Chronic Neurological Problems Outline PDF

Gbs MS 1/20/25 2 autoimmune 2 nine parkinson 1 CHRONIC NEUROLOGICAL PROBLEMS D...

Gbs MS 1/20/25 2 autoimmune 2 nine parkinson 1 CHRONIC NEUROLOGICAL PROBLEMS DR. MEGAN LIPPE ALS ADAPTED FROM DR. LARK FORD AND MRS. RUTH JOHNSON 2 OBJECTIVES 1.Differentiate the etiology, diagnostic tests, clinical manifestations, collaborative care, and nursing management of multiple sclerosis, Parkinson's disease, myasthenia gravis, and amyotrophic lateral sclerosis 2.Explain the potential impact of chronic neurological disease on physical and psychological well-being 3.Compare and contrast myasthenic and cholinergic crisis causes and differential diagnosis 4.Explain the etiology, diagnostic exams, clinical manifestations, collaborative care, and nursing management of Guillian-Barre syndrome 5.Describe the primary causes/etiology and clinical manifestations for patients with seizure disorder 6.Identify the collaborative care and nursing management of patients with seizure disorder be central 3 MULTIPLE SCLEROSIS relapsing remitting okay then not 1 4 OVERVIEW scar tiss e damage Autoimmune disease of the CNS Spine Chronic, progressive, degenerative damages Development of plaque in the white matter of the CNS Leads to demyelination of nerve fibers in brain and spinal cord 20-50 years of age; avg 30-35 years Most common CNS disease of young adults More common in women F Approx. 400,000 people in US Life expectancy from diagnosis is 25 years 5 ETIOLOGY AND PATHOPHYSIOLOGY 1 Etiology unknown Inherited susceptibility Increased prevalence in latitude to the north inflammation Limmune sheath Sys destroy 1 5 1 Inherited susceptibility Increased prevalence in latitude to the north Triggered by environmental and health factors Infection Smoking Trauma Stress Fatigue Pregnancy Poor Health Childhood obesity 2 Chronic Inflammation T cell activation triggers autoimmune response Disrupts blood-brain barrier Demyelination Antigen-antibody reactions Slower transmission causes weakness Myelin can regenerate and cause remission Gliosis in CNS Myelin cannot regenerate Lose nerve function Plaques form in white matter x̅ 6 CLINICAL MANIFESTATIONS 1 Blurred, Double Vision- Optic Neuritis Nystagmus involuntary eyewinement Muscle Weakness that can lead to Paralysis Gait and Balance Abnormalities Dizziness and Vertigo Fatigue Numbness/Tingling Spasticity Seizures rigid eye inflammation 2 Pain Hearing Loss Bladder/Bowel Dysfunction- spastic or flaccid diff swallowing I lead ti pmerminia mrius go into tags  turn Pt 2 hrs 2 Hearing Loss every Bladder/Bowel Dysfunction- spastic or flaccid Changes in Cognitive Function Depression/Emotional Changes Speech impairments Heat sensitivity (Uhthoff phenomenon) I Lhermitte’s sign- Barber chair phenomenon. Upon flexion of neck, electric shock down spine and or extremities. m.IE EEE 7 MULTIPLE SCLEROSIS DIAGNOSING Rule out other dx Cerebral spinal fluid- Increased IgG and presence of oligoclonal banding (protein in CNS) Delayed evoked potential-Test eye to brains response McDonald Diagnosing Criteria 2 demyelinating lesions in at least 2 different CNS locations (MRI) to see plaque Number of “attacks” Symptoms and findings typical of MS developing acutely/sub- acutely lasting at least 24 hours 8 PATTERNS OF MULTIPLE SCLEROSIS 9 PLAN OF CARE maximize neuromuscular function maintain independence in ADLs for as long as possible prevent infections and complications manage fatigue and anxiety optimize psychosocial well-being adjust to the illness reduce factors that precipitate exacerbations 10 NURSING MANAGEMENT 1 Monitor: Visual Acuity (apply eye patch to treat diplopia) Speech Swallowing Activity tolerance (avoid fatigue; provide rest periods) Skin integrity (immobility leads to pressure ulcers) heat sensitivity 2  1 Activity tolerance (avoid fatigue; provide rest periods) Skin integrity (immobility leads to pressure ulcers) Cognitive changes (reorient patient) Fluid intake (to avoid developing UTI) 2 Interventions Assist patient with bowel & bladder elimination Anticholinergics, catheterization, high fiber diet Diligent pain management Ensure patient safety Collaborate with PT/OT/ST Medication administration (differs for all patients) Symptom management Client education regarding triggers Provide emotional support to patient and caregivers Palliative care 11 PHARMACOLOGIC THERAPIES 1 Monoclonal Antibodies natalizumab alemtuzumab Oral therapies Furmarates (dimethyl fumarate) S1P receptor modulators (gingolimod) Platform injections Interferon B-1a Longterm prevent Interferon B-1b relapses Glatiramer acetate 2 Exacerbation Management Corticosteroids g Immunosuppi Lacerbation Bladder symptoms Anti-cholinergic (oxybutynin) tot w Spasticity corticosteroids Muscle spasm Baclofen Dantrolene diazepam musile 12 relaxant 13  Dantrolene diazepam 12 PARKINSON’S DISEASE Assess trap 13 PARKINSON’S DISEASE Chronic, progressive, neurodegenerative disorder Most common movement disorder affecting 1-2 % > 65 years Second most common neurodegenerative disorder after Alzheimer´s disease (AD) As of 2020, expected 1 million individuals diagnosed with Parkinson’s Disease More common in men (1.5 times) Average onset ages 40-70 14 ETIOLOGY AND PATHOPHYSIOLOGY 1 Cause unknown Interplay of Genetic and Environmental factors 20% with genetic link Multiple forms of secondary PD following chemical exposure or drug-exposure 2 Lack of dopamine Degeneration of dopamine-producing neurons Altered balance of dopamine and acetylcholine 15 CLINICAL MANIFESTATIONS 1 Tremor* First sign; more prominent at rest Worsens with stress and increased concentration “Pill rolling” Rigidity* shaking pill tilling Jerky quality Causes soreness, aches, fatigue, pain Akinesia/Bradykinesia* Loss of involuntary movements Stooped posture, masked face, drooling, shuffling gait 2  Loss of involuntary movements 151 Stooped posture, masked face, drooling, shuffling gait Postural Instability High risk for falls 2 Dysfunction of the Autonomic Nervous System Orthostatic hypotension; flushing; diaphoresis Depression (~50% of cases), anxiety, apathy Pain Fatigue Urinary retention Constipation Erectile dysfunction Mild cognitive impairment; can become dementia Sleep impairments REM behavior disorder (act out vivid often unpleasant dreams) Dysphagia 16 PARKINSON’S DISEASE: DIAGNOSTICS No specific test History & clinical features + Presence of TRAP & asymmetrical onset + Response to antiparkinsonian drugs 17 PLAN OF CARE maximize neurologic function help fold laundry maintain independence in ADLs for as long as possible optimize psychosocial well-being 18 NURSING MANAGEMENT 1 Administer medication at prescribed time Monitor swallowing/Prevent aspiration Provide smaller, more frequent meals Sit patient upright to eat and drink Easy to chew and swallow Maintain adequate nutrition Consult with dietician for appropriate diet Document patient’s weight high protein High cat food 2 sit p ti prevent aspiration  unintentional weight loss Consult with dietician for appropriate diet Document patient’s weight Evaluate need for high-calorie, high-protein supplements 2 Maintain client’s mobility for as long as possible Encourage exercise (yoga) Encourage use of assistive devices as disease progresses Encourage ROMs Assist with ADLs Collaborate with PT/OT/ST Fall prevention 19 NURSING MANAGEMENT 1 Promote communication for as long as possible Teach patient facial muscle strengthening exercises Encourage patient to speak slowly and to pause frequently Use alternate forms of communication Refer patient to Speech-Language pathologists Monitor client’s mental and cognitive status Observe for signs of depression and dementia Provide a safe environment (no throw rugs, encourage the use of an electric razor) Provide a list of community resources (support groups) 2 Provide support for caregivers Promote sleep hygiene Palliative care Promote immunizations (no live-attenuated) Post-op care: Deep brain stimulation Ablation of affected areas Transplantation of fetal neural tissue Monitor cognitive status Infection prevention meds mirror their environment if pt tams med be an advocate 20 8 1 for v pt be they're body 2 experiences s g with not maintaining consistently  take w food everyday 20 I mirror PHARMACOLOGICAL THERAPIES advocate 1 DOPAMINE PRECURSORS to the fad if 2 Levodopa with carbidopa (Sinemet) dopamine promoters improves function Give on empty stomach Report dyskinesia, mental status changes, palpitations, urinary difficulties Imagine.mn Drug may take weeks-months to work-let the patient know 3 DOPAMINE RECEPTOR AGONISTS- STIMULATE DOPAMINE RECEPTORS 4 Pramipexole Ropinirole Rotigotine Take with food (pramipexole) Report psychotic behaviors, drowsiness/sleep attacks May cause orthostatic hypotension Avoid alcohol/CNS depressants Assess skin-melanoma lesions 21 PHARMACOLOGICAL THERAPEUTICS: OTHER AGENTS 22 MYASTHENIA GRAVIS severe muscle weakness 23 OVERVIEW Autoimmune disease of the neuromuscular junction Characterized by fluctuating weakness of certain skeletal muscles Occurs in either gender in persons of any ethnicity 60,000 people have MG in the United States Age on onset – women after 40; men after 60 24 ETIOLOGY No known cause Autoimmune process antibodies attack acetylcholine receptors Acetylcholine is a crucial substance for nerve cell & muscle 25 1 24 antibodies attack acetylcholine receptors Acetylcholine is a crucial substance for nerve cell & muscle communication Muscle weakness- fluctuating of skeletal muscles 25 CLINICAL MANIFESTATIONS 1 Weakness progressively worsens throughout the day Rest can improve strength Progression is highly variable Can have episodes of myasthenic crisis Triggers: respiratory infection, surgery, stress, pregnancy, medications, starting corticosteroids, pain, alcohol, extreme temperatures Intact reflexes and other sensory processes 2 Ptosis* Facial paralysis Difficulty talking Difficulty swallowing or chewing Hoarse voice High risk of aspiration Problems in walking up stairs or lifting objects Difficulty breathing Fatigue Double vision 26 TABLE 58.19 COMPARISON OF MYASTHENIC AND Parasympathe CHOLINERGIC CRISES i 27 digest 28 MG: DIAGNOSTIC STUDIES Actalagintest H&P EMG-electromyography-measures muscle response to stimulation Anti-acetylcholine receptor (AChR) antibody test* (high specificity) ax tac hi mayest too little not meds to  sys worsen iii 28 am animist Anti-acetylcholine receptor (AChR) antibody test* (high specificity) Chest X-ray, Chest CT what is causing weakness Anticholinesterase test (Tensilon/Edrophonium) musile Evaluates muscle weakness before and after IV administration Complication- Sinus bradycardia. Atropine must be available on hand. May produce false-negatives & false-positives I me Isie weakness ftin little aletylcholine 29 MYASTHENIA GRAVIS – COLLABORATIVE CARE Monitor muscle weakness and tone Assess extraocular eyes movements and cardinal fields of gaze iff b w Test motor functions (touching your finger to your nose) edrophonium (Tensilon) Test: a levels of gasthenia cholinergic A drug called Tensilon is administered agent intravenously acetylcholine iii ficrisis Patient asked to perform muscle movements under physician observation Increasing weakness can indicate crisis Chest CT Scans or MRI cholinergic crisis works V worse 30 PLAN OF CARE ftp.ffs MGticmuihacctylocholi Have a return of normal muscle strength Manage fatigue v Avoid complications Maintain a quality of life appropriate to the disease course anidite 31 NURSING INTERVENTIONS Patent airway Atropine Teach foods that can be easily chewed and swallowed Aspiration precautions chiking Arrange activities that require little physical effort Plan activities of daily living to avoid fatigue Follow medication regime assist omb lotion Anticholinesterase inhibiting agents rest periods Corticosteroids (specially prednisone) used to suppress immune response Administer medications and oxygen as needed for respiratory infections 32 33 1 brain spiral card  button lower limbs w legs tip starts Administer medications infections paralyzed and oxygen as needed for respiratory diaphrapon 1 f cure chest to 32 AMYOTROPHIC LATERAL SCLEROSIS of airway Yet 33 AMYOTROPHIC LATERAL SCLEROSIS (ALS) AKA Lou Gehrig’s disease Rare progressive neurologic disorder characterized by loss of motor neurons i s muscu century megan crampM Progressive weakness and atrophy rap ALS leads to death 2 to 6 years after diagnosis Onset between 40 to 70 years of age More common in men than women More Approximately 5,000 people diagnosed with ALS every year prone No cure to 34 CLINICAL MANIFESTATIONS resp 1 Limb-onset- affects arms and legs Limb weakness Tripping, dropping things, stumbling ipf Bulbar onset- affects mouth Dysarthria pneumonia Dysphagia diff etc Drooling swallowing Remain cognitively intact I 2 Pain Ventilater Sleep disorders Spasticity and Hyperreflexia Emotional lability Depression if lose 70 Constipation Esophageal reflux resp effect 35 1 Pull keep them on Plug Venitulates  monitor Maintain patent airway failure 35 NURSING CAREfor pneumonia or respiratory 1 Facilitate communication Communication boards, texting Blinking Reduce aspiration risk and infection Early identification of respiratory insufficiency Pain management Medications Riluzole 50 mg BID (no cure slows progression) 2 Fall prevention Keep patient as active as possible Provide emotional support Emotional response to diagnosis and prognosis Assist patient through grief and grieving process Support caregiver Encourage verbalization of feelings 36 WHEN PARALYSIS SETS IN 1 Prevent infection Pneumococcal and influenza vaccine Prevent skin breakdown Turn and position every 2 hours. Keep skin dry Wash skin and dry well after each bowel movement or urination Palliative care at diagnosis 2 Prevent vein thrombosis, pulmonary embolism Elastic stockings, if ordered, especially when patient out of bed Active and passive ROM to affected limbs 3-4 times per day Provide respiratory care May require mechanical ventilation 37 38 but s's worse similar ms ALS L  2 w Estimate Provide respiratory peripheral care fing May require mechanical ventilation Reversible 37 GUILLAIN-BARRÉ SYNDROME (GBS) Autoimmune eff peripheral GUILLAIN-BARRÉ SYNDROME (GBS)nervous 38 sys weakness and Demyelinating polyneuropathy w/ acute ascending flaccid paralysis symmetric Onset 1-3 weeks following relatively benign illness Extremely rare after influenza vaccine Most pts with GBS will start to recover spontaneously at about 28 muscle days weakness Diagnostics History & clinical manifestations Progressive weakness of more than one limb PLUS diminished or absent reflexes CSF analysis Electromyography test (EMG) & nerve conduction studies tendon reflexes feet UP the 39 GUILLAIN-BARRÉ SYNDROME (GBS) body 40 NURSING & COLLABORATIVE CARE 1 Supportive Ventilator support ~ ⅓ of pts Cardiac monitoring IV immunoglobulin (IVIG) & plasma exchange Nutritional supplementation Pain 2 Monitor for infection, bowel, bladder Prevention pressure ulcers, contractures, DVT PT, OT, SLP patent monitor aspiration Maintain airway Seizure Disorder 41 Premi ia resp failure Transient, uncontrolled electrical discharge of neurons in the brain – interrupts normal function Seizures from systemic / metabolic problems are not considered seizure disorder (epilepsy) if they stop when underlying condition 42 Asending 1 paralysis button it  ge p 41 g Seizures from systemic / metabolic problems are not considered seizure disorder (epilepsy) if they stop when underlying condition is corrected 42 Systemic/Metabolic Seizures 1 Systemic Causes Acidosis Electrolyte imbalance Hypoglycemia Hypoxemia Alcohol / Barbiturate withdrawal Dehydration Water intoxication 2 Metabolic Disorder Causes Heart, lung, liver, kidney diseases Systemic Lupus Erythematosus (SLE) Diabetes Hypertension Sepsis 43 Seizure Disorder: Etiology 3.4 million in US have seizure disorder Seizure disorder has many possible causes Most common causes vary by age For Adults 20-30 years of age: Structural lesions Trauma Brain tumor Vascular disease After age 50: Stroke  After age 50: Stroke Metastatic brain tumors 1/3 of cases are idiopathic Not attributable to a specific cause 44 Pathophysiology Group of abnormal neurons seem to fire without clear cause Firing spreads to near or distant areas of brain Factors that cause abnormal firing not clear Changes in function of astrocytes may play several key roles in recurring seizures Activation of astrocytes by hyperactive neurons is one of crucial factors that causes nearby neurons to generate an epileptic discharge Genetic abnormalities may be an important factor contributing to idiopathic seizure disorders Some types of seizure disorder run in families Other types of idiopathic seizures are related to changes in specific genes 45 Seizure Phases I Prodromal Phase - sensations or behavior changes hours or days before seizure 2 Aural Phase - sensory warning Similar each time seizure occurs; considered part of the seizure Ictal Phase - from first symptoms to end of seizure activity Postictal Phase - recovery period after seizure 46 Generalized-Onset Seizures Involve both sides of brain Usually impaired awareness for few seconds to several minutes Tonic-Clonic – most common generalized-onset seizure Lose consciousness, fall to ground 46 Tonic-Clonic – most common generalized-onset seizure Lose consciousness, fall to ground Body stiffens (tonic phase) for 10-20 seconds Jerking of extremities (clonic phase) for another 30-40 seconds May have: cyanosis, excessive salivation, tongue/cheek biting, incontinence bive Postictal – muscle soreness, tired, may sleep for several hrs, no memory of seizure after seizure 47 Generalized-Onset Seizures Tonic Seizure suddenly drink sin tinic Sudden onset of increased extensor muscle tone (stiffness) Most often occur in sleep + affect both sides of body Will fall if standing fall Usually < 20 secs Clonic Seizure Begin with loss of awareness + sudden loss of muscle tone Followed by limb jerking Rare antinic 48 Generalized-Onset Seizures Atonic Seizure (drop attack) Tonic episode or paroxysmal loss of muscle tone Begins suddenly with falling to ground Last < 15 secs, can resume normal activity immediately High risk for head injury, often wear protective helmet 49 Generalized-Onset Nonmotor Seizures Absence Seizure Usually only in children, rarely beyond adolescence Typical: brief staring spell (daydream like) Often goes unnoticed – very short (< 10 secs) May occur up to 100 x / day if untreated EEG shows distinct pattern Atypical: staring spell with other manifestations  EEG shows distinct pattern Atypical: staring spell with other manifestations Eye blinking Jerking movements of lips Lasts > 10 seconds Usually continue into adulthood 50 Focal-Onset Seizures Begin in specific region of cortex in one brain hemisphere Manifestations based on function of area of brain involved Described by level of awareness Focal awareness seizures Focal impaired awareness seizures 51 Focal-Onset Seizures Focal awareness seizures Pt remains conscious + alert Unusual feelings or sensations that can take many forms Sudden / unexplainable feelings: Joy Anger Sadness Nausea May hear, smell, taste, see, or feel things that are not real 52 Focal-Onset Seizures Focal impaired seizures Pts have loss of consciousness or a change in awareness Eyes are open but cannot interact Usually last 1-2 mins May do things that can be dangerous or embarrassing Walking in traffic Removing their clothes After seizure, no memory of activities 53  Removing their clothes After seizure, no memory of activities Tired, confused May not return to normal for hrs 53 Psychogenic Seizures Resemble epileptic seizures Can be misdiagnosed as seizure disorder Proper diagnosis usually requires video-EEG monitoring History of emotional or physical abuse or traumatic event may emerge Some may have both psychogenic seizures and seizure disorder Once ID’d – treatment is psychological 54 Complications Status Epilepticus enoxitiseet.at State of continuous seizure activity or seizures in rapid succession without regaining consciousness between seizures Any seizure lasting longer than 5 mins Neurologic emergency Can occur with any type of seizure 55 Complications Severe injury and death can result from trauma during a seizure natkillsp weinoftseizveoved Many seizure deaths are a result of trauma during seizure Pts who lose consciousness are at greatest risk Sudden unexpected death in epilepsy (SUDEP) Affects about 1 in 150 with uncontrolled seizures / yr Almost always associated with tonic-clonic seizures Exact cause unknown, maybe: Respiratory dysfunction Dysrhythmias Cerebral depression Med adherence, disease awareness critical for at-risk pts 56 seizure on the ground  56 Psychosocial Complications Effect on lifestyle – most common complication of seizure disorder Ineffective coping / depression Social stigma still exists Discrimination in employment and education opportunities 57 Texas Drivers Licensing Laws Prohibited from driving: ongoing or uncontrolled seizures Must be seizure free for 3 months for cars Seizure free for 5 yrs for class A and B (big trucks, commercial vehicles) There is no provision requiring physicians to report pts who have been treated for or diagnosed as having epilepsy to a central state agency 58 Diagnostics Accurate, comprehensive description of seizures and health history Precipitating factors, antecedent events Seizure description: onset, duration, frequency, postictal state EEG May help determine type of seizure and pinpoint seizure focus Many pts don’t have abnormal findings the first time CBC, chemistries, liver/kidney functions, UA Rule out metabolic disorders CT/MRI scans Rule out structural lesion 59 Collaborative Care Most seizures don’t require emergency care Self-limiting Rarely cause bodily injury Immediate medical care if: Status epilepticus occurs Significant bodily harm occurs 60  Status epilepticus occurs Significant bodily harm occurs Event is a first-time seizure 60 Collaborative Care Seizure disorder is mainly treated with antiseizure meds Cure not possible Goal = prevent seizures with minimum toxic side effects Meds control seizures in about 70% of pts About 1/3 of pts will need to add another med Start with single med based on age/weight; type/frequency/cause of seizure Meds stabilize nerve cell membranes + prevent spread of epileptic discharge Must be taken regularly and continuously, often for life 61 Medication Management Main drugs for generalized tonic-clonic + focal onset (No single antiseizure med is clearly the most effective or best tolerated) Phenytoin (Dilantin) Divalproex (Depakote) Carbamazepine (Tegretol) Phenobarbital Antiseizure drugs should not be discontinued abruptly as this may cause seizures Many antiseizure drugs have a long half-life Can be given 1 to 2 times / day A simplified drug regimen can increase med compliance Meds should be routinely reviewed / adjusted as needed Noncompliance is a concern – often because of undesirable side effects (SE) Common SEs involve CNS and include diplopia, drowsiness, ataxia, mental slowness 62 Surgical Interventions About 30% of pts do not respond to antiseizure meds Surgery Remove epileptic focus or prevent spread of epileptic activity in brain Anterior temporal lobe resection – most common procedure 62 brain Anterior temporal lobe resection – most common procedure 80% of patients are seizure free after 5 yrs 72% still seizure free at 10 years Candidates must meet 3 requirements for surgery: Confirmed diagnosis seizure disorder Adequate drug trial without satisfactory results Defined type of seizure disorder 63 Collaborative Care Other therapies Vagal nerve stimulation – adjunct to meds when accessible focal point not identified Surgically implanted neck electrode stops excessive discharge of neurons Pt activates when senses seizure is imminent Responsive neurostimulation - continually monitored EEG to detect abnormalities Similar to cardiac pacemaker Responds to seizure activity by delivering electrical stimulation to a precise location 64 Vagal Nerve Stimulator 65 Other Therapies 1 Ketogenic diet High-fat, low-carb diet Ketones are produced and pass into brain – replace glucose as an energy source 2 Biofeedback Pt learns to maintain a certain brain wave frequency that is refractory to seizure activity Further research needed to assess effectiveness 66 Nursing Assessment History CNS trauma, tumors, infections Stroke, metabolic disorders 66 CNS trauma, tumors, infections Stroke, metabolic disorders Adherence with antiseizure medications Headaches, aura, mood or behavioral changes before seizure Anxiety, depression, loss of self-esteem, social isolation Post Seizure: Bitten tongue, soft tissue damage Hypertension, tachycardia/bradycardia Bowel incontinence Excessive salivation Urinary incontinence Injuries 67 Nursing: Acute Care Observe and record seizure – stay with pt! Ease to floor Airway Do not attempt to place any objects in pt’s mouth during seizure Turn patient to side if possible Protect from injury – pad side rails if inpatient DO NOT RESTRAIN Loosen restrictive clothing aura serve p's 68 Post-Seizure Care VS / Assessment Reposition to open/maintain airway Suctioning or O2 if needed LOC intubate 3 dead Glasgow Coma Scale low 8 Reassurance – frightening experience for pt / family Treat hypoglycemia with IV Dextrose Postictal phase: Lethargy – want to sleep Altered LOC 69 Patient Teaching Prevention of recurring seizures is major goal time it start thank dirt truth them side if pt manteing  y tinic the ic week fall 69 Patient Teaching Prevention of recurring seizures is major goal Don’t skip or stop anti-seizure meds were dint coldtarkey What to do if missed dose Instruct to report any side effects to provider Teach family/caregivers emergency management of tonic-clonic seizures Not always necessary to call ambulance or go to hospital after single seizure unless: Prolonged seizure Another seizure immediately occurs Pt sustained injuries as a result of seizure Adjusting to personal / societal limitations Job discrimination – refer to US Equal Opportunity Commission Epilepsy Foundation (EF) excellent resource www.epilepsy.com Medic alert bracelet, necklace, ID card 70 QUESTIONS? [email protected] What do do it pt you risk for aspiration Pt pt in NPO I consult physio w then then elevate hob  1/20/25 1 Dementia SHIRLEY GOMEZ, MSN, RN PH.D. STUDENT, NURSING SCIENCE UT HEALTH SAN ANTONIO [email protected] 2 Objectives 1.Define Alzheimer's disease and dementia and their impact on society 2.Describe the clinical manifestations, diagnostic studies, and collaborative management for patients with dementia 3.Describe the clinical manifestations, diagnostic studies, and collaborative management for patients with Alzheimer's disease 4.Describe the nursing management of the patient with Alzheimer's disease and dementia 3 Dementia women experience adjusted life yr higher disability uMore than 55 million people worldwide have dementia mortality due uOver 60% live in low-and middle-income countries to dementia uThere are approximately 10 million new cases yearly u7th leading cause of death uMajor cause of disability and dependency among older people worldwide uAs of 2019, global economic cost were US $1.3 trillion uWomen are increasingly affected by dementia 4 What is dementia? uA disorder represented by a decline of previous level of function uAffects function of 1 or more cognitive domains uComplex attention uExecutive function uLanguage uLearning and memory uPerceptual-motor uSocial cognition 5 The lignitive derive affects to f rition ability performing daily activities ADL 1  uGenetic Testing u 10 Collaborative Management and Nursing Care uIdentify and treat the cause uTreating risk factors (Vascular or multi-infarct Dementia (VaD)) uHypertension uDiabetes uSmoking uHypercholesterolemia uDysrhythmias ustroke u 11 Vascular Dementia uMay be caused by stroke 7 uPoor prognosis uSymptoms may be sudden and are similar to AD alatimers uMore common in men uNo treatment uStroke prevention 12 Dementia with Lewis bodies Abnormal deposits of protein a 1 uLewy bodies present synulleint in brainsters uFeatures similar to AD and Parkinson disease uMay have bradykinesia, rigidity, postural instability, hallucinations, short term memory loss, cognitive changes, sleep problems uPneumonia is common uDrugs: levodopa/carbidopa, acetylcholinesterase inhibitors uManage dysphagia and immobility uMonitor nutrition problems due to swallowing difficulties uFalls! 13 Other Causes of Dementia uNeurogenerative disorders uVascular diseases uImmunologic diseases or infections uMedications 13 uImmunologic diseases or infections uMedications uMetabolic or nutrition diseases uSystemic diseases uTrauma uTumors uVentricular disorders 14 Question 1 uWhat information should you obtain from a health history assessment? Why? c 15 Alzheimer’s Disease uAffects those 65 and older uMore than 6.2 million in U.S. uProjected to increase to 12.7 million by 2050 u6th leading cause of death in the U.S. u5th leading cause of death over 65 uIncreased burden, as of 2020 it was estimated $257 billion of unpaid care was provided uIncludes 15.3 billion hours of assistance u u 16 Alzheimer’s Disease uUnknown etiology uChronic, progressive, irreversible neurodegenerative brain disease uEarly onset = younger than 65, late-onset = over 60 uIt is NOT a normal part of aging uFamily history - genetics uCardiovascular factors uHead Trauma uFamily history of AD is an important risk factor. Persons with a first-degree relative (parent or sibling) with dementia are more likely to develop AD. Those who have more than 1 first-degree relative with dementia are at even higher risk for developing AD. u-Brain functioning depends on a good blood supply and nutrients delivered to it by that blood supply. u -Many factors increase the risk for CVD. These include diabetes, hypertension, obesity, hypercholesterolemia, and smoking. Diabetes udramatically increases the risk of developing AD and other types of dementia. Diabetes can contribute to dementia in several ways. Chronic high levels of insulin and glucose may be directly toxic to brain cells. Insulin resistance, which causes high blood glucose and can lead to type 2 diabetes, may interfere with the body s ability to break down amyloid, a protein that forms brain plaques in AD. 17 High blood glucose and high cholesterol have a role in atherosclerosis, which contributes to VaD.8 ) -Diabetes may contribute to poor memory and decreased mental function in other ways. Diabetes causes microangiopathy, which damages small blood vessels throughout the body. Ongoing damage to blood vessels in the brain may be one reason people with diabetes are at a higher risk for cognitive problems as they age. People with diabetes may lose brain volume, especially gray matter, as the disease progresses. -Professional football players and mi litary veterans who had a traumatic brain injury or posttraumatic stress disorder have an increased risk for AD and other types of dementia. First step – medical, neurologic, and psychologic history Obtain info on: Judgment Interests Repeating Difficulties with tools Forgetful? Financial affairs Appointment keeping Memory Diet and nutrition information Alcohol use Medications Physical assessment Movement and gait problems Urinary incontinence and ataxia Neuro assessment Mental status exam or screening 1st step – need a thorough exam, focus on cognitive and behavior changes. Family and significant others can provide important info. Obtain information about (1)problems with judgment; (2)reduced interest in hobbies/activities; (3)repeating questions, stories, or statements; (4)trouble learning how to use a tool or appliance; (5)forgetting the month or year; (6)problems handling financial affairs; (7)difficulty remembering appointments; and (8)consistent problems with thinking and/or memory. Include: 1. herbal supplements 2. recreational substances in the medication history 3.drugs that can impair cognition, such as analgesics, anticholinergics, psychotropics, and sedative-hypnotics 4.Movement problems suggest parkinsons 5.Dementia, urinary incontinence and ataxia = normal pressure hydrocephalus  u 17 Pathophysiology uChanges in brain structure and function uAmyloid plaques uNeurofibrillary tangles uLoss of connections between neurons uNeuron death uIncrease production of plaques made up of proteins called β- amyloid uTau proteins are altered uAmyloid plaques and tau are abundant in AD uhttps://youtu.be/0GXv3mHs9AU?si=vcGZVOCt4fdODO8A u 18 Clinical Manifestations uPathologic brain changes occur at least 15 years before symptoms u10 warning signs uMild, moderate, or severe stages uAphasia, apraxia, visual agnosia, dysgraphia uRetrogenesis u 19 10 Warning Signs 20 Health History/Assessment uHealth history uPhysical assessment uNeurologic and mental status assessment uLaboratory tests uNeuroimaging uBiomarkers uNeuropsychologic testing 21 Collaborative Management uDrug therapy uBehavior modification uModerate exercise uAssistance with functional independence 22 Stages 1.Mild Forgetfulness beyond what is seen in a normal person 2. Short-term memory impairment, especially for new learning 3. Loss of initiative and interests 4. May forget recent events or the names of people or things 5. Impatient 6. May no longer be able to solve simple math problems 7. Slowly loses the ability to plan and organize 8.Moderate 9. Memory loss and confusion become more obvious 10. Has more trouble organizing, planning, and following directions 11. May need help getting dressed 12. May start having incontinence 13. Trouble recognizing family members and friends 14. Agitation, restlessness 15. May lack judgment and begin to wander, gets lost 16. May have trouble sleeping 17. Delusions, hallucinations, paranoia 18. Behavior problems 19.Severe 20. Severe impairment of all cognitive functions 21. Little memory, unable to process new information 22. Unable to perform self-care activities 23. Often needs help with daily needs 24. May not be able to talk 25. Cannot understand words 26. May have problems eating, swallowing 27. May not be able to walk or sit up without help 28. Immobility 29. Incontinence As AD progresses, more cognitive impairments occur. These include aphasia (difficulty comprehending language and oral communication), apraxia (inability to manipulate objects or perform purposeful acts), visual agnosia (inability to recognize objects by sight), and dysgraphia (difficulty communicating by writing). Retrogenesis is the process in which the decline in AD mirrors, in reverse order, brain development that occurs from birth.13 Thus, it compares the developmental stages of childhood with the deterioration of patients with AD 21 uModerate exercise uAssistance with functional independence uAssistance and support for caregivers uCollaborate with dietitian, occupational therapist, and social worker 22 Nursing Management uAssessment uAddress challenging behavior uAssess caregiver stress level and provide support uIdentify and plan for needs (elimination, nutrition, hydration, and hygiene) uProvide patient needs uSafe environment uPromote sleep uDelegate to LPN/VN 23 Safety uFALLS! uIngesting dangerous substances uWandering uInjuring others and self uBurns uDifficulties in crisis situations 24 Communication with patients uTreat with respect and dignity uGentle touch uPatience and calm demeanor uPrepare for challenging behavior uUse gestures and pictures for directions uSimplify tasks uAvoid abstract topics uBe flexible uUse distraction uProvide reassurance 25 Question 2 uWhat are two Alzheimer’s warning signs? Describe. 26 1.10 warning signs: 1. MEMORY LOSS THAT DISRUPTS DAILY LIFE. One of the most common signs of Alzheimer s disease, especially in the early stages, is forgetting recently learned information. Others include forgetting important dates or events, asking the same question over and over again, or increasingly needing to rely on memory aids (e.g., reminder notes or electronic devices) or family members for things the person used to handle on their own. 2.CHALLENGES IN PLANNING OR SOLVING PROBLEMS. Some people living with dementia may experience changes in their ability to develop and follow a plan or work with numbers. They may have trouble following a familiar recipe or keeping track of monthly bills. They may have difficulty concentrating and take much longer to do things than they did before. 3.DIFFICULTY COMPLETING FAMILIAR TASKS. People living with Alzheimer s disease often find it hard to complete routine tasks. Sometimes they may have trouble driving to a familiar location, organizing a grocery list or remembering the rules of a favorite game. 4.CONFUSION WITH TIME OR PLACE. People living with Alzheimer s can lose track of dates, seasons and the passage of time. They may have trouble understanding something if it is not happening immediately. Sometimes they may forget where they are or how they got there. 5.TROUBLE UNDERSTANDING VISUAL IMAGES AND SPATIAL RELATIONSHIPS. For some people, vision problems are a sign of Alzheimer s. This may lead to difficulty with balance or trouble reading. They may also have problems judging distance and determining color or contrast, causing issues with driving. 6.NEW PROBLEMS WITH WORDS IN SPEAKING OR WRITING. People living with Alzheimer s may have trouble following or joining a conversation. They may stop in the middle of a conversation and have no idea how to continue, or repeat themselves. They may struggle with vocabulary, have trouble naming a familiar object or use the wrong name. 7.MISPLACING THINGS AND LOSING THE ABILITY TO RETRACE STEPS. A person living with Alzheimer s may put things in unusual places. They may lose things and be unable to go back over their steps to find them again. He or she may accuse others of stealing, especially as the disease progresses. 8.DECREASED OR POOR JUDGMENT. Individuals may experience changes in judgment or decision-making. For example, they may use poor judgment when dealing with money, or pay less attention to grooming or keeping themselves clean. 9.WITHDRAWAL FROM WORK OR SOCIAL ACTIVITIES. A person living with Alzheimer s disease may experience changes in the ability to hold or follow a conversation. As a result, they may withdraw from hobbies, social activities or other engagements. They may have trouble keeping up with a favorite team or activity. 10. CHANGES IN MOOD OR PERSONALITY. Individuals living with Alzheimer s may experience mood or personality changes. They may be easily upset at home, at work, with friends or when out of their comfort zone. 25 uWhat are two Alzheimer’s warning signs? Describe. 26 Delirium uState of confusion can develop over days or hours uMay be caused by several factors uDementia leading risk factor for delirium - - delirium risk factor for developing dementia u u 27 Delirium Mnemonic (Causes) uMnemonic for causes of Delirium uDementia, dehydration uElectrolyte imbalances, emotional stress uLung, liver, heart, kidney, brain uInfection, intensive care unit uRx drugs uInjury, immobility uUntreated pain, unfamiliar environment uMetabolic disorders u u 28 Cultural Considerations uClinical Evaluation and Neuropsychological Assessment uClinician cultural competence and awareness uGuidelines and standards (CLAS & ECLECTIC) uLiteracy uAcculturation uLinguistic diversity uTake a look! uhttps://www.alzheimersla.org/videos/telenovela/ u rel u provide regarding issues u as u such driving supervision 29 Palliative Care uCan identify challenging symptoms uProvide better management of symptoms source discomfort t A identifying tot prevent under or appropriately over trt  29 uCan identify challenging symptoms uProvide better management of symptoms uProvide better quality of life uCommon symptom management in Palliative Care uAgitation wandering imparting uSwallowing difficulties ites hard'reeding fuintal uPain uHallucinations lobe uCaregiver support dysfunction u untot pain present as depression agitation u 30 changing heavier press Caregiver Support Infers ja to uCaregivers uProvide supportive resources uFamily role changes uEffect on relationships uAssess stressors and coping strategies uCaring for the Caregiver program at UTHSCSA uUtcaregivers.org uhttps://youtu.be/jwoG-cA2XkI 31 Summary uIdentify the importance in nursing management of Dementia and Alzheimer’s patients uIdentify the importance of collaborative management uIdentify the importance of cultural considerations uIdentify the importance of supportive services uPalliative care uCaregiver support u 32 References uAlzheimer’s Association. October 1, 2024. https://www.alz.org/alzheimers-dementia/what-is-dementia uGaviola, M.A., Omura, M., Inder, K.J., Johnson, A. (2023). Caring for people with dementia from culturally and linguistically diverse backgrounds in nursing homes: A scoping review. International journal of Nursing Studies, 151, 1-13. What are you going to see, what are you going to do? Clinical manifestations, health history assessment, screening tests Treat underlying condition, specialists, PT/OT Cultural competence and awareness  1/20/25 Hypertension 1 R O Z M I N J I WA N I P H D , R N ADAPTED FROM MEGAN LIPPE PHD, RN, RUTH, R JOHNSON, MSN, RN, CMSRN Hypertension 2 LEARNING OBJECTIVES 1.Summarize the classification, etiology, and risk factors for hypertension 2.Select appropriate strategies for the prevention of hypertension 3.Recognize the clinical manifestations and diagnostic findings related to hypertension 4.Describe the collaborative care for hypertension, including drug therapy and lifestyle modifications 5.Explain the collaborative care of the older adult with hypertension 6.Prioritize the nursing management of the patient with hypertension St t b aril se 3 REVIEWING KNOWLEDGE sz a b semilunar Cardiac Anatomy & Physiology valves close Epicardium: Surrounds the heart, provides protection and support, forms the pericardium, has two layers with 30-50 mL serous fluid for lubrication. Myocardium: Cardiac muscle controlled by the autonomic nervous system. Endocardium: Lines the interior of the heart and valves. Four Chambers: Two atria (receiving chambers) and two ventricles (pumping chambers). m Four Valves: Two atrioventricular valves (tricuspid and mitral) and two semilunar valves (pulmonic and aortic). pa Lumpblindleave heart 4 REVIEWING KNOWLEDGEJenn Blood Flow and Valve Function Deoxygenated Blood Flow: From periphery to inferior and superior vena cava → right atrium → tricuspid valve → right 1  4 Deoxygenated Blood Flow: From periphery to inferior and superior vena cava → right atrium → tricuspid valve → right ventricle → pulmonic valve → pulmonary system (releases CO2, uptakes oxygen). Oxygenated Blood Flow: From pulmonary system → left atrium → mitral valve → left ventricle → aortic valve → aorta. Cintration Valve Sounds: S1 (lub) - closure of atrioventricular valves; S2 Sys (dub) - closure of semilunar valves. relax 5 FA C T O R S I N F L U E N C E C A R D I A C O U T P U T Preload (stretch)- The volume of blood in the left ventricle before contraction end of diastine preloadwasherabt to contract Afterload (squeeze)– The resistance the left ventricle has to pump against to push blood into circulation end of squeeze sublaid out Contractility – The force of the left ventricular p contraction 6 REVIEWING KNOWLEDGE Cardiac Output (CO) Definition: Volume of blood expelled from the left ventricle per minute (normal CO is 5 L/min). Formula: CO = HR x SV (Heart Rate x Stroke Volume). Factors Influencing CO: Preload, afterload, myocardial contractility. mi Stroke volume (SV): volume of blood expelled with each left ventricular contraction (~70 ml/contraction) Aunt of blood leaving Heart rate (HR) - How many times the left ventricle contracts in a PE in i ns Svestmatediastile ucl minute Left Ventricle Ejection Fraction (LVEF, ~58% or 50-65%): Partoverwhile percentage of blood pumped out of the left ventricle with each of blind heartbeat (heart contractility) https://www.osmosis.org/learn/Stroke_volume%2C_ejection_fracti leaving out on%2C_and_cardiac_output of left ventricle 7 REVIEWING KNOWLEDGE per beat BP- the force exerted by the blood against the wall of the blood vessel. 7 BP- the force exerted by the blood against the wall of the blood vessel. Definition: Force exerted by blood against the wall of blood vessels. Formula: BP = CO x SVR (Cardiac Output x Systemic Vascular Resistance). Importance: Must be adequate to maintain perfusion during activity and rest. SVR is the force opposing the movement of blood within the blood vessels 8 H Y P E R T E N S I O N P R E VA L E N C E 9 HYPERTENSION Classification and Risk Factors Primary Hypertension: Accounts for 90-95% of cases, without identifiable cause. Contributing factors include age, family history, gender, ethnicity, sodium intake, BMI, diabetes, tobacco use, and alcohol intake. Secondary Hypertension: Accounts for 5-10% of cases, with specific causes such as cirrhosis, renal disease, sleep apnea, drug-related factors, endocrine disorders, and more. Treatment is aimed at removing or treating the underlying cause Suspect in people who suddenly develop high BP. Blanks highest prevalence 10 11 C L A S S I F I C AT I O N O F H Y P E R T E N S I O N “Silent Killer” recitation A s y m p t o m a t i c U n t i l Ta r g e t O r g a n D a m a g e 2 3 Occurs 12 C L I N I C A L M A N I F E S TAT I O N & D I A G N O S T I C STUDIES Symptoms: Often asymptomatic until target organ damage occurs. May include headaches, dizziness, and visual disturbances. Diagnostic Studies: Accurate BP monitoring, laboratory tests (renal function, lipid profile, etc.), eye exams, ECG, echocardiogram, ambulatory blood pressure monitoring (ABPM). White coat BP when see doc  you ju L first tone in BP high dat i ga shy ugly I rhityftau.net 12980 1219 eft one cogan til main are is Modifiable risk factors to prevent CVD. As BP increases, so does the risk of MI, Heart failure, Stroke, Renal disease, Retinopathy Hypertensive heart disease: A risk factor for CAD, left ventricular hypertrophy caused by sustained high BP, HF heart compensatory mechanisms are overwhelmed-heart can no longer meet body s demand Cerebrovascular disease: atherosclerosis is the most common cause of cerebrovascular disease. HTN is a significant risk factor for cerebral atherosclerosis and stroke. The risk for stroke is 4 times higher Peripheral vascular disease: Intermittent claudication (ischemic leg pain precipitated by activity and relieved by rest) is a classic symptom of PVD Kidney: Nephrosclerosis: one of the leading causes of CKD. Renal disease results from ischemia caused by the narrowing of renal blood vessels Eyes: Retinal damage: Blurry vision, retinal hemorrhage, and vision loss; damage to the retinal vessels indicates concurrent damage to the heart, brain, and kidneys.  (renal function, lipid profile, etc.), eye exams, ECG, echocardiogram, ambulatory blood pressure monitoring (ABPM). Accurate BP monitoring - Clinic & ambulatory settings BP classification is based onobscene 2 or more readings accurately performed on both arms on 2 separate occasions Every 3-6 months once stable 13 GOALS 14 HYPERTENSION INTERPROFESSIONAL CARE Overall goals 1.Achieve and maintain goal BP 2.Reduce CV risk factors and target organ disease 3.Lifestyle modifications American Heart Association (AHA) Life’s Simple 8 1.Manage BP 2.Control cholesterol 3.Reduce blood sugar 4.Get active 5.Dietary changes (DASH diet) 6.Weight reduction (Weight loss of 1 kg will decrease SBP by 1 mm Hg) 7.Stop smoking 8.*Get healthy sleep 4. Drug Therapy: Antihypertensive medications such as ACE inhibitors, beta-blockers, diuretics, and calcium channel blockers. 15 D I E TA R Y S O D I U M R E D U C T I O N Healthy adults should restrict sodium intake to 2300 mg/day or less. At-risk groups should restrict sodium to 1500 mg/day or less. Most adults exceed the recommended limit: (men 4200mg/day women 3300 mg/day) AHA ”Salty Six” bread products, lunch meat and cured meats, pizza, soup, sandwiches, and poultry 16  b T.ly p Ie Ig s Ég's AHA ”Salty Six” bread products, lunch meat and cured meats, p se pizza, soup, sandwiches, and poultry rapid Teaching-reading labels (OTC drugs, foods, toothpaste) 16 NURSING MANAGEMENT breathing Prioritizing Care Assessment: Regular BP monitoring, evaluation of target organ damage, patient education on lifestyle modifications. Interventions: Medication adherence, dietary counseling, physical activity encouragement, smoking cessation support, stress reduction techniques. 17 N U R S I N G M A N A G E M E N T: E D U C AT I O N 18 G E R O N T O L O G I C C O N S I D E R AT I O N S Age-Related Changes: Loss of arterial elasticity, increased systemic vascular resistance, orthostatic hypotension, altered drug metabolism. Management: Gradual dose changes, monitoring for postprandial hypotension, careful use of NSAIDs. ØIncreased incidence with age; 90% risk age greater than 55 ØMore likely to have “white coat” HTN ØAfter-meal BP drops - Measure supine, sitting, and standing BP and HR at every visit ØNSAIDs - Risk for renal effects and hyperkalemia with ACE inhibitors, ARBs, and aldosterone antagonists 19 H Y P E R T E N S I O N D R U G T H E R A P Y: D I U R E T I C S 20 H Y P E R T E N S I O N D R U G T H E R A P Y: S Y M PAT H O LY T I C ( B E TA - A N T I A D R E N E R G I C ) 21 H Y P E R T E N S I O N D R U G T H E R A P Y: C A L C I U M C H A N N E L B L O C K E R S & VA S O D I L AT O R S 22 H Y P E R T E N S I O N D R U G T H E R A P Y: S U P P R E S S I N G RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM- RAAS 23 H Y P E R T E N S I O N D R U G T H E R A P Y: S Y M PAT H O LY T I C ( A N T I A D R E N E R G I C ) 24 1  math Dry I remember se function 22 23 S Y M PAT H O LY T I C ( A N T I A D R E N E R G I C ) 24 NURSING MANAGEMENT 1 General Nursing Management Assess HR & BP: Monitor heart rate and blood pressure regularly. Orthostatic Hypotension: Assess for symptoms of orthostatic hypotension. Serum Potassium & Electrolyte Levels: Monitor electrolyte levels, especially potassium. Renal Function: Assess renal function regularly. Fluid Volume Status: Monitor for signs of fluid volume overload or deficit. I mine fluid Bp Patient Teaching: Educate patients on medication adherence, lifestyle modifications, and potential side effects. 2 Specific Nursing Management for Drug Classes Diuretics: Consider the time-of-day administration to avoid nocturnal diuresis. Beta Blockers: Assess ECG, monitor for postural hypotension, and be cautious with nonselective blockers in respiratory disorders. Calcium Channel Blockers: Monitor for reflex tachycardia and peripheral edema. Vasodilators: Monitor for increased blood volume and systemic lupus erythematous-like syndrome. ACE Inhibitors and ARBs: Monitor for first-dose hypotension, cough, hyperkalemia, and angioedema. Adrenergic Antagonists: Monitor for drowsiness, dry mouth, and withdrawal symptoms. Antingis antagonist 25 R E S I S TA N T H T N Definition: Failure to reach goal BP in patients taking full doses of an appropriate 3-drug therapy regimen that includes a diuretic. Complications: Increases a 2- to 6-fold risk of MI and stroke. Management: Identify potential contributing factors, assess adherence, and evaluate alternative drug combinations. I 26  adherence, and evaluate alternative drug combinations. 26 N U R S I N G D I A G N O S I S & E VA L U AT I O N Nursing Diagnosis: Altered blood pressure, ineffective tissue perfusion, potential complications (stroke, MI, renal dysfunction, retinopathy), risk for fluid/electrolyte impairment, impaired nutrition. Evaluation: Achieve and maintain goal BP, understand and implement a treatment plan, and report minimal side effects of therapy. Answer: A A 56-year-old man whose father died at age 62 27 HOME BP MONITORING from a stroke. History of a close blood relative (e.g., father to son) with hypertension is associated with an 28 increased risk for developing hypertension; atherosclerosis is the most common cause of AUDIENCE RESPONSE QUESTION cerebrovascular disease. Hypertension is the major risk factor for cerebral atherosclerosis and stroke. F While performing blood pressure screening at a health fair, the nurse counsels which person is having the greatest risk for developing hypertension. a.A 56-year-old man whose father died at age 62 from a stroke b.A 30-year-old female advertising agent who is unmarried and lives alone c. A 68-year-old man who uses herbal remedies to treat his enlarged prostate gland d.A 43-year-old man who travels extensively with his job and exercises only on weekends 29 C A S E S T U D Y- H T N Patient Profile: Name: C.S. Age: 40 years Occupation: Truck driver Lifestyle: Eats mainly fast food, smokes a pack of cigarettes a day Height: 5 ft, 9 in Weight: 230 pounds Vital Signs: BP 182/104, HR 90, RR 24, Temp 97.0°F Background: C.S. attends a community health screening and No smoking, exercise, or caffeine 30 minutes prior to BP Rest quietly for 5 minutes; relax; no talking Proper size and placement of cuff important for accuracy Position arm at level of heart Use auscultatory (oscillatory) method Deflate 2 to 3 mm Hg/sec Take in both arms; note differences Use arm with highest BP for future If can t use upper arm; use forearm and radial artery or Doppler; document site Clean cuff between patients per agency policy HTN Leads to the development of cardiovascular disease (CVD); As BP increases so does the risk for complications; Increased risk, MI, HF, CVA, renal disease, vision loss  Vital Signs: BP 182/104, HR 90, RR 24, Temp 97.0°F Background: C.S. attends a community health screening and mentions he hasn't seen a healthcare provider in a long time. He smokes to pass the time and manage stress during long hours of driving. Questions: 1.What risk factors for hypertension does C.S. have? 2.What clinical manifestations of hypertension would you assess for in C.S.? 3.What complications will you assess C.S. for? 4.What diagnostic studies might you expect the healthcare provider to order for C.S.? 5.What lifestyle modifications would you recommend for C.S. to control his BP? 6.What would you teach C.S. about hydrochlorothiazide? 7.What could you do to increase C.S.’s compliance with his medication and lifestyle changes? 8.How would you evaluate the effectiveness of his treatment strategies after 3 months? 30 LEARNING OBJECTIVES 1.Summarize the classification, etiology, and risk factors for hypertension 2.Select appropriate strategies for the prevention of hypertension 3.Recognize the clinical manifestations and diagnostic findings related to hypertension 4.Describe the collaborative care for hypertension, including drug therapy and lifestyle modifications 5.Explain the collaborative care of the older adult with hypertension 6.Prioritize the nursing management of the patient with hypertension 31  arterial sclerosis 1/20/25 if plague buildup 1 ATHEROSCLEROSIS AND CORONARY ARTERY DISEASE Rozmin Jiwani PhD, RN Adapted from Megan Lippe PhD, RN, Ruth R. Johnson MSN, RN, CMSR 2 OBJECTIVES 1.Summarize the etiology and risk factors for the development of atherosclerosis, coronary artery disease, and chronic stable angina 2.Describe the nursing role in the promotion of therapeutic lifestyle changes in patients at risk for coronary artery disease 3.Explain the precipitating factors, clinical manifestations, and collaborative care to include medication therapy and nursing management of the patient with coronary artery disease and chronic stable angina 4.Describe the cardiovascular diagnostic studies potential complications, and nursing management. 5. 3 CARDIOVASCULAR DISEASE (CVD) Leading cause of death in the United States Coronary artery disease (CAD)—most common CVD CAD—asymptomatic or chronic stable angina (chest pain) Major death CAD—profound effect on perfusion Perfusion depends on the heart’s ability to generate enough cardiac output (CO) to distribute blood to all body tissues. Significant CAD negatively affects heart function; impaired CO and decreased perfusion Acute coronary syndrome (ACS) —unstable angina (UA) or myocardial infarction (MI) 4 ATHEROSCLEROSIS ETIOLOGY AND PATHOPHYSIOLOGY Chronic endothelial injury causing an inflammatory response Fatty streak- earliest lesions of atherosclerosis Fibrous plaque- the result is narrowing of the vessel. Complicated lesion-last stage, most dangerous, could cause total occlusion Collateral circulation- re-route- alternate circulation around a LAD away from 5 hard 1  occlusion Collateral circulation- re-route- alternate circulation around a blocked artery 5 ATHEROSCLEROSIS AFFECTS ALL BLOOD VESSELS But…most common: Brain- vascular dementia & stroke Carotid arteries- stroke Peripheral- PAD causing amputations Coronary arteries- Angina & MI Kidneys- CKD Eyes- ischemic eye disorders (age-related macular degeneration) Sex organs- sexual dysfunction 6 ATHEROSCLEROSIS 7 CORONARY ARTERY DISEASE (ISCHEMIC HEART DISEASE) 8 CAD MAJOR MODIFIABLE RISK FACTORS 1 High serum lipids : Total chol > 200 mg/dL bad LDL > 130 mg/dL gold HDL Men < 40 mg/dL: women < 50 mg/dL Triglycerides >150 mg/dL 2 Hypertension Diabetes- 2 to 4 times greater even those with well-controlled blood glucose levels isk for Metabolic syndrome -central obesity, HTN, abnormal lipids, high fasting glucose CAD Obesity BMI greater than 30kgm Proportional Sedentary lifestyle a a ne to degree of Tobacco use and secondhand exposure Carbon monoxide org eensag obesity physical inactivity lack of physical activity a week 9 CAD CONTRIBUTING MODIFIABLE RISK FACTORS Psychological - depression, acute and chronic stress, SNS 10 9 CAD CONTRIBUTING MODIFIABLE RISK FACTORS Psychological - depression, acute and chronic stress, SNS stimulation causes increased release of catecholamines Homocysteine-(amino acid)- high levels are linked to CAD Substance abuse –cocaine and methamphetamine can produce coronary artery spasms resulting in chest pain and MI 10 CAD NON-MODIFIABLE RISK FACTOR 1 Age –highest among middle-aged men As humans age, the incidence of CAD increases, and people over 75 are more likely to have multiple-vessel CAD. Gender- Risk increases for men over 45 and women over 55. Women are more likely than men to die after their first MI. CAD is the leading cause of death in women Genetics – genetic predisposition is a key factor in the occurrence of CAD 2 The prevalence of CAD also depends on race: Whites White males have the highest incidence and mortality of CAD Blacks Males have a higher incidence of CAD compared to Hispanic and Asian males Hispanics Have slightly lower rates of CAD than either non-Hispanic Whites or Blacks Have lower death rates from CAD than non-Hispanic Whites and Blacks Native Americans Die from heart disease earlier than expected Mortality rates for those under age 65 are twice as high as those of other Americans Sys last 711 min or more 11 OUTCOMES OF CAD new in onset Asymptomatic – maybe years Clinical manifestations not apparent in early stages Risk screening important similar to stable unstable angina angina BUT on ur rest sym more frequent lost larger than pt thrinic stable unpredictable t trt immediately 11 Clinical manifestations not apparent in early stages Risk screening important May eventually develop stable chest pain Acute Coronary Syndromes Unstable angina (UA or USA) Non-ST-elevation MI (NSTEMI) 12 ST-elevation MI (STEMI) INTERPROFESSIONAL AND NURSING CARE r 13 14 HEALTH PROMOTION PHYSICAL ACTIVITY a TIE III 15 NUTRITIONAL THERAPY Nurse should discuss nutrition at each patient encounter Fat is 25-35% total calories Mostly monounsaturated and polyunsaturated PREDIMED trial (Prevencion con Dieta Mediterranean) Mediterranean diet supplemented with extra virgin olive oil or mixed nuts vs control diet 30% reduction of CVD death, MI, stroke Prominently whole food plant-based show improvement in coronary artery angiograms 16 MEDICATION THERAPY 17 CARDIOVASCULAR DISEASE DIAGNOSTIC STUDIES 18 DIAGNOSTIC TEST AND IMAGING 19 DIAGNOSTICS 12-Lead ECG ST changes Ischemia (ST depression) Injury/cell death (ST elevation) T wave changes (inversion) New onset bundle branch block (BBB) Development of a deep or pathologic Q wave 20 DIAGNOSTIC TESTS AND IMAGING Echocardiogram wintin  atherostarctic Lipid blood thinner heartmuscle Lupo 20 DIAGNOSTIC TESTS AND IMAGING Echocardiogram Valvular structure and motion, heart chamber size and contents, ventricular and septal motion and thickness, pericardial sac and ascending aorta Contrast, M-mode, 2-dimensional, color-flow imagine, 3- dimentional Pharmacologic Echo w/ IV adenosine, dobutamine, dipyridamole or regadenoson (Lexiscan) Transesophageal Echocardiogram (TEE) May use IV Contrast 21 DIAGNOSTIC TEST AND IMAGING 22 DIAGNOSTIC TEST AND IMAGING Coronary Angiography (Cardiac Cath) Examines heart muscle, pressure readings, valves, and coronary arteries Contrast dye used with serial radiographs Percutaneous coronary intervention (PCI) such as coronary angioplasty or stent placement U.S. global coronary stent market = approx. $8.6 billion/year 23 CARDIAC CATHETERIZATION CARE 1 BEFORE PROCEDURE: 2 Allergies (latex, rubber, x-ray dye) Consent NPO Assess renal function (contrast-induced nephropathy) Generally, hold anticoagulants, diuretics, & antidiabetics Pitt procedure 3 Assess the puncture site Femoral site: keep the leg straight and bedrest if Compression Vital sign trends Neurovascular ECG more serious Assess for complications 4 24  ECG Assess for complications Fluid and monitoring on hand for catheter removal (if not done in cath lab) 4 POST-PROCEDURE: 24 RELATIONSHIPS BETWEEN CAD, CHRONIC STABLE ANGINA, AND ACS abt 25 ANGINA -CHEST PAIN make sure oz if worried angina Myocardial ischemia: demand for O2 higher than supply Usually from narrowing of coronary arteries Types: Stable (chronic, exertional) Unstable (new-onset, > 10 min) Prinzmetal’s angina (or variant angina) Transient coronary artery vasospasm Rare- heavy smokers, migraine sufferers 26 CHRONIC STABLE ANGINA (CSA) 27 OTHER FORMS OF ANGINA Microvascular angina Chest pain without significant CAD or coronary artery spasm Distal branches of coronary microcirculation More common in women Silent Ischemia Don’t know they are having a problem until MI Increased prevalence in diabetes Diabetic neuropathy Confirmed by ECG changes 28 CHRONIC STABLE ANGINA (CSA) Assess OPQRST, VS, & ECG Predictable (pain at rest is UNUSUAL and may indicate unstable angina) Pain subsides when- precipitating factors alleviated resting 1 nitroglycerin administered or I  resting nitroglycerin administered Women & older adult Atypical- dyspnea, nausea, mid-epigastric discomfort, fatigue Silent Ischemia Refers to ischemia that occurs in the absence of any subjective symptoms (consider patients with diabetes, neuropathy affecting the nerves) 29 ANGINA PRECIPITATING FACTORS Physical exertion Temperature extremes Strong emotions Heavy meal consumption Tobacco use (and environmental tobacco) Sexual activity Stimulants Circadian rhythm patterns 30 CHRONIC STABLE ANGINA: MANAGEMENT OF CARE ABCDEF A= Antiplatelet/Anticoagulant; Antianginal; Ace Inhib/ARB B= β-adrenergic blocker; BP control C= Cigarette smoking cessation, cholesterol mgmt, CCB, cardiac rehab D= Diet, DM mgmt, depression screening E= Education, exercise F= Flu vaccine 31 PHARMACOLOGIC TREATMENT 32 Nitroglycerin edu 1 Assess location, duration, intensity, and precipitating pain factors Monitor BP and pulse before and after administration Hold for hypotension (Systolic BP < 90 mm Hg or more than 30 mm Hg below baseline) minimum Side Nitroglycerin can cause effects- Dizziness, methemoglobinemia, Headache, a condition where Hypotension, hemoglobin is altered and cannotTachycardia effectively release oxygen to body tissues. This can exacerbate anemia, leading to insufficient oxygen delivery. both nitroglycerin and PDE-5 inhibitors (like sildenafil) cause vasodilation. When used together, they can lead to severe hypotension (dangerously low blood pressure), which can result in fainting, shock, or even death Hypovolemia is a condition of decreased blood volume. Nitroglycerin can further lower blood pressure by dilating blood vessels, which can lead to severe hypotension or shock in patients with uncorrected hypovolemia Nitroglycerin can increase blood flow to the brain, raising intracranial pressure. This can worsen conditions like head injuries or other situations where intracranial pressure is already elevated Nitroglycerin patches can cause burns or other injuries at the site of the patch due to the electrical current. Therefore, it is recommended to remove the patch before the procedure 32 1 mm Hg below baseline) Side effects- Dizziness, Headache, Hypotension, Tachycardia Contraindications- Severe anemia Concurrent use of PDE-5 Inhibitors (sildenafil, avanafil) Uncorrected hypovolemia Increased intracranial pressure Caution during cardioversion (remove patch) 2 Administration defyme Patches/ointment: hairless site and avoid distal extremities Do not massage into skin Short-acting ointment- 1-2 inches every 6-8 hrs Long active patch- worn 12-14 hr/day and then taken off for 10- 12 hours per day Lingual spray Lift tongue and spray under the tongue 1-2 sprays; may be repeated every 5 minutes for a total of 3 doses Sublingual (SL) keep in original container. Keep cool (not refrigerated) replace 6 months after opening to maintain potency Should taste bitter repeat every 5 min for a total of 3 doses 33 PHARMACOLOGIC TREATMENT CONT 34 PHARMACOLOGIC TREATMENT CONT Antiplatelet: aspirin, clopidogrel, ticagrelor Anticoagulants: heparin, enoxaparin, warfarin Lipid lowering (same as CAD) 1st line= statins 35 NURSING DIAGNOSES 36 PATIENT EDUCATION 37  35 36 PATIENT EDUCATION 37 OBJECTIVES 1.Summarize the etiology and risk factors for the development of atherosclerosis, coronary artery disease, and chronic stable angina 2.Describe the nursing role in the promotion of therapeutic lifestyle changes in patients at risk for coronary artery disease 3.Explain the precipitating factors, clinical manifestations, and collaborative care to include medication therapy and nursing management of the patient with coronary artery disease and chronic stable angina 4.Describe the cardiovascular diagnostic studies potential complications, and nursing management. 5. 38 QUESTIONS? I