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seCtioN i i
i

Resp i R at o R y R E S P I R AT ORYPAT h
O lO g Y

R E S P I R AT ORYPAT h O lO g Y
Rhinosinusitis

Obstruction of sinus drainage into nasal cavity

inflammation and pain over affected
area
(typically maxillary sinuses in adults A ).
Most common acute cause is viral URI;
may
cause superimposed bacterial infection, most
commonly S. pneumoniae, H. influenzae, and
M. catarrhalis.

A
Deep venous
thrombosis

Predisposed by Virchow triad:

Stasis
Hypercoagulability (e.g., defect
in coagulation cascade proteins,
most commonly factor V Leiden)
Endothelial damage (exposed
collagen triggers clotting cascade)

Rhinosinusitis. Coronal CT of the sinus shows bilateral

maxillary sinusitis (yellow arrows) and unrelated nasal septal
deviation (red arrow).

Approximately 95% of pulmonary emboli arise

from deep leg veins.
Homan signdorsiflexion of foot calf
pain. Use heparin for prevention and acute
management; use warfarin for long-term
prevention of DVT recurrence.

Pulmonary emboli
A

V/Q mismatch hypoxemia

respiratory alkalosis. Sudden-onset dyspnea,
chest pain, tachypnea. May present as
sudden death.
Types: Fat, Air, Thrombus, Bacteria, Amniotic
fluid, Tumor. Fat emboliassociated with
long bone fractures and liposuction; classic
triad
of hypoxemia, neurologic abnormalities, and
petechial rash.
Amniotic fluid embolican lead to
DIC, especially postpartum.
Gas embolinitrogen bubbles precipitate in
ascending divers; treat with hyperbaric
oxygen.

Pulmonary embolism. Note large embolus (arrows) in the

pulmonary artery.

An embolus moves like a FAT BAT.

CT pulmonary angiography is the imaging
test of choice for a PE (look for filling
defects) A B C .

Pulmonary thromboembolus.
Lines
of Zahn
are (RBCs)
interdigitating
areas of pink (platelets,
fibrin)
and red
found only in thrombi formed before death. Help distinguish
pre- and postmortem thrombi.

Obstructive lung
diseases

TYPE

Obstruction of air flow resulting in air trapping in the lungs. Airways close prematurely at high
lung volumes RV and FVC. PFTs: FEV1, FVC FEV1/FVC ratio (hallmark),
V/Q
mismatch. Chronic, hypoxic pulmonary vasoconstriction can lead to cor pulmonale.
PAThOlOgY

OThER

Chronic bronchitis
(blue bloater)

A form of COPD along with emphysema.

Hyperplasia of mucus-secreting glands in the
bronchi Reid index (thickness of gland
layer/total thickness of bronchial wall) >
50%.

Productive cough for > 3 months per year (not

necessarily consecutive) for > 2 years. Disease
of small airways.
Findings: wheezing, crackles, cyanosis (earlyonset hypoxemia due to shunting), late-onset
dyspnea, CO2 retention.

Emphysema (pink
puffer, barrelshaped chest)

Enlargement of air spaces, recoil,

compliance, DLCO resulting
from destruction of alveolar walls A .
Two types:
Centriacinarassociated with smoking
B.
Panacinarassociated with 1antitrypsin deficiency.

elastase activity loss of elastic fibers

lung compliance.
Exhalation through pursed lips to airway
pressure and prevent airway collapse during
respiration.

by thin septa seen on left. There is relative preservation of

alveoli on right.

Centriacinar emphysema. Gross specimen shows

multiple air-space cavities lined by heavy black carbon
deposits.

Asthma

Bronchial hyperresponsiveness causes

reversible bronchoconstriction. Smooth
muscle hypertrophy, Curschmann spirals
(shed epithelium forms mucus plugs), and
Leyden
Charcot-crystals (formed from breakdown of
eosinophils in sputum).

Can be triggered by viral URIs, allergens,

and stress.
Test with methacholine challenge.
Findings: cough, wheezing, tachypnea,
dyspnea, hypoxemia, I/E ratio, pulsus
paradoxus, mucus plugging.

Bronchiectasis

Chronic necrotizing infection of bronchi

permanently dilated airways, purulent
sputum, recurrent infections, hemoptysis.

Associated with bronchial obstruction, poor

ciliary motility (smoking), Kartagener
syndrome, cystic fibrosis, allergic
bronchopulmonary aspergillosis.

Restrictive lung disease

Restricted lung expansion causes lung volumes ( FVC and TLC). PFTs: FEV1/FVC
ratio
80%.
Types:
Poor breathing mechanics (extrapulmonary, peripheral hypoventilation, normal A-a gradient):
Poor muscular effortpolio, myasthenia gravis
Poor structural apparatusscoliosis, morbid obesity
Interstitial lung diseases (pulmonary diffusing capacity, A-a gradient):
Acute respiratory distress syndrome (ARDS)
Neonatal respiratory distress syndrome (hyaline membrane disease)
Pneumoconioses (anthracosis, silicosis, asbestosis)
Sarcoidosis: bilateral hilar lymphadenopathy, noncaseating granuloma; ACE and Ca2+
Idiopathic pulmonary fibrosis (repeated cycles of lung injury and wound healing with
collagen
deposition)
Goodpasture syndrome
Granulomatosis with polyangiitis (Wegener)
Langerhans cell histiocytosis (eosinophilic granuloma)
Hypersensitivity pneumonitis
Drug toxicity (bleomycin, busulfan, amiodarone, methotrexate)

Hypersensitivity
pneumonitis

Mixed type III/IV hypersensitivity reaction to environmental antigen dyspnea, cough,

chest tightneass, headache. Often seen in farmers and those exposed to birds.

Pneumoconioses

Asbestosis
B

Coal workers pneumoconiosis, silicosis, and asbestosis risk of cor pulmonale and
Caplan syndrome (rheumatoid arthritis and pneumoconioses with intrapulmonary
nodules).
Associated with shipbuilding, roofing, and
plumbing. Ivory white, calcified pleural
plaques A are pathognomonic of asbestos
exposure, but are not precancerous. Associated
with an incidence of bronchogenic
carcinoma and mesothelioma.

Affects lower lobes.

Asbestos (ferruginous) bodies are golden-brown
fusiform rods resembling dumbbells B .
Asbestos is from the roof (was common in
insulation), but affects the base (lower lobes).
Silica and coal are from the base (earth), but
affect the roof (upper lobes).

Asbestosis. Note white, calcified pleural plaques

(arrows).

Coal workers
pneumoconiosis

Prolonged coal dust exposure

macrophages laden with carbon
inflammation and fibrosis.
Also known as black lung disease.

Affects upper lobes.

Anthracosisasymptomatic condition found in
many urban dwellers exposed to sooty air.

Silicosis

Associated with foundries, sandblasting,

and mines. Macrophages respond to silica
and release fibrogenic factors, leading to
fibrosis. It is thought that silica may disrupt
phagolysosomes and impair macrophages,
increasing susceptibility to TB. Also risk
of bronchogenic carcinoma.

Affects upper lobes.

Eggshell calcification of hilar lymph nodes.

Neonatal respiratory
distress syndrome

Surfactant deficiency surface tension alveolar collapse. A lecithin:sphingomyelin ratio

< 1.5 in amniotic fluid is predictive of neonatal respiratory distress syndrome. Persistently low O2
tension risk of PDA. Therapeutic supplemental O2 can result in retinopathy of prematurity
and bronchopulmonary dysplasia.
Risk factors: prematurity, maternal diabetes (due to fetal insulin), C-section delivery (
release of fetal glucocorticoids).
Treatment: maternal steroids before birth; artificial surfactant for infant.

Acute respiratory
distress syndrome

May be caused by trauma, sepsis, shock, gastric aspiration, uremia, acute pancreatitis, or
amniotic fluid embolism. Diffuse alveolar damage alveolar capillary permeability
protein-rich leakage into alveoli and noncardiogenic pulmonary edema (normal PCWP) A .
Results in formation of intra-alveolar hyaline membrane B . Initial damage due to release of
neutrophilic substances toxic to alveolar wall, activation of coagulation cascade, and oxygenderived free
radicals.

Acute respiratory distress syndrome. Near-complete

opacification of the lungs with obscured cardiomediastinal
silhouette.

Obstructive vs. restrictive lung disease

FEV1
8

Restrictive
FEV1
80%
FVC

FVC
8

fluid (clear, frothy) and thickened hyaline membranes (pink).

Obstructive
FEV1
< 80%
FVC

Normal
FEV1
= 80%
FVC

Lung volume (L)

Acute respiratory distress syndrome. Note the alveolar

5
4

5
4

5
4

FEV1

FVC

1
0

1
Time (sec)

FEV1

FVC

1
0

1
2
Time (sec)

1
2
Time (sec)

Note: Obstructive lung volumes > normal ( TLC, FRC, RV); restrictive lung volumes < normal. In both
obstructive and restrictive, FEV1 and FVC are reduced. In obstructive, however, FEV1 is more dramatically reduced
compared to FVC, resulting in a FEV1/FVC ratio.

Pulmonary
hypertension

Normal pulmonary artery pressure = 1014 mmHg; pulmonary hypertension 25 mmHg at

rest. Results in arteriosclerosis, medial hypertrophy, and intimal fibrosis of pulmonary arteries.
Primarydue to an inactivating mutation in the BMPR2 gene (normally functions to

inhibit vascular smooth muscle proliferation); poor prognosis.

Secondarydue to COPD (destruction of lung parenchyma); mitral stenosis ( resistance

pressure); recurrent thromboemboli ( cross-sectional area of pulmonary vascular bed);

autoimmune disease (e.g., systemic sclerosis; inflammation intimal fibrosis medial
hypertrophy); left-to-right shunt ( shear stress endothelial injury); sleep apnea or living at
high altitude (hypoxic vasoconstriction).
Course: severe respiratory distress cyanosis and RVH death from
decompensated cor pulmonale.

Sleep apnea

Repeated cessation of breathing > 10 seconds

during sleep disrupted sleep
somnolence.
Normal Pao2 during the
daytime
day. Nocturnal hypoxia
systemic/pulmonary
hypertension,
arrhythmias
flutter), and sudden
death. (atrial fibrillation/

Treatment: weight loss, CPAP, surgery.

Hypoxia EPO release
Obesity
hypoventilation syndromeobesity
erythropoiesis.
(BMI 30 kg/m2) hypoventilation
Pao2

Central sleep apneano respiratory effort.

Obstructive sleep apnearespiratory effort

against airway obstruction. Associated with

obesity, loud snoring.

Lungphysical findings
ABnORmAlITY

BREATh SOUnDS

Pleural effusion

Dull

Atelectasis (bronchial
obstruction)

Dull

Toward side of lesion

Spontaneous
pneumothorax

Hyperresonant

Tension pneumothorax

lesion
Bronchial breath sounds;
late inspiratory crackles

Hyperresonant

Away from side of

Consolidation
(lobar pneumonia,
pulmonary edema)

PERCUSSIOn

Dull

FREmITUS

TRAChEAl DEVIATIOn

Lung cancer is the leading cause of cancer

Lung cancer

death.
Presentation: cough, hemoptysis, bronchial
obstruction, wheezing, pneumonic coin
lesion on x-ray film or noncalcified nodule on
CT.
In the lung, metastases (usually multiple
lesions) are more common than 1
neoplasms. Most often from breast, colon,
prostate, and bladder cancer.
Sites of metastases from lung cancer
adrenals, brain, bone (pathologic fracture),
liver (jaundice, hepatomegaly).

SPHERE of complications:
Superior vena cava syndrome
Pancoast tumor
Horner syndrome
Endocrine (paraneoplastic)
Recurrent laryngeal symptoms (hoarseness)
Effusions (pleural or pericardial)
All lung cancer types except bronchial carcinoid
are associated with smoking.
Squamous and Small cell carcinomas are
Sentral (central).

TYPE

lOCATIOn

ChARACTERISTICS

Adenocarcinoma

Peripheral

Squamous cell
carcinoma

Central

Most common lung cancer in nonsmokers and

overall (except for metastases). Activating
mutations include k-ras, EGFR, and ALK.
Associated with hypertrophic osteoarthropathy
(clubbing).
Bronchioloalveolar subtype (adenocarcinoma in
Bronchioloalveolar
subtype: situ): CXR often shows hazy infiltrates similar to
grows along
alveolar septa pneumonia; excellent prognosis.

apparent
thickening
Keratin pearls and
Hilar mass arising from bronchus; Cavitation;
intercellular bridges A .
Cigarettes; hyperCalcemia (produces PTHrP).

Small cell (oat cell)

carcinoma

Central

Undifferentiated very aggressive.

May produce ACTH, ADH, or Antibodies
against presynaptic Ca2+ channels (LambertEaton myasthenic syndrome). Amplification of
myc oncogenes common. Inoperable; treat with
chemotherapy.

Neoplasm of
neuroendocrine
Kulchitsky cells
small dark blue cells B .

Large cell carcinoma

Peripheral

Highly anaplastic undifferentiated tumor; poor

prognosis. Less responsive to chemotherapy;
removed prognosis;
surgically.metastasis ra
Excellent

Pleomorphic giant cells.

Symptoms usually due to mass efre.

carcinoid syndrome (5-HT secrefect; occasionally
tion
diarrhea, wheezing).
flushing,

Nests
neuroendocrine
cells;ofchromogranin
A .

carcinoid

Bronchial
tumor

Squamous cell carcinoma. Note sheets of large,

dysplastic squamous cells (arrows) surrounding dark, pink
keratin pearls (lower right).

hISTOlOgY

Small cell carcinoma. Sheets of dark purple tumor cells

with nuclear molding, high mitotic rate, necrosis, and salt
and pepper neuroendocrine-type chromatin.

Mesothelioma

Malignancy of the pleura associated with

asbestosis. Results in hemorrhagic
pleural effusions and pleural thickening.

Pancoast tumor

Carcinoma that occurs in apex of lung may

affect cervical sympathetic plexus, causing
Horner syndrome (ipsilateral ptosis, miosis,
and anhidrosis), SVC syndrome, sensorimotor
deficits, and hoarseness A .

Psammoma bodies seen on histology.

A
Superior vena cava
syndrome

Pancoast tumor. Chest CT demonstrates mass (arrow) at

the left lung apex.

An obstruction of the SVC that impairs blood drainage from the head (facial plethora), neck
(jugular venous distention), and upper extremities (edema). Commonly caused by
malignancy and thrombosis from indwelling catheters. Medical emergency. Can raise
intracranial pressure (if obstruction severe) headaches, dizziness, and risk of
aneurysm/rupture of intracranial arteries.

Pneumonia
TYPE

TYPICAl ORgAnISmS

Lobar

S. pneumoniae most frequently, also

Legionella, Klebsiella

Intra-alveolar exudate consolidation;

may involve entire lung A B .

Bronchopneumonia

S. pneumoniae, S. aureus, H. influenzae,

Klebsiella

Acute inflammatory infiltrates from

bronchioles into adjacent alveoli; patchy
distribution involving 1 lobe C .

Interstitial (atypical)
pneumonia

Viruses (influenza, RSV, adenoviruses),

Mycoplasma, Legionella, Chlamydia

Diffuse patchy inflammation localized to

interstitial areas at alveolar walls; distribution
involving 1 lobe D . Generally follows a
more indolent course.

Lung abscess
A

Lobar pneumonia. Dense right upper lobe consolida

with branching air-bronchograms; sharp inferior margintion

represents the horizontal fissure.

Bronchopneumonia. Note neutrophils in the alveolar

spaces.

Localized collection of pus within parenchyma.

Caused by: bronchial obstruction (e.g.,
cancer) or aspiration of oropharyngeal
contents (especially in patients predisposed to
loss of consciousness [e.g., alcoholics or
epileptics]).

ChARACTERISTICS

Bronchopneumonia (left) and lobar pneumonia

(right). Gross specimens show typical consolidation
patterns.

Interstitial pneumonia. Coarse bilateral reticular opacities,

worse on the right.

Air-fluid levels A often seen on CXR. Often

due to S. aureus or anaerobes (Bacteroides,
Fusobacterium, Peptostreptococcus).

Pleural effusions

Excess accumulation of fluid between the two pleural layers A restricted lung expansion
during inspiration.

Transudate

protein content. Due to CHF,

nephrotic syndrome, or hepatic
cirrhosis.

Exudate

protein content, cloudy. Due to malignancy,

pneumonia, collagen vascular disease, trauma
(occurs in states of vascular permeability).
Must be drained in light of risk of infection.

Lymphatic

Also known as chylothorax. Due to thoracic

duct injury from trauma, malignancy. Milkyappearing fluid; triglycerides.

A
Pneumothorax

Spontaneous
pneumothorax
Tension
pneumothorax

Pleural effusion. Blunting of the left costophrenic angle

(arrow) due to fluid in the pleural space.

Accumulation of air in the pleural space A . Unilateral chest pain and dyspnea, unilateral chest
expansion, tactile fremitus, hyperresonance, diminished breath sounds, all on the affected
side.
Accumulation of air in the pleural space A . Occurs most frequently in tall, thin, young
males because of rupture of apical blebs.
Usually occurs in setting of trauma or lung infection. Air is capable of entering pleural space but
not exiting. Trachea deviates away from affected lung
B.

Pneumothorax. CT shows

collapsed left lung.

and rightward mediastinal shift.

Tension
pneumothorax.
Note the
hyperlucent
lung
field
with low
left hemidiaphragm
(below
the field left
of view)