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17 Cards in this Set

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  • Back
Blue bloater vs. Pink Puffer
chronic bronchitis leads to blue bloater because you get hypoxic and pO2 goes down early. emphysema leads to being a "pink puffer" because he maintains his pO2
three components:
1. recurrent episodes of reversible airway obstruction that resolves spontaneously or with treatment
2. Airway hyperresponsiveness (methacholine challenge)
3. Inflammation of airways
Pathology of asthma
-edema and hyperemia of bronchial mucosa
-infiltration of bronchial mucosa with TH2 lymphocytes, mast cells, eosinophils
-increased mucus
-constriction of airway smooth muscle
-airway thickening with variable degree of fibrosis with chronic asthma
-shedding of airway epithelium
Physiologic changes with asthma
1. FEV1 and peak flow are decreased
2. air trapping in acute attack
3. increased responsiveness to methacholine and histamine
4. pO2 is normal or high initially then falls when they get tired.
Pathophysiology of smooth muscle
1. exagerrated contraction of smooth muscle
2. increased smooth muscle mass
3. increased release of inflammatory mediators
Factors that precipitate asthma
Medications (aspirin or beta blockers)
Physical exam in asthma
increased respiratory rate, increased pulsus paradoxus, wheezing in expiration, rhonchi
What will you find in arterial blood gases of asthmatic?
Acutely- respiratory alkalosis because they hyperventilate and blow off their CO2
Later, the patients will tire and get a metabolic acidosis because of increased lactic acid from muslce. CO2 might go up once they get tired. The patient will then have low pH, low pO2, and high CO2 and will need to be intubated
What might you see hematologically in asthmatics?
What do you see in the sputum of asthmatics?
Charcot-Leyden crystals and creola bodies (clusters of airway epithelial cells)
Relievers: B-adrenergics (relax airway smooth muscles and decrease mucus secretion- side effects are tachycardia and tremor), anticholinergics
Controllers: inhaled corticosteriods (decrease mediator release and decreases shedding but may cause growth retardation, bone loss, cataracts, glaucoma, oral candidiasis)
anti-leukotrienes- Montelukast and Zafirlukast are receptor antagonists and Zileuton is a lipoxygenase inhibitor. leukotrienes are involved in eosinophil recruitment and mucus secretion
-theophylline- inhibits phosphodiesterase and may be antiinflammatory. significant GI, cardiac, and CNS side effects
-Cromylyn and nedocromil
What can you use to treat nighttime asthma or chronic maintenace?
Salmeterol and formeterol because they are long acting B agonists. They are now used for chronic maintenance. They can cause sudden death
Pathophysiology of COPD
-inflammation with neutrophils and macrophages
-Destruction of alveoli due to proteases and you get collage deposition (fibrosis) in the alveoli. This fibrosis causes airway obstruction rather than restriction.
-With proteases from neutrophils you get alveolar wall destruction in emphysema and mucus hypersecretion in chronic bronchitis.
Centrilobular emphysema vs. Panlobular emphysema
Centrilobular is associated with smoking. Damage is in the respiratory bronchiole and it is worse in upper lobes.

Panlobular emphysema- associated with alpha 1 antitrypsin deficiency. Whole alveolar lobule is affected equally. Whole lobule involved.
PFT findings with chronic bronchitis
reduced FEV1 and mid flow rates but normal FVC and diffusion. ABG shows hypoxemia and hypercarbia in later stages
PFT findings with emphesyma
-reduced FEV1 and mid flow rates
-FVC decreased, RV increased, TLC increased due to hyperinflation, diffusion decreased, ABG shows normal pO2 till late stages
Important factors for survival with COPD
1. Smoking cessation
2. Bronchodilators
3. Oxygen therapy