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CPR Exam 1 > Chapter 15: Normal fetal lung development > Flashcards

Chapter 15: Normal fetal lung development Flashcards

1
Q

What is required for normal fetal lung development?

A

1. Enough space in the thoracic cavity for the lungs to grow

2. Ability to inhale

  • -Chest wall has to be able to move
  • -Must have enough amniotic fluid
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2
Q

Except for the vocal cords, the entire respiratory tree is lined by what type of epithelium?

A

Pseudostratified columnar ciliated epithelium

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3
Q

Bronchia mucosa contains population of neuroendocrine cells with neurosecretory granules containing which factors?

A
  • 1. Calcitonin
  • 2. 5HT
  • 3. Bombesin (gastrin releasting peptide)
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4
Q

Numerous mucus-secreting goblet cells and submucosal glands are dispersed throughout the walls of which parts of the respiratory tree?

A

Trachea and bronchi

BUT NOT BRONCHIOLES

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5
Q

How do normal lungs grow?

A

Normally from bronchus => alveoli (branching)

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6
Q

What 3 things do we want as our lungs grow?

A
  1. Airways to branch: larger airways will conduct the air to acinar units where gas can exchange.
  2. Rigid, open aiways
  3. Thin wall with high vascularity for gas exhchange
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7
Q

Diffusion distance between capilliary and basal lamina of the aveoli must be small.

Why?

A

Because RBC have less than one second to dump CO2 and pick up O2

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8
Q

What makes the wall of a aveoli?

A
  1. Capillaries with associated endothelium
  2. BM and interstitium.
  3. Type 1 pneumocytes line the aveolus
  4. Type 2 pneumocytes make surfactant to decrease ST and replace type 1
  5. Aveolar pores of Kohn
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9
Q

What are alveolar pores of Kohn

A

Pres that allow aveoli to share air with one another.

Only problem is that they also allow bacteria, cells, junk to pass between aveoli

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10
Q

What are the 4 congenital anomalies we will talk about?

A

1. Pulmonary hypoplasia

2. Foregut cysts

3. CPAM/CCAM (congeintal pulmonary adenomatoid malformation)

4. Pulmonary sequestration

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11
Q

Pulmonary hypoplasia occurs in utero and what are 2 major causes?

A
  1. Not enough space for lung to grow
    * d/t conginital diagphragmatic hernia that pushes abdominal organs into thorax
  2. Inability to inhale
  • oligohydramnois (not enough amnoitic fluid)
  • probs moving chest wall
  • malformation in the airway (tracheal stenosis)
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12
Q

Do babies born with pulmonary hypoplasia have a good change of living?

A

No (95% die). If the weight of the lung is less than 40% of NL => immediately die.

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13
Q

Foregut cysts are?

and where do they occur most often?

A

Cysts from of the foregut

Hilum/middle mediastinum

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14
Q

Foregut cysts are most often located where in the lungs and which classification/type is most common?

Treatment?

A

Hilum or middle mediastinum

  • Bronchogenic = most common; can also be respiratory, ESO, gastroenteric
  • Excision = curative!
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15
Q

Histology of a foregut cysts will reveal what?

How are they discovered?

A

Normal respiratory epithelium, thus it is NOT a neoplasm.

By accident d/t complications: rupture, cause infection or compress airways

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16
Q

Congenital pulmonary adenomatoid malformations (CPAM/CCAM) are caused by what?

A

“Arrested development”of pulmonary tissue that forms intrapulmonary cystic peice of abnormal lung tissue THAT connect to tracheobronchial airway and pulmonary vasculature.

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17
Q

Via which imaging modality can congenital pulmonary adenomatoid malformations be detected?

A

Fetal ultrasound

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18
Q

Congenital pulmonary adenomatoid malformation (CPAM) can be deadly due to what?

What is a complication?

A
    1. Hydrops
    1. Pulmonary hypoplasia
  • Infection or if it is large, it can cause pulmonary hypoplasia.
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19
Q

Pulmonary sequestration is what?

How is it different from CPAM?

A

Intra or extra-pulmonary peice of nonfunctioning lung tissue that forms into a bud but does NOT connect to the tracheobronchial airway and has its OWN blood supply.

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20
Q

Where do pulmonary sequestrations usually grow?

A

Lower left lobe (can be intralobular or extralobular)

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21
Q

When do intralobular pulmonary sequestration (ILS) present and what is a complication?

A

Older children and adults

Because ILS do not get air (even though they have their own BS), they have an increased liklihood of infection and abbsess formation (so come to ATN later)

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22
Q

Extralobar pulmonary sequestrations present when and come to ATN how?

How are they different from intralobular pulmonary sequestration?

A
  • Present after birth as mass lesions and come to ATN earlier bc they bb usually has other congenital foregut anomies, especially CARDIAC and UPPER GI.
  • Have their own BS, pleura and AIRWAY
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23
Q

What is atelectasis?

A

atelectasis is decreased expansion or loss of volume affecting the lungs

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24
Q

Atelectasis is a reversible disorder, except in cases caused by what?

A

Contraction atelectasis

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25
Q

What are the 3 main types of acquired atelectasis and what is each caused by?

A
  1. Resorption due to complete obstruction of airway (ex d.t a mucus plugs) => decreases air to lungs and reduce lung expansion.
  2. Compression due to an accumulation of material or air in the pleural cavity (i.e., transudate/exudate/blood or pneumothorax)
  3. Contraction due to local or fibrotic changes in the lung/ pleura prevents expansion (problem directly related to lung)
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26
Q

Which type of acquired atelectasis causes the mediastinum/trachea to shift toward the affected lung; which type causes a shift away?

A
  • Resorption —> mediastinum shifts toward affected lung
  • Compression –> mediastinum shifts away from affected lung
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27
Q

Which type of acquired atelectasia occurs in the setting of asbestosis?

A

Contraction atelectasis

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28
Q

Hemodynamic pulmonary edema is d/t due to an increase in what; most commonly occuring in what setting?

A

1. Increased hydrostatic pressure =>

Left-sided CHF

2. Or decreased in oncotic pressure

3. Or increase capillary permability (dmg to alveolar/endothelial wall)

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29
Q

What can you see in this picture?

A

Pulmonary edema: pink proteinaceious material in aveolar spaces

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30
Q

What is the histological appearance of of the alveolar capillaries in hemodynamic pulmonary edema?

A

Engorged, and an intra-alveolar transudate appears as finely granular pale PINK material

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31
Q

Where does fluid accumulate 1st in pulmonary edema due to hydrostatic pressure being greatest in these sites (dependent edema)?

A

Basal regions of the lower lobes

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32
Q

Pulmonary edema can also be due to decreased oncotic pressure, which cause “leaking out”. What 4 things can cause this?

A
    • Hypoalbuminemia
    • Nephrotic syndrome
    • Liver disease
    • Protein-losing enteropathies
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33
Q

What other mechanisms can cause the pushing out of fluid, resulting in pulmonary edema?

A
  1. Too much volume
  2. Obstruction of pulmonary vein
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34
Q

What can injure the alveolar wall => cause pulmonary edema?

A
    • Infections: bacterial pneumonia
    • Inhaled gases: high [O2] and smoke
    • Liquid aspiration: gastric contents; near drowing
    • Radiation
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35
Q

What are 2 causes of pulmonary edema that we arent sure how it results in it?

A

1. Brain injury

2. High altitude

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36
Q

How does pulmonary edema affect airflow to lungs?

A

Decrease air to lungs.

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37
Q

In long-standing pulmonary congestion (i.e., mitral stenosis), hemosiderin-laded macrophages are abundant, and what is the gross morphology of the lungs?

A

Soggy lungs become firm and brown (brown induration)

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38
Q

Differentiate acute lung injury (ALI) and acute respiratory distress syndrome (ARDS).

How are they alike?

A

ALI: abrupt hyoxemia (<300) and BILATERAL pulmonary infiltrate without cardiac failure.

ARDS is a more severe ALI that occurs as hypoxia (<200) worsens and is more severe on the ARDS spectrum.

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39
Q

How do we diagnose with Diffuse Alveolar Damage (DAD)?

A

Pathologists diagnose this as the histological manifestations of ARDS/ALI, caused by inflammation d/t increased vascular permability that occurs in both.

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40
Q

When the edema associated with pneumonia fails to stay localized and instead becomes diffuse alveolar edema what fatal condition may this lead to?

A

ARDS

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41
Q

A patient comes in who we think has ALI, what must his arterial blood gas be?

A

Less than or equal to 300 (PaO2/FiO2)

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42
Q

Describe the pathogenesis of ALI/ARDS

A
    1. Injury to the pneumocytes and pulmonary endothelium => activating endothelium
    1. Neutrophil adhere and leak into interstitium and alveoli => degranulate and release inflammatory mediatorys (proteases, ROS and cytokines)
      * Macrophage migration inhibitory factor (MIF) promotes the cycle of pro- inflammation and damage => more injury and endothelial damage
    1. Damage causes pulmonary capillaries to become leaky => accumulation of intraalveolar/interstitial edema
      * Type 2 pneumo are damaged => fucks up surfactant => fucking up gas xchange
      * Thick, protein rich edema, fibrin and debris from dead cells (necrosis) => form hyaline membranes
  • 4. Resolution of injury: damage prevents cells from preventing edema. If inflammation decreases, MO release TGF-B and PDGF to help grow fibroblast and deposit collagen => fibrosis of alveoli.
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43
Q

Following the fibroproliferative phase in ARDS, what 2 pathways may ensue and the result of each?

A
  1. Resolution: restoration of normal cell structure and fx: we can breath n shit
  2. Fibrosis: fucks up normal cell struture and is irreversible
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44
Q

What are the 3 stages of ARDS?

A
  1. Exudative: edema, hyaline and neutrophils
  2. Proliferative: fibroblast proliferate and organize and early fibrosis
  3. Fibrotic: extensive fibrosis and loss of structure of alveoli OR

Resolution of normal cell structure and function

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45
Q

What causes the formation of hyaline membrane?

A

Edema

Fibrin

Dead cells

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46
Q

What is this and what does it result in?

A

Hyaline membrane increases the distance between capillary and alveoli => decrease aeration => mismatch in how much air your breathing in vs how much is getting in lungs (ventillation:perfusion mismatch) => decrease in PaO2/FiO2

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47
Q

ALI/ARDS is more common and associated with a worse prognosis in whom?

A

Chronic smokers and alcoholics

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48
Q

During the acute stage of ALI/ARDS what is seen morphologically in the lungs?

A

1. Lungs are heavy, firm, red and boddy

2. Congestion, edema fibrin and DAD

3. Haline membrane

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49
Q

What is a pathological dx of ARDS (DADS)?

A

HIE

1. Hyaline memrbane

2. Intersitial edema

3. Epithelial necrosis

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50
Q

What is seen on radiographic imaging of patient with ALI?

A

Diffuse bilateral infiltrates

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51
Q

Pt’s with ALI will have what sx’s?

A

- Profound dyspnea and tachypnea

- Followed by ↑ cyanosisand hypoxemia

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52
Q

What is the cause of the ventilation perfusion mismatch and hypoxemia in ALI/ARDS?

A
  • Poorly aerated regions continue to be perfused
  • Perfusion = normal; but ventilation = decreased
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53
Q

ARDS is a diagnosis of exclusion using the criteria which can be remembered with mnemonic A.R.D.S.

A
  1. Abnormal CXR (bilateral lung infiltrates)
  2. Resp failure w/t 1 week of damage to aveoli (abrupt)
  3. Decreased PaO2/FiO2 (<200)
  4. Sx not d/t HF/too much fluid
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54
Q

The causes of ARDS may be remembered with “SPARTAS.”

A
  • Sepsis
  • Pancreatitis/Pneumonia
  • Aspiration
  • uRemia
  • Trauma
  • Amniotic fluid embolism
  • Shock
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55
Q

How is the diagnosis of Acute Interstial Pneumonia (AIP) different from classic ARDS.

A

Everything is the same (clinical presentation/histo) except WE DO NOT KNOW WHY IT OCCUTS

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56
Q

When do most deaths associated with Acute Interstitial Pneumonia occur?

A

Within 1-2 months

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57
Q

Which 2 obstructive lung diseases are grouped together and referred to as COPD?

A

- Chronic bronchitis

- Emphysema

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58
Q

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

A
  • OLD occurs d/t decreased airflow d/t partial/complete obstruction that causes hyper-expanded lungs.
  • Restrictive lung disease is reduced expansion of lungs and decreased total lung capacity.
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59
Q

How does the FEV1/FVC ratio differ for restrictive lung disease and obstructive lung disease?

A

RLD: normal FEV1/FVC. Both values decrease, keeping the ratio the same

OLD: Decreased FEV1 (amount of air you force out in 1 second), but normal FVC (amount of air that you can force out after taking a deep breath in) => decreases FEV1/FVC ratio

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60
Q

What are the causes of obstructive lung disease?

What are they most often caused by?

A
  • 1. COPD
  • 2. Asthma
  • 3. Bronchiectasis
  • 4. Emphysema
  • Smoking
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61
Q

What are the causes of restrictive lung disease?

A
  • 1. Pulmonary fibrosis
  • 2. Rheumatoid Arthritis
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62
Q

What is the dominant pathogenic mechanism of chronic bronchitis?

A

Irritation of the airways d/t inhalation of

  1. Tobacco smoke
  2. Dust from grain, cotton, and silica

Irritants will damage the epithelium and interfere with cilia, preventing mucus clearance.

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63
Q

Chronic bronchitis is associated with what 2 symptoms?

A

A small-airway disease where the patient has inflammation of the airway and a productive cough.

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64
Q

What is the earliest feature seen in the pathogenesis of Chronic Bronchitis; over time there is a marked increase in what cell type?

A
  • Mucus hypersecretion d/t hyperplasia of submucosal glands in the trachea and bronchi d/t inflammation => Damaged and thickens the smooth muscle of small airways => more prone to infection.
65
Q

How do we diagnose someone with chronic bronchitis?

A
  1. Persistent cough with sputum for 3 months out of 2 consecutive years.
66
Q

Long-term chronic bronchitis can lead to what??

A
  1. Bronchiectasis
  2. Squamous metaplasia and dysplasia can cause cancer

3. Death d/t respiratory infection

67
Q

Emphysema is an _________ lung disease characterized by what?

Does fibrosis occur?

A

Obstructive LD where air spaces distal to terminal bronchioles are IRREVERSIBLY damaged. Alveoli are dilated (with ↓ elasticity and ↑ compliance) whiile toxins from smoking cause airway to collapse, trapping air in the alveoli.

68
Q

What causes emphysema?

A

Smoking or air pollutants

69
Q

What does emphysema look like on XR?

A

Air trapping and hyperinflation cause enlarged lungs with a barrel chest (Increase in AP diameter)

70
Q

What is the FEV1/FVC ratio, TLC of emphysema and what does the volume-flow loop look like?

A
  1. Reduced: FEV1 decreases alot and FVC decrease
  2. TLC will increase (max volume of air into the lungs increases bc air is trapped)
  3. Chair

NL ration: 4L/5L= 80%

Emphysema: 2L/4L = 50%

71
Q

What is the clnical presentation of emphysema?

A

PINK PUFFERS

  1. Older and thin
  2. Severe dyspnea (SOB), so pts will purse lips to breath and prvent airway collapse (uses NRG so thats why pt is thin)
  3. Chest sounds are quiet
72
Q

What is the clinical presentation of chronic bronchitis?

A

BLUE BLOATERS

  1. Young, overweight and cyanotic (resp insufficiency)
  2. High hemoglobin to try to compensate
  3. Peripheral edema
  4. Rhonchi and wheezing
73
Q

Of the 4 major types of emphysema which 2 cause clinically significant airflow obstruction; which is most common?

A

1. Centriacinar(centrilobular) = most common = affects upper lungs

Most dmged d/t smoking

2. Panacinar (panlobular) = affects lower lungs

  • occurs d/t alpha-1 antitrypsin deficiency
74
Q

Where are lesions of centriacinar (centrilobular) emphysema most commonly seen and most severe?

A

Upper lobes (apical segments)

Affects proximal respirtory bronchioles, but does not affect distal alveoli

75
Q

Centriacinar (centrilobular) emphysema occurs predominantly in whom and is often associated with what other lung disorder?

A

Heavy smokers, often in assoc. w/ chronic bronchitis (COPD)

76
Q

Panacinar (panlobular) emphysema occurs most commonly where in the lungs and is associated with what underlying abnormality?

A
  • Lower lobes and anterior margins of lung, usually most severe at bases

-Entire acini are enlarged (from resp bronchile => terminal alveoli) d/t

  • α1-antitrypsin deficiency
77
Q

Which type of emphysema most likely underlies many cases of spontaneous pneumothorax in young adults?

A

Distal acinar (paraseptal) emphysema (distal alveoli are affected)

78
Q

What are some of the inflammatory mediators released by macrophages and resident epithelial cells which influence the development of emphysema?

A
  1. - Leukotriene B4
  2. - IL-8
  3. - TNF
79
Q

The pathogenesis of emphysema is related to an imbalance between which factors?

A

Proteases (i.e., elastase) and anti-proteases (α1-antitrypsin)

80
Q

α1-antitrypsin is encoded by which locus and on what chromosome?

A

Proteinase inhibitor (Pi) on chromosome 14

81
Q

Loss of elastic tissue in the walls of alveoli in emphysema causes respiratory bronchioles to do what during expiration?

A

Collapse —> preventing air from leaving

82
Q

What is the characterisitc gross morphology seen in advanced emphysema?

A
  • Enlarged lungs which often overlap the heart
  • Large alveoli seen on cut surface of fixed lungs
83
Q

Microscopically, in emphysema, the large alveoli are separated by what and have fibrosis where?

A

Thin septa w/ only focal centriacinar fibrosis

84
Q

What are complication of emphysema?

A
  1. Resp failure
  2. CAD
  3. Right heart failure (Cor pulmonale)
  4. Pneumothorax w collapsed lung
85
Q

COPD includes

A

chronic bronchitis and emphysema

86
Q

What is asthma?

A

a chronic relapsing obstructive lung disease caused by reversible bronchoaspams d/t hyper-reactive airways that undergo inflammation

87
Q

Asthma is distinguished from chronic bronchitis and emphysema by the presence of what feature?

A
  1. Reversible bronchospasm
  2. Not assx w smoking
88
Q

What are the 2 forms of asthma?

A

1. Atopic (extrinsic) asthma

2. Non-atopic (intrinsic) asthma

89
Q

Atopic (extrinsic) asthma

____ of patients

Affects what age:

Family history

Caused by:

A
  • 2/3 of patients (most common)
  • Any age; typically children
  • Runs in family
  • Type 1 hypersensitivity reaction (high IgE levels) with eosinophils, mast cells and lymphocytes caused by allergens
  • Triggered by allergens
90
Q

Non-atopic (intrinsic) asthma

____ of patients

Affects what age:

Family history:

Caused by:

A
  • 1/3 of patients
  • Older patients
  • No family history
  • D/t cold, excercise infection and normal levels of IgE, T cells and neutrophil
91
Q

What are the changes that occur in the airway of someone with asthma?

A
    1. Increase mucus production
      * ​Increase number of goblet cells
      * hypertrophy of mucus glands
    1. Chronic inflammation (eosino/MO)
    1. Thick BM
    1. Hyperplasia/hypertrophy of smooth muscle
92
Q

Early-onset allergic asthma is associated with inflammation due to what type of T cells and has good response to what tx?

A

- TH2 helper T cell inflammation

- Responds well to corticosteroids

93
Q

A fundamental abnormality in the pathogenesis of asthma is an exaggerated response by which immune cells to normally harmless enviornmental allergens?

A

TH2 response=> IL-4, 5 and 13

94
Q

What is the role of IL-4, IL-5, and IL-13 released from TH2 cells in asthmatic patients?

A

- IL-4 stimulates class switching to IgE

- IL-5 activates eosinophils

  • IL-13 stimulates mucus secretion and IgEproduction by B cells
95
Q

Other than TH2 cells what other type of T cell is seen in the late-phase reaction of asthma and what is it’s function?

A

TH17 produce IL-17 –> recruit neutrophils

96
Q

The bronchoconstriction characteristic of the early phase (immediate hypersensitivity) of asthma is triggered by what?

A

Direct stimulation of Vagal (parasympathetic) receptors by mediators from mast cells

97
Q

What causes bronchoconstriction in asthma?

A
  • 1. Leukotrienes C4-D4-E4,
  • 2. Histamine,
  • 3. Prostaglandin D2
  • 4. ACh
98
Q

What causes mucus secretion in asthma?

A
  1. Leukotrienes C, D, E-4
99
Q

What causes increased vascular permeability in asthma?

A

Leukotrienes C4, D4 and E4

100
Q

What recruits inflammatory cells in asthma?

A

Interleukins

101
Q

Which factors released from eosinophils in the late phase reaction of asthma cause damage to the epithelium?

A
  1. - Major basic protein
  2. - Esoinophil cationic protein
102
Q

Uncontrolled asthma can lead to what irreversible (?) changes?

A
  • Airway remodeling
    • Fibrosis
    • Smooth muscle hyperplasia
    • Increased goblet cells and submucosal glands
103
Q

Airways that have undergo remodeling will respond how to therapeutic agents such as bronchodilators & corticosteriods?

A

Decreased response

104
Q

What is status asthmaticus?

A

Acute SEVERE asthma attack where thick mucus plugs (Curschmann spirals) block bronchioles.

105
Q

What 2 findings do we see in status asthmaticus?

A
  1. Thick mucus plugs (Curschmanns spirals)
  2. Charcot Leyden crystals, a breakdown product of eosinophils
106
Q

There is an increased incidence of what 2 other allergic disorders in those with atopic asthma?

A

1. Allergic rhinitis

2. Eczema

107
Q

Leukotrienes C4, D4, E4 are responsible for what 3 pathogenic processes in asthma?

A

- Bronchoconstriction

- Mucus secretion

- ↑ vascular permeability

108
Q

Variants of which interleukin receptor gene is associated w/ atopy, elevated total serum IgE and asthma?

A

IL-4

109
Q

What are 2 characteristic findings in the sputum or bronchoalveolar lavage specimens in a pt w/ severe asthma?

A

- Curschmann spirals = Coiled mucus plus

  • Numerous eosinophils and Charcot-Leyden crystals composed of an eosinophil protein called galectin-10
110
Q

The characteristic histologic finding of “airway remodeling” in pt w/ asthma includes what 5 major changes?

A

- Thickening of airway wall

- Sub-basement membrane FIBROSIS

- ↑ vascularity

- ↑ in size of submucosal glandsand # of goblet cells

- Hypertrophy and hyperplasia of the bronchial wall muscle

111
Q

What are the cardinal sx’s of asthma?

A
  1. - Chest tightness
  2. - Dyspnea
  3. - Wheezing
  4. - Cough (with or w/o sputum production)
112
Q

Aspirin-sensitive asthma occurs most commonly in pt’s with what underlying disorders?

A
  1. Recurrent rhinitis (Samsters triad)
  2. Nasal polyps
113
Q

Pt’s with aspirin-sensitive asthma suffer from what sx’s during an attack?

A

1. Asthmatic attacks

2. Uticaria (hives)

114
Q

Describe how aspirin inhibiting COX plays a role in the pathogenesis of aspirin-sensitive asthma?

A

Aspirin => inhibits COX => rapid ↓ in PGE2, which normally inhibts leukotriens C4-E4 => increased vascular permability, bronchoconstriction, mucus secretion => aspirin-sensive asthma

115
Q

What is bronchiectasis?

A

Perment dilation of bronchi and bronchioles d/t destructive necrotizing inflammation of bronchi and bronchioles.

116
Q

What conditions can lead to bronchiectasis>

A

1. Allergic bronchopulmonary aspergillosis (ABPA)

2. Cystic fibrosis

3. TB (chronic infection)

4. Primary ciliary dyskinesia

117
Q

Many cases of Bronchiectasis lack any association with another disease process and therefore are what?

A

idiopathic

118
Q

What are the 2 major conditions associated with Bronchiectasis and are often both necessary for its development?

A
  1. - Obstruction
  2. - Infection
119
Q

Which 3 organisms are the most common causes of lung infection in pt with CF?

A

1. Staph aereus

2. H. influenza

3. Pseudo. aeruginosa

120
Q

In CF the primary defect in ion transport leads to defective what in the lungs?

A
  • Mucociliary action + airway obstruction by thick viscous secretions
  • Sets stage for chronic bacterial infections
121
Q

What is primary ciliary dyskinesia?

A

Mutation of motor proteins in cilia and flagella (dynien arm of microtubules)

122
Q

Half of the pt’s with primary ciliary dyskinesia have what syndrome and what is the triad of this syndrome?

A

Kartageners syndrome

  1. - Sinusitis
  2. - Bronchiectasis
  3. - Situs inversus
123
Q

Males with Kartagener Syndrome tend to be what?

A

Infertile bc sperm cannot swim

124
Q

What is allergic bronchopulmonary aspergillosis and who does it most commonly affect

A

Hypersentitivity to aspergillus infection, found in the soil, causing bronchospasm and mucus buildup in bronchi.

It most commonly affects those with asthma or CF.

125
Q

What are characteristic findings in the seurm of someone with Allergic Bronchopulmonary Aspergillosis?

A

High IgE (because it is a hypersensitivity reaction)

126
Q

How can we test to see if someone has ABPA?

A

1. Increase serum IgE

2. Positive skin test

127
Q

What is the funal hypae characteristic of asperigillus?

A

Thick mucus in bronchi

128
Q

Which stain can be used to demonstrate Aspergillus and what is seen?

A
  • Silver stain
  • Aggregates of fungal hyphae
129
Q

Bronchiectasis usually affects which lobes of the lung, particularly which air passages, and is most severe where?

A

- Lower lobes bilaterally

  • Vertical air passages
  • Distal bronchi and bronchioles
130
Q

Which lung disease will have dilated airways, sometimes up to 4x normal size?

A

Bronchiectasis

131
Q

What are the signs/sx’s of Bronchiectasis?

A
  • Bad cough w/ smelly, bloody sputum
  • Dyspnea and orthopnea in severe cases
  • Occasionaly hemoptysis, which can be massive!
132
Q

Restrictive lung diseases are also called what?

A

chronic diffuse interstitial disease

133
Q

Restrtive lung disorders make up 2 general conditions

A
    1. Chronic interstitial and infiltrative disease (pneumoconioses and interstitial fibrosis)
    1. Chest wall disorders
134
Q

What are the sign/sx’s of chronic interstitial pulmonary diseases?

A
    • Dyspnea and Tachypnea (SOB and fast-breathing)
    • End-respiratory crackles
    • Cyanosis (late)
    • NO wheezing
135
Q

What is characteristically seen on CXR of someone w/ chronic interstitial pulmonary diseases?

A

Bilateral lesion that can look like small nodules or irregular lines

Ground glass shadow

136
Q

Grossly, what is the end-stage lung seen in chronic interstitial pulmonary diseases referred to as?

A

Honeycomb lung

137
Q

What is pneumoconiosis?

A

Non-neoplastic lung response to inhaled minerals, organic dusts or air pollusion

138
Q

Only a small percentage of people exposed to inhaled pollutants develop a lung disesase. What does this suggest about pneumoconiosis?

A

There is a possible genetic component

139
Q

Development of pneumoconiosis depends on what factors?

A
    1. Amount of dust you inhale (if high and repetitive = worsens)
    1. Size of the particle (smaller particles are worse bc if 1-5um, they can reach the alveoli).
    1. Toxicity and solubility of particle (more soluble = cause more toxicity)
    1. Irritants that may damage cilia: SMOKING
140
Q

What is Coal Workers Pneumoconiosis?

A

A spectrum of diseases caused by the inhalation of coal dust

  • 1. Anthracosis (asymptomatic)
  • 2. Coal macules/nodules
  • 3. Black lung (progressive massive fibrosis)
  • 4. Caplan syndrome
141
Q

What occurs to the inhaled carbon pigment from coal, leading to Anthracosis?

A
  1. MO take up carbon pigment from coal
  2. Accumulate in CT along lymphatics in lungs or hilus
142
Q

Where are lesions (macules and nodules) of simple coal workers’ pneumoconiosis most often seen in the lungs?

A
  1. Upper lobes
  2. Upper zones of lower lobes
143
Q

Indoor use of smoky coal (bituminous) for cooking and heating is associated with what complication?↑

A

↑ risk of lung cancer

144
Q

What is the most prevalent occupational disease worldwide?

A

Silicosis, a disease resulting from inhaled silicone dioxide => chronic, progressive nodular fibrosis

145
Q

Which race has a higher risk for Silicosis?

A

African Americans

146
Q

What occurs after inhalation of silica particles; what is activated and what is released?

A

1. MO take up particles

2. Activate inflammasome

3. Release IL-1 and IL-8

147
Q

How is Silicosis different than CWP?

A

With Silicosis, you have a 2-fold risk of getting cancer

148
Q

Where in the lungs and in which LN’s are the nodules of silicosis seen?

A

Upper zones of lungs in Hilar LN

149
Q

Histologically, what is the hallmarklesion seen with silicosis?

A

Central area of WHORLED COLLAGEN nodules w/ MO located peripherally w dust

150
Q

What do you see on XR of someone with silicosis?

A

Eggshell calcification d/t calcified hilar LN

151
Q

The onset of Silicosis is often what?

A

Slow and insidious (10-30 years later)

152
Q

What is asbestosis and what is the most dangerous type of asbestos fiber?

A

Asbestosis is a interstitial and pleural disease d/t inhalation of asbestos fibers.

Amphibole: more aerodynamic and less soluble

153
Q

Who has a higher risk of developing asbestosis?

A

1. Working with insulation

2. Navy (shipyard workers)

3. Paper mill workers

4. Oil/chemical refinery workers

154
Q

What is this?

A

Abestosis

Diffuse interstitial fibrosis that is no different from disorders EXCEPT there are asbestos bodies (golden-brown, fusiform or beaded rods)

155
Q

What is the morphology of asbestos on the lungs?

A
  1. Well circumscribed pleural plaques of dense collagen, that do not contain asbestos bodies.
  2. Candlewax drippings on pleura
156
Q

Besides asbestos bodies, what else does histo of asbestosis show?

A

Hyalinzed collagen

157
Q

In contrast to other types of pneumoconiosis, where is the lungs does asbestosis typically begin?

A

Lower lobes

Subpleurally

158
Q

What is associated with asbestos exposure and can occur DECADES after, with a 10% chance of occuring?

A

Mesothelioma

CPR Exam 1 (19 decks)

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