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Hematology 2 Lec > CHAPTER 1 - HEMOSTASIS PART 6 > Flashcards

CHAPTER 1 - HEMOSTASIS PART 6 Flashcards

1
Q

From an external substance

A

ACQUIRED DEFECTS OF PLATELET FUNCTION

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2
Q
  1. Drug-related
A

• Aspirin

• NSAIDs and other COX-2 inhibitors (naproxen and ibuprofen)

• Other Antiplatelet medications: ticlopidine and clopidogrel

• Dextran

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3
Q

acytelate the cyclooxygenase enzyme

A

Aspirin

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4
Q

adding/removin one cpd to make it nonfuncitonal

A

acytelate

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5
Q

– secretes thromboxane and prostaglandin

A

cyclooxygenase enzyme

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6
Q

(stimulates the activation of plt and aggregation)

A

thromboxane and prostaglandin

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7
Q

blood donation: deferral after 14 days; plasma and plt are nonfuncitonal

A

NSAIDs and other COX-2 inhibitors (naproxen and ibuprofen)

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8
Q

.Prevent blood clotting by preventing plt aggregation

A

ticlopidine and clopidogrel

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9
Q

Administered to enhance fibrinolysis (plt clot – stabilization of coagulation – agglutinates in the bv to arrest bleeding – interacts w/ bf = not healthy)

A

Dextran

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10
Q

Side effect: reduce plt adhesion to vWF (interference to plt plug formation)

A

Dextran

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11
Q

Normal:

A

140-450 x 109/uL

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12
Q

: transient thrombocytopenia

A

100-150 x 109/uL

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13
Q

(due to medication but can go back as soon as it is eliminated)

A

: transient thrombocytopenia

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14
Q
  • abnormally low
A

• ≤ 100,000/ pL

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15
Q
  • bleeding possible
A

• 30,000-50,000/ pL

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16
Q
  • spontaneous bleeding
A

• ≤ 30,000

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17
Q
  • severe spontaneous bleeding
A

• ≤ 5,000/pL

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18
Q

-decrease in circulating platelets

A

THROMBOCYTOPENIA

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19
Q

-less than 100,000/uL

A

THROMBOCYTOPENIA

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20
Q

-increase in circulating platelets

A

THROMBOYTOSIS /THROMBOCYTHEMIA

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21
Q

-more than 450,000/uL

A

THROMBOYTOSIS /THROMBOCYTHEMIA

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22
Q

-bleeding -

A

THROMBOCYTOPENIA

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23
Q

hallmark for myeloproliferative diseases

A

Primary Thrombocytosis

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24
Q
  • polycythemia vera: thrombocytosis is in sync w/ an abnormality of the rbc
A

THROMBOYTOSIS /THROMBOCYTHEMIA

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25
Q

THROMBOCYTOPENIA

A
  1. Decreased production
  2. Blood Transfusion
  3. Increased Destruction or Consumption
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26
Q
  1. Decreased production
A

a. Megakaryocyte hypoproliferation

b. Ineffective thrombopoiesis

c. Marrow replacement (infiltration) by abnormal cells

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27
Q

a. Megakaryocyte hypoproliferation

A

a.1) Inherited/Congenital Hypoplasia

a.2) Acquired/Drug induced Hypoplasia

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28
Q

Inherited/Congenital Hypoplasia:

A
  1. May Hegglin Anomaly
  2. TAR Syndrome
  3. Fanconi Anemia
  4. Neonatal Thrombocytopenia
  5. Bernard Soulier Syndrome
  6. Wiskott Aldrich
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29
Q

-Large plt (20 um); dohle like bodies (neutrophils, monocytes)

A

May Hegglin Anomaly

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30
Q

-Mutation in MYH9 gene

A

May Hegglin Anomaly

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31
Q

Encodes for myosin heavy chain

A

May Hegglin Anomaly

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32
Q

– contractile protein in plt (imp for activation)

A

Thrombostenin

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33
Q

Causing thrombocytopenia (abnormally large plt but low in level)

A

May Hegglin Anomaly

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34
Q

-absence/hypoplasia of radial bones (small arm)

A

TAR Syndrome

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35
Q

-Mutation in RBM8A gene

A

TAR Syndrome

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36
Q

-occurs in neonates

A

Fanconi Anemia

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37
Q

-bone and visceral organ abnormalities

A

Fanconi Anemia

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38
Q

-pancytopenia (decrease in all blood cells)

A

Fanconi Anemia

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39
Q

-onset: w/in 72 hours of birth

A

Neonatal Thrombocytopenia

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40
Q
  • associated with infections with TORCH
A

Neonatal Thrombocytopenia

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41
Q

Toxoplasma, Rubella, CMV, HIV, Herpes

A

Neonatal Thrombocytopenia

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42
Q

-small platelets

A

Neonatal Thrombocytopenia

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43
Q

-absence of megakaryocytes

A

Neonatal Thrombocytopenia

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44
Q

: directly affect the fetal BM megakaryocyte

A

chlorthiazide and tolbutamide

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45
Q

-Large plt but few

A
  1. Bernard Soulier Syndrome
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46
Q

-Dense granules; small platelets

A
  1. Wiskott Aldrich
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47
Q

-suppresses BM megakaryocyte production and other cells.

A

Acquired/Drug induced Hypoplasia

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48
Q

Acquired/Drug induced Hypoplasia Examples:

A

-methotrexate, busulfan, cytosine, arabinoside, cyclosphamide, cisplatin

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49
Q

– assoc. w/ specific gene chromosomal abnormality

A

Inherited/Congenital Hypoplasia

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50
Q

: HIV treatment

A

-Zidovudine

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51
Q

side effect – severe thrombocytopenia

A

-Zidovudine

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52
Q

eliminates infection but negatively affects the healthy cells

A

-Zidovudine

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53
Q

: thrombocytosis treatment

A

-Anagrelide

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54
Q

(eliminating some platelet to go back to normal level by increasing sequestration or affecting the life span of plt)

A

-Anagrelide

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55
Q

improper administration causes thrombocytopenia

A

-Anagrelide

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56
Q

: long-term consumption may lead to thrombocytopenia

A

-Ethanol

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57
Q

bleeding may not be arrested easily

A

-Ethanol

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58
Q

: after chemotherapy, there will be pancytopenia, destroying some healthy cells

A

-Recombinant IL-2

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59
Q

restores platelet

A

-Recombinant IL-2

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60
Q

chemotherapy-induced thrombocytopenia treatment

A

-Recombinant IL-2

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61
Q

• Seen in megaloblastic anemias

A

Ineffective thrombopoiesis

62
Q

Pernicious anemia, Folic acid deficiency and Vitamin B 12 deficiency

A

Ineffective thrombopoiesis

63
Q

: affects maturation stage of cell; immature cells remained large; nucleus continue to divide but the cytoplasm will not; main cause

A

Folic acid deficiency and Vitamin B 12 deficiency

64
Q

: response will follow after 1-2 weeks

A

Vitamin replacement

65
Q

-impaired DNA synthesis = BM produce abnormal megakaryocytes

A

Ineffective thrombopoiesis

66
Q

-Platelets: decreased survival time and abnormal function

A

Ineffective thrombopoiesis

67
Q

-abnormality in the division and maturation of the megakaryocyte – even plt shedding is affected (ineffective)

A

Ineffective thrombopoiesis

68
Q

-due to infiltration of abnormal cells, inhibitors of thromobopoiesis are produced contributing to thrombocytopenia

A

Marrow replacement (infiltration) by abnormal cells

69
Q

Suppression of normal cell/megakaryocyte production - Affecting thrombopoiesis

A

Marrow replacement (infiltration) by abnormal cells

70
Q

-inhibits maturation of the megakaryocyte

A

Marrow replacement (infiltration) by abnormal cells

71
Q

: lost of platelet containing blood products and coagulation
factors

A

• Donor

72
Q

: may have alloantibodies directed against the antigens of blood products

A

• Recipient

73
Q

: dilution of px platelet

A

• Recipient

74
Q
  1. Increased Destruction or Consumption
A

a. non-immune (premature activation & consumption)

b. Immune destruction

75
Q

a. non-immune (premature activation & consumption)

A

Thrombotic Thrombocytopenic Purpura (TTP)
DIC
HUS
Infections (eg. Dengue)

76
Q

Secondary

A

non-immune (premature activation & consumption)

77
Q

caused by mechanical trauma

A

non-immune (premature activation & consumption)

78
Q

due to inflammation, infection, or gene mutation

A

non-immune (premature activation & consumption)

79
Q

does not involve the immune system

A

non-immune (premature activation & consumption)

80
Q

Gene that produces enzyme, which controls the VWF

A

(ADAMTS-13)

81
Q

responsible for cutting VWF to interact w/ plt in a normal size

A

(ADAMTS-13)

82
Q
  • has uncontrolled and very large VWF
A

Thrombotic Thrombocytopenic Purpura (TTP)

83
Q

VWF is unfolded, multimer, and hyper adhesive (creating a thrombus)

A

Thrombotic Thrombocytopenic Purpura (TTP)

84
Q

: composed of 1 VWF + plt

A
  • Hyaline thrombi
85
Q
  • thrombocytopenia: circulating plt decreases due to thrombi formation
A

Thrombotic Thrombocytopenic Purpura (TTP)

86
Q
  • aka Moschcowitz Symdrome
A

Thrombotic Thrombocytopenic Purpura (TTP)

87
Q
  • thrombocytopenia: due to simultaneous coagulation
A

Disseminated Intravascular Coagulation (DIC)

88
Q

: composed of fibrinogen + plt (plt is trapped in agglutination during coagulation concerning fibrinogen)

A
  • DIC thrombi
89
Q

: invasive bacteria in the colon that destroys mucosa lining

A
  • S.dysentiriae/E.coli 0157:H7 serotype
90
Q
  • thrombocytopenia: as soon as the colon is damaged, the endothelium of the colon releases VWF creating thrombi that may go to the renal structure
A

Hemolytic Uremic Syndrome (HUS)

91
Q

Involves the immune system, Abs, and auto-Abs

A

b. Immune destruction

92
Q
  • Acute: onset after 1-3 weeks
A

Immune (Idiopathic) Thrombocytopenic Purpura (ITP)

93
Q

Ab and Ag forms an immune complex that binds w/ plt = elimination of Gp IIb-IIIa

A

Immune (Idiopathic) Thrombocytopenic Purpura (ITP)

94
Q

-after plt is destroyed, it will be removed by the reticuloendothelial cells from the circulation

A

Immune (Idiopathic) Thrombocytopenic Purpura (ITP)

95
Q
  • unfractioned heparin administration: destroys PF4, affecting aggregation and plt destruction
A

Heparin-Induced Thrombocytopenia

96
Q

: used to test platelet aggregation

A
  • Ristocetin
97
Q

in vivo/unfractioned form administration will facilitate interaction of VWF + Gp Ib-IX causing adhesion, aggregation, and in vivo agglutination

A
  • Ristocetin
98
Q

: can cause transient tmrombocytopenia

A
  • Hematin
99
Q

: induces thrombocytopenia

A
  • Rotamine sulfate (for parasitic infection) and Bleomycin ( for bacterial infection)
100
Q

Deficiency: disintegrase + ADAMTS-13

A

TTP

101
Q

-platelets are trapped in fibrin clots

A

DIC

102
Q

-VWF involvement

A

HUS

103
Q

Disease triad: Microangiopathic Hemolytic Anemia, thrombocytopenia and neurologic abnormality

A

TTP

104
Q

onset with platelet consumption, factor V,VIII and fibrinogen reduced level

A

-acute DIC

105
Q

Due to S.dysentiriae/E.coli 0157:H7 serotype

A

HUS

106
Q

Onset on children

A

HUS

107
Q

Life threatening

A

DIC

108
Q

Characterized by: erosive damage to the colon + bloody diarrhea

A

HUS

109
Q

-no apparent cause

A

ITP

110
Q

-presence of anti-platelet ab (IgG)

A

ITP

111
Q

-develops IgG antibody specific for heparin plt factor 4 complex

A

HIT

112
Q

-due to unfractioned heparin administration

A

HIT

113
Q

abrupt onset, usually on children

A

Acute: ITP

114
Q

mumps, chicken pox, small pox, and measles

A

ITP

115
Q

Characterized by bruising, petechiae and epistaxis

A

ITP

116
Q

Drugs affecting thrombocytopenia:
- Ristocetin
- Hematin
- Rotamine sulfate
- Bleomycin

A

HIT

117
Q

: any age onset

A

Chronic ITP

118
Q

rubella, chicken pox, ruboela

A

ITP

119
Q

Characterized by: menorrhagia, epistaxis and bruising

A

ITP

120
Q

Splenic sequestration Seen in:

A

hypersplenism/splenomegaly

121
Q

(Gaucher’s, Hodgkin, Cirrhosis, Sarcoidosis, Lymphoma)

A

hypersplenism

122
Q

more plt can be sequestered, reducing the circulating plt (thrombocytopenia)

A

hypersplenism

123
Q

– removal of the spleen = low plt (thrombocytopenia)

A

splenomegaly

124
Q

THROMBOYTOSIS/THROMBOCYTHEMIA

A
  1. Primary Thrombocytosis
  2. Secondary/Reactive Thrombocytosis
125
Q

-hallmark of myeloproliferative disorders

A

Primary Thrombocytosis

126
Q

-unregulated plt production

A

Primary Thrombocytosis

127
Q

-variable size (small and large) affecting function

A

Primary Thrombocytosis

128
Q

-increased megakaryocyte production in the bm

A

Primary Thrombocytosis

129
Q

-myeloproliferative disorders: pcv, chronic myelogenous leukemia, myelofibrosis

A

Primary Thrombocytosis

130
Q

plt can exceed up to 1 million/uL

A

Primary Thrombocytosis

131
Q

-aka Essential Thrombocytopenia

A

Primary Thrombocytosis

132
Q

-does not exceed 800,000/uL

A

Secondary/Reactive Thrombocytosis

133
Q

-secondary to inflammation and trauma

A

Secondary/Reactive Thrombocytosis

134
Q

-occurs to compensate for the lost platelet (betterment of the body)

A

Secondary/Reactive Thrombocytosis

135
Q

-Ex. Childbirth, splenectomy, tissue necrosis, IDA

A

Secondary/Reactive Thrombocytosis

136
Q

-exists for a short period of time

A

Secondary/Reactive Thrombocytosis

137
Q

-normal plt morphologyand responds to normal stimuli

A

Secondary/Reactive Thrombocytosis

138
Q

→ Excessive plasma proteins lead to hyperviscosity syndrome

A

Paraproteinemias (Multiple myeloma and Waldenstrom macroglobulinemia)

139
Q

→ uremia: leads to decreased thromboxane synthesis, decreased adhesion, decreased platelet release, and decreased aggregation

A

Renal disease

140
Q

May-Hegglin

A

Megakaryocyte hypoproliferation

141
Q

in-utero exposure to certain drugs (particularly chlorothiazide diuretics and the oral hypoglycemic tolbutamide)

A

Neonatal Thrombocytopenia

142
Q

• caused by a deficiency of a disintegrin an metalloproteinase with a thrombospondi type 1 motif, member 13 (ADAMTS-13).

A

TTP

143
Q

involves the activation of both coagulation and fibrinolysis at the same time due to liberation of thromboplastic substance by damaged or abnormal cells

A

DIC

144
Q

Associated with mild febrile illnesses, certain immunizations, and gastrointestinal disturbances

A

HUS

145
Q

E. coli 0157:H7 or other Shiga/Vero toxin-producing bacteria

A

HUS

146
Q

due to presence of anti-platelet antibodies of the IgG type

A

ITP

147
Q

Most common in young females <15 y/o

A

ITP

148
Q

patient develops IgG antibody specific for heparin-platelet factor 4 complexes

A

Heparin-Induced Thrombocytopenia

149
Q

A. common side effect of unfractionated heparin administration

A

Heparin-Induced Thrombocytopenia

150
Q

seen in myeloproliferative disorders

A

Primary Thrombocytosis

151
Q

seen in splenic mobilization and in hemolytic anemias

A

Secondary/Reactive Thrombocytosis

152
Q

(deformed with dumbbell shaped nuclei; could be reversed)

A

Ineffective thrombopoiesis

Hematology 2 Lec (29 decks)

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