NURS 6501 Week 5 Knowledge Check

NURS-6501 Week 5 Knowledge Check

NURS-6501 Week 5 Knowledge Check

QUESTION1

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. NURS-6501 Week 5 Knowledge Check

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? P. 1332

 

PUD is a break or ulceration in the mucosal lining of the lower esophagus, stomach, or duodenum. This patient has several risk factors contributing to the development of PUD. Namely:

 

• Daily use of Ibuprofen for osteoarthritis pain
• High psychological stress d/t pending divorce, working, and managing 2 homes
• Smoking (35 PPY)
• Alcohol use (1-2 glasses wine/day) NURS-6501 Week 5 Knowledge Check
• Age (65)
• Coffee consumption is debated as a potential causative factor for PUD; research is not definitive at this point
• Breath test positive for urease indicates presence of pylori infection of the gastric mucosa

 

NOTE: Chronic use of NSAIDS, such as Ibuprofen for the osteoporosis suffered by this patient, suppresses mucosal prostaglandin synthesis. This, in turn, results in decreased bicarbonate secretion and mucin production. The bicarbonate is a buffer against HCl, and mucin is a component of the gut barrier. Subsequently, secretion of HCl is increased. The interaction of NSAIDS and H. Pylori can contribute to the pathogenesis of peptic ulcer as both disrupt the integrity of the mucosa. This exposes submucosal areas to gastric secretions and autodigestion, causing erosion and ulceration.

QUESTION2

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. NURS-6501 Week 5 Knowledge Check

The healthcare provider suspects the client has peptic ulcer disease.

Question:

1. What is the pathophysiology of PUD/ formation of peptic ulcers? P. 1335

The two major types of peptic ulcers are duodenal ulcers and gastric (stomach) ulcers. Both are predominately caused by H. pylori and NSAID usage. The pathophysiology of both is similar, however, in duodenal ulcers, acid and pepsin concentrations in the duodenum penetrate the mucosal barrier and lead to ulceration. In the case of gastric ulcers, duodenal reflux of bile precipitates ulcer formation by limiting the mucosa’s ability to secrete a protective layer of mucus. The pyloric sphincter may fail to respond properly allowing reflux of bile and pancreatic enzymes to damage the gastric mucosa. The damaged mucosal barrier permits hydrogen ions to diffuse into the mucosa. Here they disrupt permeability and cellular structure. A vicious cycle is then established as the damaged mucosa liberates histamine. This stimulates the increase of acid and pepsinogen production, blood flow, and capillary permeability. The disrupted mucosa becomes edematous and loses plasma proteins. The destruction of small vessels causes bleeding. NURS-6501 Week 5 Knowledge Check

Thus, the pathophysiology of the various peptic ulcer formation has similar beginnings and can diverge from there to follow a couple different pathways.  Initially:

1. Causative factors: pylori, bile salts, NSAIDS, alcohol, ischemia
2. Damaged mucosal barrier
3. Decreased function of mucosal cells, decreased quality of mucus, loss of tight junctions between cells
4. Back-diffusion of acid into gastric LEADS TO EITHER:
   1. Conversion of pepsinogen to This leads to further mucosal erosion, destruction of blood vessels and bleeding. Resulting in ulceration.
   2. Formation and liberation of This leads to local vasodilation, and resulting increased capillary permeability, loss of plasma proteins, mucosal edema, and loss of plasma into gastric lumen. This formation and liberation of histamine also increases acid secretion leading to both ulceration and muscle spasms.

NOTE: H. pylori which thrives in the presence of increased acidity also leads to mucosal injury, and thereby, ulceration.

To summarize, Peptic ulcer disease (PUD) accounts for up to 40% of cases and those at particularly high risk for PUD include alcoholics, patients on extensive NSAIDs, and those with chronic renal failure. PUD has been strongly linked to infection with Helicobacter pylori. This bacterium is responsible for the destruction of protective mechanisms in the stomach and duodenum leading to damage by stomach acid that would otherwise not be a problem. These ulcers are found more commonly in the duodenum than in the stomach, although both locations present with equal incidences of bleeding.

NURS-6501 Week 5 Knowledge Check QUESTION3

1. Scenario 2: Gastroesophageal Reflux Disease (GERD)

A 44-year-old morbidly obese female comes to the clinic complaining of “b

urning 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? 1326

 

GERD is caused by frequent acid reflux; the reflux of acid and pepsin or bile salts from the stomach to the esophagus. This, in turn, causes esophagitis, or inflammation and irritation of the esophagus. To break it down even more, when you swallow, a circular band of muscle around the bottom of your esophagus (lower esophageal sphincter or LES) relaxes to allow food and liquid to flow into your stomach. Then the sphincter closes again. If the sphincter relaxes abnormally or weakens, stomach acid can flow back up into your esophagus. This constant backwash of acid irritates the lining of your esophagus, often causing it to become inflamed. NURS-6501 Week 5 Knowledge Check

I would then explain to the patient risk factors that increase a person’s susceptibility to developing GERD, as well and factors that can aggravate acid reflux as follows:

Risk factors: Conditions that can increase your risk of GERD include:

• Obesity
• Bulging of the top of the stomach up into the diaphragm (hiatal hernia)
• Drugs or chemials that relax the LES (anti-cholinergic, nitrates, calcium channel blockers, nicotine)
• Pregnancy
• Connective tissue disorders, such as scleroderma
• Delayed stomach emptying. NURS-6501 Week 5 Knowledge Check

Factors that can aggravate acid reflux include:

• Smoking
• Eating large meals or eating late at night
• Eating certain foods (triggers) such as fatty or fried foods
• Drinking certain beverages, such as alcohol or coffee
• Taking certain medications, such as aspirin

QUESTION4

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? P. 1324-1325

The variables that contribute to an upper GI bleed in this patient include, foremost, the passing of dark, tarry stools. Additionally, nausea, sweating, weakness, and mid-epigastric pain are also symptoms of a GI bleed. Furthermore, this patient has been taking OTC antacids which generally contain aspirin. Aspirin and contribute to ulceration. NURS-6501 Week 5 Knowledge Check

Bleeding within the GI tract itself not a disease, but rather a symptom of a disease. This bleeding may be divided into upper and lower GI bleeding The gastrointestinal (GI) tract begins in the mouth and works its way down the esophagus, through the stomach, small and large intestines, and rectum, before terminating at the anus. Bleeding or hemorrhaging anywhere along this pathway may be acute or chronic and can be due to a host of factors. Bleeds from the upper GI tract are significant causes of morbidity and mortality and are much more common than lower GI bleeds. Important to note is that mortality associated with upper GI bleeds are often because of comorbidities rather than the actual bleeding itself.

Signs of upper GI bleed include:

• Melena, or dark, tarry stool that is almost black in color
• Nausea
• Hematemesis (vomiting blood)
• Weakness
• Pale skin
• Shortness of breath
• Sweating
• Alterations of consciousness
• Mild epigastric and diffuse abdominal pain

The major causes of upper GI bleeding include:

• peptic ulcer bleeding (most common) NURS-6501 Week 5 Knowledge Check
• erosive esophagitis and erosive gastritis
• esophageal inflammation (most commonly d/t acid reflux)
• esophageal varices (abnormally dilated vessels; typically seen in patients with portal hypertension and chronic liver disease and these patients are at an increased risk for hemorrhage)
• Mallory-Weiss syndrome (caused by violent coughing or vomiting; results in tear of mucous membrane most commonly where stomach and esophagus meet)
• Patients in shock due to trauma, sepsis, or organ failure can also have upper GI bleeds as a result of erosions occurring in the presence of decreased blood flow and altered acidity of the gastric
• cancer

Common risk factors for upper GI bleeding include:

• prior upper GI bleeding
• anticoagulant use
• high-dose nonsteroidal anti-inflammatory drug use
• older age

The most common conditions associated with lower GI bleeding include:

• diverticulitis (diverticular disease)
• infections
• polyps
• inflammatory bowel disease
• hemorrhoids
• anal fissures

NURS-6501 Week 5 Knowledge Check QUESTION5

1. Scenario 4: Diverticulitis

A 54-year-old schoolteacher is seeing you 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?

Diverticula are small, bulging pouches that can form in the lining of your digestive system. They are found most often in the lower part of the large intestine (colon). Diverticula are common, especially after age 40, and seldom cause problems.

The presence of diverticula is known as diverticulosis. When one or more of the pouches become inflamed, and in some cases infected, that condition is known as diverticulitis. Diverticulitis can cause severe abdominal pain, fever, nausea, and a marked change in your bowel habits. Mild diverticulitis can be treated with rest, changes in your diet and antibiotics. NURS-6501 Week 5 Knowledge Check

Symptoms

The signs and symptoms of diverticulitis include:

• Pain, which may be constant and persist for several The lower left side of the abdomen is the usual site of the pain. Sometimes, however, the right side of the abdomen is more painful, especially in people of Asian descent.
• Nausea and
• Abdominal
• Constipation or, less commonly,

When to see a doctor

Get medical attention anytime you have constant, unexplained abdominal pain, particularly if you also have a fever and constipation or diarrhea.