Topics in Gastroenterology

Renee Andreeff RPA-C,MPAS

Esophageal Motor Disorders

Results from a disruption of
neurohumoral or muscular control of
peristalsis or sphincter function.
The disorder can be primary or
secondary and can involve the
striated or smooth muscle (recall
bottom 2/3 of esophagus is smooth
muscle).

ESOPHAGEAL SMOOTH MUSCLE MOTILITY

DISORDERS

Achalasia (Greek: does not relax)

An idiopathic motility disorder
characterized by the loss of peristalsis
in the distal 2/3 of the esophagus and
impaired relaxation of the LES

Achalasia
Etiology: denervation of the esophagus, cause unknown
Symptoms: gradual onset
Dysphagia of solid foods that evolves to liquids
Substernal pain after eating; pts. Each more slowly
adopt specific maneuvers such as lifting the neck and throwing
shoulders back
PE: non-specific
Dx: Baruim Swallow : BIRDs BEAK Esophagus
Manometry (measures function of LES)
Tx: Pharmacologic intervention: Nitrates; CA+ Channel blockers (to
relax LES)
Endoscopic Intervention: Botulinum toxin (relaxes)
Pneumatic Dilation
Myotomy

GERD
Recurrent reflux of gastric contents
into the distal esophagus b/c of
mechanical or functional abnormality
of the LES.
Up to 60% of population experience it
at some point; in infants >50% have
reflux but <10% has esophagitis

GERD
Sx: Heartburn: generally worse after meals, lying down and
is often relieved by antacids
Atypical sxs: chest pain, hoarseness, cough, aspiration,
asthma, anorexia
Dx: barium swallow if pt. has dysphagia
- Endoscopy for prolonged sxs or any atypicals
Check for H. Pylori infection
Ph monitoring (manometry)
Tx: Lifestyle adjustments
Meds: 1. Antacids for mild symptoms
2. histamine (h2) blockers: first line for mild GERD
3. PPI: first line in moderate to severe GERD or those
unresponsive to H2
4. H2 at night and PPI in the daytime for those with sig.
Symptoms

GERD Complications
Chronic Inflammation
Ulcerations
Strictures
Pulmonary Involvement
Perforation
Barretts Esophagus

BARRETTS ESOPHAGUS
8-20% of patients with GERD
Acquired
Squamous epithelium replaced by
columnar epithelium from stomach
Increased risk of adenocarcinoma
Biopsy every 1-2 years

Screening
American Gastroenterological Association Risk factors considered by the AGA
include:

Age 50 years or older

Male sex
White race
Chronic GERD
Hiatal hernia
Elevated body mass index
Intra-abdominal distribution of body fat

The AGA recommends against screening

the general population with GERD.

MALLORY WEISS TEARS

Linear mucosal tear in the esophagus,
generally at the gastroesphageal junction,
that occurs with forceful vomiting or
retching causing hematemesis
Often associated with alcohol use
Sx; Bleeding-pain referred to back
Dx: endoscopy
Tx: most resolve without treatment, can
inject epinephrine or use thermal coagulate

GASTRITIS
Inflammation of the stomach
Natural Protective factors
Mucous, bicarbonate, mucosal blood flow,
prostaglandins, alkaline state,
hydrophobic layer and epithelial renewal

Gastritis is commonly secondary to infectious or

autoimmune etiologies, although it can also result from
drugs, hypersensitivity reactions, or extreme stress
reactions.
Gastropathy is commonly secondary to endogenous or
exogenous irritants, such as bile reflux, alcohol, or aspirin
and nonsteroidal antiinflammatory drugs.
However, gastropathy can also be secondary to ischemia,
stress, or chronic congestion.
"Gastritis" is a term often used by endoscopists to
describe the gastric mucosa rather than representing a
particular endoscopic entity. A gastric mucosal biopsy is
necessary to establish a definitive diagnosis of gastritis
versus gastropathy.

Gastritis
Types:
A: involving the body of the stomach
B: involves the antrum and the body

Gastritis
Causes: Erosive
a.Stress: cns injury, burns, sepsis or
surgery
b. NSAID gastritis: diminish local
prostaglandin production in the
stomach
Alcoholic: excessive intake

Gastritis
Non-erosive, non-specific
H. Pylori : spiral gram negative rod that resides beneath
the gastric mucous layer adjacent to the epithelial cells.
Non-invasive but does cause inflammation with PMNs and
lymphocytes
Transmission is person to person but mode unknown
Chronic inflammation confined to epithelium
Eradicate with antibiotic therapy (triple therapy)
Also associated with PUD
Chronic infection associated with a 2.5 fold increase in the
risk of gastric adenocarcinoma and low grade B cell gastric
lymphoma

Dyspepsia
Presence of sxs coming from UGI tract
3 patterns
1. Ulcer-like or acid dyspepsia (burning pain; epigastric
hunger-like pain; relief with food, antacids, and/or
antisecretory agents)
2. Food-provoked dyspepsia or indigestion (postprandial
epigastric discomfort and fullness, belching, early
satiety, nausea, and occasional vomiting)
3. Reflux-like dyspepsia

PEPTIC ULCER DISEASE

Def: any ulcer of the upper digestive system
Duodenal Ulcers > Gastric (peptic) Ulcers
Etiology: H. Pylori is the most common cause
Symptoms: epigastric burning, dyspepsia
Gnawing pain that radiates to the back
Relieved with food or antacids
Pain occurs 2-3 hours after eating (DU)

Duodenal Ulcers
The "classic" pain of duodenal ulcers (DU) occurs when
acid is secreted in the absence of a food buffer.
Food is usually well emptied by two to three hours after
meals, but food-stimulated acid secretion persists for three
to five hours;
Thus, classic DU symptoms occur two to five hours after
meals.
Symptoms also classically occur at night, between
about 11 PM and 2 AM, when the circadian stimulation
of acid secretion is maximal.
The ability of alkali, food, and antisecretory agents to
produce relief suggests a role for acid in symptom
generation

Peptic Ulcers
Peptic ulcers :food-provoked symptoms
epigastric pain that worsens with eating
postprandial belching
epigastric fullness
early satiety, fatty food intolerance, nausea,
and occasional vomiting.
Food-provoked symptoms in ulcer patients appear
to reflect a combination of visceral sensitization
and gastroduodenal dysmotility.

PEPTIC ULCER DISEASE

Complications: Bleeding, perforation and
penetration
Labs: Endoscopy with biopsy for HP, tissues
Treat: Lifestyle modifications (d/c smoking,
NSAIDS, alcohol)
Antacids, H2 blockers, PPI, and sucralfate
generally heal DU within 4-6 weeks and gastric
ulcers with 8 weeks.

H. Pylori Treatment
Combination Triple Therapy for HP
eradication:
PPI (BID) + amox (1000mg BID) +biaxin
(500mg BID) 7-14 days

Quadruple Threapy for cases found

resistant to Biaxin
PPI, combined with bismuth (525 mg QID) and
two antibiotics (eg, metronidazole 250 mg QID
and tetracycline 500 mg QID) given for 10 to
14 days

Zollinger-Ellison Syndrome
Rare
Presents 30-50 years of age
Gastrinoma: Tumor secretes gastrin
that results in excess acid secretion
and PUD.
Unlike PUD this is progressive/
persistent/life threatening
most commonly found in the pancreas

Zollinger-Ellison Syndrome

Z-E Syndrome Symptoms

High Gastric Acid output exceeds the
neutralizing capacity of pancreatic
bicarbonate secretion-leads to low pH
in intestines
maldigestion and malabsorption may
result in steatorrhea
Secretory Diarrhea
Abdominal pain

ZE Diagnostic tests
Gastric Acid Secretion Studies
Fasting Serum Gastrin
The upper limit of normal for serum
gastrin is 110 pg/mL. In the presence of
gastric acid (ie, a gastric pH below 5.0),
a serum gastrin value greater than 1000
pg/mL (475 pmol/L) is virtually
diagnostic of the disorder

Secretin Simulation Test

ZE Treatment
High Dose PPI
Surgery
Metastatic disease management

Gastric malignancy
Uncommon in the US, but gastric
adenocarcinoma is the most common
type of cancer worldwide
2x men vs. women,
> 40, 45-55
Strong association between this and
H. Pylori infection

Gastric Carcinoma Risk factors

ALARM SYMPTOMS
Unintended weight loss
Bleeding
Anemia
Dysphagia
Odynophagia
Hematemesis
A palpable abdominal mass or lymphadenopathy
Persistent vomiting
Unexplained iron deficiency anemia
Family history of upper gastrointestinal cancer
Previous gastric surgery
Jaundice

GASTRIC LYMPHOMA

Stomach is the most common

extranodal site for non-Hodgkins
lymphoma
Sixfold greater risk with HP infection

INTESTINAL DISEASES

CELIAC SPRUE

Small bowel malabsorption disease

Results in diarrhea, abdominal
distension, steatorrhea, weight loss
Most will not manifest as serious
symptoms; more commonly to report
chronic diarrhea, dyspepsia,
flatulence

Celiac Sprue
Etiology: immunologic response to gluten (storage protein
found in grains) that causes damage to villi making them
markedly shortened or absent.
Labs: IgA endomysial antibody and IgA tTG antibody
tests: both have > 90% sensitivity/specificity. A negative
reliably excludes the diagnosis
Tests should be done while still on gluten rich diet
Postive= small bowel biopsy

Tx: Gluten free diet (remove all wheat, rye and barley)
OATS may be okay but many are processed in facility with
other grains.
Most patients also have lactose intolerance so dairy should
be restricted.
Pt. Needs vitamin supplements

IRRITABLE BOWEL SYNDROME

Functional disorder without known
pathology
Combination of altered motility,
hypersensitivity to intestinal distension
and
psychological distress (>50% have
underlying depression, anxiety or
somatization)
15% of adult population; Females 2:1

IRRITABLE BOWEL SYNDROME

Sx: Abnormal stool frequency (> 3 BM per day
or less than 3 per week)
Abnormal stool form (lumpy or hard; loose or
watery)
Abnormal stool passage (straining, urgency, feeling
of incomplete evacuation)

Passage of mucous
Bloating or feeling of abdominal distension

IBS
Labs: R/O parasites, lactose intolerance,
bacteria
Tx: Education
Avoid Dietary Triggers
High Fiber
Antispasmotics (bentyl prior to meals),
antidiarrheals, anticonstipations,
psychotropics
Probiotics

IBS
Alarm" or atypical symptoms which are not
compatible with IBS include:
Rectal bleeding
Nocturnal or progressive abdominal pain
Weight loss
Laboratory abnormalities such as anemia,
elevated inflammatory markers, or
electrolyte disturbances

INFLAMMATORY BOWEL DISEASE

ULCERATIVE COLITIS
Def: Chronic, recurrent disease
characterized by diffuse mucosal
inflammation involving only the colon,
invariably involves the rectum, that results
in friability and bleeding (continuous
involvement)
Inflammation confined to the mucosa and
submucosa

UC
Symptoms: Flares
Diarrhea, rectal pain, rectal bleeding
HALLMARK: BLOODY DIARRHEA

Dx: history, PE for peritoneal

irritation
X-RAY: LEAD PIPE APPEARANCE

UC
Complications: blood loss, toxic megacolon,
stricture formation, carcinoma
Tx: Limit caffeine and gas producing foods
Drug Tx differs on extent of disease but
can include: mesalamine suppositories, HC
foam, antibiotics and surgery (25%)

CROHNS DISEASE
Def: Chronic, recurrent disease
characterized by patchy transmural
inflammation involving any segment of the
GI tract from mouth to anus (not
continuous)
Through the entire wall that can result in
mucosal inflammation and ulceration,
structuring, fistula development and
abscess formation

CROHNS
Sx: Diarrhea, Bleeding, abd pain (reflecting
inflammatory process), obstruction
HALLMARK SX: Fatigue, Prolonged Diarrhea with Adb
pain, wt. loss, fever (with/without bleeding)
Extraintestinal manifestation: cutaneous, eye,
rheumatologic, hepatic
Complications: Fistula development, bile salt,
malabsorption, gallstones
X-ray: String sign, assess small bowel involvement
Labs: CBC, SED, B12 along with antibodies
Tx: segmental removal, steroids, antibiotics for
complications (see chart)

Diverticular Disease
Large outpouchings of the diverticula of
the colon
Most asymptomatic, attributed to low
fiber intake
Diverticulitis is the inflammation of the
diverticula by obstruction
Diverticulitis Sx:
Tenderness LLQ, guarding, melena, N/V,
urinary symptoms
Mild to severe

Diverticulitis
Contraindication: barium enema
Water soluble contrast ok if needed

TX: Bland diet, high fiber, broad

spectrum antibiotic

Outpatient: Flagyl (500mg TID) and Cipro

(500mg BID) X 10 days
Surgery, hosp., IV tx required for
perforations and peritonitis

Appendicitis
Occurs with obstruction of the
appendix
Most common surgical emergency
Perforations and peritonitis occurs in
20%

Appendicitis
SX:
Intermittent periumbical or epigastric
pain
Will localize to RLQ (McBurneys pt)
Increases with mvmnt
Nausea and anorexia are common
Low-grade fever common

Appendicitis
Signs:
Psoas sign
Obturator
McBurneys point
Rebound tenderness
Rovsings

Appendicitis
Labs: Leukocytosis
Dx: CT
Tx: Surgery, broad spectrum
antibiotic

Cholelithiasis
10% of population >33% women >40
2/3 asymptomatic

Types of stones: cholesterol and pigment

Cholesterol: excess cholesterol molecules
(90%)
Pigment: Black: form in GB, brown: form in bile
duct

Complications: cholecystitis, pancreatitis

Cholecystitis
Obstruction of the bile duct
Sx:
colickly epigastric or RUQ pain often
after a fatty meal
Radiates to right shoulder and
subscapular pain
N/V, low-grade fevers

Cholecystitis
Labs:
>24 hours, bilirubin levels increase
Leukocytosis

Tx: surgery

Hepatitis
Acute or chronic hepatocellular damage
Most common causes of acute is viral (A)
2nd is toxins (I.e. alcohol)

Chronic: viral infection with B,C,D ;

inherited disorders like Wilsons dx;
autoimmune disorder; or hepatic effects of
systemic disease
Sx: fatigue, malaise, anorexia, nausea, teacolored urine, vague abdominal discomfort

Hepatitis A & E
Variable symptoms
Transmitted fecal-oral route
Usually self-limiting without long
term sequelae

Hepatitis A
30 day incubation period
Excreted in feces for 2 weeks before
clinical illness
About 30% of population show
exposure to disease

Hepatitis B,C,D
Transmitted parenterally or by
mucous membrane contact

Highest transmission in heterosexuals

Variable presentation
Chronic B or C will require treatment
D is only seen in conjunction with B
and is associated with a more severe
course

Hep B
Incubation 6 wks to 6 months
Onset insidious
Chronic infection increases risk of
cirrhosis and cancer

Hep B serologic patterns

HBsAG: surface antigen

first evidence of infection

Appears 1-10 weeks after infx
Usually fades 4-6 months
If present > 6 months signifies chronic infx

Anti-HBs: antibody to HBsAg; appears after

clearance of HBsAG and after immunization.
Signals recovery &immunity
IgM anti-HBc is the sole marker of HBV
infection during the window period between the
disappearance of HBsAg and the appearance of
anti-HBs

Hep B Tx
Self-limiting for most
Complete recovery 3-6 months
Chronic infection: Interferon
treatments among others Complex:
refer to GI/liver specialist

Hep C
50% of cases from IV drug use
Risk factors
Nasal cocaine use
Body piercing
Tattoos
hemodialysis

Hep C
Incubation 6-7 weeks
Clinical illness mild

Prolonged malaise and fatigue

RUQ tenderness

Some spontaneous recovery

Chronic infection is common 80% of
infections leading to cirrhosis
Interferon tx, vaccinate for A & B

Hepatitis Dx/Tx
Dx: Hep panel
Monitor: LFTs

Tx: most resolve in 3-6 months

bed rest
Interferon tx for chronic B & C

Thank you
Good Luck!!!!!!!!