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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
Q

cardiac tamponade

A

heart leaks into space between muscle and pericardium, compressing heart and impairing pumping

26
Q

describe the mechanism of hypovolemic shock

A

inadequate blood or plasma volume

27
Q

describe the mechanism of systemic inflammatory shock

A 
cytokine cascade activation
peripheral vasodilation and pooling of blood
endothelial activation/injury
leukocyte induced damage
disseminated intravascular coagulation
28
Q

what are the 3 stages of shock

A

non-progressive (reversible)
progressive
irreversible

29
Q

non-progressive shock

A

compensatory mechanisms allow for survival

30
Q

progressive shock

A

failing compensatory mechanisms
increasing tissue hypoxia
beginning lactic acidosis due to anaerobic metabolism

31
Q

irreversible shock

A

leads to death

32
Q

physical signs of inflammation

A 
rubor - redness
calor - heat
tumor - swelling
dolor - pain
functio laesa - loss of function
33
Q

VINDICATE differential diagnosis

A 
vascular
infectious
neoplasm
drugs/toxins
inflammatory
congenital/genetic
autoimmune
trauma
endocrine/metabolic
34
Q

diagnostic evaluation of sepsis

A

blood cultures
CBC (white blood cell count, platelets, hemoglobin)
CMP (electrolytes, renal function, liver function)
coagulation tests

35
Q

steps associated with empiric chemotherapy (what to do before lab results come back)

A
  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
Q

range of pathogens affected by a given drug

A

narrow spectrum- effective against a few species/classes of pathogen
broad spectrum- effective against many species/classes of pathogens

37
Q

when should narrow spectrum drugs be used

A

when the pathogen and its sensitivity to the drug are documented

38
Q

when should broad spectrum drugs be used

A

mixed infections, or when pathogen identity and sensitivities are not known
maximize probability of toxicity to pathogens

39
Q

combination chemotherapy

A

use of multiple drugs against the same pathogen

40
Q

indications for combination chemotherapy

A
  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
Q

possible sources of air in subcutaneous tissue

A

gas produced by bacteria

tissue destruction

42
Q

why is lactate elevated in septic shock?

A

tissue hypoxia from hypoperfusion

metabolic activity switches from oxidative metabolism to non oxidative or anaerobic metabolism

43
Q

sepsis therapies

A

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
Q

bacteremia

A

bacteria in the bloodstream

45
Q

source of redness

A

increased circulation to the area

46
Q

source of swelling

A

increased vascular permeability

47
Q

source of warmth

A

influx of inflammatory cells

48
Q

local inflammation

A

innate mechanisms for eradication microbes

49
Q

systemic disease

A

local defenses are enhances by increasing circulation to the area, increasing circulating neutrophils, and elevated microbial recognition molecules

50
Q

cytokines

A

soluble proteins that interact with cells to produce changes in growth/activation of immune cells, inflammation, and the immune response

51
Q

chemokines

A

soluble molecules which guide immune cells into a particular area

52
Q

TNF alpha

A

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
Q

IL-8 and IL-17

A

attract neutrophils

54
Q

IL-1B

A

fever

55
Q

intravascular thrombosis

A

key factor of local inflammation
wall off microbes, prevent spread of infection
intravascular fibrin deposition, thrombosis, and bleeding
dissemination intravascular coagulation

56
Q

disseminated intravascular coagulation

A

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
Q

what organ failure is particularly harmful in exacerbating DIC

A

liver failure

cant make clotting factors

58
Q

what is a lab test to quickly assess for DIC

A

d-dimer

59
Q

schistocytes

A

fibrin causes mechanical damage to the red blood cells

IBI Test 1 (15 decks)

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