Esophagus
What is Esophagitis?
 Inflammatory changes to the
lining of the esophagus
(squamous epithelium)
Esophagitis Symptoms:
 Dysphagia
 Chest Pain
 Odynophagia
Causes:
 GERD (#1)
 Radiation
 Pills
 Caustic Ingestion
 Eosinophilic Infiltration
 Infection
Diagnostic Tests:
 Gold Standard: Endoscopy
 Bravo Study: Ambulatory
Esophageal pH
Infectious Esophagitis:
 THINK Immunocompromised!
Agents that can cause esophagitis due to
mucosal injury:
 Bisphosphanates
 Aspirin
 Iron salts
 NSAID’s
 Potassium chloride tablets
 Quinidine
 Tetracycline
There are various scales available to
quantify esophagitis severity. The
Hetzel-Dent scale utilizes a rating of 0 to
4, with 0 indicating no abnormalities and
grade 4 indicating deep peptic
ulcerations or confluent erosions
involving more than 50% of the mucosal
surface of the distal 5 cm of esophageal
squamous mucosa
CMV (Chemo/HIV)
 Ganciclovir (5mg/kg IV q 12
hours x 3-6 weeks)

Candida
 Fluconazole 100mg/d P.O. x 1421 days
 Suspect in patients w/ DM or
recent steroid or ABX treatment

Herpetic
 Acyclovir 400mg 5x daily for 10
days
 Famciclovir 500mg BID or
Valacyclovir 500mg BID x 10 days

Eosinophilic Esophagitis:
 Affects children to adults 20-40
y.o
 Males > females (3:1)
 History of allergies, eczema,
asthma or GERD is common
 “Feline esophagus” on EGD
 Often causes solid food dysphagia
due to esophagitis and
Trachealisation – “Feline Esophagus”
dysmotility
 CBC w/ diff. reveals eosinophilia –
systemic response to something
allergic
 Consider checking tTG for celiac
disease and consider food allergy
testing
 Treat acid suppression
aggressively with PPI b.i.d. For 68 wks and may consider
Montelukast (Singulair) 10mg
daily or Budesonide susp 1mg
B.I.D.
Achalasia:
 Idiopathic motility disorder
involving loss of peristalsis in the
distal 2/3 of smooth muscle and
impaired relaxation of LES.
 Likely the result of neuronal
abnormalities
 Dysphagia (solids & liquids),
Chest Pain, Weight loss
 Age 25 and greater
 Also consider Scleroderma or late
stage Chagas’ disease (South
American Trypanosomiasis)
Esophageal Varices:
 Dilated submucosal veins that
develop in patients with
underlying Portal Hypertension /
Cirrhosis and may result in
serious upper GI bleeding in 1/3
of patients.
 Usually occurs in distal 5 cm of
esophagus
 Higher mortality rate than any
other source of UGI bleeding.
 Identified via upper endoscopy
 Actively Bleeding Treatment =
ABC’s, page GI or Surgery stat
Management:
 Emergency stabilization (fluids
IVs etc)
 Treat underlying coagulopathy (if
present)
 Endoscopy with banding or
injection sclerotherapy
 Balloon tamponade (if
hemorrhage is too vigorous)
Mallory-Weiss Tear:
 Non-penetrating mucosal tear at
the GE junction caused by
retropulsion of the gastric cardia
into the chest during repeated
vomiting/retching
 ~ 5% of GI bleeds
 Small, fresh hematemesis
 Common in young adults or those
with history of ETOH abuse
 Diagnosis is confirmed
endoscopically (EGD)
Boerhaave’s Syndrome:
 Caused by a sudden increase in
intraesophageal pressure +
negative intrathoracic pressure
caused by straining or vomiting.
 Tear most often occurs @ left
posterolateral aspect of the distal
esophagus and can extend several
centimeters.
 Often associated with alcoholism
or hx. of peptic ulcer disease
 Can lead to Mediastinitis
GERD:
 Also known as Pyrosis or old
fashioned “heartburn”
 Refers to backflow of gastric acid
and/or duodenal contents (bile
acid) into the esophagus and past
the LES (lower esophageal
sphincter) without associated
belching or vomiting.
 Affects 20% of adults who report
at least weekly episodes, 10% of
adults report daily heartburn.
Symptoms:
 History of vomiting or retching
followed by acute, severe
retrosternal chest and upper
abdominal pain.
 Odynophagia
 Fever
 Cyanosis
 Shock
Pathophysiology:
1. Impaired acid neutralization by
saliva and HCO3
2. Impaired esophageal motility
3. LES (inappropriate relaxation)
4. Hiatal hernia
5. Delayed gastric emptying
(Gastroparesis)
Typical (Esophageal) Clinical
Presentation:
 Heartburn *classic*
 Bitter taste in the throat
 Acid regurgitation
Risk Factors:
 Obesity
 Delayed gastric emptying
 Pregnancy
 Systemic sclerosis
 Hiatal hernia
 Recumbency
 Smoking
 Alcohol use
 Medication such as CCB’s,
nitrates, Theophylline
 Consuming large meals (within 3
hours before bedtime) – one of
the main things that will help
with nocturnal reflux
 Wearing tight belts
 Foods: chocolate, coffee,
peppermint, or fatty food, garlic



Dysphagia
Odynophagia
Waterbrash
Atypical (Supraesophageal)
Presentation:
 Chest pain
 Laryngitis (Hoarseness)
 Asthma
 Sinusitis
 Chronic cough
 Aspiration pneumonia
 Tooth decay
 Recurrent sore throat
 Frequent throat clearing
 Globus sensation
Treatment:
Antacids (Tums, Rolaids)  neutralize
secreted HCl
H2-receptor antagonists (H2RAs) 
block the histamine receptor,
interfering with one of
the stimulation pathways
Proton pump inhibitors (PPIs)  block
acid at its source in the proton pump of
the parietal cell. (1st Line)
 Omeprazole (Prilosec) 20 mg
 Lansoprazole (Prevacid) 15 to 30
mg
 Rabeprozole (Aciphex) 20mg
 Pantoprozole (Protonix) 40mg
 Esomeprazole Magnesium
(Nexium) 40mg

Omeprazole w/Sodium Bicarb
(Zegerid) 40mg
 Dexlansoprazole (Dexilant) 60mg
Side Effects of PPI’s: HA, diarrhea,
nausea
Prokinetic drugs (Zelnorm, Reglan)
Antireflux surgery (Nissen
Fundoplication)
Esophagitis secondary to GERD:
 Severe Reflux from GERD
(incompetent LES) can lead to
esophagitis.
Diagnostic Histology:
 Intraepithelial Eosinophils
 The severity of symptoms is not
related to the degree of histologic
esophagitis
Consequences:
 bleeding, stricture, Barrett
esophagus
Treatment: Lifestyle modification
 elevate head of bed, no bedtime
snacks
 no smoking/alcohol
 decrease meal size and fat intake
 avoid caffeine (chocolate, coffee,
tea, cola) peppermint, citrus fruit
 Medications – antacids, H2
receptor blockers, proton pump
inhibitors
Barrett’s Esophagus:
 A self-protective mechanism by
which squamous epithelium in
the distal esophagus is replaced
by columnar epithelium (gastric).
 3 types of gastric columnar
epithelium, **Intestinal
metaplasia is the type that
increases the risk of
adenocarcinoma.
 Secondary to chronic refluxinduced injury – compensation by
the body but this causes a lot of
cellular turnover
 Affects ~ 10,000 people per year
in U.S.
 5 year survival rate < 15% if you
have adenocarcinoma
 Pay attention to GERD complaints
in old, white males with truncal
obesity. (Sutton’s Law)
“Tongue” of Barrett’s
Treatment:
 long-term PPI therapy and
adherence to anti-reflux
measures
 Advised to have repeat
endoscopic surveillance at 2 to 3
year intervals
Incidence of Barrett’s evolving into
esophageal adenocarcinoma is 2 in 200.
Squamous Cell Esophageal Cancer:
 Blacks > whites
 Most prevalent worldwide
 Associated with:
 ETOH
 Tobacco abuse
 Human Papilloma Virus
 > 50% involve distal third of
esophagus
Overall 5- year survival rate is < 15% for
either form of Esophageal Cancer
Adenocarcinoma Esophageal Cancer:
 Prominent in whites
 Incidence rising
 Associated with Obesity
 Most cases arise from Barrett’s
changes and chronic GERD
 Involves distal third of esophagus
Overall 5- year survival rate is < 15% for
either form of Esophageal Cancer
More Nodular:
More Spread out:
Esophageal Web:
 A thin, diaphragm-like membrane
of squamous mucosa
 Mid to upper esophagus
 May be multiple
 Congenital or may be related to
Plummer – Vinson Syndrome
Plummer-Vinson Syndrome:
 Predominately in Caucasians
 Female > male; 40-70 years old
Esophageal “Schatzki Rings”
 Smooth, circumferential and thin
mucosal structures found at the
GE junction (distal).
 Lead to dysphagia
 Strongly associated with Hiatal
Hernias
 Suspected secondary to GERD
 Treatment = Esophageal Dilation
Esophageal Strictures:
 Most found in mid to distal
esophagus
 Majority result from chronic
inflammation and GERD
 Usually benign
 Can be associated with Barrett’s
Esophagus
 May also be caused by burns
 Pills that got stuck and
disintegrated the tissue
Predominant findings are dysphagia
with a history of iron-deficiency anemia.
Treatment: Esophageal Dilation
Balloon Method:

Maloney-Dilator Method:
Zenker’s Diverticulum:
 Protrusion of pharyngeal mucosa
@ PE junction (posterior
protrusion most common).
 Caused by loss of elasticity of UES
 Usually older patients
Symptoms:
 Halitosis
 Dysphagia
 Nocturnal Choking
Diagnosis: Barium Swallow
Tx: Surgery

Benign Esophageal Tumor:
Leiomyoma
 The most common
 Submucosal, nodular lesions
 Most are asymptomatic, although
larger lesions can cause
dysphagia.
 Endoscopic ultrasonography** is
test of choice because endoscopic
biopsies are generally
Stomach
Peptic Ulcer Disease:
 Include both Gastric and
Duodenal ulcers
 ~ 10% of adults develop PUD in
their lifetime
 Epigastric Pain (dyspepsia) often
described as gnawing, dull,
“hunger-like” discomfort.
 Most common cause of Upper GI
bleeding
Duodenal Ulcers
 5x more common, younger
patients
 Pain relieved with food or
antacids, recurs 2-4 hours after a
meal, or a strong nocturnal
component
(3) major causes :
 NSAIDS – inhibit prostaglandin
synthesis. Prostaglandins are
known to increase mucosal blood
flow, increase bicarb and mucous
secretion and stimulate mucosal
repair. Aspirin is the most
ulcerogenic NSAID (beware of BC,
Goody’s powders and Alkaseltzer).
 H. pylori – gram neg. bacillus that
resides in the mucous gel coating
the epithelial cells of the stomach.
Suspected to cause a defect in
protective barrier that can then
lead to chronic gastritis and ulcer
formation.
 Zollinger-Ellison (ZE) syndrome –
benign gastrin-secreting tumor
Gastric Ulcers
 more common in ages 55-70 ,
high association with cancer
 Pain aggravated by food and
associated with weight loss and
“fear of eating”
 Associated symptoms: Nausea,
Anorexia, Abdominal bloating,
vomiting, melena, weight loss,
hematemesis
usually located in the pancreas or
duodenal wall that results in
uninhibited secretion of gastrin
(Hypersecretion) and constant
acid production. Leads to
development of peptic ulcers in
90% of patients; diarrhea is
common. < 1% of PUD is caused
by ZE syndrome, may be
associated with MEN type 1
Complications: Perforation
Diagnosis:
 Upper Endoscopy with biopsy is
diagnostic test of choice.
 CBC, BUN if suspected GI
bleeding.
 H.pylori serology gives limited
information for active
involvement of H.pylori. Need
gastric biopsy to confirm active
infection.
 Consider checking a fasting
serum Gastrin level if peptic
disease is persistent (to r/o ZES).
Need to stop PPI therapy before
testing.
Management:
 Pharmacotherapy is directed at
reduction of acid secretion,
preserving mucosal defenses, and
eradication of H.pylori infection.
 Proton pump inhibitors are
currently the treatment of choice
for PUD, given their high safety
and efficacy profile.
 Combination antibiotic regimens
with PPI are most effective in
eradicating H.pylori.
 Regular, well balanced diets with
elimination of caffeine, sodas,
acidic foods, NSAID’s, ETOH and
smoking.
Gastritis:
 superficial inflammation and
erosions of gastric mucosa
without penetration into the
submucosa or muscularis.
 Patients are usually
asymptomatic but can progress to
dyspepsia, anorexia, nausea and
vomiting.
 Accounts for < 5% of GI bleeds.
Acute Gastritis:
 NSAIDs
 Biphosphonates
 Potassium
 Macrolides
 ETOH
 Stress
 Viruses
 Bacteria
Chronic Gastritis:
 Helicobacter pylori
 Autoimmune
 Lymphocytic
 Bile Reflux
 Eosinophilic
Gastric Cancer:
 Most neoplasms of the stomach
are malignant and most of those
are adenocarcinoma.
 Adenocarcinoma of the stomach
is the 2nd most frequent cause of
cancer world-wide.
 Incidence has declined in
Westernized countries;
attributable to improved diet and
refrigeration (has eliminated the
need for salting, smoking,
preserved foods.)
Commonly associated with:
 NSAID’s
 Prolonged stress (physiologic)
due to severe medical or surgical
illness
 Heavy ETOH consumption
 Caffeine abuse, and H.pylori.
 ** Psychological Stress
Diagnosis:
 Endoscopy with biopsies for
H.pylori.
Treatment:
 Proton Pump inhibitors and
cessation of offending
medication, ETOH, or caffeine.
Risk Factors:
 Chronic Gastritis w/ H.pylori
 National origin (Japan, Chile,
Finland)
 Diet (high sodium/nitrates)
 Blood group A
 Male>Female
 Hx of partial gastrectomy
 Family hx of gastric cancer 
autosomal dominant
Symptoms:
 Early  typically asymptomatic
 Abdominal Pain
 Weight loss/anorexia
 Generalized weakness
 GI bleeding

Early satiety
Physical Exam:
 Epigastric mass
 Enlarged mass
 Ascites
 Pelvic mass if gastric cancer has
mets to the ovaries (Krukenberg
tumor)
Diagnostic Studies:
 Endoscopy
 Upper GI series
 CEA level – elevated in 1/3 of
patients
 CBC (Hgb / Hct)
 CT abdomen to evaluate for
metastasis
Prognosis:
 Poor. 5 year survival 10%
 Sx is primary hope for cure
Pyloric Stenosis:
 Hypertrophy of the pyloric
muscle
 Affects infants around 4-6 weeks
of age
 Most common in first born
children
 5:1 male predominance
Diagnostic Tests:
 Elevated BUN d/t dehydration
 Unconjugated hyperbilirubinemia
Plain films showing gastric enlargement
and little gas in bowels

U/S is the study of choice which reveals
elongation and thickening of pylorus:
Presentation:
 Projectile vomiting after feeding,
otherwise not ill
 Vigorous/Hungry





Non-bilious vomiting
Abdominal Swelling
Weight loss
Metabolic Alkalosis due to loss of
hydrochloric acid
Physical Exam:
 “Olive” of hypertrophied muscle
 Reverse Peristalsis
Barium Upper GI study reveals a “string
sign”:

Treatment:
 Correct fluid and electrolyte
abnormalities
 Keep NPO
 Surgery (pyloromyotomy)
Small Intestine
Small Bowel Neoplasms:
 Overall very rare, <5% of GI
cancers
 Occur in most people >50 years of
age
 Adenocarcinomas, Lymphomas,
Carcinoid tumors
Complications with Increased risk of SB
cancers:
 Crohn’s: adenocarcinoma
 Familial adenomatous polyposis:
peri-ampullary adenocarcinoma
(200fold inc)
 Celiac sprue: lymphoma and
adenocarcinoma
 AIDS: non-hodgkin’s lymphoma
and kaposi’s sarcoma
 Neurofibromatosis: leiomyopma
and adenocarcinoma
 Melanoma: highest rate of mets to
SB
Small Bowel Adenocarcinoma:
 Most common malignant SB
tumor
 Most often located in
duodenum/proximal jejunum
 Ampulla of Vater m/c site
 80% of cases have already
metastasized by the time of dx. SB
surgical resection is
recommended for control of sx
 Findings: anemia/GI bleed,
Jaundice, SB obstruction, weight
loss
Small Bowel Lymphomas:
 Most common in distal SB
 Majority are non-hodgkin’s
intermediate or high grade B cell
lymphoma’s
 Findings: Abdominal pain, N/V,
anemia, weight loss, abdominal
distention, positive hemoccult
 Work-up: CT enterography, or
SBFT
 Treatment: resection,
chemo/radiation – dependent on
stage of disease (overall poor
prognosis of 20% at 5 yrs)
Small Bowel Carcinoid Tumors:
 Most common neuroendocrine
tumors from GI tract
 Slowest growing, majority are
asymptomatic and found
incidentally
 May contain serotonin,
somatostatin or gastrin
 Commonly arise in ileum
 Slow spread but >2cm mass =
mets (onset to death is ~9yrs)
 Findings: abd pain, signs of
obstruction, rectal bleeding,
change in bowel habits
 **Carcinoid Syndrome: <10% of
pts, caused by tumor secretion of
hormonal mediators, may lead to
flushing, head/neck edema,
bronchospasms, diarrhea, cardiac
(valvular) disease
 Work-Up: Plasma Chromagranin
A m/c screening test, 24 hour
urine for 5-HIAA, abd CT scan,
Octreotide scan
 Treatment: surgery
 If Carcinoid: consider resection of
hepatic mets and start octreotide
100-500mcg SC TID
Appendicitis:
Aids to Diagnosis:
 Most common surgical emergency
 H&P
 Mostly between ages 10-30
 CBC
 If untreated  gangrene and perf
 Serum Pregnancy
within 36 hours
 UA
 CT abd/pelvis
Findings:
 Initially vague periumbilical
Make NPO and consult surgery!
abdominal pain that later locates
to the RLQ
**Be aware of retrocecal appendix!
 Anorexia
 Nausea / vomiting
 +/- fever
 +/- leukocytosis
 Tenderness over McBurney’s Pt.
 Positive bounce test
Irritable Bowel Syndrome:
 Constipation, diarrhea, or
alternating with both
 Abdominal pain
 Bloating/distention
 Mucous in stool
 Sx related to stress
 Weight stable
 Must be present at least
3days/month for longer than 3
months
 Females > Males
 Ages 18-45 most common
 Food is the most common culprit
(up to 2/3 of pts associate sx with
eating a meal)
Clinical Work-Up:
 Stool for occult blood
 If diarrhea: stool for O&P, C&S
 Colonoscopy
 Consider labs for tTG, CMP, TSH,
CBC
Treatment:
 Reassurance and Education
 Stress reduction
 Regular exercise and diet
modification
 Consider use of TCA’s or SSRI’s
 Increase soluble fibers, H2O
 Stool Softeners, Laxatives,
Lubiprostone or antidiarrheals
 MAINSTAY: Psyllium husk
powder (Metamucil)
**Alarm Symptoms: weight loss and
rectal bleeding  refer to GI
Large Intestine
Diverticular Disease:
 Very common in westernized
countries where dietary fiber has
been replaced by refined carbs
 Prevalence increases with age
 Most will remain asymptomatic
 Caused by increased intra-luminal
pressures over time  small
herniation of the colon wall
 Most are found in the sigmoid
colon (smaller radius)
Diverticulitis Symptoms:
 LLQ abdominal pain
 Change in bowel habits
(constipation- 50%, diarrhea
25%)
 Rectal bleeding
 Fever, Chills
Treatment:
 Bowel rest, NPO
 Ciprofloxacin + Metronidazole or
Augmentin (2nd line)

Nausea and Vomiting
Diagnosis:
 CBC, CMP, UA, Serum pregnancy
 CT abd/pelvis (if fever or 1st
episode), DRE
 Leukocytosis is mc lab finding
 Colonoscopy contraindicated
within 6-8 wks of infection due to
inc risk of perforation
Inflammatory Bowel Disease:
 Crohn’s + Ulcerative Colitis
 1/3 of cases present in 2nd decade
of life and between the 6th and 7th
decades


Gradually increase fiber and
maintain high fiber diet
Surgery may be considered for
severe segments of diverticulosis
Complications: bleeding, abscess,
perforation
Potential risk factors:
 Family history *most important
 High level of sanitation (CD)
 Cigarette Smoking (+ CD, -UC)
 Increased sugar intake, esp CD
Signs & Symptoms of Crohn’s:
 Non bloody diarrhea
 Abdominal pain (RLQ)
 Anorexia/Weight loss
 Peri-anal abscess, fistula, chronic
fissure
 Growth retardation in children
 N/V, fever
 Erythema nodosum
 Arthralgias
 Apthous stomatitis
Signs & Symptoms of UC:
 Bloody diarrhea with mucus
 Tenesmus
 Fecal incontinence
 Abdominal Pain + Tenderness
 Feverm fatigue, loss of
appetite/weight
 Arthralgias
 Uveitis
 Skin Ulcers
 Jaundice (with primary biliary
Work-Up for Crohn’s:
 CBC: anemia, iron def, B12
malabsorption
 CMP: hypoalbuminemia
 ESR/CRP: elevated
 IBD panel: autoantibodies
 Stool Studies: C&S, O&P, Fecal fat
 Colonoscopy: to evaluate/biopsy
 Small bowel radiographs
Treatment for Crohn’s:
 Surgery
 Natalizumab (anti-TNF)
 Prednisone, 6-MP, AZA/MTX,
Budesonide, ABX,
Aminosalicylates
Treatment for Ulcerative Colitis:
 Surgery: Colectomy
 Biologics: Cyclosporine,
cirrhosis)

infliximab
Corticosteroids: Steroids (short
term), Azathiprine/6MP (long
term)
Aminosalicylates: 5-ASA’s
(mesalamine)
IBD Complications:
 Crohn’s: fistulas, abscess,
intestinal blockage,

extraintestinal disorders,
malnutrition, colon or rectal
cancer, growth retardation
 UC: severe inflammation,
perforation, megacolon,
extraintestinal disorders, colon or
rectal cancer
Colorectal Cancer:
Screening:
 Third mc type of cancer and cause
 Colonoscopy: Gold Standard
of cancer-related death
q10years
 Most colon cancers arise from
 Flexible sigmoidoscopy q5yrs
pre-existing polyps
 Double contrast barium enema
 Mean age at dx: 64
q5yrs
 CT colonography q5yrs
Risk Factors:
 FOBT qyear
 Age (>50)
 Prior hx of adenoma or carcinoma
 Family hx of CRC
 IBD
 High fat/low fiber consumption
 Beer and ale consumption
Hereditary Colorectal Cancers:
 Familial Adenomatous Polyposis
(FAP): APC gene
 Hereditary non-polyposis
colorectal cancer (HNPCC): MMR
genes
Colon Polyps:
 Mucosal neoplastic
(adenomatous)  tubular,
villous, tubulovillous, serated
 Mucosal non-neoplastic
(hyperplastic)  hyperplastic,
juvenile, inflammatory
 Submucosal lesions  lipomas,
lymphoid aggregates
Remove via colonoscopy
Pancreas
Acute Pancreatitis:
 May be related to edema or
obstruction of ampulla, reflux of
bile, direct injury to acinar cells,
biliary tract dz, cyst, abscess,
pancreas necrosis
 Most common causes in US:
Biliary Tract disease and/or
ETOH
 ABRUPT onset of deep epigastric
pain possibly associated with
radiation to the back and worse
when lying down
 Pain improved when leaning
forward
 History of prior episodes (usually
involve alcohol or consumption of
a heavy/greasy meal before
attack)
Symptoms:
 Steady/boring/severe epigastric
pain
 N/V
 Diaphoresis, weakness
 Hypotension, pallor, clammy skin
Physical Exam:
 Tender epigastric region, +/guarding/rebound/rigidity,
abdominal distention, dec bowel
sounds
 Cullens sign or Grey Turner’s sign
if severe necrotizing pancreatitis
with hemoperitoneum
Complications:
 ARDS (usually 3-7d after fluids)
 Pancreatic necrosis
 Pancreatic pseudo cyst
 Pancreatic cyst or abscess
**Necrotizing Pancreatitis in 5-10% of
Ranson Criteria on Admission
 Age greater than 55 years
 WBC greater than 16,000/ul
 Blood glucose greater than 200
mg/dl
 Serum LDH greater than 350
I.U./L
 SGOT (AST) greater than 250
I.U./L
Ranson Criteria in first 48 hours
 Hematocrit fall greater than 10%
 BUN increase greater than 8
mg/dl
 Serum calcium less than 8 mg/dl
 Arterial oxygen saturation less
than 60 mm Hg
 Base deficit greater than 4 meq/L
 Estimated fluid sequestration
greater than 6000 ml (6 liters)
 Ranson score of 0-2, minimal
mortality
 Ranson score of 3-5, 10%-20%
mortality
 Ranson score of >5 has more than
50% mortality and is associated
with more systemic
complications.
Lab Testing:
 Increased amylase and lipase (3x
normal) – lipase remains elevated
for a week, amylase for 72hours
 Leukocytosis
 Hypocalcemia
 Proteinuria
 Hyperglycemia
 Fasting TG >1000mg/dL
 ** Hct>44% or inc Serum Cr,
worry about pancreatic necrosis
 Rise of ALT may mean biliary
pancreatitis
cases and accounts for mst deaths
Imaging:
 Plain radiographs for setinal loop,
gall stones or colon cutoff sign
 Abd ultrasound for gallstones
 noncontrastCT ABD test of choice
 MRCP for repeated attacks
Treatment:
 Most resolve without tx
(supportive)
 NPO (bowel rest) & Bed rest
 NG tube if needed
 IV crystalloid resuscitation (250300 mL/hour for the first 48hrs)
 Pain meds: Meperidine or
Morphine
 Lap Chole if biliary pancreatitis
Chronic Pancreatitis:
 Prolonged inflammatory, fibrosis
of the organ
 70-80% associated with
alcoholism
 Tobacco accelerates progression
 Usually develops in 5-10% of
alcoholics
 Hallmark features = abd pain
(chronic epigastric or LUQ pain
that radiates to the back and is
unrelenting) and pancreatic
insufficiency (steatorrhea- late
finding with weight loss)
TIGAR-O: classification of chronic
pancreatitis etiology:
 Toxic Metabolic: alcohol, tobacco,
Severe Treatment:
 Supportive measures +:
 Vigorous fluid resuscitation and
check HCT q12h (if decrease then
hydration is adequate)
 TPN for7-10d
 Abx if necrosis (imipenum 500mg
IV q8h x 14d)
 If abscess  surgical drainage
Treatment:
 Low fat diet
 Alcohol abstinence
 Smoking cessation
 Analgesics (avoid narcotics if
possible)
 Pancreatic supplements (Creon,
Pancrease)- Allows them to
digest better
 Autoimmune- Corticosteroids
(Prednisone taper)
 Treat diabetes if indicated
Surgical Options:
 Drain pseudocysts
 Relieve biliary obstructions
 Rule out pancreatic CA
 ERCP- ductal dilitation/stent





hypercalcemia, chronic renal
failure
Idiopathic
Genetic: Autosomal Dominant
Autoimmune: Sjrogen, primary
sclerosing cholangitis, Type1DM,
primary biliary cirrhosis
Recurrent: post necrotic,
vascular/ischemia
Obstructive: pancreas divisum,
duct obstruction from tumors or
post trauma
Complications:
 Opioid addiction
 Pancreatic CA develops in 4%
after 20 years of condition
 >80% develop diabetes (25 years
after onset)
 Others: pseudocyst, fistula
formation, pseudoaneurysm, CBD
stenosis, splenic/portal
obstruction
Lab Testing:
 Increases in Amylase/Lipase –
remember that the longer the
abuse or deterioration of the
pancreas, the more the labs will
appear normal.
 Alkaline phosphatase
 Total bilirubin -- Elevation of
liver function tests may signal
compression of the pancreatic
portion of the bile duct by edema,
fibrosis, or tumor development.
 Sudan stain to confirm fecal fat
excretion
 Fecal Pancreatic Elastase (FPE-1)
-- An ELISA stool test that serves
as a marker of exocrine
pancreatic function (<100)
Imaging:
 Plain films show calcifications
 CT/MRI – mainstay
 MRCP (noninvasive)
 ERCP (invasive)
Pancreatic Cancer:
 2% of all cancers (5% of all CA
deaths)
 7-8% have familial relation of CA
 95% of all CA arises from
exocrine portion of pancreas
 75% are in the head, 25% in body
and tail (pain in RUQ)
Laboratory Testing:
 Most labs normal (if cancer is in
the tail)
 Elevated glucose in 10-20% cases
 CA 19-9: not sensitive for early
detection but can be useful in
diagnosis and monitoring
treatment




Mean survival 11.2 monthsdependent on staging
More common in men
More in African Americans,
Polynesians and native New
Zealanders
Rare before age 45 , but increases
sharply after the 7th decade.
Types:
 Ductal Adenocarcinoma (most
common – 90%) –arise from
epithelial cells in the exocrine
ducts
 Neuroendocrine tumors aka
carcinoid
 Cystic neoplasm if cyst and no
history of pancreatitis




Alk Phos 4-5x elevated
Bilirubin elevated
Hepatic Transaminases
(AST/ALT) elevated
Amylase/Lipase elevated
Imaging:
 Spiral CT *Best
 MRI as an alternative
 Endoscopic US
 ERCP
Treatment:
 If duodenal obstructiongastrojejunostomy
 Chemotherapy has a high
resistance and is not very
effective, alone or with radiation
 Radiation alone has little impact
Risk Factors:
 15-20% present with disease that
 Age
can be resected, local invasion
 Obesity
determines success
 Tobacco use (thought to cause 20 The Whipple Procedure:
25% of cases)
pancreaticoduodenectomy
 Chronic pancreatitis
 Prior abdominal radiation
Prognosis:
 Family History
 5 year survival with no treatment
2-5%
Symptoms:
 20-40% if resectable
 Obstructive painless jaundice (if
 If family history present,
pancreatic head) ddx is duodenal
recommend endoscopic U/S
cancer, ductal carcinoma,
and/or CT ABD starting at age 40 Enlarged gallbladder (+/- pain)
45 or 10 years before age at
 Upper abdominal pain or
which family member was
discomfort described as vague
diagnosed.
and diffuse pain (gnawing pain)
 Weight loss/ Anorexia
 Diarrhea
 New onset DM
 Thrombophlebitis (late stage)
 Sister Mary Joseph’s nodule- hard,
palpable nodule that bulges from
the umbilicus. (Results from
abdominal or pelvic metastasis)


Courvoisier sign: a palpable, non
tender gall bladder due to the
CBD becoming obstructed by a
pancreatic neoplasm
Rectum
Anorectal Abscess:
 A localized inflammatory process
that can be associated with
infections of soft tissue and anal
glands based on anatomic
location.
 Most are located in the posterior
rectal wall but can communicate
around the rectum (Horseshoe
abscess)
Presentation:
 Males> Females
 Perirectal cellulitis or erythema
 Perirectal mass by inspection or
palpation
 Localized perirectal or anal pain
often worsened with movement
or straining
 Fever and signs of sepsis with
deep abscess
 Urinary retention
Causes by infection of mucous secreting
anal glands:
 Staph aureus
 E. coli
 Bacteroides, Proteus
 Streptooccus
Diagnosis: Many people will have
predisposing underlying conditions
including:
 Malignancy/Leukemia
 Immune deficiency
 DM (check BS!)
 Recent surgery or Steroid therapy
Workup:
 Rule out necrotic process and
crepitance suggesting deep tissue
involvement
 Local aerobic/anaerobic culture
 Blood cultures if
toxic/febrile/compromised
 Possible sigmoidoscopy
 Imaging studies not indicated
unless extensive disease abscess
Treatment:
 I&D of abscess (cures in 50% of
cases)
 Debridement of necrotic tissue
 Chronic recurrence leads to
fistula formation  fistulectomy
 Local wound care/packing
 Sitz bath
Complications: Necrotizing fasciitis,
sepsis, death
Outpatient Antibiotics:
 Amoxicillin/Clavulanic acid
875/1000 mg BID
 Ciprofloxacin 750mg BID+
Metronidazole 500-750mg TID
 Clindamycin 150-300mg TID
Inpatient Antibiotics:
 Ampicillin/sulbactam (Unasyn)
1-2gm IV q6-8hrs
 Cefotetan 1-2gm IV q8h
 Piperacillin/Tazobactam
3.375gm IV q6-8h
 Imipenem 500-1000mg IV q8h
Anal Fissure:
 A fissure is a tear in the epithelial
lining of the anal canal.
 Men>Women
 Common in women before/after
childbirth
 Can occur at any age
 Most common cause of rectal
bleeding in infants
 90% posterior, 10% anterior
Acute anal fissure sx:
 Sharp burning/tearing pain
associated with bowel
movements
 BRB on toilet paper or streak of
blood on the stool
Chronic anal fissure sx:
 Pruritis ani
 Pain seldom present
 Intermittent bleeding
 Sentinel tag at caudal aspect of
fissure and hypertrophied anal
papilla at proximal end
*According to Kirby: Abx are of unproven
value but should be used in diabetics,
immunocompromised, sepsis, or those
with prosthesis or valvular heart dz.
Etiology:
 Large, hard stool passage
 Frequent defecation/diarrhea
 Bacterial infection: TB, syphilis,
gonorrhea, chancroid,
lyphogranuloma venereum
 Viral: HSV, CMV, HIV
 IBD
 Trauma
 Malignancy: Kaposis, lymphoma,
carcinoma
Treatment:
 Sitz Bath, High fiber diet, inc fluid
intake.
 Bulk producing agent
(Metamucil)
 Stool softeners (Colace, surfak)
 Local anesthetic jelly
 Nitroglycerin ointment
 Surgery (lateral sphincterotomy)
 Injection of botulinum toxin if
chronic.
Underlying disease possible if:
 Ectopically located
 Broad based/deep/purulent
 Extends proximal to dentate line

BEWARE:
 Crohns, anal TB, anal carcinoma,
can all present as ulcers so biopsy
all chronic ulcers
Anorectal Fistula:
 Chronic form of anorectal abscess
 A fistula is an inflammatory tract
with a secondary (external)
opening in the perianal skin and a
primary (internal) opening in the
anal canal at the dentate line.
 May be initial sign of Crohn’s, TB,
Neoplasm
 Managed by opening the fistula
Work-Up:
tract (fistulotomy) and curetting
 DRE to assess sphincter tone
the tract and allowing it to heal by
 Determine the presence of an
secondary intention.
extraluminal mass
 Identify an indurated track
 Palpate an internal opening or pit
Symptoms:
 Anoscopy
 Acute stage: perianal swelling,
 Proctosigmoidoscopy to exclude
pain, fever
inflammatory/neoplastic dz
 Chronic stage: history of rectal
drainage or bleeding, previous
Labs:
abscess with drainage.
 CBC
 Rectal Biopsy if IBD/malignancy
Etiology:
suspected
 Most common: nonspecific
cryptoglandular infection (skin
Imaging:
or intestinal flora)
 Colonoscopy or barium enema if
 Fistulas more common when
dx of IBD/malignancy suspected,
intestinal microorganisms are
patient <25, history of recurrent
cultured from the anorectal
fistulas
abscess
 TB, Lymphogranuloma
Treatment:
venereum, actinomycosis
 Sitz bath
 IBD
 Surgery


Trauma: sx, FB, intercourse
Malignancy: carcinoma,
leukemia, lymphoma


Broad-spectrum abx if cellulitis,
immunocompromised, valvular
heart disease, prosthesis
Stool softener/laxative
***


HIV/Diabetic pts with fistulas are
true surgical emergencies
Risk of septicemia, fournier’s
gangrene
Hemorrhoids:
 Valscular and connective tissue
 Usually located in 3 positions: R.
anterolateral, posterior/lateral,
left lateral
 Internal are above the dentate
line (painless)
 External are under the anoderm
(same sensation as skin and thus,
painful)
Grading System:
1. Bleed
2. Bleed + Prolapse, but
spontaneously reduces
3. Bleed + prolapse and needs
manual reduction
4. Incarcerates
External Symptoms: pain, pruritis,
fullness sensation, thrombosis, +/bleeding
Internal Symptoms: Bleeding (painless)
Causes:
 Lack of soluble fiber, water,
straining
 Increased intra-abdominal
pressure from pregnancy, obesity,
sitting, coughing, sneezing etc.
 Excessive cleaning, rubbing,
steroids or hemorrhoid creams
Rectal Neoplasm:
 Adenocarcinoma
Treatment:
 After confirmation via
sigmoidoscopy/colonoscopy..
 High fiber diet
 Stool softeners
 Avoid heavy lifting/straining
 Warm baths BID
 Medication for anorectal
inflammation
 Anusol-HC suppositories
 Analpram or procto-foam
W.A.S.H regimen: Warm water,
Analgesics, Stool softeners, high fiber
diet
If symptoms persist, consider surgical
referral.
Treatment:
 local excision
 low anterior resection (tumors

Anal Neoplasm:
 Squamous cell carcinoma
Melanoma
Diarrhea:
Rotavirus:
 Severe in children between 3 and
15 mos.
 Shed by feces, transmitted via
fecal / oral route
 Most common in winter months
 Incubation period of 1 – 3 days.
Symptoms last 5 – 7 days.
 Sx’s = vomiting, fever, watery
diarrhea, dehydration
Enteric Adenovirus:
 Transmitted from person to
person
 Nosocomial outbreaks do occur,
but spread to adults in
uncommon
 Year round occurrence
 Incubation period = 8 -10 days,
lasts 1 – 2 weeks
 Symptoms: low grade fever,
watery diarrhea, then brief
vomiting
Clostridium botulinum:
 Associated with improperly
prepared home-canned fruits and
vegetables.
 Responsible for 1/3 of all deaths
from food borne illness.
above 8-10 cm from anus)
Abdominal-perineal resection
Treatment:
 Chemo radiation with 5-FU and
Mitomycin or external beam
radiation
Treatment: Wide excision


Dx = Rotozyme test (viral assay)
Tx = symptomatic / supportive
with oral or IV rehydration

Dx: can detect virus on electron
microscopy
Tx: Supportive

Dx: made by history and culture
TX: Golytely bowel lavage
Clostridium perfringens:
 Found in soil and GI tract of
humans and animals
 Beef or poultry source
 Requires inadequate initial
preparation and then reheated
 Symptoms: watery diarrhea with
severe, Crampy pain w/in 8-24
hrs of ingestion
Norwalk Viruses:
 Year round occurrence
 Affects older children and adults
(usually not young children)
 Spreads rapidly via fecal / oral
route
 May also be airborne via droplets
from vomitus or contaminated
laundry.
 Incubation period = 12 – 48 hours
 Symptoms : rapid onset of
abdominal cramping, vomiting,
diarrhea
Vibrio parahaemolyticus:
 Gram (-) bacillus that survives in
water with high salt content.
 More common in summer
 Found in contaminated fish or
shellfish (raw or cooked)
 Incubation = 12 – 24 hours
 Symptoms: explosive, watery
diarrhea. Headaches, vomiting
 Resolves in 1 – 7 days


DX: history
TX: Supportive
Diagnosis : H&P
Treatment : Supportive
DX: stool culture
TX: supportive, if severe consider
tetracycline
Enterotoxigenic E. coli:
DX: History
TX: supportive, if severe, consider Cipro
 Found in contaminated water or
or Tetracycline.
food
 Spread via fecal / oral route
 Most common travelers’ pathogen
 Requires large inoculum for
disease to emerge
 Incubation period = 1 to 3 days
 Symptoms = abrupt, profuse,
large volume diarrhea (like
cholera)
Vibrio Cholerae:
 Gram negative
 Contaminated saltwater crabs
and freshwater shrimp
 Incubation period = 1 – 3 days
 Symptoms: abrupt onset of
PROFUSE, large-volume watery
diarrhea. No fever, vomiting
 Beware of rapid dehydration !!!!
Staphylococcus aureus:
 Most frequent cause of toxinmediated vomiting and diarrhea
 Transmitted via hands of food
handlers
 Problematic foods: Cole slaw,
potato salad, salad dressings, milk
products, and cream pastries
 Symptoms: Abrupt onset of
vomiting within 2 – 6 hrs of
ingestion and explosive diarrhea
with some abdominal cramping
but no fever.
Bacillus cereus:
 Gram +, spore-forming organism
found in soil
 Spores can survive extreme
temps
 Contamination occurs before
cooking
 Normally found in contaminated
rice or meat from Asian
restaurants.
Infectious Diarrhea: CCSSY +EVE
Campylobacter jejuni
 C.jejuni is the most common
bacterial pathogen that causes
bloody diarrhea in the U.S.
 Transmitted to humans from
contaminated pork, lamb, beef,
milk products, water, or exposure
to infected household pets.
 Incubation period 1 to 7 days
 Symptoms start with malaise, HA,
followed by severe abdominal
pain, fever and bloody diarrhea.
Dx: dark field microscopy
Tx: Volume replacement, may respond
to Doxycycline


Dx = History
Tx = Supportive, symptoms
normally dissipate within 24
hours.
“emesis syndrome” – severe vomiting
within 2 – 6 hours
or
“diarrhea syndrome” – foul-smelling,
profuse diarrhea 8 -16 hrs after eating
Dx: history
Tx: Supportive
DX: made by stool cultures
TX: Emycin or Cipro
 Can lead to systemic infection
Salmonella:
 Transmitted from fecally
contaminated foods and water
 Poultry products most common
 Fever & bacteremia < 10% cases
 Carrier state can exist, as some
patients carry bacteria in GB or in
urinary tract.
Shigella:
 Seasonal preference for winter.
 Fecal / oral route
 Common in dairy and egg salad
 Common in children 6 mos to 5 yr
 Incubation period 1 to 3 days
Enterohemorrhagic E.coli:
 E.coli 157:07
 Infection occurs if meat is
undercooked.
 Outbreaks in schools, daycare
centers, nursing homes
 Fecal / oral spread
 Lasts 7 to 10 days
 May be complicated by hemolytic
uremia syndrome
Yersinia enterocolitica:
 Found in stream or lake waters
and has been isolated in many
animals.
 Transmitted via contaminated
water or from human or animal
carriers.
 Most common in children
 Symptoms = bloody diarrhea,
fever and abdominal pain
Clostridium difficile:
 Most commonly affects elderly.
 Spread by fecal / oral
transmission or by contaminated
hands of healthcare workers
 Follows antibiotic use, especially:
ampicillin, amoxicillin,
cephalosporins, clindamycin and
fluoroquinolones
DX: history and + blood/stool cx’s
TX: supportive in most cases
** Antibiotics contraindicated in most
pts b/c it can increase the carrier state.
Consider Amoxil, Bactrim DS or Cipro in
immunosuppressed adults, pediatric or
adults > 65.
Dx: stool culture
Tx: supportive & Antibiotics
 Bactrim DS, Cipro, Tetracycline
 Do not use Immodium or Lomotil
DX: stool culture
TX: supportive & Cipro antibiotic
DX: stool and blood cultures
TX: Supportive, may use Bactrim or
Tetracycline for severe illness.
Treatment:
 Stop all offending antibiotics first
 Replace fluids/electrolytes (if
needed)
 Avoid anti-peristaltic agents
 Flagyl (metronidazole) 500mg
P.O. TID x 10-14 days
 Vancomycin 125mg P.O. QID x 10
days

Symptoms usually start within 1
Complications:
week of antibiotic exposure but
can range from day one to 10
 Pseudomembranous colitis
weeks post antibiotic exposure.
 Toxic megacolon
(always inquire about any abx use
 Perforations **
in the past 2-3 mos)
 Sepsis
 Recurrent diarrhea
Dx: Stool cultures for C.diff toxin (PCR,
EIA) **always order x 3
Nutritional Disorders
Obesity:
Metabolic Syndrome:
 BMI >30
 Elevated abdominal
Circumference: >40 inches (men)
 Increased abdominal
and >35 inches (women)
circumference (>40 inches (men)
and 35 inches (women):
 Triglycerides > 150 mg/dL
Increased risk of DM, HTN, early
 HDL < 40 mg/dL (men), < 50
death
mg/dL (women)
 BMIs > 40, cancer risk is 52%
 BP > 130/85
higher (men), 62% (women)
 FBS > 100 mg/dL
Etiology:
 Excess caloric intake and
sedentary lifestyle
 Genetic influences
Anorexia Nervosa:
 Weight loss leading to body
weight < 15% below expected
 In females, absence of three
consecutive menstrual cycles
 90% female
Signs/Symptoms:
 Emaciation, cold intolerance,
constipation, bradycardia,
hypotension, hypothermia
 Amenorrhea: almost always
present
 PE: loss of body fat, dry, scaly
skin, increased lanugo body hair.
Bulimia:
 Uncontrolled episodes of binge
eating at least twice weekly for 3
months
Treatment:
 Lifestyle modification: calories,
exercise, behavior therapy
 Pharmacotherapy short term
 Surgery: refer if BMI>40 or >35+
additional health related risks
Labs:
 Anemia
 Electrolyte Abnormalities
 Inc BUN/Cr
Treatment:
 behavioral therapy,
psychotherapy, family therapy,
antidepressants
 Refer for psych eval
Treatment:
 Psychotherapy: behavioral,
family, individual, group
 ?antidepressants

Prevention of weight gain by selfinduced vomiting, laxatives,
diuretics, excessive exercise
 Gastric dilatation, pancreatitis,
poor dentition, pharyngitis,
aspiration, electrolyte
abnormalities
Vitamin Deficiencies
Vitamin B1 (Thiamine)
 Found in cereals, beans, pork,
yeast, rice
 In US, seen with chronic
alcoholism
Early Findings:
 Anorexia
 Muscle cramps
 Paresthesias
 Irritability
Advanced Findings Dry Beriberi:
 Low calorie intake and inactivity
with nervous system involvement
 Peripheral involvement: both
motor and sensory-(symmetric):
pain, paresthesias, loss reflexes,
Lower>upper extremities
 Central involvement: WernickeKorsakoff Syndrome
 Wernicke encephalopathy:
nystagmus progressing to
opthalomoplegia, confusion,
truncal ataxia
 Korsakoff Syndrome:
Confabulation, amnesia, impaired
learning
Advanced Findings: Wet Beriberi:
 Very high activity levels and
eating large amounts of
carbohydrates
 Cardiovascular involvement (high
output failure), vasodilatation,
dyspnea, cardiomegaly,
pulmonary and peripheral edema
Diagnosis:
 Most commonly used lab test is to
measure the erythrocyte
transketolase activity (ETKA) and
urinary thiamine excretion
Treatment:
 50-100 mg/day IV for several
days then po, 5-10 mg/day
 50% complete resolution within
several days
Vitamin B2 (Riboflavin)
 Milk, dairy products, cereals,
meats, and dark green vegetables
 Rarely an isolated deficiency,
usually occurs with other Vitamin
B complex deficiencies
 Alcoholism, Malasorption, Celiac
sprue
 Medication interactions
 Protein-calorie undernutrition
Physical Exam Findings:
 Cheilosis/Angular stomatitis






Glossitis
Seborrheic dermatitis
Weakness
Corneal vascularization
Anemia
Diagnosis:
 Measurement of the riboflavindependent enzyme erythrocyte
glutathione reductase
 Measure the urinary excretion of
riboflavin
Treatment:
 Oral Preparation: 5-15 mg/day
po until symptoms resolve
Vitamin B3 (Niacin)
Diagnosis:
 Chocolate, oats, dates, milk,
 N-methynicotinamide in urine
cottage cheese, eggs, fish, poultry,
can be measured
bananas
 NAD and NADP can be measured,
 Absorbed in intestines
but are nonspecific
 Niacin deficiency can occur where
Treatment:
corn is the mainstay of the diet
 Niacin or niacinamide 10-150
 Occurs in industrialized countries
mg/day po
in alcoholics
Signs/Symptoms:
 Anorexia, weakness, irritability ,
mouth soreness, glossitis,
stomatitis, weight loss
 Pellagra Triad: 3 D’s 
dermatitis, diarrhea, dementia
Vitamin B6 Deficiency:
 Meats, grains, nuts, vegetables,
bananas
 Most commonly occurs in
Diagnosis:
 Plasma pyridoxal phosphate
concentration (PLP)
 Urinary excretion levels of

patients taking isoniazid,
cycloserine, penicillamine, oral
contraceptives and in alcoholics
Also occurs in the elderly, dialysis
patients, HIV patients, and
patients with rheumatoid
arthritis and liver disease
Symptoms:
 Seborrheic dermatitis, glossitis,
angular cheilitis, confusion,
somnolence (similar to other
Vitamin B deficiencies)
Vitamin B9 (Folic Acid)
 Citrus fruits, grains, legumes,
green leafy vegetables and liver
 Daily requirements are 50-100
mcg
 Poor diet, alcoholics, overcooking
of food
Signs/Symptoms:
 Megaloblastic and macrocytic
anemias
 Fatigue, HA, palpitations
 Gray hair
 Mouth ulcers
 Glossitis
Vitamin B12
 Sources: Meat/Dairy
 Causes: strict vegans, alcoholics,
elderly, pernicious anemia,
H.pylori, metformin, PPI’s
Signs/Symptoms:
 Paresthesias, numbness, tingling
 Vibration/Position sense loss
 Proprioception/Balance loss
 Dementia, Memory disturbance
Vitamin C (Ascorbic Acid)
 Fresh fruits and vegetables
 Populations affected: urban/poor,
smokers, elderly, alcoholics,
pyridoxic acid
Treatment:
 10-20 mg/day Vitamin B6
Diagnosis:
 RBC folic acid level<150 ng/ml
 Macrocytosis
 Hypersegmented neutrophils
 Elevated LDH and bilirubin
 Normal B12 levels
Treatment:
 1mg/day PO
Findings:
 Macrocytosis
 Megaloblastic anemia
 Hypersegmented neutrophils
 Low serum B12 <170
 Schilling test (rarely)
Treatment:
 IM or SQ 100mcg daily for first
week then weekly for one month
followed by monthly for life
Treatment:
 300-1000 mg/day
chronic illness
Symptoms:
 Weakness/fatigue
 Scurvy: Perifollicular
hemorrhages, petechiae, purpura,
hemarthrosis, bleeding gums,
splinter hemorrhages, corkscrew
hair
 Late symptoms: Edema, oliguria,
neuropathy, intracerebral
hemorrhage, death
Vitamin A (Retinol)
 Found in highly pigmented
vegetables as beta-carotenes and
carotenoids
 Populations: fat malabsorption
syndromes, mineral oil laxative
abuse, elderly, poor
 Most common cause of blindness
in developing countries
Diagnosis:
 Strongly suggestive: night
blindness
 Vitamin A serum levels <30-65
Treatment:
 Orally 30,000 IU QDx7days
Symptoms:
 Night blindness, Bitot’s spots and
xerosis
 Keratomalacia, blindness,
perforation
Vitamin D:
 Primary food source is fortified
milk
 Populations at risk: infants,
elderly, disabled, malabsorption
syndromes
Symptoms:
 Nonspecific muscle pain
 Rickets in children
 Osteomalacia in adults
Lab Findings:
 25-hydroxyvitamin D (25-OHD)
serum level <15-37.5
Vitamin E:
 Sources: oils, nuts, avocado
Symptoms:
 Areflexia
 Gait disturbances
 Decreased proprioception
 Decreased vibratory sensation
 Myopathy
Vitamin K:
 Populations affected: newborn
infants, alcoholics, IBD, bulimics,
cystic fibrosis
 Sources: green leafy vegetables
Major Symptom: bleeding from minor
trauma
 mucosal and subcutaneous
bleeding, epistaxis, hematoma,
menorrhagia, GI bleeding,
bleeding from gums.
Hernias
Hiatal Hernia:
 Found in 50% of patients >50
 Increases in age
 Sliding hernias more common in
women than men
 Associated with diverticulosis,
esophagitis, duodenal ulcers and
gall stones
Symptoms:
 Heartburn
 Dysphagia
 Chest Pain
 Regurgitation
 Postprandial fullness
 Dyspnea
 GI bleed
Treatment:
 600-800 IU vitamin D currently
recommended for osteoporosis
with 1200-1500 mg calcium per
day.
Diagnosis:
 Plasma vitamin E level <0.5
mg/dL
Treatment: 100-400 IU/Day
Diagnosis:
 PT/INR elevated
Treatment:
 FFP
 Reversal of warfarin effects
Work-Up:
 Upper endoscopy to exclude
abnormal metaplasia, dysplasia
or neoplasia
 Barium contrast UGI
 Upper GI endoscopy
Treatment:
 Lifestyle modifications avoiding
caffeine, chocolate, mint, CCB’s,
and anticholinergics
 Weight loss
 Avoid large quantities of food
with meals
 Sleep with head of bed elevated
 Antacids may be used to relieve
mild sx


Wheezing
Hoarseness
Classified:
1. Sliding
2. Paraesophageal
3. Mixed (rare)
4. Large- intrabdominal organs
enter hernia sac
Liver
Viral Hepatitis Symptoms:
 Prodrome often insidious:
malaise, arthralgia, fatigue,
anorexia, nausea, vomiting, lowgrade fever
 RUQ/epigastric pain,
hepatomegaly, jaundice/icterus
 Very elevated transaminases
Hepatitis A:
 Transmitted fecal-oral: shellfish,
contaminated fruit/vegetables,
 Incubation period averages 30
days
 No chronic carrier state
Hepatitis B:
 dsDNA genome
 core protein (HBcAg)
 surface protein (HBsAg
 Transmission: blood, blood
products, IVDA, sexual
 Incubation: 6 weeks to 6 months




H2 agonists: cimetidine 400mg
BID, rantidine 150mg BID
PPI’s: omeprazole 20mg QD
Prokinetic agents:
metoclopramide 10mg taken 30
min before each meal
Surgery
Diagnosis:
 AntiHAV IgM
Prevention:
 Immune globulin available
Vaccine:
 travel to endemic areas (incl.
military)
 food, sewage, daycare/nursing
home/veterinary workers
 pts with underlying chronic liver
disease
 MSM, IVDA
 children
Diagnosis:
 HBsAg: first evidence of infection
(appears before elevated LFTs)
 anti-HBsAb: appears after
clearance of HBsAg or after
vaccination
 anti-HBcAb: useful when HBsAg
cleared but antiHBsAb not yet
detectable
 HBeAg: secretory form of HBsAg.
Indicates infectivity
Prevention:
 HBIG if given w/in 7d postexposure or to newborns of
HBsAg + mothers
Vaccine:
 HBsAg alone
 all medical workers, dialysis,
domestic/sexual partners of
infected, MSM, IVDA, children
Prognosis:
 Acute mortality 0.1-1%, higher
with HDV coinfection
 Chronic in 1-2% of
immunocompetent adults
Hepatitis D:
 Only causes hepatitis in coinfection with HBV
 In chronic HepB, superinfection
with HDV = worse prognosis
Hepatitis C:
 Transmission similar to HBV –
IVDA is the most common route
 Incubation: 6-7 weeks. Often
asymptomatic
 Most frequent indication for liver
transplantation
 8-10k deaths/year
 No reliable means of prevention
Hepatitis E:
 RNA virus
 Enterically transmitted
 No carrier state
 High mortality (10-20%) in
pregnant women
 Consider if travel Hx.
Hepatitis G:
 Not important cause of liver
disease
 Chronic viremia lasting >10 yr
 1.5% of blood donors, 50% of
Diagnosis:
 anti-HCVAb
 PCR for HCV RNA - confirmatory
Prognosis: Chronic in 80%
Treatment:
 interferon alpha or peginterferon
for 24-48 weeks- depends on
viral genotype
 Ribavirin
IVDA, 30% of dialysis patients
Cirrhosis:
Complications:
 Irreversible chronic injury of liver
 Portal hypertension
parenchyma with extensive
 Variceal Bleeding
fibrosis
 Ascites
 Spontaneous Bacterial Peritonitis
Types:
 Alcoholic (Laennec’s cirrhosis)
TIPS procedure:
 Posthepatic
 Interventional radiology makes a
 Cardiac (prolonged, severe, righttunnel through the liver with a
sided CHF)
needle, connecting the portal vein
 Metabolic, Inherited, Drug-related
to one of the hepatic veins. A
metal stent is placed in this
Primary Biliary Cirrhosis (destruction of
tunnel to keep it open.
bile ducts with resulting cholestasis):
 The shunt allows the blood to
 pruritus, fatigue early
flow normally through the liver to
the hepatic vein. This reduces
 jaundice and gradual darkening of
portal hypertension, and allows
the exposed areas of the skin
the veins to shrink to normal size,
 steatorrhea
helping to stop variceal bleeding.
 lipid deposition around the eyes
(xanthelasmas) and over joints
Child-Pugh Classification of Cirrhosis **
and tendons (xanthomas).
attachment
Secondary Biliary Cirrhosis (prolonged
partial or total obstruction of common
bile duct)
Hepatocellular Carcinoma:
Work-Up:
 Fifth most common cancer world
 LFt’s
 Areas with high rates of Hep B or
 Elevated AFP
C have inc rates
 Ultrasound, CT or MRI
 Males > females
 Percutaneous biopsy is diagnostic
th
th
 Peak incidence: 5 -6 decade
Treatment:
 Early stage: curative treatment
Risk Factors:
(resection, liver transplant or
 Chronic liver disease
percutaneous ablation)
 Cirrhosis
 Intermediate stage: possible
chemoembolization
 Chronic B or C infection
 Advanced stage: no curative
 Hepatotoxins: alcohol, high dose
treatment
anabolic steroids, possibly
 End stage: palliative care
estrogen
 Systemic diseases affecting the
liver including hemochromatosis,
tyrosinemia and
alpha1antitrypsin deficiency
Symptoms:
 1/3 of patients are asymptomatic
 signs of underlying cirrhosis
present (weight loss, ascites)
 paraneoplastic syndromes
(hypoglycemia, erythocytosis,
hypercalcemia, severe diarrhea)
Gall Bladder
Cholelithiasis:
 Frequently asymptomatic
 2 Major types: cholesterol (80%)
and pigment stone
Symptoms: Biliary Colic
 pain is characteristically a severe,
steady ache or fullness in the
epigastrium or RUQ of the
abdomen
 nausea and vomiting frequently
accompany episodes of biliary
pain.
 may be precipitated by eating a
fatty meal, by consumption of a
large meal following a period of
prolonged fasting
Signs/Symptoms:
 Murphy’s sign
 Triad of RUQ pain, fever,
leukocytosis
Acute Cholecystitis:
 inflammation of the gallbladder
wall usually follows obstruction
of the cystic duct
Chronic Cholecystitis:
 almost always associated with the Diagnosis:
presence of gallstones
 mildly elevated LFTs
 thought to result from repeated
 RUQ ultrasound: gallbladder wall
bouts of subacute or acute
thickening and pericholecystic
cholecystitis or from persistent
fluid
mechanical irritation of the
 HIDA scan: 98% sensitive
gallbladder wall by stones
 Hydrops - resolution of acute
phase but duct obstruction
persists. Gallbladder overdistended with clear, mucoid fluid
 Porcelain gallbladder - d/t
calcium deposition