Session 12 - Depression & Anxiety Flashcards
Give five things which cause psychiatric disorders to occur
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
Give two overarching ways in which CNS drugs work
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
Name the three main transmission pathways in CNS?
o Noradrenergic Pathways
o Dopaminergic Pathways
o Serotonergic (5HT) Pathways
Name 5 commonly treated psychiatric illnesses
o Schizophrenia o Depression o Bipolar disorder o Eating disorders o Obsessive compulsive disorder
What is everyones lifetime risk of depression?
10%
What is the diagnosis of depression dependent on? (overarching types and length of time must have suffered)
Two weeks with
Core symptoms (2 of three needed for diagnosis)
and Secondary Symptoms
Name the three core symptoms of depression
o Low mood
o Anhedonia (lack of enjoyment)
o Decreased energy
Give four secondary symptoms of depression
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)
Give three theories for depression
Monoamine hypothesis
Neurotransmitter receptor hypothesis
Monoamine gene expression hypothesis
What is the monoamine hypothesis
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
What is the neurotransmitter receptor hypothesis
o Depression is due to abnormality in the receptors for monoamine transmission
What is neurotransmitter receptor hypothesis?
o Depression is due to abnormality in the receptors for monoamine transmission
What is the monoamine gene expression hypothesis?
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
Give three mainline drugs for depression
1st - SSRI
2nd - Serotonin+noradrenaline reuptake inhibitor
3rd - Tricyclic anti-depressants
What is the mechanism of action of SSRI?
Act with a high specificity for potent inhibition of serotonin reuptake into nerve terminals from the synaptic cleft
Only minimal effects on noradrenaline uptake
Give three common ADRs of SSRIs
Anorexia
Diarrhoea
Nausea
Give two rare ADRs of SSRIs
- Increase in suicidal ideation
- Precipitation of mania
- Tremor
- Extrapyramidal syndrome
Give a major DDI of SSRIs
Used in combination with MAOIs can cause potentially fatal serotonergic syndrome of hyperthermia and cardiovascular collapse
What is a contraindication for SNRIs
Hypertensive patients, as Venlafaxine raises blood pressure
What is the mechanism of action of SNRIs
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
Give three common ADRs to SNRIs
Anorexia, nausea, diarrhoea
Give three rare ADRs of SNRIs
Precipitation of mania tremor extrapyramidal syndromes Hypertension (INCREASES NORADRENALINE) Sleep disturbance
What is a DDI of SNRIs?
MAOIs – Used in combination can cause potentially fatal serotonergic syndrome of hyperthermia and cardiovascular collapse
How do tricyclic antidepressants work?
Block serotonin and noradrenaline reuptake. Also have affinity for H1, muscarinic and α1 and α2 receptors.
Give four contraindications for TCAs
Recent MI or arrhythmias (especially heart block)
Manic phase
Severe liver disease
Epilepsy (TCAs lower seizure threshold)
Give some ADRs for TCAs
Arrhytmia (block reuptake of NA)
Muscarinic blocking effects
a2 blockers - Postural hypotension
What monoamine oxidase inhibitor is used in depression?
MAOa
When is MAOb used?
Parkinsons
What do MAOIs do for depression?
MAOIs block the action of monoamine oxidase, the enzyme that metabolises monoamines (noradrenaline and serotonin
Three ADRs of MAOIs
Hypertension
CNS stimulation causing excitement and tremor
Dry mouth, blurred vision
What is anxiety?
o Fear out of proportion to situation
Give some symptoms of anxiety
Light headedness Dyspnoea Hot and cold flushes Nausea Palpitations Numbness Paraesthesia
What is the first line treatment for anxiety?
Light headedness Dyspnoea Hot and cold flushes Nausea Palpitations Numbness Paraesthesia
What are benzos used?
Anxiety
Status epilepticus
What is the mechanism of action of benzos?
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
Give some common ADRs of benzos 3
drowsiness, dizziness, psychomotor impairments
Give 3 rare sideeffects of nbenzoes
Amnesia, restlessness, rash
Give some other side effects of benzos
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
What do the DDIs of benzos stem from?
High protein bindign
WHat is overdose of benzos reversed by?
Overdose reversed by IV Flumazenil (antagonist at BDZ receptors)
What happens if you take benzos in preg?
o Use in late pregnancy can cause respiratory depression and feeding difficulties in baby
Teratogenic – Cleft lip and palate if exposed in utero
What is bipolar?
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
What do antidepressants cause in bipolar?
Mania
Give three types of drugs used to mood stabilisers
- Lithium
- Anti-epileptic drugs
- Atypical antipsychotics
What is lithium used for?
Mood stabiliser (Antimanic and Antidepressant activity)
Prophylaxis of Mania and Depression in bipolar disorder
Augmentation of antidepressants in unipolar depression
What is the mechanism of action?
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
Give some ADRs
Memory problems (learning new information) – 52% Thirst – 42% Polyuria – 38% Tremor (very fine) – 34% Drowsiness – 24% Weight gain – 18% Hair loss Rashes
What are the two treatments for dementia?
Acetylcholinesterase Inhibitors
NMDA Antagonists
What is first-line treatment for dementia?
Acetylcholinesterase Inhibitors
Why are Acetylcholinesterase Inhibitors used in dementia?
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.
Give some ADRs of AChinesterase inhibitors?
Nausea, vomiting, anorexia, diarrhoea (most common)
Fatigue, insomnia, headache
Bradycardia (particularly with Polypharmacy, e.g. β-blockers)
Worsening of COPD
Gastric/Duodenal ulcers
When are NMDA antagonists used?
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.
Give 5 common ADRs of NMDA antagonists?
Hypertension Dyspnoea Headache Dizziness Drowsiness
