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
