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Advanced Pathophysiology > Respiratory System > Flashcards

Respiratory System Flashcards

1
Q

Approximately 1L of oxygen is transported to cells each minute. How is most of the body’s transported?

A

bound to Hgb

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2
Q

What usually has a higher pH, venous or arterial blood?

A

Arterial blood

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3
Q

What are the conducting airways of the lower airway?

A

Larynx
Trachea
Segmental bronchi
Non-respiratory bronchioles

(no gas exchange occurs here)

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4
Q

What are the respiratory units of the lower airway?

A

Respiratory bronchioles
Alveolar ducts

(where gas exchange occurs)

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5
Q

What do Type I alveolar cells do?

A

Provide structure to the alveoli

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6
Q

What do Type II alveolar cells do?

A

Produce surfactant

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7
Q

What is surfactant?

A

A phospholipid essential to maintain alveolar patency. Decrease surface tension and facilitate gas exchange.

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8
Q

What do the narrow airways in pediatric patients predispose them to?

A

Increased risk for obstruction and increased resistance to air flow.

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9
Q

At birth newborns have about _____ of alveoli

A

1/6 to 1/8 the amount an adult has (which is 300mil)

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10
Q

At what age are alveoli matured and increased in size and number by?

A

8yrs

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11
Q

What happens to the alveoli in elderly patients?

A

Reduction of alveolar units

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12
Q

What are the two suppliers of blood supply to the lungs?

A

Bronchial artery system

Pulmonary artery system (vast network)

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13
Q

What is a normal pulmonary pressure?

A

22-25/8 mmHg

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14
Q

What are the functional components of the resp system? (4)

A
  1. Neurochemical control of ventilation
  2. Mechanics of breathing
  3. Gas transport
  4. Control of the pulmonary circulation
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15
Q

Area of neural control of ventilation is located in the:

A

Medulla and pon (aka resp center)

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16
Q

Which population has the most mucous producing glands?

A

Pediatric

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17
Q

What stimulates the muscles of inspiration?

A

Dorsal respiratory group of neurons

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18
Q

How do efferent nerve impulses travel from the brainstem to the diaphragm to stimulate muscle contraction (inspiration)?

A

via the phrenic nerve

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19
Q

What controls airway lumen diameter?

A

The ANS:
Parasympathetic: constriction
Sympathetic: dilation

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20
Q

What do central chemoreceptors respond to?

A

CO2 and pH (H+ conc)

CO2 crosses BBB and stimulates respiration

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21
Q

What do peripheral chemoreceptors respond to?

A

Decrease in O2 concentration and decreased pH

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22
Q

The pons apneustic center:

A

Stimulates/prolongs inspiration

Pattern of respiration

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23
Q

What does the pneumotaxic center of the pons do?

A

Influences rate of respiration

Inhibits the inspiration (effectively ending it)

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24
Q

How do the baroreceptors in the aortic arch and carotid bodies affect respiration?

A

When an increased BP is sensed, respiration is decreased

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25
Q

How do proprioreceptors in muscles affect respiration?

A

Respond to body movement

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26
Q

What are the main muscles of inspiration?

A

External intercostals

Diaphragm

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27
Q

What are the accessory muscles and when are they used?

A

Scalenus muscles
Sternocleidomastoid muscles

Used when main muscles are inadequate

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28
Q

What happens when the diaphragm contracts?

A

It flattens downward, increasing the volume of the thoracic cavity, and creates a negative pressure that draws gas into the lungs through the upper airways and trachea.

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29
Q

What does contraction of the external intercostals do?

A

Elevates the anterior portion of the ribs. This increases the volume of the thoracic cavity by increasing its front-to-back (anteroposterior [AP]) diameter

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30
Q

When are accessory muscles of expiration used?

A

High minute ventilation, during coughing, or when airway obstruction is present

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31
Q

How do the lungs create a small amount of negative intrapleural pressure?

A

The chest wall likes to expand out and the lungs recoil (elastic recoil)- this create negative pressure

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32
Q

Airway is resistance is dependent on:

A 
Length of tube
Radius size 
Density
Viscosity
Velocity of gas
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33
Q

What are the 3 types of deadspace?

A
  1. Anatomic- conducting airways
  2. Alveolar- ventilated but under-perfused (wasted ventilation)
  3. Physiologic- anatomic and alveolar
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34
Q

What are the 4 major steps of gas transport?

A
  1. Ventilation of the lungs
  2. Diffusion of oxygen from the alveoli into the cap blood
  3. Perfusion of systemic cap with oxygenated blood
  4. Diffusion of oxygen from systemic cap into the cells
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35
Q

What is a normal tidal volume?

A

500ml (normal breath)

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36
Q

What is ventilation?

A

The process of moving air into the lungs and distributing it to the gas exchange units for maintenance of oxygenation and removal of CO2

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37
Q

What is a major compensatory mechanism in many pulmonary diseases/disorders that impair gas exchange?

A

Elevated Hgb

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38
Q

Why is PaO2 important?

A

It is the major driving pressure that causes O2 to move from the plasma into the RBC and bind to Hgb

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39
Q

How is CO2 transported?

A
  1. Dissolved in plasma
  2. Carbamino compounds
  3. Bicarb (60%)
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40
Q

A shift to the Right of the oxyhemoglobin curve:

A

Decreases O2 affinity; aids in the release of O2 from blood to tissue

ex- acidosis, hyperthermia

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41
Q

A shift to the Left of the oxyhemoglobin curve:

A

Increases O2 affinity; tighter bonding of O2 to hemoglobin. Helps loading of O2 in the lungs but impairs delivery to tissues.

ex- alkalosis, hypothermia

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42
Q

What is the difference between hypoxemia and hypoxia?

A

Hypoxemia is deficient levels of blood oxygen and hypoxia is a decrease in tissue oxygenation

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43
Q

What is hypoxic hypoxia?

A

Decreased PaO2 despite normal O2 carrying capacity

ex- altitude, hypoventilation, airway obstruction
Give O2

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44
Q

What is anemic hypoxia?

A

Decreased O2 carrying capacity.

ex- any d/o with low Hgb

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45
Q

What is circulatory hypoxia?

A

Low CO state, O2 carrying capacity normal but blood flow reduced

ex- shock, arrest, blood loss, congestive HF

46
Q

What is histotoxic hypoxia?

A

Inability of the tissues to utilize available O2 d/t a toxic substance

ex-cyanide poisoning

47
Q

At what level does oxygenation failure most often occur?

A

Pulmonary capillary-alveolar interface

48
Q

What do irritant receptors of the respiratory epithelium sense and respond to?

A

Chemical irritants. Afferent signals from these sensory cells may initiate coughing or bronchoconstriction in those with asthma

49
Q

What is happening in a pulmonary shunt?

A

Alveoli are perfused but not ventilated. Ex- ARDS, pulm hemmorhage

(opposite deadspace where alveoli are ventilated but not perfused ex- PE, anatomical)

50
Q

Acute respiratory failure is usually a combination of what 2 things?

A
  1. Failure of respiration (leading to hypoxemia with normal or low CO2)
  2. Failure of ventilation (leading to hypercapnia)
51
Q

What are the values associated with acute respiratory failure?

A

ph: <7.30
PaCO2: >50mmHg
PaO2: <60mmHg

52
Q

Where is the lung is the area of greatest perfusion and the area of greatest ventilation?

A

Ventilation: Apices (zone 1)
Perfusion: Bases (zone 3)

53
Q

Is hypoxemia always associated with hypercapnia?

A

NO

Diffusion of CO2 in the lungs is so efficient defects that affect O2 transport don’t always affect CO2 movement

54
Q

What does hypoxic vasoconstriction in the pulmonary vessels happen in response to?

A

Alveolar hypoxia

normal compensatory mechanism

55
Q

Why does it often taken a prolonged amount of time before increasing pressures in the pulmonary system are detected?

A

The pulmonary system is a low pressure system with a capillary network that can increase to 2-3x its normal size before increases are detectable

56
Q

What value if sustained represents pulmonary hypertension?

A

PAP >25mmHg at rest

57
Q

Describe primary pulmonary hypertension

A

Rare, rapidly progressive
Women > men
Associated with portal hypertension, HIV, appetite suppressing drugs

58
Q

Describe secondary pulmonary hypertension

A

Vasoconstrictive
Obstructive (d/t hypoxic vasoconstriction)
Obliterative (loss of capillary bed)
Increased left atrial pressure

Ex-chronic bronchitis and emphysema

59
Q

PE usually:

A
  • Originate in the deep veins of the legs
  • Obstruct blood flow to the lung parenchyma
  • Occlude pulmonary artery branches
  • Causes V/Q missmatch (lungs continue to bring in O2 and adequate ventilate but are not perfused d/t blockage: deadspace)
60
Q

What is the most common lung malignancy?

A

Adenocarcinoma

61
Q

Obstructive lung disease is characterized by:

A

increased resistance to air flow

trouble getting air out/air trapping

62
Q

What are the three common classifications of obstructive lung disease?

A
  1. Wall lumen conditions
  2. Loss of lung parenchyma
  3. Obstruction of airway lumen
63
Q

What do PFTs of obstructive lung disease show?

A

FVC: Normal
FEV1: Reduced
FEV1/FVC: Reduced

64
Q

What are common obstructive lung diseases that affect the wall lumen?

A

Asthma

Bronchitis

65
Q

What are common obstructive lung diseases that are associated with loss of lung parencyma?

A

COPD/Emphysema

66
Q

What are common obstructive lung diseases that obstruct the airway lumen?

A 
Bronchiectasis
Cystic Fibrosis
Bronchiolitis 
Acute Tracheobronchial Obstruction
Epiglottitis
Croup Syndromes
67
Q

What is the pathogenesis of asthma?

A

IgE-mediated response
Mast cell and histamine release results in smooth muscle contraction causing airway constriction
Goblet cells release of mucous increases

68
Q

S/s of asthma:

A 
Wheezing
Feeling of tightness of chest
Dyspnea
Cough (dry or productive)
Increased sputum production
Hyperinflated chest
Decreased breath sounds
69
Q

What is bronchitis?

A

Acute inflammation of the trachea and bronchi

Obstructive lung disease affecting the wall lumen

70
Q

Describe chronic bronchitis:

A

Type B COPD : Blue bloater
Chronic swelling and bronchial mucosa resulting in scarring
Hypersecretion of bronchial mucous
Chronic productive cough (>3mos or >2+ yrs)

71
Q

What are some characteristics of a ‘Blue bloater’

A

(chronic bronchitis)

  • excess body fluids
  • chronic cough
  • DOE
  • Increased sputum
  • Cyanosis (late sign)
72
Q

What is emphysema?

A

Type A COPD
Destructive changes of alveolar walls and abnormal enlargement of distal air sacs. Decreased elastic lung recoil.

(Obstructive lung disease affecting the lung parenchyma)

73
Q

Young patients exhibiting signs of emphysema should be tested for :

A

alpha 1 antitrypsin deficiency

genetic component

74
Q

What are characteristics of a ‘pink puffer’?

A

(emphysema)

  • use of accessory muscles to breath
  • pursed lip breathing
  • minimal/absent cough
  • leaning forward to breath
  • barrel chest
  • digital clubbing
  • DOE (late sign)
75
Q

Describe the pathogenesis of emphysema:

A

Alveolar destruction by the realse of proteolytic enzymes from inflammatory cells such as neutrophils and macrophages.

Smoking- leads to inflammation in the lung tissue causing protelytic enzymes to damage aleveolar cells. It also inactives α1-Antitrypsin which normally protects lung tissue.

α1-Antitrypsin (α1AT) deficiency can be either congenital or “functional” as a result of oxidative inactivation

76
Q

Restrictive lung disease is characterized by:

A

Decreased compliance of lung tissue

air intake problem

77
Q

Restrictive PFTs show:

A

FVC: Reduced
FEV1: Reduced (or normal relative to air taken in??)
FEV1/FVC ratio: Normal

78
Q

Restrictive lung diseases are categorized as: (5)

A
  1. Parenchyma disorders
  2. Atelectatic disorders
  3. Pleural space disorders
  4. Neuromuscular disorders
  5. Chest wall deformities
79
Q

Patients with restrictive lung diseases’ ABGs show:

A

PaO2: decreased
PaCO2: normal or decreased
pH: elevated (alkalotic)

80
Q

Common restrictive lung disease affecting the lung parenchyma include:

A

Diffuse interstitial lung disease
Sarcoidosis
Pneumonitis
Occupational lung disease

81
Q

What is the pathogenesis of diffuse interstitial lung disease?

A

An unknown antigen activates T and B lymphocytes which activated macrophages. These macrophages recruit neutrophils and cytokines resulting in injury to Type I pneumocytes(alveolar cells) and hypertrophy/hyperplasia of Type II pneumocytes

82
Q

What three pathologic changes take place in diffuse interstitial lung disease?

A

Inflammation
Fibrosis
Destruction

83
Q

S/s of diffuse interstitial lung disease:

A 
Progressive, dyspnea
Irritating, nonproductive cough
Rapid, shallow breathing 
Clubbing 
Bibasilar end-expiratory crackles
84
Q

What is the pathogenesis of sarcoidosis?

A

Unknown trigger, most likely immunologic basis
Presence of CD4 T cells
Activation of alveolar macrophages
Development of multiple, uniform granulomas

85
Q

What is hypersensitivity pneumonitis?

A

Restrictive lung disease of the parenchyma

Also considered occupational
Genetic predisposition
Inhaled organize agent leads to inflammatory process
Antigen combines with antibody in alveolar walls (Type III hypersensitivity reaction)
Ag-Ab complex causes granulomatous inflammation leading to lung tissue injury

**Hallmark sign: diffuse pulmonary fibrosis in upper lobes

86
Q

What is pneumoconiosis?

A

Restrictive lung disease of the parenchyma
Occupational

Inahalation of inorganic dust particles
Alveolar macrophages try to engulf and remove particles by secreting lysozymes which causes damage to the alveolar walls and deposition of fibrous materials

Anthracosis (coal miners lung)
Silicosis (silica inhalation)
Asbestosis (asbestos inhalation)

87
Q

What is atelectasis? What are 3 types?

A

Collapse of lung tissue

Compression, absorption, and surfactant impairement

88
Q

What causes compression atelectasis?

A

Tumors, fluid, and air in the pleural space.

89
Q

What causes absorption atelectasis?

A

Absorption of air from obstructed or hypoventilated alveoli

Concentrated O2 or anesthetic agents

90
Q

What causes surfactant impairment?

A

Decreased production or inactivation of surfactant

Prematurity, ARDS, anesthesia, mechanical ventilation

91
Q

Briefly describe ARDS:

A

Damage to the alveolar capillary membrane causing widespread protein rich alveolar infiltrates that lead to severe dyspnea.
Disruption in oxygen transport and utilization. Unable to diffuse O2 and oxygenate causes profound hypoxemia

92
Q

What is pneumonia and what are some common causes?

A

An inflammatory reaction in alveoli and interstitium usually caused by an infectious agent.

Aspriation
Inhaled contaminants (bacteria-TB, viral, fungal)
Contamination from systemic circulation

93
Q

Pleural space disorders include:

A

Pneumothorax and pleural effusion

accumulation of air or fluid in the pleural space

94
Q

What are the 3 types of pneumothorax?

A

Primary- sponatanous; rupture of bleb in apices. common in talk thin men in their 20s-30’s
Secondary- iatrogenic or complication
Tension

95
Q

Describe a tension pneumo:

A

Traumatic build up of air in the pleural space. Air can’t exit on expiration. This leads to ipsalateral lung collapse and mediastinal deviation to the contralateral side. This decreases CO

96
Q

What are the common types of effusion? (5)

A
  1. Transudate
  2. Exudate
  3. Empyema
  4. Hemothorax
  5. Chylothorax
97
Q

What do Transudative Effusions result from:

A

High hydrostatic pressure or Low oncotic pressure

d/t low concentrations of protein and LDH within fluid

Ex- HF, cirrhosis, kidney disease

98
Q

What do Exudative Effusions result from:

A

high concentrations of protein, WBC, and LDH

Ex- malignancy, infection, sarcoidosis

99
Q

What is a chylorthorax and when might it occur?

A

Traumatic leakage of lymph fluid.

Seen in rheumatoid effusion and TB pleuritis

100
Q

What is an empyema and when might it occur?

A

Purulent fluid build up, cx growth + for Staph aureus

Complication of pneumonia or bronchial obstruction by tumor. Can be a complication of TB

101
Q

What is flail chest?

A

Fracture of the ribs at two distant sites resulting in a free floating chest wall segment that moves paradoxically (in on inspiration and out on expiration)

102
Q

In children with CF what is often a sign of poor prognosis?

A

+ pseudomonas sputum culture

103
Q

What is the gold standard test for children with CF and the diagnostic result?

A

Sweat test

Sweat chloride concentration >60mEq/L

104
Q

What is CF?

A

An autosomal recessive disorder associated with defective epithelial ion transport. This CFTR defect affects Na and water transport causes impaired mucous clearance and viscous mucous production, chronic bacterial infections, neutrophilic inflammation, bronchiectasis (cyclic)

Most affected are the lungs, pancreas, intestines, and sweat glands

105
Q

Would could CF eventually lead to?

A

Cor pulmonale

106
Q

What are the primary muscles of pediatric ventilation?

A

Diaphragm and abdomen

107
Q

Why is the very compliant lung tissue in a pediatric patient of concern?

A

Prone to overdistension

108
Q

Which obstructive lung disease are pediatric patients often affected by?

A

Bronchiolitis (RSV)

Inflammation of the bronchioles, production of thick mucus leads to airway obstruction, atelectasis, and hyperinflation

109
Q

What is epiglottitis?

A

Cellulitis of the epiglottis and adjacent soft tissue

Most commonly caused by H. influenza

110
Q

What is croup syndrome?

A

Acute viral and inflammatory disease of the larynx

111
Q

What is paroxysmal nocturnal dyspnea is a result of:

A

Fluid in the lungs

112
Q

What are the normal PFT values?

A

FVC: 4.0L
FEV1: 3.0L
FEV1/FVC: 75%

Advanced Pathophysiology (12 decks)

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