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Pulm, Critical Care > interstitial lung disease > Flashcards

interstitial lung disease Flashcards

1
Q

most common type of interstitial lung disease

WHAT ARE THE IMAGING FINDINGS?

A

idiopathic pulmonary fibrosis

CXR - bibasilar septal line thickening with reticular changes and volume loss and bronchiectasis when more severe. diffuse interstitial lung opacities and reduced lung volumes. CXR can also be normal.

NEED HRCT for diagnosis since CXR can be normal.

HRCT- shows bilateral, peripheral, and basal predominant septal line thickening with honeycomb changes

  • will show usual interstitial pneumonia
  • Biospy may not be necessary for diagnosis.
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2
Q

demographics of pts who have idiopathic pulmonary fibrosis

presentation of IPF

A

50-70 with history of smoking.

See dyspnea on exertion, progressive dypsnea, clubbing of fingers and chronic dry cough

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3
Q

CXR and physical exam of idiopathic pulmonary fibrosis

A

on CXR : see decreased lung volumes with lower posterior lung zone predominance

clubbing and early inspiratory velcro crackles, may be hypoxic

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4
Q

HRCT scan of idiopathic pulmonary fibrosis shows

A

honey combing, cystic changes, and traction bronchiectasis (at the bases and subpleural areas).

can be diagnosed by CT but if unclear can get lung biopsy which will show usual interstitial pneumonia

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5
Q

do we every use bronchoscopy with biopsy to make diagnosis of interstitial lung disease

A

no it’s not able to get adequate tissue if biopsy is needed. prefer a VATS.

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6
Q

ILD in ages 20-50 think of these differentials

A

sarcoidosis,

pulmonary histocytosis X (pulmonary langerhaan cell granulomatosis)

hypersensivity pneumonitis

LAM (if young woman)

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7
Q

if suspect ILD and silicosis, look at exposure history:

A

history of exposure to TB

job occupation

histoplasmosis

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8
Q

Subacute causes of ILD

A

chronic UIP

chronic hypersensitivity pneumonitis

asbestosis

rheumatoid arthritis, chronic scleroderma or other connective tissue disorder (dermatomyositis)

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9
Q

beryllosis

A

rocket and microchip making or fuorescent lighting

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10
Q

Why do we need to get HRCT everytime when we consider ILD?

A

because CXR is 15% negative for changes

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11
Q

pulmonary lymphangioleiomyomatosis (LAM)

A

cystic lung dx seen in young women

Presentation: present with pneumothorax (often recurrent) chylothorax, chylous ascites, hemoptysis and multiple thin walled cysts scattered diffusely in the lungs without nodules or fibrosis on imaging studies.

see elevated VEGF-D

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12
Q

pulmonary lymphangioleiomyomatosis (LAM) diagnosis

A

clinical but definitive is lung biopsy

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13
Q

pulmonary lymphangioleiomyomatosis (LAM) treatment

A

transplantation of lung

OCP and pregnancy worsen disease can also see luterine leiomyomas and renal angiomyolipomas as well

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14
Q

manfestation of Cystic fibrosis patients

A

bronchiectasis and chronic bronchitis

see _pancreatic insufficienc_y, cough, SOB and other signs of malnutrition and vitamin deficiency

Diagnosis: elevated sweat chloride testing

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15
Q

pulmonary langerhan cell histiocytosis X is

A

common in smokers seen in ages 20-50 yrs old.

HRCT findings: see diffuse thin walled cystic lung dx with upper lobe predominance

Commonly will have restrictive disease. Only see obstruction on PFTs with significant cystic dx. Will have lower DLCO

Tx: smoking cessation and can give steroids.

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16
Q

advanced sarcoidosis can have

A

cystic lung dx and bilateral hilar LAD.

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17
Q

cryptogenic organizing pneumonia (COP)

A

cough, fever, dyspnea, malaise, myalgias and presentation is similar to CAP or flu like illness. IT has an acute to subacute onset (<2 months) and see fever and they may get multiple rounds of abx

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18
Q

when do we see clubbing if the fingers?

A

IPF,

asbestosis,

CF

hypersensitivity pneumonitis

bronchiectasis

and occasionally in lung cancer.

Rarely seen in COPD or sarcoidosis

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19
Q

signs and symptoms of bronchiectasis

A

daily mucopurulent cough with significant sputum production, (cups of it)

can see rhinosinusitis, dyspnea, hemoptysis, crackles and wheezes

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20
Q

causes of bronchiectasis

A

irreversible enlargement of airways due to destruction of airway architecture;

Pathophysiology: injury to lung from prolonged irway inflammation which causes subsequent mucus stasis and leads to further airway obstruction, chronic infection and inflammation.

airway obstruction (cancer),

rheumatic dx (RA Sjogren’s)

toxic inhalation

chronic or prior infection (aspergillosis and mycobacteria)

immunodeficiency (hypogammaglobulinemia, congenital CF and

alpha 1 antitrypsin deficiency

ciliary dismotility - Kartagner’s

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21
Q

Evaluation of bronchiectasis

pathphysiology

diagnosis

labs:

A

irreversible enlargement of airways due to destruction of airway architecture;

Pathophysiology: injury to lung from prolonged irway inflammation which causes subsequent mucus stasis and leads to further airway obstruction, chronic infection and inflammation.

diagnosis of bronchiectasis is by HRCT scan of chest. See airway diameter that is greater than that of accompany vessel and lack of distal airway tapering. Can have thickened walls or cysts.

Need to figure out why bronchiectasis is present. Rule out underlying bacterial or mycobacterial infection.

Look at connective tissue dysfunction

fribrosis and ciliary dysfunction or alpha 1 anti-trypsin deficiency

CHECK:

immunoglobulin quantification

CF testing,

sputum culture (bacteria, fungai, mycobacterium and PFTs)

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22
Q

cyclophosphamide can cause

A

pulmonary toxicity with pneumonitis with symptoms of cough, fatigue and dyspnea.

NO longer use this to treat NSIP from diffuse scleroderma. Preferred to use mycophenolate mofetil for treatment

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23
Q

silicosis associated occupations are:

A

coal mining (underground and surface)

hard rock mining (Granite, slate, sandstone)

masonry,

construction glass manufacturing

ceramic production

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24
Q

clinical presentation of acute silicosis (less common)

A

symptoms within a few weeks or years after exposure rapid onset of cough, weight loss, fatigue and possible pleuritic chest pain CXR shows basilar alveolar filling pattern without rounded opacities or lymph node calcifications.

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25
Q

prognosis of acute silicosis?

A

poor prognosis with silicosis and cor pulmonale and respiratory failure and <4 year survival rate

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26
Q

clinical presentation of chronic silicosis (most common)

A

asymptomatic and slowly develops symptoms 10-30 years after silica exposure

CXR with <10 mm diameter nodular opacities that are rounded, irregular, and in mid to upper lung zones. Nodules can coalesce to form (progressive massive fibrosis) PMF with severe respiratory symptoms or cor pulmonale

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27
Q

Accelerated silicosis clinical presentation

A

asymptomatic, or slowly developing symptom within 10 years of exposure to high levels silica

It doesn’t show up within a few weeks or years (acute) but doesn’t appear after 10 or 30 years (chronic).

CXR similar to chronic silicosis increased risk for PMF (progressive massive fibrosis)

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28
Q

What is silicosis associated with?

A

increased risk for lung cancer

high risk for mycobacterial disease

associated with scleroderma and RA

airflow limitation and chronic bronchitis

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29
Q

respiratory protective devices can help

A

with prevention of disease but also can be seen in workers who use personal respiratory protection.

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30
Q

Chest imaging of chronic silicosis is

A

rounded and nodular opacities <10 mm in diameter in mid to upper lung zones

some nodules may coalesce in some pts to form progressvie massive fibrosis

see resulted retracted hila, upper lobe fibrosis, and lower lobe hyperinflation.

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31
Q

diagnosis of silicosis

A

clinical findgins, occupational history, and chest imaging and absences of other etiologies Spirometry shows mixed obstructive and restrictive impairment decreased FEV1 and FEV1/FVC ratio. PMF can be seen with sharper decline in PFTs. may need lung biopsy.

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32
Q

Treatment of silicosis

A

supportive treatment (bronchodilators and supplemental oxygen) with possible lung transplantation for end stage silicosis.

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33
Q

who gets asbestosis?

A

plumbers,

carpenters,

electricians

janitors.

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34
Q

presentation of asbestosis?

A

present 20-30 yrs post initial exposure with chronic dyspnea and see restrictive dx on spirometry without airflow obstruction

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35
Q

chest imaging findings for asbestosis?

A

see pleural plaques

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36
Q

when do pts with sarcoidosis present

A

10 or 40 yrs. See upper lobe involvement

37
Q

fibrotic radiation pneumonitis

A

dyspnea, chest pain, and see CT with volume loss and coarse reticualr/dense opacities. Pt has history of radiation therapy 12 months ago

38
Q

treatment of acute radiation pneumonitis:

A

prednisone 60 mg daily for 2 weeks followed by gradual taper

39
Q

clinical presentation of acute radiation pneumonitis:

A

antibiotic non responsive pneumonia can have fever, dyspnea, pleurtic chest pain, and cough. labs show leukocytosis have history of radiation to neck and chest 4-12 weeks ago.

40
Q

when does acute radiation pneumonitis develop?

A

4-12 weeks after radiation therapy

41
Q

how to diagnose acute radiation pneumonitis

A

after failing course of antibiotics. needs bronchoscopy to rule out infection and malignancy CT scan will show perivascular haziness and see patchy ground glass alveolar infiltrates or consolidative opacities. See “straight-line effects” of distinct boundaries where pneumonitis is from normal parenchyma.

42
Q

Long term complications of acute radiation pneumonitis

A

see fibrotic radiation pneumonitis progression after 6 to 12 months time.

43
Q

does smoking cause bronchiectasis?

A

no.

Bronchiectasis results from damage from bronchial walls from inflammation and infection.

44
Q

hypersensitivity pneumonitis is

A

repetitive inhalations of antigens in a sensitized pt which results in immunologic response that forms noncaseating granulomas and peribronchial mononuclear cell infiltration with giant cells.

extrinsic allergic alveolitis and a form of interstitial lung dx that develops after inhalation of allergens (microbes, animal/plant proteins, dust, fungi, and chemicals)

Three forms of HP.

acute HP: large exposure to inciting antigen. see fevers, cough, fatigue within 12 hrs of exposure. CXR will have diffuse micronodular dx or be normal. Hear inspiratory crackles. HRCT- d_iffuse centrallobular micronodules and ground glass opacities_. TX: remove antigen and pt feels better within 48 hrs.

Recurrence of symptoms with repeat exposure is HALLMARK.

subacute and chronic HP : lower level prolonged exposure of antigen. See cough, fatigue, weight loss and SOB. HRCT shows micronodules and ground glass opacities but ALSO evidence of septal line thickening and fibrosis. Significant long exposure shows traction bronchiectasis and honeycomb changes on CT. TX: r_emove antigens essential for treatment._

Steroids are sued in pts with severe dx.

45
Q

bird fancier’s lung is

A

chronic hypersensitivity pneumonitis - bird antigens cause problems and pt experiences cough, fatigue and weight loss and SOB.

lower level prolonged exposure of antigen.

HRCT shows micronodules and ground glass opacities but ALSO evidence of septal line thickening and fibrosis. S_ignificant long exposure shows traction bronchiectasis and honeycomb_ changes on CT.

TX: remove antigens essential for treatment.

46
Q

presentation of hypersensitivity pneumonitis

A

acute or subacute or chronic depending on duration of exposure subacute and chronic forms a present with worsening sympotms

47
Q

subacute form of hypersensitivity pneumonitis

A

resolves when antigen exposure ceases (with or without corticosteroids) people who are untreated develop interstitial fibrosis and chronic hypersensitivity pneumonitis. also 50% may have digital clubbing

48
Q

subacute cough and dypsnea and see digital clubbing. has a new pet and symptoms stop when pt is away on vacation

A

hypersensitivity pneumonitis

49
Q

history of antigen exposure and cessation of symptoms on removal of antigenic environment are major historical clues for

A

hypersensitivity pneumonitis otherwise it’s difficult to distinguish from other forms of interstitial fibrosis

50
Q

CT findings of hypersensitivity pneumonitis

A

see ground glass opacities with emphysematous changes in mid upper lung fields

51
Q

work up for hypersensitivity pneumonitis

A

need to get inhalation challenge test

if obtained BAL showing lymphocytosis

if obtained lung biopsy would show poorly formed noncaseating granulomas in the lung periphery (needed for diagnosis)

52
Q

pulmonary alveolar proteinosis PAP is a

A

diffuse lung disease of accumulation of periodic acid schiff positive lipoproteinaceous material in distal air spaces

presents similar to chronic eosinophilic pneumonia (fever progressive dyspnea, cough and weight loss)

imaging shows “bat wing” distribution. no eosinophilia

53
Q

asbestosis presentation

HRCT findings

A

plumbers, carpenters, electricians and janitors

present 20-30 years after initial exposure with chronic dyspnea (cough and wheezing are unusual)

spirometry shows restrictive pattern and no airflow obstruction

see bilateral nodular or reticular opacities and pleural plaques and clubbing of digits.

54
Q

idiopathic pulmonary fibrosis demographics

Presentation?

A

50-70 yrs old with 6 months of progressive dyspnea with exertion and chronic dry cough. No provoking factors, will have of history of smoking

see clubbing (50%) and late inspiratory velcro crackles at lung bases

History: treated for COPD without improvement, treated for CHF without improvement (crackles)

CXR - bibasilar septal line thickening with reticular changes and volume loss and bronchiectasis when more severe.

diffuse interstitial lung opacities and reduced lung volumes. CXR can also be normal.

NEED HRCT for diagnosis since CXR can be normal.

HRCT- shows bilateral, peripheral and basal predominant septal line thickening with honeycomb changes

  • will show usual interstitial pneumonia - Biospy may not be necessary for diagnosis.
55
Q

eosinophilic pneumonia is divided into

A

acute and chronic

56
Q

acute eosinophilic pneumonia presentation

A

follows a rapid course (<3 weeks) of dyspnea and seen in smokers

see hypoxemic respiratory failure

see initial neutrophilic predominent leukocytosis and subsequent eosinophilia

see BAL>25% eosinophils - diffuse alveolar damage on lung biopsy

57
Q

acute eosinophilic pneumonia

A

acute worsening of dyspnea due to high build up of eosinophils in lungs associated with smokers responds to steroids

58
Q

treatment of eosinophilic pneumonia

A

steroids

both acute and chronic eosinophilic pneumonia respond well to steroids

keep them on it for 3 months followed by taping of steroids in subsequent three months.

59
Q

labs of acute eosinophilic pneumonia

A

see initial neutrophilic predominent leukocytosis and subsequent eosinophilia

see BAL>25% eosinophils

  • diffuse alveolar damage on lung biopsy
60
Q

Difference between acute and chronic eosinophilic pneumonia

A

acute: <3 weeks, smokers, and see acute respiratory failure

chronic: >3 weeks and non smokers. don’t see respiratory failure

61
Q

Chronic eosinophilic pneumonia presentation

A

Chronic Eosinophilic Pneumonia presentation: insidious onset of fever, cough, progressive dyspnea, wheezing, weight loss. NO respiratory failure unlike AEP. see peripheral eosinophilia>6% and elevated ESR and CRP, thrombocytosis. BAL>25% eosinophils suggests this lung biopsy will show interstitial and alveolar eosinophils with multinucleated giant cells and associated bronchiolitis obliterans with organizing pneumonia.

62
Q

treatment of bronchiectasis

A

chronic productive cough and sputum - has irreverisble airway dilation. Tx of underlying cause may not lead to improvement in symptoms but could prevent further progression.

Tx is focused on airway clearance, treating infections, and preventing exacerbations. FOcus on preventing chronic or recurrent infections

Bronchodilators, inhaled steroids, and combo inhalers -help symptoms but don’t prevent future exacerbation or stop decline of lung function.

Can give antibiotics if needed

63
Q

Cystic fibrosis definition

presentation

A

autosomal rescessive dx affecting CF transmembrane regulator (CFTR) gene and dx affects homozygous pts. See abnormally thick secretions that are difficult to clear.

Changes in respiratory secretions lead to bacterial colonization of airways and chronic bacterial infection resulting in chronic inflammation, sinusitis, chronic productive cough and bronchiectasis. Also not enough lung antiproteases to counteract neutrophilic elastases so worsening of lung damage

Thickened secretions cause problems for the GI tract with bile and pancreas and so see pancreatic exocrine and endocrine deficiency, liver dx, and malabsorption and maldigestion occurs; see b_owel obstruction, distal ileal obstructive syndrome, intussusception, and rectal prolapse. can also see kyphoscoliosis and airway hyperreactivity_

spirometry will show obstructive pattern.

64
Q

CXR findings of CF pts

A

CXR: upper lobe predominant mucoid impaction

65
Q

CF diagnosis

A

Diagnostic evaluation: SCREENING test is increased chloride in sweat in sweat chloride test

family history of CF is helpful for diagnosing.

sweat chloride is less sensitive in adults and so a negative test doesn’t rule out dx

DNA testing is what confirms diagnosis and provide prognosis.

if sweat chloride is elevated then needs genetic testing. if TWO mutations are present then diagnosis is made.

If genetic testing shows 0 to 1 gene then repeat sweat chloride and expanded genetic testing is indicated.

66
Q

Diffuse parenchymal lung disease are characterized by:

initial work up

A

characteristics of presentation: non productive cough and dyspnea that is subacute or chronic without response to treatment

All suspected pulmonary parenchymal diffuse lung dx need to get: ANA, RF, anti -CCP and peptide antibodies in pts <40 yrs old.

Get a high res CT chest. and if can’t make diagnosis then consider lung biopsy

acute dypsnea and cough of short duration= think: PNA, PE, CHF, asthma onr infection.

67
Q

Pulmonary Langerhan cell histiocytosis clinical features

A

considered a part of the smoking related diffuse parenchymal lung diseases

CT scan: diffuse thin walled cysts and several pulmonary nodules in the mid and upper lung zone on HRCT. see development of pulmonary HTN.

See presence of langerhan cells with S100 and CD1a staining on tissue biopsy or transbronchial biospy

Tx: stop smoking and can give steroids.

68
Q

Other smoking related ILD or diffuse parenchymal lung diseases

A

RB- ILD or respiratory bronchiolitis- combined restrictive and obstructive dx on PFTs

Pulmonary Langerhan cell histiocytosis (histocytosis X) - restrictive dx and can be obstructive if see lots of cysts.

Desquamative intersitial pneumonia-

All have lower DLCO.

Tx all with smoking cessation and steroids

69
Q

medication that can cause ILD?

A

methotrexate can possible cause pulmonary ILD

See pulmonary fibrosis with

amiodarone

nitrofurantoin

busulfan

bleomycin

70
Q

Connective tissues disorders that can cause ILD?

A

connective tissues disorders that can cause this -

rheumatoid arthritis: bronchiolitis, organizing pneumonia, rheumatoid nodules and nonspecific interstitial PNA (NSIP) and UIP (same as IPF)

diffuse scleroderma- can cause NSIP. Treat NSIP with mycophenolate mofetil, not cyclophosphamide due to side effects.

71
Q

Prognosis with IPF?

A

IPF is progressive disorder and median survival time is 3-5 yrs.

Progression of dx is not linear but variable with periods of relative stability and then acute declines with exacerbations.

  • acute exacerbation is acute worsening of dry cough, dyspnea, of <1 month duration and see new findings of CT scan (bilateral ground glass opacities) after a period of relative stability. Need to rule out CHF and pulm edema
  • can see right sided heart failure and pulmonary HTN in severe dx.
72
Q

treatment of IPF is:

A
  • optimize comorbidities like obesity, heart failure, and sleep disordered breathing; this is common due to nocturnal hypoxemia and increased prevalance of OSA
  • treat hypoxemia with supplemental O2 as needed based on pulse oximetry.
  • with deconditioning, get pulmonary rehab to i_ncrease exercise tolerance and improve quality of life_
  • treat with nintedanib and pifenidone which target fibroblasts and this delays the IPF progression but not curative.

Needs to be followed by pulmnologist.

73
Q

IPF exacerbation is defined as:

A

acute exacerbation is a_cute worsening of symptoms (dry cough, dyspnea) <1 month duration and see new findings of CT scan_ (bilateral ground glass opacities) after a period of relative stability.

Events are triggered by infection or idiopathic.

Need to rule out pulm edema and CHF b/c of the ground glass opacities.

74
Q

Lung transplantation for IPF is for:

A

life prolonging therapy for those without cormorbidities that may limit life expectancy

  • those that don’t qualify are those who have untreatable end organ damage outside the lungs.

early referral for eligible pts is needed.

75
Q

Most common cause of death in IPF pts

A

respiratory failure.

those who need mechanical ventilation with IPF have a terrible prognosis and increased mortality

Guidelines recommend against intubation with IPF if lung transplantation is not an option and have severe exacerbation or poor performance status.

need to have advanced care planning and end of life goals of care and palliative strategies.

76
Q

NSIP or nonspecific interstitial pneumonia is

A

most common diffuse lung parenchymal disease associated with autoimmune disorders. NSIP affects younger population than IPF, can get lung transplant for this if no other end organ damage.

  • two forms of NSIP: cellular and fibrotic
  • cellular form (better prognosis and responds better to immunosuppression)

HRCT: bilateral lower lobe reticular changes and NO HONEYCOMB changes.

77
Q

NSIP HRCT findings:

A

most common form of ILD with connective tissue disorders; seen in pts <50yrs

HRCT: bilateral lower reticular changes and NO honeycomb changes. See areas of ground glass opacification.

seen in systemic sclerosis, SLE, Sjogren’s sydnrome, dermatomyositis, polymositis and undifferentiated connective tissue disorder.

78
Q

COP or cryptogenic organizing pneumonia

A

Disorder that results from injury to lung, see patchy proliferation of granulation tissue that affects the terminal bronchiole and alveolar ducts and spaceis.

-seen after a infection, radiation exposure, drug induced pneumonitis, and autoimmune diseases

presents as a “pneumonia that doesn’t respond to course of antibiotics” as it’s misdiagnosed. Has a CXR with consolidation

Need HRCT chest- see ground glass opacities or areas of alveolar consolidation resembling an infectious pneumonia and infiltrates can be migratory on repeat imaging but also see peripheral nodules and nocules along bronchovascular bundle. Don’t need to have lung biopsy.

Tx with steroids and COP improves. Relapses of COP need taping of steroids and recurrence may need a immunosuppresive therapy.

2nd line is cyclophosphamide for pts who dont’ respond with steroids or for those who are critically ill from severe COP.

79
Q

acute intestitial pneumonia is

A

rapidly progresses in days to weeks and basically cannot be distinguished from ARDS

HRCT: has pulmonary edema and open lung biopsy shows diffuse alveolar damage.

The main difference for knowing that this is acute interstitial pneumonia is that there is no precipitating reason for ARDS.

high mortality >50%, tx like ARDs with low tidal volume ventilation and give steroids but it doesn’t really help.

80
Q

What is Lofgren’s syndrome?

A

bilateral hilar LAD

migratory polyarthralgia

erythema nodosum

fever

presentation of sarcoidosis that doesn’t need biopsy

Tx with NSAIDs, no steroids.

81
Q

What does not require a biopsy for diagnosis of sarcoidosis?

A

asymptomatic bilateral hilar LAD - no fevers, malaise, night sweats to suggest malignancy

Lofgren’s sydrome - bilateral hilar LAD, migratory arthralgias, erythema nodosum and fever

Heerfordt syndrome - anterior uveitis, parotiditis, fever and facial nerve palsy

82
Q

what is Heerfordt syndrome

A

sarcoidosis that doesn’t need a biopsy for diagnosis- anterior uveitis, parotiditis, fever and facial nerve palsy

83
Q

Treatment of Sarcoidosis

A

treat with steroids but many pts don’t need to be treated.

Stage 0, I, will resolve spontaneously.

Stage II 50% will need steroids, and Stage III 80% need steroids

Decision to treat sarcoidosis depends on involvement and this is not based on radiographic findings.

Treatment is required low to mdeium dose steroid therapy on alternate days is needed.

84
Q

Sarcoidosis is

A

granulomatous disease of unknown cause that affects several organs. Seen more in AA and younger pts. 90% of pts have lung involvement.

can be asymptomatic but can have lung involvement

HRCT findings: pulmonary parenchymal dx, intrathoracic LAD alone or in combination. There can be multiple appareances they can have small nodules alongside bronchovascular bundles.

PFTs: obstructive, restrictive or both

Diagnosis: non-caseating granulomas with exclusion of infections like TB and fungi

85
Q

Complication of Sarcoidosis

A

Sarcoidosis can develop pulmonary HTN through multiple ways:

  • chronic hypoxemia
  • destruction of capillary bed so less capillary surface area
  • granulomatous inflammation of pulmonary arteries
  • compression of pulmonary arteries secondary contiguous LAD
  • pulmonary veno-occlusive dx from granulomatous inflammation and LV ventircular dysfunction from cardiac involvement

If we see pulmonary HTN see prognosis and survival time of about 3 years.

86
Q

Asbestos is associated with

A

increased risk for lung cancer regardless of smoking status.

87
Q

what causes cryptogenic organizing pneumonia COP or formly known as BOOP (bronchiolitis obliterans organizing pneumonia)

A

infection - bacterial viral PCP or mycoplasma

drugs - cocaine or amiodarone

connective tissue dx: SLE< RA, Sjogren’s and scleroderma

idiopathic pulmonary fibrosis

hypersensitivity pneumonitis

diffuse alveolar hemorrhage.

88
Q

Desqumative interstitial pneumonia

A

is one of the smoking related ILDs

  • tx stop smoking and if they are exposed to notoxious air particles.

On CT: see bilateral hazy opacities with diffuse basilar subpleural ground glass opacities. can see cysts in areas of ground glass opacities

Bronchoscopy: numberous pigmented machrophages and distal airspaces and moderate infiltration of alveolar septum by lymphocytes and plasma cells and mild alveolar septal fibrosis.

Pulm, Critical Care (30 decks)

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