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PATH30001 - Mechanisms of Disease > Lecture 5 - Pneumonia and ARDS > Flashcards

Lecture 5 - Pneumonia and ARDS Flashcards

1
Q

Describe the structure of the lung

A

Trachea
Bronchi
Bronchioles
Alveoli

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2
Q

Describe the defences in the lung

A 
• Cilia covered with mucous
beating mucous upwards
 • Alveolar macrophages
 • Neutrophils
 • Complement
 • Draining lymph nodes
 • IgA
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3
Q

Describe the presence of microorganisms in the respiratory tract

A

Lower lung: normally sterile

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4
Q

Where do infections most commonly occur in the respiratory tract?
What about the more dangerous lung infections?

A

Normally: bronchioles (bronchitis)
Serious: alveoli

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5
Q

Why is infection of the alveoli so dangerous?

A

Threatens oxygen exchange between air and blood

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6
Q

Which cells produce mucous?

Where are they?

A

Goblet cells

Interspersed in the epithelium of the respiratory tract

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7
Q

What are the cell types in the alveoli?

A

Type I pneumocytes
Type II alveolar cells
Alveolar macrophages
White blood cells (in interstitium)

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8
Q

What are Type I pneumocytes?

A

Elongated cell that forms the structure of the alveoli and the exchange epithelium

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9
Q

What are Type II alveolar cells?

A

Normally: Produce surfactant

Under pathological conditions: divide into new type I cells as a replacement

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10
Q

Where is surfactant found?

A

It is the physical lining of the type I alveolar cells

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11
Q

What is the role of alveolar macrophages?

A

Low numbers normally

Increase in the inflammatory response

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12
Q

What are the outcomes of pneumonia?

A

Recovery
Chronic inflammation
Death

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13
Q

What is pneumonia?

A

Acute inflammation of the alveoli and bronchioles

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14
Q

What are the general causes of pneumonia?

A
  1. Infectious
    • Bacterial
    • Viral
    • Fungal
  2. Non infectious
    • Chemical pneumonia (ARDS)
    • Aspiration pneumonia
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15
Q

What is chemical pneumonia normally called?

A

ARDS

Acute respiratory distress syndrome

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16
Q

What is inhalation / aspiration pneumonia?

A

Gastric, acidic contents of stomach breathed into the lung

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17
Q

Which people are most susceptible to pneumonia?

A
  • Immunocompromised people

* The elderly

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18
Q

Describe how defences are compromised, leading to pneumonia

A
  • Cilia immobilised due to smoking, loss of consciousness in acute alcohol consumption etc.
  • loss of cough reflex
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19
Q

Which people commonly die from pneumonia?

A 
People with other primary diseases, such as:
 • chronic alcoholism
 • AIDS
 • transplant immunosuppression
 • cystic fibrosis
 • cancer
 • burns
 • diabetes
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20
Q

Which are some infectious agents that cause pneumonia?

A
  • S. pneumoniae
  • Staphylococcus aureus
  • H. influenza
  • P. aeruginosa
  • Candida
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21
Q

Why is pneumonia important?

A

N° 1 killer of children worldwide

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22
Q

What are the different types of pneumonia, in terms of acquisition?

A

Community-acquired
• acute
• atypical
Nosocomial pneumonia

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23
Q

Compare symptoms of community-acquired acute and atypical pneumonia.

A

Acute: large volume of inflammatory exudate
Atypical: smaller amounts of exudate

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24
Q

What are the causes of nosocomial pneumonia?

A

Aquired in a health care setting, due to
• underlying chronic disease
• invasive procedures
• immunosuppresion

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25
Q

Which type of pneumonia is ‘necrotising’?

A

Aspiration pneumonia

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26
Q

How does pneumonia present?

A
  1. Lobar
    • large areas of the lung affected
  2. Focal
    • small areas
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27
Q

How long does acute pneumonia last?

A

Around a week

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28
Q

Why does acute inflammation occur in acute pneumonia?

A

To dilute and destroy agent of injury

29
Q

What are the main differences between acute and chronic inflammation?

A 
Chronic:
 • longer lasting
 • more variable and complex
 • necrosis
 • fibrosis
(vicious cycle)
30
Q

What are the components of acute inflammation in pneumonia?

A
  • neutrophil infiltration
  • monocytes
  • complement
  • macrophages
31
Q

Which cells are producing chemokines in acute inflammation?

What is the result of this?

A

Neutrophils

Recruitment of many other inflammatory cells

32
Q

Which cells immediately increase in number during inflammation?

A
  • neutrophils

* macrophages

33
Q

What changes occur to the vasculature in acute inflammation?

A
  • Increased permeability

* Vasodilation

34
Q

What is the result of increased vascular permeability?

A

Tissue oedema

35
Q

Compare focal and lobar pneumonia

A

Lobar: whole lobe of lung is affected uniformly
Focal: small areas affected

Affected = fluid filled

36
Q

What is the name for pus build up in pneumonia?

A

Supparative response

37
Q

Compare the appearance of the different types of pneumonia on a chest X-Ray

A
  • lobar

* bronchopneumonia

38
Q

Describe the time scale of acute pneumonia

A

1-2 days: lung heavy (blood, oedema)
2-4 days: Red hepatisation
4-8 days: Grey hepatisation
8 days onwards: Resolution

39
Q

Compare and contrast red and grey hepatisation

A

Red:
• lung red, due to erythrocytes
• lung heavy
• full of liquid & fibrin

Grey: 
 • lung grey-white
 • lung solid & heavy
 • more fibrin
 • more neutrophils
 • blood has disappeared
40
Q

What is the function of regions of oedema in the lung?

A

Non-functional

41
Q

What is stasis and congestion in the lung?

When does this happen?

A

Lung full of fluid, blood and proteins

Can not function normally

Happens around 2-4 days

42
Q

What happens in resolution of acute pneumonia?

A

Fluid reabsorbed back into alveolar epithelium and cells migrate away

43
Q

What are pores of Kohn?

A

Openings connecting alveoli together

44
Q

What are complications of lobar pneumonia?

A
  • necrosis
  • pleurisy
  • bactaraemic dissemination
45
Q

What is pleurisy?

A

Infection and inflammation of pleural cavity

46
Q

Which organs are affected in bactaraemic dissemination?

A

Endocarditis
Pericarditis
Meningitis
Nephritis

47
Q

What are the symptoms of lobar pneumonia?

A
  • malaise
  • fever
  • child
  • productive cough
  • ARDS
48
Q

What are the symptoms of ARDS?

A
  • Increased work of breathing
  • Severe hyperaemia
  • Decreased CO2 excretion
49
Q

What is the major treatment of pneumonia?

A

Antibiotics

* must be appropriate for infectious agent *

50
Q

Compare histology of acute and chronic inflammation

A

Chronic:
• Cuboid, thickened of type I alveolar cells
• Macrophages and lymphocytes

Acute:
• Blood
• Neutrophils

51
Q

What is the effect of the thick, cuboid type I alveolar cells in chronic inflammation?

A

Very poor oxygen exchange across epithelium

52
Q

What is the difference between pneumonia and ARDS?

A

ARDS:
• modern definition of acute lung injury
• high mortality rate
• severe damage to alveoli themselves, as well as surfactant
• a result of a myriad of diseases, as well as direct lung injury
• acute onset of respiratory failure
• bilateral infiltrate on Chest X ray

53
Q

What is the mortality rate of ARDS?

A

Around 40% mortality rate

54
Q

What are some causes of ARDS?

A
  • Gastric aspiration
  • Near drowning
  • Oxygen toxicity from Scuba diving
  • Gas inhalation
55
Q

What are some differences of the inflammatory response in ARDS, compared to pneumonia?

A

In ARDS:
• NECROSIS
• Lots of cellular debris due to necrosis of type I alveolar cells
• Complete denudation of the alveoli (no living cells)
• Loss of surfactant
• Formation of hyaline membrane

56
Q

What are the phases of ARDS?

A
  1. Exudative

2. Organising

57
Q

Describe the exudative phase of ARDS

A
  • very rapid oedema
  • degenerative changes to type I alveolar cells, then sloughing
  • formation of hyaline membrane
  • inflammatory infiltrate
  • (+/- thrombi)
58
Q

Describe formation of hyaline membrane

A

This occurs in ARDS
• Lots of proteins laid down
• Starts after about 2 days

59
Q

Describe the organising phase of ARDS

A

Recovery attempt of alveoli

Often leads to fibrosis

60
Q

Describe resolution of ARDS

A

Resorption of exudate

• Na/K ATPase, aquaporins resetting the osmotic balance

61
Q

What are the possible outcomes of ARDS?

A
  • Death
  • Resolution
  • End stage fibrosis
62
Q

What is end stage fibrosis?

A

‘Honeycomb lung’

• tissue

63
Q

What are some treatments of ARDS?

A
  • Mechanical ventilation (most effective)
  • Inhalation of NO
  • Anti-inflammatory drugs

Future:
• mesenchymal stem cells

64
Q

What is the effect of NO?

A

Vasodilation, increased gas exchange

65
Q

What is one of the most important anti-inflammatory drugs?

A

Glucocorticoids

66
Q

Describe the effect of mesenchymal stem cells

A 
• Increased IL-10 (suppressive cytokine)
 • decreased inflammatory cytokines
Leads to:
 • structural recovery
 • reduced pulmonary oedema
67
Q

Rapid inflammatory response in the lungs?

A

ARDS

not pneumonia

68
Q

Which cells produce surfactant?

A

Type II alveolar cells

69
Q

Which pathogens often lead to atypical pneumonia?

A
  • Mycoplasms

* Influenza virus

PATH30001 - Mechanisms of Disease (34 decks)

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