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MS2 Respiratory > 9/23- Pathology Review > Flashcards

9/23- Pathology Review Flashcards

1
Q

What are the stage of intrauterine lung develompent? Timeline?

A
  • Embryonic (26d- 5 wks)
  • Pseudoglandular (6 - 16 wks)
  • Canaliculur (17-28 wks)
  • Saccular (29 wks - birth)
  • Alveolar (35 wks - ?)
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2
Q

Histo characteristics of canalicular phase?

A

Immature acinar structures surrounded by supporting framework

  • Can see red cells in some small capillaries
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3
Q

Histology of trachea and bronchi?

A
  • Cartilage
  • C-shaped in trachea
  • Plates in bronchi
  • Submucosal glands
  • Smooth muscle
  • Lamina propria
  • Epithelium
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4
Q

What is key to distinguishing membranous from respiratory bronchiole?

A

Membranous has smooth muscle (more pink surrounding it)

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5
Q

What type of cells are type I pneumocytes?

A

Squamous epithelial cells

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6
Q

When does surfactant production by type II pneumocytes begin?

A

Saccular phase (29 wks - birth)

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7
Q

What are Pores of Kohn and Canals of Lambert?

A

Provide collateral ventilation by connecting adjacent alveoli and bronchioles

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8
Q

What comprises the pulmonary acinus? Function?

A

Functional unit of gas transfer (because all lined by alveoli; gas transfer can happen anywhere)

  • Respiratory bronchiole
  • Alveolar ducts
  • Alveoli
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9
Q

What is the epithelium in each lung structure/stage?

A
  • Bronchus: ciliated columnar (pseudostratified?)
  • Bronchioles: simple epithelial, columnar or cuboidal
  • No more goblet cells, submucosal glands, or cartilage (Lose smooth muscle going from Memb -> Resp bronchiole)
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10
Q

What are the three forms of atelectasis?

A
  • Resorption (obstructive), e.g. mucus plugs
  • Compressive, e.g. pleural effusion
  • Contraction, e.g. tumor (mesothelioma)
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11
Q

What is DAD?

A

Diffuse alveolar damage

  • Form of acute injury
  • Histologic counterpart to the clinical process of ARDS
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12
Q

What are the two types/forms of DAD?

A

1. Exudative (under 1 wk from injury/inciting event)

  • Hyaline membranes = histologic landmark! (begin 2d, peak 4-5 d); precipitated plasma protein and debris from sloughed epithelial cells

2. Proliferative (Organizing) (> 1 wk)

  • Proliferation of type 2 pneumocytes
  • Formation of granulation tissue - Fibrosis
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13
Q

What is seen here?

A

Exudative phase of DAD/ARDS

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14
Q

What are types of obstructive lung disease? Provide histologic features of each

A

Asthma

  • Goblet cell metaplasia
  • Mucus plugs
  • Muscle wall hypertrophy

Chronic bronchitis

  • Goblet cell metaplasia
  • Mucus plugs
  • Submucosal gland hypertrophy/hyperplasia

Bronchiectasis

  • Permanent dilatation of airways
  • Lower lobes
  • Destruction of muscle/elastic tissue by inflammation and fibrosis
  • Occurs in cystic fibrosis as well as others

Emphysema

  • Permanent enlargement of airspaces distal to terminal bronchiole
  • Centriacinar in smokers or panacinar in alpha 1 antitrypsin deficiency
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15
Q

What are the histological components of asthma?

A

Asthma

  • Goblet cell metaplasia
  • Mucus plugs
  • Muscle wall hypertrophy
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16
Q

What are the histological components of chronic bronchitis?

A

Chronic bronchitis

  • Goblet cell metaplasia
  • Mucus plugs
  • Submucosal gland hypertrophy/hyperplasia
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17
Q

What parts of the acinus does centriacinar emphysema involve? Panacinar?

A

Centriacinar

  • Respiratory bronchiole

Panacinar

  • Alveolar duct
  • Alveoli
  • Begins distally, but may progress to involve respiratory bronchiole
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18
Q

Is centriacinar emphysema upper or lower lobe dominant? Associations? Panacinar?

A

Centriacinar

  • Upper lobe
  • Associated with smoking

Panacinar

  • Lower lobe
  • Alpha 1 antitrypsin deficiency
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19
Q

What are the macroscopic patterns of pneumonia?

A
  • Bronchopneumonia: inflammation centered in the airways and possibly alveolar tissue just around those tissues (very patchy)
  • Lobar

Bronchopneumonia can transition to lobar pneumonia if not treated (although some very virulent organisms may start out lobar)

20
Q

T/F: A single organism can cause either bronchopneumonia and lobar pneumonia?

A

True

21
Q

What are the microscopic patterns of pneumonia?

A

For lobar pneumonia:

  1. Congestion
  2. Red hepatization
  3. Gray hepatization
  4. Resolution
22
Q

What are some complications of pneumonia?

A
  • Lung abscess
  • Empyema
  • Septicemia -> multiorgan abscess
23
Q

What is seen here?

A

Bronchopneumonia

  • Patchy; around airways
24
Q

What is seen here?

A

Lobar pneumonia

25
Q

What are complications of lung transplants?

A
  • Infections (bacterial, viral, fungal)

- Acute rejection (wks - mos)

  • International Working Formulation (A0-A4) grades rejection based on location and predominant cell type (lymphocytes early, neutrophils later?)

- Chronic rejection (3-5 yrs post-op)

  • Problem in half of transplants
  • Bronchiolitis obliterans = hallmark!; granulation tissue at level of membranous bronchioles: fibrosis +/- inflammation
26
Q

What are some organisms that frequently cause opportunistic infection (in lung transplants)?

A
  • Aspergillus: 45’ septated branches
  • Crytpococcus: budding yeast with clear halo of polysaccharide capsule
  • Pneumocystis
  • Herpes
  • CMV: can have nuclear or even cytoplasmic inclusions
  • Histoplasma
27
Q

What condition/disease involves bronchiolitis obliterans?

A
  • Acute rejection of lung transplant
  • Others?
28
Q

What are the microscopic and gross findings of UIP?

A

Microscopic:

  • Temporal heterogeneity (mature and immature fibrous tissue adjacent)
  • Honeycombing; cystic spaces filled with mucin and lined by metaplastic bronchial cells
  • Patchy fibrosis
  • Subpleural distribution

Grossly:

  • Cobblestoning of pleural surface over involved lung
29
Q

What can cause honeycombing?

A
  • UIP and other interstitial diseases
  • Infection
  • Radiation
30
Q

What are the microscopic findings of NSIP?

A

Microscopic:

  • Lymphoplasmacytic interstitial infiltrate
  • Architecture preserved!
  • Type II pneumocyte hyperplasia
  • Temporally uniform fibrosis (in contrast to UIP); no fibroblastic foci
31
Q

What are the microscopic and gross findings of asbestosis?

A

Microscopic:

  • Patchy interstitial and subpleural fibrosis (fibers stimulate release of mediators leading ot repeated cycles of inflammation/fibrosis)
  • Starts around resp bronchioles and alveolar ducts; proceeds distally
  • Fibrosis similar to UIP, but should see asbestos bodies! (asbestos fiber + iron-protein coat; look like dumbbell beaded bodies)
  • Honeycombing

Grossly:

  • Visceral pleural thickening
  • Most commonly affects lower lobes
32
Q

Where do pleural plaques commonly form?

A
  • Parietal pleura
  • Domes of diaphragm
33
Q

What are pleural plaques made of?

A

Typically acellular; don’t commonly have asbestos bodies

34
Q

What are the microscopic and gross findings of silicosis?

A
  • Early: dust-filled macrophages, lymphatic/bronchovascular distribution
  • Later: silicotic nodules (lamellar fiborsis with birefringent silica particles)
  • Uniform fibrosis begins around bronchioles
  • Can get honeycombing

Grossly: upper lobes

35
Q

What are the microscopic and gross findings of HP?

A

Acute:

  • Neutrophils in alveoli and respiratory bronchioles
  • Lasts 1-2 days

Subacute/chronic (3 characteristics you need to know!)

1. Interstitial lymphoplasmacytic infiltrate (beings around bronchioles (~100%)

2. Ill-defined, random, non-caseating granulomas (~67%)- these are more diffuse/less discrete than the granulomas of sarcoidosis

3. Patchy organizing pneumonia (60%)

36
Q

What are the microscopic findings of sarcoidosis?

A

Microscopic

  • Mutliple nodules: pleura, interlobular septa, bronchovascular structures
  • Well-formed/defined granulomas:
  • Epithelioid histioctyes
  • Multinucleated giant cells
  • Chronic inflammatory cells
  • Usually no necrosis!! (noncaseating)
  • Lung architecture preserved
  • Must rule out infectious organisms (TB, fungus) before starting to treat sarcoidosis with steroids
37
Q

What are the microscopic findings of COP?

A

Microscopic:

  • Intraluminal plugs of granulation tissue (Masson bodies) in distal airways (bronchioles, alveolar ducts, alveoli)
  • Patchy distribution; temporally homogeneous
  • Lung architecture preserved
  • Inflammation
38
Q

What are the microscopic findings of RB?

A
  • Finely pigmented (dusty brown) macrophages in respiratory bronchioles and adjacent alveolar ducts and alveoli
  • Lung architecture preserved
  • More?
39
Q

What are the microscopic findings of DIP?

A
  • Diffuse involvement of lung parenchyma
  • Large accumulation of alveolar macrophages
  • Uniform fibrotic thickening of alveolar septa (mild-moderate)
  • Chronic inflammation; overall lung architecture preserved
  • No honeycombing
40
Q

What are the ILDs associated with smoking?

A
  • RB: Respiratory Bronchiolitis
  • DIP: Desquamative Interstitial Pneumonitis
41
Q

How are lung cancers divided?

How does the treatment vary with each?

A
  • Small cell: chemo and radiation
  • Non-small cell: start with surgery if resectable
42
Q

Histological characteristics of squamous cell carcinomas?

A
  • Have stratified squamous organization
  • Commonly necrotic; can form —
  • Keratin
43
Q

Histological characteristics of adenocarcinoma?

A
  • Presence of glands
  • Mucin production (if no glands seen, may have to stain for mucin)
44
Q

What are the 2 types of AIS?

A

Adenocarcinoma in situ

  1. Mucinous
  2. Non-mucinous

(Can only say AIS if entire resection and no vascular or septal invasion.. otherwise adenocarcinoma “with lepidic growth pattern”)

45
Q

Histological characteristics of small cell carcinoma?

A
  • Hyperchromatic cells
  • Indistinct nucleoli
  • Nuclear indentation/hugging
  • Necrosis (?)
46
Q

Histological characteristics of typical carcinoid tumor?

A
  • Bland looking cells
  • Rich vascular tissue
  • Chromogranin stain shows NE
47
Q

Stain for large cell NE tumor?

A

CD56+

MS2 Respiratory (26 decks)

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