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 : BIRD’s 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 sx’s: chest pain, hoarseness, cough, aspiration, asthma, anorexia Dx: barium swallow if pt. has dysphagia

- Endoscopy for prolonged sx’s 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

Barrett’s Esophagus

BARRETT’S 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 PMN’s 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 sx’s 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-Hodgkin’s 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%)

CROHN’S 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

CROHN’S

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 (McBurney’s pt)

Increases with mvmnt

Nausea and anorexia are common

Low-grade fever common

Appendicitis

Signs: Psoas sign

Obturator

McBurney’s point

Rebound tenderness

Rovsing’s

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 Wilson’s dx; autoimmune disorder; or hepatic effects of systemic disease Sx: fatigue, malaise, anorexia, nausea, tea-colored 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: LFT’s

Tx: most resolve in 3-6 months bed rest

Interferon tx for chronic B & C

Thank you

Good Luck!!!!!!!!