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1. Infectious Diseases
2. Obstructive Lung Diseases
3. Chronic Obstructive Pulmonary Disease (COPD)
4. Restrictive Lung Disorders
Primary atypical pneumonia
Pneumocystis carinii pneumonia
-May develop as primary infection in lungs or may be secondary
-It becomes a risk after aspiration or inflammation in the lung
-Organisms enter lungs via inhalation (virus), bacteria, fungi, parasites, aspiration
-½ of pneumonia cases are believed to be viral
-Most common bacterial form is pneumococcus
-Depends on how soon treatment is started, general health of the person, and the infecting agent
-Most recover completely in a few weeks with a residual cough lasting up to 8 weeks after infection is gone
-Can be fatal in the very old, very young, and those with chronic cardiovascular or respiratory diseases
Inflammation of alveolar wall and leakage of cells, fibrin, and fluid into alveoli causing consolidation
Inflammation and purulent exudate in alveoli often arising from prior pooled secretions or irritation
Pneumonia Diagnostic Tests & Lab Values
-Chest x-ray or CT scan: shows areas of opacity
-Physical exam: Dr. listens to lungs to check for abnormal sounds (rales and crackles)
-Blood test: Increase in white blood cells
Pneumonia Clinical Features-Lobar
-High fever and chills
-Productive cough with rusty sputum
-Rales progressing to absence of breath sounds in affected lobe.
Pneumonia Clinical Features-Bronchopneumonia
-Productive cough with yellow-green sputum
Pneumonia Clinical Features-Interstitial Pneumonia (Primary Atypical Pneuomonia PAP)
-Variable fever and headache
-Nonproductive hacking cough
Pneumonia Clinical Features-Legionnaries' Disease
-Cough that may be severe enough to cause production of sputum
-Nausea, vomiting, and stomach discomfort
-Headaches, muscle aches, chest pain, and shortness of breath
1. Lung abscesses
2. Respiratory failure
3. Sepsis which may lead to organ failure
4. Acute respiratory distress syndrome (ARDS)
5. Infection in bloodstream (bacteremia)
6. Empyema (pleural space inflammation)
7. Pleural effusion (fluid accumulates in between the pleural spaces)
-Transmitted by oral droplets of myobacteria from a person with active infection that are inhaled into lungs
-Coughing, singing, or any forced respiratory movement
-Bacteria can remain in air currents for several hours, making spreading easier
-One person, on average, can affect 7 people but most do not develop active infection
-TB disease has an insidious onset, but eventually anorexia, malaise, fatigue, weight loss, fever, and night sweats occur
-Cough becomes increasingly severe and more productive
-Sputum becomes purulent and often bloody
-If left untreated, the disease destroys large portions of the lungs and other organs and death ensues
TB is an infection usually caused by mycobacterium tuberculosis. It primarily affects the lungs
2 Stages in pathogenesis (primary and secondary infection)
Tuberculosis Pathophysiology-Primary Infection
bacteria enters the lungs and cause a local inflammatory reaction -> granuloma (containing bacilli) forms at site of inflammation -> tubercle forms -> caseation necrosis develops in center of tubercle (which become walled off by fibrous tissue in a healthy person) ->by 6 to 8 weeks immune response is complete and individual has been infected but does not have active disease
Tuberculosis Pathophysiology-Secondary Infection
-Stage of active infection, often years after primary infection, usually due to decreased host immune resistance
-Bacteria multiply -> tissue destruction occurs -> cavitation occurs with formation of a large open area in the lung with erosion into the bronchi and blood vessels -> organisms spread into other parts of the lung -> infection may spread to digestive tract or pleural cavity
Tuberculosis Diagnostic Tests & Lab Values
-Skin Test: delayed skin hypersensitivity reaction
-Blood Test: based on the proportion of IFN- released in response to tuberculin compared with mitogen
1. (mitogen -- nil) and (tuberculin -- nil) are both >1.5 IU
2. percentage avian difference < 10
3. percentage tuberculin response > 15 (increased risk for LTBI) or > 30 (low risk for LTBI).
-Sputum Analysis: levels over 1.0 mU per mL
Tuberculosis Clinical Features
-Primary TB is asymptomatic
-The onset of secondary or active TB is very gradual with systemic signs usually appearing first
Tuberculosis Signs & Symptoms
-Anorexia, malaise, fatigue, and weight loss
-Afternoon low-grade fever and night sweats
-Prolonged cough becomes more severe and productive
-Sputum: purulent often with blood
1. Collapsed lung/damage to the lungs
2. Organ failure including liver damage
3. Joint damage that can lead to arthritis
4. Problems with the eyes
5. Develop drug-resistant TB
7. Improper kidney functioning/kidney failure
8. Lymph node infection
9. Bone complications
10. Cardiac tamponade (inflammationg and fluid prevent the heart from pumping effectively)
Cystic Fibrosis Etiology
-CF is a genetic disease
-Caused by a mutated CFTR gene on the 7th chromosome, transmitted as autosomal recessive disorder
-Large proportion of population is carriers with no symptoms
Cystic Fibrosis Course
-Early diagnosis and aggressive management has increased the lifespan of children with CF (mean survival age in 2006 was 37 years). However...
-Chronic cough and frequent respiratory infections increase over time
-As lung damage proceeds, hypoxia, fatigue and exercise intolerance develop
-Respiratory failure is often the cause of death
Cystic Fibrosis Pathophysiology
-Several mutations to the CFTR gene have been identified that relate to a protein involved in chloride ion transport in the cell membrane.
-This gene mutation causes a defect in the exocrine glands, which causes abnormally thick secretions.
-Lungs: mucus obstructs airflow in the bronchioles, causing air trapping with permanent damage to the bronchial walls. Stagnant mucus creates an ideal environment for bacterial growth. Infections are common and dangerous.
-Pancreas: ducts of the exocrine glands become blocked, a deficit of pancreatic digestive enzymes in the intestine results and causes malabsorption and malnutrition
-Other obstructions occur in the small intestine and in the bile ducts of the liver. This contributes to the malabsorption and malnutrition also.
-The salivary glands, sweat glands, and reproductive system (mucus obstructs vas deferens or cervix) may also be affected
Cystic Fibrosis Diagnostic Tests & Lab Values
-Genetic testing can identify the CFTR mutation
-Sweat analysis when the child is at least 2-3 weeks old can find elevated electrolyte levels
-Stool analysis for fat content and trypsin (a pancreatic enzyme)
-Lung involvement can be assessed with x-rays, pulmonary function tests and blood gas analysis
Cystic Fibrosis Clinical Features
-Steatorrhea, abdominal distension, and inability to gain weight
-Chronic cough and frequent respiratory infections
-Progression of lung damage leads to hypoxia, fatigue, and exercise intolerance
-Inability to meet common growth landmarks
Cystic Fibrosis Co-morbidities
3. Infertility in men
4. Lack of nutritional absorption
6. Cirrhosis (due to the bile duct being blocked)
7. Rectal prolapse
9. Collapsed lung
10. Chronic infections
11. Nasal polyps
12. Respiratory failure
13. Electrolyte imbalances
-Exact cause for asthma unknown
-Family history of hay fever, asthma, and eczema common
-Children living sedentary lifestyles (so staying indoors) which leads to exposure to allergens due to poor ventilation
-Increased air pollution
-Depends on the frequency and severity of attacks. Usually asthma attacks cause reversible bronchial obstruction, and most children with asthma grow out of it as their immune systems mature
-Chronic asthma may develop from irreversible damage in the lungs when attacks are frequent and severe.
-Status asthmaticus (persistent severe attack) may be fatal due to severe hypoxia and respiratory acidosis leading to cardiac arrhythmias or CNS depression
typically childhood onset and involves acute episodes triggered by type I hypersensitivity reactions to an inhaled antigen.
-adult onset and acute attacks triggered by stimuli such as respiratory infections, exposure to cold, exercise, aspirin, stress, and inhalation of irritants.
-In both types, the bronchi and bronchioles respond to the stimuli with inflammation of the mucosa with edema, bronchoconstriction, and increased secretion of thick mucus in the air passages.
-Second stage of attack: (occurs a few hours after the attack) additional chemical mediators are released causing prolonged inflammation, bronchoconstriction, and epithelial damage. This leads to obstruction of the airways and marked hypoxia.
Asthma Diagnostic Tests & Lab Values
-Spirometry measures the narrowing of bronchial tubes. FEV1 and FVC values will be reduced during an asthma attack, but tend to be fairly normal between attacks
-Peak flow meter measures how hard a person can exhale. Lower than usual peak flow readings signal that the lungs may not be working well
-Nitric oxide test measures the amount of nitric oxide in the breath. If airways are inflamed, nitric oxide levels may be elevated
Asthma Clinical Features
-Cough and marked dyspnea (Patient may be unable to talk)
-Rapid and labored breathing
-Thick and sticky mucous may be coughed up
***Respiratory failure is characterized by decreased responsiveness and cyanosis
1. Gastroesophageal reflux disease (GERD)
3. Nasal polyposis
4. Allergic rhinitis
5. Vocal cord dysfunction (rare)
6. Allergic bronchopulmonary aspergillosis (ABPA) (rare)
10. Obstructive Sleep Apnea (OSA)
-Long-term exposure to lung irritants
-Most common is cigarette smoking
-Also secondhand smoke, air pollution, chemicals
-Rarely genetic component - Alpha-1 antitrypsin deficiency
-Leads to lung damage, smoking enhances disease
COPD causes irreversible and progressive damage to the lungs. Eventually respiratory failure may result due to hypoxia, or right-sided congestive heart failure (cor pulmonale) may result due to lung disease.
alveolar walls and septae are destroyed leading to permanently inflated alveolar air spaces. The alveoli can be destroyed by a genetic deficiency of alpha1 antitrypsin (which inhibits the activity of destructive enzymes during an inflammatory response), cigarette smoking, and certain bacterial infections.
COPD Pathophysiology-Chronic Bronchitis
fibrosis and thickening of the bronchial wall occurs from constant irritation from smoking or exposure to industrial pollution. Oxygen levels are low and during coughing episodes cyanosis may occur.
an irreversible abnormal dilation of the bronchi caused by recurrent inflammation and infection in the airways. In dilated areas, large amounts of fluid constantly collect and become infected.
COPD Diagnostic Tests & Lab Values
-Pulmonary function tests: Criterion for airflow obstruction is the ratio of forced expiratory volume in 1 second (FEV1)to forced vital capacity (FVC) < 70%.
-Oximetry SaO2 value of < 90% in a COPD exacerbation suggests a need for hospital management. Saturated Oxygen level = SaO2
-Arterial blood gases
pH: less than 7.4
Condition: Respiratory Acidosis
Caused by: lung diseases such as pneumonia and COPD
-Alpha1-antitrypsin level: Sometimes decreased in patients with emphysema
COPD Clinical Features-Emphysema
-Onset is gradual
-Dyspnea first noted on exertion, then is present during rest
-Hyperventilation leading to development of "barrel chest"
-Anorexia and fatigue lead to weight loss
-Clubbed fingers and secondary polycythemia
COPD Clinical Features-Bronchiectasis
-Chronic cough and production of high levels of purulent sputum
-Rales and Rhonchi
-Weight loss, anemia, and fatigue
COPD Clinical Features-Chronic Bronchitis
-Constant productive cough
-Tachypnea and shortness of breath
-Secretions may be thick and purulent.
-Cough typically more severe in morning
-Hypoxia leading to cyanosis and hypercapnia
-Secondary polycythemia, weight loss, and systemic edema
1. Cardiovascular disease
2. Myocardial infarction
4. Lung cancer
6. Metabolic syndrome
7. Skeletal muscle loss
8. Skeletal muscle weakness
9. Weight loss
A majority of these co-morbidities exist because of the systemic inflammation that COPD causes. Cigarette smoking plays a role; however, it is not the only reason why these co-morbidities exist.
-Monitor energy exertion and ineffective breathing patterns during ADLs
-Teach proper way to breathe while moving (exhale during more strenuous part of activity)
-Practice pursed-lips breathing to open breathing tubes
-Exercises promoting relaxation and postural alteration in muscles that are involved in breathing
-Percussion and vibration techniques
-Help establish daily routines
-Monitor and evaluate the patient's psychological health and status
-Educate on ways of relieving stress, pain and fatigue
-Energy conservation techniques
-Work simplification strategies
-Strategies to decrease or prevent patient's pain
Physical therapy for CF patients includes postural drainage, percussion, and coughing techniques to ensure removal of the tenacious mucus
-Teach energy conservation techniques
-Provide assistive devices
-Teach work simplification strategies and modify activities
-Stress reduction techniques and strategies
-Side note: it is good to know which medications your patients may be taking, so you can be aware of the side effects.
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