Clinical Pathology Exam #2 (Set 2 Of 4)

Front 1

What is Hemostatic Mechanism?

Back 1

-Complex series of biochemical & physiological events that are activated to stop the loss of blood when vessels are damaged.
-Prevents minor bumps and bruises of daily life from being fatal!

Front 2

Hemostasis combination of 3 separate mechanisms are:

Back 2

1. Response of blood vessels to injury.
2. Platelet activation
3. Stimulation of clotting cascade.

Front 3

Name 2 resons why vessels constrict:

Back 3

Caused by:
1. Local muscle fiber stimulation.
2. Reflex of the sympathetic nervous system.

Front 4

What is Vascular Response?

Back 4

When artery/arteriole is damaged, the varying amounts of smooth muscles within vessels contract almost immediately.

Front 5

What is the life span of Platelets?

Back 5

5-10 days

Front 6

Platelets are only exposed to what 3 areas?

Back 6

1. Endothelium
2. Endocardium
3. Sinusoids of liver

Front 7

Platelets release what 3 products as they aggregate?
What does each do?

Back 7

1. Adenosine diphosphate (ADP) = stimulates rapid aggregation & adherence
2. Histamine & Serotonin = maintains vasoconstriction after trauma and in small vessels may control hemorrhage.
3. Phosopholipid (PLatelet Factor 3 or PF3) = important in activation of coagulation cascade and clot retraction.

Front 8

Blood clots gradually shrink over a period of time releasing trapped serum called what?

Back 8

Syneresis

(process is to decrease defect in blood vessel)

Front 9

What is the substance from platelets responsible for clot retraction?

Back 9

Thrombosthenin

Front 10

What is the Coagulation Mechanism Response?

Back 10

Result of numerous inactivated soluable proteins and other substances present in the blood stream become activated changing the physical form of blood in the region from a liquid to a semisolid substance. (these proteins & substances are: Clotting Factors)

Front 11

Clot formation is activated by one of 2 pathways. What are the 2 pathways?

Back 11

1. Intrinsic Pathway (within)
2. Extrinsic Pathway (outside)

(both effect of "Common Pathway" converting soluble fibrinogen into an insoluble fibrin strands which form a meshwork and attaches to a platelet plug)

Front 12

What is the Intrinsic Pathway? Give an example

Back 12

-Consist of factors present WITHIN the blood steam.
-These are activated *without* tissue contact.
EX: indwelling catheter

Front 13

What is the Extrinsic Pathway? Give an example

Back 13

-Activated by contact w/ cells and tissue fluid OUTSIDE the vessel
-Tissue thromboplastin (factorIII) important in this pathway.

Front 14

How long does it take for clot formation?

Back 14

Takes place in as little as 15 seconds and (if not physically disrupted) completed in 5 minutes.

Front 15

What is the job of Enzymes in clot formation?

Back 15

-They are present to destroy each clotting factor activated.
-Prevents the coagulation from spreading throughout the vascular system.

Front 16

What does Fibrinolysin do?

Back 16

Its another enzyme that is present to begin degrading the clot as it is formed.

Front 17

What is Clot Formation?

Back 17

A dynamic balance between stimulation for formation and removal.
(after damaged vessel is repaired, the clot will be removed)

Front 18

Define Thrombus:

Back 18

A clot within a vessel if it stays at the formation site.

Front 19

Define Embolus:

Back 19

If a clot detaches into the blood stream it becomes an (Thromboembolus)
**Thrombi & Emboli are common causes of heart attacks and strokes in humans and animals.

Front 20

Define Eschar:

Back 20

A blood clot that forms on the skin surface and dries. (SCAB)

Front 21

Define Hemostatic Defects:

Back 21

Leads to excessive loss of blood and are potentially fatal.

Front 22

What causes Hemostatic Defects?

Back 22

**May be either HEREDITARY or AQUIRED defects in coagulation proteins, platelets, or the vasculature.

Front 23

Clinical signs of Hemostatic Defects:

Back 23

-Most bleeding disorders in veterinary species are secondary to a disease process.*
Clinical Signs: spotting, nosebleeds, melena, prolonged bleeding @ injection or incision sites

Front 24

HEMOPHILIA A
(deficiency of Factor VIII)

Back 24

HEMOPHILIA A (deficiency of factor VIII): an abnormality in the intrinsic system. (Prothrombin consumption is deficient)

Front 25

The following are Hereditary Coagulation Defects:

Back 25

5 are listed

Front 26

HEMOPHILIA B
(deficiency of Factor IX)

Back 26

HEMOPHILIA B (deficiency of Factor IX): AKA: CHRISTMAS DISEASE
-Recessive trait, seen less freq. than hemophilia A

Front 27

FACTOR VII deficiency

Back 27

-Affected animals usually do NOT have serious bleeding tendencies
-*Note: Excessive bleeding can occur during surgeries!

Front 28

FACTOR XI deficiency

Back 28

-Dogs & Cattle
-Characterized by minor bleeding episodes
-Protracted bleeding in association w/ surgery

Front 29

VON WILLEBRAND'S Disease

Back 29

**MOST COMMON HEMOSTATIC DEFECT!
-Not a clotting factor defect
-Lack of protein available for proteins to attach to endothelium preventing/slowing clot formation
-Clinical Signs: Excessive bleeding following minor surgery, nosebleeds, gingival, penile, vaginal bleeding, GI bleeding w/ or w/o diarrhea, hematuria, prolonged estral/postpartum bleeding and umbilical cord @ birth, hematoma, lameness

Front 30

Acquired Coagulation Defects

Back 30

**Most often encountered by veterinarians