Coagulation Flashcards Preview

Modules > Coagulation > Flashcards

Flashcards in Coagulation Deck (86)
Loading flashcards...
1

Normal INR

0.8-1.2

2

Warfarin INR

2-3

3

Normal PTT

22-35 seconds

4

Vit K dependent factors

2,7,9,10
Protein C and S

5

Normal PT

Less than 14

6

Which coagulation factor is not produced by the liver?

Factor 8, made by epithelial cells

7

Mixing study

1:1 mix of patient blood and normal blood
Ordered after elevated PT or PTT
If it corrects- deficiency in factors
If doesn't correct- inhibits factors

8

What are the three main anti- platelet factors made by endothelial cells?

1. NO- vasodilates, inhibits aggregation
2. PgI2- vasodilates, inhibits aggregation
3. ADPhosphotase- degrades ADP which is released by dense granules and activates platelets

9

What are the three major anticoagulant factors made my endothelial cells?

1. Heparin like molecules- activated anti thrombin 3
2. Thrombomodulin- binds thrombin and makes it activate protein C which together with protein S ( also made by endothelial cells) inactivated factors V and VIII
3. TFPI

10

What anti fibrinolytic factor do endothelial cells secrete when activated?

Plasminogen activator inhibitors (PAI)

11

What are the receptors on platelets

1. Gp1b- binds vwf
2. GpIIb/IIIa- binds fibrin and links platelets
3. GpVI- binds collagen
4. P2Y12 and P2Y1- bind ADP
5. PAR-1- binds thrombin

12

Contents of alpha granules

White on EM
VwF, fV, fibrinogen, fVIII, PDGF, TGFb, RANTES (attracts monocytes)

13

Contents of dense bodies

ADP/ATP, Ca, serotonin

14

What other constituents are there in platelets besides granules?

Microtubles under membrane help it change shape
Has the capacity to make TXA2 when activates which aggregates platelets and causes vasoconstriction

15

Why does aspirin lower risk of thrombosis if it blocks prostacyclin and thromboxane synthesis?

Platelets cannot make more COX because can't synthesize new profit while endothelial cells can so endothelial cells can overcome the blockade

16

What are the non clotting cascade effects of thrombin and how are they propagated?

Thrombin activates PARs ( protease activated receptors) by cleaving the seven transmembrane protein and thus activating a G coupled cascade

1. Platelet activation and txa2 secretion
2. Endothelial activation to generate leukocyte adhesion molecules and tPA and NO and PGI2
3. Increase leukocyte adhesion to endothelium

17

Anti thrombin action

Bind heparin like molecules on endothelial cells or heparin drug
Inhibits factors 9,10,11,12

18

Protein c and s action

Vit K dependant ( with 2,7,9,10)
Inhibit factor 8 and 5

19

What are fibrin split products and how are they used?

Fibrin breakdown by plasmin results in D-dimers which can be used to diagnose DIC, DVT, or PE

20

How does plasminogen become plasmin

Factor 12
tPA- made by endothelial cells, most active when bound to fibrin which limits its action to recent thrombi
uPA(urokinase) - in plasma, can be cleaved to active form by streptokinases

21

How is free plasmin controlled

Bound to a2 anti plasmin in blood

22

What endothelial cell product blocks the fibrinolytic cascade?

Plasminogen activator inhibitors
Activity increase by inflammatory cytokines esp IFN y and probably responsible for intravascular thrombosis in severe inflammation

23

Primary hypercoagulability

Inherited
1. Leiden/ factor V mutation- makes resistant to protein C , increased risk venous thrombosis, change of aa residue
2. Prothrombin mutation- g to a substitution, increases prothrombin synthesis, increase risk venous thrombosis
3. Congenitally elevated homocysteine

Heterozygotes not that bad off until they have additionally acquired risk like bedrest, pregnancy, long airplane ride

24

Secondary hypercoagulability

1. Stasis or vascular injury
2. Hyperestrogenic states- oral contraceptives and pregnancy, increase hepatic synthesis of coag factors and decreased synthesis of anti thrombin III
3. Cancers - tumors can release procoagulant products like mucin from adenocarcinoma
4. Age- lower PGI2

25

What are the additives for a PT

plasma, Ca, thromboplastin (brain extract)

26

What are the additive for PTT

plasma, Ca, kaolin (XII activator), and cephalin (phospholipid layer substitute)

27

DDx for bleeding due to vascular instability/fragility

1.vit C deficiency
2.systemic amyloidosis
3. Chronic glucocorticoid use
4. inherited conditions of connective tissue
5. vasculitides (meningococcemia, infective endocarditis, rickettsial disease, typhoid, and HSP)

28

Clinical characteristics of bleeding due to vascular fragility

spontaneous petechiae and ecchymoses of skin and mucous membrane

29

Clinical characteristics of platelet disorder

easy bruising, nosebleeds, excessive bleeding from minor trauma, menorrhagia

30

Clinical characteristics of coagulation disorder

bleeding in joints and lower extremities (areas subject to trauma)