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GI and liver > PUD > Flashcards

PUD Flashcards

1
Q

background info for peptic ulcers

A

Peptic ulcers require gastric acid for their formation
Three common types: Helicobacter Pylori induced, NSAID induced, Stress-related mucosal damage (SRMD)
Most common occurrences: Stomach, Duodenum*

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2
Q

ulcer definition

A

breaks in the mucosal surface over 5mm in

size, with depth to the submucosa

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3
Q

imbalances leading to mucosal damage

A

Increased gastric acid and pepsin secretion - increased tissue breakdown
Decreased bicarbonate, blood flow, and cell regeneration - decreased natural protection

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4
Q

risk factors for PUD

A

**H. Pylori
**NSAID use (don’t overlook PRN ibuprofen or ASA)
antiplatelet medications (ACS = DAPT), Smoking, Alcohol, Gastric acid
hypersecretion, Patient non-compliance, Viral infections, Vascular insufficiency, Radiation and chemotherapy

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5
Q

H. Pylori induced PUD

A

gram negative bacteria
most remain asymptomatic
no clear link to causing dyspepsia or GERD symptoms
30-40% of US population is infected - commonly acquired during childhood
transmission occurs person-to-person via oral-oral or fecal-oral
unique pathophysiology - facilitate residence, induce mucosal injury, avoid host defenses, induced inflammatory response

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6
Q

NSAID induced PUD

A

cause direct mucosal damage - cause intermucosal hemorrhages, progress to erosions with continued use,, worse if concominant H. Pylori, inhibit PGs
take with food
gastric ulcers occur in up to 25% of patients with continued use

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7
Q

established risk factors for NSAID induced PUD

A 
Age over 65
Previous peptic ulcer
Concomitant corticosteroid
Concomitant ASA
High-dose NSAID
NSAID + other drugs - antiplatelets (compound risk), anticoagulants (compound risk), bisphosphonates (irritant), SSRIs
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8
Q

potential risk factors for NSAID induced PUD

A 
NSAID-related dyspepsia
H. pylori infection
Rheumatoid arthritis
Alcohol consumption
Cigarette consumption
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9
Q

other PUD risk factors

A

antiplatelet use - ASA (increased with other NSAIDs), clopidogrel, DAPT, Hx of GERD or PUD, CS use, over 60 YO, anticoagulant use
cigarette smoking - mechanism unclear, risk proportional to number of cigarettes

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10
Q

complications of PUD

A

upper GI bleed - H Pylori and NSAID induced, bleeding caused by erosion of ulcer into an artery
perforation into the peritoneal cavity - surgical emergency, 1/3 to 1/2 caused by NSAIDs, pain is “sudden, sharp, and severe”
gastric outlet obstruction - mechanical obstruction of the intestines

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11
Q

clinical presentation of PUD

A

pain with food? stomach ulcer
pain after food (1-3 hours)? intestinal ulcer
epigastric pain - burning, fullness, cramping, nocturnal pain (patients wake up)
may be seasonal/cyclical (relapsing/remitting)
changes in character of pain
heartburn, belching, bloating
NV associated with weight loss

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12
Q

diagnosis of PUD

A

lab tests - Hgb and Hct may be low during active bleeds, stool hemoccult, test for HPylori
esopahgogastroduodenoscopy (EGD) - can be used to acutely treat ulcers, detects 90% of ulcers, direct inspection biopsy and visualization of active ulcers and bleeding, preferred for accurate diagnosis or concerns for bleeding

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13
Q

endoscopic diagnosis of HPylori induced PUD

A

histology - gold standard, tests for active infection
culture - allows for sensitivity testing for antibiotic use, use after 2nd line treatment failure
biopsy urease - HPylori produces ammonia which leads to color change, preferred test with endoscopy, rapid results
polymerase chain reaction - tests for HPylori DNA in gastric tissue, high rate of false positives and negatives

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14
Q

nonendoscopic diagnosis of HPylori induced PUD

A

antibody tests - unable to determine active or past infection, less specific and sensitive than endoscopic tests
urea breath test - HPylori breaks down ingested labeled C-urea and exhales labeled CO2, test for active infection, hold PPI or H2RA for 1-2 weeks and bismuth or antibiotics for 4 weeks
fecal antigen - blood with HPylori, test for active antigen, medications can cause false positive but to a lesser extent

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15
Q

patient presents with ulcer like symptoms….

A

Think 1) NSAID?? 2) HPylori??
on NSAID? stop it. decrease it. still sxs? PPI or H2RA still sxs?? endoscopy
hpylori?? serology or endoscopy. ulcer?? treat or test for HPylori. yes? treat and follow up. no? NSAID? evaluate need and consider COX-2 with PPI

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16
Q

goals of PUD therapy

A

Relieve pain and heal ulcers
Prevent ulcer recurrence
Eradicate H. pylori infection
NSAID-induced: Heal ulcer, Assess medication therapy

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17
Q

nonpharm PUD therapy

A

Reduce psychological
stress
Stop smoking
Avoid foods and beverages that worsen symptoms - Spicy foods, alcohol, caffeine, etc.
Use alternative agents to NSAIDs for pain if possible
Surgery

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18
Q

pharmacologic PUD options

A 
Antacids (see GERD section)
H2RAs
PPIs
Sucralfate
Misoprostol
Antibiotics (H. pylori only)
19
Q

H2RA dosing for PUD with an active ulcer***

A

cimetidine - 800 mg QHS, 400 mg BID, 300 mg QID
famotidine - 40 mg QHS, 20 mg BID
nizatidine - 300 mg QHS, 150 mg BID
ranitidine - 300 mg QHS, 150 mg BID

20
Q

H2RA dosing for PUD maintenance***

A

cimetidine - 400-800 mg QHS
famotidine - 20-40 mg QHS
nizatidine - 150-300 mg QHS
ranitidine - 150-300 mg QHS

21
Q

PPI dosing for an active ulcer***

A

dexlansoprazole: –
esomeprazole: 20-40 mg QD/BID
lansoprazole: 15-30 mg QD/BID
omeprazole: 20-40 mg QD/BID
pantoprazole: 40 mg QD/BID
rabeprazole: 20 mg QD/BID

22
Q

PPI dosing for maintenance***

A

dexlansoprazole: –
esomeprazole: 20-40 mg QD
lansoprazole: 15-30 mg QD
omeprazole: 20-40 mg QD
pantoprazole: 40 mg QD
rabeprazole: 20 mg QD

23
Q

sucralfate MOA

A

Mucosal protectant for duodenal ulcer
When exposed to acid and alkali - breaks down to insoluble aluminum/sucrose “paste”
Adheres to ulcer to protect and allow for healing

24
Q

sucralfate dosing

A

1 g QID OR 2 g BID***
administer on an empty stomach 2 hours before or 4 hours after other meds - protect from food and affects medication absorption

25
Q

misoprostol overview

A

synthetic PGE1 - replaces PGs inhibited by NSAIDs, also causes uterine contractions
reserved for refractory NSAID-induced mucosal damage
MOA - mucosal protectant, moderately inhibits acid secretion
MUST do a pregnancy test prior to initiation in women who can become pregnant

26
Q

misoprostol dosing

A

prophylaxis of NSAID-induced ulcers - 200 mcg PO TID to QID, doses under 400 mcg/day decrease protective effects

27
Q

misoprostol AEs

A

use-limiting

GI, NV, HA, dysmenorrhea

28
Q

treatment of non-NSAID, non-HPylori PUD

A

conventional therapy: H2RAs or sucralfate for 6-8 weeks or PPIs for 4 weeks
many have ulcer recurrence within one year after initial therapy
maintenance therapy may be indicated - prevent recurrence, prevent complications, may use PPIs, H2RAs or sucralfate

29
Q

treatment of HPylori PUD

A

initial tests - for all newly diagnosed patients, for young otherwise healthy patients with dyspepsia secondary to PUD, hx of PUD with unknown HPylori status
goal = eradicate HPylori
multidrug regimens - combine acid-suppression or mucosal protection PLUS one or more antibiotics, preferred PPI based regimen if on NSAID, high relapse rates without use of antibiotics

30
Q

PPI based regimens for HPylori PUD overview

A

1st line
10-14 days recommended
BID PPI dosing better than QD

31
Q

PPI based regimens for HPylori PUD**

A 
one of:
-omeprazole 20 mg BID
-lansoprazole 30 mg BID
-pantoprazole 40 mg BID
-esomeprazole 40 mg QD or 20 mg BID
-rabeprazole 30 mg BID
PLUS: clarithromycin 500 mg BID*
PLUS:
-amoxicillin 1 g BID
OR 
-metronidazole 500 mg BID
32
Q

bismuth based regimens for HPylori PUD

A

quadruple therapy = bismuth, PPI or H2RA, 2 antibiotics
2nd line after failure of PPI based therapy or if less expensive needed initially
duratoin = 10-14 days (PPIs can be 7 days)
eradication similar to PPI based
pro: cheap
con: increased dosing complexity and minor AEs

33
Q

bismuth based regimens for HPylori PUD***

A 
One of:
-omeprazole 20 mg BID
-lansoprazole 30 mg BID
-Pantoprazole 40 mg BID
-Esomeprazole 40 mg daily or
20 mg BID
-Rabeprazole 20 mg BID
-Cimetidine 800 mg HS,
400 mg BID, 300 mg QID
-Ranitidine 300 mg HS,
150 mg BID
-Famotidine 40 mg HS,
20 mg BID
-Nizatidine 300 mg HS,
150 mg BID
PLUS one of:
-bismuth subsalicylate 525 mg QID
-bismuth subcitrate 420 mg QID
PLUS: metronidazole 250-500 QID*
PLUS one of:
-tetracycline 500 mg QID
-amoxicillin 500 mg QID
-clarithromycin 250-500 mg QID
34
Q

treatment failure for HPylori PUD

A

methods: use antibiotics not previously used, extend duration to 14 days
sequential therapy: to decrease bacterial load with antibiotics not thought to face bacterial resistance (i.e. amoxicillin) then follow-up with another antibiotic more prone to resistance (metronidazole or clarithromycin), Superior eradication rates to PPI-based 3 drug regimens, Questionable adherence issues due to mid-treatment therapy change

35
Q

sequential therapy for HPylori PUD

A

days 1-5: PPI QD or BID + amoxicillin 1 g BID

days 6-10: PPI QD or BID + metronidazole 250-500 BID + clarithromycin 250-500 BID

36
Q

overview of treatment for NSAID induced PUD

A

Prevention is key - Misoprostol or PPIs
NSAIDs therapy changes: Discontinue, Use acetaminophen or other analgesics if possible, Lower to lowest effective dose, Change to more selective COX-2 inhibitor
PPIs more effective than H2RAs, misoprostol 200mcg BID (similar efficacy to 200mcg QID dose)

37
Q

dosing for prevention of NSAID induced PUD

A 
omeprazole 20 mg QD
lansoprazole 15-30 mg QD
raberprazole 20 mg QD
pantoprazole 40 mg QD
esomeprazole 20-40 mg QD
misoprostol 200 mcg 2-4 x/day
H2RAs? no shown efficacy for prevention of NSAID induced gastric ulcers, questionable for duodenal ulcer
38
Q

overview of prevention of NSAID induced PUD

A

COX-2 specific NSAIDs: Not as high risk of causing ulcers as non-selective NSAIDs, GI protective effects not seen when also taking daily aspirin, Past agents - increased cardiovascular adverse effects, Equivalent benefit to non-selective NSAID + PPI, Will not eliminate risk for gastric ulcers
-Celecoxib: Safest in regards to CV effects, Not considered to be COX-2 selective anymore by FDA and contains the same warning for GI effects
Avoid misoprostol as first line therapy
Naproxen preferred non-selective agent due to decreased CV risk compared to others (no added benefit for GI effects)

39
Q

selection of NSAIDs for PUD prevention

A

no/low CV risk - no ASA
high CV risk - need ASA
reason for NSAID?
no ASA:
-no/low GI risk: traditional NSAID alone
-moderate GI risk: traditional NSAID + PPI/misoprostol
-high NSAID GI risk: alternative or COX-2 selective +PPI/misoprostol
using ASA:
-no/low GI risk: naproxen + PPI/misoprostol
moderate GI risk: naproxen + PPI/misoprostol
high NSAID GI risk: avoid NSAIDs and COX-2 selective

40
Q

treatment of NSAID Induced Ulcers

A

if you can discontinue NSAID - PPI, H2RA or sucralfate for 6-8 weeks
If you must continue NSAID - PPI for 8-12 weeks
-Consider COX-2 selective or nonselective NSAID that is more COX-2 specific (ie: diclofenac)
-Use lowest effective NSAID dose
-May consider continuing PPI as long as NSAID is required

41
Q

antiplatelet induced PUD

A 
prophylaxis therapy for: combination of ASA + NSAID/COX2 selective, ASA or clopidogrel in high risk patient (2+ risk factor for patients), antiplatelet + anticoag
PPI preferred but use of PPI with clopidogrel is controversial - class effect?? (some say all, others say just omeprazole/esomeprazole while pantoprazole is safe), famotidine 20 mg BID may be effective in preventing complications related to ASA
42
Q

management of PUD in the ED/ICU

A

assess hemodynamic stability (i.e. active bleed) and resuscitate as needed
endoscopy within 24 hours of presentation - can be diagnostic and therapeutic
risk of bleeding?
-low - discharge after endoscopy with antisecretory therapy
-high - needs at least 72 hours of hospitaliztion (24 ICU)
goal of therapy: maintain pH above 6
do not use H2RAs
PPIs preferred - pantoprazole 80 mg IV loading dose followed by 8 mg/hr continuously for 72 hours

43
Q

patient education

A

proper drug administration
avoidance and management of AEs
compliance with HPylori eradication treatment
avoid triggers (foods/meds) that can aggravate PUD
to reduce NSAID related complications - develop alternate pain control, avoid multiple NSAIDS including OTC

GI and liver (10 decks)

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