Thrombosis Embolism and Infarction Flashcards

1
Q

define thrombus

A

a solidification of blood contents that forms within the vascular system during life.

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2
Q

define thrombosis

A

this is a pathological process that denotes the formation of a thrombus within the noninterupted vascular system

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3
Q

what is the first aspect which contributes to the pathogenesis of thrombosis

A

endothelial injury - important in thrombi formation in the heart and arteries

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4
Q

what are the other potential bases for endothelial injury

A
radiation injury 
chemical agents: exogenous and endogenous 
bacterial toxins and endotoxins 
immunologic injuries 
neoplastic involvement
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5
Q

what are the roles of platelets in thrombosis

A

after injury to a vessel, platelets undergo three important reactions:
- adhesion
- secretion (release reaction)
- aggregation
all these processes are collectively known as PLATELET ACTIVATION

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6
Q

What happens to blood vessels during the first steps after the initial injury
VASOCONSTRICTION
PRIMARY HEMOSTASIS

A

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

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7
Q

what granules do platelets secrete

A
ADP = adenosine diphosphate 
TXA2 = thromboxane A2
Pf4 = platelet factor 4
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8
Q

how do the platelets adhere to the collagen and how do they adhere to each other

A

they adhere to the surface via von williebrand factor and Glycoprotein Ib and adhere to eachother via fibrinogen and Glycoprotein IIb-IIIa

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9
Q

what is a definceicny in GpIIb-IIIa complex called

A

glanzmanns thrombasthenia

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10
Q

what is a deficiency in GpIb called

A

Bernard-soulier syndrome

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11
Q

SECONDARY HEMOSTASIS

A

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
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12
Q

THROMBUS AND ANTITHROMBOTIC EVENTS

A

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

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13
Q

What are the two types of alterations in blood flow

A
turbulence = arterial and cardiac thrombi 
stasis = venous thrombi
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14
Q

what is the role of the alterations in blood flow towards thrombosis pathogenesis

A
  • disrupt laminar flow
  • prevent dilution of the coagulation factors
  • retard the inflow of inhibitors of clothing factor
  • promote endothelial cell activation
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15
Q

what is hypercoagulability

A
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
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16
Q

Mural thrombi

A

applied to one wall of underlying structure, occur in the capacious lumina of the heart chambers and aorta

17
Q

arterial thrombi

A

usually occlusive
may be mural
frequent in coronary, cerebral, femoral
appears grey-white and are friable (easily broken)

18
Q

when looking at histology how can you tell its a thrombus

A

lines of Zahn
pale band = fibrin and platelets
red band = RBC trapped between the fibrin

19
Q

venous thrombosis

A

invariably occlusive and appear dark red , they mostly effect veins of the lower extremities

  • deep calf
  • popliteal
  • iliac veins
20
Q

thrombophlebitis

A

inflamed and then becomes thrombosed

21
Q

arterial thrombosis

A
  • loss of pulses distal to the thrombus
  • THE 5 P’S area becoming perishing cold, pale, painful, paraesthesia
  • eventually tissue dies and gangrene results
22
Q

Symptoms of a superficial venous thrombosis (saphenous system)

A

congestion, swelling, tenderness (these rarely embolise)

23
Q

symptoms of a deep venous thrombosis

A

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

24
Q

what are some treatment options for thrombosis

A

stockings as a prevention

anticoagulant drugs which aim to prevent the clot growing any larger and to prevent or stop embolism

25
Q

what are the two anticoagulant drugs most commonly used

A

heparin (intravenously or subcutaneously

warfarin (orally) only starts to work after one day so start on heparin first

26
Q

definition of an embolism

A

a detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin

27
Q

what are some other causes of an emobolism

A

bits of tumour
foreign bodies
bubbles of air or nitrogen

28
Q

pulmonary embolism

A

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

29
Q

what is a saddle embolus

A

large emboli that lodge in the bifurcation

30
Q

what are the two pathophysiologic consequences of emboli

A

respiratory compromise
haemodynamic compromise
a large PE is one of the few causes of virtually instant death (pulseless electrical activity PEA)

31
Q

what are some signs of a small pulmonary embolism

A

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

32
Q

systemic embolism

A

refers to emboli that travel through the arterial circulation, these almost always cause infarction

  • lower extremities
  • the brain
  • viscera
  • upper limbs
33
Q

air embolism

A
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
34
Q

fat embolism

A

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

35
Q

amniotic fluid emobolsism

A

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

36
Q

infarct

A

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

37
Q

factors which influence development of an infarct

A

nature of the vascular supply
rate of development of the occlusion
vulnerability to hypoxia
oxygen content of blood

38
Q

what are the two types of infarcts

A
red (haemorrhagic):
- venous occlusions 
- in loose tissues 
- in tissues with dual circulation 
white (anaemic)
- arterial occlusions 
- solid organs 
septic or bland 
- bacteria collection
39
Q

histology of an infarction

A

ischaemic coagulative necrosis but liquefactive necrosis in the CNS
inflammatory response (hours - 7 days)
reparative response (1-2 weeks)
scaring (2weeks - 2 months)