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Exam 1 > Sepsis > Flashcards

Sepsis Flashcards

1
Q

Define SIRS

A

cytokine storm in response to a stimulus leading to multiple organ dysfunction

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2
Q

SRIS criteria

A

febrile (>38 or 100.4), or hypothermic (<36 or 96,8), tachycardia (>90), tachypnea (>20), leukocytosis or leukopenia (>12,000, <4,000)

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3
Q

Define sepsis

A

2 of the 4 SIRS criteria plus suspected or proven infection

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4
Q

Define severe sepsis

A

2 of the 4 SIRS criteria, suspected or proven infection, and end-organ dysfunction in one or more organ systems

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5
Q

Define septic shock

A

2 of the 4 SIRS criteria, suspected or proven infection, end-organ dysfunction in one or more systems, and severe hypotension (<90 or >40 decrease from baseline) despite fluid resuscitation, requires pressor therapy

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6
Q

Define refractory septic shock

A

septic shock that lasts for 1 hour despite fluid resuscitation and pressors, this is where patients often die

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7
Q

Define early sepsis (new)

A

infection based on clinical suspicion combined with RR >22, altered mentation, and/or systemic BP <100, sofa score >2

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8
Q

Define sepsis (new)

A

life-threatening organ dysfunction caused by an infection with a unregulated host response

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9
Q

Define septic shock (new)

A

vasodilation or distribution problem due to sepsis causing circulatory, cellular, and metabolic derangements, require vasopressors to maintain arterial BP of >65, lactate >2, 40% mortality vs 10% with sepsis alone,

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10
Q

Define shock

A

diminished cardiac output or reduced effective circulating blood volume, impairing tissue perfusion, leading to cellular hypoxia, reversible but can be fatal

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11
Q

Causes of shock

A

infection, anaphylaxis, cardiac abnormality, hypovolemia

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12
Q

Define multiple organ dysfunction syndrome

A

progressive illness caused either by a defined insult (primary) or as a result of the host response to an indirect insult, no universally accepted criteria, so use the SOFA score

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13
Q

28-day mortality of septic shock

A

40-70%

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14
Q

patient has a poor prognosis with sepsis if they are experiencing the following:

A

increased age, comorbidities, high APACHE II score, elevated lactate, insufficient response to vasopressors, delay in treatment

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15
Q

Infectious causes of sepsis

A

opportunistic infections, host factors such as comorbidities, indwelling devices, especially those leading to the obstruction of normal drainage, and microbial factors that allow infections to evade the immune system and produce toxins we can’t treat

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16
Q

cardiogenic shock

A

patient has MI, leads to loss of perfusion, reduced circulating volume, hypoxia, necrosis, and ultimately organ failure and death

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17
Q

hypovolemic shock

A

patient experiences trauma where they lose large volume of blood, leads to reduced circulating volume, hypoxia, necrosis, and ultimately organ failure and death

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18
Q

septic shock

A

patient has infection where overblown immune response leads to the shunting of blood away from peripheral vital organs leading to hypoxia, necrosis, and ultimately organ failure and death

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19
Q

anaphylactic shock

A

hypersensitivity leads to over exaggerated immune response against a benign invador leading to the shunting of blood, hypoxia, necrosis, organ failure, and death

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20
Q

toxic shock

A

bacteria associated with tampons lead to rapidly progressing infection leading to shunting, hypoxia, necrosis organ failure, and death within 48 hours in 65% of patients if left untreated

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21
Q

Catecholamine role in shock

A

peripheral vasoconstriction due to autonomic nervous system releasing adrenal catecholamines, shunt blood to heart and brain, lead to renal and liver failure, capillary acidosis, and hemodilution with hypovolemia

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22
Q

hemodilution with hypovolemia

A

when peripheral blood volume decreases, interstitial fluids move into the vasculature to replace this pressure, leading to dilute blood

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23
Q

DIC

A

disseminated intravascular coagulation, blood pools at site of infection, forms a clot, uses up all clotting factors in the body, leads to profuse bleeding everywhere else

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24
Q

Crepitus

A

crunching sound indicative of a friction rub between bone and cartilage

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25
Q

signs of inflammation

A

rubor, calor, tumor, dolor, functio laesa

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26
Q

differential diagnosis with leg pain

A

VINDICATE: vascular, infection, neoplasm, drugs/toxins, inflammation, congenital, autoimmune, trauma, endocrine

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27
Q

possible infections of the leg

A

cellulitis (skin), fasciitis (fascia), myositis (muscle), and osteomyelitis (bone)

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28
Q

labs collected with suspected sepsis

A

cultures, CBC, CMP, coagulation test

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29
Q

CBC

A

complete blood count, evaluates for leukocytosis or leukopenia, platelet count, and hemoglobin

30
Q

blood culture test

A

2 separate sites, anaerobic and aerobic, total of 4 bottles, if patient as an implanted device, want one from there too

31
Q

coagulation test

A

test for DIC, see if the clotting time is decreased

32
Q

CMP

A

electrolytes, renal function, and liver function

33
Q

What factors come into play when choosing an empiric drug treatment

A

site of infection, patient history

34
Q

first things you do when septic patient is admitted

A

obtain labs, take x ray, administer IV fluids, start on broad spectrum antibiotics

35
Q

slight lactate elevation on metabolic panel is a sign that

A

there is poor perfusion, patient needs a pressor, but if it is only slight, it is still reversible

36
Q

minor elevation in liver enzymes is a sign that

A

liver is being poorly perfused, this is the beginning of an acute liver injury, still reversible, do something now

37
Q

air in the subcutaneous tissue is indicative of

A

necrosis beyond the skin but before the muscle, that is fasciitis, so necrotizing fasciitis

38
Q

debridement

A

surgical procedure to scoop out necrosed tissue

39
Q

Bandemia

A

left shift in the bands, indicating excessive presence of immature white blood cells, infection is so acute and body is so desperate that WBCs are being released prematurely

40
Q

lab sign of malnutrition

A

low albumin

41
Q

low fibrinogen levels is indicative of

A

DIC

42
Q

bacteremia

A

bacteria in the blood

43
Q

sepsis therapies

A

treat underlying cause, increase BP, replace RBCs, platelets, and clotting factors if bleeding, ventilation, dialysis, corticosteroids, and nutritional support

44
Q

IL10

A

calms the immune response, down regulating inflammation

45
Q

IL7 and IL8

A

flags for help from neutrophils, attracting them to infection site

46
Q

IL1B

A

causes fever, some patients have too much of this, have periodic fever syndrome

47
Q

NLRP3

A

enhances production of IL1B, genetic defect would lead to periodic fever syndrome

48
Q

TNFalpha

A

causes leukocytes and endothelial cells to produce and release cytokines, express cell-surface molecules to improve neutrophil adhesion, and increase prostaglandinin and leukotriene production

49
Q

IL6

A

promotes clotting via tissue factor induction

50
Q

cause of hemolytic anemia in septic patients

A

consumption coagulopathy, use up all complement mediators really fast, serious sign of end-stage sepsis

51
Q

amniotic fluid embolism

A

pregnant patient experiences trauma i.e. car accident, fluid leaks from amniotic sac, travels to mother in the form of an embolism, causes DIC, obstetric emergency

52
Q

how do patients develop DIC

A

tissue factor released in response to tissue damage, leads to intrinsic pathway coagulation, platelet aggregation, decreased antithrombin, protein C, protein S, ultimately unopposed clotting

53
Q

what factor would worsen DIC

A

liver failure, patient can’t produce clotting factors, they’re already at a disadvantage, DIC will progress very quickly

54
Q

quick laboratory test for DIC

A

D dimer test, D dimer produced from the breakdown of fibrin in peripheral tissues leading to bleeding

55
Q

signs of organ failure

A

decreased urine output, altered mental status, decreased platelets, difficulty breathing, abnormal heart function, abdominal pain

56
Q

why are biofilms dangerous

A

incurable by immune system, recalcitrant to antibiotic therapy, chronic

57
Q

top pathogens that lead to sepsis

A

staph aureus, coagulase negative staph, e coli, and strep

58
Q

features of staph

A

gram positive cocci in cluster, none motile, non spore forming, catalase positive and oxidase negative, facultative anaerobe, if coagulase positive, aureus, otherwise epidermis or saprophyticus, major component of normal flora

59
Q

steps of septic shock

A

innate immune system recognizes microbes, immune factors activate endothelial cells and leukocytes, immune system over-responds, systemic endothelia damage, vasodilation, capillary leakage, multiple organ failure, death

60
Q

microbial trigger on gram - bacteria

A

lipopolysaccharide, on E coli surface, exposed and easy to recognize

61
Q

microbial trigger on gram + bacteria

A

lipoteichoic acid exposed on surface, peptidoglycan both inside and outside where it is sloughed off, and superantigens

62
Q

microbial trigger on viruses

A

nucleic acid

63
Q

PAMP

A

pathogen associated molecular patterns

64
Q

PRR

A

pattern recognition receptors

65
Q

Toll-like receptors

A

pattern recognition receptors that respond to PAMPs to release pro inflammatory cytokines

66
Q

super antigens

A

exotoxins that cross link T cell receptors to class II MHC, amplifying the t cell stimulation from its normal 1 in 10,000 to 1 in 5, resulting in massive IFN gamma and IL2 production

67
Q

IFN gamma

A

interferon gamma, proinflammatory cytokine, recruits leukocytes

68
Q

IL2

A

interleukin 2, proinflammatory cytokine, recruits leukocytes

69
Q

which bacteria produce super antigens

A

staph aureus and step pyogenes

70
Q

super antigens are best known for causing

A

toxic shock syndrome

Exam 1 (7 decks)

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