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KCSU17 Patho/Pharm Submodule 1 > Platelets > Flashcards

Platelets Flashcards

1
Q

primary job of platelet

A

hemostasis

stops the blood loss

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2
Q

which component of the cell is essential for hemostasis

A

cell membrane

covered with glycoproteins, coagulation factors, and phospholipids

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3
Q

IIb/IIIa protein

A

essential glycoprotein

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

forms stable clot

once activated they stick together

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4
Q

granules in platelet fxn

A

have vasoactive substances

causes vasoconstriction

histamine, ADP, platelet factor 4

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5
Q

activated platelet

A

degranulates, amplifies the coagulation response

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6
Q

platelet function once vessel injury occurs

A
  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
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7
Q

coagulation factors are ____ form in blood

A

inactive

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

then they go on to activate the next one

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8
Q

coagulation cascade

A

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

(extrinsic or intrinsic)

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9
Q

common coagulation pathway

A

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
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10
Q

fibrin

A

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

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11
Q

endothelial cells

A

vasodilators that line blood vessels

produce vasorelaxors: NO, ADP-ase, prostacyclin

when damaged, stops producing these cells triggering vWF expression

also expresses tissue factor

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12
Q

vonWillebrand’s factor

A

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

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13
Q

blood clot is formed bc of which process

A

coagulation cascade + platelet activation

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

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14
Q

requirements for adequate hemostasis

A
  1. integrity of small vessels
  2. adequate # and fxn of platelets
  3. normal # and fxn of coagulation factors
  4. normal amount of inhibitors
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15
Q

opposition of coagulation

A

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

coagulation inhibitors and fibrinolysis

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16
Q

coagulation inhibitors

A

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)

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17
Q

fibrinolysis

A

breaks up the clot

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

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18
Q

what activates plasminogen ?

A

release of t-PA baby endothelial cells

can be artificially done in stroke, MI

activation occurs at same time as activation of coagulation cascade

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19
Q

what tests do we use to evaluate coagulation process

A
  1. platelet count
  2. PTT
  3. PT
20
Q

platelet count

A

part of CBC

quantitive number of platelets

21
Q

PTT

A

partial thromboplastin time

measures first phase of coagulation

used to monitor dosages of UNFRACTIONATED heparin

22
Q

PT

A

prothrombin time

measures time of combined second and third phases of coagulation

monitors warfarin dosage and liver dysfunction

23
Q

Thrombocytosis

A

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

increases viscosity

24
Q

secondary thrombocytosis

A

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

25
Q

essential thromocytosis

A

occurs less commonly

don’t know why but when work up must exclude everything else

26
Q

thrombocytopenia

A

platelet deficiency

<100,000

often found with petechial bleeding

may also prevent with clotting (may cause clotting to activate too)

27
Q

6 main etiologies of thrombocytopenia

A
  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
28
Q

subtypes of anti platelet Abs in peripheral vessels

A

immune thrombocytopenia purpura

heparin induced thrombocytopenia

thrombotic thrombocytopenia purpura

29
Q

immune thrombocytopenia purpura

A

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)

30
Q

heparin induced thrombocytopenia

A

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

31
Q

thrombotic thrombocytopenia purpura

A

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)

32
Q

splenic sequestration of platelets when?

A

can occur anytime the spleen is enlarged
i.e. liver disease, CML , mono

more platelets are in the spleen than are in the blood

33
Q

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

A

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

34
Q

petechiae

A

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

35
Q

coagulation factor deficiencies

A

hereditary and rare

  1. vonWillebrand’s dx
  2. hemophilia

extensive and severe bleeding following minor trauma

36
Q

von Willebrand’s dx

A

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

37
Q

hemophilia

A

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

38
Q

these deficiencies cause bleeding deeper in the soft tissue

hematoma are large and palpable

A

coagulation factors

39
Q

unable to get bleeding to stop but eventually it does

A

platelet disorder

40
Q

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

A

coagulation deficiency

clot can still form but it isn’t held together

41
Q

disseminated intravascular coagulation

A

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)
42
Q

inherited clotting disorders/thrombophilias

A
  1. factor V lieden
  2. anti thrombin III deficiency
  3. Protein C and Protein S deficiency
43
Q

factor V leiden

A

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

44
Q

anti-thrombin III def.

A

unable to inhibit thrombin

hypercoagulabilty caused by increase in fibrin

45
Q

Protein C and Protein S def.

A

inability to inactivate factors Va and VIIIa

longer activation of 5 and 8 and hypoercoagulable state

KCSU17 Patho/Pharm Submodule 1 (12 decks)

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