COPD: Week 1 - PDF
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University of British Columbia Okanagan Campus
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This document provides notes on Chronic Obstructive Pulmonary Disease (COPD), covering its definition, causes, physiological changes, and clinical manifestations. It also discusses pulmonary function tests, acute exacerbations, and management goals. The document includes questions and answers related to COPD.
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WEEK 1 - COPD 1. What is the de nition of Chronic Obstructive Pulmonary Disease (COPD)? Preventable disease, characterized by persistent air ow limitation that is typically progressive...
WEEK 1 - COPD 1. What is the de nition of Chronic Obstructive Pulmonary Disease (COPD)? Preventable disease, characterized by persistent air ow limitation that is typically progressive 2. What changes are characteristic of emphysema & chronic bronchitis? Emphysema → Destruction of alveoli Bronchitis → Presence of chronic productive cough for 3 months in 2 successive years 3. What causes COPD (& how)? Exposure to tobacco smoke is the primary cause of COPD When cigarettes are smoked, approximately 4000 chemicals are inhaled into the lungs Nicotine stimulates the sympathetic nervous system, resulting in increased HR, peripheral vasoconstriction, BP, & cardiac workload → compounds health problems in a person with CAD Cigarette smoke further stimulates in ammatory response in the lungs, causing hyperplasia of the goblet cells in the lungs, which subsequently results in increased production of mucus Smaller airway injury leads to narrowing & obstruction of the airway Smoking reduces ciliary activity & accelerates loss of ciliated cells 4. What physiological changes occur in COPD? Chronic in ammation found in airways Air ow limitations during forced exhalation that are caused by loss of elastic recoil & are not fully reversible Air ow obstruction caused by mucus hypersecretion, mucosal edema, & bronchospasm Overactive in ammatory process 5. Describe the in ammatory process in COPD. Predominant in ammatory cells are neutrophils, macrophages, & lymphocytes In ammatory cells attract other in ammatory mediators (eg leukotrienes, interleukins) Cascading in ammatory process results in the activation of proin ammatory cytokines such as tumour necrosis factor Growth factors are brought to the area & activated, resulting in structural changes in the lungs May be further magni ed by oxidative stress (produced by cigarette smoke & other inhaled materials), adversely affects the lungs as it inactivates antiproteases After the inhalation of oxidants in tobacco or air pollution, the activity of proteases (which break down the connective tissue of the lungs) increases, & the antiproteases (which protect against the breakdown) are inhibited. Therefore, the natural balance of protease/antiprotease is tipped in favour of destruction of the alveoli & loss of the elastic recoil of the lung 6. What are bullae & blebs? Why do people with COPD develop pulmonary hypertension? fl fl fl fl fl fl fi fl fl fi fl fl fl fl Bullae → large air space in the parenchyma (large area in lung responsible for air exchange) Blebs → air spaces adjacent to pleurae Bullae & blebs are not effective in gas exchange because the capillary bed that normally surrounds each alveolus does not exist, therefore there is a signi cant VQ (ventilation-perfusion) mismatch & hypoxemia results which can subsequently lead to carbon dioxide retention Pulmonary hypertension may occur late in the course of COPD, caused by pulmonary arteries undergo vasoconstriction as a consequence of hypoxemia There structure changes, resulting in the thickening of the vascular smooth muscle as the disease advances Due to the loss of alveolar walls and the capillaries surrounding them, the pressure in the pulmonary circulation increases 7. What systemic (extrapulmonary) changes can result from COPD? Hypertrophy of the right ventricle of the heart Cor pulmonale Cachexia with a loss of skeletal muscle mass Weakness due to increased apoptosis, muscle disuse or both Chronic anemia, anxiety, & depression 8. What are the clinical manifestations (signs and symptoms) of COPD? Cough Sputum production Dyspnea becoming progressively more severe Prolonged expiratory phase Decreased breath sounds Pursed lip breathing 9. How do the clinical manifestations of COPD differ from those of asthma? fi 10. Describe the dyspnea experienced by people with COPD. Acute dyspnea is described as an sensation inextricably related to anxiety & emotional functioning 11. What positions do people with COPD often adopt to help with breathing? Sit upright with arms supported on a xed surface such as a table (tripod) 12. Why might polycythemia develop later in the development of COPD? As a result of the increased production of RBCs secondary to the bodies attempt to compensate for chronic hypoxemia 13. What FEV1/FVC ratio establishes the diagnosis of COPD? Less than 70% establishes the diagnosis of COPD PULMONARY FUNCTION TESTS 1. How are pulmonary function tests (PFTs) conducted? Conducted utilizing a spirometer Pt’s age, sex, height, & weight are entered into the PFT computer to calculate predicted values Pt inserts a mouth piece, takes a deep breath as possible, & exhales hard fast & as long as possible fi 2.What are the following pulmonary function tests used for COPD? Forced vital capacity (FVC)? ◦ Amount of air that can be quickly & forcefully exhaled after maximum inspira- tion Forced expiratory volume in the rst second of expiration (FEV1)? ◦ Amount of air exhaled in rst second of FVC; valuable clue to severity of airway obstruction FEV1/FVC? ◦ Ratio of value for FEV1 to value for FVC; useful in differentiating obstructive & restrictive pulmonary dysfunction Peak expiratory ow rate (PEFR)? ◦ Maximum air ow rate during forced expiration; aids in monitoring bronchoconstriction in asthma COPD (cont.) Return to the chapter on COPD (p. 654)… 1. What is cor pulmonale, & how can it result from COPD? Cor pulmonale is hypertrophy of the right side of the heart, with or without HF resulting from pulmonary hypertension In COPD, pulmonary hypertension is caused primarily by constriction of the pulmonary vessels in response to alveolar hypoxia, acidosis further potentiates the vasoconstriction Chronic hypoxia also stimulates erythropoiesis, which causes polycythemia & increased viscosity of the blood 2. How are acute exacerbations of COPD (AECOPD) de ned? De ned as a sustained worsening of COPD symptoms that lasts for 48 hours or longer Exacerbations are further characterized as either purulent or nonpurulent in determining the need for antibiotic therapy 3. Why is it important to identify whether a client has a purulent or nonpurulent exacerbation of COPD? In order to help determine the need for antibiotic therapy, purulent exacerbations typically necessitate antibiotic therapy 4. What causes AECOPD? Dif cult to determine, may be caused by exposure to allergens, irritants, cold air, & air pollution Half of all exacerbations are thought to be infectious in nature, many of those viral in origin 5. What vaccinations should be recommended for people with COPD? Annual in uenza vaccinations & pneumococcal vaccination should be encouraged unless the patient has a contraindication 6. How can COPD lead to acute respiratory failure? An acute exacerbation leads to increased decline in overall lung function, deterioration in health status, & risk of death Exacerbation of cor pulmonale may lead to acute respiratory failure Discontinuing bronchodilator or corticosteroid medication may also precipitate respiratory failure 7. How is depression, anxiety, & panic related to COPD? fi fi fl fl fl fi fi fi People with COPD experience higher rates of depression & anxiety 8. What assessments should a nurse perform on a client with COPD? Thorough history → tobacco consumption should be quanti ed & is typically expressed in pack years Physical examination Chest radiographic studies, although not diagnostic, can help to con rm or rule out comorbid conditions 9. How are “pack-years” calculated for people with a history of cigarette smoking? Multiplying the number of packs smoked per day by the # of years smoked 10. How is the MRC Dyspnea Scale used to assess shortness of breath & dyspnea in COPD? 11. What are the 7 primary COPD management goals? Prevent disease progression (smoking cessation) Reduce the frequency & severity of exacerbations Alleviate breathlessness & other respiratory symptoms Improve exercise tolerance Treat excaverations & complications of the disease Improve health status & quality of life Reduce associated mortality & mortality 12. How does smoking cessation slow the progression of COPD? Most signi cant factor in slowing the progression of COPD After a pt stops smoking accelerated decline in pulmonary function slows - typically improving 13. How do medications help with COPD? Can reduce intensity of symptoms or abolish them all together fi fi fi 14. Why are bronchodilators the mainstay of treatment for COPD? Bronchodilators are the mainstay of pharmacological therapy, relaxing smooth muscles in the airway reducing airway resistance & dynamic hyperin ation of the lungs 15. What are the most commonly medications used to treat COPD? Beta 2 adrenergic agonists, muscarinic medications, & methylxanthines 16. How do short-acting bronchodilators help in COPD? Improve pulmonary function, symptoms & exercise functions 17. How do long-acting bronchodilators help in COPD? Used in pts with mild to severe COPD who experience persistent symptoms Helps to prevent exacerbations 18. Why are inhaled corticosteroids (ICS) & long-acting β2 adrenergic agonists (LABAs) often combined in the treatment of COPD? Inhaled corticosteroids independently used in stable COPD has not been found to modify the long term decline of FEV1 However ICS in combination with a LABA has been found to reduce the frequency of exacerbations & to improve lung function & health status in patients who are at high risk of AECOPD 19. Why would a phosphodiesterase 4 inhibitor (e.g. Ro umilast) be prescribed for a person with COPD? The phosphodiesterase 4 inhibitor ro umilast (Daxas) is indicated as add-on therapy for reduction of in ammation with bronchodilators, for the maintenance of COPD in patients with chronic cough & sputum & frequent exacerba- tions 20. Why are oral or parenteral corticosteroids used in the treatment of COPD? Used for AECOPD treatment, they speed recovery time & reduce relapse rate 21. How does long-term oxygen therapy at home affect the prognosis for clients with COPD? Prolongs life in patients with hypoxemia 22. Which three surgical procedures have been used to manage severe COPD? (& how do they help?) Lung volume reduction surgery, reducing the size of the hyperin ated emphysematous lungs, airway obstruction is decreased Bullectomy is speci c to the patient with bullous emphysema, the surgical removal of the bulla is intended to decompress adjacent lung parenchyma Lung transplant → Last resort, better outcomes 23. What are the components of an effective pulmonary rehabilitation program? Exercise conditioning, breathing exercises, energy conservation, nutrition, smoking cessation 24. How does upper & lower extremity training improve the health of people with COPD? Can help to improve dyspnea & exercise performance Improving strength 25. How is pursed-lip breathing performed? Used to prolong exhalation, prevent bronchiolar collapse & air trapping, & assist with dyspnea. Exhalation should be at least three times longer than inhalation. Steps: fi fl fl fl fl fl ◦ Relax neck & shoulder muscles. ◦ Inhale slowly through the nose to the count of 2. ◦ Pucker lips as if whistling. ◦ Exhale slowly & gently through the lips while mentally counting to 6. ◦ Always exhale longer than inhaling. 26. How does weight loss & nutrition relate to COPD? Common with individuals diagnosed with COPD Energy expenditure is increased as a result of an increased WOB Eating becomes an effort 27. How much uid should a client with COPD take in daily? At least 2 - 3 L per day 28. What physiological changes can make COPD worse? Reduced lean body mass Decreased respiratory muscle strength 29. What medications (commonly used to treat disorders in older adults) can worsen COPD symptoms? Nonspeci c Beta Blockers → block the A2 receptors in the airway & cause bronchoconstriction Angiotensin-converting enzyme inhibitors may cause a dry cough or worsen a current cough Long term ICS use can cause local or systemic adverse effects 30. What physical characteristics of older adults can make management of COPD more dif cult? 31. How can the nurse promote effective airway clearance in a client with COPD? Facilitate deep breathing by sitting patient up to maximize use of diaphragm & prolong expiratory phase. Ensure adequate hydration (oral intake approximately 2–3 L/day, humidi ed ambient air) to liquefy secretions for easier expectoration. Teach effective cough techniques to minimize the extent of airway collapse & to enhance airway clearance. Assist with inhaled bronchodilator administration to facilitate clearance of retained secretions 32. How should a nurse support a client with COPD to improve gas exchange? Monitor respiratory & oxygenation status to assess need for intervention. Teach pursed-lip breathing to prolong expiratory phase & slow respiratory rate. Assist patient to assume position of comfort (e.g., tripod position, elevated back rest, support of upper extremities to x shoulder girdle) to maximize respiratory excursion. Administer & teach appropriate use of bronchodilators to open the airways. Teach signs, symptoms, & consequences of hypercapnia (e.g., confusion, somnolence, headache, irritability, decrease in mental acuity, increase in respiration, facial ush, diaphoresis) to recognize condition early & initiate treatment. Teach avoidance of central nervous system depressants because they further depress respirations. Administer O2 if appropriate to increase SaO2 saturation. fi fi fl fl fi fi Select O2 supply systems & devices (e.g., nasal cannula, mask) that are appropriate for patient’s ADLs (rest, sleep, exercise) to minimize effect on preferred lifestyle. 33. How can a nurse promote good nutrition in a client with COPD? Monitor caloric intake, weight, & serum albumin & protein levels to determine adequacy of intake. Provide menu suggestions for high-protein, high-calorie foods to ensure maintenance of weight. Give patient high-protein, high-calorie liquid supplements if necessary, to provide adequate calories & protein to prevent weight loss & muscle wasting. Plan periods of rest before & after food intake to assist with controlling fatigue & to compensate for blood ow diversion to the gastrointestinal tract for digestion. Refer to hospital for nancial or nutritional assistance as necessary (e.g., Meals- On-Wheels, home care) to ensure nutritional adequacy after discharge. Discuss bene t of ve to six small meals throughout the day because this reduces bloating 34. How can a nurse promote effective sleep in a client with COPD? Identify usual sleep habits & elicit reasons for dif culty sleeping to provide baseline data. Monitor patient’s sleep pattern, & note physical circumstances (e.g., pain or discomfort & urinary frequency) & psychological circumstances (e.g., fear or anxiety) that interrupt sleep to initiate appropriate interventions. Observe signs & symptoms of sleep apnea such as frequent awakenings at night or excessive daytime sleepiness, or noting a partner who complains of the patient’s snoring or gasping for air to initiate appropriate diagnostic tests & interventions. Identify patient-speci c methods of relaxation, & teach patient relaxation methods to foster sleep. Encourage exercise & activity during daylight hours to ensure improved sleep at night. Provide patients with activity that promotes wakefulness to limit daytime sleep. Instruct patients in arranging surroundings (e.g., clothing, temperature, position, noise level) to produce an environment conducive to sleep. Teach patients to avoid alcoholic beverages, caffeine products, or other stimulants before bedtime to reduce interference with sleep. 35. How can a nurse reduce the risk for respiratory infection in a client with COPD? Monitor for systemic & localized signs & symptoms of infection to determine whether an infection is present. Teach patient to assess indicators of infection: change in sputum colour, quantity, odour, & viscosity; increase in cough & dyspnea; experience of fever, chills, diaphoresis, excessive fatigue; increase in respiratory rate; & abnormal breath sounds (gurgles, wheezing) to determine whether an infection is present. Teach patient to use good h&washing & hygiene techniques & to avoid contact (when possible) with people with respiratory infections to minimize sources of infection. fi fi fi fi fl fi Encourage patient to obtain vaccination for in uenza & pneumococcal pneumonia to decrease occurrence or severity of in uenza or pneumonia. Teach proper care & cleaning of home respiratory equipment to eliminate this source of infection. Instruct patient to seek medical attention for manifestations of early infection to initiate treatment promptly. Teach patient to follow plan of care for managing exacerbations (e.g., increase uid intake, initiate antibiotics & oral corticosteroid) to initiate appropriate self- care promptly. 36. How can the health of a client with COPD be promoted? Early identi cation & treatment of respiratory tract infections is important for improving long term prognosis of COPD Avoid large crowds during in uenza season 37. What patient teaching should be provided to clients with COPD & their caregivers? Preparation of a long term care plan 38. What exercise should be recommended for a client with COPD? Walking is by far the best physical exercise for patients with COPD Coordinated walking & breathing → patient is taught to breathe in through the nose during one step, then out through pursed lips during the next two - four steps 39. What strategies can be used to conserve energy in clients with COPD? When doing ADLs (such as hair drying or shaving) the patient can assume a tripod posture & utilize a portable mirror as opposed to a standing mirror If a patient has home oxygen therapy it must be used during activities of hygiene because these activities consume energy 40. What should nurses teach clients with COPD about maintaining a healthy sex life? Use SABA before sexual activity can help control dyspnea 41. What are the psychosocial considerations for a client with COPD? Healthy coping is challenging Patients frequently have to deal with many lifestyle changes PNEUMONIA 1. What is pneumonia? Acute in ammation of the lung parenchyma caused by a microbial agent 2. What are all of the things that can cause pneumonia? Pneumonia is more likely to result when defence mechanisms become incompetent or are overwhelmed by the virulence or quantity of infectious agents fl fl fi fl fl fl Decreased consciousness depresses the cough & epiglottal re exes which may allow aspiration of oropharyngeal contents into the lungs Tracheal intubation interferes with the normal cough re ex and the mucociliary escalator mechanism The mucociliary escalator mechanism is impaired by air pollution, cigarette smoking, viral upper respiratory infections (URIs), and normal changes of aging Diseases such as leukemia, alcoholism, and diabetes mellitus are associated with increased frequency of gram negative bacilli in the oropharynx Altered oropharyngeal ora can also occur secondary to antibiotic therapy given for an infection somewhere else in the body Acquisition of Organisms that cause pneumonia can reach the lung via 3 methods: ◦ Aspiration from the nasopharynx or oropharynx. ◦ Inhalation of microbes present in the air ◦ Hematogenous spread from a primary infection elsewhere in the body 3. Why is it helpful to classify pneumonia as community-acquired or hospital- acquired? Classifying pneumonia is important because of differences in the likely causative organism and the selection of appropriate antibiotics 4. What are the factors that predispose an individual to develop pneumonia? Smoking COPD Recent use of antibiotics Conditions incurring risk of aspiration 5. What are the characteristics of community-acquired pneumonia (CAP)? De ned as lower respiratory tract infection of the lung parenchyma with onset in the community or within 2 days of a hospital stay 6. What is the de nition of hospital-acquired pneumonia (HAP)? Pneumonia occurring 48 hours or longer after hospital admission and not incubating at the time of hospitalization HAP accounts for 25 percent of all critical care unit infections Many of the organisms causing HAP enter the lungs after aspiration of particles from the patient’s own pharynx Immunosuppressive therapy and endotracheal intubation may be predisposing factors 7. Which factors increase the risk of a person developing aspiration pneumonia? History of loss of consciousness due to gag and cough re ex being depressed Tube feedings 8. What are the 3 types of aspiration pneumonia? If the aspirated material is an inert substance (e.g., barium), the initial manifestation is usually caused by mechanical obstruction of airways When the aspirated materials include toxic uids such as gastric juices, there is chemical injury to the lung with infection occurring as a secondary event - this is identi ed as chemical (noninfectious pneumonia) Bacterial infection 9. Which individuals are most at risk for opportunistic pneumonia? fi fi fi fl fl fl fl fl Patients with altered immune responses: ◦ Severe protein-calorie malnutrition ◦ Immune de ciencies ◦ Hx of transplants ◦ Treated w/ immunosuppressive medications ◦ Chemotherapy patients 10. What are the 4 stages of the disease process in pneumonia (and the characteristics of each stage)? Congestion ◦ After the pneumococcus organisms reach the alveoli via droplets or saliva, there is an outpouring of uid into the alveoli ◦ Organisms multiply, infection is spread Red hepatization ◦ There is a massive dilation of the capillaries, and the alveoli are lled with organisms, neutrophils, RBCs, and brin ◦ Lung appears red and granular Grey hepatization ◦ Blood ow decreases and leukocytes and brin consolidate in the affected part of the lung Resolution ◦ Complete resolution and healing occur if there are no complications 11. What are the typical clinical manifestations of pneumonia? Fever Chills Cough producing purulent sputum Pleuritic chest pain In the older adult may be confusion / stupor related to hypoxia 12. What sort of atypical signs and symptoms might manifest with pneumonia? Gradual onset Dry cough Extrapulmonary manifestations such as headache, myalgias, fatigue, sore throat, nausea, vomiting, and diarrhea 13. What are the complications of pneumonia? Pleurisy (in ammation of the pleura Common accompanying condition of pneumonia. Pleural effusion can occur. Usually, the effusion is sterile and is reabsorbed in 1 to 2 weeks. Occasionally, it necessitates aspiration by means of thoracentesis. Atelectasis (collapsed, airless alveoli) in one or part of one lobe may occur. These areas are usually cleared with effective coughing and deep breathing. Delayed resolution results from persistent infection and is seen on radiograph as residual consolidation. Usually, the physical ndings return to normal within 2 to 4 weeks. Delayed resolution occurs most frequently in patients who are older or malnourished or have alcohol use disorder or COPD. Lung abscess is not a common complication of pneumonia. It may be seen with pneumonia caused by S. aureus and Gram-negative pneumonias (see Lung Abscess later in this chapter). fl fl fi fl fi fi fi fi Empyema (accumulation of purulent exudate in the pleural cavity) is relatively infrequent but necessitates antibiotic therapy and drainage of the exudate by a chest tube or by open surgery. Pericarditis results from spread of the infecting organism from an infected pleura or via a hematogenous route to the pericardium (the broserous sac around the heart). Bacteremia can occur with pneumococcal pneumonia, more so in older patients. Meningitis can be caused by S. pneumoniae. The patient with pneumonia who is disoriented, confused, or somno- lent should have a lumbar puncture to evaluate the possibility of meningitis. Endocarditis can develop when the organisms attack the endocardium and the valves of the heart 14. What is empirical therapy? Therapy based on observation and experience, implemented when the exact cause is not known 15. When caring for a client with pneumonia, what should be done rst: administer the rst dose of antibiotics, or collect a sputum culture? Sputum culture should be collected rst 16. What types of pneumonia respond best to antibiotic therapy? Bacterial and mycoplasma pneumonia 17. How many days does it take for the signs and symptoms of pneumonia to improve after starting antibiotic therapy? 48 - 72 hours 18. What supportive measures should be used to treat people with pneumonia? Oxygen therapy Analgesics to treat chest pain Antipyretics such as ASA or acetaminophen for increased temp 19. What, if any, drug treatment is available for viral pneumonia? No de nitive treatment An antiviral medication, amantadine is approved for oral use in the treatment of in uenza A Flu vaccine prophylactic measure against viral pneumonia 20. What vaccinations are recommended to prevent viral pneumonia? Who should get these vaccines? Pneumococcal vaccine → indicated primarily for the individual considered at risk who has: ◦ Chronic illness ◦ Recovering from severe illness ◦ 65 years of age or older ◦ Resides in LTC facility 21. What nutritional therapy should be used in pneumonia? Fluid intake of at least 3 L / day Intake of at least 1500 calories per day Small frequent meals are tolerated better in people with dyspnea fl fi fi fi fi fi WEEK 2 - OXYGENATION MANAGING CHEST DRAINAGE 1. What are the three spaces found in the thorax? Centrally located mediastinum The right lung cavity The left lung cavity 2. What is contained in the mediastinum? Flexible partition in the center of the thoracic cavity Contains the heart, thymus gland, parts of the esophagus and trachea, and a network of nerves and blood vessels 3. What is the inner and outer membranes covering the lungs called? Parietal pleura → outer membrane Visceral pleura → inner membrane 4. How much pleural uid is produced in about 24 hours? 25 mL 5. What is the pressure in the pleural space during inhalation and exhalation? Inhalation = - 8cmH20 -4 cmH20 during expiration Negative pressure keeps lungs expanded and allows them to move in tandem with the rib cage and diaphragm during inspiration 6. What is the de nition of: Ventilation? ◦ Mechanical act of moving air into and out of the lungs Respiration? ◦ Gas exchange across the alveolar-capillary membranes 7. What is the name of the nerve that causes the diaphragm to contract? Phrenic nerve 8. What are the characteristics of pleural pain? Sharp, stabbing pain during inspiration as the pleura moves Patients will involuntarily reduce tidal volume while increasing respiratory rate to maintain ventilation while limiting the movement of the pleurae to reduce pain 9. What are two common clinical conditions that require pleural drainage? Rupture of the surface of the lung or tracheobronchial tree, allowing air and possibly serous or serosanguineous uid into the pleural space while the chest wall remains intact External penetration of the chest wall resulting from surgical intervention or trauma allowing air and blood or serosanguineous uid from damaged tissues into the pleural space 10. What is a pneumothorax? fi fl fl fl Whenever the chest wall is opened or the lung is penetrated, air enters the pleural space and the negative pressure between the pleura vanishes, allowing the lung to collapse → pneumothorax 11. What are the characteristics of a/an: Open pneumothorax? ◦ Air enters the pleural space via traumatic penetration of the chest, leaving the pleural space open to the atmosphere ◦ As long as hole is signi cantly smaller than trachea, patient may be able to tolerate the open pneumothorax for some time Closed pneumothorax? ◦ Air enters the pleural space via rupture of lung and visceral pleura, but the chest wall remains intact ◦ Air can enter the pleural space but cannot escape as easily as in open pneumothorax Spontaneous pneumothorax? ◦ Pneumothorax for no obvious reason 12. Describe the following in relation to a tension pneumothorax: What is it? ◦ When air continues to leak into the pleural space with no means of escape there will be a build up of pressure in the pleural space → serious condition known as tension pneumothorax Why is it dangerous? ◦ If pressure becomes high enough, the lung can completely collapse and the pressure can be transmitted to the mediastinum, the mediastinum can be pushed away from the affected side → can compress the great vessels and the heart itself → venous return decreased → decreased CO ◦ Mediastinal shift life threatening situation → can lead to cardiovascular collapse and death What are the signs and symptoms? ◦ Increased respiratory rate and effort ◦ Dyspnea ◦ Pleuritic chest pain (if pt able to communicate) ◦ Decreased movement of the affected side of the chest ◦ Decreased breath sounds on auscultation of the affected side ◦ Falling BP ◦ Rising pulse 13. What are the following: Subcutaneous emphysema? ◦ Feeling of crackling on palpation of the chest ◦ Indicates air has entered subcutaneous tissue Hemothorax? ◦ Collection of blood in the pleural space ◦ Typically occur after there has been an opening in the chest ◦ Disrupts normal negative intrapleural pressure Empyema? fi ◦ Accumulation of pus in the pleural space caused by pneumonia, lung abscess, or contamination of the pleural cavity Chylothorax ◦ Accumulation of lymphatic uid in the pleural space Cardiac tamponade? ◦ Following cardiac surgery or chest trauma, blood can pool in the mediastinal cavity ◦ Blood can collect between the pericardium and the heat, externally compressing the heart ◦ Life threatening if not identi ed and treated promptly because it reduces the hearts ability to accept venous return, resulting in signi cantly decreased CO 14. How much extra air or uid can a person usually tolerate in their pleural space (if they don’t have underlying lung disease)? If less than 10 percent of the pleural space is occupied by air or uid, patient will typically have few respiratory symptoms 15. What are the goals of chest drainage? Remove the uid and air as quickly as possible Prevent drained air and uid from re-entering the chest cavity Re-expand the lungs, restore normal negative intrapleural pressure 16. What should the nurse assess in regards to respirations? Rate, regularity, depth, and ease of respirations Listen for changes in breath sounds, paying particular attention to the the symmetry of sounds 17. What could cause diminished breath sounds on the side that a client has a chest tube? May indicate reaccumulation of uid on the affected side 18. How should the nurse prevent pulmonary complications (e.g. pneumonia) in clients with chest tubes? Regular pain assessments → failure to adequately manage pain can lead to hypoventilation, leading to the patient being at a much higher risk of pneumonia 19. How should a nurse teach a client to splint their incision? When the patient coughs, have them place a pillow over the incision and hug / squeeze the pillow close to the chest wall during coughing 20. What does it mean if the nurse nds that a client with a mediastinal chest tube has muf ed heart sounds? Cardiac tamponade 21. Why is it so important to assess mobility in a client with a chest drainage system? Research shows that people who get out of bed and walk around postoperatively will have fewer complications and shorter length of stay 22. How can the nurse use positioning to enhance chest drainage while the client is in bed? High or Semi-Fowler’s position to facilitate gravity drainage of pleural uid 23. When are the only occasions when a nurse should clamp the tubing on a chest tube? Locate an air leak fl fl fl fl fl fi fi fl fi fl fl Simulate chest tube removal (to assess patient's tolerance) Replace a drain Connect or disconnect an in-line autotransfusion bag 24. What does a nurse need to assess about the chest tube site/dressing? Regularly assess the chest tube insertion site, check to see if the dressing is dry / intact Palpate around the dressing and the insertion site for subcutaneous emphysema that can indicate air escaping from the pleural space and into the subcutaneous tissue 25. What should the nurse do if (1) subcutaneous emphysema develops, or (2) drainage eyelets are visible in the chest tube where it exits the chest? If subcutaneous emphysema is present: ◦ Take down the dressing and carefully inspect the site where the chest tube leaves the chest wall ◦ Look for any evidence drainage eyelets may have been pulled out of the pleural space, such as broken sutures If eyelets are visible: ◦ Chest tube will need to be repositioned In both of the above cases, notify physician 26. What should the nurse do if a client accidentally pulls out the chest tube? Cover the site with a sterile dressing and tape on three sides (prevents a tension pneumothorax) Stay with patient while a colleague calls the physician stat 27. What should a nurse assess in regards to tubing in a chest drainage system? Leaks, kinks, uid lled dependent loops Compression or occlusion and Trace the tubing from the chest wall to the collection chamber of the chest drain 28. What should the nurse do if a section of the tubing on the chest drainage system comes apart? Clean the ends with a alcohol wipe and reconnect them Ask the patient to cough a few times to push any residual air out of the pleural space 29. Why is it essential to eliminate dependent loops in tubing (between the chest tube and the drainage system)? It can change the pleural pressure and decrease uid drained to zero within 30 minutes 30. What should a nurse assess in regards to uid that has drained from a chest tube? Volume, rate, color and characteristics of the collected drainage 31. What does it mean if a chest tube suddenly has increased drainage when a postoperative client changes position? The patient has moved into a more favorable position for gravity drainage Check colour of drainage → if its dark it is old drainage, fresh drainage is more red fl fi fl fl Typically lasts for a few minutes after position change 32. What should a nurse assess regarding the water seal on a chest drainage system? To see that the water seal is lled to the appropriate level, and that the water level moves as the patient breathes (tidalling) 33. What could it mean if there is no tidaling in the water seal chamber? The tubing is kinked The tubing is clamped The patient is lying on the tubing There is a dependent, uid- lled loop in the tubing Lung tissue or adhesions are blocking the catheter eyelets No air is leaking into the pleural space and the lung has re-expanded 34. Why is it important for a nurse to assess for bubbling in the water seal chamber? Because if the air leak is not something you expected in your patient assessment, there may be a leak in the system 35. How should a nurse check for an air leak in a chest drainage system? To locate the leak, clamp the tubing with a special tubing clamp or rubber-tipped (booted) hemostat. Start by clamping the chest tube where it leaves the chest, and work your way down to the collection chamber. Leave the clamp in place no longer than ten seconds while you glance at the water seal chamber. Once the clamp is placed between the air leak and the water seal, the bubbling should stop. Proceed as follows: ◦ 1. Clamp the tube where it leaves the dressing. If the bubbling stops, the leak is likely from the lung/pleural space. However, the tube itself may be displaced. If the bubbling is new and unexpected, take down the dressing and examine to see if a drainage eyelet has moved outside the chest wall ◦ 2.If the bubbling continues when you place the clamp at the chest wall, place the clamp on the patient side of the connector between the chest tube and the tubing leading to the chest drain. If bubbling stops, the leak is between the patient and the clamp. ◦ 3. If bubbling continues, move the clamp to the other side of the connector. If bubbling stops, the leak is likely coming from the connector. fl fi fi Check to see that the tubing is attached tightly on each side of the connector and push the tubing and connector together as tightly as possible. Then look to see if bubbling stops. If necessary, replace the connector. ◦ 4. If bubbling persists when you place the clamp on the drain side of the connector, the leak could be coming from a hole or puncture in the patient tubing. ◦ 5. If bubbling does not stop after you have clamped at intervals all the way down the tubing, the drainage unit may be cracked and may need to be replaced. 36. What should a nurse assess in regards to the suction on a chest drainage system? Check suction connections and tubing routinely to ensure that the tubing is patent and the system is operating properly Check that the suction control chamber on the drain is set at the level as ordered CHEST TUBES AND PLEURAL DRAINAGE 1. How would a nurse assess for chest tube malposition? Routine monitoring to evaluate whether the chest drainage is successful by observing for tidalling in the water seal chamber, listening for breath sounds over the lung elds and measuring the amount of uid drainage 2. What causes re-expansion pulmonary edema? After a rapid expansion of a collapsed lung in patients with a pneumothorax or with evacuation of large amounts of pleural uid 3. What can cause a vasovagal response in a client with a chest tube? Too rapid removal of uid 4. How can infection at the skin site be prevented? Meticulous sterile technique during dressing changes can reduce the instances of infected sites 5. What increases the risk of pneumonia in clients with chest tubes? Not taking deep breaths Not using an incentive spirometer 6. Why are clients with chest tubes at increased risk for “frozen shoulder”? Ie shoulder dislocation From lack of range of motion exercises PLEURAL EFFUSIONS 1. What is a pleural effusion? Collection of uid in the pleural space Sign of a serious disease Frequently classi ed as transudative or exudative according to whether the protein content of the effusion is low or high 2. What conditions cause a transudative pleural effusion? Occurs primarily in nonin ammatory conditions, associated with the accumulation of protein and cell-poor uid Caused by: ◦ Increased hydrostatic pressure found in heart failure fi fl fi fl fl fl fl fl ◦ Decreased oncotic pressure found in chronic liver or renal disease 3. What conditions cause an exudative pleural effusion? Accumulation of uid and cells in an area of in ammation Results from the increased capillary permeability characteristics of the in ammatory reaction Occurs secondary to conditions such as pulmonary malignancies, pulmonary infections, pulmonary embolization, and GI disease 4. What is a thoracentesis? Procedure to remove uid from the pleural space, used to diagnose type of pleural effusion 5. What is an empyema? Pleural effusion that contains pus Caused by conditions such as pneumonia, TB, lung abscess, and infection of surgical wounds of the chest Antibiotic therapy needed to get rid of causative organism 6. What is a trapped lung? Can occur with effusions and empyema Occurs when the visceral pleura become encased with a brous peel or rind Fibrous peel causes severe pulmonary restrictions 7. What are the clinical manifestations of a pleural effusion? Progressive dyspnea and decreased movement of the chest wall on the affected side May be pleuritic pain from the underlying disease Decreased breath sounds over the affected area 8. What are the clinical manifestations of an empyema? Caused by infections such as pneumonia Pleural effusion Fever Night sweats Cough Weight loss 9. What treatments are used for a pleural effusion? Goal is to treat underlying cause Flashcards done VIDEO: PLEUR-EVAC CHEST DRAINAGE SYSTEM 1. How does the nurse ll the water-seal chamber and set up the chest drainage system? 2. Note: IH requires chest tube connections to be taped 3. How does a nurse apply suction to the chest drainage system? 4. How can the nurse visually con rm that the suction is operating correctly? fl fl fi fl fi fl fi 5. How does the nurse adjust the amount of suction that is applied to the client’s chest tube? 6. How can the clinician check that the drainage system is working correctly? 7. What does intermittent bubbling (or lack of bubbling) in the water seal chamber indicate? 8. Why would uid oscillate ( uctuate) in the water seal chamber? 9. What does it mean if the nurse observes constant bubbling in the water seal chamber (after it has been 10. connected to the suction source)? 11. What are the three functions of a water-seal chamber? 12. Watch from 5:39-7:00 (Collection Chamber) Stop at 7:00 Skip 7:00-10:24 13. How can the nurse measure the amount of chest drainage? 14. How does the nurse change drainage units (e.g., when it is full)? 15. How can a nurse take a sample of pleural uid? 16. Watch 10:24-11:40 (Troubleshooting) Stop at 11:40 Skip the remainder of the video 17. How can a nurse check to see if there is the chest catheter has been disconnected/damaged? 18. What should the nurse do if the chest drainage system is accidentally knocked over? VIDEO: P-EGGY DRAIN 1. How is the drain attached to a chest catheter? 2. How can the drain be attached to clothing? 3. How is suction applied to the drain? 4. How does air escape from the drain (if the patient has a pneumothorax)? 5. How can the nurse con rm if the patient has an air leak? 6. How can the nurse take a sample of pleural uid? VIDEO: PLEURX CATHETER SYSTEM 1. Where is the catheter placed to drain pleural uid (from the chest)? 2. What steps does the client in the video follow during the drainage procedure? 3. What should a client do if they experience discomfort/pain while draining pleural uid? 4. What is the maximum amount of uid that should be drained from the pleural space at one time? 5. What steps does the client in the video follow when the uid has nished draining from the PleurX catheter? 6. Stop at 10:37 Skip the remainder of the video (ignore the procedure to empty the bottle) VIDEO: THOPAZ DIGITAL CHEST DRAINAGE SYSTEM 1. How is the Thopaz drainage system assembled? 2. How can the nurse determine if the patient has an air leak? 3. How does the nurse measure the amount of pleural uid drainage? 4. How can the nurse tell if the system is working correctly? 5. How can the nurse take a sample of pleural uid? fl fl fi fl fl fl fl fl fl fl fl fi TRACHEOSTOMIES: IH Respiratory Care and Oxygen Therapy manual: 1. What is a tracheostomy? Surgical incision made into the trachea, creating a stoma or hole through which the airway is managed 2. What are the 6 reasons that a tracheostomy may be performed? Airway obstruction - acute or chronic To provide mechanical ventilation To prevent aspiration pneumonia Vocal cord paralysis or upper airway tumors Secretion retention Prevention VAP (Ventilator Associated Pneumonia) 3. When should a cuffed tracheostomy tube be used? To supply short-term mechanical ventilation, high ow oxygen, and to prevent the aspiration of secretions (mucus, vomit) 4. When should an uncuffed tracheostomy tube be used? Long term tracheostomy and during the tracheostomy weaning process 5. What is the main disadvantage of an uncuffed tracheostomy tube? Do not protect the lower airway from aspiration 6. What are the component parts of a tracheostomy? Outer cannula: ◦ Main portion of the tracheostomy tube that lies within the incision in the trachea Inner cannula: ◦ The inner cannula ts inside the outer cannula ◦ Inner cannula is removable to facilitate cleaning and ensure that patency of the tracheostomy is maintained ◦ Not all tracheostomies have an inner cannula Obturator ◦ Solid piece of curved plastic that is used to help the insertion of the tracheostomy tube Tracheostomy cuff ◦ Balloon that is xed to the outer cannula and sits inside the trachea ◦ When in ated, cuff minimizes the passage of air or secretions around the tracheostomy tube ◦ Helps to minimize aspirations and aids mechanical ventilation Pilot balloon ◦ Pilot balloon and pilot line are attached to the cuff in order to allow for the insertion or removal of air when in ating or de ating the cuff ◦ If pilot line or pilot balloon are damaged, the cuff will not pressurize and the entire tracheostomy tube will have to be replaced 7. For each of the following tracheostomy complications, what is the cause, and how are they managed or prevented? Mucus plugs fl fi fi fl fl fl Cause ◦ ▪ Bodies natural humidi cation system (upper airway) is bypassed when a patient breathes through a tracheostomy ◦ Management ▪ Caregiver needs to provide the patient with humidity via a tracheostomy mask to help minimize the risk of mucus plugs Bleeding ◦ Cause ▪ Irritation and in ammation of the site can cause minor bleeding ▪ Insuf cient humidity, vigorous suctioning, the presence of infection or excessive coughing may also contribute to bleeding ◦ Management ▪ Report to MRP Infection ◦ Cause ▪ Either the lung itself or stoma may become infected ▪ Natural defenses for ltration for airway are bypasses when tracheostomy present ◦ Management ▪ Be conscientious about cleanliness whenever providing trach care Tracheoesophageal stula ◦ Cause ▪ Necrosis of the tracheal wall advances into the esophagus, air is allowed to enter the stomach and stomach contents may be aspirated ◦ Management A small NG tube may be utilized to prevent this complication Tracheal stenosis ◦ Cause ▪ Prolonged tracheal intubation may result in the formation of scar tissue → may result in tracheal narrowing ◦ Management ▪ Measures to prevent tracheal stenosis include using an appropriately sized trach tube, minimal cuff pressure, limiting movement of trach tube during coughing, and preventing infection 8. In a postop client with a new tracheostomy, what assessments must the nurse perform? Monitoring VS Assessing sedative use as can cause respiratory depression Assessing for shock, hemorrhage, respiratory insuf ciency and complications related to the surgical and medical conditions Noting the colour, amount, and consistency of secretions Providing tracheal suctioning, as required Applying humidi ed oxygen to loosen secretions and prevent mucous plugging and/or infection Maintaining hydration which will help thin secretions fi fl fi fi fi fi fi Ensuring tracheostomy supplies and safety equipment is at the bedside Providing frequent position changes to increase motility of secretions and prevent atelectasis Providing patient reassurances 9. What precautions are recommended to prevent obstruction of the tracheostomy? Avoid clothing / gowns that may cover or block the tracheostomy Do no use ointments or salves on a tracheostomy site unless ordered by the physician Check the patency and cleanliness of the inner cannula regularly to avoid airway obstruction ◦ Check inner cannula for patency Q12H ◦ Change inner cannula Q24H 10. What are the signs and symptoms of respiratory distress that may occur when the patient is being weaned from a tracheostomy tube? Abnormal respiration rate and pattern Accessory muscle use Abnormal pulse and BP Abnormal skin and mucous membrane colour Abnormal ABG levels or O2 saturations 11. In Interior Health facilities, how often should routine tracheostomy care be performed? Twice daily care 12. What is the purpose of routine tracheostomy care? Prevent obstruction of the tracheostomy, infection of the site/or lungs and skin breakdown 13. What technique is used to clean around the tracheostomy site? Sterile technique 14. Does a tracheostomy always need a dressing? May not be needed for well-established trach sites if the stoma is well healed and free from rash or redness 15. What type of tracheostomies have non-disposable inner cannulas? Cuf ess trachs 16. If the nurse needs to clean the inner cannula of a tracheostomy, what solution should be used for this cleaning? Sterile water and a Q tip 17. What should the nurse do if the area surrounding the stoma becomes red, swollen, in amed, warm to the touch, or emits a foul odour? Notify MRP 18. What are the indications that a client’s tracheostomy requires suctioning? Ineffective cough demonstrated by the patient Patients with depressed LOC Thick, tenacious, immobilized secretions 19. What precautions should be used when suctioning a client’s tracheostomy? Limit actual suctioning time to no more than 15 seconds, as hypoxemia may occur fl fl Ensure that the suction catheter is the appropriate size, in general the catheter should be no larger than half the diameter of the airway it is entering 20. If a client with a tracheostomy experiences bronchospasm after suctioning, what is the nursing management? Bronchodilators Ensure pt is in semi-fowler's position AIRWAY OBSTRUCTION AND TRACHEOSTOMY (MED-SURG) 1. What may cause a partial or complete airway obstruction? Aspiration of food Foreign body Laryngeal edema following extubation Laryngeal or tracheal stenosis CNS depression Allergic reactions 2. What are the clinical manifestations of a partial or complete airway obstruction? Stridor Use of accessory muscles Suprasternal and intercostal retractions Wheezing Restlessness Tachycardia Cyanosis 3. What are the indications for a tracheostomy? Bypass an upper airway obstruction Facilitate removal of secretions Enable long term mechanical ventilation Facilitate oral intake and speech in patients who requires long term mechanical ventilation 4. What are the bene ts of a tracheostomy over an endotracheal tube? Better for long term care No tube in mouth → patient comfort and mobility can be increased, risk for long- term damage to the vocal cords is decreased 5. For each of the following tracheostomy complications, describe the causes and management (or prevention): o Abnormal bleeding ▪ Cause Surgical intervention Erosion or rupture of blood vessel ▪ Management Monitor bleeding Notify physician if bleeding continues or is excessive o Tube dislodgement ▪ Cause Excessive manipulation or suctioning fi ▪ Management Ensure ties are secure Keep obturator, hemostat, and new tracheostomy tube at bedside o Obstructed tube ▪ Cause Dried or excessive secretions ▪ Management Assess patients respiratory status Suction as necessary Maintain humidi cation Perform tracheostomy care Ensure adequate hydration o Subcutaneous emphysema ▪ Cause Air escapes from the incision to the subcutaneous tissue ▪ Management Monitor subcutaneous emphysema Reassure patient and family o Tracheoesophageal stula ▪ Cause Tracheal wall necrosis, leading to stula formation ▪ Management Monitor cuff pressure Monitor patient for coughing and choking while eating or drinking o Tracheal stenosis ▪ Cause Narrowing of tracheal lumen owing to scarring caused by tracheal irritation ▪ Management Monitor cuff pressure Ensure prompt treatment of infections Ensure ties are secure WEEK 3 DIABETES P1 fi fi fi ETIOLOGY AND PATHOPHYSIOLOGY OF DIABETES MELLITUS 1. What is diabetes mellitus (DM)? Multisystem disease related to abnormal insulin production, impaired insulin utilization, or both 2. How does DM affect Indigenous people? Indigenous populations are three to ve times more likely than the general population to develop type 2 diabetes 3. Describe normal insulin metabolism. Insulin is a hormone produced by the beta cells in the islets of Langerhans of the pancreas, under normal conditions insulin is released into the bloodstream in small pulsatile increments with increased release when food is ingested The activity of released lowers blood glucose and facilitates a stable, normal glucose range of approximately 4 - 6 mmol / L 4. What are the “counter regulatory hormones”, and what do they do? Glucagon, epinephrine, growth hormone, and cortisol Work to oppose the effects of insulin by increasing blood glucose levels via stimulating glucose production and output by the liver and by decreasing the movement of glucose into the cells 5. Which tissues of the body are insulin-independent (do not require insulin to allow the cells to take in glucose)? Blood cells Brain cells Liver 6. A lot of different terminology is used by healthcare providers to describe diabetes. Even though the current terminology is Type 1 DM, Type 2 DM, and prediabetes, you will often hear (or read in patient charts) about the following older terms. What do they refer to (note: you may need to “Google” some of these terms)? o IDDM (insulin-dependent diabetes) o NIDDM (non-insulin-dependent diabetes) o Juvenile-onset diabetes o Adult-onset diabetes 7. Compare and contrast Type 1 DM and Type 2 DM. What are the characteristics of each of these conditions (refer to Table 52-1)? Factor Type 1 Type 2 Factor Type 1 Type 2 Diabete Diabete Diabete Diabete s s s s Melitus Mellitus Mellitus Melitus fi Age of More Usually Endogen Minimal Possibly onset common >35 yr ous or excessiv ly in but can insulin absent e; young occur adequat people e but but can delayed occur at secretio any age n or reduced utilizatio Type of Signs Insidious Nutrition Thin, Obese onset and ; may go al status normal, or sympto undiagn or obese normal ms osed for abrupt, years but disease Prevalen Account Account Sympto Thirst, Frequent ce s for s for ms polyuria, ly none, 5-10% of 90% of polypha fatigue all types all types gia, recurrent of of fatigue, infection Environ Viruses, Obesity, Ketosis Prone at Resistan mental toxins lack of onset or t except factors exercise during during insulin infection Primary Absent Insulin Nutrition Essentia Essentia defect or resistanc al l l minimal e, therapy insulin decreas producti ed on due insulin to an producti autoimm on over une time, process and Islet-cell Often Absent Insulin Require Require antibodi present d for all d for es at onset some 8. What causes Type 1 DM? Progressive destruction of pancreatic Beta cells due to an autoimmune process in susceptible individuals Autoantibodies to the islet cells cause a reduction of 80 - 90 percent of normal Beta cell function before hyperglycemia and other manifestations occur 9. During the onset of Type 1 DM, what signs and symptoms usually lead a person to seek medical attention? Manifestations develop when the person’s pancreas is no longer able to produce insulin Onset usually rapid, leads person to come to the emergency department with impending / actual ketoacidosis S/S includes: ◦ Sudden weight loss ◦ Polydipsia (excessive thirst) ◦ Polyuria ◦ Polyphagia 10. What will happen if a person with Type 1 DM does not take insulin? They will develop diabetic ketoacidosis, a life-threatening condition 11. What is prediabetes? Impaired glucose tolerance Noted when a fasting or 2-hour plasma glucose is higher then normal (6.1-6.9 mmol / L) Typically no symptoms 12. Do people with prediabetes typically have symptoms of diabetes? No 13. Do people with prediabetes need to regularly test their blood glucose? Yes 14. Does the pancreas produce any insulin in Type 2 DM? Yes, the pancreas continues to produce some endogenous insulin Insulin produced is insuf cient for the needs of the body, poor utilized by the tissues or both 15. What are the 4 major metabolic abnormalities in the development of Type 2 DM? Insulin resistance Marked decrease in the ability of the pancreas to produce insulin Inappropriate glucose production by the liver Alteration in the production of hormones and cytokines by adipose tissue 16. What are the characteristics of metabolic syndrome? Metabolic syndrome (aka insulin resistance syndrome) → cluster of abnormalities that act synergistically to greatly increase the risk for cardiovascular disease Characterized by the following: ◦ Abdominal obesity ◦ Hypertension ◦ Dyslipidemia ◦ Insulin resistance ◦ Dysglycemia People with metabolic syndrome are at signi cant risk of developing DM and cardiovascular disease 17. Describe the typical onset of Type 2 DM. Typically gradual onset People typically go years without getting diagnosed with it, diagnosed via routine laboratory testing 18. What is gestational diabetes (GDM)? Develops during pregnancy Detected between 24 and 28 weeks gestation 19. After having gestational diabetes, do women usually progress to diabetes mellitus after pregnancy? Only approximately 10 percent of patients progress to DM after pregnancy Risk of developing DM in the next 5-10 years increases 20. What is the treatment for gestational diabetes mellitus (GDM)? Nutritional counselling → rst line treatment Physical activity as tolerated If above doesnt work, insulin therapy indicated 21. What sorts of medical conditions can cause secondary diabetes? Schizophrenia Cystic brosis Cushing’s syndrome Hyperthyroidism 22. Which drugs can cause secondary diabetes? Corticosteroids Phenytoin Atypical antipsychotics 23. What are the 3 classic clinical manifestations that occur at the onset of Type 1 DM? Polyuria fi fi fi fi Polyphagia Polydipsia 24. What additional signs and symptoms occur at the onset of Type 1 DM? Weight loss Weakness Fatigue Changes in visual acuity 25. What are the more common manifestations associated with Type 2 DM? Fatigue Recurrent infections Prolonged wound healing Painful peripheral neuropathy in feet LAB AND DIAGNOSTIC TESTS 1. What four methods are used to diagnose DM? Glycated hemoglobin Fasting blood glucose Random plasma glucose Two-hour plasma glucose 2. Explain how the Hemoglobin A1C (Hgb A1C) test works. Works by showing the amount of glucose that has been attached to hemoglobin molecules, which are attached to the RBC for the life of the cell Therefore, an A1c indicates the overall glucose control from the previous 90 to 120 days 3. What are the following values for Hgb A1C? o Normal (not diabetic)? Less than 6% o Prediabetes 6.0-6.4% o Ideal Hgb A1C for most people with DM? Less than 7% o Target for some people with T2DM at high risk for nephropathy? Less than 6.5% 4. How long does a person need to fast (no caloric intake) for a Fasting Plasma Glucose (FPG) test? Overnight fast 5. What are the following values of a Fasting Plasma Glucose (FPG) test? o Normal (not diabetic)? Less than 6.1 o Impaired fasting glucose (IFG)? Greater than 6.1, but less than 6.9 o Diagnostic of diabetes? Greater than or equal to 7.0 6. What is a random plasma glucose measurement? Taken at any time of the day without regard for meals 7. What is the normal value (not diabetic) for a random plasma glucose measurement? Less than 11.1 mmol / L 8. What is an oral glucose tolerance test (OGTT), and how is it used to diagnose diabetes? Glucose measurements 2 hours after drinking a glucose-containing solution MEDICATIONS 1. What is “intensive insulin therapy”, and what is the goal? Multiple basal-bolus injections in a day The goal is to achieve a near-normal glucose level of 4-7 mmol/L before meals, or 4-6mmol / L if this can be reached safely without severe hypoglycemia 2. What are the pharmacodynamics (onset/peak/duration) of the following classes of insulins? NOTE: the numbers in your medical-surgical textbook are a bit different than those in your Pharmacology textbook... To avoid confusion, you may want to only learn the values from your Pharmacology textbook. o Rapid-acting insulins (e.g. Novorapid) ▪ Onset: ▪ Peak: ▪ Duration: o Short-acting insulins (e.g. Regular) ▪ Onset: ▪ Peak: ▪ Duration: o Intermediate-acting insulins (e.g. NPH) ▪ Onset: ▪ Peak: ▪ Duration: o Glargine ▪ Onset: ▪ Peak: ▪ Duration: 3. When should bolus insulin be administered? 10-15 minutes before a meal 4. When should basal insulin be administered? Bedtime - one time a day typically 5. What is the only type of insulin that can be administered intravenously (IV)? Regular insulin 6. From what anatomical site is insulin absorbed from the fastest? Abdomen 7. What is the potential problem with injecting insulin into the thigh prior to going jogging? It can increase the rate of absorption and speed of the onset of insulin action 8. What should patients be taught about rotating injection sites... how should they do this? Lipodystrophy not a big concern anymore as human insulin reduces the risk Should advise patient to rotate injection within one particular site, such as the abdomen 9. How should patients be taught to cleanse their skin prior to insulin injection? With routine hygiene (washing with soap and water) when at home 10. How do insulin pumps work? Catheter inserted into the subcutaneous tissue and the device is programmed to deliver a continuous infusion of rapid-acting insulin 24 hours / day known as a basal rate 11. What are the bene ts of using an insulin pump? Reduces hypoglycemic episodes Helps individuals lead a more normal lifestyle 12. What is lipodystrophy? Hypertrophy or atrophy of subcutaneous tissue May occur if the same injection sites are used frequently Hypertrophy eventually regresses if the patient does not use the site for at least 6 months 13. What is the difference between the Somogyi effect and the dawn phenomenon? Somogyi effect ◦ Typically occurs in the hours of sleep ◦ Decline in blood glucose levels in response to too much insulin ◦ Counterregulatory hormones are released, stimulating lipolysis which in turn produces rebound hyperglycemia and ketosis Dawn phenomenon ◦ Characterized by hyperglycemia that is present on awakening in the morning owing to the release of counter-regulatory hormones in the predawn hours ◦ Affects the majority of people with DM 14. How do the following oral antihyperglycemic agents work? o Insulin secretagogues/sulphonylureas (e.g.Glyburide) Type 2 Diabetes Increase beta-cell insulin production in from the pancreas More insulin available in the bloodstream → more likelihood that glucose will be taken into the cells o Meglitinides (e.g. Repaglinide) Increase insulin production in the pancreas More rapidly absorbed and eliminated, increase risk of hypoglycemia Should take right before eating a meal o Biguanides (e.g. Metformin) Reduces glucose production via the liver Enhances insulin sensitivity at the tissue level and improves glucose transport into the cells First line medication for diabetes Does not promote weight gain fi o Αlpha-glucosidase inhibitors (e.g. Acarbose) Work by slowing down the absorption of carbohydrate in the small intestine Most effective in lowering postprandial blood glucose o Thiazolidinediones (e.g. Pioglitazone) AKA: TZDs or glitazones Increases glucose uptake in muscle and fat, inhibits hepatic glucose production o DPP-4 inhibitors (e.g. Sitagliptin) Enhance the incretin system, stimulate release of insulin from pancreatic beta cells, and inhibit hepatic glucose production o SGLT2 inhibitors (e.g. Canagli ozin) Enhance urinary glucose excretion o GLP-1 receptor agonists / Incretin mimetics (e.g. Liraglutide) Stimulate release of insulin, decrease glucagon secretion, increase satiety, decrease gastric emptying 15. Familiarize yourself with this additional information about diabetic medications: Why should metformin be avoided in people who have kidney disease, liver disease, heart failure, alcohol abuse (and temporarily stopped before people receive IV contrast media) ◦ IV contrast media poses a risk for acute kidney injury Which classes of oral (and non-insulin injectable) diabetic medications increase the risk of hypoglycemic episodes? NUTRITION AND EXERCISE 1. What 6 tips are included in the Diabetes Canada resource, “Just the Basics: Healthy Eating for Diabetes Management and Prevention”? Eating three meals per day at regular times and eating at intervals no more than 6 hours apart Limiting sugars and sweets such as sugar, regular pop, desserts, candies, jam, and honey Limiting the amount of high-fat food such as fried foods, chips, and pastries Eating more high bre foods Drinking water if thirsty as drink of choice Adding physical activity to the lifestyle 2. What should be the emphasis of nutritional therapy in people with Type 2 DM? Achieving glucose, lipid, and blood pressure goals 3. How does weight loss improve glycemic control in people with Type 2 DM? By increasing insulin sensitivity and glucose uptake and decreasing hepatic glucose output 4. What proportion of a diabetic person’s diet should be made up of: Protein ◦ 15-20% Fat ◦ Less than 35% Fibre ◦ 30-50g / day Carbohydrates ◦ 45%-60% fi fl 5. What is glycemic index (GI) and how is it used? Term used to describe the rise in blood glucose levels after a person has consumed carbohydrate containing foods 2. How can drinking alcohol affect a diabetic person’s blood glucose level? Inhibitory effect of alcohol on glucose production can cause severe hypoglycemia in patients taking insulin or OHAs that increase insulin secretion 3. What adverse effects can alcohol have on people who are taking diabetic medications? Risk for lactic acidosis 4. What is a “standard drink”? (You may need to Google this phrase to get a comprehensive answer) 5. What is the “plate method” of teaching healthy eating? Helps patient visualize the amount of each food group should be on the plate One half vegetables, one fourth starch, and one-fourth lled with 60-90g protein 6. How can regular physical activity support diabetes management? Exercise increases insulin sensitivity and can have a direct effect on lowering blood glucose levels 7. How much exercise (and how frequent) should people with Type 2 DM get per week? 150 minutes / week 8. How can a person with DM (who takes insulin or a sulphonylurea) avoid getting hypoglycemia when they exercise? Schedule exercise 1 hour after a meal or have a 10-15 gram carbohydrate snack before exercising 9. Why does strenuous activity sometimes cause hyperglycemia in people with DM? Can be perceived by the body as stress, causing counter-regulatory hormones to be released 10. Should people with DM exercise when: o Their blood glucose is elevated (but no urine ketones are present)? Exercise with caution o Their blood glucose is elevated and urine ketones ARE present? Postpone exercising SELF-MONITORING OF BLOOD GLUCOSE (SMBG) 1. How often should blood glucose be tested in each of these situations: Person with Type 1 DM? ◦ Three times a day Person with an insulin pump? ◦ Testing more frequent Person with Type 2 DM who is taking oral diabetic medications (or lifestyle modi cations only)? ◦ Individualized regimens Person with Type 2 DM taking once daily insulin and oral medications ◦ Once daily Person with DM is ill? ◦ Q4H fi fi 2. What surgery may be recommended for people with Type 2 DM who are obese and have dif culty meeting recommended treatment targets? Bariatric surgery NURSING MANAGEMENT 1. What subjective and objective data should be obtained when assessing a person with DM? Subjective: ◦ Constipation / diarrhea ◦ Frequent urination ◦ Depression ◦ Malaise ◦ Muscle Weakness ◦ Poor healing ◦ Thirst, hunger, nausea, and vomiting ◦ Weight loss Objective: ◦ Cataracts, soft, sunken eyeballs ◦ Dry, warm inelastic skin ◦ Rapid, deep respirations ◦ Hypotension, weak rapid pulse ◦ Dry mouth, fruit breath ◦ Altered re exes, restlessness, confusion 2. What diagnostic test results (blood and urine) should be reviewed when assessing a person with DM? 3. What are the overall goals for patients with DM? 4. What are the 3 acute situations involving patients with DM? Illness Injury Surgery 5. How can emotional or physical stressors, acute illness, injury, and surgery affect blood glucose? Results in increased blood glucose levels → hyperglycemia 6. If people with DM are ill: What should people eat and drink, even if they have a minor illness? ◦ Regular meal plan ◦ Increase the intake of noncarbohydrate containing uids (broth, water) What should people with diabetes drink if they are eating less than normal? ◦ Continue taking insulin as prescribed ◦ Supplementing food intake with carbohydrate-containing uids Should they continue to take their DM medications and insulin? ◦ Yes What should a person with DM do if they vomit more than twice in 12 hours? ◦ ED / doctor fl fi fl fl WEEK 4 DIABETES P2 ACUTE COMPLICATIONS OF DIABETES: HYPER- AND HYPO-GLYCEMIA 1. What are the causes of: o Hyperglycemia? Corticosteroids Emotional, physical stress Illness, infection Inactivity Poor absorption or lack of insulin Too little or no diabetes medication Too much food o Hypoglycemia? Alcohol intake without food Diabetes medication or food taken at wrong time Loss of weight without change in medication Too little food Too much diabetic medication Too much exercise without compensation Use of beta adrenergic blockers interfering with recognition of symptoms 2. What measures can be used to prevent: o Hyperglycemia? Accurate administration of insulin, non insulin injectables, and OHA Adherence to sick day rules when ill Checking blood glucose as ordered o Hypoglycemia? Recognize and know symptoms of hypoglycemia Accurate administration of insulin, non insulin injectables, and OHAs Checking BG as ordered DIABETIC KETOACIDOSIS 1. What is this complication? Acute metabolic complication of DM occurring when fats are metabolized in the absence of insulin Profound de ciency of insulin and is characterized by hyperglycemia, ketosis, metabolic acidosis, and dehydration More common in type 1 DM 2. How does this condition develop? fi When the circulating supply of insulin is insuf cient, glucose cannot be properly used for energy, so the body breaks down fat stores as a secondary source of fuel Ketones are acidic byproducts of fat metabolism that can cause serious problems when there is an excessive amount in the blood Ketosis alters the pH balance, causing metabolic acidosis to develop Ketonuria is a process that begins when ketone bodies are excreted in the urine During this process, electrolytes become depleted as cations are eliminated in an attempt to maintain electrical neutrality Insulin de ciency impairs protein synthesis and causes excessive protein degradation, condition results in nitrogen losses from the tissues Insulin de ciency also stimulates the production of glucose from amino acids → further hyperglycemia But because there is a de ciency of insulin, the additional glucose cannot be used and the blood glucose level rises further, adding to the osmotic diuresis. In osmotic diuresis, this additional amount of glucose enters the renal tubules and draws a large amount of water that leads to an increase in urine output. 3. What are the precipitating factors for DKA? Illness Infection Inadequate insulin dosage Insulin omission Undiagnosed DM 1 Poor self management 4. What hormones are involved in this condition? None other then insulin are listed in the textbook so idk 5. Does it occur more commonly in people with Type 1 or Type 2 DM? Type 1 6. What are the signs and symptoms of this condition? Polydipsia Polyuria Poor skin turgor Dry mucous membranes Tachycardia Orthostatic hypotension N/V Acetone is noted on the breath as a sweet, fruity odour due to the high levels of ketones in the blood Kussmauls respirations → bodys attempt to reverse metabolic acidosis 7. How does DKA affect the following diagnostic tests: o Plasma blood glucose? Above 14 mmoL o Arterial blood pH? Below 7.35 o Serum bicarbonate? Less than 15 mmol / L fi fi fi fi o Blood and/or urine ketones? Ketones in the blood and urine 8. What is the initial goal of treatment? Establish IV access and begin uid / electrolyte replacement therapy 9. What type of IV uids are usually used, in the initial treatment of DKA? Comprises an infusion of 0.45% or 0.9% NaCl IV solution at a rate to restore urine output to 30 - 60 ml / hr 10. What are the goals of uid and electrolyte replacement in DKA? Restore urine output and raise blood pressure 11. Why is hypokalemia a particular danger? Hypokalemia is a signi cant cause of preventative death during treatment of DKA Although initial serum potassium levels may be normal or high, levels may rapidly decrease once therapy starts because insulin drives potassium into the cells, causing life-threatening hypokalemia 12. What is the goal of administering IV insulin in DKA? Correcting hyperglycemia and hyperketonemia 13. Why is insulin withheld in a person with DKA until uid replacement is started and serum potassium is normal? Because insulin allows water and potassium to enter the cell along with glucose and can lead to a depletion of vascular volume and hypokalemia 14. When would IV sodium bicarbonate be administered? If severe acidosis (pH 14 mmol/L Thirst Urinary frequency HYPEROSMOLAR HYPERGLYCEMIC STATE (HHS) 1. What is this complication? fl fl fi fi fl fl Life threatening syndrome that can occur in the patient with DM who is able to produce enough insulin to prevent DKA but not enough to prevent severe hyperglycemia 2. How does this condition develop? Not enough insulin is produced, blood glucose levels climb Ketoacidosis does not occur because the body has enough insulin to prevent it 3. What hormones are involved in this condition? 4. How is HHS different from DKA? Higher blood glucose levels increase serum osmolality and produce more severe neurological manifestations such as somnolence, coma, seizures, and aphasia Typically occurs in the older patient with type 2 DM 5. What are the signs and symptoms of this condition? Neurological, see above 6. Which people are at highest risk for developing HHS? Older adult 7. How does HHS affect the following diagnostic tests: o Plasma blood glucose? Greater than 34 mmol/L o Serum osmolality? Marked increase in serum osmolarity o Blood and/or urine ketones? Minimal or absent 8. What are the nursing and medic