TRACTO

GASTROINTESTINAL
ARTURO RFAEL HEREDIA
UNIVERSIDAD NACIONAL DE UCAYALI
HOSPITAL AMAZÓNICO DE YARINACOCHA
ESOFAGO
 CONTENIDO

 1.- ANOMALÍAS CONGÉNITAS.

 2.- LESIONES ASOCIADAS A
DISFUNCIÓN MOTORA.
 3.-VARICES ESOFÁGICAS.
 4.- ESOFAGITIS.
 5.- TUMORES.
 ESÓFAGO NORMAL
 Procede de la porción craneal del
intestino anterior.
 Es reconocible hacia la 3ra semana de
gestación.
 Tubo muscular hueco muy distensible.
 Va desde la epiglotis en la faringe
(C6), hasta la unión gastroesofágica al
nivel de las vértebras T11 o T12.
 Esófago normal
 Mide entre 10 y 11 cm. En el RN.
 En el adulto 25 cm.
 Para el endoscopista inicia a 15 cm. de
los dientes incisivos y termina a 40 cm.
 Zonas de estenosis luminal: proximal en
el cartílago cricoides, en la zona media
en el cayado aórtico y en el cruce
anterior del bronquio principal izquierdo
y la aurícula izquierda; y en la porción
distal el punto en donde atraviesa el
diafragma.
 ESÓFAGO NORMAL.
 DOS ÁREAS DE ALTA PRESIÓN:
1.- EES: un segmento de 3 cm. A
nivel del músculo cricofaríngeo.
2.- EEI: 2 a 4 cm. Proximal a la unión
gastroesofágica anatómica, a nivel
del diafragma.
 Esófago normal
 La pared del esófago consiste en :
1.- mucosa: superficie lisa brillante, rosado – oscura
(epitelio, lámina propia y muscular de la mucosa).
2.- submucosa: tejido conectivo laxo, vasos
sanguíneos y linfáticos, folículos linfoides, fibras
nerviosas- plexo de Meissner y glándulas sub
mucosas.
3.- muscular propia .(circular interna y longitudinal
externa) entre las dos capas el plexo de Auerbach
4.- adventicia. El esófago carece de serosa
 ESOFAGO NORMAL
 Funciones: conducir alimentos, prev difusion
pasiva de alimentos a la sangre y evitar el
reflujo.

 GASTRINA, ACETIL COLINA, SEROTONINA,

PROSTAGLANDINA F2, MOTILINA, SUSTANCIA P,
HISTAMINA, POLIPEPTIDO PANCREATICO
AUMENTAN EL TONO DEL EEI.

 OXIDO NITRICO, PEPTIDO INTESTINAL

VASOACTIVO DISMINUYEN EL TONO
EEI
 PATOLOGIA
 Todos los trastornos tienden a
producir sintomas similares:
 ACIDEZ, DISFAGIA, DOLOR Y/O
HEMATEMESIS.

 PIROSIS, dolor urente retroesternal.

 DISFAGIA, dificultad para deglutir.
 I.- ANOMALÍAS
CONGÉNITAS:

1.- ATRESIA Y FÍSTULAS.

2.- MEMBRANAS, ANILLOS Y

ESTENOSIS.
 ATRESIAS Y FISTULAS
 Se deben corregir pronto, son
incompatibles con la vida.

 Regurgitacion inmediata.

 Ausencia o agenesia
extremadamente rara.
 ATRESIAS Y FISTULAS
 La atresia y la formacion de fistulas son mas
comunes.
 Se asocia a fistula que conecta el fondo de saco con
un bronquio y traquea.
 Se asocia a cardiopatias, enf. Neurologicas, e.
genitourinarias y malf. Gastrointestinales.
 Presencia de una sola arteria umbilical.

 ASPIRACION Y SOFOCACION PAROXISTICA CON

ALIMENTO, NEUMONIA Y DESEQUILIBRIO
HIDROELECTROLITICO
Figure 11-5. The main varieties of tracheoesophageal fistula. Possible directions
of the flow of the contents are indicated by arrows. Esophageal atresia, as
illustrated in A, is associated with tracheoesophageal fistula in more than 85% of
cases. B, Fistula between the trachea and esophagus. In C, air cannot enter the
distal esophagus and stomach. Air can enter the distal esophagus and stomach
in D, and the esophageal and gastric contents may enter the trachea and lungs.
Classification (Gross's
Anatomical Classification)
 Type A: Esophageal atresia without
tracheoesophageal fistula.
 Type B: Esophageal atresia with
proximal tracheoesophageal fistula.
 Type C: Esophageal atresia with distal
tracheoesophageal fistula (most
common type) (85%).
 Type D: Esophageal atresia with
proximal and distal fistula.
 Type E: Tracheoesophageal fistula
without atresia. (Not shown)
 MEMBRANAS, ANILLOS
Y ESTENOSIS.
LAS MEMBRANAS:
 Protrusiones de la mucosa hacia la luz.

 Rara vez sobresalen 5 mm y 2 a 4mm de

grosor.

 Origen congenito, evolucion de esofagitis de

reflujo, enfermedad ingerto contra huesped,
enfermedades vesiculosas cutaneas.
 MEMBRANAS, ANILLOS
Y ESTENOSIS.
 Sindrome de Paterson - Brown -
Kelly o Plumer - Vinson :
MEMBRANA DEL ESOFAGO
SUPERIOR, ANEMIA
FERROPENICA, GLOSITIS Y
QUEILOSIS, aumento del riesgo de
carcinoma esofagico en porcion
retrocricoidea.
 MEMBRANAS, ANILLOS
Y ESTENOSIS.

LOS ANILLOS ESOFAGICOS:

 ANILLO A, por encima de la union
escamocolumnar.

 ANILLO DE SCHATZKI O ANILLO B,

en la union escamocolumnar.
 Anillos y membranas en mujeres por
encima de los 40 a. DISFAGIA.
 MEMBRANAS, ANILLOS
Y ESTENOSIS.
 LA ESTENOSIS ESOFAGICA:
 Engrosamiento fibroso de la pared, en
particular de la submucosa.
 Lesiones congenitas, reflujo
gastroesofagico, radicacion,
esclerodermia, ingestion de causticos.

 DISFAGIA PROGRESIVA.
Anneau de Schatzki
LESIONES ASOCIADAS A
DISFUNCION MOTORA
II.- LESIONES ASOCIADAS
A DISFUNCIÓN MOTORA

1.- ACALASIA.
2.- HERNIA HIATAL.
3.- DIVERTÍCULOS.
4.- DESGARRO ( SINDROME DE
MALLORY – WEISS ).
 ACALASIA
 Acalasia significa falta de relajacion, tres
anomalias principales:

1.- APERISTALSIS.
2.- RELAJACION PARCIAL E INCOMPLETA
DEL EEI CON LA DEGLUCION.
3.- TONO EN REPOSO AUMENTADO DEL
EEI.
 ACALASIA

 En la patogenia de la acalasia
primaria, disfuncion de las neuronas
inhibidoras que contienen ON y PIV.
 Alteraciones degenerativas de la
inervacion intrinseca, nervios vagos
extraesofagicos, nucleo dorsal del
vago.
 ACALASIA
ACALASIA SECUNDARIA en:
 la enfermedad del chagas, trypanosoma
cruzi destruye el pexo mioenterico.
 Poliomielitis y ablacion quirurgica,
nucleos motores.
 Neuropatia autonomica diabetica.

 Procesos infiltrantes: NM, amiloidosis y

sarcoidosis.
 LA MAYORIA PRIMARIA DE ETIOLOGIA
INCIERTA.
 ACALASIA
MORFOLOGIA:
 En la acalasia primaria, dilatacion
progresiva del esofago por encima del
EEI.
 Los ganglios mioentericos suelen estar
ausentes en el cuerpo del esofago.
 El revestimiento mucoso, inflamacion,
ulceracion y engrosamiento fibroso.
 ACALASIA
CARACTERISTICAS CLINICAS:
 Adultos jovenes, puede aparecer durante
la lactancia o la nines.
 DISFAGIA PROGRESIVA.

 Regurgitacion nocturna y aspiracion.

 Riesgo carcinoma de celulas escamosas

5%.
 Esofagitis por candida.

 Diverticulos esofagicos

 aspiracion con neumonia u obstruccion

de las vias aereas.
Spasme de l’oesophage
 HERNIA HIATAL
 Dos patrones anatomicos :
1.- hernia deslizante o axial, 95%.
2.- hernia hiatal paraesofagica.

 Solo el 9% de los adultos sufre pirosis.

 Complicaciones son numerosas:

1.- ulceracion hemorragia y perforacion.
2.- etrangulacion u obstruccion.
 Hiatal hernia,
esophageal A
(Schatzki's) and B
rings
Hernia hiatal
This x-ray shows the upper portion of the stomach protruding through the
diaphragm (hiatal hernia).
 DIVERTICULOS
 Evaginacion de todas las capas
viscerales.

 En epocas tardias, en tres regiones:

1.- diverticulo de Zenker o
faringoesofagico, EES.
2.- diverticulo por traccion, punto medio.
3.- diverticulo epifrenico imediatamente
por encima de EEI.
 Epiphrenic
Diverticulum

• Location is usually in
distal esophagus on
lateral esophageal
wall,
• right > left
• Often associated with
hiatal hernia
• Pulsion diverticulum
• False diverticulum
 DIVERTICULO
MEDIOESOFAGI
CO
 May be formed in
response to pull
from fibrous
adhesions following
lymph node infection
(usually TB).
 True diverticulum  =
contains all 3
esophageal layers.
 Or, may form from
increased
intraluminal
pressure and be
pulsion diverticula
Zenker’s
Diverticulum·        
Pharyngoesophageal
diverticulum·        
 Occurs in older
women·         Posteriorly
at site of Killian's
dehiscence = superior
boundary is
thyropharyngeal muscle
and inferior boundary is
cricopharyngeal muscle.
 Pulsion diverticulum·
 False diverticulum =
herniation of mucosa and
submucosa through
muscular layer
Diverticule de Zenker
 DESGARROS:
SINDROME DE
MALLORY - WEISS
 Desgarros longitidinales en el
cardias gastrico o en UEG.
 Consecuencias de nauseas y vomitos
intensos.
 Falla la relajacion antes de la onda
de contraccion antiperistaltica.
 De varios milimetros a cm. Afectan
la mucusa o perforan la pared.
 DESGARROS:
SINDROME DE
MALLORY - WEISS
 Responsables del 5 a 10 % de
hemorragia.

 Tratamiento con vasoconstrictores,

transfuciones y taponamiento con
balon.

 SINDROME DE BOERHAAVE, rotura

esofagica es muy rara.
III.-VARICES
ESOFÁGICAS
 III.-VARICES
ESOFÁGICAS
 Cuando la hipertension portal es
prolongada.
 En todas las zonas de comunicacion
porta - cava.
 Sistema porta > coronarias del
estomago > plexo de venas
subepiteliales y sub mucosas > vena
acigos >circulacion sistemica.
 III.-VARICES
ESOFÁGICAS
 Cirrosis alcoholica.
 La esquistosomiasis hepatica.

 Hematemesis masiva.
 Coexisten con gastritis, desgarro
esofagico, ulcera peptica.
 Escleroterapia, taponamiento con balon.
50% mueren, mas de la mitad recidiva
en un a.
IV.- ESOFAGITIS
 IV.- ESOFAGITIS.

1.- ESOFAGITIS POR REFLIJO

(ENFERMEDAD POR REFLUJO
GASTROESOFÁGICO).

2.- ESÓFAGO DE BARRETT.

3.- ESOFAGITIS INFECIOSA Y

QUÍMICA.
 1.- ESOFAGITIS POR REFLUJO
(ENFERMEDAD POR REFLUJO
GASTROESOFÁGICO).
 Reflujo del contenido gastrico, factores
causales:

1.- disminucion del mecanismo antirreflujo,

tono el EEI: depresores del SNC,
hipotiroidismo, embarazo, trastornos
esclerosantes sistemicos, alcohol tabaco,
SNG .

2.-hernia hiatal por deslizamiento.

 1.- ESOFAGITIS POR REFLUJO
(ENFERMEDAD POR REFLUJO
GASTROESOFÁGICO).

3.- Eliminacion inadecuada del

material refluido.

4.-Retraso del vaciamiento y aumento

del contenido gastrico.

5.- Reduccion de capacidad de

reparacion de la mucosa.
 1.- ESOFAGITIS POR REFLUJO
(ENFERMEDAD POR REFLUJO
GASTROESOFÁGICO).

 Anomalias histologicas caracteristicas:

 1.- celulas inflamatorias:
EOSINOFILOS, neutrofilos, exceso de
linfocitos.
 2.- hiperplasia de la zona basal, mas
del 20% del grosor epitelial.
 3.- elongacion de las papilas con
congestion capilar.
 1.- ESOFAGITIS POR REFLUJO
(ENFERMEDAD POR REFLUJO
GASTROESOFÁGICO).

 Adultos de mas de 40 a. puede

presentarse en lactantes y ninos.

 DISFAGIA, PIROSIS, REGURGITACION

DE LIQUIDO AMARGO,
HEMATEMESIS O MELENA.
 CRISIS DE DOLOR TORACICO
INTENSO.
 2.- ESÓFAGO DE
BARRETT.
 Por RGE de larga evolucion. Riesgo de
adenocarcinoma.
 La mucosa escamosa distal es sustituida
por epitelio columnar. Dos criterios para el
dx:
1.- demostracion endoscopica de tapizado
epitelial columnar por encima de union GE.
2.- metaplasia intestinal en biopsia de
epitelio columnar.
 2.- ESÓFAGO DE
BARRETT.
 Morfologia: mucosa ROJA
ATERCIOPELADA,

 mucosa esofagica, lisa rosa palido.

 Mucosa gastrica, pardo claro mas

lustrosa.
 2.- ESÓFAGO DE
BARRETT.
 Pacientes entre 40 y 60 a.
 modo ocacional en ninos.

 Sintomas de ulceracion local,

hemorragia y estenosis.
 Adenocarcinoma, mas 3cm. De EB,
Frecuencia de 30 a 40 veces mayor.
Barrett
 3.- ESOFAGITIS
INFECIOSA Y QUÍMICA.
Causas de inflamacion esofagica:
 1.- ingestion de irritantes.

 2.- terapia antineoplasica.

 3.- infeccion: bacterias, virus, etc.

 4.- infeccion micotica.

 5.- uremia.

 6.- EICH.penfigide, epidermolisis

bullosa.
Plummer-Vinson
Mycose oesophagienne
 V.- TUMORES.
1.- TUMORES BENIGNOS.
2.- TUMORES MALIGNOS:
- CARCINOMA DE CÉLULAS
ESCAMOSAS.
- ADENOCARCINOMA.
 1.- TUMORES
BENIGNOS.
 Leiomiomas.
 Fibromas, lipomas, hemangiomas,
neurofibromas, linfangiomas.
 Polipos fibrovasculares o lipomas
pediculados.
 Papilomas escamosos.
 Condiloma.
 Polipo inflamatorio
 pseudotumor inflamatorio.
 2.- TUMORES
MALIGNOS:
 En USA el carcinoma de esofago
representa el 6% de todos los
canceres de el TGI.
 Permanecen asintomaticos hasta
estadios tardios.
 Los carcinomas de celulas
escamosas constituyen el 90%.
 Carcinoma de celulas
escamosas.
 En adultos de mas de 50 a.
 la relacion hombre/mujer varia 2:1 a
20:1.
 Zonas de alta incidencia: Iran, China
central, Sud Africa y sur de Brasil.
Incidencia annual de 100 por 100 mil.
20% de todas las muertes por cancer.
 Mas comun en raza negra.
Carcinoma de celulas escamosas.
ETIOLOGIA Y PATOGENIA.

1.- FACTORES DIETETICOS:

 Deficits de vitaminas (A, C, riboflavina,
tiamina, piridoxina).
 Deficits de oligoelementos (cinc,
molibdeno).
 Contaminacion de alimentos por Hongos.

 Contenido alto de nitritos/nitrosaminas.

 Masticar betel.
 Carcinoma de celulas
escamosas.
2.- estilos de vida:
 consumo de bebidas muy calientes.

 Consumo de alcohol.

 Uso de tabaco.

 Medio ambiente urbano.

 Carcinoma de celulas
escamosas.
 3.- trastornos esofagicos.
 Esofagitis de larga evolucion.
 Acalasia.
 Sindrome de Plummer - Vinson.
 Carcinoma de celulas
escamosas.
 4.- Predisposicion genetica.

 Enfermedad celiaca de larga

evolucion.
 Displasia ectodermica.
 Epidermolisis bullosa.
 Predisposicio racial.
 Carcinoma de celulas
escamosas.
 Mutaciones puntiformes del gen p
53.

 Mutaciones en p16 INK4,

amplificacion de ciclina D1, de C-
MYC y del receptor del factor de
crecimiento epidermal.(EGFR).
 Carcinoma de celulas
escamosas.
Morfologia:
 inicia como neoplasia intraepitelial.

 20% en el tercio superior.

 50% en el tercio medio.

 30% en el tercio inferior.

 ADENOCARCINOMA

 Se origina en la mucosa de Barrett.

Riesgo 10%.
 La mitad de todos los canceres
esofagicos.
 Hombres de raza blanca mayores de
40 a.
 tabaco, obesidad, alcohol otros
factores de riesgo.
Malformaciones
del aparato
digestivo
 HERNIA DIAFRAGM
ATICA CONGENITA
: Cadáver de recién
nacido, con prolapso
del bazo y de asas
de intestino a la
cavidad torácica
izquierda, a través
de un orificio
indicado por una
sonda metálica. El
corazón y el timo
están desplazados al
hemitórax derecho.
HERNIA DIAFRAGMATICA
CONGENITA
 Se trata de un prolapso de vísceras
abdominales en una cavidad pleural

 a través de un foramen diafragmático

póstero-lateral (foramen de Bochdalek ), que
representa un conducto pleuro-peritoneal
persistente.

 (1 en 2.000 nacimientos), en el 80% de los

casos se produce al lado izquierdo.
 FISTULA TRAQUEO-ESOF
AGICA DISTAL CON ATR
ESIA ESOFAGICA
: Tráquea abierta por la
cara anterior; en la zona
ubicada entre ambos
bronquios fuentes la
pared de la tráquea se
continúa con la del
esófago, a través de una
fistula tráqueo-esofágica
inferior. Por detrás de la
porción superior de la
tráquea se ven los bordes
del segmento superior del
esófago que está dilatado
(termina en fondo de saco
ciego).
Formas
La persistencia anómala de comunicación entre el
esófago y la tráquea tiene 3 formas más comunes:
 Fístula tráqueo-esofágica distal con atresia
esofágica: la porción esofágica superior termina en
saco ciego; la porción inferior tiene una
comunicación fistulosa con la tráquea (más del 90%).

 Fístula tráqueo- esofágica proximal con atresia

esofágica: la porción superior del esófago está
comunicada con la tráquea a través de una fístula; la
porción inferior tiene un saco ciego por arriba, y está
normalmente comunicada con el estómago por abajo
(cerca del 1% de los casos)

 Fístula tráqueo-esofágica sin atresia esofágica :

fístula entre esófago y tráquea (forma en H, cerca
del 5% de los casos).
This is a normal esophagus
with the usual white to tan
smooth mucosa seen at the
left. The gastroesophageal
junction (not an anatomic
sphincter) is at the center, and
the stomach is at the right.
The upper GI endoscopic view
of the transition from tan
squamous mucosa to pink
columnar mucosa is seen
below.
This is Candida esophagitis. Tan-yellow plaques are
seen in the lower esophagus, along with mucosal
hyperemia. The same lesions are also seen at the
upper right in the stomach.
Acute esophagitis is manifested here by increased neutrophils in
the submucosa as well as neutrophils infiltrating into the
squamous mucosa at the right.
The lower esophagus here shows sharply demarcated
ulcerations that have a brown-red base, contrasted with
the normal pale white esophageal mucosa at the far left.
Such "punched out" ulcers are suggestive of herpes
simplex infection.
A herpetic ulcer is seen microscopically to have a sharp
margin. The ulcer base at the left shows loss of overlying
squamous epithelium with only necrotic debris remaining. In
the upper GI endoscopic view below, there are rounded,
erythematous ulcerations of the lower esophagus. Biopsies
of these lesions reveals intranuclear inclusions in squamous
epithelial cells indicative of herpes simplex virus esophagitis.
This patient was immune compromised from chemotherapy.
At high magnification, the squamous mucosa at the margin of
the herpetic ulcer shows pale pink "ground glass" inclusions
within squamous epithelial cells. Some of the inclusions are
clustered together-- multinucleation is another common viral
cytopathic effect.
Here are two more sharply demarcated "punched
out" ulcerations of the mid esophagus in an
immunocompromised patient with herpes simplex
infection.
Another cause for inflammation is a so-called "Barrett's esophagus" in which
there is gastric-type mucosa above the gastroesophageal junction. Note the
columnar epithelium to the left and the squamous epithelium at the right. This is
"typical" Barrett's mucosa, because there is intestinal metaplasia as well (note
the goblet cells in the columnar mucosa).
These two endoscopic views demonstrate Barrett esophagus areas
of mucosal erythema of the lower esophagus, with islands of normal
pale esophageal squamous mucosa. If the area of Barrett mucosa
extends less than 2 cm above the normal squamocolumnar junction,
then the condition is called "short segment" Barrett esophagus, as
shown below.
This is the view of the lower esophagus seen on endoscopy.
Note the areas of dark red friable mucosa representing Barrett
esophagus. Note the polypoid mass which on biopsy proved to
be a moderately differentiated adenocarcinoma. This patient had
a 30 year history of poorly controlled gastroesophageal reflux
disease.
At the lower end of the esophagus (which has been turned inside out at
autopsy) are linear dark blue submucosal dilated veins known as varices. In
patients with portal hypertension (usually micronodular cirrhosis from chronic
alcoholism), the submucosal esophageal veins become dilated (form varices).
These varices are prone to bleed.
Here is another varix near the gastroesophageal junction that is dark red
black because it has been bleeding. (The esophagus has been turned
inside out.) The plexus of veins also involves some of the upper stomach,
but it is generically called the esophageal plexus of veins and, hence,
bleeding here is termed esophageal variceal bleeding. Endoscopic views of
esophageal varices are shown below, with dilated veins bulging into the
lower esophageal lumen.
Below the squamous mucosa is an elongated, inflamed varix.
Variceal bleeding can be massive and difficult to control.
Inflammation and hemorrhage is seen here in the
region of a ruptured varix of the esophagus.
This radiograph taken
following barium
swallow demontrates
a stricture in the lower
esophagus, with
pooling of the contrast
above the point of
stricture. Such
stricture may
complicate conditions
such as scleroderma,
gastroesophageal
reflux disease, or
carcinoma.
A history of smoking and/or alcoholism is often present in patients with esophageal
squamous carcinoma, while a history of Barrett's esophagus precedes
development of esophageal adenocarcinoma in many cases. Here, an ill-defined
mass at the gastroesophageal junction produces mucosal ulceration and
irregularity, which led to the clinical symptoms of pain and difficulty swallowing.
This irregular reddish, ulcerated exophytic mid-esophageal mass as seen
on the mucosal surface is a squamous cell carcinoma. Endoscopic views
of an ulcerated mid-esophageal squamous cell carcinoma causing
lumenal stenosis are seen below. Risk factors for esophageal squamous
carcinoma include mainly smoking and alcoholism in the U.S. In other
parts of the world dietary factors may play a role.
At high power, these infiltrating nests of neoplastic cells have abundant pink
cytoplasm and distinct cell borders typical for squamous cell carcinoma.
Esophageal carcinomas are not usually detected early and, therefore, have a
very poor prognosis.
EL ESTOMAGO
ARTURO RAFAEL HEREDIA
 EL ESTOMAGO
CONTENIDO

I.- FISIOLOGÍA DE LA MUCOSA

GÁSTRICA.
II.- ANOMALIAS CONGÉNITAS.
1.- ESTENOSIS PILÓRICA.
III.- GASTRITIS.
IV.- ENFERMEDAD ULCEROSA PÉPTICA.
V.- PROCESOS DIVERSOS.
VI.- TUMORES.
 ESTOMAGO NORMAL

 Organo sacular de 1200 a 1500 ml. De

volumen.
 Capacidad superior a 3000 ml.
 Insisura angular, angulo a lo largo de la
curvatura menor.
 5 regiones anatomicas: cardias, fundus,
cuerpo, antro y piloro.
 Pared gastrica: mucosa, submucosa,
muscular propia y serosa.
 Fisiología de la mucosa
gástrica
SECRECION DE ACIDO.
Se divide en tres fases:
 La fase cefálica: iniciada por la visión, el
sabor, el olor, la masticación y la deglución –
MEDIADA POR ACTIVIDAD VAGAL.
 La fase gástrica: estimulación de los
receptores de estiramiento, mediada por
impulsos vagales, implica liberación de
GASTRINA (células G antrales – endocrinas)
favorecida por AA, estimulación vagal.
 La fase intestinal: Intervienen varios
péptidos además de la gastrina
 SECRECION DE ACIDO.
 La acetil colina estimula la célula parietal
…receptor muscarina 3
colinérgico….aumento del calcio
citosólico ….activación de la bomba de
protones.
 La gastrina activa un receptor …aumento
del calcio citosólico en células parietales.
 La gastrina y los aferentes vagales
inducen la liberación de histamina por
las ECL, estimulando el receptor H2, VIA
MAS IMPORTANTE DE ACTIVACIÓN DE
LA BOMBA.
 PROTECCION DE LA MUCOSA.
1.- Secreción de moco.
2.- secreción de bicarbonato.
3.- barrera epitelial.
4.- flujo sanguíneo.
5.- síntesis de prostaglandinas.

LA GHRELINA, regula el crecimiento

corporal y el apetito.
 PATOLOGIA
ANOMALIAS CONGENITAS.

ESTENOSIS PILORICA, mas frecuente

en hombres, uno de cada 300 a 900
recien nacidos.
REGURGITACIÓN, VOMITOS
PERSISTENTES EN PROYECTIL SIN
BILIS, en la segunda o tercera semana.
PERISTALTISMO VISIBLE, MASA
OVOIDE.
Estenosis pilórica adquirida del adulto
 GASTRITIS

 Este diagnóstico se emplea

demasiado y se pasa por alto con
frecuencia.
 Inflamación de la mucosa gástrica.

 GASTRITIS AGUDA.
 GASTRITIS CRONICA
 GASTRITIS AGUDA
 Proceso inflamatorio agudo de
naturaleza transitoria.
 Se acompaña de hemorragia, erosión
mucosa – HDA.
 PATOGENIA: Se asocia AINES,
Alcohol, tabaco, antineoplásicos,
uremia, infecciones, estrés intenso,
isquemia y shock, intento de suicidio,
irradiación-congelación, traumatismo,
gastrectomía distal.
 GASTRITIS AGUDA
 MORFOLOGÍA, en FORMAS LEVES
edema y congestión en la lámina propia.
Epitelio intacto, algunos neutrófilos.
 Neutrófilos por encima de la membrana
basal es anormal…ACTIVIDAD.
 Daño mayor, erosión y hemorragia.
 EROSIÓN: pérdida del epitelio
superficial sin atravesar la muscular
mucosae.
 GASTRITIS AGUDA
 La hemorragia puede ocurrir de
manera independiente y genera un
punteado de manchas oscuras.
 La coexistencia de erosión y
hemorragia se denomina:
GASTRITIS HEMORRÁGICA
EROSIVA AGUDA.
 GASTRITIS AGUDA
MANIFESTACIONES CLÍNICAS:
 Asintomática.
 Dolor epigástrico variable.
 Náuseas y vómitos.
 Hemorragia franca.
 Hematemesis masiva.
 Melena.
 Pérdida de sangre potencialmente fatal.
 GASTRITIS CRÓNICA
 Cambios inflamatorios mucosos
crónicos que pueden conllevar a atrofia
mucosa y metaplasia intestinal,
generalmente en ausencia de
erosiones.
 Los cambios epiteliales se pueden
convertir en displásicos y ser la base
para desarrollo de un carcinoma.
 En occidente los cambios histológicos
indicadores de gastritis supera el 50%.
 GASTRITIS AGUDA
 Asociaciones etiológicas:
1. Infección crónica por Helicobacter pylori.
2. autoinmune – anemia perniciosa.
3. Toxicos – alcohol, humo del cigarrillo.
4. Postquirúrgicas, post antrectomía y reflujo
de bilis.
5. Motora y mecánica, obstrucción, bezoares
y atonía gástrica.
6. Radiación.
7. Procesos granulomatosos.
8. Otros.
 GASTRITIS AGUDA
 Infección por Helicobácter pylori:
1. Gastritis crónica – relación causal
fuerte.
2. Enfermedad ulcerosa péptica- RCF.
3. Carcinoma gástrico – RCF.
4. Linfoma MALT gástrico – papel
etiológico definitivo.
 GASTRITIS AGUDA
 Razgos especializados de H. pylori:

1. Motilidad mediante flagelo.

2. Elaboración de una ureasa.
3. Expresión de adhesinas
bacterianas, BabA.
4. Expresión de toxinas bacterianas,
CagA, VacA.
 GASTRITIS AGUDA
 El genoma de H. pylori tiene 1,65
millones de pares de bases.
 Codifica alrededor de 1500
proteínas.

 La interleucina 1 B, citocina
proinflamatoria potente inhibidor
poderoso de la secreción gástrica.
 GASTRITIS AGUDA
 MORFOLOGÍA:
 Infiltrado de linfocitos y células
plasmáticas en la lámina propia.
 Actividad, presencia de neutrófilos
en el epitelio.
 Cambios histológicos adicionales:
 Cambio regenerativo:
1. Metaplasia.
2. Atrofia.
3. Displasia.
 FORMAS ESPECIALES DE
GASTRITIS
 Gastritis eosinófila.
 Gastroenteropatía alérgica.
 Gastritis linfocítica.
 Gastritis granulomatosa.
 Enfermedad del ingerto contra el
huesped.
 Gastropatía reactiva.
 ENFERMEDAD ULCEROSA
PÉPTICA
 ulcera brecha en la mucosa que va
mas allá de la muscularis mucosae.

ULCERAS PÉPTICAS:
 Lesiones crónicas, a veces unicas, en
cualquier porción del aparato
gastrointestinal expuesto a la acción
de los jugos ácido pépticos.
 ULCERAS PÉPTICAS:

 Sitios de localización por orden de

frecuencia:
1. Primera porción del duodeno.
2. Estómago, normalmente en el antro.
3. Unión gastroesofágica.
4. En márgenes de gastroyeyunostomía.
5. En duodeno, estómago y yeyuno de
pacientes con SD de Zollinger – Ellison.
6. Junto a un divertículo de Meckel.
 ULCERAS PÉPTICAS:

 USA, 4 millones de personas tienen

ulceras pépticas duodenales y
gástricas.
 Cada año se diagnostica 350 000
casos nuevos.
 Se hospitaliza 180 000.
 Fallecen 5 000.
 ULCERAS PÉPTICAS:
 Características clínicas:
 DOLOR CORROSIVO, URENTE O
PUNSANTE EN EL EPIGASTRIO.
 El dolor empeora por las noches y
reaparece 1 a 3 h después de las
comidas durante el día.
 Las nauseas, vómitos, los eructos y la
pérdida de peso significativa –
CANCER.
 ULCERAS PÉPTICAS:

 Complicaciones:
1. HEMORRAGIA.
2. PERFORACIÓN.
3. OBSTRUCCIÓN.
 ULCERACIÓN GÁSTRICA AGUDA.
 PROCESOS DIVERSOS:
1. Gastropatía hipertrófica.
2. Varices gástricas.
 TUMORES
1. Benignos.
2. Malignos.
This is the normal appearance of the stomach, which has been opened along the
greater curvature. The esophagus is at the left. In the fundus can be seen the lesser
curvature. Just beyond the antrum is the pylorus emptying into the first portion of
duodenum is at the lower right. The normal appearance of the gastric fundus on
upper GI endoscopy is shown below at the left, with the normal duodenal
appearance at the right.
This is the normal appearance of the gastric antrum extending to the pylorus
at the right of center. The first portion of the duodenum (duodenal bulb) is at
the far right. In the endoscopic views below, the normal appearance of the
pylorus is seen at the left, with the first portion of the duodenum at the right.
This is the normal appearance of the gastric fundal mucosa, with short pits
lined by pale columnar mucus cells leading into long glands which contain
bright pink parietal cells that secrete hydrochloric acid.
This is a more typical acute gastritis with a diffusely hyperemic gastric
mucosa. There are many causes for acute gastritis: alcoholism, drugs,
infections, etc.
Here are some larger areas of gastric hemorrhage that could best be termed
"erosions" because the superficial mucosa is eroded away. Such erosions are
typical for the pathologic process termed gastropathy, which describes gastric
mucosal injury without significant inflammation. The findings here fit with acute
erosive gastropathy, but there are other patterns. Etiologies for the various
gastropathies can include: alcohol, drugs such as NSAIDS, stress, uremia, bile
reflux, portal hypertension, radiation, and chemotherapy.
At high power, gastric mucosa demonstrates infiltration by
neutrophils. This is acute gastritis.
A 1 cm acute gastric ulcer is shown here in the upper fundus. The ulcer is
shallow and sharply demarcated, with surrounding hyperemia. It is
probably benign. However, all gastric ulcers should be biopsied to rule out
a malignancy. The endoscopic appearance of a similar acute peptic ulcer in
the prepyloric region is seen below.
Here is a much larger 3 x 4 cm gastric ulcer that led to the resection of the
stomach shown here. This ulcer is much deeper with more irregular margins.
Complications of gastric ulcers (either benign or malignant) include pain,
bleeding, perforation, and obstruction.
Microscopically, the ulcer here is sharply demarcated, with normal gastric
mucosa on the left falling away into a deep ulcer whose base contains
infamed, necrotic debris. An arterial branch at the ulcer base is eroded
and bleeding.
The mucosa at the upper right merges into the ulcer at the left which is eroding
through the mucosa. Ulcers will penetrate over time if they do not heal.
Penetration leads to pain. If the ulcer penetrates through the muscularis and
through adventitia, then the ulcer is said to "perforate" and leads to an acute
abdomen. An abdominal radiograph may demonstrate free air with a
perforation.
The ulcer at the right is penetrating through the muscularis and approaching
an artery. Erosion of the ulcer into the artery will lead to another major
complication of ulcers--hemorrhage. This hemorrhage can be life threatening.
Chronic blood loss may lead to an iron deficiency anemia.
Gastritis is often accompanied by infection with Helicobacter pylori. This
small curved to spiral rod-shaped bacterium is found in the surface epithelial
mucus of most patients with active gastritis. The rods are seen here with a
methylene blue stain.
The strongest association with Helicobacter pylori is with duodenal peptic
ulceration--over 85% of duodenal ulcers. Seen here is a penetrating acute
ulceration in the duodenum just beyond the pylorus. An acute duodenal
ulcer is seen in two views on upper endoscopy in the panels below.
Another association with gastritis is pernicious anemia. Chronic atrophic gastritis
is associated with autoantibodies that block or bind intrinsic factor. Another type
of autoantibody demonstrated here is anti-parietal cell antibody. The bright
green immunofluorescence is seen in the paritetal cells of the gastric mucosa.
Gastric neoplasia is not uncommon. Here is a gastric adenocarcinoma. In
the U.S., most gastric cancers are discovered at a late stage when the
neoplasm has invaded and/or metastasized. ALL gastric ulcers and ALL
gastric masses must be biopsied, because it is not possible to tell from gross
appearance alone which are benign and which are malignant. In contrast,
virtually all duodenal peptic ulcers are benign.
Here is a gastric ulcer in the center of the picture. It is shallow and is
about 2 to 4 cm in size. This ulcer on biopsy proved to be malignant, so
the stomach was resected as shown here.
This is an example of linitis plastica, a diffuse infiltrative gastric
adenocarcinoma which gives the stomach a shrunken "leather bottle"
appearance with extensive mucosal erosion and a markedly thickened gastric
wall. This type of carcinoma has a very poor prognosis. The endoscopic view
of this lesion is shown below, with extensive mucosal erosion.
At autopsy, the thoracic cavity and abdominal cavity are both opened to
reveal the stomach just to the right and below the edge of liver in this
photograph. Gastric adenocarcinoma has infiltrated through the wall
and appears on the surface as irregular tan masses. The extensive
tumor in this case caused gastric outlet obstruction.
A moderately differentiated gastric adenocarcinoma is infiltrating
up and into the submucosa below the squamous mucosa of the
esophagus. The neoplastic glands are variably sized.
At higher magnification, the neoplastic glands of gastric adenocarcinoma
demonstrate mitoses, increased nuclear/cytoplasmic ratios, and
hyperchromatism. There is a desmoplastic stromal reaction to the infiltrating
glands.
This is a signet ring cell pattern of adenocarcinoma
in which the cells are filled with mucin vacuoles that
push the nucleus to one side, as shown at the arrow.
This is an immunoperoxidase stain with antibody to cytokeratin,
which is positive in the poorly differentiated neoplastic cells seen
here infiltrating through the gastric wall. Cytokeratin staining is
typical for neoplasms of epithelial origin (carcinomas).
 INTESTINO
DELGADO Y
GRUESO
APENDICE CECAL Y
PERITONEO
 CONTENIDO
 ANATOMÍA.
 VASCULARIZACIÓN.
 MUCOSA DEL INTESTINO
DELGADO.
 MUCOSA DEL COLON.
 CELULAS ENDOCRINAS.
 SISTEMA INMUNE INTESTINAL.
 FUNCIÓN NEUROMUSCULAR.
 CONTENIDO
 ANOMALÍAS CONGÉNITAS.
1. Atresia y estenosis.
2. Divertículo de Meckel.
3. Enfermedad de Hirschsprung.
 ENTEROCOLITIS.
 SINDROMES DE MALAABSORCIÓN.
 ENFERMEDAD INFLAMATORIA INTESTINAL
IDIOPÁTICA.
 PROCESOS VASCULARES.
 ENFERMEDAD DIVERTICULAR.
 OBSTRUCCIÓN INTESTINAL.
 TUMORES.
 APÉNDICE.
 PERITONEO.
Seen here is a loop of bowel attached via the mesentery. Note the extent of the
veins. Arteries run in the same location. Thus, there is an extensive
anastomosing arterial blood supply to the bowel, making it more difficult to
infarct. Also, the extensive venous drainage is incorporated into the portal
venous system heading to the liver.
This is the normal appearance of terminal ileum. In the upper frame, note the
ileocecal valve, and several darker oval Peyer's patches are present on the
mucosa. In the lower frame, a Peyer's patch, which is a concentration of
submucosal lymphoid tissue, is present. Note the folds are not as prominent
here as in the jejunum, as evidenced by the colonoscopic view below.
This is the normal appearance of small intestinal mucosa
with long villi that have occasional goblet cells. The villi
provide a large area for digestion and absorption.
This is an adhesion between loops of small intestine. Such adhesions are
typical following abdominal surgery. More diffuse adhesions may also form
following peritonitis.
This is an example of cecal volvulus. Volvulus is a twisting of the bowel. Volvulus
is most common in adults, where it occurs with equal frequency in small intestine
(around a twisted mesentery) and colon (in either sigmoid or cecum which are
more mobile). In very young children, volvulus almost always happens in the
small intestine.
The small intestinal mucosa demonstrates marked hyperemia as a result of
ischemic enteritis. Such ischemia most often results from hypotension (shock)
from cardiac failure, from marked blood loss, or from loss of blood supply from
mechanical obstruction (as with the bowel incarcerated in a hernia or with
volvulus or intussusception). If the blood supply is not quickly restored, the
bowel will infarct.
On closer inspection, early ischemic enteritis involves the tips of the villi. A
colonoscopic view of ischemic colitis with minimal overlying exudate is shown
below. In general, bowel is hard to infarct from atherosclerotic vascular
narrowing or thromboembolization because of the widely anastomosing blood
supply. Thus, most cases of bowel ischemia and infarction result from
generalized hypotension and decreased cardiac output.
The mucosal surface of the bowel seen here shows early necrosis with
hyperemia extending all the way from mucosa to submucosal and
muscular wall vessels. The submucosa and muscularis, however, are
still intact.
At higher magnification with more advanced
necrosis, the small intestinal mucosa shows
hemorrhage with acute inflammation in this case of
ischemic enteritis.
Perforation of GI tract (from lower esophagus to colon) can result in a peritonitis
as seen here at autopsy. A thick yellow purulent exudate covers peritoneal
surfaces. An ovarian carcinoma caused sigmoid colonic obstruction (the
sigmoid is the markedly dilated grey-black bowel in the pelvis seen here) with
perforation.
Neoplasms of the small intestine are uncommon. Benign tumors can
include leiomyomas, fibromas, neurofibromas, and lipomas. Seen here
at the ileocecal valve is another tumor that has a faint yellowish color.
This is a carcinoid tumor. Most benign tumors are incidental
submucosal lesions, though rarely they can be large enough to
obstruct the lumen.
The carcinoid tumor is seen here to be a discreet, though
not encapsulated, mass of multiple nests of small blue cells
in the submucosa.
At high magnification, the nests of carcinoid tumor have a typical
endocrine appearance with small round cells having small round
nuclei and pink to pale blue cytoplasm. Rarely, a malignant carcinoid
tumor can occur as a large bulky mass. Metastatic carcinoid to the
liver can rarely result in the carcinoid syndrome.
The most common neoplasm in small bowel is a metastasis as
seen here. This mass caused local obstruction. Primary sites
are often from nearby colon, ovary, pancreas, and stomach.
This adenocarcinoma arose in the ampulla of Vater. Primary small intestinal
carcinomas are very rare, but the majority of those that do occur arise in the region
of the ampulla, where they may become symptomatic through biliary or pancreatic
duct obstruction. The appearance of such a mass on
esophagogastroduodenoscopy is seen below, and following placement of a stent
for drainage.
This is a leiomyosarcoma of the small bowel. As with
sarcomas in general, this one is big and bad. Sarcomas
are uncommon at this site, but must be distinguished from
other types of neoplasms.
The large blue non-Hodgkin's lymphoma cells can be seen
infiltrating through the mucosa.
At high magnification, the non-Hodgkin's lymphoma
cells have prominent clumped chromatin and
nucleoli with occasional mitotic figures.
DIVERTICULO DE MECKEL: segmento de intestino
delgado con una evaginación en forma de dedo de guante
Congenital anomalies of bowel consist mainly of diverticulae or atresias
which are often in association with other congenital anomalies. Seen
here is the most common congenital anomaly of the GI tract--a Meckel's
diverticulum. Remember the number 2: about 2% of people have them;
they are usually located 2 feet from the ileocecal valve.
Normal small intestinal mucosa is seen at the left, and mucosa involved by
celiac sprue at the right. There is blunting and flattening of villi with celiac
disease, and in severe cases a loss of villi with flattening of the mucosa as
seen here. Celiac sprue has a prevalence of about 1:2000 Caucasians, but
is rarely seen in other races. Over 95% of affected patients will express the
DQw2 histocompatibility antigen, which suggests a genetic basis.
The small intestinal mucosa at high magnification shows marked chronic
inflammation in celiac sprue. There is sensitivity to gluten, which contains the
protein gliaden, found in cereal grains wheat, oats, barley, and rye. Removing
foods containing these grains from the diet will cause this gluten-sensitive
enteropathy to subside. The enteropathy shown here has loss of crypts,
increased mitotic activity, loss of brush border, and infiltration with lymphocytes
and plasma cells (B-cells sensitized to gliaden).
This is an example of infectious diarrhea due to Giardia lamblia
infection of the small intestine. The small pear-shaped trophozoites live
in the duodenum and become infective cysts that are excreted. They
produce a watery diarrhea. A useful test for diagnosis of infectious
diarrheas is stool examination for ova and parasites.
Ciego y orificio de AP Cecum Ascending colon

Transverse colon Splenic flexure Sigmoid colon Rectum

This is normal colonic mucosa. Note the crypts that are lined by numerous
goblet cells. In the submucosa is a lymphoid nodule. The gut-associated
lymphoid tissue as a unit represents the largest lymphoid organ of the body.
This is an example of pseudomembranous enterocolitis. The mucosal surface of
the colon seen here is hyperemic and is partially covered by a yellow-green
exudate. The mucosa itself is not eroded. Broad spectrum antibiotic usage (such
as clindamycin) and/or immunosuppression allows overgrowth of bacteria such
as Clostridium dificile or S. aureus or fungi such as Candida to cause this
appearance. The colonoscopic appearance is seen below.
This is another example of pseudomembranous
inflammation, this time in the ileum. A greenish-yellow
exudate covers most of the mucosal surface.
Microscopically, the pseudomembrane is seen to be composed of
inflammatory cells, necrotic epithelium, and mucus in which the
overgrowth of microorganisms takes place. The underlying mucosa
shows congested vessels, but is still intact.
At higher magnification, the overlying pseudomembrane at the
left has numerous inflammatory cells, mainly neutrophils.
This is the normal appearance of the appendix against the background of
the cecum. The colonoscopic view of the appendiceal orifice between the
fork of two haustral folds in the cecum is seen below.
This appendix was removed surgically. The patient presented with abdominal pain
that initially was generalized, but then localized to the right lower quadrant, and
physical examination disclosed 4+ rebound tenderness in the right lower quadrant.
The WBC count was elevated at 11,500. Seen here is acute appendicitis with
yellow to tan exudate and hyperemia, including the periappendiceal fat superiorly,
rather than a smooth, glistening pale tan serosal surface.
This is the tip of the appendix from a patient with acute appendicitis. The
appendix has been sectioned in half. The serosal surface at the left shows
a tan-yellow exudate. The cut surface at the right demonstrates yellowish-
tan mucosal exudation with a hyperemic border.
Microscopically, acute appendicitis is marked by
mucosal inflammation and necrosis.
Here, the mucosa shows ulceration and undermining
by an extensive neutrophilic exudate.
Neutrophils extend into and through the wall of the appendix in a case of acute
appendicitis. Clinically, the patient often presents with right lower quadrant
abdominal pain. Rebound tenderness is noted on physical examination. An
elevated WBC count is usually present.
A small adenomatous polyp (tubular adenoma) is seen here. This lesion is
called a "tubular adenoma" because of the rounded nature of the neoplastic
glands that form it. It has smooth surfaces and is discreet. Such lesions are
common in adults. Small ones are virtually always benign. Those larger than 2
cm carry a much greater risk for development of a carcinoma, having collected
mutations in APC, DCC, K-ras, and p53 genes over the years. The
colonoscopic appearance of rectal polyps that proved to be tubular adenomas
are seen below.
This small adenomatous polyp (tubular adenoma) on a small stalk is seen
microscopically to have more crowded, disorganized glands than the normal
underlying colonic mucosa. Goblet cells are less numerous and the cells lining
the glands of the polyp have hyperchromatic nuclei. However, it is still well-
differentiated and circumscribed, without invasion of the stalk, and is benign.
Two colonoscopic views of a small polyp that proved to be a tubular adenoma
is seen below.
This adenomatous polyp has a hemorrhagic surface (which is
why they may first be detected with stool occult blood
screening) and a long narrow stalk. The size of this polyp--
above 2 cm--makes the possibility of malignancy more likely,
but this polyp proved to be benign.
Here are multiple adenomatous polyps of the cecum. A small
portion of terminal ileum appears at the right.
This is familial polyposis in which the mucosal surface of the colon is
essentially a carpet of small adenomatous polyps. Of course, even though
they are small now, there is a 100% risk over time for development of
adenocarcinoma, so a total colectomy is done, generally before age 20.
Here is another example of polyposis with numerous small polyps covering the
colonic mucosa. In this particular case, there were osteomas of the skull, a
periampullary adenocarcinoma, and epidermal inclusion cysts. Thus, this is a
case of Gardner's syndrome. As with familial adenomatous polyposis, the
inheritance pattern is autosomal dominant.
A microscopic comparison of normal colonic mucosa on the left and that of an
adenomatous polyp (tubular adenoma) on the right is seen here. The neoplastic
glands are more irregular with darker (hyperchromatic) and more crowded nuclei.
This neoplasm is benign and well-differentiated, as it still closely resembles the
normal colonic structure.
The gross appearance of a villous adenoma is shown above the surface at
the left, and in cross section at the right. Note that this type of adenoma is
sessile, rather than pedunculated, and larger than a tubular adenoma
(adenomatous polyp). A villous adenoma averages several centimeters in
diameter, and may be up to 10 cm. On colonoscopy, a sessile polyp is seen
below.
Microscopically, a villous adenoma is shown at its edge on the left, and projecting
above the basement membrane at the right. The cauliflower-like appearance is due
to the elongated glandular structures covered by dysplastic epithelium. Though
villous adenomas are less common than adenomatous polyps, they are much more
likely to have invasive carcinoma in them (about 40% of villous adenomas).
An encircling adenocarcinoma of the rectosigmoid region is seen here. There
is a heaped up margin of tumor at each side with a central area of ulceration.
This produces the bleeding that allows detection through a stool guaiac test.
Normal mucosa appears at the right. The tumor encircles the colon and
infiltrates into the wall. Staging is based upon the degree of invasion into and
through the wall. The colonoscopic views of a smaller rectal adenocarcinoma,
but still with an ulcerated surface, are shown below.
 Below is a higher magnification of
the radiograph above.

The barium enema technique instills the radiopaque barium sulfate into the colon,
producing a contrast with the wall of the colon that highlights any masses present.
In this case, the classic "apple core" lesion is present, representing an encircling
adenocarcinoma that constricts the lumen.
 This CT image of the abdomen
demonstrates an encircling mass
involving the colon. This is a
colonic adenocarcinoma.

The encircling mass of firm adenocarcinoma in

this colon at the left is typical for
adenocarcinomas arising in the descending
colon. A change in stool or bowel habits can be
created by the mass effect. By colonoscopy, a
fungating, ulcerating mass is seen in the views
below.
Here is another example of an adenocarcinoma of colon. This
cancer is more exophytic in its growth pattern. Thus, one of the
complications of a carcinoma is obstruction (usually partial).
Colonoscopic views of another ulcerating mass, a rectal
adenocarcinoma, are seen below.
This is an adenocarcinoma arising in a villous adenoma. The surface
of the neoplasm is polypoid and reddish pink. Hemorrhage from the
surface of the tumor creates a guaiac positive stool. This neoplasm
was located in the sigmoid colon, just out of reach of digital
examination, but easily visualized with sigmoidoscopy.
The edge of the carcinoma arising in the villous adenoma is seen
here. The neoplastic glands are long and frond-like, similar to those
seen in a villous adenoma. The growth is primarily exophytic (outward
into the lumen) and invasion is not seen at this point. Grading and
staging of the tumor is done by the surgical pathologist who will
examine multiple histologic sections of the tumor.
Microscopically, a moderately differentiated adenocarcinoma of colon is
seen here. There is still a glandular configuration, but the glands are
irregular and very crowded. Many of them have lumens containing
bluish mucin.
Here is an adenocarcinoma in which the glands are much
larger and filled with necrotic debris.
At high magnification, the neoplastic glands of adenocarcinoma
have crowded nuclei with hyperchromatism and pleomorphism.
No normal goblet cells are seen.
The sigmoid colon at the right appears lighter in color than the adjacent
small intestine and has a band of taenia coli muscle running longitudinally.
Protruding from the sigmoid colon are multiple rounded bluish-gray
diverticula. Diverticula are much more common in the colon than in small
intestine, and they are more common in the left colon, and they are more
common in persons living in developed nations in which the usual diet has
less fiber.
Several diverticula are seen along the length of the descending colon.
Focal weaknesses in the bowel wall and increased lumenal pressure
contribute to the formation of diverticula.
The colon has been opened to reveal the presence of non-inflamed
diverticula. Each has an opening to the colonic lumen through a
narrow neck. Colonoscopic views of diverticula are seen below.
At low magnification, a colonic diverticulum has a central lumen with
surrounding mucosa, while the wall (lacking a muscularis) is attenuated. The
narrow neck of the diverticulum may become eroded.
The surface of the colon is hyperemic because of inflammation as a result
of diverticulitis. The erosion of the mucosa by the stool in the diverticula
can produce inflammation and hemorrhage.
This diverticulum has become inflamed and has ruptured
outward, seen as the dark brown irregular tract extending
down from the mucosal surface here.
Seen here is the anus and perianal region with prominent prolapsed true
(internal) hemorrhoids. Hemorrhoids consist of dilated submucosal veins which
may thrombose and rupture with hematoma formation. External hemorrhoids
form beyond the intersphincteric groove to produce an "acute pile" at the anal
verge. Chronic constipation, chronic diarrhea, pregnancy, and portal
hypertension enhance hemorrhoid formation. Hemorrhoids can itch and bleed
(usually bright red blood, during defacation). Seen below is on colonoscopy are
views of hemorrhoids at the anorectal junction.
 Enfermedad
inflamatoria del
intestino
Arturo Rafael Heredia
This portion of terminal ileum demonstrates the gross findings with Crohn's
disease. Though any portion of the gastrointestinal tract may be involved with
Crohn's disease, the small intestine--and the terminal ileum in particular--is most
likely to be involved. The middle portion of bowel seen here has a thickened wall
and the mucosa has lost the regular folds. The serosal surface demonstrates
reddish indurated adipose tissue that creeps over the surface. Serosal
inflammation leads to adhesions. The areas of inflammation tend to be
discontinuous throughout the bowel. The endoscopic appearance with
colonoscopy, demonstrating mucosal erythema and erosion, is seen below
This is another example of Crohn's disease involving the small intestine.
Here, the mucosal surface demonstrates an irregular nodular appearance
with hyperemia and focal superficial ulceration.
Microscopically, Crohn's disease is characterized by transmural
inflammation. Here, inflammatory cells (the bluish infiltrates) extend
from mucosa through submucosa and muscularis and appear as
nodular infiltrates on the serosal surface with pale granulomatous
centers.
At high magnification the granulomatous nature of the inflammation of
Crohn's disease is demonstrated here with epithelioid cells, giant cells,
and many lymphocytes. Special stains for organisms are negative.
One complication of Crohn's disease is fistula formation. Seen here is a
fissure extending through mucosa at the left into the submucosa toward the
muscular wall, which eventually will form a fistula. Fistulae can form between
loops of bowel, bladder, and skin. With colonic involvement, perirectal fistulae
are common.
This gross appearance is
characteristic for ulcerative
colitis. The most intense
inflammation begins at the
lower right in the sigmoid colon
and extends upward and
around to the ascending colon.
At the lower left is the ileocecal
valve with a portion of terminal
ileum that is not involved.
Inflammation with ulcerative
colitis tends to be continuous
along the mucosal surface and
tends to begin in the rectum.
The mucosa becomes eroded,
as in this photograph, which
shows only remaining islands
of mucosa called
"pseudopolyps".
At higher magnification, the pseudopolyps can be seen clearly as raised red
islands of inflamed mucosa. Between the pseudopolyps is only remaining
muscularis.
Here is another example of
extensive ulcerative colitis
(UC). The ileocecal valve is
seen at the lower left. Just
above this valve in the cecum
is the beginning of the
mucosal inflammation with
erythema and granularity. As
the disease progresses, the
mucosal erosions coalesce to
linear ulcers that undermine
remaining mucosa.
Colonoscopic views of less
severe UC are seen below,
with friable, erythematous
mucosa with reduced haustral
folds.
Pseudopolyps are seen here in a case of severe
ulcerative colitis. The remaining mucosa has been
ulcerated away and is hyperemic. A colonoscopic view
of active ulcerative colitis, but not so eroded as to
produce pseudopolyps, is seen below
Microscopically, the inflammation of ulcerative colitis is confined primarily
to the mucosa. Here, the mucosa is eroded by an ulcer that undermines
surrounding mucosa.
At higher magnification, the intense inflammation of the
mucosa is seen. The colonic mucosal epithelium
demonstrates loss of goblet cells. An exudate is present over
the surface. Both acute and chronic inflammatory cells are
present.
The colonic mucosa of active ulcerative colitis shows "crypt
abscesses" in which a neutrophilic exudate is found in glandular
lumens. The submucosa shows intense inflammation. The glands
demonstrate loss of goblet cells and hyperchromatic nuclei with
inflammatory atypia.
Crypt abscesses are a histologic finding more typical with ulcerative colitis.
Unfortunately, not all cases of inflammatory bowel disease can be classified
completely in all patients.
Over time, there is a risk for adenocarcinoma with ulcerative colitis. Here, more
normal glands are seen at the left, but the glands at the right demonstrate
dysplasia, the first indication that there is a move towards neoplasia.
Malformaciones
congénitas
HERNIA DIAFRAGMATICA CONGENITA

Se trata de un prolapso de vísceras abdominales en una cavidad pleural a través de un

foramen diafragmático póstero-lateral (foramen de Bochdalek ), que representa un
conducto pleuro-peritoneal persistente

Primitivamente las cavidades pleurales están comunicadas con la abdominal por sendos
conductos o canales pleuro-peritoneales . Normalmente estos canales se cierran por
la fusión del septum transversum con las membranas pleuro-peritoneales. La fusión
tiene lugar en la 6a y 7a semanas, primero al lado derecho; después, al izquierdo. La
fusión se produce así antes de la desaparición de la hernia umbilical fisiológica (10a
semana).

La hernia diafragmática congénita es una malformación frecuente (1 en 2.000

nacimientos), en el 80% de los casos se produce al lado izquierdo, lo que
probablemente esté relacionado con la desaparición más tardía del conducto pleuro-
peritoneal izquierdo. El prolapso de vísceras abdominales tiene lugar tan pronto se
reduce la hernia umbilical fisiológica. La cavidad pleural afectada contiene por lo
común intestino delgado, estómago, bazo y parte del colon; cuando el foramen es
grande, además, el lóbulo izquierdo del hígado. De regla hay hipoplasia y atelectasia
del pulmón correspondiente y desplazamiento del mediastino, junto con el corazón,
hacia el lado opuesto, en que no rara vez, hay hipoplasia pulmonar. El abdomen
suele estar excavado. La gravedad de la anomalía depende en último término del
grado de hipoplasia pulmonar.
FISTULA TRAQUEO-ESOFAGICA

El esófago y el árbol tráqueo-bronquial se originan a partir del intestino anterior del embrión: es un
solo tubo, que luego da origen al divertículo respiratorio, ventral, que se separa del esófago por el
tabique tráqueo-esofágico. El tabique se cierra completamente en la cuarta semana.

Formas
La persistencia anómala de comunicación entre el esófago y la tráquea tiene 3 formas más comunes:

Fístula tráqueo-esofágica distal con atresia esofágica: la porción esofágica superior termina en
saco ciego; la porción inferior tiene una comunicación fistulosa con la tráquea (más del 90%).
Fístula tráqueo- esofágica proximal con atresia esofágica:
esofágica: la porción superior del esófago está
comunicada con la tráquea a través de una fístula; la porción inferior tiene un saco ciego por
arriba, y está normalmente comunicada con el estómago por abajo (cerca del 1% de los casos)
Fístula tráqueo-esofágica sin atresia esofágica:
esofágica: fístula entre esófago y tráquea (forma en H, cerca
del 5% de los casos).

Consecuencias
En el feto la atresia esofágica impide el paso normal de líquido amniótico al tubo digestivo, con la
consecuente acumulación excesiva de líquido en el saco amniótco (polihidroamnios). En el recién
nacido el saco esofágico superior ciego tiende a llenarse con mucus, el que es aspirado vía laringe.
En la atresia con fístula inferior el estómago tiende a llenarse con aire. En la atresia con fístula
superior tiende a haber aspiración de contenido alimentario. La comunicación en H puede
determinar infecciones respiratorias a repetición.
La atresia esofágica sin fístula tiene una frecuencia de cerca del doble de la fístula sin atresia.
 
ESTENOSIS CONGENITA DEL PILORO
Se manifiesta dentro de los primeros seis meses de vida, predominantemente en
varones, con vómito en proyectil posprandial precoz, después de lo cual el
paciente queda con hambre; esto puede llevar a una alcalosis hipoclorémica.
Hay hipertrofia de las fibras circulares de la muscular propia del píloro, que
deben seccionarse quirúrgicamente por pilorotomía para corregir la
alteración funcional.
 
ATRESIA O ESTENOSIS CONGENITA DEL INTESTINO
Pueden producirse por una vacuolización incompleta en el proceso que
convierte al intestino de un cordón sólido en un tubo.
 
DUPLICACIONES
Pueden presentarse desde el esófago hasta el ano, más comunes en íleon y
yeyuno. Se observan como formaciones esféricas o tubulares adosadas al
tubo digestivo; pueden estar aisladas del lumen (quistes entéricos), o bien
comunicadas con él, formando divertículos.
Las duplicaciones pueden ser asintomáticas, o causar obstrucción intestinal o
intususcepción.
 
DIVERTICULO DE MECKEL
Es una anomalía común (5% de las autopsias). Consiste en la persistencia de un
segmento del conducto vitelino (onfalo-mesentérico). Se encuentra en el borde
antimesentérico del íleon a 60-100 cm. de la válvula ileo-cecal. Tiene 3 a 5 cm. de
longitud, con forma de dedo de guante. Histología: tiene las cuatro túnicas del
intestino. Su mucosa a veces presenta focos de mucosa de tipo gástrico.
El divertículo de Meckel generalmente es asintomático. Sin embargo, puede sufrir
complicaciones: úlcera péptica con sangramiento o perforación, intususcepción,
inflamación (diverticulitis).
 

ENFERMEDAD DE HIRSCHPRUNG (AGANGLIONOSIS)

Ausencia congénita de células ganglionares en los plexos de la pared del recto; a veces
también en segmentos superiores del intestino grueso. Es 10 veces más frecuente en
niños con síndrome de Down.
Patogenia: detención de la migración de las células de la cresta neural al intestino.
(Normalmente los neuroblastos migran en dirección céfalocaudal en el tubo
digestivo para alcanzar el recto hacia las 12 semanas del desarrollo)
El recto agangliónico está permanentemente contraído: no hay expulsión de meconio en
el recién nacido, se produce dilatación de la porción proximal (megacolon),
constipación, impactación de heces endurecidas resistentes a los enemas, distensión
abdominal. El tratamiento consiste en la remoción quirúrgica del segmento
agangliónico.
La lesión puede complicarse con una inflamación del intestino (enterocolitis) con
necrosis y ulceración del segmento dilatado proximal.
 
MALFORMACIONES ANORRECTALES
En la atresia rectal y la agenesia anorrectal el intestino termina a distancia del
piso pélvico; son la manifestación de una alteración grave en el proceso de
unión del esbozo endodérmico constituido por el intestino posterior y el
esbozo ecto-mesodérmico que concurren en la formación de los órganos
anorrectales. La corrección quirúrgica de esta anomalía es muy compleja.
En la imperforación anal el intestino termina en el piso pélvico: sólo hay
oclusión por una membrana cutánea, que corresponde a la persistencia de
la membrana anal del embrión.
 
ATRESIA DE LA VIA BILIAR
Se manifiesta por ictericia en las primeras semanas de vida. Consiste en
obliteración total o segmentaria de las vías biliares extrahepáticas.
Actualmente se considera que no corresponde a una malformación, sino a
obliteración cicatrizal postinflamatoria, presumiblemente de origen viral.
Si no se corrige quirúrgicamente en forma precoz, la enfermedad es de
curso fatal.
En el hígado se aprecia colestasia, fibrosis progresiva de los espacios porta y
proliferación y dilatación de conductillos biliares.
 
ENFERMEDAD FIBROPOLIQUISTICA DEL HIGADO
Las formas más manifiestas de la enfermedad fibropoliquística del hígado corresponden
a malformaciones de la vía biliar intrahepática acompañadas de fibrosis variable, la
mayoría con tendencia hereditaria y se asocian con riñones poliquísticos. Se pueden
dividir en tres grupos: hígado poliquístico de tipo adulto, hígado poliquístico de tipo
infantil y fibrosis hepática congénita.
Hígado poliquístico de tipo adulto
Autosómico dominante; se asocia con riñones poliquísticos de tipo adulto. El hígado
presenta múltiples quistes redondeados, macroscópicamente evidentes; estos
quistes derivan de la primera generación de conductos biliares intrahepáticos;
normalmente hay una segunda generación, que en este caso está indemne, por lo
que no hay disfunción hepatobiliar.
Hígado poliquístico de tipo infantil
Autosómico recesivo; se asocia con riñones poliquísticos de tipo infantil. Sin quistes
evidentes macroscópicamente. Histológicamente, fibrosis leve de espacios porta,
con conductos biliares alargados y anastomosados.
Fibrosis hepática congénita
Esporádica o familiar. Puede asociarse con riñones poliquísticos de tipo adulto.
Histológicamente, en los espacios porta se observan bandas de colágeno que rodean
lobulillos normales; en las bandas, numerosos conductillos biliares.
La enfermedad evoluciona con hipertensión portal por hipoplasia o compresión fibrosa
de las venas de los espacios porta.
ENFERMEDAD DE CAROLI
Sin tendencia familiar, se manifiesta a cualquier edad. Caracterizada por dilatación
sacular de conductos biliares intrahepáticos, que generalmente compromete
segmentos hepáticos.
En las cavidades se pueden formar cálculos biliares; también son susceptibles a la
infección.
 
DILATACIONES CONGENITAS DEL COLEDOCO
No presentan tendencia familiar. La forma más frecuente es el llamado quiste del
colédoco que es una dilatación concéntrica en su trayecto extraduodenal; menos
frecuentes son el divertículo coledocociano, dilatación sacular, y el coledococele,
dilatación concéntrica en la porción intraduodenal del conducto. Estas lesiones se
manifiestan por dolor, ictericia o masa abdominal. Pueden asociarse con fibrosis
hepática congénita o con dilatación de conductos intrahepáticos.
Puede manifestarse como dolor, ictericia o masa abdominal.
 
PANCREAS HETEROTOPICO
Se presenta como pequeñas masas, generalmente menores de un 1 cm., en la mucosa o
en la túnica muscular propia, más frecuentemente en duodeno, estómago y yeyuno.
Su aspecto más característico en el antro gástrico es el de una lesión solevantada
sésil, a veces umbilicada en la desembocadura de un conducto central. Histología:
formado por lobulillos de páncreas exocrino, a veces con islotes de Langerhans.