Inflammation Module 1B² PDF

INFLAMMATION  INFLAMMATION ❖ A complex biological response of vascular tissues to harmful stimuli, such as pathogens, damage cells, or irritants. ❖ Protective attempt to remove the injurious stimuli and to initiate healing process. ❖ It is a non specific response meant to serve a prote...

INFLAMMATION  INFLAMMATION ❖ A complex biological response of vascular tissues to harmful stimuli, such as pathogens, damage cells, or irritants. ❖ Protective attempt to remove the injurious stimuli and to initiate healing process. ❖ It is a non specific response meant to serve a protective function. ❖ it is classified type of exudates produced Acute- usually lasts less than 2 weeks Subacute inflammation - reactive sign of inflammation. Gradual in onset and may become a chronic or severe reaction Chronic- many months or years  CARDINAL SIGNS (PRISH) 1. Pain Due to chemical release by damage cells. 2. Swelling or edema Due to an influx of fluid into the damaged region. 3. Redness Due to vasodilation 4. Heat Due to increase in blood flow to the area 5. Loss of function (Immobility) Due to increase swelling and pain  CHARACTERISTIC OF INFLAMMATION I. VASCULAR CHANGES A. Vasodilation > Occur from arteriole level, progressing to the capillary increase blood flow redness, heat and inflammation. B. Increased permeability > Caused by movement of plasma into the tissues stasis producing swelling C. Slowing of blood flow D. Release of bradykinin > Vasoactive protein induce vasodilation, increase vascular permeability, and induce pain. CHARACTERISTIC OF INFLAMMATION 1. Initial tissue injury > Release of chemicals ▪ Bradykinins, Serotonin, act as chemical messengers Lymphokines ▪ Prostaglandin ▪ Histamine causes vasodilation 2. Blood flow increases to the injuredarea. 3. Increased capillary permeability 4. Leukocyte migration ▪ Caused by chemotaxis (chemical messenger) leads to migration of certain WBC (leukocytes) to the damaged area. ▪ 2 types of leukocyte predominantly respond: > Neutrophils- first to attack, neutralizing bacteria > Macrophages- healing process by engulfing bacteria 5. Destroyed tissue cells are replaced by identical or similar structural and functioning cells and/or fibrous tissue. > Minimize complications of the edema that accompanies inflammation. > Reduce the inflammatory response. > Monitor the systemic response. > Comfort measures such as rest, elevation, wrapping of the affected area, and administration of analgesics. Heat, cold, or both may be applied and need a physician’s order. COLD - 24 to 72 HOURS OF COMPRESSION AND HOT COMPRESS THEREAFTER FOR QUICKLY REMOVAL OF WASTE PRODUCT. A. Gastrointestinal Disorders NFLAMMATORY BOWEL DISEASE (IBD) > A group of chronic disorders: 1. Crohn's disease (i.e., regional enteritis) 2. Ulcerative colitis >This results in the inflammation or ulceration of the bowel >Unknown cause however some factors may take into consideration: a. environmental triggers (air pollutants) b. food, tobacco c. viral illness d. genetic hereditary CROHN’S DISEASE AND ULCERATIVE COLITIS  CROHN’S DISEASE (REGIONAL ENTERITIS) A subacute and chronic inflammation of the GI tract wall that extends through all layers (i.e., transmural lesion) Histopathologic changes can occur anywhere in the GI tract but it commonly occurs in the distal ileum in the ascending colon Characterized by periods of remission and exacerbation Regional enteritis/Skip lesions: diseased bowel segments are sharply demarcated by adjoining areas of normal bowel tissue Crypt inflammation and abscesses →> develop into small, focal ulcers → deepen into longitudinal and transverse ulcers which are separated by edematous patches → cobblestone appearance; inflammation extends into the peritoneum → formation of fistulas, fissures, and abscesses → interference of intestinal peristalsis because of a constricted lumen →crampy abdominal pain/tenderness/spasm; advanced disease, bowel wall thickens and becomes fibrotic (tissue doesn’t function normally) → narrowed intestinal lumen; diseased bowel loops sometimes adhere to other loops surrounding them  CLINICAL MANIFESTATION > RLQ pain and diarrhea unrelieved by defecation > Crampy abdominal pain after meals > Anorexia, weight loss, malnutrition as a result the patients tends to limit food intake to prevent further abdominal pain > Nutritional deficiencies (i.e., anemia) > Chronic diarrhea > Fever and leukocytosis (if the inflamed intestine may perforate which leads to intra-abdominal and anal abscesses) > Steatorrhea (excessive fat in feces)  Assessment and Diagnostic Findings: > Barium Study of the Upper GI Tract: String sign of the terminal ileum (a traditional conclusive diagnostic test) > Improved diagnostic exams - CT scan and MRI: highlights bowel wall thickening and mesenteric edema, also highlights obstructions, abscesses, and fistulae > Thus, CT scan is more sensitive in diagnosing Crohn's disease than Barium Studies > CBC: assess for hematocrit and hemoglobin levels (may be decreased), WBC count (may be elevated), erythrocyte sedimentation rate (may be elevated) > Albumin and protein levels may be decreased, indicating malnutrition  COMPLICATIONS ▪ Intestinal obstruction ▪ Stricture formation ▪ Perianal disease ▪ Fluid and electrolyte imbalances ▪ Malnutrition from malabsorption ▪ Fistula and abscess formation > Enterocutaneous fistula > Abnormal opening between the small bowel and skin > Most common type of small bowel fistula caused by Crohn's disease ▪ Colon cancer  ULCERATIVE COLITIS > Chronic ulcerative and inflammatory disease of the mucosal and submucosal layers of the colon and rectum > Characterized by unpredictable periods of remission and exacerbation with bouts of abdominal cramps and bloody or purulent diarrhea > Inflammatory changes begin in the rectum and progress proximally through the colon (LLQ) > Since the inflammatory process affects the inner lining of the colon only, abscesses, fistulas, obstruction, and fissures are rare. Multiple ulcerations, diffuse inflammations,desquamation/shedding at the superficial mucosa of the colon → bleeding→then mucosa becomes edematous and inflamed → muscular hypertrophy and fat deposits → the bowel narrows, shortens, and thickens Clinical Manifestations/Symptoms Diarrhea with mucus/pus/blood LLQ abdominal pain Intermittent tenesmus (cramping rectal pain) Passage of 6 or more liquid stools each day Hypoalbuminemia Electrolyte imbalances Anemia  Assessment and Diagnostic Findings: 1. Abdominal x-ray > To determine the cause of symptoms 2. Colonoscopy > Definitive test > To distinguish ulcerative colitis from other diseases of the colon with similar symptoms > May reveal friable, inflamed mucosa with exudate and ulcerations 3. Colon biopsy > To determine histologic characteristics of the colonic tissue and extent of disease 4. CT scan/MRI/Ultrasound studies > Identify abscesses and perirectal involvement 5. Fecal Occult Blood Test 6. Stool exam for parasites or microbes 7. CBC: low hematocrit, low hemoglobin, elevated WBC 8. Albumin level: low (indicating malabsorptive disorders) 9. C-reactive protein: elevated  COMPLICATIONS Toxic megacolon Inflammatory process extends into the muscular layer of the colon, inhibiting its ability to contract and resulting in colonic distention. Symptoms: fever, abdominal pain and distention, vomiting,fatigue Subtotal colectomy: if bowel perforation has not occurred, otherwise,colectomy is indicated (removal of colon) Surgery becomes necessary to relieve the effects of the disease and treat these serious complications  Medical Management (for Inflammatory Bowel Diseases: Crohn's Disease and Ulcerative Colitis) 1. Nutritional therapy Oral fluids Low-residue, high protein, high calorie diet with supplemental vitamin therapy and iron replacement IV therapy for fluid and electrolyte imbalances Cold foods (can cause cramping) and smoking are avoided since both increase intestinal motility  Medical Management (for Inflammatory Bowel Diseases: Crohn's Disease and Ulcerative Colitis) 2. Pharmacologic therapy Sedatives Immunomodulators - to alter Antidiarrheals and antiperistaltic medications immune response (Loperamide) - to rest the inflamed bowel ▪ Azathioprine (Imuran) Aminosalicylates ▪ Mercaptopurine (6-MP) ▪ Sulfasalazine (Azulfidine) ▪ Methotrexate (MTX) Sulfa-free aminosalicylates ▪ Cyclosporine (Neoral) ▪ Mesalamine (Asacol, Pentasa) Monoclonal antibodies Antibiotics ▪ Infliximab (Remicade) ▪ Metronidazole (Flagyl) ▪ Adalimumab (Humira) Corticosteroids - taken orally, intravenously, or ▪ Certolizumab pegol (Cimzia) rectally (Prednisone) ▪ Natalizumab (Tysabri)  SURGICAL MANAGEMENT 1. Indications for surgery 2. Indications for surgery from: from: CROHN'S DISEASE ULCERATIVE COLITIS: Recurrent partial intestinal obstructions Presence of colon cancer Complete intestinal obstructions Colonic dysplasia/polyps Intractable fistulas/abscesses Megacolon Total colectomy with ileostomy Severe, intractable Total removal of the colon with an ileostomy bleeding created in the abdomen Colon perforation Drainage is liquid to unformed and occurs at frequent intervals  3. Restorative proctocolectomy with ileal pouch anal anastomosis Proctocolectomy - removal of the rectum and colon Surgical procedure of choice in cases where the rectum can be preserved because it eliminates the need for a permanent ileostomy It establishes an ileal reservoir that functions as a “new” rectum, and anal sphincter control of elimination is retained. COMPLICATIONS Continent ileostomy ▪ Creation of a continent ileal reservoir (i.e., Kock pouch) by diverting a portion of the distal ileum to the abdominal wall and creating a stoma ▪ This procedure eliminates the need for an external fecal collection bag  NURSING MANAGEMENT OF A PATIENT WITH CHRONIC INFLAMMATORY BOWEL DISORDER 1. Assessment 2. Nursing Diagnoses Obtain health history Diarrhea related to the inflammatory process Assess for pain, presence of diarrhea, Acute pain related to increased peristalsis and GI inflammation fecal urgency, straining at stool Deficient fluid volume related to anorexia, nausea, and (tenesmus), nausea, anorexia, weight diarrhea loss, family history of IBD, patterns of Imbalanced nutrition: less than body requirements bowel elimination, allergies related to Monitor I&O dietary restrictions, nausea, and malabsorption Obtain daily weights Activity intolerance related to generalized weakness Anxiety related to impending surgery Assess for skin turgor Ineffective coping related to repeated episodes of Maintain normal elimination patterns diarrhea Risk for impaired skin integrity related to malnutrition and diarrhea Deficient knowledge related to the concern of the process and management of the disease 3. Planning and Goals 4. Nursing Interventions Attainment of normal bowel Administer antidiarrheal (loperamide) medications elimination patterns as prescribed Relief of abdominal pain and Administer pain medications as prescribed cramping Change into a comfortable position, apply heat (as Prevention of fluid volume deficit prescribed), divert activities, and prevent fatigue Maintenance of optimal nutrition Encourage oral fluid intake and weight Regulate IVF at prescribed rate Avoidance of fatigue Maintain optimal nutrition Reduction of anxiety Promote rest Promotion of effective coping Reduce anxiety Absence of skin breakdown Enhance coping measures Increased knowledge about the Prevent skin breakdown disease process and self-health Monitor and manage potential complications management Promote home, community-based, and transitional Avoidance of complications care Evaluate the patient's response to the interventions  APPENDICITIS Inflammation of the appendix The appendix fills with by- products of digestion and empties regularly into the cecum. Since the appendix empties inefficiently and its lumen is small, the appendix is prone to obstruction and is vulnerable to infection  Causes: > Being kinked > Being occluded with fecalith (hardened mass of stool) > Lymphoid hyperplasia (secondary to inflammation or infection) > Foreign bodies (e.g. fruit seeds) or tumors > Causes of appendicitis→appendix becomes ischemic →bacterial overgrowth →gangrene or perforation → peritonitis  Clinical Manifestations/Symptoms > Vague periumbilical pain that progresses to RLQ pain > Nausea > Anorexia > Low-grade fever > (+) McBurney point tenderness > (+) Rovsing sign - palpation of the LLQ causes pain at the RLQ > Rebound tenderness (intensification of pain when pressure is released) > Ruptured appendix = pain is consistent with peritonitis, abdominal distention develops as a result of paralytic ileus  Assessment and Diagnostic Findings: > CBC: elevated WBC and neutrophils > C-reactive protein levels are elevated > CT Scan: RLQ density or localized distention of the bowel; enlargement of the appendix by at least 6 mm is suggestive of appendicitis COMPLICATIONS > Gangrene/perforation of the appendix resulting in peritonitis, abscess formation, or portal pylephlebitis (septic thrombosis of the portal vein caused by vegetative emboli that arise from the septic intestines) > Perforation generally occurs within 6 to 24 hours after the onset of pain and leads to peritonitis  Medical/Surgical Management: > For fluid and electrolyte imbalance, dehydration, sepsis: IV fluids and antibiotics > Once appendicitis is diagnosed, immediate surgery is indicated o Surgery: Appendectomy (surgical removal of the appendix) to decrease the risk of perforation > Laparoscopic Appendectomy (faster recovery, small incisions) > For complicated appendicitis (e.g., with gangrene or perforation), the patient is typically treated with a 3- to 5- day course of antibiotics postoperatively  Nursing Management: > Relieve pain Educate on the use of an incentive spirometer > Prevent fluid volume deficit Give analgesics as prescribed > Reduce anxiety Regulate IV at prescribed rate > Prevent or treat surgical site infection Auscultate for the return of bowel sounds and > Prevent atelectasis passing of flatus (5-30 clicks/min) Incentive spirometry > Rationale: To determine if intestinal peristalsis has > Maintain skin integrity started after the operation. Also, this may signal that > Attaining optimal nutrition the patient may start on oral fluids/foods. For post-appendectomy surgery Encourage ambulation Place in high fowler position > Rationale: to reduce the risk of atelectasis and > Rationale: This reduces the tension on the venous thromboemboli formation incision and abdominal organs, helping to reduce Encourage patient to perform proper incision care, pain. It also promotes thoracic expansion, monitor for any post-op complications, and instruct to diminishing the work of breathing, and decreasing avoid heavy lifting the likelihood of atelectasis  PERITONITIS Inflammation of the peritoneum (the serous membrane lining the abdominal cavity and covering the viscera) Most common bacteria: Klebsiella, Proteus, Pseudomonas, Streptococcus  Caused by: o External sources (e.g. abdominal surgery, trauma - gunshot/stab wound) o Medical procedures such as peritoneal dialysis o Pancreatitis – if infections spreads outside the pancreas o Diverticulitis – infection of small, bulging pouches in the digestive tract (diverticulosis); if one e pouch ruptures, there is a spillage of the intestinal waste into the abdominal cavity  Categories: 1. Primary/Spontaneous bacterial peritonitis - bacterial infection of ascitic fluid; commonly in adults with liver failure 2. Secondary peritonitis - perforation/rupture of abdominal organs with spillage that affects the serous peritoneum Common causes: ▪ Perforated appendix ▪ Perforated peptic ulcer ▪ Perforated sigmoid colon caused by severe diverticulitis ▪ Volvulus of the colon ▪ Strangulation of the small intestine 3. Tertiary peritonitis - occurs as a result of a suprainfection in a patient who is immunocompromised Example: Tuberculous peritonitis  PATHOPHYSIOLOGY Inflammation, infection, ischemia, trauma, or tumor perforation → leakage of contents from abdominal organs to abdominal cavity →the normally sterile abdominal cavity gets infected with foreign substances (bacteria, gastric acid, partially digested food) →bacterial proliferation →infectious process →tissue edema and fluid exudation →fluid in peritoneal cavity becomes turbid with increasing amounts of protein, WBCs cellular debris, and blood →immediate response of the intestinal tract is hypermotility →this is soon followed by paralytic ileus with an accumulation of air and fluid in the bowel  Clinical Manifestations/Symptoms Symptoms depend on the location and extent of inflammation Constant abdominal pain which is more intense over the site of the pathological process (site of maximal peritoneal irritation) Abdomen becomes extremely tender and distended; muscles become rigid Board-like abdomen Rebound tenderness Anorexia, nausea, vomiting - caused by decreased/diminished peristalsis Fever Tachycardia Without swift and decisive intervention, clinical manifestations will mirror those of sepsis and septic shock  Assessment and Diagnostic Findings: CBC - elevated WBC for infection, hemoglobin and hematocrit levels may be, low if blood loos has occurred Serum electrolyte studies - may reveal altered levels of potassium, sodium, and chloride Abdominal x-ray: may show fluid and air levels as well as distended bowel loops Abdominal ultrasound: may reveal abscesses and fluid collections CT scan: may show abscess formation Peritoneal aspiration, culture and sensitivity studies of the aspirated fluid may reveal infection and identify the causative organisms MRI: may be used to diagnose intra-abdominal abscesses  MedicaL Management: Major focus of medical management: fluid, colloid, and electrolyte replacement Analgesic agents Antiemetic agents Intestinal intubation and suction - to relieve abdominal distention and promote intestinal function Oxygen therapy - as fluid in the abdominal cavity can cause pressure that restricts expansion of the lungs Antibiotic therapy Surgical treatment for secondary peritonitis: excision, resection with or without anastomosis, repair, drainage, fecal diversion (for extensive sepsis) Ultrasound-guided and CT-guided peritoneal drainage/aspiration of abdominal and extraperitoneal abscesses  Nursing Management: Increase fluid and food intake gradually as prescribed Must prepare for emergency surgery in case of a worsening clinical condition Monitor for signs of improving peritonitis: ❖ Decrease in temperature and pulse rate ❖ Softening of the abdomen ❖ Return of peristaltic sounds ❖ Passing of flatus ❖ Bowel movement/s Administer medications as prescribed PANCREATITIS Inflammation of pancreas and can be classified as acute (a medical emergency) or chronic (often goes undetected because the classic clinical and diagnostic findings are not always present in the early stages of the disease Pancreatitis is commonly described as autodigestion of the pancreas Caused by smoking and alcohol abuse (alcohol has a direct toxic effect on the pancreatic cells) Pancreatic duct becomes temporarily obstructed  hypersecretion of exocrine enzymes of the pancreas  enzymes enter bile duct -> enzymes are activated with bileback-up/reflux into the pancreatic duct  pancreatitis  Acute pancreatitis: o Interstitial edematous pancreatitis Affects majority of the patients Considered the milder form Characterized by a lack of pancreatic or peripancreatic parenchymal necrosis with diffuse enlargement of the gland due to inflammatory edema Edema and inflammation is confined to the pancreas o Necrotizing pancreatitis Presence of tissue necrosis in either the pancreatic parenchyma or in the tissue surrounding the gland Characterized by a more widespread and complete enzymatic digestion of the gland Enzymes damage the local blood vessels, thus, bleeding and thrombosis can occur Chronic pancreatitis o Inflammatory disorder characterized by a progressive destruction of the pancreas o Pancreatic cells are replaced with fibrous tissue due to repeated attacks of pancreatitis  Clinical Manifestations o Severe abdominal pain (caused by the irritation and edema of the inflamed pancreas) o Abdominal distention o Nausea/vomiting o Poorly defined, palpable abdominal mass o Fever o Decreased peristalsis o Jaundice o Vomiting that fails to relieve the pain or o Mental confusion nausea o Agitation o Abdominal guarding o Hypotension o Rigid/boardlike abdomen - usually a o Tachycardia threatening sign indicating peritonitis o Cyanosis o Ecchymosis in the flank or around the umbilicus  Assessment and Diagnostic Findings: o Serum amylase and serum lipase - used in making the diagnosis of acute pancreatitis; usually elevated within 24 hours of the onset of symptoms; serum amylase usually returns to normal within 2-3 days but serum lipase levels may remain elevated for a longer period o Urine amylase levels - elevated o CBC: elevated WBC o Hypocalcemia which correlates with the severity of pancreatitis o Ultrasound studies/contrast-enhanced CT scans, MRI: used to identify an increase in the diameter of the pancreas and to detect pancreatic cysts, abscesses, or pseudocysts o Chronic pancreatitis: ERCP - the most useful study in the diagnosis of chronic pancreatitis because it provides details about the anatomy of the pancreas and the pancreatic and biliary ducts  MedicaL/Surgical Management: o NPO - to inhibit stimulation of the pancreas and its secretion of enzymes o Parenteral nutrition for severe acute pancreatitis, and for those who are unable to tolerate enteral nutrition o Nasogastric suction - to relieve nausea and vomiting, decrease painful abdominal distention, and paralytic ileus o H2 antagonists: cimetidine (Tagamet), ranitidine (Zantac) To decrease pancreatic activity by inhibiting secretion of gastric acid o Proton pump inhibitors: pantoprazole (Protonix) For those who cannot tolerate or improve with H2 antagonists o Analgesics: Opioids: morphine, fentanyl (Sublimaze), hydromorphone (Dilaudid) o Antibiotics - if infection is present o Aggressive respiratory care because of the high risk of elevation of the diaphragm, effusion, and atelectasis o Placement of biliary drains (for external drainage) o Surgery: resect or debride an infected, necrotic pancreas o Surgical management for chronic pancreatitis: Pancreaticojejunostomy (aka Roux-en-Y) Side-to-side anastomosis of the pancreatic duct to the jejunum Pancreaticoduodenectomy (aka Whipple resection) Removal of the head of the pancreas, duodenum, gallbladder, and bile duct  Nursing Management: Relieve pain and discomfort  Assess for pain  Administer analgesics (opioids) as prescribed  Nonpharmacologic pain relief interventions such as proper positioning, music, distraction, and guided imagery  NPO temporarily to decrease secretion of secretin (this is a gastrointestinal hormone that stimulates the secretion of pancreatic fluids)  Nasogastric suction to relieve nausea/vomiting, treat abdominal distention, or paralytic ileus  Provide frequent oral hygiene  During the acute phase, maintain on bed rest to decrease metabolic rate and reduce secretion of pancreatic and gastric enzymes Improving breathing pattern  Semi-fowler's position to increase respiratory expansion  Frequent position changes to prevent atelectasis and pooling of secretions  Encourage use of incentive spirometry, DBE, and coughing  Improving nutritional status Monitor serum glucose levels every 4-6 hours or as prescribed Administer enteral or parenteral nutrition Diet: high carbohydrate, low protein, low fat Maintaining skin integrity Because of poor nutritional status, enforced bed rest, and restlessness, the patient is at risk for skin breakdown For post-op patients, check incision sites and monitor for presence of infection; also do appropriate wound care Monitoring and managing potential complications Monitor skin turgor and moistness of mucous membranes Weigh daily Monitor I&O Measure abdominal girth if ascites is suspected Monitor for presence of fluid and electrolyte imbalances (due to nausea&vomiting (hypokalemia), movement of vascular compartment to the peritoneal cavity, diaphoresis, fever, and use of gastric suction  Promoting home, community-based, and transitional care Educating patients about self-care Continuing and transitional care  CHOLECYSTITIS Inflammation of the gallbladder Calculous cholesystitis o A gallstone obstructs bile outflow → bile remaining on the gallbladder initiates a chemical reaction → autolysis and edema →blood vessels of gallbladder are compressed →compromised blood supply → gangrene of the gallbladder Acalculous cholecystitis o Acute gallbladder inflammation in the absence of obstruction by gallstones o May be caused by alterations in fluids and electrolytes, alterations in regional blood flow in the visceral circulation, bile stasis (lack of gallbladder contraction), and increased bile viscosity Calculi, or gallstones, usually form in the gallbladder from the solid constituents of bile  Two major types of gallstones: o Pigment stones  Form when unconjugated pigments in the bile precipitate to form stones  Cannot be dissolved and must be removed surgically o Cholesterol stones  Bile is supersaturated with cholesterol  cholesterol-saturated bile predisposes to the formation of gallstones  act as an irritant that produces inflammatory changes in the mucosa of the gallbladder  Clinical Manifestations  Biliary colic with excruciating upper right abdominal pain that Risk Factors: radiates to the back or right shoulder o 5Fs: Nausea and vomiting after a heavy meal  Fat Restlessness due to pain  Female Fever (if with cholecystitis)  Forty Jaundice - bile, which is no longer carried to the duodenum, is  Fair absorbed by the blood and gives the skin and mucous  Fertile membranes a yellow color o Cystic fibrosis Acholic/clay-colored stool - since the feces are no longer o Diabetes colored with bile pigments o Frequent changes in Dark color urine - due to excretion of bile pigments by the weight kidneys o Obesity Fat-soluble vitamin deficiency (i.e., bleeding caused by vitamin o Ileal resection or K deficiency since vitamin K is necessary for blood clotting) disease  Assessment and Diagnostic Findings  Abdominal x-ray Radionuclide imaging or Ultrasonography Cholescintigraphy  Diagnostic procedure of choice because it is  A radioactive agent is administered rapid and accurate through IV which is taken up by the  Procedure is more accurate if the patient hepatocytes and excreted rapidly through fasts overnight so that the gallbladder is the biliary tract distended  Biliary tract is scanned and images of the gallbladder and biliary tract are obtained  Oral cholecystography  Patient takes iodine-containing tablets by mouth for one/two nights in a row  iodine is absorbed from the intestine into the bloodstream removed from the blood by the liver excreted by the liver into the bile iodine, together with the bile, is highly concentrated in the gallbladder Endoscopic retrograde cholangiopancreatography (ERCP)  A fiberoptic endoscope is inserted through the esophagus to the descending duodenum Percutaneous transhepatic cholangiography  Injection of dye directly into the biliary tract  MedicaL/Surgical Management: Ursodeoxycholic acid UDCA (Ursofalk) - acts by inhibiting synthesis and secretion of cholesterol, thereby desaturating bile; this medication can reduce the size of existing stones, dissolve small stones, and prevent new stones from forming Stone removal by instrumentation  Intracorporeal lithotripsy  Stones are fragmented by laser pulse technology under fluoroscopic guidance with the use of devices that can distinguish between stones and tissue.  Electrohydraulic lithotripsy uses a probe with two electrodes that deliver electric sparks in rapid pulses, creating expansion of the liquid environment surrounding the gallstones. This results in pressure waves that cause stones to fragment Extracorporeal shock wave lithotripsy (ESWL)  Uses repeated shockwaves directed at the gallstones to fragment the stones Surgical Management: Laparoscopic cholecystectomy  Removal of gallbladder through a small incision through the umbilicus  Standard of therapy for symptomatic gallstones  Patient is often discharged from the hospital on the same day of surgery or within 1-2 days Cholecystectomy  Gallbladder is removed through a large abdominal incision (usually right subcostal)  Choledochostomy  Reserved for a patient with acute cholecystitis who may be too ill to undergo a surgical procedure  Incision is made at the common duct, usually for removal of stones. After the stones have been evacuated, a tube is usually inserted into the duct for drainage of bile until edema subsides  Laparoscopic cholecystectomy is planned for a future date after acute inflammation has resolved  Percutaneous cholecystostomy  Fine needle is inserted through the abdominal wall and liver edge into the gallbladder under guidance of ultrasound or computed tomography (CT). Bile is aspirated to ensure adequate placement of needle, and a catheter is inserted into the gallbladder to decompress the biliary tract  Nursing Management: Nursing Management Planning and goals:  Pain relief  Adequate ventilation  Intact skin and improved biliary drainage  Optimal nutritional intake  Absence of complications  Understanding of self-care routines Pre-op teachings: avoid smoking, avoid blood thinners (aspirin, NSAIDS, herbal remedies) Post-op diet: soft, low-fat diet once bowel sounds return, and advance to full, low-fat, high carbohydrate and protein diet once fully recovered (Fat restriction usually is lifted in 4-6 weeks when the biliary ducts dilate to accommodate the volume of bile once held by the gallbladder and when the ampulla of Vater again functions effectively.) Relieve pain by administering analgesics Encourage DBE and cough every hour to prevent atelectasis Instruct on the use of incentive spirometry  Nursing Management: Encourage to do early ambulation to prevent venous complications (i.e., venous thromboembolism formation) Keep dressings clean, dry, and intact Do wound care as directed Monitor for signs and symptoms of infection Monitor and manage potential complications PELVIC INFLAMMATION DISORDER Inflammatory condition of the pelvic cavity that may begin with cervicitis and may involve the uterus, fallopian tubes, ovaries, pelvic peritoneum or pelvic vascular system. Increases the risk for ectopic pregnancy, infertility, recurrent pelvic pain, tubo-ovarian abscess.  Pathophysiology ❖ Pathogenesis- unknown ❖ Presumed that organisms enter Vagina Cervical Causes: canalendocervixuterus - Gonnorheal and chlamydial ❖ After childbirth or abortion- pathogen spreads through organism (Common) tissues by lymphatics and blood vessels - CMV ❖ Pregnancy- increased blood supply needed by placenta - Bacteria, viruses, fungus or increases the risk for infection parasite ❖ Gonorrheal infection- pass through cervical canal and into uterus, where the environment (especially during menstruation) allows to multiple and spread ❖ Commonly caused by sexual transmission ❖ Can also occur with invasive procedures (Hysterectory, Emdometrial biopsy, Surgical abortion, Insertion of IUD) Risk factors: ❖ Early age at first intercourse ❖ Multiple sex partners ❖ Frequent intercourse ❖ Intercourse without condoms ❖ Sex with a partner with STD ❖ History of STDs or previous pelvic infection  Clinical Manifestations ❖ Malodorous purulent vaginal discharge ❖ Dyspareunia ❖ Lower abdominal pelvic pain MedicaL Management ❖ Tenderness that occurs after menses ❖ Anorexia ❖ Antibiotic ❖ intense tenderness upon palpation of ❖ V therapy ❖ uterus or movement of cervix (pelvic exam) ❖ NGT and suction (abdominal ❖ Fever distention or ileus) ❖ Dysuria and dyschezia ❖ Careful monitoring of v/s ❖ Anorexia ❖ Treatment of sexual partner ❖ n/v ❖ leukocytosis  Nursing Management: ❖ -Provide physical and emotional support ❖ Instruct to increase fiber diet and EOF ❖ Position to semi-Fowlers position ❖ Monitor vital signs and vaginal discharges ❖ Analgesics prescribed for pain relief ❖ Heat compress to abdomen ❖ Dispose properly the used perineal pads and discarded soiled pads ❖ Hand washing before and after contact with patient  SIMPLE VAGINITIS ❖ Inflammation of the vagina ❖ Cause vulvovaginal symptoms (itching, irritation, burning, and abnormal discharge) ❖ Urethritis may accompany vaginitis ❖ Symptoms may be aggravated by voiding and defecation RISK FACTORS ❖ Premenarche ❖ Use of oral contraceptives ❖ Pregnancy Risk Factors for Vulvovaginal ❖ Use of broad-spectrum antibiotics Infections Perimenopause/Menopause ❖ Diabetes mellitus ❖ Poor personal hygiene ❖ Low estrogen levels ❖ Tight undergarments ❖ Intercourse with infected partner ❖ Synthetic clothing ❖ Oral–genital contact (yeast can ❖ Frequent douching inhabit the mouth and intestinal tract) ❖ Allergies ❖ HIV infection  3 common types: 1. Bacterial Vaginosis 2. Candidiasis 3. Trichomoniasis 1. Bacterial Vaginosis -caused by an overgrowth of anaerobic bacteria and Gardnerella vaginalis - is not usually considered a serious condition, although associated with premature labor, premature rupture of membranes, endometritis, and recurrent urinary tract infection. Risk factors: -douching after menses -smoking -multiple sex partner -other sexually transmitted diseases (STDs)  Clinical Manifestations: ❖ More than half of patients with bacterial vaginosis do not notice any symptoms. ❖ Vaginal discharges: gray to yellowish white, fish like odor (noticeable after sexual ntercourse/ during menstruation) Medical Management: ❖ Metronidazole (Flagyl) ❖ Vaginal gel ❖ Clindamycin (Cleocin) vaginal cream or ovules (oval suppositories) ❖ Treatment of patients’ partners does not seem to be effective, but use of condoms may be helpful. 2. VULVOVAGINAL CANDIDIASIS ❖ is a fungal or yeast infection caused by strains of Candida ❖ many women are asymptomatic Clinical Manifestations: ❖ Vaginal discharges: > watery or thick, white cottage cheese like appearance > It causes pruritus and subsequent irritation Symptoms: ❖ -more severe before menstruation ❖ less responsive to ttt during pregnancy  Diagnosis: ❖ wet mount preparation ❖ gram staining Medical Management: ❖ Goal: eliminate symptoms ❖ Antifungal medications: CREAM: miconazole (Monistat), nystatin (Mycostatin), clotrimazole (Gyne-Lotrimin), and terconazole (Terazol) ORAL: fluconazole (Diflucan) ❖ treatment of sex partners is not necessary  3. Trichomoniasis vaginalis ❖ is a flagellated protozoan ❖ sexually transmitted vaginitis that is often called “trich” ❖ Trich may be transmitted by an asymptomatic carrier Clinical Manifestations: ❖ Vaginal discharge: thin (sometimes frothy), yellow to yellow-green, malodorous ❖ Vulvovaginal burning and itching  Diagnosis: ❖ culture ❖ testing of trichomonal discharge demonstrates a pH greater than 4.5 ❖ Inspection with a speculum: reveals vaginal and cervical erythema (redness) : multiple small petechiae (“strawberry spots”). Medical Management: ❖ Metronidazole or Tinidazole (Tindamax) - Most effective treatment. ❖ Tinidazole is not considered safe in pregnancy.  VULVITIS ❖ Inflammation of the vulva ❖ May occur with other disorders (diabetes, dermatologic problems or poor hygiene) Risk factors: ❖ May affect: women between 18-25 years old -Prepubescent girls ❖ Pathophysiology is unknown -Postmenopausal women Symptoms: -burning -stinging -irritation -stabbing pain -swelling Medical Management: -Antifungal and antibiotic -Cortisone cream- steroids -Do not over clean the affected area  TOXIC SHOCK SYNDROME -is an infection that usually is caused by Staphylococcus aureus organisms. -possible cause: insertion of tampons Clinical Manifestations (3 symptoms must be present for diagnosis.) Temperature greater than 102° F (38.9° C) Vomiting and diarrhea A macular (sunburn-like) rash that desquamates on palms and soles 1 to 2 weeks after illness Severe hypotension (systolic pressure less than 90 mm Hg) Shock, leading to poor organ perfusion Impaired renal function with elevated blood urea nitrogen or creatinine at least twice the upper limit of normal  Clinical Manifestations Hyperemia of mucous membrane Impaired liver function with increased total bilirubin and increased serum glutamate oxaloacetate transaminase (aspartate aminotransferase) at twice the upper limit of normal Decreased platelet count Central nervous system symptoms of disorientation, confusion, severe headache Medical Management remove tampon particles (Iodine douches, penicillinase resistant antibiotics) *recurrence may happen if organism is not completely eliminated from the body. IV therapy vasopressors (dopamine(Intropin)) Osmotic therapy  BENIGN PROSTATIC HYPERPLASIA ❖ Enlargement or hypertrophy of the prostate gland. ❖ Prostate gland enlarges, extending upward into the bladder and obstructing the outflow of urine. ❖ Most common disease in aging men. ❖ Occurs in mean older than 40 years of age Pathophysiology ❖ The cause is not well understood, but evidence suggest hormonal involvement (high estrogen level and Dihydrotestosterone DHT Level ) a metabolite of testosterone. Risk factors: ❖ Smoking ❖ Heavy alcohol consumption ❖ Obesity ❖ Diabetes ❖ HPN ❖ Western diet (high animal fat ❖ Heart and protein and refines carbs, disease low in fiber)  Clinical Manifestations ❖ Prostate: large, rubbery and nontender ❖ Hesitancy in starting urination, urinary frequency, urgency, nocturia, abdominal straining ❖ Dec. in volume and force of urination, interruption of urinary stream, dribbling Incomplete bladder emptying, Acute urinary retention (>60ml ), and recurrent UTIs ❖ Fatigue, anorexia nausea and vomiting, and pelvic discomfort are also reported, and ultimately azotemia, and renal failure Assessment ❖ Physical examination, including digital rectal examination (DRE), and health history ❖ Urinalysis to screen for hematuria and UTI-Prostate specific antigen (PSA) level is obtained if the patient has at least 10-year life expectancy and for whom knowledge of the presence of prostate cancer would change management ❖ Urinary flow-rate recording and the measurement of postvoid residual (PVR) urine. ❖ Urodynamic studies, urothrocystoscopy, and UTZ ❖ Complete blood studies including clotting studies  Medical Management ❖ Goals: improve quality of life, improve urine flow, relieve obstruction, prevent disease progression, minimize complications. ❖ -Urinary catheter- if patient unable to void ❖ Pharmacologic ttt Alpha adrenergic blockers –relaxes the smooth muscle of the bladder neck and prostate. (improve urine flow and relieves symptoms of BPH) Ex. alfuzosin (Uroxatral), terazosin (Hytrin), doxazosin (Cardura), talmusolin 5-alpha-reductase inhibitors- prevent conversion of testosterone to DHT and decrease prostate size Ex. finasteride (Proscar), dutasteride (Avodart) Use of phytotherepeutic agents and other dietary supplements are not recommended, although they are commonly used. Ex. Serenoa repens, Pygeum africanum  ❖ Minimally invasive procedures Transurethral microwave heat treatment (TUMT) – involves application of heat to prostatic tissue Transurethral needle ablation (TUNA) – uses low level radiofrequencies delivered by thin needles placed in prostate gland to produce heat that destroys prostate tissue Prostatic stents – for patients with urinary retention and with poor surgical risks ❖ Surgery Surgical resection of prostate gland Transurethral resection of the prostate (TURP) – benchmark for surgical ttt of BPH -removal of the inner portion of the prostate through an endoscope inserted through the urethra. Transurethral incision of the prostate (TUIP) -use to treat smaller prostates -cuts are made in prostate and prostate capsule to reduce constriction of urethra and decrease resistance to flow of urine out of the bladder -can be performed on an outpatient basis -lower complications