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Cellular Week 3 > Infection Term/Sepsis > Flashcards

Infection Term/Sepsis Flashcards

1
Q

Host

A

An entity in which microorganisms reside and/or replicate; an entity in which microbial pathogenesis occurs

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2
Q

Damage

A

Disruption in the normal homeostatic mechanisms of a host that alter the functioning of cells, tissues, or organs. Can be caused by host and/or microbe.

  • -Microorganisms produce mediators that can alter organ function or hijack cellular function.
  • -The host’s cellular response can cause collateral damage. For example toxic oxygen radicals released by phagocytes to kill a microbe also may impair the function or integrity of the host cells.
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3
Q

Yersinia pestis - infectious disease pathology?

A

co-opts normal function of macrophages - stops signal that they have been invaded (dampened immune response)

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4
Q

colonization

A

a state of infection that results in a continuum of damage from none to great, with the latter leading to the induction of host responses that could eliminate or retain the microbe, or progress chronicity or disease

another def: a state of host-microoranism interaction that leads to a variable amount of host damage, from minimal to great, thereby reflecting host immune responses that have the capacity to eliminate the microorganism or to promote the development of another state

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5
Q

mutualism

A

a state of infection whereby both the host and the microorganism benefit

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6
Q

commensalism

A

a state of infection that results in either no damage or clinically inapparent damage to the host, though it can elicit and immune response

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7
Q

disease

A

a clinical outcome of host damage that occurs after a threshold amount of damage has occurred

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8
Q

microbial infection

A

the acquisition of a microorganism by a host

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9
Q

virulence

A

the relative capacity of a microorganism to cause damage in a host

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10
Q

pathogen

A
    • term of 1880s
    • some have argued that this term should be eliminated from the lexicon of microbiology and infectious disses
    • so called non-pathogens were recognized as causing disease (ex. coagulase negative staphylococci and diphtherioids –both are skin flora that can cause major disease)
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11
Q

latency

A

a state of host-microorganism interaction in which a microorganism persists in a host and can be associated with damage that can be evident at the cellular or tissue level, but is not associated with disease

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12
Q

virulence factor

A

a microbial component that can damage a host

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13
Q

examples of virulence factor?

A

toxins
enzymes (often degradative - Dnase, elastase)
enzymes - catalases, phosphatoases, dismutases
proteins that impair signaling

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14
Q

opportunist

A

causes disease when the host is impaired - can be due to pharmacologic agents that alter immunity or a genetic defect

ex. aspergillus (in those that are neutropenic)

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15
Q

streptococci can cause skin infections - can also cause disease in immunocompromised pts.

A

…

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16
Q

two goals with pathogens?

A

eradicate it

limit tissue damage associated with inflamm

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17
Q

if you have a weak immune system, give therapy that enhances the immune response/inflammation to lessen disease/host damage (increase neutrophils etc)

A

…

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18
Q

if you have a too strong response, give therapy that reduces immune response/inflamm. Give steroids - can be dangerous though because they are so nonspecific!

A

…

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19
Q

host benefits, microbe does not?

A

fecal transplantation

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20
Q

host benefits, microbe neutral?

A

intestinal flora synthesizes vitamen k and host provides niche for nutrients.

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21
Q

host does not benefit, microbe does?

A

microbe causes disease

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22
Q

host does not benefit, microbe is neutral?

A

infection in dead end hosts, i.e. the organism will no longer be transmitted

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23
Q

pathogens that can cause disease in only strong immune responses?

A

helicobacter pylori
SARS associated cornavirus
whipples agent
theoretical agents

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24
Q

pathogens that cause damage across the spectrum of immune responses but damage can be enchanted by strong immune responses

A 
shigella
mycoplasma pneumoniae
mumps 
chalamydia 
trypanosoma
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25
Q

pathogens that cause damage primarily at the extremes of both immune repsonses

A

aspergillus and vaccina virus

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26
Q

pathogens that cause damage in the setting of appropriate immune responses and produce damage at both ends of the continuum of immune responses

A

staph aureus
mycobacterium tb
herpes
HIV

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27
Q

pathogens that cause damage either in hosts with weak immune responses or in the setting of normal

A

strep pneumoniae
candida albincas
arboviruses
toxoplasma gondii

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28
Q

pathogens that only cause damage in the setting of weak immune respnoses

A

staph epidermis

pneumocystis carinii

29
Q

exposrue refers to risk of contact with a microbe

A

…

30
Q

isoniazid for Tb

For tb - you have a period of latency after infection before reactivation and disease

A

..

31
Q

Neisseria meningitidies - go from exposure, to colonization, to infection (no latency).

A

..

32
Q

If you give antibiotics to a patient, the may have elevated prothrombin time. This is because wiped out normal flora that produce vitamin K!!! Produce menaquinones for vit K production.

A

…

33
Q

Reduced immune system can allow for candida albicans to grow in immune compromised individuals! (chemotherapy) We are normally colonized by them in a commensalistic relationship.

A

…

34
Q

Candida Albicans disease route

A

exposed at birth in vaginal tract
commensalism
disruption of gut epithelium
infection or diease

35
Q

definition of sepsis

A

systemic response to an infectious agent that could be bacterial (common), viral, or fungal

36
Q

typical responses in sepsis? (4)

A

change in temp (fever or hypothermia)
tachycardia
tachypnea
alteration in WBC count (typically up but can be low)

37
Q

humoral responses to sepsis

A
  • complement
  • coagulation cascade - Protease activated receptors (PAR) are the link between coagulate band inflammation. high levels of thrombin activate these receptors (PAR1) and this causes disruption of the endothelial cell-barrier function
  • pro inflammatory mediators (IL-1)
  • anti-inflamm mediatorys (IL-10)
38
Q

metabolic response to sepsis?

A

increase ACTH

glucocorticoids

39
Q

what are the benefits of bodily changes in sepsi?

A

increased WBC - fight infection
tachycardia - increase CO
tachypnea - increase ventilation
fever - temp inhibits microbial growth

40
Q

benefits of complement in sepsis

A

opsonizes organisms, pro inflamm

41
Q

benefits of pro inflamm cytokines in sepsis

A

helps to mobilize WBCs to sites of infection

42
Q

benefits of anti-inflamm mediates in sepsis

A

prevents excessive damage to tissues

43
Q

benefits of coagulation in sepsis

A

helps to seal off infection and prevent dissemination

44
Q

benefits of changes in metabolic response in infection

A

preserves normal glucose, mobilizes energy stores

45
Q

what is severe sepsis/septic shock?

A

sepsis +evidence of insufficient organ perfusion and oxygen delivery, leading to organ dysfunction.
SHOCK DOES NOT EQUAL HYPOTENSION!

46
Q

YOU DO NOT HAVE TO BE HYPOTENSIVE TO BE IN SHOCK.

A

…

47
Q

def of shock?

A

insufficient organ perfusion and oxygen delivery

48
Q

Signs of severe sepsis…

A

at least two of

  • temp >38.3 or <36
  • HR>90
  • RR >20
  • WBC >1200 or <4000 or >10% bands

and 1 sign of significant organ dysfunction

49
Q

signs of significant organ dysfunction?

A 
lactate >2 mmol/L
INR >1.6 or aPTT>60
platelets <100,000
total bilirubin >2.0 mg/dl
creatine >2.0 mg/dl
urine output <0.5 mg/kg/hr
systolic BP <90 or MAP <65
50
Q

What are the first steps in treating severe sepsis? (w/n 3 hrs of arrival - optimally w/n 1 hr)

A

initial lactate measurement
2 blood cultures prior to antibiotic. culture lines too.
broad spectrum IV
fluid resuscitation with 30 mL/kg crystalloid fluids
admit to suitable level of care (usually ICU)

51
Q

the longer you wait for tx of shock, the worse the outcome for the pt

A

…

52
Q

mortality rate for sepsis

A

30 to 35% for adults

10% for children

53
Q

pathogen associate factors in shock?

A

overgrowth and tissue invasion causes direct tissue and organ injury
bacteria also release endotoxin/exotoin (leads to both direct tissue/organ injury but also inflamm cell recruitment)

54
Q

host response to sepsis causes what factors in shock?

A

complement, coagulation, o2 and n2 radicals, proteases if excessive or uncontrolled can lead to direct tissue/ organ injury

55
Q

gram positive causes of sepsis?

A

staph aureus

strep pneumoniae

56
Q

gram negative causes of sepsis?

A

e coli
klebsiella sp.
pseudomonas aeruginosa

57
Q

usual sites of organ damage upon presentation with severe sepsis?

A

lung
kidney (usual)
liver
CNS (2nd highest)

58
Q

Lung damage from sepsis?

A

impaired gas exchange requiring exogenous o2 or ventilation

59
Q

kidney damage from sepsis?

A

impaired glomerular filtration rate as evidence by increase in creatinine

60
Q

liver damage from sepsis?

A

increase in liver enzymes - typically AST and ALT

61
Q

CNS damage from sepsis?

A

loss of consciousness
delirium
confusion

62
Q

Tx for sepsis?

A 
Hemodynamic support 
Control infection with antibiotics
Ventilation for reps failure
Nutrition 
Dialysis if renal failure
CNS support-sedation
63
Q

Antibiotic approach for sepsis? - overview

A

Most initial therapy is empirical

Delayed or inappropriate antibiotic therapy is associated with higher mortality

64
Q

choices of antibiotics for sepsis

A
  • vancomycin for gram positives + a third generation cephalosporin for gram negatives
  • if you think the pt has pseudomonas (neturopenic/on ventilator, etc) then cefipime of piperacillin/tazobactam
  • if pseudomonas is not part of your consideration, then ceftriaxone is fine
65
Q

alternatives for gram neg

A

ciproflaxacin - good for pseudomonas

carbapenems (imipenem/meropenem) - these should be used for highly resistant gram negatives (ESBLs)

66
Q

alternatives for vanco?

A

daptomycin (if worried about MRSA)

ceftriaxone(if not worried about MRSA)

67
Q

when appropriate, deescalate antibiotics to make them match the sensitivity of the organism. For example, do not need a carbapenem to treat penicillin sensitive pneumococcus

A

…

68
Q

post-sepsis immune paralysis

A

following tx, period of weeks to months where pt is vulnerable to new infection
WBC will be normal
will have defective DC’s and macrophages, buildup of trigs, and TGFbeta (antiinflamm)

Cellular Week 3 (21 decks)

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