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Coagulation > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

abnormal clot in vitro, retraction and normal plt count

A

Glanzmann Thrombasthenia

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2
Q

What is clot retraction

A

volume of a formed clot is reduced through contraction of cytoskeleton of activated plts within the clot

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3
Q

Deficiency or abnormality of the plt membrane GP IIb/ IIIa complex

A

Glanzmann Thrombasthenia

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4
Q

Petechiae, purpura, menorrhagia, GI bleeding, hematuria

A

Glanzmann Thrombasthenia

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5
Q

What levels of GP in Glanzmann thrombasthenia

A

homo severely decreased to no GP IIb/ IIIa
hetero- 50-60% of normal GP IIb/ IIIa

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6
Q

Lab test in Glantzmann Thrombasthenia

A

plts normal
lack of aggregation in response to all plt activating agents
diminished plt activity

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7
Q

How is GT treated

A

normal plt transfusion

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8
Q

What type of platelet disorder is GT

A

platelet aggregation

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9
Q

platelet disorder where GP Ib/ IX/ V complex is missing from platelet surface

A

Bernard Soulier Giant platelet syndrome

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10
Q

If there is an inability to bind to VWF, then platelets have an inability to

A

adhere to exposed subendothelial cells, causes bleeding

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11
Q

In childhood: Ecchymoses, epistaxis, gingival bleeding

A

Bernard-Soulier Giant platelet syndrome

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12
Q

How is Bernard Soulier treated

A

cannot be correct by adding plasma
afibrinolytic therapy- treat the mucosal bleeding

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13
Q

What glycoprotein defect is most often the cause of BSS

A

GP Ib alpha

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14
Q

normal ADP, epi, collagen, arachadonic
no response to ristocetin

A

What lab results can be expected from BSS

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15
Q

What is the main disorder of plt aggregation
and plt adhesion?

A

aggregation- Glanzmann Thrombsthenia
adhesion- Bernard Soulier Giant plt

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16
Q

normal plt count
mucocutaneous hemorrhage, hematuria, epistaxis, easy bruising

A

platelet secretion

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17
Q

What are dense granules

A

storage site for serotonin, nucelotides, Ca and pyrophosphate

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18
Q

Deficiency associated with albinism

A

Dense granules

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19
Q

Plt aggregation test shows an aggregation pattern affected by ADP
What deficiency is this

Arachidonic acid …
epi and low dose ADP …..
Collagen …..

A

dense granules
Arachidonic acid … no response
epi and low dose ADP …..primary wave, no secondary
Collagen ….. decreased

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20
Q

dense granule deficiency that shows defective lysosomal function

A

Hermansky-Pudlak syndrome

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21
Q

Swiss cheese plts

A

Hermansky-Pudlak syndrome

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22
Q

Dense granule deficiency that causes giant lysosomal granules

A

Chediak Higashi syndrome

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23
Q

Dense granule deficiency that causes microthrombocytopenia

A

Wiskottp-Aldrich Syndrome WAS

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24
Q

Dense granule deficiency that is autosomal recessive and causes an absence of radial bones

A

Thrombocytopenia with absent Radii syndrome
TAR

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25
Q

What are alpha granules

A

storage site for proteins produced by the megakaryocyte or present in plasma and taken up by plts

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26
Q

Primary reason for platelets to have a granular appearance

A

alpha granules

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27
Q

absence of alpha granules

A

gray platelet syndrome

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28
Q

large plts with a gray appearance

A

gray plt syndrome

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29
Q

Which part of the platelet is affect in storage pool diseases

A

dense granules

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30
Q

Deficiency that leads to lifelong mild bleeding disorder,
platelets do not adhere to collagen

A

collagen receptor deficiencies

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31
Q

What are the 3 ADP receptors

A

P2X1 - Ca ion influx
P2Y1 Ca mobilization and shape change in response to ADP

P2Y12 macroscopic plt aggregation

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32
Q

No Phospholipid flip

A

Scott syndrome
no binding of vitamin K dependent factors

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33
Q

platelets always in activated state

A

Stormorken syndrome

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34
Q

What can case acquired defects of platelet function

A

drug ingestion

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35
Q

What drug
irreversible acetylates/ inactivates cyclooxygenase

A

aspirin

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36
Q

What is not affected by aspirin

A

endothelial cells- produce nitric oxide, a plt inhibitor, making them unaffected by aspirin

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37
Q

drugs that inhibit cyclooxygenase are ____

A

reversible

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38
Q

How do P2Y12 ADP receptor inhibitors work

A

plt activation and aggregation are induced by ADP and inhibited

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39
Q

Clopidogrel, prasugrel, ticlopidine, ticagrelor, cangrelor

A

P2Y12 ADP receptor inhibitors

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40
Q

How does clopidogrel (plavix) work

A

needs to be converted to an active drug by a liver enzyme

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41
Q

CYP2C19 gene

A

clopidogrel plavix

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42
Q

Platelet drug that interferes with fibrinogen, inhibits plt aggregation

A

GP IIb/ IIIa receptor inhibitor

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43
Q

Drug used with patients under percutaneous coronary intervention

A

GP IIb/ IIIa receptor inhibitors

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44
Q

Drug that inhibits thrombin by blocking binding site on PAR-1

A

PAR-1 antagonist

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45
Q
A

P2Y12 inhibitors when taken with aspirin inhibit plt function

46
Q

platelet disorder that shows
PV, CML, ET, CMF
also decreased aggregation and secretion in response to epi, ADP and collagen

A

MPNs myeloproliferative neoplasms

47
Q

plt disfunction that arises from coating of plt membrane by paraprotein

A

multiple myeloma and waldenstrom macroglobulinemia

48
Q

causes plt activation and fragmentation in the extracorporeal circuit

A

CPB cardiopulmonary bypass surgery

49
Q

associated with hemostatic abnormalities
alcoholic cirrhosis

A

liver disease

50
Q

rare disorder where there is an absence or near absence of fibrinogen, causing abnormal platelet function

A

hereditary afrinogenemia

51
Q

platelets aggregate at lower concentrations of aggregating agents than normal

A

hyperaggregable plts

52
Q

sticky plt syndrome

A

hyperaggregable plts

53
Q

Hereditary Vascular disorder where
thin walled blood vessels with a discontinuous endothelium

A

Hereditary Hemorrhagic Telangiectasia
Rendu Osler Weber Syndrome

54
Q

giant cavernous hemangiomas (vascular tumors), present at ___

A

Hemangioma Thrombocytopenia
Kasabach Merrit Syndrome
present at birth

55
Q

hyperextensible skin, hypermobile joints, defects in collagen production

A

Ehlers-Danlos Syndrome

56
Q

allergy associated with foods, drugs, cold, insect bites, vaccinations

A

Henoch Schonlein purpura
allergic purpura

57
Q

proteins coat the plt membrane- causes abnormalities in plt aggregation, adhesion and actibation

A

paraproteinemia

58
Q

Deposition of abnormal quantities of amyloid protein in tissues

A

amyloidosis

59
Q

fibrous protein consisting of rigid, aggregated fibrils

A

amyloid

60
Q

dark flat blotches, leave ae spots, due to lack of collagen support

A

Senile pupura

61
Q

when antibodies develop to vessel wall components and create complexes that change the wall permeability

A

Drug induced vascular purpuras

62
Q

What is epistaxis

A

nose bleeds

63
Q

small pinpoint hemorrhages, 1 mm diameter

A

Petechiae

64
Q

3mm diameter, generally round

A

purpura

65
Q

1cm or larger, irregular in shape

A

eccchymoses

66
Q

Large plts- megathrombocytes
dohle like bodies in neutrophils
mostly asymptomatic
normal plt function

A

May-Hegglin Anomaly

67
Q

What is the cause of most congenital types of plt disorders

A

impaired plt PRODUCTION due to chromosomal abnormalities or genetic defects
BM does not have enough megakaryocytes

68
Q

What is the normal plt reference range

A

150-450

69
Q

What is the range for thrombocytopenia

A

<100

70
Q

What is the most common cause of clinically important bleeding?

A

thrombocytopenia

71
Q

severe neonatal thrombocytopenia that causes absence or extreme hypoplasia of radial bones

A

TAR syndrome

72
Q

BM failure causes no megakaryocytes to be produced, TPO receptor is not functioning
can develop into luekemia, aplastic anemia, myelodysplasia
petechiae and bleeding
in infants at birth

A

Congenital Amegakaryocytic thrombocytopenia

73
Q

thrombocytopenia due to incomplete megakaryocyte differentiation

normal plt functon and morphology
absent or mild bleeding

A

autosomal dominant thrombocytopeniaa

74
Q

Disorders due to decreased plt production

A

X-linked thrombocytopenia
May-Hegglin Anomaly
TAR syndrome
Congenital Amegaakaryocytic Thrombocytopenia
Autosomal dominant thrombocytopenia

75
Q

What can cause neonatal thrombocytopenia (platelet production issue)

A

TORCH syndrome infection - toxoplasmosis, rubella, CMV (most common), herpes
maternal ingestion of sulfonamides
Impaired plt production
Increased plt consumption or sequestration

76
Q

What are 3 disorders that lead to decreased plt production

A

infections, chronic alcoholism, drug induced

77
Q

Disorders that cause Immune platelet destruction

A

ITP
Immuno drug induced thrombocytopenia
neonatal immune mediated thrombocytopenia
posttransfusion Purpura
secondary thrombocytopenia, immune mediated

78
Q

What is ITP

A

immune thrombocytopenia purpura

79
Q

Distinguish ITP
acute
chronic

A

acute- kids, vaccines, infections
chronic- adults, mostly F

80
Q

onset bruising, petechiae and epistaxis on normally healthy child, they had just received a vaccine

A

Acute ITP

81
Q

What causes chronic ITP

A

IgG antibodies made against plts,

82
Q

What is menorrhagia and what condition can it be seen in

A

very heavy period, chronic ITP

83
Q

What lab test to expect with ITP

A

plt count low
plt morpho normla

BM hyperplasia
coag- abnormal if plts are non functioning

84
Q

What type of Drug induced thrombocytopenia
immune complex induced, Drug induced autoabs,
hapten induced abs, drug dependet abs

abs interact with plts only in presence of drug
haptens act as a complete antigen
no drug presence needed
heparin induced

A

dependent- abs interact with plts only in presence of drug
hapten induced-haptens act as a complete antigen
drug induced- no drug presence needed
immune complex induced-heparin induced

85
Q

What is neonatal alloimmune thrombocytopenia NAIT

A

IgG from mom crosses placenta and cause thrombocytopenia in fetus

86
Q

What is neonatal autoimmune thrombocytopenia

A

passive transfer of maternal ITP autoantibodies

87
Q

mostly patients that are multiparous, middle aged women, usually have history of a blood transfusion
1 week after transfusion shows purpura

A

PTP post transfusion purpura

88
Q

What causes PTP

A

alloantibodies to antigens on plts in transfused product

89
Q

thrombocytopenia due to loss of ADAMTS13

A

TTP
thromotic thrombocytopenic purpura
Mochcowitz syndrome

90
Q

What does ADAMTS13 do

A

cuts VWF into small pieces allowing plts to be triggered

91
Q

Who is more commonly affected by TTP

A

women 30-40

92
Q

What lab tests to expect with TTP

A

intravascular hemolysis
BM- increased megakaryocytes
schistocytes
normal coag tests

93
Q

How to treat TTP

A

infusion of plasma that are deficient of ADAMTS13
UL-VWF multimers removed

94
Q

What is HUS

A

Hemolytic Uremic syndrome
thrombotic microangiopathies caused by bacteria
mostly Shigella in kids or E. coli O157
cause damage to colon- bloody diarrhea

95
Q

What can cause adult HUS

A

immunosuppressive drugs or chemo, damaged kidneys, usually will need dialysis

96
Q

What lab results to expect with HUS

A

hemolytic anemia
renal failure
thrombocytopenia

97
Q

which is more severe HUS or TTP
in terms of thrombocytopenia
in terms of RBC anemia

A

TTP both

98
Q

What is DIC

A

coag cascade activated and traps plts in fibrin clot

99
Q

DIC and TTP
which is red and which is white clots

A

DIC-Red
TTP-White

100
Q

What causes a big spleen syndrome

A

increased level of plts make spleen sequester more, there are too many plts produced because the plt count is low in blood vessels, BM is making more to compensate

101
Q

What is the range for thrombocytosis

A

more than 450

102
Q

What is reactive thrombocytosis

A

increased plt count due to inflammation trauma or underlying condition

103
Q

What is postsplenectomy thrombocytosis

A

spleen is removed causes high plt count

104
Q

What is Kawasaki disease

A

disorder caused by inflammation of the walls of small arteries in body

105
Q

Who is most affected by Kawasaki disease

A

infants and young kids of Japanese descent

106
Q

What lab tests to expect with exercise induced thrombocytosis

A

MPDs extreme values

107
Q

What is the most common cause of thrombocytosis

A

Essential thrombocythemia ET

108
Q

What lab results to expect in ET

A

way too many megakaryocytes in BM
super high plt count
abnormal plts, clumped agranular

109
Q

Who is most affected by ET

A

middle aged/ older patients

110
Q

Digital pain, gangrene, erythromelalgia, hemorrhagic episodes

A

ET

Coagulation (7 decks)

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