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Respiratory > EXAM #1: OBSTRUCTIVE DISEASE > Flashcards

EXAM #1: OBSTRUCTIVE DISEASE Flashcards

1
Q

What is atelectasis?

A

Incomplete expansion of the lung

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2
Q

What are the four types of atelectasis?

A

1) Resorption= airway obstruction leading to incomplete expansion
2) Compression= excess matter in lung space preventing expansion
3) Patchy=microatelectasis/ loss of surfactant (post-op)
4) Contraction= fibrosis around the lung preventing full expansion

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3
Q

What is the difference between the direction of medisatinum shift in resorption and compression atelectasis?

A

Resorption= mediastinal shift TOWARD affected lung

Compression= mediastinal shift AWAY from affected lung

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4
Q

What are the two major types of pulmonary edema?

A

1) Hemodynamic distrubance

2) Microvascular injury

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5
Q

What is the most common cause of hemodyamic pulmonary edema?

A

Increased hydrostatic pressure e.g. left-sided CHF

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6
Q

What are heart failure cells?

A

Hemosiderin-laden macrophages

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7
Q

What is the mechanism of edema caused by microvascular injury?

A

1) Injury to capillaries in alveolar septa

2) Leakage of fluid and proteins

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8
Q

What is the major difference between restrictive and obstructive lung disease?

A

Obstructive= can’t get air OUT

Restrictive= can’t get air IN

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9
Q

What are the major obstructive lung diseases?

A

1) COPD
2) Asthma
3) Bronchiectasis

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10
Q

What happens to FEV1 and FVC in obstructive disease?

A
  • FEV1= decreased b/c difficulty getting air OUT
  • FVC= normal or slightly decreased

FEV1/FVC is LOW

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11
Q

What happens to FEV1 and FVC in restrictive disease?

A

Can’t get air IN, but what you do get in can go OUT

Thus, FVC is low and TLC are low–BUT, FEV1/FVC is normal

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12
Q

When does one see the sx. of emphysema i.e. how bad does the disease have to be for there to be clinical significance?

A

1/3 of pulmonary capacity impaired

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13
Q

What airways are affected in emphysema?

A

Airways DISTAL to the terminal bronchiole

Destruction of the airway WITHOUT obvious fibrosis

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14
Q

Describe the pathogenesis of emphysema.

A

1) Smoking is proinflammatory increase neutrophil recruitment and alveolar macrophage activity
2) Neutrophils/ alveolar macrophages increase elastase/protease secretion that induces tissue damage
3) Furthermore, smoking inhibits antielastase

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15
Q

What cytokines are induced by smoking to attract neutrophils to the lungs?

A

1) IL-8
2) LTB4
3) TNF

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16
Q

What is the normal alpha-1 antitrypsin phenotype?

A

PiMM

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17
Q

What is the phenotype associated with severe alpha-1 antitrypsin disease?

A

PiZZ

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18
Q

What are the different types of emphysema?

A

1) Centriacinar= center of the acinus
2) Panacinar= entire acinus
3) Paraseptal
4) Irregular

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19
Q

What type of emphysema is most associated with smoking?

A

Centriacinar

*Inhalation of smoke affects the center of the acinus the most

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20
Q

Where is centriacinar emphysema most severe in the lung?

A

Apex

*Remember that smoke rises–mnemonic to remember the apex is most affected

21
Q

What type of emphysema is most assocaited with alpha-1 antitrypsin deficiency?

A

Panacinar

*Lack of anti-protease causes damage to the entire acinus vs. just the central portion that is most exposed to smoke

22
Q

What part of the lung is most affected by panacinar emphysema?

A

Base

23
Q

What kind of emphysema is associated with bullae and pneumothorax?

A

Paraseptal/ distal acinar emphysema

24
Q

What is the surgical procedure that can aid patients with very severe emphysema?

A

Volume reduction surgery

25
Q

Anatomically, where is the inflammation of chronic bronchitis seen?

A

Larger airways

26
Q

What are the morphologic changes that are seen in chronic bronchitis?

A

1) Goblet cell metaplasia

2) Mucus hypersecretion with plugging

27
Q

What is the Reid index?

A

Gland/airway wall ratio

*Greater than 0.4= bronchitis, there has been hyperplasia of the mucous glands that cause the ratio to increase

28
Q

What are the most common pathogens to cause acute exacerbations of chronic bronchitis?

A

Bacterial= H. influenza and S. pneummoniae

Viral= Adenovirus and RSV

29
Q

What is cor pulmonale?

A

Lung disease leading to right-heart failure

*Increased PVR from lung disease causes RVH. When the right heart FAILS, this is cor pulmonale

30
Q

Outline the pathogenesis of allergic asthma.

A

1) Sensitization to inhaled allergen causes induction of TH2 CD4+ cells
2) TH2 releases cytokines i.e. IL-4, IL-5, and IL-10

31
Q

What is the role of IL-4 in allergic asthma?

A

Class switching to IgE

32
Q

What is the role of IL-5 in allergic asthma?

A

Attraction of eosinophils

33
Q

What is the role of IL-10 in allergic asthma?

A

1) Inhibition of TH1

2) Stimulation of TH2 (perpetuates TH2 response)

34
Q

When is a patient is re-exposed to their allergen/trigger, what happens?

A

1) IgE cross-links mast cells

2) Mast cell degranulation

35
Q

Outline the sequence of events that occurs following mast cell degranulation in the pathogenesis of allergic asthma.

A

1) Preformed histamine granules are released
2) Leukotrienes C4, D4, and E4 are generated
3) Major basic protein is released from eosinophils

36
Q

What is the “early phase reaction” in asthma? Late-phase?

A

Early=

  • Histamine
  • Leukotrienes C4, D4, and E4

Late=
- MBP

37
Q

Classically, what can be seen on histology of the sputum from an asthmatic patient?

A

1) Curshmann spirals

2) Charcot-Leyden crystals

38
Q

What are Cruschmann spirals?

A

Spiral-shaped mucus plugs

39
Q

What are Charcot-Leyden crystals?

A

Eosinophil derived crystals

40
Q

What is classically associated with aspirin-intolerant asthma in adults?

A

Nasal polyps

41
Q

What condition should a child with nasal polyps be worked up for?

A

Cystic Fibrosis

42
Q

How does one develop bronchiectasis?

A

1) Obstruction

2) Persistent infection–gets fibrosed OPEN

43
Q

What can cause obstructive bronchiectasis?

A

1) Tumor
2) FB
3) Secretions

44
Q

What are the genetic diseases that can cause bronchiectasis?

A

1) CF

2) Kartanganer Syndrome

45
Q

What infectious diseases cause bronchiectasis?

A

Necrotizing pneumonia

  • S. aureus
  • Klebsiella
46
Q

What is Kartagener Syndrome?

A

AR defect in dynein in cilia

47
Q

What are the classic features of Kartagener Syndrome?

A

1) Sinusitis
2) Bronchiectasis
3) Situs inversus
4) Infertility

48
Q

What are the symptoms of bronchiectasis?

A
  • Chronic productive cough
  • Dyspnea
  • Foul-smelling sputum
49
Q

What is one of the major complications of bronchiectasis?

A

Amyloidosis (AA) from chronic inflammation

Respiratory (35 decks)

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