02a: Sepsis Flashcards
2016 definition of sepsis:
Life-threatening organ dysfunction caused by a dysregulated host
response to infection
Diagnosis of SIRS requires 2 out of which 4 criteria?
- Body T (under 35C or over 39C)
- HR over 90 bpm
- RR over 20 breaths/min, aCO2 under 32 mmHg, or required mechanical ventilation
- WBC over 12,000, under 4000, or over 10% bandemia
Difference between sepsis and SIRS.
Sepsis is SIRS due to an infectious etiology
T/F: The total number of cases of sepsis and the number of patients who are dying is increasing.
True
T/F: Causes of SIRS are nearly always infectious agents.
False - could be infectious, trauma, pancreatitis, etc.
T/F: For SIRS resulting from sepsis, Gram-pos infections more frequent than Gram-neg.
True
A simple definition of (X) is “blood outside the blood vessel”. List the types of (X).
X = hemorrhage;
- Hematoma
- Petechiae
- Purpura
- Ecchymoses
(X) is the medical term for “bruise”, which is typically 1-2 (mm/cm/in).
X = ecchymoses
1-2 cm
Patients with low platelet counts develop which type of hemorrhages? They’re typically 1-2 (mm/cm/in).
Petechiae (small);
1-2 mm
List the steps of normal hemostasis.
- Arteriolar vasoconstriction
- Primary hemostasis
- Secondary hemostasis
- Anti-thrombotic events
In (primary/secondary) hemostasis, (X) factor serves as bridge between ECM proteins and platelets.
Primary;
X = von Willebrand’s
In secondary hemostasis, (X) needs to be stabilized through activation of (Y).
X = platelet plug Y = coagulation cascade (results in local fibrin deposition)
Plasminogen activaor inhibitors are (pro/anti)-coagulant.
Pro-coagulant
Thrombin is (pro/anti)-coagulant and functions to:
Pro-coagulant;
Cleaves fibrinogen
Tissue factor is (pro/anti)-coagulant and functions to:
Pro-coagulant;
Activates extrinsic clotting cascade
T/F: Under normal circumstances, endothelial cells have strong pro-thrombotic properties.
False - anti-thrombotic (quickly change to pro-thrombotic state upon injury)
Describe the anti-platelet effect of vascular wall endothelial cells.
- Physical barrier between platelet and ECM proteins)
2. Secrete prostacyclin, NO (vasodilation and inhibit platelet aggregation)
Describe the anti-coagulant effect of vascular wall endothelial cells.
Membrane has:
- Heparin-like molecules
- Thrombomodulin
- Tissue factor pathway inhibitor
Describe the fibrinolytic effect of vascular wall endothelial cells.
Cells produce tissue type plasminogen activator (tPA), enhancing breakdown of fibrin
Which pro-thrombotic factors are produced by vascular endothelial cells?
- Von Willebrand factor
- Tissue factor
- Plasminogen activator inhibitors (PAIs)
Protein C and S are (pro/anti)-coagulant and function to:
Anti-coagulant;
Inhibit clotting factors
Thrombomodulin is (pro/anti)-coagulant and functions to:
Anti-coagulant;
Binds thrombin and activates protein C
Normally, platelets circulate freely in the blood. When exposed to (X), which 3 reactions favor thrombus formation?
X = ECM proteins
- Adhesion
- Secretion
- Aggregation
A genetic deficiency in vWF (von Willebrand factor) may result in (hypercoagulation/excessive bleeding).
Excessive bleeding;
vWF serves as bridge between platelet and ECM collagen during thrombus formation
Thrombus formation: once platelets have adhered to ECM, (X) step occurs. Which two factors are important here?
X = secretion (of granule contents)
- Ca (activates coagulation cascade)
- ADP (aggregates platelets)
Heparin injected by doctors into patients is used for (pro/anti)-coagulation purposes. What’s the mechanism?
Anti-coagulation;
Binds and activates anti-thrombin
Molecule that interferes with fibrin polymerization and breaks down fibrin.
Plasmin
List the three factors that contribute to thrombus formation. Star the most crucial of these.
- Endothelial cell damage*
- Hypercoagulable state
- Abnormal blood flow (i.e. turbulent, slow)
Primary hypercoagulability state are due to
X
X = genetic alterations (mutations/deficiencies of coagulation pathway elements)
Secondary
hypercoagulability state is called this because:
It is secondary to another disease state or clinical condition.
T/F: Primary hypercoagulability more common than secondary hypercoagulability.
False - vice versa
Arterial thrombi arise at site of (X) and venous thrombi at site of (Y).
X = injury (ex: atherosclerosis) Y = stasis
(Arterial/venous) thrombus has lines of Zahn and is (more/less) firmly attached than (arterial/venous) thrombus.
Arterial;
More;
Venous
List the fate of thrombus (if patient survives).
Acronym PEDO
- Propagate (grow/occlude)
- Embolize (freed/travels)
- Dissolution (fibrinolysis lyses it)
- Organize/recanalize (fibrosis with new vascular channels)
Disseminated intravascular coagulation (DIC) is clinical condition in which:
There is widespread formation of numerous fibrin thrombi throughout the micro-vasculature
A detached intravascular solid, liquid or gaseous mass carried by the blood to a site distant from its point of origin.
Embolus
Pulmonary thromboemboli are formed from:
Deep veins of pelvis/legs
After long bone fractures, (X) emboli may form.
X = fat
(X) embolism may form secondary to changes in atmospheric pressure. This is called (Y) sickness.
X = air Y = decompression
Following tear in amniotic membrane, (X) an embolus, composed of (Y) cells, can be found in which location in (fetus/mother)?
X = amniotic fluid Y = squamous cells (from fetal skin)
Maternal pulmonary microcirculation
(X) emboli are caused by pieces of necrotic, infected tissue.
X = septic
(X) is an area of ischemic necrosis secondary to occlusion of the vasculature.
X = infarct
White, aka (X), infarcts occur in which situation(s)?
X = anemic
(End) arterial occlusion
(X) is the clinical state of systemic hypoperfusion.
X = Shock
List the five types of clinical “shock”.
- Cardiogenic
- Septic
- Hypovolemic
- Anaphylactic
- Neurogenic
Septic patients have (excess/delayed) neutrophil
apoptosis.
Delayed (cells persist longer in bloodstream)
Septic patients have (excess/delayed) lymphocyte
apoptosis.
Excess/accelerated
Sepsis mortality can be predicted quickly via SOA (sequential organ failure assessment). Which factors are considered here? How accurate is this screen?
- RR over 20/min
- Altered mentation
- Systolic BP under 100 mmHg
Accurately screens 2/3