RTRMF – BSN LEVEL III BATCH TOPAZ

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

Malabsorption Syndromes & WHAT HAPPENS IN THE BODY WHEN SOMEONE WITH
CELIAC EATS GLUTEN?
Nursing Care of Clients with 1. Gluten triggers an immune response against the
body of a person with a celiac disease. It’s called an
Hepatic Disorders autoimmune disorder
2. The immune system mistakes gluten for a pathogen.
TOPIC OUTLINE Normally the immune system only attacks foreign
Malabsorption Syndrome pathogens like viruses.
1. Celiac Sprue 3. The immune response to gluten occurs in the small
2. Short Bowel Syndrome intestine
Nursing Care of Clients with Hepatic Disorders 4. Over time this immune system attack and destroys
1. Jaundice the villi
a. Hemolytic Jaundice 5. Damage to the villi causes digestive and other
b. Hepatocellular Jaundice symptoms but it can also lead to serious malnutrition
c. Obstructive Jaundice over time
d. Jaundice due to hereditary hyperbilirubinemia
6. Damage causes by the gluten-triggered immune
2. Portal Hypertension
response will repair itself in time but only of the
3. Hepa A, B, C, D, E virus
person with celiac disease cuts our gluten entirely.

CELIAC SPRUE
(Celiac Disease) SIGNS OF CELIAC DISEASE
 Fatigue and anemia – because the normal villi of the
 Aka “Gluten-Sensitive Enteropathy” intestine cannot absorb nutrients properly, the
 A chronic disorder of the digestive tract that results person will suffer fatigue kay waray nutrition an
in inability to tolerate gliadin tissue cells, and anemia because of malabsorption
(Gliadin - the alcohol-soluble fraction of gluten)  Bone and joint pain
 They cannot tolerate Gliadin  Depression and anxiety – if you have severe fatigue,
 Gluten is a protein commonly found in wheat, rye pirme ka nala nanluluya, you feel depressed, you feel
and barley anxious
 Most patients with celiac disease tolerate oats, but  Loss of bone density
they should be monitored closely  Headaches
 They can tolerate oats, but they cannot tolerate  Mouth ulcers
wheat, rye, and barley  Acid reflux
 When people with celiac disease ingest gliadin, the  Heartburn
mucosa of their intestine is damaged by an  Numbness and tingling in the hands and feet
immunologically mediated inflammatory response,
resulting in maldigestion and malabsorption.
 Autoimmune
 Patients with celiac disease can present with failure
to thrive and diarrhea (the classical form)
 Nagkakadiarrhea kay diri man nakatolerate han
gluten, and the mucus is so thick
 However, some patients have only subtle symptoms
(a typical disease) or are asymptomatic (silent celiac
disease).

The left is the normal villi of the small intestine, and the right is
the damaged villi because of celiac disease. Kun sugad hito na
dikit dikit na, diri na ito maka absorb

ETIOLOGY

 It results from a combination of immunological

responses to an environmental factor (gliadin) and
genetic factors
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
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NCM 116 (MEDICAL-SURGICAL NURSING II) LECTURER: Dean Gasco

 Vomiting  Leg cramps

Age 9-18 Months  Muscle spasm
 Impaired Growth  Swelling of hands and feet
 Abdominal distention Vitamin Deficiencies
 Anorexia  Anemia
 Hypotonia (loss of muscle tone)  Hypomagnesemia
 Abnormal stool  Low vit D
 Mild clubbing of fingers - would occur due to anemia  Low iron
 Vomiting commonly occurring in the evening Behavioral
 Aphthous ulcers  Anxiety
 Dermatitis herpetiformis - similar to Henoch-  Depression
Schonlein Syndrome, or measles  Irritability
Older Children  Loss of interest of activities
 Symptoms diminish or disappear in adolescent  Memory loss
 Mood swings
MANIFESTATION SECONDARY TO MALABSORPTION  Panic attack
 Anemia  Suicidal
 Vitamin Deficiency Skin
 Hypocalcemia  Acne
 Hypomagnesemia  Bruising
 Hypokalemia  Dandruff
 Hypothrombonemia  Dark circle around eyes
 Eczema
 Skin cancer
 Rashes
Others
 Asthma
 Blurred vision
 Fainting
 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
Oral Symptoms
DIAGNOSTIC TEST
 Halitosis
- D-xylose absorption test
 Gum disease
- Lactose tolerance test
 Mouth sores
- Stool studies
 Mouth ulcers
- Endoscopy
 Swollen gums
- Ct scan
 Tongue sores
- Utz
Female-Specific Symptoms
- CBC
 Breast tenderness
- Pancreatic function test
 Early menopause
INTERVENTIONS
 Frequent miscarriage
 Focus on avoiding dietary substances that aggravate
 Heavy period
malabsorption.
 Infertility
 Nutrient supplementation such as water-soluble
Intestinal
vitamins, B 12 folic acid, and fat-soluble vitamins
 Acid reflux
(ADEK), calcium, iron
 Bloating
 Dietary therapy is aimed at reducing gluten intake
 Constipation
 Folic acid supplements are prescribed for patients
 Diarrhea
with tropical sprue.
 Loss of appetite
 Antibiotics (eg, tetracycline [Tetracyn], ampicillin
 Nausea and stomach pain
[Polycillin] are sometimes needed in the treatment of
Joints And Muscles
tropical sprue and bacterial overgrowth syndromes.
 Ataxia
 Antidiarrheal agents may be used to decrease
 Joint pains
intestinal spasms.
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NCM 116 (MEDICAL-SURGICAL NURSING II) LECTURER: Dean Gasco

 Parenteral fluids may be necessary to treat ○ Cramping

dehydration.
GERONTOLOGICAL CONSIDERATIONS
 The older patients may have more subtle symptoms
of malabsorption that may be extraintestinal,
including fatigue and confusion.
 Medical management may include the
administration of corticosteroids, which may cause a
host of adverse effects such as hypertension, I
hypokalemia and mood changes.
 Antibiotics _may reduce vitamin K- producing
intestinal flora, resulting in a prolonged prothrombin
time (PT)and international normalized ratio (IR)if the
patient is concurrently taking warfarin ( Coumadin).
 Urinary retention, altered mental status, or glaucoma
may occur as adverse effects of anticholinergic drug
therapy in older people.
NURSING MANAGEMENT
● The nurse provides patient and family education
regarding diet and the use of nutritional
supplements.
● It is important to monitor patients with diarrhea for
fluid and electrolyte imbalances.
● Patient education includes information about the risk
of osteoporosis related to malabsorption of calcium.
SHORT BOWEL SYNDROME
● The bowel is made up of two parts- the large
intestine, also called the colon, and the small
intestine.
● Without this duodenum and jejunum, the body can't
get enough nutrients and absorb them.
● This causes bowel troubles, like diarrhea, which can
be dangerous if you go without treatment.
CAUSES
● Short bowel syndrome in adults and children is
usually caused by surgery.
● This surgery may be done for:
○ Crohn' s disease, an inflammatory disorder
of the digestive tract
○ Volvulus, a spontaneous twisting of the
small intestine that cuts off the blood
supply and leads to tissue death.
○ Tumors of the small intestine
○ Injury or trauma to the small intestine.
○ Necrotizing Enterocolitis [premature
newborn]
○ Bypass surgery to treat obesity
Surgery to remove diseases or damaged portion of the small
intestine
• Some children are also born with an abnormality short small
intestine known as congenital short bowel
SIGNS AND SYMPTOMS
● The symptoms and short bowel syndrome can
include:
○ Abdominal pain
○ Diarrhea and steatorrhea (oily, bulky stool,
which can be malodorous)
○ Fluid depletion
○ Weight loss and malnutrition
○ Fatigue
○ Bloating
○ Heartburn
○ Persons with short bowel system syndrome
may have complications caused by
malabsorption of vitamins and minerals,
such as deficiencies in vitamins A, D,E, K, B
[Folic acid, and B12, calcium, magnesium,
iron and ZInC.
THESE MAY APPEAR AS:
● Anemia
● Hyperkeratosis (scaling of the skin)
● Easy bruising
● Muscle spasms
● Poor blood clothing
● Bone pain or osteoporosis (thinning and fragile
bones)
● Fatty liver
● Kidney stones
● Gallstones
DIAGNOSIS
● Blood tests
● Stool exam
● X-rays of your chest and belly
● Upper Gi series is also called a barium X-ray. You' II
drink a special liquid that coats your throat, stomach
and small intestine to make them stand out on the X-
ray image.
● CT scan, an X-ray that makes detailed pictures inside
your body
● Ultrasound, which uses sound waves to make images
of your organs
● Bone density test
● Liver biopsy, when doctors remove a piece of tissue
for testing. Most of the time, doctors make a small
cut on your belly and use a hollow needle to get the
cells they need. They use a CT scan or an ultrasound
to see where to place the needle. The biopsy takes
about 5 minutes, but you may need a few hours to
recover.
● Short Bowel Syndrome when there is less than 2
meters or less than 6 feet.
○ Enlargement and lengthening of the villi
found in the lining
○ Increase in the diameter of the small
intestine
○ Slow down in peristalsis or movement of
food through the small intestine.
TREATMENT
● Vitamins and minerals
● Small frequent feedings
● Extra fluids
● IV feeding tubes directly into the stomach
DRUG INCLUDE:
● Teduglutide (Gaffex), Doctors may prescribe this
hormone for adults with more serious cases of short
bowel syndrome who need IV feeding tubes.
● L-glutamine, a powder that you can mix with water
and drink.

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

● These drugs help the small intestine absorb more 5. Medications or chemical toxins such as carbon
nutrients and water. tetrachloride, chloroform, phosphorus, arsenicals,
certain medications.
JAUNDICE SIGNS & SYMPTOMS:
 Also known as Icterus, occurs when the bilirubin
1. Mildly or severely ill
concentration in the blood is abnormally elevated, all
2. Lack of appetite
the body tissues, including the sclerae and the skin,
3. Nausea
become tinged yellow or greenish-yellow.
4. Malaise
 Becomes clinically evident when the serum bilirubin
5. Fatigue
level exceeds 2.5 mg/dL (43 fmol/L).
6. Weakness
It may result from:
7. Weight loss
• Impairment of hepatic uptake.
DIAGNOSTIC FINDINGS:
• Conjugation of bilirubin.
1. The serum bilirubin concentration and the urine
• Excretion of bilirubin into the biliary system.
urobilinogen level may be elevated.
TYPES OF JAUNDICE 2. AST and ALT levels may be increased – indicating
1. Hemolytic Jaundice cellular necrosis.
2. Hepatocellular Jaundice 3. The pt may report headache, chills, and fever if the
3. Obstructive Jaundice cause is infectious.
4. Jaundice due to hereditary hyperbilirubinemia.
OBSTRUCTIVE JAUNDICE
HEMOLYTIC JAUNDICE  Obstructive jaundice resulting from extrahepatic
- The result from increased destruction of red blood obstruction may be caused by occlusion of the bile
cells in circulation or the precursors of the red blood duct from a gallstone, an inflammatory process, a
cells in the bone marrow leading to the yellowish tumor, or pressure from an enlarged organ (e.g.,
discoloration of the eyes, skin, and mucous membranes. liver, gallbladder). The obstruction may also involve
- This increased destruction of the red blood cells leads to the small bile ducts within the liver (i.e., intrahepatic
elevated levels of bilirubin in the blood obstruction); this may be caused, for example, by
(Hyperbilirubinemia). pressure on these channels from inflammatory
- Unconjugated bilirubin – type of bilirubin released in swelling of the liver or by an inflammatory exudate
hemolytic jaundice.
within the ducts themselves. Extrahepatic
- Fecal and urine urobilinogen levels are increased, but the
obstruction may be due to stones in the biliary duct.
urine is free of bilirubin.
Inflammatory process, inflammation therefore it
- Pts with this type of jaundice, unless their
swells. Tumor, at the biliary duct. Pressure from liver
hyperbilirubinemia is extreme, do not experience
(hepatomegaly) or from the gallbladder.
symptoms or complications as a result of the jaundice.
- Prolonged jaundice predisposes to the formation of - Intrahepatic obstruction it could result from stasis or
pigment stones in the gallbladder. thickening of bile (inspissation) within the
- Extremely severe jaundice (levels of free bilirubin canalicalculi and ingestion of certain medications
exceeding 20 to 25 mg/dL) poses a risk or brainstem which are cholestatic agents.
damage.
MEDICINES THAT MAY CAUSE OBSTRUCTIVE JAUNDICE:
If the bilirubin crosses the blood brain barrier is called  Phenothiazines
KERNICTERUS  Antithyroid medications
 Sulfonylureas for diabetes
CAUSES:  Tricyclic antidepressant agents
1. Severe anemia  Nitrofurantoin
2. Sickle cell anemia  Erythromycin estolate
3. Spherocytosis  Androgens and estrogens
4. Thalassemia  Propylthiouracil
5. Pyruvate kinase deficiency
 Amoxicillin-clavulanic acid
6. Glucose 6-phosphate dehydrogenase deficiency

HEPATOCELLULAR JAUNDICE OTHER CAUSES:

 It is caused by the inability of damaged liver cells to
clear normal amounts of bilirubin from the blood.
 It is caused by the inability of damaged liver cells to
clear normal amounts of bilirubin from the blood.
CAUSES:
The cellular damage may be caused by:
1. Acute or chronic hepatitis
2. Hepatoxicity
3. Cirrhosis due to alcohol
4. Other viruses that affect the liver such as yellow
fever virus, Epstein-Bar virus.
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 Gallstones in the common bile duct
 Pancreatic cancer
 Strictures of the common bile duct
 Biliary atresia absence of the biliary duct
 Cholangiocarcinoma cancer of the biliary
 Pancreatitis inflammation
 Pancreatic pseudocysts pseudocysts are false cysts in
the pancreas
SIGNS AND SYMPTOMS
 Deep orange and foamy urine because of bile
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NCM 116 (MEDICAL-SURGICAL NURSING II) LECTURER: Dean Gasco

 Light or clay-colored stools because of absence of - Hepatic venous pressure gradient (HVPG) the
bile difference between wedged hepatic venouse
 Skin may itch intensely, requiring repeated soothing pressure and free hepatic venous pressure.
- Measurement is made by inflating and deflating the
baths pruritus in skin because of the presence of bile
balloon in the tip of the catheter, introduced through
salts
internal jugular and femoral vein.
 Dyspepsia
 Intolerance to fatty foods because fat is emulsified ANATOMY OR PORTAL VENOUSE SYSTEM
by bile therefore absence of bile results to diarrhea
 AST, ALT, and GGT level rise only moderately
 Bilirubin and alkaline phosphatase levels are
elevated
DIAGNOSTIC EXAMS
 Bilirubin tests
 CBC
 Hepatitis A, B, and C tests
 MRI, CT, and Ultrasound scans
 Endoscopic Retrograde Cholangiopancreatography
(ERCP)
 Liver biopsy
COMPLICATIONS
 Bleeding
 Anemia - Portal vein is formed by the union of the superiroir
 Infectious mesenteric vein and the splenic vein just posterior to
the head of the pancrease at the level of second
 Abnormal bloating
lumbar vertebra/
 Swelling of legs
- Portal blood flow in man is about 1000 to 1200
 Liver failure ml/min
 Diarrhea
 Kidney failure CLASSIFICATION AND CAUSES:
 Constipation 1. PREHEPATIC
 Abdominal pain  Portal Vein Thrombosis
 Flatulence  Splenic Vein Thrombosis
MANAGEMENT  Massive Splenomegaly
2. HEPATIC
 Anemia-induced jaundice may be treated by
1. Presinusoidal: Schistomiasis, Congenital Hepatic
boosting the amount of iron in the blood by either
Fibrosis
taking iron supplements or eating iron-rich foods.
2. Sinusoidal: Cirrhosis of Liver, Alcoholic Hepatitis
 Hepatitis-induced jaundice requires antiviral or
3. Postsinusoidal: Hepatic Sinusoidal Obstruction (veno-
steroid medications.
occlusive syndrome) Iton Fibrosis natikang anay hito
 Obstruction-induced jaundice can be treated by fatty liver, katapos hit fatty liver- fibrosis kahuman
surgically removing the obstruction. hito Cirrhosis.
3. POSTHEPATIC
PORTAL HYPERTENSION  Budd-Chiari Syndrome
- The portal circulation in the liver is damaged or  Inferior Vena Cava Obstruction
congested.  Cardiac causes: Restrictive cardiomyopathy,
- If the blood goes to the esophagus esophageal varices constrictive pericarditis, severe congestive cardiac
may occur
failure
- The liver is congested kay impaired an circulation an
blood makadi ha peritoneal area which leads to
PATHOPHYSIOLOGY:
Ascites.
- There will be collateral distribution of blood leading to Normal Blood Flow to and from the liver depends on proper
caput medusa functioning of the:
- After the shunting from the artery to the vein o Portal Vein (70% of inflow)
mechanical obstruction. o Hepatic artery (30% of inflow)
- Then hypersplenism meaning splenomegaly leading to o Hepatic veins (outflow)
anemia, leukocytopenia and thrombocytopenia and  Portal Hypertension results either from increased
liver failure. blood flow in the portal vein or from an increased
- This is the increase pressure throughout the portal resistance to flow within the portal venous system
venous system that results from obstructions of  The most common cause of portal hypertension is
blood flow into and through the damaged liver. cirrhosis
- Elevation of hepatic venous pressure to 5mmhg then
 The pathophysiologic mechanism in cirrhosis is
the gradient exceeds 10 mmHg. Risk of variceal
increased resistance, which is intrahepatic and
bleeding the gradient is increased to 12 mmhg.
primarily sinusoidal.
MANAGEMENT OF PORTAL PRESSURE

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NCM 116 (MEDICAL-SURGICAL NURSING II)
 Portal Hypertension may also arise from pre-
sinusoidal obstruction, either outside the liver (as in
portal vein thrombosis) or within it (as in
Schistomiasis)
 In addition, lesions leading to portal hypertension
may be Postsinusoidal, either within the liver (as in
veno-occlusive disease) or distal to it (as in Budd-
Chiari Syndrome or Right Heart failure)
 Normal portal venous pressure is 5 to 10 mmHg
 Pressure rises 5 mmHg higher than the inferior vena
cava pressure
CLINICAL MANIFESTATIONS:
 Tortuous epigastric vessels that branch off the area
of the umbilicus and lead toward the sternum and
ribs (caput medusae)
 Enlarged palpable spleen
 Internal Hemorrhoids
 Bruits
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
return will cause decreased in circulating arterial blood volume
which will cause less supply of blood in the kidneys and the
glomerulus will be damaged. When the glomerulus is
damaged, Renin is released and this will activate the RAAS to
compensate for the low blood pressure to the point that it will
increase the blood pressure too much that it will lead to
hypertension. In RAAS, the kidney retains sodium which leads
to water retention therefore edema.
CAUSES OF CIRRHOSIS:
 Schistosomiasis
 Alcohol
 Fibrosis
MANIFESTATION:
 Increased abdominal girth
 Rapid weight gain due to ascites and edema
 Shortness of breath because the diaphragm is
compressed by the ascites therefore there is reduced
lung expansion
 Striae due to collateral circulation of the distended
veins
 Umbilical hernia also due to collateral circulation of
occluded veins
ASSESSMENT:
 Percuss the abdomen
 Fluid wave test
 Daily measurement of abdominal girth
 Daily measurement of body weight
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BATCH TOPAZ
LECTURER: Dean Gasco
TREATMENT OR MEDICAL MANAGEMENT
 Dietary modification
 Low sodium diet
 Diuretics (Spinorolactol)
 Bedrest
 Upright posture
 Paracentesis
 Transjugular Intrahepatic portosystemic shunt -
method in treating ascites, cannula or catheter is
inserted to the portal vein and a stent is placed as a
bypass so the flow of blood can go to the hepatic
veins and supply the digestive tract specially the
kidney.
DOCUMENTATION:
 Measuring abdominal girth
 Intake and Output
 Measure fluid electrolytes
HEPATITIS A (Infectious Hepatitis/Catarrhal Jaundice)
 It is an inflammation of the liver that is not only
severe and runs in acute course.
 This is known as infectious hepatitis because it
spreads relatively easy to individuals who have close
contact with the infected.
SIGNS & SYMPTOMS:
 Fever
 Fatigue
 Nausea
 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.
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NCM 116 (MEDICAL-SURGICAL NURSING II) LECTURER: Dean Gasco

2. The blood carries the virus to its target, the liver, 6. Alkalies, belladona and anti-emetics should be
where it lives and multiplies within the hepatocytes administered to control dyspepsia and malaise.
and Kupffer cells. NURSING MANAGEMENT
3. Virions are secreted into the bile and released in 1. Pt must be isolated (enteric isolation).
stools. HAV is excreted in large quantities 2. Pt should be encouraged to rest during the acute or
symptomatic phase.
approximately 11 days prior to the appearance of
3. Pt’s nutritional status must be improved.
symptoms or anti-HAV IgM antibodies in the blood.
4. Appropriate measures to minimize spread of the
CLINICAL MANIFESTATION:
disease must be taken.
1. Flu-like illness with chills and high fever.
5. Observe the pt for melena and check stools for the
2. Diarrhea, fatigue and abdominal pain. presence of blood.
3. Loss of appetite. PREVENTION:
4. Nausea and fever. 1. Vaccines
5. Jaundice and dark-colored urine. 2. Clean water
6. The infection in young children is often mild and 3. Safe sex
asymptomatic. 4. Personal hygiene
7. HAV does not have a chronic stage and does not 5. Sanitation
cause permanent liver damage. 6. New needles and syringes
8. Following infection, the immune system makes
HEPATITIS B (Serum Hepatitis)
antibodies against the HAV that confer immunity
 This is considered to be more serious than Hepatitis
against future infection.
A due to possibility of severe complications such as
COMPLICATIONS:
massive damage and hepatocarcinoma of the liver.
1. Progressive encephalopathy characterized by
After 5 years of contructing Hepa B, expect
drowsiness and cerebral edema.
hepatocarcinoma.
2. GIT bleeding progressing to stupor and later coma.
 It is the inflammation of the liver caused by Hepatitis
Bleeding is not responsive to vitamin K
B virus.
administration.
ETIOLOGY:
3. Clonus and hyperreflexia are later replaced by loss of
 The disease is caused by the Hepatitis B virus.
deep tendon reflexes.
 The virus has a very limited tissue tropism.
 HBV infects the liver and possibly the pancreas.
Differential Diagnosis:
 HBsAg appears in the blood 30 to 60 days after
1. Prodromal Stage
exposure and persistent for variable period of time.
 The disease must be differentiated from a variety of
INCUBATION PERIOD:
infections including:
- 50 to 189 days or 2 to 5 months with a mean equal to
1. Typhoid fever
90 days.
2. Dysentery kay mayda eni hiya diarrhea
MODE OF TRANSMISSION:
3. Malaria
- HBV can be directly transmitted by person to person
4. Infectious mononucleosis
contact via infected body fluids.
5. Acute abdominal conditions
- It can be transmitted through contaminated needles
 When the jaundice is present, Weil’s disease, yellow
and syringes. Through infected blood or body fluids
fever, infectious mononucleosis, the jaundice which
introduced at birth.
occurs in other acute infections, hemolytic jaundice
- Through sexual contact.
and surgical disease of the extrahepatic biliary tract
PATHOGENESIS:
must be considered.
- HBV primarily interferes with the functions of the
liver by replicating in liver cells, known as
DIAGNOSTIC TEST:
hepatocytes.
1. HAV and HBV – compliment fixation rate.
- During HBV infection, the host immune response
2. Liver function test
causes both hepatocellular age and viral clearance.
3. Bile examination of stool and urine samples.
- The virus replication may be as soon as 3 days from
4. SGOT (serum glutamic oxaloacetic transaminase)
acquisition, but symptoms may not be observed until
5. SGPT (serum glutamic pyruvic transaminase)
after 45 days or much longer.
6. ALT (serum alanine transaminase)
- Replication of the virus is not cytopathic or proceeds
7. IgM level
for relatively long periods without causing liver
damage.
PERIOD OF COMMUNICABILITY:
- During the acute phase of infection, the liver
 The infected patient is capable of transmitting the
parenchyma shows degenerative changes consisting
organisms from a week before until a week
of cellular swelling and necrosis, especially in
appearance of the symptoms.
hepatocytes.
TREATMENT
CLINICAL MANIFESTATIONS:
1. Bed rest is essential
1. Prodromal Stage
2. Diet must be high in carbohydrates, low in fat and
 Fever, malaise and anorexia.
low in protein.
 Nausea, vomiting, abdominal discomfort, fever and
3. Pt must take vitamin supplements, especially the B
chills.
complex group.
 Jaundice, dark colored urine, and pale stools.
4. Intravenous therapy is occasionally necessary.
 Right sided abdominal pain.
5. ISOPRINOSINE (METHOSIPRENOL) may enhance the
 Recovery is indicated by a decline of fever and
cell-mediated immunity of the Tlymphocytes.
improved appetite.

MT#: __5__
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RTRMF – BSN LEVEL III BATCH TOPAZ
NCM 116 (MEDICAL-SURGICAL NURSING II) LECTURER: Dean Gasco

COMPLICATIONS: - Urine may become dark colored and stools are clay
1. Cirrhosis colored.
2. Liver cancer
3. Fulminant Hepatitis may be fatal and manifested by 2. Clinical Jaundice Stage
severe symptoms like ascites and bleeding. - Pruritus, abdominal pain or tenderness and
DIAGNOSTIC PROCEDURES: indigestion.
1. Compliment fixation test - Yellowish discoloration of sclerodermatous
2. Radio-immunoassay-hemagglutinin test. membrane and the skin, which can last for 1 to 2
3. Liver function test weeks.
4. Bile examination in blood and urine. - Rashes, erythematous patches and urticaria. Pain,
5. Blood count tenderness of the RUQ, and enlarged and tender
6. Serum transaminase – SGOT, SGPT, ALT. liver, splenomegaly and cervical adenopathy are
7. HBsAg present.
TREATMENT: 3. Recovery Stage
1. Antiviral medication (TENOFOVIR, INTERFERON) - Most of the pt’s symptoms decrease or subside.
2. Liver transplantation Recovery commonly last for 2 to 12 weeks
PREVENTION:
1. Vaccines DIAGNOSIS:
2. Clean water 1. Hepatitis C: diagnosis depends on serologic testing
3. Safe sex for the specific antibody, one or more months after
4. Personal hygiene the onset of acute hepatitis.
5. Sanitation COMMON NURSING DIAGNOSIS:
6. New needles and syringes • Knowledge deficit
NURSING MANAGEMENT: • Low self-esteem
1. Blood donors must be screened to exclude carriers. • Body image disturbance
2. Caution must be observed in giving care to patients • Risk for infection
infected with HBV. • Impaired skin integrity
3. Hands and other skin areas must be washed • Altered nutrition: less than body requirement
immediately and thoroughly after contact with body • Social isolation
fluids.
4. Avoid injury with sharp objects or instruments. 5. HEPATITIS D
Use disposable needles and syringes only once and - Also called (DELTA VIRUS) is a small, circular RNA
discard properly virus.
5. Avoid sharing toothbrushes, razors and other - It is a replication-defective and therefore cannot
instrument that may be contaminated with blood. propagate in the absence of another virus.
6. Practice safe sex. - Hepatitis D infection occurs only in the presence of
7. Get adequate rest, sleep, and exercise and eat hepatitis B infection.
nutritious foods. - This can be transmitted by blood and blood products
8. Hepatitis B vaccines is recommended for pre- - A patient can acquire hepatitis D infection at the
exposure. same time that he/she is infected with the hepatitis B
9. HBIg should be administered within 72 hours to virus.
those exposed directly to Hepatitis B by either - A patient can also be infected with hepatitis D virus
ingestion, prick or inoculation. at any time during acute hepatitis B virus infection.

HEPATITIS C SIGNS & SYMPTOMS:

- It is a blood-borne infectious disease caused by
hepatitis C virus (HCV)
- Known as "non-A, non-B hepatitis.
- Asymptomatic, but once established, can cause
scarring of the liver (fibrosis) and eventually, cirrhosis
(advance scarring).
- With a higher rate of chronic liver disease (chronic
hepatitis
- Cirrhosis, and an increase risk for hepatocellular
carcinoma).
- Client with chronic hepatitis C are considered
infectious.
- No vaccine is available for hepatitis C.
SIGNS AND SYMPTOMS
Assessment findings are similar for the different types of
hepatitis. 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.
MT#: __5__
- 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.
Page 8 of 9
RTRMF – BSN LEVEL III BATCH TOPAZ
NCM 116 (MEDICAL-SURGICAL NURSING II) LECTURER: Dean Gasco

- Recovery commonly last for 2 to 12 weeks • Radio-immunoassay-hemaglutinin test

• Liver function test
DIAGNOSTIC PROCEDURES: • Bile examination Test
1. Compliment fixation test • Blood count
2. Radio-immunoassay-hemagglutinin test. • Serum transaminase – SGOT (Glutamic-Oxaloacetic
3. Liver function test Transaminase), SGPT (Serum Glutamic Pyruvic
4. Bile examination in blood and urine. Transaminase) , ALT (Alanine Transaminase)
5. Blood count • HBsAg
6. Serum transaminase – SGOT, SGPT, ALT. DIAGNOSIS:
7. HBsAg - Hepatitis D: detection of E antigen supports the
TREATMENT: diagnosis.
1. Antiviral medication (TENOFOVIR, INTERFERON) COMMON NURSING DIAGNOSIS:
2. Liver transplantation • Knowledge deficit
DIAGNOSIS: • Low self-esteem
- Hepatitis D: detection of intrahepatic delta or • Body image disturbance
immunoglobulin M (IgM) establishes the diagnosis. • Risk for infection
COMMON NURSING DIAGNOSIS: • Impaired skin integrity
• Knowledge deficit • Altered nutrition: less than body requirement
• Low self-esteem • Social isolation
• Body image disturbance PREVENTION:
• Risk for infection 1. Vaccines
• Impaired skin integrity 2. Clean water
• Altered nutrition: less than body requirement 3. Safe sex
• Social isolation 4. Personal hygiene
5. Sanitation
HEPATITIS E 6. New needles and syringes
 Transmitted through fecal-oral and waterborne
routes), like hepatitis A.
 Inconsistently shed in stool; therefore, detection is END
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
MT#: __5__
Page 9 of 9