Abdominal Pain (8 questions) Flashcards
Differential for LUQ pain
splenic origin
gastritis
gastric ulcer
pancreatitis
DDx LLQ pain
diverticulitis
salpingitis
ectopic pregnancy
inguinal hernia
nephrolithiasis
IBS
IBD
DDx diffuse pain
AGE
mesenteric ischeia
metabolic (DKA, porphyria)
malaria
familial mediterranean fever
bowel obstruction
peritonitis
IBS
psychosocial
DDx RUQ pain
hepatitis
cholecystitis
cholangitis
biliary colic
pancriatitis
Budd-Chiari syndrome
Pneumonia / empyema pleurisy
subdiaphragmatic abscess
DDx RLQ pain
appendicitis
salpingitis
ectopic pregnancy
inguinal hernia
nephrolithiasis
IBD
mesenteric adenitis (yersina)
DDx epigastric pain
PUD
GERD
gastritis
pancreatitis
MI
pericarditis
Ruptured AAA
DDx periumbilical pain
early appendicitis
AGE
bowel obstruction
Ruptured AAA
Referred pain: right shoulder
gallbladder, diaphragm
Referred pain: left shoulder
diaphragm
Referred pain: periumbilical
appendix
What is GERD?
when reflux of stomach contents cause troublesome symptoms &/or complications
S/Sx of GERD
- Heartburn (pyrosis), regurgitation, and dysphagia (difficulty swallowing)
- bronchospasm, laryngitis, and chronic cough.
- chest pain, nausea (rarer), odynophagia (painful swallowing; unusual usually indicates esophageal ulcer)
Chest pain: GERD vs AP
GERD pain may mimic angina pectoris, described as squeezing or burning, located substernally and radiating to the back, neck, jaw, or arms, lasting anywhere from minutes to hours. Usually occurs after meals,
How is GERD diagnosed?
symptoms alone; 2/3 of pts who have symptoms of GERD have no visible endoscopic findings (ie non-erosive reflux dz)
mgmt of GERD: empiric tx
PPIs > H2 blockers in efficacy for esophageal GERD symptoms; ALL PPIs equally effective; Antacids for acute symptom relief
mgmt of GERD: maintenance Tx
continue PPI if: GERD returns after PPI tx; erosive esophagitis; Barrett’s esophagus.
No erosive esophagitis: consider H2 blocker tx
What are Sx of Barret’s esophagitis?
Most patients are seen initially for symptoms of associated GERD, such as heartburn, regurgitation, and dysphagia.
How is Barret’s esophagitis typically discovered?
during endoscopic examinations of middle-aged and older adults
How is Barret’s esophagus Dxed?
- Two criteria must be fulfilled to make a diagnosis of Barrett’s esophagus:
- Endoscopist must document that columnar epithelium lines the distal esophagus.
- Histologic exam of biopsy specimens from columnar epithelium must reveal specialized intestinal metaplasia.
Risk associated w/Barrett’s?
Cancer!
- Absolute CA risk low: 0.1 to 2.0 percent
- BUT esophageal cancer risk is ↑at least 30-fold above that of the general population
- UTD suggests pts w/ Barrett’s esophagus have regular surveillance endoscopy to obtain esophageal biopsy spec
What causes dysphagia?
often caused by GERD
Two classifications of dysphagia
oropharyngeal dysphagia
esophageal dysphagia
What is oropharyngeal dysphagia?
“transfer dysphagia”: characterized by difficulty initiating swallow. Swallowing may be accompanied by coughing, choking, nasopharyngeal regurgitation, aspiration, & sensation of residual food remaining in the pharynx.
What is esophageal dysphagia?
characterized by difficulty swallowing several seconds after initiating a swallow and a sensation of food getting stuck in the esophagus
What should you as a provider do if you encounter dysphagia in a pt?
warrants immediate evaluation to define the exact cause and initiate appropriate therapy
Visceral vs parietal pain
Visceral: vague or dull, steady or crampy, DIFFUSE
Parietal: severe, worse with moving, LOCALIZED
What is Crohn’s disease?
Fine cobblestone ulcers in non-continuous, skip lesions. Chronic inflammation of the digestive tract. Can develop fistulas: colon, vagina, perirectum
S/S of Crohn’s
- 3-4 semi-solid stools per day
- Mucous & pus in stool
- RLQ abd’l pain
- Abdominal distention, N/V
- Low grade fever
- Weight loss
How is Crohn’s diagnosed?
- CBC, lytes, sedrate
- serum protein↓
- Stool for occult blood/fat (fat ↑)
-Colonoscopy &/or sigmoidoscopy
What is ulcerative colitis?
Chronic inflammation of the digestive tract.
Mucosal ulcerations begin in the recto sigmoid colon and spread upward in a continuous pattern, through the colon.
S/S of UC
-4-20 diarrhea stools per day
- Mucous, pus, blood in stools
- Cramps before stool.
-Fever
-Weight loss
-Periods of remission & exacerbation
Dx of UC
same as Crohn’s
Which has higher cancer risk, UC or Crohn’s?
UC
Tx of UC and Crohn’s
- Supportive with rest & nutritional support
- Bulking agents-Metamucil to reduce stools
- Vitamin & iron supplements
- Sulfasalazine (Azulfidine)-used for anti-inflammatory effects
What is C diff?
C diff colonizes the human intestinal tract after the normal gut flora have been altered by antibiotic therapy** and causes antibiotic-associated colitis
S/S of C diff
watery diarrhea up to 10 or 15x daily w/ lower abd pain & cramping, low grade fever, & leukocytosis
Diagnostics for c diff
polymerase chain reaction (PCR)
Tx of C diff
- cessation of inciting abx
- Initial tx nonsevere CDI, metronidazole 10-14 d
- Treatment of severe CDI, vancomycin 125 mg 4x QD for 10-14 days
What abx are most frequently indicated in predisposition to C diff?
fluoroquinolones, clindamycin, cephalosporins, & PCN
Causes of PUD
- H-Pylori: Breaks down mucus layer, inflammatory response, direct cellular injury
- NSAIDs: inhibit prostaglandin synthesis // Gastric Acid Hypersecretion // Impaired duodenal bicarb secretion
- steroids
- cytotoxins
- etoh
- Typically gastric or duodenal uclers
S/Sx of PUD
- Upper abdominal pain or discomfort is the most prominent symptom in patients with peptic ulcers
- Peptic ulcers can present with any of 3 dyspeptic symptom patterns:
- Ulcer-like or acid dyspepsia (burning pain; epigastric hunger-like pain; relief with food, antacids, and/or antisecretory agents)
- Food-provoked dyspepsia or indigestion (postprandial epigastric discomfort and fullness, belching, early satiety, nausea, and occasional vomiting)
- Reflux-like dyspepsia
Which is more common: duodenal or gastric ulcers?
Duodenal! 75%
Acid secretion in duodenal and gastric ulcers
duodenal: normal to high
gastric: normal to low
Main cause of duodenal ulcers vs gastric ulcers
duodenal: H. pylori
gastric: NSAIDs (including aspirin)
Peak age for duodenal vs gastric ulcers
duodenal: 40s
gastric: 50s
Duodenal vs gastric: relationship to eating food
duodenal: pain gets better, then worse 2-3 hrs later
gastric: aggravated by food - sharp pain in midepigastric region 30-60min after a meal
How can a test for H. pylori be done?
stool antigen or urea breath test
How do NSAIDs cause PUD?
Inhibition of PG synthesis
(PGs stimulate mucous cells to produce mucous, which forms protective coat over surface of stomach)
Treatment options for H. pylori
Triple therapy and quadruple therapy: a combo of PPIs and antibiotics +/- bismuth subsalicylate
Triple therapy
14 day Tx for H. pylori
- High dose PPI Q12h
- Antibiotics Q12h
- Clarithromycin 500mg AND
- Amoxicillin 1000mg OR metronidazole 500mg
Triple if not >15% resistance in area.
Quadruple Therapy
14 day Tx for H. pylori
- High dose PPI Q12h
- Bismuth subsalicylate 524mg 4x daily
- Antibiotics 4x daily
- Metronidazole 250mg AND
- Tetracycline 500mg OR doxycycline 100mg Q12h
quadruple if >15% resistance in area.
Tx of NSAID related ulcers
- Stop NSAID therapy // Confirm H Pylori negative
- Start anti-secretory therapy with H2 blockers or PPIs (faster ulcer healing w/ PPIs for 4-6 weeks
S/S that associated with upper or lower GI bleeds
o Feeling weak, light-headed, or woozy (especially if you lose a lot of blood)
o A racing heartbeat (if you lose a lot of blood)
o Cramps or belly pain // Diarrhea // Pale skin
Diagnostic approach to suspected GI bleed
o Lab testing: hemoglobin/hematocrit
o Imaging: CT angiography – useful for determining the exact location of the bleeding within the GI tract
Etiology of upper GI bleed
- PUD** (gastric/duodenal ulcer) *often times pts have an H pylori infx as well
- esophagogastric varices
S/S of upper GI bleed
- Vomiting blood or something that looks like coffee grounds
- Diarrhea or stool that look like black tar (this can happen with lower GI bleeds, too, but it is less common)
Gastric vs duodenal PUD: vomiting and stool
Gastric: more hematemesis
Duodenal: more melena
Diagnostic testing for PUD
- Antigen stool is gold std for HPyl
also
- i) Fiberoptic endoscopy
- ii) Barium contrast studies
- iii) Gastric analysis with culture for H. pylori
- iv) Stools for occult blood-not a definitive test
- v) CBC with a decreased Hgb and Hct
Etiology of lower GI bleed
diverticulosis, colitis, color cancer
Sx of lower GI bleed
Bowel movements that look bloody (this can happen with upper GI bleeds, too, but it is less common)
What is IBS?
recurrent abd pain or discomfort at least 3 days/mo in the last 3 months w/ 2+ of the following: improvement w defecation, onset a/w ∆ in freq of stool, onset associated with a change in form (appearance) of stool
Primary Sx of IBS
abdominal pain and changes in bowel habits (eg, diarrhea and/or constipation).
Abdominal pain can vary in location and severity. Patients can experience primarily diarrhea, primarily constipation, or an alternating pattern of the two; additional GI symptoms may also occur.
Tx for IBS
- Many different tx available to relieve symptoms of IBS
- monitoring of symptoms and patterns
- adjustment of the diet to increase fiber and eliminate foods that can worsen symptoms
- psychosocial therapy (since stress may aggravate IBS)
- medication.
Hemorrhoids: S/S
painless passage of bright red blood per rectum often a/w a BM, anal pruritus, anal pain a/w a thrombosed hemorrhoid, and/or fecal soilage/staining.
DDx for hemorrhoids
- anal fissures, solitary rectal ulcer syndrome, polyps, rectal prolapse, anal cancer, and proctitis.
- Suspect in patients with bright red blood per rectum, anal pruritus, and/or acute onset of perianal pain.
Tx of hemorrhoids
- Avoid constipation. Hard stool can lead to rectal bleeding and/or anal fissure.
- Increasing fiber (recommended amount of dietary fiber is 20 to 35 grams per day)
- Warm sitz baths- soak the rectal area in warm water for 10 to 15 minutes two to three times daily. Sitz baths are available in most drugstores
- Pain-relieving creams and hydrocortisone rectal suppositories may help relieve pain, inflammation, and itching, at least temporarily.
Sx appendicitis
-
Right lower quadrant (right anterior iliac fossa) abdominal pain gradual onset
- pain is typically periumbilical in nature with subsequent migration to the right lower quadrant
- Anorexia
- Nausea and vomiting
- Fever-related symptoms generally occur later in the course of illness
Common causes lower abd pain
appendicitis, ovarian cyst, diverticulitis, UTI, cholecystitis, IBS, IBD, constipation, pregnancy, PID, ruptured AAA
Labs if lower adominal pain
CBC, amylase, lipase, UA, abd XR [pelvic U/S, colonoscopy, abd CT]
McBurney’s Pt:
palpate 1/3 way btwn ISIS & umbilicus – if it elicits pain then its likely appendicitis
Rebound tenderness:
pain when hand is coming off abd
Psoas Sign:
Have pt rais leg against resistance
Rovsing’s Sign:
Press deeply in LLQ if + pain is felt in RLQ
Obturator sign:
bend knee and rotate internally
Cutaneous hyperesthesia
lift up skin and they have RLQ pain
Pancreatitis: definition
acute inflammatory process of the pancreas. should be suspected in patients w/ severe acute upper abdominal pain
What causes pancreatitis?
Gallstones block common bile duct → obstruct pancreatic juices → reflux back to pancreas causing necrosis, erosion, hemorrhage
Causes: ETOH, trauma, viral infx, duodenal ulcers, drugs
Sx pancreatitis
- Unrelenting PAIN-LUQ pain w. radiation to back, sudden intense, severe, piercing pain unrelieved by vomiting; described as “knife-like”
- Dyspnea if severe d/t diaphragmatic inflammation
- hypotension and tachycardia 2ndary to hypovolemia, third spacing
- Fevers, increased WBC, jaundice, Cullen’s sign
Lab findings in pancreatitis
- ↑ amylase: pancreatic cell injury;
- ↑ lipase: pancreatic cell injury;
- ↑ glucose - beta cell damage & not sufficient insulin to metabolize glucose;
- ↓ calcium-glucose not available due to lack of insulin so body feeds off of fatty acids—calcium binds to fatty acids so is now ↓
- ↑ C-reactive protein (CRP)
- ↑hematocrit from hemoconcentration due 3rd spacing (from inflammatory rxn)
- ↑ blood urea nitrogen (BUN) from dehydration/3rd spacing
Tx pancreatitis
NPO, Fluid replacement, pain control!,
possible: TPN, NG suctioning, Proton pump inhibitors, antibiotics, insulin
what will you likely find on PE if pancreatitis?
- Epigastrium tender to palpation.
- Abdominal distention and hypoactive bowel sounds due to an ileus secondary to inflammation
- Patients may have scleral icterus (yellow eye) due to obstructive jaundice
- Patients with severe pancreatitis may have fever, tachypnea, hypoxemia, and hypotension.
- Rarely findings suggesting the presence of retroperitoneal bleeding
- Cullen’s sign: in periumbilical region // Grey-Turner’s sign: along the flank
Normal amylase and lipase
Normal amylase 50 – 150 U/dL
Normal lipase 10 – 140 U/L
Pancreatitis: what might you see on abdominal U/S?
pancreas appears diffusely enlarged and hypoechoic
Gallstones may be visualized in the gallbladder or the bile duct
Pancreatitis: what might you see on abdominal CT?
acute interstitial edematous pancreatitis: focal or diffuse enlargement of the pancreas with heterogeneous enhancement with IV contrast
Pancreatitis: what might you see on MRI?
diffuse or focal enlargement of the pancreatic gland
How is acute pancreatitis diagnosed
-
requires the presence of two of the following three criteria:
- acute onset of persistent, severe, epigastric pain often radiating to the back,
- elevation in serum lipase or amylase to three times or greater than the upper limit of normal,
- and characteristic findings of acute pancreatitis on imaging
What is diverticulitis?
Inflammation and/or infection of a diverticulum
S/S of diverticulitis
- Abdominal pain - lower abdominal - is the most common complaint in patients with acute diverticulitis.
- Pain is left sided in approximately 85 percent of patients.
- Associated symptoms include fever, N/V, constipation, and diarrhea. ↑WBC
complications of diverticulitis
bowel obstruction, development of an abscess, fistula, or a colonic perforation into the peritoneum and peritonitis.
How is acute diverticulitis Dxed?
abdominal CT scan with oral and IV contrast to establish the diagnosis of acute diverticulitis because it has a high sensitivity and specificity for acute diverticulitis and it can exclude other causes of abdominal pain.
Tx of acute diverticulitis
in absence of complications, the treatment is antibiotics that cover bowel flora (e.g., a fluoroquinolone plus metronidazole) and bowel rest (i.e., no oral intake). Surgery is needed for perforation or abscess.
Risk factors for cholecystitis
“40, fertile, fat, female”
Signs and Symptoms of cholecystitis
-
RUQ (or epigastrium) pain, fever, and leukocytosis a/w gallbladder inflammation and is usually r/t gallstone disease
- may radiate to the right shoulder or back.
- prolonged (more than four to six hours), steady, and severe.
- possible nausea, vomiting, and anorexia.
- A positive Murphy’s sign supports the diagnosis.
Ddx of cholecystitis
benign condition of biliary colic, which presents with the same type of pain.
Acute hepatitis; Lower lobe pneumonia, PUD, pancreatitis
Benign biliary colic vs cholecystitis: duration
Pain > four to six hours should raise suspicion for acute cholecystitis.
BBC tends to crescendo then resolve (GB relaxes and stones fall back from cystic duct)
Benign biliary colic vs cholecystitis: constitutional sx
Patients with constitutional symptoms such as malaise or fever are more likely to have acute cholecystitis.
Benign biliary colic vs cholecystitis: PE and labs
Patients with biliary colic do not have signs of peritonitis on examination and have normal laboratory tests.
Dx of cholecystitis
RUQ Ultrasound
Tx of cholecystitis
cholecystectomy if symptomatic (if not symptomatic, no surgery)
