02a: Sepsis

Question 1

2016 definition of sepsis:

Answer 1

Life-threatening organ dysfunction caused by a dysregulated host
response to infection

Question 2

Diagnosis of SIRS requires 2 out of which 4 criteria?

Answer 2

1. Body T (under 35C or over 39C)
2. HR over 90 bpm
3. RR over 20 breaths/min, aCO2 under 32 mmHg, or required mechanical ventilation
4. WBC over 12,000, under 4000, or over 10% bandemia

Question 3

Difference between sepsis and SIRS.

Answer 3

Sepsis is SIRS due to an infectious etiology

Question 4

T/F: The total number of cases of sepsis and the number of patients who are dying is increasing.

Answer 4

True

Question 5

T/F: Causes of SIRS are nearly always infectious agents.

Answer 5

False - could be infectious, trauma, pancreatitis, etc.

Question 6

T/F: For SIRS resulting from sepsis, Gram-pos infections more frequent than Gram-neg.

Answer 6

True

Question 7

A simple definition of (X) is “blood outside the blood vessel”. List the types of (X).

Answer 7

X = hemorrhage;

1. Hematoma
2. Petechiae
3. Purpura
4. Ecchymoses

Question 8

(X) is the medical term for “bruise”, which is typically 1-2 (mm/cm/in).

Answer 8

X = ecchymoses

1-2 cm

Question 9

Patients with low platelet counts develop which type of hemorrhages? They’re typically 1-2 (mm/cm/in).

Answer 9

Petechiae (small);

1-2 mm

Question 10

List the steps of normal hemostasis.

Answer 10

1. Arteriolar vasoconstriction
2. Primary hemostasis
3. Secondary hemostasis
4. Anti-thrombotic events

Question 11

In (primary/secondary) hemostasis, (X) factor serves as bridge between ECM proteins and platelets.

Answer 11

Primary;

X = von Willebrand’s

Question 12

In secondary hemostasis, (X) needs to be stabilized through activation of (Y).

Answer 12

X = platelet plug
Y = coagulation cascade (results in local fibrin deposition)

Question 13

Plasminogen activaor inhibitors are (pro/anti)-coagulant.

Answer 13

Pro-coagulant

Question 14

Thrombin is (pro/anti)-coagulant and functions to:

Answer 14

Pro-coagulant;

Cleaves fibrinogen

Question 15

Tissue factor is (pro/anti)-coagulant and functions to:

Answer 15

Pro-coagulant;

Activates extrinsic clotting cascade

Question 16

T/F: Under normal circumstances, endothelial cells have strong pro-thrombotic properties.

Answer 16

False - anti-thrombotic (quickly change to pro-thrombotic state upon injury)

Question 17

Describe the anti-platelet effect of vascular wall endothelial cells.

Answer 17

1. Physical barrier between platelet and ECM proteins)

2. Secrete prostacyclin, NO (vasodilation and inhibit platelet aggregation)

Question 18

Describe the anti-coagulant effect of vascular wall endothelial cells.

Answer 18

Membrane has:

1. Heparin-like molecules
2. Thrombomodulin
3. Tissue factor pathway inhibitor

Question 19

Describe the fibrinolytic effect of vascular wall endothelial cells.

Answer 19

Cells produce tissue type plasminogen activator (tPA), enhancing breakdown of fibrin

Question 20

Which pro-thrombotic factors are produced by vascular endothelial cells?

Answer 20

1. Von Willebrand factor
2. Tissue factor
3. Plasminogen activator inhibitors (PAIs)

Question 21

Protein C and S are (pro/anti)-coagulant and function to:

Answer 21

Anti-coagulant;

Inhibit clotting factors

Question 22

Thrombomodulin is (pro/anti)-coagulant and functions to:

Answer 22

Anti-coagulant;

Binds thrombin and activates protein C

Question 23

Normally, platelets circulate freely in the blood. When exposed to (X), which 3 reactions favor thrombus formation?

Answer 23

X = ECM proteins

1. Adhesion
2. Secretion
3. Aggregation

Question 24

A genetic deficiency in vWF (von Willebrand factor) may result in (hypercoagulation/excessive bleeding).

Answer 24

Excessive bleeding;

vWF serves as bridge between platelet and ECM collagen during thrombus formation

Question 25

Thrombus formation: once platelets have adhered to ECM, (X) step occurs. Which two factors are important here?

Answer 25

X = secretion (of granule contents) 1. Ca (activates coagulation cascade) 2. ADP (aggregates platelets)

Question 26

Heparin injected by doctors into patients is used for (pro/anti)-coagulation purposes. What's the mechanism?

Answer 26

Anti-coagulation; Binds and activates anti-thrombin

Question 27

Molecule that interferes with fibrin polymerization and breaks down fibrin.

Answer 27

Plasmin

Question 28

List the three factors that contribute to thrombus formation. Star the most crucial of these.

Answer 28

1. Endothelial cell damage* 2. Hypercoagulable state 3. Abnormal blood flow (i.e. turbulent, slow)

Question 29

Primary hypercoagulability state are due to | X

Answer 29

X = genetic alterations (mutations/deficiencies of coagulation pathway elements)

Question 30

Secondary | hypercoagulability state is called this because:

Answer 30

It is secondary to another disease state or clinical condition.

Question 31

T/F: Primary hypercoagulability more common than secondary hypercoagulability.

Answer 31

False - vice versa

Question 32

Arterial thrombi arise at site of (X) and venous thrombi at site of (Y).

Answer 32

``` X = injury (ex: atherosclerosis) Y = stasis ```

Question 33

(Arterial/venous) thrombus has lines of Zahn and is (more/less) firmly attached than (arterial/venous) thrombus.

Answer 33

Arterial; More; Venous

Question 34

List the fate of thrombus (if patient survives).

Answer 34

Acronym PEDO 1. Propagate (grow/occlude) 2. Embolize (freed/travels) 3. Dissolution (fibrinolysis lyses it) 4. Organize/recanalize (fibrosis with new vascular channels)

Question 35

Disseminated intravascular coagulation (DIC) is clinical condition in which:

Answer 35

There is widespread formation of numerous fibrin thrombi throughout the micro-vasculature

Question 36

A detached intravascular solid, liquid or gaseous mass carried by the blood to a site distant from its point of origin.

Answer 36

Embolus

Question 37

Pulmonary thromboemboli are formed from:

Answer 37

Deep veins of pelvis/legs

Question 38

After long bone fractures, (X) emboli may form.

Answer 38

X = fat

Question 39

(X) embolism may form secondary to changes in atmospheric pressure. This is called (Y) sickness.

Answer 39

``` X = air Y = decompression ```

Question 40

Following tear in amniotic membrane, (X) an embolus, composed of (Y) cells, can be found in which location in (fetus/mother)?

Answer 40

``` X = amniotic fluid Y = squamous cells (from fetal skin) ``` Maternal pulmonary microcirculation

Question 41

(X) emboli are caused by pieces of necrotic, infected tissue.

Answer 41

X = septic

Question 42

(X) is an area of ischemic necrosis secondary to occlusion of the vasculature.

Answer 42

X = infarct

Question 43

White, aka (X), infarcts occur in which situation(s)?

Answer 43

X = anemic (End) arterial occlusion

Question 44

(X) is the clinical state of systemic hypoperfusion.

Answer 44

X = Shock

Question 45

List the five types of clinical "shock".

Answer 45

1. Cardiogenic 2. Septic 3. Hypovolemic 4. Anaphylactic 5. Neurogenic

Question 46

Septic patients have (excess/delayed) neutrophil | apoptosis.

Answer 46

Delayed (cells persist longer in bloodstream)

Question 47

Septic patients have (excess/delayed) lymphocyte | apoptosis.

Answer 47

Excess/accelerated

Question 48

Sepsis mortality can be predicted quickly via SOA (sequential organ failure assessment). Which factors are considered here? How accurate is this screen?

Answer 48

1. RR over 20/min 2. Altered mentation 3. Systolic BP under 100 mmHg Accurately screens 2/3