医学专业英语课件2.pptx
2023年4月21日星期五医学专业英语课件医学专业英语课件_2。 Mini Mental Status Examination gives a score of 18 out of 30. The head and neck and cardiovascular examination are unremarkable. Abdomen is benign without hepatosplenomegaly. The extremities are without edema, cyanosis, or clubbing. The neurologic examination reveals that the cranial nerves are intact, and the motor and sensory exams are within normal limits. Cerebellum examination is unremarkable and the gait is normal.Alzheimer dementia. Assess for depression and reversible causes of dementia. Acetylcholinesterase inhibitor Analysis12Table 49-1ABBREVIATED WORKUP FOR DEMENTIAComplete blood count and consider erythrocyte sedimentation rate (ESR) Chemistry panel Thyroid-stimulating hormone level Venereal Disease Research Laboratory (VDRL) HIV assay Urinalysis Serum vitamin B12 and folate levels Chest radiographElectrocardiogram CT or MRI imaging of the head 12 APPROACH TO DEMENTIAnMultiinfarct dementia: Numerous small cerebral vascular accidents, most commonly caused by atherosclerotic disease, leading to dementia.nNormal pressure hydrocephalus: Reversible form of dementia where the cerebral ventricles slowly enlarge as a result of disturbances to cerebral spinal fluid resorption. The classic triad is dementia, gait disturbance, and urinary or bowel incontinence.Table 49-2NEUROLOGICAL DISEASES IMPAIRING COGNITIVE ABILITYDISEASE CLINICAL FEATURES TREATMENT Alzheimer disease Slow decline in cognitive and behavioral ability; pathology: neurofibrillary tangles, enlarged cerebral ventricles, and atrophy Cholinesterase inhibitors such as donepezil or rivastigmine Normal-pressure hydrocephalus Gate disturbance, dementia, incontinence; enlarged ventricles without atrophy Ventricular shunting process Multi-infarct dementia Focal deficits, stepwise loss of function; multiple areas of infarct usually subcortical Address atherosclerotic risk factors, identify and treat thrombus Parkinson disease Extrapyramidal signs (tremor, rigidity), slow onset Dopaminergic agents Table 49-2 (cont)NEUROLOGICAL DISEASES IMPAIRING COGNITIVE ABILITYDISEASE CLINICAL FEATURES TREATMENT HIV defintion Systemic involvement; risk factors for acquisition; positive HIV serology Treat specific infection Neurosyphilis Optic atrophy, Argyll-Robertson pupils, gait disturbance; positive cerebro-spinal fluid serology High dose intravenous penicillinMultiple sclerosis Brainstem signs, optic atrophy, long-standing disease with exacerbations and remissions; MRI showing white matter abnormalities Recombinant interferon, corticosteroids Intracranial tumor Focal signs, papilledema, seizures Corticosteroids to reduce intracranial pressure, treat the lesion The etiology of Alzheimer dementia is an unknown but Alzheimer disease has a genetic component. The risk of developing the disease for an individual in a family with Alzheimer disease increases by a factor of 3 or 4. The gene that codes for apoprotein E seems to be associated with some prediction. The pathologic changes in the brains of Alzheimer disease patients include neurofibrillary tangles with a deposition of abnormal amyloid in the brain. Amyloid Precursor ProteinA-Neurofibrillary TanglesA- AggregationNeuron DeathBasal Forebrain and Brainstem NucleiNeurotransmitter DeficitsNeuritic PlaquesNeuron DeathCortexDemantia SyndromeMutations and vulnerability genes associated with Alzheimers diseaseGenotypeCellular effectMutationsDown syndrome(trisomy 21)Increased APP productionwith enhanced generationof AAPP mutations(varions) 21q21.1-21.3Altered APP processingresultiong in increasedproduction of AChromosome 14 (PS1mutation) 14q24.2-24.3Increased A productionChromosome 1 (PS2mutation) 1q31-32Increased A productionMutations and vulnerability genes associated with Alzheimers diseaseGenetic risk factorsChromosome 19 (ApoE-4) 19q13.2Increase A aggregationChromosome 12 (low-densitylipoprotein receptor-relatedprotein)Lipoprotein receptormediating the moleculareffects of ApoE-4Chromosome 6 (HLA-A2)HLA histocompatibilityallele regulating theinflammatory responseChromosome 17Bleomycin hydrolase;implicated in APPprocessingClassical neuritic plaque(Bielschowsky silver stain)Neurofibrillary TanglesNeurofibrillary tangles(H&E stain)Cerebral amyloid angiopathy(H&E stain)Table 49-3ALZHEIMER DISEASE CLINICAL COURSECLINICAL STAGE MANIFESTATIONS Early Mild forgetfulness, poor concentration, fairly good function, denial, occasional disorientation Intermediate Drastic deficits for recent memory, can travel to familiar locations, suspicious, anxious, aware of confusion Late Cannot remember names of family members or close friends; may have delusions or hallucinations, agitation, aggression, wandering, disoriented to time and place, need for substantial care AdvancedTotally incapacitated and disoriented, incontinent, personality and emotional changes; eventually all verbal and motor skills deteriorate, leading to need for total care nDonepezil (Aricept) and revastigmine (Exelon) are cholinesteras
