Platelets

Question 1

primary job of platelet

Answer 1

hemostasis

stops the blood loss

Question 2

which component of the cell is essential for hemostasis

Answer 2

cell membrane

covered with glycoproteins, coagulation factors, and phospholipids

Question 3

IIb/IIIa protein

Answer 3

essential glycoprotein

once activated, binds to the fibrin to connect one platelet to others

forms stable clot

once activated they stick together

Question 4

granules in platelet fxn

Answer 4

have vasoactive substances

causes vasoconstriction

histamine, ADP, platelet factor 4

Question 5

activated platelet

Answer 5

degranulates, amplifies the coagulation response

Question 6

platelet function once vessel injury occurs

Answer 6

1. to adhere to defect in vessel wall when complexed with vWF
2. release vasoconstrictors and chemicals that cause platelet aggregation (clumping)
3. initiate and propagate the coagulation

Question 7

coagulation factors are ____ form in blood

Answer 7

inactive

remain this way until they are activated by another factor in cascade

then they go on to activate the next one

Question 8

coagulation cascade

Answer 8

highly complex chain ran activated by exposure of sub endothelial tissue OR release of tissue factor

(extrinsic or intrinsic)

Question 9

common coagulation pathway

Answer 9

where they extrinsic and intrinsic pathways merge

1. activation of factor 10 (X) –> 10a
2. Xa cleaves prothrombin into thrombin
3. thrombin cleaves fibrinogen to fibrin

Question 10

fibrin

Answer 10

binds platelets and connects them to ea. other to stabilize the clot

Question 11

endothelial cells

Answer 11

vasodilators that line blood vessels

produce vasorelaxors: NO, ADP-ase, prostacyclin

when damaged, stops producing these cells triggering vWF expression

also expresses tissue factor

Question 12

vonWillebrand’s factor

Answer 12

binds platelets from bloodstream to vessel wall

grabs platelet from circulation and causes degranulation

site where platelet and coagulation factors interact

carrier protein for factor Viii

Question 13

blood clot is formed bc of which process

Answer 13

coagulation cascade + platelet activation

made up of meshwork of fibrin threads with platelets trapping RBC and WBC

Question 14

requirements for adequate hemostasis

Answer 14

1. integrity of small vessels
2. adequate # and fxn of platelets
3. normal # and fxn of coagulation factors
4. normal amount of inhibitors

Question 15

opposition of coagulation

Answer 15

occurs bc we don’t want the clot to be too big (dampens cascade)

coagulation inhibitors and fibrinolysis

Question 16

coagulation inhibitors

Answer 16

natural anticoagulants

protein C, protein S, anti thrombin III

inactive coagulation factors, stopping process

deficiencies lead to hyper coagulable state (more likely to form clots)

Question 17

fibrinolysis

Answer 17

breaks up the clot

plasminogen is activated to make plasmin, which lyses fibrin and breaks up clot

Question 18

what activates plasminogen ?

Answer 18

release of t-PA baby endothelial cells

can be artificially done in stroke, MI

activation occurs at same time as activation of coagulation cascade

Question 19

what tests do we use to evaluate coagulation process

Answer 19

1. platelet count
2. PTT
3. PT

Question 20

platelet count

Answer 20

part of CBC

quantitive number of platelets

Question 21

PTT

Answer 21

partial thromboplastin time

measures first phase of coagulation

used to monitor dosages of UNFRACTIONATED heparin

Question 22

PT

Answer 22

prothrombin time

measures time of combined second and third phases of coagulation

monitors warfarin dosage and liver dysfunction

Question 23

Thrombocytosis

Answer 23

excesss of platelets (above 400,000 - get worried when its more like 700k)

increases viscosity

Question 24

secondary thrombocytosis

Answer 24

excessive platelets that occur secondary to cytokine processes (infection or impending sepsis )

this is most common

may also be bc of iron deficiency, autoimmune, malignant

Question 25

essential thromocytosis

Answer 25

occurs less commonly don't know why but when work up must exclude everything else

Question 26

thrombocytopenia

Answer 26

platelet deficiency <100,000 often found with petechial bleeding may also prevent with clotting (may cause clotting to activate too)

Question 27

6 main etiologies of thrombocytopenia

Answer 27

1. bone marrow injury or disease causing damage to megakaryocytic (CXT, XT, alcohol) or medications (thiazide diuretics, PCN, cephalosporins, NSAIDS, H2 blockers, estrogen) 2. infiltration of bone marrow by cancer cells (leukemia or metastases) -- will affect multiple lines 3. anitplatelet antibody destroys platelets in peripheral vessels (3 subtypes) 4. splenic sequestration of larger # than usual (enlarged spleen - liver disease, CML, mono) 5. failure of stimulation of thrombopoeisis hormones 6. abnormal platelet FUNCTION

Question 28

subtypes of anti platelet Abs in peripheral vessels

Answer 28

immune thrombocytopenia purpura heparin induced thrombocytopenia thrombotic thrombocytopenia purpura

Question 29

immune thrombocytopenia purpura

Answer 29

ITP IgG Abs to platelets cause them to be tagged and trapped in the spleen Pediatric ITP - 1-6, male, occurs acutely after viral infection, resolves spontaneously Adult ITP- females, 30s-40s, occurs insidiously, req. treatment (steroid)

Question 30

heparin induced thrombocytopenia

Answer 30

autoantibody to heparin and platelet factor 4 only occurs in pts on heparin causes activation of platelet and its destruction at same time paradoxical arterial venues clot formation clots in larger arteries AND veins

Question 31

thrombotic thrombocytopenia purpura

Answer 31

TTP adult females (20-50) can be associated with infection, high levels of estrogen (Birth control) lack of an enzyme that cleaves vWF in molecules causing platelets to be consumed and activated (less numbers of free ones in blood)

Question 32

splenic sequestration of platelets when?

Answer 32

can occur anytime the spleen is enlarged i.e. liver disease, CML , mono more platelets are in the spleen than are in the blood

Question 33

why is it uncommon to see hormone failure as a cause of thrombocytopenia?

Answer 33

bc thrompoeitin can be stimulated by the bone marrow, liver, muscles or nervous tissue while erythopoeitin can only be activated by the kidneys

Question 34

petechiae

Answer 34

small breaks in the capillaries cause pin point size hemorrhages in the skin and mucous membranes

Question 35

coagulation factor deficiencies

Answer 35

hereditary and rare 1. vonWillebrand's dx 2. hemophilia extensive and severe bleeding following minor trauma

Question 36

von Willebrand's dx

Answer 36

autosomal dominant cells don't express the vWF on their cells so they are unable to attach to the platelet and clot will also have lower factor 8 levels excessive bleeding in SubQ tissues and skin after injury

Question 37

hemophilia

Answer 37

x linked recessive PRIMARILY effects males episodes of hemorrhage in joints and internal organs Hemophilia A- factor 8 def. Hemophilia B- factor 9 def. hemarthroses will cause pain and deformity

Question 38

these deficiencies cause bleeding deeper in the soft tissue hematoma are large and palpable

Answer 38

coagulation factors

Question 39

unable to get bleeding to stop but eventually it does

Answer 39

platelet disorder

Question 40

get bleeding to stop but only for a short amount of time

Answer 40

coagulation deficiency clot can still form but it isn't held together

Question 41

disseminated intravascular coagulation

Answer 41

condition where body creates and dissolves clots at the same time -- widespread intravascular clot formation and fibrinolysis this will use all the clotting factors and platelets supplied so can be terrible bc eventually can't clot at all (consumptive coagulopathy) large and widespread clotting and bleeding issue caused by 1. dx ass. with shock and tissue necrosis 2. overwhelming bacterial infections (esp. gram - endotoxin that turns on coagulation)

Question 42

inherited clotting disorders/thrombophilias

Answer 42

1. factor V lieden 2. anti thrombin III deficiency 3. Protein C and Protein S deficiency

Question 43

factor V leiden

Answer 43

most common genetic mutation in Factor V that causes it to be resistant to inactivation once activated it stays activated for a long time and clots form

Question 44

anti-thrombin III def.

Answer 44

unable to inhibit thrombin hypercoagulabilty caused by increase in fibrin

Question 45

Protein C and Protein S def.

Answer 45

inability to inactivate factors Va and VIIIa longer activation of 5 and 8 and hypoercoagulable state