GI Pathology

Digestion => Absorption => Excretion
DIGESTION
















Reverse in the digestive system =
vomiting
o Vomiting: loss of fluid +
electrolyte + acid = danger of
creating alkalosis
Too fast in the digestive system =
diarrhea
o Diarrhea: lose alkaline fluid =
danger of creating acidosis (with
chronic diarrhea)
Too slow through the digestive system =
constipation
The stomach lining is made up of
RUGAE, within the rugae, moving down
the stomach, there are gastric pits. A
number of cell types within the gastric pits
have the responsibility of creating the
gastric juices (really acidic)
One of the cell types in the stomach is
MUCOUS PRODUCING CELL – is a
mechanical barrier so the acids produced
by other cells are not going to corrode
Acids are very potent protein digestive –
breakdown protein bonds and take acids
towards amino acids
From voluntary swallowing to small
intestine = digestion
Can’t absorb proteins till it get to amino
acids
Can’t absorb carbohydrates till it gets to
mono/disaccharides
Lipids need to be broken down as close
to fatty acids.
Can absorb lipid molecules, but have to be small
Anything not small get picked up by lymphatics, go through lymphatic system
Any system where there is a transition increases chance for pathology
o Sphincters regulate introduction to next segment
o Weak sphincter b/w esophagus and stomach
Pyloric sphincter – regulate dumping contents from the stomach to small intestine
Ileocecal – last part of the small intestine, ileum, the pouch part of the beginning of the large intestine
– tells us where to find it
Smooth muscle creates peristalsis and then the valves will regulate how quickly or slowly they will be
emptied
ESOPHAGUS

GERD – Gastro (stomach) Esophageal Reflex Disease (enteral – intestine)
o Signs/Symptoms:
 Retrosternal pain (heartburn)
 Epigastric pain
 Burning sensation
 Gnawing
 Timing (key differential for heart issues)
 For gastroesophageal, going to be associated with eating and
positioning.
 Wheezing
 Difficulty breathing
o With repeated exposure, possibility of scaring. Repeated exposure with incomplete repair
strictures may form. Strictures are going to narrow the esophageal or upper part of the
stomach opening and put an imbalance in normal functioning of the passage of food from one
segment to another, reduce efficiency of peristalsis and increase possibility esophageal
weakness

The anatomy of the esophagus not designed to resist the acids of the stomach; acids will burn, irritate
causing inflammation, the esophageal epithelium
o burning
Different anatomy different function
Inflammation of the esophagus called esophagitis
o Chronic exposure to acid is going to create some type of cellular response. These cells are
going to try to adapt to the chronic exposure of the acid, and try to convert to columnar. When
you have that transition going on, called metaplasia. When metaplasia occurs, not by design,
increase chance for mutations. Increase chance for mutation, increase chance for neoplasia
(cancer)
o Increase risk for Barrett’s cancer


o
Causes:
a) *Incompetent L.E.S. (Lower Esophageal Sphincter)
a) Weak
b) Not preventing reflux
c) Caffeine, alcohol, chronic exposure to acid will weaken esophageal sphincter
b) *Hiatal Hernia (Hiatus – opening in the diaphragm, allows esophagus to enter the
stomach)








Sliding – L.E.S. is going up and down with eating & breathing.
Rolling – Esophagus stays where it is supposed to, but part of the stomach
can squeeze up, pulls everything. The valve has lost its patency, not as
effective due to additional pressure
In the esophagus the predominant epithelium is a stratified squamous
epithelium, most of the esophagus is stratified squamous.
In the stomach, it’s a columnar epithelium (simple columnar)
o Longer than they are wide
o More activity going on
o They produce gastric juices
c) Under Producing Saliva
 create esophagitis for a different reason, not from acid reflux, symptomology
will be similar
 might lead to damage up to the L.E.S. which allows for some reflux to occur.
Peristalsis – food it not being delivered effectively.
o PSNS – Promoting peristalsis
o SNS
CAT Scan – relation b/w esophagus and diaphragm
Protein stimulates gastric secretion
Treatment
o Not to lay down after eating
o Smaller, more frequent meals
o Chewing slower, completely
o Antacids – careful b/c of people w/ heartburn
 Overindulging on antacids your not going to digest proteins effectively
o Surgery (last resort)
STOMACH


PUD – Peptic (protein, pepsinogen, start in stomach) Ulcer (erosion of 1/more layers (4 layers in
digestive system)) Disease.
o 4 layers:
1. Mucosal layer (inner)
2. Submucosal (glands located)
3. Muscular layer (muscularis) (deeper)
 Halfway through to the esophagus, is smooth muscle. All the way through
the tube at least 2 layers of smooth muscle. A circular layer that can
squeeze the diameter shut or expand the diameter. The longitudinal layer
that shortens the length of the tube. Squeeze and then shorten it, is how
you get peristalsis. The stomach has the third layer. Stomach is a mixer.
Not only will the stomach reduce its diameter and shorten but allow it to
twist (3rd layer of muscle). Small intestine back to 2 layers of muscle. The
large intestine will be a bit pouched, the longitudinal layer changes a bit,
chronically short segments that create pouching.
4. Subserosa + Serosa
G-cell => produce hormone called Gastrin. Will
act on parietal cell.
Parietal Cell = HCL(Pepsinogen) + intrinsic factor
o Gastrin stimulates the parietal cells to
produce HCL
o Intrinsic factor is an important protein,
that binds to vitamin B12
 If the intrinsic factor can’t absorb
B12, can’t make red blood cells,
DNA, & can’t create myelin
Chief cell => Pepsinogen
o Pepsinogen + Acid (HCL) = Pepsin
o Pepsin is an enzyme that is now active
that breaks up peptide bonds (protein
bonds) b/w amino acids. We are after
pepsin for digestion.
Mucosal Cell => Protect from acid
o Produces mucous, mucous coats the
lining of the stomach to protect from the
acid




Common cause for PUD is from a bacteria
called:
o Helicobacter pyloris (80%, most
common cause)
 Flagellum gives this bacterium
motility. It burrows away from the acid towards the mucous. When it gets out in
the mucous starts to colonize and erodes some of the mucous. When it erodes
the mucous, the acid can be exposed to the cells and they become inflamed and
irritated. We exposed/interrupted the mucosal layer and the acids are all to start
the digestion process on the cells in the stomach, ulceration.
o NSAID’s (20%) (side effect concern)
 Break up the prostaglandin pathway (prostaglandin produced in the stomach
promote mucous production & inhibit HCL acid production)
 When taking NSAID’s with the goal of reducing pain + inflammation, your
blocking mucous production and promoting HCL acid production, creating an
imbalance
o Helicobacter pyloris (asymptomatic) + NSAID’s = Increased risk for PUD
The concern when we start erosion, relatively minor if we erode the mucosal layer. The mucosal
and epithelial layer don’t have a blood supply, so not bleeding. When you reach submucosal
layer, and into muscularis there is bleeding. Bleeding will show up in the stool. If the bleeding is
occurring in the stomach and shows up in the stool, its old blood. If the erosion is allowed to
progress will go through the mucosal, submucosal, muscularis and if allowed through the outer
layer, you have perforation. The contents of the stomach will be able to get into the peritoneum
and spread, the bacteria will go crazy. This will cause systemic infection called sepsis (leads to
shock). Shock is life threatening, drops BP means can’t deliver oxygen + nutrients to all the cells
in the body, the cells become ischemic and organ shutdown

Risk





Treatment
NSAIDS
Weakened immune system
Alcohol*
Caffeine*
Smoking*





Remove NSAID’s
Regulate alcohol, caffeine, smoking
(limit/eliminate/modified)
Manipulate acid-base balance
o Antacids would reduce the
presence/effectiveness of HCL
acid
Surgery – if concerned about perforation
Dumping syndrome – resection of the stomach (take a section out of the stomach)
o Reduce absorption of B12 vitamin
o Taking out a section of parietal cells and intrinsic factor
o Create a fluid shift in the interests of equalizing.
o A large volume of chyme introduced to the small intestine. Goal of small intestine is
absorption. If we dump a load in there, it becomes a hypertonic load, it will create a fluid
shift (first concern) in the interest of equalizing fluid balances. Fluid shifting will occur in
the intracell equilibrium. From the blood supply to small intestine. If pulling from blood
supply create hypovolemia = hypovolemic shock. Blood glucose from a dump =
hyperglycemia then hypoglycemia. Will be b/w hyper and hypoglycemia b/w meals, will
put stress on beta cells and pancreas. This stress can cause Type 2 diabetes.
GASTROENTERITIS

Tells us its stomach or intestinal inflammation
o Common cause: Infection
1. Food
2. Water
o Treatment: fluid and electrolyte replacement
o Higher up = vomiting, lower down = diarrhea
S. Aureus
o
o
o
o
o
o
o
o
o
o
E. Coli
Enterotoxin
Few hours
Cooperative on skin, part of normal flora
Issue – resistant to heat (less than 30 min of
heating)
Release exotoxin
Fast to create an immune response
Nausea (2-3hrs) -> vomiting (predominant)
(last several days) -> diarrhea
Fast, leads to upper GI
Cause - Under cooked food, water
Demand on oxygen
o
o
o
o
o
o
o
o
o
Salmonella Enterica
o
o
o
o
o
o
Endotoxin
Small intestine
2-3 days
Eggs/poultry
Sensitive to HCL
Hard to figure source, b/c take 2-3 days to
show (salmonella poisoning)
Enterotoxin
More hours (10-12hrs)
Found in undercooked food/water
Don’t have antibodies to fight when in
different region (to drink water in diff’t region)
Cause ulceration if aggressive
Ex: Pork mixed with digestive contents of
animal cause e.coli
Depend on oxygen
Diarrhea (Predominant), vomitting
Targets intestine, Increase motility
Clostridium Botulinum
o
o
o
o
1-2 days
Anaerobic
Colonized in canned food ( when dented, etc.)
Very resistant to heat/cold when switch to
sporform
o Resistant to temp, releases very toxic
chemical that targets ACH
o Paralysis
Treatment: replace electrolyte and fluids
LARGE INTESTINE



Diverticular Disease:
o The walls of the
large intestine
become weak,
and create out
pouching along
the pathway of the
intestine b/c
location for
bacterial
colonization,
 may
create
imbalance
to normal
flora
 creating
an immune response, inflammation
 repair process may leave with scaring and further weakening.
 Bouts of constipation + diarrhea (class of presentation)
Pouching visible in colonoscopy
Diverticulosis – condition of extra pouching
o Asymptomatic

Diverticulitis – further down
o Inflammation
o Cramping
o Burning
Treatment: antibacterial, damaged area may need to be surgically removed

Crohn’s Disease









Ulcerative Colitis
Present in proximal part of small intestine
Reginal (scalp lesion) enteritis (localized)
Skip lesions
Very Aggressive
Perforation
Can affect all layers in the area its irritated at
Low grade/acute, relatively constant
Chronic (granulation, scarring)
Surgery










Distal in large intestine
Cramping
Exacerbation, remission
Colon cancer
No skip lesions
Tends to be mucosal, submucosal, not all
layers (out of muscularis)
Increase risk by low fibre diet
Treatment: frequent/smaller meals, high fiber
Risk: smoking, alcohol, caffeine
Increase risk for colon cancer
COMMON

Treatment: anti-inflammatory (corticosteroids), surgery
 Problem: chronic use of corticosteroids
 Idiopathic
LIVER







Ducts – drain products from
the hepatocytes, liver cells, on
daily basis
Bile stored in gallbladder
Bile drained from right & left
hepatic duct into common
hepatic duct and join with the
pancreatic duct
Pancreatic duct will drain the
product from the bulk of the
cells in the pancreas that
produce enzymes for digestion
Bile drained R/L hepatic ducts > common hepatic duct -> join
pancreatic duct
Gallbladder = cyst, small
muscular pouch, an expansion
for storing bile
For healthy person, when food
is introduced into the small intestine, pancreatic juices (from pancreatic cells) produce alkaline filled
with enzymes (carboxypeptidase (peptidase act on peptides(protein), amylase(act on carbohydrates),
lipase(act on lipids)). Alkaline neutralizes the acid from the stomach and enzymes activated once







exposed to the mix of alkaline and acid in small intestine. Those enzymes are designed to finish the
job of digestion
Bile produced by hepatocytes –> collected by the duct system -> drained into small intestine to help
with digestion
Bile addresses small molecules of fat called micelles
Bile eliminates cholesterol
ADEK - Fat soluble
Vitamin K -> Coagulation
Vitamin K
o Activated in large intestine
o Allows osteoid to attract calcium to form mineralization
Small intestine releases hormones: CCK, Cholecystic, Secretin
o Cholecystokinin – encourages the pancreas to produce and release pancreatic juices
(enzyme + alkaline)
PANCREASE





Exocrine
Endocrine
o Makes insulin(hypoglycemic) + glucagon(hyperglycemic) = homeostasis
Auto digestion
Pancreatitis – infection/ inflammation
o Acute: short episode than treat for symptoms (respiratory and renal function are support
after cause has been removed)
o Chronic: Alcoholism (common), drugs(street drugs), abnormal duct formation, enzyme
production, high levels blood calcium, trauma – slower progression/destruction
o Invasive: damage to integrity of the pancreatic tissue than concerned about enzymes not
staying at the duct but get outside the duct. If enzymes like peptidases get outside the
duct, the will target other proteins in the body
o Autodigestions – enzymes that are not where they belong, start autodigestive process
in the pancreas
o What started as an exocrine can change to endocrine b/c start to digest the cells that
produce insulin(more concerned about insulin b/c only one that lowers blood glucose, no
back up) and glucagon (has back up)
Anything that can challenge the liver can challenge pancreas
GALLBLADDER





Stores bile
Release bile when food in small intestine
Problem: Formation of stones -> cholelithiasis (80% cholesterol, 20% +calcium++)
Cholelithiasis (chole = cholesterol),
Bile eliminates cholesterol
Ultrasound can identify stones in gallbladder

Cholecystitis
o Acute/chronic
o Hard to differentiate
o May radiate upward
o Inflamed gallbladder
o Treatment:
 Chronic – removal
of gallbladder
 Acute – wait a few
days
o Problem: when the stone
is bigger than the diameter
of the duct
o Diagnosis: Ultrasound