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GI & Liver Complications Guide

1. Cirrhosis can cause hepatic hydrothorax due to fluid shifts through diaphragmatic defects caused by low oncotic pressure from low albumin. Diverticulosis is a common cause of lower GI bleeding presenting as painless bleeding. It is seen most often in the sigmoid colon. 2. Splenic abscesses are life-threatening infections that can develop from distant sites like the heart or gallbladder. Risk factors include immunocompromise. Features include left upper quadrant pain, fever, and splenomegaly. 3. Lactose intolerance is caused by lactase deficiency resulting in undigested lactose fermentation by colonic bacteria, causing gastrointestinal symptoms after dairy. It

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0% found this document useful (0 votes)
398 views5 pages

GI & Liver Complications Guide

1. Cirrhosis can cause hepatic hydrothorax due to fluid shifts through diaphragmatic defects caused by low oncotic pressure from low albumin. Diverticulosis is a common cause of lower GI bleeding presenting as painless bleeding. It is seen most often in the sigmoid colon. 2. Splenic abscesses are life-threatening infections that can develop from distant sites like the heart or gallbladder. Risk factors include immunocompromise. Features include left upper quadrant pain, fever, and splenomegaly. 3. Lactose intolerance is caused by lactase deficiency resulting in undigested lactose fermentation by colonic bacteria, causing gastrointestinal symptoms after dairy. It

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Gi and Liver UWorld

CIRRHOSIS
Complications
- Hepatic hydrothorax
o Cirrhosis —> low albumin —> low oncotic pressure —> fluid shifts out of intravascular
space —> fluid goes through diaphragm defect (microperforations)
o This causes one sided (typically right side) pleural effusions and peripheral edema
o Similar mechanism happens with pancreatitis
LOWER GI BLEED
Diverticulosis – most common cause of lower GI bleed
- Outpouchings of the colonic wall that form at points of weakness
- Deformation in the colonic wall can cause weakness in the associated arterial supply and lead to
bleeding into the diverticular lumen
- Diverticulosis is most common in the sigmoid colon
- Diverticular bleeding is more common in the right colon
o Painless, large volume bleeding, lightheadedness, hemodynamic instability
o Irritation due to bleeding can cause urge to defecate
- Diagnosis
o Colonoscopy – indicated in the management of presumed diverticular bleed but
contraindicated in diverticulitis due to inflamed diverticula
- Treatment
o Most resolve spontaneously
o Minority require endoscopic or surgical intervention
- Seen on abdominal CT
- Plan radiographs are normal
Colonic Angiodysplasia
- Painless bleeding in the right colon
- Usually venous
- Low-volume bleeding
Colon cancer
- Chronic occult blood loss w/ abdominal pain
- Altered passage of stool and weight loss
- Gross bleeding is less likely
Hemorrhoids
- Painless rectal bleeding
- Bright red blood in the toilet bowl or on the paper
Ischemic colitis
- Sudden onset of abdominal pain and tenderness followed by rectal bleeding
- Due to inadequate perfusion of watershed areas of the colon (splenic flexure) in the setting of
nonocclusive ischemia or surgical or endovascular interventions
SPLENIC ABSCESS
- Life threatening complication from distant infection (infective endocarditis, cholecystitis)
o Consider in patients who recently underwent laparoscopic cholecystectomy for
cholecystitis
- Risk factors: immunocompromised from HIV, hematologic malignancy, or DM.
- Clinical manifestations
o LUQ pain
o High fever
o Tender splenomegaly
o Anorexia
o Weight loss
- Laboratory studies
o Leukocytosis w/ left shift
- CXR shows elevated left hemidiaphragm and/or left pleural effusion
- Diagnosis
o CT scan of the abdomen
- Treatment
o Antibiotic therapy
o Splenectomy
SPLENIC INFARCTION
- Clinical manifestations
o LUQ
o Fever and splenomegaly occasionally occur
o Underlying hypercoagulable disorder, a source of embolic disease (a-fib), a
myeloproliferative neoplasm, or hemoglobinopathy (sickle cell disease
SPLENIC VENOUS THROMBOSIS
- Occurs in the setting of portal hypertension from liver disease or pancreatitis
LACTOSE INTOLERANCE
- Caused by deficiency of intestinal lactase, an enzyme in the brush border that metabolized
dietary lactose
- Undigested lactose is metabolized by colonic bacteria, releasing hydrogen gas and other
byproducts
- Etiology/risk factors
o Asian, African, Hispanic ethnicity
o Congenital or developmental lactase deficiency
o Small intestinal infection or inflammation
 Can be precipitated by inflammatory disorders affecting the brush border –
infectious gastroenteritis, celiac disease, and Crohn disease
- Clinical features
o Gastrointestinal distress after dairy intake
 Abdominal pain
Flatulence/bloating
 +/- watery diarrhea
- Diagnosis
o Resolution of symptoms on dairy-restricted diet
o Lactose breath hydrogen test
 Detects hydrogen released from standardized dose of oral lactose – can be
diagnostic
- Management
o Dietary restriction of lactose
o Lactase replacement if dairy ingested
Stool fat measurement – helps w/ diagnosis of malabsorptive diarrhea – occurs in the setting of small-
intestine infection (giardiasis), bacterial overgrowth, chronic pancreatitis
Tumor necrosis factor inhibitors – often used for refractory UC
Endoscopic retrograde cholangiopancreatography – used to evaluate choledocolithiasis
Evaluation of upper GI – esophagogastroduodenoscopy
- When there are features suggesting bleeding (iron deficiency anemia) or malignancy (progressive
dysphagia or odynophagia)
Evaluation of lower GI – colonoscopy
- Features associated with bleeding (hematochezia) or risk factors for malignancy (age>50,
unexpected weight loss)
CHOLESTASIS
Primary sclerosing cholangitis (PSC)
- Type of acute cholangitis caused by biliary obstruction (stricture) – predisposes patients to
bacterial invasion of the normally sterile biliary tree
- Chronic disease characterized by fibrosis and structuring of the medium and large- intra-and
extrahepatic bile ducts
o Promoted cholestasis and obstruction
- Clinical features
o Usually men
o Asymptomatic
o Fatigue and pruritus
o Associated with IBD, particular ulcerative colitis (>90% of patients)
 Hematochezia
o Features of acute cholangitis – RUQ pain, fever, jaundice, hypotension, AMS)
- Laboratory/imaging
o Cholestatic liver injury (very high ALP, high bilirubin)
o Multifocal structuring/dilation of intrahepatic and/or extrahepatic bile ducts on
cholangiography (i.e. magnetic resonance cholangiopancreatography)
o Patients usually have normal ultrasonography because intrahepatic bile ducts are not
easily visible
- Liver biopsy
o Fibrous obliteration of small bile ducts with concentric replacement by connective tissue
in onion-skin pattern
- Complications
o Biliary stricture
o Cholangitis or cholelithiasis
o Cholangiocarcinoma, colon cancer, biliary cancer
o Cholestasis (low fat-soluble vitamin, osteoporosis)
- Treatment
o Endoscopic interventions for strictures
o Therapy for coexisting UC
o Antibiotics for cholangitis
o Occasionally ursodeoxycholic acid
Primary biliary cholangitis (PBC)
- Results from an immune response against the intrahepatic bile ducts
- Can present with cholestasis
- More common in women
PANCREATITIS
Acute pancreatitis
- Severe epigastric pain radiating to the back
- Elevated lipase (>3 times normal)
- Common causes: alcohol use, gallstones
o After alcohol and gallstones have been excluded (RUQ ultrasound)  consider other less
common causes
 Hypercalcemia
 Hypertriglyceridemia
- Diagnosis – 2/3 classic features
o Class symptoms (severe epigastric pain radiating to the back)
o Elevated amylase/lipase
o Characteristic imaging findings
 Patient does NOT require a CT scan if they have symptoms and lab findings
Triglyceride-induced pancreatitis
- Risk
o Triglyceride levels
 <500: minimal risk
 500-999: mild risk
 1,000-1,999: moderate risk
 >2,000: high risk
o Other risk factors: pregnancy, alcoholism, obesity, uncontrolled diabetes
- Clinical features
o Acute epigastric pain radiating to back
o +/- fever, nausea, vomiting
o Elevated serum lipase (>3 times upper limit of normal)
- Diagnosis
o Lipid panel – triglyceride level >1000mg/dL is required for diagnosis
- Management
o IV fluid hydration, pain control
o Glucose >500 mg/dL: consider insulin infusion
o Glucose <500 mg/dL or severe pancreatitis (i.e. lactic acidosis, hypocalcemia): consider
apheresis (therapeutic plasma exchange – removes triglyceride-rich plasma)
DIARRHEA
Factitious disorder
- Intentional falsification of illness in the absence of external reward (financial compensation,
disability benefits)
- Purposely cause large, voluminous stools via improper use of laxatives and can create the
appearance of diarrhea by adding fluid to the stool
- Stool osmolality
o Stool osmolality is in equilibrium with plasma osmolality
o Typically remains constant (i.e. 290 mOsm/kg) in organic GI disease
o Hypoosmolality suggests addition of water or other dilute fluid
o Hyperosmolality suggests addition of a concentrated fluid (urine)
- Stool electrolytes
o Elevated stool magnesium or phosphate levels suggest overuse of saline osmotic
(magnesium or phosphate containing) laxatives
- Stool osmotic gap
o Osmotic laxatives (lactulose, polyethylene glycol) cause a high osmotic gap diarrhea,
whereas senna and bisacodyl produce a low osmotic gap secretory diarrhea.
o 290 mOsm/kg – 2 x (stool Na + stool K)
 <50 – secretory diarrhea
 50-125 – indeterminate
 >125 - osmotic diarrhea
Celiac disease
- Tissue transglutaminase IgA antibodies
- Weight loss
- Signs of malabsorption
o Iron deficiency anemia
o Vitamin D deficiency w/ hypocalcemia
Norovirus
- Causes chronic diarrhea in immunocompromised patients (HIV, solid-organ transplant)
- 1-2 days of symptoms
- Self-limited in immunocompetent individuals
Clostridioides difficile infection (CDI)
- Development of large-volume watery stool and leukocytosis after antibiotic use
- Risk factors
o Antibiotic use
o Recent hospitalization
o IBD and other comorbid illnesses

HELICOBACTER PYLORI
- Plays a critical role in the pathogenesis of extranodal marginal zone B cell lymphomas (low-grade
B cell lymphoma of MALT) of the stomach.
- Present in 90% of patients with tumors
- Chronic inflammation from H. Pylori infection results ins timulation of large numbers of antigen-
dependent B and T cells in the gastric lamina
- Chronic activation and proliferation eventually results in a monoclonal population of B cells that
no longer depends on normal stimulatory pathways for growth
- All patients with MALT lymphomas should be tested for H. Pylori
- Treatment
o Positive H. Pylori + MALT lymphoma – quadruple therapy
o Majority of patients achieve complete remission w/ antibiotic treatment

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