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;
maycause superimposed bacterial infection, most commonly S.
pneumoniae, H. influenzae, and M. catarrhalis.
ARhinosinusitis. Coronal CT of the sinus shows bilateral
maxillary sinusitis (yellow arrows) and unrelated nasal septal
deviation (red arrow).
602seCtioN i i iRespi R at o R y R E S P I R AT ORYPAT h O lO g
Y
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)
Approximately 95% of pulmonary emboli arise from deep leg
veins.Homan signdorsiflexion of foot calf pain. Use heparin for
prevention and acutemanagement; 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
triadof hypoxemia, neurologic abnormalities, and petechial
rash.Amniotic fluid embolican lead to DIC, especially
postpartum.
Pulmonary embolism. Note large embolus (arrows) in theGas
embolinitrogen bubbles precipitate in ascending divers; treat with
hyperbaric oxygen.
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
.
B pulmonary artery.
C Pulmonary thromboembolus. Lines of Zahn are interdigitating
areas of pink (platelets, fibrin) and red (RBCs)found only in
thrombi formed before death. Help distinguish pre- and postmortem
thrombi.
Obstructive lung diseases
Obstruction of air flow resulting in air trapping in the lungs.
Airways close prematurely at highlung volumes RV and FVC. PFTs:
FEV1, FVC FEV1/FVC ratio (hallmark), V/Qmismatch. Chronic, hypoxic
pulmonary vasoconstriction can lead to cor pulmonale.
TYPE PAThOlOgY OThERChronic 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 (early- onset hypoxemia due to
shunting), late-onset dyspnea, CO2 retention. Emphysema (pink
puffer, barrel- shaped chest)
Enlargement of air spaces, recoil, compliance, DLCO resulting
from destruction of alveolar walls A .Two types:
Centriacinarassociated with smoking B . Panacinarassociated with
1-antitrypsin deficiency.
elastase activity loss of elastic fibers lung
compliance.Exhalation through pursed lips to airway pressure and
prevent airway collapse during respiration.
Bby 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.
AsthmaBronchial hyperresponsiveness causes reversible
bronchoconstriction. Smooth muscle hypertrophy, Curschmann spirals
(shed epithelium forms mucus plugs), and Charcot-Can be triggered
by viral URIs, allergens, and stress.Test with methacholine
challenge. Findings: cough, wheezing, tachypnea,
Leyden crystals (formed from breakdown ofdyspnea, hypoxemia, I/E
ratio, pulsus
eosinophils in sputum).paradoxus, mucus plugging.
BronchiectasisChronic necrotizing infection of bronchiAssociated
with bronchial obstruction, poor
permanently dilated airways, purulentciliary motility (smoking),
Kartagener
sputum, recurrent infections, hemoptysis.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.
PneumoconiosesCoal workers pneumoconiosis, silicosis, and
asbestosis risk of cor pulmonale and Caplan syndrome (rheumatoid
arthritis and pneumoconioses with intrapulmonary nodules).
AsbestosisAssociated with shipbuilding, roofing, andAffects
lower lobes.
Bplumbing. Ivory white, calcified pleuralAsbestos (ferruginous)
bodies are golden-brown
plaques A are pathognomonic of asbestosfusiform rods resembling
dumbbells B .
exposure, but are not precancerous. Associatedwith an incidence
of bronchogenicAsbestos is from the roof (was common ininsulation),
but affects the base (lower lobes).
carcinoma and mesothelioma.Silica and coal are from the base
(earth), but
Asbestosis. Note white, calcified pleural plaquesaffect the roof
(upper lobes).
A (arrows).
Coal workerspneumoconiosis
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
oxygen-derived free
radicals.Acute respiratory distress syndrome.
Near-completeABopacification of the lungs with obscured
cardiomediastinal silhouette.
Acute respiratory distress syndrome. Note the alveolar fluid
(clear, frothy) and thickened hyaline membranes (pink).
Obstructive vs. restrictive lung disease
NormalFEV1FVC = 80%
8 8
ObstructiveFEV1FVC < 80%
FEV1 FVC
RestrictiveFEV1FVC 80%
8
7 FEV1 FVC 7 7
6 6 6
Lung volume (L)5 5 5
4 4 4
3 3 3
FEV1 FVC
2 2 2
1 1 1
0 1 2 3 0
1 2 3 0
1 2 3Time (sec) Time (sec) 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 apneaRepeated cessation of breathing > 10 seconds
during sleep disrupted sleep daytimeTreatment: weight loss, CPAP,
surgery. Hypoxia EPO release erythropoiesis.
somnolence. Normal Pao2 during the day. Nocturnal hypoxia
systemic/pulmonaryhypertension, arrhythmias (atrial
fibrillation/Obesity hypoventilation syndromeobesity(BMI 30 kg/m2)
hypoventilation Pao2and Paco2 during waking hours.
flutter), and sudden death.
Central sleep apneano respiratory effort.Obstructive sleep
apnearespiratory effort against airway obstruction. Associated with
obesity, loud snoring.
Lungphysical findings
ABnORmAlITY BREATh SOUnDS PERCUSSIOn FREmITUS TRAChEAl
DEVIATIOn
Pleural effusion Dull
Atelectasis (bronchial obstruction) Dull Toward side of
lesion
Spontaneous pneumothorax Hyperresonant
Tension pneumothorax Hyperresonant Away from side of lesion
Consolidation (lobar pneumonia, pulmonary edema)Bronchial breath
sounds; Dull late inspiratory crackles
Lung cancer Lung cancer is the leading cause of 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 multiplelesions) are
more common than 1 neoplasms. Most often from breast, colon,
prostate, and bladder cancer.
carcinoid Excellent prognosis; metastasis ra Symptoms usually
due to mass ef carcinoid syndrome (5-HT secrediarrhea,
wheezing).Sites of metastases from lung canceradrenals, brain, bone
(pathologic fracture), liver (jaundice, hepatomegaly).
SPHERE of complications: Superior vena cava syndrome Pancoast
tumorHorner syndromeEndocrine (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 areSentral
(central).
TYPE lOCATIOn ChARACTERISTICS hISTOlOgY
AdenocarcinomaPeripheral Most common lung cancer in nonsmokers
andoverall (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 thickeningof alveolar walls.
Squamous cell carcinomaCentralHilar mass arising from bronchus;
Cavitation;Cigarettes; hyperCalcemia (produces PTHrP).Keratin
pearls and intercellular bridges A .
Small cell (oat cell)carcinomaCentralUndifferentiated very
aggressive.May produce ACTH, ADH, or Antibodies against presynaptic
Ca2+ channels (Lambert-Eaton myasthenic syndrome). Amplification of
myc oncogenes common. Inoperable; treat with chemotherapy.Neoplasm
of neuroendocrine Kulchitsky cells small dark blue cells B .
Large cell carcinomaPeripheralHighly anaplastic undifferentiated
tumor; poor prognosis. Less responsive to chemotherapy; removed
surgically.Pleomorphic giant cells.
Bronchial tumorre.fect; occasionally tion flushing,Nests of
neuroendocrine cells; chromogranin A .
BASquamous cell carcinoma. Note sheets of large, dysplastic
squamous cells (arrows) surrounding dark, pink keratin pearls
(lower right).
Small cell carcinoma. Sheets of dark purple tumor cellswith
nuclear molding, high mitotic rate, necrosis, and salt and pepper
neuroendocrine-type chromatin.
MesotheliomaMalignancy of the pleura associated with asbestosis.
Results in hemorrhagic pleural effusions and pleural
thickening.
Psammoma bodies seen on histology.
Pancoast tumor Carcinoma that occurs in apex of lung may affect
cervical sympathetic plexus, causing Horner syndrome (ipsilateral
ptosis, miosis, and anhidrosis), SVC syndrome,
sensorimotordeficits, and hoarseness A .
APancoast tumor. Chest CT demonstrates mass (arrow) at the left
lung apex.
Superior vena cava syndrome
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.
PneumoniaTYPE TYPICAl ORgAnISmS ChARACTERISTICSLobar S.
pneumoniae most frequently, also Legionella,
KlebsiellaBronchopneumonia S. pneumoniae, S. aureus, H. influenzae,
Klebsiella
Intra-alveolar exudate consolidation; may involve entire lung A
B .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.
Lobar pneumonia. Dense right upper lobe consolida with branching
air-bronchograms; sharp inferior marginrepresents the horizontal
fissure.C Bronchopneumonia. Note neutrophils in the alveolar
spaces.BA tion
Bronchopneumonia (left) and lobar pneumonia (right). Gross
specimens show typical consolidation patterns. ,
DInterstitial pneumonia. Coarse bilateral reticular opacities,
worse on the right.
Lung abscess
A
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]).
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. Milky- appearing
fluid; triglycerides.
APleural effusion. Blunting of the left costophrenic
angle(arrow) due to fluid in the pleural space.
PneumothoraxAccumulation 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.Spontaneous pneumothoraxTension pneumothorax
Accumulation of air in the pleural space A . Occurs most
frequently in tall, thin, young males because of rupture of apical
blebs.
B .B Tension pneumothorax. Note the hyperlucent left lung field
with low left hemidiaphragm (below the field of view)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
A Pneumothorax. CT shows collapsed left lung.
and rightward mediastinal shift.