my.ilstu.edumy.ilstu.edu/~ddwilso2/nur475/Respiratory student notes... · Web viewMay need...

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Common Respiratory Problems 1 NUR 475 – Family Nurse Practitioner III Common Respiratory Problems Cough Dyspnea Hemoptysis Asthma Bronchitis COPD Pneumonia Lung cancer Tuberculosis Obstructive Sleep Apnea Lower Respiratory Infections in Older Adults (LRI) Significant source of both morbidity and mortality in the U.S. Include: o Acute bronchitis o COPD-note Gold: Global Initiative for Chronic Obstructive Lung Disease http://www.goldcopd.com/ o Influenza o Pneumonia o TB May progress from less serious airway disease to potentially fatal parenchymal involvement before the clinician can identify and treat the original disease LRI Statistics (2001/2003) found at http://www.cdc.gov/tb/default.htm o COPD = 4th leading cause of death for persons age 65 years and older o Pneumonia + influenza = 5th leading cause of death in 2002 o TB case rate for age 65+ = 6.4 per 100,000 (2008) is the highest rate of all age groups. The number of TB cases was highest among adults ages 25 to 44 (33% of all cases)

Transcript of my.ilstu.edumy.ilstu.edu/~ddwilso2/nur475/Respiratory student notes... · Web viewMay need...

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Common Respiratory Problems 1

NUR 475 – Family Nurse Practitioner III

Common Respiratory Problems

Cough Dyspnea Hemoptysis Asthma Bronchitis COPD Pneumonia Lung cancer Tuberculosis Obstructive Sleep Apnea

Lower Respiratory Infections in Older Adults (LRI)

Significant source of both morbidity and mortality in the U.S. Include:

o Acute bronchitiso COPD-note Gold: Global Initiative for Chronic Obstructive Lung Disease

http://www.goldcopd.com/o Influenzao Pneumoniao TB

May progress from less serious airway disease to potentially fatal parenchymal involvement before the clinician can identify and treat the original disease

LRI Statistics (2001/2003) found at http://www.cdc.gov/tb/default.htmo COPD = 4th leading cause of death for persons age 65 years and older o Pneumonia + influenza = 5th leading cause of death in 2002o TB case rate for age 65+ = 6.4 per 100,000 (2008) is the highest rate of all age

groups. The number of TB cases was highest among adults ages 25 to 44 (33% of all cases)

Keep in Mind….

More so than with many other illnesses, treatment decisions and outcomes depend heavily on epidemiological factors such as

o Ageo Functional statuso General health-underlying co morbidities

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 Cough

Most common respiratory symptom and reason patients seek an office visit

Cough duration and differential diagnosiso Acute - < 3 weeks

Cough due to acute respiratory tract infection resolves within 3 weeks in the vast majority of patients (over 90%).

Pertussis should be considered in previously immunized adults with persistent or severe cough lasting more than 2-3 weeks.

Common cold (viral), influenza, acute bronchitis, B pertussis infection, exacerbations of asthma/COPD/bronchiectasis, allergic rhinitis

Consider; pneumonia, aspiration, CHF, PEo Subacute - 3-8 weeks

Post-infectious cough most common, sinusitis; exacerbation of asthma, COPD of bronchiectasis

Consider B pertussiso Chronic or Persistent - > 8 weeks

Asthma, GERD, upper airway cough syndrome (previously called post-nasal drip), chronic rhinosinusitis, chronic bronchitis, ACE-I induced cough, B pertussis, bronchiectasis

Contributing factors: smoking, trauma, living environment, work environment RED FLAG symptoms

o Copious sputum production (bronchiectasis)o Fever, sweats, weight loss, hemoptysis (TB, lymphoma, bronchial carcinoma)o Dyspnea with cough (COPD, HF, fibrotic lung disease)

Essential inquiries: Age, duration of cough, dyspnea (at rest or with exertion), inhalant exposure at work or home, other symptoms, tobacco use history, vital signs-including pulse ox, chest examination, chest x-ray if unexplained cough lasts more than 3-6 weeks.

Testing:

PPD- if at risk for TB CBC Sputum C&S CXR ECG Stop ACE-I if taking Spirometry Bronchoscopy-referral

See “Evaluation of Patient with Chronic Cough” at http://www.aafp.org/afp/2011/1015/p887.html

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Treatment-

Individuals with acute cough associated with the common cold can be treated with a first-generation antihistamine/decongestant preparation such as Clarinex-D (desloratadine + pseudoephedrine)

The newer generation of non-sedating antihistamines such as loratadine plays no role in treating cough in this setting.

The use of inhaled ipratropium bromide (Atrovent) can be helpful in attenuating the post infectious cough (Anticholinergic)

In patients with post-infectious cough, when the cough adversely affects the patient’s quality of life and when cough persists despite use of inhaled ipratropium, consider the use of inhaled corticosteroids with the recognition that this product will take about 1 week of use prior to providing significant symptom relief.

For severe paroxysms of post infectious cough, consider prescribing 30 to 40 mg of prednisone per day for a short, finite period of time (5 days) when other common causes of cough including rhinosinusitis, asthma, or GERD have been ruled out.

Central acting antitussive agents such as codeine and dextromethorphan should be considered when other measures fail.

Dyspnea

Acute Dyspnea in the Office includes algorithms by Zoorob & Campbell retrieved from http://www.aafp.org/afp/2003/1101/p1803.html

The Pathophysiology and Treatment of Dyspnea by James Hallenbeck, MD found at http://69.36.35.38/accp/pccsu/pathophysiology-and-treatment-dyspnea?page=0,3

Use of the 6-Min Walk Test: A Pro and Con Review by Daniel R. Smith, MD, FCCP found at http://69.36.35.38/accp/pccsu/use-6-min-walk-test-pro-and-con-review?page=0,3

Essential Evaluation factors: Fever, Cough, Chest pain, vital sign measurements including pulse oximetry and temperature, Cardiac and chest examination, Chest X-ray, Arterial Blood Gas measurement

Shortness of breath is a very common symptom in primary care, but diagnosing the underlying disorder is not always easy

Complete history is key

Be sure to understand what the dyspneic patient means by “shortness of breath”o Is it pain?

Cardiac chest pains are often located centrally, whereas pain in pulmonary disease may also be lateral and be aggravated by deep breathing and coughing

Does the effort required to breathe seem excessive?

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Common Respiratory Problems 4

Does the patient have a feeling of smothering or of being unable to get a satisfying breath?

Consider medication-induced causes:o Beta blockers, including timolol maleate (Timoptic) eye drops used to treat

glaucoma, may aggravate CHF or induce bronchospasm in certain patients, even those whose asthma or COPD has been subclinical. “Wheezers have more difficulty with beta blockers.”

o Diffuse interstitial fibrosis, pleural effusion, and respiratory muscle paralysis or weakness can all be due to medications

o Be alert for use of aminoglycosides, nitrofurantoin (Macrodantin), busulfan (Myleran), cyclophosphamide (Cytoxan), methotrexate, and drugs thought to induce SLE.

Obtain thorough history o Coughing and wheezingo Previous lung diseases (tuberculosis, pneumonia, asthma)o Smoking habitso Previous chest surgeryo Has the patient ever coughed blood? 

Hemoptysis associated with inflammation in 80-90% of cases, idiopathic bronchitis being the most common cause; others are bronchiectasis, tuberculosis, carcinoma, and aspergillosis and even less common are pulmonary infarction from embolic disease, left heart failure, mitral stenosis.

Bronchiectasis: chronic dilatation of a bronchus or bronchi, with a secondary infection that usually involves the lower portion of the lung.  Dilatation may be in an isolated segment or spread throughout the bronchi. (Taber’s Cyclopedic Medical Dictionary, 20th ed., 2005) Bronchiectasis is a congenital or acquired disorder of the large bronchi characterized by permanent, abnormal dilation and destruction of bronchial walls. May be caused by recurrent inflammation or infection of the airways and may be localized or diffuse. Cystic fibrosis causes ½ of all cases. Essentials of diagnosis include: chronic productive cough with dyspnea and wheezing, recurrent pulmonary infections requiring antibiotics, a preceding history of recurrent pulmonary infections or inflammation, or a predisposing condition, radiographic findings of dilated, thickened airways and scattered, irregular opacities.

o Is cough chronic?  (as with asthma, emphysema, bronchitis, especially in a smoker). Is cough productive? (amount and color of sputum)

o Environmental substances the patient may be exposed to at work and at home?o When does the patient feel dyspneic and what circumstances and activities bring

on the sensation? Dyspnea at night especially paroxysmal nocturnal dyspnea (PND)

suggests left ventricular dysfunction, particularly if progressively worsens over several months

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May feel well when they go to bed but wake up with a feeling of suffocation that is relieved by sitting up or walking around (obstructive sleep apnea)

Patients with COPD may also become dyspneic at night, but the episode is likely to occur after many hours in bed or in the early morning and is relieved by bronchodilator inhalation or expectoration of significant amounts of purulent sputum-pO2 drops at night

Asthma patients tend to get up with dyspnea shortly after lying down Exertional dyspnea may reflect cardiopulmonary disease or simply poor

conditioning Ask how long it takes for dyspnea to be relieved after ceasing activity and

whether there is associated pain Does dyspnea develops only while the patient is at rest?

o Uncommon and, unless the patient is very sick, may indicate psychogenic disease, especially in a younger patient with no history of heart or lung disease)

o Organic disease must be ruled out before diagnosing dyspnea as psychogenic. Specific stresses or personal problems occurring? When dyspnea is associated with specific postures, consider neuromuscular disease

o Patients with diaphragmatic paralysis have more difficulty breathing when lying down than when sitting

o If the intercostal accessory muscles are predominantly involved in neuromuscular deficit, the patient may be more comfortable when lying down, with dyspnea becoming exaggerated when he is seated

Physical examination

Note components of breathing cycle:o Prolonged and decreased expiration suggests airway obstructiono Rapid and shallow breathing is more typical of CHFo Irregular or very slow breathing may be due to neurologic disease

Mental status Extremities:

o Edema; DVT, CHFo Cyanosiso Digital clubbing; right-to-left intracardiac shunt, lung cancer, interstitial

pulmonary fibrosis, chronic pulmonary disease with bronchiectasis, familial clubbing, asbestosis, mesothelioma

Necko Neck vein distention (COPD, CHF, cardiac tamponade)o Thyroid enlargement o Trachea midline

Chest o Inspect;

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Hyperinflation (including barrel chest) and use of accessory muscles of breathing:  substantial COPD

o Palpate; Subcutaneous emphysema or crepitus Tactile and vocal fremitus - diminished in COPD, normal or enhanced

in CHF, absent with significant pleural effusion or a pneumothoraxo Percuss;

Dullness – consolidations or effusions Hyper-resonance – pneumothorax or bullous emphysema

o Auscultate; Absent – pneumothorax, pleural effusion, airway obstruction Stridor - upper airway obstruction, epiglotitis (stridor, drooling, fever),

croup Wheezing – asthma, COPD, pulmonary edema, pulmonary emboli Decreased - airway obstruction Inspiratory and expiratory crackles (rales) - left CHF, pulmonary

edema and pneumonia Coarse crackles - interstitial pulmonary fibrosis or significant left

ventricular failure In patients with COPD - scattered fine basilar crackles can be present

from retained secretions (often heard at very end of expiration) Heart auscultation;

o Dysrhythmiao S3 gallop: left ventricular dysfunction (would also have jugular venous

distension, liver enlargement, peripheral edema)o Increased second pulmonic sound (especially when associated with a pleural

rub) may mean pulmonary infarction, pulmonary HTN or cor pulmonaleo Distant heart sounds; COPD, obese persons, those with pericardial disease and

cardiac tamponadeo Check for scars on the chest that may indicate prior thoracic or cardiac

surgery Abdominal - hepatojugular reflex, hepatomegaly, ascites (CHF)

Differential Diagnosis

Cardiopulmonary causeso Heart diseases; CHF, CAD, dysrhythmias, pericarditis, MIo Pulmonary; COPD, new-onset asthma or exacerbation, pneumonia,

pneumothorax, PE, pulmonary edema, restrictive lung disorders, respiratory muscle dysfunction . . . Subtle interstitial disease-encompasses 180 disease entities with many not

having a specific cause: pulmonary fibrosis from Amiodarone, antineoplastic agents, environmental, infections, systemic disorders-sarcoidosis, Wegener’s granulomatosis, See Table 9-19, p. 292-Lange 2013

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Pleural effusion-a volume of fluid greater than 7-14 mL in this space is abnormal. Many mechanisms come into play: increased hydrostatic pressures in the microvascular circulation, decreased oncotic pressures in the microvascular circulation, lung collapse which decreases pleural space pressure, increased permeability of the microvascular circulation, obstruction of lymphatic drainage (neoplasm or sarcoidosis). A common presentation of many pulmonary and systemic diseases. Many are asymptomatic. Most common symptoms are dyspnea, nonproductive cough, and pleuritic chest pain.

Primary or secondary hypertension (including that following silent pulmonary embolism)

Upper airway obstruction; epiglottitis, croup, foreign body Systemic causes; anemia, hyperthyroidism, obesity, ascites, pregnancy

o May be a consequence of poor conditioning (a normally sedentary person who suddenly undertakes strenuous activity)

Psychogenic; panic attacks, hyperventilation, pain, anxiety

Diagnostic testing

CBC, complete metabolic profile Chest x-ray-What is a quality chest film? Use the RIPE mnemonic.

o Rotation. To determine the degree of rotation in a radiograph, measure the distance between the medial heads of the clavicles and the adjacent spinous processes in the upper thorax. In a truly straight film, the distances should be the same.

o Inspiration. To check for an adequate degree of inspiration, count the anterior ribs on the right. In a good radiograph, 6 anterior ribs should be visible above the right hemidiaphragm.

o Position. Identification of a gas-fluid level (often in the gastric fundus), alignment of the scapulae with the lungs, and a posteroanterior (PA) label all help establish the patient was upright.

o Exposure. A good film must have both adequate penetration of the patient and sufficient contrast to distinguish between adjacent structures of different densities. If the intervetebral disks of the lower thoracic spine are visible through the heart and the pulmonary vessels posterior to the heart on the left can be identified, the exposure is probably adequate.

Resting ECG Basic spirometry (the FEV1/FVC ratio of predicted/referenced value is the critical

measurement). Interpretation of spirometry discussed in http://www.aafp.org/afp/2004/0301/p1107.pdf

o < 30% = very severe obstructive pulmonary diseaseo 30-49% = severe obstructive pulmonary diseaseo 50-79% = moderate obstructive pulmonary diseaseo > 80% = mild obstructive pulmonary disease or may not have pulmonary disease

May need ventilation-perfusion scan, stress testing or cardiac catheterization

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Hemoptysis

Essential Inquiries: Smoking history, Fever, Cough, and other symptoms of lower respiratory tract infection, Nasopharyngeal or gastrointestinal bleeding, Chest x-ray and complete blood count

Definitionso Scant hemoptysis:  blood-tinged sputumo Frank hemoptysis:  < 600 ml of blood in 24 houro Massive hemoptysis:  > 600 ml of blood in 24 hours

History o Cougho Sputum productiono Fever, chills, night sweats, weight losso Chest paino Gurgling, wheezingo URI symptomso Smokingo Travel to Africa, Asia, South America

 Clinical Findingso Vital Signs; elevated temperature, heart & respiratory rates, hypotensiono General;  Anxiety, palloro HEENT; chest nares and oropharynx, URI signso Neck; Supraclavicular adenopathy-helps diagnosis of lung cancero Chesto Extremities:  cyanosis, clubbing, edema

Differential Diagnosiso Scant or frank:

Bronchitis Bronchiectasis Lung cancer Active TB Chronic necrotizing pneumonia PE with infarction HF

o Massive : TB Bronchiectasis Necrotizing pneumonia Lung abscess Fungal lung infection Bronchogenic cancer

Diagnostic testing

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o CXRo CBC with diffo T  & Co Coagulation profileo Chemistry profileo ABGso UA (hematuria-vasculitis)o Sputum analysiso Echo (if diastolic murmur-all diastolic murmurs are pathological)o Bronchoscopyo PPDo CT scan and/or angiography

Managemento Scant or frank bleeding

Antibiotic trial if infection present Antitussive (nonsedating dose) Treat underlying condition Oxygen prn

o Massive : Assess ABCs Oxygen (mask) Volume resuscitation Foley catheter Positioning Bronchoscopy Mild sedation (anxiety)

***Case study group #1

AsthmaExpert Panel Report 3: Guidelines for Diagnosis and Management of Asthma http://www.nhlbi.nih.gov/guidelines/asthma/asthsumm.htm

Asthma Care Quick Reference: http://www.nhlbi.nih.gov/guidelines/asthma/asthma_quickref.htm

See Lange (2013) page 243-259Essentials of diagnosis: Episodic or chronic symptoms of airflow obstruction: breathlessness, chest tightness, wheezing and cough; Complete or partial reversibility of airflow obstruction, either spontaneously or following bronchodilation therapy; Symptoms frequently worse at night or in the early morning; Prolonged expiration and diffuse wheezes on physical examination; Limitation of airflow on pulmonary function testing or positive bronchoprovocation challenge.

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Note Stepwise Approach for Managing Asthma in Adults and Children > 5 Years of Age and; Quick relief for asthma in readings.

Morbidity and Mortality32.6 million people had had an asthma diagnosis in their lifetime22.2 million people are currently diagnosed with asthma12.2 million people suffer from asthma attacks annuallyApproximately 4000 asthma-related deaths occur annuallyApproximately 11 people die from asthma each day What is asthma? “A common chronic disorder of the airways that is complex and characterized by variable and recurring symptoms, airflow obstruction, bronchial hyperresponsiveness, and underlying inflammation. “ NHLBI, 2007

Making the diagnosis….Is it asthma?History of

Recurrent wheezingRecurrent chest tightnessRecurrent coughRecurrent difficulty breathingTroublesome cough at nightCough or wheezes after exerciseSymptoms worse after exposure to airborne allergens, viral infections, smoke, pollutants or other irritantsSymptoms influenced by menstrual cycle, strong emotions such as laughing or crying

Per EPR-3: Consider the diagnosis of asthma and perform spirometry if any of these indicators are present. These indicators are not diagnostic by themselves but the presence of multiple key indicators increases the probability of the diagnosis of asthma. Spirometry is needed to make the diagnosis of asthma.

Goal of asthma therapy: Achieve controlReduce impairment

Prevent chronic and troublesome symptomsRequire infrequent use of inhaled short-acting beta2 agonist (≤ 2 days/week)Maintain (near) “normal” pulmonary functionMaintain normal activity levelsMeet patients’ expectations of and satisfaction with asthma care

Reduce riskPrevent recurrent exacerbationsMinimize need for emergency department visits or hospitalizationsPrevent progressive loss of lung functionProvide optimal pharmacotherapy with minimal or no adverse effects

Examples of Controller Drugs to Prevent Inflammation-Mainstay of asthma careInhaled Corticosteroids Leukotriene receptor

antagonists, leukotriene Mast cell stabilizers-good for kids as kids have mast cell

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modifiers releaseMometasone (Asmanex)Fluticasone (Flovent)Budenoside (Pulmocort)Beclomethasone (QVAR)Triamcinolone (Azmacort)

Montelukast (Singulair)Zafirlukast (Accolate)Zileuton (Zyflo)

Cromolyn (Intal)Nedocromil (Tilade)

Medications to Treat or Prevent BronchospasmRescue drugs for bronchospasm-takes one minute to start working Short acting beta 2 agonists such as Albuterol (Proventil), pirbuterol (Maxair), levabuterol (Xopenex-pronounced Zopenex)

To prevent bronchospasm-these are not rescue drugs, takes one hour to work Long-acting beta2-agonists such as salmeterol (Serevent)

Acute asthma flare management-Aggressive treatment of inflammation with corticosteroid, i.e., Prednisone 40-60 mg qd X 3-10 days (average 5-7 days).This takes six hours to start working and will see a change in 24 hours.

PEF-peak expiratory flow meters-handheld device, home monitoring tool PEF should be measure in the morning before administration of a bronchodilator and in the afternoon after taking a bronchodilator. A 20% change in PEF values from morning to afternoon or from day to day suggests inadequately controlled asthma. PEF values less than 200L/min indicate severe airflow obstruction.

Routine chest x-ray usually shows only hyperinflation.

Acute BronchitisDefinition:  inflammation of the tracheobronchial tree typically resulting from viral infection with adenovirus or influenza. Most are 90% viral and 10% bacterial. The most common bacterial pathogens are atypical pathogens: M. pneumonia, C. pneumoniae (not revealed by gram stain)

Cough is usually present, and mucoid sputum is produced in 1/2 of cases.

Acute Bronchitis in the Older Adult•      Most common early symptoms–   anorexia–   malaise–   headache•      Chest pain and fever can be present in severe infection•      Lung findings often unremarkable; rhonchi and wheezing may occur (esp. in COPD)Diagnosis•      Secondary bacterial infection is common following influenza and in those with COPD or immunocompromising illnesses.

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•      Most common causative bacteria are Haemophilus influenzae and Streptococcus pneumoniae.  In COPD pts, Moraxella catarrhalis. •      CXR should be performed in patients who appear ill or do not respond to initial treatment.Treatment•      General supportive therapy:–   rest–   fluids–   antipyretic-analgesic agents–   cough suppressants, if appropriate•      Antibiotic selection per sputum Gram stain and culture (ideally)Empirical Treatment•      Most common causative organisms can usually be treated with:–   amoxicillin–   second-generation cephalosporins–   erythromycin–   tetracyclines–   trimethoprim-sulfamethoxazoleProphylaxis•      For patients with severe chronic bronchitis, prophylaxis with low-dose tetracycline or TMP-SMZ may be prescribed during winter months or when an exacerbation would be life-threatening.•      Use of the influenza and pneumonia vaccines is highly recommended for age 65+, especially those with chronic disease. 

***Case study group #2

Chronic Obstructive Pulmonary Disease (COPD)Asthma is no longer part of diagnosisEssentials of Diagnosis: History of cigarette smoking; Chronic cough, dyspnea (in emphysema), and sputum production (in chronic bronchitis); Rhonchi, decreased intensity of breath sounds, and prolonged expiration on physical examination; Airflow limitation on pulmonary function testing that is not fully reversible and most often progressive. From Prescribers Letter, September 3, 2009:

RUMOR: You can’t abruptly stop Advair or Symbicort.

TRUTH:      This is only partly true.     Some patients want to stop these combo inhalers...due to warnings about an increased risk of death with long-acting beta-agonists.     Tell patients they DON’T need to taper long-acting beta-agonists (salmeterol, formoterol).     Instead, recommend switching to just an inhaled steroid.     If asthma symptoms worsen, suggest increasing the steroid dose. If this isn’t enough, suggest adding an oral leukotriene modifier like montelukast (Singulair) for asthma or an inhaled anticholinergic like

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ipratropium or tiotropium for COPD.     On the other hand, it can be important to taper inhaled steroids...to prevent severe asthma exacerbations.     Recommend tapering an inhaled steroid over 2 to 4 weeks before stopping...not because of adrenal risks but to lessen the risk of asthma exacerbations.     Keep in mind that salmeterol and formoterol should NOT be used alone for asthma. Explain that unless they are being used prophylactically to prevent exercise-induced bronchospasm, they need to be used with an inhaled steroid to reduce the potential risk of death.     If COPD symptoms worsen on a beta-agonist alone, suggest adding an inhaled anticholinergic.     Watch for patients who may be abruptly stopping an inhaled steroid because they can’t afford their meds. Emphasize the importance of taking their inhaled steroid regularly. If they can’t, try to recommend alternatives or suggest a patient assistance program

Pathogenesis-the inflammation of COPD differs from asthma so the use of anti-inflammatory medications and the response to those medications are different. The inflammation of asthma is mediated through eosinophils and mast cells. The inflammation of COPD includes neutrophils, macrophages, and CD8 T lymphocytes (Chisholm-Burns, p. 232).•      “COPD” generally includes:–   chronic bronchitis–   emphysema•      Normal aging-->  panlobular emphysema (a decrease in supporting elastic lung structure with resultant loss of alveoli)•      In the absence of lung disease, normal respiratory reserves are more than adequate to cope with the changes due to aging.•      Symptomatic disease results from centrilobular emphysematous damage to alveoli, generally due to:–   smoking–   occupational exposures•      Chronic bronchitis:  excessive bronchial mucus production and a chronic cough that persists for at least 2 successive years in the absence of any specific disease•      Mucus hypersecretion and inflammation of the bronchial mucosa --> nonuniform airway obstruction --> hypoxemia --> retention of CO2 --> cause or exacerbate pulmonary hypertension --> elevated right-sided heart pressures Diagnosis (-the dyspnea panel may be helpful here.)•      One of the most common complications of an acute exacerbation of chronic bronchitis is dyspnea secondary to Heart Failure.•      Left-sided heart failure can be triggered by the additional hypoxemia of an acute infection•      Since rhonchi and adventitious sounds are frequently present with COPD, lung auscultation is typically not diagnostic

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•      A 4th heart sound (S4) and pedal edema may be helpful diagnostic signs. Signs of cor pulmonale include increased pulmonic component of the second heart sound, jugular venous distension, hepatomegaly. •      CXR only minimally useful (pulmonary edema may be masked)• Spirometry is required to confirm the diagnosis. The presence of a postbronchodilator FEV1/FVC ratio less than 70% confirms the presence of airflow limitation that is not fully reversible. You don’t need full pulmonary function tests with lung volumes and diffusion capacity to establish the diagnosis . (Tierney)Note article differentiating asthma from COPD. Other differential diagnoses include: Asthma, HF, Bronchiectasis, TB, Obliterative Bronchiolitis, Diffuse Panbronchiolitis (GOLD document) Treatment:   Long-term therapy for elderly with COPD •      Controlling symptomsMedications

1. Short-acting bronchodilators, both beta agonists and anticholinergics, are the mainstay of therapy for COPD.

2. Long-acting bronchodilators are indicated for moderate to severe COPD. Currently two beta agonists (formoterol, salmeterol) and long-acting anticholinergic (tiotropium-Spirva) are available.

3. Inhaled corticosteroids are recommended for patients with moderate to severe COPD with frequent exacerbations (incidents which worsen symptoms).

4. Systemic corticosteroids (IV or pills) are beneficial for treatment of severe exacerbations.5. Antibiotics may be beneficial for treatment of exacerbations. (Lange 2013, p 263)

Pathogens Associated with COPD ExacerbationRespiratory Bacteria Viral (20-50%) Less common resp. bacteria

(usually in advanced disease or repeat exacerbations)

Gram positiveS. pneumonia

Gram negativeH. influenzaM. catarrhalis

Atypical pathogensM. pneumoniaC. pneumoniaLegionella spp.

RhinovirusInfluenza virus

Enterobacteriaceae spp.Pseudomonas spp. - inpatient

6. Theophylline in low doses may reduce frequency of exacerbations in patients who tolerate it (it has many side effects).

•      Maximizing independent self-care

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•      Reducing frequency of hospitalization Acute Exacerbations   •      Anticholinergic drugs, beta-adrenergic drugs, bronchodilators, corticosteroids (If baseline FEV1 < 50% of predicted, add a corticosteroid such as prednisone 40 mg qd for 10 days. Consider using an inhaled corticosteroid such as nebulized budesonide (Pulmicort) during non-acidotic exacerbations), and oxygen should be progressively employed in a stepwise fashion. Antimicrobial therapy is likely indicated when symptoms of breathlessness and cough are accompanied by altered sputum characteristics that are indicative of bacterial infection such as increased purulence and /or change in volume. Consider chest x-ray with fever and/or low SaO2. •      Verify compliance with existing therapy•      Monitor the adequacy of existing therapy (e.g., with a theophylline level-a lower dose of Theo helps improve the action of the steroid)•      Escalate existing therapy to maximal dosages•      Add new therapeutic agents directed at the presenting symptoms or apparent precipitating event•      Change mode of therapy delivery (po→IV) When to Hospitalize?•      If new oxygen therapy is prescribed or escalation of oxygen supplementation to levels that must be closely monitored•      Questionable compliance•      Intravenous therapy•      Use of nebulizer treatments more often than every 4 hours Prevention•      Smoking cessation•      Proper nutrition and hydration•      Exercise-pulmonary rehab•      Use of continuous oxygen therapy •      Prevention of pneumonia through use of flu and pneumococcal vaccine 

***Case study group #3

Pneumoniahttp://www.idsociety.org/uploadedFiles/IDSA/Guidelines-Patient_Care/PDF_Library/CAP%20in%20Adults.pdf

 Essentials of Diagnosis/Community-Acquired Pneumonia Symptoms and signs of acute lung infection: fever or hypothermia, cough with or without sputum, dyspnea, chest discomfort, sweatrs or rigors; Bronchial breath sounds or rales are frequent auscultatory findings; Parenchymal infiltrate on chest radiograph; Occurs outside of the hospital or less than 48 hours after admission in a patient who is not hospitalized or residing in a long-term care facility for more than 14 days before the onset of symptoms.

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Essentials of Diagnosis/Hospital Acquired Pneumonia Occurs more than 48 hours after admission to the hospital and excludes any infection present at the time of admission; At least two of the following: fever, cough, leukocytosis, purulent sputum; New or progressive parenchymal infiltrate on chest x-ray; Especially common in patients requiring intensive care or mechanical ventilation Pathogenesis•      Mortality in older persons:  15-70%, depending on etiology and population at risk•      Incidence:  25-44/1000 in the community; 68-114/1000 in chronic care facilities•      High co-morbidity:  80-90% of elderly pneumonia patients have one+ concomitant illnesses (DM, CV, COPD, chronic CHF, alcoholism)•      Aspiration is believed to be the most common route of infection in elderly patients•      Usual mechanism:  unapparent introduction of oropharyngeal secretions into the lung while swallowing, lying supine, or sleeping Most common organisms•      In the community:–   S. pneumonia-“Strep will kill you.” Most common cause of fatal community-acquired pneumonia.–   H. influenzae–   Atypicals: M. pneumoniae, Chlamydia pneumoniae, Legionella species•      In hospital-acquired bacterial pneumonia:–   Klebsiella pneumonia-likes alcoholics–   H. flu–   S. pneumoniae,–   Staph. Aureus Most Common Pathogens Encountered in Respiratory Tract Infections

CAP

Sinusitis ABECB Pharyngitis

Streptococcus pneumonia √ √ √Hemophilus influenza* √ √ √Moraxella catarrhalis* √ √ AtypicalsMycoplasma pneumoniaeChlamydia pneumoniaeLegionella Sp.

√ √

Streptococcus pyogenes √Viruses √ √ √ √

*Can produce Beta-lactamaseABECB=acute bacterial exacerbation of chronic bronchitisFrom: Slain, D. (2009). Infectious Disease Therapeutics: What you Must Know about Antimicrobial Therapy in the Era of Resistance.

Physical Findings•      Presentation of pneumonia in the elderly is frequently nonspecific.

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•      Poor appetite and weakness•      Slower, insidious onset•      A respiratory rate > 28 is often earliest clue.•      Fever may be blunted or absent•      Suspect pneumonia when has significant dyspnea or functional impairment Diagnosis•      Confirming diagnosis usually depends on the CXR, although an infiltrate may be obscured by pulmonary edema or not apparent until 24-48 hours after rehydration.•      Normal or mildly elevated total WBC count accompanied by a left shift in the differential is characteristic but nonspecific.•      ABGs, sputum specimen analysis TreatmentSee Lange (2013) page 267 for treatment of common organisms

•      RTO •      CXR 6 weeks after ABT done Caution with...•      Aminoglycosides:  nephrotoxic, ototoxic•      Erythromycin:  multiple drug interactions and GI intolerance•      Ciprofloxacin:  inadequate coverage of S. pneumoniae; high incidence of delirium Prevention•      May be achieved in part by vaccination against influenza and pneumococcus 

Lung Cancerhttp://www.cancer.gov/types/lung

Essentials of Diagnosis: New cough, or change in chronic cough; Dyspnea, hemoptysis, anorexia, weight loss; Enlarging nodule or mass, persistent opacity, atelectasis, or pleural effusion on chest x-ray or CT; cytologic or histologic findings of lung cancer in sputum, pleural fluid or biopsy specimen.Review of content discussed in Pathophysiology regarding pathogenesis, symptomsDiagnosis and Treatment-Lange, pp. 1595-1603. May develop pleural effusion. Can be sent home with portable chest tube.  

***Case study group #4

Tuberculosishttp://www.cdc.gov/tb/http://www.who.int/mediacentre/factsheets/fs104/en/

Essentials of Diagnosis:

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Fatigue, weight loss, fever, night sweats, and coughPulmonary infiltrates on chest x-ray, most often apical-p. 246, Imaging+ TB skin testAcid-fast bacilli on smear of sputum and sputum culture positive for M. tuberculosisCharacteristics of antituberculous drugs-Lange, 2013, p. 284 (dosages)

***Case study group #5 

Obstructive Sleep Apnea (OSA)

Essential Evaluation: Excessive sleepiness or fatigue, snoring, witnessed apnea, crowded airway, high-risk conditions (see below), polysomnogram test

Prevalence

1 in 20 adults have OSA with daytime impairment As common as adult asthma 26% of adult clinical population at-risk 32% of primary care adult patients at high-risk 30% of cardiology clinic population Mortality rate similar to breast and colon cancer, significantly lower testing rate 80-90% undiagnosed and untreated; especially women with lower BMI “Typical” OSA patient model (snoring, obese, sleepy, middle-aged male) misses up to

30% of cases

Pathogenisis

Crowded or narrow oropharynx relaxes in sleep and partially (hypopnea) or fully (apnea) obstructs airway

Airway collapse alerts carbon dioxide and oxygen levels, then stimulates the brain to cause a partial arousal

Leads to frequent arousals, sleep loss and in some cases hypoxemia Familial trend likely due to anatomical characteristics

Symptoms

Daytime; excessive sleepiness, fatigue, unrefreshing sleep, morning/nocturnal headache, decreased memory/concentration/attention/judgment, personality changes (irritable, aggressive, anxious, depressed), weight gain, sexual dysfunction

Nighttime; snoring, gasps or pauses in breathing, nocturnal choking of dyspnea, restless sleep, frequent awakenings, insomnia (W>M), mouth breathing, nocturia, nocturnal gastroesophageal reflux, nocturnal diaphoresis

Signs

Overweight/obese; BMI > 25 kg/m3 (93% sensitive, 74% specific)

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Large neck size; > 16 inches (61% sensitive, 93% specific) Crowded oropharynx; large uvula, long soft palate, lateral crowding, macroglossia,

narrow or high arched hard palate, retrognathia, micrognathia, mid-facial hypoplasia High-risk for OSA HTN; 30%, particularly newly diagnoses and drug-resistant Atrial fibrillation; 50% new onset and recurrent CHF; 26-50% CAD; 2-fold greater occurrence Nocturnal dysrhythmias; frequent Stroke/TIA;72% and increased with recurrent stroke Obesity; 40% T2DM; 23-40% and poor glycemic control Pre-operative; >70% of bariatric patients, 66% with difficult intubation Driving occupations; 3-fold increase of motor vehicle crashes

Differential diagnosis

Nighttime symptoms;o Primary snoringo Panic attackso Larygospasm (GERD)o Dsypnea due to pulmonary edemao Central sleep apneao Nonobstructive alveolar hypoventilation

Daytime symptoms;o Insufficient sleep syndromeo Narcolepsy or idiopathic hypersomniao Periodic limb movement disordero Hypothyroidismo T2DMo Depression

Key health consequences of untreated OSA

Function related; excessive sleepiness, motor vehicle crashes (3.71 relative risk, estimated 980 deaths/year), neurocognitive deficits

Disease related; HTN (OSA is an independent risk factor, JNC 7) , MI, cardiac dysrhythmias (atrial fibrillation-49%, 40% reduction in recurrence with CPAP), CHF (30-70%, 26-43% improvement in LVEF with CPAP), Stroke/TIA (57% initial, 74% recurrent), impaired glucose metabolism, obesity, depression, erectile dysfunction

20.3 deaths: 1,000 person-years

Screening

Recommend screening all adults with high-risk conditions

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Incorporate sleep questions into ROS (amount of sleep, snoring, unusual breathing in sleep, excessive sleepiness and fatigue, insomnia, unusual behaviors in sleep, drowsy driving)

Berlin Questionnaire – validated in primary care populations STOP-Bang screening tool – validated in surgical populations

Diagnostic testing

Polysomnogram CPAP titration TSH, CBC, CMP, ferritin in selected cases

Treatment

CPAP (continuous positive airway pressure); most effective, average compliance 40-60% Weight loss; 10% reduction in BMI reduces rate of apnea Oral appliances; 30-60% effective overall, more effective in mild OSA, retrognathia,

lower BMI Surgical-multiple procedures; least effective overall

Additional information

Read overview of OSA at: http://emedicine.medscape.com/article/302773-overview Dodson, K.J. (2008). Cardiovascular Effects of Sleep Apnea. The Journal for Nurse

Practitioners, 33 (6), 439-444. http://www.webmd.com/sleep-disorders/understanding-obstructive-sleep-apnea-

syndrome American Academy of Sleep Medicine website:

http://www.aasmnet.org/AboutAASM.aspx

Chronic Insomnia

First line treatment: Cognitive behavioral therapy, which includes: Stimulus control: aims to establish consistency in sleep patterns and maintain an

association of sleep with the bed and bedroom (e.g., only go to sleep when tired) Sleep restriction: limits time in bed to sleep time, gradually increasing the time spent in

bed as sleep efficiency improves Relaxation training: training to reduce somatic tension and control bedtime thought

patterns that impair sleep

Insufficient evidence on effectiveness of benzodiazepine hypnotics, melatonin, or trazodone.

See: “Management of Chronic Insomnia Disorder in Adults: A Clinical Practice Guideline From the American College of Physicians” at http://annals.org/article.aspx?articleid=2518955

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