engl BUN.edit

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DISEASES OF THEDISEASES OF THE

INTESTINEINTESTINE


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DIAREEADIAREEA

Definition >3 feces/day, > 200 g/day

Physiology:

in gastrointestinal tract 9-10 l fluids (2l ingestion, the rest

secretions);

Na - co-transport with Cl and glucose in small bowel and biliarysalts in terminal ileum; co-transport with H - HCO3; K absorbed with

H or Ca.

In colon, Na absorbed through apical membrane canals

parasimpatic is stimulating the peristalsis and electrolyte secretion;

simpatic nerves are doing the opposite.

Enteric nervous system.


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Figure 4.1 - Water fluxes through the intestineFigure 4.1 - Water fluxes through the intestine

Copyright Science Press Internet Services


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Functional design of small intestine


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Acute DiarrheaAcute Diarrhea


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DefinitionDefinition

Stool weight in excess of 200 gm/dayStool weight in excess of 200 gm/day

3 or more loose or watery stools/day3 or more loose or watery stools/day

Alteration in normal bowel movementAlteration in normal bowel movement

characterized by decreased consistency andcharacterized by decreased consistency and

increased frequencyincreased frequency

Less than 14 days in durationLess than 14 days in duration


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EpidemiologyEpidemiology

1.2-1.9 episodes per person annually in the1.2-1.9 episodes per person annually in thegeneral populationgeneral population

2.4 episodes per child


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EtiologyEtiology

ViralViral: 70-80% of infectious diarrhea in: 70-80% of infectious diarrhea in

developed countriesdeveloped countries

BacterialBacterial: 10-20% of infectious diarrhea but: 10-20% of infectious diarrhea butresponsible for most cases of severeresponsible for most cases of severe

diarrheadiarrhea

ProtozoarsProtozoars: less than 10%: less than 10%


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Viral DiarrheaViral Diarrhea

RotavirusRotavirus

Norovirus (Norwalk-like)Norovirus (Norwalk-like)

Enteric AdenovirusEnteric Adenovirus

AstrovirusAstrovirus


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RotavirusRotavirus

Leading cause of hospitalization for diarrhea inLeading cause of hospitalization for diarrhea in

childrenchildren

Most prevalent during winter seasonMost prevalent during winter season Fecal-oral transmission: viral shedding canFecal-oral transmission: viral shedding can

persist for 21 dayspersist for 21 days

Acute onset of feverAcute onset of feverfollowed byfollowed by waterywaterydiarrheadiarrhea (10-20 BM/day) and can(10-20 BM/day) and canpersist for uppersist for up

to a weekto a week


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NorovirusNorovirus

Most common cause of diarrhealMost common cause of diarrheal

outbreaks/epidemicsoutbreaks/epidemics

Multiple modes of fecal-oral transmissionMultiple modes of fecal-oral transmission Acute onset of nausea and vomiting, wateryAcute onset of nausea and vomiting, watery

diarrheadiarrhea withwith abdominal crampsabdominal cramps and canand can

persist for 1-3 dayspersist for 1-3 days


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Enteric AdenovirusEnteric Adenovirus

Primarily affects children < 4 years oldPrimarily affects children < 4 years old

Fecal-oral transmissionFecal-oral transmission

Clinical picture similar to rotavirus (Clinical picture similar to rotavirus (feverfever

and watery diarrheaand watery diarrhea))


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AstrovirusAstrovirus

Primarily affects children < 4 years old andPrimarily affects children < 4 years old and

immunocompromisedimmunocompromised

Seasonal peak in the winterSeasonal peak in the winter Fecal-oral transmission: viral shedding canFecal-oral transmission: viral shedding can

occur for several weeksoccur for several weeks

Fever, nausea and vomiting, abdominal painFever, nausea and vomiting, abdominal pain,,andand diarrheadiarrhea lasting up to a weeklasting up to a week


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Summary of Viral DiarrheaSummary of Viral Diarrhea

Most likely causeMost likely cause of infectious diarrheaof infectious diarrhea

Rotavirus and Norovirus are most commonRotavirus and Norovirus are most common

Symptoms usually includeSymptoms usually include low grade fever,low grade fever,nausea and vomiting, abdominal cramps, andnausea and vomiting, abdominal cramps, and

watery diarrheawatery diarrhea lasting up to 1 weeklasting up to 1 week

Viral shedding can occur for weeks afterViral shedding can occur for weeks aftersymptoms resolvesymptoms resolve


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Bacterial DiarrheaBacterial Diarrhea

CampylobacterCampylobacter

SalmonellaSalmonella

ShigellaShigella

Enterohemorrhagic Escherichia coliEnterohemorrhagic Escherichia coli


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CampylobacterCampylobacter

Most common bacterial pathogenMost common bacterial pathogen

Transmitted through ingestion of contaminatedTransmitted through ingestion of contaminatedfood or by direct contact with fecal materialfood or by direct contact with fecal material

Symptoms includeSymptoms include diarrhea (+/- blood),diarrhea (+/- blood),abdominal cramps (can be severe), malaise,abdominal cramps (can be severe), malaise,feverfever

Usually self-limited and does not requireUsually self-limited and does not requireantibioticsantibiotics


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SalmonellaSalmonella

Most common in children


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ShigellaShigella

Fecal-oral transmissionFecal-oral transmission Symptoms includeSymptoms include fever, abdominalfever, abdominal

cramps, tenesmus, and mucoid stoolscramps, tenesmus, and mucoid stools withwith

or withoutor withoutbloodblood Can lead to serious complicationsCan lead to serious complications Antimicrobial treatment shortens durationAntimicrobial treatment shortens duration

of illness and limits fecal sheddingof illness and limits fecal shedding


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E. ColiE. Coli O157:H7O157:H7

Transmission via contaminated food and waterTransmission via contaminated food and water

Symptoms includeSymptoms includebloody diarrheabloody diarrhea,, severesevere

abdominal pain, and sometimes feverabdominal pain, and sometimes fever Can lead to serious complicationsCan lead to serious complications

Antibiotics have no proven benefit and mayAntibiotics have no proven benefit and may

increase the risk of complicationsincrease the risk of complications


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Summary of Bacterial DiarrheaSummary of Bacterial Diarrhea

Can affect all age groupsCan affect all age groups

Fecal-oral transmission, often throughFecal-oral transmission, often through

contaminated foodcontaminated food Typical symptoms include bloody diarrhea,Typical symptoms include bloody diarrhea,

severe cramping, and malaisesevere cramping, and malaise

Antibiotic treatment not always necessaryAntibiotic treatment not always necessary


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History and Physical ExamHistory and Physical Exam

3 main goals3 main goals

Estimate the level of dehydrationEstimate the level of dehydration

Identify likely causes on the basis of historyIdentify likely causes on the basis of historyand clinical findingsand clinical findings

Determine if additional studies and/orDetermine if additional studies and/or

medications are necessarymedications are necessary


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HistoryHistory

Onset, frequency, quantity, and character ofOnset, frequency, quantity, and character ofdiarrheadiarrhea

Associated symptoms: nausea, vomiting,Associated symptoms: nausea, vomiting,fever, abdominal pain, tenesmus, malaisefever, abdominal pain, tenesmus, malaise

Recent oral intakeRecent oral intake

Signs and symptoms of dehydrationSigns and symptoms of dehydration


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Physical ExamPhysical Exam

Vitals, vitals, vitals!Vitals, vitals, vitals!

Abdominal examAbdominal exam

Presence of occult bloodPresence of occult blood

Signs of dehydrationSigns of dehydration


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Laboratory EvaluationLaboratory Evaluation

Unnecessary for patients who present within 1Unnecessary for patients who present within 1day from onset of diarrheaday from onset of diarrhea

Warning signs/symptoms: bloody diarrhea,Warning signs/symptoms: bloody diarrhea,

high fever, severe abd pain, dehydration, orhigh fever, severe abd pain, dehydration, orcomorbid conditioncomorbid condition

Fecal leukocytes followed by bacterial culture,Fecal leukocytes followed by bacterial culture,

ova & parasites, viral antigensova & parasites, viral antigens CBC, chemistriesCBC, chemistries


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Chronic DiarrheaChronic Diarrhea


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DefinitionDefinition

>3 weeks duration>3 weeks duration

Average fecal daily weight in normalAverage fecal daily weight in normal

person is 100-200grams/dayperson is 100-200grams/day


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Approach to PatientApproach to Patient

Patient should be questioned about thePatient should be questioned about the

onset, duration, pattern, aggrevantsonset, duration, pattern, aggrevants

(especially diet), relieving factors, and stool(especially diet), relieving factors, and stool

characteristicscharacteristics

Presence or absence of fecal incontinence,Presence or absence of fecal incontinence,

fever, weight loss, pain, certain exposures-fever, weight loss, pain, certain exposures-

travel, medications, contacts with diarrhea)travel, medications, contacts with diarrhea)

should be notedshould be noted


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Approach to patientApproach to patient

On physical exam, check for thyroid mass,On physical exam, check for thyroid mass,

wheezing on lung exam, heart murmurs,wheezing on lung exam, heart murmurs,

edema, hepatomeg, abdominal mass, LAD,edema, hepatomeg, abdominal mass, LAD,

perianal fistula, or anal sphincter laxity.perianal fistula, or anal sphincter laxity.


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Chronic DiarrheaChronic Diarrhea

If diagnosis is still unclear after initialIf diagnosis is still unclear after initial

encounter, further testing is requiredencounter, further testing is required

Further work up should delineate secretoryFurther work up should delineate secretory

vs. osmotic diarrhea vs. malabsorption vsvs. osmotic diarrhea vs. malabsorption vs

inflammatoryinflammatory


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Malabsorptive diarrheaMalabsorptive diarrhea

Malabsorption suspected in patients with weightMalabsorption suspected in patients with weightloss, greasy stools, glossitis, anemia, andloss, greasy stools, glossitis, anemia, andhypoalbumenimahypoalbumenima

If malabsorption suspected, a 72 hr stool specimenIf malabsorption suspected, a 72 hr stool specimenshould be sent for fecal fat determination, if +should be sent for fecal fat determination, if +suspect malabsorptionsuspect malabsorption

Causes of malabsorption include pancreaticCauses of malabsorption include pancreatic

insufficiency (confirmed by CT/pancreaticinsufficiency (confirmed by CT/pancreaticfunction tests) and disease of small intestine--function tests) and disease of small intestine--Whipples disease, tropical sprue, intestinalWhipples disease, tropical sprue, intestinallymphoma (small bowel biopsies by EGD)lymphoma (small bowel biopsies by EGD)


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Malabsorptive Diarrhea-MucosalMalabsorptive Diarrhea-Mucosal

MalabsorbtionMalabsorbtion

Celiac sprue-hypersensitivity to glutenCeliac sprue-hypersensitivity to gluten

Tropical sprue-infectious disease ofTropical sprue-infectious disease of

unknown origin, seen in Indianunknown origin, seen in Indian

subcontinent, Asia, West Indies, North &subcontinent, Asia, West Indies, North &

South America, central and southern Africa,South America, central and southern Africa,

and Central Americaand Central America

--


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Mucosal MalabsorptiveMucosal Malabsorptive

Tropical Sprue-tx with tetracycline andTropical Sprue-tx with tetracycline andfolic acidfolic acid

Whipples->infection form Treponema-Whipples->infection form Treponema-

whippelii.whippelii. Diagnosed by + biopsy for PASDiagnosed by + biopsy for PAS

macrophagesmacrophages

Associated symptoms includeAssociated symptoms includehypersomnolescence, arthralgias, fever,hypersomnolescence, arthralgias, fever,hypotension, and LADhypotension, and LAD


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Intraluminal MalabsorbtionIntraluminal Malabsorbtion

Other-Most commonly results from pancreaticOther-Most commonly results from pancreaticexocrine insufficiency when >90% of pancreaticexocrine insufficiency when >90% of pancreaticsecretory function is lostsecretory function is lost

Most commonly due to ethanol abuseMost commonly due to ethanol abuse Other causes include cystic fibrosis, pancreaticOther causes include cystic fibrosis, pancreatic

duct obstructionduct obstruction

Also SBO where bacteria deconjugate bile acids,Also SBO where bacteria deconjugate bile acids,

impairing fat digestionimpairing fat digestion SBO one can see low B12, high folate, andSBO one can see low B12, high folate, and

megaloblastic anemiamegaloblastic anemia


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Secretory vs OsmoticSecretory vs Osmotic

Secretory vs Osmotic check stool osmoticSecretory vs Osmotic check stool osmotic

gapgap

290-2x[NAstool + Kstool]290-2x[NAstool + Kstool]

If < 50, diarrhea falls under secretoryIf < 50, diarrhea falls under secretory

categorycategory


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Secretory DiarrheaSecretory Diarrhea

Characterized by watery, large-volumeCharacterized by watery, large-volume

fecal outputs that are typically painless andfecal outputs that are typically painless and

persist with fastingone may do a 24 hrpersist with fastingone may do a 24 hr

stool quant.-should exceed one liter and notstool quant.-should exceed one liter and not

decrease with fastingdecrease with fasting

Usually stool pH is neutral, and fecal fatUsually stool pH is neutral, and fecal fat

test is negativetest is negative


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Secretory diarrheaSecretory diarrhea

If secretory diarrhea confirmed, recommendIf secretory diarrhea confirmed, recommend

checking serum should be sent for:checking serum should be sent for:

Gastrin (gastrinoma), VIP(VIPOMA),Gastrin (gastrinoma), VIP(VIPOMA),

glucagon (glucogonoma), serotonin (carcinoid),glucagon (glucogonoma), serotonin (carcinoid),

calcitonin, histamine, and prostaglandinscalcitonin, histamine, and prostaglandins

-if overproduction of one of these mediators is-if overproduction of one of these mediators isdocumented,documented,abdominal CT scan isabdominal CT scan isrecommendedrecommended


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Carcinod present with watery diarrhea,Carcinod present with watery diarrhea,flushing, skin changes, bronchospasm, andflushing, skin changes, bronchospasm, andcardiac murmurs which are all symptomscardiac murmurs which are all symptoms

caused by secretion of serotonin, histamine,caused by secretion of serotonin, histamine,catecholamines, kinins, and prostaglandinscatecholamines, kinins, and prostaglandinsby the tumor massesby the tumor masses

1/3 pts with carcinoid present with diarrhea1/3 pts with carcinoid present with diarrheaalonealone


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Medullary carcinomas of thryoidMedullary carcinomas of thryoid

(spontaneous or part of MENIIA) cause(spontaneous or part of MENIIA) cause

secretory diarrhea because of the release ofsecretory diarrhea because of the release of

calcitonincalcitonin


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Sectretory DiarrheaSectretory Diarrhea

Other conditions to consider include:Other conditions to consider include:

Diseases like Crohns ileitis or resection ofDiseases like Crohns ileitis or resection of


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SECRETORY DIARRHEASECRETORY DIARRHEA

TABLE 4-5. TYPICAL FEATURES OF SECRETORY DIARRHEA

Voluminous, watery stools

Little or no fecal osmotic gap, stool pH near 7.0

Usually persists during fasting

Usually no pus, blood, or excess fat in stools

TABLE 4-6. MECHANISMS AND CAUSES OF SECRETORY DIARRHEA

Reduction in mucosal surface area


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Reduction in mucosal surface area

Postresection diarrhea

Short-bowel syndrome

Extensive mucosal disease and Inflammation

Viral gas troenteritis

Celiac disease

Whipple s disease

Crohn`s disease

Lymphoma

Absence of ion transport mechanism

Congenital chloridorrhea

Bacterial toxins

Cholera

Enterotoxigenic Escherichia coli

Shigella

Staphylococcus

Clostridium perfringens

Luminal secretagogues

Bile acids

Fatty acids, hydroxy-fatty acids

Phenolphthalein, ricinoleic acid, bisacodyl

Circulating secretagogues

Gastrin (Zollinger-Ellison syndrome)

Vasoactive intestinal polypeptide (VIPoma, ganglioneuroma, neuroblastoma, pheochromocytoma)

Calcitonin, prostaglandins (medullary carcinoma of the thyroid)

Somatostatin (somatostatinoma)

Glucagon (glucagonoma)

Serotonin, kinins (carcinoid tumor)

Thyroxine (hyperthyroidism)

Histamine (mastocytosis)


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Osmotic DiarrheaOsmotic Diarrhea

Most common cause is lactase deficiencyMost common cause is lactase deficiency

Magnesium ingestion or factitious laxativeMagnesium ingestion or factitious laxative

abuseabuse

Intraluminal maldigestion is also seen inIntraluminal maldigestion is also seen in

cirrhotics and bile duct obstruction-there iscirrhotics and bile duct obstruction-there is

impaired delivery of bile salts to smallimpaired delivery of bile salts to small

intestine, leads to poor micelle formationintestine, leads to poor micelle formation

with ingested fatswith ingested fats

CRONIC DIARRHEA I i iCRONIC DIARRHEA I i i


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CRONIC DIARRHEA -Investigation-CRONIC DIARRHEA -Investigation-

Blood: ESR; hemoleucograme ( anemia,

inflammation); proteinograme (hyposerinemia)

Rectosigmoidoscopy, Colonoscopy with/without

biopsy/ UGI endoscopy ( celiac disease )

Rx: small bowel/barium enema

Chronic diarrhea: Abdominal X-Ray, US/ CT

TABLE 5-3. DIAGNOSTIC STUDIES FOR FECAL INCONTINENCE


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Tests Information Obtained

Sigmoidoscopy Inflammation, strictures, tumors

Anorectal manometry Sphincter pressures

Rectal sensation, compliance

External sphincter responses

Pelvic floor neurophysiology External sphincter electromyography

Puborectalis electromyography

Pudendal nerve conduction

Proctography Rectal capacity

Anorectal angle

Perineal descent

Retention of contrast

Anal ultrasonography Anal sphincter integrity


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CONSTIPATIONCONSTIPATION

1.1. DefinitionDefinition

2.2. PathogenesisPathogenesis

3.3. Risk factorsRisk factors

4.4. Diagnosis and differential diagnosisDiagnosis and differential diagnosis5.5. Treatment approachesTreatment approaches


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1. Definition

The patients view:

The following perceptions,

Need for straining (52%)

Hard pellet-like stools (44%)

Inability to defecate when desired (34%)

Infrequent defecation (33%)

The clinical view: ROME-CRITERIA (at least 2 in any 12week period);

< 3 bowel movements (BM) per week

Hard stools in > 25% of BMs

Sense of incomplete evacuation in >25% of BMs

Excessive straining in >25% of BMs

The necessity of digital manipulation

2 C


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2. Causes

Extrinsic

Inadequate dietary fiber, fluid

Ignoring urge to defecate

Structural

Colorectal: neoplasm,stricture,ischemia,volvulus,diverticular disease

Anorectal: inflammation, prolapse, rectocele,fissure, stricture

Systemic

Hypokalemia

Hypercalcemia

Hyperparathyroidism

Hypothyroidism

Diabetes mellitus

Addisons disease

Pregnancy

Neurological


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Neurological

CNS: Parkinson's disease, Multiple sclerosis, trauma, ischemia, tumor

Sacral nerves: trauma, tumor

Autonomic neuropathyAganglionosis ( Hirschsprungs disease )

Drugs

Analgesics

Anticholinergics

Anticonvulsants

Antihistamines

Antihypertensive

Chemotherapeutic agents

Diuretics

Metal ions

Uncertain Pathophysiology

Irritable bowel syndrome, Slow transit constipation (STC)

3 Risk factors


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3.Risk factors

Risk situations, groups and factors:

Infants and children

People older than 55 yrs

Recent abdominal or perianal/pelvic surgery

Late pregnancy

Limited mobility

Inadequate diet (fluid or fiber)

Medications especially in the elderly

Laxative abuse

Terminal care patients

Travel

History of chronic constipation

4


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4.

4. Diagnosis and differential diagnosis

History takingPhysical examination

Diagnostic techniques

History taking


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History taking

Check for age of onset ( sudden or long term)

Check for ROME- II criteria

Check for neurological disorders

Check for psychiatric conditions

Check for family history of constipation?

Physical examination

Palpation of abdomen ( tumour )

Percussion ( check for gases)

Rectal palpation

Consistency/impaction

Presence of non-fecal masses or abnormalities (tumors, hemorrhoid,

fissures)

Presence of blood

Sphincter tone

Diagnostic techniques


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Stool analysis

Weighing 3 days; < 100g avg means constipation

Abdominal x-rays

Radiological or endoscopic investigation

Colon tumour, stenosis

Abdominal echography

Tumour mass

Anorectal function testsManometry

Electromyography

Rectal mucosal biopsy

Colonic transit time (radiopaque marker)


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Major alarm symptoms especially in patients >50yrsMajor alarm symptoms especially in patients >50yrs

New onset constipationNew onset constipation

AnemiaAnemia

Weight lossWeight loss

Anal blood lossAnal blood loss

Positive occult blood testPositive occult blood test

Sudden changes in defecation pattern andSudden changes in defecation pattern and

appearance of stoolappearance of stool

Barium proctography in a healthy subject (A)


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Barium proctography in a healthy subject (B)


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Barium proctography in a healthy subject (C)


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Barium proctography in a healthy subject (D)


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DEFECOGRAFIADEFECOGRAFIA


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-

Distal bowel in Hirschsprung`s diseaseDistal bowel in Hirschsprung`s disease


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Distal bowel in Hirschsprung s diseaseDistal bowel in Hirschsprung s disease


M i t f i fl t b lM i t f i fl t b l1


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Main types of inflammatory bowelMain types of inflammatory bowel

disease (IBD)disease (IBD)

Ulcerative colitisUlcerative colitis

Crohns diseaseCrohns disease

2


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Specific IBD syndromesSpecific IBD syndromes

ProctitisProctitis

ProctosigmoiditisProctosigmoiditis

Left-sided ileitisLeft-sided ileitis IleitisIleitis

IleocolitisIleocolitis

24


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(reproduced with permission, the AGA Teaching Project, 1992)

Geographical distribution of IBD

25


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Ethnic prevalence of IBDEthnic prevalence of IBD

Ethnic Group

Prevalence

(per 105)

(after Kurata et al, 1992)

0

10

20

30

40

50

White Black Hispanic Asian Other

Incidence of IBD with respect to age26


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(reproduced with permission from Wells Medical Ltd, Binder 1993)

Incidence of IBD with respect to age

and sex

Patterns of IBD incidence in previous27


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(reproduced with permission from Wells Medical Ltd, Binder 1993)

Patterns of IBD incidence in previous

decades


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Def. chronic idiopathic inflammation ofcolon starting from rectum

Epidemiology:

2-10 / 100.000 loc (USA),

maximum15-25 (secondary 55-65);

Women more than males;

Smoking more common;

Ethnic Jews

28


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Aetiological theories of IBDAetiological theories of IBD

GeneticGenetic

SmokingSmoking

DietaryDietary InfectionInfection

ImmunologicalImmunological

Psychological?Psychological?

Recent controversies in theRecent controversies in the29


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Recent controversies in theRecent controversies in the

pathogenesis of IBDpathogenesis of IBD

GeneticsGenetics

Mycobacterium paratuberculosisMycobacterium paratuberculosis Measles virusMeasles virus

30


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Genetic factorsGenetic factors

It is estimated that between 10 and 20 genesIt is estimated that between 10 and 20 genes

are involvedare involved

Susceptibility loci have been located onSusceptibility loci have been located on

chromosomes 3, 7, 12 and 16chromosomes 3, 7, 12 and 16

The genetic contribution to the aetiology ofThe genetic contribution to the aetiology of

both Crohns disease and ulcerative colitisboth Crohns disease and ulcerative colitis

is polygenic NOT Mendelianis polygenic NOT Mendelian

Pathological and anatomical featuresPathological and anatomical features 23


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g

distinguishing ulcerative colitis from Crohnsdistinguishing ulcerative colitis from Crohns

diseasedisease

Clinical presentation ofClinical presentation of12


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Clinical presentation ofClinical presentation of

ulcerative colitisulcerative colitis

Bloody diarrhoeaBloody diarrhoea

FeverFever

Cramping abdominal painCramping abdominal pain

Weight lossWeight loss

Frequency and urgency of defecationFrequency and urgency of defecation

TenesmusTenesmus

General malaiseGeneral malaise


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InvestigationInvestigation

ColonoscopyColonoscopy

E d i f t f l ti

3


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Endoscopic features of ulcerative

colitis

(reproduced with permission, Schilleret al, 1986)

Figure 4.1a - Endoscopic features of activeFigure 4.1a - Endoscopic features of activeulcerative colitisulcerative colitis


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Figure 4.1b - Endoscopic features of activeFigure 4.1b - Endoscopic features of activeulcerative colitisulcerative colitis


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Figure 4.2 - Ulcerative colitis in remissionFigure 4.2 - Ulcerative colitis in remission


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Figure 4.3 - Severe ulcerative colitisFigure 4.3 - Severe ulcerative colitis


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Figure 4.4 - Severe ulcerative colitis withFigure 4.4 - Severe ulcerative colitis withpseudopolypspseudopolyps


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pseudopolypspseudopolyps


i i


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Barium enemaBarium enema

Lab: ex stools cultureLab: ex stools culture

Lab: anemia, high sedimentation rate,Lab: anemia, high sedimentation rate,

Low Na, K,Low Na, K,

High creatinine, blood ureea, renal failureHigh creatinine, blood ureea, renal failure

Radiological features of acute4


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Radiological features of acute

ulcerative colitis

(from Wilson et al, 1991)

Radiological features of chronic5


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(from Wilson et al, 1991)

Radiological features of chronic

ulcerative colitis

A t i l l ti f l ti liti

6


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Anatomical location of ulcerative colitis

Intestinal complications ofIntestinal complications of7


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Intestinal complications ofIntestinal complications of


FibrosisFibrosis

Shortening of the colonShortening of the colon

BleedingBleeding

StrictureStricture

Bowel perforationBowel perforation

Toxic megacolonToxic megacolon

Systemic complications ofSystemic complications of8


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Systemic complications ofSys e c co p c o s o


ArthritisArthritis

IritisIritis

Erythema nodosumErythema nodosum

Pyoderma gangrenosumPyoderma gangrenosum

Sclerosing cholangitisSclerosing cholangitis

Aphthous stomatitisAphthous stomatitis

Thromboembolic disordersThromboembolic disorders

Ri k f ith l ti liti

9


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Risk of cancer with ulcerative colitis

(reproduced with permission, the AGA Teaching Project, 1992)

10


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Risk of colectomy with pancolitisRisk of colectomy with pancolitis

1% per yearFollowing years

3% each yearFollowing 4 years

9%Year of diagnosis

Risk of colectomyDisease duration

Relapse of ulcerative colitisRelapse of ulcerative colitis11


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e pse o u ce ve co sp

during pregnancyduring pregnancy

Trimester(after Willoughby & Truelove, 1980)

Relapse in

pregnant

women withUC, who were

remission at

conception

(%)

0

5

10

15

1st 2nd 3rd Post-partum

M P b l iM P t b l i d C h d C h

31


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M. ParatuberculosisM. Paratuberculosis and Crohnsand Crohns

diseasediseaseMycobacterium paratuberculosisMycobacterium paratuberculosis has beenhas beenthought to have an aetiological role inthought to have an aetiological role inCrohns disease as:Crohns disease as: it causes a similar disease in the smallit causes a similar disease in the smallintestine in cattle (Johnes disease)intestine in cattle (Johnes disease) it can be found in milkit can be found in milk it can be found in Crohns diseaseit can be found in Crohns disease tissue,tissue,although it is also found in otheralthough it is also found in other tissuestissues

M l i d IBDM l i d IBD

32


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Measles virus and IBDMeasles virus and IBD

Measles virus has been associated with CrohnsMeasles virus has been associated with Crohns

disease due to:disease due to: good epidemiological links betweengood epidemiological links between

perinatal measles infection and subsequentperinatal measles infection and subsequent

Crohns diseaseCrohns disease a possible increase in the incidence ofa possible increase in the incidence of

CrohnsCrohns disease in children of mothers whodisease in children of mothers who

had measles during pregnancyhad measles during pregnancy tissue studies suggest a higher thantissue studies suggest a higher than expectedexpected

proportion of patients withproportion of patients with Crohns diseaseCrohns disease

(Forbes, 1997)

Clinical presentation of CrohnsClinical presentation of Crohns21


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pp

diseasedisease DiarrhoeaDiarrhoea

Abdominal painAbdominal pain

BleedingBleeding

PyrexiaPyrexia Weight lossWeight loss

FistulaeFistulae

Perianal diseasePerianal disease General malaiseGeneral malaise

I ti tiI ti ti


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ColonoscopyColonoscopy

E d i f C h

13


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reproduced with permission, Schilleret al, 1986)

Endoscopic appearance of Crohns

disease

Figure 4.15 - Severe Crohn`s colitisFigure 4.15 - Severe Crohn`s colitis


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Figure 4.19 - Cutaneous opening of a perirectalFigure 4.19 - Cutaneous opening of a perirectalfistulafistula


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Figure 4.20 - Typical perianal changes of Crohn`sFigure 4.20 - Typical perianal changes of Crohn`sdiseasedisease


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CROHNS DISEASECROHNS DISEASE

R di lR di l


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-Radiology--Radiology-

Radiological features of Crohns14


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(reproduced with permission

from McGraw-Hill)

(courtesy of Dr Sten Norby

Rasmussen, Denmark)

disease

A t i l l ti f C h di

15


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Anatomical location of Crohns disease

Intestinal complications ofIntestinal complications of16


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p


FistulaeFistulae

AbscessesAbscesses

AdhesionsAdhesions

StricturesStrictures

ObstructionObstruction


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Risk of cancer with Crohns disease

18


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Risk of cancer with Crohn s disease

and ulcerative colitis

(adapted from Hamilton, 1985, with permission)

Systemic complications ofSystemic complications of19


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ArthritisArthritis

GallstonesGallstones

MalabsorptionMalabsorption

Lactase deficiencyLactase deficiency

Vitamin BVitamin B

1212 deficiencydeficiency

Renal stone formationRenal stone formation

Differences in clinical presentation betweenDifferences in clinical presentation between22


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ulcerative colitis and Crohns diseaseulcerative colitis and Crohns disease

* **Pus

* **Mucus** * *Blood

Stools

** * *Diarrhoea

**Fever

* ** * *General malaise

* * **Pain

Symptoms

Crohns diseaseUlcerative colitis

The number of * symbols indicates the frequency with which each

symptom is present


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Intestinal SemiologyIntestinal Semiology


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Intestinal SemiologyIntestinal Semiology

As you could kill timewithout injuring eternity

Henry David Thoreau

Colorectal cancer D f A i d i di d l d


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Def: Acquired genetic disease, due to prolongedDef: Acquired genetic disease, due to prolongedexposure to carcinogensexposure to carcinogens

EpidemiologyEpidemiology The 4th malignant localization after lungs, stomach, sin. 10% of total deaths by cancer in developed countries Increase cases of morbidity and mortality, affecting

1:20 persons with a growth of economic standards. sex: more frequent in men than women race: white > black, asian Geographical variability: increase > 30/100.000 in

North America, West Europe, Australia, New Zeeland;

decrease in less developed countries. In Romania - 15-20/100.000 Age: exponential rise over 50 years of age Increased risk factors: high caloric report, sedentarism,

beer consumption,(smoking = adenomes)

Colorectal cancer-Etiopathogenesis


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Genetic FactorsGenetic Factors

Hereditary genetic anomalies (hereditary CCR - 25% of totalCCR); sporadic CCR, non-hereditary (75%).

Hereditary genetic anomalies confirm an increased susceptibility

for cancer.

Sporadic form: multi-stage process of carcinogenization with

accumulation of genetic anomalies under the action ofenvironemental factors,hereditary playing a minor role.

2 major forms of hereditary CCR: a) polyposis cancer ,syndroms

of familial adenomatosis polyposis- 1% cancer; b) HNPCC:

hereditary non-polyposis colorectal cancer - 5% din CCR

Molecular genetic events in evolution of colon cancer


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Genetic alterations in progression to colorectal cancer


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Genes altered in colon cancer


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TABLE 3 - 10. GENES ALTERED IN COLON CANCER

Gene ChromosomeSporadic tumors withalterations, %

Class Function

K - ras 12 50 Protooncogene Signal transduction

APC 5 60 Tumor supressor ?Cell adhesion

DCC 18 70 Tumor supressor ?Cell adhesion

p53 17 75 Tumor supressor Cell cycle control (G1/S arrest)

hMSH2 2DNA Mismatchrepair

Maintains fidelity of DN Areplication

hMLH1 3 DNA Mismatchrepair

Maintains fidelity of DN Areplication


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Colorectal Cancer - symptomatology-


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age >50 years, more frequent in men than in females.

Personal history: RCUH (post-colecystectomy) Family history- familial polyposis syndrome and Lynch

ASYMPTOMATIC-(the rate of doubling of the tumors of 2 years) Abdominal coilcative pain -subocclusive/occlusive syndrom

Change in bowel habits: constipation/false diarrhea Inferior digestive tract hemorrhage (rectorhagia) SG: weight loss/ important asthenia (anemia), loss of appetite S. given by distant causes: hepatic metastasis- jaundice; increase in

abdominal volumn carcinomatous ascites

Colorectal Cancer objectiveexamination-


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examination

normal

palpation: Tumoral formation (more often if of suboclusive

phenomenon)

SG: cashexia/ iron deficiency anemia picture: palor/ asthenie

headache/tachycardia, anginal pain/ platonychia

Hepatomegaly MTS hepatic/ increase in abdominal volume because ofcarcinomatous ascites

RECTAL TOUCH IS A PART OF GENERAL CLINICAL

EXAMINATION.

Mucocutaneous pigmentation in Peutz-Jeghers syndromeMucocutaneous pigmentation in Peutz-Jeghers syndrome


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Colorectal Cancer Paraclinical exploration


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Digestive endoscopy: anuloscopy, flexibil

rectosigmoidoscopy , colonoscopyEssential exam for diagnosis of intestinal

disease, completed with a histological exam

and therapy.

Flexible sigmoidoscopic view of the distal rectumFlexible sigmoidoscopic view of the distal rectum


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Colorectal Cancer paraclinical

l i


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exploration

Radiological examination of the colon is realized withBaSo4 through barium enema done with simple or double

contrast method.

Some Rx on empty bowel may show obstacle.

Colorectal Cancer paraclinical

l ti


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exploration

Barium enema

Colonic PolyposisColonic Polyposis


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Barium enema with double contrastBarium enema with double contrast


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Computerized Tomographic examination (ECHO) forComputerized Tomographic examination (ECHO) forevaluation of local extension and MTSevaluation of local extension and MTS


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Computerized Tomographic examination(ECHO) ForComputerized Tomographic examination(ECHO) Forevaluation of local extension and MTSevaluation of local extension and MTS


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Colorectal Cancer


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EEPIDEMIOLOGYIncidence in the world

Fourth malignantlocalization after lungs,stomach and breasts.

1023 000 new annual

cases and 529.000deaths

10% of total deaths dueto cancer in developingcountries.


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Europe in 2000highest increasedincidents 300.000new cases

Czech Republic,Czech Republic,Hungary, Slovakia,Hungary, Slovakia,Germany haveGermany haveincidents muchincidents muchhigher ( 2x thanhigher ( 2x thanUSA in general)USA in general)

N t i i th t d f l t l ( ll t ti tiN t i i th t d f l t l ( ll t ti ti


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Net increase in the tendency of colorectal cancer (all statisticNet increase in the tendency of colorectal cancer (all statistic

reports).reports).

Increase in colorectal cancer incidents with proximal localizationIncrease in colorectal cancer incidents with proximal localization

0

500000

1000000

1975 1990 1996 2003

with 4016 deaths in 2002 (OMS report) Romania registered awith 4016 deaths in 2002 (OMS report) Romania registered a


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( p ) g( p ) g

mortality rate of 11,3/100 000.mortality rate of 11,3/100 000.


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For both localizations levels of mortality presented an intentionalFor both localizations levels of mortality presented an intentional

increase of constancy and continuity, with a higher increased rate forincrease of constancy and continuity, with a higher increased rate for

colon cancer.colon cancer. In the last 40 years mortality doubled, an important increase inIn the last 40 years mortality doubled, an important increase in

comparison with other European countries.comparison with other European countries.

0

2

4

6

8

10

12

1969 1975 1996 2002

Mortalitate

Territorial distribution of mortality levels (standardized indicators) forTerritorial distribution of mortality levels (standardized indicators) for

colon and rectal cancer.colon and rectal cancer.


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Incidents higher in western part of the cities and in Bucharest.Incidents higher in western part of the cities and in Bucharest.

The study which took place between 1994-1996 using data acquiredThe study which took place between 1994-1996 using data acquiredfrom city hospitals from Moldova revealed a higher level of mortalityfrom city hospitals from Moldova revealed a higher level of mortalityfor colon cancer for cities Neam ,Galai, Botoani.for colon cancer for cities Neam ,Galai, Botoani.


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IRITABLE BOWEL SYNDROME


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Functionalgastrointestinaldisorders - a

frequent cause forreferral togastroenterologist

EpidemiologyEpidemiology


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-Prevalence: 10%-20% (5 and 65%);

-more frequent in women; (2:1);

-all age affected.

-20 - 30% presented to doctor

-1%-3% - GP consultation

SYMPTOMS BASED DEFINITION -whichdefinition?-


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DEFINITION -which definition?-


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DEFINITION -LIMITS-

S t b d d fi iti d t th


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Symptoms based definition due to the

absence of a specific biologic marker. Overlap between the definition of irritable

bowel syndrome and other functional

disorders. The present definition are not able to

differentiate between the subgroups of

IBS patients. The present definition criteria seem to

have a different gender sensibility.

ROME II DEFINTION

At l t 12 k hi h d t t b ti i


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At least 12 weeks or more, which need not to be consecutive, in

the proceeding 12 months of abdominal discomfort or pain that

has two out of three features: 1. Relieved with defecation; and/or

2. Onset associated with a change in frequency of stool; and/or

3. Onset associated with a change in form (appearance) of stool.

Symptoms that cumulatively Support the Diagnosis of Irritable

Bowel Syndrome:

Abnormal stool frequency (> 3 bowel movements/day and less than 3

bowel movements per week);

Abnormal stool form (lumpy/hard or loose/watery stool);

Abnormal stool passage (straining, urgency, or feeling of incomplete

evacuation);

Passage of mucus;

Bloatin or feelin of abdominal distension

DEFINITION


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Functional intestinal disorder in which

abdominal discomfort or pain is

associated with defecation or a changein bowel habit and with features of

disordered defecation.

PATHOPHYSIOLOGY

-MECANISMS-


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Digestive motility disorders;

Visceral hypersensibility;

Involvement of intestinal infection; Alimentary intolerance and allergy;

Alteration of perception due topsychiatric disorders.

PATHOGENIC MECANISMS- Intestinal hypersensibility -


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COMORBIDITY


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About 50% of IBS patients from primary care and gastroenterologyclinics have at least one comorbid somatic symptom.

Comorbidity substantially alters the quality of life of IBS patients and

adds an additional cost for its treatment.

The presence of commorbidity was suggested to be a new diagnosticcriterion.

Specific comorbide somatic condition are Fibromyalgia, Chronic

fatigue syndrome, Chronic pelvic pain, Temporo-mandibular joint

disorder. Overlap with other functional gastrointestinal disorders: functional

dyspepsia, non-cardiac chest pain, functional anorectal pain, fecal

incontinence.

COMORBIDITY


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Overlap with psychiatric disorders such as: depressive syndromes,

anxiety disorder, somatisation.

Figure 5.33 - Visceral sensationsFigure 5.33 - Visceral sensations


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Anorectal manometryAnorectal manometry Anorectal manometry catheterAnorectal manometry catheter


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Anorectal manometry cathetery Distal balloon 320 mlDistal balloon 320 ml

DiagnosisDiagnosis


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Alarm symptoms

onset in elderly;

increasing intensity;

waking up the patient;

fever;

Weight loss;

rectoragia;

Exclusion of other disease

INVESTIGATIONSINVESTIGATIONS


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Sedimentation rate, hemoleucogramSedimentation rate, hemoleucogram

Proctoscopy 45 ani)

coproculturecoproculture

Occult blood lossOccult blood loss

Colon spasticColon spastic


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N-benzoyl-L-tyrosyl-para-aminobenzoic acidN-benzoyl-L-tyrosyl-para-aminobenzoic acid


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Points to be discussed.Points to be discussed.

IntroductionIntroduction


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Introductiont oductio

ClinicalClinical

DifferentialsDifferentials

WorkupWorkup

TreatmentTreatment

Introduction:

Clinical term that encompasses defects occurring during the


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Clinical term that encompasses defects occurring during the

digestion and absorption of food nutrients by the gastrointestinal

tract.

The digestion or absorption of a single nutrient component

may be impaired, as in lactose intolerance in lactasedeficiency.

When a diffuse disorder such as celiac disease affects the

intestine, the absorption of almost all elements is impaired.

Pathophysiology:Patho

physiology:3 major phases of digestion and absorption of food3 major phases of digestion and absorption of food

t i lt i l


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materials.materials.

Luminal phaseLuminal phase: dietary fats, proteins, and carbohydrates: dietary fats, proteins, and carbohydratesare hydrolyzed and solubilized by secreted digestiveare hydrolyzed and solubilized by secreted digestive

enzymes and bile.enzymes and bile.

Mucosal phaseMucosal phase: relies on the integrity of the brush-border: relies on the integrity of the brush-bordermembrane of intestinal epithelial cells to transport digestedmembrane of intestinal epithelial cells to transport digested

products from the lumen into the cells.products from the lumen into the cells.

Post absorptive phasePost absorptive phase: reassembled lipids and other key: reassembled lipids and other keynutrients are transported via lymphatic and portalnutrients are transported via lymphatic and portal

circulation from epithelial cells to other parts of the body.circulation from epithelial cells to other parts of the body.

Pathophysiology of bacterial overgrowthPathophysiology of bacterial overgrowth


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Pathophysiology of lactase deficiencyPathophysiology of lactase deficiency


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Clinical:Clinical: symptomatologysymptomatology


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DiarrheaDiarrhea Diarrhea is the most common symptomatic complaint.Diarrhea is the most common symptomatic complaint. Diarrhea frequently is watery, reflecting the osmotic load receivedDiarrhea frequently is watery, reflecting the osmotic load received

by the intestine.by the intestine. Bacterial action producing hydroxy fatty acids from undigested fatBacterial action producing hydroxy fatty acids from undigested fat

also can increase net fluid secretion from the intestine, furtheralso can increase net fluid secretion from the intestine, further

worsening the diarrhea.worsening the diarrhea. SteatorrheaSteatorrhea

Steatorrhea is the result of fat malabsorption.Steatorrhea is the result of fat malabsorption. The hallmark of steatorrhea is the passage of pale, bulky, andThe hallmark of steatorrhea is the passage of pale, bulky, and

malodorous stools.malodorous stools.

Such stools often float on top of the toilet water and are difficult toSuch stools often float on top of the toilet water and are difficult toflush. Also, patients find floating oil droplets in the toiletflush. Also, patients find floating oil droplets in the toiletfollowing defecation.following defecation.

Weight loss and fatigueWeight loss and fatigue Weight loss is common and may be pronounced; however, patientsWeight loss is common and may be pronounced; however, patients

may compensate by increasing their caloric consumption, maskingmay compensate by increasing their caloric consumption, maskingweight loss from malabsorptionweight loss from malabsorption


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weight loss from malabsorption.weight loss from malabsorption.

The chance of weight loss increases in diffuse diseases involvingThe chance of weight loss increases in diffuse diseases involving

the intestine, such as celiac disease and Whipple disease.the intestine, such as celiac disease and Whipple disease.

Flatulence and abdominal distensionFlatulence and abdominal distension Bacterial fermentation of unabsorbed food substances releasesBacterial fermentation of unabsorbed food substances releases

gaseous products, such as hydrogen and methane, causinggaseous products, such as hydrogen and methane, causingflatulence.flatulence.

Flatulence often causes uncomfortable abdominal distention andFlatulence often causes uncomfortable abdominal distention andcramps.cramps.

EdemaEdema Hypoalbuminemia from chronic protein malabsorption or fromHypoalbuminemia from chronic protein malabsorption or from

loss of protein into the intestinal lumen causes peripheral edema.loss of protein into the intestinal lumen causes peripheral edema.

Extensive obstruction of the lymphatic system, as seen in intestinalExtensive obstruction of the lymphatic system, as seen in intestinallymphangiectasia, can cause protein loss.lymphangiectasia, can cause protein loss.

With severe protein depletion, ascites may develop.With severe protein depletion, ascites may develop.

AnemiaAnemia Depending on the cause, anemia resulting from malabsorption canDepending on the cause, anemia resulting from malabsorption can

be either microcytic (iron deficiency) or macrocytic (vitamin B-12be either microcytic (iron deficiency) or macrocytic (vitamin B-12deficiency)deficiency)


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deficiency).deficiency).

Iron deficiency anemia often is a manifestation of celiac disease.Iron deficiency anemia often is a manifestation of celiac disease.

Ileal involvement in Crohn disease or ileal resection can causeIleal involvement in Crohn disease or ileal resection can causemegaloblastic anemia due to vitamin B-12 deficiency.megaloblastic anemia due to vitamin B-12 deficiency.

Bleeding disordersBleeding disorders Bleeding usually is a consequence of vitamin K malabsorption andBleeding usually is a consequence of vitamin K malabsorption and

subsequent hypoprothrombinemia.subsequent hypoprothrombinemia.

Ecchymosis usually is the manifesting symptom, althoughEcchymosis usually is the manifesting symptom, althoughoccasionally, melena and hematuria occur.occasionally, melena and hematuria occur.

Metabolic defects of bonesMetabolic defects of bones Vitamin D deficiency can cause bone disorders such as osteopeniaVitamin D deficiency can cause bone disorders such as osteopenia

or osteomalacia.or osteomalacia.

Bone pain and pathological fractures may be observed.Bone pain and pathological fractures may be observed.

Malabsorption of calcium can lead to secondaryMalabsorption of calcium can lead to secondaryhyperparathyroidism.hyperparathyroidism.

Neurological manifestationsNeurological manifestations Electrolyte disturbances such as hypocalcemia andElectrolyte disturbances such as hypocalcemia and

hypomagnesemia can lead to tetany, manifesting as the Trousseauhypomagnesemia can lead to tetany, manifesting as the Trousseausign and the Chvostek signsign and the Chvostek sign


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sign and the Chvostek sign.sign and the Chvostek sign.

Vitamin malabsorption can cause generalized motor weaknessVitamin malabsorption can cause generalized motor weakness

(pantothenic acid, vitamin D) or peripheral neuropathy (thiamine),(pantothenic acid, vitamin D) or peripheral neuropathy (thiamine),a sense of loss for vibration and position (cobalamin), nighta sense of loss for vibration and position (cobalamin), nightblindness (vitamin A), and seizures (biotin).blindness (vitamin A), and seizures (biotin).

Physical findings:Physical findings: GeneralGeneral

Patients may have orthostatic hypotension.Patients may have orthostatic hypotension.

FatigueFatigue

Signs of weight loss, muscle wasting, or both may be present.Signs of weight loss, muscle wasting, or both may be present.

Patients may have signs of loss of subcutaneous fat.Patients may have signs of loss of subcutaneous fat.

Abdominal examinationAbdominal examination The abdomen may be distended, and bowel sounds may beThe abdomen may be distended, and bowel sounds may be

hyperactive.hyperactive.

Ascites may be present in severe hypoproteinemia.Ascites may be present in severe hypoproteinemia.

Dermatological manifestationsDermatological manifestations Pale skin may reveal anemia.Pale skin may reveal anemia.

Ecchymosis due to vitamin K deficiency may beEcchymosis due to vitamin K deficiency may be


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Ecchymosis due to vitamin K deficiency may beEcchymosis due to vitamin K deficiency may bepresent.present.

Dermatitis herpetiformis, erythema nodosum, andDermatitis herpetiformis, erythema nodosum, andpyoderma gangrenosum may be present.pyoderma gangrenosum may be present.

Pellagra, alopecia, or seborrheic dermatitisPellagra, alopecia, or seborrheic dermatitis

Neurological examinationNeurological examination Motor weakness, peripheral neuropathy, or ataxia mayMotor weakness, peripheral neuropathy, or ataxia may

be present.be present.

The Chvostek or Trousseau sign may be evident due toThe Chvostek or Trousseau sign may be evident due tohypocalcemia or hypomagnesemia.hypocalcemia or hypomagnesemia.

Cheilosis, glossitis, or aphthous ulcers of theCheilosis, glossitis, or aphthous ulcers of themouthmouth

Peripheral edemaPeripheral edema

TABLE 5-33. SELECTED SYMPTOMS AND SIGNS OF NUTRIENT DEFICIENCIES

Symptoms or sign Possible nutrient deficiencyWeakness, weight loss, musclewasting

Protein, calorie

Pallor Folate, iron, vitamin B12Follicular hyperkeratosis Vitamin A, vitamin CPerifollicular petechiae Vitamin C


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Perifollicular petechiae Vitamin C

DermatitisProtein, calorie, niacin, riboflavin, zinc,vitamin A, essential fatty acids

Bruising, purpuraEasily plucked, alopecia Vitamin C, vitamin KCorkscrew hairs, coiled hair Protein, zinc, biotin

Night blindness, keratomalacia,photophobia

Vitamin C, vitamin A

Conjunctival inflammation Vitamin AGlossitis Vitamin A, riboflavinBleeding or receding gums, mouthulcers

Riboflavin, niacin, folate, vitamin B12,protein

Decreased taste Vitamin A, vitamin C, vitamin K, folateBurning or sore mouth and tongue Zinc, vitamin A

Angular stomatitis or cheilosisVitamin B12, vitamin C, niacin, folate,iron

Tetany Riboflavin, niacin, pyridoxine, iron

Paresthesias Calcium, magnesiumLoss of reflexes, wrist drop, foot drop,loss of vibratory and position sense

Thiamine, pyridoxine

Vitamin B12, vitamin EDementia, disorientation Niacin, vitamin B12Ophthalmoplegia Vitamin E, thiamineDepression Biotin, folate, vitamin B12


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Massive small-bowel resection can causeMassive small-bowel resection can causesignificant malabsorptionsignificant malabsorption

TABLE 5-16. PREDICTED NUTRITIONAL OUTCOME IN PATIENTS WHO HAVE HAD MASSIVEINTESTINAL RESECTIO N


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Remaining Jejunal length, cm Colon Nutritional outcome

0-50 - TPN

+ TPN

51-100 - IVFM/TPN

+ Modified oral diet

101-150 - Regular or modified oral diet

+ Regular diet

151-200 - Modified oral diet

+ Regular diet

>200 - or + Regular diet


Differentials:Differentials:


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ZollingerZollinger-Ellison Syndrome-Ellison Syndrome

Other Problems to be ConsideredOther Problems to be Considered::

Amino acid deficiencies (cystinuria)Amino acid deficiencies (cystinuria)Cystic fibrosisCystic fibrosis

Hartnup diseaseHartnup disease

Tropical jejunitisTropical jejunitisWhipple diseaseWhipple disease

Workup :
http://www.emedicine.com/MED/topic2437.htmhttp://www.emedicine.com/MED/topic2437.htmhttp://www.emedicine.com/MED/topic2437.htmhttp://www.emedicine.com/MED/topic2437.htmhttp://www.emedicine.com/MED/topic2437.htmhttp://www.emedicine.com/MED/topic2437.htm


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TABLE 5-32. INITIAL EVALUATION OF PATIENT WITH POSSIBLEMALABSORPTION

History and Physical ExaminationInitial blood tests Follow-up laboratory tests

Complete blood count Serum ironProthrombin time Serum folate

Standard electrolytes Serum vitamin B12Calcium Serum vitamin AMagnesium Plasma 25-hydroxy vitamin DBlood urea nitrogen Urinary oxalate excretionCreatinine Stool for Sudan stainAlkaline phosphatase Stool for ova and parasites

CholesterolTotal protein and albumin

Imaging studiesImaging studies::

Small bowel barium studies.Small bowel barium studies.


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CT-scan of the abdomen.CT-scan of the abdomen.

Endoscopic retrograde cholangiopancreatogramEndoscopic retrograde cholangiopancreatogram

Plain abdominal x-ray film.Plain abdominal x-ray film.

Other studiesOther studies::

Tests of fat malabsorption.Tests of fat malabsorption.

D-xylose test.D-xylose test.

Test of carbohydrate absorption.Test of carbohydrate absorption.

Test of bile salt absorption.Test of bile salt absorption.

Schilling test.Schilling test.

ProceduresProcedures::

Upper endoscopy with small bowel mucosal biopsyUpper endoscopy with small bowel mucosal biopsy


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Upper endoscopy with small bowel mucosal biopsypp py p y Establishing a definitive diagnosis of malabsorption of theEstablishing a definitive diagnosis of malabsorption of the

mucosal phase often can be achieved by histologicalmucosal phase often can be achieved by histologicalexamination of biopsied mucosal specimens obtained duringexamination of biopsied mucosal specimens obtained duringroutine upper endoscopy.routine upper endoscopy.

Examples of conditions that can be diagnosed this way includeExamples of conditions that can be diagnosed this way includeceliac sprue, giardiasis, Crohn disease, Whipple disease,celiac sprue, giardiasis, Crohn disease, Whipple disease,amyloidosis, abetalipoproteinemia, and lymphoma.amyloidosis, abetalipoproteinemia, and lymphoma.

Histologic FindingsHistologic Findings:: Depending on the cause, theDepending on the cause, thehistologic features of malabsorption vary.histologic features of malabsorption vary. A frequently encountered histologic finding isA frequently encountered histologic finding is villousvillous

atrophyatrophy, which is seen in celiac disease,, which is seen in celiac disease, tropicaltropicalspruesprue,, viral gastroenteritisviral gastroenteritis,, bacterial overgrowthbacterial overgrowth,,

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