Alimentary Prophylaxis Flashcards

1
Q

What is the word for the movement of enteric organisms across the bowel wall?

A

Translocation

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2
Q

What is multiorgan failure?

A

Persistent inflammation and progressive dysfunction of 2 or more organ systems

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3
Q

What is the gut hypothesis?

A

Splanchnic hypo perfusion caused but hypoperfusion –> sepsis –> SNS activation –> splanchnic vasoconstriction

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4
Q

How much of the splanchnic blood supply goes to the gastric mucosa?

A

70-90%

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5
Q

What are the risk factors for stress ulcer bleeding?

A
Mechanical ventilation over 24 hours
Coagulopathy: platelets less than 50k, INR greater than 1.5, PTT greater than 2x control
Burns involving more than 30% of body
Shock
Sepsis
Trauma
TBI
Renal failure
Steroid therapy
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6
Q

What is clinically significant bleeding in the ICU?

A

A drop in bp or hgb by more than 2

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7
Q

What is the ph goal for using acid blockers in ICU?

A

Ph above 4

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8
Q

What are the 3 mechanisms of protection against microbial invasion in the alimentary tract?

A
  1. Stomach acid
  2. Mucosal barrier of bowel wall
  3. Reticuloendothelial system on extra luminal side of bowel wall
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9
Q

How long does ranitidine last?

A

6-8h

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10
Q

What is the typical dosing of ranitidine?

A

50 mg IV q 8h

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11
Q

How long does famotidine last?

A

20 mg lasts 10-15 hours

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12
Q

How are H2 blockers cleared?

A

Renally

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13
Q

What can happen if patients with renal failure is given H2 blockers intravenously?

A

They may accumulate and cause neurotoxicosis: confusion, agitation, seizures

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14
Q

What are the risks of using H2 blockers?

A

Infectious gastroenteritis
c. Dif
Aspiration pneumonia

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15
Q

What is MOA of PPI?

A

Binds irreversibly to the membrane proton pump and prevents gastric acid secretion

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16
Q

What are the advantages of ppi over H2 blockers?

A
  1. Greater reduction in acidity
  2. Longer duration of action
  3. Responsiveness does not diminish with continued usage
  4. Metabolized by the liver
17
Q

What are the risks of using PPI?

A

Higher risk of infectious gastroenteritis

Higher incidence of hospital acquired pneumonia and C.dif

18
Q

Which drug do PPI’s inhibit?

A

Clopidogrel because they are both metabolized by the same P450 enzyme.
Can reduce clopidogrel effect through competitive inhibition

19
Q

What is the disadvantage to sucralfate?

A

It binds other drugs in the lumen and inhibits their absorption

20
Q

Which drugs does sucralfate bind in the lumen?

A
Warfarin
Theophylline 
Tetracycline
Cipro
Norfloxacin
Digoxin
Ketoconazole 
Phenytoin
Ranitidine
Thyroxin
21
Q

Which drug (sucralfate or h2/PPI) was shown to cause less adverse events?

A

Sucralfate

22
Q

What are the benefits of enteral tube feeds?

A
  1. Trophic to gastric mucosa

2. Raises ph

23
Q

What is believed to be the inciting event in hospital acquired pneumonia?

A

Aspiration of mouth secretions into the upper airways

24
Q

What bacteria is the mouth of a critically ill patient usually populated with?

A

Aerobic gram negative bacilli: Pseudomonas,

25
Why do critically ill patient get colonization of pathogenic organisms in their mouth?
The epithelial receptors change
26
What is the change in micro flora in the mouth directly correlated with?
The severity of illness
27
Who benefits most from chlorhexidine washes of the mouth?
Cardiac patients
28
What is chlorhexidine most effective against?
Gram positives
29
What is selective oral decontamination?
Direct application of antibiotic to the buccal mucosa
30
What is the formula of SOD?
Gentamicin (gram negatives) Colistin (candida) Vanc (gram positives)
31
What are the benefits of SOD.
1. Reduced incidence of hospital acquired pneumona 2. Reduced incidence of bacteremia by gram negatives 3. Decline of tracheal colonization
32
What is the SDD formula?
10 ml of polymixin, tobramycin, amphotericin
33
Who is SDD recommended for?
ICU patients who will stay for more than 72 hours because it takes a week to decontaminate the gut
34
What organ metabolizes PPi?
Liver
35
What drug should not be used with PPi?
Plavix because it decreases its anti platelet activity