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Systemic Pathology > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Acute respiratory distress syndrome occurs in response to?

A

Direct insults

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2
Q

Examples of these are?

A

Chest trauma, gastic contents, toxic gases

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3
Q

In the exudative or acute phase of ACRDS, where is the primary injury?

A

Vascular endothelium or alveolar epithelial cells

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4
Q

During the exudative or acute phase there is damage to what cells? What does this cause?

A

Type 2 pneumocytes leading to surfactant inactivation and hyaline membrane formation

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5
Q

During the organizing phase of ACRDS what cells attempt to repair the damage?

A

Type 2 epithelial cells proliferate

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6
Q

What happens in mild cases of ACRDS? Progressive?

A

Resolution, progressive cases show intra-alveolar fibrosis leading to marked thickening of the septa

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7
Q

What is the usual cause of mortality in progressive ACRDS

A

Secondary bronchopneumonia

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8
Q

How does respiratory distress syndrome of the newborn differ?

A

Surfactant disturbance is primary

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9
Q

What is the most common cause of respiratory distress syndrome in newborns?

A

Hyaline membrane disease, the alveolar cells do not produce surfactant

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10
Q

What happens to those cells without surfactant?

A

Hypoxia and hyaline membrane formation

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11
Q

What is the treatment for this disease?

A

Antenatal corticosteroids given at birth that stimulate surfactant production

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12
Q

Emphysema usually occurs in conjunction with?

A

Chronic bronchitis

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13
Q

What is the most common form of emphysema>

A

Centriacinar or centrolobular

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14
Q

What areas are affected by panacinar emphysema>

A

Alveoli throughout the lung are uniformly enlarged

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15
Q

Panacinar emphysema is associated with a deficiency in what enzyme?

A

Alpha-1-antitrypsin

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16
Q

Smoking stimulates the formation of what enzyme?

A

Elastase, it also destroys its inhibitor

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17
Q

What do patients develop when they have alpha-1-antitrypsin deficiency?

A

Panlobular emphysema and cirrhosis of the liver

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18
Q

Polymorphisms in what gene determine susceptibility to COPD? Why?

A

TGFB gene, these determine the response of mesenchymal cells to injury

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19
Q

Does tissue destruction occur with or without fibrosis in emphysema?

A

Without due to lack of mesenchymal cells

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20
Q

What is the key to diagnosis of emphysema?

A

Limited ability to expire

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21
Q

Define chronic bronchitis clinically

A

Persistent cough with sputum production occurring for at least 3 months in 2 consecutive years without any identifiable cause

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22
Q

What happens in large airway disease?

A

Smoking and other irritants cause hyper secretion of mucus in large airways with secondary infection

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23
Q

What is the morphologic basis of airflow obstruction?

A

Small airway disease

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24
Q

What type of cell change is seen in small airway disease?

A

Goblet cell metaplasia

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25
Q

What happens in the most severe cases of small airway disease?

A

Bronchiolitis obliterans, obliteration of the lumen of the vessel

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26
Q

Pink puffers tend to have mild or severe emphysema and bronchitis?

A

Severe emphysema and mild bronchitis

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27
Q

What happens to the lungs of pink puffers?

A

They have reduced elasticity and trouble exhaling, patients overventilate

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28
Q

What are the 3 hallmarks of asthma?

A
  1. Intermittent and reversible airway obstruction
  2. Chronic bronchial inflammation with eosinophils
  3. Bronchial smooth muscle hypertrophy
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29
Q

What are 3 causes of extrinsic or atopic asthma

A
  1. Genetic predisposition to type 1 hypersensitivity reactions
  2. Airway inflammation
  3. Bronchial hyperresponsiveness to various stimuli
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30
Q

In extrinsic asthma antigens lead to what type of cell reaction?

A

TH2 cell reaction

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31
Q

When does the early immediate response of asthma begin?

A

Within a hour of antigen inhalation and leads to bronchioconstriction by muscle contraction

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32
Q

What attracts the cells that involved in the late phase?

A

Mast cell cytokines

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33
Q

In asthma, the bronchioles are blocked with mucus containing?

A

Curschmann’s spirals

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34
Q

What types of inflammatory cells are present, what structures are present derived from these cells?

A

Eosinophils, Charcot-Layden crystals

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35
Q

Severe cases of asthma can lead to?

A

Heart failure

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36
Q

What is the term for persistent paroxysm that can be fatal?

A

Status asthmaticus

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37
Q

Cystic fibrosis occurs as a result of?

A

Abnormal function of chloride channel proteins encoded by the CF transmembrane conductance regulator gene

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38
Q

Decreased chloride excretion leads to?

A

Increased reabsorption of sodium ions and water which causes thick, obstructive mucus

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39
Q

How do you diagnose cystic fibrosis?

A

Elevated chloride levels in sweat

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40
Q

What happens in cystic fibrosis aside from the pulmonary manifestations?

A

Hepatic cirrhosis and impaired intestinal digestion and absorption

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41
Q

What are the hallmarks of chronic interstitial or restrictive lung diseases?

A

Reduced compliance, dyspnea, damage to alveolar walls

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42
Q

What do patients often develop?

A

Respiratory faiure

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43
Q

In idiopathic pulmonary fibrosis what is the histologic pattern?

A

Usual interstitial pneumonia

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44
Q

What cells are injured in idiopathic pulmonary fibrosis? They produce a certain substance resulting in?

A

Type 1 pneumocytes. Produce TGF-beta-1 which turns fibroblasts into myofibroblasts

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45
Q

When fibroblasts turn into myofibroblasts, this causes excess deposition of?

A

Collagen

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46
Q

What is the only definitive treatment for idiopathic pulmonary fibrosis?

A

Lung transplant

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47
Q

What is pneumoconiosis?

A

Non-neoplastic lung reactions to inhalation of mineral dusts

48
Q

The most dangerous particles are of what size

A

1-5 micrometers

49
Q

What causes lung injury in pneumoconiosis?

A

After macrophages ingest the particles, they release toxic agents

50
Q

Anthracosis is caused by?

A

Inhalation of the silica in coal

51
Q

Who get asymptomatic pulmonary anthracosis?

A

Urban dwellers and coal miners

52
Q

Where does the inhaled carbon accumulate in asymptomatic anthracosis?

A

Perilymphatic connective tissue and the lymph nodes

53
Q

Simple coal works pneumoconiosis may develop into?

A

Centrolobular emphysema

54
Q

Once large nodules coalesce, what can happen?

A

Complicated CWP or progressive massive fibrosis AKA black lung disease

55
Q

The large black scars in this disease cause?

A

Respiratory dysfunction, pulmonary hypertension, and cor pulmonale

56
Q

Silicosis is caused by?

A

The crystalline forms of silica, specifically quartz

57
Q

What will you see in the early stages of silicosis?

A

Tiny nodules caused by macrophages releasing fibrogenic mediators

58
Q

When do patients with silicosis begin to experience shortness of breath?

A

When the the nodules coalesce resulting in progressive massive fibrosis

59
Q

Silicosis is linked to increased susceptibility to?

A

Tuberculosis and cancer

60
Q

Asbestosis is caused by?

A

Asbestos fibers, specifically those that are straight, stiff, and long (amphiboles).

61
Q

Asbestosis can lead to?

A

Cor pulmonale, lung carcinoma, and mesothelioma

62
Q

What is sarcoidosis?

A

A multi system disease characterized by non-caseous granulomas in many organs

63
Q

What causes it?

A

A disordered immune response in those who are genetically susceptible

64
Q

What is a major feature in most cases of sarcoidosis?

A

Bilateral hilar lymphadenopathy or lung disease

65
Q

What oral feature may be enlarged in sarcoidosis?

A

The parotid gland leading to xerostomia

66
Q

Those with sarcoidosis will show elevated levels of what 5 things?

A

Angiotensin-converting enzyme, ESR, calcium, vitamin D, and alkaline phosphatase

67
Q

What is the skin test for sarcoidosis?

A

Kveim-Siltzbach

68
Q

What is the most common test for sarcoidosis?

A

Transbronchial lung biopsy

69
Q

How is sarcoidosis treated?

A

Corticosteroids, steroid sparing agents, antimalarial agents

70
Q

A small number of people with sarcoidosis develop?

A

Progressive fibrosis and cor pulmonale

71
Q

What is the most common etiologic agent of pneumonia?

A

Streptococcus pneumoniae

72
Q

Bronchopneumonia involves how much of the parenchyma?

A

Patchy parts, not the whole thing

73
Q

Lesions seen in bronchopneumonia contain what cells? What areas does this exudate fill?

A

Neutrophils. The exudate fills bronchi, bronchioles, and alveoli

74
Q

Lobar pneumonia infects how much of the parenchyma?

A

A large area, as much as an entire lobe

75
Q

What happens in the first stage of lobar pneumonia?

A

Congestion along with vascular dilatation and intra-alveolar fluid exudate

76
Q

What happens in the second stage of lobar pneumonia?

A

Red hepatization, obliteration of the alveolar spaces by red blood cells, neutrophils and fibrin

77
Q

What happens in the third stage?

A

Grey hepatization, the fibrosuppurative exudate persists while the red cells disintegrate

78
Q

What is the fourth stage?

A

Resolution, the exudate is digested

79
Q

What affect does influenza type C have on the respiratory system?

A

Mild respiratory illness

80
Q

How is influenza type A divided into types?

A

based on the antigens on its surface, H for hemagluttinin and N for neuraminidase

81
Q

What is H5N1?

A

A type of influenza type A that causes severe respiratory illness

82
Q

What is H7N9?

A

A type of influenza type A that causes severe respiratory illness

83
Q

Patients with SARS-CoV go on to develop what respiratory condition?

A

Severe acute respiratory syndrome

84
Q

What is aspiration pneumonia?

A

A necrotizing fatal pneumonia in those who aspirate stomach contents

85
Q

What kind of bacteria are involved in aspiration pneumonia?

A

Usually aerobic

86
Q

What is a common complication in those that survive the initial episode of aspiration pneumonia?

A

Fatal abscess formation

87
Q

Tuberculosis is the leading cause of death in what illness?

A

AIDS

88
Q

What bacteria is usually involved in TB?

A

Mycobacterium tuberculosis

89
Q

What happens in the earliest stages of primary TB?

A

The bacteria replicate within macrophages

90
Q

What symptoms do patients experience in this time, the 1st 3 weeks?

A

Either have no symptoms or are mildly ill

91
Q

After 3 weeks, mycobacterial agents cause what to happen?

A

Activate TH1 cells to produce IFN-gamma, this makes macrophages bactericidal

92
Q

What cells form epithelioid granulomas and cause caseous necrosis?

A

TH1 cells

93
Q

When macrophages are activated by IFN-gamma they produce what cytokine?

A

TNF, causes monocytes to become epithelioid cells

94
Q

In primary TB what develops at the initial site of involvement?

A

The Ghon focus

95
Q

When bacilli spread via airways this is called?

A

Miliary TB

96
Q

What is the gold standard for diagnosing TB?

A

Culture

97
Q

What else can be used in the mean time since cultures take time?

A

Acid fast stains and PCR

98
Q

When the CD4 count dips below what level can primary progressive TB become an issue?

A

Less than 200

99
Q

What two mycobacteria cause problems in the last stages of AIDS?

A

Avium and intracellulare

100
Q

What is the most common cause of cancer mortality worldwide?

A

Lung carcinoma

101
Q

What are the 4 major histologic types of lung cancer?

A

Adenocarcinoma, small cell carcinoma, large cell carcinoma, and squamous cell carcinoma

102
Q

Which of the 4 is the most common?

A

Adenocarcinoma

103
Q

Where do most lung cancers begin?

A

Near the hills in primary, secondary, and tertiary bronchi

104
Q

What structures are seen in well differentiated squamous cell carcinomas?

A

paving stone like epithelial cells with intercellular bridges and keratin pearls

105
Q

How often does lymph node spread occur in lung squamous cell?

A

Often

106
Q

Which of the 4 types has the worst prognosis?

A

Small cell carcinoma

107
Q

What is the term for the appearance of cells in small cell carcinoma>

A

Oat cells

108
Q

Cells in small cell carcinoma resemble what cell?

A

Neuroendocrine, some may even produce hormones and neuron-specific enolase

109
Q

What is the most common type of cancer in non-smokers?

A

Adenocarcinoma

110
Q

What is the precursor to adenocarcinoma?

A

AAH or atypical adenomatous hyperplasia

111
Q

What are the 4 most common sites of metastasis for lung cancer?

A

Adrenal gland, liver, bone, brain

112
Q

Lung cancer is known for paraneoplastic syndromes, what hormones are produced as a result of this in small cell carcinomas?

A

ADH and ACTH

113
Q

What hormones are produced in squamous cell carcinomas?

A

PTH and hypercalcemic agents

114
Q

What two osseous changes are strongly linked with lung cancer?

A

Finger clubbing and hypertrophic osteoarthropathy

115
Q

What is the most common site of metastases?

A

Lung, secondary tumors in the lung are the most common types of lung cancer

116
Q

What is compression atelectasis and what causes it?

A

Lungs collapse due to pressure in the pleural cavity. Due to fluid effusion in CHF, pneumothorax, blood

117
Q

What is contraction atelectasis?

A

Fibrosis in the lung hampers expansion, irreversible

Systemic Pathology (11 decks)

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