Resp Pathology Flashcards
What disorders can precipitate the Adult Respiratory Distress Syndrome (ARDS)?
- Infection: sepsis*, diffuse pulmonary infections*, gastric aspiration*
- Trauma: lung injury, head injury*, burns, radiation • Inhalation: oxygen, smoke, irritants
- Chemical injury: heroin, salicylate, barbiturate, paraquat
- Haematology: transfusions, DIC
- Other: pancreatitis, uremia, CP bypass, hypersensitivity reactions (50% of ARDS cases associated with *)
What is the pathogenesis of ARDS?
- Diffuse alveolar capillary damage, variety of insults, initiated by different mechanisms.
- Capillary injury causes inc. vascular permeability, alveolar flooding & oedema, fibrin exudation, formation of hyaline membranes, loss of diffusion capacity, abnormalities of surfactant.
- Consequence of uncontrolled activation of acute inflammatory response; most injury by neutrophils
- Macrophages alternative source of injury
What are the outcomes of ARDS?
Death, survival with organisation and scarring
What are the pathological features of asthma?
- Increased airway responsiveness to variety of stimuli
- Episodic bronchoconstriction
- Bronchial wall inflammation
- Increased mucus
Asthma may be categorised as atopic or non-atopic. What are the characterisitcs of each of these types?
Atopic:
- IgE mediated type 1 hypersensitivity (allergen sensitisation)
- Environmental allergen triggers, e.g. house dust mite, pollens, dander, foods
- Family history common
- Skin test positive to allergen
- RAST shows allergen sensitivity
Non-atopic:
- Hyperirritiability of bronchial tree (no allergen sensitiation, skin test usually negative)
- FHx uncommon
- Triggers - resp infection 2° viruses common
- Inhaled air pollutants may contribute - SO2, ozone, NO2)
In atopic asthma, what happens in the early-phase reaction?
Allergen exposure →IgE
• Re-exposure→mast cell degranulation with release of cytokines/mediators
→Bronchoconstriction (via subepithelial vagal/parasympathetic receptors)
→Mucus production
→Vasodilation with increased vasc permeabiliy
What is the definition of emphysema?
A lung condition characterised by irreversible enlargement of the airspaces distal to the terminal bronchiole accompanied by destruction of their walls without obvious fibrosis
Describe the pathogenesis of emphysema
- Mild chronic inflammation (NØs & MØs), mediator release (LTB4, IL-8, TNF), causes damage and sustains inflammation
- Protease-antiprotease imbalance - destructive effect of high protease activity in pts with low anti-protease activity
- Oxidant-antioxidant imbalance - abundant reactive O2 species in smoke depletes antioxidant mechanisms
What are the potential complications of emphysema?
- Bullous lung disease
- Expiratory airflow limitation
- Infection
- Respiratory failure
- Pneumothorax
- Cor pulmonale, CCF (“pink puffers”)
What organisms cause community-acquired pneumonia?
- Bacterial - Strep pneumonia, H influenza, Moraxella catarrhalis, S aureus, Klebsiella & Pseudomonas
- Atypical organisms - Mycoplasma, Chlamydia spp, Coxiella burnetti (Q fever), Legionella pneumonia
- Viral - RSV, parainfluenza, influenza A & B, adenovirus, SARS, H1N1
What are some potential complications of pneumonia?
Abscess formation, empyema, bacteraemia/bacterial dissemination (endocarditis, pericarditis, meningitis, kidney/brain abscess), sepsis, respiratory failure
How do the clinical features of atypical pneumonias differ from classic pneumonias?
- Moderate sputum, no physical findings of consolidation, only moderate increase in WBCs
- Cough not prominent, usual features are fever, HA, myalgia
- Lower mortality cf classic pneumonia
What is secondary tuberculosis?
Pattern of disease that arises in a previously sensitised host
How may infection occur in secondary tuberculosis?
- May follow shortly after primary infection (<5%)
- Reactivation of latent organisms - typically in areas of low disease prevalence
- Reinfection - typically in areas of high disease prevalence
Describe the pathological features in the lung of secondary infection with TB
- Site - apical UL in secondary
- Areas of inflammation/granuloma/multinucleated giant cells
- Central caseous necrosis
- Cavitation
- Healing with fibrosis and calcification
+/- Complications include tissue destruction, erosion of blood vessels, miliary spread, pleural effusion
