Hemodynamic Disorders 2

Front 1

What is hemostasis?

Back 1

A normal physiologic process maintaining blood in a fluid, clot-free state in normal vessels while inducing a rapid and localized hemostatic plug at sites of vascular injury.

Front 2

Hemostasis relies on what 3 components?

Back 2

1. Vascular endothelium

2. Platelets

3. Coagulation cascade

Front 3

What is a thrombus?

Back 3

A permanent hemostatic plug composed of platelets, fibrin (from the liver as fibrinogen), and trapped blood cells

Front 4

What is thrombosis? What are the 3 primary inciting causes?

Back 4

Inappropriate activation of blood clotting in an uninjured vessel or after a minor injury.

Influences = Virchow's Triad:

1. Endothelial injury (most important) - exposure of endothelial cell contents promotes clotting

2. Abnormal blood flow (2nd most important)

3. Hypercoaguability

Front 5

Some causes of endothelial injury

Back 5

- Trauma (bad IV)

- Vasculitis (infection, immune mediated)

- Metabolic (vit E deficiency)

- Neoplasia

- Toxins (bacterial endotoxin)

Front 6

2 Types of Abnormal blood flow

Back 6

Stasis and turbulence. Both:

- Disrupt laminar flow = platelets contact endothelium

- Prevent activated clotting factor dilution by fresh blood

- Slow inflow of clot factor inhibitors, therefore allowing thrombi buildup

- Promote endothelial cell activation

Note: stasis causes thombosis more often in veins and heart; turbulence more often in arteries

Front 7

What is hypercoagulability?

Back 7

- Any alteration of the coagulation pathway that predisposes thrombosis

- Ie: inflammation

Front 8

Characteristics of arterial thrombi

Back 8

- Non-occlusive in the heart and aorta, may be occlusive in smaller arteries

- Firmly attached at origin with downstream tail

- Form bc of endothelial damage and accumulate platelets and fibrin, but not RBCs

- Pale gray red

- Laminated: Lines of Zahn (due to alternating layers of pale platelets/fibrin and RBCs)

Front 9

Characteristics of venous thrombi

Back 9

- Generally occlusive (slower blood flow)

- Less firmly attached with upstream tails

- Red soft gelatinous

- RBCs encorporated bc of slower blood flow

- Looser fibrin/platelet net

- Tend to form when stasis

Front 10

How can cardiac valvular thrombi form?

Back 10

1. Septic - form vegetations on heart valves composed of thombi and bacteria/fungi; ususally associated with systemic infection

2. Sterile - when in a hypercoagulative state

Front 11

2 reasons why thrombi are significant

Back 11

1. Obstruction of vessels

2. Source of thromboembolism

Front 12

What is DIC?

Back 12

Disseminated Intravascular Coagulation: a complication of diffuse activation of coagulation in the microcirculation. Can be caused by many things (ie sepsis, cancer).

Leads to diffuse circulatory insufficiency, especially in the brain, heart, lungs, kidney.

Rapid consumption of platelets/clotting factors due to formation of so many thrombi. This causes consumptive coagulopathy and widespread hemorrhage.

Front 13

What does DIC look like?

Back 13

Hemorrhage! But you can't really tell it was DIC just by looking. (Can diagnose histologically.)

Front 14

4 potential fates of a thrombus

Back 14

1. Propagation causing vessel obstruction

2. Embolization to other sites

3. Dissolution by fibrinolysis

4. Organization and recanalization (endothelial cells and smooth muscle cells grow and create a channel through the thrombus, re-establishing vascular flow)

Front 15

What is an embolism?

Back 15

The passage of any intravascular solid, liquid or gaseous mass by blood to a site distant from it origin. May lodge into a smaller vessel and create a vascular occlusion that leads to ischemic necrosis of tissue (infarction).

IE: 99% are thromboembolism - fragments of thrombi, also can be fat from long bone fracture, neoplasm, bacteria from abscesses, heartworms/flukes, fibrocartilage from degenerate intervertebral discs

Front 16

Where do cardiac thromboemboli usually lodge?

Back 16

Usually at the aortic termination. IE: feline aortic thromboembolism ("saddle thrombus")

Front 17

Where do arterial and venous thromboemboli usually lodge?

Back 17

Arterial: The nearest bifurcation (IE: intestinal infarction from cranial mesenteric arteritis in horses)

Venous: Usually lodge in the lungs (pulmonary infarction/right sided heart failure)

Front 18

What is infarction?

Back 18

Ischemic necrosis of an area caused by obstruction of its arterial supply. Almost all infarction is due to vascular occlusion by thrombosis or thromboembolism. (Other causes are vascular compression or torsion.) Infarcted areas undergo coagulative necrosism (except the brain = liquefactive necrosis). Repair is usually through scar formation.

Front 19

What factors determine that severity of arterial or venous infarction?

Back 19

- Tissue or organ supplied (brain most susceptible)

- Amount of collateral circulation

- Speed of onset (rapid more serious)

Front 20

How does necrosis differ from arterial and venous infarction?

Back 20

Arterial: Rapid ischemic necrosis

Venous: Slowly developing ischemic necrosis (also edema and congestion)

Front 21

What is shock?

Back 21

Systemic hypofusion resulting from either reduced cardiac output or reduced effective circulating blood volume. Not a primary disease.

Front 22

3 categories of shock

Back 22

1. Cardiogenic shock: failure of heart to adequately pump blood

2. Hypovolemic shock: reduced circulating blood volume

3. Blood maldistribution: widespread peripheral vasodilation resulting in more vessel volume than blood to fill it