M.S lecture from sir Pañgan


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  • M.S lecture from sir Pañgan

    1. 1. Gerontological Nursing COGNITIVE AND NEUROLOGICAL FUNCTION Jose Karlo M. Pañgan,RN, MAN ` Week NINE
    2. 2. CENTRAL NERVOUS SYSTEM (CNS) Brain Spinal CordPERIPHERAL NERVOUS SYSTEM Cranial Nerves Spinal Nerves Somatic Nervous System Autonomic Nervous System Reflex Arc
    3. 3. NeuronShrinkage in neuron size and gradual decrease in neuron numbers.Structural changes in dendrites.Deposits of lipofuscin granules, neuritic plaque and neurofibrillary bodies within cytoplasm and neuron.Loss of myelin and decreased conduction
    4. 4. Changes in precursors necessary for neurotransmitter synthesis.Change in receptor sites.Alteration in enzymes that synthesize and degrade neurotransmittersSignificant decrease in neurotransmitter.
    5. 5. MotorMuscular atrophy – decrease in muscle bulkDecrease in electrical conduction system
    6. 6. Decrease in electrical conductionAtrophy of taste budsAlteration in olfactory nerve fibersAlteration in nerve cells of vestibular system of inner ear, cerebellum, and proprioception.
    7. 7. Altered electrical conduction of the nerve due to myelin lossAltered reflexes response (ankle, superficial reflexes
    8. 8. Disruption of stage 3 and 4 of the sleep cycle
    10. 10. Slowing of autonomic nervous system response as a result of structural changes in basal ganglia.
    11. 11. Reduction in the turnover of CSF.
    12. 12. Most common mental disorder in the older adults.Between the ages of 80 and 84, 17% of men and 22% of women have severe depression.By age 85, the percentage of older persons with depressive symptoms equalizes.Not a normal consequence of aging.A significant risk for suicide.
    13. 13. Changes in feelings or mood, described as feeling sad, hopeless, pessimistic or “blue” lasting most of the day.Fatigue, constipation, psy chomotor retardation, depressed mood, loss of interest, energy, libido or pleasure, changes in appetite, weight and sleeping pattern.
    14. 14. Common response to serious illness of any kind (MS, hypothyroidism, SLE, Hepatitis, AIDS, anem ia)Drugs (Amphetamines, analgesics, narcotics, anti HPN, anti-microbials, anti-Neoplastics, anti- parkinsonian, barbiturates, benzodiazepines, dig oxin, hypoglycemics, phenothizides, steroids, sul fonamides)
    15. 15. PSEUDODEMENTIA – depression masquerading as DEMENTIAPSEUDODELIRIUM – term used when an older adult is seem to be with an acute confusion found to be due to depression.
    16. 16. Anti-depressants  Trazodone  First line of treatment  Mild to moderate agitation  25-50 mg  SSRI  Paroxetine (Paxil), Sertraline (Zoloft), and Fluoxetine (Prozac) – agitation.  Benzodiazepine – reserved for acute conditions  Lorazepam (Ativan) – 0.25 mg to 1 mg orally or IM  Oxazepam – 5-10 mg  Buspirone – anxiety triggered agitation  Anti-epileptic Or Anti-convulsants  Carbamazepine (tegretol) 4-8 mcg/ml  Valproic acid
    17. 17. Transient, organic mental syndrome characterized by reduced level of consciousness, reduc ed ability to maintain attention, perceptua l disturbances and memory impairment.
    18. 18. ONSET: Short (hours to days)LOCATION: occur in all areas (frequently precipitates hospital admission)RISK FACTORS: Advanced age, CNS diseases, infection, polypharma cy, GIT, GUT, CPD sensory changes
    19. 19.  Medical conditions that causes DeliriumIN THE BRAIN – stroke, trauma, meningi tis, and vascular disorder.OUT THE BRAIN – endocrine dysfunction, organ failure, infections, meta bolic disorders, shock, burns, dehydration, and nutritional deficiency.
    20. 20. MEDICATIONSIN THE BODY – opiates, anticholinergic medications, steroids, p sychoactive drugs, OTC cold drug preparations.OUT THE BODY – alcohol withdrawal, steroid withdrawal, SSRI withdrawal.
    21. 21. Change: Recent onset and fluctuate during the course of the day.Difficulty maintaining concentration or attention to external stimuliLanguage disturbance (slurred, forced or rambling speech)Disorganized thinking (tangenital reasoning and conversation)Disturbances of consciousness.Change in cognition
    22. 22. Early assessment Delirium rating scale Delirium symptom interview Identification of risk factors Delirium, visual impairments, severe illness, cognitive impairments and high BUN and Creatinine.
    23. 23.  NON-PHARMACOLOGIC INTERVENTION  Removing bladder catheters  Improving nutritional intake  Providing reality orientation PHARMACOLOGIC  Decreasing sensory overstimulation or deprivation AND NON PHARMACOLOGIC  Reassuring the older adult and his or her family members. INTERVENTIONS PHARMACOLOGIC  Agitations and hallucination – Haloperidol  Alcohol withdrawal symptoms – benzodiazepines
    24. 24. Is a syndrome of gradual and progressive cognitive declineAlteration in memoryCharacterized by a loss of cognition and at least one of the following  Ability to speak coherently and understand language (APHASIA)  Ability to recognize or identify objects (AGNOSIA)  Ability to execute motor activities (APRAXIA)  Ability to think abstractly, make sound judgment, and plan and carry out complex tasks
    25. 25. Phenomenon that occurs when other pathologic condition masquerade as dementia.Medications, ethyl alcohol intoxication or withdrawal, metabolic disorders (thyroid disorders, Vitamin B12, hyponatremia, hypercalcemi a, hepatic and renal dysfunction) depression, delirium, CNS neoplasms, chronic subdural hematoma, normal pressure hydrocephalus.
    26. 26. Progressive neurodegenerative disease characterized by the presence of neurofibrillary tangles composed of misplaced proteins within the brain, cortical amyloid plaques, and granulovascular degeneration of neurons in the pyramidal cell layer of the hippocampus.
    27. 27. GeneticsViralAgeHead injuryEnvironmental exposuresNutritional factors
    28. 28. Individual’s repeated questions and statementsForgetfulnessIncreasing problem with orientation and geographic disorientationMemory lossLanguage deteriorationImpaired ability to mentally manipulate visual informationPoor judgmentConfusionRestlessnessMood swingsPersonality changes
    29. 29. MRIPET
    30. 30. No cure for ADCognex  Cholinesterase inhibitors  Monitor the patient’s liverDonepezil (Aricept)RivastigmineGalantamine (Reminyl)Gingko Biloba – herbal plant extract  Enhances the cognitive performance  Vitamin supplementation
    31. 31. Preserving the dignity and promoting independenceMaintaining the cognitive and global function early in the disease process.
    32. 32. Loss of cognitive function resulting from ischemic, hypoperfusive or hemorrhagic brain lesions from a CVDAbrupt onset of dementiaMulti infarct dementia (Multiple strokes in CT or MRI present)Focal neurological findingsLow-density areas indicate vascular changes in white matterUnchanged personalityEmotional problem
    33. 33. Arteriosclerosis, blood dyscrasias, cardiac decompensation, hypert ension, atrial fibrillation, cardiac valve replacement, systemic emboli.
    34. 34. Symptoms depends on the location of the infarct  Impaired learning and impaired retention of new information  Impaired handling new tasks  Impaired reasoning ability  Impaired spatial ability and orientation  Impaired language.
    35. 35. CT Scan and MRI
    36. 36. Donepezil – improving cognition and function, clinical global impression and ability to perform ADLs.Nimodipine – short term benefit for VAD
    37. 37.  Clinical features persist over long period of time resulting in severe dementia Lewy bodies and Lewy neuritis found in brain structures  Found in the Lewy brainstem, diencephalon, basal ganglia and cerebral cortex body  Lewy bodies : are abnormal dementia aggregates of protein that develop inside nerve cells in Parkinsons disease (PD) and Alzheimers disease (AD) and some other disorders.
    38. 38. advanced ageDepressionconfusion or psychosis while taking levodopa,facial masking of individuals with PD
    39. 39. Prominent fluctuations in attention and ability to communicate.More visual-spatial processing impairments and Clinical subcortical dementia. manifestations:EPS: rigidity, bradykinesia, flexed posture, shuffling gait.
    40. 40. Symptomatic reliefCholinesterase MANAGEMENT: inhibitors
    41. 41. Presence of frontal brain Fronto-temporal area atrophy in lobe dementia CT or MRI
    42. 42. Clinical Manifestations: Frontal or aphasic variants – changes in personality and social cognition, disinhibition s, loss of Diagnostics – CT empathy, changes in scan or MRI eating pattern, stereotypic behavior. Fluent or non fluent aphasia.
    43. 43. Management 3-10 years No specific treatment
    44. 44. Assessment Glasgow coma scale Mental status examination Pupil examination Neurologic assessment Behavioral assessment
    45. 45. Individualized care for each patientsMonitor and maintain physical healthAdapt the environmentCommunicate in a simple, direct mannerProvide cues for reality orientationMaintain social interaction and self esteem.
    46. 46. Sundowning syndromeWanderingParanoia and suspiciousnessHallucinations and DelusionsCatastrophic ReactionsResources
    47. 47. Primary cause: UnknownOther causes: viral infection, disequilib rium between dopamine and acetylcholine, ence phalitis, arterioscler osis, and carbon monoxide poisoning, stroke, i nfections.
    48. 48. Tremors pillrolling tremors Resting tremorsCogwheel rigidityBradykinesia, AkinesiaPropulsive gait ( begins walking, then starts running forward unable to stop until he or she falls or runs into something.)Festinating gait ( small steps)Retropulsion ( walking and falling backward)
    49. 49. Freezing (a phenomenon where the individual appears to be glued to the floor.)Mask like facial expression (flat affect)Emotional lability, depressionFatigueSoft, monotonous voiceShaky small handwritingExcessive sweating, seborrhea, lacri mation, constipation, decre ased sexual activity.
    50. 50. Diagnostics EEG Symptoms improve with antiparkinsonian drugs
    51. 51. Aimed: relieving clinical manifestations, increasing individual’s ability to perform ADL’s and decreasing the risk for injury.MEDICATIONS Anticholinergics Cogentin (Benztropine) Akineton (Biperiden) Artane (Trihexyphenidyl)  MAO  Dopaminergics
    52. 52.  Monitor v/s, urine output and bowel sounds Observe for involuntary movements Advise the client to avoid Nursing alcohol, cigarette, caffeine and aspirin. Intervention for Prevent and relieve side effects: the  Dry mouth : hard candy, ice pharmacologic chips, sugarless chewing gum  Photophobia: sunglasses management:  Urinary retention: void before taking the drug  Increased intraocular pressure: routine eye examinations
    53. 53.  Levodopa Carbidopa with Levodopa (Sinemet) Nursing Interventions:  Side effect: Orthostatic Hypotension  Monitor client’s vital signs and ECG  Check for weakness, dizziness or syncope.  Advise the client to practice gradual change of position.  Reddish brown urine and perspiration  Harmless but clothes may be stained.  Impaired voluntary movement – takes weeks or months to be controlled.
    54. 54.  Symmetrel (Amantadine HCL) - dopaminergic Parlodel (Bromocriptine Mesylate) Requip (Ropinizole HCL) Nursing Interventions:  Report signs of skin lesion, seizure or depression.  Report lightedness when changing positions.  Avoid alcohol  Advise the client not to abruptly stop the drug without notifying the health care provider.
    55. 55. Ablation (destruction)Deep brain stimulationTransplantation
    56. 56.  Provide a safe environment Provide measures to increase mobility:  Physical therapy, Assistive devices Encourage independence in self care activities. Improve communication abilities. Maintain Adequate Nutrition Avoid constipation and maintain adequate bowel elimination.
    57. 57. VisionLose of tone of the eye lids and become lax – ptosis of the eyelids, redundancy of the skin, and malposition of the eyelids.Conjunctiva – thins and yellow in appearance.
    58. 58. Sclera – develop brown spots  Arcus senilis – surrounding rings made up of fat deposits at the cornea.  Pupil – decrease in size and loses some of its ability to constrict.  Limit the amount of light entering the eye.Lens – increases in rigidity and density affecting the eye’s ability to transmit and focus light.
    59. 59. Peripheral vision decreases, night vision diminishes and sensitivity to glare increases.Difficulty in identifying cool colors: blue, green and violet.Vitreous humor loses transparency and increases the scattering of light. (causes Floaters- dots, wigly lines or clouds)Flashers – jagged lines; vit. Fluid rubs eyes or pulls retina.
    60. 60. Decline in the visual acuity Presbyopia – inability to focus nearby objects.
    61. 61. Group of degenerative eye diseases in which the optic nerve is damaged by high intraocular pressure (IOP) resulting in blindness due to nerve atrophy.
    62. 62. Race (African Americans, Asian American and Alaska Natives)eye traumasmall corneasmall anterior chamberFamily historyCataractsSome Medications
    63. 63. Cause: Unknown, results from a papillary blockage that limits the flow of aqueous humor causing an increase in IOP.
    64. 64. More common, occurs gradually.90% of all primary glaucomaDegenerative changes in Schlemm’s canal obstruct the escape of aqueous humor.
    65. 65. Peripheral vision loss gradually and painlesslyTired eyesSeing Halos around lightsWorse symptoms experience in the morning.
    66. 66. Symptoms associated with StressMedical emergency and the patient should seek emergency help immediately. Severe eye pain in one eye red eye Blurred vision Nausea and Vomiting Seeing colored halos around the lights Bradycardia Pupil dilation Steamy appearance of cornea
    67. 67. When drainage angle is damage by eye injury or other specific conditions.Medications (steroids), tumors, in flammation, or abnormal blood vessels.
    68. 68. Diagnosis: Gonioscopy – direct exam Tonometer – to measure IOP (Normal : 10-21 mmHg)
    69. 69. Aimed to reduce IOP.MedicationsSurgery: Iridectomy for Acute Glaucoma Treatment TrabeculoplastyChronic Glaucoma – Medications and eyedropsConcern: Safety
    70. 70.  Medical follow-up and eye medication will be required for the rest of your life. Eyedrops must be continued as long as prescribed, even the absence of symptoms Avoid driving 1-2 hours after the administration of miotics Prevent complications Bright lights and darkness are not harmful There is no apparent relationship between the vascular hypertension and ocular hypertension. Report any reappearance of symptoms Avoid the use of mydriatric or cyclopegic drugs. (atropine)
    71. 71. Clouding of the normally clear and transparent lens of the eyes.Cause by Oxidative damage to lens proteins that occurs with aging.  Other causes:  Heredity  diabetes  poor nutrition  hypertension  excessive exposure to sunlight  cigarette smoking  high alcohol intake  Eye trauma.
    72. 72. Senile Cataract – due to normal aging process as early as 40Traumatic Cataract Types of – hard Cataract blow, puncture, cut or burn.Secondary
    73. 73. With gradual loss of vision (blurred, misty or dimmed) Complaints of being fuzzy, sensitive to glare and halo-effect around lights.No pain or discomfortDecrease night visionYellowing of the lens.trouble distinguishing colorsPupil changed into cloudy white.Decreased visual acuity.Recurrent eyeglass prescription changes.
    74. 74. Improved visual acuity, depth perception.Complications: Surgery retinal detachment, in fection and macular edema.
    75. 75. Avoid rubbing or pressing on the eye.Avoid bending at the waist or lifting heavy objects for at least 1 ACTIVITIES month NOT TO DOAvoid straining with AFTER A bowel movements CATARACTAvoid taking showers SURGERY and shampooing hair for specified time as instructed.Limit reading.
    76. 76. Sleep on back or unaffected side.Apply metal eye shield at night.Wear glasses indoorsProper handwashing
    77. 77. Most common cause of blindness for those over age 60.Damage or breakdown of the macula and subsequent loss of central vision due to Macular Degeneration.
    78. 78. Dry (Nonexudative) – involutional macular degeneration. Breaking down or thinning of macular tissue related to the aging process. Types: Gradual vision loss.Wet (exudative) – rapid and severe vision loss. Abnormal blood vessels form and hemorrhage.
    79. 79. Difficulty performing tasks (reading and sewing)Decreased central visionSeeing images are Signs and distorted Symptoms:Decreased color vision (colors look dim)Central Scotoma (sometimes)
    80. 80. Photodynamic Therapy – a special laser to seal leaking blood vessels.Retinal Cell TransplantationMedications: Treatment Ranibizumab (Lucentis) Bevacizumaba Pegaptanib
    81. 81. Auricle – becomes elongated, with a wrinkled appearance.Auditory canals – narrowsHairs lining the canal becomes coarser and stiffer.Cerumen glands atrophyTympanic membrane – dull, retracted and gray appearance.Degeneration of the ossicular joints in the middle earDecreased vestibular sensitivity.
    82. 82. Age related balance decline Decreased sensory input, slowing of motor responses and musculoskeletal limitations.
    83. 83. Reversible, overlooked cause of conductive hearing loss.Cause: physiologic changes with aging – atrophic changes in the Cerumen sebaceous and apocrine Impaction glands.Impaired communication – social isolation and depression.
    84. 84. Hearing loss, feeling of fullness in the ear, itching and tinnitus.Intervention Read the protocol for cerumen removal page 740
    85. 85. Is the annoying combination of both conductive and sensorineural hearing loss.Subjective sensation in the ear, defined as the ringing, buzzing or hissing.Cause: noise, toxins, cochlear nerve and age related changes in the organs of hearing.
    86. 86. SubjectiveObjective – rareUnilateral – associated with more serious diseases (Meniere’s disease)
    87. 87. Treat the correctable problems.Softening loud sounds through improved acousticUse a protective ear plugsAvoid ototoxic substances (foods, drugs)
    88. 88. sensorineural hearing lossThe most common form of hearing loss in older adult.Bilateral, difficulty hearing high pitched tones and conversational speech.
    89. 89. Increasing volume on television or radio.Tilting head toward the person speakingCupping hand around the ear.Watching the speaker’s lipsSpeaking loudlyNot responding when spoken to
    90. 90. Focus on aural rehabilitation and facilitation of communication.Aural rehabilitation Auditory training speech and reading training hearing aids.
    91. 91. should not be considered as a normal part of aging.Benign paroxysmal positional vertigo (BPPV) – severe episodes of vertigo precipitated by a particular change in head position.Ampullary dysequilibrium – vertigo or disequilibrium associated with rotational head movements.
    92. 92. Macular disequilibrium – vertigo precipitated by a change of head position in relation to the direction of gravitational force.Vesicular ataxia of aging – constant feeling of imbalance with ambulation.Meniere’s disease – an uncommon disease seen most often in older women, characterized with severe vertigo accompanied and usually preceded by tinnitus and progressive low frequency sensorineural hearing loss.
    93. 93. Pharmacological treatment Anti-vertiginous drugs Meclizine (antivert) Diphenhydramine (Benadryl) May cause drowsiness, avoid alcoholic beverages Diuretic Hydrochlorothiazide (Hydrodiuril) Remove the excess endolymph fluid
    94. 94. No complete cureMeasures to reduce dizziness Move slowly Avoid bright glaring Nursing lights (quiet darkened interventions room is preferred) For Vertigo If vertigo occurs during ambulation lie down immediately and hold the head still.