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RESPIRATORY VIVAS2010-1, 2007-2, 2006-1, 2003-2What is the pathological definition of emphysemaAbnormal permanent enlargement of the air spaces distal to the terminal bronchioleDestruction of alveolar wallsNo obvious fibrosisDescribe the pathogenesis of emphysemaProtease – antiprotease theoryAlveolar wall destruction results from an imbalance between proteases (mainly elastase) and antiproteasesElastases from neutrophils (also macrophages, mast cells, pancreas, bacteria)Anti-elastases: 1 antitryspin (from serum and macrophages) is a major protease inhibitorAny stimulus that ↑ number of leukocytes (neutrophils / macrophages) in lung or release of their elastase containing granules ↑ elastocytic activityStimulated neutrophils also release oxygen free radicals which inhibit 1 antitryspin activity meaning process of elastic tissue destruction is uncheckedWhat is the role of cigarette smoke?Smokers have ↑ neutrophils & macrophages in alveoli, – smoking stimulates neutrophil chemotactic factor (e.g. IL-8), nicotine is chemotactic, smoke activates alternative complement pathway, activates macrophages to recruit neutrophilsSmoking stimulates release of neutrophil elastase, proteinase 3, Catepsin GSmoking ↑ elastase activity in macrophages (not inhibited 1 antitryspin )Reactive oxygen species in cigarette smoke deplete glutathione and superoxide dismutaseIndividuals with hereditary deficiency of 1 antitryspin develop emphysema, and at a younger age if they smokeNote: centri-acinar distribution due to impaction of smoke particles in small bronchi / bronchioles with neutrophil influx. Differs to pan-acinar emphysema associated with 1 antitryspin deficiency and chronic low level proteolysis from neutrophils in transit through the lung circulation.What are the anatomical types 2007-2 2006-1Centriacinar (centilobular) 95%Central/proximal parts of acini affectedDistal alveoli spared except in severe diseaseMore common/severe in upper lobes/apicesOccurs in heavy smokers, often associated with chronic bronchitisPanacinarUniform enlargement from respiratory bronchiole distallyTends to occur at lower zonesAssociation with 1 antitryspin deficiencyDistal acinar (paraseptal): near the pleura, adjacent to scars/fibrosisIrregular emphysema: Also associated with scarring, usually asymptomaticWhat cancers can smoking predispose to? 2003-2Oropharyx, larynx, lung, oesophagus, stomach, pancreas, bladder2009-2What disorders can precipitate the Adult Respiratory Distress Syndrome, ARDS?Infection:? sepsis*, diffuse pulmonary infections*, gastric aspiration*Trauma:? lung injury, head injury*, burns, radiationInhalation:? oxygen, smoke, irritantsChemical injury:? heroin, salicylate, barbiturate, paraquatHaematology:? transfusions, DICOther:? 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.Pro-inflammatory > anti-inflammatory mediator imbalanceActivated macrophages recruit neutrophils (IL-8) and activate endothelium (IL-1, TNF)Capillary injury causes inc. vascular permeability, alveolar flooding & oedema, fibrin exudation, formation of hyaline membranes, loss of diffusion capacity, abnormalities of surfactantConsequence of uncontrolled activation of acute inflammatory response w/ most injury by neutrophilsWhat are the outcomes of ARDS?Death or survival of acute phaseSurvival with organisation and scarringResolutionInterstitial fibrosisDeath, often from super imposed infection 2007-2, 2007-1, 2006-1Describe the pathogenesis of atopic asthmaAsthma is a chronic relapsing inflammatory disorder characterised by paroxysmal reversible broncospasm due to smooth muscle hyperplasiaMucus secretion also a featureAtopic asthma (most common) is caused by a classic type I hypersensitivity reactionInitial sensitisation to allergens (antigens), e.g. pollen, dust mites, foods, animal danderRe-exposure triggers Ag-IgE-mast cell => release of (preforemed and new formed) mediatorsMediators: IL-1, IL-6, TNF, NO, bradykininsDirectly or via neuronal reflexes: causes bronchospasm, mucus production, increased vascular permeability, inflammatory cell recruitmentLate phase occurs (after hours) due to recruited leukocytes (eosinopils, lymphocutes, neutrophils, monocytes) causing persistent bronchospasm, oedema and epithelial damage and lossRepeated bouts cause airway remodelling with: bronchial SMC and mucus gland hypertrophy/hyperplasia, increased vascularity, increased subepithelial collagen deposition2009-1Describe the relationship between asbestos exposure and malignant mesotheliomaIncreased incidence among people with heavy exposure to asbestos (Lifetime risk 10%)Asbestos bodies found in increased numbers in lungs of patients with mesotheliomaLong latent period for mesothelioma (25-45 yrs).No increased risk in asbestos workers who smoke (in contrast to asbestos related lung carcinoma) Asbestos workers more at risk of dying from lung carcinoma (especially if they smoke)Where can malignant mesothelioma arisePleura, peritoneum, pericardium, tunica vaginalis, genital tract2011-1, 2003-1 (atypical)What organisms commonly cause community acquired pneumonia?BacterialStreptococcus pneumoniae (pneumococcus)Haemophilus influenzaMoraxella catarrhalisStaphlococcus aureusLegionella pneumophiliaOthers: Klebsiella pneumonia, Pseudomonas Atypical pneumoniaMycoplasma pneumoniaChlamydia sppCoxielle burnetti (Q feverViral: RSV, parainfluenzavirus, influenza A+B, adenovirus, SARS virusHow do atypical pneumonias differ from classical (typical) bacterial pneumoniasModerate amount sputumNo physical findings of consolidationOnly moderate elevation of WCCNo alveolar infiltratePatchy inflammatory changes largely confined to alveolar septa and pulmonary interstitium i.e. interstitial nature of the inflammation vs alveolar exudates in classical pneumomiaDifferent clinical presentation: few localising signs, cough often absent, typical symptoms are fever, headache, myalgiaLower mortality cf bact pneumonia (severe disease uncommon)2011-1, 2005-1How is legionella pneumonia contracted? Artificial aquatic environment e.g. water cooling tower, water supply tubingInhalation of aerosolised dropletsOr aspiration of contaminated drinking water2005-1What groups of patients are at risk of legionella infectionUnderlying co-morbidities: cardiac, renal, immune, hematologicTransplant patients especiallySmokers, chronic lung and elderlyHow is legionella diagnosedUrinary antigen or fluorescent Ab test on sputumCulture is gold standard (special medium)PCR2011-2, 2009-1, 2005-1Describe the structure of the influenza virus.Single stranded RNA8 helices bound by a nucleoprotein that determines the type of virusSpherical capsule: lipid bilayer studded with viral haemaglutinin and neuraminadaseWhat are the types and subtypes?ABC determined by the nucleoprotein: Type A mutates, B and C do notHaemagglutinin and neuraminidase (determined by proteins on the bilipid envelop)E.g. H5N1 – 60% mortality due to ability to spread throughout the body b/c the avian H5 is cleaved (activated) by tissue proteases, not only in the lung as per the usual strains What is the pathological basis of pandemics and epidemics?Epidemics (new cases in a certain population):Occurs when there are changes in the haemaglutinin or neuraminase proteins allowing escape for host antibodiesBy antigenic driftClearing the infection requires cytotoxic T cell and innate immune responsePandemics (widespread epidemic across multiple populations/geography)Haemaglutinin and neuraminase proteins completely replaced by recombination of RNA segments with those from animal virusesAntigenic shiftHow does the influenza virus cause pneumonia 2009-1Attachment of virus to upper respiratory tract epitheliumNecrosis of cells followed by inflammatory responseInterstitial inflammation with outpouring of fluid into alveoliSecondary infection by bacteria (e.g. Staph or Strep)How does the immune system specifically attack the influenza virus 2005-1Antibody mediated cellular immunity: Cytotoxic (CD8+) T cellsInnate immunity: Macrophages via specific anti-influenza proteins (Mx1) ................
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