Respiratory Flashcards

(117 cards)

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
What happens in the most severe cases of small airway disease?
Bronchiolitis obliterans, obliteration of the lumen of the vessel
26
Pink puffers tend to have mild or severe emphysema and bronchitis?
Severe emphysema and mild bronchitis
27
What happens to the lungs of pink puffers?
They have reduced elasticity and trouble exhaling, patients overventilate
28
What are the 3 hallmarks of asthma?
1. Intermittent and reversible airway obstruction 2. Chronic bronchial inflammation with eosinophils 3. Bronchial smooth muscle hypertrophy
29
What are 3 causes of extrinsic or atopic asthma
1. Genetic predisposition to type 1 hypersensitivity reactions 2. Airway inflammation 3. Bronchial hyperresponsiveness to various stimuli
30
In extrinsic asthma antigens lead to what type of cell reaction?
TH2 cell reaction
31
When does the early immediate response of asthma begin?
Within a hour of antigen inhalation and leads to bronchioconstriction by muscle contraction
32
What attracts the cells that involved in the late phase?
Mast cell cytokines
33
In asthma, the bronchioles are blocked with mucus containing?
Curschmann's spirals
34
What types of inflammatory cells are present, what structures are present derived from these cells?
Eosinophils, Charcot-Layden crystals
35
Severe cases of asthma can lead to?
Heart failure
36
What is the term for persistent paroxysm that can be fatal?
Status asthmaticus
37
Cystic fibrosis occurs as a result of?
Abnormal function of chloride channel proteins encoded by the CF transmembrane conductance regulator gene
38
Decreased chloride excretion leads to?
Increased reabsorption of sodium ions and water which causes thick, obstructive mucus
39
How do you diagnose cystic fibrosis?
Elevated chloride levels in sweat
40
What happens in cystic fibrosis aside from the pulmonary manifestations?
Hepatic cirrhosis and impaired intestinal digestion and absorption
41
What are the hallmarks of chronic interstitial or restrictive lung diseases?
Reduced compliance, dyspnea, damage to alveolar walls
42
What do patients often develop?
Respiratory faiure
43
In idiopathic pulmonary fibrosis what is the histologic pattern?
Usual interstitial pneumonia
44
What cells are injured in idiopathic pulmonary fibrosis? They produce a certain substance resulting in?
Type 1 pneumocytes. Produce TGF-beta-1 which turns fibroblasts into myofibroblasts
45
When fibroblasts turn into myofibroblasts, this causes excess deposition of?
Collagen
46
What is the only definitive treatment for idiopathic pulmonary fibrosis?
Lung transplant
47
What is pneumoconiosis?
Non-neoplastic lung reactions to inhalation of mineral dusts
48
The most dangerous particles are of what size
1-5 micrometers
49
What causes lung injury in pneumoconiosis?
After macrophages ingest the particles, they release toxic agents
50
Anthracosis is caused by?
Inhalation of the silica in coal
51
Who get asymptomatic pulmonary anthracosis?
Urban dwellers and coal miners
52
Where does the inhaled carbon accumulate in asymptomatic anthracosis?
Perilymphatic connective tissue and the lymph nodes
53
Simple coal works pneumoconiosis may develop into?
Centrolobular emphysema
54
Once large nodules coalesce, what can happen?
Complicated CWP or progressive massive fibrosis AKA black lung disease
55
The large black scars in this disease cause?
Respiratory dysfunction, pulmonary hypertension, and cor pulmonale
56
Silicosis is caused by?
The crystalline forms of silica, specifically quartz
57
What will you see in the early stages of silicosis?
Tiny nodules caused by macrophages releasing fibrogenic mediators
58
When do patients with silicosis begin to experience shortness of breath?
When the the nodules coalesce resulting in progressive massive fibrosis
59
Silicosis is linked to increased susceptibility to?
Tuberculosis and cancer
60
Asbestosis is caused by?
Asbestos fibers, specifically those that are straight, stiff, and long (amphiboles).
61
Asbestosis can lead to?
Cor pulmonale, lung carcinoma, and mesothelioma
62
What is sarcoidosis?
A multi system disease characterized by non-caseous granulomas in many organs
63
What causes it?
A disordered immune response in those who are genetically susceptible
64
What is a major feature in most cases of sarcoidosis?
Bilateral hilar lymphadenopathy or lung disease
65
What oral feature may be enlarged in sarcoidosis?
The parotid gland leading to xerostomia
66
Those with sarcoidosis will show elevated levels of what 5 things?
Angiotensin-converting enzyme, ESR, calcium, vitamin D, and alkaline phosphatase
67
What is the skin test for sarcoidosis?
Kveim-Siltzbach
68
What is the most common test for sarcoidosis?
Transbronchial lung biopsy
69
How is sarcoidosis treated?
Corticosteroids, steroid sparing agents, antimalarial agents
70
A small number of people with sarcoidosis develop?
Progressive fibrosis and cor pulmonale
71
What is the most common etiologic agent of pneumonia?
Streptococcus pneumoniae
72
Bronchopneumonia involves how much of the parenchyma?
Patchy parts, not the whole thing
73
Lesions seen in bronchopneumonia contain what cells? What areas does this exudate fill?
Neutrophils. The exudate fills bronchi, bronchioles, and alveoli
74
Lobar pneumonia infects how much of the parenchyma?
A large area, as much as an entire lobe
75
What happens in the first stage of lobar pneumonia?
Congestion along with vascular dilatation and intra-alveolar fluid exudate
76
What happens in the second stage of lobar pneumonia?
Red hepatization, obliteration of the alveolar spaces by red blood cells, neutrophils and fibrin
77
What happens in the third stage?
Grey hepatization, the fibrosuppurative exudate persists while the red cells disintegrate
78
What is the fourth stage?
Resolution, the exudate is digested
79
What affect does influenza type C have on the respiratory system?
Mild respiratory illness
80
How is influenza type A divided into types?
based on the antigens on its surface, H for hemagluttinin and N for neuraminidase
81
What is H5N1?
A type of influenza type A that causes severe respiratory illness
82
What is H7N9?
A type of influenza type A that causes severe respiratory illness
83
Patients with SARS-CoV go on to develop what respiratory condition?
Severe acute respiratory syndrome
84
What is aspiration pneumonia?
A necrotizing fatal pneumonia in those who aspirate stomach contents
85
What kind of bacteria are involved in aspiration pneumonia?
Usually aerobic
86
What is a common complication in those that survive the initial episode of aspiration pneumonia?
Fatal abscess formation
87
Tuberculosis is the leading cause of death in what illness?
AIDS
88
What bacteria is usually involved in TB?
Mycobacterium tuberculosis
89
What happens in the earliest stages of primary TB?
The bacteria replicate within macrophages
90
What symptoms do patients experience in this time, the 1st 3 weeks?
Either have no symptoms or are mildly ill
91
After 3 weeks, mycobacterial agents cause what to happen?
Activate TH1 cells to produce IFN-gamma, this makes macrophages bactericidal
92
What cells form epithelioid granulomas and cause caseous necrosis?
TH1 cells
93
When macrophages are activated by IFN-gamma they produce what cytokine?
TNF, causes monocytes to become epithelioid cells
94
In primary TB what develops at the initial site of involvement?
The Ghon focus
95
When bacilli spread via airways this is called?
Miliary TB
96
What is the gold standard for diagnosing TB?
Culture
97
What else can be used in the mean time since cultures take time?
Acid fast stains and PCR
98
When the CD4 count dips below what level can primary progressive TB become an issue?
Less than 200
99
What two mycobacteria cause problems in the last stages of AIDS?
Avium and intracellulare
100
What is the most common cause of cancer mortality worldwide?
Lung carcinoma
101
What are the 4 major histologic types of lung cancer?
Adenocarcinoma, small cell carcinoma, large cell carcinoma, and squamous cell carcinoma
102
Which of the 4 is the most common?
Adenocarcinoma
103
Where do most lung cancers begin?
Near the hills in primary, secondary, and tertiary bronchi
104
What structures are seen in well differentiated squamous cell carcinomas?
paving stone like epithelial cells with intercellular bridges and keratin pearls
105
How often does lymph node spread occur in lung squamous cell?
Often
106
Which of the 4 types has the worst prognosis?
Small cell carcinoma
107
What is the term for the appearance of cells in small cell carcinoma>
Oat cells
108
Cells in small cell carcinoma resemble what cell?
Neuroendocrine, some may even produce hormones and neuron-specific enolase
109
What is the most common type of cancer in non-smokers?
Adenocarcinoma
110
What is the precursor to adenocarcinoma?
AAH or atypical adenomatous hyperplasia
111
What are the 4 most common sites of metastasis for lung cancer?
Adrenal gland, liver, bone, brain
112
Lung cancer is known for paraneoplastic syndromes, what hormones are produced as a result of this in small cell carcinomas?
ADH and ACTH
113
What hormones are produced in squamous cell carcinomas?
PTH and hypercalcemic agents
114
What two osseous changes are strongly linked with lung cancer?
Finger clubbing and hypertrophic osteoarthropathy
115
What is the most common site of metastases?
Lung, secondary tumors in the lung are the most common types of lung cancer
116
What is compression atelectasis and what causes it?
Lungs collapse due to pressure in the pleural cavity. Due to fluid effusion in CHF, pneumothorax, blood
117
What is contraction atelectasis?
Fibrosis in the lung hampers expansion, irreversible