BON qualifications M masters in NSG A- accredited nsg org (PNA) S seven (1 chairman, 6 members) I immediately resign upon appointment

ent N not convicted of any crime P pecuniary interest, absence of T 10 yrs experience (last 5 years hr in RP) C citizen & resident of RP

Ex. Papavarine Hcl Prophantheline Bromide (Profanthene) c.) Vasodilator NTG d.) Antacid Maalox e.) H2 receptor antagonist -Ranitidin(Zantac) to decrease pancreatic stimulation f.) Ca gluconate to decrease pancreatic stimulation

DEAN qualification Chief nurse & Director > RN + MAN + 5 yrs experience in nsg

Nurse Licensure Exam 1. Cert of Good Moral Char (Optional) 2. Proof holder of Fil citizenship Birth cert. 3. Proof BSN degree Transcript with scanned picture done by reg

2. Withold food & fluid aggravates pain (total NPO) 3. Assist in Total Parenteral Nutrition (TPN) or hyperalimentation Complications of TPN Infectionmaintain a strict aseptic technique Pulmonary Embolismcheck all connection to system Hyperglycemia Hyperkalemia 4. Institute stress mgt tech a.) DBE b.) Biofeedback 5. Comfy position -Knee chest or fetal lie position 6. If pt can tolerate food, give increase CHO, decrease fats, and moderate CHON 7. Complications: Chronic hemorrhagic pancreatitis, Peritonitis, Septicemia, Shock

PANCREATITIS
acute or chronic inflammation of pancreas leading to pancreatic edema, hemorrhage & necrosis due to auto digestion (self-digestion). Bleeding of pancreas - Cullens sign on umbilical area PEPTIC ULCER DISEASE (PUD) excoriation / erosion of submucosa & mucosal lining due to: a.) Hyper secretion of acid pepsin b.) Decrease resistance to mucosal barrier Incidence Rate: 1. Men 40 55 yrs old 2. Aggressive persons/ type A personality 3. Hereditary Predisposing factors: 1. Hereditary 2. Emotional 3. Smoking vasoconstriction GIT ischemia 4. Alcoholism stimulates release of histamine = Parietal cell release Hcl acid = ulceration 5. Caffeine tea, soda, chocolate 6. Irregular diet 7. Rapid eating 8. Ulcerogenic drugs NSAIDS, aspirin, steroids, indomethacin, ibuprofen Indomethacin -S/E corneal cloudiness. Needs annual eye check up. NSAID and steroids= gastropathy 9. Gastrin producing tumor or gastrinoma Zollinger Ellisons syndrome 10. Microbial invasion helicobacter pylori. Metronidazole (Flagyl)

Predisposing factors: 1. Chronic alcoholism 2. Hepatobilary disease 3. Obesity 4. Hyperlipidemia 5. Hyperparathyroidism 6. Drugs Thiazide diuretics,aspirin, pills, Pentamidine HCL (Pentam) for clients with AIDS, 7. Diet increase saturated fats S/Sx: 1. Severe Midepigastrium epigastric pain radiates from back & flank area (left upper quadrant) -24-48 hrs. Aggravated by heavy meals/eating, accompanied by DOB 2. N/V 3. Tachycardia 4. Palpitation due to pain (abdominal guarding) 5. Dyspepsia /indigestion (rigid board like abdomen) 6. Decrease bowel sounds 7. (+) Cullens sign -ecchymosis of umbilicus hemorrhage 8. (+) Grey Turners spots ecchymosis of flank area 9. Hypocalcemia Diagnosis: Serum amylase & lipase increase Urine lipase increase Serum Ca decrease Nursing Mgt: 1. Meds a.) Narcotic analgesic -Meperidine Hcl (Demerol) Dont give Morphine SO4 will cause spasm of the sphincter of ODDI. b.) Smooth muscle relaxant/ anticholinergic

SITE PAIN

GASTRIC ULCER Antrum or lesser curvature > 30 min 1 hr after eating > epigastrium > gaseous & burning >not usually relieved by food & antacid >Eating leads to pain Normal gastric acid secretion common hematemesis Wt loss a. stomach cancer b. hemorrhage

DUODENAL ULCER Duodenal bulb >2-3 hrs after eating >mid epigastrium >cramping & burning pain >usually relieved by food & antacid >12 MN 3am pain >Eating lessens pain Increased gastric acid secretion Not common Melena Wt gain a. perforation

HYPERSECRETION VOMITING HEMORRHAGE WT COMPLICATIONS

Diagnosis: Endoscopic exam Stool from occult blood (+) Gastric analysis Gastric Ulcer: normal gastric acid secretion Duodenal: increased gastric acid secretion GI Series-confirm presence of ulceration Nursing Mgt: 1. Diet bland, non irritating, non spicy 2. Avoid caffeine & milk/ milk products > Increase gastric acid secretion 3. Administer meds Antacids > ACA Aluminum containing antacids Magnesium containing antacids H2 receptor antagonist: o Ranitidine (Zantac) SE: fever o Cimetidine (Tagamet)hastens the effect of oral anticoagulants o Famotidine (Pepcid) SE: fever -Avoid smoking decrease effectiveness of drug Nursing Mgt: Administer antacid & H2 receptor antagonist (Cimetidine) 1hr apart Cemetidine decrease antacid absorption & vise versa Cytoprotective agents o Sucralfate (Carafate) -Provides a paste like subs that coats mucosal lining of stomach o Misoprostol (Cytotec) SE: menstrual spotting Sedatives/ Tranquilizers -Valium, lithium Anticholinergics / Antispasmodic o Atropine SO4 o Prophantheline Bromide (Profanthene) NOTE: Pt has history of hpn crisis with peptic ulcer disease. Rn should not administer alka seltzer-has large amount of Na. Surgery: subtotal gastrectomy -Partial removal of stomach. Billroth I (Gastroduodenostomy) Removal of of stomach & anastomoses of gastric stump to the duodenum Billroth II (Gastrojejunostomy) Removal of -3/4 of stomach & duodenal bulb & anastomostoses of gastric stump to jejunum. Before surgery for BI or BII -Do vagotomy (severing of vagus nerve) & pyloroplasty (drainage) first.

Nursing Mgt: Monitor NGT output or drainage immediately post op-bright red o Immediately post op should be Bright Red o Within 36-48h output is yellow green o After 48h output is Dark Red due to HCl acid Administer meds: o Analgesic o Antibiotic o Antiemetics Maintain patent IV line VS, I&O & bowel sounds Complications: o Hemorrhage hypovolemic shock Late signs anuria o Peritonitis o Paralytic ileus most feared o Hypokalemia o Thrombophlebitis o Pernicious anemia o Septicemia

Dumping syndrome
common complication rapid gastric emptying of hypertonic food solutions CHYME leading to hypovolemia. Sx of Dumping syndrome: 1 Dizziness 2 Diaphoresis 3 Diarrhea 4 Palpitations Nursing mgt: o Avoid fluids in chilled solutions, sweets (fluids must be taken after meals) o Small frequent feedings-6 equally divided feedings o Diet decrease CHO, moderate fats & CHON o Flat on bed 15 -30 minutes after q feeding

prevent infection

Type 1 (IDDM) Juvenile onset type Brittle disease Predisposing Factors Hereditary (total destruction of pancreatic cells) Related to viruses Drugs o Lasix o Steroids Related to carbon tetrachloride toxicity Signs and Symptoms Polyuria Polydypsia Polyphagia Glycosuria Weight loss Anorexia nausea and vomiting Blurring of vision Increase susceptibility to infection Delayed/poor wound healing Treatment Insulin therapy Diet Exercise Complication: Diabetic Ketoacidosis - due to severe hyperglycemia leading to severe CNS depression Mgt for Complication > Assist in mechanical ventilation > Administer 0.9 NaCl followed by .45 NaCl (hypotonic solutions) to counteract dehydration and shock > Monitor strictly vital signs, intake and output and blood sugar levels > Administer medications as ordered Insulin therapy (regular acting insulin/rapid acting insulin peak action of 2 4 hours) Sodium Bicarbonate to counteract acidosis Antibiotics to

Type 2 (NIDDM) Adult onset Maturity onset type Obese over 40 years old Predisposing Factors Obesity because obese persons lack insulin receptor binding sites Signs and Symptoms Usually asymptomatic Polyuria Polydypsia Polyphagia Glucosuria Weight gain Treatment Oral Hypoglycemic agents Diet Exercise Complications : HYPER OSMOLAR NON KETOTIC COMA - Hyperosmolar: increase osmolarity (severe dehydration) - Non ketotic: absence of lypolysis (no ketones) Mgt for Complication > Assist in mechanical ventilation > Administer 0.9 NaCl followed by .45 NaCl (hypotonic solutions) to counteract dehydration and shock > Monitor strictly vital signs, intake and output and blood sugar levels > Administer medications as ordered Insulin therapy (regular acting insulin/rapid acting insulin peak action of 2 4 hours) Antibiotics to prevent infection

Types of Insulin

Color & consistency

Peak 2-4 6-12 12-24

Rapid Intermediate Long acting

Clear Cloudy Cloudy

Diagnostic Procedures for DM FBS is increased (3 consecutive times with signs

or polyuria, polydypsia, polyphagia and glucosuria confirmatory for DM)

Random Blood Sugar is increased Oral glucose tolerance test is increased most sensitive test

Alpha Glycosylated Hemoglobin is increased

III. CONVALESCENT/RECOVERY PHASE3-12

months.

CHRONIC RF irreversible loss of kidney function....

Pathognomonic sign: (+) rebound tenderness Pain at Rt. iliac region-- MCBURNEYS point site of surgical incision Late sign due pain tachycardia Rovsings sign elicited by palpating the left lower quadrant; this paradoxically causes pain to be felt in the right lower quadrant. Treatment: - appendectomy 24 45 Dont give analgesic pre-diagnosis will mask pain Presence of pain means appendix has not ruptured. Avoid heat application will rupture appendix. Complications: Peritonitis & Septicemia

Predisposing factors: 1. DM 2. HPN 3. Recurrent UTI/ nephritis/ pyelonephritis 4. Exposure to renal toxins Stages of CRF 1. Diminished Reserve Volume asymptomatic Normal BUN & Crea, GFR < 10 30% 2. Renal Insufficiency 3. End Stage Renal disease

ACUTE RENAL FAILURE

sudden immobility of kidneys to excrete nitrogenous waste products & maintain F&E balance due to a decrease in GFR. (N 125 ml/min)

Predisposing factors: Pre renal cause - decrease blood flow Intra-renal cause involves renal pathology = kidney problem Post renal cause involves mechanical obstruction

Stages: Initiation period begins with the initial insult and ends when oliguria develops

I. OLIGURIC STAGE (1-2 weeks) - involves

passage of urine < 400ml/day.

II. DIURETIC PHASE 2-3 weeks Increased

amount of urine