Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

16 Cards in this Set

  • Front
  • Back
How is platelet production stimulate?
When Plates dec.=fewer MPL receptors for TPO (constituitively made and abs by adeq. platelet number) causeing free TPO to increase, stims Stem Cells and Megakaryocytes
MPL, the binder of TPO (to keep free TPO level down when platelets are in plenty) works through which communication System
Jak/STAT (Jak2, Stat5)
& MAP Kinases
Why do platelets have receptor for Collagen
--Which platelet Factors help with this
When vessel damaged, the collagen is exposed and platelets can begin to work there
--think Thromboxane A2 & Serotonin----
Describe Step 1 of Hemostasis
Vascular Spasm (direct myogenic-NO neurons reqd.)
-Smooth MM. contracts indep.
-P.Factors Serotonin and Thromboxane A2 help
(serotonin may be impt for headache where vessels constrict)
Describe Step 2 of Hemostasis (2 steps)
Formation of a Platelet Plug--collagen exposed
1-VonWF-binds BETWEEN Plate Rec and Collagen.
2-Bind of Platelet Integrin Rec. to diff part of Collagen
=activation of platelet
-swelling and podocyts
In Step 2, after platelets are activated, they contract (release Ca+ from ER) causing Granules to Leave and the Plates Stick to the Vessels and to Each other. What are two important factors in platelets for the stickiness
Thromboxane A2 and ADP
--note, Thromboxane can be blocked by Aspirin (acetylminophen)
What are 3 essential steps of Step 3 of Homeostasis. The Blood Coagulation Step resulting in Clot Retraction
1. Formation of Prothrombi Activator
2. Activation of Thrombin
3. Creation of Fibrin from Fibrinogen (constituitively produced by liver, like TPO)
Name & Describe Step 4 of hemostasis
Repair of Damage
-PDGF--stims fibroblasts to grow in area
-Fibroblasts diff into smooth muscle and contract to close hole (note, bleeding may have ceased as early as end of step 2)
Which Step do the following occur
-excess fluid in clot removed/clot solidified
--new platelets reqd to contract fibrin polymer
These occur during Step 3--Blood Coagulation

-this is the clot retraction phase
Which two factors are Required to get rid of the Clot
1. Plasminogen --constituitively made by liver/floats inactively
2. tPA--Tissue Plasminogen Activator--released by damaged tissue.

note, circulating plasminogen stays inactive by inhibitio of tPA inhibitor in the blood)
Fibrin form Fibrinogen is made via what
--initially makes Fibrin,
Later, it chews up Fibrin clot indirectly via Plasmin
How does Thrombin indirectly chew up Fibrin Cloat (which it initially helped form)?
What intermediate Pr/Factor is required
Thrombin activates Protein C
Protein C INactivates tPA inhibitor (tissue plasminogen inhibitor)
activated tPA turns Plasminogen to Plasmin, which lyses Fibrin
In un-injured Blood Vessel, name 3 features of membrane that prevent unwanted clot formation
1. Smooth Surface prevents rupture of plates
2. Glycocalyx is neg, repels plates
3. Thrombomodulin
List 4 Chemicals that limit clotting
1. Fibrin, binds Thrombin, prevents it from working
2. Prostacyclin (PGI2)--vasodilates, limits Plate aggreg
3. Antithrombin III -- works as anticoagulant when thrombin binds to it
4. Heparin --from mast cells, inc. antithrombin efficacy.
Most important part of hemostasis for stopping bleeding in small breaks
Platelet Plug
(NOt the clot,which forms next)
How can Fibrin, the stuff that makes clots, limit blood clotting?
Fibrin binds thrombin. Thrombin cannot work then and will not further activate fibrinogen to form fibrin. This is the fate of 80+% of Thrombin once clot is formed