EXAM #2: Chapters 8, 12, 13, 20, 21, 22 Flashcards
(40 cards)
Thrombocytosis
Platelets
Hemostasis
Stopping blood flow
NORMAL: blood usually fluid, seals broken blood vessel’s (clot forms)
ABNORMAL: not clotting
Thrombus
Blood clot
lysis
Loosening, separation
thrombocytopenia
Blood clot deficiency
Thrombocytes (platelets)
NORMAL: 150,000-400,000
Stored in spleen Lives 8 to 10 days Disc shaped for clotting Meds (NSAIDS) stick to life of platelets Antiplatelets: don't stick very well
<150,000 = risk for bleeding
> 400,000 = clotting too much
Mediators of Hemostasis
- Chemicals produced by platelets
- Released after injury to start clotting
- Help platelet stick
- Stimulate wound healing
- Help platelet stick to the vessel wall
- Constrict blood vessels
Hemostasis phases
Phase 1/Primary:
- Vasospasms and Constrictions = reduces blood flow, temporary fix
- Endothelial injury
- Vascular spasm/vasoconstriction of smooth muscle in vessel wall)
- Decrease blood flow
- Short-lived/localized
Phase2/Platelet:
- Release of Vonwillebrand’s Factor (makes everybody stick together) by epithelial cells (lining of vessel walls) and platelets.
- Platelets secreate ATP = Aggregations = (everybody sticks)
- Aggregated platelets release thromboplastin (Factor III).
- Platelet Plug (NOT a clot yet!)- platelets clumped together
Phase3/Coagulation: (2 ways)
- Extrinsic pathway-injury outside the cell
- Intrinsic pathway-injury inside the cell
- Activates X Factor (common pathway):
- *Prothrombin to Thrombin (without thrombin, can’t aggregate) then Fibrinogen to Fibrin.
*MUST HAVE X FACTOR TO MAKE CLOT!
- **Prothrombin—>Thrombin—>
- –> Fibrinogen—>Fibrin= CLOT***
Hemostasis 1st Phase
1st Phase/Primary:
*Vasospasms and Constrictions = reduces blood flow, temporary fix
- Endothelial injury
- Vascular spasm/vasoconstriction of smooth muscle in vessel wall)
- Decrease blood flow
- Short-lived/localized
Hemostasis 2nd Phase
2nd Phase/Platelet:
*Release of Vonwillebrand’s Factor (makes everybody stick together) by epithelial cells (lining of vessel walls) and platelets.
- Platelets secreate ATP = Aggregations = (everybody sticks)
- Aggregated platelets release thromboplastin (Factor III).
- Platelet Plug (NOT a clot yet!)- platelets clumped together
Hemostasis 3rd Phase
Phase3/Coagulation: (2 ways)
*EXTRINSIC pathway-injury outside the cell
*INTRINSIC pathway-injury inside the cell
- Activates X Factor (common pathway):
- *Prothrombin to Thrombin (without thrombin, can’t aggregate) then Fibrinogen to Fibrin.
*MUST HAVE X FACTOR TO MAKE CLOT!
- **Prothrombin—>Thrombin—>
- –> Fibrinogen—>Fibrin= CLOT***
Extrinsic pathway
PT value
* Occurs in tissues (“extrinsic” to blood)
- Clotting process for chemical shortcut
- VERY RAPID-
takes 10-15 seconds (Quick patch process measured by value of PT) - Production of thrombin is low and resulting clot is small
- 2 ways to get a clot-
A tissue problem or a vascular problem - Not Antithrombolytics (PT/PTT)
PT and PTT
(Extrinsic Pathway)
NOT ANTITHROMBOLYTICS
*PT: Warfarin (Coumadin) “Rat poison”
Takes twice as long to clot
don’t want client to clot too fast.
Measure with labs
- PTT: Heparin
Prolongs bleeding time
Measure with labs
Intrinsic pathway-PTT
(Phase 3/Coagulation)
(Intrinsic pathway) Phase 3/Coagulation
- Collagen in the blood vessel wall activates
- Slower (five-10 minutes) but measured in seconds as a PTT lab value
- Large amounts of Thrombin = Larger clot
PT and INR
Assessment of Extrinsic coagulation
- Used to monitor clients taking certain meds as well as to help diagnose clotting disorders
*(evaluate oral anticoagulation therapy:
Warfarin (Coumadin) = PT/INR
PTT & aPTT
- activated partial thromboplastin time
- Assessment of intrinsic coagulation used to monitor Heparin
- Lab values: NORMAL range 25-35 seconds
Common Pathway (Phase III)
- Factor X active- Prothrombin activator (without it cannot clot!!)
Fibrinolysis V
- Occurs in response to Enzyme Plasmin (digest/degrades Fibrin)
- T-PA Tissue plasminogen activator converts plasminogen to plasmin
- Plasmin digest clot (synthetic T-PA used in strokes, sometimes heart attacks)
- If injury was not completely healed then client at risk for bleeding
- Do not give in surgery or brain bleed
- No Foley catheter or IV after med
- Thrombolytic-at risk for bleeding
Factors that affect Coagulation
- Vit K deficiency (necessary for synthesis and regulation of components that make a clot, without it you will bleed; stored in liver).
- Liver disease-causes hemostasis disorder = defects in Coagulation, Fibrinolysis, and Platelet number/function. (Liver cirrhosis = going to bleed)
- Babies get Vit K shot at birth
- Green, leafy veg has Vitamin K
Platelet disorders:
Thrombocytopenia: platelets <150,000
- Causes: Hypersplenism, Autoimmune disorders, Hypothermia, Viral/Bacterial infections that cause DIC (disseminated intravascular coagulation)
- check PT, PTT, platelets if client is bleeding
< 50,000-hemorrhage from minor trauma (IV stick)
<15,000-spontaneous bleeding (petechiae)
<10,000-severe bleeding (doctor wouldn’t let them in surgery; need platelet transfusion)
Bleeding disorders
- Platelets (low or high) defect and platelet function
- Coagulation factors
- Vessel integrity (blood vessel defect) inherited or acquired
Hypercoagulability
Clotting too much
Inherited (diseases) or Acquired (over a lifetime)
- Increase platelet function-Increased number, Endothelial injury (Von Willebrand’s too much), Increased Procoagulation factors or Decreased Anticoagulation factors
Inherited: Hypercoagulation
Associated with Venus thrombosis
Deficiency Protein C or S
Protein C and S work together to in activate Factor V (cause clot) and stop villa (causes clot) in order to stop the clot
So if there is not enough C or S clots are more probable
Protein C deficiency = DVT
Protein S deficiency = risk of arterial thrombosis
Factor V Leiden (FVL) deficiency
AKA Activated Protein C resistance = Clotting
Genetic mutation of Factor V which causes resistance to the action of protein C
(unable to stop the clot; C would normally stop clot from continuing)