Git Disorders2( Need To Review Changes)

Chronic Inflammatory Bowel Disease

Chronic Inflammatory Bowel Disease Ulcerative Colitis chronic inflammatory disease of the rectum and colon may lead to ulcerations and cause bleeding causes: unknown, possibly related to infectious process, stress, food allergies occurs in adolescents, young adults (20-40 y.o) S/SX: profuse watery diarrhea (20 stools / day) containing blood, mucus and pus cramping pain at R lower quadrant, flatulence   w/ eating electrolyte loss may lead to metabolic acidosis Diagnostic test : x-ray, sigmoidoscopy, colonoscopy, occult blood in the stool, fecalysis – pus, mucus

Chronic Inflammatory Bowel Disease Regional Enteritis (Crohn’s disease) non-specific inflammation of the small bowel , usually the terminal ileum , chac. by cobble stone-like ulcerations along the mucosa, with thickening of intestinal wall and formation of scar tissue S/SX : severe abdominal pain, cramps (RLQ) mild diarrhea (semi-formed stool)  WBC, fever, anorexia, malaise, wt. loss may lead to fistula formation or intestinal obstruction long history of diarrhea  dehydration a mass can be felt in the area of the appendix and cecum Complications : perforation, polyps, fistula, strictures

Chronic Inflammatory Bowel Disease Management: place on NPO during acute stage, IV fluids, TPN Diet:  protein,  calorie, bland, low residue diet avoid whole grain, nuts, raw fruits except banana, excess milk, raw vegetables, tough meats, fried or highly seasoned meats avoid gas-producing or irritating foods and milk products small, frequent feedings Vit. supplements (A,D,E,K) avoid too hot, too cold foods  fluid intake (3L/day) promote bed rest (  intestinal motility), quiet, comfortable stress-free environment antibiotics for infection anticholinergics, antidiarrheals -  gastric motility and cramping keep perianal skin clean and dry, proper hygiene

Management of Chronic Inflammatory Bowel Disease

Diverticulosis / Diverticulitis Diverticulum – outpouching or formation of sacs in the musculature of the intestine Diverticulosis – the condition of being afflicted with diverticulum Diverticulitis – inflammation of the diverticulum most common in the sigmoid colon Risk factors : diet low in fiber and high in refined and processed foods age (over 40 yrs.) chronic constipation S/Sx: crampy pain in left lower quadrant of the abdomen constipation, alternating with diarrhea fever  WBC Diagnostic Test – barium enema

Diverticulosis / Diverticulitis Management : acute episodes : NPO, antibiotics, IV fluids, low fiber, low residue diet ongoing care : high fiber, high-roughage diet, laxatives, anti-spasmodics surgery : bowel resection with or without temporary colostomy keep pt. on NPO until pain subsides then liquid diet keep on bed rest to  intestinal motility observe for complications of perforation or peritonitis

Diverticulosis / Diverticulitis Measures to control divertoculosis: High fiber diet – fruits, raw vegetables, whole wheat, cereals Take stool softeners – metamucil  stress in lifestyle  daily fluid intake Avoid activities that  intraabdominal pressure Avoid nuts, fruits and vegetables w/ seeds to prevent seeds from lodging in the intestinal pouches and causing infection

Hernia a protrusion of an organ or structure from its normal cavity through a congenital or acquired defect or opening a hernia may contain peritoneal fat, a loop of intestine, a section of a bladder or a portion of the stomach Reducible hernia if the protruding structure or organ can be returned by manipulation back to its own cavity Irreducible hernia or incarcerated hernia when the protruding structure is stuck and cannot be returned Strangulated hernia when the blood supply to the structure w/in the hernia becomes occluded  necrosis and gangrene if intestines are involved  lead to intestinal obstruction

Causes and Risk Factors 1. Defect in the integrity of the muscular wall A. Congenital B. Weak muscle strength - obese & malnourished patients C. Injury or trauma D. Aging - muscle tissue infiltrated with fatty & connective tissue 2. Increase Intra-abdominal Pressure Obesity Frequent heavy lifting Frequent straining - urinary flow obstruction - constipation Chronic “coughers” - asthmatic patients - chronic bronchitis Obesity Frequent heavy lifting C. Frequent straining - urinary flow obstruction - constipation D. Chronic “coughers” - asthmatic patients - chronic bronchitis

Types of Hernia Indirect inguinal hernia when a loop of the intestine passes through the abdominal ring to the inguinal canal caused by  in intraabdominal pressure w/c forces the intestines to be pushed into a congenital defect failure of the processus vaginalis to close during fetal development Direct inguinal hernia one that passes through the posterior inguinal wall in an area of muscular weakness caused by  intraabdominal pressure against a weak posterior inguinal wall more common in men, more difficult to repair Femoral hernia the loop of intestine passes through the femoral ring and down the femoral canal  due to congenital weakness of femoral ring muscle appears as a round bulge below the inguinal ligament more common in women, high incidence of strangulated hernia

Types of Hernia Umbilical hernia when a loop of intestine passes through the umbilical ring caused by failure of the umbilicus to close at birth or by a defect in the umbilical scar, which opens in adult life when there is  intraabdominal pressure such as in pregnancy, intestinal obstruction, chronic cough Incisional hernia one that occurs through an old surgical incision caused by the failure of the resected and approximated muscles and fascial tissues to heal properly because of wound infections, drains or poor physical condition  intraabdominal pressure  push the organ or tissue through the weakened scar

Hernia Clinical Manifestations lump, bulge, or mass in the groin, around the umbilicus or protruding from an old surgical incision swelling that appears after coughing, straining, lifting or other vigorous exertion palpation of the hernia will reveal soft and nodular or smooth edges the swelling may disappear when the person lies down and reappear on standing or coughing strangulated hernia – may cause severe pain and symptoms of intestinal obstruction such as nausea, vomiting and distention Medical Management Surgery – Herniorrhaphy – the herniating tissues are returned to the abdominal cavity and the defect in the fascia or muscle is closed with sutures Strangulated hernia  resection of the area of gangrene and do anastomosis

Hernia Nsg. Management: Post-operative nursing care give food or fluids as tolerated monitor post-op urinary elimination apply ice bags if scrotal edema occurs Patient teaching : report any early signs of wound infection (redness, discomfort) that may weaken the surgical repair any post-operative echymosis will disappear in a few days sexual functioning is not affected by surgery restrict driving for 2 weeks avoid heavy lifting, pulling or pushing for 6 weeks

Hemorrhoids/ Anal Fissure Hemorrhoids : dilated veins under the mucous membranes in the anal area, may either be internal or external Anal fissure : linear ulceration on the margin of the anus Predisposing factors : straining at stool – constipation pregnancy portal hypertension congestive heart failure Complications: bleeding - strangulation thrombosis - infection S/Sx : pain and pruritus around the anus abdominal distention - urinary retention blood in stool

GRADE I - bleeding on defecation, - no prolapse GRADE II – there’s prolapse but reduce spontaneously

GRADE III – with prolapse and reduced manually GRADE IV – cannot be reduced, incarcerated

Management ointment / suppositories to shrink hemorrhage warm sitz bath surgery – hemorrhoidectomy : excision of dilated veins fissurectomy : excision of fissure provide analgesics for pain relief, ice packs or warm compress give low-residue, soft diet as tolerated for 1 st week post-op then include vegetable and fruits force fluids 2,500-3,000 ml / day watch out for symptoms of anal stricture (  pain with BM, difficulty passing stool) and report to physician

Health Teachings B. Drink 6-8 glasses of water per day Regular exercise walking, swimming 1. EASING CONSTIPATION Eat more high fiber food cereals vegetables fresh fruits, prune juice May take over the counter fiber supplement - fibrosine - metamucil

2. DEVELOP GOOD BOWEL HABITS Sit on the toilet only as long as necessary Avoid straining – prevent irritation that leads to swelling Use the toilet at a fixed time – like when you wake up 3. AVOID FOODS WHICH COULD CAUSE LOCAL IRRITATION Spicy food Alcohol 4. TRY TO AVOID LIFTING HEAVY WEIGHTS

Intestinal Obstruction 90% of bowel obstructions occur in the small bowel, esp. in the ileum, - narrowest segment has a high mortality rate if not diagnosed and treated w/in 24 hrs. Etiology and Risk factors : Mechanical Factors 1. Adhesions most common cause may form after abdominal surgery fibrous bands of scar tissue can become looped over a portion of the bowel the presence of multiple adhesions increases the risk of obstruction

Etiology and Risk factors (cont.) 2. Hernia an incarcerated hernia may or may not cause obstruction, depending on the size of the hernial ring a strangulated hernia is always obstructed bec. the bowel cannot function when its blood supply is cut off 3. Volvulus twisting of the bowel 180 o twist can cause obstruction and ischemia  infarction of the bowel 4. Intussusception is a telescoping of the bowel (slipping of a section of bowel into an adjacent section) often associated w/ a tumor of the large bowel 5. Cancer chief cause of obstruction in the large bowel

Etiology and Risk factors (cont.) B. Neurogenic Factor Paralytic Ileus – lack of peristaltic activity - prevents forward flow of intestinal contents - commonly occurs after abdominal surgery C. Vascular Factors - when the blood supply to any part of the body is interrupted, the part ceases to function 1. Complete occlusion ( Mesenteric infarction) Mesenteric thrombosis - usual cause is an embolus - causes intense abdominal pain –-- due to ischemia  bowel necrosis and gangrene and sepsis - other s/sx: fever,  WBC, signs of shock - surgical intervention must be done immediately 2. Partial occlusion (Abdominal angina) - usually results from atherosclerosis of the mesenteric arteries - pain develop 15-30 mins after eating -  need for O2 - manifestation arise when interruption in blood flow/supply is sufficient to compromise bowel function

Pathophysiology Normally 7-8 liters of electrolyte-rich fluids is secreted by the bowel, and most of the fluid is reabsorbed bowel obstruction  this fluid is partially retained w/in the bowel and partially eliminated by vomiting  severe  in circulating blood volume  hypotension, hypovolemic shock ,  renal blood flow (oliguria),  cerebral blood flow (  LOC) Fluids and air collect proximal to the site of obstruction  distention Distension causes a temporary  in peristalsis as the bowel attempts to force the material through the obstructed area After a few hours --- the bowel becomes flaccid Greater pressure w/in the bowel reduces its absorptive ability ,   fluid retention in the bowel

Pathophysiology (cont.) The bowel wall becomes permeable to bacteria and bowel organisms enter the peritoneal cavity  peritonitis and infection  pressure in the bowel wall, slows arterial blood flow and  blood supply  necrosis, sepsis, perforation and peritonitis Bacterial proliferation in the strangulated or necrotic bowel  release of endotoxins into the peritoneal cavity & systemic circulation  Septic Shock and Death

Clinical Manifestations 4 Cardinal Signs of Complete Small Bowel Obstruction Abdominal pain Vomiting Absolute constipation Distention Severe distention may raise the diaphragm  inhibit respiration  Hypoxia and Dyspnea At first, vomitus is semidigested food and chyme, later becomes watery and contains bile. Finally, the client vomits dark fecal material Signs of dehydration and hypovolemic shock Electrolyte imbalances (  Na, K, Cl) and metabolic acidosis Signs of peritonitis – rigid abdomen, fever,  bowel sounds

Interventions Surgery – to relieve the obstruction, remove the ischemic bowel and establish patency type of surgery depends on the type of obstruction and location - bowel resection, colostomy, ileostomy Nursing Interventions: replace fluids and electrolytes (IV w/ NaCl, K, NaHCO3) an NGT is inserted and attached to suction to relieve the vomiting and distention ( GI decompression ) Assess and measure emesis and drainage from NGT (document color, odor, consistency and volume)

Interventions (cont.) monitor VS closely and WOF signs of shock monitor UO < 30 ml/hr.  hypovolemia inform MD if distention occurs during post-op period report signs of paralytic ileus post-op semi-fowler’s position, deep breathing, coughing, turn to sides administer antibiotics as ordered emotional care comfort measures (oral care)

Cancer of the Colon 70% of cases occur in the rectosigmoid area Risk Factors: Age > 50, family history of cancer history of ulcerative colitis, polyps Diet -  fat, food additives, low-fiber chronic constipation S/Sx: constipation, blood in stool vague-dull pain anorexia, wt. loss, weakness, anemia signs of obstruction hemorrhage, perforation Dx :rectal exam (palpable tumor) - sigmoidoscopy, colonoscopy - barium enema - stool exam for occult blood Management : surgery : colon resection, colectomy, colostomy : abdomino-perineal resection (removal of anus and rectum) with a permanent colostomy Radiation therapy Chemotherapy

Duke’s Classification of Colorectal Cancer Stage A: confined to bowel mucosa- 5 year survival rate Stage B: invading muscle wall Stage C: lymph node involvement Stage D: metastases

Surgeries for Colorectal Cancer Right Hemicolectomy Resection or removal of ascending colon and hepatic flexure Ileum is anastomosed (connected) to the transverse colon Left Hemicolectomy Resection of splenic flexure, descending colon and sigmoid colon Transverse colon is anastomosed to the rectum Anterior Rectosigmoid Resection Resection of part of descending colon, the sigmoid colon, and upper rectum Descending colon anastomosed to remaining rectum Abdominoperineal Resection Resection of sigmoid colon and rectum Proximal end of descending colon is brought out through the abdominal wall to form a permanent colostomy Obstruction or perforation of the colon usually requires a temporary colostomy, followed later by closure of the colostomy

Nursing Care of Patient Experiencing Bowel Surgery Pre-operative Care Preventing infection a. give low-residue diet several days before surgery b. give clear liquids on day prior to surgery c. give prescribed antibiotics d. give prescribed enema and laxatives 2. Teaching a. describe deep-breathing and coughing exercises b. explain use of siderails to facilitate turning in bed w/o exerting pull on abdomen

Nursing Care of Patient Experiencing Bowel Surgery Post-operative care Promoting oxygenation encourage turning and deep breathing exercises encourage pt to be active Maintaining fluid and electrolyte balance maintain patency of NGT tube & record amount of drainage accurately maintain prescribed flow of IV fluids monitor for signs of fluid deficit (dry skin & mucous membranes, decreased skin turgor)

Post-operative Care (cont.) 3 . Promoting elimination monitor for signs of returning peristalsis (passage of flatus, bowel sounds) encourage ambulation monitor character of initial stool 4. Promoting comfort give good oral hygiene until oral fluids are taken freely give analgesics on a fairly regular basis during the 1 st 48 hrs to prevent severe pain 5. Teaching drink at least 2000 ml of fluid daily to avoid constipation avoid use of laxatives without medical approval—stool softeners or metamucil may be used drink prune juice or fruit juices daily avoid heavy lifting for at least 6 weeks after surgery

Colostomy Care: a. skin care - use of effective skin barriers or wafers to prevent skin irritation; cleanse with mild soap and water using cotton cloth b. odor control - avoid foods known to cause odor; dairy products, fish, eggs, and cabbage; use of pulverized charcoal, sodium bicarbonate, deodorant tablet c. control of gas -avoid carbonated beverages and gas forming foods d. diet - avoid overeating; chew food thoroughly; prevent diarrhea or constipation e. colostomy irrigation- to stimulate peristalsis; to establish a regular pattern of evacuation

Functions of the Liver 1. Carbohydrate, protein, fat metabolism Carbohydrate metabolism glycogen formation (glycogenesis) and storage glycogen – the form of glucose that can be stored by the body – when there is excess glucose intake b. Protein Metabolism Convert protein to glucose – when there is  carbohydrate intake (protein catabolism) Protein synthesis- produce the following plasma proteins: albumin – responsible for maintaining colloid oncotic pressure Alpha & beta globulins (immunoglobulins) clotting factors I, II, V, VII, IX, X C – reactive protein and enzymes Transferrin 3) formation of needed amino acids (transamination) 2) glucose formation – where there is  glucose intake glycogen is broken down to glucose (glycogenolysis) new glucose is formed from amino acids, lactic acids and glycerol (gluconegenesis)

Functions of the Liver(cont.) c. Fat metabolism Oxidation of fatty acids for energy Ketone formation – by-product of fat metabolism synthesis of cholesterol and phospholipids formation of triglycerides from dietary lipids, and excessive dietary carbohydrates & proteins (lipogenesis) formation of lipoproteins 2. Production of Bile Salts Bile – water, cholesterol, phospholipids, bile salts, bile pigment (bilirubin) protein & electrolytes, metabolites of drugs that need to be excreted Bile Salts – necessary for breakdown & absorption of fats, cholesterol and fat–soluble vitamins liver secretes 700 ml. of bile daily

Functions of the Liver(cont.) 3. Bilirubin Metabolism Hemoglobin Globin Heme Iron Protoporphyrin  indirect or converted by liver enzyme unconjugated bilirubin glucoronyl transferase (fat-soluble, cannot be  excreted by the kidneys) direct or conjugated bilirubin (water soluble)  secreted in the bile to the duodenum reabsorbed by the liver  bilirubin metabolized to urobilinogen excreted into the urine (by bacterial action)  excreted into the feces as stercobilin

Functions of the Liver(cont.) 4. Detoxification of endogenous and exogenous substances Ammonia – a major toxic product produced by bacteria in the GIT and also produced by the liver from deamination or removal of amino group (NH 2 ) from amino acids - ammonia is detoxified by conversion to urea – which is excreted by the kidneys steroid hormones – (estrogen, progesterone, testosterone, cortisone, aldosterone) - are in activated by the liver when there is increased production Drugs are detoxified by the liver barbiturates, sedatives are inactivated by the liver prevent toxicity of drugs

Functions of the Liver(cont.) 5. Storage of Minerals and Vitamins Vit. A, D, B 12 , E, K Iron in the form of ferritin is stored to resupply iron for hemoglobin formation copper 6. Reservoir of blood when venous blood volume increase and cannot be handled by the right side of the heart – excess blood can accumulate in the liver 7. Remove bacteria , damaged RBC, other foreign substances from the blood by phagocytosis - Kupffer cells (macrophages that stay in the liver)

Gallbladder is a saclike organ that lies on the inferior surface of the liver primary function is to store and concentrate bile between meals bile flows from the liver through the hepatic duct  cystic duct  gallbladder  mucosa of the gallbladder wall readily absorbs water and electrolytes, leaving a high concentration of bile salts, bilirubin and cholesterol (90 ml. of bile) within 30mins. after eating  presence of fat molecules in the duodenum stimulate release of hormone cholecystokinin  stimulate contraction of the gallbladder and the Sphincter of Oddi relaxes  forcing bile into the duodenum

Diagnostic Tests 1. UTZ of the liver to identify hepatic tumor, hematoma, abscesses identify the cause of jaundice preparation of the pt.: NPO 8-12 hours before the procedure 2. CT Scan of the Abdomen place pt. on NPO 8-12 hours before the procedure if contrast medium is to be used – assess allergies to iodine 3. Biopsy of the Liver to determine the cause of liver disease a needle is inserted through the chest or abdomen into the liver and a small piece of tissue is removed for study Vit. K IV may be given for several days before procedure to prevent bleeding instruct client to hold his breath and remain still and do not move to prevent the needle to slip and tear the liver covering

Diagnostic Tests (cont.) 3. Liver Biopsy (cont.) NPO 6 hours before procedure, a sedative is given 30mins. before procedure CT scan or UTZ guided needle biopsy 8 th or 9 th intercostal space - usual area of biopsy After procedure: monitor PR, BP, RR q 30 mins. then hourly for 24 hours. monitor for bleeding in the biopsy site advise pt. to lie on the R side with small pillow or blanket under the costal margin place pt. on CBR for 24 hours after the test 4. Paracentesis or peritoneal tap to remove peritoneal fluid for lab. test or to drain large volumes of ascitic fluid when there is resp. distress, cardiac dysfunction, severe abdominal discomfort maintain sterile technique have the pt. void before procedure to prevent puncture of bladder obtain consent monitor v.s. urine output, monitor for bleeding

Liver Abscess may result from a variety of organisms including E. coli, staphylococcus, streptococcus, Pseudomonas, Proteus, and Klebsiella, Entamoeba histolytica (Amoebiasis) may also occur in pts. with decreased immune function such as in leukemia, neutropenia Pathophysiology abscesses can occur as either singular large abscess or multiple small abscesses the organisms originate in various areas of the body & reach the liver through the biliary tract, vascular or lymphatic system the organisms may also be introduced by penetrating injuries to the liver lead to liver tissue destruction and abscess (pus) formation  disrupt hepatic function If untreated, they continue to  in size and can perforate into the peritoneal cavity (peritonitis) or pleural cavity

Liver Abscess (cont.) S/sx: – caused by the infectious process fever , temp 38.8 – 41 0 c , chills cough, difficulty breathing diaphoresis right upper abdominal quadrant pain and tenderness anorexia, nausea, vomiting, wt. loss signs of peritonitis - board-like abdomen, distention of abdomen altered hepatic function: hepatomegaly, jaundice & pruritus, splenomegaly, abdominal distention, ascites Amoebiasis – bloody, mucoid diarrhea, abdominal pain, rectal tenesmus, dehydration, hypotension Diagnostic Tests leukocytosis,  ESR – due to infection  serum alkaline phosphatase, SGOT, SGPT  bilirubin (hyperbilirubinemia) UTZ, CT scan

Liver Abscess (cont.) Medical Mgt. supportive measure – F & E replacement and control of temp. elevation surgical drainage of abscess and antibiotics Metronidazole (Flagyl), Chloroquine, Emetine for amoebic abscesses Nursing Mgt. provide adequate fluids and nutrition provide comfort measures for fever, pruritus - coal sponge baths - prevention of dry skin - use of soft linens - provide cool environment frequent oral hygiene pt. education complete dose of medications (several weeks to months) to prevent recurrence monitor for signs of recurrence or worsening hepatic function  cirrhosis proper hygiene, drink clean water and avoid uncooked foods

Liver Tumors Primary Hepatic Carcinoma may arise w/in the liver cell (hepatocellular) or the bile duct cell (cholangiocellular) chronic liver disease from Hepatitis B or cirrhosis may predispose individuals to primary liver cancer Metastatic Tumor of the Liver more common than primary tumor cancer cells may come from the GIT, lungs, breasts, kidneys and melanomas of the skin Pathophysiology Cancer cells compress the surrounding normal liver cells and may spread by invading the portal veins cause hemorrhage by extension into the vascular tissue of the liver cause necrosis – by depriving normal hepatic tissue of adequate circulation Tend to grow rapidly and metastasize to the lungs, spleen, kidney, pancreas, adrenal glands

Liver Tumors (cont.) S/Sx: depends on the extent of tumor growth, hepatocellular damage, and liver failure enlarge R upper quadrant masses, hepatomegaly, epigastric fullness, pain or discomfort wt. loss, abnormal liver function tests, weakness ascites, hepatic failure, jaundice, fever Diagnostic tests: blood studies -  ESR,  Hgb, RBC (anemia), hyperbilirubinemia  alkaline phosphatase,  AST,  ALT,  blood glucose, hypoalbuminemia Alpha – fetoprotein (AFP) – a special blood test used to help diagnose primary liver cancer (500 ng/ml – 50mg/ml) CT scan, UTZ liver biopsy

Liver Tumors (cont.) Medical Management 1. Supportive measures – if the tumor is far advanced at the time of diagnosis Control of pain & other discomforts Paracentesis – to decrease ascites Low sodium diet Restrict protein intake – to  ammonium production 2. Surgery – removal of solitary tumors - Liver transplant 3. Chemotherapy Done to decrease or slow down tumor growth Ex. 5- FU (5- flurouracil), Doxorubicin, mitomycin 4. Radiation therapy May occasionally be used to control pain Does not contribute to survival

Liver Tumors (cont.) Nursing Management Help pt. cope with anxiety & fear, provide emotional support Provide care when liver failure progresses – fluid volume excess, pain, pruritus, alteration in LOC & thought process Care of pt. having hepatic resection/surgery Pre – operative care Administer Vit. K and other vitamins, fluid therapy & blood transfusion Bowel preparation Post operative care Close monitoring (VS, UO, I&0, ABG, electrolytes, CBC) WOF for signs of hypovolemia, shock, sepsis and cardio/pulmo complications Administer glucose, albumin, blood replacement Restrict protein – to  ammonia Maintain chest tube drainage to water–sealed bottle Promote turning, coughing, splinting, proper positioning (Fowler’s position) Adequate pain control Frequent mouth care, pt. on NPO, with NGT to suction Encourage ambulation (4 th post day) Feeding started (5 th post–op day) – maintain adequate intake ,  protein

Jaundice there is excess bilirubin in the blood leading to distribution of bilirubin to the skin, mucous membranes and other body fluids and tissues, giving them yellowish discoloration occurs when bilirubin level is > 2.5 mg/dl Bilirubin in the skin causes pruritus (itching) Causes : intrahepatic cholestasis (stasis of bile w/in the liver) due to drug interactions extrahepatic abstruction – obstruction of hepatic, gallbladder or common bile duct, gallbladder stones, pancreatisis, cancer of pancreas hepatocellular damage – interference w/ the uptake, conjugation and excretion of bilirubin into bile

Hepatitis acute inflammatory disease of the liver caused by a virus (most common), bacteria or toxic or chemical injury Types: Toxic Hepatitis injury to the liver cells caused by alcohol, drugs, industrial chemical and toxins Ex. Industrial toxins – Carbon tetrachloride, chlorinated tetracarbons cleaning agents, solvents to remove paint Drugs – acetaminophen (paracetamol) – large doses Tetracycline Rifampicin, Isoniazid (INH) Phenytoin Chemotherapy drugs

Toxic Hepatitis (cont.) Pathophysiology: Damage to the liver  - fatty infiltrations  altered liver function - necrosis  - stasis of bile (cholestasis) can lead to - inflammation liver failure S/Sx : anorexia nausea, vomiting, lethargy, weakness jaundice (icterus), hepatomegaly, liver tenderness  AST,  ALT – the higher the enzyme levels, the more severe the cellular damage to the liver  bilirubin in blood and urine low albumin, prolonged PT

Toxic Hepatitis (cont.) Medical Mgt.: identify the toxic agent and remove or eliminate it insert NGT and do gastric lavage and cleansing of the bowel supportive medical care of the symptoms present Nsg. Mgt.: promote comfort, maintain fluid & electrolyte balance promote well- balanced diet promote rest pt. teaching - proper use of chemicals at home - avoid exposure to chemical in the work environment - proper use of drugs, follow doctor’s advice

Viral Hepatitis 4 types: Hepatitis A, Hepatitis B, non-A, non-B hepatitis, Delta hepatitis

Viral Hepatitis(cont.) Virus invades portal tracts (blood vessels going to the liver) and lobules of liver, causing inflammation and destruction of parenchymal cells  hyperplasia of Kupffer cells (phagocytes)  damage cells are gradually phagocytized and cell regeneration occurs S/Sx: Pre-icteric (before yellowish discoloration appears) – last for 1 week flu like symptoms (malaise, fever, chills) dull pain and tenderness in RUQ of abdomen, liver enlargement nausea and vomiting dyspepsia, anorexia headache weakness wt. loss

Viral Hepatitis(cont.) Icteric (2-3 weeks ) – starts with jaundice jaundice (yellow sclera & skin esp. palms and soles of the feet clay colored stools, dark – amber urine,  urine bilirubin and  urobilinogen Pruritus Fatigue, anorexia, abdominal tenderness, weakness Abnormal liver function test (  AST, ALT, bilirubin),  alkaline phosphatase Post icteric (2-4 months) – begins with disappearance of jaundice resolving jaundice gradual return of appetite & energy Medical Mgt.: (no specific medical treatment) - rest, symptomatic support - F/E replacement -antihistamine for pruritus interventions to prevent transmission – Vit. K replacement antiemetic for vomiting

Viral Hepatitis(cont.) Nsg. Interventions: prevent transmission of infection handwashing, good personal hygiene Hep. A - use disposable eating utensils/dishes or separate them Hep. B – Hep. B immune globulin, Hep. B vaccine to exposed persons universal precautions aseptic technique CBR, calm, restful environment avoid administering drugs toxic to the liver proper skin care (pruritus), comfort measures encourage well-balanced diet, adequate nutrients /calories  fluid intake, avoid fatty foods Instruct pt. to avoid sexual activity, avoid alcohol intake, not to share personal items, not to donate blood

Liver Cirrhosis a chronic, degenerative disease of the liver causing inflammation destruction, fibrotic regeneration and hepatic insufficiency  loss of liver function 2x common in men than women, 40-60 years old. Predisposing/ Precipitating factors: malnutrition effects of alcohol abuse chronic impairment of bile excretion – biliary obstruction in the liver and common bile duct (gallbladder stones) necrosis from hepatotoxins or viral hepatitis chronic congestion heart failure Pathophysiology: liver cell damage result in inflammation & hepatomegaly attempts at regeneration eventually result to fibrosis and a small nodular liver hepatic function is slowly impaired obstruction of venous channels blocks hepatic blood flow and cause portal hypertension

Liver Cirrhosis (cont.) S/Sx - early : anorexia, nausea, indigestion aching or heaviness in right upper quadrant weakness & fatigue Late signs : abnormal liver function tests:  bilirubin, AST, ALT, alkaline phos. intermittent jaundice, pruritus edema, ascites, prominent abdominal wall veins,  albumin bleeding tendencies, prolonged prothrombin time,  plt. ct. anemia: folic acid deficiency,  RBC production,  RBC destruction in spleen frequent infection,  WBC Nsg. Interventions: 1. Reduce metabolic demands on the liver provide bed rest eliminate ingestion of toxic substances to the liver: sedatives opiates, alcohol, acetaminophen  activities

Liver Cirrhosis (cont.) 2. Provide adequate nutrition & hydration Low – protein, high-carbohydrate, high calorie, sodium- restricted diet multiple vitamin therapy restrict fluids & sodium if there is edema or ascites provide mouth care before meals monitor I/O, daily wt. 3. Prevent infection encourage good personal hygiene reverse isolation assess for signs of urinary/esp. infection encourage deep breathing/position changes 4. Protect pt. from bleeding monitor urine, stool, gums, skin for signs of bleeding/ bruising avoid injections, apply pressure to venipuncture sites for at least 5 mins. Monitor prothrombin time, bleeding time Teach pt. to use soft toothbrush, avoid constipation Prevent scratching from pruniturs, proper skin care Administer Vit. K as ordered

Complications of Liver Cirrhosis 1. Ascites abnormal intraperitoneal accumulation of watery fluid containing small amounts of protein due to :  colloid asmotic pressure from  albumin prod. by liver  capillary hydrostatic pressure from portal hypertension Na and H 2 O retention S/sx: abdominal enlargement,  wt. fatigue abdominal discomfort, respiratory difficulty Med. Mgt. (depending on severity of ascites) Na+ & fluid restriction (500-1000 ml/day) diuretic therapy (aldactone/ spirinolactone) salt-poor albumin transfusion to restore plasma volume placement of LeVeen Shunt (catheter to remove fluid from peritoneum to vena cava) Paracentesis – used for diagnosis or when fluid volume compromise comfort & breathing

Complications of Liver Cirrhosis (cont.) Nursing Interventions to  ascites & increase/promote comfort maintain on bed rest fluid & Na restriction monitor I/O, daily wt. measure abd. girth every shift maintain on high-Fowlers for max. respiration support abdomen with pillows administer diuretics, salt-poor albumin IV as ordered - monitor for signs of CHF, pulmonary edema, dehydration, electrolyte imbalance, hypersensitivity reaction Assist with Paracentesis have the client void before the procedure high –fowlers position during the procedure monitor pt. for hypovolemia & electrolyte imbalance observe puncture wound for leakage & signs of infection

Complications of Liver Cirrhosis (cont.) 2. Hepatic Encephalopathy cerebral dysfunction assoc. with severe liver disease inability of the liver to metabolize substances that can be toxic to the brain such as ammonia , which is produced by the breakdown of protein in the intestinal tract S/Sx: Asterixis- flapping hand tremors ---early sign  LOC – lethargy progressing to coma  mental status, confusion, disorientation dullness, slurred speech behavioral changes, lack of interest in grooming/ appearance twitching, muscular incoordination, tremors Fetor hepaticus elevated serum ammonia level

Complications of Liver Cirrhosis (cont.) Interventions: a. )  ammonia production  dietary protein to 20-40 g/day, maintain adequate calories  ammonia formation in the intestine – give laxative, enema as ordered and Neomycin -  bacterial ammonia production b.) Protect pt. from injury side rails up turning to side assess mental status, LOC proper positioning (semi-Fowler’s) prevent aspiration c.) Prevent further episodes of encephalopathy low protein diet prescribed medications avoid constipation ( to  ammonia production by bacteria in the GIT) early signs of encephalopathy (restlessness, slurred speech, dec. attention span)

Complications of Liver Cirrhosis (cont.) 3. Esophageal Varices distention of the smaller blood vessels of the esophagus as a result of portal hypertension – due to obstruction of venous circulation w/in the damaged liver the  portal venous pressure causes blood to be forced into these vessels – become tortous and fragile blood vessel become prone to injury by mechanical trauma from ingestion of coarse food and acid pepsin erosion which may result in bleeding bleeding may also occur as a result of coughing, vomiting, sneezing, straining at stool or any physical exertion that  abdominal venous pressure S/Sx: upper GI bleeding - blood in vomitus (hematemesis) - melena massive hemorrhage signs/symptoms of hypovolemic shock

Complications of Liver Cirrhosis (cont.) Medical Management: find the source of bleeding – esophagoscopy, angiography control bleeding – gastric lavage, administration of antacid via NGT surgery – ligation and shunts insertion of Sengstaken–Blakemore tube with gastric and esophageal balloon that are inflated to stop bleeding has a nasogastric suction tube to remove blood in the stomach the balloon is deflated periodically to prevent ulceration to the gastric mucosa if the balloon ruptures or the tube dislodged – deflate the balloon and remove immediately

Cholelithiasis Cholelithiasis – stone formation in the gallbladder Cholecystitis – inflammation of the gallbladder that can be acute or chronic and is usually precipitated by gallstones, can also be caused by bacterial infection Choledocholithiasis – stones in the common bile duct Gallstones – composed primarily of cholesterol, bile salts, calcium, bilirubin and proteins Etiology/causes: (4x more common in women) Metabolic factors –  serum cholesterol level in situations like obesity, pregnancy, diabetes, hypothyroidism 75% of gallstones are cholesterol stones 25% of gallstones are bilirubin stones – consists of bilirubin pigment stones – occurs in persons with hemolytic disease 2. Biliary stasis – leading to stagnation of bile in the gall bladder  leads to excessive absorption of water w/c allows the salts to precipitate and form mixed stones

Cholelithiasis (cont.) Inflammation of the biliary tract cause the bile constituents to become altered and the inflamed gallbladder mucosa absorbs more of the bile acids  results to formation of cholesterol stones Stones may lodge anywhere in the biliary tract  cause obstruction  lead to jaundice and poor absorption of fats may cause pressure, subsequent necrosis and infection of the walls of the biliary tract may stimulate spasm and pain a stone can block the entrance of pancreatic fluid and bile into the duodenum  cause pancreatitis Predisposing Factors: 5 F’s Female Fat (obese) Fair complexion Forty (age 40 and above) Fertile (multipara)

Cholelithiasis (cont.) Pathophysiology Clinical Manifestations Stasis of bile  Stone formation Obstruction of bile flow  total and conjugated serum bilirubin   urinary bilirubin,  urine urobilinogen Impairment of fat - jaundice, pruritus, dark amber urine absorption bec. of impaired Vit. K absorption – prolonged PT  bile in the intestine - bleeding tendencies intolerance to fatty foods - indigestion - nausea - eructation (bleching) - vomiting clay–colored stools Smooth muscle contractions biliary colic – RUQ pain in the gallbladder & bile duct - severe pain- radiate to back & R shoulder Acute or chronic – chills, fever, elevated WBC, N/V Inflammation of the gallbladder Acute Cholecystitis  May lead to perforation & peritonitis

Impacted stone Acute Cholecystitis swollen edematous vascular

Cholelithiasis (cont.) Dx: Abdominal Ultrasound, HBT UTZ Management: low – fat diet weight reduction dissolution therapy (chenodeoxycholic acid) - dissolves stones Surgery: Cholecystectomy (removal of gall bladder and cystic duct) removal of stones in common bile duct - placement of T- tube to maintain duct patency during healing

Cholelithiasis (cont.) Nsg. Interventions: provide pain relief – analgesics, anti-spasmodic drugs Give antibiotics as ordered Post op-care – place pt. in semi-fowler’s position Encourage coughing, deep breathing, turning to prevent atelectasis Change dressing as needed (bile is very irritation to the skin) Care for the T – tube – avoid tension and obstruction of tubing measure amt. of drainage ( 200-1000 ml/day for 1 st several days) Clamp as ordered in 3-4 days, before meals to allow bile to drain into duodenum, assess tolerance Usually removed 10-12 days post-op Advance from clear liquids to low-fat diet as tolerated

Pancreas produce 2,000 ml. of secretions daily, composed of: electrolyte solution w/ a high concentration of bicarbonate digestive enzymes – secreted by the acinar cells in the pancreas Pancreatic enzymes Trypsinogen – converted by enterokinase to trypsin – breakdown polypeptides into peptides and amino acids Amylase – hydrolyzes starch (carbohydrates) into maltose, lactose and sucrose Lipase – catalyzes splitting of fats into glycerol and fatty acids The release or secretion of pancreatic enzymes are stimulated by hormones released from the duodenum: a). secretin b). cystokinin – pancreozymin (CCK – PZ) - these hormones are stimulated by the presence of food in the intestine

Acute Pancreatitis Pancreatitis – a serious inflammatory disorder of the pancreas that can be acute or chronic Acute Pancreatitis can occur as a single episode or as recurrent attacks the pancreas returns to normal after successful treatment except for alcohol- induced pancreatitis Causes: alcoholism biliary tract disease – gallstones in the biliary tract that cause obstruction of the pancreatic duct Post-operative abdominal or non-abdominal surgery blunt abdominal trauma infections esp. viral Drugs (antihypertensives, diuretics, antibiotics, immunosupresstants, oral contraceptives Intestinal disease such as duodenal ulcers, regional enteritis Unknown

Acute Pancreatitis (cont.) Pathophysiology: reflux of bile, obstruction of pancreatic duct, ischemia, anorexia, trauma, endotoxins and exotoxins from bacteria or microorganisms  stimulate activation of proteolytic enzymes Ex. Trypsinogen  trypsin inside the pancreas  Auto digestion - trypsin and other proteolytic enzymes digest pancreatic and other surrounding tissues and cell membranes  edema, interstitial hemorrhage, parenchymal cell necrosis in the pancreas

Acute Pancreatitis (cont.) Summary of major Pathologic events that occur in Acute Pancreatitis Altered glucose Stress response Metabolism  cardiac (hyperglycemia) contractility  Release of Acute Pancreatitis release of Insulin kinin Vasodilation (activated by trypsin) Obstruction of edema, distention of Shock bile flow capsule, obstruction of pancreatic flow Exudate of blood and protein into Hypovolemia Altered bilirubin peritoneal space metabolism Pain Peritonitis  gastrointestinal Fever function

Acute Pancreatitis (cont.) Complications of Acute Pancreatitis hypotension, shock Anemia due to blood loss Atelectasis, pleural effusion, ARDS, respiratory failure Peptic ulcers, gastritis Hemorrhage, pancreatic abscess, ascites Hyperglycemia S/Sx: severe abdominal pain (epigastric or LUQ) - more intense when pt. is lying supine nausea, vomiting, low grade fever abdominal distension and rigidity & tenderness,  bowel sounds Signs of dehydration (poor skin turgor, dry mouth, tachycardia Jaundice – obstruction of common bile duct Purplish discoloration of the flank area (Grey Turner’s sign) or the periumbilical area ( Cullen’s sign ) – due to hemorrhagic necrosis of pancreas

Acute Pancreatitis (cont.) Diagnostic test:  serum enzyme levels a.) serum amylase greater than 300 units – indicate acute pancreatitis b.) serum lipase greater than 1.5 units  WBC, Anemia (  Hgb,  RBC),  bilirubin abdominal x-ray, UTZ Medical Management place pt. on NPO – to decrease stimulation of pancreatic secretion  to rest the pancreas insertion of NGT – to decompress the bowel and relieve abdominal distention and allow to drain fluid and electrolyte replacement pain relief (analgesics, anti-inflammatory drugs) Drugs (antibiotic, somatostatin -  pancreatic secretion) Monitor blood glucose levels (insulin may be given)

Acute Pancreatitis (cont.) Nursing Interventions 1. Maintain fluid & electrolyte balance – I& O, V.S, daily wt. Hemodynamic measurements measure urine output accurately, foley catheter care monitor for signs of shock maintain correct IVF infusion rates 2. Promote nutrition - NPO, provide oral care - gradual diet from clear liquids – low fat, bland diet, small frequent feedings - monitor for nausea, vomiting, pain - TPN 3. Controlling discomfort pain relievers every 3-4 hrs. position on side-lying, Knee-chest position., or sitting position to decrease pain relaxation techniques, deep breathing exercises, guided imaginary

Acute Pancreatitis (cont.) 4. providing self-care prevent skin breakdown, pressure sores provide adequate rest periods assist or perform self-care for the patient during the acute stage 5. Patient teaching prevent future attacks by avoiding alcohol, maintaining a nutritious diet, low-fat, bland diet, avoid caffeine small frequent feedings regular follow-up

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