New Stuff in Newly appeared questions Flashcards
(68 cards)
What did the following people talk about:
- Winnicott
- Carl Jung
- Melanie Klein
- Sigmund Freud
- Wilfred Bion
- Karen Horney
- Erving Goffman
- Siegfried Foulkes
- Barton
Winnicott - Good enough mother, transitional object
Carl Jung - Collective unconscious, archetype, anima, animus
Melanie Klein - Paranoid-schizoid position, depressive position, splitting
Sigmund Freud - Free association, transference, ego, super-ego, id, eros, thanatos, defense mechanisms, oedipus Complex, the unconscious
Wilfred Bion - Basic assumption group
Karen Horney - Womb envy
Erving Goffman - Total institution
Siegfried Foulkes - Foundation matrix
Barton - Institutional Neurosis
Freud introduced the topography of the mind in what publication?
What were the three areas he split the mind into, and what did each entail?
The interpretation of dreams.
Conscious
Preconscious
Unconscious
The conscious system: part of the mind that is aware.
The preconscious system: information that is known and can potentially be brought into consciousness.
The unconscious system: this area of the mind was outside conscious awareness. It operates on the primary process thinking, which means it is aimed at wish fulfilment. It is governed by the pleasure principle. It has no concept of time, and denies the existence of negatives, and is irrational as it allow the existence of contradictions.
What does AUDIT test for?
What does CAGE test for?
Which is the tool of choice for primary care?
AUDIT is used in primary care settings as it accurately detects both alcohol dependence and hazardous drinking. CAGE is good at detecting dependence only.
AUDIT is used in primary care settings.
Serotonin syndrome:
- Characteristic triad?
- Most reliable diagnostic finding?
- Three features nearly always present?
- Onset?
- Most frequent drug interaction causing this?
- Treatment?
- Triad= neuromuscular abnormalities (clonus, myoclonus), altered mental state, autonomic dysfunction.
- Most reliable finding: neuromuscular abnormalities (clonus/myoclonus)
- Three features always present: hyper-reflexia, muscular rigidity and clonus
- Onset usually acute/rapid
- Treatment: can range from supporitve with benzos and IV fluids to use of 5HT-2A antagonist such as cyproheptadine
Neuroleptic malignant syndrome Cause? (both what drug types and biochemically) Onset? Treatment? Mortality rate? Risk factors?
Caused usually by antipsychotics.
Thought to be due to dopamine blockade messing up thermo-regulatory system
Onset more gradual than SS but usually within 2 weeks of initial treatment; also with rapid dose reductions and abrupt withdrawal of anticholinergics
Mortality rate can be up to 20%
Treatment not always necessary. Involves removing antipsychotic; consider benzo, bromocriptine, dantrolene
Risk Factors: young male physical exhaustion dehydration previous and FH of NMS organic mental disorder low serum iron rasied CK comorbid substance misuse high loading dose faster rate of loading high potency sudden withdrawal
Differences between NMS and SS Onset Course Neuromuscular findings Reflexes Pupils
NMS onset is within 2 weeks of offending medication, SS has an acute onset (within 24 hours of drug administration)
SS usually rapidly resolves. NMS is a gradual
CLonus and tremor in SS
diffuse rigidty in NMS
Reflexes increased in SS, decreased in NMS
Mydriasis in SS, normal in NMS
Which antipsychotic is linked to pathological gambling?
There is evidence in the form of case reports suggesting there may be an association between aripiprazole and pathological gambling.
This makes sense since the only antipyschotic with some dopamine agonist features is Aripiprazole (D2 agonist)
Three medications that have been trialled in pathological gambling
SSRIs
Mood stabilisers
Naltrexone
Advice is to use whichever comorbid disease is present e.g. mood stabiliser if BPAD, SSRI is OCD or depressed, naltrexone if pathalogical gambling associated with other impulse-control disorders
What are the three key limbs of diagnosis of anorexia?
What is atypical?
- Energy restriction leading to low body weight
- Fear of gaining weight
- Disturbed body image
Atypical describes presentation not quite meeting full criteria e.g. a lady who is very thin, starving herself but recognises that she is thin
What is the DSM-V guide to diagnosis of anorexia, with further subdivision
Similar to three key limbs:
- Energy intake restriction relative to requirement, leading to significant reduced body weight (BMI <18.5 is a guide)
- Disturbed body image or persistent lack of recognition of the seriousness of the current low body weight
- Intense fear of gaining weight or becoming fat
Further divided into:
- Restricting type (weight loss attained through diet, fasting and exercise alone, within previous 3 months)
- Binge eating/purging type (in previous 3 months, purging or binge-eating)
Severity criteria for anorexia
Mild = BMI > 17
Moderate = BMI 16-16.99
Severe - BMI 15 - 15.99
Extreme = BMI <15
Remember normal BMI Underweight is < 18.5 Normal 18.5-25 Overweight 25-30 Obese over 30
Relationship to person and schizophrenia
Relationship to person with schizophrenia Risk of developing schizophrenia (lifetime risk) General population 1% First cousin 2% Uncle/aunt 2% Nephew/niece 4% Grandchildren 5% Parents 6% Half sibling 6% Full Sibling 9% Children 13% Fraternal twins 17% Offspring of duel matings (both parents had schizophrenia) 46% Identical twins 48%
When do the initial signs and symptoms of alcohol withdrawal become apparent?
Symptoms?
When do they diminish?
How many people progress to DTs? What is it? When occur?
Risk factors
Treatment of all the above; how does this relate to alcohols effect on GABA
The initial signs and symptoms of withdrawal begin from 6 to 48 hrs after drinking stops. They usually peak between 10-30 hours (McIntosh 2004).
Initial symptoms include: - sweating, agitation, nausea, tremor, irritability, and in a small number of cases transient hallucinations. These initial symptoms usually diminish by 48hrs.
5% progress to DTs.
More serious: severe agitation, tremor, hallucinations. occurs 2-4 days following alcohol cessation. mortality 1-5%.
risk factors : abnormal liver function, old age, severity of withdrawal symptoms, concurrent medical illness, heavy alcohol use
Alcohol enhances the effect of GABA on GABA-A, resulting in decreased overall brain excitability. Chronic exposure to alcohol results in a compensatory decrease of GABA-A neuroreceptor response to GABA. As a result when people stop drinking their brains become very excitable. For this reason benzodiazepines are the main stay of treatment.
NICE guidelines for:
- Short term insomnia
- Long term insomnia
SHORT TERM (<4 weeks)
Short-acting benzodiazepines temazepam, loprazolam, lormetazepam.
Non-benzodiazepines (the ‘z-drugs’) zopiclone, zolpidem, and zaleplon (all are short acting).
Diazepam is not generally recommended, but it can be useful if insomnia is associated with daytime anxiety
LONG TERM
Refer to psychological services for a cognitive or behavioural intervention.
Pharmacological therapy is generally not recommended for the long-term management of insomnia but may be considered for immediate relief of symptoms.
If prescribing medication, use the lowest effective dose for the shortest period possible. The exact duration will depend on the underlying cause but should not continue for longer than 2 weeks. Up to 4 weeks’ use may occasionally be required, but continued use should always be re-assessed after 2 weeks.
For people over 55 years of age with persistent insomnia, consider treatment with a modified-release melatonin. The recommended initial duration of treatment is 3 weeks. If there is a response to treatment, it can be continued for a further 10 weeks.
Tremor in lithium
Toxicity?
Long term lithium use?
Lithium toxicity = Coarse, intention tremor
Long term lithium use = Fine, physiological tremor
Night terrors:
- What age do they occur?
- Boys vs girls?
- How long does an episode last?
- when does it begin?
- what happens?
- how are they different to nightmares?
- in children age 3-12 and most often when a child is 3-4
- equal between boys and girls
- 1 to 15 minutes
- 1 to 3 hors after sleep has begun
- intesne crying and distress, unresponsive to external stimuli
- nightmares occur during REM, night terrors during stage 3-4 NREM, there is no recall in night terrors, the onset in sleep of night terror is early (vs late), and the associated autonomic arousal is far greater in night terrors
What is the Wechsler Adult Intelligence Test? Ages used? Four index scores? Two scores gained? Average score?
Most commonly used intelligence test in clinical practice.
Between 16 and 90
Verbal Comprehension Index
Perceptual Reasoning Index
Working Memory Index
Processing Speed Index
Full scale IQ
General ability Index
Average score is 100, meaning you are on 50th centile (50% of people score above and 50% score below)
PTSD:
- What are cortisol levels doing?
- Two structures implicated?
- Lower than normal; attributed to chronic adrenal exhaustion
- Amygdala and hippocampus
How does the ICD-10 differentiate mania from hypomania?
DSM?
In the ICD-10 hypomania is differentiated from mania by duration and symptoms. Hypomania is an elevated mood for a minimum of 4 days. Mania requires a minimum of 7 days.
The DSM-IV differentiates between mania and hypomania by stipulating that hypomania occurs without any marked social or occupational interference.
What three features would suggest mania rather than hypomania?
Flight of ideas
Psychotic symptoms
Loss of social inhibitions
Go through the B vitamins
Vitamin B1 = thiamine Vitamin B2 = riboflavin Vitamin B3 = niacin Vitamin B5 = pantothenic acid Vitamin B6 = pyridoxine Vitamin B7 = biotin Vitamin B9 = folic acid Vitamin B12 = cyanocobalamin
What are the features of vitamin B3 deficiency? Who gets it?
Vitamin B3 is Niacin.
Deficiency leads to Pellagra.
Pellagra = 3ds; dermatitis, diarrhoea, dementia.
Alcoholics get it, but much less commonly than B1 deficiency (i.e. wernickes/korsakoff syndrome)
Describe the DSM-IV clusters of personality disorders.
What is the big difference between this and ICD-10.
Cluster A (MAD)
Paranoid
Schizoid
Schizotypal
Cluster B (BAD)
Narcissistic
Borderline
Antisocial
Histrionic
Cluster C (SAD)
Obsessive compulsive
Dependent
Avoidant
. One important exception is that in the ICD-10, schizotypal personality disorder is not grouped with the personality disorders. Instead it is grouped with schizophrenia and referred to as Schizotypal disorder.
Drugs and pregnancy/breastfeeding?
Antidepressants
Psychotics
Mood stabiliers
Sedatives
Drug class Suggested in pregnancy Suggested in breastfeeding
Antidepressants: PREGNANCY Fluoxetine, sertraline, amitriptyline, imipramine, (avoid paroxetine, clomipramine, and all MAOI) BREASTFEEDING Sertraline
Antipsychotics PREGNANCY Olanzapine, quetiapine, haloperidol, clozapine, chlorpromazine BREASTFEEDING Olanzapine
Mood stabilisers
PREGNANCY
Avoid if at all possible, antipsychotic with mood stabilising properties is preferred
BREASTFEEDING
Avoid if possible and use antipsychotics instead. Valproate is recommended if essential
Sedatives
PREGNANCY Promethazine (widely used but little data)
Benzodiazepines (probably not teratogenic but avoid in late pregnancy due to floppy baby syndrome)
BREASTFEEDING
For anxiety - Lorazepam
For insomnia - Zolpidem
