FUNCTION OF LIVER

GLUCOSE METABOLISM
One of the livers primary jobs is to store energy in the form of glycogen, which is made from a type of sugar called glucose. The liver
removes glucose from the blood when blood glucose levels are high. Through a process called glycogenesis, the liver combines the glucose
molecules in long chains to create glycogen, a carbohydrate that provides a stored form of energy. When the amount of glucose in the blood falls
below the level required to meet the bodys needs, the liver reverses this reaction, transforming glycogen into glucose.

AMMONIA CONVERSION
Use of amino acid from protein for gluconeogenesis result in the formation of ammonia as a byproduct. The liver converts this metabolically
generated ammonia into urea. Ammonia produced by the bacteria in the intestine is also removed from portal blood for urea synthesis. In this way,
the liver converts ammonia, a potential toxin, into urea, a compound that is excreted in the urine.



PROTEIN METABOLISM
It synthesizes almost all of the plasma proteins ( except gamma globulin ) including albumin, alpha globulins and beta globulins, blood
clotting factors, specific transport proteins, and most of the plasma lipo protein. Vitamin K is required by the liver for synthesis of prothrombin and
some other clotting factors. Amino acid are used by the liver for protein synthesis

FAT METABOLISM
Fatty acids can be broken down for the production of energy and ketone bodies. Ketone bodies are small compounds that can enter the
blood stream and provide a source of energy for muscles and other tissues. Breakdown of fatty acids into ketone bodies occurs primarily when the
availability of glucose for metabolism is limited. Fatty acids and their metabolic products are all used for the synthesis of cholesterol, lecithin,
lipoproteins, and other complex lipids.

VITAMINS AND IRON STORAGE
Vitamin A, B, and D and several of the B-complex vitamins are stored in large amounts in the liver. Certain substances, such as iron and
copper are also stored in the liver.

DRUG METABOLISM
Metabolism generally results in loss of activity of the medication, although in some cases activation of the medication may occur. One of the
important pathways for medication metabolism involves conjugation of the medication with a variety of compounds to form substances that are
more soluble. The conjugated products maybe excreted in the feces or urine similar to bilirubin excretion. Bioavailability is the fraction of the
administered medication that actually reaches the systemic circulation. The bioavailability of an oral medication can be decreased if the medication
is metabolized to a great extent by the liver before it reaches the systematic circulation; this is known as first pass effect.

BILE FORMATION
Bile is continuously formed by the hepatocytes and collected in the canaliculi and bile ducts. It is composed mainly of water and electrolytes
such as Sodium, Potassium, Calcium, Chloride and Bicarbonate, and it also contains significant amounts of Lecithin, Fatty Acid, Cholesterol,
Bilirubin and Bile Salts. Bile is collected and stored in the gall blader and is emptied into the intestine when needed for digestion. The functions of
bile are excretory, as in the excretion of bilirubin; bile also serves as an aid to digestion through the emulsification of fats by bile salts. Bile salts are
synthesized by the hepatocytes from cholesterol. After conjugation or binding with amino acids (taurine and glycine), they are excreted into the bile.
The bile salts, together with cholesterol and lecithin, are required for emulsification of fats in the intestine, which is necessary for efficient digestion
and absorption. Bile salts are then reabsorbed, primarily in the distal ileum, into portal blood for return to the liver and are again excreted into the

bile. This pathway from hepatocytes to bile to intestine and back to the hepatocytes is called the enterohepatic circulation. Because of the
enterohepatic circulation, only a small fraction of the bile salts that enter the intestine are excreted in the feces. This decreases the need for active
synthesis of bile salts by the liver cells.

BILIRUBIN EXCRETION
Bilirubin is a pigment derived from the breakdown of hemoglobin by cells of the reticuloendothelial system, including the Kupffer cells of the
liver. Hepatocytes remove bilirubin from the blood and chemically modify it through conjugation to glucuronic acid, which makes the bilirubin more
soluble in aqueous solutions. The conjugated bilirubin is secreted by the hepatocytes into the adjacent bile canaliculi and is eventually carried in the
bile into the duodenum. In the small intestine, bilirubin is converted into urobilinogen, which is in part excreted in the feces and in part absorbed
through the intestinal mucosa into the portal blood. Much of this reabsorbed urobilinogen is removed by the hepatocytes and i s secreted into the
bile once again (enterohepatic circulation). Some of the urobilinogen enters the systemic circulation and is excreted by the kidneys in the urine.
Elimination of bilirubin in the bile represents the major route of excretion for this compound. The bilirubin concentration in the blood may be
increased in the presence of liver disease, when the flow of bile is impeded (ie, with gallstones in the bile ducts), or with excessive destruction of
red blood cells. With bile duct obstruction, bilirubin does not enter the intestine; as a consequence, urobilinogen is absent from the urine and
decreased in the stool.


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. There are three types of cirrhosis or scarring of the liver:

Alcoholic cirrhosis: the scar tissue characteristically surrounds the portal areas. This is most frequently due to chronic alcoholism and is the most
common type of cirrhosis.

Postnecrotic cirrhosis: There are broad bands of scar tissue as a late result of a previous bout of acute viral hepatitis.

Biliary cirrhosis: Scarring occurs in the liver around the bile ducts. This type usually is the result of chronic biliary obstruction and infection
(cholangitis); it is much less common than the other two types.

The portion of the liver chiefly involved in cirrhosis consists of the portal and the periportal spaces, where the bile canaliculi of each lobule
communicate to form the liver bile ducts. These areas become the sites of inflammation, and the bile ducts become occluded with inspissated



(thickened) bile and pus. The liver attempts to form new bile channels; hence, there is an overgrowth of tissue made up largely of disconnected,
newly formed bile ducts and surrounded by scar tissue. Clinical manifestations include intermittent jaundice and fever. Initially the liver is enlarged,
hard, and irregular, but eventually it atrophies.

COMPENSATED CIRRHOSIS: Liver function may continue for sometimes even with significant scarring but metabolic abnormalities may occur
such as coagulation defects and malnutrition.

DECOMPENSATED CIRRHOSIS: progression of failure with significant complication such as portal hypertension with bleeding varices, ascites,
peritonitis, hepatorenal syndrome and enphalopathy.

Ascites
Jaundice
Weakness
Muscle wasting
Weight loss
Clubbing of fingers
Purpura due to decrease platelet count
Spontaneous breathing
Epistaxis
Hypotension
Sparse body hair
White nails
Gonadal atrophy

CLINICAL MANIFESTATION
Liver enlargement
Portal obstruction and ascites
Infection and peritonitis
Gastrointestinal varices
Edema
Vitamin deficiency and anemia
Mental deterioration




DIAGNOSTIC EXAM

Serum Bilirubin: Bilirubin result from the breakdown of hemoglobin
-elevated because of cellular disruption, or biliary obstruction, causing jaundice
Aspartate aminotransferase/alanine aminotransferase (AST/ALT): detects liver damage
-increase because of cellular damage and release of enzymes. Most specific indicator of Hepatitis as cause
Alkaline phosphate (ALP): enzyme found in high concentration in the liver cells forming the bile ducts as well as in other tissues
-elevated in biliary obstruction
Serum albumin: Protein of the highest concentration in plasma. Transport substances such as bilirbin, calcium, progesterone and drugs and
regulate osmotic pressure of blood, keeping fluid from leaking out into tissue.
-because albumin is made by the liver, decrease serum albumin may result from liver disease. Also be explained by malnutrition or low protein diet
Immunoglobulin (Ig) A, G and M: protein found in blood or other bodily fluids used by the immune system to identify and neutralize foreign object,
such as bacteria and virus
-levels are increase
Complete blood count: screening test which typically includes HgB, Hct, RBCcount, platelet count, WBC count
-HgB, Hct and RBCs count may be decrease because of bleeding or RBC distruction. Anemia is seen in hypersplenism and iron deficiency.
Leucopenia may be present as a result of hypersplenism.
Prothrombin time (PT): measures length of time required for blood sample to clot.
-prolonged of decrease production of clotting proteins and fat soluble of vitamin K deficiency leading to easy bleeding
Fibrinogen and other clotting factor: used to monitor the progression of liver disease over time
-deacrease; chronically low level seen in end stage liver disease
Blood urea nitrogen (BUN): urea is the end product of protein metabolism formed in the liver from amino acid and from ammonia compounds
-elevation indicates breakdown of blood protein and possible kidney dysfunction because of diuretic use in treatment of ascites
Serum ammonia: product of breakdown of protein which is normally converted to urea and excreted
-elevated due to inability to convert ammonia to urea
Serum glucose: one of the simple sugars in the blood which serves as primary energy source for cells
-low blood glucose(hypoglycemia) suggest impaired synthesis of glycogen from glucose(glucongenesis)

Electrolytes: substances that dissociate into ions in solution and acquire the capacity to conduct electricity. Common electrolytes include Na, K, Cl,
Ca, and Phosphate.
-low K (hypokalemia) may reflect increase aldosterone, although various imbalances may occur. Low Ca (hypokalcemia) may occur because of
impaired absorption of vitamin D.
Nutrient studies: evaluate nutritional status
-deficiency of Vitamin A, B, C and K; folic acid and iron may be noted
Viral test: determine if cirrhosis is caused by viral Hepatitis
-Hepa B, C or D may be present
OTHERS:
Abdominal ultrasonography: diagnostic technique that uses sound waves to produce an image of internal body structure
-may first assessment performed in individual with suspected liver disease to detect ascites and enlarge liver and spleen. It can also identify biliary
duct obstruction or bile stone.
Liver biopsy: biopsy can be performed via percutaneous, transjugular, laparoscopic, open operative. Samples are obtained for microscopic
evaluation
-detects fatty infiltrates, fibrosis, destruction of hepatic tissues, tumors and associated ascites
Percutaneous transhepatic cholangiography (PTHC): X-ray procedure where dye is injected directly into the drainage system of the liver. If
necessary, catheter may be inserted to allow the bile to drain into a collection bag outside the body or into the small intestine.
-shows whether there is blockage in the liver or the bile ducts that drain it. May be done to differentiate causes of jaundice or to perform biliary
drainage.
Hepatobiliary iminodiacetic acid (HIDA) scan: the client is given a radioactive tracer IV that is excreted by the liver into bile ducts
-identifies blockage in the biliary system
Urine and stool urobilinogen: serves as guide for differentiating live disease, hemolytic disease, and biliary obstruction.
-may or may not be present






DRUG
CLASSIFICATION/
DRUGS
MECHANISM OF
ACTION
INDICATION
SIDE EFFECTS/
ADVERSE EFFECTS
KEY NURSING CONSIDERATION
HISTAMINE H
2

RECEPTOR
ANTAGONISTS
cimetidine(Tagamet)
famotidine(Pepcid)
ranitidine(Zantac)
Decreases amount of
HCL produced by
stomach by blocking
action of histamine on
histamine receptors of
parietal cells in the
stomach

Hyper secretion of
stomach acids
Gastro esophageal
reflux
Short term for
duodenal ulcers
Long term prophylaxis
of duodenal ulcer
Prevention of upper GI
bleed

Confusion
Headache
Nausea
Diarrhea/constipation
Depression
Rash
Blurred vision
Hepatic/renal toxicity
Blood dyscrasia
Dont take with antacid
Inform provider of GI bleeding
No smoking, alcohol and NSAID
No to coffee, spices, chocolate and peppermint
Encourage to wear loose clothing.
Elevate head at least 6inches
Emesis or stool with blood, REPORT!
K-SPARRING
DIURETICS
spironolactone
(Aldactone)
triamterene (Dyrenium)
amiloride (Midamor)

Promote excretion of
Na and H
2
0 but retains
K in the distal renal
tubule
To decrease ascite Nausea
Diarrhea
Dizziness
Headache
Cry mouth
Rash
Photo sensitivity
Monitor i&O and daily weight
Check for fluid and electrolyte ibalance
Review for HR, BP
Evening dose not recommended for elderly
Take with/after meals in the morning
Increase risk of hypostatic hypotension
Cancel alcohol and cigarette
COLCHICINE


Decrease leukocyte
motility, phagocytosis,
lactic acid production
resulting in decrease
urate crystal deposits,
inflammatory process
Anti-inflammatory
agent.
Increase survival time
in patient with mild to
moderate cirrhosis
Oliguria
Hypersensitivity
Nasea
Vomiting
Anorexia
Cramps
Diarrhea
renal &hepatotoxicity
blood dyscrasia
Monitor i&O
Monitor CBC every 3months
Evaluate for signs of toxicity
Discontinue if patient experiences GI distress
Take with meal
Never mix with D5 water
Avoid any OTC preparation containing alcohol


DRUG STUDY

Beta adrenergic
blocker
propranolol(Inderal)
timolol(Blocadren)
metoprolol(Betaloc)
Binds with b1 and b2
adrenergic receptors
and prevent release of
catecholamine
Decrease cardiac
contractility
Decrease rennin
release
Decrease sympathetic
output
P: reduction venous
pressure, reduction
of esophageal
varices bleeding

Hypertension, angina,
MI
Fatigue
Weakness
Dizziness
Impotence
AE: bradycardia
Brochial constriction
BP too low
Agranulocytosis

Assess bradycardia
Caution on asthma, COPD and DM patient
Monitor BP
Rise slowly to reduce orthostatic hypertension
Avoid activity that requires increase alertness


Silybum marianum
(herb milk thistle)

Protects liver cell from
toxic damage,
antioxidant
Lowering cholesterol
levels
Reducing insulin
resistance in people
with type 2 diabetes
who also have
cirrhosis
Reducing the growth
of cancer cells in
breast, cervical, and
prostate cancers
Liver cirrhosis
Chronic hepatitis
Gall bladder disorder


lactulose (Cephulac) Acidification of feces
in bowel and trapping
of ammonia causing
its elimination in feces
constipation Nausea
Anorexia
Cramping
Diarrhea
Increase fluid, fiber and exercise
Mointor I&O and bowel sound
Bitter in taste: give with milk/juice
Be aware on electrolyte imbalance
VITAMIN K
Phytonadione
(AquaMEPHYTON)
For adequate blood
clotting factors
Vitamin K
malabsorption

Headache
Nausea
Hemolytic anemia
hyperbilirubinemia
Assess for bleeding: emesis, stool, urine
Assess PT during treatment
Monitor for bleeding, HR and BP
Use soft toothbrush
Avoid using floss and electric razor
Instruct to avoid IM injections














SURGICAL MANAGEMENT
Living Donor Liver Transplantation
a piece of healthy liver is surgically removed from a living person and transplanted into a recipient, immediately after the recipients diseased liver
has been entirely removed.
ANY MEMBER OF THE FAMILY, PARENT, SIBLING, CHILD, SPOUSE OR A VOLUNTEER CAN DONATE THEIR LIVER. THE CRITERIA FOR A
LIVER DONATION INCLUDE:
Being in good health
Having a blood type that matches or is compatible with the recipient's
Having a charitable desire of donation without financial motivation
Being between 18 and 60 years old
Being of similar or bigger size than the recipient
Before one becomes a living donor, the donor must undergo testing to ensure that the individual is physically fit. Sometimes CT scans or MRIs are
done to image the liver. In most cases, the work up is done in 23 weeks
THERE ARE THREE TYPES OF LIVER TRANSPLANTATION METHODS. THEY INCLUDE:
Orthotopic transplantation, the replacement of a whole diseased liver with a healthy donor liver.
Heterotrophic transplantation, the addition of a donor liver at another site, while the diseased liver is left intact.
Reduced-size liver transplantation, the replacement of a whole diseased liver with a portion of a healthy donor liver. Reduced-size liver transplants
are most often performed on children.




ST. FERDINAND COLLEGE
COLLEGE OF HEALTH SCIENCES
Calamagui 1
st
, Ilagan 3300, Isabela
Tel. No. (078) 622-3110

CHS is a holistic department with dynamic staff that intend to produce a globally
competitive health care provider

IN PARTIAL FULFILLMENT OF THE COURSE
REQUIREMENT IN NURSING CARE
MANAGEMENT 103

Prepared by:

Lerma CABANIT
Allan John CASTILLEJO
Faye Mie Velasco
BSN-III

To be checked by:

MS. CRYSTAL PAGUIRIGAN,RN,MSN
Instructress