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First Aid 2014 > RESPIRATORY: 604 - 605 > Flashcards

RESPIRATORY: 604 - 605 Flashcards

1
Q

What is the main problem in obstructive lung disease?

A

Obstruction of air flow - can’t get air out of the lungs

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2
Q

What happens to the residual volume and forced vital capacity in obstructive lung disease?

A

RV increases and FVC decreases

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3
Q

What is forced vital capacity (FVC)?

A

Maximal expiration

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4
Q

What are the significant PFT’s in obstructive lung disease?

A

Extremely decreased FEV1
Decreased FVC
Decreased FEV1/FVC ratio (hallmark)
V/Q mismatch

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5
Q

Name the major complication in obstructive lung disease.

A

Chronic, hypoxic pulmonary vasoconstriction can lead to cor pulmonale

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6
Q

What is cor pulmonale?

A

Enlargement and failure of the right ventricle of the heart as a response to pulmonary hypertension

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7
Q

What are the 4 types of obstructive lung disease?

A
  1. Chronic bronchitis
  2. Emphysema
  3. Asthma
  4. Bronchiectasis
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8
Q

Describe the pathophysiology of chronic bronchitis.

A

Hyperplasia of mucus-secreting glands in the bronchi leads to mucus plugs obstructing the airway

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9
Q

What is the classic description of a patient with chronic bronchitis?

A

Blue bloater

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10
Q

What clinical findings are associated with chronic bronchitis?

A
  1. Productive cough
  2. Wheezing
  3. Crackles
  4. Cyanosis
  5. Late-onset dyspnea
  6. CO2 retention
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11
Q

What type of cough is diagnostic for chronic bronchitis?

A

Productive cough for > 3 months per year (not necessarily consecutive) for > 2 years

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12
Q

Which airways are primarily affected in chronic bronchitis?

A

Small airways

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13
Q

What is the Reid index?

A

Thickness of gland layer/total thickness of bronchial wall

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14
Q

What complications are patients with chronic bronchitis at risk for?

A

Infection and cor pulmonale

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15
Q

What is the Reid index in patients with chronic bronchitis?

A

> 50%

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16
Q

Describe the pathologic changes in emphysema.

A

Destruction of alveolar walls leads to enlargement of air spaces, decreased recoil, and increased compliance

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17
Q

Why do emphysema patients exhale through pursed lips?

A

To increase airway pressure and prevent airway collapse during respiration

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18
Q

What are the two types of emphysema and what are they associated with?

A
  1. Centriacinar - smoking

2. Panacinar - alpha1-antitrypsin deficiency

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19
Q

What is chronic bronchitis usually linked to?

A

Smoking

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20
Q

What are two mechanisms by which emphysema leads to air trapping?

A
  1. Loss of elastic recoil and subsequent collapse of small airways
  2. Imbalance of proteases and antiproteases
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21
Q

Is emphysema more a physical or physiologic obstruction?

A

Physiologic

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22
Q

What is the most important antiprotease in the lung?

A

Alpha1-antitrypsin

23
Q

Why does the lung need antiproteases?

A

To protect the lung tissue from proteases from inflammation stimulated by alveolar macrophages

24
Q

Why does smoking lead to emphysema?

A

Lots of toxic debris –> increased activity of alveolar macrophages –> increased inflammation –> increased protease activity

25
Q

Is asthma reversible or irreversible?

A

Reversible

26
Q

What is asthma?

A

Bronchial hyperresponsiveness causing reversible bronchoconstriction

27
Q

Describe three histologic findings in asthma.

A
  1. Smooth muscle hypertrophy
  2. Curschmann spirals (shed epithelium forms mucus plugs)
  3. Charcot-Leyden crystals (formed from breakdown of eosinophils in sputum)
28
Q

List 5 causes of asthma.

A
  1. Allergens
  2. Viral URI’s
  3. Stress
  4. Exercise
  5. Aspirin
29
Q

What type of hypersensitivity reaction is asthma?

30
Q

What sort of immune response does asthma induce?

31
Q

Name 3 key interleukins (and what they do) involved in asthma.

A

Th2 induces the release of:

  1. IL-4 - induces class switching from IgG to IgE
  2. IL-5 - recruits eosinophils
  3. IL-10 - promotes the Th2 response and inhibits the Th1 response
32
Q

How do we test for asthma?

A

Methacholine challenge

33
Q

What are the clinical findings in asthma?

A

Cough, wheezing, tachypnea, dyspnea, hypoxemia, pulsus paradoxus, mucus plugging, decreased I/E ratio

34
Q

Describe the pathophysiology in bronchiectasis.

A

Chronic necrotizing infection of bronchi leads to permanently dilated airways which leads to loss of tone allowing for air to be trapped since it has trouble accelerating and be expelled

35
Q

What are 5 things associated with bronchiectasis?

A
  1. Bronchial obstruction
  2. Poor ciliary motility (smoking)
  3. Kartagener syndrome (defect in dynein arm of cilia)
  4. Cystic fibrosis
  5. Allergic bronchopulmonary aspergillosis
36
Q

What are some clinical findings in bronchiectasis?

A

Purulent sputum, recurrent infections, hemoptysis

37
Q

What is the main problem in restrictive lung disease?

A

Problem with filling the lung (restricted expansion)

38
Q

What happens to FVC and TLC in restrictive lung disease?

A

Both decrease

39
Q

What is the signature PFT’s in restrictive lung disease?

A

FEV1/FVC ratio > 80%

40
Q

What are the two types of restrictive lung disease and how do you characterize each?

A
  1. Poor breathing mechanics - extrapulmonary, peripheral hypoventilation, normal A-a gradient
  2. Interstitial lung diseases - decreased pulmonary diffusing capacity, increased A-a gradient
41
Q

In terms of restrictive lung disease caused by poor breathing mechanics, what are two subcategories of deficits?

A
  1. Problem with the muscles - e.g. polio, myasthenia gravis

2. Problem with the physical structure - e.g. scoliosis, morbid obesity

42
Q

What are 10 interstitial lung diseases that can lead to restrictive lung disease?

A

2 respiratory distress syndromes:

  1. Acute respiratory distress syndrome
  2. Neonatal respiratory distress syndrome

2 from outside toxins

  1. Drug toxicity (bleomycin, busulfan, amiodarone, methotrexate)
  2. Pneumoconioses

2 hypersensitivity reactions

  1. Hypersensitivity pneumonitis
  2. Goodpasture syndrome

3 that cause granulomas

  1. Sarcoidosis
  2. Granulomatosis with polyangiitis (Wegener’s)
  3. Langerhans cell histiocytosis

1 ???
1. Idiopathic pulmonary fibrosis

43
Q

What is damaged in neonatal respiratory distress syndrome?

A

Hyaline membrane

44
Q

What is sarcoidosis?

A

Systemic disease involving non-caseating granulomas in multiple organs

45
Q

What are some of the findings in sarcoidosis?

A

Bilateral hilar lymphadenopathy, increased ACE, hypercalcemia, dyspnea or cough

46
Q

Why is there hypercalcemia in sarcoidosis?

A

Granulomas have 1 alpha hydroxylase so they upregulate vitamin D activity leading to increased serum calcium levels

47
Q

Describe what happens in idiopathic pulmonary fibrosis.

A

Repeated cycles of lung injury and wound healing with increased collagen deposition - TGF beta from injured pneumocytes induces fibrosis

48
Q

What are some of the drugs that can cause interstitial lung disease?

A

Bleomycin, busulfan, amiodarone, methotrexate

49
Q

What is hypersensitivity pneumonitis?

A

Mixed type III/IV hypersensitivity reaction to organic environmental antigen

50
Q

What are 5 clinical findings in hypersensitivity pneumonitis?

A
  1. Dyspnea
  2. Cough
  3. Chest tightness
  4. Headache
  5. Fever
51
Q

What two groups of people is hypersensitivity pneumonitis often seen in?

A
  1. Farmers

2. Those exposed to birds

52
Q

How do we treat hypersensitivity pneumonitis?

A

Remove the exposure

53
Q

When does hypersensitivity pneumonitis lead to interstitial lung disease?

A

When it is a chronic exposure (leads to interstitial fibrosis)

First Aid 2014 (24 decks)

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