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secondary Flashcards

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1
Q

severe form of bleeding that requires
immediate intervention and transfusion.

A

hemorrhage

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2
Q

APTT’s result is shortened
if the plasma is incubated with a surface
activating substance such as kaolin

A

prekallikrein (fletcher factor) deficiency

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3
Q

results in poor contact –phase
reactions

A

absence of HMWK

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4
Q

Prolonged APTT

A
  • HMWK def
  • Factor XI def
  • Factor VIII (Hemophilia A)
  • Factor IX (Hemophilia B)
  • Factor X
  • Factor II (Afibrino)
  • DIC
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5
Q

Originally described in 1953

A

Factor XI (Hemophilia C; Rosenthal Syndrome)

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6
Q

autosomal recessive

A
  • Prekallikrein
  • Factor VII
  • Factor X
  • Factor V
  • Afibrinogenemia
  • Hypofibrinogenemia
  • Factor XIII
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7
Q

Autosomal dominant

A
  • Factor XI
  • VWD
  • Dysfibrinogenemia
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8
Q

Presents mild to moderate bleeding.

A

Factor XI

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9
Q

Factor XI treatment

A

frequent transfusion of fresh plasma

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10
Q

Represents the first inherited disorder of the intrinsic
cascade to which a clinical bleeding syndrome is attributed

A

Factor XI

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11
Q

Prevalent in Jewish population

A

Factor XI

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12
Q

Clinical syndromes of Factor XI

A

epistaxis, hematuria and menorrhagia.

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13
Q

LABORATORY FINDINGS for factor XI

A

^ APTT corrected by aged serum and adsorbed plasma

One stage PT and BT are not affected

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14
Q

First scientifically described in 1803

A

Factor VIII:C

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15
Q

sex-linked disorder transmitted on an
X chromosome by carrier women to their
sons. Inherited Disorders of Coagulation: Intrinsic Pathway Disorders

A

Factor VIII

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16
Q

most vulnerable parts of the patient with hemophilia A

A

Joints of the knee, elbow, ankle and shoulder

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17
Q

LABORATORY FINDINGS for hemophilia A

A

^ APTT corrected by adsorbed plasma but not with aged serum

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18
Q

Tx for hemophilia A

A

Cryoprecipitate product infusion to replace factor VIII:C

For milder cases, administration of 1-desamino-8-D-arginine-vasopressin (DDAVP)

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19
Q

used or reserved especially for life threatening situations

A

Porcine factor VIII:C and prothrombin factor components

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20
Q

Represents approximately 14% of hemophilia cases in the
United States

A

Factor IX deficiency

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21
Q

Milder form of hemophilia than factor VIII:C deficiency

A

Factor IX deficiency

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22
Q

Deficiency reduces thrombin production and may lead to
soft tissue bleeding that is indistinguishable from
hemophilia A

A

Factor IX deficiency

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23
Q

Three variants of the disease based on antigenic reactivity
of factor IX

A

Cross-reactive material positive (CRM+),
cross-reactive material negative (CRM-), cross-reactive
material reduced (CRMR)

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24
Q

LABORATORY FINDINGS of heophilia B

A

^ APTT corrected with aged serum but not with adsorbed plasma

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25
tx for factor IX deficiency
Administration of commercial concentrate products Plasma exchange with normal donor plasma
26
VWD was described in what year
in 1926
27
produces a prolonged bleeding time and evidence of vascular fragility
VWD
28
demonstrated that the vWF portion of the VIII complex is reduced or absent in this disease
Zimmerman
29
clinical symptoms of patient with VWD
easy bruising, epistaxis, menorrhagia and hemorrhage from tooth extraction
30
LF for VWD
^ BT Inc APTT Decrease activity of VIII:C Abn ristocetin
31
Tx for VWD
✓Infusion of cryoprecipitate ✓Infusion of commercial factor VIII:C ✓Intravenous DDAVP administration.
32
A very rare disorder that occurs in 1 for every 500,000 individuals
Factor VII deficiency
33
Patients are vulnerable to thrombotic events
Factor VII deficiency
34
LF for factor VII
Dx based on family history ^ PT Normal TCT and APTT
35
tx for factor VII deficiency
Infusion of donor plasma, serum components or commercial concentrates containing prothrombin complex
36
It is inherited as autosomal trait that is incomplete recessive but shows high penetrance
Factor X deficiency
37
The disorder is uncommon in the general population
Factor X deficiency
38
LF for Factor X
^ APTT, PT, Stypven time Abn Prothrombin utilization PT is corrected by serum but not with adsorbed plasma
39
tx for factor X deficiency
FFP or Prothrombin complex concentrates are used for therapy
40
Factor V deficiency was discovered by professor owren's in what year?
1944
41
An autosomal recessive trait which is most commonly demonstrated by homozygotes and is mild to silent in heterozygotes
Factor V deficiency
42
Also described as deficient in conjunction with factor VIII deficiency due to genetic defect traced to chromosome 18
Factor V deficiency
43
Factor V laiden mutation was discovered in what year
1993
44
Screening for the presence of APCR is easily performed by clottable assays utilizing modified APTT & Russell’s viper venom time methods.
Factor V laiden mutation
45
May be inherited as a deficiency or a dysfunction
Factor II deficiency
46
new and very common inherited thrombophilic syndrome was described: activated protein C resistance (APCR)
Factor V laiden mutation
47
LF for Factor II
^ APTT and one stage PT Normal TCT
48
diagnostic test procedures for factor II deficiency
Two-stage prothrombin method and immune based factor assay using antiprothrombin antisera
49
Tx for factor II
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.
50
A recessive and severe condition type of fibrinogen I deficiency
Afibrinogenemia
51
LF for afibrinogenemia
▪ Prolonged bleeding time, PT, APTT & TT ▪ Abnormal platelet adhesion and aggregation Extrinsic & Common Pathway Disorder: Factor I (Fibrinogen) Deficiency
52
tx for afibrinogenemia
- cryoprecipitate - FFP however volume overload is concerned - whole blood transfusion
53
tx for hypofibrinogenemia
Cryoprecipitate & FFP are the treatment of choice for this condition.
54
Substitution of amino acids in fibrinogen’s polypeptide chains is the striking feature of this disorder
DYSFIBRINOGENEMIA
55
LF for dysfibrinogenemia
▪ 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.
56
An autosomal recessive trait in which only homozygotes express the syndrome. * Patients exhibit spontaneous bleeding and poor wound healing processes with unusual scar formation
Factor XIII deficiency
57
tx for factor XIII deficiency
Infusion of donor plasma or commercial purified, lyophilized placental factor XIII
58
decreased level of plasma contact factors secondary to hepatic immaturity; insufficient levels of antithrombin III and plasminogen; expression of a unique fetal fibrinogen which behaves differently as to matured ones
Neonatal hepatic disease
59
produce by normal flora of the GIT and absorbed
Vitamin K
60
Vit K Deficiency is due to
(1) absence of normal flora in GIT due to intake of broad spectrum antibiotics, (2) absorption is decreased as seen in obstructive jaundice, (3) if antagonistic drug like coumarin is taken by the patient
61
Intravenous anticoagulant most commonly used in clinical medicine
heparin
62
It is used extensively in preventing fibrin deposition on intravenous tubing devices residing in vessels
heparin
63
water soluble and administered orally. It interferes with the carboxylation of vitamin K dependent procoagulants in the liver by interrupting the enzymatic phase of this reaction.
warfarin
64
Nonfunctional proteins that circulates in the plasma as a result of warfarin activity is referred to as
proteins induced by vitamin K antagonist
65
It results in consumption of coagulation proteins and platelets into thrombi which are deposited locally or widely in the circulation
DIC
66
substance produced by the body that inhibit coagulation.
Circulating anticoagulant
67
Patients having this kind of acquired disorder have increased levels of fibronogen
Circulating anticoagulant
68
Acute DIC has a mortality rate of
60-80%.
69
Progress of DIC may be controlled by
plasmin or thrombin.
70
LF for DIC
prolonged APTT, TCT & PT, decreased platelet count, fibrinogen level and antithrombin III, elevated FSP and fibrin monomers, positive D-dimer.

hema312 (12 decks)

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