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(OMS2) CPR II Exam 2 > (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 so that there is easy exchange

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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 pluripotent)

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10
Q

What is the function of alveolar pores (of Kohn)?

A

“holes” that 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 taking up the space by the lungs)

Impaired ability to inhale (eg. oligohydraminos from renal agenesis, 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 asymptomatic and 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)?

What are the complications?

A

“Arrested development” (stuck at a stage) of pulmonary tissue branching from the tracheobronchial tree with formation of intrapulmonary cystic masses that repeats itself; can be detected via US

can lead to hydrops fetalis, pulmonary hypoplasia (since the CPAM is taking up the space for the lung to grow) or get infected later in life

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16
Q

What are pulmonary sequestrations?

A

Nonfunctioning lung tissue that forms as an aberrant accessory“lung bud”, not connected to the tracheobronchial tree unlike CPAM

*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, but they are non functional so they do not tend to get blood flow

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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, appears as a mass in the chest or abdomen

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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 - parenchyma does not get air = 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 and prevents it from expanding

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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” –> as in left sided heart failure (backing to pulm circ. = too much blood in pulm .circuit = leak out = pulm edema)

“Leaking out” –> pulmonary vessels cannot keep blood in and it leaks out in the lungs (e.g. low albumin/oncotic pressure)

Injury to alveolar wall

Unsure mechanisms (neurologic, high altitude pulmonary edema)

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32
Q

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

A

Acute onset

Hypoxemia (PaO2/FiO2 <300)

Bilateral infiltrates

No evidence of cardiac failure

33
Q

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

A

Abrupt onset of symptoms

Hypoxemia (PaO2/FiO2 <200)

Bilateral infiltration

Non cardiac in nature

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 is the pathophysiology of ARDS?

A

Fluid leaks into the endothelium from the capillary into the alveoli > damage to the Type 1 and 2 pneumocytes > debris forms hyaline deposits on the alveoli

37
Q

What is the pathology?

A

Diffuse alveolar damage (DAD)

Edema + Fibrin + Cell debris = HYALINE MEMBRANES

38
Q

What are the three stages of ARDS?

A
  1. Exudate
  2. Proliferative
  3. Fibrotic
39
Q

What occurs during the exudative stage of ARDS?

A

Edema

Hyaline membranes

Neutrophils

40
Q

What occurs during the proliferative stage of ARDS?

A

Fibroblast proliferation

Organizing pneumonia

Can lead to resolution or Early fibrosis

41
Q

What occurs during the fibrotic stage of ARDS?

A

Extensive fibrosis

Loss of normal alveolar architecture

42
Q

ARDS : resolution

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

A

Resolution OR Fibrosis (irreversible)

43
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

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 restrictive lung disease?

A

aka interstitial lung dz, characterized by volume restriction (stiff lungs) = cannot fill the lung

FEV1/FVC ratio is normal or increased (both are reduced BUT the ratio is not necessarily 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

Smoke chemicals cause inflammation and mucus production

  • Mucus hypersecretion (mucinous layer with goblet cell hyperplasia/hypertrophy) > cillia is “drowning” and cannot get rid of the debris/chemicals
  • predisposes to more inflammation and infection
50
Q

What is the criteria for diagnosing 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 are the complications of chronic bronchitis?

A

Squamous cell metaplasia of the bronchi > dysplasia > carcinoma

Bronchiectasis

Death for respiratory infection

53
Q

What is the pathology?

A

Emphysema

*Notice the extremly dilated spaces within the lung parynchema

54
Q

Why is emphysema considered an obstructive process?

A

There is a compressed duct proximal to the alveolar sac > causes the destruction of the alveolar sacs that define emphysema

Smoking induced emphysema: centriacinar emphysema (upper lobes)

55
Q

What is the clinical presentation of emphysema?

A

Clear but enlarged lungs on CXR

“Barrel chest”

FEV1/FVC ratio is reduced

56
Q

What does “blue bloaters” refer to?

A

Chronic bronchitis (actually the initial stage of emphysema)

cyanotic and edematous (rhonchi - mucus)

compensation still going on so Hgb is elevated

57
Q

What does “pink puffers” refer to?

A

Emphysema

Older and thin, severe dyspnea, pursed lips trying to prolong expiratory wheezing

58
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

59
Q

What is an alpha1-antitrypsin deficiency?

A

Lungs LACK alpha1-antitrypsin coating coded by Pi gene on Cr.14 (Homozygous mutatnt is PIZZ)

This leaves lungs vulnerable to damage by neutrophil elastase > panacinar emphysema (lower lobes since it contacts more elastase from the capillaries in the setting of decreased a1-antitrypsin)

presents as dyspnea + cirrhosis in genetically susceptible individuals

60
Q

Describe the type of emphysema associated with each image

A
61
Q

Alpha1 antitrypsin deficiency demonstrates a ___________ emphysema pattern

A

BASILAR panacinar

62
Q

What are the complications of emphysema?

A

Respiratory failure

Pneumothorax with lung collapse

CAD

Right heart failure (cor pulmonale)

63
Q

What are the basic mechanisms of asthma?

A

Inflammation > airway hyperresponsiveness + airway obstruction (reversible)

64
Q

What are the classifications of asthma?

A

Atopic (extrinsic)

Non-atopic (intrinsic)

65
Q

Describe atopic asthma

A

2/3 of all patients

May be any age, usually children

FH of asthma

triggered by allergies, Elevated IgE levels (type I hypersensitivity)

Triggers may include a variety of allergens

66
Q

Describe the pathogenesis of atopic asthma

A

TH2 > interleukins > recruit inflammatory cells

TH2 > leukotrienes C4, D4, E4 > bronchoconstriction, increased vascular perm, mucus secretion

Mast cell cross linked to IgE > histamine

67
Q

Describe non-atopic asthma

A

1/3 of all patients

Often older pts

NORMAL IgE levels

Triggers include cold, exercise, infection

68
Q

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

A

High potential for irreversible airway remodeling with each subsequent asthma attack

69
Q

What are some of the results of airway remodeling?

A

Fibrosis

Smooth muscle hyperplasia

Increased goblet cells and submucosal glands

*now irreversible

70
Q

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

A

DECREASED response to therapeutic agents:

Bronchodilators

Corticosteroids

71
Q

What is status asthmaticus?

A

Unremitting, potentially fatal asthma attack

Characterized by bronchial occlusion by thick mucus

*Hallmark = curschmann spirals (coiled mucus plugs) and Charcot Leyden crystals (eosinophlic crystals) found in mucus

72
Q

What is aspirin-sensitive asthma?

A

Unique sensitivity to aspirin that induces asthma

Highly associated with: nasal polyps and recurring rhinitis (Samter’s triad)

73
Q

What is the pathogenesis of aspirin sensitive asthma?

A

Aspirin inhibits COX-1 > AA accumulates > becomes Leukotriene C4, D4, E4

74
Q

What is bronchiectasis?

What conditions predispose to bronchiectasis?

A

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

ABPA, Cystic Fibrosis, Chronic Infection (TB), Primary ciliary dyskinesia

75
Q

Describe the path of cystic fibrosis

A

CFTR gene is affected

Chloride transport is impaired > cells absorb extra Na+,Cl and H20 instead of lubricating the mucus –> Leads to dehydrated mucus that forms plugs > predispose to infection > bronchiectasis

76
Q

What is kartagener’s syndrome?

A

Aka Primary ciliary dyskinesia –> Dysfunction of dynein arm of microtubules –> impaired ciliary function

Triad of : Sinusitis, bronchiectasis, situs inversus

dextrocardia (cillia helps rotate the organs in utero)

***Often male infertility (sperm cannot swim)

77
Q

What is this pathology?

A

Allergic Bronchopulmonary Aspergillosis (ABPA)

78
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

(OMS2) CPR II Exam 2 (19 decks)

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