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21. CPR Exam 1 > 18. Pulmonary Path 1 > Flashcards

18. Pulmonary Path 1 Flashcards

1
Q

Threre are 5 stages of normal fetal lung development, starting with the embyronic lung bud, and what are the final 4 stages?

A

Pseudoglandular
Canalicular
Saccular
Alveolar

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2
Q

In the alveolar stage is where terminal buds grow, what can one determine via the stage of lung development?

A

Age of the fetus

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3
Q

There are important requirements for normal lung development including adequate space in the thoracic cavity and the ability to?

A

INHALE

chest wall must be able to move and there must be enough amniotic fluid present

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4
Q

Larger airways conduct air to the terminal acinal units for proper?

A

gas exchange

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5
Q

The trachea and bronchus are rigidly open and patent and end at respiratory bronchioles which have thin walls with high vascularity for?

A

gas exchange to occur

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6
Q

The trachea histologically consists of cartilage, a submucosa, a smooth muscle layer, a lamina propria, and respiratory epithelium which contains? 4

A

Pseudostratified ciliated epithlium which contains:
Goblet (mucous cells)
Cilia
Ciliated columnar cells
(*all to keep the airways open and clean)

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7
Q

The lung parenchyma (functioning part) contains bronchioles, blood vessels, and most importantly, abundant?

A

Alveoli (white space where gas exchange occurs)

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8
Q

Histologically, lung parenchyma consists of erythrocytes which are extremely red/hot pink/purple within capillaries. Also type 1 and 2 pneumocytes can be seen. What distance needs to be minimal?

A

The distance between capillaries and alveolar in order to allow for quick gas exchange (takes less than 1s to dump CO and pick up O2)

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9
Q

In alveolar structure, there are capillaries with endothelium and a basement membrane with interstitium. What are the main jobs of Type 1 and 2 Pneumocytes?

A

Type 1: cover 95% of alveoli and facilitate gas exchange (flattened plate like)
Type 2: Produce surfactant and replace type 1 (stem cell action) when needed

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10
Q

What in the lung alveoli allow aeration (redundant) but also allow bacterial, cells and exudate to travel between alveoli?

A

Alveolar pores of Kohn

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11
Q

What congenital abnormality causes 1/2 of mortality in babies?

A

Pulmonary hypoplasia

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12
Q

Pulmonary hypoplasia can be caused by reduced space in the thoracic cavity (diaphragmatic hernia/tumors) or by the impaired ability to inhale via what 3 mechanisms?

A

Chest wall motion disorders
Airway malformations (tracheal stenosis)
Oligohydramnios

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13
Q

Oligohydramnios can be caused by renal agenesis as seen in Potters sequence, what occurs during this?

A

there is renal agenesis which causes a lack of fetal urine leading to lack of amniotic fluid and lung hypoplasia

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14
Q

A fetal lung should be at the same level of the bottom of the heart, there is high mortality (up to 95%); if the lung weight is less than 40% what occurs in the neonatal period?

A

immediate death

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15
Q

What arise from an abnormal detachment of primitive forgut and are most often located in the hilum or middle mediastinum (bronchogenic-MC)?

A

Foregut cysts

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16
Q

Foregut cysts can be respiratory, esophageal or gastroenteric and are often seen incidentally, 3 of the complications include?

A

Rupture
Infection
*Airway compression

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17
Q

Excision for foregut cysts is curative. What is the classification for the cysts, which has a single ‘balloon’ wall, with not other cysts, but fluid inside?

A

Foregut cysts are classified as SIMPLE cysts

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18
Q

Congenitla pulomanary (cystic) adenomatoid malformation (CPAM/CCAM) is known as arrested development of pulmonary tissue with formation of?

A

intrapulomnary cycstic masses

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19
Q

CPAM communicated with the tracheobronchial tree and can be detected on fetal U/S. It can be deadly due to hydrops or pulmonary hypoplasia and can get?

A

infected later in life (or incidentally found)

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20
Q

CPAMs should be taken out during gestation (in utero) because it competes for?

A

normal thoracic space, causing lung hypoplasia

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21
Q

What are nonfunctioning lung tissue that forms as an abberant accessory “lung bud”?

A

Pulmonary sequestrations

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22
Q

Pulmonary sequestations are typically in the left lower lobe (so both R/L lungs have 3 lobes), they are characterized by a lack of any connection to the airway system and an independent?

A

arterial supply from the aorta or its branches

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23
Q

Pulmonary sequestrations may be intralobar or extralobar depending on whether budding occurs before or after?

A

pleura is established

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24
Q

What type of sequestration lacks airway perfusion, does not have its own pleura, making them susceptible to infection and abcess formation?

A

Intralobar pulmonary sequestrations ILS

seen in older children and adults with recurrent location infection or bronchiectasis

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25
Q

Extralobar pulmonary sequestrations (ELS) usually presents after birth with other congenital malformations (heart). They have independent vessles and (sometimes airways), and come to attention as mass lesions in the chest. What is the main difference between ELS and ILS

A

ELS has its own pleura while ILS does not!

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26
Q

What is the main difference between the lesions in CPAM and pulmonary sequestrations?

A

CPAMs are within the lung connected to tracheobronchial airways and pulmonary vasculature which sequstrations have NO connection to pulmonary vasc or trach tree (usually only have independent vessels off aorta)

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27
Q

Acquired atelectasis (collapse) refers to incomplete expansion of the lungs (neonatal) or to the collapse of previously inflated lung, producing areas of relatively airless pulmonary parenchyma, seen in?

A

Adults

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28
Q

What occurs due to complete airway obstruction with graudal resorption of air, reducing lung expansion/causing collapse?

A

Resorption Atelectasis

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29
Q

Resorption atelectasis is commonly due to excessive secretions or exudates within small bronchi, what occurs anatomically in resorption atelectasis?

A

mediastinum shifts towards the affected lung b/c lung volume is diminished

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30
Q

What tpy eof atelectasis is not related to the lung, and is due to accumulated material in the pleural cavity compressing the lung parynchema?

A

Compression atelectasis

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31
Q

Compression atelectasis occurs when volumes accumulate such as transudate, exudate blood or air, causing the mediastinum to shift?

A

away from the affected lung (opposite resorption atelectasis)

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32
Q

What is the most common type of acquired atelectasis which is due to fibrotic or other innate restrictive processes in the pleura or peripheral lung, restricting lung expansion?

A

Contraction atelectasis (mediastinal shift toward affected lung)

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33
Q

What is pink material (interstitial fluid) in alveolar spaves which decreases aeration and gas exchange?

A

Pulmonary edema

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34
Q

Pulmonary edema is caused by many influences. Physiologically, what are the two main ways edema occur?

A

Increased hydrostatic pressure = forces fluid out (result of L heart failure)
Decreased oncotic pressure (hypoalbuminemia) = loses fluid through equilibrium across a semipermeable membrane

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35
Q

Pulmonary edema causes heavy, wet lungs, leading to decreased oxygenation because the diffusion barrier is increased. Leads to granular pink proteinaceous material in alveolar spaces initially, chronically leads to brown firm lungs due to interstitial fibrosis and ?

A

hemosiderin laden macrophages (heart failure cells)

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36
Q

Pulm edema is also caused by microvascular (alveolar) injury, including bacterial pneumonia, sepsis, smoke inhalation and?

A

aspiration (near drowning)

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37
Q

What can also cause pulmonary and cerebral edema causing death extremely quick?

A

High altitude pulmonary edema (HAPE)

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38
Q

What is characterized by abrupt onset of significant hypoxemia and bilateral pulmonary infilitrates in the absence of cardiac failure?

A

Acute lung injury ALI

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39
Q

What is the manifestation of worsening hypoxemia, or severe ALI?

A

Acute Respiratory distress syndrome ARDS

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40
Q

What is known as the histological manifestation of ALI/ARDS, which are both associated with inflammation associated increases in pulmonary vascular permeability, edema and epithelial cell death?

A

Diffuse Alverolar Damage (DAD)

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41
Q

ARDS has an abrupt onset of symptoms (infection, physical injury, inhaled irritants, chemical injury, hematologic conditions). Hypoxemia is important, what PaO2/FiO2 is needed to be considered ARDS?

A 
PaO2 (amount of blood in circulation)
FiO2 (fraction of O2 being breathed in)
= arterial blood gas
is less than or equal to 200
(ALI requires less than 300)
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42
Q

Along with a PaO2/FiO2 of less than 200, ARDS is non cardiac in nature and or not secondary to a heart condition and often will see what on CXR?

A

cloud CXR with bilateral infiltrates

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43
Q

ARDS can result from insults from the respiratory system or from circulation. Increased alveolar capillary permeability cause fluid leak and alveolar damage. What biochemically causes the inc. permeability?

A

Disrupted VE-cadherin bonds

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44
Q

ALI/ARDS is initiated by injury of pneumocytes and pulm endothelium causing an increasing cylce of inflammation and pulmonary damage. What is the first stage?

A

Endothelial activation

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45
Q

Endothelial activation occurs when there is a respiratory or systemic (sepsis) insult to pneumocytes sense by resident macrophages. What happens next, after endothelial activation?

A

Neutrophilic adhesion and extravastion, releasing mediators such as PAF, leukotriences and proteases to recruit more

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46
Q

After neutrophilic extravasion, accumulation of intralaveolar fluid occurs, damaging type 2 pneumocytes causing surfactant related issues. The protein rich fluid and dead epithelial cells forms? (characteristic of ALI/ ARDS)

A

hyaline membranes

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47
Q

After formation of hyaline membranes, resolution of injury occurs if inflammation lessens and macrophages and clean everything up with fibrogenic factors such as? (2)

A

TGFB

PDGF

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48
Q

In acute ARDS, lungs are heavy, firm, red and boggy and exhibit congestion, edema, inflammation, fibirin deposition and?

A

Diffuse aveolar damage

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49
Q

Alveolar hyaline membranes consist of fibrin-rich edema fluid mixed with cytoplasmic and lipid remnants of necrotic epithelial cells (protein rich exudate). Usually granulation tissue resolves post injury, but sometimes there is fibrotic?

A

thickening of alveolar septa

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50
Q

Edema + fibrin + cell debris =?

A

Hyaline membranes

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51
Q

When there are hyaline membranes which thicken the diffusion distance between capillaries and alveoli, there is decreased aeration causing ventilation?

A

perfusion mismatch =(decreased PaO2/FiO2)

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52
Q

ARDs has multiple stages: 1) exudative - edema. hylaline membranes, neutrophils. 2) proliferative: fibroblast proliferation, organizing pneumonia, early fibrosis 3) fibrotic: extensive fibrosis, loss of normal alveolar structure. Which stage do 40% of people with ARDS die?

A

The exudative stage

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53
Q

After fibroproliferative phase, 2 pathways may result: 1) resolution, type 2 pneumocytes restore and normal cellular struction/fucntion 2) fibrosis causing distruction/distortion of cell structure which does what to the alveoli?

A

Shrinks the alveoli (fibrosis)

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54
Q

Clinically ALI/ARDS present cyanosis, hypoxemia, respiratory failure, and the appearance of diffure bilateral infiltrates. What two sx are characteristic of ARDS/ALI?

A

Dyspnea

Tachypnea

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55
Q

To clinically diagnose ARDS is must be acute onset, bilateral infiltrates, hypoxemia and exlusion of heart failure. Pathologic diagnosis via hyaline membranes, interstitial edema and epithelial necrosis. What is the main difference between ARDS and acute interstitial pneumonia (AIP)?

A

AIP has same clinical and histological presentation except it CANNOT be attributed to a specific etiology (idiopathic)

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56
Q

What lung disease is characterized by an increase in resistance to airflow due to partial or complete obstruction at any level from the trachea and larger bronchi to the terminal and respiratory bronchioles?

A

Obstructive lung diseases

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57
Q

What lung disease is characterized by reduced expansion of lung parenchyma and decreased total lung capacity?

A

Restrictive lung disease

58
Q

Obstructive lung disease occurs during decreased flow, and have a low FEV1/FVC ratio (forced expiratory volume to forced vital capacity), have hyperexpanded lungs and dilated alveoli/air trapping. The 3 major causes includ bronchiectasis, and?

A

COPD = (Emphysema & chronic bronchitis)

Asthma

59
Q

Restrictive lung disease is volume restricted, has a normal FEV1/FVC but a reduced FVC. Scarring between alveoli and reduced lung volume can be seen. What are the 2 most common causes?

A

Pulmonary Fibrosis
Rheumatoid Arthritis
(chest wall DOs such as obesity, kyphoscoliosis)

60
Q

Obstructive pulm dz is usually caused by smoking injury. Emphysema is alveolar wall destruction/overinflation, chornic bronchitis is productive cough w airway inflammation and asthma is reversibile obstruction d/t bronchial?

A

Hyperresponsivenss triggered by allergens, infections, etc

61
Q

When comparing chronic bronchitis compared to a normal airway, one can see mucus hypersecretion, inflammation and infection. Also, smooth muscle is hyperplastic and thickened and extra goblet cells (hyperplasia) which cause?

A

theyre proliferative and increase mucus, damaging cilia and drowning under the excess mucus

(thickened SM/mucus causes shrunken dimention of airway = chronic bronchitis)

62
Q

Chronic bronchitis is diagnosed by having a persisten cough with sputum production for?

A

3 months out of 2 consecutive years

63
Q

The predominant pathophysiologic mechanism of chronic bronchitis is thick mucous gland hyperplasia leading to?

A

damage to airway epithelium

Note: reid index - measures thickness of mucous glands- not used normally

64
Q

Common complications of chronic bronchitis include bronchietasis, death from respiratory infection and most importantly?

A

squamous metaplasia causing dysplasia which can form squamous carcinoma over time

65
Q

There is marked narrowing of bronchioles caused by mucus plugging, inflammation, and fibrosis, in most severe cases there may be obliteration of the lumen d/t fibrosis known as?

A

bronchiolitis obliterans

66
Q

What is characterized by irreversible enlargement of the airspces distal to the terminal bronchiole, accompanied by destruction of their walls without obvious fibrosis?

A

Empysema

(Primary abnormality is d/t large dilated alveoli d/t duct compression) this can cause dec in gas exchange d/t dilation

67
Q

Clinical presentation of emphysema include hyperlucent airways/hyperinflation with enlarged lungs on CXR, reduced FEV1/FVC ration and what type of chest?

A

Barrel chest with increased anterior posterior dimention

68
Q

People with dilated alveoli in emphysema are typically pink puffers; older and thin with a hx of smoking, flattened diaphragm, with what other common symptoms?3

A

dyspnea
wheezing
cough
(hunched over breathing through pursed lips)

69
Q

Chronic bronchitis pts are known as blue bloaters; overweight, cyanotic, elevated hemoglobin, peripheral edema and what other common symptoms? (2)

A

Rhonchi

Wheezing

70
Q

A-1 antitrypsin is synthesized in the liver and secreted into the bloodstream to coat the lungs, to inhibit neutrophil elastase. Neutrophil elastase is produced by WBC to?

A

break down harmful bacterial and can potentially damage lungs

71
Q

If the Pi locus on chr14 is polymorphic, and you are homozygous for Z allele, there is a high chance you will be A-1 antitrypsin deficient. What occurs in this disease?

A

A1 Antitrypsin is produced in the liver but is trapped, causing liver damage, and it is not able to go to the lungs to coat them causing lung damage

72
Q

Where will most of the damage be in an emphysemic lung with AAT deficiency?

A

Basilar panacinar emphysema is seen with AAT becuase blood is pulled down by gravity

73
Q

What accelerates emphysema in patients with AAT deficiency?

A

SMOKING

74
Q

Based on the segments of the respiratory units that are involved, emphysema is classified into 4 major types: centriacinar, panacinar, paraseptal and ?

A

Irregular

75
Q

Distal acinar/ paraseptal emphysema occurs in the distal acinus in the upper half of the lungs. Contain airspaces that may form cyst like structures-blebs. It is commonly the underlying lesion in?

A

spontaneous pneumothorax in the young

76
Q

What type of emphysema is uniform destruction and enlargement of the entire acini from the respiratory bronchiole to the terminal blind alveoli?

A

Panacinar or panlobular

77
Q

Panacinar or panlobular emphysema occurs everywhere and is most severe at the base, associated with?

A

AAT deficiency

78
Q

What type of emphysema causes destruction and enlargement of the central or proximal parts of the acini, (respiratory bronchioles), sparing the DISTAL alveoli?

A

Centriacinar or centrilobular emphysema

79
Q

Centriacinar or centrilobular emphysema is predominantly in the upper lobes and apices, MC form of emphysema (95%) and is seen in?

A

HEAVY smokers with COPD

80
Q

What type of emphysema is the acinus irregular involved, with invariable scarring and clinically insignificant?

A

Irregular emphysema (localized)

81
Q

AAT def is encoded by proteinase inhibitor gene Pi on chr 14, Z allele is associated with dec circulating AAT, diagnose with serum testing of AAT, who is most likely to have it?

A

Homozygous PiZZ individuals

82
Q

Common complications of emphysema include respiratory failure, pneumothorax with lung collapse, coronary artery disease, and ?

A

right heart failure - cor pulmonale

83
Q

Microscopically, abnormally large alveoli are separated by thin septa with only focal.

A

centriacinar fibrosis

84
Q

Bronchiolitis, asthma, bronchiestasis, and chronic bronchitis are all in the bronchus while emphysema is seen in the?

A

Acinus (SMOKE)

85
Q

What is a chronic disorder of the conducting airways, usually caused by an immunological reaction, which is marked by episodic bronchoconstriction due to increased airway sensitivity to stimuli, inflammation of the bronchiole walls, and increased mucus secretion?

A

Asthma

86
Q

There are 3 main components associated with obstructive pulmonary disease - Astham, including recurrent airway obstruction with reversivle component, airway hyperresponsivness and?

A

airway inflammation

87
Q

Asthma is not associated with smoking, airway inflammation causes increased mucus, smooth muscle thickening, causing airway hyperresponsivness and obstruction leading to the?

A

clinical symptoms

88
Q

There are two types of asthma, atopic (extrinsic) and non-atopic (intrinsic). Which of the two is more common?

A

Atopic asthma

89
Q

Atopic asthma occurs in 2/3 of patients who are any age, but typically in childhood. There is a family history of astma, triggers including a variety of allergens. What type of reaction is atopic?

A

classic example of IgE-mediated type 1 hypersensitivity d/t environmental allergens (pollen)

90
Q

Elevated IgE levels as seen in atopic asthma, where you see high levels of lymphocytes, mast cells, and ?

A

eosinophils

91
Q

Non atopic asthma is less common and seen in 1/3 of patients, often older patients whose IgE levels are usually normal (t lymp, neutrophils), triggers for nonatopic include? 3

A

cold
exercise
viral resp. infection

92
Q

In atopic asthma, there is increased mucus, basement membrane, smooth muscle, glands and lamina propria which contains Mø, neutrophils, eosinophils, mast cells and lymphocytes- most importantly?

A

Th2 cells!

93
Q

A fundamental abnormality in asthma is an exaggerated Th2 response to normally harmless environmental antigens. What occurs when allergens elicit a Th2 response?

A

IL4 to make IgE from B cells, IgE antibody goes to mast cell via IgE Fc receptor, upon second encounter with allergen= mast cell degranulation & eosinophil degranulation

94
Q

Th2 leads to IL4 (IgE), IL5 (eosinophils), IL13 (stimulates bronchial submucosal glands to secerete mucous and IgE B cells to make more). The early/immediate phase is dominated by bronchoconstriction, increased mucus production and? 2

A

variable degrees of vasodilation

increased vascular permeability

95
Q

The following cause what effect of asthma?

Leukotrienes C4-D4-E4, histamine, prostaglandin D2, acetylcholine

A

Bronchoconstriction

96
Q

The following cause what effect of asthma?

mucus secretion

A

Leukotrience C4D4E4

97
Q

The following cause what effect of asthma?

increased vascular permeability

A

Leukotrienes C4D4E4

98
Q

The following cause what effect of asthma?

Recruitment of inflammatory cells

A

Interleukins

99
Q

In the late phase reaction hours later after the asthma attack, it is dominated by leukocytes (eosinophils/neotrophils) that were recruited to the site of reaction- release additional mediators to intiate late phase. Name two factors released that cause epithelium damage

A

Major basic protein

Eosinophil cationic protein

100
Q

What is a characteristic histological finding of asthma known as progressive structural changes to airways with characteristic histologic findings including: fibrosis, smooth muscle hyperplasia and increased goblet/submucosal glands?

A

Airway remodeling (may be IRREVERSIBLE) thickening of the airway wall

101
Q

Repeated bouts of asthma lead to airway remodeling causing a decreased response to what two therapeutic agents due to excessive fibrosis?

A

Bronchodilators

Corticosteroids

102
Q

In what type of asthma are patients lungs distended by overinflation and contain small areas of atelectasis?

A

Status asthmaticus (airways full of mucus)

103
Q

Status asthmaticus is unremitting and a potentially fatal asthma attack, seen with bronchial occlusion by thick mucus, and coiled mucus plugs called?

A

Curschmann Spirals - characteristic of this severe asthma

104
Q

Status asthmaticus, along with curschmann spirals, histologically has eosinophils and their breakdown product which are known as?

A

Charcot Leyden Crystals

105
Q

Atopic asthma is comprised of 3 factors: genetics, immunity, and the environment. genetics associated with season allergies and eczema- may be linked to various alleles controlling factors like adrenergic receptors, and what other 2?

A

IgE and cytokines like IL13 (strongest/most consisten association with asthma)

106
Q

The environment is an important factor in atopic asthma- it is a disease of industrialized societies (pollution/lack of allergen exposure at an early age), also if a child has an early infection then they are prone to?

A

develop asthma later on

107
Q

What type of asthma is associated with nasal polyps and recurrent rhinitis (samter’s triad)?

A

Aspirin-Sensitive Asthma (unique sensitivity, cross reacts with other NSAIDs)

108
Q

Aspirin sensitive asthma occurs when one takes aspiring, and it blocks cyclooxygenase production, shunting the main production to 5-lipoxygenase, causing an increased production in?

A

Leukotrienes C4D4E4 = Bronchospasm**

109
Q

Patients with atopic asthma are more likely to have other allergic disorders like allergic rhinitis and?

A

eczema

110
Q

What is a disease in which destruction of smooth muscle and elastic tissue by chronic necrotizing inflammatory infections leads to permanent dilation of bronchi and bronchioles?

A

Bronchiectasis

111
Q

Bronchietasis is the end stage process of many processes such as infection, obstruction, allergic bronchpulmonary aspergillosis (ABPA), chornic infection (Tb), primary ciliary dyskinesia and?

A

cystic fibrosis

112
Q

Cystic fibrosis is abnormal function or loss of epithelial chloride channel (CFTR) on chromosome 7. When someone has CF, the CFTR gene is not function leading to loss of eflux of chloride, causing what?

A

increase influx of Na/H20 leading to dehydrated, thick mucous = increased infection with S. Aureus, Haemophilus influenzae and burkolderia cepacia

113
Q

What is an AR disorder where there is dysfunction of dynein arm of microtubules, causing recurrent infections and retention of secretions?

A

Primary Ciliary Dyskinesia

114
Q

half of the patients with Primary Ciliary Dyskinesia also have Kartageners syndrome, which is characterized by sinusitis, bronchiectasis and ***?

A

situs inversus (organs do not rotate everything is on opposite side)

115
Q

Primary Ciliary Dyskinesia lack of microtubule function is vital to motlilty of various cell populations including cilia and flagella, what are flagella most needed for?

A

SPERM = male infertility

116
Q

What is an exaggerated hypersensitivity response to aspergillus infection overlying chronic lung disease?

A

Allergic bronchopulmonary aspergillosis (ABPA)

117
Q

Patients with ABPA have a background/history of asthma or cystic fibrosis and increased IgE on serum testing with a positive skin test. What can be seen histologically?

A

Thick, dark mucus in bronchi

***Fungal Hypahe acute branching which is characteristic of aspergillus (w eosinophils)

118
Q

What type of stain demostrates aggregates of fungal hyphae assoc w aspergillus?

A

Silver stain

119
Q

Obstruction and infection are the major conditions assoc with bronchiestasis. It usually affects the lower lobes bilaterally (vertical airways), most severe in the distal bronchi and?

A

bronchioles

120
Q

In bronchietasis, the airways are dilated sometimes up to four times normal size, almost to the pleural surfaces, appear cystic with filled?

A

mucopurulent secretions (may be inflam exudation in the walls, pseudostratification of columnar cells/squamous metaplasia, necrosis= abcesses)

121
Q

Bronchiectasis clincally presents as a persistent severe cough, fever orthopnea, dyspnea, cyanosis and abundant purulent sputum that is ?

A

foul smelling and bloody

122
Q

Restrictive lung disease (chronic diffuse interstitial disease) is due to chronic interstitial and infiltrative diseases such as pneumoconiosis or interstitial fibrosis and also?

A

chest wall disorders

123
Q

What was originally coined to describe the nonneoplastic lung reaction to inhalation of mineral dusts encountered in the workplace, which now also includes diseases induced by organic as well as inorganic particulates and chemical fumes and vapors?

A

Pneumoconioses

124
Q

Pneumoconioses is rxn of the lungs to inhaled mineral or organic dust, mainly seen in occupational exposure or?

A

air pollution (urban environments)

125
Q

Exaggerated response in Pneumoconioses in some individuals indicate a possible ?

A

genetic component

126
Q

Pneumoconioses is worse if exposure is high and repetitive (work), if there is impaired ciliary clearance due to smoking (inc. accumulation of dust in lungs), and the size of the particle determines?

A

how deeply into the lungs the particles go IE:
1-3um = reach alveoli
3-5um= mid respiratory tract
5-10um= upper respiratory tract

127
Q

What is a sprectrum of disease due to inhaled coal dust including anthracosis, coal macules/nodules, and progerssive massive fibrosis (most severe least common)?

A

Coal workers pneumoconiosis (most patients will not have progressive dz)

128
Q

Simple coal workers pneumoconiosis is characterized by coal macules and somewhat larger coal nodules. Concentration in the upper lobes and upper zones of lower lobes adjacent to respiratory bronchioles, give rise to what dz?

A

centrilobular emphysema

129
Q

Complicated coal workers pneumoconiosis = prodressive massive fibrosis occurs on a background of simple disease and takes years to develop with larger 1cm or greater blackened scars of dense collagen and pigment. Center of the lesion is often?

A

necrotic due to ischemia

130
Q

What disease results from inhaled silicon dioxide due to mining/quarry work or concrete repair and demolition?

A

Silicosis (takes decades)

131
Q

Silicosis has an insidious onset and can occur years after exposure is no longer present. May progress to massive pulmonary fibrosis and has a two fold risk of developing?

A

Cancer as opposed to CWP

Note: increased risk of Tb w some SOB

132
Q

Histologic hallmark lesion of silicosis is characterized by a central area of whorled, dense collagenous nodules with a more peripheral zone of dust laden macrophages, also may be calcification around the hilar lymph nodes known as?

A

eggshell calcifications (on radiographic findings)

133
Q

What is an interstitial and pleural disease resulting from inhalation of asbestos fibers?

A

Asbestosis

134
Q

Asbestosis is commonly seen in insulation workers, shipyard navy workers, paper mill workers, and oil/chemical refinery workers. It has many disease presentations including pleura: fibrosis/plaques, effusions mesothelioma, Lung: interstitial fibrosis carincoma and?

A

extrapulmonary neoplasms (lots of human disease—> laryngeal, ovarian)

135
Q

What is the more pathogenic form of asbestosis due to the tiny, straight size of the fibers that are able to enter?

A

Amphiboles (serpentine fibers less pathogenomic)

136
Q

Asbestosis is marked by diffuse pulmonary interstitial fibrosis with WHAT, which are pathognomonic, golden brown, fusiform or beaded rods-dumbell shapped-with translucent center and consist of asbestos fibers coated with iron containing proteinaceous material?

A

Asbestos bodies

137
Q

In contrast to coal workers and silicosis, asbestosis begins in the lower lungs and?

A

works its way up

138
Q

What are rare single bodies of asbestos found in healthy people?

A

ferruginous bodies

139
Q

What is the most common manifestation of asbestos exposure which are well circumscribed plaques of dense collagen often calcified, without asbestos bodies, occur with exposure?

A

Pleural plaques

140
Q

Pleural plaque formation in asbestosis, u can see hyalinized collagen histologically and what kind of drippings on the pleura?

A

Candlewax drippings (large fibrocalcific plaques on pleural surface)

141
Q

What is a fatal cancer associated with asbestos exposure occuring decades after exposure with a lifetime exposure risk as high as 10%?

A

mesothelioma (pleural)

21. CPR Exam 1 (26 decks)

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