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acute nd pt 2
patho exam 3
| Question | Answer |
|---|---|
| spinal cord injury damage may be... | temporary or permanent |
| can axon regrowth occur in a spinal cord injury? | yes |
| spinal cord injury | laceration of nerve tissue by bone fragments or complete transection or crushing of cord, partial transection or crushing of the cord or bruising, prolonged ischemia and necrosis |
| laceration of nerve tissue by bone fragments or complete transection or crushing of cord causes... | irreversible loss of all sensory and motor function at and below the level of the injury |
| partial transection or crushing of the cord or bruising may... | allow recovery of some functions |
| prolonged ischemia and necrosis can cause... | permanent damage |
| spinal cord injury treatment | physical therapy, occupational therapy |
| chronic neurological diseases | hydrocephalus, dementia, alzheimers, multiple sclerosis, parkinsons, huntingtons, als, seizure disorders |
| causes of hydrocephalus | excess cerebrospinal fluid (CSF) accumulated at skull (usually more production than reabsorption), if cranial sutures have not closed head enlarges (infant) |
| what does hydrocephalus damage depend on? | rate of the pressure |
| two types of hydrocephalus | non communicating or obstructive hydrocephalus, communicating hydrocephalus |
| non-communicating hydrocephalus | normal flow of CSF is blocked |
| communicating hydrocephalus | problem on absorption on CSF through subarachnoid villi |
| hydrocephalus signs and symptoms | increase in CSF, scalp veins look dilate |
| hydrocephalus diagnostic test | CT scan or MRI (determine the size of the ventricles and locate the obstruction) |
| hydrocephalus treatment | surgery, shunt |
| what does the increase in CSF from hydrocephalus in infants cause? | increase in head size |
| what does the increase in CSF from hydrocephalus in adults cause? | increase in ICP- strong headaches |
| what does a shunt do when treating hydrocephalus? | placed at lateral ventricle that moves CSF from ventricle and places it in pericardial cavity |
| dementia | chronic (persistent) disorder of mental processes; memory disorders, personality changes, impaired reasoning |
| what is dementia caused by? | brain disease or injury |
| onset of dementia | slow, progressive onset with impairments in abstract thinking and memory loss |
| what is the dementia diagnosis based on? | clinical manifestations and progressive nature of illness |
| causes of dementia | illnesses, head trauma, alzheimer disease (AD), vascular dementia |
| alzheimer dementia is what percent of dementia cases? | more than 50% |
| vascular dementia | changes in thinking following series of small strokes |
| brain changes in alzheimer disease | shrinkage of cerebral cortex, enlarged ventricles, shrinkage of hippocampus |
| clinical manifestations of dementia | slow, progressive decline of cognitive function, increasing cognitive impairments over years; progressive changes in mobility |
| dementia patients are eventually... | unable to care for self or communicate |
| caregivers of individuals with dementia | initiate formal dementia evaluations, manage symptoms and monitor effects of management, provide emotional and financial support |
| dementia diagnosis | complete physical and neurologic examination |
| dementia treatment | Regular monitoring of health and cognitive status; Reinforcing orientation x3; Encouraging establishment of advance directives; Breaking instructions into simple steps; Alternating activities with rest to prevent fatigue; pharmacologic interventions |
| treatment of dementia will only... | delay progression of symptoms |
| multiplic sclerosis | progressive demyelination of the neurons in the brain spinal cord and cranial nerves- autoimmune |
| what does the loss of myelin in ms interfere with? | conduction of impulses in affected fibers |
| what does the interference of conduction of impulses in affected fiber caused by the loss of myelin in ms affect? | motor, sensory and autonomic fibers |
| what does the loss of myelin in ms occur in? | diffuse patches in the nervous system |
| types of ms | varies in effects, severity and progression |
| ms earliest lesions | inflammatory response, loss of myelin in white matter of brain or spinal cord |
| ms plaques | larger areas of inflammation and demyelination; develop later, become visible in x-ray |
| ms recurrence | 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 |
| when does multiple sclerosis onset occur? | between 20-40 |
| cause of multiple sclerosis | unknown; genetic tendency |
| multiple sclerosis signs and symptoms | manifestation determined by area of demyelination |
| multiple sclerosis diagnostic test | MRI |
| multiple sclerosis treatment | no definitive treatment |
| parkinson disease | idiopathic, chronic, progressive degenerative disorder of the CNS |
| what kind of manifestations does parkinson disease have? | motor, nonmotor, neuropsychiatric |
| who does parkinson disease affect? | individuals over age 50 (male) |
| second most common neurodegenerative disorder | parkinson disease |
| parkinson symptoms | tremors, bradykinesia, rigidity, postural instability |
| bradykinesia | slow movements |
| conditions that cause secondary parkinsonism | head trauma, toxins, metabolic disorders, infections, multiple strokes in basal ganglia, atypical antipsychotics and antiemetics |
| decreased risk of parkinson disease | cigarette smoking, caffeine intake; high blood urate levels |
| pathogenic mechanisms of parkinson disease | proteolytic stress, oxidative stress, mitochondrial dysfunction, inflammation |
| proteolytic stress parkinson disease | accumulation and aggregation of proteins, lewy bodies |
| oxidative stress parkinson disease | generation of reactive oxygen species (ROS), depletion of glutathione; increase in iron levels |
| mitochondrial dysfunction parkinson disease | decreased mitochondrial complex activity (by 30-40%) |
| inflammation parkinson disease | over activation of microglia, excess production of neurotoxic factors |
| clinical manifestations of parkinson disease | insidious onset, motor features, nonmotor features |
| clinical manifestations of parkinson disease: motor features | tremor, rigidity from increased muscle stiffness and tone, cogwheeling, bradykinesia, postural instability |
| clinical manifestations of parkinson disease: motor features: tremors | "pill-rolling" resting tremor of hand; tremor of lips, chin, jaw, tongue, legs |
| clinical manifestations of parkinson disease: nonmotor feeatures | fatigue, sleep disturbances; olfactory dysfunction; pain; autonomic dysfunction; neuropsychiatric symptoms |
| clinical manifestations of parkinson disease: nonmotor feeatures: neuropsychiatric symptoms | cognitive dysfunction, dementia, psychosis, hallucinations; mood disorders, depression, anxiety |
| parkinson disease treatment | Pharmacologic replenishment with dopaminergic drugs, Deep brain stimulation, Complementary and supportive therapies |
| huntington disease | Progressive, incurable, neurodegenerative disease of brain; autosomal dominant inherited |
| what does huntington disease cause? | uncontrolled involuntary movements; dementia; and behavior changes |
| huntington disease onset of symptoms | ages 35-44 years; duration: mean of 19 years |
| huntington disease primary cause of death | pneumonia, cardiovascular disease |
| huntington disease pathology | Gross atrophy in caudate nucleus and putamen accompanied by selective neuronal loss and gliosis; Neuronal loss in cerebral cortex; Varying degrees of atrophy in other areas in midbrain and cerebellum; Shrinkage of brain (in volume) |
| huntington disease etiology and pathology | mutation in huntington gene (HTT) on short arm of chromosome 4 |
| huntington disease clinical manifestations | involuntary movements, cognitive impairment, behavioral changes |
| huntington disease clinical manifestations: involuntary movements | Parkinson features; Akinetic-rigid syndrome; Dysarthria; Dysphagia; Abnormal eye movements; Tics |
| huntington disease clinical manifestations: cognitive impairment | Short term memory loss; Impaired intellectual function; Dementia; Psychiatric manifestations |
| huntington disease clinical manifestations: behavioral changes | Irritability, moodiness, depression, OCD; Untidiness; Antisocial behavior; Apathy |
| huntington disease diagnosis | Genetically proven by family history; Clinical presentation MRI or CT scan measure brain atrophy; Referral to neurologist who specializes in HD |
| huntington disease treatment | reduce symptoms and improve quality of life |
| Amyotrophic Lateral Sclerosis | progressive neurodegenerative disease |
| what does Amyotrophic Lateral Sclerosis cause? | weakness, disability, and death within 3-5 years |
| what is als also known as? | lou gehrig's disease |
| als neurodegeneration | Upper motor neurons in corticospinal tract Lower motor neurons in anterior horn cells of spinal cord |
| als risk factors | age and family history |
| als etiology and pathogenesis | No direct mechanism determined; Similar to prion disease or malignancy; Motor axons die by wallerian degeneration |
| als Pathways that lead to axonal degeneration and cell death | Oxidative stress; Mitochondrial dysfunction; Defeat of axonal transport; Abnormal growth factor expression; Exitotoxicity |
| als clinical manifestations | Insidious onset; Slowly progressive, painless weakness in one or more body parts; Upper motor neuron signs and symptoms Lower motor neuron signs and symptoms; Bulbar dysfunction |
| als diagnosis | Based primarily on clinical manifestations; Diagnostic tests |
| als diagnostic tests | electromyography, nerve conduction studies, MRI or CT scan of brain and spinal cord, muscle or nerve biopsy, genetic, blood tests |
| seizure activity | Abnormal electrical discharges within brain |
| what does seizure activity result in? | Involuntary movements- May encompass entire body or just certain muscle groups; Changes in level of consciousness, behavior, or sensory perception |
| seizure activity clinical manifestations | Loss of conscious awareness of environment; Varying patterns of muscular rigidity and relaxation; Aura |
| phases of generalized seizures | tonic phase, clonic phase, postictal period |
| phases of generalized seizures: 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 |
| phases of generalized seizures: clonic phase | 60-90 seconds; Alternating muscular contraction and relaxation in extremities; Hyperventilation; Eyes roll back, froth at mouth |
| phases of generalized seizures: postictal period | Decreased level of consciousness; sleepy; Quiet and relaxed breathing; Gradual regaining of consciousness |
| Clinical manifestations of status epilepticus | Life threatening condition (especially chronic seizures); Enhanced and sustained electrical activity over 30 minutes; Increased neuronal excitation with reduced inhibition |
| seizure disorders diagnosis | Laboratory tests; EEG; Lead level, toxicology screening; CT scan or MRI and angiography |
| seizure disorders laboratory tests | Complete blood cell count; Blood chemistry; Urine culture; Lumbar puncture |
| seizure disorders treatment | Antiseizure medications; Surgical intervention |
Created by:
camrynfoster