Pulmonary Pathology 2 Flashcards

1
Q

wWhat occurs in chronic bronchitis?

A

mucus hypersecretion, inflammation, and infection

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2
Q

how is chronic bronchitis defined from a clinical standpoint?

A

persistent cough with sputum production for 3 months out of 2 consecutive years

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3
Q

what is the pathophysiology of chronic bronchitis?

A

mucous gland hyperplasia–> damage to airway epithelium

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4
Q

what are 5 consequences of chronic bronchitis?

A

1) bronchiectasis 2) hypoxia 3) squamous metaplasia–> dysplasia–> carcinoma 4) pulmonary hypertension and cor pulmonale 5) death from respiratory infection

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5
Q

what is emphysema?

A

an irreversible airspace enlargement occurring distal to the terminal bronchiole

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6
Q

which type of emphysema is caused by smoking?

A

centrilobular

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7
Q

where does smoking-related emphysema dilation start?

A

respiratory bronchiole

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8
Q

what are some clinical presentations of emphysema?

A

enlarged lungs on CXR- barrel chest; diminished breath sounds with prolonged expiratory wheezes

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9
Q

why is there elevated hemoglobin in chronic bronchitis?

A

when you smoke, you are exposed to CO, this created carboxy hemoglobin, which does not carry O2. so the oxygen dissociation curve shifts to the left. And we create more hemoglobin to compensate

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10
Q

what type of emphysema does alpha-1 antitrypsin deficiency cause?

A

panacinar

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11
Q

what two patterns should you be aware of in cases of alpha-1 antitrypsin deficiency?

A

1) alveoli with panacinar destruction 2) lung with predominantly basilar panacinar emphysema

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12
Q

what is the primary means for diagnosing alpha-1 antitrypsin deficiency?

A

serum testing for alpha-1AT

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13
Q

what are the complications associated with emphysema? (4)

A

pneumothorax, respiratory failure, CAD, pulmonary HTN and cor pulmonale

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14
Q

what are the 3 components of asthma?

A

1) recurrent airway obstruction with a reversible component 2) airway hyper-responsiveness 3) airway inflammation

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15
Q

what cells are you likely to associate with atopic asthma?

A

eosinophils, mast cells, and lymphocytes

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16
Q

what cells are you likely to associate with non-atopic asthma?

A

t lymphocytes and neutrophils

17
Q

why is long-term asthma control important?

A

asthma has some very deleterious long term effects such as airway remodeling

18
Q

what occurs in airway remodeling due to long term asthma?

A

fibrosis, smooth muscle hyperplasia, increased goblet cells and submucosal glands

19
Q

what is the crisis condition associated with severe asthma?

A

status asthmaticus

20
Q

what is occurring in status asthmaticus?

A

unremitting, potentially fatal asthma attack–> bronchial occlusion by thick mucous

21
Q

what are the histologic features associated with status asthmaticus?

A

coiled mucus plugs aka “Curschmann spirals” and charcot leyden crystals

22
Q

how does aspirin-sensitive asthma occur?

A

when you block cyclooxygenase it will shunt arachidonic acid down the lipoxygenase pathway

23
Q

what triad is associated with aspirin -sensitive asthma?

A

samter’s triad

24
Q

what makes up samter’s triad?

A

nasal polyps, recurrent rhinitis, aspirin sensitive asthma

25
Q

what is bronchiectasis?

A

dilated bronchus with a tiny air passageway bc of all the mucus; dilated bronchi extended to pleural surface

26
Q

what are examples of diseases that are associated with bronchiectasis?

A

cystic fibrosis, primary ciliary dyskinesia, allergic bronchopulmonary aspergillosis

27
Q

what is occurring in primary ciliary dyskinesia?

A

dysfunction of the dynein arm of microtubules

28
Q

what syndrome is associated with primary ciliary dyskinesia?

A

kartagener’s syndrome

29
Q

what triad makes up kartagener’s syndrome?

A

sinusitis, bronchoiectasis, and situs inversus

30
Q

what is allergic bronchopulmonary aspergillosis?

A

exaggerated hypersensitivity response to aspergillus infection overlying chronic lung disease