Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

therapeutics V > Gastrointestinal and Intra-abdominal Infections > Flashcards

Gastrointestinal and Intra-abdominal Infections Flashcards

(77 cards)

Start Studying
1
Q

What type of organism is C. difficile?

A

Gram-positive, spore-forming, obligate anaerobic bacillus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How is C. difficile transmitted?

A

Fecal-oral route via ingestion of spores, often healthcare-associated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which C. difficile strain is associated with higher severity?

A

BI/NAP1/027 strain – more virulent, associated with worse outcomes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which antibiotics are high risk for CDI?

A

Fluoroquinolones, clindamycin, 3rd/4th generation cephalosporins, carbapenems.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are non-antibiotic risk factors for CDI?

A

Age ≥ 65, hospitalization, immunosuppression, GI surgery, acid suppression, chemotherapy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are hallmark symptoms of CDI?

A

Profuse, watery or mucoid green diarrhea and abdominal pain; may also see fever and leukocytosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is CDI diagnosed?

A

≥3 unformed stools in 24 hours + lab confirmation using NAAT, GDH antigen + toxin assay.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do you interpret: GDH + / Toxin – / NAAT + ?

A

Indicates potential CDI; positive NAAT suggests toxigenic strain. Treat if clinical signs are present.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How is non-severe CDI classified?

A

WBC ≤ 15,000/mcL and SCr < 1.5 mg/dL.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How is severe CDI classified?

A

WBC > 15,000/mcL or SCr > 1.5 mg/dL.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is fulminant CDI?

A

CDI with hypotension, shock, ileus, or toxic megacolon.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are first-line treatments for initial non-severe CDI?

A

Fidaxomicin 200 mg PO Q12H x 10 days or vancomycin 125 mg PO Q6H x 10 days.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

When is metronidazole used in CDI?

A

Only for fulminant CDI as adjunct or if other options unavailable.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is first recurrence of CDI treated?

A

Fidaxomicin (standard or extended), vancomycin, or vancomycin taper/pulse if previously used.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is second recurrence of CDI treated?

A

Change therapy again (e.g., switch agent, consider extended fidaxomicin, taper/pulse vancomycin).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is fulminant CDI treated?

A

Vancomycin 500 mg PO Q6H + metronidazole 500 mg IV Q8H ± rectal vanco if ileus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the role of bezlotoxumab in CDI?

A

Monoclonal antibody that binds toxin B; reduces recurrence risk. Given IV once during treatment.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the fecal microbiota products for recurrence prevention?

A

Rebyota (rectal admin) and Vowst (oral capsules) given after treatment.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are potential limitations of FMT products like Rebyota and Vowst?

A

Cost, availability, delivery method (rectal or multi-capsule oral regimen), side effects.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How should patients be counseled on probiotics for CDI prevention?

A

Probiotics are not strongly supported; may interact with antibiotics. If used, space from antibiotics and choose reputable strains (e.g., Lactobacillus, Saccharomyces).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What type of organism is C. difficile and what is its clinical significance?

A

C. difficile is an anaerobic, Gram-positive, spore-forming bacillus. It causes infectious diarrhea, often associated with antibiotic use.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the major risk factors for developing CDI?

A

Recent antibiotic use, age ≥65, hospitalization, immunocompromised state, GI surgery, and acid suppression.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How is CDI diagnosed?

A

≥3 unformed stools in 24 hours and positive lab testing (NAAT or GDH + toxin assay); imaging for severe/fulminant cases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How is CDI classified as non-severe, severe, or fulminant?

A

Non-severe: WBC ≤15,000, SCr <1.5. Severe: WBC >15,000 or SCr >1.5. Fulminant: shock, ileus, or toxic megacolon.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are first-line treatments for initial CDI episodes?
Fidaxomicin or vancomycin; metronidazole only used in fulminant cases or if other agents are unavailable.
26
How is recurrent CDI treated?
Use a different first-line agent, tapered/pulsed vancomycin, extended fidaxomicin, or bezlotoxumab for recurrence prevention.
27
What are options for CDI recurrence prevention?
Bezlotoxumab (monoclonal antibody) or microbiota-based products like Rebyota and Vowst after antibiotic treatment.
28
What is the first-line antibiotic for initial non-severe and severe CDI?
Fidaxomicin 200 mg PO BID for 10 days.
29
What is an alternative to fidaxomicin for CDI?
Vancomycin 125 mg PO QID for 10 days.
30
When is metronidazole used in CDI treatment?
Used only in fulminant CDI as adjunct to vancomycin or if first-line agents are unavailable.
31
What is the mechanism of action of fidaxomicin?
Inhibits RNA polymerase, resulting in bactericidal activity against C. difficile with minimal impact on normal gut flora.
32
What is the mechanism of action of vancomycin?
Inhibits bacterial cell wall synthesis by binding D-Ala-D-Ala terminus of cell wall precursors.
33
What is the mechanism of action of metronidazole?
Forms free radicals that damage DNA in anaerobic bacteria.
34
What is the advantage of fidaxomicin over vancomycin?
Lower recurrence rates and narrower spectrum activity; preserves normal gut microbiota.
35
What is bezlotoxumab and when is it used?
A monoclonal antibody against C. difficile toxin B; used with antibiotics to prevent recurrence.
36
What are the most important patient-specific risk factors for developing CDI?
Age ≥65, antibiotic exposure, hospitalization, GI surgery, acid suppression, chemotherapy, immunosuppression.
37
Which antibiotics are most associated with increased risk of CDI?
Clindamycin, fluoroquinolones, cephalosporins (especially 3rd/4th gen), carbapenems.
38
What symptoms should prompt CDI testing?
≥3 unformed stools in 24 hours and no other obvious cause.
39
Why should repeat testing for cure not be performed in CDI?
NAAT and antigen tests may remain positive even after clinical resolution.
40
When should empiric CDI therapy be started before test results?
In fulminant cases with high suspicion, start empiric therapy without delay.
41
What are common treatment options for recurrent CDI?
Vancomycin taper/pulse, fidaxomicin (standard or extended), fecal microbiota transplant (FMT), or bezlotoxumab.
42
What are preferred oral agents for CDI and why?
Fidaxomicin and vancomycin are preferred due to minimal systemic absorption and direct activity in colon.
43
What are key counseling points for CDI medications?
Take all doses as prescribed, monitor for symptom improvement, maintain hydration, and isolate if hospitalized.
44
What are the two major categories of intra-abdominal infections (IAIs)?
Uncomplicated (confined within a single organ) and complicated (extend beyond organ, may cause peritonitis).
45
What are common types of intra-abdominal infections?
Appendicitis, diverticulitis, cholecystitis, cholangitis, peritonitis, intra-abdominal abscesses.
46
Which patient population is at highest risk for spontaneous bacterial peritonitis (SBP)?
Patients with cirrhosis and ascites due to bacterial translocation.
47
How do patients with SBP typically present?
Fever, abdominal pain/tenderness, altered mental status, hypotension.
48
How is SBP diagnosed?
Ascitic fluid with PMN count ≥250 cells/mm³; cultures help identify pathogen.
49
What are the most common pathogens in SBP?
E. coli, Klebsiella pneumoniae, Streptococcus spp.; typically monomicrobial.
50
What is the treatment for SBP?
Cefotaxime or ceftriaxone IV; treat for 5 days.
51
What are the most common pathogens in secondary peritonitis?
Polymicrobial: Enterobacterales, anaerobes (Bacteroides), Streptococcus spp., and sometimes Enterococcus.
52
How does secondary peritonitis present?
Abdominal pain, fever, nausea, vomiting, leukocytosis; may have diffuse tenderness and imaging evidence.
53
What are the treatment pillars for secondary peritonitis?
Source control (e.g., drainage, surgery) and empiric broad-spectrum antibiotics.
54
What empiric IV antibiotics are appropriate for complicated IAI with no drainage possible?
Piperacillin-tazobactam, cefepime + metronidazole, or meropenem.
55
What are oral antibiotic options for step-down therapy in IAI?
Amoxicillin-clavulanate or ciprofloxacin + metronidazole, based on local susceptibility data.
56
What oral regimen covers Enterococcus faecalis, E. coli, and Bacteroides fragilis?
Amoxicillin-clavulanate.
57
What oral regimen covers E. coli and Enterobacter cloacae?
Ciprofloxacin + metronidazole.
58
What oral regimen covers VRE, E. coli, Proteus, Bacteroides, and Peptostreptococcus?
Linezolid + ciprofloxacin + metronidazole.
59
What oral regimen covers Streptococcus anginosus, Pseudomonas, and Enterococcus?
Ciprofloxacin + amoxicillin or ciprofloxacin + metronidazole + amoxicillin.
60
What oral regimen covers Enterobacter cloacae, Citrobacter freundii, and Bacteroides fragilis?
Ciprofloxacin + metronidazole.
61
How are intra-abdominal infections (IAIs) classified?
As uncomplicated (within a single organ) or complicated (involves peritoneal cavity, may require drainage or surgery).
62
What are the most common pathogens associated with intra-abdominal infections?
Enterobacterales (e.g., E. coli), anaerobes (e.g., Bacteroides fragilis), Streptococcus spp., and sometimes Enterococcus.
63
What is the typical presentation of spontaneous bacterial peritonitis (SBP)?
Fever, abdominal pain, altered mental status, hypotension, and ascitic PMN ≥250 cells/mm³.
64
What is the empiric treatment for spontaneous bacterial peritonitis (SBP)?
Cefotaxime or ceftriaxone IV for 5 days.
65
What is the role of source control in secondary peritonitis?
Surgical or percutaneous intervention is essential to remove the infection source (e.g., abscess, perforated bowel).
66
What empiric IV therapies are used in complicated secondary peritonitis?
Piperacillin-tazobactam, cefepime + metronidazole, or meropenem.
67
What oral regimens can be used for step-down therapy in IAI?
Amoxicillin-clavulanate or ciprofloxacin + metronidazole, tailored to susceptibility data.
68
What empiric IV antibiotic regimens are appropriate for complicated IAI?
Piperacillin-tazobactam, cefepime + metronidazole, or meropenem.
69
What oral antibiotic regimens are appropriate for step-down IAI therapy?
Amoxicillin-clavulanate or ciprofloxacin + metronidazole, based on pathogen susceptibility.
70
What agents cover anaerobes in IAI?
Metronidazole, piperacillin-tazobactam, and carbapenems (e.g., meropenem).
71
What is the role of vancomycin in IAI?
Not typically used unless MRSA or VRE is a concern; rarely needed empirically in IAI.
72
What is the mechanism of action of piperacillin-tazobactam?
Piperacillin inhibits bacterial cell wall synthesis; tazobactam inhibits beta-lactamases.
73
What is the mechanism of action of cefepime?
A 4th generation cephalosporin that inhibits bacterial cell wall synthesis.
74
What is the mechanism of action of metronidazole?
Forms free radicals in anaerobic organisms that damage DNA and cause cell death.
75
What is the mechanism of action of meropenem?
A carbapenem that inhibits bacterial cell wall synthesis and resists most beta-lactamases.
76
What is the mechanism of action of ciprofloxacin?
A fluoroquinolone that inhibits DNA gyrase and topoisomerase IV, disrupting bacterial DNA replication.
77
What is the mechanism of action of amoxicillin-clavulanate?
Amoxicillin inhibits cell wall synthesis; clavulanate inhibits beta-lactamase enzymes.

therapeutics V (29 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions