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DT3- EXAM 2 > Respiratory Review/ interstitial disease (6)- Melissa** > Flashcards

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

1
Q

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.

A

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

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2
Q

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

A

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

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3
Q

How many terminal bronchioles constitute a pulmonary lobule?

A

3-5 terminal bronchioles

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4
Q

What structures constitute an acinus? (3)

What is another name for this structure?

A
  • Terminal respiratory unit*
    1. respiratory bronchioles
    2. alveolar ducts
    3. alveolar sacs
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5
Q

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?

A
  • pseudo stratified, ciliated, tall (simple) columnar epithelium lines most of the resp tree
  • vocal cords are lined by simple squamous epithelium
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6
Q

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

A

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.

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7
Q

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?

A

Type I pneumocytes: 95% of alveolar surface

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

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8
Q

Describe the arterial supply to the lung:

A

Double supply
Pulmonary AA’s: form heart
Bronchial AA’s: from aorta

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9
Q

List three pulm defense mechanisms:

A
  1. Nasal clearance (sneeze, cough, blow nose)
  2. Trachiobroncheal clearance (epithelial mucocilliary action)
  3. Alveolar Clearance (phagocytosis by alveolar MQs)
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10
Q

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

A
  1. ETOH + smoking both interface with MQ phagocytosis

2. Smoking destroys mucocilliary apparatus

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11
Q

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

A
  • CF

- Bronchial obstruction

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12
Q

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

A
  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.
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13
Q 
Define restrictive lung disease. 
How does the disease influence the following: 
1. TLC
2. FEV1
3. FVC
4. FEV1 : FVC Ratio
A

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
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14
Q

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

A
  1. obesity
  2. kyphosis
  3. polio
  4. pleural disease
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15
Q

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

A
  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)

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16
Q

What are the components of the interstitium?

A

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
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17
Q

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)

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

–CXR: diffuse infiltrate

–Ultimate sequelae:
Cor Pulmonale + Honeycomb Lung

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18
Q

Describe the primary pathogenesis mechanism

associated with Idiopathic Pulmonary Fibrosis/ Usual Interstitial Pneumonia (IPF)/(UIP)

A

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

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19
Q

What is a fibroblastic focus and what causes its formation?

With what is it assc?

A

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

*Asstd with IPF/UIP

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20
Q

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

A

Morphology:
“cobblestone” pleural surface
Regions affected:
LOWER LOBES

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21
Q

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

A

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

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22
Q

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

A
  • Honeycomb lung refers to dense fibrosis + cystic spaces lined by TYPE II pneunocytes
  • Associated with IPF/UIP, severe asbestosis
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23
Q

What is meant by temporal heterogeneity?

With which disease is it associated?

A

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

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24
Q

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

A
  1. fibroblastic foci
  2. dense fibrosis
  3. honeycombing
  4. temporal heterogeneity
  5. mild/ moderate inflammation
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25
Q

IPF/UIP:
Age of onset
Tx/prognosis

A

40-70yoa

Tx/Prog: ONLY TRANSPLANT; mean survival= 3 years

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26
Q

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

A

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

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27
Q

Describe the CELLULAR morphology of NIP:

A

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

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28
Q

Describe the FIBROSING morphology of NIP:

A

Diffuse/ patchy fibrosis

WITHOUT temporal heterogeneity, no fibroblastic foci, no honeycomb

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29
Q

NIP:
Age of onset
Sx
Tx/ prognosis

A

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

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30
Q

Cryptogenic Organizing Pneumonia (COP):

Describe the pathogenesis

A

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

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31
Q

Describe the morphology of COP

A

MASSON BODIES in bronchioles and alveoli
=polypoid plugs of loose fibrous CT
(All lesions are same age)

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32
Q

COP:
CXR
Tx/prognosis

A

CXR: peribronchial consolidation (may involve Hilar nodes)

Tx/ prog: steroids for 6+mos; spontaneous resolution

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33
Q

What is Pneumoconiosis?

What are three examples of this type of disease?

A

Diffuse interstitial disease from chronic inhalation of particles

  1. Coal workers pneumoconiosis
  2. silicosis
  3. asbestos related disease
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34
Q

What are the 4 factors influencing the outcome of ALL pneumoconiosis?

A
  1. amount of toxin inhaled
  2. size of particle (small are worse! 1-5um)
  3. solubility/ physiochemical properties
  4. smoking = damage to mucociliary apparatus
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35
Q

What are two reasons why smaller particles are more dangerous or cause pneumoconiosis?

A
  1. lodge deeper in air smaller terminal airways

2. can reach toxic levels

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36
Q

What are the three degrees of Coal Workers Pneumoconiosis; who can get this disease (3)?

A
  1. Asymptomatic Anthracosis
  2. Simple CWP
  3. Complicated CWP (progressive massive fibrosis)

Can affect smokers, miners, urban dwellers

37
Q

Describe the morphology of asymptomatic anthracosis: (3)

A
  • carbon particles & pigmented MQs in pulm lymphatics

- NO CELLULAR RXN

38
Q

SIMPLE CWP:

  • -morphology
  • -Which part of the lung is affected?
  • -What might this disease cause?
A

Carbon laden MQs form macules –> nodules (w. Collagen)

  • Affects resp bronchioles of UPPER LOBES
  • May cause emphysema
39
Q

Describe the morphology of COMPLEX CWP:
What do the lesions contain?
What is the end stage of this disease called?
Three buzz words?

A
  • 2+ cm Black lesions w/ NECROTIC centers
  • Lesions contain COLLAGEN and CARBON
  • PROGRESSIVE MASSIVE FIBROSIS (PMF) = end stage

necrosis, collagen, carbon

40
Q

Describe the typical clinical course for CWP; which populations are at risk (3)?

A
  • Typically benign & does not usually progress to PMF

Population: smokers, miners, urban dwellers

41
Q

What is Caplan Syndrome?

What are the hallmarks of the disease? (2)

A
  • Pneumoconiosis + RA
  • RAPID GROWING LUNG NODULES (may mistake for tumor)
  • (Central necrosis w/ surrounding fibroblast, MQ, collagen matrix)
42
Q

What are the two morphologies of silicon dioxide particles? How do they induce disease?

A
  1. Crystalline (BAD)
  2. Amorphous (typically quartz; not as severe)

Silica inhaled–> Activate MQs–> release mediators–> fibrosis ensues decades after exposure

43
Q

What are 4 of the mediators released by MQs in response to silica?

A
  1. IL1
  2. TNF
  3. ROS
  4. Fibrogenic cytokines
    =fibrosis
44
Q

Describe the morphology of SILICOSIS (2):

Where in the lungs does it manifest?

A
  • UPPER LUNG ZONES*
    1. SCARS: concentric hyalinized collagen inside dense capsule
    2. EGG SHELL calcifications*: (fibrosis of hilar nodes + pleura)

4 C’s: concentric collagen in capsules and calcifications

45
Q

Silicosis:
Population/ prevalence?
CXR?

What are two diseases that this condition predisposes patients to get?

A

Sandblasters, miners
#1 OCCUPATIONAL DISEASE WORLD WIDE
- CXR: nodules in upper lung zones
- Predisposed to TB and malignancy

46
Q

List 4 potential sequelae of asbestos:

Which is most common?

A

1: FIBROUS PLEURAL PLAQUES

  1. pleural effusion
  2. interstitial fibosisis
  3. malignancy: extrapulm tumors, bronchogenic carcinoma»> mesothelioma
47
Q

What are the two types of Asbestos fibers?
How do they cause disease?
Which one is worse?

A 
#1: SERPENTINE 
Soluble curly fibers--> bronchocillary removal
  1. AMPHIBOLE FIBERS
    MORE PATHOGENIC; LESS COMMON
    Stiff, brittle fibers–> lodge in deep lung tissue
48
Q

What are the two ways in which asbestos can be carcinogenic?

A
  1. carcinogens bind asbestos

2. activates MQs to release ROS–> TOOMAH!

49
Q

Describe how asbestos fibers cause fibrosis

Where in the lung does this happen (early vs. late disease)?

A

Cause MQs release chemotactic/ fibrogenic mediators

EARLY: Acini (respi bronchioles etc)
LATER: Diffuse Interstitial Fibrosis (like IPF/UIP), HONEYCOMBING, extends to pleura

50
Q

What are asbestos bodies?

What do they look like?

A
  • Asbestos fibers with proteins +/- Fe
  • Golden brown, fusiform/ beaded dumbbell looking rods with translucent center

Ferruginous bodies contain Fe

51
Q

What is the most common manifestation of asbestosis in the lungs? What are they made up of (2)? Do these structures contain asbestos bodies?

A

Pleural Plaques:

  • Dense collagen, Ca++
  • DO NOT CONTAIN ASBESTOS BODIES
52
Q

Asbestos Related Disease:
Onset is how long after exposure?
CXR: where do you see densities?

A

Onset: 20 years after exposure
CXR:densities in LOWER LOBES

53
Q

List three causes of therapy induced restrictive lung disease and the mechanism by which they cause disease:

A

Bleomycin: direct damage to lung tissue

Amiodarone + radiation: pneumonitis (pulm fibrosis)

54
Q

What are the two granulomatous restrictive lung diseases?

A
  1. sarcoidosis

2. hypersensitivity pneumonitis

55
Q

Refresh your memory: what is a granuloma?

A

Infectious or noninfectious organized collection of MQs (epithelioid cells/ histiocytes)

56
Q

How is sarcoidosis diagnosed?
List 4 immunological dysfunctions associated with the disease?
What genetic mutations are associated with this disease?

A

Dx of exclusion; bronchoscopes give ^ diagnostic yield

Immunological dysfunction:

  1. ^ CD4+ T cells
  2. ^ IL2, IL8
  3. ^ IFN-g, TNF
  4. ^ MQ inflammatory protein

Genetic mutations: HLA-A1, HLA-B8

57
Q

Describe the microscopic morphology of sarcoidosis:

What FOUR things do the sarcoid granulomas include?

A

Noncaseating granulomas–> fibrous scars
The granulomas include:
1. Tight epithelioid cells
2. Langhan (giant) cells
3. Schaumann bodies (Ca/protein)
4. Asteroid bodies (sellate inclusions inside giant cells)

58
Q

How does sarcoidosis manifest in the lung/ mediastinum?

A
  • “bilateral hilar lympadenopathy”
  • granulomas in resp. lymphatics, bronchi, vasculature
    (all of the tubes– carrying blood lymph or gas!)
59
Q

How does sarcoid manifest in liver and spleen? (2)

A
  • splenic involvement without enlargement

- liver granulomas in portal tracts

60
Q

Does sarcoid affect bone marrow; if so where?

A
  • granulomas in marrow of hands and feet
61
Q

Describe how sarcoid can affect skin and eyes:

A

skin: nodules/ plaques/ lesions (it varies)
eyes: iritis, dacroadenitis

62
Q

What is Mikulicz Syndrome? (4)

A

Sarcoidosis effecting GLANDS (First 3 must be bilateral):

  1. parotid
  2. submaxillary
  3. sublingual
  4. lacrimal gland

(bilateral salivary glands involved + lacrimal)

63
Q

Patient population that gets sarcoidosis (2)?
Sx
CXR
Tx/Prognosis–who has the best prognosis?

A

Population: AA women (10X); southeastern US
Sx: mimic lung cancer
CXR: “bilateral hilar lymphadenopathy”
Prog: Best if hilar/ pulm involvement only, not systemic

64
Q

Hypersensitivity Pneumonitis:
Pathogenesis? (2)
Why is early dx critical?

A

Hypersensitivity to INHALED Ags: type III or IV

  • **NOT assc with ^^^ eos.
  • Can cause interstitial fibrosis if not diagnosed or treated early!*
65
Q

Three examples of hypersensitivity pneumonitis + their associated Ag:

A
  1. Farmer’s lung: thermophilic actinomyocytes
  2. Pigion Breeder’s lung: proteins from feathers or poops
  3. Humidifier Lung: thermophilic bacteria from heated H2O
66
Q

How does early hypersensitivity pneumonitis look on histo?

What if it is left untreated?

A

LOOSE NONCASEATING granumomas –> honeycombing if not treated

67
Q

Describe how acute hypersensitivity pneumonitis presents:

What about late stage/ untreated?

A

Acute:
- 4-6 hours after re-exposure to Ag see fever, dyspnea, cough + nodular infiltrate on CXR

Chronic/ untreated:
- cyanosis; decreased lung capacity (restrictive disease)

68
Q 
Describe ACUTE Eosinophilic Pneumonia: 
What causes the disease? 
How is it diagnosed?
Clinical presentation? 
Treatment?
A

Hypersensitivity to INHALED antigens

  • Dx: BAL (lavage) 25%+ EOS
  • Clinical: RAPID fever/dyspnea/hypoxemia–> Resp Failure
  • TX: Steroids
69
Q 
Describe SIMPLE pulmonary eosinophilia/ Loffler's Syndrome: 
Cause? 
Blood finding? 
Morphology? 
Tx/prognosis?
A

Hypersensitivity to FOOD or DRUG (#1 Sulfadrug)

Morphology:

  • ^^ eos in BLOOD
  • lung lesions with eos and giant cells @ septae

Tx/Prog: Benign/ self limiting

70
Q

Describe SECONDARY Pulmonary Eosinophilia:
Cause?
Common clinical comorbidities/ associations (2)?
Prognosis?

A

Hypersensitivity to INFECTION (parasitic, bacterial, fungal)
C: commonly associated with asthma, aspergillosis allergy
Prog: can lead to CHRONIC lung injury and FIBROSIS

71
Q

Three parasites known to cause secondary pulm eosinophilia?

A
  1. schistosoma
  2. wuchereria
  3. strongyloides
72
Q

Chronic Eosinophilic Pneumonia:
Cause?
morphology?
Tx/prog?

A

Related to AUTOIMMUNE disease
Morphology:
- peripheral lung consolidation
- lymphs + EOS infiltrate septae + alveoli

Tx: responds well to steroids

73
Q

What is pulmonary alveolar proteinosis (PAP)?
What are the three subtypes?
Which is most common?

A

Protein material accumulates in lung (^ lung size/weight)
#1: Acquired
2. Congenital
3. Secondary

74
Q

Acquired PAP:

Describe the pathogenesis

A

90% of all cases

GM-CSF Auto Abs–> DECREASE MQ fxn–> SURFACTANT + Proteins accumulate in alveolar space

75
Q

Congenital PAP:
Describe pathogenesis.
What is the prognosis?

A
  • FATAL WITHOUT LUNG TRANSPLANT (Death 3-6mos)*
  • Rare cause of NRDS
  • Associated with various gene mutations
76
Q

Secondary PAP:

With what is this disease associated? (3)

A

Associated with silicosis, malignancy, immunodeficiency

77
Q

Describe the morphology of all PAP subtypes: (2)

A
  • PAS + precipitate and consolidation

- (+/-) cholesterol clefts

78
Q

Who gets PAP?
Clinical presentation/ CXR?
Tx/ Prog?

A 
Mostly ADULTS***
CP: PRODUCTIVE GELLY COUGH!!!
CXR: scattered consolidation 
Tx: Use BAL to give GM-CSF therapy
Prog: can cause respiratory failure; esp in congenital type
79
Q

What are the two interstitial lung diseases associated with smoking?

A
  1. Desquamative interstitial pneumonitis
  2. Respiratory Bronchiolitis
    (really the same disease with RB being worsened DIP)
80
Q

Desquamative Interstitial Pneumonitis

vs Respiratory Bronchiolitis Assc Interstitial Disease: how do they differ in terms of morphology?

A

DIP: pigment laden MQs in alveoli only

RB-ILD: pigment laden MQs in alveoli, bronchioles and peribronchiolar areas + Fibrosis

81
Q

Desquamative Interstitial Pneumonitis (DIP) + Respiratory Bronchiolitis Assc Interstitial Disease (RB-ILD) :
Population affected?
Tx?

A

Middle aged male smokers

TX: steroids + smoking cessation

82
Q

Triad that should make you think respiratory bronchiolitis?

A
  1. Inflammation
  2. Liver fibrosis
  3. Pigmented MQs
83
Q

1 respiratory disease worldwide

A

silicosis

84
Q

Two restrictive diseases that present in the LOWER lobes? Two in the UPPER lobes?

A

-Upper: Silicosis, Coal Workers

-Think of lower as MORE SEVERE!
asbestos, IPF– the same two that cause honeycomb

85
Q

Condition assc with “temporal heterogeneity”

A

IPF

86
Q

Three hypersensitivity related pneumonitis conditions:

A
  1. “hypersensitivity” pneumonitis
    (type III, IV –> granulomas)
  2. Acute eosinophilic pneumonitis
    (inhaled antigens)
  3. Simple pulmonary eosinophilia
    (ingested antigens –> go to GI first and spread to lungs)
87
Q

What are the four eosinophilic pnuemonitis conditions?

What are their very broad causes

A
  • acute (inhaled allergen)
  • simple (ingested antigen)
  • secondary (infection)
  • chronic (AI disease)
88
Q

Of the four eosinophilic pneumonitis conditions, which can lead to a chronic/ fibrotic disease?

A
  • acute
  • secondary

(simple, chronic are self limiting)

89
Q

“Bronchoscope gives high diagnostic yield”

A

sarcoidosis

DT3- EXAM 2 (19 decks)

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