HEPATOBILIARY

Pancreas Endocrine function:

- Insulin (produced by beta-cells)
- Glucagon (produced by alpha-cells)
- Somatostatin (produced by delta-cells, regulates insulin
and glucagon)

Exocrine function:
- Pancreatic amylase (for carb digestion)
- Pancreatic lipase (for fat digestion)3

Pancreatic duct - Narrow, one-way (bile cannot enter)

Cholecystokinin
Manifestations when bile is not
released from gallbladder (due to
obstruction of cystic duct)
Types of Jaundice
Diagnostic Test
LIVER CIRRHOSIS
Compensated Cirrhosis
Progression of Alcoholic Cirrhosis
- Duct obstruction leads backflow of pancreatic amylase
and lipase causing autodigestion and increase serum
lipase/amylase
- Secreted when fat is ingested
- Contracts gallbladder and relaxes sphincter of Oddi
- Steatorrhea (fat not emulsified)
- Fat-soluble vitamins not used: A – eyes blurry, D – bones
brittle, E – skin impaired integrity, K – blood not clotting
- Clay-colored stool (no urobilinogen to give color)
- Urine tea/dark yellow (bile mixes in circulation giving it
its color)
- Jaundice (bilirubin circulates to eye vessels)
- Pruritus (bilirubin circulates to vessels in skin)
1. Hemolytic: increased RBC destruction
2. Hepatocellular: damaged hepatocytes cannot process
bilirubin
3. Obstructive: bile not released due to gallstone
Endoscopic Retrograde Cholangiopancreatography
- NPO for 8 hrs
- Sedation
- WOF: post-op gag reflex (returns after 1-2 hours)
- WOF: possible perforation (bleeding, shock)
Causes
- Hepatotoxic drugs (post-necrotic)
- Virus/Bacteria (post-necrotic)
- Duct obstruction (biliary)
- CHF (cardiac cirrhosis, high pressure leading to
backflow, leads to hepatomegaly, then cell death)
- Laennec’s cirrhosis (chronic alcoholism)
- Anoxia (ischemia)
- 80% of cases
- Asymptomatic for about 10 years
- Liver can still function normally
1. Healthy Liver
2. Alcoholic Fatty Liver (fat accumulation)

Complication: due to PORTAL
HYPERTENSION and reduced
ONCOTIC PRESSURE due to low
albumin production
Dx of Portal HPT:
- Hepatic vein pressure
measurement via catheter
insertion in
antecubital/femoral artery
- Hepatic venous pressure
gradient >10mmHg
- Portal vein catheterization
3. Alcoholic Hepatitis (inflammation)
4. Alcoholic Cirrhosis (fibrosis, collagen replacement,
irreversible)
Hepatocytes become scarred and hard, increasing the pressure
that blood must overcome to pass through the liver. Signs and
symptoms arise from backflow of blood into:
1. Esophagus
- Causes esophageal varices
- Painless hematemesis (esophagus has soft-tissue)
- Melena (blood ingested)
- Shock (due to blood loss)
2. Spleen
- Splenomegaly
3. Rectum
- Painful hemorrhoids
4. Peritoneal cavity
- Ascites (+) shifting dullness due to water accumulation
- Umbilical hernia (umbilicus protrudes)
5. Kidneys
- Decreased perfusion known as hepatorenal syndrome
leading to edema (hands and feet)
6. Blood vessels of stomach
- Spider angioma (due to collateral circulation)
7. Brain
- Ammonia not excreted causing hepatic encephalopathy
(confused, memory loss, coma, asterixis)
8. Mouth
- Ammonia not excreted causing stomatitis
Intervention/Management
Ascites Management
Esophageal Varices Management
1. Semi-fowler’s: patient is edematous
2. Protein intake: high if no encephalopathy, ascites or
edema (to prevent muscle wasting), low if otherwise
3. Low sodium: aggravates edema
4. Diuretics: check BP and potassium
5. WOF: bleeding (Vit. K as ordered)
6. WOF: Hepatic encephalopathy
7. Administer antibiotics (metronidazole, neomycin):
prevents protein synthesis of bacteria
8. Lactulose: decreases pH and ammonia
9. Avoid opioids, sedatives, barbiturates
10. Paracentesis: to drain ascites (empty bladder first)
11. WOF: varices, hemorrhoids
12. Sengstaken-Blakemore tube: to stop bleeding of
esophageal varices. Scissors at bedside if ever balloon
pops.
Nutrition:
- Low sodium
- Salt-substitute (lemon juice, oregano, thyme)
- Fluid not restricted unless poor sodium concentration is
present
Pharmacologic:
- Diuretics (spironolactone as first-line, furosemide)
- May cause: hypovolemia, hyponatremia, hypokalemia,
hypochloremic alkalosis
- Salt-poor albumin or colloidal therapy
Bed rest
Paracentesis
- Not routine for ascites anymore
- Used when not responding to diuretics and nutritional
treatment; or very large ascites
- 5-6L removed when ascites is severe
Transjugular Intrahepatic Portosystemic Shunt assisting with
paracentesis
- Best but high cost
Document and Monitor
- I&O
- Abdominal girth
- Daily weight
- Respiratory status (fluid compresses thoracic cavity)
- Serum ammonia, creatinine, electrolytes
Prone to rupture (decreased Vit. K, high risk for bleeding)
10-30% mortality rate when bleeding starts

Hepatic Encephalopathy and Coma
CHOLELITHIASIS/CHOLECYSTITIS
Risk Factors
Diagnostic Test
SS: hematemesis, melena, shock
Dx: Endoscopy, UTZ, CT angiography
- No heavy muscular exertion or straining
- Blood transfusion
- Sengstaken-Blakemore tube: balloon tamponade
through nose. Usually intubated first, lasts for 12hrs or
less
- Octreotide (immediate bleeding control, may cause
hypoglycemia and abdominal cramps) or vasopressin
(causes splanchnic vasoconstriction) before endoscopy
- Note: vasoconstrictors are always contraindicated in
CAD!
- Beta-blockers: reduces portal pressure, reduces risk for
bleeding
- Nitrates (isosorbide): vasodilation
- Endoscopic sclerotherapy: uses injectable sclerosing
agent (sodium morrhuate, ethanolamine oleate)
- Endoscopic variceal ligation (banding): first-line
- Direct surgical ligation
Toxic substances, such as ammonia, enters circulation, crosses
BBB, excites GABA neurotransmission (causes CNS depression
due to inhibitory effect)
- Sleepiness
- Asterixis (hands flapping when dorsiflexed)
- Constructional apraxia (cannot draw simple figures)
Treatment:
- Lactulose (to eliminate ammonia). WOF: watery
diarrhea which indicates overdose. Via NGT or enema if
comatose
- IV glucose (to prevent protein breakdown)
- Antibiotics (reduce ammonia-forming bacteria in colon)
Acute form: due to stone
Chronic from: due to fibrosis
Acalculous form: due to virus/bacteria (E. coli, Strep), or bile
stasis
Made up of cholesterol or unconjugated pigments of bile
5F’s
- Female, Fat, Forties, Fertile, Fair
- Basically increased in cholesterol synthesis
Cholecystography
- Dye used (assess for allergy)
- Eat fat the night before
- NPO at midnight
 - Dysuria normal post-op (due to dye excretion)
Manifestations 1. Indigestion: bile not released
2. Pain at RUQ, right shoulder, right scapula: gallbladder
contracts but cannot release bile
3. Belching, flatulence: increased HCL and CO2
4. Mass at RUQ may be palpated
5. Murphy’s sign (+): pain during inhalation using hook
method)

Other symptoms when bile not released from gallbladder are

the same.
Interventions 1. N&V: NPO (if no N&V, diet is low fat and low gas-
forming food), antiemetics as ordered
2. Anticholinergics: limits HCl production
3. Analgesic: no morphine (constricts Oddi), Demerol
(Meperidine) is hepatotoxic
4. Ursodeoxycholic acid/ Chenodeoxycholic acid: to
dissolve cholesterol stones
5. Percutaneous mono-octanoin and methyl tertiary butyl:
dissolves stone
6. Surgery: cholecystectomy & choledocholithotomy (post-
op splinting, monitor T-tube drain and clamp 2-4 hrs
after eating, limit fat intake)

PANCREATITIS Inflammation and scarring of the pancreas due to autodigestion

(duct is narrowed, thus, enzymes cannot escape)
Causes - Stones (obstructs ampulla of Vater)
- Trauma
- Infection
- Alcohol
Manifestations mainly due to 1. Pain: mid-epigastric, back, LUQ, aggravated when eating
increased pancreatic duct pressure (pancreas contracts but cannot release enzyme), (+)
(enzymes not released into abdominal guarding kasi nga masakit bhie
duodenum) 2. Weight loss: cannot digest nutrients (no lipase, amylase
from pancreas)
3. N&V: due to compression of food pathway
4. Decreased bowel sounds: due to compression
5. (+) Cullen’s: blue umbilicus (destruction of blood
vessels)
6. (+) Turner’s: blue flank
7. Increased serum amylase and lipase: backflows into
blood vessels
8. Hypocalcemia: breakdown of pancreatic fat releases
fatty acids and binds to calcium
9. Stridor
10. ARDS: due to increased capillary permeability
Diagnosis 1. Upper abdominal pain

Management:
Nursing Diagnoses for Impaired
Liver Function
Nursing Diagnoses for post-op
Gallbladder surgery
Nursing Diagnoses for Pancreatitis
2. 3x more serum amylase and lipase than upper limit
3. CT, MRI
4. CRP, ESR
1. H2 antagonists
2. PPI
3. Analgesia (parenteral opioids); hydromorphone,
fentanyl
4. NPO: stimulates secretion
5. NGT: decrease stomach acid
6. Monitor glucose: hyperglycemia (cannot secrete insulin)
1. Activity Intolerance related to fatigue, lethargy, and
malaise
2. Impaired nutritional Intake related to anorexia
3. Impaired skin integrity related to pruritus, jaundice, and
edema
4. Risk for injury related to altered clotting mechanism
5. Disturbed body image related to abdominal distention
6. Acute confusion related to increased serum ammonia
7. Impaired breathing related to restricted thoracic
expansion secondary to ascites
1. Acute pain related surgical incision
2. Impaired nutritional status related to inadequate bile
secretion
1. Acute pain related to pancreatic stimulation
2. Impaired nutritional status related to impaired
pancreatic secretions
3. Fluid and electrolyte imbalance related to fluid shifting