BSN – 3G

MEDICAL SURGICAL NURSING 2:

METABOLIC AND ENDOCRINE
DISORDERS PART 1

LIVER DISORDERS

Liver

Manifestation of Hepatic Dysfunction:

a. jaundice – clinically evident when serum
FUNCTIONS: bilirubin level exceeds 2.5 mg/dl
• Glucose metabolism b. portal hypertension
− convert glucose to glycogen c. ascites
− glycogen to glucose – glycogenolysis d. esophageal varices - varicosities that
− gluconeogenesis develop from elevated pressure in the
• Ammonia conversion veins that drain into the portal system.
e. hepatic encephalopathy and coma
− converts metabolically generated
ammonia into urea to be excreted to
HEPATITIS
the urine
• inflammation of the liver
• Protein metabolism
• Fat metabolism
Types:
− fatty acids are broken down for
1. Hepatitis A - Hepatitis A virus
energy and ketone bodies
Transmission: fecal-oral route
• Vitamin and iron storage
• Virus is found in the stool 2 weeks
− vitamins A, B and B- complex
before the onset of signs and
vitamins and D
symptoms; one week before the
• Bile formation onset of jaundice.
− bile salts with cholesterol and lecithin Immunoglobulin M (IgM) appears in the
are required for the emulsification of serum as the stool becomes negative for the
fats in the intestine which is virus (there is no chronic carrier state of HAV)
necessary for efficient digestion and
absorption 2. Hepatitis B – HBV a DNA virus
Transmission:
Diagnostic examination • Perinatal by infected mothers
a. liver function test
• Percutaneous (IV, needle-stick
− transaminase are sensitive indicator punctures)
of injury to the liver cells.
• Exposure to contaminated blood
▪ ALT – alanine
and blood products
aminotransferase
• Sexual transmission
▪ AST – aspartate
(HBsAg – hepatitis B surface antigen is
aminotransferase
detected to client who are HBV positive)
▪ GGT - gamma-glutamyl
transferase
3. Hepatitis C – HVC is an RNA virus that is
b. Liver biopsy
transmitted percutaneously common
method of transmission is sharing of
contaminated needles and paraphernalia
among drug user

1|P age
PREPARED BY: AMMP
4. Hepatitis D – Hepatitis D or delta hepatitis is
a defective single stranded RNA virus that
cannot survive on its own. HDV requires the
helper function of HBV to replicate
5. Hepatitis E – HEV is an RNA virus that is
transmitted by fecal-oral route. (drinking
contaminated water)
Symptoms
Acute phase:
✓ malaise, anorexia, fatigue, nausea,
occasional vomiting,
✓ Abdominal pain (RUQ)
✓ Liver enlargement
✓ Jaundice when bilirubin diffuses into the
tissues
✓ Dark urine
✓ Clay colored stool
✓ Pruritus – due to accumulation of bile
salts beneath the skin
Complications
• Hepatocellular carcinoma – chronic hepatitis
B
• Hepatic failure
• Cirrhosis of the liver
Diagnostic Studies
• Hepatitis A:
o anti-HAV IgM - acute infection
o anti-HAV IgG - previous infection and
long term immunity or immunization
• Hepatitis B: HBsAg (hepatitis B surface
antigen) - positive in chronic carrier
o Anti-HBs (antibody to surface antigen)-
marker of response to vaccine
• Hepatitis C: Anti-HCV (antibody to hepatitis C)
– marker for acute or chronic infection with
HCV
• Hepatitis D: anti-HDV, HDV Ag (hepatitis D
antigen) – infection with hepatitis D
Management
(there is no specific treatment or therapy for
acute viral hepatitis)
Emphasis on management
• Rest for liver to regenerate
• Well-balanced diet –high calorie, high
protein, high carbohydrate, low fat
• Avoid alcohol and drugs detoxified by
the liver
• Vitamin supplement
Drug therapy: (Supportive)
• Antiemetics, benadryl - if client needs
sedative
• a- interferon - it has an effect on the viral
replication cycle
Prevention:
• Immunization for hepatitis A, B virus
• Hepatitis B Immune globulin (HBIG)-
given to exposed persons to HBV who
never had Hepatitis B and have never
received hepatitis B vaccine
(needlestick, transmucosal, perinatal
exposure(infants born to HBV-infected
mothers)
• Proper disposal of excreta
• Water sanitation
• Proper disposal of syringes and needles
• Proper screening for blood donors
NONVIRAL HEPATITIS
A. TOXIC HEPATITIS
• cause: - exposure to hepatotoxic
chemicals, medications, botanical
agents
B. DRUG-INDUCED HEPATITIS
FULMINANT HEPATIC FAILURE
• is the clinical syndrome of sudden and
severely impaired liver function in a
previously healthy person.
• The generally accepted definition is that
fulminant hepatic failure develops within 8
weeks after the first symptoms of jaundice.
LIVER CIRRHOSIS
• chronic, progressive, irreversible, widespread
destruction of hepatic cells, with scar tissue
replacing healthy tissue.
Forms:
a. Alcoholic (Laennec’s or portal) – results
from malnutrition especially protein
malnutrition
b. postnecrotic cirrhosis – a complication
of viral, toxic hepatitis
2|P age
PREPARED BY: AMMP
 c. biliary cirrhosis – scarring occurs in the
liver around the bile ducts

Pathophysiology
• Hepatocyte necrosis leads to development of
scar tissue which in turn disrupts blood flow.
This leads to an increase in pressure in the
portal circulatory system – portal
hypertension

Symptoms
✓ Fatigue, weakness, decrease appetite, dull
right upper quadrant, pruritus, fetor b. ascites
hepaticus, asterixis • Portal hypertension and the resulting
✓ Jaundice, anemia, memory impairment increase in capillary pressure and
✓ Testicular atrophy, menstrual irregularities obstruction of venous blood flow
✓ Peripheral neuropathies through the damaged liver are
contributing factors.
Complications
a. Portal hypertension
• increase pressure throughout the portal
venous system that results from
obstruction of blood flow into and
damage liver

Symptoms:
✓ Increased abdominal girth
✓ Rapid weight gain
✓ Shortness of breath
✓ Fluid waves on palpation
✓ Distended veins visible over the
abdominal wall
✓ Fluid and electrolyte imbalance

c. esophageal varices
• are varicosities that develop from
elevated pressure in the veins that drain
into the portal system, found in the
submucosa of the lower esophagus.

3|P age
PREPARED BY: AMMP
 Management
a. portal hypertension
− shunt (portacaval shunt, transjugular
intrahepatic portosystemic shunt)

b. bleeding esophageal varices

− Blakemore Sengstaken tube (Balloon
tamponade)
− Sclerotherapy
− gastric lavage
− Endoscopic Variceal Ligation
(Esophageal Banding Therapy)
− vasopressin injection

d. hepatic encephalopathy
• is the neuropsychiatric manifestation of
hepatic failure associated with portal
hypertension and the shunting of blood
from the portal venous system into the
systemic circulation (ammonia enters
the brain and excites peripheral
benzodiazepine-type receptor and
stimulate GABA. GABA causes
depression of the CNS producing sleep
and behavioral patterns)

Symptoms:
✓ Mental status changes – alteration in
mood and sleep
✓ Disorientation
✓ Asterixis – involuntary flapping of the
hands
✓ Hand writing becomes difficult
✓ Constructional apraxia
✓ Fetor hepaticus
✓ Reflexes disappear
✓ Flaccid extremities
✓ Coma

4|P age
PREPARED BY: AMMP
 • Ammonia is produced in the GIT when
protein is broken down by bacteria.
• Normally liver converts ammonia into
glutamine which is stored in the liver, and is
converted to urea and excreted through the
kidney)

Additional principles of management of hepatic

encephalopathy include the following:
✓ Neurologic status is assessed frequently
✓ Mental status is monitored by keeping a
daily record of handwriting and
arithmetic performance.
✓ I&O and body weight are recorded each
day.
✓ Vital signs are measured and recorded
every 4 hours.
✓ Potential sites of infection (peritoneum,
lungs) are assessed frequently.
✓ Serum ammonia level is monitored daily.

c. ascites GALLBLADDER DISORDERS

− Restriction of sodium and water
− Diuretics and albumin CHOLECYSTITIS
− Paracentesis • acute inflammation of the gallbladder
− Peritoneal venous shunt ( Le Veen shunt)
Causes:
✓ Stone, bacteria, cystic duct obstruction,
burns
✓ distention and inflammation.
Inflammation is sterile but within 24
hours gut organism can be cultured from
the gallbladder.

Symptoms:
✓ Pain, tenderness, rigidity of the right
upper quadrant
✓ Nausea, vomiting
✓ Bile remaining in the gallbladder initiates
a chemical reaction; autolysis and
edema occur; and the blood vessels in
the gallbladder are compressed,
compromising its vascular supply.
✓ Gangrene → perforation, may result.
✓ Acalculous cholecystitis describes acute
gallbladder inflammation in the absence
of obstruction by gallstones.

CHOLELITHIASIS
• presence of stone in the gallbladder

d. hepatic encephalopathy Types of Stones:

(ammonia is a CNS depressant) • Cholesterol stone
− Lactulose – bind with ammonia and • Pigment stones
excrete with the stool
− Neomycin sulfate
− Enema
− Low protein diet

5|P age
PREPARED BY: AMMP
Symptoms:
✓ Triad manifestations: Pain, jaundice, Gallbladder Disorders (Management)
fever ✓ ERCP
✓ Jaundice when there is obstruction of ✓ Cholecystectomy (laparoscopic or the
the common bile duct traditional method)
✓ Dark colored urine, stool is clay colored ✓ Extracorporeal-shock wave lithotripsy
or pale ✓ Pharmacologic agents:
✓ Steatorrhea, a tendency to bleed and o UDCA and CDCA
juandice – when total obstruction o Analgesic
occurs. o Anticholinergic
✓ Enlarged liver if obstruction lasts for o Fat-soluble vitamins
more than few hours o Bile salts
✓ Dietary management – low-fat diet
Gallbladder Disorders (Diagnosis)
• Ultrasound examinations
• CT scan to detect ductal stones
• ERCP – endoscopic retrograde
cholangiopancreatography
− visualization of the gallbladder, cystic
duct, common hepatic duct and
common bile duct

PANCREATIC DISORDERS

PANCREATITIS
• inflammation of the pancreas, can be acute or
chronic

Causes:
✓ Alcohol
✓ Gallbladder disease
✓ Viral infections, doudenal ulcer,
pancreatic cancer

• Acute Pancreatitis is caused by premature

activation of digestive enzyme, which leads to
autodigestion of surrounding tissues,
resulting to severe edema, interstitial
hemorrhage and necrosis.

Two main types of Acute Pancreatitis:

• Interstitial edematous pancreatitis - lack
of pancreatic or peripancreatic
parenchymal necrosis with diffuse
enlargement of the gland due to
inflammatory edema
• Necrotizing pancreatitis - there is
presence of tissue necrosis in either the
pancreatic parenchyma or in the tissue
surrounding the gland.

6|P age
PREPARED BY: AMMP
• Self-digestion of the pancreas by its own Management
proteolytic enzymes, principally trypsin, ✓ Endoscopy – to drain cysts, remove
causes acute pancreatitis. pancreatic stones, correct stricture
• Gallstone obstructs the flow of pancreatic ✓ Surgery
juice → reflux of bile → pancreatic duct → ▪ Pancreaticojejunostomy (Roux-en-Y)
activates the pancreatic enzymes gastric bypass
• Activation of the enzymes → vasodilation → ▪ Pancreaticoduodenectomy (Whipple
increased vascular permeability → necrosis resection)
→ erosion → hemorrhage

Symptoms
✓ Abdominal pain at epigastrium, left upper
quadrant with possible radiation to the back.
Pain is aggravated with alcohol intake
✓ Nausea, vomiting, low grade fever
✓ Hypotension, tachycardia
✓ Cullen’s sign – bluish discoloration of the
periumbilical area
✓ Grey Turner’s sign – bluish discoloration of
the left flank.

Management
✓ Analgesia – morphine
✓ Platelet activator agonist (Lexipafant) reduce
mortality if given in 48hrs
✓ NPO, Correction of fluid and blood loss
✓ Parenteral nutrition for patients with severe
cases
✓ Nasogastric suctioning to relieve nausea and
vomiting, abdominal distention
✓ Histamine 2 antagonist (ranitidine) to
decrease pancreatic activity
✓ Proton pump inhibitors for those who can not ✓ Instruct client to avoid alcohol
tolerate H2 antagonist ✓ Low fat diet
✓ Respiratory care, oxygen inhalation therapy ✓ Treatment for DM

CHRONIC PANCREATITIS
• progressive destruction of the pancreas,
acinar atrophy, cells are replaced by fibrous
tissue resulting to obstruction of the
pancreatic and common bile ducts

Symptoms
✓ Recurring severe abdominal pain and back ,
vomiting
✓ Weight loss
✓ Malabsorption, impaired fat and protein
digestion
✓ Steatorrhae (stool with high fat content)

Diagnostic Examination
✓ ERCP – endoscopic retrograde
cholangiopancreatography
✓ MRI
✓ Glucose tolerance test
✓ Lundh test – measurement of trypsin and
lipase; use to investigate steatorrhea

7|P age
PREPARED BY: AMMP