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PHRM 865 > Exam 3 - Intraabdominal infections/C.Diff infections > Flashcards

Exam 3 - Intraabdominal infections/C.Diff infections Flashcards

1
Q

2 types of intraabdominal infections?

A

Peritonitis or abscess

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2
Q

definition of peritonitis

A

acute, inflammatory response of the PERITONEAL LINING in response to bacterial invasion, chemical irritation, irradiation, or foreign body injury

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3
Q

definition of abscess

A
  • PURULENT collection of fluid separated from surrounding tissue by fibrinous capsule
  • contains necrotic debris, bacteria, neutrophils
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4
Q

what part of the GI tract has a lot of anaerobes in their normal flora

A

colon

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5
Q

what is the etiology of secondary peritonitis

A
  • results from a focal disease process within the abdomen
  • bacteria usually enter the peritoneum as a result of disruption of the integrity of the GI tract by disease, injuries, surgery, or from local lesions of the female genital tract
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6
Q

Biliary tract or female genital tract:
has 0 normal flora?

has lots and lots normal flora?

A

biliary: 0

female genital: hella normal flora

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7
Q

in the STOMACH, bacterial counts increase up to 10^5-7 organisms/mL in what situations?

A

when LOW acid!

achlorhydria, H2 antagonists, PPIs, antacids, gastric cancer, gastric outlet

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8
Q

Super common bacterial species of intraabdominal infections?

A

E.Coli
Streptococcus
B.Fragilis/other bacteriodes
Clostridium

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9
Q

Intraabdominal infections have pseduomonas infections in what most situations?

A

in situations where the pt caught the infection in the hospital

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10
Q

Pathophys of intraabdomial infections:

NORMALLY peritoneal fluid is STERILE, ___ in protein and leukocytes, and contains no _______

A

LOW in protein/leukocytes

no fibrinogen

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11
Q

Pathophys of intraabdomial infections:
Serous fluid containing leukocytes/high protein concentration, and fibrinogen moves into peritoneum:
Fibrinogen polymerizes forming _____

A

adhesions (by forming plaques of fibrinous exudates on the inflamed peritoneal surface and begins to form adhesions)

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12
Q

What is “third spacing”

A

it is a fluid and protein shift – fluid moves to the peritoneal cavity

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13
Q

“Third spacing”: (decreased or increased)
_____ circulating blood volume
_____ cardiac output
_____ blood pressure

A

decreased
decreased
decreased…

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14
Q

Systemic GI responses to an intraabdominal infection?

A

initially diarrhea then bowel paralysis because of low perfusion –> distention b/c no poops

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15
Q

Systemic cardio responses to intraabdominal infections?

A

fluid going into peritoneal = decrease circulating blood volume/decrease venous return/decreased cardiac output/hypotension/

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16
Q

Systemic renal responses to intraabdominal infections?

A

decreased renal perfusion = acute renal failure

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17
Q

Systemic metabolic responses to intraabdominal infections?

A

increased energy demands deplete glycogen stores = catabolism of muscle/fat =weight loss

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18
Q

Role of facultative bacteria or anaerobes?

has virulence factors and are responsible for abscesses

A

anaerobes

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19
Q

Role of facultative bacteria or anaerobes?
produce extracellular enzymes to promote tissue invasion
and
provide environment conductive to growth for other bug

A

facultative
(these bugs use up the O2 which helps anaerobes grow)
(also they make enzymes to help anaerobes to get in)

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20
Q

Common symptoms of intraabdominal infections?

A 
stomach pain (distension)
Thirst (bc fluid in abdomen)
Decreased urination (bc ^)
cant pass gas/feces
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21
Q

Treatment of Secondary Peritonitis intraabdominal infections? (pharm and non-pharm)

A

collect cultures!! AEROBIC AND ANAEROBIC

empiric therapy to cover enterbacteriaceae and bacteriodes species

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22
Q

what two bugs are to cover empirically for Secondary Peritonitis intraabdominal infections?

A

enterbacteriaceae and bacteriodes species

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23
Q

what drugs typically cover anaerobes

we rarely have to do susceptibility testing for anaerobes

A

metronidazole
beta lactams + lactamase inhibitors
carbapenems

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24
Q

For intraabdominal infections: HEALTHCARE ASSOC.

want to have empiric therapy against _______ when..
[previous cephalosporin therapy,
pts who are immunocompromised,
if infection source is biliary tract,
pt has valvular hear disease or prosthetic intravascular material]

A

enterococci

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25
Enterococci is typically covered by what 3 drugs?
ampicillin pip/tazo vanc
26
General Treatment guidelines for intraabdominal infections? (2 things)
1 -- DRAIN IT -- surgery | 2 -- Antimicrobial therapy (enterbacteriaceae and bacteriodes)
27
Examples of Primary Peritonitis?
Kids -- nephrotic syndrome/post necrotic cirrhosis Adults: hepatic failure/ascites Alcoholic cirrhosis CAPD (infection with peritoneal dialysis)
28
Primary Peritonitis: | if hepatic failure -- what is the most common pathogen?
E.Coli
29
Primary Peritonitis: | if Peritoneal dialysis -- what is the most common pathogen?
staphylococci (skin flora) | streptococci
30
Primary Peritonitis: | if kids -- what is the most common pathogen?
Strep pneumoniae
31
Etiology of C.Diff bugs?
gram + anaerobic SPORE forming
32
what is BI/NAP1/027 - a type of _____ - a _____ strain
a type of C.Diff | virulent
33
BI/NAP1/027: - hypo or hyper sporulating - decreased or increased toxins A/B
hyper | increased
34
BI/NAP1/027: | has increased disease severity and has high resistance to _______
fluoroquinolones
35
Definition of CDI (C.Diff infection): presence of unexplained new- onset diarrhea: ___ or more _____ stools in _____ hours ALSO positive stool test for _______ or any histopathologic findings revealing pseudomembranous
3 or more UNFORMED stools 24 hours + test for C. Diff toxins
36
what are the 4 critical components of C. Diff infection pathogenesis
disruption of colonic microflora source of C.Diff (endogenous flora or exogenous source) organism must have potential to produce toxin multiple diff. individual risk factors
37
what are risk factors for C Diff infection
``` abx use (the longer the higher risk) duration of hospitalization advanced age physical proximity to a C Diff pt presence of a comorbidity use of PPIs or H2RAs chemo surgery immunosuppresion/HIV poor serum antibody response to c. diff toxins ```
38
what clinical markers indicate SEVERE C.Diff?
leukocytosis > 15,000 | or SCr > 1.5
39
Treatment of CDI: | Initial episode - non-severe?
``` vanc fidoxamicin or metro (last line) ```
40
Treatment of CDI: | Initial episode - severe?
vanc | fidoxamicin
41
Treatment of CDI: | Initial episode - fulminant?
vanc + metronidazole | may give rectally
42
Treatment of CDI: | First recurrence
vanc (give vanc differently - tapered) | fidoxamicin (if vanc used 1st)
43
Treatment of CDI: | Second or subsequent recurrence
vanc tapered vanc + rifampin or rifamixin?? (check ya notes) or poop transplant
44
what is the monoclonal antibody for C.Diff and how does it work
Bezlotoxumab | binds to toxin B
45
what is a complicated intra-abdominal infection
infections contained within the peritoneal cavity (extends from the diaphragm to the pelvis) or the retroperitoneal space) extends below the hollow viscus organ into the peritoneal space and are associated with peritonitis or abscess formation
46
secondary peritonitis etiology
bacteria usually enter the peritoneum as a result of disruption of the integrity of the GI tract by diseases, injuries, surgery, or from local lesions of the female genital tract
47
bacterial drug reactions in intraabdominal infection
bacterial counts can increase 10 ^ 5-7 in h2 antagonists, PPI, antacids, gastric cancer, gastric outlet obstruction, hemorrhage
48
most frequent organism in intra-abdominal infections
p. aeruginosa
49
what increased levels of normal flora can lead to complicated intra-abdominal infections
- e. coli - strep - bacteroides
50
intra-abdominal infection pathogenesis
Inoculum causes bacteria to disseminate --> serous fluid containing leukocytes, high protein concentration, and fibrinogen move into peritoneum --> fibrinogen polymerizes forming plaques of fibrinous exudates on the inflamed peritonieal surface and begins to form adhesions
51
bacterial synergy in intraabdominal infection
combination of aerobic and anaerobic organisms are more lethal than infections caused by either alone
52
diagnostric studies for intra abdominal infection
- peripheral leukocytosis (>15-20,000) with left shift - elevated hematocrit and BUN - distention - ct - blood culture
53
overall treatment option for intra abdominal infection
surgery and antimicrobial therapy
54
surgery treatment for intra abdominal infection
stop continuing bacterial contamination by repairing perforations and resection or removal of infected organs; remove foreign material COLLECT AEROBIC AND ANAEROBIC SPECIMENS FOR GRAM STAIN, CULTURE, SUSCEPTIBILITY TESTING
55
when to begin antimicrobial therapy for intra abdominal infection
begin empiric IV therapy immediately after obtaining appropriate cultures
56
what should empiric therapy cover for intra abdominal infection
enterobacteriaceae and bacteroides
57
treatment for intra abdominal infection: mild to moderate severity single agents
cefoxitin ertapenem tigecycline
58
treatment for intra abdominal infection: mild to moderate severity combo agents
cefazolin, cefuroxime, ceftriaxone, cefotaxime, cirpo, or levo in combo with metronidazole
59
treatment for intra abdominal infection: high risk or severe single agents
imipenem meropenem doripenem pip/tazo
60
treatment for intra abdominal infection: high risk or severe combo agents
cefepime, ceftazidime, cipro, or levo in combo with metronidazole
61
empiric therapy for healthcare-associated intra-abdominal infections
``` meropenem doripenem imipenem pip/tazo ceftazidime + metronidazole cefepime + metronidazole ```
62
empiric enterococcal therapy for intra abdominal infection
ampicillin pip/tazo vanc

PHRM 865 (59 decks)

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