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  • VSlides
  • Read Jayraj's boss notes alongside this

Pathology

Case 1

  • Physical examination
    • Pulse - irregularly irregular
    • ECG - AF; irregularly irregular with no P wave
    • Auscultation - pandiastolic murmur, left lateral position with bell. Opening snap with diastolic rumble.
      • NB: A/V stenosis OR pulmonary/aortic incompetence causes diastolic murmur (due to turbulence); A/V incompetence OR pulmonary/aortic stenosis causes diastolic murmur
    • Mitral stenosis causes pressure overload - causing dilatation of the left atrium (after initially become smaller due to concentric hypertrophy; because then it fails)
      • Pressure builds up in the lungs as a result - dyspnoea etc
    • Lungs: bibasal crepitations
    • CXR: elevation of the left main bronchus (due to left atrium pushing it upwards)
    • Pulmonary shadow enlargement due to pulmonary arterial hypertension
    • Upper lobe blood diversion (over 15 mmHg)
    • Shadows → Interstital pulmonary oedema (25mmHg), fine diffuse shadowing in lung fields & Kerley B-line (oedematous interlobular septa (peripherally, 1cm long)
      • Alveolar (>30 mmHg): fluid in alveolar space (white out of the region). Hilar region: Bat's wing appearance
    • Pleural effusion: loss of costophrenic margin
    • Bulging of heart → pushing on right main bronchus
    • Prominent left atrial appendage → causes raising of left main bronchus
  • Echo: thickened valves
  • Cardiac catheterisation
    • There is a pressure differential between LA and LV during diastole (due to stenosis)
  • History
    • Recurrent bacterial tonsillitis --> repeated rheumatic fever (GAS; strep throat/skin infection) --> RF --> RHD
      • Cross reaction of antibodies
      • RF (2-3 weeks after strep throat, 3% progression esp. ATSI): Pancarditis: sydenham's chorea, erythema marginatum, subcutaneous nodules, migratory polyarthritis
      • Valvular inflammation, chronic (worsened with GAS infection), scarring/deformity
      • Thickening and retraction of leaflets, commissural fusion (causes fishmouth; stenosis), thickening and fusion of chordae tendinae, calcification; chamber dilatation

Case 2

Infective endocarditis

  • Due to abnormal valve with transient bacteraemia
  • Colonisation and invasion of valve or mural endocardium by microorganisms
    • Staph aur. is very virulent, don't need a damaged valve
  • Vegetations and tissue destruction
  • Esp. streptococci and staphylococci
  • TRIAD
  1. Fever
  2. New or changing murmur
  3. Embolic phenomena
  • Indications for prophylactic antibiotics: only for RHD in indigenous
  • TOE: better picture of the valves than transthoracic
    • LA thrombi
    • MV vegetations (TOE for 2mm, TTE ≥5mm)
    • aortic dissection
    • IE
  • Blood culture: 3 samples, each are 2 bottles (anaerobic and aerobic), from different sites at different times
  • FBC: raised white cells (neutrophils), ESR and CRP, low Hb (anaemia of chronic disease; normochromic, normocytic, or destruction of red cells going through abnormal valve),
  • Pansystolic murmur
  • CXR:
    • air-fluid interface with a meniscus due to septic emboli from tricuspid valve, causing abscesses (can see white ring of collagen around the outside of the abscess; necrotic core)
    • bronchopleural fistula causes pus within pleural space (CXR looks like a glass filled up)
  • Digital infarcts due to septic emboli
  • Peripheral stigmata: ossler's nodes, janeway's lesions and splinter haemorrhages
  • Vegetation: fibrin, platelets, red cells and bacteria

Slide: aortic endocarditis

  • Thickened valve leaflet
  • Bright pink material with darker areas on the free edge
    • Fibrin (pink) and bacterial colonies (blue)
    • Dystrophic calcification of the valve
    • lymphocytes/neutrophils are at the base of the leaflet, not at the site of the infection

Slide: lung

  • Septic emboli
  • Top left = alveoli/air spaces
  • Bottom right = consolidation with dark purple spaces, inflammatory cells (neutrophils-multilobed nuclei; pus), fibrin around bacterial colonies (abscess formation)

Physiology

  • Wiggers Diagram IT.png
  • See this page: HMA/Lectures/Mechanical events of_the cardiac cycle
  • Ejection fraction = StrokeVol/EDV = (EDV-ESV)/EDV = 1-(ESV/EDV)
  • Heart rate increase = systolic pressure increase
  • Preload increase = stroke volume increase (Starling's law), ejection fraction increases, systolic + diastolic (a little) pressure (a lot) inc, raises both EDV and ESV
  • Contractility increase = ESV decrease, higher systolic pressure
  • Afterload increase: systolic pressure increases, stroke volume decreases, end systolic volume increases
  • Increased heartrate alone causes increased systolic pressure with decreased stroke volume (due to decreased ejection time)