Pancreas: Acute Pancreatitis

Ø Pancreas

- fish-shaped organ extending from duodenal curve to the spleen

- both an endocrine and exocrine gland

- pancreatic cells - empty into duodenum at the hepatopancreatic papilla; secrete enzymes which digest fats, carbohydrates and proteins

- alpha cells secrete glucagon to promote liver glycogenolysis and gluconeogenesis which ultimately increases blood glucose level

- beta cells secrete insulin

Acute Pancreatitis

- Inflammation of the pancreatic tissue due to premature activation of the pancreatic digestive enzymes

- Auto digestion

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- Etiology:

- Alcoholism

- Hyperlipidemia

- Biliary tract disease or obstruction

- Trauma

- Infection

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- Injuries to the pancreas causes abnormal activation of the proteolytic enzymes: trypsin, chemotrypsin, elastase

- Destruction of tissues in and around the pancreas – autodigestion

- Damage tissues could lead to perforation and abscess

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- Clinical Manifestation

- Pain unrelenting and sometimes vague; may radiate to chest and back

- Jaundice

- Wt loss

- low grade fever anorexia

- Steatorrhea and dark urine

- Grey Turner’s sign- dicoloration of the flank

- Cullen’s sign – discoloration in the umbilicus area

- Pleural effusion

- Peritonitis

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- Diagnostics

- Upper GI series shows delayed in gastric emptying and enlarged duodenum due to edema of the head of the pancreas

- Endoscopic cholangiopancreatography can confirm pancreatits

- CT scan may show tumors and abcess

- Elevated AST,ALT, Bilirubin, lactate dehydrogenase, glucose levels, WBC

- Decrease protein, potassium, calcium

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- Management

- Analgesics

- Anticholinergic

- Insulin

- Prophylactic antibiotics

- H2 antagonist to decrease HCl thus decrease pancreatic enzymes

- IV fluids

- NGT lavage

- Biliary drainage

- Nursing interventions

- manage pain

- monitor breathing patterns disturbances

- monitor nutritional status

- oral care when NPO

- if eating is allowed, diet high in proteins and carbohydrates and low in fat

- monitor fluid and electrolyte balances

- monitor vital signs

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Cholelithiasis

• Cholelithiasis

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- Formation or presence of stone in the gallbladder

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- Risk factor: 4 F (female, fat, forty, fertile)

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- Types of gallstones:

- Cholesterol stones – 50% cholesterol by wt

- Pigment stones – bile pigments often caused by stasis of bile

- - Clinical Manifestations

- Intolerance to fatty foods

- Nausea and vomiting

- Pain in right upper quadrant

- Positive Murphy’s sign

- Low grade fever

- Steatorrhea

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- Diagnostics:

- Cholecystogram, CT scan, Ultrasound

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- Elevated unconjugated bilirubin, WBC, Amylase, lipase

- Management

- Analgesics (demerol)

- Antiemetics

- Oral dissolution therapy- ursodeoxycholic acid

- Surgery:

- Extracorporeal Shockwave lithotrypsy

- Laparoscopic laser cholecystectomy

- Abdominal cholecystectomy

- Percutaneous cholecystolithotomy

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Nursing Interventions:

- Same as cholecystitis

Gallbladder: Cholecystitis

Ø Gallbladder

- A sac like organ approximately 7-10 cm long

- The left and right hepatic ducts transport bile to the gallbladder

- Acts as a reservoir of bile max of 40-70ml

- Concentrates bile by absorbing salts and water

- Responds to ingestion of fats by releasing bile to duodenum through sphincter of Oddi

- If surgically removed, biliary ducts enlarged and takes over its function but cannot consistently respond to ingestion of fatty foods

v

• Cholecystitis

- Inflammation of the gallbladder

- Can be acute or chronic

- Affects more in women than in men 3:1 ratio

- Risk factors:

- Gallstones

- Surgery

- Trauma

- Obesity

- Long term dietary fasting

- Infection

- Clinical Manifestation

- Acute:

- Abdominal pain

- Nausea and vomiting

- High fever

- Positive Murphy’s sign

- Flatulence and belching

- Vague non specific abdominal pain

- Chronic:

- Low grade fever

- Jaundice

- Steatorrhea

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- Diagnostics

- Ultrasound

- Imaging – CT scan

- Blood studies – elevated AST, WBC, serum bilirubin, alkaline phosphatase, lactete dehydrogenase

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- Management

- Anti cholinergic (prophantheline bromide) to relax smooth muscles and prevent biliary contraction

- Narcotics (meperidine) releive pain and decrease spasm

- Antiemetics

- Oral gallstone dissolving drugs ( chenodeoxycholic acid) if cause is gallstone

- Surgery

- Cholecystectomy

- T- tube insertion

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- Nursing Management

- Low fat diet- broil or grill food instead of frying

- Weight reduction

- Monitor serum levels and signs of peritonitis

- Monitor I/O, electrolytes, V/S

- Wound care after surgery: instruct client to report sings of inflammation, avoidance of heavy lifting, avoid driving for at least 6 weeks to prevent strain on wound

- Care of T –tube:

- Keep tube below site of wound

- Change dressing at least daily

- Empty T-tube drainage bag at same time of the day

- Attach T-tube on clothing or abdomen to prevent pulling

- Inform pt that drainage is 300- 500 ml for 1^st 24 hrs, 200 ml after 3-4 days

Esophageal Varices

Esophageal Varices

- dilated and tortuous vessels of in the esophagus

- Risk Factor

§ Irritation from gastric acid

§ Vomiting

- Etiology: increase pressure in the portal venous system

- Clinical Manifestations

§ Hematemesis

§ Melena

§ Ascites

§ Jaundice

§ Abdominal vein distention

§ Hemorrhoids

- Diagnostics

§ Guaiac test

§ Ultrasound

§ Endoscopy

- Management

§ Vasopressin to induce vasoconstriction and prevent hemorrhage

§ Nitroglycerine for vasodilation in the peripheries to reduce pressure

§ Beta blockers

§ IV fluids

§ Oxygen

§ Sclerotherapy

§ Endoscopic variceal ligation

§ Balloon Tamponade

· Sengstaken-Blakemore tube – triple lumen tube with ports for inflation of esophageal balloon, inflation of gastric balloon and aspiration of gastric contents

· Minnesota Tube – same as above but with another lumen for aspiration of the esophageal contents

· Linton Tube – single lumen tube with only two ports

- Nursing Intervention

§ Client is on NPO

§ Monitor Hgb and Hct

§ Monitor VS and urine output

§ Monitor level of consciousness

§ Assess for respiratory distress especially after insertion of balloon- if it occurs deflate balloon immediately

§ Keep scissors at bedside all times to cut immediately the balloon tube if respiratory distress occurs

§ Monitor amount of drainage

§ Watch out for signs of shock

Liver Cirrhosis

v Liver Cirrhosis

- Chronic, progressive disease characterized by inflammation, fibrosis, and degeneration of the liver cells

- Destroyed liver cells are replaced by scar tissues resulting to malfunction of liver

- Occurs more in men than women. Ages 40-60

- Types:

- Laenec’s cirrhosis – alcohol and malnuttrition

- Post necrotic – viral hepatitis

- Post billary obstruction- bile reflux

- Clinical manifestation

- Fatigue, anorexia, n&v, indigestion, weight loss, flatulence

- Hepatomegaly, pain in RUQ, hard nodular liver

- Increase abdominal girth:ascites,

- Changes in mood, alertness and mental ability

- Gynecomastia, decrease pubic hair in males

- Amenorrhea in females

- Jaundice

- Easy bruising and bleeding

- Muscle atrophy

- Anemia

- Asterixis – liver flap. Primary concern

- Hypercholesterolemia

- Palmar erythema

- Pruritus – deposition of bile salts in the skin

- Portal hypertesion resulting to esophageal varices

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- Caput medusa – dilated abdominal veins due to congestion of superficial vein shunting to umbilical area

- Diagnostics:

- AST, ALT, LDH, Bilirubin – increase

- Urobilirubin in the urine

- Prolonged PT

- Decrease serum albumin, fibrinogen, platelets

- Cholangiopancreatography reveals common bile duct obstruction

- Biopsy confirms cirrrhosis

- Ultrasound shows liver damage

- Management

- Potassium sparing diuretics

- Salt poor albumin to restore plasma volume

- Vitamin K to bring Prothrombin time close to normal

- Vitamin B complex

- Lactulose to decrease serum ammonia level and improve encephalopathy

- Propanolol to decrease portal pressure in cases of esophageal varices

- Antiemetics but cautious in usage for it requires liver for dtoxification

- Paracentesis for pt with ascites

- Leveen shunt for ascites

- Sengstaken- blakemore tube for esophageal verices

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- Nursing management:

- Encourage small frequent meal

- Low Na for ascites

- High calorie, low fat, low protein diet

- ADEK and folic acid supplements

- Prevent infection- use electronic razors

- Prevent bleeding and assess for esophageal varices

- Administer diuretics

- Measure abdominal girth daily

- Avoidance of alcohol

Liver: Hepatitis

Ø Liver

- Located at the upper right quadrant of the abdomen

- Stellate reticuloendothelial (Kupffer) cell – destroys worn out WBC and RBC, bacteria and other foreign matter

- Hepatocytes produce bile stored in the gallbladder

- Functions:

- Carbohydrate, lipid, protein metabolism

- Process drugs and hormones

- Excretion of bilirubin and bile salts

- Activation of Vit D

- Storage of ADEK, iron, copper

- Phagocytosis

• Hepatitis

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- Inflammation of the liver due to damage with hepatic cells degeneration and necrosis

- Caused by infection, hepatotxins like medications

- Viral hepatitis involves widespread inflammation of the liver and the most common cause of hepatitis

- 5 types of hepatitis virus are named: Hepatitis Virus A, B, C, D, and E

- Other types of hepatitis are alcoholic hepatitis and toxic non viral hepatitis

- Hepatitis A

- IP: 15-45 days

- Fecal- oral route

- Often occurs in crowded living conditions

- From contaminated foods

- Hepatitis B

- IP: 50-180 days

- Transmitted by blood and body fluids

- Often by contaminated needles

- Polygamous sexual contact

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- Hepatitis C

- IP: 7-50 days

- Transmission same as HBV

- 40 % of cases leads to chronic liver disease

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- Hepatitis D

- IP: 14-56 days

- Same as HBV

- Co infects people w/ HBV

- Commonly seen in drug abuser

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- Hepatitis E

- IP: 15-64 days

- Fecal oral route, usually water-borne

- Alcoholic hepatitis

- Caused by heavy alcohol ingestion

- Often leads to liver cirrhosis

- Toxic non viral hepatitis

- Exposure to hepatotoxic drugs paracetamol, aspirin, isoniazid, tetracycline

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- Clinical manifestations (divided into 3 stages)

- Pre-icteric stage

- Fatigue, malaise, anorexia, nausea and vomiting, constipation or diarrhea, abdominal discomfort, RUQ pain, weight loss, hepatomegaly

- Elevated AST, ALT, and bilirubin

- Icteric stage

- Jaundice, pruritus, fatigue, malaise, n&v, large tender liver

- Dark urine, light colored stools

- Post icteric stage

- Fatigue, decreasing jaundice, improved appetite

- Decreasing of hepatomegaly, stool and urine color return to normal

- Diagnostics

- Serum AST, ALT, bilirubin, blood glucose,

- Liver biopsy

- Ultrasound

- Specific diagnostics for Viral hepatitis

- Hepatitis A

- HAV on stool before onset of dse

- Presence of anti HAV(IgM) confirms dx in acute stage

- Anti HAV (IgG) indicates previous infection HAV and provides lifelong immunity

- Hepatitis B

- Hepatitis B surface antigen indicates acute infection

- Hepatitis B e antigen (HBVeAg) infection disappears before jaundice

- Antibody to HB surface antigen indicates immunity and HBV vaccination

- Hepatitis C

- HCV antigen and antibodies

- ELISA

- Hepatitis D

- HDV antibodies titer

- Hepatitis E

- Anti HEV

- Management: based on presenting signs and symptoms

- Dramamaine for severe nausea

- IVF to prevent dehydration

- Vit B complex

- Vit K

- Nursing intervention

- Small frequent meals of low Na, low fat, moderate to high protein, high CHO,

- Bed rest for 1-2 weeks gradually increasing activity as tolerated

- Skin care

- Abstain from alcohol

- Increase fluid intake

- Administer medications as ordered

- Give daily vitamins supplements