ABDOMINAL PAIN
Location
Work-up
Acute pain syndromes
Chronic pain syndromes

Epigastric Pain
PUD
GERD
MI
AAA- abdominal aortic aneurysm
Pancreatic pain
Gallbladder and common bile duct obstruction

Right Upper Quadrant Pain
Acute Cholecystitis and Biliary Colic
Acute Hepatitis or Abscess
Hepatomegaly due to CHF
Perforated Duodenal Ulcer
Herpes Zoster
Myocardial Ischemia
Right Lower Lobe Pneumonia

Left Upper Quadrant Pain
Acute Pancreatitis
Gastric ulcer
Gastritis
Splenic enlargement, rupture or infarction
Myocardial ischemia
Left lower lobe pneumonia

Right lower Quadrant Pain
Appendicitis
Regional Enteritis
Small bowel obstruction
Leaking Aneurysm
Ruptured Ectopic Pregnancy
PID
Twisted Ovarian Cyst
Ureteral Calculi
Hernia

Left Lower Quadrant Pain
Diverticulitis
Leaking Aneurysm
Ruptured Ectopic pregnancy
PID
Twisted Ovarian Cyst
Ureteral Calculi
Hernia
Regional Enteritis

Periumbilical Pain
Disease of transverse colon
Gastroenteritis
Small bowel pain
Appendicitis
Early bowel obstruction

Diffuse Pain
Generalized peritonitis
Acute Pancreatitis
Sickle Cell Crisis
Mesenteric Thrombosis
Gastroenteritis
Metabolic disturbances
Dissecting or Rupturing Aneurysm
Intestinal Obstruction
Psychogenic illness

Referred Pain
Pneumonia (lower lobes)
Inferior myocardial infarction
Pulmonary infarction

TYPES OF ABDOMINAL PAIN
Visceral
originates in abdominal organs covered by peritoneum
Colic
crampy pain
Parietal
from irritation of parietal peritoneum
Referred
produced by pathology in one location felt at another location

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WORK-UP OF ABDOMINAL PAIN
HISTORY
Onset
Qualitative description
Intensity
Frequency
Location - Does it go anywhere (referred)?
Duration
Aggravating and relieving factors

WORK-UP
PHYSICAL EXAMINATION
Inspection
Auscultation
Percussion
Palpation
Guarding - rebound tenderness
Rectal exam
Pelvic exam

WORK-UP
LABORATORY TESTS
U/A
CBC
Additional depending on rule outs
amylase, lipase, LFT’s

WORK-UP
DIAGNOSTIC STUDIES
Plain X-rays (flat plate)
Contrast studies - barium (upper and lower GI series)
Ultrasound
CT scanning
Endoscopy
Sigmoidoscopy, colonoscopy

Common Acute Pain Syndromes
Appendicitis
Acute diverticulitis
Cholecystitis
Pancreatitis
Perforation of an ulcer
Intestinal obstruction
Ruptured AAA
Pelvic disorders

APPENDICITIS
Inflammatory disease of wall of appendix
Diagnosis based on history and physical
Classic sequence of symptoms
abdominal pain (begins epigastrium or periumbilical area, anorexia, nausea or vomiting
followed by pain over appendix and low grade fever

DIAGNOSIS
Physical examination
low grade fever
McBurney’s point
rebound, guarding, +psoas sign
CBC, HCG
WBC range from 10,000-16,000
SURGERY

DIVERTICULITIS
Results from stagnation of fecal material in single diverticulum leading to pressure necrosis of mucosa and inflammation
Clinical presentation
most pts have h/o diverticula
mild to moderate, colicky to steady, aching abdominal pain - usually LLQ
may have fever and leukocytosis

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CHOLECYSTITIS
Results from obstruction of cystic or common bile duct by large gallstones
Colicky pain with progression to constant pain in RUQ that may radiate to R scapula
Physical findings
tender to palpation or percussion RUQ
may have palpable gallbladder

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PANCREATITIS
History of cholelithiasis or ETOH abuse
Pain steady and boring, unrelieved by position change - LUQ with radiation to back - nausea and vomiting, diaphoretic
Physical findings;
acutely ill with abdominal distention, ¯ BS
diffuse rebound
upper abd may show muscle rigidity

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PEPTIC ULCER PERFORATION
Life-threatening complication of peptic ulcer disease - more common with duodenal than gastric
Predisposing factors
Helicobacter pylori infections
NSAIDs
hypersecretory states

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SMALL BOWEL OBSTRUCTION
Distention results in decreased absorption and increased secretions leading to further distention and fluid and electrolyte imbalance
Number of causes
Sudden onset of crampy pain usually in umbilical area of epigastrium - vomiting occurs early with small bowel and late with large bowel

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RUPTURED AORTIC ANEURYSM
AAA is abnormal dilation of abdominal aorta forming aneurysm that may rupture and cause exsanguination into peritoneum
More frequent in elderly
Sudden onset of excrutiating pain may be felt in chest or abdomen and may radiate to legs and back

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PELVIC PAIN
Ectopic pregnancy
PID
UTI
Ovarian cysts

CHRONIC PAIN SYNDROMES
Irritable bowel syndrome
Chronic pancreatitis
Diverticulosis
Gastroesophageal reflux disease (GERD)
Inflammatory bowel disease
Duodenal ulcer
Gastric ulcer

IRRITABLE BOWEL SYNDROME
GI condition classified as functional as no identifiable structural or biochemical abnormalities
Affects 14%-24% of females and 5%-19% of males
Onset in late adolescence to early adulthood
Rare to see onset > 50 yrs old

SYMPTOMS
Pain described as nonradiating, intermittent, crampy located lower abdomen
Usually worse 1-2 hrs after meals
Exacerbated by stress
Relieved by BM
Does not interrupt sleep
critical to diagnosis of IBS

DIAGNOSIS
ROME DIAGNOSTIC CRITERIA
3 month minimum of following symptoms in continuous or recurrent pattern
  Abdominal pain or discomfort relieved by BM & associated with either:
Change in frequency of stools
and/or
Change in consistency of stools

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DIAGNOSTIC TESTS
Limited - R/O organic disease
CBC  with diff
ESR
Electrolytes
BUN, creatinine
TSH
Stool for occult blood and O & P
Flexible sigmoidoscopy

MANAGEMENT
Goals of management
     - exclude presence of underlying organic
     disease
     - provide support, support, & reassurance
Dietary modification
Pharmacotherapy
Alternative therapies

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CHRONIC PANCREATITIS
Alcohol major cause
Malnutrition - outside US
Patients >40 yrs with pancreatic dysfunction must be evaluated for pancreatic cancer
Dysfunction between 20 to 40 yrs old R/O cystic fibrosis
50% of pts with chronic pancreatitis die within 25 yrs of diagnosis

SYMPTOMS
Pain - may be absent or severe, recurrent or constant
Usually abdominal, sometimes referred upper back, anterior chest, flank
Wt loss, diarrhea, oily stools
N, V, or abdominal distention less reported

DIAGNOSIS
CBC
Serum amylase (present during acuteattacks)
Serum lipase
Serum bilirubin
Serum glucose
Serum alkaline phosphatase
Stool for fecal fat
CT scan

MANAGEMENT
Should be comanaged with a specialist
Pancreatic dysfunction
    - diabetes
    - steatorrhea & diarrhea
    - enzyme replacement

DIVERTICULOSIS
Uncomplicated disease, either asymptomatic or symptomatic
Considered a deficiency disease of 20th century Western civilization
Rare in first 4 decades - occurs in later years
Incidence - 50% to 65% by 80 years

SYMPTOMS
80% - 85% remain symptomless - found by diagnostic study for other reason
Irregular defecation, intermittent abdominal pain, bloating, or excessive flatulence
Change in stool - flattened or ribbonlike
Recurrent bouts of  steady or crampy pain
May mimic IBS except older age

DIAGNOSIS
CBC
Stool for occult blood
Barium enema

MANAGEMENT
Increased fiber intake - 35 g/day
Increase fiber intake gradually
Avoid
popcorn
corn
nuts
seeds

GASTROESOPHAGEAL REFLUX DISEASE
Movement of gastric contents from stomach to esophagus
May produce S & S within esophagus, pharynx, larynx, respiratory tract
Most prevalent condition affecting GI tract
About 15% of adults use antacid > 1x/wk

SYMPTOMS
Heartburn - most common (severity of does not correlate with extent of tissue damage)
Burning, gnawing in mid-epigastrium worsens with recumbency
Water brash (appearance of salty-tasting fluid in mouth because stimulate saliva secretion)
Occurs after eating may be relieved with antacids (occurs within 1 hr of eating - usually large meal of day)

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DIAGNOSIS
History of heartburn without other symptoms of serious disease
Empiric trial of medication without testing
Testing for those who do have persistent or unresponsive heartburn or signs of tissue injury
CBC, H. pylori antibody
Barium swallow
Endoscopy for severe or atypical symptoms

MANAGEMENT
Lifestyle changes
smoking cessation
reduce ETOH consumption
reduce dietary fat
decreased meal size
weight reduction
elevate head of bed 6 inches

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MEDICATIONS
Antacids with lifestyle changes may be sufficient
H2-histamine receptor antagonists in divided doses
approximately 48% of pts with esophagitis will heal on this regimen
tid dosing more effective for symptom relief and healing
long-term use is appropriate

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MAINTENANCE THERAPY
High relapse rate - 50% within 2 months, 82% within 6 months without maintenance
If symptoms return after treatment need maintenance
Full dose H2RA for most patients with nonerosive GERD
Proton pump inhibitors for severe or complicated

INFLAMMATORY BOWEL DISEASE
Chronic inflammatory condition involving intestinal tract with periods of remission and exacerbation
Two types
Ulcerative colitis (UC)
Crohn’s disease

ULCERATIVE COLITIS
Chronic inflammation of colonic mucosa
Inflammation diffuse & continuous beginning in rectum
May involve entire colon or only rectum (proctitis)
Inflammation is continuous

CROHN’S DISEASE
Chronic inflammation of all layers on intestinal tract
Can involve any portion from mouth to anus
30%-40% small intestine (ileitis)
40%-45% small & large intestine (ileocolitis)
15%-25% colon (Crohn’s colitis)
Inflammation can be patchy

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SYMPTOMS
Both have similar presentations
Abdominal pain may be only complaint and may have been intermittent for years
Abdominal pain and diarrhea present in most pts
Pain diffuse or localized to RLQ-LLQ
Cramping sensation - intermittent or constant

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PHYSICAL EXAMINATION
May be in no distress to acutely ill
Oral apthous ulcers
Tender lower abdomen
Hyperactive bowel sounds
Stool for occult blood may be +
Perianal lesions
Need to look for fistulas & abscesses

DIAGNOSIS
CBC
Stool for culture, ova & parasites, C. difficile
Stool for occult blood
Flexible sigmoidoscopy - useful to determine source of bright red blood
Colonoscopy with biopsy
Endoscopy may show “skip” areas
May be difficult to distinguish one from other

MANAGEMENT
Should be comanaged with GI
5-aminosalicylic acid products
Corticosteroids
Immunosuppressives
Surgery

DUODENAL ULCERS
Incidence increasing secondary to increasing use of NSAIDs,  H. pylori infections
Imbalance both in amount of acid-pepsin production delivered form stomach to duodenum and ability of lining to protect self

RISK FACTORS
Stress
Cigarette smoking
COPD
Alcohol
Chronic ASA & NSAID use

GENETIC FACTORS
Zollinger-Ellison syndrome
First degree relatives with disease
Blood group O
Elevated levels of pepsinogen I
Presence of HLA-B5 antigen
Decreased RBC acetylcholinesterase

INCIDENCE
About 16 million individuals will have during lifetime
More common than gastric ulcers
Peak incidence; 5th decade for men, 6th decade for women
75%-80% recurrence rate within 1yr of diagnosis without maintenance therapy
>90% of duodenal ulcers caused by H.pylori

SYMPTOMS
Epigastric pain
Sharp, burning, aching, gnawing pain occurring 1! - 3 hrs after meals or in middle of night
Pain relieved with antacids or food
Symptoms recurrent lasting few days to months
Weight gain not uncommon

DIAGNOSIS
CBC
Serum for H. pylori
Stool for occult blood

MANAGEMENT
2 week trial of antiulcer med - d/c NSAIDs
If H. pylori present - treat
If no H. pylori & symptoms do not resolve after 2 wks refer to GI for endoscopy
Antiulcer meds
H2RA; associated with 75%-90% healing over 4-6week period followed by 1 yr maintenance
inhibits P-450 pathway; drug interactions

MANAGEMENT (CONT)
Proton pump inhibitors
daily dosing
documented improved efficacy over H2-RA blockers
Prostagladin therapy - misoprostol
use with individuals who cannot d/c NSAIDs

GASTRIC ULCERS
H. pylori identified in 65% to 75% of patients with non-NSAID use
5% - 25% of patients taking ASA/NSAID develop gastric ulcers (inhibits synthesis of prostaglandin which is critical for mucosal defense)
Malignancy cause of

OTHER RISK FACTORS
Caffeine/coffee
Alcohol
Smoking
First-degree relative with gastric ulcer

SYMPTOMS
Pain similar to duodenal but may be increased by food
Location - LUQ radiating to back
Bloating, belching, nausea, vomiting, weight loss
NSAID-induced ulcers usually painless - discovered secondary to melena or iron deficiency anemia

DIAGNOSIS
CBC
Serum for H. pylori
Carbon-labeled breath test
Stool for occult blood
Endoscopy

MANAGEMENT
Treat H.pylori if present
Proton pump inhibitors shown to be superior to H2-RA
Need to use proton pump inhibitor for up to 8 wks
Do not need maintenance if infection eradicated and NSAIDs d/c’d
Consider misoprostol if cannot d/c NSAID