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MHD VI: Pulm > 11.20: Pulm II > Flashcards

11.20: Pulm II Flashcards

1
Q

What is the issue in obstructive pulmonary disease?

A
  • **PROBLEM WITH EXHALATION
  • Increase in resistance to airflow from partial/complete obstruction at any level
  • Decreased FEV1
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2
Q

What is problem in restrictive pulmonary disease?

A
  • **Problem with ability of chest wall
  • Expansion or compliance
  • Can be problem with chest wall, parenchyma, or fibrotic lung
  • Decreased TLC
  • Normal FEV1
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3
Q

What is reduced FEV1 indicative of? Normal?

A

Reduced: Obstructive airway disease
Normal: Restrictive airway disease

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4
Q

What is FEV1?

A

How much of a forced inspiration is expired in 1st second of exhalation

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5
Q

What are examples of obstructive lung diseases?

A
  1. Emphysema
  2. Chronic bronchitis
  3. Asthma
  4. Bronchiectasis
  5. Tumor / foreign body
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6
Q

What are examples of restrictive lung diseases?

A 
Chest wall disorders
1. Polio
2. Obesity
3. Pleural disease 
4. Kyphoscoliosis
Interstitial/Infiltrative disease:
1. ARDS
2. Dust diseases
3. Interstitial fibrosis
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7
Q

What is FVC?

A

“Forced vital capacity”

  • Total amount inhaled during forced inspiration
  • How much expired in first second is FEV1
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8
Q

What is included in vital capacity (VC)?

A

VC = TV + IRV + ERV

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9
Q

What is included in total lung capacity (TLC)?

A

TLC = TV + IRV + ERV + RV

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10
Q

What is included in functional residual capacity (FRC)?

A

FRC = RV + ERV

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11
Q

What is spirometry?

A
  • Clinical measure of inspiratory / expiratory volume and rate
  • Inspiration on bottom of graph
  • Expiration on top of graph
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12
Q

What are the COPDs?

A

“Chronic obstructive pulmonary disorders”

  1. Chronic Bronchitis
  2. Emphysema
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13
Q

Key characteristic of asthma?

A
  • INTERMITTENT and REVERSIBLE airway obstruction
  • Muscle layer has become hypersensitive to a stimulus
  • Bronchial inflammation with eosinophils
  • Increased mucus production
  • Bronchial smooth muscle hypertrophy
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14
Q

What is bronchial inflammation with eosinophils characteristic of?

A
  • Asthma
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15
Q

Symptoms of asthma?

A
  1. Wheezing
  2. Chest tightness
  3. Breathlessness
  4. Cough
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16
Q

Stimuli of asthma?

A
  1. Infections
  2. Cold Air
  3. Exercise
  4. Environmental irritants
  5. Stress
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17
Q

What is a main mechanism for increased asthma in Western world?

A
  • Body shifts to making more IgE than IgG/M due to limited exposure to environmental infections / toxins
  • IgE is key factor in development of asthma and other hypersensitivity disorders
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18
Q

What is atopic asthma?

A
  • Immune mediated Type I hypersensitivity rxn involving IgE bound to mast cells
  • Begins in childhood and triggered by allergens
  • General predisposition to this response
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19
Q

How can atopic asthma be detected?

A
  • Skin test for allergen rxn
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20
Q

What is non atopic asthma?

A
  • Triggered by non-immune mechanisms
  • Viral inflammation of mucosa increasing sensitivity of subepithelial vagal receptors or irritants
  • Skin an serum tests are NEGATIVE
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21
Q

During which type of asthmatic process are skin tests positive?

A

Atopic

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22
Q

Important causes of drug induced asthma?

A

Aspirin

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23
Q

Pathogenesis of asthma?

A
  • Toxin initially enters body and APC presents to T cell
  • T cell produces IL 3/5 recruiting EOSs
  • T cell produces IL 4 causing B cell to produce IgE
  • Next time antigen enters body it is primed for brisk, stronger response via vagal receptors causing constriction
  • Mucus cells degranulate and produce more mucus
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24
Q

What do IL3/5 cause?

A
  • Chemotaxis of EOSs

- Released by T cells in interaction with irritant causing atopic asthma

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25
Q

What does IL4 cause?

A
  • B cell to release IgE

- IL4 Released by T cell in atopic asthma

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26
Q

What is status asthmaticus?

A
  • Prolonged bout of asthma responding poorly to treatment
  • Persistent hyperinflation of the lungs on autopsy
  • Bronchial mucus casts from degranulation of mucus glands can also be seen
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27
Q

What are Curschmann spirals?

A
  • Dying epithelial cells coated by mucin giving spiral appearance on microscopy
  • Characteristic of status asthmaticus
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28
Q

What are Charcot leyden crystals?

A
  • Seen in status asthmaticus

- Caused by degranulation EOSs leading to granule precipitate

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29
Q

What are Curschmann spirals and Charcot leyden crystals indicative of?

A
  • Status asthmaticus
30
Q

What changes occur in chronic asthma?

A
  1. Smooth muscle proliferation beyond usual thin layer
  2. Sub mucosa becomes layers with EOSs
  3. Thickening of basement membrane
31
Q

What is thermoplasty?

A
  • Clinical procedure in which smooth muscle from chronic asthma is burned off to decrease hyperplasia in bronchial tree
  • Once it has burned it will no longer be able to constrict
32
Q

How can asthma cause cor pulmonale?

A
  • Vasoconstriction of lungs leading to right heart failure
33
Q

What is chronic bronchitis?

A
  • Disease of large airways: trachea / bronchi

-

34
Q

Difference between bronchi and bronchiole?

A
  • Bronchi have cartilage, bronchioles do not

- Bronchi have mucus glands, bronchioles do not

35
Q

What is emphysema a disease of?

A
  • Destruction and loss of recoil in (acinus) area is distal to bronchioles resulting in abnormal enlargement of spaces
  • Acinus: respiratory bronchiole, alveolar ducts, alveoli
36
Q

What constitutes the acinus?

A
  1. Respiratory bronchiole
  2. Alveolar ducts
  3. Alveoli
37
Q

Clinical definition of chronic bronchitis?

A
  • Persistent productive cough for at least 3 consecutive months in at least 2 consecutive years
  • Biopsy is not needed
38
Q

Who is at risk for chronic bronchitis?

A
  1. Smokers
  2. Urban dwellers, smog
  3. Middle aged men
39
Q

What is the REID index?

A
  • Measurement of gland to wall ratio from epithelial basement membrane to cartilage
  • 40%
  • Leads to obstruction of airway and productive cough
40
Q

Complications seen in chronic bronchitis?

A
  1. Cor pulmonale with CHF
  2. Infections: low flow
  3. Bronchogenic carcinoma: squamous metaplasia as cells adapt that can become carcinogenic
41
Q

What is emphysema a destruction of?

A
  • Alveolar septa between alveolar sacks
  • Leads to destruction of capillaries
  • Leads to destruction of individual sack units into larger sacks
42
Q

What are the 4 types of emphysema?

A
  1. Centriacinar - Smokers, upper lobes
  2. Panacinar
  3. Distal acinar
  4. Irregular
43
Q

Characteristics of centriacinar emphysema?

A
  • Seen in smokers
  • Upper lobes of respiratory bronchioles
  • Upper lobes because smoke rises to upper lobes
  • **Coal workers pneumoconiosis does similar thing
44
Q

Characteristics of panacinar emphysema?

A
  • Lower lobe involvement
  • Alpha1 antitrypsin deficiency is classic disease
  • Whole acinus involved
45
Q

Characteristics of distal acinar emphysema?

A
  • Distal acinus along pleura and lobular septa
  • Occurs adjacent to areas of fibrosis or scarring
  • Can form VERY LARGE air space that can become cysts/bullae
  • Can lead to spontaneous pneumothorax
46
Q

What is compensatory emphysema?

A
  • One portion of lung that is agenic with otherside overcompensating by inflating
47
Q

What is bullous emphysema?

A
  • VERY large are cavities in lung

- Danger is that they will rupture

48
Q

When is interstitial emphysema seen?

A

Trauma

49
Q

Pathogenesis of emphysema?

A

“Protease/antiprotease theory”

  • Mild chronic inflammation from macs, CD8 T cells, and neuts
  • Toxin (Tobacco) activates neuts to produce elastase
  • Elastase digests elastin in lung
  • Body products anti elastase: alpha1 antitrypsin
50
Q

What is alpha1 antitrypsin?

A
  • Body produces this to combat elastase produced in development of emphysema from neutrophil elastin production
  • A1AT is trying to stop damage from smoking but eventually can lose
  • In deficiency, any injury will cause emphysema
51
Q

What is hyperinflated lung with bullae characteristic of?

A

Emphysema, not status asthmaticus because of the bullae

52
Q

What are PiMM / PiZZ?

A

PiMM: normal phenotype of alpha 1 antitrypsin
PiZZ: abnormal phenotype of alpha 1 antitrypsin of which 80% develop emphysema

53
Q

Age difference in emphysema vs. bronchitis?

A

Emphysema seen in older patients usually > 50yo

54
Q

Dyspnea difference in emphysema vs. bronchitis?

A
  • Severe and early onset in emphysema
55
Q

Cough difference in emphysema vs. bronchitis?

A

Bronchitis: Early, lots of sputum
Emphysema: Late onset, scant sputum: fewer mucus glands in acinar area

56
Q

Infections more common in bronchitis or emphysema?

A

Bronchitis demonstrates repeated infections

57
Q

What is a blue bloater?

A

Patient with bronchitis

58
Q

What is a Pink puffer?

A
  • Patient with emphysema

- Because of way they purse way in breathing allowing to push out air

59
Q

What is bronchiectasis?

A

PERMANENT dilation of bronchi and bronchioles caused by destruction of muscle and elastic tissue
- This is usually caused by necrotizing inflammation

60
Q

What can lead to bronchiectasis?

A
  1. TB: #1 cause
  2. Tumor
  3. CF
  4. Kartagener Syndrome
61
Q

Pathogenesis of bronchiectasis?

A
  • OBSTRUCTION leading to impaired clearing mechanisms
  • POOLING of secretions distal to obstruction
  • Leads to INFLAMMATION with necrosis, fibrosis, and eventual dilatation
62
Q

Primary defect in CF?

A
  • Defect in chloride transport channel causing accumulation of viscous secretions obstructing the airways
  • This pulls NaCl into cells with water following
  • Mucus becomes very dry and cement like
  • Leads to airway damage and high susceptibility to infections
63
Q

Genetics of CF?

A
  • CFTR protein product found on chromosome 7

- Autosomal recessive transmission

64
Q

What is kartagener syndrome?

A
  • Defective cilia preventing from removal and escalation of mucus
  • Dynein arms are missing from cilia
65
Q

Various diseases associated with kartagener?

A
  1. Sinusitis from lack of cilia in nose
  2. Bronchiectasis
  3. Infertility
  4. Situs inversus
66
Q

What is situs inversus?

A

Heart and other organs are transposed through sagittal plane to opposite from normal

67
Q

Complications of bronchiectasis?

A

 Respiratory insufficiency
 Cor pulmonale
 Brain abscesses
 Amyloidosis

68
Q

Summary of emphysema?

A

 Destruction and dilatation of acini
 Centriacinar: smoking
 Panacinar: alpha 1 antitrypsin deficiency
 “Pink Puffers”

69
Q

Key facts of chronic bronchitis?

A 
 Cough
 Hypersecretion of mucus
 Smoking, pollutants
 Small airway disease
 “Blue bloaters”
70
Q

Key issues with Bronchiectasis?

A

 Damage to and dilatation of bronchial wall
 Permanent
 Infections, purulent mucus

71
Q

Key facts of bronchial asthma?

A 
 Episodes of bronchospasm
 Atopic or allergic
 Nonatopic (viruses and pollutants)
 Eosinophils, mucus plugs
(Charcot-Leyden crystals and
Curschmann’s spirals)

MHD VI: Pulm (20 decks)

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