03 - Lung Flashcards
Atelectasis
Definition
Mechanisms
Loss of lung volume due to inadequate expansion of air spaces. Results in hypoxia due to shunting of inadequately oxygenated blood into systemic circulation.
a. Resorption Atelectasis – obstruction prevents air from reaching distal airways and lungs do not inflate distal to the obstruction Airway obstruction prevents lung inflation. AIRWAY obstruction!
b. Compression Atelectasis (AKA Passive or Relaxation Atelectasis) – accumulations of blood, fluid or air in pleural cavity cause collapse of adjacent lung tissue; commonly caused by the pleural effusions of congestive heart failure. Space-occupation of plural cavity prevents lung inflation (air, fluids, tumors) When there is something occupying CHEST CAVITY!
c. Microatelectasis (AKA Nonobstructive Atelectasis) – loss of lung expansion; most important cause is loss of surfactant. Lack of surfactant prevents lung inflation. Usually in infants who are born prematurely and don’t produce enough surfactant and lungs do not inflate.
d. Contraction Atelectasis (AKA Cicatrization Atelectasis) – localized or generalized fibrotic changes in the lung or pleura hampers expansion and increases elastic recoil during expiration Fibrosis (scarring) prevents lung expansion. Reduces stretchiness/expansion
Obstructive lung diseases
Definition
Hallmarks
List
Airway disease characterized by limitation of airflow, usually resulting from an increase in resistance due to partial or complete airway obstruction. Does not require an obstruction! Just reduction of airflow!
1. Hallmark of obstructive lung diseases is decreased expiratory flow rate.
- Expiratory obstruction may result from:
a. Anatomic airway narrowing (asthma)
1) An anatomic change producing physical obstruction
b. Loss of elastic recoil (emphysema)
1) Produces functional obstruction
Asthma (extrinsic, intrinsic)
Chronic obstructive pulmonary diseases (emphysema, chronic bronchitis)
Bronchiectasis
Asthma
Definition
S/S
Disease characterized by episodic, reversible bronchospasm resulting from an exaggerated bronchoconstrictor response to various stimuli. May reverse spontaneously or after treatment. Both acute and chronic. Chronic disease with episodic/acute attacks.
Clinical Signs and Symptoms (both types)
a. Episodic acute attacks – 1 to several hours (usually rapid onset)
b. Severe dyspnea with wheezing – difficult to inhale, more difficult to exhale (gasping)
c. Status asthmaticus = persistent attack (days to weeks) – can be lethal.
d. Best Q to ask to determine severity of asthma = how many trips to emergency room have you taken due to asthma? Never been? = manageable
Asthma
Histologic morphology
a. Bronchi and Bronchial Walls
1) Mucous plugs in bronchi – plugs contain Curshmann spirals (whorls of shed epithelium), eosinophils and Charcot-Leyden crystals (crystals formed from eosinophil proteins)
2) Inflammation with edema, hyperemia and inflammatory infiltrate composed of eosinophils (up to 50% of infiltrate), mast cells, basophils, macrophages, lymphocytes, plasma cells, and some neutrophils.
3) Mucous gland hyperplasia
4) Hypertrophy and hyperplasia of bronchial smooth muscle and increased collagen deposition below basement membrane.
5) Bronchoconstriction can be temporary and break, but it will cause hyperplasia of smooth muscle
b. Lungs – overinflated
Asthma
Complications
Tx/prognosis
a. In severe disease, progressive hyperinflation leads to emphysema.
b. Recurrent bacterial infections are common and may lead to chronic bronchitis or pneumonia. Increased risk of infections w/o tx
c. Mucus plugs and exudate contribute to development of bronchiectasis.
Treatment and Prognosis
a. Treatment is multidisciplinary, depending on triggers.
b. Commonly used therapies include inhaled bronchodilators, inhaled and systemic corticosteroids, and leukotriene blockers. (as well as oral medications more recently and are usually anti-inflammatory in nature)
c. May be disabling but is usually controllable.
Extrinsic asthma
Ds mech
Pathogenic mediators
1) Disease mechanism – IgE-mediated type I hypersensitivity reaction induced by exposure to an extrinsic antigen. Usually response to inhaled antigen
2) Pathogenic Mediators
a) Leukotriene C4, D4 and E4 – prolonged bronchoconstriction, increased vascular permeability and increased mucin production (mucous)
b) Prostaglandin D2- bronchoconstriction and vasodilation (general inflammation + brochoconstriction)
c) Eosinophil Chemotactic Factor, Neutrophil Chemotactic Factor and Leukotriene B4 – recruitment of eosinophils and neutrophils (histamine. Eosinophils!!! > type I reaction!!!
d) Tx treat episodic symptoms! Eosinophils and mucous are still present!
Extrinsic asthma
Clinical profile
3) Clinical Profile
a) Onset is most often in first 2 years of life (atopic type).
b) Patients often have other signs of allergic reactions. (hives, rhinitis)
c) Positive family history is common.
d) Often less severe than intrinsic type, can usually be well managed.
e) Child may outgrow disease
Intrinsic asthma
Ds mech
Clinical profile
1) Disease mechanism
a) Triggering mechanism is nonimmune. No recognition of antigen and host response
b) Triggering stimuli include aspirin, pulmonary infection (especially viral), cold, psychological stress, exercise, and inhaled irritants. Stimuli appear to trigger abnormal autonomic response. Even smoke, which may have irritant that can cause bronchoconstriction. Lots of things can trigger this.
c) Although the pathogenesis is not well understood, intrinsic asthma may be due to a fundamental defect in autonomic regulation. (abnormal autonomic response)
2) Clinical Profile
a) Onset is usually in adulthood, after age 35. (rarely seen in children)
b) Symptoms are more persistent and often more severe than extrinsic type. Clinical symptoms are not easily managed. Most do not outgrow and can be hard to manage.
c) More frequently leads to status asthmaticus. Persistent asthmatic attack that last more than 24hrs and can be life threatening!
d) Avoiding triggers/stimulus of attack is suggested.
Chronic Obstructive Pulmonary Diseases (COPD)
Definition
List
A term to describe persistent and irreversible (permanent) airflow obstruction
Emphysema
Chronic bronchitis
Emphysema
Definition
Epidemiology
Permanent enlargement of the air spaces distal to the terminal bronchioles accompanied by destruction of their walls. (walls do not grow back! Causes permanent reduction in surface area for gas exchange, limitation due to loss of elasticity, minor airways)
Epidemiology
1) Common disease. Incidence at autopsy is reported as high as 50%.
2) Disease is more common in men, especially the centriacinar type.
3) Strong association between heavy smoking and emphysema.
Emhysema
Gross morphology/manisfestations
e. Gross Morphology – the lungs are enlarged, pale, hypercrepitant and pillowy.
1) Morphological manifestations
a) Enlarged lungs
b) Pillowy lungs
c) Pale lungs
d) Hypercrepitant lungs (crackly noises when you press on lungs, when “fresh”)
e) “Blebs”
f) Grey spots = anthracosis!
Emphysema
S/S
1) Dyspnea is usually the first symptom.
2) Onset is insidious and the course progressive.
3) Cough and wheezing may also be initial complaints, especially if patient has underlying chronic bronchitis.
4) Without bronchitis, classic presentation is barrel chest (enlarged chest), dyspnea, hyperventilation and prolonged expiration. Often referred to as “pink puffers.”
a) Pure emphysema
5) With pronounced chronic bronchitis, presentation differs. There is often cough with purulent sputum. They have less dyspnea and less hyperventilation, resulting in hypoxia and cyanosis. Often referred to as “blue bloaters.”
a) Emphysema + chronic bronchitis
b) Poor gas exchange due to mucous in airways
c) Do not hyperventilate
d) Wheezing due to chronic bronchitis (mucous), productive cough
Emphysema
Tx
Prognosis
Treatment
1) Lifestyle changes
2) Management of infections by prevention (fluids!) and antibiotic therapy
3) Oxygen
4) Bullectomy and/or lung volume reduction surgery (surgically remove most damaged lung)
5) Asthma medications are used today as well
Prognosis – death from emphysema is related to
1) Pulmonary failure with respiratory acidosis, hypoxia and coma
2) Right-sided congestive heart failure
a) From chronic cor pulmonale
3) When you destroy walls of lungs, you increase resistance in lungs and can cause right respiratory failure or right heart failure
Chronic Bronchitis
Definition
A clinical disease characterized by persistent productive cough for at least 3 consecutive months in at least 2 consecutive years. (major airways, mucous blockage, chronic cough)
Chronic Bronchitis
Pathogenesis
1) Single most important causative factor is smoking.
2) Other causative factors include other air pollutants, such as sulfur dioxide and nitrogen dioxide.
3) Hypersecretion of mucus starts in the larger airways.
4) Airflow obstruction occurs due to
a) Inflammation, fibrosis and narrowing of bronchioles (small airway disease)
b) Coexistent emphysema
c) Mucous! Hyperplasia of mucous glands and hypersecretion/ongoing secretion of mucous. Increased mucous clogs airways and can trap bacteria leading to infection.
