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Pathophysiology Exam 3 > Respiratory System > Flashcards

Respiratory System Flashcards

1
Q

What are the upper respiratory airways?

A

-nasopharyngeal

-larynx

-tracheobronchial tree

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2
Q

What does the nasopharyngeal airway consist of?

A

-nose (primary air intake)

-mouth (alternate airway)

-lined with mucous membranes

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3
Q

What does the larynx do in upper airways?

A

-connects oropharynx and trachea

-vocal cords (folds and elongated opening-glottis)

-epiglottis (when swallowing closes over pharynx)

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4
Q

What does the tracheobronchial tree consist of?

A

-trachea

-bronchi

-bronchioles

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5
Q

What do lobules do in the lungs?

A

-gas exchange

-terminal bronchioles/ alveolar ducts/ sacs

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6
Q

What does alveoli do in the lungs?

A

-terminal air space of respiratory tract

-lined with epithelial tissue

-Type I and II cells

-alveolar macrophages

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7
Q

What are Type I Alveolar cells

A

squamous cells form barrier between air and alveolar wall

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8
Q

What are type II alveolar cells?

A

-cuboid cells: produces pulmonary surfactant

-decreases surface tension in alveoli

-phospholipid

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9
Q

What are alveolar macrophages?

A

responsible for removal of foreign agents

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10
Q

What is a pulmonary vasculature?

A

pulmonary and bronchial circulation

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11
Q

What happens in the pulmonary circulation?

A

-pulmonary artery carries poorly oxygenated venous blood to lung capillaries for gas exchange

-pulmonary veins carry freshly oxygenated blood into left side of heart

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12
Q

What happens in bronchial circulation?

A

-distributes blood to the connecting airways

-provides blood supply to the lung structure

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13
Q

What are the Pleura and Pleural cavity?

A

-double layered serous membrane

-lines thoracic cavity

-encases lungs, thoracic wall, mediastinum, and diaphragm

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14
Q

What is the thoracic cavity potential space for?

A

inflammatory exudate to accumulate

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15
Q

What is pleural effusion?

A

abnormal collection of fluid or exudate in pleural cavity

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16
Q

What is ventilation?

A

the mechanism of breathing

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17
Q

What is breathing controlled by?

A

medulla oblongata in the lower brain

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18
Q

What monitors blood levels of CO2, O2, and blood pH?

A

chemoreceptors in the medulla, carotid arteries, and aorta

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19
Q

What is CO2 narcosis?

A

-in people with chronic hypercarbia

-people who no linger respond to stimulus and rely upon decreased blood oxygen to increase ventilation

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20
Q

What is the main chemical that determines the rate of breathing?

A

CO2

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21
Q

What happens when there is too much CO2 in the blood?

A

breathing rate increases

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22
Q

Decreased pressure inside chest compares to:

A

air pressure outside chest

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23
Q

What must combine for adequate oxygenation of the blood?

A

ventilation (V) and perfusion (Q)

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24
Q

What is the normal ventilation-perfusion match?

A

a ratio of 4:5 or also written as 0.8 (gold standard value)

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25
Q

To optimize oxygenation in the client with unilateral pneumonia, how would the nurse position the client and why? (V-Q Matching Example)

A

-position the patient in a downward position where their airways are open

-a more gravity downward position

-“GOOD lung down”

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26
Q

Perfusion of blood in the lungs is gravity-dependent. What does this mean?

A

more blood will be found in lower areas of the lungs

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27
Q

What is Atelectasis?

A

-incomplete expansion of a lung or part of a lung

-caused by airway obstruction or compression to lung tissue

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28
Q

What are the causes of Atelectasis?

A

-immobility

-decreased LOC

-medications

-decreased rate/ depth of breathing

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29
Q

What is Hemothorax?

A

blood collection in chest cavity

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30
Q

What happens to the pleural cavity when lungs are fully expanded?

A

-normally empty space between visceral and parietal pleura

-with pleural effusion, there is abnormal fluid collection between visceral and parietal pleura

-lung expansion decreases when pleural effusion occurs

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31
Q

Clinical Manifestations- Atelectasis

A

-increased temp

-decreased mobility

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32
Q

What is lung compliance and why does it matter?

A

-elastin/ collagen fibers give elasticity to lungs and help provide elastic recoil

-lung compliance helps to push air out of alveoli and airways

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33
Q

What are obstructive pulmonary disease characteristics?

A

-inspiration (airways open)

-expiration (airways narrow)

-alveoli hyper-inflated by trapped air

-increased lung compliance

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34
Q

What are the types of obstructive pulmonary disease?

A

-asthma

-emphysema

-chronic bronchitis

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35
Q

Asthma Etiology

A

-hypersensitivity lung response to stimuli

-leading risk factor= genetic predisposition for hypersensitive response to common allergens

-chronic inflammation of bronchial mucosa

36
Q

What does chronic inflammation of bronchial mucosa lead to?

A

-bronchioles hypersensitive o inhaled substances

-airway constriction

-airflow limitation (reversible)

37
Q

What happens when lungs lose its elasticity?

A

it has trouble getting air out of the lungs as fast as it should and air that is inhaled sits in the lungs and becomes stale

38
Q

Environmental Etiology- Peds

A

-air pollution

-home stress

-cockroach agent

-cat exposure

-lack of healthcare

-vitamin D insufficiency

39
Q

Environmental Etiology- Adults

A

-respiratory infections

-esophageal reflux

-obesity

-tobacco smoke

40
Q

What is primary prevention of asthma?

A

avoidance of asthma risk factors

41
Q

Why is asthma categorized as an obstructive pulmonary disease?

A

because its underlying feature is airway obstruction that worsens in the expiratory phase

42
Q

Asthma involves alveolar damage and air trapping that leads to what?

A

alveolar hyperinflation with eventual alveolar destruction

43
Q

Asthma vs COPD

A

-both: airflow limitation is a characteristic

-asthma: reversible

-COPD: irreversible

44
Q

Asthma Pathogenesis

A

-hypersensitivity cause increased Immunoglobulin E antibody response to inhaled substance

-increased histamine and leukotriene: bronchoconstrictor

45
Q

Asthma- Symptoms

A

-severe dyspnea

-chest tightness

46
Q

Asthma- Signs

A

-expiratory wheezing

-tachycardia

-tachypnea

-decreased arterial oxygen sat

-respiratory acidosis: alarm for impending respiratory failure

47
Q

What do arterial blood gases indicate?

A

elevated pCO2 and decreased pH

48
Q

Status Asthmaticus

A

-unresponsive to treatment

-worsening hypoxemia and acidosis

-can be fatal

49
Q

What is COPD?

A

-chronic and recurrent obstruction of airflow

-emphysema + chronic bronchitis often coexist

-irreversible functional change

50
Q

What are risk factors for COPD?

A

-tobacco

-air pollution

-poor nutrition

-advanced age

51
Q

What are the genetic factors of COPD?

A

-Alpha: 1 anti trypsin autosome recessive defect

-AAT: antiprotease enzyme protects lungs tissue and bile ducts

52
Q

What are COPD structural changes?

A

-bronchioles lose their shape and become clogged with mucus

-walls of alveoli are destroyed, forming fewer larger alveoli

53
Q

Emphysema Pathophysiology

A

-mucosal inflammation

-alveoli destroyed

-airway collapse

-air trapped in alveoli

-decreased alveolar surface area for gas exchange

54
Q

What does tobacco smoke inactivate?

A

the alpha-1 antitrypsin that normally protects airway tissue

55
Q

What is an example of metaplasia?

A

a reversible change when an adult cell is REPLACED by a different type of cell in the same category

56
Q

Emphysema- Clinical Manifestations

A

-dyspnea

-cough

-barrel chest

-increase pCO2

-Xray: flat diaphragm

57
Q

Chronic Bronchitis- Chronic airway inflammation

A

-defined by: Coughing > 3 months x 2 years

-common etiologies involve cigarette smoking and air pollution

-often leads to recurrent respiratory infections

58
Q

Why do individuals with COPD develop polycythemia?

A

they have chronic hypoxemia which causes the brain to feel the need to make more RBCs but it will eventually clot

59
Q

What is Pneumonia?

A

-infectious or non infectious inflammation of lung parenchyma, bronchi, and/ or alveoli

-8th leading cause of death

-increased risk in older adults or anyone with debilitating conditions

60
Q

What are the Pneumonia types?

A

typical and atypical

61
Q

What is typical pneumonia?

A

bacteria cause inflammation and fluid exudate in alveoli air spaces

62
Q

What is atypical?

A

virus and mycoplasma infection in alveoli septal area and lung interstitium

63
Q

Typical pneumonia risk factors

A

-age > 65

-immune compromised

-recent antibiotics

-comorbidities

-recently hospitalized

-smoking

-diabetes mellitus

64
Q

Atypical pneumonia risk factors

A
  • immunocompromised

-close quarters

-smoking

-children/adolescents

-late summer/fall

65
Q

Typical Pneumonia- Etiology

A

-streptococcus pneumonia

-legionella pneumophilia

66
Q

Atypical Pneumonia- Etiology

A

Mycoplasma pneumoniae

67
Q

Typical Pneumonia- Clinical Manifestations

A

-temp > 100.4 F.

-rales, rhonchi, wheezes

-elevated WBC

-cough often with purulent sputum

-dyspnea

-muscle aches

-abdominal pain

68
Q

Atypical Pneumonia- Clinical Manifestations

A

-less signs of infection than typical form

-hacking cough

-fever

-fatigue

-lack of purulent sputum

69
Q

What are risk factors for Tuberculosis?

A

-malnutrition

-immunosuppression

-advanced age

-poor sanitation

-crowded living conditions

70
Q

PPD Skin Tests

A

-test for TB

-positive test

-does NOT differentiate between active and past infection

71
Q

What does. false negative for a PPD Skin Test indicate?

A

too immunocompromised

72
Q

TB Pathophysiology

A

-begins with inhalation of tubercle bacillus

-infection spreads vis lymph and blood

-infection walled off

-can be dormant for years

-becomes active when immunocompromised

73
Q

TB Clinical Manifestations

A

-low grade fever

-cough

-frothy/ bloody sputum

-night sweats

-anorexia

-weight loss due to metabolic demands of infection

74
Q

Cystic Fibrosis (CF)

A

-autosome recessive disorder of Chromosome 7

-carrier gene identified

-75% diagnosed by age 1

75
Q

What are chloride transport defects in epithelial tissue? (CF)

A

-airways: mucus plugs

-pancreas: nutrient malabsorption

-sweat ducts: salty skin crystals

-vas deferens: male infertility

76
Q

Cystic Fibrosis- Pathophysiology

A

-development of bull in lung tissue

-pneumothorax

-hemoptysis

-pulmonary hypertension

-progressive and irreversible lung deterioration

77
Q

Cystic Fibrosis- Clinical Manifestations

A

-frequent respiratory infections

-persistent coughing

-audible wheezing

-dyspnea

-thick sputum

78
Q

What is Hypoxemia?

A

-below normal oxygen in blood

79
Q

Hypoxemia- Etiology

A

-ventilation disorders

-hypoventilation

-impaired gas exchange

-inadequate circulation

-dysfunction of nervous system

80
Q

Hypoxemia- Manifestations

A

-cyanosis

-bluish discoloration of skin and mucous membrane

-dark skin- inspect oral mucosa

81
Q

Indications for arterial blood gases`

A

-clients with serious/ critical illness or injury

-acid base status

-adequacy of ventilation

-adequacy of oxygenation

82
Q

Acid- Base Normal Values

A

-pH: 7.35-7.45

-paCO2: 35-45 mm Hg

-HCO3-: 22-26 mEq/L

-paCO2: 80-100 mm Hg

83
Q

What are the steps of an arterial blood gas assessment>

A

1- check pH

  1. check paCO2
  2. check HCO3
84
Q

What are basic results of arterial blood gas assessments?

A

-respiratory acidosis

-respiratory alkalosis

-metabolic acidosis

-metabolic alkalosis

85
Q

Respiratory vs Metabolic Disorder

A

-if paCO2 is abnormal, problem is respiratory

-if HCO3 is abnormal, problem is metabolic

86
Q

What are some respiratory acidosis causes?

A

-hypoventilation

-sedation

-anesthesia

-respiratory arrest

-paralysis of respiratory muscle

-airways obstruction

87
Q

What are some respiratory alkalosis causes?

A

-hyperventilation

-hypoxemia

-anemia

-fever

-psychological dyspnea

-anger

Pathophysiology Exam 3 (6 decks)

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