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Spinal C disorder
Peripheral Nervous and Sys and Spinal Cord disorders
Question | Answer |
---|---|
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. |