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Pathology 15: The Lung
Why do aspirated foreign materials (vomit, blood, foreign bodies) tend to lodge in right
lung more than left? Diff b/t bronchiole and bronchi? What is acinus (3parts)? What is a
lobule?
a. because it is more vertical and more directly in line w/ the trachea
b. bronchi have cartilage in walls and submucosal glands; bronchioles don't
c. alveolar sacs, alveolar ducts, and respiratory bronchiole (resp unit)
d. cluster of 3-5 terminal bronchioles w/ appended acini
What is the microscopic structure of the alveolar walls (layers)? What function (s) of type
II pneumocyte? What are pores of Kohn? Most common malig in women and lethal
visceral-M/F?
a. capillary endothelium, basement membrane, interstitial space, alveolar epithelium
(type I pneumocytes (95%) and type II (5%), alveolar macrophages (in epithelial),
and surfactant
b. responsible for synthesis of surfactant and repair of alveolar epithelium (by giving
rise to new type I pneumocytes)
c. perforations in alveolar walls that llow movement of exudate and bacteria
d. Lung cancer (even more than breast)
What is cause of pulmonary hypoplasia? of Foregut cysts? What type of foregut cyst is
most common? What is pulmonary sequestration and what are 2 types?
a. caused by compression of developing lung ie from oligohydramnions or congen
diaphragmatic hernia
b. caused by abnormal detachment of primitive foregut; bronchogenic most common
c. presence of lung tissue w/o normal connection to airway system: extra lobar (in
thorax or mediastinum) and intralobar (assoc w/ recurrent infection or
bronchiectasis)
What is atelectasis? 3 kinds, their causes, position of mediastinum, and reversibility?
a. incomplete expansion of lungs (neonatal) or collapse of prev inflated lung
b. resorption (obstruction)- caused by mucus plugs or exudates w/ asthma, chronic
bronchitis, bronchiectasis, aspiration of foreign body; mediastinum-TOWARD
problem; reversible
c. compression- pleural cavity filled w/ fluid, tumor, blood, air (pneumothorax);
mediastinum- AWAY from affected lung; reversible
d. contraction- from local/gen fibrotic changes in lung preventing expansion; not
reverseable
2 causes of pulmonary edema? What is most common cause of hemodynamic? Where
does fluid tend to accumulate and what 2 histologic findings may occur with it?
a. hemodynamic changes (increased hydrostatic pressure) and increased capillary
permeability (usually from injury from infection)
b. left-sided heart failure most common; fluid accum in base of lungs (more
hydrostatic pres)
c. "heart failure" cells (hemosiderin-laden alveolar macrophages) and 'brown
induration' (brown fibrous thickening of lung)
What is an acute lung injury (ALI)? What called when severe? What’s that
associated with? If causal infectious agent can't be identified, what classified as?
a. abrupt onset of hypoxemia and diffuse pulmonary infiltrate in the absence of
cardiac failure
b. Acute respiratory distress syndrome (ARDS) if severe; assoc w/ Sepsis;
c. if etiologic assoc absent--> acute interstitial pneumonia (AIP)
7. Macroscopic appearance of lung in ALI? Characteristic microscopic findings (2)?
What is cause of pathogenesis in ARDS though to be and what is role of immune system?
a. lungs are heavy, firm, red, and boggy; also exhibit congestion
b. diffuse alveolar damage and waxy hyaline membrane (from mixed fibrin rich
edema fluid and lipid/cytoplasmic remnants of necrotic epithelial cells)
c. in ARDS the integrity of alveolar capillary membrane barrier (epithelium and/or
endothelium) is compromised; though by imbalance of pro-inflamm. and antiinflamm
d. 30 min post insult, IL-8 recruits neutrophils that adhere endothelium (enhanced
by TNF and IL-8) and then become stiff and trapped in lungs, then release
products that damage
8. What is the clinical presentation of person w/ acute lung injury? What is presentation of
functional abnormalities?
a. dyspnea and tachypnea, increased cyanosis and hypoxemia, resp failure, diffuse
bilateral infiltrates on radiograph, poor response to O2 therapy (mismatch), stiff
lung if no resolve
b. functional abnorm not evenly distributed: regions of infiltration, of consolidation,
of collapse, and normal regions--> causes ventilation-perfusion mismatch (40%
mortality)
9. 2 categories of noninfectious diffuse pulmonary diseases? What characterized by?
Causes? Results on pulmonary function tests?
a. obstructive- increased resistance to airflow from part/full obstruction; asthma,
chronic bronchitis, bronchiectasis, emphysema, bronchiolitis; dec max airflow on
forced expiration
b. restrictive- reduced expansion of lung parenchyma and dec total lung capacity;
chest wall disorders (poliomyelitis, obesity, kyphoscoliosis), chronic
interstitial/infiltrative diseases; have reduced total lung capacity, compliance, and
expiratory flow norm or reduced proportionally [phys: FEV1/FVC increased]
10. Why are emphysema and chronic bronchitis often clinically grouped together? Anatomic
site involved? Why is asthma distinguished separately?
a. the occur at similar levels (acinar-emph; bronchus-chronic bronc), are triggered
by smoking, and small airway disease is a component of both- together make
COPD
b. asthma is has reversible component (bronchospasm); COPD irriversible
11. What is emphysema? 4 types? Which assoc w/ obstruction? Characteristics of each
type (where occur, assoc w/, etc)? Which is asymptomatic?
a. irreversible enlargement of airspaces distal to terminal bronchiole accompanied
by destruction of their walls without obvious fibrosis
b. Centriacinar(centrilobular)- most common type to cause obstruction; involves
Proximal part of acini(resp bronchiole); lesions more common in apical
segments; assoc w/ smoking
c. Panacinar(panlobular)- causes obstruction; uniform enlargement of entire acini;
lesions more common in lower zone of lungs; assoc w/ alpha1-antitrypsin
deficiency
d. Distal acinar(paraseptal)- prox acinis okay, distal part involved; cyst-like enlarged
airspaces occuring near areas of fibrosis; severe in upper lung; assoc. w/spon
pneumothorax
e. Irregular (airspace enlargement w/ fibrosis)- due to scaring; asymptomatic
12. What leads to the destructive process in emphysema? What is most common normal
alpha1-antitrysin allele?How does smoking lead to pathogenisis in emphysema (2)?
a. destruction from protease-antiprotease imbalance and imbalance of oxidantsantioxidants
b. 99.9% have an M allele (ppl w/ homozygous Z allele tend to get panacinar)
c. Smoke causes accumulation of neutrophils and macrophates in alveoli (nicotine is
a chemoattract), neutrophils/macrophages release proteases, macrophage
elastases not inhibited by anti-trypsinase (cause damage)
i. tobaco causes increased ROS and neutrophils cause oxidative damage to
alpha-1 antitrypsinase (fxnal deficiency)--> neutrophil proteases not
inactvated either!
13. What are 4 contributors to airflow obstruction in emphysema?
a. goblet cell metaplasia (mucus plugs), loss of elastic recoil (from elastases),
inflammatory infiltrate in walls of bronchioles, and thickening of walls from
smooth m. hypertrophy
14. What is morphologic apperance of emphysema? What is clinical presentation? Key to
diagnosis? 3 main causes of death in these ppl? Cause-obstructive overinflation?
Interstitial emphysema?
a. voluminous lungs (upper 2/3 more severely affected) w/ abnormally large alveoli
that have lost attachment to outer wall of small airways
b. dyspnea (first), weightloss, 'barrel-chested, dyspneic, hunched over, pursed lips,
hyperinflammation' --> Pink puffer
c. 1) respiratory acidosis=> coma, 2) cor pulmonale (R. sided heart failure), and
3)pneumothorax=> massive lung collapse
d. air trapped in lung by obstruction from tumor or foreign object (air can get in, not
out), or conginital lobar overinflation in infants
e. air in connective stroma due to alveolar tear (common), chest wound, or irritant
gas inhlation
15. What defines chronic bronchitis? 3 possible sequalae? What is initating factor, earliest
feature, and late feature?
a. persistent cough w/ sputum production for at least 3 months in last 2yrs w/o
identifyable cause
b. progression to COPD, cor pulmonale, dysplasia leading to cancerous
transformation
c. long standing irritant (smoke; also dust, silica); hypersecretion of mucus in large
airways and hypertrophy of submucosal glands earliest feaure
d. later- marked increase in goblet cells of small bronchi and bronchioles=xs mucus
16. What is role of infection in chronic bronchitis? What are morphologic features of
chronic bronchitis? Clinical presentation?
a. secondary role (doesn't initiate, but may prolongue)
b. bronchi and trachea have lymphocytic infiltrate and enlargment of mucous glands
(measured by Reid index); bronchioles obliterated by fibrosis (broniolitis
obliterans)
i. emphysema=>metaplasia; bronchitis=>hyperplasia of goblet cells
c. presistent productive cough, eventual dyspnea and COPD-hypercapnia,
hypoxemia, mild cyanosis ("blue bloater")
17. What is asthma? What are 3 hallmarks of the disease? 2 main different forms and
causes? 2 other?
a. chronic inflammatory disorder of airways causing recurrent episodes of weezing,
breathelessness, chest tightness, cough (esp night/early morn) from
bronchoconstriction
b. increased airway responsiveness to stimuli, episodic bronchoconstriciton,
increased mucus
c. atopic (most common; type 1 IgE-mediated hypersensitivity; allergic; positive
skin test); non-atopic (neg skin test; hyperirritable bronchial tree often assoc w/
viral infection)
d. Drug induced (aspirin- less lipoxygenase=bronchoconstrict) and occupational
18. What are major etiologic factors in atopic asthma? type of immune response that
occurs? What happens to the airways over time?
a. genetic predisposition to type I hypersensitivity (elevated IgE) and exposure to
environmental triggers leading to development of TH2 response
b. TH2 releases IL-4=> B cell IgE production, IL-5=> eosinophils, and IL-13=>
mucus production; IgEs coat mast cells and subsequent antigen exposure leads to
crosslinked IgE and degranulation=> early rxn (vasodilation, bronchoconstrict);
late-rxn eotaxin and chemokines (recruit eosinophils, neutrophils, Tcells)=>
eosinophil MBP=> tissue damage
c. "airway remodeling"- hypertrophy/hyperplasia of bronch smooth m., epithelial
injury, increased vascularity, increased gland hypertrophy, deposition of subep
collagen
19. What chromosome has susceptibility loci for asthma? What other genetic polymorphisms
implicated in asthma? Most striking macroscopic findings? Histologic?
a. chromosme 5q (related to IgE regulation and mast cell and eosinophil
growth/diff)
b. class II HLA alleles (reason IgEs bind to only some things), ADAM-33, B2
adrenergic receptor gene, IL-4 receptor gene, chitinases
c. macro- occlusion of bronchi/bronchioles by thick mucus plugs and lungs
overdistended w/ small areas of atelectasis
d. micro- Curschmann spirals (whorls of shed epithelium w/ mucus), CharcotLeyden crystals(eosinophils bound to protein), and airway remodeling
20. What is bronchiectasis characterized by? What congenital conditions may it develop
in assoc with? Infections it may develop w/? Other possible causes?
a. PERMANENT dilation of bronchi/bronchioles caused by destruction of muscle
and elastic tissue, resulting from or assoc w/ chronic necrotizing infections (need:
infection+obstruct)
b. cystic fibrosis, intralobar sequestration of lung, primary ciliary
dyskinesia/Kartagener
c. necrotizing pneumonia caused by bacteria (M. tuberculosis, S. aureus, H.
infleunza, Pseundomonas), viruses (HIV, influenza, adenovirus), and fungi
(aspergillus)
d. bronchial obstrution (tumor, foreign body, mucus impaction) and other
conditions: RA, SLE, IBD, and post-transplant
21. What leads to bronchiectasis in cystic fibrosis? What is Kartagener syndrome? Where
does brochiectasis affect lungs most? Morphologic appearance? Clinical presentation?
a. mutated CFTR channel leads to viscus mucus that is susceptible to infections;
recurrent infections destroy smooth m., elastic tissue, and cause dilation/fibrosis
b. occurs in 50% of ppl affected with primary ciliary dyskinesia (absent/shortened
dynein arms); signs are bronchiectasis, sinusitis, situs inversus or partial
laterization abnorm, sperm dysmotility
c. infections tend to affect lower lobes bilaterally, esp in more vertical air passages
(TB is an exception to this trend)
d. airways dilated up to 4x normal; intense acute/chronic inflammatory exudate w/
extensive areas of necrotizing ulceration, squamous metaplasia, and eventual
fibrosis
e. severe persistent cough, expectoration of foul-smelling, sometimes bloody sputum
(worse after positional change), dyspnea and orthopnea
22. What are chronic restrictive diseases characterized by? Symptoms of ppl w/ these? Lab
and radiographic findings? What are late stage restrictive diseases referred to as?
a. inflammation and fibrosis of pulmonary connective tissue
b. dyspnea, tachypnea, end-inspiratory crackles, eventual cyanosis
c. reduced CO diffusion capacity, lung volume, and compliance; radiograph:
bilateral infiltrative lesions in form of small nodules, irreg lines, or ground-glass
shadows
d. end-stage lung or honey-comb lung
23. 5 categories of restrictive lung diseases? What is idiopathic pulmonary fibrosis?
Currently believed cause? What is the driver of this process and why? What is
Caveolin-1?
a. fibrosing diseases, granulomatous diseases, pulmonary eosinophilia, smokingrelated interstitial diseases, and pulmonary alveolar proteinosis
b. IPF = crytogenic fibrosing alveolitis; caused by repeated cycles of epithelial
activation/injury by some unidentified agent (usually via Th2 repsonse)
c. TGF-β1 drives process: it negatively regulates caveolin-1 as well as telomerase,
which causes epithelial apoptosis and repair (abnormal forming fibroblastic foci);
d. an endogenous inhibitor of pulmonary fibrosis and TGF-β1 (caveolin-1 decreased
in IPF)
24. What is gross appearance of lungs in IPF? Where most affected? Microscopic hallmark
and earliest lesion? What does dense fibrosis eventually lead to? Pulm artery changes?
Outlook?
a. pleural surface is cobblestoned from scar retractions; cut surface is firm, white,
rubbery
b. lower-lobe distributed in subpleural regions and interlobular septa
c. Hallmark- patchy interstitial fibrosis; earliest lesion= fibroblastic foci (prolif
fibroblasts)
d. fibrosis eventually leads to alveolar destruction and formation of cystic spaces
lined by type II pneumocytes= honeycomb fibrosis
e. pulmonary artery changes from HTN- intimal fibrosis and medial thickness
f. BAD!! mean survival is only 3 yrs and lung transplant only therapy
25. What histologic pattern of fibrosis must be found for diagnosis of IPF? What is
nonspecific interstitial pneumonia? Why is nonspecific interstitial pneumonia (NSIP)
important to recognize? What morphologic features are not present?
a. pattern referred to as Usual Interstitial Pneumonia (UIP, essentially described
above)
b. diffuse interstitial lung disease (fibrosing) of unknown etiology whose biopsies
fail to show diagnostic features of any other well-characterized interstitial
diseases
c. important to recognize b/c MUCH better prognosis than UIP (pattern of IPF)
d. can have cellular and fibrosing patterns; IMPORTANT: fibroblastic foci and
honeycombing are absent in NSIP!
26. What is another name for cryptogenic organizing pneumonia? Radiograph findings?
Histologic findings? How treated and what is it usually caused by?
a. bronciolitis obliterans organizing pneumonia
b. subpleural or peribronchial patchy areas on radiograph
c. presene of polypoid plugs of loose connective tissue (Masson bodies) in alveolar
ducts, alveoli, and bronchioles (fibrosis all same age); NO interstitial fibrosis or
honeycomb lung
d. can accompany inflammation or infection
27. What systemic diseases can cause pulmonary involvment? Most common patterns? What
is found in RA, in Scleroderma, in SLE?
a. SLE, scleroderma, rheumatoid arthritis, deratomyositis-polymyositis, mixed
connective tissue disease
b. NSIP, UIP (as in IPF), vascular sclerosis, organizing pneumonia, and bronchiolitis
i. Keyword: fibrosis
c. RA- chronic pleuritis, diffuse interstitial fibrosis (NSIP or UIP), intrapulmonary
rheumatoid nodules, and pulmonary HTN
d. scleroderma- diffuse interstitial fibrosis (generally NSIP)
e. SLE- patchy and transient infiltrates, occasional lupus pneumonitis
28. What does the term pneumoconioses (fibrosing disease) mean? What extrinsic factors
does development of one of these diseases depend on (4)?
a. non-neoplastic lung reaction to inhalation of organic/inorganic particulates,
vapors, fumes
b. the amount of dust retained by lung and airways, the size/shape/buoyancy of
particles, particle solubility/reactivity, and additional effects from other irritants
29. What 3 factors determine quantity of dust is retained in lungs? Most dangerous particles?
How does size of particles affect disease presentation? What inhaled mineral effect
worsened by smoking?
a. dust concentration in air, duration of exposure, and effectiveness of clearance
mech
b. particles from 1-5 um diameter b/c reach terminal airways and settle in linings!
c. smaller particles- soluble so tend to accum to toxic levels in pulm fluids more
quickly= acute lung injury; larger one resist dissolve-chronic fibrosing
collagenous pneumoconioses
d. asbestos
30. Major culprit in Coal Workers Pneumoconiosis (CWP)? 3 forms of lung findings?
Morphologic findings in each? What does coal dust increase incidence of (independent of
smoking)?
a. carbon dust
b. asymptomatic anthracosis- pulm lesion from inhaled carbon pigment
c. simple CWP -coal macules(1-2cm containing coal laden macrophages) and coal
nodules (larger containing coal laden macrophages and collagen); Upper lobe
involvement, can cause centrilolobular emphysema in time
d. Complicated CWP- progressive massive fibrosis w/ intensly blackened scars >2
cm made of dense collagen and pigment (req many years to develop)
e. generally benign but does increase incidence of chronic bronchitis and
emphysema
31. What is most prevalent chronic occupational disease in the world? 2 professions affected?
What is causitive agent and how does it cause fibrosis?
a. Silicosis- inhalation of crystalline silicon dioxide (silica); sandblasters and mine
workers
b. quartz (a crystalline silica); silica causes macrophage activation and release of
mediators
32. What are early morphologic findings of silicosis in lung? Later? Radiographic findings
in lymph nodes and lung? What histologic findings? Infection susceptible to?
Carcinogenic?
a. tiny blackened nodule in upper zone
b. progress to hard collagenous scars (may undergo cavitation or softening)
c. nodes- eggshell calcification (radioleucent middle; opaque edge); lung-fine
nodularity in upper zones on radiograph
d. lesion histo-concentric layers of hyalinized collagen surrounded by dense
collagen capsule; nodules reveal 'birefringent' silica particles w/ polarized light
e. tuberculosis yes; carcinogenic maybe
33. What 6 things is exposure to asbestos associated with? What are 2 geometric forms and
characteristics of each? Where does inital asbestos injury tend to occur?
a. localized fibrous plaques, pleural effusions, parenchymal interstitial fibrosis
(asbestosis), lung carcinoma, mesothelioma, laryngeal/colon neoplasms
b. serpentine (less pathogenic b/c more flexible and soluble; dont get as deep in
lung) and amphibole (more pathogenic b/c stiff and less soluble; invade deeper
lungs & penetrate)
c. at bifurcations of small airways/ducts (macrophages try to clear and instead are
activated to release fibrogenic mediators leading to chronic deposition)
34. What are the morphologic features of asbestosis in lung? How differentiated from UIP?
Part of lung most often inolved? Most common manifestation of asbestos and location?
a. diffuse pulmonary interstitial fibrosis with presence of asbestos bodies (golden
brown, fusiform/beaded rods w/ translucent center coated by iron material (from
macrophages))
b. has fibrosis and progression to honeycomb of UIP; asbestos bodies only
difference
c. Lower lobes most involved (contrast to other forms of pneumoconiosis)
d. pleural plaques- plaques of dense collagen most freq on anterior or postlat of
parietal pleura and over domes of diaphragm (NO asbestos bodies)
35. Which cancer risks are assoc w/ concommittant asbestosis and smoking? What do chest
x-rays of asbestosis reveal? Possible disease progression?
a. lung carcinoma risk is further increased by smoking; mesothelioma risk doesn’t
synergize with cigarette smoke
b. x-rays show irregular linear densities particularly in lower lobes w/ honeycomb in
advanced; pleural plaques will appear as circumscribed densities
c. can progress to respiratory failure, cor pulmonale, and death
36. Which lung tends to be involved in radiation-induced pneumonitis? What is sarcoidosis
characterized by? 2 most commonly involved structures? How diagnosed?
a. lung within the radiation port
b. noncaseating granulomas in many tissues and organs
c. bilateral hilar lymphadenopathy or lung involvement (90% cases)
d. via exclusion (other fungal and microbial diseases that produce granulomas [like
hypersensitivity pneumonitis] ruled out)
37. What immune, genetic, and environmental factors may contribute to sarcoidosis?
What are morphologic findings and what tissues involved?
a. immune- accumulation of CD4+ cells, increased Th1 cytokines, recruitment of
Tcells and macrophages (also demonstrate hypergammaglobinemia and anergy to
skin tests like PPD)
b. genetic- assoc w/ HLA genotype; environ- possibly infection but not proven
c. noncaseating granulomas that may have Schaumann bodies (calcium) and asteroid
bodies (stellate inclusions) inside;
d. Lungs, lymph nodes (enlarged, calcified), spleen and liver (scattered granulomas),
bone marrow (usually phalanges), skin lesions, eyes (iritis, glaucoma, opacity),
gland enlargement, muscle weakness
38. Where do lung granulomas tend to occur in sarcoidosis? When do most cases of
sarcoidosis come to clinical attention?
a. primarily along lymphatics, bronchi, and blood vessels
b. when person seeks help for resp abnormality (SOB, chest pain) or constitutional
symptoms
39. What is hypersensitivity Pneumonitis (granulomatis)? Why is it important to recognize
hypersensitivity pneumonitis early? How different from asthma? What is causal agent
in Farmer's, Pigeon breeder's and Humidifer lung? Type of hypersensitivity?
a. immunologically mediated lung disorder from exposure to inhaled organic agent
b. because you can prevent it from progressing to chronic fibrotic lung disease by
removing environmental agent
c. hypersensitivity pneuonitis tends to involve alveoli insead of bronchi
i. although both involve antigen-antibody complex formation (at least atopic
asthma does), HP also requires a longer exposure time than asthma before
it occurs; asthma has an immediate hypersensitivity stage
d. Farmers- thermophilic actinomycetes; pigeon- serum, excreta, or feathers of bird;
humidifier- thermophilic bacteria in heated water reserves
e. Type III (evidenced by specific antibodies in serum and
complement/immunoglobulins in vessel walls); Some type IV as well
(granulomas suggest delayed-type hypersensitivity)
40. 3 characteristic histologic changes in hypersensitivity pneumonitis? What can it progress
to? What are different forms of pulmonary eosinophilia?
a. interstitial pneumonitis, noncaseating granulomas, and interstitial fibrosis,
honeycombing, and obliterative bronchiolitis (in late stages)
b. can progress to resp failure, dyspnea, and cyanosis w/ decreased lung
capacity/compliance
c. acute eosinophilic pneumonia w/ resp failure, simple pulmonary
eosinophilia(striking shadows on CT, but benign), Tropical eosinophilia
(microfilariae), idiopathic, secondary, chronic diagnosed by exclusion
41. 2 types of smoking-related interstitial diseases? Characterized by? Clinical features?
a. Desquamative interstitial pneumonia- large collection of macropages w/ dusty
brown pigment (smokers' macrophages); insidious onset of dyspnea and clubbed
digits
b. Respiratory bronchiolitis-associated interstitial lung disease- smokers'
macrophages in first and second order resp bronchioles; more mild dyspnea and
cough
42. What radiologic findings characterize pulmonary alveolar proteinosis? Histologic? 3
classes of PAP and cause of each? Morphologic findings? Symptoms and treatment?
a. bilateral patchy asymmetric pulmonary calcifications
b. accumulation of acellular surfactant in the intra-alveolar and bronchiolar spaces
c. Acquired- autoimmune production of anti-GM-CSF antibody (GM-CSF needed
to clear surfactant); congenital- mutations needed for surfactant (ABCA3, SP-B,
SP-B); secondary-hematopoetic disorders, malignancies, immunodeficiencies
d. peculiar homogenous granular precipitate in alveoli making them confluent w/
turbid fluid; stain with PAS and surfactant proteins present; Lungs increased size
and weight
e. cough w/ gelatinous chunks of sputum, progressive dyspnea, resp insufficiency
f. treat w/ whole-lung lavage (wash out); GM-CSF therapy helps some
43. Origin of blood clots in pulmonary artery? Who is at risk? Primary vs secondary risk
factors for hypercoagulable state (increased risk of embolus)? What does response to PE
depend on (5)?
a. emboli from deep veins of legs;
b. ppl w/ underlying cardiac disase, cancer, or immobilized (ie after a hip fracture)
c. Primary- Factor V Leiden, prothrombin mutations, Antiphospholipid syndrome;
secondary- obesity, recent surgery, cancer, oral contraceptive, pregnancy
d. extent to which vessel is obstructed, size of occluded vessel(s), number of emboli,
status of cardiovascular system, and release of vasoactive factors
44. 2 main pathophysiologic consequences of pulmonary emboli? 2 causes of death from PE?
Who tends to get infarcts as a consequence? Location? Appearance? How is PE
distinguished from post-mortum clot?
a. Most commonly they cause no symptoms! Otherwise, respiratory compromise
(non-perfusion) and hemodynamic compromise (pulm HTN)
b. sudden death (as w/ saddle embolism) from embolus or acute cor pulmonale
c. older ppl w/ already inadequate circulation (heart/lung disease); lower lobes of
lungs
d. classically hemorrhagic infarct that progresses from red-blue, to red-brown
(hemosiderin), to gray-white (fibrous replacement)
e. lines of Zahn in pulmonary embolism (from being in flowing blood)
45. What symptoms may someone who survives PE present with? Radiograph findings and
lab findings? Sequalae?What is important to note in someone w/ small PE? Prophylaxis?
a. severe chest pain, dyspnea, shock, fever, increased serum lactate dehydrogenase
b. may look normal or may have wedge-shaped infiltrate; diagnose w/ spiral CT or
ventilation perfusion scan
c. overtime unresolved emboli lead to: pulm HTN, pulm vasc sclerosis, cor
pulmonale
d. small emboli frequently precede a large one (30% chance of second)
e. early ambulation in post-op, compressive stockings for bedridden, anticoag, IVC
filter
46. At what fraction of systemic pressure does pulmonary pressure become pulm htn? 5
similar disorders associated with it? 5 common causes?
a. 1/4th systemic; pulmonary arterial HTN, PH w/ left heart disease, PH w/ lung
disease, PH from chronic thrombotic/embolic disease, miscellaneos PH
b. chronic and restrictive lung disease, congenital/acquired heart defect, recurrent
thromboemboli, connective tissue disease (systemic sclerosis), obstructive sleep
apnea (fat)
47. What is mutated in familial pulmonary HTN and how does it cause disease? What is
cause of pulmonary HTN in secondary forms?
a. bone morphogenic protein receptor type 2 (BMPR2); causes apoptosis of smooth
m. in vessels, so when 1 allele lost= vascular thickening and HTN
b. endotelial cell dysfxn from sheer mechanical injury or from biochemical injury
48. What 3 morphologic features are found in PH regardless of cause? What vessels
prominently affected? What is presentation of PH caused by drugs or HIV? Clinical
presentation/course?
a. medial hypertorphy of muscular and elastic arteries, atheromas of pulmonary
artery, and right ventricular hypertrophy
b. arterioles and small arteries (40-300um diameter)
c. Plexiform lesion- tuft of capillary formations is present producing a network or
web
d. dyspnea and fatigue progressing to cyanosis, severe resp distress, right ventricular
hypertrophy, and death from cor pulmonale
49. 3 pulmonary hemorrhagic syndromes? What is cause of Goodpasture? What is unusual
about the population affected? What are morphologic findings and clinical sequalae?
a. goodpasture syndrome, idiopathic pulmonary hemosiderosis, vasculitis-assoc
hemorrhage (hypersensitivity angiitis, Wegener granulomatosis, SLE)
b. autoantibodies against α3 chain of type IV collagen in basement membrane of
glomeruli and alveoli
c. autoimmune cause that is predominantly in males in 20s (smoking also related)
d. Lungs- necrotic hemorrhagic interstitial pneumonitis (red-brown consolidation,
focal necrosis of alveolar walls, intra-alveolar hemorrhage); kidney- cresenteric
glomerulonephritis; NOTE: linear immunofluorescence in both organs
50. Who does idopathic pulmonary hemosiderosis occur in? What are 2 diagnosticly
important features for Wegener Granulomatosis?
a. young children
b. capillaritis and scattered poorly formed noncaseating granulomas (unlike those of
sarcoidosis that are well formed)
51. What is pneumonia? 5 factors that can lower local defences increases risk? 3 important
facts to keep in mind when thinking about it? 7 pneumonia syndromes?
a. any infection of the lung parenchyma
b. loss/suppresion of cough reflex, injury to mucociliary apparatus, accumulation of
secretions (in obstructive diseases), interference w/ phagocytic action of
macrophages, pulmonary congestion and edema
c. one type of pneumonia sometimes predisposes to another, hematogenous spread
from one organ to another can occur, patients w/ chronic disease acquire terminal
pneu in hospital
d. community acquired acute, community acquired atypical, hospital acquired,
aspiration, chronic, necrotizing/lung abscess, pneumonia in immunocompromised
52. Most common cause of community-acquired acute pneumonia? How diagnosed? What is
most common bacterial cause of acute exacerbations of COPD? Characteristics? other
diseases caused?
a. Streptococcus pneumoniae (pneumococcus); sputum gram-stain reveals gram +,
lancet-shaped diplocci
b. Haemophilus influenzae; gram neg bacteria that causes life-threatening acute
lower resp infection and meningitis in kids; comm pneumo in adults (3rd most?)
c. NOTE: type b H. influenzae is major encapulated problem; has pili, proteases that
degrade IgA, factors that disorganize ciliary beating
53. 2nd most common cause of acute exacerbations of COPD? 3 most common causes of
otitis media in children? Who generally affected by S. aureus pneumonia? Most freq
gram neg pneu? Most frequent hospital-acquired pneu?
a. Moraxella catarrhalis
b. S. pneumoniae, H. influenzae, M. catarrhalis
c. children and adults secondary to viral illness, IV drug abusers
d. Klebsiella pneumoniae (esp in malnourished like chronic alcoholics)
e. P. aeruginosa
54. Where does legionella pneumophila thrive? Who’s particularly succeptible to this type
of community pneumonia? 2 patterns of bacterial pneumonia and type of
consolidation in each?
a. artificial aquatic environment (water-cooling towers)
b. organ transplant recipients
c. bronchopneumonia- patchy consolidation of the lung; lobar pneumoniafibrosuppurative consolidation of large portion or entire lobe
55. 4 stages of inflammatory response in lobar pneumonia and morphology of each?
Morphology of bronchopneumonia? 3 major complications? Clinical presentation?
a. congestion (lung heavy, boggy, red, w/ intra-alveolar fluid and many bacteria),
red hepatization (massive exudation w/ neutrophils, redcells, fibrin= red firm
airless lung w/ liver consistency); gray hepatization (disintegratin of RBCs to
fibrinosuppurative exudate, gray brown); resolution (enzymatic digestion and
resorption)
b. suppurative, patchy, multilobular, bilateral, basal lesions that are dry, granular,
and yellow
c. tissue necrosis and abscess formation, empyema(spread to pleural cavity), and
bacteremic dissemination (endocarditis, meningitis, supp arthritis)
d. abrupt onset of fever, shaking chills, productive cough and occasional hemoptysis
56. What makes an atypical pneumonia atypical? Most common causal organism? What
is predominat histologic pattern? Major clinical manifestations?
a. = viral or Mycoplasma; only moderate sputum, no physical findings of
consolidation, only moderate elevation in whites, and lack of alveolar exudate,
architecture not distorted
i. TB is a whole other genus
b. Mycoplasma pneumoniae (esp children and young adults) (often viral causes too)
c. interstitial nature of inflammatory rxn, virtually localized w/in walls of alveoli
d. generally mild compared to typicals; fever, headache, muscle aches/pain; can
have 2ndary bacterial infection
57. What is structure of influenza virus and how does this result in epidemics and
pandemics? Strain of avian influenza of concern? Morphologic presentation of viral resp
infections?
a. 8 helical ssRNA segments in envelope w/ hemagglutinin and neuramidase on
outside
b. epidemic- mutation in H or N that allows virus to escape host antibodies
(antigenic drift); pandemic- both H and N replaced via recomb w/ RNA segs of
other species (antigenic shift)
c. H5N1 (usually spread through domestic birds) – H5 allows all tissues to be
infected
d. mucosal hyperemia and swelling w/ predom lymphocytic infiltrate and mucus
oversecrete; can have swelling of vocal chords in laryngotracheobronchitis or
bronchiolitis
58. Who is most commonly infected by human metapneumovirus (MPV)? Presentation?
What is causal agent of SARS? How first transmitted to humans? Symptoms and
diagnosis?
a. young children, elderly, and immunocompromised
b. severe bronchiolitis and pneumonia that may require hospitalization
i. resembles RSV
c. an unidentified coronavirus; via wild masked palm civets eaten in China
d. dry cough, malaise, fever, progressing to SOB, tachypnea, and 10% die
e. diagnosed via detection of the coronavirus by PCR or detection of antibodies to
virus (serum, sputum)
59. Who commonly affected by hospital-acquired pneumonia (3)? Most common cause? 2
others? What is most commonly found on culture for aspiratoin pneumonia? sequalae?
a. immunosuppressed, on prolongued antibiotics, or have invasive devices (cath,
ventilator)
b. Most commonly P. aurginosa; also gram neg rods (enterobacteriaceae) and S.
aureus (NOT S. pneumoniae)
c. more than one organism (aerobes more than anaerobes); death or lung abscess
60. What is a pulmonary abscess? What organisms are most commonly isolated? 3
common anaerobes? Major mechanisms abscess acquired through? = Primary
cryptogenic if no other cause
a. local suppurative process characterized by necrotic lung tissue
b. aerobic and anaerobic streptococci, S. aureus, many gram negative organisms
c. those found in oral cavity normally: Bacteroides, fusobacterium, peptococcus
d. aspiration of infective material (most common; alcoholic, coma, sinusitis,
gingivodental sepsis), from preceding lung infection, septic embolism, neoplasia,
trauma, spread from neighboring organs or via hematogenous route
61. Where are abscesses from aspiration most common? From pneumonia? septic? What is
cardinal histologic change in all abscesses? What can continual infection lead to? How
diagnosed? Complications?
a. more common on right and single; from pneumonia tend to be multiple, diffuse,
basal; embolic can be any part of lung and multiple
b. suppurative destruction of lung parenchyma w/ central area of cavitation
c. large, fetid, green-black pool of necrotic debris-gangrene of lung
d. diagnosed only by radiology;
e. complicated by infection of pleural cavity, hemorrhage, and brain abscess
62. What types of organisms tend to cause chronic pneumonia? 3 features of the fungal
causes? Where (geographic) is each fungal cause most frequent?
a. those that form granulomas: bacteria (M. tuberculosis) and fungi
b. Histoplasmosis, blastomycosis, and coccidiodomycosis: all cause granulomatous
disease in lungs, all are thermally dimorphic, and all have specific geographic
location
c. Histo- by Ohio and Mississippi rivers and Caribbean, [prof. owl teaches History]
d. Blasto- central and SE US,
[cannon blasts surrounding the Alamo]
e. Coccidio- SW and far west US and Mexico (10% get San Joaquin Valley fever)
63. How is histoplasmosis capsulatum aquired (2 sources)? Clinical presentation resembling
tuberculosis(4)? Morphologic presentation? How diagnosed?
a. from inhalation of dust particles of soil contaminated w/ bird or bat droppings
b. self-limited laatent disease, can lead to chronic secondary lung disease involving
lung apices, localized lesions in extrapulmonary sites, and wide disseminated
immunocompromise
c. epitheliod granulomas undergo caseous necrosis; undergo fibrosis to 'tree-bark'
lesions
d. diagnosed by culture or ID of fungus in tissue lesions
64. 3 clinical forms of Blastomyces dermatitidis infection? What type of granuloma?
morphology? Type of immune response to Coccidioides immitis? Morphologic
presentation?
a. pulmonary blastomycosis, disseminated blastomycosis, and primary cutaneous
(rare)
b. suppurative granuloma; budding yeast w/ thick, double contoured cell wall,
mult nuclei
c. delayed-type hypersensitivity; granulomaous lesions similar to histo and
macrophages filled w/ nonbudding spherules of endospores
65. What is most common and serious complication in immunocompromised ppl?
Commonly causal organisms? Leading cause of morbidity and mortality in HIV?
a. pulmonary infiltrate (with or w/o signs of infection)
b. bacteria (P. aeruginosa, mycobacteria, Listeria), viruses (CMV, HSV), fungi (P.
jiroveci, candida, aspergillus, cryptococcus)
c. Pulmonary disease
66. 3 principles to keep in mind when thinking about HIV pulmonary disease? Most
common pathogens involved in HIV resp infections?
a. resp infections often caused by the "usual" pathogens of resp tract, disease can
still have non-infectious etiology (Kaposi sarcoma, lung cancer), CD4 + count
defines risk to infections of specific organisms (bacteria if >200,
pneumocysitis<200, myco avium<50)
b. S. pneumoniae, S. aureus, H. influenzae, and gram neg rods like P. aeruginosa
67. Most common indications for lung transplantation (4)? When must both lungs be
replaced? 2 main complications and morphology with each?
a. end-stage emphysema, idiopathic pulmonary fibrosis, cystic-fibrosis, and
idiopatic/familial arterial hypertension
b. bilat if chronic infection present
c. Pulmonary infections (generally bacterial in 3-12th month post transplant) and
rejection (acute-inflammatory infiltrate around small vessels or airways; chronicbroncholitis obliterans (partial or complete occlusion of small airways by
fibrosis))
Tumors
68. Do most smokers get lung cancer? Who has greater susceptibility to carcinogens found in
cigarettes? Does it help to quit?
a. 10% of smokers get lung cancer (but 90% of all lung carcinomas happen to smokers)
b. Women are more susceptible to lung cancer
c. Cessation of smoking for 10 years reduces risk, but not to control levels
i. risk persists for 30 years
69. Which type of cancer tends to involve the genes 3p, p53, BCL2, C-KIT, and MYCN/MYCL?
a. Small cell lung carcinoma has involvement of these genes
[small numbers=> small
cell]
70. What about the genes p16 INK4a, p53, EGFR, and KRAS?
a. These genes are most commonly affected in any non-small cell lung carcinoma
71. What gene is known for causing familial clustering through increased metabolization of
procarcinogens?
a. The P-450 gene CYP1A1 may increase an individual’s metabolization of cigarette
procarcinogens
72. How do characteristics of small cell carcinomas versus non-small cell carcinomas compare?
a. Small cell carcinomas are almost always metastatic and have a high initial response to
chemotherapy
b. Non-small cell carcinomas are the opposite (less often metastatic, less responsive)
73. To which organ is lung cancer most likely to metastasize?
a. The adrenal glands are involved in more than half of metastases
i. Other possibilities: liver, brain, & bone
74. What is the most common type of lung cancer? Where do they originate? What substances do
they express?
a. Adenocarcinomas are the most common;
b. Adenocarcinomas are usually more peripherally located compared to other carcinomas
c. they are usually positive for TTF-1 and mucin
75. What type of cancer is bronchioalveolar carcinoma? What is its key feature? Which subtype, in
turn, tends to spread aerogenously?
a. Bronchioalveolar carcinoma is a type of adenocarcinoma
b. Its key feature is a lepidic growth pattern: it grows along preexisting structures
c. Mucinous bronchioalveolar carcinoma tends to spread aerogenously  you’ll suffocate
76. How is squamous cell carcinoma histologically identified?
a. Squamous cell carcinoma is characterized by keratinization and/or intracellular bridges
77. Which two carcinomas are closely correlated with smoking history?
a. Squamous cell and small cell carcinomas almost always occur in smokers
78. Which carcinoma is most likely to ectopically secrete hormones? What carcinoma causes
hypercalcemia? Through what intermediates?
a. The highly malignant small cell carcinoma was the culprit in our SIADH case
b. Exception: Hypercalcemia is usually due to squamous cell carcinoma
i. caused by parathyroid hormone, PTH related peptide, prostaglandin E, and
some cytokines
[think: calcium plating]
79. Which cancer type probably represents squamous/adeno-carcinomas that have become very
undifferentiated? What do you call a cancer with combined histology of 2+ types?
a. Large cell carcinoma is perhaps just a mix of de-differation
b. Combined carcinoma has combined histology
80. How would you stage a cancer that is invading the mediastinum and heart, with ipisilateral hilar
or peribronchial nodal involvement? What defines N2?
a. This cancer would receive an T4 N1 M0
b. T4 or N3 always = IIIb
c. N2+ requires local metastasis to mediastinal or subcarinal lymph nodes
81. How would you stage a cancer of 3-7 cm in size or that involved main stem bronchus, visceral
pleura, or lobar atelectasis? [no nodal involvement]
a. This describes a T2 N0 M0 cancer
b. T2 with nothing else = stage Ib
82. What is the difference between stage IIb and IIIa?
a. IIb = T2N1 or T3N0
b. IIIa = T3N1 or T3N2
83. Which neuroendocrine tumor obstructs bronchi and sometimes fans out along the perbronchial
tissue as a collar button lesion? What rare syndrome can they produce? What other cancer
causes this syndrome?
a. Carcinoid tumors—penetrate the bronchial wall to cause obstruction
b. Carcinoid syndrome is a rare complication: intermittent attacks of diarrhea, flushing,
cyanosis
c. Carcinoid syndrome is actually more commonly seen in patients with small cell
carcinoma, simply because small cell carcinoma itself is so much more common
84. What miscellaneous tumor tends to produce connective tissue, specifically cartilage, that is
visible as a coin lesion on chest films?
a. Lung hamartoma
85. What is the growth pattern of metastasis to the lung?
a. Multiple discrete nodules “cannonball lesions” scatterred throughout all lobes
86. Asbestos workers are vulnerable to which pleural tumor? How does it look? List some
important histology:
a. Malignant Mesothelioma
b. Spindle and cuboidal cells invade adipose tissue
c. Stain features favoring diagnosis: acid mucopolysaccharide; keratin; calretinin, WT-1,
cytokeratin 5/6, and D2-40; long microvillia and abundant tonofilaments w/absent
microvillous rootlets; lack of epithelial glycoprotein antigens
[we have to kare for our asbestos workers]
87. How can you differentaite solitary fibrous tumor from malignant mesothelioma? Where are
solitary fibrous tumors located?
a. Solitary fibrous tumors are positive for CD34 and keratin-negative
b. pleura
[Alternate]
88. What is most freq diagnosed cancer in world and most common cause of cancer mortality
worldwide? Peak age of incidence? 3 factors in smoking that affect risk of carcinoma?
a. Lung cancer; 50-60s
b. amount of daily smoking, tendency to inhale, and duration of smoking habit
89. Typical mutation in lung cancer? Environmental factors linked to lung cancer (4)? Genes
most linked to small cell lung carcinoma? non-small cell? Type of lung cancer in nonsmokers?
a. G:C>T:A mutations in p53 caused by benzo[a]pyrene in smoke
b. smoking (cigarettes and cigars(less)), ionizing radiation (ie uranium in miners),
asbestos, indoor air polution-radon (esp in miners)
c. small cell: C-Kit, MYCN, MYCL, p53, 3p, RB, BCL2; non-small- EGFR, KRAS,
p16INK4a
d. in non-smoking women- adenocarcinomas w/ EFGR mutations, but no KRAS or
p53
90. 3 types of precursor lesions to lung carcinoma? 4 types of lung cancer? Most common in
women? 2 groupings based on likelihood metastases and chemo response? Most assoc w/
smoking (2)?
a. squamous dysplasia and carcinoma in situ, atypical adenomatous hyperplasia, and
diffuse idiopathic pulmonary neuroendocrine cell hyperplasia
b. Adenocarcinoma (most common in women and in some studies men), squamous
cell carcinoma, small cell carcinoma, large cell carcinoma; NOTE: can have more
than 1
c. small cell carcinomas (almost always metastatic, high response to chemo) and
non-small cell carcinomas (less often metastatic, less responsive to chemo)
d. small cell carcinoma and squamous cell carcionoma
91. Where in lung do tumors tend to arise? Which tend to arise more peripheral/distally?
Which carcinoma often preceded by precursors? Appearance of tumors? Where
metastasize to?
a. in and about the hills; adenocarcinomas can occur more perish/distal
b. Squamous cell carcinomas tend to come from precursors
c. tumors tend to be gray-white and firm; may have hemorrhage or necrosis
d. lymph- tracheal, bronchial, mediatinal nodes; hematog- adrenals (most), liver,
brain, bone
92. What type of differentition in adenocarcinoma? Most common cancers of who? What are
majority of them positive for? What is morphology for bronchioalveolar form? What
precursor?
a. gladular; most common cancers of women and non-smokers
b. positive for thyroid transcription factor-1 (TTF-1) and 80% have mucin
c. pure bronchioalveolar growth pattern that grow along PREEXISTING structures
without destruction (lepidic); can be nonmucinous (better) or mucinous (worse
prognosis)
d. thought to arise from atypical adematous hyperplasia that then progresses to
bronchioalveolar carcinoma and can transform into invasive adenocarcinoma
93. Who is sqamous cell carcinoma most commonly found in? Histologic features it is
characterized by? Most common mutation?
a. men and close assoc w/ smoking history
b. presence of keratinization(squamous pearls) and/or intercellular bridges
c. highest freq mutation in p53 (others: RB1, p16(INK4a), EGFR, HER-2/NEU)
94. Histologic appearance of small cell carcinomas? What findings on EM? What markers
suggest a neuroendocrine origin?Relation to smoke? MOST COMMON assoc ectopic
hormone production
a. small cells w/ scant cytoplasm, ill-defined cell borders, finely granular nuclear
chromatin ('salt and pepper' pattern), abscent nucleoli; high mitotic count and
necrosis common
b. EM shows dense-core neurosecretory granules;
c. markers- chromogranin, synaptophysis, CD57; smoking increases risk!
95. Morphologic findings of large cell carcinoma? What is neuroendocrine variant
characterized by? Secondary symptoms/pathology from lung tumors (6)?
a. undifferentiated epithelial tumor that lacks cytology of small-cell, gladular, or
squamous tumors; cells have large nuclei, prominent nucleoli, and moderate
cytoplasm
b. variant recognized by organoid nesting, trabecular, rosette-like, and palisading
patterns
c. partial obstruction (emphysema), complete obstruction (atelectasis), severe
suppurative bronchitis or bronchietasis, pulmonary abscess, SVC syndrome,
pleuritis/pericarditis
96. Most aggressive lung tumors incurable by surgical means? Major presenting complaints
in lung cancer? Which lung tumor does not metastasize? 2 patters w/ slightly better
prognosis?Table15-11
a. small cell carcinoma
b. cough, weight loss, chest pain, and dyspnea
c. bronchioalveolar does not; adenocarcinoma and squamous cell better (local
longer)
d. NOTE: KRAS mutation assoc w/ worse prognosis regardless of treatment
97. Hormone products that can be elaborated by lung tumors (7)? 2 hormones most secreted
predominately by small cell? 1 by squamous cell? What do apical lung tumors cause?
a. ADH, ACTH, PTH, PTHrP, Calcitonin, Gonadotropins, Serotonin/bradykinin
b. small cell- ADH and ACTH; sqamous- those producing hypercalcemia (PTH,
PTHrP)
c. Pancost tumors- compress cervical symp plexus causing combo: pain in ulnar
nerve distribution and Horner syndrome (ptosis, miosis, anhidrosis)
98. 3 neuroendocrine tumors of lung? What is all pulm neuroendocrine cell hyperplasia
secondary to? 2 types of carcinoid tumors and differences? 2 morphologic patterns of
growth? Symp carcinoid?
a. tumorlets (small, inconsequential), carcinoids, and small/large cell carcinomas
b. typical (no mutations in p53, or BCL2 and BAX abnormalities, low mitoses, no
necrosis) and atypical (mutations in p53, Bcl2, BAX, more mitoses, necrosis
present)
c. growth ino lumen of main stem broncus or penetration through bronchial wall to
fan out collarbutton lesion;both have microscopic organoid, trabecular,
palisading, or rosette look
d. intermittent attacks of diarrhea, flushing, cyanosis (syndrome); also cough
hemoptysis
99. Apperance of hamarotma on radiography? What is most common tissue in these?
Microscopic findings in inflammatory myofibroblastic tumor? 2 tumors most likely to
grow into lungs?
a. incidental round lesion of radio-opacity (coin lesion); nodule of cartilage most
common
b. prolif of spindle-shaped fibroblasts, myofibroblasts, lymphocytes, plasma cells
c. esophageal carcinomas and mediastinal lymphomas
d. NOTE: lung is most common site of metastatic neoplasms (from both blood and
lymph)
100.
What is most common cause for pathologic involvement of pleura? 2 important
primary disorders? 5 causes of pleural effusion?
a. mst often it is a secondary complication of some underlying disease
b. primary intrapleural bacterial infectins and primary pleural neoplasm
(mesothelioma)
c. increased hydrostatic pressure (congest <3 fail), increased vascular permeability
(pneumonia), decreased osmotic pressure (nephrotic synd), increased intrapleural
negative pressure (atelectasis), and decreased lymph drainage (mediastinal
carcinomas)
101.
Common causes of inflammatory pleuritis? What is empyema and when does it
occur? What is hemorrhagic pleruitis caused by? What is most common cause of
hydrothorax? Hemo-? chylo?
a. inflammatory diseases in lungs (pneumonia, tuberculosis), lung infarcts, lung
abscesses, bronchiectasis, and radiation therapy
b. purulent yellow-green creamy exudate from bacterial seeding of pleural space
(gen from spread of intrapulmonary infection); tends to undergo fibrosis
c. caused by hemorrhagic diatheses, rickettsial disease, and neoplastic involvement
(sanguinous inflammatory exudate; must diff from hemothorax)
d. hydro- clear and straw colored non-inflammatory fluid caused often by heart
failure; hemo- most often from ruptured aortic aneurysm, chylo- thoracic duct
trauma or obstruct
102.
What are pneumothoraxes most commonly associated with (3)? What are 3 forms
and their cause
a. emphysema, asthma, and tuberculosis
b. spontaneous (can complicate lung disease or can be idiopathic from rupture of
apical subpleural blebs), traumatic (chest wall injury), tension (defect acts as flap>air trapped in)
103.
What is most common cause of pleural tumors? What exudate do these tend to
produce? What is microscopic appearance of solitary fibrous tumor? How diff from malig
mesothelioma?
a. secondary metastatic involvement (often from Breast and Lung)
b. tend to cause serous or serosanguineous effusion (often containing neoplastic
cells)
c. confined; consists of fibrous tissue with whorls of reticulin and collagen fibers
and interspersed spindle cells;
d. tumor cells are CD34+ and keratin-negative (diff from meso) and no relation to
asbestos
104.
What causes increased risk of malig mesotheliomas? What doesn't? What is
macroscopic appearance of these tumors? 3 microscopic patterns?
a. asbestos exposure increases risk; smoking does not (in contrast to lung cancer)
b. diffuse pink gelatinous tumor that spreads widely in plerual space (lots effusion)
c. Epithelioid (cuboidal, columnar, or flattened cells), sarcomatoid(spindle cells
resembling fibrosarcoma), and mixed (has both of other 2)
105.
How can epithelioid type of mesothelioma be distinguished from lung
adenocarcinoma(5)? What other mesothelioma strongly linked to asbestos? Clinical
presentation of mesothelioma?
a. meso stains positive for acid mucopolysaccharide, lacks staining for epithelial
glycoprotein antigens, stains for perinuclear keratin, stians for calretinin, EM (no
lamellar bodies)
b. peritoneal mesothelioma highly related
c. present with chest pain, dyspnea, and recurrent pleural effusions; metast to hilar
nodes