Metabolic Disorders

METABOLIC DISORDERS ANATOMY OF ANATOMY AND PHYSIOLOGY (ACCESSORY DIGESTIVE SYSTEM) Accessory organs 1. Salivary glands -

Three pairs of major salivary glands o Parotid, submandibular, and sublingual glands) and numerous smaller ones secrete saliva into the oral cavity o Saliva contains water, mucus, and enzyme amylase. Functions of saliva include the following: o o o o

It has a cleansing action on the teeth. It moistens and lubricates food during mastication and swallowing. It dissolves certain molecules so that food can be tasted. It begins the chemical digestion of starches through the action of amylase, which breaks down polysaccharides into disaccharides.

2. Liver -

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located primarily in the right hypochondriac and epigastric regions of the abdomen, just beneath the diaphragm functional units of the liver are lobules with sinusoids that carry blood from the periphery to the central vein of the lobule. common hepatic artery – carries freshly oxygenated blood to the liver hepatic portal vein - Blood that is rich in nutrients from the digestive tract is carried to the liver Hepatocytes perform most of the functions attributed to the liver Kupffer cells that line the sinusoids are responsible for cleansing the blood of microorganisms and other waste products

Liver functions include the following: o o o o o o o o o o o o o

Secretion of bile synthesis of bile salts synthesis of plasma protein storage – glycogen (from glucose), vitamins A, B, D, iron and copper detoxification (drugs, alcohol, hormones) excretion carbohydrate, lipid and protein metabolism filtering manufacture of fibrinogen and prothrom bin manufacture of heparin aids in the destruction of aging RBC, manufacture of vitamin A Regulation of blood volume by storing up to 400 cc of blood

3. Biliary tract Common bile duct – composed of cystic duct from the gallbladder and hepatic duct from the liver o Transport bile from liver and gallbladder to duodenum when food is present in small intestine Cystic duct – leads from GB to CBD; passageway for bile to and from the GB o When duodenum is empty, sphincter closes, causing bile from the liver to flow through the cystic duct into the GB o During digestion, sphincter opens as the GB contracts, forcing the bile through the cystic duct to the common bile duct into the duodenum

Gallbladder -

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pear-shaped sac that is attached to the visceral surface of the liver by the cystic duct it is stimulated to contract by cholecystokinin (a hormone secreted by the small intestine in response to the presence of fat)

principal function of the gallbladder is to serve as a storage reservoir for bile o Bile - yellowish-green fluid produced by liver cells. The main components of bile are water, bile salts, bile pigments, and cholesterol. o Bile salts - act as emulsifying agents in the digestion and absorption of fats o Cholesterol and bile pigments from the breakdown of hemoglobin are excreted from the body in the bile.

*** without bile, fat is not digested and the stools become clay-colored 4. Pancreas -

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The pancreas has both endocrine and exocrine functions Joins with the bile duct at the duodenum The endocrine portion o consists of the scattered islets of Langerhans  secrete the hormones insulin (beta cells) and glucagon (alpha cells) The exocrine portion is the major part of the gland o It consists of pancreatic acinar cells that secrete digestive enzymes  Pancreatic enzymes include amylase, trypsin, peptidase, and lipase

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Pancreatic secretions are controlled by the hormones secretin and cholecystokinin.

DIAGNOSTICS A. Laboratory Studies 1. LIVER FUNCTION TESTS  a.

Over 70% of the parenchyma of the liver may be damaged before liver function tests become abnormal

Pigment studies    

Parameters of hepatic ability to conjugate and excrete bilirubin Abnormal in liver and gallbladder disorders Client must fast for 4 hours NV: direct (conjugated) bilirubin – 0.2 – 0.4 mg/dl (increases with hepatocellular injury or obstruction) : indirect (unconjugated) bilirubin - <0.8 mg/dl (increases with hemolysis of RBC) : total bilirubin – 1. 0 – 1.2 mg/dl (increases with biliary obstruction) : Urine bilirubin – 0 (increases with biliary obstruction)

b. Serum albumin   

Proteins are produced by the liver and can diminish in hepatic disease Decreased serum albumin results in generalized edema NV: 3.5 – 5.5 g/dL (reduced with hepatocellular injury)

c. Coagulation studies (Prothrombin time – PT, partial thromboplastin time – PTT)  

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May be prolonged in hepatic disease, PTT is prolonged due to lack of Vit C. NV: PT: 9.5 – 12.0 seconds, (increase with chronic liver disease (cirrhosis) or Vit. K deficiency) PTT – 20-45 seconds (increase with severe liver disease or heparin therapy) Put specimen in ice, apply pressure to site for 5 mins (15 mins for clients with anticoagulant

d. Liver enzymes 

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NV: AST: Aspartate Aminotransferase(SGOT) – 10-40 units, ALT: Alanine Aminotransferase (SGPT) – 5-35 units (both increases with hepatocellular injury) LDH (Lactic dehydrogenase): 165 – 400 units (elevated with hypoxic and primary liver injury) Alkaline Phosphatase NV: 32-92U/L (increases with biliary obstruction and cholestatic hepatitis)

e. Blood ammonia  

Converts ammonia to urea, with liver disease ammonia levels rise NV: 15-40 mg/dl

B. Diagnostic and Imaging Studies

1. Abdominal xray

2. Liver scan 

Question about allergy to seafoods or iodine

3. Cholecystogram and cholangiogram 

For GB and bile duct visualization

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Instruct to have a fat-free diet evening before exam Ingestion of dye in tablet form (Telepaque tablets) check for iodine and shelfish allergies NPO after dye ingestion X-rays followed by ingestion of high fat meal followed by further X-rays

4. Celiac axis arteriography 

Liver and pancreas visualization; check for seafood allergies

5. Liver Biopsy    

Administer Vit K to decrease chance of hemorrhage, NPO morning of exam Sedative administration just before exam Teach client he will be asked to hold his breath for 5 to 10 seconds Performed at bedside, supine position, lateral with upper arms elevated

C. Other Test

1. PARACENTESIS 

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Needle aspiration of abnormal fluid accumulated fluid in the abdominal cavity (ascites) for analysis or therapeutic measure Patient in semi-fowler’s or sitting position Empty bladder prior to procedure to avoid accidental perforation

HEPATIC DISORDERS AND MANAGEMENT 1. LIVER CIRRHOSIS -

A chronic, progressive disease of the liver characterized by diffuse damage to cells with fibrosis and nodular regeneration

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Repeated destruction of hepatic cells causes the formation of scar tissue

Type: a. Laennec’s cirrhosis – result of alcoholism and poor nutrition b. Biliary cirrhosis – result of chronic biliary obstruction and infection c. Postnecrotic cirrhosis – result of previous hepatitis Complications: a. Portal hypertension o A persistent increase in pressure within the portal vein that develops as a result of obstruction to flow b. Ascites o Accumulation of fluid within the peritoneal cavity that results in venous congestion of hepatic capillaries o Capillary congestion leads to plasma leaking directly from the liver surface and portal vein c. Bleeding esophageal varices o

fragile, thin walled, distended esophageal veins become irritated and rupture

o Usually found in the submucosa of the lower esophagus; may lead to hemorrhage

Interventions for esophageal varices and cirrhosis A. Shunts – to relieve portal hypertension – last resort intervention for portal hypertension and esophageal varices o Portacaval – blood diverted from portal circulation to vena cava o Splenorenal – blood diverted from splenic vein to left renal artery o

Transjugular intrahepatic portosystemic shunt (TIPS) – shunt is between the portal and systemic venous system using a metallic stent

B. Insertion of Sengstaken-Blakemore tube with 3 openings o Esophageal balloon o Gastric balloon o Gastric aspiration lumen 

gastric balloon – applies pressure at the cardioesophageal junction to compress gastric varices and to decrease blood flow to the esopahgeal varices; a traction is applied to maintain the gastric balloon in place

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esophageal balloon – directly compresses esophageal varices

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gastric aspiration port/lumen – used in lavage and

o if bleeding is not stopped , the esophageal balloon is inflated to 24 to 45 mmHg o a radiograph of the upper abdomen is used to confirm placement C. Insertion of Minnesota tube

o Four-lumen gastric tube; same as Sengstaken – Blakemore tube but with an added lumen for esophagopharyngeal secretion Things to remember in the use of Sengtaken – Blakemore and Minnesota tube

a. Check patency and integrity of all balloons before insertion, label each lumen b. Position client in the upright or Fowler’s position for insertion; immediately after insertion prepare for radiography to verify placement c. Maintain head elevation once tube is in place d. Double clamp the balloon ports to prevent air leaks e. Keep scissors at the bedside at all times ; monitor for RD and if it

occurs immediately cut the tubes to deflate balloons f. Prevent ulceration or necrosis of the esophagus by releasing esophageal pressure as prescribed g. Monitor for increased bloody drainage that may indicate persistent bleeding h. Monitor for esophageal rupture 

Drop in blood pressure, increased heart rate, and back and upper abdominal pain; report to the AP immediately

D. Assist in the administration of iced saline irrigations to achieve vasoconstriction of varices E. Administer Vasopressin (Pitressin) by IV or intraarterial infusion as prescribed to induce vasoconstriction and bleeding. Have NTG available for administration to prevent vasoconstriction of coronary arteries F. Instruct client to avoid activities that increase vasovagal responses G. Endoscopic injection (Sclerotherapy) – causes veins to become fibrotic H. Endoscopic variceal ligation – ligation of varices with an elastic rubber band to slough off the varices d. Coagulation defects o Decreased synthesis of bile fats in the liver prevents the absorption of fat soluble vitamins (ADEK) o Without Vit. K, blood coagulation factors 2,7,9,10, the client is prone to bleeding

e. Jaundice o Liver is unable to metabolize bilirubin o All tissues including th sclera are yellow or greenish yellow because of an increased concentration of bilirubin in the blood f. Portal systemic encephalopathy o Characterized by altered LOC, neurological symptoms, impaired thinking, and neuromuscular disturbances g. Hepatorenal syndrome o Renal failure associated with hepatic failure o Sudden decrease in UO, elevated BUN and CREA, decreased urine sodium excretion, and increased urine osmolarity Assessment 1. Anorexia and weight loss 2. Early morning nausea and blood tinged vomitus 3. Dyspepsia 4. Flatulence and changes in bowel habits 5. Emaciation, fatigue, jaundice 6. Abdominal pain and tenderness 7. Ascites 8. Peripheral edema, dry skin and rashes 9. Petechiae or ecchymosis 10.Spider angiomas on the nose, cheeks, upper thorax and shoulders 11.Hepatomegaly 12.Protruding umbilicus, dilated abdominal veins 13.Fetor hepaticus – fruity, musty breath odor of chronic liver disease 14.Asterixis (liver flap) – a coarse tremor characterized by rapid nonrhythmic extension and flexion in the wrist and fingers 15. Delirium

Interventions

1. Elevate HOB to minimize SOB 2. High protein diet if ascites and edema are absent and no signs of impending coma 3. Provide vitamin supplements 4. Restrict sodium and fluid intake 5. Initiate enteral feedings or TPN, administer diuretics as prescribed

6. Monitor I and O and electrolyte balance 7. Weigh client and measure abdominal girth daily 8. Monitor for LOC; assess for precoma state (tremors and delirium) 9. Monitor for asterixis 10.Monitor gastric intubation to assess bleeding or esophagogastric balloon tamponade to control bleeding varices 11.Administer low sodium antacids and blood products as prescribed 12.Monitor coagulation laboratory results; admin vit K as prescribed 13.Administer lactulose -

To decrease the pH of the bowel decreases ammonia production by bacteria in the bowel  facilitate excretion of ammonia

14. Administer Neomycin (Mycifradin)  inhibit protein synthesis in bacteria 

decrease production of ammonia 15.Avoid narcotics, sedatives and barbiturates and any hepatotoxic drugs or substances 16.Alcohol restriction 17. Prepare for paracentesis  remove excess fluid in the abdomen

18.Prepare for surgical shunting PORTAL HYPERTENSION -

an increase in the blood pressure within a system of veins called the portal venous system due to an obstruction to flow.

Pathophysiology -

veins come from the stomach, intestine, spleen and pancreas  merge into the portal vein  then branches into smaller vessels and travels

through the liver vessels in the liver are blocked cause high pressure in the portal system  the blood backs up and finds other ways to flow back to the heart then to the lungs, where it gets rid of waste products and picks up oxygen  blood can travel to the veins in the esophagus (esophageal varices)  in the skin of the abdomen, and the veins of the rectum and anus (hemorrhoids) to get around the blockages in the liver. CAUSES 1. Liver cirrhosis

2. blood clots in the portal vein 3. Schistosomiasis SYMPTOMS •

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Gastrointestinal bleeding o Black, tarry stools or blood in the stools o Vomiting of blood due to the spontaneous rupture and hemorrhage from varices. Ascites (an accumulation of fluid in the abdomen) Encephalopathy or confusion and forgetfulness caused by poor liver function. Reduced levels of platelets, blood cells that help form blood clots, or white blood cells, the cells that fight infection.

Diagnosis 1. physical exam of the abdomen or the anus o based on the presence of ascites or of dilated veins or 2. Various lab tests, X-ray tests and endoscopic examinations may also be used. Treatment 1. most causes of portal hypertension cannot be treated Prevention and Management of Complications 1. Endoscopic therapy o first line of treatment for variceal bleeding and consists of either banding or sclerotherapy  Banding is a procedure A. uses rubber bands to block off the blood vessel. Sclerotherapy is occasionally used when banding cannot be used and is a procedure in which a solution is injected into the bleeding varices to cause them to scar. 2. Medications

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beta blockers (nadolol or propranolol) A. reduce the pressure in varices and further reduce the risk of re-bleeding lactulose A. treat confusion and other mental changes associated with encephalopathy.

3. Lifestyle Changes

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Do not use alcohol or street drugs. Do not take any over-the-counter or prescription drugs without first consulting your doctor or nurse. (Some medications may make liver disease worse.) eating a low-sodium (salt) diet. A. No more than 2 grams of sodium per day Reduced protein A. required if confusion is a symptom

4. Transjugular intrahepatic portosystemic shunt (TIPS) o

a stent (a tubular device) in the middle of the liver that connects the hepatic vein with the portal vein.

5. Distal splenorenal shunt (DSRS) o

connects the vein from your spleen to the vein from your left kidney in order to reduce pressure in the varices and control bleeding

CHOLELITHIASIS -

solid deposits of cholesterol or calcium salts that form in your gallbladder or nearby bile ducts can be caused by increased concentration and precipitation of bile substances (cholesterol, bile acids, bile pigments)

Risk Factors 1. Metabolic factors – obesity, pregnancy, diabetes, hypothyroidism 2. Biliary stasis 3. Biliary system inflammation

Symptoms 1.Chronic indigestion. o

Nausea, gas, bloating, diaphoresis and sometimes abdominal pain  made worse after you eat high-fat foods

2.Upper abdominal pain Sudden, steady and moderate to intense pain in your upper middle or upper right abdomen may signal a gallbladder attack o Severe R upper quadrant abdominal pain radiating to the back and right shoulder o The pain may occur one to two hours after eating but may also occur at other times — even at night. It can last about 30 minutes to several hours o

3.Nausea and vomiting 4.Fever Symptoms of Bile Duct Obstruction 1. 2. 3.

Pain and fever due to inflammation Yellowing of your skin and the whites of your eyes (jaundice) Clay-colored stools

Types of gallstones 1. Cholesterol gallstones -

often yellow in color, are composed mainly of undissolved cholesterol o other components, such as calcium and bilirubin, the residue from the breakdown of red blood cells o 80 percent of gallstones are cholesterol stones.

2. Pigment gallstones -

These small, dark brown or black stones form when your bile contains too much bilirubin tend to form in people with conditions like o cirrhosis, biliary tract infection and sickle cell anemia (result in excess bilirubin forming)

Contributors to Gallstones Formation 1. Too much cholesterol.

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if your bile contains more cholesterol than can be dissolved, the cholesterol may form into crystals and eventually into stones

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Cholesterol in your bile has no relation to the levels of cholesterol in your blood cholesterol-lowering drugs don't help prevent gallstones.

2. Incomplete or infrequent gallbladder emptying -

bile may become too concentrated and contribute to the formation of gallstones Eating too little fat or going long periods without eating, such as skipping breakfast, also can decrease gallbladder contractions

3. Sex -

Women between the ages of 20 and 60 o female hormone estrogen causes more cholesterol to be excreted in bile o Pregnancy, which causes estrogen levels to rise, also increases the risk o birth control pills and hormone therapy (HT) both increase bile cholesterol levels and decrease gallbladder emptying

4. Body weight o

As your body mass index (BMI) increases, so does your risk of developing gallstones.

5. Diet 

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Low-calorie, rapid-weight-loss diets tend to disrupt your bile chemistry and may cause your gallbladder to contract less often bariatric surgery A. increases risk of gallstones

6. Age o

chance of developing gallstones increases with age. People older than 60 years of age are more likely to have gallstones than are those who are younger.

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American Indians have the highest incidence of gallstones in the United States. Mexican-Americans also are at increased risk.

7. Ethnicity

Tests and diagnosis 1. Medical history and a Physical exam.

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check for jaundice of your skin or the whites of your eyes and will feel (palpate) your abdomen to see if it's tender

2. Blood tests -

CBC, elevated liver enzymes, elevated bilirubin

3. Ultrasonography -

the best way to detect gallstones in your gallbladder and sometimes in the common bile duct.

4. Computerized tomography (CT) scan -

uses a series of computer-generated X-rays to provide a comprehensive view of your internal organs.

5. Radionuclide scan (cholescintigraphy) -

small amount of a radioactive tracer material through your veins (intravenously), followed by a scan of the gallbladder to see if the tracer material gains access to the gallbladder. If it doesn't, a stone is likely blocking the opening of the gallbladder or cystic duct.

6. Endoscopic retrograde cholangiopancreatography (ERCP 7. Endoscopic ultrasound (EUS) Complications of gallstones may include: 1. 2.

Blockage of the common bile duct Inflammation of the pancreas -

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Pancreatitis is likely to cause an intense, constant pain in your upper abdomen that may radiate to your back or chest The pain is usually worse when you lie flat and better when you sit up or bend forward

Gallbladder cancer

Treatments and drugs 1.

Surgery a. cholecystectomy o Laparoscopic surgery  laparoscope is inserted o Open surgery  best option in severe cases  used when the gallbladder walls are thick and hard, the gallbladder is obviously infected, or there is scar tissue from earlier abdominal operations  A Penrose drain maybe inserted through the incision

b. Cholecystostomy – opening of gallbladder to remove stones, bile or pus c. Choledocostomy – opening into the CBD to remove obstructing stones; a T-tube is inserted into the duct and connected to drainage Post-op Care -

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Semi-fowler’s position Prevent kinking or twisting of tubes Position drainage bottle as ordered ; usually kept on bed at same level as gallbladder Observe and recosr amount and character of drainage (expect 500-1,000 ml/day at first) Check orders regarding clamping of T-tube before/after meals Check orders regarding fluid replacement of drainage Provide low-fat, high carbohydrate, high protein diet Note color changes of skin, sclera and stool as indicators of improved bile flow after T-tube removal o Jaundice should lessen o Stool should slowly progress from light to dark Protect skin around incision from drainage and leakage o Apply coat of zinc oxide or petroleum jelly o Change dressing frequently o If drainage amount remains large, record finding (may indicate fistula) Monitor for pain intensity

Nonsurgical options -

Bile salt tablets o ursodiol (Actigall), chenodeoxycholic acid (chenodiol) o dissolves cholesterol stones over a period of time Sound wave therapy (extracorporeal shock wave lithotripsy) o uses high-frequency sound waves to break up gallstones Percutaneous electrohydraulic lithotripsy o A small probe is inserted into the catheter to deliver short bursts of energy to break up the stones Topical gallstone dissolution o small catheter is inserted into the gallbladder. A solution that dissolves cholesterol gallstones is then delivered through the catheter into the gallbladder over a several hour period

Prevention • •

Maintain a healthy body weight o Avoid losing more than 1/2 to 2 pounds a week. Avoid crash diets or a very low intake of calories — less than 800 calories a day.

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Be active. Make sure that you exercise regularly. Choose a low-fat, high-fiber diet

CHOLEDOCHOLITHIASIS -

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Choledocholithiasis is the presence of a gallstone in the common bile duct. The stone may consist of bile pigments or calcium and cholesterol salts Gallstone in the bile duct; Bile duct stone; Bile calculus; Biliary calculus

Causes, incidence, and risk factors 1. History of gallstone 2. Client who had their gallbladder removed Symptoms •

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Abdominal pain in the right upper or middle upper abdomen that may: o Come and go o Be sharp, cramping, or dull o Spread to the back or below the right shoulder blade o Get worse after eating fatty or greasy foods o Occurs within minutes of a meal Fever Loss of appetite Jaundice (yellowing of skin and whites of eyes) Nausea Vomiting

Signs and tests Abdominal CT scan Abdominal ultrasound Endoscope retrograde cholangiography (ERCP) Endoscopic ultrasound Magnetic resonance cholangiopancreatography (MRCP) Percutaneous transhepatic cholangiogram (PTCA Bilirubin Liver function tests Pancreatic enzymes Treatment • Surgery to remove the gallbladder and stones • ERCP and a procedure called a sphincterotomy, which makes a surgical cut into the muscle in the common bile duct • • • • • • • • •

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Complications • • •

Biliary cirrhosis Cholangitis Pancreatitis

CHOLECYSTITIS -

Inflammation of the GB that may be acute or chronic Acute inflammation is associated with gallstones Chronic cholecystitis – results when inefficient bile emptying and GB wall disease cause a fibrotic and contracted GB Acalculus cholecystitis – occurs in the absence of gallstones and is related to bacterial invasion via the lymphatic or vascular systems

Assessments 1. Nausea, vomiting, indigestion, belching, flatulence 2. Epigastric pain that radiates to the scapula 2 to 4 hours after eating fatty foods and may persist for 4 to 6 hours 3. Pain localized in RUQ 4. Guarding, rigidity, and rebound tenderness 5. Mass palpated in the RUQ 6. Murphy’s sign (cannot take a deep breath when the examiner’s finger’s are pressed below the hepatic margin) 7. Fever, tachycardia 8. Signs of dehydration Biliary Obstruction 1. Jaundice 2. Dark orange and foamy urine 3. Steatorrhea and clay-colored feces 4. Pruritus Interventions 1. 2. 3. 4.

NPO during nausea and vomiting Maintain nasogastric decompression as prescribed for severe vomiting Administer antiemetics for nausea and vomiting Analgesics as prescribed to relieve pain and reduce spasm Alert: Morphine sulphate and codeine sulphate o Avoided because they can cause spasm in the Sphincter of Oddi and increase the pain

5. Antispasmodics (anticholinergics) to relax smooth muscles 6. Instruct to eat low fat meal in small amounts 7. Avoid gas-forming foods PANCREATITIS -

Acute or chronic inflammation of the pancreas with associated escape of pancreatic enzymes into surrounding tissue Autodigestion of the pancreas

Precipitating Factors 1. 2. 3. 4. 5. 6. 7.

Trauma Alcohol abuse Biliary tract disease Viral or bacterial disease Hyperlipidemia, hypercalcemia, cholelithiasis, hyperparathyroidism Ischemic vascular disease Peptic ulcer disease

ACUTE PANCREATITIS Assessment o Abdominal pain – sudden onset ; midepigastric or L upper quadrant with radiation to the back o Pain is aggravated by a fatty meal, alcohol or lying in a recumbent position o Abdominal tenderness and guarding, nausea, vomiting, weight loss o Cullen’s sign – discoloration of the abdomen and periumbilical area o Turner’s sign – bluish discoloration of the flank o Absent or decreased bowel sounds o Elevated WBC, glucose, bilirubin, ALP, urinary amylase o Increased serum amylase and lipase, decreased serum calcium, elevated bilirubin Interventions o NPO, hydration with IVF o TPN for severe nutritional depletion o Supplemental preparations and vitamins and minerals to increase caloric intake if prescribed o Maintain NGT to decrease gastric distention and suppress pancreatic secretion o Administer meperidine hydrochloride (Demerol) as prescribed for pain – does not cause spasm of the sphincter of Oddi o Antacids to neutralize gastric secretions; H2 receptor antagonists  decrease HCL secretion and prevent activation of pancreatic enzymes o Anticholinergics to decrease vagal stimulation, GI motility and inhibit pancreatic enzyme secretion o Instruct to avoid alcohol o Advise to see AP if acute abdominal pain, jaundice, clay-colored stools, or dark urine develops o Low-fat bland diet and small frequent meals CHRONIC PANCREATITIS Assessment

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Abdominal pain, LUQ mass Steatorrhea and foul-smelling stools Weight loss, muscle wasting, jaundice s/s of diabetes mellitus

Interventions o Diet: limit fat and protein intake o Avoid heavy meals, avoid alcohol o Provide supplemental preparations and vitamins and minerals to increase caloric intake o Administer pancreatic enzymes as prescribed to aid in the digestion and absorption of fat and protein o Administer insulin or oral hypoglycaemic medications as prescribed to control DM