Peptic ulcer disease Flashcards

1
Q

What is ulcer?

A

Ulcer is a break in the continuity of epithelial surface

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2
Q

Where is peptic ulcer seen?

A

Peptic ulcer develops in/close to acid secreting areas in stomach (gastric ulcer) and proximal duodenum (duodenal ulcer). Can occur in the esophagus or in Meckel’s diverticulum.

Peptic ulcer : from lower esophagus > stomach/duodenum > rarely ileum adjacent to Meckel’s diverticlum

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3
Q

How does peptic ulcer occur?

A
  • Peptic ulcers are produced by the imbalance between gastro-duodenal mucosal defense mechanisms and damaging forces of gastric acid and pepsin together with superimposed injury from environmental or immunologic agents (spicy food)
  • mucous membrane lining the digestive tract erodes and cause break down of tissue which manifests clinically as burning pain in the the upper middle part of the abdomen
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4
Q

Gastric ulcer or duodenal ulcer is more common?

A

Duodenal ulcer

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5
Q

List the age group for gastric ulcer and duodenal ulcer
List the male:female predilection in which ulcer

A

Gastric ulcer :
Age group : 55-70 years old
M:F : Female predominance

Duodenal ulcer :
Age gorup : 30-55 year old
M:F : Male predominance

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6
Q

Etiology of peptic ulcer disease

A
  • Helicobacter pyori infection (80%)
  • Worsened by drugs (NSAID, Aspirin, Corticosteroid)
  • Smoking, alcohol, stress, diet
  • Acid hyper secretory state (Zollinger Ellison Syndrome : islet cell pancreas produce gastrin)
  • Head injury, Intracranial tumor/infections : Cushing ulcer (increase in intracranial pressure lead to overstimulation of vagus nerve, increase in gastric acid secretion leading to gastro-duodenal ulcer
  • Severe Burns : Curling’s ulcer (reduce plasma volume lead to ischemia and necrosis of gastric mucosa casing it to slough off)
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7
Q

Possible damaging actions of H.pylori ?

A

1) increase gastric acid secretion
2) loss of protective mucous layer
3) increased secretion of pepsinogen and gastrin
4) decreased duodenal bicarbonate secretion

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8
Q

NSAIDs induced ulcer

A
  • long time use of NSAID are more commonly associated with gastric ulcers than duodenal ulcer
  • complications of patient : more commonly ulcer related which can irritate the lining of stomach and small intestine
  • Action : inhibit the production of enzyme cyclo-oxygenase (COX) that produces prostaglandins and these hormone like substances help protect stomach lining from chemical and physical injury
  • Examples : aspirin, ibuprofen, naproxen, ketoprofen
  • celecoxib, etorocoxib less likely cause gastric ulcer (COX 2 inhibitor)
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9
Q

Effects of smoking on peptic ulcer disease

A
  • Increased rate of gastric emptying
  • Diminished pancreatic bicarbonate secretion
  • Decreased duodenal pH
  • Reduced mucosal blood flow
  • Inhibition of mucosal prostaglandins
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10
Q

Clinical features of peptic ulcer disease

A
  • Recurrent epigastric pain which is burning pain and gnawing (hunger pain)
  • may be symptomless
  • occasional dyspepsia (indigestion)
  • acid/water brash
  • complications : hemorrhage, perforations, pyloric obstruction (stenosis) with vomiting
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11
Q

Symptoms of PUD

A
  • Burning pain
  • Nausea
  • Unexplained weight loss
  • Appetite changes
  • Vomiting
  • Low blood cell count (anemia)
  • Frequent burping or hiccuping
  • Bloating
  • Water brash
  • Hematemesis (vomiting of blood)
  • Melena
  • Blood in the stools
  • Stomach pain wakes you up at night
  • An early sense of fullness with eating
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12
Q

Gastric vs duodenal ulcer

A

Duodenal ulcer :
- burning, gnawing, aching, hunger-like pain, primarily in the epigastric region.
- pain may occur or worsen when stomach is empty, usually 2-3 hours after a meal
- can occur at night between 11pm and 2am when acid tends to be the greatest
- feel better when eat or drink and then worse 1 or 2 hours later (duodenal ulcer)
- Relieving factor is eating

Gastric ulcer :
- epigastric region
- pain soon after eating
- feel worse when you eat or drink
- not relieved by eating or taking antacids
- relieving factors is vomiting

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13
Q

Complications of peptic ulcer disease

A
  • gastrointestinal bleeding : (most common complication)
    ulcer erodes one of the blood vessels
    — slow blood loss : anemia
    — severe blood loss : hospitalization or blood transfusion
  • perforation : erosion in gastro intestinal wall by ulcer leads to spillage of stomach/intestinal content into the abdomina cavity.
    — perforation at anterior surface of stomcah : acute peritonitis (initially chemical then later bacterial peritonitis
    — first sign : sudden intense abdominal pain
    —perforation at posterior : pancreatitis (pain often radiates to the back
  • Penetration : ulcer continues into adjacent organs (liver and pancreas)
  • Scar tissue : scaring and swelling causes narrowing in duodenum and gastric outlet obstruction (pyloric stenosis).
    —- patient often presents with severe vomiting (obstruction of food through digestive tract causing fullness easily and to vomit and lose weight.
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14
Q

Investigations done on peptic ulcer disease

A

1) Endoscopy (choice of investigation)
2) Barium studies (may be done before endoscopy)
3) Gastric acid/serum gastrin levels
4) Biopsy
5) Blood test (show anemia)
6) Stool (occult blood)

H.pylori can be diagnosed by
- non invasive tests: serology, fecal antigen assay, urea breath test
- invasive tests : biopsy urease test, histology, culture

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15
Q

Management of peptic ulcer disease

A

1) Dietary modifications (frequent small meals with no fried foods)
2) Smoking cessation
3) Alcohol moderation

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16
Q

Treatment of peptic uler disease

A

1) acid neutralizaing / inhibitory drugs
2) mucosal protective agents
3) eradication of h.pylori

acid neutralizing / inhibitory drugs
- antacids : neutralize existing stomach acidd and can provide rapid pain relief
- H2 receptor antagonist (histamine blocker) : reduces HCL release into digestive tract, reduces ulcer pain, encourage healing (EXAMPLES : RANITIDINE, FAMOTIDINE, CIMETTIDINE)
- Proton up inhibitor (PPI) :
(1) reduces acid by blocking the action of pumps in acid secreting cells. (EXAMPLES : OMEPRAZOLE, LANSOPRAZOLE, RABEPRAZOLE, ESOMEPRAZOLE)
(2) promote healing of peptc ulcer
(3) inhhibit h.pylori

mucosal protective agents
- promotes healing by enhancing the mucosal defense mechanism
- NOT USED AS 1ST LINE TREATMENT (ppi and h2 blocker is more effective)
- EXAMPLES : BISMUTH SUBSALICYLATE, MISOPROSTOL (INDICATED IN PT WITH NSAID THERAPY THAT CANNOT BE WITHDRAWN)

H.Pylori infection
- Triple Therapy for 7 days (90 % effective + little risk of relapse)
- 2 antibiotics and 1 ppi (AMOXICILLIN, CLARITHROMYCIN, OMEPRAZOLE)
antibiotics :
- AMOXICILLIN (1mg BD)
- CLARITHROMYCIN (500mg BD)
- METRONIDAZOLE (USED IN PT WITH PENICILLIN SENSITIVITY)
ppi :
- OMEPRAZOLE (20mg)
- LANSOPRAZOLE (30mg)
- PANTOPRAZOLE (40mg)
- RABEPRAZOLE (20mg)

17
Q

Surgery

A

Vagotomy : cutting branch of vagus nerve that signals stomach for secretion of gastric acid
Antrectomy : distal 3rd of stomach is excised (pyloric antrum)
Pyloroplasty : widen the lower part of stomach so that stomach contents can empty into duodenum
Tying off an artery : -
Gastroduodenal anastomosis : end to end joining of upper part of stoamch and duodenum after resecting lower stomach

18
Q

Time period of healing of gastric and duodenal ulcer

A
  • Duodenal ulce : 4 weeks
  • Gastric ulcer : 8 weeks