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Pathophysiology > lungs > Flashcards

lungs Flashcards

1
Q

toxic gases, organic dusts, inorganic dusts

A

pulmonary fibrosis

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2
Q

rheumatologic diseaase

A

pulmonary fibrosis

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3
Q

chronic inflammation, alveolar epithelialization, mylofibroblast proliferation

A

pulmonary fibrosis

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4
Q

MC idiopathic lung disorder, men over 60, survive 2-4yrs

A

idiopathic pulmonary fibrosis

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5
Q

PE diffuse inspiratory crackles

A

idiopathic pulmonary fibrosis, pulmonary edema, vial pneumonia

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6
Q

damage airway epithelium, cilia, alveoli

A

toxic gases

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7
Q

burning of eyes, nose, throat

A

toxic gases

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8
Q

inhaled inorganic dust particles

A

pneumoniciosis

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9
Q

MC silicosis, asbestosis, coal worker/black lung

A

Pneumoconiosis

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10
Q

Pneumoconiosis cough

A

productive

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11
Q

proinflammatory cytokines released, inflammation, scarring of alveolocapillary membrane, and pulmonary fibrosis

A

Pneumoconiosis

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12
Q

organic dust particles

A

Hypersensitivity pneumonitis/ extrinsic allergic alveolitis

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13
Q

type 3 hypersens, IgG, granuloma

A

Hypersensitivity pneumonitis/ extrinsic allergic alveolitis

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14
Q

Granulomatous disorders
CT disorders
Goodpasture’s syndrome

A

Systemic disorders affecting airways, lungs, and lung parenchyma

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15
Q

Excess water in the lungs from capillary hydrostatic pressure (from heart failure), oncotic pressure, and permeability (from injury) so pts have dyspnea, orthopnea, hypoxemia, and inc work of breathing

A

Pulmonary edema

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16
Q

MCC is left sided heart disease

A

Pulmonary edema

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17
Q

PE- inspiratory crackles, dullness to percussion at lung bases, and ventricular dilation (S3 gallop)

A

Pulmonary edema

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18
Q

MC predisposing factors- genetics, sepsis, and multiple traumas

A

Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) or noncardiogenic pulmonary edema

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19
Q

exudative phase, proliferative phase, then fibrotic phase

A

Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) or noncardiogenic pulmonary edema

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20
Q

predisposing factors: heart disease, ARDS, inhalation of toxic gases

A

pulmonary edema

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21
Q

rare but life threatening complication that can occur after relief of upper airway obstruction

A

postobstructive pulmonary edema; neg press pulmonary edema

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22
Q

dyspnea, wheezing, low VQ, dec FEV1

A

Obstructive pulmonary disease

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23
Q

Mucous plug

A

asthma, bronchiectasis, COPD

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24
Q

IRREVERSIBLE if left untreated

A

asthma

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25
Q

bronchospasm is not reversible by usual trmt

A

Status asthmaticus-

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26
Q

3rd leading cause of death in the US

A

COPD

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27
Q

6th leading cause of death in the world

A

COPD

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28
Q

Risk factors: tobacco, dust and chemicals, indoor air pollution, anything that affects lung growth during gestation and childhood

A

COPD

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29
Q

Mucous plugs narrow airways so air trapping and hyperinflation occur

A

copd

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30
Q

chronic bronchitis type of cough

A

productive

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31
Q

polycythemia

A

chronic bronchitis

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32
Q

Gas exchange airways are permanently enlarged and alveolar walls are destroyed WITHOUT fibrosis so we lose elastic recoil

A

Emphysema

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33
Q

Barrel chest & pts lean forward to increase lung capacity

A

emphysema

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34
Q

MCC smoking emphysema

A

sec

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35
Q

centriacinar, panacinar

A

emphysema

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36
Q

Elastin breakdown, imbalance of protease and antiprotease, oxidative stress, apoptosis of lungs structural cells

A

emphysema

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37
Q

MCC short term disability in the US

A

Respiratory tract infections

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38
Q

6th leading cause of death in the US

A

pneumonia

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39
Q

Different microorganisms causes this pneumonia

A

CAP

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40
Q

Seasonal, mild, self limiting infection of LRT

A

Viral pneumonia

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41
Q

Viral pneumonia type of cough

A

productive

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42
Q

PE= crackles, inc tactile fremitus (vibratory tremors on chest palpation), egophony (inc voice resonance on auscultation)

A

Viral pneumonia

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43
Q

Virus destroys epithelial cells, invades goblet cells, destroys bronchial epithelium, prevents mucous from being cleared, bronchial walls become red and WBC come in

A

Viral pneumonia

44
Q

Leading cause of death worldwide from a curable infectious disease

A

tb

45
Q

night sweats

A

tb

46
Q

caseous necrosis

A

tb

47
Q

Must use at least 4 drugs for 18 months; check at 6 months to see if it’s working

A

tb

48
Q

MCC aspiration

A

Abscess and cavitation

49
Q

Abscess and cavitation cough type

A

productive

50
Q

chronic PRODUCTIVE cough with foul smelling and purulent sputum

A

Bronchiectasis, Abscess and cavitation

51
Q

Acute infection or inflammation of airways/bronchi usually after a viral illness

A

Acute bronchitis

52
Q

Acute bronchitis cough type

A

nonproductive

53
Q

Has similar sx to pneumonia, but no pulmonary consolidation and chest infiltrates… chest x ray is normal

A

Acute bronchitis

54
Q

Virchow’s triad: venous stasis, venous endothelial damage, hypercoagulability

A

pe

55
Q

high vq

A

pe

56
Q

Workload of right ventricle is increased so right ventricular hypertrophy occurs

A

PAH

57
Q

First induction: chest radiography shows enlarged pulmonary arteries on R heart border or R ventricular hypertrophy on ECG

A

PAH

58
Q

Hoarseness

A

Laryngeal cancer

59
Q

2-3% of all cancers in the US

A

Laryngeal cancer

60
Q

MCC of cancer death in the US

A

Lung cancer/bronchogenic carcinomas

61
Q

MCC of cancer death in the US

A

Lung cancer/bronchogenic carcinomas

62
Q

85% of all lung cancers

A

Non small cell lung cancer

63
Q

Squamous cell carcinoma

A

nonproductive cough or hemoptysis

64
Q

Adenocarcinomas-

A

tumors from glands; asymptomatic OR pleuritic chest pain and SOB

65
Q

Non small cell lung cancer types

A

squamous cell, adenocarcinoma, large cell

66
Q

chemo and radiation are not helpful so palliative care is best option

A

Large cell carcinomas/ undifferentiated

67
Q

MC and WORST prognosis cancer

A

Small cell carcinoma/Oat cell carcinoma

68
Q

1st manifestation: paraneoplastic syndrome- t cells attack body’s own CNS

A

Small cell carcinoma/Oat cell carcinoma

69
Q

Rare and are NOT related to smoking

A

Bronchial carcinoid tumors

70
Q

Asymptomatic; we can cure these if they have not spread

A

Bronchial carcinoid tumors

71
Q

Associated with asbestos

May take 20-40 years to appear

A

Mesothelialomas

72
Q

TNM classification system of CA

A

T: extent of primary tumor
N: nodal involvement
M: extent of metastasis

73
Q

MC pain caused by pulm disease

A

pleural pain

74
Q

chest wall pain-

A

from costochondritis- inflammation of costochondral junction; reproducable

75
Q

hypercapnia due to _______ ventilation of alveoli

A

hypo

76
Q

easily overlooked as normal breathing and ventilation may appear normal

A

hypercapnia

77
Q

how can we inc hypoventilatio of alveoli

A

inc rate and depth of breathing

78
Q

MCC hypoxemia

A

vq mismatch

79
Q

normal vq

A

0.8-0.9

80
Q

would we die 1st from hypoxemia or hypercapnia

A

hypoxemia

81
Q

MV=

A

TV*RR

82
Q

maintain arterial CO2 at

A

40 mmHg

83
Q

MC post op problems: atelectasis, pneumonia, pulmonary edema, PE

A

acute resp failure

84
Q

MCC of hospital admission from hypercapnia and hypoventilation

A

Respiratory difficulty

85
Q

hypo or hypoerventilaion in flail chest

A

hypo

86
Q

PE= No or decreased breath sounds and hyperresonance to percussion on affected side

A

tension pneumothorax

87
Q

PE= decreased breath sounds and dullness to percussion

A

empyema

88
Q

Caused by Staph aureus, E. coli, Anaerobic bacteria, Klebsiella pneumonia (think SEAK) so we want to treat with antimicrobial meds

A

empyema

89
Q

PEEP

A

aspiration

90
Q

fever and leukovytosis, sydpnea, cough

A

atelectasis

91
Q

deep breathing

A

atelectasis

92
Q

high resolution CT

A

Bronchiectasis, idiopathic pulm fibrisos

93
Q

MC in children, but can also occur in adults with chronic bronchitis or viral infection from inhaling toxic gases

A

bronchiolitis

94
Q

bronchiolitis cough

A

nonproductive

95
Q

MC after lung transplant

A

Bronchiolitis obliterans

96
Q

dec perfusion at the alveolocapillary membrane

A

pulm fibrosis

97
Q

Injury to pulmonary capillary endothelium, inc capillary permeability, inflammation, surfactant inactivation, edema, atelectasis

A

Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) or noncardiogenic pulmonary edema

98
Q

prolonged exposure to high conc of supplpemental O2

A

oxygen toxicity

99
Q

reduce inspired O2 conc to less than 60 %

A

oxygen toxicity

100
Q

life threatening complication that can oocur after relief of upper airway obstruction

A

POPE postobstructive pulm edema; negative pressure pulm edema

101
Q

Acute lung inflammation and alveolocapillary injury

A

Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) or noncardiogenic pulmonary edema

102
Q

poor resp with O2 supplementaion

A

Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) or noncardiogenic pulmonary edema

103
Q

resp alkalosis, metabolic acidosis, resp acidosis

A

Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) or noncardiogenic pulmonary edema

104
Q

early detection is key

A

Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) or noncardiogenic pulmonary edema

105
Q

MC: asthma, chronic bronchitis, emphysema, COPD

A

Obstructive pulmonary disease

Pathophysiology (17 decks)

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