5 - Gastric Disorders
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Questions and Answers

In the context of chronic gastritis stemming from autoimmune disease, what is the MOST likely underlying mechanism contributing to the observed neurological symptoms?

  • Autoantibody-mediated destruction of parietal cells, resulting in impaired intrinsic factor production and vitamin B12 malabsorption. (correct)
  • Hypersecretion of hydrochloric acid triggering vagal nerve dysfunction and impaired neurotransmitter synthesis in the central nervous system.
  • Malabsorption of iron due to chronic inflammation, inducing iron-deficiency anemia and subsequent neurological sequelae.
  • Direct neuronal invasion by _Helicobacter pylori_, leading to demyelination and axonal degradation.

A patient with chronic gastritis presents with glossitis, peripheral neuropathy, and gait ataxia. Which of the following interventions directly addresses the pathophysiological origin of these manifestations?

  • Recommend a gluten-free diet to reduce intestinal inflammation and improve nutrient assimilation.
  • Administer broad-spectrum antibiotics to eradicate potential enteric pathogens exacerbating mucosal inflammation.
  • Initiate high-dose proton pump inhibitor therapy to mitigate gastric acid secretion and promote mucosal healing.
  • Prescribe intramuscular injections of cobalamin (vitamin B12) to circumvent impaired absorption and replenish depleted stores. (correct)

A patient diagnosed with acute gastritis following prolonged NSAID use is prescribed a proton pump inhibitor (PPI). What is the MOST critical mechanism by which PPIs facilitate gastric mucosal healing in this scenario?

  • Irreversible inhibition of the H+/K+-ATPase pump, suppressing gastric acid secretion and reducing mucosal irritation. (correct)
  • Sequestration of reactive oxygen species, mitigating oxidative stress and preventing further cellular damage.
  • Neutralization of gastric acid, creating an alkaline environment conducive to epithelial regeneration.
  • Stimulation of prostaglandin synthesis, enhancing mucosal blood flow and cytoprotection.

In managing a patient with acute gastritis secondary to ingestion of a strong alkali, which intervention is MOST contraindicated?

<p>Administration of a weak acid solution to neutralize the alkali. (C)</p> Signup and view all the answers

A patient undergoing radiation therapy for esophageal cancer develops acute gastritis. What is the primary pathophysiological mechanism by which radiation induces gastric mucosal damage?

<p>Direct cytotoxic effects on rapidly dividing gastric epithelial cells, impairing mucosal regeneration. (D)</p> Signup and view all the answers

A patient with a history of chronic Helicobacter pylori gastritis is undergoing eradication therapy with clarithromycin, amoxicillin, and a proton pump inhibitor. What is the MOST critical mechanism of action of clarithromycin in this therapeutic regimen?

<p>Inhibition of bacterial protein synthesis by binding to the 50S ribosomal subunit, impairing bacterial growth. (B)</p> Signup and view all the answers

A patient with chronic atrophic gastritis is at increased risk for gastric adenocarcinoma. Which of the following cellular or molecular events is MOST closely associated with this increased risk?

<p>Epigenetic silencing of DNA repair genes, leading to accumulation of somatic mutations. (B)</p> Signup and view all the answers

Following a partial gastrectomy, a patient develops dumping syndrome. What is the primary pathophysiological mechanism underlying the early phase of this syndrome?

<p>Rapid gastric emptying of hyperosmolar chyme into the small intestine, causing fluid shifts and intestinal distension. (C)</p> Signup and view all the answers

A patient with severe acute gastritis presents with hematemesis and signs of hypovolemic shock. After initial resuscitation, which diagnostic procedure is MOST appropriate to identify the source and severity of the bleeding?

<p>Esophagogastroduodenoscopy (EGD) with possible hemostatic intervention to directly visualize and treat the bleeding site. (A)</p> Signup and view all the answers

A researcher is investigating novel therapeutic targets for chronic gastritis. Which of the following molecular pathways, if inhibited, would MOST likely reduce inflammation and promote mucosal healing?

<p>Activation of the nuclear factor kappa B (NF-κB) signaling pathway. (A)</p> Signup and view all the answers

In the context of a perforated peptic ulcer, which pathophysiological cascade most accurately describes the progression from initial insult to potential systemic sequelae?

<p>Serosal breach → peritoneal contamination → localized peritonitis → systemic inflammatory response syndrome (SIRS). (D)</p> Signup and view all the answers

A patient presents with a rigid, board-like abdomen and severe upper abdominal pain radiating to the shoulder. Initial management includes NPO status and nasogastric (NGT) insertion. What is the PRIMARY rationale for these interventions in the immediate management of this patient?

<p>To decrease intra-abdominal pressure and prevent further contamination of the peritoneum. (C)</p> Signup and view all the answers

Following a Billroth II procedure, a patient reports experiencing episodes of lightheadedness, diaphoresis, and abdominal cramping approximately 30 minutes after meals. Which of the following mechanisms BEST explains the pathophysiology underlying these symptoms?

<p>Rapid influx of hyperosmolar gastric contents into the small intestine. (B)</p> Signup and view all the answers

In the management of H. pylori eradication therapy, which of the following accurately describes the rationale for including bismuth subsalicylate in a quadruple therapy regimen?

<p>Bismuth subsalicylate potentiates the antimicrobial effects of other antibiotics and inhibits urease activity. (C)</p> Signup and view all the answers

A patient with a history of peptic ulcer disease is prescribed a highly selective vagotomy. Which of the following physiological outcomes is the MOST anticipated result of this procedure?

<p>Targeted reduction of gastric acid secretion with preservation of antral motor function. (A)</p> Signup and view all the answers

A patient who underwent a Billroth I gastroduodenostomy several years ago presents with anemia and signs of malabsorption. Which of the following pathophysiological mechanisms is the MOST likely contributing factor to these findings?

<p>Accelerated gastric emptying leading to inadequate mixing of chyme with pancreatic enzymes and bile. (D)</p> Signup and view all the answers

Which of the following diagnostic modalities provides the MOST definitive assessment for confirming the presence of H. pylori-induced peptic ulcer disease and simultaneously allows for histopathological evaluation to rule out malignancy?

<p>Upper endoscopy with biopsy. (C)</p> Signup and view all the answers

In managing a patient with a perforated duodenal ulcer, initial resuscitation includes intravenous crystalloid administration. Which of the following hemodynamic parameters should be MOST aggressively targeted during the initial phase of resuscitation, considering the risk of exacerbating peritoneal contamination?

<p>Systolic blood pressure (SBP) of 90-100 mmHg, balancing perfusion with minimizing leakage from the perforation. (A)</p> Signup and view all the answers

A patient with chronic peptic ulcer disease is prescribed a proton pump inhibitor (PPI). What is the underlying mechanism of action of PPIs in reducing gastric acid secretion?

<p>Irreversible inhibition of the H+/K+-ATPase pump on parietal cells. (D)</p> Signup and view all the answers

Which of the following dietary modifications is MOST appropriate for a patient recovering from a bleeding peptic ulcer to minimize gastric irritation and promote mucosal healing?

<p>Frequent small meals avoiding spicy foods, alcohol, and caffeine. (D)</p> Signup and view all the answers

In the pathophysiology of Peptic Ulcer Disease (PUD), which intricate interplay of factors predominantly determines the progression from mucosal integrity to ulcer formation, considering both aggressive and protective mechanisms at a molecular level?

<p>A multifactorial etiology involving impaired somatostatin release affecting gastric acid inhibition, coupled with increased gastrin-releasing peptide (GRP) activity escalating pepsinogen secretion, while concurrently depleting trefoil factors essential for mucosal repair. (C)</p> Signup and view all the answers

How does the chronic erosion characteristic of chronic peptic ulcers manifest at the cellular level, differentiating it from acute ulcers, and what are the implications for long-term tissue remodeling?

<p>The erosion in chronic ulcers extends through the muscularis mucosa, stimulating fibroblast proliferation and collagen deposition, resulting in substantial fibrosis and potential stricture formation. (C)</p> Signup and view all the answers

Given the range of diagnostic findings in gastritis, how does the interpretation of gastric analysis data differentiate between various etiologies, and what are the clinical implications?

<p>Differentiating between achlorhydria, hypochlorhydria, and hyperchlorhydria through gastric analysis aids in discerning atrophic gastritis, pernicious anemia, and Zollinger-Ellison syndrome respectively, informing targeted management strategies. (C)</p> Signup and view all the answers

What are the implications of administering Misoprostol, a cytoprotective drug, in the context of peptic ulcer disease, and under what specific conditions is its use absolutely contraindicated, considering its mechanism of action at the cellular level?

<p>Misoprostol, a synthetic prostaglandin E1 analog, is strictly contraindicated during pregnancy due to its potential to induce uterine contractions, leading to abortion or premature labor. (B)</p> Signup and view all the answers

How does Sucralfate exert its cytoprotective effect in managing peptic ulcers, and what patient-specific factors must be considered to mitigate its most common adverse effect, especially in the context of polypharmacy?

<p>Sucralfate forms a viscous gel to coat the ulcer crater, protecting it from acid and pepsin; constipation can be managed by adequate hydration and dietary fiber, but caution is needed with concurrent use of aluminum-containing antacids in patients with renal dysfunction. (D)</p> Signup and view all the answers

Considering the multifaceted nursing management of gastritis, what are the specific rationales behind advising patients to avoid alcohol and smoking, and how do these recommendations correlate with the underlying pathophysiology of the condition?

<p>Alcohol and smoking are strictly contraindicated due to their direct toxic effects on gastric mucosa, impairing mucosal defense mechanisms, increasing acid secretion, and exacerbating inflammation, thus hindering healing and potentially leading to chronic disease. (D)</p> Signup and view all the answers

In cases of gastritis complicated by hemorrhage, what are the critical considerations for fluid resuscitation, hemodynamic monitoring, and transfusion management, taking into account the potential risks and benefits of different resuscitation strategies?

<p>In hemorrhagic gastritis, a balanced resuscitation approach is advocated, incorporating crystalloids, colloids, and blood products as needed, guided by continuous hemodynamic monitoring and assessment of end-organ perfusion, while carefully considering the risks of over-resuscitation and transfusion-related complications. (D)</p> Signup and view all the answers

When managing gastritis with concurrent vomiting, what is the underlying rationale for instituting NPO status alongside intravenous fluid administration and antiemetic therapy, considering the physiological mechanisms involved in gastric motility and fluid balance?

<p>Implementing NPO status reduces gastric distension and stimulation of the vomiting center, while IV fluids correct dehydration and electrolyte imbalances, and antiemetics mitigate nausea and vomiting, thus facilitating gastric mucosal healing by reducing irritation and acid exposure. (A)</p> Signup and view all the answers

How does Vitamin B12 deficiency, consequent to conditions like pernicious anemia often associated with chronic gastritis, impact cellular function at a molecular level, and what specific neurological manifestations arise from this deficiency?

<p>Vitamin B12 deficiency disrupts myelin synthesis due to impaired methylmalonyl-CoA mutase and methionine synthase activity. This leads to impaired neuronal transmission, causing peripheral neuropathy, subacute combined degeneration of the spinal cord, and cognitive dysfunction. (A)</p> Signup and view all the answers

Considering the recommendation to avoid spicy foods, caffeine, and large heavy meals in managing gastritis, what is the evidence-based rationale behind these dietary modifications in relation to the underlying pathophysiology of gastric inflammation and acid secretion?

<p>Spicy foods, caffeine, and large heavy meals are avoided as they can stimulate gastric acid secretion, increase gastric motility, and delay gastric emptying, thereby exacerbating mucosal inflammation and symptoms in gastritis. (D)</p> Signup and view all the answers

In the context of Stress-Related Mucosal Disease (SRMD), which pathophysiological mechanism most accurately differentiates Cushing's ulcer from Curling's ulcer?

<p>Cushing's ulcers are characterized by the disruption of the gastric mucosal barrier due to ischemia induced by increased intracranial pressure, commonly found in head trauma patients. Curling's ulcers, on the other hand, are associated with severe burns leading to hypovolemia, reduced gastric blood flow, and subsequent mucosal damage. (A)</p> Signup and view all the answers

Which of the following clinical scenarios would most strongly suggest a diagnosis of Zollinger-Ellison syndrome over a typical duodenal ulcer?

<p>A patient presenting with recurrent duodenal ulcers refractory to high-dose proton pump inhibitors (PPIs), accompanied by diarrhea and elevated fasting serum gastrin levels that paradoxically increase after secretin stimulation. (C)</p> Signup and view all the answers

How does the pathophysiology of pain differ between gastric and duodenal ulcers in relation to food intake, and what underlying mechanisms account for these differences?

<p>Gastric ulcer pain worsens 30-60 minutes after eating due to gastric acid secretion stimulated by food intake, eroding the ulcerated mucosa, whereas duodenal ulcer pain is alleviated by food because it buffers gastric acid, reducing mucosal irritation until gastric emptying occurs. (B)</p> Signup and view all the answers

A patient with a history of chronic NSAID use presents with signs of upper gastrointestinal bleeding, including melena and hematemesis. Endoscopy reveals multiple gastric ulcers and a single duodenal ulcer. What is the most likely mechanism by which NSAIDs contribute to the formation of these ulcers?

<p>NSAIDs inhibit cyclooxygenase (COX) enzymes, reducing the synthesis of prostaglandins, which normally inhibit gastric acid secretion, increase bicarbonate production, and enhance mucosal blood flow, resulting in impaired mucosal protection and increased ulcer susceptibility. (B)</p> Signup and view all the answers

What factors most critically determine whether a patient with a bleeding peptic ulcer requires surgical intervention rather than continued endoscopic and medical management?

<p>The severity and persistence of bleeding, the failure of endoscopic hemostasis, and hemodynamic instability despite aggressive resuscitation. (D)</p> Signup and view all the answers

In a patient presenting with symptoms of gastroparesis and a history of recurrent peptic ulcers, each unresponsive to standard treatments, which diagnostic procedure is most crucial for differentiating between mechanical gastric outlet obstruction and a motility disorder?

<p>A gastric emptying study using scintigraphy to quantify the rate of gastric emptying, differentiating between delayed emptying due to obstruction versus dysmotility. (B)</p> Signup and view all the answers

A patient with a known history of peptic ulcer disease presents with sudden, severe abdominal pain, rigidity, and signs of peritonitis. Based on the likely diagnosis, what initial imaging modality is most appropriate to confirm the suspected complication?

<p>Plain abdominal radiographs to look for free air under the diaphragm, indicating perforation. (A)</p> Signup and view all the answers

A patient being treated for a duodenal ulcer develops symptoms of acute upper gastrointestinal bleeding. After initial resuscitation, which of the following is the most appropriate next step in managing this patient?

<p>Perform an upper endoscopy to visualize the bleeding site, assess the severity of bleeding, and attempt endoscopic hemostasis. (A)</p> Signup and view all the answers

In the management of peptic ulcer disease, what is the rationale behind using bismuth-containing quadruple therapy as a first-line treatment option for Helicobacter pylori eradication, especially in regions with high clarithromycin resistance?

<p>Bismuth has intrinsic antibacterial properties against H. pylori and is less susceptible to resistance compared to other antibiotics like clarithromycin, making it a reliable component in regions where clarithromycin resistance is prevalent. (B)</p> Signup and view all the answers

In the context of gastric ulcers, what is the most critical distinction that mandates biopsy of the ulcer margins during endoscopy?

<p>To rule out malignancy, as gastric ulcers can be associated with gastric cancer, and biopsy allows for histological examination of the tissue. (D)</p> Signup and view all the answers

Flashcards

Gastritis

Inflammation of the stomach lining (gastric mucosa).

Acute Gastritis

Gastritis that appears suddenly and lasts for a short duration.

Chronic Gastritis

Gastritis that develops slowly and persists over a long period.

Causes of Acute Gastritis

Irritating foods, contaminated foods, overuse of NSAIDs, alcohol, radiation, or ingestion of strong acids/alkalis.

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Causes of Chronic Gastritis

Ulcers, H. pylori, autoimmune diseases, smoking, and alcohol.

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Symptoms of Acute Gastritis

Abdominal discomfort, headache, nausea/vomiting, anorexia, and hiccupping.

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Symptoms of Chronic Gastritis

Anorexia, heartburn, belching, sour taste, nausea/vomiting, and B12 deficiency.

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Treatment for Acute Gastritis

Remove the cause, antiemetics, antacids, H2 antagonists, NPO until nausea subsides, bland diet.

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Treatment for Chronic Gastritis

Bland diet, small frequent meals, antacids, anticholinergics, antibiotics for H. pylori.

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Symptoms of Vitamin B12 Deficiency

Red, smooth, sore tongue, numbness, paresthesia, weakness, and ataxia.

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Gastritis diet

Regeneration of the stomach lining, avoid spicy foods, caffeine, and large meals.

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Pernicious Anemia Treatment

Monthly intramuscular injections of Vitamin B12.

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Pain Relief for Gastritis

Antacids that reduce pain. Example: Aluminum Hydroxide with Magnesium Trisilicate.

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Achlorhydria

Absence of hydrochloric acid in gastric secretions.

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Hypochlorhydria

Low levels of hydrochloric acid in gastric secretions.

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Hyperchlorhydria

High levels of hydrochloric acid in gastric secretions.

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Gastritis Diet

Non-irritating foods and bland diet.

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Vomiting Management in Gastritis

Rest, NPO status, IV fluids, antiemetics.

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Hemorrhage Management in Gastritis

IV fluids, monitor vital signs, and possible blood transfusion.

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Peptic Ulcer Disease (PUD)

Erosion of the GI mucosa from the digestive action of HCl and pepsin.

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Stress-Related Mucosal Disease

Acute ulcers that develop after major physiological stress like trauma or surgery.

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Cushing's Ulcer

Stress ulcer common in patients with head and brain injuries.

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Curling's Ulcer

Stress ulcer frequently observed about 72 hours after extensive burns.

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Gastric Ulcer Location

Ulcer located in the lesser curvature of the antrum.

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Duodenal Ulcer Location

Ulcer located in the first 1-2 cm of the duodenum.

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Gastric Ulcer Secretion

Gastric acid secretion that is normal to decreased.

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Duodenal Ulcer Secretion

Gastric acid secretion that is hypersecreted.

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Zollinger-Ellison Syndrome

Rare condition with severe peptic ulcers, gastric acid hypersecretion & elevated gastrin levels.

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Duodenal Ulcer Pain

Pain occurs 2-4 hours after meals and is relieved by food

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Hemorrhage in PUD

Most common complication of peptic ulcer disease.

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PUD Perforation

Penetration of an ulcer through the stomach or duodenal wall, leading to leakage into the peritoneal cavity.

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Perforation Manifestations

Sudden, severe abdominal pain, rigid abdomen, rapid breathing, and absent bowel sounds.

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Endoscopy Use

Direct visualization of the gastric and duodenal mucosa, allowing for biopsy sampling.

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Serum IgG Test

Noninvasive test to confirm H. pylori infection with high sensitivity.

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Pre-Gastric Analysis Prep

Withholding food/fluids and certain medications before gastric analysis.

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PUD Nursing Management

Creating a calm environment and ensuring sufficient physical and emotional rest.

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Dietary Restrictions for PUD

Foods that irritate the stomach, high-roughage foods, and large meals consumed infrequently.

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Billroth I (Gastroduodenostomy)

Partial removal of the stomach with connection to the duodenum.

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Billroth II (Gastrojejunostomy)

Partial removal of the stomach w/ connection to the jejunum.

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Vagotomy

Severing the vagus nerve to reduce gastric acid production.

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Study Notes

Gastritis

  • Gastritis is an inflammation of the gastric or stomach mucosa.
  • Gastritis is classified as either acute or chronic.

Acute Gastritis

  • Irritating and/or contaminated foods can cause acute gastritis.
  • Overuse of aspirin and NSAIDS can lead to acute gastritis.
  • Excessive alcohol intake and radiation therapy increase risk of acute gastritis.
  • Ingestion of strong acid & alkali can cause acute gastristis.
  • Clinical manifestations include abdominal discomfort, headache, and lassitude.
  • Nausea, vomiting, anorexia, and hiccuping are clinical signs of acute gastritis.
  • Management includes removing the original cause and treating the manifestations.
  • Pt should take antiemetics and antacids or H2 receptor antagonists.
  • Pt should be NPO until nausea and vomiting subside.
  • Pt diet should include decaffeinated tea, gelatin, toast, & simple bland foods when food is tolerated.
  • Pt should avoid spicy foods, caffeine, & large heavy meals.

Chronic Gastritis

  • Ulcers of the stomach can cause chronic gastritis.
  • Helicobacter pylori bacteria and autoimmune diseases like pernicious anemia may cause chronic gastritis.
  • Smoking & alcohol are factors in chronic gastritis.
  • Anorexia, heartburn, belching, a sour taste in the mouth, nausea, and vomiting are indicators of chronic gastritis.
  • Vitamin B12 deficiency is noted with a red, smooth, sore tongue, numbness, paresthesia, weakness, and ataxia.
  • A bland diet of small frequent meals, antacids, anticholinergics, and sedatives can help.
  • Clarithromycin (Baxin), metronidazole (Flagyl), and omeprazole (Prilosec) may be prescribed if H. pylori infection is present.
  • A corticosteroid may be prescribed for parietal cell regeneration
  • Vitamin B12 IM may administered monthly for pernicious anemia.
  • Pain can be reduced with Al(OH)3 with Mg Trisilicate (Gaviscon).

Assessment and Diagnostic Findings for Gastritis

  • GI x-ray series can be used for assessment.
  • Endoscopy with histological exam obtained through biopsy can provide a definitive diagnosis.
  • Achlorhydria is the absence of HCI.
  • Hypochlorhydria indicated low levels of HCI.
  • Hyperchlorhydria means there are high levels of HCI.
  • A Complete Blood Count (CBC) may demonstrate the presence of anemia.
  • Medical management includes antibiotics, antacids, Hâ‚‚R blockers and PPIs.
  • Cytoprotective drugs can also be used for medical management.
  • E.G., Misoprostol (Cytotec) should not be used by pregnant women.
  • Sucralfate (Carafate) has a common side effect of constipation

Nursing Management for Gastritis

  • Modify diet, and promote an optimal diet of Non-irritating foods and bland diet.
  • Avoid alcohol and smoking because they are contraindicated to all forms of gastritis.
  • Stop medications that induce gastritis
  • Offer small, frequent meals.
  • Avoid overeating.
  • If the patient is vomiting, rest, maintain NPO status, administer IV fluids, and antiemetics.
  • If there is hemorrhaging, administer IV fluids, monitor vital signs, and prepare for possible blood transfusion (BT) management.

Peptic Ulcer Disease (PUD)

  • PUD is a condition characterized by erosion of the GI mucosa resulting from the digestive action of HCI and pepsin.
  • Decreased mucous secretion can be caused by stress and stimulants.
  • Increased HCI and pepsin secretion can be caused by less blood flow and irritants.
  • The damage of mucous membranes creates ulcers.

Types of PUD

  • Acute PUD is associated with superficial erosion and minimal inflammation.
  • Acute PUD has a short duration and resolves quickly when the cause is removed.
  • Chronic PUD is long-duration eroding through the muscular wall with the formation of fibrous tissue.
  • Stress-Related Mucosal Disease (physiologic stress ulcers) are acute ulcers that develop following a major physiologic insult such as trauma or surgery.
  • Cushing's ulcer is common in patients with head injury and brain trauma.
  • Curling's ulcer is frequently observed about 72 hours after extensive burns.
  • Chronic PUD presents continuously for many months or intermittently, and has a high incidence of perforation.

Location of PUD

  • A gastric ulcer is located on the lesser curvature of the antrum.
  • Gastric secretion is normal to decreased.
  • Gastric ulcers are more frequent in women.
  • Peak age of onset for gastric ulcers is 50 – 60 years.
  • Duodenal ulcers are located in the 1st 1 - 2 cm of the duodenum.
  • Hypersecretion is noted with duodenal uclers.
  • Duodenal ulcers are more common in men.
  • Peak age of onset for duodenal ulcers is 35 – 45 years.
  • H. pylori, chronic alcoholism, and chronic gastritis can cause gastric ulcers.
  • Bile reflux, smoking and certain drugs (such as NSAIDS, corticosteroids and/or aspirin) can cause gastric ulcers.
  • H. pylori, and alcohol & smoking are causitive factors in duodenal ulcers.
  • Zollinger-Ellison syndrome is a rare condition characterized by severe peptic ulcerations, gastric acid hypersecretion, elevated serum gastrin levels.
  • Zollinger-Ellison syndrome is characterized by benign or malignant tumor of the pancreas or duodenum.

Signs & Symptoms of PUD

  • Pain after 1½ - 2 hours after a meal is characteristic of a gastric ulcer.
  • Eating may worsen pain.
  • Pain is described as burning or gaseous with gastric ulcers.
  • Pain is at the high left epigastrium.
  • Weight loss and hemorrhage are more likely to occur with gastric ulcers.
  • Pain 2 - 4 hours after a meal is characteristic of a duodenal ulcer.
  • Eating may relieve pain.
  • Pain is described as burning or cramplike with duodenal ulcers.
  • Pain is at the midepigastrium.
  • Pt often awakens 1 – 2 AM.
  • Duodenal ulcers may cause weight gain.
  • Occurring continuously for a few weeks or months and then disappear for a time, only to recur some months later is characteristic of duodenal ulcers.

Complications of PUD

  • Hemorrhage is the most common complication of PUD.
  • Perforation is the penetration of ulcer into the serosal surface, resulting to spillage of either gastric or duodenal contents into the peritoneal cavity.
  • Perforation is considered the most lethal complication of PUD.
  • Sudden, severe upper abdominal pain and shoulder pain are characteristics of PUD.
  • A rigid, boardlike abdomen indicates PUD resulting from a perforated ulcer.
  • Shallow and rapid breathing and absent bowel sounds can indicate PUD.

Diagnostic Studies and Treatment for PUD

  • Endoscopy allows for a direct viewing of the gastric and duodenal mucosa.
  • Endoscopy also allows tissue sample collection for biopsy study.
  • Serum immunoglobulin G (IgG) is a noninvasive procedure of confirming H. pylori infection.
  • Serum immunoglobulin G (IgG) is 90% - 95% sensitive for H. pylori infection.
  • NPO for 8 – 12 hours is necessary for Gastric Analysis.
  • Drugs affecting gastric secretions should be withheld for 24 – 48 hours before Gastric Analysis.
  • No smoking in the morning before the test.
  • An NG tube is inserted, and gastric contents are aspirated.
  • Histalog and Pentagastrin are administered.
  • The normal serum gastrin level is 1.5 mEq/L (1.5 mmol/L)
  • Elevated serum gastrin level and elevated gastric acid secretion indicate PUD.
  • Ensure adequate rest (for both physical and emotional), provide a quiet and calm environment.
  • Stop all drugs that cause ulceration.
  • Avoid foods that may irritate gastric mucosa (hot, spicy foods and pepper, alcohol, carbonated drinks, tea, coffee, and broth [meat extracts]).
  • Avoid foods high in roughage, such as fruit, salad, and vegetables.
  • Implement small frequent feedings (6x a day).
  • HELIVAX, Metronidazole (Flagyl), and Tetracycline are used for drug therapy.
  • Hâ‚‚R blockers, PPI and Cytoprotective (Bismuth subsalicylate [Pepto-Bismol])are used for drug therapy.
  • Monitor vital signs with especial attention to BP (every 15 – 30 min) for Hemorrhage and Perforation
  • Refer to the physician if the patient has signs of Hemorrhage and Perforation
  • Maintain NPO for patients that are suffering from Hemorrhage and Perforation
  • Insert NGT and administer IV fluid replacement (lactated Ringer's solution).
  • Blood transfusion may be required.
  • Billroth I or Gastroduodenostomy: is partial gastrectomy with removal of the distal two-thirds of the stomach and anastomosis of the gastric stump to the duodenum.
  • Billroth II or Gastrojejunostomy: is partial gastrectomy with removal of the distal two-thirds of the stomach and anastomosis of the gastric stump to the jejunum.
  • Vagotomy is severing of the vagus nerve.
  • Truncal vagotomy: severs the main trunk of vagus nerve.
  • Selective vagotomy: cuts the vagus nerve at a particular branch
  • Vagotomy decreases gastric acid production
  • Dumping syndrome occurs as a surgical complication due to accelerated gastric emptying when hyperosmolar gastric contents rapidly pass into the intestine.
  • A patient experiences diarrhea, abdominal pain, borborygmi, nausea, vomiting, flushing, weakness, palpitations, diaphoresis, lightheadedness, and syncope 15 – 20 mins after eating, as the manifestations of dumping syndrome.
  • Reactive hypoglycemia (Postprandial Hypoglycemia) can occur due to the uncontrolled gastric emptying of a bolus of fluid high in carbohydrate into the small intestine.
  • Sweating, weakness, mental confusion, palpitations, tachycardia, and anxiety are the manifestations of Postprandial Hypoglycemia.

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