COPD Flashcards
Primary treatments for asthma
prevention: identify and avoid or remove triggers
secondary treatment for asthma
medications: preventative intent
antileukotrienes - LT’s stimulate inflammatory response
mast cell stabilizers to decrease histamines
anti-inflammatories (e.g. flovent)
low dose prednisone
bronchodilators: long-acting (atrovent = ipratroprium bromide)
tertiary treatment for asthma
rescue/relief medications: epinephrine, short-acting bronchodilators
anti-inflammatories (corticosteroids) IV, PO, or nebs
anticholinergics (short-acting) to produce smooth muscle relaxation and decrease mucus production
List and briefly explain the complications of COPD
Respiratory failure: decreased hypoxic drive (with O2 therapy) –> hypoventilation –> hypoxemia –> increased WOB –> exhaustion
also increased CO2 –> acidosis –> respiratory depression –> hypoventilation etc. as above
Pneumothorax: especially with emphysema because alveoli rupture –> blebs formed –> rupture –> air into pleural cavity
Polycythemia –> risk for thrombosis
Pneumonia: secondary infection
Cor pulmonale
peptic ulcer and gastroesophageal reflux - usually side effects of corticosteroid meds
Differentiate between emphysema and chronic bronchitis re: physical appearance, lab/dx findings, and respiratory assessment
Physical appearance:
CB has cyanosis, no barrel chest, overweight
E is “pink,” barrel chested, thin
Lab/Dx findings:
CB has congestion and cardiomegaly on x-ray, high RBC, Hct, and Hgb, high PaCO2, and low PaO2
E has hyperinflation on x-ray with increased intercostal margins with normal RBC, Hct and Hgb until late stages
Respiratory assessment:
CB has dyspnea, wheezing, sputum, and cough with adventitous lung sounds
E has little to no cough, little wheezing or sputum or dyspnea but decreased breath sounds
Briefly explain the pathophysiology of asthma
trigger/reactive airway –> histamine and inflammation cause smooth muscle contraction and increased WBC, increased capillary permeability, mucus secretion and edema –> bronchoconstriction and increased WOB –> insensible fluid loss and decreased intake –> mucus plugs and atelectasis –> hypoxemia –> tachycardia, tachypnea and restlessness –> increased O2 needs –> increased WOB (etc.)
Describe the pathogenesis of chronic bronchitis
Usually due to smoking: chronic bronchial irritation and inflammation –> bronchial edema and spasm, cough and mucus –> air obstruction, dyspnea, infection –> hypoxemia, hypercapnea
Describe the pathogenesis of emphysema
smoking –> alpha anti-trypsin deficiency or increase in proteolytic activity in lungs –> decreased elasticity of lungs –> alveolar septal destruction –> air trapping distal to air obstruction –> hypoxemia, hypercapnea
Explain the pathogenesis of cor pulmonale as a complication of COPD
hypoxemia leads to vasoconstriction (attempt to shunt blood to areas with more O2) –> increased resistance leads to hypertension of pulmonary vessels –> increased pressure in right ventricle and atrium of heart –> right CHF
Normal respiratory drive: which substance and where are the chemoreceptors?
Central chemoreceptors in medulla - respond to changes in CO2
Where are the peripheral chemoreceptors and what do they respond to?
Aortic arch and carotid sinuses - respond to changes in O2
Normally, inspiration is active/passive (?) and expiration is active/passive (?)
Inspiration is active (contraction of diaphragm) and expiration is passive (elastic recoil)
Explain the relationship between hypoxia and erythropoiesis
hypoxia –> stimulates kidneys to secrete erythropoietin, a hormone which stimulates RBC production by bone marrow –> increases RBC production
Briefly describe the anatomy of the bronchi re: degree of cartilage present
Incomplete rings of cartilage in the primary bronchi –> plates of cartilage in secondary bronchi –> no cartilage in tertiary and terminal bronchioles
Effect of SNS/PSNS and histamine vs. epinephrine on airways
SNS and epinephrine –> bronchodilation
PSNS and histamine –> bronchoconstriction
Briefly describe Cystic Fibrosis
genetic disorder in which there is abnormal production of thick, viscid mucus that interferes with respiratory and GI function
Briefly describe bronchiectasis
abnormal dilation of bronchi - secondary to another pulmonary disorder, e.g. infection in clients with chronic bronchitis
In COPD, patients have more difficulty with _______ than ________. (inhalation/exhalation)
more difficulty with exhalation due to air trapping
Common triggers of acute asthma attack
cold, stress, exercise, viruses, emotions
Emphysema caused by alpha antitrypsin deficiency or old age tends to be _______.
Panacinar (diffuse)
Emphysema in which septal deterioration results from smoking tends to be ________.
Centriacinar
