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MDTI > Platelets > Flashcards

Platelets Flashcards

1
Q

artery vs vein clots

A

artery: predominetly composed of platelets, pale red in color, inhibited by aspirin, likely to occur in setting of turbulence
vein: composed of clotting factors,erythrocytes, and platelets

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2
Q

artery vs vein clots

A

artery: predominetly composed of platelets, pale red in color, inhibited by aspirin, likely to occur in setting of turbulence
vein: composed of clotting factors,erythrocytes, and platelets

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3
Q

shape of resting vs activated platelets

A

resting: smooth, round
activated: irregular, sticky (if on surface, look like over easy egg)

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4
Q

what are platelets lacking?

A

nuclei (what they have is what they get. very little protein production)

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5
Q

factors secreted by artery endothelial that inhibits platelets activation

A

NO & PGI2 (Prostaglandin I2). make platelets more resistant to activation by increasing cAMP levels

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6
Q

von Willebrand factor (VWF)

A

molecular glue with binding sites for platelet surface and collagen. works to adhere platelets to site of vessel damage. necessary for adhesion at the flow rates seen in arteries

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7
Q

role of collagen in vessel damage

A

platelets stick to collagen fibrils and become activated.

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8
Q

role of tissue factor in vessel damage

A

activates platelets indirectly via thrombin production

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9
Q

what factors are secreted by activated platelets that recruit more platelets to the clot?

A

ADP & TxA2

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10
Q

relationship of platelets to the clotting cascade

A

support the ten-ase and prothrombinase complexes since the negatively charged lipids on their outer membrane act as the rxn surface

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11
Q

what is the main integrin responsible for cohesion in platelets?

A

alpha 2b beta 3

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12
Q

what is the main integrin responsible for cohesion in platelets?

A

alpha 2b beta 3

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13
Q

platelet activation GPCR agonist ligands

A

TxA2, locally generated thrombin, ADP released from platelet granules

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14
Q

what are platelets lacking?

A

nuclei (what they have is what they get. very little protein production)

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15
Q

factors secreted by artery endothelial that inhibits platelets activation

A

NO & PGI2 (Prostaglandin I2). make platelets more resistant to activation by increasing cAMP levels

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16
Q

von Willebrand factor (VWF)

A

molecular glue with binding sites for platelet surface and collagen. works to adhere platelets to site of vessel damage. necessary for adhesion at the flow rates seen in arteries

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17
Q

role of collagen in vessel damage

A

platelets stick to collagen fibrils and become activated.

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18
Q

role of tissue factor in vessel damage

A

activates platelets indirectly via thrombin production

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19
Q

what factors are secreted by activated platelets that recruit more platelets to the clot?

A

ADP & TxA2

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20
Q

relationship of platelets to the clotting cascade

A

support the ten-ase and prothrombinase complexes since the negatively charged lipids on their outer membrane act as the rxn surface

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21
Q

how do platelets aggregate?

A

upon activation, platelets activate surface integrins via GPCR signals. Once activated, these proteins display fibrinogen receptors, which cross link platelets

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22
Q

what is the main integrin responsible for cohesion in platelets?

A

alpha 2b beta 3

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23
Q

GPCR signals after platelet activation

A

agonists of platelet activation bind to the GPCR on the platelet, which then signal downstream causing a rise in intracellular Ca levels. This triggers activation of the integrin via the binding of talin protein to integrin

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24
Q

platelet activation GPCR agonist ligands

A

TxA2, locally generated thrombin, ADP released from locally damaged cells

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25
Q

TxA2

A

pro platelet activation ligand generated by platelets. one of the most potent activators of platelets.

26
Q

Production pathway of TxA2

A

phosphatidylcholine (PC) –> arachidonate –> PGG2 (via COX-1) –> PGH2 –> TxA2

27
Q

COX-1

A

enzyme that converts arachidonate to PGG2. inhibited by aspirin

28
Q

aspirin mechanism

A

irreversibly inhibits Cox1 so that platelets are not activated via TxA2 and clotting is inhibited.

29
Q

progenitor of platelets

A

megakaryocytic from common myeloid progenitor

30
Q

how do megakaryocytics produce platelets?

A

spit out long psuedopods called pro-platelets, which produce platelets at tips. process isn’t entirely understood, but needs to have made everything the platelet will need in its life.

31
Q

final cytokine in megakaryocyte generation?

A

TPO

32
Q

Thrombopoieton (TPO)

A

prinicple cytokine regulating the platelet count

33
Q

where is TPO produced

A

constitutively in liver & somewhat in kidney

34
Q

TPO receptor

A

MPL, expressed on megakaryocytic and on platelets

35
Q

what happens when the platelet count falls?

A

free TPO levels increase (amount that makes it to bone marrow increases), stimulating increased megakaryocytopoiesis.

36
Q

what is a normal platelet count?

A

150-400,000

37
Q

how long do platelets last?

A

10 days

38
Q

thrombocytopenia

A

low platelet count

39
Q

functions of platelet

A

contribute to homeostasis, regulate platelet production (TxA2), promote activation of factors 2/10 (lipophospholipids)

40
Q

pathophysiology of ITP

A

antibodies that recognize epitopes on surface of platelets (integrin, etc), reticuloendothelial system then phagocytoses antibody bound platelets

41
Q

petechiae

A

pin head size hemorrhages which reflect the absence of platelets

42
Q

typical symptoms of bleeding due to platelet defect (inability to form platelet plugs)

A

petechiae/ecchymoses, epistaxis/menorrhagia, skin and mucus membrane bleeding, immediate bleeding

43
Q

typical symptoms of bleeding due to coagulation defects (inability to form thrombin and fibrin)

A

deep spreading hematomas, hemarthroses, retroperitoneal bleeding, delayed bleeding when an inadequate fibrin clot breaks down prematurely (platelet clot occurs, but it is not great and is broken down quickly by plasmin)

44
Q

why does application of pressure stop bleeding?

A

creates local stasis so that coagulation factors can accumulate and work faster

45
Q

mechanism of death from coronary artery occlusion

A

atherosclerotic plaques bulge into vessel and restrict flow. eventually plaque ruptures into vessel, exposing blood to tissue factor, collagen, oxidized lipids. causes rapid pile up of platelets in already constricted area

46
Q

causes of thrombocytopenia

A

failure of production, reduced survival/increased destruction, increase pooling in spleen

47
Q

causes of decreased platelet production

A

decreased megakaryocytes and/or ineffective production

48
Q

thrombocythemia

A

neoplastic thrombocytosis. clonal disorder or malignancy driving platelet production. JAK gain of function mutation.&raquo_space;1million

49
Q

clinical features of ITP (Immune thrombocytopenic purport)

A

autoimmune disorder, more common in women, chronic in adult, acute in kids, petechiae and ecchymoses at low platelet counts.

50
Q

physical and lab findings of ITP

A

low platelet counts, rest of CBC is normal, spleen size is usually normal, fatal bleeding is rare (platelets that are present are normal, there are just fewer of them)

51
Q

pathophysiology of ITP

A

antibodies that recognize epitopes on surface of platelets (integrin, etc), reticuloendothelial system then phagocytoses antibody bound platelets

52
Q

ITP treatments

A

inhibit phagoctye mediated clearance of Ab coated platelets (steroids, splenectomy, IVIG), decrease antibody production (steroids, rituximab), impair T/B cell interactions (steroids, immunosuppresants), enhance platelet production (TPO mimetics)

53
Q

how do steroids inhibit phagocytosis of platelets?

A

they down regulate Fc receptors on surface of megakaryocytes

54
Q

rituximab

A

drug that binds to CD20 (on B cells) and reduces the B cell population.

55
Q

drug induced thrombocytopenia

A

drug sticks to glycoprotein on platelet surface, Ab recognizes drug.glycoprotein complex, Ab covered platelets destroyed by RES (quinine is example drug). worse upon second exposure

56
Q

causes of increased sequestration of platelets

A

typically 1/3 of all platelets reside in spleen, so when spleen enlarges, so does this %.

57
Q

glanzmann’s thrombasthenia

A

alpha2 beta3 deficiency that leads to defect in platelet aggregation

58
Q

thrombocytosis

A

elevated platelet count (>450k), normal platelets, no problems with bone marrow. commonly acquired after splenectomy, iron deficiency, inflammatory states, etc. sometimes inherited as TPO/MPL mutations

59
Q

thrombocythemia

A

neoplastic thrombocytosis. clonal disorder or malignancy driving platelet production. JAK gain of function mutation.&raquo_space;1million

60
Q

functions of TPO

A

stimulate megakaryocyte maturation & promote platelet release (bound to platelets via MPL when platelet levels are normal)

MDTI (42 decks)

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