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CPR II > (14.1) Pulmonary Pathology (Singh) > Flashcards

(14.1) Pulmonary Pathology (Singh) Flashcards

1
Q

Describe the progression of normal fetal lung development

A

Embryonic (lung bud) –> Pseudoglandular –> Canalicular –> Saccular –> Alveolar

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2
Q

What are the clinical uses for knowing the stage of fetal lung development?

A

Knowing the stage can help the clinician determine the age of the fetus

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3
Q

What are the requirements for normal fetal lung development?

A
  • Space in the thoracic cavity
  • Ability to inhale (chest call must be able to move, and there must be enough material (amniotic fluid) present to inhale
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4
Q

What are the main structures you will see histologically of the trachea and main bronchi?

A

Cartilage

Glandular tissue

Respiratory epithelium

Smooth muscle layer

Lamina propria

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5
Q

Describe what you would encounter with a low-power image of lung parenchyma

A

Alveoli

Blood vessels

Bronchioles

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6
Q

Describe what you would encounter with a high-power image of lung parenchyma

A

Erythrocytes

Macrophages

Type 1/2 pneumocytes

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7
Q

What is CRUCIAL to the sucessful oxygen exchange occuring in the lungs?

A

A very THIN layer between the circulating erythrocytes and alveolar lumen

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8
Q

Describe the function of Type I pneumocytes

A

Facilitate gas exchange

*Support and line the alveoli

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9
Q

Describe the function of Type II pneumocytes

A

Product surfactant

Replace type 1 pneumocytes

***THEY ARE MODIFIED STEM CELLS HOW COOL IS THAT WOWOWOW

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10
Q

What is the function of alveolar pores?

A

Allow aeration but also bacteria/cells/exudate to travel between alveoli

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11
Q

What is this pathology?

A

Pulmonary hypoplasia

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12
Q

What causes pulmonary hypoplasia?

A

Reduced space in the thoracic cavity (eg. diaphragmatic hernia)

Impaired ability to inhale (eg. oligohydraminos, airway malformation, chest wall motion disorders)

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13
Q

What is the mortality rate of pulmonary hypoplasia?

A

HIGH! (up to 95%)

If lung weight is <40%, immediate death occurs in neonatal period

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14
Q

What are foregut cysts?

A

Detached outpouchings of foregut

Seen along hilum and mediastinum

Can be respiratory, esophageal or gastroenteric

Often seen incidentally; complications include rupture, infection, or airway compression

Tx: Excision is curative

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15
Q

What is congenital pulmonary adenomatoid malformation (CPAM)?

A

“Arrested development” of pulmonary tissue with formation of intrapulmonary cystic masses

aka, a specific type of pulmonary tissue decides to only make a certain type of tissue for the rest of it’s life

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16
Q

What are pulmonary sequestrations?

A

Nonfunctioning lung tissue that forms as an aberrant accessory“lung bud”

*Typically found in the region of the left lower lobe

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17
Q

How are pulmonary sequestrations characterized?

A

Lack of connection to the tracheobronchial tree

Independent (systemic) arterial supply

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18
Q

What is this image an example of?

A

Intralobar pulmonary sequestration (ILS)

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19
Q

What are intralobar pulmonary sequestration (ILS)s susceptible to?

A

Lack of airway perfusion makes ILS’s susceptible to infection and absess formation

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20
Q

What is this an example of?

A

Extralobar pulmonary sequestrations (ELS)

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21
Q

How are extralobar pulmonary sequestrations (ELS) different from ILS?

A

ELS have their own PLEURA

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22
Q

What comes to attention sooner…

ILS or ELS?

A

ELS

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23
Q

Describe the differences between these congenital anomalies:

CPAM/CCAM

vs

Pulmonary sequestraion

A

CPAM/CCAM = INTRApulmonary cystic malformation w/ CONNECTION to tracheobronchial airways and pulmonary vasculature

Pulmonary sequestration = INTRA or EXTRA pulmonary lung tissue with NO CONNECTION to pulmonary vasculature or tracheobronchial tree

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24
Q

What is atelectasis?

A

Partial or complete collapse of the lung

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25
Q

What are the three major types of atelectasis?

A
  • Resorption
  • Compression
  • Contraction
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26
Q

What causes resorption atelectasis?

A

Airway obstruction with gradual resorption of air reduces lung expansion

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27
Q

What causes compression atelectasis?

A

Accumulated material in pleural cavity compresses the lung parenchyma

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28
Q

What causes contraction atelectasis?

A

Fibrotic or other innate restrictive process in the pleura or peripheral lung restricts lung expansion

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29
Q

What is the LEAST common form of atelectasis?

A

Contraction atelectasis

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30
Q

What pathologic process is occuring here?

A

Pulmonary edema

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31
Q

What are the major causes of pulmonary edema?

A

“Pushing out” –> left sided heart failure

“Leaking out” –> liver disease

Injury to alveolar wall

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32
Q

What are the clinical criteria for acute lung injury (ALI)?

A

Acute onset

Hypoxemia

Bilateral infiltrates

No evidence of cardiac failure

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33
Q

What is the clinical criteria for acute respiratory distress syndrome (ARDS)?

A

Worsening hypoxemia

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34
Q

What is diffuse alveolar damage (DAD)?

A

Histologic manifestation of ARDS

35
Q

What is the pathology?

A

Acute respiratory distress syndrome (ARDS)

36
Q

What are the clinical indications of acute respiratory distress syndrome (ARDS)?

A
  • Abrupt obsent of symptoms
  • Hypoxemia (PaO2/FiO2) <200
  • Bilateral infiltrates
  • Non-cardiac in nature
37
Q

What is the pathology?

A

Diffuse alveolar damage (DAD)

Edema + Fibrin + Cell debris = HYALINE MEMBRANES

38
Q

Describe the histologic differences b/w a normal lung and a lung w/ hyaline membranes

A

Lung w/ hyaline membranes has THICKENED walls that make oxygen exchange nearly impossible

This is what accounts for the decreased PaO2/FiO2 values observed

39
Q

What are the three stages of ARDS?

A
  1. Exudate
  2. Proliferative
  3. Fibrotic
40
Q

What occurs during the exudative stage of ARDS?

A

Edema

Hyaline membranes

Neutrophils

41
Q

What occurs during the proliferative stage of ARDS?

A

Fibroblast proliferation

Organizing pneumonia

Early fibrosis

42
Q

What occurs during the fibrotic stage of ARDS?

A

Extensive fibrosis

Loss of normal alveolar architecture

43
Q

ARDS : resolution

After the fibroproliferative phase, 2 pathways may ensue… what are they?

A

Resolution OR Fibrosis (irreversible)

44
Q

What is acute interstitial pneumonia (AIP)?

A

Same clinical presentation as ARDS

Same histology as ARDS/DAD

***​CANNOT BE ATTRIBUTED TO A SPECIFIC ETIOLOGY

45
Q

What is a restrictive lung disease?

A

Volume restriction

FEV1/FVC is normal

FVC is reduced

(FEV=force expiratory volume, FVC=forced vital capacity)

46
Q

What is obstructive lung disease?

A

Decreased flow

LOW FEV1/FVC ratio

***(FEV=force expiratory volume, FVC=forced vital capacity)

47
Q

What are examples of obstructive pulmonary diseases?

A

Emphysema

Chronic bronchitis

Asthma

48
Q

What is the most common cause of COPD/Chronic bronchitis?

A

Smoking

49
Q

Describe what is occuring during a chronic bronchitis state

A
  • Mucus hypersecretion
  • Inflammation
  • Infection

*Typically is a response to cigarrette smoke

50
Q

Define:

Chronic bronchitis

A

Persistent cough w/ sputum production for 3 months out of 2 consecutive years

51
Q

What is the predominant pathophysiologic mechanism of chronic bronchitis?

A

Mucous gland hyperplasia

52
Q

What is the pathology?

A

Emphysema

*Notice the extremly dilated spaces within the lung parynchema

53
Q

Why is emphysema considered an obstructive process?

A

There is a compressed duct proximal to the alveolar sac

54
Q

What is the clinical presentation of emphysema?

A

Enlarged lungs on CXR

“Barrel chest”

FEV1/FVC ratio is reduced

55
Q

What does “blue bloaters” refer to?

A

Chronic bronchitis

56
Q

What does “pink puffers” refer to?

A

Emphysema

57
Q

What is alpha1-antitrypsin?

A

Alpha1-antitrypsin coats the lungs protecting them from neutrophil elastase

Neutrophil elastase is produced by white blood cells to break down harmful bacteria

58
Q

What is an alpha1-antitrypsin deficiency?

A

Lungs LACK alpha1-antitrypsin coating

This leaves lungs vulnerable to damage by neutrophil elastase

59
Q

Describe the type of emphysema associated with each image

A
60
Q

Alpha1 antitrypsin deficiency demonstrates a ___________ emphysema pattern

A

BASILAR panacinar

61
Q

What are the basic mechanisms of asthma?

A
62
Q

What are the classifications of asthma?

A

Atopic (extrinsic)

Non-atopic (intrinsic)

63
Q

Describe atopic asthma

A

2/3 of all patients

May be any age, usually children

FH of asthma

Elevated IgE levels (type I hypersensitivity)

Triggers may include a variety of allergens

64
Q

Describe non-atopic asthma

A

1/3 of all patients

Often older pts

NORMAL IgE levels

Triggers include cold, exercise, infection

65
Q

Why is it SO important to make sure your asthmatic patients’ have “controlled” asthma?

A

High potential for irreversible airway remodeling

66
Q

What are some of the results of airway remodeling?

A

Fibrosis

Smooth muscle hyperplasia

Increased goblet cells and submucosal glands

67
Q

Pharmacologically, what is a huge problem in patients that have undergone airway remodeling?

A

DECREASED response to therapeutic agents:

Bronchodilators

Corticosteroids

68
Q

What is status asthmaticus?

A

Unremitting, potentially fatal asthma attack

Characterized by bronchial occlusion by thick mucus

*Hallmark = curschmann spirals (coiled mucus plugs)

69
Q

What is aspirin-sensitive asthma?

A

Unique sensitivity to aspirin that induces asthma

Highly associated with: nasal polyps and recurring rhinitis

70
Q

What is bronchiectasis?

A

Necrotizing inflammatory response that is an end stage process of multiple processes that can include infection or obstruction

71
Q

Describe the path of cystic fibrosis

A

CFTR gene is affected

Chloride transport is affected

W/out it, cells absorb extra Na+ and H20 –> Leads to dehydrated mucus

72
Q

What is kartagener’s syndrome?

A

Aka Primary ciliary dyskinesia

–> Dysfunction of dynein arm of microtubules

Triad of : Sinusitis, bronchiectasis, situs inversus

***Often male infertility

73
Q

What is this pathology?

A

Allergic Bronchopulmonary Aspergillosis (ABPA)

74
Q

What is allergic bronchopulmonary aspergillosis (ABPA)?

A

Exaggerated hypersensitivity response to Aspergillus infection overlying chronic lung disease

–> Background of asthma or CF

-Increased IgE on serum testing, positive skin test

***Thick mucus in bronchi

75
Q

What is pneumoconiosis?

A

Reaction by the lungs to inhaled mineral or organic dust

*occupational exposure, air pollution

76
Q

Name the pathology

A

Coal worker’s pneumoconiosis

77
Q

What is silicosis?

A

Disease resulting from inhaled silicon dioxide

*mining/quarry work/concrete repair/demolition

78
Q

Describe the histologic findings for silicosis

A

Dense collagenous nodules

79
Q

Describe the radiographic findings of silicosis

A

Eggshell calcifications

(calcified hilar lymph nodes)

80
Q

What populations are at risk for asbestosis exposure?

A

Insulation workers

Shipyard workers

Paper mill workers

Oil or chemical refinery workers

81
Q

What are histologic hallmarks of asbestos inhalation?

A

Asbestos bodies

82
Q

What is this pathology?

A

“Candlewax drippings” on pleura w/ asbestosis infiltration

83
Q

What cancer is highly associated with asbestos exposure?

A

Mesothelioma

84
Q
A

CPR II (30 decks)

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