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Year2-Common MentalDisorders &Neurovascular ConditionsCommon Mental Disorders ILOs • Describe and apply the basic clinical features of depressive disorder including the diagnostic criteria. • List causes and risks of developing a major depressive disorder, including both physiological and psychological (psychodynamic model) elements. • Describe the basic clinical features of Generalised Anxiety disorder (GAD) including the diagnostic criteria. • List causes and risks of developing GAD, including both physiological and psychological (psychodynamic model) elements. • Identify the importance of non-pharmacological treatments for depression and GAD, including psychological therapies, green/social prescribing, and physical activities. • Summarise basic mechanisms of action, side effects, contraindications, and withdrawal effects of antidepressant drugs, including SSRIs, SNRIs, tricyclics and MAOIs. • Summarise the basic mechanisms of action, side effects and withdrawal effects of drug treatments of GAD. • Discuss the placebo effect and its role in both clinical trials and practice. • Discuss the relationship between poverty, social inequality and mental health. • Recognise the impact that global changes may have on local health and wellbeing. Depressive Disorder • Depression- state of low mood & aversion to activitythat can have anegative effect on person’s thoughts, behaviours, feelings,world view & physical wellbeing • Feelings of sadness, tearfulness, emptiness or hopelessness • Angry outbursts, irritability orfrustration, even oversmall matters • Loss of interest or pleasurein most orall normal activities, such as sex, hobbies orsports • Sleep disturbances, including insomnia or sleeping too much • Tiredness and lack of energy, so even small tasks takeextra effort • Reduced appetite and weight loss orincreased cravings forfood and weight gain • Anxiety, agitation or restlessness • Slowed thinking, speaking or body movements • Feelings of worthlessness orguilt, fixating on past failures or self-blame • Trouble thinking, concentrating, making decisions and remembering things • Frequent orrecurrent thoughts of death, suicidal thoughts, suicide attempts or suicide • Unexplained physical problems, such as back pain or headaches • Increase in MAOenzyme • Suppresses immune systemMoving/speaking slowly- psycho-motorretardation Movingaround alotmore- psychomotor agitation 9. Suicidalideation Causes& Risksof MajorDepressive Disorder Development • Riskincreasedinparticularmedical conditions: Modern view: Environmentalstress • Hypothyroidism Internal stress • Addison’sdisease Stresshormones- reduces glucocorticoid hormones, reduces brainGFs, reduces monoamines&increasesproinflammatorycytokines • MS HPA axis dysregulation • Influenza Impairmentofkeybrainstructures • Post-stroke Reducedmonoamines Reducednerve growth factors • Menopause Immune or inflammatory activation • Alcohol/druguse Dorsal neuralsystem is underactive- psychomotor agitation, apathy& deficits in attention & working memory • Sideeffect ofsomedrugs: Ventralneuralsystem is overactive- depressed mood Amygdalais impairedwhereby itprefers to process negative stimulirather thanpositive; • Corticosteroids usuallythere is bilateralenlargementindepression • Beta blockers Hippocampus maybe small tobeginwith,but itshrinksasdepressiondevelops; thisis • Statins due toreducesBDNFwhichreduces neurogenesis(memory isimpaired) Anabnormal hippocampus & amygdala maintainabnormal levels ofglucocorticoids, BDNF • Oral contraceptives(progestogens) & cytokines • Isotretinoin • Inteferon alpha • Geneticelement aswell Chronic stress causesexcessive release of CRH bythe hypothalamus CRHcauses pituitarytorelease excess ACTH ACTHcauses adrenalcortex torelease excess glucocorticoids e.g. cortisol Increasedglucocorticoids dysregulates amygdalafunction Increasedadrenalactivity causesincreasessympathetictone byrelease ofADR which causesrelease ofpro-inflammatory cytokinesintothe bloodstream Thepro inflammatorycytokinin& glucocorticoids cause increases MAO whichdegrades more5HT,Nadr & dopamine• Catecholamines- • Dopamine • Nadr- relevant to depression;binds to alpha2 receptor • Adr • Indoleamines: • Serotonin- relevant to depression (90% isfound in the enteric chromaffin cells in theGIT • Less severe depression- PHQ-9 score of <16 • Guided self-help • Group CBT • Group behaviouralactivation (BA) • Individual CBT • Individual BA • Group exercise • Group mindfulness and meditation • Interpersonal psychotherapy (IPT) • SSRIs • Counselling • Short-term psychodynamic psychotherapy (STPP) • Moresevere depression- a PHQ-9 score of ≥16 • CBT + antidepressant • Individual CBT Treatment-Non- • Individual BA • Antidepressant medication • SSRIor Pharmacological • SNRI or • Another antidepressant ifindicated based on previous clinical and treatment history • Individual problem-solving &Drug • Counselling • STPP • IPT • Guided self-help • Group exerciseMAOIs-Monoamine oxidaseinhibitors • Monoamineoxidasebreaksdown 5HT,Nadr&dopamine in concentrationof these NTsinthesynapse (whichtendtobe lowindepression) • Used muchlessfrequently thantricyclic antidepressantsor SSRIsdue tothe dietaryanddruginteractions • Examples: • Tranylcypromine • Phenelzine • Isocarboxazid • Moclobemide • Cdiet,the levelscangetvery highquicklywhichleadstoHTN astyraminecausesreleaseofNadrwhichincreasesBP& HR • GAD-generalised anxietydisorder • Diagnosis: • Persistentfearorworry • &≥3 ofthe following: • Poorconcentration • Restlessness • Fatigue • Muscle tension • Initial insomnia GAD • Symptoms for>6 months • Diagnosis exclusion: • Alcoholorstreetdrug misuse • Hyperthyroidism • Phaeochromoctyoma-benigntumourof adrenal medulla whichcauses persistentHTN &anxietydueto greatreleaseof catecholaminesintothe circulation • Psychological symptoms: • Constantworries, intrusive thoughts • Feelingsofapprehension& dread • Poor concentration • Ifsevere- depersonalisation(bodyfeels as if itis melting away) & derealisation (surroundings becomedream like & faraway) • Physical symptoms: • Tremor • Sweatiness • Butterflies GAD • Drymouth • Palpitations • Musculartension Symptoms • Tensionheadache- due tomuscle tensionin frontalis muscles bilateral& tender onpalpation • Hyperventilation- difficulty taking a breath,atypicalchestpain • Atypical chest pain- sharp, stabbing pain oftenleftsided &does not radiate(needto differentiate thisfrom ACSpain) • Behavioural symptoms: • Putting things offbecause ofanxiety • Avoiding particularsituations • Self-medication- drugs & alcoholtorelieve anxiety ;acts ofGABAa receptors (so dobenzodiazepines) • GenesxEnvironment • FDR-2.5xriskincreased • Genes: • GWAS • transportergene e.g. serotonin Causes&Risks ofGAD • Overactive amygdala-partof temporallobe whichprocessesemotionaldata Development • Childhoodtrauma-parental rejectionor over-control • Major lifestress-threatevents such as physicalillness orunemployment • Threatlife events-anxiety • Loss lifeevents-depression • 1.Recognition &Diagnosis of GAD • 2.Offer treatmentin primary care • Psychological therapy e.g. CBT • Pharmacological therapysuchas SSRIs or benzodiazepines (≤2 weeks) • Selfhelp • Online self education Approachto • Shareddecisionmaking • 3.Nonresponsive GAD • Review&offeralternativetreatments • 4.Review& offerreferralto secondary care • person stillhas symptoms,thenreferto the specialist mentalhealthservices • 5.Care inspecialistmental health services • ThoroughassessmentTreatment-Non- Pharmacological&Drug • Psychological Treatment • Medication • Ifnotsevere-lifestyle changes are advised before drugs/psychological treatment • Exercise • Work/life balance • Avoidexcess caffeine &otherstimulant drugs • Avoidexcess alcohol • Mosteffective:psychological+ meds in comparisontoalonePsychologicalTherapy • Counselling • CBT-structured approach,mostwidelyused • Mindfulness-armof CBT • CBT: • Identifies unhelpful patternsofthinking e.g. catastrophising & howthesecausefeelingsofanxiety • Replace unhelpful beliefs withmore elastic &balancedones • Focusesoncurrent problemsratherthanpast • ‘e.g.crowdedplaces;graded exposureecificenvironmental trigger • 12-15 1-hoursessions over4 months • 60% respondtothisDrugT reatment • 1 line- SSRIs(antidepressant) • Tricyclic antidepressants- but have moresideeffects • Mirtazapine, duloxetine,venlafaxine,imipramine(antidepressants) • Pregabalin (lessunderstood) • Benzodiazepinese.g. diazepam/valium • However,very addictive &developpharmacologicaltolerance& withdrawalso itbecomes extremely difficult to get them off >6weeks of usage,thus limited to 2 weeks only SSRIs • Selectiveserotonin reuptakeinhibitor • Inanxiety, thereisnot enough5HT in thesynapse therefore blocking the reuptakemeans more 5HT is in symptomspse therefore more 5HT canbindto thepost-synaptic terminaltohelpalleviate anxiety • Types: • Escitalopram • Paroxetine • Sertraline • Fewer side effects&safe inoverdose incomparisonto older drugssuchastricyclic antidepressants • Whattotell patients: • Cantake 1-2 weekstowork • Not addictive • 70% effective • Ifeffective, continue for ≥6 months; ifyoustopbefore relapse rates are higher • Side effects: • GI disturbance(most common, usually transient) • Sexualdysfunction • Dizziness • Drymouth • Loss ofappetite • Sweating • Feeling agitated • Insomnia • Mildwithdrawaleffectsoccasionally sotaper downdoserather thanabruptlytaking them offAntidepressants • Mirtazapine-blocks pre-synaptic alpha-2 autoreceptors • Duloxetine-SNRI;inhibits Nadr reuptake • Venlafaxine-SNRI;inhibits Nadr reuptake • Imipramine-tricyclic antidepressantPregabalin • Anticonvulsant • Used inepilepsy &neuropathicpain • StructurallysimilartoGABA • Bindsto alpha 2delta subunit of Ca2+ channels • Reducesrelease of neurotransmitterssuchas glutamate,Nadr&substance P • Sideeffects: • Abdominal distension • Appetite abnormal • Impairedconcentration • Confusion • Constipation • Dry mouth • Manymore…(checkBNF)Benzodiazepines • GABAareceptor- transmembrane ligand-gatedionchannelreceptor • 5 subunits arounda central Cl- • Alpha, beta, gamma, delta, p • GABA binds tothe binding pocket betweenthe alpha & betasubunits whichcauses Cl- toflow intothe neuron • This reduces the chances ofanactionpotentialfrom being firedas Cl- causeshyperpolarisation • Benzodiazepines binds between alpha & gamma subunit which potentiates the action of GABA • Reduces chances ofAP firing by increased Cl- influx& thus hyperpolarisesthe neuron • Side effects: • Alertness decreased • Ataxia • Confusion • Dizziness • Drowsiness • Headache • Manymore…(check BNF) • Placebo- • Anytherapy which has no specific activityfor the condition being treated • Contains no activeingredient • Has no direct physiological effect • Dummy orsham treatment • Placeboeffect- • Anyfavourable psychological orpsychophysiological effect produced byplacebos • Change in symptom(s) not directlyattributableto drugs ortreatment underinvestigation because it occurs in placebo treated controls • In clinical trials,does thetreatment causean improvement over& abovethat due to a placebo alone? Considerethics • Differencebetween treatment & placebo groups • Placebowashout- • Placebo administered fora specificperiod beforecommencing the study • Ifpossiblefor pps to be taken offtheirexistingtreatments before commencing the study,washout enables theireffects Placebo to be removed beforebeginning the investigation • Washout enables identification of high degreeplacebo responders & maywish to exclude them from the study Effect • Nocebo effect- • Adverse psychological orpsychophysiological effects produced byplacebos • Howthe placeboeffectworks- • Expectancies: • Idea that wecan makeourselves better through our beliefs & expectations of the treatment we are going to receive • Morelikelyforgood to happen if you believeit will do you good,than ifyou believe it will do you bad • Outcome expectancies- beliefs that treatments will havepositiveeffects on health • Patient relatedself-efficacy expectancies- • Beliefs that one takes actions necessary for successful disease management • Believe that meds or exercisewill do you good, then disease is managed betterthan if you didn’t believe this • Conditioning- associating experiences of previous health care with positive outcomes • Reduced anxiety- interactions with HCPs when receiving placebo can lessen anxiety; can have positive impression on things like pain • Psychophysiological mechanisms- e.g.releaseofendorphins & endogenous opioids can increasedopamine production (PD) Poverty ,SocialInequality &MentalHealth • People with severe & enduring mentalillhealthareatgreater risk of poorer physicalhealth & reduced life expectancy compared to the generalpopulation • Poverty & socialinequalityhave direct & indirect effects on social, mental& physicalwellbeing of an individual • Health inequalities- avoidable & unfair differences in health status & determinants between groups of people due to factors such as: • Their demographic, socioeconomicstatus & where they live& work • Diseaseprevalence, access to, experience & quality of care & support • Disadvantage can startbefore a child is born & impact future generations • Mental illnessis closely associated with many forms of inequalities • Health inequalities are generally caused by the inequalities in society e.g. environment we live & work in, poor working conditions etc. • Children facing multiple risks havean increased risk of childhood mentalillheath • Compared to the general population, peoplewith mentalillness also havephysicalconditions • Living inmore deprived areasaremorelikely to have physicalhealth conditions • Protective factors to buffer the impact of adverseconditions on health include socialsupport & employment conditions • People living with mental illness are more likelyto: • Havehigher rates of poverty,homelessness, unemployment & social isolation • Live inless safe neighbourhoods,have less access to health foods & health-related activities • People with mental health facemany challenges in gaining & maintaining employment including stigma • Health Behaviours & Mental Ill Health- • Smoking,alcohol & substance misusearecommon among living with mental ill health • Complexsocialfactors &stresses impact people’s psychologicalwellbeing &health behaviours • Many health behaviours are seen as coping & survivalmechanisms despite their impact being damaging to health • Smoking remains the largest single cause of preventable deaths in England • People living with severe mentalillhealth (40.5%) are3xmore likelythan thegeneralpopulation (14.9%) to smokeMCQs• What isthemechanismofactionofduloxetine? • A) Tricyclicantidepressant • B) GABAa potentiator • C) Blocksalpha 2 autoreceptors • D) Noradrenaline reuptake inhibitor • E) Serotoninreuptakeinhibitor • Howmanysubunits doestheGABAareceptorhave? • A) 2 • B) 3 • C) 4 • D) 5 • E) 6• What typeofheadache cana patient withGAD get? • A) Sinusheadache • B)Cluster headache • C) Theydon’t tend togetheadaches • D)Tensionheadache • E) Migraine • Whichone ofthese drugs is a selective serotonin reuptakeinhibitor? • A) Venlafaxine • B)Mirtazapine • C) Alteplase • D)Duloxetine • E) Escitalopram• A42-year-old man,wholived alone,booked a follow-upappointment tosee hisGP.Due tothe COVID-19 pandemic,he had beenself- isolating at homeforseveralmonths.Afterthe easing of the lockdown,hestillpreferredtostayat home and was afraidtogoout. Priortothe pandemic,he went througha difficult divorce withongoing issueswith respecttothecustody of his children. Unfortunately,he lost his job ashis workplace were unable toofferhim apositiongoing forward. He had receiveda telephoneconsultation4 weekspriorwithhis GP andwas diagnosedwith moderatedepression.He was referredfor computerised cognitivebehavioural therapyandadvised toincrease hislevelsof exercise. Unfortunately,his mental healthwasdeteriorating andhestartedtohave difficultysleeping andearlymorning awakening,andfleeting thoughts that hewould be 'betteroffgone' but withnoactive suicidal plans.He stated he didnot wishtobe referredforpsychological treatments suchas one-to-onecognitive behavioural therapy,ashefoundthemdifficult toengage with. HisGPdiscussedthe next stepin managing his depression. What treatment should he be offered? • A)Citalopram • B) Mirtazapine • C)Venlafaxine • D)Refertothe localcrisisresolutionteam • E) Refertoa structuredexerciseprogrammeNeurovascular Conditions ILOs • Describe the structure and function of the brainstem and cranial nerves. • Define stroke and differentiate between different types of strokes, such as ischaemic and haemorrhagic. • Explain the epidemiology and risk factors leading to stroke and discuss how personal health improvement can reduce stroke risk. • Identify key elements of neurological symptoms with sudden onset (e.g. facial/muscle weakness or headache) and discuss possible underlying differentials. • Evaluate the use of the F.A.S.T screening tool in patients with suspected stroke. • Describe how to assess a suspected stroke patient, including history and examination. Explain the rationale of this assessment. • Explain impairments to speech, movement, and memory caused by stroke and their relation to anatomical lesions within the brain. • Describe the basic mechanisms of action, side effects, and contraindications, of drugs used to manage stroke with particular focus on thrombolysis in acute ischaemic stroke. • Explain long-term management of stroke with regards to speech and language therapy, physical disability, memory loss, and the role of care givers (both paid and unpaid). • Discuss the role of secondary prevention and rehabilitation in recovery from stroke. • Discuss the five main models of disability and apply them to stroke patients with differing symptoms.Brainstem&CranialNerves • Need toknow: • Where eacharises • Where eachexits the skull • Whether nerve is motor, sensory or mixedinfunction • Whether ithasparasympathetic fibres or not • Brainstem: Brainstem& • Split into midbrain, pons & medulla oblongata • Contains axons of neurons connecting higher& lower brain regions & the ascending & descending tracts that connect theSC with the cerebral cortex Cranial • Also contains nucleiof most cranial nerves (nerves can be seen as theyexit the brainstem) • Reticularformation (concerned with pain perception,control of consciousness & regulation ofCV & respiratory systems) is located within the brainstem Nerves • Connects brain to spinal cord • Regulates unconscious bodyfunctions such as breathingand HR Functions • Balance,coordination &reflexes • CranialNerves: • 12 pairs arisefrom the brain • 10 arise from the brainstem • I- Olfactorynerve- smell • II- Optic nerve- vision • III- Oculomotornerve- motor innervation to the structures within thebonyorbit • IV- Trochlearnerve- innervates superior oblique muscle • V- Trigeminalnerve- sensory to the face,motorthemuscles – split into:ophthalmic, maxillary, mandibular • VI- Abducens nerve- innervates lateral rectus muscle • VII- Facial nerve- sensory &motorfunction, tastefrom anterior2/3 oftongue, PNS to glands • VIII- Vestibulocochlear nerve- balance & hearing • IX- Glossopharyngeal nerve- swallowing reflex, taste from posterior1/3 of tongue, gag reflex • X- Vagus nerve- supplies head,neck,thorax,abdomen,gag reflex,cough reflex • XI- Accessory nerves– innervates sternocleidomastoid & trapezius • XII- Hypoglossal nerve- innervates tonguemuscles (intrinsic &extrinsic)except palatoglossus Stroke&ItsTypes • Stroke (WHOdefinition)- clinicalsyndrome characterisedby rapid onset offacialor globalcerebral deficit lasting >24 hours or leadingtodeathwithno other apparent causethana vascular one • Types: • Ischaemic (85%)- loss ofbloodsupply tothebrain • Haemorrhagic(15%)- • Intracerebal • Subarachnoid- presents as headaches, vomiting, LoC • TIA- transient ischaemic attack • Duetoocclusionofvesselwhichreperfuses • Short lived(<1hour) • Resolves withinafewhours • Symptomsfully resolve<24 hours • NOTa stroke • >100,000 strokes/yearin the uk • 1 in every 5 minutes • >1.2million strokesurvivors • Every 2seconds, someonein the worldis having a stroke • 4 biggest killer in theworld • >400 strokes/year in children • 1/3survivors willbedepressedafter Epidemiology • >8/10 areeligiblefor emergency clot busting treatment(thrombolysis) but only 1/10receive it • 2/3survivors leavehospital with a disability • £26bn/yearRisk Factors • Ischaemic stroke: • Generalriskfactorsforcardiovasculardisease: • Age • Hypertension • Smoking • Hyperlipidaemia • Diabetesmellitus • Riskfactorsforcardioembolism-atrialfibrillation • Haemorrhagicstroke: • Age • Hypertension • Arteriovenousmalformation • anticoagulationtherapy • Troublespeaking and understanding what others are saying- A person having a stroke maybe confused, slur words or maynot be able to understand speech. • Numbness,weakness or paralysis in the face, armor leg- This often affects just one side of the body.The person can try to raise both arms overthe head. If one arm begins to fall, it maybe a sign Neurological ofa stroke. Also,one side ofthe mouth maydroop when trying to smile. Symptoms • Problems seeing in oneor both eyes- The person may suddenly have blurred orblackened vision in one orboth eyes.Or the person maysee double. • Headache- A sudden, severe headache maybe a symptom of a stroke. Vomiting, dizziness and a change in consciousness may occur with the headache. • Tbalance or coordination.aving a stroke may stumble orloseFAST ScreeningT ool • Cantheysmile?enonone side? • Arms-cantheyraisebotharms &keepthemthere? • Speech-is theirspeechslurred? • Time-call999 ifanyofthe signs are shown • DoNOTtake themtoA&E yourself,bycalling999, stroke unitASAP forurgent treatmentLesionsTreatmentforIschaemicStroke • Reperfusiontherapy • tPA • Thrombectomy • TPA: • Tissueplasminogenactivator- fibrin-> plasmin • 1mg/kgover 1 hour • Has tobe given<4.5 hoursfromonsetor canbe givenupto9 hoursafter onsetifimaging showsa salvageablepenumbra • Clot buster- breaks downclottoallow reperfusion • Increases risk ofhaemorrhage • Cancause angioedema whichisanallergic response tothe drug • Causes unilateralswelling oflips & tongue • Thrombectomy: • Stent retriever whichphysicallyremovestheclot • <6hours fromonset,iffavourableimaging canbedonewhiting 24hours • UsuallydoneiftPA didnotwork • Limitedaccess, only10-15% eligible, and 2-3%actuallytreated • Catheter angiogramusedtoguide throughfemoral artery • Dye isinjectedtoshowocclusion& then reperfusiononceclotis removed • Fluidmanagement- • Regular assessment forfluid statusinhospitaltoensure patientsare normovolaemic • Hypovolaemia canworsenischaemic penumbra and increase the riskofinfection, DVT, constipation& delirium • Over hydrationcancause cerebraloedema,cardiacfailure,hyponatraemia • Oral hydration for those who can swallow • IV hydrationiftheycan’t swallow • Glycaemiccontrol- • Controlbloodsugar especiallyifNBM • Post stroke, patients with hyperglycaemia have increasedmortalitydueto increases LongT erm tissueacidosis fromanaerobic metabolism • 4-11mmol/L target Management • BP management- ofStroke • Anti-hypertensives onlyforthose whohavehypertensiveemergencies • This is because loweringit toomuchcancompromise collateralbloodflow tothe affectedregionthuscause irreversibletissueinfarction • IV labetalol,nicardipine &clevidipine • Feeding assessment- • Screenfor swallowing functionasdysphagia is commonafterstroke • Reducerisk ofaspiration • NGtube ifnotsafe toswallow • Newstrategy- • Neuroplasticity- re-establishneuronalconnectionsbetween neurons Secondary Prevention & Rehabilitation • Identifythe cause • Atherothromboembolism-clotfromcarotidoraortic archorintracranial atherosclerosis • Cardioembolic-clotfromheart • Smallvessel disease-causedby HTN,diabetes& increasingage;occlude small perforated cause weaknesshebasal ganglia;causelacunar strokeswhichaffectcorticospinaltractsthus • Miscancellous rarecauses-usually inyoungerpatientssuchasaortic dissection • Medications • Aspirin-for2weeks,theswitchtoclopidogrel • Statin • BPmanagement • Screenforcarotidstenosis • If≥50%->carotidendertorectomy(1-2daysafterstroke) • KEY-ifpatient hasatrialfibrillation,give themananti-coagulant ratherthanananti-platelet • DOACs • Rehabilitation: • Discharge planningfromday 1 • Goal orientated • Family,home circumstances, driving considered • Community follow ups • Back towork • ST& LTgoals, family, patient& MDT • Achievement at home tomaximise participationindailylife ModelsofDisability • Social model- • People with disabilities are no different to those without,but people become disabled bythe environment around them rather than their impairment. Through makingsocietymore inclusive and supportivewe can promote participation in community. • Medical model- • Focuses on an individual’s impairment,causing dependencybetween disabled peopleand those without disabilities. There maybe abelief that individuals with disabilities need to be‘cured’ortreated through medical interventions beforetheycan participate in the community. Additionally, people with these beliefs may view people with disabilities as unableto make their own decisions. • Charity model- • Communities can view people with disabilities as not having the capacityto live independently.Therefore,peoplewith disabilities must be‘cared for’in separate facilities to the rest of thecommunity. This can bedisempowering, disheartening,and portray people with disabilities as victims. • Rights-based model- • Disabilityis based on asocial construct notion ofdisabilitywhich demands that impairment maynot be taken as an excuseforviolation of an individuals’human rights. It regards the barriers in society as discriminatory and provides avenues forindividuals with disabilities to complain as they have the right to equal opportunities and participation in society.Peoplewith disabilities are viewed as having the abilityto claim theirrights and makedecisions that affect theirlives.MCQs• Whichcranialnerve innervates thelateral rectusmuscle? • A) CNXI • B) CNIX • C) CNVI • D) CN III • E) CNX • Patient Xsuffers froma stroke, withadetected clot intheir posterior cerebralartery.Whichpresentationarethey likelytohave? • A) Loss ofsenseofsmell • B) Agitation& irrationalbehaviour • C) Lack ofpainjudgement • D) Broca’saphasia • E) Wernicke’s aphasia• PatientY has hadan ischaemic stroke. Within how many hoursarethey eligiblefor alteplase? • A)2 hours • B) 3hours • C) 3.5 hours • D)4 hours • E) 4.5 hours • PatientZhas suffered froman ischaemic stroke. They have newonsetofnystagmus.Which artery is most likely to be occluded? • A)Anteriorinferiorcerebellar • B) Posterior inferior cerebellar • C) Vertebral • D)Anteriorcerebellar • E) Posterior cerebellar• A76-year-oldfemalepresents withsuddenonsethemiparesis affecting theleftface, armand leg.On examinationyounoteleftsided hemiparesis,and aleft homonymous hemianopia. Whichis the bestassessmenttool for differentiating betweenstrokeand strokemimics? • A)FAST • B) PESI • C)PERC • D) ROSIER • E)2 levelsWells ScoreStudyTips  Anatomy  TBL structure  Notetaking/flashcards  Revision-  Mid Sem  Endof Sem  Resources  WellbeingQuestions?Feedback • https://app.medall.org/feedbac flow?keyword=cde5b65cced89 40d2ec30d65&organisation=m anchester-meded