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Respiratory Block > Obstructive Disease > Flashcards

Obstructive Disease Flashcards

1
Q

Obstructive disease parameters are:

A

FEV1 is reduced,

FEV1/FVC is reduced

TLC is increased due to increase in the trapped air

FVC is also reduced or normal

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2
Q

What is vital capacity?

A

The Inspiratory capacity + tidal volume + expiratory capacity

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3
Q

What does obstructive disease affect?

A

It affects the airways (partial or extensive obstruction).

Can be partial obstruction vs complete obstruction.

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4
Q

What happens to parameters in restrictive diseases?

A

TLC is reduced due to decreased capacity in inhalation

FEV1 is reduced or normal

FEV1/FVC is usually increased or normal. (>80%)

Forced Vital Capacity is reduced due to the reduction in inspiration.

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5
Q

What do restrictive diseases affect and what do they involve?

A

It affects parenchyma, difficulty exapanding, most often caused by ARDS

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6
Q

What is COPD?

A

It is chronic bronchitis and emphysema together. Early symptoms aren’t present. Not fully reversible

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7
Q

Describe bronchitis

A

There is the hyper-secretion of goblet cells in the bronchial wall. Hypertrophy of the submucosal mucous secreting cells. Causes there to be obstruction in the airways

In the small airways there is increased goblet cells in the smaller airways

Airflow obstruction or increased obstruction in the airways due to the increased mucous glands.

Small airway fibrosis basically.

Airflow obstruction.

There is also inflammatory response which is CD8+ response–>airflow obstruction. Damage to the airway.

Reid Index > 0.5 (50%)

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8
Q

What are the clinical features of Bronchitis?

A

Blue bloaters ( mucus traps CO2)

causes Pa Co2 to increase, and PaO2 to decrease

Productive cough for more than 3 months in 2 years

can be cor pulmonale

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9
Q

What is emphysema

A

Emphysema is due to basically there being destruction of alveolar sacs. Results in excessive air trapping and causes there to be loss of elastic recoils.

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10
Q

What are the 4 different causes of emphysema?

A

Due to imbalance and of proteases and anti-proteases, smoking, AIAT deficiency.

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11
Q

What happens in imbalance of proteases and antiproteases?

A

Inflammation causes there to be protease release by the neutrophils and macrophages. A1AT causes neutralization. Lack of the enzyme causes there to be increased neutrophils.

Smoking is the most common cause of emphysema –> centri-acinar (upper lobes)

Hereditary AIAT Deficiency: pan-acinar.

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12
Q

AIAT effects on the liver:

A

the mis-folded proteins cause them to be stuck in the liver, causing them to be struck in the ER of hepatocytes

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13
Q

What are the clinical features of emphysema?

A

They are pink puffers, barrel chest, loss of alveoli. Dyspnea and cough with minimal sputum

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14
Q

What is the definition and pathogenesis of asthma

A

Asthma is reversible bronchoconstriction, and is caused by type 1 hypersensitivity.

Allergens induce there to be Th2 cells in CD4+ cells. These release release IL-4 and IL-5. IL-4 causes IgE switching. IL-5 is causes eosinophil attraction and IL-10 (attracts TH2 and inhibits TH1).

The second time there is a IgE induced reaction–> causes there to be leukotrienes (CDE4 release) and histamine release.

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15
Q

What are the clinical aspects of asthma?

A

They are dyspnea, productive cough and dyspnea. Productive cough can cause there to be wither Curschmann Spirals, or there can be Eosinophilic crystals ( Charcot-Leyden Crystals)

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16
Q

What can asthma be caused by?

A

Allergic rhinitis, Eczema, an a family history of Atopy.

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17
Q

What happens in early phase asthma?

A

Vascular permeability, edema, and bronchoconstriction and mucus production.

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18
Q

What happens in late phase of the asthma reaction?

A

What happens in the late phase is that major basic protein from the Eosinophils damages cells and causes bronhoconstritcion

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19
Q

What is severe non-responsive asthma called?

A

Status asthmaticus

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20
Q

What is the cause of bronchiectasis?

A

It is basically when there is permanent dilation of bronchi and bronchioles due to several reasons:

Can be because of

  1. CF
  2. Ciliary dyskinesea
  3. Necrotizing pneumonia
  4. local obstruction
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21
Q

How can CF cause there to bronchiectasis?

A

CF can cause bronchiectasis as the impaired chloride channels can cause an increase in mucus production, causing there to be more infections ==> increased destruction of the bronchial tissue.

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22
Q

How can primary ciliary dyskinesia cause there to be an bronchiectasis?

A

The dynein arm mutation can cause there to be lack of ciliary movement, which can caused increased infections.

23
Q

What is Kartagener’s Syndrome?

A

Kartagener’s is when there is the triad: situs invertus, sinusitis, bronchiectasis , infertile of male

24
Q

What is morphology of bronchiectasis?

A

Dilated airways with thick purulent mucus, MC lower lobes near pleural folds, and necrotizing inflammation

25
Q

What are clinical features of bronchiectasis?

A

severe persistent cough with cupfulls of mucous. Hemoptysis. Antibiotic treatment

26
Q

What is the pathophysiology, pathogenesis, and morphology of interstitial lung?

A

Heterogenous chronic interstitial (restrictive) disease that cause diffuse and chronic bilateral fibrotic changes that mainly affect the alveolar interstitium.

27
Q

What do all they advanced stages of interstitial lung disease cause?

A

Honey comb lung.

28
Q

Clinical Features of interstitial lung disease

A

There is ground glass appearance and hypoxemia and hypercapnia

29
Q

Idiopathic Pulmonary Fibrosis/Cryptogenic Fibrosis definition

A

Patchy chronic bilateral fibrotic changes of unknown etiology

30
Q

What is the predicted etiology?

A

It is basically repetitive micro-injuries to ageing alveolar epithelium by environment.

31
Q

Pathogenesis:

A

Loss of senescent Type 2 cells

32
Q

Morphology of Idiopathic interstitial lung disease?

A

Injured pneumocytes causes there to be reaction from TGF B, which causes there to be fibrosis of the lung.

33
Q

What are the clinical features of interstitial lobar pneumonia?

A

There is bilateral fibrosis of the lungs, and with sub-pleural patches, and it causes honeycombing at later disease stages

34
Q

What are the other clinical features present for pumonary fibrosis/ cryptogenic fibrosing alveolitis?

A

Is in males >50 years old, 3-5 year prognosis. insiduous dyspnea on exertion,
dry cackles/ velcro rales at the lung bases
Honeycombing
Dx of exclusion (usual interstitial pneumonia)

35
Q

What is treatment of the idiopathic fibrinogenic interstitial pneumonia?

A

lung transplant

36
Q

Non-specific interstitial pneumonia definition, morphology

A

When there is bilateral fibrotic changes that are often associated with collagen vascular disorders such as rheumatoid arthritis

37
Q

What is the morphology of non-specific interstitial pneumonia?

A

Cobble stoned pleural retraction, rubber white areas of fibrosis, mainly lower lobe/interlobar septa/subpleural space.

38
Q

What are the microscopic features of non-specific interstitial pneumonia?

A

is in middle aged females (73% 10 year survival)

HCRT–> bilateral patchy ground glass infiltrates

39
Q

Treatment is

A

corticosteroids, immunosuppressives, and lung transplant

40
Q

Pneumoconiosis

A

It is interstitial fibrosis dues to occupational exposure, requires chronic exposure to small particles that are fibrogenic: alveolar macrophages engulf the particles and induce fibrosis

41
Q

What are the different types of pneuomoconioses?

A
  1. Coal workers:
  2. Silicosis:
  3. berylliosis:
  4. Asbestosis:
42
Q

What does coal worker’s pneumoconiosis cause?

A

When coal is phagocytosed by dust cells –> aggregates in the interstitium and causes –> dilation of the respiratory bronchioles

43
Q

Silicosis

A

Sandblasters and silica miners. Fibrotic nodules in the upper lobes of the lung

44
Q

Asbestosis

A

Asbestosis: insulating materials cause this Phagocytosis of asbestos by dust cells. –> no digestion–> asbestos fibers coated by iron and protein. Release of TNF alpha and IL-1 to stimulate fibroblasts to deposit connective tissue

45
Q

What does CWP present as?

A

Simple, 1-4 mm blackcoal dust macules (collagen and macrophages) in the upper lobe.

In complicated cases, macules coalesce into nodules –> respiratory impairment

46
Q

Silicosis

A

Concentric whorls of collagen fibers with peripheral mononuclear cells = silicotic nodules. Upper lobe hilar nodes and pleura

47
Q

Asbestosis

A

Bilateral diffuse interstitial fibrosis in lower lobes.

Calcium plaques in the pleura.

Asbestos bodies (look like screw in the bronchiolar walls/ alveoalr space

CXR pleural plaques swwnin the anterior and posterolateral parietal pleura and domes of the diaphragm.

48
Q

For CWP, what are the clinical features?

A

They are SOB and cough

49
Q

What are the clinical features of silicosis?

A

They are eggshell like calcification of hilar lymph nodes

and increases risk of TB

50
Q

Asbestosis clinical features?

A

There is association with mesothelioma

51
Q

What are the causes of sarcoidosis?

A

It is basically when there is formation of non-caseating granulomas. Can be due to CD4+ T-helper cells and cause to an unknown antigen

52
Q

Morphology of sarcoidosis

A

Macroscopic: bilateral peripheral lymphadenopathy (hilar and mediastinal lymph nodes)

53
Q

Microscopic

A

Non-caseating (non-necrotizing) GRANULOMA.

Asteroid Bodies: stellate inclusion w/giant cells

Schaumann Bodies: concretions with calcium and proteins

54
Q

What are the clinical features?

A

Nonsmoking adults <40 years of, african american females most common.

HRCT–> bilateral hilar lymphadenopathy (potato nodes

Associated with Bell’s Palsy,a facial droop.

Respiratory Block (12 decks)

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