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Clin Med B 2 > Interstitial lung diseases > Flashcards

Interstitial lung diseases Flashcards

1
Q

what is the lung interstitium

A

Lung interstitium is the region of the alveolar wall exclusive of and separating the basement membranes of alveolar epithelial and pulmonary capillary endothelial cells.

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1
Q

what is interstitial lung disease categorized by

A
  • a group of pulmonary disorders (>200) characterized by a similar pathology with an insidious and progressive presentation of :
  • damaged alveoli and surrounding tissue
  • dyspnea on exertion
  • dry cough
  • late inspiratory rales
  • CXR with septal thickening and reticulonodular changes
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2
Q

what structures are affected by ILD

A

a collection of support tissues within the lung that includes:
* alveolar epithelium
* pulm capillary endothelium
* alveolar basement membrane
* perivascular tissues
* perilymphatic tissues

(Layman’s Terms: the tissue and space around the air sacs of the lungs)

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3
Q

what is the frequency of ILDs in the following diagnoses:
- idiopathic pulmonary fibrosis
- occupational and environmental
- sarcoidosis
- drug and radiation

A
  • idiopathic pulmonary fibrosis - 55%
  • occupational and environmental - 26%
  • sarcoidosis - 10%
  • drug and radiation - 1%
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4
Q

what is the pathophysiology of ILD

A

injury to the alveolar epithelial or capillary endothelial cells (alveolitis) leads to progressive, irreversible scarring and stiffness of lung parenchyma

this results in poor O2 exchange

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5
Q

what is included in lung parenchyma

A

bronchioles, alveoli and capillaries

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6
Q

what is the mechanism of ILD

A

repetitive and/or excessive injury followed by dysregulation of tissue repair

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7
Q

what can cause dysregualtion of tissue repair

A

genetic predisposition
autoimune d/o
superimposed diseases

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8
Q

what are the two histopathological categories of ILD

A

granulomatous lung disease
inflammation/fibrosis

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9
Q

what occurs during granulomatous lung disease

A

accumulation of T lymphocytes, macrophages, and epithelioid cells¹ organized into discrete structures (granulomas) within in the lung parenchyma

granulomas then become fibrotic

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10
Q

what occurs during inflammation/fibrosis of the lung

A

repetitive injury results in chronic inflammation leading to fibrotic alveoli

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11
Q

what are possible eitologies of ILD

A

medication related
environmental
infectious
primary pulm disorders
systemic disroders

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12
Q

what is the onset time line of the majority of ILD

A

chronic - months to years

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13
Q

what is the MC age of presentation in ILD

A

20-40

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14
Q

what about a patients social history would increase risk of ILD

A

smoking
occupational or environmental exposure

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15
Q

if a patients ILD is onset days-weeks what is likely the etiology

A
  • allergy
  • acute interstitial pneumonia
  • hypersensitivity penumonitis
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16
Q

what are symptoms associated with ILD

A

fatigue
weight loss
worsening dyspnea (MC)
nonproductive cough (MC)

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17
Q

when would you see extrapulmonary symptoms in ILD

A

only if it is associated with a connective tissue disorder

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18
Q

what physical exam findings are associated with ILD

A
  • cachexia
  • tachypnea
  • late inspiratory rales (often heard first bibasilar in posterior axillary line, less common in granulomatous)
  • rhonchi (aka sonorus rhonchus)
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19
Q

what does late ILD present as on PE

A
  • digital clubbing
  • pulm HTN
    also this:
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20
Q

what would a CXR show in ILD

A

bibasilar reticular and/or reticulonodular pattern with honeycombing in late stage

honeycombing indicates poor prognosis

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21
Q

what is the preferred imaging for ILD

A

HRCT (she said we dont really need to know what it shows for this_)

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22
Q

what would you order to workup ILD

A
  • PFTs includeing:
  • spirometry
  • DLco
  • pulse ox
  • 6MWT
  • ABG
  • EKG
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23
Q

how do ILDs resent on spirometry

A

most are restrictive but if sarcoidosis or hypersensitivity then will be obstructive.

also shows obstructive if mixed w COPD

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24
Q

what DLco is common in ILD

A

< 80% DLco is common in ILD but not specific

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25
Q

how does pulse ox and ABG ususally present in ILD

A

normal until late disease

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26
Q

what would a 6MWT show in ILD

A

desaturation <88% during 6 minute walk test (6MWT) is associated with increased mortality

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27
Q

what would you see in a ILD pt on EKG

A

normal unless pulm HTN:

pulm HTN: right axis deviation, evidence of right ventricular hypertrophy or right atrial enlargement

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28
Q

what additional specialty workup can be done in ILD

A
  • bronchoalveolar lavage
  • lung biopsy

(these arent done often)

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29
Q

what is a bronchoalveolar lavage and how does it present in ILD

A
  • obtains samples of cells and pulmonary fluid for assessment of cell count, cultures and cytologic analysis
  • BAL in ILD is usually nonspecific²
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30
Q

when is a lung biopsy used in ILD workup and what would you evaluate in the biopsy?

A
  • last resort to confirm/stage disease
  • the histopathologic pattern is evaluated in combination with the clinical information to determine the diagnosis
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31
Q

what is the managment goals for an asymptomatic ILD patient

A

reduce risk factors (smoking cessation, remove offending agent)

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32
Q

what is the managment goals for symptomatic ILD patients

A
  • remove offending agent (if known)
  • manage hypoxemia (oxygen)
  • suppression of inflammatory process (steroids)
  • improve quality of life (pulmonary rehab)
  • manage complications (pulmonary hypertension and cor pulmonale¹)
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33
Q

what is the term used to describe RV enlargement, dysfunction and subsequent failure

A

cor pulmonale

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34
Q

when is supplemental oxygen indicated in ILD and what is the treatment goal

A
  • indicated at <88% O2 (at rest or with exertion)
  • goal - 90-92%
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35
Q

what pharmacotherapy is suggested to decerase inflammation in ILD

A

glucocorticoids (prednisone) for 4-12 weeks and then if patient is stable, they can be tapered down over another 4-12 weeks

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36
Q

if there is no improvement in inflammation with glucocorticoids, what other pharmacotherapy is initiated for ILD

A

immunosuppressent will be added to steroid. such as:
- cyclophosphamide
- azathioprine
- mycophenolate mofetil

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37
Q

what is included in pulmonary rehabilitation in ILD treatment

A

we learned this already but just in case!

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38
Q

how often should ILD patients follow up

A

every 3-6 months

during visits they should:
- reassess symptoms, PFTs
- monitor for comorbid conditions

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39
Q

what is patient education that should be given about ILD

A
  • fibrosis is irreversible
  • compliance is vital to slow progression
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40
Q

what is the pathophysiology theory about idiopathic pulmonary fibrosis

A
  • An epithelial-fibroblastic disease, in which endogenous or environmental stimuli disrupt the homeostasis of alveolar epithelial cells leading to abnormal epithelial cell repair and fibrosis
  • Excessive production and dysregulation of myofibroblasts
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41
Q

what are clinical findings of idiopathic pulmonary fibrosis

A

gradual onset of exertional dyspnea with nonproductive cough

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42
Q

what is the MC onset and demographic for idiopathic pulmonary fibrosis

A

MC onset 55-60y/o with slight male predominance

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43
Q

what PE findings are in idiopathic pulmonary fibrosis

A

fine inspiratory rales/crackles with or without digital clubbing

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44
Q

what is found on PFT studies for Idiopathic pulmonary fibrosis

A
  • restrictive PFT pattern
  • reduced DLco
  • hypoxemia worsened with exercise
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45
Q

what radiologic findings are seen in idiopathic pulmonary fibrosis

A

HRCT scan typically shows:
* bibasilar, reticular opacities
* traction bronchiectasis
* honeycombing

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46
Q

what must you do to observe histology of idiopathic pulmonary fibrosis

A

open or VATS biopsy to obtain histology results

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47
Q

what does histology show in idiopathic pulmonary fibrosis

A

alternating areas of healthy lung, interstitial inflammation, fibrosis, and honeycomb change

fibrosis will predominate over inflammation

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48
Q

how do you manage idiopathic pulmonary fibrosis

A
  • glucocorticoids NOT recommended
  • antifibrotics - nintedanib or pirfenidone
  • refer for lung transplant!!
  • encourage patients to apply for clinical trials!
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49
Q

what type of drug is nintedanib

A

tyrosine kinase inhibitor

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50
Q

what type of drug is pirfenidone

A

anti-inflammatory agent, antifibrotic agent

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51
Q

what do antifibrotics (nintedanib and pirfenidone) do to treat idiopathic pulmonary fibrosis

A

do not reverse fibrosis but can prevent further scarring!

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52
Q

what are the risks and CI of antifibrotics

A

high risk of drug induced liver injury and CI in liver disease

must monitor LFTs prior to therapy and then Q monthly for 6 months then Q 3 months

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53
Q

what may be associated with acute exacerbations of idiopathic pulmonary fibrosis

A

COVID-19 mRNA vaccine

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54
Q

what is the new class of agent being studied that has both antifibtoric and immunomodulatory effects

A

phosphodiesterase 4B inhibitors

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55
Q

what is sarcoidosis

A

an inflammatory disease, of unknown etiology¹, characterized by the presence of noncaseating² (non-necrotizing) granulomas involving two or more organ systems

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56
Q

what is the MC organs effected in sarcoidosis

A
  1. lungs including mediastinal lymph nodes (MC)
  2. skin and eyes
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57
Q

who is sarcoidosis MC in

A

African american women and Northern Europeans

age onset 20-60 (seriously, come on. )

58
Q

how does sarcoidosis tend to present in african american females? how is it different from presentation in NE descent?

A

AA women - acute, severe disease

NE - mild, chronic disease

59
Q

what are presentation findings in sarcoidosis

A
  • dyspnea and cough x 2-4 weeks
  • ROS with fever, fatigue, night sweats and weight loss.
  • lung exam normal
60
Q

when in sarcoidosis would you see wheezing on lung exam?

A

only if there is endobronchial involvement or traction bronchiectasis due to scarring

61
Q

what are the findings of the skin in sarcoidosis

A
  • erythema nodosum (LE panniculitis)
  • lupus pernio (vesicular rash on cheeks/nose)
  • maculopapular lesions (MC chronic form of disease)
62
Q

what all should be done during an eye PE for sarcoidosis

A

PE should include visual acuity, tonometry, slit lamp, and fundoscopic testing

63
Q

what ocular findings present in sarcoidosis

A
  • anterior or posterior granulomatous uveitis
  • conjunctival lesions and scleral plaques
  • may lead to blindness if untreated
64
Q

how does anterior ganulomatous uveitis present

A

insidious onset, +/-pain, slight photophobia, blurred vision

65
Q

how does posterior ganulomatous uveitis

A

painless, floaters, loss of visual field, scotomas, decreased vision

66
Q

when is topical opthalmic steroids contraindicated?

A

when dendritic lesions are found in the eye. this indicates herpes and can make it worse

67
Q

what initial labs should be ordered in a patient with sarcoidosis

A
68
Q

what lab findings present in sarcoidosis

A
  • hypercalcemia (5%) or hypercalciuria (20%)
  • elevated ESR
  • Elevated ACE levels (40-80%)
69
Q

what causes hypercalcemia or hypercalciuria in sarcoidosis patients

A

Granulomas produce 1,25 dihydroxyvitamin D which increases intestinal absorption of Ca - ultimately results in a suppressed PTH

70
Q

what causes elevated ACE levels in sarcoidosis patients

A
  • Pulmonary granulomas secrete ACE
  • Consider: ACEI use will produce low ACE level in the presence of sarcoidosis
71
Q

what do PFT sudies show in sarcoidisis

A
  • DLco (most sensitive) reduced diffusing capacity (<80%)
  • spirometry - nonspecific (can be restrictive, obstructive or normal)
  • 6MWT - depends on severity of disease ( diminished distance and exercise induced hypoxemia. )
72
Q

what does a CXR show in sarcoidosis (consider each stage)

A
73
Q

what does an HRCT scan show in sarcoidosis

A
  • adenopathy >2cm in the short axis
  • infiltrates that are patchy or confluent
74
Q

what would a biopsy show in sarcoidosis

A

noncaseating granulomas

75
Q

what would bronchoalveolar lavage show in sarcoidosis

A
  • increased lymphocytes
  • high CD4/CD8 cell ratio
76
Q

what would you use to assess for caridac involvement in sarcoidosis? how common is cardiac involvement

A

found in 5% of patients

use EKG, 24hr holter monitor, and/or echo

77
Q

DDX for pulmonary sarcoidosis

A
78
Q

what are indications for treatment for sarcoidosis

A

basically anything

79
Q

what is the treatment for advanced pulmonary fibrosis secondary to sarcoidosis

A

lung transplant is their only hope:/

80
Q

what is the prognosis for sarcoidosis

A
  • Spontaneous remission within 2-5 years occurs in most patients
  • A chronic sarcoid disease state, leads to worse outcomes
81
Q

how often should patients with sarcoidosis follow up

A

yearly!
PFTS, Chemistry panel, CXR, EKG

82
Q

what are additional historical questions that may be asked when assessing occupational/environmental lung disease

A
83
Q

what would uncomplicated vs complicated Occupational/Environmental Lung Disease look like on PFT?

A

uncomplicated - restrictive pattern with decreased DLco
complicated - obstructive pattern with deceased DLco

84
Q

what is pneumoconiosis and what are the 3 types

A

A chronic fibrotic lung disease caused by the inhalation of inorganic dusts
1. coal minors lung
2. silicosis
3. asbestosis

85
Q

what is the treatment for pneumoconiosis

A

supportive for all three types

86
Q

what is the presentation for pneumoconiosis

A

Presentation ranges from asymptomatic disorders with diffuse nodular opacities on CXR to severe, symptomatic, life-shortening disorders

87
Q

what is the pathophysiology of coal workers pneumoconiosis

A

Pathophysiology - alveolar macrophages ingest inhaled coal dust leading to the formation of “coal macules”, usually 2–5 mm in diameter

88
Q

what is the clinical presentation of simple coal workers pneumoconiosis

A

Simple: asymptomatic, minimal changes on PFT, small (<1 cm) rounded opacities on CXR

89
Q

what is the clinical presentation of complicated coal workers pneumoconiosis

A

Complicated: symptomatic, diminished lung function on PFT, nodules ≥1 cm in diameter generally confined to the upper half of the lungs

90
Q

what type of occupation would expose someone to silica

A

Rock mining, coal mining (via rock dust), quarrying, stone cutting, tunneling, masonry, sandblasting, pottery

91
Q

what is silicosis

A

Silicosis is a fibronodular lung disease caused by inhalation of dust containing crystalline silica

92
Q

what is the pathophysiology of silicosis

A

Pathophysiology - alveolar macrophages ingest the particles inducing an inflammatory response resulting in cell damage and fibroblast release leading to fibrosis

93
Q

what is the clinical presentation of acute silicosis

A
  • occurs in heavily exposed environments
  • few weeks to years after exposure
  • cough, SOB, pleuritic pain, weight loss, fatigue
94
Q

what is the clinical presentation for chronic silicosis

A
95
Q

hat does the PE for silicosis show

A

rales

96
Q

what does imaging CXR show for simple silicosis

A

Simple Silicosis - multiple small (< 10 mm) nodules that are scattered diffusely throughout the lungs but may be more prominent in the upper lung fields.

97
Q

what does imaging CXR show for complicated silicosis

A

Complicated Silicosis bilateral upper lobe masses, which are formed by the coalescence of nodules

98
Q

what foes a CT show in silicosis

A

small nodules are seen coalesced into larger masses

99
Q

what does silicosis increase the risk of

A
  • TB due to alveolar macrophage dysfunction
  • all patients should have yearly tuberculin skin test and screening CXR
100
Q

what is asbestos

A

A group of minerals that are shaped like long, thin fibers and used in insulation for pipe, cements, textile, spackling on walls, patching, gaskets, sheet material, ceiling tiles in homes or schools

101
Q

what is asbestosis

A

A nodular interstitial fibrosis occurring in workers exposed to asbestos fibers over many years

102
Q

what is the pathophysiology of asbestosis

A

asbestos fibers are inhaled and completely or partially ingested by macrophages depending on the size of the fiber resulting in an inflammatory response, fibroblast proliferation and chronic scarring

103
Q

when do symptoms appear for asbestos and what are they

A
  • after 20 years of latency
  • Dyspnea on exertion (MC symptom and progressive over time)
104
Q

what will the physical exam present as in asbestosis

A
  • bibasilar, fine end-inspiratory crackles
  • clubbing (<1/2 of patients)
105
Q

what does CXR show in asbestosis

A
  • linear (reticular) opacities (often seen first)
  • multinodular parenchymal opacities of various size and shape
  • pleural plaques
  • honeycomb changes in advanced cases
106
Q

what parts of the lungs are most affected in asbestosis? what parts are generally spared?

A

Visceral pleura may be fibrotic and associated with parietal pleural plaques, while the central portions of the lung are relatively spared

107
Q

why should you order a HRCT when suspecting asbestosis

A

up to 30% of asbestos exposed patients have normal CXR and abnormal CT

108
Q

what is used in asbestosis suspicion if HRCT is not diagnostic? what will it show?

A

Bronchoalveolar Lavage (BAL)

will show asbestos bodies even in patients who are asymptomatic

109
Q

what does a lung autopsy show in patients with asbestosis

A

small, stiff lungs with fibrosis in the subpleural regions of the lower lobes

110
Q

what is additional management of asbestosis

A

Smoking cessation is important due to increased risk of lung carcinoma, especially mesothelioma

111
Q

what is hypersensitivity pneumonitis

A

aka: extrinsic inflammatory alveolitis

A nonatopic, nonasthmatic inflammatory pulmonary disease resulting from exposure to inhaled organic antigens leading to an acute illness

112
Q

what is the pathophysiology of hypersensitivity pneumonotis

A

immune-mediated disorders characterized by diffuse inflammation of interstitial lung, terminal bronchioles, and alveol

113
Q

this is overwhelming but may be good to look at

A
114
Q

what is the clinical presentation of acute hypersensitivity pneumonitis

A
  • flu like illness (fever, chills, malaise, cough, chest tightness, dyspnea, HA)
  • onset within hours following exposure
  • gradual improvement 12 hours - several days after removal of exposure
115
Q

what does CXR show in acute hypersensitivity pneumonitis

A

a poorly defined micronodular or diffuse interstitial pattern

116
Q

what is the clinical presentation of subacte/chronic hypersensitivity pneumonitis

A
  • Insidious onset of productive cough, dyspnea, fatigue, anorexia, and weight loss
  • onset over weeks to months
  • progresses to persistent cough and dyspnea
117
Q

what are the CXR findings for subacute/chronic hypersensitivity pneumonitis

A

progressive fibrotic changes with loss of lung volume and coarse linear opacities are common

118
Q

why is prompt diagnosis important in hypersensitivity pneumonitis

A
  • Symptoms can be reversible if the offending antigen is detected and removed early in the course of illness
  • Continued exposure may lead to progressive disease
119
Q

what is the management for hypersensitivity pneumonitis

A
  • Treatment consists of identification and avoidance of offending agent
  • Oral corticosteroids can be useful, especially in severe or protracted cases
120
Q

what is radiation lung injury

A

The lung is an exquisitely radiosensitive organ that can be damaged by external beam radiation therapy.

121
Q

what are the factors that determine the degree of pulmonary injury in radiation lung injuries

A
  • Volume of lung irradiated
  • Dose and rate of exposure
  • Other potentiating factors such as concurrent chemotherapy, previous radiation therapy in the same area, and simultaneous withdrawal of corticosteroid therapy
122
Q

radiation therapies of which cancers are MC in radiation lung injuries

A
  • breast cancer (10%)
  • lung cancer (5–15%)
  • lymphoma (5–35%)
123
Q

what is the pathogenesis of radiation lung injury

A

unknown
possibly a hypersensitivity reaction

124
Q

what are the two phases of the pulmonary response to radiation

A
  • an acute phase (radiation pneumonitis)
  • chronic phase (pulmonary radiation fibrosis)
125
Q

what is the onset of radiation lung therapy

A

Onset: 2-3 months (range 1-12 months) after completion of radiation therapy

126
Q

what is the clinical presentation of radiation lung disease

A
  • insidious onset of dyspnea, intractable dry cough, chest fullness or pain, weakness, and fever
  • In severe disease, respiratory distress and cyanosis occur that are characteristic of ARDS
  • Inspiratory rales may be heard in the involved area
127
Q

what is found on CXR for radiation lung injury

A
  • alveolar or nodular opacities limited to the irradiated area
  • Air bronchograms are often observed
128
Q

what is the treatment for radiation pneumonitis

A

Treatment is supportive; steroids may be given

129
Q

what is pulmonary radiation fibrosis

A
  • Most common in patients who receive a full course of radiation therapy for cancer of the lung or breast
  • May occur with or without prior hx of radiation pneumonitis
130
Q

what is the clinical presentation of pulmonary radiation fibrosis

A

most patients are asymptomatic, although slowly progressive dyspnea may occur

131
Q

what is found on imaging for pulmonary radiation fibrosis

A
  • obliteration of normal lung markings
  • dense interstitial and pleural fibrosis
  • reduced lung volumes
  • tenting of the diaphragm
  • sharp delineation of the irradiated area
132
Q

what is the treatment for pulmonary radiation fibrosis

A
  • No specific therapy is proven effective
  • Corticosteroids have no value
133
Q

what are connective tissue diseases

A
  • autoimmune disorders of unknown etiology that lead to inflammation and damage to the connective tissues:
  • skin, fat, muscle, joints, tendons, ligaments, bone, cartilage, and even the eye, blood, and blood vessels
134
Q

what are the MC CTDs associated with ILD

A
  • Progressive Systemic Sclerosis
  • Rheumatoid Arthritis
  • Systemic Lupus Erythematosus
  • Sjögren Syndrome
  • Polymyositis and Dermatomyositis
135
Q

what are clinical findings suggestive of CTDs

A

musculoskeletal pain, weakness, fatigue, fever, joint pain or swelling, photosensitivity, Raynaud’s phenomenon, pleuritis, dry eyes, dry mouth

136
Q

what usually precedes, the pulmonary symptoms or the CTD symptoms?

A

Pulmonary symptoms occasionally precede the more typical systemic manifestations of CTD’s by months or years

137
Q

How many drugs today are known to cause drug induced ILD

A
  • > 350 drugs
  • known to cause lung disease
138
Q

how does the onset vary with drug induced ILD

A
  • abrupt and fulminant (days-wks) OR insidious (wks - months)
  • The drug may have been taken for several years before a reaction develops
  • Symptoms may begin weeks to years after the drug has been discontinued
139
Q

what are the MC symptoms in drug induced ILD

A
  • exertional dyspnea
  • nonproductive cough
140
Q

what are some common drugs that cause drug induced ILD

A
141
Q

what is the treatment of drug induced ILD

A

Treatment - discontinuation of any possible offending drug and supportive care

142
Q

YAY! youre done, flip for doggo!!

A

Clin Med B 2 (44 decks)

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