Chapter 22

Question 1

normal hemostasis

Answer 1

Blood usually fluid

Seals broken blood vessels

Question 2

abnormal hemostasis

Answer 2

Inappropriate clotting: too much

Insufficient clotting: too little

Question 3

hemostasis

Answer 3

stopping blood flow

Question 4

mediators of hemostasis

Answer 4

chemicals produced by platelets

Question 5

mediators of hemostasis is released at an injury to

Answer 5

Start clotting by reacting with blood proteins
Help platelets stick together 
Stimulate wound healing
Help platelets stick to vessel wall
Constrict blood vessels

Question 6

requirements for blood clotting process

Answer 6

Presence of platelets produced in the bone
marrow
Von Willebrand factor generated by the
vessel endothelium
Clotting factors synthesized in the liver
using vitamin K

Question 7

stages of hemostasis

Answer 7

1. vessel spasm
2. platelet plug formation
3. blood coagulation
4. fibrin clot

Question 8

vessel spasm

Answer 8

Constriction
– Endothelial Injury initiates
– Vascular spasm/ Vascular Vasoconstriction of the smooth muscle in the vessel wall
• decreased Blood Flow
– Short Lived and Localized

Question 9

platelet plug formation

Answer 9

– Release of von Willebrand’s Factor
• By Endothelial Cells & Platelets
- adhesion of platelets to exposed collagen fibers
– platelets become activated and secrete Adenosine diphosphate (ADP) (Promotes Aggregation), then attract more platelets
– Result: Platelet Plug (not a clot)

Question 10

blood coagulation

Answer 10

Two ways to get there
• Extrinsic Pathway
• Intrinsic Pathway
• Ultimately Both end in X Factor to activate 
Factor Xa - (Common Pathway)
– Prothrombin to Thrombin 
– Fibrinogen to fibrin

Question 11

without thrombin, what cannot occur?

Answer 11

aggregation

Question 12

extrinsic pathway

Answer 12

• occurs in the tissues (outside the vessel)
• clotting process to take a chemical shortcut
• takes 10-15 secs, measured by value PT
  production of thrombin is low, clot is small

Question 13

intrinsic pathway

Answer 13

• collagen in blood vessel wall activates
• 5-10 minuets but measured as a PTT lab value
• larger amounts of thrombin, large clot

Question 14

Factor X (active)

Answer 14

Prothrombin Activator

without it - Cannot clot

Question 15

Factor V Complex

Answer 15

Prothrombin to Thrombin

without it - cannot clot

Question 16

conversion of Thrombin (enzyme)

Answer 16

accelerates the
formation of Fibrin threads from Fibrinogen
(Factor I) that creates insoluble blood clot

Question 17

common pathway of hemostasis

Answer 17

factor X (active) -> factor V complex + calcium -> conversion of prothrombin to thrombin -> converts fibrinogen to fibrin-> fibrin clot; both extrinsic and intrinsic pathways will end up in the common pathway.

Question 18

clot retraction and dissolution

Answer 18

retraction- actin and myosin contract, pull out the fibrin, serum is squeezed out of the clot, clot shrinks
dissolution- Enzyme Plasmin Digests Clot

Question 19

alterations of coagulation

Answer 19

vitamin K deficiency, liver disease

Question 20

vitamin K

Answer 20

Vitamin K is necessary for synthesis and
regulation of components that make a clot
(stored in liver) fat-soluble vitamin (no vitamin K-> you will bleed/ inability to clot)

Question 21

liver disease

Answer 21

– Causes a broad range of hemostasis disorders -
– Many Coagulation factors made or stored in
liver
– Causes defects in coagulation, fibrinolysis, and
platelet number and function
- ppl w liver disease are very prone to bleeding bc their liver does not make the clotting factors

Question 22

Thrombocytopenia

Answer 22

platelet count <150,000/mm^3

• <50,000- hemorrhage from minor trauma
• <15,000- spontaneous bleeding
• <10,000- severe bleeding

Question 23

causes of Thrombocytopenia

Answer 23

Hypersplenism, autoimmune disease,
hypothermia, and viral or bacterial infections
that cause DIC (disseminated intravascular
coagulation)

Question 24

platelets

Answer 24

live 8–10 days in circulation
– Many are stored in the spleen
– Released when needed
– Normal Value 150,000 - 400,000 *need to know this 
– Disc-shaped essential for clotting

Question 25

Hypercoagulability

Answer 25

states are either inherited or acquired
increased platelet function - increase in number, increase in procoagulation and decrease in anticoagulation during an endothelial injury

Question 26

Inherited hypercoagulation

Answer 26

Usually associated with venous thrombosis;
Deficiency of Protein C or S
factor V Leiden

Question 27

protein C and S

Answer 27

work together to
inactivate factors Va(cause clot) and
VIIIa(causes clot) (in order to stop the
clot) So if there is not enough C or S clots
are more probable

Question 28

protein C deficiency

Answer 28

common DVT

Question 29

Protein S deficiency

Answer 29

risk of ARTERIAL

thrombosis

Question 30

Factor V Leiden (FVL) (Deficiency)

Answer 30

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)

Question 31

most common acquired increase in clotting

Answer 31

- Smoking
– Disseminated Cancer
– Diabetes
– Obesity
– Can also be related to other Diseases
• Polycythemia Vera (too many RBC)
• Sickle Cell Disease
Most common Female Acquired 
– Use of Oral Contraceptives

Question 32

Hypercoagulability due to increased platelet 
function results in

Answer 32

platelet adhesion,
formation of platelet clots, and disruption of
blood flow.

Question 33

causes of increased platelet function

Answer 33

disturbances in flow, endothelial
damage, and increased sensitivity of
platelets to factors that cause adhesiveness
and aggregation.

Question 34

thrombocytopenia

Answer 34

Results from a decrease in platelet production,
increased sequestration of platelets in the
spleen, or decreased platelet survival
can be due drugs (chemo, heparin), idiopathic (cant be identified), immune system/infections, radiation therapy, autoimmune

Question 35

Von Willebrand Disease

Answer 35

• Defect in vWF (does not allow platelets to aggregate)
  – Normal platelet Count with prolonged bleeding
  – Affects men and women
  – Multiple variants (3 variations)

Question 36

hemophilia

Answer 36

 Most common X-linked genetic disease
 Female cases rare
 Lack of Clotting Factors prevents stable clot
 Hemophilia A >80% of all hemophiliacs (aka
classic, Factor VIII or A)
 Hemophilia B aka Christmas Disease (Factor IX)

Question 37

Disseminated 
Intravascular Coagulation (DIC)

Answer 37

 Complex, acquired disorder: clotting and
hemorrhage simultaneously occur
– Sepsis, cancer, trauma, blood transfusion, shock
 Endothelial damage or Tissue Damage is
primary initiator
 Results in Clotting that leads to Bleeding

Question 38

anticoagulant drugs

Answer 38

Heparin
• binds to AT to produce an anticoagulant effect
– Coumadin drugs interfere with vitamin K action of the liver
(oral)

Question 39

antiplatelet drugs

Answer 39

(inhibits platelet plug formation)
– Aspirin
• Decrease platelet adherence and may increase bleeding
• Clopidogrel (Plavix) - Prevention of platelet
aggregation
 Thrombolytic Drugs
– Plasminogen activators are used to lyse thrombi in vivo

Question 40

antithrombotic therapy - aspirin

Answer 40

– Administration results in irreversible inhibition
of the platelet enzyme cyclooxygenase, which is
needed for proper platelet aggregation
– This reduces the “stickiness” of platelets
– Affects last for the lifetime of the platelets – 7-10
days
– NSAID drugs such as ibuprofen compete for
cycloxygenase and may be used in conjunction
with aspirin

Question 41

Plavix (clopidogrel)

Answer 41

a specific
inhibitor of ADP-induced platelet
aggregation