Disorders of the GB, Pancreas

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Disorders of the GB, Pancreas Liver

• Dee Tanner, RN, MSN
• NUR 310

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Gallbladder Review

• Part of biliary system (liver)
• Pear shaped
• RUQ- rests on posterior surface of liver
• Bile reservoir/ digests fats

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Common Gallbladder Disorders/Terms

• Cholecystitis-Inflammation of the GB (acute/
  chronic) GB becomes edematous
• 4 fs
• Biliary Colic- actual contraction of the GB
  following ingested fatcannot release bile due to
  obstruction by stones/sludge.
• Cholelithiasis- biliary calculi/stonesformed
  from solid constituents in bile
• may occur together or separate

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Clinical Manifestations ofGB Disorders

• Symptoms due to disease/irritation of the GB or
  bc of obstruction of the bile passages.

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Clinical Manifestations

• May be asymptomatic unless acute attack or with
  calculi- silent
• Pain/Tenderness in RUQ (radiates to R. scapula or
  shoulder)
• Severe and steady, persistent
• Wakes at night usually 3-6 hrs after meal
• Associated with ingestion of fatty foodor heavy
  meal

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Assessment Findings

• Wt. loss from food intolerance
• Heartburn, flatulence
• Restlessness
• N, V, fever, decreased BS or abd rigidity
• Pain worse when try to lie down or reclining
• ? Murphys sign- inspiratory arrest

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Assessment Cond

• If bile cannot escape and there is complete
  obstruction or with chronic Dz expect
• Jaundice if common bile duct obstructed
• Dark, tea-colored, foamy urine.
• Fatty stools (steatorrhea) decreased digestion of
  fats
• Clay colored stools- see above
• Pruritis- itching r/t bile salts on the skin.

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Diagnostics for Diagnosis

• H P- Least invasive testing first. Ask the pt
• GB Ultrasound- most common test
• 90 accurate in detecting stones
• CT scan
• ERCP (endoscopic retrograde cholangiopancreatograp
  hy) visualization of GB, pancreas,etc. using
  endoscope.
• Labs ? WBC, Amylase, Lipase, Bilirubin

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Cholecystitis Treatment

• Symptomatic therapy- (treat symptoms)
• MEDS-----
• Pain management- tx w/ narcotics- Demerol.
• Nausea management- N/G tube- gastric
  decompression- almost immediate relief- let abd
  rest.
• Antispasmodics/Anti-cholinergics- decrease
  secretions biliary contractions ex Atropine,
  Bentyl.
• Pruritis- Questran- Powder mix with milk of
  juice, binds to bile salts in the intestine and
  excretes them thru stool.

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Cholelithiasis Non- Surgical Treatment

• Non-surgical treatment- depends on MD and pt.
  condition.
• Medical Dissolution Therapy-med tx used for pts
  with small stones poor surgical candidates.
  Expensive and may take several years to dissolve.
  Ex- Actigall, UDCA.
• ERCP- endoscopy-clear stones from biliary tree
  using basket retrieval- mechanical lithotripsy
• Lithotripsy- busts stones using high energy shock
  waves- takes 2 hours.

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Surgical Mgmt

• Cholecystectomy-removal of GB open or closed
  procedure Penrose drain may be inserted. One of
  the most common surgeries in US! Out-pt basis.
• Cholecystostomy-opening draining of GB
• Choledochotomy-opening into common duct T tube
  inserted until edema subsides connected to
  gravity drainage tubing

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ERCP with stone retrieval
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Post-op Nsg. Interventions for GB Disorders

• Semi-Fowlers position
• Keep NPO- slowly progress diet as tol. Start with
  cl liquids-low fat/protein, high carb.
• IVF- to prevent fld/electrolyte imbalance
• N/G tube to suction until return of bowel sounds
• Analgesics/Nausea meds
• Turn, Cough and Deep breathe
• Early ambulation

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Post-op Nsg. Cond

• Care of biliary drainage/dressing- if lap chole
  may have band aids only.
• Observe for Infection
• T tube-measure drainage (300-500 first 24 hrs)
  observe for obstruction clamp 1 hour before
  meals, unclamp 1 hr after meal ck leakage of
  bile into peritoneal cavity (N/V, pain in RUQ,
  clay colored stools)
• Penrose drain
• Frequency of dressing change, skin Montgomery
  straps
• Patient Family teaching- diet, wound care,
  activity

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Pancreas

• Fish shaped/nodular gland
• LUQ behind stomach across posterior wall
• Secretes-enzymes, insulin, glucagon
• Made up of endocrine (secretes into systemic
  circulation) and exocrine (secretes thru a duct)
  tissue

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Exocrine Functions of Pancreas

• Secretes enzymes-Trypsin, break down proteins
  into amino acids
• Lipase digest fats into fatty acids and
  phospholipids
• Amylase digests carbohydrates
• Enzymes are produced when vagal stimulation
  occurs or when food enters the stomach
• Enzymes are transported to the duodenum via the
  common bile duct (the sphincter of Oddi must
  relax for this to occur- no MSO4).

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Pancreatitis

• Acute- sudden onset and sudden cessation
• Chronic- progressive process usually r/t ETOH
  abuse
• Pain may be r/t ETOH ingestion (most common
  cause) or heavy meal
• Pain is caused by autodigestion of the pancreas
• Treatment aimed at pain relief decreasing
  secretion of pancreatic enzymes
• Remember pain relief is 1!!

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Acute Pancreatitis

• Sudden, severe, upper abdominal pain (usually
  LUQ) may radiate to back bc of pancreas position
• NV, fever, jaundice, decreased bowel sounds
• Gray Turners sign
• Cullens Sign
• Paralytic ileus if small intestines come in
  contact with irritating acids
• Elevated amylase (first 24 hours).
• Elevated lipase levels (elevates after 24 hours
  and stays up for week or more).
• Hyperglycemia- decrease in insulin secretion
• Elevated Triglycerides- release of fatty acids by
  lipase
• Causes- 2 most common are ETOH abuse most
  common), gallstone disease, trauma, or unknown
  causes/idiopathic
• ETOH ABUSE- Acetaldehyde is a byproduct of
  alcohol metabolism and is toxic to the pancreas

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Cullens Sign
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Pancreatitis Cond

• Bile reflux into the pancreas occurs if
  gallstones obstruct the common bile duct and bile
  contributes to attacks of acute pancreatitis.
• The activated proteolase (trypsin and elastase)
  and lipases break down tissue and cell membranes,
  causing edema, vascular damage, hemorrhage, and
  necrosis.

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Two types of Acute Pancreatitis (distinguished by
clinical course)

• Interstitial Vs. Hemorrhagic
• Interstitial inflammation confined to the
  pancreas. Which becomes engorged with
  interstitial fluid and has small foci of necrosis
  surrounded by inflammatory cells, which release
  amylase

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• Hemorrhagic (goes out into the tissues) when
  interstitial pancreatitis becomes worse, the
  pancreas becomes necrotic, and there is bleeding
  into the organ and surrounding retro-peritoneal
  space. Major abdominal vessels may be digested
  by pancreatic enzymes.
• Toxic enzymes and inflammatory mediators (TNF-a,
  IL-I?, IL-6, IL-8, IL-10, C5a, ICAM, substance P)
  are released into the bloodstream and cause
  injury to vessels and other organs (lungs and
  kidneys)
• Myocardial depression and shock can develop
  secondary to release of vasoactive peptides.
  These systemic effects are major causes of
  multiple-organ failure and mortality.

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Diagnostics for Diagnosis

• H P
• Amylase/Lipase/Blood Glucose/Electrolytes levels
• ERCP, x-ray, ultrasound, CT- may show dilated
  intestine or gallstones

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Treatment for Pancreatitis

• Hydration- IVFs- electrolytes albumin blood
• NG tube to suction
• NPO to reduce pancreatic secretions then advance
  to small frequent meals (bland) no stimulants-
  caffeine
• Pain medication (Demerol- no MO!)
• Respiratory assessment
• TPN
• Treatment of infections
• BS control with SS

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Complications

• Alcohol withdrawal complicates attempts to treat-
  watch for! Ask when was your last drink.
• Pancreatic abscess
• Pancreatic pseudo cysts
• Multiple organ failure

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Chronic Pancreatitis

• Progressive, destructive changes- fibrosis
• Often due to alcohol abuse
• Hyperglycemia due to development of diabetes-
  entire organ becomes damaged and cannot secrete
  insulin as needed.
• May or may not cause increased amylase levels
• Treatment no cure- promote health, dietary
  control with PO pancreatic enzymes with meals and
  stop alcohol consumption!

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Hepatitis- Toxic Viral

• itis means inflammation
• Toxic hepatitis drugs, ETOH, industrial toxins
  or poisons
• Viral Hepatitis Types A B C D E G
• Hepatitis A- most common type

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Viral Hepatitis

• Inflammatory process of the liver tissue is
  inflamed, liver cells die, Kupffer cells enlarge
• Speed of onset course of illness vary with the
  kind and strain of the virus but characteristics
  of disease and tx are essentially the same
• Inflammation, degeneration regeneration occur
  simultaneously
• Tissue is inflamed, liver cells die, Kupffer
  cells enlarge

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Phases of Hepatitis

• Many are asymptomatic
• Preicteric phase before jaundice occurs
• Icteric jaundice phase
• Posticteric jaundice is resolving
• Anicteric without jaundice

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Preicteric Phase

• lasts up to 21 days
• N, V, D or Constipation
• Anorexia
• RUQ pain
• Fever
• Malaise
• Arthralgia
• Hepato, splenomegaly

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Icteric Phase

• Lasts up to 4 weeks
• Jaundice- bilirubin diffuses into tissues
• Tea colored urine
• Clay colored stools
• Pruritis
• GI symptoms, fatigue hepatomegaly continue

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Posticteric Phase

• Lasts 2 to 4 months
• Jaundice is resolving
• Malaise
• Relapses may occur
• Some Hepatomegaly

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Hepatitis A (HAV)

• RNA virus
• Transmission fecal-oral route
• Usually fecal contaminated drinking H20 or food
  such as poor sanitation, poor hygiene
• Risk Usually under developed countries or
  infected food handlers
• Incubation period 15-50 days
• Treatment prevention, Hep A vaccine Immune
  globulin (IG)
• Almost all will recover completely

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Hepatitis B (HBV)

• DNA virus
• Transmission- percutaneous (needle stick) or
  exposure to blood, blood products or body fluids
  through contaminated instruments, vaginal
  secretions, semen, saliva, tears, perinatal,
  etc.)
• Risk health care workers, IV drug users,
  frequent blood transfusions, multiple sex
  partners.
• Can live on a dry surface for 7 days teach dont
  share razors, toothbrushes, etc.
• Treatment prevention, Hep B vaccine (95
  effective)

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Hepatitis C (HCV)

• RNA Virus
• Transmission IV drug use most common, perinatal,
  blood/blood product exposure.
• Risk blood transfusions before 1992, dialysis,
  health care workers, prisoners, multiple sex
  partners.
• Treatment No vaccine available (YET)
• More infectious than HIV (co infection)
• Progression

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Hepatitis D (HDV)

• Delta Hepatitis- defective single strand RNA
  virus
• Occurs only in those infected with HBV (relies on
  HBV replication- cant replicate independently).
• Transmission Sexual, needles.
• Treatment prevention on HBV
• Super infection HBV/HDV

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Hepatitis E (HEV)

• RNA virus
• Transmitted fecal-oral route (usually
  contaminated drinking water)
• Risk underdeveloped countries or after natural
  disasters contaminate water

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Hepatitis G (HGV)

• RNA virus
• Risk usually coexists with other hepatitis
  viruses
• Transmission blood/blood products, sexual
  intercourse
• Treatment

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Diagnostic Studies

• History Physical
• LFTs Elevated ALT, AST
• Elevated Serum Bilirubin
• Elevated Urinary Bilirubin
• Prolonged PT
• Decreased Albumin
• Elevated Alkaline Phosphatase
• Liver biopsy

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Nursing Management

• Similar regardless of type
• Rest- BR with BRP
• Diet As tolerated with high calorie intake- big
  breakfast.
• Offer small, frequent meals- high carb, protein,
  low fat. Avoid ETOH!
• Supplemental tube feedings as needed
• Vitamin supplements

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Drug Therapy

• Use meds to treat virus symptoms nausea,
  vomiting, constipation, diarrhea, pain, itching.
  Examples Benadryl, Tigan, Dramamine, etc.
• No phenothiazines- toxicity
• Chronic HBV HCV give anti-virals such as
  Interferon, Epivir, Ribavirin

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Teaching Home Care

• Most treated at home
• Encourage good hand washing
• Stress Prevention of illness with vaccines
• Rest and increase activity gradually
• Diet as tolerated
• Bleeding complications
• Regular Follow-ups
• Sexual Intercourse
• No sharing of personal items
• Side effects of drugs