Thrombosis Embolism and Infarction Flashcards
define thrombus
a solidification of blood contents that forms within the vascular system during life.
define thrombosis
this is a pathological process that denotes the formation of a thrombus within the noninterupted vascular system
what is the first aspect which contributes to the pathogenesis of thrombosis
endothelial injury - important in thrombi formation in the heart and arteries
what are the other potential bases for endothelial injury
radiation injury chemical agents: exogenous and endogenous bacterial toxins and endotoxins immunologic injuries neoplastic involvement
what are the roles of platelets in thrombosis
after injury to a vessel, platelets undergo three important reactions:
- adhesion
- secretion (release reaction)
- aggregation
all these processes are collectively known as PLATELET ACTIVATION
What happens to blood vessels during the first steps after the initial injury
VASOCONSTRICTION
PRIMARY HEMOSTASIS
constriction of BVs
platelets then adhere to the exposed collagen and undergo a change in shape and become square.
they then release their granules into the lumen which in turn recruits more platelets
this results in the formation of a homeostatic plug
what granules do platelets secrete
ADP = adenosine diphosphate TXA2 = thromboxane A2 Pf4 = platelet factor 4
how do the platelets adhere to the collagen and how do they adhere to each other
they adhere to the surface via von williebrand factor and Glycoprotein Ib and adhere to eachother via fibrinogen and Glycoprotein IIb-IIIa
what is a definceicny in GpIIb-IIIa complex called
glanzmanns thrombasthenia
what is a deficiency in GpIb called
Bernard-soulier syndrome
SECONDARY HEMOSTASIS
When several layers have been formed tissue factor is released
- phospholipid complex expression which leads to the activation of thrombin
- this in turn causes fibrin polymerisation which acts as a strong glue
THROMBUS AND ANTITHROMBOTIC EVENTS
This newly formed mass could grow to occlude the vessel but the release of:
t-pa (fibrinolysis)
thrombomodulin - acts by blocking the coagulation cascade so there is no more build up
PREVENTS THIS
What are the two types of alterations in blood flow
turbulence = arterial and cardiac thrombi stasis = venous thrombi
what is the role of the alterations in blood flow towards thrombosis pathogenesis
- disrupt laminar flow
- prevent dilution of the coagulation factors
- retard the inflow of inhibitors of clothing factor
- promote endothelial cell activation
what is hypercoagulability
an alteration of the blood coagulation mechanism that In some what predisposes thrombosis. Primary = genetic Protein C and S deficiency Secondary = acquired Bed rest, tissue damage, MI, Carcinoma
Mural thrombi
applied to one wall of underlying structure, occur in the capacious lumina of the heart chambers and aorta
arterial thrombi
usually occlusive
may be mural
frequent in coronary, cerebral, femoral
appears grey-white and are friable (easily broken)
when looking at histology how can you tell its a thrombus
lines of Zahn
pale band = fibrin and platelets
red band = RBC trapped between the fibrin
venous thrombosis
invariably occlusive and appear dark red , they mostly effect veins of the lower extremities
- deep calf
- popliteal
- iliac veins
thrombophlebitis
inflamed and then becomes thrombosed
arterial thrombosis
- loss of pulses distal to the thrombus
- THE 5 P’S area becoming perishing cold, pale, painful, paraesthesia
- eventually tissue dies and gangrene results
Symptoms of a superficial venous thrombosis (saphenous system)
congestion, swelling, tenderness (these rarely embolise)
symptoms of a deep venous thrombosis
foot and ankle oedema, humans sign (dorsiflexion of the foot and pain in the calf as a result)
could be auto symptomatic and recognised only when they have embolised
what are some treatment options for thrombosis
stockings as a prevention
anticoagulant drugs which aim to prevent the clot growing any larger and to prevent or stop embolism
what are the two anticoagulant drugs most commonly used
heparin (intravenously or subcutaneously
warfarin (orally) only starts to work after one day so start on heparin first
definition of an embolism
a detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin
what are some other causes of an emobolism
bits of tumour
foreign bodies
bubbles of air or nitrogen
pulmonary embolism
occlusion of a large or medium sized pulmonary artery is embolic in origin until proven otherwise
most occur in the large deep veins of the lower leg
what is a saddle embolus
large emboli that lodge in the bifurcation
what are the two pathophysiologic consequences of emboli
respiratory compromise
haemodynamic compromise
a large PE is one of the few causes of virtually instant death (pulseless electrical activity PEA)
what are some signs of a small pulmonary embolism
occlusion can put some strain on the heart which can be evident on an ECG
chest X-ray may disclose a pulmonary infarct as a wedge shaped infiltrate
systemic embolism
refers to emboli that travel through the arterial circulation, these almost always cause infarction
- lower extremities
- the brain
- viscera
- upper limbs
air embolism
the pressure of air or gas within the circulation obstruct vascular flow and damage tissues BAROTRAUMA can happen during delivery or abortion caisson disease (scuba divers treated in recompression chamber) or decompression sickness
fat embolism
minute globules of fat can often be demonstrated in the circulation following
- fractures of the shafts of long bones
- soft tissue traumas and burns
- fat embolism syndrome
mechanical obstruction and chemical obstruction (free fatty acids released from fat globules result in toxic injury to the vascular endothelium)
for histology used frozen sections and fat stains
characterised by:
- pulmonary insufficiency
- neurologic symptoms
- anaemia and thrombocytopenia
symptoms appear after the latent 24-72 hour period and there is a sudden onset of tachypnoea, dyspnoea, and tachycardia, irritability and restlessness
amniotic fluid emobolsism
infusion of amniotic fluid into the lateral circulation
pulmonary circulation POST MORTUM would contain epithelial squares from foetal skin and other things
- profound respray difficulty (Depp cyanosis and cardiovascular shock
- followed by convulsions and profound coma
infarct
an area of ischaemic necrosis cause by the occlusion of arterial supply or venous drainage in a particular tissue
two causes:
thrombosis and embolism
twisting of vessels and vasospasm
factors which influence development of an infarct
nature of the vascular supply
rate of development of the occlusion
vulnerability to hypoxia
oxygen content of blood
what are the two types of infarcts
red (haemorrhagic): - venous occlusions - in loose tissues - in tissues with dual circulation white (anaemic) - arterial occlusions - solid organs septic or bland - bacteria collection
histology of an infarction
ischaemic coagulative necrosis but liquefactive necrosis in the CNS
inflammatory response (hours - 7 days)
reparative response (1-2 weeks)
scaring (2weeks - 2 months)
