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73 Cards in this Set

  • Front
  • Back
q
Pulm Edema
Congestion-increased blood because of decreased blood flow
hyperemia (active process, increased blood flow)

Two catagories
Cardiogenic (increased hydrostatic pressure)

Noncardiogenic (increased vascular permeabilty)

Increased fluid in alveoli, decreased ventilation

Macroscopically
fluid in lungs, become heavy
When sectioned-fluid oozes out (glistening surface)

Alveolar septi which are congested
normally look clear (gas) but this is filled with pink a cellular "protein" fluid.
RBC- congestion
q
Heart Failure Cells
Chronic
Microhemmoraghes
Alveolar macrophages breakdown RBCS
brown pigment-hemo (heart failure cells cus commonly associated with CHF)
.q
ARDS
Majority of cases
Pulm infection, sepsis, trauma, aspiration (more than half of cases)

Looks very similar to pulm edema, damage to alveolar capillaries and alevolar epithelia cells --> increased fluid in alveolar space

Aspiration (gastric juices)
.q
Hyaline Membranes in DAD
Characteristic amourphous dense hyaline membranes

decreased lung function, mortality increase, can have fibrosis
q
Pulm Embolus
multiple causes of emboli
Fat emboli (fractures in bones)
Air emboli (deep sea diving)

Multiple fates of thrombis, not just embolise
density in lumen
q
Pulm Embolus
Occludes major pulmonary arteries

complication of sudden death

Primary thrombus in lung is very rare
Clot in lung is almost going to be embolic
q
Pulm Embolus
Formed from thrombi
blood flowing
see a striated layered appearance

WBCs, fibrins, blood
q
Pulm Embolus
Layered appearance

Lines of Zahn
When die, blood stops flowing, postmortem emboli, not important

Lines of zahn suggest premortem clots
q
Organizing Pulm Embolus
Organazing, recanulize the clots
Big proximal--> sudden death
Small, peripheral, recannulize, left with pulm hypertension or decreased vascularization
q
Pulm Hemorrhagic Infarct
Organazing, recanulize the clots
Big proximal--> sudden death
Small, peripheral, recannulize, left with pulm hypertension or decreased vascularization

triangular profile
apex pointing toward the hilum
hemmoraghic-bloody
q
Hemorrhagic pulmonary infarct
small white outline
fibrous layer. reorganization
q
Resolving Pulmonary Infarct
white outline,
reorganization
q
Ashtmatic Lung Autopsy
lungs are hyperinflated at death
cus lungs are almost touching at the midline
q
Bronchial Mucous Plug in Asthma
Die of status asthmaticus (severe asthma attack)

here we have a lot of muscos giving a tree like appearance
q
Asthma
Left to Right
basophilic mucus
epithelium
asthma developed hypertrophy
small dark nuclei are inflammatory cells
eosinophils are commonly present (red appearance)
q
Centrilobular Emphysema
classically associated with cig smoke
more proximal "central" acinus which are affected
q
Centrilobular Emphysema
destruction of alveolar septi and enlargement of the are space
q
Centrilobular Emphysema
tends to affect the upper lobe first
q
Centrilobular Emphysema
enlarged alveolar space
septi have been destroyed
q
Panilobular Emphysema
associated with the genetic disorder
characteristic entire acinus
q
Panacinar Emphysema
affects lower lobe more prominently
q
Bronhiectasis
dilation of airways
caused by destruction of muscle and elastic tissue
two etiologies
obstruction
chronic inflammation
can trace out larger airways but narrow closer to the entierior
q
Bronchiectasis
dont see normal structure (smooth muscle, epi cells etc)

but overrun with inflammatory process which causes everything to become messed up
q
Pneumoconiosis
Results from restrictive lung disease
decreased vital capactiy, decreased oxygen diffusion

Silicosis: occupation exposure (sandblaster, coal worker)
inhaled--> macrophage response--> release of stuff that cause fibroblast to respond--> nodules--> can enlarge

Asbestosis (interstitial fibrosis)
same process but not nodular
get interstitial fibrosis which impairs oxygenation

coal worker (carbon inhalation)


(inhalation of inorganic or organic substance-->fibrosis and scarring

Silicosis
silicotic nodule
pink-fibrosis
peripheral- lots of inflammatory cells
q
Asbestos Body
Long, cylindrical

when trying to remove it
gets coated with protein (iron)
stain with prussian blue
q
Asbestosis
thickened interstium

asbestos-associate with malignancy
lung cancer and mesothelioma
q
big lung mass
qq
SCLC
cig smoke, centrally located, advance stage disease at time of diagnosis

therfore not surgical canidate
good for treatment
but very aggressive (5% 5 year)
q
SCLC
sea of blue
small, mostly nucleus, very little cytoplasm,

oval, elongated (spindle shaped)
Highly mitotic
q
SCLC
nuclei are fragile, tend to smear out
small cells, rapidly dividing, often has necrosis
q
Adenocarcinoma
peripherally located tihink adenocarcinoma
well circumfrence
q
Adenocarcinoma (bronchioloalveolar carcinoma)
has a pneumonic pattern (looks like a pneumonia)
q
Adenocarcinoma
Two features
1)formed glands (central lumen, tumor cells line the lumen)
2) mucous
q
Adenocarcinoma
example of the gland
q
presence of mucin, or mucin production represented by this clear area
q
Squamous Cell Carcinoma in Left Mainstem Bronchus
centrally located, firm (not like SCLC)
q
Squamous Cell Carcinoma
Two features
1- squamus pearls "layered"(concentric arrangement of cells)
Become keratinized
2)skinny white areas are the intracellular ridges
.
Squamous Cell Carcinoma
Two features
1- squamus pearls "layered"(concentric arrangement of cells)
Become keratinized
2)skinny white areas are the intracellular ridges
q
Metastatic Carcinoma

not related to slide
Large cell carcinoma
not sclc
not adeno
not squamous
q
Mesothelioma
these cells line your pleura cavity, peritineol, and pericardial

takes decades layer after asbestos exposure
tumor arises in the pleura
grows and surroundes the lungs
thick rind of tissue
q
Mesothelioma
doesnt have a good chracteristic
q
hyaline membranes in DAD
q
Saddle Embolus
q
Pulm Embolus
q
Embolus in Pulmonary Artery
q
Recanalized Pulmnary Embolus
q
Hemorrhagic Pulmnary Infarct
q
Hemorrhagic Pulmonary Infarct
q
Eosinophilia in Bronchus in Asthma
q
Asthmatic Bronchitis
q
Panlobular Emphysema
q
Bronchiectasis
q
Bronchiectasis
q
Silicosis
Note refracile material under polarized light
q
Coal Miners Lung
q
Asbestos Body
q
Ferruginous Body
same as the asbestos body but with iron and prussian blue stain
q
SCLC
q
Squamous Cell Carcinoma
q
Squamous Cell Carcinoma of Bronchus
q
Mesothelioma
q
mesothelioma
Pulmonary Congestion and Edema
Station #1: Pulmonary congestion and edema
Pulmonary edema can result from hemodynamic disturbances (cardiogenic pulmonary edema) or from direct increases in capillary permeability, owing to microvascular injury (see Table 15-1)
Pathologic findings:
1. Congested lung appears dark red/brown macroscopically
2. Microscopic appearance of pulmonary edema: engorged capillaries and pink
proteinaceous material within alveoli
3. Microscopic appearance of chronic pulmonary congestion: “heart failure cells”
(hemosiderin-laden macrophages within alveolar spaces)
ARDS/ Diffuse Alveolar Damage (DAD)
Station #2: Adult Respiratory Distress Syndrome/Diffuse alveolar damage (DAD)
DAD is pathologic correlate to clinical “adult respiratory distress syndrome” (ARDS) Common reaction to lung injury from a variety of different causes (see Table 15-2)
Pathology: Diffuse damage to alveolar capillaries and lining epithelium with formation of “hyaline membranes” – pink material composed of fibrin-rich proteinaceous material and lipids
In ARDS, type I cells undergo necrosis as a result of diffuse cell injury. Intra-alveolar edema follows, after which there is formation of hyaline membranes composed of proteinaceous exudates and cell debris. Type II pneumocytes proliferate to line the alveolar spaces.
Pulm Embolism
Station #3: Pulmonary embolism
Embolus is defined as “occlusion of a blood vessel by a mass of material that is transported in the bloodstream.”
- Most commonly involves thrombus, called a “thromboembolus”
- Vast majority of pulmonary emboli arise from DVT of legs Conditions predisposing to DVT/PE:
- Immobility and bed rest
- Post-operative period
- Pregnancy and post-partum period
- Oral contraceptives
- Nephrotic syndrome
- Severe burns and trauma
- Disseminated malignancy
Clinical effects:
- Large massive emboli (“saddle emboli”): Sudden death
- Medium sized emboli
i. Healthy persons: hypoxemia
ii. Individuals with CHF/lung disease: pulmonary infarct
- Small emboli:
i. Few emboli: may undergo thrombolysis
ii. Numerous: pulmonary hypertension
Pulmonary Infarct
Station #4: Pulmonary infarct
PE usually causes infarction only in patient with pre-existing heart or lung disease, such that pulmonary circulation is already compromised
Grossly appears as a wedge-shaped, hemorrhagic, raised areas with the apex pointing to the hilum of the lung and the base at the pleural surface
Asthma
Station #5: Asthma
Individuals dying of an asthmatic attack (status asthmaticus) show hyper-inflated lungs Microscopic:
1. bronchial smooth muscle hypertrophy
2. hyperplasia of mucous glands
3. mucous plugs
4. inflammation (particularly eosinophils)
COPD
Station #6:COPD
Emphysema: Abnormal permanent enlargement of airspaces distal to the terminal bronchiole, accompanied by destruction of their walls and in the absence of fibrosis
- Centrilobular: Chronic smoking
- Panacinar: Alpha-1-antitrypsin deficiency
Chronic bronchitis: No characteristic pathologic findings, but defined clinically (persistent productive cough for at least 3 months in at least 2 consecutive years)
Bronchiectasis
Station #7: Bronchiectasis:
Permanent dilation of airways caused by destruction of muscle and elastic tissue, usually associated with chronic necrotizing infections and/or obstruction
- Not a single disease but a result of other disease processes
- Grossly, dilated bronchi/bronchioles may be traced from hilum to pleura Associated diseases: Bronchial obstruction (tumor, foreign body, etc), infections such as necrotizing pneumonia, cystic fibrosis, immotile cilia syndrome (Kartagener’s syndrome)s
Pneumoconioses
Station #8: Pneumoconioses
Lung disease secondary to inhaled organic and inorganic particles
Coal worker’s pneumoconiosis (anthracosis): exposure to coal (carbon), often associated with exposure to silica or tuberculosis
Silicosis: Chronic pulmonary fibrosis with silicotic nodules
Asbestosis: Inhaled asbestos fibers causing pulmonary fibrosis
a.
Asbestos bodies: Coated with iron and protein (“ferruginous bodies”)
Asbestos-related lung disease
Station #9: Asbestos-related lung disease
Localized pleural fibrous plaques: usually asymptomatic, flat fibrous thickening of pleura Asbestosis: Intersitial lung disease (fibrosis)
Carcinoma of the lung
Mesothelioma
Lung Cancer
Station #10: Lung cancer (Carcinoma of the lung)
Four main histologic types:
1. Small cell carcinoma (20-25%): Small undifferentiated cells, marked mitotic
activity, frequently necrotic
a. Paraneoplastic syndromes: Cushing syndrome (ACTH), SIADH,
Eaton-Lambert syndrome
2. Squamous cell carcinoma (25-40%): Centrally-located, composed of polygonal cells with intracellular bridges and “keratin pearls”
a. Paraneoplastic hypercalcemia (due to PTH-related hormone)
3. Adenocarcinoma (25-40%): Peripherally-located, gland-forming neoplasm
4. Large cell carcinoma (10-15%): Large undifferentiated cells showing neither
squamous nor glandular differentiation
Prognosis largely depends on stage of disease and histologic subtype/grade
EGFR (epidermal growth factor receptor): Activating mutations of the tyrosine kinase domain of EGFR are important in adenocarcinomas, as those adenocarcinoma with mutated EGFR may be treated with tyrosine kinase inhibitors (gefitinib or erlotinib).
Mesothelioma
Station #11: Mesothelioma
Malignant neoplasm of mesothelium (visceral or parietal pleura, or sometimes arising in the peritoneum)
- Strong association with prior asbestos exposure
- Grossly, mesothelioma diffusely involves the pleura and encases the lung
- Poor prognosis, with 50% of patients dying within 1 year