psych vol 1 Flashcards
delerium overview
acute, transient and reversable state of confusion, usually as a result of other organic processes. highly fluctuant cognition.
2 types- hyperactive and hypoactive
hyper- agitation, delusion, hallucinatio wandering and aggression
hypo- lethargy, slowness, excessive sleeping, inattention
aertiology and risk factors for delerium
pretty much anything can lead to it.
change location
constipation, drugs infection ect.
Ax, Ix, Rx delirium
acute mental test score- assess cognition and can be used to chart progress.
4ats can be used.
DSM5- disturbance in attention, developed over short period of time, congative disturbance, not better explained by anything else, as a consequence of another acute condition
confusion screen (bloods, urinanalysis imaging- think CT hear chext x-ray to ax for infection.)
identify and rx underlying cause.
gentle re-orientation, ensure sensory needs are met (glasses etc)
overview of dementia
irreversable, progressive decline of more than one aspect of higher brain function (conc, mem, language personality, emotion) - no impairment of consiousness
4 types
alzheimers- amyloid plaques + neurfibrilliary tangles
fronto temportal- tau protein defect- neuro tangles
vasc- small vessel disease- stepwise deterioration
lewy body- parkinsons associated.
differential diagnosis of dementia
prion- creutzfeldt-jakob disease
HIV- related cognative decline
normal pressure hydrocephalus
depression
pathology of the different types of dementias
alzheimers- beta amyloid is cleaved by Beta not alpha secretase- resulting in different length proteins to normal- causes toxicity
Fronto temportal- tau proteins are hyperphosphorylated causing them to alter shape and cause tangles
Vasc- diffuse small vessel disease
Lewy- the lewy bodies that are normally in the substansia nigra spread to different areas of the brain causing dementia type symptoms
diagnosis and management of dementia
exculde other diagnosis
use cognative assessmenet tool (10 point cognative screener etc)
collateral history - slow onset of symtoms as opposed to big decline.
Mx: consider anticholinesterase inhibitors, memantadine.
reduce polypharmacy
elderly care psychaitrist
S+S and risk factor for dementia
mem loss, comm issues, reasoning issues, decision making issues, dysphasia, coordination diffs
risk factors:
age, mild cognstive impairment
Learning disability (downs syndrome espesially)
genetics
cvs diseases
PD
lower educational attainment
depression
alchol, TBI
prognosis of dementia different types
alzhimers 8-10 year
vasc 5
lewy- 5-8 years
FTD- 7-13
substance misue disorder alcohol definition.
risk factors for developing AMD
impaired ability to stop or control alcohol use despite adverse social, occupational or health consequences, encompassess alcohol abuse, dependence and addiction.
RF: early age drinking (before 15)
genetics + environment
mental health and history of trauma.
diagnosis of alcohol misuse disorder.
DSM-5 criteria at least 2 is mild, 4 is mod, 6 is severe.
remission is when no criteria other than cravings are present for 3/12 (early) or 12/12 (late)
larger amounts than intended, or longer time
desire to cut down but unnsuccesful attempts
sig time obtaining, using and recovering from alcohol
craving
recurrent use leading to social responsibility faiures
continued use despite persistent/ recurring social/ psych problems cause/worsened by alcohol (above is two seperate ones)
giving up social activities (work, school, recreational) for more alcohol
alcohol use is hazardous situations
tolerance
withdrawal
what makes a drug addictive.
what are the brain changes in alcohol misuse disorder
crosses BBB, acts on pleasure pathway
the shorter the half life the more addicive.
in detox- give long half life drugs that have the same effect.
alcohol acts on GABAa receptors + antagnoises NMDA
inhibits cells from firing
- downreg of gaba, + upreg NDMA (presence of alcohol firing rates return to normal)
in abscence of alcohol- balance shifts to excitation and physical symptoms emerge (seziures agitation etc etc)
peaks / binges of alcohol are more damaging than long term low level use.
what are the types of alcohol users
hazadarous- binging 20 units in one go. men 33-50 years women 15-25 years
harmful- no dependency features and function well, but exceed 50 units a week- they wake up yellow in liver faliure
dependant user- the obvious
overview of delerium tremens and detoxing
severe alcohol withdrawal syndrome - medical emergency 48-96 hrs after last drink last 1-5/7. 5% mortality
overactivity ad glutamate NMDA receptors. more common in the elderly + acutely ill.
S+S- confusion (sundwoning) autonomic hyperactivity (fever, swet tacy, htn) visual/ tacile hallucinations (snakes etc)
Rx: in HDU
IV pabrinex (wernicks prevention) - parenterally always.
benzoz (loraz), halloperidol.
general Detox management: benzoz- chlordiazepoxiade or diazepam (long half lifes)
lorazapam if liver faliure slow 7-10/7 wean.
what is wernicks encephalopathy
a thiamine deficiency caused by inhibition of uptake by alcohol + inefficient use.
need thiamine in the metabolism of glucose
no thiamine- no brain food- bad- leads to haemmorhage- wernickes is a medical emergency.
S+S- ataxia, nystagmus opthalmoplegia. coma, confusion, hypothermia + tension.
Rx: IV pabrinex BD for 5-7/7 continue OD after this untill no further immprovement.
untreated wernickes leads to korsikoffs- which is irreversable and bad.
must give pabrinex before glucose- as if give glucose you will use up the last bit of it and you could induce wernickes.