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GI/Hepatic > SUP and Bleeding > Flashcards

SUP and Bleeding Flashcards

1
Q

What is the pathophysiology of stress ulcers?

A

decreased splanchnic blood flow secondary to hypovolemia, reduced cardiac output, proinflammatory mediator release, increased catecholamine release, and visceral vasoconstriction

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2
Q

What are additional factors contributing to the pathophysiology of stress ulcers?

A

decreased gastric mucosal bicarbonate production, decreased gastric emptying of irritants and acidic contents, acid back-diffusion, reperfusion injury follow restoration of blood flow after hypoperfusion

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3
Q

What is the most common cause of GI bleeds in the ICU?

A

Stress ulcers

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4
Q

When does superficial mucosal damage generally begin to occur after ICU admission?

A

within 1-2 days

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5
Q

When is stress ulcer prophylaxis not recommended?

A

in the non-ICU setting

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6
Q

What are the major risk factors for SUP?

A
  1. mechanical ventilation ≥ 48 hours
  2. Platelets < 50,000 and/or INR > 1.5
  3. Hx of GI ulceration or bleeding within past year
  4. burns > 35% BSA
  5. severe head or spinal cord injury
  6. multiple trauma
  7. perioperative transplant period
  8. low intragastric pH
  9. surgery lasting > 4 hours
  10. acute lung injury
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7
Q

What are the other risk factors?

A
  1. sepsis
  2. ICU stay > 1 week
  3. occult bleeding
  4. ≥ 250 mg/day of hydrocortisone or equivalent
  5. hepatic failure
  6. acute kidney injury
  7. hypotension
  8. anticoagulation
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8
Q

What are the treatment goals for SUP?

A
  1. prevent any bleeding

2. reduce acid secretion (pH > 4) or increase protective factors

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9
Q

What factors determine which agents to give for SUP?

A
  1. functioning GI tract
  2. adverse effects
  3. cost
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10
Q

What is the MOA of sucralfate?

A

forms a complex with positively charged proteins to form a substance that coats the stomach to protect gastric mucosa

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11
Q

In which patients should sucralfate not be used?

A

Renal dysfunction (it can cause aluminum toxicity)

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12
Q

What is sucralfate’s role in therapy?

A

Not a first line option

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13
Q

Which two treatment options require a functioning GI tract?

A

sucralfate and antacids

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14
Q

What is the MOA of antacids?

A

neutralize stomach acid

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15
Q

How often are antacids dosed?

A

q1-2h

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16
Q

What are the ADRs associated with antacids?

A

constipation, diarrhea, electrolyte abnormalities

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17
Q

What are antacids’ role in SUP?

A

Avoid use - last line option

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18
Q

Which two products can lead to toxicity in renal failure patients?

A

aluminum and magnesium

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19
Q

What is a major concern with antacids and an NG tube?

A

It can clog the NG tube

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20
Q

Which two H2RAs are available via IV?

A

Ranitidine and famotidine

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21
Q

What is the MOA of H2RAs?

A

inhibits histamine receptors of the gastric parietal cells to ultimately inhibits gastric acid secretion

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22
Q

What is the typical dosing of H2RAs?

A

BID dosing with renal adjustments

23
Q

What are the major ADRs of H2RAs?

A

mental status changes and thrombocytopenia

24
Q

Which H2RA should be avoided due to a high number of drug interactions>

A

cimetadine

25
Which PPIs are available via IV?
Esomeprazole and pantoprazole
26
What is the MOA of PPIs?
suppress the parietal cells H+/K+ ATP pump to raise gastric pH
27
What are the major ADRs of PPIs?
diarrhea, constipation, nausea, nosocomial pneumonia, and c-diff
28
What is the role of therapy for PPIs?
first line
29
Which sign/symptom indicates treatment failure of SUP?
hematemesis
30
What are the monitoring parameters for SUP?
signs and symptoms of bleeding
31
When should SUP therapy be discontinued?
1. when risk factors resolve | 2. before transferring to the general floor
32
What are the four categories of GI bleeds?
1. upper 2. lower 3. occult 4. obscure
33
What is an upper GI bleed?
pharynx to ligament of Treitz
34
What is the most common GI bleed?
Upper (4 times more common than lower)
35
What is an occult GI bleed?
unknown to the patient
36
What is an obscure GI bleed?
unknown location in GI tract
37
What are the two types of GI bleeds?
variceal and non-variceal
38
What is a variceal bleed?
esophageal or gastric varices that rupture
39
What is non-variceal bleeding caused by?
peptic ulcers (H. pylori), stress ulcers, aspirin, NSAID use, and Mallory-Weiss tears
40
What are the signs and symptoms of a GI bleed?
1. hematemesis 2. melena 3. hematochezia 4. N/V 5. anemia 6. tachycardia 7. hypotension 8. fatigue 9. weakness 10. abdominal pain 11. hemodynamic instability
41
What is the initial priority in a GI bleed?
hemodynamic status/stability
42
When should fluids or a blood transfusion be given?
when Hg falls below 7
43
What are the two diagnostic exams for GI bleed?
esophagogastroduodenoscopy for upper GI bleed and colonoscopy for lower GI bleed
44
When should the EGD or colonoscopy be performed
When the patient is stable (ideally in the first 24 hours)
45
What treatments can be performed during the EGD or colonoscopy?
1. sclerotherapy (high saline drug) 2. thermal coaptive therapy 3. hemostatic clip placement
46
What is the most efficacious therapy for GI bleed?
sclerotherapy + copative therapy
47
What is the pharmacological treatment of a GI bleed?
1. remove contributing meds 2. give fluids or transfusion 3. discontinue anticoagulants and use reversal agents 4. acid suppression therapy
48
What is the goal pH to prevent clot dissolution?
≥ 6
49
What medications should be used for acid suppression?
PPIs (IV options: esomeprazole and pantoprazole)
50
What is the typical dosing for IV PPIs?
80 mg bolus, followed by 8 mg/hr infusion x 72 hours
51
How long should PPI therapy be continued post-endoscopy?
72 hours
52
How long should oral PPI therapy be continued for a non-H. pylori bleed?
6-8 weeks
53
What happens if you can't stop NSAID therapy?
Switch to COX-2 selective agent like celecoxib
54
When can aspirin be resumed for a secondary prevention?
as soon as possible after bleeding stops (usually 7 days)

GI/Hepatic (4 decks)

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