VIRANotes Transcriptions

Gen Path: GIT part 2

PPT: Doc Aira

SMALL & LARGE INTESTINES - Occurs when a segment of the intestines telescopes into the
immediately distal segment pulling with it its mesentery
A. INTESTINAL OBSTRUCTION:
Causes:
- SI are MOST often involved due to its relatively narrow
lumen. 1. Adults- may be due to an intraluminal tumor which serves as
the point of traction
1. Hernias – protrusion of a serosa-lined pouch of peritoneum (hernia
2. Infants & children – no underlying defect
sac) thru a weakened part of the wall of the peritoneal cavity
Some are associated with rotavirus infection
Acquired hernias:
- telescoping of 1 segment into another  obstruction 
MOST commonly occur anteriorly
infarction
1. inguinal canal - in infants – usually normal GIT
2. femoral canal - in adults – usually due to an intraluminal mass
3. 3.umbilicus
4. surgical scars
B. VASCULAR DISORDERS
External herniationincarceration  strangulation
infarction/necrosis Blood supply of the SI & LI:

2. Adhesions 1. Areas of bowel supplied by the superior mesenteric artery (SMA)

Causes: a. most of the SI

b. ascending and transverse colon up to the left colic flexure
1. Surgical procedures
(splenic flexure)
2. Infections
c. SMA & inferior mesenteric artery (IMA) overlap at the
3. Peritoneal inflammation- endometriosis
splenic flexure
Adhesions could be:
- Splenic flexure is a WATERSHED area
a. between bowel segments
b. adhesion to the abdominal walls 2.Areas of bowel supplied by the inferior mesenteric artery (IMA)
c. adhesion to the operative sites
a. descending & sigmoid colon
Internal herniation- when fibrous bridges create a closed loop through b. proximal rectum
which intestinal segments can slide and be trapped c. upper half of the anal canal

-fibrous adhesions could be a congenital Types of Infarction:

3. Volvulus- complete twisting of a bowel segment about its 1. Transmural infarct

mesenteric base of attachment
- Can cause both luminal & vascular compromise
- Most common location: sigmoid colon
- features of obstruction & infarction are present
- Full-thickness hemorrhagic infarction
- Usually involves small part of the small bowel
- Usually due to thrombosis of the SMA
- Splenic flexure is the site of greatest risk

2. Mural infarction – infarction of the mucosa & submucosa

Process:
1. complete twisting of a loop of bowel about its mesenteric 3. Mucosal infarction – infarction not extending beyond the
base muscularis mucosa
2. obstruction
3. infarction Both mural & mucosal infarctions are due to hypoperfusion states (e.g.
shock)
4. Intussusception

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 VIRANotes Transcriptions
Gen Path: GIT part 2
PPT: Doc Aira

Causes of acute ischemia involving small bowel ANGIODYSPLASIA

A. Acute mesenteric ischemia (50% of cases) - malformation of the submucosal & mucosal blood vessels
- MOST common location- cecum and right colon
1. 1.due to embolism from the left side of the heart to the SMA
- Usually occurs in the elderly
(atrial fibrillation is the MOST common predisposing
- Increase wall stress in the cecum & right colon (because of
arrythmia)
the increased diameter) stretches the underlying vessels
2. 2.due to thrombosis of the SMA
- Angiodysplasia prevalence is < 1% in adult population
B. Nonocclusive ischemia (25% of cases) - Accounts for 20% of major episodes of lower intestinal
bleeding which may be chronic & intermittent or acute &
1. Hypotension secondary to heart failure (MOST COMMON) massive.
2. Hypovolemic shock
3. Patient taking digitalis (? vasospasm) MALABSORPTION

C. Mesenteric vein thrombosis (25%of cases) - Presents as chronic diarrhea

- Defective absorption of fats, proteins, carbs, electrolytes,
1. Thrombosis state- polycythemia vera minerals, vitamins (fat water-soluble) and water
2. Extension of renal cell carcinoma into the vena cava - Hallmark is STEATORRHEA- excessive fecal fat, bulky, frothy,
greasy, yellow or clay-colored stool
Pathogenesis:
Disturbance in any of the four phases of nutrient absorption, namely:
Two phases:
1. intraluminal digestion- proteins, fats & carbs
1. hypoxic injury – onset of vascular injury
2. reperfusion injury- initiated by restoration of the blood Diseases:
supply
1. chronic pancreatitis
The greatest damage occurs 2. cystic fibrosis
3. primary bile acid malabsorption
- free radical production
4. inflammatory bowel dse
- Neutrophilic infiltration
- Release of inflammatory mediators (TNF) 2. terminal digestion – occurs in the brush borders of the SI

Clinical findings of small bowel infarction Hydrolysis of carbs (disaccharidase) & peptides (peptidases)

a. sudden onset of diffuse abdominal pain- pain is Diseases:

disproportionate to the PE findings
b. bowel distention 1. celiac dse
c. bloody diarrhea 2. tropical sprue
d. ileus (absent bowel sounds) 3. autoimmune enteropathy
e. NO rebound tenderness early in infarction 4. disaccharidase def
f. profound neutrophilic leucocytosis 5. viral, bacterial & parasitic gastroenteritis
g. positive stool guaiac test 6. Inflammatory bowel dse

3. transepithelial transport- occurs in the SI

Differential diagnosis: Nutrients, fluids & electrolytes are transported across & processed

1. Acute appendicitis Diseases:

2. perforated ulcer
1. celiac dse
3. acute cholecystitis
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 VIRANotes Transcriptions
Gen Path: GIT part 2
PPT: Doc Aira

2. tropical sprue - Tissue transglutaminase (tTG; deaminating enzyme) in the

3. primary bile malabsorption lamina propria plays a pivotal role in producing celiac dse
4. carcinoid syndrome 1. 1. It deaminates mucosally absorbed gluten to produce
5. autoimmune enteropathy deaminated & negatively charged alpha gliadin
6. abetalipoproteinemia peptide
7. viral, bacterial, parasitic gastroenteritis 2. Deamidated gliadin peptides stimulate the immune
8. inflammatory bowel dse system
- they are phagocytosed by antigen-processing
4. lymphatic transport of absorbed lipids
cells in the lamina propria
Disease: - they are presented in complex with HLA-DQ2 or
HLA-DQ8 to gluten specific CD4 helper T cells
1. Whipple disease
CD4 T cells produce cytokines that release matrix proteases causing
General symptoms of malabsorption: cell death & degradation in the epith cells loss of villous surface in
the SI
1. diarrhea- from nutrient malabsorption & excessive intest
secretion Clinical findings:
2. flatus
3. abdominal pain 1. Steatorrhea
4. weight loss 2. weight loss
5. other symptoms related to vitamin & mineral def 3. failure to thrive in infants & children
4. pallor- combined anemias
5. findings related to water-soluble vit def

DIARRHEA Morphology:

Four major categories: - increased intraepithelial lymphocytosis, crypt hyperplasia &

villous atrophy
1. Secretory- characterized by isotonic stool & persists during fasting

2. Osmotic diarrhea-due to excessive osmotic forces exerted by

unabsorbed luminal solutes

- This abates with fasting

3. Malabsorptive diarrhea-associated with steatorrhea; relieved by

fasting

4. Exudative diarrhea- due to inflammatory dse, presence of purulent

bloody stools that continue during fasting

WHIPPLE DISEASE

CELIAC DISEASE - Rare, multivisceral chronic dse

- Caused by a gram (+) actinomycete, Tropheryma whippelii-
- Inappropriate immune response to gluten in wheat products PCR or culture
- Occurs at any age
Microscopic findings:
Pathogenesis:
1. blunting of villi of the SI
- Inappropriate T-cell & IgA-mediated response against gluten
in genetically predisposed persons
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 VIRANotes Transcriptions
Gen Path: GIT part 2
PPT: Doc Aira

2. foamy macrophages in the lamina propria which obstruct
lymphatics & reabsorption of chylomicrons 
malabsorption of fats
- The foamy macrophages contain PAS-positive diastase-
resistant granules that represent lysosomes stuffed
with partially digested bacteria
3. bacteria-laden macrophages can accumulate within
limited dse would trigger an overwhelming immune
response chronic inflammatory dse
Pathogenesis:
Both dses result from a combination of:
1. defects in host interaction with intestinal microbiota

mesenteric LN, synovial membranes of affected joints, 2. intestinal epith dysfunction

cardiac valves & brain 3. aberrant mucosal immune responses

Clinical findings: Triad: .

1. diarrhea CROHN DISEASE

2. weight loss Morphology:

3. malabsorption
Most common sites: (but may occur in any sites)

1. terminal ileum
INFLAMMATORY BOWEL DISEASE (IBD) 2. ileocecal valve

- Chronic condition resulting from inappropriate mucosal 3. cecum

immune response but these are NOT autoimmune dses Characteized by: presence of multiple, separate, sharply delineated
- More common in females, teens & early 20’s areas of dse SKIP lesions
- More common among Azkenazi Jews
- Long-term feared complication is development of neoplasia - Apthous ulcer- earliest lesion progress to multiple
ulcers coalesce forming serpentine ulcers oriented along
Two conditions:
the axis of the bowel
1. Crohn disease (CD) - Cobblestone appearance of the mucosa
2. Ulcerative colitis (UC) - Presence of fissures fistula tracts
- Thickened & rubbery intest wall
Distinction between these two depends on: - Creeping fat- extension of mesenteric fat to the serosal
a. Distribution of affected sites surface

b. morphologic expression of disease Microscopic:

1. Crohn dse/regional enteritis- may involve any area of the GIT tract & 1. abundant neutrophilic infiltrates
is typically transmural 2. damaged crypt epithelium; cyrpt abscesses
2. Ulcerative colitis – affects the colon & rectum & extends only to the 3. distorted mucosal architecture

mucosa & submucosa 4. epithelial hyperplasia- presence of gastric antral glands

( pseudopyloric metaplasia)
5. when Paneth cells are found in the left colon where Paneth
cells are normally absent- Paneth cell metaplasia
Hygiene theory: suggests that:
Noncaseating granuloma is a hallmark of Crohn dse (seen in 35% of
1. Improved food storage conditions & decreased food
cases) but the ABSENCE of granuloma should not preclude its
contamination may be related to increasing incidence of IBD
diagnosis.
2. Reduced frequency of enteric infectionsinadequate devt
Metastatic Crohn disease- cutaneous granulomas that form nodules
of regulatory processes that limit mucosal immune
responsesinfection with pathogens that should cause self-

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 VIRANotes Transcriptions
Gen Path: GIT part 2
PPT: Doc Aira

ULCERATIVE COLITIS Effect: absence of coordinated peristaltic contractions of the affected

colon (remains contracted) functional obstruction dilatation of
Morphology:
the colon (megacolon) proximal to the affected segment
- involves the colon (pancolitis) & rectum (ulcerative
Diagnosis:
proctosigmoiditis/ ulcerative proctitis)
- broad –based ulcers Document the absence of ganglion cells in the affected segment
- mucosal atrophy (contracted appearance)
- inflammatory process- limited to the mucosa
1. H&E stain of biopsies
- pseudopolyps- islands of regenerating mucosa
2. Immunohistochemical stains for acetylcholinesterase –
- toxic megacolon- damage of muscularis propria
ganglion cells stain positive
(neuromuscular defect)
Clinical findings:

1. failure to pass meconium

CONGENITAL ANOMALIES
2. obstructive constipation
1. Intestinal atresia- commonly affects duodenum
Complications:

2. Imperforate anus- MOST common form of congenital intestinal 1. enterocolitis- fluid % electrolyte imbalance
atresia 2. perforation peritonitis

3. Meckel diverticulum- Most common type of diverticulum Treatment: surgical resection of aganglionic segment
- solitary, located on the antimesenteric side of SI
- Rule of 2’s:
- Common location- 2 ft of the ileocecal valve
- About 2 cms in length
READ THE MICROPRINTS, TABLES, CHARTS & DIAGRAMS IN YOUR
- 2 x more common in males than females
BOOK, THIS COULD MAKE THE DIFFERENCE.
- lined by 3 layers of intestinal mucosa
- -due to failed involution of the vitelline ducts THANK YOU!
- symptoms may mimic acute appendicitis or intestinal obst

4. Hirschprung dse (congenital aganglionic megacolon)

- Incidence – 1/5000; 10% in patients with Down symdrome
(genetic component); penetrance is incomplete
- Pathology:
a. when migration of neural crest cells from cecum to
rectum is prematurely arrested
b. when ganglion cells undergo premature death
- affected distal segment lacks both:
1. Meissner submucosal ganglia
2. Auerback myenteric plexus

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