GASTROINTESTINAL

Gastritis is a condition where the lining of the stomach becomes inflamed and irritated. It can
be caused by factors such as bacterial infection, excessive alcohol consumption, long-term use
of certain medications, or stress. Symptoms of gastritis may include stomach pain, indigestion,
nausea, vomiting, and feeling full.
The etiology of gastritis refers to the underlying causes or factors that contribute to the
development of the condition. There are several potential etiological factors for gastritis,
including:

Helicobacter pylori infection: This bacterium is a common cause of gastritis. It can colonize the
stomach lining and trigger an immune response, leading to inflammation.
Nonsteroidal anti-inflammatory drugs (NSAIDs): Regular or long-term use of NSAIDs like aspirin
or ibuprofen can irritate the stomach lining, leading to gastritis.
Excessive alcohol consumption: Alcohol can irritate and inflame the stomach lining, causing
gastritis.
Autoimmune disorders: In some cases, the body's immune system mistakenly attacks the cells
of the stomach lining, leading to autoimmune gastritis.
Bile reflux: When bile flows back into the stomach from the small intestine, it can cause
irritation and inflammation of the stomach lining.
The pathophysiology of gastritis involves the mechanisms and changes that occur within the
body leading to the inflammation of the stomach lining. The specific pathophysiology can vary
depending on the underlying cause, but in general, it involves:

Disruption of the protective mucosal barrier: The stomach lining has a protective layer of mucus
that shields it from the corrosive effects of stomach acid. Factors like H. pylori infection or
NSAID use can disrupt this barrier, allowing acid and other irritants to damage the lining.
Inflammatory response: The presence of irritants or infection triggers an immune response,
leading to the release of inflammatory mediators. These mediators cause blood vessels in the
stomach lining to dilate and become more permeable, allowing immune cells to infiltrate the
area.
Tissue damage and repair: The inflammation and immune response can lead to damage to the
stomach lining. This can result in erosions or ulcers in severe cases. The body initiates a repair
process, involving cell regeneration and tissue healing.
Pain in gastritis can vary in type and severity. Commonly, patients experience a dull, burning, or
gnawing pain in the upper abdomen, typically around the center or slightly to the left. The pain
may be aggravated by eating certain foods, especially spicy or fatty ones. In some cases, the
pain may radiate to the back or chest. The intensity of pain can range from mild discomfort to
severe and debilitating. Pain in gastritis is often described as "epigastric pain," referring to the
area between the chest and the belly button.

It's important to note that the type and severity of pain can vary among individuals, and some
individuals with gastritis may not experience any pain at all. Other symptoms such as nausea,
vomiting, and bloating may also be present in addition to pain. Proper diagnosis and evaluation
by healthcare professionals are essential to determine the specific etiology, pathophysiology,
and appropriate management of gastritis
Gastritis - Risk Factors
◦ Drug-Related Gastritis: Drugs contribute to the development of
acute and chronic gastritis. NSAIDs, including aspirin, and
corticosteroids inhibit the synthesis of prostaglandins that are
protective to the gastric mucosa.
◦ Diet: Dietary indiscretions can also result in acute gastritis
◦ Prolonged damage induced by repeated alcohol abuse results in
chronic gastritis. Eating large quantities of spicy, irritating foods and
metabolic conditions such as renal failure can also cause acute
gastritis.
◦ Helicobacter pylori: An important cause of chronic gastritis is
Helicobacter pylori infection.
Other Risk Factors: Although not as common, other risk factors of
chronic gastritis have been identified. Bacterial, viral, and fungal
infections, including Mycobacterium species, cytomegalovirus (CMV),
and syphilis, are associated with chronic gastritis.

In acute gastritis the symptoms include anorexia, nausea and

vomiting, epigastric tenderness, and a feeling of fullness.

PEPTIC ULCER
Peptic Ulcer Disease
• Peptic ulcer disease (PUD) is a condition characterized by erosion of
the Gl mucosa resulting from the digestive action of HCI acid and
pepsin.

As described in the section on gastritis, a variety of agents are known

to damage the mucosal barrier (Helicobacter pylori, medication-
induced injury, lifestyle factors, duodenal ulcers, stress-related
mucosal disease.

◦ Clinical Manifestations
◦ The discomfort generally associated with gastric ulcers is located
high in the epigastrium and occurs about 1 to 2 hours after meals.
◦ The pain is described as "burning" or "gaseous." If the ulcer has
eroded through the gastric mucosa, food tends to aggravate rather
than alleviate the pain. For some patients, the earliest symptoms are
due to a serious complication such as perforation.
◦ The symptoms of duodenal ulcers occur when gastric acid comes
in contact with the ulcers. With meal ingestion, food is present to help
buffer the acid.
◦ Symptoms of duodenal ulcers occur generally 2 to 5 hours after a
meal.
◦ The pain is described as "burning" or "cramplike." It is most often
located in the mid epigastric region beneath the xiphoid process.
Duodenal ulcers can also produce back pain.
Not all patients with gastric or duodenal ulcers experience pain or
discomfort. Silent peptic ulcers are more likely to our in older adults
and those taking NSAIDs.

Peptic Ulcer Disease

◦ Complications
◦ Hemorrhage: Hemorrhage is the most common complication of PUD.
Duodenal ulcers account for a greater percentage of upper Gl bleeding
episodes than gastric ulcers.
◦ Perforation: Perforation is one that can cause death /harm
complications of PUD. Perforation is commonly seen in large
penetrating duodenal ulcers.
◦ Gastric Outlet Obstruction: Both acute and chronic PUD can result in
gastric outlet obstruction. Obstruction in the distal stomach and
duodenum is the result of edema, inflammation, or pylorospasm and
fibrous scar tissue formation.

Peptic Ulcer Disease

◦ Diagnostic Studies
◦ Endoscopy is the most accurate diagnostic procedure.
◦ direct viewing of the gastric and duodenal mucosa.
◦ Biopsy of the antral mucosa and testing for urease (rapid urease testing) is
considered the gold standard for diagnosis of [Link] infection.
◦ Noninvasive tests include stool testing or breath testing.
do not distinguish between past and current infections.
◦ The urea breath test can identify active infection.
◦ Laboratory tests, including a CBC, liver enzyme studies, serum
amylase determination, and stool examination, should be performed.
drug therapy (Proton pump inhibitors, H2-receptor blockers, Antibiotics
for H. Pylori, Cytoprotective drugs, Antacids, Anticholinergics)

◦ Hemorrhage. vital signs changes and an increase in redness of the

aspirate often signal massive upper GI bleeding.
◦ With bleeding, the patient's pain often decreases because the
blood helps neutralize the acidic gastric contents.
It is important to maintain the patency of the NG tube so that blood
clots do not obstruct the [Link] the tube becomes blocked, the patient
can develop abdominal distention.

◦ NURSING IMPLEMENTATION
◦ ACUTE INTERVENTION:
◦ Perforation: With perforation, the patient complains of sudden,
severe abdominal pain.
◦ ***Perforation is manifested by a rigid, boardlike abdomen; severe
generalized abdominal and shoulder pain; drawing up of the knees; and
shallow, grunting respirations.
◦ The bowel sounds that may have been previously normal or
hyperactive may diminish and become absent. When the patient with
an ulcer demonstrates these changes, suspect perforation and notify
the health care provider immediately.
◦ Take vital signs promptly and record them every 15 to 30 minutes.
◦ Temporarily stop all oral or NG drugs and feedings until you can
notify the health care provider and a definitive diagnosis is made. If
perforation does exist, anything taken orally can add to the spillage
into the peritoneal cavity and increase discomfort.
◦ When perforation is confirmed, antibiotic therapy begins.
When the perforation fails to seal spontaneously, surgical or
laparoscopic closure is necessary and is performed as soon as
possible.

◦ ACUTE INTERVENTION:
◦ Gastric Outlet Obstruction: Gastric outlet obstruction can happen
at any time. It is most likely to occur in the patient whose ulcer is
located close to the pylorus.
◦ The onset of symptoms is usually gradual.
◦ Constant NG aspiration of stomach contents can help relieve
symptoms. This allows edema and inflammation to subside and
permits the normal flow of gastric contents through the pylorus.
◦ Regular irrigation of the tube with a normal saline solution per
institutional policy may facilitate proper functioning.
It may also be helpful to reposition the patient from side to side so
that the tube tip is not constantly lying against the mucosal surface.

◦ To check for ongoing obstruction, clamp the NG tube

intermittently and measure the gastric aspirate. It is important to
maintain accurate intake and output records, especially of the gastric
aspirate.
When conservative treatment is not successful, surgery is performed
after the acute phase has passed.

◦ PATIENT & CAREGIVER TEACHING GUIDE

◦ Include the following instructions when teaching the patient and
caregiver about the management of PUD.
◦ dietary modifications, and avoidance of foods that may cause
epigastric distress. This may include black pepper, spicy foods, and
acidic foods.
◦ Avoid cigarettes. promoting ulcer development, smoking delays
ulcer healing.
◦ Reduce or eliminate alcohol intake.
◦ Avoid OTC drugs unless approved by the health care provider.
• Many preparations contain ingredients, such as aspirin, that should
not be taken unless approved by the health care provider. Check with
the health care provider regarding the use of nonsteroidal anti-
inflammatory drugs.
Do not interchange brands drugs
Take all medications as prescribed.
◦ It is important to report any of the following:
◦ Increased nausea or vomiting
◦ Increased epigastric pain
◦ Bloody emesis or tarry stools
Stress can be related to signs and symptoms of PUD.
Share concerns about lifestyle changes and living with a chronic
illness.

LOWER GASTROINTESTINAL
PROBLEMS
INFLAMMATORY BOWEL DISEASE
◦ Inflammatory bowel disease (IBD) is a chronic inflammation of the Gl tract.
It is characterized by periods of remission interspersed with periods of
exacerbation. The exact cause is unknown, and there is no cure.
◦ IBD is classified as either.
◦ Crohn's disease or ulcerative colitis based on clinical manifestations.
◦ As the name suggests, ulcerative colitis is usually limited to the
colon.
◦ Crohn's disease can involve any segment of the Gl tract from the
mouth to the anus.
Both ulcerative colitis and Crohn's disease commonly occur during the
teenage years and early adulthood, and both have a second peak in
the sixth decade.

INFLAMMATORY BOWEL DISEASE

◦ Complications
◦ Patients with IBD experience both local (confined to the GI tract)
and systemic (extraintestinal)complications.
◦ GI tract complications include hemorrhage, strictures, perforation
(with possible peritonitis),fistulas, and colonic dilation (toxic
megacolon).
◦ Patients with toxic megacolon are at risk of perforation and may
need an emergency colectomy.
◦ Toxic megacolon is more common with ulcerative colitis.
◦ Hemorrhage may lead to anemia and is corrected with blood
transfusions and iron supplements.
◦ Perineal abscess and fistulas occur in up to a third of patients
with Crohn's disease.
The incidence and severity of C. difficile infection in patients with IBD
are increasing.

INFLAMMATORY BOWEL DISEASE

◦ Complications
◦ Nutritional problems are especially common in Crohn's disease when
the terminal ileum is involved.
◦ Bile salts and cobalamin are exclusively absorbed in the terminal ileum.
◦ Thus, disease in the terminal ileum can result in fat malabsorption
and anemia.
◦ Patients with a history of IBD are considered at increased or high
risk for colorectal cancer. In addition, those with Crohn's disease are
at increased risk for small intestinal cancer.
◦ Some people with IBD suffer from systemic complications,
including joint, eye, mouth, kidney, bone, vascular, and skin problems.
Circulating factors such as cytokines trigger inflammation in these
areas.
Routine liver function tests are important because primary sclerosing
cholangitis, a complication of IBD, can lead to liver failure.

LIVER, PANCREAS, AND BILIARY TRACT PROBLEMS

Certainly! Hepatitis is a condition that involves inflammation of the liver. It can be caused by
different factors, including viruses, alcohol, certain medications, or autoimmune diseases. The
most common types of hepatitis are caused by viruses, such as hepatitis A, B, C, D, and E.
Here's a simplified explanation of each type of viral hepatitis:
[Link] A: It is usually transmitted through contaminated food or water. Symptoms may
include fatigue, nausea, vomiting, abdominal pain, and yellowing of the skin and eyes
(jaundice). It typically resolves on its own without long-term effects.
[Link] B: It is transmitted through contact with infected blood, unprotected sex, or
from an infected mother to her baby during childbirth. Symptoms may include fatigue,
abdominal pain, dark urine, jaundice, and joint pain. Some people may develop a
chronic infection that can lead to liver damage over time.
[Link] C: It is transmitted through contact with infected blood, often through sharing
needles or other drug paraphernalia. Many people with hepatitis C may not have
symptoms initially, but it can lead to chronic infection, liver cirrhosis, or liver cancer over
time.
 [Link] D: This type only occurs in people who already have hepatitis B. It is transmitted
through contact with infected blood or sexual contact. It can cause more severe liver
damage than hepatitis B alone.
[Link] E: It is transmitted through contaminated food or water, similar to hepatitis A. It
is more common in developing countries and usually resolves on its own, but it can be
more severe in pregnant women.
The common symptoms of viral hepatitis include fatigue, abdominal pain, loss of appetite,
nausea, vomiting, dark urine, pale stools, and jaundice (yellowing of the skin and eyes).
Treatment for viral hepatitis depends on the type and severity. Some cases may resolve on their
own, while others may require antiviral medications, rest, and supportive care. Vaccines are
available to prevent hepatitis A and B. It's important to consult with healthcare professionals for
proper diagnosis, treatment, and prevention strategies.
Remember, this is a simplified explanation, and there is more detailed information available
about each type of hepatitis

DISORDERS OF THE LIVER

◦ HEPATITIS
◦ Viral Hepatitis
◦ Hepatitis A Virus
◦ Hepatitis B Virus
◦ Hepatitis C Virus
◦ Hepatitis D Virus
◦ Hepatitis E Virus
◦
◦ Autoimmune, Genetic, And Metabolic Diseases
◦ Autoimmune Hepatitis
◦ Wilson's Disease
◦ Hemochromatosis
◦ Primary Biliary Cirrhosis
◦ Nonalcoholic Fatty Liver Disease and Nonalcoholic Steatohepatitis

Cirrhosis

DISORDERS OF THE LIVER- VIRAL HEPATITIS

◦ Collaborative Care
◦ Well-balanced diet
◦ Vitamin supplements
◦ Rest degree of strictness varies
◦ Avoidance of alcohol intake and drugs detoxified by the liver.
◦ Drug Therapy: There are no drug therapies for the treatment of
acute hepatitis A infection. Treatment of acute hepatitis B is indicated
only in patients with severe hepatitis and liver failure.
◦ In persons with acute hepatitis C, treatment with pegylated
interferon within the first 12 to 24 weeks of infection decreases the
development of chronic hepatitis C.
Supportive drug therapy may include antiemetics for nausea, such as
prochlorperazine (Compazine), promethazine (Phenergan), or
ondansetron (Zofran).

CIRRHOSIS
Cirrhosis is a chronic progressive disease of the liver characterized by
extensive degeneration and destruction of the liver cells.
• The development of cirrhosis is an insidious, prolonged course,
usually after decades of chronic liver disease.

◦ Clinical Manifestations
◦ Early Manifestations: The onset of cirrhosis is usually insidious, and
gradual.
◦ Early symptoms include fatigue. Many patients with normal liver
function (compensated cirrhosis) may not be aware of their liver
condition. The diagnosis may not be discovered until later, when they
manifest symptoms of more advanced liver disease.
◦ Later Manifestations: Later symptoms may be severe and result
from **liver failure and portal hypertension.
◦ Jaundice, peripheral edema, and ascites develop gradually.
Other late symptoms include skin lesions, hematologic disorders,
endocrine disturbances, and peripheral neuropathies.
In the advanced stages, the liver becomes small and nodular.

◦ Clinical Manifestations
◦ Jaundice: Jaundice results from the functional derangement of liver
cells and compression of bile ducts by connective tissue overgrowth.
Jaundice occurs as a result of the decreased ability to conjugate and
excrete bilirubin. The jaundice may be minimal or severe, depending
on the degree of liver damage.
◦ Skin Lesions: Various skin manifestations are commonly seen in
cirrhosis.
◦ Spider angiomas (telangiectasia or spider nevi) are small, dilated blood
vessels with a bright red center point and spiderlike branches. They
occur on the nose, cheeks, upper trunk, neck, and shoulders.
Palmar erythema (a red area that blanches with pressure) is located on the
palms of the hands. Both of these lesions are attributed to an increase
in circulating estrogen as a result of the damaged liver's inability to
metabolize steroid hormones.

◦ Complications
◦ Major complications of cirrhosis are
◦ portal hypertension with resultant esophageal and gastric varices
◦ peripheral edema and ascites,
◦ hepatic encephalopathy (mental status changes, including coma),
hepatorenal syndrome.

In simpler terms, hepatic encephalopathy occurs when the liver is not able to remove toxins,
particularly ammonia, from the blood. The increased ammonia affects the brain and causes
problems with its functioning. This can lead to a range of symptoms, including confusion,
changes in behavior, and difficulties with thinking and coordination. Managing the underlying
liver disease, reducing ammonia levels, and treating precipitating factors are important in the
management of hepatic encephalopathy.
◦
◦
◦
◦ Complications

◦ Clinical manifestations of encephalopathy are changes in

neurologic and mental responsiveness; impaired consciousness; and
inappropriate behavior, ranging from sleep disturbances to lethargy to
deep coma.
Changes may occur suddenly because of an increase in ammonia in
response to bleeding varices or infection or gradually as blood
ammonia levels slowly increase.
◦
◦ Hepatic Encephalopathy:
A characteristic manifestation of hepatic encephalopathy is asterixis
(flapping tremors).
series of rapid flexion and extension movements of the hands.
Impairments in writing involve difficulty in moving the pen or pencil
from left to right and apraxia (the inability to construct simple figures).
Other signs include hyperventilation, hypothermia, and grimacing and
grasping reflexes.

Fetor hepaticus (musty, sweet odor of the patient's breath) occurs in

some patients with encephalopathy. This odor is from the
accumulation of digestive by-products that the liver is unable to
degrade.

Hepatorenal Syndrome: Hepatorenal syndrome can our in patients with

decompensated cirrhosis. It is a type of renal failure with advancing
azotemia, oliguria, and intractable ascites. In this syndrome, the
kidneys have no structural abnormality.

CIRRHOSIS
◦ Diagnostic Studies
Patients with cirrhosis have abnormalities in most of the liver function
studies. Enzyme levels, including alkaline phosphatase, AST, ALT, and
y-glutamyl transpeptidase (GGT), are initially elevated because of their
release from damaged liver cells.

◦
Collaborative Care
Ascites: Management of ascites focuses on sodium restriction,
diuretics, and fluid removal.
◦ Ascites:
A paracentesis (needle puncture of the abdominal cavity) may be
performed to remove ascitic fluid or to test the fluid for infection
(spontaneous bacterial peritonitis).
Peritoneovenous shunt is a surgical procedure that provides
continuous reinfusion of ascitic fluid into the venous system. Its use
has almost been eliminated because of the high rate of complications.

CIRRHOSIS
◦ Collaborative Care
◦ Hepatic Encephalopathy: The goal of management of hepatic
encephalopathy is the reduction of ammonia formation.
◦ Ammonia formation in the intestines is reduced with lactulose, a
drug that traps ammonia in the gut. It can be given orally, as an
enema, or through a nasogastric (NG) tube.
◦ The laxative effect of the drug expels the ammonia from the colon.
◦ Antibiotics such as rifaximin may also be given, particularly in
patients who do not respond to lactulose.
Constipation should be prevented.

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