WorksheetsFIBRINOLYOSIS & THROMBOSIS part 2
Total questions: 32
Worksheet time: 16mins
Body’s natural response to vascular injury
Physiological thrombosis
Pathological thrombosis
Conditions that predispose an individual to thrombosis
Environmental
Inherited
Acquired
Physiological thrombosis
Pathological thrombosis
Which is NOT part of the Pathogenesis of Thrombosis?
Deficiencies of antithrombotic factors
Fibrinolytic defects
Platelet abnormalities
all can be a part of pathogenic thrombosis
Surgery
Immobilization
Pregnancy
Hormone replacement therapy
Heparin treatment
The following can cause _______
Environmental
Coagulation Abnormalities
Inherited
Coagulation Abnormalities
Acquired
Coagulation Abnormalities
all of the above
Cancer
Nephrotic syndrome
Antiphospholipid antibodies
Myeloproliferative disease
Hyperviscosity syndrome
Vasculitis
The following can cause _______
Environmental
Coagulation Abnormalities
Inherited
Coagulation Abnormalities
Acquired
Coagulation Abnormalities
all of the above
Naturally occurring clotting inhibitors
Made in liver
Inhibitory action of _______ is increased when it binds to heparin
deficiency associated with thrombosis
Antithrombin (AT)
Heparin cofactor II
Protein C
Protein S
Naturally occurring clotting inhibitors
Coagulation inhibitor
Acts against thrombin
deficiency alone is not associated with thrombosis
Antithrombin (AT)
Heparin cofactor II
Protein C
Protein S
Naturally occurring clotting inhibitors
Vitamin K dependent
Made in liver
(deficiencies cause thrombosis)
Antithrombin (AT)
Heparin cofactor II
Protein C
Protein S
Naturally occurring clotting inhibitors
Clotting factor inhibitor
thrombin-thrombomodulin complex
Antithrombin (AT)
Heparin cofactor II
Protein C
Protein S
Naturally occurring clotting inhibitors
Clotting factor inhibitor
cofactor
Antithrombin (AT)
Heparin cofactor II
Protein C
Protein S
the decreased ability of activated protein C to inactivate factor V.
Activated Protein C Resistance
APC-R
Lupus anticoagulant/antiphospholipid syndrome
single point mutation (G20210A)
Factor XII, PK, and HMWK deficiency
most common risk factor associated with inherited venous thrombosis among Caucasians
Activated Protein C Resistance
APC-R
Lupus anticoagulant/antiphospholipid syndrome
single point mutation (G20210A)
Factor XII, PK, and HMWK deficiency
genetic defect in factor V gene (Factor V Leiden)
Activated Protein C Resistance
APC-R
Lupus anticoagulant/antiphospholipid syndrome
single point mutation (G20210A)
Factor XII, PK, and HMWK deficiency
Causes an increase in concentration of plasma prothrombin
Risk of venous thromboembolism increases as the plasma prothrombin level
Thrombotic episodes develop early, before the age of 40
Activated Protein C Resistance
APC-R
Lupus anticoagulant/antiphospholipid syndrome
single point mutation (G20210A)
Factor XII, PK, and HMWK deficiency
Prolonged PTT
strangely Cause thrombosis instead of bleeding
Activated Protein C Resistance
APC-R
Lupus anticoagulant/antiphospholipid syndrome
single point mutation (G20210A)
Factor XII, PK, and HMWK deficiency
Which of the following is an inherited thrombotic disorder?
Dysfibrinogenemia
Tissue factor pathway inhibitor (TFPI) deficiency
Hyperhomocysteinemia
all of the above
◦Patients produce antibodies to phospholipids β2-glycoprotein I (β2GPI) or apolipoprotein (apo)
Activated Protein C Resistance
APC-R
Lupus anticoagulant/antiphospholipid syndrome
single point mutation (G20210A)
Factor XII, PK, and HMWK deficiency
Antibody to reagent phosphoplipid (APTT)
PTT prolonged, not corrected by addition of normal plasma in a mixing study
Activated Protein C Resistance
APC-R
Lupus anticoagulant/antiphospholipid syndrome
single point mutation (G20210A)
Factor XII, PK, and HMWK deficiency
Which is INCORRECT about Specific Factor Inhibitor?
Usually IgG immunoglobulins or abnormal proteins produced secondary to a disease process.
usually cause bleeding
not corrected by addition of normal plasma in a mixing study
Inhibit the coagulation process by specifically inactivating coagulation factors.
Purpose:
thin the blood so that thrombosis will not occur or so that the blood can flow around blood clots which have formed
Coumadin therapy
Heparin therapy
makes vitamin K dependent factors (II, VII, IX, & X) inactive
Coumadin therapy
Heparin therapy
peak effect is 36 -72 hours after administration
Coumadin therapy
Heparin therapy
at first can be thrombogenic because the effect of the drug is delayed until the coagulation factors are cleared from circulation (72-96 hours)
Long Term treatment
Coumadin therapy
Heparin therapy
Wafarin is the most common drug used
Administered orally
Monitored by Prothrombin time (PT)
Coumadin therapy
Heparin therapy
inhibits thrombin formation by inhibiting factor X activation
quickly cleared from the body
Coumadin therapy
Heparin therapy
peak effect is 2 - 4 hours
Coumadin therapy
Heparin therapy
Administered by injection
given for short term therapy
Coumadin therapy
Heparin therapy
Monitored by APTT
Therapeutic range: 1.5 - 2.5 times the normal APTT value
Coumadin therapy
Heparin therapy
Therapeutic goal 2 - 2.5 times normal PT value
Coumadin therapy
Heparin therapy
overdose
administer protamine sulfate
Coumadin therapy
Heparin therapy
overdose
administer vitamin K
Coumadin therapy
Heparin therapy
Which is NOT a characteristic of Heparin Induced Thrombocytopenia (HIT)?
Thrombocytopenia
Hypercoaglution
cause by antibody activation of platelets
Life-Threatening Thrombosis
causes bleeding and clotting simultaneously (similar to DIC)
