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TFPI
Tissue factor pathway inhibitor
Heparin sulfate
Blood thinner, inc antithrombin
Thrombomodulin
Modulates thrombin by stopping it, activates protein C
EPCR
Endothelium protein C receptor: works with thrombomudulin to activate protein c decreasing 5 and 8
TPA
Tissue plasminogen factor : precursor to plasmin, eats clots
VWF
bonds to collagen, stabilizes factor 8
Adamts13
Kills vwf multimers
PAI-1 or TPAI-1
Plasminogen activator inhibitor: controls TPA (tissue plasminogen activator) from activating and eventually breaking down clots, blocks TPA until a clot needs to be broken down
TAFI
Thrombin activatable fibrinolysis inhibitor: protects fibrin clot from lysis
TXA2
Thromboxane A2: stimulates plt activation and aggregation
In vitro coag inhibitors
EDTA, citrate, oxalate, heparin
In vivo coag inhibitors
Heparin warfarin
Coagulation COFACTORS
3, 8, 5
Prothrombin/vit K factors
10 9 7 2 C S
Fibrinogen factors
5, 8, 13
Contact factors
11, 12, PK, HMWK
what else does thrombin do
when thrombin is low: aggregates
when thrombin is too high, activates protein C to degrade 5 and 8
PT
Extrinsic pathway
inovin reagent
11-14
Warfarin/oral coumodin affects this test (K factor 7)
PTT
Intrinsic pathway
Actin FSL reagent
23-35
Heparin affects it (factor 8)
A2 antiplasmin/ alpha 2 plasmin inhibitor
Inhibits plasmin
Arterial thrombus
White clots
From wbcs and plts
Activates monos, plts, and macrophages within fatty plaque
Cause of 80% myeloid infarction and strokes
^HS-CRP, homocysteine, lipids , fibrinogen
Venous thrombus
Red thrombi
Damage to EC and RBCs trapped in clot behind valve
Emboli move from legs to lungs
TTC
Thrombin-thrombomodulin complex: involves thrombomodulin which activates EPCR to activate protein CS
Antithrombin
Works with heparin (PTT affected)
Degrades thrombin, 12, 11, 10, 9
Acquired antithrombin deficiency
Decrease in antithrombin levels: from overconsumption
Decrease in antithrombin = more clots
Liver disease (no liver, no antithrombin)
Nephrotic syndrome (antithrombin leak in urine)
Prolonged heparin use (too much heparin is bad)
DIC
Congenital antithrombin deficiency
90% Type 1: low amount
10% Type 2: not functional
Lupus anticoagulant
Ab that binds to phospholipids: causes clots to form
Factor 5 Leiden
Protein C resistance
Glutamine for arginine mutation, prevents factor 5 from being degraded, clots form
Prothrombin G20210A mutation
G2A = guanine to adenine
Actually increase prothrombin
Which increase thrombin = more clots
Increases VENOUS thrombosis
Markers for thrombosis
HS-CRP (predicts cardiovascular disease risk)
Homocysteine (arterial damage and plaque, also seen in def B12)
Fibrinogen (inc in fibrinogen and cholesterol, inc risk)
Antiphospholipid syndrome
1) Lupus anticoagulant (inc PTT)
2) anticardiolipin
3) anti beta 2 glycoprotein
Rheumatoid arthritis, SLE, after bacterial infection/antibiotics