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X Clin Med II Exam 2 > Interstitial Lung Disease > Flashcards

Interstitial Lung Disease Flashcards

1
Q

Interstitial Lung Disease

A

Group of pulmonary disorders that cause progressive scarring of lung tissue surrounding the alveoli
Generally irreversible
Process of fibrosis and inflammation (not infectious)

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2
Q

Causes of interstitial lung disease

A

Idiopathic, autoimmune (dermatomyositis, RA), exposure to hazardous material or drugs (nitrofurantoin, methotrexate)

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3
Q

Sxs of interstitial lung disease

A

Progressive dyspnea on exertion
Persistent non-productive cough
*wheezing and chest pain (uncommon)
Extra pulm sxs (may suggestive connective tissue disease-MSK pain, weakness, joint pain, fevers, dry eyes)

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4
Q

What is seen on the physical exam in interstitial lung disease?

A

Crackles (usually at bases): velcro
Inspiratory squeaks (high pitched rhonchi)
Cor pulmonale: later stages
Cyanosis (only advanced disease)
Digital clubbing (advanced)
Extra pulm: associated with different disease like erythema nodusum of Gottrons papules)

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5
Q

Gold standard for diagnosis of ILD

A

Tissue biopsy (HRCT gives highest yield as non-invasive test)

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6
Q

What abnormal CXRs suggest ILD?

A

(10% have normal ones)
Ground glass appearance (early usually)
Reticular “netlike” (most common), nodular or mixed opacities
Honeycombing

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7
Q

What does honeycombing indicate?

A

Poor prognosis

Alveoli breakdown and become cystic and aren’t functional

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8
Q

What is HRCT used for?

A

Greater diagnostic accuracy than CXR
See distribution and pattern of disease in lung
Compare to old CT

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9
Q

Serologic studies in ILD

A

Rule out subclinical autoimmune disease (start with ANA and Rf and maybe more like anti-ds-DNA)
If hemorrhage or systemic sxs, evaluate for vasculitis (ANCA)
Sed rate and CRP not helpful

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10
Q

PFTs of ILD

A

Most are associated with restrictive defect (but might not see early on)
Decreased TLC
Decreased FEV1 and FVC but proportional so FEV1/FVC normal or increased

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11
Q

What should you do if the PFTs show a restrictive or normal pattern?

A

Obtain a DLCO (if low then consistent with ILD)

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12
Q

What is DLCO?

A

Diffusing Capacity of Lungs for Carbon monoxide (reduced might be the only finding in early disease)
Measures quantity of CO transferred each minute from alveoli to RBCs in pulm caps
Normal is 80% predicted

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13
Q

What does low DLCO signify?

A

Alveolar damage, impaired gas exchange and therefore less delivery of O2 into bloodstream

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14
Q

What might be seen on ABG in ILD?

A

Might be normal or show hypoxemia or respiratory alkalosis

May beed exercise testing with serial ABGs

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15
Q

What is bronchoalveolar lavage?

A

Minor extension of bronchoscopy
Allows sampling from distal airways and alveoli
Cell counts, cultures and cytology
Not typically performed with HRCT findings consistent with IPF

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16
Q

Indications for a lung biopsy

A

Specifying diagnosis (<50, weight loss, hemoptysis, signs of vasculitis)
Atypical or rapidly progressing HRCT findings or progressive disease
Unexplained extrapulm manifestation
Excluding neoplasm or infection that can mimic ILD
ID more treatable process than originally suspected
Predict likelihood of response to therapy

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17
Q

Contraindication for lung biopsy

A

Honeycombing (b/c poor prognosis so biopsy won’t change the management)

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18
Q

Transbronchial biopsy

A

During bronchoscopy, biopsy forceps passes through bronchoscope (helpful for central locations and not periphery)

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19
Q

Surgical biopsy

A

Done under anesthesia with 1 lung ventilated (larger sample)
Video assisted thorascopic surgery
Thoracotomy (5-6 cm incision to more pain after)

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20
Q

Endobronchial u/s-guided transbronchial needle aspiration

A

Special bronchoscope used to evaluate and mediastinal lymph nodes
Anesthesia
Especially useful if sarcoid suspected

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21
Q

Epidimiology of Idiopathic pulmonary fibrosis

A 
(50-85)
Males > females
Most common
If familial then present earlier
Poor prognosis (2-5 yr survival)
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22
Q

Presentation of idiopathic pulmonary fibrosis

A

Gradual onset of exertional dyspnea and non-productive cough (>6 mos)
Velcro crackle (inspiratory)
Digital clubbing

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23
Q

Diagnostics seen in IPF (CXR, HRCT, PFTs, echo)

A 
6 minute walk test for baseline
CXR: peripheral reticular opacities in bases, honeycombing
HRCT sees the same
PFTS: restrictive pattern
Don't need biopsy, bronchoscopy/BAL
Pulmonary HTN seen on echo
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24
Q

HRCT is used in IPF to determine if…

A

UIP pattern
Probable UIP pattern
Indeterminate UIP pattern
Alternative diagnosis

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25
Q

What is a surgical lung biopsy + BAL used for in IPF

A

If there is not a definitive UIP pattern

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26
Q

Tx for IPF

A 
Consult pulmonologist (not many choices tho)
Treat for GERD even if no sxs 
Nintedanib (TKI)
Pirfenidone
Quit smoking and vaccines
Supplement O2 prn
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27
Q

Use of pirfenidone in IFP

A

Reduces lung fibrosis through downregulation of production of growth factors and procollagens

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28
Q

Who is Ivan IPF?

A

Male
60ish
Common man with not much PMH
Smoker

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29
Q

Where does sarcoidosis mainly occur?

A

Lungs and intrathoracic lymph nodes (central predominance)

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30
Q

What do the non-caseating granulomas in sarcoidosis secrete?

A 
1/25 dihydroxyvitamin D so high serum levels (and Ca elevated too)
Secrete ACE (acts as cytokine)
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31
Q

Epidimiology of sarcoidosis

A

Seen more in African Americans
Slight female predominance
20-40

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32
Q

Presentation of sarcoidosis

A

DOE, chest pain, cough, hemoptysis is rare

Systemic complaints in about half

33
Q

Extra pulmonary findings in sarcoidosis

A

Erythema nodosum, lupus pernios, granulomatous uveitis, arthralgias

34
Q

What is seen on the diagnostics for sarcoidosis?

A

Restrictive patterns on PFTs (but 20% can be obstructive)
May only see isolated reduced DLCO
Adenopathy on CXR

35
Q

Lab testing for sarcoidosis

A

Elevated serum ACE in 60%
Elevated Ca, hypercalciuria
Elevated alkaline phosphatase

36
Q

Is a biopsy needed for sarcoidosis?

A

Usually (EBUS-TBLB is fine)

37
Q

Staging for sarcoidosis

A

Based on CXR

0: normal
1: hilar adenopathy
2: hilar adenopathy and diffuse infiltrates
3: only diffuse parenchymal infiltrates
4: pulmonary fibrosis

38
Q

When do pts usually start needing tx for sarcoidosis?

A

When stage 2 and symptomatic

39
Q

Tx for sarcoidosis

A

High dose corticosteroids (taper over 6 mos-PJP prophylaxis)
Methotrexate is non steroid alternative
Chroloquine/hydroxychloroquine for cutaneous lesions, neurologic, hypercalcemia
Lung transplant stage 4

40
Q

Most common pattern of LAD in sarcoidosis

A

Bilateral symmetrical hilar and right parenchymal mediastinal adenopathy

41
Q

Who is Sally Sarcoidosis?

A 
Female
African American
30s
Non smoker
(she has hilar adenopathy and shes an ACE)
42
Q

What is pneumoconiosis?

A

General term for lung disease caused by inhalation and deposition of mineral dust
Asbestosis, silicosis and pneumoconiosis

43
Q

What characterizes silicosis?

A

Fibronodular lung disease

Due to inhalation of silica dust (alpha quartz or silicon dioxide)

44
Q

Occupations at risk for silicosis

A

Mining, construction, granite cutting, pottery making

45
Q

CXR for sarcoidosis

A

Enlarging opacities even after exposure eliminated (can cavitate so rule out TB)

46
Q

PFTs for silicosis

A

Mostly restrictive pattern

Massive fibrosis leading to severe restriction

47
Q

Chronic simple silicosis

A

10-12 yrs exposure (may be asymptomatic)
Non-progressive when exposure is eliminated
Hilar node calcification (eggshell pattern)
Small round opacities (silicotic nodules) on CXR

48
Q

Chronic complicated silicosis

A

> 20 yrs exposure
Progressive even after eliminate exposure
Exam: tachypnea, prolonged expiration, rhonchi, wheezing,cyanosis and cor pulmonale (advance)
Digital clubbing uncommon

49
Q

What might benefit acute phase of silicosis?

A

Corticosteroids

50
Q

Tx for silicosis

A

Consult pulmonologist
Smoking cessation
No specific therapy to alter disease course
Vaccinate, treat latent TB because increased risk
Maybe lung transplant if candidate

51
Q

Who is Sam silicosis?

A 
Male
Miner
Indeterminate age
Smoker making things worse
(has eggshell calcifications)
52
Q

Epidimiology of asbestosis

A

Usually presents after 15-20 yrs exposure (dose dependent)
40-75 usually
Males more

53
Q

Occupations at risk for asbestosis

A

Construction (old building demo), auto mechanics, pipe fitters, plumbers, welders, janitors, shipyard, biolermakers

54
Q

Asbestos and lung cancer

A

Asbestors is linked to lunger cancer and malignant mesothelioma
Smoking increases the risk

55
Q

Physical exam of asbestosis

A 
No specific sxs
Insidious onset of dyspnea, reduced exercise tolerance
Dry cough
End-inspiratory rales
Digital clubbing (30-40%)
56
Q

CXR asbestosis

A

Opacities in lower lungs, thickened pleura and calcified pleural plaques (reliable indicator)–usually in diaphragmatic pleura or parietal pleura of ribs 6-9

57
Q

Open lung biopsy for asbestosis

A

Usually not indicated but would be definitive (histology shows fibrosis and asbestos bodies in light microscope)

58
Q

PFTs asbestosis

A

Restrictive pattern (use to follow progression)

59
Q

Tx of asbestosis

A

Consult pulm (long term O2)
Immunotherapy drugs and steroids not effective
Want to eliminate progression or sxs and reduce risk of lung disorders
Vaccine for influenza and pneumovax

60
Q

What is mesothelioma?

A

Form of cancer almost always associated with asbestos exposure
Mesothelium is protective lining that covers most organs

61
Q

Characteristics of mesothelioma

A

May be short term exposure (1-2 yrs)
Most common in pleura but can be peritoneum or pericardium
Not caused by smoking
6-12 month survival after presentation

62
Q

Who is Al asbestosis?

A 
Male
50ish
Pipefitter
Smoker making things worse
(has pleural plaques)
63
Q

What is granulomatosis with polyangiitis (GPA)?

A

Auto-immune mediated systemic vasculitis of small-medium vessels
ANCA associated vasculitis
Multisystem

64
Q

What characterizes GPA?

A

Necrotizing granulomas of upper and lower respiratory tracts

65
Q

Epidimiology of GPA

A

Northern European descent
Men and women
35-55
Relapse common by 5 yrs

66
Q

History in GPA

A

Recurrent respiratory infections

Nonspecific constitutional sxs (B sxs-fever, weight loss and night sweats, loss of appetite, fatigue)

67
Q

Organ manifestations of GPA

A 
Ocular involvement
ENT (saddle nose! sinusitis, rhinitis)
Pulmonary (infiltrates and cough common, dyspnea etc)
MSK
Renal
Nervous system peripheral
Skin (about half of people)- blistering purpura
Cardiac
68
Q

Diagnostic images in GPA

A

CXR: variable but maybe nodules that cavitate
CT chest: stellate shaped peripheral pulmonary arteries (sign of vasculitis), feeding vessels leading to nodules and cavities, alveolar hemorrhage

69
Q

Bronchoscopy in GPA

A

Usually not indicated unless hemorrhage or need for therapeutic intervention

70
Q

Lab studies in GPA

A

ESR/CRP usually elevated
CBC/CMP: normocytic anemia, thrombocytosis, leukocytosis, renal involvement
UA: proteinuria if renal, RBC casts
C-ANCA (antineutrophil cytoplasmic antibody)
Maybe RF and ANA

71
Q

Initial tx of GPA

A

Cyclophosphamide (immunosuppressant) and corticosteroids
Watch for toxicites: cardiac, heme, renal, GI
Consult rheum and pulm

72
Q

What is hypersensitivity pneumonitis?

A

Inflammatory syndrome of lung caused by repetitive inhalation of antigens in susceptible host
No predilections
Bacteria/fungi, proteins, chems, environmental stuffs

73
Q

Difference between hypersensitivity pneumonitis and the rest

A

This is reversible!! (but recovery make take a couple yrs)

74
Q

History of hypersensitivity pneumonitis

A

flu-like syndrome within hours of exposure if acute
Insidious onset of productive cough, dyspnea, fatigue over wks if subacute
Progressive dyspnea, cough, fatigue if chronic

75
Q

Physical exam of hypersensitivity pneumonitis

A

Diffuse, fine bibasilar crackles, fever, tachypnea, muscle wasting, clubbing

76
Q

What is seen on imaging in hypersensitivity pneumonitis?

A

Interstitial inflammation, honeycombing, centrilobular fibrosis, peribronchiolar fibrosis

77
Q

Tx for hypersensitivity pneumonitis

A

Consult pulm
Avoidance
Acute doesn’t need therapy
Corticosteroids can speed recovery when severe (so used in chronic)
Bronchodilators, antihistamines, inhaled corticosteroids can be adjuncts

78
Q

Complications of ILD

A 
Pul HTN
Cor pulmonale/cardiovascular disease (hypertrophy or dilation of right ventricle associated with lung disease)
Pneumothorax
PE
Pulm infection
Elevated cancer risk
Progressive respiratory insufficiency

X Clin Med II Exam 2 (6 decks)

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