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| back 1 PANCREAS |
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| back 2 Acute Pancreatitis- Etiology |
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| back 15 SIGNS AND SYMPTOMS OF PANCREAS |
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| back 16 Collaborative Problems and Potential Complications PANCREAITIS |
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| back 17 PANCREAITIS |
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| back 18 DIAGNOSTIC TESTS Chronic Pancreatitis |
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Histamine Antagonists | back 19 THERAPUTIC TX Chronic Pancreatitis |
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| back 20 Chronic Pancreatitis |
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| back 21 Chronic Pancreatitis: SIGNS AND SYMPTOMS |
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| back 22 DIAGNOSIS Chronic Pancreatitis |
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| back 23 Chronic Pancreatitis TX |
front 24 What is a major symptom of chronic pancreatitis? A.Recurrent attacks of severe upper abdominal and back pain accompanied by vomiting B.Fever, jaundice, confusion, and agitation C.Ecchymosis in the flank or umbilical area D.Abdominal guarding | back 24 A.Recurrent attacks of severe upper abdominal and back pain accompanied by vomiting Chronic pancreatitis has recurrent attacks of severe upper abdominal and back pain accompanied by vomiting. Acute pancreatitis presents with fever, jaundice, confusion, agitation, ecchymosis in the flank or umbilical area, and abdominal guarding. |
front 25 COPD | back 25 refers to diseases that obstruct air flow and commonly includes chronic bronchitis and emphysema (airflow limitation) |
front 26 Exacerbation and co-morbidity contributes to the clinical manifestations | back 26 contributes to the clinical manifestations |
front 27 Presents with 3 cardinal signs and symptoms –Dyspnea –Chronic cough –Sputum production Less common signs
| back 27 COPD SIGNS AND SYMPTOMS |
front 28 cigarette, air pollution, allergy, autoimmunity, infection, occupational exposure, aging etc. Excessive mucous production resulting in chronic cough is characteristic of chronic bronchitis. | back 28 RISK FACTOR FOR COPD |
front 29 Inflammatory changes leads to mucociliary dysfunction & bronchial constriction Increase production of mucus with a chronic cough that persists for at least 3 months of the year for 2 consecutive years With continued irritation epithelial cells die, destroying their Celia Goblet cells hypertrophy creating more tenacious mucus The inability to clear the airway of excess mucus causes susceptibility to infections | back 29 CHRONIC BRONCHITIS |
front 30 Repeated infections lead to airways showing scarring, stenosis and obstruction
| back 30 CHRONIC BRONCHITIS |
front 31 Productive cough, exertional dyspnea, and wheezing Over time, hypoxemia (PaO2 <60 mm Hg or O2 saturation <88%) may develop with hypercapnia (PaCO2 >45 mm Hg) leading to respiratory acidosis. Because of their reduced oxygen saturation they start to retain fluid. polycythemia develops as a result of increased production of red blood cells as the body attempts to compensate for chronic hypoxemia. the resp. acidosis , polycythemia and < O2 leads to the constant cyanosis and bloated appearance and that’s why chronic bronchitis is referred to as “blue bloaters” | back 31 CLINICAL MANIFESTATIONS COPD |
front 32 Degenerative, nonreversible disease characterized by –Destruction of the alveoli –Enlargement of the distal airspaces –Breakdown of alveolar walls leads to loss of alveolar recoil+ decrease ventilation Breathing out is the main problem | back 32 Pulmonary Emphysema |
front 33 Thin, emaciated body frame Dyspnea on exertion, later at rest Shortness of breath and “air hunger” Chronic productive cough Classic “barrel chest” indicating constant lung over inflation and overwork of chest muscles used for breathing (diaphragm). Dilatation and destruction of lung tissue distal to terminal bronchioles. It leads to air trapping and an increase in total lung capacity. There is also a loss of alveolar tissue, reducing capacity for gas exchange. Carbon dioxide clearance is not impaired to the same extent as chronic bronchitis, usually because patients increase their respiratory effort and ventilation, the pt. Is not usually cyanotic Instead you will observe a pinkish skin color and that is why they are called “pink puffers” | back 33 Clinical Manifestations: Pulmonary Emphysema |
front 34 H&P CXR, CT scan Pulmonary function tests ABGs Pulmonary test to rule out TB or malignancy | back 34 Diagnostic Eval. Of COPD |
front 35 Elevated Hct - to low oxygenation levels Hypoxemia-low PO2 less than 80mmHg Hypercapnia- high PCO2 -45 mmHg Resp acidosis | back 35 LABS COPD |
front 36 The nurse reviews the arterial blood gases of a patient. Which result would indicate the patient has later stage COPD? pH 7.32, PaCO2 58 mm Hg, PaO2 60 mm Hg, HCO3 30 mEq/LnpH 7.30, PaCO2 45 mm Hg, PaO2 55 mm Hg, HCO3 18 mEq/L pH 7.40, PaCO2 40 mm Hg, PaO2 70 mm Hg, HCO3 25 mEq/L pH 7.52, PaCO2 30 mm Hg, PaO2 80 mm Hg, HCO3 35 mEq/L | back 36 ABGS COPD Answer: A Rationale: In later stage COPD, the patient will have a low or low normal pH, a high normal or above normal PaCO2, and a high normal or above normal HCO3-. This indicates compensated respiratory acidosis, as the patient has chronically retained CO2 and the kidneys have conserved HCO3- to increase the pH to near or within the normal range. |
front 37 This image shows multiple cystic areas caused by destruction of lung tissue typical of emphysema. | back 37 Lung Severe Emphysema: |
front 38 The chest cavity is opened at autopsy to reveal numerous large bullae apparent on the surface of the lungs in a patient dying with emphysema. Bullae are large dilated airspaces that bulge out from beneath the pleura. Emphysema is characterized by a loss of lung parenchyma by destruction of alveoli so that there is permanent dilation of airspaces | back 38 BULLAE |
front 39 nCan improve survival in patients with advanced COPD who have hypoxemia, (low blood oxygen levels) nThis treatment can improve a patient's exercise tolerance and ability to perform on psychological tests which reflect different aspects of brain function and muscle coordination | back 39 HOME OXYGEN THERAPY COPD |
front 40 Increasing the concentration of oxygen in blood also improves the function of the heart and prevents the development of Cor pulmonale. Monitor amount of oxygen given. No more than 3L is recommended. Why? | back 40 Some patients cannot maintain this effort and their carbon dioxide levels rise. This stimulates respiratory drive for a time, but then they become desensitized to it and they depend on hypoxemia to drive ventilation. Oxygen can also lessen sleeplessness, irritability, headaches, and the overproduction of red blood cells. n Continuous oxygen therapy is recommended for patients with low oxygen levels at rest, during exercise, or while sleeping. nReview Oxygen delivery system (NC, Mask etc..) |
front 41 Suppressed respiratory drive and low O2 Fire Oxygen toxicity | back 41 COMPLICATIONS OF OXYGEN THERAPY |
front 42 COPD MEDICATIONS Bronchodilators Methylxanthines Corticosteroids or Steroids Antibiotics Expectorants Diuretics Digitalis Leukotriene Inhibitors Tranquilizers Pain meds Cough suppressants (codeine, etc.) Sleeping pills (barbiturates, etc.) | back 42
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front 43 Surgical removal of large air spaces called bullae that are filled with stagnant air May be beneficial in selected patients Recently, use of lasers to remove bullae has been suggested | back 43 BULLECTOMY |
front 44 nHas been successfully employed in some patients with end-stage COPD. n In the hands of an experienced team, the 1-year survival in patients with transplanted lungs is over 70 percent. | back 44 LUNG TRANSPLANT |
front 45 Help to overcome the conditions which cause dyspnea, anxiety and allergic reactions Smoking cessation Oxygen therapy Breathing retaining Airway clearance techniques Improve capacity for physical exercise and activities of daily living Frequent rest periods Diet : Offer small frequent meals; high calorie, high protein 2-3L fluid unless contraindicated IV/PO Daily weights n Intermittent mechanical ventilatory support relieves dyspnea and rests respiratory muscles in selected patients. nPurse lip breathing techniques | back 45 PULMONARY REHABILITATION |
front 46 Continuous positive airway pressure (CPAP) is used as an adjunct to weaning from mechanical ventilation to minimize dyspnea during exercise. Relaxation techniques may also reduce the perception of ventilatory effort and dyspnea | back 46 Breathing exercises and breathing techniques, such as pursed lips breathing and relaxation Place in high Fowler’s position or seated on the bedside with the arms folded on the over bed table to promote full lung expansion (Tripod) Keeping air passages reasonably clear of secretions is difficult for patients with advanced COPD. Re: Some commonly used methods for mobilizing and removing secretions are already discussed. |
front 47 nAvoid smoking environment nBreathing toxic fumes such as glue, paint etc. nAerosol products other than meds nGoing to places with polluted atmosphere nAvoid people with infections etc.. | back 47 C: IS FOR CONTROLLED ENVIROMENT |
front 48 Highly communicable disease Caused by mycobacterium tuberculosis –Rod shaped, gram+, acid fast bacillus (AFB) http://en.wikipedia.org/wiki/Mycobacterium | back 48 WHAT IS TB? |
front 49 Spread by airborne droplet from an affected person during –Coughing –Speaking –Laughing –Sneezing Another person breathes in the bacteria & becomes infected Close quarters | back 49 TRANSMISSION OF TB |
front 50 The tuberculosis bacterium invades the alveoli and begins to multiply forming a tubercle lesion The body’s defense mechanism encapsulate the tubercle leaving a scar. May continue to grow to form granulomas or cheese like mass called caseation This is what is seen on a CXR and is called the Ghon tubercle or primary lesion Primary lesions form, they may become dormant, but can be reactivated and become a secondary infections when re-exposed to the bacterium | back 50 Pathophysiology TB |
front 51 www.anatomy.unimelb.edu.au/museum/collection.html | back 51 Dissected, preserved lung with tuberculosis TB |
front 52 Close contact with infected person Live in areas where TB in common HIV infections, immune system diseases The elderly Homeless, poor, crowded living conditions Poor access to heath care Illicit drug use Health care professional | back 52 WHOS AT RISK TB |
front 53 TB has an insidious onset and many pts are not aware of the symptoms until the disease is well advanced Fever, night sweats, malaise Anorexia and weight loss Cough non productive at first, but later produces yellow mucoid sputum Hemoptysis Pleuritic chest pain and tightness Dyspnea if severe lung involvement | back 53 CLINICAL MANIFESTATIONS OF TB |
front 54 H&P especially for pts at risk Tests: Sputum smear and C&S –AFB x 3 samples are usually obtained for an acid-fast smear . (May aspirate gastric fluid if unable to obtain specimen) –The sputum test confirms the diagnosis of TB because Chest X-rays –Determines the presence of Ghon tubercles or lesions on the lungs and the extent of the disease (cheesy caseations) –Indicates presence and extent of disease process but cannot differentiate active from inactive form – WBC and ESR increased A + reaction is noted if the induration is greater than 5mm This means that the patient has had contact with tubercle bacillus. It does not mean that active disease is present in the body . (antibodies are now present) Check for vaccination with BCG | back 54 DIAGNOSTIC TESTS TB |
front 55 ¨Goal of treatment is to prevent transmission, control symptoms, and prevent progression of the disease ¨6-12 months, may be as long as 24 months ¨2-4 meds Given concurrently ¨Mycobacteria grow slowly, resistance is common vImproper or noncompliant use of treatment programs may cause the development of mutations in the tubercle bacilli resulting in a multidrug resistant strain of TB (MDR-TB (+) Mantoux test, (-) CXR, and at risk for the disease are treated prophylactically to prevent development of active TB Isoniazid (INH) for 9-12 months | back 55 Medical management TB |
front 56 Combination drug therapy is most effective –It destroys the organism and minimize development of multiple drug resistant strain of the bacilli –After TB meds have been given for 2-3 weeks, the risk of transmission is reduced greatly | back 56 ACTIVE TB |
front 57 Drug of choice Take with meals if GI upset otherwise take one hr before or 2hr after meals. Absorption is decreased if given with food Avoid antacids exp. Aluminum based – decrease absorption Peripheral neuritis – drug is usually given with Vitamin B6 (Pyridoxine) to prevent this side effect Hepatitis Nausea, vomiting, diarrhea, stomach pain Avoid foods with tyramine – aged cheese, smoked fish, tuna, sauerkraut, avocado etc. Combined with INH will make you sicker | back 57 Drugs for TB : INH Isoniazid |
front 58 150-300mg , maximum dose 600mg /day S/S: hepatotoxicity, hepatitis, blood dyscrasias Steven Johnson’s syndrome Red/orange stain to urine, feces, saliva, skin, sputum, sweat and tears .. | back 58 Rifampin (+ INH) |
front 59 15mg/kg po daily or 50mg /kg twice weekly when use in combination with other TB drugs. Max. 1200mg/day S/S: optic neuritis leading to color blindness (exp.Red- Green) Peripheral neuritis; GI irritation Gouty arthritis from ^ uric acid levels | back 59 Ethambutol/myambutol |
front 60 Bactericidal. Kills mycobacterium present in macrophages S/S: hepatotoxicity, thrombocytopenia Hyperuricemia- gout (hot painful, swollen big toe, ankle or knee) Gi irritation | back 60 Pyrazinamide (PZA |
front 61 Not used as much theses days; has now been replaced by Ethambutol S/S GI upset, fever, rash, hepatitis Fluid retention because of high sodium content 150mg/kg/day | back 61 Para-Aminosalicylic Acid |
front 62 Antibiotics- aminoglycosides IM/ IV S/S: nephrotoxicity 8th cranial nerve damage- ototoxicity | back 62 Streptomycin |
front 63 Maintain prescribed isolation precautions Diet high carbohydrate, protein, iron & Vit. C. Small frequent meals. Stress food & meds combinations Check for vaccination with BCG vaccine (Bacille Calmette-Guerin Vaccine) Lifestyle changes Review other nursing measures in the Hinkle chapter. | back 63 NURSING MANAMGEMENT TB |
front 64 Rheumatoid arthritis (RA) is a chronic disease in which various joints in the body are inflamed, leading to swelling, pain, stiffness, and the possible loss of function. Rheumatoid arthritis should not be confused with other forms of arthritis, such as osteoarthritis or arthritis associated with infections. Rheumatoid arthritis is an autoimmune disease in which the body's immune system attacks joints and other tissues. The pattern of joints affected is usually symmetrical, involves the hands and other joints, and is worse in the morning. Rheumatoid arthritis is a systemic (body-wide) disease, involving other body organs, whereas osteoarthritis is limited to the joints. Both forms of arthritis can be crippling. Synovitis Synovium Thickens, Fluid Accumulates Destructive Pannus Erodes Joint Cartilage, Destroys Joint Bone Pannus Converted to Bony Tissue Joint Deformity Other Connective Tissue Affected | back 64 RHEUMATOID ARTHRITIS |
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front 98 Early Symptoms Bilateral, Symmetrical Joint Inflammation Reddened, Warm, Swollen, Stiff, Painful Stiffness After Resting Activity Decreases Pain and Stiffness Low Grade Fever, Weakness, Fatigue, Anorexia Late Symptoms Joint Deformity Secondary Osteoporosis | back 98 SIGNS AND SYMPTOMS RA |
front 99 Unknown Genetic Predisposition Environmental Abnormal Autoimmune Response – Antibodies (Rheumatoid Factor) some environmental or biologic trigger, such as a viral infection or hormonal changes | back 99 ETIOLOGY RA |
front 100 Health history: include onset of and evolution of symptoms, family history, past health history, and contributing factors Functional assessment Arthrocentesis X-rays, bone scans, CTs, and MRIs Tissue biopsy Blood studies | back 100 Patient Assessment and Diagnostic Findings RA |
front 101 Rheumatoid Factor (RF) Red Blood Cell (RBC) C4 Complement Decreased Erythrocyte Sedimentation Rate (ESR) Antinuclear Antibody (ANA) C-reactive Protein (CRP) | back 101 DIAGNOSIS RA |
front 102 Medication Disease-modifying Antirheumatic Drugs (DMARDs) Sulfasalazine (Azulfidine) Leflunomide (Arava) Etanercept (Enbrel) Adalimumab (Humira) Methotrexate -antineoplastic Gold salts- antiflammatory effect Prednisone NSAIDs – Indocin, motrin, naprosyn etc. Salicylates -ASA COX -2 Inhibitor- Celebrex Heat/Cold Balanced Rest and Activity Surgery – Total Joint Replacement | back 102 Therapeutic Interventions RA |
front 103 Acute Pain Disturbed Body Image Fatigue Self-care Deficit Impaired Physical Mobility Deficient Knowledge Ineffective coping | back 103 NURSING DIAGNOSIS RA |
front 104 Disease Process Medication Management Rest and Exercise Vocational Counselor Community Resources | back 104 PATIENT EDUCATION HR |
front 105 Major goals may include: Relief of pain and discomfort Relief of fatigue Promotion of restorative sleep Increased mobility Maintenance of self-care Improved body image Effective coping Absence of complications | back 105 Nursing Process: The Care of the Patient with a Rheumatic Disease—Planning |
front 106 Autoimmune Disease More than 80 autoimmune diseases 75% of autoimmune diseases affect women One of the top 10 causes of death in women 65 and younger Lupus: Wolf | back 106 Systemic Lupus Erythematosus (SLE) |
front 107 1.4 million cases of lupus in the USA 90% are women 80% diagnosed between 15 and 45 years of age 50% have organ-threatening disease to kidneys, heart, lungs, liver, CNS, and hematopoetic system. | back 107 INCIDENCE OF LUPUS |
front 108 Definition: Chronic, inflammatory disturbance caused by an exaggerated production of “auto-antibodies.” Immune complexes and fibrin deposit in blood vessels, collagen, and in organs Can result in necrosis of glomerular capillaries | back 108 Systemic Lupus Erythematous |
front 109 Abnormal Antibodies Immune Complex Formation Complement System Activation Affects Connective Tissue | back 109 Pathophysiology SYSTEMIC LUPUS ERYTHEMATOUS |
front 110 Disturbance is probably caused by some combination factors of: 1. Genetic 2. Hormonal 3. Environmental | back 110 Immuno-Regulatory SYSTEMIC LUPUS ERYTHEMATOUS |
front 111 Genetics: Occurs in families by no gene isolated yet. Hormonal: Estrogen metabolism is abnormal, flares with pregnancy and post-partum and post-menopausal HRT Environmental: Sunlight, stress, burns, infection, antibiotics | back 111 SYSTEMIC LUPUS ERYTHEMATOUS |
front 112 Drugs: Hydralazine (Apresoline) Procainamide (Pronestyl) Isoniazid (INH) Chloropromazine (Thorazine) Anticonvulsants NOTE: Usually if taken away, process goes away. | back 112 SYSTEMIC LUPUS ERYTHEMATOUS |
front 113 Systemic Lupus Erythematous (SLE) Multiple organs affected 1 test will not diagnose – Watch signs/symptom Discoid Lupus erythematous Mild involving skin of face, neck, cheeks, etc.. Rarely progresses to Systemic Lupus Drug induced lupus Symptoms go away when triggering drug is removed | back 113 TYPES OF LUPUS |
front 114 NOTE: Not a specific syndrome – varies from patient to patient
| back 114 HISTORY/PHYSICAL LUPUS |
front 115 Note: 4 or more symptoms simultaneously or serially Most common sites are: Cutaneous Muscle Tissue Lining of the lungs (pleurisy) Pericarditis Nervous system Kidneys | back 115 CLINICAL MANIFESTATIONS LUPUS |
front 116 80% have Skin Manifestations: Skin: butterfly rash across the cheeks and bridge of the nose (40% of patients) Diffuse maculopapular rash upon sun exposure (flat pimple like) Discoid lesions (round like coins) Both can itch, burn and cause “red palms” Alopecia Ulcers (Nasal or oral) - 35% of patients Pruritus | back 116 ASSESSMENT LUPUS |
front 117 Polyarthralgia | back 117 MUSCOSKELETAL LUPUS |
front 118 Atherosclerosis Cardiovascular disease – Cardiac Precautions | back 118 CARDIOPULMONARY LUPUS |
front 119 Renal Disease (50% of patients) 50% with proteinuria, cellular casts | back 119 RENAL LUPUS |
front 120 Lupus Nephritis – leading cause of death followed by cardiac involvement Develop High Blood Pressure | back 120 Lupus Nephritis |
front 121 Seizures
(15%) | back 121 CENTRAL NERVOUS SYSTEM LUPUS |
front 122 Caused by antibodies attacking blood cells Anemia (98%) with reticulocytosis (excessive RBC’s, but immature) Leukopenia (80%) – Highly prone to infections (lymphs
<4000 Thrombocytopenia (36%) platelets <100,000 | back 122 Hematologic LUPUS |
front 123 Dysphagia | back 123 GI SYMPTOM LUPUS |
front 124 Biopsy | back 124 DIAGNOSTIC TESTS LUPUS |
front 125 Fatigue Fever without infection Weight Loss | back 125 ASSOCIATE SYMPTOMS LUPUS |
front 126 ELEVATED: Note: Falls faster when lots of antibodies (gamma globulins) are attached. Positive Serum Tests: High + ANA (occurs when the body is fighting own DNA – in autoimmune diseases) +LE Prep – 75% of those with lupus will have these cells-lots of false+ tests. | back 126 DIAGNOSTIC STUDIES LUPUS |
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