The document discusses conditions of the liver including its functions, health history focus, clinical assessment, diagnostics, liver biopsy, manifestations of liver damage, ascites, esophageal varices, hepatic encephalopathy, and other manifestations such as vitamin deficiency, hepatitis, and hepatic cirrhosis. The liver's key roles include glucose metabolism, protein metabolism, drug and hormone metabolism, and bile formation. Clinical assessment focuses on signs of liver damage like jaundice, bleeding, edema. Liver function tests and biopsy are important diagnostics. Complications include ascites, varices, encephalopathy.
3. FUNCTIONS OF THE LIVER
Glucose Metabolism
Ammonia Conversion
Protein Metabolism
Fat Metabolism
Drug and Hormone Metaboliism
Vitamin and Iron Storage
Bile Formation
Bilirubin Excretion
4. FOCUS OF HEALTH HISTORY
exposure to hepatotoxic substance
Infection (e.g. hepatitis, leptospirosis)
Alcohol and drug use
Sexual proctices
Familial history
History suggesting liver damage
6. DIAGNOSTICS
Liver function test
Alanine aminotransferase (ALT)
aspartate aminotransferase (AST)
gamma-glutamyl transferase (GGT)
Alkaline phosphatase
Lactose degydrogenase
Bleeding time
Clotting time
Serum albumine
Serum ammonia
7. ALT levels increase
primarily in liver disorders and
may be used to monitor the
course of hepatitis or cirrhosis
or the effects of treatments
that may be toxic to the liver
AST is present in tissues that
have high metabolic activity;
therefore, the level may be
increased if there is damage
to or death of tissues of
organs such as the heart, liver,
skeletal muscle, and kidney
Increased GGT levels are
associated with cholestasis
but can also be due to
alcoholic liver disease.
9. LIVER BIOPSY
Liver biopsy is the removal of a small amount
of liver tissue, usually through needle
aspiration.
Bleeding and bile peritonitis after liver biopsy
are the major complications; therefore,
coagulation studies are obtained, their values
are noted, and abnormal results are treated
before liver biopsy is performed
10. OTHER DIAGNOSTICS
Abdominal X-ray
CT scan
MRI
Laparoscopy
Barium study of
esophagus
Cholecystogram and
cholangiogram
Celiac axis
arteriography
Measurement of portal
pressure
Esophagoscopy/endoscopy
Electroencephalogram
Ultrasonography
Endoscopic retrograde
cholangiopancreatography(
ERCP)
11. MANIFESTATIONS OF LIVER DAMAGE
Jaundice, resulting from increased bilirubin
concentration in the blood
Hemolytic
Hepatocellular
Obstructive
Portal hypertension, ascites, and varices,
resulting from circulatory changes within the
diseased liver and producing severe GI
hemorrhages and marked sodium and fluid
retention
12. MANIFESTATIONS OF LIVER DAMAGE
Nutritional deficiencies, which result from the
inability of the damaged liver cells to
metabolize certain vitamins
responsible for impaired functioning of the
central and peripheral nervous systems and for
abnormal bleeding tendencies and to synthesize
proteins
Hepatic encephalopathy or coma, reflecting
accumulation of ammonia in the serum due
to impaired protein metabolism by the
diseased liver
18. ASCITES
Transjugular intrahepatic portosystemic shunt (TIPS)
TIPS is the treatment of choice
for refractive ascites. It is
extremely effective in
decreasing sodium retention,
improving the renal response to
diuretic therapy, and preventing
recurrence of fluid accumulation
To reduce portal hypertension,
an expandable stent is inserted
to serve as an intrahepatic
shunt between the portal
circulation and the hepatic vein
19. ASCITES
Nursing Management
Monitor intake and output, abdominal girth, and
daily weight to assess fluid status
monitorsserum ammonia and electrolyte levels to
assess electrolyte balance, response to therapy,
and indicators of encephalopathy
Instruct to avoid alcohol
Encourage adherence to dietary regimen
Monitor signs of infection, hemorrhage, and pain
Provide skin care with edema
22. CAUSES OF BLEEDING
Lifting heavy objects
straining at stool;
sneezing,
coughing, or
vomiting;
esophagitis;
irritation of vessels by
poorly chewed foods
or irritating fluids;
reflux of stomach
contents (especially
alcohol).
Salicylates and any
medication that erodes
the esophageal mucosa
or interferes with cell
replication also may
contribute to bleeding.
25. MANAGEMENT
Monitor for signs of
bleeding that may lead
to hypovolemia
IV fluid replacement
Blood transfusion
Insert IFC to monitor
I&O
Vasopressin if no
conntraindication
Propanolol (Inderal)
26. MANAGEMENT
Baloon Tamponad
(Sangstaken Blakemore Tube)
pressure is exerted on the cardia (upper orifice of
the stomach) and against the bleeding varices by
a double-balloon tamponade (Sengstaken-
Blakemore tube)
Management
1. Monitor for esophageal Injury/rupture
2. Monitor for the color of gastric and
esophageal aspirate
3. Monitor for signs of aspiration
4. Monitor for signs of mucosal damage
5. Keep a pair of scissors at bedside
6. Stay with the patient to alleviate anxiet
27. MANAGEMENT Endoscopic Sclerotherapy
Injection of sclerosing agent into esophageal
varices through an endoscope promotes
thrombosis and eventual sclerosis, thereby
obliterating the varices.
Management
1. observe for bleeding,
2. perforation of the esophagus,
3. aspiration pneumonia,
4. esophageal stricture.
5. Antacids, histamine-2 antagonists such
as cimetidine [Tagamet], or proton
pump inhibitors such as pantoprazole
[Protonix] may be administered
28. MANAGEMENT
Esophageal banding
(Variceal Band Ligation)
a modified endoscope loaded with an elastic
rubber band is passed through an overtube
directly onto the varix (or varices) to be
banded. After the bleeding varix is suctioned
into the tip of the endoscope, the rubber band
is slipped over the tissue, causing necrosis,
ulceration, and eventual sloughing of the varix.
29. MANAGEMENT
Surgical Bypass procedures
Blood Going to the Liver is shunted to other
different venous system in such a way that it
will not enter the liver and it will cause
reduction of portal pressure
Management is the same for any
other abdominal surgery
31. HEPATIC ENCEPHALOPATHY
It is caused by the increase of Ammonia in
the blood in patients with Liver disease.
Hepatic coma represents the most advanced
stage of hepatic encephalopathy.
Causes including synergistic effects of other
chemicals (ie, serotonin) with ammonia, and
the generation of endogenous
benzodiazepines or opiates
32. HEPATIC ENCEPHALOPATHY
Sources of ammonia includes
Metabolism of proteins
Formed by the bacteria in the large intestine
Bleeding
AMMONIA is converted to UREA by the liver
33. HEPATIC ENCEPHALOPATHY
Other causes of
Hepatic
encephalopathy
excessive diuresis,
dehydration,
infections, surgery,
fever, and
some medications
34. HEPATIC ENCEPHALOPATHY
The earliest symptoms
of hepatic
encephalopathy
include minor mental
changes and motor
disturbances
slightly confused and
unkempt and
has alterations in
mood and sleep
patterns
sleep during the day
35. HEPATIC ENCEPHALOPATHY
Normal level of consciousness with
periods of lethargy and euphoria;
reversal of day–night sleep patterns
Asterixis; impaired writing and ability
to draw line figures. Normal EEG.
Increased drowsiness; disorientation;
inappropriate behavior; mood swings;
agitation
Asterixis; fetor hepaticus. Abnormal EEG
with generalized slowing.
Stuporous; difficult to rouse; sleeps most
of time; marked confusion; incoherent
speech
Asterixis; increased deep tendon reflexes;
rigidity of extremities. EEG markedly
abnormal.
Comatose; may not respond to painful
stimuli
Absence of asterixis; absence of deep
tendon reflexes; flaccidity of extremities.
EEG markedly abnormal.
38. HEPATIC ENCEPHALOPATHY
Management
LACTULOSE
(CEPHULAC)
(1) ammonia is kept in
the ionized state,
resulting in a decrease
in colon pH, reversing
the normal passage of
ammonia from the
colon to the blood;
(2) evacuation of the
bowel takes place,
which decreases the
ammonia absorbed
from the colon; and
(3) the fecal flora are
changed to organisms
that do not produce
ammonia from urea
39. HEPATIC ENCEPHALOPATHY
Nursing Management
Maintain a safe
environment
Monitor for potential
complication
Limit Protein intake,
give high biologic
protein
Prevent formation of
ammonia
Provide small frequent
feedings and frequent
snacks of complex
carbohydrate
Substitute vegetable
protein over animal
protein
40. OTHER MANIFESTATIONS OF
HEPATIC DYSFUNCTION
Edema and Bleeding
Vitamin Deficiency
Metabolic
Abnormalities
Pruritus and skin
changes
41. VITAMIN DEFICIENCY
Vitamin A deficiency, resulting in night blindness and eye
and skin changes
Thiamine deficiency, leading to beriberi, polyneuritis, and
Wernicke-Korsakoff psychosis
Riboflavin deficiency, resulting in characteristic skin and
mucous membrane lesions
Pyridoxine deficiency, resulting in skin and mucous
membrane lesions and neurologic changes
Vitamin C deficiency, resulting in the hemorrhagic lesions of
scurvy
Vitamin K deficiency, resulting in hypoprothrombinemia,
characterized by spontaneous bleeding and ecchymoses
Folic acid deficiency, resulting in macrocytic anemia
42. HEPATITIS
Inflammation of the liver due to the presence
of virus
Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis D
Hepatitis E
46. HEPATIC CIRRHOSIS
Cirrhosis is a chronic disease characterized by
replacement of normal liver tissue with
diffuse fibrosis that disrupts the structure and
function of the liver
47. HEPATIC CIRRHOSIS
3 types of cirrhosis
Alcoholic cirrhosis, in which the scar tissue
characteristically surrounds the portal areas. This is most
frequently caused by chronic alcoholism and is the most
common type of cirrhosis.
Postnecrotic cirrhosis, in which there are broad bands of
scar tissue. This is a late result of a previous bout of acute
viral hepatitis.
Biliary cirrhosis, in which scarring occurs in the liver
around the bile ducts. This type of cirrhosis usually results
from chronic biliary obstruction and infection (cholangitis);
it is much less common than the other two types.
48. HEPATIC CIRRHOSIS
Liver enlargement
Abdominal pain
Portal Obstruction and Ascites
Indigestion and altered bowel function
Infection and Peritonitis
hepatorenal syndrome,
Gastrointestinal Varices
Edema
Vitamin Deficiency and Anemia
Mental Deterioration
55. BILE
Bile is composed of water and electrolytes
(sodium, potassium, calcium, chloride, and
bicarbonate) along with significant amounts
of lecithin, fatty acids, cholesterol, bilirubin,
and bile salts. The bile salts, together with
cholesterol, assist in emulsification of fats in
the distal ileum. They are then reabsorbed
into the portal blood for return to the liver,
after which they are once again excreted into
the bile
57. CHOLELITHIASIS
Caused by
Bile pigments
Cannot be dissolved, thus, must be surgically
removed
Cholesterol
decreased bile acid synthesis and increased
cholesterol synthesis in the liver, resulting in bile
supersaturated with cholesterol, which precipitates out
of the bile to form stones
People at risk are
FAT FERTILE FEMALE at FORTY
58. CHOLELITHIASIS
Clinical manifestation
Gall bladder stones may be silent producing no
symptoms
Epigastric distress, such as fullness, abdominal
distention, and vague pain in the right upper
quadrant of the abdomen, may occur. This
distress may follow a meal rich in fried or fatty
foods.
59. CHOLELITHIASIS
Clinical manifestation
Problems may occur if the stones irritate any of
the part of the biliary tree
Cholecystitis
Choledochocystitis
Biliary colic and pain
Murphy’s sign
Pain medication
Jaundice
Change in urine and stool color
Vitamin deficiency
61. Management
Low fat diet
Non-gas forming foods
Avoid milk and milk
products
Avoid alcoholic
beverage
Lithotripsy
Laparoscopic
Cholecystectomy
rest, IV fluids,
nasogastric suction,
Ursodeoxycholic acid
(UDCA) and
chenodeoxycholic acid
(chenodiol or CDCA)
have been used to
dissolve small,
radiolucent gallstones
composed primarily of
cholesterol.
It acts by inhibiting the
synthesis and secretion
of cholesterol, thereby
64. CHOLELITHIASIS
Management
Routine Preop
Teaching
Routine Postop
activities
T-tube(Bile drainage)
Monitor for bile
peritonitis
Monitor for bleeding
Manage Pain
Early ambulation
Monitor for GI
symptoms
Fluids and Electrolyte
management
NG suction
Improve respiratory
status
Deep breathing and
coughing
Skin care
Improve Nutritional
67. THE PANCREAS
Hormones secreted by the
pancreas
Alpha & Beta cells of the
Islet of Langerhans
Somatostatin
Glucagon
insulin
68. THE PANCREAS
Factors affecting secretions of pancreatic
enzymes are
CCK
Vagal nerve stimulation
Duodenal distention
69. PANCREATITIS
Characterized by inflammation of the
pancreas
Increased secretion of digestive enzymes
Auto-digestion of the pancreas
Enzyme damages up to the blood vessels
leading to bleeding and thrombosis
70. PANCREATITIS
Risk factors
Biliary tract disease
Alcoholism
Blunt trauma
Viral or bacterial infection
Duodenitis
The most common
cause of death in
pancreatitis is SHOCK
71. PANCREATITIS
Clinical Manifestation
Severe pain is the
major symptom of
pancreatitis
the pain occurs in the
midepigastrium
occurring 24 to 48
hours after a very
heavy meal or alcohol
ingestion
Abdominal distension
Decreased peristalsis
Nausea and Vomiting
Cullen’s sign
Signs of shock
Fever
72. PANCREATITIS
Diagnostics
Elevated serum amylase and Lipase
Serum amylase falls after 48 to 72 hrs
Serum lipase remains high in 5 to 7 days
Elevated urinary amylase
Elevated serum glucose
Ultrasound
Contrast CT scan
Drop in HgB and Hct
High fecal fat contents
73. PANCREATITIS
Management
Put patient on NPO
during acute phase
Initiate parenteral
nutrition
NG suction
H2R antagonist or
PPI’s
Opioid analgesics
Fluid and electrolyte
correction
Blood transfusion
I&O
Insulin
Respiratory Care
High fowlers
Deep breathing
O2 inhalation
Surgical intervention
Low fat/Low protein diet
during the post-acute
phase
Avoid caffeine and
alcohol
74. PANCREATITIS
Focus of assessment
History of pain, food intake and alcohol
consumption
Assess for bowel sound and respiratory status
History of nausea, vomiting & characteristics of
stool
Monitor renal functioning
Signs of fluid and electrolyte disturbance
Necrosis of pancreas
Shock and multiorgan damage
