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MS2 Respiratory > 9/23- Pathology Review > Flashcards

9/23- Pathology Review Flashcards

(47 cards)

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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?

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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?

21
Q

What are the microscopic patterns of pneumonia?

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A

For lobar pneumonia:

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

What are some complications of pneumonia?

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

What is seen here?

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A

Bronchopneumonia

  • Patchy; around airways
24
Q

What is seen here?

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A

Lobar pneumonia

25
What are complications of lung transplants?
- 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
What are some organisms that frequently cause opportunistic infection (in lung transplants)?
- **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
What condition/disease involves bronchiolitis obliterans?
- Acute rejection of lung transplant - Others?
28
What are the microscopic and gross findings of UIP?
_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
What can cause honeycombing?
- UIP and other interstitial diseases - Infection - Radiation
30
What are the microscopic findings of NSIP?
_Microscopic_: - **Lymphoplasmacytic** interstitial infiltrate - Architecture **preserved**! - **Type II** pneumocyte **hyperplasia** - **Temporally uniform** fibrosis (in contrast to UIP); no fibroblastic foci
31
What are the microscopic and gross findings of asbestosis?
_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
Where do pleural plaques commonly form?
- Parietal pleura - Domes of diaphragm
33
What are pleural plaques made of?
Typically acellular; don't commonly have asbestos bodies
34
What are the microscopic and gross findings of silicosis?
- **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
What are the microscopic and gross findings of HP?
_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
What are the microscopic findings of sarcoidosis?
_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
What are the microscopic findings of COP?
_Microscopic:_ - **Intraluminal plugs** of **granulation tissue** (Masson bodies) in **distal** airways (bronchioles, alveolar ducts, alveoli) - **Patchy** distribution; **temporally homogeneous** - Lung architecture **preserved** - Inflammation
38
What are the microscopic findings of RB?
- **Finely pigmented** (**dusty** brown) macrophages in respiratory bronchioles and adjacent alveolar ducts and alveoli - Lung architecture **preserved** - More?
39
What are the microscopic findings of DIP?
- 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
What are the ILDs associated with smoking?
- **RB**: Respiratory Bronchiolitis - **DIP**: Desquamative Interstitial Pneumonitis
41
How are lung cancers divided? How does the treatment vary with each?
- Small cell: chemo and radiation - Non-small cell: start with surgery if resectable
42
Histological characteristics of squamous cell carcinomas?
- Have stratified squamous organization - Commonly necrotic; can form --- - Keratin
43
Histological characteristics of adenocarcinoma?
- Presence of glands - Mucin production (if no glands seen, may have to stain for mucin)
44
What are the 2 types of AIS?
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
Histological characteristics of small cell carcinoma?
- Hyperchromatic cells - Indistinct nucleoli - Nuclear indentation/hugging - Necrosis (?)
46
Histological characteristics of typical carcinoid tumor?
- Bland looking cells - Rich vascular tissue - Chromogranin stain shows NE
47
Stain for large cell NE tumor?
CD56+

MS2 Respiratory (26 decks)

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