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Spinal C disorder

Peripheral Nervous and Sys and Spinal Cord disorders

QuestionAnswer
Myasthenia Gravis autoimmune disease which affects the neuromusclar junctions
Myasthenia Gravis causes? fluctuating weakness of certain skeletal muscle groups
How does Myasthenia Gravis work? autoimmune process, antibodies attack Ach (acetylcholine) receptors, which then decrease # of receptors at neuromusclar jcn, prevents Ach molecules from attaching and stimulating muscle contraction
causes of Myasthenia Gravis coexisting autoimmune disorder, strong association with hyperthyroidism, hyperplasia of the thymus gland
Clinical Manifestations and Complications of Myasthenia Gravis decrease ability to move eyes and eyelids, decrease chewing ability, decrease ability to swallow, decreased abilty to speak, decreased ability to breath
Cholinergic Crisis Occurs with overdose of anticholinesterase drugs (too much cholinesterase inhibition ), S/S: muscle fasciculation(rapid twitching motion), sweating, increased salivation constricted pupils. Have atropine (choinergic antagonist) avai
What counteracts cholinergic crisis? atropine
Guillain Barre form of polyneuritis, acute, rapid progression, thought to be autoimmune disorder, potentially fatal.
how does Guillain Barre work? immune response involving peripheral nerves. the syndrome occurs after stimuli attck the immune sys. T-cells become sensitize to myelin, loss of myelin, edema and inflammation of affected nerves
clinical manifestations of Guillain Barre weakness of lower extremities, parasthesia, paralysis, hypotonia, areflexia, altered sensory preception:pain tingling
Complications of Guillain Barre RESPIRATORY FAILURE (Paralysis in GB is ascending), respiratory infections may need intubation and ventilation, UTI, immobility can cause: paralytic ilius, muscle atrophy, DVT, PE, skin breakdown
how to diagnose Guillain Barre history & clinical signs, EMG (electromyography) and nerve conduction, studies show greatly decreased velocity. White cell count - leukocytosis and LP (lumbar puncture) - CSF has increased protein without increased in cell count
therapies of Guillain Barre Plasmapheresis - remove antibodies that been form, and high dose of IV immunoglobulins
Multiple Sclerosis (MS) cause unknown, autoimmune process (t cells become activated and migrate to CNS and disrupt BBB ( blood brain barrier), antigen antibody rxn triggers inflammatory response and then demyelination of axons. plaque forms & its scattered throughout CNS
clinical manifestations of Multiple Sclerosis (MS) motor s/s - weakness or paralysis of lumbs, trun or head, diplopia (double vision), spasticity of affected muscles. Sensory sysmptoms - numbness tinlging, scotomas, blurred visions, vertigo, tinnitis, decreased hearing, chronic neuropathic pain,
drug therapy for Multiple Sclerosis (MS) immunosupressove agemts redice freq of relapse (azathioprine, cyclosporin (also used for antirejection agent for tranplant agents)
drug therapy for Multiple Sclerosis (MS)cont corticosteroids to reduce inflmmations in acute exacerbations (prednisone)
drug therapy for Multiple Sclerosis (MS)cont antispasmodics (dantroline, baclofen)
drug therapy for Multiple Sclerosis (MS)cont anticonvulsants for parasthesia (tegratol)
drug therapy for Multiple Sclerosis (MS)cont eta blocker for tremors (primidone, clonazepam (antiseizure med)
drug therapy for Multiple Sclerosis (MS)cont immunomodulators for exacerbations (interferon (cancer))
drug therapy for Multiple Sclerosis (MS)cont anticholinergics for bladder problems (propantheline)
Amyotropic lateral sclerosis, Lou Gherigs Disease cause unknown, degernations and loss of motor neurons in brain and spinal cord - dead motor neurons = no transport of signals to muscles
Course of Amyotropic lateral sclerosis, Lou Gherigs Disease gradual progressive death of motor neurons, muscle wasting, pralysis, death within 2-5 years
Clinical Manifestations of Amyotropic lateral sclerosis, Lou Gherigs Disease weakness of upper extremities, dysarthria, dysphagia, muscle wasting
Diagnostic Procedures for Amyotropic lateral sclerosis, Lou Gherigs Disease Creatine Kinase level is elevated, and EMG (electromyography) shows muscle fasciculation
Drug therapy for Amyotropic lateral sclerosis, Lou Gherigs Disease Riluzole - mechanism is unknown, but it extends survival time, also ntispasmodics:baclofen, dantrolene, and diazepam.
Created by: starr8904
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