SMALL

INTESTINE
ZOO115 - Histology
SMALL INTESTINE

> divided into:

- duodenum (25-30 cm)
- jejunum (about first two-fifths of the
rest)
- and ileum
> the three segments merge imperceptibly and
have the same basic histological organization
> the principal site of absorption of food
products from gastrointestinal tract. (Total
length in man= 4 to 6m )
THE MUCOSA

> has various structural features which

considerably increase the luminal surface
area

> support the main function of the small

intestine - the absorption of the degraded
components of the food.
THE MUCOSA

Plicae circulares (of Kerkering)

- macroscopically visible, crescent-
shaped folds of the mucosa and
submucosa
- extend around one-half to two-thirds of
the circumference of the lumen of
the small intestine.
THE MUCOSA

Plicae circulares (of Kerkering)

- permanent structures, i.e. their
presence
does not depend on the state of
distension of the small intestine.
- are absent from the first few
centimetres
of the duodenum and the distal part
of
the ileum.
- increase the surface area of the
mucosa
THE MUCOSA
Intestinal villi (~1 mm long)
- increase the surface area by a factor of
~ ten.
- surface of the villi is formed by a
simple
columnar epithelium.
- Each absorptive cell or enterocyte of
the
epithelium forms numerous microvilli

(1 µm long and about 0.1 µm wide).

- Microvilli increase the surface area by
THE MUCOSA
Crypts of Lieberkühn
- openings of simple tubular glands
between the intestinal villi
- extend through the lamina propria
down
to the muscularis mucosae.
- Paneth Cells are (bottom of the
crypts)
- release a number of
antibacterial
substances, among them
lysozyme, and are thought to
THE MUCOSA
Crypts of Lieberkühn
- function: the secretion of "intestinal
juice" (about 2 liter/day),
- the only enzymes which can be
demonstrated in the intestinal juice
are
enteropeptidase (or enterokinase),

- activates the pancreatic

enzyme t
trypsin, and small amounts of
amylase.
THE MUCOSA
> endocrine cells secreting:
- Cholecystokinin stimulates the
secretion of digestive enzymes in
the pancreas and the contraction
of the gall bladder.
- Secretin stimulates the pancreas to
release "pancreatic juice", which
is
rich in bicarbonate ions. Secretin
also amplifies the effects of
cholecystokinin.
LAMINA PROPIA
> similar to the lamina propria of the
stomach, unusually cell rich.
> lymphocytes often invade the epithelium
or form solitary lymphoid nodules in
the
lamina propria.
> lymph nodules may form longitudinal
aggregations of 30-50 nodules in the
lamina propria of the ileum.
> These large aggregations are called
Peyer's patches.
MUSCULARIS MUCOSAE
- has two layers and extends into the
intestinal villi, where the smooth muscle
cells form a longitudinal bundle in the
centre of the villi.
- inner circular muscle and the outer ]
longitudinal muscle
SMALL INTESTINE

mucosa

submucosa

Muscularis
externa
SMALL INTESTINE
Small Intestine Disorders
Small intestine cancer
Small intestine obstruction ("high" mechanic ileus)
Obstruction from external pressure
Obstruction by masses in the lumen
Paralytic ileus Maropthisis
Crohn's disease Celiac disease
Carcinoid Meckel's
Diverticulum
Gastric dumping syndrome Mesenteric
ischemia Inguinal hernia Short
bowel syndrome
Infectious diseases
- Giardiasis
- Scariasis
- Tropical sprue
- Tapeworm infection
Coeliac disease
> is caused by a reaction to gliadin, a gluten
protein found in wheat.
> Upon exposure to gliadin, the enzyme tissue
transglutaminase modifies the protein, and
the
immune system cross-reacts with the bowel
tissue, causing an inflammatory reaction.
> That leads to flattening of the lining of the small
intestine, which interferes with the absorption
of nutrients.
> The only effective treatment is a lifelong gluten-
free diet.
> Biopsy of small
bowel showing
coeliac disease
manifested by
blunting of villi, crypt
hyperplasia, and
lymphocyte
infiltration of crypts,
consistent with
Marsh classification
III.
> normal small intestinal lining

> cross-section of healthy villi which project upward - like

slender fingers.

> When susceptible individuals with Celiac Sprue ingest

grains containing gluten (wheat, barley, and rye), a reaction
occurs in which the body is tricked into believing that these
villi are foreign, like an infecting virus.

> The body mistakenly mounts a counterattack by mobilizing

millions of white blood cells to attack the villi.
> biopsy of a patient with Celiac Sprue before treatment.

> tthe normal finger-like villi have been eroded away.

> The surface is flattened.

> The numerous black dots reflect an increase in white blood

cells which have come to attack the intestinal lining.

> By restricting gluten from the diet, the white blood cell
attack diminished and the villi can grow back and restore
normal absorption of nutrients.
Angiosarcoma

Microscopic view of the small intestinal mucosa adjacent to

the perforation.

Foci of small
intestinal mucosal
glands are seen,
surrounded by a
pleomorphic
cellular infiltrate
of malignant cells
and extensive
hemorrhage
(H&E, O.M ×100).
Title: Jejunal enteropathy associated
with human immunodeficiency virus
infection: quantitative histology.

By: P A Batman, A R Miller, S M Forster, J R

Harris, A J Pinching, and G E Griffin
SUMMARY
Jejunal biopsy specimens from 20 HIV positive male
homosexual patients were analysed and compared with
those of a control group to determine whether the
abnormalities were caused by the virus or by opportunistic
infection. The degree of villous atrophy was estimated
with a Weibel eyepiece graticulate, and this correlated
strongly with the degree of crypt hyperplasia, which was
assessed by deriving the mean number of enterocytes in
the crypts. The density of villous intraepithelial
lymphocytes fell largely within the normal range, either
when expressed in relation to the number of villous
enterocytes or in relation to the length of muscularies
mucosae. Villous enterocytes showed mild non-specific
abnormalities. Pathogens were sought in biopsy sections
and faeces.
SUMMARY
Crypt hyperplastic villous atrophy occurred at all
clinical stages of HIV disease and in the absence of
detectable enteropathogens. An analogy was drawn
between HIV enteropathy and the small bowel changes
seen in experimental graft-versus-host disease. It is
suggested that the pathogensesis of villous atrophy is
similar in the two states, the damage to the jejunal
mucosa in HIV enteropathy being inflicted by an immune
reaction mounted in the lamina propia against cells
infected with HIV.
RESULTS
> biopsy specimens showed variable degrees of villous
blunting and broadening, or were normal.
> villous enterocytes showed only mild focal nuclear
irregularity.
> Vacoulation of apical cytoplasm of enterocytes was
seen in some areas of a few biopsy specimens.
> Micosal crypts in some specimens seemed to be
elongated.
> apoptopic cells were observed in very few crypts.
> there was a mild or moderate increase in the density of
lymphocytes and plasma cells.
Fig. 1. Jejunal
mucosa from patients
with ARC showing
mild atrophy of villi
and hyperplasia of
crypts. Surface
enterocutes show
mild nuclear
irregularity.
Fig. 2. Jejunal
mucosa from patients
with AIDS showing
severe atrophy of villi
and hyperplasia
crypts
DISCUSSION
> The specimens exhibited a tendency of crypt
hyperplasia. There was no correlation between
the degree of crypt hyperplasia and the clinical
stage of HIV disease.
> There was a highly significant inverse
correlation between S:V and mean crypt length
in biopsy specimens from HIV antibody positive
subjects – that is, atrophy of villi correlated
strongly with hyperplasia of crypts.