Pulmonary Pathology Part I: Pulm Edema, Chronic Bronchitis, Emphysema, Asthma Flashcards
What is the term for the functional unit of the lung consisting of the respiratory bronchiole and associated alveolar ducts and alveoli?
Acinus
Blood-air interface
The “space” between the endothelium and the type-1 pneumocyte/epithelium
Examples of congenital lung pathology?
Agenesis/hypoplasia
Tracheo-Esophageal (TE) fistula
Pulmonary vascular anomalies
Neonatal Respiratory Distress Syndrome (N.R.D.S.)
Embryonic Development of Lung: T or F?
A. Surfactant begins to be produced at 20 weeks
B. Alveoli begin to develop at 36 weeks
C. Alveolar ducts begin to develop at 30 weeks
D. Lung buds are an outgrowth of the foregut
A. False. about 25 weeks
B. True
C. False. 24 weeks
D. True
Pulmonary hypoplasia in the neonate may be secondary to:
- Space-occupying lesions in the uterus
- Congenital diaphragmatic hernia
- Many others
The most common type of TE fistula?
What is the baby’s response to feeding?
Esophageal atresia with distal TE fistula
Food comes back up without going into the lungs
T or F? Neonatal Respiratory Distress Syndrome
A. Primary defect is lung had not yet developed alveoli
B. Etio: Oversedation of mom, head injury @ delivery, aspiration of blood/amnio fluid, Intra-uterine hypoxemia
C. Fibrous tissue forms from lack of surfactant
D. Tx = surfactant delivery or maternal Tx with steroids
A. False. lung will not open b/c no surfactant
B. True
C. False. Hyaline membranes form
D. True
Atelectasis: Reabsorption, Compression, or Contraction?
A. can be from a pleural effusion or pneumothorax.
B. can be from a diffuse lung fibrotic process.
C. can be from a bronchial obstruction, such as a tumor.
D. results from underperfused tissue
A. Compression
B. Contraction
C. Reabsorption
D. Contraction
Other than cardiogenic and non-cardiogenic, additional causes of Pulmonary Edema?
- Fluid overload (renal failure, iatrogenic)
- Hypoalbuminemia (liver disease, Nephrotic syndrome, severe malnutrition)
- Lymphatic obstruction (cancer)
- Injury to the capillaries of the alveolar septae
- Infectious agents (i.e. Mycoplasma pneumonia)
- Liquid aspiration (gastric contents, near-drowning)
- Gas inhalation (too much oxygen, smoke)
- Chemotherapeutic agents (Bleomycin)
- High altitude sickness
T or F: Pathologic mechanisms of pulmonary edema. A. Decreased venous pressure B. Decreased oncotic pressure C. Venous obstruction D. Alveolar injury
A. False. increased venous pressure
B. False. increased oncotic pressure
C. False. Lymphatic obstruction
D. True
Pathophysiology of Pumonary Edema
- Capacity of the lymphatics to absorb and drain interstitial fluid is exceeded
- Architecture of the alveolar epithelial cells breaks down.
- Fluid entering the alveolar spaces reduces or halts gas exchange.
Pulmonary Edema: Cardiogenic or NON-cardiogenic?
A. Direct injury to the lung parenchyma
B. Failure of the heart to remove fluid from lung circulation
C. ARDS is this type of pulmonary edema
A. NON-cardiogenic
B. Cardiogenic
C. NON-cardiogenic
In addition to the typical pathophysiology of pulmonary edema, what additional feature is present in the pathophysiology of ARDS?
How easily are symptoms of ARDS resolved?
Decrease in surfactant production
exudates and diffuse tissue destruction of ARDS are not easily resolved
Etiology of ARDS?
Commonly due to
Sepsis, Widespread lung infections (pneumonia, TB), Gastric aspiration, Mechanical trauma (lung trauma, head trauma)
Also may be
Multi-organ failure, Burns, Inhaled gases and chemicals, ~ 20% no identified risk factor
Immune Response to ARDS?
If the immune system is intact, the damaging effects are balanced by:
•Antioxidants
•Anti-proteases
•Anti-inflammatory cytokines
Histopathology of ARDS?
Damage/death of
Type 1 Epith–lining the membrane of lungs and/or Endothel–lining blood vessel
**Increased permeability of pulmonary bv (capillary)
Type 2 Epith
**decreased surfactant production
Neuts produce oxidants, proteases, PAF, leukotrienes
T or F? ARDS
A. Most deaths due to sepsis
B. 15% mortality rate, esp in young
C. Transudative fluid only leaks into alveoli
D. Often progresses to multi-system organ failure, death
A. True
B. False. 30 –70% mortality rate increases w age
C. False. Also fibrin, protein, cells, etc.
D. True
Sn/Sx of ARDS?
Dyspnea, Tachypnea, Cyanosis, Respiratory fail/acidosis, Bilateral fluid on CXR
T or F: Acute Interstitial Pneumonia
A. Same as ARDS except not 2ndary to something else
B. Describes localized acute lung injury
C: Etio: Gastric aspiration, lung infections
A. True
B. False. Widespread acute
C. False. No known etiology
Obstructive or Restrictive? A. Less compliance/volume/gas exchange/cyanosis B. Hyperexpansion on CXR C. Ground glass on CXR D. Air trapping/wheezing
A. Restriction
B. Obstruction
C. Restriction
D. Obstruction
Obstructive or Restrictive? A. Has 2 categories (1) chest wall disorders (2) acute or chronic interstitial and infiltrative dz B. Affects small airway expiration C. More lucency, less density on CXR D. More opacity, more density on CXR
A. Restrictive
B. Obstructive
C. Obstructive
D. Restrictive
Emphysema, Chronic Bronchitis, or Asthma?
A. Chest tightness, dysp, wheeze, cough w/w/o sputum
B. Dyspnea, cough, wheeze, wt loss
C. Chronic small airway obstrxn –> repeated infections
D. Etio: Tobacco smk, smog, dust fr: grains, cotton, silica
A. Asthma
B. Emphysema
C. Asthma
D. Chronic Bronchitis
Emphysema, Chronic Bronchitis, or Asthma?
A. Damages airway epithelium, inhibits macrophages
B. Xtra lg lungs/acini, loss of elastic recoil, apical blebs
C. Hyper-secretion of mucus in the large airways, inflamm
D. Bronchospasm and wheezing from the small airways
A. Chronic Bronchitis
B. Emphysema
C. Chronic Bronchitis
D. Asthma
Emphysema, Chronic Bronchitis, or Asthma?
A. Pink puffer, pulse ox normal
B. Blue bloater, hypercapnia, hypoxemia
C. Often exists concomitant with emphysema
D. May develop corpulmonale, CHF
A. Emphysema
B. Chronic Bronchitis
C. Chronic Bronchitis
D. Emphysema and Chronic Bronchitis
