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KC Fall 17 ID > SIRS/Sepsis > Flashcards

SIRS/Sepsis Flashcards

1
Q

How do viruses proliferate

A

invade host cells and take over cells’ machinery (can’t reproduce)

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2
Q

Virus consists of

A

DNA OR RNA, surrounding protein coat (capsid), opt: lipoprotein envelope

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3
Q

A viruses 3 methods of affecting cell

A

lyse host cells to spread, remain latent incorporated in host genome, cause oncogenic change

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4
Q

4 facts about viruses that make them hard to kill

A
  1. intracellular: evade humoral immune system
  2. easily mutate (new strands, body w/o immunity)
  3. disguise themselves (take part host cell memb camo)
  4. target our own immune cells for destruction
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5
Q

Describe prion’s and their effects

A

No genome, produce progressive wasting disease of CNS, replicate and add up w/in neuron

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6
Q

What happens to body in Prion disease, S/S

A

progressive non-inflamm neuron degeneration, leads to ataxia, dementia, death, no treatment

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7
Q

What typically causes GU disease and atypical pneumonia

A

mycoplasma (bacteria)

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8
Q

Describe mycoplasma

A

no cell wall, bacteria causes disease w/o cellular invasion

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9
Q

What 3 ABX categories is mycoplasma sensitive to

A

E-mycins, tetracycline, quinolone ABX

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10
Q

How do you see spirochetes

A

dark field microscopy

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11
Q

Spriochetes: Gram result?, can they move?, shape?

A

GNR (gram neg rods), motile, corkscrew shape

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12
Q

What causes syphilis (Treponema)

A

spirochetes

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13
Q

what causes GI disease (H. pylori)

A

spirochetes

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14
Q

what causes lyme disease (Borrelia)

A

spirochetes

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15
Q

What 2 diseases does mycoplasma cause

A

GU disease and atypical pneumonia

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16
Q

describe chlamydiae

A

obligate intracellular parasite, obtain energy from host cell

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17
Q

what does chlamydiae cause

A

GU infection, atypical pneumonia

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18
Q

3 ABX to treat chlamydiae

A

tetracyclines, macrolides, some quinolone ABX

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19
Q

Describe Rickettsiae

A

intracellular parasites, usually spread by insect vector

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20
Q

What does Rickettsiae cause

A

vascular cell infection/vasculitits

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21
Q

What ABX use for Rickettsiae

A

tetracyclines

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22
Q

Mycobacteria: description, how to see, where in body

A

GPR (weakly), acid fast-retain dye after alcohol wash, slow growing intracellular parasites of macrophages

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23
Q

what 3 diseases does mycobacteria cause

A

TB, MAC, leprosy

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24
Q

Nocardia/Actinomyces description

A

weakly GP filament bacteria, slow growing; work well in pts with T-cell immune dysfunction

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25
Q

What does Nocardia/Actinomyces cause

A

severe infection/abscess (require long term treatment)

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26
Q

Pts with T-cell immune dysfunction should watch out for what bacteria

A

Nocardia/Actinomyces

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27
Q

What bacteria is intracellular parasite of macrophages

A

mycobacteria

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28
Q

list 3 gram positive rods

A

Uncommon: Diptheria, Corynebacteria, Listeria

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29
Q

List 3 gram positive cocci

A

Enterococcus (including VRE), staphylococcus (epidermidis and aureus)

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30
Q

what is grouped by carbohydrate capsules A-D

A

streptococci

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31
Q

What hemolysis blood agar: alpha incomplete, beta complete, gamma none

A

streptococci

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32
Q

Skin colonizer and potential pathogen (bacteria)

A

Staphylococcus

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33
Q

Gram status and description of staphylococcus epidermidis

A

gram positive cocci

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34
Q

patients with DM, IVDA, or HD patients might have what colonized in their nares

A

Staphylococcus aureus

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35
Q

What has abscesses with low intenral pH and has enzymes to retard body’s defense mech

A

staphylococcus aureus

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36
Q

What produces enterotoxins (scalded skin syndrome and TSS)

A

staphylococcus aureus

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37
Q

what is increasingly becoming resistant to all beta-lactams

A

staph

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38
Q

Features of gram negative bacteria

A

cell wall with lipopolysaccharide to strongly induce cytokines (like TNF)

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39
Q

List some GN bacteria

A

haemophilus species, klebsiella species, pseudomonas species, eschherichia coli, enterobacter, Moraxella, serratia, slamonella, shiegella, proteus, neisseria

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40
Q

2 ways anaerobes cause infection

A

contaminate of sterile sites with heavy load of anaerobes (aspiration pneumonia), infection of tissues with poor vascular supply and low tissue oxygen concentration (diabetic ulcers)

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41
Q

What pathogen infection generally implies a polymicrobial infection

A

anaerobic infection

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42
Q

2 examples of anaerobes

A

clostridium species, bacteroides fragilis

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43
Q

3 clues for presence of anaerobic infection

A

foul odor, presence of gas (x-ray or crepitus), mixed GN and GP cultures, esp on aerobic culture

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44
Q

6 common fungi

A

Candida, Histoplasma, Coccidiomycosis, Cryptococcus, aspergillus, pneumocystis jiroveci

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45
Q

Fungi found in mouth, skin, blood (fungemia)

A

Candida

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46
Q

fungi found in cavitary lung or systemic dz, endemic to ohio river valley

A

Histoplasma

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47
Q

endemic to desert SW, cause pneumonia, meingitis

A

Coccidiomycosis

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48
Q

insidious meningitis, space occupying lesions or pulm disease (fungi)

A

Cryptococcus

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49
Q

fungi found in lungs, sinuses

A

aspergillus

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50
Q

opportunistic infection in pts with t-cell immunodef (fungi)

A

Pneumocystis jiroveci

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51
Q

What 2 components do both innate and adaptive immunity have

A

humoral immunity and cellular immunity

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52
Q

5 innate defenses of immune system

A

mucociliary clearance, skin/epithelium, phagocytic cells (neutrophils), toll-like receptors (transmemb receptors recognize diff compon of microbes), complement (protein activated by immune complex or surf proteins, enhances opsonization, phagocytosis, lysis)

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53
Q

Upon activing complement cascade what are the 4 steps that happen

A

Deposite complement on microbial surface, local inflammation/leaky capillaries, drill pores in surface cause cell lysis, recruit WBC

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54
Q

What type of immunity is complement

A

Humoral

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55
Q

relationship of mnocytes and macrophages

A

start as monocytes and differentiate into macrophages

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56
Q

3 roles of monocytes/macrophages

A

phagocytosis and presentation of ingested antigens to lymphocytes; secretion of proteolytic enzymes, oxygen radiacals, and cytokines (further inflame and call attn. to site of inf); debris clean-up

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57
Q

3 examples of graunlocytes

A

Polymorphonuclear cells (PMN)/neutrophils, eosinophils, basophils

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58
Q

what cell releases cytoplasmic graunles containg proteolytic enzymes (also actively phagocytic cell)

A

PMN or netuorphils

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59
Q

3 roles of lymphocytes

A

destroy cells identified by antibodies, defend against viral pathogens, recognize and kill tumor cells/abn cells/cells inf w/ intracellular pathogens (like viruses)

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60
Q

list 3 types of lymphocytes

A

Natural killer cells, B lymp, T lymph

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61
Q

Difference between T and B lymph

A

T matures in thymus, B matures in bone marrow

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62
Q

what type of cell secretes cytokines (like IL and TNF) to be general activator of inflammation and immune response

A

Lymphocytes

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63
Q

Role of central lymphoid tissues, bone marrow and thymus

A

finishing school for B and T lymphocytes, they must mature appropriately in order to leave the organ (otherwise destroyed)

64
Q

Role of B lymphocyte

A

circulate in body to find antigens, if recognized then cell proliferates and ramps up immunoglobulin production (humoral immun)

65
Q

Role of T lymphocytes

A

recognize protein antigens on MHC so if foreign antigens are identified T lymp seeks out and kills invader or cell infected by pathogen (cellular immun)

66
Q

List the 5 types of immunoglobulins secreted by B lymph specific to each invader

A

IgA, IgG, IgM, IgD, and IgE

67
Q

What stimulates humoral immunity

A

complement cascade

68
Q

3 things antibodies (immunoglobulins) do

A

recognize and bind microbe to inactivate it, binding to microbe and facilitate phagocytosis, recognize foreign proteins and kill it

69
Q

principal antibody molec for infectious agents, smaller remains elevated longer (Antibody)

A

IgG

70
Q

large antibody, elevates quickly in acute infection, macroglobulin (Antibody)

A

IgM

71
Q

increased in allergic individuals (Antibody)

A

IgE

72
Q

antibody for things we inhale or eat

A

IgA

73
Q

antibody found on cell memb of b lymph

A

IgD

74
Q

2 types of T-lymp and what they do (general)

A

CD4 and CD8: kill body’s own cels that were invaded

75
Q

What adaptive defense component is vital in organizing immune system

A

CD4 T-lymphocytes

76
Q

Helper T cell vs cytotoxic t cell

A

Helper: help B lymph and phagocytic cells make antibodies and lyse
Cytotoxic: kill lyse intracellular microbes

77
Q

Humoral Innate Immunity

A

pattern receptors, complement, enzymes, cytokines

78
Q

Cellular innat eimmunity

A

phagocytes, NK cells (all must be tagged)

79
Q

Humoral adaptive immunity

A

antibodies, cytokines

80
Q

Cellular adaptive immunity

A

T and B cells

81
Q

adaptive immunity lag time for proliferation of lymphocytes to respond to antigen

A

> 1 week

82
Q

5 parts of peripheral lymphoid tissues

A

spleen, lymph nodes, tonsils, appendiz, MALT/GALT (mucosa-assoc lymphoid tissues of gut, lung, reproductive systems)

83
Q

Areas that function as localized meeting places to expose antigens to immune cells and promote cell-cell interactions

A

peripheral lymphoid tissues

84
Q

Direction that lymph enters the nodes

A

afferent channel

85
Q

What do t-cells do to B cells in lymph nodes

A

t cells present antigens to b cells after phagocytosis and b cells pump out antibodies into efferent lymph flow

86
Q

maturation site of b lymphocytesq

A

bone marrow

87
Q

areas to provide “first look” and are active in humoral immunity

A

MALT, appendix, tonsils

88
Q

antibodies of newborn process

A 
maternal antibodies (most IgG) cross placenta stored in fetal tissues, first few months of life
exception: preemies, chronic viral disease
89
Q

What contains IgA and what does it help with

A

colostrum and breast milk, decreases diarrheal illness in newborn

90
Q

Hypersensitivity Rxns (4)

A

Type 1: anaphylactic, II: cytotoxic, III: immune complex, IV: delayed hypersensitivity or cell-mediate dhypersensitivty

91
Q

if someone has autoimmune hemolytic anemia, RH hemolytic disease, or glomerulonephritis what hypersensitivity rxn they might have

A

cytotoxic (type II): antibodies bind to cell or tissue antigens (causes complement mediated lysis of cell)

92
Q

rheumatoid arthritis, lupus, glomerulonephritis could cause this hypersensitivity rxn

A

type 3: immune complex (complex deposited in tissues, causes tissue damage)

93
Q

TB skin test, fungal an dparasitic infections, contact dermitits might cause which hypersensitivity rxn

A

type 4: delayed hypersensitivyt, t-lymph are sensitized, lymphokines cause inflammation and activat emacrophages

94
Q

4 types of drugs for immune suppression

A

cytotoxic drugs (heavy), anti-metabolite drugs (mod), corticosteroids, immune globulins

95
Q

at risk for what if defect in humoral immunity

A

encapsulated organisms (Neisseriak, H flu, pneumococcus0

96
Q

at risk for what if defect in neutrophil #/func

A

bacterial and fungal infetion

97
Q

at risk for what if defect in t cell immunity

A

pathogens that replicate w/in host cells

98
Q

3 agents for inflammation and the 4 s/s

A

physical (temp), chemical, microbiologic

calor, dolor, rubor (redness), tumor (swelling)

99
Q

3 effects of infalmmation

A

capillary dilation, increased capillary permeability, attraction of leukocytes

100
Q

When and where are C-reactive protein and ferritin produced

A

The acute inflammatory process in the liver (these are acute phase reactants)

101
Q

Negative effect of inflammation/acute inflammatory process

A

pus, tissue destruction, fibrous tissue (scar)

102
Q

essential to making immune response happen, type of regulatory proteins

A

cytokines

103
Q

what molecule activates or inhibits actions of lcal cells in immune system (large enough quantiies can mediate systemic response)

A

cytokines

104
Q

Where is systemic response first typically found

A

in lungs (b/c get 100% of blood)

105
Q

Systemic inflammatory response syndrome (SIRS) defeintino

A

response by body to insults, can cause dysfunction, organ failure, death

106
Q

HR and RR requirement for SIRS to be met

A

HR >90, RR>20 or pCO2< 32

107
Q

Temp and WBC requriemtn for SIRS to be met

A

Temp>100.4 (38C) or <96.8 (36C); WBC>12k or <4k or >10% immature bands

108
Q

4 categories of shock

A

distributive, cardiogenic, hypovolemic, obstructive

109
Q

If someone has sepsis what type of shock are you worried about

A

distributive shock

110
Q

stages of shock

A

preshock (compensated: sweaty, inc HR, RR, BP), shock (can’t compensate, organ dysfunc s/s: tachycardia, dyspnea), end stage shock (end0organ dysfunc, pt death)

111
Q

shock s/s

A

tachycardda, dyspnea, restlessness, diaphoresis, etabolic acidosis, oliguria, cool clammy skin

112
Q

s/s of end stage shock

A

anuria/acute renal failure, academia decrease cardiac output, restlessness becomes agitation, obtundation and coma

113
Q

infection with altered organ function is

A

sepsis

114
Q

most common cause of ICU death

A

septic shock

115
Q

3 steps in sepsis pathogenesis

A

Endotoxin or cell wall products
1) induce pro-inflam cytokines (IL-1 and TNF-alpha)
which activate neutorphils and endothelial cells
2) damaging endothelium and making it leaky
systemic inflame activates
3) coagulation pathways causing widespread microthrombi, tissue ischemia, depletionof natural anitocauglants

116
Q

cardiac and lung status during sepsis

A

cardiac: func sub-optimal, vasodilates, BP falls - end organ hypoperfusion
lungs: ARDS due to cytokine induced increaesin pulm cap perm

117
Q

what does gram neg sepsis often produce

A

coagulopathy

118
Q

hematologic result of sepsis

A

thrombocytopenia, leukocytosis, leukopenia (alcoholics, elderly), coagulopathy (gram neg sepsis), 10% DIC

119
Q

3 other manifestations of sepsis

A

renal dysfunction, GI bleeding (b/c coagulopathy and thrombocytopenia), hypoglycemia (cause AMS, Sz)

120
Q

studies for sepsis

A

full physical exam, CBC, chemistries, blood, urine, sputum culture, wound culture, CSF exam, radiology

121
Q

What is the MOST IMPORTANT thing you can do for sepsis (and other things)

A

choose appropriate empiric antimicrobial (other things: fluids, O2, glucose control, steroid therapy)

122
Q

what is the strongest predictor of mortality in spesis

A

time to initaitno of appropriate antimicrobial therapy

123
Q

Empiric ABX therapy for sepsis if Pseudomonas not a consideration

A

vancomycin with: cephalosporin 3-4 gen, beta-lactam/beta-lactamase inhibitor, carbapenem

124
Q

Empiric ABX therapy for sepsis if Pseudomonas IS a consideration

A

vancomycin with: antipseduomonal cephalosporin, anti-pseudomonal carbapenem, anti-pseudomonal beta-lactam/beta-lcamase inhibor, fluorquinolone, aminoglycoside, monobactam

125
Q

alcoholism predisposed to what 2 micro-organisms

A

klebsiella, strep pneumo

126
Q

Diabetes predisposed to what 2 micro-organisms

A

Pseduomonas, strep pneumo

127
Q

Splenic dysfunction predisposed to what 3 micro-organisms

A

Strep pneumo, H. flu, Neisseria meningitis

128
Q

Neutropenia predisposed to what 2 micro-organisms

A

GNR from gut, Pseudomonas

129
Q

diseases found on skin

A

staph, strep

130
Q

diseases found on DM ulcers

A

staph, strep, gram neg, pos, anaerboes

131
Q

diseases found on burns

A

strep, staph, pseudomonas (love burns!!)

132
Q

diseases found on urine

A

enteroic gram neg (e coli), gramp pos (enterococcus)

133
Q

diseases found on lungs CAP

A

typical: strep pneumo, h flu, staph aureus
atypical: microplasma, legionella, clamidia

134
Q

diseases found on lungs HAP/VAP

A

all CAP typical and pseudomans and other gram neg

135
Q

diseases found on lines

A

gramp pos: staph, strep

136
Q

diseases found on heart

A

strep, staph (stpah=#1)

137
Q

diseases found on abdomen

A

gram neg, anerobe

138
Q

Albumin/Hetastarch/dextran

A

plasma expanders w/ high MW that increase plasma oncotic pressure

139
Q

first choice treatment in distributive shock like sepsis

A

levophed/norepinephrine

140
Q

treatment for cardiogenic shock

A

dobutamine

141
Q

useful adjunct in severe septic shock, 2nd line

A

vasopressin

142
Q

when to intubate

A

RR>30, mental status changes, hemodynarmic nistabiilty

143
Q

what is bedside echocardigoraphy used for

A

assess myocardial function during sepsis

144
Q

Defintion TPN

A

IV feeding of critically ill pt

145
Q

ANC value for neutropenic

A

<1500

146
Q

Febrile Neutorpenia requirements

A

fever, ANC<1500

147
Q

what is neutropeniac pt at HIGH risk for

A

fungal and bacterial infection (common sites: skin, perirectal, genital mucosa)

148
Q

when is febrile neutropenia seen

A

following CTX, XRT, cancer, aplastic anemic, toxins, drugs

149
Q

s/s febrile neutorpnia

A

not typical inf symp b/c not enough neutrophils to cause symp

150
Q

work-up for febrile neutropenia to search for infection

A

CXR, pan-culture, and additional studies guided by PE findings

151
Q

work-up for febrile neutropenia (5)

A

blood cultures (10-15 min apart), urinalysis w/ culture and sensitivity, culture of wound or catheter discharge (if wet), sputum (gram stain and culture), stool for clostridium difficile

152
Q

treatment and precautions for febrile neutropenia (general)

A

skin and oral care, avoid rectal manipulation, start bowel regimen; gowns/glvoes/mask, no flowers, diet restriction (no raw)

153
Q

treatment (pharm) for febrile neutropenia

A

Broad sprectum ABX (start w/in 1 hr of culture)
If fever fails to improve w/in 4-5 days add empiric anti-fungal
Filgrastim (Neupogen) or Pegfilgrastim (Neulasta): granulocyte colony0stiulaitng factors (improve cytotoxicity of neutrophils) (use only in some pts)

154
Q

what is febrile neutropenia prognosis dependent on

A

recovery of adequate neutrophil numbers: rapid initaiton of appropriate empiric ABX: moratlity 4-30%

155
Q

What 3 diseases do spirochetes cause

A

syphilis (treponema), GI disease (H. pylori), lyme disease (Borrelia)

KC Fall 17 ID (4 decks)

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