03c: Hemostasis

Question 1

What are the key steps to preventing blood loss?

Answer 1

1. Vasoconstriction
2. Platelet plug
3. Fibrin clot

Question 2

List the machinery involved in vasoconstriction.

Answer 2

1. Neurogenic (fastest)
2. Myogenic (fast)
3. Humoral (slow)

Question 3

Examples of neurogenic vasoconstriction:

Answer 3

Spinal reflex, pain response

Question 4

Examples of myotonic vasoconstriction:

Answer 4

Smooth muscle contracts (response to trauma)

Question 5

Examples of humoral vasoconstriction:

Answer 5

Substance (i.e. Serotonin) release locally

Question 6

Once blood extravasates in vessel injury, which steps take place?

Answer 6

1. Endothelial cells produce VWF factor
2. VWF binds collagen
3. Platelets stick to VWF

Question 7

What’s the “release reaction”?

Answer 7

Platelet adhesion (bound to VWF) causes exocytosis of granule contents

Question 8

(X) acts as a bridge in formation of platelet plug.

Answer 8

X = collagen

Between endothelial tissue and platelets

Question 9

Release reaction involves in exocytosis of which substance(s)?

Answer 9

1. Ca
2. Serotonin
3. ADP
4. Enzymes targeting platelet phospholipids

Question 10

Which substance released by (X) specifically aids in increasing platelet aggregation?

Answer 10

ADP released by

X = platelets

Question 11

How does release reaction affect vasoconstriction?

Answer 11

1. Serotonin promotes vasoconstriction

2. Enzymes act on platelet phospholipids and produce TA2 (thromboxane A2)

Question 12

Thromboxane A2, released by (X), has which effect(s)

Answer 12

Not released directly by platelets, but formed by action of enzymes released by platelets;

1. Vasoconstriction
2. Increase platelet aggregation

Question 13

What’s the reason behind platelet aggregation?

Answer 13

Platelets stuck to VWF change surface characteristics (express receptors) that bind other platelets

Question 14

Easy bruising, without severe hemorrhagic issues, can be a sign of (excess/defecit):

Answer 14

Defecit in platelet adhesion due to decreased VWF (production issues)

Question 15

What’s considered primary hemostasis?

Answer 15

Vasoconstriction and platelet plug formation

Question 16

What’s considered secondary hemostasis?

Answer 16

Fibrin clot formation

Question 17

What’s thrombocytopenic purpura?

Answer 17

Shortage of thrombocytes (platelets), resulting in medium-sized lesions under skin

Question 18

Patients without primary hemostasis will show (X) on which part(s) of body?

Answer 18

X = lesions under skin

Usually legs/feet

Question 19

Small lesions under skin are called:

Answer 19

Petechiae

Question 20

Medium lesions under skin are called:

Answer 20

Purpura

Question 21

Large lesions under skin are called:

Answer 21

Ecchymoses

Question 22

In secondary hemostasis, what substance is being produced by (X) to increase platelet aggregation?

Answer 22

Nothing produced to increase aggregation!

Endothelial cells secrete prostacyclins to DECREASE aggregation

Question 23

In clot formation, what prevents the platelet plug from continuing to spread and grow?

Answer 23

Prostacyclins produced by endothelial cells in secondary hemostasis

Question 24

What’s hemophilia?

Answer 24

Lack of secondary hemostasis (incapable of forming strong, firm clot)

Question 25

T/F: Fibrin is a plasma protein that's always in the circulation.

Answer 25

False - fibrinogen is

Question 26

Describe process that converts (X) to fibrin.

Answer 26

X = fibrinogen 1. Thrombin cleaves it into fibrin monomers 2. Monomers spontaneously polymerize into long chains (fibrin polymer)

Question 27

T/F: Covalent bonds support the fibrin clot.

Answer 27

True

Question 28

(X) reinforces fibrin clot by inserting (Y) bonds.

Answer 28

``` X = Fibrin Stabilizing Factor XIII Y = covalent ```

Question 29

Thrombin is what kind of protein?

Answer 29

Protease

Question 30

T/F: Thrombin is a plasma protein that's always in the circulation.

Answer 30

False - Prothrombin is

Question 31

Extrinsic clotting pathway stimulated by:

Answer 31

External trauma that causes blood to escape from the vascular system.

Question 32

Intrinsic clotting pathway stimulated by:

Answer 32

Trauma inside the vascular system

Question 33

Intrinsic pathway factors come from:

Answer 33

Already in blood

Question 34

Extrinsic pathway factors come from:

Answer 34

Endothelial cells

Question 35

Which post-translational modification of clotting factors must occur for successful coagulation?

Answer 35

1. Addition of second COOH at all Glu residues 2. Ionize to COO- 3. Both bind Ca

Question 36

Describe MOA of Warfarin.

Answer 36

Vit K analog (non-functional) that inhibits enzyme responsible for clotting factor post-translational modification

Question 37

The (extrinsic/intrinsic) clotting pathway is faster.

Answer 37

Extrinsic

Question 38

Removal of Fibrin after healing is carried out by:

Answer 38

Plasmin

Question 39

Which cell(s) secrete(s) plasmin?

Answer 39

Not secreted by cell; inactive precursor (Plasminogen) circulates in blood.

Question 40

Which factor(s) facilitate breakdown of fibrin by (X)?

Answer 40

X = plasmin 1. Tissue plasminogen activator (tPA) 2. Urokinase

Question 41

tPA is used in the ER to treat:

Answer 41

Coronary thrombosis; enhances clearance of coronary artery clot

Question 42

Aspirin has which effect on clotting? How?

Answer 42

Reduce clotting; inhibits cyclooxygenase (no production of TA2) and slows platelet adhesion, aggregation, vasoconstriction

Question 43

Which ion is crucial for proper clotting? When taking blood samples, we prevent clotting by:

Answer 43

Ca; container has Ca chelator (EDTA/citrate) that binds all Ca and prevents clotting

Question 44

Prompt hemolysis of many RBC will cause (increase/decrease) in circulating bilirubin for the few days following.

Answer 44

Increase

Question 45

T/F: Sickle cell disease can cause hypo proliferative anemia.

Answer 45

False - RBC breakdown too fast

Question 46

T/F: Renal failure can cause hypo proliferative anemia.

Answer 46

True

Question 47

T/F: G6PD deficiency can cause hypo proliferative anemia.

Answer 47

False - RBC breakdown too fast

Question 48

T/F: Marrow damage (chemotherapy/radiation) can cause hypo proliferative anemia.

Answer 48

True

Question 49

(Thalassemia/hereditary spherocytosis) can cause hypo proliferative anemia.

Answer 49

Thalassemia

Question 50

What's thrombomodulin? How does it affect clot formation?

Answer 50

Epithelial transmembrane receptor that binds Thrombin; reduces coagulation

Question 51

(X) is a protein that (stimulates/inhibits) coagulation by which mechanism? Its activity is enhanced over 1000x by (Y).

Answer 51

X = antithrombin III Inhibits coagulation by binding and inhibiting thrombin Y = heparin

Question 52

Protein C is activated by (X) and (stimulates/inhibits) coagulation.

Answer 52

X = thrombin (when bound to thrombomodulin receptor) Inhibits