RTRMF – BSN LEVEL III BATCH TOPAZ

NCM 116 (MEDICAL-SURGICAL NURSING II) LECTURER: Dean Gasco

Malabsorption Syndromes & 4. Over time this immune system attack and destroys the
villi
Nursing Care of Clients with 5. Damage to the villi causes digestive and other
symptoms but it can also lead to serious malnutrition
Hepatic Disorders over time
6. Damage causes by the gluten-triggered immune
TOPIC OUTLINE response will repair itself in time but only of the person
Malabsorption Syndrome with celiac disease cuts our gluten entirely.
1. Celiac Sprue
2. Short Bowel Syndrome SIGNS OF CELIAC DISEASE
Nursing Care of Clients with Hepatic Disorders  Fatigue and anemia – because the normal villi of the
1. Jaundice intestine cannot absorb nutrients properly, the person
a. Hemolytic Jaundice will suffer fatigue kay waray nutrition an tissue cells,
b. Hepatocellular Jaundice and anemia because of malabsorption
c. Obstructive Jaundice  Bone and joint pain
d. Jaundice due to hereditary hyperbilirubinemia
 Depression and anxiety – if you have severe fatigue,
2. Portal Hypertension
pirme ka nala nanluluya, you feel depressed, you feel
3. Hepa A, B, C, D, E virus
anxious
 Loss of bone density
CELIAC SPRUE
(Celiac Disease)  Headaches
 Mouth ulcers
 Aka “Gluten-Sensitive Enteropathy”  Acid reflux
 A chronic disorder of the digestive tract that results in  Heartburn
inability to tolerate gliadin  Numbness and tingling in the hands and feet
(Gliadin - the alcohol-soluble fraction of gluten)
 They cannot tolerate Gliadin
 Gluten is a protein commonly found in wheat, rye and
barley
 Most patients with celiac disease tolerate oats, but they
should be monitored closely
 They can tolerate oats, but they cannot tolerate wheat,
rye, and barley
 When people with celiac disease ingest gliadin, the
mucosa of their intestine is damaged by an
immunologically mediated inflammatory response,
resulting in maldigestion and malabsorption. The left is the normal villi of the small intestine, and the right is
 Autoimmune the damaged villi because of celiac disease. Kun sugad hito na
 Patients with celiac disease can present with failure to dikit dikit na, diri na ito maka absorb
thrive and diarrhea (the classical form)
ETIOLOGY
 Nagkakadiarrhea kay diri man nakatolerate han gluten,
and the mucus is so thick  It results from a combination of immunological
 However, some patients have only subtle symptoms (a responses to an environmental factor (gliadin) and
typical disease) or are asymptomatic (silent celiac genetic factors
disease). 1. Immune Mechanisms
2. Genetic Factors
3. IgA Deficiency: Children are 20x more likely to
develop celiac disease
4. Can be triggered by surgery

CLINICAL MANIFESTATIONS:
Age 3-9 Months
 Irritability
 Severe Diarrhea
 Vomiting
Age 9-18 Months
 Impaired Growth
 Abdominal distention
 Anorexia
 Hypotonia (loss of muscle tone)
 Abnormal stool
WHAT HAPPENS IN THE BODY WHEN SOMEONE WITH CELIAC  Mild clubbing of fingers - would occur due to anemia
EATS GLUTEN?  Vomiting commonly occurring in the evening
1. Gluten triggers an immune response against the body  Aphthous ulcers
of a person with a celiac disease. It’s called an  Dermatitis herpetiformis - similar to Henoch-Schonlein
autoimmune disorder Syndrome, or measles
2. The immune system mistakes gluten for a pathogen. Older Children
Normally the immune system only attacks foreign  Symptoms diminish or disappear in adolescent
pathogens like viruses.
3. The immune response to gluten occurs in the small MANIFESTATION SECONDARY TO MALABSORPTION
intestine  Anemia
 Vitamin Deficiency

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RTRMF – BSN LEVEL III BATCH TOPAZ
NCM 116 (MEDICAL-SURGICAL NURSING II) LECTURER: Dean Gasco

 Hypocalcemia  Asthma
 Hypomagnesemia  Blurred vision
 Hypokalemia  Fainting
 Hypothrombonemia  Dizziness
 Hear loss
 Hypertension
 Hypothyroidism
 Night sweats

COMPLICATIONS
 Risk for malignant disease is increase
 Adenocarcinoma of oropharynx esophagus, pancreas,
small and large bowel
 Enteropathy associated t cell lymphoma
 T or B cell non Hodgkin lymphoma
DIAGNOSTIC TEST
- D-xylose absorption test
- Lactose tolerance test
- Stool studies
- Endoscopy
- Ct scan
- Utz
- CBC
Oral Symptoms
- Pancreatic function test
 Halitosis
INTERVENTIONS
 Gum disease
 Focus on avoiding dietary substances that aggravate
 Mouth sores
malabsorption.
 Mouth ulcers
 Nutrient supplementation such as water-soluble
 Swollen gums
vitamins, B 12 folic acid, and fat-soluble vitamins
 Tongue sores
(ADEK), calcium, iron
Female-Specific Symptoms
 Dietary therapy is aimed at reducing gluten intake
 Breast tenderness
 Folic acid supplements are prescribed for patients with
 Early menopause
tropical sprue.
 Frequent miscarriage
 Antibiotics (eg, tetracycline [Tetracyn], ampicillin
 Heavy period
[Polycillin] are sometimes needed in the treatment of
 Infertility
tropical sprue and bacterial overgrowth syndromes.
Intestinal
 Antidiarrheal agents may be used to decrease
 Acid reflux
intestinal spasms.
 Bloating
 Parenteral fluids may be necessary to treat
 Constipation
dehydration.
 Diarrhea
GERONTOLOGICAL CONSIDERATIONS
 Loss of appetite
 The older patients may have more subtle symptoms of
 Nausea and stomach pain
malabsorption that may be extraintestinal, including
Joints And Muscles
fatigue and confusion.
 Ataxia
 Medical management may include the administration
 Joint pains
of corticosteroids, which may cause a host of adverse
 Leg cramps
effects such as hypertension, I hypokalemia and mood
 Muscle spasm
changes.
 Swelling of hands and feet
 Antibiotics _may reduce vitamin K- producing intestinal
Vitamin Deficiencies
flora, resulting in a prolonged prothrombin time
 Anemia
(PT)and international normalized ratio (IR)if the patient
 Hypomagnesemia
is concurrently taking warfarin ( Coumadin).
 Low vit D
 Urinary retention, altered mental status, or glaucoma
 Low iron
may occur as adverse effects of anticholinergic drug
Behavioral
therapy in older people.
 Anxiety
NURSING MANAGEMENT
 Depression
● The nurse provides patient and family education
 Irritability
regarding diet and the use of nutritional supplements.
 Loss of interest of activities
● It is important to monitor patients with diarrhea for
 Memory loss
fluid and electrolyte imbalances.
 Mood swings
● Patient education includes information about the risk
 Panic attack
of osteoporosis related to malabsorption of calcium.
 Suicidal
Skin
 Acne SHORT BOWEL SYNDROME
 Bruising ● The bowel is made up of two parts- the large intestine,
 Dandruff also called the colon, and the small intestine.
 Dark circle around eyes ● Without this duodenum and jejunum, the body can't
 Eczema get enough nutrients and absorb them.
 Skin cancer ● This causes bowel troubles, like diarrhea, which can be
 Rashes dangerous if you go without treatment.
Others CAUSES

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RTRMF – BSN LEVEL III BATCH TOPAZ
NCM 116 (MEDICAL-SURGICAL NURSING II) LECTURER: Dean Gasco

● Short bowel syndrome in adults and children is usually ○ Increase in the diameter of the small intestine
caused by surgery. ○ Slow down in peristalsis or movement of food
● This surgery may be done for: through the small intestine.
○ Crohn' s disease, an inflammatory disorder of TREATMENT
the digestive tract ● Vitamins and minerals
○ Volvulus, a spontaneous twisting of the small ● Small frequent feedings
intestine that cuts off the blood supply and ● Extra fluids
leads to tissue death. ● IV feeding tubes directly into the stomach
○ Tumors of the small intestine
○ Injury or trauma to the small intestine. DRUG INCLUDE:
○ Necrotizing Enterocolitis [premature ● Teduglutide (Gaffex), Doctors may prescribe this
newborn] hormone for adults with more serious cases of short
○ Bypass surgery to treat obesity bowel syndrome who need IV feeding tubes.
Surgery to remove diseases or damaged portion of the small ● L-glutamine, a powder that you can mix with water
intestine and drink.
● These drugs help the small intestine absorb more
• Some children are also born with an abnormality short small nutrients and water.
intestine known as congenital short bowel
JAUNDICE
 Also known as Icterus, occurs when the bilirubin
SIGNS AND SYMPTOMS
concentration in the blood is abnormally elevated, all
● The symptoms and short bowel syndrome can include:
the body tissues, including the sclerae and the skin,
○ Abdominal pain
become tinged yellow or greenish-yellow.
○ Diarrhea and steatorrhea (oily, bulky stool,
 Becomes clinically evident when the serum bilirubin
which can be malodorous)
level exceeds 2.5 mg/dL (43 fmol/L).
○ Fluid depletion
It may result from:
○ Weight loss and malnutrition
• Impairment of hepatic uptake.
○ Fatigue
• Conjugation of bilirubin.
○ Cramping
• Excretion of bilirubin into the biliary system.
○ Bloating
○ Heartburn TYPES OF JAUNDICE
○ Persons with short bowel system syndrome 1. Hemolytic Jaundice
may have complications caused by 2. Hepatocellular Jaundice
malabsorption of vitamins and minerals, such 3. Obstructive Jaundice
as deficiencies in vitamins A, D,E, K, B [Folic 4. Jaundice due to hereditary hyperbilirubinemia.
acid, and B12, calcium, magnesium, iron and
ZInC. HEMOLYTIC JAUNDICE
- The result from increased destruction of red blood cells
THESE MAY APPEAR AS: in circulation or the precursors of the red blood cells in
● Anemia the bone marrow leading to the yellowish discoloration of
● Hyperkeratosis (scaling of the skin) the eyes, skin, and mucous membranes.
● Easy bruising - This increased destruction of the red blood cells leads to
● Muscle spasms elevated levels of bilirubin in the blood
● Poor blood clothing (Hyperbilirubinemia).
● Bone pain or osteoporosis (thinning and fragile bones) - Unconjugated bilirubin – type of bilirubin released in
● Fatty liver hemolytic jaundice.
● Kidney stones - Fecal and urine urobilinogen levels are increased, but the
● Gallstones urine is free of bilirubin.
- Pts with this type of jaundice, unless their
DIAGNOSIS hyperbilirubinemia is extreme, do not experience
● Blood tests symptoms or complications as a result of the jaundice.
● Stool exam - Prolonged jaundice predisposes to the formation of
● X-rays of your chest and belly pigment stones in the gallbladder.
● Upper Gi series is also called a barium X-ray. You' II - Extremely severe jaundice (levels of free bilirubin exceeding
drink a special liquid that coats your throat, stomach 20 to 25 mg/dL) poses a risk or brainstem damage.
and small intestine to make them stand out on the X-
ray image. If the bilirubin crosses the blood brain barrier is called
● CT scan, an X-ray that makes detailed pictures inside KERNICTERUS
your body
● Ultrasound, which uses sound waves to make images CAUSES:
of your organs 1. Severe anemia
● Bone density test 2. Sickle cell anemia
● Liver biopsy, when doctors remove a piece of tissue for 3. Spherocytosis
testing. Most of the time, doctors make a small cut on 4. Thalassemia
your belly and use a hollow needle to get the cells they 5. Pyruvate kinase deficiency
need. They use a CT scan or an ultrasound to see 6. Glucose 6-phosphate dehydrogenase deficiency
where to place the needle. The biopsy takes about 5
HEPATOCELLULAR JAUNDICE
minutes, but you may need a few hours to recover.
 It is caused by the inability of damaged liver cells to
clear normal amounts of bilirubin from the blood.
● Short Bowel Syndrome when there is less than 2
 It is caused by the inability of damaged liver cells to
meters or less than 6 feet.
clear normal amounts of bilirubin from the blood.
○ Enlargement and lengthening of the villi
found in the lining CAUSES:
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RTRMF – BSN LEVEL III BATCH TOPAZ
NCM 116 (MEDICAL-SURGICAL NURSING II) LECTURER: Dean Gasco

The cellular damage may be caused by:  Skin may itch intensely, requiring repeated soothing
1. Acute or chronic hepatitis baths pruritus in skin because of the presence of bile
2. Hepatoxicity salts
3. Cirrhosis due to alcohol  Dyspepsia
4. Other viruses that affect the liver such as yellow fever  Intolerance to fatty foods because fat is emulsified by
virus, Epstein-Bar virus. bile therefore absence of bile results to diarrhea
5. Medications or chemical toxins such as carbon
 AST, ALT, and GGT level rise only moderately
tetrachloride, chloroform, phosphorus, arsenicals,
 Bilirubin and alkaline phosphatase levels are elevated
certain medications.
DIAGNOSTIC EXAMS
SIGNS & SYMPTOMS:
 Bilirubin tests
1. Mildly or severely ill
 CBC
2. Lack of appetite
3. Nausea  Hepatitis A, B, and C tests
4. Malaise  MRI, CT, and Ultrasound scans
5. Fatigue  Endoscopic Retrograde Cholangiopancreatography
6. Weakness (ERCP)
7. Weight loss  Liver biopsy
DIAGNOSTIC FINDINGS: COMPLICATIONS
1. The serum bilirubin concentration and the urine  Bleeding
urobilinogen level may be elevated.  Anemia
2. AST and ALT levels may be increased – indicating  Infectious
cellular necrosis.  Abnormal bloating
3. The pt may report headache, chills, and fever if the  Swelling of legs
cause is infectious.
 Liver failure
OBSTRUCTIVE JAUNDICE  Diarrhea
 Obstructive jaundice resulting from extrahepatic  Kidney failure
obstruction may be caused by occlusion of the bile duct  Constipation
from a gallstone, an inflammatory process, a tumor, or  Abdominal pain
pressure from an enlarged organ (e.g., liver,  Flatulence
gallbladder). The obstruction may also involve the small MANAGEMENT
bile ducts within the liver (i.e., intrahepatic obstruction);  Anemia-induced jaundice may be treated by boosting
this may be caused, for example, by pressure on these the amount of iron in the blood by either taking iron
channels from inflammatory swelling of the liver or by supplements or eating iron-rich foods.
an inflammatory exudate within the ducts themselves.  Hepatitis-induced jaundice requires antiviral or steroid
Extrahepatic obstruction may be due to stones in the medications.
biliary duct. Inflammatory process, inflammation  Obstruction-induced jaundice can be treated by
therefore it swells. Tumor, at the biliary duct. Pressure surgically removing the obstruction.
from liver (hepatomegaly) or from the gallbladder.
- Intrahepatic obstruction it could result from stasis or PORTAL HYPERTENSION
thickening of bile (inspissation) within the canalicalculi - The portal circulation in the liver is damaged or
congested.
and ingestion of certain medications which are
- If the blood goes to the esophagus esophageal varices
cholestatic agents.
may occur
- The liver is congested kay impaired an circulation an
MEDICINES THAT MAY CAUSE OBSTRUCTIVE JAUNDICE:
blood makadi ha peritoneal area which leads to Ascites.
 Phenothiazines - There will be collateral distribution of blood leading to
 Antithyroid medications caput medusa
 Sulfonylureas for diabetes - After the shunting from the artery to the vein mechanical
 Tricyclic antidepressant agents obstruction.
 Nitrofurantoin - Then hypersplenism meaning splenomegaly leading to
anemia, leukocytopenia and thrombocytopenia and liver
 Erythromycin estolate
failure.
 Androgens and estrogens
- This is the increase pressure throughout the portal
 Propylthiouracil venous system that results from obstructions of blood
 Amoxicillin-clavulanic acid flow into and through the damaged liver.
- Elevation of hepatic venous pressure to 5mmhg then
OTHER CAUSES: the gradient exceeds 10 mmHg. Risk of variceal
 Gallstones in the common bile duct bleeding the gradient is increased to 12 mmhg.
MANAGEMENT OF PORTAL PRESSURE
 Pancreatic cancer
- Hepatic venous pressure gradient (HVPG) the
 Strictures of the common bile duct difference between wedged hepatic venouse pressure
 Biliary atresia absence of the biliary duct and free hepatic venous pressure.
 Cholangiocarcinoma cancer of the biliary - Measurement is made by inflating and deflating the
 Pancreatitis inflammation balloon in the tip of the catheter, introduced through
 Pancreatic pseudocysts pseudocysts are false cysts in internal jugular and femoral vein.
the pancreas
ANATOMY OR PORTAL VENOUSE SYSTEM

SIGNS AND SYMPTOMS

 Deep orange and foamy urine because of bile
 Light or clay-colored stools because of absence of bile

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NCM 116 (MEDICAL-SURGICAL NURSING II) LECTURER: Dean Gasco

DIAGNOSTIC EXAM:
 Ultrasound
 MRI
 Doppler
 CT Scan
TREATMENT OR MEDICATION:
 Medication to control hypertension
 Diuretic
 To decrease fluid retention

ASCITES
 Ascites in portal hypertension
 Portal hypertension is because of cirrhosis
Portal hypertension will cause splanchnic vasodilation that in
- Portal vein is formed by the union of the superiroir return will cause decreased in circulating arterial blood volume
mesenteric vein and the splenic vein just posterior to which will cause less supply of blood in the kidneys and the
the head of the pancrease at the level of second glomerulus will be damaged. When the glomerulus is damaged,
lumbar vertebra/ Renin is released and this will activate the RAAS to compensate
- Portal blood flow in man is about 1000 to 1200 ml/min for the low blood pressure to the point that it will increase the
blood pressure too much that it will lead to hypertension. In
CLASSIFICATION AND CAUSES: RAAS, the kidney retains sodium which leads to water retention
1. PREHEPATIC therefore edema.
 Portal Vein Thrombosis
 Splenic Vein Thrombosis CAUSES OF CIRRHOSIS:
 Massive Splenomegaly  Schistosomiasis
2. HEPATIC  Alcohol
1. Presinusoidal: Schistomiasis, Congenital Hepatic  Fibrosis
Fibrosis
2. Sinusoidal: Cirrhosis of Liver, Alcoholic Hepatitis MANIFESTATION:
3. Postsinusoidal: Hepatic Sinusoidal Obstruction (veno-  Increased abdominal girth
occlusive syndrome) Iton Fibrosis natikang anay hito  Rapid weight gain due to ascites and edema
fatty liver, katapos hit fatty liver- fibrosis kahuman hito  Shortness of breath because the diaphragm is
Cirrhosis. compressed by the ascites therefore there is reduced
3. POSTHEPATIC lung expansion
 Budd-Chiari Syndrome  Striae due to collateral circulation of the distended
 Inferior Vena Cava Obstruction veins
 Cardiac causes: Restrictive cardiomyopathy,  Umbilical hernia also due to collateral circulation of
constrictive pericarditis, severe congestive cardiac occluded veins
failure
ASSESSMENT:
PATHOPHYSIOLOGY:  Percuss the abdomen
Normal Blood Flow to and from the liver depends on proper  Fluid wave test
functioning of the:  Daily measurement of abdominal girth
o Portal Vein (70% of inflow)  Daily measurement of body weight
o Hepatic artery (30% of inflow)
o Hepatic veins (outflow) TREATMENT OR MEDICAL MANAGEMENT
 Portal Hypertension results either from increased  Dietary modification
blood flow in the portal vein or from an increased  Low sodium diet
resistance to flow within the portal venous system  Diuretics (Spinorolactol)
 The most common cause of portal hypertension is  Bedrest
cirrhosis  Upright posture
 The pathophysiologic mechanism in cirrhosis is  Paracentesis
increased resistance, which is intrahepatic and  Transjugular Intrahepatic portosystemic shunt -
primarily sinusoidal. method in treating ascites, cannula or catheter is
 Portal Hypertension may also arise from pre-sinusoidal inserted to the portal vein and a stent is placed as a
obstruction, either outside the liver (as in portal vein bypass so the flow of blood can go to the hepatic veins
thrombosis) or within it (as in Schistomiasis) and supply the digestive tract specially the kidney.
 In addition, lesions leading to portal hypertension may DOCUMENTATION:
be Postsinusoidal, either within the liver (as in veno-  Measuring abdominal girth
occlusive disease) or distal to it (as in Budd-Chiari  Intake and Output
Syndrome or Right Heart failure)  Measure fluid electrolytes
 Normal portal venous pressure is 5 to 10 mmHg
 Pressure rises 5 mmHg higher than the inferior vena HEPATITIS A (Infectious Hepatitis/Catarrhal Jaundice)
cava pressure  It is an inflammation of the liver that is not only severe
and runs in acute course.
CLINICAL MANIFESTATIONS:  This is known as infectious hepatitis because it spreads
 Tortuous epigastric vessels that branch off the area of relatively easy to individuals who have close contact
the umbilicus and lead toward the sternum and ribs with the infected.
(caput medusae)
SIGNS & SYMPTOMS:
 Enlarged palpable spleen
 Fever
 Internal Hemorrhoids
 Fatigue
 Bruits
 Nausea

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RTRMF – BSN LEVEL III
NCM 116 (MEDICAL-SURGICAL NURSING II)
 Loss of appetite
 Jaundice (yellowing of the skin or eyes)
 Stomach pain
 Vomiting
 Dark urine, pale stools, and diarrhea
ETIOLOGY
 It is caused by a VIRUS. The virus is resistant to a
temperature of 132.4 F (56 C) for 30 minutes.
INCUBATION PERIOD:
 Ranges from 15 to 60 days, or 3 to 5 weeks, with a
mean of incubation period of 25 days.
SOURCE OF INFECTION:
 Discharges from the alimentary tracts of infected
person and human blood are the chief source of
infection. And if you are eating, you can tell it is
contaminated (milk, water, and seafoods
 It has been approved to be present in the urine or in
the nasopharynx, but it has been found in the blood.
MODE OF TRANSMISSION:
 The virus can be transmitted through the oralfecal
pathway:
1. Ingestion of contaminated drinking water or ice,
uncooked fruits and vegetables, and fruits and vegetables
grown in or washed with contaminated water.
2. Contamination of food or drinks by infected food
handlers.
 The most frequent modes of transmission have been
through blood or blood products and by the use of
improperly sterilized syringes, needles and other
instruments subject to contamination with blood and
those used for skin puncture.
PATHOLOGY/PATHOGENESIS:
1. Following ingestion, HAV enters the blood stream
through the epithelium of the oropharynx and the
intestines.
2. The blood carries the virus to its target, the liver, where
it lives and multiplies within the hepatocytes and
Kupffer cells.
3. Virions are secreted into the bile and released in stools.
HAV is excreted in large quantities approximately 11
days prior to the appearance of symptoms or anti-HAV
IgM antibodies in the blood.
CLINICAL MANIFESTATION:
1. Flu-like illness with chills and high fever.
2. Diarrhea, fatigue and abdominal pain.
3. Loss of appetite.
4. Nausea and fever.
5. Jaundice and dark-colored urine.
6. The infection in young children is often mild and
asymptomatic.
7. HAV does not have a chronic stage and does not cause
permanent liver damage.
8. Following infection, the immune system makes
antibodies against the HAV that confer immunity
against future infection.
COMPLICATIONS:
1. Progressive encephalopathy characterized by
drowsiness and cerebral edema.
2. GIT bleeding progressing to stupor and later coma.
Bleeding is not responsive to vitamin K administration.
3. Clonus and hyperreflexia are later replaced by loss of
deep tendon reflexes.
Differential Diagnosis:
1. Prodromal Stage
 The disease must be differentiated from a variety of
infections including:
1. Typhoid fever
2. Dysentery kay mayda eni hiya diarrhea
3. Malaria
4. Infectious mononucleosis
5. Acute abdominal conditions
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BATCH TOPAZ
LECTURER: Dean Gasco
 When the jaundice is present, Weil’s disease, yellow
fever, infectious mononucleosis, the jaundice which
occurs in other acute infections, hemolytic jaundice
and surgical disease of the extrahepatic biliary tract
must be considered.
DIAGNOSTIC TEST:
1. HAV and HBV – compliment fixation rate.
2. Liver function test
3. Bile examination of stool and urine samples.
4. SGOT (serum glutamic oxaloacetic transaminase)
5. SGPT (serum glutamic pyruvic transaminase)
6. ALT (serum alanine transaminase)
7. IgM level
PERIOD OF COMMUNICABILITY:
 The infected patient is capable of transmitting the
organisms from a week before until a week
appearance of the symptoms.
TREATMENT
1. Bed rest is essential
2. Diet must be high in carbohydrates, low in fat and low
in protein.
3. Pt must take vitamin supplements, especially the B
complex group.
4. Intravenous therapy is occasionally necessary.
5. ISOPRINOSINE (METHOSIPRENOL) may enhance the
cell-mediated immunity of the Tlymphocytes.
6. Alkalies, belladona and anti-emetics should be
administered to control dyspepsia and malaise.
NURSING MANAGEMENT
1. Pt must be isolated (enteric isolation).
2. Pt should be encouraged to rest during the acute or
symptomatic phase.
3. Pt’s nutritional status must be improved.
4. Appropriate measures to minimize spread of the
disease must be taken.
5. Observe the pt for melena and check stools for the
presence of blood.
PREVENTION:
1. Vaccines
2. Clean water
3. Safe sex
4. Personal hygiene
5. Sanitation
6. New needles and syringes
HEPATITIS B (Serum Hepatitis)
 This is considered to be more serious than Hepatitis A
due to possibility of severe complications such as
massive damage and hepatocarcinoma of the liver.
After 5 years of contructing Hepa B, expect
hepatocarcinoma.
 It is the inflammation of the liver caused by Hepatitis B
virus.
ETIOLOGY:
 The disease is caused by the Hepatitis B virus.
 The virus has a very limited tissue tropism.
 HBV infects the liver and possibly the pancreas.
 HBsAg appears in the blood 30 to 60 days after
exposure and persistent for variable period of time.
INCUBATION PERIOD:
- 50 to 189 days or 2 to 5 months with a mean equal to
90 days.
MODE OF TRANSMISSION:
- HBV can be directly transmitted by person to person
contact via infected body fluids.
- It can be transmitted through contaminated needles
and syringes. Through infected blood or body fluids
introduced at birth.
- Through sexual contact.
PATHOGENESIS:
- HBV primarily interferes with the functions of the liver
by replicating in liver cells, known as hepatocytes.
- During HBV infection, the host immune response
causes both hepatocellular age and viral clearance.
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NCM 116 (MEDICAL-SURGICAL NURSING II) LECTURER: Dean Gasco

- The virus replication may be as soon as 3 days from SIGNS AND SYMPTOMS
acquisition, but symptoms may not be observed until Assessment findings are similar for the different types of
after 45 days or much longer. hepatitis. PROGRESS IN THREE STAGES:
- Replication of the virus is not cytopathic or proceeds
for relatively long periods without causing liver 1. Prodromal Stage
damage. - May complaint of easy fatigue, anorexia, body malaise,
- During the acute phase of infection, the liver headache.
parenchyma shows degenerative changes consisting of - Arthralgia, myalgia, photophobia, and nausea and
cellular swelling and necrosis, especially in vomiting
hepatocytes. - Changes in pt. senses of smell and taste. - moderate
CLINICAL MANIFESTATIONS: fever from 37.8-38.9 C.
1. Prodromal Stage - Urine may become dark colored and stools are clay
 Fever, malaise and anorexia. colored.
 Nausea, vomiting, abdominal discomfort, fever and
chills. 2. Clinical Jaundice Stage
 Jaundice, dark colored urine, and pale stools. - Pruritus, abdominal pain or tenderness and
 Right sided abdominal pain. indigestion.
 Recovery is indicated by a decline of fever and - Yellowish discoloration of sclerodermatous membrane
improved appetite. and the skin, which can last for 1 to 2 weeks.
- Rashes, erythematous patches and urticaria. Pain,
COMPLICATIONS: tenderness of the RUQ, and enlarged and tender liver,
1. Cirrhosis splenomegaly and cervical adenopathy are present.
2. Liver cancer 3. Recovery Stage
3. Fulminant Hepatitis may be fatal and manifested by - Most of the pt’s symptoms decrease or subside.
severe symptoms like ascites and bleeding. Recovery commonly last for 2 to 12 weeks
DIAGNOSTIC PROCEDURES:
1. Compliment fixation test DIAGNOSIS:
2. Radio-immunoassay-hemagglutinin test. 1. Hepatitis C: diagnosis depends on serologic testing for
3. Liver function test the specific antibody, one or more months after the
4. Bile examination in blood and urine. onset of acute hepatitis.
5. Blood count COMMON NURSING DIAGNOSIS:
6. Serum transaminase – SGOT, SGPT, ALT. • Knowledge deficit
7. HBsAg • Low self-esteem
TREATMENT: • Body image disturbance
1. Antiviral medication (TENOFOVIR, INTERFERON) • Risk for infection
2. Liver transplantation • Impaired skin integrity
PREVENTION: • Altered nutrition: less than body requirement
1. Vaccines • Social isolation
2. Clean water
3. Safe sex HEPATITIS D
4. Personal hygiene - Also called (DELTA VIRUS) is a small, circular RNA virus.
5. Sanitation - It is a replication-defective and therefore cannot
6. New needles and syringes propagate in the absence of another virus.
NURSING MANAGEMENT: - Hepatitis D infection occurs only in the presence of
1. Blood donors must be screened to exclude carriers. hepatitis B infection.
2. Caution must be observed in giving care to patients - This can be transmitted by blood and blood products
infected with HBV. - A patient can acquire hepatitis D infection at the same
3. Hands and other skin areas must be washed time that he/she is infected with the hepatitis B virus.
immediately and thoroughly after contact with body - A patient can also be infected with hepatitis D virus at
fluids. any time during acute hepatitis B virus infection.
4. Avoid injury with sharp objects or instruments. 5. Use
disposable needles and syringes only once and discard SIGNS & SYMPTOMS:
properly - Assessment findings are similar for the different types
5. Avoid sharing toothbrushes, razors and other of hepatitis. Signs and symptoms progress in three
instrument that may be contaminated with blood. stages.
6. Practice safe sex. 1. Prodromal Stage
7. Get adequate rest, sleep, and exercise and eat - May complaint of easy fatigue, anorexia, body malaise,
nutritious foods. headache.
8. Hepatitis B vaccines is recommended for pre-exposure. - Arthralgia, myalgia, photophobia, and nausea and
9. HBIg should be administered within 72 hours to those vomiting
exposed directly to Hepatitis B by either ingestion, - Changes in pt. senses of smell and taste. - moderate
prick or inoculation. fever from 37.8-38.9 C.
- Urine may become dark colored and stools are clay
HEPATITIS C colored.
- It is a blood-borne infectious disease caused by 2. Clinical Jaundice Stage
hepatitis C virus (HCV) - Pruritus, abdominal pain or tenderness and
- Known as "non-A, non-B hepatitis. indigestion.
- Asymptomatic, but once established, can cause - Yellowish discoloration of sclerodermatous membrane
scarring of the liver (fibrosis) and eventually, cirrhosis and the skin, which can last for 1 to 2 weeks
(advance scarring). - Rashes, erythematous patches and urticaria.
- With a higher rate of chronic liver disease (chronic - Pain, tenderness of the RUQ, and enlarged and tender
hepatitis liver, splenomegaly and cervical adenopathy are
- Cirrhosis, and an increase risk for hepatocellular present.
carcinoma). 3. Recovery Stage
- Client with chronic hepatitis C are considered - Most of the pt’s symptoms decrease or subside.
infectious. - Recovery commonly last for 2 to 12 weeks
- No vaccine is available for hepatitis C.

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RTRMF – BSN LEVEL III BATCH TOPAZ
NCM 116 (MEDICAL-SURGICAL NURSING II) LECTURER: Dean Gasco

DIAGNOSTIC PROCEDURES: COMMON NURSING DIAGNOSIS:

1. Compliment fixation test • Knowledge deficit
2. Radio-immunoassay-hemagglutinin test. • Low self-esteem
3. Liver function test • Body image disturbance
4. Bile examination in blood and urine. • Risk for infection
5. Blood count • Impaired skin integrity
6. Serum transaminase – SGOT, SGPT, ALT. • Altered nutrition: less than body requirement
7. HBsAg • Social isolation
TREATMENT: PREVENTION:
1. Antiviral medication (TENOFOVIR, INTERFERON) 1. Vaccines
2. Liver transplantation 2. Clean water
DIAGNOSIS: 3. Safe sex
- Hepatitis D: detection of intrahepatic delta or 4. Personal hygiene
immunoglobulin M (IgM) establishes the diagnosis. 5. Sanitation
COMMON NURSING DIAGNOSIS: 6. New needles and syringes
• Knowledge deficit
• Low self-esteem
• Body image disturbance END
• Risk for infection
• Impaired skin integrity
• Altered nutrition: less than body requirement
• Social isolation

HEPATITIS E
 Transmitted through fecal-oral and waterborne routes),
like hepatitis A.
 Inconsistently shed in stool; therefore, detection is
difficult. Because sometimes it is not seen in stool.
 Fulminant liver failure may cause death.
 Pregnant Women are at a much higher risk of dying
from fulminant liver failure.
 The great majority of patient who recover from acute
infection do not continue to carry HEV and cannot pass
the infection to others.

SIGNS & SYMPTOMS:

 Assessment findings are similar for the different types
of hepatitis. Signs and symptoms progress in three
stages.
1. Prodromal Stage
- May complaint of easy fatigue, anorexia, body
malaise, headache
- Arthralgia, myalgia, photophobia, and nausea and
vomiting
- Changes in pt. senses of smell and taste. -moderate
fever from 37.8-38.9 C.
- Urine may become dark colored and stools are clay
colored.
2. Clinical Jaundice Stage
- Pruritus, abdominal pain or tenderness and
indigestion.
- Yellowish discoloration of sclerodermatous membrane
and the skin, which can last for 1 to 2 weeks.
- Rashes, erythematous patches and urticaria.
- Pain, tenderness of the RUQ, and enlarged and tender
liver, splenomegaly and cervical adenopathy are
present.
3. Recovery Stage
- Most of the pt’s symptoms decrease or subside.
- Recovery commonly last for 2 to 12 weeks.

TREATMENT:
1. Antiviral medication (TENOFOVIR, INTERFERON)
2. Liver transplantation
DIAGNOSTIC TEST:
• Compliment Fixation Test
• Radio-immunoassay-hemaglutinin test
• Liver function test
• Bile examination Test
• Blood count
• Serum transaminase – SGOT (Glutamic-Oxaloacetic
Transaminase), SGPT (Serum Glutamic Pyruvic
Transaminase) , ALT (Alanine Transaminase)
• HBsAg
DIAGNOSIS:
- Hepatitis D: detection of E antigen supports the
diagnosis.

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