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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
Describe mean platelet volume for platelet evaluation
Varies between analyzer, anticoagulant, and storage time | Presence of cell fragments and large platelets
26
What is the concentration of platelets like when there is thrombocytopenia?
Concentration is lower than the LRL
27
What breeds a predisposed to thrombocytopenia?
Greyhounds | Shiba Inus
28
What does thrombocytopenia reflect?
A pathologic process, it is not a diagnosis
29
What is present if the thrombocytes are less than 30,000/μL?
``` Petechiae and ecchymosis Mucosal bleeding (epistaxis, hematochezia, melena), hematuria, and hyphema ```
30
What are causes of pseudo-thrombocytopenia?
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
31
What is a thrombocytopenia shift/sequestration?
Reversibly distributed platelets in vascular systems (spleen)
32
What does thrombocytopenia shift/sequestration result in?
Mild or moderate thrombocytopenia Splenomegaly Severe hypothermia Endotoxemia
33
What are causes of decreased production of platelets?
``` Generalized BM or MK-specific process Idiopathic thrombocytopenia of CKCS Drugs (predictable and dose-dependent; idiosyncratic) Infectious Marrow replacement (myelophthisis) ```
34
What infections caused decreased production of platelets?
Direct infection of MK (BVD and canine distemper) Myelosuppressive cytokinesm (EIA) Unclear (parvo, canine monocytic ehrlichiosis) FeLV
35
What kinds of marrow replacement cause decreased production of platelets?
Bone marrow neoplasia | Myelonecrosis
36
What is the cause of platelet destruction?
Immune-mediated thrombocytopenia (IMT) Drug induced IMT IMT associated to infection Neonatal alloimmune thrombocytopenia
37
What is found with IMT?
Platelet surface-associated immunoglobulin
38
What happens to platelets with IMT?
Destruction by MPS
39
What does IMT result from?
Defective immune system | Defective platelets
40
Describe idiopathic or primary IMT
Not associated to a detected disease It could be autoimmune Common in dogs Ab may target MKs
41
What is the criteria for diagnosis of drug induced IMT?
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
42
What are drugs that can cause drug induced IMT?
Gold salts, sulfonamides (dogs) Methimazole and proplyrhiouracil (cats) Penicillin and TMS (horses)
43
What are infections that can cause IMT?
``` Acute canine ehrlichiosis Other Ehrlichia and Anaplasma Rocky Mountain Spotted Fever Histoplasmosis, Leishmaniasis Distemper or modified virus vaccination Equine infectious anemia Babesiosis ```
44
What must neonatal alloimmune thrombocytopenia be differentiated from?
Other causes especially sepsis
45
Describe IMT caused by neoplasia
May include immunologic mechanisms | Lymphoma
46
Descibe IMT caused by systemic immune mediated disease (i.e. SLE)
SLE: evidence of increase PSAIg | Evan's syndrome: IMHA with IMT described in dogs
47
What can cause thrombocytopenia dilution?
``` Blood loss (acute and severe) Hemodilution ```
48
Describe thrombocytopenia associated with blood loss
Thrombocytopenia could be due to consumption | Mild to moderate and self-limiting
49
What are causes of thrombocytopenia via consumption?
Platelet activation with accelerated consumption or use Disseminated intravascaulr coagulation (DIC) Drugs or foreign material Evenomation Vasculitis or endocarditis
50
What results from platelet activation with accelerated consumption or use?
Localized intravascular coagulation
51
What is a potent platelet activator?
Thrombin
52
Describe idiopathic thrombocytopenia of CKCS
Congenital Common in the breed Macrothrombocytopenia No clinical bleeding problem
53
What is thrombocytopenia do to infectious causes frequently associated to?
Endotoxemia
54
What are bacteria that can cause thrombocytopenia?
Ehrlichia and Anaplasma spp
55
What is a fungi that can cause thrombocytopenia?
Histoplasma spp
56
What are protozoa that can cause thrombocytopenia?
Leishmania, Babesia, and Theileria spp.
57
How do infectious causes result in decreased platelet production?
Direct infection Immune suppression BM inflammation
58
How does Anaplasma platys cause thrombocytopenia?
Infect platelets Clinical or subclinical Mild parasitemia PCR diagnosis
59
What neoplasma can cause thrombocytopenia?
Carcinomas Sarcomas Lymphomas Leukemias
60
How do neoplasms cause decreased production of platelets?
Myelophthisis Myelodysplasia Estrogen secretion Chemotherapy
61
How do neoplasms cause consumtpion of platelets?
DIC | Vasculitis or thrombosis
62
How do neoplasms cause destruction of platelets?
Secondary IMT | Hemorrhage, sepsis
63
How do neoplasms cause sequestration of platelets?
Splenomegaly or heptomegaly | Organ congestion
64
How does hypophosphatemia cause thrombocytopenia?
Hyperalimentation Decreased platelet survial Decreased platetlet ATP
65
How does anaphylaxis cause thrombocytopenia?
Mechanism incompletely characterized Inflammatory mediators DIC Immune-complex interaction with platelets
66
What is thrombocytosis?
Platelet concentration greater than URL
67
What can cause thrombocytosis?
Redistribution or increased production (hemic neoplasias)
68
What is the cause of physiologic thrombocytosis?
Redistribution
69
What causes an increased production of platelets?
``` Inflammation (IL-6 induced TPO production) Nonhemic malignant neoplasia Iron deficiency Vinca alkaloids Rebound (recovery from thrombocytopenia) Postsplenectomy Blood loss Hypercortisolemia ```
70
What are the functions of platelets?
``` Primary hemostatic plug Adhesion Aggregation Degranulation Facilitation of coagulation Clot retratction ```
71
How do platelets cause adhesion?
Perturbed endothelium or exposed subendothelium | Via vWF binding to GPIb
72
What are the agonists that cause aggregation with platelets?
ADP Collagen PAF Thrombin
73
What are the high affinity sites for cagulation?
Enzymes Cofactors Zymogen
74
What is involved with the contractile process of clot retraction?
Activated platelets GPαIIbβ3 via fibrinogen Actin and myosin
75
What is the standardized primary hemostasis test?
BMBT
76
What is the BMBT procedure?
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
What can BMBT detect?
Only moderate to marked primary hemostasis defects
78
What could it mean if BMBT is prolonged (>4-5 minutes)?
``` Thrombocytopenia Thrombocytopathia (platelet dysfunction) vWD Anemia Vascular disease Antiplatelet drugs Afibrinogenemia ```
79
What is von Willebrand Factor responsible for?
Platelet adhesion | Platelet aggregation
80
What is vWF produced by?
Endothelial cells
81
What does vWF from with Factor VIII?
Noncovalant complexes
82
What is the purpose of the noncovalent complexes formed by vWF and factor VIII?
It is protective and a stabilizer for factor VIII
83
What is the most common hereditary bleeding disorder of dogs?
von Willebrand disease
84
What is type 1 vWD?
All vWF multimers are present in decreased concentration | Dioberman Pinchers and many other breeds
85
What is type 2 vWD?
Deficiency of vWF with disproportionate decrease of large multimers German Shorthaired Pointers, German Wiredhaired Pointers, and horses
86
What is type 3 vWD?
Absence of all multimers | Chesapeaks Bay Retrievers, Dutch Kooikers, Scottish Terriers, Shetland Sheepdogs
87
What are the clinical and lab findings of vWD?
``` 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
What should be used to analyze vWF?
Sodium citrate or EDTA
89
How long is the vWF antigen stable at room temperature?
8 hours
90
What is coagulation?
Interconnected series of reactions that forms thrombin, which converts soluble fibrinogen into soluble fibrin
91
What are the enzymatic factors involved in coagulation produced by?
Hepatocytes
92
What enzymatic facotrs are vitamin k dependent?
2, 7, 9, and 10
93
Which enzymatic factor is sex-linked (x chromosome)?
Factor 9
94
What are the nonenzymatic factors involved in coagulation?
Tissue factor Fibrinogen FV and FVIII (cofactors)
95
What is tissue factor?
Cofactor for FVII | Major activator of coagulation in vivo
96
What is fibrinogen?
Positive acute phase protein produced by hepatocytes
97
What are FV and FVIII (cofactors)?
Markedly accelerate coagulation | Facilitates surface attachment of other factors
98
Which nonenzymatic factor is sex-linked?
FVIII
99
When are FV and FVIII consumed?
During coagulation
100
What is the extrinsic pathway initiated by?
Tissue factor that activated factor VII
101
What does the extrinsic pathway initiate?
``` Common pathway (factor X) Intrinsic pathway (factor 9) ```
102
What is the extrinisc pathway important in?
Initiating thrombin generation
103
What is the intrinsic pathway initiated by?
HMWK, PK, and factor 12 contacting negatively charged surfaces
104
What does the intrinsic pathway start?
Common pathway by activating factor 10
105
What is the intrinsic pathway inhibited by?
ATIII (2, 9, 10, 11)
106
What is the intrinsic pathway activated by?
Factor 7a, which activates factor 9
107
What does thrombin activate in the intrinsic pathway?
Factors 5, 8, and 11
108
What is the common pathway initiated by?
Activation of factor 10
109
What does the common pathway lead to?
Formation of thrombin from prothrombin
110
What does thrombin do in the common pathway?
Forms fibrin monomers and them multimers cross linked by factor XIIIA
111
What is the common pathway inhibited by?
AT3
112
What is antithrombin 3 produced by?
Hepatocytes
113
What does AT3 do?
Binds, inactivates and removes coagulation factors (most importantly 2a, 9a, and 10a)
114
What is AT3 markedly enhanced by?
Heparin
115
What kind of sample is needed to determine the ACT (activated coagulation/clotting time)?
Whole blood
116
What is ACT?
Screening coagulation test that evaluates surface activation (intrinsic and common)
117
What can increase the ACT?
Thrombocytopenia
118
What can ACT be used to monitor?
Heparin therapy
119
What does the activated partial thromboplastic time (aPTT) screen for?
Intirinsic and common pathways
120
What is the sample needed for aPTT?
Citrated blood (plasma)
121
What does prothrombin time screen for?
Extrinsic and common pathways
122
What is the samples needed for prothrombin time?
Citrated blood (Plasma)
123
What does PT test?
Ca, phospholipids, and TF
124
What does thrombin time asses?
Transformation of fibrinogen in fibrin without the interference of thrombin generation
125
What is the sample neededfor thrombin time?
Citrated blood (plasma)
126
What is the test done for TT?
Thrombin is added to the sample
127
What does it mean if there is prolonged time with a TT?
``` Hypofibrinogenemia or afibrinogenemia Increased consumption, localized coagulation, or DIC Hereditary deficiency Dysfibrinogenemia Heparinized sample Increased FDPs Paraproteinemia ```
128
What are proteins induced by vitamin K antagonism (PIVKA)?
Incomletely carboxylated vit K dependednt factors | Due to antagonism, deficiency, absence of vit K
129
What is used to test PIVKA?
Thrombotest PT
130
What is a thrombotest PT?
A modified PT test with added FV and fibrinogen so that it detects activity of factors 2, 7, and 10
131
What does it mean if the thrombotest PT is prolonged?
VitK antagoism or deficiency Other acquired and hereditary coagulopathies Cats with hepatic, biliary, or inflammatory bowel diseases Heparin
132
What does it mean if there is decreased ATIII activity?
Hypercoagulable states Decreased production Loss due to protein-losing nephropathy or severe hemorrhage Consumption (DIC, spesis, heparin)
133
What does it mean if there is decreased ATII?
Decreased production Loss due to protein losing nephropathy Consumption (DIC, sepsis, heparin)
134
What is fibrinolysis?
Enzymatic degradation of fibrin
135
What does fibrinolysis counteract?
Coagulation
136
When is fibrinolysis initiated?
At the same time as coagulation
137
Where does fibrinolysis happens?
On the hemostatic plug
138
What does plasmin do?
Degrades fibrin, fibrinogen, FVa, FVIIIa, vWF, HMWK
139
What is plasmin inhibited by?
Plasmin inhibitor
140
What is plasmin cleared by?
Liver
141
What is plasmin activated by?
tissue-plasminogen activator
142
What is used to assess fibrinolysis?
Fibrin and fibrinogen degradation products (FDPs)
143
What are FDPs cleared by?
Lvier Phagocytes Kidneys
144
What are effects of increased FDPs?
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
What do FDPs detect?
Increased fibrinolysis due to excessive coagualtion | May also detect increased fibrinogenolysis
146
What is the sample needed to look at FDPs?
``` Serum: special tubes with thrombin or Botrox atrox venom Citrated plasma (24 hours at 4 deg C) ```
147
What are interpretive considerations (false results) of FDPs?
Serum samples: FDPs incorporated into the clots Generation of FDPs during blood collection Unspecificty of test
148
What are interpretive considerations (increased) of FDPs?
``` Higher concentration in equine neonates Localized intravascular coagualtion DIC Sepsis and inflammatory conditions Hemorrhagic fluid from body cavities Hyperplasminemia leading to increased fibrinolysis ```
149
What does D-dimer detect?
Increased fibrinolysis due to excessive coagulation | Factor 13a cross-linked fibrin
150
What is the sample used for D-dimer?
Citrated plasma
151
What can biopsy and histology of blood vessels show?
Vasculitis and thrombosis | Diseases involving small vessels
152
How can you diagnose vessel disorders?
Gross examination Serology Imagining Biopsy
153
What are causes of large vessel disorders?
Surgical and nonsurgical traumas Invasion Aneurysms Anomalies
154
What are causes of small vessel disorders?
Vasculitis | Vasculopathies
155
What are examples of blood disorders?
Impaired primary hemostatsis Impaired secondary hemostasis Excessive fibrinolysis: DIC and come envenomations
156
What is the bleeding pattern seen with a primary hemostasis problem or small vessels?
Petechiae and ecchymosis | Hemorrhages through mucosal surfaces
157
What is the bleeding pattern seen with a secondary hemostasis problem?
Subcutaneous hematomas and hemorrhage into blood cavities | Hemorrhages through mucosal surfaces
158
What are some predisposing factors to bleeding disorders?
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
``` What is the diagnosis? PT= WRI PTT= WRI FDPs= WRI TT= WRI Platelets= WRI BMBT= Prolonged ```
Functional platelet problem: vWD or thrombopathia
160
``` What is the diagnosis? PT= WRI PTT= WRI FDPs= WRI TT= WRI Platelets= decreased BMBT= Prolonged ```
Thrombocytopenia with or without platelet functional problems
161
``` What is the diagnosis? PT= Prolonged PTT= Prolonged FDPs= WRI TT= Prolonged Platelets= WRI BMBT= WRI or Prolonged ```
Hepatic disease
162
What does hepatic disease cause defects in?
Production and clearing of procoagulants, anticoagulants, profibrinolytics, and antifibrinolytics
163
What tests determine hepatic disease and what is the result?
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
``` What is the diagnosis? PT= WRI PTT= Prolonged FDPs= WRI TT= WRI Platelets= WRI BMBT= WRI ```
Acquired: hepatic disease, heparin contamination, heparin therapy, VitK antagonism Inherited: hemophilias A and B F11 deficiency
165
``` What is the diagnosis? PT= Prolonged PTT= WRI FDPs= WRI TT= WRI Platelets= WRI BMBT= WRI ```
Hepatic or heptobiliary disease, VitK antagonism
166
``` What is the diagnosis? PT= Prolonged PTT= Prolonged FDPs= WRI TT= WRI Platelets= WRI BMBT= WRI ```
VitK antagonism, hepatic disease
167
``` What is the diagnosis? PT= Prolonged PTT= Prolonged FDPs= Increased TT= Prolonged Platelets= Decreased BMBT= Prolonged ```
Typical of fulminant consumptive coagulopathy
168
What is consumptive coagulopathy?
The process of accelerated or unbalanced coagulation that leads to destruction or removal of procoagulant moleucles DIC
169
What can you expect to find with consumptive coagulopathy?
``` 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
What is dilutional coagulopathy?
Dilution of blood components by colloid fluids, crystalloid fluids, plasma-poor packed erythrocytes, or oxyglobin solution
171
What can cause the inhibition of functional factors?
Heparin | FDPs
172
What is thrombosis?
Formation of thrombi within vascular system | Shift of equilibrium between prothrombic factors and antithrombic factors
173
What are the potential hemostatic abnormailites caused by thrombosis?
``` Increased D-dimers Increased FDPs Decreased ATIII Thrombocytopenia Increased tt: decreased fibrinogen ```

Clinical Pathology (16 decks)

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