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Pathology > Hemostasis, Thrombosis, Hemorrhage > Flashcards

Hemostasis, Thrombosis, Hemorrhage Flashcards

1
Q

Hemostasis

A

Interaction of endothelium, platelets, and coagulation cascade

  • maintain blood in a fluid, clot-free state
  • induce rapid and localized “hemostatic plug”
  • anticoagulant activities occur to limit extend of the plug (fibrinolysis)
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2
Q

Pathogenic hemostasis

A

Thromosis

  • inappropriate activation of normal hemostatic processes
  • formation of a clot in uninjured vasculature
  • thrombotic occlusion of a vessel after relatively minor injury
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3
Q

Sequence of events with vascular injury

A
  • vasoconstriction
  • primary hemostasis
  • secondary hemostasis
  • reorganization and formation of a permanent plug
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4
Q

Vasoconstriction

A

Transient arteriolar vasoconstriction after initial endothelial injury that exposes collagen of the subendothelial matric (ECM)

  • occurs due to local nerve reflex and release of endothelin by endothelial cells
  • helps limit escape of RBCs and proteins from damaged areas
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5
Q

Primary hemostasis

A

Platelets adhere to exposed ECM via von Willebrand factor –> platelets activate, change shape –> release of secretory granules –> form primary hemostatic plug

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6
Q

Secretory granules

A

ADP and thromboxane A2

- cause vasoconstriction and promote further platelet aggregation

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7
Q

vWF

A

Released immediately from adjacent endothelial cells

- aids platelet binding to collagen (procoagulant)

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8
Q

Secondary hemostasis

A

Local activation of the coagulation cascade
- tissue factor (thromboplastin) secreted by adjacent endothelial cells
- thromboplastin initiates clotting cascade
= fibrin polymerization and cementing platelets into definitive secondary plug

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9
Q

Thrombin

A

Makes fibrin

  • made from fibrinogen (always found in blood)
  • thrombin puts fibrinogen together = fibrin, nonsoluble, cements everything together
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10
Q

Counter-regulatory mechanisms

A

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

  • tissue type plasminogen activator (t-PA) = fibrinolytic
  • thrombomodulin: interferes with the clotting cascade
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11
Q

Thrombosis

A

Formation of a blood clot (hemostatic plug) due to either inappropriate activation of normal hemostasis or formation of a clot in a vessel after injury
- due to other abnormal process that block a vessel

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12
Q

Fibrinolysis

A

Process of limiting the hemostatic process at the site of injury
- release of tissue plasminogen activator (t-PA) and thrombomodulin by adjacent endothelium

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13
Q

What 2 properties does endothelium have?

A
  • antithrombotic

- prothrombotic

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14
Q

Antithrombotic properties

A

Acts as a barrier between blood and subendothelial collagen

  • block platelet aggregation (antiplatelet)
  • interfere with coagulation cascade by inactivating thrombin and factors Xa and IXa (anticoagulant)
  • actively lyse clots (fibrinolytic)
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15
Q

Prothrombotic properties

A

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

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16
Q

Normal endothelium

A

Prevents platelets and coagulation factors from meeting highly thrombogenic subendothelial ECM
- nonactive platelets do not adhere to uninjured endothelium

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17
Q

Antiplatelet mechanisms of endothelium

A

Activated platelets are inhibited from adhering to surrounding uninjured endothelium by endothelial prostacyclin (PGI2) and NO –> potent vasodilators and inhibitors of platelet aggregation
- express ADPases –> ADP needed for platelet aggregation

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18
Q

Anticoagulant mechanisms of endothelium

A

Heparin-like molecules (cofactors) from endothelium act indirectly with and inactivate several coagulation factors (thrombin, IXa, Xa, XIa, XIIa)

  • thrombomodulin acts indirectly –> binds to thrombin and converts it from procoagulant to anticoagulant
  • source for tissue factor pathway inhibitor: cell surface protein that complexes with and inhibits several proteins of the clotting cascade (VIIa and Xa)
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19
Q

Fibrinolytic effects of endothelium

A

Endothelial cells synthesize tissue-type plasminogen activator (t-PA)

  • promotes fibrinolytic activity
  • clears fibrin deposits from endothelial surfaces
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20
Q

Properties of platelets

A

Central role in normal hemostasis

  • smallest components of mammalian blood (2-4 um)
  • are NOT cells! membrane bound, no nucleus when unactivated
  • originate from bone marrow megakaryocytes
  • glycoprotein receptors (integrins) bind to exposed collagen –> vWF bridges integrins and exposed collagen (adhesion)
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21
Q

What do platelets come in contact with after vascular injury?

A
  • collagen
  • proteoglycans
  • fibronectin
  • other adhesive glycoproteins
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22
Q

What 3 reactions do platelets undergo after contact with ECM?

A
  • adhesion and shape change
  • secretion (release reaction)
  • aggregation
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23
Q

What 2 granules do platelets contain?

A

Alpha granules and dense bodies

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24
Q

Alpha granules

A

Express adhesion molecule P-selectin

- contain fibrinogen, fibronectin, factor V, VIII, vWF, PDGF, TGF-B

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25
Q

Dense bodies

A

Delta granules

- contain ADP, ATP, ionized Ca, histamine, serotonin, epinephrine

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26
Q

Properties of activated platelets

A

Activated platelets have spiny processes that protrude from cell membranes

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27
Q

Platelet activation process

A

Undergo change in shape –> secrete granule contents, express surface phospholipid complex –> aggregate (thromboxane A2) = reversible primary hemostatic plug via thrombin binding to surface receptors and binding 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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28
Q

Thrombocytopenia

A

Lack of platelets

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29
Q

Secondary hemostasis

A 
Blood clot (thrombus) forms thru the action of a cascade of proteolytic reactions involving 20 different substances
- most are liver-synthesized plasma glycoproteins
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30
Q

3rd step of hemostatic process

A

Cascade of enzymatic conversions that turn inactive proenzymes into activated enzymes

  • culminates in formation of thrombin
  • thrombin converts fibrinogen (soluble plasma protein) precursor into insoluble protein fibrin
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31
Q

Each reaction in the pathway results from the assembly of a complex composed of ___

A
  • an enzyme: activated coagulation factor
  • a substrate: proenzyme from of coagulation factor
  • a cofactor: reaction accelerator
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32
Q

Components of coagulator cascade are assembled on _______

A

A phospholipid complex, held together by Ca ions

- clotting remains localized to sites where assembly can occur (on surface of activated platelets or endothelium)

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33
Q

EDTA

A

Binds all Ca in the blood

- enzymes in clotting cascade cannot stick together due to wrong charges (anticoagulant)

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34
Q

What are the clotting factors that require vitamin K as a cofactor?

A

10, 9, 7, 2

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35
Q

What 2 diagnostic tests are used to test the clotting cascade?

A
  • PT: extrinsic pathway

- PTT: intrinsic pathway

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36
Q

Intrinsic pathway

A

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

37
Q

Extrinsic pathway

A

Initiated by tissue factor

- cellular lipoprotein exposed at site of tissue injury

38
Q

FDP

A

Fibrin degradation products

  • diagnoses DIC, elevated levels measured as fibirn d-dimers
  • fibrin split products that act as weak anticoagulants
  • degrades fibrinogen
  • any free plasmin in circulation is bound and neutralized by a-2-antiplasmin
39
Q

DIC

A

Disseminated intravascular coagulopathy

  • widespread clot formation
  • seen clinically as a bleeding animal because all clot factors are used up
  • diagnostically look for large numbers of FDP and no platelets
40
Q

Plasminogen

A

Found in circulation, cleaved to plasmin by tissue plasminogen activator (t-PA)

  • tissue type-PA is synthesized by endothelial cells –> active when attached to fibrin meshwork –> activity blocked by PA inhibitor (PAI)
  • plasmin breaks down fibrin and interferes with polymerization
41
Q

______ is an important process in the regulation of hemostasis

A

Fibrinolysis

- FDP

42
Q

Extravasation

A

Escape of blood from blood vessels

- always antemortem!!

43
Q

Does hemorrhage occur after death?

A

NO

44
Q

Hemorrhage per rhexis

A

Rapid flow of blood through breaks in vessel wall

- due to cut, rupture, etc

45
Q

Hemorrhage per diapedesis

A

Oozing of blood thru holes in vessel wall

  • vessel is intact morphologically, but RBCs are still leaking out
  • due to severe passive congestion, shock, etc
46
Q

Hematoma

A

Enclosed accumulation of blood in a tissue

  • bulging, rounded area of hemorrhage
  • can be insignificant (bruise) or cause death (intracranial hematoma)
47
Q

Petechiae

A

1-2 mm hemorrhage in the skin, mucous membranes, or serosal surface of organ
- associated with locally increased intravascular pressure, thrombocytopenia, defective platelet function, clotting factor deficits

48
Q

Ecchymoses

A

2 mm - 1 cm SQ hemorrhage

- associated with same processes as petechiae, especially in trauma

49
Q

Purpura

A

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

  • associated with same as petechiation
  • trauma, local vasculitis, increased vascular fragility
  • petechia/ecchymoses become overlapped and get close together forming purpura
50
Q

Suffusive

A

Hemorrhage along a natural plane (area of least resistance)

- paintbrush hemorrhage

51
Q

Hemorrhage

A

Large accumulation of blood in a body cavity

  • hemothorax: blood in thorax
  • hemopericardium: pericardial sac
  • hemoperitoneum: peritoneal cavity
  • hemarthrosis: joint or synovial cavity
52
Q

Fate of hemorrhage

A

RBCs are phagocytized and enzymatically degraded

- porphyrin release from hemoglobin produces color

53
Q

What are the 3 colors of hemorrhage?

A
  • hemoglobin: red/blue
  • bilirubin: blue/green
  • hemosiderin: gold/brown
54
Q

Clot

A

Contracts which causes separation of serum from coagulum

55
Q

Coagulum

A

Lysed and removed, if small

- organized by connective tissue

56
Q

Serum

A

Resorbed and removed

  • form seroma: large area of fluid in a tissue
  • seromas are great growth media for bacteria
57
Q

Rate and amount

A
  • > 1/3 blood volume lost quickly: hypovolemic shock –> exsanguination
  • <1/3 blood volume lost quickly: compensation and survival
  • slow blood loss: compensatory changes
58
Q

Hypovolemic shock

A

Hypoxic conditions occur due to loss of blood
- all capillary beds dilate to get blood = dilution of blood –> hypovolemic shock, blood is sequestered to capillary beds leading to widespread shock

59
Q

What 3 areas will cause death from hemorrhage, even if blood loss is minimal?

A

Brain, pericardium (cardiac tamponade), lungs

60
Q

How much blood can be lost for the animal to survive and compensate?

A

If lost slowly, an animal can lose as much as 1/2 blood volume over weeks/months and still be able to compensate

61
Q

Methods of compensation

A
  • RR increases to help oxygenate
  • hematopoiesis in bone marrow
  • extramedullary hematopoiesis
  • limit exercise to keep O2 consumption low
  • may die acutely if over exerted
62
Q

Hematuria

A

Bloody urine

63
Q

What are the 3 conditions that create thrombosis?

A
  • endothelial injury
  • abnormal blood flow
  • hypercoagulability
64
Q

Thrombosis

A

Pathological formation of a clot (thrombus) within the cardiovascular system

  • leads to interference with blood flow (turbulence, stasis)
  • result in infarction, passive congestion, or embolism
65
Q

Infarction

A

Blockage of arterial supply due to thrombus

- whatever is after the blockage will die

66
Q

Embolism

A

Fragment of thrombus that breaks off and lodges somewhere distal

67
Q

Causes of thrombosis

A
  • change in blood flow (slow down)
  • change in blood viscosity
  • loss of vascular endothelial smoothness
  • endothelial injury
  • hyperactive states of platelets (parturition, sepsis, surgery, massive trauma)
  • proteinuria (renal disease)
68
Q

Endothelial injury

A

Endothelial cell damage and exposure of subendothelial collagen

  • vasoconstriction follows –> platelet aggregation –> activation of clotting cascade
  • platelet plug is formed, held together by polymerized fibrin
69
Q

Turbulent blood flow

A

arterial and cardiac thrombosis via endothelial injury and countercurrent/local areas of stasis

70
Q

Stasis

A

Major factor in venous thrombi

71
Q

____ and _____ disrupt laminar flow and bring platelets into contact with endothelium

A

Stasis and turbulence

  • prevents dilution of clotting factors by fresh flowing blood
  • retards inflow of clotting factor inhibitors
72
Q

Blood hypercoagulability

A

Least common cause of thrombosis

  • humans: any alteration in coagulation pathways that predisposes to thrombosis
  • commonly a secondary cause in all species
73
Q

Primary hypercoagulability

A

Mutation in factor V gene

- affects 2-15% of caucasian population as recurrent deep venous thrombosis

74
Q

Secondary hypercoagulability

A

Acquired

  • DIC
  • disseminated cancers: release of procoagulant tumor products
  • certain glomerular diseases (loss of anti-thrombin III)
75
Q

Post-mortum clot

A

After death, blood clots in vessels and forms a mold in the shape of the vessel (or heart chamber)

  • shiny, gelatinous
  • fills entire chamber
  • removes easily
  • red, may be yellow plasma near surface and red at base
76
Q

Thrombus characteristics

A
  • rough surface and attached to vessel wall
  • difficult to remove
  • pale color due to protein and fibrin
  • early thrombi may be red
77
Q

Microscopic thrombus

A
  • attached to wall

- laminations: alternating pale layers of platelets admixed with fibrin and darker layers containing more RBCs

78
Q

Venous thrombus

A

Occurs at sites with blood stasis, extending in the direction of blood flow (toward the heart)

79
Q

Arterial thrombus

A

Begin at site of endothelial injury or turbulence (ex: vessel bifurcation)

  • grow in retrograde direction from point of attachment
  • ex: saddle thrombus in cat
80
Q

Vegetative thrombus

A

Most common on mitral (left AV) valve

  • tend to travel in general circulation (kidneys)
  • occur on semilunar and right AV valves –> travel to lungs or general circulation
81
Q

Verminous thrombus

A

Caused by parasites

82
Q

Mural thrombus

A

Attached to the endocardium

83
Q

Septic thrombus

A

Bacterial colonization of a thrombus

- causes or is a result of bacteremia

84
Q

What are the 4 outcomes of thrombosis?

A
  • propagation
  • embolization
  • dissolution/resolution
  • organization and recanalization
85
Q

Propagation

A

Thrombus may accumulate more platelets and fibrin leading to vessel obstruction

86
Q

Embolization

A

Thrombus may dislodge and travel to other sites, forming thromboemboli

87
Q

Dissolution/resolution

A

Thrombi may be removed by fibrinolytic activity

- drugs available for this

88
Q

Organization and recanalization

A

May induce inflammation and fibrosis (organization), will eventually become recanalized
- possible formation of collateral circulation

89
Q

Recanalization

A

Re-establish blood flow or be incorporated into a thickened vascular wall

  • thrombus converted to fibrous connective tissue (scar tissue)
  • may contract over time

Pathology (19 decks)

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