1. Stressors of the Gallbladder, Pancreas And Liver
GI Stressors II
McKevney 4/08, rev Borrero 11/09

2. Topics Choleycystitis Pancreatitis & Pancreatic Cancer Cirrhosis
Hepatitis
Liver Cancer
Liver Transplantation
NCLEX Time

3. Gallbladder Function- storage depot for bile
Cholecystitis- inflammation of the gallbladder wall, acute infection
Cholelithiasis- presence of gallstones
When food enters the duodenum, the gallbladder contracts and the sphicter of Oddi relaxes (valve in the common bile duct), allowing bile to enter the intestine.
Cholecystitis- inflammation of gallbladder usually develops in assoc. with gallstones. But can occur from bacterial invasion or biliary spasm. Jaundice, bile obstruction not common. Blockage of bile flow from GB
Gallbladder becomes fibrotic and contracted, which result in decreased motility and deficient absorption.
3x4” pear shaped hollow organ underside of liver
Cholelithiasis- over time the concentration of bile in the gallbladder may result in insoluble stones, especially if bile contains high amounts of cholesterol.
Result of abnormal metabolism of bile salts and cholesterol
Over 20 million americans have G.B. disease, many have surgery within 1 year of diagnosis. Female, Fat and Forty- many get gall bladder problems.
Cholesterol stones form and block drainage of bile from gallbladder, which causes spasm, GB becomes inflamed, edematous and distended. This congestion leads to changes in GB circulation which eventually causes necrosis. Bacterial growth also develops.

4. Cholecystitis:Pathophysiology
The most common cause is cholelithiasis; obstructing the cystic and or common bile ducts.
Can be acute or chronic
Bile is used for digestion of fats. It’s produced in the liver and stored in the gallbladder.
Acute- gallstones partially/completely obstruct CBD
Chronic Cholecystitis- results from inefficient emptying of bile by gallbladder and gallbladder muscle wall disease persists.
Chronic- may be caused by or lead to formation of gallstones (cholelithiasis)
The most common cause is cholelithiasis obstructing the cystic and or common bile ducts. (Bile flow from the gallbladder to the duodenumThe most common cause is cholelithiasis obstructing the cystic and or common bile ducts. (Bile flow from the gallbladder to the duodenum)

5. Gallbladder
Pancreatitis and Cholangitis (inflammation of common bile duct) can occur as complications of cholecystitis.
Pancreatitis and cholangitis result from backup of bile throughout biliary tract.
Bile obstruction leads to jaundice.
Nonsurgical management- diet and drug therapy.
Jaundice- yello discoloration of skin and mucus membranes and icterus= yellow discoloration of sclera can occur in clients with acute cholecystitis, but is most commonly seen in clients with chronic gallbladder inflammation .
Impeded or obstructed flow caused be edema of ducts or gallstones contributes to extrahepatic obstructive jaundice.
Jaundice in cholecystitis may also be caused by direct liver involvement. The inflammation of the liver’s bile channels or bile ducts may cause intrahepatic obstructive jaundice, resulting in an increase in circulating levels of bilirubin, the principal pigment of bile.
When the concentration of bilirubin in the blood increases to greater than 2mg/dl, jaundice occurs.
Excessive bile salts accumulate on the skin causing pruritis (itching) or a burning sensation.
In a person with obstructive jaundice, the normal flow of bile into duodenum is blocked. Bilirubin is unable to reach the large intestine, where it is converted to urobilinogen- which accounts for the normal brown color of stool, clay – colored feces results.
Water soluble bilirubin is normally excreted by kidneys in urine, when an excess in circulating bilirubin occurs, the urine becomes dark and foamy because of the kiney’s efforts to clear the bilirubin.
Chenodiol- blocks liver synthesis of cholesterol, decreases biliary cholesterol levels leading to gradual dissolving of floating cholesterol gallstones.

6. Risk Factors More common in females (Remember 4Fs) High-fat diets
Obesity (impaired fat metabolism, high cholesterol)
Genetic predisposition
Older than 60 years
Type 1 diabetes (high triglycerides)
Low-calorie, liquid protein diets
Rapid weight loss (increases cholesterol)
Trauma, Surgery, Immobilty
Pregnancy
HRT
Fat, fertile, Female,

7. Diagnostic Procedures
RUQ ultrasound
Abdominal x-ray- calcified gallstones
ERCP- Endoscopic Retrograde Cholangiopancreatography
Hepatobiliary scan (assesses patency of biliary duct system
Elevated WBC
Increase serum bilirubin levels
Increased LFTS; AST, ALT, Alkphos, LDH
Serum cholesterol elevated above 200 mg/dL
ultrasound visualizes gallbladder edema
Elevated WBC indicates inflammation
AST- aspartate aminotransferase (recheck labs)
ALT-
LDH- lactate dehydrogenase
ERCP- Endoscopic Retrograde Cholangio Pancreatopography.- Direct visualization of biliary tree via endoscope passed through sphicter of Oddi: CBD, pancreatic and hepatic ducts can be visualized. Stone retrieval also possible.

8. Nursing Assessment S/S of Acute Cholecystitis
Patient complains of sharp RUQ pain radiating to right shoulder
Intense pain after eating a high fat meal
Increased HR, pallor, diaphoresis
Rebound tenderness
Nausea, vomiting, anorexia
Dyspepsia, eructation, and flatulence
Fever, chills
Steatorrhea, light colored stools
Light colored bowel movements
Fat soluble vitamin deficiency
With obstructive jaundice, bilirubin can’t reach large intestines where it is converted to urobilinogen- which accounts for normal brown color of stool.
Water soluble bilirubin is normally excreted by kidneys as urine, when an excess of circulating bilirubin occurs, the urine becomes dark and foamy because of the kidney’s efforts to clear the bilirubin.
Familial tendency for cholelithiasis
Bile is needed for absorption of fats/fat soluble vitamins in intestines

9. Nursing Diagnoses Acute Cholecystitis
Acute pain
Impaired gas exchange
Risk for infection
Knowledge deficit

10. Cholecystitis
Diet therapy: NPO or modify diet by avoiding high fat or high volume meals. These measures decrease stimulation of gallbladder.
IV Hydration
Drug therapy:
Acute pain: opioids: meperidine HCL (Demerol), not Morphine Sulfate
Antispasmodics or anticholinergics: Atropine or dicyclomine (Bentyl)
Anti-emetics
Antispasmodics- relax smooth muscles preventing biliary contraction , minimizes sevretions and assists in reduction of apin. Antiemetics such as tigan are also ordered.
MSO4 causes biliary spasm and constrict the sphinctor of Oddi

11. Surgical Interventions
Open Choleycystectomy
Laproscopic Cholecystectomy
Laparoscopic- Ambulatory surgery, usual pre op tests and pt. NPO. Dr. make a 10mm midline puncture at the umbilicus. The abdominal cavity is insufflated with 3-4 L Co2 A trocar catheter is inserted, through which a laparoscope is infused.This is attached to a video camera. The surgeon makes3 small punctures through which to intoduce laparoscopic forceps to manipulate the gallbladder. A laser is used to dissect the gallbladder away from the liver bed and to close off the cystic artery and duct. The surgeon extracts the gallbladder through midline puncture site.
Traditional surgery- not used very often any more. Subcostal incision removes gallbladder, explores ducts and inserts a t-tubedrain to ensure patency of duct.

12. Nursing Interventions S/P Cholecystectomy
Lap vs.Open Cholecystecomy
LOC
Vital signs
Pulmonary Hygiene (cough deep breath, ambulate, turn and postion incentive spirometer)
Splinting to reduce pain
Pain management
Monitor wound incision /S/S of infection
Monitor T-tube drainage (initially bloody, then green-brown bile)
T-tube initially may drain >400ml/day then should gradually decrease
Advantages??

13. Care of the T-tube
Report sudden increases in drainage or amounts exceeding 1000ml/day
Keep drainage bag below level of GB
Inspect surrounding skin
Maintain flow by gravity
Never irrigate, clamp or aspirate without MD order
Clamp 1 to 2 hours ac and pc
Monitor and document the client’s response to food
Normal darinage is about 400ml pe r day
Assess drainage- serous to green bilious liquid by 2-3rd postop day, gradually decrease in amt
After several days of drainage, the tube may be clamped for an hour befora and after meals to deliver bile to the duodenum to aid in digestion
Change dsg QD

14. Nursing Interventions: Patient Education
Dietary counseling:
Low fat diet
Weight reduction
Fat-soluble vitamins and bile salts to enhance absorptions and aid digestion
Avoid gas-forming foods
Smaller more frequent meals
Activity precautions 4-6 weeks
Care of T-tube

15. Pancreatitis and Pancreatic Cancer

16. Function of Pancreas
Pancreas has both exocrine and endocrine functions
Exocrine: secretes pancreatic enzymes to break down starch, proteins, and fats
Endocrine function: Islet of Langerhans:
B cells secrete insulin and
A cells secrete glucagon
What’s the difference?
The pancreas is a long, slender gland lying behind the stomach and in front of the first and second lumbar vertebrae. It consists of the head, body and tail. The anterior surfaces covered by the peritoneum. The pancreas contains both lobes and lobules. The pancreatic duct extends along the gland and enters the duodenum through the common bile duct.
Exocrine- term applied to glands whose secretion reaches an epithelial surface either directly or through a duct. It is the exocrine function of the pancreas that contributes to the process of digestion.
Early activiation of these enzymes in the pancreas cause inflammation: lipase, trypsin, elastase. Amylase,
Endocrine glans secrete products into EC space and pass through membranes into blood eg. hormones
Exocrine glands-eg digestive enzymes,, sweat glands, sebaceous glands

17. Pathophysiology Pancreatitis is an autodigestion of the pancreas
Can result in inflammation, necrosis, and hemorrhage
Acute pancreatitis is an inflammation of the pancreas resulting from activated pancreatic enzymes autodigesting the pancreas
Severity varies but the overall mortality rate is 10% to 20% r/t hypotension, fluid/electrolyte imbalance, and shock
Chronic pancreatitis progressive destruction of the pancreas. Mortality rate up to 50%
Pancreatitis is an inflammatory process of pancreas, resulting in autodigestion of organ by its own enzymes. Ranges from mild to severe, severe form of pancreatitis is characterized by diffusely bleeding pancreatic tissue, fibrosis and death. Mortality is 10% due to hypotension, fluid/lyte imbalance and shock.
Lipolysis- fatty acids are released and combine with calcium and cause hypocalcemia.
Necrosis of blood vessels can occur- leads to generalized hemorrhaging, which can lead to shock and death.
Complications- Jaundice- occur from swelling of head of pancreas which impedes blood flow through common ile duct.
Transient hyperglycemia- from release of glucagon and decreased release of insulin from damage to islet cells.
Pleural effusion- enzymes from peritoneal cavity go to pleural cavity via lymph channels, atelectasis and pneumonia can occur.

18. Digestive enzymes for starch, protein, and fat Endocrine function:
What would you expect to see if the pancreas isn’t functioning properly??
Exocrine function:
Digestive enzymes for starch, protein, and fat
Endocrine function:
Insulin and glucagon
Transient hyperglycemia
Mid epigastric pain

19. Diagnostic Testing for Pancreatitis
Elevated serum amylase, lipase, elastase
Elevated trypsin
Elevated urine amylase
Elevated serum glucose
Serum calcium and magnesium levels are decreased
Serum liver enzymes and bilirubin levels are elevated- hepatobiliary involvement
WBC elevated
CT scan with contrast
Several theories explain the triggering mechanisms leading to enzyme release p.1404 Iggy
Rises in enzymes means pancreatic cell injury
Glu= pancreatic cell injury, CHO metabolism impaired, decreased insulin release

20. Nursing Assessment Monitor mental status
Monitor VS- Elevated T, P. R, decreased BP.
Dyspnea, or resp. complications
Sudden onset of severe pain
Epigastric pain radiating to back, left flank, or shoulder
Not relieved with vomiting
Some relief in fetal position
Abdominal tenderness, guarding, rigidity.
Palpable mass if cyst is present
Possible changes in behavior r/t ETOH withdrawal.
Pain may be relieved in fetal position, Worse when lying down or with eating
Pleural effusions, atelectasis, PN
Pain is intense and continuous. Pain is in mid-epigastrum. Frequently acute in onset(24 to 48 hrs. after heavy meal or alcohol ingestion.
May be more severe after meals and unrelieved by antacids. May be accompained by abd. Distension.
Pt. appears acutely ill. Board like abdo., soft without peritonitis
Ecchymosis in flank or around umbilicus, which may indicate severe hemorrhagic pancreatitis.
n/v, fever jaundice, mental confusion, agitation.
Hypotension related to hypovolemia and shock.
Acute renal failure common.
May develop tachycardia, cyanosis and cold, clammy skin.
Resp. distress and hypoxia.
Dyspnea, tachypnea, abnormal blood gas values. Diffuse pulmonary infiltrates.Hypocalcemia, hyperglycemia and DIC
Dx- based on history of abd. Pain, known risk factors and elevated serum lipase and amylase, most indicative.

21. Nursing Assessment Nausea and vomiting Weight loss
Signs and symptoms of inflammation or peritonitis
Ecchymosis on the flanks (Turner’s sign)
Bluish periumbilical discoloration (Cullen’s
sign)
Generalized jaundice
Paralytic ilieus
Hyperglycemia

22. Nursing Diagnoses Pain r/t Fluid volume deficit r/t
Altered nutrition r/t
Ineffective breathing pattern r/t

23. Pancreatitis Nursing Interventions
P- Pain: Morphine or Dilaudid
A- Antispasmodic drugs motility
N- NPO/NGT suction- pancreas to rest, TPN
C- Calcium, hypocalcemia, replace Ca
R- Replace F/E- NG losses and fluid shift
E- Endocrine & Enzymes
A- Antibiotics- with fever
S- Steroids- corticosteroids during acute attacks
C- Calcium- monitor levels and look for clinical signs, replace as needed.
R- Replace Fand E- NG losses plus- fluid shifts into peritoneum. TPN if NPO over 7-10 days 3.
Medications administered
Pancreatic enzymes: pancreatic and panrelipase take with meals for fat and protein digestion
Education: take ac or c meals, swallow wihout chewing to minimize oral irritation, mix powder forms in applesauce or fruit e in protein containing foods. Wipe lips to avoid skin irritation
Anticholinergics,glucagon,histamine inhibitors- all decreas vagal stimulation, decrease GI motility and inhibit pancreatic secretions
E- Endocrine- control of hyperglycemia- insulin, glucagon, calcitonin and somatastatin sometimes used.
Other interventions may include heparin, peritoneal dialysis to remove toxic substancesand peritoneal tap for fluid collection which impairs resp. dynamics no oral intake to inhibit pancreatic stimulation
Anticholinergics- atropine (Bentyl)
Vitamin supplements
Monitor blood glucose levels and administer insulin as needed
Monitor hydration levels orthostatic blood pressure,
I&O, lab values, weights
morphine sulfate is not used: can cause spasms in the pancreas(spincter of Oddi)

24. Pancreatitis Nursing Interventions
Monitor for hypocalcemia:
Tetany
Trousseau’s sign (hand spasm when BP cuff is inflated)
Chvostek’s sign (facial twitching when facial nerve is tapped)
Tetany: A combination of signs and symptoms, due usually to low calcium, that can include:

25. Complications of Pancreatitis
Pancreatic Infection: Pseudocyst or Abscess
Type 1 diabetes
Left lung effusion and atelectasis
DIC- Monitor bleeding times
Acute Renal Failure
ARDS- Shock
Paralytic Ileus
** Pulmonary failure accounts for more than 50% of the deaths that occur within the first 7 days of the disease
ARDS, pulmonary failure accounts for half of all deaths within 7 days of disease.
DIC- hypercoagulation of blod, development of microthrombi.
Shock- peripheral vasodialtion, from vasoactive substances.
Acute renal failure- in response to hypovolemia.
Paralytic ileus- from release of pancreatic enzymes into abdominal cavity.

26. Chronic Pancreatitis Types: 1.Chronic Calcifying Pancreatitis (CCP)
2.Chronic Obstructive Pancreatitis- develops from inflammation, spasm and obstruction of sphincter of Oddi.
The primary cause of chronic pancreatitis in the older adult is chronic alcoholism
Age related changes reduce the older person’s ability to process alcohol
Psychosocial interventions?
Progressive, destructive disease, remissions and exacerbations
Goals: relief of pain, prevention of recurrence of attacks, prevention of complications and nutritional support
S&S , TX similar to acute with inclusion of pancreatic enzymes replacemnet
Risk factor for pancreatic cancer
Chronic- progressive, destructive disease of pancreas, characterized by remission and exacerbations (recurrence). This may develop after repeated episodes of alcohol induced pancreatitis.
CCP alcohol induced- protein precipitates and plug ducts and leads to obstruction, cell replacement and ulceration.
Pathophysiologic changes- loss exocrine function decreased secretion of aqueous bicarb and enzymes.
Aqueous component- neutralizes duodenal contents and pancreatic enzymes that are essential to normal digestion and absorption.
When pancreatic enzyme secretion is reduced more than 8%, malabsorption of fats occurs- steatorrhea, pale, bulky, frothy, stools with an offensive odor.
This malabsorption of fats also leads to wt. loss, muscle wasting and general debilitation.
Loss of endocrine function- diabetes.
Pulmonary complications- effusion and infiltrates. ARDS may develop.
Loss of exocrine function

27. Pancreatic Cancer Vague symptoms
Usually diagnosed in late stages after liver or gallbladder problems
Cause is unknown
Occurs years of age
Risk factors
30k case/year= to # die yearly
<20% survive longer that 1 year
<5% survive for 5 years because occult malignancy, hidden

28. Diagnostic Procedures
Serum amylase and lipase elevated
Serum alkaline phosphate and bilirubin levels elevated
CEA (Carcinoembryonic antigen elevated) CT
ERCP: Most definitive test, analysis of aspirate, placement of a drain or stent for biliary drainage
Abdominal paracentesis: Test for malignant cells
Nursing interventions for paracentesis; consent, specimen to lab, assess/monitor insertion site

29. Nursing Assessment Pancreatic Cancer
Monitor vital signs
Monitor for signs of biliary obstruction (Jaundice-late sign, clay colored stools and dark urine-earlier sign)
Nursing Diagnoses…..
Chemotherapy: Monitor for myelosuppression and pancytopenia
Radiation: Monitor fatigue and diarrhea
Anorexia and weight loss
Prep for possible surgery
The liver releases bile salts into the stool, giving it a normal brown color. You may have clay-colored stools if you have a liver infection or if the flow of bile out of the liver is blocked.
Yellow skin (jaundice) often accompanies clay-colored stools.
NSG DX- Acute Pain
Imbalance Nutrition: Less than body requirements

30. Surgical Procedures Whipple procedure:
Removal of the head of the pancreas, duodenum, parts of the jejunum and stomach, gallbladder, and possibly the spleen
The pancreatic duct is connected to the common bile duct and the stomach is connected to the jejunum
Post-op care
Extensive procedure- radical pancreaticoduodectomyPrevent complications: CV, Pulm, GI wound, Metabolic (Unstable DM, Renal failure)

31. Postoperative Care Whipple Surgery
LOC
Vital signs
Respiratory status: Incentive spirometer, O2
IVF
Pain Management : PCA Opioids
Monitor NG -tube
Surgical drainage: Protect the surgical sites
Semi-fowlers: facilitate lung expansion and to decrease stress on the suture line
Monitor glucose levels and administer insulin prn
Provide nutritional support
Standard post-op care for GI surgery
facilitate lung expansion and to decrease stress on the suture line

32. Complications Whipple Procedure
1.Fistulas
Due to breakdown of a site of anastomosis
2.Peritonitis
Internal leakage of corrosive pancreatic fluid
Elevated WBCs, fever, abdominal pain, rebound tenderness, alteration in bowel sounds, shoulder pain
Administer antibiotics
3. Venous thromboembolism: most common complication of pancreatic cancer
Monitor pulses and for areas of warmth and tenderness
Administer anticoagulants
Venous compression

33. LIVER DISORDERS HEPATITIS CIRRHOSIS OF THE LIVER LIVER CANCER
TRANSPLANTATION

34. Functions of the Liver 1.Bile production: essential for fat metabolism
2.Protein metabolism: Breaks down amino acids ammonia urea excreted via kidneys
3.Phagocyte system: removes toxins and breaks down old RBCs
Kupffer cells remove bacteria and toxins
Liver is a very large and vascular organ The portal circulatory system bringd blood to the liver from the stomsch. Intestines, spleen and pancreas

35. Functions of the Liver 4.Synthesizes albumin
5.CHO Metabolism: storage of glycogen
6.Storage of fat soluble vitamins A,D,E,K
7.Steroid and drug metabolism
8.Clotting: prothrombin and fibrinogen
Vit K can’t be absorbed due to decrease synthesis of bile fats in the liver. Without Vit K, clotting factors 2,7,9, and 10 are not produced in sufficient quantities, bleeding and bruising occurs.
Many drugs are metabolized by liver: barbs, opioids, sedatives, amphetamines
Liver dysfunction- What symptoms would you expect to see?
What symptoms would you expect to see?
Clotting factors
Infection
Swelling: decreased albumin levels
Vitamin deficits
Digestive problems
Unable to rid body of toxins
Blood flow problems/portal vein
Increased bilirubin

36. Lab Findings in Liver Disease
Elevated AST(aspartase
aminotransferase)
Elevated ALT (alanine aminotransferase)
Elevated LDH (lactate dehydrogenase) and ALP (alkaline phosphatase)
Elevated serum bilirubin
Increased total serum protein-acute
Decreased total serum protein- chronic
Decreased serum albumin (normal 3-5 g/dl)
Prolonged PT/INR
Elevated serum ammonia
INR>2

37. Liver Lab Results LAB TESTS NORMAL RESULTS LIVER DISEASE AST 5-40 u/L
ALT
8-20 u/L
LDH
units/L
Alkaline Phosphatase
u/L
Bilirubin
mg/dl
Total Protein
g/dl
Normal
Ammonia
15-45 mg/dl PT
seconds
Prolonged
INR
Albumin
3-5 g/dl 

38. Viral Hepatitis-Facts
Acute (short- term)-inflammation of the liver
Chronic (long- term) debilitating with increasing severity of symptoms
Each year 250,000 in US become infected
Persons with hepatitis are carriers and can spread disease without showing any symptoms of the disease
Never donate blood, body organs or tissues
Hepatitis B vaccine for all health care workers
Mandated that all cases of hepatitis are reported to the health department
Hepatitis A vaccine for high risk population
Several types- all Inflammation of the liver

39. High Risk Behaviors HBV, HCV
Failure to follow Universal/Standard Precautions
Dirty needles, sharp instruments, body piercing, tattooing, sharing drug paraphernalia and personal hygiene tools
Unprotected sex, multiple sex partners and/or anal sex
Unscreened blood transfusions (before 1992)
Hemodialysis
Poor hand hygiene with food preparation by a person infected with hepatitis
Traveling in underdeveloped countries and using tap water
Living in crowded environments: prisons, dormatories, universities, long-term care facilities, military housing
Chronic HCV or chronic HBV leading cause of ESLD and most common and leading reason for transplantation in US

40. Type Route of Transmission Risk Factors HAV Oral-fecal route
Ingestion of contaminated food
(shellfish) or water
HBV
Blood
Drug abuse
Sexual contact
Healthcare work
HCV
HDV
Co-infection with HBV
HEV
Contaminated water
A- GI distress, flu like Run its course
B Anorexia, NV, Fever, fatigue, RUQ pain, Dk urine, light stool, joint pain, jaundice
C Asymtomatic for yrs until blod test is done or liver impairment signs appear, similar to B
D Often asymptomatic, coinfects with HBV, trnasmitted parenterally
E Resembles A
Chronic hep- inflammation longer than 6mos. Usually occurs with B or C. Liver bx for dx. Increases risk for liver Ca

41. Diagnostic testing
Serological markers: Identify presence of virus. +HBsAg for longer than six months indicates chronic hepatitis and/or hepatitis carrier status
Clotting factors
Hepatitis antibody serum test: Indicates immunity and effectiveness of vaccine ( + HBsAb)
X-rays : hepatomegaly, ascites, spleen enlargement
Liver biopsy: Most definitive test that identifies the degree of liver damage
Nursing: consent, explain procedure, have patient lie on affected surgical side for short period of time after biopsy)
HBsAg- Considered infectious as long as present in blood
HBsAb- shows recovery and immunity to hepatitis B (after immunization)
Liver bx- done in ASU percutaneously if no clotting issues.

42. Nursing Assessment Hepatitis
Monitor for signs and symptoms:
Flu-like symptoms and RUQ abdominal pain, N&V
HBV presents with hepatomegaly and possible obstruction
Signs of obstruction: light colored stools, dark urine, jaundice, elevated bilirubin and liver enzymes
Flu-like symptoms (headache, fatigue, low grade fever, RUQ abdominal pain, nausea and vomiting

43. Nursing Assessment Hepatitis
Assess skin color and sclera
Pain in muscles joints and abdomen
Fever, malaise, increased fatigue, nausea and vomiting
Clay colored stools
Dark urine
Rashes, pruritis

44. Hepatitis A
Mild course, spread fecal-oral route Sources: Contaminated water Shellfish from contaminated water Infected food handlers Oral/anal sex Incubation: days Symptoms:
Most common type
Hepatitis A vaccine recommended for hi risk pts: travel abroad, health care workers, food handlers where HAV is high. Ig is given immediately after exposure
Lifetime immunity with 2 doses.
Most HAV is killed by disinfectants
S&S mild, flu like URI, LGT
Anorexia
Symptoms clear, but pt may have residual liver damage. Symptoms may subside in 3-7 days

45. Hepatitis B
HBV spread by percutaneous/permucosal route by contamination with blood or serous fluid.
Incubation days
Sources: sexual contact,sharing needles, tattooing, body piercing, accupuncture, perinatal
Symptoms:
Nurses and other health care workers vaccinated
Infants vaccinated
Can’t give blood until 1 year p tattoing, piercing
Symptoms: similar to other viral syndromes, malaise, nausea, abdominal discomfort, icterus, dark urine, enlarged tender liver, possible jaundice
Can progress to fulminant- mortality 80%

46. Hepatitis- Other Causes
Direct toxic hepatitis- alcohol abuse, tylenol toxicity, industrial toxins
Idiosyncratic toxic hepatitis- may occur during or shortly after exposure to drug
Eg. Halothane, Methyldopa, Isoniazid
Toxic hep- results in necrosis and fatty infiltration of liver. Industrial toxins ( carbon tetrachloride) have a direct toxic effect on liver
Idiosncratic- produces changes similar to thiose found in viral hepatitis
Complication- necrosis

47. Nursing Interventions
Medications: Used sparingly to promote hepatic rest
Antivirals- Lamivudine (Epivir HBV)
Interferon for HBV and HCV
Assess for side effects of interferon:
Flu-like symptoms
Alopecia
Bone marrow suppression
Monitor CBC
Administer antiemetics
Provide comfort measures
Immunomodulating drug
Blocks virus from replicating, renal toxicity
Antiemetics- tigan and dramaimine ok, compazine not.
Check all meds for liver toxicity
Antivirals- SE myopathy, muscle weakness and aching

48. Nursing Interventions
Contact Precautions Hepatitis A,E
Universal/Standard Precautions for HBV,HCV ,HDV
Limit activity: bedrest, initially to promote hepatic healing
Patient Education
Dietary Education: High carbohydrate, high calorie, low-moderate fat, low-moderate protein WHY?
Teach good personal hygiene, safe practices for preparing and dispensing foods
Mandatory reporting of viral hepatitis to health dept
Goal- patient will gradually increase activity to prior level
Rest promotes healing of liver
Void fatty or fried foods- increases nausea
Small frequent meals to promote nutrition and healing
Meds used sparingly for hepatic rest and regeneration of tissue
Disease transmission and exposure and transmission
Hepatitis vaccine
Universal/Standard Precautions
Needleless systems
Handwashing!
Traveling: drink bottled water in underdeveloped countriesNo alcohol, no OTC meds for 3-12mos
Avoid sex until antibody testing results are negative
Hep A- do not prepare food for others
Supplemental vitamins

49. Complications
Chronic hepatitis B, C, D: increases risk for liver cancer
Fulminating Hepatitis: Fatal. Liver cells cannot regenerate and progressive liver necrosis occurs. Hepatic encephalopathy and death occur
Cirrhosis of the liver: Scarring causes injury to the liver
Liver failure
Liver Cancer
If liver cells fail to regenerate, progresses to necrotic process, results in severe, frequently fatal form, fulminant hep. Hepatic encephalopathy, death

50. Cirrhosis of the Liver
Extensive scarring of the liver caused by necrotic injury or a chronic reaction to inflammation over a prolonged period of time
Risk Factors
4 Types- Laennec’s, Postnecrotic, Biliary, Cardiac
Cirrhosis- chronic progressive liver condition..Destruction of hepatocyte In the end stages, it is essentially an irreversible reaction to hepatic inflammation and necrosis
RF- alcohol, direst toxic effect on liver cells. Autoimmune hepatitis, Steatohepatitis, (fat/chol deposits in liver). Drugs and toxins, Biliary disease, CV disease
Episodes of chronic hepatitis will do permanent injury and scarring to the liver and RF for liver Ca.
Can be life-threatening but can be controlled if discovered early
Laennac’s- most common type, caused by longterm alcohol use. The liver becomes enlarged, firm in early disease, smaller and nodular in end stage disease.
Postnecrotic- caused by massive hepatic cell necrosis, usually from acugte viral hepatitis
Biliary - caused by chronic biliary obstruction, bile stasis and infla,,ation. The liver becomes fibrotic.
Cardiac- caused by severe or chronic HF. The liver becomes enlarged and congested with venous blood, resulting in cell necrosis from anoxia.
Without transplant, usually fatal

51. Diagnostic Procedures
Liver biopsy
EGD: Esphagastroduodenoscopy: detect esophageal varices
LABS to be monitored??
WHY??
Serum liver enzymes
Serum bilirubin
Serum albumin
CBC, WBC, Platelets: all decreased due to anemia
PT/INR
Ammonia levels (normal 5-110mg/dL) rise when cirrhosis prevents the conversion of ammonia to urea for excretion
Creatinine levels (normal 0.6 to 1.2mg/dL may increase
Liver Biospy (Most definitive) identifies the extent of cirrhosis
EGD: Esphagastroduodenoscopy: detect esophageal varices
Decreased absorption of fat soluble vitamins- K, No factor II, VII, IX X

52. Nursing Assessment Cirrhosis of the Liver
Monitor vital signs
LOC-Neuro
Pulmonary GI
Integumentary GU
Coagulation defects
Fetor hepaticus-liver breath-end stage
Inability of liver to synthesize albumin
Fruity, musty odor caused by damaged liver
Generalized weakness, weight loss
Resp- dyspnea, hyperventilation, hypoxemai
GI- loss of appetite, clay colored stools, abd pain, ascites. RUQ mass, tenderness

53. Nursing Assessment Petechiae red pinpoint and red-purple lesions,
Ecchymosis, nose bleeds, hematemesis
Spider angiomas red spider -like lesions of face, upper thorax, and shoulders
Dependent peripheral edema of extremities and sacrum
Asterixis- tremors liver flapping tremor of the wrist and fingers
Complications of portal hypertension
Asterixis- Low Ca

54. Management of Cirrhosis
Non-surgical Diet- low Na, low protein, moderate fat restriction, high carb, high calories, vitamins TPN often necessary Meds-Aldactone, Lactulose, Neomycin, antacids Paracentesis Esophagogastric balloon tamponade Injection sclerotherapy STOP alcohol Surgical Peritovenous shunt or LaVeen shunt Endoscopic band ligation
Non surgical- to control ascites Limit protein(500mg-2G) to keep ammonia levels low. Ammonia is a byproduct of protein metabolism Fluid restriction-1L-1500mL/day
Aldactone- K sparing diuretic, reduces ascites and decreases aldosterone levels
Monitor EKG, lytes, I&O, K levels, bradycardia, muscle twitching. Assess for hyponatremia: confusion, lethargy and apprehension
Lactulose (Cehulac)-promotes excretion of ammonia in stool and lowers pH. Lower pH converts ammonia to ammonium ion, non absorbable that is excreted in feces. Lactulose also pulls water into the bowel lumen, increasing the number of daily stools. Maintain stool chart, F&E. Goal- 2-4 soft stools per day
Neomycin- ant infective- reduces intestinal bacteria, decreases ammonia production. Nephrotoxic, ototoxic and neurotoxic
Neomycin-broad spectrum AB, intestinal antiseptic, destroys normal flora, diminishes protein breakdown and decreases rate of ammonia breakdown
Paracentesis- inserion of trocar catheter into abd at bedside to remove ascitic fluid from peritoneal cavity
Blakemore Tube:- for bleeding esophageal varices. Balloon is inflated and stops bleeding. Pitressin a vosoconstrictor may be ordered to stop bleeding
Injection sclerotherapy- via endoscope, a sclerosing agent may be injected to stop bleeding.
Shunt- drains ascites through a one way valve into a tube that terminates in the SVC. Pt loses weight, decrease in abd girth, and have increased urine output. .

55. Complications of Cirrhosis
Portal Hypertension
Ascites
Bleeding esophageal varices
Coagulation defect
Jaundice
Hepatic encephalopathy
Hepatorenal syndrome
1, Portal HTN- Increase in pressure in portal vein. Blood flows back into spleen, causing splenomegaly, ascites, esophageal varices, prominent abd veins and hemorrhoids
2. Accumulation of free fluid containing almost pure plasma in the abd
3. Bleeding varices- blood backs up into esophageal and gastric vessels. These vessels are fragile, thin walled and will blees
4.Coag defect- due to cirrhosis, dec in synthesis of bile fats in liver, preventing absorpion of fat soluble Vit K.. Pt susceptible to bruising and bleeding
5. Jaundice- Liver cannot metabolize bilirubin
6. Hepatic encephalopathy- Altered LOC, impaired thinking and neuromuscular disturbances. A/R/O impaired ammonia metabolism. Liver can’t convert ammonia to urea.. 5 stages- from prodromal (subltle changes) to coma.
7.Hepatorenal- Primary cause of death in end stage cirrhosis. Manifested by sudden decrease in urine flow, elevated BUN and creat. Impaired urine osmolarity.. Progressive oliguria and renal failure
Monitor LOC, Level of orientation, Recent memory
Monitor F/E
Monitor bleeding Chart 62-2Normal Ammonia mg/dL
Sleepdisturbance, mood disturbances, mental status changes, speech problems- early
Acute and reversbible in early stages
Late- ALC, impaired thinking, neuromuscular problems

56. Bleeding esophageal varices
Hematemesis and melena
Dx: endoscopy, CT, ultrasound, barium swallow, LFTs
Tx: O2, IVF, Blood transfusions, I&O, Balloon tamponade, saline lavage, endoscopic tamponade, vasopressin (Pitressin)
One of the major causes of death in pts with cirrhosis.
Esophageal varices are dilated, toruous veins ususally found in submucosa of the lower esophagus. 2nd to portal hypertension.

57. Nursing Diagnoses Altered mental status Ineffective breathing pattern
Excess fluid volume
Risk for impaired skin integrity
Risk for infection
Chronic pain
Risk for imbalanced nutrition

58. Portal Hypertension
Portal hypertension results from the abnormal blood flow pattern in liver created by cirrhosis. The increased pressure is transmitted to collateral venous channels. Sometimes these venous collaterals are dilated. Seen here is "caput medusae" which consists of dilated veins seen on the abdomen of a patient with cirrhosis of the liver.
library.med.utah.edu/WebPath/LIVEHTML/LIVER061.html

59. Treatment for Cirrhosis of Liver
Injection sclerotherapy: varices are sclerosed
TIPS: Transjugular intrahepatic portosystemic shunt – placement of a portal shunt for esophageal varices
Surgical bypass shunting procedures:
Last resort: Ascites is shunted from the abdominal cavity to the superior vena cava
Liver Transplantation

60. Hepatic Encephalopathy and Coma
Early symptoms- minor mental changes and motor disturbances
Progression to changes in LOC, difficult to arouse, asterixis
Hyperactive reflexes then flaccid
Progression to seizures and coma
Encephalopathy is a complication of liver disease, occurs with liver failure and may result from the accumulation of ammonia and other toxic metabolites in blood
Coma represents most severe stage of encephalopathy. Ammonia accumulates because liver cannot convert to urea
Early symptoms: unkempt, altered sleep patterns, sleep during day, awake at night.
Asterixis-flapping tremor of hands
Tx- lactulose, decrease protein intake, enemas, IVF, vitamins, O2. Monitor ammonia levels

61. Hepatic Coma Jaundice Profound anorexia Coagulation defects
Renal failure
Electrolyte disturbances
Hypoglycemia
Infection
Encephalopathy
Tx: Liver transplant, blood products, corticosteroids

62. Concept Map: Impaired Liver Function
Ineffective breathing pattern
Body Image Disturbance
Activity Intolerance
Excess fluid volume
Imbalanced Nutrition, Less than Body Requirements
Risk for injury
Impaired Skin Integrity
Nursing Diagnoses
Observe for potential bleeding complications
Labs
Monitor PT/INR PTTDiet: Low Na, Low fat, Low protein
Small frequent meals
Supplemental vitamin enriched drinks
Replace vitamins: liver unable to store
If serum Na is low, patient will be put on a fluid restriction
Medications are administered sparingly: liver toxicity
Diurectics: monitor for hypokalemia and hypotention
H2 receptor antagonist: stress ulcer
Lactulose- promote excretion of ammonia via stool
Neomycin and metronidazole (Flagyl) removes intestinal bacteria which produces ammonia
Platelets
Injury- Assess LOC, cognitive level, orientation. Monitor restlessness and agitation. Obtain and record sample of handwriting.. Assess neuro signs, DTRs and ability to follow directions.
Provide safe environment, prevent falls.. Stimulate and orient pt. frequently, avoid restraints. Monitor meds- esp hypnoticss, sedatives and analgesics. Monitor ammonia levels
2. Body Image- encourage pt to verbalize reactions and feeling re changes. Assess coping strategies. Encourage and assist pt in making decisions about his care. ID resources to help pt: clergy, counselor
3. GI Bleeding- Monitor VS, LOC, stool and emesis for occult or frank bleeding. Monitor Hgb and Hct. Avoid activities that increase intra-abdominal pressure.
Monitor H&H ,Blood transfusions
4. Activity intolerance- assist with ADLS and hygiene. Encourage rest.Elevate HOB during meals to increase comfort.
5. Administer meds prescribed to reduce ammonia: lactulose, antibiotics
6. Skin- assess degree of discomfort related to pruritis and edema. Keep fingernails short. Provide frequent skin care. Skin care will remove waste products deposited on skin. T&P frequently.Provide oral hygien..
Comfort measures: HOB elevated 30 degrees

63. Liver Cancer HCC- hepatocellular carcinoma most common of liver cancer
Most liver tumors are unresectable
5 year survival rate is less than 9%.
Clinical manifestations
Rare in US, 2% of all cancers. The cancer is common in Africa.
S&S- jaundice, ascites, bleeding, encephalopathy. Elevated LFTs.
Because of high vascularity of the liver, common site for mets from primary Ca of esophagus, stomach, colon, rectum, breasts, lungs or malignant melnoma.

64. Risk Factors Cirrhosis Metastasis from another site Dx
AFP: Alpha-fetoprotein tumor marker
Liver enzymes ALP elevated
Liver biospy: definitive diagnosis

65. Treatment For Liver Cancer
Chemotherapy via an surgically implanted infusion pump
Liver transplantation
Portions of a liver are transplanted and will regenerate
Transplantation surgery- 12 hours
Immunosuppressant drugs
Steroids
Monitor for infection and organ rejection

66. Indications for Liver Transplant
Primary or secondary biliary cirrhosis
Chronic active hepatitis with cirrhosis
Liver abscesses
Fatty liver infiltrates
Liver Ca
Indicated for diseases with irreversible damage
Not commonly performed on pts with mets because Ca is likely to recur
Not considered candidates: hepatorenal syndrome, AIDS, sepsis, repeated episodes of esophageal varices or active alcoholism

67. Liver Transplant Complications
1. Graft rejection
Manifestations of graft rejection are:
Fever
Tachycardia
RUQ or flank pain
Dimished bile flow through t-tube or change in bile color
Increased bilirubin
Increased jaundice
Occurs most often 1-2 wks post-op.
Meds: cyclosporin A, Imuran, prednisone.