Flashcards in GI 6/25 Deck (568):
Indications for ERCP:
-suspected biliary obstruction
-discovery of otherwise undetectable common duct stone
-diagnosis and treatment of pancreatic duct obstruction
-diagnosis of primary sclerosing cholangitis (MRCP a non-invasive, safe alternative)
-treatment of choledocholithiasis with cholangitis
-further evaluation of abnormal biliary or pancreatic duct imaging (from CT/MRCP/EUS)
ERCP is contraindicated in acute pancreatitis, except in the following conditions?
-ascending cholangitis (bacterial infection causing cholangitis)
MRCP can be used for?
-diagnose bile duct obstruction
-diagnose chronic pancreatitis
-assess a lack of clinical improvement in acute pancreatitis
-test of choice fro primary sclerosing cholangitis
What are the indications for EUS?
-staging of malignancy of the GI tract, biliary tree and pancreas
-diagnosis of chronic pancreatitis
-diagnosis and treatment of complications of pancreatitis
-tissue sampling of organs adjacent to the GI tract
providing access to pancreatic duct or biliary tree
What are the indications for an EGD?
-evaluation of painful swallowing (odynophagia)
-determining the presence of a peptic ulcer (instead of UGI series or after UGI negative)
-Workup of GERD if initial treatment fails or alarm signs
-Dysphagia (if needed after barium swallow)
-Foreign body (evaluation/removal)
-Evaluation of small bowel disease (Celiac)
-Persistent dyspepsia despite treatment (normal EGD is a prerequisite for diagnosing non-ulcer dyspepsia)
-Placement of feeding tube or drains
What are the 3 categories of dysphagia?
-Transfer disorders (oropharyngeal)
*neurologic deficits/muscle dysfunction (stroke, parkinson's, ALS)
-Anatomic or structural
*failure of effective peristalsis and/or failure of LES relaxation
What is the first test usually performed in the workup of dysphagia?
*preferred in new-onset dysphagia with liquids or neuro symptoms
What are the reasons barium swallow is performed prior to EGD in evaluation of dysphagia?
-Increased risk of perforation when EGD performed in a patient with diverticula or high-grade obstruction
-Information may preclude the need for EGD
-Provides information for type and severity of underlying lesion
What is the test of choice if a patient with history of reflux, presents with slight-to-moderate dysphagia for solids?
-pre test probability ishigh for stricture secondary to chronic reflux
When is esophageal manometry performed in the evaluation of dysphagia?
only if dysphagia persists after negative barium swallow and EGD studies
What are the characteristic pathologic findings of achalasia?
-neuronal denervation and ganglion cell degeneration of myenteric plexus
-absence of organized peristalsis in the esophageal body
-LES does not relax completely with swallowing
-Often LES has elevated resting pressure
What are the characteristic clinical features of achalasia?
-dysphagia for solids and liquids
-long standing symptoms, usually years
-regurgitation of food, especially at night
-no age or gender predilection
How to diagnose achalasia?
*bird-beak narrowing distally, long transit time
*2nd test to confirm diagnosis and exclude tumor (pseudoachalasia)
*shows absence of normal peristalsis, often with non-relaxing LES
-rapid onset of symptoms of dysphagia (achalasia)
-age > 60 years
-profound weight loss
-tumor at the esophagastric junction
What is the preferred treatment for achalasia?
-pneumatic dilation (preferred)
*5% risk of perforation
-Botox injection may be an alternative
*effective in 65% of patients
*need repeat injection in 6-12 months
What is diffuse esophageal spasm (DES)?
simultaneous, nonperistaltic contraction of the esophagus, often precipitated by cold or carbonated liquids
This is a cause of DES, even in the absence of symptoms?
A classic corkscrew pattern seen on barium swallow is indicative of what disorder?
How to diagnose DES?
-Barium swallow (generally normal, but may show corkscrew esophagus)
*reveals excess, simultaneous (nonperistaltic) contractions in the distal esophagus with normal LES relaxation
What is the treatment of DES?
Reassurance is most important
*If further treatment required
1. Diltiazem or Imipramine
2. Isosorbide or Sildenafil
3. Botox injection
What type of problem causes slowly progressive dysphagia for solids and then to liquids?
What is a likely cause of anatomic obstruction of the esophagus in younger patients?
In older patients?
-Younger --> Schatzki ring
-Older --> cancer (esophageal or extrinsic compression) or peptic stricture
Common finding with Schatzki ring?
What is the treatment for Schatzki ring?
-Dilation (bougie method or through-the-scope hydrostatic balloon)
*PPIs started after dilatation
What anatomic problem causes slowly progressive intermittent dysphagia to solid food?
Schatzki ring (lower esophageal ring)
presents with a history of slowly progressive, constant (not intermittent) dysphagia for solid foods
What are the causes of esophageal stricture?
-Chronic acid reflux (most common)
-Lye ingestion (ingested decades before)
Diagnosis and treatment of esophageal stricture?
-Dilation, PPI's if from reflux
rare disorder, results in dysphagia in post-menopausal women and is associated with iron-deficiency
What is the most sensitive test in diagnosing Hereditary Hemochromatosis?
serum transferrin saturation
- > 45-50%
What is the calculation for stool osmotic gap?
290-2 x (stool sodium + stool potassium)
Evaluate findings of stool osmotic gap?
-gap > 100 --> osmotic diarrhea
-gap less than 50 --> non osmotic
How is the diagnosis of microscopic colitis made?
biopsies of the colon -->
-predominance of intraepithelial lymphocytes with few neutrophils or eosinophils in the lamina propria of the colonic mucosa (lymphocytic colitis)
-thickened subepithelial collagen band (collagenous colitis)
Neurologic problems involving the swallowing and/or esophageal peristaltic mechanism cause this type of dysphagia presentation
dysphagia to solids and liquids from the time of onset
-examples: stroek, parkinsonism, bulbar palsy (lower motor neuron - ALS, MS), pseudobulbar palsy (UMN - ALS)
Test of choice if aspiration suspected secondary to dysphagia (neurologic dysfunction)
3-phase barium swallow
term for shiny, hard, thickened skin
-called systemic sclerosis when it involves internal organs
Most common connective tissue disease involving the esophagus
Diffuse Systemic Sclerosis (SSc)
*more than 80% of patients have involvement of the esophagus
What is the LES pressure in patients with dysphagia due to SSc?
"wide open" --> low or no tone/pressure
-peristalsis --> very weak to absent in the distal 2/3 of the esophagus
-causes severe acid reflux change to the esophagus
Dysphagia in SSc is caused by any 1 or a combination of 3 problems:
Workup for dysphagia in SSc?
*esophagitis --> PPI therapy, f/u EGD in 2-3 months to confirm adequate PPI dose
*stricture --> EGD with dilation
-occurs most commonly in men, age 20-40 years
-leading symptom is recurrent attacks of dysphagia with food impaction
-IgE elevated in 2/3 of patients
eosinophilic esophagitis (EoE)
Laboratory findings in eosinophilic esophagitis?
-IgE elevated in 2/3 of patients
-peripheral eosinophilia (30% of patients)
What is the EGD finding in EoE?
-scalloped appearance with longitudinal furrows, ridges or rings (trachealization)
-dense eosinophilic infiltration of the esophageal epithelium ( > 15 eos/HPF)
Treatment of EoE?
-Swallowed fluticasone (bid) or viscous budesonide --> usually response within 1 week
-PPI may be helpful in those with concomitant reflux
Common causes of odynophagia?
Common causes of pill-induced esophagitis?
-Doxycycline (teenager with acne)
Diagnosis of pill-esophagitis?
-discontinue offending agent
Common OI's leading to esophagitis?
-Candida (treated with fluconazole)
-Herpes simplex virus
What drugs interact with PPI's?
-Decrease absorption and serum levels: thyroxine and itraconazole/ketoconazole
-Increase absorption: digoxin
What are some of the short term effects of PPI's?
-CAP (appears more likely within 30 days of starting therapy, and especially within 48 hours)
What are some of the long term effects of PPI's?
-Fracture risk increased
-Hypomagnesemia (muscle spasms, arrhythmias, seizures)
Occurs when PPI's are stopped abruptly after several months?
rebound acid hypersecretion
What is the clinical presentation of GERD?
-persistent, nonproductve cough, especially with hoarseness
-continual clearing of the throat
-feeling of fullness in the throat
-commonly worse at night
What are the "alarm" signals in a patient with GERD symptoms?
These indicate the need for what?
-Blood in stool
-Family history of PUD
-Iron deficiency anemia
-Abnormal physical exam
-Long duration of frequent symptoms, especially in Caucasian males > 50 years old
-Failure to respond to full doses of PPI
*EGD should be performed if: Alarm symptoms or Barrett esophagus (suspected)
What diagnostic test may be helpful for atypical GERD?
24-hour esophageal pH monitor
For how long is severe GERD treated?
And with what?
-Indefinitely (particularly if evidence of esophagitis)
What is the cause/pathology of GERD?
-transient relaxation of LES
-vagally mediated reflex, physiologic mechanism of belching
-hiatal hernia is a risk factor for GERD
LES pressure is increased by what agents?
LES pressure is decreased by what agents?
-progesterone (pregnancy increases GE reflux)
Most non-cardiac chest pains (70%) are caused by this?
What are the extraesophageal manifestations of GERD?
-frequent sore throat
-hoarseness, laryngitis, clearing of the throat
-loss of dental enamel
-exacerbation of asthma
-VCD (vocal cord dysfunction)
GERD is associated with what 2 respiratory disorders?
spasm of the vocal cords with associated inspiratory stridor
Diagnostic workup and treatment for a GERD patient without alarm signs?
trail of PPI's --> EGD if treatment fails
Check this in patients with GERD symptoms who do not respond to PPI's?
-medications that may delay gastric emptying (CCB's, antihistamines, narcotics, TCA's, anticholinergics)
What are the indications for antireflux surgery (fundoplication)?
-refractory to medical treatment
-young patients with severe disease
-alternative to long-term PPI's
What percentage of patients who undergo fundoplication (reflux surgery) will still require PPI's?
In patients with GERD, what study must be done before antirflux surgery?
*results may influence the performance of the fundopliction
What is the pathologic definition of Barrett esophagus?
change in cell type caused by chronic reflux
squamous --> specialized intestinal metaplasia (columnar epithelium with goblet cells)
What cancer is associated with Barrett's esophagus?
-30x the normal rate if present
-0.52% per year
-risk related to the length of time present, presence of hiatal hernia, degree of dysplasia, concurrent smoking
What follow-up is indicated in patient's with Barrett's esophagus?
-No dysplasia --> 3-5 years
-Low-grade dysplasia --> 6-12 months
-High-grade dysplasia --> 3 months
*eradication therapy now recommended over surveillance
What is the treatment of choice for Barrett's with high-grade dysplasia?
Discuss the differences between adenocarcinoma and squamous cell cancer of the esophagus?
Adenocarcinoma (most common)
-occurs in the distal 1/3 of the esophagus
-Risk factor: Barrett's esophagus
Squamous cell carcinoma
-occurs in the proximal 2/3 of the esophagus
-Risk factor: Tobacco, alcohol (most important-syngergistic), achalasia, lye stricture, Plummer Vinson syndrome
Treatment for esophageal cancer?
-Small and localized --> surgical resection
-Large or metastasized --> combination chemotherapy (cisplatin + 5FU) + radiation therapy prior to surgery
*combination = 2 year survival of 38% (vs. 10% with radiation therapy alone)
Define Zenker diverticulum
-outpouching of the upper esophagus
-presents with foul-smelling breath and may regurgitate food eaten several days earlier
-most common cause of transfer dysphagia
Most common cause of transfer dysphagia, but can also cause transport dysphagia
condition in which patients will be noted to have extremely high gastrin levels ( > 500)
achloryhydria (autoimmune gastritis) or pernicious anemia
*due to loss of inhibitory effect
What is the clinical presentation of dyspepsia?
What are the possible diagnostic/treatment approaches to dyspepsia?
-Test and treat if H. pylori positive
-Conduct a PPI treatment trial
-Order EGD if alarm symptoms or failure of therapy
When should you test for H. pylori?
-any prior history of PUD, complicated or uncomplicated, and especially duodenal ulcer
-current findings on EGD show ulcer disease, erosive gastritis, or duodenitis
-MALT lymphoma is present; and/or
family history of gastric cancer
Is the CLOtest accurate if a patient is taking a PPI?
What other H. pylori tests are affected by PPI's?
-No. Less sensitive if on PPI's
-Other Rapid Urease tests (RUT's) are also affected by PPI's
Which type of H. pylori test is not good for checking effectiveness of treatment?
-PPV less than 50%
-can stay positive for years after treatment
Define Non-ulcer dyspepsia
recurrent upper abdominal pain with a normal EGD
Define Type A Gastritis?
-Autoimmune, Atrophic, pernicious Anemia, Achlorhydria
-affects the proximal stomach (fundus and body only)
What is the pathophysiology of pernicious anemia?
-autoantibodies against both intrinsic factor and parietal cells --> pernicious anemia --> achlorhydria with secondary hypergastrinemia ( levels > 1000)
Define Type B Gastritis?
-most common form of chronic gastritis (80%)
-usually occurs secondary to chronic infection with H. Pylori --> treatment results in resolution of gastritis
Oral medications which require gastric acid for optimal absorption?
Name some common causes of erosive gastropathy?
-Severe physiologic stress
Where is stress-related mucosal damage (SRMD) commonly seen?
*avoided with H2 antagonists, PPI's, early feedings
What is the most effective treatment of SRMD?
continuous infusion of an H2 receptor antagonist or PPI
H. Pylori infection can lead to these complications?
-gastric B-cell (MALT) lymphoma
Which type of patient's should be treated for H. Pylori?
Only symptomatic patients with:
-history of gastric/duodenal ulcer
-personal/family history of gastric cancer
-personal history of MALT lymphoma
What is the gold standard for H. pylori testing?
histologic examination of biopsied antral mucosa (obtained during EGD)
What type of H. pylori testing is first line for checking effectiveness of treatment and also to identify active disease?
Urease breath test (UBT)
-H. pylori breaks down urea --> ammonia + CO2
-95% sensitivity and specificity
This is a good method to determine primary diagnosis of H. pylori and is the best test for checking effectiveness of treatment?
Fecal antigen test (FAT)
-can be used if patient on PPI therapy
H. pylori testing which is no longer recommended due to low PPV?
How long should PPI's be stopped prior to CLOtest and urease breath test?
PPI's interfere with this type of H. pylori testing?
urease test (any)
What is a common medical regimen for H. pylori infection?
Triple therapy (2 antibiotics + PPI)
-OCLAM (BID x 14 days) --> 80% cure rate
*Clarithromycin 500 mg
*Amoxicillin 1 gm
What are alternative H. pylori treatments?
What are the indications for post-treatment testing in H. pylori?
-History of H. pylori associated ulcer
-Persistent dyspepsia despite the test-and-treat strategy
-H. pylori-associated MALT lymphoma
-Resection of early gastric carcinoma
When should post-treatment testing for H. pylori be performed ?
No sooner than 4 weeks after completion of treatment
What is the most common cause of peptic ulcer disease?
Helicobacter pylori infection
What are the 4 well-confirmed causes of PUD?
-H. pylori infection (50%)
-High acid-secreting states (Zollinger-Ellison, accounts for 1-3% of cases)
-Crohn disease of the duodenum/stomach
What is the prevalence of ulcers in patients on chronic NSAID therapy?
What are the treatment options in PUD in patients requiring NSAIDs?
-Nonacetylated NSAIDs (salsalate)
-NSAIDs that are non-acidic prodrugs (nabumetone; Relafen)
-NSAIDS with PPI or prostaglandin E analog (misoprostol)
What are the risk factors for conventional NSAID-induced PUD?
-first 3 months of use
-history of ulcer disease or prior UGIB
-cardiac disease/concurrent ASA use
-concurrent steroid use
How does smoking affect PUD?
exacerbates the ulcer (in both gastric and duodenal PUD)
-decreases healing rate
-increases recurrence and perforation rate
What is the relationship to PUD with:
-Alcohol --> ulcerogenic
-Corticosteroids --> not ulcerogenic but double the risk of serois NSAID-associated GI complication (bleeding risk may be 10-fold)
How is PUD diagnosed?
-Younger, healthy patients -->
*trial H2 blocker or PPI
*test-and-treat is also acceptable
-All other patients --> EGD
In what situations is EGD always indicated for PUD?
-symptoms include dysphagia or odynophagia
-Abnormal UGI (barrium swallow) or CT scan
-Family history of duodenal ulcer disease
How is perforated gastric/duodenal ulcer diagnosed?
-AXR (upright) --> air in peritoneal space
*EGD and UGI contraindicated until perforation is excluded
In what situation is Sucralfate the drug of choice in nonbleeding PUD?
-also binds PO4
-used in short term --> leads to aluminum accumulation and metabolic bone disease if used long term
What are the indications for surgery in PUD?
-UGIB (most common)
*5% cannot be stopped with endoscopy
-Gastric outlet obstruction
*initial treatment balloon dilation
*25% surgery indicated
-Recurrent/refractory ulcers (rare)
-Zollinger-Ellison syndrome (ZES)
*surgery for underlying gastrinoma)
Most common cause of duodenal ulcers?
Most common cause of gastric ulcers?
What is the association between gastric ulcers and gastric cancer?
No associated risk
-examine all nonhealing ulcers via EGD with 6 biopsy samples to r/o cancer
What is the main cause of bleeding ulcers in the U.S.?
*risk is dose related
Name 4 EGD findings that indicate increased risk for rebleed of a peptic ulcer?
-Larger size of the ulcer
-Active bleeding at time of endoscopy (risk of rebleed 55%)
-Visible vessels on a non-bleeding ulcer (increases the risk for rebleed to 43%)
-Visible clot (rebleed risk = 22%)
What is the best initial treatment of an actively bleeding peptic ulcer (or adherent clot/visible vessel)?
combination therapy consisting of:
-injection (epinephrine or sclerosant)
-thermal/laser coagulation or hemoclip
Causes telangiectasias on the skin, buccal and nasal mucosa and throughout the GI tract, lungs, and brain?
Osler-Weber-Rendu (hereditary hemorrhagic telangiectasia)
-Causes dark melanin spots on the lips, buccal mucosa and the hands and feet
-most patients have polyps that can occur anywhere from the stomach to the rectum
Peutz-Jeghers syndrome (PJS)
Define Zollinger-Ellison Syndrome (ZES)?
-occurs when a gastrinoma --> causes refractroy (usually duodenal bulb) ulcers and diarrhea +/- steatorrhea
-Duodenum (50%), Pancreas (25%), 90% found in ZE triangle (porta hepatis, mid-duodenum, head of pancreas)
-80% sporadic form and 20% associated with MEN type I
What is the most common presentation of ZES?
What is the first step in diagnosis of ZES?
-Serum gastrin level
*while patient off PPI
-Elevated Gastrin --> CT, EUS, Somatostatin receptor imaging
What is the treatment for ZES?
*50% cured with resection of primary tumor (if no evidence of metastatic disease)
-PPI therapy (usually higher dose and increased long term)
What are other conditions associated with elevated Gastrin levels?
-Chronic type A gastritis
-Achlorhydria (caused by PPI)
What is a complication of persistently high gastrin levels?
What is the usual cause of gastric carcinoid?
Chronic hypergastrinemic states
What are the type carcinoids?
Based on cause of hypergastrinemic state
-Type 1 (70-80%)
*Autoimmune gastritis/pernicious anemia
-Type 2 (5%)
*ZES when it occurs as part of MEN type I
-Type 3 (20%)
*Spontaneous (most aggressive)
What are the 4 significant malignancies of the stomach?
-Adenocarcinoma (most common, 95%)
-GIST (gastrointestinal stromal tumors; leiomyosarcoma)
What are the clinical and environmental risk factors for gastric cancer?
-Chronic H. pylori infection
-Metaplastic (chronic) atrophic gastritis
-Menetrier disease ( = large stomach folds from epithelial cell hyperplasia)
-Adenomatous gastric polyps (rare)
Distal gastric cancer is more strongly associated with what environmental risk factors?
-diet low in fruits and vegetables
-diet high in dried, smoked, and salted foods
-foods rich in nitrates and nitrites
What skin condition is most commonly associated with gastric cancer?
-commonly seen in Type II DM and obesity
Carcinoid may be associated with which skin condition?
What is the relationship of alcohol/gastric ulcers to gastric cancer?
No relationship to gastric cancer
How do you rule out gastric cancer in a patient with a nonhealing gastric ulcer?
Endoscopy with multiple biopsies
-tumor markers (CEA and AFP) are not useful in early gastric cancer
What are the most common postgastrectomy syndromes?
-blind loop syndrome
-afferent loop syndrome
What is the clinical presentation of dumping syndrome?
postprandial vasomotor symptoms (palpitations, sweating, lightheadedness)
What are the 2 types of Dumping syndrome?
-occurs 30 minutes after eating
-uncertain etiology (hyperosomolality of food and fluid shifts in the small bowel)
-occurs 90 minutes after eating
-due to hypoglycemia
What is the treatment for dumping syndrome?
-restrict sweets and lactose containing foods
-separate liquid and solid intake by at least 30 minutes
-encourage frequent small meals that are high in protein and complex carbohydrates
What is Blind Loop Syndrome?
-Manifested by fat and B12 malabsorption
-bacterial overgrowth in a loop
-Diagnosis --> low D-xylose absorption test
What is the presentation of Afferent Loop Syndrome?
-Abdominal bloating and pain 20 minutes - 1 hour after eating
-Vomiting relieves symptoms
Highly variable gastric emptying is seen in this patient population?
*Type I > Type II
*emptying may be fast, slow, normal
What is the clinical presentation for gastroparesis?
Nausea, vomiting, early satiety and predisposition for bezoars
What are the causes of gastroparesis other than DM?
-autonomic dysfunction (amyloid neuropathy
-infiltrative process of the smooth muscles (scleroderma, amyloidosis)
-antecedent viral infection (particularly norovirus and rotavirus)
-CNS disorder (stress, MS, parkinsonism, tumor, cord injuries)
What is the best diagnostic test for suspected gastroparesis?
-rule out obstruction first
-Gastric emptying study (to confirm)
What is the treatment for gastroparesis?
-dietary modification (low-fat, low-residue; multiple small meals)
-tight control of blood glucose
-symptom management (anti-emetics)
-metoclopramide (FDA warning for long-term use, extrapyramidal side effects may become permanent)
-domperidone (widely used outside the US)
Medication which can be used in the short term setting for gastroparesis?
-similar in structure to motilin
-stimulates gastric motility
-not very useful as long term agent
This is a complication in both UC and Crohn disease?
When are barium enemas contraindicated in IBD?
Describe the findings in Crohn disease?
-Lesions → Focal, Skip, Deep
-Clinical course → Indolent
-Prednisone response → Less responsive
-Granulomas → Pathgnomonic
-Rectal involvement → Rectal sparing in 50%
-Perianal disease → Abscesses, fistulas
-Small Bowel Involvement → > 50%
Describe the findings in Ulcerative Colitis?
-Lesions → Shallow, continuous
-Clinical course →More acute
-Prednisone response → Very responsive
-Granulomas → None
-Rectal involvement → Rectum always involved
-Perianal disease → None
-Small Bowel Involvement → Backwash ileitis in less than 10% of patients
Sulfasalazine is ineffective in which types of CD?
Disease of the small bowel
What are the side effects of metronidazole?
Peripheral sensory neuropathy
-seen in doses > 10 mg/kg
Describe the mechanism of action of sulfasalazine?
-split by bacterial action in the colon → mesalamine (active component) + sulfapyridine
What are the common side effects to sulfasalazine?
-reversible infertility in men, leukopenia, headache
-sulfapyridine has highly reactive sulfa moiety leading to symptoms of sulfa-intolerance
When is metronidazole used in IBD?
perianal abscesses and fistulas
What are the indications for monoclonal antibodies in patients with IBD?
-Moderate to severe Crohn disease
-Fistulous Crohn disease
What is the use/effect of Budesonide in IBD?
-released mostly in the ileum and ascending colon
-90% first pass effect → fewer systemic side effects
What should be monitored in patients on Budesonide?
Yearly bone mineral density
What medications are used in IBD?
-Azathioprine and its metabolite, 6-mercaptopurine
-Infliximab, adalimumab, and certolizumamb (monoclonal antibody to TNF-alpha)
-Methotrexate and Cyclosporine
Prednisone-sparing drugs useful in both Crohn and UC but usually take 3-4 months to take effect?
Azathioprine and 6-mercaptopurine
Major side effect with Azathioprine and 6-mercaptopurine?
Bone marrow suppression
-monitor monthly CBC
What are the side effects of monoclonal antibodies used in IBD?
-TB reactivation, HBV (potential)
-Positive ANA (55%)
-Severe fungal infections
-Lymphoma and MS (have also been described)
Testing required prior to initiating monoclonal antibodies in IBD?
-Hepatitis B testing
-All age-appropriate vaccinations
Drugs which are proven to decrease relapse rate in CD?
Which drugs are proven to decrease the relapse rate in UC?
Describe the relationship with smoking cessation in UC and CD?
-CD → decreases relapse rate
-UC → increases relapse rate
What is the relationship of Crohn disease to cancer?
increased risk of GI cancer (especially long-standing disease or Crohn colitis)
What medication is recommended for the treatment of Crohn disease in pregnancy?
Monoclonal antibodies, TNF-alpha inhibitors
What is the colorectal cancer screening recommendation in a patient with CD?
-start screening 8-10 years after diagnosis
-repeat every 1-2 years
Common associated disease process associated with CD?
-70% have abnormal bone density
-due to chronic disease, vitamin D deficiency, and/or steroids
What are the colonoscopy and biopsy findings in CD?
-skip lesions (apthous and deep transmural ulcers)
Biopsy finding in CD that is rarely found but pathognomonic if present?
Classic but uncommon feature seen in the terminal ileum on small bowel follow through in CD?
-only a small lumen upon which contrast can be visualized passing through
What is the significance of an "apple-core" lesion?
How does it differ from the string sign?
-usually indicates cancer if anywhere outside of terminal ileum in the colon
Serologic marker which is positive in CD? and UC?
-CD --> ASCA
-UC --> p-ANCA
What are some of the complications of terminal ileum involvement in CD?
-B12 deficiency, Nutrient malabsorption
-Calcium oxalate kidney stones
-Diarrhea (Bile acid-induced)
-Hypocalcemia (from vitamin D malabsorption)
What type of gallstones occur in CD?
Amount of bowel resection associated with B12 malabsorption?
greater than 60 cm
What GU complication can arisei n a patient with Crohn's of the terminal ileum?
Calcium oxalate kidney stones
What is the usual etiology of diarrhea in CD patients with > 100cm of distal ileum removed?
Less than 100 cm removed?
Treatment for both?
-Greater than 100 cm --> steatorrhea from greatly decreased proximal gut concentration of bile salts
*synthesis does not keep up with GI losses with the loss of distal ileum resorption
*Treatment: Low-fat diet
-Les than 100 cm --> bile acid-induced diarrhea
*escape absorption in terminal ileum and stimulate colonic salt and water secretion by the colon
*Treatment: bile acid sequestrants (cholestyramine, colestipol)
What is the treatment for mild CD?
5-ASA, slow release
-progression to other medications if response inadequate
What is the role of Prednisone in CD?
Used only in flairs
-recommended is less than 3 months because of side effects
What steroid is preferred in CD?
-1st line drug for mild-to-moderate disease of ileum or ileocecal disease
What are the indications for Metronidazole in CD? and UC?
-CD --> fistulas and perianal disease
-UC --> fulminant disease with peritonitis
When is surgery most beneficial in CD?
-if involvement limited to colon --> colectomy
* > 60% have no recurrence
CD treatment with only Colon involvement?
-5-ASA drugs (second choice because more expensive)
CD treatment with any ileum or small bowel involvement?
CD treatment: only ileum or small bowel involvement?
slow-release Mesalamine or Budesonide
CD treatment with fistula or perianal disease?
-6-MP can also be used
CD treatment with steroid dependence?
6-MP, azathioprine or mAB
CD treatment for incomplete small bowel obstruction?
What are the findings of UC on colonoscopy?
-uniform, contiguous mucosal inflammation with shallow ulcers
-always involves/starts in the rectum and extends proximally
-confined to the colon
What serological marker may be found in 70-80% of patients with UC?
-little clinical use
-low sensitivity and specificity
Describe the extraintestinal manifestations of UC
-Iritis/episcleritis/uveitis (HLA B-27+)
-RF negative peripheral polyarthritis (types 1 and 2)
-Ankylosing spondylitis (also HLA B27+)
-Apthous ulcers of mouth
-Primary sclerosing cholangitis (PSC, HLA-B8+)
-Skin lesions (erythema nodosum and pyoderma gangrenosum-which correlates with disease activity)
Disease associated with UC that presents with jaundic, itching, cholestatic LFT's?
primary sclerosing cholangitis
-occurs in 5% of UC patients
-Diagnosis --> US, MRCP (string of beads)
How to diagnose primary sclerosing cholangitis?
-MRCP --> string of beads
*multifocal strictures of intrahepatic bile ducts
What is the relationship of UC to cancer?
-risk increases 8 years after onset of symptoms
-Pancolitis patients (20 years: 5-10%, 50 years: 12-20%)
What factors increase the risk of cancer in UC patients?
-Duration of UC
-Extent of UC (pancolitis is highest risk, ulcerative proctitis = no risk)
-Persistent mucosal inflammation
What is the colon cancer screening for UC patients?
-Pancolitis --> started 8 years after diagnosis
-Left sided colitis --> started 15 years after diagnosis
*Every 1-2 years cancer colonoscopy screening
What is the treatment for moderate-severe UC?
-Distal: rectal corticosteroids; oral or rectal 5-ASA
-Extensive: Oral 5-ASA
-Distal: Oral or rectal corticosteroids
-Extensive: Oral corticosteroids
What is the only curative treatment for UC?
-difficult, so reserved for cancer or dysplasia
What are the indications for surgery in UC patients?
-complication from therapy
-dysplasia in a mass lesion
-growth retardation in children
-high grade dysplasia in a flat lesion
What is the treatment for mild UC?
*suppository for proctitis
*enema for proctosigmoiditis
What is the initial treatment for moderate-severe UC flare?
What is the treatment for fulminant UC?
-Infliximab or Cyclosporine
-Colectomy if symptoms persist > 48 hours
What is maintenance therapy for UC?
-Sulfasalazine or Mesalamine for 2 or more years
-frequent recurrences/steroid dependence --> Azathioprine or 6-MP
*may take 3-4 months to show effect
What UC treatment is better for short term remission or long term remission in combination with Azathioprine?
greater than 200-350 g/day of stool
*normal 150-180 grams
*small, loose stools are not considered diarrhea
*normal frequency 3-21 stools/week
How is diarrhea classified?
Duration of symptoms
-Acute: less than 2 weeks
-Persistent: 2-4 weeks
-Chronic: greater than 1 month
What tests are done for the workup of acute diarrhea?
-Check diet and travel history (first)
-Labs: guaic test, fecal WBC's
What tests are indicated if fecal WBC's are elevated?
-Culture and sensitivity exam (C+S)
-Ova + Parasite (especially with travel history)
-Sigmoidoscopy with biopsy (+/-)
What are the treatments generally used for invasive diarrhea?
-Macrolides for Camylobacter (resistant to quinolones)
-Metronidazole for amebiasis
Two causes of invasive diarrhea in which antibiotics are contraindicated?
-E. coli O157:H7
What finding on stool evaluation suggests invasive diarrhea?
Elevated Fecal WBC's
What are common causes of invasive diarrhea?
-Amebic GI infections
What is a possible adverse consequence of treating infectious diarrhea due to E. Coli O157:H7 with antibiotics?
What type of symptoms will E. Coli O157:H7 result in?
What is the most common cause of traveler's diarrhea?
Enterotoxigenic E. Coli
Vibrio vulnificus can cause severe disease (skin infections and sepsis) in which group of patients?
-Chronic liver disease
What is the current treatment of choice in patients with severe C. difficile diarrhea?
What antibiotics are especially likely to cause C. diff colitis?
*any antibiotic may cause it
C. diff colitis may occur up to this time period after antibiotic exposure?
Diagnosis of C. diff colitis?
assay for C. diff cytotoxin
Define severe disease in C. diff colitis?
-WBC > 15,000
-Cr. increase by > 50%
What is the treatment for mild C. diff colitis?
When is severe C. diff colitis considered complicated?
*if any are present
What is the recommendation for treatment of first recurrence of C. diff?
-Metronidazole (or Vancomycin)
*repeat first regimen
*relapse occurs in 25% of patients
*metronidazole c/i for > 2 relapses
What infection control precautions must be used on patients with C. diff diarrhea?
Isolation with contact precautions
*hand gels do not kill spores (only hand washing)
What is the diagnosis and treatment of Cryptosporidium induced diarrhea?
-Acid fast stain of stool (small round red organisms)
-Treatment (HIV patients) --> ART + Nitazoxanide
What is the most common cause of viral gastroenteritis in children?
What infectious cause of viral gastroenteritis is associated with clams, oysters and waterborne?
-"winter vomiting disease"
-Diagnosis --> ELISA
-Common on cruise ships
Describe the clinical presentation of acute severe UC?
-greater than 10 BM's/day
What is the treatment for acute severe UC?
-Workup for infectious/other causes of abdominal pain
*stool studies (Shigella, Salmonella, C. diff, Campylobacter)
*AXR (rule out perforation)
*3 day trial to assess response
What is the further treatment of acute severe UC after a 3 day trial of IV corticosteroids?
-Complete response --> transition to oral steroids
-Partial response --> continue x 5-7 days and reassess
-No response -->
*Rescue therapy (cyclosporine or infliximab) --> if no response --> colectomy
What are the indications for adding Vancomycin in febrile neutropenia?
-suspected catheter-associated blood stream infection
-Gram positive bacteremia (while awaiting final culture identification)
-Colonization with MRSA
-Skin or soft tissue infection
Define chronic diarrhea?
loose stools > 200-250 g/day for > 1 month
What are the types of chronic diarrhea?
What is the stool osmotic gap in secretory diarrhea?
less than 25-50
What are some causes of secretory diarrhea?
-Enterotoxins from E. coli, cholera, and S. aureus
-Villous adenomas (rare cause)
-VIPomas that produce vasoactive intestinal peptide
What is the result of a 24-48 hour fast in secretory diarrhea?
*except in fatty acid-
*bile acid-related diarrheas
What is the result of a 24-hour fast in osmotic diarrhea
great improvement or near resolution
What are common causes of osmotic diarrhea?
-lactase deficiency (most common)
-Mg-containing laxatives and antacids
-non- or poorly absorbable carbohydrates (xylitol, lactulose, sorbitol, fructose)
-nutrient malabsorption (pancreatic insufficiency, celiac disease, bacterial overgrowth)
What are causes of diarrhea secondary to increased motility?
-antibiotic associated diarrhea
In an AIDS patient without fever and diarrhea, what organisms are on your differential list?
-Cryptosporidia (usual cause)
In an AIDS patient with fever and diarrhea, what organisms are on your differential list?
What are the causes of diabetic diarrhea?
-Diabetic foods rich in sorbitol (erroneously labeled "sugarless)
-Visceral autonomic neuropathy (especially suspect this in incontinent diabetic patients)
-Malabsorption (less common)
*celiac disease (present in 5% of diabetics
*bacterial overgrowth (treat with metronidazole and amoxicillin-clavulanate)
-Pancreatic exocrine insufficiency (more common in DM due to pancreatic disease)
What tumor causes the majority of cases of carcinoid syndrome?
primary tumor in the midgut
*ileum and proximal colon
When do symptoms of GI carcinoid tumors typically arise?
only when the primary tumor has metastasized to the liver
*vasoactive mediators are released directly into the bloodstream and cannot be deactivated by the liver
What is the clinical presentation of carcinoid syndrome?
-crampy, explosive diarrhea
What vitamin deficiency can occur in carcinoid syndrome?
-tryptophan is a precursor of niacin
-symptoms: pellagra (diarrhea, dermatitis, dementia), scaly rash, thickened tongue, angular cheilitis, mental status change
How do you diagnose carcinoid?
-24 hour urine 5-HIAA
*a breakdown product of 5-hydroxytryptamine
*will be > 25 (normal less than 10)
What are the symptoms of visceral autonomic neuropathy?
-Delayed gastric emptying (gastroparesis)
-Postural decrease in blood pressure
-Anhidrosis (inability to tolerate heat, lack of functioning sweat glands)-especially in lower extremities
-Urinary overflow incontinence
Cause of chronic diarrhea which presents with normal colonoscopy and abnormal histologic examination?
-do not progress to IBD
-Budesonide is first line treatment
Explain the workup in stage 1 of chronic diarrhea
-Weight of stool/day
-Fecal leukocytes x 3
-3-day fecal fat (or if Sudan stain is positive, do the fecal fat)
-Serum chemistry and thyroid profile
-Stool O and P
-C. difficile toxin assay
-Lactose free diet (if at all suggestive by history)
Explain the workup in stage 2 of chronic diarrhea
-Immunoabsorbent assay for Giardiasis
-Steatorrhea confirmed --> US or CT for pancreatic calcification
-Diabetic --> lactulose breath test for bacterial overgrowth
-if > 1000 g/day stool --> check VIP
-Check for laxative abuse (stool osmotic gap)
Explain the workup in stage 3 of chronic diarrhea
EGD and colonoscopy
-significant number of patients with all results negative --> idiopathic chronic diarrhea
What lab tests are done in the workup of malabsorption?
-serum iron (all low)
Malabsorption can be differentiated into these categories?
-decreased mucosal transport
*something wrong with intestinal uptake
*not enough digestive enzymes
What are causes of malabsoprtion due to decreased mucosal transport?
-Other Small bowel disease
-common variable immune deficiency with hyogammaglobulinemia
Define Celiac disease
autoimmune intestinal disorder in which there is an altered gut mucosal response to dietary gluten (wheat, barley, malt, rye) --> small bowel villous atrophy and crypt hypertrophy --> malabsorption
What are the extraintestinal manifestations of Celiac Disease?
-IDA (most common presentation; iron absorbed mostly in duodenum)
-Abnormal serum aminotransferases
-Dental enamel defects
What is a rare late complication of Celiac disease?
Define Dermatitis herpetiformis
Characterized by intensely itchy vesiculopapular eruptions on the face, trunk, buttocks, sacrum, and extensor surfaces of elbows and knees
How do you diagnose Celiac Disease?
-Evidence of malabsorption (steatorrhea, weight loss, IDA)
-Positive antibody test (tissue transglutaminase or antiendomysial)
-Positive response to gluten-free diet (clinical, chemical, histological and immunological)
-Abnormal small bowel biopsy (confirms diagnosis)
What are the antibody tests for Celiac disease?
-Tissue transglutaminase (tTG) antibody
-IgA antiendomysial Ab
*but not good with IgA deficiency
What are the limitations of EGD/small bowel biopsy in Celiac disease?
Many small bowel diseases can demonstrate villous atrophy
What is the treatment for Celiac disease?
Gluten Free Diet (GFD)
What are the treatment options/considerations in Celiac disease that does not respond to GFD?
-Dietary noncompliance (most common)
Variant of celiac disease which shows flattened mucosa with large masses of sub-epithelial eosinophilic hyaline material in the lamina propria on small bowel biopsy?
*one of the most common causes of GFD failure in suspected celiac patients
What is the presentation/treatment of Tropical sprue?
-Endemic to Caribbean, South Africa, Venezuela, India and SE Asia
-biopsy: partial villous atrophy
-Megaloblastic anemia often present
-Treatment: Tetracycline/Doxycycline x 3-6 months
What is the clinical presentation of Whipple Disease?
TETRAD of symptoms:
-Arthralgias (most common preceding symptom)
What is the causative agent in Whipple disease?
What is the histologic finding in Whipple disease?
small bowel biopsy
-positive PAS staining bacterial remnants
*can also check CSF PCR for T. whipplei
What is the treatment for Whipple disease?
-Ceftriaxone or IV PCN x 14 days
-TMP/SMX x 1 year
*Relapse often manifests with CNS symptoms
What is the diagnosis and treatment for eosinophilic gastroenteritis?
-Diagnosis: n/v/d, abdominal pain, weight loss and Peripheral eosinophilia (must r/o strongyloides first as can cause peripheral eosinophilia)
-Treatment: Corticosteroids x 2-6 weeks and avoidance of causative foods
When is short bowel syndrome more likely to occur?
less than 2 feet (60 cm) of bowel remaining
-especially if proximal jejunum and/or distal ileum are removed
This is often required in small bowel syndrome when less than 100 cm bowel left and loss of ileocecal valve?
What are common complications in short bowel syndrome?
-Calcium oxalate kidney tones (secondary to steatorrhea)
-Gastric acid hypersecretion
What is the treatment for short bowel syndrome?
-low fat diet
-small frequent meals
What are the 2 main causes of malabsorption due to decreased digestion?
-Bile acid deficiency
What are causes of malabsorption due to pancreatic insufficency?
How to identify pancreatic insufficiency?
Qualitative stool exam
-reveals undigested muscle fibers, neural fat, split fat, and low levels of fecal elastase
What must be ruled out in a patient older than 55 with pancreatic insufficiency?
What are causes of malabsorption due to bile acid deficiency?
-Ileal resection ( > 100 cm) or disease that decreases bile acid uptake
-Severe liver disease
*decreases production of bile acids
*increased acid production --> precipitation of bile acids
*breakdown of bile acids --> useless for fat digestion
What is the best indicator of malabsorption?
What is the best screening test for steatorrhea?
-3-day, quantitative fecal fat measurement
*defined as > 14 g/d
What is the significance of a normal D-xylose absorption test in a patient with steatorrhea?
-Normal test --> mucosal transport in small bowel is normal
*probable pancreatic insufficiency
-Low result --> probable small bowel disease --> proceed with small bowel biopsy
What laboratory abnormalities if associated with steatorrhea indicate small bowel malabsorption problem?
-low serum carotene
What are some important causes of bacterial overgrowth?
-Structural abnormalities (diverticula, fistula, strictures, after ileocecal resection)
*decreased peristalsis in DM and scleroderma
-Achlorhydria (acid kills bacteria before entering small bowel)
What is the diagnosis in patients with:
-Elevated Folate level
-Decreased B12 level
-makes more folate but decreases B12 absorption
Bacterial overgrowth is associated with what dermatologic condition?
-50% of patients
-100% had long-term resolution of symptoms with 10 day course of Rifaximin (nonabsorbable antibiotic)
How do you diagnose bacterial overgrowth as a cause of diarrhea?
Lactulose hydrogen breath test (hydrogen breath test or C14-clycocholate breath test)
Quantitative culture from small bowel
What are the treatment options for bacterial overgrowth?
-Rifaximin (nonabsorbable antibiotic that stays in the digestive tract)
-Amoxicillin-Clavulanate or combination of antibiotics (Cephalexin + Metronidazole)
*treated for 2 weeks on, 1 week off until symptoms resolve
What symptoms are associated with this degree of bowel resection?
> 60 cm of terminal ileum --> B12 deficiency
60-100 cm of terminal ileum --> bile acid induced diarrhea
> 100 cm of terminal ileum --> bile acid deficiency and fat malabsorption
Most cases of constipation are due to what?
What common gynecologic surgery leads to constipation in 5% of patients?
-leads to refractory constipation in 5% of patients
What are the most common causes of fecal incontinence?
-Pelvic floor injuries (childbirth)
What is the clinical presentation of fecal impaction?
sudden onset of watery stools/incontinence in a person with chronic constipation
-abdominal pain or discomfort associated with disturbed defecation
-abdominal pain improved with defecation
-symptoms are continuous or intermittent
-NO NOCTURNAL or organic symptoms
-Response to physical or emotional stimuli (nonspecific)
-Association to childhood psychological or physical trauma
What other diagnoses should be excluded prior to diagnosing a patient with IBS?
*33% of patients do not improve with lactose-free diet because of concurrent IBS
What are the risk factors for colon cancer?
-Age > 50
-Adenomatous polyps (current or past)
-Diets high in calories and animal fat
What are the hereditary risk factors for colon cancer?
-1st degree relatives with colon cancer or adenomatous polyps
-Familial polyposis syndromes
-Hereditary, nonpolyposis colon cancer (HNPCC)
Endocarditis with what organisms should prompt colonoscopy to search for colon cancer?
What size and histologic features of colon adenomas are considered "advanced features" with increased malignant potential?
-presence of high-grade dysplasia
-presence of villous histology
-size > 10 mm
What is the relationship between hyperplastic polyps and colon cancer?
no malignant potential and contain no features of dysplasia
What is the follow up recommendation for colon cancer?
- 1-2 small tubular adenomas with low grade dysplasia
repeat colonoscopy 5-10 years after initial polypectomy
What is the follow up recommendation for colon cancer?
- 3-10 adenomas, or 1 adenoma > 1 cm, or any adenoma with villous features or high-grade dysplasia
repeat colonoscopy every 3 years
What is the follow up recommendation for colon cancer?
- > 10 adenomas
repeat colonoscopy less than 3 years
*consider possibility of underlying familial syndrome
What is the follow up recommendation for colon cancer?
- sessile adenomas that are removed piecemeal
repeat colonoscopy in 2-6 months to verify complete removal
What are the 4 familial (or hereditary) polyposis syndromes?
-Familial adenomatous polyposis (FAP)
Which 2 familial polyposis syndromes have the highest risk of cancer?
-Familial adenomatous polyposis (FAP)
*both adenomatous polyps
Define Familial Adenomatous polyposis
-hundreds of adenomas in the colon
-100% risk of cancer if not treated
-often require prophylactic proctocolectomy by age 20
-after colectomy --> develop duodenal cancer
-increased risk of secondary malignancies (ampullary adenomas and carcinomas)
-Giant gastric tumors are common (but benign)
Define Gardner syndrome
-variant of FAP with more extraintestinal benign growths
-risk of cancer is 100%
-Osteomas and soft tissue tumors
-Treatment: colectomy early
Define Peutz-Jeghers syndrome
-multiple hamartomatous polyps throughout the small bowe, occasionally in the colorectum and stomach
-melanotic pigmentation (freckles) on the lips and buccal mucosa
-abdominal pain (intussusception or bowel obstruction due to large polyp)
Define Hereditary nonpolyposis colon cancer
-HNPCC, "Lynch Syndrome"
-occurrence of a HNPCC-associated cancer (colorectal, endometrial, small bowel, ureter or renal pelvis) in at least 3 (one is a 1st degree relative of the other two) 1st degree relatives over at least 2 generations, and with at least 1 person diagnosed before age 50
-Women --> increased risk for ovarian and endometrial cancer
At what age does screening begin for HNPCC?
Under what circumstances should periodic colonoscopy be started at age 40?
Increased risk patients
-1st degree relative with colon cancer or adenomatous polyp (start 10 years prior to index case)
What common colon problem in older patients is an indication for colonoscopy?
-wait 6 weeks for resolution of acute inflammation to avoid risk of perforation
FOBT is negative in what percentage of patient's with colon cancer?
What role do CEA levels play in colon cancer?
useful for surveillance and recurrence only
What is the most common location of colon cancer metastasis?
-via the portal circulation
*if involves the rectum --> bypasses portal circulation --> lung, bone, brain mets without liver
What are the treatment options for colon cancer?
*1st treatment option
-Chemotherapy - FOLFOX
*(5FU + Leucovorin (LV) + Oxaliplatin)
*effective only for stage III and locally advance stage II
*useful for rectal lesions only
What are the 4 types of diverticular disease?
-Asymptomatic diverticulosis (most common)
-Painful diverticulosis (contraction of hypertrophied colonic muscle)
What is the most common cause of colonic bleeding in the elderly?
-Angiodysplasia (2nd most common)
*results in more severe bleeding
Laboratory finding which indicates presence of UGIB?
BUN/Cr ration > 30:1
-indicates blood is being digested and breakdown products are being absorbed
What is the most common pathophysiologic cause of divertculitis?
What may be seen on abdominal CT scan in a patient with diverticulitis?
-areas of thickened sigmoid colon or pericolic fluid accumulation
What is the treatment of moderate-severe diverticulitis?
1. Dual drug therapy (better)
-GN aerobic coverage --> Aminoglycoside or Cipro
-GN anaerobic coverage --> Metronidazole or Clinda
2. Single-drug therapy
What is the treatment of mild diverticulitis?
If able to drink without peritoneal signs: Outpatient
-Ciprofloxacin or TMP/SMX
How to diagnose Meckel's Diverticulum?
Technetium uptake scan
-less than 50% have gastric mucosa
Test of choice in patient with recurrent melanotic stools, with negative EGD/CSP?
video capsule endoscopy
What is the most common cause of small intestine obstruction?
post operative adhesions
What is the most common cause of colonic obstruction?
What are the 4 types of intestinal ischemia?
-Ischemic colitis (most common)
-Chronic mesenteric ischemia
-Acute mesenteric ischemia (70% mortality)
-Mesenteric venous thrombosis
What is "thumbprinting" and when is it seen?
-submucosal hemorrhage and edema (mildest injury)
-seen on AXR or barium enema
-lasts only for a few days
What is the treatment for ischemic colitis?
What is the clinical presentation of chronic mesenteric ischemia?
-Abdominal pain after meals
-Weight loss (from tolerating only smaller meals)
What is another name for chronic mesenteric ischemia?
What is the diagnostic process for chronic mesenteric ischemia?
-MRA or CT angiogram
*good sensitivity for proximal lesions
What is the treatment for chronic mesenteric ischemia?
surgical bypass or angioplasty
What is the pathophysiology of acute mesenteric ischemia?
thromboemboli in a mesenteric artery --> loss of blood flow to the corresponding small intestine and/or ascending colon
Patients with acute mesenteric ischemia often have these associated problems?
*because symptoms likely secondary to thromboemboli
Acute mesenteric ischemia + elevated lactic acid
Diagnosis and treatment of acute mesenteric ischemia?
-Treatment: surgical resection
What are the most common causes of pancreatitis in the US?
1. Alcohol abuse
-Hypertriglcyeridemia ( > 1,000)
-Obstruction of pancreatic duct (pancreatic cancer)
Which medications can cause acute pancreatitis?
-HIV drugs (pentamadine, didanosine)
-Diuretics (furosemide, thiazides)
-Antibiotics (tetracycline, sulfa)
-6-MP, L-asparaginase, valproic acid
What happens to serum amylase and lipase levels over time with acute pancreatitis?
-Amylase decreases within 2-3 days
-Lipase decreases after 7 days
What 2 relationships do high triglyceride levels have with acute pancreatitis?
-High TG levels --> normal amylase levels
-High TG levels ( > 1,000) --> acute pancreatitis
The severity of pancreatitis is directly related to what factor?
the degree of necrosis
-infected --> mortality 30%
-not infected --> mortality 10%
What are multiorgan failure indicators used to assess severity?
-Heart: SBP less than 90; tachycardia > 130 bpm
-Lungs: PO2 less than 60 mmHg
-Renal: progressive azotemia or oliguria (less than 50 mL/hr)
-CNS: altered sensorium
-Metabolic: low calcium ( less than 8 ) and ablumin (less than 3.2)
Cullen and Turner sign when seen indicate this in acute pancreatitis?
severe necrotizing pancreatitis
What is Cullen sign?
faint blue discoloration around the umbilicus --> hemoperitoneum
What is Turner sign?
bluish-reddish-pruple or greenish-brown discoloration of the flanks --> tissue catabolism of hemoglobin from retroperitoneal blood dissecting along tissue planes
When is pancreatic necrosis considered severe?
if > 30% of pancreas is necrotic
What is the APACHE II score that indicates severe pancreatitis?
How is pancreatic necrosis best confirmed?
CT or MRI
What masses may develop due to acute pancreatitis?
What is their timeline, and what is their treatment?
Acute fluid collections
What is the timeline/significance/treatment of acute fluid collections in the pancreas?
-50% of patients
-within 48 hours
-usually resolve spontaneously
-can cause pleural effusion, high in amylase
What is the timeline/significance/treatment of necrotic tissue in the pancreas?
-occurs in the first 1-2 weeks
-may simulate pseudocyst --> differentiated with US
-Serious; may require drainage
What is the timeline/significance/treatment of infected necrosis in the pancreas?
-Diagnose: CT guided biopsy, culture
-Treatment: drainage (endoscopic or CT guided) or surgery within 2 weeks
What is the timeline/significance/treatment of pseudocyst in the pancreas?
-less than 10% of patients
-requires minimum of 4 weeks to develop after attack
-Treatment is drainage/surgery
*Size > 5 cm --> will not resolve on its own
*Time: if persists > 3-6 months and causes symptoms --> drainage
-Remove if rapidly enlarging --> rupture carries high mortality
*w/o hemorrhage = 15%, with hemorrhage = 60%
What is the timeline/significance/treatment of abscess in the pancreas?
-occurs after 4-6 weeks
-AXR --> "soap bubble sign"
-presents with fever and septic shock
-Diagnosis: CT guided aspirate
-Treatment: immediate surgical or radiological debridement
What is the first test in the workup of the etiology of acute pancreatitis?
gallbladder US --> rule out gallstones
What is the nutritional recommendation in patients with acute pancreatitis?
early enteral feeds
-have been shown to be superior to TPN
Laboratory finding which indicates unresolved pancreatitis/complication?
Elevated amylase at 10 days
Complication of acute and chronic pancreatitis which presents with gastric varices in the absence of esophageal varices?
splenic vein thrombosis
What is the criteria for resumption of oral feeds in acute pancreatitis?
-bowel sounds present and passing flatus/stools
-not requiring narcotics
-patient is hungry and wants to eat
What are other causes of elevated amylase?
-increased salivary amylase
What is the treatment for suspected infected necrotizing pancreatitis?
-CT guided aspirate with culture
*if no infection --> supportive care
What is the clinical presentation of chronic pancreatitis?
-initial, asymptomatic phase, followed by recurrent bouts of abdominal pain
-late in disease (80-90% of endocrine/exocrine function lost) --> steatorrhea and DM
-increases risk of pancreatic cancer 2-fold
What i the classic diagnostic triad for chronic pancreatitis?
TRIAD, present in less than 20% and only in late disease
What is the preferred initial test used in the workup of chronic pancreatitis?
-diagnosis confirmed if ductal dilation, atrophic, calcification
*Secretin stimulation test
can be used if still high index of suspicion
What are some complications of chronic pancreatitis?
-gastric varices (from splenic vein thrombosis)
What is the treatment of chronic pancreatitis?
-alcohol and tobacco cessation
-pancreatic enzyme supplimentation
*must have enteric coating of be administered with PPI/H2 blocker
-decreasing dietary fat
What is the presentation/lab findings/diagnosis/treatment of autoimmune pancreatitis?
-50% present with obstructive jaundice (simulating cancer of the panceras)
-Serum IgG4 usually > 2 x normal
-Diagnosis: CT abdomen -->
*mass in the head of the pancreas or diffuse enlargement (sausage-shaped pancreas)
*Strictures (bile duct or pancreatic duct)
-Treatment: Prednisone, Immunomodulators if relapse
Concurrent findings associated with autoimmune pancreatitis?
-mediastinal fibrosis and adenopathy
-IgG4 associated cholangitis
What are the classic symptoms of pancreatic carcinoma?
-unexplained upper abdominal pain (gnawing quality)
How is pancreatic cancer treated if there are metastases? Without metastases?
-Supportive care, experimental chemotherapy
-Pancreaticoduodenectomy (whipple resection) and evaluate lymph nodes for metastasis
-Adjuvant chemotherapy (survival improved 3 months)
*5FU or gemcitabine
*5 year survival 30% if node negative, 10% if node positive
When is ERCP indicated in pancreatic cancer?
stent placement to palliate biliary obstruction
What are the clinical findings in glucagonoma?
-scaly necrolytic erythema
-plasma glucagon (by RIA) usually > 1,000
What are the 3 causative factors of cholelithiasis?
-Abnormal bile secreted by the liver (lithogenic-supersaturated with cholesterol)
-Accelerated nucleation of microcrystals to macrocrystals
-Defective gallbladder emptying
What is the composition of most gallstones?
-75% radiolucent cholesterol (pure or mixed)
-25% bile pigment stones
What is the recommended treatment of cholelithiasis?
Symptomatic --> elective cholecystectomy
-70% will have recurrent symptoms
Asymptomatic --> observation
-only 20% will develop symptoms
What should you investigate in the patient who persists in having RUQ pain after cholecystectomy or with symptoms of cholangitis?
common duct blockage/stone
What is the triad for acute cholangitis?
-TRIAD (biliary colic, fever, jaundice)
-SC (AMS, bacteremia, shock)
What is the treatment for acute cholangitis?
-ERCP or drain placement
*if suppurative cholangitis present
What is the treatment for emphysematous cholecystitis?
-emergent laporotomy with cholecystectomy
*avoid ceftriaxone --> increases biliary sludge
What is the imaging finding of porcelain gallbladder?
-XR --> calcified outline
*requires open cholecystectomy to rule out cancer
What are precipitating causes of hepatic encephalopathy in cirrhotic patients?
-Hypovolemia (diarrhea, vomiting, diruetic use, excessive paracentesis)
-Excessive nitrogen load (GI bleeding, constipation, high protein diet)
-Hypokalemia and metabolic alkalosis
-Hypoxia and hypoglycemia
-Infection (pneumonia, UTI, SBP)
-Portosystemic shunting (surgical/radiographic placed shunts)
Define primary biliary cirrhosis
-slow onset, typically complain of itching (first on palms and soles)
-70% have associated autoimmune diseases
*Sjogren's, scleroderma, autoimmune thyroiditis, limited scleroderma
-Antimitochondiral antibody (90%)
-nonsuppurative, progressive, destructive cholangitis
-Inflamed bile ducts --> obstructive jaundice, elevated alkaline phosphatase and liver cirrhosis
What is the hallmark test for primary biliary cirrhosis?
Antimitochondrial antibodies (90%)
-not a good indicator of disease activity
This laboratory finding is present in 95% of patients with primary biliary cirrhosis and frequently leads to the diagnosis?
Elevated Alkaline Phosphatase
-2-5 tx increased
How is PBC confirmed?
-granulomas (florid duct lesions)
-often findings are nonspecific
PBC: What is the best, proven treatment for early disease?
For late disease?
-Early disease --> Ursodiol (ursodeoxycholate-synthetic bile acid)
-Late disease --> liver transplant
What supportive treatments are used in PBC?
-Pruritis --> cholestyramine
-Osteomalacia --> vitamin D and Calcium
-Malabsorption --> decreased dietary fat
What are the AAAABC's of PBC?
Antimitochondrial Antibody Attack --> elevated Alkaline phosphatase --> obstructive Biliary lesions --> Cirrhosis
Define Primary Sclerosing Cholangitis
-typically occurs in males (70%)
-Strong association with UC (75% of patients)
-Inflammation and sclerosis of entire biliary tract (intra and extrahepatic ducts) --> obstructive jaundice and cirrhosis
-8-15% will develop cholangiocarcinoma
*CA 19-9 elevated in 80% of these patients
All patients diagnosed with PSC should have this screening test performed?
-rule out UC
Recently diagnosed UC patient with persistently elevated alkaline phosphatase and bilirubin (cholestatic pattern)?
Which diseases have elevated hepatic copper?
How is the diagnosis of PSC made?
MRCP, ERCP or transhepatic cholangiography
-"beaded" appearance of bile ducts
Liver biopsy --> "onion skin" fibrosis in portal triads
What is the treatment for PSC?
*prior recommendations for ursodeoxycholic acid, but no longer recommended due to poor efficacy and side effects
Jaundice + increased alkaline phosphatase + chronic diarrhea
-MRCP or ERCP to rule out
Describe differences between PBC and PSC?
-UDCA effective: Yes
-IBD: Yes, UC
-Cancer: UC --> 8-15% risk of cholangiocarcinoma
-UDCA effective: No
Liver enzyme that will be more elevated in alcoholic hepatitis?
-due to damage to mitochondria
-less liver specific than ALT
LFT pattern in NAFLD
ALT:AST > 2:1
-damage is more liver specific
Next test if liver transaminases elevated
-If still elevated --->
*Hepatitis A, B, C
*Iron studies with ferritin
Define Hepatitis A virus
-easily transmitted by fecal-oral route and sexually
-no transplacental transmission
-Occassionally get prolonged cholestasis (with increased bilirubin and alkaline phosphatase)
How to diagnose HAV?
high titers of anti-HAV IgM in serum
-IgG indicates previous infection
With what confections can hepatitis A become fulminant?
chronic Hepatits B and Hepatitis C
What is the post-exposure prophylaxis for Hepatitis A?
-instead of immunoglobulin
HBV: what is the significance of HBsAg?
-means you are producing Hepatitis B virus
-acute or chronic
HBV: what is the significance of HBeAg?
-correlates with the quantity of intact virus --> infectivity --> liver inflammation
-appears several weeks after the illness
What is the only Hepatitis Virus composed of DNA?
What serologic marker should be tested to determine acute HBV infection during the "window period?"
HBV is associated with which autoimmune condition?
Polyarteritis Nodosa (20-30%)
Are hepatitis B vaccines safe for pregnant patients?
-to ensure effectiveness, check HBsAb after vaccine has been given
What is the treatment for newborn delivered from mother with HBV?
HBIG + vaccination
-5-10% chance of transplacental transmission
What is the diagnosis and management of a patient with HBsAg?
-Carrier or early active infection
-Follow closely (if already infected, neither HBIG or vaccination will help)
What is the treatment for sexual contact with an HBV infected person?
HBIG --> vaccination
The likelihood of developing chronic HBV is inversely related to this?
-infants --> 90%
-children 1-5 --> 25-50%
-children and older adults --> 5%
Describe the 2 carrier states in HBV?
Inactive carrier state
-asymptomatic with normal LFTs
-can develop severe exacerbations of HBV
Medication which can be given to stunt HBV replication in immunocompromised carriers?
What is the HCC risk with chronic HBV?
-2% per year
-20% lifetime risk
What is the screening recommendation for HCC in HBV patients?
-CT or MRI can also be used
When is treatment for HBV recommended?
-HBV DNA > 20,000
-ALT > 2x ULN
*Treatment is delayed 3-6 months for newly diagnosed HBeAg+ patients to see if seroconversion takes place
When is the treatment for HBV + cirrhosis recommended?
-compensated cirrhosis --> HBV DNA > 2,000
-decompensated cirrhosis --> HBV DNA > 200
What are the two most common liver diseases in the US?
-NAFLD (most common)
Most common genotype in HCV?
Genotype 1 ( > 70%)
-less responsive to treatment than other genotypes
Hepatitis rule of 2's
-2% of the population
-2% risk of needlestick transmission (though some say 5%+)
-2% risk of neonatal transmission
-2% risk of spousal transmission
-2% cirrhotics with HCV develop hepatoma each year
In the US, what percentage of patients with HIV are coinfected with HCV?
-progress faster to cirrhosis with concurrent infection
What extrahepatic diseases are associated with HCV?
-Small vessel vasculitis with glomerulonephritis and neuropathy
-Porphyria cutanea tarda (PCT)
Porphyria cuteanea tarda is associated with what hepatic condition?
-not associated with HBV
What serology should be checked 2-4 months after HCV exposure or episode of Hepatitis C?
-to ensure disease has not become chronic
What test confirms that a previous hepatitis C infection did not become chronic?
What percentage of HCV infections become chronic?
-25% --> end stage cirrhosis (after 20-25 years)
-1-4% --> HCC
How often should screening for HCC be performed in HCV patients?
every 6 months
-US, CT, MRI
What is the number 1 reason for liver transplantation in the US?
With which chronic hepatitis infection is mixed cryoglobulinemia strongly associated?
How does it present?
-Chronic HCV infection (55% of patients)
-small vessel (leukocytoclastic) vasculitis
-rash --> "palpable purpura" or "crops" of purple papules
What is the treatment of hepatitis C genotype 1?
Pegylated INF-alphay (weekly injections, decreases risk of HCC)
Protease inhibitors (telaprevir/boceprevir)
*added for Genotype I
How to measure the treatment response in HCV?
-no response noted (decreased by 2 log units) in 12 weeks --> d/c thearpy
-those who respond
*Genotype 1 --> treat for 1 year
*Genotype 2-3 --> treat for 6 months
What is the major side effect of Ribavrin therapy?
Which virus does hepatitis D require to replicate?
Sudden decompensation in a patient with chronic HBV?
Hepatitis D infection
-Diagnose --> anti-HDV IgM
-Immunity to HBV implies immunity to HDV
Hepatitis E is associated with which risk factor?
Pregnancy (3rd trimester)
-very high risk for fulminant hepatitis
What are the causes of chronic hepatitis?
-ANA +/- anti-ds DNA
-Hepatitis D (only with HBV)
What test has an 80% rate of specificity for autoimmune hepatitis?
anti-SMA (smooth muscle antibody)
-more specific than ANA
What test has replaced anti-SMA for autoimmune hepatitis?
anti-Actin antibody (AAA)
-higher specificity and sensitivity
What is the treatment for autoimmune hepatitis?
Prednisone/budesonie +/- Azathioprine
-rapid reversal of symptoms and increased survival
What medication can exacerbate autoimmune hepatitis and is contraindicated?
What drugs are commonly associated with drug-induced hepatitis?
How does alcohol intake affect liver toxicity from acetaminophen?
Increases risk for severe hepatic toxicity or liver failure
-Alcohol --> ramps up cytochrome P-450 and depletes glutathione
What are the factors that potentiate acetaminophen liver damage?
-chronic alcohol use
-one time heavy alcohol use
What is the most common cause of fulminant hepatitis in the US?
What enzyme level will be disproportionately high in alcoholic liver disease?
-GGT (induced by alcohol)
*AST:ALT = 2:1 (AST always less than 300)
What are the hepatic side effects associated with OCP's?
-benign hepatic adenoma
-peliosis hepatis (blood-filled sinusoids)
-focal nodular hyperplasia of the liver
What is nonalcoholic fatty liver disease (NAFLD)?
-specturm of steatosis (fatty degeneration), steatohepatitis, fibrosis and cirrhosis
-75-80% of cyrptogenic cirrhosis is due to NAFLD
-LFT's opposite that of alcoholic liver disease (AST:ALT = 1:2)
What are the NAFLD associations?
-DROP (Dyslipidemia, insulin Resistence, Obesity, elevated blood Pressure)
-DM, type II
-Prolonged IV Hyperalimentation
What is the treatment for NAFLD?
*not proven treatment
Chronic liver disease associated with HCC?
-alpha-1 antitrypsin deficiency
-alcoholic liver disease
Carries a high risk for HCC, found in raw peanuts or raw peanut butter, especially in Asia
What is the most common of HCC in the US?
Alcoholic liver disease
-75% concurrent HCV infection
What is the most likely diagnosis in a patient with tender hepatomegaly, an RUQ bruit, bloody ascites, a high alkaline phosphatase, and a very elevated alpha-fetoprotein level?
What are common HCC paraneoplastic syndromes?
*due to parathyroid-like hormone produced by the tumor
*due to tumor's high metabolic needs or, more rarely, IGF II
What treatment reduces the risk of HCC in HCV patients?
What are the treatment guidelines for HCC?
-Resect a solitary tumor without vascular invasion
*best if consider for liver transplant
-Even with advanced disease, there are multiple treatment options
*radiofrequency ablation, transarterial chemoembolization, oral-targeted therapies
What are the causes of cirrhosis?
-Alcohol (most common cause in US)
-Hepatitis (B and C)
-Post-necrotic (drugs and toxins)
-Cardiac causes (primarily sever, prolonged right-sided CHF-which is rare)
What are the common findings of cirrhosis?
-Gynecomastia and testicular atrophy
-Asterixis (in hepatic encephalopathy)
Bleeding risk of esophageal varices is best correlated with what aspects of the varices?
What drug class is used for prophylaxis against bleeding with large esophageal varices?
What do you do with small esophageal varices?
Nonselective BB (Propanolol)
-prescribed for all patients with med-large varices regardless of bleeding status
No intervention required for small varices
Which drugs and which endoscopic therapies are used for active variceal hemorrhages?
-endoscoping banding or sclerotherapy (primary therapy)
-Somatostatin and its analog Octreotide
*given parenterally in conjunction with endoscopic therapy
*proven benefit when used in conjunction
Why are antibiotics given to cirrhotics with GI bleed?
Which antibiotics are used?
-Prevent SBP, AKI, decrease mortality
-3rd generation cephalosporins or Fluorquinolones
What drug is given to a cirrhotic patient with a history of variceal hemorrhage to decrease the chance of rebleeds?
Propanolol or Nadolol
What are the main uses for TIPS?
-Variceal rebleed (recurrent)
-Intractable ascites secondary to cirrhosis
*increased mortality if MELD > 15-18
What is the mechanism of Lactulose?
-disacharide, commonly used as osmotic laxative
-passes through the upper GI tract and is broken down by colonic bacteria into organic acids
-excess H+ in the proximal colon:
*inhibits coliform bacterial growth and thereby decreases NH3 production, and
*traps NH3 as inactive NH4+
Alternative treatment for hepatic encephalopathy?
-Rifaxamin, metronidazole, rifampin
What is a key finding in Hepatorenal syndrome?
Urin Na less than 10
If the PT is prolonged in an alcoholic and is easily corrected with vitamin K, what does this indicate?
-corrected with IM vitamin K
What is the cause of chylous ascites?
-trauma, tumors (especially Lymphoma), TB and filariasis
tumor, trauma, TB (rarely)
(chylous) lymphatic obstruction
What is the calculation for SAAG?
Serum to Ascites Albumin Gradient
-SAAG = Serum albumin - Ascitic albumin
What is a common complication of TIPS?
*not recommended in elderly patients because they are most susceptible
What is bilirubinuria an indication of?
-only conjugated bilirubin is excreted in urine
-bilirubin is conjugated in the liver
What hereditary liver disease has increased unconjugated bilirubin?
-autosomal dominant, variable penetrance
-7% of population
-Jaundice is variable --> brought on by stress, fasting, alcohol ingestion
-due to absence glucuronyl transferase
When does jaundice in Gilbert syndrome typically occur?
-Physical stress (surgery, exertion, infection)
What is the treatment for AAT deficiency?
-pooled human AAT infusions
What are the two types of Hemochromatosis?
-HFE gene association
-secondary to blood tranfusions (sickle cell, sideroblastic, thalassemia)
What is the risk of hepatocellular cancer in a patient with cirrhosis caused by hemochromatosis?
-higher than any other cause
What is the treatment for Hemochromatosis?
-goal ferritin level 50-100
Define Wilson Disease?
-AR genetic disorder, caused by impaired copper excretion into bile
-Decreased levels of ceruloplasmin
-presents with liver disease or neurologic/psychiatric dysfunction in adolescents
-Other symptoms: arthritis (chondrocalcinosis)
What is a pathognomonic finding in Wilson disease?
-diagnosed by slit-lamp examination
What is the confirmatory test in Wilson disease?
-shows high liver copper level
*also seen in PBC and PSC
What is the treatment of Wilson disease?
-Chelation with Penicillamine (must give supplimental pyridoxine) --> decreases copper levels
*low dose penicillamine
*low copper diet (
*Liver transplant cures Wilson's disease
This is the best time for surgery in pregnant patients with severely symptomatic gallstones?
Important viral infection which occurs in the 3rd trimester?
Hepatitis E --> fulminant hepatitis
-20% fatality rate
What is the diagnosis and treatment?
-Pregnant patient in 3rd trimester
-modest elevation of AST/ALT/Bilirubin
-encephalopathy, hypoglycemia, preeclampsia, pancreatitis, DIC, renal faiulre
Fatty Liver of Pregnancy
-due to microvescicular fat deposition in liver
Treatment --> early delivery required
Which patients should be considered for a liver transplant?
-almost all patients with irreversible end-stage acute and chronic liver disease
-MELD > 20
What is the usual cause of jaundice in persons less than 30 years old?
-Acute viral hepatitis
*85-90% less than 30 years old
*50-70% in age range
-Obstructive pattern (common duct stone or pancreatic cancer)
*80% in age range
What is the next step following ultrasound in jaundice workup:
-dilated common bile duct and stones
What is the next step following ultrasound in jaundice workup:
-dilate common bile duct and no stones
CT or EUS (think pancreatic cancer)
What is the next step following ultrasound in jaundice workup:
-dilated intrahepatic ducts
What is the next step following ultrasound in jaundice workup:
-dilated ducts and testing to exclude PSC
What is the next step following ultrasound in jaundice workup:
-no dilated ducts
What is the timeframe for development of vitamin deficiency:
-Water soluble vitamins, magnesium, zinc
What is the timeframe for development of vitamin deficiency:
-Vitamin A and D (selenium and chromium)
What is the timeframe for development of vitamin deficiency:
-Iron and cobalt
What is the timeframe for development of vitamin deficiency:
Major cause of blindness in developing countries?
Vitamin A deficiency
-first sign is night blindness
Common populations which develop Vitamin B1 (thiamine) deficiency?
-Normochromic normocytic anemia
-Sore throat with hyperemic mucosa and glossitis
-seborrheic dermatitis (perianal/scrotal area)
-Precipitated by phenothiazines or TCA's
Vitamin B2 deficiency (Riboflavin)
-precipitated by INH, Cycloserine, Penicillamine
Vitamin B6 (pyridoxine) deficiency
-Neuropathy (Pins and needles) --> loss of vibration and propioception
Vitamin B12 (cobalamin) deficiency
-Pellagara (dermititis, dementia, diarrhea)
Niacin deficiency (Nicotinic acid)
-made from tryptophan
-Petechial hemorrhages and ecchymoses
-hyperkeratotic papules around hair follicles
-hemorrhages into muscles and joints
-Splinter hemorrhages in the nail beds
Vitamin C deficiency (ascorbic acid)
Petechiae are associated with what vitamin deficiency?
Vitamin C (ascorbic acid)
What does Vitamin D deficiency cause in children? adults?
-Children --> Rickets
-Adults --> Osteomalacia
Explain how vitamin D is produced and altered in the body?
-Most vitamin D is synthesized in the skin (from a protovitamin D + sunlight) but some is absorbed from the gut
-Vitamin D --> converted to 25(OH)-D in the liver --> 1, 25 (OH)2-D (active form) in the kidney
*decreased absorption of calcium from the gut
*decreased calcium resorption from the kidney
What are the main causes of decreased 1,25-(OH)2-D?
-Decreased production in skin
-Elderly: decreased skin synthesis at age > 70
-Winter: decreased sun exposure
-Decreased intestinal absorption: steatorrhea, insufficient dietary intake
What are the findings associated with excessive continuous ingestion of vitamin B6?
-normal motor and sensory function
-absent positional and vibratory sensation
What is the main side effect of Vitamin E overdose?
potentiation of oral anticoagulants
What is the main side effect of Vitamin C overdose?
-increased incidence of oxalate renal stones
-impaired B12 absorption
What is the main side effect of Niacin overdose?
What is a catastrophic effect of refeeding syndrome?
cardiac failure (with rapid refeeding)
What is the treatment:
Gallstones with no symptoms?
no treatment indicated
What is the treatment:
Gallstones with typical biliary symptoms?
What is the treatment:
Gallstones with atypical/non-biliary symptoms?
Treat more likely etiology
What is the treatment:
Biliary symptoms without gallstones?
What is the treatment for anal fissures?
-Nitroglycerin (topical cream)
*improves blood flow to the anal area to promote wound healing
*used in patients refractory to NTG
-Other conservative therapies
*increased fluid and fiber intake
*keeping the area clean and dry
What is the clinical presentation of peritoneal dialysis related peritonitis?
-Abdominal pain (80%)
-Fever > 37.5 (99.5F) (50%)
-PE: Abdominal/rebound tenderness, cloudy abdominal fluid
How to diagnose PD-related peritonitis?
- > 100 WBC's (highly suggestive)
* >50% neutrophils strongly favors diagnosis regardless of WBC
-Culture is confirmative (80-95%)
*Gram stain is usually negative
What is the treatment of PD related peritonitis?
3rd or 4th generation cephalosporin (or an Aminoglycoside)
What are etiologies of Budd-Chiari syndrome?
-Myeloproliferative diseases (PCV)
-Malignancy (HCC-most common)
-Pregnancy or postpartum state
-Space-occupying liver lesions
What is the clinical presentation of Acute Budd-Chiari Syndrome?
-Most common in Women
-Severe RUQ pain, hepatmegaly
-Rapid development of jaundice and ascites
-Variceal bleeding, encephalopathy
What is the clinical presentation of Subacute/chronic Budd-Chiari syndrome?
-May be asymptomatic for weeks to months
-Abdominal pain, hepatomegaly, ascites
-Lower-extremity edema, cirrhosis
-Jaundice and encephalopathy less common
What is the diagnostic process for Budd-Chiari syndrome?
-Doppler US liver, CT, MRA --> decreased hepatic flow
-SAAG > 1.1
-Venography (gold standard) --> venous occlusion and "spider-web" pattern of collaterals
What is the treatment for Budd-Chiari syndrome?
-TIPS (if not responding to other therapies)
What are high risk procedures for bacterial endocarditis?
-Dental manipulation of gingival tissue or periapical region of teeth or perforation of oral mucosa
-Respiratory tract procedures with incision or biopsy
-Procedures in patients with ongoing GI/GU tract infection or infected skin or musculoskeletal tissue
When is bacterial endocarditis prophylaxis indicated?
Amoxicillin, Cephalexin, Ceftriaxone, Clindamycin, Azithromycin
GI/GU prophylaxis (Etnerococcus)
-Amoxicillin, Ampicillin, Vancomycin
Skin/musculoskeletal tissue prophylaxis (Staph/Strep)
-Vancomycin, Clindamycin (suspected MRSA)
What is the appropriate test in a HCV patient who presents with liver mass > 1 cm on surveillance US?
MRI or CT
-increased sensitivity and specificity
-helps to differentiate malignant nodules from regenerative nodules associated with cirrhosis
What is the treatment for recurrent variceal bleed?
-Repeat EGD (if early)
*can be used if bleeding continues despite 1st attempt at EGD
-TIPS or shunt surgery
Complication which occurs in 50% of patients with Roux-en-Y gastric bypass (RYGB) surgery?
What are common non-pancreatic causes of lipase elevation?
This test is more sensitive for diagnosing Schatzki ring than EGD?
-rings are not easily visualized on EGD unless lower esophagus is widely distended
What is the diagnosis/treatment of suspected perforation of sigmoid colon?
-CT scan with water-soluble contrast
*obtain if AXR negative and suspicion is high
What are the most common causes of modest elevations in AST/ALT?
-Drug induced hepatitis
-Hepatitis B, C
-ETOH abuse (AST/ALT > 2:1)
-Consider fatty liver disease (AST/ALT less than 1, --> obtain RUQ US)
What is the differential of continued elevation of aminotransferases after negative initial testing?
Hepatic (less common causes of liver disease)
-alpha 1 antitrypsin
*if all still unrevealing --> Liver biopsy
What are common findings in Boerhaave's syndrome (esophageal rupture)?
-forceful vomiting --> chest pain, respiratory distress
-CXR --> mediastinitis --> subcutaneous emphysema (present in only 30% of patients)
-Pleural effusion (usually on the left)
Cause of acute left upper quadrant pain in young AAM?
splenic vein thrombosis
-Diagnosis --> confirm sickle cell with Hgb electrophoresis
-Treatment --> supportive care
What are the clinical symptoms of PBC?
-fatigue with excessive daytime somnolence
-Pruritis (worse at night)
-RUQ abdominal pain
-Xanthomas and xanthelasmas (due to increased cholesterol)
-Metabolic bone disease (osteoporosis and osteomalacia) (20-30% of patients ***)
What are the laboratory findings in PBC?
-Increased LFT's (especially alkaline phosphatase)
-AMA positive (95% of patients)
-ANA positive (70%) of patients
-Hypercholesterolemia (especially HDL)
What conditions are associated with PBC?
-life threatening infection common in patients with hematologic malignancies (leukemia) who become neutropenic after chemotherapy
-fever + RLQ abdominal pain + nause with/without vomiting + watery or bloody diarrhea
typhlitis (due to:)
-intestinal mucosal injury (from cytotoxic drugs)
-inability of host to prevent microorganism invasion
What is the diagnosis/treatment of typhlitis?
-fluid-filled and distended cecum with thickened wall
-intramural air or edema
C. diff toxin assay
-should be checked and empiric treatment started
-Empiric antibiotics (including C. diff coverage)
-Surgery for complicated typhlitis
*Antifungal therapy should be added if fever persists > 72 hours
What is the treatment of ascites due to portal hypertensions with SAAG > 1.1 (due to Cirrhosis)?
-Avoid NSAID, ACE, ARB
-Sodium restriction 2g/day
Serum Sodium > 120
-Furosemide / Spironolactone
-Increase dose weekly as needed
-Max dose 160 mg / 400 mg
What is the treatment of ascites due to portal hypertensions with SAAG > 1.1 (due to Cirrhosis) and serum sodium less than 120?
-Vasopressin receptor antagonists
What medication can be used in patients with cirrhotic refractory ascites (on max diuretics) and hypotension?
What are the treatment options in patients with cirrhotic refractory ascites (on max diuretics)?
-Large volume paracentesis
*with albumin if > 5L removed
What is the treatment for the second recurrence of C. diff?
Pulsed tapering oral vancomycin x 6-7 weeks
What is the treatment for subsequent relapses (> 2) of C. diff infection?
-Consider fecal microbiota transplant
What is the diagnostic workup for suspected factitious diarrhea?
1. 24 hour stool specimen
-solid vs. liquid stool (further workup indicated)
2. Liquid stool
-sodium, potassium, osmotic gap
-less than 250 --> rule out water added to stool
- > 400 --> check urea and Cr. to rule out urine added to stool
- 250-400 --> Osmotic gap
4. Osmotic gap
- less than 75 --> secretory laxative use
*comprehensive laxative screen (saline, senna, bisacodyl)
- > 75 --> laxative use with unmeasured solute
*measure fecal fat
*rule out ingestion (lactulose, sorbitol, mineral oil, magnesium sulfate, polyethylene glycol)
What is a possible colonoscopic finding in chronic laxative use?
What is the most likely cause of NAFLD resulting in hepatomegaly?
-increased leptin and decreased adipnectin that affect hepatic insulin sensitivity