Pulmonary 1 and 2 Flashcards
1
Q
Lungs are a. ——– grams each (——– is slightly heavier)
A
200-250, right lung
2
Q
a. Lungs have a ———- (pulmonary & bronchial)
A
dual blood supply
3
Q
a. Vocal cords – lined by
A
stratified squamous epithelium
4
Q
a. The large airways (larynx, trachea, bronchi) are lined by
A
pseudostratified, ciliated, columnar epithelium, with mucus glands (mucosal and submucosal), neuroendocrine cells and cartilage
5
Q
a. Alveoli – 2 cell types:
A
i. flat, type I pneumocytes (95%)
ii. cuboidal, type II pneumocytes (produce surfactant)
6
Q
a. Alveolar-Capillary wall –
A
basement membrane and strands of interstitial connective tissue
7
Q
i. upper airway –
A
filtering function
8
Q
ii. lower airway –
A
mucociliary apparatus
9
Q
iii. lymphoid tissues –
A
cellular & humoral immunity
10
Q
iv. alveolar macrophages
A
Know that this is a thing I guess….
11
Q
- Hemoptysis -
A
coughing up blood
12
Q
- Dyspnea -
A
difficulty breathing, perception of needing to breathe deeper and faster (aka; shortness of breath)
13
Q
- Atelectasis –
A
collapse or loss of lung volume – inadequate expansion of airspaces
14
Q
- Pneumothorax -
A
air in the pleural space, leads to collapse of the lung
15
Q
- Pleural effusion -
A
fluid in the pleural space
16
Q
a. Transudate -
A
low protein fluid, caused by increased venous pressure (CHF)
17
Q
b. Exudate -
A
high protein fluid, with or without inflammatory cells, caused by increased vascular permeability (damage), pneumonia is an example
18
Q
- Empyema –
A
suppuration (purulence) in pleural cavity, often related to bacterial infection
19
Q
- Pulmonary edema; Accumulation of fluid in the lungs, first in the interstitial tissues, then filling the air spaces
Causes:
A
a. increased intravascular pressure (CHF)
b. hypoproteinemia (low protein)
c. vascular damage (infections, autoimmune diseases)
20
Q
II. PULMONARY THROMBOEMBOLI
A
A. Usually from the DEEP veins of the legs or pelvic veins
Small emboli may cause only minimal damage
Larger emboli cause hemorrhage or infarction
Very large emboli lodge at the bifurcation of pulmonary arteries (“saddle” embolus), can cause sudden death
21
Q
Pulmonary thromboemboli: Predisposing factors:
A
– chronic illness
– prolonged bed rest (immobility)
– hypercoagulable state
– deep vein thrombophlebitis
22
Q
B. CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
A
Group of diseases that causes chronic airflow obstruction
23
Q
4 disorders of COPD
A
- Emphysema
- Chronic bronchitis
- Bronchiectasis
- Asthma
Overlap iscommon
24
Q
emphysema/chronic bronchitis often known as
A
COPD
25
A. Emphysema: permanent enlargement of the small air spaces due to
destruction of alveolar septae
26
A. Emphysema: clinically -
dyspnea, cough, prolonged exhalation (“pink puffers”)
27
A. Emphysema: pathogenesis -
imbalance between protease and anti-protease enzymes
28
A. Emphysema: Smoking is a
MAJOR cause of this imbalance
29
A. Emphysema: Centriacinar - involves the central portion of the
lobule, may progress to bullae,
| usually affects upper lobes, typically associated with smoking,
30
A. Emphysema: Panacinar- involves the
entire respiratory lobule and usually involves the lower lobes, associated with α-1-AT deficiency
31
Chronic Bronchitis: 1. cough with sputum production at least
3 consecutive months for 2 consecutive years
32
Chronic Bronchitis: 2. often occurs with
emphysema, May have hypoxemia, cyanosis (“blue bloaters”)
33
Chronic Bronchitis: 3. Pathogenesis-
chronic irritation and infections
34
Chronic Bronchitis: 4. Pathology -
increased mucus glands, chronic inflammation, fibrosis and narrowing of the airways
35
Chronic Bronchitis: 5. Predisposing factors for chronic bronchitis and emphysema:
* cigarette smoking - causes mucus gland hyperplasia, increases smooth ms tone, inhibits cilia, inhibits phagocytosis, and squamous metaplasia
* atmosphere pollutants
* infection(s)
* genetic factors - CF, α-1-AT deficiency (esp. emphysema)
36
A. Bronchiectasis: 1. chronic infection with permanent
(large) airway dilation
37
A. Bronchiectasis: 2. clinically -
cough, fever, expectoration, dyspnea
38
A. Bronchiectasis: 3. complications -
abscess, pneumonia, bronchopleural fistula, empyema
39
A. Bronchiectasis: 4. Predisposing factors -
bronchial obstruction, scarring, CF, other COPD
40
A. Bronchiectasis: 5. Pathology -
dilated distal bronchi, variable inflammation
41
A. Asthma:
| 1. increased irritability of
smooth muscle in bronchi and bronchioles
42
A. Asthma: 2. leads to
reversible contraction
43
A. Asthma: 3. initiating factors -
allergies, infections, exercise, drugs, emotions
44
A. Asthma: 4. Clinically -
wheezing, long exhalation, hyperinflation of lungs
45
Bone marrow tranplant: allows for
More aggressive treatment (should be WBC lecture, but I'm lazy).
46
5. Atopic asthma (extrinsic, allergic) -
environmental antigen, often family history
47
6. non-Atopic asthma - initiated by
infection, emotional stress, air pollutants
48
7. Pathology asthma - mucus gland
hypertrophy and hyperplasia, smooth muscle hypertrophy, inflammation with eosinophils and type 2 helper T cells
49
8. Asthma Pathogenesis - antigen binds to
surface IgE on mast cells releasing a large number of mediators, including histamine and leukotrienes
50
Asthma 9. Attack may subside
spontaneously, bronchodilators for immediate relief (albuterol), Controller medications (corticosteroids)
51
A. PNEUMONIA
| 1. General:
one of the leading causes of death
a. often complicates other chronic debilitating diseases
b. any organism can cause pneumonia in the right setting
c. bacterial, viral, fungal, parasites
52
2. Bacterial Pneumonia: Predisposing factors:
a. loss of cough reflex
b. injury to cilia
c. decreased phagocytosis
d. pulmonary edema
e. immunocompromised condition
f. Clinically - cough, dyspnea, fever, chills, sputum production
53
Bacterial pneumonia 2 major types:
Bronchopneumonia
| Lobar pneumonia
54
Bronchopneumonia:
patchy process, begins around the small bronchi
| - common in the very young & old
55
Lobar pneumonia - involves an
entire lobe
- Streptococcus pneumoniae in 90% of cases
- healthy adults
56
Bacterial pneumonia: Early stage -
‘red hepatization’ - purulent exudate with many red blood cells
57
Bacterial pneumonia: Later stage -
‘grey hepatization’ - exudate with fibrin and macrophages
58
Bacterial pneumonia: Outcome -
complete resolution or a scar
59
i. Complications of Pneumonia:
abscess, pleuritis, pericarditis, bacteremia
60
Recent day medical breakthrough
ALL survival rate 90+%, years ago was a death sentence.
61
3. Viral or Interstitial Pneumonia:
| a. caused by
viruses & Mycoplasma pneumoniae
| b.
62
Viral or Interstitial Pneumonia:
| clinically -
fever, H/A, dry cough, myalgia
| c.
63
Viral or Interstitial Pneumonia:
| pathology -
interstitial inflammation, mononuclear cells, congestion and hyaline membranes (diffuse alveolar damage)
64
. ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)
| 1. same histologic features as
interstitial pneumonia
| 2.
65
. ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS): many causes:
shock, infections, trauma, drug overdose, irritants, aspiration, fat embolism
66
. ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS): 3. injury to the
endothelium and alveolar epithelium
67
. ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS): 4. increased
endothelial permeability (leaky)
68
PULMONARY ABSCESS
| 1. clinically -
cough, fever, purulent sputum
69
PULMONARY ABSCESS: 2. predisposing factors:
bronchiectasis, aspiration, septic emboli, airway obstruction, dental sepsis
70
PULMONARY ABSCESS: 3. course -
scar, may progressively enlarge or cavitate (make a hole in the tissues)
71
TUBERCULOSIS (TB): species:
1. Mycobacterium tuberculosis
72
TUBERCULOSIS (TB): 2. infects about ----- of the world
1/3
73
TUBERCULOSIS (TB); 3. most common infectious cause of
death in the world (about 3 million deaths/year)
74
TUBERCULOSIS (TB): 4. since 1992 # of US cases has been declining
Exceptions:
HIV infection, overcrowding, poor living conditions, immigrants
75
TUBERCULOSIS (TB): 5. bacterial properties
bacillus (rod), aerobe, non-motile, slow growing
has waxy coat - resists acid destaining
Acid Fast Bacillus (AFB)
76
TUBERCULOSIS (TB): 6. Pathology -
caseating granuloma - classic tissue reaction
77
TUBERCULOSIS (TB): 7. Pathogenesis - acquired by
inhalation
Cavitary TB
Apex
Significant Scarring
May seed the large airways, lymph nodes or blood
Direct extension to the pleura - effusion
78
TUBERCULOSIS (TB): 8. Disease Course – 90-95% resolve
a. infection may become inactive or progress
b. inactive infection may reactivate many years later if immunity wanes
c. may widely disseminate (miliary TB) and involve many other organs
d. reactivation – induces type IV hypersensitivity, tissue necrosis
79
Ghon lesion -
site of early TB infection
80
Ghon complex - TB-
parenchymal lesion + hilar lymph nodes
81
Note: granulomatous inflammation is found in other processes - TB is the classic, but is associated with many
fungal infections, of which histoplasmosis is the most common, esp in Ohio.
82
Another conditions with granulomatous inflammation:
sarcoidosis
83
II. LUNG CANCER
| 1. leading cause of
cancer deaths in men & women in the US
84
Lung cancer: 2. risk factors:
cigarette smoking**
asbestos
radon gas
nickel, chromates, pollutants, lung scar
85
Lung cancer: 3. Clinical:
cough, weight loss, chest pain, hemoptysis, dyspnea
some lung tumors produce hormones (or hormone like substances) such as ADH, ACTH, PTH and others –paraneoplastic syndrome
86
Lung cancer: 4. Pathology: major cell types
```
squamous cell carcinoma (25-30%)**
adenocarcinoma (30-35%)
small cell (oat cell) (20-25%)**
large cell (10-15%)
others: mesothelioma (asbestos), carcinoid
```
87
Lung cancer: 5. Prognosis for lung cancer –
16% 5-year survival (all types), if localized when found 45%
88
PNEUMOCONIOSES:
| 1. Definition –
a group of lung disorders caused by inhalation of dusts
89
PNEUMOCONIOSES: 2. The size, shape, and concentration of particles are
important factors
90
PNEUMOCONIOSES: 3. Particles 1-5 um diameter are the
most dangerous
91
PNEUMOCONIOSES: 4. Inhaled particles induce
fibrosis (scarring)
92
PNEUMOCONIOSES: 5. Coal Worker’s pneumoconiosis
nodular or diffuse fibrosis with coal macules
| “progressive massive fibrosis” – ongoing fibrosis and lung destruction
93
PNEUMOCONIOSES: 6. Silicosis -
most prevalent occupational disease in the world
94
PNEUMOCONIOSES: 7. Other Occupational/Environmental causes,
also drugs, immunologic associations
95
PNEUMOCONIOSES: 8. Idiopathic Pulmonary Fibrosis (IPF) –
unknown etiology
96
PNEUMOCONIOSES: 9. restrictive lung disorders -
reduced lung capacities
| ARDS, interstitial lung diseases are other examples
97
PNEUMOCONIOSES: 10. Many other interstitial lung diseases -
inflammation & fibrosis, hypersensitivity pneumonitis, sarcoidosis, others
