COPD and Restrictive Lung Disease Flashcards

0
Q

What can cause both inspiratory and expiratory obstructive lung disease?

A

Fixed intra or extra thoracic obstruction

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1
Q

What can cause inspiratory obstructive lung disease?

A

Snoring

Foreign body

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2
Q

What can cause an expiratory obstructive lung disease?

A
Asthma
COPD 
Bronchiectasis
Bronchiolitis
Broncheomalacia
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3
Q

What is the mechanism of obstruction in asthma?

A

Bronchospasm
Inflammation
Mucus

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4
Q

What is the mechanism of obstruction in chronic bronchitis?

A

Bronchospasm
Inflammation
Mucus

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5
Q

What is the mechanism of obstruction in emphysema?

A

Loss of lung elastic recoil

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6
Q

What are the main symptoms of obstructive lung disease?

A

Dyspnea
Cough - in asthma and chronic bronchitis, not emphysema
Wheezing

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7
Q

What are some important questions to ask a patient with suspected obstructive lung disease?

A

Dyspnea - when did it start and get worse
Cough - productive?
Smoking history
History of allergy
History of wheezing - not in pure emphysema

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8
Q

What are physical findings to focus on when evaluating patients with obstructive lung disease?

A

RR
Cyanosis - 5 grams unsaturated hemoglobin/100 cc of blood, more hemoglobin shows this more readily, rarely in asthma or emphysema
Decreased breath sounds (asthma indicate attack, common in emphysema), wheezing or rhonchi (rare inspiratory in stable asthma or COPD, expiratory more common, no rhonchi in emphysema)
Rales should not be heard - dry suggest restriction like fibrosis

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9
Q

What is the alveolar air equation?

A

PAO2 = 150 - (PaCO2/.8)

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10
Q

What is the hallmark of obstructive lung disease?

A

FEV1/FVC less than 70% AND FEV1 less than 80%

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11
Q

What is the Ddx of a fixed obstruction?

A

Laryngeal carcinoma
Thyromegaly
Vocal cord asthma

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12
Q

What is the Ddx of a variable extra thoracic obstruction?

A

Obstructive sleep Alena
Tracheomalacia
Inhibits inspiratory limb of flow volume loop

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13
Q

What is the Ddx of a variable intrathoracic obstruction?

A

Asthma
COPD
Bronchiectasis
Affects expiratory limb on flow volume loop

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14
Q

What DLCO means patient will develop arterial hypoxemia with exercise?

A

<45%

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15
Q

When is an ABG ordered?

A

When FEV1 less than or equal to 30-40% predicted

Normal pCO2 of 41 is bad sign in someone with asthma - developing respiratory acidosis (should be lower)

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16
Q

What ABGs are present in COPD?

A

Emphysema usually has pCO2 < 45 and moderate hypoxemia (60-70) on room air at rest
Chronic bronchitis have pCO2 > 45 and pH only marginally low due to compensatory metabolic alkalosis, pO2 often <7.31) indicates acute worsening of COPD with worsening CO2 retention

17
Q

What are interstitial lung diseases?

A

Affect both alveolar and interstitial compartments

Lead to restriction

18
Q

What are the five categories of ILDs?

A
Idiopathic interstitial pneumonias
Connective tissue diseases
Drug induced diseases
Other systemic disorders
Occupational and environmental exposures
Last two are granulomatous
19
Q

What are signs and symptoms of ILDs?

A

Dyspnea
Tachypnea more prominent with exercise
Normal PaCO2, decreased PaO2, increased A-a gradient
Exercise induced hypoxemia sensitive for early disease

20
Q

Crackles, clubbing, cyanosis

A

Interstitial lung disease

21
Q

Wheezes, prolonged expiratory phase, distant breath sounds

A

Obstructive lung disease, including asthma

22
Q

Tachycardia, chest pain, leg swelling, syncope

A

Pulmonary emboli

23
Q

S3 gallop, bibasilar inspiratory crackles, PND, orthopnea

A

Cardiac disease

24
Q

Pale conjunctiva, tachycardia

A

Anemia

25
Q

What are HRCT findings and what do they indicate?

A

Ground glass appearance - alveolitis which can be reversible

Dense lines and honey combing - fibrosis, irreversible

26
Q

What are common causes of drug induced ILD?

A

Chemo - bleomycin, busulfan, cyclophosphamide, methotrexate, nitrosoureas
Cardiac - procainemide, amiodarone
, hydralazine
Antibiotics - isoniazid, nitrofurantoin*
Illicit drugs - heroine, cocaine

27
Q

Where are crackles less common?

A

Sarcoidosis

28
Q

Where is clubbing especially predominant?

A

IPF

Asbestosis

29
Q

What is loffgren’s syndrome?

A
Erythema nodosum (painful nodular panniculitis and vasculitis), bilateral hilar adenopathy and arthralgias
Associated with sarcoidosis
30
Q

What is Heerfordts syndrome?

A

Facial nerve palsy, parotidis, uveitis

Associated with sarcoidosis

31
Q

What is the natural history of sarcoidosis?

A

Therapy withheld until evidence of vital organ dysfunction - then corticosteroids, with or without immunosuppressants
1/3 spontaneously remit in 3 yrs, 1/3 progress over 5-10 yrs, 1/3 remain stable

32
Q

What mimics sarcoidosis?

A

Berylliosis - a pneumoconiosis

33
Q

How is hypersensitivity pneumonitis a mimic?

A

Acute resemble pneumonia
Subacute resemble tb
Chronic resemble IPF

34
Q

What are the shared clinical features of pneumoconioses?

A

Inhalation of inorganic material
Linear dose response
Long latency
Symptoms and disease limited to respiratory system
No known treatment except removal from exposure
Very slow progression

35
Q

What are connective tissue diseases associated with ILD?

A
SLE
RA
Systemic sclerosis / CREST syndrome
Sjogrens
Dermatomyositis / poly myosotis
36
Q

What are hallmarks of connective tissue diseases and ILD?

A

Underlying disease usually present before lung involvement
Multisystem involvement
Younger age of onset

37
Q

What is idiopathic pulmonary fibrosis?

A

Chronic progressive dyspnea and cough, restrictive lung physiology, and UIP histologic pattern
Characterized not by inflammation, but by chronic fibroproliferation due to abnormal lung tissue wound healing
Rare in children, typically over 50, common in men and smokers
Exclude other ILD causes
Peripheral distribution
Reticulations in lower lobes, honeycombing and traction bronchiectasis

38
Q

Why is it important to distinguish IPF from other ILDs?

A

IPF is the most lethal and doesn’t respond to corticosteroids and immunosuppressants
Only possible treatment is transplant but this is rare

39
Q

What is the molecular basis for the familial form of IPF?

A

AS pattern with incomplete penetrate
Same presentation as clinical IPF but earlier age of onset
Heterozygous mutations in genes encoding telomerase
Mutations in gene encoding surfactant proteins A2 and C