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patho exam 3
acute ND and neurodevelopment disorders
| Question | Answer |
|---|---|
| central nervous system consists of | brain and spinal cord |
| central nervous system: association neurons | contained entirely within the CNS, usually relays from afferent to efferent |
| peripheral nervous system consists of | cranial and spinal nerves |
| peripheral nervous system: afferent and efferent nerves | afferent (sensory): dendrites distal to CNS and axons proximal efferent (motor): dendrites proximal to CNS and axons distal |
| motor and sensory cortices | brain is responsible for motor function |
| neurodevelopment disorders | impairments of brain function occurring as brain develops: language, coordination, attention, behavior |
| brain tumors: development | fast and never related to overgrowing of neurons |
| brain tumors are | Space occupying lesions that cause increase in intracranial pressure |
| Benign and malignant tumors can be life threatening because | of the pressure it cases and depends of how easy it is to be removed |
| largest category of primary malignant tumor | gliomas |
| Primary malignant tumors | rarely metastasize outside the CNS (BBB) |
| Secondary brain tumor | metastasizing from breast of lung tumor - don't know why they metastasize to brain |
| pathophysiology of primary malignant brain tumor | Usually no well define Invasive and have irregular projections into adjacent tissue Usually inflammation around the tumor |
| etiology of primary malignant brain tumor | Brainstem and cerebellar tumors are common in young children Adults; more frequently in the cerebral hemisphere |
| Signs and symptoms of primary malignant brain tumor | Seizures are often a sign Headaches, vomiting, lethargy, irritability, personality and behavior changes, possible unilateral facial paralysis (bc only one side has tumor), visual problem Do not cause the systemic signs of malignancy |
| treatment of primary malignant brain tumor | May cause damage to normal CNS tissue Surgery if accessible chemotherapy and radiation |
| Infections - Meningitis | Inflammation of the meninges (the three layers that cover the brain) |
| meninge layers | Skull Dura mater Arachnoid: where CF moves and gives space for vasculature to penetrate the brain Pia mater: first |
| Different age groups are | susceptible to different causative organisms - may be secondary to other infections |
| young adults: meningitis | Most often due to haemophiles influenzae bacteria (more often in the fall or winter) |
| Children and young adults: meningitis | Neisseria meningitides or meningococci- classic meningitis pathogen Frequently carried in the nasopharynx of asymptomatic carriers Spread by respiratory droplets (later winter/early spring) |
| older adults: meningitis | Streptococcus pneumonia - major cause |
| signs and symptoms of meningitis | Sudden onset is common Severe headache Back pain Photophobia Nuchal rigidity Kerning sign - move legs Brudzinski sign - move neck Vomiting, irritability, lethargy, fever and chills with leukocytosis Progressing to stupor or seizures |
| diagnostic test of meningitis | Examination of CSF (lumbar puncture) Identify causative organism |
| treatment of meningtitis | Aggressive antimicrobial therapy Specific treatment for ICP and seizures Glucocorticoids (stop inflammation) Vaccines are available for some types of meningitis |
| Infection - Brain Abscess usually occurs when | bacteria or fungi enter the brain tissue after an infection or severe head injury |
| Infection - Brain Abscess | Pus-filled swelling in the brain Localized infection (frontal and temporal lobes) Necrosis of the brain tissue and surrounding edema May spread from organism in the E,T,L, sinuses May be from septic emboli, acute bacterial site of injury or surgery |
| Infection - Encephalitis is | Infection of parenchymal (nerve or glial cells) or CT of the brain and spinal cord |
| Infection - Encephalitis is due to | Necrosis and inflammation development in brain tissue, result in permanent damage |
| Infection - Encephalitis may include | Viral infections Bacterial infections Autoimmune disorders Allergic reactions |
| early sign of Encephalitis | severe headache, stiff neck, lethargy, vomiting, seizures, fever |
| diagnosis of Encephalitis | imaging tests, CSF analyses |
| infections that can cause neuro problems | tetanus, Herpes Zoster (shingles) |
| tetanus is caused by | clostridium tetani |
| Make sure everyone is up to date on | their tetanus vaccine!! |
| what is unique about tetanus | Spores can survive in soil (years) |
| in tetanus, exotoxin enters nervous system and causes | Tomic muscle spasm Jaw stiffness Difficult to swallowing Stiff neck Headache and skeletal muscle spasm Respiratory failure |
| Herpes Zoster (shingles) is caused by | varicella-zoster in adults |
| Herpes Zoster (shingles) occurs | years after primary infection of varicella |
| what does Herpes Zoster (shingles) usually affect | one cranial nerve or one dermatome |
| Herpes Zoster (shingles) inflicts | pain, paresthesia, vesicular rash |
| If antiviral drugs started within 48 hours of onset... | pain is significantly reduced |
| Lesion and pain persist for | a few weeks |
| vaccine available for Herpes Zoster (shingles) | chicken pox |
| head injuries | May involve skull fracture Induce hemorrhage and edema Direct injury to brain tissue Injury can be mild or life threatening |
| Concussion (minimal brain trauma) cause | reversible interference with brain function, sudden excessive movement of the brain |
| concussions are a result of | mild blow to the head or whiplash-type injury |
| what follows a concussion | Amnesia and headaches |
| concussion recovery | usually within 24 hours without permanent damage |
| Contusion | Bruising of brain tissue, rupture of small blood vessel (inflammation and edema) |
| contusion is caused by | Blunt blow to the head- possible residual damage |
| closed head injury | Skull is not fractured in injury Brain tissue is injured and blood vessel may be ruptured Extensive damage may occur when head is rotated |
| open head injury | Skull is damaged Involves fractures or penetration of the brain |
| depressed skull fractures involve | displacement of a piece of the bone below the levels of the skull |
| depressed skull fracture | Compression of brain tissue Blood supply to area often impaired- pressure to brain |
| basilar fractures occur at | the base of the skull |
| basilar fractures are a leakage of | CSF through ears or nose is possible |
| basilar fractures may occur | when the forehead hits windshield |
| Contrecoup injury | area of the brain contralateral to the site of direct damage is injured, as brain bounces off the skull |
| Contrecoup injury may be secondary to | acceleration or deceleration injuries |
| Head Injury is | trauma to brain tissue |
| head injuries cause | loss of function in part of body controlled by the area of the brain |
| cell damage and bleeding lead to | inflammation and vasospasm around injury site |
| hematoma's are classified by | their location in relation to the meninges |
| Signs and symptoms of head injuries | Focal signs General signs of increased ICP Seizures Cranial nerve impairment may occur Otorrhea or rhinorrhea Fever |
| Diagnostic/treatment of head injuries | MRI or CT to determine the extent of the brain injury Glucocorticoids agents - decrease edema Abx - reduce infections Surgery - reduce ICP Oxygen - to protect remaining brain tissue |
| spinal cord injury damage may be | temporary or permanent |
| spinal cord injury axon regrowth | may occur |
| spinal cord injury due to | 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 causes | permanent damage |
| treatment for spinal cord injury | PT or OT |
| hydrocephalus is caused by | excess CSF accumulates at skull - usually more production than reabsorption if cranial sutures have not closed, the head enlarges (infant) |
| hydrocephalus depends on | the rate of pressure that the CSF is putting on the brain |
| two types of hydrocephalus | non-communicating or obstructive hydrocephalus - flow is blocked communicating hydrocephalus - problem on absorption of CSF through subarachnoid villi |
| where is CSF drained | subarachnoid villi |
| signs and symptoms of hydrocephalus | increase in CSF scalp veins looks dilate |
| diagnostic test for hydrocephalus | CT scan or MRI - determine the size of ventricles and locate the obstruction |
| treatment for hydrocephalus | surgery shunt - drains the CSF |
| dementia is a | neurocognitive disorder |
| dementia | chronic disorder of mental processes |
| dementia is caused by | brain disease or injury |
| dementia includes | memory disorders, personality changes, impaired reasoning |
| dementia has a | slow, progressive onset with impairments in abstract thinking and memory loss |
| dementia diagnosis is based on | CMs and progressive nature of illness complete physical and neurologic examination |
| causes of dementia | illnesses head trauma alzheimer disease (AD) - more than 50% of dementia cases vascular dementia - changes in thinking following series of small strokes |
| CMs of dementia | slow, progressive decline of cognitive functioning AD versus vascular dementia increasing cognitive impairments over years - eventually unable to care for self or communicate progressive changes in mobility |
| caregivers of individuals with dementia | initiate formal dementia evaluations manage symptoms and monitor effects of management provide emotional and financial support |
| treatment for dementia | Regularly monitor health and cognitive status Reinforce orientation to person, place, time Breaking instructions into simple steps Alternating activities with rest to prevent fatigue Providing pharmacologic interventions |
| providing pharmacologic interventions will only | delay progression of symptoms |
| multiple sclerosis can be caused by | Progressive demyelination of the neurons in the brain spinal cord and cranial nerves - autoimmune Loss of myelin interferes with conduction of impulses in affected fibers |
| MS may affect | motor, sensory and autonomic fibers |
| MS occurs in | diffuse patches in the NS |
| 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 of MS causes | additional areas of the CNS to become affected |
| MS onset | between 20-40 |
| MS causes | unknown |
| MS has a | genetic tendency |
| signs and symptoms of MS | manifestation determined by area of demyelination |
| diagnostic test of MS | MRI |
| treatment of MS | no definitive treatment |
| parkinson disease (PD) is an | idiopathic, chronic, progressive degenerative disorder of the CNS |
| PD has | motor, nonmotor, and neuropsychiatric manifestations |
| PD affects | individuals over 50, male |
| PD is the | second most common neurodegenerative disorder |
| parkinsonism symptoms | tremors, bradykinesia, rigidity, postural instability |
| PD conditions that cause secondary parkinsonism | Head trauma Toxins Metabolic disorders Infections Multiple strokes in basal ganglia Atypical antipsychotics and antiemetics |
| decreased risk for PD | Cigarette smoking, caffeine intake High blood urate levels |
| pathogenic mechanisms | proteolytic stress, oxidative stress, mitchondrial dysfunction, inflammation |
| proteolytic stress | accumulation and aggregation of proteins, lewy bodies |
| oxidative stress | Generation of ROS Depletion of glutathione; increase in iron levels |
| mitochondrial dysfunction | Decreased mitochondrial complex activity (by 30-40%) |
| inflammation | Overactivation of microglia Excess production of neurotoxic factors |
| CMs of PD | insidious onset motor features nonmotor features |
| motor features of PD | tremor - pill rolling resting tremor of hand, tremor of lips, chin, jaw, tongue, legs rigidity from increased muscle stiffness and tone cogwheelings bradykinesia postural instability |
| nonmotor features of PD | Fatigue, sleep disturbances Olfactory dysfunction Pain Autonomic dysfunction Neuropsychiatric symptoms |
| neuropsychiatric symptoms of PD | Cognitive dysfunction, dementia, psychosis, hallucinations Mood disorders, depression, anxiety |
| treatment of PD | Pharmacologic replenishment with dopaminergic drugs Deep brain stimulation Complementary and supportive therapies |
| huntington disease (HD) is | progressive, incurable, degenerative disease of brain |
| HD is inherited | autosomal dominantly |
| HD causes | uncontrolled involuntary movements; dementia; and behavior changes |
| HD onset of symptoms | ages 35-44 years |
| duration of HD symptoms | mean of 19 years |
| primary causes of death in HD | pneumonia and cardiovascular disease |
| pathology of HD | 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) |
| etiology and pathogenesis | Mutation in huntington gene (HTT) on short arm of chromosome 4 |
| caudate atrophy seen in | HD |
| CMs of HD | involuntary movements, cognitive impairments, behavioral changes |
| HD involuntary movements | Parkinsonian features Akinetic-rigid syndrome Dysarthria (problem with speech) Dysphagia (problem with swallowing) Abnormal eye movements Tics |
| HD cognitive impairments | Short term memory loss Impaired intellectual function Dementia Psychiatric manifestations |
| HD behavioral changes | Irritability, moodiness, depression, OCD Untidiness Antisocial behavior Apathy |
| diagnosis of HD | Genetically proven family history Clinical presentation MRI or CT scan measure brain atrophy Referral to neurologist who specializes in HD |
| treatment of HD | Reduce symptoms and improve quality of life |
| amyotrophic lateral sclerosis (ALS) is a | progressive, neurodegenerative disease |
| ALS causes | weakness, disability and death within 3-5 years |
| ALS is aka | lou gehrig's disease |
| neurodegeneration of ALS | upper motor neurons in corticospinal tract lower motor neurons in anterior horn cells of spinal cord |
| 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 wallerian degeneration |
| pathways that lead to axonal degeneration and cell death in ALS | Oxidative stress Mitochondrial dysfunction Defect of axonal transport Abnormal growth factor expression Excitotoxicity |
| CMs of ALS | Insidious onset Slowly 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 CMs |
| diagnostic tests of ALS | Electromyography Nerve conduction studies MRI or CT scan of brain and spinal cord Muscle or nerve biopsy Genetic Blood tests |
| seizure activity happens due to | abnormal electrical discharges within brain |
| seizure activity results in | involuntary movement and/or behavior and sensory alterations |
| involuntary movements due to seizure activity | may encompass entire body or just certain muscle groups |
| seizure activity causes changes in | level consciousness, behavior or sensory perception |
| CMs of seizure disorders | Loss of conscious awareness of environment Varying patterns of muscular rigidity and relaxation Aura |
| phases of generalized seizures | tonic phase, clonic phase, postical period |
| tonic phase lasts | 15-60 seconds |
| tonic phase includes | Muscular rigidity Sudden loss of consciousness Pupils fixed dilated Increased metabolic demands Hypoxia - skin pallor and cyanosis Urinary and bowel incontinence |
| clonic phase lasts | 60-90 seconds |
| clonic phase includes | Alternating muscular contraction and relaxation in extremities Hyperventilation Eyes roll back, froth and mouth |
| postical period | Decreased level of consciousness; sleepy Quiet and relaxed breathing Gradual regaining of consciousness |
| CMs of status epilepticus | Life threatening conditions Enhanced and sustained electrical activity over 30 minutes Increased neuronal excitation with reduced inhibition |
| diagnosis of seizure disorders | laboratory tests, EEG, lead level, toxicology screening, CT scan or MRI and angiography |
| laboratory tests for seizure disorders | Complete blood cell count Blood chemistry Urine culture Lumbar puncture |
| treatment for seizure disorders | antiseizure medications, surgical intervention |
Created by:
leh195