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Pulmonology Exam 2 > Restrictive lung disease > Flashcards

Restrictive lung disease Flashcards

1
Q

PAINT classification for Restrictive Lung Diseases

A
  • Pleural
  • Alveolar
  • Interstitial
  • Neuromuscular
  • Thoracic cage
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2
Q

Intrinsic Lung Diseases

A
  • Cause inflammation or scarring of the lung
    tissue (interstitial lung disease)
  • Can be caused by exudates in the air
    spaces (such as pneumonia) leading to
    pneumonitis
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3
Q

Examples of Intrinsic Lung Diseases:

A
  • Sarcoidosis
  • Idiopathic Pulmonary Fibrosis
  • Pneumoconiosis
  • Drug or Radiation Induced Interstitial Disease
  • Pneumonitis
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4
Q

Clinical presentation of Intrinsic Lung Diseases:

A
  • Progressional exertional dyspnea
  • Dry cough
  • Possibly hemoptysis, wheezing, chest
    pain
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5
Q

Physical examination
findings of Intrinsic Lung Diseases:

A
  • Insidious progression of
    dyspnea (all RLDs)
  • 3 C’s: cough, clubbing, coarse
    crackles on auscultation
  • can also have no abnormal
    findings
  • Skin manifestations in some
    with rheumatoid Dz
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6
Q

Intrinsic Lung Diseases diagnostic evaluation:

A
  • Routine labs fail to show much
  • Can do Reumatologic testing
  • Reticular, nodular,
    reticulonodular pattern on CXR
  • CT and US use
  • possible Bx, lavage, etc
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7
Q

Extrinsic lung Diseases:

A
  • Typically extrapulmonary causes
  • Obesity
  • Kyphoscoliosis
  • Pectus excavatum
  • Pleural diseases
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8
Q

Clinical presentation for Extrinsic lung Diseases:

A
  • Depends on etiology
  • younger could be asymptomatic
  • Older: dyspnea, decreased exercise tolerance,
    respiratory infections
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9
Q

Physical examination findings for Extrinsic lung Diseases

A

3 C’s
- Possible Kyphosis (or other spinal abn)
- Increased BMI
- Pleural DO’s: decreased tactile fremitus, dull to percuss, decreased breath sounds
- Accessory muscle use, rapid shallow breathing, paradoxical breathing

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10
Q

Diagnostic Evaluation of Extrinsic lung Diseases:

A
  • Elevated creatinine kinase shows possible myositis, resulting in muscle weakness
    and restrictive lung Dz
  • CXR for chest wall deformities, possible basal atelectasis and/or low volumes with
    muscle DOs
  • possible Bx, lavage, etc
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11
Q

Restrictive Lung Disease treatments (Dependent on cause!)

A
  • Steroids in acute exacerbations: ie prednisone
  • Immunosuppressive and Cytotoxic agents: ie cyclophosphamide
  • Supplemental 02
  • Diet and exercise recommendations
  • Pulmonary rehab
  • Weight loss
  • Surgical correction
  • Extreme : lung transplant
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12
Q

A _____ is a collection of cells
that are new tissue and typically in
response to a cut, infection,
laceration, etc

A

granuloma

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13
Q

Sarcoidosis

A

noncaseating granulomas in the lung (i.e not necrotic)
- May Contain “star shaped structure”
aka Asteroid, Or possibly
Schaumann bodies on Bx

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14
Q

Multisystem granulomatous disorder

A

-Characterized by noncaseating granulomas
in involved organs, most common in the lungs
(90% of cases)
-Typically, affects young adults

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15
Q

Clinical Presentation of Sarcoidosis

A

Presents with one or more of the following
-Bilateral hilar adenopathy
-Pulmonary reticular adenopathies
-Skin, joint, and or eye lesions
- Frequently found incidentally on routine CXR before
symptoms, Most asymptomatic!

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16
Q

PE for sarcoidosis is ____

A

likely going to be normal (may have wheezing if
bronchi are involved, could have crackles)

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17
Q

Sarcoidosis diagnostic labs

A
  • CBC, CMP, ESR, CRP can be done, but not specific
  • TB skin test only to exclude mycobacterium
  • Bx done in most cases, the least invasive the better!
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18
Q

Sarcoidosis imaging & other testing

A

Lung imaging is essential to diagnosis (initial Xray
followed by CT)
Bilateral hilar adenopathy is classic finding
Pulmonary Function Tests- Obtained in ALL patients:
20% abnormal in early dz, 40-70% in late dz

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19
Q

Diagnosis of sarcoidosis

A

One definitive test doesn’t exist
1. Clinical and radiographic elements consistent with
Sarcoidosis
2. Exclusion of other diseases
3. Pathology consistent with noncaseating granulomas

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20
Q

Tx of sarcoidosis

A

-No definitive monitoring regimen has been identified
-Tx depends, some require none
-Monitor extrapulmonary disease

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21
Q

Idiopathic Pulmonary Fibrosis- (IPF)

A

Most common type of idiopathic interstitial pneumonia (IIP)
- a specific form of chronic fibrosing interstitial pneumonia
- Bilat fibrosis, inspiratory bibasilar crackles, >60, unknown cause
Spontaneously occurring diffuse parenchymal lung disease

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22
Q

Idiopathic Pulmonary Fibrosis
Pathogenesis pathogenesis

A

Complex
Likely Cycles of epithelial cell injury and dysregulated repair

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23
Q

Risk Factors for Idiopathic Pulmonary Fibrosis

A

-No known cause
-Strongest association with cigarette smoking
-Exposure to stone, wood, organic dusts possible risk factors
-GERD may contribute via microaspiration (difficult to assess due to high
frequency of GERD in general population)

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24
Q

Idiopathic Pulmonary Fibrosis clinical presentation

A

-6th -7th decade
-H/O cigarette smoking
-Gradual onset of dyspnea on
exertion, nonproductive cough
over several months
-Fatigue, fever, myalgias,
arthralgias (can happen but rarely
reported)

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25
Q

Idiopathic Pulmonary Fibrosis PE

A

-Bibasilar crackles, may be unilateral in early dz (usually absent)
-Finger clubbing in 45-75%, manifestation of advanced disease

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26
Q

Idiopathic Pulmonary Fibrosis Labs

A

-Tests to R/O rheumatologic diseases and other autoimmune disorders
ie ANA, RA, anti-CCP
-Pulmonary Function Tests- Show restrictive pattern (which is what?)
-CXR- Reticular pattern (nonspecific, also found in other interstitial lung dz
or heart failure)
-CT- Peripheral bibasilar reticular opacities, honeycomb changes possibly
ie Clusters of cystic airspaces, can be on all fibrosis CT’s or CXR
Lung biopsy if previous evaluation does not help with diagnosis

27
Q

Diagnosis Criteria of Idiopathic Pulmonary Fibrosis

A

-Exclusion of other known causes of interstitial lung disease
-Usual expected pattern on CT scan (“honeycombing”)
-Lung biopsy- if all others fail!

28
Q

Idiopathic Pulmonary Fibrosis TX

A
  • Traditionally immunosuppression drugs
  • Now antifibrotics help: pirfenedone for example to slow progression
29
Q

Pneumoconiosis ie Occupational Lung Disease

A

Lung Reaction from inhalation and deposition of inorganic particles & mineral dust
(most common: asthma, bronchitis, bronchiolitis, hypersensitivity pneumonitis, acute
toxic inhalant syndromes, pneumoconiosis and tumors)

30
Q

Pneumoconiosis- Divided by Exposure type

A

Fibrogenic - silica, asbestos, coal, talc
Benign or Inert- iron, tin barium
Granulomatous - beryllium
Hard Metal - cobalt

31
Q

4 Criteria for Diagnosis of Occupational Lung Disease

A
  1. Documented exposure to agent known to induce disease
    2 Defined latent period between exposure and development of the disease
  2. Clinical features consistent with recognized features of the diseases
  3. Exclusion of other diseases that could be responsible
32
Q

Pneumoconiosis presentation

A

Progressive dyspnea on exertion, progressive
nonproductive cough (proceed radiographic findings)

33
Q

Pneumoconiosis Evaluation

A

● Aimed at confirming exposure history, exclude other causes
● Evaluating level of respiratory impairment
● Labs - no specific labs, may help exclude other causes
● CXR- defined by width and depends on offending agent- can be small round or irregular opacities
● CT- Differ depending on offending agent

34
Q

Diagnosis of Pneumoconiosis

A

Made clinically, biopsy if unable to clinical diagnosis

35
Q

Pneumoconiosis treatment

A

-Supportive and depends on the agent (ie- beryllium is avoid further exposure, supportive care, steroids, and watch for progression of disease)
-Lung transplant (eventually)
-Stop contact with substance
-Workmen’s compensation
Since there is no known cure, efforts should be placed on prevention (there has been great strides in this and decreases significant in the past
20-30/40 years)

36
Q

Workup for Silicosis

A

Type of Individual Pneumoconiosis
(Quartz, granite, sandstone)
Occupations at risk: mining, quarrying, drilling, sandblasting
CT scan (+) for B/L perilymphatic sharp marginated nodules
Hilar and mediastinal lymph node enlargement
TB occurs preferentially in patients with silicosis

37
Q

Workup for Coal Workers Pneumoconiosis (CWP)

A

(Silica free coal dust particles)
-CWP has similar features of Silicosis on imaging but due to characteristic
Pathologic findings of large black masses (black lung) as a result is
classified as a separate disease
-On CT reticular opacities with honeycombing
-Associated with bronchogenic carcinoma

38
Q

Workup for Talcosis

A

Talc powder
Occupational Exposure: ceramic, paper, plastics, rubber, paint, cosmetics
On imaging, small rounded opacities similar to silicosis
Potentially contaminated with asbestos

39
Q

Workup for Asbestosis

A

Primary Occupational Exposure: asbestos mining, milling
Secondary Occupational Exposure: insulation work, brakes, shipbuilding,
Construction, textiles
Nonoccupational, indirect, bystander: air pollution, among households
Latent period of 20-30 years from exposure to visible plaque formation
Malignant Mesothelioma - strongly linked to asbestos exposure
Latent period of 30-45 years common
Pleural plaque most common manifestation of asbestos exposure

40
Q

Radiation-induced Lung Injury

A

ie Radiation Pneumonitis
Associated with radiation primarily for cancer treatment
Clinical pneumonitis occurred in:
- Irradiation Tx of lung, breast or hematologic malignancies.
Radiation causes changes in the cells, which then leads to
fibrosis

41
Q

Radiation-induced Lung Injury: factors influencing development

A

● Method of irradiation
-Trying to improve methods of targeting dose to diseased tissue,
sparing healthy tissue
-Volume of lung irradiated
-Dosage of radiation
-Time-dose factor (ie tx 1 or 2 times daily)
● Concurrent chemotherapy
Known chemotherapy agents sensitize to radiotherapy
● Other factors
Prior irradiation, volume loss due to lung collapse, younger age,
smoking hx, interstitial lung Dz, COPD, females, endocrine therapy for
breast CA, glucocorticoid withdrawal
● Radiation Recall: Prior radiation before antineoplastic agent = pneumonitis

42
Q

Phases of Radiation-induced Lung Injury

A

Immediate phase: hrs to days after exposure; usually asymptomatic;
Pulmonary edema from leukocytic infiltration and Increased capillary
permeability
Latent phase: thick secretions develop, decreased ciliary function
Third Phase: (acute exudative phase) clinically=radiation pneumonitis:
occurs 3-12 wks p exposure pulmonary capillaries narrow
microvascular thrombosis from sloughing endothelial and epithelial cells
Fourth Phase:(intermediate phase) hyaline Membrane dissolution, fibroblasts
migrate into alveolar walls
Final Phase: FIBROSIS: Early as 6 months p radiation; can progress for years;
Decreased lung volume, chronic infx may develop

43
Q

Radiation-induced Lung Injury presentation

A

-Acute radiation pneumonitis sxs develop approx. 4-6 wks p exposure; Late
or fibrotic are 6-12 months out.
-Includes nonproductive cough, dyspnea usually with exertion, low grade
fever; chest pain; malaise and wt loss

44
Q

Physical Exam Findings with Radiation-induced Lung Injury

A

-At times-Crackles or pleural rub (auscultation can be normal)
-Dullness to percussion if pleural effusion present (10%).
-erythema may be present at radiation area
-Tachypnea, cyanosis, or signs of pulmonary HTN in advanced cases

45
Q

Diagnosis of Radiation-induced Lung Injury

A

History taking!!!
CXR - likely normal; severity dependent
CT - Preferred, more sensitive
Nuclear Medicine Scans - under investigation
Bronchoscopy for eval if other issues.
PFTs - used to differentiate with COPD

46
Q

Radiation-induced Lung Injury Treatment

A

-Many studies of many different drugs are being done
-Some recommend steroids if symptomatic and subacute, not for all cases. Otherwise supportive care: ie cough meds, treat comorbid Dz

47
Q

Acute Interstitial Pneumonitis

A

Rare, acute, interstitial pneumonia- similar to ARDS

48
Q

Pathophysiology of Acute Interstitial Pneumonitis

A

-Diffuse alveolar damage (unknown cause)
-Starts with acute exudative, organizing proliferative and healed phases.
-temporally uniform lesions- injury occurs at single point in time. (unlike
some other interstitial diseases).

49
Q

Clinical Presentation for Acute Interstitial Pneumonitis

A

● Rapid onset
● Prodrome illness last 7-14 days ***
● Common presentation
○ Fever, cough, progressive severe shortness of breath
● Hypoxia at presentation
● Physical exam is (+) for tachypnea and diffuse crackles
● Most will require intubation and mechanical ventilation

50
Q

Hamman-Rich syndrome AKA

A

Acute Interstitial Pneumonitis

51
Q

Acute Interstitial Pneumonitis workup includes:

A

-Exclude cardiogenic causes for pulmonary edema (BNP and
Echocardiogram)
-Labs - Usually help identify alternative causes, elevated WBC common,
recommended checking for other connective tissue diseases.
-ABGs - moderate to severe hypoxemia (Similar to ARDS)
-CXR - Diffuse bilateral opacification (Similar to ARDS) Ground glass
appearance
-Microbiological Studies - generally to R/O infection causes (ie flu)

52
Q

Acute Interstitial Pneumonitis diagnosis

A

Based on Two Findings
1. Presence of a clinical syndrome of idiopathic ARDS
2. Pathologic confirmation of diffuse alveolar damage

53
Q

Acute Interstitial Pneumonitis treatment

A

-Supportive care -MAIN
-Glucocorticoids, broad spectrum antibiotics if unsure it’s not an infection
-Mortality in hospital is high

54
Q

Risks for Drug Induced Lung Damage

A

Genetics
Exposures to meds or environmental factors
Comorbid Dz
Could be a combination of the above

55
Q

Drug induced Lung Damage: general principles

A
  1. Nonspecific presentation clinically
  2. Injury occurs with variable latency from drug initiation
  3. Lung injury is often dose dependant
  4. Pulm toxicity may be unrelated to the drug’s pharmacological properties
  5. Acute, subacute and chronic reactions may be caused by a drug
  6. A variety of histopathologic patterns may be induced by a drug
  7. Dx of drug induced injury is often made by exclusion
  8. Resolution of injury may occur with drug discontinuation alone
  9. Rechallenge with the suspected culprit drug is NOT recommended.
56
Q

Chemotherapeutic drugs that
cause Lung Damage:

A

Cytotoxic Antibiotics (ie- bleomycin)
Alkylating agents (ie- cyclophosphamide)
Antimetabolites (ie- methotrexate in higher
doses)
Nitrosoureas (ie-carmustine)
Molecularly targeted agents (ie-erlotinib)
Monoclonal antibodies (ie-rituximab,
cetuximab)
All-trans retinoic acid
Interleukin-2
Procarbazine
Taxanes
Vinca alkaloids

57
Q

Non-Chemotherapeutic drugs
that cause Lung Damage

A

B-Adrenergic Receptor Blockers
Amiodarone
Hydralazine
HCTZ
Procainamide
Statins
Anticonvulsants
Aspirin
Antirheumatic and anti-inflammatory drugs
NSAIDS
Methotrexate (in lower doses)
D-Penicillamine
Gold Salts
Sulfasalazine and mesalazine
Biologic agents
Immunosuppressants
Nitrofurantoin
Antimicrobial drugs
Interferons
Opiates and illicit drugs

58
Q

Obesity Hypoventilation Syndrome
(OHS)

A

○ Obesity can decrease lung volumes, respiratory muscle strength, and respiratory drive. Increases work. Sleep apnea makes worse

59
Q

Pathophysiology of Obesity Hypoventilation Syndrome (OHS)

A

Usually Dx after pt becomes hypercapnic, there is a more
mild form. Decreased FRC, ERV and TLC. More affecting men due to where fat
forms

60
Q

Clinical presentation of Obesity Hypoventilation Syndrome (OHS)

A

BMI >30, Sleep apnea usually present, R heart
failure from pulm HTN, other comorbidities.
○ What are other comorbidities?

61
Q

Obesity Hypoventilation Syndrome (OHS) Dx

A

PFT’s, chest X Ray, EKG, echo, R/O other
diseases, CMP, CBC, thyroid, Toxicology, polysomnogram
○ What does the body do and what will you see on these tests?

62
Q

Obesity Hypoventilation Syndrome (OHS) treatment

A

○ Weight loss (How?)
○ Intermittent noninvasive respirations (what is this?)

63
Q

Kyphoscoliosis

A

“Thoracic Cage Syndrome”

64
Q

Neuromuscular Disorders affecting the lungs

A

Cervical Spine Injury
Diaphragmatic
Weakness or Paralysis
Myasthenia Gravis

Pulmonology Exam 2 (5 decks)

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