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Pathology > Exam 1: Hemostasis, Thrombosis, and Hemorrhage > Flashcards

Exam 1: Hemostasis, Thrombosis, and Hemorrhage Flashcards

1
Q

What is bleeding stopped by?

A

Hemostasis

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2
Q

Describe what happens in hemostasis

A

Complex interaction of endothelium, platelets, and the coagulation cascade
These processes maintain blood in a fluid, clot-free state in normal blood vessels
They can also induce a rapid and localized “hemostatic plug” at the site of vascular injury
Anticoagulant activities also occur to limit the extent of the plug–process of fibrinolysis

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3
Q

What is the pathologic correlate to hemostasis?

A

Thrombosis, but it is considered to be an inappropriate activation of normal hemostatic processes

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4
Q

What is the sequence of events with vascular injury?

A

Vasoconstriction
Primary hemostasis
Secondary hemostasis
Reorganization and formation of a permanent plug

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5
Q

What are the different ways vasoconstriction can occur?

A

Transient arteriolar vasoconstriction after initial endothelial injury that exposes collagen of the subendothelial matrix (ECM)
Vasoconstriction due to local nerve reflex and release of endothelin by endothelial cells

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6
Q

What does vasoconstriction help do?

A

Limit the escape of RBCs and proteins from damaged areas

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7
Q

Describe primary hemostasis

A

Platelets adhere to exposed ECM via von Willebrand factor
Platelets undergo activation
Platelets release secretory granules (ADP and thromboxane A2, cause vasoconstriction and promote further platelet aggregation)
Form primary hemostatic plug

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8
Q

Describe secondary hemostasis

A

Local activation of the coagulation cascade
Tissue factor is secreted by adjacent endothelial cells
Thromboplastin initiate the clotting cascade
Results in fibrin polymerization and cementing platelets into a definitive secondary plug

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9
Q

What happens with counter-regulatory mechanisms?

A

Release of compounds that limit that hemostatic process to the site of injury

  • –tissue type plasminogen activator (fibrinolytic)
  • –thrombomodulin (interferes with the clotting cascade)
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10
Q

What is thrombosis?

A

Formation of a blood clot due to either inappropriate activation of normal hemostasis or formation of a clot in a vessel after injury
Can also be due to other abnormal processes that can block a blood vessel and lead to death

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11
Q

What is fibrinolysis?

A

The process of limiting the hemostatic process at the site of injury
Includes the release of tissue plasminogen activator and thrombomodulin by adjacent endothelium

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12
Q

What is endothelium?

A

Cells that line blood vessels

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13
Q

What are the antithrombotic properties of endothelium?

A

Normally acts as a barrier between blood and subendothelial collagen

  • –Block platelet aggregation
  • –Interfere with coagulation
  • –Actively lyse clots
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14
Q

What are the prothombotic properties of endothelium?

A

Injury or activation of endothelial cells can result in procoagulant phenotypes that augment local clot formation

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15
Q

What are the effects of antithrombotic properties of endothelium?

A

Antiplatelet effects
Anticoagulant effects
Fibrinolytic effects

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16
Q

Describe the antiplatelet properties of endothelium

A

Intact endothelium prevents platelets and coagulation factors from meeting the highly thrombogenic subendothelial ECM

  • –Non-active platelets do not adhere to the uninjured endothelium
  • –Activated platelets are inhibited from adhering to surrounding uninjured endothelium by endothelial prostacyclin and NO
  • –Endothelial cells also express ADPases (ADP is needed for platelet aggregation)
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17
Q

Describe the anticoagulant properties of endothelium

A

Heparin-like molecules from endothelium act indirectly with and inactivate several coagulation factors
Thrombomodulin from endothelium also acts indirectly, binding to thrombin and converting it from a procoagulant to an anticoagulant
Major source for tissue factor pathway inhibitor- a cell surface protein that complexes with and inhibits several proteins of the clotting cascade

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18
Q

What are the fibrinolytic effects of endothelium?

A

Endothelial cells synthesize tissue-type plasminogen activator

  • –Promotes fibrinolytic activity
  • –Clears fibrin deposits from endothelial surfaces
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19
Q

What are properties of platelets?

A

Play a central role in normal hemostasis
Smallest components of mammalian blood
They are not cells; membrane-bound smooth discs with no nucleus
Originate from bone marrow megakaryocytes as the end products of cytoplasmic and membrane protrusions
Their surface has several glycoprotein receptors called integrins that bind to exposed collagen

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20
Q

What do platelets do after vascular injury?

A

They encounter ECM constituents that are normally sequesterd beneath an intact endothelium

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21
Q

What are the 3 general reactions platelets undergo on contact with ECM?

A

Adhesion and shape change
Secretion (release reaction)
Aggregation

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22
Q

What are the 2 types of granules that platelets contain?

A

Alpha granules and dense bodies (delta granules)

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23
Q

Describe alpha granules

A

Express the adhesion molecule P-selectin

Contain fibrinogen, fibronectin, factor V, Factor VIII, vWF, PDGF, and TGF-β

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24
Q

Describe dense bodies

A

Contain ADP, ATP, ionized Ca, histamine, serotonin, epinephrine

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25
Q

What do activated plates have?

A

Spiny processes that protrude from cell membranes

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26
Q

Describe platelet activation

A

Activated platelets undergo change in shape
Secrete granule contents and express surface phospholipid complex
Aggregate and form reversible primary hemostatic plug
—Thrombin binds to surface receptors and binds to fibrinogen to integrins on surface
Contract irreversibly to form secondary hemostatic plug
—Thrombin converts fibrinogen to fibrin
—FIbrin “mortars” in place

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27
Q

What is thrombocytopenia?

A

Lack of platelets

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28
Q

Describe the coagulation cascade

A

Secondary hemostasis
A blood clot forms through the action of a cascade of proteolytic reactions
Third component of the hemostatic process
Major contributor to thrombosis
Cascade of enzymatic conversions that turn inactive proenzymes into activated enzymes
Culminates in the formation of thrombin
Thrombin then converts the soluble plasma protein fibrinogen precursor into the incoluble protein fibrin

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29
Q

What does each reaction in the coagulation cascade result from?

A

The assembly of a complex composed of an enzyme (activated coagulation factor), a substrate (proenzyme form of coagulation factor), a cofactor (reaction accelerator)

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30
Q

How are the components that result it in the coagulation cascade assembled?

A

Assembled on a phospholipid complex and held together by Ca ions

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31
Q

What is the intrinsic pathway initiated by?

A

Initiated in vitro by activation of the Hageman factor (factor XII)

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32
Q

What is the extrinsic pathway initiated by?

A

Tissue factor (a cellular lipoprotein exposed at site of tissue injury)

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33
Q

Besides coagulation, what does the activation of the clotting cascade also initiate?

A

The fibrinolytic cascade that limits the final size of the clot

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34
Q

What happens to plasminogen in fibrinolysis?

A

Plasminogen is in circulation and is cleaved to plasmin by tissue plasminogen activator

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35
Q

What does plasmin do?

A

Breaks down fibrin and interferes with its polymerization

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36
Q

What can fibrin split products act as?

A

Weak anticoagulants

37
Q

What is an important process in the regulation of hemostasis?

A

Fibrinolysis

38
Q

What is extravasation?

A

Escape of blood from blood vessels

39
Q

What is hemorrhage per rhexis?

A

Rapid flow of blood through breaks in vessel wall

40
Q

What is hemorrhage per diapedesis?

A

Oozing of blood through holes in the vessel wall

41
Q

What is a hematoma?

A

Enclosed accumulation of blood in a tissue (bulging, rounded area of hemorrhage)

42
Q

What is petechiae?

A

1-2 mm hemorrhage in the skin, mucous membranes, or serosal surface of an organ

43
Q

What is petechiae associated with?

A

Locally increased intravascular pressure, thrombocytopenia, defective platelet function, or clotting factor deficits

44
Q

What are ecchymoses?

A

2mm - 1cm SQ hemorrhage

45
Q

What is ecchymoses associated with?

A

Locally increased intravascular pressure, thrombocytopenia, defective platelet function, or clotting factor deficits, especially trauma

46
Q

What is purpura?

A

More than 1 cm hemorrhage in the skin, mucous membrane, or serosal surface

47
Q

What is purpura associated with?

A

Locally increased intravascular pressure, thrombocytopenia, defective platelet function, or clotting factor deficits
Also trauma, local vasculitis, increased vascular fragility

48
Q

What is paintbrush hemorrhage?

A

Hemorrhage along a natural plane

49
Q

What is suffusive hemorrhage?

A

Hemorrhage along a natural plane

50
Q

What is hemorrhage?

A

A large accumulation of blood in a blood cavity

51
Q

What is the fate of hemorrhage?

A

RBCs are phagocytized and enzymatically degraded by mφ
Porphyrin release from hemoglobin produces color
Clot

52
Q

What is the process of color changes with hemorrhage?

A

Hemoglobin (red-blue)
Bilirubin (blue-green)
Hemosiderin (gold-brown)

53
Q

What is a clot?

A

Contracts which causes separation of serum from coagulum

54
Q

Describe coagulum

A

Lysed and removed

Can become organized by connective tissue

55
Q

Describe serum

A

Reabsorbed and removed
Form seroma (large area of fluid in a tissue)
Seromas can be excellent growth media for bacteria

56
Q

What does the significance of a hemorrhage depend on?

A

Amount, rate, and location

57
Q

What happens if more than 1/3 of blood volume is lost quickly?

A

Hypovolemic shock which leads to exsanguination

58
Q

What happens if less than 1/3 of blood volume is lost quickly?

A

Possible compensation and survival

59
Q

What happens with slow blood loss?

A

Compensatory changes

60
Q

What happens if the location of the hemorrhage is in the brain, pericardium, or lungs?

A

Interference with organ normal function

61
Q

How much blood volume can be lost if blood is lost slowly?

A

As much as 1/2 of blood volume over weeks to months and the animal is able to compensate

62
Q

What occurs when an animal is trying to compensate for blood loss?

A

RR may increase to help oxygenate better
Hematopoiesis in bone marrow
Extramedullary hematopoiesis
Animals will limit exercise to keep O2 consumption low

63
Q

What is thrombosis?

A

Pathological formation of a clot with the cardiovascular system

64
Q

What may thrombosis lead to?

A

Interference with blood flow

—Turbulence and stasis

65
Q

What may thrombosis result in?

A

Infarction, passive congestion, or embolism (fragment of thrombus that breaks off and lodges somewhere distal

66
Q

What are causes of thrombosis?

A 
Change in blood flow (slow down)
Change in blood viscosity
Loss of vascular endothelial smoothness
Endothelial injury
Hyper reactive states of platelets
Proteinuria
67
Q

Describe what happens with endothelial injury

A

Endothelial cell damage and exposure of subendothelial collagen
Vasoconstriction follows and then platelet adhesion, aggregation, and activation of the clotting cascade
A platelet plug is formed which is often held together by polymerized fibrin

68
Q

What does turbulence of blood flow contribute to?

A

Arterial and cardiac thrombosis by causing endothelial injury and by forming countercurrent and local areas of stasis

69
Q

What is stasis?

A

A major factor in the development of venous thrombi

70
Q

What do stasis and turbulence do?

A

Disrupt laminar flow and bring platelets into contact with endothelium
Prevents dilution of clotting factors by fresh flowing blood
Retard inflow of clotting factor inhibitors

71
Q

Describe secondary blood hypercoagulability

A

Disseminated intravascular coagulation (DIC)
Disseminated cancers- release of procoagulant tumor products
Certain glomerular diseases (loss of anti-thrombin III)

72
Q

What is a postmortem (PM) clot?

A

When an animal dies, blood clots in vessels and forms a mold in the shape of the vessel

73
Q

Describe what a PM clot is like

A

Shiny and gelatinous
Fills entire chamber
Removes easily
Usually red, but may have yellow plasma near the surface and be red at the base

74
Q

Describe thrombus

A

Rough surface and attached to vessel wall
Difficult to remove
Usually pale color due to protein and fibrin
Early thrombi may be red

75
Q

What is a current jelly clot?

A

Homogenous red

76
Q

What is a chicken fat clot?

A

Homogenous yellow (plasma)

77
Q

What is the microscopic appearance of thrombus?

A

Attached to wall

Lamination- alternating pale layers of platelets admixed with some fibrin and darker layers containing more RBCs

78
Q

Where does a venous thrombi\us usually occur?

A

At sites with blood stasis, extending in the direction of blood flow

79
Q

Where does an arterial thrombus begin?

A

At site of endothelial injury or turbulence

80
Q

Where is a vegetative thrombus most common? Where else can one occur?

A 
On mitral (left AV) valve and it tends to travel in general circulation (kidneys)
It can also occur on semilunar and R AV valves and it tends to travel to lungs or general circulation
81
Q

What is verminous thrombus caused by?

A

Parasites

82
Q

What is a mural thrombus?

A

Attached to endocardium

83
Q

What is a septic thrombus?

A

Bacterial colonization of a thrombus; causes or is a result if bacteremia

84
Q

What are the outcomes of thrombosis?

A

Propagation
Embolization
Dissolution/resolution
Organization and recanalization

85
Q

What is propagation?

A

Thrombus may accumulate more platelets and fibrin leading to vessel obstruction

86
Q

What is embolization?

A

Thrombus may dislodge and travel to other sites, forming thromboemboli

87
Q

What is dissolution/resolution?

A

Thrombi may be removed by fibrinolytic activity

88
Q

What may organization and recanalization induce?

A

Inflammation and fibrosis and eventually become recanalized (re-established blood flow or be incorporated into a thickened vascular wall)

89
Q

What happens with recanalization?

A

Thrombus converted to fibrous connect tissue

May contract over time

Pathology (16 decks)

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