VIVA: Pathology - Respiratory Flashcards
Describe the pathogenesis of thrombotic pulmonary embolism (PE)
- PEs originate from deep vein thrombosis* (95% from lower limb)
- Fragmented thrombi from DVTs are carried through the venous system and into the right side of the heart before lodging in the pulmonary arterial vasculature*, including the main pulmonary artery, pulmonary artery bifurcation or smaller branching arteries
*needed to pass
What are the symptoms and signs of pulmonary embolism?
- Clinical manifestations depend on size and location of the thrombus in the pulmonary vasculature
- Most PEs (60-80%) are small and produce no symptoms or signs
- Symptoms include pleuritic chest pain, dyspnoea, cough, haemoptysis and collapse/syncope*
- Signs include hypoxaemia, tachypnoea, hypotension, fever, acute right heart failure, pleural rub, shock, sudden death*
*total of 5 symptoms and signs to pass
List two other types of emboli
2 to pass:
- Fat (bone marrow)
- Air, other gas
- Amniotic fluid
- Foreign body (e.g. fragment of catheter)
Describe the pathogenesis of ARDS
Type of acute lung injury:
- Initial injury to alveolar capillary membrane* (endothelium)
- Acute inflammatory response* (neutrophil-mediated)
- Results in increased vascular permeability* and alveolar flooding
- Fibrin deposition
- Formation of hyaline membranes
- Widespread surfactant abnormalities* (damage to type II pneumocytes)
- Eventually leads to organisation with scarring
*3/4 needed to pass
What conditions are associated with the development of ARDS?
- Infection*: sepsis, diffuse pulmonary infection, gastric aspiration
- Physical/injury: head trauma, pulmonary trauma, fractures, near drowning, burns, radiation
- Inhaled irritants: O2 toxicity, smoke, irritant gases and chemicals
- Chemical injury: opiates, barbiturates, paraquat, acetylsalicylic acid, gastric aspiration
- Haematological conditions: multiple transfusions, DIC
- Other: pancreatitis, uraemia, cardiopulmonary bypass, hypersensitivity, organic solvents, drugs
*needed to pass + 2 other categories with 1 example each
What is the definition of asthma?
Asthma is a chronic disorder of the conducting airways, usually caused by immunological reaction, which is marked by:
- Episodic bronchoconstriction* due to increased airway sensitivity to a variety of stimulation
- Inflammation* of the bronchial walls
- Increased mucus secretion*
*needed to pass
Describe the pathogenesis of acute atopic asthma
- Classic example of IgE-mediated (type I) hypersensitivity*
- Atopic triggers: environmental allergens (e.g. dust, pollens, dander, food)
- On re-exposure to antigen, the Ag induces cross-linking of IgE bound to Fc receptors on mast cells
- Mast cells degranulate* and release preformed mediators that act directly and via neuronal reflexes to induce bronchospasm, increased vascular permeability, mucus production, and recruitment of leucocytes
*needed to pass
What are the potential triggers agents for non-atopic asthma?
2 to pass:
1. Non-atopic:
- Respiratory viruses
- Air pollutants
- Exercise
- Cold
2. Drug-induced (e.g. aspirin)
3. Occupational triggers:
- Fumes (e.g. epoxy resins, plastics)
- Organic and chemical dusts (e.g. wood, cotton, platinum)
- Gases (e.g. toluene)
- Other chemical (e.g. formaldehyde, penicillin products)
4. Asthmatic bronchitis in smokers
Name the main inflammatory cells involved in the pathogenesis of asthma
Wide range of inflammatory cells are involved, including (2 to pass):
- Lymphyocytes
- Eosinophils
- Mast cells
- Macrophages
- Neutrophils
How is asthma categorised pathologically?
2/4 to pass:
1. Atopic:
- Most common
- IgE-mediated (type I) hypersensitivity reaction
- Also involves TH2 cells
- Characterised by an immediate (bronchoconstriction) and late-phase (inflammation) reactions
- TH2 cytokines including IL-4, IL-5 and IL-13 are important mediators (IL-17 and IL-9 in some)
2. Non-atopic:
- No evidence of allergen sensitisation and negative skin test
- Family Hx is rare
3. Drug-induced (e.g. aspirin)
4. Occupational (e.g. epoxy fumes)
Name some common triggers of asthma
Atopic:
- Environmental factors (e.g. dust, pollens, food) in synergy with other pro-inflammatory cofactors such as respiratory viral infection
- Positive family Hx and skin test for allergens
Non-atopic:
- Triggers are less clear
- Viral respiratory infections (e.g. rhinovirus, parainfluenza, RSV)
- Inhaled air pollutants (e.g. smoking, sulfur dioxide, ozone, nitrogen dioxide)
- Exercise-induced
- Exposure to cold
What are the pathological features of acute asthma?
3/4 to pass:
- Increased airway responsiveness
- Episodic bronchoconstriction
- Bronchial wall inflammation
- Increased mucus
What happens in the early phase reaction in atopic asthma?
- Allergen exposure* produces IgE
- Re-exposure triggers mast cell degranulation and cytokine release
- Mediators induce bronchoconstriction, mucus production, and vascular changes (vasodilation, increased vascular permeability)
*needed to pass + concept
What is bronchiectasis?
Bronchiectasis is a disease characterised by permanent dilation of bronchi* and bronchioles caused by the destruction of the smooth muscle and elastic tissue *, resulting from or associated with chronic necrotising infections *
Also involves scarring and persistent infection
*needed to pass
What conditions are associated with the development of bronchiectasis?
4 examples to pass:
1. Congenital/hereditary:
- Cystic fibrosis
- Immunodeficiency
- Ciliary dyskinesia
- Kartagener’s syndrome
2. Post-infectious (necrotising pneumonia):
- Staph aureus
- Haemophilus
- TB
- Pseudomonas
- Adenovirus
- HIV
- Influenza
- Fungi
- Aspergillosis
3. Bronchial obstruction:
- Tumour, foreign body, mucous impaction
4. Other:
- Rheumatoid arthritis
- SLE
- Inflammatory bowel disease
- Post transplantation
5. Idiopathic (25-50%)
Name some risk factors for pulmonary embolism
- Primary*:
- Factor V Leiden
- Antiphospholipid syndrome
- Prothrombin mutations - Secondary*:
- Obesity
- OCP
- Cancer
- Immobilisation
- Long haul flights
- Pregnancy
- Indwelling central venous line
- Hip fracture
*1 primary and 3 secondary needed to pass
Outline the natural history and spectrum of TB
- Primary infection
- Primary complex* formed:
- Local caseation
- Ghon complex is primary TB with mediastinal nodes - Primary complex may heal (organisms not viable) or lead to latent lesion (organisms viable)
- Latent period* OR progressive primary TB (latter may lead to miliary TB)
- Latent lesion can be reactivated leading to secondary TB* (reinfection may also lead to secondary TB)
- Secondary TB occurs as localised (pulmonary or extrapulmonary) caseating destructive lesions OR progressive secondary TB
- Progressive secondary TB may lead to miliary TB*
*needed to pass
