Podcast
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?
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?
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?
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?
In managing a patient with acute gastritis secondary to ingestion of a strong alkali, which intervention is MOST contraindicated?
A patient undergoing radiation therapy for esophageal cancer develops acute gastritis. What is the primary pathophysiological mechanism by which radiation induces gastric mucosal damage?
A patient undergoing radiation therapy for esophageal cancer develops acute gastritis. What is the primary pathophysiological mechanism by which radiation induces gastric mucosal damage?
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?
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?
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?
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?
Following a partial gastrectomy, a patient develops dumping syndrome. What is the primary pathophysiological mechanism underlying the early phase of this syndrome?
Following a partial gastrectomy, a patient develops dumping syndrome. What is the primary pathophysiological mechanism underlying the early phase of this syndrome?
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?
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?
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?
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?
In the context of a perforated peptic ulcer, which pathophysiological cascade most accurately describes the progression from initial insult to potential systemic sequelae?
In the context of a perforated peptic ulcer, which pathophysiological cascade most accurately describes the progression from initial insult to potential systemic sequelae?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
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?
In the context of Stress-Related Mucosal Disease (SRMD), which pathophysiological mechanism most accurately differentiates Cushing's ulcer from Curling's ulcer?
In the context of Stress-Related Mucosal Disease (SRMD), which pathophysiological mechanism most accurately differentiates Cushing's ulcer from Curling's ulcer?
Which of the following clinical scenarios would most strongly suggest a diagnosis of Zollinger-Ellison syndrome over a typical duodenal ulcer?
Which of the following clinical scenarios would most strongly suggest a diagnosis of Zollinger-Ellison syndrome over a typical duodenal ulcer?
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?
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?
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?
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?
What factors most critically determine whether a patient with a bleeding peptic ulcer requires surgical intervention rather than continued endoscopic and medical management?
What factors most critically determine whether a patient with a bleeding peptic ulcer requires surgical intervention rather than continued endoscopic and medical management?
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?
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?
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?
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?
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?
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?
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?
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?
In the context of gastric ulcers, what is the most critical distinction that mandates biopsy of the ulcer margins during endoscopy?
In the context of gastric ulcers, what is the most critical distinction that mandates biopsy of the ulcer margins during endoscopy?
Flashcards
Gastritis
Gastritis
Inflammation of the stomach lining (gastric mucosa).
Acute Gastritis
Acute Gastritis
Gastritis that appears suddenly and lasts for a short duration.
Chronic Gastritis
Chronic Gastritis
Gastritis that develops slowly and persists over a long period.
Causes of Acute Gastritis
Causes of Acute Gastritis
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Causes of Chronic Gastritis
Causes of Chronic Gastritis
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Symptoms of Acute Gastritis
Symptoms of Acute Gastritis
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Symptoms of Chronic Gastritis
Symptoms of Chronic Gastritis
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Treatment for Acute Gastritis
Treatment for Acute Gastritis
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Treatment for Chronic Gastritis
Treatment for Chronic Gastritis
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Symptoms of Vitamin B12 Deficiency
Symptoms of Vitamin B12 Deficiency
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Gastritis diet
Gastritis diet
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Pernicious Anemia Treatment
Pernicious Anemia Treatment
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Pain Relief for Gastritis
Pain Relief for Gastritis
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Achlorhydria
Achlorhydria
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Hypochlorhydria
Hypochlorhydria
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Hyperchlorhydria
Hyperchlorhydria
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Gastritis Diet
Gastritis Diet
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Vomiting Management in Gastritis
Vomiting Management in Gastritis
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Hemorrhage Management in Gastritis
Hemorrhage Management in Gastritis
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Peptic Ulcer Disease (PUD)
Peptic Ulcer Disease (PUD)
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Stress-Related Mucosal Disease
Stress-Related Mucosal Disease
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Cushing's Ulcer
Cushing's Ulcer
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Curling's Ulcer
Curling's Ulcer
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Gastric Ulcer Location
Gastric Ulcer Location
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Duodenal Ulcer Location
Duodenal Ulcer Location
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Gastric Ulcer Secretion
Gastric Ulcer Secretion
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Duodenal Ulcer Secretion
Duodenal Ulcer Secretion
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Zollinger-Ellison Syndrome
Zollinger-Ellison Syndrome
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Duodenal Ulcer Pain
Duodenal Ulcer Pain
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Hemorrhage in PUD
Hemorrhage in PUD
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PUD Perforation
PUD Perforation
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Perforation Manifestations
Perforation Manifestations
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Endoscopy Use
Endoscopy Use
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Serum IgG Test
Serum IgG Test
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Pre-Gastric Analysis Prep
Pre-Gastric Analysis Prep
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PUD Nursing Management
PUD Nursing Management
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Dietary Restrictions for PUD
Dietary Restrictions for PUD
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Billroth I (Gastroduodenostomy)
Billroth I (Gastroduodenostomy)
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Billroth II (Gastrojejunostomy)
Billroth II (Gastrojejunostomy)
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Vagotomy
Vagotomy
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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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