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CPR II Exam #1 > Pulmonary Pathology I > Flashcards

Pulmonary Pathology I Flashcards

1
Q

In order for normal lung development, the infant must have:

A

Space within the thoracic cavity.

Ability to inhale.

  • chest wall must be able to move.
  • enough amniotic fluid must be around to inhale.
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2
Q

What is the progression of bronchus to alveolus during development? (6 steps)

A 
Bronchus
Terminal bronchiole
Respiratory bronchiole
Alveolar duct
Alveolar sac
Alveolus
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3
Q

Where do larger airways conduct air within the respiratory tree for gas exchange?

A

Terminal acinar units

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4
Q

What cells exist within the alveolar sac and septum?

A

RBCs
Type I and type II alveolar cells
Fibroblasts
Mo

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5
Q

Function of type I vs. type II pneumocytes cells

A

Type I - facilitates gas exchange

Type II - produce surfactant and replace type I pneumocytes

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6
Q

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

A

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

This allows aleoli to “share air” so they aren’t reliant only on their own aeration.

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7
Q

Pulmonary hypoplasia (3)

A

Reduced space within the thoracic cavity.
-diaphragmatic hernia, tumors, GI, etc. Anything that limits thoracic cavity space.

Impairment of ability to inhale.

  • oligohydramnios (renal agenesis).
  • airway malformation (tracheal stenosis).
  • chest wall motion DOs.

High mortality (95%)

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8
Q

How does immediate death in the neonatal period occur in pulmonary hypoplasia?

A

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

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9
Q

Foregut cysts (4)

A

Detached outpounchings of foregut seen along hilum and mediastinum.

Can be respiratory, esophageal, or gastroenteric.

Often incidental, complication include rupture, infection or airway compression. Mucous-filled.

Excision is curable.

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10
Q

Congenital pulmonary adenomatoid malformation (CPAM) occurs how?

Features: (4)

A

“Arrested development” of pulmonary tissue w/ formation of intrapulmonary cystic masses. There are 5 types depending on the stage of lung development.

Communicates w/ tracheobronchial tree.
Can be detected on fatal ultrasound.
Can be deadly due to hydrops or pulmonary hypoplasia.
Can become infected later in life.

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11
Q

Pulmonary sequestrations

A

Non-functioning lung tissue that forms as an aberrant accessory “lung bud”.
-usually in LLL.

Characterized by a lack of connection to the tracheobronchial tree AND an independent (systemic) arterial supply.

May be intralobar or extralobar, based on whether the budding occurs before or after the pleura is established.

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12
Q

Intralobar pulmonary sequestration (ILS) (2)

A

May present in older kids and adults.

Lack of airway perfusion makes these susceptible to infection and abscess formation.

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13
Q

Extralobar pulmonary sequestration (ELS) (3)

A

Usually presents after birth w/ other congenital abnormalities.

Independent vessels, *pleura, and possibly airways.

Become noticable as mass lesions in the chest or abdomen.

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14
Q

Which pulmonary seuestration (ILS/ELS) is associated w/ older kids/adults or at birth?

A

ILS as an older kid/adult, ELS as a newborn.

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15
Q

Which pulmonary seuestration (ILS/ELS) is associated w/ its individual pulmonary vasculature AND pleura?

A

ELS

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16
Q

Which pulmonary seuestration (ILS/ELS) is associated w/ tracheobronchial tree?

A

ELS

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17
Q

Resorption atelectasis

A

Airway obstruction w/ gradual resorption of air reduces lung expansion (apex lowers).

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18
Q

Compression atelectasis

A

Accumulated material in pleural cavity compresses lung parenchyma (base rises).

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19
Q

Contraction atelectasis

A

Fibrotic or other restrictive process in pleura or peripheral lung restricts expansion.

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20
Q

Where does fluid accumulate in pulmonary edema?

A

Interstitial fluid occurs in alveolar spaces.

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21
Q

3 causes of pulmonary edema from “pushing out”

A

LSHF

Volume overload

Pulmonary v. obstruction

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22
Q

3 causes of pulmonary edema from “leaking out”

A

Hypoalbuminemia

Nephrotic syndrome

Liver Dz

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23
Q

4 causes of pulmonary edema from injury to alveolar wall

A

Bacterial pneumonia

Sepsis

Smoke inhalation

Aspiration

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24
Q

What 2 other processes can cause pulmonary edema via an unknown mechanism?

A

Neurogenic (brain injury)

High altitude

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25
Q

High altitude pulmonary edema (HAPE) leads to accumulation of what substance in the alveolar spaces?

A

A pink proteinaceous material.

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26
Q

Which 2 diseases exist within the ARDS spectrum?

A

Acute lung injury (ALI)

ARDS

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27
Q

Acute lung injury (ALI) SX

Level of hypoxemia:

A

Acute onset, hypoxemia and BL infiltrates.
No evidence of cardiac failure.

< 300 PaO2/FiO2

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28
Q

ARDS onset:

Level of hypoxemia:

On CXR:

Cardiac involvement?

A

Abrupt onset.

<200 PaO2/FiO2

BL infiltrates on CXR.

Non-cardiac in nature.

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29
Q

4 “steps” of development ARDS

A
  1. Endothelial activation
  2. Adhesion/extravasation of neutrophils
  3. Accumulation of intraalveolar fluid and formation of hyaline membranes
  4. Resolution of injury
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30
Q

Diffuse alveolar damage (DAD) leads to _____.

How?

A

Hyaline membranes.

Edema + fibrin + cell debris accumulation.

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31
Q

Ventilation-perfusion mismatch in hyaline membranes

A

The membranes are damaged -> decreased aeration -> ventilation-perfusion mismatch (decreased PaO2/FiO2)

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32
Q

ARDS: stages of progression (3)

A
  1. Exudate: edema, hyaline membranes, neutrophils.
  2. Proliferative: fibroblast proliferation, organizing pneumonia and early fibrosis.
  3. Fibrotic: extensive fibrosis, loss of normal alveolar architecture.
33
Q

After the proliferative phase of ARDS occurs, what 2 pathways may ensue?

A

Resolution: restoration of normal cellular structure and function.

Fibrosis: destruction and distortion of normal cellular structure -> irreversible damage.

34
Q

3 pathologic features of ARDS

A

Hyaline membranes

Interstitial edema

Epithelial necrosis

35
Q

Acute interstitial pneumonia (AIP)

A

Same clinical presentation as ARDS.

Same histology as ARDS/DAD.

Cannot be attributed to a specific etiology.

36
Q

Restrictive lung DZ PFT features (3)

A

Volume restriction

FEV1/FVC normal

FVC reduced

37
Q

Obstructive lung DZ PFT features (2)

A

Decreased flow

Low FEV1/FVC ratio

38
Q

3 components of chronic bronchitis

A

Mucous secretion

Inflammation

Infection

39
Q

Chronic bronchitis diagnosis

A

Perisistent cough w/ sputum production for 3 mo. out of 2 consecutive yrs.

40
Q

Pathological mechanism of chronic bronchitis

A

Mucous gland hyperplasia leading to damaged airway epithelium.

41
Q

3 outcomes of chronic bronchitis

A

Squamous metaplasia -> dysplasia -> carcinoma

Bronchiectasis

Death from respiratory infection

42
Q

Clinical presentation of emphysema (CXR, physical, PFT)

A

Enlarged lungs on CXR

Barrel chested

FEV1/FVC ratio is reduced

43
Q

Alpha1-antitrypsin deficiency’s pathology exist at which 2 sites?

What kind of emphysema exists in AAT?

A

Lungs lack of a1-antitrypsin coating, making them available to damage by neutrophil elastase.
Abnormal a1-antitrypsin can become trapped in Liver.

Basilar panacinar emphysema.

44
Q

Types of emphysema for:

Spontaneous PTX

a1-AT deficiency

COPD

Localized

A

Spontaneous PTX: distal acinar or paraseptal

a1-AT deficiency: panacinar or panlobular

COPD: centrilobular, centriacinar or proximal acinar

Localized: irregular

45
Q

What gene on what chromosome is associated w/ AAT?

What allele is associated w/ low circulating AAT?

Homozygous PiZZ individuals can lead to developing which kind of emphysema?

Manner of DX?

A

Pi (proteinase inhibitor) on chr. 14.

Z allele

Panacinar emphysema

Serum testing

46
Q

4 major complications of emphysema

A

Respiratory failure

Pneumothorax w/ lung collapse

RHF (cor pulmonale)

CAD

47
Q

3 components of Asthma

A

Recurrent airway obstruction w/ reversible component

Airway hyper-responsiveness

Airway inflammation

48
Q

Atopic (Extrinsic) Asthma

Proportion of pts.:

Age group:

Family Hx?

IgE levels:

Triggers:

A

Proportion of pts.: 2/3 of pts.

Age group: can be any age, mainly childhood.

Family Hx? Yes.

IgE levels: elevate (type I hypersensitivity) w/ eosinophils, MCs and lymphocytes.

Triggers: many things.

49
Q

Non-atopic (Intrinsic) Asthma

Proportion of pts.:

Age group:

Family Hx?

IgE levels:

Triggers:

A

Proportion of pts.: 1/3 of pts.

Age group: often older.

Family Hx? No.

IgE levels: typically normal IgE, but has T cells and neutrophils.

Triggers: cold, exercise, infection.

50
Q

4 mediators of the bronchoconstriction component of asthma

A

Leukotrienes C4-D4-E4

Histamine

PGD2

ACh

51
Q

1 mediator of the mucous secretion component of asthma

A

Leukotrienes C4-D4-E4

52
Q

1 mediator of the increased vascular permeability component of asthma

A

Leukotrienes C4-D4-E4

53
Q

1 mediator family of the recruitment of inflammatory cells component of asthma

A

Interleukins

54
Q

Airway remodeling histologic findings (3)

A

Progressive structural changes to airways w/ characteristic histological findings:

  • fibrosis
  • SM hyperplasia
  • increased goblet cells and submucosal glands
55
Q

Is airway remodeling reversible?

A

Can be, and can lead to decreased response to therapeutic agents like BDs and steroids.

56
Q

Status asthmaticus

A

Unremitting, potentially fatal asthmatic attack

  • bronchial occlusion by thick mucous
  • coiled mucous plugs: “Curschmann spirals”
  • Eosinophil and breakdown product Charcot-Leyden crystals
57
Q

The genetic contribution to atopic asthma is associated w/:

A

Seasonal allergies and eczema.

Might also be linked to allele controlling factors like IgE, cytokines (IL-4), ARs, etc.

58
Q

The environmental contribution to atopic asthma is associated w/:

A

DZs of industrialized societies, like pollution or lack of allergen exposure at early age.

Early infection.

59
Q

Aspirin-sensitive asthma

A

Associated w/ nasal polyps and recurrent rhinitis.

  • unique sensitivity to aspirin
  • cross reacts w/ other NSAIDs
60
Q

Bronchiectasis is considered a _______ inflammatory response.

It is the end stage process of what processes?

A

Necrotizing inflammatory response.

End stage process of infection, obstruction, ABPA (Aspergillosis), CF, Tb, primary ciliary dyskinesia.

61
Q

Kartagener’s syndrome: Primary ciliary dyskinesia

DZ is caused by a dysfunction of what?

It includes a triad of what SX?

What associated problem exists in males?

A

Dysfunction of dynein arm of microtubules.

Triad - sinusitis, bronchiectasis and situs inversus.

Male infertility.

62
Q

Allergic bronchopulmonary aspergillosis (ABPA) def:

What DZ processes may exist in the “background”? (2)

What is increased on skin testing?

What exists in the bronchi?

Associated w/:

A

Exagerrated hypersensitivity response to Aspergillosis infection overlying chronic lung DZ.

Asthma or CF.

Increased IgE, w/ positive skin test.

Thick mucous in bronchi w/ fungal hyphae.

Associated w/ advanced bronchiectasis.

63
Q

What stain demonstrates the fungal hyphae of Aspergillosis?

A

Silver stain

64
Q

Chronic interstitial lung DZ is a:

A

Restrictive lung DZ

65
Q

Pneumoconiosis def:

A

Reaction by the lungs to inhaled mineral or organic dust via occupational exposure or air pollution.

A genetic predisposition may elicit an exaggerated response.

66
Q

3 factors that may worsen pneumoconiosis

A

High/repetitive exposure

Small particulate matter

Impaired ciliary clearance - smoking**

67
Q

Coal workers’ pneumoconiosis is a disease due to:

What are 3 components of the DZ’s spectrum?

Is this DZ progressive?

A

Due to inhaled coal dust.

Anthracosis
Coal macules/nodules
Progressive massive fibrosis

Most pts. will not have progressive DZ.

68
Q

Silicosis def:

What is unique about its onset?

What can it progress to?

What risk is associated w/ Silicosis?

A

Results from inhaled silicon dioxide from mining work or concrete repair/demo.

Insidious onset, may occur after exposure is gone.

Can progress to masse pulmonary fibrosis.

2-fold risk of developing cancer.

69
Q

What is found on histology of Silicosis?

CXR?

A

Dense collagenous nodules.

Eggshell calcifications (calcified hilar LNs).

70
Q

Asbestosis is an ______ and ______ disease.

A

Interstitial and pleural.

71
Q

Occupations w/ risk correlation to asbestos exposure:

A

Insulation workers
Shipyard workers (Navy)
Paper mill workers
Oil/chemical refinery workers

72
Q

What are the DZ manifestations of Asbestosis in the pleura vs. the lung?

A

Pleura: fibrosis, plaques, effusions and mesothelioma.

Lung: interstitial fibrosis, carcinoma.

Extrapulmonary neoplasms.

73
Q

What are “Candlewax drippings”?

A

They show hyalinized collagen on pleural plaques in a pt. w/ Asbestosis.

74
Q

Mesothelioma may occur when?

What is the lifetime exposure risk?

A

Might occur decades post exposure.

Lifetime exposure risk is as high as 10%.

75
Q

Most common cause of compression atelectasis is:

A

Pleural effusions

76
Q

Why is emphysema considered an obstructive lung disease?

A

The alveolar duct becomes compressed and constricted, along with damage to the alveoli.

77
Q

How can sepsis lead to ARDS?

A

Increased capillary permeability via mediators can damage the VE-cadherin bonds and lead to fluid leaking into the alveolus

78
Q

Chronic bronchitis SX vs Emphysema

A

Chronic bronchitis - overweight, cyanosis, elevated Hb, edema, rhonchi and wheezing.
“Blue bloater”

Emphysema - thin, severe dyspnea, quiet chest, hyperinflated lungs
“Pink puffer”

CPR II Exam #1 (30 decks)

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