4235992
| Questão | Responda |
| What are the emotional symptoms of depression? (2) | 1) Mood 2) Thought disorder |
| What are the biological symptoms of depression? (2) | 1) Anhedonia (no reward feeling) 2) Motivational impairments |
| What are the cognitive symptoms of depression? (2) | 1) Difficulty in decision making 2) Poor concentration |
| Which mood disorder is bipolar? | Manic depression |
| What are the four main characteristics of mania? | 1) Less sleep required 2) Excessive exuberance, enthusiasm and confidence etc 3) Behaviours inappropriate to circumstance 4) Disorders of thought (psychosis) |
| What are the two main possible causes of depression? | 1) Monoamine theory 2) Neuroplasticity/degeneration |
| What monoamines are thought to be affected in the monoamine theory? | Functional deficit of 5-HT and NA (possibly DA) |
| What evidence is there in support of the monoamine theory? (5) | 1) Current anti-depressants target MA system 2) Good link between MA and mood 3) Measurements in some patients show MA deficit 4) Depleting 5-HT can induce a relapse into depression 5) Genetic evidence for 5-HT depletion |
| What evidence is there against the monoamine theory? | 1) Amphetamine and cocaine lack efficacy 2) Some patients are resistant to treatment 3) Improvements are delayed (3-4weeks) 4) Non-pharmacological treatments have efficacy |
| Why does a varying response to treatment not necessarily undermine the monamine theory? | Depression is a heterogenous disorder with a complex pathology - i.e. low mood is common symptom but cause may vary |
| What is neuroplasticity/neurodegeneration in depression caused by? | 1) Genes - 40% genetic vulnerability 2) Environmental stress |
| How can stress lead to neurodegeneration? (3) | 1) Increase detrimental transcription via cortisol release 2) Increase detrimental transcription via inhibiting NA, 5-HT and BDNF 3) Increase neural apoptosis via glutamate release |
| How does stress lead to the release of cortisol? | CRF (Corticotropin releasing factor) released from the hypothalamus ACTH (adrenocorticotropic hormone) released from pituitary Cortisol released from adrenal cortex |
| How does glutamate release lead to cell death? | Over activation of NMDA receptors leads to excitotoxicity |
| How does detrimental gene transcription lead to depressive symptoms? (2) | 1) Increased neural apoptosis 2) Decreased neurogenesis |
| Which area of the brain can neuro-degeneration be seen in depressed patients? | Hippocampus |
| What are the three ways of increasing monoamine function in the CNS? | 1) Enzyme inhibitors 2) Uptake blocker 3) Block pre-synaptic autoreceptors |
| What is moclobemide? | Inhibitor of MAO |
| What is fluoxetine (prozac) | Uptake inhibitor |
| What is Mitrazapine? | Receptor blocker |
| What are the four types of typical anti-depressants? | 1) MAO 2) Tricyclic Antidepressants (TCA) 3) SSRI 4) NARI (Selective Noradrenaline Re-uptake Inhibitors) |
| What is the mechanism of MAOI? | Prevents breakdown of monoamine |
| Which monoamine(s) does MAOa prefer? | 5-HT |
| Which monamine(s) does MAOb prefer? | DA and NA |
| At which other receptors can MAOI act and cause side effects? | M1 a1 H1 5-HT2 |
| What is the CHEESE reaction? | If MAO gets too low tyramine enters blood and displaces NA causing a hypertensive crisis |
| Why are reversible MAOI better than irreversible MAOI? | Reversible MAOI can be displaced in places where substrate is high (eg in the gut) but still act where substrate is low (eg in brain for depression). Less likely to cause side effects/cheese reaction. |
| What is the therapeutic index for MAOI like? | Moderate |
| Give an example of a irreversible and a reversible MAOI? | 1) Iproniazid 2) Moclobemide (MAOaI) |
| What is the mechanism for TCAs? | Block re-uptake of 5-HT and/or NA |
| Which adrenoreceptor do TCAs also effect? What side effects does this lead to? | a2-adrenoreceptor - dry mouth, sympathetic effects |
| Which other receptors can TCAs target? What does this effect? | Histamine (drowsiness) Muscarinic actions a1-adrenergic 5-HT2 - weight gain (antagonism) effects sleep wake cycle |
| What is the therapeutic index of TCAs like?What can this lead to? | Low TI - leads to cardiotoxicity - tachycardia, arrythmias and hypotension |
| What is the only way of preventing death once an overdose has been taken? | Prevent TCAs from being absorbed from the gut. |
| Which opioid agonist reacts badly with TCAs? | Tramidol |
| On which MA does clomipramine act? | 5-HT, not and SSRI as it have many sites of action despite being fairly selective |
| On which MA does amitriptyline act? | NA/5-HT |
| Which MA does desipramine act on? | NA |
| Why do SSRIs show less side effects? | Doesn't bind to or act at any other receptors |
| What are the 5 benefits of SSRIs? | 1) No cholinergic side effects 2) No interaction with food 3) Less weight gain 4) Reduced drug interactions 5) Low toxicity in overdose |
| Which 5-HT receptor is responsible for mediating weight gain? | 5-HT2C (anatgonism causes weight gain) |
| What are the 5-HT side effects caused by SSRIs? | 1) Nausea 2) Anorexia 3) Insomnia 4) Sexual dysfunction 5) 5-HT syndrome (similar to ecstasy overdose) |
| Through which 5-HT receptor is nausea mediated? | 5-HT3 |
| Through which 5-HT receptor is Anorexia mediated? | 5-HT2 |
| Through which 5-HT receptors is weight loss mediated? | 5-HT2 |
| Through which 5-HT receptors is sexual dysfunction mediated? | 5-HT2 |
| What are the 5 atypical types of anti-depressants? | 1) SNRI 2) 5-HT2 antagonist + SSRI 3) 5-HT2 antagonist +SNRI/SSRI 4) a2-adrenoreceptor antagonist + 5-HT antagonist 5) Agomelatine |
| What is.... (4) Who ... it used for? What does ... increase? VENLAFAXINE | SNRI Severely depressed, hypersomnic, weight gaining atypical depressives Increases NA |
| TRAZEDONE | SSRI + 5-HT2 antagonist Treats anxiety, improves slow wave sleep, causes sedation and can reduce sexual function Reduces 5-HT2 activity |
| MITRAZAPINE | a2 adrenoreceptor (Gi/o) and 5-HT antagonist Via a2 >> Increases NA and 5-HT by blockade of presynaptic inhibition. 5-HT >> 5-HT3 = Nausea 5-HT2 = sexual dysfunction, reduced anxiety and sleep enhancement |
| What is agomelatine? | Melatonin agonist, 5-HT2 antagonist |
| Explain how mirtrazapine works and why the effects of elevated 5-HT works mainly through 5-HT1 receptors? | a2 - adrenoreceptor antagonist component blocks autoreceptors on NA cells. This leads to increased release of NA which acts on 5-HT system (and NA system) increasing activity. 5-HT2 and 5-HT3 postsynaptic (to 5-HT neuron) are blocked by mitrazapine so 5-HT1 mediates effect of increased 5-HT. |
| How is electroconvulsive therapy performed? | 1) Patient anaesthetised, electrodes inserted, seizure induced |
| What are the changes that come about from ECT? (2) | 1) Increase in MA conc. 2) Changes in MA receptor function a2-adreno. and 5-HT2 downregulated. |
| What are the three theories as to why onset of antidepressants are delayed? | 1) Neurochemical and neuroadaptive 2) Neuroplasticity and neurogenesis 3) Cognitive |
| Describe the two parts of the Neurochemical and neuroadaptive theory (receptor activation) | 1) Activation of somatodendritic autoreceptors (5-HT1a and a-2 adreno) leads to decreased neuronal firing. 2) Activation of pre-synaptic autoreceptors (5-HTb/d, a-2 adreno) leads to decreased neurotransmitter release. |
| Explain the neuroplasticity/neurogenesis theory. | Chronic activation of receptors leads to down regulation - only at that point is there a real increase in the concentration of the MA at the synapse. |
| Explain the cognition theory (2) | 1) Hippocampal neurogenesis - delayed onset as neurons take a while to grow 2) Post synaptic receptor adaptation takes a while |
| With a placebo what percentage of patients see a response in 8 weeks? | 30%-60% |
| How do you treat mild/moderate depression? | Cognitive Therapy |
| How do you treat severe depression? | Drugs |
| What is the first line of drugs? | SSRI |
| What is usually the second line? | MAO-I |
| How longs should you take ADs following remission? | 6-12 months |
| With which type of drugs are you most likely to see 'discontinuation syndrome' | SSRIs |
| In how many patients does discontinuation syndrome occur in? | 1 in 3 |
| What are the symptoms of discontinuation syndrome? (5) | Dizziness, anxiety, mood disturbance, GI disturbance and 'flu-like symptoms' |
| Is discontinuation syndrome more common with paroxetine or fluoxetine? | Paroxetine |
| Over what time scale do concentration of paroxetine and fluoxetine need to be reduced? | 6-8 weeks |
| What is Lithium Carbonate | A mood stabilising drug |
| What is lithium carbonate most effective and controlling but why does the patient need careful monitoring? | Mania - potential toxicity |
| How does Lithium carbonate work? (3) | 1) Effects G-protein signalling - prevents transduction of signalling 2) Interacts with inositol monophosphates and reduces IP3 pathway signalling 3) Inhibits glycogen synthase kinase 3 - GSK3 - reduces phosphorylation of key enzymes |
| What is valproic acid and how can it be used to reduce mania? | 1) Anti-epileptic 2) Weak GABA-T inihbitor - increases inhibitory neurotransmission with some effect on Na+ channels with acute use |
| What is Carbamazepine and how does it help treat mania? | 1) Derived from TCAs 2) Use dependent block of Na+ channels |
| What is olanzapine | Atypical antipsychotic mixed D2 and 5-HT2 antagonist |
| BIPOLAR DISORDER What are the first and second line treatments for.. ACUTE MANIC EPISODES | 1) Lithium/Carbamazepine 2) Valproate |
| PROPHYLAXIS | 1) Lithium/olanzapine 2) Carbamazepine |
| What are combination treatments for bipolar disorder? | antidepressant SSRI + antiepileptic/antipsychotic |
| With prophylactic treatment: What are the relapse percentages after 1) With treatment after 1 year? 2) With treatment after 5 years? 3) Without treatment after 1 year? | 1) 40% 2)90% 3) 80% |
| What else can SSRIs be used to treat? (5) | 1) OCD 2) Panic disorder 3) Social phobia 4) Anxiety disorders 5) Eating disorders (bulimia/binge-eating) |
| What can TCAs (name one specifically) be used to treat other than depression? | 1) Analgesic agent 2) Migraine phrophylaxis drug Amytryptyline (NA/5-HT) |
| What can 5-HT/NA reuptake inhibitors be used for other than depression (eg Duloxetine) | Chronic pain management eg due to chemotherapy or damaged nerve endings |
| What is a drug that could be used to treat depression with a rapid onset? | Ketamin |
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