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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
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

45
Q

what is a complicated intra-abdominal infection

A

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
Q

secondary peritonitis etiology

A

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
Q

bacterial drug reactions in intraabdominal infection

A

bacterial counts can increase 10 ^ 5-7 in h2 antagonists, PPI, antacids, gastric cancer, gastric outlet obstruction, hemorrhage

48
Q

most frequent organism in intra-abdominal infections

A

p. aeruginosa

49
Q

what increased levels of normal flora can lead to complicated intra-abdominal infections

A
  • e. coli
  • strep
  • bacteroides
50
Q

intra-abdominal infection pathogenesis

A

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
Q

bacterial synergy in intraabdominal infection

A

combination of aerobic and anaerobic organisms are more lethal than infections caused by either alone

52
Q

diagnostric studies for intra abdominal infection

A
  • peripheral leukocytosis (>15-20,000) with left shift
  • elevated hematocrit and BUN
  • distention
  • ct
  • blood culture
53
Q

overall treatment option for intra abdominal infection

A

surgery and antimicrobial therapy

54
Q

surgery treatment for intra abdominal infection

A

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
Q

when to begin antimicrobial therapy for intra abdominal infection

A

begin empiric IV therapy immediately after obtaining appropriate cultures

56
Q

what should empiric therapy cover for intra abdominal infection

A

enterobacteriaceae and bacteroides

57
Q

treatment for intra abdominal infection: mild to moderate severity single agents

A

cefoxitin
ertapenem
tigecycline

58
Q

treatment for intra abdominal infection: mild to moderate severity combo agents

A

cefazolin, cefuroxime, ceftriaxone, cefotaxime, cirpo, or levo in combo with metronidazole

59
Q

treatment for intra abdominal infection: high risk or severe single agents

A

imipenem
meropenem
doripenem
pip/tazo

60
Q

treatment for intra abdominal infection: high risk or severe combo agents

A

cefepime, ceftazidime, cipro, or levo in combo with metronidazole

61
Q

empiric therapy for healthcare-associated intra-abdominal infections

A 
meropenem
doripenem
imipenem
pip/tazo
ceftazidime + metronidazole
cefepime + metronidazole
62
Q

empiric enterococcal therapy for intra abdominal infection

A

ampicillin
pip/tazo
vanc

PHRM 865 (59 decks)

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