INTRODUCTION

The small intestine is the longest segment of gastro

intestinal tract,accounting for about two thirds of the total length. It
extends from the pyrolus to the ileocaecal junction.it is divided into
duodenam, jejunam and ileum. It is 6 mt long and 2.5-3 cm in
diameter. Surface area of the human small intestine mucosa averages
30 Sq metre.The main functions are digestion and absorption.It
receives bile juice and pancreatic juice through the pancreatic duct .
 SMALL INTESTINAL DISORDERS

 Celiac disease
 Chron’s disease
 Diverticular disease
 Gastroenteritis
 Intestinal Obstruction
 Malabsorption Syndrome
 Intestinal cancer
 CELIA DISEASE
DEFINITION
Celiac disease is a genetically predisposed auto immune disease in
which ingestion of gluten in diet causes immune-mediated mucosal damage in the
small intestine resulting in malabsorption and growth failure.
EPIDEMIOLOGY
 can develop at any age after child starts eating foods contain that gluten and
affects 1 in 100 persons world wide.
 Children with a first-degree relative having celiac disease have an increased risk
of developing celiac disease.
ETIOLOGY
 Genetic predisposition,ingestion of gluten,mucosal damage
 Presence of human Leukocyte antigen HLA DQ2 and DQ8 present in(25-30%
population)increases the risk by 3%
 Normal mucosa Flat mucosa

This Photo by Unknown Author is licensed under CC BY

PATHOPHYSIOLOGY
Etiological factors
Ingestion of gluten in diet
Immune reaction to gluten
Antibody formation &
Lymphocyte infiltration
Mucosal damage
Villus atrophy and flat mucosa
Malabsorption&osmotic diarrhea
Malnutrition and growth failure
MARSH CLASSIFICATION

Stage 0 : Normal mucosa

Stage 1 : Increased number of intra-epithelial lymphocytes
Stage 2 : Proliferation of crypts of lieberkuhn
Stage 3 : Partial or Complete villus atrophy
Stage 4 : hypoplasia of the mucosa
CLINICAL FEATURES
 Chronic diarrhoea
 Malabsorption
 Abdominal Distension
 Pain abdomen
 Vomiting
 Constipation
 Anorexia
 Ulcers
EXTRA INTESTINAL CLINICAL FEATURES

 Failure to thrive/poor weight gain/weight loss

 Short stature
 Delayed puberty
 Iron deficiency anemia
 Fatigue Osteoporosis
 Dental enamel defects
 Peripheral Neuropathy
 Dermatitis herpetiformis (itchy skin rashes)
CLINICAL TYPES
Typical CD : GI symptoms, malabsorption, growth failure
Atypical CD : No GI symptoms, extra-intestinal clinical
features
Silent CD : No symptoms,mucosal damage present,
diagnosed on investigations
Potential CD : No symptoms,no mucosal damage
diagnosed on serology and tests.
COMPLICATIONS
 Poor weight gain
 Malnutrition,iron deficiency anemia,Short stature
 Delayed puberty
 Celiac crisis,neurologic dysfunction
This Photo by Unknown Author is licensed under
CC BY
DIAGNOSTIC EVALUATION
 History collection
 Physical examination
 Anti tissue transglutaminase IgA antibodies titre 10 times upper normal limit
 IgA endomysial antibody
 Duodenal biopsy
 Gluten free diet- clinical improvement
DIFFERENTIAL DIAGNOSIS
 Post enteritis malabsorption
 Malnutrition
 Toddler’s diarrhoea
 Giardiasis
 Rare_ IBD, cystic fibrosis, immunodeficiency
MANAGEMENT
Avoiding gluten in diet
MANAGEMENT DURING CRISIS
 IV rehydration
 Monitor & Treat hypoglycemia
 Management of electrolyte imbalances ,Micronutrients
 IV cortici steroids,Antibiotics
 Gluten & Lactose free diet
 Blood and blood products
AVOID- wheat,rye,barley,oats,pasta,pizza,bread,baked goods
(cookies,cakes)
 CROHN’S DISEASE
DEFINITION
Cronh’s disease is an idiopathi,chronic,transmural
inflammatory process of the bowel that can affect any part of the
gastrointestinal tract from the mouth to the anus.
Most cases involve the small bowel,particularly the terminal
ileum.
PREVALENCE
 Common in western industrialized nations
 Males and females equally affected
 Smokers - high risk to develop
 Tends to develop initially in teens & twenties
ETIOLOGICAL FACTORS
 Mutations in the NOD2/CARD gene
 Anomalies in the XBP1 gene
 Environmental factors- organisms stimulates poorly regulated immune
response
 Smoking
 Microbes- Mycobacterium avium subspecies, paratuberculosis
CLASSIFICATION
According to area it affects
 Ileocolic crohn’s disease-(ileum & large intestine)-50%
 Crohn’s ileitis- 30%
 Crohn’s colitis - 20%
ACCORDING TO PROGRESSION

1.Stricturing
Disease causes narrowing of the bowel which may lead to bowel
obstruction.
2.Penetrating
Disease causes abnormal passage ways between the bowel and other
structures such as skin.
3.Inflammatory
Disease causes inflammation without causing strictures or fistulae.
 PATHOPHYSIOLOGY
Antigenic stimulation
Intestinal mucosa Gut immune system
Physiologic inflammation

Normal host Susceptible host(gene,envt)

Limited inflammation Uncontrolled inflammation

Healing with no tissue Extensive tissue injury

injury
Manifestations of signs & symptoms
 CLINICAL MANIFESTATIONS
 Diarrhoea, colicky abdominal pain, flatulence, dysphagia,weight
loss
 In severe cases- diarrhoea is bloody, contains mucus & occurs 10-20
times/day
Extra intestinal symptoms- Increase the risk of blood clots leads to
DVT, pulmonary embolism, auto immune hemolytic anemia.
COMPLICATIONS
 Stricture formation,thromboembolism
 Intestinal obstruction,small bowel cancer
 Fluid electrolyte imbalance
 Malnutrition,fistula & abscess formation
 SYSTEMIC COMPLICATIONS

JOINTS - Peripheral arthritis,ankylosing spondylitis,sacroiliitis,

finger clubbing
SKIN - Erythema nodosum,pyoderma gangrenosum,
thromboembolism
MOUTH- Ulcer
EYE - Conjunctivitis,uvetis,episcleritis
OTHERS- Gallstones,kidneystones,primary sclerosing,cholangitis,
osteoporosis.
 DIAGNOSTIC FINDINGS

 History collection & physical examination

 CBC, ESR, Serum chemistries
 Genetic studies
 Stool for occult blood
 Stool culture
 Capsule endoscopy
 Radiologic studies with barium contrast
 MANAGEMENT
NUTRITIONAL THERAPY
Oral fluids, high protein, high calorie diet with supplemental
vitamin therapy, iron replacement.
Parenteral nutrition if needed.
Avoid _ cool foods & smoking.
PHARMACOLOGIC THERAPY
 Aminosalicylates
 Antimicrobial agents (metronidazole )
 Corticosteroids drugs (prednisolone)
 Immunosuppressants
(Azathioprine,mercaptopurine,methotrexate,infliximab)
 Hydrocortisone- severe attack
 SURGICAL THERAPY
75 % Of patients needs surgery and many produce remission
and recurrence. The indications are as follows
 Drainage of abdominal abscess
 Failure to respond to conservative therapy
 Fistulas
 Inability to decrease corticosteroids
 Intestinal obstruction
 Massive haemorrhage
 Perforation
 Suspicion of carcinoma
TOTAL COLECTOMY WITH ILEOANAL RESERVOIR
The combination of the two procedures is performed
approximately 8 -12 wks apart. The initial procedure includes
colectomy, rectal mucosectomy, ileal reservoir construction ,ileoanal
anastomosis and temporary ileostomy.
The second surgery involves closure of the ileostomy to
direct stool towards the new reservoir.
TOTAL PROCTOCOLECTOMY WITH PERMANENT
ILEOSTOMY
It is the one stage operation involving the removal of the
colon, rectum and anus with closure of the anus. The end of the
terminal ileum is brought out through the abdominal wall and forms a
stoma.
TOTAL PROCTOCOLECTOMY WITH CONTINENT
ILEOSTOMY

The distal segment of the ileum is surgically split,a fold is

made and one way valve is created and sutured into place on the
abdomen. The pouch acts as a reservoir and is drained at regular
interval by insertion of catheter.
 DIVERTICULAR DISEASE

DEFINITION
Diverticular disease refers to the bulging pouch like
herniations (diverticula)in the GI wall push the mucosal lining through
the surrounding muscle.
Common sites- sigmoid colon
Typical sites- duodenum, jejunum
TYPES
1.Diverticulosis- presence of non inflammed diverticula
2.Diverticulitis - the inflammation of the diverticulum.
PREVALENCE
 Western , industrialized populations
 Consume of low fiber diet, high carbohydrate diet
 Incidence rises with increasing age & obesity
 Affects 5 % of the us population by age 40yrs &
 50% By age of 80 yrs
ETIOLOGY
1. High luminal pressures from a deficiency in dietary fiber intake
2. Loss of muscle mass and collagen with the aging process
 PATHOPHYSIOLOGY
lack of dietary fiber
slow down of transmit time
reabsorption of more water
decreased stool size
increased intraluminal pressure
diverticula formation
retention of stools & bacteria in the diverticulum
infection & inflammation of diverticula
formation of fecalith
inflammation and perforation
peritonitis and bleeding
TYPES
1.Extra luminal diverticula
2.Intraluminal diverticula
3.Juxta papillary diverticula
EXTRA LIMINAL DIVERTICULA
Produce outside the wall of the duodenum
INTRALUMINAL DIVERTICULA
1.Intraluminal diverticula protrude into the inside of the wall
of the duodenum.
2. Rare condition
3.Caused by congenital abnormality
4.Bulging sacs develops inside of the duodenum
JUXTA PAPILLARY DIVERTICULA
Arises within 2 to 3 cm of the ampulla of vater.

CLINICAL MANIFESTATIONS
 Abdominal pain,
 Nausea, vomiting, diarrhoea
 Fever, chills, anorexia
 Feeling of fullness early on during a meal
 Bloating loud rumbling sounds accused by gas
If untreated leads to septicemia
COMPLICATION
ACUTE
 Haemorrhage,
 perforation - leads to general peritonitis,
local suppuration
CHRONIC
 Pericolic abscess- leads to fistula & local
suppuration
Stricture- intestinal obstruction
Most common cause of GI hemorrhage
DIAGNOSTIC FINDINGS
 History collection
 Physical examination
 Complete blood cell count, blood culture, ESR
 Urine analysis
 Ultrasound,
 abdominal X-ray
 CT scan with contrast, MRI
 Capsule endoscopy

DIFFERENTIAL DIAGNOSIS
Perforated neoplasm, small bowel ulceration, large polyps
MEDICAL MANAGEMENT
General management
1.Bed rest , initially clear fluid, then high fiber low fat diet
2.severe symptoms- nil per oral, IVFluid administration,
naso gastric suctioning
Medicines
1.Broad spectrum antibiotics
2.opoids for pain relief
3.anti spasmodics - propantheline bromide, oxyphency
climine
4.stool softeners -Dulcolax
SURGICAL MANAGEMENT
Abscess- CT guided percutaneous drainage

Surgery

1. One stage resection and primary end anastomosis

2. Multi stage procedure for complications such as obstruction or
perforation.
 GASTRO ENTERITIS
DEFINITION
Gastroenteritis is inflammation of the gastro intestinal tract,
involving the stomach, intestine or both. Usually resulting in
diarrhoea ,abdominal cramps, nausea, and possibly vomiting.
frequently termed as “stomach flu” or “gastric flu”.
CAUSES
 Bacteria - bacterial toxins (10-20 %)
Eg. E.coli , vibrio cholerae, salmonella,
shigella etc
 Virus - rota virus, Astro virus, enteric
adenovirus(70%)
 Parasite - Giardia, entamoeba,
strongyloides,cryptosporidium
 Chemicals - lead poisoning
 Drugs - eg. Antibiotics
INFECTIOUS GASTRO ENTERITIS
E.Coli infection
common problem for travellers to countries with poor sanitation.
Camphylobacter infection
 found in animal faeces
 infection caused by contaminated food, water, under cooked
meat ,improper hand washing
Cryptosporidium infection
parasites are found in the bowels of human’s and animals .
Infection caused by swimming in contaminated pool and accidently
swallowing water.
Salmonellosis and Shigellosis
CLINICAL MANIFESTATIONS
 Nausea, vomiting, diarrhoea
 Anorexia, fever, headache,
 Abnormal flatulence, abdominal pain, cramps, melena
 Fainting and weakness, heart burn.

Complications
Dehydration- fluid and electrolyte imbalance
High fever- blood 7 mucus in diarrhoea, blood in vomit, severe abdominal
pain, swelling
DIAGNOSIS
 History collection
 Physical examination
 CBC, serum electrolytes, BUN
 Acid base status
 Stool examination and culture

MANAGEMENT
 Bed rest, increased fluid intake
 Oral rehydration solution
Severe dehydration- IV Fluids, monitoring intake and output
Medicines
Doxycycline, Tetracycline, Norfloxacin, ciprofloxacin,
Metronidazole, Trimethoprim, Ofloxacin, Azithromycin,
Erythromycin.
Injections- Inj. Ceftriaxone ,Inj.Cefotaxime

PREVENTION
 Proper hand washing
 Maintain good environmental sanitation
 Drinking boiled water
 MALABSORPTION SYNDROME
Definition
Mal absorption is failure of the intestinal mucosa to absorb single or
multiple nutrients efficiently. Absorption of amino acids, fats, sugars, or
vitamins may be impaired resulting in an inadequate movement of nutrients
from the small intestine to the blood stream or lymphatic system.
Causes
1.Digestive failure caused by enzyme deficiencies
2.Structural defects
3.Mucosal abnormality
4.Infective agents
5.Systemic diseases affecting GIT
Causes
1.Digestive failure caused by enzyme deficiencies
-Pancreatic insufficiencies, bile salt insufficiency
2.Structural defects
-IBD, Obstruction, fistula, diverticula, stricture
3.Mucosal abnormality
-celiac disease
4.Infective agents
-Intestinal tuberculosis, parasites
5.Systemic diseases affecting GIT
-Hypo/Hyperthyroid, DM, Malnutrition
PATHOPHYSIOLOGY
In celiac disease
presence of dietary gluten

injury to the mucosal villi

loss of absorptive surface

mucosa appears flat

deficiency in absorption

Occurrence of symptoms
Lactose deficiency
Lactose is an enzyme that splits non absorbable lactose
(disaccharide ) into absorbable monosaccharide,
Glucose and galactose.
Production may be deficient or another intestinal may inhibit the
enzyme.
Malabsorption may occur after gastrectomy

poor mixing of chyme with gastric secretion

post surgical malabsorption

In Zollinger Ellison Syndrome
increased acidity in duodenum

inhibits release of cholecystokinin

stimulates pancreatic enzyme secretion

pancreatic enzyme deficiency leads to

decrease breakdown of nutrients and malabsorption

A
Clinical manifestations
1.Gastro intestinal –weight loss, diarrhoea, flatulence
steatorrhea, glossitis, cheilosis, stomatitis.
2.Hematologic_ Anemia, haemorrhage tendency.
3.Musculoskeletal_Bone pain, tetany, weakness, muscle
cramps, muscle wasting
4.Neurologic_ Altered mental status, parasthesias,
peripheral neuropathy, Night blindness
5.Intugumentary_ bruising, dermatitis, brittle nails ,
hair thinning and loss
6.Cardiovascular_ Hypotension, Tachycardia, peripheral
edema
DIAGNOSTIC STUDIES
 History collection
 Physical examination
 Qualitative measurement of faecal material for fat
 D-xylose absorption -excretion test(carbohydrate absorption)
 3 kinds of breath test
 Bile acid breath test-bile salt malabsorption
 Triolein breath test- measures carbon dioxide excretion after ingestion of a
radioactive triglyceride
 Excretion of breath hydrogen- after ingestion of lactose
Sensitive, specific and non invasive test for lactose deficiency
Laboratory studies
*CBC,PT, serum vit –A, and carotene levels, serum
electrolytes, cholesterol, calcium.
*pancreatic function test
X-ray, ultrasound, endoscopy, capsule endoscopy, CT
Small intestine biopsy
Treatment
 Replacement of fluids, electrolytes, and nutrients
 Supplementation include-vitamins, minerals
 Diet_ Reducing gluten intake
 Antibiotics-(tetracycline, Inj.Ampicillin)
 Anti diarrheal agents
 INTESTIONAL OBSTRUCTION
DEFINITION
Intestinal obstruction occurs, when the intestinal contents cannot
pass through the gastro intestinal tract. The obstruction may occur in the small
intestine or colon and can be partial or complete.
CLASSIFICATION
1.Mechanical (dynamic)
Bowel capable of contracting normally or excessively proximal to a local
site of obstruction.
2.Non-Mechanical(adynamic)
Peristalsis may be absent or present in non-propulsive form (mesenteric
vascular occlusion, Pseudo obstruction).
Pseudo obstruction
It is an apparent mechanical obstruction of the intestine without
demonstration of obstruction by radiologic methods.
Causes
1.Dynamic
Gall stone, impaction of foreign bodies, obstruction
( worms ),stricture, malignancy, adhesion, hernia, intussusception.
2.Adynamic
Paralytic ileus, mesenteric vascular occlusion,
Pseudo obstruction, intra abdominal abscess, peritonitis.
Pathophysiology
obstruction in the small intestine
inhibition of movement of chyme
accumulation of the intestinal contents
near obstruction( fluid +gas)
Distention reduces absorption of fluids &
stimulates intestinal secretions
bacterial flourish stimulates additional secretion of fluids
Intraluminal pressure increase
increased capillary permeability
Cont..
extravasation of fluids & electrolytes into the
peritoneal cavity peritonitis

reduction in arterial & capillary pressure

hypotension & hypovolemic shock

inadequate blood supply

intestinal tissues become ischemic , necrotic

and rupture
Classification
On the basis of nature
1.Acute
2.chronic
3.Acute on chronic
4.Sub acute
On the basis of obstruction
1. Simple Mechanical
2. Strangulated
3. Closed loop
On the basis of etiology
1.Extraluminal
2.Intramural (causes from the wall)
3.Intraluminal (causes in the wall)
Acute obstruction
Usually occurs in small bowel, with sudden onset of symptoms.
Chronic obstruction
Usually seen in large bowel ,absolute constipation followed by
distension.
Acute on Chronic obstruction
Starts in large bowel but gradually involves in the small
intestine.
Simple mechanical obstruction
- Blockage occurs without vascular compromise
- Intussusception or shortening of the colon
I
Strangulated obstruction
1.Obstruction with compromised blood flow, occurs 25% of
patients with small bowel obstruction.
2.Usually associated with hernia, volvulus and intussusception.
3.It can progress to Infarction and gangrene in little as 6hrs.
4.venous obstruction occurs first, followed by arterial occlusion
resulting in rapid ischemia.
5.Ischemic bowel becomes edematous and infarcts leading to
gangrene and perforation.
In large bowel obstruction strangulation is rare.
Closed loop obstruction
 Specific type of obstruction
 Two point along the course of the bowel are obstructed at a single location thus
forming a closed loop.
Clinical manifestations
Cardinal features
 Pain-occurs suddenly &severe, colicky, centred
 Vomiting- interval, frequency depends on site
 Distension- depends on site
 Constipation
Others
visible peristalsis, bloating, fatigue, infrequent urination, dehydration,
hypokalemia, pyrexia, abdominal tenderness.
Diagnosis
 History collection
 Physical examination- borborigymi
 Radiological examination
_ abdominal x ray, CT Scan, sigmoidoscopy &colonscopy
Laboratory studies
CBC, BUN, Serum electrolytes, RFT
Medical management
*Decompression of bowel through a nasogastric tube.
*IVFluids replacement ,in needed electrolyte
replacement
*parenteral nutrition
Surgical management
*If the patient condition not improved deteriorates surgery is
performed.
*Resection and anastomosis( partial or total colectomy,ileostomy)
 SMALL INTESTINE CANCER
Definition
Small intestine cancer is a rare disease where cells in the
tissue of the small intestine change. They grow out of control and can
form a mass or tumour.
INCIDENCE
According to American cancer society, IN-US 2023
12,070 people diagnosed small intestine cancer 2,070 people, will die
of small intestine cancer.
Etiological and risk factors
 Exact cause not known
Several things can increase the chance of getting
 Age (average age at diagnosis is 60)
 Slightly higher risk in men
 Some genetic disorders
 Smoking and alcohol use
 High fat diet
 Living or working near large quantities of chemicals
Types of Small Intestine Cancer
1.Adenocarcinoma
These make up an estimated 30-40%. An adenocarcinoma starts
in the lining of the small intestine. At first it may look like a small ,
non cancerous growth called a polyp but over time it can turn into
cancer.
2.Sarcoma
Cancerous cells develop in the soft tissue of the small intestine.
3.Carcinoid tumour
These slow growing cancers often take root in the lower section
of the small intestine. They might also affect your appendix or rectum.
These tumors give off large amounts of certain body chemicals like
serotonin.
4.Gastrointestinal stromal tumors
Rare form of small intestine cancer. More than half of them
start in the stomach.
5.Intestinal lymphomas
A lymphoma is a cancer that starts in the lymphnodes. People
who develop them often have a type of immunodeficiency disorder.
Clinical Manifestations
Earlier stages- abdominal pain and discomfort
Others
Nausea, abdominal cramp, bloating, Appetite loss
In severe conditions
Fatigue, weight loss, weakness, Vomiting, anemia
and diarrhoea, blood or black stools, lump in the abdomen, Jaundice.
Diagnostic evaluation
History collection, Physical examination, CBC, LFT
X-ray, CT, MRI, PET, endoscopy, Barium swallow, capsule endoscopy,
Single Balloon enteroscopy, Spiral Enteroscopy.
TREATMENT
The treatment depends on the type of cancer and its
stages
SURGERY
surgical removal of the affected section and anastomosis of
the cut ends of the intestine.
CHEMOTHERAPY
Combination of medication used to kill fast
growing cells.
5 fluorouracil, Oxaliplatin, Irinotecan, Capecitabine
Targeted drug therapy
Focus on specific weakness present within cancer cells, used
for certain types of small bowel cancer, including gastro intestinal
stromal tumor amd lymphoma.
Immunotherapy
Helps to improve the immune system to fight against cancer.
Body’s immune system to might not attack cancer because the cancer
cells produce proteins that blind the immune system cells.
Possible nursing diagnosis
 Acute pain
 Deficient fluid volume
 Risk for infection
 Risk for imbalanced nutrition less than body requirement
 Diarrhoea
 Constipation
 Anxiety
 Knowledge deficient
 Impaired skin integrity
Conclusion
patients should be educated on the importance of dietary habits,
signs and symptoms of dehydration, and hand washing techniques, and
environmental sanitation focusing on preventive actions.