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t/f: stress induced ulcers are associated with a prior GI disease
false. not associated with prior GI disease. clinical outcome depends on severity of the current underlying disease
gastric acid secretions are normal except in which diseases?
sepsis and CNS injury (cause increase in gastric acid secretion)
how can you differentiate SUP and PUD
SUP= asymptomatic (indistinguishable from NSAID)
- superficial lesions in fundus and body (acid producing)
- perforations are RARE
- bleeding from superficial capillaries
PUD= characteristic sx
- some deep lesions in antrum and duodenum (not acid producing
- perforations COMMON
- bleeding from one large vessel
Curlings vs Cushings vs Drug induced ulcers
Curling's: burn pts. single lesion in duodenum that goes below muscle
Cushing: head trauma/ increased intracranial pressure. can happen anywhere, may perforate wall of viscus
Drug: looks same as stress ulcer!! dx based on clinical setting
RISK FACTORS FOR SUD
CSLN
critically ill with:
1. coagulopathy (plts <50k, INR>1.5, PTT >2x)
2. shock (<90)
3. chronic Liver disease
Neurocritical pt (brain, hemorrhage)
pathophys of stress induced ulcers
critical illness increases catecholamines and hypovolemia-> lower CO-> hypoperfusion which causes...
lower bicarb, lower blood flow, lower GI motility, acid back diffusion
==== acute stress ulcer
gold standard for stress ulcer dx
endoscopy
for stress ulcers, what do we want to maintain gastric pH above?
want to maintain above 4, ideally above 5-7
pharm options for SUD prophylaxis
H2RAs and PPIs
(want to maintain pH above 4, so sucralfate and antacids arent rlly effective)
H2RAs route for SUD prophylaxis
- via NG tube or PN
- IV push or continuous infusion
continuous infusion is more effective tho! NEED renal dosage adjustments (CrCl <30ml/min)-> give less
H2RAs ADEs
diarrhea
headache, drowsy, fatigue, confusion
thrombocytopenia!!! (4-7 days after initiation)
which SUD tx can lead to thromobcytopenia (less platelets)
H2RAs (also can cause fatigue and drowsiness)
t/f: if platelet count is <50k, you may consider switching PPI to H2RA
false. H2RA is the one that might induce thrombocytopenia
which SUD prophylaxis may be more helpful in pts with erosive esophagitis
PPIs
prophylaxis pantoprazole for SUD
administration and dose
pantoprazole IV: unstable in solution, needs dedicated line w filter. only stable for 12hrs
- 40mg daily
[compare to bleeding ulcer which was 80 bolus then 8mg/hr]
which PPIs are available as suspensions
omep, lanso, eso, panto
PPIs ADEs/ increased risk/ clinical pearls
well tolerated but may have headache, diarrhea, ab pain
risk: c. diff, pneumonia, osteoporosis
omep/eso: phenytoin, warfarin, diazepam (increases levels bc inhibits cyp2c19), also clopidogrel (attenuates/worsens)
t/f: all critically ill pts should be treated with SU prophylaxis
false. adults who are enterally fed and are at low risk for stress related UGIB do not need SUP
when is stress ulcer prophylaxis needed?
pts with 1+ risk factors
- coagulopathy
- shock
- chronic liver disease
- neurocritical
pt has 1+ risk factors and needs SUP. what is different in administration based on if their gut works
EN: give H2RA/PPI EN. if NG then stop suction 2hrs after administration
gut doesnt work: give IV
which SUP needs to be adjusted based on kidney fxn? how do you know when to adjust it?
H2RAs need to be adjusted if CrCl is <30ml/min
- give less
[also remember cimetidine has more DDIs]
dosing for the following for SUP
pantoprazole
esomeprazole
omeprazole
lansoprazole
famotidine
cimetidine
pantoprazole and esomeprazole: 40mg IV/NG/PO qd
omep: 40mg PO or NG qd
lanso: 30mg PO or NG qd
famotidine: 20mg IV/NG/PO BID!!
cimetidine: 300mg IV/PO/NG q6hrs!!!
remember H2RAs need adjustment if CrCl<30
and cimetidine has a lot of DDIs
when are PPIs required OVER H2RAs in SUD
1. recent UGIB
2. hypersecretory states (ex: ZES)
3. erosive esophagitis
4. HP infections
when do you d/c SUP prophylaxis?
- no more risk factors present
- before TO of ICU to prevent inappropriate prescribing