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Adv patho exam 5 study guide 20
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Adv patho exam 5 study guideChronic bronchitis - hypersecretion of mucus and chronic productive cough that lasts for at least 3
months of the year and for at least 2 consecutive years
Emphysema - Abnormal permanent enlargement of the gas-exchange airways accompanied by
destruction of alveolar walls without obvious fibrosis
Risk factors for COPD - - Tobacco smoke
- Occupational dusts and chemicals
- Air pollution both indoor and outdoor
- Any factor affecting lung growth during gestation and childhood
-genetic and epigenetic susceptibilities
-an inherited mutation in the a1-antitrypin gene can cause COPD at an early age - without smoking
Patho of COPD - Large central airways, smaller peripheral airways and lung parenchyma are affected by
Chronic irritant exposure recruits neutrophils, macrophages, and lymphocytes to the lung - progressive
damage from inflammation and oxidative stress and Ap optic and autophagic cell death
Airway damage causes - Narrowing
Alveolar damage causes - Widening
Chronic bronchitis - infection or inflammation of the large airways or bronchi, self-limiting
Caused by viruses
,Cough, fever, pain behind sternum that is aggravated by coughing
Treatment - antitussive agents
Emphysema - Abnormal permanent enlargement of the gas-exchange airways accompanied by
destruction of alveolar walls without obvious fibrosis
Loss of lung elasticity - abnormal enlargement of the airspace's distal to the terminal bronchioles
Destruction of the alveolar walls and capillary beds
Enlargement of the airspaces leads to hyperinflation of the lungs
Two recognized causes of emphysema - Smoking, which in cities lung injury
An inheritied deficiency of AAT, an anti protease enzyme that protects the lung from injury
Most people with clinically diagnosed emphysema before the age of 40 have an a2-antitrypsin disorder
patho of emphysema - Emphysema results from the breakdown of elastin and other alveolar wall
components by enzymes, called proteases which digest proteins
Antiprotease enzymes, including AAT, protect the lung
Cigarette smoke and other irritants stimulate the movement of inflammatory cells into the lungs,
resulting in increased release of elastase and other proteases - in smokers in whom COPD develops,
antiprotease production and release may be inadequate to neutralize the excess protease production
, Dyspnea - subjective sensation of uncomfortable breathing
Severe - flaring, accessory muscles, retraction
Dyspnea on exertion - SOB with activity
Orthopnea - when lying down
Paroxysmal nocturnal dyspnea - awakening at night and gasping for air, must sit up or stand up
Treatment and management of pneumo - Chest tube with water seal drainage
Needle aspiration
Carnia - Ridge where the trachea divides into the right and left bronchi
Function - coughing and airway narrowing
Aging and the pulm system - Loss of elastic recoil
Stiffening of the chest wall
Alterations in gas exchange
Increase in flow resistance
Alveoli tend to lose alveoli wall tissue and capillaries
Dec in PaO2 and diminished ventilator reserve, causing a dec in exercise tolerance
Dec in resp muscle strength and endurance
Pulmonary edema - Excess water in the lungs from disturbances of capillary hydrostatic pressure,
capillary oncotic pressure, or capillary permeability
Most common cause - left heart dx
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