Case in Review 2 Flashcards
Main causes of COPD
- Smoking
- toxic chemicals
- Alpha-1 antitrypsin deficiency
Pathophysiology of COPD
- Persistent narrowing of small airways when pt has emphysema, chronic obstructive bronchitis
- Leads to a decrease in the rate of exhaled air (OBSTRUCTIVE)
- Most common cause is cig smoking
- Irreversible
COPD age affected
Adult 40-50, takes years to develop
How do you evaluate airflow?
Spirometry
- the ratio of forced expired volume in 1 second (FEV1) to the forced vital capacity (FVC) is <0.70 after administration of a bronchodilator, airway obstruction is indicated
COPD symptoms
mild cough with clear sputum -> SOB during exertion -> weight loss -> barrel chest
Pathophysiology of Asthma
-Airways narrow in response to certain stimuli
- Reversible
- Chronic inflammatory disease of airways
Bronchi receptors sense the presence of a substance and stimulate bronchi muscles to contract or relax (altering airflow)
- Difficulty exhaling (OBSTRUCTIVE)
Early phase reaction of asthma
(Minutes)
Antigen exposure causes it to cross-link IgE mast cells causing the release of preformed mediation.
Results in bronchoconstriction, excess mucus, and edema.
Inflammatory cell recruitment
Late phase reaction of asthma
(hours)
Recruited immune cells cause long-term inflammation.
Airway remodeling.
Main causes of asthma
- Allergens/irritants (tobacco smoke)
- Exercise
- Infections: bronchitis, pneumonia, colds
- Aspirin
Main causes of pneumonia
- Bacteria, viruses
Symptoms of asthma
Sudden onset when exposed to trigger
- wheezing
- SOB
- Cough
Symptoms of pneumonia and age
Develop over several days
Adults 65+ and young kids
-Productive cough (sputum)
- Angina
- Chills
- Fever
- SOB
Pathophysiology of pneumonia
- Pathogen colonizes nasopharynx and reaches alveoli via microaspiration
-Infection of alveoli and surrounding tissues - Fluid/pus in alveoli
Changes in lung/airways with restrictive lung disease
- Lungs become stiff, and more effort is needed to expand when inhaling
- Decrease in the volume of air that lungs can hold,
- Lose elasticity
- Harder to INHALE
- Does NOT cause wheezing
Ex: sarcoidosis (granulomas in lungs)
Changes in lung/airways with obstructive lung disease
- Airway is narrowed, with high resistance of airflow
- Airways widen during inhalation and air can be pulled in, airways narrow during exhalation and air cant be exhaled from lungs quickly (wheezing)
- Dyspnea occurs when too much air is left in the lungs after inhaling
- Hard to EXHALE
Ex: asthma, COPD
How can pulmonary hypertension from COPD cause pitting edema, elevated jugular venous pressure, and hyperinflated lungs?
How can cor pulmonae from COPD cause pitting edema, elevated jugular venous pressure, and hyperinflated lungs?
What are some of the environmental factors that can cause COPD?
- Smoking
- Pollution
- Dust/ fume exposure in the workplace
How do we know that there are genetic factors that predispose an individual to COPD?
-B/c a non-smoker can develop COPD
- There are clusters in families
What genetic factors have been linked to COPD?
-Alpha-antitrypsin deficiency (AATD)
There are other parts of the genome that have been associated with COPD
Epidemiology of COPD; why is it important for a HCP to learn about COPD?
- Common worldwide
- Prevalence is correlated with increasing age, lower socioeconomic status, and smiling
- Prevalent in M and F
- Annual death rates are steadily rising in US
- Economic burden
- 4th leading COD worldwide
What type of disease is COPD?
Complex disorder; environmental and genetic factors involved
What is emphysema?
- Permanent enlargement of air spaces distal to the terminal bronchioles
- Destruction of lung tissues, limiting gas exchange
What is the connection b/t inflammation and emphysema?
Cause emphysema and proteolytic destruction of the lung connective tissue:
- imbalance b/t protease and anti-protease systems in the lungs
- Macrophages MMP
- Neutrophil elastase and destruction of elastin
- cig smoking -> induced infl. -> trigger cycle of protease release and lung destruction