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1

4 statges of hemostasis

HUGE SLIDE BUT THE BASIS AND INTRO INTO ALL THAT FOLLOWS

 

  1. VASCULAR CONSTRICTION- limits the flow of blood to the area of injury
  2. PLATELETS become ACTIVATED by thrombin and aggregate at the site if injury (temp loose PLATELET PLUG). Fibrinogen is responsible for stimulating platelet clumping (platelets bind to collagen that becomes exposed following rupture of the endothelial lining of vessles)
  3. Activated platelets release ADENOSINE-5'-DIPHOSPHATE (ADP) and TXA2 (which activates additional platelets), SEROTONIN, PHOSPHOLIPIDS, LIPOPROTEINS, and other proteins important for the coagulation cascade. Activated platelets change their shape to accomodate the formation of the plug.
  4. to insure stability of the initial loose platelet plug, a FIBRIN MESH (CLOT), forms and entraps the plug. if the plug contains only platelets it is termed WHITE THROMBUS, if red blood cells are present it is called RED THROMBUS.

The clot must be dissolved in order for normal blood flow to resume following tissue repair. the dissolution of the clot occures through the action of PLASMIN

2

test that knowledge

initial phase if hemostasis


vascular constriction

3

to test that knowledge

platelets become activated by what?


thrombin

4

to test that knowledge

what is responsible for stimulating platelet clumping


fibrinogen

5

to test that knowledge

activated platelets release what?

(6)


ADP

TXA2

Serotonin

Phospholipids

Lipoproteins

other proteins

6


to test that knowledge

which protein released by activated proteins, activates additional platelets

TXA2

7


to test that knowledge

what forms to entrap the plug to insure stability


Fibrin mesh (clot)

8

to test that knowledge

  1. If the plug contains only platelets it is called what?
  2. If it containd RBC ot is called what

  1. white thrombus
  2. red thrombus

9

to test that knowledge

dissolution of the clot occurs through the action of what?


plasmin

10


Whooooo made it time for an easy question to make you feel smart again!

1+1=?

2

11

picture time

now that you feel better. draw me a pic representation of what you want your edothelial layer to look like with a break and blood in the middle

keep this we'll expand

12

Physiology, pathophysiology, and pharmacology of hemostasis

what is the patho for adhesion of platelets

 

  1. Damage to endothelial surface → subendothelial collagen exposure
  2. production/release of vWF form endothelial cells
  3. vWF anchors platelets to subendothelial collagen vascular wall

vWF= Von Willebrad factor

13

you now know the adhesion of plateletes draw it!!!

  1. Damage to endothelial surface → subendothelial collagen exposure
  2. production/release of vWF from endothelial cells
  3. vWF anchors platelets to subendothelial collagen vascular wall

Hint expand your 1st pic

14


What is the most common inherited coagulation defect


Von Willebrands Disease

15

what is tx for Von Willebrands disease

DDAVP- it releases vWF from endothelial cells

or

Give FFP

16

Physiology, pathophysiology, and pharmacology of hemostasis

patho of the activation of plateletes

  1. prothrombin → thrombin (IIa) which activates platelets
  2. Shape changes and realease of mediators (TXA2 and ADP)
  3. TXA2 and ADP promote platelet aggregation

17

now that you know the patho for activation of platelets draw it!!!

  1. prothrombin → thrombin (IIa) which activates platelets
  2. Shape changes and realease of mediators (TXA2 and ADP)
  3.   TXA2 and ADP promote platelet aggregation

18

Physiology, pathophysiology, and pharmacology of hemostasis

What is the patho for aggregation of platelets

  1. TXA2 and ADP "uncover" fibrinogen receptor (GPIIb/IIIa)
  2. this allows fibrinogen (I) to bind to the receptor and further aggregate platelets

19

  1. TXA2 and ADP "uncover" fibrinogen receptor (GPIIb/IIIa)
  2. this allows fibrinogen (I) to bind to the receptor and further aggregate platelets

 

yep your going to draw it!!! try putting all of the drawings together

20

After platelets aggregate , __1__ is woven into plateets and cross-linked (water soluble >stable)

the cross linkage requires fibrin stabilizing factor __2__

 

  1. fibrin
  2. XIII

21


mechanism of action aspirin and NSAID's


COX 1 inhibition: reduction in TXA2

 

22


All procoagulants (clotting factors) are produced in the ___1___,  with the exception of what 3? and where are they produced?

 

  1. liver
  • tissue factor or thromboplastin (III)- released from traumatized cells
  • Ca++(IV)- diet
  • vWF (VIII:vWF)- vascular endothelial cells

23


whhat are the vit K dependent factors

 

  • II
  • VII
  • IX
  • X
  • protein C
  • Protein S

24


what are the roman numerics for the following clotting factors

  • fibrinogen
  • prothrombin
  • tissue factor/thromboplastin
  • Von Willibrands factor

  •     fibrinogen- I
  •     prothrombin- II
  •     tissue factor/thromboplastin III
  •     Von Willibrands factor VIII:vWF

25


tissue factor/thromboplastin (III) comes from where?

Vascular wall and extravascular cell memerane; released from traumatized cells

26


clotting cascade TISSUE FACTOR PATHWAY (Extrinsic)

(Factor III)

  • Damage occurs from outside of blood vessel → triggers release of tissue factor
  • Tissue factor comes in contact with factor VII
  • Complexed with Ca++ on platelet → activates factor X

27


clotting cascade TISSUE FACTOR PATHWAY (Extrinsic)

  • Damage occurs from outside of blood vessel → triggers release of tissue factor
  • Tissue factor comes in contact with factor VII
  • Complexed with Ca++ on platelet → activates factor X

put this whole cascasde into a picture

28


what is the primary physiologic initiator of coagulation

(in the extrinsic pathway)


tissue factor

29

the tissua factor pathway (extrinsic pathway) is measured by what?

PT test

30


how to remember the Extrensiv pathway


you can buy the extrinsic pathway for $0.37 (III, VII)