Exam 3 - Intraabdominal infections/C.Diff infections Flashcards Preview

Therapeutics V Spring 2019 (P3 Spring) > Exam 3 - Intraabdominal infections/C.Diff infections > Flashcards

Flashcards in Exam 3 - Intraabdominal infections/C.Diff infections Deck (44):
1

2 types of intraabdominal infections?

Peritonitis or abscess

2

definition of peritonitis

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

3

definition of abscess

-PURULENT collection of fluid separated from surrounding tissue by fibrinous capsule
-contains necrotic debris, bacteria, neutrophils

4

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

colon

5

what is the etiology of secondary peritonitis

- 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

6

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

has lots and lots normal flora?

biliary: 0

female genital: hella normal flora

7

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

when LOW acid!
achlorhydria, H2 antagonists, PPIs, antacids, gastric cancer, gastric outlet

8

Super common bacterial species of intraabdominal infections?

E.Coli
Streptococcus
B.Fragilis/other bacteriodes
Clostridium

9

Intraabdominal infections have pseduomonas infections in what most situations?

in situations where the pt caught the infection in the hospital

10

Pathophys of intraabdomial infections:
NORMALLY peritoneal fluid is STERILE, ___ in protein and leukocytes, and contains no _______

LOW in protein/leukocytes
no fibrinogen

11

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

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

12

What is "third spacing"

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

13

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

decreased
decreased
decreased...

14

Systemic GI responses to an intraabdominal infection?

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

15

Systemic cardio responses to intraabdominal infections?

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

16

Systemic renal responses to intraabdominal infections?

decreased renal perfusion = acute renal failure

17

Systemic metabolic responses to intraabdominal infections?

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

18

Role of facultative bacteria or anaerobes?
has virulence factors and are responsible for abscesses

anaerobes

19

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

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

20

Common symptoms of intraabdominal infections?

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

21

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

collect cultures!! AEROBIC AND ANAEROBIC

empiric therapy to cover enterbacteriaceae and bacteriodes species

22

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

enterbacteriaceae and bacteriodes species

23

what drugs typically cover anaerobes
(we rarely have to do susceptibility testing for anaerobes)

metronidazole
beta lactams + lactamase inhibitors
carbapenems

24

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]

enterococci

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)