Busy. Please wait.

show password
Forgot Password?

Don't have an account?  Sign up 

Username is available taken
show password


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.
We do not share your email address with others. It is only used to allow you to reset your password. For details read our Privacy Policy and Terms of Service.

Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.

Remove ads
Don't know
remaining cards
To flip the current card, click it or press the Spacebar key.  To move the current card to one of the three colored boxes, click on the box.  You may also press the UP ARROW key to move the card to the "Know" box, the DOWN ARROW key to move the card to the "Don't know" box, or the RIGHT ARROW key to move the card to the Remaining box.  You may also click on the card displayed in any of the three boxes to bring that card back to the center.

Pass complete!

"Know" box contains:
Time elapsed:
restart all cards

Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how



Multiple Sclerosis Autoimmune disorder causing demyelination of the white matter anywhere in CNS - spares peripheral nerves Life expectancy - 35 yrs post dx. Patho:Optic nerves,Chiasm and tracts,Cerebrum,Brain stem,Cerebellum,Spinal cord.
Multiple Sclerosis Clinical Manifestations Diplopia Nystagmus Scanning speech Muscle weakness Muscle spasms Paralysis Gait/coordination problems Paresthesias
MS Diagnosis CT- plaques MRI - 2 lesions Elevated immunoglobulin’s in CSF (IgG)
MS Treatment (No cure) Immunosuppressive agents Corticosteroids Anti-spasmodics to decrease spasticity Plasmapheresis
Myasthenia Gravis Deficit of acetylcholine at myoneural junction produces chronic progressive weakness of muscles Autoimmune destruction likely cause Thymus gland frequently enlarged IgG antibody to acetylcholine myoneural junction - diminished transmission
Myasthenia Gravis 2-3X more common in women 20-30 peak age of onset
Myasthenia Gravis Etiology pathophysiology Onset is slow Precipitated by Hormonal disturbances Emotional stress Infections Trauma Medications
Myasthenia Gravis Common Symptoms Speaking, Chewing, Swallowing Problems Fatigue after exercise of muscle group Eye muscle weakness diplopia, ptosis Facial muscle weakness aspiration risk Proximal limb weakness later All muscle weakness is worse with effort and improves with rest.
Myasthenia Gravis Diagnosis Tensilon testing PET scan EEG EMG Blood work History and clinical symptoms
Myasthenia Gravis Treatment Anticholinesterase medications Prostigmin Mestinon Corticosteroids Imuran Cytoxan Thymectomy Plasmapheresis during crisis
Plasmapheresis (plasma exchange) Removal of patients plasma and plasma components Produces a temporary reduction in the antibodies Does not treat the underlying abnormality
Myasthenia Gravis Life Threatening Complications Myasthenia Crisis Undiagnosed or under medicated Stress or infection Severe muscle weakness - respiratory insufficiency Tensilon will improve symptoms
Cholinergic Crisis Too much medication N&V, diarrhea, cramps hypotension Tensilon to distinguish from Myasthenia Crisis Atropine to reverse Respiratory support may be needed
Myasthenia Gravis Patient Education Avoid extreme temperatures Avoid exposure to infections Avoid emotional stress Avoid medications that could precipitate an exacerbation Signs and symptoms of crisis
Myasthenia Gravis Adequate nutrition Peak muscle strength while eating Frequent small meals Soft/semisolid IV fluids Enteral feedings
Parkinson’s disease Etiology pathophysiology Basal ganglia disorder of dopamine deficiency is most common origin May result from head trauma, medications, post encephalitis Dopamine decreases, acetylcholine no longer inhibited
Parkinson’s disease Clinical Manifestations Tremors Rigidity Bradykinesia Gait disturbances Postural disturbances Heat intolerance Urinary retention Constipation Dysphagia Depression Sleep disorders Cognitive disorders Memory deficits Personality changes Psychosis Acute confusio
Parkinson’s disease Complications Respiratory tract infections Urinary tract infections Skin breakdown Falls Adverse affects of medications
Parkinson’s Treatment Levodopa is most common Dopamine replacement Antiparkinsons/antiviral agent MAO inhibitor- inhibits dopamine metabolism Anticholinergic medications for tremor Stereotactic procedures
Amyotrophic Lateral Sclerosis (ALS) Loss of motor neurons in the spinal cord and brain stem Death of nerve cells Atrophic changes of muscle fibers Autoimmune disease (theory)Free radical damage (theory)Cell injury and neuronal degeneration (theory)
Amyotrophic Lateral Sclerosis (ALS) Disease progression Peak onset 40-50; M/F ratio 3/2 Strong evidence to support genetic component Progressive loss of motor function Intelligence & sensation remain intact! Total supportive care No cure
Amyotrophic Lateral Sclerosis (ALS) Supportive care Treat symptoms NG tubes Mechanical ventilation EOL counseling
Spinal Cord Injury (SCI) “Think first, SCI are forever.” Mechanisms of injury hyperextension - acceleration/deceleration hyperflexion - neck propelled forward Axial compression - force down from top Flexion-rotation - shearing plus accel/decel
Spinal Cord Injury (SCI) Fractures may or may not be present Subluxation = atlas, axis dislocation (C1, C2)
Degree of Injury Complete cord involvement Results in total loss of sensory and motor function below level of lesion (injury) Incomplete (partial) cord involvement Results in a mixed loss of voluntary motor activity and sensation and leaves some tracts intact
Terminology of SCI Quadriplegia (4) and Paraplegia (2) Cord concussion - temporary disruption Cord contusion - bruising, temporary Cord compression – pressure; need surgery Laceration - tearing Transection - severing
Spinal Shock Temporary neurologic syndrome Reflexes Loss of sensation Flaccid paralysis below level of injury
Neurogenic Shock Loss of vasomotor tone caused by injury Loss of sympathetic nervous system innervation causes Peripheral vasodilation Venous pooling ↓ Cardiac output
Clinical Manifestations of SCI Autonomic Hyperreflexia (Dysreflexia) Sudden massive uncompensated CV response to stimulation of SNS: severe hypertension Life threatening
Diagnosis of SCI X-ray CT scan MRI
Treatment of SCI Immobilization Decompression and surgical fixation Steroids Nutrition Respiratory support Skin, bowel and bladder management Life time rehabilitation program
Clinical Manifestations Immediate post injury problems include Maintaining a patent airway Adequate ventilation Adequate circulating blood volume Preventing extension of cord damage (secondary damage)
Clinical Manifestations Respiratory System Respiratory complications closely correspond to level of injury
Clinical Manifestations Respiratory System Cervical and thoracic injuries cause paralysis of Abdominal muscles Intercostal muscles Patient cannot cough effectively Leads to atelectasis or pneumonia
Clinical Manifestations Urinary System Urinary retention common Bladder is atonic and over distended
Clinical Manifestations Gastrointestinal System njury level above T5, primary GI problems related to hypomotility Injury level of T12 or below neurogenic bowel
Clinical Manifestations Integumentary System Consequence of lack of movement is skin breakdown Pressure ulcers can occur quickly Can lead to major infection or sepsis
Clinical Manifestations Thermoregulation Poikilothermism Adjustment of body temp to room temp.Occurs in spinal cord injuries bc sympathetic nervous system interruption prevents peripheral temp sensations from reaching hypothalamus.
Clinical Manifestations Thermoregulation Don’t forget health promotion,disease prevention,&patient education!
Cranial Nerve Disorders Bell’s palsy (CN VII) Unilateral paralysis of the facial muscles Trigeminal neuralgia (CN V) Chronic disease Severe facial pain
Etiology Pathophysiology Cranial Nerve Disorders Inflammation Infection Viral
Clinical Manifestations Trigeminal neuralgia Pain
Clinical Manifestations Bell’s palsy One-sided facial paralysis Loss of corneal reflex Loss or impairment of taste Increased tearing from lacrimal gland
Treatment Trigeminal neuralgia Anticonvulsants—Tegretol, Dilantin Microvascular decompression Rhizotomy
Treatment Bell’s Palsy Corticosteroids—prednisone Antivirals Eye patch/protective glasses
Created by: LauraHall