Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

HEMATOLOGY 2 > DISORDERS OF SECONDARY HEMOSTAS > Flashcards

DISORDERS OF SECONDARY HEMOSTAS Flashcards

1
Q

is a severe form of bleeding that requires immediate intervention and transfusion

A

hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the inherited disorders of coagulation: intrinsic pathway disorders

A

prekallikrein (fletcher factor deficiency)
high molecular weight kininogen (fitzgerald factor) deficiency
factor XI deficiency (hemophilia C; rosenthal syndrome)
Factor VIII;C deficiency (hemophilia A; classic hemophilia)
Factor IX deficiency (hemophilia B; christmas disease)
von willebrand’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the inherited disorders of coagulation: extrinsic and common pathway disorders

A

factor VII (proconvertin; stable factor) deficiency
factor X (stuart-power factor) deficiency
Factor V deficiency (owren’s disease; labile factor deficiency
Factor II (Prothrombin) Deficiency
Fibrinogen (factor I) deficiency
Factor XIII (fibrin stabilizing factor) deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

acquired disorders of coagulation

A

hepatic disease
vitamin K deficiency
therapeutic anticoagulation
circulating anticoagulant (inhibitory) substance
massive transfusion effects
disseminated intravascular coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

pre-kallikrein (fletcher factor) deficiency is believed to be transmitted as _____ trait

A

autosomal recessive trait

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

laboratory findings of prekallikrein (fletcher factor) deficiency is similar to what factor deficiency

A

factor XII deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

laboratory findings of prekallikrein is similar to factor XII deficiency except for

A

APTT result as it is shortened if the plasma is incubated with a surface activating substance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the surface activating substance being talk about in shortened APTT result of incubated plasma

A

kaolin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

refers to the absence of HMWK in poor contact-phase reactions, a deficiency of kinin formation (active forms derived from kininogen), and defective fibrinolysis reaction

A

High Molecular Weight Kininogen (Fitzgerald
Factor) Deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

active form derived from kininogen

A

kinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

lab findings in High Molecular Weight Kininogen (Fitzgerald
Factor) Deficiency

A

APTT results typically are prolonged
other tests are within normal limits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

factor XI deficiency is what type of hemophilia

A

hemophilia C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

hemophilia C, what is the general name

A

rosenthal syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

factor XI deficiency is originally describe on what year

A

1953

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

factor XI deficiency

what is the mode of inheritance

A

autosomal dominant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

describe the bleeding of factor XI deficiency

A

mild to moderate bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

TX of factor XI deficiency( Hemophilia C; Rosenthal Syndrome

A

fresh plasma infusions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

this deficiency represents the first inherited disorder of the intrinsic cascade to which a clinical bleeding syndrome is attributed

A

factor XI deficiency (Rosenthal syndrome; hemophilia C)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

this deficiency is very prevalent in jewish population

A

Factor XI Deficiency (Hemophilia C; Rosenthal Syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

clinical findings of patients with factor XI Deficiency (Hemophilia C; Rosenthal Syndrome))

A
  • patients present mild bleeding tendencies which usually respond to therapy
  • most patients are symptomatically “silent” until stressed by trauma or surgery
  • clinical syndromes may include episodes of epistaxis, hematuria, and menorrhagia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

laboratory findings of Factor XI Deficiency (Hemophilia C; Rosenthal Syndrome)

A

prolonged APTT which is corrected by aged serum
one stage PT and bleeding time are not affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

prolonged aptt in factor XI deficiency is corrected using

A

aged serum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

therapy for Factor XI Deficiency (Hemophilia C;
Rosenthal Syndrome)

A

no specific blood component exist to treat factor XI deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

factor VIII:C deficiency (hemophilia A; classic hemophilia )

is first scientifically described on what year

A

1803

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

factor VIII:C deficiency ; hemophilia A; classic hemophilia

what is the disease called

A

royal disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

mode of inheritance of factor VIII:C deficiency hemophilia A; classic hemophilia

A

sex-linked (X chromosome)

mother to son

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

the entire molecule as it circulates in the plasma. Composed of VIII:C and VIII:vWF portions noncovalently bound

A

VIII/vWF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

portion of molecule responsible for binding to endothelium and supporting normal platelet adhesion and function. Tested by bleeding time

A

VIII:vWF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

portions of molecule acting in intrinsic system as cofactor to factor Ixa (with Ca++) in the conversion of factor X to Xa. Tested by PTT

A

VIII:C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

antigenic property of procoagulant portion as measured by immunologic monoclonal antibody techniques

A

VIIC:Ag

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Factor VIII-related antigen, which is a property of the large vWF portion of
the molecule and measured by immunologic techniques of Laurell rocket or
immunoradiometric assay.

A

VIIIR:Ag

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Ristocetin cofactor activity, which is factor VIII related activity required for
aggregation of human platelets with ristocetin in in vivo aggregation studies

A

VIIIR:RCo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Bleeding diathesis arises from decreased or defective factor VIII:C.

A

Hemophilia A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Joints of the knee, elbow, ankle and shoulder are the most vulnerable
parts of the patient

A

Hemophilia A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Repeated hemarthroses can cripple and deform the patient.

A

Hemophilia A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

✓Tragically, 70% of hemophiliacs treated before 1984 are ___ and
have died from ___

A

HIV positive and
have died from AIDS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

lab findings of hemophilia A

A

prolonged APTT but corrected by adsorbed plasma but not with aged serum

level so of factor VIII:C differ in the daughters of
carrier females (maternal carrier) and the daughters
of hemophiliacs (paternal carriers).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

__ product infusion to replace factor VIII:C

A

Cryoprecipitate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

hemophilia A

For milder cases, administration of pharmacologic agent such
as __ may be
substituted for donor component.

A

1-desamino-8-D-arginine-vasopressin (DDAVP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

hemophilia A

Intravenous administration of DDAVP rise plasma levels of
plasma factor VIII:C how manytimes

A

threefolds to sixfolds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

used to monitor therapeutic progress of
patients with hemophilia A

A

factor assays

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Patients who have developed antibodies against factor VIII:C
may be given with ____ component to purge the antibody from plasma. But this was believed to be ineffective

A

plasma pheresed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

__ components are
used or reserved especially for life threatening situations.

A

Porcine factor VIII:C and prothrombin factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Factor IX Deficiency is also called as

A

hemophilia B; Christmas disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Factor IX Deficiency represents approx ____ of hemophilia cases in the US

A

14%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Milder form of hemophilia than factor VIII:C deficiency

A

Factor IX Deficiency (Hemophilia B; Christmas Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q
  • Deficiency reduces thrombin production and may lead to soft tissue bleeding that is indistinguishable from
    hemophilia A.
A

Factor IX Deficiency (Hemophilia B; Christmas Disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Three variants of the factor IX deficiency based on antigenic reactivity
of it:

A

cross reactive material positive (CRM+)

cross reactive material negative (CRM-)
cross reactive material reduced (CRMr)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

lab findings of hemophilia B

A

prolonged aptt which is corrected with aged serum but with not adsorbed plasma

specific factor IX assay - used for diagnosis and to assess actvity levels during therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

therapy for hemophilia B

A

administration of commercial concentrate products

plasma exchange with normal donor plasma have been performed to achieved 50% to 100% activity levels and to prevent cardiac overload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Factor XI Deficiency (Hemophilia C; Rosenthal
Syndrome)

mode of inheritance

A

autosomal dominant hemophilia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

year 1926, ____ described this disorder at autosomal dominant disorder that produces a prolonged bleeding time and evidence of vascular fragility

A

eric von willebrand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Caused by defects in both in factor VIII:C and VIIIR:Ag of factor VIII complex.

A

von willebrand disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

In 1971, __ demonstrated that the vWF portion
of the VIII complex is reduced or absent in von willebrand disease

A

Zimmerman

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Platelets in von Willebrand’s plasma, in contrast to platelets in normal plasma, do not aggregate in the presence of __.

A

ristocetin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Patients demonstrate easy bruisability, epistaxis, menorrhagia and hemorrhage from tooth extraction

A

von Willebrand’s Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

It is the most frequently inherited disorder.

A

von Willebrand’s Disease

58
Q

type of von willebrand disease

A

homozygous “double heterozygous”
heterozygous I
heterozygous II (subtype IIa IIb)

59
Q

from the type of von willebrand disease, which one is the autosomal recessive

A

homozygous

60
Q

from the type of von willebrand disease, which one has the a severe effect

A

homozygous

61
Q

effect of heterozygous von willebrand disease

A

variably; mild to moderate

62
Q

effect of heterozygous II

A

variable

63
Q

a predominant plasma protein of the extrinsic coagulation pathway

A

factor VII (proconvertin; stable factor) deficiency

64
Q

mode of inheritance of factor VII (Proconvertin; Stable Factor) deficiency

A

autosomal recessive genetic abnormality with intermediate expression

65
Q

a very rare disorder that occurs in 1 every 500,000 individuals

A

Factor VII (Proconvertin; Stable Factor) Deficiency

66
Q

what are the variants of Factor VII (Proconvertin; Stable Factor) Deficiency

A

CRM+ AND CRIM R

no negative in factor VII deficiency

67
Q

In factor VII deficiency, the Correlation between ___ and ___ are poor.

A

clinical tendency and activity
levels

68
Q

patients are vulnerable to thrombotic events

A

Factor VII (Proconvertin; Stable Factor) Deficiency

69
Q

lab findings of factor VII deficiency

A

diagnosis is based on family history
prolonged PT
normal thrombin clotting time and APTT
chromogenic substrate procedures measure the ability of factor VII to cleave factor X
increased levels of factor X in pregnant women

70
Q

therapy for factor VII deficiency

A

Infusion of donor plasma, serum components or commercial concentrates containing prothrombin complex (Autoplex T preparations).

71
Q

it is inherited as autosomal trait that is incomplete recessive but shows high penetrance

A

factor X (stuart-prower factor) deficiency

72
Q

factor X (stuart-prower factor) deficiency

does it have immune variants?

A

yes

73
Q

the disorder is uncommon in the general population

A

factor X - stuart prower deficiency

74
Q

in Factor X (Stuart- Prower Factor) Deficiency,
the symptoms of patients having the disorder are variable

true or false

A

true

75
Q

lab findings of Factor X (Stuart- Prower Factor) Deficiency

A

prolonged APTT, PT, and stypven time
prothrombin utilization is abnormal
PT is corrected by aged serum but not with adsorbed plasma

76
Q

Therapy for factor X deficiency

A

✓FFP or Prothrombin complex concentrates are used for therapy

77
Q

Factor V Deficiency, what’s the disease called?

A

owren’s disease; labile factor deficiency

78
Q

Factor V Deficiency (Owren’s Disease; Labile Factor Deficiency)

discovered in 1944 by

A

Professor Owen

79
Q

mode of inheritance of factor V deficiency

A

autosomal recessive

80
Q

also described as deficient in conjunction with factor VIII deficiency due to genetic defect traced to chromosome 18

A

Factor V Deficiency (Owren’s Disease; Labile Factor Deficiency)

81
Q

FACTOR V LAIDEN MUTATION (_______)

it’s like some sort of code

A

R506Q

82
Q

In 1993, a new and very common inherited
thrombophilic syndrome was described:

A

activated protein C resistance (APCR)

83
Q

FACTOR V LAIDEN MUTATION (R506Q)

Molecular defect (single point mutation) was identified involving the transition of a guanine (G) to adenine (A) at nucleotide __

A

1691 of factor V gene.

84
Q

FACTOR V LAIDEN MUTATION (R506Q)

Mutation results in the substitution of __at number 506

A

arginine (R) with glutamine (Glu)

85
Q

factor V laiden mutation

Screening for the presence of APCR is easily performed
by clottable assays utilizing __

A

modified APTT & Russell’s
viper venom time methods.

86
Q
  • May be inherited as a deficiency or a
    dysfunction.
A

Factor II (Prothrombin) Deficiency

87
Q

Hemarthroses in patients are rare

A

Factor II (Prothrombin) Deficiency

88
Q

Factor II (Prothrombin) Deficiency

can aspirin be administered

A

nope, can cause serious bleeding

89
Q

lab findings for Factor II (Prothrombin) Deficiency

A

▪ APTT & one-stage PT will be prolonged.
▪ TCT (Thrombin clotting time) is normal.
▪ Two-stage prothrombin method and immune based factor assay using antiprothrombin antisera are the
diagnostic test procedures.

90
Q

therapy for Factor II deficiency

A

➢Infusion of FFP is the usual choice of treatment.
➢Vitamin K concentrates may also be given to patients but there is a risk of thrombosis after administration

91
Q

FibrInogen (Factor I) Deficiency

defect may result to the following conditions

A

afibrinogenemia
hypofibrinogenemia
dysfibrinogenemia

92
Q

–inherited lack of fibrinogen.

A

Afibrinogenemia

93
Q

inherited deficiency of fibrinogen.

A

Hypofibrinogenemia

94
Q

–inherited production of dysfunctional
fibrinogen molecule.

A

Dysfibrinogenemia

95
Q

____ __ aid in the differentiation
between inherited and acquired forms of fibrinogen deficiency

A

History and clinical features

96
Q

AFIBRINOGENEMIA

mode of inheritance

A

recessive and severe condition

97
Q

Patients having this condition have nearly undetectable
amounts of fibrinogen

A

AFIBRINOGENEMIA

98
Q
  • Patients’ platelets appear affected in that prolonged bleeding time may be measured. (Platelets have a
    surface receptor for fibrInogen, and fibrinogen
    apparently is necessary for platelets to function in vivo)
A

AFIBRINOGENEMIA

99
Q

LABORATORY FINDINGS of afibrinogenemia

A

▪ Prolonged bleeding time, PT, APTT & TT
▪ Abnormal platelet adhesion and aggregation

100
Q

therapy for afibrinogenemia

A

➢Treatment requires administration of
cryoprecipitate
➢FFP may be used; however, volume overload is a
major concern.
➢Whole blood transfusions may be required if
significant bleeding has occurred.

101
Q

Patients possess 20-100 mg/dL level of fibrinogen
(normal range: 200-400 mg/dL).

A

HYPOFIBRINOGENEMIA

102
Q

mode of inheritance of hypofibrinogenemia

A

Inherited as heterozygous, autosomal recessive
disorder.

103
Q

TX FOR hypofibrinogenemia

A

Cryoprecipitate & FFP are the treatment of choice for
this condition

104
Q

Molecular structure of fibrinogen is said to be normal for what type of fibrinogen deficiency

A

hypo and afib

105
Q

mode of inheritance of dysfibrinogenemia

A

Inherited as an autosomal dominant trait

106
Q

Patients demonstrate abnormal fibrinogen function but usually
have normal levels in antigenic assay.

A

DYSFIBRINOGENEMIA

107
Q
  • Substitution of amino acids in fibrinogen’s polypeptide chains is the striking feature of dysfibrinogenemia, which may result in:
A
  1. Inability to submit proteolysis by thrombin, because the cleavage sites are inappropriate.
  2. Peculiar behaviour during polymerization stages secondary to aberrant charge distribution across the molecule.
  3. Addition of inappropriate side groups that affect reactivity.
  4. Persistence of fetal fibrinogen into adulthood
108
Q

lab findings for dysfibrinogenemia

A

▪ Normal PT, APTT
▪ Normal bleeding time and platelet function tests
▪ Normal quantitative level of fibrinogen
▪ Mild to markedly prolonged thrombin time
▪ Prolonged ReptilaseR
(venom) clotting time.

109
Q

Factor XIII (Fibrin-Stabilizing Factor) Deficiency

mode of inheritance

A

autosomal recessive trait in which only homozygotes express the syndrome

110
Q
  • Patients exhibit spontaneous bleeding and poor wound
    healing processes with unusual scar formation
A

Factor XIII (Fibrin-Stabilizing Factor) Deficiency

111
Q

Factor XIII (Fibrin-Stabilizing Factor) Deficiency

all patients should avoid what medication

A

aspirin

112
Q

lab findings for factor XIII deficiency

A

▪ Patients have inadequate cross-linking of fibrin which
results in an unstable and friable clot with excessive
red cell “fall out”.
▪ Condition cannot be evaluated in the presence of
heparin
▪ Specific Factor XIII assays are available but are not
suitable for routine clinical use.
▪ Immunologic Factor XIII procedures are available to
measure quantities of the said factor

113
Q

therapy for factor XIII deficiency

A

➢Infusion of donor plasma or commercial purified, lyophilized placental factor XIII.

114
Q

Liver disorders present two challenges

A

decreased synthesis of coagulation, lyses, and inhibitory proteins

impaired clearance of activated hemostatic component

115
Q

there is a decreased level of
plasma contact factors secondary to hepatic immaturity

A

Neonatal hepatic disease

116
Q

Neonatal hepatic disease resultsto

A

there is a decreased level of
plasma contact factors secondary to hepatic immaturity

insufficient levels of antithrombiin III and plasminogen

expression of a unique fetal fibrinogen which behaves differently as to matured ones

117
Q

is produce by normal flora of the GIT and
absorbed.

A

vitamin K

118
Q

vitamin K deficiency is due to

A

absence of normal flora in GIT due to intake of broad spectrum antibiotics

absorption is decreased as seen in obstructive jaundice

if antagonistic drug like coumarin us taken by the patient

119
Q

is used to asses levels of vitamin K dependent factors in the new born

A

one stage PT

120
Q

Intravenous anticoagulant most commonly used in clinical medicine

A

heparin

121
Q
  • It is used extensively in preventing fibrin deposition
    on intravenous tubing devices residing in vessels.
A

heparin

122
Q

It is a mucopolysaccharide that acts in conjunction
with antithrombin III to inhibit most of serine
proteases in the coagulation pathways.

A

heparin

123
Q

heparin

  • It is metabolized by the liver and has a half-life of approximately ____ hours
A

3 hrs

124
Q

Coumarin Drugs (Oral anticoagulants)
* Discovered in __

A

Wisconsin

125
Q

is most frequently used coumarin which is
water soluble and administered orally

A

warfarin

126
Q

It interferes with the carboxylation of vitamin K dependent
procoagulants in the liver by interrupting the
enzymatic phase of this reaction.

A

coumarin drugs

127
Q

Nonfunctional proteins that circulates in the plasma as a result of warfarin activity is referred to as

A

proteins induced by vitamin K antagonist (PIVKA)

128
Q

substance produced by the
body that inhibit coagulation

A

Circulating anticoagulant

129
Q

circulating anticoagulant’s Stimuli include

A

infusion of blood or blood products,
release of tumor substances into the circulation and
autoimmune disorders

130
Q

Patients having this kind of circulating anticoagulant have increased levels of fibrinogen (as seen in ___)

A

DIC, coagulation and lytic disorders

131
Q

laboratory testing for circulating anticoagulant (inhibitory) substance includes

A

FSP agglutination test,
measurement of fibrin monomers,
platelet counts,
fibrnogen levels, APTT & PT.

132
Q

Massive transfusion can jeopardize hemostatic competency because:

A

excessive quantities of infused citrates
donor product is incompatible to recipient’s system
deficient labile clotting factors or platelets in stored blood

133
Q

is considered as sensitive indicator of
depressed platelet function in extensively transfused
patients

A

bleeding time

134
Q

are less sensitive but useful in deciding
whether to supplement therapy with cryoprecipitate
or FFP in masiive transfusion effect

A

APTT and PT

135
Q

A complication of other primary disorders.

A

Disseminated Intravascular Coagulation

136
Q
  • It results in consumption of coagulation proteins and
    platelets into thrombi which are deposited locally or
    widely in the circulation.
A

Disseminated Intravascular Coagulation

137
Q

do Disseminated Intravascular Coagulation has age preference?

A

no age or gender preference for this disorder

138
Q

acute Disseminated Intravascular Coagulation has a mortality of

A

60-80%

139
Q

progress of DIC may be controlled by

A

plasmin or thrombin

140
Q

lab result of Disseminated Intravascular Coagulation reveals

A

prolonged APTT, TCT, PT
decrease PLT COUNT, FIBRINOGEN LEVEL, ANTITHROMBIN III,
elevated FSP and FIBRIN MONOMERS and POSITIVE D-DIMER

141
Q

THERAPY for DIC

A

replacement therapy with blood components are necessary following acute DIC

Infusion of FFP, PC, and CRYOPRECIPITATE may be used

complete profile of coagulation and lysis should be performed at clinically determined intervals to assess this syndrome during management

142
Q
A

HEMATOLOGY 2 (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions