Defense Repair & Scenarios

Question 1

pulmonary defense mechanisms in the steady state

Answer 1

*non-pathogenic “harmless” particles are captured and eliminated by:
-cough reflex
-airway mucus → mucociliary escalator
-surfactant proteins → alveolar macrophages

Question 2

pulmonary defense mechanisms against pathogens

Answer 2

*pathogenic particles are recognized by the immune system and initiate inflammation:
-binding to secretory IgA
-direct killing by macrophages, surfactant proteins
-activation of dendritic cells
-recruitment of PMN and monocytes

*the resulting cytokine release can injure the healthy alveolar cells and basement membrane, resulting in epithelial damage [when widespread, called “diffuse alveolar damage”]

Question 3

lung microbiome

Answer 3

*the airways are not a sterile environment:
-like oral flora, but a much smaller biomass
-can be altered by antibiotic usage
*probably significant in some diseases (asthma, cystic fibrosis)
*uncertain significance in other diseases (COPD, sarcoidosis, pulmonary fibrosis, etc)

Question 4

pulmonary physiology of aging

Answer 4

*decreases in:
-chest wall compliance
-respiratory muscle strength
-FEV1, FVC, diffusing capacity

*increases in:
-lung compliance
-FRC, RV, closing volume
-dead space ventilation
-A-a gradient

Question 5

pulmonary physiology of pregnancy

Answer 5

*pregnancy demands increased metabolism
*key physiologic changes:
-mechanical effects of the enlarging uterus
-increased ventilatory requirements
-increased circulatory requirements

Question 6

lung volumes in pregnancy

Answer 6

*spirometry should be NORMAL
*TLC decreases minimally (<5%)
*FRC decreases by 20-30% (combination of reduced ERV and RV)

Question 7

respiratory gas exchange in pregnacny

Answer 7

*does not significantly change
*minute ventilation increases by 20-50%:
-required to support increased metabolism
-consists of a 30-50% increase in TIDAL VOLUME
-rises quickly in first trimester, then minimally
-likely mediated by increased progesterone, causing hyperventilation
*“normal” ABG values are NOT NORMAL in pregnancy

Question 8

pulmonary physiology of obesity

Answer 8

*excess (maladaptive) adipose tissue:
-mechanical effects: increased work of breathing, decreased respiratory system compliance, decreased FRC
-biochemical effects: increased oxygen consumption, promotion of alveolar hypoventilation

Question 9

PFTs in obesity

Answer 9

*spirometry is usually normal
*reduced FRC:
-TLC, RV are usually normal, but in extreme cases there can be restriction
-there is a significant decrease in ERV
*diffusing capacity is usually normal

Question 10

obesity and hypercapnia

Answer 10

*obesity can lead to chronic hypercapnia (elevated PCO2); aka chronically hypoventilating

Question 11

obesity-hypoventilation syndrome - criteria

Answer 11

1. obesity
2. sleep disordered breathing (OSA in 90%)
3. hypoventilation (daytime PCO2 >45)
4. no other causes for hypoventilation

Question 12

obesity-hypoventilation syndrome - clinical features

Answer 12

*symptoms: sleepiness, morning headache, dyspnea
*mechanism incompletely understood
*associated with increased morbidity and mortality
*treatment with nocturnal positive airway pressure (PAP)

Question 13

pulmonary physiology at high altitude

Answer 13

*at high altitude, % oxygen is the same, but the PRESSURE is much lower
*increased minute ventilation & cardiac output:
-increased PaCO2 → RESPIRATORY ALKALOSIS
-increased pulmonary blood flow

Question 14

pulmonary physiology of exercise

Answer 14

*oxygen consumption increases → carbon dioxide production increases → minute ventilation increases

Question 15

pulmonary physiology of exercise - phases

Answer 15

*phase 1: immediate, learned vs. neural
*phase 2: eliminating the aerobically produced CO2
*phase 3: eliminating the anaerobically produced CO2
*phase 4: metabolic acidosis directly stimulates chemoreceptors