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patho
chronic neurological diseases ch 32
| Question | Answer |
|---|---|
| hydrocephalus | excess cerebrospinal fluid (CSF) accumulates at the skull (usually more production than reabsorption) if cranial sutures have not closed head enlarges (infants) damage depends on the rate of the pressure |
| two types of hydrocephalus | non communicating or obstructive hydrocephalus: flow is blocked communicating hydrocephalus: problem w absorption on CSF through subarachnoid vili |
| hydrocephalus signs and symptoms | increase in CSF scalp veins look dilated |
| hydrocephalus diagnosis | CT scan or MRI determine the size of the ventricles and locate the obstruction |
| hydrocephalus treatment | surgery shunt |
| dementia | -chronic (persistent) disorder of mental processes -caused by brain disease or injury -memory disorders, personality changes, impaired reasoning -slow, progressive onset with impairments in abstract thinking and memory loss |
| diagnosis of dementia | based on CM and progressive nature of the illness |
| causes of dementia | illnesses head trauma alzheimer disease (more than 50% of dementia cases) vascular dementia (changes in thinking following a series of small strokes) |
| brain changes in Alzheimers disease | misfolded proteins causing impaired action potentials. causes shrinking of the brain and enlargement on the ventricles |
| CM of dementia | slow, progressive decline of cognitive functioning AD versus vascular dementia increasing cognitive impairments over years (eventually cant care for self or communicate) progressive changes in mobility |
| caregivers of people with dementia | initiate formal dementia evaluations manage symptoms and monitor effects of management provide emotional and financial support |
| diagnosis of dementia | complete physical and neurological examination |
| treatment of dementia | monitoring of health and cognitive status reorienting to person, place, time Encouraging advance directives instructing with simple steps Alternating activities with rest to avoid fatigue Providing medication interventions (only to delay progress) |
| multiple sclerosis | -Progressive demyelination of the neurons in the brain, spinal cord, and cranial nerves - autoimmune -Loss of myelin interferes with the conduction of impulses in affected fibers -May affect motor, sensory, and autonomic fibers |
| how does MS occur in the nervous system? | Occurs in diffuse patches in the nervous system types of MS: vary in effect, severity, and progression |
| earliest lesions of MS | Inflammatory response Loss of myelin in the white matter of the brain or spinal cord |
| Plaques of MS | Larger areas of inflammation and demyelination Develops later, becomes visible in X-ray |
| recurrence of MS | -Initial inflammation may subside -Neural function may return to normal for a short period of time -Each recurrence causes additional areas of the CNS to become affected |
| etiology of MS | Onset between 20-40 Causes is unknown Genetic tendency |
| signs and symptoms of MS | Manifestation is determined by the area of demyelination |
| diagnostic test of MS | MRI |
| Treatment of MS | no definitive Tx |
| Parkinson's Disease | Idiopathic, chronic, progressive degenerative disorder of the CNS Has motor, non-motor, and neuropsychiatric manifestations Affects individuals over age 50 (male) The second most common neurodegenerative disorder |
| parkinsons disease symptoms | Tremors Bradykinesia Rigidity Postural instability |
| conditions that cause secondary Parkinsonism (same signs but different cause) | Head trauma Toxins Metabolic disorders Infections Multiple strokes in the basal ganglia Atypical antipsychotics and antiemetics (prevent vomiting and nausea) |
| what causes a decreased risk of Parkinsons | Cigarette smoking, caffeine intake High blood urate levels |
| Pathogenic mechanisms of parkinsons | proteolytic stress oxidative stress mitochondrial dysfunction inflammation |
| proteolytic stress (parkinsons) | Accumulation and aggregation of proteins Lewy bodies |
| oxidative stress (parkinsons) | Generation of reactive oxygen species (ROS) Depletion of glutathione; increase in iron levels |
| mitochondrial dysfunction (parkinsons) | Decreased mitochondrial complex activity (by 30-40%) |
| inflammation (parkinsons) | Overactivation of microglia Excess production of neurotoxic factors |
| clinical manifestations of parkinson's | Insidious onset Motor features non-motor features |
| motor features of parkinsons | -Tremor (Pill-rolling resting tremor of head, Tremor of lips, chin, jaw, tongue, and legs) -Rigidity from increased muscle stiffness and tone -Cogwheeling (ratchet, jerky resistance when moving pts leg) -Bradykinesia -Postural instability |
| non-motor features of parkinsons | Fatigue, sleep disturbances Olfactory dysfunction Pain Autonomic dysfunction Neuropsychiatric symptoms (Cognitive dysfunction, dementia, psychosis, hallucinations, Mood disorders, depression, anxiety) |
| treatment of parkinsons | Pharmacological replenishment with dopaminergic drugs (increase dopamine levels) Deep brain stimulation Complementary and supportive therapies |
| Huntington's disease | -Progressive, incurable, neurodegenerative disease of the brain; autosomal dominant inherited -Causes uncontrollable involuntary movements, dementia, and behavioral changes |
| huntington's disease age | Onset of symptoms: ages 35-44 years Duration: mean of 19 years |
| huntington's primary cause of death | pneumonia cardiovascular death |
| huntington's disease pathology | -Gross atrophy in the caudate nucleus and putamen accompanied by selective neuronal loss and gliosis -Neuronal loss in the cerebral cortex -Varying degrees of atrophy in other areas of the midbrain and cerebellum -Shrinkage of the brain (in volume) |
| etiology of huntington's diease | mutation in the huntington gene (HTT) on the short arm of chromosome 4 |
| CM of huntingtons disease | involuntary movements cognitive impairments behavioral changes |
| involuntary movement CM of huntingtons | Parkinsonian features Akinetic-rigid syndrome Dysarthia Dysphagia Abnormal eye movements Tics |
| cognitive impairments CM of huntingtons | Short-term memory loss Impaired intellectual function Dementia Psychiatric manifestations |
| behavioral changes CM of huntingtons | Irritability, moodiness, depression, OCD Untidiness Antisocial behavior Apathy |
| diagnosis of huntingtons disease | Genetically proven family history Clinical presentation MRI or CT scan to measure brain atrophy Referral to a neurologist who specializes in HD |
| treatment of huntingtons disease | reduce symptoms and improve quality of life |
| amyotrophic lateral sclerosis (ALS) | Progressive neurodegenerative disease Causes weakness, disability, and death within 3-5 years Also known as Lou Gehrig’s disease |
| neurodegeneration of ALS | Upper motor neurons in the corticospinal tract Lower motor neurons in anterior horn cells of the spinal cord |
| amyotrophic lateral sclerosis (ALS) AKA | Lou Gehrig's disease |
| risk factors of ALS | Age and family history |
| etiology and pathogenesis of ALS | No direct mechanism determined Similar to prion disease or malignancy Motor axons die by Wallerian degeneration |
| pathways that lead to axonal degeneration and cell death ALS | Oxidative stress Mitochondrial dysfunction Defect of axonal transport Abnormal growth factor expression Excitotoxicity |
| CM of ALS | Insidious onset Slow progressive, painless weakness in one or more body parts Upper motor neuron (UMN) signs and symptoms Lower motor neuron (LMN) signs and symptoms Bulbar dysfunction |
| diagnosis of ALS | Based primarily on clinical manifestations Diagnostic tests (Electromyography, Nerve conduction studies, MRI or CT scan of the brain and spinal cord, Muscle or nerve biopsy, Genetic, Blood tests) |
| seizure disorders result from | seizure activitiy |
| seizure activity | Abnormal electrical discharge within the brain results in involuntary movements and/or behavior and sensory alterations changes in level of consciousness, behavior, or sensory perception |
| involuntary movements of seizure activity | May encompass the entire body or just certain muscle groups |
| CM of seizures | Loss of conscious awareness of the environment Varying patterns of muscular rigidity and relaxation Aura |
| phases of generalized seizures | tonic phase clonic phase postictal period |
| tonic phase | 15-60 seconds Muscular rigidity Sudden loss of consciousness Pupils fixed and dilated Increased metabolic demands Hypoxia (Skin pallor and cyanosis) Urinary and bowel incontinence |
| clonic phase | 60-90 seconds Alternation of muscular contraction and relaxation in the extremities Hyperventilation Eyes roll back, froth at the mouth |
| postictal period | Decreased level of consciousness; sleepy Quiet and relaxed breathing Gradual regaining of consciousness |
| CM of status epilepticus | Life-threatening condition Enhanced and sustained electrical activity over 30 minutes Increased neural excitation with reduced inhibition |
| diagnosis of seizure disorders | Laboratory tests (Complete blood cell count , Blood chemistry, Urine culture, Lumbar puncture) EEG Lead level, toxicology screening CT scan or MRI and angiography |
| Treatment of seizure disorders | anti-seizure medication surgical intervention |
Created by:
ago24