9. Hypercoagulable States

Question 1

Thrombosis

Answer 1

Blood clot (thrombosis) with a non-traumatized blood vessels

Question 2

Etiology of venous thromboembolism (VTE)

Answer 2

Virchows triad:

Endothelial injury: pro-coagulation changes - down regulation of thrombomodulin (TM), antifibronolytic effects

Abnormal blood flow: turbulence, stasis

Hyper coagulability: inherited or acquired

Question 3

Venous thromboembolism

Answer 3

Most common clinical presentation of venous thrombosis

DVT

PE

Question 4

Pathogenesis of DVT

Answer 4

Decrease flow of oxygenated blood in veins causes hypoxia endothelial state

Coagulation cascade begins

Calf DVTS asymptomatic - skeletal muscle pump helps prevent DVTs by moving blood past the valves

Proximal DVTs - symptomatic and can embolism to form PE

Question 5

Hypercoagulable states

Answer 5

Primary (genetic) - prothrombin mutation can be positive (too much) or negative (not enough thrombin). If we do not make thrombin: fibrinogen will not convert to fibrin

Secondary (acquired):
Prolonged bed rest/immobilization
Myocardial infarction
Tissue injury (surgery, fracture, burn)
Prosthetic cancer valves
Disseminated intramuscular coagulation (DIC)

Question 6

Atrial vs venous thrombosis

Answer 6

Atrial

Source: aortic plaques, aortic mitral valves, heart chambers
Disease: acute coronary syndrome (ACS) ischemic stroke, limb claudication/ischemia (lower extremity have extreme pain

Venous

Source: combination of factors in virchow triad, vein valves
Disease: DVT, PE

Question 7

Fate of thrombus

Answer 7

Propagation - thrombus enlargement by added fibrin and platelets

Embolization - dislodging and transporting elsewhere

Dissolution - activation of fibronlytic factors (tPA)

Organization and recanalization - growth of endothelial cells, SMC and fibroblasts, lysosomal enzymes digest center of thrombus

Question 8

Phlebitis

Answer 8

Benign self-limited disorder

If larger veins get involved (superficial vein thrombosis ) SVT - spread into deep vein system (DVT) - PE

Question 9

Superficial phlebitis

Answer 9

Inflammation

Can cause pain and inflammation involving a vein in the absence of thrombus

Question 10

Superficial thrombophlebitis

Answer 10

Combination of inflammation and formation of thrombus

Presence of symptoms of venous inflammation and confirmed thrombosis of tributary veins

Question 11

Superficial vein thrombosis (SVT)

Answer 11

Thrombosis of axial veins (femoral) can Cause thromboembolism

Question 12

Risk factors/causes venous thrombosis.thromboembolism

Answer 12

Venous stasis

Abnormalities of coagulation or fibronlysis

Endothelial dysfunction

Question 13

Disseminated intravascular coagulation (DIC)

Answer 13

Systemic process with potential for causing thrombosis or hemhorrage

Causes: 
Sepsis
Malignancy (pancreatic, gastric, ovarian, brain tumors)
Trauma to CNS - endothelial dysfunction
Obstetrical complications

Question 14

Pathophysiology of DIC

Answer 14

Coagulation and fibrinolysis becomes abnormally (often massively) activated in blood vessels

Ongoing coagulation and fibrinolysis

Must have underlying condition

Question 15

Embolus

Answer 15

Traveling detached intravascular material

Question 16

Types of embolisms

Answer 16

Pulmonary thromboembolism - for DVTs

systemic thromboembolism - from intracranial thrombi

Fat embolism - soft tissue crash or skeletal injury

Air embolism - circulating gas bubbles

Question 17

Infarction

Answer 17

Occlusion of either arterial supple or venous drainage - ischemic necrosis

Majority are due to thrombosis/embolism

Question 18

Influential factors in infarction development

Answer 18

Anatomy of vascular supply - existence of an alternative blood supply

Rate of occlusion - slowly developing - collateral blood supply (angiogenesis = formation of new blood vessels)

Tissue vulnerability to hypoxia