Fluid hemodynamics disorders II Flashcards
thrombus
pathological process
platelets+fibrin+cellular elements (RBC’s)
attached to vessel wall
mainly ante-mortem only
Clot
ante-mortem (extravascular) or post-mortem (intravascular)
RBC’s+ coagulation factors
not attached to vessel wall
NO platelet activation
post-mortem clot composition
coagulation factors and erythrocyte only
gross appearance of postmortem clot
- “Currant jelly clot”-> dark to red black, smooth and shiny surface, rubbery, uniform, molded to shape of vessel, NOT ATTACHED, increased RBS
- “Chicken-fat clot”-> yellow, results from settling and separation of RBC’s and plasma, supernatant, no/few RBC’s.
thrombus gross appearance
heterogeneous
arterial thrombi
pale, grey-tan, dry, friable, concentric layers, attached to vessel wall
venous thrombi
red (lots of red cells), friable, attached to vessel wall, can be confused with clot, often occlusive
composition of thrombus
fibrin, platelets, WBC, RBC, +/- bacteria
- more organized than clots, attached to vessel wall
- laminated (lines of Zahn)-> arterial thrombi, alternating layers of platelets/fibrin (pale) and RBC (dark)
criteria for thromus
- formation: ante-mortum
- cause: endothelial injury
- attachment: vessel wall
- consistency: dry
- surface: granular, rough
- vascular endothelium: damaged, rough
- organization: partial
- structure: laminated
criteria for PM clot
formation: post-mortem
cause: stagnant blood in dead animal
attachment: none
consistency: moist
surface: smooth, glistening
vascular endothelium: smooth, intact
organization: none
structure: homogenous
virchow’s triad
- endothelial injury/dysfunction
- alterations in normal blood flow
- turbulence
- stasis - hypercoagulability
- primary
- secondary
endothelial injury
heart: endocardium-> infarction, infection (myocarditis), immune reactions
valves: inflammation, prostheses (on edges-> vegetations)
arteries: ulcerated, atherosclerotic plaques, vasculitis
other causes: radiation, bacterial agents, chemical agents, catheter
alterations blood flow
turbulence
stasis
turbulence
arterial and cardiac thrombi
stasis
venous thrombi
mechanism:
-flow of blood is laminar: platelets in axial stream
-stasis &turbulence disrupt laminar flow, platelets, contact endothelium
-prevent dilution of activated clotting factors by fresh blood
-retard inflow of inhibitors of coagulation, permit build-up of thrombi
-promote endothelial cell activation
examples in alteration of blood flow
- aneurysms-> abnormal dilatation of vessels
- MI: necrotic myofibers do not contract
- ulcerated atherosclerotic plaques: local turbulence
- hyperviscosity syndrome (polycthemia)-> slow blood flow
hypercoagulability: primary
genetic defects/deficiencies
- factor V leiden
- prothrombin mutation
- elevated homocysteine levels
- antithrombin III def.
- protein C/S deficiency
- defects in fibrinolysis
hypercoagulability: secondary
acquired hypercoagulability states
- oral contraceptives
- cancer-> procoagulant tumor products (pancreatic cancer-> migrating thrombophlebitis)
- aging-> increased platelet aggregation
- heparin-induced thrombocytopenia
- anti-phospholipid antibody syndrome (lupus)
fate of a thrombus
propagation-> gets larger and moves towards heart
detachment (embolization)
lysis/dissolution
retraction-> incorporated into vessels
organization with fibrosis
recanalization: formation of capillary channels through thrombus with blood flow through lumina
types of thrombi
arterial
venous
vegetations
arterial thombi
occlusive
coronary, cerebral, femoral arteries
venous thrombosis
thrombophelbitis
- red, or stasis thrombi
- more red cells, fewer platelets
- most in deep veins of legs (pulmonary emboli)
embolism
detached intravascular solid, liquid, or gaseous masses carried by the blood stream to distant sites
- fibrinous (thrombo) emobolus-> derived from fibrin thrombus, accounts for most emboli (99% emboli)
- deep venous thrombosis to pulmonary embolism
- cardiac thrombi to brain
- atheromatous debris
- bacterial (septic) embolus
- fat embolus: sequel to bone fracture
gas embolus
rapid decompression > gas out of solution > gas bubbles
parasitic embolus
parasites in circulation (e.x filarial nematodes)
neoplastic embolus
metastasis involves entry into an dispersion by circulation
fibrocartilaginous embolus
ruptured vertebral disc fragments
amniotic fluid embolus
tear in placenta and infusion of amniotic cells into circulation
foreign bodies
bullets, catheters, hairs
pulmonary emboli
-often arise from thrombi in deep veins of lower legs
-most are CLINICALLY SILENT
-sequela:
sudden death
pulmonary hemorrhage
pulmonary infarction
pulmonary hypertension
why is it hard to infarct the lungs?
dual blood supply
-saddle embolus
systemic emboli
emboli traveling in arterial circulation
-others arise from aneurysms, atherosclerotic plaques
where do 80% of systemic emboli arise?
intracranial mural thrombi
-associated with: left ventricular wall infarcts or dilated left atria
atrial fibrillation
infarction
localized ischemic necrosis resulting from sudden reduction either of arterial blood supply or of venous drainage
types of infarctions
red
white
causes of infarcts
Arterial thrombi/thromboemboli
-local vasospams
-extrinsic vascular compression (tumor)
Expansion of antheromas with hemorrhage within plaque
Mechanical-> torsions (testis or bowel), entrapment in hernia sac
Vascular compromise by edema (anterior compartment syndrome)
most common cause of infacrts
arterial thrombi/thromboemboli
white infarcts
arterial occlusions in solid tissue (tissue to dense for seepage of blood into infarcted area)
- grossly pale
- more common
- mainly embolic
- well defined borders
- if wedged-shaped-> apex points towards focus of occlusion
red infarcts
hemorrhagic
- grossly red
- may occur with venous occlusion
- when blood flow is re-established after arterial occlusion
- previously congested tissue, sluggish venous outflow
- tissue with dual blood supplies: pulmonary, small intestine, liver
- septic infarcts
common sites of infarction from arterial emboli
brain retina heart (left ventricle) kidney small intestine lower leg
microscopic features
- coagulative necrosis (expect brain), sharply demarcated
- +/- occluded vessels, +/- congestion
- congestion and leukocyte influx in adjacent tissue, later fibrosis
outcome of infarcts are dependent on
-tissue susceptibility->brain
collateral circulation-> kidneys versus muscle
dual blood supply: lung, liver
