Sepsis

Front 1

4-step process of normal hemostasis?

Back 1

1. Arteriolar vasoconstriction
2. Primary hemostasis
3. Secondary hemostasis
4. Thrombosis and anti-thrombotic events

Front 2

What occurs in step 1 of hemostasis - arteriolar vasoconstriction?

Back 2

The smooth muscles of the vessel contract and cause more matrix proteins to be exposed in the lumen

Front 3

What occurs in step 2 of hemostasis - primary hemostasis?

Back 3

platelets adhere to the matrix proteins and release their granules to cause aggregation

Tissue factor is expressed on endothelial cells, which activates the clotting cascade

Front 4

What allows platelets to adhere to the matrix proteins/collagen in primary hemostasis?

What do platelets release to cause aggregation in primary hemostasis?

Back 4

Adhesion = von willebrand factor

Secretion = Ca++ and ADP

Thromboxane A2 released by platelets

Front 5

After tissue factor is expressed and the coagulation cascade begins, what occurs during secondary hemostasis?

Back 5

Multiple steps in the clotting cascade result in thrombin cleaving fibrinogen to produce fibrin deposition between platelets

Front 6

After secondary hemostasis occurs, what is next?

Back 6

The body begins to release factors to break down the clots

Front 7

What properties of the endothelial cells are anti-platelet and contribute to step 4 -Thrombosis and anti-thrombotic events

Back 7

1. physical barrier = endothelial cells normally shield matrix/vWF from platelets

2. nitric oxide - vasodilator

3. prostacyclin PGI2 - inhibits aggregation

Front 8

What properties of the endothelial cells are anti-coagulant and contribute to step 4 -Thrombosis and anti-thrombotic events

Back 8

1. heparin-like molecules

2. thrombomodulin

3. tissue factor pathway inhibitor

Front 9

How does thrombomodulin function as an anticoagulant? (2 ways)

Back 9

1. It binds thrombin. This prevents thrombin from converting fibrinogen to fibrin

2. Thrombin+Thrombomodulin activates Protein C. Protein C (and protein S) degrades coagulation factors.

Front 10

How do heparin-like molecules function as an anticoagulant?

Back 10

Bind anti-thrombin III which inactivates thrombin and coag factors

Front 11

How does tissue factor pathway inhibitor function as an anticoagulant?

Back 11

Made by endothelial cells to inactivate thrombotic factors

Front 12

How does plasmin participate in thrombosis?

Back 12

plasminogen is cleaved by plasminogen activator to form plasmin which then:

-interferes with polymerization of fibrin.

-breaks down fibrin

Front 13

What properties of the endothelial cells are fibrinolytic and contribute to step 4 -Thrombosis and anti-thrombotic events

Back 13

tissue type plasminogen activator - these activate plasminogen to plasmin which breaks down fibrin

Front 14

What are plasminogen activator inhibitors

Back 14

Released by the endothelial cell to block plasminogen activator (PA).

This prevents PA from activating plasmin and breaking down fibrin; maintains the thrombus

Front 15

Lines of zahn?

Back 15

sign of arterial thrombosis

Front 16

Define each of the following with respect to the fate of thrombi:

1. Propagate
2. Embolize
3. Dissolution
4. Organize and recanalize

Back 16

PEDO:

1. Propagate – grow, may occlude
2. Embolize – breaks free travels to other sites
3. Dissolution – fibrinolysis may lyse the thrombus
4. Organize and recanalize – granulation tissue shrinks the thrombus, new vascular channels form

Front 17

Common causes of

1. Pulmonary thromboemboli
2. Fat emboli
3. Air emboli

4. Amniotic fluid emboli
5. Septic emboli

Back 17

1. Pulmonary thromboemboli – come from the deep veins of the pelvis or legs
2. Fat emboli – after long bone fractures
3. Air emboli – decompression sicknes

4. Amniotic fluid emboli – following tear in amniotic membranes
5. Septic emboli – fragments of necrotic, infected tissue

Front 18

Janeway lesions?

Back 18

Septic emboli resulting from the release of vegetations on heart valve into circulation: cause small infarcts on extremities

Front 19

Hemorrhagic or "red" infarct?

Back 19

Occur where there is an infarct of tissue but blood gets to the tissue by another means:

– Dual blood supply such as lung
– Reperfusion by unblocked vessel

– Watershed areas

Front 20

White or anemic infarct?

Back 20

Occlusion of an end arteriole

Front 21

Explain that the concept excess production of a single mediator does not cause sepsis.

Back 21

Many mediators are released during sepsis. Therapy for one mediator has never improved outcomes

Front 22

How are each of the following disfunctional in sepsis:

1. Lymphocytes

2. Neutrophils

Back 22

1. Lymphocytes – accelerated apoptosis in several organs and the blood
2. Neutrophils – decreased apoptosis so that they persist longer in the circulation

"Dysregulated apoptosis contributes to the pathogenesis of sepsis by early removal of those cells which should not be removed i.e. lymphocytes, and delayed removal of those cells which should be removed i.e. neutrophils."

Front 23

Mechanism of each type of shock:

1. cardiogenic

2. hypovolemic

3. neurogenic

4. anaphylactic

5. septic

Back 23

1. cardiogenic - heart cant meet demand

2. hypovolemic - not enough blood/plasma

3. neurogenic - loss of vascular tone

4. anaphylactic - systemic vasodilation

5. septic - excess inflammation and DIC

Front 24

SIRS definition and criteria

Back 24

Systemic Inflammatory Response Syndrome

2 or more of the following are needed
1.Temperature >38° or < 36 °C
2.Heart rate > 90 beats/minute
3.Respiratory rate >20 or PaCO2 < 32mm Hg
4.WBC >12K or < 4K/mm3, or >10% bands

*LOs don't say to know the criteria fyi

Front 25

Describe the differences between the Systemic Inflammatory Response Syndrome (SIRS) and
sepsis.

Back 25

SIRS denotes the presence of systemic inflammation (can have many causes).

Sepsis is SIRS caused by an infection

Front 26

Define:

1. Sepsis
2. Septic Shock
3. Severe Sepsis

Back 26

1. Sepsis – SIRS due to an infection
2. Septic Shock – Shock due to sepsis
3. Severe Sepsis – Sepsis causing failure of at least one organ system

Front 27

Define:

1. Petechiae
2. Purpura
3. Ecchymosis

4. Hematoma

Back 27

1. Petechiae - small one to 2 mm hemorrhages
2. Purpura - slightly larger hemorrhages, typically greater than 3 mm in size
3. Ecchymosis - large subcutaneous hematomas, one to 2 cm; aka bruise

4. Hematoma - hemorrhage which is enclosed within a tissue; can be any size/significance