Scenario 1: Peptic Ulcer
A 65-year-old female comes to the clinic with a complaint of abdominal pain in the epigastric area. The pain has been persistent for two weeks. The pain described as burning, non-radiating and worse after meals. Denies N&V, weight loss or obvious bleeding. She admits to frequent belching with bloating.
PMH: seasonal allergies with Chronic Sinusitis, positive for osteoarthritis,
Meds: Claritin 10 mg po daily, ibuprofen 400-600 mg po prn pain
Family Hx-non contributary
Social history: Separated recently pending divorce; stressful situation with trying to manage two homes. Works as a Legal Assistant at a local law firm. She has 35 PPY of smoking, drinks 1-2 glasses of wine a day, and 6-7 cups of coffee per day. She denies illicit drug use, vaping or unprotected sexual encounters.
Breath test in the office revealed + urease.
The healthcare provider suspects the client has peptic ulcer disease.
Questions:
1. Explain what contributed to the development from this patient’s history of PUD?
Your Answer:
The excessive release of gastric acid and the resulting breakdown of the stomach’s protective mucosal Request Unlock barrier are the root causes of peptic ulcer disease, manifesting as inflammation and ulceration of the mucosal lining. Duodenal, stomach, and stress ulcers are the three kinds of ulcers. H. pylori infection and long-term usage of NSAIDS have been linked to ulcers in the duodenum and stomach. The patient’s positive urease result suggested they were infected with H. pylori, which raised their likelihood of developing PUD. PUD risk factors include the patient’s history of using NSAIDs, the patient’s age, the patient’s current smoking status, the patient’s current drinking status (more than one or two glasses of wine per day), and the patient’s current psychological stress levels. The interaction of NSAIDs and H. Pylori may influence peptic ulcer pathogenesis. Coffee and alcohol cause more acid to be produced, eroding the mucosal lining and promoting more inflammation. Nicotine reduces stomach mucosal prostaglandin production, making the mucosa more prone to ulceration.
Scenario 1: Peptic Ulcer
A 65-year-old female comes to the clinic with a complaint of abdominal pain in the epigastric area. The pain has been persistent for two weeks. The pain described as burning, non-radiating and worse after meals. Denies N&V, weight loss or obvious bleeding. She admits to frequent belching with bloating.
PMH: seasonal allergies with Chronic Sinusitis, positive for osteoarthritis,
Meds: Claritin 10 mg po daily, ibuprofen 400-600 mg po prn pain
Family Hx-non contributary
Social history: Separated recently pending divorce; stressful situation with trying to manage two homes. Works as a Legal Assistant at a local law firm. She has 35 PPY of smoking, drinks 1-2 glasses of wine a day, and 6-7 cups of coffee per day. She denies illicit drug use, vaping or unprotected sexual encounters.
Breath test in the office revealed + urease.
The healthcare provider suspects the client has peptic ulcer disease.
Question:
1. What is the pathophysiology of PUD/ formation of peptic ulcers?
In peptic ulcer disease, the protective mucosal barrier of the stomach is compromised, leading to inflammation and ulceration of the Request Unlock mucosa. Due to PUD risk factors, duodenal acid, and pepsin concentrations can breach the mucosal barrier and produce ulcers. The duodenal acid environment is ideal for the growth of H. pylori. Disruption of the gastrointestinal (GI) tract’s inner lining due to gastric acid production or pepsin causes PUD. It penetrates the stomach epithelium down to the muscularis propria layer. It often affects the stomach and the first part of the duodenum. It is well-documented that H. pylori colonizes the stomach mucosa and causes inflammation there. Acidity and stomach metaplasia are facilitated by H. pylori’s interference with bicarbonate production.
Scenario 2: Gastroesophageal Reflux Disease (GERD)
A 44-year-old morbidly obese female comes to the clinic complaining of “burning in my chest and a funny taste in my mouth”. The symptoms have been present for years but patient states she had been treating the symptoms with antacid tablets which helped until the last 4 or 5 weeks. She never saw a healthcare provider for that. She says the symptoms get worse at night when she is lying down and has had to sleep with 2 pillows. She says she has started coughing at night which has been interfering with her sleep. She denies palpitations, shortness of breath, or nausea.
PMH-HTN, venous stasis ulcers, irritable bowel syndrome, osteoarthritis of knees, morbid obesity (BMI 48 kg/m2)
FH:non contributary
Medications: Lisinopril 10 mg po qd, Bentyl 10 mg po, ibuprofen 800 mg po q 6 hr prn
SH: 20 PPY of smoking, ETOH rarely, denies vaping
Diagnoses: Gastroesophageal reflux disease (GERD).
Question:
1. If the client asks what causes GERD how would you explain this as a provider?
Your Answer:
The symptoms of GERD are caused by acid from the stomach traveling back up into Request Unlock the esophagus. The hallmark of pyrosis is a burning feeling below the breastbone, which most people call heartburn. In someone who has just eaten, this may be accompanied by regurgitation. Some drugs (calcium channel blockers), a hiatal hernia, and obesity may all cause the lower esophageal sphincter (LES) to relax, allowing stomach contents to enter the lower esophagus and potentially cause inflammation and erosion of the esophagus.
Scenario 3: Upper GI Bleed
A 64-year-old male presents the clinic with complaints of passing dark, tarry, stools. He stated the first episode occurred last week, but it was only a small amount after he had eaten a dinner of beets and beef. The episode today was accompanied by nausea, sweating, and weakness. He states he has had some mid epigastric pain for several weeks and has been taking OTC antacids. The most likely diagnosis is upper GI bleed which won’t be confirmed until further endoscopic procedures are performed.
Question:
1. What are the variables here that contribute to an upper GI bleed?
Your Answer:
Explicit, bright red bleeding in emesis or black, granular digested blood (often known as Request Unlock “coffee grounds”) in the stool are telltale signs of bleeding in the esophagus, stomach, or duodenum, all parts of the upper gastrointestinal (GI) tract. Drugs (nonsteroidal anti-inflammatory medicines [NSAIDs]), aspirin, selective serotonin reuptake inhibitors, antiplatelet and anticoagulant medications, malignancy, arteriovenous malformations, and peptic ulcers may all contribute to the development of upper gastrointestinal bleeding.
Scenario 4: Diverticulitis
A 54-year-old schoolteacher is seeing your today for complaints of passing bright red blood when she had a bowel movement this morning. She stated the first episode occurred last week. The episode today was accompanied by nausea, sweating, and weakness. She states she has had some LLQ pain for several weeks but described it as “coming and going”. She says she has had a fever and abdominal cramps that have worsened this morning.
Diagnosis is lower GI bleed secondary to diverticulitis.
Question:
1. What can cause diverticulitis in the lower GI tract?
Herniations of the mucosa, or Request Unlock saclike protrusions of mucosa through the muscular layers of the colon wall, are what we call diverticula. Infection of the diverticula is the root cause of diverticulitis. If undigested food or feces becomes lodged in one of the pouches, it might lead to an infection. The feces bacteria may then proliferate and spread, leading to an illness. Fever, leukocytosis, and lower left quadrant discomfort manifest when diverticula become inflamed or abscesses form.