Brainscape's Knowledge GenomeTM

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


See full index

pathology > hemostasis and thrombosis > Flashcards

hemostasis and thrombosis Flashcards

1
Q

thrombosis

A

inappropriate activation of normal processes in uninjured vessels or thrombotic occlusion of a vessel after relatively minor injury

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

hemorrhage

A

defects in hemostatic plug formation

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

four stages of normal hemostasis

A

1 - vasoconstriction after injury to epithelium
2 - primary hemostasis - platelet aggregation
3 - secondary hemostasis - coagulation cascade (clot)
4 - thrombus and anti-thrombotic events

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

role of endothelial cells

A

maintain blood fluidity

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

how do endothelial cells regulate vessel tone?

A
  • secrete endothelia - vasoconstriction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how do endothelial cells prevent platelet aggregation and promote vasodilation?

A
  • secrete prostacyclin, nitric oxide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how do endothelial cells act as anticoagulants?

A

1 - prevent interaction with adhesive proteins such as collagen, vWF, tissue factor
2 - modulate fibrinolysis by synthesizing both plasminogen activator (tPA) and plasminogen activator inhibitor (PAI)

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

what is tissue factor?

A
  • membrane protein
  • in smooth muscle, fibroblasts, macrophages
  • initiates coagulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

prothrombotic properties of endothelial cells

A
  • synthesis, storage, release of vWF
  • storage and release of FVIII
  • synthesis of tissue factor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

primary hemostasis (the three A’s)

A

1 - adhesion - to subendothelium mediated by vWF at site of injury
2 - activation - metabolic - membrane shape change, surface GPIIb/IIIa alteration
3 - aggregation - fibrinogen cross-links via GPIIb/IIIa

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

concept of anti-platelet therapy

A
  • prevention of inappropriate platelet activation to prevent stroke, ischemic heart disease, re-stenosis after angioplasty or stent.
  • aspirin irreversibly inhibits platelet cyclo-oxygenase-1 (COX-1)
  • NSAIDs reversibly inhibit COX-1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Clopidogrel

A
  • anti platelet therapy

- blocks ADP receptor

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

Abciximab

A
  • anti platelet therapy

- blocks GPIIb/IIIa

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

Where is VonWillebrand factor synthesized and stored?

A

endothelial cells and megakaryocytes (in platelet a granules)

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

vWF secretion and stimulation

A
  • secretion is constitutive from endothelium into plasm
  • stimulated by thrombin, fibrin, histamine, DDAVP from endothelium
  • from platelet a granules in megakaryocytes when they are activated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

functions of vWF

A
  • adhesion
  • aggregation (bind to GPIIb/IIIa
  • FVIII binding - protects FVIII from proteolytic cleavage and brings it to site of hemorrhage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

vitamin k dependent coagulation enzymes

A

factors 2, 7, 9, 10

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

what are the three lab coagulation pathways?

A
  • intrinsic
  • extrinsic
  • common (both feed into it)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what starts the lab intrinsic pathway?

A

factors XII and XIIa

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

what starts the lab extrinsic pathway?

A

TF and VIIa - stimulate X to Xa conversion directly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

the lab common pathway starts with the conversion of:

A

X to Xa

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

what from the lab intrinsic pathway stimulates the first step of the lab common pathway?

A

VIIIa and Ca

23
Q

what stimulates the conversion from fibrinogen to fibrin in the lab common pathway?

A

Ca

24
Q

what stimulus the conversion from fibrin to cross-linked fibrin in the lab common pathway?

A

factor XIII

25
Q

what starts the in-vivo coagulation pathway?

A

TF + Factor VIIa

26
Q

prothrombin is also known as

A

factor II

27
Q

thrombin is also known as

A

factor IIa

28
Q

what stimulates the conversion of fibrinogen to fibrin in the in-vivo pathway?

A

thrombin (IIa)

29
Q

what stimulates the conversion of fibrin polymers to a fibrin clot in the in-vivo pathway?

A

factor XIII

30
Q

what enzyme is known as the master conductor?

A

thrombin (IIa)

31
Q

how does factor XIII work?

A

stabilizes fibrin clot by cross linking lysine and glutamine side chains of fibrin to form homopolymers

32
Q

four elements of the quaternary complex:

A

1 - enzyme
2 - cofactor
3 - phospholipid surface
4 - calcium ions

33
Q

what does coumadin do?

A

blood thinner - antagonizes vitamin k, which inhibits factors 2, 7, 9, 10

34
Q

what are the body’s three anticoagulant mechanisms?

A
  • antithrombin system
  • protein C system
  • fibrinolytic system
35
Q

describe antithrombin action

A

AT + heparins neutralize thrombin and factors IX, X, XI, XII

36
Q

describe protein C system

A
  • thrombomodulin binds thrombin and protein C

- activated protein C and protein S inactivate factors V and VIII

37
Q

describe the fibrinolytic system

A

plasminogen from the liver cleaves fibrin and fibrinogen

38
Q

name four inherited hemorrhage disorders, their defect, mode of inheritance, and frequency

A

1 - vonWillebrand’s disease, vWF, autosomal dominant, .1-1%
2 - hemophilia A, factor VIII, x-linked, 1/10,000 males
3 - hemophilia B, factor IX, x-linked, 1/50,000 males
4 - hemophilia C, factor XI, autosomal recessive, 1/100,000

39
Q

four acquired hemorrhage disorders

A

1 - blood loss - platelet and clotting factor depletion
2 - excess anticoagulation - decrease or inhibition of factors
3 - disseminated intravascular coagulation (DIC) - consumption of clotting factors or platelets
4 - inhibitors - antibodies to clotting factors

40
Q

Bernard Soulier syndrome

A
  • hemorrhage disease
  • deficiency of GPIB
  • AR
41
Q

Glanzmann’s Thrombasthenia

A
  • hemorrhage disease
  • deficiency of GPIIbIIIa
  • AR
42
Q

thrombosis: Virchow’s Triad

A
  • endothelial injury
  • abnormal blood flow
  • hypercoagulability
43
Q

APC resistance/factor V mutation

A
  • AA replacement at one of three APC cleavage sites in factor Va molecule
  • factor V inactivation takes ten times longer so there is persistent thrombin generation and a hypercoagulable state
44
Q

prothrombin 20210 mutation

A

second most common explanation for hyper coagulability

45
Q

disseminated intravascular coagulation causes and treatment

A

causes - bacterial sepsis, viremia, trauma, tissue necrosis, leukemia, obstetric accidents
treatment - treat underlying condition, break DIC cycle with heparin

46
Q

heparin-induced thrombocytopenia syndrome

A
  • antibodies that bind PF4/heparin/platelets causing clotting
  • depletion of platelet count
  • generally important when treating with heparin and it causes pre-existing clots to get worse
  • avoid by using low molecular weight heparin
47
Q

antiphospholipid antibody syndrome (Hughes Syndrome)

A
  • causes thrombosis, thrombocytopenia
  • possibly activates platelets directly, inhibits PGI2, or inhibits proteins C or S
  • treatment - warfarin, heparin, steroids
48
Q

PT prolonged by

A
  • deficiencies of VII, X, V, II, fibrinogen
49
Q

important application of PT

A
  • monitor warfarin therapy because warfarin interferes with vitamin k dependent factors II, VII, IX, X
50
Q

reagents added for PT

A
  • recombinant TF
  • Ca2+
  • phospholipid
51
Q

reagents added for PTT

A
  • contact activator

- phospholipid

52
Q

PTT prolonged by

A
  • deficiencies in VIII, IX, XI, XII, (HMWK, pre-kallikrein)

- unfractionated heparin, lupus anticoagulant, factor inhibitors

53
Q

what are mixing studies?

A
  • when prolonged PT or PTT - used to figured out whether it is a factor deficiency or the presence of an anticoagulant
  • if fresh pooled normal plasma (PNP) mixed with patient plasma corrects PT/PTT, it is a factor deficiency
  • if PT/PTT does not correct it is an anticoagulant which also inhibits the added factor in the PNP.

pathology (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions