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.
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
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.
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.
5
Q
Q: What is the mood stabilizer of choice for bipolar disorder?
A
A: Lithium.
6
Q
Q: What is an alternative mood stabilizer to lithium for bipolar disorder?
A
A: Valproate.
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).
8
Q
Q: How is depression in bipolar disorder managed?
A
Talking therapies.
Fluoxetine is the antidepressant of choice.
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).
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).
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.
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A: A disorder in which a person holds a delusion that a friend or partner has been replaced by an identical-looking impostor.
13
Q
Q: What are the four types of child abuse?
A
Neglect
Emotional abuse
Physical abuse
Sexual abuse
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
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
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
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’)
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.
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
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
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.
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.
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.
24
Q
Q: What is the most common cause of chronic pancreatitis?
A
A: Around 80% of cases are due to alcohol excess.
25
Q: What other causes, besides alcohol, can lead to chronic pancreatitis?
Genetic causes (e.g., cystic fibrosis, haemochromatosis)
Ductal obstruction (e.g., tumours, stones, structural abnormalities like pancreas divisum and annular pancreas)
26
Q: What are the typical symptoms of chronic pancreatitis?
Pain, usually worse 15-30 minutes following a meal
Steatorrhoea (fatty stools)
Diabetes mellitus (typically develops more than 20 years after symptoms begin)
27
Q: How long after the onset of pain do symptoms of pancreatic insufficiency, such as steatorrhoea, usually develop?
A: Symptoms typically develop between 5 and 25 years after the onset of pain.
28
Q: What imaging tests are used to diagnose chronic pancreatitis?
Abdominal x-ray (shows pancreatic calcification in 30% of cases)
CT scan (more sensitive for detecting pancreatic calcification with 80% sensitivity and 85% specificity)
29
Q: What functional test can be used to assess exocrine function in chronic pancreatitis?
A: Faecal elastase may be used to assess exocrine function if imaging is inconclusive.
30
Q: What is the management of chronic pancreatitis?
Pancreatic enzyme supplements
Analgesia
Antioxidants (limited evidence, but one study suggests benefit in early disease)
31
Q: What is Cotard syndrome?
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.
32
Q: What is De Clerambault's syndrome also known as?
A: De Clerambault's syndrome is also known as erotomania.
33
Q: What belief does a person with De Clerambault's syndrome hold?
A: The patient believes that a famous person is in love with her.
34
Q: What is delusional parasitosis?
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.
35
Q: What are some common tools used to assess the degree of depression?
Hospital Anxiety and Depression (HAD) scale
Patient Health Questionnaire (PHQ-9)
36
Q: What is the scoring system for the Hospital Anxiety and Depression (HAD) scale?
14 questions (7 for anxiety, 7 for depression)
Each item is scored 0-3
Depression severity:
0-7: Normal
8-10: Borderline
11+: Case
37
Q: How is depression severity defined in the updated NICE guideline?
Less severe depression (score <16 on PHQ-9)
More severe depression (score ≥16 on PHQ-9)
38
Q: What are the DSM-5 criteria for diagnosing Major Depressive Disorder (MDD)?
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
39
Q: How long should a patient refrain from driving after a coronary artery bypass graft (CABG)?
A: 4 weeks off driving.
40
Q: How long should someone refrain from driving after an acute coronary syndrome event?
A: 4 weeks off driving, or 1 week if successfully treated by angioplasty.
41
Q: What are the DVLA guidelines for a patient with epilepsy or seizures?
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.
42
Q: What are the DVLA guidelines for stroke or TIA?
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.
43
Q: What is the typical presentation of fibromyalgia?
Widespread chronic pain, lethargy, cognitive impairment (e.g., "fibro fog"), sleep disturbance, headaches, and dizziness.
44
Q: What is the diagnostic approach for fibromyalgia?
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.
45
Q: What are the management strategies for fibromyalgia?
A psychosocial and multidisciplinary approach.
Aerobic exercise (strongest evidence base), cognitive behavioural therapy (CBT), and medications such as pregabalin, duloxetine, and amitriptyline.
46
Q: At what age is head banging considered normal behavior in children, and when might it indicate a concern?
Normal behavior for a 2-year-old.
If it persists beyond 3 years, it could be a sign of autism.
47
Q: What is the minimum duration for mania to be diagnosed?
A: Mania lasts for at least 7 days.
48
Q: What is the minimum duration for hypomania to be diagnosed?
A: Hypomania lasts for less than 7 days, typically 3-4 days.
49
Q: What speech and thought patterns are common in both hypomania and mania?
A: Pressured speech, flight of ideas, and poor attention are common.
50
Q: What behavioral symptoms are common to both hypomania and mania?
A: Common behaviors include insomnia, loss of inhibitions (e.g., sexual promiscuity, overspending, risk-taking), and increased appetite.
51
Q: What is insomnia as defined by the DSM-V?
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.
52
Q: What is the difference between acute and chronic insomnia?
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.
53
Q: How is the diagnosis of insomnia primarily made?
A: Diagnosis is primarily through patient interview, looking for the presence of risk factors. Sleep diaries and actigraphy may also aid diagnosis.
54
Q: When might polysomnography be considered for diagnosing insomnia?
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.
55
Q: What are the short-term management strategies for insomnia?
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.
56
Q: What hypnotic drugs are recommended for insomnia treatment?
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.
57
Q: What is the guidance on using hypnotics for insomnia?
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.
58
Q: What are some genetic causes of learning difficulties?
A: Fragile X syndrome and Down's syndrome are genetic causes of learning difficulties.
59
Q: Which congenital infections can lead to learning difficulties?
A: Cytomegalovirus, toxoplasmosis, and rubella can cause learning difficulties.
60
Q: What birth-related factors can contribute to learning difficulties?
A: Hypoxia, rhesus haemolytic disease, and intraventricular haemorrhage can lead to learning difficulties.
61
Q: What metabolic disorders are associated with learning difficulties?
A: Phenylketonuria (PKU), maple syrup urine disease, and homocystinuria are metabolic disorders that can cause learning difficulties.
62
Q: What are vasomotor symptoms, and how common are they during menopause?
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.
63
Q: What urogenital changes may occur during menopause?
A: Around 35% of women may experience vaginal dryness, atrophy, and urinary frequency.
64
Q: What psychological symptoms may be seen during menopause?
A: Anxiety and depression may affect around 10% of women, and short-term memory impairment is also common.
65
Q: What are some longer-term complications associated with menopause?
A: Longer-term complications include osteoporosis and an increased risk of ischaemic heart disease.
66
Q: What is the management for a paracetamol overdose?
Activated charcoal if ingested < 1 hour ago
N-acetylcysteine (NAC)
Liver transplantation if severe
67
Q: What is the management for a salicylate overdose?
Urinary alkalinization with IV bicarbonate
Haemodialysis
68
Q: What is the treatment for opioid/opiates overdose?
A: Naloxone
69
Q: What is the management for a benzodiazepine overdose?
A: Flumazenil, but generally only used for severe or iatrogenic overdoses due to seizure risk.
70
Q: How is a tricyclic antidepressant overdose managed?
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
71
Q: What is the management for a lithium overdose?
Mild-moderate toxicity: Volume resuscitation with normal saline
Severe toxicity: Haemodialysis
Sodium bicarbonate may be used, but evidence is limited
72
Q: What is the treatment for warfarin overdose?
A: Vitamin K and prothrombin complex
73
Q: What is the management for heparin overdose?
A: Protamine sulphate
74
Q: How should a beta-blocker overdose be managed?
If bradycardic, use atropine
For resistant cases, use glucagon
75
Q: What is the management for ethylene glycol poisoning?
Fomepizole (first-line)
Ethanol (used previously)
Haemodialysis for refractory cases
76
Q: How is methanol poisoning treated?
Fomepizole or ethanol
Haemodialysis
77
Q: What is the treatment for organophosphate insecticide poisoning?
A: Atropine; the role of pralidoxime is still unclear.
78
Q: What is the management for digoxin toxicity?
A: Digoxin-specific antibody fragments
79
Q: How is iron overdose treated?
A: Desferrioxamine, a chelating agent
80
Q: What is the treatment for lead poisoning?
A: Dimercaprol and calcium edetate
81
Q: What is the management for carbon monoxide poisoning?
100% oxygen
Hyperbaric oxygen
82
Q: How is cyanide poisoning treated?
A: Hydroxocobalamin, or a combination of amyl nitrite, sodium nitrite, and sodium thiosulfate.
83
Q: What mental health problem is commonly seen in around 60-70% of women within 3-7 days following birth?
A: 'Baby-blues'
84
Q: What are the characteristic symptoms of the 'baby-blues'?
A: Anxiety, tearfulness, and irritability. It is more common in primips (first-time mothers).
85
Q: What is the usual onset and peak time for postnatal depression?
A: Postnatal depression affects around 10% of women, with most cases starting within a month and peaking at 3 months.
86
Q: What is puerperal psychosis, and how common is it?
A: Puerperal psychosis affects around 0.2% of women, with onset usually within the first 2-3 weeks following birth.
87
Q: What are the features of puerperal psychosis?
A: Features include severe mood swings (similar to bipolar disorder) and disordered perception, such as auditory hallucinations.
88
Q: What is the initial management for 'baby-blues'?
A: Reassurance and support, with a key role for the health visitor.
89
Q: What is the management for postnatal depression?
A: Reassurance, support, and possibly cognitive behavioural therapy. Severe cases may require SSRIs such as sertraline or paroxetine, which are considered safe for breastfeeding.
90
Q: What is the treatment for puerperal psychosis?
A: Admission to hospital is usually required, ideally in a Mother & Baby Unit. There is a 25-50% risk of recurrence in future pregnancies.
91
Q: What SSRIs are preferred for treating postnatal depression in breastfeeding mothers?
A: Sertraline and paroxetine are preferred due to their safety during breastfeeding, with paroxetine recommended by SIGN for its low milk/plasma ratio.
92
Q: Why is fluoxetine generally avoided for postpartum depression treatment?
A: Fluoxetine is avoided due to its long half-life, which can be a concern for breastfeeding infants.
93
Q: What are Schneider's first-rank symptoms of schizophrenia?
A: Schneider's first-rank symptoms include auditory hallucinations, thought disorders, passivity phenomena, and delusional perceptions.
94
Q: What are some thought disorders associated with schizophrenia?
Thought insertion
Thought withdrawal
Thought broadcasting
95
Q: What are passivity phenomena in schizophrenia?
A: Experiences where bodily sensations, actions, impulses, or feelings are controlled or influenced by external forces or others.
96
Q: What are some other features of schizophrenia?
Impaired insight
Negative symptoms (e.g., anhedonia, alogia, avolition)
Incongruity/blunting of affect
Social withdrawal
Neologisms (made-up words)
Catatonia
97
Q: What is anhedonia in schizophrenia?
A: Anhedonia is the inability to derive pleasure from activities that are normally enjoyable.
98
Q: What is alogia in schizophrenia?
A: Alogia refers to poverty of speech, where the individual speaks very little or provides minimal responses.
99
Q: What is avolition in schizophrenia?
A: Avolition is poor motivation or a lack of drive to engage in purposeful activities.
100
101
What is the most common cause of superior vena cava (SVC) obstruction?
Lung cancer
102
What is the most common symptom of superior vena cava (SVC) obstruction?
Dyspnoea
103
What are some common features of superior vena cava (SVC) obstruction?
Swelling of the face, neck, and arms; conjunctival and periorbital oedema; headache (often worse in the mornings); visual disturbance; pulseless jugular venous distension
104
Which malignancies are most commonly associated with superior vena cava (SVC) obstruction?
Small cell lung cancer and lymphoma
105
What are other causes of superior vena cava (SVC) obstruction?
Metastatic seminoma, Kaposi's sarcoma, breast cancer, aortic aneurysm, mediastinal fibrosis, goitre, and SVC thrombosis
106
What is the treatment of choice for superior vena cava (SVC) obstruction in many cases?
Endovascular stenting
107
When might radical chemotherapy or chemo-radiotherapy be preferred over endovascular stenting in the management of SVC obstruction?
In certain malignancies such as lymphoma and small cell lung cancer
108
Is there strong evidence supporting the use of glucocorticoids in the treatment of SVC obstruction?
No, the evidence base is weak, but they are often given.
109
What is circumstantiality in thought disorders?
The inability to answer a question without giving excessive, unnecessary detail, but eventually returning to the original point.
110
What is tangentiality in thought disorders?
Wandering from a topic without returning to it.
111
What are neologisms in thought disorders?
New word formations, which might include the combining of two words.
112
What are clang associations in thought disorders?
When ideas are related to each other only by the fact they sound similar or rhyme.
113
What is word salad in thought disorders?
Completely incoherent speech where real words are strung together into nonsense sentences.
114
What is Knight's move thinking, and in which condition is it a feature?
A severe type of loosening of associations with unexpected and illogical leaps from one idea to another, featured in schizophrenia.
115
What is flight of ideas and in which condition is it a feature?
A thought disorder with leaps from one topic to another but with discernible links between them, featured in mania.
116
What is perseveration in thought disorders?
The repetition of ideas or words despite an attempt to change the topic.
117
What is echolalia in thought disorders?
The repetition of someone else's speech, including the question that was asked.
118
What causes Wernicke's encephalopathy?
Thiamine deficiency, most commonly seen in alcoholics, and also caused by persistent vomiting, anorexia nervosa, stomach cancer, and dietary deficiency.
119
What is the classic triad of symptoms in Wernicke's encephalopathy?
Ophthalmoplegia/nystagmus, ataxia, and encephalopathy.
120
Where do petechial haemorrhages occur in Wernicke's encephalopathy?
In a variety of structures in the brain including the mamillary bodies and ventricle walls.
121
What are the features of Wernicke's encephalopathy?
Oculomotor dysfunction, nystagmus (most common ocular sign), ophthalmoplegia (lateral rectus palsy, conjugate gaze palsy), gait ataxia, encephalopathy (confusion, disorientation, indifference, inattentiveness), peripheral sensory neuropathy.
122
What are the investigations for Wernicke's encephalopathy?
Decreased red cell transketolase and MRI.
123
What is the treatment for Wernicke's encephalopathy?
Urgent replacement of thiamine.
124
What syndrome may develop if Wernicke's encephalopathy is not treated?
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.
125
What is the most common cause of blindness in the UK?
Age-related macular degeneration (ARMD).
126
What is the key feature of age-related macular degeneration (ARMD)?
Degeneration of the central retina (macula), usually bilateral, with the formation of drusen.
127
What are the main risk factors for developing age-related macular degeneration (ARMD)?
Advancing age, smoking, family history, hypertension, dyslipidaemia, and diabetes mellitus.
128
What is the greatest risk factor for ARMD?
Advancing age.
129
What is the difference in risk of ARMD between patients aged 65-74 years and those older than 75 years?
The risk of ARMD increases 3 fold for patients aged older than 75 years.
130
How does smoking affect the risk of ARMD?
Current smokers are twice as likely to experience ARMD-related visual loss compared to non-smokers, and ex-smokers have a slightly increased risk.
131
What are the two traditional forms of macular degeneration?
Dry macular degeneration (atrophic) and wet macular degeneration (exudative or neovascular).
132
What is the most common type of age-related macular degeneration?
Dry macular degeneration (90% of cases).
133
What is characteristic of wet macular degeneration?
Choroidal neovascularisation and leakage of serous fluid and blood, leading to rapid vision loss.
134
What is the recent updated classification of age-related macular degeneration?
Early age-related macular degeneration (non-exudative, age-related maculopathy) and late age-related macular degeneration (neovascularisation, exudative).
135
What are the clinical features of age-related macular degeneration?
Subacute onset of visual loss, reduced visual acuity, difficulty with dark adaptation, fluctuations in visual disturbance, photopsia, glare, and visual hallucinations (Charles-Bonnet syndrome).
136
What sign on Amsler grid testing may be observed in ARMD?
Distortion of line perception.
137
What is seen on fundoscopy in dry ARMD?
Drusen (yellow areas of pigment deposition in the macular area), which may become confluent to form a macular scar in late disease.
138
What is seen on fundoscopy in wet ARMD?
Well-demarcated red patches representing intra-retinal or sub-retinal fluid leakage or haemorrhage.
139
What is the initial investigation of choice for ARMD?
Slit-lamp microscopy, often accompanied by colour fundus photography.
140
When is fluorescein angiography used in ARMD?
If neovascular ARMD is suspected, to guide intervention with anti-VEGF therapy.
141
What is optical coherence tomography used for in ARMD?
To visualise the retina in three dimensions and reveal areas of disease not visible with microscopy alone.
142
What treatment was shown to reduce the progression of dry ARMD in the AREDS trial?
A combination of zinc and antioxidant vitamins A, C, and E.
143
What is the role of anti-VEGF agents in the treatment of wet ARMD?
Anti-VEGF agents, such as ranibizumab, bevacizumab, and pegaptanib, limit progression and can stabilise or reverse visual loss in wet ARMD.
144
When should anti-VEGF therapy ideally be initiated in wet ARMD?
Within the first two months of diagnosis.
145
What is the role of laser photocoagulation in ARMD treatment?
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.
146
What is the most common cause of admissions to child and adolescent psychiatric wards?
Anorexia nervosa.
147
What percentage of patients with anorexia nervosa are female?
90%.
148
What age group is most commonly affected by anorexia nervosa?
Teenage and young-adult females.
149
What is the prevalence of anorexia nervosa?
Between 1:100 and 1:200.
150
What are the DSM-5 diagnostic criteria for anorexia nervosa?
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.
151
Are BMI and amenorrhoea specifically mentioned in the DSM-5 criteria for anorexia nervosa?
No, they are no longer specifically mentioned.
152
What is the first-line treatment for adults with anorexia nervosa according to NICE guidelines?
Individual eating-disorder-focused cognitive behavioural therapy (CBT-ED), Maudsley Anorexia Nervosa Treatment for Adults (MANTRA), or specialist supportive clinical management (SSCM).
153
What is the first-line treatment for children and young people with anorexia nervosa according to NICE guidelines?
Anorexia-focused family therapy.
154
What is the second-line treatment for children and young people with anorexia nervosa according to NICE guidelines?
Cognitive behavioural therapy (CBT).
155
What is the prognosis of patients with anorexia nervosa?
Up to 10% of patients may eventually die due to the disorder.
156
What are some characteristic clinical features of anorexia nervosa?
Reduced body mass index, bradycardia, hypotension, enlarged salivary glands.
157
What physiological abnormalities are commonly seen in anorexia nervosa?
Hypokalaemia, low FSH, LH, oestrogens, and testosterone; raised cortisol and growth hormone; impaired glucose tolerance; hypercholesterolaemia; hypercarotinaemia; low T3.
158
What is the DSM-V definition of Attention Deficit Hyperactivity Disorder (ADHD)?
ADHD is defined as a condition incorporating features of inattention and/or hyperactivity/impulsivity that are persistent, with developmental delay required for diagnosis.
159
What is the prevalence of ADHD in the UK?
ADHD has a UK prevalence of 2.4%, and is more common in boys than in girls (M:F 4:1).
160
At what age are most children diagnosed with ADHD?
Most children are diagnosed between the ages of 3 and 7.
161
What is the diagnostic criteria for ADHD in children up to the age of 16?
Six of the features of inattention and/or hyperactivity/impulsivity must be present.
162
What is the diagnostic criteria for ADHD in individuals aged 17 or over?
Five of the features of inattention and/or hyperactivity/impulsivity must be present.
163
What are some common features of inattention in ADHD?
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
What are some common features of hyperactivity/impulsivity in ADHD?
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
What is the recommended approach to managing ADHD according to NICE?
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
When should drug therapy be considered for ADHD?
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
What is the first-line pharmacotherapy for ADHD in children?
Methylphenidate, given on a six-week trial basis.
168
What are some side effects of methylphenidate in children?
Abdominal pain, nausea, dyspepsia, and monitoring of weight and height every 6 months.
169
What should be done if there is an inadequate response to methylphenidate in children?
Switch to lisdexamfetamine.
170
What is the treatment approach for ADHD in adults?
Methylphenidate or lisdexamfetamine are first-line options, with a switch between the two if no benefit is seen.
171
What cardiotoxic risks are associated with ADHD medications?
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
What is important when diagnosing ADHD due to its overlap with other conditions?
A thorough history and clinical examination are key to distinguishing ADHD from other psychiatric and physical conditions.
173
What is Autism Spectrum Disorder (ASD)?
Autism is a neurodevelopmental condition characterized by qualitative impairment in social interaction and communication, along with repetitive stereotyped behaviours, interests, and activities.
174
What is the prevalence of ASD?
The prevalence of ASD is estimated to be 1-2%, with it being three to four times more common in boys than girls.
175
What percentage of children with ASD have an intellectual disability?
Around 50% of children with ASD have an intellectual disability.
176
What are some clinical features of Autism Spectrum Disorder?
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
What other conditions are commonly associated with ASD in children?
Attention deficit hyperactivity disorder (35%) and epilepsy (18%).
178
What is the goal of managing Autism Spectrum Disorder?
The goal is to increase functional independence, improve social skills and communication, decrease disability and comorbidity, and aid families.
179
What are some non-pharmacological therapies for ASD?
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
What pharmacological interventions may be used in managing ASD?
SSRIs (to reduce repetitive behaviours, anxiety, and aggression), antipsychotic drugs (to reduce aggression and self-injury), and methylphenidate (for ADHD).
181
What role does family support and counselling play in managing ASD?
Parental education on how to interact with the child, understanding their behaviour, and accepting it are key aspects of family support.
182
What are the features of beta-blocker overdose?
Bradycardia, hypotension, heart failure, and syncope.
183
How should bradycardia caused by a beta-blocker overdose be managed?
Atropine should be administered.
184
What treatment may be used in resistant cases of beta-blocker overdose?
Glucagon may be used in resistant cases.
185
Is haemodialysis effective in beta-blocker overdose?
No, haemodialysis is not effective in beta-blocker overdose.
186
What is the first-line management for binge eating disorder in adults according to NICE?
NICE recommends a 'binge-eating-disorder-focused' guided self-help programme.
187
What should be offered if guided self-help for binge eating disorder is unacceptable, contraindicated, or ineffective after 4 weeks?
If guided self-help is ineffective, NICE recommends offering group eating-disorder-focused cognitive behavioural therapy (CBT-ED).
188
What characterizes bulimia nervosa?
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
What are the DSM-5 diagnostic criteria for bulimia nervosa?
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
What are physical signs associated with bulimia nervosa?
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
What are the diagnostic criteria for bulimia nervosa?
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
What is the first-line treatment for bulimia nervosa in adults according to NICE?
NICE recommends bulimia-nervosa-focused guided self-help for adults.
193
What should be offered if bulimia-nervosa-focused guided self-help is ineffective after 4 weeks?
NICE recommends considering individual eating-disorder-focused cognitive behavioural therapy (CBT-ED) if guided self-help is ineffective.
194
What is the recommended treatment for children with bulimia nervosa?
Children should be offered bulimia-nervosa-focused family therapy (FT-BN).
195
What is the role of pharmacological treatment in bulimia nervosa?
Pharmacological treatments have a limited role, with a trial of high-dose fluoxetine being licensed for bulimia, but long-term data is lacking.
196
What are the CNS features of synthetic cannabinoid toxicity?
CNS features include agitation, tremor, anxiety, confusion, somnolence, syncope, hallucinations, changes in perception, acute psychosis, nystagmus, convulsions, and coma.
197
What are the cardiac features of synthetic cannabinoid toxicity?
Cardiac features include tachycardia, hypertension, chest pain, palpitations, and ECG changes.
198
What renal complication can occur with synthetic cannabinoid toxicity?
Acute kidney injury can occur.
199
What muscular symptoms are associated with synthetic cannabinoid toxicity?
Muscular symptoms include hypertonia, myoclonus, muscle jerking, and myalgia.
200
What are other features of synthetic cannabinoid toxicity?
Other features include cold extremities, dry mouth, dyspnoea, mydriasis, vomiting, and hypokalaemia.
201
What is Charles-Bonnet syndrome (CBS)?
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
What are the common risk factors for Charles-Bonnet syndrome?
Advanced age, peripheral visual impairment, social isolation, sensory deprivation, and early cognitive impairment.
203
What ophthalmological conditions are most commonly associated with Charles-Bonnet syndrome?
Age-related macular degeneration, followed by glaucoma and cataract.
204
What is the prevalence of Charles-Bonnet syndrome in individuals with severe visual impairment?
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
How long do hallucinations last in most individuals with Charles-Bonnet syndrome?
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
What is the mechanism of action of cocaine?
Cocaine blocks the uptake of dopamine, noradrenaline, and serotonin.
207
What are the cardiovascular adverse effects of cocaine?
Coronary artery spasm, myocardial ischaemia/infarction, tachycardia, bradycardia, hypertension, QRS widening, QT prolongation, and aortic dissection.
208
What are the neurological adverse effects of cocaine?
Seizures, mydriasis, hypertonia, and hyperreflexia.
209
What are the psychiatric effects of cocaine?
Agitation, psychosis, and hallucinations.
210
What other adverse effects can cocaine cause?
Ischaemic colitis, hyperthermia, metabolic acidosis, and rhabdomyolysis.
211
What is the first-line management for most cocaine-related problems?
Benzodiazepines.
212
What is the treatment for chest pain in cocaine toxicity?
Benzodiazepines and glyceryl trinitrate.
213
What should be done if myocardial infarction develops in cocaine toxicity?
Primary percutaneous coronary intervention.
214
How is hypertension managed in cocaine toxicity?
Benzodiazepines and sodium nitroprusside.
215
What is the controversy regarding beta-blockers in cocaine toxicity?
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
What is the most common cause of dementia in the UK?
Alzheimer's disease, followed by vascular and Lewy body dementia.
217
What is a common issue in the diagnosis of dementia?
Diagnosis can be difficult and is often delayed.
218
What assessment tools are recommended by NICE for non-specialist settings?
10-point cognitive screener (10-CS) and 6-Item cognitive impairment test (6CIT).
219
What assessment tools are not recommended by NICE for non-specialist settings?
The abbreviated mental test score (AMTS), General practitioner assessment of cognition (GPCOG), and the mini-mental state examination (MMSE).
220
What MMSE score suggests dementia?
A score of 24 or less out of 30.
221
What blood tests are commonly sent in primary care to exclude reversible causes of dementia?
FBC, U&E, LFTs, calcium, glucose, ESR/CRP, TFTs, vitamin B12, and folate levels.
222
What is the role of neuroimaging in dementia diagnosis?
To exclude other reversible conditions (e.g. subdural haematoma, normal pressure hydrocephalus) and provide information on aetiology to guide prognosis and management.
223
What did the 2011 NICE guidelines state about structural imaging in dementia?
Structural imaging was said to be essential in the investigation of dementia.
224
What PHQ-9 score defines 'less severe' depression according to the 2022 NICE guidelines?
A PHQ-9 score of < 16.
225
What PHQ-9 score defines 'more severe' depression according to the 2022 NICE guidelines?
A PHQ-9 score of ≥ 16.
226
What does NICE recommend for managing less severe depression?
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
What are the first-line treatment options for less severe depression according to NICE?
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
What are the preferred treatment options for more severe depression according to NICE?
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
What is recommended when switching from citalopram, escitalopram, sertraline, or paroxetine to another SSRI?
A direct switch is possible.
230
What is recommended when switching from fluoxetine to another SSRI?
Withdraw fluoxetine and leave a gap of 4-7 days before starting a low dose of the alternative SSRI.
231
What is recommended when switching from an SSRI to a tricyclic antidepressant (TCA)?
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
What is recommended when switching from citalopram, escitalopram, sertraline, or paroxetine to venlafaxine?
A direct switch is possible, with caution if paroxetine was used.
233
What is recommended when switching from fluoxetine to venlafaxine?
Withdraw fluoxetine and start venlafaxine at a low dose 4-7 days later.
234
What are the primary classifications of eating disorders?
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
What is the definition of anorexia nervosa?
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
What are the criteria for anorexia nervosa?
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
What characterises bulimia nervosa?
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
What are the criteria for bulimia nervosa?
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
What characterises binge eating disorder?
Binge eating disorder involves recurrent episodes of binge eating, but unlike bulimia nervosa, there are no consistent inappropriate compensatory behaviours.
240
What are the criteria for binge eating disorder?
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
What is the diagnosis and treatment approach for eating disorders?
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
What are the complications of untreated eating disorders?
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
What are the neurological clinical features of ecstasy poisoning?
Agitation, anxiety, confusion, ataxia.
244
What are the cardiovascular clinical features of ecstasy poisoning?
Tachycardia, hypertension.
245
What electrolyte imbalance is associated with ecstasy poisoning?
Hyponatraemia, which may result from either syndrome of inappropriate ADH secretion or excessive water consumption.
246
What is a key metabolic feature of ecstasy poisoning?
Hyperthermia and rhabdomyolysis.
247
What is the management for ecstasy poisoning?
Supportive care, and dantrolene may be used for hyperthermia if simple measures fail.
248
What is the central feature of anxiety according to NICE?
Excessive worry about a number of different events associated with heightened tension.
249
What are some important physical causes to consider when diagnosing anxiety disorders?
Hyperthyroidism, cardiac disease, and medication-induced anxiety (e.g., salbutamol, theophylline, corticosteroids, antidepressants, and caffeine).
250
What is the first step in the management of Generalised Anxiety Disorder (GAD) according to NICE?
Education about GAD and active monitoring.
251
What is the second step in the management of GAD?
Low-intensity psychological interventions, such as individual non-facilitated self-help, individual guided self-help, or psychoeducational groups.
252
What is the third step in the management of GAD?
High-intensity psychological interventions, such as cognitive behavioural therapy (CBT) or applied relaxation, or drug treatment.
253
What is the first-line drug treatment for GAD recommended by NICE?
Sertraline (an SSRI).
254
What should be offered if sertraline is ineffective for GAD?
An alternative SSRI or a serotonin-noradrenaline reuptake inhibitor (SNRI), such as duloxetine or venlafaxine.
255
What drug is recommended if SSRIs or SNRIs are not tolerated in GAD?
Pregabalin.
256
What warning should be given to patients under 30 years starting treatment for GAD?
The increased risk of suicidal thinking and self-harm, with weekly follow-up recommended for the first month.
257
What is the first step in the management of panic disorder according to NICE?
Recognition and diagnosis.
258
What is the second step in the management of panic disorder?
Treatment in primary care, which may involve cognitive behavioural therapy or drug treatment.
259
What is the first-line drug treatment for panic disorder recommended by NICE?
SSRIs.
260
What should be offered if SSRIs are contraindicated or ineffective after 12 weeks for panic disorder?
Imipramine or clomipramine.
261
What are the major complications of iron overdose?
Metabolic acidosis, erosion of gastric mucosa leading to GI bleeding, shock, hepatotoxicity, and coagulopathy.
262
How is iron overdose management guided?
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
What is the management for patients who ingested less than 40mg/kg elemental iron and are asymptomatic?
They can be observed at home.
264
What is the management for patients who ingested more than 40mg/kg elemental iron or are symptomatic?
They require medical assessment with serum iron levels measured 2-4 hours post-ingestion and an abdominal x-ray.
265
What is the decontamination procedure of choice for iron overdose?
Whole bowel irrigation, especially for patients who ingested > 60mg/kg elemental iron or have undissolved tablets on abdominal x-ray.
266
Is activated charcoal effective in treating iron poisoning?
No, activated charcoal is ineffective in iron poisoning.
267
When is desferrioxamine indicated in iron overdose?
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
What may be required if whole bowel irrigation is not effective or iron is adhered to the gastric wall?
Endoscopy or surgery may be required.
269
What is the common use of lithium?
Lithium is most commonly used prophylactically in bipolar disorder and as an adjunct in refractory depression.
270
What is the therapeutic range for lithium?
The therapeutic range for lithium is 0.4-1.0 mmol/L.
271
How is lithium primarily excreted?
Lithium is primarily excreted by the kidneys.
272
What are the two theories for lithium's mechanism of action?
Lithium interferes with inositol triphosphate formation and with cAMP formation.
273
What are the common adverse effects of lithium?
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
How should lithium levels be monitored?
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
How often should thyroid and renal function be checked in patients on lithium?
Thyroid and renal function should be checked every 6 months.
276
What should be issued to patients on lithium therapy?
Patients should be issued with an information booklet, alert card, and record book.
277
When does lithium toxicity generally occur?
Lithium toxicity generally occurs following concentrations > 1.5 mmol/L.
278
What factors can precipitate lithium toxicity?
Dehydration, renal failure, and drugs such as diuretics (especially thiazides), ACE inhibitors/angiotensin II receptor blockers, NSAIDs, and metronidazole.
279
What are the features of lithium toxicity?
Coarse tremor (as opposed to fine tremor at therapeutic levels), hyperreflexia, acute confusion, polyuria, seizure, and coma.
280
How is mild-moderate lithium toxicity managed?
Mild-moderate toxicity may respond to volume resuscitation with normal saline, IV fluids with isotonic saline, until euvolemic, then typically twice maintenance rate.
281
What should be monitored in lithium toxicity management?
Serum sodium should be monitored closely (every 4 hours with serial lithium concentrations) if there is concern about lithium-induced nephrogenic diabetes insipidus.
282
When is haemodialysis required in lithium toxicity?
Haemodialysis may be needed in severe toxicity.
283
How can sodium bicarbonate be used in lithium toxicity management?
Sodium bicarbonate is sometimes used to increase the alkalinity of the urine, promoting lithium excretion, although there is limited evidence to support this.
284
What are the psychoactive symptoms of LSD intoxication?
Psychoactive symptoms include variable subjective experiences, impaired judgement, amplification of current mood (euphoria or dysphoria), agitation, appearing withdrawn, and drug-induced psychosis.
285
What are the somatic symptoms of LSD intoxication?
Somatic symptoms include nausea, headache, palpitations, dry mouth, drowsiness, and tremors.
286
What signs are associated with LSD intoxication?
Signs of LSD intoxication include tachycardia, hypertension, mydriasis, paresthesia, hyperreflexia, and pyrexia.
287
What are the complications of massive LSD overdoses?
Massive overdoses can lead to respiratory arrest, coma, hyperthermia, autonomic dysfunction, and bleeding disorders.
288
How is LSD toxicity diagnosed?
The diagnosis is mainly based on history and examination, as most urine drug screens do not detect LSD.
289
What is the management for agitation in LSD intoxication?
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
What is the management for LSD-induced psychosis?
LSD-induced psychosis may require antipsychotics.
291
How is massive LSD ingestion managed?
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
Why is activated charcoal and gastric emptying of limited clinical value in LSD toxicity?
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
What is the mechanism of action of nitrous oxide when inhaled?
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
What are the psychological symptoms of nitrous oxide misuse?
Psychological symptoms include euphoria, altered perception of reality, hallucinations, anxiety, and paranoia.
295
What are the neurological symptoms of nitrous oxide misuse?
Neurological symptoms include dizziness, headache, incoordination, numbness, and tremors.
296
What physiological effects are associated with nitrous oxide misuse?
Physiological effects include hypoxia, hypothermia, elevated heart rate, and elevated blood pressure.
297
What are the long-term effects of nitrous oxide misuse?
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
How does chronic nitrous oxide exposure lead to vitamin B12 deficiency?
Chronic exposure leads to vitamin B12 deficiency due to its interference with vitamin B12 metabolism.
299
How does chronic nitrous oxide exposure lead to vitamin B12 deficiency?
Chronic exposure to nitrous oxide oxidises and inactivates vitamin B12, leading to deficiency.
300
What neurological impairment can result from persistent nitrous oxide misuse?
Persistent misuse can lead to subacute combined degeneration of the spinal cord, resulting in irreversible neurological impairments.
301
What physical harm can result from inhaling nitrous oxide from containers or balloons?
The act of inhaling gas from containers or balloons poses a risk of lung damage, barotrauma, and frostbite.
302
What characterises obsessive-compulsive disorder (OCD)?
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
What are obsessions in OCD?
Obsessions are unwanted intrusive thoughts, images, or urges that repeatedly enter a person’s mind.
304
What are compulsions in OCD?
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
What is the peak age of onset for OCD?
The peak age of onset for OCD is between 10-20 years.
306
What are some risk factors for developing OCD?
Risk factors include family history, age (peak onset 10-20 years), pregnancy/postnatal period, and a history of abuse, bullying, or neglect.
307
How does NICE recommend classifying OCD impairment?
NICE recommends classifying impairment into mild, moderate, or severe using the Y-BOCS scale.
308
What are the treatment options for mild OCD?
For mild OCD, low-intensity psychological treatments, such as cognitive behavioural therapy (CBT) with exposure and response prevention (ERP), are recommended.
309
What are the treatment options for moderate OCD?
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
What are the treatment options for severe OCD?
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
What is exposure and response prevention (ERP) in the treatment of OCD?
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
How long should an SSRI be continued for OCD treatment?
If the SSRI is effective, it should be continued for at least 12 months to prevent relapse and allow time for improvement.
313
How does the duration and dose of SSRIs in OCD treatment compare to depression?
SSRIs usually require a higher dose and longer duration (at least 12 weeks) for an initial response in OCD compared to depression.
314
What are some features of opioid misuse?
Features of opioid misuse include rhinorrhoea, needle track marks, pinpoint pupils, drowsiness, watering eyes, and yawning.
315
What are some complications of opioid misuse?
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
What is the emergency management for opioid overdose?
The emergency management for opioid overdose includes IV or IM naloxone, which has a rapid onset and relatively short duration of action.
317
What are some harm reduction interventions for opioid misuse?
Harm reduction interventions include needle exchange programs and offering testing for HIV, hepatitis B & C.
318
How is opioid dependence typically managed?
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
What are the first-line treatments for opioid detoxification according to NICE?
NICE recommends methadone or buprenorphine as the first-line treatment for opioid detoxification.
320
What is the mechanism of action of methadone in opioid detoxification?
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
What is the mechanism of action of buprenorphine in opioid detoxification?
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
How is compliance monitored in opioid detoxification?
Compliance in opioid detoxification is monitored using urinalysis.
323
How long should detoxification last in an inpatient/residential setting versus the community?
Detoxification should last up to 4 weeks in an inpatient/residential setting and up to 12 weeks in the community.
324
When should activated charcoal be administered in the case of a paracetamol overdose?
Activated charcoal should be administered if the patient presents within 1 hour of ingestion to reduce absorption of the drug.
325
When should acetylcysteine be given in the case of a paracetamol overdose?
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
How should acetylcysteine be administered for paracetamol overdose?
Acetylcysteine should now be infused over 1 hour, rather than the previous 15 minutes, to reduce the risk of adverse effects.
327
How should an anaphylactoid reaction to acetylcysteine be managed?
If an anaphylactoid reaction occurs, stop the infusion and then restart it at a slower rate.
328
What are the King's College Hospital criteria for liver transplantation in cases of paracetamol liver failure?
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
What defines a staggered overdose in paracetamol ingestion?
A staggered overdose is defined as one in which all the tablets were not taken within 1 hour.
330
What is the ICD-11 classification of personality disorders based on?
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
What are the characteristics of mild personality disorder according to ICD-11?
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
What is the defining feature of a personality disorder according to ICD-11?
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
What are the key domains of personality disorder trait domains in ICD-11?
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
What are the three clusters of personality disorders in the previous classification system?
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
What are some treatments for personality disorders?
Treatments for personality disorders include psychological therapies, such as dialectical behavior therapy, and treatment for any coexisting psychiatric conditions.
336
What are the key features of post-traumatic stress disorder (PTSD)?
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
What is the recommended management for PTSD following a traumatic event?
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
Is debriefing recommended after a traumatic event?
No, single-session interventions like debriefing are not recommended following a traumatic event.
339
What are some drug treatments used for PTSD, and when should they be considered?
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
What is the definition of a pseudohallucination?
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
Are pseudohallucinations included in the ICD-10 or DSM-5?
No, pseudohallucinations are not specifically mentioned in either the ICD-10 or DSM-5.
342
How are pseudohallucinations viewed in clinical practice?
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
Can pseudohallucinations occur in healthy individuals?
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
In which situations are pseudohallucinations most commonly seen?
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
What is a key concept in salicylate overdose management?
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
What are common features of salicylate overdose?
Hyperventilation, tinnitus, lethargy, sweating, pyrexia, nausea/vomiting, hyperglycaemia and hypoglycaemia, seizures, and coma.
347
What is the treatment for salicylate overdose?
General treatment includes ABC management, activated charcoal, urinary alkalinization with intravenous sodium bicarbonate to enhance aspirin elimination, and haemodialysis.
348
What are the indications for haemodialysis in salicylate overdose?
Serum concentration > 700 mg/L, metabolic acidosis resistant to treatment, acute renal failure, pulmonary oedema, seizures, and coma.
349
Why do salicylates cause sweating and pyrexia?
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
What are selective serotonin reuptake inhibitors (SSRIs) commonly used for?
SSRIs are considered first-line treatment for the majority of patients with depression.
351
Which SSRIs are preferred in clinical practice?
Citalopram and fluoxetine are currently the preferred SSRIs. Sertraline is also useful post-myocardial infarction due to its safer profile in this context.
352
What are the main adverse effects of SSRIs?
Gastrointestinal symptoms are the most common side effect, and there is an increased risk of gastrointestinal bleeding, especially in patients taking NSAIDs.
Hyponatraemia
353
What should be prescribed with SSRIs if a patient is also taking an NSAID?
A proton pump inhibitor should be co-prescribed to reduce the risk of gastrointestinal bleeding.
354
What precautions should be taken when prescribing SSRIs to children and adolescents?
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
What is the concern regarding citalopram and the QT interval?
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
What SSRIs are more prone to drug interactions?
Fluoxetine and paroxetine have a higher propensity for drug interactions.
357
What should be done if SSRIs are prescribed with NSAIDs, warfarin, or triptans?
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
What should be the follow-up after starting antidepressant therapy?
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
How long should patients continue SSRI therapy after remission?
Patients should continue SSRI therapy for at least 6 months after remission to reduce the risk of relapse.
360
How should SSRIs be discontinued?
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
What are common discontinuation symptoms of SSRIs?
Increased mood changes, restlessness, difficulty sleeping, unsteadiness, sweating, gastrointestinal symptoms (pain, cramping, diarrhea, vomiting), and paraesthesia.
362
What are the risks of using SSRIs during pregnancy?
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
What causes serotonin syndrome?
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
What are the key features of serotonin syndrome?
Key features include neuromuscular excitation (hyperreflexia, myoclonus, rigidity), autonomic nervous system excitation (hyperthermia, sweating), and altered mental state (confusion).
365
How is serotonin syndrome managed?
Management is supportive, including intravenous fluids and benzodiazepines. More severe cases may require serotonin antagonists such as cyproheptadine or chlorpromazine.
366
What are the early features of a tricyclic overdose?
Early features include dry mouth, dilated pupils, agitation, sinus tachycardia, and blurred vision due to anticholinergic effects.
367
What are the severe features of a tricyclic overdose?
Severe features include arrhythmias, seizures, metabolic acidosis, and coma.
368
What ECG changes are seen in tricyclic overdose?
ECG changes include sinus tachycardia, widening of the QRS interval, and prolongation of the QT interval.
369
What ECG changes are seen in tricyclic overdose?
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
How is a tricyclic overdose managed?
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
What is somatisation disorder?
Somatisation disorder involves multiple physical symptoms present for at least two years, with the patient refusing to accept reassurance or negative test results.
372
What is illness anxiety disorder (hypochondriasis)?
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
What is functional neurological disorder (conversion disorder)?
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
What is a dissociative disorder?
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
What is factitious disorder (Munchausen's syndrome)?
Factitious disorder, also known as Munchausen's syndrome, involves the intentional production of physical or psychological symptoms by the patient.
376
What is malingering?
Malingering is the fraudulent simulation or exaggeration of symptoms with the intention of obtaining financial or other gain.
377
What is the mechanism behind alcohol withdrawal?
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
When do symptoms of alcohol withdrawal typically start?
Symptoms of alcohol withdrawal typically start 6-12 hours after the last drink and may include tremor, sweating, tachycardia, and anxiety.
379
When do seizures and delirium tremens peak in alcohol withdrawal?
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
How is alcohol withdrawal managed?
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
Why is lorazepam preferred over chlordiazepoxide in patients with liver cirrhosis?
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
What is the primary difference between typical and atypical antipsychotics?
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
What are some examples of typical antipsychotics?
Haloperidol and chlorpromazine are examples of typical antipsychotics.
384
What are some examples of atypical antipsychotics?
Clozapine, risperidone, and olanzapine are examples of atypical antipsychotics.
385
What are common extrapyramidal side effects (EPSEs) of typical antipsychotics?
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
How can acute dystonia (e.g., torticollis or oculogyric crisis) be managed?
Acute dystonia may be managed with procyclidine.
387
What are the side effects specific to elderly patients taking antipsychotics?
Elderly patients taking antipsychotics have an increased risk of stroke and venous thromboembolism.
388
What are other common side effects of antipsychotics?
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
According to NICE guidelines (2009), what is the first-line treatment for schizophrenia?
Oral atypical antipsychotics are considered first-line treatment for schizophrenia.
390
What therapeutic approach should be offered to all patients with schizophrenia, according to NICE guidelines?
Cognitive behavioural therapy (CBT) should be offered to all patients with schizophrenia.
391
Why is cardiovascular risk-factor modification important in the management of schizophrenia?
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
What factors are associated with a poor prognosis in schizophrenia?
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
What are the different types of subdural haematomas (SDH) based on their age, and how do they present clinically?
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
How is acute subdural haematoma managed?
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
How is chronic subdural haematoma managed?
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.
396
Q: What neurotransmitter do benzodiazepines enhance, and how do they affect chloride channels?
A: Benzodiazepines enhance the effect of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) by increasing the frequency of chloride channels.
397
Q: What are the main uses of benzodiazepines?
A: Sedation, hypnotic, anxiolytic, anticonvulsant, muscle relaxant.
398
Q: How long does the Committee on Safety of Medicines advise prescribing benzodiazepines?
A: Benzodiazepines should be prescribed only for a short period of 2-4 weeks.
399
Q: What is the BNF's advice on how to withdraw a benzodiazepine?
A: The dose should be reduced in steps of about 1/8 (range 1/10 to 1/4) of the daily dose every fortnight.
400
Q: What is a suggested withdrawal protocol for patients experiencing difficulty with benzodiazepine withdrawal?
A: Switch patients to the equivalent dose of diazepam, reduce the dose of diazepam every 2-3 weeks in steps of 2 or 2.5 mg, and the time needed for withdrawal can vary from 4 weeks to a year or more.
401
Q: What condition can occur if patients withdraw too quickly from benzodiazepines, and when might it occur?
A: Benzodiazepine withdrawal syndrome, which may occur up to 3 weeks after stopping a long-acting drug.
402
Q: What are the features of benzodiazepine withdrawal syndrome?
A: Insomnia, irritability, anxiety, tremor, loss of appetite, tinnitus, perspiration, perceptual disturbances, seizures.
403
Q: What is a significant risk associated with clozapine, and what monitoring is essential during treatment?
A: Clozapine carries a significant risk of agranulocytosis, and full blood count monitoring is essential during treatment.
404
Q: In what situation should clozapine be used according to the BNF?
A: Clozapine should be introduced if schizophrenia is not controlled despite the sequential use of two or more antipsychotic drugs (one of which should be a second-generation antipsychotic drug), each for at least 6-8 weeks.
405
Q: What are the adverse effects of clozapine?
A: Agranulocytosis (1%), neutropaenia (3%), reduced seizure threshold (can induce seizures in up to 3% of patients), constipation, myocarditis (a baseline ECG should be taken before starting treatment), hypersalivation.
406
Q: When might dose adjustment of clozapine be necessary?
A: Dose adjustment of clozapine might be necessary if smoking is started or stopped during treatment.
407
Q: What factors suggest depression over dementia?
A: Short history, rapid onset, biological symptoms (e.g. weight loss, sleep disturbance), patient worried about poor memory, reluctant to take tests, disappointed with results, mini-mental test score: variable, global memory loss (dementia characteristically causes recent memory loss).
408
Q: What is electroconvulsive therapy used for?
A: Electroconvulsive therapy is a useful treatment option for patients with severe depression refractory to medication (e.g. catatonia) and those with psychotic symptoms.
409
Q: What is the only absolute contraindication for electroconvulsive therapy?
A: Raised intracranial pressure.
410
Q: What are the short-term side effects of electroconvulsive therapy?
A: Headache, nausea, short-term memory impairment, memory loss of events prior to ECT, cardiac arrhythmia.
411
Q: What are the long-term side effects of electroconvulsive therapy?
A: Some patients report impaired memory.
412
Q: What are the normal stages of grief according to a popular model?
A: Denial, Anger, Bargaining, Depression, Acceptance.
413
Q: What are the features of atypical grief reactions?
A: Delayed grief (more than 2 weeks before grieving begins) and prolonged grief (grieving reactions taking up to and beyond 12 months).
414
Q: What is Othello's syndrome?
A: Pathological jealousy where a person is convinced their partner is cheating on them without any real proof, accompanied by socially unacceptable behaviour linked to these claims.
415
Q: What are typical features of post-concussion syndrome?
A: Headache, fatigue, anxiety/depression, dizziness.
416
Q: What is Seasonal affective disorder (SAD)?
A: Depression that occurs predominately around the winter months.
417
Q: How should SAD be treated according to NICE guidelines for mild depression?
A: Begin with psychological therapies and follow up with the patient in 2 weeks.
418
Q: What should be done if there is no improvement in SAD after psychological therapies?
A: An SSRI can be given if needed.
419
Q: What is Section 2 under the Mental Health Act?
A: Admission for assessment for up to 28 days, not renewable, with an application made by an Approved Mental Health Professional (AMHP) or the nearest relative, based on the recommendation of 2 doctors.
420
Q: What is Section 3 under the Mental Health Act?
A: Admission for treatment for up to 6 months, renewable, with an application made by an AMHP and 2 doctors who have seen the patient within 24 hours. Treatment can be given against the patient's wishes.
421
Q: What is Section 4 under the Mental Health Act?
A: A 72-hour emergency assessment order, used when a Section 2 would involve an unacceptable delay, and often changed to a Section 2 upon arrival at the hospital.
422
Q: What is Section 5(2) under the Mental Health Act?
A: Allows a doctor to detain a voluntary patient in hospital for up to 72 hours.
423
Q: What is Section 5(4) under the Mental Health Act?
A: Allows a nurse to detain a voluntary patient in hospital for up to 6 hours.
424
Q: What is Section 17a under the Mental Health Act?
A: Supervised Community Treatment (Community Treatment Order) that allows a patient to be recalled to hospital for treatment if they fail to comply with conditions, such as taking medication.
425
Q: What is Section 135 under the Mental Health Act?
A: A court order that allows the police to break into a property and remove a person to a Place of Safety.
426
Q: What is Section 136 under the Mental Health Act?
A: Allows the police to take someone found in a public place who appears to have a mental disorder to a Place of Safety for up to 24 hours while a Mental Health Act assessment is arranged.
427
Q: What is sleep paralysis?
A: Sleep paralysis is a condition characterized by transient paralysis of skeletal muscles occurring upon awakening or falling asleep, thought to be related to the paralysis that naturally occurs during REM sleep.
428
Q: What are the features of sleep paralysis?
A: Features include paralysis occurring after waking up or shortly before falling asleep, and hallucinations such as images or speaking during the paralysis.
429
Q: How is sleep paralysis managed?
A: If troublesome, clonazepam may be used.
430
Which antipsychotic is best for reduced side effects eg prolacinaemia
arpiprazole
431
Side effects of TCAs
antagonism of histamine receptors
drowsiness
antagonism of muscarinic receptors
dry mouth
blurred vision
constipation
urinary retention
antagonism of adrenergic receptors
postural hypotension
lengthening of QT interval
432
What is the treatment for moderate/severe tardive dyskinesia
Tetrabenazine
433
What should be done in terms of antidepressant medication when undergoing ECT
should be reduced but not stopped
434
What side effect is common for SNRIs and needs to be monitored
hypertension - blood pressure
435
When cant you use chlordiazepoxide for alcohol withdrawal
if they have liver problems - use lorazepam instead
436
437
438
