Client with Alzheimers Disease Form of dementia characterized by progressive, irreversible deterioration of general intellectual functioning Begins with

h memory loss, initially subtle until progresses to being more noticeable; course includes deteriorating cognition and judgment with eventual physical decline and total inability to perform ADL Risk factors older age female family history Exact cause is unknown; theories include loss of transmitter stimulation, genetic defects, viral and autoimmune cases Warning signs include Memory loss affecting ability to function in job Difficulty with familiar tasks Problems with language, abstract thinking Disorientation, changes in mood and personality Types and Changes in brain Familial (follows inheritance pattern) and sporadic Early-onset (<65) Older-onset (>65) Loss of nerve cells and presence of neurofibrillary tangles and amyloid plaques Progressive brain atrophy Manifestations : Stage I Appears healthy and alert Cognitive deficits are undetected Subtle memory lapses, personality changes Seems restless, forgetful, uncoordinated Stage II Memory deficits more apparent Less able to behave spontaneously Wandering behavior, deterioration in orientation to time and place Changes in sleeping patterns, agitation, stress Trouble with simple decisions Sundowning: increased agitation, wandering, disorientation in afternoon and evening hours Echolalia, scanning speech, total aphasia at times, apraxia, astereognosis, inability to write Becomes frustrated and depressed

Stage III Increasing dependence with inability to communicate, loss of continence Progressive loss of cognitive abilities, falls, delusion, paranoid reactions Average life expectancy is 7 years from diagnosis to death, often from pneumonia, secondary to aspiration Collaborative Care No cure Supportive care for client and family Diagnostic Tests Diagnosis by ruling out other conditions including depression, hypothyroidism, infection, stroke EEG shows slow pattern in later stages of disease MRI and CT scan: shrinkage of hippocanthus Positron emission tomography (PET):visualizes brain activity and interactions Folstein Mini-Mental Status: instrument reflecting loss of memory and cognitive skills Medications Cholinesterase inhibitors used to treat mild to moderate dementia Tacrine hydrochloride (Cognex) Donepezil hydrochloride (Aricept) Rivastigmine (Exelon) Medications to treat depressions Tranquilizers for severe agitation

 Thioridazine (Mellaril) Haloperidol (Haldol) Antioxidants: vitamin E, anti-inflammatory agents, estrogen replacement therapy in women Complementary Therapy Massage, herbs, ginko biloba, Coenzyme Q10 Art therapy, music, dance Nursing Care &Health Promotion Intensive, supportive nursing interventions directed at physical and psychosocial responses to illness Maintain functional abilities Maintain safety of client and caregiver Nursing Diagnoses Impaired Memory Include written or verbal reminders Use cues to deal with memory loss Chronic Confusion Anxiety Hopelessness Caregiver Role Strain Client with Multiple Sclerosis Description Chronic demyelinating disease of CNS associated with abnormal immune response to environmental factor Initial onset followed by total remission making diagnosis difficult Most persons have disease with periods of exacerbations and remissions Progression of disease with increasing loss of function Incidence is highest in young adults (20 40); onset between 20 50 Affects females more than males More common in temperate climates Occurs mainly in Caucasians Pathophysiology Autoimmune response to prior viral infection Inflammation destroys myelin leading to axon dysfunction Myelin sheaths of white matter of spinal cord, brain, optic nerve destroyed in patches called plaques Demyelination slows and distorts nerve conduction resulting in absence of impulse transmission Neurons in spinal cord, brain stem, cerebrum, cerebellum, and optic nerve affected Recurrent demyelination and plaque formation result in scarring of glia and degeneration of axons Disease follows different courses, most common is the relapsing-remitting type Stressors trigger MS: febrile states, pregnancy, physical exertion and fatigue; and these also can trigger relapses Manifestations Fatigue Optic nerve involvement: blurred vision, haziness Brain stem involvement: nystagmus, dysarthria (scanning speech), cognitive dysfunctions, vertigo, deafness Weakness, numbness in leg(s), spastic paresis, bladder and bowel dysfunction Cerebellar: nystagmus, ataxia, hyptonia Blindness Collaborative Care Focus is on retaining optimum functioning, limiting disability Diagnostic Tests Neurological exam, careful history Lumbar puncture with CSF analysis: increased number of T lymphocytes; elevated level of immunoglobulin G (IgG) Cerebral, spinal optic nerve MRI: shows multifocal lesions CT scan of brain: changes

 PET: measures brain activity Evoked response testing of visual, auditory, somatosensory impulses show delayed conduction Medications ACTH Glucocorticosteroids Immunosuppressants: azathioprine (Imuran), cyclophosphamide (Cytoxan) Cychophosphamide Antispasmodics to treat muscle spasms Medications to deal with bladder problems: anticholinergics or cholinergics depending on problem experienced by client Rehabilitation Physical therapy to maintain abilities and deal with spasticity Nursing Care Education and support of client dealing with chronic disease with unpredictable course Health Promotion Client needs to develop strategies to deal with fatigue, exacerbations Prevention of respiratory and urinary tract infections Nursing Diagnoses Fatigue Self care deficits Home Care Education Referral to support group and resources Referral to home health agencies when condition requires Bells Palsy Description Disorder of seventh cranial nerve and causes unilateral facial paralysis Occurs between age of 20 60 equally in males and females Cause unknown, but thought to be related to herpes virus Manifestations Numbness, stiffness noticed first Later face appears asymmetric: side of face droops; unable to close eye, wrinkle forehead or pucker lips on one side Lower facial muscles are pulled to one side; appears as if a stroke Prognosis Majority of person recover fully in few weeks to months Some persons have residual paralysis Diagnosis based on physical examination Collaborative Care Corticosteroids are prescribed in some cases but use has been questioned Treatment is supportive Nursing Care Teaching client self-care: prevent injury and maintain nutrition Use of artificial tears, wearing eye patch or taping eye shut at night; wearing sunglasses Soft diet that can be chewed easily, small frequent meals