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Sepsis Recap Flashcards

1
Q

Define SIRS

A

Systemic inflammatory response syndrome.
Widespread inflammatory response to an infectious or non-infectious insult

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2
Q

Define sepsis (old def)

A

SIRS + documented or suspected infection

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3
Q

Define sepsis (new def)

A

life-threatening organ dysfunction caused by a dysregulated host response to infection.
Organ dysfunction is defined as SOFA (or q SOFA) score >/= 2

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4
Q

Define severe sepsis (old def)

A

Sepsis + evidence of organ dysfunction

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5
Q

Define severe sepsis (new def)

A

No such thing! All sepsis is “severe” now.

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6
Q

Define septic shock (old def)

A

Sepsis + hypotension that is not responsive to fluid therapy

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7
Q

Define septic shock (new def)

A
  • a subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone.

Vasopressors required to maintain MAP >65

AND

Lactate >2 in the absence of hypovolemia

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8
Q

Define MODS

A

multiple organ dysfunction syndrome.

Sepsis/SIRS + more than one organ dysfunction.

Increase in SOFA score of >/= 2 points.

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9
Q

What are the components of a SOFA score?

A
  • Respiration: based on PaO2/FiO2 ratio
  • Coagulation: based on platelet count
  • Liver: based on bilirubin
  • Cardiovascular: based on MAP
  • CNS: based on Glasgow coma scale
  • Renal: based on creatinine and urine output
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10
Q

What are the components of a qSOFA score?

A

3 categories not requiring lab work, score 0 or 1

RR >22/min
Altered mentation
Systolic BP <100mmHg

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11
Q

List 8 other findings of organ dysfunction with sepsis/SIRS that are not accounted for with a SOFA score.

A
  1. Hyperglycemia
  2. Hypoglycemia
  3. GI signs (V/D)
  4. Cardiac dysfunction (arrhythmias, impaired contractility)
  5. Immune dysregulation (CARS)
  6. Mitochondrial dysfunction
  7. Vascular leak/increased vascular permeability
  8. Hypoalbuminemia
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12
Q

What are the 4 basic steps in sepsis treatment?

A
  1. Identification
  2. Administer broad spectrum antibiotics (within 1 hr of ID)
  3. Systemic Stabilization
  4. Source Control
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13
Q

List the 5 major catecholamine receptors.

A

α1

α2

β1

β2:

dopaminergic (D receptors)

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14
Q

What are the effects of stimulation of alpha 1 (α1) receptors?

A

vasoconstriction (arterial and venous)
mild positive inotrope

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15
Q

What are the effects of stimulation of alpha 2 (α2) receptors?

A

primarily vasoconstriction, but vasodilation of vital organs

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16
Q

What are the effects of stimulation of beta 1 (β1) receptors?

A

Positive inotrope and chronotrope

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17
Q

What are the effects of stimulation of beta 2 (β2) receptors?

A

Vasodilation of vital organs
Bronchodilation

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18
Q

What are the effects of stimulation of Dopaminergic (D) receptors?

A

vasodilation of smooth muscle (renal, splanchnic, coronary, cerebrovascular).

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19
Q

What are the primary receptors stimulated by norepinephrine?

A

Primarily α
mild β (increases SVR)

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20
Q

What are the primary receptors stimulated by epinephrine?

A

Non selective α and β

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21
Q

What are the primary receptors stimulated by Dopamine?

A

Low dose (1-5mcg/kg/min): dopaminergic receptors

Mid dose (5-10): primarily β1, some α (positive inotrope/chronotrope with mild increase in SVR)

High dose (10-20): primarily α1 (vasoconstriction), lower GI blood flow

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22
Q

What are the primary receptors stimulated by dobutamine?

A

Beta only (β 1 > β 2)

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23
Q

What are the primary receptors stimulated by vasopressin?

A

V1: vasoconstriction

V2: found in the renal collecting duct, increases water reabsorption (increases aquaporin channels in the duct)

V3: stimulate release of ACTH from the pituitary

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24
Q

According to the Surviving Sepsis Guidelines, what is the preferred vasopressor for septic shock?
List the other options in order of preference.

A
  1. Norepinephrine
  2. Epinephrine
  3. Vasopressin
  4. Dopamine
  5. Phenylephrine- not really recommended at all anymore
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25
Q

Which of these are indications for administering steroids to a septic patient?

  • Low random cortisol level
  • Decreased “delta” cortisol on an ACTH stimulation test
  • Hypotension that is poorly responsive to fluid and vasopressor therapy
  • Fever
  • Early severe ARDS (PaO2/FiO2 <200)
A
  • Hypotension that is poorly responsive to fluid and vasopressor therapy
  • Early severe ARDS (PaO2/FiO2 <200)
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26
Q

What are 6 other measures that can be considered in a septic patient with hypotension poorly responsive to fluid therapy, vasopressors, and hydrocortisone?

A
  1. Positive inotropes (dobutamine, pimobendan?)
  2. Blood transfusion if indicated (higher transfusion threshold)
  3. Mechanical ventilation
  4. Colloid therapy if hypoalbuminemic or requiring high dose crystalloids
  5. Bicarbonate therapy if severely acidotic (pH < 7.1)
  6. Calcium supplementation if severely hypocalcemic
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27
Q

Amoxicillin:

MOA:
Cidal or static:
Spectrum:

A

MOA:
B-lactam.
Inhibit cell wall synthesis by binding to and inhibiting penicillin binding proteins (which catalyze cross linking of glycopeptides that form the cell wall).

Cidal or static: Cidal

Spectrum: G (+), G (-), anaerobes

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28
Q

Cefotaxime:

MOA:
Cidal or static:
Spectrum:

A

MOA:
B-lactam (3rd gen cephalosporin).
Inhibit cell wall synthesis.

Cidal or static: Cidal

Spectrum: G (-)

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29
Q

Metronidazole:

MOA:
Cidal or static:
Spectrum:

A

MOA: Inhibit RNA and DNA synthesis

Cidal or static: Cidal

Spectrum: Anaerobes

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30
Q

Enrofloxacin:

MOA:
Cidal or static:
Spectrum:

A

MOA: Inhibit DNA gyrase

Cidal or static: Cidal

Spectrum: G(-)

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31
Q

Azithromycin:

MOA:
Cidal or static:
Spectrum:

A

MOA: Inhibit protein synthesis via the 50S subunit

Cidal or static: Static

Spectrum: G (+), mycoplasma

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32
Q

Chloramphenicol:

MOA:
Cidal or static:
Spectrum:

A

MOA: Inhibit protein synthesis via the 50S subunit

Cidal or static: Static

Spectrum: G (+), G (-), anaerobes

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33
Q

Clindamycin:

MOA:
Cidal or static:
Spectrum:

A

MOA: Inhibit protein synthesis via the 50S subunit

Cidal or static: Static (except at high doses)

Spectrum: G (+), anaerobes

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34
Q

Tetracycline:

MOA:
Cidal or static:
Spectrum:

A

MOA: Inhibit protein synthesis via the 30S subunit

Cidal or static: Static

Spectrum: G (+), G (-), anaerobes

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35
Q

Amikacin:

MOA:
Cidal or static:
Spectrum:

A

MOA: Inhibit protein synthesis via the 30S and 50S subunits

Cidal or static: Cidal

Spectrum: G (-), staph

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36
Q

Suflas:

MOA:
Cidal or static:
Spectrum:

A

MOA: Inhibit folic acid synthesis 🡪 impaired protein and nucleic acid metabolism

Cidal or static: Static

Spectrum: G (+), G (-), anaerobes

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37
Q

Define cMax:

A

peak concentration of a drug after administration

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38
Q

Define MIC

A

lowest concentration of an antibiotic with no evidence of bacterial growth.

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39
Q

Define Breakpoint

A

The approximate concentration of the drug that can be achieved safely in the plasma given the clinically accepted dose and route (takes into account pharmacology of the drug)

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40
Q

How can you use the breakpoint and MIC to choose the best antibiotic for your patient?

A

Subtract Breakpoint from MIC- choose drug with largest number.
Use higher doses (if safe) if you absolutely have to use drugs with breakpoint near the MIC.

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41
Q

Explain time dependent antibiotics.

A

Time dependent antibiotics are those where the amount time spent above MIC is the major determinant of effectiveness (generally given multiple times daily).

Try to keep the concentration at 2-4 x MIC over dosing interval.

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42
Q

Explain concentration dependent antibiotics.

A

Concentration dependent antibiotics are those where the height of cMax is the major determinant of effectiveness (generally given once daily).

cMax should be at least 10-12 x the MIC to be effective.

Concentration dependent antibiotics often have a “post antibiotic effect” in which killing continues after the antibiotic concentration has dropped below MIC.

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43
Q

Examples of time dependent antibiotics.

A

B-lactams
vancomycin
clindamycin
macrolides

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44
Q

Examples of concentration dependent antibiotics.

A

aminoglycosides
fluoroquinolones

45
Q

Choose the correct words in the sentence.

An antibiotic with a HIGH volume of distribution is typically (MORE/LESS) lipophilic.
Because of this, it has a (HIGHER/LOWER) concentration in the tissues and a (HIGHER/LOWER) concentration in the blood.
These are typically eliminated/cleared by the (KIDNEYS/LIVER).
These would work (WELL/NOT WELL) for a prostate infection.

A

An antibiotic with a HIGH volume of distribution is typically MORE lipophilic.

Because of this, it has a HIGHER concentration in the tissues and a LOWER concentration in the blood.

These are typically eliminated/cleared by the LIVER.

These would work WELL for a prostate infection.

46
Q

Choose the correct words in the sentence.

An antibiotic with a LOW volume of distribution is typically (MORE/LESS) lipophilic.
Because of this, it has a (HIGHER/LOWER) concentration in the tissues and a (HIGHER/LOWER) concentration in the blood.
These are typically eliminated/cleared by the (KIDNEYS/LIVER).
These would work (WELL/NOT WELL) for a prostate infection.

A

An antibiotic with a LOW volume of distribution is typically LESS lipophilic.

Because of this, it has a LOWER concentration in the tissues and a HIGHER concentration in the blood.

These are typically eliminated/cleared by the KIDNEYS.

These would work WELL/NOT WELL for a prostate infection.

47
Q

Why should you generally not use a bacteriostatic antibiotic in combination with a bacteriocidal antibiotic?

A

Most bacteriocidal antibiotics require growth of the organism or formation of a protein to be effective.
Most bacteriostatic antibiotics inhibit protein synthesis or microbial growth.
Use of one would inhibit effectiveness of the other.

48
Q

What are the mechanisms by which bacteria acquire resistance?

A

Random mutation by individual bacteria
Natural selection: survivors live to replicate
Transformation
Transduction
Conjugation

49
Q

Discuss transformation in terms of resistance.

A

Recipient cell uptakes naked DNA from a donor cell

50
Q

Discuss transduction in terms of resistance.

A

Bacteriophage transfers the DNA

51
Q

Discuss conjugation in terms of resistance.

A

Transfer by direct contact between cells (sex)

52
Q

What is the most common type of antimicrobial resistance in veterinary medicine?
What adjustments have we made to try to combat this?

A

B-lactamases (break up the B-lactam ring of the B-lactam abx)

Add clavulanic acid to the B-lactam antibiotics (ie Unasyn, Timentin, Clavamox)- more resistant to B-lactamases.

53
Q

List/explain 4 ways to help avoid antimicrobial resistance

A
  1. De-escalate: if infection is life-threatening, start with a broad spectrum/aggressive antibiotic at highest dose that is safe (dead bugs don’t mutate) and then de-escalate to one drug or a lower tier of drugs once culture results are available. Also, shorten courses of antibiotics where appropriate.
  2. Design: choose the most appropriate antibiotic for the given bacteria and site (narrow spectrum)
  3. Decontaminate: reduce spread of bacteria between patients or from one area of the patient to another (bandages, gloves/gowns, hand washing, etc)
  4. Choose cases that warrant antibiotics carefully, do not use antibiotics when not indicated (ie pancreatitis, FLUTD without UTI, fever without evidence of infection).
54
Q

What are the general changes in efficacy as you go from first to second to third generation cephalosporins?

A

First generation is mainly gram +, little gram –

Second generation is equal

Third generation is mainly gram -, little gram +

55
Q

What are factors to consider when choosing an antibiotic regimen for your patient?

A
  • Likely pathogens (including likelihood of resistance)
  • Spectrum of activity of your antibiotic
  • Culture/sensitivity results (if available)
  • Side effects to the patient
  • Concurrent illnesses (ie hypoalbuminemia, renal disease)
  • Ability to penetrate into the affected area
  • Frequency/method of administration and ability of owners to comply
  • Duration of therapy
  • Cost?
56
Q

List 5 factors in critically ill patients that can affect pharmacokinetics of antibiotic therapy.

A
  1. Increased vascular permeability increases the volume of distribution (mostly for hydrophilic abx) 🡪 decreased plasma concentrations
  2. Increased drug clearance (shorter half life) due to increased cardiac index and fluid therapy increasing renal perfusion
  3. Decreased drug clearance if decreased renal or hepatic function is present 🡪 toxic effects
  4. Hypoalbuminemia 🡪 higher unbound fraction of antibiotics that are usually protein bound (none of the common ones we use)
  5. Impaired antibiotic penetration into tissues when septic shock is present (impaired microcirculation)
57
Q

Define hospital acquired/nosocomial infection

A

Infection that is contracted in-hospital (neither present or incubating when a patient is admitted)

Infection that develops at least 48 hours after hospitalization without proven prior incubation.

Infection occurring up to 3 days after discharge or within 30 days of a surgical procedure.

58
Q

List possible methods to reduce hospital acquired/nosocomial infections

A
  • Isolation of patients with known contagious infections
  • Hand washing/gloves
  • HEPA air filters
  • Sterilization of surgical equipment (steam or gas, avoid “cold sterile”)
  • Disinfect cages between patients
  • Sterile technique and wide clipping of fur when placing indwelling catheters (IV, urinary, or other)
  • Appropriate care of tubes after placement (ie Urinary catheter care)
  • Avoid disconnecting IV catheters, wipe injections ports prior to injections
  • Good nursing care to avoid bed sore wounds
59
Q

What are the main components of innate immunity?

A
  • Anatomic and physical barriers
  • Phagocytic and cytotoxic cells (granulocytes, NK lymphs, monocytes, macrophages, dendritic cells)
  • Inflammatory mediators
  • Complement
60
Q

What are the main components of acquired immunity?

A

B-lymphocytes (plasma cells produce antibiodies, Memory B-cells remember for next time)

T-lymphocytes (Cytotoxic T-cells, Helper T-cells, regulatory T-cells): recognize “non-self” cells after exposure

Antigen presenting cells (Macrophages, B-lymphs, dendritic cells)

61
Q

Draw a basic immunoglobulin molecule

A
62
Q

List the types of hypersensitivity reactions.

A

Type 1: Immediate, IgE mediated, T cell dependent

Type 2: Cytotoxic hypersensitivity

Type 3: Ag:Ab complexes

Type 4: delayed hypersensitivity. T cell mediated.

63
Q

Discuss type 1 hypersensitivity reactions and give an example.

A

immediate
IgE mediated, T-cell dependent 🡪 eosinophil recruitment 🡪 anaphylaxis

(ie any allergic reaction- vaccine, anaphylaxis, insect bite)

64
Q

Discuss type 2 hypersensitivity reactions and give an example.

A

cytotoxic hypersensitivity.
Antibodies formed against target antigens on cell membranes.

Complement mediated (ie IMHA, ITP)

Ab dependent cytotoxic (ie transfusion reactions)

Ab mediated of cell surface receptors (ie Myasthenia gravis)

65
Q

Discuss type 3 hypersensitivity reactions and give an example.

A

Ag:Ab complexes deposit in tissues 🡪 activate complement and induce acute inflammatory response.

(ie lupus, glomerulonephritis- esp Lyme)

66
Q

Discuss type 4 hypersensitivity reactions and give an example

A

delayed hypersensitivity.
T-cell mediated.
Intracellular parasites and soluble proteins 🡪 24-72 hour later, macrophage/monocyte response.
Requires previous sensitization to Ag.
(ie TB test, poison ivy)

67
Q

What is the classic initiator of sepsis?

A

LPS (gram -) binding to LPS binding protein on macrophages

68
Q

List the main pro-inflammatory mediators involved with sepsis:

A

TNFa
IL-1
IL-6
IL-8
IL-12
IF-g

69
Q

List the main anti-inflammatory mediators involved with sepsis:

A

IL-4
IL-10
TGF-b
glucocorticoids

70
Q

What is the difference between C-reactive protein and Activated Protein C? Do they go up or down with sepsis?

A

C-reactive protein: acute phase protein, increased in sepsis

Activated Protein C: anticoagulant protein, decreased in sepsis

71
Q

What is the best biomarker to use to determine sepsis from non-infectious SIRS?

A

We have not found one yet…

72
Q

List the positive acute phase proteins.

A

Increased during inflammation

  • Mannose binding protein
  • Fibrinogen
  • Haptaglobin
  • C-reactive protein
  • Serum amyloid A
  • AGP (alpha 1 acid glycloprotein)
  • Ceruloplasmin
73
Q

List the negative acute phase proteins.

A

decreased during inflammation

Albumin
Antithrombin: body becomes pro-thrombotic
Transferrin: less iron transport = less iron available for bacteria

74
Q

Discuss mannose binding protein

A

Positive acute phase protein

binds to mannose on bacteria, opsonizes them, initiates complement (lectin pathway)

75
Q

Discuss fibrinogen

A

Positive acute phase protein

increased in early inflammation, low levels indicate excessive coagulation/DIC

76
Q

Discuss Haptoglobin

A

Positive acute phase protein

inhibits microbial iron uptake

77
Q

Discuss C -reactive protein

A

Positive acute phase protein

binds to LPS on cell walls, opsonizes bacteria, activates classical pathway of complement

78
Q

Discuss serum amyloid A.

A

Positive acute phase protein

recruits immune cells

79
Q

Discuss AGP (alpha 1 acid glycloprotein)

A

Positive acute phase protein

Steroid carrier

80
Q

Discuss ceruloplasmin

A

Positive acute phase protein

carries copper, inhibits microbe iron uptake

81
Q

Define AMPs

A

antimicrobial peptides.

Present on mucosal surfaces to inhibit microbes.

Examples- digestive enzymes, enzymes that disrupt cell membranes, bind essential elements for bacteria, act as decoys for microbial attachment.

82
Q

Define PRRs

A

Pattern recognition receptors.

Expressed on immune cells to recognize patterns that are associated with pathogens or cell damage/danger.

83
Q

Define PAMPs

A

Pathogen associated molecular patterns.

Produced only by microbes, not the host.

84
Q

Define MAMPs

A

Microbial associated molecular patterns.

A more accurate term for PAMPs, as some of them are expressed by non-pathogens.

85
Q

Define DAMPs

A

Danger associated molecular patterns.

Expressed by endogenous cells in response to damage/infection or altered self.

86
Q

Define alarmins

A

another term for DAMPs

87
Q

Define CARS

A

Compensatory anti-inflammatory response syndrome.

Adaptive response to the excessive pro-inflammatory state with sepsis.

Can provide appropriate balance, or be over-exuberant 🡪 immunoparalysis and apoptosis of self cells.

88
Q

What conditions have been documented to lead to MODS?

A

Shock
sepsis
trauma
pancreatitis
ischemia (GDV, other volvulus)
auto-immune disease (ie IMHA)
heat stroke

89
Q

List organs/systems that can be affected by MODS

A

GI tract
Lungs
Cardiac
Liver
Kidneys
CNS
Coagulation
Mitochondria
Adrenal

90
Q

Effects of MODS on the GI tract

A

bacterial overgrowth, loss of mucosal barrier function (translocation), impaired motility, electrolyte abnormalities, vomiting/diarrhea.

91
Q

Effects of MODS on lungs

A

primary injury (pneumonia, contusions), increased permeability 🡪 ALI/ARDS

92
Q

Effects of MODS on the heart

A

myocardial dysfunction, arrhythmias

93
Q

Effects of MODS on the liver

A

impaired
gluconeogenesis/glycogenolysis (hypoglycemia)
reduced synthetic/metabolic functions
cholestasis (hyperbilirubinemia)
coagulopathy

94
Q

Effects of MODS on the kidneys

A

impaired perfusion and loss of GFR from afferent and efferent vasodilation (less common), renal cell apoptosis (histopath usually normal!) 🡪 increased renal values, decreased urine output

95
Q

Effects of MODS on the CNS

A

encephalopathy/depressed mentation

96
Q

Effects of MODS on the coagulation

A

activation of endothelium and platelets 🡪 hypercoagulable state 🡪 possible DIC

97
Q

Effects of MODS on the mitochondria

A

impaired cellular energy production (“cytopathic hypoxia”)

98
Q

Effects of MODS on the adrenals

A

CIRCI

99
Q

Define heatstroke

A

A form of hyperthermia associated with systemic inflammatory response leading to a syndrome of multiple organ dysfunction with encephalopathy.

100
Q

What are ways that the body typically copes with heat stress?

A
  • Peripheral vasodilation/central vasoconstriction to increase heat loss
  • Panting
  • Acute phase response protects against tissue injury and promotes repair
  • Heat shock proteins help cells compensate for acute episodes of hyperthermia
101
Q

List the 4 mechanisms of heat dissipation:

A
  1. conduction
  2. convection
  3. radiation
  4. evaporation
102
Q

Define conduction as a mechanism of heat dissipation

A

body loses heat by direct contact with a cooler object

103
Q

Define convection as a mechanism of heat dissipation

A

transfer of heat to cooler air as it passes over the body

104
Q

Define radiation as a mechanism of heat dissipation

A

body releases heat into the environment

105
Q

Define evaporation as a mechanism of heat dissipation

A

body loses heat by converting water into a vapor

106
Q

List endogenous predisposing factors for heatstroke

A
  • obesity
  • cardiovascular disease
  • neuro/neuromuscular dz
  • thick haircoat
  • upper airway abnormalities
107
Q

List exogenous predisposing factors for heatstroke

A
  • lack of acclimatization
  • high environmental temperature and/or humidity (esp with limited ventilation/shade)
  • water deprivation
  • medications (diuretics, B-blockers, phenothiazines)
108
Q

Explain your basic initial treatment/monitoring plan for a patient with heat stroke.

A
  • Active cooling until 103.1 F (cool water/fan, IVF)
  • Rehydration if dehydrated
  • Cardiovascular support if shocky (fluid therapy +/- pressors)
  • Intubation/Oxygen as indicated if dyspneic
  • Monitor of BG/supplementation with dextrose as indicated
  • Antibiotics if GI translocation is suspected
  • GI protectants
  • Medications for cerebral edema if indicated (once hydrated)
  • Monitoring of urine output
  • Transfusions may be needed if clinical coagulopathy
109
Q

List negative prognostic indicators that have been identified for patients with heat stroke.

A
  • Altered mental status (coma at presentation or progressive decline in mental status after admission)
  • Hypothermia at presentation
  • Hypoglycemia
  • Prolonged PT/PTT or other evidence of - DIC
  • Persistent hypotension
  • Elevated creatinine or oliguria despite fluid resuscitation
  • Ventricular arrhythmias
  • Elevated bili
  • Delayed admission to the hospital (>90 min)
  • Seizure activity
  • Obesity
  • High levels of high mobility group box-1 protein (humans)
  • Poor response to aggressive therapy in the first 12-24 hours

Boards Review (14 decks)

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