Thrombosis, Embolism and Infarction Flashcards
What is thrombosis ?
A pathological process.
It denotes the formation of a thrombus within the non-interrupted vascular system.
What is a thrombus ?
A thrombus is a solidification of blood contents that forms within the vascular system DURING LIFE.
Pathogenesis of thrombosis
Endothelial injury
Alterations in normal blood flow
Hypercoagulability
Give examples of where thrombus develops
Left ventricle (at sites of MI)
On ulcerated plaques in advanced atherosclerosis
Injured endocardium (cardiac surgery)
Valves with inflammatory valve disease, and prosthetic valves.
State some causes of endothelial injuries
Radiation injury
Chemical agents (exogenous and endogenous)
Bacterial toxins or endotoxins
Immunological injuries
Neoplastic involvement
State the role of platelets in thrombosis
After injury to a vessel, platelets undergo 3 important reactions :
- Adhesion
- Secretion
- Aggregation
Describe primary haemostasis
- Platelet adhesion
- Shape change
- Granule release
- Recruitment
- Aggregation
Problem with : von Willebrands factor
Causes von willebrands disease
Problem with : GpIb
Causes Bernard-Soulier Syndrome
Problem with : GpIIb-IIIa
Causes Glanzmann’s Thrombasthenia
Describe secondary haemostasis
- Tissue Factor
- Phospholipid Complex Expression
- Thrombin Activation
- Fibrin Polymerisation
State alterations in blood flow
Turbulence
Stasis
Turbulence
Contributes to development of arterial and cardiac thrombi
Stasis
Contributes to venous thrombosis
What do turbulence and stasis do ?
Disrupt laminar flow
Prevent the distribution of coagulation factors
Retard the inflow of inhibitors of clotting factors
Promotes endothelial cell activation
What is hyper-coagulability ?
Can be defined as an alteration of the blood coagulation mechanism that in some ways predisposes thrombosis.
Causes of Hyper-coagulability
Primary (genetic)
Secondary (acquired)
Describe primary cause of hyper-coagulability
Mutation in factor V gene
Anti-thrombin III deficiency
Protein C and S deficiency
Describe the secondary cause of hyper-coagulability
2 risk groups
High risk
Low risk
High risk for hyper-coagulability
Bed rest (immobilisation)
MI
Tissue damage
Carcinoma
Prosthetic valves
DIC
Low risk for hyper-coagulability
AF
Cardiomyopathy
Nephrotic Syndrome
Oral Contraceptive
Sickle cell anaemia
Smoking
Phlebothrombosis
Venous thrombosis
Mural Thrombi
Solidification of blood contents occurring in the chambers of the heart/aorta
Arterial thrombi
Usually occlusive
May be mural
Frequent in arteries
Grey, white and friable
State the common places for arterial thrombi
(most common last)
Coronary
Cerebral
Femoral
Describe the histological appearance of thrombus
Venous thrombosis
Invariably occlusive and dark
Affects the veins of the lower extremities (90%)
State where venous thrombi form
Deep calf
Femoral
Popliteal
Iliac veins
State the fates of the thrombus
5 Fates
- Resolution
- Embolisation to lungs
- Organised and incorporated into wall
- Organised and recanalised
- Propagation towards heart
Clinical correlations of thrombi
Cause obstruction of arteries and veins
Provide possible sources of emboli
5 P’s of Arterial Thrombosis
Area becomes :
- Perishing cold
- Pale
- Painful
- Paraesthesia
- Pulse loss (distal to thrombus)
What happens due to arterial thrombosis ?
Eventually tissue dues and gangrene results
Symptoms of superficial venous thrombosis
Congestion
Swelling
Pain
Tenderness (rarely embolism)
Symptoms of deep venous thrombosis
Foot and ankle oedema
Homan’s sign
Hofman’s sign
Discomfort in the calf muscles on forced dorsiflexion of the foot with the knee straight.
Treatment for thrombosis
Stockings (prevention)
Anticoagulant drugs
Function of anticoagulant drugs
Prevent the clot form growing any larger and to prevent/stop an embolism
State the 2 main forms of anticoagulant drugs
Heparin
Warfarin (oral)
What is an embolus ?
A detached intravascular solid, liquid or gaseous mass that is carried by the blood to a distant site from its point of origin.
Thromboembolism
99% of all emboli arise in thrombi
What do rare forms of emboli include ?
Fragments of :
- Bone/marrow
- Atheromatous debris
- Fat droplets
- Bits of tumour
- Foreign bodies
- Bubbles of air or nitrogen
Pulmonary embolism
Occlusion of a large/medium sized pulmonary artery
> 95% arise in thrombi within large deep veins of lower leg
Saddle embolism
Rare type of acute pulmonary embolism (PE) that can lead to sudden hemodynamic collapse and death
Lines of Zahn
Thick bands formed by nested platelets wrapped in fibrin.
CHARACTERISTIC of thrombus
Large PE
(pulmonary embolism)
Virtually instantaneous death
Pulsless Electrical Activity
Smaller PE
(pulmonary embolism)
Acute respiratory and cardiac problems
How to detect pulmonary embolism ?
Pulmonary Lung Scanning (using RADIO-NUCLEOTIDES)
ECG - occlusion puts strain on heart
Chest X-ray : wedge shaped infiltrate
SPIRAL CT
Systemic embolism
Emboli that travel through the arterial circulation
80-85% arise from thrombi within the heart
State the major sites of lodgement of systemic embolisms
Lower extremities (70-75%)
The brain (10%)
Viscera (10%)
Upper limbs (7-8%)
Air embolism
Presence of bubbles of air or gas within circulation.
This obstructs vascular flow and damages tissues.
Barotrauma
Air embolism
Causes of air embolism
Delivery/abortion
Performance of pneumothorax
Injury to the lung or chest wall
Caisson disease or compression sickness
Who does Caisson disease affect ?
Scuba and deep sea divers
Workers engaged in underwater tunnelling
(if individual decompresses too rapidly, then helium and nitrogen tend to persist to form gaseous emboli)
Acute form of air embolism
The bends/ the chokes
Chronic form of air embolism
Caisson disease
Treatment of air embolism
Recompression chamber
Fat embolism
Minute globules of fat can be demonstrated in circulation following :
- Fractures of shafts of long bone
- Soft tissue trauma and burns
Fat embolism syndrome
1% of individuals with severe skeletal injury
Pathogenesis of fat embolism
Mechanical obstruction
Chemical injury
Fat embolism histology
Rounded holes appearing in vascular spaces
Characteristics of fat embolism
Pulmonary insufficiency
Neurological symptoms
Anaemia and Thrombocytopenia
Onset of symptoms of fat embolism
24-72 hour period
- tachypnea
- dyspnea
- tachycardia
- irritability
- restlessness
Amniotic fluid embolism
Rare complication of labour
Maternal mortality (86%)
Infusion of amniotic fluid into maternal circulation
Pulmonary microcirculation contents
Epithelial squames from foetal skin
Presentation of amniotic fluid embolism
Respiratory difficulty
Convulsions
Profound coma
Infarction
Area of ischaemic necrosis caused by occlusion of blood supply
Main causes infarcts
Thrombosis
Embolism
Other causes of infarcts
Twisting of vessels
Vasospams
Traumatic rupture
Factors that influence the development of infarct
Nature of vascular supply
Rate of development of occlusion
Vulnerability to hypoxia
Oxygen content of blood
State the 3 types of infarct
Red
White
Septic
Red infarct
Haemorrhage
- venous occlusions
- in loose tissues
- in tissues with dual circulation
White infarct
Anaemic
- arterial occlusions
- solid organs
State dual supply
Liver
Hand
Intestines
State single supply
Kidneys
Spleen
Time of Ischaemic coagulative necrosis
Minutes to Days
Time of inflammatory response
Hours to 7 days
Time of restorative response
1-2 Weeks
Time of scarring
2 weeks to 2 months
