Gupta - Pathology/Histology Flashcards
(126 cards)
1
Q
What is the pathogenesis of silicosis?
A
2
Q
What are the obstructive lung diseases (4)?
A
- Emphysema
- Chronic bronchitis
- Asthma
- Bronchiectasis
- Lung does not empty; air is trapped
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)
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
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)
6
Q
What do you see here?
A
Barrel chest: characteristic of emphysema
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
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
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
10
Q
What is this?
A
Normal respiratory epithelium
11
Q
What is this?
A
Normal lung CT
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
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
14
Q
What is this?
A
- Paraseptal emphysema (exact cause unknown)
- Distal acini adjacent to interlobular septa and pleura affected
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
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
17
Q
What is this?
A
- Giant cell inclusions -> asteroid bodies
1. Not specific for sarcoidosis, and can occur in other granulomatous diseases
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)
19
Q
What is this?
A
-
Hypersensitivity pneumonitis
1. Plug of organizing pneumonia with accompanying lymphocytic inflammation
20
Q
What is this arrow pointing at?
A
Ciliated cells
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
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
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
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
25
What is this?
- Complicated CWP
- "Black lung”
- Whole mount thin slice of lung shows pigmented areas of progressive massive fibrosis in the upper lobe (arrows)
26
What is a T-E fistula? Which one is the most common? What are some acquired causes?
- 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)
27
What do you see here?
- Idiopathic pulmonary fibrosis
- Subpleural, net-like reticulations
28
What is this?
- Microscopic appearance of _bronchiectasis_
- Airway dilation (arrow) accompanied by surrounding fibrosis and luminal pus
29
What do you see here? Which one is more pathogenic?
- 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)
30
What is this?
- Microscopic appearance of chronic bronchitis
- Lymphocytes (arrow) surround the bronchial epithelium
31
Normal respiratory epithelium. Appreciate it.
Good job!
32
What is rhinitis?
- Inflammation of the nasal mucosa
- Most commonly attributed to Rhinovirus
- Presents as common cold
- Repeat bouts can create nasal polyps (edema, inflam)
33
What are these?
- _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)
34
What do you see here?
- Micro appearance of **UIP** -\> severely affected areas show:
1. Densely collagenized fibrosis (arrows) and
2. Honeycomb cysts lined by metaplastic bronchiolar epithelium (asterkisks)
35
What are the 3 types of emphysema?
- _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
36
What is A1AT deficiency?
- 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_
37
What type of atelectasis do you see here?
- _Compression pneumothorax_
- Left pneumothorax from chest wall trauma resulting in left lung collapse and rightward mediastinal shift
38
What is asthma? What are the 2 types?
- 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.)
39
What is hypersensitivity pneumonitis?
- 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
40
What is the arrow on the left pointing to? What about those on the right?
- Ciliated cells on the left
- Club/clara cells on the right
41
What is this?
- _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
42
What is silicosis?
- 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
43
What do you see here?
- Gross appearance of _paraseptal emphysema_
- Markedly enlarged subpleural airspaces, known as _bullae_ (arrow) are prone to rupture -\> can result in pneumothorax
44
What is this?
- Microscopic appearance of panacinar emphysema
- Relatively uniform dilation of all parts of the acini
45
What is complicated CWP?
- Aka, **p****rogressive 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_
46
What is the Reid index?
- 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_
47
What do you see here?
- 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_
48
What is this?
- _Hypersensitivity pneumonitis_
- Lymphocytic interstitial inflammation and fibrosis centered on a bronchiole (arrow)
49
What do you see here?
- Microscopic appearance of IPF -\> manifests histologically as usual interstitial pneumonia (UIP)
- Features patchy interstitial fibrosis (arrows) that is most severe subpleurally
50
What is this?
- 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_
51
What is parenchymal interstitial fibrosis (asbestosis)?
- 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
What are chronic interstitial/restrictive lung diseases?
- 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
What are these?
- _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
What do you see?
Usual interstitial pneumonia (UIP)
55
What is this cell?
Macrophage
56
What do you think is going on here?
Occupational lung disease (pneumoconiosis)
57
What is the triad of aspirin-intolerant asthma?
- Seen in 10% of asthmatic adults
1. Asthma
2. Aspirin induced bronchospasm
3. Nasal polyps
58
What are the 3 types of CWP?
- _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
What part of the lung is the dependent region?
- 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
What is this?
Cryptogenic organizing pneumonia
61
What is this?
- 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
What is the pathogenesis of CWP (image)?
63
What is this?
- _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
What are these arrows pointing at? What is the difference b/t the pt on the left and that on the right?
- _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
What is the difference between these CXR's?
- 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
What do you see here?
- Asbestos-related disease
- Circumscribed plaques of dense collagen (arrows) most often arise on the parietal pleura and diaphragmatic domes
67
What kind of cells do you see here? What is inside of them?
Club/clara cells -\> vacuoles inside
68
What do you see here?
- Gross appearance of _bronchiectasis_
- Cylindrically dilated airways (arrows) extend almost to the pleura
69
What are the gross and microscopic features of asthma?
- _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
What is the pathogenesis of asbestosis?
71
What do you see?
- _Sarcoidosis_
1. Granulomas (arrow) surrounding a bronchiole
72
What type of atelectasis do you see here?
- _Resorption atelectasis_
- Tumor obstructing the R mainstem bronchus has resulted in markedly reduced right lung volume and rightward mediastinal shift
73
What do you see here?
- Microscopic appearance of chronic bronchitis
- Goblet cells (arrows) are markedly increased in this small bronchus
74
What are the causes, mechs, and shifts associated with the 3 different types of atelectasis (table)?
75
What do you see here?
- 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
What is this?
- _Angiofibroma_:
1. Benign tumor of the nasal mucosa composed of large blood vessels and fibrous tissue
2. Presents with profuse epistaxis (nose bleeds)
77
What do you see here?
- _Simple coal workers pneumoconiosis_
- Coal dust macule (arrow; 1-2 mm diameter) with dilated adjacent airspaces (localized emphysema)
78
What is this?
- _Cryptogenic organizing pneumonia_ (micro appearance)
- Intra-alveolar plugs of loose fibro-connective tissue (arrows)
79
What are some non-neoplastic asbestos-related disorders?
- Diffuse pleural fibrosis
- Benign pleural effusions
- Pleural plaques
- Parenchymal interstitial fibrosis (_asbestosis_)
80
What are these arrows pointing at?
Club (clara) cells
81
What is this?
- Gross appearance of _centriacinar emphysema_ (upper lobes of the lung)
- Enlarged airspaces with tissue destruction is evident, particularly at the apex (arrow)
82
How does extrinsic asthma work?
- _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
What do you see here?
- **Hypersensitivity pneumonitis**
- _Ill–defined granuloma_ composed of a few giant cells and histiocytes (arrow) surrounded by lymphocytes
84
What is this?
- Birefringent silica particles under polarized light
- Silicosis (pneumoconiosis)
85
What is this?
- _Sarcoidosis granulomas_:
1. Composed of epithelioid histiocytes and giant cells (arrows)
2. Typically well-formed and non-necrotizing
86
What do you see here? Star? Arrow?
- _Allergic rhinitis_: type I hypersensitivity (associated with asthma and eczema)
- _Star_ = inflammatory infiltrate
- _Arrow_ = Charcot-Leyden crystals
87
What is this?
Panacinar emphysema -\> characteristic of A1AT deficiency (entire acinus affected)
88
What do you see here?
- _Angiofibroma_:
1. Benign tumor of the nasal mucosa composed of large blood vessels and fibrous tissue
2. Presents with profuse epistaxis (nose bleeds)
89
What are the 2 primary mechanisms of increased resistance to air flow in obstructive disease?
- Loss of elastic recoil in the lung: emphysema
- Airway obstruction/narrowing: asthma, bronchiectasis, chronic bronchitis
90
What is the pulmonary interstitium composed of?
- BM of endo and epi cells, collagen fibers, elastic tissue, and fibroblasts
91
What do you see here? What might cause it?
- 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
What is the normal structure of an acinus?
- The acinus is comprised of the structures distal to a terminal bronchiole (between dashed red lines) -\> respiratory bronchiole, alveolar ducts and sacs
93
What are the 2 categories of intersitital/restrictive diseases? Provide examples (4 & 2).
- _Fibrosing_:
1. Idiopathic pulmonary fibrosis
2. Collagen vascular disease-associated
3. Pneumoconioses
4. Drug/radiation pneumonitis
- _Granulomatous_:
1. Sarcoidosis
2. Hypersensitivity pneumonitis
94
What is the pathogenesis of hypersensitivity pneumonitis (image)?
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
What is this?
- 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
What do you see?
- Laminated calcified concretions -\> **Schaumann bodies**
1. Not specific for sarcoidosis and can occur in others granulomatous diseases
97
What is this?
Type II pneumocyte hyperplasia after alveolar injury
98
What is bronchiectasis?
- _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
What is this?
- _Sarcoidosis granulomas_ (arrows):
1. Tend to be distributed along the bronchovascular bundles and interlobular septa
100
What are the causes of bronchiectasis?
- _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
What is emphysema?
- 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
What do you see here?
- Gross appearance of _asthma_
- _Mucous plug_ (arrow) within a bronchus
103
What do you see here?
Normal alveoli
104
What is beryllium pneumoconiosis?
- 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
What do you see here?
- Microscopic appearance of chronic bronchitis
- Submucosal gland (arrow) hypertrophy (\>40% of wall)
106
What is the major cytokine involved in the pathogenesis of IPF?
TGF-beta from injured pneumocytes: induces fibrosis
107
What do you see here?
- 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
What are these?
- Micro appearance of _asthma_
- Asthmatic mucous sometimes forms tight coils known as **Curschmann spirals** (arrows)
- You can also get these in cervical specimens
109
What is sarcoidosis? How would you diagnose it?
- 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
What is this?
- Idiopathic pulmonary fibrosis
- Patchy interstitial fibrosis (white arrow) that is most severe subpleurally
- Orange arrow: intervening normal tissue
111
What are the micro findings with hypersensitivity pneumonitis?
- Airway-centered interstitial lymphocytic inflammation
- Loosely formed, ill-defined granulomas
- Interstitial fibrosis and organizing pneumonia
- _Eosinophils are not a feature_
112
What is COP?
- _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
What is IPF? How does it prevent? Tx?
- _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
What do you see here?
- 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
What are these arrows pointing at?
- EM: surfactant–containing _lamellar bodies_ (in a type II pneumocyte)
116
What do you see?
- Silicosis (pneumoconiosis)
- Dense collagenized nodule (arrow) with surrounding lymphocytes
117
What do you see here?
Hemosiderin-laden macrophages
118
What is Virchow's triangle?
- Stasis
- Endothelial damage
- Hypercoagulable state
119
What is a PE? Epi?
- 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
What % of PE's cause infarction? Why?
- 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
What is this?
- 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
What do you see here?
- **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
What is this?
- **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
What do you see here?
- **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
What is this?
- **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
Describe the path of blood through the pulmonary/CV circuit.
- 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
