Ch 22

Front 1

What is hemostasis?

Back 1

Physiological process that lead to the stoppage of bleeding from an injured vessel

Front 2

3 stages of hemostasis

Back 2

1. Vascular construction

2. Formation of the plates plug/ temporary clot through platelets aggregation

Front 3

Final stage of hemostasis

Back 3

Blood coagulation/ formation of definitive clot

Front 4

What is the first and 2nd steps in vascular constriction?

Back 4

1. Reflex Vasoconstriction

2. Platelets arrival and release of vasoconstriction mediators .

3. Release of Prostacyclin ( vasodilation) from endothelium.

Front 5

What does reflex vasoconstriction do?

Back 5

Provides temporary slowing down of the blood flow.

Front 6

Vasoconstriction mediators

Back 6

1. Platelets release Thromboxane A2

(TXA2) =vasoconstriction

2. Serotonin = vasoconstriction

3. Endothelin is potent vasoconstrictor

4. Prostacyclin (Prostaglandin)

from endothelium

Prostacyclin=vasodilation is released to Prevent platelets from aggregating in uninjured areas.

Front 7

Function of prostacyclin ( prostaglandin)

Back 7

Can vasoconstrict or vasodilate

Front 8

Stages of formation of platelets plugs

Back 8

1. Platelets ( Alpha and Dense granules).

2. Von Willebrand factor ( transports factor VIII) released from endothelium to help with adhesion to collagen fibers.

3. Thromboxane and ADP activates and signals platelets to come to the area.

4. Platelets arrive and accumulate.

5. Fibrinogen binds to platelets receptor sites to form loose plug. Platelets plug.

Front 9

Alpha granules include

Back 9

Clotting factors and adhesion proteins.

P Selectin

• Fibrinogen

Von Willebrand Factor (VWF)

Factor V

• Factor VIlI

Platelet Factor IV (heparin bindin

• Fibronectin

Platelet Derived Growth Factor (PDGF)

Transforming Factor-alpha (TGF- alpha)

Front 10

Dense granules include

Back 10

• ADP

• ATP

• Calcium

• Histamine ( vasoconstriction mediators)

Serotonin

Epinephrine

Front 11

Blood coagulation cascades?

Back 11

Intrinsic: slower 1-6 min Activated in circulation by Factor XII

Extrinsic: Rapid: trauma at vessel site which releases Tissue Factor and activates Factor VII.

Front 12

Terminal factor in intrinsic system ( blood or vessel injury) and extrinsic system ( tissue factor) ?

Back 12

Factor X

Front 13

What activates prothrombin?

Back 13

Factor X + Ca ++ ions

Front 14

Prothrombin converts to …

Back 14

Thrombin

Front 15

What activities fibrinogen?

Back 15

Back (Definition)

Front 16

Stable clot in the vessel?

Back 16

Fibrin ( monomer to polymer).

Front 17

Organ plays major role in blood clotting factors?

Back 17

Liver

Front 18

Natural anticoagulation factors?

Back 18

Protein C, S, antithrombin

Front 19

Factors produced by hepatocytes in a liver?

Back 19

Fibrinogen

Prothrombin

Factors: V, VIl, IX, X, xI, xII

Front 20

What factors inactivates Protein C?

Back 20

Factor V, VIII helps to decrease the amount of thrombus formation

Front 21

Protein C deficiency causes?

Back 21

Increased risk of thrombosis or thromboemboly.

Front 22

Function of protein S?

Back 22

Acceleration function of protein C

Front 23

Fibrinogen is needed for ?

Back 23

For activation of

Pro-coagulation factor of Fibrin for clot formation

Front 24

Prothrombin is needed for..

Back 24

Conversion of thrombin

Front 25

Antithrombin is needed for

Back 25

Inactivates coagulation factors to neutralize Thrombin

Front 26

Lack of Protein C and S causes …

Back 26

Hypercoagubility state / higher risk of developing thromboemboly

Front 27

Vitamin K helps to synthesize?

Back 27

Vitamin K

Synthesis:

II, VII, IX, X

Prothrombin

Protein C

Front 28

Clot dissolution is known as?

Back 28

Fibrinolysis

Front 29

Plasminogen is activated by?

Back 29

Plasminogen activator

Front 30

Plasminogen converts to …

Back 30

Plasmin to break the clots ( Factors V, VII, VII, Prothrombin,

Fibrinogen).

Front 31

Plasmin inactivated by…

Back 31

Plasmin alpha inhibitor

Front 32

Thrombocytosis

Back 32

Hypercoagulability state- increased platelets function

Front 33

Types of thrombocytosis

Back 33

Primary - nothing underlying ( Defect of thrombopoietin receptor; Causes increased levels of free thrombopoietin)

Secondary- smth causes problems ( Seen with disease states that increase thrombopoietin)

Front 34

Secondary Thrombocytosis causes?

Back 34

CA, RA, chronic inflammatory infection, causes of tissues damage.

Front 35

Something that stimulates trombopoietin to…

Back 35

Increase amount of RBC

Front 36

Normal feedback system

Back 36

Platelets decreased -

Increased Unbound TPO

Stimulates Megakaryocytes Production

Platelets Increased

• Decreased unbound TPO

Inhibition of Megakaryocyte Production

Front 37

Primary Thrombocytosis main cause?

Back 37

Myeloproliferative disorder

Stem cells makes more platelets than balance system can handle on a negative feedback

Can be the cause of defects on the platelets receptor- inhibiting ability of TPO to attach to the receptor- free TPO- unbound TPO is going to stimulate bone marrow to make more megakaryocytes to increase the platelets

Front 38

Increased numbers of platelets and their form causing

Back 38

Causes increased risk of blood clots and because of the abnormal form - bleeding

Front 39

Protein C and S made in a liver is to …

Back 39

To anticoagulate , to inactivate clotting factors

Protein C

Inactivates Factor V and VIlI

Protein S

Accelerates the action of Protein C

Front 40

Goal of Protein C, S ?

Back 40

To prevent blood clots in a body

Goal:

Prevent thromboembolism

Front 41

Protein C and S deficiency causes?

Back 41

• Increased risk for blood clots

Front 42

What is Factor V Leiden?

Back 42

It’s a mutation in the blood clotting Factor V

Because of the mutation protein C cannot shut it down

Factor V Leiden resistant to protein C and will not respond

Causes risks of blood clots.

Risk population:

Pregnancy

Front 43

Protein C deficiency caused by ?

Back 43

Congenital

Liver failure

Vitamin K deficiency

Malignancy

Front 44

Protein S deficiency causes?

Back 44

Autoimmune disorder

Front 45

Treatment for Inherited Hypercoagulability Disorders

Back 45

Anticoagulation treatment

Front 46

Acquired Hypercoagulabilit Causes

Back 46

Immobility

MI

Cancer

Smoking

Surgery

Obesity

Heart failure

Especially cancer

Hormone replacement

Oral contraception

Front 47

Coagulation factor deficiencies-inherited

Back 47

Von Willebrand

Hemophilia A ( factor VIII deficiency)

Front 48

Von Willebrand hallmark

Back 48

Hereditary

Can’t form clots/ Clotting

Cascade interrupted

Transports factor VIII

Risk at bleeding ( nose bleed, dental procedure)

Bleeding in the presence of normal platelet counts- hallmark

Front 49

Hemophilia A Factor 8 deficiency

Back 49

Hereditary

X Linked

Recessive

Affects males

Spontaneous bleeding in soft tissue/GI Tract

Front 50

Factor 8 and Coagulation Factor Deficiencies-Inherited

Back 50

You have to differentiate is it a primary true deficiency in hemophilia A of factor 8 or is it a secondary as a result of Von Willebrand.

Front 51

If it’s a hemophilia A , liver and endothelial lining are not making factor 8. Not enough factor 8 being made- primary cause.

Back 51

If it’s plenty of factor 8 being made and it’s a transport problem . It becames a secondary cause as deficiencies in Von Willebrand.

Front 52

Acquired Bleeding Disorders

Vitamin K deficiency

Clotting factors not working

Back 52

Reasons:

Not enough vitamin k in a diet

Intestinal problem ( bacteria will not be present to break down for Vit K)

Use of antibiotics ( destroyed intestinal flora)

Liver disease ( liver can’t store vitamin k)

Can be seen in newborns ( they don’t have established intestinal flora)

Factors II, VII, IX, X not functional

Front 53

Bleeding Associated with Platelet Disorders

Thrombocytopenia=LOW PLATELETS

Causes

Back 53

Primary immune thrombocytopenic purpura ( idiopathic thrombocytopenia purpura) is a result of antibody attack glycoproteins on platelets

Autoimmune disorder

Receptors involved: 3 B 1B 3 A

These receptors are targeted for destruction. It will caUse an excessive amount of platelets distraction and will cause thrombocytopenia.

Front 54

Purpura

Back 54

Discoloration on the skin because of platelets distraction

Risks of bleeding gums,

Nose bleed

Menstrual bleeding

GI bleeding

Front 55

Disseminated Intravascular Coagulation : problems

Back 55

1. Excessive amount of coagulation

2. Excessive amount of bleeding

Front 56

Coagulation part of DIC

Back 56

Increased bleeding

Excessive coagulation

Tissue injury

• Obstetric complications

• Malignant neoplasms

• Infections (especially gram-negative sepsis)

• Trauma

• Surgery

• Burns

• Hypotension

ENDOTHELIAL CELL INJURY

• Infections

• Immune complex deposition

• Burns

• Hypoxia

• Acidosis

• Shock

• Vasculitis

Activation of both clotting cascades - excessive clotting. Thrombin generation. Thrombin goes unchecked. excessive amount of fibrin production. Fibrin will produce clots: • Ischemic tissue injury

• Microangiopathic hemolytic anemia ( intravascular).

DIC causes the destruction of natural coagulants: Anti- Thrombin III.

With excessive amount of clotting, plasmin (fibrinolysis) gets activated.

Plasmin will destroy clotting factors ( V, VIII, fibrinogen, platelets). No more left for other clotting mechanisms- people will bleed.