Sepsis Flashcards
what is responsible for elevated plasma white cell count?
IL-6 and IL-1
TNF - Il1 and IL6 = leuokocyte production
characteristic of IL17 and chemokines
more adaptive immune response and chemokines will modify the leukocyte trafficking
is loss of blood volume associated with septic shock?
no - this is a part of hypoalemic shock
septicemia
sepsis with positive blood culture (used to identify whether there is bacteria in the blood or not
blood poisoning - especially when caused by bacteria or their toxins
most of the time the blood culture is negative - even if have sepsis
bacteremia
bacteria in blood
TLR4
pattern recognition receptor - activation leads to activation of the innate immune system
SOFA
*REQUIRE LAB TESTS
Sequential [sepsis-related] organ failure assessment score
0-4 (4 being severe)
organ dysfunctin represented by an increase in SOFA score of 2 points or more
T/F sepsis is a syndrome shaped by pathogen factors and host factors (sex, race, age, co-morbitites, environment)
True
qSOFA
aka
‘quick’ SOFA - ‘sepsis-3’ - looking at it in terms of three criteria
Respiratory rate of 22/min or greater
altered mentation (mental status)
systolic blood pressure of 100 mmHg or less
- quick because ‘bedside’ and do not need to run lab tests
coagulation factor 5
co-factor for coagulation cascade - protein C patwhay acts on this by inhibiting it
- if mutation or deficeint -
components of basic hemostatic plug
- exposure of collagen and other extracellular matrix molecules
- activated platelets
- tissue factor and fibrin from coagulation cascade
what does activated protein C target?
targets the coagulation co-factors
- make a bunch of fibrin if dont have the protein C???
DIC
Disseminated Intravascular Coagulation = consumptive coagulation
COMPLICATION OF AN UNDERLYING ILLNESS - not a disease itself
- so much clotting occuring that patient actually at risk for too much bleeding - using up antithrombotic factors (protein C) and pro-thrombotic factors
plasmin
activated by tPA - this is a ant-thrombotic factor
- inhibits the formation of clots
petachiae
cutaneous hemmorrhage, thrombocytopenia, DIC
- frequent complication of severe sepsis
- small clots in the cutaneous microvasculature- often leading to amputation of limbs or digits
PAI-1
PLASMINOGEN ACTIVATOR INHIBITOR supresses fibrinolysis (breaking down clots- as plasmin is major component of breaking down clots) and promotes the formation of the fibrin clots through the fibrinolytic response to infection
hemorrhage
blood outside the vessel
hematoma
type of hemmorage (blood outside the vessel) but enclosed within a space like subdural (brain) and retroperitoneal (abdominal space)
bruises
bleeding into the extracellular space
petachiae, purpura, ecchymosis are all?
bruises - type of hematoma where the bleeding is occurring in the extracellular space
the order of these is smallest to largest
generalizations of the protein C pathway
anti-thrombotic - CONTROLLING THROMBIN
anti-inflammatory
neuroprotective
*in DIC - there is A LOSS OF ANTI-THROMBOTIC CAPACITY OF PROTEIN C (usually it is inhibiting the coagulation co factors)
Factor 5 Leiden
mutant - protein C pathway does not work now
change in allele where the protein C needs to bind to control the thrombin
three ways compliment can become activated
- alternative pathway - spontaneous C3 activation - MICROBE MEDIATED
- classical pathway - Antigen/antibody complex - ANTIBODY MEDIATED
- lectin pathway - CARBOHYDRATE MEDIATED serum lectins bind pathogen mannose
all will deposit c3b on the microbe
Kinin system
resulting in bradykinin formation - very potent vasoactive peptide responsible for vasodilation, pain transmission, smooth muscle cell contraction