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People and Illness 18:00 2440051B@student.gla.ac.ukToday… 1. Intro to psychiatry terminology 2. Depression 3. ADHD 4. Alcohol use disorders 5. Dementia 6. DeliriumExams are soon - focus on the important stuffDefinitions in your ILOS 1 Psychosis: an altered relationship with reality Delusion: a false belief held with absolute conviction and out of keeping with the patients culture, social and religious beliefs e.g. partner is cheating on you Hallucination: perception in the absence of a stimulus, perceive objective space with the qualities of normal perceptions e.g. you see a person in an empty roomDefinitions NOT in your ILOS (but Glasgow exams…) Pseudo-hallucination: usually auditory, true externally sited hallucinations, but with insight into their imaginary nature Illusion: misperceptions of external stimuli, most likely when the general level of sensory stimulation is reduced e.g. someone with dementia interpreting a chair in an empty room as a person Illusion vs hallucination? Illusion has an external stimulus, hallucination does notDefinitions in your ILOS 2 Symptom: subjective complaint from an individual Syndrome: conditions characterised by a particular symptom profile Disease: condition with specific aetiology and pathogenesis Disorder: a deviation from the accepted standard of normal (?) e.g. hypertension - a BP of 90/60 might be considered “low” as compared to the accepted “normal” of 120/80Definitions in your ILOS 3 Mood: a persons emotion or feeling - this is patient-reported Affect: how you perceive a patient's mood Depression: a pathological lowering of mood that affects a person's ability to complete activities of daily living, characterised by low mood, anhedonia and/or fatigue Bipolar Disorder: a mood disorder characterised by experiences of hypomania/mania and depression and different timesDefinitions in your ILOS 4 Addiction: characterised by an inability to stop using a drug; failing to meet social obligations with some withdrawal/tolerance Harmful Use: a pattern of alcohol consumption that is causing mental or physical damage ● >35 units women ● >49 units men Dependence Disorder: A cluster of behavioural, cognitive and physiological features that typically include a strong desire to drink alcohol and difficulty controlling its sue.Changes of Brain in Adolescence ● Increase in cortical grey matter from back to front ● Limbic system develops before prefrontal cortex ● Prefrontal cortex: proliferation during early adolescence followed by myelination and synaptic pruning Limbic system -> prefrontal cortex means adolescents priorities reward seeking behaviours > executive planning/risk assessmentSynaptic Pruning Initially, large amounts of proliferation in prefrontal cortex but eventually unused synapses are “pruned” to make the brain more efficient “Use it or Lose it” If you learned French at age 9 and didn’t practice, those synapses are now gone. BUT it means your brain can carry out more complex tasks/focus longerADHD ADHD: A behavioural disorder characterised by hyperactivity, impulsivity and inattention which can lead to functional impairment such as psychological, social, education or occupational difficulties.ADHD Features Features: ● Hyperactivity - restlessness, fidgeting or overactivity ● Inattention - short attention span or being easily distracted ● Impulsivity - acting without forethought, poor awareness of danger, accident proneADHD Risk Factors ● Genetic (later) ● Familial environmental influence e.g. parents with ADHD ● Premature/traumatic birth ● Maternal exposure to heavy metals ● Maternal substance misuseADHD Features Diagnosis ● Inattention + six or more symptoms of hyperactivity/impulsivity present for at least 6 months prior to assessment ● Apparent before age 7 ● Excessive for the child's age and development ● Pervasive i.e. evident in more than one environment e.g. home, school, clubs ● Symptoms worse in afternoonADHD Investigations 1. History - risk factors, developmental history, feeding patterns APPARENT BEFORE AGE 7 2. Conner’s Questionnaire (for parents + teachers) PERVASIVE 3. Additional Tests a. Hearing + vision b. Height + weight (psychostimulants risk anorexia) c. Blood pressure (CV risk and psychostimulants)ADHD Co-morbidities ● Tourette’s Syndrome ● Anxiety ● Sleep disorders ● Behavioural difficulties ● Learning difficultiesADHD Pharmacological Management Psychoeducation ± 1. Psychostimulant e.g. methylphenidate, dexamphetamine 2. Atomoxetine 3. Adrenergics e.g. clonidine, guanficine Methylphenidate i.e. ritalin ADHD Mechanism: inhibits dopamine reuptake transporter. Maintains high dopamine in Pharmacological Management synaptic cleft Dexamphetamine Mechanism: 1. Inhibits dopamine reuptake transporter 2. Targets VMAT2, releasing dopamine into synaptic cleft 3. Inhibits MAO at higher concentrationsPsychostimulants SIDE EFFECT METHOD TO OVERCOME 1. Faltering Growth 1. Drug Holidays (increase calories at weekend + don’t take medication) 2. CV/HR irregularities 2. Monitoring of CV risk factor 3. Anorexia 3. Eat large breakfast before taking medication Mechanism: Noradrenaline reuptake Atomoxetine inhibitor. Increasing noradrenaline in the synaptic cleft of pre-frontal cortex. Side effects: ● Nausea/vomiting ● Excessive tiredness ● Headaches ● Insomnia ● Hepatic impairment (monitor LFTs) Mechanism: alpha-2 adrenergic Adrenergics e.g. receptor agonist clonidine, Side Effects guanficine ● Dizziness ● Sedation ● Hypotension When psychostimulants are not tolerated anymore.Depression ● Biological symptoms: ○ Diurnal variation ○ Insomnia, nightmares, vivid dreams ● Low mood ○ Loss of libido ● +/- anhedonia ○ Loss of appetite/weight loss ● +/-fatigue ○ Constipation, amenorrhoea ● Everyday >2 weeks ○ Cognitive symptoms: ○ Reduced concentration ○ Negative thoughts ○ Reduced self esteem, confidence ○ Guilt ○ Hopelessness ○ SuicidalityWhy does it We don’t know. happen? Monoamine Hypothesis “Depression results from a deficiency of one or more of the three monoamines e.g. dopamine, norepinephrine, serotonin” Important in anti-depressants pharmacology. Management of Depression Biological 1. Cessation of depressants e.g. alcohol 2. Regular exercise 3. Antidepressants 4. Adjunctive drugs e.g. lithium (if no response to two antidepressants) 5. Electroconvulsive therapy (ECT; if depression life threatening or non-responsive) Psychological 1. Eduction and regular follow up 2. CBT Social 1. Financial: benefits eligibility, debt counselling 2. Employment: change of employment or acquiring a job 3. Housing: adequate, secure tenancy 4. Young children: child-care support Management of Depression MOST COMMONLY… CBT + antidepressant NICE “Do not routinely offer antidepressants as a first-line treatment, unless that is the person’s preference.” Anti-Depressants 1. Selective Serotonin Reuptake Inhibitors (SSRIs) e.g. citalopram, sertraline 2. Serotonin/Noradrenaline Reuptake Inhibitors (SNRIs) e.g. duloxetine 3. Monoamine Oxidase Inhibitors (MAOIs) e.g. selegiline 4. Tricyclic Acid Antidepressants (TCAs) e.g. amitriptyline SSRIs Mechanism: inhibits seorotoning reuptake transporters in presynaptic neurones.Increases serotonin in synaptic cleft. Side Effects (SSRIS) Serotonin Syndrome SIADH Rocking (Movement Disorders) Insomnia Sexual dysfunction MOAIs Mechanism: Inhibits monoamine oxidase. Decreases breakdown of epineprine, norepinephrine, serotonin and dopamine, increasing levels of these monoamines in synaptic cleft. Don’t eat cheese. DONT LEARN: MAO enzymes in gut and breakdown tyramine. Inhibiting enzymes leads to accumulation of tyramine (found in fermented foods). Tyramine accumulates and is taken up at synapses -> catecholamine crisis. SNRIs Mechanism: inhibit serotonin and noradrenaline reuptake in the synaptic cleft. Increases the levels of these monoamines. Side effects (similar to SSRIs) TCAs Mechanism: inhibition of serotonin and noradrenalin reuptake in the synaptic cleft. Increases serotonin and noradrenaline. Also… target histamine, muscarinic receptors leading to a widespread effect - LOTS OF SIDE EFFECTS therefore rarely used anymore. Side effects (similar to SSRIs)Alcohol Physiology Three mechanisms: 1. ADH 2. MEOS 3. Catalase Don’t complicate it.1. ADH Disulfuram target ● Most ethanol takes this pathway ● Formation of acetate is rate limiting step ● Excess alcohol -> Acccumulation of acetaldehyde Acetaldehyde causes hangover type symptoms2. MEOS ● Kicks in during periods of EXCESS drinking ● Basically, a different pathway (different enzymes) with the same outcome3. Catalase ● <2% of ethanol goes through this pathway ● ?more of a role in the brain where there is less ADH ● AGAIN… just a different enzyme pathway of the same equationAlcohol ICD-10 Classification for Alcohol Dependence Syndrome Features of dependency must be evident over 12 months but diagnosis can be made with continuous alcohol use for 1 month. 3+ symptoms: • Strong internal drive to use alcohol ○ Loss of control ○ Increasing priority given over other activities ○ Persistence despite knowledge of consequences • Tolerance • Withdrawal symptoms following cessation • Repeated use to alleviate withdrawal symptoms Classified into mild, moderate and severe depending on the number of criteria met.Alcohol withdrawal A variable presentation. Stages 1. (6-12 hours) Minor withdrawal symptoms e.g. tremor, anxiety, headache, NV, sweating 2. (12-24 hours) Alcoholic hallucinosis 3. (24-48 hours) Alcohol withdrawal seizures - GTC 4. (48-72 hours) Delirium Tremens Treatment aim? STOP DELIRIUM TREMENSAlcohol Withdrawal Diagnosis of Alcohol Withdrawal Any three of the following: • Tremor of outstretched hands, tongue or eyelids • Sweating • Nausea, retching or vomiting • Tachycardia or hypertension • Anxiety • Psychomotor agitation • Headache • Insomnia • Malaise or weakness • Transient visual, tactile or auditory hallucinations or illusions • Grand mal convulsionsManagement Alcohol Withdrawal Management of Delirium Tremens 1. Admit to medical unit 2. IV fluids 3. IV thiamine to combat Wernicke-Korsakoff Syndrome 4. Prophylactic phenytoin/carbamazepine if there is a hx of alcohol withdrawal seizures Specific Drug Treatment: DiazepamThiamine + Wernicke’s Encephalopathy Thiamine Deficiency causes Wernicke’s Encephalopathy. If left untreated can lead to Korsakoff Syndrome. DON’T LEARN: Thiamine (B1) involved in cerebral metabolism. Deficiency leads Classic Triad of Wernicke’s Encephalopathy: 1. Eyes: nystagmous, bilateral lateral rectus palsies, to neuronal cell death in mammilary conjugate gaze palsies bodies and thalamus. 2. Ataxia: broad based gait, cerebellar signs 3. Cognitive change: acute stupor + coma, later causes amnestic syndrome with confabulation WKS - more chronic problem you’re trying to prevent DT - deal with it now, medical emergencyLong term medical management of harmful drinking ● Naltrexone: opioid antagonist, blocks pleasurable effects of alcohol, making it easier to stop ● Acamprosate: increases GABA and supresses serotonin ● Disulfiram: reacts with alcohol to cause aldehyde and ● histmaine release causing an unpleasant intoxication ORAL THIAMINE: should always be prescribed in heavy drinkers to prevent Wernicke's Encephalopathy NOTE: IV thiamine in acute settingAlcohol Related Liver Disease See Gastroenterology teachingDementia Dementia: progressive global decline in cognitive function, without impairment of consciousness Four types to know: 1. Alzheimer’s Disease 2. Vascular Dementia 3. Dementia with Lewy Bodies 4. Frontotemporal DementiaAlzheimer’s Disease ● Risk factors: repeated head injury, family history, hypothyroidism ● Neurofibrillary tangles (Tau protein) and amyloid plaques in hippocampus and cerebral cortex (frontal and temporal) ● Presentation ○ Short term memory loss (autobiographical memory often preserved) ○ Dysphasia ○ Dyspraxia ○ Behavioural changes e.g. wandering ○ Psychotic symptoms ○ Apathy ● Clinical features: Progressive decline ● Management (improvement of symptoms) ○ Cholinesterase inhibitions e.g. rivastigmine, donepazil (these are shown to SLOW PROGRESSION) ○ Memantine (NMDA antagonist)Vascular Dementia ● Multiple small infarcts or small vessel disease ● Associated with cardiovascular risk factors ● After a stroke ● Presentation ○ Gait disturbance ○ Personality change ○ Labile mood ○ Urinary symptoms ○ Insight preserved ● Clinical features: stepwise progression, cardiovascular risk factors ● Management: modify cerebrovascular risk factorsDementia with Lewy Bodies ● Lewy bodies in cerebral cortex made of alpha synuclein ● Presentation ○ Fluctuating dementia ○ Delirium ○ Parkinsonism ○ Visual Hallucination ○ Sleep disorders ● Clinical features: progressive disease ● Management: rivastigmine might improve symptomsFrontotemporal Dementia ● Atrophy of frontotemporal lobes, without histology of Alzheimer's Disease ● Presentation - DISHINHIBITION ○ Stereotyped behaviours ○ Personality change ○ Loss of insight ○ Expressive dysphasia ○ Preserved memory ○ Primitive reflexes ● Clinical features: ○ Slow progression ○ Family history ○ Women>men with early onset (<70)Dementia vs DeliriumHow many grams of ethanol are contained in 1 unit? A. 5g B. 8g C. 12g D. 10g E. 2g How many grams of ethanol are contained in 1 unit? A. 5g B. 8g C. 12g D. 10g E. 2g Annoying thing to learn but was in my lecture notes. You’ll either know it or not.Which of the following is an NMDA receptor antagonist? A. Atomoxetine B. Rivastigmine C. Memantine D. Donepazil E. MethylphenidateWhich of the following is an NMDA receptor antagonist? A. Atomoxetine B. Rivastigmine C. Memantine D. Donepazil E. MethylphenidateWhich of the following is used in the assessment of ADHD? A. Addenbrooke’s Questionnaire B. MoCA C. AUDIT D. Conner’s Questionnaire E. CAGE questionnaireWhich of the following is used in the assessment of ADHD? A. Addenbrooke’s Questionnaire cognition B. MoCA cognition C. AUDIT Alcohol Use Disorders Identification Test D. Conner’s Questionnaire E. CAGE questionnaire Screening questions for alcohol misuseWhich is not a feature of depression? A. Low mood B. Anhedonia C. Pervasive D. Everyday for >2 weeks E. FatigueWhich is not a feature of depression? A. Low mood B. Anhedonia C. Pervasive D. Everyday for >2 weeks E. Fatigue “Pervasive” is part of the diagnostic workup of ADHD, not dementia.A 10 year old boy has recently been diagnosed with ADHD. His mother is concerned is innattention is affecting his education and is interest in starting medication. Which of the following medications risks growth faltering in this young boy? A. Acamprosate B. Clonidine C. Guanficine D. Atomoxetine E. MethylphenidateA 10 year old boy has recently been diagnosed with ADHD. His mother is concerned is innattention is affecting his education and is interest in starting medication. Which of the following medications risks growth faltering in this young boy? A. Acamprosate B. Clonidine C. Guanficine D. Atomoxetine E. Methylphenidate Stimulants e.g. ritalin, dexamphetamine cause hepatitis suppression. Growth can be maintained through drug holidays and having a calorie dense breakfast before taking medication for the day.What is the weekly limit for alcohol intake for adults in the UK? A. 14 units for women, 22 units for men B. 21 units for women, 21 units for men C. 14 units for women, 14 units for men D. 21 units for women, 14 units for men E. 18 units for women, 18 units for menWhat is the weekly limit for alcohol intake for adults in the UK? A. 14 units for women, 22 units for men B. 21 units for women, 21 units for men C. 14 units for women, 14 units for men D. 21 units for women, 14 units for men E. 18 units for women, 18 units for menEleanor wakes up after a night out during her first week of university. She has a sore head and feels nauseous. What compound is responsible? A. Acetaldehyde dehydrogenase B. NADH C. Acetaldehyde D. Acetyl CoA E. CatalaseEleanor wakes up after a night out during her first week of university. She has a sore head and feels nauseous. What compound is responsible? A. Acetaldehyde dehydrogenase B. NADH C. Acetaldehyde D. Acetyl CoA E. Catalase Remember: the conversion of acetaldehyde to acetate is the rate limiting step. When alcohol is consumed in excess, acetate cannot be produced at a high enough rate. Acetalyde therefore accumulates. Questions that could be easy MEQs but you might not have thought to revise Stages of change as a treatment for alcohol use disorders Label it. Define each stage. From “Alcohol Use Disorders” Lecture 2021Questions that could be easy MEQs but you might not have thought to revise Kubler Ross Model (Stages of Grief) 1. Denial 2. Anger 3. Bagaining 4. Depression 5. Acceptance Questions that could be easy MEQs but you might not have thought to revise Know a couple of these steps. “Give 3 examples of the 12 principles of AA as a therapy for Alcohol Dependency.” From “Alcohol Use Disorders” Lecture 2021 Questions that could be easy MEQs but you might not have thought to revise Know a couple of these steps. “Give 3 examples of the 12 principles of AA as a therapy for Alcohol Dependency.” From “Alcohol Use Disorders” Lecture 2021Questions that could be easy MEQs but you might not have thought to revise Genes that put someone at higher risk of ADHD ● DRD4 ● SLC6A3/DAT1 ● DRD5 ● 5HTT ● HTR1B Feedback Form Please include my name somewhere “Emma Ball” 2d&organisation=glasgow-neuro-f259ab17-2be5-4c52-a2ab-ccee66ee66c120a8c7707e