Lungs Part 1 Flashcards
1
Q
How many breaths does one breath per minute?
A
12-20
2
Q
How many lobes does each lung have?
A
right-3
left-2
3
Q
What are the structures of the lung from largest to smallest?
A
trachea, bronchus, bronchioles, terminal bronchioles, acinus
4
Q
What are acini?
A
structures distal to terminal bronchioles
alveolar duct and multiple alveoli
5
Q
Describe Type I pneumocytes?
A
95% of alveolar surface, have pores of Kohn
6
Q
What are pores of Kohn?
A
pores within the type I pneumocytes
this is where diffusion, edema and bacteria occur
7
Q
What are Type II pneumocytes?
A
pneumocytes for surfactant and repair
8
Q
What are pulmonary alveolar macrophages?
A
sparse macrophages within the lung
9
Q
What parts of the lung do pathologies involve?
A
airways, vasculature, interstitum
10
Q
What is atelectasis?
A
collapsed lung because of multiple alveoli collapse (decreases lung volume)
11
Q
What happens to the blood with atelectasis?
A
blood from pulmonary arteries get shunted to pulmonary veins without oxygen, which can cause hypoxia
12
Q
What are the different types of atelectasis?
A
resorption, compression, contraction
13
Q
What is resorption atelectasis?
A
when an obstruction prevents air from reaching distal airways
14
Q
What happens to the air left in the lungs?
A
it eventually becomes absorbed and the alveolae collapse
15
Q
What part of the lung collpases in resorption atelectasis?
A
it depends on the level of obstruction, could be the entire lung, complete lobe or one or more segments
16
Q
What is the most common cause of resorption atelectasis?
A
mucous or mucopurulent plug
17
Q
When does resorption atelectasis occur?
A
postoperatively, can also complicate bronchialasthma, bronchiectasis, chronic bronchitis, tumor or foreign body aspiration
18
Q
What is compression atelectasis also called?
A
passive or relaxation atelectasis
19
Q
What is compression atelectasis?
A
when there is an accumulation of fluid, blood or air within the pleural cavity, which mechanically collapses the lung
20
Q
What is compression atelectasis most commonly caused by?
A
CHF
21
Q
What can compression atelectasis follow?
A
pleural effusion (fluid in the lungs)
22
Q
What is basal atelectasis?
A
a condition from elevated position of the diaphragm
23
Q
Who commonly gets atelectasis?
A
bed ridden patients, patients with ascites, during or after surgery
24
Q
What is contraction atelectasis?
A
a condition when either lcoal or generalized fibrotic changes in the lungor pleura hamper expansion and increase elastic recoil during expiration
25
Which type of atelectasis is reversible?
compression and resorption, as long as it is prompt to prevent hypoxemia and superimposed infection of the lung
26
What does acute lung injury manifest as?
acute onset dyspnea, hypoxemia, development ofbilateral pulmonary infiltrates on the chest radiograph
27
What is acute respiratory distress syndrome?
a clinical syndrome caused by diffuse alveolar capillary and epithelial damage
28
What is ARDS characterized by?
usually characterized by rapidonset of life-threatening respiratory insufficiency, cyanosis and severe arterial hypoxemia that is refractory to oxygen therapy and can progress to multisystem organ failure
40% lethal, 6-12 month survival
29
What is the histologic manigestation of ARDS?
diffuse alveolar damage
30
How does ARDS occur?
a multitude of clinical settings or indirect injury
31
What are the two barriers that are compromised in ARDS?
microvascular endothelium and alveolar epithelium
32
What types of immune cells are seen in ARDS?
lots of neutrophil chemotactic and activating agent by pulmonary macrophages
33
What is obstructive pulmonary disease characterized by?
limitation of airflow, usually resulting from an increase in resistance caused by partial or complete obstruction at any level
34
What is restrictive pulmonary disease characterized by?
reduced expansion of lung parenchyma accompanied by decreased total lung capacity
35
What are the major diffuse obstructive disorders?
emphysema, chronic bronchitis, bronchiectasis, asthma
36
What is the forced vital capacity for those with diffuse obstructive disorders?
normal or slightly decreased
37
What is the expiratory flow rate for those with diffuse obstructive disorders?
significantly decreased
38
The ratio of expiratory flow rate to forced vital capacity is what?
decreased
39
What does expiratory obstruction result from?
anatomic airway narrowing, loss of elastic recoil
40
What is the ratio of diffuse restrictive diseases?
FVC is reduced, expiratory flow rate is normal or reduced or slightly lowered
the ratio is normal
41
What are the restrictive defects that occur during two general conditions?
chest wall disorders in the presence of normal lungs
| acute or chronic interstitial lung diseases
42
What are the types of expiratory obstruction diseases?
emphysema, chronic bronchitis, bronchiectasis, asthma
43
What is emphysema characterized by?
abnormal permanent enlargement of air spaces distal to the terminal bronchioles, accompanied by destruction of their walls without significant fibrosis
44
What is the diagnosis for emphysema?
morphologic tissue destruction
45
What kind of inflammatory cells accumulate in emphysema?
increase in proteases, increase in ROS, decrease in normal anti-proteases, but no fibrosis
46
What does emphysema do to the acini? What happens because of that?
enlarges the acini, resulting in decreased surface area which leads to decreased gas exchange which results in dyspnea
47
What are the two types of emphysema?
centriacinar and panacinar
48
Which type of emphysema is more common?
centriacinar
49
What happens in centriacinar emphysema?
the central acini get destroyed, but spares the distal lobule
50
Where is centriacinar emphysema located most commonly?
lung apices
51
Who is at risk for centriacinar emphysema?
chronic smokers
52
What happens in panacinar emphysema?
acini are uniformly destroyed, most commonly in lower lungs
53
What deficiency do those with panacinar emphysema?
alpha1-antitrypsin deficiency
54
What does alpha1-antitrypsin do?
normally functions as a protease inhibitor, but when there are less of them, there is an increase in protease activity
55
What accelerates the destruction of panacinar emphysema?
smoking
56
What are risks of emphysema?
smoking, genetics, air pollution
57
What immune cells are seen in emphysema?
neutrophils, macrophages and lymphocytes
58
Why is smoking a risk for emphysema?
ROS from smoke and released from WBCs, oxidant and antioxiant imbalances (causes tissue damage)
59
What is a chemoattractant for WBCs?
nicotine
60
What are the resulting symptoms of emphysema?
progressive dyspnea, cough, hyperventilation, wheezing, weight loss
61
What kind of immune cells are seen in chronic bronchitis?
neutrophils, macrophages, lymphocytes
62
What occurs during chronic bronchitis?
there is hypersecretion of mucus because of hypertrophy/hyperplasia of mucous glands and increased sputum
63
What are the risks of chronic bronchitis?
smoking, air pollutants, males, age 40-65
64
What are the symptoms of chronic bronchitis?
pronounced and productive cough lasting more than 3 consecutive months in more than 2 consecutive years
dyspnea, wheezing, cyanosis, cor pulmonale, recurrent infections, green/yellow sputum
65
What is COPD?
a mix of chronic bronchitis and emphysema
66
Describe the "pink puffer"
pathologic diagnosis, permanent enlargement and destruction of airspaces distal to the terminal bronchiole
older and thin, severe dyspnea, quiet chest, X-Ray, hyperinflation with flattened diaphragm
67
Describe "blue bloater"
clinical diagnosis, daily productive cough for 3 months or more in at least two consecutive years
overweight and cyanotic, elevated hemoglobin, peripheral edema, wheezing
68
Describe the symptoms of COPD that is predominantly bronchitis.
```
40-45 years,
mild dyspnea (late),
copious sputum cough (late),
infections common,
repeated respiratory insufficiency,
cor pulmonale,
increased airway resistance,
normal elastic recoil,
blue bloater
prominent vessels, large heart
```
69
Describe the symptoms of COPD that is predominantly emphysema?
```
50-75 years
severe, early dyspnea
late scanty sputum of cough
occasional infection
terminal respiratory insufficiency
rare, terminal cor pulmonale
airway resistance is normal
low elastic recoil
hyperinflation, small heart
```
70
What are the shared risks of COPD?
smoking and air pollution
71
What happens to the airflow in those with COPD? What are symptoms that follow this?
irreversible obstruction to airflow, prominent wheezing, possible pulmonary HTN
72
What kind of lung disease is asthma?
obstructive (bronchoconstriction)
73
What happens to the lung tissue in asthmatics?
smooth muscle hypertrophies or is hyperactive, inflammation and increase in mucous
74
What happens to the airflow in those with asthma?
reversible airway obstruction, wheezing, dyspnea, cough, chest tightness
75
What are the characteristics of asthmatics?
difficulty inhaling and exhaling, occurs in morningand evening, curschmann spirals, charcot-leyden crystals, various stimuli
76
Where is there an increased prevalence of asthma?
westernized world
77
What is atopic asthma?
Type I hypersensitivity, caused by allergens
78
What is non-atopic asthma?
bronchial hyper-responsiveness, non-allergic stimuli
79
Which type of asthma is more common?
atopic asthma
80
What are the triggers for atopic asthma?
environmental antigens like dust, dander, food, pollen
81
What is atopy?
a common condition, eczema/urticaria, allergic rhinitis, hyperreactive skin test
82
What causes non-atopic asthma?
viral URTI infection, pneumonia, exercise,cold air, aspirin, inhaled irritants, physiological stress
83
What happens histologically with non-atopic asthma?
bronchial inflammation, hyper-responsiveness
84
Do we know what causes non-atopic asthma?
no, it's idiopathic, no allergen trigger, no family history
85
What are the physiological symptoms of chronic asthma?
bronchial narrowing, hypertrophy of bronchial smooth muscles, fibrosis, increased submucosal glands, mucous plugs, increased submucosal vascularity
86
What happens to the acini of chronic asthma?
progressive hyperinflation, dysfunctional expiration, can be lethal, no response to bronchodilators or steroids
87
What can happen when there is obstruction in chronic asthmatics?
necrotizing infection, lung cancer, tuberculosis, chronic bronchitis, foreign bodies, impacted mucus, cystic fibrosis, permanent dilation of bronchial tree, destroys tissue (CT and musculature)
88
Where is chronic asthma located?
lower lobes
localized: foreign bodies
bilateral cystic fibrosis, Kartagener syndrome
89
What are features of chronic asthma?
episodes of severe coughing, hemoptysis and foul/purulent sputum
90
What kind of lung disease is bronchiectasis?
an obstructive lung disease that is caused by necrotizing infections that destroy supporting elastic tissue and muscle
91
Is bronchiectasis primary or secondary?
secondary because it is persisting to infection or obstruction caused by a variety of conditions
92
Once bronchiectasis develops, what is the characteristic symptoms complex?
cough and expectoration of copious amounts of purulent sputum
93
What does diagnosis of bronchiectasis depend on?
appropriate history, radiographic demonstration of bronchial dilation
94
What are the conditions that commonly predispose to bronchioectasis?
bronchial obstruction, congenital or hereditary conditions, necrotizing or suppurative pneumonia
95
What are common causes of bronchial obstruction for bronchioectasis?
tumors, foreign bodies, occasionally impaction of mucus
96
What can bronchioectasis complicate?
atopic asthma and chronic bronchitis
97
What are examples of congenital or hereditary conditions that can cause bronchiectasis?
cystic fibrosis, immunodeficiency, Kartagener syndrome
98
What is cystic fibrosis?
widespread severe bronchiectasis that results from obstruction caused by secretion of abnormally viscid mucus, which predisposes them to infections of bronchial tree
99
How is bronchiectasis associated with immunodeficiency states?
immunoglobulin deficiencies, localized or diffuse bronchiectasis is likely to develop of an increased susceptiblity to repeated bacterial infections
100
What is Kartagener syndrome?
a rare autosomal recessive disorder that is frequently associated with bronchiectasis and sterility in males
101
What are the structural abnormalities of Kartagener syndrome?
abnormal cilia,
102
What happens when there are abnormal cilia in Kartagener syndrome?
this impairs mucociliary clearance in the airways, leading to persistent infections and reduce the mobility of spermatozoa
103
What are the organisms that cause pneumonia in Kartagener syndrome?
staph aureus or kleibsella, this predisposes patients to bronchiectasis
104
Which type of bronchiectasis is a significant cause of morbidity in endemic areas?
post-tuberculosis bronchiectasis
105
What are the symptoms of Kartagener syndrome?
bronchiectasis, chronic sinusitis, situs inversus
106
What is situs inversus?
inverted chest and abdominal organs
107
What is ascites?
accumulation of fluid in the peritoneal cavity that causes abdominal swelling
