Alterations of pulmonary System 2.

Define and describe the common cause and signs dyspnea Dyspnea is a sign of pulmonary disorder. It is a subjective experience of breathing discomfort The experience comes from physiological, psychological, social and environment factors and, may induce secondary physiological and behavioural response. Described as breathlessness, air hunger, SOB and laboured breathing Caused by: Pulmonary disease, pain, heart disease, trauma and anxiety The severity of the experience of dyspnea may not correlate to the severity of underlying disease. 3. Define and compare orthopnea and paroxysmal nocturnal dyspnea (PND). Orthopnea is dyspnea when a person lies flat. -lying flat redistributes the body` s water which causes the abdominal contents to exert pressure on the diaphragm and decrease the efficiency of the respiratory muscles. PND is the same thing but happens when a person is sleeping which causes the pressure on the diaphragm. -both can be somewhat improved by having the person sit or stand up or by supporting the upper body with pillows. 4. Describe abnormal breathing patterns. Normal breathing- is rhythmic and effortless -resting ventilator rate is 8-16 times a minute -tidal volume is 400-800ml -short expiratory pause occurs with each breath Abnormal breathing-the rate depth, regularity and effort of breathing changes in response to physiological and pathophysiologic condition -patterns of breathing adjust to minimize the work of respiratory muscles (i)strenuous exercise-metabolic acidosis induces Kussmaul respiration slight increase in ventilator rate, very large tidal volume

-no expiratory pause -laboured breathing-when there is an increased work in breathing especially if airways is obstructed -large obstruction of airway-get slow ventilator rate, large tidal volume, increase effort, prolonged inspiration and expiration -small obstruction-(asthma)- rapid ventilator rate, small tidal volume, increase effort, prolonged expiration, wheezing Causes-pulmonary fibrosis stiffens the chest wall and lungs, shock, cerebral hypoxia, anxiety Cheyne-Stokes Respirations alternating periods of deep and shallow breathing -apnea for 15-60seconds then followed by ventilations that increase in volume until a peak is reached then volume decreases apnea is present Causes-decrease blood flow to brain-this slows impulses sending information to respiratory center in brain 5. Compare and contrast the manifestations and causes of hypoventilation and hyperventilation. Hypoventilation-is the inadequate alveoli ventilation to meet demands -occurs when minute volume is reduced -caused by alterations in pulmonary mechanics or in the neurologic control of breathing -the CO2 removal is slower than CO2 production therefore there is an increase in CO2 in blood Paco-increase causes hypercapnia which causes respiratory acidosis Hyperventilation-alveoli ventilation exceeding metabolic demands -lungs take CO2 out faster than CO2 produced -decrease Paco -respiratory alkalosis -increase respiratory rate and volume-occurs with anxiety or head injury Paco- how much CO2 in arterial blood 6. Define the followings term used to describe the signs and symptoms of pulmonary disease: hypercapnia, hypocapnia, coughing, hemoptysis, cyanosis, pain, clubbing and sputum. Hypercapnia-where arterial blood CO2 level is increased above normal levels

-Paco increases because CO2 removal is slower than CO2 production level level is greater than 44mm Hg results in respiratory acidosis Hypocapnia lungs remove CO2 faster than CO2 is produced by cellular metabolism- results in decrease in Paco2 (less than 36 mm Hg) or respiratory alkalosis Hypocapnia is caused by hypoventilation of alveoliHypoventilation is caused by depression of respiratory center by drugs or disease of medulla Coughing a protective reflex that helps clear airways by an explosive expiration -presence of inhaled particles, mucus, inflammation or a foreign body initiates cough reflex by stimulating the irritant receptors in the airway -cough reflex consists of inspiration, closure of glottis and vocal cords which causes a sudden forceful expiration that removes offending matter Hemoptysis- expectoration of blood or bloody secretions -blood with coughing usually bright red, has alkaline pH, frothy sputum -usually indicates infection that damages bronchi or lung condition (pneumonia) Cyanosis-bluish discolouration of the skin and mucous membrane caused by increase amount of desaturated or reduced hemoglobin in blood -happens when 5g of hemoglobin is desaturated Peripheral cyanosisSlow blood circulation in the fingers and toes caused by poor circulation and cold temperatures. It is not a good indicator of respiratory distress. Pain Pain caused by pulmonary disorder originates in pleura, airway or wall. Infection or inflammation of parietal pleura causes sharp stabbing pain when pleura stretches. Pleural pain common with pulmonary infarction (tissue death). Pulmonary pain can be central chest pain that is worse after coughing in people with infection inflammation of trachea. Clubbing Enlargement at the end of the digits. Based on extension of nail bed hypertrophy and amount of change in nail. Painless, associated with chronic hypoxemia (Cystic fibrosis, lung abscess, CHD).

Sputum Change in amount, colour and consistency provides info about progression of diseases and effectiveness of therapy. Analysis of microscopic appearance of sputum helps identify cellular debris or microorganism, helps aid diagnosis and therapy. Compare and Contract acute cough and chronic cough acute cough a cough that resolves itself within 2 to 3 weeks of onset of illness or resolved within treatment of the illness. Usually caused by upper respiratory tract infection, pneumonia, allergies and bronchitis Chronic cough-persists for more than three weeks, 7 to 8 weeks may be more appropriate time frame because acute cough can be prolonged in some cases of viral infections. Caused by postnasal drainage problems, asthma, gastroesophageal reflux disease and some medications. Smoking is the most common cause of chronic cough for smokers. Differentiate among ischemia, hypoxia and hypoxemia. Hypoxemia- reduced oxygenation of arterial blood (reduced PA 02) caused by respiratory alterations. Hypoxia-reduced oxygenation of cells and tissues. Caused by alteration of other systems as well as respiratory alterations Hypoxemia can lead to tissue hypoxia. Hypoxia can be caused by other abnormalities unrelated to alteration of pulmonary function. Ischemia a local state in which the cells are temporarily deprived of blood supply. They remain alive but cannot function properly. Characterize the causes, signs, and symptoms of pulmonary edema pulmonary edema is excess water in the lungs. The most common cause is left-sided heart disease where left ventricle fails Vascular volume redistributes it to the lungs, causing an increase in pulmonary capillary by hydrostatic pressure. When the hydrostatic pressure is greater than oncotic fluid moves into the interstitial space. When the flow of fluid out of the capillaries exceeds the lymphatic system ability to remove it and you get pulmonary edema. Signs and symptoms dyspnea physical exam may reveal inspiratory crackles and dullness to percussion over the lung base. Severe edema- you see pink frothy sputum, lung compliance decreases which leads to decreased tidal volume. Characterize the signs and symptoms of the following lung conditions that are caused by pulmonary disease or injury: aspiration, atelectasis, bronchiectasis, bronchiolitis, bronchiolitis obliterans,

pneumothorax, pleural effusion, pleurisy, hemothorax, empyema, abscess, fibrosis, chest wall restriction, flail chest, toxic gas exposure, pneumoconiosis, silicosis, and allergic alveolitis. Aspiration passage of fluid and solid particles into the lungs. Clinical manifestations include sudden onset of choking, coughing, vomiting, dyspnea and wheezing. Can lead to read Karen infection and permanent dilation of bronchus Atelectasis- collapse of lung tissue, developed after surgery clinical manifestations - similar to pulmonary infection including dyspnea, cough, fever and leukocytosis. Bronchiectasis- persistent abnormal dilation of the bronchi cystic fibrosis common cause in children. Adult- conjunctivitis with other respiratory conditions Symptoms- chronic productive cough from childhood illness or infection. Associated with recurrent lower respiratory tract infection and expectoration of large amounts of foulsmelling sputum,clubbing of fingers and decreased lung capacity and expiratory flow rate. Bronchiolitis inflammatory obstruction of the small airway or bronchioles -mostly children.

Client presents with rapid ventilator rates, use of accessory muscles, fever, dry cough, hyper inflated chest and a decrease in ventilation. Bronchiolitis obliterans -a fibrotic process that occludes airway and causes permanent scarring of the lungs Signs and symptoms- same as Bronchiolitis Emphysema- presence of microorganisms and cellular debris in the pleura space- complication of surgery Signs and symptoms- cyanosis, fever, tachycardia, cough and pleura pain Breathing sounds are decreased directly over the emphysema Pneumothorax - presence of air or gas in the pleura space caused by a rupture in visceral pleura. Lung collapses toward that hilium. Signs and symptoms- sudden pleura pain, tackypnea and dyspnea. Absent or decreased breath sounds and hyperresnance to percussion on the affected side. Pleural Effusion-presence of fluid in the pleural space Signs-dyspnea, compression atelectasis with impaired ventilation and pleural pain -physical examination shows decrease in breath sounds and dullness to percussion on affected side -a pleural friction rub can be heard over areas of inflamed pleura h) Hemothorax-is a pleural effusion where the fluid is blood in pleural space Signs- same as g

i)Abscess-is a circumscribed area of suppuration and destruction of lung parenchyma -have production of copious amounts of foul smelling sputum, occasionally hemoptysis -other clinical manifestations include fever, cough, chills and pleural pain j) Fibrosis-excess amount of fibrous or connective tissue in the lung -marked loss of lung capliance -difficult for lungs to ventilate Primary symptom is increase dyspnea or exertion -physical exam show diffuse inspiratory crackles K) Chest Wall Restriction-when chest wall is deformed, traumatized, immobilized- the work of breathing increases and ventilation may be compromised because of decrease in tidal volume Signs and Symptoms- decrease in tidal volume l) Flail chest- type of chest wall destruction several consecutive ribs. m) toxic gas exposure- Inhalation of gaseous irritation. Symptoms- burning of the eyes, nose, throat, coughing, chest tightness and dyspnea Hypoxemia is common. Pneumoconiosis- change in the lung caused by inhalation of inorganic dust particles Signs and symptoms- cough, chronic sputum production, decrease in lung volume, dyspnea and hypoxemia. Allergic alveolitis inhalation of organic dust lung inflammation or pneumonia occurred after prolonged exposure. Signs and symptoms-fever cough chill dyspnea. Describe how inhaling toxic or allergenic substances causes respiratory dysfunction. When toxic substances are inhaled the particles can cause damage to the airway, epithelium, mucus secretion, inflammation, ciliary damage, pulmonary edema. Some toxic substances can damage cells that are involved with oxygen exchange as a part of respiratory process. Allergenic substances like dust cause lung inflammation. When this happens lymphocyte and inflammatory cells enter the lung tissue which release variety of autoimmune and inflammatory cytokines. Describe the sequence of events in the pathophysiology of acute respiratory distress syndrome (ARDS) See Figure 26-7 page 688

Describe the pathophysiology of the obstructive pulmonary disease: asthma

Cell and cellular elements lead to inflammation of the bronchial mucosa and hyperresponsivness of the airway including mast cells, eosinphils, basophils, macrophages, neutrophils and lymphocytes. Inflammatory mediators released by cells increase capillary permeability and stimulate smooth muscle contraction and increase mucous production. Early Asthmatic response Antigen is exposed to mucosa, activates B cells to produce antigen-specific IgE. Cross- linking of IgE molecules with the antigen on the surface of mast cell cause mast cell degradation with the release of inflammatory mediators . Mediatory cause vasodilation, increased capillary permeability, mucosal edema, bronchial smooth muscle contraction- mucus secretion from mucosal goblet cells with narrowing of the airway and obstruction to airflow. Other inflammatory cytokines alter muscarinic receptor function and increase levels of acetylcholine which causes smooth muscle contraction mucus secretion. Discuss the role of inflammation in asthma. See question above

Describe the pathophysiology of chronic obstructive pulmonary disease (COPD): emphysema and chronic bronchitis chronic bronchitis- hyper secretion of mucus and productive cough for three months of the year. Inhaled irritant causes airway inflammation in the broad shield wall. Continual inflammation \causes bronchial edema and increases the size and number of mucus gland and goblet cells in the airway epithelium. The thick mucus can be cleared because of impaired ciliary function. The defense mechanisms are therefore compromised, increasing risk for pulmonary infection and injury. This process affects the large bronchi but eventually all airways are involved. The thick mucus and hypertrophied bronchial smooth muscle constricts the airway and leads to obstruction. Emphysema enlargement of gas exchange airway accompanied by destruction of Alveolar wall without obvious fibrosis. Obstruction results from change in lung tissue. Begins with destruction of alveolar septa which eliminate part of the capillary bed and increases the volume of air in the acinus. There is alveolar destruction and loss of normal elastic recoil of the bronchi. Alveolar destruction produces large air spaces within lung parenchyma and air spaces adjacent to pleurae (blebs). Blebs are effective in gas exchange and result in significant ventilation perfusion

mismatching and hypoemia. Expiration is difficult because loss of elasticity recoil reduces the volume of air that can be expired and air trapped in the lungs. Describe the pathophysiology of respiratory tract infections: bacterial pneumonia, viral pneumonia, tuberculosis and acute bronchitis. Pneumonia- infection of the lower respiratory tract caused by bacteria, virus, parasite Bacterial pneumoniaMostly caused by aspiration of oropharyngeal secretion. These bacteria have capsules that make phagocytosis by alveolar macrophages more difficult and have an ability to release variety of toxins which damage airway. Viral pneumoniaUsually mild and lead to bacterial infection by damaging ciliated epithelial cells which prevent pathogens from reaching lower airway. Viruses destroy ciliated epithelial cell. These destroyed cells prevent mucus clearance. Tuberculosis- highly contagious. Infection caused by an acid-fast bacillus that affects the lungs Transmitted by airborne droplets, when bacteria are inhaled into the lungs they multiply and cause localized nonspecific lung inflammation. This causes activation of alveolar macrophages. The phagocytes engulf the bacteria and begin the body's defense mechanisms which isolate the bacteria. The macrophages contain the bacteria, forming granulomatous lesions called a tubercle. Tissue in the tubercle die forming material called ceseation necrosis. Collagenous scar tissue grows around the tubercle isolating the bacteria. This stops the bacteria from multiplying. The bacteria may remain dormant for life. Acute bronchiolitisAcute section or inflammation of the airway or bronchi. Caused mostly by virus. There was no explanation of patho. Describe the pathophysiology of pulmonary vascular disease: pulmonary embolism and pulmonary hypertension. Pulmonary embolism- occlusion of a portion of the pulmonary vascular bed by embolus The effect of the embolus depends on the size of the affected vessel, the nature of the embolus, and obstruction of blood. Embolus with infarction an embolus that causes infarction of a part of lung tissue

Embolus without infarction- an embolus that does not cause permanent lung injury Massive occlusion- an embolus that occludes a major portion of pulmonary circulation Multiple pulmonary emboli- multiple emboli may be chronic or recurrent. Obstruction of the pulmonary vasculature leads to increase pulmonary artery pressure Pulmonary hypertension- pulmonary artery pressure 25 mm Hg. Endothelial dysfunction with overproduction of Vasoconstrictor. Vascular growth factors are released that cause changes in the vascular smooth wall called remodeling. Angiotensin two, serotonin, electrolyte transporter mechanism, and nitric oxide play a role in this disorder. Together these resolve in fibrosis in the thickening of vessel walls with luminal narrowing and abnormal vasoconstriction. These changes cause resistance to pulmonary artery blood flow thus increasing the pressure in the pulmonary artery. As resistance and pressure increases the workload of the right ventricle increases and subsequent right ventricle hypertrophy. See figure 26 15 Describe the different types of lung cancer. Lung cancer arises from the epithelium of the respiratory tract. Primary lung cancer arises from cells that line the bronchi within the lungs called bronchogenic carcinoma- caused by mutilated epithelial stem cells. Two main categories of lung cancer 1) Non-small cell lung cancer 2) Neuroendocrine tumors of the lungs Non-small cell lung cancer has three types 1)Squamous cell carcinoma- tumors are located near the hila and project into bronchi . 2)Adenocarcinoma- tumor arising from the gland. 3)Large cell carcinomas- these cells are large and contain darkly stained nuclei. These arise centrally and can grow to distort the trachea and cause widening of the carina. Neroendocrine tumors of the lungs Small cell carcinomas central in origin range from 6 to 8 um. Tumor show a rapid rate of growth and tend to metastasize early and widely, these cells have a worse prognosis. They idolize from neuroendocrine cells that contain neurosecretory granules thus small cell carcinoma is often associated with ectopic hormone production.