Mind Flashcards

Question

What is PTSD?

Answer 1

- frightening and overwhelming flashbacks - especially if suffered abuse/neglect as a child or abuse or violence as an adult - other symptoms involve avoidance, numbing and being on guard

Answer 2

this is an ongoing state of excessive anxiety lacking any clear reason or focus. it affects 2% of the population. difficult to control. Symptoms include: - restless/irritable/muscle tension/'keyed up' a lot of the time - tired easily - difficulty concentrating - mind goes blank quite often - insomnia Risk factors: - low SES - childhood maltreatment and conduct problems

Answer 3

- 5-HT - GABA - CRF - CCK

Answer 4

- mediates postsynaptic inhibitory transmission - receptor subtypes: GABAa GABAb GABAc - activation of GABAa receptors increases chloride conductance - GABA is a NT present in almost all brain areas. Mainly interneurons, some longer pathways Ligands acting at allosteric sites on GABA receptor complex: - barbiturates - benzodiazepines - neurosteroids - alcohol these act by modulating the effects of GABA. Alcohol and barbiturates also have many other sites of action.

Answer 5

- relationship between anxiety and 5-HT not simple - many receptor subtypes located presynaptically - some drugs act on reuptake mechanisms or are parietal agonists - prolonged effects of drugs may be different from initial effects e.g. SSRIs desensitise 5-HT auto receptors, resulting in increased release of 5-HT

Answer 6

- Serotonin - there are 5-HT cell bodies in the raphe nuclei in the pons and medulla. The rostral nuclei project to the cerebral cortex, limbic system and the hippocampus. The caudal nuclei project to the`medulla and the spinal cord. There are different receptor subtypes (1-7) with many subdivisions. The 5-HT receptor activation can be excitatory or inhibitory

Answer 7

- sleep/wakefulness - mood - nociception - temperature regulation - feeding

Answer 8

- 5-HT1A receptors control raphe cell firing | - 5-HT1B/D receptors control 5-HT release at terminals

Answer 9

- released from the hypothalamus - controls release of ACTH - NT in CNS, especially in amygdala

Answer 10

- hippocampus - basal ganglia - amygdala - bed nucleus and stria terminals - dorsal periaqueductal grey

Answer 11

- benzodiazepines - SSRIs - 5-HT1A receptor agonists - 5HT2/3 receptor antagonists - beta blockers - GABApentin (neurontin) - others e.g. MDMA, psilocybin

Answer 12

- anxiolytic - anticonvulsant - centrally acting muscle relaxants - sedative - amnesic tolerance develops have a higher therapeutic index than barbiturates

Answer 13

``` anxiety insomnia alcohol withdrawal status epilepticus spasticity premedication prior to general anaesthesia ```

Answer 14

- drowsiness - ataxia - increased appetite - decreased stage 4 REM sleep - occasional hostility - can cause confusion in the elderly

Answer 15

They are very addictive and dependence develops. Withdrawal syndrome is seen on cessation from long-term intake. Compulsive use can develop after a long duration of administration. They are recommended for short term prescription only because of these reasons, not more than 6 weeks.

Answer 16

benzodiazepine antagonists flumazenil binds to benzodiazepine receptors but doesn't alter the actions of GABA has a short half life

Answer 17

- block B-adrenergic receptor - decrease heart rate and blood pressure - useful in decreasing autonomic symptoms of anxiety - eg propranolol

Answer 18

- experimentally CRF found to be involved in behaviour associated with anxiety - CSF concentrations in CRF raised during anxiety, post traumatic stress and alcohol withdrawal - activation of CRF receptors found to cause anxiety-related behaviour CRF antagonists - experimentally, antagonists at CRF receptors appear to be anxiolytic - most available at present do not enter the brain well after systemic administration - synthesis of new compounds may provide an important breakthrough

Answer 19

- hormone released from the intestine - signals satiety at the end of a meal - now known to be a NT in the CNS - most abundant peptide transmitter in the CNS - co-released with other transmitters e.g. monoamines Infusion of CCK causes feelings of anxiety in a proportion of normal volunteers. CCK precipitates panic attacks in susceptible people. There is some evidence that these effects are due to peripheral actions of CCK. CCK antagonists may be useful in anxiety, there are ongoing pre-clinical studies.

Answer 20

- out of proportion with the stressful situation - persistent when stressful stimuli has gone - appears for no apparent reason when there are no stressors

Answer 21

- HPA axis - cortisol - when hyperactive affects most MH conditions - increase blood sugar, suppress immune system direct sympathetic (parasympathetic) system - pro-inflammatory - reduced neurotrophic (BDNF): small hippocampus, reduced near-genesis

Answer 22

- physical examination - TFTs - glucose - FBC - U&Es - LFTs - ESR - B12/Folate - Ca

Answer 23

- excessive unreasonable fear, by prince or anticipation of a specific object or situation - exposure provokes anxiety response, with to without panic attacks - avoidance - inside present - interferes with life! - exclude other mental disorder, medical conditions, primary drugs and alcohol misuse

Answer 24

- social phobia - fear of scrutiny or criticism, by others - avoidance of social situations - may present with blushing, hand tremor, nausea, urgency of micturition - low self-esteem - sometimes convinced non-psychological - many progress to panic attacks

Answer 25

- coffee - tobacco - OTC

Answer 26

- promethazine - Z-drugs (ZZoplicone) - benzodiazepines - melatonin (insomnia)] - propranolol - pregablin

Answer 27

- challenge reactions to anxiety-provoking safety seeking behaviours - proof that dysfunctional thought processes are unrealistic

Answer 28

- CBT - systemic desensitisation - sustained exposure

Answer 29

- neurofibrillary tangles within neurone - extra-cellular senile plaques - neuronal depletion in cerebral cortex and hippocampus - shrunken brain - swollen ventricles - thickened and deep sulci - grey matter ribbon is thinner

Answer 30

- early onset, rare - most common gene on Chr21 and is APP - can have a little bit cut off it at 40aa which can form Abeta and then form the plaques - prenesilins - swedish families - mirror of downs syndrome?: extra version of Chr21 and an extra APP

Answer 31

mutations associated with familial, early onset AD

Answer 32

- late onset (LOAD) - much more common - >65 years - >5% over 65, >40% over 80 - global phenomenon, not to do with where you live etc - just about living long enough for it to surface - nothing to do with genetics - ApoE gene is a risk factor but not DETERMINING factor; these are plasma cholesterol transport proteins and are three different alleles of this (E2, E3, E4) - 1 is increase, 2 even more, 3 even more

Answer 33

- as death form other diseases go down, deaths with Ad increase - this may be because people are living longer so more are getting it - drain on budgets and time - as we get older pathology accumulates in our brain, eventually taking us over the threshold of being able to be diagnosed with dementia

Answer 34

a test that goes on for a while patient given a list of words to remember and they are tested after 2 minutes hard to make a global test - difficult to fairly translate between languages

Answer 35

- APP, Abeta, secretases | - tau, GSK3b, etc

Answer 36

extracellular deposito of Abeta fibrils

Answer 37

amyloid precursor protein APP

Answer 38

Abeta is cleaved form APP by secretase enzymes; alpha, beta and gamma. They have an intracellular C-terminus and an N-terminus sticking out. In healthy patients alpha secretase cleaves APP forming fragments and no harm is one. The problem is if it gets excessively chopped by beta secretase and then gamma so we end up with tiny fragments which form plaques from the Abeta. these can be 40 or 42 aa in length

Answer 39

- used increasingly with Abeta in diagnostics - smal molecules have been developed which can cross the BBB and bin selectively to amyloid plaques (can see loads in AD patients) - this is a way of visualising amyloid load in live patients - if we had a way of getting rid of them this would be very useful, but at the minute we don't

Answer 40

- tau is part of the neuronal cytoskeleton - it is essential as a type of scaffolding for neurone and we all have it - it is bad if the tau is hyperphosphorylated - if there is too much phosphorylation the filamentous tau protein crinkles up into a tangle - there are filaments inside neurone and the cerebral cortex

Answer 41

- tangled tau clumps into little balls | - healthy tau looks like neat parallel railway tracks

Answer 42

- filaments ar ein the neve cell processes - it wants to keep it in tact and going to where it should with connections - if the filaments become defective and tangles, the axon with become pathological and may die - the neurone might live but the circuit won't work - some phosphorylation is normal but too much is not

Answer 43

- the amyloid is not only found in plaques, can also be found around blood vessels - Abeta40 is clustered around the vessel - Abeta-42 forms a messy corona around that - they are very distinct - in someone who has it, they tend to have both 40 and 42. - vascular is also pathological and damaging but not as bad as in plaques

Answer 44

CHOLINESTERASE INHIBITORS - donezepil - rivastigmine - galantine - memantamine (NMDA receptor antagonist) - immunotherapy

Answer 45

- the cholinergic system is involved in memory - Ach major transmitter in circuit son memory - many people with MCI will see an improvement with cholinesterase inhibitors, but not all

Answer 46

- we know that Abeta is the problem and it is a protein - if we can make an antibody to it then it'll find the Abeta in the plaques and prevent them forming and could event rid of them - did a trial but some people died so it was terminated (Elan vaccine trial) - as the surviving patients died over the years their brains were examined and although some of them had completely got rid of their plaques, their MMSE scores were still at 0 (the lowest! highest/normal is 31) - this shows that one the damage is done it is too late to sort it - closing the stable door but the horse has already left. it is too late when the AD has become symptomatic.

Mind Flashcards

(70 cards)