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Pulmonology > Gupta - Pathology/Histology > Flashcards

Gupta - Pathology/Histology Flashcards

1
Q

What is the pathogenesis of silicosis?

A
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2
Q

What are the obstructive lung diseases (4)?

A
  • Emphysema
  • Chronic bronchitis
  • Asthma
  • Bronchiectasis
  • Lung does not empty; air is trapped
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3
Q

What do you see?

A
  • Example of busulfan toxicity
    1. Mild interstitial fibrosis accompanied by:
    a. Lymphocytic inflammation and
    b. Type II pneumocyte hyperplasia (arrows)
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4
Q

What is drug/radiation pneumonitis?

A
  • A variety of drugs, especially chemotherapeutic agents, can cause pulmonary fibrosis
  • Radiation to the chest causes pulmonary fibrosis
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5
Q

What do you see here?

A
  • Liver biopsy showing pink PAS positive hyaline granules
  • Pink globules IN the cytoplasm
  • Sign of A1AT deficiency -> A1AT is a misfolded mutant protein that accumulates in the endoplasmic reticulum of the hepatocytes (and may even lead to liver cirrhosis)
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6
Q

What do you see here?

A

Barrel chest: characteristic of emphysema

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7
Q

What is this?

A
  • Gross appearance of bronchiectasis: regardless of the cause, this will be the general gross appearance
  • This case shows saccular dilation of the airways (arrows) with surrounding fibrosis
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8
Q

What are the histologic manifestations of chronic bronchitis?

A
  • Submucosal gland hypertrophy of large airways
    1. Increased Reid index (% of submucosa composed of glands)
  • Increase in goblet cells in smaller airways
  • Chronic (lymphocytic) airway inflammation (plasma cells)
    1. Acute: neutrophils
  • Peribronchial fibrosis
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9
Q

What are the arrows pointing to?

A
  • Type II pneumocytes (hobnail-shaped)
    1. Post-injury and destruction of normally abundant type I pneumocytes, type II pneumos are the main cell type involved in repair
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10
Q

What is this?

A

Normal respiratory epithelium

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11
Q

What is this?

A

Normal lung CT

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12
Q

What are the gross and microscopic findings with IPF?

A
  • Gross findings:
    1. Patchy interstitial fibrosis
    2. Predominant lower lobe subpleural distribution
  • Microscopic findings (usual interstitial pneumonia):
    1. Fibroblast foci
    2. Collagenized areas
    3. Mild lymphocytic inflammation
    4. Intervening areas of normal lung
    5. Honeycombing in advanced cases
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13
Q

What do you see here? What are each of the arrows pointing to?

A
  • Fetal lungs: look VERY DIFFERENT
    1. Sacculation
    2. Bronchi
    3. Pulmonary artery
  • Saccular stage is where the transition starts to begin making surfactant (26-32 weeks) -> the one to KNOW
  • Branching tubes from the foregut give rise to the trachea, bronchi and bronchioles
  • Alveoli start to differentiate around 7 months, and there are 3 stages:
    1. Glandular – thick walls, lots of interlobular and intralobular CT and a cuboidal epithelium
    2. Saccular stage (26-32 weeks) – transition to flat, type 1 alveolar cells and type 2 cells (surfactant!!)
    3. Alveolar stage – reduction of interstitial tissues and increasing capillaries
  • At birth, the lungs are not histologically “mature” -> this happens around age 8
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14
Q

What is this?

A
  • Paraseptal emphysema (exact cause unknown)
  • Distal acini adjacent to interlobular septa and pleura affected
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15
Q

What are pneumoconioses? What are the 4 types?

A
  • Non–neoplastic lung reaction to inhaled dusts (chronic exposure)
  • Mineral dusts:
    1. Coal
    2. Silica
    3. Asbestos
    4. Berylliosis
  • Others: chemical fumes/vapors
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16
Q

What is chronic bronchitis? How is it defined?

A
  • Defined clinically -> persistent cough with sputum at least 3 months in at least 2 consecutive years
  • Inhaled substances such as tobacco smoke cause chronic irritation resulting in mucous hypersecretion
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17
Q

What is this?

A
  • Giant cell inclusions -> asteroid bodies
    1. Not specific for sarcoidosis, and can occur in other granulomatous diseases
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18
Q

What is centriacinar emphysema? What is is characteristic of?

A
  • Affects central portion of acinus while sparing distal alveoli
  • Characteristic of the emphysema associated w/heavy smoking (upper lobes)
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19
Q

What is this?

A
  • Hypersensitivity pneumonitis
    1. Plug of organizing pneumonia with accompanying lymphocytic inflammation
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20
Q

What is this arrow pointing at?

A

Ciliated cells

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21
Q

What are the causes of hypersensitivity pneumonitis?

A
  • Thermophilic bacterial Ags
    1. Farmer’s lung
    2. Mushroom worker’s lung
    3. Humidifier lung
    4. Hot tub lung
  • Animal proteins
    1. Bird fancier’s lung
    2. Mollusk shell HP
  • Fungal Ags
    1. Malt worker’s lung
    2. Cheese washer’s lung
    3. Paprika splitter’s lung
    4. Maple bark stripper’s lung
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22
Q

What is simple CWP?

A
  • Little/no pulmonary dysfunction
  • Upper lobe predominant
  • Coal dust macules (1 – 2 mm diameter)
    1. Accumulation of dust adjacent to respiratory bronchioles ± dilated adjacent alveoli (localized emphysema)
  • Coal dust nodules (0.3 – 1 cm diameter)
    1. Carbon-laden macrophages with collagen
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23
Q

What diseases other than IPF can show UIP histologically? How does this affect IPF diagnosis?

A
  • Collagen vascular disease- associated frequently show UIP histologically (see attached image):
    1. Rheumatoid arthritis, scleroderma, mixed connective tissue disease, and others
  • Because UIP can occur in diseases other than IPF, the diagnosis of IPF is one of exclusion
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24
Q

What is atelectasis? What are the 3 types, and what causes them?

A
  • Collapse of previously inflated lung resulting in relatively airless pulmonary parenchyma -> loss of lung volume caused by inadequate expansion of air spaces
    1. Resorption: obstruction, i.e. mucus (postoperatively, asthma, bronchiectasis, chronic bronchitis, tumor, foreign body aspiration)
    2. Compression: accumulated fluid in pleural cavity, i.e., pleural effusion in CHF, pneumothorax, or elevated diaphragm in pregnancy or ascites
    3. Contraction: fibrotic changes
  • Need to know what kind of a mediastinal shift you are going to get, and what causes it
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25
Q

What is this?

A
  • Complicated CWP
  • “Black lung”
  • Whole mount thin slice of lung shows pigmented areas of progressive massive fibrosis in the upper lobe (arrows)
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26
Q

What is a T-E fistula? Which one is the most common? What are some acquired causes?

A
  • Failure of the fetal respiratory tract to separate from the GI tract (ventral wall of the foregut) from which it derives can result in tracheoesophageal fistula
    1. Branching tubes from the foregut give rise to the trachea, bronchi and bronchioles
  • Rare, but most common is fistula between lower part of the esophagus and the trachea (top of esophagus ends in a pouch)
  • Acquired causes of TE fistula:
    1. Esophageal tumor -> cancer that starts to erode into the trachea
    2. Surgery (tracheostomies and NG tubes)
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27
Q

What do you see here?

A
  • Idiopathic pulmonary fibrosis
  • Subpleural, net-like reticulations
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28
Q

What is this?

A
  • Microscopic appearance of bronchiectasis
  • Airway dilation (arrow) accompanied by surrounding fibrosis and luminal pus
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29
Q

What do you see here? Which one is more pathogenic?

A
  • EM appearance of asbestos
  • Among this gp of fiber-forming silicates, types of asbestos that form curly flexible fibers (left) are more easily ingested by macros, and less pathogenic than those that form straight, stiff fibers (right)
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30
Q

What is this?

A
  • Microscopic appearance of chronic bronchitis
  • Lymphocytes (arrow) surround the bronchial epithelium
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31
Q

Normal respiratory epithelium. Appreciate it.

A

Good job!

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32
Q

What is rhinitis?

A
  • Inflammation of the nasal mucosa
  • Most commonly attributed to Rhinovirus
  • Presents as common cold
  • Repeat bouts can create nasal polyps (edema, inflam)
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33
Q

What are these?

A
  • Asbestos bodies
  • In addition to macrophage ingestion, the body tries to destroy asbestos fibers by coating them with iron–containing proteinaceous material
    1. Results in golden brown beaded rods with translucent fiber cores (arrows)
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34
Q

What do you see here?

A
  • Micro appearance of UIP -> severely affected areas show:
    1. Densely collagenized fibrosis (arrows) and
    2. Honeycomb cysts lined by metaplastic bronchiolar epithelium (asterkisks)
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35
Q

What are the 3 types of emphysema?

A
  • Centriacinar: associated with heavy smoking, and predominantly in the upper lobes
  • Panacinar: whole acinus, not necessarily the whole lung
    1. Associated with α1-antitrypsin deficiency (can’t get out of the liver to go to the lung and protect it)
    2. Predominantly lower lung zones
  • Paraseptal: on the pleura of the lung
    1. Probably underlies spontaneous pneumothorax in young adults
    2. –Kind of young male who is very tall and thin and comes in with a pneumothorax; get bullous lesions on the edge of the lung that rupture
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36
Q

What is A1AT deficiency?

A
  • Rare cause of emphysema – causes panacinar
  • Liver cirrhosis may also be present
  • A1AT is a misfolded mutant protein that accumulates in the endoplasmic reticulum (ER) of the hepatocytes
  • Genetics: PiM is the normal allele; two copies normally expressed (PiMM)
    1. PiZ and PiS is the most common clinically relevant mutations
    2. PiMZ heterozygotes have low levels of circulating A1AT; usually ok unless they smoke
    3. PiZZ homozygotes are at risk for panacinar emphysema and liver cirrhosis
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37
Q

What type of atelectasis do you see here?

A
  • Compression pneumothorax
  • Left pneumothorax from chest wall trauma resulting in left lung collapse and rightward mediastinal shift
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38
Q

What is asthma? What are the 2 types?

A
  • Chronic inflammatory disorder of the airways
  • Increased airway responsiveness to a variety of stimuli
    1. Extrinsic: type I hypersensitivity reaction to inhaled allergen
    2. Intrinsic: non-immunologic reaction (precipitated by respiratory infection, stress, exercise, cold, drugs like aspirin, etc.)
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39
Q

What is hypersensitivity pneumonitis?

A
  • Immunologically mediated lung disorder due to prolonged exposure to inhaled organic dusts
  • Affected individuals abnormally sensitized to antigen in inhaled dust
  • Chronic form is a type IV (delayed type) hypersensitivity response
  • Progression to fibrosis prevented by removal of environmental antigen
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40
Q

What is the arrow on the left pointing to? What about those on the right?

A
  • Ciliated cells on the left
  • Club/clara cells on the right
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41
Q

What is this?

A
  • Honeycomb lung (via hypersensitivity pneumonitis)
    1. Can be caused by persistent exposure to a triggering environmental antigen
    2. Represents the end stage of a variety of chronic interstitial fibrosing lung diseases
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42
Q

What is silicosis?

A
  • Caused by inhalation of SiO2 (silica)
  • Sandblasters, mine workers, stone cutters: decades of exposure -> progressive nodular fibrosis
  • Predominantly upper lobes and hilar nodes
  • Silica ingestion by macros causes release of fibrogenic mediators, resulting in hard collagenous nodules
  • Polarizing microscopy demonstrates birefringent silica particles
  • INC TB susceptibility likely related to impaired macrophage function
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43
Q

What do you see here?

A
  • Gross appearance of paraseptal emphysema
  • Markedly enlarged subpleural airspaces, known as bullae (arrow) are prone to rupture -> can result in pneumothorax
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44
Q

What is this?

A
  • Microscopic appearance of panacinar emphysema
  • Relatively uniform dilation of all parts of the acini
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45
Q

What is complicated CWP?

A
  • Aka, progressive massive fibrosis
    1. Lung function compromised
    2. Develops in background of simple CWP over many years -> progression from simple to complicated not well understood
    4. Black scars composed of pigment and dense collagen
    5. Associated with rheumatoid arthritis
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46
Q

What is the Reid index?

A
  • Ratio of the thickness of the mucous gland layer to the thickness the thickness of the wall between the epithelial basement membrane and cartilage (normal = 0.4) is increased in chronic bronchitis
  • Serous (for humidification) and mucinous (to prevent infection) glands
  • Anything above 50% counts as an elevated Reid Index
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47
Q

What do you see here?

A
  • Microscopic appearance of asthma
  • Asthmatic mucous often has Charcot-Leyden crystals (arrow) formed from the disintegration of eosinophils
    1. From major basic protein of eosinophils (if there are enough eosinophils, there will be charcot-leyden crystals)
  • Mostly going to see these in chronic allergic rhinitis
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48
Q

What is this?

A
  • Hypersensitivity pneumonitis
  • Lymphocytic interstitial inflammation and fibrosis centered on a bronchiole (arrow)
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49
Q

What do you see here?

A
  • Microscopic appearance of IPF -> manifests histologically as usual interstitial pneumonia (UIP)
  • Features patchy interstitial fibrosis (arrows) that is most severe subpleurally
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50
Q

What is this?

A
  • Microscopic appearance of paraseptal empysema
  • Distal airspaces (arrow) immediately beneath the pleural show marked dilation – cause unknown
  • Histologically, the location is going to be the most helpful
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51
Q

What is parenchymal interstitial fibrosis (asbestosis)?

A
  • A non-neoplastic asbestos-related diseases
  • Slowly progressive dyspnea
  • Usually requires heavy prolonged asbestos exposure
  • Latency period typically 20 + years
  • Injury initially to respiratory bronchioles and alveolar ducts
  • In attempting to ingest and clear fibers, macrophages release fibrogenic mediators -> results in fibrosis of adjacent alveoli
52
Q

What are chronic interstitial/restrictive lung diseases?

A
  • Heterogeneous group of diseases characterized by dyspnea and reduced total lung capacity (TLC)
  • Interstitium often involved
  • Disease progression results in diffuse scarring (end-stage honeycomb lung)
53
Q

What are these?

A
  • Asbestos bodies
  • Easier to detect w/a histochemical stain for iron (Prussian blue), which stains the iron–rich coating on the asbestos fibers blue (arrow)
54
Q

What do you see?

A

Usual interstitial pneumonia (UIP)

55
Q

What is this cell?

A

Macrophage

56
Q

What do you think is going on here?

A

Occupational lung disease (pneumoconiosis)

57
Q

What is the triad of aspirin-intolerant asthma?

A
  • Seen in 10% of asthmatic adults
    1. Asthma
    2. Aspirin induced bronchospasm
    3. Nasal polyps
58
Q

What are the 3 types of CWP?

A
  • Coal Workers Pneumoconiosis (CWP
    1. Anthracosis: innocuous inhaled carbonaceous pigment engulfed by macros that accumulates in CT along lymphatics and in lymphoid tissue
    2. Simple CWP
    3. Complicated CWP (progressive massive fibrosis)
59
Q

What part of the lung is the dependent region?

A
  • Lowest part of the lung in relation to gravity
  • In this region, smaller volumes mean the alveoli are more compliant (distensible), and capable of wider O2 exchanges with the external environment
60
Q

What is this?

A

Cryptogenic organizing pneumonia

61
Q

What is this?

A
  • Micro appearance of usual interstitial pneumonia (UIP)
  • Fibroblast foci: localized areas of fibroblastic proliferation (arrows on the right) -> believed to be sites of recent injury
  • Arrow on the left is pointing at lymphocytes
62
Q

What is the pathogenesis of CWP (image)?

A
63
Q

What is this?

A
  • Organizing pneumonia following acute respiratory distress syndrome (ARDS)
  • Alveolar duct plugging by loose fibro-connective tissue (arrows) is similar to histologic appearance of COP, making clinical input essential
64
Q

What are these arrows pointing at? What is the difference b/t the pt on the left and that on the right?

A
  • Alveolar macros: ingest and destroy 1–5 µm particles that reach the alveoli
  • As compared to a non–smoker (left), note the number of ingested particles in a crack cocaine user (right)
  • Can be along the alveoli, but are often in the middle
65
Q

What is the difference between these CXR’s?

A
  • Normal on the left -> loss of elastic recoil in centriacinar emphysema on the right
    1. Manifests as hyperinflation -> over 11 posterior ribs are seen, the diaphragms are flattened and there is enlargement of the retrosternal airspace
66
Q

What do you see here?

A
  • Asbestos-related disease
  • Circumscribed plaques of dense collagen (arrows) most often arise on the parietal pleura and diaphragmatic domes
67
Q

What kind of cells do you see here? What is inside of them?

A

Club/clara cells -> vacuoles inside

68
Q

What do you see here?

A
  • Gross appearance of bronchiectasis
  • Cylindrically dilated airways (arrows) extend almost to the pleura
69
Q

What are the gross and microscopic features of asthma?

A
  • Gross features:
    1. Overinflation
    2. Mucous plugs (increased goblet cells and mucin)
  • Microscopic features:
    1. Thickened basement membrane
    2. Submucosal gland hypertrophy
    3. Bronchial wall smooth muscle hypertrophy
    4. Eosinophil–rich inflammatory infiltrate
70
Q

What is the pathogenesis of asbestosis?

A
71
Q

What do you see?

A
  • Sarcoidosis
    1. Granulomas (arrow) surrounding a bronchiole
72
Q

What type of atelectasis do you see here?

A
  • Resorption atelectasis
  • Tumor obstructing the R mainstem bronchus has resulted in markedly reduced right lung volume and rightward mediastinal shift
73
Q

What do you see here?

A
  • Microscopic appearance of chronic bronchitis
  • Goblet cells (arrows) are markedly increased in this small bronchus
74
Q

What are the causes, mechs, and shifts associated with the 3 different types of atelectasis (table)?

A
75
Q

What do you see here?

A
  • Gross appearance of panacinar emphysema
  • In this thin slide whole mount section tissue destruction with airspace dilation is most severe in the lower lobe
  • If a smoker comes in with panacinar emphysema -> what are you going to ask? Family history?
76
Q

What is this?

A
  • Angiofibroma:
    1. Benign tumor of the nasal mucosa composed of large blood vessels and fibrous tissue
    2. Presents with profuse epistaxis (nose bleeds)
77
Q

What do you see here?

A
  • Simple coal workers pneumoconiosis
  • Coal dust macule (arrow; 1-2 mm diameter) with dilated adjacent airspaces (localized emphysema)
78
Q

What is this?

A
  • Cryptogenic organizing pneumonia (micro appearance)
  • Intra-alveolar plugs of loose fibro-connective tissue (arrows)
79
Q

What are some non-neoplastic asbestos-related disorders?

A
  • Diffuse pleural fibrosis
  • Benign pleural effusions
  • Pleural plaques
  • Parenchymal interstitial fibrosis (asbestosis)
80
Q

What are these arrows pointing at?

A

Club (clara) cells

81
Q

What is this?

A
  • Gross appearance of centriacinar emphysema (upper lobes of the lung)
  • Enlarged airspaces with tissue destruction is evident, particularly at the apex (arrow)
82
Q

How does extrinsic asthma work?

A
  • Type 1 hypersensitivity is beginning w/subsequent re-exposure leading to IgE-mediated activation of mast cells
    1. Inflammation damages and perpetuates bronchoconstriction
  • Parents probably have asthma (underlying genetic cause); have it when they’re younger, it goes away as they go through adolescence, then comes back with older age
  • Gets worse each time because it is happens faster
83
Q

What do you see here?

A
  • Hypersensitivity pneumonitis
  • Ill–defined granuloma composed of a few giant cells and histiocytes (arrow) surrounded by lymphocytes
84
Q

What is this?

A
  • Birefringent silica particles under polarized light
  • Silicosis (pneumoconiosis)
85
Q

What is this?

A
  • Sarcoidosis granulomas:
    1. Composed of epithelioid histiocytes and giant cells (arrows)
    2. Typically well-formed and non-necrotizing
86
Q

What do you see here? Star? Arrow?

A
  • Allergic rhinitis: type I hypersensitivity (associated with asthma and eczema)
  • Star = inflammatory infiltrate
  • Arrow = Charcot-Leyden crystals
87
Q

What is this?

A

Panacinar emphysema -> characteristic of A1AT deficiency (entire acinus affected)

88
Q

What do you see here?

A
  • Angiofibroma:
    1. Benign tumor of the nasal mucosa composed of large blood vessels and fibrous tissue
    2. Presents with profuse epistaxis (nose bleeds)
89
Q

What are the 2 primary mechanisms of increased resistance to air flow in obstructive disease?

A
  • Loss of elastic recoil in the lung: emphysema
  • Airway obstruction/narrowing: asthma, bronchiectasis, chronic bronchitis
90
Q

What is the pulmonary interstitium composed of?

A
  • BM of endo and epi cells, collagen fibers, elastic tissue, and fibroblasts
91
Q

What do you see here? What might cause it?

A
  • Nasal polyp with stromal edema (S) and scattered inflammatory cells (mostly eosinophils- Eo)
    1. E= respiratory epithelium
  • Edematous, inflamed nasal mucosa
  • Causes: repeat bouts of rhinitis, cystic fibrosis, and aspirin-intolerant asthma (asthma + aspirin induced bronchospasm + nasal polyps -> seen in 10% of asthmatic adults)
92
Q

What is the normal structure of an acinus?

A
  • The acinus is comprised of the structures distal to a terminal bronchiole (between dashed red lines) -> respiratory bronchiole, alveolar ducts and sacs
93
Q

What are the 2 categories of intersitital/restrictive diseases? Provide examples (4 & 2).

A
  • Fibrosing:
    1. Idiopathic pulmonary fibrosis
    2. Collagen vascular disease-associated
    3. Pneumoconioses
    4. Drug/radiation pneumonitis
  • Granulomatous:
    1. Sarcoidosis
    2. Hypersensitivity pneumonitis
94
Q

What is the pathogenesis of hypersensitivity pneumonitis (image)?

A
  1. Antigen
  2. Inhalation of organic dust antigen
  3. Ag binds pre-existing ab’s in alveoli OR phagocytosis of Ag by alveolar macros
  4. 4-6 hrs complement fixation and neutrophil exudation (edema -> ACUTE HP)

OR

interstitial lympho infiltrate and granulomas (CHRONIC HP)

95
Q

What is this?

A
  • Microscopic appearance of asthma
  • Epithelial basement membrane thickening (arrow) with eosinophilic inflammation (asterisk)
  • Allergic rhinitis and nasal polyps possible
  • Recurrent mucous plugging can also cause bronchiectasis
96
Q

What do you see?

A
  • Laminated calcified concretions -> Schaumann bodies
    1. Not specific for sarcoidosis and can occur in others granulomatous diseases
97
Q

What is this?

A

Type II pneumocyte hyperplasia after alveolar injury

98
Q

What is bronchiectasis?

A
  • Permanent airway dilation associated with smooth muscle and elastic tissue destruction
  • Repeated cycles of airway obstruction and inflammation lead to fibrosis of airway walls
99
Q

What is this?

A
  • Sarcoidosis granulomas (arrows):
    1. Tend to be distributed along the bronchovascular bundles and interlobular septa
100
Q

What are the causes of bronchiectasis?

A
  • Congenital/hereditary conditions
    1. Cystic fibrosis: chloride transport defect leads to thick, obstructive secretions
    2. –Immotile cilia syndromes (Kartagener): interferes with bacteria clearance (dynein arm defect; sperm don’t work well either)
  • Necrotizing pneumonia (e.g. Mycobacteria, Staph)
  • Bronchial obstruction (e.g. tumors, foreign bodies)
    1. A lot of these things boil down to obstruction (mucous, tumors, dead cells from necrosis)
  • Increased mucous can lead to increased risk of infection
101
Q

What is emphysema?

A
  • Abnormal permanent enlargement of airspaces accompanied by destruction of their walls -> imbalance between proteases and anti-proteases
    1. A1AT should neutralize proteases release by inflammatory cells
    2. Excessive inflammation or absent/inactive A1AT leads to destruction of elastic tissue
  • Fibrosis is not a significant feature
  • Classified according to portion of acinus affected
102
Q

What do you see here?

A
  • Gross appearance of asthma
  • Mucous plug (arrow) within a bronchus
103
Q

What do you see here?

A

Normal alveoli

104
Q

What is beryllium pneumoconiosis?

A
  • Beryllium miners and workers in the space industry
  • Non-caseating granulomas in the lung, hilar lymphnodes and systemic organs
  • Increased risk of lung cancer
105
Q

What do you see here?

A
  • Microscopic appearance of chronic bronchitis
  • Submucosal gland (arrow) hypertrophy (>40% of wall)
106
Q

What is the major cytokine involved in the pathogenesis of IPF?

A

TGF-beta from injured pneumocytes: induces fibrosis

107
Q

What do you see here?

A
  • Pattern of diffuse interstitial fibrosis in asbestosis
    1. Similar to UIP, but distinguishable by the presence of asbestos bodies (depicted in high magnification inset on right)
108
Q

What are these?

A
  • Micro appearance of asthma
  • Asthmatic mucous sometimes forms tight coils known as Curschmann spirals (arrows)
  • You can also get these in cervical specimens
109
Q

What is sarcoidosis? How would you diagnose it?

A
  • Systemic disease of unknown cause characterized by non-necrotizing granulomatous inflammation
    1. Commonly affects hilar lymph nodes, lungs, skin
    2. Insidious onset of shortness of breath, cough, and/or constitutional symptoms
    3. Unpredictable course; usually responds to steroids
  • Cell–mediated response to as yet unidentified antigen
  • BAL fluid shows increased CD4:CD8 ratio (> 2.5) due to increase in CD4+ (helper) T-lymphocytes
  • Must exclude other causes of granulomatous inflam, esp mycobacterial and fungal infections
  • Incidence varies geographically and by gender
110
Q

What is this?

A
  • Idiopathic pulmonary fibrosis
  • Patchy interstitial fibrosis (white arrow) that is most severe subpleurally
  • Orange arrow: intervening normal tissue
111
Q

What are the micro findings with hypersensitivity pneumonitis?

A
  • Airway-centered interstitial lymphocytic inflammation
  • Loosely formed, ill-defined granulomas
  • Interstitial fibrosis and organizing pneumonia
  • Eosinophils are not a feature
112
Q

What is COP?

A
  • Cryptogenic organizing pneumonia: intra-alveolar rather than interstitial process
    1. Polypoid plugs of loose organizing connective tissue in bronchioles, alveolar ducts, and alveoli
    2. Organizing connective tissue all of same age and underlying architecture preserved
  • Steroid-responsive
  • Similar histologic pattern seen in resolving acute lung injury (ALI)/infection, distal to obstruction (see attached image)
113
Q

What is IPF? How does it prevent? Tx?

A
  • Idiopathic pulmonary fibrosis: repeated cycles of injury by as yet unidentified agent, resulting in diffuse fibrosis
  • Presents insidiously as dyspnea on exertion and dry cough with gradually deteriorating course
    1. Must rule out secondary causes of fibrosis like drugs and radiation
  • No current effective medical treatment
114
Q

What do you see here?

A
  • Microscopic appearance of centriacinar emphysema
  • Central portion of acinus (arrows) has abnormally large airspaces with club–shaped alveolar septa that appear to be “free floating”
115
Q

What are these arrows pointing at?

A
  • EM: surfactant–containing lamellar bodies (in a type II pneumocyte)
116
Q

What do you see?

A
  • Silicosis (pneumoconiosis)
  • Dense collagenized nodule (arrow) with surrounding lymphocytes
117
Q

What do you see here?

A

Hemosiderin-laden macrophages

118
Q

What is Virchow’s triangle?

A
  • Stasis
  • Endothelial damage
  • Hypercoagulable state
119
Q

What is a PE? Epi?

A
  • Blood clots in the pulmonary arteries are almost always emboli (50,000 deaths/year in U.S.)
  • Usual source is deep leg vein thrombi (DVT)
  • Usually a complication of underlying disorder
    1. Immobilization
    2. Hypercoagulable states
  • Most of these will not be of clinical consequence
  • If you are on birth control pills, don’t smoke
120
Q

What % of PE’s cause infarction? Why?

A
  • Only 10%
  • Consequences depend on size of embolus and status of circulation
    1. Adequate CV func: bronchial arterial supply sufficient to sustain lung tissue distal to small peripheral emboli
    2. Inadequate pulmonary circulation: due to underlying cardiac or pulmonary disease results in infarction -> typically hemorrhagic due to dual circulation of the lung
121
Q

What is this?

A
  • Gross appearance of a saddle PE
  • A large pulmonary embolus (arrow) that lodges at the bifurcation of the pulmonary arteries can result in sudden death due to acute cor pulmonale
  • Post-mortem vs. actual emboli: post-mortem has a lot of fat (chicken fat), whereas real clot more fibrous (white)
  • Lines of Zahn
122
Q

What do you see here?

A
  • Gross PE with early infarction
  • Bronchial arterial circulation was insufficient to sustain lung tissue distal to these small pulmonary emboli (arrow), resulting in a wedge–shaped hemorrhagic infarct (line)
    1. Wedge-shaped infarct due to tree-like branching of the vessels
123
Q

What is this?

A
  • Micro PE w/early infarction
  • Infarcted lung tissue distal to a pulmonary embolus shows alveolar hemorrhage (arrow) and coagulative necrosis of the alveolar septa (asterisk)
    1. Any blue is just remains -> not live cells anymore (lymphos)
124
Q

What do you see here?

A
  • Resolving pulmonary infarction; gross appearance
  • After 48 hours, infarcted lung tissue begins organizing and becomes a paler red–brown (arrows) due to the conversion of hemorrhage into hemosiderin by macrophages and will eventually form a contracted scar
  • Macros have come in to break down the RBC’s
125
Q

What is this?

A
  • Non-thrombotic PE, micro appearance
  • Non-thrombotic sources of PE include:
    1. Air
    2. Bone marrow
    4. Fat (long-bone fractures)
    5. Amniotic fluid, and
    6. Foreign material, as in this example resulting from illicit intravenous drug use in which cellulose plugs a small artery (arrow)
126
Q

Describe the path of blood through the pulmonary/CV circuit.

A
  • Deoxygenated blood is transported to the lung by the pulmonary arteries and oxygenated blood returns to the heart via the pulmonary veins
  • See attached image

Pulmonology (18 decks)

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