Gastroenterology pearls

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GI Bleeding

Quick Tips

LGIB or positive FOBT in pt >40 yo is CRC until proven otherwise.

Approx. 80% UGIB resolve spontaneously w/ supportive therapy.

Small bowel bleed—hematochezia or melena.

Colonic bleed—positive FOBT or hematochezia.

To evaluate GIB—take vitals, H&P (note anticoag meds or NSAIDS/asa), resuscitation (IV fluids/transfuse), rectal exam/heme occult test.

Melena is really smelly and distinctive. Other causes of dark stool—bismuth, iron, spinach, charcoal, licorice.

If lower GIB is suspected, first r/o UGIB because the test can be performed quickly and easily and if negative, f/u with colonoscopy.

Presentation & Dx Tests: any of the following +/- signs of volume depletion or sxs of anemia—fatigue, pallor, exertional dyspnea

Hematemesis- vomiting blood, usually upper GIB source; order an upper GI endoscopy

“Coffee-grounds” emesis- usu. UGIB but slower bleed since blood has time to clot

Melena- black, tarry, liquid stool d/t degradation of Hgb by bacteria in colon most often d/t UGIB or possibly ascending colon bleed.  Tests- UGD and if negative, colonoscopy.

Hematochezia- bright red blood per rectum, usu. LGIB—colon or rectum or an UGIB that is bleeding rapidly.  

If UGIB often pt is hemodynamically unstable—decreased BP, tachycardia, postural changes in BP or HR.  

Tests- first r/o hemorrhoids then order colonoscopy to look for polyps or CRC, esp. in pt >50 yo.

Occult blood in stool- may occur from any site along GI tract.  Tests- colonoscopy and if negative, EGD.

Causes of GIB:

Upper- peptic ulcer dz, reflux esophagitis, esophageal/gastric varices, Mallory-weiss tear, Dieulafoy’s vascular malformation, aortoenteric fistula (rare cause usu. s/p aortic aneurysm/graft), neoplasm

Lower- diverticulosis , angiodysplasia, Crohn’s dz or Ulcerative colitis, CRC or polyps, ischemic colitis, hemorrhoids/anal fissure

Treatment: depends upon the cause and severity of GIB

Hemodynamically unstable- ABCs, supplemental O2, IV fluids

Labs- Hgb, Hct, PT, PTT, platelet count; monitor Hgb Q 4-8h

Upper GIB- EGD w/ coagulation of bleeding vessel or ligation of bleeding vessel if rebleed.

Lower GIB- colonoscopy w/ polyp excision/cautery, last resort surgical resection of area

Diseases of the Colon

Colorectal CA (CRC)- #3 most common CA in US                                                                               

Colonoscopy most sensitive and specific test for CRC, best dx choice for pt with positive FOBT

CEA- serum marker not used for screening but good to monitor recurrence surveillance

Liver most common site of metastasis

Risk factors: age >50, adenomatous polyps—villous greater potential for malignancy than tubular, larger polyp size, greater number of polyps, Inflammatory Bowel Dz—UC>>Crohn’s, pos fam hx, major polyposis syndrome.

Familial Adenomatous Polyposis: autosomal dominant, hundreds of polyps in the colon, risk CRC 100% by 30-40yo, 

prophylactic colectomy is tx of choice

Hereditary Nonpolyposis CRC: Lynch Syndrome I or II—early onset CRC w/o prior polyposis, Lynch II has CRC plus early occurrence of many other cancers at various sites.

Clinical Features CRC: abdominal pain, CRC most common cause of large bowel obstruction in adults, weight loss, blood in stool or asymptomatic

Treatment: surgical resection of tumor containing bowel and regional lymphatics, colonoscopy at 1 year and then Q 3 years, monitor CEA level Q 3-6 months, 90% recurrences occur within 3 years of surgery 

Diverticulosis- inner layer of colon bulges through area of focal weakness in wall often d/t increased intraluminal pressure as a result of low fiber diet and constipation

Risk factors: low fiber diet, positive family hx, age

Most commonly found in sigmoid colon

Clinical Features: usually asymptomatic (80-90%) found on colonscopy or vague LLQ discomfort, bloating, constipation/diarrhea 

Barium enema dx test of choice

Treatment: high fiber diet


a) painless rectal bleeding—usually minimal and stops spontaneously or 

b) diverticulitis

Diverticulitis- erosion of diverticula d/t fecal impaction 

Clinical features: fever, LLQ pain, leukocytosis

Dx via CT abdomen/pelvis with oral and IV contrast; barium enema and colonoscopy are contraindicated d/t risk of perforation!

Abdominal X-rays helpful to r/o other causes of LLQ pain- ileus or obstruction or perforation

Treatment: first episode treat with IV abx, bowel rest—NPO, IV fluids, surgery if sx persist greater than 3-4 days; subsequent episodes surgery is recommended

 Acute Mesenteric Ischemia: usually d/t decreased blood supply to the bowel via the superior mesenteric vessels

Decreased blood supply may result from arterial embolism (50%), arterial or venous thrombosis, or from splanchnic vasoconstriction 2/2 low cardiac output

Mortality 60-70% overall, 90% if bowel infarction occurs

Clinical features: acute onset severe abdominal pain disproportionate to physical findings/abdominal exam is benign, anorexia, vomiting, mild GI bleeding, and peritonitis, sepsis, shock in advanced cases 

Dx via mesenteric angiography

Treatment: supportive IV fluids, Abx; direct intra-arterial infusion of papaverine (vasodilator) during angiography for all arterial causes of AMI, thrombolytics/embolectomy may be used or surgery if bowel is infarcted

Diseases of the Liver

Cirrhosis- fibrosis of the liver d/t chronic liver injury or disease replaces damaged or dead hepatocytes resulting in nodules /disruption of liver architecture

Cirrhosis leads to a) portal HTN  ascites, peripheral edema, splenomegaly, gastric/esoph varices and b) hepatocellular failure  impaired liver fx, decreased albumin synthesis, decreased clotting factor synthesis

Childs-Pugh classification is used to estimate hepatic reserve in liver failure and predict morbid/mortality based upon presence/severity of ascites, bilirubin level, encephalopathy, nutritional status and albumin level.

Causes of Cirrhosis: Alcoholic liver dz, Chronic Hep B or C infxn, acetaminophen toxicity, autoimmune hepatitis, hemochromatosis, Wilson’s dz, a-1-antitrypsin deficiency, NASH

Clinical features: asymptomatic early on, later presents with sxs of complications of cirrhosis such as ascites, varices, gynecomastia, testicular atrophy, palmar erythema, spider agiomas, hemorrhoids, caput medusae (distension of abdominal wall veins). 

Varices 2/2 portal HTN: present with massive hematemesis, melena; 90% esophageal—Tx hemodynamic stabilization (fluids, maintain BP), perform emergent EGD for dx, long-term tx beta blockers to prevent rebleeding or sclerotherapy/banding

Ascites: accumulation of fluid in peritoneal cavity d/t inc hydrostatic pressure from portal HTN and reduced oncotic pressure from low albumin levels abdominal distension, shifting dullness, fluid wave on exam; dx abdominal U/S or dx paracentesis, Tx—rest, low Na diet, furosemide and spironolactone, therapeutic paracentesis if SOB, early satiety or tense ascites is present.  

Hepatic encephalopathy: increased toxic metabolite levels in the brain (esp. ammonia) lead to altered mental status, decreased mental fx/confusion, asterixis (flapping hand tremor), rigidity/hyperreflexia, fetor hepaticus (musty breath); Tx lactulose to prevent further absorption of ammonia and neomycin to kill bowel flora that produce ammonia, limit dietary protein intake <30-40mg/day

Hepatorenal syndrome: progressive renal failure in advanced liver dz 2/2 renal hypoperfusion d/t vasoconstriction of renal vessels azotemia, oliguria, hyponatremia, hypotension, low urine sodium <10mEq/L, liver transplantation is the only cure

Other complications of cirrhosis : spontaneous bacterial peritonitis (infected ascitic fluid), hyperestrinism (d/t inability of liver to process hormones appropriately), coagulopathy 2/2 decreased syn of clotting factors usu manifest as increased PT (must treat with fresh frozen plasma), hepatocellular carcinoma 

Viral Hepatitis

Five main categories viral Hep: Hep A, B, C, D, E.  Hepatitis may also be caused by EBV, CMV, HSV.

Transmission: fecal-oral route—HAV, HEV; parenteral—HBV, HCV (think IVDU); sexually/perinatal—HBV.  Hep D requires infection with Hep B to be transmitted.  HBV, HCV, HDV are chronic forms of hepatitis.  

Clinical features: acute hepatitis ( duration < 6 months), asymptomatic or jaundice, dark-colored urine d/t conjugated hyperbilirubinemia, RUQ pain, N/V, fever, malaise, hepatomegaly most severe presentation is fulminant liver failure, which occurs more commonly in Hep B, D, or E.

Clinical features: chronic hepatitis (duration >6 months), may be asymptomatic or present with late complications of hepatitis—cirrhosis or hepatocellular CA.  Chronic hepatitis occurs most often after HCV infection (80%) or after HBV infection (1-10%).  Risk of cirrhosis or HCC is 25-40% in chronic HBV, 10-25% in chronic HCV

Acute Pancreatitis

Diagnostic Clues:  acute onset of upper abdominal pain, often radiating to the back, pain that worsens after eating, nausea, vomiting


Gallstones (45%)

EtOH (35%)



Mumps (and other viral and parasitic infections)


Scorpion stings

Hyperlipidemia (triglycerides >1000)/Hypercalcemia


Drugs (valproic acid, HCTZ)

Labs: serum amylase and lipase (lipase more specific to pancreatitis), LFTs—ID gallstones as cause, hyperglycemia, hypoxemia and leukocytosis may also be present

Treatment:  find and eliminate cause if possible, supportive care (IVF, pain medications, bowel rest, other measures as needed), Ranson’s criteria can be used to estimate mortality

Prognosis: Determined by Ranson’s criteria—glucose  >200, Age >55, LDH >350, AST >250, WBC >16,000; if  >7 criteria mortality is 100%, >5 criteria—40%

Other GI Topics to Review

We suggest also looking over information on inflammatory bowel diseases diagnosis and treatment.

1. Ascites: A transudation of fluid into the peritoneum

Diagnostic Clues:  positive fluid wave & shifting dullness; abdominal paracentesis can be both diagnostic and therapeutic

Routine tests ordered on ascitic fluid:  cell count, albumin, Gram stain and culture, glucose -- must also collect serum albumin near time of paracentesis to allow calculation of serum-ascites albumin gradient (SAAG)

SAAG =  ascitic fluid [albumin] – serum [albumin]

If SAAG > 1.1 portal hypertension

Causes:  cirrhosis, splenic or portal vein thrombosis, large hepatic mets,

right heart failure, Budd-Chiari syndrome

If SAGG < 1.1 protein leakage

Causes:  nephrotic syndrome, tuberculosis, malignancy

WBC > 500 or PMNs > 250 indicate infection begin empiric therapy

with broad spectrum antibiotics pending C&S results 

Gastroesophageal Reflux Disease (GERD)

retrograde flow of stomach contents into the esophagus

Presentation- retrosternal pain/burning after eating, worse with lying down, may mimic cardiac chest pain, waterbrash-reflex salivary hypersecretion, cough

Diagnosis- endoscopy with bx or upper GI series (barium contrast study to look for complications such as strictures or ulcerations cannot dx GERD itself)

Causes- primarily 2/2 decreased LES tone, decreased esophageal motility, gastric outlet obstruction, presence of hiatal hernia and dietary factors (Etoh, tobacco, high-fat foods, coffee) may also contribute

Complications- erosive esophagitis, peptic stricture, esophageal ulcer, barrett’s esophagus dysplastic change in esophageal mucosa from squamous to columnar epithelium, increased risk adenocarcinoma

Treatment- diet modification, antacids, H2 blocker, PPI