DISORDERS OF SMALL AND

LARGE INTESTINE
 MALABSORPTION
• Diminished intestinal absorption of one or more
dietary nutrients
• Commonly associated with steatorrhea, an increase in
stool fat excretion of >6% of dietary fat intake.lactose
intolerance isnt
• Form differential diagnosis for diarrhoea
• Diarrhoea as a smptom-decrease in stool consistency,
an increase in volume, an increase in frequency , or any
combination of these three change
• As a sign-quantitative increase in stool water or weight
of >200–225 mL or gram per 24 h on western diet
 Etiology of malabsorption
• Inadequate digestion
– Postgastrectomya
– Deficiency or inactivation of pancreatic lipase
• Exocrine pancreatic insufficiency Chronic
pancreatitis Pancreatic carcinoma
• Drugs—orlistat
• Reduced intraduodenal bile acid
concentration/impaired micelle formation
– Liver disease
• Parenchymal liver disease
• Cholestatic liver disease
– Bacterial overgrowth in small intestine:
Anatomic stasis
• Afferent loop Stasis/blind
• Loop/strictures/fistulae
• Functional stasis -Diabetes,Scleroderma
– Interrupted enterohepatic circulation of bile salts
• Ileal resection
• Crohn's diseasea
• Drugs (bind or precipitate bile salts)—neomycin,
cholestyramine, calcium carbonate
Impaired mucosal absorption/mucosal loss or
defect
– Intestinal resection or bypassa
• Inflammation, infiltration, or infection:
• Crohn's , Amyloidosis , Sclerodermaa Lymphomaa
Eosinophilic enteritis ,Mastocytosis Tropical sprue
,Celiac disease Collagenous sprue Whipple's
disease ,Radiation enteritis , Folate and vitamin B12
deficiency
• Impaired nutrient delivery to and/or from
intestine:
– Lymphatic obstruction
• Lymphoma ,Lymphangiectasia
– Circulatory disorders -
• Congestive heart failure ,Constrictive pericarditis
,Mesenteric artery atherosclerosis ,Vasculitis
• Endocrine and metabolic disorders
– Diabetes ,Hypoparathyroidism,Adrenal insufficiency
,Hyperthyroidism ,Carcinoid syndrome
 Signs and symptom of malabsorption
• Weight loss/malnutrition
• Diarrhoea-
• Flatus-fermentation of unabsorbed carbohdrate
• Glossitis,cheilitis,stomatitis-FE,B12,folate def
• Abdominal pain
• Bone pain-vitD,B12,folate,osteoporosis
• Tetany,paraesthesia-ca,mg malabsoption
• Azotemia,hypotension-fluid,electrolte depletion
• Bleeding-vitamin K def,hypothrombinemia
• Peripheral neuropathy-VITB12,thiamine deficiency
• Decreased libido,amenorrhoea-decreased
protein,decreased calories,secondar
hypopituirism
• Dermatitis-ZN,vit A,essential ats deicency
• Weakness-electrolyte depletion,anemia
• Night blindness,xeropthalmia-vit A
 Inflammatory bowel disease(IBD)
• immune-mediated chronic intestinal condition of
two types
– Ulcerative colitis (UC) and
– Crohn's disease (CD
• Most affected are jews and white people
• UC is more common in women
• Smoking and appendectomy thought to be
protective against UC
• Peak age is 15-30 and a second one at 60-80yrs
 Etiology and pathogenesis
• At risk is genetically predisposed individuals
• exogenous factors (e.g composition of normal
intestinal microbiota )
• Endogenous host factors (e.g., intestinal
epithelial cell barrier function, innate and
adaptive immune function) interact
• This causes a chronic state of dysregulated
mucosal immune function that is further
modified by specific environmental factors (e.g.,
smoking, enteropathogens)
 Ulcerative colitis
• Mucosal disease that involve rectum and
extend proximally to involve all or part of
colon
• 20% entire colon
• 40-50%-rectum and rectosigmoid
• 30-40% extend beyond sigmoid colon but not
entire colon
 Crohns disease
• Affect any part of GIT from anus to mouth
• 30-40% small intestine only
• 40-55% have both small and large intestine
• 15-20% colitis
• Unlike UC,spares rectum
• Segmental involvement
• Perirectal fistulas,fissures,abscess,anal stenosis in
1/3rd of patients
• May involve pancrease and liver
• Transmural involvement
• Apthous or small ulcer
• Cobblestone appearance of the intestine
• Focal inflammation and formation of fistula
tracts which will resolves b fibrosis and
stricturing of the bowel
• bowel wall thickens and becomes narrowed
and fibrotic, leading to chronic, recurrent
bowel obstructions
 Symptoms UC
• diarrhea, rectal bleeding, tenesmus, passage of mucus, and
crampy abdominal pain.
• The severity of symptoms correlates with the extent of
disease
• Fresh blood,tenesmus/urgency if rectum involved
• If disease extends beyond rectum blood is mixed with stool
or grossly blood diarrhoea
• Inflammed intestines lead to reduced transit times.with
severe disease patients pass liquid stool containing
mucus,ecal matter and blood
• Diarrhoea is nocturnal or post prandial
• Vague central andominal pain also present,severe pain if
disease severe
• Other smptoms of moderate or severe disease include
anorexia, nausea, vomiting, fever, and weight loss
• Laboratory =increased CRP,ESR,platelets,WBCS with
reduced albumin
• Complications
– Toxic megacolon-severe UC attacks ,bowel wall thins and
the mucosa is severely ulcerated.transverse or right colon
with a diameter of >6 cm. this may lead to perforation.
– Catastrophic hemorrhage
– Malignant strictures
 Crohns disease
• Two patterns fibrostenotic obstructing pattern or a
penetrating fistulous pattern
• Site of disease influences presentation
• Ileocolitis-
– commonest site is terminal ileum
– chronic history of recurrent episodes of right lower
quadrant pain and diarrhea
– right lower quadrant pain, a palpable mass, fever, and
leukocytosis. This ma mimic appendicitis.Pain is usually
colicky; it precedes and is relieved by defecation
– Low grade fever
– Weightloss-diarrhea, anorexia, and fear of eating
• inflammatory mass may be palpated in the right
lower quadrant of the abdomen. The mass is
composed of inflamed bowel, adherent and
indurated mesentery, and enlarged abdominal
lymph nodes
• Bowel obstruction -early stages of disease, bowel
wall edema and spasm produce intermittent
obstructive manifestations
• persistent inflammation gradually progresses to
fibrostenotic narrowing and stricture
• Fistula formation-bladder,skin,
• Jejunoileitis-Extensive inflammatory disease is
associated with a loss of digestive and
absorptive surface, resulting in malabsorption
and steatorrhea. Nutritional deficiencies can
also result from poor intake and enteric losses
of protein and other nutrients.
• Colitis and Perianal Disease-present with low-
grade fevers, malaise, diarrhea, crampy
abdominal pain, and sometimes hematochezia
• Laboratory,endoscopy and radiology-elevated
CRP,ESRlow albumin,anemia,leucoctosis
• Colonoscopy-rectal sparing, aphthous
ulcerations, fistulas, and skip lesions.
• Complications
– Fistula formation and perforation
– Intrabdominal or pelvic abscess
– intestinal obstruction, massive hemorrhage,
malabsorption, and severe perianal disease.
 ulcerative crohns
Gross blood in stool Yes Occasionally
Mucus Yes Occasionally
Systemic symptoms Occasionally Frequently
Pain Occasionally Frequently
Abdominal mass Rarely Yes
Significant perineal disease No Frequently
Fistulas No Yes
Small intestinal obstruction No Frequently
Colonic obstruction Rarely Frequently
Response to antibiotics No Yes
Recurrence after surgery No Yes
ANCA-positive Frequently Rarely
ASCA-positive Rarely Frequently
Endoscopic
Rectal sparing Rarely Frequently
Continuous disease Yes Occasionally
 Differential diagnosis
• Bacterial –
salmonella,shigella,E.coli,Campylobacter
• Mycobacterial-Tuberculosis
• Parasite-amoeba
• Virus-HIV,HSV,CMV
• Inflamamtory-appendictis,diverticultis,ischemic
• Neoplastic-metastatic,lymphoma
• Drugs-chemotherapy,NSAIDS
 Extraintestinal manifestations of IBD
• Dermatologic-
– erythema nodosum
– Pyoderma gangrenosum
• Rheumatologic
– -peripheral arthritis
– Ankylosing arthritis
• Ocular-
– Episcleritis,conjuctivitis,
• Primary sclerosing cholangitis (PSC) both intrahepatic and
extrahepatic bile duct inflammation and fibrosis, frequently
leading to biliary cirrhosis and hepatic failure;
approximately 5% of patients with UC have PSC, but 50–
75% of patients with PSC have IBD.
 treatment
• 5-ASAs AGENT
– e.g sulfasalazine,mesalazine. Are mainstay of
management.
– effective at inducing and maintaining remission in UC.
• moderate-to-severe UC benefit from oral or parenteral
glucocorticoids.
• Prednisone is usually started at doses of 40–60 mg/d
for active UC that is unresponsive to 5-ASA therapy.
• Parenteral glucocorticoids may be administered as
hydrocortisone, 300 mg/d, or methylprednisolone, 40–
60 mg/d.
• Others
– Methotrexate
– Azathioprine and
– 6mercaptopurine
• Biologics-anti-TNF eg infliximab,
 DIARRHOEA
• Upto 9L of fluid enter GIT in a day but only 200ml
excreted
• Diarrhoea-increased frequency and
consistency(unformed)
• Types
– Acute if less than 2 weeks
– Persistent if 2-4 weeks
– chronic if more than 4 weeks
• Causes
– Infections in 90%
– Others medicine,toxins,endocrine,tumors,ischemic
 INFECTIOUS DIARRHOEA
• 90% of all diarrhoea
• Commonly associated with fever,abdominal pain
and vomiting
• Acquired by fecoral transmission or ingestion of
food and water contaminated by human or
animal faeces
• Fecal microflora/normal flora suppresses growth
of pathogenic bacteria.
• disturbance e.gthrough antibiotic use leads to
diarrhoea through overgrowth of pathogenic
bacteria or reduced digestive function
• Infection occurs when ingested agents
overwhelm hosts immunity which include
– Gastric acid
– Digestive enzymes
– Mucus secretions
– Peristalsis
– Suppressive resident flora
• enterotoxigenic or enteroadherent pathogens
produce profuse watery diarrhoea. Associated
with marked vomiting but minimal or no fever.
• Cytotoxin producing microrganism all cause
high fever,abdominal pain
• Enterohaemorrhagic and enteroinvasive
bacteria and as well as entamoeba histolytica
causes bloody diarrhoea(dysentry)
 pathogenesis
a)Toxin producer(enterotoxigenic)-profuse
diarrhoea due to small
bowel hypersecretion occurs a few hours after
ingestion
preformed toxins eg bacillus
cereus,staphlococcus aureus.
b)Enteroadherent –enteropathogenic and
enteroadherent eg E.COLI,Giardia
c)Cytotoxin producers
C.difficileenetrohaemorrhagic E.coli
• Invasive organism
– Minimal inflammation eg rotavirus
– Variable inflammation eg
salmonellacampylobacter,yersinia
– Severe inflammation-shigella,E.histolytica,enetroinvasive
E.Coli
• Other causes of diarrhoea
• Drugs-NSAIDSanti-hypertensives,chemotherpay
• Ischemic colitis->50 year old,initially watery then
bloody diarrhoea
• Other toxins-organophosphate,mushroom
• Others-diverticulitis,graft versus host disease
 investigations

• If acute,short lived no need for tests

• But if any of below investigate via stool
microscopy
– Fever
– Immunosuppressed
– Increased WBC in stool
– Immunosppressed and elderly
• Tests include
– Stool analysis and culture
– Immunoassay-C.difficile
– Antigens-salmomella,rotavirus,norovirus
 treatment
• Mild,non febrile diarrhoea –antidiarrhoea eg
loperamide
• Moderatel ill-as above and add oral rehydration
• Severely ill,febrile or dysentry emperic therap
with fluoroquinolones eg ciprofloxacin
• If parasitic like amoeba,giardia use metronidazole
• For all dehydrated patients use oral rehdration or
IV fluid
 Chronic diarrhoea
• Secretory
• Osmotic
• Steatorrheal
• Inflammattory
• Dysmotile causes
• Factitional
• iatrogenic
 Chronic diarrhoea

• Medications-increase secretion and motility,changed gut flora

increased cell death or inflammation
• Osmotic-increased stool osmotic gap.symptoms decrease with
fasting.-ve fecal fat
– A)Lactose intolerance in 75% of non white population.may develop
after infection eg gastroenteritis(GE).present with bloating,abdominal
discomfort,diarrhoea moreso after ingesting milk/products.treatment
is avoid lactose
– Others –lactulose,sorbitol,fructose use
• Malabsoprtion-positive fecal fat,increased fecal osmotic gap
– i)Celiac disease in genetically predisposed patients who react to
gliadin found in gluten(wheat protein).small bowel
inflammation,infiltrate and crypt hyperplasia,villous atroph leads to
impaired absorption across the intestine
 • May cause iron and folate deficiency,osteoporosis
• Diagnosed via positive anti-endomsial antibodies
• Long term risk of small bowel lymphoma/adenocarcinoma
– ii)pancreatic insufficiency in chronic pancreatitis
– Iii)bacterial overgrowth e.g post gastric
bypass,slceroderma,diabetes mellitus,
– Iv)decreased bile acid-decreased synthesis in
cirrhosis,cholestasis
– V)short bowel from resection
– Vi)tropical sprue
– Vii)crohn disease
– Viii)whipples disease
• Inflammatory diarrhoea-positive fecal white blood
cells.fever,abdominal pain and bloody diarrhoea
– Infections-parasitic e.g cryptosporidium,isospora.TB,cmv
– Inflammattory bowel disease-crohns
– Radiation enetritis,ischemic etc
• Secretory diarrhoea-normal osmotic gap.no change
after overnight fasting.
– Hormone-carcinoid,VIPoma,thyroid,zollonger ellison
– Laxative abuse
– Neoplasm-carcinoma,lymphoma
– Decreased bile absorption eg post ileal resection
• Motility diarrhoea due to increased GUT
motility time-normal osmotic gap
– Irritable bowel syndrome
– Diabetic
– Scleroderma
– Hyperthyroidism
 investigations
• Fecal occult blood,white blood cells,+lactoferrin
then do stool culture or colonoscopy
• If positive fecal fat only investigate for
malabsoprtion eg celiac,pancreatitis,
• If none of above and has normal osmotic gap
consider motility/secretory and do colonoscopy
or ct scan,hormone levels to rule out tumors
• If high osmotic gap-consider laxative abuse or
lactose intolerance
 constipation
• Straining,hard/lumpy stool,incomplete evacuation,manual
evacuation of stool or frequency of stool <3/week
• If acute consider obstruction e.g sigmoid
volvulus,stricture,adhesion etc
• Etiology moreso for chronic constipation
– Functional-slow transit eg diabetic gastroparesis
– Medication-opiod,CCB,NSAIDS,TCA,antipsychotic
– Metabolic/endocrine –hypothroid,DM,electrolyte e.g low
Ca,Mg,K
– Neurologic-parkinsons,spinal cord injury,autonomic neuropath
• Investigate for the specific cause
• Incase of red signs e.g weight loss,anemia colonoscopy.ct
scan abdomen
 treatment
• Bulk laxative-increase stool bulk and motility
eg methylcellulose,isphaghula husk
• Osmotic laxative-increase fecal water volume
eg lactulose,Mg/Na phosphate
• Stimulant laxative-increase gastric motility e.g
senna,bisacodyl
• Enema/suppositories-phosphate,mineral
oil,soap etc.given rectally
 Adynamic ileus
• Loss of intestinal peristalsis in absence of
mechanical obstruction
• Precipitants include intrabdominal
surgery,peritonitis,severe medical
illness,hypokalemea
• Symptoms include
nausea/vomiting,hiccups,abdominal
discomfort,absent bowel sounds