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HEM Exam 1 > Platelet Production and Function > Flashcards

Platelet Production and Function Flashcards

1
Q

what kind of cells do megakaryotes develop from?

A
  • hematopoietic stem cells
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2
Q

where do hematopoietic stem cells reside?

A
  • in the bone marrow
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3
Q

stem cell gives rise to

A
  • early bilineage progenitors that are able to undergo erythrocyte or megakaryocytic differentiation
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4
Q

Meg-CFCs begin

A
  • endomitosis
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5
Q

what happens in endomitosis

A
  • DNA replication continues

- neither nucleus nor cell undergoes division

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6
Q

what does endomitosis produce?

A
  • a polyploid cell
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7
Q

after endomitosis, what happens with megakaryoctes?

A
  • they undergo cytoplasmic maturation
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8
Q

process of cytoplasmic maturation

A
  • increase in size
  • fill with platelet-specific granules
  • expand content of cytoskeletal proteins
  • develop invaginated membrane system
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9
Q

thrombopoietin function

A
  • the physiologically relevant regulator of platelet production
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10
Q

what is the TPO receptor

A
  • C-Mpl
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11
Q

C-Mpl is located on

A
  • megakaryocytes

- platelets

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12
Q

binding of TPO to its receptor does what

A
  • prevents apoptosis of megakaryocytes

- increases their number, size, and ploidy

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13
Q

additional of TPO to CD34+ cells in culture results in

A
  • majority of cells becoming megakaryocytes

- shedding platelets

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14
Q

synthesis of TPO is

A
  • static
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15
Q

TPO is made in

A
  • the liver
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16
Q

plasma TPO concentrations are regulated by

A
  • platelet production rates
  • platelet mass
  • MK mass
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17
Q

process of TPO regulation

A
  • platelets and MKs expression c-Mpl receptors that bind and clear TPO from circulation
  • thus regulate free TPO levels
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18
Q

integrins are

A
  • heterodimeric transmembrane molecules that cells use to both bind to and respond to extracellular matrix proteins
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19
Q

integrins composed of

A
  • alpha and beta subunits
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20
Q

integrins link

A
  • extracellular matrix

- intracellular cytoskeleton

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21
Q

clustering of integrins leads to

A
  • signaling into the cell
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22
Q

signaling in the cell also causes

A
  • activation of other integrins
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23
Q

major platelet glycoproteins that are integrins

A
  • a2B1

- A2bB3

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24
Q

another name for a2B1

A
  • GPIa-IIa
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25
Q

GPIa-IIa binds

A
  • collagen
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26
Q

another name for a2bB3

A
  • GPIIb-IIIa
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27
Q

GPIIb-IIIa binds

A
  • fibrinogen
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28
Q

platelet glycoproteins that are not integrins

A
  • GP Ib-IX-V

- GPVI

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29
Q

GP Ib-IX-V binds

A
  • von Willebrand factor
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30
Q

GPVI activates

A
  • platelets by binding to collagen
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31
Q

platelet plug formation

A
  • adhesion
  • activation
  • aggregation
  • secretion
32
Q

adhesion

A
  • platelets stick to injured vessel wall via GP Ib-IX-V (1b-9-5) binding to vWF
33
Q

activation

A
  • resting platelets come into contact with agonists that bind receptors
  • signaling occurs
  • platelets change shape, secrete, and activate their GP IIb-IIIa integrins
34
Q

aggregation

A
  • platelets stick to each other via fibrinogen bridges binding to activated GP IIb-IIIa
35
Q

secretion

A
  • platelets release granular contents and potentiate clotting
36
Q

platelet activators examples

A
  • thrombin
  • thromboxane
  • collagen
  • ADP
37
Q

thrombin receptor

A
  • PAR-1
38
Q

type of receptor that PAR-1 is

A
  • GPCR
39
Q

what is the ligand of PAR-1

A
  • it’s own proteolyzed N-terminus
40
Q

importance of thrombin

A
  • most potent platelet agonist
41
Q

how is thromboxane produced

A
  • arachidonic acid -> TxA2

- by COX1

42
Q

COX1 reversibly blocked by

A
  • NSAIDS
43
Q

COX1 irreversibly blocked by

A
  • aspirin
44
Q

thromboxane receptor - type of receptor

A
  • GPCR
45
Q

what keeps the platelets from sticking to normal endothelium?

A
  • nitric oxide
  • ecto-ADPase
  • prostacyclin
46
Q

nitric oxide

A
  • vasodilator
47
Q

Ecto-ADPase

A
  • chews up ADP to prevent platelet activation
48
Q

how is prostacyclin produced

A
  • arachadonic acid -> prostacyclin

- via COX-1 and COX-2

49
Q

prostacyclin

A
  • vasodilator

- inhibits platelet activation

50
Q

membrane of platelets after activation

why?

A
  • turned inside out

- so the negative charges are on the outside

51
Q

what anchors themselves to the now neg charged platelet membrane?

A
  • coagulation proteins with gamma carboxyl groups
52
Q

qualitative platelets disorders diagnosed by

A
  • a prolonged bleeding time

- or PFA 100 time

53
Q

PT in platelet qualitative disorders

A
  • normal
54
Q

PTT in platelet qualitative disorders

A
  • normal
55
Q

TT in platelet qualitative disorders

A
  • normal
56
Q

DDX of qualitative platelet disorders

A
  • congenital

- acquired

57
Q

DDx of congenital qualitative platelet disorders

A
  • Bernard-Soulier

- Glanzmann’s thrombaesthenia

58
Q

Bernard-Soulier defect in

A
  • Ib-IX on platelet surface
59
Q

result of Bernard-Soulier

A
  • no adhesion
60
Q

Ddx of acquired qualitative platelet disorders

A
  • uremia
  • drugs
  • herbs
  • myeloproliferative diseases
61
Q

drugs that induce qualitative platelet disorders

A
  • ASA

- NSAIDS

62
Q

symptoms of platelet dysfunction

A
  • same defects as primary hemostasis
  • petechiae
  • mucocutaneous bleeding
63
Q

mucocutaneous bleeding is

A
  • oozing and bruising
64
Q

mucocutaneous bleeding is NOT

A
  • hematomas

- bleeding into joints

65
Q

abnormal platelet activation results in

A
  • arterial occlusion
66
Q

with splenic enlargement and when platelets go there to hang out, what happens with the TPO levels?

A
  • they stay the same
67
Q

collagen receptors

A
  • GP Ia/IIa

- GP VI

68
Q

adhesion to collagen mediated by

A
  • GPIa/IIa
69
Q

GPVI acts in complex with

to cause

A
  • FcR gamma

- platelet activation

70
Q

ADP released by

A
  • damaged RBCs
71
Q

ADP secreted by

A
  • activated platelets
72
Q

ADP receptors

A
  • P2Y12

- P2Y1

73
Q

type of receptor P2Y12, P2Y1

A
  • GPCR
74
Q

P2Y12 target of

A
  • anti platelet drugs
75
Q

Glanzmann’s defect in

A
  • IIb/IIIa
76
Q

result of Glanzmann’s

A
  • no aggregation

HEM Exam 1 (22 decks)

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