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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
What do activated plates have?
Spiny processes that protrude from cell membranes
26
Describe platelet activation
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
27
What is thrombocytopenia?
Lack of platelets
28
Describe the coagulation cascade
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
29
What does each reaction in the coagulation cascade result from?
The assembly of a complex composed of an enzyme (activated coagulation factor), a substrate (proenzyme form of coagulation factor), a cofactor (reaction accelerator)
30
How are the components that result it in the coagulation cascade assembled?
Assembled on a phospholipid complex and held together by Ca ions
31
What is the intrinsic pathway initiated by?
Initiated in vitro by activation of the Hageman factor (factor XII)
32
What is the extrinsic pathway initiated by?
Tissue factor (a cellular lipoprotein exposed at site of tissue injury)
33
Besides coagulation, what does the activation of the clotting cascade also initiate?
The fibrinolytic cascade that limits the final size of the clot
34
What happens to plasminogen in fibrinolysis?
Plasminogen is in circulation and is cleaved to plasmin by tissue plasminogen activator
35
What does plasmin do?
Breaks down fibrin and interferes with its polymerization
36
What can fibrin split products act as?
Weak anticoagulants
37
What is an important process in the regulation of hemostasis?
Fibrinolysis
38
What is extravasation?
Escape of blood from blood vessels
39
What is hemorrhage per rhexis?
Rapid flow of blood through breaks in vessel wall
40
What is hemorrhage per diapedesis?
Oozing of blood through holes in the vessel wall
41
What is a hematoma?
Enclosed accumulation of blood in a tissue (bulging, rounded area of hemorrhage)
42
What is petechiae?
1-2 mm hemorrhage in the skin, mucous membranes, or serosal surface of an organ
43
What is petechiae associated with?
Locally increased intravascular pressure, thrombocytopenia, defective platelet function, or clotting factor deficits
44
What are ecchymoses?
2mm - 1cm SQ hemorrhage
45
What is ecchymoses associated with?
Locally increased intravascular pressure, thrombocytopenia, defective platelet function, or clotting factor deficits, especially trauma
46
What is purpura?
More than 1 cm hemorrhage in the skin, mucous membrane, or serosal surface
47
What is purpura associated with?
Locally increased intravascular pressure, thrombocytopenia, defective platelet function, or clotting factor deficits Also trauma, local vasculitis, increased vascular fragility
48
What is paintbrush hemorrhage?
Hemorrhage along a natural plane
49
What is suffusive hemorrhage?
Hemorrhage along a natural plane
50
What is hemorrhage?
A large accumulation of blood in a blood cavity
51
What is the fate of hemorrhage?
RBCs are phagocytized and enzymatically degraded by mφ Porphyrin release from hemoglobin produces color Clot
52
What is the process of color changes with hemorrhage?
Hemoglobin (red-blue) Bilirubin (blue-green) Hemosiderin (gold-brown)
53
What is a clot?
Contracts which causes separation of serum from coagulum
54
Describe coagulum
Lysed and removed | Can become organized by connective tissue
55
Describe serum
Reabsorbed and removed Form seroma (large area of fluid in a tissue) Seromas can be excellent growth media for bacteria
56
What does the significance of a hemorrhage depend on?
Amount, rate, and location
57
What happens if more than 1/3 of blood volume is lost quickly?
Hypovolemic shock which leads to exsanguination
58
What happens if less than 1/3 of blood volume is lost quickly?
Possible compensation and survival
59
What happens with slow blood loss?
Compensatory changes
60
What happens if the location of the hemorrhage is in the brain, pericardium, or lungs?
Interference with organ normal function
61
How much blood volume can be lost if blood is lost slowly?
As much as 1/2 of blood volume over weeks to months and the animal is able to compensate
62
What occurs when an animal is trying to compensate for blood loss?
RR may increase to help oxygenate better Hematopoiesis in bone marrow Extramedullary hematopoiesis Animals will limit exercise to keep O2 consumption low
63
What is thrombosis?
Pathological formation of a clot with the cardiovascular system
64
What may thrombosis lead to?
Interference with blood flow | ---Turbulence and stasis
65
What may thrombosis result in?
Infarction, passive congestion, or embolism (fragment of thrombus that breaks off and lodges somewhere distal
66
What are causes of thrombosis?
``` Change in blood flow (slow down) Change in blood viscosity Loss of vascular endothelial smoothness Endothelial injury Hyper reactive states of platelets Proteinuria ```
67
Describe what happens with endothelial injury
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
What does turbulence of blood flow contribute to?
Arterial and cardiac thrombosis by causing endothelial injury and by forming countercurrent and local areas of stasis
69
What is stasis?
A major factor in the development of venous thrombi
70
What do stasis and turbulence do?
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
Describe secondary blood hypercoagulability
Disseminated intravascular coagulation (DIC) Disseminated cancers- release of procoagulant tumor products Certain glomerular diseases (loss of anti-thrombin III)
72
What is a postmortem (PM) clot?
When an animal dies, blood clots in vessels and forms a mold in the shape of the vessel
73
Describe what a PM clot is like
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
Describe thrombus
Rough surface and attached to vessel wall Difficult to remove Usually pale color due to protein and fibrin Early thrombi may be red
75
What is a current jelly clot?
Homogenous red
76
What is a chicken fat clot?
Homogenous yellow (plasma)
77
What is the microscopic appearance of thrombus?
Attached to wall | Lamination- alternating pale layers of platelets admixed with some fibrin and darker layers containing more RBCs
78
Where does a venous thrombi\us usually occur?
At sites with blood stasis, extending in the direction of blood flow
79
Where does an arterial thrombus begin?
At site of endothelial injury or turbulence
80
Where is a vegetative thrombus most common? Where else can one occur?
``` 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
What is verminous thrombus caused by?
Parasites
82
What is a mural thrombus?
Attached to endocardium
83
What is a septic thrombus?
Bacterial colonization of a thrombus; causes or is a result if bacteremia
84
What are the outcomes of thrombosis?
Propagation Embolization Dissolution/resolution Organization and recanalization
85
What is propagation?
Thrombus may accumulate more platelets and fibrin leading to vessel obstruction
86
What is embolization?
Thrombus may dislodge and travel to other sites, forming thromboemboli
87
What is dissolution/resolution?
Thrombi may be removed by fibrinolytic activity
88
What may organization and recanalization induce?
Inflammation and fibrosis and eventually become recanalized (re-established blood flow or be incorporated into a thickened vascular wall)
89
What happens with recanalization?
Thrombus converted to fibrous connect tissue | May contract over time

Pathology (16 decks)

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