Chronic Obstructive Pulmonary Disease and Lung Abscess Flashcards

1
Q

Emphysema
Chronic bronchitis
Asthma

Overlaps

A

Alveolar wall destruction and overinflation

Productive cough and airway inflammation

Bronchial hyperresponsiveness from allergens and infections

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2
Q

Emphysema def and acini shape

A

Abnormal dilitation from the level of the terminal bronchiole on down and permanent and not associated with scar

Acini are roughly spherical and 7 mm in diameter…this is where gas exchange occurs

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3
Q

Centri
Pana
Distal
and Irregular

A

Central - middle…central acinus is abnormally dilated up

Panacinar - entire

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4
Q

Emphysema

Etiology and patho

A

Smoking…and rarely alpha-1-antitrypsin def…smoking increases elastase which leads to elastic damage…due to neutrophil recruitment

antitrypsin def…decrease antielastase and more elastic damage…this also happens in smoking

Protease-antiprotease theory

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5
Q

Emphysema microscopic pathology and gross

A

Gross - panacinar/centroacinar

Destruction of bronchial walsl

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6
Q

Clinical features of emphysema

A

1st sx - shortness of breath

Only reliable finding is slowing of forced expiration

“pink puffer” - puffing, working hard, good oxygenation, thin

Relatively decent oxygenation

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7
Q

Chronic bronchitis etiology and patho

A

Smoking, airpollution, infection

Large vs. small airway change airflow obstruction and role of infections…in small airways, will feel more SOIB

Obstructive chronic bronchitis - if you add the SOB

Chronic asthmatic bronchitis - coughing up stuff with variable wheezing

Most important aspect is the sputum production***

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8
Q

Chronic bronchitis gross vs. microscopic

A

Mucinous plugs

Increase in size of submucosal glands, goblet cell hyperplasia, mucous plugging, and inflammation of msall airways

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9
Q

Chronic bronchitis clinical

A

Sputum production

DOE with eventual ABG changes…will stop exercising and comfortable being hypoxic

Blue bloaters - overweight person becoming more blue

Exacerbations - mucous becomes infected and pours out all of the sudden

Most common basteria is heamophilus influenza

LT comps - pulmonary hypertension…right sided heart failure…core pulmomaly?

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10
Q

Asthma patho

A

Depends on subtype

Atopic - IgE mediated hypersensitivity intitial and subsequent exposure to offending allergen

Non atopic - not IgE but secondary to virus or chemicals

Drug induced - aspirin

Occupational - industrial chemicals

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11
Q

Non atopic

Drug induced

Occupational

patho

A

Virus, cold, or stress lower the threshold of responsiveness of the bronchi

Aspirin blocks the COX and tips balance toward leukotrienes

Many mechanisms

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12
Q

Asthma gross pathology

A

Mucous plugging

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13
Q

Asthma microscopic patho

A

Overall thickening of airway wall

Subbasement membrane thicening

Increased vasculairty

increase in size of submucosal glands

Hypertrophy and hyperplasia of smooth muscle wall of bronchus

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14
Q

Asthma clinical

A

Classic attack - sudden onset of cough, SOB and wheezing

Often lasts several hours and can last for several hours

Dx can be aided by increase in airway obstruction, prolonged exp, and increase in blood eosinophil couns

Status asthmaticus may persist for days or weeks and if severe can produce cyanosis and death

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15
Q

Bronchiectasis etiology, patho

A

Obstruction, congenital, infection

Obstruction and infection

Bronchi seen grossly out to the pleura

Inflammation, fibrosis and loss of the linign epithelium

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16
Q

Bronchiectasis clinical

A

Cough with large volumes of foul sputum

Long standing fever

17
Q

Lung abscess etiology, gross path, mciro path, clinical dcourse

A

Most common is aspiration oneumonia, septic emboli, or cancer

Single or multiple, small or large depends on etiology - “lung gangrene”…single - aspiration…multiple - septic emboli in both lungs

Classic finding is suppurative destruction of pung parenchyma within the central cavity

Course - like bronchiectasis…confrim dx using radiologically…rule out cancer