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Flashcards in Resp Pathology Deck (15)
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1
Q

What disorders can precipitate the Adult Respiratory Distress Syndrome (ARDS)?

A
  • 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 *)
2
Q

What is the pathogenesis of ARDS?

A
  • 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
3
Q

What are the outcomes of ARDS?

A

Death, survival with organisation and scarring

4
Q

What are the pathological features of asthma?

A
  • Increased airway responsiveness to variety of stimuli
  • Episodic bronchoconstriction
  • Bronchial wall inflammation
  • Increased mucus
5
Q

Asthma may be categorised as atopic or non-atopic. What are the characterisitcs of each of these types?

A

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)
6
Q

In atopic asthma, what happens in the early-phase reaction?

A

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

7
Q

What is the definition of emphysema?

A

A lung condition characterised by irreversible enlargement of the airspaces distal to the terminal bronchiole accompanied by destruction of their walls without obvious fibrosis

8
Q

Describe the pathogenesis of emphysema

A
  • 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
9
Q

What are the potential complications of emphysema?

A
  • Bullous lung disease
  • Expiratory airflow limitation
  • Infection
  • Respiratory failure
  • Pneumothorax
  • Cor pulmonale, CCF (“pink puffers”)
10
Q

What organisms cause community-acquired pneumonia?

A
  • 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
11
Q

What are some potential complications of pneumonia?

A

Abscess formation, empyema, bacteraemia/bacterial dissemination (endocarditis, pericarditis, meningitis, kidney/brain abscess), sepsis, respiratory failure

12
Q

How do the clinical features of atypical pneumonias differ from classic pneumonias?

A
  • 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
13
Q

What is secondary tuberculosis?

A

Pattern of disease that arises in a previously sensitised host

14
Q

How may infection occur in secondary tuberculosis?

A
  1. May follow shortly after primary infection (<5%)
  2. Reactivation of latent organisms - typically in areas of low disease prevalence
  3. Reinfection - typically in areas of high disease prevalence
15
Q

Describe the pathological features in the lung of secondary infection with TB

A
  • 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