Transcript Liver and Pancreas

LIVER and PANCREAS
DYSFUNCTION
Valerie Gumangan, RN, ACNP
PANCREAS

Exocrine



Secretes digestive
enzymes into the
small intestines
Breakdown of CHO,
protein, and fats
Endocrine



Produces hormones
Insulin
Glucagon
EXOCRINE FUNCTION

CCK: Cholecystokinin


Secretin




Stimulus for enzyme
secretion
Secretion of bicarb and
water
Lipase: Fats
Amylase: Carbohydrates
Trypsin: Proteins
EXOCRINE FUNCTION



90% of pancreatic
digestive enzymes are
proteolytic
Trypsin
Chymotrypsin


splits proteins into
peptones
Elastase

Breakdown elastic
tissue
EXOCRINE FUNCTION

Amylolytic



Breakdown of
carbohydrates
Amylase
Lipolytic



Breakdown of fats
Lipase
Phospholipase A
ENDOCRINE FUNCTION
Islet of Langerhans
 Alpha cells


Beta cells


Glucagon: ↑ blood
glucose
Insulin: ↓ blood
glucose
Delta cells

Somatostatin
PANCREATITIS



Inflammation of the
pancreas
Autodigestion of the
pancreas by
pancreatic enzymes
Cellular destruction
and organ damage
ACUTE PANCREATITS

Acute



Mild or Nonhemorrhagic
Severe or
Hemorrhagic
Fulminant
EPIDEMIOLOGY



185,000 cases each
year
150,000 cholelithiasis
or sustained alcohol
abuse
African-Americans
are at ↑ risk
CAUSES







Alcohol consumption
Gallstones
Pancreatic
obstruction
Drugs and toxins
Hyperlipidemia
Family history
Trauma and
iatrogenic factors
SIGNS and SYMPTOMS

Severe abdominal pain







Epigastrium radiating to
midback
Not relieved by vomiting
Fever, malaise
Nausea, vomiting
Rigid and distended
Rebound tenderness
Absent or diminished
bowel sounds
SIGNS and SYMPTOMS

Dyspnea and
Tachypnea


Grey Turner’s sign


Large ecchymosis
appearing in the
flanks
Cullen’s sign


Pulmonary infiltrates
Ecchymosis in
umbilical area
Hypovolemic Shock
DIAGNOSTIC FINDINGS

Serum Amylase


Serum Lipase



Normal (23-85 u/L)
Normal (0-160 u/L)
Serum trypsinogen:
elevated
Urinary amylase:
elevated
DIAGNOSTIC FINDINGS




Hematocrit: initially
elevated then later
decreased
WBC: elevated
C-reactive protein:
elevated
Liver function tests:
elevated
DIAGNOSTIC FINDINGS




Sodium and
Potassium: decreased
Blood glucose:
elevated
Serum Calcium:
decreased
Albumin and
Magnesium:
decreased
DIAGNOSTIC FINDINGS





Abdominal and Chest X-ray
CT scan, Ultrasound, MRI
Endoscopic Retrograde
Cholangiopancreatography
(ERCP)
Aspiration biopsy
Stool studies: steatorrhea
COMPLICATIONS

Hypovolemic shock




3rd spacing
Hemorrhage
Vomiting
Decreased protein
intake
COMPLICATIONS

Pulmonary
complications




Atelectasis
Acute lung injury
Pleural effusion
ARDS
COMPLICATIONS

Cardiovascular


Release of myocardial
depressant factor
Pancreatic
pseudocyst


Cavity next to
pancreas
Filled with necrotic
products
COMPLICATIONS

Pancreatic abscess




2-4 weeks after
episode
Necrosis of tissue
Relocation of bacteria
Hypocalcaemia can
occur with severe
disease
COMPLICATIONS

Fluid and electrolytes



Vomiting
NG suction
Redistribution of fluids
TREATMENT

Pain Management




IV opioid analgesics
Dilaudid IV PCA
Demerol and
Morphine IV
GI rest


Decrease stimulation
of pancreas
Nasogastric tube
insertion
TREATMENT




Fluid and Electrolyte
replacement
Cessation of alcohol
consumption
Nutrition: enteral
versus parenteral
Surgery if there is
biliary obstruction
TREATMENT

Respiratory




Oxygen
Monitor oxygen
saturation
Arterial blood gas
Ventilator support
TREATMENT

Fluid volume deficit





IV fluids
Plasma expanders
Vasopressors
Blood replacement
Strict intake and output
TREATMENT

Fluid and electrolyte
imbalance



LR or IV maintenance
fluid containing K+
Calcium gluconate
Hypocalcemia


Chvostek’s sign
Trousseau’s sign
TREATMENT

Pseudocyst, abscess
or fistula



Monitor for signs and
symptoms of shock
Prepare patient for
surgery
Watch for infections
post-operatively
TREATMENT



Biliary drainage tube
Surgical debridement
ERCP





Sphinceterotomy
Gallstone removal
Stent placement
Balloon dilatation
Laparoscopic
cholecystectomy with
CBDE
MEDICATIONS

Viokase


Pancrease


Replace pancreatic
enzymes
Replace pancreatic
enzymes
Glucagon

Treat hypoglycemia
NURSING IMPLICATIONS

Vital signs



Laboratory values



Hypovolemic shock
Sepsis
Amylase, Lipase
BMP
Fluid and electrolytes



NPO
NGT
Nutrition
NURSING IMPLICATIONS




Administer pain
medication
Monitor blood
glucose
Monitor intake and
output
Daily weight
CHRONIC PANCREATITIS


Persistent
inflammation of the
pancreas
Scarring and
calcification of the
pancreatic ducts
CAUSES


70% is caused by
alcohol abuse
20% is caused by
obstruction, trauma,
metabolic
disturbances
SIGNS & SYMPTOMS

80% of pancreatic
destruction causes



Malabsorption
resulting in nutritional
deficits
Diarrhea and
steatorrhea
Impaired glucose
regulation
DIAGNOSTIC FINDINGS



LFT, CMP, CBC, ESR
Stool studies
Abdominal CT scan


Abdominal US


Images organ, detect
inflammation
Detect inflammation and
calcifications
ERCP

looks for stones
TREATMENT




GI rest
Pain control
No Alcohol
Daily weight
TREATMENT



Low fat, protein, and
high carbohydrate
diet
Oral pancreatic
enzymes
Monitor blood
glucose
TREATMENT



Replacement of fat
soluble vitamins
Octreotide
(Sandostatin)
Celiac plexus block
LIVER FUNCTION

Glucose metabolism



Ammonia conversion



Glycogenolysis
Gluconeogenesis
Ammonia to urea
Urea excreted in the
urine
Protein metabolism

Synthesis of plasma
proteins
LIVER FUNCTION

Fat metabolism


Vitamin and iron
storage




Fatty acids broken
down for energy
Vitamin A,B,D, and Bcomplex vitamins
Bile formation
Bilirubin excretion
Drug metabolism
LIVER FUNCTION TESTS





ALT: Alanine
aminotransferase
ALP: Alkaline
phosphotase
AST: Aspartate
aminotransferase
Bilirubin
Albumin
LIVER PANEL




Total Protein
GGT: Gammaglutamyl transferase
LDH: Lactic acid
dehydrogenase
Prothrombin time
HEPATIC DYSFUNCTION




Primary liver disease
Obstruction of bile
flow
Altered hepatic
circulation
Acute or chronic
CAUSES

Toxicities:





Chemicals, Plants,
Drugs
Bacterial invasion
Nutritional deficiency
Autoimmune
Hepatitis
Viruses

Hepatitis A,B,C,D,E
CHRONIC LIVER DISEASE



12th leading cause of
death in the United
states among young
and middle-aged
adults
40% associated with
alcohol use
Cirrhosis
SIGNS & SYMPTOMS






Jaundice
Portal hypertension
Ascites and varices
Nutritional
deficiencies
Hepatic
encephalopathy
Coma
JAUNDICE




Bilirubin level >2.5
mg/dL
All body tissue
become tinged yellow
Hepatocellular
jaundice
Obstructive jaundice
PORTAL HYPERTENSION



Increased pressure
through portal
venous system
Obstructed blood
flow through
damaged liver
Commonly
associated with liver
cirrhosis
PORTAL HYPERTENSION

GI bleeding





Black tarry stool
Hematemesis
Encephalopathy
Coagulopathy
Ascites
ASCITES




Backup of venous
blood flow from portal
HTN
Failure to metabolize
aldosterone
Movement of fluid
from vessels to
peritoneal space
Accumulation of
albumin-rich fluid
HEPATIC ENCEPHALOPATHY



Life-threatening
complication of liver
disease
Liver unable to
detoxify toxic
byproducts of
metabolism
Ammonia is the
major etiologic factor
of encephalopathy
HEPATIC ENCEPHALOPATHY





Mental changes
Motor disturbances
Altered mood and
sleep patterns
Asterixis “liver flap”
 Flapping tremor of
the hands
Constructional
apraxia
VIRAL HEPATITIS




Systemic, viral
infection
Necrosis and
inflammation of liver
cells
Altered liver function
5 definitive types of
viral hepatitis

Hepatitis A, B, C, D, E
HEPATITIS A


Hepatitis A Virus
Fecal-oral
transmission




Poor sanitation
Person-person
contact
Water and food borne
Incubation

15-50 days
SIGNS and SYMPTOMS
Hepatitis A Phases
 Preicteric






Flu-like symptoms
Fatigue
Loss of appetite
Nausea
Cough
Joint pain
SIGNS and SYMPTOMS

Icteric







Jaundice
Dark colored urine
RUQ pain
Itchy skin
Clay-colored stools
Poor appetite
Some preicteric
symptoms subside
SIGNS and SYMPTOMS

Post icteric phase


Things start to return
to normal
Fatigue can remain
HEPATITIS A



Mild with recovery
No carrier state
Doesn’t usually lead
to chronic state
HEPATITIS A
Prevention
 Hand washing
 Safe water supplies
 Proper sanitation
 Sewage disposal
 HAV vaccination
Medical Management
 Bed rest during acute
stage
 Small frequent meals
 Supplemental IV with
glucose
 Gradual progressive
ambulation
HEPATITIS B





Hepatitis B Virus
Parenteral
transmission
Intimate contact with
carriers
Perinatal: mother to
baby
Occupational hazard
to health care
workers
HEPATITIS B





Incubation: 28-160
days
Symptoms: rash and
arthralgias
Outcome: may be
severe
Carrier state possible
Increased risk of
chronic hepatitis
HEPATITIS B
Prevention
 Hand washing
 Wear gloves when
handling body fluids
 safe sex
 HBV vaccination
 Hepatitis B
Immunoglobulin
Medical management
 Alpha-interferon
 Lamivudine (Epivir)
and adefovir
(Hepsera)
 Bed rest until s/s
subside
 Restrict activities
 Adequate nutrition
HEPATITIS B PANEL



HBsAg: Hepatitis B
surface antigen
HBsAb or Anti-HBs:
Hepatitis B surface
antibody
HBcAb: Hepatitis B
core antibody
HEPATITIS C





Hepatitis C Virus
Blood transfusion
transmission
Exposure to
contaminated blood
Intimate contact with
infected partner
Increased risk for
STDs
HEPATITIS C





Incubation: 15-160
days
Symptoms: similar to
HBV. Less severe
and anicteric
Chronic carrier state
Can lead to chronic
liver disease
Increased risk for
cancer
HEPATITIS C


No benefit from rest,
diet, or vitamin
supplements
Antiviral agents



Interferon (Intron-A)
Ribavirin (Rebetol)
Side effect: hemolytic
anemia
HEPATITIS D





Delta agent
HBV surface antigen
required for replication
Incubation: 21-140
days
Symptoms: similar to
HBV
Can lead to carrier
state, chronic active
hepatitis, and cirrhosis
HEPATITIS E






Hepatitis E Virus
Fecal-oral
transmission
Low risk for person to
person contact
Incubation: 15-65
days
Symptoms: Similar to
HAV
Severe in pregnant
women
HEPATITIS G and GB VIRUS C






Non A-E virus
Incubation: 14-145
days
2 isolates of same
virus
Autoantibodies are
absent
Still too many
unknowns
Persistent infection
TOXIC HEPATITIS


Resembles viral
hepatitis
Exposure to toxic
chemicals



Medications
Botanicals
Remove causative
agent
TOXIC HEPATITIS





Anorexia, nausea,
vomiting
Jaundice
Hepatomegaly
No effective antidotes
Delay in treatment
can result in
increased severity
DRUG INDUCED HEPATITIS



Most common cause
of acute liver failure
50% of all cases in
the U.S.
Acetaminophen has
been identified as the
leading cause of
acute liver failure
DRUG INDUCED HEPATITIS


Onset is abrupt
Early symptoms


Late symptoms


Fever, chills, rash,
arthralgia, pruritus,
anorexia
Jaundice, dark urine,
enlarged and tender liver
Treatment

Short course of highdose corticosteroids
TREATMENT





Rest
Small, frequent
meals
Low protein, fat, and
high carbohydrate
IV fluid containing
dextrose as needed
Monitor labs