Emphysema Chronic Bronchitis
Definition destruction of alveolar walls and
enlargement of the airspaces distal to the
terminal bronchioles, including the
respiratory bronchioles, alveolar ducts
and alveoli (Hillegas); permanent,
irreversible dilation of airways distal to
the terminal bronchioles
Etiology Smoking, Alpha1-antitrypsin deficiency,
air pollution
(A1-antitrypsin – stops elastase from
breaking down elastin)
Smoking + antitrypsin deficiency =
imbalance between proteases → tissue
breakdown → antiprotease enzymes
Continuous irritants – damage to alveolar
walls
Pathogenesis Irritant (smoking) → inflammation →
neutrophils and macrophages → produce
elastase → breakdown of elastin → V/Q
mismatch → hypoxemia → dyspnea
COMPENSATORY MECHANISM
Polycythemia, inc viscosity and
vasoconstriction → slowness of
bloodflow → inc CO → inc workload of
heart → pulmonary hypertension → cor
pulmonale → enlargement of the heart
Signs and Dyspnea on exertion, ↓ BS, wheezing,
Bronchiectasis
presence of a chronic productive
cough for 3 months in each of two
successive years
Smoking, air pollution
Irritant (smoking/pollution) →
proximal airway affectation (goblet
cell hyperplasia, mucus gland
hypertrophy) → inc secretion &
inflammation → thickening of
bronchial lumen → airway
obstruction & narrowing →
chronic hypoxemia 2 to V/Q
mismatch
COMPENSATORY MECHANISM
Polycythemia, inc viscosity and
vasoconstriction → slowness of
bloodflow → inc CO → inc
workload of heart → pulmonary
hypertension → cor pulmonale →
enlargement of the heart
Dyspnea, coughing c scanty and
irreversible dilation of one or more
bronchi with chronic inflammation and
infection
Idiopathic, complication of a prior lung
infection or injury to the bronchial wall
Localized – d/t intraluminal obstructive
process or airway tumor, extrinsic
compression from lung tumor or lymph
adenopathy, aspergilloma, sarcoidosis,
interstitial fibrosis, tuberculosis,
infections
Damaged airways → inflammation →
bronchospasm → airway obstruction →
infection → excess thick mucus
 Bronchial wall weakness/injury
ff infection or inhalation
 Traction from adjacent lung
fibrosis → airway is pulled
outward by local retractile
forces resulting in fixed dilation
of airways
 Bronchial lumen obstruction d/t
tumors or fibrotic structures in
the airways
MC: cough c chronic sputum production
Symptoms prolonged expiratory phase, barrel-chest
deformity c inc rib angle, hypertrophy of
accessory mm, hyperinflated lungs,
flattened diaphragm, cachexia, inc TLC
RV, hypercapnia, pursed-lip breathing,
hoover’s sign
Primary PT Dyspnea
Problem
Treatment Smoking cessation, B2 agonists, oxygen
therapy, bullectomy, lung transplantation
Additional Notes: Subtypes of Emphysema
 Centrilobular – proximal dilation
of the respiratory bronchioles,
(N) alveolar sacs and ducts; MC:
upper lobes and posterior
portions of lungs, 1st and 2nd
order respiratory bronchioles
 Panlobular/panacinar – dilation
of all the respiratory airspaces in
the acinus; assoc c anti-trypsin
deficiency; MC: bases
 Distal acinar
(subpleural/paraseptal) - dilation
of airspaces underneath the
apical pleura, assoc c apical
bullae; MC: periphery
 Irregular – mixed, mc assoc c
infection
purulent secretions (MC
pathogens: S. pneumoniae, H.
influenza), wheezing, prolonged
expiratory phase, ↓ BS, barrel-
chest, use of accessory mm,
pursed-lip breathing, cyanosis,
jugular vein distention, edema,
lung hyperinflation, flattened
diaphragm,
Dyspnea, impaired airway
clearance
Smoking cessation, health and
nutrition education,
bronchodilators, anti-
inflammatory agents, secretion
clearance techniques,
Chronic bronchitis may lead to the
formation of misshapen or large
alveolar sacs with reduced space
for oxygen and carbon dioxide
exchange. The client may develop
cyanosis and pulmonary edema.
Mucous plugs and narrowed
airways cause air trapping and
hyperinflation on expiration.
During inspiration the airways are
pulled open, allowing gas to flow
past the obstruction. During
expiration decreased elastic recoil
of the bronchial walls results in
collapse of
the airways and prevents normal
expiratory airflow
Pathogenesis:
greatest in the morning, hx of lung
infection, hemoptysis, dyspnea, sinusitis,
cilia dysfunction, signet-ring sign (HRCT-
“when the
internal luminal diameter of one or
more bronchi exceeds the diameter of
the adjacent pulmonary artery), tram-
track (parallel-thickened walls), crackles
Impaired airway clearance
Bronchodilators, oxygen therapy,
antibiotic therapy, increased hydration,
surgical resection
Types of Bronchiectasis
 Cylindrical - characterized by
smooth, parallel bronchial walls
that fail to taper progressive in
their distal course and often end
squarely and abruptly
 Varicose or varicoid -
characterized by bronchi that
are distorted and
bulging
 Saccular/cystic - characterized
by bronchial dilation that
increases
progressively toward the lung
periphery, almost to the pleura,
where the bronchus has a
ballooned outline, most severe
 *Imbalance between proteases leads to
the loss of lung parenchyma and elastic
recoil → dilation of airways, premature
airway closure and air trapping and inc
residual volume
*D/t intrinsic pulmonary damage →
hyperinflation of lungs → dysfunction of
diaphragm → respiratory failure
Chronic inflammation results in
structural changes and narrowing
of the small airways. Chronic
inflammation also
results in destruction of lung
parenchyma, the respiratory
bronchioles, and alveoli → dec
lung recoil → reduce the ability of
the airways to remain open
during expiration, which leads to
air trapping, hyperinflation
and progressive airflow limitation
*COPD Severity (Hillegas, Table 6-
6)

Lung CA Tuberculosis Pneumonia

Definition malignant growth of abnormal
epithelial cells arising in a bronchus
Etiology Smoking, genetics, passive smoking,
diet, occupational agents
Pathogenesis Squamous Cell CA - arises from the
bronchial mucosa after repeated
inflammation or irritation caused by
cancer stimuli; MC assoc c smoking,
arises in the segmental or
Mycobacterium tuberculosis
infection spread by droplet nuclei,
which are aerosolized by coughing,
sneezing or speaking
Mycobacterium tuberculae
DRTB – resistant to one of HRZE
MDRTB – HR resistant
XDRTB – HRZE resistant, 1 of 2nd
defense
Inhalation → <10% reach the alveoli
→ phagocytosis of the bacilli by
alveolar macrophages →
complement system activation →
inhibition of intracellular increase in
Inflammatory process of the lung
parenchyma (begins c a lower
respiratory tract infection) where gas
exchange occurs that progresses
beyond inflammation and develops into
infection
CAP - mc: S. pneumoniae, L.
pneumophila, H. influenza, S. aureus
HAP - infections in the lower respiratory
tract with an onset of 72 hours or more
after hospitalization (MC: Pseudomonas
aeruginosa)
Bacteria & microbes through inhalation
and aspiration → inc edema fluid →
PMN leukocytes for phagocytosis →
deposition of fibrin in the inflamed area
→ specific Ab to fight bacteria
 subsegmental bronchi and may extend
into the bronchial lumen → atelectasis
& pneumonia; these tumors often
cavitate
Small Cell CA – aka oat cell CA, often
presents as a centrally located lesion;
(+) hilar or lymph node involvement;
spreads through submucosa,
metastasize widely; produces
hormones
Adenocarcinoma – most common;
located in the periphery of the lung,
may cause carcinogenic pleural effusion
Large Cell CA – subpleural in location,
may cause compression of lung tissue
Signs and Weight loss, loss of appetite, cough,
Symptoms chest pain, digital clubbing, dypnea,
unresolving pneumonia
Primary PT Problem Dyspnea
Treatment Chemotherapy, radiation, surgery,
palliative therapy
Ca2 by glycolipid of bacterial cell Virus → localizes in respiratory
wall → survival and replication of epithelial cells → destruction of cilia
the bacilli → cell-mediated and and mucosal surface → loss of
humoral immunity develops to mucociliary function → (predispose to
destroy tubercle bacilli → bacterial pneumonia) → alveoli →
accumulation of macrophages at the edema, hemorrhage, hyaline
site of lesion → granulomatous membrane formation → ARDS →
lesions → caseous necrosis hypoxemia
production in the center of the
lesion → fibrotic healing of some
lesions, inflammation and necrosis
of other lesions → damage to
surrounding tissues → caseous
materials liquefy → invasion and
destruction of bronchial walls and
blood vessels forming cavities →
multiplication of tubercle bacilli
within the cavity → drainage of the
liquefied caseous material into the
bronchi → discharge into the
environment
Weight loss, loss of appetite, fever, Bacterial pneumonia – abrupt onset,
night sweats, productive cough for 2 lobar consolidation, high fever, chills,
weeks, hemoptysis, malaise, chest dyspnea, tachypnea, productive cough,
pain, dyspnea, anorexia, weakness, pleuritic pain, leukocytosis
ARDS Viral pneumonia – insidious onset, low
fever, dyspnea, tachypnea,
nonproductive cough, myalgia, normal
WBC
Dypsnea Dyspnea
1st line: HRZES Antibiotics, oxygen therapy
 HRZE – 1st 2 months
 HR – last 4 months
nd
2 line: Fluoroquinolones

Additional Notes: MC site of metastasis: CNS → liver →
adrenal gland → pancreas → bones →
GU system → thyroid → spleen
Lung CA Staging
 Stage 1- Surgery
A – T1N0M0
B – T2NM0
 Stage 2 – Chemotherapy
A – T1N1M0
B – T2N1M-, T3N0M0
 Stage 3A - +/- surgery
T1-3N2M0, T3N1M0
 Stage 3B – No surgery
T4N0-2M0, T1-4N3M0
 Stage 4 – Terminal
Any T, Any N M1 = Palliative
Pleural Effusion
Definition Accumulation of fluid in the pleural
cavity
Etiology Transudate PE – CHF, LVHF, cirrhosis,
nephrotic syndrome, pericardial
disease, myxedema pulmonary emboli,
peritoneal dialysis, atelectasis
Exudative PE – malignancy, altered
Vaccine
Chemo + rifampin for 6 mos –
alternative
ATS Classification of TB Aspiration pneumonia – spilling of
0 – no exposure gastric contents or foreign matter
1 – exposure s evidence below vocal cords (within 2 hours)
2 – latent
3 – active
4 – inactive
5 – suspect
Patient Classification of TB
New – never had tx for <4 wks
Relapse – cured but (+) smear
RAD – stop tx for >2 mos, but
returns (+) smear
Tx failure – (+) smear even after 5
mos tx
Transfer-in – transfer of facility
Tests for TB
AFB – MC test
C/S – gold standard
Skin test/Mantoux/PPD
*Bacillus Calmette Guerin – pedia
EPTB
Pneumothorax Hemothorax
Entry of free air in the pleural space Presence of blood in the pleural space
Idiopathic, trauma, secondary Penetrating wounds or crushed injuries
pneumothorax, iatrogenic to the thorax
 lymphatic drainage, infections, TB, SLE,
RA
Pathogenesis Transudate PE – ↓ oncotic pressure, ↑
hydrostatic pressure
Exudative PE – ↑ permeability of the
pleural surfaces that allows protein and
excess fluid to move into the pleural
space
Signs and Dyspnea, pleuritic chest pain, dry
Symptoms nonproductive cough, ↓ BS, pleural
friction rub
Primary PT Problem Dyspnea, atelectasis
Treatment Thoracocentesis, thoracoscopy
Additional Notes: Normal pleural fluid: 5-10
Empyema – large infected pleural
effusion
Transudative – low protein content
Exudative – high protein content
Open PTX – air in the pleural space Blood in the pleural space →
communicates freely with the compression of the underlying lung
outside environment → unable to tissue → prevents lung expansion →
maintain negative pleural space residual blood becomes nonelastic
pressure fibrous tissue → restrictive pleural rind
Tension PTX – air can enter the → fibrothorax
pleural space but cannot escape the
external environment → collapse of
involved lung
Spontaneous PTX – tall, thin young
men who grow faster than their
pleura → bleb formation
Secondary PTX – 2 to diseased lungs
Iatrogenic PTX – 2 to medical
procedures
↓BS, dyspnea, ↓ lung volumes, ↑ ↑ V/Q mismatch, ↓ lung compliance
V/Q mismatch, sudden sharp pain,
severe dyspnea, coughing,
mediastinal shift to C/L half of
thorax, ↑ RR, lung collapse,
flattened diaphragm, hypoxemia,
hypercapnia, systemic hypotension,
shock
Atelectasis Atelectasis
CTT, deep diaphragmatic breathing Decortication, CTT
exercises, oxygen supplement
MC in the lower lobes
Lymph drainage in the pleural space -
chylothorax