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Perio Exam 2 > Pulmonary 1 and 2 > Flashcards

Pulmonary 1 and 2 Flashcards

1
Q

Lungs are a. ——– grams each (——– is slightly heavier)

A

200-250, right lung

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2
Q

a. Lungs have a ———- (pulmonary & bronchial)

A

dual blood supply

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3
Q

a. Vocal cords – lined by

A

stratified squamous epithelium

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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

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5
Q

a. Alveoli – 2 cell types:

A

i. flat, type I pneumocytes (95%)

ii. cuboidal, type II pneumocytes (produce surfactant)

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6
Q

a. Alveolar-Capillary wall –

A

basement membrane and strands of interstitial connective tissue

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7
Q

i. upper airway –

A

filtering function

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8
Q

ii. lower airway –

A

mucociliary apparatus

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9
Q

iii. lymphoid tissues –

A

cellular & humoral immunity

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10
Q

iv. alveolar macrophages

A

Know that this is a thing I guess….

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11
Q
  1. Hemoptysis -
A

coughing up blood

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12
Q
  1. Dyspnea -
A

difficulty breathing, perception of needing to breathe deeper and faster (aka; shortness of breath)

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13
Q
  1. Atelectasis –
A

collapse or loss of lung volume – inadequate expansion of airspaces

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14
Q
  1. Pneumothorax -
A

air in the pleural space, leads to collapse of the lung

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15
Q
  1. Pleural effusion -
A

fluid in the pleural space

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16
Q

a. Transudate -

A

low protein fluid, caused by increased venous pressure (CHF)

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17
Q

b. Exudate -

A

high protein fluid, with or without inflammatory cells, caused by increased vascular permeability (damage), pneumonia is an example

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18
Q
  1. Empyema –
A

suppuration (purulence) in pleural cavity, often related to bacterial infection

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19
Q
  1. 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)

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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

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21
Q

Pulmonary thromboemboli: Predisposing factors:

A

– chronic illness
– prolonged bed rest (immobility)
– hypercoagulable state
– deep vein thrombophlebitis

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22
Q

B. CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)

A

Group of diseases that causes chronic airflow obstruction

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23
Q

4 disorders of COPD

A
  1. Emphysema
    1. Chronic bronchitis
    2. Bronchiectasis
    3. Asthma

Overlap iscommon

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24
Q

emphysema/chronic bronchitis often known as

A

COPD

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25
Q

A. Emphysema: permanent enlargement of the small air spaces due to

A

destruction of alveolar septae

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26
Q

A. Emphysema: clinically -

A

dyspnea, cough, prolonged exhalation (“pink puffers”)

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27
Q

A. Emphysema: pathogenesis -

A

imbalance between protease and anti-protease enzymes

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28
Q

A. Emphysema: Smoking is a

A

MAJOR cause of this imbalance

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29
Q

A. Emphysema: Centriacinar - involves the central portion of the

A

lobule, may progress to bullae,

usually affects upper lobes, typically associated with smoking,

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30
Q

A. Emphysema: Panacinar- involves the

A

entire respiratory lobule and usually involves the lower lobes, associated with α-1-AT deficiency

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31
Q

Chronic Bronchitis: 1. cough with sputum production at least

A

3 consecutive months for 2 consecutive years

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32
Q

Chronic Bronchitis: 2. often occurs with

A

emphysema, May have hypoxemia, cyanosis (“blue bloaters”)

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33
Q

Chronic Bronchitis: 3. Pathogenesis-

A

chronic irritation and infections

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34
Q

Chronic Bronchitis: 4. Pathology -

A

increased mucus glands, chronic inflammation, fibrosis and narrowing of the airways

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35
Q

Chronic Bronchitis: 5. Predisposing factors for chronic bronchitis and emphysema:

A
  • 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)
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36
Q

A. Bronchiectasis: 1. chronic infection with permanent

A

(large) airway dilation

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37
Q

A. Bronchiectasis: 2. clinically -

A

cough, fever, expectoration, dyspnea

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38
Q

A. Bronchiectasis: 3. complications -

A

abscess, pneumonia, bronchopleural fistula, empyema

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39
Q

A. Bronchiectasis: 4. Predisposing factors -

A

bronchial obstruction, scarring, CF, other COPD

40
Q

A. Bronchiectasis: 5. Pathology -

A

dilated distal bronchi, variable inflammation

41
Q

A. Asthma:

1. increased irritability of

A

smooth muscle in bronchi and bronchioles

42
Q

A. Asthma: 2. leads to

A

reversible contraction

43
Q

A. Asthma: 3. initiating factors -

A

allergies, infections, exercise, drugs, emotions

44
Q

A. Asthma: 4. Clinically -

A

wheezing, long exhalation, hyperinflation of lungs

45
Q

Bone marrow tranplant: allows for

A

More aggressive treatment (should be WBC lecture, but I’m lazy).

46
Q
  1. Atopic asthma (extrinsic, allergic) -
A

environmental antigen, often family history

47
Q
  1. non-Atopic asthma - initiated by
A

infection, emotional stress, air pollutants

48
Q
  1. Pathology asthma - mucus gland
A

hypertrophy and hyperplasia, smooth muscle hypertrophy, inflammation with eosinophils and type 2 helper T cells

49
Q
  1. Asthma Pathogenesis - antigen binds to
A

surface IgE on mast cells releasing a large number of mediators, including histamine and leukotrienes

50
Q

Asthma 9. Attack may subside

A

spontaneously, bronchodilators for immediate relief (albuterol), Controller medications (corticosteroids)

51
Q

A. PNEUMONIA

1. General:

A

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
Q
  1. Bacterial Pneumonia: Predisposing factors:
A

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
Q

Bacterial pneumonia 2 major types:

A

Bronchopneumonia

Lobar pneumonia

54
Q

Bronchopneumonia:

A

patchy process, begins around the small bronchi

- common in the very young & old

55
Q

Lobar pneumonia - involves an

A

entire lobe

  • Streptococcus pneumoniae in 90% of cases
  • healthy adults
56
Q

Bacterial pneumonia: Early stage -

A

‘red hepatization’ - purulent exudate with many red blood cells

57
Q

Bacterial pneumonia: Later stage -

A

‘grey hepatization’ - exudate with fibrin and macrophages

58
Q

Bacterial pneumonia: Outcome -

A

complete resolution or a scar

59
Q

i. Complications of Pneumonia:

A

abscess, pleuritis, pericarditis, bacteremia

60
Q

Recent day medical breakthrough

A

ALL survival rate 90+%, years ago was a death sentence.

61
Q
  1. Viral or Interstitial Pneumonia:

a. caused by

A

viruses & Mycoplasma pneumoniae

b.

62
Q

Viral or Interstitial Pneumonia:

clinically -

A

fever, H/A, dry cough, myalgia

c.

63
Q

Viral or Interstitial Pneumonia:

pathology -

A

interstitial inflammation, mononuclear cells, congestion and hyaline membranes (diffuse alveolar damage)

64
Q

. ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)

1. same histologic features as

A

interstitial pneumonia

2.

65
Q

. ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS): many causes:

A

shock, infections, trauma, drug overdose, irritants, aspiration, fat embolism

66
Q

. ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS): 3. injury to the

A

endothelium and alveolar epithelium

67
Q

. ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS): 4. increased

A

endothelial permeability (leaky)

68
Q

PULMONARY ABSCESS

1. clinically -

A

cough, fever, purulent sputum

69
Q

PULMONARY ABSCESS: 2. predisposing factors:

A

bronchiectasis, aspiration, septic emboli, airway obstruction, dental sepsis

70
Q

PULMONARY ABSCESS: 3. course -

A

scar, may progressively enlarge or cavitate (make a hole in the tissues)

71
Q

TUBERCULOSIS (TB): species:

A
  1. Mycobacterium tuberculosis
72
Q

TUBERCULOSIS (TB): 2. infects about —– of the world

A

1/3

73
Q

TUBERCULOSIS (TB); 3. most common infectious cause of

A

death in the world (about 3 million deaths/year)

74
Q

TUBERCULOSIS (TB): 4. since 1992 # of US cases has been declining
Exceptions:

A

HIV infection, overcrowding, poor living conditions, immigrants

75
Q

TUBERCULOSIS (TB): 5. bacterial properties

A

bacillus (rod), aerobe, non-motile, slow growing
has waxy coat - resists acid destaining
Acid Fast Bacillus (AFB)

76
Q

TUBERCULOSIS (TB): 6. Pathology -

A

caseating granuloma - classic tissue reaction

77
Q

TUBERCULOSIS (TB): 7. Pathogenesis - acquired by

A

inhalation
Cavitary TB
Apex
Significant Scarring
May seed the large airways, lymph nodes or blood
Direct extension to the pleura - effusion

78
Q

TUBERCULOSIS (TB): 8. Disease Course – 90-95% resolve

A

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
Q

Ghon lesion -

A

site of early TB infection

80
Q

Ghon complex - TB-

A

parenchymal lesion + hilar lymph nodes

81
Q

Note: granulomatous inflammation is found in other processes - TB is the classic, but is associated with many

A

fungal infections, of which histoplasmosis is the most common, esp in Ohio.

82
Q

Another conditions with granulomatous inflammation:

A

sarcoidosis

83
Q

II. LUNG CANCER

1. leading cause of

A

cancer deaths in men & women in the US

84
Q

Lung cancer: 2. risk factors:

A

cigarette smoking**
asbestos
radon gas
nickel, chromates, pollutants, lung scar

85
Q

Lung cancer: 3. Clinical:

A

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
Q

Lung cancer: 4. Pathology: major cell types

A 
squamous cell carcinoma (25-30%)**
		adenocarcinoma (30-35%)
		small cell (oat cell) (20-25%)**
		large cell (10-15%)
		others: mesothelioma (asbestos), carcinoid
87
Q

Lung cancer: 5. Prognosis for lung cancer –

A

16% 5-year survival (all types), if localized when found 45%

88
Q

PNEUMOCONIOSES:

1. Definition –

A

a group of lung disorders caused by inhalation of dusts

89
Q

PNEUMOCONIOSES: 2. The size, shape, and concentration of particles are

A

important factors

90
Q

PNEUMOCONIOSES: 3. Particles 1-5 um diameter are the

A

most dangerous

91
Q

PNEUMOCONIOSES: 4. Inhaled particles induce

A

fibrosis (scarring)

92
Q

PNEUMOCONIOSES: 5. Coal Worker’s pneumoconiosis

A

nodular or diffuse fibrosis with coal macules

“progressive massive fibrosis” – ongoing fibrosis and lung destruction

93
Q

PNEUMOCONIOSES: 6. Silicosis -

A

most prevalent occupational disease in the world

94
Q

PNEUMOCONIOSES: 7. Other Occupational/Environmental causes,

A

also drugs, immunologic associations

95
Q

PNEUMOCONIOSES: 8. Idiopathic Pulmonary Fibrosis (IPF) –

A

unknown etiology

96
Q

PNEUMOCONIOSES: 9. restrictive lung disorders -

A

reduced lung capacities

ARDS, interstitial lung diseases are other examples

97
Q

PNEUMOCONIOSES: 10. Many other interstitial lung diseases -

A

inflammation & fibrosis, hypersensitivity pneumonitis, sarcoidosis, others

Perio Exam 2 (20 decks)

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