Lecture 5 - Pneumonia and ARDS Flashcards Preview

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

Flashcards in Lecture 5 - Pneumonia and ARDS Deck (69):
1

Describe the structure of the lung

Trachea
Bronchi
Bronchioles
Alveoli

2

Describe the defences in the lung

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

3

Describe the presence of microorganisms in the respiratory tract

Lower lung: normally sterile

4

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

Normally: bronchioles (bronchitis)
Serious: alveoli

5

Why is infection of the alveoli so dangerous?

Threatens oxygen exchange between air and blood

6

Which cells produce mucous?
Where are they?

Goblet cells
Interspersed in the epithelium of the respiratory tract

7

What are the cell types in the alveoli?

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

8

What are Type I pneumocytes?

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

9

What are Type II alveolar cells?

Normally: Produce surfactant

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

10

Where is surfactant found?

It is the physical lining of the type I alveolar cells

11

What is the role of alveolar macrophages?

Low numbers normally
Increase in the inflammatory response

12

What are the outcomes of pneumonia?

Recovery
Chronic inflammation
Death

13

What is pneumonia?

Acute inflammation of the alveoli and bronchioles

14

What are the general causes of pneumonia?

1. Infectious
• Bacterial
• Viral
• Fungal

2. Non infectious
• Chemical pneumonia (ARDS)
• Aspiration pneumonia

15

What is chemical pneumonia normally called?

ARDS
Acute respiratory distress syndrome

16

What is inhalation / aspiration pneumonia?

Gastric, acidic contents of stomach breathed into the lung

17

Which people are most susceptible to pneumonia?

• Immunocompromised people
• The elderly

18

Describe how defences are compromised, leading to pneumonia

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

19

Which people commonly die from pneumonia?

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

20

Which are some infectious agents that cause pneumonia?

• S. pneumoniae
• Staphylococcus aureus
• H. influenza
• P. aeruginosa
• Candida

21

Why is pneumonia important?

N° 1 killer of children worldwide

22

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

Community-acquired
• acute
• atypical
Nosocomial pneumonia

23

Compare symptoms of community-acquired acute and atypical pneumonia.

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

24

What are the causes of nosocomial pneumonia?

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

25

Which type of pneumonia is 'necrotising'?

Aspiration pneumonia

26

How does pneumonia present?

1. Lobar
• large areas of the lung affected

2. Focal
• small areas

27

How long does acute pneumonia last?

Around a week

28

Why does acute inflammation occur in acute pneumonia?

To dilute and destroy agent of injury

29

What are the main differences between acute and chronic inflammation?

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

30

What are the components of acute inflammation in pneumonia?

• neutrophil infiltration
• monocytes
• complement
• macrophages

31

Which cells are producing chemokines in acute inflammation?
What is the result of this?

Neutrophils
Recruitment of many other inflammatory cells

32

Which cells immediately increase in number during inflammation?

• neutrophils
• macrophages

33

What changes occur to the vasculature in acute inflammation?

• Increased permeability
• Vasodilation

34

What is the result of increased vascular permeability?

Tissue oedema

35

Compare focal and lobar pneumonia

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

Affected = fluid filled

36

What is the name for pus build up in pneumonia?

Supparative response

37

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

• lobar
• bronchopneumonia

38

Describe the time scale of acute pneumonia

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

39

Compare and contrast red and grey hepatisation

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

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

Non-functional

41

What is stasis and congestion in the lung?
When does this happen?

Lung full of fluid, blood and proteins

Can not function normally

Happens around 2-4 days

42

What happens in resolution of acute pneumonia?

Fluid reabsorbed back into alveolar epithelium and cells migrate away

43

What are pores of Kohn?

Openings connecting alveoli together

44

What are complications of lobar pneumonia?

• necrosis
• pleurisy
• bactaraemic dissemination

45

What is pleurisy?

Infection and inflammation of pleural cavity

46

Which organs are affected in bactaraemic dissemination?

Endocarditis
Pericarditis
Meningitis
Nephritis

47

What are the symptoms of lobar pneumonia?

• malaise
• fever
• child
• productive cough
• ARDS

48

What are the symptoms of ARDS?

• Increased work of breathing
• Severe hyperaemia
• Decreased CO2 excretion

49

What is the major treatment of pneumonia?

Antibiotics
* must be appropriate for infectious agent *

50

Compare histology of acute and chronic inflammation

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

Acute:
• Blood
• Neutrophils

51

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

Very poor oxygen exchange across epithelium

52

What is the difference between pneumonia and ARDS?

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

What is the mortality rate of ARDS?

Around 40% mortality rate

54

What are some causes of ARDS?

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

55

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

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

What are the phases of ARDS?

1. Exudative
2. Organising

57

Describe the exudative phase of ARDS

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

58

Describe formation of hyaline membrane

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

59

Describe the organising phase of ARDS

Recovery attempt of alveoli
Often leads to fibrosis

60

Describe resolution of ARDS

Resorption of exudate
• Na/K ATPase, aquaporins resetting the osmotic balance

61

What are the possible outcomes of ARDS?

• Death
• Resolution
• End stage fibrosis

62

What is end stage fibrosis?

'Honeycomb lung'
• tissue

63

What are some treatments of ARDS?

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

Future:
• mesenchymal stem cells

64

What is the effect of NO?

Vasodilation, increased gas exchange

65

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

Glucocorticoids

66

Describe the effect of mesenchymal stem cells

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

67

Rapid inflammatory response in the lungs?

ARDS
(not pneumonia)

68

Which cells produce surfactant?

Type II alveolar cells

69

Which pathogens often lead to atypical pneumonia?

• Mycoplasms
• Influenza virus