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Medicine > Interstitial Lumg Diseases > Flashcards

Interstitial Lumg Diseases Flashcards

1
Q

What is it meant by diffuse parnchymal lung diseases?

A

group of disorders based
lung disease.
9/26/2022
on similar clinical, radiographic, physiologic, and pathologic changes that affect the alveolar walls and often the related small airways and distal pulmonary vasculature.

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2
Q

What is the main symptoms of DPLDs?

A

shortness of breath

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3
Q

Is DPLDs bilateral of unilateral?

A

Imaging studies will typically demonstrate bilateral rather than unilateral lung disease.

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4
Q

If the FEV1/FVC ratio low?

A

Obstructive diseases ( asthma or copd)

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5
Q

If the FEV1/FVC ratio high ?

A

Restrictive disease

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6
Q

If the FEV1/FVC ratio low and DLCO is normal or increased?

A

Asthma or chronic bronchitis

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7
Q

If the FEV1/FVC ratio low and DLCO is decreased?

A

Emphysema

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8
Q

If the FEV1/FVC ratio normal or high and DLCO is normal or increased?

A

Chest wall weakness ( sclerosis)

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9
Q

If the FEV1/FVC ratio normal or high and DLCO is decreased?

A

ILD ( DPLDs): gramulomas diseases

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10
Q

High DLCO without pulmonary diseases?

A

Polycythemia

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11
Q

Low DLCO without pulmonary disease?

A

Anemia

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12
Q

If there is only low levels of DLCO, what is the diagnosis?

A

Pulmonary hypertension

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13
Q

The best time to improve sclerosis?

A

Spinal surgery while the patient is 1 and half year.

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14
Q

What is thr normal ranges of pft?

A

FEV1/FVC = > 70%
DLCO= 80-120
FVC =< 80%

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15
Q

What is the radiological diagnosis of IPF?

A

UIP ( usual interstitial pneumonia)

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16
Q

ILD ( interstitial lung diseases) are divided into those with a known cause or those which are idiopathic, mention the known causes?

A

Known Causes or Association:
1-Drug-induced: Examples: amiodarone,
methotrexate( to decrease the side effect we should give him folic acid the next day),
nitrofurantoin, chemotherapeutic agents.

2- Radiation-related: May occur 6 weeks to months following radiation therapy.( we should ask about that in a history)

3- Occupation-related: Asbestosis or silicosis.

4- Connective Tissue Disease-related: Rheumatoid arthritis, systemic sclerosis,
Polymyositis/dermatomyositis.

5- Granulomatous Disease-related: Sarcoidosis, Hypersensitivity pneumonitis or TB.

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17
Q

ILD ( interstitial lung diseases) are divided into those with a known cause or those which are idiopathic, mention the idiopathic causes?

A

 Unknown Causes or Association:
1-Chronic Process: Idiopathic pulmonary fibrosis.

2-Acute to Subacute Process: Acute interstitial pneumonia or Cryptogenic organizing pneumonia.

3- Smoking-related: respiratory bronchiolitis-associated interstitial lung disease (RB-ILD),
desquamative interstitial pneumonia (DIP), and pulmonary Langerhans cell histiocytosis (PLCH) occur almost exclusively in individuals who are current smokers.
9/26/2022
6

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18
Q

Woman 33 years old comes with shortness of breath and has spontaneous pneumothorax and chylous effusion, on chest CT shows cystic disease, what is the diagnosis?

A

Lymphangioleiomyomatosis.

Which Affects women in their 30s and 40s.
Associated with spontaneous pneumothorax and chylous effusions.
Chest CT shows cystic disease.

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19
Q

Treatment of Lymphangioleiomyomatosis?

A

Lung transplant

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20
Q

What is Chronic eosinophilic pneumonia?

A

Chest radiograph shows
“radiographic negative” heart failure, with peripheral alveolar
infiltrates predominating. Other findings may include peripheral blood eosinophilia and eosinophilia on bronchoalveolar lavage.

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21
Q

Man with 39 years old comes with chest ct shows CRAZY PAVING pattern, what is the diagnosis?

A

Pulmonary alveolar proteinosis: Median age of 39 years, and males
predominate among smokers but not in nonsmokers.

Diagnosed using bronchoalveolar lavage, which shows proteinaceous material in and
around alveolar macrophages. Chest CT shows “crazy paving” pattern.

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22
Q

How to treat Chronic eosinophilic pneumonia?

A

Supportive treatment like oxygen, Diuretics, exercise digoxin and anyicouglation.

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23
Q

How to treat Pulmonary alveolar proteinosis?

A

Whole lung lavage( wash out the lungs using saline).

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24
Q

Patients with ILD commonly come to clinical attention in one of the
following ways?

A

1-Symptoms of progressive chronic SOB with exertion or a persistent nonproductive
cough.

2-Pulmonary symptoms associated with another disease, such as a connective
tissue disease.

3-History of occupational exposure (eg, asbestosis, silicosis).

4-An abnormal chest imaging study.

5-Lung function abnormalities on simple office spirometry, particularly a
restrictive pattern (ie, reduced total lung capacity and forced vital capacity).

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25
Q

What are the most common symptoms in ILD and what is important in history?

A

1- Age and Gender.

2-Nonproductive cough and dyspnea with (subacute to chronic course) are
the most common presenting symptoms of a DPLD.

3-When DPLD is suspected, questions should focus on determining the onset
of symptoms, system review (CTD related symptoms), past medical
history, medications, exposures ( occupations, home environment, hobbies, and other activities) and smoking history.

26
Q

What to find in physical examination in patents with ILD?

A

The physical examination of patients with ILD is usually nonspecific.

1-In patients with connective tissue disorders, findings may include Raynaud
phenomenon, skin thickening, sclerodactyly, inflammatory arthritis, or
tenosynovitis.

This is very important **
2- Resting and exertional pulse oximetry. It is common for patients with DPLD to
have normal resting pulse oximetry while > 4% drop in O2 saturation suggestive
of ILD.

3- Lung examination: is frequently abnormal in ILD, but the findings are generally
nonspecific. Crackles or “velcro rales” are present on chest examination in most
forms of ILD.

4-Signs of right sided heart failure suggestive of long standing ILD.

27
Q

What is coarse crackles?

A

Air within fluid ( the fluid is thick like sputum)

28
Q

How to differentiate early and late fine crackles?

A

Make him cough by using auscultation.

29
Q

What is the investigation needed in DPLD patients?

A

1-The first and PFT.

2- HIGH RESOLUTION CT( HRCT) is the best: scan
of the chest (slice thickness 1-2
mm) is the best imaging study to
identify abnormalities that can
help diagnose the underlying
disease.

30
Q

The most common form in chest x-ray in ILD?

A

Reticulondular

31
Q

When to screen for serologic testing?

A

The American Thoracic Society guidelines recommend screening all
patients with DPLD with an antinuclear antibody (ANA), rheumatoid
factor, and anti-cyclic citrullinated peptide antibody appropriate in the
following:

1-Younger patients, in particular those younger than 40 years of age.
2-Patients with symptoms of an underlying rheumatologic disorder.
3-Patients with a family history of autoimmune or rheumatologic
disease.

32
Q

What to do if pulmonary function tests and HRCT are insufficient for making the diagnosis?

A

the physician must consider the risks and benefits of eithe:
1-bronchoscopic or
2- surgical lung biopsy,
including the patient’s general health and risk of intervention.

33
Q

What is it meant by granuloma?

A

a small area of chronic inflammation.

Granulomas form when immune cells clump together and create tiny nodules at the site of the infection or inflammation. A granuloma is the body’s way: to contain an area of bacterial, viral or fungal infection so it can try to keep it from spreading; or. to isolate irritants or foreign objects.

34
Q

What is Sarcoidosis?

A

multisystem granulomatous disorder.

1- It commonly affects young adults.
2-It is a common disease of unknown etiology that is often detected
on routine chest X-ray.

3-Typically presents with bilateral hilar lymphadenopathy, pulmonary infiltration and skin or eye lesions.
4- Typical sarcoid granulomas consist of focal accumulations of
epithelioid cells, macrophages and lymphocytes, mainly T cells.

35
Q

******There is t a picture for clinical features of Sarcoidosis.

A
36
Q

Why a patient with sarcoidosis comes with hypercalcaemia?

A

due to increased production of 1,25-dihydroxy vitamin D by granuloma that increase the activation of inactive form of vitamin D 25-hydroxlase

37
Q

What are the symptoms of sarcoidosis in pulmonary?

A

Pulmonary involvement may be an i
ncidental finding,
cough,
exertional SOB and
vague chest discomfort are common presentations.

38
Q

What are the stages of Sarcoidosis?

A

1-Stage I: BHL (usually symmetrical); paratracheal nodes often enlarged:
Often asymptomatic but may be associated with erythema nodosum
and arthralgia.
The majority of cases resolve spontaneously within
1 year

2-Stage II: BHL and parenchymal infiltrates :
Patients may present with breathlessness or cough.
The majority of
cases resolve spontaneously.

3- Stage III: parenchymal infiltrates without BHL:
Disease less likely to resolve spontaneously ( require treatment).

4- Stage IV: pulmonary fibrosis:
Can cause progression to ventilatory failure, pulmonary hypertension
and cor pulmonale.( end stage)

(BHL = bilateral hilar lymphadenopathy)

39
Q

What is L̈fgren’s Syndrome?

A

It is a triad and a typical combination of:
1-bilateral hilar lymphadenopathy,
2-erythema nodosum,
3-arthralgia( ankle joint)
R- and fever.
 Has excellent prognosis as
usually resolves spontaneously
without the need for treatment.

40
Q

What is The treatment of L̈fgren’s Syndrome?

A

Reassurance

41
Q

What are the investigations for Sarcoidosis?

A

 Imaging. Chest X-ray is the initial modality for staging, followed by HRCT
for assessment of parenchymal involvement.

 CBC. There may be cytopenia , mild normochromic, normocytic anemia
with raised ESR.

 Biochemistry. Calcium Level as activated macrophages in lung and lymph
nodes are able to hydroxylate vitamin D leading to increased intestinal
absorption of dietary calcium.

 Serum ACE level. Less specific, so used for disease monitoring.

Lung function tests. Showed restrictive pattern as disease progress.

 Biopsy. Non-caseating granulomas.

42
Q

What is the treatment of Sarcoidosis?

A

Pulmonary Sarcoidosis has good prognosis, spontaneous remission within 6 months.

 Systemic treatment is indicated for hypercalcemia and extrathoracic major organ
involvement, particularly neurological, cardiac, progressive pulmonary or ocular
disease resistant to topical therapy. 

1-First-line treatment is with Prednisone 0.5 mg/ kg for 4–6 weeks, gradually tapering to
a maintenance dose for at least 12 months. 

2-Alternative immunosuppressants, including methotrexate.

3-  Lung transplantation should be considered for suitable patients with stage IV disease
and respiratory failure.

43
Q

What is Hypersensitivity Pneumonitis (HP)?

A

Hypersensitivity pneumonitis (HP) is caused by an allergic reaction
affecting the small airways and alveoli in response to an inhaled
antigen.

***Cigarette smokers have a lower risk of developing HP due to
decreased antibody reaction to the antigen, but once established,
smoking may lead to a more chronic or severe disease course.

44
Q

What is inspiratory squeaks?

A

End-inspiratory wheezing

45
Q

What are the clinical features of Hypersensitivity Pneumonitis (HP)?

A

HP can be categorized according to the time course of symptoms, as determined by
duration and intensity of exposure.

1- Symptoms include weight loss, malaise, dyspnea and cough.

2- Auscultation reveals inspiratory squeaks due to bronchiolitis, and bilateral fine
crackles.

Levels of symptoms:

1-Acute: symptom onset 4–6h following exposure. Fever is common and patients may be mistakenly diagnosed with a chest infection. Resolution occurs 24–48h following
removal from the inciting antigen.

2-Subacute: usually occurs with intermittent or lower-level exposure. Improvement is
seen in weeks to months following removal from exposure.

3-Chronic: usually no history of preceding acute symptoms. Insidious onset of
respiratory and constitutional symptoms is typical. Finger clubbing may be present.
Progression to irreversible fibrosis is associated with increased mortality.

46
Q

The most important in HP in a history, we need to know about offending exposure or the specific antigen)

A
47
Q

What to find in HRCT in HR patients?

A

Mosaic pattern

48
Q

Patient with Pigeon Fancier, what is he going to develop?

A

HP

49
Q

What is the treatment of HR.

A

The key to successful treatment is avoidance of exposure to the
inciting antigen (if known) and this may be achieved by changes in
work practice.

 Pigeon fancier’s lung is more difficult to control, as affected
individuals remain strongly attached to their hobby.

 Prednisone should be initiated in patients whose symptoms persist
despite withdrawal from the causative antigen, and in severe disease.

 Established fibrosis will not resolve and, in some patients, the
disease may progress inexorably to respiratory failure.

50
Q

When can we do lung transplant in HR patients?

A

Only If the exposure known cause known or the antigen known 

51
Q

What is Idiopathic Pulmonary Fibrosis (IPF)?

A

IPF is the most common of the idiopathic interstitial pneumonias.

It is a progressive and ultimately fatal disease of unknown cause.

Affecting old ages >50 years.

It is thought that repetitive injury to the alveolar epithelium, caused by currently unidentified environmental stimuli, leads to the
activation of several pathways responsible for repair of the damaged
tissue.

52
Q

the diagnostic confirm for HR patients?

A

Biopsy

53
Q

What are the presenting symptoms IPF?

A

insidious onset of progressive
dyspnea that may be accompanied by cough, with or without sputum
production.

54
Q

What are the examination of IPF?

A

1- chest shows bi-basal end inspiratory crackles
(velcro rales) .
2- finger clubbing.

  1. Acute form (fulminant) called Hamman-Rich Syndrome.
55
Q

What the investigation of IPF?

A

1-PFT usually show a restrictive pattern (FEV1/FVC ratio >70%) with
reduced total lung volumes and capacity. However, spirometry may
be normal in early disease.

2- Serological tests, Bronchoalveolar lavage and possible lung biopsy
»> To Rule out alternative diagnosis (as it is disease of exclusion).

3-Chest X-ray shows small-volume lungs with increased reticular
shadowing at the bases but may be normal in early disease.

56
Q

What is the imaging of choice in IPF? and what are going to find?

A

HRCT is the imaging modality of choice.
A confident diagnosis of IPF may be made in
patients with:

1-Basal distribution.

2-Subpleural reticulation: reticulation is
most evident in the lung peripheries.

3-Traction bronchiectasis: the fibrotic
process distorts the normal lung
architecture, pulling the airways open and
causing bronchiectasis.

4-Honeycombing: there are basal layers of
small, cystic air-spaces with irregularly
thickened walls composed of fibrous
tissue.

57
Q

How much time will IPF patients will survive?

A

2-5 years

And Mortality is increased following acute exacerbations.

58
Q

What are the contraindication dugs in IPF?

A

1-Immunosuppression is generally avoided in IPF and

2-steroids are no longer recommended in confirmed disease.

59
Q

What is the treatment of IPF?

A

1- Pirfenidone, an antifibrotic agent, has been shown to slow the rate of
FVC decline, with the most common side-effects being a reversible
photosensitive rash and gastrointestinal disturbance.

2- Other treatments include Nintedanib, an intracellular inhibitor of tyrosine
kinases.

60
Q

The only hope for IPF patients is Lung Transplant.

A

Medicine (13 decks)

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