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Pathology > Inflammatory Lung Disease > Flashcards

Inflammatory Lung Disease Flashcards

1
Q

Type 1 pneumocytes

A
  • Cover 95% of alveolar surface

- Act like endothelial cells

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2
Q

Type 2 pneumocytes

A
  • Synthesise surfactant

- Involved in repair of alveolar epithelium through ability to give rise to type 1 cell

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3
Q

Alveolar constituents

A
  • Type 1 & 2 pneumocytes
  • Resident macrophages
  • Capillaries
  • Rare monocytes, other WBCs
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4
Q

Pnemonias

A

Respiratory disorders involving acute inflammation of the lung structures, such as the alveoli and bronchioles, classified as infectious or non infectious

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5
Q

Infectious pneumonia, causative agents

A
  • Bacterial (most commonly)
  • Viral
  • Fungal
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6
Q

Non-infectious pneumonia causative agents

A
  • Chemical pneumonia (ingestion/inhalation of irritating substances
  • Inhalation pneumonia (also called aspiration pneumonia)
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7
Q

Pneumonia risk factors

A
  • Immuno compromised patients
  • Alcoholics
  • Transplant immunosuppression
  • Pregnancy
  • Cystic fibrosis
  • Autoimmune disease
  • Burns
  • Cancer
  • Chemo
  • Old or young age
  • Chronic steroids
  • Diabetes
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8
Q

Innate lung defences

A
  • Mucus blanket (cilia and cough reflex)
  • Phagocytosis-alveolar macrophages or recruited neutrophils
  • Complement- C3b, MAC
  • Draining lymph nodes- initiation of immune response
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9
Q

Acquired lunge defences

A
  • Secreted IgA in alveoli
  • IgM and IgG in alveolar fluid- activate complement and opsonise
  • Accumulation of T-cells- viral infection
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10
Q

Causes of impaired lung function

A
  • Loss/suppression of cough reflex from coma, anaesthesia, neuromuscular disorders, drugs, chest pain- can lead to aspiration of gastric contents
  • Injury to muco-ciliary apparatus- smoke, viral infection, inhalation of hot/corrosive gases, genetic abnormalities
  • Interference with phagocytic/antibacterial action of alveolar macrophages- alcohol, smoke, anoxia, O2 intoxication, genetic abnormality
  • Accumulation of secretions, e.g. cystic fibrosis, bronchial obstruction (e.g. tumour), stroke
  • Pulmonary congestion or oedema, due to chronic heart disease
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11
Q

Community-acquired acute pneumonia

A

Large volume of inflammatory exudate in alveoli and airways, phlegm

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12
Q

Community-aqcuired atypial pneumonia

A

Smaller amounts of exudate-patchy-in alveolar interstitium

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13
Q

Nosocomial pnuemonia (hospital aqcuired)

A

Due to chronic disease and/or immunosuppression and invasive procedures and resistant organisms

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14
Q

Chronic pneumonia

A

Fungal species, intracellular bacteria

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15
Q

Pneumonia in immunocompromised host

A

Viral, bacterial or fungal

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16
Q

Aspiration pneumonia

A

Necrotising

  • Mostly in debilitated patients, those who aspirate gastric contents
  • Chemical and bacterial
17
Q

Lobar pneumonia symptoms

A
  • Acute onset, malaise (tiredness), fever, chills, productive cough
  • Chest pain secondary to pleurisy
  • ARDS (acute respiratory distress syndrome)
18
Q

Lobar pneumonia complications

A
  • Tissue destruction and necrosis
  • Spread of infection and inflammation to pleural cavity=pleurisy
  • bacteraemic dissemination
  • endocarditis, pericarditis, meningitis, nephritis
19
Q

Features on chronic inflammation in the lung

A
  • collection of chronic inflammatory cells
  • destruction of parenchyma where normal alveoli are replaced by spaces lined by cuboidal epithelium
  • replacement by connective tissue
20
Q

Acute Respiratory Distress Syndrome (ARDS) -a severe Acute Lung Injury(ALI)

A
  • AKA shock lung, traumatic wet lungs, diffuse alveolar damage- high mortality
  • it is the effect of wide-spread, diffuse damage to alveolar capillaries and/or alveolar epithelium and alveolar surfactant layer
  • Can arise as a complication of diverse situations- direct injury to lungs or systemic disorders
21
Q

ARDS causes

A
  • gastric aspiration
  • pulmonary contusion, penetrating lung injury
  • ionising radiation
  • near drowning
  • inhalation injury
  • reperfusion pulmonary oedema after lung transplant
  • oxygen toxicity (SCUBA divers)
22
Q

ARDS progression- exudative phase

A

D1: interstitial/alveolar oedema, degenerative changes in type 1 alveolar epithelium, start of interstitial infiltrate-lymphocytes, plasma cells, macrophages
D2: sloughing type 1 cells- bare basement membrane, hyaline membranes begin
D4-5: peak of hyaline membrane formation
D7: peak of interstitial inflammatory infiltrate, type 2 alveolar epithelial cells proliferate and spread along basement membrane, thrombi in alveolar capillaries and pulmonary arterioles

23
Q

ARDS progression- organising phase

A

From D14:

  • interstitial inflammation and type 2 hyperplasia persists
  • macrophages breakdown hyaline membrane and debris
  • interstitial fibroblasts proliferate, produce collagen
24
Q

ARDS outcomes- resolution

A
  • Complete recovery and restoration of normal lung function
  • Alveolar exudate and hyaline membrane resorbed
  • Normal alveolar epithelium restored
  • Fibroblast proliferation ceases
  • Extra collagen metabolised- broken up and destroyed
25
Q

ARDS outcomes- end stage fibrosis

A
  • Exudate associated with tissue destruction, i.e. the hyaline membranes-large amounts of scar tissue produced
  • lung architecture remodelled, multiple cyst-like spaces= honeycomb lung
  • spaces separated from each other by fibrous tissue, lined with type 2 epithelium, bronchiolar epithelium or squamous cells
26
Q

ARDS treatment

A
  • Mechanical ventilation
  • Inhalation of NO
  • High O2 concentrations-toxic
  • Surfactant therapy
  • Anti-inflammatory drugs-glucocorticoids
  • Treatment is difficult- 40-60% mortality

Pathology (23 decks)

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