Inflammatory Lung Disease Flashcards
Type 1 pneumocytes
- Cover 95% of alveolar surface
- Act like endothelial cells
Type 2 pneumocytes
- Synthesise surfactant
- Involved in repair of alveolar epithelium through ability to give rise to type 1 cell
Alveolar constituents
- Type 1 & 2 pneumocytes
- Resident macrophages
- Capillaries
- Rare monocytes, other WBCs
Pnemonias
Respiratory disorders involving acute inflammation of the lung structures, such as the alveoli and bronchioles, classified as infectious or non infectious
Infectious pneumonia, causative agents
- Bacterial (most commonly)
- Viral
- Fungal
Non-infectious pneumonia causative agents
- Chemical pneumonia (ingestion/inhalation of irritating substances
- Inhalation pneumonia (also called aspiration pneumonia)
Pneumonia risk factors
- Immuno compromised patients
- Alcoholics
- Transplant immunosuppression
- Pregnancy
- Cystic fibrosis
- Autoimmune disease
- Burns
- Cancer
- Chemo
- Old or young age
- Chronic steroids
- Diabetes
Innate lung defences
- Mucus blanket (cilia and cough reflex)
- Phagocytosis-alveolar macrophages or recruited neutrophils
- Complement- C3b, MAC
- Draining lymph nodes- initiation of immune response
Acquired lunge defences
- Secreted IgA in alveoli
- IgM and IgG in alveolar fluid- activate complement and opsonise
- Accumulation of T-cells- viral infection
Causes of impaired lung function
- 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
Community-acquired acute pneumonia
Large volume of inflammatory exudate in alveoli and airways, phlegm
Community-aqcuired atypial pneumonia
Smaller amounts of exudate-patchy-in alveolar interstitium
Nosocomial pnuemonia (hospital aqcuired)
Due to chronic disease and/or immunosuppression and invasive procedures and resistant organisms
Chronic pneumonia
Fungal species, intracellular bacteria
Pneumonia in immunocompromised host
Viral, bacterial or fungal
Aspiration pneumonia
Necrotising
- Mostly in debilitated patients, those who aspirate gastric contents
- Chemical and bacterial
Lobar pneumonia symptoms
- Acute onset, malaise (tiredness), fever, chills, productive cough
- Chest pain secondary to pleurisy
- ARDS (acute respiratory distress syndrome)
Lobar pneumonia complications
- Tissue destruction and necrosis
- Spread of infection and inflammation to pleural cavity=pleurisy
- bacteraemic dissemination
- endocarditis, pericarditis, meningitis, nephritis
Features on chronic inflammation in the lung
- collection of chronic inflammatory cells
- destruction of parenchyma where normal alveoli are replaced by spaces lined by cuboidal epithelium
- replacement by connective tissue
Acute Respiratory Distress Syndrome (ARDS) -a severe Acute Lung Injury(ALI)
- 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
ARDS causes
- gastric aspiration
- pulmonary contusion, penetrating lung injury
- ionising radiation
- near drowning
- inhalation injury
- reperfusion pulmonary oedema after lung transplant
- oxygen toxicity (SCUBA divers)
ARDS progression- exudative phase
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
ARDS progression- organising phase
From D14:
- interstitial inflammation and type 2 hyperplasia persists
- macrophages breakdown hyaline membrane and debris
- interstitial fibroblasts proliferate, produce collagen
ARDS outcomes- resolution
- 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
