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MHD > Obstructive Lung Diseases > Flashcards

Obstructive Lung Diseases Flashcards

1
Q

What is the main problem in obstructive pulmonary disease?

A

Limitation of airflow in expiration

Increase in resistance due to partial or complete obstruction

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2
Q

How is the FEV1/FVC ratio affected in obstructive diseases?

A

FEV1 is reduced

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3
Q

What are the four main obstructive pulmonary diseases?

A

Asthma
Chronic Bronchitis
Emphysema
Bronchiectasis

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4
Q

Which of the obstructive pulmonary diseases are known as COPD?

A

Chronic bronchitis

Emphysema

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5
Q

Asthma

What is the main problem? Where are how does the obstruction occur?

A

Intermittent and reversible airway obstruction

Due to a hyperresponsive tracheobronchial tree

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6
Q

Asthma

Symptoms

A

Wheezing
Breathlessness
Chest tightness
Cough

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7
Q

Why have asthma rates increased dramatically in recent years?

A

Hygiene hypothesis is one idea (eradication of infections leads to alteration of immune homeostasis)

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8
Q

What are some stimuli that could induce asthma attacks?

A 
Infections
Environmental irritants
Cold air
Stress
Exercise
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9
Q

What is Atopic Asthma?

A

Immune mediated asthma. Type I hypersensitivity rxn involving IgE bound to mast cells.

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10
Q

What is Non-Atopic Asthma?

A

We don’t know the cause, but it is presumed to be caused by a hyperreactive bronchial tree

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11
Q

What drug may cause drug-induced asthma? What symptoms might this cause?

A

Aspirin

Recurrent rhinitis and nasal polyps
Urticaria

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12
Q

What may cause occupational asthma?

A

Need repeated exposure to the irritating agent
Fumes
Organic chemical dusts
Gases

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13
Q

Describe the pathogenesis of Atopic Asthma

A

Allergen comes in, gets presented to a T cell. Activate a Th2 cell to produce IL-3, IL-5 (Brings in eosinophils), and IL-4 (to induce B cells to make IgE against the allergen)

When the allergen enters again, mast cells with IgE on surface will degranulate quickly, cause bronchoconstriction, and cause mucus cells to release more mucus

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14
Q

What is status asthmaticus?

A

Prolonged hyperinflation of the lungs

May appear with mucus casts plugging up the entire bronchial tree

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15
Q

What are Curschmann spirals?

A

Seen in asthma
Degranulated inflammatory cells and dying epithelial cells covered in mucin
Have a spiral architecture

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16
Q

What are Charcot-Leyden crystals?

A

They are crystals seen on H&E from the degranulation of eosinophils (bi-lobed nuclei, very pink cytoplasm)

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17
Q

In chronic asthma, what histological changes would you expect to see?

A

Thickening of the basement membrane

Smooth muscle changes and hypertrophy

Eosinophils present

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18
Q

What are some complications of asthma?

A 
Status asthmaticus
Emphysema
Chronic bronchitis
Pneumonia
Bronchiectasis
Cor pulmonale
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19
Q

What is the clinical definition of Chronic Bronchitis?

A

Persistent productive cough for at least 3 consecutive months in at least 2 consecutive years

20
Q

Who is most likely to get Chronic Bronchitis?

A

Smokers
Urban dwellers (smog)
Middle-aged men

21
Q

What part of the respiratory system is affected by Chronic Bronchitis?

A

The larger airways (the bronchi)

22
Q

Describe the pathogenesis of Chronic Bronchitis

A

In smokers, the mucociliary escalator will have increased mucus production to trap more irritants. The body will increase production of the glands and they will become thicker. Inflammation and fibrosis occurs. Leads to a productive cough and may lead to obstruction

23
Q

What are some important consequences of Chronic Bronchitis?

A

Cor pulmonale with R heart failure
Infections
Bronchogenic carcinoma

24
Q

What is emphysema?

A

Destruction of the walls of airspaces distal to the terminal bronchioles, causing PERMANENT ABNORMAL ENLARGEMENT of those airspaces

25
Q

What are the 4 types of emphysema?

A

Centriacinar
Panacinar
Distal acinar
Irregular

26
Q

Centriacinar Emphysema

Who tends to acquire this disease? Where does it happen in the lungs?

A

Smokers

Upper lobes of the lungs

27
Q

Panacinar Emphysema

Where does it happen in the lungs?

A

Lower lobes, more towards the alveolar sacs and alveoli

28
Q

Panacinar Emphysema

What deficiency is commonly associated with it?

A

Alpha-1-antitrypsin deficiency

29
Q

Distal Acinar Emphysema

Where does it happen in the lungs?

A

Distal acinus, along pleura and lobular septa

30
Q

Irregular emphysema

Where does it happen in the lungs?

A

Acini are irregularly involved

No pattern to the dilatations seen

31
Q

Describe the pathogenesis of Emphysema and the protease-antiprotease theory

A

Smoking produces free radicals, which activate PMNs. The PMNs release elastase to digest elastin all over the lung. The body’s compensatory mechanism to prevent damage is the release alpha-1-antitrypsin (an anti-elastase). When a person keeps smoking, elastase will be more prevalent than alpha-1-antitrypsin and cause destruction of the acinus and formation of large sac-like structures

32
Q

How will the alveoli look on histological section with emphysema?

A

The alveoli will be very distended with large “grocery bag” sacs

33
Q

Alpha-1-Antitrypsin Deficiency

What is the normal phenotype? What is the abnormal phenotype?

A

Normal – PiMM

Abnormal – PiZZ
80% of PiZZ pts develop emphysema

34
Q

Blue bloaters are associated with what disease?

A

Bronchitis

35
Q

Pink puffers are associated with what disease?

A

Emphysema

36
Q

Bronchitis vs. Emphysema

Which has a productive cough?

A

Bronchitis (it affects the bronchi, where mucus can be produced)

37
Q

Bronchitis vs. Emphysema

Which causes more infections?

A

Bronchitis (more mucus production provides a great place for bacteria to grow)

38
Q

Bronchitis vs. Emphysema

Which is more likely to cause cor pulmonale?

A

Bronchitis

39
Q

Bronchitis vs. Emphysema

Which has worse elastic recoil?

A

Emphysema

40
Q

Why do emphysema patients become cachectic?

A

Pink puffers
Purse their lips for breathing
Work of breathing is increased, so they often get weakness and wasting of the body due to their chronic illness

41
Q

What is Bronchiectasis?

A

Permanent dilatation of bronchi and bronchioles caused by destruction of muscle and elastic tissue caused by chronic necrotizing inflammation

42
Q

Describe the pathogenesis of Bronchiectasis

A

Obstruction in the airway leads to impaired clearing mechanisms and pooling of secretions distal to that obstruction.

Leads to inflammation of the airway with necrosis, fibrosis, and eventual dilatation

43
Q

What are two genetic disorders that could lead to Bronchiectasis?

A

Cystic fibrosis

Kartagener syndrome

44
Q

What is the pathological issue in cystic fibrosis? How does this cause bronchiectasis?

A

Chloride channel (CFTR) dysfunction. Cannot bring H2O out into mucus, so you get thick mucus that is difficult to clear from the airways

Autosomal recessive

45
Q

Kartagener Syndrome

What is the primary pathological issue?

A

Primary ciliary dyskinesis

Absence/shortening of the dynein arms prevents proper functioning of the cilia

MHD (57 decks)

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