Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Gastroenterology Exam 1 > Peptic Ulcer disease and Gastritis > Flashcards

Peptic Ulcer disease and Gastritis Flashcards

1
Q

mucosal defect in the gastrointestinal tract (gastric or duodenal) exposed to acid and pepsin secretion

A

peptic ulcer disease

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

Epithelial cell damage and regeneration with or no associated inflammation

  • secondary to endogenous or exogenous irritants
A

Gastropathy

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

precursor to PUD and it is clinically difficult to differentiate the two. it denotes inflammation assoicated with mucosal injury

  • Histologic diagnosis
  • usually due to H.pylori (infectious) or other conditions
A

Gastritis

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

cuases of non H.pylori gastritis

A

Chemical gastritis (acute and chronic)

  • alcohol-induced gastritis
  • drug-induced gastritis (e.g, NSAID)
  • reflux (due to duodenal juice or bile) gastritis
  • other chemical gastritis

Radiation
allergic
autoimmune
duodenitis

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

Prostaglandins- the primary factor mediating cytoprotection

  • Stimulate bicarbonate and mucus production
  • help maintain adequate mucosal blood flow

Prostaglandin deficiency is final common pathway to injury

A

Mucosal cytoprotection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  • Ulcerated lesion in the mucosa of the stomach or duodenum
  • types: Gastric, duodenal
A

Peptic Ulcers

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

signs and symptoms of PUD?

A
  • Epigastric pain is most common symptom
  • pain described as gnawing or burning
  • may radiate to the back (consider penetration)
  • occurs 1-3 hours after meals or at night
  • relieved by food, antacids (duodenal) or vomiting (gastric)
  • dyspepsia including belching/bloating
  • hematemesis or melena with GI bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

alarm symptoms of PUD?

A

require early/urgent endoscopy

  • > 50 yrs old
  • bleeding
  • anemia
  • early satiety
  • unexplained weight loss
  • dysphagia or odynophagia
  • recurrent vomiting
  • family hx of GI cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Complications of PUD?

A
  • bleeding- most common complication
  • gastric outlet obstruction
  • perforation- may lead to free perforation or posterior perforation into pancreas with secondary pancreatitis #1 cause of pneumoperitoneum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
  • More common than gastric ulcers
  • always non-malignant
  • almost always in bulb (except for hypersecretory states (zollinger ellison syndrome or gastrinoma)
  • patient will report feeling better after eating= weight gain
A

Duodenal ulcer considerations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
  • although almost always benign, has malignant potential
  • therefore, repeat endoscopy recommended after course of acid suppresion
  • document healing, biopsy for malignancy
  • patient feel worse with eating= weight loss
A

gastric ulcer

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

NSAID induced gastritis or ulcers are frequently?

A

“silent”

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

which NSAIDs is considered High risk for development of PUD?

A
  • Piroxicam/ Feldene
  • ketorolac/ toradol
  • indomethacin/ indocin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Patients at risk for NSAID-induced PUD

A
  • Prior hx of an adverse GI event (ulcer hemorrhage) increase risk four to five fold
  • age > 60 increases risk five to sixfold
  • high (more than twice normal) dosage of a NSAID increases risk 10fold
  • concurrent use of glucocorticoids increases risk four to fivefold
  • concurrent use of anticoagulants increases risk 10-15fold
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
  • Spiral shaped, gram (-) rod with flagella
  • most common cause of PUD
  • transmission route fecal-oral
  • secrets urease–> convert urea to ammonia
  • produces alkaline environment enabling survival in stomach
A

H. Pylori

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

Differentiating between H.pylori and NSAID- induced ulcer

A

Ulcers associated with H.pylori

  • More oftne in duodenum
  • often superficial
  • less severe GI bleeding

Ulcers associated with NSAIDS

  • More often in stomach
  • often deep
  • more severe GI bleeding
  • sometimes asymptomatic
16
Q

Physical exam findings in PUD?

A

Uncomplicated

  • epigastric tenderness
  • bowel sounds -normal
  • rectal exam may show melena/ guaiac +stoll from occult blood loss
  • signs of peritonitis with perforation

GI bleed

  • look for signs of volume depeletion: tachycardia, hypotenstion, orthostatics, skin tugor, MM appearance
  • look for signs of anemia: conjunctiva or skin pallor, new heart murmur
17
Q

diagnosis of peptic ulcer disease?

A
  • Upper endoscopy with biopsy: diagnostic test of choice
  • endoscopy with biopsy: gold standard in diagnosing H. pylori infection
  • urea breath test: noninvasive. H.pylori converts labeled urea into labeled carbon dioxide
  • H.pylori stool antigen: useful in diagnosing H.pylori & confirming eradication after therapy
  • serologic antibodies: only useful in confirming H.pylori infection not eradication (antibodies can stay elevated long after eradication
18
Q
  • Endoscopy indicated in the following high risk patients?
A
  • > 50 years old with new onset dyspepsia
  • dyspepsia with dysphagia and/or weight loss
  • evidence of GI bleeding
  • failed appropriate trial of empiric therapy
  • using NSAIDs or other high risk meds
  • signs of UGI tract obstruction (early satiety, vomiting)
  • genetic background assoc. with increased UGI malignancies
19
Q
  • useful for intial diagnosis + confimation of eradication
  • sensitivity and specificity over 90% (false positives are rare)
  • urease activity iis present in the stomach in those infected with H. pylori
  • ingest urea labeled with radioactive carbon
  • hydrolysis or urea–> labeled carbon dioxide
  • rapidly absorbed into bloodstream and within a few minutes, appears in breath
  • false negative with PPI, bismuth, antibiotics
A

Urea breath test

20
Q
  • Useful in initial diagnosis + confirmation of eradication
  • test requires collection of stool samply- size of acorn
  • performed in lab
  • requires little preparation, however patients may not be compliant with collecting sample
  • false negative PPI, bismuth, antibiotics
  • test 4 weeks after treatment
A

H. pylori stool antigen test

21
Q
  • office based test that is faster but less acurate than lab-based Elisa tests
  • sensitivity and specificity of approx 90%
  • not useful for evaluating eradication- antibody levels can persist for long time, need serial titers to evaluate
  • ELISA to detect IgG antibodies to H.pylori (does not determine if active H.pylori infection)
A

serology

22
Q

when is serology testing useful?

A
  • patients who never received H.pylori treatment
  • symptomatic patients not using NSAIDS- if negative serology- unlikely PUD
    not useful in elderly populations to detect active disease prevalence; populations with low disease prevalence
23
Q

treatment for non H.pylori PUD?

A

OTC neutralizers

  • Aluminum and magnesium hydroxide salt (Maalox, mylanta) - not used in treatment but pts may have used them
  • calcium carbonate
  • bismuth subsalicylate (binds to ulcer base forming a protective coat, has anti-inflammatory and bacteriocidal properties- can cuase dark stools

H2 blockers
PPIs
Surgery

24
Q
  • Selectively block receptors on parietal cells reducing acid secretion
  • used primarily in ulcer disease not associated with H. pylori
  • famotidine, cimetidine
  • treatment duration is 6-8 wk
  • not #1 treatement option (that PPI)
A

H2 blockers (most OTC)

25
Q

Side effects of Cimetidine

A
  • Elderly patients- confusion
  • young males- impotence +/- gynecomastia
  • may alter levels of other drug- warfarin
  • may alter renal function requiring lower doses
  • likely not a first choice but is available otc
26
Q
  • Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump
  • relieve pain and heal peptic ulcers more rapidly than H2 blockers
  • drugs in this class are equally effective
  • treatment length depends on location, etiology and complications
  • omeprazole, lansoprazole, pantoprazole
A

Proton pump Inhibitors

PPI> H2 blocker in efficacy for NSAID related PUD

27
Q

what if you can’t d/c the NSAIDs in PUD?

A
  • try to get to the lowest dose that is tolerable
  • sucralfate: binds proteins in exudates and forms viscous adhesive that protects GI lining
  • misoprostol: prostaglandin analog- protects lining of GI tract by replacing depleted prostaglanding E1. Prevents peptic ulcers in patients taking NSAIDs
  • misoprostol and lansoprazole for high risk patients taking nonselective NSAIDS
28
Q

Surgical options for non-H.pylori PUD?

A
  • antrectomy with vagotomy
  • truncal vagotomy with pyloroplasty
  • highly selective vagotomy
29
Q

H.Pylori triple therapy treatment? Quadruple therapy?

A
  • triple therapy for 14 days is treatment of choice
  • clarithromycin based triple therapy (PPI + clarithromycin +amoxicillin) substitute metronidazole in pen allergic
    * bismuth based quadruple= bismusth subsalicylate+tetracycline +metronidazole +PPI
30
Q

why doesn’t treatment?

A
  • # 1 =adequate patient compliance
31
Q

failure treatment for PUD?

A
  • Retest for presence of H.pylori (can’t use serology)
  • retreat if positive
  • reinforce compliance and education
  • switch treatment if you trust they took the previous treatment correctly (treat with PPI, lefofloxacin and amoxicillin- 10 days)
32
Q

Subsequent management of DU, GU?

A
  • DU: don’t repeat EGD unless symptoms persist
  • GU: surveillance EGD in 8-12 weeks
33
Q
  • Neuroendocrine tumors that produce gastrin
  • symptoms similar to typical peptic ulcer
  • symptoms may be controlled by standard doses of antisecretory drug
  • patients may not be tested for hypergastrinemia
  • most patients are diagnosed between the ages of 20 and 50
  • gastrinomas can be sporadic or associated with multiple endocrine neoplasia type 1
A

Zollinger Elison Syndrome

34
Q

red flags of ZES?

A
  • multiple ulcers
  • diarrhea (significant diarrhea)
  • ulcer in atypical site (usually in the bulb and antrum of stomach; Would see in body, lower abdomen)
  • resistant ulcer
  • enlarged folds
  • severe esophagitis
  • family hx of MEN 1
35
Q

diagnosis ZES?

A
  • fasting gastrin level (usually 3x higher than normal level)
  • secretin stimulation test (secretin will normally suppress gastrin release, in ZES, gastrinoma cells are stimulated by secretin)
  • imaging
36
Q

ZES treatment

A

Omeprazole effectively controlled acid output in all patients

Gastroenterology Exam 1 (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions