Peptic Ulcer Disease - Gastrointestinal

Snapshot
A 45-year-old male presents to the clinic for black stool for the past day. He reports intermittent epigastric pain that is worse with food intake for the past 4 months. The pain is described as dull, 6/10, nonradiating and improves with antacids. He reports a 5-lb. unintended weight loss but denies diarrhea, constipation, cancer history, or fevers. A physical examination is unremarkable.
Introduction
Clinical definition characterized by erosion and defects in the mucosal lining of the stomach, duodenum, and sometimes the lower esophagus that persist as a function of the acid or peptic activity in gastric juice gastric ulcers describe ulcers occurring at the stomach duodenal ulcers describe ulcers occurring at the duodenum duodenal ulcers abdominal pain is relieved with food intake the majority (90%) of cases are secondary to Helicobacter pylori gastric ulcers abdominal pain is exacerbated with food intake the leading causes are H. pylori followed by nonsteroidal anti-inflammatory drugs (NSAIDs) Epidemiology demographics ulcer incidence increases with age H. pylori is the predominant cause of peptic ulcer disease (PUD) worldwide increasing prevalence of NSAID-related PUD due to widespread use of aspirin and NSAID risk factors NSAIDs smoking stress age Pathogenesis development of ulcers is secondary to the disruption of normal protective mechanisms of the gastric mucosa (e.g., bicarbonate) H. pylori secretion of urease creates an alkaline environment which allows for the survival of the bacteria inflammatory cytokines inhibit parietal cell acid secretion causing gastric ulcers at the pyloric antrum, somatostatin production is reduced and gastric production is increased, leading to metaplasia of the duodenal cells and causing duodenal ulcers NSAIDs mechanism of action blocks the function of cyclooxygenase-1 (COX-1), which is essential for the production of prostaglandins that stimulates the secretion of mucous that protects the gastric mucosa also inhibits stomach mucosa cell proliferation and mucosal blood flow other causes stress from serious illness gastric ischemia metabolic disturbances vasculitis gastrinoma (Zollinger-Ellison syndrome) Associated conditions Zollinger-Ellison syndrome suspect in patients with refractory duodenal ulcers Behcet disease Crohn disease
Presentation
Symptoms abdominal pain most commonly at the upper quadrants belching vomiting weight loss poor appetite bloating hematemesis melena Physical exam abdominal tenderness peritoneal signs if perforation
Evaluation
Diagnostic testing diagnostic approach diagnosis is primarily based on clinical presentation and preemptive treatment, confirmation of the diagnosis is made via endoscopy imaging esophagogastroduodenoscopy (EGD) gold standard of diagnosis indicated in patients who show no symptom improvement following few weeks of treatment allows for direct visual identification and allows for evaluation of the location and severity of the disease biopsy is important for the differentiation between benign ulcers and malignancy abdominal and chest radiographs may be useful in detecting pneumoperitoneum secondary to perforation positive findings include air-fluid levels with bowel dilation or free air studies urease breath test best initial test noninvasive and allows for the detection of H. pylori infection complete blood count often normal serum gastrin can be used to evaluate Zollinger-Ellison syndrome
Differential
Gastric malignancy differentiating factors lesions will appear different on endoscopy and will be confirmed via biopsy Chronic pancreatitis differentiating factors may have characteristic disease history and will present with calcifications on abdominal imaging
Treatment
Management depends on disease etiology and severity H. pylori-induced PUD clarithromycin, amoxicillin, and pantoprazole for 7-14 days clarithromycin, amoxicillin, pantoprazole, and metronidazole for 7-14 days NSAID-induced PUD stop NSAID use introduce proton pump inhibitor (PPI) use Bleeding ulcers resuscitation with IV fluids and/or blood products IV PPI endoscopic therapy with either cautery, endoclip or epinephrine injection Surgery indicated in patients with perforated ulcer and/or hemorrhage requires IV antibiotics and PPI prior to repair other indications include PUD refractory to medical therapy and Zollinger-Ellison syndrome
Complications
Bleeding Perforation manage with broad spectrum antibitoics, PPI, and emergency surgery Obstruction Malignancy

Blood, Plasma, Serum	Reference Range
ALT	8-20 U/L
Amylase, serum	25-125 U/L
AST	8-20 U/L
Bilirubin, serum (adult) Total // Direct	0.1-1.0 mg/dL // 0.0-0.3 mg/dL
Calcium, serum (Ca²⁺)	8.4-10.2 mg/dL
Cholesterol, serum	Rec: < 200 mg/dL
Cortisol, serum	0800 h: 5-23 μg/dL //1600 h: 3-15 μg/dL 2000 h: ≤ 50% of 0800 h
Creatine kinase, serum	Male: 25-90 U/L Female: 10-70 U/L
Creatinine, serum	0.6-1.2 mg/dL
Electrolytes, serum
Sodium (Na⁺)	136-145 mEq/L
Chloride (Cl^-)	95-105 mEq/L
Potassium (K⁺)	3.5-5.0 mEq/L
Bicarbonate (HCO₃^-)	22-28 mEq/L
Magnesium (Mg²⁺)	1.5-2.0 mEq/L
Estriol, total, serum (in pregnancy)
24-28 wks // 32-36 wks	30-170 ng/mL // 60-280 ng/mL
28-32 wk // 36-40 wks	40-220 ng/mL // 80-350 ng/mL
Ferritin, serum	Male: 15-200 ng/mL Female: 12-150 ng/mL
Follicle-stimulating hormone, serum/plasma	Male: 4-25 mIU/mL Female: premenopause: 4-30 mIU/mL midcycle peak: 10-90 mIU/mL postmenopause: 40-250
pH	7.35-7.45
PCO₂	33-45 mmHg
PO₂	75-105 mmHg
Glucose, serum	Fasting: 70-110 mg/dL 2-h postprandial:<120 mg/dL
Growth hormone - arginine stimulation	Fasting: <5 ng/mL Provocative stimuli: > 7ng/mL
Immunoglobulins, serum
IgA	76-390 mg/dL
IgE	0-380 IU/mL
IgG	650-1500 mg/dL
IgM	40-345 mg/dL
Iron	50-170 μg/dL
Lactate dehydrogenase, serum	45-90 U/L
Luteinizing hormone, serum/plasma	Male: 6-23 mIU/mL Female: follicular phase: 5-30 mIU/mL midcycle: 75-150 mIU/mL postmenopause 30-200 mIU/mL
Osmolality, serum	275-295 mOsmol/kd H₂O
Parathyroid hormone, serume, N-terminal	230-630 pg/mL
Phosphatase (alkaline), serum (p-NPP at 30° C)	20-70 U/L
Phosphorus (inorganic), serum	3.0-4.5 mg/dL
Prolactin, serum (hPRL)	< 20 ng/mL
Proteins, serum

Hematologic	Reference Range
Bleeding time	2-7 minutes
Erythrocyte count	Male: 4.3-5.9 million/mm³ Female: 3.5-5.5 million mm³
Erythrocyte sedimentation rate (Westergren)	Male: 0-15 mm/h Female: 0-20 mm/h
Hematocrit	Male: 41%-53% Female: 36%-46%
Hemoglobin A1c	≤ 6 %
Hemoglobin, blood	Male: 13.5-17.5 g/dL Female: 12.0-16.0 g/dL
Hemoglobin, plasma	1-4 mg/dL
Leukocyte count and differential
Leukocyte count	4,500-11,000/mm³
Segmented neutrophils	54%-62%
Bands	3%-5%
Eosinophils	1%-3%
Basophils	0%-0.75%
Lymphocytes	25%-33%
Monocytes	3%-7%
Mean corpuscular hemoglobin	25.4-34.6 pg/cell
Mean corpuscular hemoglobin concentration	31%-36% Hb/cell
Mean corpuscular volume	80-100 μm³
Partial thromboplastin time (activated)	25-40 seconds
Platelet count	150,000-400,000/mm³
Prothrombin time	11-15 seconds
Reticulocyte count	0.5%-1.5% of red cells
Thrombin time	< 2 seconds deviation from control
Volume
Plasma	Male: 25-43 mL/kg Female: 28-45 mL/kg
Red cell	Male: 20-36 mL/kg Female: 19-31 mL/kg

Cerebrospinal Fluid	Reference Range
Cell count	0-5/mm³
Chloride	118-132 mEq/L
Gamma globulin	3%-12% total proteins
Glucose	40-70 mg/dL
Pressure	70-180 mm H₂O
Proteins, total	< 40 mg/dL

Sweat	Reference Range
Chloride	0-35 mmol/L
Urine
Calcium	100-300 mg/24 h
Chloride	Varies with intake
Creatinine clearance	Male: 97-137 mL/min Female: 88-128 mL/min
Estriol, total (in pregnancy)
30 wks	6-18 mg/24 h
35 wks	9-28 mg/24 h
40 wks	13-42 mg/24 h
17-Hydroxycorticosteroids	Male: 3.0-10.0 mg/24 h Female: 2.0-8.0 mg/24 h
17-Ketosteroids, total	Male: 8-20 mg/24 h Female: 6-15 mg/24 h
Osmolality	50-1400 mOsmol/kg H₂O
Oxalate	8-40 μg/mL
Potassium	Varies with diet
Proteins, total	< 150 mg/24 h
Sodium	Varies with diet
Uric acid	Varies with diet
Body Mass Index (BMI)	Adult: 19-25 kg/m²