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What is the esophagus problem for the ff complaint?
Pain with swallowing
What is the esophagus problem for the ff complaint?
Choking or coughing
- Oropharyngeal or neurologic.
- Needs a PEG
What is the esophagus problem for the ff complaint?
Difficulty swallowing liquids and solids
What is the esophagus problem for the ff complaint?
Intermittent solid food
What is the esophagus problem for the ff complaint?
Progressive solid food
Sticture or malignancy
What is the diagnostic workup of choice for dysphagia with solids?
- EGD is the procedure of choice
- PPI is not appropriate since dysphagia usually requires more workup.
- Consider Barium Swallow if it sounds like a motility problems such as dysphagia with cold water
What are the motility disorders of the esophagus?
- Diffuse esophageal spasm
What is the pathophysiology of Achalasia?
- No peristalsis
- Elevated LES pressure
- Failure of LES to relax completely, thus unable to open up completely
What are the sx of Achalasia?
- Dysphagia for both solids and liquids
- Delayed regurgitation
- Nocturnal cough, aspiration
- Occasional chest pain
How do you diagnose Achalasia?
- Barium swallow
- Motility study
You may have to do all three of them in the order above
What do you expect to see on each of the procedures in workup for Achalasia?
- Barium Swallow:
- Dilated esophagus -- degree of dilation corrlating with duration
- "Bird bead" distal esophagus
- Delay in emptying
- Retained food in esophagus
- Dilated esophagus/retained food
- Performed to rule out tumor at GE junction
- Showing no organized peristalsis
- Non-relaxing, high-pressure LES
What is pseudoachalasia?
- AKA secondary achalasia
- The presentation of achalasia due to malignancy
- Clinical features: Age > 60, short duration of semptoms, profound weight loss
- Barium swallow and manometry may be exactly the same as regular achalasis
What is the treatment for achalasia?
- No medical treatment
- Standard would be pneumatic dilation -- 5% risk of rupture due to the very large balloon used.
- Surgical -- laparoscopic myotomy
- Endoscopic botox for high risk pt - relief may last 6-8 months
Once you see the result of the barium swallow and recognize Achalasia, what should you order?
EGD and manometry
What causes a "corkscrew esophagus?"
What is Diffuse Esophageal Spasm (DES)?
- Intermittent dysphagia for solids and liquids (especeially cold liquids)
- Chest pain -- atypical for angina
- Barium swallow -- usually normal but can show "corkscrew"
Once you see "corkscrew," you have obtained the diagnosis
How do you workup Esophageal spasm?
- EGD very low yield
- 24-hr pH probe -- some cases are due to atypical reflux
- Motility -- diagnostic criteria for DES, but also low yield
- Most of time, no additional workup needed once you see the "corkscrew" on the esophagram.
What is the treatment for DES (Diffuse Esophageal Spasm)?
- Trial PPI
- Anti-spasm agents
- Calcium channel antagonists
- Reassurance - go for this first if the patient is anxious
What are the mechanical or structural causes of dysphagia?
- Lower esophageal ring
- Stricture or esophagitis
What is the Schatzki ring?
What is the common complaint?
What is the treatment?
- They will show a dilated esophagus with an indentation just above the diaphragm
- Lower esophageal ring
- Intermittent solid food dysphagia
- Often for steak, chicken
- Often regurgitates for relief
- Always have hiatal hernia, but unknown if reflux plays a role, but it is becoming commonif not standard, to put on PPI after dilation
- Treatment: Dilation
- So, answer is endoscopic dilation, then PPI
Describe the presentation of Esophageal Strictures
What is the most common cause?
What type food (solid vs. liquid) causes dysphagia?
What is the pattern of dysphagia?
What is the treatment?
- Most common cause: Reflux
- Solid food dysphagia; can be progressive
- Not intermittent
- Treatment: Endoscopic dilation
- Misc. causes: Radiation, lye ingestion, NG tube trauma, pill-induced
- Esophagogram will show esophagus with smooth tapered area
What is Eosinophilic esophagitis?
What type of food causes dysphagia?
Who is usually affected?
What is the associated history of those affected?
How is it diagnosed?
What is the treatment?
- Solid food dysphagia - esp food impaction
- Young males
- Often history of allergy, asthma
- EGD shows "ringed" esophagus and biopsy reveals infiltrate of eosinophils
- Treat: PPI and ingested fluticasone
Describe the effect of Scleroderma on the esophagus
- causes incompetent LES, poor peristalsis
- At risk for severe GERD
- Dysphagia can be due to esophagitis, stricture, or just poor motility
- Work up if dysphagia: Barium swallow and EGD - if unable to swallow, do barium swallow, otherwise go straight to EGD
- Important to assess for GERD complications -- Barretts? Esophagitis?
- Only treatment id PPI -- dilate if stricture
What causes Odynophagia?
- Rare for common entities of stricture, i.e.,Schatzki ring
- More common causes are infections and medications
- Infections: CMV, Candida, herpes
- Medication-induced: ASA, NSAIDs, doxycycline, KCl, FeSO4, alendronate, quinidine
What are the Factors in Pathogenesis of GERD
- LES - defective or transient relaxation
- Hiatal hernia
- Poor esophageal clearance
- Delayed gastric emptying
- Association with BMI -- Weight gain leads to more reflux
Describe the workup of GERD:
- EGD if alarm symptoms, especially dysphagia, weight loss, heme+ shools
- 24-hour pH study -- helpful in atypical cases, like refreactory symptoms and normal EGD, or atypical symptoms like cough, hoarseness
What are indications for endoscopy in GERD?
- Failure to respond to treatment
- Long history of symptoms, esp. in males
- Guide to long term treatment plan
- Alarm symptoms, like dysphagia
- Barrett's confirmation, follow-up
When is a 24-hour pH study helpful?
It confirms the diagnosis of reflux when EGD and PPI did not confirm it.
When is it best to take PPI?
Best when taken fasting before a meal, i.e., before breakfast
What are complications of GERD?
- Ulcerative esophagitis
- Barrett's esophagus
What interventions would you do on a pt with Ulcerative Esophagitis?
- Start with PPI qd
- Re-scope to assess healing and exclude Barrett's esophagitis in 3-6 months
- If persistent esophagitis: change PPI to bid
- Indefinite maintenance treatment
When is GERD surgery indicated?
- Surgery is Fundoplication
- The following will need surgery:
- Young patient, definite GERD, intolerant of PPIs
- Any patient -- refractory regurgitation leading to cough, asthma, aspiration pneumonia
Does funduplication cure Barrett's?
What is the treatment for Benign Esophageal Stricture?
- Dilation can be accomplished safely
- Peptic strictures will require long-term medication use
- PPI provides better relief than standard dose histamine-2 receptor antagonists
What is Barrett's esophagus?
- Change in cell type of esophagus in response to chronic injury from GERD
- Biopsy showing "Specialized intestinal epithelium" has to be present above the GE junction to call it Barrett's
- Symptoms are 20 to complications like strictures, esophagitis -- this are indications for EGD
- Predominantly in white males; mean age 60
- Associated with adenocarcinoma of esophagus --which is rarely seen in absence of Barrett's
- Treat as if severe reflux -- PPI (even if asymptomatic)
- Endoscopic surveillance biopsies
A pt presents with c/o 10-year history of GERD symptoms, was diagnosed with GERD in the past. What intervention is needed?
Endoscopy to evaluate for Barrett's esophagus
How do you follow a pt with a long history of reflux, now with an EGD showing Barrett's confirmed by biopsy, but no dysplasia?
Repeat EGD and biopsies in one year, and if still negative for dysplasia, EGD every 3 years
What do you do with a pt with Barrett's esophagus and low-grade dysplasia?
What about if with high-grade dysplasia?
- Bring back in 6 months for EGD and biopsy for low grade dysplasia.
- If high grade -- look up recent recommendations
Briefly discuss Squamous cell esophageal cancer
- Location in proximal 2/3 of esophagus
- Smoking and alcohol are risk factors
- Other risk factors: lye stricture, other head and neck malignancy
Briefly discuss Adenocarcima of esophagus
- Location is distal 1/3 of esophagus
- Related to reflux and Barrett's
How do you workup Esophageal cancer?
- Start with EGD and biopsy
- Stage with both endoscopic ultrasound and CT abdomen and chest
- (endscopic u/s good for showing mets to regional nodes while CT good for showing mets to liver)
- Treat: surgery if localized
- XRT + Cistplatin + 5FU
- Then Neoadjuvant tx before surgery
Describe the workup for dyspepsia
- Test and treat H. pylori
- DC NSAIDs
- Trial PPI
- EGD if with alarm sx, failure of tx, or over 55 and new-onset sx
What is H. Pylori?
- Spiral, flagellated GNR
- Lives in mucous layer
- Mucosal invasion rare
- Chronic, nonspecific gastritis
- Infiltration PMN + lymphocytes
- Has urease
What malignancy may regress with treatment of H. Pylori?
MALT lymphoma of the stomach
H. pylori has been causally linked to what diseases?
- gastric adenocarcinoma
- gastric B-cell lymphoma
- MALT lymphoma
When do you check for H. pylori?
- any prior history of PUD
- EGD shows gastritis, or ulcer
- MALT lymphoma
- Family history of gastric cancer
- Dyspeptic symptoms -- test and treat, if age less than 50 and no alarm symptoms
How do you look for H. pylori?
What is the best test to test for eradication?
Breath test and stool antigen are best test for eradication
- if doing a scope anyway, do CLOtest or mucosal biopsy
- If no need for EGD: H. pylori ELISA, breath test, stool antigen test
What are limitations in the test for H. pylori?
- If patient is taking a PPI, this suppresses the bacteria. The CLOtest may be false negative, and the same for the breath test.
- Stool test should still be accurate.
- Use the stool test if patient cannot be taken off PPI
Patient has to be off PPI for 2-3 weeks if doing breath test.
What can happen after H. pylori is eradicated?
Reflux symptoms may worsen secondary to increased acidity (H. pylori reduces gastric acidity)
What are causes of PUD?
- H. pylori
- Zollinger-Ellison syndrome
When do complications from NSAID use usually occur?
What are other risk factors
- first 3 months of admintistration
- Advanced age
- History of ulcer disease
- Concomittant steroids
Diagnosis of PUD
- Empiric treatment with PPI
- H. Pylori ELISA and treat if positive
- Endoscopy if with alarm symptoms
Indications for Endoscopy
- Dysphagia and odynophagia
- Suspected ulcer
- Follow-up healing of gastric ulcer
- UGI bleeding
- Abnormal UGI series or CT
- Epigastric pain
- Anemia, iron deficiency (start workup from below)
- Some occulrt GI bleeding
- Follow-up gastric adenoma, carcinoid
What is the usual treatment for PUD due to H. pylori?
- PPI + bismuth + metronidazole + tetracycline
- PPI + amoxicillin + clarithromycin
- PPI + metronidazole + clarithromycin
- PPI should be bid
After treatment for H. pylori, what else do you need to do?
follow-up in few months for stool test to check for eradication
When do you do EGD on a pt who is actively bleeding?
What is the risk of rebleeding if the following are seen on EGD?
What is the role of PPI in UGI hemorrhage?
Use for 72 hours in any patient with endoscopic therapy
What is Osler-Weber-Rendu?
- Hereditary Hemorrhagic Telengiectasia
- Telangiectasia of fingers and nasal and oral mucosa
- History of nosebleeds
What is Peutz-Jeghers?
- Pt presents with perioral pigmentation
- Hamartomas of GI tract can bleed
What is Zollinger-Ellison syndrome?
How does it present?
What is the workup?
- Chronic diarrhea accompanied either by bad esophagitis or peptic ulcer diseaseUlcer disease of UGI tract
- Due to non-beta islet cell tumor or pancreas or duodenal wall
- Marked increase gastric acid and elevated serum gastrin
- 20% has MEN-1
- Workup: Somatostatin-receptor scintigraphy and endoscopic ultrasound (EUS)
How does the patient with Zollinger-Ellison syndrome present?
chronic diarrhea + bad esophagitis or bad peptic ulcer disease
What is the workup for Zollinger-Ellison Syndrome?
- Somatostatin-receptor scintigraphy
- Endoscopic ultrasound (EUS)
Surgical exploration if can't find lesion
What is the most common of increased gastrin?
achlorhydria - no acid means no inhibition of gastrin secretion
When should you be suspicious of ZE (Zollinger-Ellison syndrome)?
- Recurrent ulcer and no other factors
- Recurrent complicated ulcer
- Duodenal ulcer and big folds in stomach
- Duodenal ulcer and diarrhea combination
- Chronic diarrhea and gastritis despite omeprazole
Name some malignancies of the stomach
- GIST-stromal tumor
Describe the presentation and behavior of Gastric Carcinoid
- Single or multiple polypoid lesions in fundus or body of stomach
- Common gastrin elevation
- Benign behavior
- Least common GI site
- Very rare to have carcinoid syndrome with this
Describe the presentation of Gastric Adenocarcinoma?
- Usually diagnosed after symptoms
- Most with symptoms are advanced
- Abdominal pain, nausea, satiety, wt. loss
- Most common of the gastric neoplasms -- with recent trend of increase in proximal stomach near junction of esophagus and stomach
Briefly discuss Gastric Lymphoma
- Most common form is Diffuse Histiocytic Lymphoma
- Better prognosis than adenocarcinoma
- MALT - related to H. pylori
What is the treatment of MALT lymphoma?
- omeprazole/amoxicillin/clarithromycin and F/U
- Repeat endoscopy in a few months
Describe the diagnosis and staging of Gastric Cancer
- Endoscopy, brush, and biopsy
- -- CT and EUS for staging
- -- most have regional nodes or direct invasion
Describe the treatment and survival for Gastric cancer
- Surgical resection if possible
- - node-negative: 5-year survival 85-90%
- - node-positive: 5-10%
How do you diagnose Gastroparesis?
- Gastric emptying scan
- Always exclude obstruction with EGD
- More prevalent in DM type 1
What is the treatment of gastroparesis?
- Improve diabetes control
- Diet: liquid if severe, low fiber
- E-mycin -- not indicated, but does cause strong gastric contractions (only good for 1 or 2 uses)
- Gastric pacemaker?
Briefly describe some characteristics of Crohn's disease
- Symptom onset in 20s
- Overt bleeding is unusual
- Perirectal symptoms or lesions
- Symptoms often prolonged, diagnosis delayed
- Family history in 10-20%, association with smoking
How do you diagnose Crohn's disease?
- - patchy disease, aphthous and deep ulcers, strictures, fistula
- - Colonic disease -- rectal sparing, skip lesions, perirectal disease
- - ileal disease
- CT or CT enterography: shows small bowel or colonic inflammation or thickening
- UGI with small bowel: String sign -- ileal disease
- Granulomas not common, but diagnostic
What are "bear claw ulcers"?
Wide claw-shaped ulcers found only in Crohn's
What are complications related to Ileal disease/resection in Crohn's disease?
- Calcium oxalate kidney stones
- Pigment gallstones
- B12 deficiency
- Hypocalcemia and Vit D malabsorption
- Bile acid induced diarrhea (seen if less than 100 cm resected) Tx: cholestyramine
- Steatorrhea 20 to depleted bile acids (more than 100 cm resected, Tx: low-fat diet and medium-chain triglycerides)
What is the treatment for diarrhea in a pt with Crohn's who had less than 100 cm of ilem resection?
How about in one with more than 100 cm resected?
- Less than 100 cm resected causes "bile acid-induced diarrhea.
- Tx: cholestyramine
- More than 100 cm resected causes Steatorrhea 20 to depleted bile acids.
- Tx: low-fat diet and medium-chain triglycerides
What is the first line treatment for mild to moderate Crohn's disease?
How do you treat Crohn's?
- Mild disease : mesalamine, sulfasalazine, budesonide
- Acute flares: prednisone
- Immunocompromisint drugs?
How do you use Sulfasalazine in the treatment of Crohn's?
- Only use in Crohn's disease of the colon
- Split by colonic bacteria to 5-ASA and sulfpyridine
- Not very effective in small bowel, only in colon
- Use in acute or maintenance
- Sulfa portion can cause side effects and allergy -- leukepenia, oligspermia
How do you use Mesalamine (5-ASA) in treament of Crohn's?
- Oral and enema preparations
- Oral forms have delayed absorption
- -- Useful for Crohn's even if small bowel disease and UC, or Crohn's of the colon
- -- Use in acute or maintenance
What is a side effect of Mesalamine (5-ASA)?
How do you use Budesonide in the treatment of Crohn's?
- Use in ileal Crohn's
- For mild to moderate disease
- This is an option to mesalamine
What is the role of Immunosuppressants in IBD?
- Azathioprine, 6MP and methotrexate
- Value as steroid-sparing
- Maintenance agent
- Takes 3-4 months to start working
- Probably more useful for Crohn's disease, but can be used in UC
- Side effect: BM suppression, esp. WBC -- follow the CBC
What is the role of Tumor Necrosis Factor (TNF) antagonists in the treatment of Crohn's?
- Infliximab, adalimumab and certolizumab
- Indications: Fistulous Crohn's, moderate-to-severe active Crohn's and refractory UC
- Generally requires ongoing treatment
- Screen for TB before treating
- Arthralgias are very common after start of treatment
When do you use Metronidazole in Crohn's?
How about in UC?
- Crohn's: Perianal abscess, fistula
- UC: Only if peritonitis, toxic megacolon, pouchitis
Side effects, especially neuropathy limits long term use
What is useful for treatment of perirectal fistula in Crohn's?
Discuss the role of the ff meds -- mesalamine, steroids, infliximab, 6MP, Flagyl
- Infliximab is most helpful
- If symptoms weren't severe, could also use Flagyl and 6MP, but would take longer to respond
- Mesalamine and steroids would never help fistulous disease
Treatment for Crohn's exacerbation involving the colon only?
Mesalamine, also sulfasalazine
Treatment for Crohn's exacerbation involving the small bowel?
Treatment for Crohn's exacerbation involving a fistula or perianal?
Treatment for Crohn's exacerbation with acute small bowel obstruction?
Treatment for Crohn's exacerbation in a steroid-dependent patient?
- 6MP (or azathioprine)
Briefly describe UC
Uniform, continuous, mucosal inflammation, may be shallow ulcers, nothing deep
What are the main symptoms of UC?
- Bloody diarrhea and abdominal pain - main symptoms
- Variable extent
- -- Proctitis - Rectum only
- -- Proctosigmoiditis
- -- Extensive colitis (pancolitis)
- Contstitutional symptoms are common
What are the extraintestinal manifestations of UC?
- Peripheral polyarthritis (RF negative)
- Ankylosing spondylitis (HLA-B27)
- Skin lesions (E. nodosum, pyoderma)
- Eye: Iritis, episcleritis, uveitis
- *HLA association tends not to improve with colitis treatment
- *Not unique to UC, seen with Crohn's
A pt with history of Crohn's or UC presents with abnormal LFTs. What would be your differential?
What test would you order?
- Primary Sclerosing Cholangitis
- -- this can occur even after colectomy
Order ultrasound or MRCP
What is the recommended screening for colon ca in a patient with UC?
Colonoscopy q 2 years after 10 years, and q 1 year after 20 years
- High grade dysplasia -- colectomy
- Any mass lesion or cancer -- colectomy
What is the treatment for mild UC?
Sulfasalazine, 5-ASA, topical
What is the treatment for moderate-to-severe UC?
What is the treatment for fulminant UC?
- IV fluids
What is the maintenance treatment for UC?
Sulfa and 5-ASA decrease recurrence
What is the treatment for persistent UC with frequent steroids?
Azathioprine or 6-MP
What is the treatment for refractory UC?
- Don't forget surgery
How would you treat UC with the extent below?
- a. Suppository mesalamine
- b. Enema (hydrocortisone or mesalamine)
After topical treatment, may still need oral maintenance
What are the indications for surgery in UC?
- Intractable disease
- Growth retardation in children
- Toxic megacolon
- Massive hemorrhage
- Suspected cancer, high-grade dysplasia
A patient comes in with UC flare, what test should you include in your initial workup?
Describe features that favor Crohn's vs. UC
Crohn's: Lesions are focal, skip, deep; granulomas are present (not always there, but pathognomonic); with rectal sparing, and absecess or fistula on perianal disease.
UC: Lesions are shallow, continuous; no granulomas, always involve the rectum, no perianal disease
- Colonoscopy is usual method to assess
- Very little role for barium enema
- Never BE in acute illness
- Crohn's patients should quit smoking
- Most UC patients are non-smokers
Define the following:
a. Acute diarrhea
b. Persistent diarrhea
c. Chronic diarrhea
- acute -- up to 14 days
- persistent -- 14-30 days
- chronic -- 30 days
What is Traveler's diarrhea?
Prevention and treatment?
- Definition: Occurs during or within 10 days of travel
- Attack rate: up to 40%
- Most common organism: Enterotoxigenic and enteroadherent E. coli (ETEC and EAEC)
- Lasts 3-5 days
- Prevention is key
- Prevent with bismoty subsalicylate or lactobacillus
- Treat: Bactrim, doxycycline, fluroquinolone, rifaximin
- No treatment needed after acute phase
What are the common infectious/invasive causes of acute diarrhea?
- Salmonella (sickle cell, achlorhyrida)
- Campylobacter (most common)
- Yersinia (joint pains, rash)
- E. Coli 0157:H7
What causative organism causes diarrhea with joint pains and rash?
What organism is associated with infectious diarrhea in patients with sickle cell and/or achlorhydria
Briefly discuss Campylobacter jejuni and diarrhea.
What is the preferred treatment?
What is it associated with?
- Most common bacterial colitis
- 90% with diarrhea and fever
- Abdominal pain and bloody stools are common
- Assoc with Guillain-Barre
- Tx: E-mycin and azithromycin preferred. Cipro works but increasing resistance
- No treatment if mild
Discuss the management of Salmonella-induced diarrhea
When do you treat?
- Same sx as campylobacter - bloody diarrhea
- Treat if severe sepsis or underlying medical or immune disorder
- Resistance in ampicillin and Bactrim (but ok to use if sensitive)
- Ciprofloxacin effective, higher relapse
- Tx: Levofloxacin for 5-7 days
Presentation and treatment of Shigella-induced diarrhea?
- Very bloody diarrhea
- Only small inoculum is needed
- Tx: ampicillin unless PCN-allergic or community has resistance
- Bactrim effective
- Fluoroquinolone good choice if acquired in developing country
Discuss Hemorrhagic E. coli (0157:H7)
What part of the colon is involved?
- Contaminated beef
- Sporadic and epidemic disease
- Bloody diarrhea, often n/v
- Right colon involved
- Associated with complicated HUS and TTP
- Don't treat with antibiotics -- patients treated with antibiotics can develop HUS
- Tx: supportive measures only
When do you use antibiotic in patient with diarrhea?
- Empiric antibiotic treatment if severe: > 8 stools per day, bloody. fever, volume depletion, severe enough for admit, immunocompromised
- Empiric tx -- flouroquinolone
What is the treatment for Amoebiasis?
- Metronidazole + iodoquinol
- Then add paronomycin afterwards to get rid of the luminal phase of any amoeba remaining
Discuss Amebic Liver Abscess
- most common extraintestinal manifestation
- Usually a traveller or recent immigrant who presents with Fever, RUQ pain, WBC > 10,000
- Concurrent diarrhea in approx 1/3
- Abnormal LFTs common; alk p in 75%
- Rare increase in bili
- Multiple abscesses
- Complications: Rupture into chest, peritoneum
What is the usual presentation of Giardiasis?
- Scenario: Travel (mountain streams), daycare workers
- Presentation: Acute, sub-acute, and chronic. Foul-smelling diarrhea, bloating, diarrhea, cramps, malabsorption, weight loss
- Giardia is hardy in cold water and resistant to chlorine
How do you treat Giardia?
Is there eosinophilia?
- Tx: Metronidazole and tinidazole
- Dx: Stool antigen
- No eos
- No systemic symptoms
- No fecal leucocytes
What is the difference between secretory and osmotic diarrhea?
Secretory: Daily stool volume > 1 L daily, continues even if pt fasts, solute gap <50
Osmotic: daily stool volume < 1L/day, stops when pt fasts, solute gap > 50
What is osmotic diarrhea?
- Resolves with fast, gap > 50
- Lactose intolerance is a common cause
- Assoc with Nutrient malabsorption -- pancreatic disease or celiac disease
How do you manage severe acute pancreatitis?
What is the the preferred route of feeding?
What is the role of antibiotics in acute pancreatitis, and when is it recommended?
What is the role of antibiotics in mild to moderate acute pancreatitis?
When is pancreatic debridement recommended?
- Enteral feeding is the preferred route of providing nutrition in patients with severe acute pancreatitis
- Imipenem therapy is only helpful in acute pancreatitis when there is evidence of pancreatic necrosis.
- Pancreatic necrosis is diagnosed by a contrast-enhanced CT scan that shows nonenhancing pancreatic tissue.
- In patients with noninfected pancreatic necrosis, antibiotics may decrease the incidence of sepsis, systemic complications (for example, respiratory failure), and local complications (for example, infected pancreatic necrosis or pancreatic abscess).
- Prospective trials have shown no benefit from antibiotic use in acute pancreatitis of mild to moderate severity but may lead to development of nosocomial infections with resistant pathogens.
- Pancreatic débridement is recommended only in patients with pancreatitis and infected pancreatic necrosis.
What are the sx?
- Malabsorption due to small bower atrophy of villi
- -Dermatitis herpetoformis
- -Iron deficiency anemia
- -Diarrhea, wt loss, malabsorption, osteoporosis, infertility, unexplained LFTs
- - Tissue transglutaminase*
- - Antiendomysial Ab*
- - Antigliadin Ab
- Treatment: Gluten-free diet
What is the organism?
- Tropheryma Whipplii
- Sx: weight loss, arthralgias, abdominal pain, diarrhea, malabsorption
- Dx: endoscopy with small bowel biopsy
- Bx: Foamy macrophages, bacterial remnants stain with PAS stain
- Tx: Ceftriaxone, then TMP for 1 year
- May relapse with CNS sx
How do you evaluate for malabsorption?
Best screening test?
What is the gold standard and what amount is relevant?
- Steatorrhea: the best indicator
- Sudan Stain: best screening test
- Serum carotene: less specific
- Quatitative fecal fat is gold standard (> 14 g/day)
- Pancreatic insufficiency has the most fat.
Malabsorption symptoms with Fe deficiency will point to what diagnosis?
How about if it's B12 deficiency?
What does a normal test mean?
What next after low D-xylose?
What do you do if D-xylose is normal?
- Normal D-xylose excludes small bowel disease (urine > 5 gm after 25 gm oral dose)
- Low D-xylose: small bowel disease, poor gastric emptying, bacterial overgrowth, ascites, renal insufficiency, old age
- Biopsy if low D-xylose
If normal D-xylose, do trial of pancreatic enzymes
- Structural abnormalities: Diverticula, prior surgery
- Motility disorders: Diabetes, scleroderma
- Symptoms: diarrhea, steatorrhea, abdominal distension, wt. loss
- Diagnosis: Lactulose breath test,
- Empiric tx: Tetracyclline, Augmentin, or rifaximin 400 mg tid for 7 days
- Pearl: Increased folic acid but high MCV from B12 deficiency
Irritable Bowel Syndrome
- -abdominal pain relieved by defecation
- -altered stool frequency
- -altered stool form
- -abdominal distention
- -no organic symptoms
- -no nocturnal symptoms
- -symptoms more than 3 months
- -no iron deficiency or anemia
What would you order if a 45 year old patient presents with initial onset of IBS?
Do a colonoscopy. IBS onset is usually in the early 20's.
What is it?
- Chronic, watery diarrhea
- Middle-aged to elderly female
- Associations: NSAIDs, autoimmune disease
- Know how to make diagnosis: need colonoscopy or sigmoidoscopy of normal looking mucosa
- Does not evolve into UC or Crohn's
Colon Cancer Risk Factors
- Age > 50
- Hx adenoma
- 1st degree relatives
- Familial polyposis
- UC or Crohn's (after they've had the disease for 10 years or more)
- Hereditary nonpolyposis: HNPCC
- Diet of High-fat, low fiber
- Risk of cancer: size > 2 cm, sessile base, multiple polyps, villous
- No malignant potential: hyperplastic polyps
- Tx: Remove at colonoscopy and follow closely
Colonoscopy follow-up intervals:
When do you follow in 10, 5, or 3 years?
- If no polyp, or hyperplastic, can f/u in 10 years.
- One or two adenomas, then 5 years
- Repeat colonoscopy in three years for any of the ff:
- 3-10 adenomas found
- Any adenoma larger than 10 mm
- Any adenoma with villous eratures
- Any adenoma with high-grade dysplasia
What is it?
What would you advise patient once diagnosis is confirmed?
What is Gardner syndrome?
What is the second most common cause of death in FAP? What would you recommend to avoid this?
- Autosomal dominant
- Hundres of adenomas
- 100% cancer risk
- -scope to confirm diagnosis
- -Elective proctocolectomy by age 20
- Gardner Syndrome: Same as FAP except bone lesions -- osteomas, soft tissue tumors
- After proctocolectomy, recommend UGI endoscopy every few years to evaluate for duodenal polyp. Duodenal cancer -- the second most common cause of death
- Screen family members
Familial Polyposis Syndromes
What is is?
- Peutz-Jeghers syndrome
- -Hamartomatous polyps GI tract
- -Pigmentation on lips
- -Can bleed or obstruct
- -Main clinical problem early: Small bowel obstruction from intussusception
- -Clinical problems later: At risk for different malignancies
Hereditary Non-Polyposis Colon Ca
What is it?
After it's diagnosed, what else do you do?
When do you start screening?
- HNPCC or Lynch syndrome
- Colon Ca in three 1st degree relatives over 2 generations, one with dx < 50 years old
- Right sided colon cancers
- Screen for other malignancies: endometrial, renal, ureteral, gastric
- Start screening early -- Colonoscopy at 25
Colon Ca: TNM I, Duke's A
What is the extent?
Treatment and followup?
- Cancer confined to the mucosa and submucosa
- About a quarter of cases
- 5-year survival -- 93%
- No treatment after resection, but careful follow-up
- Colonoscopy followup after a year
Colon Ca: TNM II, Duke's B
Extent of involvement?
- Cancer extends into or through the muscularis, but no lymph node involvement
- About 30% of cases
- 5-year survival: 72 to 85%
- Chemo if locally advanced
Colon Ca: TNM III, Duke's C
Extent of disease?
- Cancer extends into lymph nodes
- 26% of cases
- 5-year survival: 44 to 83%
- Treat with FOLFOX: 5FU + leucovorin + oxaplatin
Colon Ca: Stage IV
- Spread into liver
- Poor prognosis
What are indications for colonoscopy?
- Occult bleeding
- Iron-deficiency anemia
- Gross lower GI bleeding (not hemorrhoidal in young)
- Abnormal barium enema
- Adenomatous polyp on flexible sig or in past
- History of colon ca
- Family history of colon ca
- Bacteremia; Strep bovis, Clostridium septicum
- Ischemic colitis
- After an acute attack of diverticulitis: 4-8 weeks later
What is ist?
- Most frequent congenital GI anomaly
- Cause of half of GI bleeds in children and young children
- Can cause obstruction, intussusception
- Not seen on barium enema, rarely on UGI series
- Dx: technetium scan
Lower GI Bleed
Most common cause?
- Diverticulosis - most common, painless
- Colon cancer or polyp (and post-polypectomy)
- Ischemic colitis: Always with pain
- Upper source; duodenal ulcer
- Meckel diverticulum - in young patient
- Anorectal source
Hereditary Hemorrhagic Telangiectasia
- Telangiectasias on physical exam and family history
- History of epistaxis
- Family history of GI bleeding or epistaxis
- AVMs (multiple) of GI tract -- more upper than lower
What is the best test for obscure GI bleeding? - meaning that upper and lower caused have been excluded. An angiogram woul only be helpful if very active bleeding; for instance, a postive tagged RBC scan
Who is at risk?
- Severe abdominal pain followed by severe bloody diarrhea
- Usually pain in the LLQ
- Involves watershed area -- splenic flexure
- Low-flow state, not embolic
- At risk: CHF, hypovolemic
- Treatment: Bowel rest, IV fluid, possible antibiotics
- Usual resolution > 50%
- Dx: colonoscopy
- No angiogram
- Young patients: workup for Protein C deficiency, Antithrombin III def
- Females: oral contraceptives
- Cocaine use
- Pseudoephedrine users
- Long-distance runners
Chronic Mesenteric Ischemia
Triad of sx?
- Classic triad:
- 1. Abdominal pain after meals - 30 min. after meals
- 2. Decreased pain with smaller meals and weight loss
- 3. Abdominal bruit
- Diagnosis: mesenteric angiogram -- CT angiogram, or MR angiogram
- Acute, severe abdominal pain
- Symptoms out of proportion to exam
- Vomiting, diarrhea, occult blood (not gross)
- Acidosis, elevated amylase
- Dx: Angiogram
What is the appropriate recommendation for recurrent pancreatitis with negative US, except for sludge?
- Amylase 3X normal
- Lipase peaks later
- Hemoconcentration - a bad indicator
- Bili > 3 and increased ALT suggest common bile duct stone
Acute Pancreatitis Management
- NPO, aggressive IV fluids
- NG tube if ileus or vomiting
- Tx: Imipenem if necrosis on CT, otherwise no antibiotic
- Feed: jejunal feeding is superior and safe
What size is not drainable?
When do you drain it?
- Can be seen in acute or chronic
- Usually 2 to 4 weeks after acute episode
- Can spontaneously resove
- Size > 5 cm unlikely to resolve, need drainage or surgery after acute episode
- Size ≤ 5 cm can be observed rather than surgery, etc.
- Can be complicated -- infection, hemorrhage
- Consider if delayed recurrence of pain with another elevation of amylase
When do you do ERCP?
When do you recommend lap chole?
- Early ony if ongoing biliary sepsis, biliary obstruction, cholangitis, rising bili
- Later for other cases; suspected due to CBD stone, unknown cause, Ca of pancreas
- Timing of lap chole -- can be done early but wait until pancreatitis has subsided
What fecal test?
Is there a long term risk?
What is the classic diagnostic triad?
When do you do MRCP?
- Early: recurrent pain episodes
- Late: Steatorrhea and diabetes (80-90% function lost)
- Fecal fat can be very high (40-100 gm/d)
- Increased risk of pancreatic cancer
- Dx: calcification on KUB - not usually seen, but significant if present
- CT and EUS: Best second step
- Classic diagnostic triad: Pancreatic calcifications, diabetes, steatorrhea
- MRCP: visualizes pancreatic and bile ducts. Order before the invasive ERCP if suspicious of CBD stone
What are the risk factors?
Workup of mass?
What's the recommendation if no mets?
When is the pt resectable or non-resectable?
- Risk factors: Smoking, chronic pancreatitis, DM
- 5th leading cause of cance deat in U.S.
- Presentation: Jaundice, abdominal or back pain, and weight loss
- Most located at head of pancreas
- Elevated CA 19-9
- If mass: CT-guided biopsy, or needle biopsy at EUS
- If no mets: Consider eval for surgery.
- Resectable if: no mets, no encasement of vessels. If either of these are present, then non-resectable.
- If mets or local vascular invasion: ERCP + stent to give palliation of the jaundice.
- Gemcitabine: Improves survival, reduces pain and improves QOL
Pigment stones in gallbladder
When can it occur?
What are not considered symptoms?
- Can occur in bile duct with chronic infection: Clonorchis, strictures, cholangitis
- Can occur in gallbladder with hemolysis
- Can occur in Crohn's pts, with ileal disease or ileal resection
- 50% radio-opaque
- Symptoms: Pain is epigastric or RUQ. Constant for 20-60 minutes. Nausea and vomiting. (dyspepsia, heartburn, and fatty food are not sxs)
- Ultrasound: 90% sensitive
- HIDA for acute cystic duct obstruction
- Treatment if symptomatic: cholecystectomy
- If asymptomatic: no treatment. Bile acid never used
- Common duct stones: ERCP
Common bile duct gallstones
What kind of stones?
- Cholangitis: Charcot's triad -- abd pain, fever and chills, jaundice
- Pigmented stones or cholesterol
- Management: Antibiotics, endoscopic sphincterotomy, surgery if ERCP unable to pull out stone
- Pain and increased LFT's
- Immediate post-op: Think bile duct leak
- Any delay (think months to years later): Think Choledocholithiasis, need ERCP
When would you use it?
- MR cholangiography: Sensitivity for CBD stones about same as ERCP
- Use when index of suspicion is low to moderate -- i.e., if pt with pancreatitis, CBD stone mildly dilated but bili is normal
- If high index of suspicion, go straight to ERCP
Primary biliary cirrhosis
Usual patient affected?
What other associated disorders?
Findings on physical exam?
What is the natural history (survival) of the disease?
Treatment for the disease?
When to refer for transplant?
What is the best test for diagnosis?
- Middle-aged women
- Main symtoms: Fatigue, pruritus, often suspected based on symptoms alone
- Often asymptomatic
- Autoimmune disorders are common (Sjogren's, CREST, thyroiditis)
- PE: Xanthelasma, skin hyperpigmentation, hepatomegaly, other signs of liver disease
- -Increased alk phos (can be marker) and GGT
- -Anti-mitochondrial Ab
- -Increased cholesterol (HDL)
- -Increased IgM
- -Bili usually normal
- Liver biopsy required to establish dx
- - nonsuppuratie destruction of small bile ducts
- - reduced biliary excretion
- - accumulation of bile acids and copper
- - early stage: (I) chronic inflammatory cells and granulomas adjacent to damaged bile ducts
- Natural History
- - Asymptomatic: survival 10-16 years
- - Asymptomatic: Survival 7 years
- Symptom treatment:
- - Pruritus: Cholestyramine
- - Metabolic bone disease: Calcium, Vit D, estrogen, bisphosphonates
- - Malabsorption: Restrict dietary fat, medium-chain triglycerides
- - Steatorrhea
- - Wt. loss
- - At risk for deficiency of fat-soluble vitamins -- most importanc clinically is D
- - Liver failure
- Treatment for PBC: UDCA (Ursodeoxycholic acid)
- Poor prognosis if Bilirubin increasing -- refer for liver transplant
- Best test for diagnosis: anti-mitochondrial antibody
Serologic markers in liver disease -- what is prominent in the following?
- Primary biliary cirrhosis: Anti-mitochondrial Ab 90% pos; anti-smooth muscle Ab neg
- Autoimmune chronic active hepatitis: Anti-smooth muscle Ab pos; anti-mitochondrial Ab occ pos at low titers
- Drug-induced chronic active hepatitis: Anti-mitochondrial Ab occ pos; Anti-smooth muscle Ab neg
What medications can commonly cause cholestatic liver disease?
Primary Sclerosing Cholangitis
Age of onset?
- Male to female 2:1
- Average age: 45
- 75% have IBD, esp UC
- No relation to severity of colitis
- Often asymptomatic at first
- Later Sx: Weakness, fatigue, itching, jaundice, cholangitis
- -increased Alk Phos
- -Mild increase AST and ALT
- -Bili usually normal
- -Positive pANCA
- Tests: MRCP and ERCP show multiple strictures of intra= and extrahepatic bile ducts. Do MRCP first with suspected PSC
Primary Sclerosing Cholangitis management and course
Course of disease?
Intervention for end-stage disease?
Treatment for pruritus?
- Slow, indolent course
- 5-year survival: 60-70%
- Most will progress to liver failure
- Cholangiocarcinoma in 10%
- Liver transplant for end-stage disease
- Ursodeoxycholic acid may help pruritus
- Stricture dilation
- No benefit from colitis treatment or colectomy
- These pts have significant colon cancer risk, more than just colitis -- go to every year colonoscopy
What is the associated disease and lifetime risk?
What other disease associations?
- Associated PSC: more commonly men
- -Lifetine risk of cancer: 10%
- -Time with PSC before Ca: Variable
- Other associations: choledochal cysts, clonorchis sinensis
- Sx: painless jaundice, pruritus
- Labs: Alk phos, GGT > transaminases
- - CA 19-9 > 100% in 80%
- ERCP: brush cytology 50% yield
- Use CT, MRI, EUS if needed
- If mass found early and procedures above non-diagnostic, may have to do surgery
Alcohol-induced hepatitis labs?
What to send out for increased ALT?
How do you workup persistent increased LFT?
- ALT more liver-specific than AST
- Alcohol AST:ALT 3:1
- Viral hepatitis ALT > AST
- Workup for increased ALT: full set biochemical -- Alk phos, direct and indirect bili, albumin, PT, CBC
- Persistent increase: Hepatitis panel, Fe, TIBC, Ferritin
Presentation of acute and chronic HBV?
- Only hepatitis DNA virus
- Incubation 1-6 mos
- Transmission: Sexual contact, IV drugs, vertical mother to newborn
- Activates cellular immune response
- Vigor of immune response determines course
- Acute HBV:
- - Usually acute infection asymptomatic
- - Can present as serum sickness due to immune complex disease with fever, urticaria, arthralgias
- - Glomerulonephritis, vasculitis, PAN
- Chronic HBV:
- - nonspecific sx
- - malaise, fatigue, anorexia
What labs are seen initially and later?
What marker becomes undetectable later?
What marker is seen during the window period?
What is the risk of chronic HBV?
What is the risk of chronic symptoms?
- Initial rise HBsAg
- Later anti-HBc
- HBsAg usually becomes undetectable
- Window period: Anti-HBc IgM
- HBeAg correlates with intact virus and infectivity
- Risk of chronic HBV inversely related to age
- - 90% infants infected at birth
- - 25-50% children age 1-5
- - 1-5% oder children and adults
- Development of clinical disease relates to age:
- - 10% of children have sxs
- - 30% adults over 30 have sxs
Hepatitis B markers
Marker for acute infection?
Marker for acute infection and chronic carrier?
Remote infection, immunized marker?
Window, remote infection, false pos?
More than one infection?
- Acute infection: HBsAg
- Acute infection and Chronic, carrier: HBsAg and HBcAb
- Remote infxn, immunized: HBsAb
- Remote infection: HBcAb, HBsAb
- Window, remote infection, false pos: HBcAb
- More than one infection: HBsAg, HBcAb, HBsAb
Chronic Active Hep B
What do the markers look like?
- Most have HBsAg
- Usually HBeAg (in the U.S.)
- Positive HBcAb IgG
- High levels of HBV DNA
HBV Chronic Carrier
Clinical and lab presentation?
- Termed non-replicative state
- HBsAg persists
- HBcAb present
- HBV DNA present at low levels
- Inflammatory response minimal
Hepatitis B Vaccines
What is the indication?
What do you give post-exposure?
What do you check for vaccine effect?
What population will have a reduced response to the vaccine?
- Recombinant vaccines
- Indicated pre- and post-exposure: prophylaxis
- Post exposure: Give HBIG too
- Check HBsAb for effect
- Reduced response in cirrhosis, chronic renal failure, immunosuppressed
- Immunocompetent patients: 90-95% develop Ab
- Chronic hemodialysis patients: 50-60% develop Ab
What do you give a newborn whose mother is HBsAg?
HBIG and vaccine at birth
Treatment of HBV
Whom to treat?
Options for treatment?
Which treatment has the highest risk of developing resistance?
- Any HBeAg+, and eAg- with HBV DNA, and compensated cirrhosis with HBV DNA greater and 2000
- Options for treatment: Interferon, lamivudine, adefovir, entecavir, telbivudine
- Lamivudine has highest risk of developing resistance
HBV and Liver Transplantation
What s the indication?
What medication to give after transplantation?
- Liver failure with Hep B is an indication for liver transplant
- High rate of recurrent infection (up to 100%)
- Give long-term HBIG, lamivudine
What is the lifetime risk for HCC?
- Lifetime risk HCC around 20%; therefore screen with alpha-fetoprotein and US q 6 months
- Risk of HCC varies with viral load: increased risk with HBV DNA > 10,000 copies/ml
Lab for acute infection?
- RNA virus
- Incubation 15-50 days
- Acute infection: Anti-HAV IgM
- Travel or working in high-risk contries
- Children in communities with high rates of disease (> 2 yr)
- Individuals with high-risk behavior
- Patients with chronic liver disease
HCV molecular biology
- Single-stranded RNA
- Genotype 1: 70% U.S. infection
- Prone to mutation - genetic diversity
Treatment of health care worker after needle stick?
- Sexual transmission is low. Monogamous relationship 10-20 years -- 5%
- Household contact -- extremely low
- Maternal infant transmission: < 5%
- Health care worker needle stick: 5-10% from known infected pt. No treatment needed after needle stick
HCV clinical spectrum
What is the incubation period?
- Acute infection: only 25-35% have sxs
- Rare, fulminant liver failure
- Incubation period: 7 weeks (range 3-20)
- Chronic phase
- - 30% carriers: no sxs and normal LFTs
- - 50% no sxs and abnormal LFTs
- - 20% clinical liver dz with sx
HCV Extrahepatic Disease
- Small vessel vasculitis
- Most common cause:
- - Essential mixed cryoglobulinemia
- - Skin rash: Purpura, vasculitis, urticaria
- - Joint, muscle aches
- - Porphyria cutanea tarda
- - Neuropathy and glomerulonephritis associated with cryoglobulinemia
What is the rash above, and what disease association?
Porphyria Cutanea tarda which is associated with Hepatitis C
What do you do if positive in low-risk pt?
- If positive in low-risk pt, confirm with Recombinant Immunoblot Assay or HCV-RNA
- HCV-RNA by PCR: Useful in response to tx, confirm diagnosis
- Liver bx: Assess severity, presence cirrhosis
- ALT usually > AST
Indications for treatment?
What are adverse effects of tx?
What is the most common genotype in the U.S.? How long do you treat?
What do you follow during treatment?
Who has poor response to treatment?
Who has the best response to treatment?
What is a side-effect of ribavirin?
What do you do if with mild side-effect (of ribavirin)?
What other preventive measure in pt with HCV?
- Pegylated interferon with weight-based ribavirin
- Indication: Abnormal LFTs, moderate fibrosis on bx
- Adverse effects: Flu sx, leucopenia, low platelets, fatigue, depression*
- *Be careful with pt with depression before treatment. Do not give interferon. Depression has to be under good control for fear of suicide.
- Genotype I: most common in U.S., has lowest response to treatment, treat for 1 year
- Genotype II and III: has better response, treat typically shorter for 24 weeks
- Follow HCV-RNA for treatment
- Overweight pt has poor response
- Best response: Female, less than 40, less fibrosis on biopsy
- Ribavirin side-effect: Hemolytic anemia
- Can use EPO if respoding but Hgb < 10
- Vaccinate for HBV and HAV
HCV and HIV
How do you treat the HCV?
What is the response rate?
What HIV med do you not co-administer?
- Tx: PEG interferon and ribavirin
- Only 27% sustained virologic response at 72 weeks
- No co-administration of didanosine
HCV and Hepatocellular CA
What is the median interval from dx to ca?
Long term intervention?
- Known complication
- Median interval: 30 years
- Surveillance: US and alpha-fetoprotein q 6 months
- RNA virus, requires HBV
- found in IV drug abuse, high-risk HBsAg carriers
- Can be severe if superinfects HBV carrier
- Diagnosis: Anti-HDV IgM
Who is at risk?
- Fecal-oral spread like HAV
- Far East, Africa, Central America
- Contamination of water supply
- No chronic state
- High-risk fulminant in pregnancy (mortality 20%)
Autoimmune Chronic Hepatitis
Who is commonly affected?
- Young women, 50% autoimmune disease
- Acute, fulminant, or indolent
- Can be asymptomatic or nonspecific sx
- Anti-smooth muscle Ab -- 80%
- Low titer AMA, ANA
- Elevation of gamma globulin
- Tx: Prednisone and azathioprine
Drug-Related Liver Disease
- Chronic hepatitis: Methyldopa, nitrofurantoin, phenytoin
- Cholestasis: Oral contraceptives, anabolic steroids, chlorpromazine, erythromycin
- Fulminant hepatitis: Ketoconazole, INH
- Indolent cirrhosis: Methotrexate
Drug-Related Liver disease
Acetaminophen toxicity -- who is at risk?
- - Glutathione reduces toxic metabolite
- - Glutathione depletion-- toxin accumulates- treat with N-acetylcysteine acutely after checking acetaminophen level
- Chronic, moderate-to-heavy alcohol induces cytochrome p450 and depletes glutathione. Therefore, at risk for toxicity at relatively low levels; e.g., dose < 4 gm a day
- Other risks: dieting, weight loss, gastric bypass, malnutrition
Who is at risk?
What is the usual presentation?
- Young women
- Oral contraceptives and Glycogen Storage Disease
- Typically solitary lesion
- Can cause RUQ pain and rare complications like rupture/hemopritoneum
Alcohol Liver Disease?
- Macrovesicular fat accumulation
- Women more susceptible
- GGT disproportionately high
- AST:ALT = 3:1
- AST less than 300
Non-Alcoholic Fatty Liver Disease (NAFLD)
What is the diagnostic test?
- Also known as Non-alcoholic steatohepatitis (NASH)
- Typical pt: Obese, diabetic female, hyperlipidemia
- Can cause hepatomegaly, RUQ pain
- Mild increase: ALT > AST
- Ultrasound: Fat, diffuse
- Can cause fibrosis, cirrhosis
Associated with what risk factors?
Who is at risk?
How do you decrease risk?
- Hepatomegaly, RUQ bruit
- Labs: High alk phos, hypercalcemia, high alpha-fetoprotein
- 75% prior cirrhosis - any type
- Developing countries: HBV acquired at birth
- Highest risk: non-whites
- Rising incidence overall
- Leading U.S. causes: HCV, HBV, ETOH
- HCV with cirrhosis: Cancer develops 1-4% per year
- INF Tx may decrease risk of HCC
- Surveillance: AFP (alpha-fetoprotein) and ultrasound q 6 months
- Criteria for liver transplant
- Common causes: ETOH, HBV, HCV
- Uncommon causes: Post-necrotic (drug), biliary disease, R-sided CHF, A1AT, hemochromatosis, Wilson's, schistosomiasis
- Variceal hemorrhage
- 30% mortality, 30% cirrhotics bleed
- Risk of bleeding higher for larger varices
- Primary prevention: beta blockers
- Acute treatment: Banding (or sclero) and ocreotide infusion
- Treatment failure: TIPS
- Antibiotics to prevent SBP (if with ascites)
- Hepatic encephalopathy
- Hepatorenal syndrome
- -Oliguric renal failure
- -Renal vasoconstriction
- -Often iatrogenic, poor survival
- -Urinary Na < 10-Attempt volume expansion
- Many precipitating factors: GI bleed, pneumonia, high protein intake, low K, sedatives, alkalosis
- Hyperreflexia, asterixis
- Treat: Lactulose, antibiotics -- neomycin or metronidazole
Explain ascites fluid workup
- - Bloody: Ca
- - Cloudy: infection
- - Milky: lymphatic obstruction
- Serum albumin - Ascitic albumin
- - Difference > 1.1 = portal hypertension
- - Difference < 1.1 = TB, nephrotic syndrome, pancreatitis, peritoneal carcinomatosis
Causes of Serum/Ascites albumin > 1.1
- Portal HTN
- Liver failure
- Budd-Chiari syndrome
- Right heart failure
Causes of Serum/Ascites albumin < 1.1
- TB peritonitis
- Nephrotic syndrome
- Peritoneal carcinomatosis
Key Concepts: Ascites
- Dietary Na restrictionis vital
- Cirrhosis is most common vause
- Spironolactone is diuretic of choic
- Avoid NSAID, ASA, aminoglycosides
Contraindications to TIPS:
- CHF, encephalopathy are contraindications
- Low platelets, transplant candidate are not contraindications
Spontaneous Bacterial Peritonitis
What are the risk factors?
Criteria for diagnosis?
- Risk factors: Prior SBP, bili > 2.5, fluid protein < 1, UGI hemorrhage
- Criteria for diagnosis: > 250 neutrophils on paracentesis
- Common organisms: E. coli, S. pneum, Klebsiella
- Initial treatment: Cefotaxime
- Give IV albumin: less renal impairment and lower mortality
When to suspect SBP?
- Unexplained leukocytosis
- Unexplained renal failure
- Hepatic Encephalopathy
- Abdominal pain not always present
- *Have a low threshold for doing paracentesis on pt with tense ascites and any sx such as confusion, fever
- Unconjugated hyperbilirubin (indirect, without bilirubinuria)
- Jaundice after physical stress, fasting
- Common, hereditary condition
- Autosomal dominant
- Genetic or acquired
- C282Y mutation 0.44% of U.S. non-Hispanic white population
- Autosomal recessive
- Abnormal increased intestinal Fe absorption
- Fe deposition: Liver, heart, pancrease, pituitary
- Associated with arthritis
- Sx: Hepatomegaly 95%, hyperpigmentation 90%, diabetes 65%, arthropathy 40%, Cardiac 15%
- Dx: Fe saturation, ferritin, HFE gene (use if Fe sat and ferritin are positive)
- Screen family members
- Treat with phlebotomy, try to get ferritin level around 50
- Autosomal recessive
- Presents: Adolescents with liver, neuro, personality change
- Impaired excretion of copper
- Serum Ceruloplasmin is low
- Urinary copper is high
- Slit lamp exam show Kayse-Fleisher ring
- Liver biopsy: high copper, but this is also seen in PBC and PSC
Liver Disease During Pregnancy
Labs with hyperemesis?
Presentation of Intrahepatic cholestasis of pregnancy?
When during pregnancy is the best time for surgery?
- Hyperemesis: Mild increase AST/ALT first trimester
- Intrahepatic cholestasis of pregnancy: Itching, late in pregnancy, increased ALT/AST, ↑↑Alk Phos, and Bili
- Gallbladder and CBD stones: Pain, abnormal U/S, 2nd trimester is best for surgery
- Viral hepatitis E can be severe
Fatty Liver of Pregnancy
When does it occur?
What is the treatment?
- Microvesicular fat deposition
- Occurs in last trimester
- Abdominal pain, nausea, vomiting
- Encephalopathy, hypoglycemia -- due to rapid liver failure
- Pruritus is rare
- Complications: Fulminant liver failure, encephalopathy, jaundice, hypoglycemia, coagulopathy
- Modest elevation of AST/ALT/Bili
- Tx: Prompt delivery
- Consider for any pt with end-stage, acute/chronic disease or with HCC
- End-stage disease: Bili > 10, Alb < 2.5, INR 2
- Refractory sx: pruritus, encephalopathy, ascites
- Assess with MELD: Includes bilie, INR, and creat
A liver biopsy showing onionskin fibrosis with lymphocytic infiltration, suggests?
Describe gastroenteritis due to Staph aureus
Onset of symptoms?
Staphylococcus aureus produces illness indirectly via a specific enterotoxin. Patients present with rapid onset of symptoms, usually within 30-60 minutes of ingestion. Patients typically experience nausea and cramps followed by vomiting. Duration of symptoms is short, usually 24-48 hours. Since humans are the principal reservoir for Staphylococcus, uncooked foods that require extensive handling, such as salads, eggs, dressings and sandwich meat, are the most common sources. Staphylococcus aureus also causes dermatologic lesions, such as pustules and abscesses, which, when present on the skin of food handlers, can be a source of contamination. In addition, Staphylococcus aureus is present in cows; therefore, milk and cheese products that are not adequately refrigerated can also cause illness.
Describe gastroenteritis due to Bacillus cereus
Onset of symptoms?
Duration of illness?
Bacillus cereus is another organism that causes illness via the production of enterotoxins. 2 enterotoxins are produced by these spore-forming bacteria, 1 that is heat stable and another that is inactivated by heat (heat labile). The heat stable species causes primarily vomiting, while the heat labile form results predominantly in diarrhea. Intoxication caused by Bacillus cereus is most commonly associated with foods - classically rice - that have been reheated after having been left at room temperature. Illness usually occurs within a few hours of ingestion and usually resolves within 24 hours.
Describe gastroenteritis due to Clostridium perfringens
What is the gram-stain characteristic?
Onset of symptoms?
- Gram-positive, rod-shaped, anaerobic
- Clostridium perfringens is also a toxin-producing organism. Cramping and diarrhea are the most common symptoms of illness caused by C. perfringens. Nausea also occurs, but vomiting is rare. Inadequately heated meat products are the most common source. Onset of symptoms occurs within 12 hours of ingestion, and symptoms usually abate in a day.
Describe the intestinal effect of Giardial lamblia infection.
Onset of symptoms?
Mode of transmission?
Giardia lamblia is a protozoon that causes upper intestinal enteritis marked by fatigue, chronic diarrhea, steatorrhea, colicky abdominal pain, and bloating. Infection can occur with ingestion of a single cyst, and symptoms generally appear within 1 week of exposure. Fecal contamination of drinking water is a common source of infection, as is person-to-person infection via hand-to-mouth contact with the feces of an infected individual. Outbreaks have occurred in institutional facilities such as day care centers by this method. Diagnosis of Giardia lamblia can be made by visualization of trophozoites or cysts in appropriately prepared fecal specimens.
Primary biliary cirrhosis
What is it?
What is the diagnostic triad?
- Primary biliary cirrhosis is a chronic progressive cholestatic liver disease of unknown cause.
- Occurs predominantly in women (80% to 90% of cases) between 40 and 60 years of age.
- The diagnostic triad associated with primary biliary cirrhosis includes a cholestatic liver profile, positive antimitochondrial antibody titers, and compatible histologic findings on liver biopsy.Serum alkaline phosphatase level is usually elevated ten times or more above normal.
What is chronic intestinal pseudo-obstruction?
Chronic intestinal pseudo-obstruction is characterized by chronic or recurrent episodes of abdominal pain, distention, nausea, vomiting and obstipation; the disorder may be due to myopathic causes (such as scleroderma) or neuropathic causes (such as amyloidosis, diabetes mellitus, and paraneoplastic syndromes).
How do you treat unresectable metastatic hepatocellular carcinoma?
Sorafenib is beneficial in treating patients with unresectable hepatocellular carcinoma.
How do you treat primary biliary cirrtosis?
- Ursodeoxycholic acid therapy is indicated for early-stage primary biliary cirrhosis and may reduce the rate of liver transplantation and prolong survival in affected patients.
- Treatment with ursodeoxycholic acid improves the biochemical profile, reduces pruritus, decreases progression to cirrhosis, and delays the need for liver transplantation if begun at an early stage of disease. The data are more conflicting for later stages of disease. Therapy is usually continued indefinitely.
How do you evaluate a pt with hematochezia who is younger than 40 years of age and low risk for colonic neoplasia?
Patients at low risk of colonic neoplasia may undergo evaluation for hematochezia with flexible sigmoidoscopy rather than colonoscopy.
How do you manage recurrent hepatitis C after liver transplantation?
- a liver biopsy is indicated to distinguish between rejection and recurrent HCV infection
- HCV is known to recur in the transplanted liver almost immediately after surgery if the patient was viremic at the time of transplant. As a result, some degree of inflammation is to be expected and in some patients early histologic injury as the HCV establishes itself in the new liver. In a small percentage of patients, the HCV can recur very quickly and aggressively a few months after liver transplantation, a condition termed rapidly recurring cholestatic hepatitis C, which carries a poor prognosis. Fortunately, most patients have a much more benign course, with approximately 30% still developing recurrent cirrhosis within 5 to 10 years after transplantation. Identifying those patients who show histologic injury in the liver graft and initiating therapy in these patients is important.
When do you suspect a diagnosis of Hereditary Nonpolyposis Colorectal Cancer?
Most patients with HNPCC are identified from their medical history. The diagnosis should be suspected in persons who have multiple family members with cancers of the colon, endometrium and ovaries, small bowel, ureter, renal pelvis, and pancreaticobiliary system. The Amsterdam II clinical criteria for HNPCC use the 3-2-1 rule: three relatives with an HNPCC-associated cancer, two generations affected, one person diagnosed before age 50 years.
Explain the management of patients with HNPCC:
- Management of patients with HNPCC or those who are considered at risk for the disease consists of colonoscopy every 1 to 2 years beginning at age 20 to 25 years or 10 years before the age at diagnosis of the youngest family member diagnosed with colon cancer.
- Annual colonoscopy is recommended after age 40 years.
- The risk for gynecologic malignancies is greatly reduced in affected women who undergo prophylactic hysterectomy and salpingo-oophorectomy, and many physicians advocate surgery for women who no longer wish to bear children.
- Women who do not choose prophylactic surgery should have a pelvic examination with endometrial sampling, transvaginal ultrasonography, and measurement of serum CA-125 every 1 to 2 years from age 30 years. Screening for urinary tract cancers with urine cytology and renal ultrasonography should also be performed every 1 to 2 years beginning at age 30 years.
Management of pt with UC or Crohn's.
When do you start to screen for malignancy?
The annual cancer risk is estimated to be 1% to 2% per year after 8 years of disease, and, therefore, colonoscopic surveillance should be started in patients who have had inflammatory bowel disease for 8 years or longer. For patients with inflammation limited to the left colon, recommendations vary, with some authorities initiating surveillance after 15 years' duration of disease. If dysplasia is detected on biopsy in a patient with colitis, the risk for colon cancer is markedly increased even at sites distant from the site of biopsy; colectomy should, therefore, be considered even in the absence of a preoperative cancer diagnosis.
What are the three classic findings in chronic pancreatitis?
- Abdominal pain that is usually mid-epigastric
- Postprandial diarrhea
- DM secondary to pancreatic endocrine insufficiency
What antiendomysial antibodies?
a marker for celiac disease
How do you manage gastric adenocarcinoma?
Upper endoscopy is often the first test performed to establish the diagnosis. CT scanning is often the next step to evaluate for metastatic involvement, but it cannot accurately assess the depth of disease in early lesions. Conversely, endoscopic ultrasonography is the most reliable preoperative test for assessing depth of invasion, but it is poor at determining distant metastases. Positron emission tomography may be used preoperatively to follow-up suspicious but nondiagnostic abnormalities detected on CT scan
How do you evaluate nonalcoholic steatohepatitis?
Patients with metabolic syndrome and persistently elevated liver enzyme concentrations, despite adequate treatment of its components, should undergo liver biopsy.