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CPR II Exam 2 > Chapter 15: The Lung - Restrictive through Diseases of Vascular Origin > Flashcards

Chapter 15: The Lung - Restrictive through Diseases of Vascular Origin Flashcards

1
Q

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

A
  • Dyspnea and Tachypnea
  • End-respiratory crackles
  • Cyanosis (late)
  • NO wheezing
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2
Q

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

A
  • Bilateral lesions that take form of small nodules, irregular lines, or
  • Ground-glass shadows
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3
Q

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

A

Honeycomb lung

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4
Q

Which 2 chronic interstitial lung diseases are categorized as granulomatous?

A
  • Sarcoidosis
  • Hypersensitivity pneumonitis
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5
Q

What are some of the enviornmental and occupational factors which may be associated with Idiopathic Pulmonary Fibrosis?

A
  • Cigarette smoking
  • Expsoure to metal fumes and wood dust
  • Occupations such as: farming, hair-dressing, and stone-polishing
  • GERD has also been implicated
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6
Q

Loss-of-function mutations in which 2 genes has been implicated in Idiopathic Pulmonary Fibrosis?

A
  • TERT
  • TERC

*Encode components of telomerase

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7
Q

Some cases of Idiopathic Pulmonary Fibrosis are associated with a genetic variant leading to ↑ secretion of which mucin?

A

MUC5B

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8
Q

Idiopathic pulmonary fibrosis is a disease most common in which age group?

A

>50 yo

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9
Q

The histologic pattern of fibrosis seen in Idiopathic Pulmonary Fibrosis is referred to as what; can be diagnosed based on its characteristic appearance via what imaging modality?

A

- Usual interstitial pneumonia (UIP)

  • On CT
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10
Q

Microscopically, what is the hallmark of Idiopathic Pulmonary Fibrosis; there is coexistence of what?

A
  • Patchy interstitial fibrosis***, which varies in intensity and age
  • Coexistence of early (fibroblastic foci) and late (collagenous) lesions
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11
Q

In Idiopathic Pulmonary Fibrosis the formation of cystic spaces lined by hyperplastic type II pneumocytes or bronchiolar epithelium is known as what?

A

Honeycomb fibrosis

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12
Q

The earliest lesions in Idiopathic Pulmonary Fibrosis contain exuberant what?

A

Fibroblastic proliferation (fibroblastic foci)

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13
Q

Diagnosis of Idiopathic Pulmonary Fibrosis requires what?

A

Classic findings on high-resolution CT or pulmonary biopsy

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14
Q

What are the initial sx’s of Idiopathic Pulmonary Fibrosis and the later sx’s with progression?

A
  • Early —> ↑ dyspnea on exertion and dry cough
  • Later –> hypoxemia, cyanosis and clubbing
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15
Q

What is the prognosis and only definitive therapy for Idiopathic Pulmonary Fibrosis?

A
  • Median survival = 3 years after Dx
  • Lung transplantation
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16
Q

Why is it important to recognize pt’s with Nonspecific Interstitial Pneumonia?

A

Have much better prognosis than those w/ UIP

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17
Q

What is the morphology of both the cellular and fibrosing patterns of Nonspecific Interstitial Pneumonia?

A
  • Cellular = mild to moderate chronic interstitial inflammation; in UNIFORM or patchy distribution
  • Fibrosing = diffuse or patchy fibrotic lesions of roughly the SAME age
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18
Q

What is a major morphological difference between the lesions of Nonspecific Interstitial Pneumonia and Idiopathic Pulmonary Fibrosis?

A

In NSIP the lesions are at roughly SAME stage of development

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19
Q

What 4 morphologial findings are absent in Nonspecific Interstitial Pneumonia?

A
  • NO fibroblastic foci
  • NO honeycombing
  • NO hyaline membranes
  • NO granulomas
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20
Q

Which population is most likely to be affected by Nonspecific Interstitial Pneumonia?

A

Female NON-smokers in their 6th decade of life

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21
Q

What are the key features of Nonspecific Interstitial Pneumonia seen on high-resolution CT?

A

Bilateral, SYMMETRIC, predominantly lower lobe reticular opacities

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22
Q

How do patients with Cryprogenic Organizing Pneumonia present and what is seen radiographically?

A
  • Cough and dyspnea
  • Patchy SUBpleural or peribronchial areas of airspace consolidation
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23
Q

What is the hallmark histology seen with Cryprogenic Organizing Pneumonia?

A
  • Polypoid plugs of loose organizing CT (Masson bodies) within alveolar ducts, alveoli, and often bronchioles
  • “Balls of Fibroblasts”
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24
Q

Prognosis and Tx of Cryprogenic Organizing Pneumonia?

A
  • Some recover spontaneously
  • Most need oral steroids x 6 months + for complete recovery
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25
Q

Cryprogenic Organizing Pneumonia is most often caused by what?

A

As a response to infection or inflammatory injury to the lungs

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26
Q

Which 3 autoimmune/CT disease can manifest as interstital lung disease?

A
  • Rheumatoid arthritis
  • Systmic sclerosis (scleroderma)
  • SLE
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27
Q

Inhalation of particles, pneumoconiosis, stimulate what inside the lung which lead to progression of disease?

A

Resident INNATE immune cells

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28
Q

Inhalation of coal dust may be a part of what 4 diseases?

A
  • Anthracosis
  • Coal macules/nodules
  • Progressive massive fibrosis –> “Black lung”
  • Caplan syndrome
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29
Q

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

A

Engulfed by alveolar or interstitial macrophages, which then accumulate in the CT along lymphatics in lungs or in hilus

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30
Q

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

A

Upper lobes and upper zones of lower lobes

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31
Q

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

A

↑ risk of lung cancer

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32
Q

What is the most prevalent occupational disease worldwide?

A

Silicosis

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33
Q

Which race has a higher risk for Silicosis?

A

African American

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34
Q

Which form of silica (crystalline/amorphous) is the most fibrogenic?

A

Crystalline (i.e., quartz, cristobalite, and tridymite)

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35
Q

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

A
  • Particles phagocytosed by macrophages
  • Activate the inflammasome
  • Leads to release of inflammtory mediators, IL-1 and IL-18
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36
Q

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

A
  • Hilar LN’s
  • Upper zones of lungs
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37
Q

Histologically, what is the hallmark lesion seen with silicosis?

A

Central area of WHORLED COLLAGEN fibers w/ a peripheral zone of dust-laden macrophages

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38
Q

Thin sheets of calcification may occur in the LN’s of pt with silicosis and are seen radiographically as what?

A

Eggshell calcification

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39
Q

Silicosis is associated with an increased susceptibility to what infection; why?

A

TB; impaired ability of pulm. macrophages to kill phagocytosed mycobacteria

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40
Q

The onset of Silicosis may occur in what 3 ways (classification/duration)?

A
  • Slow and insidious = 10-30 yrs after exposure
  • Accelerated = within 10 yrs
  • Rapid = week to months after intense exposure to fine dust high in silica
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41
Q

Pt’s with Silicosis have double the risk for developing?

A

Lung cancer

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42
Q

Which asbestos fiber (serpentine or amphibole) is the most dangerous and pathogenic?

A

Amphibole = more aerodynamic and less soluble

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43
Q

Which property of asbestos fibers accounts for the remarkable synergy btw tobacco smoking and development of lung carcinoma in asbestos workers?

A

Toxic chemicals ca be adsorbed onto the fibers

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44
Q

Asbestosis is marked by diffuse pulmonary interstital fibrosis, indistinguishable from other causes, except for the presence of?

A

Asbestos bodies –> Golden-brown, fusiform or beaded rods

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45
Q

In asbestosis, inorganic particulates may become coated with iron-protein complexes and are called what?

A

Ferruginous bodies

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46
Q

Most common manifestation of asbestos exposure seen on the anterior and posterolateral aspects of the parietal pleura and over the dome of the diaphragm?

Known as?

A
  • Well-circumscribed plaques of dense collagen, often calcified
  • “Candlewax drippings”
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47
Q

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

A

Lower lobes and subpleurally

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48
Q

Which cytotoxic drug used in cancer therapy may lead to pulmonary damage and fibrosis?

A

Bleomycin

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49
Q

What is the most common clinical pattern/organs of involvement seen with Sarcoidosis?

A
  • Bilateral HILAR lymphadenopathy and Lung involvement
  • Eye and skin lesions are 2nd in frequency
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50
Q

What is the CD4/CD8 T-cell like in pt’s with Sarcoidosis?

A
  • CD4/CD8 T-cell ratios range from 5:1 to 15:1
  • Suggests pathogenic involvement of CD4+ helper T cells
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51
Q

Which cytokine found in the bronchoalveolar fluid of pt with Sarcoidosis is a marker of disease activity?

A

TNF

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52
Q

Pt’s with Sarcoidosis have abnormal immune responses including anergy to what?

A

Common skin test Ags such as Candida or tuberculosis PPD

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53
Q

Which 2 HLA genotypes are associated with Sarcoidosis?

A
  • HLA-A1
  • HLA-B8
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54
Q

What is the characterisic finding in the tissues of pt with Sarcoidosis?

A

Non-caseating (Non-necrotizing) granulomas composed of clustered epitheloid macrophages, often w/ giant cells

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55
Q

What are 2 characteristic morphological findings within giant cells of pt with Sarcoidosis?

A
  • Laminated concentrations of Ca2+ and proteins = Schaumann bodies
  • Stellate inclusions known as asteroid bodies
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56
Q

Why is there a high diagnostic yield of bronchoscopic biopsies for Sarcoidosis?

A

Relatively high frequency of granulomas in the bronchial submucosa

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57
Q

Which LN’s are most frequently affected by Sarcoidosis?

A

Hilar and mediastinal

58
Q

Which 3 sites other than lungs and LN’s are also commonly affected by Sarcoidosis and what is seen in each?

A
  • Spleen - may be enlarged; granulomas often form small nodules
  • Liver - may be enlarged; scattered granulomas often in portal triad
  • Bone marrow - lesions w/ tendency for phalangal bones of hands and feet; small areas of bone resorption within marrow cavity w/ widening of the bony shafts
59
Q

What 3 types of skin lesions may be encountered in Sarcoidosis?

A
  • Subcutaneous nodules
  • Erythema nodosum
  • Flat, slightly red and scaling, resembling those of SLE
60
Q

Scattered granulomas associated with Sarcoidosis may be found in the liver, most often where?

A

Portal triads

61
Q

What is the ocular involvement in some cases of Sarcoidosis?

A
  • Iritis or uveitis, either uni- or bilaterally
  • Corneal opacities, glaucoma, and total vision loss may occur
  • Often accompanied by inflammation of the lacrimal glands w/ suppression of lacrimation
62
Q

Bilateral sarcoidosis of the parotid, submaxillary, and sublingual glands constitutes a combined uveoparotid involvement designated as what?

A

Mikulicz syndrome

63
Q

Muscle involvement in Sarcoidosis may be asymptomatic, but weakness, tenderness, aches, and fatigue should prompt consideration of what?

A

Occult Sarcoid Myositis

64
Q

Majority of pt’s with Sarcoidosis will present due to what signs/sx’s?

A
  • Insidious onset of respiratory abnormalities (i.e., SOB, cough, chest pain, hemoptysis)
  • Constitutional sx’s –> fever, fatigue, weight loss, night sweats
65
Q

Elevated serum levels of what enzyme and ion may be seen in Sarcoidosis?

A
  • ↑↑↑ ACE
  • ↑ 1ᾳ-hydroxylase –> hypercalcemia
66
Q

What is the prognosis of Sarcoidosis; how does death most often occur?

A
  • 60-70% recover w/ minimal or no residual manifestations
  • 20% have permanent loss of lung function or vision
  • 10-15% die of cardiac or CNS damage
67
Q

Hypersensitivity pneumonitis primarily involves what structures in the lungs in constrast to asthma?

A
  • Alveolar walls; granulomatous rxn to inhaled Ags
  • Asthma = conducting airways
68
Q

Why is history so important in the diagnosis of Hypersensitivity Pneumonitis?

A
  • Disorders such as Pigeon breeder’s lung and Humidifier or air-conditioner lung are in this class
  • Pet birds and moldy basements are easily missed unless asked about specifically
69
Q

Presence of noncaseating granulomas in 2/3’s of pt’s with hypersensitivity pneumonitis suggests what type of hypersensitivity rxn?

A

T-cell mediated (type IV)

70
Q

Farmers lung is due to exposure to dusts generated from humid, warm, newly harvested hay that permits rapid proliferation of which spores?

A

Thermophilic actinomycetes

71
Q

The histologic changes of hypersensitivity pneumonitis are characteristically centered around which lung structures?

A

Bronchioles

72
Q

What are 3 histomorphological changes seen with hypersensitivity pneumonitis?

A
  1. Interstitial pneumonitis w/ lymphocytes, plasma cells, and macrophages
  2. Noncaseating granulomas
  3. Interstital fibrosis w/ fibroblastic foci, honeycombing, and obliterative bronchiolitis (late stages)
73
Q

How soon after exposure to antigenic dust do sx’s of hypersensitivity pneumonitis appear; last how long; what are the sign’s/sx’s?

A
  • Appear 4-6 hours after exposure; lasting 12 hours to days
  • Sx’s = recurring fever, dyspnea, cough, and leukocytosis
74
Q

What is seen on CXR of pt with hypersensitivity pneumonitis and what will PFT’s show?

A
  • CXR = micronodular interstitial infiltrates
  • PFT’s = acute restrictive disorder
75
Q

Why is it important to recognize the diseases of hypersensitivity pneumonitis as far as prognosis goes?

A
  • If unresolved —> chronic fibrotic lung disease, respiratory failure w/ dyspnea and cyanosis and a ↓ TLC and compliance
  • If exposure removed = sx’s and disease resolve
76
Q

What is the most striking morphological finding in Desquamative Interstitial Pneumonia?

A

Large # of macrophages w/ abundant cytoplasm containing dusty brown pigment (smoker’s macrophages) in the airspaces

77
Q

Some of the macrophages in desquamative interstitial pneumonia contain lamellar bodies which are what?

A

Vacuoles of surfactant from necrotic type II pneumocytes

78
Q

What is the morphology of the alveolar septa in desquamative interstitial pneumonia and they are lined by what?

A

Thickened septa lined by plump, cuboidal pneumocytes

79
Q

Desquamative interstitial pneumonia most often presents in which age group associated w/ what risk factor; what are the sign’s/sx’s?

A
  • Men or women in the 4th or 5th decade; virtually all of whom smoke
  • Insidious onset of dyspnea + dry cough over weeks to months, often with clubbing of digits = restrictive lung disease presentation
80
Q

Patients with desquamative interstitial pneumonia often have an excellent response to what; what is the prognosis like?

A
  • Steroids and cessation of smoking
  • Excellent prognosis
81
Q

Respiratory bronchiolitis-interstitial lung disease is part of a spectrum with desquamative interstitial pneumonia, except when does it present and what are the sx’s like?

A
  • Earlier presentation (3rd-4th decades)
  • Less symptomatic; still has restrictive pattern w/ similar sx’s
82
Q

Hallmark of respiratory bronchiolitis-interstitial lung disease is presence of pigmented intraluminal macrophages where?

A

First- and second-order respiratory bronchioles

83
Q

Patchy submucosal and peribronchiolar infiltrate of lymphocytes and histiocytes in a smoker is characteristic of what disease?

A

Respiratory bronchiolitis-interstitial lung disease

84
Q

Pulmonary Langerhans Cell Histiocytosis is most commonly seen in whom?

A

Young smokers; who improve after smoking cessation

85
Q

Imaging of the chest in pt w/ Pulmonary Langerhans Cell Histiocytosis will show what?

A

Cystic and nodular abnormalities

86
Q

Peripheral cysts of Pulmonary Langerhans Cell Histiocytosis may rupture and cause what?

A

Pneumothorax

87
Q

The langerhans cells of Pulmonary Langerhans Cell Histiocytosis will stain positive for what and negative for?

A
  • Positive for S100, CD1a and CD207 (langerin)
  • Negative for CD68
88
Q

In some cases of Pulmonary Langerhans Cell Histiocytosis, the Langerhans cells show neoplastic change due to activating mutation in what?

A

Serine/threonine kinase BRAF

89
Q

Major histology and cell types of Pulmonary Langerhans Cell Histiocytosis?

A
  • Eosinophils
  • Langerhans cells (immature dendritic cells)
  • Varying fibrosis and cysts
90
Q

Pulmonary Alveolar Proteinosis (PAP) is a rare disorder related to which defects?

A
  • Defects in granulocyte-macrophage CSF (GM-CSF)

or

  • Pulmonary macrophage dysfunction = accumulation of surfactant in the intra-alveolar and bronchiolar spaces
91
Q

Pulmonary Alveolar Proteinosis (PAP) is characterized by what radiologic findings?

A

Bilateral PATCHY asymmetric pulmonary opacifications

92
Q

Autoimmune Pulmonary Alveolar Proteinosis (PAP) occurs primarily in whom and is due to antibodies against what?

A
  • Primarily adults; represents 90% of PAP cases
  • Antibodies against GM-CSF
93
Q

Loss of GM-CSF signaling seen in Pulmonary Alveolar Proteinosis (PAP) causes what?

A

Blocks terminal differentiation of alveolar macrophages impairing their ability to catabolize surfactant

94
Q

Pulmonary Alveolar Proteinosis (PAP) can be treated how if autoimmune vs. secondary?

A
  • Autoimmune = SQ injections of GM-CSF
  • Secondary = Tx the underlying disorder
95
Q

Secondary Pulmonary Alveolar Proteinosis (PAP) is uncommon and associated with what other disorders?

A
  • Hematopoietic disorders
  • Malignancies
  • Immunodeficiency disorders
  • Lysinuric protein intolerance (inborn error of metabolism)
  • Acute silicosis
96
Q

Hereditary Pulmonary Alveolar Proteinosis (PAP) is extremely rare and occurs in whom?

97
Q

Pulmonary Alveolar Proteinosis (PAP) is characterized by what morphological changes within the alveoli?

A
  • Homogenous, granular precipitate containing surfactant proteins
  • Causing focal-to-confluent consolidation of large areas of the lungs w/ minimal inflammation
98
Q

What is found in the alveolar precipitate of Pulmonary Alveolar Proteinosis (PAP) and what does it stain positive for?

A
  • Cholesterol clefts and surfactant proteins
  • Stains (+) for PAS
99
Q

What is the standard of care and provides underlying benefit for pt’s with Pulmonary Alveolar Proteinosis (PAP) regardless of cause?

A

Whole-lung lavage

100
Q

How do adult pt’s with Pulmonary Alveolar Proteinosis (PAP) present (signs/sx’s)?

A

Cough + andundant sputum w/ chunks of gelatinous material

101
Q

What is the most frequently mutated gene in surfactant disorders and via what inheritance pattern?

A

Autosomal recessive disorder assoc. w/ ABCA3

102
Q

Small lamellar bodies with electron dense cores are diagnostic for which mutation causing a surfactant dysfunction disorder?

A

ABCA3 mutation

103
Q

Fractures of which bone cause a particularly high risk for PE?

A

Hip fractures

104
Q

What are some primary and secondary hypercoagulable states that are risk factors for PE?

A
  • Primary = factor V Leiden, prothrombin mutations, and antiphospholipid syndrome
  • Secondary = obesity, recent surgery, cancer, OC use, and pregnancy
105
Q

Which type of emboli are often seen in pt’s who die after chest compressions performed during CPR?

A

Small bone marrow emboli

106
Q

Indwelling central venous lines can act as a nidus for formation of what type of thrombi, with what complication?

A

Right atrial thrombi, which can embolize to lungs

107
Q

PE have what 2 deleterious pathophysiologic consequences?

A
  • Respiratory compromise due to the non-perfused, although ventilated, segment
  • Hemodynamic compromise due to ↑ resistance to pulmonary blood flow caused by the embolic obstruction
108
Q

In pt’s w/ adequate CV function, which arterial supply sustains the lung parenchyma following PE; what is seen (hemorrhage/infarction)?

A
  • Bronchial arterial supply
  • Hemorrhage may occur WITHOUT infarction
109
Q

Majority of infarcts associated w/ PE affect which lobes and occur as (single/multiple) lesions?

A
  • Lower lobes
  • Multiple lesions
110
Q

How can a PE be distinguished from a postmortem clot?

A

Presence of the lines of Zahn in the thrombus

111
Q

Infarction associated with PE is most often seen in whom?

A

Pt’s w/ inadequate CV function

112
Q

How does pulmonary infarction appear morphologically in the early stages and what is seen on the apposed pleural surface?

A
  • Hemorrhagic as raised, red-blue area
  • Pleural surface covered by fibrinous exudate
113
Q

What occurs 48 hours after pulmonary infarct and what are the morphological changes as time progresses?

A
  • Red cells begin to lyse –> infarct becomes paler and eventually red-brown as hemosiderin is produced
  • Over time, fibrous replacement begins at margins as a gray-white peripheral zone —> contracted scar
114
Q

If a pulmonary infarct is caused by an infected embolus, there may be intense neutrophilic inflammatory rxn, and these lesions are knowna as what?

A

Septic infarcts

115
Q

What is electromechanical dissociation in regards to the clinical presentation of a large pulmonary embolus?

A

ECG has a rhythm, but no pulses are palpated due to no blood entering pulmonary aterial circulation

116
Q

If pt survives after a sizable pulmonary embolus the clinical syndrome may mimic what other condition, with what associated signs/sx’s?

A
  • May mimic MI
  • Severe chest pain + dyspnea + shock
117
Q

What are the associated signs/sx’s of a pulmonary infarct?

A
  • Dyspnea
  • Tachypnea
  • Fever
  • Chest pain
  • Cough + hemoptysis
118
Q

Fibrinous pleuritis associated with pulmonary infarcts may produce what PE finding?

A

Pleural friction rub

119
Q

How soon can pulmonary infarct be seen on CXR and what is seen?

A
  • 12-36 hours
  • Wedge-shaped infiltrate
120
Q

Via which imaging modality is the diagosis of PE usually made?

A

Spiral CT angiography

121
Q

What are complications which may develop due to small pulmonary which are unresolved; greater risk for developing what?

A
  • Pulmonary HTN
  • Chronic cor pulmonale
  • Pt’s have 30% chance of suffering 2nd embolus
122
Q

Talc embolisms are common in whom?

A

IV drug users

123
Q

Pulmonary HTN is defined as mean pulmonary artery pressure ≥______mmHg at rest

A

≥25 mmHg at rest

124
Q

What are the 5 classification of pulmonary HTN as classified by the WHO?

A
  1. Pulmonary arterial HTN - primarily vascular disease
  2. 2’ to left-heart failure
  3. 2’ to chronic pulmonary parenchymal disease or hypoxemia
  4. 2’ to thromboembolic pulmonary HTN
  5. Multifactorial
125
Q

List 5 common causes of pulmonary HTN

A
  1. Chronic obstructive or interstitial lung disease (group 3)
  2. Congenital or acquired heart disease (group 2)
  3. Recurrent thromboemboli (group 4)
  4. Autoimmune disease (group 1)
  5. Obstructive sleep apnea (also group 3)
126
Q

Idiopathic pulmonary HTN has what type of inheritance pattern?

A

Autosomal Dominant w/ incomplete penetrance

127
Q

Inactivating germline mutations in which gene has been implicated in familial pulmonary HTN?

A

BMPR2 gene

128
Q

Haploinsufficiency for BMPR2 leads to what pathologic changes causing pulmonary vascular thickening and occlusion?

A

Proliferation of endothelial cells AND vascular smooth m. cells

129
Q

What are the hallmark morphological changes of pulmonary muscular and elastic arteries and right ventricle seen with all forms of pulmonary HTN (list 3)?

A
  • MEDIAL hypertrophy of the pulmonary and elastic arteries
  • Pulmonary arterial ATHEROSCLEROSIS
  • RV hypertrophy
130
Q

Which vessels are most prominently affected by pulmonary HTN and what’s seen morphologically?

A

Arterioles and small arteries = striking MEDIAL hypertrophy and INTIMAL fibrosis

131
Q

What type of lesions are small, vascular channels (tufts of capillary) that may be seen with severe, long standing pulmonary HTN?

A

Plexiform lesions

132
Q

Idiopathic pulmonary HTN is most commonly seen in whom?

A
  • Women who are 20-40 yo
  • Occasionally young children
133
Q

What is the usual cause of death that ensues within 2-5 years of symptomatic idiopathic pulmonary HTN?

A

Decompensated cor pulmonale often w/ superimposed thromboembolism and pneumonia

134
Q

In Goodpasture Syndrome autoantibodies destroy the glomerular BM in renal glomeruli and pulmonary alveoli giving rise to what disease in each system?

A
  • Rapidly progressive glomerulonephritis (RPGN)
  • Necrotizing hemorrhagic interstitial pneumonitis
135
Q

Which sex and age group is most often affected by Goodpasture Syndrome?

A

Males in the teens or 20’s; majority are active smokers

136
Q

Which 2 HLA subtypes are associated with Goopasture Syndrome?

A

HLA-DRB1*1501 and *1502

137
Q

What is the histology of the damage to alveolar walls in Goodpasture Syndrome?

A

Focal necrosis w/ hemosiderin-laden macrophages

138
Q

What is the most common cause of death in pt with Goodpasture Syndrome?

139
Q

Most cases of Idiopathic Pulmonary Hemosiderosis occur in whom and how does it present?

A
  • Most often young children; but some cases in adults
  • Insidious onset of productive cough, hemoptysis, and anemia assoc. w/ diffuse pulmonary infiltrations
140
Q

Tx for Idiopathic Pulmonary Hemosiderosis?

A

Long-term immunosuppression w/ prednison or azathioprine

141
Q

What are the diagnostically important features of Polyangiitis w/ Granulomatosis (Wegener), especially in contrast to Sarcoidosis?

A
  • Capillaritis and scattered, POORLY formed granulomas
  • Granulomas of sarcoidosis are rounded and well-defined
142
Q

Which biopsy technique may provide the only tissue necessary for diagnosis of Polyangiitis w/ Granulomatosis (Wegener)?

A

Transbronchial biopsy

CPR II Exam 2 (23 decks)

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