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Clinical Pathology > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

What is involved in primary hemostasis?

A

Platelets

Vessel

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2
Q

What is involved in secondary hemostasis or coagulation?

A

Coagulation factors

Vessel

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3
Q

What is involved in tertiary hemostasis or fibrinolysis?

A

Fibrinolytic molecules

Vessel

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4
Q

What are platelets?

A

Small fragments of megakaryocyte cytoplasm

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5
Q

Describe the composition of platelets

A

Phospholipid membrane with glycoproteins
Open canalicular system of membrane invaginations
Cytoskeleton is a peripheral microtubule ring and is made of actin and mysoin
Tubular system of ER
α-granules
Dense granules
Glycogen and mitochondria

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6
Q

What is the function of the platelet membrane?

A

Coagulation and cell to cell interaction

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7
Q

What is the function of the open canalicular system of membrane invaginations in platelets?

A

Substance trafficking between platelet and plasma

Increase platelet surface

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8
Q

What does the tubular system of ER in platelets do?

A

Stores Ca for platelet activation and thromboxane production

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9
Q

What do α-granules play a role in?

A

Hemostasis

Angiogenesis

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10
Q

What are the dense granules in platelets?

A 
Ca
Mg
ADP
ATP
Serotonin
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11
Q

What do glycogen and mitochondria do for platelets?

A

Energy

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12
Q

What plays a role in megakaryopoiesis and thrombopoiesis?

A

Thrombopoietin and other cytokines

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13
Q

Where do megakaryopoiesis and thrombopoiesis occur?

A

Bone marrow
Spleen
Lung

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14
Q

What happens with megakaryopoiesis and thrombopoiesis?

A

Platelets are released directly into the blood

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15
Q

Where is thrombopoietin made?

A

Hepatocytes (dog)
Renal tubular epithelium
BM stromal cells

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16
Q

What is TPO expressed?

A

Constitutively

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17
Q

What is the plasma concentration of TPO dependent on?

A

MPL receptor numbers present in platelets and megakaryocytes

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18
Q

How does inflammation/IL-6 impact TPO?

A

IL-6 leads to TPO expression in the BM

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19
Q

What are reticulated platelets?

A

Young platelets
Increased RNA
Less than 24 hours in dogs

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20
Q

What does the concentration of platelets depend on?

A 
Production
Consumption
Destruction
Shift/sequestration
Dilution
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21
Q

What are the methods of evaluating platelets?

A

Blood smear
Blood sample
Platelet count
Mean platelet volume

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22
Q

Describe a blood smear for platelet evaluation

A

Platelet estimation

Morphologic abnormalities

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23
Q

Describe a blood sample for platelet evaluation

A

EDTA (not heparin)
Citrate, theophylline, dipyridamole, and adenosine (CTAD tubes) may be useful for cats
8 hours at RT and 48 hours at 4 deg C
Check for platelet clumping

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24
Q

What can be used for platelet count for platelet evaluation?

A

Impedance counters
Optical or layer flow cytometers
QBC
Hemocytometer

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25
Q

Describe mean platelet volume for platelet evaluation

A

Varies between analyzer, anticoagulant, and storage time

Presence of cell fragments and large platelets

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26
Q

What is the concentration of platelets like when there is thrombocytopenia?

A

Concentration is lower than the LRL

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27
Q

What breeds a predisposed to thrombocytopenia?

A

Greyhounds

Shiba Inus

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28
Q

What does thrombocytopenia reflect?

A

A pathologic process, it is not a diagnosis

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29
Q

What is present if the thrombocytes are less than 30,000/μL?

A 
Petechiae and ecchymosis
Mucosal bleeding (epistaxis, hematochezia, melena), hematuria, and hyphema
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30
Q

What are causes of pseudo-thrombocytopenia?

A

Not all of the platelets were counted
In vitro platelet activation or aggregation
Presence of large platelets in impedance counters
Cold agglutinins, or anticoagulant-induce, antibody mediated agglutination

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31
Q

What is a thrombocytopenia shift/sequestration?

A

Reversibly distributed platelets in vascular systems (spleen)

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32
Q

What does thrombocytopenia shift/sequestration result in?

A

Mild or moderate thrombocytopenia
Splenomegaly
Severe hypothermia
Endotoxemia

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33
Q

What are causes of decreased production of platelets?

A 
Generalized BM or MK-specific process
Idiopathic thrombocytopenia of CKCS
Drugs (predictable and dose-dependent; idiosyncratic)
Infectious
Marrow replacement (myelophthisis)
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34
Q

What infections caused decreased production of platelets?

A

Direct infection of MK (BVD and canine distemper)
Myelosuppressive cytokinesm (EIA)
Unclear (parvo, canine monocytic ehrlichiosis)
FeLV

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35
Q

What kinds of marrow replacement cause decreased production of platelets?

A

Bone marrow neoplasia

Myelonecrosis

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36
Q

What is the cause of platelet destruction?

A

Immune-mediated thrombocytopenia (IMT)
Drug induced IMT
IMT associated to infection
Neonatal alloimmune thrombocytopenia

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37
Q

What is found with IMT?

A

Platelet surface-associated immunoglobulin

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38
Q

What happens to platelets with IMT?

A

Destruction by MPS

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39
Q

What does IMT result from?

A

Defective immune system

Defective platelets

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40
Q

Describe idiopathic or primary IMT

A

Not associated to a detected disease
It could be autoimmune
Common in dogs
Ab may target MKs

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41
Q

What is the criteria for diagnosis of drug induced IMT?

A

PSAIg present
Plasma Ab bind in vitro to platelets only in presence of the drug
Resolution after drug is discontinued
Relapse after drug is reintroduced

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42
Q

What are drugs that can cause drug induced IMT?

A

Gold salts, sulfonamides (dogs)
Methimazole and proplyrhiouracil (cats)
Penicillin and TMS (horses)

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43
Q

What are infections that can cause IMT?

A 
Acute canine ehrlichiosis
Other Ehrlichia and Anaplasma
Rocky Mountain Spotted Fever
Histoplasmosis, Leishmaniasis
Distemper or modified virus vaccination
Equine infectious anemia
Babesiosis
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44
Q

What must neonatal alloimmune thrombocytopenia be differentiated from?

A

Other causes especially sepsis

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45
Q

Describe IMT caused by neoplasia

A

May include immunologic mechanisms

Lymphoma

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46
Q

Descibe IMT caused by systemic immune mediated disease (i.e. SLE)

A

SLE: evidence of increase PSAIg

Evan’s syndrome: IMHA with IMT described in dogs

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47
Q

What can cause thrombocytopenia dilution?

A 
Blood loss (acute and severe)
Hemodilution
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48
Q

Describe thrombocytopenia associated with blood loss

A

Thrombocytopenia could be due to consumption

Mild to moderate and self-limiting

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49
Q

What are causes of thrombocytopenia via consumption?

A

Platelet activation with accelerated consumption or use
Disseminated intravascaulr coagulation (DIC)
Drugs or foreign material
Evenomation
Vasculitis or endocarditis

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50
Q

What results from platelet activation with accelerated consumption or use?

A

Localized intravascular coagulation

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51
Q

What is a potent platelet activator?

A

Thrombin

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52
Q

Describe idiopathic thrombocytopenia of CKCS

A

Congenital
Common in the breed
Macrothrombocytopenia
No clinical bleeding problem

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53
Q

What is thrombocytopenia do to infectious causes frequently associated to?

A

Endotoxemia

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54
Q

What are bacteria that can cause thrombocytopenia?

A

Ehrlichia and Anaplasma spp

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55
Q

What is a fungi that can cause thrombocytopenia?

A

Histoplasma spp

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56
Q

What are protozoa that can cause thrombocytopenia?

A

Leishmania, Babesia, and Theileria spp.

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57
Q

How do infectious causes result in decreased platelet production?

A

Direct infection
Immune suppression
BM inflammation

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58
Q

How does Anaplasma platys cause thrombocytopenia?

A

Infect platelets
Clinical or subclinical
Mild parasitemia
PCR diagnosis

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59
Q

What neoplasma can cause thrombocytopenia?

A

Carcinomas
Sarcomas
Lymphomas
Leukemias

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60
Q

How do neoplasms cause decreased production of platelets?

A

Myelophthisis
Myelodysplasia
Estrogen secretion
Chemotherapy

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61
Q

How do neoplasms cause consumtpion of platelets?

A

DIC

Vasculitis or thrombosis

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62
Q

How do neoplasms cause destruction of platelets?

A

Secondary IMT

Hemorrhage, sepsis

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63
Q

How do neoplasms cause sequestration of platelets?

A

Splenomegaly or heptomegaly

Organ congestion

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64
Q

How does hypophosphatemia cause thrombocytopenia?

A

Hyperalimentation
Decreased platelet survial
Decreased platetlet ATP

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65
Q

How does anaphylaxis cause thrombocytopenia?

A

Mechanism incompletely characterized
Inflammatory mediators
DIC
Immune-complex interaction with platelets

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66
Q

What is thrombocytosis?

A

Platelet concentration greater than URL

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67
Q

What can cause thrombocytosis?

A

Redistribution or increased production (hemic neoplasias)

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68
Q

What is the cause of physiologic thrombocytosis?

A

Redistribution

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69
Q

What causes an increased production of platelets?

A 
Inflammation (IL-6 induced TPO production)
Nonhemic malignant neoplasia
Iron deficiency
Vinca alkaloids
Rebound (recovery from thrombocytopenia)
Postsplenectomy
Blood loss
Hypercortisolemia
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70
Q

What are the functions of platelets?

A 
Primary hemostatic plug
Adhesion
Aggregation
Degranulation
Facilitation of coagulation
Clot retratction
71
Q

How do platelets cause adhesion?

A

Perturbed endothelium or exposed subendothelium

Via vWF binding to GPIb

72
Q

What are the agonists that cause aggregation with platelets?

A

ADP
Collagen
PAF
Thrombin

73
Q

What are the high affinity sites for cagulation?

A

Enzymes
Cofactors
Zymogen

74
Q

What is involved with the contractile process of clot retraction?

A

Activated platelets
GPαIIbβ3 via fibrinogen
Actin and myosin

75
Q

What is the standardized primary hemostasis test?

A

BMBT

76
Q

What is the BMBT procedure?

A

Small cut that is 5 mm x 1 mm of the upper lip
Start timing when the cut is made (1-5 minutes)
Remove excess blood with a filter paper without disturbing the cut
The end point is when no blood is transferred to the filter paper

77
Q

What can BMBT detect?

A

Only moderate to marked primary hemostasis defects

78
Q

What could it mean if BMBT is prolonged (>4-5 minutes)?

A 
Thrombocytopenia
Thrombocytopathia (platelet dysfunction)
vWD
Anemia
Vascular disease
Antiplatelet drugs
Afibrinogenemia
79
Q

What is von Willebrand Factor responsible for?

A

Platelet adhesion

Platelet aggregation

80
Q

What is vWF produced by?

A

Endothelial cells

81
Q

What does vWF from with Factor VIII?

A

Noncovalant complexes

82
Q

What is the purpose of the noncovalent complexes formed by vWF and factor VIII?

A

It is protective and a stabilizer for factor VIII

83
Q

What is the most common hereditary bleeding disorder of dogs?

A

von Willebrand disease

84
Q

What is type 1 vWD?

A

All vWF multimers are present in decreased concentration

Dioberman Pinchers and many other breeds

85
Q

What is type 2 vWD?

A

Deficiency of vWF with disproportionate decrease of large multimers
German Shorthaired Pointers, German Wiredhaired Pointers, and horses

86
Q

What is type 3 vWD?

A

Absence of all multimers

Chesapeaks Bay Retrievers, Dutch Kooikers, Scottish Terriers, Shetland Sheepdogs

87
Q

What are the clinical and lab findings of vWD?

A 
Mild to severe mucosal bleeding
Hemarthrosis and hematomas in horses
Absence of petechiae
Prolonged BMBT
Possibly decreased PTT due to decrease of factor VIII
88
Q

What should be used to analyze vWF?

A

Sodium citrate or EDTA

89
Q

How long is the vWF antigen stable at room temperature?

A

8 hours

90
Q

What is coagulation?

A

Interconnected series of reactions that forms thrombin, which converts soluble fibrinogen into soluble fibrin

91
Q

What are the enzymatic factors involved in coagulation produced by?

A

Hepatocytes

92
Q

What enzymatic facotrs are vitamin k dependent?

A

2, 7, 9, and 10

93
Q

Which enzymatic factor is sex-linked (x chromosome)?

A

Factor 9

94
Q

What are the nonenzymatic factors involved in coagulation?

A

Tissue factor
Fibrinogen
FV and FVIII (cofactors)

95
Q

What is tissue factor?

A

Cofactor for FVII

Major activator of coagulation in vivo

96
Q

What is fibrinogen?

A

Positive acute phase protein produced by hepatocytes

97
Q

What are FV and FVIII (cofactors)?

A

Markedly accelerate coagulation

Facilitates surface attachment of other factors

98
Q

Which nonenzymatic factor is sex-linked?

A

FVIII

99
Q

When are FV and FVIII consumed?

A

During coagulation

100
Q

What is the extrinsic pathway initiated by?

A

Tissue factor that activated factor VII

101
Q

What does the extrinsic pathway initiate?

A 
Common pathway (factor X)
Intrinsic pathway (factor 9)
102
Q

What is the extrinisc pathway important in?

A

Initiating thrombin generation

103
Q

What is the intrinsic pathway initiated by?

A

HMWK, PK, and factor 12 contacting negatively charged surfaces

104
Q

What does the intrinsic pathway start?

A

Common pathway by activating factor 10

105
Q

What is the intrinsic pathway inhibited by?

A

ATIII (2, 9, 10, 11)

106
Q

What is the intrinsic pathway activated by?

A

Factor 7a, which activates factor 9

107
Q

What does thrombin activate in the intrinsic pathway?

A

Factors 5, 8, and 11

108
Q

What is the common pathway initiated by?

A

Activation of factor 10

109
Q

What does the common pathway lead to?

A

Formation of thrombin from prothrombin

110
Q

What does thrombin do in the common pathway?

A

Forms fibrin monomers and them multimers cross linked by factor XIIIA

111
Q

What is the common pathway inhibited by?

A

AT3

112
Q

What is antithrombin 3 produced by?

A

Hepatocytes

113
Q

What does AT3 do?

A

Binds, inactivates and removes coagulation factors (most importantly 2a, 9a, and 10a)

114
Q

What is AT3 markedly enhanced by?

A

Heparin

115
Q

What kind of sample is needed to determine the ACT (activated coagulation/clotting time)?

A

Whole blood

116
Q

What is ACT?

A

Screening coagulation test that evaluates surface activation (intrinsic and common)

117
Q

What can increase the ACT?

A

Thrombocytopenia

118
Q

What can ACT be used to monitor?

A

Heparin therapy

119
Q

What does the activated partial thromboplastic time (aPTT) screen for?

A

Intirinsic and common pathways

120
Q

What is the sample needed for aPTT?

A

Citrated blood (plasma)

121
Q

What does prothrombin time screen for?

A

Extrinsic and common pathways

122
Q

What is the samples needed for prothrombin time?

A

Citrated blood (Plasma)

123
Q

What does PT test?

A

Ca, phospholipids, and TF

124
Q

What does thrombin time asses?

A

Transformation of fibrinogen in fibrin without the interference of thrombin generation

125
Q

What is the sample neededfor thrombin time?

A

Citrated blood (plasma)

126
Q

What is the test done for TT?

A

Thrombin is added to the sample

127
Q

What does it mean if there is prolonged time with a TT?

A 
Hypofibrinogenemia or afibrinogenemia
Increased consumption, localized coagulation, or DIC
Hereditary deficiency
Dysfibrinogenemia
Heparinized sample
Increased FDPs
Paraproteinemia
128
Q

What are proteins induced by vitamin K antagonism (PIVKA)?

A

Incomletely carboxylated vit K dependednt factors

Due to antagonism, deficiency, absence of vit K

129
Q

What is used to test PIVKA?

A

Thrombotest PT

130
Q

What is a thrombotest PT?

A

A modified PT test with added FV and fibrinogen so that it detects activity of factors 2, 7, and 10

131
Q

What does it mean if the thrombotest PT is prolonged?

A

VitK antagoism or deficiency
Other acquired and hereditary coagulopathies
Cats with hepatic, biliary, or inflammatory bowel diseases
Heparin

132
Q

What does it mean if there is decreased ATIII activity?

A

Hypercoagulable states
Decreased production
Loss due to protein-losing nephropathy or severe hemorrhage
Consumption (DIC, spesis, heparin)

133
Q

What does it mean if there is decreased ATII?

A

Decreased production
Loss due to protein losing nephropathy
Consumption (DIC, sepsis, heparin)

134
Q

What is fibrinolysis?

A

Enzymatic degradation of fibrin

135
Q

What does fibrinolysis counteract?

A

Coagulation

136
Q

When is fibrinolysis initiated?

A

At the same time as coagulation

137
Q

Where does fibrinolysis happens?

A

On the hemostatic plug

138
Q

What does plasmin do?

A

Degrades fibrin, fibrinogen, FVa, FVIIIa, vWF, HMWK

139
Q

What is plasmin inhibited by?

A

Plasmin inhibitor

140
Q

What is plasmin cleared by?

A

Liver

141
Q

What is plasmin activated by?

A

tissue-plasminogen activator

142
Q

What is used to assess fibrinolysis?

A

Fibrin and fibrinogen degradation products (FDPs)

143
Q

What are FDPs cleared by?

A

Lvier
Phagocytes
Kidneys

144
Q

What are effects of increased FDPs?

A

Prolonged PT, aPTT, TT, ACT
Impairs platelet function
Compete with fibrinogen for thrombin
Compete with fibrinogen for paltelet binding sites
Associate with fibrin monomers and may disrupt polymerization

145
Q

What do FDPs detect?

A

Increased fibrinolysis due to excessive coagualtion

May also detect increased fibrinogenolysis

146
Q

What is the sample needed to look at FDPs?

A 
Serum: special tubes with thrombin or Botrox atrox venom
Citrated plasma (24 hours at 4 deg C)
147
Q

What are interpretive considerations (false results) of FDPs?

A

Serum samples: FDPs incorporated into the clots
Generation of FDPs during blood collection
Unspecificty of test

148
Q

What are interpretive considerations (increased) of FDPs?

A 
Higher concentration in equine neonates
Localized intravascular coagualtion
DIC
Sepsis and inflammatory conditions
Hemorrhagic fluid from body cavities
Hyperplasminemia leading to increased fibrinolysis
149
Q

What does D-dimer detect?

A

Increased fibrinolysis due to excessive coagulation

Factor 13a cross-linked fibrin

150
Q

What is the sample used for D-dimer?

A

Citrated plasma

151
Q

What can biopsy and histology of blood vessels show?

A

Vasculitis and thrombosis

Diseases involving small vessels

152
Q

How can you diagnose vessel disorders?

A

Gross examination
Serology
Imagining
Biopsy

153
Q

What are causes of large vessel disorders?

A

Surgical and nonsurgical traumas
Invasion
Aneurysms
Anomalies

154
Q

What are causes of small vessel disorders?

A

Vasculitis

Vasculopathies

155
Q

What are examples of blood disorders?

A

Impaired primary hemostatsis
Impaired secondary hemostasis
Excessive fibrinolysis: DIC and come envenomations

156
Q

What is the bleeding pattern seen with a primary hemostasis problem or small vessels?

A

Petechiae and ecchymosis

Hemorrhages through mucosal surfaces

157
Q

What is the bleeding pattern seen with a secondary hemostasis problem?

A

Subcutaneous hematomas and hemorrhage into blood cavities

Hemorrhages through mucosal surfaces

158
Q

What are some predisposing factors to bleeding disorders?

A

Breed: might help diagnose inherited diseases
Age: young, prompt inherited
Gender: hemophilia A F8 deficiency and Hemophilia B F9 deficiency, males are not carries only affects; females can be carriers or affected

159
Q 
What is the diagnosis?
PT= WRI
PTT= WRI
FDPs= WRI
TT= WRI
Platelets= WRI
BMBT= Prolonged
A

Functional platelet problem: vWD or thrombopathia

160
Q 
What is the diagnosis?
PT= WRI
PTT= WRI
FDPs= WRI
TT= WRI
Platelets= decreased
BMBT= Prolonged
A

Thrombocytopenia with or without platelet functional problems

161
Q 
What is the diagnosis?
PT= Prolonged
PTT= Prolonged
FDPs= WRI
TT= Prolonged
Platelets= WRI
BMBT= WRI or Prolonged
A

Hepatic disease

162
Q

What does hepatic disease cause defects in?

A

Production and clearing of procoagulants, anticoagulants, profibrinolytics, and antifibrinolytics

163
Q

What tests determine hepatic disease and what is the result?

A

PT, aPTT, TT, ACT: Decreased production
FDPs and D-dimers: decreased clearance, intravascular coagualtion
Thrombocytopenia: sequestration, decreased production
BMBT: thrombocytopenia, thrombopathia
Fibrinogen, ATIII: decreased production, consumption

164
Q 
What is the diagnosis?
PT= WRI
PTT= Prolonged
FDPs= WRI
TT= WRI
Platelets= WRI
BMBT= WRI
A

Acquired: hepatic disease, heparin contamination, heparin therapy, VitK antagonism
Inherited: hemophilias A and B F11 deficiency

165
Q 
What is the diagnosis?
PT= Prolonged
PTT= WRI
FDPs= WRI
TT= WRI
Platelets= WRI
BMBT= WRI
A

Hepatic or heptobiliary disease, VitK antagonism

166
Q 
What is the diagnosis?
PT= Prolonged
PTT= Prolonged
FDPs= WRI
TT= WRI
Platelets= WRI
BMBT= WRI
A

VitK antagonism, hepatic disease

167
Q 
What is the diagnosis?
PT= Prolonged
PTT= Prolonged
FDPs= Increased
TT= Prolonged
Platelets= Decreased
BMBT= Prolonged
A

Typical of fulminant consumptive coagulopathy

168
Q

What is consumptive coagulopathy?

A

The process of accelerated or unbalanced coagulation that leads to destruction or removal of procoagulant moleucles
DIC

169
Q

What can you expect to find with consumptive coagulopathy?

A 
3 or more of:
Thrombocytopenia
Prolonged PT and/or PTT
Increased FDPs and/or increased d-dimer
Decreased fibrinogen concentration
Decreased ATIII
RBC fragments
170
Q

What is dilutional coagulopathy?

A

Dilution of blood components by colloid fluids, crystalloid fluids, plasma-poor packed erythrocytes, or oxyglobin solution

171
Q

What can cause the inhibition of functional factors?

A

Heparin

FDPs

172
Q

What is thrombosis?

A

Formation of thrombi within vascular system

Shift of equilibrium between prothrombic factors and antithrombic factors

173
Q

What are the potential hemostatic abnormailites caused by thrombosis?

A 
Increased D-dimers
Increased FDPs
Decreased ATIII
Thrombocytopenia
Increased tt: decreased fibrinogen

Clinical Pathology (16 decks)

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