Psychiatric Disease Flashcards

1
Q

Name some other secondary symptoms of depression

A

Reduced appetite, sleep disturbance, feeling of hopelessness
Reduced concentration, irritability, reduced libido, risk of self harm, suicide
Can also have psychotic symptoms

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2
Q

Name the 3 hypotheses of depression pathophysiology

A

Mono amine hypothesis (low serotonin, low NA )
Neurotransmitter receptor hypothesis (abnormality in receptors)
Gene expression mono amine hypothesis (molecular functioning)

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3
Q

MoA of SSRIs

A

Block 5HT reuptake at presynaptic so increases 5HT time in synaptic cleft. (Selective)

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4
Q

MoA TCAs

A

Inhibit neurotransmitter reuptake (NA and 5HT)

Blocking of receptors (Muscarinic, a1 adrenergic, histaminic)

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5
Q

MoA SNRIs

A

At low doses, inhibits 5HT reuptake

At high doses, inhibits NA reuptake

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6
Q

Describe pharmacokinetics of SSRIs ( and a contraindication)

A

Once daily dosage as long elimination half life
Well absorbed orally
Metabolised by Cyt P450
Reduce dosage in hepatically impaired

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7
Q

Name common ADRs of SSRIs that would normally settle down after 10-14 days

A

Nausea
Anorexia
Vomiting

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8
Q

What is a rare but severe ADR of SSRIs ?

A

Precipitation of mania

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9
Q

TCAs pharmacokinetics

A

Well absorbed orally
Lipid soluble
Long half life
Liver metabolism, renal excretion

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10
Q

Name some ADRs for TCAs

A

CNS: sedation, autonomic: dry mouth/blurred vision
CVS: increased HR, postural hypotension, severe arrythmias
GI: constipation

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11
Q

What is a problem with TCAs ?

A

Too easy to intentionally OD and cause cardiac problems eg arrythmias

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12
Q

SNRIs are second or third line. Why?

A

All side effects of SSRIs plus increased BP, dry mouth, sleep disturbances etc.
Also, relatively short half life so maya have withdrawal.

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13
Q

Define psychosis

A

Lack of contact w reality

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14
Q

Symptoms of paranoid schizophrenia (by symptom category)

A

Positive- hallucinations, delusions, thought disorders, abn behaviour
Negative- blunted affect, social withdrawal, poverty of thought and speech
Cognitive- selective attention, poor memory, reduced abstract thought
Affective- anxiety and depression

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15
Q

What is the most popular theory for pathophysiology of schizophrenia?

A
Dopamine theory (too much dopamine)
However, this only explains positive symptoms
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16
Q

Name the 4 main dopaminergic pathways

A

Mesolimbic (emotional response and behaviour)
Mesocortical (important in arousal and mood)
Nigrostriatal (key motor pathway damaged in PD)
Tuberoinfundibular (hypothalamus and pituitary)

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17
Q

What are the 2 other theories for explaining schizophrenia?

A

Increased 5HT function
Decreased cortical glutamate

Mechanisms are unclear in both

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18
Q

Typical (first gen.) antipsychotics: give an example drug in this class

A

Haloperidol

Chlorpromazine

19
Q

Atypical antipsychotics: give an example of a drug in this class

A

Olanzapine, Clozapine

20
Q

Name the core symptoms in depression

A

Low energy, low mood, anhedonia

21
Q

Actions of all antipsychotics

A

Sedation and tranquilisation

22
Q

Which class of antipsychotic is less likely to cause extrapyramidal side effects?

A

Atypical (eg olanzapine)

23
Q

Typical antipsychotics can cause which two specific severe ADRs

A

EPS- eg tardive dyskinesia

Neuroleptic malignant syndrome (potentially fatal reaction)

24
Q

Give an advantage of typical APs over atypical and a situation in which you would use haloperidol

A
More sedating (act mainly against positive symptoms)
Haloperidol can be safely used in emergencies
25
Q

Atypical anti psychotics ADRs vary bw drugs, Name possible ADRs

A

Significant Weight gain ( implications eg CVS risk eg non adherence)
Sedation
Increased Prolactin
Sexual dysfunction

26
Q

Toxicity of anti psychotics can cause

A

CNS depression

Cardiac toxicity (arrythmias)
Sudden cardiac death
27
Q

MoA typical Antipsychotics (eg haloperidol)

A

Competitive inhibitors at a variety of receptors

But main anti psychotic effects due to high affinity comp. inhibition of D2 receptors (also probably causes EPS/td)

28
Q

MoA of atypical anti psychotics

A

Blockade of both 5HT(2) receptors and D2 receptors

29
Q

What symptoms characterise the anxiety disorders?

A
Fear is out of proportion to situation
Avoidance
Fear dying/going crazy (due to X)
Physical fight or flight type symptoms 
(light headed, SOB, nausea, palpitations, numbness, pins and needles)
30
Q

Outline treatment options for anxiety disorders

A

CBT

Pharmacological only if severe

31
Q

MoA benzodiazepines

A

full agonist enhancing GABA via GABA-BDZ receptor complex

Increases Cl- in so inhibitory

32
Q

Pharmacokinetics of benzodiazepines

A

Oral admin. Reaches peak plasma conc within 30-90 mins
Highly lipid soluble
Long half life
Renal excretion

33
Q

ADRs benzodiazepines

A

Tolerance and dependence (hence short course then not again)

Common- drowsy, dizzy, dry mouth

34
Q

Benzodiazepines are toxic in pregnancy. What issues due they cause?

A

Cleft lip and palate

Resp depression

35
Q

Treatment of benzodiazepine OD

A

IV flumazenil

36
Q

Name 3 classes of mood stabilisers

A

Lithium salts
Anti epileptics
(Atypical anti psychotics)

37
Q

What are some manic symptoms?

A

Feeling unusually excited/happy/optimistic or irritable
Over activity. Reduced concentration and attention span
Poor sleep leading to exhaustion
Rapid speech, jumping from one idea to another
Poor judgement (eg overspending). Increased interest in sex
Psychotic symptoms- hallucinations, grandiose delusions

38
Q

Lithium salts ADRs

A
Reduction in memory / concentration
Thirst, polyuria
Tremor
Drowsiness
Weight gain
39
Q

Lithium salts other systems ADRs

A

Nephrotoxic

Hypothyroid

40
Q

What monitoring do patients on lithium salts require? (systems ADRs)

A

Renal excretion - check e GFR

Check thyroid function (thyrotoxic)

41
Q

MoA lithium salts

A

Theories

Competes w electrolytes for channels
Neurotransmitter effects (eg Li raises 5HT)
Second messenger systems
42
Q

Toxic effects of lithium

A

N&V
Coarse tremor
Cognitive impairment
Agitation/restlessness

43
Q

How can lithium toxicity be managed?

A

Increase fluids
Eg IV fluids
Haemodialysis