Concepts of Gastrointestinal and Hepatobiliary Disorders

Explain what contributed to the development of this patient’s history of PUD?

PUD is distinguished by a breach in the mucosa that extends to the submucosa or deeper layers. PUD primarily affects gastric and duodenal mucosa. Peptic ulcer disease originates from an array of etiologies. However, the most common etiologies include NSAID use, alcohol, and H. pylori (McCance & Huether, 2019).

Concepts of Gastrointestinal and Hepatobiliary Disorders

In the case scenario, the patient apparently has all these predominant etiologies. For instance, her urease test is positive, which points to H. pylori, and she uses ibuprofen, an NSAID. She also takes wine. Additional risk factors for her PUD development include smoking and emotional stress following a pending divorce.

What is the pathophysiology of PUD/ formation of peptic ulcers? 

Peptic ulcer disease stems from an imbalance between gastric mucosa’s destructive and protective factors. Protective factors include GI mucus, bicarbonate, mucosal blood flow, tight intercellular junctions, cell renewal and restitution, and prostaglandins E, F, and I (McCance & Huether, 2019). Gastrointestinal mucosa, for instance, protects against mucosal damage, lubricates against friction, and controls the diffusion of hydrogen ions.

On the other hand, aggressive factors include acid, pepsin, bile, pancreatic enzymes, and H.pylori. With the destruction of the mucosal layer, the bicarbonate production is decreased resulting in enhanced susceptibility of the deep layers to acidity (McCance & Huether, 2019). Several factors alter this balance, including NSAIDs, H. pylori, alcohol, steroids, psychological stress, and genetic factors.

 If the client asks what causes GERD how would you explain this as a provider?

GERD is a condition that develops following the backflow of stomach contents into the esophagus. The exact cause related to the development of GERD is unknown. However, it is stipulated that GERD stems from a multifactorial etiology. For instance, motor abnormalities, esophageal dysmotility, impaired tone of the lower esophageal sphincter, delayed gastric emptying, and transient lower esophageal sphincter relaxation, have been identified (Clarrett & Hachem, 2018).

Additionally, anatomical factors such as hiatal hernia and an increase in intraabdominal pressure, as in the case of obesity, predispose to GERD. Other risk factors correlated with GERD symptoms include smoking, alcohol consumption, pregnancy, age greater than 50 years, connective tissue disorders, low socioeconomic status, and drugs such as anticholinergics, benzodiazepines, and calcium channel blockers (Clarrett & Hachem, 2018).

What are the variables here that contribute to an upper GI bleed?

Upper GI bleeding implies gastrointestinal bleeding that originates proximal to the ligament of Treitz. According to McCance and Huether. (2019), upper GI bleeding accounts for 70 to 80% of all gastrointestinal bleeding. In the scenario presented, variables that contribute to the diagnosis of an upper GI bleed include age, passing dark tarry stools, history of antiacids, and mid-epigastric pain for several weeks.

An age greater than 60 years increases the risk of gastrointestinal bleeding, while the passage of black tarry stool predominantly originates from upper GI bleeding. Finally, antiacid use and mid-epigastric pain are associated with peptic ulcer disease, the most common cause of upper GI bleeding.

What can cause diverticulitis in the lower GI tract? 

Diverticula refers to sac-like protrusions in the colonic wall (Strate & Morris, 2019). These outpouchings are a consequence of the weakness of the outer muscle layer of the colonic wall. Diverticulitis refers to the inflammation or infection of these sac-like protrusions. The distinct cause of diverticulitis is unclear.

However, several factors contribute to the risk of diverticulitis, including increased pressure from constipation, abdominal obesity, and smoking (Strate & Morris, 2019). Similarly, diet plays a significant role in the development of diverticulitis, particularly high-fat, red meat, and low-fiber diet (Strate & Morris, 2019). Finally, exposure to drugs such as opioids, steroids, and NSAIDs increases the risk of diverticulitis.

References

  • Clarrett, D. M., & Hachem, C. (2018). Gastroesophageal reflux disease (GERD). Missouri Medicine115(3), 214–218. https://www.ncbi.nlm.nih.gov/pubmed/30228725
  • McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). Mosby.
  • Strate, L. L., & Morris, A. M. (2019). Epidemiology, pathophysiology, and treatment of diverticulitis. Gastroenterology156(5), 1282-1298.e1. https://doi.org/10.1053/j.gastro.2018.12.033

Concepts of Gastrointestinal and Hepatobiliary Disorders Assignment Instructions

Q&A.
Knowledge Check
Short essay answers.
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Learning Resources
Required Readings (click to expand/reduce)

McCance, K. L. & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). St. Louis, MO: Mosby/Elsevier.

Chapter 38: Structure and Function of the Renal and Urological Systems including Summary Review
Chapter 39: Alteration of Renal and Urinary Function (stop at Fluids and electrolytes); Summary Review
Chapter 41: Structure and Function of the Digestive System (stop at Tests of digestive function); Summary Review
Chapter 42: Alterations of Digestive Function (stop at Cancer of the digestive track); Summary Review
Osna, N. A., Donohue, T. M., Jr., & Kharbanda, K. K. (2017). Alcoholic liver disease: Pathogenesis and current management. Alcoh

QUESTION 1

  1. 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?

QUESTION 2

  1. 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? 

QUESTION 3

  1. 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? 

 

QUESTION 4

  1. 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?

QUESTION 5

  1. 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 inthe lower GI tract?