Case Studies 3 and 4 - Weebly



Case Studies 3 and 4Laura LangenhopWright State UniversityCase Studies 3 and 41.Which of the following processes can produce postoperative hypotension? Explain your rationale. Bold the correct answer. A. Hypovolemia secondary to blood lossB. SepsisC. Adrenal insufficiencyD. Perioperative myocardial infarctionE. All of the abovePost-operative hypotension can occur through multiple channels. Hypovolemia, sepsis, adrenal insufficiency, and perioperative myocardial infarction are processes that can produce postoperative hypotension. Hypovolemia secondary to acute blood loss can produce post-operative hypotension. An increase in blood loss causes the body to compensate with tachycardia in order to maintain an adequate cardiac output (Laine, 2012). Tachycardia can only persist for a certain amount of time before the body decompensates and hypotension occurs. A decrease in hemoglobin and hematocrit may not decrease initially, but can occur over a period of 72 hours after the acute blood loss as extravascular volume travels into the vascular space (Laine, 2012). Hypovolemia is common following surgery when acute blood loss and extravascular volume manifest (Laine, 2012). If left untreated, hypotension can occur. Sepsis has been known to cause hypotension. Reasons are multifactorial. First, myocardium dysfunction occurs in 40% of patients and can be systolic, diastolic, or biventricular in nature (Ely & Goyette, 2005). Myocardium dysfunction occurs with the release of cytokines and TNF-alpha mediators causing myocardial ischemia followed by reperfusion injury (Ely & Goyette, 2005). Myocardial dilation, ventricular changes, and changes on a patient’s electrocardiogram are suspected to be potential consequences of myocardial dysfunction with subsequent hypotension (Ely & Goyette, 2005). The common response from a person with hypotension is vasoconstriction of the systemic vasculature. In sepsis, a patient is in a state of vasodilation. Blood vessels are unable to properly respond to vasopressors and intravenous fluids causing hypotension (Ely & Goyette, 2005). Nitric oxide in the smooth muscle and endothelium are increased by cytokine activity, causing increased vasodilation and decreasing systemic vascular resistance ultimately causing continued hypotension (Ely & Goyette, 2005). The adrenal gland is important to the hemodynamic stability of a patient. The adrenal cortex releases mineralocorticoids and glucocorticoids in order for glucose to be more readily available and for extracellular volume to be sustained (Marino, 2014). The adrenal medulla releases catecholamines in order to stabilize circulation (Marino, 2014). Adrenal insufficiency can be dormant until a physiologic stressor such as surgery or infection occurs. When patients have adrenal insufficiency, they can become hemodynamically unstable with hypotension being one of the signs (Marino, 2014). Adrenal insufficiency can be due to the inhibition of the hypothalamic-pituitary level or inhibition of the adrenal gland. When adrenal insufficiency is present, the patient experiences hypotension (Marino, 2014). A perioperative myocardial infarction can occur without symptoms when a patient is under anesthesia, while at the same time electrocardiogram and creatine-kinase levels have the inability to be specific and sensitive in their testing because of the co-existence of muscular injury from surgery (Landesberg, Beattie, Mosseri, Jaffe, & Alpert, 2009). A perioperative myocardial infarction develops within two to three days of surgery and is detected between day three and five following surgery (Landesberg et al., 2009). Tachycardia is the most common cause of oxygen demand perioperatively. Following a surgical procedure, hypovolemia and bleeding can cause hypotension due to increased myocardial demand. A myocardial infarction increases the demand on the myocardium and decreases the supply of oxygen throughout the body (Landesberg et al., 2009). Ischemia and hypervolemia leads to myocardial decompensation subsequently producing hypotension (Landesberg et al., 2009). 2. Which of the following is the most appropriate method to diagnose BMAH? Explain your answer. A. Cortrosyn stimulation testB. CT scan of adrenal glandsC. CT scan of adrenal glands and Cortrosyn stimulation testD. Random plasma cortisol levelThe first method in diagnosing bilateral massive adrenal hemorrhage is a computed tomography (CT) scan of the adrenal glands. A CT scan of the adrenal glands is a quick and reliable test for the diagnosis of BMAH (Green & Cohen, 2010). In the instance of BMAH, the adrenal glands have an oval shape, are hyper-dense in structure, and appear to be between two to five centimeters in diameter (Green & Cohen, 2010). The adrenal glands’ crura are thickened. There is reduction in size and density over time. A CT scan of the adrenal glands will show enlarged adrenal glands with high attenuation (Green & Cohen, 2010; Liew et al., 2012). A Cortrosyn stimulation test is another reliable test in confirming the diagnosis of BMAH. The hypothalamus produces a corticotrophin-releasing hormone that in turn causes that anterior pituitary gland to release adrenocorticotrophic hormone (ACTH), producing activity of the adrenal gland (Marino, 2014). Cortisol is therefore released from the adrenal cortex. Normal production of cortisol is 15-25 mg/day in a normal non-stressed individual and up to 350 mg/day for a patient under physiologic stress (Marino, 2014). In patients who remain hypotensive in spite of fluid resuscitation and vasopressor initiation, the diagnosis of adrenal insufficiency should be suspected (Marino, 2014). An ACTH stimulation test is completed by first drawing the patient’s cortisol level at baseline. A baseline cortisol level less that 10 mcg/dL is evident of adrenal insufficiency (Marino, 2014). The patient is then given an intravenous synthetic ACTH dose. After an hour of the ACTH administration, another cortisol level is drawn. If the cortisol level does not increase more that 9 mcg/dL of the baseline cortisol level, suspicion of adrenal insufficiency should be considered (Marino, 2014). 3. Which of the following can occur in patients with primary adrenal insufficiency? Explain your answer. A. Electrolyte abnormalitiesB. HypotensionC. Mental status changeD. Abdominal painE. All of the aboveElectrolyte abnormalities, hypotension, mental status change, and abdominal all occur in primary adrenal insufficiency. The first issue that can arise from adrenal insufficiency is electrolyte abnormalities. The adrenal gland is divided into the outer cortex and the inner medullary zone (Tucci & Sokari, 2014). The adrenal cortex is subdivided into the zona fasiculata, zona reticularis, and zona glomerulosa (Tucci & Sokari, 2014). The zona fasiculata and zona reticularis produce glucocorticoids and androgens. The zona glomerulosa produces mineralcorticoids. The most important mineral-corticoid produced is aldosterone (Tucci & Sokari, 2014). In the presence of adrenal insufficiency aldosterone production is decreased. Inadequate levels of aldosterone released from the adrenal gland cause hypovolemia, hyponatremia, hyperkalemia, and hypotension (Lin & Denker, 2012). In patients with primary adrenal insufficiency, 80% have hyponatremia and 40% have hyperkalemia (Arlt, 2012). The decrease in aldosterone primarily causes hyponatremia. The inability to release anti-diuretic hormone results in a mild form of Syndrome of Inappropriate Secretion of Anti-Diuretic Hormone (SIADH) (Arlt, 2012). Hypercalcemia is also common in untreated adrenal insufficiency due to the uptake of calcium in the renal tubule and gut (Arlt, 2012). Hypotension also occurs in patients with adrenal insufficiency. Hypotension occurs as a result of decreased myocardial contractility as well as a decreased response to catecholamines (Liew, Sheehy, Wood, & Coursin, 2012). The glucocorticoids released by the adrenal gland facilitate catecholamine release, such as norepinephrine and epinephrine, in order to maintain blood pressure. Cardiovascular integrity also is a result of proper glucocorticoid release (Liew et al., 2012). When an improper amount of glucocorticoids is released cardiovascular integrity is compromised and ultimately hypotension occurs (Liew et al., 2012). Postural hypotension may progress to hypovolemic shock in patients if left untreated (Arlt, 2012).Adrenal insufficiency also mimics vague symptoms of acute abdominal pain, abdominal tenderness, fever, nausea, and vomiting (Arlt, 2012). In some cases, patients present to the emergency department with decreased levels of consciousness that can quickly worsen to a coma (Arlt, 2012). Changes in mental status in patients with primary adrenal insufficiency are likely related to abnormal electrolytes. Hyponatremia alone has been known to cause mental status changes in individuals (Arlt, 2012). Surgery, illness, infection, or an increase in glucocorticoid inactivation can cause an adrenal crisis (Alrt, 2012). Treatment of such a crisis requires volume resuscitation, glucocorticoid initiation, and continuous hemodynamic monitoring (Arlt, 2012). 4. Which of the following is not a risk factor for developing BMAH? Explain your rationale.A. Postoperative stateB. CoagulopathyC. Thromboembolic diseaseD. DiabetesE. SepsisThere are often multifactorial reasons why a patient can experience bilateral massive adrenal hemorrhage (BMAH). The adrenal gland receives blood flow from the phrenic artery, adrenal artery, and the subcapsular plexus (Egan, Larkin, Ryan, & Waldron, 2009). Adrenal hemorrhage can occur from hypotension, vascular engorgement, and vascular stasis (Egan et al., 2009). Diabetes is not a risk factor for developing bilateral massive adrenal hemorrhage. Postoperative state, coagulopathy, thromboembolic diseases are risk factors for BMAH. Like sepsis, following surgery there is an inflammatory response that occurs within the body. Adrenal insufficiency in a postoperative patient occurs when the body is unable to produce adequate amounts of cortisol in the face of acute stress (Marik & Zaloga, 2005). In a patient with heparin-induced thrombocytopenia (HIT), coagulopathy is a risk factor for BMAH. Patients with HIT experience a decrease in platelet levels following administration of heparin or low-molecular weight heparin following surgery or for deep vein thrombosis prophylaxis (Rosenberger et al., 2011). HIT is mediated by an antibody effect. The patient may experience a 50% drop in platelets as well as a formation of a new thrombus within 14 days of the heparin administration (Rosenberger et al., 2011). The patient becomes prone to a hypercoaguable state. Risk for hemorrhage as well as bleeding is increased. The adrenal gland promotes an atmosphere of venous and arterial thrombosis leading to a high risk of BMAH (Rosenberger et al., 2011).Thromboembolic disease, as with Antiphospholipid Syndrome (APS), is another risk factor for adrenal hemorrhage (Silverio, Caetano, Gomes, & Sequeira, 2012). Two mechanisms have been proposed as the rationale behind adrenal hemorrhage in the presence of thromboembolic diseases. The first is that the adrenal gland is rich in arterial supply and lacks in venous drainage. Because of the physiology of adrenal gland, there is risk for pockets of turbulence and local stasis of blood (Silverio et al., 2012). In the event of thrombosis, arterial blood pressure in the affected area increases, followed by hemorrhaging. The second mechanism is that the adrenal gland cells are rich in cholesterol (Silverio et al., 2012). In patients with APS, production of antibodies that attack lysobiphosatidic acid in the adrenal cortex causes an increase in cholesterol, the release of lysosomal proteinases, endothelial dysfunction and the production of small thrombi (Silverio et al., 2012). The thrombi travel, like in the first mechanism, leading to increased arterial pressure in the adrenal arteries resulting in hemorrhage (Silverio et al., 2012). Sepsis is also a risk for adrenal insufficiency. It has been reported that up to 60% of patients with severe sepsis and septic shock develop adrenal insufficiency (Marino, 2014). Patients with sepsis suffer from critical illness-related corticosteroid insufficiency. During sepsis, an inflammatory response occurs throughout the whole body. There is suppression of the hypothalamus and pituitary gland causing adrenal insufficiency (Marino, 2014). Therefore, a patient with sepsis is at a higher risk of developing adrenal insufficiency (Marino, 2014). 5. Which of the following statements regarding the long-term management of patients with BMAH is correct? Explain your answer.A. Glucocorticoid therapy is needed only during acute illnessB. Patients should be discharged on maintenance doses of oral glucocorticoids and mineralocorticoids.C. Patients do not need mineralocorticoid therapy.D. Adrenal function is likely to recover over 4 to 6 months with no further need for glucocorticoids.Patients with bilateral massive adrenal hemorrhage should be discharged on both maintenance doses of oral glucocorticoids and mineral-corticoids. Initially, if adrenal crisis is suspected, a bolus dose of hydrocortisone should be administered. Hydrocortisone is then prescribed every six hours for a total dose of 300 mg/day (Rosenberger et al., 2011). Once symptoms and hemodynamics stabilize, the patient may begin taking an oral regimen. Glucocorticoids are prescribed at morning and at nighttime to mimic cortisol secretion. Hydrocortisone is typically prescribed between 15-25 mg in order to resemble the daily cortisol production (Liew et al., 2012). Prednisolone and Dexamethasone may be ordered in place of hydrocortisone for patients who are non-compliant or who experience afternoon fatigue. In the state of Ohio, the advanced practice registered nurse (APRN) can prescribe glucocorticoids (The Ohio Board of Nursing, 2014). Mineralcorticoids, such as Fludrocortisone (Florinef), are initiated and maintained at a dose of 0.1mg/day (Liew et al., 2012). Mineralcorticoids promote reabsorption of sodium and loss of potassium in the renal distal tubules (Rosenberger et al., 2011). Side effects of this medication are hypertension, edema, and hypokalemia. It is important to monitor electrolytes, plasma renin, and blood pressure when prescribing these medications (Liew et al., 2012). In the state of Ohio, the advanced practice registered nurse (APRN) can prescribe glucocorticoids (The Ohio Board of Nursing, 2014).Case Study 4A 46 year-old male comes into the emergency department complaining of nausea and vomiting he has experienced over the past month. The patient states in the past 24 hours he has started to vomit a small amount of bright red blood. The patient states the nausea and vomiting persist throughout the day with no consistency in their presence. The patient’s nausea subsides following consumption of a small amount of food. The patient denies being awakened during the night with nausea. The patient does state he has abdominal pain described as “achy” and “gnawing” in the epigastric area. The patient does admit to feeling fatigued. The patient has taken over the counter ibuprofen 400 mg for the pain every six hours for the past couple of weeks with minimal relief. The patient states his stool has not changed in consistency or color over the past month. The patient denies taking any prescribed medications currently. The patient admits to drinking between two to three glasses of coffee a day. The patient is a vegetarian and states he eats healthy. There has been no unplanned weight loss or weight gain within the last month. The patient is a social drinker, drinking two glasses of wine a week. The patient states he recently changed jobs. The patient traveled to the Caribbean on a cruise where he visited three different islands one month prior to admission. The patient denies being sexually active. Physical examination reveals active bowel sounds. There is no pain on light, moderate and deep palpation. There is negative murphy and McBurney’s signs. The patient’s last bowel movement was this morning. Test results as are follows: WBC 8.5, RBC 4.69, H/H 8.2/26, Platelets 226, Na 139, K 4.1, Cl 105, CO2 26, BUN 16, Cr. 1.38, Ca 9.4, INR 1.0. Urinalysis was negative. Abdominal ultrasound was negative for acute bleed of cholelithiasis. Vital signs are as follows: 97.9 Fahrenheit, HR 110 normal sinus rhythm, BP 98/60, RR 16, SpO2 96% on RA. 1. What are the differential diagnoses for this patient?The differential diagnoses for this patient are peptic ulcer disease (PUD), gastroesophogeal reflux disease (GERD), acute gastritis, gastric ulcer, esophagitis, and acute gastrointestinal bleed. Peptic ulcer disease is the first differential diagnosis for this patient. A peptic ulcer is a tear in the gastric or the duodenal mucosa. The tear occurs due to an increased amount of acid and pepsin (Valle, 2012). Men between the ages of 30 and 55 years of age and patients taking non-steroidal anti-inflammatory drugs (NSAIDS) are at an increase risk of developing peptic ulcer disease (Valle, 2012).Peptic ulcer disease (PUD) originates from an imbalance of the protective and aggressive factors of the gastrointestinal tract (Lew, 2012). In the presence of gastrin and pepsin, the patient’s defense mechanisms are impaired. Ulcers form causing discomfort in the epigastric area. In patients with peptic ulcer disease, complaints of burning, dull, and gnawing pain are present (Lew, 2012). Burning subsides by consuming food. In this specific case study, the symptoms of burning pain and nausea subside with food consumption. The patient also has a long-standing history of taking NSAIDs for headache with increased consumption for his abdominal pain. The last possible issue the patient may be dealing with is Helicobacter Pylori (H. Pylori) causing the patient’s peptic ulcer disease. The patient recently went on a cruise and explored different countries, consuming meals in various places. H. Pylori can develop through an oral to oral or fecal to oral route (Ferri, 2015). One must consider the possibility of the patient developing H. Pylori based on his recent travels. The patient’s most likely diagnosis is peptic ulcer disease (Lew, 2012). There are 400,000 Americans that are admitted each year to the hospital with upper gastrointestinal bleeding related to PUD (Tintanalli et al., 2011). Isotonic saline, packed red blood cells, and a proton pump inhibitor infusion are warranted at times when hemodynamic instability is seen. It is at times hard to differentiate between peptic ulcer disease and acute gastritis. The major difference in these two states is that gastritis often comes with a massive upper gastrointestinal bleed, whereas PUD does not. PUD also is almost always described as a burning pain in the epigastric area (Tintanalli et al., 2011). The patient’s symptoms in this case study are more consistent with peptic ulcer disease. Infection is the most common cause of acute gastritis (Valle, 2012). Unlike the patient in this case study, acute gastritis is associated with a sudden onset of epigastric pain, nausea, and vomiting (Valle, 2012). Neutrophils, hyperemia, and edema are noted on the histology report of these patients. Elderly individuals, alcoholics, and immunocompromised patients may be affected by gastritis. Other causes of acute gastritis are polypectomy and mucosal injection with India ink (Valle, 2012). Streptococci, staphylococci, escherichia coli, proteus, and haemophilus species are all common pathogens for acute gastritis. Though acute gastritis is a possible diagnosis in this case study, given the time frame and onset of symptoms, there is most likely another cause of this patient’s dyspepsia (Valle, 2012). Esophagitis is considered to be inflammation of the esophagus proceeded either by GERD or infiltrates from the mucosa caused by a food allergy (Bennett, Dolin, & Blaser, 2015). Patients who are immunocompromised are predominantly those who are affected by esophagitis. Rarely will a patient who is otherwise healthy get esophagitis. Typical pathogens include candidiasis, cytomegalovirus, herpes simplex virus, and human immunodeficiency virus (Bennett, Dolin, & Blaser, 2015). Non-infectious forms of esophagitis are caused by GERD, ingestion of corrosives, long-standing use of NSAIDS, and mucositis from medications such as antibiotics that come in capsule form (Bennett, Dolin, & Blaser, 2015). Patients will present to the emergency department or primary care offices with complaints of pain with swallowing. Patients can experience worsened pain by eating foods that are high in acid. Weight loss, nausea, and vomiting are other common presented signs and symptoms. In this specific case, the patient does not have pain on swallowing or difficulty swallowing. The patient does however have a history of taking NSAIDS as well as nausea and vomiting, so the diagnosis cannot be ruled out without imaging. The patient is also not immunocompromised and does not have a history of GERD making this diagnosis rare (Bennett, Dolin, & Blaser, 2015). Acute gastrointestinal bleed is the last differential diagnosis. The patient in this case developed hematemesis following a month of nausea and vomiting. Upper gastrointestinal bleeding occurs from many different disease states. Peptic ulcer disease, portal hypertension, vascular anomalies, Mallory Weiss tears, gastritis, and esophagitis are a few common causes of acute gastrointestinal bleeding (McQuaid, 2014). Patients can present with tachycardia and hypotension, revealing to the provider severe acute blood loss. Resuscitation efforts with isotonic saline and packed red blood cells should be administered in order to prevent further compromise of the patient’s hemodynamic instability. The patient in this case has a lower hemoglobin and hematocrit with tachycardia reflective of a more severe acute GI bleed (McQuaid, 2014). Proper fluid resuscitation should be performed to stabilize the patient. Once the patient is stable, the focus can be on the causes of the bleeding. 2. What are the two major causes of peptic ulcer disease?The two major causes of peptic ulcer disease are long-term use of non-steroidal anti-inflammatory medications and H. Pylori (McQuaid, 2014). Within a year there is a two to five percent likelihood of a duodenal ulcer originating from long-term NSAID use causing serious complications (Ferri, 2015). Patients who are at risk for serious complications are patients taking NSAIDs in combination with aspirin, anticoagulants, or corticosteroids (Valle, 2012). NSAIDs inhibit prostaglandins by reversing the inhibition of COX-1 and COX-2 enzymes. Aspirin also causes inhibition of COX-1 and COX-2 enzymes as well as platelet aggregation. The issue with COX-1 enzymes is they cause a cytoprotection to the mucosal lined layer of the stomach and duodenum. As the enzymes that protect the layer are inhibited, the risk for ulcer is increased (Laine, 2012). The use of aspirin alone doubles the risk of developing bleeding in a patient with peptic ulcer disease. H. Pylori increases the risk of peptic ulcer disease by three times when the patient is taking NSAIDs or aspirin (Ferri, 2015). The etiology of H. Pylori is unknown, but most believe it originates from oral to oral or fecal to oral route. Food contamination is also a possibility. H. Pylori invades the mucosal layer of the duodenum and gastric area causing vulnerability to acid peptic damage (Ferri, 2015). It is important to detect signs and symptoms of H. Pylori early as well as obtain a proper history and physical in order to prevent malignancies from arising (Ferri, 2015). 3. What imaging/testing should be ordered for this patient?The gold standard for the diagnosis of peptic ulcer disease is an esophagoduodenoscopy (EGD). The sensitivity and specificity are greater than 95% for visualization of an ulcer, and endoscopy allows the viewing of other potential abnormalities and allows biopsy of appropriate lesions (Laine, 2012). Also, an EGD is more sensitive and specific than barium studies of the upper gastrointestinal system (McQuaid, 2014). During an EGD, the physician is looking for sources of bleeding, malignancy ulcers, and esophagitis (McQuaid, 2014). The patient in this case study will have an EGD completed because of the acute GI bleed. The patient also had recent travel outside of the country placing him at risk for ingesting contaminated food. With a possible diagnosis of H. Pylori, the gastroenterologist will order histology, rapid urease testing, culture and polymerase testing. In a patient that does not have an active GI bleed and shows no evidence of bleeding, an EGD may not be recommended (Chey & Wong, 2007). In this case, the nurse practitioner will order antibody testing, urea breath tests, and fecal antigen tests. The antibody testing is widely used and has a good negative predictive value (Chey & Wong, 2007). Urea breath tests have a great positive and negative predictive value regardless of H. Pylori prevalence, however reimbursement for this testing and availability are not consistent (Chey & Wong, 2007). Fecal antigen testing also tests active H. Pylori infection with good negative and positive predictive value (Chey & Wong, 2007). Fecal antigen testing is also convenient for follow-up appointments (Atherton & Blaser, 2012). The urea breath test is an accurate way of identifying H. Pylori if the patient has not been prescribed a PPI within the last two weeks prior to the EGD. A urea breath test is inexpensive and does not require an EGD (Atherton & Blaser, 2012). Histology with biopsies should be taken in a patient who has been taking a PPI. A urea breath test does not need to be performed on the individual since the test results will be skewed (Chey & Wong, 2007). The sensitivity of the urea breath test can decreased by 25% if a patient has been taking a PPI, bismuth, and antibiotics (Chey & Wong, 2007). Culturing during an EGD results in highly specific testing, but is not as sensitive as the rapid urea breath tests and histology (Chey & Wong, 2007). Finally, a polymerase chain reaction (PCR) can also be completed with high specificity for H. Pylori. A PCR has been shown to detect up to 20% on H. Pylori cases from gastric biopsies (Chey & Wong, 2007). In the event that the patient has symptoms of bowel perforation, penetration, or obstruction from peptic ulcer disease, a computed tomography (CT) scan should be obtained (Laine, 2012). The specificity of a CT scan to rule-out bowel obstruction, penetration, or perforation is 95% with a sensitivity of 64% (Zissin, Osadchy, & Gayer, 2009). Though not a first choice in testing peptic ulcer disease, a CT scan can be done to rule out complications of surrounding organs (Laine, 2009; Zissin, Osadchy, & Gayer, 2009). 4. What are the treatment options for this patient?Stabilization of this patient is the first step in treatment. In a patient with active bleeding, two 18-gauge large bore intravenous catheters should be inserted for proper resuscitation with isotonic saline and packed red blood cells. In a patient with a coagulopathy, reversal of certain clotting factors may be warranted. A proton pump inhibitor infusion is typically started in order to aid in the suppression of gastric or duodenal ulcers that have formed (Ferri, 2015). As stated above, an EGD should be completed within 24 hours of hospital admission in order to diagnose the peptic ulcer as well as to biopsy if necessary (Chey & Wong, 2007). Once a patient is diagnosed with peptic ulcer disease associated with NSAID use, the next step is to stop medications that are causing the ulcer (Chey & Wong, 2007). NSAIDs should be stopped. This patient takes in a moderate amount of coffee a day and a moderate amount of alcohol a week. Education on the benefits of reducing caffeine and alcohol intake can lead to decreased acid production and symptoms (McQuaid, 2014). In patients with a diagnosis of peptic ulcer disease, with no sign of H. Pylori, a proton pump inhibitor (PPI) is the recommended drug of choice in treating these patients (McQuaid, 2014). Proton pump inhibitors bind to the acid-secreting enzymes and cause malfunction and inactivation. After four weeks of treatment with a PPI, 90% of duondenal ulcers have been shown to effectively heal whereas 90% of gastric ulcers have been shown to heal after eight weeks (McQuaid, 2014). The other treatment choice for PUD is an H2-receptor antagonist. Unfortunately, H2-receptor antagonists are not the drug class of choice in treating peptic ulcer disease. Proton pump inhibitors suppress 90% of acid secretion in a one day, whereas H2-receptor antagonists only suppress 65% (McQuaid, 2014). Therefore it is recommended to prescribe a proton pump inhibitor for four weeks in a patient with peptic ulcer disease. If given PPIs for longer than recommended treatment, the advanced practice registered nurse should be aware of the effects on the patient. Long-term use can cause a decreased Vitamin B12, iron, and calcium absorption and place patients at risk for clostridium difficile (McQuaid, 2014; Chey & Wong, 2007). In the state of Ohio, the advanced practice registered nurse can prescribe proton pump inhibitors and H2-receptor antagonists (The Ohio Board of Nursing, 2014). The first line combination of medications to administer to this patient is a PPI twice daily, 500 mg of Clarithromycin twice daily, and one gram of amoxicillin twice daily for 10 to 14 days (Chey & Wong, 2007). Metronidazole can be substituted for amoxicillin in patients with penicillin allergy. Another alternative treatment is 525 mg of bismuth subsalicylate four times a day, metronidazole 250 mg four times a day, tetracycline 500 mg four times a day, ranitidine 150 mg twice daily, and a PPI twice daily prescribed orally and for 10-14 days. The triple therapy combination has been shown to eradicate the disease by 75-90% (Chey & Wong, 2007). In the state of Ohio, the advanced practice registered nurse can prescribe the triple and quadruple therapy for patients with H. Pylori (The Ohio Board of Nursing, 2014). ReferencesArlt, W. (2012). Disorders of the adrenal cortex. In D. L. Longo, D. L. Kasper, J. L. Jameson, A. S. Fauci, S. L. Hauser, & J. 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