Week 2 - B - Direct self Harm, Huntingtons disease, Depression and bipolar questions and ECT Flashcards

1
Q

When talking to a patient, should you use the term deliberate self harm or attempted suicide?

A

Deliberate self harm is the term that should be used

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2
Q

Where is suicides more common? What gender is it more common? When is this not the case?

A

Sucidies are more common in countries further from the equator ie northern europe

They are more common in males in all countries bar finland

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3
Q

What is the risk of suicide in the 12 months after deliberate self harm?

A

1% risk of suicide

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4
Q

By what mechanism is Huntington’s disease inherited? A - Autosomal dominant B – Autosomal recessive C -X-linked recessive D – X-linked dominant E – Multifactorial Inheritance

A

A - autosomal dominant

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5
Q

If your patient has an autosomal dominant condition, what are the chances that their child will get it?A – 100% B – 25% C – 75% D – 12.5% E – 50%

A

E - 50%

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6
Q

The phenomoen in which each generation develops a genetic disease at an earlier age is called: A- Acceleration B – Penetrance C – Anticipation D – Heritability E – Transformation

A

C - Anticipation

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7
Q

Huntingtons disease first described thoroughly in 1872 by George Huntington, although there were some mentions in the literature before this What is its inheritance? What cause huntingtons disease?

A

It is an autosomal dominant condition

It is caused by a trinucleotide expansion of the CAG nucleotide chain on chromosome 4 due to a mutation in huntingitn gene which codes for the huntingtin protein

CAG normally codes for glutamine so more CAG means more glutamine which causes the huntingtin gene to be misshapen

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8
Q

How many CAG repeats are normal in the huntingin gene on chromsome 4? How many will most defintely cause diseasee? How many repeats usually can cause juvenile huntingtins disease?

A

Normally, the CAG segment is repeated 10 to 35 times within the gene.

In people with Huntingtons, the CAG segment is repeated 36 to more than 120 times.

People with more than 40 almost definitely develop Huntingtons with people with more than 60 CAG repeats developing juvenile huntingtons

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9
Q

What percentage of the UK have bipolar 1? A – 0.5% B – 1% C – 2%

A

1% of the Uk have bipolar I 2% of the UK have bipolar II

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10
Q

Which of these symptoms would be inconsitnet with mania with psychotic symptoms? * A – normal sleep pattern * B – irritability instead of elation * C – delusional idea that they are being monitored by the police * D - physical aggression * E – flight of ideas

A

A - normal sleeping pattern

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11
Q

Which of these can be a feature of hypomania? A – hearing a voice saying ‘you are special’ B – hearing a voice saying ‘ everone is watching you’ C – paranoid delusions D – impulsive overspending E – self-neglect causing dehydration

A

The first three psychotic symptoms, the last one is either severely manic, or severely depressed

D – impulsive overspending is hypomania

Hypomania still have some level of function without the psychotic symptoms , mania you kindve lose the ability to take personal care of yourself

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12
Q

How is bipolar disorder inherited? A – autosomal dominant B – recessive C – xlinked D – multifactorial E – no

A

D - multifactorial

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13
Q

Is genetic testing for bipolar disorder useful? A – yes B- No

A

B - no

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14
Q

CASE EXAMPLE 1: A 25 year old woman presents with a 2 month history of low mood, loss of interest, lethargy. She is finding it increasingly difficult to cope with work, takes more than 2 hours to get to sleep and even then wakens repeatedly through the night. She denies any previous similar episodes. 4 months ago her husband left her and she has since been living alone; her parents and family are 200 miles away. a) What is the likely diagnosis?

A

Her likely diagnosis is depression

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15
Q

b) What are the three main groups of antidepressants? Name a specific example from each group. How do they differ in their mechanisms of action?

A

Monoamine reuptake inhibitors * SSRIs - sectively block the reuptake of serotonin in the synaptic celft (citalopram, fluoxetine, paroxeine) * SNRIs - block the reuptake of noradrenaline and serotonin in the synapctic cleft (duloxetine,) * TCAs - block the reuptake of monoamine in the synaptic cleft - mainly serotonin and noradrenaline MAOI - block the degradation of monoamines via the monoamine oxidase enzyme (phenelzine - irreversible) Atypicals - mirtazapine (Noradrenergic & specific serotonergic antidepressant) & bupropion (dopamine uptake inhibitor)

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16
Q

c) How would you decide which group of antidepressants to prescribe from in this situation?

A

First line is SSRI’s. Also think about patients past medical history, drug history and age/gender. Tell her the possible side effects, how long it takes to work and whether they are addictive.

17
Q

When is a treatment considered non-responsive?

A

Non-responsive treatment to an anti-depressant occurs after inadequate or no response after six weeks of use at the maximum or best tolerated dose of the drug

18
Q

She is prescribed fluoxetine, but re-attends one month later – she is no better. e) What factors may have contributed to her non-response?

A

Should take 4-6 weeks for antidepressants to work She may have been non-compliant Dose also may be too low

19
Q

After a further month’s prescription of fluoxetine she has still not improved. She is then prescribed paroxetine 50mg per day, but again does not improve after 2 months. f) What non-pharmacological treatment options are there?

A

Cognitive behavioural therapy Interpersonal therapy

20
Q

What treatment can be considered for severe, life-threatening depression and when a rapid response is required, or when other treatments have failed?

A

This would be electroconvulsive therapy

21
Q

g) How would you decide what antidepressant to prescribe next?

A

Would probably be chossing betweena typicals, TCAs and SNRIs Inform the patient of the pros and cons of each

22
Q

She is prescribed imipramine and responds very well to this. She is able to return to work and feels she is functioning at her normal level. She asks how long she should continue to take imipramine. h) How would you answer her question?

A

After recovery from depression, continue treatment for at least 6 months before stopping

23
Q

Seven years later she re-presents with a further depressive episode following the death of her mother. i) How would you decide which anti-depressant to prescribe

A

Would probably use imipramine as she responded well to this last time

24
Q

How long should she take the imipramine for in this case?

A

Take it for at least 12-24 months

25
Q

CASE EXAMPLE 2: A 25 year old woman has had two previous episodes of depression which have responded well to anti-depressants. She now presents with a 2-week history of increased energy, racing thoughts, overactivity and reduced sleep. She appears grandiose at interview, has flight of ideas and speaks of having invented a machine that will make her millions. a) What is the likely diagnosis?

A

Her most likely diagnosis is bipolar disorder

26
Q

What factors in her history and presentation would influence the decision to commence him on a mood stabilizer?

A

She has had periods of depression and mania meaning she needs to be on a mood stabiliser

27
Q

What would be the first line mood stabilizer to use? What is its mechanism of action?

A

Lithium carbonate It acts as a glycogen synthase kinase 3 B inhibitor or by blocking the phosphatidylinositol pathway

28
Q

d) What would you tell her about common side effects and signs of toxicity?

A

Side effects - GI upset, fine tremor, sedation, diabetes insipidus causing polyuria, hypothyrodism, hypoparathyroidism, ankle swelling Toxicity - vomiting , diarrhoea, ataxia, coarse tremor drowsiness, convulsions, coma VERY IMPORTANT TO KEEP HYDRATED WHEN ON LITHIUM OR CAN BECOME TOXIC

29
Q

e) What investigations are routinely monitored during the course of therapy?

A

Monitor U&Es and lithium levels 3 monthly Check TFTs 6 monthly

30
Q

f) If this drug is not tolerated or is ineffective, what alternatives are there?

A

Anti-convulants - carbamezapine, sodium valproate, lamortigine or Anti-psychotics

31
Q

The initial choice of drug is effective and provides a period of relative stability. 2 years later, she presents to say that she and her husband want to have a child. g) What advice would you give her about whether to discontinue the drug or continue it through pregnancy?

A

Congenital abnormalities can occur when the mother is taking lithium. Can also cause heart arrhythmias in the child. However if the mother was going to come off the drug then there is a 50% chance of relapse. Need to monitor the drug levels very closely very frequency if taking lithium throughout pregnancy

32
Q

What heart anomalies is the use of lithium during pregnancy associated with?

A

Ebstein’s anomaly is a congenital heart defect in which the septal and posterior leaflets of the tricuspid valve are displaced towards the apex of the right ventricle of the heart.