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PC705 Module 3 Exam Study Guide Exam and All Correct Answers Updated.

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Components of neural-muscular control of breathing - Answer Medulla: generates impulses to respiratory muscles Phrenic nerve: innervates diaphragm. Originates from C3, C4, C4 nerve roots in spinal cord Process of gas exchange/diffusion in the lungs - Answer 1. O2 passes through alveoli's thin lining into capillary network 2. CO2 moves out of capillary network 3. CO2 is exhaled as the partial pressure in alveoli is higher than PP of external environment 4. O2 attaches to RBCs, which travel back to the heart via the pulmonary vein 2 components of normal ventilation - Answer 1. Air-conduction (ventilation) 2. Gas-exhange functions (respiration) Ventilation-Perfusion Ratio (V/Q) - Answer Indicates adequate ventilation and sufficient perfusion of blood to alveoli. 1) Decreased: indicates ventilation problem, pneumonia, asthma, ARDS, alveolar collapse, pulmonary AV communication, pulm edema 2) Increased: indicates perfusion problem, PE, non-embolic obstruction by tumor, radiation therapy, cardiovascular shock, emphysema Normal V/Q is 0.8 V/Q Ratio Values - Answer Normal is 0.8. Lower at base of lungs (more blood flow), higher at apex (less blood flow). Ventilation is approx. 4L/min, perfusion approx 5L/min. >0.8: ventilation exceeds perfusion <0.8: poor ventilation

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PC705 Module 3 Exam Study Guide
Exam and All Correct Answers 2025-
2026 Updated.
Components of neural-muscular control of breathing - Answer Medulla: generates impulses
to respiratory muscles

Phrenic nerve: innervates diaphragm. Originates from C3, C4, C4 nerve roots in spinal cord



Process of gas exchange/diffusion in the lungs - Answer 1. O2 passes through alveoli's thin
lining into capillary network

2. CO2 moves out of capillary network

3. CO2 is exhaled as the partial pressure in alveoli is higher than PP of external environment

4. O2 attaches to RBCs, which travel back to the heart via the pulmonary vein



2 components of normal ventilation - Answer 1. Air-conduction (ventilation)

2. Gas-exhange functions (respiration)



Ventilation-Perfusion Ratio (V/Q) - Answer Indicates adequate ventilation and sufficient
perfusion of blood to alveoli.

1) Decreased: indicates ventilation problem, pneumonia, asthma, ARDS, alveolar collapse,
pulmonary AV communication, pulm edema

2) Increased: indicates perfusion problem, PE, non-embolic obstruction by tumor, radiation
therapy, cardiovascular shock, emphysema

Normal V/Q is 0.8



V/Q Ratio Values - Answer Normal is 0.8. Lower at base of lungs (more blood flow), higher at
apex (less blood flow). Ventilation is approx. 4L/min, perfusion approx 5L/min.

>0.8: ventilation exceeds perfusion

<0.8: poor ventilation



Physiology of obstructive pulm. disorders - Answer obstruct airflow; makes difficult to exhale
air completely from lungs. Increased airway resistance due to narrowed/blocked airways.

,Obstructive pulmonary disorder diagnostics - Answer -Spirometry: decreased FEV 1. Ratio
<70% indicates obstruction

-Peak flow meter: asthma monitoring

-CXR, CT



Physiology of restrictive pulmonary disorders - Answer Reduces the total lung capacity (TLC)
by limiting expansion.

-Stiff lungs or chest wall impairs inhalation; mechanical restriction; decreased lung volumes

-Pulmonary fibrosis, sarcoidosis, obesity hypoventilation syndrome, scoliosis, neuromuscular
disorders (ALS, myasthenic crisis, cholinergic crisis)



Restrictive pulm disorder symptoms - Answer SOB especially w/ activity, rapid shallow
breathing (compensatory), fatigue, weakness, cyanosis



Restrictive pulm disorder diagnostics - Answer -Spirometry: normal or increased FEV 1/ FVC
ratio

Decreased TLC

-Lung volume tests: measure residual volume & TLC using plethysmography

-CT to detect fibrosis, pleural thickening



Obstructive pulm disorder symptoms - Answer Chronic cough w/ or without mucus,
wheezing, chest tightness, SOB on exertion, prolonged exhalation



Pathophys of emphysema - Answer -Inflammation of mucosa

-Alveolar wall destruction leads to loss of elastic recoil

-Alveoli merge into larger air spaces, reducing surface area for gas exchange

-Bronchioles collapse on exhalation due to loss of structural support

-Lungs become chronically hyperinflated with increased residual volume (air trapping)

-Diaphragm flattens over time, reducing efficiency



Types of emphysema - Answer 1) Centriacinar (centrilobular): most common. Affects central
portions of acini, commonly in lower lobes. Associated w/ smoking

2) Panacinar (panlobular): affects entire acinus, commonly in lower lobes. Linked to alpha-1
antitrypsin deficiency

, Alpha-1 Antitrypsin Deficiency - Answer Genetic disorder resulting from deficiency of alpha
1-antitrypsin, a protective agent for the lung; allows unchecked destruction of lung tissue by
neutrophil elastase. The body doesn't produce enough AAT, which is produced in the liver. Rare,
typically affects younger people, inherited; autosomal recessive. Increases patient's risk for
developing panacinar emphysema even in the absence of smoking, and can also cause liver
disease.



Role of neutrophils & macrophages in emphysema - Answer Their release of elastase &
proteases contributes to tissue damage in alveoli. Elastase breaks down elastin, a protein in the
connective tissue. Protease breaks down proteins in body or skin.



Diagnostics & testing for emphysema - Answer -Reduced FEV 1 values

-Test the forced vital capacity (FVC)

-FEV 1:FVC ratio <70%: increased residual volume due to air trapping.

-Gas exchange impairment: reduced O2 levels due to hypoxemia, increased CO2 levels
(hypercapnia)



Clinical signs & symptoms of emphysema - Answer -SOB/dyspnea, chronic cough, wheezing,
chest tightness, weight loss & muscle wasting in advanced cases.

-"Pink puffer"



Complications of emphysema - Answer -Pulmonary HTN

-Cor pulmonale: R-sided heart failure caused by pulm. HTN

-Pneumothorax due to rupture of bullae and collapse

-Total respiratory failure



Pathophys of chronic bronchitis - Answer -Inflammatory mediators like cytokines recruit
immune cells, causing persistent inflammation that damages tissue

-Macrophages, neutrophils, CD8+ T-cells dominate response

-Interleukins (IL-8) attract neutrophils, tumor necrosis factor-alpha --> amplifies inflammation

-Proteases cause tissue destruction, airway remodeling

-Goblet cell hyperplasia increases mucus production, blocking airways

-Impaired ciliary function, fibrosis in airway walls, smooth muscle hypertrophy

-Narrowed airways & trapped air cause dyspnea, impaired gas exchange

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