Assignment

Applied medicine
 Assignment
Submitted To: Dr. Asad

Submitted By: Dr.

Sap Id: 70059756

Semester: MID 5th

1. Case 1

2. Gastric ucer
 Definition
 Etiology
 Clinical features
 Pathogenesis
 Stages
 Diagnosis
 Differential diagnosis
 Treatment
 Complications
 Prevention
 Prognosis
 Risk factors
Case 2
Peptic ulcer
 Definition
 Etiology
 Clinical features
 Pathogenesis
 Stages
 Diagnosis
 Differential diagnosis
 Treatment
 Complications
 Prevention
 Prognosis
 Risk factors
 CASE 1
History:
 A 23 years old male visited clinic with complains of an upper abdominal pain, heartburn,
nausea and sometimes vomiting. He was in usual state of health 5 days back when he
started having epigastric pain. Pain aggravated at night after taking large meal. He was
fond of fried and spicy food. He had a family history of peptic ulcer disease. He denied
cigarette smoking.
Past medication history
 He was using Synflex (naproxen) to relieve pain from past 2 days, but no significant effect.
Then he decided to consult doctor.
Past medical history: Past medical history reveals the absence of any disease in the patient.
Family history: Patient’s father had a history of peptic ulcer disease.
Diagnosis of peptic ulcer
 According to the provided information, patient’s laboratory tests were done. Serological
and Urea breadth test confirmed H. pylori positive infection in the patient.
Medication therapy
Brand Generic Strength Frequency
Amoxil Amoxicillin 1g BID
Clarithro Clarithromycin 250mg BID
Risek Omeprazole 40mg OD
Glamet Ranitidine 150mg BID
Mucaine suspension Aluminium hydroxide 120ml 1 tsp TID
Drug related interventions
a. Take Omeprazole before meal.
b. There is no need of ranitidine (H2 receptor antagonist) at this stage of patient. Triple
drug therapy is followed in the patient. As, PPIs and Mucaine syrup is already
added in medication to relieve burning sensation so, Glamet is skipped from
therapy.
Dietary modifications
a. Omega-3 polyunsaturated fatty acids should be added as they have an anti-
inflammatory effect and protect stomach from ulcers.
b. Avoid spicy food.
c. Avoid late night meals.
d. Take healthy balanced diet having low cholesterol.
e. Take plenty of water and fresh juices.
Lifestyle modifications
a. Avoid lying down in bed immediately after meal.
b. Elevate head of bed.
c. Avoid stress
Outcomes
Patient used the medicine regularly, routine tests and monitoring was done and patient was
improved on follow-up. He was advised to visit in case of any complication.
 ULCERS
Definition:
Peptic ulcers are open sores that develop on
the inside lining of your stomach and the upper
portion of your small intestine. The most
common symptom of a peptic ulcer is stomach
pain.
Peptic ulcers include:
 Gastric ulcers that occur on the inside
of the stomach
 Duodenal ulcers that occur on the
inside of the upper portion of your
small intestine (duodenum)
 The most common causes of peptic ulcers
are infection with the bacterium
Helicobacter pylori (H. pylori) and long-term use of nonsteroidal anti-inflammatory drugs
(NSAIDs) such as ibuprofen (Advil, Motrin IB, others) and naproxen sodium (Aleve). Stress
and spicy foods do not cause peptic ulcers. However, they can make your symptoms worse.
Etiology:
Peptic ulcer disease (PUD) has various causes; however, Helicobacter pylori-associated PUD and
NSAID-associated PUD account for the majority of the disease etiology.
Causes of Peptic Ulcer Disease
Common
 H. pylori infection: H. pylori infection
is more prevalent among those with
lower socioeconomic status and is
commonly acquired during childhood.
The organism has a wide spectrum of
virulence factors allowing it to adhere
to and inflame the gastric mucosa. This
results in hypochlorhydria or
achlorhydria, leading to gastric
ulceration.
 NSAIDs: The secretion of
prostaglandin normally protects the
gastric mucosa. NSAIDs block
prostaglandin synthesis by inhibiting
COX-1 enzyme resulting in a decrease
in gastric mucus and bicarbonate production and a decrease in mucosal blood flow.
 Medications
Rare
 Zollinger-Ellison syndrome
 Malignancy (gastric/lung cancer, lymphomas)
  Stress (Acute illness, burns, head injury)
 Viral infection
 Vascular insufficiency
 Radiation therapy
 Crohn disease
 Chemotherapy
Epidemiology
 PUD is a global problem with a lifetime risk of development ranging from 5% to 10%.
 Overall, there is a decrease in the incidence of PUD worldwide due to improved hygienic
and sanitary conditions combined with effective treatment and judicious use of NSAIDs.
 Duodenal ulcers are four times more common than gastric ulcers. Also, duodenal ulcers
are more common in men than in the woman.
Clinical features
 Burning stomach pain
 Feeling of fullness, bloating or belching
 Intolerance to fatty foods
 Heartburn
 Nausea
 Vomiting or vomiting blood — which may appear red
or black
 Dark blood in stools, or stools that are black or tarry
 Trouble breathing
 Feeling faint
 Nausea or vomiting
 Unexplained weight loss
 Appetite changes
Pathophysiology:
 The mechanism of occurrence of PUD results
from an imbalance between gastric mucosal
protective and destructive factors. Risk factors
predisposing to the development of PUD:
 H. pylori infection
 NSAID use
 First-degree relative with PUD
 Emigrant from a developed nation
 African American/Hispanic ethnicity
 With peptic ulcers, there is usually a defect
in the mucosa that extends to the
muscularis mucosa. Once the protective
superficial mucosal layer is damaged, the
inner layers are susceptible to acidity.
Further, the ability of the mucosal cells to
secrete bicarbonate is compromised.
 H. pylori is known to colonize the gastric
mucosa and causes inflammation. The H.
pylori also impairs the secretion of
bicarbonate, promoting the development of acidity and gastric metaplasia.
Diagnosis:
Diagnosis of PUD requires history taking, physical examination, and invasive/noninvasive
medical tests.
History
A careful history should be obtained and noted for the presence of any complications. Patient
reporting of epigastric abdominal pain, early satiety, and fullness following a meal raise suspicion
of PUD. The pain of gastric ulcers increases 2 to 3 hours after a meal and may result in weight
loss, whereas the pain of duodenal ulcers decreases with a meal which can result in weight gain.
Any patient presenting with anemia, melena, hematemesis, or weight loss should be further
investigated for complications of PUD, predominantly bleeding, perforation, or cancer.
Physical Exam
A physical exam may reveal Epigastric abdominal tenderness and signs of anemia.
Investigations
1. Esophagogastroduodenoscopy (EGD): Gold standard and most accurate diagnostic test
with sensitivity and specificity up to 90% in diagnosing gastric and duodenal ulcers. The
American Society of Gastrointestinal Endoscopy has published guidelines on the role of
endoscopy in patients presenting with upper abdominal pain or dyspeptic symptoms
suggestive of PUD. Patients over 50 years of age and new onset of dyspeptic symptoms
should get evaluated by an EGD. Anyone with the presence of alarm symptoms should
undergo EGD irrespective of age.
2. Barium swallow: It is indicated when EGD is contraindicated.
3. Complete blood work, liver function, and levels of amylase and lipase
 4. Serum gastric is ordered if Zollinger Ellison syndrome is suspected
5. Helicobacter pylori testing:
 Serologic testing
 Urea breath test: High sensitivity and specificity. It may be used to confirm eradication
after 4 to 6 weeks of stopping treatment. In the presence of urease, an enzyme produced by
H.pylori, the radiolabeled carbon dioxide produced by the stomach is exhaled by the lungs.
 Antibodies to H.pylori can also be measured
 Stool antigen test
 Urine-based ELISA and rapid urine test
 Endoscopic biopsy: Culture is not generally recommended as it is expensive, time-
consuming, and invasive. It is indicated if eradication treatment fails or there is suspicion
about antibiotic resistance. Biopsies from at least 4-6 sites are necessary to increase
sensitivity. Gastric ulcers are commonly located on the lesser curvature between the antrum
and fundus. The majority of duodenal ulcers are located in the first part of the duodenum.
6. Computerized tomography of the abdomen with contrast is of limited value in the diagnosis
of PUD itself but is helpful in the diagnosis of its complications like perforation and gastric outlet
obstruction.
Differential diagnosis:
 Acute Cholangitis
 Acute Cholecystitis
 Biliary Colic
 Acute Coronary Syndrome
 Acute Gastritis
 Cholecystitis
Treatment:
Medical treatment
 Antisecretory drugs used for PUD include H2-receptor antagonists and the proton pump
inhibitor (PPIs). PPIs have largely replaced H2 receptor blockers due to their superior
healing and efficacy. PPIs block acid production in the stomach, providing relief of
symptoms and promote healing.
 Treatment may be incorporated with calcium supplements as long-term use of the PPIs can
increase the risk of bone fractures. NSAIDs induced PUD can be treated by stopping the
use of NSAIDs or switching to a lower dose. Corticosteroid, bisphosphonates, and
anticoagulants should also be discontinued if possible. Prostaglandin analogs (misoprostol)
are sometimes used as prophylaxis for NSAID-induced peptic ulcers.
 First-line treatment for H. pylori-induced PUD is a triple regimen comprising two
antibiotics and a proton pump inhibitor. Pantoprazole, clarithromycin, and metronidazole
or amoxicillin are used for 7 to 14 days.
 Antibiotics and PPIs work synergistically to eradicate H. pylori.The antibiotic selected
should take into consideration the presence of antibiotic resistance in the environment. If
first-line therapy fails, quadruple therapy with bismuth and different antibiotics is used.
Refractory disease and surgical treatment
  Surgical treatment is indicated if the patient is unresponsive to medical treatment,
noncompliant, or at high risk of complications.
 A refractory peptic ulcer is one over 5 mm in diameter that does not heal despite 8-12
weeks of PPI therapy.
 The common causes are persistent H/pylori infection, continued use of NSAIDs or
significant comorbidities that impair ulcer healing or other conditions like gastrinoma or
gastric cancer.
 If the ulcer persists despite addressing the above risk factors, patients can be candidates for
surgical treatment. Surgical options include vagotomy or partial gastrectomy.
Complications:
 Upper gastrointestinal bleeding
 Gastric outlet obstruction
 Perforation
 Penetration
 Gastric cancer
Complication Cause

ulcer wears away the stomach or small intestine and breaks the
bleeding
blood vessels there

ulcer breaks through the lining and stomach wall, causing bacteria,
perforation
acid, and food to leak through

inflammation and infection of the abdominal cavity due to

scar tissue can form as a result of the ulcers and keep food from
blockage
leaving the stomach or duodenum

Prevention
 Protect yourself from infections
 Use caution with pain relievers.
Prognosis:
 The prognosis of PUD is excellent after the underlying cause is successfully treated.
Recurrence of the ulcer may be prevented by maintaining good hygiene and avoiding
alcohol, smoking, and NSAIDs.
 Unfortunately, recurrence is common wth rates exceeding 60% in most series. NSAID
induced gastric perforation occurs at a rate of 0.3% per patient per year. However, unlike
the past, mortality rates for peptic ulcer disease have decreased significantly.
Risk factors:
 Smoke. Smoking may increase the risk of peptic ulcers in people who are infected with H.
pylori.
 Drink alcohol. Alcohol can irritate and erode the mucous lining of your stomach, and it
increases the amount of stomach acid that's produced.
 Have untreated stress.
 Eat spicy foods.