LIVER CIRRHOSIS / HEPATIC ENCEPHALOPATHY

Hepatic encephalopathy occurs in liver cirrhosis due to the liver's impaired ability to detoxify harmful
substances, especially ammonia. In cirrhosis, damaged liver tissue hinders blood flow through the
organ, reducing its ability to remove toxins from the bloodstream. Ammonia, produced by gut
bacteria and protein metabolism, accumulates in the blood and crosses the blood-brain barrier,
leading to neurotoxic effects. Additionally, cirrhotic patients may develop portal hypertension,
causing blood to bypass the liver (portosystemic shunting) and allowing toxins to circulate freely. This
disruption in detoxification results in altered mental status and neurological impairment characteristic
of hepatic encephalopathy.

A. One of the physical manifestations foe patients with hepatic encephalopathy is ASTERIXIS.
To assess asterixis in hepatic encephalopathy, ask the patient to extend their arms, dorsiflex their
wrists, and spread their fingers, maintaining this position for 10-30 seconds. A positive sign is the
presence of flapping, jerky hand movements caused by an inability to maintain sustained posture,
indicating a motor control abnormality.

B. Recommended diet: For hepatic encephalopathy, the recommended diet focuses on reducing
ammonia production while maintaining nutrition. Protein intake should be monitored, around 1.2-1.5
g/kg/day, with emphasis on plant-based or dairy proteins as they are less likely to produce ammonia
than animal proteins.

Foods to avoid include high animal protein diet such as red meat, high-sodium processed foods, and
alcohol, as they can worsen liver function and increase ammonia levels.

STOMATITIS

Stomatitis is inflammation of the mucous membranes in the mouth, leading to symptoms such as
pain, swelling, redness, and sores or ulcers. It can affect the lips, tongue, gums, and inner cheeks,
making eating, drinking, and speaking uncomfortable. Stomatitis may be caused by infections (viral,
bacterial, fungal), irritants (such as tobacco, alcohol, or spicy foods), allergic reactions, or systemic
conditions like autoimmune diseases or nutritional deficiencies. Common types include aphthous
ulcers (canker sores) and herpes stomatitis. Treatment depends on the cause and may involve topical
medications, mouth rinses, or managing underlying conditions to reduce inflammation and promote
healing.

The care plan should include the intervention LIKE Encourage foods with neutral or cool
temperatures. This helps reduce irritation to the already inflamed mucous membranes and makes
eating more comfortable. Spicy foods can exacerbate the condition, and alcohol-based mouthwashes
can further irritate the oral mucosa. Inspecting the mouth for fungal infections should be done more
frequently than once a week, as chemotherapy increases the risk for opportunistic infections like oral
thrush.

The most appropriate intervention for a client with stomatitis is a soft, bland diet helps prevent
further irritation to the already inflamed and sensitive oral mucosa, promoting comfort and healing.
Drinking hot tea or gargling with antiseptic wash could worsen inflammation and discomfort. An
electric toothbrush may be too harsh on delicate oral tissues and can cause further injury or
discomfort.

The correct oral hygiene practice the nurse must include when teaching a client with stomatitis is
Regular brushing with a soft-bristle toothbrush and gentle flossing are crucial to maintain oral hygiene
and prevent infection, but care should be taken to avoid trauma to inflamed tissues. Self-
examinations should be more frequent, especially in clients with ongoing oral issues. Wearing loose
dentures can cause irritation and exacerbate lesions, and mouthwash with alcohol should be avoided,
as it can further irritate and dry out the mucous membranes, worsening stomatitis.
HIATAL HERNIA

A hiatal hernia occurs when part of the stomach pushes up through the diaphragm into the chest
cavity. Normally, the diaphragm separates the chest from the abdomen, with the esophagus passing
through an opening called the hiatus to connect to the stomach. In a hiatal hernia, the upper part of
the stomach moves through this opening, which can lead to symptoms like heartburn, acid reflux,
chest pain, and difficulty swallowing. The condition is often associated with factors such as obesity,
aging, and increased abdominal pressure. Treatment may include lifestyle changes, medications to
reduce acid, and in severe cases, surgery.

The nurse should teach the client with hiatal hernia to avoid Lying down immediately after eating can
worsen heartburn by allowing stomach acid to reflux into the esophagus. Instead, the client should
remain upright for at least 1-2 hours after meals. The other interventions, such as taking small,
frequent bland meals (B), raising the head of the bed (C), and taking H2-receptor antagonist
medications (D), are appropriate for managing heartburn and reducing acid reflux symptoms
associated with hiatal hernia.

ACUTE GASTRITIS

Acute gastritis is a sudden inflammation of the stomach lining, often caused by factors such as
excessive alcohol consumption, prolonged use of NSAIDs, infection (particularly Helicobacter pylori),
stress, or bile reflux. It leads to symptoms like upper abdominal pain, nausea, vomiting, bloating, and,
in severe cases, gastrointestinal bleeding. The inflammation occurs when the protective mucous
barrier of the stomach is weakened, allowing stomach acid to irritate the lining. Diagnosis is typically
made through clinical evaluation, endoscopy, or testing for H. pylori. Treatment focuses on removing
the underlying cause, using antacids or proton pump inhibitors to reduce acid production and
allowing the stomach to heal.

Indomethacin is a nonsteroidal anti-inflammatory drug (NSAID) that can irritate the gastric mucosa
and worsen acute gastritis by increasing the risk of gastrointestinal bleeding and ulcers. NSAIDs are
generally avoided in patients with gastritis or other gastrointestinal issues. The other medications—
digoxin, furosemide, and propranolol are not typically associated with direct irritation of the gastric
lining, though they may still require careful monitoring for other reasons.

CHRONIC GASTRISTIS

Chronic gastritis is a long-term inflammation of the stomach lining that develops gradually over time.
It occurs when the protective mucous layer of the stomach becomes weakened or damaged, allowing
digestive acids to irritate the stomach lining. Common causes include persistent infection with
Helicobacter pylori, prolonged use of NSAIDs, excessive alcohol consumption, or autoimmune
disorders where the body attacks its own stomach cells. Symptoms can include indigestion, upper
abdominal pain, nausea, vomiting, and loss of appetite. Chronic gastritis increases the risk of stomach
ulcers, bleeding, and, in severe cases, stomach cancer. Treatment focuses on eliminating the cause,
reducing stomach acid, and promoting healing.

The correct combination of medications for eradicating H. pylori in a patient with chronic gastritis is
ANTIBIOTIC, PROTON PUMP INHIBITOR AND BISMUTH. This combination is commonly used to treat H.
pylori infection. Antibiotics are used to kill the bacteria, proton pump inhibitors reduce stomach acid
to promote healing, and bismuth helps protect the stomach lining and enhances antibiotic
effectiveness. Corticosteroids, aspirin, and NSAIDs are not appropriate because they can irritate the
stomach lining and worsen gastritis.

Chronic gastritis, particularly when associated with Helicobacter pylori infection or autoimmune
gastritis, can lead to damage of the stomach lining, specifically the parietal cells. These cells produce
intrinsic factor, which is essential for the absorption of vitamin B12 in the small intestine. A deficiency
in intrinsic factor results in poor absorption of B12, leading to pernicious anemia. Over time, this can
cause symptoms like fatigue, weakness, and neurological changes. Other vitamins like A, C, and E are
not as directly affected by chronic gastritis.

Intrinsic factor, produced by the parietal cells in the stomach, is necessary for the absorption of
vitamin B12 (cobalamin) in the small intestine. In chronic gastritis, particularly autoimmune gastritis,
the destruction of parietal cells leads to a lack of intrinsic factor, resulting in impaired B12 absorption
and pernicious anemia. Pernicious anemia, as it is specifically linked to the loss of intrinsic factor
rather than direct destruction of B12 or increased acid production.

PEPTIC ULCER DISEASE

Peptic ulcer disease (PUD) is a condition characterized by open sores or ulcers that develop on the
inner lining of the stomach (gastric ulcers) or the upper part of the small intestine (duodenal ulcers).
These ulcers form when the protective mucous layer of the digestive tract is eroded, allowing
stomach acid to damage the underlying tissue. Common causes include infection with Helicobacter
pylori and long-term use of NSAIDs, which weaken the mucosal lining. Symptoms include burning
stomach pain, bloating, and nausea. Treatment typically involves antibiotics (for H. pylori), acid-
reducing medications, and lifestyle changes to promote healing.

Helicobacter pylori (H. pylori) is a spiral-shaped bacterium, often described as having a helical or
corkscrew form. It is a gram-negative organism, meaning it has a thin peptidoglycan layer and an
outer membrane. This unique shape allows H. pylori to penetrate the mucus layer that lines the
stomach, enabling it to colonize the gastric epithelium and contribute to conditions such as gastritis
and peptic ulcers.

In the stomach lining, the parietal cells release hydrochloric acid, and the chief cells release
pepsinogen, which both play a role in peptic ulcer disease. Therefore, the correct answer is:

 Hydrochloric acid helps create an acidic environment necessary for digestion and activates
pepsinogen into pepsin.
 Pepsinogen is an inactive precursor that, when activated to pepsin in the presence of acid,
breaks down proteins in the stomach. Both of these substances can contribute to the
development of peptic ulcers when there is an imbalance between aggressive factors (like
acid) and protective factors in the gastric mucosa.

Helicobacter pylori can live in the stomach’s acidic conditions because it secretes urease. Urease is an
enzyme that breaks down urea into ammonia and carbon dioxide. The ammonia produced helps to
neutralize the gastric acid in the immediate environment surrounding the bacterium, creating a more
favorable pH for its survival.

A patient with ulcer may be ordered with UREA breath test. In this test, the patient ingests a urea
solution labeled with a specific carbon isotope (usually carbon-13 or carbon-14). If Helicobacter pylori
is present in the stomach, it will metabolize the urea into ammonia and carbon dioxide. The carbon
dioxide is then absorbed into the bloodstream, transported to the lungs, and exhaled. The presence
of increased levels of this labeled carbon dioxide in the patient's breath indicates that H. pylori is
present in the stomach.

VAGOTOMY maybe indicated for patients with PUD. A patient has vagotomy with antrectomy to treat
a duodenal ulcer. Postoperatively, the patient develops dumping syndrome. Dumping syndrome
occurs when food, especially high-sugar content, moves too quickly from the stomach into the small
intestine. This is common after gastric surgery, such as a gastric resection, as the normal regulation of
gastric emptying is disrupted. Symptoms, including nausea, bloating, diarrhea, and abdominal cramps,
typically occur shortly after eating, as described by the patient.
In dumping syndrome, the statement made by the patient that indicates further dietary teaching is
necessary is “I should eat bread with each meal.” While bread can be part of a diet, it's important for
patients with dumping syndrome to be cautious with carbohydrate intake, particularly simple
carbohydrates, which can exacerbate symptoms. Instead, they should focus on complex
carbohydrates and protein-rich foods. The other statements reflect appropriate strategies for
managing dumping syndrome: eating smaller, more frequent meals), lying down after eating, and
avoiding fluids with meals are all recommended practices to help reduce symptoms.

After endoscopy, the patient indicated PUD. The most appropriate teaching point the nurse should
provide to the patient with peptic ulcer disease (PUD) is: Alcohol can irritate the stomach lining and
increase acid production, which may exacerbate ulcer symptoms and hinder healing. Excessive milk
intake is not recommended and may actually stimulate acid production. Pureed diet is not necessary
for all patients with PUD; a balanced diet is typically encouraged unless specific symptoms warrant it.
Medications will allow the patient to maintain their current diet, which may not be realistic, as dietary
modifications may be necessary for symptom management.

Patient with PUD can be treated with H2-receptor blockers. The statement H2 blockers block
histamine which causes the chief cells to decrease the secretion of hydrochloric acid is misleading
as H2 blockers primarily act on the parietal cells in the stomach to block histamine receptors, which
reduces the secretion of hydrochloric acid. While it indirectly affects the chief cells, the primary action
is on the parietal cells. Ranitidine and famotidine are indeed types of H2 blockers. Antacids can
interfere with the absorption of H2 blockers if taken together, so they are often recommended to be
spaced apart.