Morphology of Hemodynamic Disorders Flashcards
What are the two categories that make up simple changes in blood flow
Hyperemia
Congestion
What is hyperemia
Increased blood flow due to arteriolar dilation
How can tissue affected by hyperemia be described
erythemic (red)
What is congestion
Reduced venous outflow
Can be systemic or local
How can tissue affected by congestion be described
Cyanotic
Congestion and hyperemia - which is active v passive
Congestion - passive
Hyperemia - active
Hemorrhage:
Extravasation of blood into tissues, body cavities, or externally
What are some general causes of hemorrhage (think categories)
Trauma
Vit K deficiency
Vasculitis
Aneurism rupture
Heriditary
How can hemorrhage be heriditary
Genetic coag factor defect
Platelet function is altered
Purpura:
purplish or brownish-red discoloration of the epidermis due to hemorrhage
Petechia
Pinpoint hemorrhage, smallest lesion that is grossly visible
Ecchymosis:
Larger (>1cm) focus of hemorrhage
Description of hemorrhage into body cavities -
hemo- + cavity
ex: hemothorax, hemopericardium, etc
Hematoma:
localized collection of clotted blood found in tissue space
(extravascular coagulation)
Thrombosis:
Pathologic presentation of normal hemostatic pathways
Occurs within intact blood vessels
Needs to be distinguished from a post-mortem clot at necropsy
Hemoptysis:
Blood or blood-stained sputum
Ew.
Hematochezia:
fresh blood in feces
Usually indicates bleed in lower GI - blood was not exposed to stomach acid
Melena:
Black tarry blood in feces
What % of their blood can healthy animals stand to loose
20%
What is the name for the unholy thrombotic trinity
Virchow’s Triad
What are the components of Virchow’s Triad
Hypercoagulability (blood composition)
Stasis (flow)
Vessel wall injury (vasculature)
How does endothelial injury contribute to thrombosis
Damage alters blood flow and can lead to coagulation
How does alteration in blood flow lead to thrombosis
Stasis brings platelets into contact with the endothelium –> activation
Turbulence causes damage
How does a change in blood composition lead to thrombosis
Increased # of platelets –> hypercoagulability
Elevated fibrin levels
Decreased anti-thrombin levels
Post-mortem clot morphology
Easily removed
Cast of vessel
Dark red, gelatinous
Shiny, smooth
Area of yellow if RBCs settle out
Arterial thrombi morphology
Form in areas of rapid blood flow
Attached to sites of endothelial damage
Retrograde growth
Pale/grey
Dry, friable
Alternating layers of fibrin and platelets
Venous thrombi morphology
Areas of slow flow
Attached to area of injury
Grow in direction of blood flow
Form in casts BUT not easy to remove
Firm, moist, red
What are the possible ‘fates of thrombi
Propagation
Dissolution
Embolization
Organization
Recanalization
Propagation:
continues to grow
Dissolution:
Clot dissolved by fibrinolysis
Embolization:
Dislodges and travels somewhere else (thromboembolism)
Organization:
conversion to fibrous connective tissue
Recanalization:
small vessels form in the thrombis to re-establish blood flow
Infarction:
Occlusion due to thrombis and thromboembolism
Ischemia:
Hypoxia due to loss of blood supply
Morphology of infarcts
Wedge shaped, poorly defined when fresh
White infarct morphology
Arterial occlusion in solid tissues/organs
red infarct morphology
Can be venous or arterial
Venous - loosely organized tissue (lungs)
Arterial - in tissues with secondary collateral blood supply, may have originally been white
WHat do bland vs septic infarct refer to
etiology
Bland infarct:
Sterile, most common
Septic infarct:
Contaminated with bacteria, can produce an abscess
