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Pathology II > Exam 3 - Respiratory > Flashcards

Exam 3 - Respiratory Flashcards

1
Q

Accumulated alveolar macrophages. Cells that are filled with hemosiderin deposits (brown induration)

A

Hear failure cells

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2
Q

What offers protection against edema in the wall fo the lungs?

A

Tight junctions of endothelial and epithelial cells

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3
Q

Common causes of pulmonary edema

A
  1. Any condition that contributes to pulmonary HTN
  2. Hypoalbuminemia (reduced oncotic pressure)
  3. Lymph obstruction
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4
Q

What condition(s) contributes to pulmonary HTN? And what can pulmonary HTN lead to?

A

Left side heart failure & Mitral stenosis (etc.)

Leads to: Pulmonary edema

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5
Q

What are causes of Hypoalbuminemia (reduced oncotic pressure)? And what can that lead to?

A

Liver disease, nephrotic syndrome, severe burns

May lead to pulmonary edema

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6
Q

What can cause lymphatic obstruction? And what is the concern?

A

Tumors, renal disease, congestive heart failure.

The concern is pulmonary edema

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7
Q

What can cause pulmonary emboli and infarcts?

A 
Any factor that leads to systemic thrombosis including:
Cardiac disease
Immobilization
Trauma
Surgery
Burns
Cancer
Hypercoagulability states
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8
Q

What is ARDS

A

Adult respiratory distress syndrome aka Lung Shock

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9
Q

Diffuse alveolar and capillary damage contribute to increased permeability, accumulated fluid and respiratory failure.

On plain film, you would see fluid filled, firm, red, boggy lungs.

A

ARDS (adult respiratory distress syndrome)

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10
Q

Causes of ARDS?

A 
Most common: sepsis
Chemical and thermal injury
Oxygen toxicity
Severe lung infections
Near drowning
Narcotic overdose
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11
Q

Atelectasis

A

Decrease in lung volume for whatever reason

“incomplete expansion of the lungs,”
Greek: ateles “imperfect, incomplete,” literally “without an end,” (from a-, privative prefix, + telos “completion”) + ektosis “extention

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12
Q

Why does atelectasis happen in neonatals?

A

Stillborn where lungs are airless or secondary deficiencies of surfactant leads to collapsed alveoli

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13
Q

What is acquired atelectasis?

A

Either obstructive (absorptive) or compressive

Obstructive: airways blocked by foreign bodies, tumors, secretions
Compressive: contributing causes include pneumothorax and hydrothorax

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14
Q

In obstructive atelectasis, what way does the mediastinum shift?

A

Toward affected side

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15
Q

In compressive atelectasis, what way does the mediastinum shift?

A

Away from affected side

E.g. pneumothorax and hydrothorax

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16
Q

A group of chronic pulmonary disorders that restrict ventilation (airflow)

A

COPD (chronic obstructive pulmonary disease)

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17
Q

Characteristics of COPD?

A

Narrowing of bronchi and bronchioles, chronic or episodic patterns and dyspnea during symptomatic stages

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18
Q

What are major disease characterized by COPD?

A

Emphysema

Chronic bronchitis

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19
Q

What is common characteristic in emphysema in terms of the alveoli?

A

Enlargement of alveoli and reduced pulmonary elasticity

E.g. like an office building with a bunch of cubicles — take out some of the cubicle walls and you make the spaces bigger

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20
Q

A serum enzyme produced in the liver protects against action of Proteoglycan enzymes derived from leukocytes activated within lung

A

Alpha-1-antitrypsin (anti-elastase)

This is associated with the pathogenesis of emphysema

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21
Q

What is the enzymatic hypothesis associated with the imbalanced actions of proteases and protease inhibitors within the lung?

A

Alpha-1-antitrypsin

Reduced antitrypsin activity includes tobacco smoke and hereditary deficiency of alpha-1-antitrypsin

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22
Q

Whatare the anatomical patterns of emphysema?

A

Centrilobular — most common
Panlobular — most severe
Other types: paraseptal and irregular (patchy)

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23
Q

What are first signs of emphysema?

A
  • Progressive dyspnea
  • Cough but NOT productive
  • Weight loss because breathing burns calories
24
Q

dyspnea

A

Difficult or labored breathing

25
Q

What are advanced signs of emphysema?

A
  • Lungs become hyperinflated “barrel chest”
  • X-ray shows reduced pulmonary density
  • Prolonged expiration
  • Pts compensate by overventilating “pink puffers”
26
Q

One cause of mortality for people with emphysema is pneumothorax which is associated with the rupture of

A

Bullae

27
Q

4 causes for mortality of emphysema

A
  • pneumothorax
  • Cor pulmonale with increased risk for heart failure
  • respiratory acidosis - decreased ventilation lead to elevated CO2
  • increased vulnerability to respiratory infection
28
Q

Pink puffer

A

Emphysema

Lungs become hyperinflated which contributes to “barrel chest” and depressed diaphragm. Pts overcompensate by overventilating and elevating intrapulmonary pressures, thus they are well oxygenated.

29
Q

Blue bloater

A

Chronic bronchitis

Respiratory dysfunction with cyanosis combined with increased risk for heart failure and edema

30
Q

Persistent productive cough for 3+ months for 2 consecutive years in the absence of other causes

A

Chronic bronchitis

31
Q

Pathogenesis and risk factors of chronic bronchitis

A

Bronchiolitis — small airways disease — interferes with pulmonary ventilation

Risk factors: air pollution, cigarette, pulmonary infection 2˚

32
Q

Recurrent infections of chronic bronchitis contribute to squamous cell

A

Metaplasia with loss of cilia. So the secretions are “trapped” and can’t get bumped out by the cilia (because you lost your cilia)

33
Q

What is another name for bronchial asthma? And what is it?

A

paroxysmal dyspnea

Chronic inflammatory disorder of airways leading to recurrent episodes of wheezing, breathlessness, chest tightness, cough.

34
Q

What are the 2 classes of bronchial asthma/paroxysmal dyspnea? and which one is associated with being IgE mediated?

A

Extrinsic — reaginic, atopy** IgE mediated (type I hypersensitivity)
Intrinsic — non-reaginic, idiosyncratic

35
Q

Chronic necrotizing infection of bronchi and bronchioles lead to permanent dilation of air passages with pooling of secretions

A

Bronchiectasis

Usually 2˚ and seen as the “end stage” of other disease

36
Q

Pathogenesis of bronchiectasis

A

Infection

  • bronchial obstruction may contribute to secretions building up and being a medium for infection
  • reduced cilia movement
  • necrotizing infections such as measles, staph or pertussis, TB
37
Q

Infection of lung parenchyma

A

Pneumonia, pneumonitis

38
Q

Acute bacterial infections give rise to exudates that fill alveolar spaces with ________ of affected pulmonary tissue

A

Consolidation, solidification

39
Q

4 types of acute bacterial pneumonia infections

A
  • Lobar pneumonia - 4 stages/phases of progression
  • Bronchopneumonia - caused by staph and strep, more common in the very young or old with pre-existing disease
  • Acute necrotizing pneumonia - sudden onset, rapid progression, high mortality
  • Acute interstitial pneumonitis or primary atypical pneumonia “PAP” - mild
40
Q

Acute bacterial infections uniformly affect a large region of the lung, this is called _______ pneumonia

A

Lobar

90% due to pneumococcus

41
Q

Name 4 stages of lobar pneumonia

A

Congestion — inflammation with dilation of alveolar capillaries
Red hepatization — exudates fill alveolar spaces = productive cough
Gray hepatization — consolidation persists, RBCs lysed, antibodies to bacteria form, symptoms persist
Resolution — recovery, exudates lysed, drop in temp

42
Q

Acute necrotizing pneumonia caused by what organisms or conditions?

A

Plague
Anthrax “wool-sorters disease”
Legionnaire’s disease

43
Q

Primary atypical pneumonia (PAP) is also called

A

Acute interstitial pneumonitis (AIP)

44
Q

Etiology of acute interstitial pneumonitis?

A

Mycoplasma pneumoniae

45
Q

What are the symptoms of acute interstitial pneumonitis?

A

Mild, acts like a chest cold

46
Q

Tuberculosis leaves behind granulomas and causes what kind of necrosis?

A

Caseous necrosis and liquefaction, so the infected tissue is destroyed

47
Q

1˚ or 2˚ TB? Early stages free of symptoms

A

1˚ and then 2-3 weeks delayed hypersensitivity and cell immunity develop

48
Q

1˚ or 2˚ TB? Occurs in “sensitized” subjects who have had prior TB infection

A

2˚ and caseous necrosis lesions are commonly localized in lung apex

49
Q

What pulmonary infection is characterized by Ghon complex?

A

1˚ (childhood) tuberculosis

50
Q

What are examples of fungal infections of the lung?

A
  • Histoplasmosis 🦇
  • Coccidiomycosis
  • Candida
51
Q

What is it called when you inhale suspended particles and that causes lung damage and scarring?

A

Pneumoconiosis

52
Q

What specific named dust/breathable chemicals can cause pneumoconiosis (3)?

A

Silicosis - silicon dioxide particles
Asbestosis - fibers are visible as ferruginous bodies
Anthracosis - coal (carbon) dust

53
Q

Most 1˚ lung tumors are

A

Carcinomas

54
Q

What kind of cancer tumor arises in bronchial mucosa

A

Bronchogenic carcinoma

55
Q

What is associated with most lung cancer?

A
  • Cigarette smoke
  • Inhaled industrial carcinogens: radon, asbestos, arsenic, etc
  • Pulmonary scars: abscesses, surgery, infarcts
56
Q

4 histological types of Bronchogenic carcinoma (note which ones are related to cigarettes, which ones aren’t)

A

Squamous cell *cigarette smoking
Small cell “oat cell” *cigarette smoking
Adenocarcinoma - non-cigarette
Large cell

Pathology II (7 decks)

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