NURS 5315: Advanced Pathophysiology Hematologic Module 4 Questions with 100% Correct Answers
What is the peripheral zone of platelet?
Outermost layer. Made of phospholipids. Contains many receptors responsible for platelet adhesion and aggregation
What is the sol-gel of the platelet
It is t...
NURS 5315: Advanced Pathophysiology
Hematologic Module 4 Questions with 100%
Correct Answers
What is the peripheral zone of platelet?
Outermost layer. Made of phospholipids. Contains many receptors responsible for platelet adhesion
and aggregation
What is the sol-gel of the platelet
It is the outermost layer made of possible if it contains many receptors responsible for platelet
adhesion and aggregation
What is the organelle zone of platelets
Innermost layer contains calcium dense granules and alpha granules
What are the four phases of platelet plug formation?
Activation, adherence, aggregation, and secretion
What is the first step or phase of platelet plug formation and explain
Activation is the first step. In physiological states. Platelets circulate without adhering to the intact
endothelium. An injury to the endothelium exposes thev WF, fibronectin, collagen and from
thrombospondin.. Collagen is a potent activator and when the sub endothelial collagen is exposed by
an injury. The platelets become charged AKA activated. Platelets and become aware of the injury and
undergo a shape change that increases their ability to adhere to the site of injury.
The second step in platelet plug formation is
Adherence is a process by which platelets attached to the injured endothelium. Adherence begins
with the vWF. Circulating vWF binds to the exposed subendothelial collagen and to the GP Ib/IX/V
receptors on circulating platelets. Collagen then binds with the GP VI receptor. The binding of collagen
with the GP VI receptor results in the activation of the GPIIb/IIIa and GPIa/IIa receptors. vWF then
binds with the GPIIb/IIIa receptors and collagen further binds with the GPIa/IIa receptors. This
collective binding anchors the platelets in place
The third step in platelet plaque formation is
Aggregation- is the process by which platelets bind to one other. There are multiple GPIIb/IIIa
receptors on one platelet and when activated (as described above) they have a greater affinity for
fibrinogen. Fibrinogen is able to bind to two GPIIb/IIIa receptors simultaneously and thereby bind
platelets together
The fourth step in platelet plug formation is
Secretion- during this phase the platelet granules release their contents.
a. ADP- enhances adhesion, activates platelets and recruits platelets
b. Serotonin recruits platelets.
c. Fibronectin and thrombospondin are proteins which stabilize platelets that are adhered to the site
of injury.
d. Thromboxane A2- is a product of the arachidonic acid pathway but is stored inside the platelet too.
It causes vasoconstriction and enhances platelet aggregation.
e. Growth factors promote tissue repair however they have a role in the development of
atherosclerosis.
,The final step in platelet plug formation
The platelet plug is stabilized by fibrin and XIIIa which are the end products of the coagulation
cascade.
What is the extrinsic pathway arms of the coagulation cascade
Extrinsic pathway is considered the primary pathway of coagulation. It is activated when Tissue Factor
is exposed at the site of injury. The process starts with a vascular injury which results in the exposure
of Tissue Factor (III) which has a cell receptor for factor VII. (As a side note lipid filled macrophages in
atherosclerotic plaques contain a large amount of tissue factor which increases the likelihood of
arterial thrombus formation from plaque ruptures). Once exposed TF binds with VII to form the
TF/VIIa complex. TF/VIIa activates X = Xa. Activated factor Xa binds with activated Va and calcium to
form the prothrombinase complex. The prothrombinase complex converts factor II (prothrombin) to
activated factor IIa (thrombin). Thrombin (activated factor IIa) then moves on to activate 4 factors. It
activates factor I (fibrinogen) to activated factor Ia (fibrin) and it also activates factors V, VIII & XIII.
You can see the action of thrombin on your screen marked with blue lines. Fibrin (activated factor Ia)
is placed over the platelet plug and activated factor XIIIa stabilizes the fibrin.
What is the intrinsic pathway arms of the coagulation cascade
The clinical significance of the intrinsic pathway is not entirely understood, because a deficiency of
factor XII (Hageman factor) does not cause bleeding. As such the intrinsic pathway's main function is
thought to be one which enhances the extrinsic pathway. This pathway is activated when the blood is
exposed to negative charges which are found on the molecules of ADP and ATP. This exposure
activates factor XII (Hageman factor). Activated factor XIIa then activates factor XI. Activated factor
XIa activates IX. Activated factor IXa then activates factor X. Activated factor Xa then forms the
prothrombinase complex in the common pathway.
Coagulation Cascade Key Plasma Proteins
1.Tissue Factor
2.VII
3.X
4 .Prothrombinase Complex
5. Prothrombin
6. Thrombin
7 .Fibrinogen
8. Fibrin
9. XIII
10. XII
11. VIII
12. IX
13. Antithrombin
14. Protein C
15. Protein S
16.t-PA
1. Initiator of extrinsic pathway.
2. Forms complex with tissue factor (III) and activates factors IX and X
3. Activates Prothrombin through activated Xa form
4. (prothrombin and activated factors X and V) that activates prothrombin into thrombin
5. Factor II, source of thrombin that activates fibrinogen
6. cleaves the extracellular domain of G-protein-coupled protease-activated receptors (PARs),
thereby initiating transmembrane signaling.
7. moves between the beta and gamma regions but is removed during the formation of serum;
precursor of fibrin clot
, 8. Used to stabilize clot
9. Fibrin - stabilizing factor - cross links fibrin through XIIIa to strengthen clot
10. Hageman Factor. Initiator of intrinsic pathway
11. VIIIa is a component of tenase complex
12. IXa is a component of tenase complex, activates factor X
13. it inhibits thrombin and several activated clotting factors (e.g., VIIa, IXa, Xa, XIa, XIIa).
14. in the circulation binds to thrombomodulin in a thrombin-dependent manner and is converted to
activated protein C
15. degrades factors Va and VIIIa
16. a serine protease that reaches maximal enzymatic activity after binding to fibrin and
proteolytically activates plasminogen to plasmin
What is the coagulation cascade
The coagulation cascade is the second arm of hemostasis. This process involves quite a few steps and
there are many players involved. It can be difficult to follow and understand. This first slide show the
coagulation process in a simplified manner. The two arms of the coagulation cascade are activated,
followed by multiple enzymatic processes, the two arms then converge into the common pathway
and the final product of this process is the formation of fibrin which stabilizes the platelet plug.
There are a total of twelve coagulation factors, and a number of additional proteins which function to
control coagulation and dissolve clots. All twelve coagulation factors are plasma proteins and the
majority of them are produced by the liver. Because they are produced by the liver individuals with
liver disease such as cirrhosis, acute hepatic failure, or hepatocyte damage of any kind (temporary or
chronic) are likely to be deficient in these factors and at an increased risk of bleeding.
How was the platelet plug process altered with aspirin?
Inhibits the formation of TX a two by blocking Cox one pathway of arachidoic pathway
How is the platelet plug process altered with clopidogrel?
P2Y12 receptor is blocked from ADP - thus allowing cAMP to continue to prevent platelet aggregation
How does warfarin altered coagulation?
Vitamin K is blocked from becoming vitamin k reductase, and carboxylation of vitamin K dependent
clotting factors is unable to occur.
How does low molecular weight heparin alter coagulation?
-cannot inhibit thrombin, but can only inhibit clotting factor Xa
-They inhibit activated Xa and prevent the formation of the prothrombinase complex and
consequently thrombin. They do have some effect on antithrombin but to a much lesser extent than
heparin.
How does factor X a inhibitors alter coagulation
These drugs (fondaparinux, apixiban, rivaroxaban) increase antithrombin's affinity for Xa.
Antithrombin neutralizes Xa and thereby prevents the formation of the prothrombinase complex and
thrombin.
How does direct thrombin inhibitors altered coagulation
Drugs in this class include dabigatran and argatroban. The inhibition of thrombin prevents the
activation of fibrinogen and XIII. The active form of fibrinogen is fibrin which supports the platelet
plug. XIIIa cross links with fibrin to provide stabilization to the platelet plug.
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