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Psychiatry > Management Mood Disorders > Flashcards

Management Mood Disorders Flashcards

1
Q

what is overgeneralising?

A

-ve automatic thought/thinking error:

rules from isolated incidents then applied in all cases

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2
Q

What is dichotomous thinking?

A

-ve automatic thought/thinking error:

all or nothing/black and white thinking

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3
Q

What is selective abstractation?

A

-ve automatic thought/thinking error:

focuses on one negative detail and colours entire experiences

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4
Q

What is personalisation?

A

-ve automatic thought/thinking error:

relate external events to self without cause (or little cause)

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5
Q

What is minimisation or magnification?

A

-ve automatic thought/thinking error:

overestimate magnitude of undesirable events (or opposite)

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6
Q

What is arbitary evidence?

A

-ve automatic thought/thinking error:

draw a conclusion in context or no/contrary evidence

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7
Q

What is emotional reasoning?

A

-ve automatic thought/thinking error:

i feel bad/guilty therefore i am bad or should feel guility

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8
Q

What is shoulds and musts?

A

-ve automatic thought/thinking error:

have rigid views of how themselves or other should be

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9
Q

What is ECT used for? 4 reasons

A

Severe depressive illness or refractory depression. (depressive stupor e.g. can’t eat/drink)
Catatonia.
A prolonged or severe episode of mania. (not improved medications)
Schizophrenia psychosis

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10
Q

What are the contraindications to ECT

A

Absolute - raised ICP

Relative - CVD (e.g. HTN/aneurysms), RS (e.g. pnuemonia), cerebrovascular (stroke)

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11
Q

Describe usual treatment schedule for ECT

A

3X a week, reduced to twice then once as improvements show to limit cognitive problems
Catatonia usually resolves after 3-5 treatments
Treatment depression usually 6-12 times

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12
Q

What are the main risks/side effects ECT? (4)

A

impairment cognition - period of confusion immediately after ECT
Memory loss - usually improves after couple wks and majority cognitive functions improve thereafter, sometimes permanent
medical complications - heart problems
physical symptoms - nausea/vomiting/headache/muscle ache/jaw pain.

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13
Q

What kinds of ECT are more effective?

A

increased dose is more effective - needs to cause a seizure

bilateral ECT is more effective than unilateral

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14
Q

What is the general mechanism of action of antidepressants?

A

broadly they work by:
-blocking reuptake of monoamine neurotransmitters (5HT/Na/DA)
-preventing the breakdown of monoamine neurotransmitters
= increasing neurotransmitter availability

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15
Q

List 5 SSRI’s

A

Selective serotonin reuptake inhibitors:

  • fluoxetine
  • paroxetine
  • citalopram
  • sertraline
  • fluvoxamine
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16
Q

List 9 disorders in which SSRI’s are used

A 
Depression
Panic disorder
social anx. disorders
PTSD
OCD
Chronic pain
Eating disorder
Premature ejaculation
Stroke recovery
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17
Q

What is the specific mechanism of SSRI’s?

A

Inhibit reuptake of 5-HT and most can increase synaptic 5HT within hours

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18
Q

How long does it take SSRI’s to work usually - how is this related to the concentration of 5-HT in the synapse?

A

can take 2-3wks to improve mood and by the time the mood has improved 5HT conc. is normal again.
-increase in extracellular 5HT stimulates 5HT autoreceptors (which work to inhibit 5HT release) to inhibit firing, however chronic occupancy of autoreceptors causes them to desensitise which leads to normal firing again
= seroteonergic transmission in presence of reuptake blockade
= even more pumped out
(NB not too little 5HT in depression but 5HT neurotransmission may be dysregulated)

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19
Q

Describe how to start SSRI’s

A

almost all can be started off at therapeutic dose from day 1

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20
Q

Are SSRI’s safe in overdose?

A

relatively safe

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21
Q

Are SSRI’s tolerated well?

A

Usually, side effects generally improve over time

22
Q

Which enzyme do some SSRI’s inhibit e.g. fluoxetine/paroxetine

A

CYP450 so there may be some interactions with drugs in the same pathway

23
Q

What are the adverse effects of SSRI’s

A

Sexual dysfunction - can be reversed using 5HT antagonist or 5HT autoreceptor agonist
GI - nausea/dyspepsia/constipation/diarrhoea
Short term anxiety common
In those under 25yrs there’s an increased risk of suicide/self harm in the first few weeks

24
Q

List 5 tricyclic antidepressants

A

Amitryptilline, clomipramime, imipramime, nortryptilin, dosulipin

25
Q

What are tricyclic antidepressants used for?

A

hospitalised or severe depression

26
Q

what is the mechanism of tricyclic antidepressants?

A
  • serotonin-norepinephrine reuptake inhibitors by blocking serotonin and norepinephrine transporters = increase conc. of serotonin and noepinephrine.
  • also block histamine and muscarinic ACh receptors thus acting as antihistamines and anticholinergics too
27
Q

What are the concerns regarding tricyclic antidepressants?

A
  • require more individualised dose titration and at higher doses patients may need ECG monitoring (can cause GT prolongation)
  • contraindicated after an MI
28
Q

What are the adverse effects of tricyclic antidepressants?

A 
constipation
dry mouth
blurred vision
effects on cardiac function
postural hypotension (adrenergic and cholinergic blockade)
NOT safe in overdose
29
Q

List three monoamine oxidase inhibitors

A

phenelzine
isocarboxide
tranycypromide

30
Q

When are MAOI’s used?

A

less commonly, atypical depression
3rd/4th line
- due to drug/dietary reactions

31
Q

What is the mechanism of action of monoamine oxidase inhibitors?

A

inhibit monoamine oxidase A& B; MAOB so increase storage and availability for NA and 5-HT release
BUT MAO A metabolises NA 5HT and tyramine
MAO B metabolises DA, tyramine and phenylethylamine

32
Q

What is the main interaction to be wary of with MAOI’s?

A

Tyramine, this is usually inactivated in the gut by MAO’s and can get a hypertensive crisis with tyramine food and some drugs

33
Q

What foods/drugs contain tyramine? which antidepressant can interact with these?

A

MOAI’s
Food: cheese/yoghurt/yeast extract/meat/alcohol/broad beans/pickled herring
Drugs: sympathomimetics(inc. OTC) e.g. adrenaline/clonidine, pethidine

34
Q

what is the link with dopamine and antidepressants?

A
  • Many antidepressants have effects on DA and extrapyramidal side effects can occur such as tremor/dystonia/akathisia
  • Some antipsychotics may be antidepressants at low doses probs due to DA antagonism
  • DA plays a key role in reward and motivation and probs plays some role in pathophysiology depression (unknown whether cause or effect)
35
Q

What is GABA?

A
  • this is the main inhibitory neurotransmitter in mammalian brains (although in developing brains = excitatory)
  • when GABA binds to GABA receptors = opening of ion channels to let Cl- in and K+ out = hyperpolarisation
36
Q

What kind of receptor type is GABAa receptor? what are agonists of this receptor? what antagonises this receptor?

A

ligand-gated ion channel
Agonist: ethanol/benzodiazepines/propofol/anaesthetics
Antagonist: Flumazenil

37
Q

What kind of receptor type is GABAb receptor? what are agonists of this receptor?

A

G-protein coupled receptor (opens channels via intermediate g proteins)
Agonists: Baclofen, propofol

38
Q

List GABA-transaminase inhibitors

A

phenelzine, valproate, vigabetrin

39
Q

List GABA analogues

A

Pregabalin, gabapentin

40
Q

what are mood stabilisers?

A

most are anticonvulsant drugs

41
Q

What are mood stabilisers effective in?

A

more effective at lowering manic episodes than lifting depressive
(most people with bipolar disorder dont have long term stable mood)

42
Q

list the three types of mood stabilisers and give examples

A 
Anticonvulsant drugs:
-carbamazepine
-valproate, semisodium valproate
-lamotrigine
Atypical antipsychotics (SGA):
-olanzepine
-risperidone
-aripripazole
-quetiapine
Others:
-lithium carbonate
-nimodipine (Ca2+ channel blocker)
43
Q

How do anticonvulsants work as mood stabilisers?

A

probably exert effect via increasing inhibitory neurotransmission in the brain

44
Q

How does lamotrigine work as a mood stabiliser?

A

probably by blocking sodium channels, although it doesnt work directly via GABA the overall effect is a decrease in excitability and cell firing

45
Q

what are the mechanisms of lithium?

A
  • inhibits 5HT autoreceptors
  • increase in anti-apoptotic factor Bcl-2
  • inhibition of glycogen synthase kinase 3
  • depletion of inositol
  • upregulation of glutamate reuptake
46
Q

what are the disadvantages of using lithium in practice

A
  • increase in incidence of adverse effects and risk inadvertant toxicity
  • toxicity in overdose (effective therapeutic dose 0.4-1mmol/l)
  • problems with poor adherance
  • requires blood monitoring (thyroid/kidney) monthly?
47
Q

describe the mechanism of first generation antipsychotics

A

DA blockade in the mesolimbic circuits (efficacy related to affinity for D2 receptors), adverse effects are due to DA blockade in nigrostriatal (extrapyramidal) and tuberoinfundibular pathways (hyperprolactinaemia)

48
Q

describe the two mechanisms of second generation antipsychotics

A

1) increase in D2 receptor binding affinity so increase in efficacy
2) increase in 5HT2c, 5HT2a, 5HT1a receptor binding affinity so increase in antipsychotic efficacy (but drowsy/metabolic syndrome)

49
Q

What is a SNRI and an example

A

Serotonin–norepinephrine reuptake inhibitor, venlafaxine/duloxetine

50
Q

What is the mechanism of mirtazepine and when would you use it?

A

It is a noradrenergic and specific serotonergic antidepressant (NaSSA) that acts by antagonizing the adrenergic alpha2-autoreceptors and alpha2-heteroreceptors as well as by blocking 5-HT2 and 5-HT3 receptors. It enhances, therefore, the release of norepinephrine and 5-HT1A-mediated serotonergic transmission. Mirtazapine also exhibits significant antagonism at H1-receptors, resulting in sedation. Mirtazapine has no effects on the reuptake of either NE or 5-HT and has only minimal activity at dopaminergic and muscarinic receptors.

would use if someone needed sleep/appetite help

Psychiatry (26 decks)

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