Respiratory Review/ interstitial disease (6)- Melissa** Flashcards Preview

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Flashcards in Respiratory Review/ interstitial disease (6)- Melissa** Deck (89)
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1

How many lobes are in the right and left lung respectively?
Describe why aspirated objects are more likely to lodge in the right lower lobe than in the left lung.

Right lung = 3 lobes
Left Lung - 2 lobes
Left has Less Lobes!!!
*Right main stem bronchus is vertical--easier route for aspirated objects*

2

Describe the progression of the bronchial tree; where are cartilage and submucosal glands found?

Trachea--> Bronchi--> Bronchioles (*No cartilage or submucosal glands)--> Terminal Bronchioles--> Acinus (respiratory bronchioles+ alveolar ducts + alveolar sacs)

3

How many terminal bronchioles constitute a pulmonary lobule?

3-5 terminal bronchioles

4

What structures constitute an acinus? (3)
What is another name for this structure?

*Terminal respiratory unit*
1. respiratory bronchioles
2. alveolar ducts
3. alveolar sacs

5

What type of epithelium lines (most of) the respiratory tree?
What area in the tree is NOT lined by this type of epithelium?
What type of epithelium lines this area?

- pseudo stratified, ciliated, tall (simple) columnar epithelium lines most of the resp tree
- vocal cords are lined by simple squamous epithelium

6

Where do we find mucus secreting goblet cells and glands in the respiratory tree?
What disease state causes excessive formation of goblet cells?

Cartilaginous airways (Trachea and bronchi) have goblet cells and glands

*ASTHMA causes excessive formation of goblet cells and glands--may cause tumor like clusters. If you see cilia on biopsy assume benign.

7

What are the two cell types that make up the alveolar epithelium? Which one constitutes most of the epithelium? What roles does each cell play?

Type I pneumocytes: 95% of alveolar surface

Type II pneumocytes: 5% alveolar surface; produce surfactant and participate in repair

8

Describe the arterial supply to the lung:

*Double supply*
Pulmonary AA's: form heart
Bronchial AA's: from aorta

9

List three pulm defense mechanisms:

1. Nasal clearance (sneeze, cough, blow nose)

2. Trachiobroncheal clearance (epithelial mucocilliary action)

3. Alveolar Clearance (phagocytosis by alveolar MQs)

10

How do ETOH and smoking compromise our resp. defense mechanisms? (2)

1. ETOH + smoking both interface with MQ phagocytosis

2. Smoking destroys mucocilliary apparatus

11

What are two important examples of how pulmonary congestion and edema can compromise pulm. defense?

- CF
- Bronchial obstruction

12

Describe examples of conditions in which patients are predisposed to lung infection: (3)

1. Viral infection predisposes to bacterial infection
2. All other forms of immunosuppression including splenic insufficiency
3. **Also: He doesn't say it but FOR SURE CF cause the bugs live in all of the extra slime.

13

Define restrictive lung disease.
How does the disease influence the following:
1. TLC
2. FEV1
3. FVC
4. FEV1 : FVC Ratio

Restrictive lung disease refers to REDUCED EXPANSION of lung parenchyma--caused by either diseased lung tissue itself or chest wall probs.

1. TLC: decreases
2. FEV1: decreases (MAY stay same)
3. FVC: decreases THE MOST
4. FEV1: FVC ratio INCREASES/ is normal

14

What are 4 chest wall disorders that can cause restrictive lung disease?

1. obesity
2. kyphosis
3. polio
4. pleural disease

15

What exactly IS interstitial lung disease?
How does it effect lung capacity and DLCO?
How common is it?

1. Inflammation or fibrosis of lung CT/ alveolar septal interstitium-->
2. DECREASED lung capacity, compliance, and volume
3. INCREASED diffusion barrier = DECREASED DLCO

~15% non infectious pulm disease
(So far less common than COPD spectrum)

16

What are the components of the interstitium?

Includes basically everything EXCEPT vessels and pneumocytes!
1. BM of endothelial and epithelial cells
2. collagen
3. proteoglycans
4. fibroblast
5. mast cells, lymphs, monocytes

17

Restrictive disease: symptoms
What is heard on auscultation and observed on PE?
What is seen on CXR?
What is the ultimate sequelae of these diseases? (2)

--Dyspnea/tachypnea--> cyanosis
***FINE DRY CRACKLES AND CLUBBING!!!!***

--CXR: diffuse infiltrate

--Ultimate sequelae:
Cor Pulmonale + *Honeycomb Lung*

18

Describe the primary pathogenesis mechanism
associated with Idiopathic Pulmonary Fibrosis/ Usual Interstitial Pneumonia (IPF)/(UIP)

Telomerase dysfxn --> excess apoptosis --> Constant Inflammation/repair (TNFa) --> FIBROBLASTIC FOCI in lung

19

What is a fibroblastic focus and what causes its formation?
With what is it assc?

Proliferation caused by constant inflammation and healing (mediated by TNFa)

*Asstd with IPF/UIP

20

Describe the gross morphology of IPF/UIP--which area of the lungs does this disease primary affect?

Morphology:
"cobblestone" pleural surface
Regions affected:
*LOWER LOBES*

21

Describe the microscopic morphology of IPF/UIP; how does it change from early to late disease? (2)

Morphology:
Fibroblastic foci--> honeycombing
*lesions will demonstrate TEMPORAL HETEROGENEITY and MILD/MODERATE INFLAMMATION*

22

What is honeycomb lung and with which diseases is it associated (2)?

- Honeycomb lung refers to dense fibrosis + cystic spaces lined by TYPE II pneunocytes

- Associated with IPF/UIP, severe asbestosis

23

What is meant by temporal heterogeneity?
With which disease is it associated?

Abrupt transition from healthy to diseased tissue in the fibrotic lung--associated with IPF/UIP

24

What are the 5 dead giveaways Sigdel gave in class that should ALWAYS point to IPF/UIP?

1. fibroblastic foci
2. dense fibrosis
3. honeycombing
4. temporal heterogeneity
5. mild/ moderate inflammation

25

IPF/UIP:
Age of onset
Tx/prognosis

40-70yoa
Tx/Prog: ONLY TRANSPLANT; mean survival= 3 years

26

Nonspecific Interstitial Pneumonia (NIP):
How is this disease defined?
What are its two morphologies? Better prognosis?

Lacks histo features of other interstitial diseases
Two morphologies:
1. cellular (better prognosis)
2. fibrosing

27

Describe the CELLULAR morphology of NIP:

uniform mild/moderate interstitial inflammation (better prognosis)
- no fibrobastic foci, honeycomb, temporal heterogeneity

28

Describe the FIBROSING morphology of NIP:

Diffuse/ patchy fibrosis
WITHOUT temporal heterogeneity, no fibroblastic foci, no honeycomb

29

NIP:
Age of onset
Sx
Tx/ prognosis

46-55 yoa
Sx: cough + dyspnea for mos
Tx/ prog: steroids; good prognosis

30

Cryptogenic Organizing Pneumonia (COP):
Describe the pathogenesis

Response to ANY sort of infection/ inflammation; most commonly infections.