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Pathophysiology > 27. Pulmonary Alterations > Flashcards

27. Pulmonary Alterations Flashcards

1
Q

subjective experience of breathing discomfort often described as breathlessness, air hunger, shortness of breath, or labored breathing

A

dyspnea

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2
Q

Most severe signs of dyspnea

A
  • nostril flaring - use of accessory muscles - retraction of supercostal and intercostal muscles (common in children)
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3
Q

dyspnea that occurs when an individual lies flat (ABD contents exert pressure on diaphragm)

A

orthopnea

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4
Q

Orthopnea is common in what condition

A

heart failure

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5
Q

occurs when individuals w/ pulmonary or cardiac disorders awake at night gasping for air and have to sit or stand to relieve dyspnea

A

paroxysmal nocturnal dyspnea (PND)

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6
Q

protective reflex that helps clear airways by an explosive expiration

A

cough

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7
Q

coughing up blood or bloody secretions

A

hemoptysis

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8
Q

normal/rhythmic/effortless breathing

A

eupnea

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9
Q

breathing pattern characterized by increased ventilatory rate, very large tidal volumes, and no expiratory pause

A

Kussmaul respiration (hyperpnea)

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10
Q

amount of air inspired and expired in a single breath

A

tidal volume

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11
Q

causes of Kussmaul respiration

A

strenuous exercise or metabolic acidosis

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12
Q

breathing pattern characterized by alternating periods of deep and shallow breathing

A

Cheyne-Stokes respirations

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13
Q

Explain the rhythm of Cheyne-Stokes respirations

A
  • increased levels of CO2 -> tachypnea - CO2 levels decrease -> leads to apnea until CO2 accumulates again
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14
Q

causes of Cheyne-Stokes respirations

A

any condition that reduces blood flow to the brainstem -> slows impulses sending info to respiratory centers of brainstem

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15
Q

inadequate alveolar ventilation in relation to metabolic demands (CO2 removal does not keep up w/ CO2 production)

A

hypoventilation

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16
Q

PaCO2 is greater than 44 mmHg

A

hypercapnia (increased CO2 levels) -> leads to respiratory acidosis

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17
Q

alveolar ventilation exceeds metabolic demands (lungs remove CO2 faster than it is produced)

A

hyperventilation

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18
Q

PaCO2 less than 36 mmHg

A

hypocapnia (decreased CO2 levels) -> leads to respiratory alkalosis

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19
Q

bluish discoloration of the skin and mucous membranes caused by increased amounts of desaturated or reduced Hgb in the blood; late symptom of deoxygenation

A

cyanosis

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20
Q

peripheral vs central cyanosis

A
  • peripheral: often caused by poor circulation due to intense peripheral vasoconstriction (best seen in nail beds) - central: caused by decreased arterial oxygenation (low PaO2) from pulmonary disease or cardiac right-to-left shunts (best seen in buccal mucosa and lips)
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21
Q

selective bulbous enlargement of the end of a digit

A

clubbing

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22
Q

7 causes of hypercapnia

A
  • depression of respiratory center by drugs - diseases of the medulla - abnormalities of spinal conducting pathways (spinal cord disruption) - diseases of NMJ or respiratory muscles (MG or MD) - thoracic cage abnormalities - large airway obstruction (tumors/sleep apnea) - increased work of breathing or physiologic dead space
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23
Q

hypoxia vs hypoxemia

A
  • hypoxia: reduced O2 in cells - hypoxemia: reduced O2 in blood
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24
Q

pathological condition which results when the alveoli of the lungs are perfused (Q) with blood as normal, but ventilation (the supply of air or V) fails to supply the perfused region -> low V/Q

A

pulmonary shunt

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25
Q

V/Q mismatching results in what?

A

hypoxemia

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26
Q

air in the pleural space caused by a rupture in the visceral pleura

A

pneumothorax

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27
Q

occurs unexpectedly in healthy individuals between 20-40 y/o and is caused by spontaneous rupture of blebs on the visceral pleura

A

primary (spontaneous) pneumothorax

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28
Q

type of pneumothorax caused by chest trauma

A

secondary pneumothorax

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29
Q

air pressure in the pleural space = barometric pressure; air drawn into pleural space on inspiration is forced out on expiration

A

open (communicating) pneumothorax

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30
Q

one-way valve that permits air to enter on inspiration but prevents escape during expiration (causes mediastinal shift) -> life threatening

A

tension pneumothorax

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31
Q

results from fracture of several consecutive ribs in more than one place or fracture of sternum and several consecutive ribs

A

flail chest

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32
Q

Describe chest wall movement w/ flail chest

A

paradoxical movement - chest wall moves in on inspiration - chest wall moves out on expiration

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33
Q

presence of fluid in the pleural space

A

pleural effusion

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34
Q

Name 5 types of pleural effusion drainage

A
  • transudative (hydrothorax): watery drainage from intact capillaries - exudative: WBC and protein - empyema: pus-like drainage - hemothorax: bloody drainage - chylothorax: milky lymphatic drainage and fat droplets
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35
Q

diseases characterized by airway obstruction that is worse w/ expiration (more force is required to expire a given volume of air and emptying of the lungs is slowed)

A

obstructive lung diseases

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36
Q

3 most common obstructive lung diseases

A
  • asthma - emphysema - chronic bronchitis
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37
Q

chronic inflammatory disorder of the bronchial mucosa that causes bronchial hyper-responsiveness, constriction of airways, and variable airflow obstruction

38
Q

Describe an acute asthmatic response

A
  • inhaled Ag binds to mast cells covered w/ preformed IgE - mast cells release mediators - mediators induce bronchospasm, edema from increased capillary permeability, and mucous secretion (goblet cells) - dendritic cells process and present Ag to Th2 -> produce ILs - eosinophils activated -> damage respiratory epithelium - neutrophils add to inflammation and airway obstruction
39
Q

clinical manifestations of asthma attack

A
  • chest constriction - expiratory wheezing - dyspnea - nonproductive cough - prolonged expiration - tachycardia - tachypnea
40
Q

decrease in systolic BP during inspiration of more than 10 mmHg; may be seen during asthma attack

A

pulses paradoxus

41
Q

considered acute severe bronchospasm if asthma symptoms not reversed by usual treatment -> can lead to death

A

status asthmaticus

42
Q

reversible bronchospasm

43
Q

irreversible bronchospasm

A

chronic bronchitis and emphysema

44
Q

COPD includes what 2 disorders

A

chronic bronchitis and emphysema

45
Q

hyper-secretion of mucus and chronic productive cough for at least 3 months of the year for at least 2 consecutive years

A

chronic bronchitis

46
Q

pathogenesis of chronic bronchitis

A
  • chronic irritation from inhaled substances/irritants such as tobacco smoke - inflammation causes bronchial edema, hyper-secretion of mucus (goblet cells), and smooth muscle hypertrophy w/ fibrosis, and bacterial colonization of airways
47
Q

clinical manifestation of chronic bronchitis

A
  • productive cough (classic) - prolonged expiration - cyanosis - chronic hypoventilation - polycythemia - cor pulmonale
48
Q

abnormal permanent enlargement of gas-exchange airways accompanied by destruction of alveolar walls without obvious fibrosis

49
Q

primary emphysema is inherited and linked to what deficiency

A

a1-antitrypsin deficiency

50
Q

pathogenesis of emphysema

A
  • destruction of alveoli through breakdown of elastin within the septa (increased protease activity) - loss of elastin = loss of recoil of bronchial walls - produces large air spaces within lung parenchyma (bullae)
51
Q

mucous plugs and narrowed airways cause ____; leads to hyperinflation of alveoli and hyper-expansion of chest

A

air trapping

52
Q

clinical manifestations of emphysema

A
  • dyspnea - wheezing - barrel chest (classic) - prolonged expiration
53
Q

diseases characterized by decreased compliance of lung tissue (takes more effort to expand lungs during inspiration)

A

restrictive lung disease

54
Q

collapse of lung tissue

A

atelectasis

55
Q

caused by external pressure exerted by tumor, fluid, or air in the pleural space or by ABD dissension on portions of lung -> cause alveoli to collapse

A

compressive atelectasis

56
Q

caused by removal of air from obstructed or hypoventilated alveoli or from inhalation of concentrated O2 or anesthetic agents

A

absorption atelectasis

57
Q

persistent abnormal dilation of bronchi

A

bronchiectasis

58
Q

diffuse inflammatory obstruction of the small airways or bronchioles occurring most commonly in children

A

bronchiolitis

59
Q

excessive amount of fibrous or connect tissue in the lung; can be caused by formation of scar tissue after active pulmonary disease, in association w/ autoimmune disorders, or by inhalation of harmful substances

A

pulmonary fibrosis

60
Q

autosomal recessive defect on chromosome 7 that causes defective epithelial chloride ion transport and deficient Na in airways, bile ducts, pancreas, and sweat ducts

A

cystic fibrosis

61
Q

Explain pathogenesis of cystic fibrosis

A

Defective CFTR causes buildup of Cl inside airway epithelial cells -> Na enters cells to create NaCl -> water enters cells to offset salts -> external mucous becomes thick -> difficulty breathing and increased bacterial infections

62
Q

3 clinical manifestations of cystic fibrosis

A
  • chronic lung inflammation - chronic lung infections - GI malabsorption
63
Q

excess water in the lung

A

pulmonary edema

64
Q

3 causes of pulmonary edmea

A
  • left heart failure: causes increased pulmonary capillary hydrostatic pressure - injury to capillary endothelium: movement of fluid and protein from capillary to alveoli - blockage of lymphatics: inability to remove excess fluid from interstitial space
65
Q

2 primary features of acute respiratory distress syndrome (ARDS)

A
  • acute lung inflammation - diffuse alveolar-capillary injury
66
Q

Pathogenesis of ARDS

A
  • acute lung injury -> inflammation and neutrophil aggregation w/ release of mediators and complement - platelet activation -> micro thrombi in pulmonary circulation -> decreased flow to lungs -> pulmonary HTN and V/Q mismatch - damage to alveolar and endothelial cells -> disrupts alveolocapillary membrane -> fluid enters interstitial space -> impaired surfactant production and atelectasis
67
Q

3 phases of ARDS

A
  • exudative phase: pulmonary edema and hemorrhage w/ severe impairment of ventilation - proliferative phase: proliferation of type II pneumocytes; formation of hyaline membrane - fibrotic phase: tissue remodeling (destruction of alveoli and bronchioles)
68
Q

Final result of ARDS

A

acute respiratory failure - hypoxemia - hypercapnia - acidosis

69
Q

acute infection or inflammation of the airways or bronchi (usually self-limiting)

A

acute bronchitis

70
Q

most common and lethal cause of outpatient and inpatient pneumonias

A

streptococcus pneumoniae (pneumococcus)

71
Q

pathologic course of pneumonia

A
  • aspiration of bacteria -> adherence to alveolar macrophages - inflammatory response - consolidation of lung parenchyma - leukocyte infiltration (neutrophils and macrophages) - phagocytosis in alveoli - resolution of infection
72
Q

clinical manifestation of bronchitis vs pneumonia

A
  • both cause fever, chills, cough, malaise - pneumonia will show signs of pulmonary consolidation (inspiratory crackles) and infiltrates on Xray
73
Q

infection caused by Mycobaterium tuberculosis; airborne transmission

A

tuberculosis (TB)

74
Q

occlusion of portion of pulmonary vascular bed by an embolus; obstruction occurs distal to clot location; most commonly caused by DVT

A

pulmonary embolism (PE)

75
Q

clinical manifestation of PE

A

sudden onset of symptoms - pleuritic chest pain - dyspnea - tachypnea - tachycardia - unexplained anxiety - massive occlusion = pulmonary HTN and shock

76
Q

mean pulmonary A. pressure greater than 25 mmHg at rest

A

pulmonary artery HTN (PAH)

77
Q

PAH is associated w/ what conditions

A
  • COPD - interstitial fibrosis - obesity-hypoventilation syndrome
78
Q

pathogenesis of PAH

A
  • conditions cause chronic hypoxemia and chronic acidosis - Pulmonary A. vasoconstriction - increased pulmonary A. pressure - intimal fibrosis and hypertrophy of medial smooth muscle layer of pulmonary As.
79
Q

right ventricular enlargement caused by PAH

A

cor pulmonale

80
Q

Explain how PAH causes cor pulmonale

A
  • resistance and pressure in pulmonary A. increases - workload of RV increases - leads to hypertrophy of RV and right heart failure
81
Q

primary risk factor for laryngeal cancer

A

tobacco smoking; further increased risk w/ alcohol consumption

82
Q

non-small cell lung cancer that originates from the main stem bronchus; slow growing

A

squamous cell carcinoma

83
Q

non-small cell lung cancer that usually originates in the peripheral regions of pulmonary parenchyma; moderate growth rate

A

adenocarcinoma

84
Q

non-small cell lung cancer that grows rapidly and arises centrally to distort trachea and cause widening carina

A

large cell carcinoma

85
Q

neuroendocrine lung cancer that has the highest correlation w/ smoking and arise centrally (hilar/mediastinal); very rapid growing and poor prognosis

A

small cell carcinoma

86
Q

3 conditions associated w/ pulmonary shunting/low V/Q

A

low ventilation of perfused areas - atelectasis - asthma - pulmonary edema

87
Q

1 condition associated w/ alveolar dead space/high V/Q

A

pulmonary emboli

88
Q

ventilation is adequate but perfusion to lung tissue is not

A

alveolar dead space

89
Q

2 conditions associated w/ alveolar capillary membrane barrier slowing diffusion of O2

A
  • emphysema: decrease surface area - chronic bronchitis: thickened alveolar capillary membrane w/ edema and fibrosis
90
Q

list 4 pulmonary diagnostic tests

A
  • arterial blood gas (ABG) - pulmonary function test (PFT) - sputum analysis - bronchoscopy
91
Q

Formation of fibrous tissue or nodules in the lungs due to chronic environmental exposure

A

pneumoconiosis

92
Q

Types of people at high risk for pneumonia and TB

A
  • nursing home pts - prisoners - COPD - TB = pneumonia + pts w/ HIV

Pathophysiology (20 decks)

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