - De Clerembault’s syndrome)
  • Othello syndrome (believe partner is unfaithful)
  • Fergoli syndrome (>/= 2 people are same person changing disguises to deceive)
  • Folle a deux (shared delusions/hallucinations between people)
  • Factitious disorder (consciously pretending you have a medical illness)
378
Q

What are the investigations for delusional disorder?

A
  • Full history, collateral history + MSE

- Exclude organic causes

379
Q

What are the differentials for delusional disorder?

A
  • Substance-induced
  • Dementia + delirium
  • Hypochondriasis
  • Mood disorders with delusions
  • Body dysmorphia
  • Paranoid personality disorder
  • Schizo
  • OCD
380
Q

What is the management of delusional disorder?

A
  • Consider admission (if high risk to self, to other or from others)

Biological (limited evidence)

  • Antipsychotics (poor evidence)
  • SSRI (cover other potential missed differential)
  • BDZ (for anxiety)

Psychological:

  • Individual CBT
  • Psychoeducation

Social:

  • Social skills training
  • Psychoeducation
  • Family therapy
381
Q

What is acute psychosis?

A

Sudden onset psychosis (tend to lack insight), resolving in <3 months

382
Q

What are the signs and symptoms of acute psychosis?

A

Same as schizophrenia

383
Q

What are the investigations/differentials of acute psychosis?

A
  • Organic - demential or delirium
  • Substance misuse (steroids)
  • BPAD/depression
  • Schizo
  • Personality disorder
384
Q

What is the management of acute psychosis?

A

Bio:

  • Short term antipsychotic/BDZ eg. high dose olanzapine (acute behavioural disturbance)
  • Antidepressants/mood stabalisers useful to prevent relapse eg. low dose aripiprazole

Pycho:

  • Specific social issues
  • Reality - orientated, adaptive, supportive psychotherapy

Eg 1st line “start low, go slow”

  • Low dose aripiprazole
  • Education and support
385
Q

What can steroids cause?

A

Depression

Psychosis

386
Q

What is a better prognosis of acute psychosis?

A
  • Better prognosis if short interval between onset and full-blown symptoms
  • Better prognosis if perplexity or confusion, good premorbid social and occupational functioning, blunted affect
387
Q

What is schizoaffective disorder?

A

A group of disorders in which BOTH affective and schizo (psychotic) symptoms are prominent equally (50/50) but do not justify a full diagnosis of either schizo or depression/manic episodes

Manic type:

  • Both schizo and manic symptoms prominent (develop at the same time)
  • Single episode. or recurrent disorder (majority manic episodes)

Depressive type:

  • Both schizo and depressive symptoms prominent (develop at the same time)
  • Single episode. or recurrent disorder (majority depressive episodes)
388
Q

What is the duration of schizoaffective disorder?

A
  • Psychotic states to persis for >/= 2 weeks without concurrent affective symptoms
  • Requires 2 episodes of psychosis:
    1. 1 episode lasting >2 weeks without mood disorder symptoms
    2. 1 episode requires obvious overlap of mood and psychotic symptoms
389
Q

What is the management of schizoaffective disorder?

A
  • Treat as per schizo (add a mood stabiliser if the affective component is not being controlled)

BPAD (mania + depression):

  • 1st line: fluoxetine (SSRI) + olanzapine (antipsychotic)
  • 2nd line: lamotragine
390
Q

What is schizo?

A

A severe mental illness characterised by disintegration of the process of thinking, of contact with reality, and of emotional responsiveness

  • Hallucinations - a perception in the absence of stimulus
  • Delusion - a fixed, false belief, held despite evidence to the contrary (not explained by the patient’s background)
391
Q

What are the signs and symptoms of schizo?

A

(A) >/= 1 Scheider’s 1st rank symptoms, >/= 1 month duration:

  • Delusions (false and fixed beliefs)
  • Passivity (delusions of control)
  • Thought disorders: thought insertion, thought withdrawal, thought broadcasting
  • Auditory disorder: thought echo, 3rd person voice, running commentary

OR

(B) >/=2 of the following:

  • Paranoid = persistent hallucinations in any modality
  • Hebephrenic = incoherent or irrelevant speech (neologisms, Knight’s move thinking)
  • Catatonic = catatonic behaviour (excitement, posturing, waxy flexibility, negativism, mutism, stupour)
  • Simple = negative symptoms (apathy, paucity of speech, blunted/incongruent emotional response)

AND

(C) Present, most of the time, >/= 1 month

AND

(D) Not causes by substance use or organic disease

392
Q

What is residual schizo?

A

Previous schizo (+ve & -ve S/S) –> just -ve symptoms

393
Q

What are the positive and negative symptoms of schizo?

A

+ve:

  • hallucinations
  • delusions
  • Due to excess domapines in the mesolimbic tracts
  • ve:
  • apathy
  • social withdrawal
  • due to declined dopamine in the mesocortical tracts
394
Q

What is the progression and clinical pattern or schizo?

A

Prodrome / At-risk mental state / ARM (negative symptoms dominant):

  • social withdrawal
  • loss of interest in work and relationships

Acute phase (positive symptoms dominant):

  • delusions
  • hallucinations
  • thought inteference

Chronic phase: (negative symptoms dominant):

  • apathy
  • blunted affect
  • social withdrawal
  • anhedonia
  • poverty of thought/speech
395
Q

What are the subtypes of schizo?

A

Paranoid:

  • most common
  • prominent delusions
  • prominent hallucinations

Hebephrenic/disorganised:

  • mainly focused on speech/thought
  • disorganised mood and speech
  • neologism, knights move thinking
  • inappropriate affect

Catatonia:

  • psychomotor disturbance
  • stupor, waxy flexibility (retain any shape you put into them), automatic obedience, forced grasping, opposition

Simple:

  • negative symptoms only
  • apathy
  • social withdrawal
396
Q

What is the aetiology of schizo?

A

1% of UK pop
M=F
15-45 y/o onset

397
Q

What are the investigations fro schizo?

A
  • Collateral history
  • Physical exam
  • Bloods (FBC, U&E, LFT, VDRL, 5-HIAA)
  • Urine (Drug screen and MSU)
  • MRI (hypofunction in the prefrontal cortex)
  • Rating scale - Brief Psychiatric Rating Scale
  • ADL Assessment and Housing and Finance
398
Q

What are the differentials of schizo?

A
  • Organic - substance misuse, demential, delirium, epilepsy, steroids, tumours
  • Acute/transient psychotic episodes
  • Mood disorder - depression and mania can cause psychotic symptoms
  • Schizo affective disorder - schizophrenic and affective symptoms develop together and are balanced
  • Persistent delusional disorder - only delusions
  • Schizotypal disorder - eccentricity with abnormal thoughts
399
Q

What is the management of schizo?

A

Urgent = crisis resolution team and home treatment team

Not-urgent = early intervention in psychosis team (>14 y/o, CAMHS can tx = 17 y/o)

  • psychosis is toxic, the longer a patient is psychotic, the more is will affect them
  • early treatment leads to a better prognosis
  • Aim to keep duration of untreated psychosis <3 months
  • Tx: antipsychotics, psychosocial interventions

Rapid tranq:

  • 1st line: Lorazepam (oral –> IM)
  • 2nd line: Haloperidol (5mg) + Lorazepam (1mg)
400
Q

When would you admit someone with schizo?

A
  • Suicide/homocide risk
  • Lack capacity
  • Significant medication changes
  • Severe symptoms
  • Failure of OPD (outpatient department) treatment
  • Address comorbid conditions
401
Q

What is the bio management of schizo?

A

1st line: (6 weeks, atypical antipyschotics, “start low, go slow”:

  • (LESS STRONG, LESS SIDE EFFECTS) Aripiprazole (initial akanthisia), quetiapine (sedation, weight gain)
  • (STRONGER, MORE SIDE EFFECTS) Olanzapine (weight gain), Risperidone (hyperprolactinemia, EPSEs, sedation)
  • 1st: low-dose aripirazole / high-dose olanzapine + education and support
  • Augmentation: BDZ (diazepam) if non-acute anxiety, Mood stabaliser (lithium) if schizoaffective disorder suspected
  • Non-compliance: once monthly IM depot injection (zuclophenthixol decanoate 200mg depot injection)

2nd line: (6 weeks, typical antipsychotics)

3rd line: (treatment resistance, clozapine)
- Failure to respond to >/2 antipsychotics, at least one if atypical, each given at a therapeutic dose for at least 6 weeks

402
Q

What is the psychological management of schizo?

A

1st line: CBT (offer to all patients, regardless of level of schizo)

  • at least 16 sessions
  • emphasis of testing reality

1st line: Family therapy (if needed, esp if young)

  • at least 10 sessions
  • to help control the highly expressed emotions of schizo (helps family cope)
403
Q

What is a good prognostic indicator for schizo?

A
  • Sudden onset, late
  • Stressful event
  • No FHx
  • Higher IQ
404
Q

What is a bad prognostic indicator for schizo?

A
  • Gradual onset, early
  • Lack of precipitant
  • FHx
  • Low IQ
405
Q

What is a bad prognostic indicator for schizo?

A
  • Gradual onset, early
  • Lack of precipitant
  • FHx
  • Low IQ
406
Q

What is the monitoring protocol for a patient with schizo?

A

Baseline measurements before starting an anti-psychotic:

  • Basic obs: weight, wast circ, pulse and BP
  • Bloods: FBC, U&E, LFTs, fasting BM, HbA1c, lipid profile, prolatin (more frequently in clozapine)
  • Assessment of any movement disorders
  • Assessment of nutritional status, diet and physical activity (CVD assessment)
  • ECG (if CVD risk present or recommended by the chosen medication)

Monitoring - there is a high risk of CVD in patients on schizo meds:

  • response to treatment and side-effects
  • emergence of movement disorders
  • adherence
  • overall physical health

Monitoring apps at:

1) 1,2,3,4,5,6 weeks = weight + waist
2) 12 weeks = weight, waist, HR, BP
3) Annual = weight, waist, HR, BP

Basic obs:

  • weight and waist circumference (weekly for 6 weeks, at 12 weeks, annual thereafter)
  • Pulse and BP (at 12 weeks, annual thereafter)
407
Q

What is huntingdon’s disease?

A

Autosomal dominant (50% chance of children inheriting the condition)

Onset 30-50 years old:
- Trinucleotide expansion disorder –> genetic anticipation = onset and severity may be younger and greater in successive generations

408
Q

What gene is affected in huntingdon’s disease?

A

HTT/huntingtin gene

409
Q

What are the signs and symptoms of huntingdon’s disease?

A

Picture: clumsy, speech difficulties

  • Movement: chorea, speech/swallowing, stumbling/clumsiness
  • Cognitive: organising tasks, flexibility, impulse control, learning new information, difficulty concentrating
  • Psychiatric: depression, irritablity/mood swings, suicide in 9% of cases, personality change
  • Lack of insight: they don’t care that anything is wrong - tends to indicate organic pathology
410
Q

What are the investigations for huntingdon’s disease?

A
  • Genetic analysis (HTT gene)

- MMSE may be normal

411
Q

What is the aetiology of frontotemporal dementia (inc. picks disease)?

A

Atrophy of fronto-temporal regions

  • early onset - 40-60 y/o
  • 60% sporadic, 40% autosomal inheritence
412
Q

What are the signs and symptoms of frontotemporal dementia (inc. picks disease)?

A

3 clinical presentation:

(1) frontotemporal dementia: frontal lobe syndrome (disinhibition, social/personality changes)
(2) Semantic dementia: progressive loss of understanding of verbal and visual meaning
(3) Progressive non-fluent aphasia: 1st, naming difficulties and 2nd, mutism

Memory tends to be affected much later unlike AD which is the first thing affected

413
Q

What are the investigations for frontotemporal dementia (inc. picks disease)?

A

1) Cognitive impairment:
- Screening –> AMTS (<7 suggest cognitive impairment), GPCOG (GP assessment of cognition)
- Detailed –> Addenbrooke’s (ACE-R - 100 questions, MMSE - not widely used, MoCA)

2) Dementia/delirium screen:
- TFTs (hypo –> cognitive decline)
- LFTs (Korsakoff’s)
- U&Es and dipstick (infection, diabetes)
- HbA1c (diabetes)
- Vitamin B12 and folate

Further tests:

  • Alzheimers: FDG-PET, CSF, MRI (grey matter atrophy, wide ventricles & sulci, temporal lobe atrophy)
  • Vascular: ECG (AF with emboli), MRI/CT
  • Lewy body: FP-CIP SPECT, I-MIBG
  • Frontotemporal: FDG-PET, perfusion SPECT, MRI (frontal lobe shrinkage)

Memory assessment clinical referral after GP:

  • Take collateral history and check bloods
  • Risk assess the patient
  • Cognitive assessment - MMSE
  • Brain scan (check organic pathology)
414
Q

What is the management of frontotemporal dementia (inc. picks disease)?

A

Biological:
- Antidepressants (treat frontal lobe syndrome)

Psychosocial:

  • Same as AD
  • OT, SALT, physiotherapy
415
Q

What is the prognosis of frontotemporal dementia (inc. picks disease)?

A

Death in 5-10 years

416
Q

What is the pathology of frontotemporal dementia (inc. picks disease)?

A

2 pathologies with no correlation to clinical presentation:

(1) Tau positive - Pick’s bodies (hyperphosphorylated tau) = Pick’s disease (3R), CBD (4R), PSP (4R)
(2) Tau negative - no Tau = FTLD-U (frontotemporal lobar dementia with Uniquinated inclusions)

417
Q

What is the aetiology of Vascular dementia?

A

Infarcts cause by thromboemboli or narrowing of arteries due to HTN

418
Q

What are the risk factors of Vascular dementia?

A

Same as CVD RFs:

  • Age
  • Male
  • Obesity
  • Lack of exercise
  • Smoking
  • AF
  • DM
  • HTN
  • CVA history (stroke, TIA)
419
Q

What are the signs and symptoms of Vascular dementia?

A
  • Sudden onset (may follow CVA), stepwise deterioration
    1st: emotional and minor changes (labile emotion - tearful –> elation)
    2nd: cognitive deficit
  • Focal neuro signs (S/S reflect site of infacrt)
  • Co-morbid depression
  • Relatively preserved personality
420
Q

What are the investigations of Vascular dementia?

A

1) Cognitive impairment:
- Screening –> AMTS (<7 suggest cognitive impairment), GPCOG (GP assessment of cognition)
- Detailed –> Addenbrooke’s (ACE-R - 100 questions, MMSE - not widely used, MoCA)

2) Dementia/delirium screen:
- TFTs (hypo –> cognitive decline)
- LFTs (Korsakoff’s)
- U&Es and dipstick (infection, diabetes)
- HbA1c (diabetes)
- Vitamin B12 and folate

Further tests:

  • Alzheimers: FDG-PET, CSF, MRI (grey matter atrophy, wide ventricles & sulci, temporal lobe atrophy)
  • Vascular: ECG (AF with emboli), MRI/CT
  • Lewy body: FP-CIP SPECT, I-MIBG
  • Frontotemporal: FDG-PET, perfusion SPECT, MRI (frontal lobe shrinkage)

Memory assessment clinical referral after GP:

  • Take collateral history and check bloods
  • Risk assess the patient
  • Cognitive assessment - AMTS/ACE-R
  • Brain scan (check organic pathology)
421
Q

What is the management of Vascular dementia?

A

Biological:

  • Daily aspirin (if indicated due to CVA/AF risk)
  • Reduce risk factors (exercise, less alcohol, treat HTN, stop smoking, treat AF, control DM)

Psychosocial:
- Same as AD

422
Q

What is the aetiology of Lewy body dementia (BLD)?

A
  • Lewy body = alpha-synclein with ubiquitin
  • Spectrum of diseases including Lewy bodies
    > In parkisons, LB are found in the brainstems
    > In LBD, LB are found in the brainstem, cingulate gyrus and neocortex
423
Q

What are the risk factors of Lewy body dementia (BLD)?

A
  • Age

- Unknown

424
Q

What are the signs and symptoms of Lewy body dementia (BLD)?

A

> /= 2 of 3, general gradual decline:

  • Fluctuating confusion with marked variations in alertness levels (has some lucid intervals unlike other dementias)
  • Vivid visual hallucinations (Lilliputin hallucinations) - animals or humans
  • Parkinsonims (shuffling gait, bradykinesia, rigidity, animia)
  • Frequent falls
  • Comorbid depression
425
Q

What are the investigations of Lewy body dementia (BLD)?

A

1) Cognitive impairment:
- Screening –> AMTS (<7 suggest cognitive impairment), GPCOG (GP assessment of cognition)
- Detailed –> Addenbrooke’s (ACE-R - 100 questions, MMSE - not widely used, MoCA)

2) Dementia/delirium screen:
- TFTs (hypo –> cognitive decline)
- LFTs (Korsakoff’s)
- U&Es and dipstick (infection, diabetes)
- HbA1c (diabetes)
- Vitamin B12 and folate

Further tests:

  • Alzheimers: FDG-PET, CSF, MRI (grey matter atrophy, wide ventricles & sulci, temporal lobe atrophy)
  • Vascular: ECG (AF with emboli), MRI/CT
  • Lewy body: FP-CIP SPECT, I-MIBG
  • Frontotemporal: FDG-PET, perfusion SPECT, MRI (frontal lobe shrinkage)

Memory assessment clinical referral after GP:

  • Take collateral history and check bloods
  • Risk assess the patient
  • Cognitive assessment - MMSE
  • Brain scan (check organic pathology)
426
Q

What is the management of Lewy body dementia (BLD)?

A

Bio:
1st line: Ach inhibitors (Donepezil or Rivistigmine)
- Do not offer antipsychotics (increased risk of cerebrocascular disease)

Psychosocial:
- Same as AD

427
Q

What is dementia?

A

Acquired, chronic, and progressive cognitive impairment, sufficient to impair ADLs

428
Q

What is the epidemiology of of demnetia?

A
  • <65 y/o = early onset dementia

- Alzheimers dementia (70%) > Vascular dementia > Lewy body dementia

429
Q

What are the signs and symptoms of general dementia?

A

1st: forgetfulness (stepwise or progressive)
2nd: Disorientation (time –> place –> person)
- wandering
- delusions
- calling out
- sleep-disturbance
- hallucinations
- inappropriate behaviour/aggression

430
Q

What is BPAD?

A

Behaviour and psychological symptoms of dementia

1) Mood changes
2) Abnormal behaviour
3) Hallucinations/delusions

431
Q

What do different MMSE scores mean?

A

24-30 = no impairment
18-23 = mild cognitive impairment
< 18 = severe cognitive impairment

432
Q

What are the investigations for dementia?

A

1) Cognitive impairment:
- Screening –> AMTS (<7 suggest cognitive impairment), GPCOG (GP assessment of cognition)
- Detailed –> Addenbrooke’s (ACE-R - 100 questions, MMSE - not widely used, MoCA)

2) Dementia/delirium screen:
- TFTs (hypo –> cognitive decline)
- LFTs (Korsakoff’s)
- U&Es and dipstick (infection, diabetes)
- HbA1c (diabetes)
- Vitamin B12 and folate

Further tests:

  • Alzheimers: FDG-PET, CSF, MRI (grey matter atrophy, wide ventricles & sulci, temporal lobe atrophy)
  • Vascular: ECG (AF with emboli), MRI/CT
  • Lewy body: FP-CIP SPECT, I-MIBG
  • Frontotemporal: FDG-PET, perfusion SPECT, MRI (frontal lobe shrinkage)

Memory assessment clinical referral after GP:

  • Take collateral history and check bloods
  • Risk assess the patient
  • Cognitive assessment - MMSE
  • Brain scan (check organic pathology)
433
Q

How to determine the difference between delirium and dementia?

A
  • Confusion Assessment Method (CAM)

- Observational Scale of Level of Arousal (OSLA)

434
Q

What is cannabis?

A

Active ingredient delta-9-tetrahydrocannabinol

  • Grass/weed - made from dried cannabis leaves
  • Hash - squidgy, brown-black lump made from resin and flowes
  • Skunk and sinsemilla - particularly strong varieties (MOST COMMONLY USED)
435
Q

What are the signs and symptoms of cannabis addiction?

A

Effects largely depend on expectations and original mood state:

  • Euphoria, relaxation to paranoia, anxiety and panic
  • Perceptual/time distortion, hunger pangs
  • Nausea and vomitting (‘greening’)
436
Q

What are the investigations for cannabis addiction?

A

Urine drug screen - in urine for up to 4 weeks

437
Q

What is the pharmacokinetics of cannabis?

A
  • Smoking –> peak at 30 mins, last 2-5 hours

- PO –> slower onset, last longer

438
Q

What is the management of cannabis addiction?

A
  • Abstinence (in those with major mental illness)

- Clinical experience suggest that irregular use can be free from major problems

439
Q

What is the background, prognosis and risk of cannabis addiction?

A

Acute implications:

  • paranoia, panic attacks, accidents associated with delayed reaction time (driving)
  • cannabis can precipitate an episode of psychosis or schizo

Chronic implications:
- dysthymia, anxiety/depressive illness, amotivational syndrome

No physical dependancy:
- there is a mild withdrawal syndrome in heavy users eg. insomnia, anxiety, irritability

440
Q

What are hallucinogenic drugs?

A

Hallucinogens produce psychological (heightened perseption, illness) and psychological (dilated pupils, peripheral vasoconstriction, increased temp) effects but NO DEPENDANCE

LSD: (lysergic acid diethylamide, acid)

  • Affect DA and 5-HT transmitter systems
  • Impregnated on tabs –> trips last up to 12 hours (perceptual changes and euphoria)

Phencyclidine (PCP, angel dust):

  • liquid or powder–> snorted or smoked in a joint
  • associated with violent outburst and ongoing psychosis

Ketamine (special K):

  • anaesthetic effect can lead to unknowingly self-harming
  • unique anaesthesia in that in blocked cortical awareness of pain
  • Small doses = dissociation
  • Large doses = hallucinations, synaesthesia

Magic mushrooms (liberty cap/psylocybin semilanceata):

  • eaten raw or drunk (cooked, dried and made into a drink)
  • small doses = euphoria
  • large doses = hallucinations similar to LSD
  • tolerance develops so continued use unlikely
441
Q

What are the signs and symptoms of hallucinogenic addiction?

A
  • Visual illusions, hallucinations, depersonalisation, derealisation
  • Synaesthesia ( experience sensation in another modality - eg. hear a smell)
  • Behavioural toxicity (ie. acting on drug-induced beliefs such as being able to fly)

Side effects:

  • LSD: acute SEs due to behavioural toxicity, chronic SEs include flashbacks, anxiety and depression
  • Ketamine - LARGE amounts –> nausea, ataxia, slurred speech
  • Magic mushrooms - behvaioural toxicity, accidental poison consumption
  • Phencyclidine - serotoninergic/cholinergic effects (confusion/violence)
442
Q

What is the epidemiology of cig smoking?

A

14.7% in the UK smoke

443
Q

What are the investigations for cig smoking?

A

CO level of = 10ppm indicates abstinence from smoking

444
Q

What is the management of cig smoking?

A

Very brief advice (VBA) - offer at any interaction in any healthcare setting:

  • ask about current and past smoking behaviour
  • provide verbal and written information on risks of smoking and benefits of stopping smoking
  • risks: cancer, bronchitis, COPD, hosp admission
  • Benefits of stopping: cost savings, better heath
  • advise options for quitting smoking including behavioural support and medication
  • refer the person to their local stop smoking service
  • If they do not want to quit, enquire to a harm reduction policy

1st advice:

  • stopping is best done through behavioural support + medication
  • set a quit date, and commit to it
  • the first few days are often the most difficult (may experience withdrawal), but passes by 3-4 days - stop smoking but use NRT)

2nd medications: (depends on individual preference, cannot give NRT in combo with meds):

1) NRT (lozenges, mouth spray, patches)
- start on agreed quit date
- patches (24 hour) useful if: smoking shortly after waking, on combo NRT

2) Varenicline:
- Mechanism: partial nicotine receptor agonist
- Dose: 1mg, BD, titrated up from 500mcg OD over 1 week. (started 7-14 days before quit date, whilst they are still smoking)
- Contraindications: <18y/o, renal disease

3) Bupropion:
- Mechanism: selective Da and NA reuptake inhibitor
- Dose: 150mg BD, titrated up from 150mg OD over 1 week (started 7-14 days before quit date, whilst they are still smoking, max use 7-9 weeks)
- Contraindications: <18y/o, seizures, CNS disorders, eating disorder, BPAD, cirrhosis

3rd FOllow-up:

  • 2 weeks if on NRT, 3-4 weeks if on medications
  • Measure CO levels 4 weeks after quitting
  • Check progress, withdrawal symptoms
  • Of relapse, or partial relapse, provide encouragement and set new quit date
445
Q

What are benzodiazepines?

A

Uses: sedation, hypnotic, anxiolytic, anticonvulsant, muscle relaxant

  • should only be used for a short time (2-4 weeks)
  • Risks:
    1) Short-term: drowsiness, reduced concentration
    2) Long-tern: cognitive impairment, anxiety and depression, sleep, disruption, dependance
446
Q

What are the signs and symptoms of BDZ addiction?

A

Similar to alcohol:

  • calm and mild euphoria
  • slurred speech, ataxia, stupor
447
Q

What happened during an BDZ overdose?

A
  • Resp depression (TREAT with IV flumazenil)

- Low GCS, low BP, mydriasis, hyporeflexia

448
Q

What are the S/S BDZ withdrawal?

A
  • ANXIETY (biggest SE)
  • insomnia
  • tachnyponea
  • tremor
  • hyperreflexia
  • palpitations
  • derealisation
  • irritability
  • tachycardia
  • tinnitus
  • seizures
  • delusions
  • depersonalisation
  • ataxia
  • sweating
  • mydriasis
  • depression
  • anterograde amnesia

Sudden withdrawal can lead to a delirium tremens like picture

449
Q

What is the management of BDZ addition?

A
  • Address underlying need for BDZ
  • Address long term complications of use (cognitive impairment, anxiety, depression, insomnia)
  • Check willingness to withdraw from use and weather it can be done successfully in primary care

Withdrawal management:

(1) slow-dose reduction
(2) switch to equivalent dose of diazepam, and slow-dose reduction used in: difficult to physically taper down the dose, on short-acting potent BDZ such as lorazepam

450
Q

What advice do you give to BDZ addiction?

A
  • If done properly, there will be few, if any, withdrawal side effects:
    (1) anxiety is most common side effect and is normal
    (2) treat with non-pharma management (relaxation breathing techniques)
  • may take 3m to 1y or longer
  • assess driving risk and advise cannot drive on certain levels of BDZs
451
Q

What is the withdrawal process of BDZ addiction?

A
  • 1/8th daily dose reduction every 2 weeks

- Estimated time = 30-60 weeks

452
Q

What are long-acting BDZ?

A

Chlordiazepoxide, diazepam

453
Q

What are the different types of stimulants?

A
  1. Cocaine (Charlie, coke, snow)
    - Intranasal or IV
  2. Crack cocaine (rock, base, freebase)
    - inhalational
    - Immediate, extreme high –> wears off quickly (5-10 mins)
    - highly addictive
  3. Amphetamine (speed)
    - IV, PO, intranasal
    - Withdrawal medications include dexamphetamine
  4. Khat (quat, chat)
    - Mild stimulant, used in east african communities
    - causes psychosis
  5. Ectasy (3,4-methylenedioxymethamphetamine, E, MDMA)
    - causes seretonin release and blocks reuptake
    - hallucinogenic as well as stimulant properties
    - S/S: inital 3 hour rush, agitation relieved by dancing/movement, bruxism (teeth-grinding)
    - Hangover at 24-48 hours (fatigue, anorexia, depressed mood)

Potentiate neurotransmission and increase cortical excitability –> increased alertness, endurance, diminished need for sleep and subjective sense of well-being

454
Q

What are the signs and symptoms of stimulant addiction?

A
  • Increased alertness, endurance and confidence
  • Risky behaviour
  • Unpleasant crash period (dysphoria and lethargy)
455
Q

What are the side effects of cocaine?

A

No dependence but can become a habit:

  • Acute: arrhythmia, intense anxiety, hypertension –> CVA, impulsivity, impaired judgment
  • Chronic: nasal septum necrosis, foetal damage, panic and anxiety, delusions, psychosis
456
Q

What are the side effects of cocaine?

A

No dependence but can become a habit:

  • Acute: arrhythmia, intense anxiety, hypertension –> CVA, impulsivity, impaired judgment
  • Chronic: nasal septum necrosis, foetal damage, panic and anxiety, delusions, psychosis
457
Q

What are the side effects of amphetamines?

A

Very regular use associated with dependance:

  • Acute: tachycardia, arrhythmia, hyperpyrexia, irritability, post-use depression
  • Quasi-psychotic state with visual, auditory and tactile hallucinations
458
Q

What are the side effects of ecstasy?

A

Tolerance but no dependence:

  • Acute: increased sweating, nausea, vomiting, diminished potency despite increased libido
  • Death associated with dehydration and hyperthermia (some chronic liver and cognitive issues)
459
Q

What are the stages of cocaine withdrawal?

A

2 stages:

(1) Crash phase - from 3 hours - depression, exhaustion, agitation, irritability
(2) Withdrawal: - cravings, irritability, anergia, poor concentration, insomnia, slowed movements (can last 1-10 weeks)

460
Q

What are the investigations for stimulant addiction?

A
  • Urine drug screen - cocaine in urine for up to 5-7 days
461
Q

What is the management for stimulant addiction?

A
  • Harm reduction

- Short-term withdrawal symptoms relief as an inpatient with BDZ

462
Q

What are opiates?

A

Derived from poppy seed, papaver somniferum types:

  • Heroin
  • Pethidine
  • Morphine, diamorphine
  • Codeine, dihydrocodeine

Heroin profile (mu) opiate agonist –> immediate euphoria, diminished pain sensation, feelings of detachment

Routes:

  • smoking
  • sniffing
  • oral
  • IV
  • IM or SC
463
Q

What are the signs and symptoms of opiate addiction?

A

Local complications:

  • Abscess
  • Cellulitis
  • DVT
  • Emboli

Systemic complications:

  • septecaemia
  • infective endocarditis
  • blood-bourne infection
  • increased risk of overdose

Intoxication symptoms:

  • euphoria and warmth –> sedation, bradycardia
  • Overdose: miosis + low RR (treat with naloxone which is an opiate antagonist, immediate start of withdrawal symptoms)
  • Low-dose SEs: constipation, anorexia, decreased libido
464
Q

What are the withdrawal symptoms of opiate addiction?

A

Begins 6 hours after injection, peak 36-48 hours, last 5-7 days:

  • raving, nausea, insomnia, agitation
  • Flu-like symptoms
  • Runs - D+V, macrimation, rhinorrhoaea
  • Goose-flesh - pilomotor unit erection, yawning
  • Mydriasis (dilation)
465
Q

What are the investigations of opiate addiction?

A
  • Physical exam (establish baseline physical state)
  • Urine drug screen (2 days in urine)
  • U&E (features of malnutrition)
  • FBC (anaemia due to malnutrition or signs of infection)
  • LFTs (may impact medication dosing)
  • Blood bourne infections (RPR, hepatitis serology, HIV test)
466
Q

What is the management of opiate addiction?

A

General recommendations:

1) Appointment a key worker (single point of contact) and develop a care plan:
- agreed treatment and recovery goals
- specific, clear, action to be taken to achieve those goals
- clarity about who is takeing the actions
- monitoring of progress
2) Harm reduction:
- needle exchanges for IVDUs
- Offer vaccinations and testing for blood-bourne pathogens
3) Health education:
- smart recovery
- narcotic anonymous

Discuss if they want to undergo Opioid Substitution therapy (OST) withdrawal or maintenance regimen:

1st) maintenance - the goal = stabilise lifestyle and reduce harm
2nd) detoxification - the goal = detoxification and abstinence

Replacement: 
Methadone - long acting synthetic opiate(liguid)
Bupronopephrine - partial opiate
antagonist (sublingual)
Lofexidine - alpha 2 antagonist
467
Q

What is Opioid substitution therapy?

A

Admission may be necessary:

1st) OST given in controlled environment for 3-6months
2nd) if suitable, take home some medications

Maintenance:

1st) Methadone (liquid) or buprenorphine (sublingual)
- if still using heroin –> low-dose methadone
- If wanting to stop heroin completely –> high-dose methadone or buprenorphine
- Offer naloxone to take home with them and training on when/how to use it

Detoxification: (must be committed to stopping)

  • Must be on stable OST maintenance before you start detox
  • Last 12 weeks as an outpatient
  • Inform them they will lose tolerance so if they start again, they should take a lot less
  • 1st line: Methadone (liquid) or buprenorphine (sublingual) and offer naloxone to take home with them and training on when/how to use it
  • 2nd line: Lofexidine (alpha 2 agonist), indications: rapid detox, mild dependance, preference

Withdrawal symptom medications:

  • Clonidine or lofexidine (alpha 2 agonist)
  • Anti-diarrheals (loperamide), anti-emetics (metoclopramide)

Ultra-rapid detoxing regimens do exist but are not pleasant and not routinely offered (using naloxone)

468
Q

What us the follow up protocol for opiate addiction?

A

With drugs and alcohol services for at least 6 months:

  • Look for signs of withdrawal
  • ECG (QTc) for those with methadone
  • Check other drug use (urine drug screens)
  • CBT (to reduce relapse chance)
  • Contingency management (through frequent screening –> less frequent screenings as time goes on) - incentive for -ve drug test results, urinalysis preferred
469
Q

What is Alzheimer’s?

A
  • Most common form of dementia with steady progression

- APP= amyloid precursor protein

470
Q

What is the normal physiology of amyloid?

A
  1. APP cleaved by alpha-secretase
  2. sAPP(alpha) released and the C83 fragment remains
  3. C83 is then digested by (gamma)-secretase
  4. Products are then removed
471
Q

What is the pathophysiology of amyloid?

A
  1. APP cleaved by beta-secretase
  2. sAPP(beta) released and the C99 fragment remains
  3. C99 is then digested by (gamma)-secretase releasing (beta)-amyloid (Alpha-beta) protein
  4. Alpha-beta protein forms the toxic aggregates
472
Q

What is the normal physiology of Tau?

A
  • Tau proteins is a soluble protein present in axons

- Tau important for assembly and stability of microtubules

473
Q

What is the pathophysiology of tau?

A
  1. Hyperphosphyrylated tau is insoluble –> self-aggregates
  2. The self-aggregates from neurofibrillary tangles (neurotoxic)
  3. The tangles result ultimately in microtubule instability and neurotoxic damage to neurones
474
Q

What is the normal physiology of Inflammation?

A
  • Microglial cells are specialist CNS macrophages
475
Q

What is the pathophysiology of inflammation?

A
  1. Increased inflammatory mediators and cytotoxic proteins
  2. Increased phagocytosis
  3. Decreased levels of neuroprotective proteins
476
Q

What are the signs and symptoms of Alzheimer’s dementia?

A

Present due to 4 key elements of pathophysiology:

  • Atrophy from neuronal loss
  • Plague formation
  • Neurofibrillary tangle formation
  • Cholinergic loss

Presentation:

  • Amnesia (recent memories loss first)
  • Aphasia (problems finding the correct words, muddled, disjointed speech without disturbance to illelect)
  • Agnosia (difficulty remembering faces)
  • Apraxia (difficulty dressing and doing skilled tasks, despite normal motor functioning)

BPSD= mood change, abnormal behaviour, hallucinations/delusions

477
Q

What are the investigations for Alzheimer’s?

A

1) Cognitive impairment:
- Screening –> AMTS (<7 suggest cognitive impairment), GPCOG (GP assessment of cognition)
- Detailed –> Addenbrooke’s (ACE-R - 100 questions, MMSE - not widely used, MoCA)

2) Dementia/delirium screen:
- TFTs (hypo –> cognitive decline)
- LFTs (Korsakoff’s)
- U&Es and dipstick (infection, diabetes)
- HbA1c (diabetes)
- Vitamin B12 and folate

Further tests:

  • Alzheimers: FDG-PET, CSF, MRI (grey matter atrophy, wide ventricles & sulci, temporal lobe atrophy)
  • Vascular: ECG (AF with emboli), MRI/CT
  • Lewy body: FP-CIP SPECT, I-MIBG
  • Frontotemporal: FDG-PET, perfusion SPECT, MRI (frontal lobe shrinkage)

Memory assessment clinical referral after GP:

  • Take collateral history and check bloods
  • Risk assess the patient
  • Cognitive assessment
  • Brain scan (check organic pathology)
478
Q

What are the bad prognostic indicators of Alzheimer’s?

A
  • Male
  • Depression
  • Behavioural problems
  • Severe focal cognitive deficit
479
Q

What are the good prognostic indicators of Alzheimer’s?

A

Female

480
Q

What is the bio management of Alzheimer’s?

A

1st: Anticholinesterases (mild to moderate AD:)
- Donepezil - reversible AcH inhibitor
- Galantamine - reversible AcH inhibitor
- Rivastigmine - pseudo-reversible AChe inhibitor and butylcholinesterase (BChe) inhibitor

2nd: (moderate or 1st line in severe AD) - NMDA (glutamate) partial receptor antagonist
- Memantine - use-dependant non-competitve NMDA receptor blocker with low channel affinity

481
Q

What is the social management of Alzheimer’s?

A

1st: Structural group cognitive stimulation sessions (mild to moderate AD)
- Exclude depression of GAD (pseudo-dementia)
- Other: group reminiscence therapy, validation therapy, multisensory therapy

482
Q

What is the social management of Alzheimer’s?

A
  • Explain diagnosis (“AD causes dementia which describes a set of symptoms including memory loss and difficulties with thinking, problem-solving or language. AD is a physical disease that affects the brain”)
  • Optimise health in other areas (eg. hearing aids)
  • Identify future wishes (eg. advance directives, lasting power of attorney)

Follow-up: every 6 months with yourself and a single named care manager with a clearly defined care plan

General: always wear ID, Dossett Boxes, change gas to electricity, assistive technology in the house

Carers: identify and support any carers involved (signpost information and support, carer’s assessment)

Social support: personal care support, meal support, day centre availability

Legally required: to form DVLA and insurers

483
Q

What needs monitoring when prescribing anticholinesterases?

A

1st: ECG

Side effect:
- GI (N&V, diarrhoea, anorexia), other (fatigue, dizziness, headache)

Absolute contraindications:

  • Anticholinergics (block ACh from binding)
  • Beta-blockers
  • NSAIDs
  • Muscle relaxants

Relative contraindications:

  • asthma
  • COPD
  • GI disease
  • Bradycardia
  • sick sinus syndrome
  • AV block
484
Q

What is somatisation disorder?

A
  • multiple physical SYMPTOMS present for at least 2 years

- patient refuses to accept reassurance or negative test results

485
Q

What is illness anxiety disorder (hypochondriasis)?

A
  • persistent belief in the presence of an underlying serious DISEASE, e.g. cancer
  • patient again refuses to accept reassurance or negative test results
486
Q

What is conversion disorder?

A
  • typically involves loss of motor or sensory function
  • the patient doesn’t consciously feign the symptoms (factitious disorder) or seek material gain (malingering)
  • patients may be indifferent to their apparent disorder - la belle indifference - although this has not been backed up by some studies
487
Q

What is dissociation disorder?

A
  • dissociation is a process of ‘separating off’ certain memories from normal consciousness
  • in contrast to conversion disorder involves psychiatric symptoms e.g. Amnesia, fugue, stupor
  • dissociative identity disorder (DID) is the new term for multiple personality disorder as is the most severe form of dissociative disorder
488
Q

What is a factitious disorder?

A
  • also known as Munchausen’s syndrome

- the intentional production of physical or psychological symptoms

489
Q

What is malingering?

A

fraudulent simulation or exaggeration of symptoms with the intention of financial or other gain

490
Q

Neologism

A

new word formations, which might include the combining of two words

491
Q

Clang associations

A

when ideas are related to each other only by the fact they sound similar or rhyme.

492
Q

Word salad

A

completely incoherent speech where real words are strung together into nonsense sentences

493
Q

Knight’s move

A

severe type of loosening of associations, where there are unexpected and illogical leaps from one idea to another. It is a feature of schizophrenia

494
Q

Flight of ideas

A

thought disorder where there are leaps from one topic to another but with discernible links between them.

495
Q

Preservation

A

repetition of ideas or words despite an attempt to change the topic

496
Q

Echolalia

A

repetition of someone else’s speech, including the question that was asked.

497
Q

Tangentially

A

wandering from a topic without returning to it.

498
Q

Circumstantiality

A

inability to answer a question without giving excessive, unnecessary detail. However, this differs from tangentiality in that the person does eventually return the original point.

Year 5 - Fatty (4 decks)

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