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HEMATOLOGY 2 > DISORDERS OF FIBRINOLYTIC SYSTEM and THROMBOTIC DISORDERS > Flashcards

DISORDERS OF FIBRINOLYTIC SYSTEM and THROMBOTIC DISORDERS Flashcards

1
Q

it comprises an inactive proenzyme, plasminogen, which can be converted to the active enzyme, plasmin, which in turn degrades fibrin into soluble fibrin degradation products.

A

fibrinolytic system

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2
Q

excessive amounts of plasminogen activators from damaged cells/malignant cells

A

primary fibrinolysis

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3
Q

secondary fibrinolysis is can be caused by

A

DIC; uncontrolled, inappropriate formation of fibrin within the blood vessels

example:
infection
neoplasm
snake bite
HTR

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4
Q

the disorder of fibrinolytic system can impair the breakdown of fibrin resulting in a build-up of fibrin thus resulting to __

A

thrombosis

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5
Q

Plasminogen Deficiency

what are its subclassification

A

plasminogen deficiency type 1
plasminogen deficiency type II

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6
Q

subclassification of plasminogen deficiency which is the True plasminogen deficiency (hypoplasminogenemia)

A

plasminogen deficiency type 1

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7
Q

subclassification of plasminogen deficiency wherein there’s Proportionate decrease in both level of plasminogen and its activity

A

plasminogen deficiency type I

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8
Q

cause of plasminogen deficiency type I

A

congenital plasminogen deficiency is caused by MUTATIONS in the PLG gene

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9
Q

this gene provides instructions for making a protein called plasminogen

A

PLG gene

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10
Q

dx for plasminogen deficiency 1

A

genetic testing
research studies

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11
Q

other name for plasminogen deficiency type I

A

hypoplasminogenemia
plasminogen deficiency, type I

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12
Q

subclassification of plasminogen deficiency wherein the level of immunoreactive plg is normal whereas the specific functional activity is markedly reduced because of abnormalities in the variant plg molecule

A

plasminogen deficiency type II

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13
Q

refers to an increased tendency to develop thrombi or emboli

A

thrombosis

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14
Q

thrombosis is sometimes called as ____

A

hypercoagulable state

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15
Q

thrombosis is a multifaceted disorder resulting from abnormalities in blood flow, such as

A

stasis
abnormalities in the coagulation system
plt function
leukocyte activation molecules
blood vessel wall

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16
Q

predisposition to thrombosis

A

thrombophilia

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17
Q

abnormality of blood coagulation that increases the risk of thrombosis

A

thrombophilia

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18
Q

thrombophilia, it may be due to ____

A

physical, biological, and chemical events

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19
Q

thrombophilia, it may be due to physical, biological, and chemical events such as :

A

acute or chronic inflammation
inappropriate or uncontrolled plt activation
uncontrolled triggering of the plasma coagulation system
inadequate control of coagulation-impaired fibrinolysis

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20
Q

classification of thrombosis

A

venus and arterial thrombosis

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21
Q

what are the venous thrombosis

A

deep vein thrombosis
portal vein thrombosis
renal vein thrombosis
jugular vein thrombosis
budd chiari syndrome
paget-schroetter disease
cerebral venous sinus thrombosis

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22
Q

formation of blood clot within a deep bein

A

deep vein thrombosis

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23
Q

affects the superficial leg veins from the iliac, poplietal, and femoral veins of the upper leg and calves

A

deep vein thrombosis

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24
Q

signs of deep vein thrombosis

A

swelling, pain, and redness in the affected area especially the entire legs

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25
Q

form of venous thrombosis affecting the hepatic portal vein which can lead to portal hypertension and reduction of supply to the liber

A

portal vein thrombosis

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26
Q

obstruction of the renal vein by a thrombus

A

renal vein thrombosis

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27
Q

jugular vein thrombosis may occur during __

A

infection, malignancy, or infusion of the intravenous drug`

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28
Q

conditions associated with jugular vein thrombosis

A

systemic sepsis, pulmonary embolism, papilledema

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29
Q

this is the form of thrombosis present abdominal pain, hepatomegaly and ascites

A

budd-chiari syndrome

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30
Q

there is a blockage of the inferior vena cava by a thrombus

A

budd-chiari sundrome

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31
Q

conditions that usually occurs after exercise

A

paget schroetter disease

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32
Q

there is an obstruction of the upper extremity vein by a thrombus

A

paget schroetter disease

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33
Q

rare form of thrombosis which result from a blockage of the diural venous sinuses by a thrombus

A

cerebral venous sinus thrombosis

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34
Q

cerebral venous sinus thrombosis has the same symptoms of ___

A

stroke, headache, and abnormal vision

35
Q

it is the formation of accumulation of thrombi within an artery known as

A

atherosclerotic plaque

36
Q

arterial thrombosis is also known as

A

atherothrombosis

37
Q

it causes infarction to different organs in the body

A

arterial thrombosis

38
Q

arterial thrombosis is common to _____% patient not receiving anticoagulant therapy
ex, MI or stroke

A

5%

39
Q

suspected when thrombotic events occur in young adults and their unusual sites (mesentery, renal, or axillary veins )

A

genetic or congenital thrombosis

40
Q

it involved the alteration of guanine to adenine at the base of the 20210 of the 3` untranslated region of prothrombin gene

A

prothrombin 20210 mutation

41
Q

prothrombin 20210 mutation is found in __ % with clotting disorder

A

10%

42
Q

second most common inherited thrombophilic tendency in patients with family history of DVT

A

prothrombin 20210 mutation

43
Q

associated with higher levels of prothrombin, averaging to 130%

A

prothrombin 20210 mutation

44
Q

prothrombin 20210 mutation is linked to other clotting events such as

A

coronary artery disease
venous clots
etc

45
Q

hyperhomocysteinuria

deficient in 3 enzymes

A

methionine synthase
cystathionine-B-synthase
5, 10 methyltetrahydrofolate reductase

46
Q

increased level of homocysteine

A

hyperhomocysteinemia

47
Q

may predispose to arterial thrombosis and venous thromboembolism

A

hypercysteinuria

48
Q

May be due to deficiency in enzymes that will
hydrolyze homocysteine in several end products

A

Hyperhomocysteinuria

49
Q

Plasma homocysteine levels are ≥10 fold in
homozygous cystathionine-ß-synthase deficiency.

true or false

A

true

50
Q

inherited cause of hyperhomocysteinuria

A

low levels of an enzymes necessary for the
conversion of homocysteine to cysteine which increase the risk of
a clotting event.

51
Q

acquired event of hyperhomocysteinuria

A

advance age and diet

52
Q

factor V leiden mutation is also called as

A

activated protein C resistance

53
Q

factor V Leiden Mutation or
Activated Protein C Resistance

is identified on what year

A

1993

54
Q

factor V Leiden Mutation or
Activated Protein C Resistance

it was identified in 1993 as the tope leading cause of

A

blood blots among white population

55
Q

The most common genetic risk of factor for
blood clots.

A

Factor V Leiden Mutation or
Activated Protein C Resistance

56
Q

The mutation happens in Factor V protein,
which is known as the

A

Leiden protein

57
Q

Factor V Leiden Mutation or
Activated Protein C Resistance

The mutated plasma protein is resistant to
regulation by _____that is why
clotting is uncontrolled

A

activated protein C

58
Q

posses only the Leiden
protein and an 80-fold increased risk of clotting qdisorder compared to the general unaffected
population

A

Factor V Leiden homozygotes

59
Q

are believed to
produced about 50% of Leiden protein and have 5-7 fold increased risk of clotting disorder compared to the
general population

A

Factor V Leiden heterozygotes

60
Q

OTHER FACTOR V MUTATION:

A

Factor V Cambridge mutation
Factor V Hongkong mutation

61
Q

Elevated levels of other clotting factors as a prociagulant can
also be associated with increased risk of
thrombosis

list the mentioned clotting factors

A
  • Factor VIII
  • Factor IX
  • Factor XI
  • Factor I
  • vWF
62
Q

A serine protease inhibitor (serpin) that
neutralizes thrombin, Factor Ixa, Xa, Xia & XIIa.

A

ANTITHROMBIN

63
Q

ANTITHROMBIN

Its activity is enhanced by

A

unfractionated heparin, LMW heparin, and systemic entasaccharide

64
Q

First of the plasma coagulation control protein
to be identified and first assayed in the
laboratory

A

ANTITHROMBIN

65
Q

Acquired antithrombin deficiency

A
  • Liver disease
  • Nephrotic syndrome
  • Prolonged heparin therapy
  • Oral contraceptives
  • DIC (AT is rapidly consumed)
66
Q

Congenital antithrombin deficiency

A

Defect in heparin binding sites causing
severe clotting tendencies that usually
presents in early stage of life

67
Q

2 types of antithrombin deficiency

A

type I and II AT deficiency

68
Q

this type of AT deficiency refers to the genetic alteration usually
leads to drastic decrease levels in AT

A

Type I AT deficiency

69
Q

this type of AT deficiency refers to the genetic alteration leads to
abnormal function of the plasma protein.

A

type II AT deficiency

70
Q

type of protein C deficiency wherein there’s low protein C levels
and activity.

A

Type I Protein C deficiency

71
Q

type of protein C deficiency wherein there’s ow protein C
activity due to genetic alteration of protein C
sequence resulting to abnormal functioning.

A

Type II Protein C deficiency

72
Q

this protein C deficiency appears in newborn infants.

A

Homozygous Protein C Deficiency

73
Q

Homozygous Protein C Deficiency
can cause what type of purpura

A

purpura fulminans in children

74
Q

caused by rapid drop in protein C and factor VII resulting to temporary super clotting state in the extremities

A

warfarin induced skin necrosis

75
Q

can also cause neonatal purpura fulminans which is
clinically indistinguishable from Protein C deficiency.

A

protein S deficiency

76
Q

a type of protein S deficiency wherein there’s a proportional
decrease in the level and activity of Protein S

A

type I protein S deficiency

77
Q

a type of protein S deficiency wherein the levels of the free and bound forms are normal, but there is an abnormal function due to genetic alteration in the gene sequence

A

type II protein S deficiency

78
Q

a type of protein S deficiency wherein there’s a normal level to total protein S but with clinically significant decrease in free protein S levels

A

type III protein S deficiency

79
Q

Deficiency leads to increased thombi formation
due to low/deficient activity to inhibit thrombin

A

Heparin Cofactor II Deficiency

80
Q

type of heparin cofactor II deficiency where in there’s a decreased in both levels and
functional capacity

A

type I (quantitative)

81
Q

type of heparin cofactor II deficiency where in there’s a decreased in functional
capacity but with normal levels of heparin
cofactor II.

A

type II (qualitative)

82
Q

Small thrombomodulin fragments circulates in
soluble form in plasma of healthy individuals.

A

thrombomodulin Deficiency

83
Q

thrombomodulin Deficiency

increased levels are seen in patients with ___

A

venous and arterial clotting conditions and
DIC

HEMATOLOGY 2 (18 decks)

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