Pathophysiology Exam #3 Flashcards Preview

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Flashcards in Pathophysiology Exam #3 Deck (167)
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1

The precursor to fibrin is?

fibrinogen

2

Hemocytoblast Stem Cell become Myeloid Stem Cells which become Megakaryoblast which form Megakaryocytes......each Megakaryocytes can fragment into how many platelets?

2000 - 5000

3

The precursor cell for platelets is?

Megakarycote--->platelets are formed from the fragments of them

4

Platelets are anuclear...what does this mean?

-they cannot multiply and divide(they have no nucleus)
-Bone marrow (BM) has to be constantly producing and moving those platelets from the BM into the circulation to maintain an adequate circulating level of platelets

5

What is the normal circulating concentration and the lifespan of platelets?

• Normal circulating concentration:
150,000 – 450,000/μL (could also use mm3)
• Half-life: 8 – 12 days

6

What are six things that are found in the cytoplasm of platelets?

-Contractile proteins
-ER and Golgi apparatus
-Mitochondria
-PGs and TXA2 synthesis
-Fibrin-stabilizing factor synthesis
-Growth factors

7

What are three contractile proteins found in the cytoplasm of platelets?

-actin
-myosin
-thrombosthenin

8

What is the function of the ER and Golgi apparatus that is found in the cytoplasm of platelets?

-Ca++ storage and enzyme synthesis

§ Ca is very important in the coagulation cascade (both intrinsic and extrinsic pathways of the coag cascade)
§ ER ribosomes will produce enzymes that are needed for coag
§ Golgi apparatus will further process the enzymes needed

9

What is the function of the mitochondria found in the cytoplasm of platelets?

ADP and ATP synthesis

§ ADP itself actually aids in the aggregation of platelets, as well as recruitment of other platelets

10

What is the function of the Fibrin-stabilizing factor?

§ Once you get to the final clot, the final fibrin fibers, the fibrin−stabilizing factor enhance the bonds between the fibrin fibers and create a stronger clot

11

What is the function of the Growth factors found in the cytoplasm of platelets?

cause vascular endothelial cells, vascular smooth muscle cells, and fibroblasts to grow and divide for repair of damaged blood vessels.

§ When you have an injury and platelets respond, those growth factors are released from the platelets which helps aid in the healing of that damaged tissue

12

What makes up the cell membrane of platelets?

-Glycoprotein coating
-Phospholipids
-Receptors

13

What is the characteristics of the Glycoprotein coating of the platelet cell membrane?

o Glycoprotein coating that prevents adherence to normal vascular endothelium, but causes adherence to
injured endothelium.
§ Very important because this prevents the platelets from adhering to normal vascular endothelium; platelets will not adhere to NORMAL vasc endothelial cells.
§ Anything that’s causes injury to the vasc endothelium, will activate the platelets and they will respond to the damaged vasc endothelium

14

What is the role of the phospholipids found in the platelet cell membrane?

Plays important role in the clotting cascade

15

What is important about the receptors found in the platelet cell membrane?

o Numerous receptors involved in platelet plug formation and coagulation
o When individuals have clotting disorders, that are r/t platelets; it’s the receptors themselves that are dysfunctional or deficient which leads to the coagulopathy

16

What is the definition of hemostasis?

prevention of blood loss

17

How is hemostasis achieved and in what order does it occur(5)?

1. Vascular constriction
2. Platelet plug formation
3. Blood coagulation/blood clot
4. Fibrin formation and repair of injured vessel
5. Clot lysis

18

What are four ways in which Vascular Constriction achieves hemostasis?

• TRAUMA CAUSES VASCULAR CONSTRICTION, WHICH DECREASES BLOOD LOSS
• VASCULAR SMOOTH MUSCLE SPASM
o The greater the trauma to the blood vessel (BV), the greater the spasm
o EX: Nick yourself shaving in the bathroom; you think your going to bleed to death while a crushing injury or severed limb: because of the greater degree of injury, the greater degree of vasospasm
• PAIN AND SNS REFLEXES: VASOCONSTRICTION
o NE is released from the postganglionic symp fibers
o EPI/NE released from the adrenal medulla
o causing activation of alpha1 receptors of the vasc smooth muscle; causing vasoconstriction
• PLATELETS → TXA2 → VASOCONSTRICTION
§ When platelets become activated they release thromboxane A2 (TxA2)
§ TxA2 is also a very very potent vasoconstrictor

19

Platelet plug is the second way in which Hemostasis occurs...what are the characteristics of Platelet plug?

• PLATELETS CONTACT DAMAGED VASCULAR ENDOTHELIUM AND COLLAGEN IN BLOOD VESSEL WALL
o Swell, exude pseudopods
§ pseudo = false; pod = foot
o Actin, myosin, thrombosthenin contract: release active clotting factors
o Platelets then become sticky and aggregate; adhere to collagen and von Willebrand factor (vWF) in blood vessel wall
§ vWF has to be present for the platelets to stick to the collagen in the BV wall
§ vWF is a protein secreted by the BV endothelial cells; it mediates platelet adhesion to the BVs by
forming a bridge between the collagen and the platelets
§ von Willebrand factor binds to both platelet membrane receptors and collagen in the vascular wall to
form the bridges
o ADP and TxA2 secretion: activation of other platelets
v ADP and TxA2 actually combine with receptors on other platelets and recruit them to come play along
o More and more platelets aggregate and are activated and form the platelet plug in the vasc wall
o Eventually the platelets will Express fibrinogen receptors; and the fibrinogen receptors will bind with
the fibrinogen
v the fibrinogen forms bridges between the fibrinogen receptors of the platelets to form platelet plug
o Fibrin threads form in platelet plug
o Platelet plug may seal small blood vessels injury
o However, Large injury also requires blood
coagulation/blood clot

20

Some people are born with a deficit or a complete absence of vWF; and they will need surgery.
Q: What will you do to correct that problem?

Administer vWF; they have vWF concentrate that you can admin; can also admin cryo

21

The third stage of hemostasis is Blood coagulation/Blood clot....what are its characteristics?

• BEGINS: 1-2 MIN. FOR MINOR TRAUMA AND 15 – 20 SEC. FOR MAJOR TRAUMA
• 3 – 6 MIN. TEAR IN VESSEL FILLED WITH CLOT
• CLOT RETRACTS IN 20 – 60 MIN.: CLOSES TEAR(APPROXIMATES) MORE AND AIDS IN HEALING
• NORMALLY THERE’S A BALANCE BETWEEN PROCOAGULANTS AND ANTICOAGULANTS
o Normal conditions: anticoagulants predominate
o After injury: procoagulants predominate
o However, procoagulants predominance should be
localized to the area of the injury; you do not
want systemic procoagulant predominance

22

There are three steps of coagulation in relation to hemostasis...what is the the first step?

1. Activation of blood coagulation factors and formation of PROTHROMBINASE (PROTHROMBIN ACTIVATOR)

23

There are three steps of coagulation in relation to hemostasis...what is the the second step?

2. Prothrombinase converts PROTHROMBIN TO THROMBIN

24

There are three steps of coagulation in relation to hemostasis...what is the the third step?

3. Thrombin converts FIBRINOGEN TO FIBRIN FIBERS = Enmesh platelets, blood cells, and plasma to form the clot

25

What is the final outcome of step 1 of coagulation?

Prothrombinase is the final outcome of step 1 of coagulation

26

There are two pathways for prothrombinase formation in step one...what are they?

-Extrinsic (tissue factor) pathway
-Intrinsic (contact activation) pathway

27

What are the characteristics of the Extrinsic pathway

v Its called extrinsic because the damage is EXTERNAL to the BV
v Once tissue is damaged, that causes the release of thromboplastin; released from the traumatized tissue
v Thromboplastin along with Factor VII and Ca ions activate Factor X
v Activated Factor X, Factor V, platelet phospholipids, and Ca ions activate prothrombinase (the final outcome of step 1 of the coagulation pathway.

28

In step one of coagulation, what initiates the action of the extrinsic clotting pathway, and what is the final outcome of it?

-tissue damage(trauma)
-Prothrombinase

29

In step one of coagulation, what initiates the action of the intrinsic clotting pathway, and what is the final outcome of it?

-contact w/ collagen of damage bv activates factor xii
-Prothrombinase

30

Do both the intrinsic and the extrinsic pathways lead to the same result?

yes; Note that beginning with activation of Factor X, both become a common pathway