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Therapeutics 5 Kappa Epsilon > 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

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)

20
Q

Common symptoms of intraabdominal infections?

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

22
Q

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

A

enterbacteriaceae and bacteriodes species

23
Q

what drugs typically cover anaerobes

we rarely have to do susceptibility testing for anaerobes

A

metronidazole
beta lactams + lactamase inhibitors
carbapenems

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

25
Q

Enterococci is typically covered by what 3 drugs?

A

ampicillin
pip/tazo
vanc

26
Q

General Treatment guidelines for intraabdominal infections? (2 things)

A

1 – DRAIN IT – surgery

2 – Antimicrobial therapy (enterbacteriaceae and bacteriodes)

27
Q

Examples of Primary Peritonitis?

A

Kids – nephrotic syndrome/post necrotic cirrhosis
Adults: hepatic failure/ascites
Alcoholic cirrhosis
CAPD (infection with peritoneal dialysis)

28
Q

Primary Peritonitis:

if hepatic failure – what is the most common pathogen?

A

E.Coli

29
Q

Primary Peritonitis:

if Peritoneal dialysis – what is the most common pathogen?

A

staphylococci (skin flora)

streptococci

30
Q

Primary Peritonitis:

if kids – what is the most common pathogen?

A

Strep pneumoniae

31
Q

Etiology of C.Diff bugs?

A

gram +
anaerobic
SPORE forming

32
Q

what is BI/NAP1/027

  • a type of _____
  • a _____ strain
A

a type of C.Diff

virulent

33
Q

BI/NAP1/027:

  • hypo or hyper sporulating
  • decreased or increased toxins A/B
A

hyper

increased

34
Q

BI/NAP1/027:

has increased disease severity and has high resistance to _______

A

fluoroquinolones

35
Q

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

A

3 or more
UNFORMED stools
24 hours

+ test for C. Diff toxins

36
Q

what are the 4 critical components of C. Diff infection pathogenesis

A

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
Q

what are risk factors for C Diff infection

A 
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
Q

what clinical markers indicate SEVERE C.Diff?

A

leukocytosis > 15,000

or SCr > 1.5

39
Q

Treatment of CDI:

Initial episode - non-severe?

A 
vanc
fidoxamicin
or metro (last line)
40
Q

Treatment of CDI:

Initial episode - severe?

A

vanc

fidoxamicin

41
Q

Treatment of CDI:

Initial episode - fulminant?

A

vanc + metronidazole

may give rectally

42
Q

Treatment of CDI:

First recurrence

A

vanc (give vanc differently - tapered)

fidoxamicin (if vanc used 1st)

43
Q

Treatment of CDI:

Second or subsequent recurrence

A

vanc tapered
vanc + rifampin or rifamixin?? (check ya notes)
or poop transplant

44
Q

what is the monoclonal antibody for C.Diff and how does it work

A

Bezlotoxumab

binds to toxin B

Therapeutics 5 Kappa Epsilon (27 decks)

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