PUD and ZES - Free MCQ Practice Test with solutions, NEET PG Medicine

• In case of gastrinoma showing metastasis the diagnostic sensitivity of octreoscan is 80-100%.
• In contrast in primary gastrinoma. Endoscopic ultrasound shows a sensitivity of 80-100% versus octreoscan which shows a sensitivity of 67-86%. (The given figures are quoted from Harrison page 2240, Harrison 20th ed.).

• Cetuximab is the first line treatment for Menetrier's disease. Other agents like octreotide, H₂ receptor antagonists yield varying results.
• The rare gastropathy is characterised by foveolar cell hyperplasia and marked reduction in oxyntic cells, parietal cells and chief cells.

Zollinger Ellison Syndrome is a tumour of G cells. Due to presence of chronic hypergastrinemia there is a resultant marked gastric acid hypersecretion and growth of the gastric mucosa.
The gastric acid hypersecretion characteristically causes peptic ulcer disease, often refractory and severe, as well as diarrhea.
Clinical features:

1. Abdominal pain (70-100%)
2. Diarrhea (37-73%)
3. Gastroesophageal reflux disease (GERD) (30-35%)

Most common site of ZES (50-70%) is the duodenum, followed by the pancreas (20-40%) and other intraabdominal sites (mesentery, lymph nodes, biliary tract, liver, stomach, Ovary).
Work up:

1. The secretin provocative test is usually positive, with the criterion of a > 120-pg/mL increase over the basal level having the highest sensitivity (94%) and specificity (100%).
2. Fasting hypergastrinemia, and Fasting stomach pH < 2 when off anti-secretory drugs.
3. Plasma ionized calcium
4. Serum prolactin levels
5. Plasma PTH and GH levels
6. Increased Basal acid output

Tumour localisation in ZES :Endoscopic USG > portal venous sampling > octreo-scan. Pointers to presence of ZES:

1. Peptic ulcer disease (PUD); with diarrhea
2. P.U.D in an unusual location or with multiple ulcers
3. P.U.D refractory to treatment or persistent; PUD associated with prominent gastric fold
4. P.U.D associated with findings suggestive of MEN 1 (endocrinopathy, family history of ulcer or endocrinopathy, nephrolithiases)
5. P.U.D without Helicobacter pylori present.

• Majority of Duodenal ulcers occur due to H. pylori and NSAID-induced injury leading to decreased prostaglandins.
• DUs occur most often in the first portion of the duodenum (> 95%), with -90% located within 3 cm of the pylorus.
• They are usually < 1 cm in diameter with depth at times reaching the muscularispropria.
• The base of the ulcer often consists of a zone of eosinophilic necrosis with surrounding fibrosis.
• The reason for the reduction in the frequency of DUs is likely related to the decreasing frequency of Helicobacter pylori due to eradication therapy.

ELISA test has sensitivity of 80% and has been replaced by C-13 urea breath test and fecal antigen immunoassay. Both have sensitivity of > 90%.
Endoscopy is not indicated to diagnose H. pylori in most circumstances. Hence though rapid urease test is having a comparable sensitivity and higher specificity, it is an invasive test Sensitivity of various diagnosis tests

In assessment of response to treatment, non-invasive tests are preferred. Breath urea test will be done but can be false negative if done within 4 weeks of antibiotic treatment.

• H. pylori releases urease enzyme which converts urea to ammonia and ammonia stimulates G cells of stomach which inturn stimulates parietal cells and cause excess secretion of acid. This acid travels into stomach & duodenum a causes peptic ulcers.
• H. pylori is a type 1 carcinogen, which, if present in stomach for long term can cause cancer called MALTOMA (Mucosa Associated Lymphoid Tumor), which is a B-type NHL.

Long-term acid suppression, especially with PPIs, has been associated with

1. A higher incidence of community-acquired pneumonia
2. Community and hospital acquired Clostridium difficileassociated disease.
3. A population-based study revealed that long-term use of PPIs was associated with the development of hip fractures in older women. The absolute risk of fracture remained low despite an observed increase associated with the dose and duration of acid suppression
4. PPIs may exert a negative effect on the anti-platelet effect of clopidogrel. The mechanism involves the competition of the PPI and clopidogrel with the same cytochrome p450 (CYP2C19).

Ulcer located along the lesser curve of the stomach and posterior duodenal bulb are at greater risk for severe bleeding and rebleeding due to the proximity of the left gastric artery and gastro-duodenal artery, respectively. The mortality rate for bleeding peptic ulcers is approximately 6%-7%.

Type A is autoimmune gastritis with antibodies against parietal cells whereas the gastritis caused by H. Pylori is referred to as type B gastritis.

• Breath urea test: The patient drinks a solution of urea labeled with the nonradioactive isotope 13C and then blows into a tube. If urease is present, the urea is hydrolyzed and labeled carbon dioxide is detected in breath samples.
• After first line course of antibiotics, breath urea test can be performed and if it turns negative that indicates eradication of Infection.
• In case the test is still positive, second line antibiotics should be started.

• On examination of vitals where BP is low and pulse is increased, CVA is ruled out as stroke presents with Cushing reflex (Bradycardia and hypertension).
• Pulmonary embolism develops in setting of hypercoagulable state which is unlikely as he is taking aspirin for long time
• Since patient is taking aspirin, it cuts the risk of Ml and there is no history of chest pain or ECG findings given
• The diagnosis points to gastric ulcer with bleed in lieu of history of aspirin intake plus passage of black stools plus features of shock due to blood loss.

Helicobacter Pylori leads to type B gastritis characterized by hypergastrinemia and hyperchlorhydria.

• Geriatric age group presentation is a risk factor for coronary artery disease. Chest pain can be misleading. The breathlessness and bradycardia and hypotension point towards myocardial infarction.
• Hence the initial evaluation at presentation should be ECG.
• Second-degree heart block (intermittent AV block) may occur as a transient abnormality in inferior wall MI
• Although many patients have a normal pulse rate and blood pressure within the first hour of STEMI, about one-fourth of patients with anterior infarction have manifestations of sympathetic nervous system hyperactivity (tachycardia and/or hypertension), and up to one-half with inferior infarction show evidence of parasympathetic hyperactivity (bradycardia and/or hypotension).

The agents used with the greatest frequency include amoxicillin, metronidazole, tetracycline, clarithromycin, and bismuth compounds. Multiple drugs have been evaluated in the therapy of H. pylori. No single agent is effective in eradicating the organism. Combination therapy for 14 days provides the greatest efficacy. A shorter course administration (7-10 days), although attractive, has not proved as successful as the 14-days regimens.

Surgery is more often required for treatment of an ulcer-related complication.

1. Hemorrhage is the most common ulcer-related complication, occurring in 15 - 25% of patients. Bleeding may occur in any age group but is most often seen in older patients (sixth decade or beyond). Patients unresponsive or refractory to endoscopic intervention will require surgery (-5% of transfusion-requiring patients).
2. Free peritoneal perforation occurs in 2 - 3% of DU patients. Concomitant bleeding may occur in up to 10% of patients with perforation, with mortality being increased substantially. Peptic ulcer can also penetrate into adjacent organs, especially with a posterior DU, which can penetrate into the pancreas, colon, liver, or biliary tree.
3. Pyloric channel ulcers or DUs can lead to gastric outlet obstruction in 2 - 3% of patients. This can result from chronic scarring or from impaired motility due to inflammation and/or edema with pylorospasm. If a mechanical obstruction persists, endoscopic intervention with balloon dilation may be effective. Surgery should be considered if all else fails.

• Dietary modification is the cornerstone of therapy for patients with dumping syndrome.
• Small, multiple meals devoid of simple carbohydrates coupled with elimination of liquids during meals is important.
• Antidiarrheals and anticholinergic agents are complementary to diet. Pectin, which increases the viscosity of intraluminal contents, may be beneficial in more symptomatic individuals.
• Acarbose, an alpha-glucosidase inhibitor that delays digestion of ingested carbohydrates, has also been shown to be beneficial in the treatment of the late phases of dumping.
• The somatostatin analogue octreotide has been successful in diet-refractory cases

• Helicobacter pylori eradication has reduced complications and recurrence of peptic ulcer. Due to low socio-economic status and Feco-oral contamination favoring spread of H. Pylori the incidence in India is high.
• The physician's goal in treating PUD is to provide relief of symptoms (pain or dyspepsia), promote ulcer healing, and ultimately prevent ulcer recurrence and complications. The greatest impact of understanding the role of H. pylori in peptic disease has been the ability to prevent recurrence. Documented eradication of H. pylori in patients with PUD is associated with a dramatic decrease in ulcer recurrence to <10 - 20% as compared to 59% in GU patients and 67% in DU patients when the organism is not eliminated. Eradication of the organism may lead to diminished recurrent ulcer bleeding.

Most gastrinomas (50 - 70%) are present in the duodenum, followed by the pancreas (20 - 40%) and other intraabdominal sites (mesentery, lymph nodes, biliary tract, liver, stomach, ovary).

•  The diagnosis of ZES requires the demonstration of inap-propriate fasting hypergastrinemia, usually by demonstrating hypergastrinemia occurring with an increased basal gastric acid output (BAO) (hyperchlorhydria).
• Chronic unexplained diarrhea also should suggest gastrinoma.
• Approximately 20 - 25% of patients with ZES have MEN 1, and in most cases hyperparathyroidism is present before the gastrinoma. These patients are treated differently from those without MEN 1; therefore, MEN 1 should be sought in all patients by family history and by measuring plasma ionized calcium and prolactin levels and plasma hormone levels (parathormone, growth hormone).

Misoprostol can trigger uterine contractions and hence contraindicated in a pregnant lady.

• Phlegmonous means a diffuse spreading inflammation of or within connective tissue. In the stomach, it implies infection of the deeper layers of the stomach (submucosa and muscularis).
• Phlegmonous gastritis is an uncommon form of gastritis caused by numerous bacterial agents, including streptococci, staphylococci, Proteus species, Clostridium species, and Escherichia coli.
• Phlegmonous gastritis usually occurs in individuals who are debilitated. It is associated with a recent large intake of alcohol, a concomitant upper respiratory tract infection, and AIDS.
• As a result, purulent bacterial infection may lead to gangrene. Phlegmonous gastritis is rare. The clinical diagnosis is usually established in the operating room, as these patients present with an acute abdominal emergency requiring immediate surgical exploration. Without appropriate therapy, it progresses to peritonitis and death.

Most sensitive & specific method for identifying Zollinger Ellison syndrome is demonstration of an increased fasting serum gastrin concentration (> 150 pg/mL)

Abdominal angina is defined as the (postprandial pain that occurs in individuals with mesenteric vascular occlusive disease such that blood flow cannot increase enough to meet visceral demands). The classic feature is abdominal pain, which occurs a few minutes after eating and slowly subsides over next few hours. Gradually, most patients develop fear of eating and lose significant weight. A history of peripheral vascular disease and significant smoking is common.

• 10% of patients may seek medical attention for the treatment of postvagotomy diarrhea. This complication is most commonly observed after truncal vagotomy.
• This is due to a motility disorder from interruption of the vagal fibers supplying the luminal gut. Other contributing factors may include decreased absorption of nutrients, increased excretion of bile acids, and release of luminal factors that promote secretion. Diphenoxylate or loperamide is often useful in symptom control.

• Viral infections can cause gastritis. Cytomegalovirus (CMV) is a common viral cause of gastritis. It is usually encountered in individuals who are immunocompromised, including those with cancer, immunosuppression, transplants, and AIDS. Gastric involvement can be localized or diffuse.
• Fungal infections that cause gastritis include Candida albicans and histoplasmosis. Gastric phycomycosis is another rare lethal fungal infection. The common predisposing factor is immunosuppression.

• Because of gravity, the inciting agents lie on the greater curvature of the stomach. This partly explains the development of acute gastritis distally on or near the greater curvature of the stomach in the case of orally administered NSAIDs. However, the major mechanism of injury is the reduction in prostaglandin synthesis. Prostaglandins are chemicals responsible for maintaining mechanisms that result in the protection of the mucosa from the injurious effects of the gastric acid.
• H pylori gastritis typically starts as an acute gastritis in the antrum, causing intense inflammation, and over time, it may extend to involve the entire gastric mucosa resulting in chronic gastritis.

GUs tend to occur later in life than duodenal lesions, with a peak incidence reported in the sixth decade. More than one- half of GUs occur in males and are less common than DUs, perhaps due to the higher likelihood of GUs being silent and presenting only after a complication develops.

• Pernicious anemia is associated with auto-immune gastritis. The auto-antibodies against the parietal cells will lead to achlorhydria. This type of gastritis spares the antrum and involves mainly the body.
• Gastric acid plays an important role in feedback inhibition of gastrin release from G cells. Achlorhydria, coupled with relative sparing of the antral mucosa (site of G cells), leads to hyper gastrinemia. Gastrin levels can be markedly elevated (> 500 pg/mL) in patients with pernicious anemia. Hypergastrinemia and achlorhydria may also be seen in non-pernicious anemia-associated type A gastritis.

• Endoscopic ultrasound permits imaging of ZES with high degree of resolution (<5 mm). This modality rules out small neoplasms in pancreas.
• In imaging modalities for ZES: best answer is EUS > octreoscan > MRI > USG
• The secretin provocative test is usually positive, with the criterion of a > 120-pg/mL increase over the basal level having the highest sensitivity (94%) and specificity (100%).

Type A gastritis is characterized by achlorhydria due to autoimmune destruction of parietal cells. The feedback leads to increased gastrin.

• Signs and symptoms arise from the rapid emptying of hyperosmolar gastric contents into the small intestine, resulting in a fluid shift into the gut lumen with plasma volume contraction and acute intestinal distention.
• Release of vasoactive GI hormones (vasoactive intestinal polypeptide, neurotensin, motilin) is also theorized to play a role in early dumping.
• Early dumping takes place 15 - 30 minutes after meals and consists of crampy abdominal discomfort, nausea, diarrhea, belching, tachycardia, palpitations, diaphoresis, light headedness, and, rarely, syncope.
• Late phase of dumping is due to hypoglycemia from excessive insulin release.