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Year 6 > Psych > Flashcards

Psych Flashcards

1
Q

Q: What is bipolar disorder?

A

A: A chronic mental health disorder characterised by periods of mania/hypomania alongside episodes of depression.

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2
Q

Q: What are the two types of bipolar disorder?

A

Type I disorder: Mania and depression (most common)
Type II disorder: Hypomania and depression

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3
Q

Q: What defines mania and hypomania?

A

Both terms refer to abnormally elevated mood or irritability.

Mania involves severe functional impairment or psychotic symptoms lasting 7 days or more.
Hypomania involves decreased or increased function lasting 4 days or more.

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4
Q

Q: What is the key differentiating feature between mania and hypomania?

A

A: The presence of psychotic symptoms (e.g., delusions of grandeur or auditory hallucinations) suggests mania.

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5
Q

Q: What is the mood stabilizer of choice for bipolar disorder?

A

A: Lithium.

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6
Q

Q: What is an alternative mood stabilizer to lithium for bipolar disorder?

A

A: Valproate.

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7
Q

Q: How is mania/hypomania managed in bipolar disorder?

A

Consider stopping antidepressants if the patient is taking one.
Antipsychotic therapy (e.g., olanzapine or haloperidol).

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8
Q

Q: How is depression in bipolar disorder managed?

A

Talking therapies.
Fluoxetine is the antidepressant of choice.

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9
Q

Q: What are the co-morbidities associated with bipolar disorder?

A

A: Increased risk of diabetes, cardiovascular disease, and COPD (2-3 times higher).

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10
Q

Q: What should be done if symptoms suggest hypomania in a patient with bipolar disorder?

A

A: NICE recommends a routine referral to the community mental health team (CMHT).

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11
Q

Q: What should be done if there are features of mania or severe depression in a patient with bipolar disorder?

A

A: An urgent referral to the community mental health team (CMHT) should be made.

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12
Q

Q: What is Capgras syndrome?

A

A: A disorder in which a person holds a delusion that a friend or partner has been replaced by an identical-looking impostor.

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13
Q

Q: What are the four types of child abuse?

A

Neglect
Emotional abuse
Physical abuse
Sexual abuse

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14
Q

Q: What features should raise suspicion of sexual abuse in a child?

A

Persistent dysuria or anogenital discomfort without medical explanation
Gaping anus in a child during examination without medical explanation
Pregnancy in a young woman aged 13-15 years
Hepatitis B or anogenital warts in a child aged 13-15 years

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15
Q

Q: What are features suggesting sexual abuse in a child?

A

Persistent or recurrent genital or anal symptoms associated with emotional or behavioral changes
Anal fissure with no explanation from conditions like constipation or Crohn’s disease
STI in a child younger than 12 years (without evidence of vertical or blood transmission)
Sexualized behavior in a prepubertal child

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16
Q

Q: What features should raise suspicion of physical abuse in a child?

A

Any serious or unusual injury with an absent or unsuitable explanation
Cold injuries in a child with no medical explanation
Hypothermia in a child without a suitable explanation
Oral injury in a child with an absent or unsuitable explanation

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17
Q

Q: What are some factors that point towards child abuse?

A

Story inconsistent with injuries
Repeated attendances at A&E departments
Delayed presentation
Child with a frightened, withdrawn appearance (‘frozen watchfulness’)

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18
Q

Q: How is chronic fatigue syndrome (CFS) diagnosed?

A

A: Diagnosed after at least 3 months of disabling fatigue affecting mental and physical function more than 50% of the time in the absence of other diseases that may explain the symptoms.

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19
Q

Q: What are the central features of chronic fatigue syndrome?

A

Fatigue is the central feature, along with:

Sleep problems (insomnia, hypersomnia, unrefreshing sleep, disturbed sleep-wake cycle)
Muscle and/or joint pains
Headaches
Painful lymph nodes without enlargement
Sore throat
Cognitive dysfunction (difficulty thinking, inability to concentrate, memory impairment, word-finding difficulties)
Physical or mental exertion worsening symptoms
General malaise or ‘flu-like’ symptoms
Dizziness
Nausea
Palpitations

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20
Q

Q: What investigations does NICE recommend for chronic fatigue syndrome?

A

A large number of screening blood tests to exclude other pathologies, including:

FBC
U&E
LFT
Glucose
TFT
ESR
CRP
Calcium
CK
Ferritin
Coeliac screening
Urinalysis

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21
Q

Q: When is a diagnosis of chronic fatigue syndrome typically made?

A

A: A diagnosis is typically made if symptoms persist for 3 months.

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22
Q

Q: How is chronic fatigue syndrome managed?

A

Refer to a specialist CFS service if diagnostic criteria are met and symptoms have persisted for 3 months.
Energy management strategy.
Physical activity and exercise under supervision of an ME/CFS specialist team.
Cognitive behavioural therapy (supportive rather than curative).
Graded exercise therapy is not recommended by NICE.

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23
Q

Q: What is chronic pancreatitis?

A

A: Chronic pancreatitis is an inflammatory condition that can affect both the exocrine and endocrine functions of the pancreas.

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24
Q

Q: What is the most common cause of chronic pancreatitis?

A

A: Around 80% of cases are due to alcohol excess.

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25
Q

Q: What other causes, besides alcohol, can lead to chronic pancreatitis?

A

Genetic causes (e.g., cystic fibrosis, haemochromatosis)
Ductal obstruction (e.g., tumours, stones, structural abnormalities like pancreas divisum and annular pancreas)

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26
Q

Q: What are the typical symptoms of chronic pancreatitis?

A

Pain, usually worse 15-30 minutes following a meal
Steatorrhoea (fatty stools)
Diabetes mellitus (typically develops more than 20 years after symptoms begin)

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27
Q

Q: How long after the onset of pain do symptoms of pancreatic insufficiency, such as steatorrhoea, usually develop?

A

A: Symptoms typically develop between 5 and 25 years after the onset of pain.

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28
Q

Q: What imaging tests are used to diagnose chronic pancreatitis?

A

Abdominal x-ray (shows pancreatic calcification in 30% of cases)
CT scan (more sensitive for detecting pancreatic calcification with 80% sensitivity and 85% specificity)

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29
Q

Q: What functional test can be used to assess exocrine function in chronic pancreatitis?

A

A: Faecal elastase may be used to assess exocrine function if imaging is inconclusive.

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30
Q

Q: What is the management of chronic pancreatitis?

A

Pancreatic enzyme supplements
Analgesia
Antioxidants (limited evidence, but one study suggests benefit in early disease)

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31
Q

Q: What is Cotard syndrome?

A

A: Cotard syndrome is a rare mental disorder where the affected patient believes that they (or part of their body) is either dead or non-existent.

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32
Q

Q: What is De Clerambault’s syndrome also known as?

A

A: De Clerambault’s syndrome is also known as erotomania.

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33
Q

Q: What belief does a person with De Clerambault’s syndrome hold?

A

A: The patient believes that a famous person is in love with her.

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34
Q

Q: What is delusional parasitosis?

A

A: Delusional parasitosis is a rare condition where a patient has a fixed, false belief (delusion) that they are infested by ‘bugs’ such as worms, parasites, mites, bacteria, or fungus.

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35
Q

Q: What are some common tools used to assess the degree of depression?

A

Hospital Anxiety and Depression (HAD) scale
Patient Health Questionnaire (PHQ-9)

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36
Q

Q: What is the scoring system for the Hospital Anxiety and Depression (HAD) scale?

A

14 questions (7 for anxiety, 7 for depression)
Each item is scored 0-3
Depression severity:
0-7: Normal
8-10: Borderline
11+: Case

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37
Q

Q: How is depression severity defined in the updated NICE guideline?

A

Less severe depression (score <16 on PHQ-9)
More severe depression (score ≥16 on PHQ-9)

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38
Q

Q: What are the DSM-5 criteria for diagnosing Major Depressive Disorder (MDD)?

A

Five (or more) of the following symptoms must be present during the same 2-week period:

Depressed mood or loss of interest/pleasure
Significant weight change or appetite disturbance
Insomnia or hypersomnia
Psychomotor agitation or retardation
Fatigue or loss of energy
Feelings of worthlessness or excessive guilt
Diminished ability to think, concentrate, or indecisiveness
Recurrent thoughts of death or suicidal ideation

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39
Q

Q: How long should a patient refrain from driving after a coronary artery bypass graft (CABG)?

A

A: 4 weeks off driving.

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40
Q

Q: How long should someone refrain from driving after an acute coronary syndrome event?

A

A: 4 weeks off driving, or 1 week if successfully treated by angioplasty.

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41
Q

Q: What are the DVLA guidelines for a patient with epilepsy or seizures?

A

First unprovoked seizure:
6 months off if no structural abnormalities on brain imaging and no epileptiform activity on EEG.
12 months off if these conditions are not met.
Established epilepsy or multiple unprovoked seizures:
Must be seizure-free for 12 months to qualify for a driving licence.
If seizure-free for 5 years (with medication if necessary), a ‘til 70’ licence is usually restored.
Epilepsy medication withdrawal:
Must not drive during withdrawal and for 6 months after the last dose.

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42
Q

Q: What are the DVLA guidelines for stroke or TIA?

A

Stroke or TIA: 1 month off driving; may not need to inform DVLA if no residual neurological deficit.
Multiple TIAs over a short period: 3 months off driving and must inform DVLA.

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43
Q

Q: What is the typical presentation of fibromyalgia?

A

Widespread chronic pain, lethargy, cognitive impairment (e.g., “fibro fog”), sleep disturbance, headaches, and dizziness.

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44
Q

Q: What is the diagnostic approach for fibromyalgia?

A

Clinical diagnosis, sometimes using the American College of Rheumatology classification criteria.
If a patient is tender in at least 11 of the 18 tender points, fibromyalgia is more likely.

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45
Q

Q: What are the management strategies for fibromyalgia?

A

A psychosocial and multidisciplinary approach.
Aerobic exercise (strongest evidence base), cognitive behavioural therapy (CBT), and medications such as pregabalin, duloxetine, and amitriptyline.

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46
Q

Q: At what age is head banging considered normal behavior in children, and when might it indicate a concern?

A

Normal behavior for a 2-year-old.
If it persists beyond 3 years, it could be a sign of autism.

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47
Q

Q: What is the minimum duration for mania to be diagnosed?

A

A: Mania lasts for at least 7 days.

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48
Q

Q: What is the minimum duration for hypomania to be diagnosed?

A

A: Hypomania lasts for less than 7 days, typically 3-4 days.

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49
Q

Q: What speech and thought patterns are common in both hypomania and mania?

A

A: Pressured speech, flight of ideas, and poor attention are common.

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50
Q

Q: What behavioral symptoms are common to both hypomania and mania?

A

A: Common behaviors include insomnia, loss of inhibitions (e.g., sexual promiscuity, overspending, risk-taking), and increased appetite.

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51
Q

Q: What is insomnia as defined by the DSM-V?

A

A: Insomnia is difficulty initiating or maintaining sleep, or early-morning awakening that leads to dissatisfaction with sleep quantity or quality, despite adequate time and opportunity for sleep, resulting in impaired daytime functioning.

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52
Q

Q: What is the difference between acute and chronic insomnia?

A

A: Acute insomnia is typically related to a life event and resolves without treatment, while chronic insomnia is diagnosed if a person has trouble sleeping at least three nights per week for 3 months or longer.

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53
Q

Q: How is the diagnosis of insomnia primarily made?

A

A: Diagnosis is primarily through patient interview, looking for the presence of risk factors. Sleep diaries and actigraphy may also aid diagnosis.

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54
Q

Q: When might polysomnography be considered for diagnosing insomnia?

A

A: Polysomnography may be considered in patients with suspected obstructive sleep apnoea or periodic limb movement disorder, or when insomnia is poorly responsive to conventional treatment.

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55
Q

Q: What are the short-term management strategies for insomnia?

A

A: Identify potential causes (e.g., mental/physical health issues, poor sleep hygiene), advise against driving while sleepy, and recommend good sleep hygiene (no screens before bed, limited caffeine intake, fixed bedtimes). Only consider hypnotics if daytime impairment is severe.

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56
Q

Q: What hypnotic drugs are recommended for insomnia treatment?

A

A: Short-acting benzodiazepines or non-benzodiazepines (e.g., zopiclone, zolpidem, zaleplon) are recommended. Diazepam is not recommended but can be used for insomnia linked to daytime anxiety.

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57
Q

Q: What is the guidance on using hypnotics for insomnia?

A

A: Use the lowest effective dose for the shortest period, review after 2 weeks, and consider referral for cognitive behavioral therapy (CBT). If the first hypnotic does not work, do not prescribe another one. Repeat prescriptions are typically not given.

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58
Q

Q: What are some genetic causes of learning difficulties?

A

A: Fragile X syndrome and Down’s syndrome are genetic causes of learning difficulties.

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59
Q

Q: Which congenital infections can lead to learning difficulties?

A

A: Cytomegalovirus, toxoplasmosis, and rubella can cause learning difficulties.

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60
Q

Q: What birth-related factors can contribute to learning difficulties?

A

A: Hypoxia, rhesus haemolytic disease, and intraventricular haemorrhage can lead to learning difficulties.

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61
Q

Q: What metabolic disorders are associated with learning difficulties?

A

A: Phenylketonuria (PKU), maple syrup urine disease, and homocystinuria are metabolic disorders that can cause learning difficulties.

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62
Q

Q: What are vasomotor symptoms, and how common are they during menopause?

A

A: Vasomotor symptoms, such as hot flushes and night sweats, affect around 80% of women and can occur daily, continuing for up to 5 years.

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63
Q

Q: What urogenital changes may occur during menopause?

A

A: Around 35% of women may experience vaginal dryness, atrophy, and urinary frequency.

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64
Q

Q: What psychological symptoms may be seen during menopause?

A

A: Anxiety and depression may affect around 10% of women, and short-term memory impairment is also common.

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65
Q

Q: What are some longer-term complications associated with menopause?

A

A: Longer-term complications include osteoporosis and an increased risk of ischaemic heart disease.

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66
Q

Q: What is the management for a paracetamol overdose?

A

Activated charcoal if ingested < 1 hour ago
N-acetylcysteine (NAC)
Liver transplantation if severe

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67
Q

Q: What is the management for a salicylate overdose?

A

Urinary alkalinization with IV bicarbonate
Haemodialysis

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68
Q

Q: What is the treatment for opioid/opiates overdose?

A

A: Naloxone

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69
Q

Q: What is the management for a benzodiazepine overdose?

A

A: Flumazenil, but generally only used for severe or iatrogenic overdoses due to seizure risk.

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70
Q

Q: How is a tricyclic antidepressant overdose managed?

A

IV bicarbonate for severe toxicity to reduce risk of seizures and arrhythmias
Avoid class 1a (e.g. Quinidine) and class III (e.g. Amiodarone) antiarrhythmics
Dialysis is ineffective
First-line management of tricyclic-induced arrhythmias is correcting acidosis

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71
Q

Q: What is the management for a lithium overdose?

A

Mild-moderate toxicity: Volume resuscitation with normal saline
Severe toxicity: Haemodialysis
Sodium bicarbonate may be used, but evidence is limited

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72
Q

Q: What is the treatment for warfarin overdose?

A

A: Vitamin K and prothrombin complex

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73
Q

Q: What is the management for heparin overdose?

A

A: Protamine sulphate

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74
Q

Q: How should a beta-blocker overdose be managed?

A

If bradycardic, use atropine
For resistant cases, use glucagon

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75
Q

Q: What is the management for ethylene glycol poisoning?

A

Fomepizole (first-line)
Ethanol (used previously)
Haemodialysis for refractory cases

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76
Q

Q: How is methanol poisoning treated?

A

Fomepizole or ethanol
Haemodialysis

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77
Q

Q: What is the treatment for organophosphate insecticide poisoning?

A

A: Atropine; the role of pralidoxime is still unclear.

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78
Q

Q: What is the management for digoxin toxicity?

A

A: Digoxin-specific antibody fragments

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79
Q

Q: How is iron overdose treated?

A

A: Desferrioxamine, a chelating agent

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80
Q

Q: What is the treatment for lead poisoning?

A

A: Dimercaprol and calcium edetate

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81
Q

Q: What is the management for carbon monoxide poisoning?

A

100% oxygen
Hyperbaric oxygen

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82
Q

Q: How is cyanide poisoning treated?

A

A: Hydroxocobalamin, or a combination of amyl nitrite, sodium nitrite, and sodium thiosulfate.

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83
Q

Q: What mental health problem is commonly seen in around 60-70% of women within 3-7 days following birth?

A

A: ‘Baby-blues’

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84
Q

Q: What are the characteristic symptoms of the ‘baby-blues’?

A

A: Anxiety, tearfulness, and irritability. It is more common in primips (first-time mothers).

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85
Q

Q: What is the usual onset and peak time for postnatal depression?

A

A: Postnatal depression affects around 10% of women, with most cases starting within a month and peaking at 3 months.

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86
Q

Q: What is puerperal psychosis, and how common is it?

A

A: Puerperal psychosis affects around 0.2% of women, with onset usually within the first 2-3 weeks following birth.

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87
Q

Q: What are the features of puerperal psychosis?

A

A: Features include severe mood swings (similar to bipolar disorder) and disordered perception, such as auditory hallucinations.

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88
Q

Q: What is the initial management for ‘baby-blues’?

A

A: Reassurance and support, with a key role for the health visitor.

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89
Q

Q: What is the management for postnatal depression?

A

A: Reassurance, support, and possibly cognitive behavioural therapy. Severe cases may require SSRIs such as sertraline or paroxetine, which are considered safe for breastfeeding.

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90
Q

Q: What is the treatment for puerperal psychosis?

A

A: Admission to hospital is usually required, ideally in a Mother & Baby Unit. There is a 25-50% risk of recurrence in future pregnancies.

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91
Q

Q: What SSRIs are preferred for treating postnatal depression in breastfeeding mothers?

A

A: Sertraline and paroxetine are preferred due to their safety during breastfeeding, with paroxetine recommended by SIGN for its low milk/plasma ratio.

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92
Q

Q: Why is fluoxetine generally avoided for postpartum depression treatment?

A

A: Fluoxetine is avoided due to its long half-life, which can be a concern for breastfeeding infants.

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93
Q

Q: What are Schneider’s first-rank symptoms of schizophrenia?

A

A: Schneider’s first-rank symptoms include auditory hallucinations, thought disorders, passivity phenomena, and delusional perceptions.

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94
Q

Q: What are some thought disorders associated with schizophrenia?

A

Thought insertion
Thought withdrawal
Thought broadcasting

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95
Q

Q: What are passivity phenomena in schizophrenia?

A

A: Experiences where bodily sensations, actions, impulses, or feelings are controlled or influenced by external forces or others.

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96
Q

Q: What are some other features of schizophrenia?

A

Impaired insight
Negative symptoms (e.g., anhedonia, alogia, avolition)
Incongruity/blunting of affect
Social withdrawal
Neologisms (made-up words)
Catatonia

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97
Q

Q: What is anhedonia in schizophrenia?

A

A: Anhedonia is the inability to derive pleasure from activities that are normally enjoyable.

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98
Q

Q: What is alogia in schizophrenia?

A

A: Alogia refers to poverty of speech, where the individual speaks very little or provides minimal responses.

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99
Q

Q: What is avolition in schizophrenia?

A

A: Avolition is poor motivation or a lack of drive to engage in purposeful activities.

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100
Q
A
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101
Q

What is the most common cause of superior vena cava (SVC) obstruction?

A

Lung cancer

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102
Q

What is the most common symptom of superior vena cava (SVC) obstruction?

A

Dyspnoea

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103
Q

What are some common features of superior vena cava (SVC) obstruction?

A

Swelling of the face, neck, and arms; conjunctival and periorbital oedema; headache (often worse in the mornings); visual disturbance; pulseless jugular venous distension

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104
Q

Which malignancies are most commonly associated with superior vena cava (SVC) obstruction?

A

Small cell lung cancer and lymphoma

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105
Q

What are other causes of superior vena cava (SVC) obstruction?

A

Metastatic seminoma, Kaposi’s sarcoma, breast cancer, aortic aneurysm, mediastinal fibrosis, goitre, and SVC thrombosis

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106
Q

What is the treatment of choice for superior vena cava (SVC) obstruction in many cases?

A

Endovascular stenting

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107
Q

When might radical chemotherapy or chemo-radiotherapy be preferred over endovascular stenting in the management of SVC obstruction?

A

In certain malignancies such as lymphoma and small cell lung cancer

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108
Q

Is there strong evidence supporting the use of glucocorticoids in the treatment of SVC obstruction?

A

No, the evidence base is weak, but they are often given.

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109
Q

What is circumstantiality in thought disorders?

A

The inability to answer a question without giving excessive, unnecessary detail, but eventually returning to the original point.

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110
Q

What is tangentiality in thought disorders?

A

Wandering from a topic without returning to it.

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111
Q

What are neologisms in thought disorders?

A

New word formations, which might include the combining of two words.

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112
Q

What are clang associations in thought disorders?

A

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

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113
Q

What is word salad in thought disorders?

A

Completely incoherent speech where real words are strung together into nonsense sentences.

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114
Q

What is Knight’s move thinking, and in which condition is it a feature?

A

A severe type of loosening of associations with unexpected and illogical leaps from one idea to another, featured in schizophrenia.

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115
Q

What is flight of ideas and in which condition is it a feature?

A

A thought disorder with leaps from one topic to another but with discernible links between them, featured in mania.

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116
Q

What is perseveration in thought disorders?

A

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

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117
Q

What is echolalia in thought disorders?

A

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

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118
Q

What causes Wernicke’s encephalopathy?

A

Thiamine deficiency, most commonly seen in alcoholics, and also caused by persistent vomiting, anorexia nervosa, stomach cancer, and dietary deficiency.

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119
Q

What is the classic triad of symptoms in Wernicke’s encephalopathy?

A

Ophthalmoplegia/nystagmus, ataxia, and encephalopathy.

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120
Q

Where do petechial haemorrhages occur in Wernicke’s encephalopathy?

A

In a variety of structures in the brain including the mamillary bodies and ventricle walls.

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121
Q

What are the features of Wernicke’s encephalopathy?

A

Oculomotor dysfunction, nystagmus (most common ocular sign), ophthalmoplegia (lateral rectus palsy, conjugate gaze palsy), gait ataxia, encephalopathy (confusion, disorientation, indifference, inattentiveness), peripheral sensory neuropathy.

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122
Q

What are the investigations for Wernicke’s encephalopathy?

A

Decreased red cell transketolase and MRI.

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123
Q

What is the treatment for Wernicke’s encephalopathy?

A

Urgent replacement of thiamine.

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124
Q

What syndrome may develop if Wernicke’s encephalopathy is not treated?

A

Korsakoff’s syndrome, leading to Wernicke-Korsakoff syndrome, characterized by antero- and retrograde amnesia and confabulation in addition to the symptoms of Wernicke’s encephalopathy.

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125
Q

What is the most common cause of blindness in the UK?

A

Age-related macular degeneration (ARMD).

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126
Q

What is the key feature of age-related macular degeneration (ARMD)?

A

Degeneration of the central retina (macula), usually bilateral, with the formation of drusen.

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127
Q

What are the main risk factors for developing age-related macular degeneration (ARMD)?

A

Advancing age, smoking, family history, hypertension, dyslipidaemia, and diabetes mellitus.

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128
Q

What is the greatest risk factor for ARMD?

A

Advancing age.

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129
Q

What is the difference in risk of ARMD between patients aged 65-74 years and those older than 75 years?

A

The risk of ARMD increases 3 fold for patients aged older than 75 years.

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130
Q

How does smoking affect the risk of ARMD?

A

Current smokers are twice as likely to experience ARMD-related visual loss compared to non-smokers, and ex-smokers have a slightly increased risk.

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131
Q

What are the two traditional forms of macular degeneration?

A

Dry macular degeneration (atrophic) and wet macular degeneration (exudative or neovascular).

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132
Q

What is the most common type of age-related macular degeneration?

A

Dry macular degeneration (90% of cases).

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133
Q

What is characteristic of wet macular degeneration?

A

Choroidal neovascularisation and leakage of serous fluid and blood, leading to rapid vision loss.

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134
Q

What is the recent updated classification of age-related macular degeneration?

A

Early age-related macular degeneration (non-exudative, age-related maculopathy) and late age-related macular degeneration (neovascularisation, exudative).

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135
Q

What are the clinical features of age-related macular degeneration?

A

Subacute onset of visual loss, reduced visual acuity, difficulty with dark adaptation, fluctuations in visual disturbance, photopsia, glare, and visual hallucinations (Charles-Bonnet syndrome).

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136
Q

What sign on Amsler grid testing may be observed in ARMD?

A

Distortion of line perception.

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137
Q

What is seen on fundoscopy in dry ARMD?

A

Drusen (yellow areas of pigment deposition in the macular area), which may become confluent to form a macular scar in late disease.

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138
Q

What is seen on fundoscopy in wet ARMD?

A

Well-demarcated red patches representing intra-retinal or sub-retinal fluid leakage or haemorrhage.

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139
Q

What is the initial investigation of choice for ARMD?

A

Slit-lamp microscopy, often accompanied by colour fundus photography.

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140
Q

When is fluorescein angiography used in ARMD?

A

If neovascular ARMD is suspected, to guide intervention with anti-VEGF therapy.

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141
Q

What is optical coherence tomography used for in ARMD?

A

To visualise the retina in three dimensions and reveal areas of disease not visible with microscopy alone.

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142
Q

What treatment was shown to reduce the progression of dry ARMD in the AREDS trial?

A

A combination of zinc and antioxidant vitamins A, C, and E.

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143
Q

What is the role of anti-VEGF agents in the treatment of wet ARMD?

A

Anti-VEGF agents, such as ranibizumab, bevacizumab, and pegaptanib, limit progression and can stabilise or reverse visual loss in wet ARMD.

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144
Q

When should anti-VEGF therapy ideally be initiated in wet ARMD?

A

Within the first two months of diagnosis.

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145
Q

What is the role of laser photocoagulation in ARMD treatment?

A

It slows progression in cases of new vessel formation but carries a risk of acute visual loss, especially in sub-foveal ARMD, so anti-VEGF therapies are usually preferred.

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146
Q

What is the most common cause of admissions to child and adolescent psychiatric wards?

A

Anorexia nervosa.

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147
Q

What percentage of patients with anorexia nervosa are female?

A

90%.

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148
Q

What age group is most commonly affected by anorexia nervosa?

A

Teenage and young-adult females.

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149
Q

What is the prevalence of anorexia nervosa?

A

Between 1:100 and 1:200.

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150
Q

What are the DSM-5 diagnostic criteria for anorexia nervosa?

A
  1. Restriction of energy intake leading to a significantly low body weight. 2. Intense fear of gaining weight or becoming fat, even though underweight. 3. Disturbance in body weight or shape perception, undue influence of body weight on self-evaluation, or denial of the seriousness of low body weight.
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151
Q

Are BMI and amenorrhoea specifically mentioned in the DSM-5 criteria for anorexia nervosa?

A

No, they are no longer specifically mentioned.

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152
Q

What is the first-line treatment for adults with anorexia nervosa according to NICE guidelines?

A

Individual eating-disorder-focused cognitive behavioural therapy (CBT-ED), Maudsley Anorexia Nervosa Treatment for Adults (MANTRA), or specialist supportive clinical management (SSCM).

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153
Q

What is the first-line treatment for children and young people with anorexia nervosa according to NICE guidelines?

A

Anorexia-focused family therapy.

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154
Q

What is the second-line treatment for children and young people with anorexia nervosa according to NICE guidelines?

A

Cognitive behavioural therapy (CBT).

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155
Q

What is the prognosis of patients with anorexia nervosa?

A

Up to 10% of patients may eventually die due to the disorder.

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156
Q

What are some characteristic clinical features of anorexia nervosa?

A

Reduced body mass index, bradycardia, hypotension, enlarged salivary glands.

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157
Q

What physiological abnormalities are commonly seen in anorexia nervosa?

A

Hypokalaemia, low FSH, LH, oestrogens, and testosterone; raised cortisol and growth hormone; impaired glucose tolerance; hypercholesterolaemia; hypercarotinaemia; low T3.

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158
Q

What is the DSM-V definition of Attention Deficit Hyperactivity Disorder (ADHD)?

A

ADHD is defined as a condition incorporating features of inattention and/or hyperactivity/impulsivity that are persistent, with developmental delay required for diagnosis.

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159
Q

What is the prevalence of ADHD in the UK?

A

ADHD has a UK prevalence of 2.4%, and is more common in boys than in girls (M:F 4:1).

160
Q

At what age are most children diagnosed with ADHD?

A

Most children are diagnosed between the ages of 3 and 7.

161
Q

What is the diagnostic criteria for ADHD in children up to the age of 16?

A

Six of the features of inattention and/or hyperactivity/impulsivity must be present.

162
Q

What is the diagnostic criteria for ADHD in individuals aged 17 or over?

A

Five of the features of inattention and/or hyperactivity/impulsivity must be present.

163
Q

What are some common features of inattention in ADHD?

A

Does not follow through on instructions, reluctant to engage in mentally intense tasks, easily distracted, finds it difficult to sustain tasks, often forgetful, often loses things necessary for tasks.

164
Q

What are some common features of hyperactivity/impulsivity in ADHD?

A

Unable to play quietly, talks excessively, does not wait their turn, leaves seat when expected to sit, is often ‘on the go’, interrupts others, answers prematurely, runs and climbs in inappropriate situations.

165
Q

What is the recommended approach to managing ADHD according to NICE?

A

A holistic approach, with a ten-week ‘watch and wait’ period followed by referral to secondary care if symptoms persist. Treatment is tailored to the individual.

166
Q

When should drug therapy be considered for ADHD?

A

Drug therapy is considered a last resort, usually for those aged 5 or more, when symptoms are severe or don’t respond to other interventions.

167
Q

What is the first-line pharmacotherapy for ADHD in children?

A

Methylphenidate, given on a six-week trial basis.

168
Q

What are some side effects of methylphenidate in children?

A

Abdominal pain, nausea, dyspepsia, and monitoring of weight and height every 6 months.

169
Q

What should be done if there is an inadequate response to methylphenidate in children?

A

Switch to lisdexamfetamine.

170
Q

What is the treatment approach for ADHD in adults?

A

Methylphenidate or lisdexamfetamine are first-line options, with a switch between the two if no benefit is seen.

171
Q

What cardiotoxic risks are associated with ADHD medications?

A

All ADHD medications are potentially cardiotoxic, so a baseline ECG should be performed, and a cardiologist should be consulted if there is any relevant medical history or concerns.

172
Q

What is important when diagnosing ADHD due to its overlap with other conditions?

A

A thorough history and clinical examination are key to distinguishing ADHD from other psychiatric and physical conditions.

173
Q

What is Autism Spectrum Disorder (ASD)?

A

Autism is a neurodevelopmental condition characterized by qualitative impairment in social interaction and communication, along with repetitive stereotyped behaviours, interests, and activities.

174
Q

What is the prevalence of ASD?

A

The prevalence of ASD is estimated to be 1-2%, with it being three to four times more common in boys than girls.

175
Q

What percentage of children with ASD have an intellectual disability?

A

Around 50% of children with ASD have an intellectual disability.

176
Q

What are some clinical features of Autism Spectrum Disorder?

A

Impaired social communication and interaction, such as playing alone, failure to regulate social interaction with nonverbal cues, and social isolation. Repetitive behaviours, interests, and activities, including stereotyped motor mannerisms and inflexible adherence to routines.

177
Q

What other conditions are commonly associated with ASD in children?

A

Attention deficit hyperactivity disorder (35%) and epilepsy (18%).

178
Q

What is the goal of managing Autism Spectrum Disorder?

A

The goal is to increase functional independence, improve social skills and communication, decrease disability and comorbidity, and aid families.

179
Q

What are some non-pharmacological therapies for ASD?

A

Early educational and behavioural interventions such as Applied Behavioural Analysis (ABA), TEACCH, Early Start Denver Model (ESDM), and Joint Attention Symbolic Play Engagement and Regulation (JASPER).

180
Q

What pharmacological interventions may be used in managing ASD?

A

SSRIs (to reduce repetitive behaviours, anxiety, and aggression), antipsychotic drugs (to reduce aggression and self-injury), and methylphenidate (for ADHD).

181
Q

What role does family support and counselling play in managing ASD?

A

Parental education on how to interact with the child, understanding their behaviour, and accepting it are key aspects of family support.

182
Q

What are the features of beta-blocker overdose?

A

Bradycardia, hypotension, heart failure, and syncope.

183
Q

How should bradycardia caused by a beta-blocker overdose be managed?

A

Atropine should be administered.

184
Q

What treatment may be used in resistant cases of beta-blocker overdose?

A

Glucagon may be used in resistant cases.

185
Q

Is haemodialysis effective in beta-blocker overdose?

A

No, haemodialysis is not effective in beta-blocker overdose.

186
Q

What is the first-line management for binge eating disorder in adults according to NICE?

A

NICE recommends a ‘binge-eating-disorder-focused’ guided self-help programme.

187
Q

What should be offered if guided self-help for binge eating disorder is unacceptable, contraindicated, or ineffective after 4 weeks?

A

If guided self-help is ineffective, NICE recommends offering group eating-disorder-focused cognitive behavioural therapy (CBT-ED).

188
Q

What characterizes bulimia nervosa?

A

Bulimia nervosa is characterized by episodes of binge eating followed by intentional vomiting or other purgative behaviours such as the use of laxatives, diuretics, or excessive exercise.

189
Q

What are the DSM-5 diagnostic criteria for bulimia nervosa?

A

The criteria include recurrent episodes of binge eating, a sense of lack of control over eating, recurrent inappropriate compensatory behaviour (e.g., self-induced vomiting, laxative misuse, excessive exercise), binge eating and compensatory behaviours occurring at least once a week for three months, self-evaluation unduly influenced by body shape and weight, and the disturbance not occurring exclusively during anorexia nervosa.

190
Q

What are physical signs associated with bulimia nervosa?

A

Recurrent vomiting may lead to erosion of teeth and Russell’s sign (calluses on the knuckles or back of the hand due to repeated self-induced vomiting).

191
Q

What are the diagnostic criteria for bulimia nervosa?

A

Eating, recurrent inappropriate compensatory behaviour (e.g., self-induced vomiting, laxative misuse, excessive exercise), binge eating and compensatory behaviours occurring at least once a week for three months, self-evaluation unduly influenced by body shape and weight, and the disturbance not occurring exclusively during anorexia nervosa.

192
Q

What is the first-line treatment for bulimia nervosa in adults according to NICE?

A

NICE recommends bulimia-nervosa-focused guided self-help for adults.

193
Q

What should be offered if bulimia-nervosa-focused guided self-help is ineffective after 4 weeks?

A

NICE recommends considering individual eating-disorder-focused cognitive behavioural therapy (CBT-ED) if guided self-help is ineffective.

194
Q

What is the recommended treatment for children with bulimia nervosa?

A

Children should be offered bulimia-nervosa-focused family therapy (FT-BN).

195
Q

What is the role of pharmacological treatment in bulimia nervosa?

A

Pharmacological treatments have a limited role, with a trial of high-dose fluoxetine being licensed for bulimia, but long-term data is lacking.

196
Q

What are the CNS features of synthetic cannabinoid toxicity?

A

CNS features include agitation, tremor, anxiety, confusion, somnolence, syncope, hallucinations, changes in perception, acute psychosis, nystagmus, convulsions, and coma.

197
Q

What are the cardiac features of synthetic cannabinoid toxicity?

A

Cardiac features include tachycardia, hypertension, chest pain, palpitations, and ECG changes.

198
Q

What renal complication can occur with synthetic cannabinoid toxicity?

A

Acute kidney injury can occur.

199
Q

What muscular symptoms are associated with synthetic cannabinoid toxicity?

A

Muscular symptoms include hypertonia, myoclonus, muscle jerking, and myalgia.

200
Q

What are other features of synthetic cannabinoid toxicity?

A

Other features include cold extremities, dry mouth, dyspnoea, mydriasis, vomiting, and hypokalaemia.

201
Q

What is Charles-Bonnet syndrome (CBS)?

A

CBS is characterised by persistent or recurrent complex hallucinations (usually visual or auditory), occurring in clear consciousness, typically against a background of visual impairment, with preserved insight and no significant neuropsychiatric disturbance.

202
Q

What are the common risk factors for Charles-Bonnet syndrome?

A

Advanced age, peripheral visual impairment, social isolation, sensory deprivation, and early cognitive impairment.

203
Q

What ophthalmological conditions are most commonly associated with Charles-Bonnet syndrome?

A

Age-related macular degeneration, followed by glaucoma and cataract.

204
Q

What is the prevalence of Charles-Bonnet syndrome in individuals with severe visual impairment?

A

It is thought to occur in 10-30% of individuals with severe visual impairment, and the prevalence in visually impaired people is between 11 and 15%.

205
Q

How long do hallucinations last in most individuals with Charles-Bonnet syndrome?

A

Around a third find the hallucinations unpleasant or disturbing, and 88% had CBS for 2 years or more, with only 25% resolving after 9 years.

206
Q

What is the mechanism of action of cocaine?

A

Cocaine blocks the uptake of dopamine, noradrenaline, and serotonin.

207
Q

What are the cardiovascular adverse effects of cocaine?

A

Coronary artery spasm, myocardial ischaemia/infarction, tachycardia, bradycardia, hypertension, QRS widening, QT prolongation, and aortic dissection.

208
Q

What are the neurological adverse effects of cocaine?

A

Seizures, mydriasis, hypertonia, and hyperreflexia.

209
Q

What are the psychiatric effects of cocaine?

A

Agitation, psychosis, and hallucinations.

210
Q

What other adverse effects can cocaine cause?

A

Ischaemic colitis, hyperthermia, metabolic acidosis, and rhabdomyolysis.

211
Q

What is the first-line management for most cocaine-related problems?

A

Benzodiazepines.

212
Q

What is the treatment for chest pain in cocaine toxicity?

A

Benzodiazepines and glyceryl trinitrate.

213
Q

What should be done if myocardial infarction develops in cocaine toxicity?

A

Primary percutaneous coronary intervention.

214
Q

How is hypertension managed in cocaine toxicity?

A

Benzodiazepines and sodium nitroprusside.

215
Q

What is the controversy regarding beta-blockers in cocaine toxicity?

A

The American Heart Association issued a warning against beta-blockers due to the risk of unopposed alpha-mediated coronary vasospasm, but many cardiologists have since questioned this recommendation.

216
Q

What is the most common cause of dementia in the UK?

A

Alzheimer’s disease, followed by vascular and Lewy body dementia.

217
Q

What is a common issue in the diagnosis of dementia?

A

Diagnosis can be difficult and is often delayed.

218
Q

What assessment tools are recommended by NICE for non-specialist settings?

A

10-point cognitive screener (10-CS) and 6-Item cognitive impairment test (6CIT).

219
Q

What assessment tools are not recommended by NICE for non-specialist settings?

A

The abbreviated mental test score (AMTS), General practitioner assessment of cognition (GPCOG), and the mini-mental state examination (MMSE).

220
Q

What MMSE score suggests dementia?

A

A score of 24 or less out of 30.

221
Q

What blood tests are commonly sent in primary care to exclude reversible causes of dementia?

A

FBC, U&E, LFTs, calcium, glucose, ESR/CRP, TFTs, vitamin B12, and folate levels.

222
Q

What is the role of neuroimaging in dementia diagnosis?

A

To exclude other reversible conditions (e.g. subdural haematoma, normal pressure hydrocephalus) and provide information on aetiology to guide prognosis and management.

223
Q

What did the 2011 NICE guidelines state about structural imaging in dementia?

A

Structural imaging was said to be essential in the investigation of dementia.

224
Q

What PHQ-9 score defines ‘less severe’ depression according to the 2022 NICE guidelines?

A

A PHQ-9 score of < 16.

225
Q

What PHQ-9 score defines ‘more severe’ depression according to the 2022 NICE guidelines?

A

A PHQ-9 score of ≥ 16.

226
Q

What does NICE recommend for managing less severe depression?

A

NICE recommends considering the least intrusive and least resource-intensive treatment first, with antidepressants not routinely offered as first-line unless the patient’s preference is for them.

227
Q

What are the first-line treatment options for less severe depression according to NICE?

A

Guided self-help, group cognitive behavioural therapy (CBT), group behavioural activation (BA), individual CBT, individual BA, group exercise, group mindfulness and meditation, interpersonal psychotherapy (IPT), selective serotonin reuptake inhibitors (SSRIs), counselling, short-term psychodynamic psychotherapy (STPP).

228
Q

What are the preferred treatment options for more severe depression according to NICE?

A

A combination of individual cognitive behavioural therapy (CBT) and an antidepressant, individual CBT, individual behavioural activation (BA), antidepressant medication (SSRI, SNRI, or another antidepressant based on previous history), individual problem-solving, counselling, short-term psychodynamic psychotherapy (STPP), interpersonal psychotherapy (IPT), guided self-help, group exercise.

229
Q

What is recommended when switching from citalopram, escitalopram, sertraline, or paroxetine to another SSRI?

A

A direct switch is possible.

230
Q

What is recommended when switching from fluoxetine to another SSRI?

A

Withdraw fluoxetine and leave a gap of 4-7 days before starting a low dose of the alternative SSRI.

231
Q

What is recommended when switching from an SSRI to a tricyclic antidepressant (TCA)?

A

Cross-tapering is recommended, where the current drug dose is reduced slowly while the dose of the new drug is increased slowly, except for fluoxetine, which should be withdrawn, with a 4-7 day gap before starting the TCA at a low dose.

232
Q

What is recommended when switching from citalopram, escitalopram, sertraline, or paroxetine to venlafaxine?

A

A direct switch is possible, with caution if paroxetine was used.

233
Q

What is recommended when switching from fluoxetine to venlafaxine?

A

Withdraw fluoxetine and start venlafaxine at a low dose 4-7 days later.

234
Q

What are the primary classifications of eating disorders?

A

The primary classifications are anorexia nervosa, bulimia nervosa, and binge eating disorder, along with other specified and unspecified feeding or eating disorders (OSFED/UFED).

235
Q

What is the definition of anorexia nervosa?

A

Anorexia nervosa is defined by a restriction of energy intake relative to requirements, leading to a significantly low body weight, with an intense fear of gaining weight or becoming fat, and a disturbance in the perception of one’s body weight or shape.

236
Q

What are the criteria for anorexia nervosa?

A
  1. Restriction of food intake leading to a significantly low body weight.
  2. Intense fear of gaining weight or persistent behavior to avoid it.
  3. Disturbance in the perception of body weight or shape, undue influence of body weight on self-worth, or persistent denial of the seriousness of the low body weight.
237
Q

What characterises bulimia nervosa?

A

Bulimia nervosa is characterised by recurrent episodes of binge eating followed by inappropriate compensatory behaviours, such as vomiting, laxative misuse, or excessive exercise, to prevent weight gain.

238
Q

What are the criteria for bulimia nervosa?

A
  1. Recurrent episodes of binge eating with a sense of lack of control.
  2. Recurrent inappropriate compensatory behaviours to prevent weight gain.
  3. Both binge eating and compensatory behaviours occur at least once a week for three months.
  4. Self-worth is overly influenced by body shape and weight.
239
Q

What characterises binge eating disorder?

A

Binge eating disorder involves recurrent episodes of binge eating, but unlike bulimia nervosa, there are no consistent inappropriate compensatory behaviours.

240
Q

What are the criteria for binge eating disorder?

A
  1. Recurrent episodes of binge eating.
  2. At least three of the following: eating more rapidly than normal, eating until uncomfortably full, eating large amounts when not physically hungry, eating alone due to embarrassment, and feeling disgusted, depressed, or guilty after eating.
  3. Marked distress regarding binge eating.
  4. Binge eating occurs at least once a week for three months.
241
Q

What is the diagnosis and treatment approach for eating disorders?

A

Diagnosis is based on clinical evaluation considering medical history, physical examination, and diagnostic criteria. Early detection and a multidisciplinary approach involving medical, psychological, and nutritional support are crucial for optimal outcomes.

242
Q

What are the complications of untreated eating disorders?

A

Untreated eating disorders can lead to severe physical complications like cardiac arrhythmias, electrolyte imbalances, osteoporosis, and increased mortality risk, as well as psychological complications including depression, anxiety, and a higher risk of self-harm or suicide.

243
Q

What are the neurological clinical features of ecstasy poisoning?

A

Agitation, anxiety, confusion, ataxia.

244
Q

What are the cardiovascular clinical features of ecstasy poisoning?

A

Tachycardia, hypertension.

245
Q

What electrolyte imbalance is associated with ecstasy poisoning?

A

Hyponatraemia, which may result from either syndrome of inappropriate ADH secretion or excessive water consumption.

246
Q

What is a key metabolic feature of ecstasy poisoning?

A

Hyperthermia and rhabdomyolysis.

247
Q

What is the management for ecstasy poisoning?

A

Supportive care, and dantrolene may be used for hyperthermia if simple measures fail.

248
Q

What is the central feature of anxiety according to NICE?

A

Excessive worry about a number of different events associated with heightened tension.

249
Q

What are some important physical causes to consider when diagnosing anxiety disorders?

A

Hyperthyroidism, cardiac disease, and medication-induced anxiety (e.g., salbutamol, theophylline, corticosteroids, antidepressants, and caffeine).

250
Q

What is the first step in the management of Generalised Anxiety Disorder (GAD) according to NICE?

A

Education about GAD and active monitoring.

251
Q

What is the second step in the management of GAD?

A

Low-intensity psychological interventions, such as individual non-facilitated self-help, individual guided self-help, or psychoeducational groups.

252
Q

What is the third step in the management of GAD?

A

High-intensity psychological interventions, such as cognitive behavioural therapy (CBT) or applied relaxation, or drug treatment.

253
Q

What is the first-line drug treatment for GAD recommended by NICE?

A

Sertraline (an SSRI).

254
Q

What should be offered if sertraline is ineffective for GAD?

A

An alternative SSRI or a serotonin-noradrenaline reuptake inhibitor (SNRI), such as duloxetine or venlafaxine.

255
Q

What drug is recommended if SSRIs or SNRIs are not tolerated in GAD?

A

Pregabalin.

256
Q

What warning should be given to patients under 30 years starting treatment for GAD?

A

The increased risk of suicidal thinking and self-harm, with weekly follow-up recommended for the first month.

257
Q

What is the first step in the management of panic disorder according to NICE?

A

Recognition and diagnosis.

258
Q

What is the second step in the management of panic disorder?

A

Treatment in primary care, which may involve cognitive behavioural therapy or drug treatment.

259
Q

What is the first-line drug treatment for panic disorder recommended by NICE?

A

SSRIs.

260
Q

What should be offered if SSRIs are contraindicated or ineffective after 12 weeks for panic disorder?

A

Imipramine or clomipramine.

261
Q

What are the major complications of iron overdose?

A

Metabolic acidosis, erosion of gastric mucosa leading to GI bleeding, shock, hepatotoxicity, and coagulopathy.

262
Q

How is iron overdose management guided?

A

It is guided by the total amount of iron ingested (elemental iron/kg) and the presence or absence of symptoms like abdominal pain, diarrhoea, vomiting, or lethargy.

263
Q

What is the management for patients who ingested less than 40mg/kg elemental iron and are asymptomatic?

A

They can be observed at home.

264
Q

What is the management for patients who ingested more than 40mg/kg elemental iron or are symptomatic?

A

They require medical assessment with serum iron levels measured 2-4 hours post-ingestion and an abdominal x-ray.

265
Q

What is the decontamination procedure of choice for iron overdose?

A

Whole bowel irrigation, especially for patients who ingested > 60mg/kg elemental iron or have undissolved tablets on abdominal x-ray.

266
Q

Is activated charcoal effective in treating iron poisoning?

A

No, activated charcoal is ineffective in iron poisoning.

267
Q

When is desferrioxamine indicated in iron overdose?

A

It is indicated in patients with serum iron level > 90umol/l, or in patients with serum iron level 60-90umol/l who are symptomatic or have persistent iron on abdominal x-ray despite whole bowel irrigation, or in any patient with shock, coma, or metabolic acidosis.

268
Q

What may be required if whole bowel irrigation is not effective or iron is adhered to the gastric wall?

A

Endoscopy or surgery may be required.

269
Q

What is the common use of lithium?

A

Lithium is most commonly used prophylactically in bipolar disorder and as an adjunct in refractory depression.

270
Q

What is the therapeutic range for lithium?

A

The therapeutic range for lithium is 0.4-1.0 mmol/L.

271
Q

How is lithium primarily excreted?

A

Lithium is primarily excreted by the kidneys.

272
Q

What are the two theories for lithium’s mechanism of action?

A

Lithium interferes with inositol triphosphate formation and with cAMP formation.

273
Q

What are the common adverse effects of lithium?

A

Nausea/vomiting, diarrhoea, fine tremor, nephrotoxicity (polyuria secondary to nephrogenic diabetes insipidus), thyroid enlargement (leading to hypothyroidism), T wave flattening/inversion on ECG, weight gain, idiopathic intracranial hypertension, leucocytosis, hyperparathyroidism and resultant hypercalcaemia.

274
Q

How should lithium levels be monitored?

A

Lithium levels should be checked 12 hours post-dose. After starting lithium, levels should be performed weekly and after each dose change until concentrations are stable, then every 3 months. After a dose change, levels should be checked weekly until stable.

275
Q

How often should thyroid and renal function be checked in patients on lithium?

A

Thyroid and renal function should be checked every 6 months.

276
Q

What should be issued to patients on lithium therapy?

A

Patients should be issued with an information booklet, alert card, and record book.

277
Q

When does lithium toxicity generally occur?

A

Lithium toxicity generally occurs following concentrations > 1.5 mmol/L.

278
Q

What factors can precipitate lithium toxicity?

A

Dehydration, renal failure, and drugs such as diuretics (especially thiazides), ACE inhibitors/angiotensin II receptor blockers, NSAIDs, and metronidazole.

279
Q

What are the features of lithium toxicity?

A

Coarse tremor (as opposed to fine tremor at therapeutic levels), hyperreflexia, acute confusion, polyuria, seizure, and coma.

280
Q

How is mild-moderate lithium toxicity managed?

A

Mild-moderate toxicity may respond to volume resuscitation with normal saline, IV fluids with isotonic saline, until euvolemic, then typically twice maintenance rate.

281
Q

What should be monitored in lithium toxicity management?

A

Serum sodium should be monitored closely (every 4 hours with serial lithium concentrations) if there is concern about lithium-induced nephrogenic diabetes insipidus.

282
Q

When is haemodialysis required in lithium toxicity?

A

Haemodialysis may be needed in severe toxicity.

283
Q

How can sodium bicarbonate be used in lithium toxicity management?

A

Sodium bicarbonate is sometimes used to increase the alkalinity of the urine, promoting lithium excretion, although there is limited evidence to support this.

284
Q

What are the psychoactive symptoms of LSD intoxication?

A

Psychoactive symptoms include variable subjective experiences, impaired judgement, amplification of current mood (euphoria or dysphoria), agitation, appearing withdrawn, and drug-induced psychosis.

285
Q

What are the somatic symptoms of LSD intoxication?

A

Somatic symptoms include nausea, headache, palpitations, dry mouth, drowsiness, and tremors.

286
Q

What signs are associated with LSD intoxication?

A

Signs of LSD intoxication include tachycardia, hypertension, mydriasis, paresthesia, hyperreflexia, and pyrexia.

287
Q

What are the complications of massive LSD overdoses?

A

Massive overdoses can lead to respiratory arrest, coma, hyperthermia, autonomic dysfunction, and bleeding disorders.

288
Q

How is LSD toxicity diagnosed?

A

The diagnosis is mainly based on history and examination, as most urine drug screens do not detect LSD.

289
Q

What is the management for agitation in LSD intoxication?

A

Agitation from a ‘bad trip’ should be managed with supportive reassurance in a calm, stress-free environment. If ineffective, benzodiazepines are the medication of choice.

290
Q

What is the management for LSD-induced psychosis?

A

LSD-induced psychosis may require antipsychotics.

291
Q

How is massive LSD ingestion managed?

A

Massive ingestions should be treated with supportive care, including respiratory support and endotracheal intubation if needed. Hypertension, tachycardia, and hyperthermia should be treated symptomatically. Hypotension should be treated initially with fluids and subsequently with vasopressors if required.

292
Q

Why is activated charcoal and gastric emptying of limited clinical value in LSD toxicity?

A

Because LSD is rapidly absorbed through the gastrointestinal tract, activated charcoal administration and gastric emptying are of little clinical value by the time a patient presents to the emergency department.

293
Q

What is the mechanism of action of nitrous oxide when inhaled?

A

Nitrous oxide acts as a dissociative anaesthetic by blocking NMDA receptors, impairing the perception of pain and inducing a state of euphoria and relaxation. It also causes the release of endogenous opioids and dopamine, contributing to its addictive potential.

294
Q

What are the psychological symptoms of nitrous oxide misuse?

A

Psychological symptoms include euphoria, altered perception of reality, hallucinations, anxiety, and paranoia.

295
Q

What are the neurological symptoms of nitrous oxide misuse?

A

Neurological symptoms include dizziness, headache, incoordination, numbness, and tremors.

296
Q

What physiological effects are associated with nitrous oxide misuse?

A

Physiological effects include hypoxia, hypothermia, elevated heart rate, and elevated blood pressure.

297
Q

What are the long-term effects of nitrous oxide misuse?

A

Long-term effects include vitamin B12 deficiency, subacute combined degeneration of the spinal cord, psychological issues (e.g., mood disorders and anxiety), and physical harm (e.g., lung damage, barotrauma, and frostbite).

298
Q

How does chronic nitrous oxide exposure lead to vitamin B12 deficiency?

A

Chronic exposure leads to vitamin B12 deficiency due to its interference with vitamin B12 metabolism.

299
Q

How does chronic nitrous oxide exposure lead to vitamin B12 deficiency?

A

Chronic exposure to nitrous oxide oxidises and inactivates vitamin B12, leading to deficiency.

300
Q

What neurological impairment can result from persistent nitrous oxide misuse?

A

Persistent misuse can lead to subacute combined degeneration of the spinal cord, resulting in irreversible neurological impairments.

301
Q

What physical harm can result from inhaling nitrous oxide from containers or balloons?

A

The act of inhaling gas from containers or balloons poses a risk of lung damage, barotrauma, and frostbite.

302
Q

What characterises obsessive-compulsive disorder (OCD)?

A

OCD is characterised by the presence of either obsessions (unwanted intrusive thoughts, images, or urges) or compulsions (repetitive behaviours or mental acts), but commonly both. These symptoms cause significant functional impairment and/or distress.

303
Q

What are obsessions in OCD?

A

Obsessions are unwanted intrusive thoughts, images, or urges that repeatedly enter a person’s mind.

304
Q

What are compulsions in OCD?

A

Compulsions are repetitive behaviours or mental acts that a person feels driven to perform. These can be overt (e.g., checking if a door is locked) or covert (e.g., repeating a phrase in one’s mind).

305
Q

What is the peak age of onset for OCD?

A

The peak age of onset for OCD is between 10-20 years.

306
Q

What are some risk factors for developing OCD?

A

Risk factors include family history, age (peak onset 10-20 years), pregnancy/postnatal period, and a history of abuse, bullying, or neglect.

307
Q

How does NICE recommend classifying OCD impairment?

A

NICE recommends classifying impairment into mild, moderate, or severe using the Y-BOCS scale.

308
Q

What are the treatment options for mild OCD?

A

For mild OCD, low-intensity psychological treatments, such as cognitive behavioural therapy (CBT) with exposure and response prevention (ERP), are recommended.

309
Q

What are the treatment options for moderate OCD?

A

For moderate OCD, a choice of either an SSRI (any SSRI for OCD, fluoxetine specifically for body dysmorphic disorder) or more intensive CBT (including ERP) is recommended. Clomipramine may be considered if the person prefers it or has had a previous good response.

310
Q

What are the treatment options for severe OCD?

A

For severe OCD, patients should be referred to the secondary care mental health team for assessment. In the meantime, combined treatment with an SSRI and CBT (including ERP) or clomipramine may be considered.

311
Q

What is exposure and response prevention (ERP) in the treatment of OCD?

A

ERP is a psychological method where a patient is exposed to an anxiety-provoking situation (e.g., having dirty hands) and prevented from engaging in their usual safety behaviour (e.g., washing hands). This helps confront anxiety, leading to the extinction of the response over time.

312
Q

How long should an SSRI be continued for OCD treatment?

A

If the SSRI is effective, it should be continued for at least 12 months to prevent relapse and allow time for improvement.

313
Q

How does the duration and dose of SSRIs in OCD treatment compare to depression?

A

SSRIs usually require a higher dose and longer duration (at least 12 weeks) for an initial response in OCD compared to depression.

314
Q

What are some features of opioid misuse?

A

Features of opioid misuse include rhinorrhoea, needle track marks, pinpoint pupils, drowsiness, watering eyes, and yawning.

315
Q

What are some complications of opioid misuse?

A

Complications include viral infections (HIV, hepatitis B & C) from sharing needles, bacterial infections (e.g., infective endocarditis, septic arthritis, necrotising fasciitis) from injection, venous thromboembolism, overdose leading to respiratory depression and death, psychological issues (e.g., cravings), and social problems (e.g., crime, prostitution, homelessness).

316
Q

What is the emergency management for opioid overdose?

A

The emergency management for opioid overdose includes IV or IM naloxone, which has a rapid onset and relatively short duration of action.

317
Q

What are some harm reduction interventions for opioid misuse?

A

Harm reduction interventions include needle exchange programs and offering testing for HIV, hepatitis B & C.

318
Q

How is opioid dependence typically managed?

A

Opioid dependence is managed by specialist drug dependence clinics, with options for maintenance therapy or detoxification. GPs with a specialist interest may also offer similar services.

319
Q

What are the first-line treatments for opioid detoxification according to NICE?

A

NICE recommends methadone or buprenorphine as the first-line treatment for opioid detoxification.

320
Q

What is the mechanism of action of methadone in opioid detoxification?

A

Methadone is a full agonist of the mu-opioid receptor, fully activating these receptors in the brain to relieve withdrawal symptoms and cravings. It has a long half-life.

321
Q

What is the mechanism of action of buprenorphine in opioid detoxification?

A

Buprenorphine is a partial agonist of the mu-opioid receptor and an antagonist of the kappa-opioid receptor. It partially activates mu-opioid receptors to alleviate cravings and withdrawal symptoms. It has a strong affinity for mu-opioid receptors, displacing other opioids and preventing their effects.

322
Q

How is compliance monitored in opioid detoxification?

A

Compliance in opioid detoxification is monitored using urinalysis.

323
Q

How long should detoxification last in an inpatient/residential setting versus the community?

A

Detoxification should last up to 4 weeks in an inpatient/residential setting and up to 12 weeks in the community.

324
Q

When should activated charcoal be administered in the case of a paracetamol overdose?

A

Activated charcoal should be administered if the patient presents within 1 hour of ingestion to reduce absorption of the drug.

325
Q

When should acetylcysteine be given in the case of a paracetamol overdose?

A

Acetylcysteine should be given if:

  • The plasma paracetamol concentration is on or above a single treatment line on the nomogram, regardless of risk factors for hepatotoxicity.
  • There is a staggered overdose or doubt over the time of ingestion.
  • The patient presents 8-24 hours after ingestion of more than 150 mg/kg of paracetamol, even if the plasma paracetamol concentration is not yet available.
  • The patient presents > 24 hours after ingestion with jaundice or hepatic tenderness, and ALT is elevated.
    Acetylcysteine should be continued if the paracetamol concentration or ALT remains elevated.
326
Q

How should acetylcysteine be administered for paracetamol overdose?

A

Acetylcysteine should now be infused over 1 hour, rather than the previous 15 minutes, to reduce the risk of adverse effects.

327
Q

How should an anaphylactoid reaction to acetylcysteine be managed?

A

If an anaphylactoid reaction occurs, stop the infusion and then restart it at a slower rate.

328
Q

What are the King’s College Hospital criteria for liver transplantation in cases of paracetamol liver failure?

A

The criteria for liver transplantation include:

  • Arterial pH < 7.3, 24 hours after ingestion, or
  • All of the following:
    • Prothrombin time > 100 seconds
    • Creatinine > 300 µmol/l
    • Grade III or IV encephalopathy
329
Q

What defines a staggered overdose in paracetamol ingestion?

A

A staggered overdose is defined as one in which all the tablets were not taken within 1 hour.

330
Q

What is the ICD-11 classification of personality disorders based on?

A

The ICD-11 classification of personality disorders is based on severity, categorizing them as mild, moderate, or severe. This provides a more flexible and comprehensive understanding of personality pathology.

331
Q

What are the characteristics of mild personality disorder according to ICD-11?

A

Mild personality disorder involves some impairments in functioning, often limited to specific areas of life, such as intimate relationships or work. Symptoms may be noticeable to others but do not cause pervasive distress or dysfunction. The individual may still maintain relatively stable relationships and occupational roles.

332
Q

What is the defining feature of a personality disorder according to ICD-11?

A

The defining feature of a personality disorder is a persistent pattern of cognition, emotional experience, behavior, and interpersonal functioning that deviates from cultural expectations, resulting in significant problems or dysfunctions in various aspects of life, including relationships, work, or social functioning.

333
Q

What are the key domains of personality disorder trait domains in ICD-11?

A

The key trait domains in ICD-11 include:

  • Negative Affectivity: Tendency to experience negative emotions like anxiety, depression, guilt, and anger.
  • Detachment: Avoidance of social interactions and emotional withdrawal.
  • Dissociality: Disregard for others’ rights, lack of empathy, and difficulty forming prosocial relationships.
  • Disinhibition: Impulsivity, risk-taking, and difficulty controlling behaviors.
  • Anankastia: Preoccupation with orderliness, control, and perfectionism.
  • Borderline Pattern: Emotional instability, unstable relationships, fluctuating identity, and impulsivity.
334
Q

What are the three clusters of personality disorders in the previous classification system?

A

The three clusters of personality disorders are:

  • Cluster A: ‘Odd or Eccentric’ (Paranoid, Schizoid, Schizotypal)
  • Cluster B: ‘Dramatic, Emotional, or Erratic’ (Antisocial, Borderline, Histrionic, Narcissistic)
  • Cluster C: ‘Anxious and Fearful’ (Obsessive-compulsive, Avoidant, Dependent)
335
Q

What are some treatments for personality disorders?

A

Treatments for personality disorders include psychological therapies, such as dialectical behavior therapy, and treatment for any coexisting psychiatric conditions.

336
Q

What are the key features of post-traumatic stress disorder (PTSD)?

A

The key features of PTSD include:

  • Re-experiencing: Flashbacks, nightmares, and distressing intrusive images.
  • Avoidance: Avoiding people, situations, or circumstances related to the traumatic event.
  • Hyperarousal: Hypervigilance, exaggerated startle response, sleep problems, irritability, and difficulty concentrating.
  • Emotional numbing: Feeling detached and unable to experience emotions.
  • Depression, drug or alcohol misuse, anger, and unexplained physical symptoms.
337
Q

What is the recommended management for PTSD following a traumatic event?

A

For mild symptoms lasting less than 4 weeks, watchful waiting may be used. Trauma-focused cognitive behavioral therapy (CBT) or eye movement desensitization and reprocessing (EMDR) therapy may be used for more severe cases. Drug treatments should not be used routinely but may include venlafaxine or SSRIs such as sertraline. In severe cases, risperidone may be recommended.

338
Q

Is debriefing recommended after a traumatic event?

A

No, single-session interventions like debriefing are not recommended following a traumatic event.

339
Q

What are some drug treatments used for PTSD, and when should they be considered?

A

Drug treatments for PTSD, such as venlafaxine or SSRIs like sertraline, should not be routinely used as a first-line treatment but may be considered in more severe cases. In particularly severe cases, risperidone may be used.

340
Q

What is the definition of a pseudohallucination?

A

A pseudohallucination is a false sensory perception in the absence of external stimuli where the affected person is aware that they are hallucinating. Unlike true hallucinations, the person recognizes that the experience is not real.

341
Q

Are pseudohallucinations included in the ICD-10 or DSM-5?

A

No, pseudohallucinations are not specifically mentioned in either the ICD-10 or DSM-5.

342
Q

How are pseudohallucinations viewed in clinical practice?

A

Many specialists view hallucinations as existing on a spectrum, from mild sensory disturbances to full-blown hallucinations. Pseudohallucinations are typically benign, and patients may need reassurance that they are normal and not indicative of a mental illness.

343
Q

Can pseudohallucinations occur in healthy individuals?

A

Yes, an example of pseudohallucinations is hypnagogic hallucinations, which can occur when transitioning from wakefulness to sleep and are experienced as vivid auditory or visual hallucinations. These are fleeting and can happen to anyone, though the person recognizes they are not real.

344
Q

In which situations are pseudohallucinations most commonly seen?

A

Pseudohallucinations are commonly seen in individuals who are grieving, but they can also occur in other contexts, such as during sleep transitions or under certain stressors.

345
Q

What is a key concept in salicylate overdose management?

A

Salicylate overdose leads to a mixed respiratory alkalosis and metabolic acidosis. Early stimulation of the respiratory center causes respiratory alkalosis, while later, the direct acid effects of salicylates combined with acute renal failure lead to acidosis. In children, metabolic acidosis tends to predominate.

346
Q

What are common features of salicylate overdose?

A

Hyperventilation, tinnitus, lethargy, sweating, pyrexia, nausea/vomiting, hyperglycaemia and hypoglycaemia, seizures, and coma.

347
Q

What is the treatment for salicylate overdose?

A

General treatment includes ABC management, activated charcoal, urinary alkalinization with intravenous sodium bicarbonate to enhance aspirin elimination, and haemodialysis.

348
Q

What are the indications for haemodialysis in salicylate overdose?

A

Serum concentration > 700 mg/L, metabolic acidosis resistant to treatment, acute renal failure, pulmonary oedema, seizures, and coma.

349
Q

Why do salicylates cause sweating and pyrexia?

A

Salicylates uncouple oxidative phosphorylation, which decreases adenosine triphosphate (ATP) production, increases oxygen consumption, and leads to increased carbon dioxide and heat production, resulting in sweating and pyrexia.

350
Q

What are selective serotonin reuptake inhibitors (SSRIs) commonly used for?

A

SSRIs are considered first-line treatment for the majority of patients with depression.

351
Q

Which SSRIs are preferred in clinical practice?

A

Citalopram and fluoxetine are currently the preferred SSRIs. Sertraline is also useful post-myocardial infarction due to its safer profile in this context.

352
Q

What are the main adverse effects of SSRIs?

A

Gastrointestinal symptoms are the most common side effect, and there is an increased risk of gastrointestinal bleeding, especially in patients taking NSAIDs.

353
Q

What should be prescribed with SSRIs if a patient is also taking an NSAID?

A

A proton pump inhibitor should be co-prescribed to reduce the risk of gastrointestinal bleeding.

354
Q

What precautions should be taken when prescribing SSRIs to children and adolescents?

A

SSRIs should be used with caution in children and adolescents. Fluoxetine is the drug of choice when an antidepressant is indicated for this age group.

355
Q

What is the concern regarding citalopram and the QT interval?

A

Citalopram and escitalopram are associated with dose-dependent QT interval prolongation. They should not be used in patients with congenital long QT syndrome, pre-existing QT interval prolongation, or in combination with other drugs that prolong the QT interval. The maximum dose is 40 mg for adults, 20 mg for patients over 65, and 20 mg for those with hepatic impairment.

356
Q

What SSRIs are more prone to drug interactions?

A

Fluoxetine and paroxetine have a higher propensity for drug interactions.

357
Q

What should be done if SSRIs are prescribed with NSAIDs, warfarin, or triptans?

A

SSRIs should not normally be offered with NSAIDs unless co-prescribed with a proton pump inhibitor. For warfarin/heparin, mirtazapine may be considered as an alternative. Triptans should be used cautiously due to an increased risk of serotonin syndrome.

358
Q

What should be the follow-up after starting antidepressant therapy?

A

Patients should be reviewed by a doctor after 2 weeks. For those under 25 years or at increased risk of suicide, review should be done after 1 week.

359
Q

How long should patients continue SSRI therapy after remission?

A

Patients should continue SSRI therapy for at least 6 months after remission to reduce the risk of relapse.

360
Q

How should SSRIs be discontinued?

A

The dose should be gradually reduced over a 4-week period, except for fluoxetine, which does not require tapering. Paroxetine has a higher incidence of discontinuation symptoms.

361
Q

What are common discontinuation symptoms of SSRIs?

A

Increased mood changes, restlessness, difficulty sleeping, unsteadiness, sweating, gastrointestinal symptoms (pain, cramping, diarrhea, vomiting), and paraesthesia.

362
Q

What are the risks of using SSRIs during pregnancy?

A

SSRIs may increase the risk of congenital heart defects if used during the first trimester and can lead to persistent pulmonary hypertension of the newborn if used during the third trimester. Paroxetine has an increased risk of congenital malformations, particularly in the first trimester.

363
Q

What causes serotonin syndrome?

A

Serotonin syndrome can be caused by monoamine oxidase inhibitors (MAOIs), SSRIs, St John’s Wort (especially when taken with SSRIs), tramadol, ecstasy, and amphetamines.

364
Q

What are the key features of serotonin syndrome?

A

Key features include neuromuscular excitation (hyperreflexia, myoclonus, rigidity), autonomic nervous system excitation (hyperthermia, sweating), and altered mental state (confusion).

365
Q

How is serotonin syndrome managed?

A

Management is supportive, including intravenous fluids and benzodiazepines. More severe cases may require serotonin antagonists such as cyproheptadine or chlorpromazine.

366
Q

What are the early features of a tricyclic overdose?

A

Early features include dry mouth, dilated pupils, agitation, sinus tachycardia, and blurred vision due to anticholinergic effects.

367
Q

What are the severe features of a tricyclic overdose?

A

Severe features include arrhythmias, seizures, metabolic acidosis, and coma.

368
Q

What ECG changes are seen in tricyclic overdose?

A

ECG changes include sinus tachycardia, widening of the QRS interval, and prolongation of the QT interval.

369
Q

What ECG changes are seen in tricyclic overdose?

A

ECG changes include sinus tachycardia, widening of the QRS interval, and prolongation of the QT interval. A QRS interval > 100 ms is associated with an increased risk of seizures, while a QRS > 160 ms is associated with ventricular arrhythmias.

370
Q

How is a tricyclic overdose managed?

A

Management includes intravenous (IV) bicarbonate for hypotension or arrhythmias, especially if the QRS interval is widened > 100 ms or there is a ventricular arrhythmia. Class 1a and 1c antiarrhythmics, as well as class III drugs like amiodarone, should be avoided. IV lipid emulsion can be used to bind free drug and reduce toxicity. Dialysis is ineffective.

371
Q

What is somatisation disorder?

A

Somatisation disorder involves multiple physical symptoms present for at least two years, with the patient refusing to accept reassurance or negative test results.

372
Q

What is illness anxiety disorder (hypochondriasis)?

A

Illness anxiety disorder is a persistent belief in the presence of an underlying serious disease (e.g., cancer), with the patient refusing to accept reassurance or negative test results.

373
Q

What is functional neurological disorder (conversion disorder)?

A

Functional neurological disorder involves loss of motor or sensory function, with the patient not consciously feigning symptoms (as in factitious disorder) or seeking material gain (as in malingering). Patients may show la belle indifference, although this is not always supported by studies.

374
Q

What is a dissociative disorder?

A

A dissociative disorder involves separating certain memories from normal consciousness, leading to psychiatric symptoms like amnesia, fugue, and stupor. Dissociative identity disorder (DID) is the most severe form and was previously known as multiple personality disorder.

375
Q

What is factitious disorder (Munchausen’s syndrome)?

A

Factitious disorder, also known as Munchausen’s syndrome, involves the intentional production of physical or psychological symptoms by the patient.

376
Q

What is malingering?

A

Malingering is the fraudulent simulation or exaggeration of symptoms with the intention of obtaining financial or other gain.

377
Q

What is the mechanism behind alcohol withdrawal?

A

Chronic alcohol consumption enhances GABA-mediated inhibition in the CNS and inhibits NMDA-type glutamate receptors. Alcohol withdrawal leads to the opposite: decreased GABA inhibition and increased NMDA glutamate transmission.

378
Q

When do symptoms of alcohol withdrawal typically start?

A

Symptoms of alcohol withdrawal typically start 6-12 hours after the last drink and may include tremor, sweating, tachycardia, and anxiety.

379
Q

When do seizures and delirium tremens peak in alcohol withdrawal?

A

Seizures in alcohol withdrawal peak at 36 hours, while delirium tremens typically peaks 48-72 hours after the last drink, with symptoms including coarse tremor, confusion, delusions, auditory and visual hallucinations, fever, and tachycardia.

380
Q

How is alcohol withdrawal managed?

A

First-line treatment for alcohol withdrawal includes long-acting benzodiazepines (e.g., chlordiazepoxide or diazepam), typically administered as part of a reducing dose protocol. Lorazepam may be preferred in patients with hepatic failure or liver cirrhosis, as it is metabolized through glucuronidation, which is less affected by liver function. Carbamazepine is also effective, while phenytoin is not as effective for alcohol withdrawal seizures.

381
Q

Why is lorazepam preferred over chlordiazepoxide in patients with liver cirrhosis?

A

Lorazepam is preferred in patients with liver cirrhosis because it is metabolized through glucuronidation, a process less affected by liver function. Chlordiazepoxide, on the other hand, is metabolized via the cytochrome P450 system, which is impaired in cirrhosis and can lead to prolonged drug accumulation and increased risk of toxicity.

382
Q

What is the primary difference between typical and atypical antipsychotics?

A

Typical antipsychotics primarily act as dopamine D2 receptor antagonists, blocking dopaminergic transmission in the mesolimbic pathways. Atypical antipsychotics act on a variety of receptors, including D2, D3, D4, and 5-HT receptors.

383
Q

What are some examples of typical antipsychotics?

A

Haloperidol and chlorpromazine are examples of typical antipsychotics.

384
Q

What are some examples of atypical antipsychotics?

A

Clozapine, risperidone, and olanzapine are examples of atypical antipsychotics.

385
Q

What are common extrapyramidal side effects (EPSEs) of typical antipsychotics?

A

Extrapyramidal side effects include parkinsonism, acute dystonia (e.g., torticollis, oculogyric crisis), akathisia (severe restlessness), and tardive dyskinesia (involuntary movements like chewing or pouting of the jaw).

386
Q

How can acute dystonia (e.g., torticollis or oculogyric crisis) be managed?

A

Acute dystonia may be managed with procyclidine.

387
Q

What are the side effects specific to elderly patients taking antipsychotics?

A

Elderly patients taking antipsychotics have an increased risk of stroke and venous thromboembolism.

388
Q

What are other common side effects of antipsychotics?

A

Other side effects include antimuscarinic effects (dry mouth, blurred vision, urinary retention, constipation), sedation, weight gain, raised prolactin (which can lead to galactorrhoea), impaired glucose tolerance, neuroleptic malignant syndrome (characterized by pyrexia and muscle stiffness), reduced seizure threshold (greater with atypicals), and prolonged QT interval (particularly with haloperidol).

389
Q

According to NICE guidelines (2009), what is the first-line treatment for schizophrenia?

A

Oral atypical antipsychotics are considered first-line treatment for schizophrenia.

390
Q

What therapeutic approach should be offered to all patients with schizophrenia, according to NICE guidelines?

A

Cognitive behavioural therapy (CBT) should be offered to all patients with schizophrenia.

391
Q

Why is cardiovascular risk-factor modification important in the management of schizophrenia?

A

Close attention to cardiovascular risk-factor modification is important due to the high rates of cardiovascular disease in patients with schizophrenia, which are linked to antipsychotic medication and high smoking rates.

392
Q

What factors are associated with a poor prognosis in schizophrenia?

A

Strong family history, gradual onset, low IQ, prodromal phase of social withdrawal, and lack of obvious precipitant are associated with a poor prognosis in schizophrenia.

393
Q

What are the different types of subdural haematomas (SDH) based on their age, and how do they present clinically?

A

Acute SDH: Symptoms develop within 48 hours of injury, with rapid neurological deterioration. Features include headache, confusion, and potential focal neurological deficits. CT imaging shows a hyperdense crescentic collection.

Subacute SDH: Symptoms appear within days to weeks post-injury, with gradual progression.

Chronic SDH: Common in the elderly, symptoms develop over weeks to months. Patients may not recall a specific head injury. Symptoms include confusion, lethargy, memory loss, and cognitive impairment. CT imaging shows a hypodense crescentic collection.

394
Q

How is acute subdural haematoma managed?

A

Acute subdural haematomas are managed based on size and clinical presentation. Small or incidental cases can be observed conservatively. Larger or symptomatic haematomas may require monitoring of intracranial pressure or surgical decompression, such as decompressive craniectomy.

395
Q

How is chronic subdural haematoma managed?

A

If small and asymptomatic, chronic subdural haematomas can be managed conservatively with observation, with the possibility of spontaneous resolution. If symptoms such as confusion, neurological deficits, or severe imaging findings occur, surgical intervention with burr holes may be required.

Year 6 (10 decks)

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