Thrombosis Embolism and Infarction Flashcards
What is a thrombus?
A solidification of blood contents that forms in the vascular system during life. (Blood clots at wounds do not count)
Name the three pathological features that lead to the development of a thrombus?
Endothelial Injury, Abnormal blood flow and hypercoagulation
Endothelial damage in important formation of thrombi where? and name some examples
- In heart and aorta.
- Some examples are thrombi developed of the left ventricle at sites of myocardial infarction and on ulcerated plaques in advanced atherosclerosis.
How can the endothelial become damaged?
Radiation Injury, Both endogenous and exogenous chemical agents, Bacterial toxins/endotoxins, Immunological Injuries, Neoplastic involvement (tumours)
Describe the role of platelets after injury to vessel
- Adhesion (to exposed collagen with help of von Williebrand’s factor)
- Secretion (of granules such as ADP, thromboxane A2 and Pf4 which recruits more platelets)
- Aggregation (fibrin helps adhesion)
WBC’s and RBC’s can become trapped in thrombus causing occlusion
Name some disorders that occur with deficiency of GpIIb-IIIa and GpIb
GpIIb-IIIa - Glanzmann’s Thromboasthenia
GpIb - Bernard-Soulier Syndrome
Results in inability to form clots
What are the two abnormal types of blood flow and what to they contribute to?
Turbulence (blood flow in all directions, not linear) - development of arterial and cardiac thrombi
Stasis (low blood flow) - venous thrombosis
Describe how the turbulence and stasis blood flow contribute to formation of thrombi
- Disrupt laminar flow
- Prevent dilution of coagulation factors
- Retard the inflow of inhibitors of clotting factors
- Promote endothelial cell activation
Define hypercoagulation
Alternation of the blood coagulation mechanism that in some way predisposes thrombosis
What is primary hypercoagulation?
Its genetic and can be because of;
- Mutation in factor V gene
- Antithrombin III deficiency
- Protein C and S deficiency
What is secondary hypercoagulation?
It is acquired and can be;
High risk - Result of bed rest, myocardial infarction, tissue damage, DIC
Lower risk - AF, cardiomyopathy, oral contraceptive, sickle cell anaemia and smoking.
What are the three different morphology of thrombi?
Mural thrombi (chambers of heart or aorta), Arterial Thrombi, Venous Thrombosis (Phlebothrombosis
Describe some of the features of arterial thrombi
- Usually occlusive, may be mural and are frequently seen (in order of commonality) Coronary, cerebral and femoral. Grey-white
Describe the histological appearance of a thrombus
Key - Lamination’s called lines of Zahn. These are pale bands of fibrin and platelets with red bands of RBC’s
Describe some of the features of venous thrombosis (Phlebothrombosis)
- Can be occlusive and are dark red.
- 90% of time effect veins of lower limbs (deep calf, femoral, popliteal and illiac)
What is Thrombophelbitis
When a vein becomes very inflamed and then thrombosed
Describe the fate of thrombi
- Resolved (using drugs)
- Embolization to lungs
- Incorporated into wall, narrowing lumen
- Organisation and recanalization
Describe the clinical appearance of arterial thrombosis
Importance - Obstruction and sources of emboli
Presentation - Lose of pulses distal to thrombus, 5P’s (pulseless, perishing cold, pale, painful and parasthesia) and tissue eventually dies and gangrene results
Describe the clinical correlations of venous thrombosis
Superficial - Congestion, swelling, pain and tenderness but rarely embolise.
Deep - Foot and ankle oedema, Homans’ sign but also could be asymptomatic until it embolised.
Describe some of the treatments for thrombosis
Prevention - Stockings (squeeze deep veins)
Anticoagulant drugs - Warferin (oral) or Heparin (i.v or s.c). Warfarin takes a day to start working so given as after treatment, heparin used for quick effects.
What is an embolus? What percent arise from thrombi?
The detachment of intravascular solid, liquid or gaseous mass carried by blood to a site distant from origin. 99% arise from thrombi so unless otherwise stated, it usually means thromboembolism.
Rare forms of emboli include fragments of what?
Bone/bone marrow Atheromatous debris Fat Bits of tumour Bubbles of air/nitrogen
Describe the classifications of embolism
Pulmonary embolism, Systemic embolism Amniotic fluid embolism Air embolism Fat embolism
Describe some of the features of a pulmonary embolism
Occlusion of a large/medium pulmonary artery is embolic until proven otherwise. Over 95% of pulmonary emboli arise from thrombi from large deep leg veins.
What is a saddle embolus?
A large embolism that bifurcation of the main pulmonary artery - causes instant death.
Pulmonary embolism results in what?
Respiratory compromise and haemodynamic compromise. It is one of the few things that cause instantaneous death.
Smaller pulmonary emboli may cause?
Acute respiratory and cardiac problems;
Chest pain, dyspnoea (difficulty breathing), shock, increased LDH and haemoptysis (coughing up blood)
How can you diagnose pulmonary emboli?
X-ray, X-ray with radionucleotides and some occlusion can put strain on the heart which is picked up on ECG
Describe some of the features of Systemic Embolism
- Emboli that travels through arterial circulation.
- 80%ish arise from thrombi within heart
- Less common sources include ulcerated atherosclerotic plaque and aortic aneurysm etc
- Most common sites of lodgement are lower extremities (70-75%), brain (10%), viscera and then upper limb
Describe some of the features of air embolism
- Presence of bubbles within circulation that obstruct vascular flow and damage tissue (barotrauma)
- Can occur; In delivery or abortion, performance of a pneumothorax, injury to chest wall or decompression sickness (Caisson disease)
Describe some of the features of Caisson disease
- Rapid decompression causes helium and nitrogen to persist and form a gaseous emboli. Effects scuba divers.
Treatment - Recompression chamber
Describe some features of fat embolism
- Small globules of fat in circulation
- Can occur with long bone fractures and less common soft tissue trauma and burns.
Pathenogenesis - Mechanical obstruction (microagregates of neutral fat causing occlusion) and chemical injury (free fatty acids released from fat cause toxic injury to endothelium)
Describe some of the clinical features of fat embolisms
Characterised by; Pulmonary insufficency, neurological symptoms (irritability, restlessness which progresses to delerium and coma) and anaemia and thrombocytopenia.
Symptoms only appear 24-72hrs after injury.
Describe some of the features of amniotic fluid embolism
Rare complication but cause of maternal mortality. Caused by infusion of amniotic fluid into mother’s circulation.
Patients pulmonary micocirculation at postmortem contains - Epithelial squames, lanugo hair, fat from vernix caseosa and mucin from baby respiratory/GI
what is the clinical presentation of amniotic fluid embolism
Resp difficulty (deep cyanosis and cardiovascular shock), followed by convulsions and the coma.
What is infarction and what are the main causes and some other causes
Occlusion of vascular supply to tissue causing cell death. Main causes are thrombosis or embolism (99%). Other causes can be vasospasm, expansion of atheroma, compression of vessel etc
What are some of the factors that influence development of an infarct?
Nature of vascular supple (kidneys and spleen have single blood supply)
Rate of development of occlusion
Vulnerability to hypoxia (brain can only last 3-4mins without air, where are myocardial cells are up to 30mins)
Oxygen content of blood
Describe the different types of infarct
Red (haemorrhagic) - venous occlusion
White (anaemic) - arterial occlusions
Septic/bland - collection of bacteria causing blockage of BV.
Describe the histology of infarction
Ischaemic coagulation necrosis (mins-days)
Inflammatory response (hours-7 days)
Reparative response (1-2 weeks)
Scaring (2weeks-2 months)
