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Advanced Patho UC Exam #2 > Hemostasis & Blood Coagulation > Flashcards

Hemostasis & Blood Coagulation Flashcards

1
Q

Thrombocytes develop from ______ progenitor cells

A

megakaryocytes

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2
Q

Platelets synthesize what? Store what?

A

enzymes, ATP, ADP, prostaglandins, histamine, serotonin, thromboxane A2, clotting factors

Also store calcium ions

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3
Q

Functions of platelets

A
  • initiate the coagulation cascade to stabilize the platelet plug
  • Fibrin-stabilizing factor binds fibrin molecules into meshwork
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4
Q

vWF

what is it?
what does it carry?

A

Glycoprotein that acts as bridging molecule at sites of vascular injury for normal platelet adhesion

vWF binds collagen when it’s exposed beneath endothelial cells d/t damage to the blood vessel (rem. both endothelium and platelets release vWF)

Carries factor VIII (antihemophilic factor A) to circulation

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5
Q

Normal platelet count is

A

150K to 400K

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6
Q

If platelet count is below ______ then what is this called?

A

100K thrombocytopenia

<50,000 = r/f hemorrhage from minor trauma 
<20,000 = r/f spontaneous bleeding
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7
Q

Cell membranes of platelets have glycoproteins on surface that do what?

Also contain phospholipids that do what?

A

REPULSE ADHERENCE TO ‘NORMAL’ ENDOTHELIUM AND PROMOTE ADHERENCE TO INJURED ENDOTHELIUM

-phospholipids that activate several stages in the blood clotting cascade

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8
Q

How long do platelets live? Eliminated how?

A

8-10 days and are eliminated through spleen macrophage system and liver kupffer cells

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9
Q

Sequence of hemostasis? What activates the coagulation cascade? 5 steps

A

1- vascular injury leads to vasoconstriction

2-formation of a platelet plug (primary hemostasis)

3-tissue factor activates coagulation cascade - fibrin strands sew plug and make it stronger

4-formation of a blood clot (secondary hemostasis) - permanent plug

5-clot retraction and clot dissolution (fibrinolysis) - wound repair and formation of fibrous tissue

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10
Q

FUNCTIONS OF PLATELETS (4 of them)

A
  • Help regulate blood flow into a damaged site by inducing VASOCONSTRICTION
  • Initiate platelet-to-platelet interactions, resulting in the formation of a PLATELET PLUG
  • ACTIVATE THE COAGULATION CASCADE to stabilize the platelet plug
  • INITIATE REPAIR processes including clot retraction and clot dissolution (fibrinolysis)
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11
Q

Important biochemicals released from platelet granules?

A

Thromboxane A2
ADP
vWF

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12
Q

Platelet biochemical thromboxane A2 function?

A
  • is a prothrombotic
  • it is PRODUCED BY activated platelets
  • STIMULATES ACTIVATION OF NEW PLATELETS
  • INCREASES PLATELET AGGREGATION
  • CAUSES VASOCONSTRICTION
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13
Q

Platelet biochemical ADP function?

A
  • is a prothrombotic
  • PLATELET ACTIVATION
  • stimulate shape change
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14
Q

Platelet biochemical vWF function?

A
  • acts as an anchor
  • endothelial cells attached to collagen
  • ACTS AS BRIDGING MOLECULE AT SITES OF VASCULAR INJURY FOR NORMAL PLATELET ADHESION
  • under high sheer conditions - promotes platelet aggregation
  • carries factor VIII in circulation
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15
Q

After injury: intravascular ______ ______ ______ reducing blood flow. Platelets are responsible for much of the ________ by means of ________.

A

smooth muscle contracts

vasoconstriction by means of thromboxane A2

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16
Q

Platelet plug formation 3 steps

A

ADHESION, ACTIVATION, AGGREGATION

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17
Q

ADHESION of platelet plug is mediated by?

A

the binding of the platelet surface receptor glycoprotein-Ib (GPIb) to vWF

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18
Q

ACTIVATION of platelet plug occurs how?

A

smooth spheres change to spiny projections and degranulation occurs (called platelet-release reaction). This results in the release of various potent biochemicals.

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19
Q

AGGREGATION is facilitated by?

What happens during clot retraction?

A

fibrinogen bridges b/w receptors on the platelets

-clot retraction: fibrin strands shorten and become denser and stronger to approximate the edges (edges of blood vessel wall come together)

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20
Q

See slide 46 steps?

A

starts with injured vascular surface –>platelets swell –> change shape –> contractile proteins contract (release granules) –> become sticky –> adhere to collagen & vWF –> secrete ADP and thromoxane A2 –> activates nearby platelets –> cycle continues

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21
Q

vWF factor is
1-essential for platelet activation
2-necessary for platelet adhesion
3-needed to stimulate platelet aggregation
4-required for Hageman factor to degrade platelets

A

2-necessary for platelet adhesion

*remember that vWF is found in the sub-endothelial matrix, and can be released by endothelial cells and platelets

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22
Q

Clotting factors

A 
FACTOR I = FIBRINOGEN
FACTOR II = PROTHROMBIN
FACTOR III = TISSUE THROMBOPLASTIN 
FACTOR IV = CALCIUM 
Factor V = proaccelerin 
Factor VII = proconvertin
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23
Q

FACTOR I = ______. Where is it synthesized and what is it converted to? Function?

First factor in ______? Activates what?

A

fibrinogen is synthesized in the liver and converted to fibrin by thrombin enzyme

The function of fibrin = threadlike protein fibers that trap RBCs, platelets & fluid during clotting. Fibrin is the 1st factor in intrinsic coagulation, and activates factor XII.

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24
Q

FACTOR II = prothrombin. Where is it synthesized in the presence of ______. Converted to?

A

Synthesized in the liver in the presence of vitamin K, and converted to thrombin during coagulation.

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25
Q

FACTOR III = tissue thromboplastin. Required for? Released by?

A

released from damaged tissue, required to initiate second phase = the extrinsic pathway

Also catalyzes the conversion of prothrombin to thrombin

26
Q

FACTOR IV =

A

CALCIUM - REQUIRED THROUGHOUT THE ENTIRE CLOTTING SEQUENCE

27
Q

FACTOR VIII =

A

antihemophilic factor A = vWF IS THE CARRIER FOR FACTOR VIII

28
Q

Calcium and vitamin K deficiency can cause a problem with _____

A

clotting

29
Q

Fibrin is…

A

threadlike protein fibers that trap RBCs, platelets, and fluid during clotting

30
Q

CALCIUM IS REQUIRED FOR…

A

MULTIPLE STEPS IN THE PROCESS TO ACTIVATE CLOTTING FACTORS

31
Q

VITAMIN K ESSENTIAL IN THE…

A

SYNTHESIS OF CERTAIN CLOTTING FACTORS IN THE LIVER

32
Q

SEQUENCE OF EVENTS IN BLOOD CLOT FORMATION

*Injury to the blood vessel induces formation of what? Steps from here with this first thing…

What does prothrombin attach to?

What assists in clot retraction?

A

1- injury to the blood vessel wall or to blood induces formation of PROTHROMBIN ACTIVATOR - release of Tissue thromboplastin

2- prothrombin activator changes PROTHROMBIN TO THROMBIN

  • this is DEPENDENT ON ADEQUATE CALCIUM
  • prothrombin attaches to platelets adherent to injured area

3- Thrombin changes FIBRINOGEN TO FIBRIN
-fibrin meshes with blood cells, platelets and plasma to form the clot

4- Clot retraction, assisted by platelets, expresses serum. Remember serum is plasma without clotting factors, such as fibrinogen. Plasma can clot, serum cannot.

33
Q

INTRINSIC PATHWAY

  • includes which factors?
  • activated when?
A

Factors XII, XI, IX, and VIII

-is activated when the Hageman factor (Factor XII) contacts sub-endothelial substances exposed by vascular injury

34
Q

EXTRINSIC PATHWAY

  • which factors
  • is activated when?
A

FACTOR VII, FACTOR III

  • IS THE MOST DOMINANT - is a faster pathway b/c it’s shorter
  • IS ACTIVATED WHEN THE TISSUE FACTOR (TISSUE THROMBOPLASTIN) IS RELEASED BY DAMAGED ENDOTHELIAL CELLS
35
Q

Both the intrinsic and extrinsic pathways lead to…what factors are included? What happens in this pathway?

A

A COMMON PATHWAY (factors X, V, II)

  • prothrombin to thrombin
  • fibrinogen to fibrin
36
Q

Three essential steps in synthesis of blood clot? Reiterate what is on clotting paper.

A

1- injury to the blood vessel wall or to blood induces formation of PROTHROMBIN ACTIVATOR

2- prothrombin activator changes PROTHROMBIN TO THROMBIN

  • this is DEPENDENT ON ADEQUATE CALCIUM
  • prothrombin attaches to platelets adherent to injured area

3- Thrombin changes FIBRINOGEN TO FIBRIN
-fibrin meshes with blood cells, platelets and plasma to form the clot

37
Q

ENDOTHELIUM PREVENTS THE FORMATION OF SPONTANEOUS CLOTS IN NORMAL VESSELS BY SEVERAL ANTICOAGULANT MECHANISMS?

A

-PRODUCTION OF NITRIC OXIDE (NO) AND prostacyclin I2 (PGI2) or prostaglandin, thrombin inhibitors (ANTITHROMBIN III), tissue factor inhibitors (tissue factor pathway inhibitors), and degrading activated clotting factors (THROMBOMODULIN-PROTEIN C)

38
Q

control of clotting - what can fibrin do?

A

FIBRIN in clot absorbs excess thrombin

39
Q

ANTI-THROMBIN III in controlling clotting can do what?

A

inactivate excess thrombin

40
Q

Heparin in controlling clotting does what? Enhances what? Released by?

A

heparin is produced by basophils and mast cells, and enhances the activity of antithrombin III

41
Q

COUMADIN acts by…to control clotting

A

acts by competing with vitamin K and inhibits the production in the liver of prothrombin and other clotting factors

42
Q

PLASMINOGEN (also called?) does what to control clotting. Released from?

A

(profibrinolysin) is activated and becomes plasmin (fibrinolysin)

  • plasminogen activator is released by damaged tissues, which then activate plasmin
  • plasminogen activators are used clinically to dissolve coronary artery clots in pts with acute MIs

-plasmin degrades fibrin clots

43
Q

Bone marrow aspiration usually from?

A

sternum or pelvis

44
Q

How is the intrinsic pathway activated

A

through exposed endothelial collagen

45
Q

How is the extrinsic pathway activated

A

release of tissue factor from damaged endothelial cells after external damage

46
Q

Blood tests of intrinsic pathway

A
  • whole blood clotting time: time it takes for whole blood to clot in the test tube (9-15 minutes normally)
  • PTT (partial thromboplastin time): clotting in test tube is initially prevented by removing calcium, and this measures the time for re-calcified citrated plasma to clot in the test tube
47
Q

Blood tests of the extrinsic pathway (shorter pathway) - remember extrinsic pathway starts d/t presence of?

What is normal?

A

Presence of tissue thromboplastin

  • PT (prothrombin time): is the time needed for recalcified citrated plasma to clot in the presence of tissue thromboplastin – “pro time” adds the critical tissue ingredient (tissue thromboplastin) that is necessary to start off the extrinsic pathway
  • normal PT is 11-15 seconds
  • INR (international normalized ratio) = PT test/PT normal *normal is 0.9-1.3; and people on anticoagulation like Warfarin or eliquis (apixaban) should have INR = 2-3 or 2.5-3.5
48
Q

Platelet function test assesses what?

A

number of platelets

49
Q

What is normal “bleeding time” which assess platelet function

Remember this tends to be normal when?

A

2-7 minutes

Tends to be normal in coagulation disorders of the extrinsic and intrinsic pathway? Idk how?

If it is prolonged, it usually suggests a defect in platelet function.

50
Q

PTT and PT tests are useful to do what?

A

distinguish extrinsic and intrinsic coagulation disorders

51
Q

In liver failure, Coumadin or heparin therapy what will happen to PT and PTT values?

A

both the PT and PTT will be abnormal

52
Q

Blood cell counts go above or below adult levels at birth?

A

increase (d/t trauma of birth and cutting umbilical cord), and these levels decline during childhood

53
Q

What is the major cause of increased RBC production in newborn/fetus? What does this result in?

A

HYPOXIC INTRAUTERINE ENVIRONMENT STIMULATES ERYTHROPOIETIN PRODUCTION

THIS RESULTS IN POLYCYTHEMIA OF THE NEWBORN

54
Q

Large number of what in full-term neonates?

A

Large number of immature erythrocytes (reticulocytes) are in full-term neonates

55
Q

In full-term and premature infants what is the lifespan of RBCs?

A

full-term 60-80 days; premature 20-30 days

56
Q

Children have more ______ lymphocytes d/t frequent viral infections

A

atypical

57
Q

Neutrophil count at birth is?

A

high and rises during the first days of life

after two weeks levels fall to below or around adult, and by four years old the same as adult

58
Q

Which wbcs are high the first year of life?

A

eosinophils (also higher in children) and monocytes

59
Q

Platelet count in full-term newborn vs adult?

A

about the same

60
Q

Humoral immune system and lymphocyte function with age?

A

lymphocyte function declines, and humoral immune system is less responsive

Advanced Patho UC Exam #2 (5 decks)

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