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BHSC 2203 - Patho > Unit 7 - Respiratory Disorders > Flashcards

Unit 7 - Respiratory Disorders Flashcards

1
Q

What are the 4 functions of respiration?

A
  1. Ventilation
  2. Perfusion
  3. Diffusion
  4. Circulation
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2
Q

What are the 3 things that can cause respiratory failure?

A
  1. Hypoventilation
  2. Impaired diffusion
  3. Pleural disorders
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3
Q

What are the three things that can cause hypoventilation (that would result in respiratory failure)?

A
  1. Depression of respiratory centre
  2. Disease of respiratory muscles or nerves
  3. Thoracic cage disorders
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4
Q

How can thoracic cage disorder cause hypoventilation?

A
  • SCOLIOSIS - a curve in the backbone will impair the movement of the ribs –> impairs breathing, there will be uneven expansion
  • KYPHOSIS (humpback) - issue with the expansion of the ribs = less expansion of the chest = compromises ventilation
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5
Q

What 4 things can result in impaired diffusion (that would cause respiratory failure)?

A
  1. Pneumonia
  2. Interstitial lung disease
  3. ARDS (acute respiratory distress syndrome)
  4. Pulmonary edema
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6
Q

What are characteristics of pneumonia?

A
  • fluid accumulation in the lungs
  • expansion will be compromised
  • less surface area for diffusion
  • respiratory membrane will be thicker = harder to breathe
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7
Q

What are the characteristics of interstitial lung disease?

A
  • Alveoli now have thick membranes

- harder to breathe b/c diffusion distance would be increased and diffusion would be compromised

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8
Q

What are the characteristics of pulmonary edema?

A
  • mitral valve stenosis (left ventricular failure)

- fluid in the lungs = less diffusion

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9
Q

What are the two pleura of the lungs?

A
  1. Parietal pleura

2. Visceral pleura

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10
Q

What does the pleural cavity contain?

A

Contains a thing layer of serous fluid

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11
Q

What is the functional significance of the serous fluid in the pleural cavity?

A

Allows for chest expansion of the lungs

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12
Q

What are the three kinds of pleural space disorders?

A
  1. Pneumothorax
  2. Pleural effusions
  3. Fibrothorax
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13
Q

What happens if air enters the pleural space?

A

Atmospheric air pressure is greater than alveoli pressure

= compress the alveoli (atelectasis)

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14
Q

What are the 4 different kinds of pleural effusions?

A
  1. Hydrothorax
  2. Empyema
  3. Chylothorax
  4. Hemothorax
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15
Q

What kind of fluid is in the pleural space in a hydrothorax?

A

Serious fluid

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16
Q

What kind of fluid is in the pleural space in an empyema?

A

Pus

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17
Q

What kind of fluid is in the pleural space in a chylothorax?

A

Lymph

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18
Q

What kind of fluid is in the pleural space in a hemothorax?

A

Blood

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19
Q

What is building around the lungs when a fibrothorax happens?

A

Connective tissue

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20
Q

What happens during a pneumothorax?

A

Air enters the pleural cavity

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21
Q

Why is a pneumothorax bad?

A

Air takes up space

  • restricts lung expansion
  • alveoli can collapse b/c the atmospheric pressure is higher than alveolar pressure
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22
Q

What are the two kinds of pneumothoraxes?

A
  1. Spontaneous
    - air filled blister on the lung ruptures
  2. Traumatic
    - air enters through chest injuries
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23
Q

What is an OPEN traumatic pneumothorax?

A

Air enters pleural cavity through the wound on inhalation and leaves on exhalation

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24
Q

What is a TENSION traumatic pheumothorax?

A

Air enters pleural cavity through the wound on inhalation but CANNOT leave on exhalation

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25
Q

Why can the alveoli collapse if there is a breach of the pleural cavity (pneumothorax)?

A

Atmospheric pressure is higher than alveolar pressure

- presses the alveoli shut

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26
Q

True or false:

If an open pneumothorax is small, it will heal be itself

A

True

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27
Q

True or false:

If an open pneumothorax is large, it will only heal if fixed by surgeons

A

True

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28
Q

What will a patient experience (S/S) with a tension pneumothorax?

A

Pain and tension!

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29
Q

How can a tension pneumothorax result in death?

A

Inferior vena cava can collapse

- if there is a LOT of pressure in the RIGHT lung, it can collapse the vein

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30
Q

What are three features of a pneumothorax?

A
  1. Tracheal shift
  2. Cardiac compression
  3. Lung deflation
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31
Q

True or False:

Trachea will shift towards the injury in a pneumothorax

A

FALSE!

  • trachea will shift AWAY from the injury
  • atmospheric air will push against the lungs, heart, and trachea
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32
Q

What will the lung look like if x-rayed when the patient has a pneumothorax?

A

When the lung is collapsed, there is a lot of tissue and the lung looks WHITE (it has become more dense)

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33
Q

What are the two manifestations of respiratory failure?

A
  1. Hypoxemia

2. Hypercapnia

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34
Q

What are the characteristics of hypoxemia?

A
  • PO2 < 60 mmHg
  • cyanosis results
  • leads to impaired function of vital centers
  • activation of sympathetic system
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35
Q

What happens to the patient (S/S) the sympathetic nervous system responds to low oxygen?

A
  1. Agitated, combative behaviour, euphoria, impaired judgement
  2. Convulsion, delirium
  3. Stupor, coma
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36
Q

Why do patients develop hypotension and bradycardia when in a hypoxemic state?

A

As oxygen levels decrease, the neurons on the sympathetic nervous system start to fail, the compensation mechanisms fail (loss or compensation or decompensation)

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37
Q

What are the characteristics of hypercapnia?

A
  • PCO2 > 50 mmHg

- respiratory acidosis develops

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38
Q

What are the S/S of hypercapnia/respiratory acidosis?

A
  • increased RR
  • decreased nerve firing
  • carbon dioxide narcosis (tremors, confusion, convulsion, coma)
  • decreased muscle contraction
  • vasodilation (headache, warm flushed skin)
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39
Q

What are 4 obstructive airway disorders?

A
  1. Bronchial asthma
  2. COPD (chronic bronchitis and emphysema)
  3. Bronchiectasis
  4. Cystic fibrosis
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40
Q

Why is asthma not classified as COPD?

A

It is episodic, not chronic

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41
Q

Why does respiratory obstruction happen more easily in children than adults?

A

Airways are MUCH smaller, therefore, an obstruction will happen much more easily

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42
Q

What are the two respiratory obstruction that occur in children that increase airway resistance?

A
  1. Extrathoracic airway obstructions

2. Intrathoracic airway obstructions

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43
Q

What happens in an extrathoracic airway obstruction?

A
  • Prolonged INSPIRATION
  • INSPIRATORY STRIDOR
  • Patient has difficulty expanding rib cage outward during inspiration
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44
Q

Where does extrathoracic airway obstructions occur?

A

UPPER airways

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45
Q

Where does intrathoracic airway obstuctions occur?

A

LOWER airways

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46
Q

What happens in an intrathoracic airway obstruction?

A
  • prolonged EXPIRATION
  • WHEEZING
  • patient has difficulty pulling ribs inward during expiration
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47
Q

When does stridor occur?

A

Occurs in the extrathoracic airways during INSPIRATION

  • When an object is obstructing the upper conducting tube
  • Air is forced through a very small space
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48
Q

Which airways EXPAND during inspiration (2)?

A
  1. Alveoli (intrathoracic airway)

2. Bronchi (intrathoracic airway)

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49
Q

What airways constrict during inspiration?

A

EXTRAthoracic airways

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50
Q

When does wheezing occur?

A

Occurs in the intrathoracic airways during EXPIRATION

  • Pressure in the lungs is going up
  • Bronchi construct during expiration
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51
Q

What are 2 upper airway obstructive disorders in children?

A
  1. Croup

2. Epiglottitis

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52
Q

What is a lower airway obstructive disorder in children?

A

Acute bronchiolitis

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53
Q

What kind of pitch is associated with stridor?

A

High pitched sound on inspiration

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54
Q

What is croup caused by?

A

Influenza virus - characterized by inspirational stridor

- Cough sounds brassy

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55
Q

When is croup most prevalent in children? Why?

A

3 months to 3 years of age

- B/c their airways are very narrow

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56
Q

What is the recommendation for a child that is experiencing croup?

A

Take a walk in the cold air, in the winter months

- Maybe cold air reduces inflammation in the airways(?)

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57
Q

What are the classifications of asthma (2)?

A
  1. Extrinsic

2. Intrinsic

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58
Q

What is extrinsic asthma?

A

Allergic reaction

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59
Q

What is intrinsic asthma?

A

Attacks precipitated by non-allergic factors

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60
Q

What are some examples of factors that trigger intrinsic asthma (6)?

A
  • Exercise
  • Psychologic stress
  • Chemical irritants
  • Air pollution
  • Bronchial infection
  • Aspirin
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61
Q

What facilitates the change in the diameter of the airway?

A

Smooth muscle!

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62
Q

What happens to airway resistance when the smooth muscles of the airways contract?

A

Increases

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63
Q

What happens to airway conductance when the smooth muscles of the airways relax?

A

Increases

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64
Q

What is the most common form of asthma in children?

A

Extrinsic asthma

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65
Q

Describe the process of extrinsic (atopic) asthma.

A
  1. Allergen present
  2. Mast cells release inflammatory mediators
  3. WBCs enter region and release more inflammatory mediators
  4. Histamine causes dilation of vessels (red and swollen)
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66
Q

How long does it take for inflammatory mediators from mast cells to cause an acute response in atopic (extrinsic) asthma?

A

10 – 20 minutes

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67
Q

When will the late phase response of airway inflammation occur in atopic (extrinsic) asthma?

A

4 – 8 hours

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68
Q

What does extrinsic (atopic) asthma involve?

A
  • Type 1 hypersensitivity

- Have abundant IgE

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69
Q

What airways are affected in asthma?

A

Intrathoracic airways (not the alveoli)

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70
Q

What kind of cells interacts with IgE during an extrinsic asthma attack?

A

BASOPHIL (mast cells)

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71
Q

Describe the steps involved when IgE interacts with basophils (mast cells)

A
  1. IgE on basophil membrane acts as receptors for the allergen
  2. Granules in the basophils contain histamine
  3. When allergen interacts with the IgE on the basophil cell membrane – Degranulation occurs -> histamine is released
  4. Histamine mediates inflammation in the airway wall
  5. Mucus secretion and multiplication of muscle cells
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72
Q

What are the effects after histamine is released (4)?

A
  • Glands are bigger and more numerous (result of inflammation)
  • Basement membrane is thickened
  • Smooth muscle hyperplasia (at expense of lumen)
  • More glands produce more mucus (further obstructing airway)
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73
Q

How can we treat broncho asthma (4)?

A
  1. Bronchodilators
  2. Corticosteriods
  3. Humidifying air
  4. Anti-histamine
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74
Q

What do bronchodilators do (2)?

A
  • Open lumen

- Relaxes smooth muscles of airway

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75
Q

What do corticosteroids do?

A
  • Reduce inflammation
  • Reduce mucus production
  • Reduce growth of smooth muscle
  • Increases airway conductance
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76
Q

Give an example of a bronchodilator

A

Ventolin

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77
Q

Give an example of a corticosteroid

A

Flowvent

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78
Q

What are the manifestations of asthma (3)?

A
  1. Bronchial smooth muscle constriction
  2. Mucosal edema
  3. Hypersecretion of mucus
79
Q

What are some causes of intrinsic (nonatopic) asthma (4)?

A
  1. Hypersensitivity to bacteria or viruses infecting respiratory system
  2. Exercise, hyperventilation, cold air
  3. Inhaled irritants triggering inflammation or vagal reflex
  4. Aspirin and other NSAIDs causing abnormal arachidonic acid metabolism
80
Q

Why does intrinsic (nonatopic) asthma occur frequently when a person is exercising (4)?

A
  • There is a lot of water loss (breathing out heavily)
  • Na+ remains
  • Concentration of ECF increases
  • In vulnerable people, the smooth muscle will depolarize more readily
    = Bronchospasm
81
Q

What is Ventolin similar to?

A

Epinephrine and nonepinephrine

- Sympathetic system is triggered = bronchodilation

82
Q

What do the parasympathetic neurotransmitters cause in the bronchi?

A

Bronchoconstriction!

  • Vagus nerve stimulated
  • Released AcH
  • Causes bronchoconstriction (only in thoracic cavity)
83
Q

How can aspirin result in intrinsic (nonatopic) asthma?

A

ASA decreases inflammation – but if someone has an abnormal reaction to it, it can cause bronchoconstriction

84
Q

What are the 2 chronic obstructive pulmonary disorders (COPD)?

A
  1. Emphysema

2. Chronic obstructive bronchitis

85
Q

What is emphysema?

A

COPD – enlargement of air spaces and destruction of lung tissue

  • Decreased delivery of gases down into the lower airways
  • Decreased exhalation of CO2 OUT of the system
86
Q

What is Chronic Obstructive Bronchitis?

A

COPD – obstruction of the small airways

  • Decreased delivery of gases down into the lower airways
  • Decreased exhalation of CO2 OUT of the system
87
Q

Why do alveoli enlarge in emphysema (4)?

A
  • Alveoli lose connective tissue fibers (collagen and elastin)
  • Adjacent alveoli become fused (to form 1 BIG alveoli)
  • Poor gas exchange
  • Smaller surface area for gas exchange
88
Q

What is the pathophysiology behind emphysema?

A

An imbalance of trypsin and antitrypsin activity in alveoli
(When there is inflammation, trypsin is released from neutrophils. Trypsin breaks down elastin and leads to emphysema)
- Trypsin breaks down proteins of the foreign material in the lungs

89
Q

Why does the body produce antitrypsin?

A

Antagonizes trypsin so that it does NOT digest the wall of the alveoli
Some people cannot produce ENOUGH antitrypsin
- Would lead to destruction of the alveoli

90
Q

What kind of cell inside the alveoli secretes trypsin?

A

Neutrophils

91
Q

Why is it more likely that if you’re a smoker that you’ll have emphysema?

A

Smoking reduces the ability of the cells to produce mucus (simple squamous), so more things get into the lungs. More neutrophils are needed to get rid of these foreign particles. More neutrophils releasing trypsin means that there isn’t enough antitrypsin being secreted = destruction of alveolar wall

92
Q

What are the risk factors of emphysema?

A
  1. Aging
  2. Smoking
  3. Inhalation of polluted air
  4. Genetic mutation of defective antitrypsin
93
Q

Why is it very unlikely that a child will have emphysema?

A

They haven’t lived long enough for the destruction of the walls of the alveoli

94
Q

What is radial traction?

A

Return of alveoli to normal size upon exhalation

95
Q

What happens to radial traction if there is a breakdown in elastin?

A

Radial traction decreases

96
Q

What happens to the concentration of CO2 in alveoli if there is a breakdown of elastin (3)?

A
  • There would be a retention of stale air in the alveoli
  • Increase in CO2 in alveoli –> higher CO2 in the blood
  • Excessive stimulation of CENTRAL chemoreceptors
97
Q

What happens to the muscles of ventilation if there is an increased concentration of CO2 in the alveoli (4)?

A
  • Central chemoreceptors are stimulated frequently
  • Person will breathe faster and more strongly
  • Muscles (diaphragm, external intercostals) will build up
  • Person will become BARREL CHESTED
98
Q

Why is an emphysema patient (pink puffer) usually lean?

A

They expend a lot more energy to breathe (more effort) and the muscles for breathing (are built up) and require a lot of energy

99
Q

True or False:

Emphysema patient’s (pink puffers) usually develop cyanosis

A

FALSE – they DON’T usually develop cyanosis because they are NOMOXIC (they don’t lack oxygen) – they just can’t get RID of CO2

100
Q

What are the S/S of a pink puffer (emphysema) (6)?

A
  • Increase RR to maintain oxygen levels
  • Dyspnea (increased ventilator effort)
  • Increase use of accessory muscles
  • Pursed-lip breathing
  • Unequal chest expansion
  • DRY COUGH
101
Q

Why does a pink puffer purse their lips?

A

Allows them to inhale and exhale more deeply

102
Q

What is the body positioning of a pink puffer?

A

Usually sit leaning a little forward (increases the ability for the chest to expand)

103
Q

What is the normal breadth:depth ratio of the chest? What is it in a pink puffer?

A

Normal = 2:1 (breatdth:depth)

Pink puffer = 1:2 = VERY deep chest, instead of a wide chest

104
Q

What is chronic bronchitis?

A

Chronic irritation of the airways

- Patients will WHEEZE

105
Q

What does chronic irritation of the airways cause (4)?

A
  1. Increased number of mucus cells
  2. Mucus hypersecretion
  3. Inflammatory infiltration of bronchiolar wall
  4. Fibrosis of bronchiolar wall (scarring)
106
Q

What is chronic bronchitis characterized by (2)?

A
  1. PRODUCTIVE cough

2. Cough over 3 consecutive months for 2 consecutive years

107
Q

What are the S/S of a blue bloater (chronic bronchitis) (6)?

A
  • Excessive airway secretions
  • Cannot increase RR enough to maintain oxygen levels
  • CYANOSIS
  • Polycythemia
  • Cor pulmonale
  • Obesity
108
Q

Why are blue bloaters (chronic bronchitis) typically obese?

A
  • Because of respiratory distress, they are not physically active
  • Because of hypoxia, they have less oxygen to facilitate burning of energy
109
Q

Why do blue bloaters experience polycythemia?

A
  • Kidneys sense reduced oxygen in the blood and release EPO
  • EPO increases the # of RBCs in circulation
  • If they have TOO many RBCs, the heart has to work harder to push the thick blood
110
Q

What is cor pulmonae and why is it seen in blue bloaters (chronic bronchitis)?

A
  • Increase in polycythemia = thick blood
  • COR PULMONALE is the difficulty in pushing thick blood through the lungs (heart failure arising from lung failure)
  • Patient might experience RIGHT sided heart failure because the heart is not strong enough to push the thick blood through the small capillaries in the lungs
111
Q

What are 4 clinical features of emphysema (pink puffers)?

A
  • Progressive loss of lung tissue
  • Weight LOSS
  • Mild hypoxemia, no hypercarbia
  • Few secretions
112
Q

What are 6 clinical features of chronic bronchitis (blue bloater)?

A
  • Chronic airway inflammation
  • Obese
  • Hypoxemia and hypercarbia
  • Increased hematocrit
  • Cor pulmonale
  • Lots of secretions
113
Q

What triggers central chemoreceptors to increase RR?

A

HIGH CO2 levels

114
Q

What triggers peripheral chemoreceptors to increase RR?

A

LOW O2 levels

115
Q

What is bronchiectasis?

A

Infection and inflammation that destroy smooth muscle in airways, causing permanent damage
Classified under COPD
- Could be congenital or result from a tumor or infection

116
Q

What are the clinical features of bronchiectasis (6)?

A
  • Cough
  • Purulent sputum
  • Hemoptysis
  • Chronic sinusitis
  • Clubbing of fingers
  • Coarse crackles
117
Q

What is hemoptysis?

A

Bloody saliva

118
Q

What is cystic fibrosis caused by?

A

A recessive disorder in chloride transport proteins

- Cystic fibrosis transport regulator (CFTR)

119
Q

What is the average life expectancy of a patient with cystic fibrosis? What is the typical maximum age of life?

A
  • Most people don’t live to be 40 years old

- Life expectancy is 28 years old

120
Q

Explain the pathophysiology behind cystic fibrosis.

A
  • High concentrations of NaCl in the sweat
  • Less Na+ and water in respiratory mucus and in pancreatic secretions
  • Results in thick, sticky mucus
  • Patient gets airway obstructions and respiratory infections (recurrent)
  • Could lead to obstruction of pancreatic and biliary ducts
121
Q

Explain the relationship between the watery fluid and CFTR in cystic fibrosis

A
  • Epithelial cells in bronchi tree secrete mucus (traps foreign particles)
  • Watery fluid covers surface of epithelial cells to prevent mucus from sticking
  • Fluid is rich in chloride (Na+ follows, and water follows Na+)
  • If there is not enough CFTR (transport proteins), then not able to transport enough chloride
  • Watery fluid becomes sticky –> mucus is even stickier
    Bacteria will feed on the mucus, individuals get a LOT of respiratory infections
122
Q

If a person has cystic fibrosis, what other areas of the body are affected (instead of the lungs) (3)?

A
  • Pancreas (Pancreatic duct blockage)
  • GI tract (GI infections)
  • Sweat glands
123
Q

What is the management for patients with cystic fibrosis (4)?

A
  • Patient lies on their belly, back is tapped to release some of the mucus
  • Anti-biotics
  • Early and good management increase life expectancy
  • Gene therapy – insert correct gene
124
Q

How is the GI system affected if a person has cystic fibrosis (4)?

A
  1. Pancreatic duct may become blocked
  2. Not able to secrete digestive enzymes into the GI tract
  3. Ineffective digestion/absorption of nutrients
  4. Pancreatic enzymes digest the PANCREAS!
125
Q

What 4 things do restrictive pulmonary disorders include?

A
  1. Chest wall (stiffness and deformity)
  2. Pleural (inflammation or space-occupying processes)
  3. Parenchymal (fibrosis, atelectasis)
  4. Acute respiratory distress syndrome (ARDS)
126
Q

In restrictive pulmonary disorders, __________ is usually normal

A

FEV1

127
Q

What is a parenchymal disorder?

A

Something is wrong with the alveoli themselves

128
Q

What is ARDS (acute respiratory distress syndrome) triggered by?

A

Injury to the respiratory membrane

- Inflammation follows leading to changes to the respiratory membrane

129
Q

What does ARDS result in?

A

Reduced diffusion of gases across the respiratory epithelium

130
Q

What is meconium and how does it affect newborn breathing?

A

Fetal feces
- If there is hypoxia in the uterus the fetus will produce a lot of fecal matter (into the amniotic fluid)
- Going to cause injury to the membranes of the fetal lungs
= Infant respiratory distress syndrome

131
Q

How is adult respiratory distress syndrome different than fetal?

A

Happens when adults are working in an industry with a lot of particles in the air (dust, glass)

  • Causes injury to the membranes of the lungs
  • Thickens alveolar membrane, results in less diffusion
132
Q

What are the characteristics of ARDS (3)?

A
  • Injury to respiratory membrane leads to fibrosis
  • Pulmonary capillaries become leaky (leads to pulmonary edema)
  • Surfactant synthesis decreases (leads to atelectasis)
133
Q

What are the clinical results of ARDs (3)?

A
  1. Higher WOB
  2. Shunting of blood
  3. Hypoxemia
134
Q

What gets inflamed with pneumonia (2)?

A
  1. Alveoli

2. Bronchioles

135
Q

What are the two major forms of pneumonia?

A
  1. Typical

2. Atypical

136
Q

Describe typical (alveolar) pneumonia

A
  • Usually resulting from bacteria in the alveoli

- Fluid collects in the alveoli

137
Q

Describe atypical (interstitial) pneumonia

A
  • Occurs as a result of viral or mycoplasma infections

- Alveolar septum or interstitium thickens

138
Q

What makes up the thickness of the alveolar membrane? How thick is it?

A
  1. Thin film of fluid
  2. Type 1 cells (alveolar membrane)
  3. Basement membrane
  4. Endothelial cells of the capillaries
    - Approx. 0.5 micrometers in thickness
139
Q

During pneumonia, what happens to the thickness of the membrane and the diffusion ability of the gases?

A 
Membrane = thickens
Diffusion = decreases
140
Q

Describe how atypical pneumonia is different from typical pneumonia

A
  • NO fluid in the alveoli
  • Caused by viruses and mycoplasma (smallest type of bacteria, no cell wall)
  • Agents affect the basement membrane
  • Inflammation causes the basement membrane to thicken
  • Harder for gases to diffuse
141
Q

What 4 things can cause pneumonia?

A
  1. Bacteria
  2. Viruses
  3. Fungi
  4. Bacteria-like organisms
142
Q

True or False:

WBCs are found in the lumen of typical (alveolar) pneumonia

A

TRUE!

143
Q

True or False:

RBCs do not escape into the lumen in typical pneumonia

A

False!

RBCs DO escape into the lumen of the alveolus in typical pneumonia

144
Q

What happens to the secretions of typical pneumonia if RBCs escape into the lumen of the alveolus?

A

Sputum will be tinged red

145
Q

In atypical pneumonia where are WBCs found?

A

Alveolar septum

146
Q

Why is fibrinous exudate formed in atypical pneumonia?

A

From damage being done to septum

  • fibrin is a by-product of bleeding
  • this coats the alveolar membrane increasing it’s thickness
147
Q

What are the manifestations of pneumonia (3)?

A
  1. Lobar
  2. Bronchopneumonia
  3. Interstitial
148
Q

What is affected in lobar pneumonia?

A

Affects an entire lobe of the lung

149
Q

What is the distribution pattern in bronchopneumonia?

A

Patchy distribution over more than one lobe

150
Q

What thickens in interstitial pneumonia?

A

Alveolar septum or interstitium thickens

151
Q

What are the manifestations of bronchopneumonia?

A
  • decreases overall function of the alveoli of the lungs
  • SOB
  • not ALL of the alveoli are affected
152
Q

How many lobes does the right lung have? Left lung?

A

Right lobe = 3 lobes

Left lobe = 2 lobes

153
Q

During lobar pneumonia, which lobe is usually affected the most?

A

INFERIOR LOBE of RIGHT lung

154
Q

Why is the inferior lobe of the right lung most often affected in lobar pneumonia?

A

Right bronchi is STEEPER than the left one

- objects (infectious agents) are more likely to fall into right lobe more easily

155
Q

What does it mean for a lung to get consolidated?

A

It gets sticky

  • alveoli are not able to receive much air
  • then alveoli don’t receive much blood
  • Patient’s feel SOB because of no gas exchange
156
Q

True or False:

In lobar pneumonia, the whole bunch (group) of alveoli are affected

A

True

- the whole bunch will solidify or consolidate

157
Q

What is affected in interstitial pneumonia?

A

Alveoli septum

- entire lung is affected

158
Q

Why do patient’s experience SOB and WOB in interstitial pneumonia?

A

Alveolar walls are thicker - gas exchange is impaired

- alveoli are CLEAR (not fluid filled)

159
Q

Describe the pathogenesis of typical pneumonia

A
  1. Infection
    2, Inflammation
  2. Serous exudate
  3. Congestion; productive cough
160
Q

What are the S/S of pneumonia?

A
  • fever, chills, malaise, prostration
  • cough
  • SOB (dyspnea)
  • rapid breathing (tachypnea)
161
Q

What is prostration?

A

Extreme exhaustion

162
Q

What is empyema?

A

Collection of pus in a cavity of the body

example: lungs!

163
Q

What are the 6 complications of pneumonia?

A
  1. Pleural fibrosis
  2. Empyema
  3. Abscesses
  4. Bronchiectasis
  5. Interstitial fibrosis
  6. Cysts
164
Q

What is a long term complication of inflammation in the lungs?

A

Fibrosis

  • can spread into pleural membranes (makes them fuse together)
  • HARD to breathe
165
Q

What are abscesses in the lungs?

A

Large areas of inflammatory tissue

- can become a restrictive lung disease

166
Q

What is parenchyma?

A

The functional tissue of an organ

167
Q

Is bronchiectasis a restrictive or obstructive lung disease?

A

Obstructive

  • bronchioles get eaten away, they can collapse
  • alveoli that serve these bronchioles will lack oxygen
168
Q

What happens to the alveolar membrane in interstitial fibrosis?

A

Increase in thickness

169
Q

Why do cysts occur in the lungs?

A

Inflammation has destroyed tissue and is replaced by fluid

- those areas are not available for gas exchange

170
Q

What are the systemic effects of pneumonia?

A
  • affects appetite
  • temperature regulation
  • muscles get broken down b/c of all of the cytokines
171
Q

What is the world’s foremost cause of death from a single infectious agent (besides HIV)?

A

Tuberculosis

172
Q

What is tuberculosis caused by?

A

Mycobacterium tuberculosis hominis

173
Q

What communities in BC have big problems with TB?

A

First nations communities

174
Q

What are the characteristics of the agent of TB that make it hard to fight (3)?

A
  1. Protective waxy capsule
  2. Can stay alive in “suspended animation” for years
  3. Drug-resistant forms have developed
175
Q

What are the steps in an initial TB infection?

A
  1. TB bacteria inhaled
  2. Bacteria are ingested by macrophages in lungs
  3. Macrophages present them to T cells
    4a. Activated T cells kill bacteria
    4b. Activated T cells stimulate macrophages to kill bacteria more efficiently
176
Q

How long does it take to develop a (+) TB test after the initial infection?

A

3 - 6 weeks

- detectable IN BLOOD

177
Q

What is formed after the initial TB infection?

A

Granulomatous lesion (Ghon Focus)

178
Q

What does a Ghon Focus contain (3)?

A
  1. Macrophages
  2. T cells
  3. Inactive TB bacteria
179
Q

If a patient has a Ghon Focus in their lung, are they contagious?

A

Not necessarily

- if the patient does not have any ACTIVE TB, then they are NOT contagious

180
Q

When is it possible for a Ghon focus to resolve?

A

If the patient is a child and the child fights off the infection
- adults cannot fight it off

181
Q

What is sometime deposited into the Ghon focus that would make it easy to see on an x-ray?

A

Calcium deposits

- surrounded by fibrous capsule

182
Q

What are the 3 stages of TB?

A
  1. Primary TB
  2. Miliary TB
  3. Secondary TB
183
Q

When is Primary TB seen in patients?

A

When they have not been previously exposed

- seen in infants and children under the age of 5 (most often)

184
Q

When is Miliary TB seen in patients?

A

Rarely

- in primary and post-primary TB in individuals with compromised immune systems

185
Q

What happens during secondary TB?

A

Lung is getting destroyed

- other organs are destroyed too (they travel throughout the body)

186
Q

What two things can happen after a primary TB infection?

A
  1. Bacteria are isolated in Ghon foci (inactive and not contagious)
  2. If immune response is inadequate, bacteria multiply in the lungs (leads to progressive primary TB)
187
Q

What do Miliary TB lesions look like in the body?

A

Like grains of millet in the tissues (stuff you feed budgies)

188
Q

How does Miliary TB affect other body tissues?

A

Bacteria may erode blood vessels and spread throughout the body

189
Q

What stage of TB is the stage of active infection?

A

Secondary TB

190
Q

Why may a secondary TB infection occur?

A

Follows reinfection of previously healed primary lesions

191
Q

Signs of _____ accompany secondary TB.

A

Chronic pneumonia

192
Q

What are the clinical manifestations of secondary TB?

A
  • productive cough (with purulent sputum - often bloody)
  • anorexia
  • malaise
  • fatigue
  • weight loss
  • fever and night sweats
193
Q

What is main cause behind the clinical manifestations of secondary TB?

A

Release of cytokines

BHSC 2203 - Patho (13 decks)

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