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Tory Davis PA-C January 2010. Colon Disorders and GI Neoplasms. Colon Disorders. Anorectal Disorders Fissure Fistula Hemorrhoid IBS- Irritable Bowel Syndrome Diverticular Disease IBD- Inflammatory Bowel Disease Crohn’s disease Ulcerative Colitis. GI Neoplasms. Esophageal Stomach

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colon disorders
Colon Disorders

Anorectal Disorders

Fissure

Fistula

Hemorrhoid

IBS- Irritable Bowel Syndrome

Diverticular Disease

IBD- Inflammatory Bowel Disease

Crohn’s disease

Ulcerative Colitis

gi neoplasms
GI Neoplasms

Esophageal

Stomach

Colorectal / anorectal

Pancreatic

Hepatic

anal fissure
Anal Fissure

Acute longitudinal tear or chronic ovoid ulcer in anal epithelium. Located posterior or anterior midline.

Pain, severe with defecation

Sometimes bleed

Often result from laceration with secondary infection.

Pain  internal sphincter spasm decreased blood supply perpetuating fissure

anal fissure tx
Anal Fissure Tx

Reduce local trauma: stool softener, fiber

Protect: zinc oxide, glycerin suppository

Relieve pain: topical anaesthetic (benzocaine, lidocaine), warm sitz bath

Surgical (last choice)‏ - internal sphincterotomy

anorectal fistula
Anorectal Fistula

Tube-like tract with one opening in anal tract and other in perianal skin

Usually a chronic condition arising from acute perirectal abscess

Constant to intermittent drainage of purulent or serosanguinous fluid

+/- pain, depends on if infected

Exam 1+ openings, +/- palpable cordlike tract. Probe to see depth, direction

Tx: Surgical- deroof or seal with fibrin glue

hemorrhoids
Hemorrhoids

Aka “Piles”

Dilated veins of hemorrhoidal plexus in lower rectum

Dentate line divides internal from external hemorrhoids

Locations: L lateral, R anterior, R posterior zones

Often asymptomatic, sometimes itching or protrusion.

External: can thrombose. Ow!

Internal: often bleed after BM

hemorrhoids1
Hemorrhoids

Internal-

graded I- IV

I – remain internal

II – prolapse with strain, reduce spontaneously

III. Require manual reduction after BM

IV. Won’t go back

thrombosed hemorrhoid
Thrombosed Hemorrhoid

Results in perianal hematoma

Acute onset of exquisite pain

Firm blue/purple perianal nodule

Tx with sitz baths, analgesics

If able in 1st 24-48h, excision gives immediate relief

tx non thrombosed hemorrhoids
Tx Non-thrombosed hemorrhoids

Symptomatic

Sitz baths

Witch hazel compress

phenylephrine 0.25% (Preparation H)

Anesthetic oint

Surgical: photocoag, rubber band ligation, hemorrhoidectomy

irritable bowel syndrome1
Irritable Bowel Syndrome

Poorly understood, but real.

Characterized by recurrent upper and lower GI sx, varying abd pain, constipation and/or diarrhea, abd bloating

ibs pathophys
IBS Pathophys

No consistent motility abnormality

Some pts demonstrate abnl gastrocolic reflex with  colonic activity

Maybe  gastric emptying

But even in demonstrated abnormality, sx don’t correlate

Excess mucus production even in absence of mucosal injury

more pathophys
More pathophys

Hypersensitivity to normal amounts of intraluminal stretch.

 perception of pain with normal amounts of intestinal gas

Can be exacerbated by hormonal fluctuations (incr prostaglandins with menses causes more pain)

ibs s s
IBS S & S

Abdominal pain related to or relieved by defecation

Change in stool frequency and/or consistency

Mucus in stool

Sensation of incomplete evacuation

slide16
S & S

Onset teens or 20s

Irregular, recurrent bouts

Sx usually do NOT affect sleep

Sx are triggered by stress, also by some foods

Varies per patient

extra intestinal sx
Extra-intestinal sx

Fibromyalgia

Headache

Dyspareunia

TMJ syndrome

Anxiety

Depression

constipation predominant
Constipation predominant

Constipation alternates with nl BMs

Clear-white mucus

Colicky or dull constant pain

Often relieved by BM

Eating may trigger sx

Bloating, flatulence, eructation, nausea, dyspepsia, heartburn

diarrhea predominant
Diarrhea predominant

Diarrhea immediately after eating, especially after rapid eating

Pain, bloating, rectal urgency

Incontinence happens

differential diagnosis
Differential Diagnosis

Lactose intolerance

Diverticular dz

Drug induced

Drug abuse

Biliary tract dz

Bacterial enteritis

Parasites

Early IBD

Ischemic colitis, esp if age > 60

Hypothyroid

Malabsorption syndromes

rome criteria
Rome Criteria

Standardized sx-based criteria for dx

Three months of the following sx:

Abdominal pain/discomfort relieved by defecation or assoc with change in freq/consistency of BM

Disturbed defecation involving at least 2 of these:

Altered stool frequency, form or passage

Passage of mucus

Bloating or feeling of abdominal distention

red flags
Red Flags

Onset after age 50

Weight loss

Progressive dysphagia

S/S bleeding or dehydration

Steatorrhea

Recurrent vomiting

Fever

 ESR or CRP

Anemia, leukocytosis

Hypokalemia

Strong FHx colon cancer

Blood or pus in stool

physical exam
Physical exam

Patient appears healthy

Abd +/- tender, esp LLQ

Possibly palpable tender sigmoid

Nl DRE- no occult blood

Females: nl pelvic exam (r/o ovarian tumor/cyst, infection, endometriosis)‏

ibs testing
IBS testing

ONLY if objective abnormalities: consider abd US or CT, barium enema

Stool cx, O&P - ONLY if supporting travel hx or fever, hematochezia or acute onset of diarrhea

ibs tx
IBS tx

Sympathetic understanding, patience, explain condition and address fears

Diet:

Normal, moderate sized meals eaten slowly.

 gas-producing food. Consider  lactose

Eliminate sorbitol, mannitol in pts with diarrhea

Dietary fiber to bulk up and soften stool, but start low, go slow or you’ll worsen sx

ID stressors, mood d/o, or anxiety and address them

ibs drugs
IBS Drugs

Anticholinergics to reduce spasm

Serotonin receptor modulators

ibs drugs1
IBS Drugs

Loperamide (Immodium) for diarrhea

TCAs for bloating, constipation, abd pain

Down-regulates spinal cord and cortical afferent pathways from intestine

Peppermint- relaxes smooth muscle spasm. Significant improvement in clinical studies.

Ginger- digestive aid

Aloe vera for constipation

Fennel – reduces bloating.

slide29
IBD

2 distinct disease entities

Only about 10% are “indeterminate colitis” Usually fairly easy to differentiate

Both

Cause bloody diarrhea

Are characterized by chronic, relapsing and remitting inflammation of various sites of the GI tract

Have inflammation from cell-mediated immune response in GI mucosa

ibd epi
IBD Epi

Gender equal, all ages, but peak incidence ages 14-24

UC has 2nd peak 50-70

Most common in people of N. European or Anglo-Saxon origin.

1st degree relatives 4-20x increased risk

Smoking increases Crohn’s risk, but decreases risk of ulcerative colitis

ibd extra intestinal manifestations
IBD Extra-Intestinal Manifestations

Common to BOTH Crohn’s and UC

1. Disorders which parallel IBD flares

Peripheral arthritis, episcleritis, aphthous stomatitis, erythema nodosum

2. Disorders probably resulting from IBD but appear independent of flares

Ankylosing spondylitis, sacroiliitis, uveitis, primary sclerosing cholangitis.

Can appear years before IBD sx, and should prompt eval for IBD!

ibd extra intestinal manifestations1
IBD Extra-Intestinal Manifestations

3. Consequences of disrupted bowel physiology (primarily seen in severe Crohn’s of small bowel)‏

Malabsorption (causing B12 and mineral deficiencies), anemia, clotting disorders, bone demineralization, kidney stones, hydroureter & hydronephrosis (from ureteral compression by inflammatory process)‏

Factors in all 3 categories can increase risk of thromboembolic disease

crohn s disease1
Crohn’s Disease

Chronic transmural inflammatory dz, usually effects distal ileum and RIGHT colon, but can occuranywhere along GI tract

Segmental rather than continuous (UC)

Not symmetric

Can have significant perirectal lesions, but rare rectal bleeding

crohn s pathophys
Crohn’s pathophys

Inflammation of crypts small abscesses & aphthoid ulcers which deep longitudinal and transverse ulcers with mucosal edema

Transmural spread of inflam lymphedema, bowel wall thickening

Severe inflam muscle hypertrophy, fibrosis, strictures (can cause obstruction)

crohn s pathophys1
Crohn’s pathophys

Abscesses common, and resulting fistulas can penetrate nearby structures

Bowel loops, bladder (can pee poop), psoas muscle (peritonitis sx), enterocutaneous

Granulomas- Pathognomonic. Found in liver, lymph nodes, all layers of bowel wall

crohn s pathophys2
Crohn’s pathophys

Discontinuous affected segments of bowel sharply demarcated from normal areas (“skip areas”)‏

Where is it?

35% ileum alone

45% ileum + colon

<20% colon alone, usually spares rectum

Uncommon in esoph, stomach, duodenum (but can be there)

crohn s s s
Crohn’s S&S

Chronic diarrhea w/ abd pain, fever, anorexia, wt loss

Tender abdomen with mass or fullness

Gross rectal bleeding RARE

One third with significant perianal disease: fissures, fistulas, abscesses

crohn s s s1
Crohn’s S&S

Can present w/ acute abd- looks like appendicitis or obstruction

Recurrent disease sx vary- Pain common with simple recurrence and with abscess

Severe flare: pt is SICK: marked tenderness, guarding, rebound

Segmental stenosis can bowel obstruction with colicky pain, abd distention, vomiting

Perforation not uncommon. Enterovesicular perf causes pneumaturia. Draining cutaneous fistulas

crohn s dx
Crohn’s Dx

To diagnose, you must first suspect!

Suspect in

pt w/ inflam or obstructive sx

pts w/ perianal fistulas

pts w/ unexplained arthritis, fever, anemia, erythema nodosum,

kiddos with growth retardation

work up and dx
Work-up and Dx

Pt presents w/ acute abd:

flat & upright plain films, abd CT to find obstruction, abscess, fistula, and to r/o other cause (ie appendicitis)‏

Consider pelvis U/S for female with predom lower abd/pelvic sx

work up and dx1
Work-up and Dx

Less acute pres:

GI series with small bowel follow-thru and spot films of terminal ileum

Considered diagnostic if shows stricture, fistulas or separation of bowel loops

work up and dx2
Work-up and Dx

If symptoms predominantly colonic (ie diarrhea)

Order barium enema which may show:

Barium reflux into terminal ileum

Irregularity and nodularity of bowel wall

Wall stiffness and thickening

Narrowed lumen

Or colonoscopy with bx, sampling for enteric pathogens and visualization of terminal lumen

slide44
Labs

CBC to monitor for anemia, leukocytosis

CMP to monitor liver function, check for hypoalbuminemia, electrolyte abnormalities

ESR, CRP- nonspecific, but useful serially to monitor disease status

crohn s prognosis
Crohn’s Prognosis

Rare cure

Intermittent exac/remit

Severe dz can be debilitating, severe pain and dysfunction

Dz related mortality low, with most caused by GI cancers (small bowel, colon)‏

ulcerative colitis1
Ulcerative Colitis

Chronic, inflammatory, ulcerative disease arising in colonic mucosa, most often characterized by bloody diarrhea

Only in the colon.

Continuous, not segmental

Symmetric

Not perirectal. No abscesses. No fistulas.

uc pathophysiology
UC Pathophysiology

Begins in rectum

Can remain localized (ulcerative proctitis), or extend to involve entire colon

Inflammation affects mucosa and submucosa only, with sharp border between healthy/diseased tissue

more uc patho
More UC patho

Fulminant colitis: transmural extension of ulceration (NB this is the only time UC is transmural)ileus & peritonitis

Colon loses muscular tone and dilatesTOXIC MEGACOLON

uc s s
UC- S&S

Bloody diarrhea of varied intensity & duration. Asymptomatic periods

Insidious onset of attack

 urge to defecate

Mild low abd cramps

Blood/mucus in stools

Can start s/p infection (ie amebiasis)‏

uc s s1
UC S&S

When ulceration confined to rectosigmoid:

Stool generally normal to hard

Rectal discharges of mucus loaded with RBCs and WBCs accompany or occur between bowel movements.

Systemic sx mild or absent

uc s s2
UC S&S

When ulceration extends proximally:

Stools looser, more frequent (>10/day)‏

Severe cramps, rectal tenesmus

No night respite (diff from IBS or psychogenic diarrhea)

Stools watery, or all blood and pus

Severe:

Systemic sx include malaise, fever, anemia, anorexia, and wt loss

Can cause hemorrhage requiring transfusion

uc diagnosis
UC Diagnosis

Typical sx by hx, particular attn to extra-intestinal S&S or hx prev similar attacks

Need to distinguish from Crohn’s, other causes of acute colitis (infection, ischemia)

uc testing
UC Testing

Labs: same as Crohn’s

Stool cx

Microscopy of fresh poop for Entamoeba histolitica

Recent hosp or abx? Check C. diff toxin stool assay

Sigmoidoscopy- permits visualization, but can’t distinguish between Crohn’s and UC

w u fulminant sx
W/U fulminant sx

Flat and upright abd xray: look for toxic megacolon

NO SCOPES (perf risk!)‏

CBC, ESR, lytes, PT/PTT, type and cross

Watch closely for progressive peritonitis

Serial abdominal films to follow course

uc prognosis
UC Prognosis

Usually chronic with remit/relapse

10% recover completely from initial event

10% have initial presentation with fulminant colitis; can die

Risk of colon cancer

Proportional to duration of sx and amt of colon affected, but NOT to disease activity

colon cancer in uc
Colon Cancer in UC

Begins to appear about 7 yr from illness onset in pt w/ extensive disease

Cumulative likelihood :

3% at 15 yrs, 5% at 20 yrs, 9% at 25 yrs

Regular colonoscopies after 8-10 yrs of disease

ANY grade of dysplasia is high risk to progress to cancer, and colectomy is advised

5 aminosalicylic acid 5 asa
5-aminosalicylic acid(5-ASA)‏

Blocks production of leukotrienes and prostaglandins

Only active intraluminally

Sulfasalazine

Start low, go slow.

Add folate supplement.

Check CBC, LFTs serially

corticosteroids
Corticosteroids

For acute flares- not ideal for maint

Until sx remit (7-28 days) then taper

immunomodulating agents azathioprine
Immunomodulating agents- Azathioprine

Inhibit T cell function

Good & effective long term- may  steroid needs. Takes 1-3 months to reach efficacy

Monitor for bone marrow suppression

3-5% develop high fever or pancreatitis – do NOT retry

Rare hepatotoxicity, check LFTs q 6 mo

immunomodulating agents
Immunomodulating agents

Methotrexate –

For severe dz not responsive to steroids, failed azathioprine.

Cyclosporine- blocks lymphocyte activation

For severe UC unresponsive to steroids, pts who may o/w need colectomy

In Crohn’s, used for refractory fistulas or pyoderma

Reserve use, and don’t use >6 mo. Renal toxicity, seizures, opportunistic infection

anticytokine drugs
Anticytokine drugs

Infliximab, CDP571, CDP870, adalimumab

Antibodies against TNF

slide64
ALSO

Antibiotics

Useful in Crohn’s, not UC

Help heal fistulas

Metronidazole or Cipro

Probiotics

Supportive Care

crohn s tx
Crohn’s Tx

General: cramps/diarrhea  loperamide (except in acute/severe)‏

Mild: 5-ASA, abx

Moderate: steroids, transition to maint

Obstruction: add NG suction, IV fluids, parenteral nutrition

Usually resolves in few days

crohn s tx1
Crohn’s Tx

Fulminant/abscess: toxic appearance, fever, persistent vomiting, rebound

IV fluids, abx, surgical or percutaneous drainage

No steroids till infection controlled

Fistulas: abx, if no response in 3-4 weeks, add immunomodulator

crohn s surgery
Crohn’s Surgery

70% ultimately will have surgery- but reserve for recurrent obstruction, intractable fistula/abscess

Resection ameliorates, does NOT cure

Further surgery required in 50% of cases

Recurrence is likely, even if all disease is removed

uc tx
UC Tx

General

Limit raw fruits and veggies

Try milk-free

Loperamide prn

Mild Left Sided disease

5 ASA enema/suppository (kind of topical tx)

Steroid enema

Maybe oral 5-ASA

uc tx1
UC Tx

Moderate-Extensive Disease

Inflammation proximal to splenic flexure

Oral and enema 5-ASA

+/- steroids

Severe- >10 bloody stools daily, tachycardic, febrile, severe abd pain

High dose IV steroids

IV fluids

+/- blood transfusion

Monitor for toxic megacolon

uc tx2
UC Tx

Fulminant colitis

Discontinue all anti-diarrheals

NPO with NG suction

Aggressive IV fluids and lytes

High dose IV steroid

Abx- cipro and metronidazole

If no improvement in 24-48h, surgery to avoid perfsepsisdeath

uc surgery
UC Surgery

1/3 of pts with extensive UC ultimately get colectomy

Total proctocolectomy = Cure

No recurrence, and all colon cancer risk is removed

what are they
What are they?

Diverticuli are saclike mucosal outpouchings protruding from a tubular structure (the colon, in this case.)‏

True diverticulum- contains all layers of parent structure (including muscle)

False diverticulum- Mucosal projection thru muscular layer.

aka pseudodiverticulum

diverticul osis
Diverticulosis

Presence of multiple pseudodiverticuli in the colon.

Likely result of lifelong low fiber diet

Usually asymptomatic, but sometimes inflame or bleed

Usually in sigmoid, but can be anywhere in large colon

Uncommon under age 40. every 90 yo has them.

slide75
Why?

Increased intraluminal pressure causes mucosal extrusion thru weak points in muscular layer of bowel. Usually next to intramural vasculature

Why? – area of weakness, there is already a hole there

s s diverticulosis
S & S Diverticulosis

70% asymptomatic. Usually incidental finding

15-25% become inflamed and painful (diverticulitis)‏

10-15% painless bleeding. Likely caused by erosion of adjacent vasculature by local trauma (hard stool)

diverticulosis tx
Diverticulosis Tx

Reduce segmental spasm. High fiber diet, supplement with psyllium seed or bran

Tx of diverticular bleed:

75% stop spontaneously but many will bleed enough to require transfusion. Tx of bleeding is surgical. Colonoscopic epi, heat or laser.

diverticul itis
Diverticulitis

Inflammation of a diverticulum

Usually in sigmoid

Micro or macro perforation releases intestinal bacteria

Localized inflammation in 75%

Remaining 25% can lead to abscess, free intraperitoneal perforation, bowel obstruction, fistulas to bladder, small bowel,etc

diverticulitis s s
Diverticulitis S & S

Abdominal pain

LLQ tenderness

Fever

+/- peritoneal signs

If obstructed, n/v, abdominal distention

Bleeding is rare

Fistula can present as pneumaturia, feculent vaginal discharge, cutaneous or myofascial infection

slide80
Dx

High suspicion in known diverticulosis

ABD CT with oral and IV contrast

Need to r/o other causes, like appendicitis, colon CA, ovarian CA

Labs: CBC shows leukocytosis

diverticulitis tx
Diverticulitis TX

Mild-Rest, liquid diet, oral abx, go home.

cipro 500 mg BID or

amox/clavulanate 500 mg TID PLUS metronidazole 500 mg QID

Sx subside quickly. Proceed to low fiber diet for 1 month

Barium enema in 2-4 weeks to eval colon

Then back to high fiber diet

tx severe diverticulitis
Tx- severe diverticulitis

Severe pain, fever, leukocytosis, or if taking prednisone (can cause  risk of perf)‏

Bed rest, NPO, IV fluids, IV abx

Ceftazidime 1 g q 8h PLUS

Metronidazole 500mg q 6-8h

May do CT guided percutaneous drainage of abscess

surgery
Surgery

Free perforation

General peritonitis

No improvement or increase in fever or pain/tenderness on above measures after 48h

Resect involved segment of colon

surgery who else
Surgery- Who else?

2+ previous diverticulitis attacks

Persistent tenderness

Endoscopic or imaging signs of cancer

Dysuria with diverticulitis in male or in female with hysterectomy (no barrier between/may have fistula)

cancer in the gi tract
Cancer in the GI Tract

Cancer: unregulated cell growth (neoplasm) plus the ability to invade distant tissues (malignancy)‏

Cancer arises usually from rapidly dividing or damaged tissue

Entire GI tract susceptible:

esophageal cancer
Esophageal Cancer

13,500 cases and 12,500 deaths overall annually

Squamous cell- Most common type

Adenocarcinoma- 2nd most common

Other esophageal tumors: spindle cell, verrucous, pseudosarcoma, sarcoma, malignant melanoma

3% are metastases

squamous cell
Squamous cell

8k cases annually

In US

4-5x more common in blacks

2-3x more common in males

Risk factors: alcohol ingestion, tobacco use (any form), achalasia, HPV infection, ingestion of caustic or hot liquids, irradiation, esophageal webs

esophageal adenocarcinoma
Esophageal Adenocarcinoma

Usually in distal esoph

4x more common in whites

>50% of esoph CA in whites

Smoking!

But not alcohol

Most cases develop from Barrett’s esophagus

esoph ca s s
Esoph CA S&S

Earliest stages- no sx

Dysphagia when lumen <14 mm

Progressive from solids, semisolids, liquids, saliva.

Wt loss- universal, even with good appetite

esoph ca s s1
Esoph CA S&S

Compression of nerves by mass effect

Recurrent laryngealhoarseness

SympatheticHorner’s sign (ptosis, miosis, anhidrosis, enophthalmosis, anisocoria)‏ - usually unilateral

Elsewhere spinal pain, hiccups, paralysis of diaphragm

Dyspnea from malignant pleural effusion or pulmonary metastases

esoph ca dx
Esoph CA Dx

If suspicious, endoscopy with bx

If confirmed

CT chest/abd to assess spread

Endoscopic U/S to assess depth of tumor and regional node involvement

CBC, lytes, LFTs

prognosis
Prognosis

Average- 5 year survival <5%

If restricted to mucosa, 80% survival

If in submucosa, 50%

With extension into muscularis, 20%

Extension to adjacent structure, 7%

Distant metastasis, 3%

treatment
Treatment

Stage 0, I, some II- surgical resection only, no benefit to chemo or radiation

Stage II, III- Preoperative radiation/chemo to  size, then surgery

Surg: en bloc resection of whole tumor with clean margins, all potentially malignant lymph nodes, part of prox stomach to get draining lymphatics, then gastric pull-up with esophogastric anastomsis.

If no surg, both chemo & rad

Stage IV- palliation, no surgery

palliation support
Palliation & Support

Relieve obstruction to allow oral intake

Stent, dilation, radiation, laser coag

Nutritional support. Enteral or parenteral supplementation. Consider early surgical/endoscopic placement of feeding tubes to allow feeding when esoph blocked

End-of-life decisions made early

gastric cancer
Gastric Cancer

21k cases, 12k deaths

95% gastric adenocarcinoma

2nd MC cancer worldwide

Multifactorial etiology; H. Pylori causative in most cases

types of gastric adenocarcinoma
Types of Gastric Adenocarcinoma

Classified by gross appearance

1. Protruding- polypoid. Better prog b/c detected sooner

2. Penetrating- ulcerated tumor

3. Superficial spreading- spreads along mucosa or infiltrates superficially within stomach wall

gastric ca s s
Gastric CA S&S

Initially nonspecific dyspepsia

Later:

Early satiety (gets full really easy)

If tumor obstructs peptic outlet or if stomach non-distensible

Dyspepsia

If tumor obstructs esoph outlet

Weight loss

Hematemesis, melena with secondary anemia

Sometimes primary sx are from mets (jaundice, bone fracture, ascites)‏

physical exam1
Physical Exam

May be normal, or you may find

Heme positive stool

Epigastric mass

Adenopathy – umbilical, L supraclavicular, L axillary

Hepatomegaly

gastric ca dx
Gastric CA Dx

Endoscopy with multiple bx and brush cytology

CT chest/abd for spread- if CT neg, endoscopic U/S

CBC, lytes, LFTs- to assess hydration, anemia, liver mets

prognosis1
Prognosis

Overall 5 year survival 5-15%

In mucosa only 80%

In local nodes 20-40%

More widespread, fatal within 1 year

treatment1
Treatment

Depends on spread and pt preference

Surgery- If ca limited to stomach and local nodes only, gastrectomy with local node removal results in 10 month survival (vs 3-4 without)‏

Extensive node involvement or metspalliation

polyps
Polyps

Mass of tissue arising from bowel wall, protruding into lumen

Pedunculated or sessile

Occur in rectum, sigmoid, with decreasing frequency toward cecum

Usually no symptoms

Concern: malignant transformation in previously benign adenomatous polyp

polyp s s and dx
Polyp S&S and Dx

Usually no sx

If any, rectal bleeding

Most found incidentally on colonoscopy

Tx: snare or electrosurgical bx during colonoscopy

If incomplete removal, laparotomy

If deep invasion into muscularis, eval for colon cancer

Monitor with serial scopes

colorectal cancer

The most common malignant esophageal tumor is squamous cell carcinoma, followed by adenocarcinoma. Symptoms are progressive dysphagia and weight loss. Diagnosis is by endoscopy, followed by CT and endoscopic ultrasound for staging. Treatment varies with stage and generally includes surgery with or without chemotherapy and radiation. Long-term survival is poor except for those with local disease.

(See also the American College of Gastroenterology\'s practice guidelines for esophageal cancer.)‏

Esophageal cancer accounts for about 13,500 cases and 12,500 deaths in the US annually.

Squamous cell carcinoma: About 8000 cases occur annually in the US. It is more common in parts of Asia and in South Africa. In the US, it is 4 to 5 times more common among blacks than whites, and 2 to 3 times more common among men than women.

The most common malignant esophageal tumor is squamous cell carcinoma, followed by adenocarcinoma. Symptoms are progressive dysphagia and weight loss. Diagnosis is by endoscopy, followed by CT and endoscopic ultrasound for staging. Treatment varies with stage and generally includes surgery with or without chemotherapy and radiation. Long-term survival is poor except for those with local disease.

(See also the American College of Gastroenterology\'s practice guidelines for esophageal cancer.)‏

Esophageal cancer accounts for about 13,500 cases and 12,500 deaths in the US annually.

Squamous cell carcinoma: About 8000 cases occur annually in the US. It is more common in parts of Asia and in South Africa. In the US, it is 4 to 5 times more common among blacks than whites, and 2 to 3 times more common among men than women.

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Colorectal Cancer

130k cases, 57 k deaths

Incidence rises after 40, peaks 60-75

70% in rectum/sigmoid

95% adenocarcinoma, usually transformation within adenomatous polyp. 80% sporadic, 20% heritable

Barrett\'s Esophagus

Barrett\'s Esophagus

Squamous Cell Carcinoma of the Esophagus

Squamous Cell Carcinoma of the Esophagus

Table 1

Table 1

Adenocarcinoma: Adenocarcinoma occurs in the distal esophagus. Its incidence is increasing; it accounts for 50% of esophageal carcinoma in whites. It is 4 times more common among whites than blacks. Alcohol is not an important risk factor, but smoking is contributory. Adenocarcinoma of the distal esophagus is difficult to distinguish from adenocarcinoma of the gastric cardia invading the distal esophagus.

Most adenocarcinomas arise in Barrett\'s esophagus, which results from chronic gastroesophageal reflux disease and reflux esophagitis. In Barrett\'s esophagus, a metaplastic, columnar, glandular, intestine-like mucosa replaces the stratified squamous epithelium of the distal esophagus during the healing phase of acute esophagitis.

Other malignant tumors: Less common malignant tumors include spindle cell carcinoma (a poorly differentiated variant of squamous cell carcinoma), verrucous carcinoma (a well-differentiated variant of squamous cell carcinoma), pseudosarcoma, mucoepidermoid carcinoma, adenosquamous carcinoma, cylindroma (adenoid cystic carcinoma), primary oat cell carcinoma, choriocarcinoma, carcinoid tumor, sarcoma, and primary malignant melanoma.

Metastatic cancer constitutes 3% of esophageal cancer. Melanoma and breast cancer are most likely to metastasize to the esophagus; others include cancers of the head and neck, lung, stomach, liver, kidney, prostate, testis, and bone. These tumors usually seed the loose connective tissue stroma around the esophagus, whereas primary esophageal cancers begin in the mucosa or submucosa.

Symptoms and Signs

Early-stage esophageal cancer tends to be asymptomatic. When the lumen of the esophagus becomes constricted to < 14 mm, dysphagia commonly occurs. The patient first has difficulty swallowing solid food, then semisolid food, and finally liquid food and saliva; this steady progression suggests a growing malignant process rather than a spasm, benign ring, or peptic stricture. Chest pain may be present, usually radiating to the back.

Weight loss, even when the patient maintains a good appetite, is almost universal. Compression of the recurrent laryngeal nerve may lead to vocal cord paralysis and hoarseness. Compression of sympathetic nerves may lead to Horner\'s syndrome, and nerve compression elsewhere may produce spinal pain, hiccups, or paralysis of the diaphragm. Malignant pleural effusions or pulmonary metastasis may cause dyspnea. Intraluminal tumor involvement may produce odynophagia, vomiting, hematemesis, melena, iron deficiency anemia, aspiration, and cough. Fistulas between the esophagus and tracheobronchial tree may produce lung abscess and pneumonia. Other findings may include superior vena cava syndrome, malignant ascites, and bone pain.

Lymphatic spread to internal jugular, cervical, supraclavicular, mediastinal, and celiac nodes is common. The tumor usually metastasizes to lung and liver and occasionally to distant sites (eg, bone, heart, brain, adrenal glands, kidneys, peritoneum).

Diagnosis

There are no screening tests. Patients suspected of having esophageal cancer should have endoscopy with cytology and biopsy. Although barium x‑ray may demonstrate an obstructive lesion, endoscopy is required for biopsy and tissue diagnosis.

Patients in whom cancer is identified require CT of the chest and abdomen to determine extent of tumor spread. If results are negative for metastasis, endoscopic ultrasound should be performed to determine the depth of the tumor in the esophageal wall and regional lymph node involvement. Findings guide therapy and help determine prognosis.

Basic blood tests, including CBC, electrolytes, and liver function, should be performed.

Prognosis and Treatment

Prognosis depends greatly on stage, but overall is poor (5‑yr survival: < 5%) because many patients present with advanced disease. Patients with cancer restricted to the mucosa have about an 80% survival rate, which drops to < 50% with submucosal involvement, 20% with extension to the muscularis propria, 7% with extension to adjacent structures, and < 3% with distant metastases.

Treatment decisions depend on tumor staging, size, location, and the patient\'s wishes (many choose to forgo aggressive treatment).

General principles: Patients with stage 0, I, or IIa disease (see Table 1: Tumors of the GI Tract: Staging Esophageal Cancer ) respond well to surgical resection; chemotherapy and radiation provide no additional benefit. Those with stage IIb and III have poor survival with surgery alone; response and survival are enhanced by preoperative (neoadjuvant) use of radiation and chemotherapy to reduce tumor volume prior to surgery. Patients unable or unwilling to undergo surgery may receive some benefit from combined radiation and chemotherapy. Radiation or chemotherapy alone is of little benefit. Patients with stage IV disease require palliation and should not undergo surgery.

Adenocarcinoma: Adenocarcinoma occurs in the distal esophagus. Its incidence is increasing; it accounts for 50% of esophageal carcinoma in whites. It is 4 times more common among whites than blacks. Alcohol is not an important risk factor, but smoking is contributory. Adenocarcinoma of the distal esophagus is difficult to distinguish from adenocarcinoma of the gastric cardia invading the distal esophagus.

Most adenocarcinomas arise in Barrett\'s esophagus, which results from chronic gastroesophageal reflux disease and reflux esophagitis. In Barrett\'s esophagus, a metaplastic, columnar, glandular, intestine-like mucosa replaces the stratified squamous epithelium of the distal esophagus during the healing phase of acute esophagitis.

Other malignant tumors: Less common malignant tumors include spindle cell carcinoma (a poorly differentiated variant of squamous cell carcinoma), verrucous carcinoma (a well-differentiated variant of squamous cell carcinoma), pseudosarcoma, mucoepidermoid carcinoma, adenosquamous carcinoma, cylindroma (adenoid cystic carcinoma), primary oat cell carcinoma, choriocarcinoma, carcinoid tumor, sarcoma, and primary malignant melanoma.

Metastatic cancer constitutes 3% of esophageal cancer. Melanoma and breast cancer are most likely to metastasize to the esophagus; others include cancers of the head and neck, lung, stomach, liver, kidney, prostate, testis, and bone. These tumors usually seed the loose connective tissue stroma around the esophagus, whereas primary esophageal cancers begin in the mucosa or submucosa.

Symptoms and Signs

Early-stage esophageal cancer tends to be asymptomatic. When the lumen of the esophagus becomes constricted to < 14 mm, dysphagia commonly occurs. The patient first has difficulty swallowing solid food, then semisolid food, and finally liquid food and saliva; this steady progression suggests a growing malignant process rather than a spasm, benign ring, or peptic stricture. Chest pain may be present, usually radiating to the back.

Weight loss, even when the patient maintains a good appetite, is almost universal. Compression of the recurrent laryngeal nerve may lead to vocal cord paralysis and hoarseness. Compression of sympathetic nerves may lead to Horner\'s syndrome, and nerve compression elsewhere may produce spinal pain, hiccups, or paralysis of the diaphragm. Malignant pleural effusions or pulmonary metastasis may cause dyspnea. Intraluminal tumor involvement may produce odynophagia, vomiting, hematemesis, melena, iron deficiency anemia, aspiration, and cough. Fistulas between the esophagus and tracheobronchial tree may produce lung abscess and pneumonia. Other findings may include superior vena cava syndrome, malignant ascites, and bone pain.

Lymphatic spread to internal jugular, cervical, supraclavicular, mediastinal, and celiac nodes is common. The tumor usually metastasizes to lung and liver and occasionally to distant sites (eg, bone, heart, brain, adrenal glands, kidneys, peritoneum).

Diagnosis

There are no screening tests. Patients suspected of having esophageal cancer should have endoscopy with cytology and biopsy. Although barium x‑ray may demonstrate an obstructive lesion, endoscopy is required for biopsy and tissue diagnosis.

Patients in whom cancer is identified require CT of the chest and abdomen to determine extent of tumor spread. If results are negative for metastasis, endoscopic ultrasound should be performed to determine the depth of the tumor in the esophageal wall and regional lymph node involvement. Findings guide therapy and help determine prognosis.

Basic blood tests, including CBC, electrolytes, and liver function, should be performed.

Prognosis and Treatment

Prognosis depends greatly on stage, but overall is poor (5‑yr survival: < 5%) because many patients present with advanced disease. Patients with cancer restricted to the mucosa have about an 80% survival rate, which drops to < 50% with submucosal involvement, 20% with extension to the muscularis propria, 7% with extension to adjacent structures, and < 3% with distant metastases.

Treatment decisions depend on tumor staging, size, location, and the patient\'s wishes (many choose to forgo aggressive treatment).

General principles: Patients with stage 0, I, or IIa disease (see Table 1: Tumors of the GI Tract: Staging Esophageal Cancer ) respond well to surgical resection; chemotherapy and radiation provide no additional benefit. Those with stage IIb and III have poor survival with surgery alone; response and survival are enhanced by preoperative (neoadjuvant) use of radiation and chemotherapy to reduce tumor volume prior to surgery. Patients unable or unwilling to undergo surgery may receive some benefit from combined radiation and chemotherapy. Radiation or chemotherapy alone is of little benefit. Patients with stage IV disease require palliation and should not undergo surgery.

The primary risk factors are alcohol ingestion and tobacco use (in any form). Other factors include achalasia, human papillomavirus, lye ingestion (resulting in stricture), sclerotherapy, Plummer-Vinson syndrome, irradiation of the esophagus, and esophageal webs. Genetic causes are unclear, but 50% of patients with tylosis (hyperkeratosis palmaris et plantaris), an autosomal dominant disorder, have esophageal cancer by age 45, 95% by age 55.

The primary risk factors are alcohol ingestion and tobacco use (in any form). Other factors include achalasia, human papillomavirus, lye ingestion (resulting in stricture), sclerotherapy, Plummer-Vinson syndrome, irradiation of the esophagus, and esophageal webs. Genetic causes are unclear, but 50% of patients with tylosis (hyperkeratosis palmaris et plantaris), an autosomal dominant disorder, have esophageal cancer by age 45, 95% by age 55.

colorectal ca risk factors
Colorectal Ca risk factors

Ulcerative colitis

Diet

Low fiber -fiber speeds colonic transit, reduces exposure to carcinogens

High in animal protein

High fat

Theory: Fats increase anaerobes in colon which convert bile to

High in refined carbs

Smoking

Genetic factors

genetic risk factors hereditary polyp syndromes look ups
Genetic risk factors: hereditary polyp syndromes(Look-ups)‏

Polyposis coli (Familial Adenosis Polyposis - FAP)‏

Hereditary Non-Polyposis Colon CA (HNPCC)‏

Peutz-Jeghers Syndrome

Familial Juvenile Polyposis Coli

Found during family medical history

Generally warrant more frequent screening

s s depend on location
S&S-depend on location

R colon- bleeding (occult or melena)  anemia fatigue/weakness

Large lumen, liquid contents, so rare obstruction

L colon- Constipation alt with diarrhea or stool freq. Partial or complete obstruction with abd pain can be initial presentation

Smaller lumen, semisolid contents. CA can encircle bowel.

Sigmoid or rectal- tenesmus, ribbon stools

screening for colorectal cancer
Screening For Colorectal Cancer

Very large part of primary care practices

Screening method and frequency based on risk assessment, average or high

Average Risk:

No 1st order relatives with colon CA

No prior Hx colon CA or polyps

No Hx IBD

High Risk: Yes to any of the above

colon ca screening
Colon CA Screening

Modalities:

Fecal Occult Blood Testing (FOBT)‏

Sigmoidoscopy

Colonoscopy

slide112
FOBT

FOBT alone reduces mortality from colon CA by 33%

Sensitivity single FOBT is 30%

Annual FOBT screen 92% sensitive

2% of positive FOBT have CA

Problems with FOBT:

Misses non-bleeding polyps

Reduces mortality only 30%

Many false positives

sigmoidoscopy
Sigmoidoscopy

Sigmoidoscopy reaches 60 cm to splenic flexure

Misses about ½ of colon

Reduces mortality by 60%

Screen every 5 years

If polyps or lesions found must do colonoscopy

colonoscopy
Colonoscopy

Colonoscopy most sensitive screen

Finds most polyps

Can remove by bx simultaneously

Requires conscious sedation

Risk of perforation, other hazards

Not usually an office procedure

Prep

slide115
DCBE

Double Contrast Barium Enema

Screens entire colon

No sedation required

Some cramping

Prep required

Must do colonoscopy if lesions found

virtual colonoscopy
Virtual colonoscopy

Virtual colonoscopy using computer-enhanced spiral CT scan

Initial studies in screening populations showed high sensitivity similar to colonoscopy

If lesions found, need colonoscopy anyway

Still must do prep

No bx possible

capsule colonoscopy
Capsule Colonoscopy

Pill or Capsule Colonoscopy easier on patient

Prep, then swallow pill

Recording sensors attached to abdomen

Results downloaded and reviewed after 6-8 hours

No manipulation of camera possible

Colonoscopy for biopsy of lesions

Limited data to date, not recommended, yet

average risk
Average risk

Average Risk: screen all pts >50 y.o. Choices:

Offer FOBT or FIT yearly. If positive, then colonoscopy

Offer sigmoidoscopy every 5 years. If positive, then colonoscopy

Offer colonoscopy every 10 years

Offer DCBE every 5 years

high risk patient screening
High-Risk Patient Screening

For High Risk pts begin to screen age 40

1st order relative screen every 3-5 years

Genetic syndromes- more frequent screening. Likely will be followed by specialist

screening for colorectal cancer1
Screening For Colorectal Cancer

Overall screening efforts very poor

And liability very high…

65% of all cases found when symptomatic, not at screening

prognosis2
Prognosis

10 year survival

CA limited to mucosa 90%

Extension thru bowel wall 70-80%

With positive nodes 30-50%

With metastases <20%

colorectal cancer tx
Colorectal Cancer Tx

Surgical- wide resection of tumor, plus regional lymph drainage with reanastomosis

Adjuvant chemo  survival by 10-30%

If no surgical cure option, consider palliative surgery, or tumor debulking measures (lessen obstructive sx)

follow up
Follow-up

Colonoscopy q year x 5 yrs, then q 3 yrs

H&P, CBC, LFTs q 3 months x 3 yrs, then q 6 months x 2 yr

small intestine tumors
Small Intestine Tumors

Less than 5% all GI cancers

Many benign tumors: adenomas, leiomyomas, lipomas, angiomas

Increased risk malignancy with Crohn’s Dz, celiac disease

Adenocarcinoma, lymphoma

Presentation: recurrent cramping abd pain, periodic small bowel obstruction (SBO), intussusception, chronic bleeds

small intestine tumors1
Small Intestine Tumors

Diagnose with CT and DCBE

Usually out of reach of colonoscope or EGD

Exploratory laparotomy for biopsy

Stage as colon cancer

Treat with surgical resection, +/- radiation or chemo for debulking

anorectal cancer
Anorectal cancer

Usually adenocarcinoma

Mets to lymphatics of rectum and inguinal nodes

Risk factors: HPV, chronic fistulas, irradiation, receptive anal intercourse,

Screening with Pap/HPV testing

Tx: wide local excision, chemo and rad

pancreatic cancer
Pancreatic Cancer

30,500 cases, 29,000 deaths

Most are exocrine tumors, primarily ductal adenocarcinoma

80% found in head of pancreas

Mean age 55, 2x more common in males

Risk: smoking, chronic pancreatitis, longstanding DM, some heredity

pancreatic cancer1
Pancreatic Cancer

Usually no symptoms until lesion too advanced to resect

Symptoms non-specific, with large DDx

Weight loss, pain, anorexia, fatigue, dyspepsia, reflux, jaundice

Severe upper abd pain, radiates to back, relieved by forward lean or fetal position

Obstructive jaundice and resulting pruritis in 80-90%

slide129
S&S

Palpable mass, ascites in 20%

Left supraclavicular lymphadenopathy (Virchow\'s node)‏

90% have locally advanced dz w/ retroperitoneal structure involvement, regional lymph spread, or mets at time of pres

diagnosing pancreatic cancer
Diagnosing Pancreatic Cancer

U/S initially to show ducts, stones, masses

CT better defines tumor, and vascular involvement

MRI great for vasculature

Biopsy: transcutaneous, ERCP, guided fine-needle aspiration

prognosis tx
Prognosis/tx

Overall, <2% survival

80-90% unresectable (mets or invasion of major blood vessels)‏

If resectable- Whipple procedure (pancreaticoduodenectomy) with adjuvant chemo+ rad 40% 2 yr and 25% 5 yr survival if node negative

treatment2
Treatment

Appropriate end-of-life care: managing death, hospice care, etc

Sx Control!

PAIN- opioids (without concern for addiction as barrier to effective pain control)‏

hepatic cancer
Hepatic cancer

Liver is common place for metastasis for many primary cancers, esp from GI tract, breast, lung, pancreas.

Mets more common than primary hepatocellular carcinoma

Primary cancer14k deaths annually in US

Primary liver cancer more common in pts with cirrhosis, common in areas with prevalent Hep B & C infections

Risk  100 fold in chronic hep B carriers

liver ca s s
Liver Ca S&S

Initially nonspecific: abd pain, fever

PE may show RUQ mass, or BIG, hard, tender liver

Hepatic bruits with pleuritic pain

Late: jaundice, hepatic encephalopathy

primary liver cancer
Primary Liver Cancer

Dx with

imaging: U/S, MRI or abd CT w/ contrast

Labs: AFP

Liver bx for definitive dx

Overall 2 year survival <5%

IF tumor is <2cm and localized to one lobe, can try resection or transplant. Chemo/rad NO help.

hepatic ca prevention
Hepatic Ca Prevention

Hep B vaccination

Prevent cirrhosis

Screen pts with cirrhosis for CA

AFP and liver U/S q 6-12 mo

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