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CV487 > Class 3 respiratory: Obstructive airway disorders > Flashcards

Class 3 respiratory: Obstructive airway disorders Flashcards

1
Q

COPD pathophysiology

A

-Decrease in the exhaled air flow caused by a narrowing or obstruction of the airways
-e.g., emphysema, chronic bronchitis, bronchiectasis (Abnormal widening of the bronchi or their branches, causing a risk of infection)

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2
Q

Levels of COPD

A

-Many patients have overlapping features of damage at both the acinar level (emphysema) and bronchial level (bronchitis)

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3
Q

COPD is caused by

A

-COPD is the result of long-term heavy cigarette smoking; about 10% of pts are non-smokers

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4
Q

COPD elastic recoil is

A

Low

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5
Q

What happens in COPD?

A

-Bronchial wall becomes inflamed and fibrosed, with breakdown of alveolar tissue and loss of elasticity, mucus secretion, airway obstruction, air trapping

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6
Q

Emphysema definition & pathophysiology

A

-Loss of lung elasticity
-Enlargement on alveoli due to air trapping; hyperinflation of lungs and increased Total Lung Capacity
-“over-inflation” enlargement of airspaces unaccompanied by destruction

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7
Q

Manifestations of emphysema

A

-Barrel chest, accessory muscles, pursed lip breathing, tripod
-Weight loss and anorexia
-Prolonged expiratory phase, wheezes, decreased breath sounds

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8
Q

Emphysema features

A

-Patient is often thin and elderly
-Little sputum produced
-Edema and overt HF are rare complications

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9
Q

About emphysema

A

-“Pink puffers”
-Caused by destruction of pulmonary connective tissue
-Characterized by permanent enlargement of air sacs and rupture of interalveolar walls
-Expiration is difficult causing hyperinflation

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10
Q

Emphysema inspection

A

-Increased AP diameter
-Barrel chest
-Accessory muscles, tripod position
-SOBOE
-Respiratory distress, tachypnea
-Decreased breath sounds, prolonged expiration, muffled heart sound d/t overdistension of the lungs

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11
Q

Chronic bronchitis

A

-Blue bloaters
-Inflammed airway
-Characterized by hypersecretion of mucus and chronic productive cough for at least 3 months

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12
Q

Pathophysiology of chronic bronchitis

A

-Inspired irritants result in airway inflammation with infiltration of neutrophils, macrophages and lymphocytes
-Continued bronchial inflammation leads to bronchial edema and increases the size and number of mucous glands leading to the production of thick tenacious mucus

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13
Q

Chronic bronchitis is often..

A

Combined with emphysema

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14
Q

Manifestations of chronic bronchitis

A

-Productive cough; classic sign
-Dyspnea, wheezing, prolonged expiration, cyanosis, hypoventilation, polycythemia, & cor pulmonale
-Barrel chest

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15
Q

Manifestation differences between bronchitis & emphysema (cough, dyspnea, wheezing, barrel chest, cyanosis, hypoventilation polycthemia & cor pulmonale)

A

-Productive cough is a classic sign in bronchitis & late in infection with emphysema
-Dyspnea is late in course with bronchitis and common in emphysema
-Wheezing is intermittent in bronchitis and common with emphysema
-Barrel chest is occasional in bronchitis and a classic sign in emphysema
-Cyanosis is common in bronchitis & uncommon in emphysema
-Hypoventilation, polycythemia, & cor pulmonale are common in bronchitis & late in course with emphysema

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16
Q

Primary bronchitis manifestations

A

Dyspnea, hypoxia, cyanosis & peripheral edema

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17
Q

About bronchitis

A

-Excessive mucus secretion
-Inflammation of bronchi with partial obstruction of bronchi by secretions or constrictions
-Sections of lung distal to obstruction may be deflated
-Acute or chronic

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18
Q

Bronchitis inspection

A

-Hacking, rasping cough productive of thick mucoid sputum
-Chronic: dyspnea, fatigue, cyanosis, possible clubbing of fingers

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19
Q

Bronchitis auscultation

A

-Normal vesicular & voice sounds
-Chronic: prolonged expiration

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20
Q

Bronchitis adventitious sounds

A

Crackles over deflated areas. Wheeze may be present

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21
Q

Pneumonia definition

A

-Infection of the lower respiratory tract caused by bacteria, viruses, fungi, protozoa, or parasites
-Defined in 2 ways:
-Location in the lungs
-Lobar Pneumonia (occurs in one lobe of the lung).
-Bronchopneumonia (tends to be patchy).
-Origin of Infection
-Community-acquired (pneumonia contracted outside the hospital)
-Hospital-acquired pneumonia – nosocomial; particularly gram-negative bacteria and staphylococci

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22
Q

Pathophysiology of pneumonia

A

-Macrophages release tumor necrosis factor-alpha and interleukin-1 from macrophages (inflammation)
-Inflammatory mediators and immune complex damage bronchial mucous membranes and alveolar-capillary membranes causing alveoli to fill with infectious debris and exudate causing lung damage and consolidation
-Accumulation in the acinus leads to dyspnea and V/Q mismatching and hypoxemia

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23
Q

How pneumonia is aquired

A

-Acquired through: aspiration, inhalation and hematogenous

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24
Q

Manifestation of pneumonia

A

-Sudden onset of fever, chills, productive cough of purulent sputum and pleuritic chest pain
-Confusion or stupor (related to hypoxia) may be predominant

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25
Q

Inspection: Pneumonia

A

increased work of breathing, cough, changes in perfusion and oxygenation

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26
Q

Auscultation: Pneumonia

A

may have decreased breath sounds or bronchial breath sounds or crackles

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27
Q

Lab values for pneumonia

A

Complete Blood Count (CBC), C-Reactive Protein (CRP), Electrolytes, Arterial Blood Gas (ABG)

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28
Q

Pneumonia complications

A

-Pleurisy (inflammation of the pleura)
-Pleural Effusion
-Atelectasis
-Empyema
-Pericarditis
-Endocarditis

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29
Q

Lobar pneumonia

A

-Infection in lung parenchyma leaves alveolar membrane edematous and porous, and so red blood cells (RBCs) and white blood cells (WBCs) pass from blood to alveoli; causes hypoxemia

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30
Q

Inspection of lobar pneumonia

A

Increased respiratory rate. Guarding and lag on expansion on the affected side. Children: sternal retraction, nasal flaring.

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31
Q

Palpation: Lobar pneumonia

A

Chest expansion decreased on the affected side

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32
Q

Auscultation: Lobar pneumonia

A

-Breath sounds louder with patent bronchus, as if coming directly from the larynx. Voice sounds have increased clarity, bronchophony, egophony, whispered pectoriloquy present
-Children: diminished breath sounds may occur early in pneumonia

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33
Q

Adventitious sounds: Lobar pneumonia

A

Crackles, fine to medium

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34
Q

Pneumonias may..

A

Turn into ARDS and lead to sepsis

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35
Q

TB

A

-Infection caused by mycobacterium tuberculosis, an acid-fast bacillus that affects the lungs
-Can have a latent period

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36
Q

TB pathophysiology

A

-Airborne droplets
-In immunocompromised people, it is contained by the immune system and results in latent TB infection (LTBI)
-After latent period in the upper lobe, bacilli are inspired into the lungs; activating alveolar macrophages and neutrophils
-May lay dormant but can also be reactivated

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37
Q

Manifestations of TB

A

-LTBI is asymptomatic
-Cough with purulent sputum, hemoptysis, weight loss, night sweats, fever, fatigue, anorexia, chest pain

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38
Q

Lab values for TB

A

-CBC, acid-fast bacilli (AFB)

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39
Q

About TB

A

-Initial complex is acute inflammatory response; macrophages engulf bacilli but do not kill them. Tubercle forms around the bacilli
-Scar tissue forms, and lesion calcifies
-Previously healed lesions are reactivated. Dormant bacilli now multiply, producing necrosis, cavitation, and caseous lung tissue (cheese like appearance)
-Apex of lungs has the most damage

40
Q

TB subjective data

A

-Initially no symptoms, manifested as positive result of skin test or on radiograph
-Progressive tuberculosis involves weight loss, anorexia, easy fatigability, low-grade afternoon fevers, night sweats.
-Patients may have pleural effusion, recurrent lower respiratory infections

41
Q

TB inspection

A

Cough initially nonproductive, later productive of purulent, yellow-green sputum, may be blood-tinged. Dyspnea, orthopnea, fatigue, weakness.

42
Q

TB palpation

A

Skin moist from night sweats

43
Q

TB auscultation

A

Normal or decreased vesicular breath sounds.

44
Q

TB adventitious sounds

A

Crackles over upper lobes are common, persist after full expiration and cough

45
Q

Pulmonary embolism

A

-Outside the lung problem
-Occlusion of the pulmonary vascular bed by an embolus

46
Q

PE pathophysiology

A

-Embolism with or without infarction, massive occlusion, or multiple pulmonary embolism
-Obstruction of the pulmonary vasculature leads to pulmonary HTN

47
Q

PE causes

A

Capillaries to leak into the alveoli (pink frothy sputum)

48
Q

PE pathophysiology

A

-Release of neurohumoral substances and inflammatory mediators; increased vasoconstriction
-Leads to pulmonary HTN (increased pulmonary after load), can lead to RV dilation
-Absent blood flow causes V-Q mismatch (dead space) and decrease surfactant production resulting in atelectasis contributing to hypoxemia

49
Q

Manifestations of a PE

A

-Sudden onset of pleuritic chest pain, dyspnea, tachypnea, tachycardia and anxiety
-Occasional syncope or hemoptysis
-Pleural friction rub, pleural effusion, fever and leukocytosis

50
Q

PE auscultation

A

Crackles

51
Q

PE lab values

A

CBC, d-dimer, troponin, BNP level, ABG

52
Q

PE subjective data

A

Chest pain, worse on deep inspiration, dyspnea

53
Q

Inspection of PEs

A

Apprehensiveness, restlessness, anxiety, mental status changes, cyanosis, tachypnea, cough, hemoptysis, PaO2 < 80 on pulse oximetry. Arterial blood gases show respiratory alkalosis

54
Q

Palpation PEs

A

Diaphoresis, hypotension

55
Q

Auscultation: PEs

A

Tachycardia, accentuated pulmonic component of S2 heart sound

56
Q

PE adventitious sounds

A

Crackles, wheezes

57
Q

Pulmonary arterial HTN

A

-High PA pressures and typically associated with COPD

58
Q

Pathophysiology of arterial HTN

A

-Vascular growth factors cause fibrosis and thickening of vessel walls with luminal narrowing
-Increased PVR (after load) the RV has to pump against; reducing gas exchange and lung volumes
-Increases workload of the RV leading to RV hypertrophy, followed by failure (Cor Pulmonale)

59
Q

Characterization of pulmonary arterial HTN

A

-Characterized by endothelial dysfunction with overproduction of vasoconstrictors (such as thromboxane and endothelin), decreased production of vasodilators (prostacyclin and nitric oxide)

60
Q

Clinical manifestations of pulmonary arterial HTN

A

-Abnormal CXR
-Fatigue, chest discomfort, tachypnea, and dyspnea
-Peripheral edema, JVD, precordial heave, louder S2

61
Q

Cor pulmonale

A

-RV enlargement (hypertrophy, dilation, or both) leading to right sided HF
-Caused by PAH

62
Q

Pathophysiology of cor pulmonale

A

-Develops due to chronic pressure overload in the RV
-Increased work of the RV leading to failure

63
Q

Manifestations of cor pulmonale

A

-Heart may appear normal at rest but with exercise CO falls
-Louder S2 (closure of the pulmonic valve)
-Murmur of the tricuspid valve
-JVD, hepatosplenomegaly, and peripheral edema

64
Q

Respiratory dysfunction in the pediatric patient

A

Upper & lower respiratory tract disease

65
Q

Approach to acute respirology

A

-Upper respiratory tract: Croup, epiglottitis
-Lower respiratory tract: Bronchiolitis/respiratory syncytial virus (RSV), pneumonia, asthma
-Upper/lower respiratory tract: Foreign body

66
Q

Upper respiratory tract diseases

A

-Diseases above the thoracic inlet
-Characterized by inspiratory stridor, hoarseness, and suprasternal retractions

67
Q

Differential diagnosis of stridor for upper respiratory tract diseases

A

-Croup
-Epiglottitis
-Foreign body aspiration

68
Q

Croup

A

-Paroxysmal attacks (spasms of the larynx)
-Etiology: Influenza A&B, RSV, allergic component

69
Q

Croup manifestations

A

-Hoarse voice, barking cough, stridor, SOB, anxiety
-Onset at night

70
Q

Croup diagnostic methods

A

Clinical diagnosis
Chest x-ray (Steeple sign from subglottic narrowing)

71
Q

Epigolittitis

A

-Acute, severe, and rapid progressive swelling
-Rare, usually occurs in 2-8 year olds
-Etiology: Bacterial (H. influenza type b)

72
Q

Epiglottitis manifestations

A

-Abrupt onset-rapid progression
-Excessive drooling, stridor, SOB, anxiety, difficulty swallowing, tripod position
-Cherry red, swollen epiglottis
-Medical emergency

73
Q

Diagnostic methods of epiglottitis

A

Clinical diagnosis
Avoid examining the throat to prevent further respiratory exacerbation

74
Q

Epiglottitis big signs

A

Tripod & drooling combined mean airway is occluding

75
Q

Lower respiratory tract diseases

A

-Obstruction of airways below thoracic inlet, produces more expiratory sounds
-Classic symptom is wheezing

76
Q

Common differential diagnosis of wheezing

A

-Bronchiolitis: First episode of wheezing
-Pneumonia: Fever, cough, fatigue
-Asthma: Recurrent wheezing episodes, identifiable triggers

77
Q

Bronchiolitis/respiratory syncytial virus (RSV)

A

-Acute viral infection of lower respiratory tract (small bronchioles), with resultant trapping of air
-Epidemiology: Infants, peak at 6 months

78
Q

Bronchiolitis/respiratory syncytial virus (RSV) etiology

A

Respiratory syncytial virus

79
Q

Bronchiolitis/respiratory syncytial virus (RSV) manifestations

A

-Coughing, wheezing, acute respiratory distress followed by rapid recovery, tachypnea, tachycardia, retractions, poor air entry

80
Q

Investigation of bronchiolitis/respiratory syncytial virus (RSV)

A

Chest x-ray
Nasopharyngeal swab
CBC

81
Q

Pneumonia

A

-Inflammation of pulmonary tissue associated with consolidation of alveolar spaces
-Common in infancy and early childhood
-Etiology: Viral agents: RSV and influenza virus

82
Q

Manifestations of pneumonia

A

-Increased work of breathing (intercostal, suprasternal, subcostal, nasal flaring and use of accessory muscles)
-Cyanosis, tachypnea, respiratory fatigue, crackles, wheezing, decreased air entry on affected side

83
Q

Diagnostic methods of pneumonia

A

Clinical diagnosis
Chest x-ray

84
Q

Asthma

A

-Lower airway disorder characterized by heightened airway reactivity with bronchospasm & obstruction
-Unknown etiolgy, 75% have family hx

85
Q

Asthma manifestations

A

-Anxiety, accessory muscle use, cough, crackles, cyanosis, SOB, tachypnea, tachycardia, & wheezing

86
Q

Asthma classifications

A

-Mild: Occasional attacks <2/week
-Moderate: more frequent with persistent coughing, decreased activity tolerance
-Severe: Daily & nocturnal symptoms, frequent ER visits

87
Q

Diagnostic methods of asthma

A

Clinical diagnosis
Pulmonary functional studies

88
Q

Asthma progression

A

Wheeze can develop into crackles if asthma progresses to pulmonary edema

89
Q

About asthma

A

Complex response characterized by bronchospasm, and inflammation, edema in walls of bronchioles, and secretion of highly viscous mucus into airways

90
Q

Asthma inspection

A

-During severe attack: Increase RR, SOB w audible wheezing, accessory neck muscles, apprehension, cyanosis, intercostal indrawing. Labored & prolonged expiration.
-When asthma is chronic, barrel chest may develop

91
Q

Auscultation of asthma

A

Diminished air movement. Breath sounds decreased, with prolonged expiration. Voice sounds decreased

92
Q

Adventitious sounds + asthma

A

Bilateral wheezing on expiration; sometimes inspiratory and expiratory wheezing

93
Q

Foreign body aspiration

A

-Child usually presents after sudden episode of coughing or choking while eating with subsequent wheezing coughing or stridor
-Usually in <5 years old

94
Q

Foreign body aspiration manifestations

A

-Symptoms depend on: extent, size and composition of object, elapsed time since, location, degreee and duration of airway blockage
-Suddent respiratory distress
-Abnormal respiratory sounds
-Coughing, gagging, agitation
-Cyanosis

95
Q

Diagnostic methods of foreign body aspiration

A

Clinical diagnosis
X-ray
Bronchoscopy
Larygoscopy (then remove with forceps)

96
Q

Respiratory infections account for…

A

majority of acute illness in children

CV487 (15 decks)

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