What is Peptic Ulcer Disease?
gastric pits that contain the parietal, chief cells,
PUD is ulcer formation in the lining of the upper
GI tract that affects mainly the mucosal lining of
the stomach, duodenum or esophagus.
Three Types of Peptic Ulcers:
 Gastric Ulcers: located inside the
stomach
 Duodenum Ulcer: located inside the
duodenum which is the first part of the
small intestine
 Esophageal Ulcer: located inside the
lower part of the esophagus
*this lecture will concentrate on gastric and
duodenum ulcers
How do these ulcers form? Acid production
and breakdown of the defense system of the
mucosal lining.
Anatomy of Stomach
Role of the stomach: liquefies the food by
churning it and release acids and enzyme such
as HCL
(hydrochloric
acid)
and pepsin to break down food.
Layers of the stomach:
Mucosa: top layer of the mucosa that releases
mucous rich in bicarbonate that protects the
lining from the stomach acid. It also contains
and g-cells.
 Parietal cells: release hydrochloric acid
along with intrinsic factor
 Chief cells: release pepsinogen which
mixes with hydrochloric acid and
becomes PEPSIN
 G-cells: release gastrin
Submucosa: made up of connective tissue,
nerves, vessels
Muscularis externa (has 3 smooth muscle
layers) : function is to perform peristalsis which
pushes food down through the GI tract
Serosa: outer layer that has connective tissue
that connects to surrounding organs
Pylorus: opening from the stomach to the first
part of the small intestine (the duodenum). It is
a muscular like structure that allows food to
flow into the small intestine.
Duodenum: first part of the small intestine
Key Players in Peptic Ulcer Disease:
Result of PUD: The hydrochloric acid and
pepsin in the stomach that normally works to
digest food starts to erode the mucosal lining
because the defense mechanisms of the
stomach are disrupted or the amount of acid is
excessive. In a sense, the stomach starts to
digest itself.
The body tries to keep a fine balance between
the amounts of stomach acid and defense
mechanisms that protect the stomach from
ulcer formation.
To function normally and prevent ulcers, the
stomach has to have the good with the ugly
because although they don’t really get along
they need each other to perform digestion.
I like to break the key players into two teams.
The GOOD team which is the defense system
and the UGLY team which is the toxic system.
Good:
 the defense system of the stomach. The
defense system protects the stomach
lining so food can be digested. It takes a
lot of effort to digest food so it can go
through the lower GI tract.
Key Players in the Defense System:
 Bicarbonate (HCO3): coats the gastric
layer and protects the cells from acids
 Prostaglandins: regulates perfusion to
stomach, causes stomach cells to release
mucous rich in bicarb, controls acid
amounts via the parietal cells
*Anything that affects these “key players”
increases the chances of ulcer formation…see
the villains below.
Ugly:
 the toxic system of the stomach. It does
the ugly/dirty work by breaking down the
food…if the “good”/defense wasn’t in
place the stomach in a sense would
digest itself.
Key Players in the Toxic System:
 Hydrochloric acid via parietal cells
 Pepsin via chief cells
Villains: main causes of Peptic Ulcer
Disease
 H. pylori: a bacterial infection (discussed
more below)
 NSAIDs usage
So, what happens when acid penetrates the
mucosa of the stomach? When the mucosal
lining is damaged histamine is released and
this is a catch 22 because it signals to the
parietal cells to release more HCL…so you
get even more toxic acid in the stomach which
continues to erode the damaged area.
Causes of Peptic Ulcers:
 *Ba
cterial infection due to Helicobacter
pylori (H. pylori):
Per CDC.gov: 90% of duodenal ulcers and
up to 80% of gastric ulcers are caused by h.
pylori (Helicobacter Pylori: Fact Sheet For
Health Care Providers 1).
These bacteria are spiral-shaped which
helps them invade the GI mucosa.
How can h. pylori live in the acidic conditions of
the stomach? Because it secretes urease
and this breakdown UREA which produces
ammonia to neutralize the acid. In addition,
the ammonia causes more damage to the
mucosal lining.
It is most likely spread from consuming
something contaminated with h. pylori via fecal
to oral or oral to oral.
 *NSAIDs (long term usage):
Think of how NSAIDS work: they work to
decrease the production of prostaglandins.
Prostaglandins cause us to feel pain,
inflammation, fever etc. Remember the
stomach uses prostaglandins to keep the
stomach protected by promoting the stomach
cells to release mucous rich in bicarb,
regulates acid amount via parietal cells, and
perfusion to stomach. NSAIDs inhibit them
from working.
Therefore, if a patient takes NSAIDs for a long
period of time the defense system of the
stomach is broken down….hence risk for ulcer
formation.
 Zollinger-Ellison Syndrome: tumor
formation that causes increased release
 of gastrin which increases stomach acid
production.
*most common
Other factors that can increase susceptibility:
smoking, alcohol, genetics, NOTE: stress and
certain foods do not causes ulcers but can
irritate them and prolong their healing.
Treatment for PUD:
 Medications: proton pump inhibitors,
antibiotics, Histamine receptor blockers,
antacids, bismuth subsalicylates
 Severe cases due to chronic ulcer
formation:
 Surgery:
 Vagotomy: cutting parts of
the vagus nerve to prevent it
from stimulating the gut to
produce hydrochloric acid
 Pyloroplasty: performed
when there is scarring to the
pylorus (specifically from
chronic duodenal ulcers) that
can cause an obstruction in
the opening of the duodenum
from the stomach so GI
contents can NOT flow into
the small intestine.
 Gastric resection: (various
types) removal of the
diseased parts of the stomach
 Watch for dumping
syndrome post-opt:
stomach is not able to
regulate the movement
of food due to the
removal of sections of
the stomach (usually the
pyloric valve and
duodenum) so it enters
into the small intestine
too fast before the
stomach can finish
digesting it. The food will
act hypertonically and
cause water from the
blood to enter jejunum
(see more below).
Diagnosed:
For ulcers from H. Pylori:
 Blood or stool test
 UREA breath test: patient will ingest a
urea tablet and if h. pylori is present it will
break down urea into ammonia
and carbon dioxide. Breath samples will
be analyzed for abnormally high carbon
dioxide levels.
Scope of the stomach (EGD)
Upper GI series: patient will drink barium which
will coat the stomach and x-rays will be taken
to assess for ulcers
CT scan of the abdomen with contrast
Complications of Peptic Ulcer
Disease
GI bleeding, formation of holes in the stomach
at the site of ulceration which is perforation and
this can lead to peritonitis, bowel blockage in
the pylorus due to chronic ulceration from a
duodenal ulcer, and increased risk of GI cancer
Signs and Symptoms of PUD
Mainly: Indigestion and Epigastric
pain….described as burning, dull, or gnawing
pain
Gastric Ulcers
 Food makes pain worst (pain 1-2 hours
after eating)
 Report of pain dull and aching
 Weight loss
 Severe: vomit blood more common
Duodenal Ulcers
  Pain happens when stomach empty…
food makes it BETTER (pain 3-4 hours
after eating)
 Wake in middle of night with pain
 Report of pain gnawing
 Weight normal
 Severe: tarry, dark stool from GI bleeding
Nursing Interventions for Peptic
Ulcer Disease
Goals: assessing, monitor, educate, and
administering meds per physician’s order
Assessing:
 Bowel sounds: hyper/hypoactive or
absent, palpation for tenderness, inspect
for bloating or mass, assess vital signs
 Ask patient when do you experience
stomach pain? Does eating help it or
make it worst? Do you awake with pain in
the middle of the night?
 Assess medical history: taking what
medications? NSAIDS,
salicylates, corticosteroids,
anticoagulant…make ulcer worst), any
history of being diagnosed with h. pylori
or any one in your family have it, smoking
, drinking alcohol or caffeine products
(prevents ulcer from healing and can
exacerbate ulcers)
Monitoring: for complications of peptic
ulcer disease or surgery
 GI bleeding: pale skin, mucous
membranes, increased HR and
decreased BP, bloating or mass in
abdomen, dark/tarry stool, vomiting blood
that is red or dark like coffee ground
(seen this and it looks just like it)
….collecting occult blood in stool per MD
order
 Perforation/Peritonitis: severe abdominal
pain with bloating, vomiting, fever,
increase HR and respirations
 Obstruction in pylorus: due to scarring for
ulceration….cause vomiting, abdominal
pain, bloating
 Dumping Syndrome: if surgery for
treatment of PUD, especially gastric
resection.
 What is dumping syndrome? Parts
of the stomach have been removed.
The stomach is not able to regulate
the movement of food due to the
removal of sections of the stomach
(usually the pyloric valve and
duodenum) so it enters into the
small intestine too fast before the
stomach can finish digesting it. The
food will act hypertonically and
cause water from the blood to enter
jejunum.
 Early dumping (happens 15-
30 minutes after eating):
fluid shifts and this causes
small bowel distention and
increased bowel motility. The
patient will have: nausea,
bloating, and diarrhea.
 In addition, from the quick
shifting of fluid the heart tries
to compensate so the patient
may experience hypotension,
syncope, dizzy.
 Late dumping (3 hours after
eating): the food that has
entered into the small
intestine is high in
carbs/sugars (body was
unable to break it down
because it entered into the
small intestine too early). This
will cause the pancreas to
release insulin. The patient
will experience signs and
symptoms
of hypoglycemia like sweating,
weak, dizzy.
Note: patients can have both or just one type
of dumping
Patient education on how to decrease signs
and symptoms:
 eat many small meals rather than 3 large
ones
 lie down for 30 minutes after eating
 eat without drinking fluids….wait 30
minutes after meals and then consume
liquids
 avoid sugary food and drinks
 eat food high in protein, fiber, and low-
carbs
DIET for Ulcers:
Avoid spicy, acidic foods(tomato/citric
juices/fruits), foods with caffeine, chocolate,
soft drinks , fried foods, alcohol
Consume a low-fiber diet that is bland and eat
to digest, eat white rice, bananas etc.
Medications
 Proton-pump inhibitors
 Histamine-receptor blockers
 Bismuth Subsalicylates
 Mucosal healing
 Antacids
 Antibiotics
Antacid Medications Help Basic Peptic Alimen
ts
Antacids: neutralizes the stomach acid
 Types: Magnesium Hydroxide, Calcium
Carbonate…these are chewed thoroughly
and then swallowed
 Interferes with MANY drugs: antibiotics,
mucosal healing, H2 blockers so always
give alone and allow for 1-2 hours before
administering other medications
Mucosal healing: Sucralfate “Carafate” lines
the stomach and adheres to the ulcer site and
protects it from acids and enzymes. Take on
empty stomach…hour before eating….don’t
give at same time as antacids or H2 blockers
*Histamine-receptor blockers: H2 blockers
“Ranitidine HCL “Zantac” or Famotidine
“Pepcid”
 End in “tidine”
 How do they work? They block
histamine. When histamine is released it
causes the parietal cells to release HCL
but this response will be blocked so
gastric acid secretion will be decreased.
Avoid giving at the same time with antacids or
Carafate. Instead give 30-45 minutes apart.
*Bismuth Subsalicylates: Pepto-
Bismol….used for h.pylori infections by
covering the site of the ulcer and keeps the
stomach acid away. It is used with antibiotics,
PPIs, or H2 blockers for treatment.
*Proton-pump Inhibitors (PPIs): decreases
stomach acid and help the protect stomach
lining
 *used with h.pylori infection along with
antibiotics
 Types: “Omeprazole “Prilosec” or
Pantoprazole “Protonix”…drugs
 end in “prazole”
 How do they work? Attaches to the
“proton pump” on the parietal cells which
is the hydrogen/potassium (H+, K+)
ATPase enzyme and blocks the release
of hydrogen ions. These ions would
mixed with the chloride ions and form
gastric acid but this is blocked so there is
decrease in gastric acid.
*Antibiotics: used if h. pylori is causing the
ulcer formation: various regime ordered by
physician. They are used with PPIs or bismuth
subsalicylate or H2 blockers
 Types: Clarithromycin (Biaxin),
Metronidazole (Flagyl), Tetracycline,
Amoxicillin (Amoxil)
*used to treat h. pylori infections
 Digestion starts in the mouth when food is
chewed. Then it is swallowed. The food is then
squeezed down into the esophagus and the
lower esophageal sphincter relaxes to let the
food into the stomach and then it CLOSES
again to prevent the food from back
flowing. Parietal and chief cells are stimulated
GERD NCLEX Review from the food to produce acid and digestive
enzymes to break down the food. In GERD, the
acids and food can flow back into the
esophagus.

Key Players in GERD

Esophagus: the tube that connects to the
stomach to allow food to enter into the
stomach. It squeezes food down into the
stomach each time we swallow and the lower
esophageal sphincter opens. It plays a role in
GERD if the esophagus is unable to perform
this role correctly due to impaired motility.

 Lower esophageal sphincter: collection

of circular muscles at the end of the
What is GERD? esophagus that closes and prevents toxic
acids and GI contents from flowing back
GERD stands for Gastroesophageal Reflux into the esophagus once it enters the
Disease and it is a chronic condition where stomach. The LES can become:
stomach contents flows back up into the
esophagus which is mainly due to a  weak from pressure: due
damaged/weak lower esophageal sphincter. to delayed gastric
emptying (anticholinergics can
GERD is sometimes referred to as “acid reflux delay gastric emptying), hiatal
disease” as well. hernia, pregnancy, obesity,
overeating (stomach distention), or
Some people have random episodes of acid medications: antihistamines,
reflux and it goes away, but GERD is when it calcium channel blockers,
occurs more than twice a week for a long antidepressants, sedatives,
period of time. smoking

Why is GERD happening? In a nutshell, the  How does a hiatal hernia

LES (lower esophageal sphincter) is not cause GERD? A hiatal hernia
staying closed but opening. This allows happens when the stomach
backwash of stomach contents and acids into pushes through a weak
the esophagus, and this leads to major irritation diaphragm and sits on top of
to the esophagus. See below the reasons for a it. All the stomach should be
weak/damaged LES. below the diaphragm and the
esophagus should be above
First let’s cover what happens in normal the diaphragm. When a hernia
swallowing: forms there is pooling of
gastric acid/contents in the
Physiology of swallowing food: herniated area and this
 increases pressure and
causes the LES to become
weak.
 closes at irregular times due to
impaired motility
Esophageal mucosal lining: erodes and
becomes damaged over time from the constant
backwash of acids/contents and ulcer/sores
form…hence “esophagitis”….complications:
esophageal cancer, Barrett’s esophagus,
narrowing of the esophagus, bleeding
Stomach Acid & Contents: erodes the
esophagus….if the acid and contents makes it
pass the upper esophageal sphincter it can
enter into the lungs causing pneumonia,
aggravate asthma signs and symptoms,
coughing, ear infections, voice changes,
chronic cough, and night time
coughing…..called laryngopharyngeal reflux
(GERD can lead to this)
Complications of GERD
 Inflammation of the esophagus
(increased risk of cancer from the chronic
inflammation)
 Narrowing of the esophagus: strictures
 Lung problems: asthma, pneumonia,
voice changes, wheezing, fluid in the
lungs
 Barrett’s esophagus: lining of the
esophagus is replaced with similar lining
that makes up the intestinal lining…
increase risk of cancer.
Signs and Symptoms of GERD
Note: not all people with GERD will have
heartburn but may have chronic cough,
recurrent pneumonia, regurgitation of food
 Gastric pain (upper)
 Excess regurgitation of food… bitter taste
in the back of the throat
 Regular, occurring burning sensation in
the chest or abdomen (it can be so
intense it feels similar to a MI)
 Dry cough (frequent)…worst at night
 Nausea
 Problems Swallowing…feels like a lump
is in the throat
 Lung Infections
How is GERD Diagnosed?
 Endoscopy: used to assess the
esophagus for changes…erosions,
strictures etc.
 Esophageal Manometry: looks at the
function of the esophagus’ ability to
squeeze the food down and how to the
lower esophageal sphincter closes
 pH monitoring: measures the acid
amounts in the esophagus for a 24 hour
period as the patient performs normal
activities of daily living…small tube stays
in the esophagus to help measure the
acid amounts
Treatment of GERD: lifestyle changes,
medications, surgery such as: fundoplication
which is where the fundus of the stomach is
placed around the lower part of the esophagus
(most severe cases)
Nursing Interventions for GERD
 Assess patient for signs and symptoms of
GERD, educating, administering
medications per MD order
Assess quality and characteristic of the pain
and differentiate the signs and symptoms from
a heart attack?
Assess for other signs and symptoms rather
than heartburn…do they have respiratory
changes, dry cough that is worst when lying
down, hoarseness of the voice? Is the pain
aggravated when eating a heavy meal? What
food makes it worst? (help develop a diet plan
to decrease signs and symptoms) What
medications are they taking?
Assess for signs and symptoms of aspiration?
Coughing, voice changes, lower oxygen
saturation, increase respiration, abnormal lung A person can have many of these outpouching
sounds areas which are called diverticula or a single
one which is called diverticulum. Typically,
Education for GERD when a patient has a single diverticulum they
are at risk for developing more herniated sac
 Eat small meals rather than large ones areas.
(prevents over eating)
Signs and Symptoms of
 Avoid foods that relax the LES: greasy,
fatty, ETOH, soft drinks (increase Diverticulosis
pressure on the LES and cause
regurgitation), and coffee, Patients are usually asymptomatic until they
peppermint/spearmint develop a complication. If a patient does have
signs and symptoms they may experience:
 Avoid eating right before bed (last meal
should be 3 hours before bed)  change in bowel pattern (sudden
constipation/diarrhea)
 Sit up after eating for at least 1 hour
 abdominal bloating
 Weight loss
*The patient may attribute these signs and
 Smoking cessation
symptoms to something else.
 Watch acidic foods: citrus and tomatoes
Many patients find out they have this disease
Medications for GERD at random. For example, they have a lower GI
series performed for another reason and they
 Antacids, H2 blockers, PPIs, prokinetics find out they have multiple diverticula in the
Antacids: neutralizes acid sigmoid colon OR the patient experiences a
complication of diverticulosis (as noted below).
 Types: Magnesium Hydroxide, Calcium
Carbonate…these are chewed thoroughly
and then swallowed
Interferes with MANY drugs: PO antibiotics,
mucosal healing, H2 NCLEX Review for
Diverticulosis and Diverticulitis
Diverticulosis and diverticulitis are two types
of diverticular disease. DiverticulITIS is a
complication of diverticulosis. Therefore, for a
person to develop diverticulitis they must first
have diverticulosis.

What is Diverticulosis? Diverticulosis is the

formation of hollow sac cavities throughout the
intestinal wall. These outpouching sacs can
form anywhere throughout the intestine but are
most commonly found in the sigmoid colon of
the large intestine.
Main Points about Diverticulosis:
Co
mplication of Diverticulosis
Diverticular Bleeding….why?
 Surrounding the diverticulum are arteries
that supply the intestinal wall. Overtime,
these walls thin and the arteries become
very superficial within the diverticulum
 wall. The artery wall can become weak  Not all people who have diverticulosis will
overtime and eventually lose integrity develop diverticulitis
which leads to GI bleeding or the
 Possibly due to stool getting stuck in the
diverticulum ruptures. Many patients will
herniated pouches due to
experience painless bleeding and
straining/constipation. Patients who
bright blood in the stool/rectum.
consume low fiber diets have hard stools
DiverticulITIS: inflammation of the that stay in the colon longer. These stools
diverticulum…hence the herniate sacs are harder to push out which increases
becomes inflamed (more is discussed below). pressure in the intestine and this leads to
This can lead to abscess, rupture of the the stool getting stuck in the out-
diverticula which leads to peritonitis and sepsis. pouching.
 Another possibility: The increased
Strictures/bowel obstruction: narrowing of
pressure in the colon causes a tear in the
the bowel wall that leads to bowel obstruction.
diverticulum which leads to infection and
This can be due to chronic episodes of
inflammation. This allows bacteria to
diverticulitis or the presence of acute
migrate in the out-pouching and cause
inflammation. Fecal matter or food can get
infection.
stuck in this narrowing which causes
obstruction. Complications of Diverticulitis
Fistula: intestinal wall weakens so much that it  Abscess: herniated pouch becomes full of
creates an opening that acts as a channel or infection and is swollen with pus. Patient
passage to other organs, such as another will have major symptoms (fever, high
intestine or another organ. Most common type WBC, intense abdominal pain, nausea,
of fistula with diverticulitis/osis fever)
is colovesicular (fistula from intestine to
bladder).  Rupture of Diverticulum: sac tears open
and spills it contents into the abdominal
Causes of Diverticulosis cavity. This leads to peritonitis.
 Obstruction due to the inflammation of
Not fully understood: It is possibly due the tissue or scarring of the tissue
to increased pressure in the colon due to
constipation/straining during bowel  Fistula formation
movements which is most likely due to
consuming a diet low in fiber. Signs and Symptoms of
Diverticulitis
 Low fiber diets don’t bulk the stool like
high-fiber diets. Instead, the stools are
smaller and drier. This requires the
intestines to work harder to push the stool
through the system and out the anus.
Due to this, certain areas of the intestinal
wall start to herniate overtime.
 Increases with age and tends to run in
families
What causes Diverticulitis?
Again not fully understood:
 Nursing Interventions for
Diverticulitis
Monitor GI system and diet status closely:

During initial phase of moderate to severe

diverticulitis…physician may prescribe IV
antibiotics (oral if case is mild) to kill the
infection and diet will be NPO…bowel rest so
healing can begin.

 MD may order TPN/IV fluids or fat

emulsions to help with nutrition
 Nurses role: administering medications,
monitoring weights/hydration status, vital
Rememb signs, signs of peritonitis…abdominal
er: “Pouch” pain/tenderness, unrelenting fever,
bloating, increased HR, RR),
Pain in abdomen…mainly in the left lower administering pain medication for
quadrant abdominal pain
Observe abdominal bloating and blood in stool As signs and symptoms decrease: advance
patient’s diet per MD order to clear liquids and
Unrelenting cramping type pain then low-fiber foods (NOTE: this is the only
time a person with diverticulosis needs to
Constipation consume a low-fiber diet)

High temperature  Clear liquids are anything that are clear

that you can see through like Jello,
Diagnosed: broths, apple juice etc.
 Low-fiber foods: White rice, cooked fruits
 Colonoscopy or vegetable without seeds or skin,
 CT scan of the abdomen with contrast eggs…Why no high-fiber foods
yet? Bowel needs to rest and work very
Treatment: little…low-fiber foods allow this to
happen.
 Most cases are treated with IV or oral
Once recovered: needs to consume high fiber
antibiotics and bowel rest with slow
foods (fresh fruits and vegetables, beans, oats
introduction of foods as signs and
and other grains)…keeps stools soft and
symptoms decrease.
bulky…decreases episodes of constipation
 Drainage of the abscess in the affected
diverticulum  Drink plenty of fluids (2-3 L) to keep
hydrated as tolerated (of course patients
 For reoccur cases: Partial colectomy
with heart failure and renal failure need to
(bowel resection): remove diseased
watch fluid intake per MD order)
portion of the colon….if multiple surgeries
are required where healthy bowel cannot  Goal to avoid constipation: MD may
be reconnected right away the patient prescribe Psyllium (Metamucil)…mix in 8
may need a temporary colostomy until it oz water and have the patient drink it.
heals and then it will be reconnected.
  Psyllium works by absorbing water from
the intestine which in turns makes stool
easier to pass (softer and bulker)
 Probiotics
 It was once thought that patients with
diverticulosis should avoid seeds, nuts
etc. but now research is showing patients
do not have to avoid seeds (pumpkin,
sunflower), nuts, fruit/veg with seeds
unless they are intolerant to them
already.
 blockers…. so always give alone and
allow for 1-2 hours before administering
other medications
Histamine-receptor blockers: decreases
secretion of gastric acid
 Types: “Ranitidine HCL “Zantac” or
Famotidine “Pepcid”
 End in “tidine”
 Short-term or PRN basis
 How do they work? They block
histamine. When histamine is released it
causes the parietal cells to release HCL
but this response will be blocked so
gastric acid secretion will be decreased.
 Avoid giving at the same time with
antacids or Carafate
Proton-pump Inhibitors (PPIs): decreases
stomach acid and helps esophagus heal
 Types: “Omeprazole “Prilosec” or
Pantoprazole “Protonix”
 end in “prazole”
 Long-term usage but there are risks:
increased risk for bone fractures
 How do they work? Attaches to the
“proton pump” on the parietal cells which
is the hydrogen/potassium (H+, K+)
ATPase enzyme and blocks the release
of hydrogen ions. These ions would
mixed with the chloride ions and form
gastric acid but this is blocked so there is
a decrease in gastric acid.
Prokinetics: prevent delayed gastric emptying
by improving pressure in LES and peristalsis of
the GI tract:
 Types: “Bethanechol” Urecholine or
Reglan “Metoclopramide”
eliac Disease NCLEX Review
What is Celiac Disease? An autoimmune, GI
disorder where when gluten is ingested, which
is found in wheat barley, grains, and rye
products, it causes damage to the small
intestine, specifically the intestinal villi.
Key Points about Celiac Disease
 Wheat is a problem for patients with
Celiac Disease. There are several
proteins in wheat and one of them is
called GLUTEN.
 Gluten itself is constructed of a group of
proteins called gliadin and
glutenin. Gliadin is the problem with
Celiac Disease.
 Celiac Disease tends to be genetic and
occurs in both children and adults.
 Celiac Disease is different from a wheat
allergy or gluten sensitivity in that it can
cause similar signs and
symptoms BUT there isn’t the same
extensive damage to the small intestine
as in Celiac Disease.
 No cure: follow gluten-free diet for life
 Celiac disease causes damage to the
small intestine due to an autoimmune
response. The body sees the protein
Gliadin as a foreign invader because it
can NOT be broken down correctly.
Key Players in Celiac Disease
Gliadin and the amino acids that make up
the protein:
Gliadin is a wheat prolamin which is a plant
storage protein that is high in the amino acids,
particularly proline and glutamine.
What do amino acids do? They help store that aid in the absorption of the nutrients by
and transport nutrients and give the protein its increasing the surface area for absorption.
structure. The body can’t break down the They are surrounded by are a network of blood
amino acids correctly. Therefore, it crosses the vessels that easily take the nutrient collected
gut cells and causes an immune response. from the food and allows it in the blood stream.
Each villus contain cells called enterocytes
What does the body do NORMALLY with which help absorb nutrients and aid in
proteins? Normally, the body will take digestion.
proteins, which start out as long amino acid
chains, and break them down into single amino
acids. The GI cells will then use them
appropriately. However, the amino acids
(proline and glutamine) of Gliadin can NOT be
broken down into a single amino acid but stay
as a small collection of amino acids
called peptides (this is what causes the
immune response).

The enterocytes which are found in the villi

allows them to cross and the immune system
doesn’t like this and views it as a bacteria or
virus and attacks.
Immune System: sends immune cells to kill
the Gliadin. The Gliadin reacts with TTG
(Tissue Transglutaminase) enzyme and
antibodies are formed by the immune cells to
fight the gliadin because the body thinks it is
bad. The antibodies formed are:
 Tissue Transglutaminase Antibodies
(tTg)
 Antibody IgA
 Endomysial antibody (EMAs)
NOTE: in the process of doing this “warfare”
between the immune system and glidian the
VILLI of the small intestine are damaged.
Intestinal Villi: found in the small intestine and
normally look like little finger-like projections
From recurrent immune system overdrive from
fighting the gluten entering the body, the
villi LOSES its finger-like like projections and
become FLAT (see the top picture in the
image above). This LEADS TO DECREASE
SURFACE AREA FOR ABSORPTION. Hence,
the patient is going to experience malnutrition.
**All of this tends to occur in the jejunum of the
small intestine
Signs and Symptoms of Celiac
Disease
“MALNOURISHED”
Mouth ulcers
Anemia
Lactose intolerance (can’t break down lactos)
Nausea/vomiting
Osteo change (thinning, fractures)
Unexplained slow growth, delay puberty
(children) and weight loss
Rashes (very itchy dermatitis herpetiformis…
elbows, backside, and knees)
Irregular periods, irritable (depression) (loss of
nutrients)
Signs and symptoms of Celiac Disease
by asking patient when they notice the most
oblivious signs and symptoms and to list what
foods they eat on a regular basis…( do they
have bloating abdomen, diarrhea/constipation,
irritable, depression, or mental fog after eating
foods with gluten?)
Patient needs to keep a food dairy along with
the signs and symptoms and the nurse should
assess the diet log (look for foods that contain
gluten)

Stools: greasy and odorous Skin, teeth, weight (normal vs abnormal)

Hair loss Family history

Enamel changes to the teeth (yellow or brown Ability to read food labels and the patient’s or
spot and deformity) families’ knowledge about gluten

Diarrhea

Diagnosing Celiac Disease

Blood tests are used to check for antibodies:

 Tissue Transglutaminase Antibodies

(tTG-IgA)
 IgA serum
 IgA Endomysial antibody (EMA)
And/OR Endoscopy: a biopsy will look at the Educate: AVOID ALL FOOD CONTAINING
villi for abnormalities GLUTEN (watch foods with hidden gluten) and
substitute with foods that do not contain gluten
Complications of Celiac Disease
More than ever grocery chains and restaurants
 Malnourishment (bone, skin, teeth, health are carrying more and more gluten free foods
mental, growth, reproductive problems) to help people enjoy foods they normally
couldn’t and food labels will say GLUTEN
 Cancer (lymphoma) FREE- like this:
 Villi take time to heal BUT sometimes the
villi never heal back (condition called
refractory celiac disease) and the patient
suffers from constant malnourishment
and will need IV supplementation.
Nursing Interventions for Celiac
Disease
Assessing
 Other Interventions:

Implementing the GF diet and making sure

food trays are GF and that patient and family
understand the importance of following the
gluten-free diet

Administering per MD order supplements to

help with any vitamin deficiencies

Always read food labels and pay close

attention to the ingredients

Foods Without Gluten

 Plain Meats (fish, beef, chicken, turkey
etc.)
 Grains: Rice, Corn, Soy, Millet, Quinoa,
Tapioca, Chia, Buckwheat (most of these
are used as substitutes for baking as in
cakes, breading on meats, pasta etc.)
 Vegetables and Fruits
 Nuts, Beans, Legumes
 Dairy (not malt)….however watch dairy
because many patients with Celiac
Disease may be lactose intolerant
Foods with GLUTEN TO AVOID
 Wheat (anything that says wheat expect
buckwheat)
 Barley
 Malt
 Beer
 Pasta Noodles
 Rye
 Seasonings, soups
 Anything with breading that doesn’t say
GF
 Anything that looks like bread: croutons,
crackers, breads, dough, cookies, most
cereals, oats unless they say GF
*most processed foods have gluten