Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
33 Cards in this Set
- Front
- Back
|
Define dyspnea and orthopnea.
|
Dyspnea is the shortness of breath/ the feeing of struggling to get enough air. Orthopnea is dyspnea when lying down.
|
|
|
Describe the characteristics of Kussmaul respirations
|
Induced by strenuous exercise or metabolic acidosis. Characterized by a slightly increased ventilatory rate, very large tidal volumes, and no expiratory pause.
|
|
|
3. Relate respiratory rate to the development of hypocapnia and hypercapnia.
|
Hypoventilation causes CO2 removal to not keep up with CO2 production, causing CO2 arterial blood level to increase causing hypercapnia (PaCO2 more than 44mmHg) and respiratory acidosis. Hyperventilation removes lung CO2 faster than production, decreasing PaCO2 less than 36mmHg(Hypocapnia) resulting in respiratory alkalosis
|
|
|
4. Describe the respiratory condition that leads to pathologic changes in the finger tips.
|
Clubbing is the selective bulbous enlargement of the end of a digit. Usually painless, clubbing is commonly associated w/ diseases causing chronic hypoxemia like lung cancer, bronchiectasis, cystic fibrosis, pulmonary fibrosis, lung abscess, and congenital heart disease. Can sometime be seen in lung cancer w/o hypoxemia.
|
|
|
7. Identify the most common cause of pulmonary edema.
|
Heart disease
|
|
|
8. Name the pathological condition involving infection the pleural cavity.
|
Pneumothorax or Empyema
|
|
|
9. Describe the features of a typical lung abscess.
|
A swollen area within body tissue, containing an accumulation of pus. It is a circumscribed area of suppuration and destruction of lung parenchyma. Abscess is most commonly caused by aspiration, Klebsiella, or Staphylococcus. Abscess is usually associated with alcohol abuse, seizure disorders, general anesthesia, and swallowing disorders. Clinical manifestations include fever, cough, chills, sputum production, and pleural pain. Treatment includes administration of appropriate antibiotics and chest physical therapy or bronchoscopy.
|
|
|
10. Describe acute respiratory distress syndrome.
|
Acute lung inflammation and diffuse alveolocapilary injury. Most common predisposing factors are sepsis and multiple traumas. All disorders causing ARDS cause massive pulmonary inflammation that injures the alveolcapillary membrane and produces severe pulmonary edema, shunting, and hypoxia. Initial lung injury also damages to alveolar.
|
|
|
11. Identify the causes of pulmonary edema in adult respiratory distress syndrome (ARDS).
|
Inflammatory mediators extensively damage the alveolocapillary membrane and greatly increase capillary membrane permeability allowing fluids, proteins, and blood cells to leak from capillary bed into the pulmonary interstitium and alveoli causing the edema.
|
|
|
12. Explain how do restrictive and obstructive lung diseases affect expiration.
|
Airway obstruction causes more force to expire a given volume of air. Major diseases are asthma, chronic bronchitis, and emphysema. Dyspnea occurs and decreased forced expiratory volume. Restrictive decreased compiance of lung tissue and increased work of breathing. It has increased respiratory rate and decreased tidalvolume. Affect alveolocapillary membrane and caused decreased diffusion of oxygen from alveoli into blood resulting in hypoxemia.
|
|
|
13. Identify the immunoglobulin that may contribute to the pathophysiology of asthma.
|
IgE
|
|
|
14. Identify the inflammatory mediators that are produced as a result of asthma.
|
Histamine, interleukins, prostaglandins, leukotrienes, and nitric oxide.
|
|
|
15. Predict the most successful treatment for asthma.
|
Management of asthma begins with avoidance of allergens and irritants and patient education with home peak-flowmeter. Oral corticosteroids and inhaled beta-agonists are treatments for acute attacks. Chronic management is regular use of anti-inflammatory medications such as inhaled corticosteroids, etc.
|
|
|
17. Describe how cigarette smoking contributes to the development of emphysema.
|
Inhaled oxidants in tobacco smoke inhibit the activity of endogenous antiproteases and stimulate inflammation with increased activity of the proteases. Balance is tipped toward alveolar destruction and loss of normal elastic recoil of the bronchi. It inflames airway epithelium and release cytokines that inhibit the normal endogenous antiproteases and eventually breakdown elastin.
|
|
|
18. Describe the pathophysiology of chronic bronchitis.
|
Inspired irritants result in airway inflammation with infiltration of neutrophils, macrophages, and lymphocytes into the bronchial wall. Continual brochial inflammation causes bronchial edema and increases the size and number of mucous glands and goblet cells in the airway epithelium. Thick tenacious mucus is produced and cannot be cleared because of impaired ciliary function, increasing susceptibility to pulmonary infection and injury. Dyspnea and productive cough occur and eventually airways collapse early in expiration trapping gas in distal portions of lung. Ventilation-perfusion mismatch occurs along with hypoxemia and hypoventilation and hypercapnia.
|
|
|
19. Identify the normal range of blood pressure in the pulmonary (not bronchial) arteries.
|
15-20
|
|
|
20. Define transudative effusion of the pleura.
|
Pleural effusion is presence of fluid in pleural space by migration of fluids and other blood components through walls of intact capillaries bordering the pleura. Pleural that enter the pleural space from intact blood vessel that trasudative are watery. Disorders associated are cardiovascular disease that causes high pulmonary capillary pressure, liver or kidnea disease and hypoproteinemia
|
|
|
21. Relate abnormal ventilation-perfusion ratio and the development of hypoxemia.
|
Abnormal ventilation-perfusion ratio is most common cause of hypoxemia. V/Q is 0.8-0.9 that is normal because perfusion is somewhat greater than ventilation. Mismatching can occur and poor perfusion results in factor for hypoxemia.
|
|
|
24. Describe major clinical manifestations of pneumonia.
|
Upper respiratory infection, which is often viral. Fever, chills, productive or dry cough, malaise, pleural pain, and sometime dyspnea and hemoptysis. Physical examination may show signs of pulmonary consolidation, such as dullness to percussion, inspiratory crackles, increased tactile fremitus, egophony, and whispered pectoriloquy. Sepsis
|
|
|
26. Relate pulmonary hypertension to alteration in the pulmonary capillaries.
|
Pulmonary arteriolar vasoconstriction occurs in PH and is caused by congestive heart failure. Firbosis and thickening of vessel wall also take place, causing resistance to pulmonary artery blood flow increasing pulmonary arterial pressure. Right ventricle increases its workload and develops hypertrophy followed by failure.
|
|
|
27. Describe the clinical manifestations of a patient with emphysema.
|
Productive cough, dyspnea, wheezing, history of smoking, barrel chest, prelong expiration, chronic hypoventilation, polycythemia, cor pulmonale
|
|
|
28. Define hypoxemia versus hypoxia.
|
Hypoxemia is abnormally low oxygen concentration in blood. Hypoxia is deficiency in amount of oxygen reaching tissues.
|
|
|
30. Describe the clinical presentations of squamous cell carcinoma of the lung.
|
Tumors located typically near the hilum and project into bronchi. Obstructive manifestations are nonspecific and include nonproductive cough or hemoptysis. Pneumonia and atelectasis are associated with squamous cell carcinoma. Chest pain is a late symptom with larger tumors. Remain fairly well localized and tend not to metastasize until late. Preferred treatment is surgical resection although when metastasis occurs survival rate decreases dramatically. Adjunctive radiation and chemotherapy improve outcomes.
|
|
|
31. Describe the most common paraneoplastic syndrome associated with small cell lung cancer.
|
Ectopic hormone production
|
|
|
32. Describe pneumoconiosis and its cause.
|
Any change in lung caused by inhalation of inorganic dust particle, usually in the workplace. Most common causes are dusts of silica, asbestos, and coal. Others include talc, fiberglass, clays, mica, slate, cement, cadmium, beryllium, tungsten, cobalt, aluminum, and iron. Deposition of any of these leads to chronic inflammation with scarring of the alveolar capillary membrane leading to pulmonary fibrosis. These dust deposits are permanent and lead to progressive pulmonary deterioration. Clinical manifestations include cough, chronic sputum, dyspnea, decreased lung volume and hypoxemia.
|
|
|
33. Describe a specific treatment for silicosis.
|
Usually palliative and focuses on preventing further exposure especially in the workplace.
|
|
|
34. Justify whether of not persons with alpha 1-antitrypsin deficiency are predisposed to emphysema.
|
Primary emphysema is commonly linked to an inherited deficiency of the enzyme -antitrypsin. Deficiency increases likelihood of emphysema because proteolysis in lung tissues is not inhibited.
|
|
|
35. Describe the most common route of transmission of tuberculosis from person to person.
|
Airborne droplets
|
|
|
36. Diagnose whether or not a pulmonary artery pressure of 20 mmHg is within normal range.
|
Within normal range
|
|
|
37. Predict whether or not chronic pulmonary hypertension can lead to cor pulmonale.
|
Primary or secondary pulmonary hypertension causes Cor pulmonale
|
|
|
Primary or secondary pulmonary hypertension causes Cor pulmonale
|
HIV
|
|
|
39. Define the normal arterial blood gas values for PaO2 and PaCo2.
|
PaCO2= 35-45mmHg
PaO2= 90-100mmHg |
|
|
40. Predict whether or not Mycobacterium tuberculosis can remain dormant and walled off as tubercles in the lungs for life, but may or may not be reactivated if the patient’s immune system is impaired.
|
Can be reactivated
|
