NU 545
Unit 5 Study Guide
Advanced Pathophysiology
University of South Alabama.
This document provides a focused
study guide
It summarizes key concepts, lecture highlights, and
exam-relevant material to support efficient last-minute
review. The guide is structured to help students
reinforce understanding, identify weak areas, and prepare
confidently for the assessment.
, 1
Exam 5 Study Guide (Chapter 35-40)
1. Know type I and Type II alveolar cells (page 1147)
a. Alveoli are the primary gas exchange units of the lungs
b. O2 enters blood, CO2 removed
c. Lung epithelial cells provide protective interface & are essential for as exchange,
preventing entry of foreign agents, regulating water & ion transport, mechanical
stability of alveoli
d. 2 major types of epithelial cells in alveolus
i. type I
1. provide structure
ii. type II
1. secrete surfactant
a. a lipoprotein that coats the inner surface of alveolus &
facilitates expansion during inspiration (this lowers alveolar
surface tension at end expiration—prevents lung collapse).
b. Decrease proinflammatory mediators, preventing oxidative
injury, regulate role of fibroblasts in airway remodeling
c. Bacteriostatic & function as opsonins
2. Role of surfactant in the lungs-infants and adults
a. Adults (page 1147)
i. Surfactant secreted by type II cells
1. Lipoprotein that coats the inner surface of the alveolus & facilitates
its expansion during inspiration, which lowers alveolar surface
tension at end expiration (prevents lung collapse aka atelectasis)
2. Surfactant proteins contribute to control of lung inflammation by
decreasing release of pro-inflammatory mediators, remodeling
3. Bacteriostatic & function as opsonins in presenting pathogens to
alveolar macrophages
4. Surfactant w/ alveolar macrophages work together w/ pulm
microbiome to prevent lower lung infection
b. Infants (page 1203)
i. Lipid protein mixture prod by type II cells & is critical for maintaining
alveolar expansion
ii. Produced by 20-24 weeks gestation
iii. Secreted by fetal airways by 30 weeks
3. Know Chronic Bronchitis-pathophysiology, etiology, prevention, clinical manifestations,
treatment, complications (page 1181-1183)
a. Inspired irritants promote bronchial inflammation bronchial edema, increases in
size & # of mucous glands & globlet cells in airway & epithelium, smooth muscle
hypertrophy w/ fibrosis, narrowing of airways
b. Hypersecretion of thick, tenacious mucous occurs & cannot be cleared b/c of
impaired ciliary function
c. Increases risk for infection
d. Initially only affects larger bronchi but eventually all airways are involved
e. Obstruction ventilation – perfusion mixmatch w/ hypoxemia
f. Clinical manifestations (figure 36.3)
i. Productive cough
, 2
1. Classic sign
ii. Dyspnea
1. Late
iii. Wheezing
1. intermittent
iv. History of smoking
1. common
v. Barrel chest
1. occasionally
vi. Prolonged expiration
1. always
vii. Common:
1. Cyanosis
2. Chronic hypoventilation
3. Polycythemia
4. Cor pulmonale
g. Eval & treatment
i. Pulmonary function test
1. Airway obstruction
a. Decreased FEV1
b. Progression & unresponsive to bronchodilators
2. Hypoxemia & hypercapnia
ii. Prevention of COPD
iii. Steroids as a last resort
4. Know gas exchange in the lungs
a. Conducting airway terminates in the respiratory (terminal) bronchioles, alveolar
ducts, & alveoli
b. Thin walled structures participate in gas exchange & the clusters of alveoli = acinus
c. Bronchioles from 16th through 23rd divisions contain increasing numbers of alveoli
and = respiratory bronchioles
d. The walls of respiratory bronchioles = very thin w/ epithelial layer devoid of cilia &
goblet cells, very little smooth muscle fiber, thin elastic connective tissue
e. Bronchioles end in alveolar ducts – lead to sacs of numerous alveoli
f. Alveoli = main primary gas exchange units of lungs
i. O2 enters blood
ii. CO2 removed
g. Pores of Kohn
i. Permit air to pass through septa from alveolus to alveolus
1. Promotes collateral ventilation & even distribution of air
h. Lungs epithelial cells provide a protective interface w/ environment & are essential
for adequate gas exchange preventing entry of foreign agents, regulating ion & water
transport, & maintain mechanical stability of the alveoli
5. How is the patient’s alveolar ventilation measured? (page 1150)
a. Arterial blood gas to measure PaCO2
6. Know asthma (adult and childhood)- pathophysiology, etiology, prevention, inflammatory
mediators, clinical manifestations, treatment (acute and chronic), complications
a. Adult (page 1179-1181)
, 3
i. Chronic inflammatory disorder of bronchial mucosa that causes bronchial
hyperrresponsiveness, constriction of the aiways, variable airflow
obstruction that is reversible
ii. Pathophysiology
1. Episodic attacks of bronchospasm, bronchial inflammation, mucosal
edema, and increased mucous production
2. Early asthmatic response – acute bronchoconstriction that reaches
maximum in first 30 min & resolves w.i 1-3 hrs
a. Dendritic cells present the antigen to T helper cells TH2
release cytokines
i. Vasodilation
ii. Increased capillary permeability
iii. Mucosal edema
iv. Bronchial smooth muscle contraction
(bronchospasm)
v. Tenacious mucous secretion
3. Late asthmatic response
a. Begins 4–8 hours after the early response w/ increase in
hyperresponsiveness
b. Chemotactic recruitment of lymphocytes, eosinophils,
basophils, neutrophils, and lymphocytes occurs
i. Bronchospasm
ii. Edema
iii. Mucous secretion & airway obstruction
iv. Airway scarring
1. From eisinophil
v. Increased bronchial hyperresponsiveness
1. From release of neuropeptides
vi. Impaired mucociliary function with accumulation of
mucous and cellular debris, forming plugs in the
airways
1. From damage to ciliated epithelial cells
vii. Decreased Treg cells
viii. Leads to airway remodeling if left untreated
4. Aiway obstruction increased resistance to airway & decreased flow
rates
a. Airtrapping results intrapleural & alveolar gas pressure &
decreased alveolar perfusion
b. Hypoexemia w/o Co2 retention more hyperventilation
CO2 decreases & pH increases decreased TV w/ increased
CO2 retention & resp acidosis
iii. Clinical manifestations
1. Asymptomatic between attacks
2. Chest constriction, expiratory wheezing, dyspnea, nonproductive
coughing, prolonged expiration, tachycardia, tachypnea
3. Pulsus paradoxus (decrease in SBP during inspiration of more than
10 mmHg)
a. During inspiration & expiration
4. Status asthmaticus
a. Bronchospasm not reversed by usual measures
Unit 5 Study Guide
Advanced Pathophysiology
University of South Alabama.
This document provides a focused
study guide
It summarizes key concepts, lecture highlights, and
exam-relevant material to support efficient last-minute
review. The guide is structured to help students
reinforce understanding, identify weak areas, and prepare
confidently for the assessment.
, 1
Exam 5 Study Guide (Chapter 35-40)
1. Know type I and Type II alveolar cells (page 1147)
a. Alveoli are the primary gas exchange units of the lungs
b. O2 enters blood, CO2 removed
c. Lung epithelial cells provide protective interface & are essential for as exchange,
preventing entry of foreign agents, regulating water & ion transport, mechanical
stability of alveoli
d. 2 major types of epithelial cells in alveolus
i. type I
1. provide structure
ii. type II
1. secrete surfactant
a. a lipoprotein that coats the inner surface of alveolus &
facilitates expansion during inspiration (this lowers alveolar
surface tension at end expiration—prevents lung collapse).
b. Decrease proinflammatory mediators, preventing oxidative
injury, regulate role of fibroblasts in airway remodeling
c. Bacteriostatic & function as opsonins
2. Role of surfactant in the lungs-infants and adults
a. Adults (page 1147)
i. Surfactant secreted by type II cells
1. Lipoprotein that coats the inner surface of the alveolus & facilitates
its expansion during inspiration, which lowers alveolar surface
tension at end expiration (prevents lung collapse aka atelectasis)
2. Surfactant proteins contribute to control of lung inflammation by
decreasing release of pro-inflammatory mediators, remodeling
3. Bacteriostatic & function as opsonins in presenting pathogens to
alveolar macrophages
4. Surfactant w/ alveolar macrophages work together w/ pulm
microbiome to prevent lower lung infection
b. Infants (page 1203)
i. Lipid protein mixture prod by type II cells & is critical for maintaining
alveolar expansion
ii. Produced by 20-24 weeks gestation
iii. Secreted by fetal airways by 30 weeks
3. Know Chronic Bronchitis-pathophysiology, etiology, prevention, clinical manifestations,
treatment, complications (page 1181-1183)
a. Inspired irritants promote bronchial inflammation bronchial edema, increases in
size & # of mucous glands & globlet cells in airway & epithelium, smooth muscle
hypertrophy w/ fibrosis, narrowing of airways
b. Hypersecretion of thick, tenacious mucous occurs & cannot be cleared b/c of
impaired ciliary function
c. Increases risk for infection
d. Initially only affects larger bronchi but eventually all airways are involved
e. Obstruction ventilation – perfusion mixmatch w/ hypoxemia
f. Clinical manifestations (figure 36.3)
i. Productive cough
, 2
1. Classic sign
ii. Dyspnea
1. Late
iii. Wheezing
1. intermittent
iv. History of smoking
1. common
v. Barrel chest
1. occasionally
vi. Prolonged expiration
1. always
vii. Common:
1. Cyanosis
2. Chronic hypoventilation
3. Polycythemia
4. Cor pulmonale
g. Eval & treatment
i. Pulmonary function test
1. Airway obstruction
a. Decreased FEV1
b. Progression & unresponsive to bronchodilators
2. Hypoxemia & hypercapnia
ii. Prevention of COPD
iii. Steroids as a last resort
4. Know gas exchange in the lungs
a. Conducting airway terminates in the respiratory (terminal) bronchioles, alveolar
ducts, & alveoli
b. Thin walled structures participate in gas exchange & the clusters of alveoli = acinus
c. Bronchioles from 16th through 23rd divisions contain increasing numbers of alveoli
and = respiratory bronchioles
d. The walls of respiratory bronchioles = very thin w/ epithelial layer devoid of cilia &
goblet cells, very little smooth muscle fiber, thin elastic connective tissue
e. Bronchioles end in alveolar ducts – lead to sacs of numerous alveoli
f. Alveoli = main primary gas exchange units of lungs
i. O2 enters blood
ii. CO2 removed
g. Pores of Kohn
i. Permit air to pass through septa from alveolus to alveolus
1. Promotes collateral ventilation & even distribution of air
h. Lungs epithelial cells provide a protective interface w/ environment & are essential
for adequate gas exchange preventing entry of foreign agents, regulating ion & water
transport, & maintain mechanical stability of the alveoli
5. How is the patient’s alveolar ventilation measured? (page 1150)
a. Arterial blood gas to measure PaCO2
6. Know asthma (adult and childhood)- pathophysiology, etiology, prevention, inflammatory
mediators, clinical manifestations, treatment (acute and chronic), complications
a. Adult (page 1179-1181)
, 3
i. Chronic inflammatory disorder of bronchial mucosa that causes bronchial
hyperrresponsiveness, constriction of the aiways, variable airflow
obstruction that is reversible
ii. Pathophysiology
1. Episodic attacks of bronchospasm, bronchial inflammation, mucosal
edema, and increased mucous production
2. Early asthmatic response – acute bronchoconstriction that reaches
maximum in first 30 min & resolves w.i 1-3 hrs
a. Dendritic cells present the antigen to T helper cells TH2
release cytokines
i. Vasodilation
ii. Increased capillary permeability
iii. Mucosal edema
iv. Bronchial smooth muscle contraction
(bronchospasm)
v. Tenacious mucous secretion
3. Late asthmatic response
a. Begins 4–8 hours after the early response w/ increase in
hyperresponsiveness
b. Chemotactic recruitment of lymphocytes, eosinophils,
basophils, neutrophils, and lymphocytes occurs
i. Bronchospasm
ii. Edema
iii. Mucous secretion & airway obstruction
iv. Airway scarring
1. From eisinophil
v. Increased bronchial hyperresponsiveness
1. From release of neuropeptides
vi. Impaired mucociliary function with accumulation of
mucous and cellular debris, forming plugs in the
airways
1. From damage to ciliated epithelial cells
vii. Decreased Treg cells
viii. Leads to airway remodeling if left untreated
4. Aiway obstruction increased resistance to airway & decreased flow
rates
a. Airtrapping results intrapleural & alveolar gas pressure &
decreased alveolar perfusion
b. Hypoexemia w/o Co2 retention more hyperventilation
CO2 decreases & pH increases decreased TV w/ increased
CO2 retention & resp acidosis
iii. Clinical manifestations
1. Asymptomatic between attacks
2. Chest constriction, expiratory wheezing, dyspnea, nonproductive
coughing, prolonged expiration, tachycardia, tachypnea
3. Pulsus paradoxus (decrease in SBP during inspiration of more than
10 mmHg)
a. During inspiration & expiration
4. Status asthmaticus
a. Bronchospasm not reversed by usual measures
