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279 Cards in this Set

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What is a normal swallowing time?
12 seconds
How do you listen for the swallow?
Auscultate over the epigastrum
What is a primary concern if dysphagia is prolonged?
This is difficulty swallowing from impeded flow of liquids, solids or both from the pharynx of the stomach.
What can dysphagia result in?
tracheal aspiration of ingested material, oral secretions or both.
This is when there is difficulty moving ingested material from the oropharynx into the esophagus. It results from abnormal function proximal to the esophagus.
Oropharyngeal Dysphagia
Difficulty initiating swallowing, nasal regurgitation, tracheal aspiration followed by coughing is seen with?
The patient's history in oropharyngeal dysphagia.
What type of patients is oropharyngeal dysphagia normally observed?
Patients with neurologic conditions or muscular disorders that affect the skeletal muscle.
This is when a patient has difficulty passing food down the esophagus.
Esophageal dysphagia
What two things can a esophageal dysphagia result from?
Motility disorder or mechanical obstruction.
Achalasia, diffuse esophageal spasms, systemic sclerosis are types of what kind of disorder? resulting in ?
These are types of motility disorder resulting in Esophageal Dysphagia
Peptic stricture, esophageal cancer, lower esophageal rings, eosinophilic esophagitis, extrinsic compression are all types of what? resulting in?
These are mechanical obstructions resulting in Esophageal Dysphagia
When examining a patient, what do you look for in the past medical history/family history/review of systems to identify esophageal/swallowing disorders?
PMH/FH/ROS - Look for Neuromuscular, GI or Connective Tissue Disorders.
What are three major red flags in regards to esophageal/swallowing disorders?
1. Symptoms of complete obstruction

2. Weight loss due to dysphagia

3. New Focal neurological deficits, objective weakness
This is an outpouching of the mucosa through the muscular layer of the esophagus.
Esophageal Diverticula
What are the three types of esophageal diverticula?

Midesophageal (traction)

This is a diverticulum of the mucosa of the pharynx above the upper sphincter of the esophagus.
Zenker's Diverticula
What could be witnessed with Zenker's diverticulum?
May have regurgitation of food when the person bends or lies down, halitosis, protrusion in the neck.
This is a type of esophageal diverticula that is caused by motility disorders or from scarring due to mediastinal or pulminary TB, typically asymptomatic.
Midesophageal (Traction)
This is a type of esophageal diverticula located above the diaphragm, usually accompany a motility disorder, and it is typically asymptomatic.
This is a ring like narrowing of the distal esophagus at the squamocolumnar junction.
Schatzki's Ring
Schatzki's Rings are almost always associated with what?
hiatal hernias
With these intermittent dysphagia of solids is seen, it is not progressive, reflux symptoms are common.
Schatzki's Ring
When does a schatzki's ring usually become symptomatic?
Usually symptomatic when the esophageal lumen is under 12 mm in diameter.
This is a thin mucosal membrane that grows across the lumen, more common in the upper esophagus, may be multiple, can be congenital or associated with dermatologic conditions.
Esophageal Web
What is the dermatologic condition associated with esophageal webs?
Plummer-Vinson Syndrome
This syndrome is characterized by symptomatic webs and iron deficiency anemia in females.
Plummer-Vinson Syndrome
This is a spontaneous rupture of the esophagus. Usually related to vomiting, retching or swallowing large contents. Distal esophagus is the most common site of rupture. Mediastinitis usually develops.
Boerhaave's Syndrome
With this you can see symptoms of-

chest and abdominal pain, vomiting, hematemesis, shock

Subcutaneous emphysema

Hamman's Sign - Mediastinal crunch synchronous with the heartbeat - Because of the gas that is there.
Boerhaave's Syndrome
How do you diagnose Boerhaave's Syndrome?
Chest and abdominal X-Rays for mediastinal air, pleural effusions or mediastinal widening. Esophagography confirms the diagnosis.
How do you treat Boerhaave's syndrome?
1. Broad spectrum ABX

2. Fluid resuscitation for shock

3. Surgical repair
This is a neurogenic motility disorder characterized by impaired esophageal peristalis, a lack of lower esophageal sphincter (LES) releaxation during swallowing and elevation of LES pressure at rest.
These are the pathologic feature of what?

1. Inflammatory response with T-Lymphocytes

2. Loss of Ganglion Cells

3. Fibrosis
The symptoms for this usually start in the 20's, there is dysphagia for solids and liquids, it is usually localized to the cerbical and xiphoid areas. Regurgitation is nocturnal, with chest pain, weight loss and heartburn.
When you do a barium swallow with fluoroscopy, you will see a Bird's beak - smooth tapering of the distal esophagus leading to a closed LES, dilation of the esophagus proximal to LES.
All patients diagnosed with Achalasia should have what?
an upper endoscopy
This results from a tumor at the esophago-gastric junction or an adjacent area. This is suspected if the endoscope does not pass from the LES into the stomach or passes with great resistance.
What are the most effective treatment options for achalasia?
Pneumatic dilation and surgical myotomy.
This is the most effective nonsurgical treatment option for achalasia.
Pneumatic dilation
After pneumatic dilation is performed to treat achalasia all patients should receive what?
A gastrograffin study followed by a barium swallow to exclude perforation.
This is vigorous nonpropulsive esophageal contractions, hyperdynamic contractions or elevated LES pressure. Typically causes substernal chest pain with and without dysphagia. Dysphagia for both solids and liquids is involved.
Esophageal spasm
What will be seen with a barium swallow in esophageal spasm?
Disordered simultaneous contractions with poor progression of a food bolus.
How do you manage esophageal spasm?
Nitrates and calcium channel blockers

Botulinum Toxin injection
What are the two types of esophagitis?
Pill induced esophagitis

Eosinophilic esophagitis
This is due to prolonged mucosal contact, most likely to occur if pills are swallowed without water or while supine. Symptoms include retrosternal chest pain, adynophagia, and dysphagia usually within hours of taking pills.
Pill Induced Esophagitis
What are the most common agents associated with Pill induced esophagitis?
How do you prevent pill induced esophagitis?
Healing typically occurs rapidly when agent is stopped.

Prevention includes taking pills with 4oz of water and remaining upright for 30 minutes after ingestion.
This is more common in men than women, it is associated with a history of atopic condition in approximately half of those affected, dysphagia for solid food; usually with history of food impaction, may have associated eosinophilia or elevated IgE levels.
Eosinophilic Esophagitis
What is required for diagnosis of eosinophilic esophagitis?
Endoscopy with biopsy and histologic evaluation
What may be seen with eosinophlic esophagitis? 3 things.
Multiple fine concentric rings

May have Whitish Papules

May have Exudates
Who do you refer a patient to if they have eosinophilic esophagitis?
Allergist - for evaluation for other atopic disorders, food and environmental allergies.
What is a Tx for eosinophlic esophagitis?
Protein Pump Inhibitor for improvement of GERD or undergo esophageal pH monitoring.
Upper GI bleeds occur above the ?
Ligament of Treitz
This is vomiting of red blood usually from an arterial source or varix?
This is vomitting of dark brown blood or granular material that resembles coffee grounds.
Coffee ground emesis
Coffee ground emesis results from what?
An upper GI bleed that has slowed or stopped with covnerstion of red Hb to brown hematin by gastric acid.
Upper GI bleeding is more likely and usually more severe in what two types of patients?
1. Chronic Liver Disease

2. Hereditary Coagulation Disorders
ROS in upper GI bleeds should address what?
Pain, weight loss, easy bleeding or bruising, previous GI studies, symptoms of anemia.
PMH in upper GI should address what?
Previous GI conditions, bleeding or clotting disorders, liver disease, drug use that increases likelihood of bleeding or liver disease.
What is the first thing you do when evaluating an upper GI bleed?
What in the NGT indicates active upper
GI bleed?
Bloody nasogastric aspirate.
Coffee ground material in the NGT suggests what?
bleeding that has slowed or stopped.
What are four things to do with Upper GI bleeding?
1. Secure the airway if needed.

2. IV Fluid resuscitation

3. Blood transfusion if needed

4. Angiographic or endoscopic hemostasis if needed

5. Inpatient admission
This is a nonpenetrating mucosal laceration of the gastroesphageal junction. It ranges in size from 0.5-4cm, caused by retching, vomiting, hiccupping, coughing. This results most commonly in hematemesis, +/- melena.
Mallory-Weiss Syndrome
Alcohol is a major risk factor for this. You see this a lot in patients who are alcoholics. You can also see this in patients who may complain of dark brown stools.
Mallory-Weiss Syndrome
These are dilated veins in the distal esphagus or proximal stomach caused by elevated pressure in the portal venous system. Normal pressure is 3-6mmHG, portal hypertension occurs when the gradient exceeds 10mmHG. Bleeding usually occurs when the portal/systemic gradient is over 12mmHG.
Esophageal Varices
What is the most common cause of portal hypertension?
liver cirrhosis
This can have sudden, painless, upper GI bleeding, distal esophagus bleeding is greater than gastric fundus, bleeding can be massive or slow and chronic resulting in anemia. This is diagnosed by endoscopy. In diagnostics it is important to check for coagulopathies.
Esophageal Varices
How do you manage Esophageal varices?
1. ABC's:
Endoctracheal intubation for airway
Fresh frozen plasma or platelets
Prophylactic IV Ceftriaxone

2. Endoscopic bonding or inejction Sclerotherpay with IV octreotide - Terlipressin if available.

3. Balloon Tube Tamponade

4. Transjuglar intrahepatic portosytemic shunting (TIPS) procedure
This is most common between the ages of 50 and 80 and has two main histologic types - Squamous cell, and Adenocarcinoma.
Esophageal Cancer
What do you give with band ligation Tx to reduce rate of recurrent bleeding when TX esophageal varices?
Nonselective Beta Blocker - Propanolol
Squamous cell esophageal cancer is most common in ?
The proximal 2/3rds of the esophagus
What are the primary risk factors for squamous cell esophageal cancer?
Alcohol ingestion and tobacco use
Adenocarcinoma esophageal cancer is more common in ?
The distal third of the esophagus
Adenocarcinoma esophageal cancer usually arises from?
Barrett's esophagus
Squamous cell esophageal cancer is more common in?
African Americans
Adenocarcinoma Esophageal cancer is more common in?
This is when the normal squamous epithelium of the distal esophagus is replaced by metaplastic columnar, glandular, intestine like mucosa. It results from healing of acute gastritis in the presence of chronic stomach acid (GERD). Patients require long term Tx of GERD and endoscopic surveillance for malignant transformation.
Barrett's Esophagus
What two cancers metastasize to the esophagus most commonly.
Melanoma and Breast Cancer
What are two signs of esophageal cancer?
1. Dysphagia for solids first, then semi-solids, then liquids and saliva

2. Weight loss is a key feature
Patients with suspected esophageal cancer should have what?
endoscopy with cytology and biopsy
This is more common in women. The risk factors include:
Increasing age, obesity, rapid weight loss, insulin resistance/diabetes, hyperlipidemia, diseases that disrupt bile acid resorption - Crohn's, Terminal ileum resection, Prolonged fasting, pregnancy.
What are the six F's associated with colelithiasis?
Female, Fat, Forty, Fertile, Fair, Flatulent
When does cholelithiasis become symptomatic?
When a stone becomes lodged in the cystic duct.
These frequently occur due to too much cholesterol and not enough bile salts.
What is the Presentation of cholelithiasis?

Onset - Often after a meal
Provocation - Eating makes worse
Quality - Dull, steady
Region - Epigastric or RUQ
Radiation - Right scapula (boas sign)
Relief - Time
Severity - Varies by patient
Time - Waxes and wanes, 30min - 6hours
When imaging the gall bladder, what is seen with cholelithiasis?
Stones, Sludge, GB wall thickening over 3 mm, CBD dilatation.
What is the medical TX of cholelithiasis?
Cheno- and ursodeoxycholic acids - bile salts that can be given up to 2 years. Most effective for people with functioning gallbladders and small stones. HELPS TO REDUCE THE RISK OF GALLSTONES FOLLOWING RAPID WEIGHT LOSS.
What is the surgical TX of cholelithiasis?
Laparoscopic cholecystectomy, Post-cholecystectomy syndrome. Surgery is only called for if cholelithiasis is symptomatic.
People with this are susceptible to cholelithiasis?
Sickle Cell Anemia
This is a complication of cholelithiasis that is a common bile duct stone.
This is a complication of cholelithiasis. It is when a stone erodes through the GB wall into duodenal bulb causing obstruction, the most common site is the ileocecal valve.
Gallstone ileus
This is characterized by inflammation of the gallbladder, steady, severe RUQ pain, Nausea and vomiting are HALLMARK, fever
Acute cholecystitis
This is a risk factor for acute cholecystitis. It usually occurs in patients within 2-4 weeks of major surgery or critically ill patients with no PO intake for a prolonged period of time. Associated with multisystem organ failure, trauma, burns, and/or sepsis.
Acalculous cholecystitis
The pathophysiology of acute cholecystitis can lead to infection from what?
EEEK bugs:

E. Coli
Enterobacter cloacae
Klebsiella spp.
Acute Cholecystitis Presentation:

Very symptomatic - 75% of patients have vomiting.

Onset - Often after a meal
Provocation - Eating makes worse
Quality - Dull, Steady
Region - Epigastric to RUQ
Radiation - Right scapula (boas)
Relief - Vomiting
Severity - Varies by patient
Time - Constant, 12-18 hours
What is the gold standard in imaging for acute cholecystitis but not always done?
Hepatic iminodiacetic acid scan (HIDA scan)
How do you TX acute cholecystitis?
Pain meds - classically meperidine (demerol) - not the best choice. Morphine/Dilaudid, although dilaudid is 8 times more powerful than morphine.
Broad spectrum ABX - Amp/Levo/Flagyl
What do the labs look like in acute cholecystitis?

CBC - Leukocytosis, 12,000-15,000/mcL

LFT's - Often elevated
The labs with choledocholithiasis will show what?
Elevated conjugated bilirubin
Elevated Alk Phos

Ultrasound - CBD dilatation > 10mm
This is infection of biliary tree usually due to obstruction. Potentially life threatening.
This is an infection due to obstruction seen with choledocholithiasis, structure, neoplasm, extrinsic compression - pancreatitis, pancreatic pseudocyst. Gram negative organisms mostly seen when involved with this.
What is the presentation with cholangitis?
Charcot's triad - RUQ pain, Fevers and rigors, Jaundice

Reynold's Pentad - Altered mental status, hypotension
What is the Tx for cholangitis?
Broad spectrum ABX

Biliary Decompression: ERCP w/sphincterotomy, Percutaneous Transhepatic Cholangiogram w/stenting, Laparotomy w/T-tube placement.
This is when there is multiple inflammatory fibrous thickening of bile duct walls resulting in strictures. Progressive obstruction possibly leading to cirrhosis and liver failure.
Primary Sclerosing Cholangitis
What is the presentation for primary sclerosing cholangitis?
Progressive jaundice - Itching from bile salts, dark urine, fatigue, clay-colored stool, weight loss.
What do you see with the diagnostic studies in Primary sclerosing cholangitis?
Labs - LFTs - Elevated alkaline phosphatase, elevated bilirubin

Imaging - Reveals "beads on a string" appearance on contrast study.
What is the Tx for Primary sclerosing cholangitis?
Steroids and ABX
This is inflammation of the pancreas.
This is when there is an inflammatory episode thought to be due to the escape of activated enzymes into surrounding tissues. By definition the gland returns to normal once the underlying cause is removed.
Acute Pancreatitis
This is when there is destruction of parenchyma, fibrosis, and calcification, Leads to loss of endocrine and exocrine tissue, may have acute or chronic exacerbation.
Chronic Pancreatitis
What are the three main things associated with pancreatitis?


Scorpion Bites
What is the pneumonic for Pancreatitis?
Scorpion Bite
Mumps (viral infection)
What is the primary pathophysiology behind pancreatitis?
It is thought to be a result of auto digestion by inappropriately activated pancreatic enzymes.
What is the Presentation of pancreatitis?

Onset - Abrupt in onset
Provocation - Walking, lying supine
Quality - Steady, boring, severe
Region - Epigastric
Radiation - Back
Relief - Walking
Severity - Varies by patient
Time - Constant
What is seen in the physical exam of acute pancreatitis?
Often with fever
May be hypotensive
Jaundice in 20%
RUQ tenderness often without guarding/rebound
Grey Turner's Sign
Cullen's Sign
What is seen with the diagnostics in acute pancreatitis?
Lab - Amylase/Lipase - Will be elevated in 90% of cases - Lipase

Calcium - <7mg/dL - correlates with severe disease

Imaging - Plain film - May show gallstones, "sentinel loop" segment of air filled small intestine in LUQ.
What is the Tx for acute pancreatitis?
NGT if vomitting
Analgesia - Dilaudid
Electrolyte correction
+/- ABX (if evidence of infected pancreatic necrosis)
Surgery (to debride necrotic tissue)
IR drainage (if abscess)
Acute Pancreatitis - Ranson's Criteria: On admission on diagnosis (when 3 or more are present, may indicate a complicated course). What are these?
Age > 55
WBC > 16,000 mcL
Blood glucose > 200 mg/dL
Serum LDH > 350 units/L
AST > 250 units/L
Acute Pancreatitis - These are supplemental to Ranson's Criteria - Development in the first 48 hours indicates a worsening prognosis if you see these things.
Hct drop > 10%
BUN Increase >5 mg/dL
Arterial Po2 < 60 mm Hg
Serum Calcium < 8 mg/dL
Fluid sequestration > 6 L
Base deficit > 4 mEq/L
What are the complications associated with Acute pancreatitis?
Necrotizing pancreatitis accounts for most of the deaths


Abscess formation

Pseudocyst formation

Chronic pancreatitis develops in 10% of acute cases
What is the presentation of chronic pancreatitis?

Onset - Persistent or recurrent
Provocation - Walking, lying supine
Quality - Steady, boring
Region - Epigastric
Radiation - Back
Relief - Walking
Severity - Varies by patient
Time - 2 hours to 2 weeks
What do you see in the diagnostic studies with chronic pancreatitis?
Amylase/Lipase - May be normal secondary to pancreatic burnout

Glucose - May be elevated from endocrine burnout

Vitamin B12 deficiency in 40%

ERCP - Most sensitive - dilated ducts, intraductal stones, strictures, or pseudocysts
What is the TX for chronic pancreatitis?
Stop Alcohol!
Insulin for DM
Pancreatic enzyme replacement
Low fat diet
H2 blockers or PPI - helps reduce lipase inactivation by stomach acids
Surgery for severe prolonged/refractory pain
Pancreatic Cancer - 90% are ________ of the pancreas arising from the duct cells.
75% of pancreatic neoplasms are located in the ?
Head of the pancreas
What is a big sign that there may be pancreatic cancer?
New onset DM after the age of 50.
What are the risk factors of pancreatic cancer?
African American
Chronic Pancreatitis
Prior abdominal radiation
Family hx
Male to Female 3:2
In pancreatic cancer, of the head of the pancreas, 70% of patients show no symptoms until the tumor does what?
Impinges on never fibers
What two things are seen in the presentation of pancreatic cancer in the head of the pancreas?
Painless Jaundice

Courvoisier's Sign - Palpable, nontender distended GB.
With pancreatic cancer of the body or tail of the pancreas, what are two presentations?
Weight loss and pain in 90%

Migratory thrombophlebitis (Trousseau's syndrome)
With pancreatic cancer what is seen with the imaging studies?
CT - Can detect a mass in 80% of cases

ERCP - Allows for pancreatic biopsy

MRI - For staging
What is the Tx for Pancreatic Cancer?


Head - Whipple procedure (pancreaticoduodenectomy)

Tail - Distal resection

Both - Stenting for symptomatic relief, multiple chemotherapy protocols, analgesia
This is classified as symptoms or mucosal damage produced by the abnormal reflux of gastric contents into the esophagus.
This is GERD that is seen with episodes postprandially, short lived, asymptomatic, not during sleep.
Physiologic reflux
This is GERD that has symptoms or/of mucosal injury, and is nocturnal.
Pathologic reflux
What are the five contributing factors to GERD?
1. Incompetent lower esophageal sphincter

2. Hiatal hernia

3. Irritant effects of refluxate

4. Abnormal esophageal clearance

5. Delayed gastric emptying
This occurs when the pressure gradient between the LES and the stomach is lost.
What are the secondary causes of LES incompetence?
Scleroderma like diseases

Myopathy associated with chronic intestinal pseudo-obstruction



Anticholinergic drugs

Smooth muscle relaxants

Surgical damage to LES
What are the conditions when gastric reflux is more likely to occur?
1. Gastric volume is increased

2. Gastric contents are near the gastro-esophageal junction.

3. Gastric pressure is increased
1/3 of patients with GERD have?
Diminished peristaltic clearance
What are the clinical manifestations of GERD?


What are other symptoms of GERD besides heartburn, regurgitation and dysphagia?
Chest pain, water brash or hypersalivation "foaming at the mouth", Globus sensation, odynophagia, nausea
What is recommended for patients with esophageal GERD along with troublesome dysphagia?
endoscopy with biopsy should be performed at presentation
What is used as the first step to diagnose GERD?
You check the response to antisecretory therapy:

Symptomatic response to antisecretory therapy to PPIs or H2 antagonists is frequently considered to support the presumptive diagnosis of GERED
This is when you have squamous epithelium in the esophagus being replaced by metaplastic columnar epithelium containing goblet and columnar cells.
Barret's Esophagus
What is the Tx for Barret's Esophagus?
PPI, surgical fundoplication
This is a GERD complication that is seen with solid food dysphagia, most are located in the gastro-esophageal junction.
Peptic Stricture
What is the Tx for peptic stricture?
Dilation of stricture with flexible weighted bougies.
How do you Tx mild symptomatic GERD?
Lifestyle modifications

Dietary modifications

Anatacids and nonprescription histamine-2 receptor antagonists
How do you Tx moderate GERD?
H2 receptor antagonist (ranitidine 150 mg twice daily) or PPI (Omeprazole 20 mg)

PPIs are often chosen as first line therapy, trial off at 8 weeks with good clinical response.
What are the Tx options for severe symptoms or erosive disease associated with GERD?

Repeat endoscopy every 8-12 weeks to determine if healing has occurred.

Barret's esophagus and peptic stricture - continuous therapy

Surgical fundoplication - is suggested for patients with erosive disease who are intolerant or resistant to PPIs
This is a term used to denote conditions where there is histological evidence of inflammation involving the gastric mucosa.
This is epithelial or endothelial damage WITHOUT inflammation.
What is the most common cause of erosive gastropathy?
NSAIDS, alcohol, stress due to severe medical or surgical illness and portal hypertension
Acute gastritis (neutrophils, edema, hyperemia) are caused by?
Most common causes are infectious. H. Pylori, also seen in immunocompromised patients.
Type A gastritis is found where and associated with what?
Type A gastritis (fundus and body, non antral) - Pernicious anemia
Type B gastritis is found where and is associated with what?
Type B gastritis (antral-predominant) more common - H. Pylori
What are the clinical manifestations of gastritis?
Generally reflect the underlying syndrome rather than the gastric injury itself.

Abdominal pain


Epigastric pain


What is the Tx for gastritis?
Aimed at sequelae and not the underlying inflammation

Appropriate antibiotics, antifungals, antivirals, antiparasitics

Various medical therapies for chronic conditions

Pernicious anemia - B12 supplementation
This occurs when there is a break in the mucosal surface > 5mm in size with depth to submucosa arises when the normal mucosal defense factors are impaired or overwhelmed by acid and pepsin.
Gastric and Duodenal Ulcers
What are the major causes of PUD?
NSAID use and H. Pylori infection

Less common causes include - Zollinger-Ellison syndrome CMV, systemic mastocytosis, crohn's disease, lymphoma and medications (other than NSAIDS)
Duodenal ulcers are usually associated with what?
H. pylori infection and NSAID induced injury. > 95% occur in the first portion of the duodenum.
Most of these are distal to the junction between the antrum and the secretory mucosa. H. Pylori and NSAID induced injury are associated. These can represent malignancy.
Gastric Ulcers
What is a major clinical manifestation with PUD?
Two thirds of symptomatic patients report epigastric discomfort that may localize to the RUQ, LUQ, or hypochondrium. This may radiate to the back.
With this pain is often described as a burning, gnawing, or hunger like feeling. Duodenal Ulcer "classic" symptoms occur when acid is secreted in the absence of food - usually 2-5 hours after meals or on an empty stomach, can also occur 11pm-2am when circadian stimulation of acid secretion is maximal.
PUD clinical manifestation
DU pain is often relieved when?
Eating and or using antacids or antisecratory agents.
GU pain is ?
more severe, occuring soon after meals and is less frequently relieved by food or antacids.
PUD diagnostic studies
Endoscopy is procedure of choice

Barium upper GI series in pts with uncomplicated dyspepsia


Urea breath test

Stool antigen test
This is the most common cause of non hemorrhagic GI bleeds/bleeding is most common complication.
PUD complications - Perforation (sudden diffuse abdominal pain). Penetration - ulcer bed tunnels into adjacent organs, DU - ?, GU - ?
DU - Panceras
GU - Liver
How do you Tx PUD?
First thing - Discontinue use of NSAIDS

Antisecretory agent DU 2-4 weekis, GU 4-6 weeks

Eradication of H. Pylori infection with triple therapy (14 days) - Bismuth + Metronidazole + Tetracycline


Ranitidine + Tetracycline + Clarithroymycin or Metronidazole


Omeprazole + Clarithromycin + Amoxicillin or Metronidazole

Eliminate irritants smoking and alcohol
This is an ulceration of the upper jejunum, with hypersecretion of gastric acid, and is associated with non beta islet cell tumors of the pancreas.
Zollinger-Ellison Syndrome
This syndrome is caused by gastrin secreting gut neuroendocrine tumors (gastrinomas). Result in hypergatrinemia and acid hypersecretion. 80% arise within the "gastrinoma triangle" bounded by the porta hepatis, the neck of the pancreas and the third portion of the duodenum.
Zollinger-Ellison Syndrome
What is the humoral agent responsible for ZES?
What are three clinical manifestations of ZES?
> 90% of pts develop peptic ulcers

Diarrhea in about 1/3 of pts

What diagnostic studies do you use in ZES?
Serum gatrin assays (fastings) - May save patients life if caught early

Secretin stimulation test

Tumor identification
What is the most common cause of morbidity and mortality in pts with ZES?
Metastatic gastrinoma
What is the Tx for ZES?
High dose PPI (omeprazole 60mg daily)

Sporatic: Surgery - Tumor resection with intent to cure

MEN1: Medical Therapy

Chemotherapy for metastatic gastrinoma is limited due to uncertainty with efficacy and toxicity
What is the most important predictor of survival with ZES?
The presence of hepatic metastases
What has a dismal prognosis with gastric cancer?
Diffusely spreading (linitus plastica) tumor that spreads through the submucosa resulting in rigid, atonic stomach with thickened folds
What has a good prognosis in gastric cancer?
Superficially spreading or early gastric cancer mucosa or submucosa, no mets
Where are most stomach cancers located?
Most are located in the antrum but increasing incidence of proximal tumors of the cardia and fundus
What is a strong risk factor for gastric cancer?
Chronic H. Pylori infection
What are the most common presenting symptoms with gastric cancer?
Weight loss - anorexia, nausea, early satiety, abdominal pain, dysphagia

Abdominal pain - epigastric, vague, mild (early), severe and constant (disease progression)
What is a sign of spread to the lymphatics in gastric cancer?
Left supraclavicular adenopathy (Virchow's Node) - most common PE finding of metastatic disease in gastric cancer.

Periumbilical node - Sister Mary Joseph Node

Left Axillary Node - Irish Node
What are signs of Peritoneal spread in gastric cancer?
enlarged ovary - Krukenberg's tumor

Mass int he cul de sac on rectal exam - Blumer's shelf

Ascites can be 1st indication of peritoneal carcinomatosis

Palpable liver mass - metastasis
What is the gold standard diagnostic study for stomach cancer?
Endoscopy with cytologic brushings and biopsies
What is the Tx for gastric cancer?
Curative surgical resection

Radical surgical resection for curative intent
What type of stomach cancer has a bad prognosis?
Diffuse and signet ring type have worse prognosis than intestinal type.
What is the 2nd most common gastric malignancy?
What is the Tx of lymphoma?
H. Pylori eradication

IE or IIE low-grade Surgical resection, radiation

IE or IIE high grade Surgical resection, CHOP chemotherapy
These are neuroendocrine tumors that are uncommon and often benign, but associated with stomach cancer.
Carcinoid tumors
These are uncommon, most common of these is the gastrointestinal stromal tumor. Leiomyomas and schwannomas are also associated.
Mesenchymal tumors
What is the Tx for carcinoid and mesenchymal tumors?
Surgery in all pats with tumors that are symptomatic > 3cm are increasing in size or are suspicious on Endoscopic ultrasound.
There is a high risk of mets with carcinoid and mesenchymal tumors when?
the tumors are > 5cm, have irregular borders, cystic spaces.
This is a fibrosing nodular condition that disrupts the entire normal architecture of the liver?
With this form of cirrhosis you usually see AST elevated, AST>ALT by a factor of at least two,
Alcoholic liver disease
Chronic Hep B and C, as well as drug toxicity, can result in what?
This is an autoimmune destruction of the small intrahepatic bile ducts and cholestasis.
Primary Biliary Cirrhosis
The risk factors for this are obesity, DM, hypertriglyceridemia, corticosteroid use, cushing's disease, PCOS. Patients may be asymptomatic or have RUQ pain and hepatomegaly, elevated ALT/AST and Alk Phos.
Nonalcoholic Fatty Liver Disease - A type of cirrhosis
What is the gold standard for diagnosing Nonalcoholic Fatty Liver Disease?
Liver Biopsy
This is an autosomal recessive disorder, associated with cirrhosis, it is a mutation of the HFE gene of chromosome 6, It results in increased accumulation of iron as hemosiderin in the liver, pancreas, heart, adrenals, testes, pituitary and kidneys, rarely recognized before the age of 50, associated with abnormal LFTs, elevated plasma iron and elevated serum ferritin
What is the Tx for hemochromatosis?
Avoid iron rich foods and perform phlebotomy
This is an automsomal recessive disorder linked to chromosome 13 associated with cirrhosis, that is characterized by excessive deposits of copper in the liver and brain.
Wilson's Disease
You must consider this in any child or young adult with hepatitis, Coombs Negative Hemolytic Anemia, Portal HTN, Neurologic or Psychiatric Disturbances.
Wilson's Disease
This is associated with increased urinary copper excretion or low serum ceruloplasmin levels and elevated hepatic copper concentrations.
Wilson's disease
What is the pathologic feature of Wilson's disease?
Kayser-Fleischer Rings, Brownish or Gray Green Corneal Ring.
How do you Tx Wilson's disease?
Restrict dietary copper and use oral penicillamine and pyridoxine which chelates the copper.
This is associated with cirrhosis, regenerating nodules are not larger than original lobules, noldues <3mm in diameter. Most common with cirrhosis due to alcohol.
These are larger nodlues associated with cirrhosis, up to several centimeters in diameter, may contain central veins.
What typically occurs before liver failure is manifested clinically?
Typically about 80-90% of the liver parenchyma must be destroyed before liver failure is manifested clinically.
What are the symptoms of cirrhosis?
Weight Loss
Abdominal Pain
Muscle Cramps
Skin Rashes, Pruritus
Increasing Abdominal Girth
What is seen in the skin exam with cirrhosis?
Palmar erythema
Vascular spiders (angiomas, telangectasias)
Glossitis and Cheilosis
Scleral icterus
What might be see non the nails in cirrhosis?

Terry's Nails - Proximal 2/3 of the nail plate appears white, distal 1/3 is red

Muehrcke's Nails - Paired horizontal white bands separated by normal color.
What is seen on the abdominal exam with cirrhosis?
Caput Medusa
What is seen in the neurological exam with a patient who has cirrhosis?
Signs of ecephalopathy
Day/Night Reversal
What are signs not seen in skin, neurological or nails associated with cirrhosis?
Testicular Atrophy
Kayser Fleischer Ring
Venous Hum
Peripheral edema
Fetor Hepaticus - breath that smells like a freshly opened corpse
This is the gold standard test for cirrhosis, but it is only performed when thorough noninvasive serologic and radiologic evaluation has failed to confirm the diagnosis.
Liver biopsy
How do you TX Cirrhosis?
Most importantly stop Alcohol
Avoid hepatotoxic drugs - NSAIDS
Must have adequate nutritional support
Give ferrous sulfate for Iron def. anemia
Give Vit. B12 or folate for macrocytic anemia
Coagulopathy: Vit K or Fresh Frozen Plasma
If fluid retention is present then restrict salt
Pt should receive vaccinations Hep A and B, Pneumococcal and yearly influenza
What are absolute contraindications for liver transplant as TX for cirrhosis?
Other malignancies, Advanced cardiopulmonary disease, multisystem organ failure, sepsis, active alcohol or drug use.
What are complications associated with cirrhosis?
Portal HTN, Ascites, Spontaneous Bacterial Peritonitis, HepatoRenal Syndrome, Hepatic encephalopathy
This results from increased resistance to portal flow due to scarring, narrowing and compression of the hepatic sinusoids. The main complication of this is varices.
Portal Hypertension
This in patients with cirrhosis is usually due to portal hypertension, hypoalbuminemia, peripheral vasodilation, increase renin and angiotensin levels and sodium retention.
What should be done with ascitic fluid?
Cell count, culture, and measurement of the ascitic albumin level.
How do you manage ascites?
Dietary restriction of sodium to 2000 mg/d

Diuretic Therapy - Spironolactone +/- lasix, goal of weight loss in patients without peripheral edema is 1-1.5lb/d

Large volume paracentesis - draining 4-6 liters

Transjugular intrahepatic portosystemic shunt (TIPS) - Stent between hepatic and portal vein, increases renal sodium excretion and control of ascites in 75% of patients. Beware of hepatic encephalopathy.
E. coli and streptococcus are the most frequent causes of what?
Bacterial peritonitis
How do you Tx bacterial peritonitis?
1. Pending isolation of ogranism cover with broad spectrum ABX - Ceftriaxone, Cefotaxime, Amoxicillin, Clavulanate

2. Supplement with IV albumin

3. Norfloxacin 400 mg once daily as prophylaxis has been shown to decrease recurrent peritonitis. If you can't handle floroquinolone use bactrim instead.
This is seen in 10% of patients with cirrhosis and massive ascites, it is characterized by azotemia, and liver transplant is the best TX of choice.
Hepatorenal syndrome
This is CNS dysfunction caused by the liver failing to detoxify noxious agents of gut origin.
Hepatic encephalopathy
What are the precipitants of encephalopathy?
GI tract bleeding
Potassium deficiency
Portosystemic shunting
Medications with ammonium in them
What are the clinical features of hepatic encephalopathy?
Day/Night Reversal, Asterixis, Intellectual impairment, Coma
What are the Stages of Encephalopathy?
I - Mild Confusion
II - Drowsiness
III - Stupor
IV - Coma
How do you TX hepatic encephalopathy?
If patient can not eat then withhold dietary protein, with oral intake, limit protein to 60-80g/d, controls and prevent GI bleeding, Purge blood from GI tract (NGT or Lactulose) - Lactulose acidifies colon content, acification favors the formation of ammonium ion which is not absorbable, Initiate AX that limit ammonia producing flora - RIFAXIMIN or METRONIDAZOLE, avoid opioids and sedatives - anything that will cause constipation.
Measure of mortality risk in patients with with End-Stage Liver Disease; Useful for Predicting Complications & Determining Priority for Donor Livers
Child-Turcotte-Pugh & Model for End-Stage Liver Disease (MELD)
This is the most common type of liver cancer - it is a malignant neoplasm that arise from the parenchymal cells.
Hepatocellular cancer
What are the symptoms of liver cancer?
Deterioration of a formerly stable cirrhotic patient
Weight loss, Weakness
New Onset Ascites
What are the signs of liver cancer?
Tender Liver, +/- Palpable Mass, +/- Bruit over Tumor, +/- Friction Rub if Liver Capsule is involved
No one test is a clear diagnosis for liver cancer, but this shows up in 70% of patients?
Alpha fetoprotein elevated in up to 70% of patients with hepatocellular
What is the gold standard for diagnosis of liver cancer?
Liver biopsy
What is the screening and prevention of liver cancer?
Monitoring for hepatocellular CA is recommended for patients with chronic Hep B or cirrhosis due to Hep C or alcohol use with alpha fetoprotein and US every 6 months.
What is the TX for liver cancer?
Surgical resection, adjuvent chemotherapy, immunotherapy and/or treatment of chronic hepatitis

Pain Management

Palliative Care

Possible Liver Transplant
This means inflammation of the liver.
What are the presenting symptoms of all types of viral hepatitis?
Loss of appetite
Abdominal Pain - RUQ and/or epigastrim
Clay-colored bowel movements
Joint Pain
What is considered infectious Hepatitis?
What is considered serum, viral hepatitis?
Hep B, D
What is considered Non A Non B Hepatitis?
E and C
What types of hepatitis are transfered via feces and are occured through the fecal oral route?
A and E
What types of hepatitis are blood/blood-derived body fluids
B, C, and D
What types of hep are associated with chronic infection?
What types of hep are associated with percutaneous permucosal transmission?
What types of hep do you use pre/post exposure immunization?
What types of hep do you use blood donor screening, and risk behaviour modification?
What types of hep do you have to ensure safe drinking water?
What is the incupation period for Hep A?
Avg 30 days, range 15-50 days.
This is spread via close personal contact, contaminated food, water, blood exposure (rare)
Hep A
How is acute infection diagnosed in hep A?
HAV-IgM in serum by EIA - Elisa test
Past infection, i.e. immunity determined by detection of ?
In Hep A highest attack rates are in?

In Hep A who serves as a reservoir of infection?
Highest attack rates are in 5-14 year olds

Children serve as a reservoir of infection
What three types of people are at increased risk of hep a?

Homosexual men

Injecting drug users
This is an established cause of chronic hepatitis and cirrhosis?
Hep B
an antigen of the DNA core of the hepatitis B virus, indicating the presence of replicating hepatitis B virus.
hepatitis B core antigen (HBcAg)
an antigen of hepatitis B virus sometimes present in the blood during acute infection, usually disappearing afterward but sometimes persisting in chronic disease.
hepatitis B e antigen (HBeAg)
a surface coat lipoprotein antigen of the hepatitis B virus, peaking with the first appearance of clinical disease symptoms. Tests for serum HBsAg are used in the diagnosis of acute or chronic hepatitis B and in testing blood products for infectivity.
es immunity.
hepatitis B surface antigen (HBsAg)
Hepatitis B chronic infection is very high in ?
children infected at birth
If you have had immunization you will have what with Hep B?
If you have had infection and/or immunization you will have with Hep B?
anti- HBC and HBS
What is the first response IgM with Hep B?
IgM anti-HBc
What are the high risk body fluids associated with Hep B?
Blood, serum, wound exudates, semen
Asian populations are infected with? and it puts them at increased risk of liver disease.
genotype C
Immune Active Phase is defined by the presence of elevated HBV DNA levels, with or without HBeAg and evidence of active liver inflammation (ALT elevated or active inflammation on liver histology)
< 40 yrs. of age may have spontaneous seroconversion
40 yrs. Of age less likelihood of seroconversion
Reactiviton Phase of Chronic HBV = elevated HBV DNA and liver inflammation should be treated
used as a general marker of infection
HBsAg -
used to document recovery and/or immunity to HBV infection.
HBsAb -
marker of acute infection.
anti-HBc IgM -
Hep B marker - past or chronic infection.
indicates active replication of virus and therefore infectiveness.
HBeAg -
virus no longer replicating. However, the patient can still be positive for HBsAg which is made by integrated HBV.
Anti-Hbe -
indicates active replication of virus, more accurate than HBeAg especially in cases of escape mutants. Used mainly for monitoring response to therapy.