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Pulmonary > Pulm 2 > Flashcards

Pulm 2 Flashcards

1
Q

What is honeycomb lung?

A

End stage lung -final result of many interstitial lung diseases

Severe fibrosis with architectural remodeling resulting in large arispaces with thick fibrous walls

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2
Q

What is this?

A

Honeycomb lung- end stage lung

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3
Q

What is this?

A

HOneycomb lung

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4
Q

What are common featurs of interstitial lung diseases?

A

Decreased compliance

Decreased lung volumes

Impaired diffusion

Devlopment of pulm HTN

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5
Q

How does fibrosis happen?

A

Abnromal repair with replacement by dense connective tissue and loss of normal architecture

Pathogenesis is poorly udnerstood, but linked to inflammation and abnormal wound healing

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6
Q

What is the interstitium of the lung?

A

Basement membrane of endothelial and epithelial cells, fibroblasts, collagen fibers, and elastic tissue

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7
Q

What do we see here?

A

Interstitial lung disease

Normal is :

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8
Q

what is Usual interstitial pneumonia (UIP)?

A

Age = 50+

Insiduous onset with exertional dyspnea and chronic evolution

Complications include pulm HTN, cor pulmonale and cardiac failure

Assoc. with collagen vascular disorder or autoimmune, but most ar idiopathic

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9
Q

What is Idiopathic pulmonary fibrosis (IPF)?

A

UIP pattern on histology plus idiopathic disease clinically

UIP = Usual interstitial pnuemonia

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10
Q

What do you see on hisotlogy in UIP?

A

PATCHY fibrosis, most pronounced beneath plura next to interlobular septa

Fibrosis has TEMPORAL HETEROGENEITY - not all same age -> Fibroblast focus = region on loose blue-gray connective tissue adjacent to an area of dense collagenous scar (new and old fibrosis next to each other)

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11
Q

What is a fibroblast focus?

A

Region of loose blue-gray connective tissue (new fibrosis) next to an area of dense collagenous scar (old fibrosis)

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12
Q

What do we see here?

A

Patchy fibrosis with subpleural predominance

UIP

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13
Q

What do we see here?

A

Patchy fibrosis

Severe alternates with spared lung

UIP

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14
Q

What do we see here?

A

Fibroblast focus - odl and new fibrosis

UIP

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15
Q

How do you treat UIP?

A

Steroids provide minimal benefit

3 years or less survival mean

Transplant may be an option

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16
Q

What is Non-specific Interstitial Pneumonia (NSIP)?

A

Similar to UIP clinically, but seen in younger patients

Improved prognosis over UIP especially at 5 years

Cellular has better prognosis than fibrosing subtype

Responds better to steroids

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17
Q

What do we see in NSIP on histology?

A

Cellular: diffuse chronic inflammatory cell infiltrates without significant alveolar expansion; no fibrosis

Fibrosing: diffuse interstitial fibrosis with uniform appearance; fibrosis is all same age (temporally uniform); lung architecture preserved

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18
Q

What is this?

A

Cellular NSIP - uniform involvement of lung by chronic interstitial inflammation

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19
Q

What is this?

A

Fibrosing NSIP - uniform involvement of lung by fibrosis of the same age

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20
Q

What is lymphocitic interstitial pneumonia (LIP)?

A

Rare- seen in patients with sjogren’s syndrome and HIV

Rarely idiopathic

Presents as cough/dyspnea

Radiology classically shows diffuse ground glass changes with cysts

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21
Q

What do you see in microscopy on LIP?

A

Small mature lymphocytes with variable numbers ofplasma cells expandign the alveolar septa

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22
Q

What do we see here?

A

LIP

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23
Q

What is sarcoidosis??

A

Multisystemic disease of unknown origin with lung involvement in 90% of cases

Classic: Interstitial/nodular lung infiltrates and bilateral hilar adenopathy

20-40 years; Females, 90% black

Elevated serum ACE

Most people recover

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24
Q

What do you see clinically in sarcoidosis?

A

Lungs: either no gross lesion or 1-2 cm nodules, often in bronhial submucosa

LN: hilar or mediastinal lymph nodes

Liver/spleen: microscopic involvement

Bone: xray changes in 20% in small bones

Skin: 30-50% involvement

Eye: iritis or iridocyclitis in 20-50%

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25
Q

How does sarcoidosis appear morphologically?

A

NON-NECROTIZING epithelioid granulomas

Tightly packed epithelioid cells, giant cells, and T cells adjacent to bronchioles aroudn broncovascular bundle

Diffuse interstitial fibrosis in small number of cases

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26
Q

What do we see here?

A

Sarcoidosis

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27
Q

What do we see here?

A

Non-caseating granuloma

Sarcoidosis

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28
Q

How do you diagnose sarcoidosis?

A

Diagnosis of exclusion as other things can casue it (infeciton, hypersensitivity pneumonitis)

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29
Q

What is hypersensitivity pneumonitits (extrinsic allergic alveolitis)?

A

Inhalation of organic antigen

Acute: within hours of exposure -not well described

Chronic: extended exposure, may be progressive with fibrosis (type 3 and 4 hypersensitivity combination)

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30
Q

What is the inciting event in hypersensitivity pneumonitis?

A

Typically due to exposure to thermophillic bacteria or fungi

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31
Q

What is the classic triad of hypersensitivity pneumonitis?

A

Chronic bronchiolitis/interstitial pneumonia

Poorly formed/vague granulomata

Organizing pneumonia

Long standing chronic disease may evolve into diffuse fibrosis

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32
Q

What do we see here?

A

Bronchiocentric pattern of inflammation in hypersensitivity pneumonitis

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33
Q

What do we see here?

A

Hypersensitivity pneumonitis

Peribronchiolar inflammation with airway remodeling

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34
Q

What do we see here?

A

Poorly formed granuloma

Hypersensitivtiy Pneumonitis

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35
Q

What is respiratory bronchiolitis and respiratory bronchiolitis-associated interstitial lung disease (RB-ILD)?

A

RB is accumulation of macrophages in smokers with granular brown pigment in small airways

RB-ILD is RB on biopsy plus clinical symptoms of interstitial lung disease (and no other findings)

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36
Q

What do we see here?

A

Respiratory bronchiolitis

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37
Q

What is desquamative interstitial pneumonia (DIP)?

A

Similar to RB-ILD but disease is more diffuse and with more severe symptoms

Adults typically with insiduous shortness of breath

Exclusively seen in smokers

X-ray shows bilateral lower lobe, gorudn glass infiltrates

Tx with steroids and smoking cessation

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38
Q

What do you see microscopically in DIP?

A

Diffuse collections of intraalveolar macrophages containing finely granular brown pigment

Minimal involvement of alveolar septa; no significant firosis

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39
Q

What do we see here?

A

DIP

Desquamative interstitial pneumnia

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40
Q

What do we see here?

A

Smoker’s macrophages with finely granular brown pigment

Seen in Desquamative interstitail Pneumonia (DIP)

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41
Q

What is langerhans cell histiocytosis?

A

Seen exclusively in cigarette smokers (males)

Bronchiolocentric fibrosis with stellate scar formation

Variable numbers of langerhans cells, eosinophils

S-100, CD1a positive

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42
Q

What do we see here?

A

Stellate airway centerd fibrosis of langerhans cell histiocytosis

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43
Q

What do we see here?

A

Langerhans cells, eosinophils, and pigmented macorphages of langerhans cell histiocytosis

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44
Q

What do we see here?

A

Birbeck graule characteristic of histiocytes

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45
Q

What is a ferruginous body?

A

General term referring to any inorganic substance with a coating of iron and protein - graphite, ceramic, iron, etc

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46
Q

What is an asbestos body?

A

Ferruginous body formed on an asbestos fiber - characterized by clear internal core and beaded ferruginous coating

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47
Q

What are manifestations of asbestos disease?

A

Pleural fibrosis and/or pleural plaques (bilateral, calcified)

Pulmonary parenchymal fibrosis (asbestosis) leading to end stage fibrosis (honeycomb lung)

Malignancies (lung carcinoma, mesothelioma)

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48
Q

What are pleural plaques?

A

Well circumscribed plaques of desne collagen, often with calcium, on parietal pleura and dome of diaphragm, doesn’t contain asbestos body, but rare if no asbestos history

May induce pleural effusion, no symptomatology typically

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49
Q

What do we see here?

A

Benign plaques - parietal and diaphragmatic pleura

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50
Q

What is asbestosis?

A

Diffuse interstitial fibrosis secondary to asbestos exposure (heavy)

Initial injury at bifurcations of small airway and ducts

Fibrosis begins aroudn respiratory bronchioles and alveolar ducts, extending distally, causing honeycomb lung

Begins in lower lubs and subleurally and proresses upwards

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51
Q

What do we see here?

A

Honeycomb on left, normal on right

Asbestosis

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52
Q

What do we see here/

A

Asbestosis - mimics UIP

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53
Q

What do we see here?

A

Giant cell reaction to asbestos bodies

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54
Q

What do we see here?

A

Asbestos bodies

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55
Q

What is silicosis?

A

Chronic occupational lung disease casued by exposure to free silica dust

Seen in miners, glass manufacturers, sand blasters, and stone cutters

INgestion of silica by alveolar macrophages -> damage initiates inflammatory response

Marked by silicotic nodules that enlarge and obstruct airways and blood vessels

Increased susceptibility to TB: Silicotuberculosis

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56
Q

How does silicosis appear grossly?

A

Early, tiny, discrete pale to black nodules in upper lungs

NOdules have stellate shape at edges

Fibrosis present at hilar nodes and pleura - eggshell calcificaiton

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57
Q

What do we see here?

A

Silicosis

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58
Q

How does silicosis appear microscopically?

A

Early - small nodules of fibroblastas and histiocytes with abudnant cilia

Onion-skin fibrosis typically

Become more hyalinized over time with proressive massive fibrosis

Later is hyalinized and condensed collagene needle-like spicules with pointed ends

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59
Q

What do we see here?

A

Subpleural silicotic nodule

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60
Q

What do we see here?

A

Silicotic nodule

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61
Q

What do we see here?

A

Silicotic nodule with lamellar fibrosis

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62
Q

What dow e see here?

A

Silica under polarized light

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63
Q

What is coal worker’s pneumoconiosis?

A

Coal macules and coal nodules scattered throughout lung

Seen in upper lobe and upper lower lobe, near respiratory bronchioles

Minimal symptoms, but 10% develop progressive massive fibrosis

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64
Q

What is progressive massive fibrosis?

A

Complicated coal worker’s pneumoconiosis -> intensely blackened scars contianing dense collagen and pigment; may be necrotic

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65
Q

What is caplan syndrome?

A

Rheumatoid arthritis and pneumoconicosis cause rapidly developing nodular pulmonary lesions identical to rheumatoid nodules typically seen in soft tissue

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66
Q

What do we see here?

A

Simple coal workers pneumonconiosis

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67
Q

What do we see herE?

A

Simple coal worker’s pneumonconiosis

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68
Q

What do we see here?

A

Black lung

Progressive massive coal worker’s pneumoconiosis

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69
Q

What do we see here?

A

Massive progressive coal worker’s pneumoconiosis

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70
Q

What is IIP?

A

Idiopathic interstitial pneumonias

Acute, chronic or sub-actue

Respiratory symptoms are non-specific

RESTRICTIVE (Decreased FVC< TLC, preserved FEV1/FVC ratio, decreased DLCO, and incerased A-a gradient)

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71
Q

What are fibrotic changes on chest x-ray in interstitial lung disease?

A

Traction bronchiectasis

Reticular densities

Honeycombing

Cysts

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72
Q

What do we see here?

A

Traction bronchiectasis

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73
Q

What do we see here?

A

Reticular abnormalities

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74
Q

What do we see here?

A

Honeycombing and Cysts

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75
Q

What are inflammatory radiographic changes you see in interstitial lugn disease?

A

Ground glass opacity

Consolidation

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76
Q

What do we see here?

A

Ground glass opacity of inflammatory interstitial lung disease

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77
Q

What do we see ehre?

A

Consolidation of inflammatory interstitial lung disease

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78
Q

What is IPF?

A

Idiopathic pulmonary fibrosis

Usual interstitial pneumonia is the histoopathology pattern

Most common of the IIPs

Most deadly (90% mortality)

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79
Q

Who gets IPF?

A

Older people

Males more than females

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80
Q

What are salient clinical features of IPF?

A

Subacute or chronic

Insidious onset of dyspnea

Cough
Rales

Clubbing

Restrictive PFTs (TLC, FVC)

Impaired gas exchagne (DLCO, A-a gradient)

There is no diagnostic blood test

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81
Q

What do you suspect here?

A

IPF - idiopathic pulmonary fibrosis

Basal, peripheral, subpleural

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82
Q

What do we see here?

A

IPF on the right, normal on left

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83
Q

What is the prognosis for IPF?

A

Very bad

Things that are worse:

Pulmonary HTN

Low DLCO

Decrease PFT’s over 6 months

Desaturation to SpO2 < 88%

Fibroblast foci on surgical lung biopsy

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84
Q

How do you treat IPF?

A

Nothign works

Lung transplant is only good option

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85
Q

Which IIP has the best prognosis?

A

COP (Cryptogenic Organizing Pneumonia)

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86
Q

What does Interstitial Lung Disease indicate about the prognosis for a patient with a connective tissue disorder?

A

Worsens prognosis

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87
Q

What is the interstitial lung disease seen in connective tissue diseases?

A

Nonspecific interstitial pneumonia

Specific histologic pattern (uniform)

Young patients, associated with Systemic scleroderma, Dermatomyosytis, polymyositis

Good response to therapy: fair prognosis

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88
Q

Who gets sarcoidosis?

A

20-40 years old; (second peak in Japan and Scandanavia in women > 50)

Females:Males 2:1

More prevalent in blacks (more common, and present more severe, and with extrapulmonary disease)

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89
Q

What is the proposed mechanism of sarcoidosis?

A

genetically predisposition

Cell mediated immune response to one or more unidentified antigens

Hallmark of sarcoidosis = epithelioid granulomas

CD4 driven process

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90
Q

What cell type drives the disease in sarcoidosis?

A

CD4 T cells

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91
Q

What is needed in order to diagnose sarcoidosis

A

BIOPSY

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92
Q

What is Lofgrens Syndrome?

A

Sarcoidosis syndrome

Erythema nodosum, hilar adenopathy, uveitis

Patients are symptomatic from erythea nodosum and arthralgias, seek medical attention -> good prognossis

BAL shows acticated CD4 lymphocytes

Bizarre, explosive manifestation; resolves

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93
Q

What ist he relationship between the respiratory tract and sarcoidosis?

A

Occurs at some time in essentially all patients (90% is sole manifestation)

Dyspnea, cough, chest pain in many; hyperreactivity in 20%, obstructive disease in up to 30%

Interstitial lung disorder involving alveoli, blood vessels, bronchioles (T cell alveolitis)

Bronchoscopic lung biopsy diagnostic in > 80% of patients

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94
Q

What do you see here?

A

Stage 1 sarcoidosis

bilateral hilar adenopathy

seen in 50% of patients; no respiratory symptoms

60-80% have spontaneous remission

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95
Q

What do you see here?

A

Stage 2 sarcoidosis

Lymph node involvement + interstitial infiltrates

In 25% of patients

Have symptoms of fever, weight loss, dyspnea

50-60% have spontaneous remission

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96
Q

What do we see here?

A

Stage 3 sarcoidosis

15% of patients

Significant respiratory impairment

<30% have spontaneous remission

Non-productive cough; restrictive disease

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97
Q

What do we see here?

A

Stage 4 sarcoidosis

5% of patients

Chronic respiratory impairment

High mortality rate

Restrictive lung disease, may develop pulmonary HTN, may become colonized with aspergillus

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98
Q

Where in the lung lobes do you typically see infiltartion in sarcoidosis?

A

Upper lung zones

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99
Q

What do you see on pulmonary funciton tests in sarcoidosis?

A

Restriciton more common

Gas transfer defect is likely

OBstruction may be present with or without bronchodilator response (endobronchial disease and/or reactive airway)

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100
Q

How is the lymphoid system involved in sarcoidosis?

A

1/3 have palpable lymph nodes (Cervical, axillary, epitrochlear, inguinal)

Discrete, movable, nontender

Non ulcerative

Extrapulmonary nodes more frequently seen in blacks

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101
Q

What is the relationship between sarcoidosis and the larynx?

A

1-5% of patinets

Hoarseness, dyspnea, stridor

Epiglottos most commonly involved

Localized edmea and erythema with punctate nodules and mass lesions

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102
Q

What is the relationship between sarcoidosis and the eye?

A

1/3 of patinets

Uveitis, chorioretinitis, vitreous opacities, keratoconjunctivitis

lacrimal gland enlargement

MOre frequenlty seen in women

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103
Q

What is the relationship between the heart and sarcoidosis?

A

Ventricular arrhytmias

Sudden death in young males

Heart block, supraventricular arrhytias and CHF/cardiomyopathy

EKG recommended

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104
Q

What ist he relationship between sarcoidosis and the skin?

A

21% of patients

Erythema nodosum is most comon

Maculopapular eruptions, skin plaques, alopecia, subcutaneous nodules

Lupus pernio characteristic - most common in black women, associated with bone scysts and pulmonary fibrosis

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105
Q

What do you see her?

A

Erythema nodosum

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106
Q

What is the relationship between sarcoidosis and MSK?

A

Arthropathy in 25-40%

Arthralgias may occur without radiographic changes, effusions, or erythema

BOne involvement uncommon

Muscle involvment common ((weakness, aches)

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107
Q

What is neruosarcoidosis?

A

CNS involvemnet in sarcoidosis (less than 10%)

Prediliciton for base of the braine (CN inovlvement (Facial palsy, optic neuropathy), hypthalamic and pituitary)

More common in women

Space occupying lesions

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108
Q

What are endocrine manifestations of sarcoidosis?

A

Hypercalcemia in 2-10% (more common in men)

Hypercalcuria in 6-30%

Due to dysregulated production of 1,25-dihydroxyvitamin D3 (calcitriol) by activated macrophages and granulomas

Can cause nephrocalcinosis, renal stones, and renal failure

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109
Q

What is the relationship between sarcoidosis and liver/spleen/kidney?

A

granulomas found in 50-80% of liver biopsy specimens

hepatomegaly in <20%

abnormla LFTs common

SPlenomegaly

Interstitial nephritis is rare

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110
Q

How do you work up a diagnosis of sarcoidosis?

A

Histological confirmation

Assess extent and severity of organ ivolvemnt

Asses likelihood of stability or progression

Determine if therapy will be of benefit

Diagnosis is of exclusion (clinical picture + histology + not something else)

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111
Q

How do you choose a biopsy site for sarcoidosis?

A

Transbronchial lung biopsy is recommended (low risk)

Lymph nodes when palpable

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112
Q

What are prognostic factosr that indicate a likelihood of spontaneous remission of sarcodiosis?

A

Erythema nodosum and acute inflammatory manifestations

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113
Q

What are adverse prognostic factors for sarcoidosis?

A

Lupus pernio

Chronic uveitis

Age > 40 at onset

Chronic hypercalcemia

Nephrocalcinosis

Black race

Cystic bone lesions

Neurosarcoidosis

Cardiac sarcoidosis

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114
Q

How do you treat sarcoidosis?

A

No treatment

If any, corticosteroids

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115
Q

What is on the differential of a sarcoidosis diagnosis?

A
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116
Q

What is a difference bwetween water soluble vs insoluble respiratory irritants?

A

Soluble : immediate effect on Upper respiratory tract and bronchi

INsoluble: delayed effect on alveoli to cause pulmonary edema

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117
Q

What pattern of fibrosis do you see in with coal dust in the lungs?

A

Progressive massive fibrosis

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118
Q

What pattern of fibrosis do you see with silica dust in the lugns?

A

Nodular fiboriss (silicosis)

Progressive massive fibrosis

Can get TB as a complication

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119
Q

What pattern of fibrosis do you see wiht asbestos dust in the lungs?

A

Diffuse fibrosis (asbestosis)

As a complicaiton, you can get lung cancer

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120
Q

What is pneumoconiosis?

A

Pulmonary disease caused by the inhalation of dusts

Classfiied by type of dust (inorganic, organic), and/or type of pathology (fibrosis, granulomas)

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121
Q

What does inorganic dust cause in the lung?

A

Pnemoconiosis

Dose related

Predictable response

Acts like direct toxicant

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122
Q

What are features of inorganic dust-related lung disease (pneumoconiosis)?

A

Dose related

Predictable response

Acts like direct toxicant

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123
Q

What is the result of organic particle-related lung disease?

A

Hyeprsensitivity pneumonitis

Idiosyncratic

prior exposure

Acts like antigen

124
Q

What is pneumoconiosis: silicosis?

A

Results from inhalation of silica; seen in miners, sand-blasters, metal polishing, etc; found in quartz

ingestion by alveolar macrophage; damages macrophage; autolysis of cells and reingestion of particel; disruption of immune cells = susceptibility to TB; releases fibrogenic mediateos and forms silicotic nodules

125
Q

What do we see here?

A

Silicosis: silicotic nodule consisting of hyaline collagine arranged in whorled pattern

126
Q

Whgat are clinical syndromes that can result from silicosis?

A

Simple nodular silicosis

Progressive massive fibrosis

Silico-tuberculosis

127
Q

Where do the nodules of silicosis tend to migrate to?

A

Upper lobes

Hilar nodes (upper)

128
Q

What is progressive massive fibrosis in silicosis?

A

Cavitating PMF, moves upwards in lobes

129
Q

What arde diseases seen in coal miners?

A

Anthracosis

Simple coal workers pneumoconicosis

Complicated coal workers pneumoconicosis (progressive massive fibrosis)

130
Q

What is anthracosis?

A

Asymptomatic carbon dust in lugns

Seen in urban dwellers, coal miners, smokers

Hardly a disease

131
Q

What od we see here?

A

ANthracosis - harmless deposition seen in urban dwellers, smokers

132
Q

What is simple CWP?

A

Greater exposure to coal

NO pulmonary dysfunction, except may be associated with emphysema

Macules aggregates of pigment + macrophages

NOdules may be larger

Contain collagen

133
Q

WHat are three diseases seen with asbestos?

A

Pleural plaque

Interstitial lung disease (asbestosis)

Malignancy (lung carcinoma, pleural mesothelioma, carcinoomas elswehre in respiratory tract)

134
Q

What is a pleural plaque?

A

acellular plaque on parietal pleura

NOt assoicated with pulmonary dysfunction

Good indicator of asbestos exposure

Occasional finding at autopsy

135
Q

Whgat is this?

A

Asbestos plerual plaque

136
Q

What is asbestosis??

A

Diffuse interstitial lugn disease resulting from inhalation of asbestos

Disffuse interstitial fibrosis and asbestos bodies

Progressive respiratory impairment

Lower lobes, shaggy heart

137
Q

What is this?

A

Asbestosis

138
Q

What are the treatments available for and the prognosis of inorganic dust disease (pneumoconicosis)?

A

NO treatment

Early recognition to stop exposure

May still progress after exposrue stops

139
Q

What is RADS (reactive ariways dysfucntion syndrome)?

A

Development of respiratory symptoms in minutes or hours after single accidental inhalation of high concentration of irritant, gas, aerosol, or particles

FOllowed by asthma-like symptoms and airway hyperresponsiveness for prolonged period

140
Q

What is byssinosis?

A

Breathing in cotton dust or dusts from other vegetable fibers such as flax, hemp, or sisal while at work

When sensitized can have asthma-ilke condition after beign exposed

141
Q

WHat is unique about hte structure of pulmonary vessels?

A

Thin walled vessels, compliant, distensible

Can handle entire cardiac output wihtout high pressures

142
Q

What are features of the pulmonary circulation (pressure, resistance)?

A

Low pressure, low resistance

143
Q

What are systolic and diastolic pulmonary artery pressures?

A

25/10

144
Q

How do you measure mean pulmonary artery pressure and mean left atrial pressure?

A

Swan Ganz Catheter

145
Q

What is the pulmonary vascular response to exercise?

A

Increased cardiac output results in a decrease in mean pulmonary vascular resistance

Recruits new vessels, distends previously perfused vessels

High capacity, high compliance, low pressure, low resistnace

146
Q

Which zone of hte lung undergoes most changes during exercise?

A

Zone 1 -> increased blood flow; V/Q ratio nears 1 (rather htan 3.3) in zone 1

147
Q

What is the pulmonary vascular response to hypoxia?

A

Vasoconstriciton in response to alveolar PO2 of 60-70 mmHg

Protective mechanism: decreases perfusion to poorly ventilated areas in order to reduce the V/Q mismatch

don’t see global abnormalities really

148
Q

How does hypoxic pulmonary vasoconstriction occur?

A

Hypoxia inhibits pulmonary artery smooth muscle K+ channel

Ca++ influx and results in smooht muscle contraction

Hypoxia causes decreased NO production

Effects of pH are additive (acidemia causes vasoconstriction too)

149
Q

What are normal mediators of pulmonary vascular tone?

A

Endothelin

Nitric oxide

Arachidonic Acid metabolism products (PGI2 and TXA2)

150
Q

What are the effects of the arachadonic acid metabolism products on pulmonary vascular tone?

A

Thromboxane = constriction

Prostacyclin = dilation

151
Q

What defines pulmonary hypertension??

A

mPAP > 25 mmHg at rest and > 30 mmHg during exercise

152
Q

What are the three factors that lead to pulmonary hypertnesion/

A

Endothelial injury leading to intimal hyperplasia

Abnormal flos (in situ thrombosis)

Smooth muscle hypertrophy

All lead to vbvascular remodeling

153
Q

What is the clinical progression of pulmonary hypertension?

A
154
Q

What is cor pulmonale?

A

Right sided heart failure

ENlargement of the right ventricle due to high BP in the lungs, typicalyl caused by chronic lung disease

155
Q

What are some underlyign causes of pulmonary hypertension?

A

Venous congestion

Destruction of microvasculature

Increased blood flow

Hereditary

Mechanical arterilal obstruciton

Hypoxic vasoconstriciton

Obliteration of vessels

Idiopathic

156
Q

What do you see in idiopathic pulmonary hypertension?

A

Medial hypertrophy

INtimal hyperplasia

Plexiform lesions

Neo-muscularization

In situ thrombosis

Women more than men

Age 20-45 years

Median survival is < 3 years

Requires aggressive therapy with multiple drugs

157
Q

Who gets idiopathic pulm HTN?

A

Women

Age 20-45 years

158
Q

What gene is involved in a heritable form of pulm HTN?

A

BMPR2 (bone morphogneic receptor type 2)

Loss of inhibitory control

Cuases dysegulated endothelial repair, thickening, smooth muscle hypertrophy

159
Q

What are some causes of group 1 pulm HTN?

A

Idiopathic

Genetic
Connective tissue diseases
HIV

Portopulmonary

Schistosomiasis (most common in developing countries)

Hemoglobinopathy

Drugs/toxins (cocaine, methamphetamine, fen-phen)

160
Q

What is gropu 2 pulm HTN?

A

Caused by left sided heart disease’

Increased back presure from left atrium

Mitral stenosis and left ventricular systolic failure

Treat underlying cardiac disease

161
Q

What is Group 3 pulm HTN?

A

Hypoxia associated conditions

INterstitial lugn disease, COPD, obstructive sleep apnea, chest wall disorders, obesity

Hypoxic pulm vasoconstriction

Destruciton of alveolar surface area due to scarring/emphysema

RV failure can lead to cor pulmonale

NEeds treatment of underlying disease and correciotn of hypoxia

162
Q

What is group 4 pulm HTN?

A

Chronic thromboembolic

Multiple and recurrent PEs

Occlusion of blodo vessels wtih clots gives rise to increasing PVR

Needs anticoagulation and surgery (thromboendarterectomy)

163
Q

What are clinical features of pulmonary HTN?

A

Exertional dyspnea

Exertional fatiuge

Chest pain, palpitations, light headedness

Syncope

Lower extremity edema

Raynaud’s PHenomenon

164
Q

What can you see on physical exam in a patient with pulmonary HTN?

A

Lower extremity edema, JVD, hepatomegaly, ascites

Loud P2, RV heave

Right sided S3 (mid diastolic)

Right sided S4 (pre systolic)

Systolic murmor of tricuspid regurg

Graham Steell murmor of pulmonary insufficiency

165
Q

What diagnostic tests do you order when you suspect pulmonary HTN?

A

Chest Xray

See hilar prominaence

Pruning of vessels

Underlying COPD, ILD

166
Q

What do we see here?

A

CXR of Pulmonary HTN

167
Q

What is the best diagnosit test for gropu 2 pulm HTN?

A

Echo - non-invasive heart ultrasound to check heart function (group 2 is caridac related)

168
Q

What do we see here?

A

Echo in pulm HTN

169
Q

WHat is the gold standadr for diagnosis of pulmonary HTN?

A

Right heart cath (swan ganz)

170
Q

Why do you order a ventilation/perfusion scan when you suspect pulmonary HTN?

A

To check for thromboembolic causes -> CURABLE

171
Q

How do you treat pulmonary HTN?

A

Essentially counter the effect of vasoconstrictors in the pulmonary vasculature

Blocking endothelin receptor (endothelin receptor antagonist)

Augment nitric oxide

Augment prostacyclin (PGI2) - analogs

172
Q

What are the components of Virchow’s Triad?

A

Stasis

Venous injury

Hypercoagulability

173
Q

What is a mnemonic to remember the risk factors for thromboembolism?

A

SIT CALM

Surgery
Immobilizaiton

Trauma/Thrombophilia

CHF

Age

“Lines” -catheters

Malignancy

174
Q

What is the most common genetic risk factor for thrombophilia?

A

Factor V Leiden Mutation

175
Q

What is the relationship between malignancy and thromboembolisms?

A

Pro-coagulant effects of tumor; immobility, presence of catheters

176
Q

What is the relationship between DVT and pulmonary embolism?

A

79% of PE patients have DVT

50% of patients with DVT get PEs

Femoral vein is common

177
Q

What pathophysiologic defect occurs in PEs?

A

Dead spacing

178
Q

Why is there hypoxemia in PEs?

A

Chemical mediators released by thrombi (serotonin) can cause small airway constriction (low V/Q - like a shunt)

Surfactant produciton is impaired (collapse of alveoli - atelectasis -> low V/Q units)

Impaired cardiac output -> increased O2 extraction -> decreased venous SpO2

179
Q

What are typical symptoms of PE?

A

Dyspnea at rest or exertion

Pleuritic pain

Cough

Orthopnea

Calf or thigh pain/swelling

Wheezing

180
Q

What are signs on PE for PE?

A

Tachycardia

Tachypnea

Hypotension (if massive)

JVP

Decreased breath sounds, dullness, sometimes wheezing

Extremities for DVT, Homan’s sign

181
Q

What are diagnostic modalities for PE?

A

ABGs

ECG

D-Dimer

Imaging

182
Q

What do you see on arterial blood gases in PEs?

A

Respiratory alkalosis (Tachypnea)

A-a gradient (hypoxemia in low V/Q units)

Metabolic acidosis (lactic acidosis) if massive PE

183
Q

How can an EKG help diagnose PE?

A

Non-specific ST/T changes

Sinus tachycardia

Maybe a RBBB or RAD with massive PE

S1Q3T3

184
Q

What is the usefulness of d-dimer in PE diagnosis?

A

Very sensitive (good negative predictive value) - Normal rules out PE

Not very specific - can be anything else

185
Q

What can you find on CXR in a patient with PE?

A

Normal CXR is classic

Can see hampton’s hump, enlarged pulm artery, westermark’s sign, or plerual effusions

186
Q

How does an ultrasound help diagnose PE?

A

Can identify a DVT if it s there

187
Q

How can a V/Q scan help diagnose PE?

A

Normal VQ scan effectively rules out PE - > negative predictive value is almost 100%

188
Q

What are pros and cons of CT angiogram for PE diagnosis?

A

Very good image of vasculature and parenchyma

Cons: IV contrast exposes patients to radiation and also is nephrotoxic

189
Q

What lesion do you characteristically see in primary pulmonary hypertension

A

Plexiform lesion

190
Q

When do you see plexiform lesions?

A

Primary pulmonary hypertension, not in secondary

191
Q

What is a plexiform lesion?

A

Dilated segment of artery consisting of numerous slits like vascular channels

Primary Pulmonary HTN

192
Q

What pulmonary signs do you see pathologically in Wegener’s Granulomatosis?

A

Irregular areas of necrosis

Vasculitis

193
Q

What is Churg-Strauss syndrome?

A

Triad of asthma, eosinophilia, and vasculitis

Male=Female; ~50 year olds

Neuropathy, cardiac, lung, sinonasal involvement; Renal involvement NOT common

Lung Xray with multifocal infiltrates (change over time)

194
Q

What do you see on lung pathology in Churg-Strauss?

A

Histology: asthmatic bronchitis, eosinophilic pneumonia, extravascular stellate granulomas, vasculitis

Granulomas = palisaded histiocytes and multinucleated ginat cells, center necrosed with eosinophils

Vasculitis of arteris, veins, or capillaries

195
Q

What od we see here?

A

Granulomas of Churg-Strauss

Centers have necrosis with prominent eosinophils.

196
Q

What is microscopic polyangiitis?

A

MPA = pauci-immune vasculitis restricted to arterioles, venules, and capillaries

Glomrulonephritis, fever, myalgia and arthralgia, weight loss, ear, nose throat symptoms, skin involvement

pANCA positive

197
Q

What do you see in lung pathology in microscopic polyangiitis?

A

Diffuse alveolar hemorrhage with neutrophilic capillaritis

No granulmoas, giant cells, eosiniophilia

No Ig deposits

198
Q

What do we see here?

A

Neutrophilic capillaritis

Characteristic of microscopic polyangiitis, but also:

collagen vascular disease (lupus), Wegener’s, Goodpasture’s, Antiphospholipid Ab sydnrome, drug reaction, infection

199
Q

What is diffuse alveolar hemorrhage?

A

Rare, but life-threatening complication of immune disorders

May present wiht fulminant respiratory failure

Hemoptysis

200
Q

What is the most common cause of lung cancer?

A

Tobacco

Risk related to duration and amount of smoking

Not just nicotine: polycyclic aromatic hydrocarbons, tobacco-specific nitrosamines

201
Q

Who is more at risk for lung cancer, men or women?

A

Women

202
Q

What are non-smoking risks for lung cancer?

A

Environmental/passive tobacco smoke

Radiation exposure (radon gas)

Air pollution)

cooking oil fumes and indoor coal/biomass burning

Prior lung disease

203
Q

What is the most common cancer from asbestos exposure?

A

Lung cancer, NOT mesothelioma

204
Q

What is the most common presentation of lung cancer?

A

Pulmonary nodules

Asymptomatic itself, but in a high risk patient it is cancer until proven otherwise

205
Q

What do we see here?

A

Pulmonary nodule - cancer until proven otherwise

206
Q

How do you evaluate a solitary pulmonary nodule?

A

common X-ray finding

Most are benign

Spiculated border is suggested of lung cancer

Smooth border can be benign or malignant

Cavitation may also benign or malignant

207
Q

How do you diagnose primary lugn canncer?

A

Sputum cytology

bronchoscopy cytology

Transthoracic needle aspiration and cytology

Biopsy

208
Q

What are histologic types of lung cancer?

A

Small cell

Non small cell (squamous cell, adenocarcinoma, large cell)

209
Q

What ist he most predominant non-small cell carcinoma?

A

Adenocarcinoma

210
Q

What are characteristics of squamous cell tumors?

A

Central location

may be cavitary

Strong association with smoking

211
Q

What are characteristics of adenocarcinomas of lung?

A

Typically peripheral

Most in current or former smokers, but it is the most common tumor in non-smokers

212
Q

What is lepidic adenocarcinoma (adenocarcinoma in situ)?

A

Lines alveolar spaces

may be indolent, with slow progression

May be multicentric

Can look like pneumonia

213
Q

What is this?

A

Lepidic adenocarcinoma

214
Q

What is squamous cell carcinoma of the lung?

A

Bulky, invades adjacent structures

Main stem or lobar bronchi, seen broncoscopically

Mets may be later

May cavitate

215
Q

What is large cell lung cancer?

A

Subtype of non-small cell lung cancer

present as bulky tumors

May be aggressive with poor prognossi

216
Q

What are carcinoid tumors?

A

Well-differentiated neuroendocrine tumors

Arise in central airways, present with wheezing, cough, and obstructive pneumonia

Better survival than small cell and non-small cell carcinomas

Can produce carcinoid syndrome, especially when metastasis

217
Q

What is small cell carcinoma?

A

Has strongest association with smoking

Arises from pulmonary neuroendocrine cells

Typically present as central, perihilar masses and are associated iwth mediastinal lymphadenopathhy

218
Q

What do we see here?

A

Small cell on left, non-small cell on right

219
Q

What symptoms do you see in small cell carcinoma?

A

Paraneoplastic syndromes (release hormones)

Mets are extremely common at presentation

Poor survival

220
Q

How does lung cancer present?

A

Most present at advanced stage, not good

Early lung cancers are asymptomatic

Detected as nodule on CXR or as symptoms (no bueno)

221
Q

What symptoms are seen with lung cancer?

A

Airway symptoms (more commoni with squamous cell): cough, hemoptysis, dyspnea, post-obstructive pneumonia

Pleural symptoms (chest pain, effusion)

Mediastinal spread (hoarseness, diaphragm paralysis, SVC syndrome)

Distant spread (headache, weakness, seizure, bone pain, abdominal pain)

Other: (anorexia, weight loss, clubbing, paraneoplastic syndromes

222
Q

What are pancoast tumors?

A

Lung cancers originating in the apex of the lung (superior sulcus or pancoast tumor)

Arm pain, weakness, due to brachial nerve involvement

Can cause Horner’s Syndrome: ptosis, meiosis, anhidrosis (due to cervical sympathetic invasion)

223
Q

What do we see here?

A

Pancoast tumor (patient’s left side)

224
Q

What paraneoplastic syndromes are common in lung cancer?

A

(seen in small cell carcinomas)
Cushing
SIADH

Eaton-Lambert myasthenic syndrome

Hypercalcemia is common in squamous cell carcinoma

Clubbing seen in any NSCLC

225
Q

How is small cell lung cancer staged?

A

Limited : confined to single hemithorax

Extensive: spread beyond hemithorax

226
Q

How is nonsmall cell lung cancer staged?

A

TNM system

227
Q

Why do we stage lung cancer?

A

Gives us prognostic value:

5 yr survival:

Stage I : 60-70%

Stage II : 30-50%

Stage III : 10-20%

Stage IV: <10%

228
Q

How do we treat NSCLC?

A

Is it resectable

Is it operable

Only surgery can cure

229
Q

How do we treat lung cancers?

A

Surgery

Radiation

Chemo

230
Q

What are the precursor lesions for lung cancers?

A

Squamous cell (squamous dysplasia and then carcinoma in situ)

Adenocarcinoma (Atypical adenomatous hyperplasia first)

Carcinoids (diffuse idiopathic pulmonary neuroendocrine cell hyperplasia first)

231
Q

What is the most common carcinoma of the lung?

A

Adenocarcinoma

then squamous cell carcinoma

232
Q

What are centraly located lung tumors?

A

squamous cell

Small cell

233
Q

what are peripherally located lung tumors?

A

Adenocarcinoma

Large cell

234
Q

Who gets squamous cell carcinoma?

A

Men, smokers

235
Q

What is this?

A

Squamous cell carcinoma in situ of the lung

236
Q

What systemic symptoms can you see in squamous cell carcinoma?

A

Hypercalcemia is the classic paraneoplastic syndrome

237
Q

What can you see grossly/on CXR in squamous cell carcinoma of the lung?

A

Cavitation

238
Q

What do we see here?

A

Squamous cell carcinoma of the lung

239
Q

What is this?

A

Keratin “pearl” characteristic of squamous cell carcinoma of the lung

240
Q

What is the characteristic histological finding of squamous cell carcinoma of the lung?

A

Keratin pearl

241
Q

What lung cancer is associated with EGFR mutations?

A

Adenocarcinoma

242
Q

What is atypical adenomatous hyperplasia?

A

Type II pneumocyte proliferation and/or clara cell proliferation

243
Q

What is this?

A

Atypical adenomatous hyperplasia

244
Q

What is broncioalveolar carcinoma (BAC) aka Adenocarcinoma in situ?

A

Entirely tumor cell sgrowign along existing alveolar septa (lepidic growth)

Non-mucinous

Important classificaiton for prognosis (almost 100% vs 60% of conventional adenocarcinomas)

245
Q

What tumors have “ground glass” CXR appearance?

A

Bronchioalveolar carcinoma aka Adenocarcinoma in situ

246
Q

What do we see here?

A

Adenocarcinoma in situ (aka BIC)

Like AAT but larger

247
Q

What is minimally invasive adenocarcinoma?

A

Adenocarcinoma 3 cm or less; with lepidic growth and invasion

Solitary and discrete

Good prognosis

248
Q

What is this?

A

Minimally invasive adenocarcinoma (MIA); like adenocarcinoma in situ, but invasive to one focus

Solitary and discrete, by definition

249
Q

What are invasive lung adenocarcinomas?

A

most of adenocarcinomas

Typically glandular o papillary in structure

Solid

Peripheral with pleural puckering

250
Q

What is large cell carcinoma?

A

Undifferentiated malignant epithelial tumor

Large nuclie, prominent nucleoli, moderate cytoplasm

251
Q

What are small cell carcinomas?

A

Men, median age = 60

99% in smokers, very agressive with early mediastinal lymph node involvement

paraneoplastic (ADH, ACTH, PTH, Calcitonin, Gonadotropins, serotonin)

252
Q

What are defining features of small cell carcinomas on pathology?

A

Gross: central/hilar, well-defined borders

Histologically: minimal cytoplasm, nuclear molding

253
Q

What do you see here?

A

Neurosecretory granules that can be seen in neuroendocrine tumors of the lung

254
Q

How do carcinoid tumors appear on histology?

A

Organoid, trabecular, palisaiding, ribbon or rosette-like arrangements of cells

Eosinophilic cytoplasm

Typical: <2 mitoses per 10 hpfs

Atypical: 2-10 mitoses per 10 hpf

255
Q

What is the most common site of metastases?

A

The lung!

256
Q

How do metastases typically present in the lung?

A

Multiple, discrete nodules scattered throughout lungs

257
Q

What is SVC syndrome?

A

Gradual insidious compression/obstruciton of SVC

Bronchiogenic carcinoma is responsible for ~80% of SBC syndrome

Not good prognosis

258
Q

What are the most common pleural tumors?

A

Metastatic more common than primary

259
Q

What is malignant mesothelioma?

A

Majority due to asbestos exposure, not related to cigarette smoking

Men >>> women

Long latency period

260
Q

How do malignant mesotheliomas present grossly?

A

Multiple small nodules that coalesce into a confluent rind

261
Q

What od we see here?

A

Malignant mesothelioma

262
Q

What are the three subtypes of mesothelioma?

A

Epithelial

Sarcomatoid

Bi-phasic

263
Q

What supplies blood to the pleura?

A

Intercostal arteries = parietal pleura

Bronchial arteries = visceral pleuraW

264
Q

What is the venous drainage of hte pleura?

A

Systemic veins = parietal pleura

Pulmonary veins = visceral pleura

Typically low pressure systems. In heart failure => pulm venous pressure increase, backup of blood. bad

265
Q

where do parietal lymphatics drain?

A

Internal mammary chain anteriorly and internal intercostal chain posteriorly

266
Q

Wehre do visceral pleura lymphatics drain?

A

Hilar and milddle mediastinal LNs

267
Q

What is exudate?

A

Altered permeability of pleural membrane results in increased leakage of fluid and protein into pleural space

Result of inflammation or tissue disruption

268
Q

What is Transudate?

A

Increased hydrostatic pressure and/or decreased colloid oncotic pressure

Typically teh result of fluid-avid states (CHF, cirrhosis, nephrotic syndrome)

269
Q

How can you detect effusions?

A

Decreased breath sounds, fremitus; dullness to percussion

CXR

CT (w/ contrast)

Bedside ultrasound

270
Q

When should you tap a pleural effusion?

A

Always except:

Less than 10mm of layering of free-flowing liquid on lateral decubitus

CHF with improvement with treatment

271
Q

What is thoracentesis?

A

CXR guided or US guided

Done at one interspace below loss of fremitus and dullness

Pt upright

Big needle over the rib

272
Q

What do you test for in the plerual fluid?

A

Protien, LDH, glucose

Cell count, differential

pH

Blood culture, gram stain

Cytology

AFB smear and culture

May do albumin, amylase, cholesterol, triglycerides and hematocrit

273
Q

What are Light’s Criteria?

A

None met = transudate

Any met = exudate

Pleural fluid/serum protein ratio > 0.5

Plerual fluid/serum LDH ratio > 0.6

Plerual fluid LDH > 2/3 of upper limit of normal

274
Q

What are transudative effusions?

A

CHF

Hepatic hydrothorax

Nephrotic syndrome
Peritoneal dialysis

Hypoalbuminemia

Urinothroax

SVC syndrome

275
Q

What causes transudateive pleural effusion?

A

Increased hydrostaic pressure (CHF)

Decreased plasma oncotic pressure (hypoproteinemia, nephrotic syndorme, end stage liver disease)

Movement of transudative abdominal fluid (ascites)

276
Q

What is hepatic hydrothorax?

A

Connection between thorax and abdomen + ascitic fluid

Right side is more common than left

Fluid is transudate

Tx the ascites

277
Q

What are exudative effusions?

A

Infectious

Malignant

Collagen vascular disease (RA, SLE)

Pulm Embolism
Post Cardiac Injury Syndrome (PCIS, Dressler’s)

Asbestos
Chylothorax

Endocrine
Abdominal origin

278
Q

What are parapneumonic effusions?

A

Simple - NBD, treat hte pneumonia

Complicated - have to drain

Empyema - emergency

279
Q

What are signs and symptoms of pleural effusion?

A

Dypsnea, pleuritic chest pain, fever

Dull to percussion, decreased breath sounds, plerual friction rub

280
Q

What differentiates empyema from pleural effusions?

A

High protein and LDH = exudate

Very low pH, very low glucose, pus = infectious

Wont always have bugs evident

Need to drain fully, treat with antibiotics and monitor for resolution

281
Q

What are the types of pleural effusions?

A

Simple: pH > 7.2, no pus or bacteria present, no loculations

Complex: loculated, low pH

Empyema: pus, + Gram stain, + culture

282
Q

What can cause pneumothorax?

A

Parietal entry: trauma, iatrogenic

Visceral entry: rupture of lung cyst, complication of mech. ventalation, necrosis due to toumor, infection, iatrogenic

283
Q

What are causes of spontaneous pneumothorax?

A

Primary: tall, thin, smokers, wiht sub-pleural blebs

Secondary: to emphysema, PCP< CF, abscess, LCH, LAM

284
Q

What is tension pneumothorax?

A

Air in pleural space under positive pressure from a one-way valve effect

Collapsed lung, redued venous return, hemodynamic changes/emergency

285
Q

What is ARDS?

A

Acute Respiratory Distress Syndrome

286
Q

What are features of ARDS?

A

Refractory hypoxemia, bilateral infiltrates, low lung compliance, increased wight at autopsy, No left atrial hypertension

287
Q

What is the threshold for ARDS vs ALI?

A

ARDS = PaO2/FIO2 < 200

ALI = PaO2/FIO2 < 300

288
Q

What are the causes of ARDS?

A

Sepsis

Pneumonia

Aspiration
Pancreatitis

Trauma

Burns

Transfusions

Toxic inhalation

289
Q

Why do people die with ARDS?

A

They typically have multiorgan system failure

290
Q

What is the pathophysiology behind ARDS?

A

Diffuse alveolar damage

Failure of alveolar capillary membrane (Flooding of alveolar airspaces with proteinaceous fluid

Activated neutrophils and macrophages release proinflammatory cytokines (TNFAα, IL1, and IL8)

O2 derived free radicals lead to injury

291
Q

What are the phases of ARDS?

A

Exudative

Proliferative

Fibrotic

292
Q

Is imaging useful in ARDS?

A

Not really - snowstorm like appearance.

293
Q

How do you manage ARDS?

A

Treat underlyign cause

Lung protective strategy of lung ventilation (avoid volutrauma nad barotrauma)

Provide supportive care

294
Q

Is mechanical ventilation/Oxygen good for ARDS?

A

Can worsen lung injury

Over distention of alveoli that can induce inflammation

Repetitive alveolar collapse and opening causes shear stress

Oxygen can generate free radicals

295
Q

What is DAD?

A

Diffuse Alveolar Damage = histologic finding

296
Q

What is AIP?

A

Acute Interstitial Pneumonia

(idiopathic diffuse alveolar damage)

297
Q

What is diffuse alveolar damage?

A

Caused by diffuse alveolar capillary/epithelial dmaage

Rapid onset of severe life-threatening respireotary insufficeincy, cyanosis, and severe areterial hypoxemia

Refractory to O2 therapy

May lead to extrapulmonary multisystem organ failure

CXR show diffuse alveolar inflitration

298
Q

How does DAD occur?

A

Injury to vascular endothelium and alveoli results in excess vascular fluid and protein leakage (early on) and then cellular necrosis, epithelial hyeprplasia, inflammaiton, and fibrosis (late)

299
Q

What is the pathognomonic finding in DAD?

A

Hyaline membranes

As well as exudate into alveoli (pulmonary edema, hemorrhage)

300
Q

What are gross findings of ARDS lungs early on?

A

Wet, boggy, airless, heavy

301
Q

What do we see here?

A

Exudative phase of diffuse alveolar damage

Interstitial and alveolar edema, fibrin exudation, and hyaline membranes

Mild inflammation

302
Q

What do you think when you see hyaline membranes?

A

Diffuse alveolar damage (ARDS)

303
Q

What is eosinophilic pneumonia?

A

Intra-alveolar fibrin, macrophages, abundant eosinophils, and eosinophil microabscesses

+/- an organizing pneumonia

Sensitive to steroids

304
Q

What is acute eosinophilic pneumonia?

A

May present with respiratory failure clinically (ARDS)

May not have periopheral blood eosinohpilia

Asthma history ist ypically not present

has hyaline membranes essentially identical to those of DAD, PLUS eosinophilia

305
Q

What is organizing pneumonia?

A

“airspace organization” is loose connective tissue in alveoli seen commonly in lung injury as the lung attempts ot repiar

Can be primary (OP pattern), component of another process (HSP, acute pneumonia), or secondary (tumor, granuloma, etc)

306
Q

What does oganizing pneumonia look like histologically?

A

Patchy, bronchiolocentric organizing pneumonia +/- fibroblastic plugs

minimal chornic ifnlammation in adjacent alveoli

Intervening lung is more or less normal

NO other findings

307
Q

What od we see here?

A

Organizing fibroblastic tissue within airspaces (organizing pneumonia)

Pulmonary (2 decks)

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