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Hematalogy Lecture > Test 6: Coagulation Disorders > Flashcards

Test 6: Coagulation Disorders Flashcards

1
Q

Severe bleeding that require physical intervention

A

Hemorrhage

-Systemic-thrombocytopenia or platelet disorders
-anatomic-coagulopathies

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2
Q

recurrent, chronic bruising in multiple locations

A

Purpura

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3
Q

nosebleeds that are reoccurring that last more than ten minutes.

A

epistaxis

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4
Q

Is acquired or congenital coagulapathies more common?

A

acquired (can be acute or chronic)

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5
Q

Examples of acquired coagulopathies

A

-ACOTS
-Liver disease
-Disorders of Fibrinogen
-DIC
-Vit K deficiency
-Heparin
-Lupus Anticoagulants
-Acquired deficiency of Factor VIII

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6
Q

Most fatal cause of hemorrhage

A

Acute Coagulopathy of Trauma-Shock (ACOTS)

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7
Q

triggered by a combination of acute inflammation, platelet activation, tissue factor release, hyopthermia, acidosis, and hypoperfusion- all elements of systemic shock.

A

Acute Coagulopathy of Trauma-Shock (ACOTS)

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8
Q

What is the treatment for Acute Coagulopathy of Trauma-Shock (ACOTS)?

A

-massive RBC transfusion protocol
-FFP- 1:4, or 1:1
-Platelet concentrate
-Activated prothrombin complex concentrate (PCC)
-Cryoprecipitate or fibrinogen concentrate

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9
Q

ACOTS treatment of FFP is given until all coag. factors are at a min of _____%

A

30

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10
Q

What are the risks of FFP transfusion for ACOTS treatment?

A

TACO (transfusion-associated circulatory overload) and TRALI (transfusion-related acute lung injury)

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11
Q

Why can liver disease be associated with coagulation disorders?

A

majority of coagulation factors are synthesized in the liver, and for clearing circulating plasminogen activators and activated clotting factors.

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12
Q

In liver disease, which factors are the first to decrease?

A

Vit. K dependant factors (II, VII, IX, X), followed by Factor V*
(Factor VII is the first to show decreased activity)

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13
Q

Platelets can be effected by liver disease. _______ of pt show thrombocytopenia due to sequestration and shortened survival.

A

1/3

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14
Q

_____________ (acute phase reactant) elevates in early liver disease.

A

Fibrinogen

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15
Q

In moderate or sever liver disease, fibrinogen is coated with ________, interfering with its ability to perform -dysfibrinogenemia.

A

sialic acid

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16
Q

Dysfinrinogenemia ther is _________ PT and ___________ Reptilase Time Test.

A

prolonged, extremely prolonged

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17
Q

If Vit. K is decreased and factor V is decreased it means that…

A

the problem is not a Vit. K deficiency, rather a problem with the liver

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18
Q

Reptilase skips factor ____ and goes straight to ____.

A

VII, X?

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19
Q

What is seen in a blood smear with a pt that has liver disease?

A

Macrocytes, target cells, and acanthocytes

BUT normoblastic in bone marrow

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20
Q

Liver disease will have __________ plt

A

decreased

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21
Q

liver disease will cause _________ PT, PTT, and TCT tests.

A

prolonged

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22
Q

Fibrinogen will be __________ with liver disease.

A

decreased

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23
Q

FDP will be ___________ with liver disease.

A

Increased

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24
Q

D-Dimer will be ___________ with liver disease.

A

normal

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25
Q

liver disease treatment?

A

-treat underlying disease
-give FFP for bleeding episodes
-Vit. K therapy
-therapeutic plt
-antithrombin concentrate
-recombinate activated factor VII
-provide generalized supportive care

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26
Q

Hereditary disorders of fibrinogen can be due to…

A

quantitative or qualitative abnormalities of either fibrinogen or fibrin stabilizing factor

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27
Q

Acquired disorders of fibrinogen occur ________ to other pathologic events

A

secondary

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28
Q

What is the indirect method of fibrinogen assay?

A

Use Thrombin Time (TT); add thrombin to pt’s PPP. The longer it takes to clot, the less fbg it has (semi-quantitative)

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29
Q

What is the direct method of fibrinogen assay?

A

use “Fbg assay” with standard curve (utilizes highly diluted samples and excessive amount of thrombin reagent) so pt’s clotting time can be extrapolated.

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30
Q

Reference range for Indirect method of Fibrinogen?

A

15-20 seconds

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31
Q

Reference range for direct method of Fibrinogen?

A

200-400 mg/dL

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32
Q

_____________ is a quantiative deficeicny of fibrinogen due to a lack of synthesisi by the liver resulting in severe hemorrhages.

A

Afibrinogenemia

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33
Q

What is the treatment for Afibrinogenemia?

A

replacement therapy with cryoprecipitate (rich in factor I and VIII) or fresh frozen plasma (FFP) to raise blood fibringoen levels above 60 mg/dL

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34
Q

_____________ is a qualitative abnormality in the structure and function of the fibrinogen molecule.

A

Dysfibrinogenemia

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35
Q

With dysfibrinogenemia, finrinogen levels are __________, and TCT is ___________.
Post-traumatic and post-operative bleeding is common.

A

decreased, prolonged

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36
Q

What are the three hereditary disorders of fibrinogen?

A

-Afibrinogenemia
-Dysfibrinogenemia
-Factor XIII deficiency

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37
Q

What is used for diagnosis of Factor XIII deficiency?

A

5M urea solution test (Chromogenic assay???)

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38
Q

__________ deficiency can be clinically severe with moderate to sever bleeding. Delayed bleeding and wound healing is often observed after trauma

A

Factor XIII

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39
Q

What test results come back normal with Factor XIII deficiency?

A

APTT, PT, and TCT

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40
Q

Refers to a deposition of large amounts of fibrin throughout the microcirculation which results in a pathological activation of coagulation pathways.

A

Disseminated Intravascular Coagulation (DIC)

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41
Q

_______ is life-threatening result of concurrent in vivo activation of both coag and fibrinolytic systems.

A

DIC

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42
Q

DIC:

Ongoing thrombosis uses up coag. factors and plts, yielding name “______________”, and then clots cause further tissue necrosis (including strokes).

A

Consumptive Coagulopathy

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43
Q

DIC is triggered by _____________ which activates platelets, catalyzes fibrin formation, and consumes control proteins.

A

circulating thrombin

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44
Q

What are the coagulation tests for DIC?

A

(everything is abnormal)
-decreased platelet count
-PT, APTT, and TCT are prolonged
-FDP and D-Dimer are elevated
-Dcreased fibrinogen level
-shistocytes and incrased RDW

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45
Q

causes of DIC…

A

snake bite, spetic shock, major tissue necrosis, cytotoxic drugs, crush injuries, heat stroke with hypovolemia and retained dead fetus syndrome. (last two are usally chronic DIC triggers.)

*all these conditions release massive amounts of tissue thromboplastin

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46
Q

Acute DIC develops within hours, what are the symptoms?

A

hemorrhage and purpura, plus gangrene from thromboses. 60-80% mortality rate.

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47
Q

________ DIC occurs in pt. with pre-existing thrombotic tendency or event, and hemorrhage less frequent problem (because chronic nature allows liver and b.m. some time to try and compensate for “over-consumption”)

A

Chronic

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48
Q

what is the treatment for chronic thrombotic DIC?

A

Give low-dose heparin IV drip to stop intavascular clotting, unless contradicted by certain conditions (head injury, surgery, etc.)

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49
Q

What is the treatment for acute hemorrhagic DIC?

A

give FFP or cryoprecipitate, and plt. concentrates (to replenish Fbg and plts.)

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50
Q

What is the new treatment for DIC?

A

antifibrinolytics (Amicar = aninocaproic acid, or its analong)

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51
Q

What are the STAT treatments for DIC?

A

-treat underlying disorder for both acute and chronic
-treat for shock complications

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52
Q

How often are acute DIC pts retested?

A

every 15 minutes

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53
Q

What test rules out DIC with 90% certainty?

A

negative D-Dimer

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54
Q

Positive FDP = some type of __________ is going on (don’t know if N. or abnormal), but suggests DIC

A

fibrinolysis

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55
Q

Pos. D-Dimer = “normal” _____________ going on, so points to some type of thrombosis (may be DIC)

A

fibrinolysis

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56
Q

Vit. K is coF that is required for final carboxylation activating factors: _____________ in the liver.

A

II, VII, IX, X, C, S, Z

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57
Q

Vit. K is fat-soluble vit. that is found in green vegetables and is also produced by normal __________.

A

gut flora

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58
Q

antagonistic drug of Vit. K?

A

Coumadin, et al.

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59
Q

who is at risk for Vit. K deficiency?

A

sterile guts with antibiotic use, newborns (lack of E. coli and Bacteroides), absorption syndromes like obstructive jaundice or Crohn’s disease.

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60
Q

Vit. K deficiency can be caused by hemorrhagic (not hemolytic) disease of the newborn that can occur in the first few days of life due to what confluence factors?

A

-sterile gut
-reduced Vit. k stores
-functional immaturity of liver
(In the U.S. it is standard practice to inject baby with H2O-soluble analog of Vit. K shortly after birth)

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61
Q

symptoms of Vit. K deficiency?

A

-mucocutaneous bleeds
-epistaxis and easy bruising*
-greater deficiency = greater bleeding*

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62
Q

treatment for Vit. K deficiency?

A

-treat underlying disease
-administer vitamin K
-give FFP if severe bleeding occurs

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63
Q

Why is bleeding normal with Vit. K deficiency?

A

it is not a plt. problem
(doesn’t effect primary homeostasis)

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64
Q

Vit. K deficiency:
APTT is __________. Which factors are being affected?

A

prolonged

II, IX, and X

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65
Q

Vit. K deficiency:
PT is __________. Which factors are being affected?

A

prolonged

II, VII

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66
Q

__________ binds to Antithrombin, greatly enhancing its ability to bind and inactivate thrombin.

A

Heparin

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67
Q

-Used in the treatment of thrombosis and following a major surgery to prevent emboli
-A fast and potent form of anticoagulation
-APTT is the most commonly used test to monitor UFH

A

Heparin

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68
Q

LMWH is monitored by the __________ assay.

A

anti-Xa
-PT and TCT also prolonged

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69
Q

Is the thrombin time (TCT or TT) assay affected by heparin?

A

yes!

70
Q

What can be done if heparin is suspected of interfering in a TCT result?

A

-treat the sample with Hepzyme or
-prepare a dilution made with protamine sulfate and saline
the repeated TCT corrects (at least somewhat) if haparin was in the sample
**This is NOT a way of monitoring heparin therapy!

71
Q

An alternative method to test for fibrinogen activity (snake venom instead of thrombin reagent)

A

Reptilase time

72
Q

Reptilase time is similar to TT (TCT) except reptilase reagent is added to plasma instead of thrombin to activate proteolytic conversion of ________ to _________.

A

fibrinogen, fibrin

73
Q

Reference range for Reptilase time?

A

18-22 seconds

74
Q

RT (reptilase time) is insensitive to _________ and is useful for detecting hypofibrinogenemia or dysfibrinogenemia
-prolonged in the presence of FDPs

A

heparin

75
Q

Dysfibrinogenemia or Afibrinogenemia:
TT = __________
RT = __________

A

Infinitely prolonged.
Infinitely prolonged

76
Q

Hypofibrinogenemia:
TT = __________
RT = __________

A

Prolonged,
Prolonged

77
Q

Heparin:
TT = __________
RT = __________

A

Prolonged,
normal

78
Q

most well-known for the non-specific circulating inhibitors

A

Lupus Anticoagulants (Antiphospholipid antibodies)

79
Q

Lupus Anticoagulants:
___________ are directed against the phospholipid portion of phospholipoprotien components found in APTT reagent (prevents them from being used as a stable surface to build the clot upon)

A

autoantibodies

80
Q

Lupus Anticoagulants:
_______ can be affected in severe cases, but PTT is the primary test.

A

PT

81
Q

LAs prolong clotting times in _______, but trigger thromboses in _____. (possibly via complement fixation against the Ab-phospholipid complex in vivo?)

A

vitro, vivo

82
Q

Lupus Anticoagulants:
Prlonged dRVVT = __________
normal dRVVT =___________

A

probable LA
no LA

83
Q

LA workup:

A
  1. mixing study with normal plasma
  2. If no correction… do dRVVT (dilute Russell Viper Venom Time) screening clotting time test.
    Use low [phospholipid], so if LA present, it will NOT be overwhelmed by autoantibodies, and clotting time will be prolonged due to its effects.
  3. Plt neutralization test (confirmatory assay)
84
Q

this test quantitates the LA by determining how much thromboplastin (or reagent-grade plts.) it takes to overwhelm the LA antibody

A

Platelet neutralization test

-follow with specialty immunoassays for specific inhibitors

85
Q

Acquired disorder of Factor VII are primarily due to the presence of ____________ inhibitors of VII.

A

autoimmune

86
Q

Most common antibody is to Factor _____.

A

VIII
-AutoAbs to factors V, VII, XI, and XIII have al been observed

87
Q

symptoms of antibody to Factor VII?

A

may or may not have bleeding tendency, depending upon severity.

88
Q

treatment for antibody to Factor VIII?

A

-treat with steroids to depress autoAb.
-give massive factor replacement or appropriate blood component if bleeding occurs.

89
Q

what drug therapy can cause Acquired inhibition of Factor XIII?

A

tuberculosis drug, isoniazid

90
Q

Acquired inhibition of Factor XIII:
PT, APTT, TCT are all _______.

A

normal

91
Q

how is Acquired inhibition of Factor XIII confirmed?

A

with 5M urea solution test and chromogenic factor assay

92
Q

Factor X deficiencies rarely occurs. Usually found in people with an autoimmune disease known as ___________. PT, APTT, RVVTT are all ____________.

A

amylodosis, prolonged

93
Q

What are the top three most common hereditary coagulation disorders?

A
  1. von Willebrand disease
  2. Hemophilia A (factor 8)
  3. Hemophilia B (factor 9)
94
Q

Von Willebrand Disease is a _____________ bleeding disorder caused by a quantitative or structural abnormality of vWF.

A

mucocutaneous

95
Q

vWD dominant or recessive?

A

can be either depending on mutation sub-type

96
Q

What is the primary function of vWF?

A

to mediate platelet adhesion
-also serves as the factor VII carrier molecule

97
Q

How common is vWD?

A

1 in 1,000

98
Q

What is the most common inheerited coagulopathy of all as a group?

A

vWD

(Group O blood type expresses least amount of vWF.

99
Q

What is the most common inhibitor and deficiency?

A

Factor 8

(lab purchases factor 8 deficient plasma instead of single factor plasmas)

100
Q

What does 1B95 bind to?

A

Von Willebrands factor

101
Q

Currently there are ___ subs types of vWD.
A slight decease in factor _____ is secondary to decreased vWF

A

7, VIII

102
Q

Each vWF monomer has 4 structural domains. What does each domain bind to?

A

-factor VIII
-Gp1b/V/IX
-Gp2b3a
-collagen

103
Q

Because vWF carries factor _____, it helps concentrate it at an injury site.

A

VII

104
Q

What cleaves vWF?

A

Adams 13

105
Q

What are the symptoms of Von Willebrand Disease (vWD)?

A

-Epitaxis (nose bleeds)
-Easy bruising
-Excessively lengthy post -op. bleeding
-Bleeding after tooth extraction
-Bleeding from mucous membranes
-GI bleeds

106
Q

Assay that detects vWF binding to GP1b/IX, used as a screening for this vWD.

A

Ristocetin Induced Plt. Agglutination (RIPA test)

107
Q

What results are seen in Ristocetin Induced Plt. Agglutination (RIPA test) with a pt that has vWD?

A

decreased (or sometime absent) response with ristocetin in classic plt. aggregation

108
Q

After screening for vWD by RIPA test, what further testing should be performed?

A

-VWF Activity Immunoassay and VWF Collagen Binding Assay and/or Ristocetin CoFactor Assay (RCoF)

109
Q

RCoF assay is just RIPA (Ristocetin Induced Plt. Agglutination) with what two modifications?

A
  1. use optical aggregometry
  2. Use standard dilutions of N., fixed, reagent-grade plts. to derive a reference curve of ristocetin-induced agglutination times. Since the vWF activity of these dilutions is known, the pt’s sample can be plotted on the curve and their vWF functional activity then extrapolated.
110
Q

___________ is the definitive diagnostic test for vWD. If further detail on vWF multimer distribution defects is needed, then agarose gel elp is done.

A

RCoF

111
Q

-Two assays used together to gain more information about VWF
-Offers more precision that RCoF Assay
-Involves a monoclonal antibody specific for VWF epitope, and analyzes the collagen adhesion ability
-both reflect VWF activity rather than concentration

A

VWF Activity Immunoassy and VWF Collagen Binding Assay

112
Q

vWD:
APTT is….

A

slightly prolonged. (slightly decreased factor VIII goes along with decreased vWF

113
Q

vWD:

PT is …..

A

Normal. (slt. decreased factor VIII does not affect extrinsic pathway

114
Q

vWD:

Bleeding time (PFA-100) is …

A

Prolonged. (vWF needed for plt. adhesion)

115
Q

vWD:

Factor VIII activity assay is…

A

slt. decreased. (slt. deceased factor VIII goes along with decrased vWF)

116
Q

vWD:

vWF:Ag EIA is…

A

Decreased. (Activity and mass of vWF can be decreased in this disease)

117
Q

vWD:

RIPA and RCoF is…

A

Decreased

Note: Ristocetin aggregation absent in BSS, and VARIABLE in vWD (but usually decreased in vWD)

118
Q

Why isn’t blood components used for vWD treatment?

A

blood components don’t have much vWF and purification removes whats there.

119
Q

What is the treatment for vWD?

A

-Pressure and ice packs for localized hemorrhages
-DDAVP (induces vWF release from endogenous stores)
-Estrogen- along with DDAVP
-Commercial factor VII (used with severe vWD)

120
Q

The goal for drug therapy with vWD is to reach ______% activity. How is drug therapy managed?

A

75
using serial runs of RCoF assay and vWF Ag EIA

121
Q

Inherited bleeding disorder. Deficiency in Factor VIII:C (vWF is normal!)

A

Hemophilia A or Classic Hemophilia

122
Q

How common is Hemophilia A?

A

1 in 10,000

123
Q

What is VIII:C?

A

Factor VIII/vWF complex that circulates in plasma

124
Q

What is the functional role of vWF?

A

to carry factor VIII around

125
Q

What is the functional role of VIII:C?

A

cofactor in factor X activation

126
Q

How is Hemophilia A inherited?

A

X-linked

127
Q

What are the three categories for Hemophilia A?

A

-severe = <1% Factor 8 activity
-Moderate = 1-5% factor 8 activity
-mild = 5-20% factor 8 activity

128
Q

Why do carriers of Hemophilia A usually have no bleeding problems?

A

carriers average about 50% of normal Factor 8 activity
-Normal range 50-150%

129
Q

What are the symptoms of Hemophilia A?

A

-Hemarthroses* (bleeding into joints)
-easy bruising
-mucous membrane hemorrhages
-sever postoperative bleeding
-unexplained severe spontaneous hemorrhages*(post-circumcision or umbilical stump)
-hematuria
-GI bleeds

130
Q

Hemophilia A coagulation profile:

A

-Normal bleeding time
-Normal PT and APTT if case is mild
-Prolonged APTT if VIII:C level is <20% normal level

131
Q

Treatment for Hemophilia A?

A

-Cryoprecipitate (rich in fibrinogen and VIII)
-Concentrated factor VIII:C complex

132
Q

Hemophilia A:

20% of severely affected pts. develop ____________ inhibitors to factor VIII.

A

alloantibody

133
Q

Hemophilia A Inhibitors:

Most are _____, non-complement-fixing, warm-reacting antibodies (reactive at 37 degrees C)

A

IgG

134
Q

With Hemophilia A pts:

What is expected when plasma factor VIII activity fails to increase after therapy?

A

Hemophilia A Inhibitors (incidence is not predictable)

135
Q

Can be used to quantify any factor inhibitor, but most often used for FVIII

A

Bethesda Titer Assay

136
Q

How is Bethesda Titer Assay done?

A

Pts PPP is mixed with known amount of factor VIII, serially diluted, and incubated for 2 hours. The residual amount is tested and compared with results from control mixture.

137
Q

Bethesda Titer Assay:

Titer of inhibitor is dilution that inhibits ____% of factor VIII in assay

A

50

138
Q

What is the treatment for Hemophilia A Inhibitors?

A

-Massive doses Factor VIII concentrate-
-Porcine Factor VIII (in life-threatening situations)
-Recombinate Factor VIIa (bypasses factor VIII)
-Prothrombin Complex Concentrate (PCC)
-Plasmapheresis and immunosuppresive drugs- done in conjuction with factor concentrates.

139
Q

Prothrombin Complex Concentrate (PCC) contains activated Factors II, VII, IX, X; thus works by?

A

turning on extrinsic pathway and bypassing Factor VIII

140
Q

What is clinically indistinguishable from severely deficient Factor IX?

A

VIII

141
Q

There are ______ types of Hemophilia B (or Christmas disease) and they vary tremendously in severity.

A

3

142
Q

How is Hemophilia B inherited?

A

X-linked

carries usually do not have symptoms

143
Q

What is the most important symptom of Hemophilia B?

A

hemarthroses and unexplained spontaneous bleeds

144
Q

Treatment for Hemophilia B?

A

-Monoclonally purified Factor IX concentrates
-Prothrombin Complex Concentrate (PPP)

145
Q

How does Prothrombin Complex Concentrate (PCC) work?

A

bypasses need for factor IX

146
Q

What factors does PCC contain?

A

II,VII, IX, X

147
Q

What are the lab results for Hemophilia B?

A

APTT: prolonged
PT: Normal
Bleeding time: usually normal
Factor IX activity assay: variable decrease (definition of the disease)

148
Q

Factor deficiencies without clinical bleeding?

A

-12
-Pre-K (PK) (PTT is corrected with koalin reagent and incubation)
-HMWK (HK)

149
Q

Factor 12 is unique in that it dose NOT cause bleeding problems. What does it cause instead?

A

Thrombotic events because lack of factor XIIa means major mechanism for triggering fibrinolysis is lost.

150
Q

Why cant a deficiency in Factor XIII be detected by a normal screening method?

A

Because it is outside the intrinsic and extrinsic pathways tested by the usual PTT and PT screening tests.

151
Q

What are the three major natural anti-coagulant mechanisms that control thrombus formation.

A

-antithrombin (AT-III, or AT)
-Protein C Pathway
-Fibrinolytic system

152
Q

AT deficiency causes spontaneous….

A

thrombotic episodes

153
Q

What are the two types of AT deficiency?

A

type-I (decrease in molecule - quantitative
type-II (decrease in activity-qualitative)

154
Q

How is AT deficiency treated?

A

heparin, because heparin will potentiate action of whatever small amount of AT is present.

155
Q

Protein C and Protein S are _____________ liver proteins.

A

K-dependent

156
Q

Protein C and Protein S act as cofactors required for the inactivation of which coag. factors?

A

VIIIa and Va

157
Q

Without protein C or S, pt. is permanently in a ____________ state.

A

hypercoagulable

158
Q

How is protein C and protein S deficiency treated?

A

-protein C administration and OACs (OACs do decrease endogenous protein C, bu that effect is outweighed by the fact that they combat the overall hypercoagulablity tendency)

159
Q

What testing is used for Protein C and Protein S deficiencies?

A

-clot-based, chromgenic, and EIA assays

160
Q

What is the most common genetic mutation causing increased thrombosis in Caucasians?

A

Factor V Leiden (FVL)

161
Q

Factor V Leiden (FVL) occurs in up to _____% of pts. with thrombotic histories.

A

50

162
Q

Factor V Leiden (FVL) causes a condition called…

A

“Activated Protein C Resistance” (APCR)

163
Q

Factor V Leiden (FVL):

With this unusually resistant Factor Va, pt. is permanently in a ___________ state.

A

hypercoagulable

164
Q

Testing for Factor V Leiden?

A

clot-based and rocket IEP* assays, and confirmatory PCR assay

165
Q

For our purposes, Factor V Leiden and APC resistance are synonymous, why?

A

approx. 90% APC-resistant pts. have the Factor V Leiden mutation.

166
Q

What pts. have significantly increased complications with FVL?

A

pregnant women. Ex: pre-eclampsia, stillbirth, and recurrent spontaneous abortion

“double-hit”

pregnant women are hypercoagulable to begin with due to increased Fbg

167
Q

a translocation mutation causing elevated levels of prothrombin
2nd most common genetic mutation causing increased thrombosis in Caucasians.

A

Prothrombin G20210A mutation

-PRC assay now available

168
Q

What does Prothrombin G20210A cause?

A

slightly increased factor II levels (at around 115-130%) but for some reason this puts pt. permanently in a hypercoagulable state (for venous thromboses)

169
Q

What pts have significantly increased complication rates with Prothrombin G20210A? same as in _____?

A

pregnant women, FVL

170
Q

Treatment for Hypercoagulablity disorders:
For severe acute episodes?
For long-term maintenance?

A

Heparin

Warfarin and its derivatives

Hematalogy Lecture (35 decks)

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