Care Plan LC pathophysiology Disease & Brief Pathology: Peptic Ulcer disease

Nursing Assessment Guide STUDENT NAME: Danielle Keasling MEDICATION ORDERS: List ALL medication orders. administration. Include dose, route, frequency & time of *Nexium 40mg IV daily given at 1800 *Regular sliding scale * Magnesium 250mg tablet 1 tablet po BIDWM 0800, 60 0 1700 60-149 0 * Lisinopril 5mg tablet 2 tabs po daily 1000 150-199 200-249 2 4 * Jevity 1000mL q20hrs 0100 250-299 6 * Xopenex 2.5/0.5mL 1 vial q4-6hrs 300-349 8 * Morphine 2mg/ml q1hr prn pain 350 10 *Ativan 2mg/ml IV 0.5mg PRN sleep 60 give oj or 1 amp d50 IV and call Dr *Metoprolol 5mg/5mL IV q6h PRN if bp 140 do not use if bp 130 or pulse 90 350 give insulin and call dr *Phenergan 25mg/mL 12.5mg IV q4h PRN n/v * Zofran 4mg/2mL 2mg IV q4h PRN nausea vomiting INSTRUCTIONS FOR DIAGNOSTIC DIVISIONS: Organize related data together so that it flows easily and in a natural progression. Include pertinent tests and give the date(s) & results if abnormal. DIAGNOSTIC DIVISIONS ACTIVITY CIRCULATION COMFORT ELIMINATION: BLADDER ELIMINATION: BOWEL FOOD/FLUID HYGIENE FUNCTIONAL CODE: 0 = completely independent 1 = use of equipment/device 2 =supervision/stand-by assist 3 = assist. of person & equip. 4 = completely dependent FUNCTIONAL STATUS (see Code): Bathing Nail Care Dressing Peri Care Hair Care Oral Care Shaving Toileting NEUROSENSORY RESPIRATION SAFETY Allergies: Codeine, Pneumonia Vac SLEEP/REST EGO INTEGRITY SOCIAL INTERACTION SEXUALITY TEACHING/LEARNING (Discuss learning needs, capabilities, strengths, &/or barriers to learning.) Source(s) of data: Signature & title: Date: Pathophysiology Disease & Brief Pathology: Peptic Ulcer disease Tobacco smoking, not eating properly, blood group, spices and other factors that were suspected to cause ulcers until late in the 20th century, are actually of relatively minor importance in the development of peptic ulcers. A major causative factor (60% of gastric and up to 90% of duodenal ulcers) is chronic inflammation due to Helicobacter pylori that colonizes the antral mucosa. The immune system is unable o clear the infection, despite the appearance of antibodies. Thus, the bacterium can cause a chronic active gastritis (type B gastritis), resulting in a defect in the regulation of gastrin production by that part of the stomach, and gastrin secretion can either be decreased resulting in hypo- or achlorhydria or increased. Gastrin stimulates the production of gastric acid by parietal cells and, in H. pylori colonization responses that increase gastrin, the increase in acid can contribute to the erosion of the mucosa and therefore ulcer formation. Studies have shown eating cabbage or cabbage juice can increase the mucosa lining in the stomach. Another major cause is the use of NSAIDs (see above). The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 (cox-1), which is essential for the production of these prostaglandins. Newer NSAIDs (celecoxib, rofecoxib) only inhibit cox-2, which is less essential in the gastric mucosa, and roughly halve the risk of NSAID-related gastric ulceration. As the prevalence of H. pylori-caused ulceration declines in the Western world due to increased medical treatment, a greater proportion of ulcers will be due to increasing NSAID use among individuals with pain syndromes as well as the growth of aging populations that develop arthritis.The incidence of duodenal ulcers has dropped significantly during the last 30 years, while the incidence of gastric ulcers has shown a small increase, mainly caused by the widespread use of NSAIDs. The drop in incidence is considered to be a cohort- phenomena independent of the progress in treatment of the disease. The cohort-phenomena is probably explained by improved standards of living which has lowered the incidence of H. pylori infections. Glucocorticoids lead to atrophy of all epithelial tissues. Their role in ulcerogenesis is relatively small. Smoking leads to atherosclerosis and vascular spasms, causing vascular insufficiency and promoting the development of ulcers through ischemia. Nicotine contained in cigarettes can increase parasympathetic nerve activity to the gastrointestinal tract by acting on the nicotinic receptors at synapses - increased stimulation to the enterochromaffin-like cells and G cells increases the amount of histamine and gastrin secreted and therefore increases the acidity of the gastric juice. A family history is often present in duodenal ulcers, especially when blood group O is also present. Inheritance appears to be unimportant in gastric ulcers. Gastrinomas (Zollinger Ellison syndrome), rare ...................................................continued..................................................................