anatomy, physiology & pathology of SI,

1. Diseases of colon and rectum:
Diseases of small intestine
Name: Nur Aisyah binti Idris

2. Contents
• Anatomy
• Physiology
• Disorder:
– Crohn’s disease
– Intestinal tuberculosis
– intestinal ameobiosis
– Campylobacter
– Salmonellosis
– Diverticula
– mesenteric ischemia
– Intestinal fistula
– Celiac disease
– Bacterial overgrowth
– neoplasm

3. Anatomy
• Small intestines extends from pylorus to
ileocaecal junction.
• Practical purposes- starting from
duodenojejunal flexure till caecum.
• Small intestine consists of proximal 2/5
jejunum & distal 3/5 ileum.6m in length
• Jejunum reside in the left side of the
peritoneal cavity & ileum on the right side.

4. Anatomy
A. Duodenum:
 Retro-peritoneal
 Supplied by the celiac artery & SMA
B. Jejunum:
 Occupies upper left of the abdomen
 Thicker wall and wider lumen than the
ileum
 Mesentery has less fat and forms only 1-2
arcades
C. Ileum:
 Occupies the lower right; has more fat and
forms more arcades
 Contains Payer’s patches
 Ileum & jejunum is supplied by the SMA
Mesenteric border of the
intestine gets more blood supply
compared to anti-mesenteric
border

5. • Venous drainage
through sup. Mesenteric
vein
Lymphatics:
• Lymph drainage occur
through lymphatic vessel
• Lymhmesenteric
LNcisterna
chylithoracic ductLt
subclavian vein
Nerve supply:
• Parasympathetic- vagus
• Sympathetic- splanchnic

7. Function
• Digestion and absorption
• Metabolism of plasma lipoproteins
• Endocrine function
• Immune function

8. CROHN’S DISEASE
• Regional enteristis
• Chronic full thickness
inflammatory process
• More prevalent in
Ashkenazi Jewish
• Female > male, 2x higher
smokers
• Breast feeding is
protective
Aetiology
• Incompletely understood
but involve interplay of
genetic & environmental
factor.
• Familial association (30x
in siblings / 13 x in 1st
degree relatives).(
NOD2/CARD15 gene)
• smoking
• Higher socioeconomic
status

9. pathogenesis
 CD is associated with a defect in
suppressor T cells, which act to
prevent escalation of
inflammatory process

10. Pathology
• Terminal ileum mc involve.
• Macroscopic: fibrotic thickening
of intestinal wall with a narrow
lumen & fat wrapping, dilated
bowel proximal to stricture &
deep mucosal ulceration,
cobblestne app., transmural
inflammation, skip lesion.
• Microscopic: focal area of chronic
inflm. Involving all layers with
lymphoid aggregates & non
caseating giant cell granuloma.
Clinical features
• Intermittent colicky lower abd.
Pain, diarrhea, weight loss.
Extraintestinal manifestation
• Related to disease
activity:Erythema nodosum,
pyoderma
gangrenosum,arthropathy, eye
complication, apthous ulceration,
amyloidosis.
• Unrelated to disease activity: Gall
stone, renal calculi, primary
sclerosing cholangitis, chronic
active hepatitis, sacroilitis
complication
• Colitis, rectal disease,
obstruction, hollow viscus
fistulae, nutritional deficiencies.

11. Investigation:
• CBC, endoscopic, imaging.
Treatment:
• Steroid, Antibiotic, aminoglycoside,
Immunomodulatory agents,
Monoclonal antibody, Nutritional
support, surgery.
Prognosis:
• No cure for the disease
• 10-20% come with relapses &
recurrent
• But repeated treatment & surgical
procedures give good prognosis
Non-operative management of Crohn’s
Disease:
Endoscopic treatment
 balloon dilatation of fibrostenotic
disease  symptomatic improvement
Indication for surgery
• Recurrent intestinal obstruction
• Bleeding
• Perforation
• Failure of medical therapy
• Intestinal fistula
• Fulminant colitis
• Malignant changes
• Perianal disease
Great range of operation is performed
depending on disease pattern
• Ileocaecal resection
• Segmental resection
• Colectomy& ileorectal anastomosis
• Subtotal colectomy & ileostomy
• Temporary loop ileostomy
• Proctocolectomy
• strictureplasty

12. Intestinal Tuberculosis
• It is secondary to pulmonary
tuberculosis.
• Commonly involve in ileoceacal
region
• Types:
– Ulcerative
– Hyperplastic
• Clinical features:
– Abdominal pain
– Diarrhea
– Abdominal distension
– Nonspecific symptoms
• Signs
– Malnourished & pale
– Visible peristalsis
– Distended bowel loop
– Rolled up omentum
– Mass in RIF/ lumbar region
• Management
– No int. obstruction ATT
– Obstruction:
• Solitary stricturoplasty
• Multiple at long interval
stricturoplasty
• Multiple at short
segmentresection
– Surgical treatment of hyperplastic TB
• Limited resection
• ATT
• Nutritional supplementation
• Blood transfusion

13. Comparison of two form of intestinal tuberculosis
ulcerative hyperplastic
Aetiology
Site
Virulence of organism
Resistance of body
Pathology
Clinical features
Complications
Investigation
Barium studies
CXR & sputum AFB
Scndry to pulm. TB
Terminal ileum
More virulent
Very poor
Multiple ulcerations in the
terminal ileum with/ wo LN
involvement. Ulcers are
transverse. Serosa reddened &
edematous
Symps. Of TB, diarrhea, blood &
mucus in stool
Acute: ulcer perforation
Chronic: healing ulcer result in
stricture of terminal ileum 
SAIO
Demonstrate strictures
Positive
It may be primary intestinal TB, due
to M. Bovis.
Ileocaecal region
Less virulent
Good
Low grade, chronic continuous
inflammation involving IC region.
Abd. Pain & diarrhea (initially)
Fever, weight loss & SAIO (later)
Nodular, mobile, firm mass in RIF
which later produces SAIO
Demonstrate: contracted caecum,
pulled up caecum, luminal obs.,
obtuse IC angle
negative

14. Intestinal ameobiasis
• An infection with Entamoeba
histolytica.
• Transmitted through
contaminated drinking water
• Can cause colonic ulcer
described as ‘bottlenecked’
• Ulcer have yellow necrotic
floor, from which blood & pus
exude.
• Can mimic UC
• Pericolitis is common & may
result adhesion int. obst.
• Ameobiasis may cause liver
absceses & amoeboma
• Clinical features:
– Bloody diarrhea
– Severe hemorrhage
– Stricture
– Perforation
• Inv: endoscopic biopsies or
fresh hot stool
• Treatment: metronidazole
400-600mg TID x 10days
• Diloxanide furoate 500mg TID
for 10days
• Surgery is frought with danger
as the bowel is to friable.

15. campylobacter
• Infection with
Campylobacter jejuni
• Mc form gastroenteritis in
UK
CF
– Dairrhea
– Abd. Pain
– Mimic acute abdomen
• May also resemble UC
• INV: stool culture
• Treatment: supportive,
usually resolve w/o
antiboitic
Yersinia
• Yersinia enterocolitica
• Infect terminal ileum,
appendix, a.colon, mesenteric
LN
• Can cause a granulomatous
inflammatory process (mimic
CD)
• CF:
– Fever
– Gastroenteritis
– Persistterminal
ileitisperforate
• INV: stool culture, serological
• Treatment: normally self
limiting, respond to
cotrimoxazole/
chloramphenical

16. Salmonellosis, typhoidsalmonellosis
• Salmonella are family of gram –ve rods
• Salmonella GE typically caused by s.
enteritidis from poultry (self
limiting)headache, fever & watery
diarrhea.
• When
severehospitalization+antibiotic+iv
fluid
• Diagnosis: stool culture
typhoid
• Typhoid feverS.typhi
• CF:
– Fever
– Abd.pain after IP(10-20 days)
– Distension, diarrhea,
splenomegaly, ‘rose spots’ on
abdomen.
• Complication
– Paralytic ileus
– Intestinal haemorrhage
– Perforation
– Cholecystitis
• Invasion of systemic circulationsevere
gram-ve sepsis & septic shock
• Metastatic sepsis
– Septic arthritis
– Osteomyleitis
– Encephalitis
– DIC
– pancreatitis
• Perforation of typhoid ulcer (3rd week)
• Diagnosis: culture of blood or stool
• Treatment: antibiotic-chloramphenicol
• Perforation-surgery to wash out & closed
perforated ulcer

17. Diverticula
• Hollow out-pouchings
• Common structural abnormality
occur from esophagus-
rectosigmoidal junction.
• classified:
– Congenital-all 3 coats of bowel are
present in the wall (Meckel’s
Diverticulum)
– Acquired-no muscularis layer
present ( sigmoid diverticula)
Jejunal diverticula
• Arises from the mesenteric side of
the bowel
• Can vary in size & multiple
• Clinical features:
– asymptomatic
– Malabsorption
– Acute abdominal emergency
(perforate)
• Investigation:
– Radiological imaging
• Treat:
– elective resection of affected small
bowel
– If perforate  resection &
anastomosis & stoma formation.

18. Meckel’s diverticulum
• A persistent remnant of
vitellointestinal duct
• Present in about 2% of
population
• Found on antimesenteric side of
ileum at 2feet from IC valve and
2inches long
• 20% cases heterotrophic
epithelium
• It contains all 3 coats & have its
own blood supply.
• Vulnerable to obstruction &
inflammation.
• If MD in an inguinal / femoral
hernia Littre’s hernia
• Can present clinically:
– Hemorrhage
– Diverticulitis
– Intussusception
– Chronic ulceration
– Intestinal obstruction
– Perforation
• Treat:
 Meckel’s diverticulectomy
 Should not amputated its base &
invaginate
 Should excise by resecting &
suturing at the base or liner
stapler cutter
 If base is indurated limited
small bowel resection +
anastomosis

19. Mesenteric ischemia
• Mesenteric vascular disease
classified as acute intestinal
ischemia:
– With/w/o occlusion,
– venous, chronic arterial,
– central / peripheral
• Superior mesenteric vessel most
likely to be affected by
embolization/thrombosis.
• Occlusion of SMA thrombosis
• Middle colic artery emboli lodge
• Inferior mesenteric involvement
clinically silent
• Sources of embolization of SMA:
– LA ass. With fibrillation, mural
MI, artheromatous plaque from
aortic aneurysm, mitral valve
vegetation ass. With
endocarditis
• Primary thrombosis:
artherosclerosis, thromboangitis
obliternas
• Primary thrombosis of SMV occur in
association: factor v leiden, Portal
HTN, portal pyaemia, sickle cell
disease, women take OCP
• Occlusion hemorrhagic
infarctionintestine & its
mesentery become swollen &
edematous blood stained fluid
exudes peritoneal cavity & bowel
lumen
• Main trunk SMA infarction covers
area from duodonejejunal flexure to
splenic flexure

20. • CF: sudden onset of acute
abdominal pain ( atrial
fibrillation/atherosclerosis),
persistent vomiting &
defecation (early), then
passaged of altered blood
hypovolemic shock
• O/E: mild abdominal
tenderness , rigidity (late)
• Pain central & out of
propotion of physical findings
• Inv: CBC- profound neutrophil
leukocytosis
• Abdominal radiograph-
absence of gas in the
thickened small intestine,
presence of gas bubble in
mesenteric vein
• Treatment: early cases:
resuscitate, embolectomy via
the ileocolic artery/
revascularization of SMA
• Late cases: resected affected
bowel, anticoagulation should
be give early in post-op period
• Iv alimentation required 
extensive enterctomy
• Selected cases small bowel
transplantation

21. Intestinal fistula
• Abnormal
communication
between 2 portion of
intestine, between
intestine & other
hollow vicus/ skin of
abd. Wall
• Involve skin &
intestines
enterocutaneous fistula
• Classification
– Anatomical
• Internal: colovesical fistula
• External: duodenal, jejunal
fistula
• Mixed: crohn’s disease
– Depending on contents
• Low output: <200ml
• Moderate output 200-500ml
• High output: >500ml

22. • Etiology:
– Iatrogenic
– Stump blow out
– Inadequate resection of
diseased segment
– Instrumentation
– spontaneous
• Management:
– Recognition and etiology
– Phase of stabilisation
– Nutrition
– Investigative phase
– Phase of definitive
management:
• Surgery
• Skin care
• Abdominal wall defect

23. Celiac disease
• Most common cause of
malabsorption in UK
• Characterised by
hypertrophic small bowel
mucosa + atrophic villi &
deep cypts
• Caused by gluten
• Genetic association with
HLA B8
• Children: steartorrhea &
growth retardation
• Adults: diarrhea, loss of
weight, anaemia
Diagnose:
– endoscopy duodenal biopsy
– Antiendomysial antibody
tests
• Increased risk of SB
lymphoma &
adenocarcinima
• Extraintestinal mnfstn:
dermatitis herpetiformis,
neurological problem
Treatment: withdrawn gluten
from diet
• Surgery malignancy

24. Tumors
• Small bowel tumors are rare
• Benign
– Peutz-jeghers syndrome
• Malignant
– Adenocarcinoma
– Carcinoid tumor
– Lymphoma
– GIST
Benign
• Majority of small bowel neoplasm
are benign
• Adenomas, lipomas,
hemangiomas, neurogenic
tumors
• Frequently asymtomatic &
identified incidentally
• Can present with intersusception,
small bowel obstruction,
bleeding, anaemia
• Inv: capsule endoscopy & small
bowel endoscopy
• Symptomatic lesion can be
treated by small bowel resection
& anastomosis.

25. Peutz-jeghers syndrome
• Autosomal dominant disease
• Melanosis of the mouth & lips
& multiple hamartomatous
tumour like malformation.
• Melanin spot also can occur
on digits & perianal skin.
• Gene STK11 on chromosome
19
• Consequence of complication
of bowel obstruction &
development of wide range of
cancers
• Malignant changes rarely
occur
• Resection may be indicated:
– Heavy & persistent
bleeding
– Intususception
– Heavy involve segments of
small intestine
• May be remove by enterotomy
/ laparotomy snared via a
colonoscope

26. Malignant
• Rare & classically present late
• Often diagnose after surgery for
small bowel obstruction
• 4 types that account over 99% of
small bowel malignancies.
Adenocarcinoma
• More often found in jejunum
than ileum
• Etiology unknown but mc in pt :
CD, coeliac disease, FAP & Peutz
Jeghers syndrome
• CF: anaemia, overt GI bleeding,
intususception, obstruction
• Prognosis: poor espcially pt with
CD
• Treatment: resection of 5cm of
non involved bowel either side of
lesion & the affected mesentery
• Right hemicolectomy if tumors at
distal ileum.

27. Carcinoid tumor
• Neuroendocrine tumor occur throughout GIT
• Mc appendix, ileum, rectum
• Arise from Kulchitsky cells at the base of
intestinal crypts
• Primary: usually small, significant LN metastases
• May produce dense fibrosis in surrounding
tissues distortion & scarring of bowel
• Can produce vasoactive peptides: serotonin,
histamine, prostaglandin, kallikrein,
• Liver mets carcinoid syndrome become
evident
CF:
• reddish-blue cyanosis, flushing attacks, diarrhea,
borborygmi, asthmatic attack, pulmonary &
tricuspid stenosis
Inv:
• octreotide scanning extent of disease
• Plasma markers tumor bulk (chromogranin A
concentration) disease recurrence
Treatment: primary surgical resection
• Mets hepatic resection
• Octreotide can be give to prevent carcinoid
crisis
• Tumors not sensitive to chemo /radiotherapy
Lymphoma
• Small bowel lymphoma may be primary,
mc secondary to systemic lymphoma.
• Mc in pt CD & immunodeficiency
syndromes
• Hodgkin’s lymphoma rare to affect
small bowel
• Most western type of lymphoma  non-
hodgkin’s type B lymphoma
• CF: anemia, bleeding, perforation,
anorexia, weight loss
• T-cell lymphoma pt with coeliac
disease
• CF: worsening diarrhea, PUO, local
obstructive symptoms
• Mediterranean lymphoma north Africa,
middle east
• Burkitt’s lymphoma aggressively affect
IC region ( children)
• Treatment: chemotherapy
• Surgery : obstruction, perforation ,
bleeding

28. GIST
• Mesenchymal tumors
• Distinction between benign
& malignant is difficult
• Increase in size & high level
of c-kit (CD117) staining ass.
With malignant potential
• Mc found in stomach, can
also found in other parts of
gut
• Mc 50-70 years
• Unknown cause but pt with
neurofibromatosis may
have risk to develop
• CF: asymptomtic, lethargy,
pain, nausea, haematemesis,
melaena
Treatment:
• surgery removing GIST
(radioresistant)
• Glivec (imatinib) tyrosine
kinase inhibitor, effective in
advanced cases

29. Short bowel obstructuion
aetiologies
• Intarluminal:foreign
bodies, gallstones,
meconium
• Intramural: tumor, CD
• Extrinsic: adhesion,
carcinomatosis, hernias

30. Pathophysiology

31. Clinical features
• Colicky abd. Pain
• Nausea
• vomiting (proximal)
• Obstipation
• Continous passage of
flatus /stool beyond 6-12
hrs (partial)
• Abd distaention ( distal
ileum)
• Bowel sound-
hyperactive(initial)decr
ease
• Lab: mild leukocytosis
• Hemoconcentration
• Electrolytes abnornal
• Strangulated:
– Abd pain disproportionate
to degree of abd. Finding
– Tachycardia
– Localised abd.tenderness
– Fever
– Leukocytosis
– acidosis

32. Diagnosis
• Plain abdominal x-ray
• CT scan

34. Treatment

35. References
• Bailey & love short practice
• Manipal manual surgery
• Schwartz 10th edition.

36. Thank you 