Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pulmonary: Clin Med II B > ILD > Flashcards

ILD Flashcards

1
Q

this word means “in between”

A

Interstitium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

lung interstitium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

a group of pulmonary disorders (>200) characterized by a similar pathology with an insidious and progressive presentation

A

Interstitial Lung Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are the insidious and progressive presentation of Interstitial Lung Disease? (5)

A
  1. damaged alveoli and surrounding tissue
  2. dyspnea on exertion (DOE)
  3. persistent dry cough
  4. late inspiratory rales on PE
    - results from forced opening of alveoli
  5. CXR - septal thickening and reticulonodular changes (MC)
    - occasionally ILD will be found incidentally during work-up for another condition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What structures are affected by ILD’s?

A
  1. a collection of support tissues within the lung that includes:
    - alveolar epithelium
    - pulmonary capillary endothelium
    - alveolar basement membrane
    - perivascular tissues
    - perilymphatic tissues

the tissue and space around the air sacs of the lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

MC presentations of ILD

A
  1. Idiopathic pulmonary fibrosis (IPF)
  2. Occupational and environmental
  3. Sarcoidosis
  4. Drug and radiation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

pathophys of ILD

A

Injury to the alveolar epithelial or capillary endothelial cells (alveolitis) –> progressive, irreversible scarring and stiffness of lung parenchyma –> poor O2 exchange

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

pathogenesis of ILD

A
  1. repetitive and/or excessive injury
    - FOLLOWED BY
  2. dysregulation of tissue repair
    - genetic predisposition
    - autoimmune d/o
    - superimposed disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

accumulation of T lymphocytes, macrophages, and epithelioid cells organized into discrete structures within in the lung parenchyma
becomes fibrotic
which type of histopathological category?

A

Granulomatous Lung Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

repetitive injury results in chronic inflammation leading to fibrotic alveoli
which type of histopathological category?

A

Inflammation and Fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the 2 histopathological categories of ILD?

A
  1. Granulomatous Lung Disease
  2. Inflammation and Fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

etiologic ddx of ILD

A
  1. medication related, environmental, infectious, primary pulmonary disorders, systemic disorders
  2. Requires a thorough PAST/PRESENT history
    - medication history
    - social history - occupational exposure to organic and inorganic compounds
    - family/past medical history - connective tissue disorders, infectious processes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

onset of ILD? presentation of each?

A

Onset is varied
1. Acute - days to weeks
- Allergy, acute interstitial pneumonia, hypersensitivity pneumonitis
2. Subacute - weeks to months
- drug-induced, sarcoidosis
3. Chronic - months to years
- majority of ILD’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

age of presentation of ILD

A
  1. 20-40 y/o - majority
  2. > 60 - Interstitial Pulmonary Fibrosis (IPF)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

social history that can cause ILD

A
  1. Smoking (past or present) increases risk
  2. Occupational and environmental exposure
    - strict chronological history of possible exposures
    - compare severity of symptoms during exposure vs non-exposure periods of time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

MC symptoms of ILD

A
  1. dyspnea, cough
    - often progressive in nature; wheezing - uncommon
    - nonproductive (“dry”)
    hemoptysis rare
  2. General - fatigue, weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Extrapulmonary symptoms only if ILD is associated with what disorders? what are the sx?

A

CT disorders
MSK pain, weakness, fatigue, fever, joint pains or swelling, photosensitivity, Raynaud phenomenon, pleuritis, dry eyes, and dry mouth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

PE findings of ILD

A
  1. General - varies based upon severity of condition
    - normal or varying SOB, cachexia and fatigued
  2. Respiratory
    - tachypnea
    - late inspiratory rales
    - rhonchi (aka sonorous rhonchus) - heard with associated bronchiolitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

late inspiratory rales in ILD is often heard where?

A

first bibasilar, in the posterior axillary line

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

late respiratory rales is less common in what type of ILD

A

granulomatous disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

rhonchi (aka sonorous rhonchus) is heard with what associated disorder?

A

bronchiolitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

PE findings of late ILD

A
  1. Digital clubbing
  2. Pulmonary Hypertension
    - Loud P2 component of the 2nd heart sound
    - a fixed split S2
    - a holosystolic tricuspid regurgitation murmur
    - pedal edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

work-up needed for ILD (tools only, not including additionals)

A
  1. CXR / HRCT
  2. PFT
    - spirometry
    - DLco
    - Pulse ox
    - ABG
    - 6MWT
  3. EKG
  4. CBC, CMP, UA, (ANA & RF)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

bibasilar reticular and/or reticulonodular pattern with honeycombing in late stage
what is this indicative of?

A

ILD
honeycombing indicates poor prognosis
indicates small cystic spaces with fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

which imaging option is better for ILD

A

HRCT (no contrast) > CXR
findings can help you narrow the ILD differential diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what diagnostic tool may assess severity of ILD and narrows DDx

A

PFT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

most ILDs are what type of lung disease (obstructive/restrictive)? what would it show on spirometry?

A

restrictive

reduced TLC
reduced TLC → reduction in FEV1 and FVC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

few ILDs will show (obstructive/restrictive) patterns, will reduced FEV1/FVC ratio. what is a common ILD with this type of lung disease?

A

obstructive
sarcoidosis (50%), hypersensitivity pneumonitis, ILD mixed with COPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

which diagnostic tool helps Assess the transfer of gas (O2/CO) from the lung to the blood cells? what would ILD look like?

A

DLco
< 80% DLco is common in ILD but not specific

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

often obtained to confirm results of Pulse Ox
performed at rest and after exertion
what type of diagnostic tool is this?

A

ABG
resting ABG often normal in early disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what criteria for 6MWT is associated with increased mortality

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

EKG of ILD

A
  1. normal unless pulmonary hypertension (PH)
    - pulm HTN: right axis deviation, evidence of right ventricular hypertrophy or right atrial enlargement
  2. Consider evaluation for PH if clinical presentation is consistent with disease.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

additional specialty work-up for ILD

A
  1. Bronchoalveolar Lavage (BAL)
    - during flexible bronchoscopy
    - gets samples of cells and pulmonary fluid for assessment of cell count, cultures and cytologic analysis
    - usually nonspecific
  2. Lung Biopsy
    - last resort to confirm dx and/or stage disease
    - histopathologic pattern is evaluated in combination with the clinical information to determine the diagnosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

ILD management goals

A

Is the patient symptomatic?
1. asx - reduce risk factors (remove offending agent and smoking cessation)
2. symptomatic
- remove offending agent (if known)
- manage hypoxemia - oxygen
- suppression of inflammatory process - steroids
- improve quality of life - pulm rehab
- manage complications - PH and cor pulmonale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

ILD tx

A
  1. Remove offending agent - Adjust meds, Change jobs
  2. Supplemental oxygen
    - Goal: O2 sat 90-92%
  3. Glucocorticoids - prednisone
    - reduce inflammation - reduce scarring/fibrosis
    - mainstay despite low success rate and lack of controlled studies
  4. If no improvement –> + immunosuppressant
    - cyclophosphamide, azathioprine or mycophenolate mofetil (Cellcept)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

indications for supplemental oxygen

A
  • hypoxemia - O2 sat ≤ 88% at rest or with exertion
  • Dose is determined by performing pulse ox testing (at rest and with exertion) while slowly titrating supplemental oxygen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

after starting a steroid for ILD, what is the management afterwards? any consequences if done incorrectly?

A
  • Pt is reevaluated after 4-12 wks
  • if stable / improved, tapered to 0.25–0.5 mg/kg and is maintained at this level for an additional 4–12 wks
  • Rapid tapering or a shortened course can result in recurrence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

a program of exercise, education, and support to help patients function at the highest level possible

A

Pulmonary rehabilitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

components of Pulmonary rehabilitation

A

Exercise - close monitoring of VS
Breathing techniques
Nutrition
Relaxation
Emotional and group support
Learning more about your medications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

monitoring for ILD

A

Follow up every 3-6 months
1. reassess sx, PFT (spirometry, DLCO, pulse ox)
2. monitoring for development of comorbid conditions
- hypoxemia, pulmonary hypertension, thromboembolic disease, COPD, heart failure, obstructive sleep apnea, depression
3. evaluate the clinical course and identify patients who develop accelerated deterioration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

pathophys of 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

clinical findings of idiopathic pulmonary fibrosis

A
  1. gradual onset of DOE w/ nonproductive cough
    - MC onset 55-60 y/o with slight male predominance
  2. fine inspiratory rales/crackles with or without digital clubbing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

PFT of idiopathic pulmonary fibrosis

A

often reveals a restrictive pattern on PFT , a reduced DLCO and hypoxemia that is exaggerated or elicited by exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

imaging findings of Idiopathic Pulmonary Fibrosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Idiopathic Pulmonary Fibrosis Often requires this diagnostic work-up? findings?

A
  1. biopsy
  2. alternating areas of healthy lung, interstitial inflammation, fibrosis, and honeycomb change
    - Fibrosis predominates over inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

management for Idiopathic Pulmonary Fibrosis

A
  1. Antifibrotics (FDA approved)
    - nintedanib (Ofev) - tyrosine kinase inhibitor
    - pirfenidone (Esbriet) - anti-inflammatory; antifibrotic agent
    - Doesn’t reverse fibrosis but can prevent further scarring
  2. Lung transplant even while attempting meds
  3. COVID-19 mRNA vax - benefit of vaccine outweighs risk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

caution + CI w/ Antifibrotic Therapy
monitoring?

A

High risk of drug induced liver injury; CI in severe liver disease
monitor LFT’s before therapy, q1m x 6 months then q3m

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what novel class of agents with both antifibrotic and immunomodulatory effects are in trial and have shown benefits for IPF

A

phosphodiesterase 4B (PDE4B) inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

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

A

Sarcoidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Sarcoidosis MC affects what organ? 2nd MC?

A

MC organ affected - lungs (including mediastinal LN)
2nd MC organs affected - skin, eye

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

a mass of granulation tissue, typically produced in response to infection, inflammation, or the presence of a foreign substance.

A

granuloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

sarcoidosis MC in who and at what age?

A
  1. African Americans (AA) and Northern European (NE) descent MC
  2. Onset - 20-60 years of age
  3. Research shows a genetic component to dz that protects some pts and predisposes others
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

in what ethnic groups is sarcoidosis more severe and more mild?

A
  1. AA’s - acute, severe disease
    - women > men
  2. NE’s - mild, chronic disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Dyspnea & cough x 2-4 wks
ROS - insidious fatigue, fevers, night sweats, wt. loss
lung exam will likely be normal
what is the dx based on these pulmonary findings?

A

Sarcoidosis

55
Q

sarcoidosis lung exam will likely be normal, but when wheezing is heard what does that indicate?

A

endobronchial involvement or traction bronchiectasis due to scarring

56
Q

> 90 % of sarcoidosis patients develop what clinical finding?

A

lung involvement

57
Q

A lower-extremity panniculitis with painful, erythematous nodules

A

Erythema nodosum

58
Q

Violaceous rash on the cheeks or nose

A

Lupus pernio

59
Q

MC chronic skin lesion of sarcoidosis

A

Maculopapular lesions

60
Q

what ocular findings can be found with sarcoidosis

A

Anterior/posterior granulomatous uveitis
Conjunctival lesions and scleral plaques
May lead to blindness if left untreated

61
Q

Erythema nodosum, Lupus pernio, Maculopapular lesions are skin findings for what dx

A

sarcoidosis

62
Q

insidious onset, +/-pain, slight photophobia, blurred vision
what type of uveitis is seen in sarcoidosis

A

anterior

63
Q

painless, floaters, loss of visual field, scotomas, decreased vision
what type of uveitis is seen in sarcoidosis

A

posterior

64
Q

lab findings of sarcoidosis

A
  1. Hypercalcemia (5%), hypercalciuria (20%)
  2. Elevated ESR - Inflammatory response in tissues affected
  3. Elevated ACE (40-80% pts with active dz)
    - ACE elevation is not sensitive / specific for sarcoidosis
65
Q

granulomas produce what which increases intestinal absorption of Ca - ultimately results in a suppressed PTH

A

1,25 dihydroxyvitamin D

66
Q

what secretes ACE that causes elevated ACE levels in sarcoidosis

A

Pulmonary granulomas
ACE is naturally produced in the lung endothelium

67
Q

Consider using what med that will produce low ACE level in the presence of sarcoidosis

A

ACEI

68
Q

PFT findings of sarcoidosis

A
  1. DLco is the most sensitive test - reduced (<80%)
  2. Spirometry - normal, restrictive or obstructive
  3. 6MWT - expected results depends on severity
    - diminished distance, exercise induced hypoxia
69
Q

CXR characterization for sarcoidosis

A
  1. Staged characterization (radiographic staging) of lung involvement
    - Stage I - hilar adenopathy alone
    - Stage 2 - adenopathy + infiltrates
    - Stage 3 - infiltrates alone
    - Stage 4 - fibrosis
  2. Usually the infiltrates are predominantly found in the upper lobes
70
Q

adenopathy >2 cm in the short axis
patchy reticular nodularity infilatrates
confluent nodularity infiltrates

these HRCT findings support which dx?

A

Sarcoidosis

71
Q

what is needed to confirm sarcoidosis dx? Findings?

A
  1. biopsy
    - transbronchial bx via bronchoscopy for pulmonary granuloma
    - extrapulmonary location is ok: skin lesion, palpable LN
    - lung and/or mediastinal LN bx via thoracoscopy - only if atypical on imaging or less invasive testing is indeterminate
  2. histologic finding - noncaseating granulomas
    - r/o infection or malignancy
72
Q

Bronchoalveolar lavage Shows increased lymphocytes, high CD4/CD8 cell ratio
what is the dx?

A

sarcoidosis

73
Q

how to look for cardiac involvement in sarcoidosis? what would you see?

A
  1. EKG, 24 hour holter monitor, Echo
    - cardiac sarcoidosis seen in 5% of patients
    - Evidenced by: restrictive cardiomyopathy, cardiac dysrhythmias, and conduction disturbances
    cardiomyopathy, cardiac dysrhythmias, and conduction disturbances
74
Q

tx indications for sarcoidosis

A

hypercalcemia
iritis
uveitis
arthritis
CNS involvement
cardiac involvement
granulomatous hepatitis
cutaneous lesions other than erythema nodosum
progressive pulmonary lesions
severe constitutional symptoms

75
Q

standard care for acute sarcoidosis
second-line?

A

Standard - oral/topical glucocorticoids
Second-line - immunomodulators (MTX, hydroxychloroquine, azathioprine)

76
Q

Chronic disease is defined by ?

A

a lack of resolution within 2-5 years

77
Q

For patients with advanced pulmonary fibrosis, _____ _____ remains the only hope for long-term survival

A

lung transplantation

78
Q

prognosis for sarcoidosis

A
  1. Spontaneous remission within 2-5 years occurs in most patients
    - Likelihood of remission decreases with higher disease staging
  2. A chronic sarcoid disease state, leads to worse outcomes
79
Q

referral and f/u for sarcoidosis

A
  1. Referral
    - Ophthalmology at onset and yearly
    - Refer to cardiology, pulmonology ect. based upon organs affected
  2. Follow up
    - Minimum yearly exam
    - Yearly PFT’s, chemistry panel, CXR and EKG - may be ordered more frequently based upon patient symptoms and response to treatment
80
Q

types of Occupational and Environmental Lung Disease

A
  1. Pneumoconiosis
    - Coal workers pneumoconiosis
    - Silicosis
    - Asbestosis
  2. Pneumonitis
  3. Radiation Injury
81
Q

what MUST be taken to discover underlying workplace or general environmental exposure of occuptional/environmental lung disease

A

A careful “exposure” history

82
Q

Why is knowledge of occupational or environmental etiology so important?

A

without proper knowledge of exposure, d/c exposure can’t occur = inadequate response to therapy = worsening course of disease and poorer outcomes

83
Q

additional historical questions for occuptional/environmental lung disease

A

the presence of visible dusts or chemical odors
the size and ventilation of workspaces
use of respiratory protective equipment
similar complaints in co-workers
correlation between symptoms and exposure
hobbies
home characteristics
exposure to secondhand smoke
proximity to traffic or industrial facilities

84
Q

what testing can be misleading due to ILD complicated by environmentally induced asthma/COPD

A

PFT

85
Q

uncomplicated and complicated diseases would display what patterns and DLco in PFTs?

A
  • uncomplicated disease - restrictive pattern and a decreased DLCO
  • complicated disease - obstructive pattern with decreased DLCO
86
Q

A chronic fibrotic lung disease caused by the inhalation of inorganic dusts

A

Pneumoconiosis

87
Q

presentation of pneumoconiosis ranges from ?

A
  • asx disorders w/ diffuse nodular opacities on CXR to severe, symptomatic, life-shortening disorders
  • Treatment for each is supportive
88
Q

aka “black lung”

A

Coal Workers Pneumoconiosis

89
Q

pathophys of Coal Workers Pneumoconiosis

A

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

90
Q

what are the 2 types of Coal Workers Pneumoconiosis

A
  1. Simple: asx, minimal changes on PFT, small (<1 cm) rounded opacities on CXR
  2. Complicated: symptomatic, diminished lung function on PFT, nodules ≥1 cm in diameter generally confined to the upper half of the lungs
91
Q

Silicosis exposure from what occupations/actions?

A

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

92
Q

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

A

silicosis

93
Q

pathophys of silicosis

A

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

94
Q

presentation of acute vs chronic silicosis

A
  1. acute
    - occurs in heavily exposed environments
    - few weeks to years after exposure
    - cough, SOB, pleuritic pain, weight loss, fatigue
  2. chronic silicosis
    - results from long-term, less intense exposure
    - may take 15-20 years to develop symptoms or radiographic changes
95
Q

what are the types of chronic silicosis

A
  1. simple silicosis- asymptomatic or exertional dyspnea and cough with sputum production
  2. complicated silicosis - cough, SOB, loss of appetite, wt loss, malaise/fatigue
96
Q

PE of silicosis

A

rales

97
Q

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

A

simple silicosis

98
Q

bilateral upper lobe masses, which are formed by the coalescence of nodules
what is the dx

A

complicated silicosis

99
Q

in a silicosis CT chest, small nodules are seen coalesced into ?

A

larger masses

100
Q

silicosis pts are at an increased risk for what other condition? why? what is their maintenance then?

A
  1. pulmonary TB
  2. Silica causes alveolar macrophage dysfunction.
    - initial immune response to TB is through alveolar macrophages
  3. annual tuberculin skin test (PPD) and screening CXR
101
Q

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

A

Asbestos

102
Q

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

A

Asbestosis

103
Q

pathophys 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

104
Q

presentation of asbestosis

A
  1. sx - only after latent period of +20 years
  2. Dyspnea on exertion (DOE) - MC, progressive with time
  3. PE - may be normal
    - bibasilar, fine end-inspiratory crackles
    - clubbing (<½ of patients)
105
Q

linear (reticular) opacities (often seen first)
multinodular parenchymal opacities of various size and shape
pleural plaques
honeycomb changes in advanced cases
what is the dx?

A

Asbestosis

106
Q

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

A

asbestosis

107
Q

most sensitive imaging for asbestosis. why is CXR not enough?

A
  1. High Resolution CT (HRCT) - more sensitive
  2. up to 30% of asbestos exposed pts have normal CXR and abnormal CT
  3. All findings on CXR can be seen with more clarity on HRCT
108
Q

used only if HRCT isn’t diagnostic for asbestos
what is this diagnostic work-up?
what would be shown?

A

Bronchoalveolar Lavage (BAL)
BAL fluid will show asbestos bodies
even in asx pts

109
Q

autopsy shows small, stiff lungs with fibrosis in the subpleural regions of the lower lobes
what is this condition?

A

asbestosis

110
Q

Smoking cessation is esp important in asbestosis due to increased risk of lung carcinoma, especially ____

A

mesothelioma

111
Q

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

A

Hypersensitivity Pneumonitis
aka: extrinsic inflammatory alveolitis

112
Q

pathophys of Hypersensitivity Pneumonitis

A

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

113
Q
  1. Flu like illness with fever, chills, malaise, cough, chest tightness, dyspnea, and headache
    - Onset - within hours following significant exposure
    - Course - gradual improvement within 12 hours to several days following exposure removal
    - May recur following re-exposure
    what is this dx?
A

acute Hypersensitivity Pneumonitis
hx is vital

114
Q

CXR shows a poorly defined micronodular or diffuse interstitial pattern
what is this dx?

A

Hypersensitivity Pneumonitis

115
Q
  1. Insidious onset of productive cough, dyspnea, fatigue, anorexia, and weight loss
    - Onset - over weeks to months
    - Course - progresses to persistent cough and dyspnea

which ILD dx

A

Subacute/ Chronic Hypersensitivity Pneumonitis

116
Q

Hypersensitivity Pneumonitis sx can be reversible if ?

A

offending antigen is detected and removed early in the course of illness

117
Q

management/tx for Hypersensitivity Pneumonitis

A
  1. tx consists of identification and avoidance of offending agent
  2. Oral corticosteroids can be useful, especially in severe or protracted cases
118
Q

the degree of Radiation Lung Injury is determine by several factors:

A
  1. Volume of lung irradiated
  2. Dose and rate of exposure
  3. Other potentiating factors:
    - concurrent chemotherapy
    - previous radiation therapy in same area
    - simultaneous withdrawal of corticosteroid therapy
119
Q

Radiation lung injury occurs in associated radiation therapy for what cancers

A

breast cancer (10%)
lung cancer (5–15%)
lymphoma (5–35%)

120
Q

Two phases of the pulmonary response to radiation are common:

A

an acute phase (radiation pneumonitis)
chronic phase (pulmonary radiation fibrosis)

121
Q

presentation of Radiation Pneumonitis

A
  1. Onset: 2-3 months (range 1-12 months) after completion of radiation therapy
  2. Clinical presentation
    - 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
122
Q

CXR
alveolar or nodular opacities limited to the irradiated area
Air bronchograms are often observed
what is the dx

A

Radiation Pneumonitis

123
Q

tx for Radiation Pneumonitis

A

supportive; steroids may be given

124
Q

Pulmonary Radiation Fibrosis Most common in patients who receive a ?

A

full course of radiation therapy for cancer of the lung or breast
May occur with or without prior hx of radiation pneumonitis

125
Q

presentation of Pulmonary Radiation Fibrosis

A

most patients are asymptomatic, although slowly progressive dyspnea may occur

126
Q

radiographic findings include of pulmonary radiation fibrosis

A
  1. obliteration of normal lung markings
  2. dense interstitial and pleural fibrosis
  3. reduced lung volumes
  4. tenting of the diaphragm
  5. sharp delineation of the irradiated area
127
Q

tx for Pulmonary Radiation Fibrosis

A

No specific therapy is proven effective
Corticosteroids have no value

128
Q

these disorders are autoimmune disorders of unknown etiology that lead to inflammation and damage to the connective tissues:

A

Connective Tissue Disorders
skin, fat, muscle, joints, tendons, ligaments, bone, cartilage, and even the eye, blood, and blood vessels

129
Q

CTD’s most commonly associated with ILD:

A

Progressive Systemic Sclerosis
RA
SLE
Sjögren Syndrome
Polymyositis and Dermatomyositis

130
Q

Patients with ILD should always be evaluated for ?

A

clinical findings suggestive of a CTDs
musculoskeletal pain, weakness, fatigue, fever, joint pain or swelling, photosensitivity, Raynaud’s phenomenon, pleuritis, dry eyes, dry mouth

131
Q

what symptoms occasionally precede the more typical systemic manifestations of CTD’s and what is its timing?

A

Pulmonary symptoms
by months or years

132
Q

MC sx of Drug Induced ILD

A

DOE and nonproductive cough

133
Q

Many classes of drugs have the potential to induce diffuse ILD, but what are some common ones?

A
  1. antiarrhythmics
  2. antibacterials
  3. antineoplastics
  4. antirheumatics
  5. phenytoin
134
Q

presentation and tx of drug-induced ILD

A
  • In most cases, the pathogenesis is unknown
  • The drug may have been taken for years before a reaction
  • sx may begin weeks to years after the drug has been d/c
  • tx - d/c any possible offending drug and supportive care

Pulmonary: Clin Med II B (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions