Path-Thrombosis, Emboli, Infarct, Shock

Front 1

What is a Thrombosis?

Back 1

An organized clot caused by damage to endothelial lining of vessels

Front 2

Factors in Thrombogenesis?

Back 2

*Endothelial injury - Promotes platelet adhesion & activates clotting factors

*Change in blood flow - platelets in contact with endothelium for longer periods of time

*Hypercoagulative state (ie bed rest, cancer, estrogens)

Front 3

Steps of Thrombogenesis:
What happens during Primary Hemostatis?

Back 3

1) Platelet adhesion (due to exposed breaks in endothilium, stagnant blood, etc)
2) Platelets change shape
3) Granule release (ADP, TXA2) from platelets
4) Recruitment of platelets
5) Aggregation to form primary hemostatic plug - loose clot

Front 4

Steps of Thrombogenesis: What happens during Secondary Hemostatis?

Back 4

1) Tissue Factor (from exposed endothelium) triggering intrinsic coagulation cascade
2) Phospholipid complex expression induced by platelets triggers extrinic coag. cascade
3) Thrombin activation (from coag. cascade)
4) Fibrin polymerization to form secondary clot

Front 5

What is Vichow’s triad in thrombosis?

Back 5

Causes of thrombogenesis: Endothelial injury, hypercoagulability, and abnormal blood flow

Front 6

What are the characteristics of arterial thrombi?

Back 6

Composed primarily of platelets and fibrine with mixed layers of RBS's - "lines of Zahn" (BE ABLE TO RECOGNIZE SLIDE).
**White or Conglutination thrombi

Front 7

What causes vasoconstriction in a endothelial injury and why is this important?

Back 7

Endothelin is released by cells surrounding the damages endothelial cells. Important to reduced blood flow the the local area to diminish loss

Front 8

What is an example of a drug (brand name) that prevents platelet clotting to prevent thrombogenesis?

Back 8

Plavix

Front 9

What is the role of Nitrous Oxide (NO)?

Back 9

Prevent coagulation

Front 10

What is von Willebrand's factor?

Back 10

A coagulation factor - without it, patients will have increased bleeding

Front 11

Describe a venous thrombi?

Back 11

Starts on endothelium & swells the vein
Appears gelatinous yet friable (easily crumbled)
"Statis or red coagulation thrombi"
Is Trosseu's sign - related to cancer

Front 12

How do you tell difference between post-mortem and pre-mortem clots?

Back 12

Post-mortem: rubbery, gelationous & forms "cast" of the vessel, looks like "currant jelly" or chicken fat if clear

Front 13

What is a mural clot?

Back 13

Thrombus on the wall that does not occule lumen of vessel, usually in heart(common in MI)

Front 14

What is an occlusive clot?
Where found usually?

Back 14

Clots that occludes lumen.
In order of frequency for each:
Arterial: Coronary, cerebral, iliac, femoral
Venous: deep calf, femoral, popliteal, iliac

Front 15

Clots on the heart valves are called?

Back 15

Vegetations

Front 16

DIC stands for?

Back 16

Disseminated Intravascular Coagulation - microcirulatory thromboses

Front 17

Hypercoagulable states - that is meant by primary and secondar causes?

Back 17

Primary causes of hypercoagulation are GENETIC causes.
Secondary are acquired (ie CA, MI, bed rest, tissue damage, Rx, etc)

Front 18

What is an embolism?

Back 18

Usually DETATCHED thrombus - an intravascular solid, liquid or gaseous mass carried from origin to a distant site.

Front 19

Common causes of emboli?

Back 19

Lack of moving - Plane trips, long periods of immobility - followed by movement that gets blood moving again to move clot

Front 20

What is a pulmonary embolism?
Where do they originate?
Result?

Back 20

-A clot that prevents or reduces blood to the lungs

-95% start in leg veins
-Large=sudden death by pulmonary A occlusion
-Small- infaction; insufficient circulation to bronchials

Front 21

What is a systemic emboli? Origin? Result?

Back 21

-A detached thrombus in arterial circulation
-Arices from from l. side of heart, aorta or Mj Aa.
-Infarction, most often in brain (CVA), lower extr., spleen & kidneys

Front 22

What's a gas embolism?

Back 22

A bubble in the circulatory system. Ex: Decompression sickness from dissolved N in blood forms bubble due to change in pressure.

Front 23

Define "Bends" & "Chokes"

Back 23

Bends: Nitrogen bubbles in joints, cause intense pain

Chokes: N bubbles form in lungs, causing respirtory distress

Front 24

What is a fat emboli? Origin?

Back 24

It's a loose piece of fat in circulatory system from trauma to fatty tissue (ie bone marrow from broken bone; liposuction) or by chylomicrons of fat formed in veins

Front 25

What is an Amniotic Embolism?
Tx?

Back 25

Amniotic fluid that gets into blood stream of mother following delivery, causing DIC and shock. High chance of death. Tx: Heparin, even though bleeding to death, to stop DIC

Front 26

What is Infarction?

Back 26

Localized ischemic necrosis due to occlusion of arterial supply or venous drainage

Front 27

What is an Anemic infarct?
Where does it occur?

Back 27

Arterial & solid tissue occlusions leadind to ischemic necrosis.
"White" infarct
Occurs in heart, spleen, kidneys

Front 28

What is a Hemorrhagic infarct?
Where does it occur?

Back 28

Venous occlusion leading to necrosis - also in tissues where blood can collect or is congested to to blocked veins
"Red" infarct
Occurs in lung, intestine, brain & liver

Front 29

What are septic and bland infarcts?

Back 29

Infarcts where bacterial inflammation is present are called septic. If there's no bacteria, it's called bland.

Front 30

What's the gross morphology of an infarct? Microscopic?

Back 30

Gross appearance: wegde-shape, apex toward occlusion & exteral part of organ forms base

Microscopic: ischemic coagulative necrosis

Front 31

What affects the degree of damage in an infarction?

Back 31

1) General status of blood and CV system
2) Anatomic pattern of arterial supply in individual
3) Rate of dev. of occlusion (time for collateral circulation development)
4) Vulnerability of tissue to ischemia

Front 32

What are the Gross and Microscopic damage done from MI during:
0-2 hrs?

Back 32

None in first ~1/2 hr - reversal cell injury changes only

Front 33

What are the Gross and Microscopic damage done from MI during:
4-12 hrs?

Back 33

G: Occasionally dark mottling

M: begining coag. necrosis of fibers; edema; hemmorage

Front 34

What are the Gross and Microscopic damage done from MI during:
12-48 hrs?

Back 34

G: Dark mottling

M: Ongoing coag. necrosis of mucles; polyleukocyte infiltrate

Front 35

What are the Gross and Microscopic damage done from MI during:
2-4 days?

Back 35

G: Yellow-brown with dark border, tissue soft
M: Lysis of muscle fibers, granulation of tissue at periphery

Front 36

What are the Gross and Microscopic damage done from MI during:
4-10 days?

Back 36

G: Tan to bright yellow with hyperemic border. Tissue gets softer
M: Tissue replaces with granulation tissue

Front 37

What are the Gross and Microscopic damage done from MI during:
4-6 WEEKS?

Back 37

G: Pearly white or gray, firm

M: Fibrous scar tissue

Front 38

Define Shock

Back 38

A set of syndroms characterized by inadequate perfusion leading to imbalance between metabolic needs of vital organs and the available blood flow

Front 39

Describe hypovolemic shock

Back 39

Reduction in blood volume from external loss of blood plasma or water or from internal loss (e.g., massive exudation or internal hemorrhage)

Front 40

Describe Cardiogenic shock

Back 40

Decrease in cardiac output due to infarction, myocaridal disease, arrythmia or cardiac tamponade

Front 41

Describe septic shock

Back 41

Overwhelming bacterial infection causes peripheral vasodilation & pooling of blood and/or DIC due to endothelial cell injury.

Front 42

Describe Neurogenic shock

Back 42

Anesthesia or spinal cord injury causes pheripheral vasodilations with pooling of blood.

Front 43

Result of shock?

Back 43

Causes generalized celular damage, especially in brain, heart, lungs, kidneys. Also adrenals GI tract & liver

Chemical mediators are produced that result in complement activation, fever, and in high concentration can learn to DIC