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Semester 5 - Farmocology > Session 12 - Depression & Anxiety > Flashcards

Session 12 - Depression & Anxiety Flashcards

1
Q

Give five things which cause psychiatric disorders to occur

A

o Genetic vulnerability to the expression of the disease
o Live events (divorce, bereavement)
o Individuals personality, coping skills, social support
o Environmental influences (e.g. viruses during pregnancy, toxins, other diseases)
o Biopsychosocial Model
 Predisposing, precipitating and perpetuating factors

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2
Q

Give two overarching ways in which CNS drugs work

A

o Agonists or Antagonists of neurotransmitter receptors
 May be competitive for neurotransmitter binding site
 May mimic or block at these sites
o Inhibitors of regulatory enzymes
 Those that make or break down neurotransmitters
 Less common
 MOA inhibitors

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3
Q

Name the three main transmission pathways in CNS?

A

o Noradrenergic Pathways
o Dopaminergic Pathways
o Serotonergic (5HT) Pathways

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4
Q

Name 5 commonly treated psychiatric illnesses

A 
o	Schizophrenia
o	Depression
o	Bipolar disorder
o	Eating disorders
o	Obsessive compulsive disorder
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5
Q

What is everyones lifetime risk of depression?

A

10%

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6
Q

What is the diagnosis of depression dependent on? (overarching types and length of time must have suffered)

A

Two weeks with
Core symptoms (2 of three needed for diagnosis)
and Secondary Symptoms

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7
Q

Name the three core symptoms of depression

A

o Low mood
o Anhedonia (lack of enjoyment)
o Decreased energy

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8
Q

Give four secondary symptoms of depression

A 
o	Decreased appetite
o	Sleep disturbance
o	Hopelessness (Depressive Cognition) 
o	Physical aches and pains
o	Irritability
o	Self harm or suicidal ideas or acts
	10% with a history of recurrent, severe depression commit suicide
o	Can have psychotic symptoms
o	Early morning wakening – (2 hours before normal waking time)
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9
Q

Give three theories for depression

A

Monoamine hypothesis
Neurotransmitter receptor hypothesis
Monoamine gene expression hypothesis

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10
Q

What is the monoamine hypothesis

A

o Depression is due to a deficiency of monoamine neurotransmitters (Noradrenaline and Serotonin)
o Monoamine Oxidase Inhibits (MAOIs) block the enzyme monoamine oxidase from destroying the neurotransmitters
o However if this were true anti-depressants would work instantly.. So maybe it’s due to Theory 2

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11
Q

What is the neurotransmitter receptor hypothesis

A

o Depression is due to abnormality in the receptors for monoamine transmission

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12
Q

What is neurotransmitter receptor hypothesis?

A

o Depression is due to abnormality in the receptors for monoamine transmission

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13
Q

What is the monoamine gene expression hypothesis?

A

o Deficiency in molecular functioning
o Hypothesised problem within the molecule events distal to receptor

However, growing evidence exists that despite apparently normal levels of monoamines and receptors that these system do not respond normally

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14
Q

Give three mainline drugs for depression

A

1st - SSRI
2nd - Serotonin+noradrenaline reuptake inhibitor
3rd - Tricyclic anti-depressants

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15
Q

What is the mechanism of action of SSRI?

A

 Act with a high specificity for potent inhibition of serotonin reuptake into nerve terminals from the synaptic cleft
 Only minimal effects on noradrenaline uptake

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16
Q

Give three common ADRs of SSRIs

A

Anorexia
Diarrhoea
Nausea

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17
Q

Give two rare ADRs of SSRIs

A
  • Increase in suicidal ideation
  • Precipitation of mania
  • Tremor
  • Extrapyramidal syndrome
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18
Q

Give a major DDI of SSRIs

A

Used in combination with MAOIs can cause potentially fatal serotonergic syndrome of hyperthermia and cardiovascular collapse

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19
Q

What is a contraindication for SNRIs

A

 Hypertensive patients, as Venlafaxine raises blood pressure

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20
Q

What is the mechanism of action of SNRIs

A

 Inhibit the reuptake of both serotonin and noradrenaline, thus potentiating neurotransmitter activity in the CNS
 Dose dependent
 Low dose blocks Serotonin
 High dose blocks Noradrenaline

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21
Q

Give three common ADRs to SNRIs

A

Anorexia, nausea, diarrhoea

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22
Q

Give three rare ADRs of SNRIs

A 
Precipitation of mania
 tremor
extrapyramidal syndromes
Hypertension (INCREASES NORADRENALINE)
Sleep disturbance
23
Q

What is a DDI of SNRIs?

A

 MAOIs – Used in combination can cause potentially fatal serotonergic syndrome of hyperthermia and cardiovascular collapse

24
Q

How do tricyclic antidepressants work?

A

 Block serotonin and noradrenaline reuptake. Also have affinity for H1, muscarinic and α1 and α2 receptors.

25
Q

Give four contraindications for TCAs

A

 Recent MI or arrhythmias (especially heart block)
 Manic phase
 Severe liver disease
 Epilepsy (TCAs lower seizure threshold)

26
Q

Give some ADRs for TCAs

A

Arrhytmia (block reuptake of NA)
Muscarinic blocking effects
a2 blockers - Postural hypotension

27
Q

What monoamine oxidase inhibitor is used in depression?

A

MAOa

28
Q

When is MAOb used?

A

Parkinsons

29
Q

What do MAOIs do for depression?

A

 MAOIs block the action of monoamine oxidase, the enzyme that metabolises monoamines (noradrenaline and serotonin

30
Q

Three ADRs of MAOIs

A

 Hypertension
 CNS stimulation causing excitement and tremor
 Dry mouth, blurred vision

31
Q

What is anxiety?

A

o Fear out of proportion to situation

32
Q

Give some symptoms of anxiety

A 
	Light headedness
	Dyspnoea
	Hot and cold flushes
	Nausea
	Palpitations
	Numbness
	Paraesthesia
33
Q

What is the first line treatment for anxiety?

A 
	Light headedness
	Dyspnoea
	Hot and cold flushes
	Nausea
	Palpitations
	Numbness
	Paraesthesia
34
Q

What are benzos used?

A

Anxiety

Status epilepticus

35
Q

What is the mechanism of action of benzos?

A

 Act at a distinct receptor site on GABA Chloride channel
 Exert effects through structure known as GABA-BDZ receptor complex
 Benzodiazepins only bind to BDZ receptor of which there are 2 main groups – high and low affinity
 High affinity group – important in anxiolytic, hypnotic and anticonvulsant effects of BDZs
 Binding of GABA or Benzodiazepines enhance each other’s binding, acting as positive allosteric effectors
 Increases Chloride current into the neurone, increasing threshold for action potential generation

36
Q

Give some common ADRs of benzos 3

A

drowsiness, dizziness, psychomotor impairments

37
Q

Give 3 rare sideeffects of nbenzoes

A

Amnesia, restlessness, rash

38
Q

Give some other side effects of benzos

A

 Sedation
 Tolerance with chronic use (need to increase dose)
 Dependence/Withdrawal with chronic use can get withdrawal effects (insomnia, agitation, anxiety)
 Confusion, impaired co-ordination
 Aggression
 Abrupt withdrawal – seizure trigger

39
Q

What do the DDIs of benzos stem from?

A

High protein bindign

40
Q

WHat is overdose of benzos reversed by?

A

 Overdose reversed by IV Flumazenil (antagonist at BDZ receptors)

41
Q

What happens if you take benzos in preg?

A

o Use in late pregnancy can cause respiratory depression and feeding difficulties in baby
 Teratogenic – Cleft lip and palate if exposed in utero

42
Q

What is bipolar?

A

o High genetic component
o Depression and hypomania/mania
o Feeling unusually excited, happy, optimistic or feeling irritable
o Overactive
o Poor concentration and short attention spam
o Poor sleep
o Rapid speech, jump from one idea to another
o Poor judgement (overspending)
o Increased interest in sex
o Psychotic symptoms – hallucinations, grandiose delusions

43
Q

What do antidepressants cause in bipolar?

A

Mania

44
Q

Give three types of drugs used to mood stabilisers

A
  • Lithium
  • Anti-epileptic drugs
  • Atypical antipsychotics
45
Q

What is lithium used for?

A

 Mood stabiliser (Antimanic and Antidepressant activity)
 Prophylaxis of Mania and Depression in bipolar disorder
 Augmentation of antidepressants in unipolar depression

46
Q

What is the mechanism of action?

A

 Electrolytes and channels – May compete with Mg2+ and Ca2+ channels
 Neurotransmitters – Lithium increase 5HT. Chronic Lithium may reduce 5HT receptor sites
 Second messenger systems – Lithium attenuates the effects of neurotransmitters on their receptors, without altering receptor density

47
Q

Give some ADRs

A 
	Memory problems (learning new information) – 52%
	Thirst – 42% 
	Polyuria – 38% 
	Tremor (very fine) – 34% 
	Drowsiness – 24%
	Weight gain – 18% 
	Hair loss
	Rashes
48
Q

What are the two treatments for dementia?

A

Acetylcholinesterase Inhibitors

NMDA Antagonists

49
Q

What is first-line treatment for dementia?

A

Acetylcholinesterase Inhibitors

50
Q

Why are Acetylcholinesterase Inhibitors used in dementia?

A

Ach plays a role in arousal, memory, attention and mood. NICE guidance advises medication be made available for mild and moderate dementia. Treatment slows own the progression of Alzheimer’s Disease, giving you ~1 year extra at home before residential care.

51
Q

Give some ADRs of AChinesterase inhibitors?

A

 Nausea, vomiting, anorexia, diarrhoea (most common)
 Fatigue, insomnia, headache
 Bradycardia (particularly with Polypharmacy, e.g. β-blockers)
 Worsening of COPD
 Gastric/Duodenal ulcers

52
Q

When are NMDA antagonists used?

A

Licensed for moderate to severe dementia and is usually well tolerated. Common side-effects include: hypertension, dyspnoea, headache, dizziness, drowsiness. Usually a 2nd line treatment.

53
Q

Give 5 common ADRs of NMDA antagonists?

A 
	Hypertension
	Dyspnoea
	Headache
	Dizziness
	Drowsiness

Semester 5 - Farmocology (27 decks)

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