Sepsis Flashcards

1
Q

what is responsible for elevated plasma white cell count?

A

IL-6 and IL-1

TNF - Il1 and IL6 = leuokocyte production

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2
Q

characteristic of IL17 and chemokines

A

more adaptive immune response and chemokines will modify the leukocyte trafficking

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3
Q

is loss of blood volume associated with septic shock?

A

no - this is a part of hypoalemic shock

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4
Q

septicemia

A

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

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5
Q

bacteremia

A

bacteria in blood

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6
Q

TLR4

A

pattern recognition receptor - activation leads to activation of the innate immune system

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7
Q

SOFA

A

*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

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8
Q

T/F sepsis is a syndrome shaped by pathogen factors and host factors (sex, race, age, co-morbitites, environment)

A

True

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9
Q

qSOFA

aka

A

‘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

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10
Q

coagulation factor 5

A

co-factor for coagulation cascade - protein C patwhay acts on this by inhibiting it
- if mutation or deficeint -

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11
Q

components of basic hemostatic plug

A
  1. exposure of collagen and other extracellular matrix molecules
  2. activated platelets
  3. tissue factor and fibrin from coagulation cascade
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12
Q

what does activated protein C target?

A

targets the coagulation co-factors

- make a bunch of fibrin if dont have the protein C???

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13
Q

DIC

A

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

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14
Q

plasmin

A

activated by tPA - this is a ant-thrombotic factor

- inhibits the formation of clots

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15
Q

petachiae

A

cutaneous hemmorrhage, thrombocytopenia, DIC

  • frequent complication of severe sepsis
  • small clots in the cutaneous microvasculature- often leading to amputation of limbs or digits
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16
Q

PAI-1

A
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
17
Q

hemorrhage

A

blood outside the vessel

18
Q

hematoma

A

type of hemmorage (blood outside the vessel) but enclosed within a space like subdural (brain) and retroperitoneal (abdominal space)

19
Q

bruises

A

bleeding into the extracellular space

20
Q

petachiae, purpura, ecchymosis are all?

A

bruises - type of hematoma where the bleeding is occurring in the extracellular space
the order of these is smallest to largest

21
Q

generalizations of the protein C pathway

A

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)

22
Q

Factor 5 Leiden

A

mutant - protein C pathway does not work now

change in allele where the protein C needs to bind to control the thrombin

23
Q

three ways compliment can become activated

A
  1. alternative pathway - spontaneous C3 activation - MICROBE MEDIATED
  2. classical pathway - Antigen/antibody complex - ANTIBODY MEDIATED
  3. lectin pathway - CARBOHYDRATE MEDIATED serum lectins bind pathogen mannose

all will deposit c3b on the microbe

24
Q

Kinin system

A

resulting in bradykinin formation - very potent vasoactive peptide responsible for vasodilation, pain transmission, smooth muscle cell contraction