N444: Test 6

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N444: Test 6 by Mind Map: N444: Test 6

1. Respiratory Assessment

1.1. A&P Review

1.1.1. Functions UR: Warms, filters air LR: Gas exchange Oxygen to tissues Carbon dioxide out to air (works with circulatory)

1.1.2. Structures Lungs Pleura Mediastinum Lobes 2 on left 3 on right Bronchi/bronchioles Alveoli Site of gas exchange Lubricated by surfactant Three types

1.1.3. Ventilation Inspiration 1/3 of cycle Contraction Increases space of diaphragmatic chamber Lowers ITP Air enters lungs, inflates them Expiration 2/3 of cycle Relaxation of diaphragm >> UPWARD movement >> Increases ITP Pushes air out of lungs Inadequate ventilation Decreased compliance Increased resistence

1.1.4. Perfusion R/T to ventilation Oxygen to hemoglobin Delivery of oxygen to tissues Cellular respiration Signs of hypoxemia Cyanotic or darker nail beds or sclera Pale and clammy skin

1.1.5. V/Q ratio V = Ventilation Movement of air into/out of lungs Q = Perfusion Filling pulmonary capillaries w/blood Entire output of RV Gas exchange @ alveoli Adequate V/Q ratio Matched ventilation + perfusion

1.2. Gerontological Differences

1.2.1. Decreased secretions

1.2.2. Weaker lungs

1.2.3. Weaker chest muscles that calcify

1.2.4. Decreased airway diameter

1.2.5. Increased immunosuppression

1.3. Assessment

1.3.1. History Dyspnea Clubbing Cyanosis Accessory muscle use Cough Sputum production Chest pain RR rate per minute WOB Lung sounds Normal Adventitious

1.3.2. Lung volumes & capacities TV = Air of each breath Use spirometer Measure several breaths IRV = Max volume inhaled during normal INH ERV = Max volume exhaled during normal EXHL VC: TV + IRV + ERV FEV: Volume exhaled forcefully / sec

1.3.3. Pulse oximetry Non-invasive Oxygen saturation of HgB in blood Normal is 95%+ May be unreliable (so still check ABGs) Check machine if running unusually low**

1.4. Diagnostics

1.4.1. Pulmonary function tests

1.4.2. ABGs

1.4.3. Sputum tests

1.4.4. CXR, CT, MRI

1.4.5. Fluroscopic stuies

1.4.6. Radioisotope procedures

1.4.7. Bronchoscopy Scope test Conscious sedation May cough up blood No red juice or soda Interferes w/interpretation

1.4.8. Thorascopy

1.4.9. Thoracentesis Pleural effusion Monitor site for excess bleeding or fluid Pain management needed

1.4.10. Biopsies


2.1. Overview

2.1.1. Airflow limitation that isn't fully reversible Progressive decrease of oxygen flow to all tissues R/T abnormal inflammation caused by toxins Airways, lungs, pulmonary vasculature Scar tissue forms Airway obstruction Lung tissue damage r/t damaging substances Altered vasculature >> vessel damage

2.1.2. Fourth leading COD (12th leading CO disability)

2.1.3. Made of disease(s) that cause airflow obstruction Chronic bronchitis Emphysema (either or)

2.1.4. No longer includes asthma (but may be comorbid)

2.2. Risk Factors

2.2.1. Tobacco smoke 80%+ of ALL cases Damages alveoli Destroys cilia (defenses) Most important risk factor 8 years of smoking or more (especially) May also include passive smoking (second-hand) Smoking cessation Ask about pack-year history Confined areas = increased damage

2.2.2. Non-modifiable Ambient air pollution Occupational hazards Genetics Alpha-antitrypsin

2.3. Pathophysiology

2.3.1. COPD Defining characteristics At least 3 mo over 2 consecutive years Aggravating, persistent cough Irritation of airways Inflammation, hypersecretion of mucus Proliferation of mucus-secreting glands & goblet cells >> Clogs the airway Structural changes Reduced ciliary fxn Thickened bronchial walls Narrowed bronchial airways Mucus plugging Damaged, fibrosed alveoli Diminished alveolar macrophage fxn

2.3.2. Emphysema Distension of air spaces beyond terminal bronchioles Destruction of alveolar walls Decreased alveolar surface area Increased "dead space" Impaired oxygen diffusion [NO GAS EXCHANGE IS HAPPENING!] Pulmonary capillary bed reduced Increased vascular resistence Increased pulmonary artery pressure Ultimately causes hypoxemia, cor pulmonale** Other manifestations 2:1 AP ratio instead of 1:2 May not report problems w/breathing b/c feels normal Tripod position helps SOB (or Semi-Fowler's position)

2.4. Clinical Manifestations

2.4.1. Appearance Pink puffer Severe COPD Thin with low muscle mass Puffing r/t "air hunger" Troubling removing CO2 Pursed lip breathing Blue bloater Appear blue-tinged, dusky Bronchitis Mucus blocks airway Hypoxemia

2.4.2. Slumped over appearance Energy conservation Tripod position for gas exchange

2.4.3. Will appear to be in distress WILL NOT COMPLAIN It feels normal Monitor frequently r/t increased CO2, low oxygen

2.4.4. Chronic cough w/sputum

2.4.5. Dyspnea Exertion Rest Orthopnea

2.4.6. Weight loss

2.4.7. Large neck muscles

2.4.8. Slow moving

2.4.9. Shallow respiration

2.4.10. Easily tired

2.4.11. Cor pulmonale

2.4.12. Clubbing

2.4.13. Prolonged expiration

2.4.14. Wheezing

2.5. Medications

2.5.1. Bronchodilators e.g. Mucomyst Opens vessels

2.5.2. Corticosteroids Treats inflammation May cause increased blood glucose* Monitor diabetics

2.5.3. Others

2.5.4. Oxygen Promote oxygenation w/o hypercapnia Oxygen is still a medication

2.5.5. Nursing care Shake MDI before admin Mouth care after MDI

2.6. Nursing Process

2.6.1. Assessment H&P Diagnostics Pulmonary function ABGs (precise) CXR Alpha-antitrypsin screen

2.6.2. Diagnoses Ineffective gas exchange Impaired airway clearance Ineffective breathing pattern Activity intolerance Deficient knowledge Ineffective coping

2.6.3. Collaboration RR failure Acidosis Hypercapnia Atelectasis Pulmonary infection Pneumonia Pneumothorax Pulmonary HTN Cor pulmonale** "R-sided heart failure" R/T pulmonary disease Changes that occur Dysrhythmias

2.6.4. Planning Smoking cessation Activity tolerance Self-care Coping Adherence Absence of complications

2.6.5. Interventions Gas exchange Medications Reduce irritants Directed coughing or "huff" coughing CPT Breathing exercises Supplemental O2 Activity tolerance Rehabilitation Pacing activities Exercises Walking aids to conserve energy Collaborate approach Nutrition Weights PO intake & supplements Avoid foods that cause bloating Don't drink before/during meals Mouth care Give bronchodilator 30 min before meal Others Realistic goals Avoid extreme temps Coping strategies Complications Education Patho Meds Procedures When/how to seek help Asepsis Avoid irritants Lifestyle changes* Health promotion NO smoking! Vaccinations Avoid high-exposure areas Medication compliance

2.6.6. Evaluation WOB easier? Voice need for meds? Compliant? No complications? Acidosis Cor pulmonale Pneumonia Pneumothorax Increase in FEV? Usually decreased w/COPD R/T fact they can't get rid of air

3. LRT Disorders

3.1. Pneumonia

3.1.1. Classifications CAP Late fall and winter Influenza HAP Preventible Costly PCP HIV-associated Immunosuppression Aspiration

3.1.2. Pathophysiology Microbes enter lungs From URT From bloodstream Inflammation of lung tissue Automatic response to invader Creates exudate, increased WBCs Impaires adequate V and diffusion of gases V/Q mismatch occurs Poorly oxygenated blood returns to heart Moves systemically >> hypoxemia

3.1.3. Risk factors Lifestyle Smoking Alcohol Unsterile equipment HCPs Age Immobility (supine) Post-op Immunosuppression Cough reflex MV/trachs

3.1.4. Clinical manifestations Mucopurulent sputum Congestion Sore throat Orthopnea/SOB Fatigue Poor appetite Cyanosis Cough Diaphoretic "Wet" lung sounds Corse Rhonchi

3.1.5. Alternative presentations Bacterial Chills Fever Pleuritic pain Tachypnea Accessory muscles Rapid, bounding pulse Viral Relative bradycardia >> Given elevated temperature

3.1.6. Medical management Antibiotics Determined by Gram stain Not indicated for viral Primary or secondary infection Supportive care RR Dehydration Inflammation O2 + IVF, then antibiotic

3.1.7. Nursing process Assessment Findings Secretions Cough Tachypnea SOB Concomitant Heart failure* Risk for shock Diagnoses Ineffective airway clearance Activity intolerance Risk for FVD Imbalanced nutrition Deficient knowledge Collaborative Continuing symptoms after therapy Shock RR failure Atelectasis Pleural effusion Confusion Superinfection Planning Airway clearance Energy conservation Fluid volume Nutrition Patient understanding No complications Interventions 2-3L per day* Humidified oxygen Coughing CPT Semi-Fowler's Rest Nutrition

3.2. Tuberculosis

3.2.1. Overview M. tuberculosis (acid-fast bacillus) Affects 1/3 of world Leading COD r/t infection On the rise in USA Immigration HIV Drug resistance* Decreased detection by HCPs Lack of funding

3.2.2. Pathophysiology Inhale microbe via droplet Travels to lungs, and may enter bloodstream (miliary) Inflammatory response Latent TB (infection) Active TB (disease

3.2.3. Transmission Person-to-person via droplet 1 cough = 3000 droplets Longer life in darker places Killed via direct sunlight Can remain in air for hours!

3.2.4. Risk factors Close contact Immunocompromised Inadequate health care Comorbidities Immigration Institutionalization Substandard housing HCPs!

3.2.5. Manifestations Low-grade fever Dry cough Night sweats Fatigue Weight loss Anorexia MP sputum or hemoptysis

3.2.6. Diagnostics TB skin test/Mantoux Indicator Unreliable* 0.01cc Read w/i 72 hrs Infected if: TB skin test + CXR = massive consolidation Mycobacterium + Symptoms +

3.2.7. Medications INH* Rifampin Pyrazinamide Ethambutol Nursing care Monitor liver fxn!! INH only for infection All 4 meds, daily for four weeks Then, INH + R for 4-7 months

3.2.8. Nursing Process Assessment H&P S/S Breath sounds Diagnoses Ineffective airway clearance Deficient knowledge Activity intolerance Isolation r/t droplet precautions Collaborative Malnutrition ADRs Multidrug resistance Spread of infection Planning/Goals Patent airway Knowledge Adherence Activity tolerance No complications

4. Neurodegenerative

4.1. Overview

4.1.1. CNS & PNS

4.1.2. Progressive neuron loss

4.1.3. Slow, progressive onset

4.1.4. Mostly home-health

4.2. Parkinson's

4.2.1. Decreased dopamine Substantia nigra in basal ganglia Rigidity, bradykinesia, tremors Postural instability

4.2.2. Risk factors Onset @ age 50 Males > females Family trend Head trauma Environmental Smoking Metals Herbicides Radiation Viral infxn Encephalitis AIDS Caucasian

4.2.3. Nursing care Assessment Degree of disability & function Emotional response/coping Home health Fall risk assessment Complications Manifestations Medications Care plan Mobility Self-care Bowel elimination Swallowing/nutrition Assistive devices Communication Coping Diagnoses Impaired verbal communication Constipation r/t muscle weakness Adult FTT r/t depression Imbalanced nutrition : <TBR Chronic sorrow Impaired mobility Self-care deficit

4.2.4. Manifestations 4 cardinal signs Tremor Rigidity Bradykinesia Postural instability ANS symptoms Psych changes Hypokinesia Micrographia Dysphonia Shoulder pain*

4.2.5. Complications RTIs UTIs Skin rbeakdown MSKT injuries r/t falls Dyskinesia Orthostatic hTN

4.2.6. Diagnostics H&P (at least 2 signs) PET & SPECT Labs, imaging = not useful

4.2.7. Medical care Control symptoms and promote function Cannot prevent progression Individualized care Medications Levadopa* Anti-cholinergics Antivirals (Symmetrel) Dopamine agents (Requip) MAOIs COMI (Comtan) Antidepressants Antihistamines Surgery Stereotactic procedures Neural transplant Deep brain stimulation

4.3. Alzheimer's

4.3.1. Pathophysiology Neuropathological/biochemical changes Tangles: Non-fxn neurons Plaques of amyloid protein Shrinkage of cerebral cortex r/t neuronal damage Cells that use ACH (deficiency)

4.3.2. Senile dementia

4.3.3. Confirmed via brain biopsy

4.4. ALS

4.4.1. "Lou Gehrig's disease" Unknown cause May be caused by excess glutamate (MSG) Amyotrophic Atrophy of muscle fibers Sclerosis Hardening Anterior and lateral columns

4.4.2. Risk factors Autosomal dominant in 5-10% 40-60 years old Males > females before age 60 Environmental toxins UV rays Carbon monoxide

4.4.3. Nursing process Assessment Muscle weakness Skin status Nutritional status RR status Support system Urinary/bowel status Plan of care Support Independence Communication ROM Repositioning Skin care ADLs Medications Diagnoses Anxiety RR-related Communication Decisional conflict r/t vent Impaired resilience Risk for aspiration

4.4.4. Manifestations Variable Fatigue Progressive weakness Cramps, twitching Atrophy Spasticity Regurgitation Problems laughing, talking, etc

4.4.5. Complications

4.4.6. Diagnosed by S/S EMG, muscle biopsy MRI

4.4.7. Nursing care Focused at function & QOL One medication: RIlutek Baclofen Dantrium Valium (anti-spasmodic) Active & passive ROM

4.5. MD

4.5.1. Incurable, inherited

4.5.2. Pathologic features Degeneration, loss of muscle Variation in muscle fiber size (contractures) Phagocytosis, regeneration Muscle replaced by CT Will also have elevated muscle enzymes

4.5.3. Nursing process Assessment MSKT Joint mobility CV, RR status Plan of care Promote function Enhance QOL Diagnoses Constipation Fatigue Nutrition Skin integrity

4.5.4. Diagnostics Blood or urine Exercise tests EMG, ECG, PFT

4.5.5. Medications Supportive only Muscle relaxants Baclofen Flexaril

4.5.6. Medical care Supportive Promote activity & QOL Supportive devices Spinal fusion sx

4.6. Huntington's

4.6.1. Premature death of basal ganglia cells Also affects cerebellum, cortex Unknown etiology R/T abnormal glutamine in nucleus >> Cell death

5. Neurological

5.1. Meningitis

5.1.1. Two forms Septic/bacterial Viral (less common) HIV Mono Immunosuppression

5.1.2. Inflammation with IICP Infected CSF Edema Brain compression IICP

5.1.3. Clinical manifestations Headache & fever (1st) Nuchal rigidity Positive K and B signs Photophobia Rash Change in LOC Acute fulminant infection Only 10% Death w/i few hours High temp w/lesions Dehydration, shock, seizures

5.1.4. A&D CT (brain stem herniation) MRI Lumbar puncture Cloudy Low glucose High protein High WBC Bacterial culture Gram stain*

5.1.5. Risk factors Lack of vaccination Close settings Tobacco use URI Otitis media/mastoiditis Immunosuppression

5.1.6. Prevented by vaccination!

5.1.7. Treatment Medications IV Vanc + Cephalosporin Decadron r/t inflammation IV fluids Phenytoin r/t seizures Antimicrobial prophlaxis Rifampin Cipro Rocephin

5.1.8. Nursing care Frequent neuro checks Injury Daily weights Labs Electrolytes Urine labs r/t SIADH Immobility Isolation Support

5.2. Brain abscess

5.2.1. Collection of pus and brain parenchyma

5.2.2. Purulent, usually bacterial

5.2.3. Higher risk w/poor immunity Otitus media Rhinosinusitis

5.2.4. Manifestations Headache esp. in AM Fever Vomiting r/t pressure Neuro efects base on area S/S IICP DLOC, seizures

5.2.5. A&D Neuroimaging MRI or CT aspiration Blood cultures CXR if lung infection EEG for brain activity, blood loss

5.2.6. Risk factors Immunosuppressed Cranial surgery Head injury Tongue piercing

5.2.7. Prevention Prompt treatment of risk factors

5.2.8. Treatment C&S >> antibiotics Corticosteroids for inflammation, edema Antiseizure meds

5.2.9. Nursing care Frequent, ongoing neuro checks Response to treatment Client safety Support

5.3. Encephalopathies

5.3.1. HSV Local necrotizing hemorrhage Edema >> Nerve body degeneration Most common cause of acute encephalitis HSV-1 HSV-2 Clinical manifestations Based on location HA Fever Confusion Changes in LOC A&D EEG shows temporal lobe alteration* LP MRI Viral cultures PCR for HSV-1 bands Treatment ASAP, for up to 3 weeks Antiviral agents

5.3.2. Arthropod-borne Transmission Primary (birds) Vector (mosquito) Secondary (human) Blood tests are slow Manifestations Early, flu-like Seizures for SL >> WN St. Louis West Nile A&D MRI LP IgM antibody Viral RNA in PCR Treatment Manage symptoms Siezures IICP Interferon w/SL Experimental for WN

5.3.3. Fungal Immunocompromised usually Certain areas, professions Respiratory risk Manifestations F/HA/M** Meningeal signs Cranial nerve dysfunction Skin lesions Seizures Associated w/stroke A&D H/O immunosuppression LP Serologic test w/antibody Blood cultures Lung biopsy r/t inhalation MRI for secondary Treatment Amphotericin B Maintenance

5.3.4. CJD Very rare, incurable Caused by prions TSE Manifestations Onset around age 50 Late psych symptoms Deterioration Ataxia Vision changes Paralysis 6-month survival A&D CSF has proteinase inhibitor EEG w/specific pattern MRI of basal ganglia Confirmed only through biopsy/autopsy

5.3.5. VCJD Human variation of BSE Manifestations Early psych symptoms Lays dormant for ~10yrs Onset at age 27 Affective changes S/C impairment Limb pain, muscle spasms/rigidity Incoordination Sleep disturbance 22 month survival A&D MRI: bilat hyperintensity of posterior thalamus Tonsillar biopsy*** shows prions Treatment Progressive, fatal Opiates for pain Meds for myoclonus

5.4. Autoimmune

5.4.1. MS Immune-mediated Progressive Demyelinating CNS Genetic Manifestation Relapses, exacerbations Parasthesias Coordination problems LOB Pain Vision changes A&D MRI LP Urodynamic studies Neuropsych testing Treatment Interferon Glatiramer acetate (Copaxone) Methylprednisone IV Symptom treatment Nursing care Memory aids Structured environment Relaxation Temperature Assistive devices

5.4.2. Myasthenia gravis Autoimmune Impaired muscle transmission Voluntary muscle weakness Manifestations Diplopia, ptosis Facial muscle weakness Swallowing impairment Speech General weakness A&D ACHI test MRI scan for enlarged thymus SEMG for delay in transmission Treatment Cholinesterase inhibitor Corticosteroids Cytotoxic meds Immunomodulating therapy Plasmapharesis Thymectomy Complications MG CG Nursing care Meds with food, on time Ocular strategies Maintain temp Aspiration

5.4.3. GBS Autoimmune Acute PN myelin attack Rapid Usually after virus Recovery phase* Manifestations Ascending weakness Bulbar weakness Tachy or brady HTN or htn Unaltered LOC A&D Symmetric weakness w/upward progression History of VI Changes in VC, NIF LP shows only elevated protein Nerve conduction Nursing care ICU observation High risk for RR distress Plasmapheresis IVIG** Cardiac dysrhythmias