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IBI Test 1 > B3.002 Sepsis > Flashcards

B3.002 Sepsis Flashcards

1
Q

what is the less recent progression of sepsis?

A

SIRS
sepsis
severe sepsis
septic shock

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2
Q

what is SIRS

A

systemic inflammatory response syndrome

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3
Q

what occurs in SIRS

A

cytokine storm

  • release large quantities of cytokines
  • can cause multiple organ dysfunction bc these cytokines can be both harmful and toxic
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4
Q

what are the criteria for SIRS?

A 
2 of the 4:
fever or hypothermia (>100.4 or <96.8)
tachycardia (>90)
tachypnea (>24)
leukocytosis (>12,000), leukopenia (<4000) or left shift (>10% immature band cells)
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5
Q

what are the criteria for sepsis?

A

SIRS

suspected or proven infection

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6
Q

what are the criteria for severe sepsis?

A

SIRS
suspected or proven infection
end organ dysfunction in one or more organ systems

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7
Q

what are the criteria for septic shock?

A

SIRS
suspected or proven infection
end organ dysfunction
hypotension despite adequate fluid resuscitation, requiring pressor therapy

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8
Q

what is a pressor?

A

increases BP by stimulating vasoconstriction

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9
Q

what are the criteria for refractory septic shock?

A 
SIRS
infection
end organ dysfunction
hypotension despite fluids
hypotension lasts for more than 1 hour despite fluids and pressors
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10
Q

what is the sepsis continuum that is now more widely accepted?

A

early sepsis
sepsis
septic shock

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11
Q

what is a SOFA score?

A 
sequential (sepsis related) organ failure assessment
based on test variables from:
respiratory  (PaO2/FIO2)
coagulation (platelets)
liver (bilirubin)
cardiovascular (hypotension)
CNS (Glasgow coma score scale)
renal (creatinine/urine output)
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12
Q

what is the APACHE II scale?

A

severity of disease classification system based on lab test results

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13
Q

what is the significance of a SOFA score of 2?

A

<2 has 3% risk of mortality

>2 is associated w poor outcomes and 18-24% mortality

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14
Q

what is septic shock?

A

vasodilation or distribution problem due to sepsis causing circulatory, cellular, and metabolic derangements

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15
Q

what is the process of shock?

A

diminished cardiac output or reduced effective circulating blood volume which impairs tissue perfusion and leads to cellular hypoxia

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16
Q

what are some causes of shock?

A

infection - due to inflammatory cytokines and a vasodilatory response
anaphylaxis
cardiac abnormality - heart cant pump properly
hypovolemia - losing blood volume from bleeding out

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17
Q

what is the difference between primary and secondary multiple organ dysfunction syndrome?

A

primary : result of a defined insult

secondary : result of an indirect insult due to the host’s response

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18
Q

why is the frequency of septic shock increasing?

A

more aggressive surgery
more resistant organisms
more immune compromise from disease and medications
increased elderly living w chronic diseases (AIDS)
widespread use of catheters/medical devices (implantable)

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19
Q

28 day mortality of septic shock

A

40-70%

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20
Q

what factors are associated with a poor prognosis in the event of sepsis?

A 
increased age
comorbid medical conditions
high APACHE II score
elevated lactate
insufficient response to vasopressors
delay in treatment
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21
Q

what are some infectious causes of sepsis?

A

opportunistic infections (don’t cause disease in immunocompetent hosts)
host factors (comorbid diseases)
indwelling lines/catheters/foreign bodies (obstruction of drainage)
microbial factors
-invading the immune system
-produce toxins (cant always be treated)

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22
Q

what are some common classes of shock?

A

cardiogenic
hypovolemic
septic

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23
Q

what are some rare classes of shock

A

anaphylactic
neurogenic
toxic

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24
Q

describe the mechanism of cardiogenic shock

A

failure of myocardial pump resulting from intrinsic myocardial damage, extrinsic compression, or obstruction to outflow

25
cardiac tamponade
heart leaks into space between muscle and pericardium, compressing heart and impairing pumping
26
describe the mechanism of hypovolemic shock
inadequate blood or plasma volume
27
describe the mechanism of systemic inflammatory shock
``` cytokine cascade activation peripheral vasodilation and pooling of blood endothelial activation/injury leukocyte induced damage disseminated intravascular coagulation ```
28
what are the 3 stages of shock
non-progressive (reversible) progressive irreversible
29
non-progressive shock
compensatory mechanisms allow for survival
30
progressive shock
failing compensatory mechanisms increasing tissue hypoxia beginning lactic acidosis due to anaerobic metabolism
31
irreversible shock
leads to death
32
physical signs of inflammation
``` rubor - redness calor - heat tumor - swelling dolor - pain functio laesa - loss of function ```
33
VINDICATE differential diagnosis
``` vascular infectious neoplasm drugs/toxins inflammatory congenital/genetic autoimmune trauma endocrine/metabolic ```
34
diagnostic evaluation of sepsis
blood cultures CBC (white blood cell count, platelets, hemoglobin) CMP (electrolytes, renal function, liver function) coagulation tests
35
steps associated with empiric chemotherapy (what to do before lab results come back)
1. establish evidence of infection and probable site 2. obtain culture and susceptibility specimens 3. propose microbiological diagnosis 4. determine the need for empiric therapy 5. initiate chemotherapy
36
range of pathogens affected by a given drug
narrow spectrum- effective against a few species/classes of pathogen broad spectrum- effective against many species/classes of pathogens
37
when should narrow spectrum drugs be used
when the pathogen and its sensitivity to the drug are documented
38
when should broad spectrum drugs be used
mixed infections, or when pathogen identity and sensitivities are not known maximize probability of toxicity to pathogens
39
combination chemotherapy
use of multiple drugs against the same pathogen
40
indications for combination chemotherapy
1. for enhanced therapeutic effect 2. to allow use of lower doses of individual drugs to minimize toxicity to patient 3. to delay development of resistance 4. for the treatment of mixed infections 5. to initiate therapy in life threatening situations when the pathogen is not known
41
possible sources of air in subcutaneous tissue
gas produced by bacteria | tissue destruction
42
why is lactate elevated in septic shock?
tissue hypoxia from hypoperfusion | metabolic activity switches from oxidative metabolism to non oxidative or anaerobic metabolism
43
sepsis therapies
treat underlying cause increased blood pressure (IV fluids, vasopressors, inotropes) blood product (packed RBCs, platelets, clotting factors) ventilator support w oxygen dialysis for renal failure corticosteroids for adrenal failure nutritional support
44
bacteremia
bacteria in the bloodstream
45
source of redness
increased circulation to the area
46
source of swelling
increased vascular permeability
47
source of warmth
influx of inflammatory cells
48
local inflammation
innate mechanisms for eradication microbes
49
systemic disease
local defenses are enhances by increasing circulation to the area, increasing circulating neutrophils, and elevated microbial recognition molecules
50
cytokines
soluble proteins that interact with cells to produce changes in growth/activation of immune cells, inflammation, and the immune response
51
chemokines
soluble molecules which guide immune cells into a particular area
52
TNF alpha
causes leukocytes and vascular endothelial cells to: - produce and release other cytokines - express cell surface molecules to improve adhesion of neutrophils - increase inflammatory production of prostaglandins and leukotrienes
53
IL-8 and IL-17
attract neutrophils
54
IL-1B
fever
55
intravascular thrombosis
key factor of local inflammation wall off microbes, prevent spread of infection intravascular fibrin deposition, thrombosis, and bleeding dissemination intravascular coagulation
56
disseminated intravascular coagulation
consumption coagulopathy or microangiopathic hemolytic anemia serious sign of end stages of sepsis consumption of platelets and clotting factors due to tissue injury, endothelial damage, or both
57
what organ failure is particularly harmful in exacerbating DIC
liver failure | cant make clotting factors
58
what is a lab test to quickly assess for DIC
d-dimer
59
schistocytes
fibrin causes mechanical damage to the red blood cells

IBI Test 1 (15 decks)

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