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Circulatory disorders - Coggle Diagram

- - - - Mod trans & serofibrinous exudate = intermediate (cont fibrinogen) = clear to straw, watery & fibrin strands/clots
        
        Exudate = many prot & cells = watery > solid
        
        Transudate & Serous exudate = low prot & cells = straw/watery
  - - - = decr plasma prot (esp albumin produced by hepatocytes)
      - = hypoalbuminaemia > decr production or excessive loss
      - Starvation, kwashiorkor, GI disorders, water intox, verminosis
    - - Red ability lymphatic syst to remove slight excess of norm accum ISF
      - Localised
      - Lymphangitis, congenital lymphatic aplasia/hypoplasia, lymphatic obstruction or compression
    - - Liver cirrhosis, chronic heart failure, iatrogenic fluid admin overload
      - Incr blood vol in microvasculature
        
        Active or passive
        
        Local or generalised
    - - Subleth injury to capil endothelial cells > localised rel mediators that cause vasodilation & incr microvasc perm
        
        Localised oedema = dilute inflam resp
        
        Localised by can be multifocal dep on cause
      - Vascular leakage ass w/ inflam
        
        Infections agents > viruses, bacteria, rickettsia
        
        Immune mediated > type III hypersensitivity
      - Toxins > bacterial endotoxins & exotoxins
      - Burns & trauma > localised oedema
      - Fluid of oedema dur to endothelial cell injury cont sml amts fibrinogen > polymerise > translucent strands fibrin = modified transudate
      - Pulpy kidney
  - - - Active (arteriolar dilation & engorgement of vascular bed)
        
        Acute
      - Physio = exercise & path = inflam
      - = incr vol blood in tiss/org due to incr blood flow to tiss/org
      - Redder than norm & warm
    - - = incr vol blood in tiss/org due to impaired venous drainage of tiss/org
      - Passive
        
        Acute/chronic
        
        Chronic - vein gradually compressed by enlarging neoplasm/abscess
        
        Form of anastomoses
        
        Cant anastomose = fibrosis to ameliorate incr pressure
        
        Cyanotic induration of liver > chronic RIGHT heart failure
        
        Chronic pulmonary congestion > primary LEFT heart failure
        
        Gravity induced chronic congestion of dep tissues inactive/recumbent animals = hypostasis
      - Systemic (congestive heart failure) or localised (obstruction of lumen of draining vein)
      - Redder than normal & cool
    - - Vascular stasis in chronic passive congestion
        
        Thrombosis > congestion
        
        Endothelial injury > haemorrhage > cell death due to hypoxia
      - Oedema ass w/ both
- - - - Stasis
        
        Shock
        
        Prolonged GA or recumbency
        
        Veins
        
        Hyper viscosity syndromes
      - Turbulence
        
        Bifurcations of arteries
        
        Aneurysms
        
        Heart chambers
    - - Arteriothrombi
      - Phlebothrombi
      - Incr stim of clotting cascade (DIC) or decr inhibition of cascade
    - - Viral infection
      - Parasitic migrations
      - Atherosclerosis
      - Chemical injury
      - Electrical injury
      - Arteriosclerosis
      - Trauma
  - - - Endothelium isolates thrombus
      - Capils grow through att > phagocytes & fibroblasts enter
      - Material cant be removed incorp into fibrous CT > scar
      - Reorganised & recanalised
- - - - Acute = dark-red, haemorrhagic
      - Sub-acute = pale, swollen
      - Chronic = pale, sunken
    - - Collateral blood supply = less susceptible
      - Dual blood supply = lease susceptible
      - Fxnal end arteries = v susceptible
    - - Occlusion of arterial > area ischeaemia
      - Occlusion of venous = area congestive hypoxia
- - - - Excessive host response
      - SIRS
        
        Systemic vasodilation
        
        Complement activation
        
        Decr myocardial contractibility
        
        Systemic leukocyte adhesion
        
        DIC
      - Release of endotoxin
      - MODS
      - Gram neg septicaemia (endotoxic shock)
      - Death
  - - - Refle compensatory mechanisms > maint perf vital orgs
      - Arteriolar constriction in non-vital orgs
      - Catecholamines & cortisol
    - - Persistent tissue hypoperf > hypoxia, decr ATP prod, anaerobic glycolysis, metabolic acidosis
      - Vasomotor resp blunted > pooling in microcirc
      - DIC starts
    - - Wspread sublethal & lethal cell injury > lysosomal enzyme rel > irrev cycle
      - Damage to intestinal wall > gram neg enterobacteria > septic shock
      - Complete renal shutdown