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PATH201 lectures > lecture 12 - pulmonary infections > Flashcards

lecture 12 - pulmonary infections Flashcards

1
Q

What are the mechanisms of evading pulmonary defences

A

Attachment to and entry into epithelial cells in LRT
Release of toxins - enhance infection by impairing ciliary activity
Resistance to killing phagocytosis

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2
Q

Define URTI

A

Upper Respiratory Tract Infection
- sore throat, tonsillitis, pharyngitis, laryngitis, sinusitis and common cold
- mostly caused by viruses

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3
Q

Define LRTI

A

Lower Respiratory Tract Infections
- Infection of lung tissue -> pneumonia or TB
Mostly caused by bacteria some virus

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4
Q

Describe the etiology of pneumonia

A

Infection of lung tissue
- compromised immune system
- compromised local defences (loss or suppression of cough reflex, ciliary impairment, thick mucus obstruction, interference with phagocytes (macrophages), pulmonary congestion and edema, preceding URTI

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5
Q

Describe lobar pneumonia

A

Entire lung lobe affected

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6
Q

Describe bronchopneumonia

A

Infection in bronchi and bronchioles - spreads to adjacent lung tissue in patchy manner - no necessarily confined to one lobe or lung

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7
Q

Describe classification by etiological agent

A
  • Determines treatment
  • Can’t always be identified
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8
Q

Describe classification by clinical setting

A
  • Narrows down suspected organisms
    (CA, HA, Aspiration pneumonia, immunocompromised hosts)
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9
Q

Describe Community Acquired (CA) pneumonia

A

Bacterial or viral - follows URTI (viral) - lobar or broncho
- Streptococcus pneumoniae most common (90-95% cases)
- haemophilus influenza, staph aureus, mycoplasma pneumoniae

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10
Q

What are the stages of lobar pneumonia

A
  • Congestion (day 1)
  • Red hepatization (days 2-4)
  • Grey hepatization (days 5-8)
  • resolution
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11
Q

Describe the congestion stage

A

Dilated and congested capillaries in alveolar walls
Proteinaceous, fibrin rich fluid in alveolar spaces(increased permeability)

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12
Q

Describe the red hepatization stage

A

Fibrous exude, neutrophils and RBC in alveolar spaces (solid alveoli)
Capillaries still congested

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13
Q

Describe the grey hepatization stage

A

Fibrinous exudate has macrophages and few neutrophils
- Macrophages contain hemosiderin (brown haemoglobin derived pigment from phagocytosis of extravasated RBC)
Alveolar wall congestion subsided

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14
Q

Describe the resolution stage

A

Enzymatic digestion of exudate occurs - expectoration and phagocytosis (macrophages)

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15
Q

What ae the complication of bacterial pneumonia

A

In elderly and already ill
- pleural effusion
- empyema (puss build up)
- lung abscess (necrotic core)
- Respiratory and circulatory failure (ARDS)

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16
Q

What is Acute Respiratory Distress Syndrome (ARDS)

A

Rapid wide spread inflammation in lungs
- injury of pneumocytes and pulmonary endothelial cell activation -> increased capillary permeability and fibrin-rich fluid fills alveoli
- 40% mortality rate - decreased quality of life common

17
Q

Describe Community Acquired (CA) viral pneumonia

A
  • Usually cause URTI but may spread to LRT
  • ‘atypical pneumonia’ (viruses) - inflammatory exude in alveoli walls rather than spaces and predominantly mononuclear cells instead of neutrophils (some bacteria may cause)
18
Q

What are the predisposing factors of CA pneumonia

A

Extremes of age, malnutrition, chronic diseases

19
Q

Describe Tuberculosis

A

Caused by Mycobacterium tuberculosis
- transmits through prolonged contact (cough, sneeze etc.) - latent or extrapulmonary TB can’t be transmitted

20
Q

Describe Mycobacterium tuberculosis

A
  • Aerobic bacillus (fast-acid - resists gram stain)
  • Lipid capsule
  • Visualised in Ziehl-Neelsen stain (pink)
  • Better detected by PCR
21
Q

Describe TB response 3 weeks after infection

A

T-cell mediated response
- Enter hilar (draining) lymph nodes - presented to APC and T cells differentiate into TH1 cells
- Produce IFN- gamma - activates macrophages and enhances bactericidal power
- Macrophages (‘epithelioid cells’)secrete TNF -> further monocyte and macrophage recruitment - aggregate to form TB granulomas
- Granulomas develop central caseous necrosis - tissue damage as result of immune response and cytokine release

22
Q

Describe the TB granuloma

A
  • Specific type of chronic inflammation (can be formed in reaction to foreign body)
  • Persistent activation of T cell-mediated response by difficult to irradiate organism
23
Q

What makes up a TB granuloma

A

Healing attempted around granuloma (fibrosis)
‘Collar’ of activated T lymphocytes
Activated macrophages (epithelioid cells)
Giant cells (fusion of multiple macrophages)
Necrosis - caseous necrosis

24
Q

Describe primary infection of TB

A

Ghon focus - develops granulomas and caseating necrosis (TH1 response)
- Deep in midzone of lung
Hilar lymph nodes involved in initial infection also develop granulomas and caseation
Together Ghon complex

25
Q

What are the 3 outcomes of primary TB infection

A
  • Acquired immunity (90%) - TH1 response halts infection -> killing of organism and Ghon complex heals by fibrosis (calcified detection on X-ray)
  • Latent TB - remain dormant waiting to reactivate when host immunity drops
  • Progressive primary TB - infection progresses and ongoing immune response -> extensive caseation necrosis and lung tissue damage (mostly immunosuppressed/elderly)
26
Q

What is secondary TB (chronic)

A

Reactivation or re-exposure to bacilli in previously sensitized host -> rapid mobilization of vigorous immune reaction
-> large granulomas with extensive tissue damage - massive central caseous necrosis surrounded by fibrosis

27
Q

Where are secondary lesions usually

A

Apical parts of lungs - oxygen tension is highest (aerobic bacteria)

28
Q

Why is secondary TB also called ‘cavitary’

A

extensive tissue destruction can destroy adjacent bronchial walls -> coughing up of bacteria-laden caseous material, leaving empty cavities in lungs
- ‘open’ lesions are infectious

29
Q

Describe the diagnosis of active TB

A
  • identifying M. tuberculosis in clinical sample (definitive)
  • Clinical findings (cough, sputum, fever etc.)
  • Chest X-ray (Indicative)
  • Mantoux test (TST) or Interferon-Gamma Release Assay (IGRA)
30
Q

Does the TST differentiated between latent and active

A

No - active diagnosed through presence of symptoms

31
Q

Describe false negative/positive TST results

A

False-negative - viral infections, malnutrition or immunosuppression
False-positive - prior BCG vaccination

32
Q

Go over IGRA

A
  • blood test
  • measures immune reactivity (TH1 cells) - produce interferon-gamma
  • should remain positive after successful treatment
    less likely to give false-positive
33
Q

What is the treatment of TB

A
  • multiple-drug therapy
  • 2 phase for active
    • intensive - bactericidal (4 drugs for 2 months)
    • Confirmation - sterilization (2 drugs for 4 months)
  • latent - one over 9 months (under 40)
  • Second-line antibiotics available for multi-drug resistant TB

PATH201 lectures (15 decks)

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