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74 Cards in this Set

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Bronchiectasis
Path: irreversible distension of the bronchi; chronic necrotizing infection, affects bronchi and bronchioles --> abnorm dilatation of airways, basal segments have worst drainage
Causes:
1. Obstructive bronchiectasis – localized (distal to obstruction), anything that plugs the bronchus (mucus, tumor, inhaled object, etc)
2. Non-obstructive bronchiectasis – localized or generalized, caused by:
a. infection (eg RSV)
b. defect in immune defenses
i. Kartegener Syndrome --> inherited syndrome where cilia are immobile so pts are at risk for recurrent
respiratory infections (triad of changes: dextrocardia +/- situs inversus, bronchiectasis, sinusitis)
ii. Hypogammaglobulinemia --> absence of IgA
iii. other immune compromise)
HISTOPATH
dilation of airways
severe necrotizing acute and chronic inflamm
sq metaplasia, fibrosis, abscess
CLIN
cough, fever, abundant purulent sputnum, obstructive resp insuff (dyspnea/cyanosis), cor pulmonale, metastatic brain abscess, amyloidosis
Lobar Pneumonia
Pneumonia – generic inflammation and consolidation of pulmonary parenchyma.
lobar pneumonia – consolidation of entire lobe (classic cause = strep pneumoniae (pneumococcus, klebsiella)
bronchopneumonia – scattered foci in one or several lobes
Path: viral infn --> thin, watery bronchial secretions --> sweeps S. pneumo (NF of nasopharynx) into alveoli and provides nice environment to grow.
Presentation: acute onset fever and chills. Often community acquired.
Rusty colored hemoptysis. May have pain if pleura is involved.
Histo: lots of acute inflammatory cells (neutrophils aka PMNs –
segmented nuclei) in the alveoli.
With treatment, this resolves to normal lung architecture.
red hepatization (PMN and RBCs)
gray hepatization (fibrinopurulent exudate)
Tuberculosis
Primary tuberculosis
Gross: parenchymal lesion = Ghon lesion + hilar lymph involvement = Ghon complex - parenchymal subpleural lesion and caseous LN draining the focus, caseating granuloma w acid fast bacilli, usu asx w fibrosis adn calcificiation of lesion, old calcified lesion may contian infective organisms for decades
Histo caseating/necrotizing granulomatous formation.
[RIGHT] Secondary Tuberculosis (Cavitary & Miliary TB)
rare progression w cavitation, TB pneumonia, miliary TB
Invasive Aspergillosis
Path: infection with Aspergillus (fungus)
3 types:
1. invasive aspergillosis – almost exclusively opportunistic. invades blood vessels -->
occlusion/thrombosis --> lung tissue infarction
2. aspergilloma – “fungus ball”, grows in previously formed cavity; usually asymptomatic
3. allergic bronchopulmonary aspergillosis – unusual immune response to aspergillus in asthmatics
[RIGHT] invasive aspergillosis caused the area of
necrosis and infarction and central cavitation.
Aspergillus spp.
Septae hyphae branching @ 45 degrees
Causes allergic bronchopulmonary aspergilosis
Aspergillomas (preexisting cavities)
Invasive infection in immunosuppressed patients
Pneumocystis (carinii) jiroveci
silver stain of pneumocystitis cysts – “target shaped”
Path: infection is associated w/ immunosuppression – most common causes of infectious pneumonia in AIDS pts.
[RIGHT] alveoli filled w/ foamy proteinaceous exudates --> contains the organism interstitium is thickened, contained inflammatory infiltrates (plasma cells &
lymphocytes)
Cytomegalovirus Pneumonitis
one example of viral pneumonia – features: interstitial infiltrates, necrosis of Type I pneumocytes, sometimes hyperplasia of Type II pneumocytes, hyaline membrane formation CMV features – interstitial infiltrate (lymphocytes), alveoli lined w/ Type II cells, alveolar cells infected have 3 key features: gigantic, single basophilic
nuclear inclusion, and many cytoplasmic basophilic inclusions. Occurs in immunocompromised pts.
Lung Abscess
Causes: most common = anaerobic bacteria from oropharynx (assoc w/ depressed consciousness); requires 2 necessary conditions: 1) poor hygiene/periodontal disease to get high bacteria levels and 2) impaired cough
* alcoholics often have both.
Presentation: cough, fever, large amounts of foul-smelling sputum, pleuritic chest pain, hemoptysis
Histo: liquefactive necrosis w/ lots of neutrophils over time, fibrous wall forms around it.
focal suppurlative inflamm w tissue necrosis
staph, strp, g neg, anaerobe
complications: extentions into pleural cavity, hemorrhage, septic embolism, sec amyloidosis
Diffuse Alveolar Damage:
Terminology – Diffuse alveolar damage refers to the pattern of injury
Acute Respiratory Distress Syndrome = clinical syndrome that occurs w/ DAD
Causes: non-thoracic trauma, infection, aspiration, drugs
Acute (Exudative) Phase
Path: edema, +/- hemorrhage, fibrinous exudate, hyaline membrane, mild interstitial inflamm, fibrin microthromi; injury to endothelial cells --. protein rich fluid leaks into interstitium & destroys Type I pneumocytes --> now
can leak into alveolar spaces --> proteins form fibrin precipitates --> hyaline membranes; Type II pneumocytes
proliferate & replace Type I cells; inflammatory cells accumulate in interstitium.
Patients may either recover or progress to end-stage fibrosis (honeycomb lung)
Organizing Phase (repair)
type II pnemocyte hyperplasia, sq metaplasia, interstitial/airspace fibroblastic prolif (fibrosis)
fibroblast proliferation in alveolar walls & can still see hyaline membranes of acute phase.
This has the potential to return to normal lung tissue, but some pts will progress to end-stage fibrosis.
Alveolar Proteinosis (aka Lipoproteinosis)
Pts tend to have: compromised immunity, cancer (esp hematologic – could cause Ab to form against GF which results in impaired macrophage fxn), respiratory infections, inorganic dust exposure
Histo: interstitial architecture intact, with little/no inflammation
alveoli are filled w/ eosinophilic, lipid-rich material – surfactant (macrophages regulate surfactant
production, so macrophage dysfunction --> excess surfactant production)
note: looks like pulmonary edema, so be sure to read info provided.
Goodpasture Syndrome
Triad: 1. diffuse alveolar hemorrhage
2. glomerulonephritis
3. cytotoxic antibody to a component of basement membranes
Histo: air spaces are filled w/ RBC (fresh, eosinophilic), hemosiderin-laden
macrophages (suggests previous intra-alveolar hemorrhage)
[RIGHT] immunofluorescence highlights IgG Antibodies
Eosinophilic Pneumonia
Presence of eosinophils w/in alveolar spaces.
Multitude of causes: 1. idiopathic
2. secondary eosinophilic pneumonia (due to an underlying disease)
-infections (esp parasites), drug hypersensitivity or allergic rxns, Churg-Strauss syndrome, asthma
Asthma
Histo: secretions in bronchial lumen; smooth m hyperplasia in bronchial wall; mucus gland hyperplasia
paroxysmal contraction of bronchial sm muscle in response to various stimuli
inc mucous secretion
rev airway narrowing
EXTRINSIC
atopic (allergic) - Type I (IgE)
occupational - Type I
allergic bronchopulm aspergillosis - type I and III
INTRINSIC
nonatopic (nonreaginic) - unknwn
Pharm (asprin) - dec PG, inc LKT
alltypes of asthma may be precipitated by cold, stress, excercise
Gross: overinflated lungs, patchy atelectasis, airways w mucus plugs
Histopath: edema, inflamm w eosinophils (bronchitis-olitis), hypertrophy of sm muscle and mucous glands; Curschmann's spirals (whorled mucous plugs), Charcot-Leyden crystasl ( of eosin. membranes)
CLIN:
acute dyspnea, wheez, rev (spont or tx)
Chronic Bronchitis
Persistent cough w sputnum production for 3 mo in at least 2 consecuative yrs
Chronic bronchitis is almost always associated w/ smoking
Path: smoke --> irritation to bronchial mucosa --> squamous metaplasia
Histo: hyperplasia & hypertrophy of mucus cells, increase in mucus glands: serous glands --> chronic productive cough bronciolitis, secondary infections
Reid index > .5 – equals width of mucus glands / total wall thickness
hyperemia and edema of mucous membrane
mucinous secretions/casts filling airways
mucous gland hyperplasia
bronchial/bronchilar mucous plugging
bronchial epi w sq and goblet-cell metaoplasia, inflamm, fibrous
BLUE BLOATER: copious mucoid sputum, hypercapnia, cyanosis, pulm HTN, cor pulmonale (RHF), periph edema, secondary bact inf, episodes of astma
Emphysema
Causes: 1. most often smoking: causes increases # neutrophils which release proteases +/- inhibits alpha-1 antitrypsin
2. more rarely hereditary alpha-1 antitrypsin deficiency (young non-smoker)
Histo: air-spaces are distended throughout the lung due to
widespread destruction of lung parenchyma; alveolar septa are thin
and delicate
dec gas-exchange area
red diffusion capacity
sm airway collapse
airflow obstruction
PINK PUFFER: exertional dyspnea, min cough, min sputnum, use accessory musc, astheic wasting, barrel chest, hyperresonance, depressed diaphragm, inc static lung volume, inc resitance to air flow, minimal blood-gas, changes
Hypersensitivity Pneumonitis
Bronchocentric inflammatory changes (bronchocentric – caused by something inhaled)
Histo: poorly formed non-caseating granulomas are present in 2/3 of cases.
Anthracosilicosis
Pneumoconiosis – inhalation of inorganic dusts (carbon, silica, beryllium, asbestos)
Anthracosilicosis – a pneumoconiosis occurring due to inhalation of both silica and carbon.
[LEFT] black material is fibrosis containing carbon particles (silica --> fibrosis; carbon doesn’t causes fibrosis as much)
Fibrous plaque:
- asbestos caused fibrosis to form on pleura
- pearly white color
- smooth and/or nodular surface
Sarcoidosis
Etiology is unknown – related to hyperresponsive CD4 cells.
Occurs more often in African Americans, Scandinavians, and Irish.
Histo: multiple non-caseating granulomas (vs Wegners = caseating) – involves interstitium rather than air spaces,
contains macrophages and giant cells centered around bronchi and blood vessels (! vasculitis) & follows lymphatics
- asteroid bodies – inclusions w/in giant cells w/ star-like appearance
- schaumann bodies – calcifications w/in giant cells
Lab: would expect no infectious microorganisms, !ACE, !urinary Ca
CXR: may be picked up incidentally in asymptomatic pt, usually bilat hilar
adenopathy +/- interstitial pulmonary infiltrates
Dx usually made on biopsy
CLINICAL MANIFESTATIONS
May be asymptomatic (incidental on chest x-ray)
Isolated cutaneous or ocular lesions
Peripheral lymphadenopathy / hepatosplenomegaly
Insidious onset with respiratory and constitutional symptoms (fever, night sweats, weight loss)
Acute onset with fever, erythema nodosum, polyarthritis
Usually lung involvement with hilar adenopathy (characteristic chest x-ray)
Elevated serum IgG and calcium
Mikulicz’s syndrome: Sarcoidosis with ocular and salivary gland involvement
Usual Interstitial Pneumonitis (UIP)
Histo: *key* is patchy lung remodeling – both spatial and temporal heterogeneity;
frequently subpleural distribution.; given fibrosis and dilation, gross appearance is “honeycomb”
Etiology is unknown; unresponsive to treatment, pts --> respiratory distress
Cryptogenic Organizing Pneumonia (COP) aka Bronchitis Obliterans Organizing Pneumonitis (BOOP)
Many etiologies, “idiopathic” is possible as well, but a cause is usually uncovered.
Histo: bronchiole lumen is filled w/ tissue w/ loose, fibrous, organizing
appearance. *key* is patchy fibrosis w/in the lumen of the air spaces of any size.
Tx: steroids is successful.
BOOP
Common response to:
infection, inflammation, toxins, drugs, collagen-vascular disease
HISTOPATHOLOGY
Loose fibrous plugs within bronchioles
Organizing pneumonia
CLINICAL MANIFESTATIONS
Cough, Dyspnea, Resent respiratory tract infection, Gradual improvement/steroid therapy
Desquamative Interstitial Pneumonia (DIP)
Almost exclusively seen in cigarette smokers; gets better if pt quits + steroid therapy.
Histo: lung architecture maintained
macrophages (golden-brown pigmented and flecked black from cigarettes) w/in the alveoli
diffuse alveolar septae undergo fibrosis chronic inflammation of interstitium
Lymphoid Interstitial Pneumonia (LIP)
Associated with these conditions: HIV, Sjogren’s syndrome, SLE, RA, chronic active hepatitis
Histo: major thickening of interstitium (much more interstitium than airspace)
lots of inflammatory cells: lymphocytes, plasma cells, macrophages
Lymphoid hyperplasia of mucosa associated lymphoid tissue may occur, and rarely may progress to
malignant lymphoma.
Eosinophilic Granuloma (Langerhans cell histiocytosis)
LCH can occur in many parts of the body; this is the adult pulmonary presentation.
RF: heavily associated w/ cigarette smoking, more commonly occurs in women.
CXR – numerous bilat. nodules (<2cm) – a discrete finding w/in
surrounding normal lung tissue
Histo: old lesions undergo cystic degeneration and fibrosis.
Langerhans cells under EM [RIGHT] contain Birbeck granules
Pneumothorax is a possible presentation.
Pulmonary Lymphangiomyomatosis
Path: abnormal smooth muscle proliferation, affecting lung, mediastinal, retroperitoneal LNs and major lymphatic ducts.
Occurs in women of childbearing age under some hormonal control (oophrectomy or hormone therapy may improve condition)
Gross: looks like emphysema (is pt a smoker or AAT def?)
Histo: smooth muscle cells are haphazardly arranged (lack parallel orientation)
Theorized to be a form of tuberous sclerosis.
Wegener Granulomatosis
A systemic disease. 2 main pulmonary features: granulomas and vasculitis.
Path: autoimmune d/o w/ production of Abs against neutrophils --> neutrophil activation --> multiple pathologic manifestations.
Respiratory Manifestations: cough, hemoptysis, pleuritis
Head & Neck: sinusitis, nasal disease, otitis media, hearing loss,
Other: arthralgias, fever, skin lesions, weight loss, peripheral subglottic stenosis, ear pain, cough, oral lesions.
neuropathy, CNS changes, pericarditis
Kidneys: renal failure
[LEFT] Granuloma – granulomatous inflammation (mix of
inflammatory cells), central necrosis that is oddly shaped
(“geographic necrosis”), fibrosis
[RIGHT] Vasculitis – elastin stains black, both internal and external
elastic laminae are disrupted by inflammation of vessel wall.
Churg-Strauss Syndrome
An artery (not necessarily the lung).
Characteristics changes of asthma – syndrome defined by: asthma
peripheral blood eosinophilia
vasculitis (especially w/ eosinophils, Systemic vasculitis
Often associated with Asthma
Anti-neutrophilic cytoplasmic antibodies, Eosinophilic pneumonia, eosinophilic vasculitis, Treatment: Steroids
Pulmonary Hamartoma
2 key components: cartilage and respiratory epithelium.
Gross: Subpleural location, pretty well circumscribed
and demarcated. White color = cartilage composition.
This is benign and there is some debate over whether it is
even neoplastic. They can occur elsewhere, and usually
asymptomatic.
Squamous Cell Carcinoma
Most common paraneoplastic syndrome associated with squamous cell carcinoma is hypercalcemia secondary to tumor production of a parathyroid-like hormone.
Gross: Endobrachial lesion (may cause obstructive of SVC) -->
central location; border is irregular and it is infiltrating across
bronchial wall --> malignant.
Histo: keratin pearls (squamous cell)
One of the 2 main cancers associated w/ cigarette smoking (other is small cell carcinoma of the lung).
Adenocarcinoma
Among lung cancers, a non-smoker would be most likely to develop an adenocarcinoma.
Gross: peripheral location, characteristics of malignancy (irregular border, infiltrates surrounding tissue).
Histo: columnar cells organizing into glandular spaces ! mucin
Bronchioloalveolar carcinoma – subtype that grows along pre-existing
lung architecture
Small Cell Carcinoma of the Lung
Strongly
Strongly associated w/ smoking. Multiple paraneoplastic syndromes associated. Very aggressive.
Histo: - lesion is at a central location.
- very cellular w/ little differentiation (anaplastic) – no gland formation, no keratin production, no mucin production.
derived from neuroendocrine cells (can be used to mark tumor for dx)
Carcinoid Tumor
May occur in non-smokers. A paraneoplastic syndrome:
Carcinoid syndrome --> serotonin
Gross: more circumscribed. shown here, tumor occludes
bronchus --> pneumonia occurs distal to the occlusion.
Histo: tends to form central lesions. uniform appearance.
Also neuroendocrine, but less aggressive than small cell carcinoma.
Can metastasize, but less likely.
Mesothelioma
Associated w/ asbestos exposure
Gross: thickened pleura
Metastatic Lung Cancer
many types of cancers frequently metastasize to the lung
Gross: multiple hard lesions
congenital cysts
most common
cystic spaces lined by bronchial type epithelium
contain mucinous secretions or air
anywhere in lung
connction w airway may not be apparent
complications
infection (abscess)
rupture (hemorrhage, hemoptysis, pneumothorax)
bronchopulmonary sequestration
congenital anomaly
segment of lung tissue without connection to airway system
blood supply from aorta or branches
A) extralobar sequestration
most common in infants
assoc w other congenital anomalies
outside the lung anywhere in thorax or mediastinum
B) intralobal sequestration
most common in adults
assoc w recurrent infections
wi lung parenchyma
Atelectasis
incomplete expansion of lung or collapseo fpreviously inflated lung
reduces oxygenation
predisposes to infection
obstructive (absorption)
compressive
patchy (micro-atelectasis)
contraction atelectasis
obstructive atelectasis
excessive secretion
asthma, chronic bronchitis
foreign body aspiration
blood
bronchial neoplasm
compressive atelectasis
expansion of pleural space by fluid (effusion = CHF, neoplasm), blood = rupture of aneurysm; by air = pneumothorax
patchy atelectasis
loss of surfactant
neonatal RDS
ARDS
contraction atelectasis
lung parenchymal fibrosis
pleural fibrosis
irreversible
pulmonary congestion and edema
hemodynamic
cause:
inc hydrostatic pressure (LHF, volume overload, PV obstruction, etc)
dec oncotic pressure, hypoalbuminemia
lymphatic
Path: accum of fluid in depndnt basal regions of lower lobes, gross = heavy, wet lungs
Hist: engorged capillaries, granular pink precipitate in alv spaces, microhemorrhages, hemosiderin-laden mphage, interstitial fibrosis (chronic)
pulmonary congestion and edema
due to microvascular injury
capillary hydrostatic pressure not elevated
primary inj to vasc endothelium or alv epitheluum
leakage of fluids into interstitial space and then alv space
cause:
infection, inhaled gas, liquid asp, drugs/chem, shock, trma, sepsis, radiation, pancreatitis, uremia, TTP, DIC
ARDS
acute respiratory failure
dec lung compliance
hypoxemia refractory to oxygen
bilat radiologic opacities
frequent superimposed infections
progression to multi-organ failure
mortality over 50%
Pulmonary embolism
chest pain, tachypnea, dyspnea, hemoptysis, unremarkable CXR
most common source = DVT
other: pelvic v. thrombi, foreign body emboli, bonemarrow emboli, amniotic fluid emboli, air
predisposing factos:
Sequele:
resp compromise - ventilated segment not perfused
hemodynamic compromise - inc resistance to pulm blood flow (vasoconstriction)
outcome depends on size of embolus and adequacy of bronchial circ
lrg emboli - saddle embolus = sudden death, CV collapse
sm emboli - asx, transient chest pain, hempptysis
pulm infarction: hemorrhage, pleural based, wedge shaped, fibrous exudeate on pleural surface, contracted scar w resolution, predom lower lobes
Tx: fibronolytic agents
Dx: perfusion lung scan, pulm angiography
venous stasis, hypercoagulable state, endothelial injry
thromboemboli
RF: immobile, obesity, pregnancy, estrogenic OC, herediatry clotting D/O
pulm HTN
inc pulm vasc resitance leading to elev pulm arterial pressure
primary and secondary
histopath: arterosclerosis, lrg elastic arteris, concentric intimal fibrosis and medial hypertrphy, medium-sized arteries and sm arterioles, thrombotic arteriopathy (eccentric intimal fibrosis and recanalization), veno-occlusive disease (venous sclerosis and muscularization)
primary pulm HTN
uncommon
kids, young women
progression to severe resp insuff, cor-pulmonale, death
plexogenic pulm arteriopathy: prom in primary HTN and congenital heart disease w L--> R shunt
pathogen unknwn,
dx by exclusion
tx: vasodilators, heart-lung transplant
secondary HTN
COPD
interstitial lung disease
L-sided heart disease
recurrent PE
COPD
chronic/recurrent airflow obstruction
narrowed airways, loss of elastic
cause:
chronic bronchitis (bronchus), bronchiectasis (bronchus), asthma (bronchus), bronchioltis (bronchioles), emphysema (acinus)
atopic asthma
most common
triggered by environmental agents
childhood
fam hx
other atopic disease (allerguc rhinitis, urticaria)
IgE mediated hypersensitivity rxn
Acute ph:
mast cells (histamine, chemotactic) and secondary mediators (LKT, PG D2, ctk) --> bronchospasm, edema, mucus secretion
late ph:
recruit neutrophils, basophils, eosinophils, monocytes, persistent bronchospasm, edema, epi cell necrosis
nonatopic asthma
resp tract infection, chem, drugs
no fam hx
no IgE hypersensitivity rxn
etiology unknw
status asthmaticus
hypoxia, hypercapnia, acidosis, fatal
Kartagener syndrome
inherited AR defect w immotile cilia (absecne of dynein arms)
dextocardia, sinusistis, bronchiectasis
recurrent resp tract inf
sterility (abnorm cilia
assoc w bronchiectasis
bronchopneumonia
cause:
staphylococci, streptococci, pneumococci, H inf, pseudomos, coliform
Gross;
focal patchy palpable consolidation an dsupprualtion
HISTOPATH:
acute suppurative exudate in airspaces and airways
abscess (aggressive disease)
infants, elderly
complete resolution or fibrous scarring
interstitial pneumonitis
peribronchiolar and interstitial inflamm wo consolidation (atyp pneumonia)
patchy, diffuse
interstitial edema and mononuclear (lymphs) infiltrate
alveolar damage w acute inflamm and hyaline membranes
may lead to ARDS
mycoplasma pneumonia
Atypical pneumonia
Tracheobronchitis
peribronchial, peribronchiolar and interstitial mononuclear inflammation

children & young adults
Ureaplasma urealyticum perinatal pneumonia
tuberculus granuloma
epitheloid cells
zone of FB and lymphocyte
langerhan's giant cells
central caseating necrosis
secondary pulm tuberculosis
reactiv of old TB
apices of lung (hi O2 pressure)
fever, nt sweat, wt loss, productive cough, hemoptysis)
dx: culture
histoplasma capsulatum
Small yeast
Narrow-based bud
Multiply within macrophages
Dx: direct visualization & capsular Ag in body fluids and urine
Endemic in Ohio and Mississippi river valleys and Caribbean (bird/bat droppings
coccidiodes immitis
Thick-walled nonbudding large spherule with endospores
Like Histoplasmosis and TB may present as asymptomatic pulmonary disease (60%), progressive pulmonary disease, or miliary disease
Endemic in SW US
blastomyces
Round to oval thick-wall yeast
Broad-based bud
Similar pathology with histoplasmosis and coccidiomycosis
Endemic in central and SE US
cryptococcus neoformans
Small yeast
Thick mucoid capsule (mucicarmine positive)
Cerebromeningeal dissemination from primary pulmonary focus
Harbored in GI tract of pigeons/birds
mucor
Broad irregular non-septae hyphae, 90 degrees brunching
Nasal, pulmonary, and disseminated infections
Diabetes / leukemia patients
diffuse interstitial lung disease
interstitial inflamm (alv septae)
dyspnea, dec diffusion capacity, ced lung vol, dec compliance (stiff lung), CXR = diffuse infiltrate = ground-glass shadow
pathogen:
inhaled/bloodborn toxin
epi/endo inj
recruit/active of inflamm cells
release of inj oxidantand ctk and FGF, IL-1
interstitial fibrosis and chr inflamm
Caplan's syndrome
RA and CWP
faster progression/more severe
nodular lesions w central necrosis and periph fibrohistiocytic inflamm
also in silicosis and asbestosis
silicosis
HISTOPATHOLOGY
Nodular fibrosis
Hyalinized whorls of collagen
Scant inflammation
Birefringent silica particles
Coalescence of nodules / large areas of dense scars (progression even after cessation of exposure)
Concomitant anthracosis
RADIOLOGY: Eggshell calcification on chest x-ray
asbestosis
Mineral fibers containing silica
curled flexible serpentines
straight stiff amphiboles (more pathogenic)
ferruginous bodies (iron coating)
Pathogenesis
Fibers ingested by macrophages
activation of macrophages and neutrophils
release of enzymes and fibrogenic cytokines
Deposition in interstitium and lymphatics
direct stimulation of fibroblast collagen
Diffuse interstitial fibrosis (asbestosis)
Pleural effusions / fibrous adhesions
Hyalinized fibrocalcific pleural-plaques
Strong association with malignant mesothelioma and bronchogenic carcinoma
Cigarette smoking acts synergistically increasing the risk of carcinoma (not mesothelioma)
Progressive fibrosis even after cessation of exposure
pulmonary alveolar proteinosis
CLINICAL MANIFESTATION
Cough
Sputum (chunks of gelatinous material)
Progressive respiratory difficulty
Diffuse pulmonary opacification on chest x-ray
HISTOPATHOLOGY
Alveolar spaces filled with dense, amorphous, PAS-positive, lipid containing, surfactant-like material
Hyperplastic pneumocytes
Focal necrosis
No inflammation
Impaired activity of alveolar macrophages with overproduction of surfactant (decreased GM-CSF)
Association with exposure to irritants and recurrent RTI (fungi/Nocardia)
Progressive respiratory insufficiency or resolution
Treatment: Repeated BALs
pulmonary alveolar proteinosis
CLINICAL MANIFESTATION
Cough
Sputum (chunks of gelatinous material)
Progressive respiratory difficulty
Diffuse pulmonary opacification on chest x-ray
HISTOPATHOLOGY
Alveolar spaces filled with dense, amorphous, PAS-positive, lipid containing, surfactant-like material
Hyperplastic pneumocytes
Focal necrosis
No inflammation
Impaired activity of alveolar macrophages with overproduction of surfactant (decreased GM-CSF)
Association with exposure to irritants and recurrent RTI (fungi/Nocardia)
Progressive respiratory insufficiency or resolution
Treatment: Repeated BALs
pancoast's tumor
Superior sulcus tumor
2-5% patients with bronchogenic cancer
Usually squamous cell, rarely small cell
T3 lesion by definition, with or without nodal involvement
Usual initial symptom is pain, sometimes upper extremity weakness
Invasion of brachial plexus about 40% incidence at presentation
Superior Vena Cava Syndrome
SVC obstruction most commonly by bronchogenic carcinoma
early sxs of facial fullness, facial and arm edema
dilated veins over anterior chest, jugular veins, then veins of the arm and face
usually responds nicely to treatment of underlying cancer (radiation or chemotherapy depending on type)
bronchial carcinoid
low-grade malignant tumors
thought to be derived from neurosecretory cell line
not strongly linked to smoking, and occurs more in younger patients
“atypical” carcinoid has a worse prognosis
usually cured by resection
Account for about 2% of lung cancers
SIADH
Most common paraneoplastic syndrome in SCLC
Approx 5-10% patients present with SIADH
Additional 40-50% can be shown to have subclinical abnormalities compatible with SIADH (radioimmunoassay for ADH)
Source of ADH may be primary tumor or its met
PTH-like hormone secretion
Hypercalcemia is more common from this cause than from skeletal mets
Unusual in SCLC - and if present consider presence of mixed (NSCLC component or other cause of hypercalcemia)
Eaton-Lambert Syndrome
Clinical picture is similar to MG with proximal easy fatigability > muscle weakness
Symptoms more prominent in lower extremities
EMG clearly distinguishes from MG
facilitation of muscular action potentials with repeated stimulation
Unlike other neuromyopathies, usually responds to treatment of the tumor