Hemostasis - Karius Flashcards

1
Q

Hemostasis

A

Steps taken by the body to limit blood loss

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2
Q

4 Steps of hemostasis

A
  1. vascular spasm
  2. formation of a platelet plug
  3. formation of a blood clot
  4. repair of damage
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3
Q

Platelet

A

Cell fragment from megakaryocyte

150000-300000/um3 normal range

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4
Q

Production of platelets

A

Thrombopoietin

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5
Q

Thrombopoietin

A
TPO
Protein hormone
Chr 3
JAK2/STAT5
Amine terminal is like erythropoietin (EPO)
Carboxyl end: prolongs half-life
Produced by liver, kidney
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6
Q

Control of thrombopoietin secretion

A

Continually secreted

Platelets bind thrombopoietin (mpl) receptor

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7
Q

Thrombopoietin binds to

A

mpl (CD-110) receptor

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8
Q

High number of platelets and thrombopoietin secretion

A

Lots of TPO bound to mol receptor on platelets
Internalize TPO and destroy it
Not much free to act on megakaryocytes

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9
Q

Low number of platelets and thrombopoietin secretion

A

Little bound to platelets
Not being destroyed
Lots free

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10
Q

Main fxn thrombopoietin

A

Increase differentiation of stem cells and maturation rate

All cell lines

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11
Q

Mutation in TPO receptor

A

Cause polycythemia vera

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12
Q

Polycythemia vera

A

Platelets unable to internalize and destroy the TPO so is action becomes continuous

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13
Q

Platelets have actin and myosin

A

Cell contraction

Empty vesicles

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14
Q

Platelets contain

A
Actin and myosin
Mitochondria
Remnants of the ER
Cyclooxgenase
Fibrin stabilizing factor
Platelet-derived growth factor
Serotonin (5-HT)
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15
Q

On platelet membrane

A

Glycoproteins
Phospholipids
Receptors for collagen

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16
Q

Platelet glycoproteins

A

When activated, sticky

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17
Q

Platelet phospholipids

A

Platelet factor 3

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18
Q

Primary causes of vascular spasm

A

Myogenic

Platelet factors

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19
Q

Myogenic causes of vascular spasm

A

Direct response to injury

No neurons, reflexes involved

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20
Q

Platelet causes of vascular spasm

A

Serotonin

Thromboxane A2

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21
Q

Factors contributing to the vascular spasm

A

A neural reflex initiated by the mechanical injury and pain
–neither necessary or sufficient for spasm to occur
MINOR

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22
Q

Formation of platelet plug

A

Damage to vessel wall and collagen is exposed
Platelets will bind to collagen
Von Willebrand factor
Binding of platelet receptor (integrin) to collagen

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23
Q

Von Willebrand factor

A

Plasma protein

Bind between collagen and platelet (receptor)

24
Q

Activation of platelet

A

Platelet swells

Extend podocytes

25
Q

Last steps of formation of platelet plug

A

Platelets swell
Contraction
Granules leave platelet
Platelets stick to vessel wall and to each other (thromboxane A2 and ADP)

26
Q

If cut is small enough

A

Platelet plug may be all that is required

27
Q

3 essential steps for blood coagulation

A
  1. Formation of prothrombin activator
  2. Activation of thrombin
  3. Creation of fibrin from fibrinogen
28
Q

Clot retraction

A
Get rid of excess fluid within clot
Solidify clot
Platelets required
-bind fibrin polymer together
-actin and myosin in platelet - contraction
Also requires calcium
29
Q

Blood clot parts

A

Platelets
RBCs
Fibrin strands

30
Q

Platelets are required

A

To stabilize the clot and cause clot retraction

31
Q

Platelet-derived growth factor

A

Secreted by platelets
Stimulate fibroblast to grow into area
Fibroblasts differentiate into smooth muscle to close the hole

32
Q

Plasminogen

A

Made by liver
Floating in plasma
Not active form

33
Q

Activation of plasminogen

A

Tissue plaminogen activator

34
Q

Tissue plaminogen activator

A

Released by damaged tissue

Activation is inhibited by tPA inhibitor (blood)

35
Q

tPA can convert

A

plasminogen to plasmin

36
Q

Plasmin

A

Breaks down fibrin to remove the clot

37
Q

How do blood vessels prevent clotting?

A

Smooth surface - prevent platelets from rupturing

Membrane proteins - glycocalyx and thrombomodulin

38
Q

Glycocalyx

A

Membrane protein that repels platelets (prevent clotting)

39
Q

Thrombomodulin

A

Membrane proteins that changes thrombin activity to prevent clotting

40
Q

4 Chemicals that limit clotting

A

Fibrin - binds thrombin
Prostacyclin
Antithrombin III
Heparin

41
Q

Fibrin

A

Binds thrombin and prevents it from working

42
Q

Prostacyclin

A

Made at time of injury by endothelial cells
Vasodilation
Limit platelet aggregation

43
Q

Antithrombin III

A

When thrombin binds to it, works as anticoagulant

44
Q

Heparin

A

Derived from mast cells

Increases antithrombin efficacy

45
Q

When Protein C is activated

A

Inactivated factors V and VIII

46
Q

Thrombocytopenia

A

Platelet plug failure

47
Q

Cause of thrombocytopenia

A

Stem cell damage
Leukemia
TPO or mpl gene mutation

48
Q

Platelet count for spontaneous bleeding

A

< 25,000

49
Q

Vitamin K deficiency

A

Fat soluble vitamin made by gut bacteria
Required for production of prothrombin and 3 other factors
Neonates are often K deficient (no gut bacteria yet)
Any thing that impairs absorption of fats can render an adult deficient

50
Q

Hemophilia

A

Genetic absence of a clotting factor

Most common Factor VIII

51
Q

Most common hemophilia

A

Factor VIII def

52
Q

vonWillebrands disease

A

Congenital absence of vWF

Impairs both platelet function and clot production

53
Q

Acquired forms of impaired clotting include:

A

Thrombocytopenia

Vit K deficiency

54
Q

Causes of inappropriate clotting

A
Blood vessels have rough surface
Blood stasis (slow moving)
Disseminated intravascular coagulation
55
Q

Protein C total absence

A

Severe pro-thrombotic state, child dies in infancy

56
Q

APC resistance

A

Leiden mutation (single point mutation)
Factor V mutated
Cannot be inactivated by APC
First signs often in young adulthood, particularly pregnancy

57
Q

Clinical relevance of APC resistance (protein C)

A

1% US population will experience thrombosis
Of them, 64% have some form of APC resistance
Effects vary