1

GIT
Acute diarrheal diseases (ADD)
1. Definition:
Acute diarrhoea is passing more than 3 watery stools in a day of less than
14 days duration and without blood in stool; blood in stool is called
dysentery.
Diarrhea for > 14 days is called persistent diarrhoea
2. WHO classification of Diarrhoea:
1. Acute watery diarrhea
2. Persistent diarrhea
3. Dysentery
4. Diarrhea in severe malnutrition
3. Etiological agents :
1. Bacterial:
1. Enterotoxigenic e. Coli
2. Shigellae
3. Salmonellae
4. Vibrio cholerae
5. Campylobacter jejuni
6. Clostridium difficile
2. Viral: Rotavirus important cause for diarrhea in infants
3. Parasitic agents: Cryptosporidium
4. Protozoans: Amoeba; Giardia
4.

Transmission:
1. Rota virus, shigella and e.coli

: person to person

2. Cholera

: food and water

3. Salmonella and camphylobacter

: food poison

2
4. Clostridium difficile
5.

: antibody associated

Pathogenesis:
1. Toxin mediated
2. Invasive
3. Osmotic
4. Increased motility
Toxin: Eg.
1. Rota virus:
a. Activates intracellular signal transduction
b. Inhibits Na, Cl coupled transport
c. Eflux of Cl
2.

E.coli:
a. Activates adenylate cyclase
b. Increases intracellular cyclic AMP
c. Pumps out Na and Cl

E.coli: types:
a. ETEC: Enterotoxigenic
Fimbrial adherence; toxin mediated chloride shift
b. EPEC: Enteropathogenic
Adherence and effacement; cell injury
c. EIEC: Enteroinvasive
Shigella like toxin; invasion and cell necrosis
d. EHEC: Enerohemolytic
Can result in Hemolytic uremic syndrome
Invasion:
1. Shigella: Invasion, mucosal destruction and exudation

3
2. E.Coli: Enteroinvasive
Osmotic:
Eg: lactose intolerance; unabsorbed food produce osmotic pressure to
water into lumen
Motility disorder:
Eg: irritable bowel syndrome
6. Risk factorsfor diarrhea in infants:
1. Age: infants for more susceptible for viral diarrheas
2. Measles: direct infection and secondary bacterial infection
3. Malnutrition: immune and vit.A deficiency
4. Breast feeding: lack of breast feeding leads to increased risk for ADD
5. Formula feeding: bottle feeding is an important source of infection
6. Vit.A deficiency: epithelium is defective to provide barrier of infection
7. Zinc deficiency: leads to lack of local immunity
8. Race lactase deficiency common in Caucasians
7. Role of Zinc:
1. Biochemical functions:
1. Component of enzymes like: carbonic unhydrase, alcohol
dehydrogenase, alkaline Phosphatase, carboxy peptidase, superoxide
dismutase etc.
2. Essential for insulin storage and secretion by b cells.
3. It is required for maintaining vit a level in serum.
4. It is required for wound healing by unknown mechanism.
5. Gusten is a zinc containing protein and is important for taste
sensation.
6. Zinc plays important roles in growth and development, the immune
response, neurological function, and reproduction.
2. Role of Zinc in diarrhoea

4
1. Improved absorption of water and electrolytes by the intestine,
2. Faster regeneration of gut epithelium,
3. Increased levels of enterocyte brush border enzymes,
4. Enhanced immune response,
8. Behavioral factors:
1. Failure to breast-feed exclusively for the first 4-6 months of life
2. Using infant bottles
3. Unsafe water
4. Improper hand washing
5. Open air defecation
9. Malnutrition and diarrhea:
Diarrhea produce malnutrition; malnutrition in turn produce immune
deficiency and increases diarrheal episodes and hence a vicious cycle is set
up.
10. Signs and symptomsof ADD:
Main symptom of diarrhoea is dehydration. The disease is classified by WHO
according to degree of dehydration as follows:

Category

General
conditio
n

Thirst

Eye signs

Skin
pinch

Urine
output

Pulse

Fontanel

No
dehydtration

Alert

Absent

Moist; not
sunken;

Quick
recoil

Normal

Normal

AF normal

Slow
recoil

reduce
d

Fast

Depresse
d

Tenting

Nil

Rapid

Much

Plan A

Some
dehydration

tears +

Irritable

Incresae
d

Plan B

Severe

Dry;
sunken;
Tears less

Lethargi

Absent

Very dry;

5
dehydration
Plan C

Severe
disease

due to
lethargy

deeply
sunken;
no tears

on
pinch

and
Thread
y

depressed

In addition to signs of severe dehydration child may have:

unconsciousness; convulsions; cyanosis; no feeding; high fever etc

Plan C

11. Treatment: (WHO guidelines)

Plan A: ADD with no dehydration:
1. Mother care which consists of:
1. Treat fever with paracetamol
2. Continue breast feeding
3. Give more foodthan usual to prevent malnutrition
4. Give extra home available fluids- HAF
a. Juices; Buttermilk; Rice water; coconut water; Rice, cereal,
dhal; kanji.
b. Do not give plain water, salt and water or glucose water
5. Give Oral rehydration solution if available:
Give as much as the child wants until diarrhoea stops. As a
guide, after each loose stool, give:
a. Children under 2 years of age: 50-100 ml per diarrheal
episode (not per Kg)
b. Children aged 2 up to 10 years: 100-200 ml

c. Older children and adults: as much fluid as they want.

6. Zinc supplementation:
10 mg for <6mo; 20 mg for >6 mo for 14 days
Plan B: Treatment of Some dehydration:

6
Plan B is for child with some dehydration. It is a supervised management
with ORT in a ORT corner of an health facility.
ORT: 75 to 100 ml/kg to be given in 4 hours and then reassess the child; if
the dehydration has been corrected continue as in Plan A; if dehydration
remains same give one more Plan B treatment; If child has worsened to
severe dehydration refer the child to hospital for Plan C management while
continuing ORT.
Plan C: Hospital management:
a. Simplified IV management: Give Ringer Lactate 100 ml/kg as follows:

Age
Infants
(under 12 months)
Older

First give
30 ml/kg
in:

Then give
70 ml/kg in:

1 hour

5 hours

30 minutes

21/2 hours

b. Electrolytes
Hyponatremia:
<130 m.eq/l; 3% NaCl for rapid correction as per deficit;
mi;d hyponatremia may be correcte by ORS itself.
Hypernatremia:
>150 m.eq /l; continue ORS which will correct
hypernatremia slowly
Hypokalemia:
<3 m.eq/l; Iv KCL carefully adjusting the dose according to
deficit.
Hyperkalemia:
1. >6 meq/l
Acidosis: correct by IV soda bicarb as per deficit
12. Other treatments:
i. Zinc:
1. 10 mg for <6m 20 mg for >6 m for 14 days
ii. Probiotics:

7
1. Produce microbial lactase
2. Competes with pathogenic bacteria
3. Increase immune effect
4. Provide acidity
5. Protects cancer and allergy?
iii. Drugs:
1. No role of antibiotics as infantile diarrhea is mainly viral and
self limiting.
2. Give Co-trimoxazole if cholera is suspected; suspect cholera if
there is large explosive rice water stools; effortless vomiting;
severe dehydration in a short time; H/O > 3 admissions for
severe diarrhea in the community or 1 death due to diarrhea.
3. Give Nitazoxanide if giardiasis is foung in microscopy; Recently
Nitazoxanide has been found to have some role role in treating
Rota virus infection.
4. If Shigella is found positive in stool culture: give quiolones or
furazolidine
iv. Vomiting:
Ondensitran 2 mg stratum
v. Anti secretary agents: Racecodotril:
a. Enkephalinaze inhibitor
b. Anti secretory
c. Under evaluation
13. Complications
1. Shock kidney- ARF
2. Intra cerebral thrombosis
3. Hemolytic uremic syndrome
4. Hypoglycemia
5. Paralytic ileus

8
6. PEM
7. 14. Lab
1. Electrolytes
2. Stool microscopy
3. Stool culture
4. Stool reducing substance
5. CBC

8. 16.

Prevention strategies

1. Breast feeding
2. Improved weaning practices
3. Proper use of water
4. Hand washing
5. Disposing feces properly
6. Effectiveness of measles vaccination
9. 17.

New developments

10.
super-ors: contains amino acid instead og glucose; rice based ORS
contains rice powder instead of glucose; they try to more energy and
nutrition; but increase the cost.
11.

Rotavirus vaccine: given at 2,4,6 months of age

12.18. Note (WHO):

a. Cholera should be suspected when a child older than 5 years or an
adult develops severe dehydration from acute watery diarrhoea
(usually with vomiting), or any patient older than 2 years has acute
watery diarrhoea when cholera is known to be occurring in the area.
13.
14.
Oral Rehydration Therapy
1.
Oral rehydration takes advantage of glucose-coupled sodium transport,
a process for sodium absorption which remains relatively intact in infective
diarrheas due to viruses or to enteropathogenic bacteria, whether invasive
or enterotoxigenic. Glucose enhances sodium, and secondarily, water
transport across the mucosa of the upper intestine.For optimal absorption,
the composition of the rehydration solution is critical.
2.
Low Osmolality ORS:
a. Studies have shown that the efficacy of ORS for treatment of children
with acute diarrhoea is improved by reducing its sodium concentration
to 75 mEq/l, its glucose concentration to 75 mmol/l, and its total
osmolarity to 245 mOsm/l. This compares to the original solution which
contained 90 mEq/l of sodium with a total osmolarity of 311 mOsm/l.
There has been a concern that the original solution, which is slightly
hyperosmolar when compared with plasma, may risk hypernatraemia
(high plasma sodium concentration) or an increase in stool output,
especially in infants and young children
b. The formula for low osmolality ORS recommended by WHO and
UNICEF contains:

15.Reduced
osmolarit
y ORS
19.Sodium
chloride
23.Anhydrous
Glucose
27.Potassium
chloride
31.Trisodium
citrate,
dihydrate
35.

39.

16.
g

20.
2
24.
1
28.
1
32.
2

36.

40.

17.Reduce
d
osmolar
ity ORS
21.Sodium
25.Anhydro
us
Glucose
29.Chloride

33.Potassiu
m

37.Citrate
41.Total
Osmolari
ty

43.
3.

How to prepare:
i. Mix one full pocket of ORS in 1000 ml of safe water and use it in 24
hours
4.
Amount of ORS to be given:
44.

Plan A: No dehydration:

45.
Give as much fluid as the child wants until diarrhoea stops. As a
guide, after each loose stool, give:
II. Children under 2 years of age: 50-100 ml (a quarter to half a
large cup) of fluid;
III. Children aged 2 up to 10 years: 100-200 ml (a half to one large
cup);
IV. Older children and adults: as much fluid as they want.
46.

Plan B: Some dehydration:

47.
75 to 100 ml/kg in 4 hours; after correcton of dehydration Continue
as in no dehydration

18.
m

22.
7
26.
7
30.
6
34.
2
38.
1
42.
2

5.
48.

6.

Super ORS:

To provide more energy without increasing osmolality trials are

being done to use rise powder, amino acid in the place of glucose.
They would be costlier routine ORS.
Advantages of low osmolarity WHO Oral Rehydration Solution.
a. Composites Standard ORS solution
i. Sodium
90 (mEq or mmol/L
ii. Chloride
80
iii. Potassium
20
iv. Citrate
10
v. Glucose
111
vi. Total osmolarity
311
b. Limitations of standard ORS:
i. Does not decrease stool volume
ii. Does not decrease frequency
iii. Does not decrease severity
iv. Does not stop diarrhoea
v. Potential risk of hypernatremia in children with noncholera
diarrhoea
vi. May provide too much Sodium to edematous children
c. Advantage of new low osmolarity ORS:
i. Reduction in need for unscheduled IV therapy ( 35% in
metaanalysis)
ii. Significant red in vomiting (30%)
iii. Reduction in stool output (20%)
iv. Reduction in duration of diarrhoea
v. No risk of hyponatremia
7.
Advantage of citrate over bicarbonate:
1. The particular advantage of citrate containing ORS (over bicarbonate
containing ORS) is its stability in tropical countries, where - up to
temperatures of 60C - no discoloration occurs. A shelf-life of 2-3 years
can be assumed without any particular storage precautions.
2. Bircarbonate is hygroscopic and absorbs moisture and get spoiled on
storage whereas citrate is less hygroscopic
3. WHO has currently recommended citrate-based ORS to replace
bicarbonate. Sodium citrate at 2.5 g/ltrs will give a concentration of
10meq/ltr of citrate.
4. Advantages of citrate-based ORS are: it increases shelf life, improves
taste, cheaper, sodium absorption in high output diarrhoea and no
soiling of pockets.
49.
50.
LACTOSE INTOLERANCE

51.
a. Lactase a disccharidase is essential for digestion of lactose into
monosacharides before absorption;

b. Types:
a.

Secondary lactase deficiency is lactase deficiency that results from

small bowel injury, such as acute gastroenteritis, persistent diarrhea,

b. Congenital lactase deficiency is extremely rare and has a genetic

origin.
c. Clinical:
a. Lactose containing milk feed produce abdominal distension, increased
bowel sounds, abdominal colic and explosive watery stools
b. Acidity of the stools produce perianal excopriations
c. Withdrawl of lactose containing feeds relieves the symptoms
d. Challenge feed with lactose formula precipitates the symptoms
d. Confirmatory tests:
a. Measurement of carbohydrate in the stool using the Clinitest reagent
for reducing substances is a simple screening test and can be
performed at the bedside.
b. The test is easily performed by combining 10 drops of water with 5
drops of stool and then adding a Clinitest tablet. The color change can
be quantified as trace to 4+ using a color sheet provided by the
manufacturer. Only 2+ or higher should raise the possibility of sugar
malabsorption. Sucrose is not a reducing sugar and requires hydrolysis
with hydrochloric acid before analysis
c. Disaccharidase activities can be assayed in mucosal biopsy specimens.
c. Stool pH, obtained easily with pH paper, lower than 5.6 is also
suggestive of carbohydrate malabsorption
d. Osmotic diarrhea may be seen with carbohydrate malabsorption.
e. The breath hydrogen test: A rise in hydrogen excretion of greater
than 20 ppm from baseline is consistent with carbohydrate
malabsorption
52.
e. Management:
a. Lactose free formula from soy milk is an alternate feed
b. Live-culture yogurt contains bacteria that produce lactase enzyme and
is therefore tolerated by patients with lactase deficiency
c. A tablet with lactase activity can also be ingested with meals.
53.
54.
ACUTE HEPATITIS:
a. Hepatitis can be divided into two subgroups according to its duration:
Acute hepatitis lasting less than six months
Chronic hepatitis lasting longer than six months.
b. Causes of acute hepatitis:

a. Infectious viral hepatitis, such as hepatitis A, hepatitis B, hepatitis C,

hepatitis D and hepatitis E.
b. Other viral diseases, such as glandular fever and cytomegalovirus.

c. Severe bacterial infections.

d. Amoebic infections.
e. Medicines, eg paracetamolpoisoning and halothane (an anaesthetic).
f. Toxins: alcohol and fungal toxins
g. Parasites: Liver fluke
h. Autoimmune: Reye sydrome
i. Metabolic: hemochromatosis; Cystic fibrosis, Wilsons disease
c. Investigations:
55.Acute liver injury caused by the hepatotropic viruses manifests in three
main functional liver biochemical profiles namely
56.
1 . Cell injury and inflammation
57.
2. Cholestasis
58.
3. Defecetive synthetic function
1.60.

1. Tests for Acute liver cell injury (parenchymal disease) in viral

a. ALT alanine transaminase aminotransferase
i.
Normal value: 5-45 U/L
ii.
Can be raised up to 50 x normal. When they are this high it
suggests viral hepatitis,
iii.
Normal levels in infants are 2 x that of adults
iv.
During liver damage, ALT is released into serum causing
raised levels that may remain high for weeks or months.
Levels will be raised before jaundice appears.
v.
More specific for liver damage than AST.
b. AST aspartate transaminase
i.
Normal: 5-45 U/L
ii.
Levels can go as high as 20 x normal.

59.

62.

63.2. Test for Cholestasis (obstructive disease)

64. 1. The serum levels of total and conjugated bilirubin and
serum bile acids are elevated
65.
2. ALP alkaline phosphatise: Normal 25-110 U/L
66.
3. Gamma-GT GGT: Normal: <65 U/L

61.

69.
68.

67.

3. 3. Synthetic function:
Prolonged prothrombin time,
High INR,
Low serum albumin levels,
Hypoglycemia,
Lactic acidosis,
Hyperammonemia
70.
4. Tests for the severity of the liver disease:
i.
Hypoglycemia,
ii.
Hyperammonemia,
iii.
Electrolyte imbalance,
iv.
Continued hyperbilirubinemia,
v.
Marked hypoalbuminemia,
vi.
Prolonged PT or in unresponsive to parenteral administration of
vitamin K
a.
b.
c.
d.
e.
f.

vi.

1.
2.
3.
4.
5.
6.
7.
1.
2.
3.
4.
5.
6.
7.

Fractionation of the total serum bilirubin level: A predominant

elevation in the conjugated bilirubin level provides a relatively
sensitive index of hepatocellular disease and hepatic excretory
dysfunction
vii.
Liver Biopsy:
1. it is not routinely done in acute hepatitis;
2. Liver biopsy may be recommended for the initial
assessment of disease severity in patients with chronic
hepatitis B or chronic hepatitis C.;
3. pathological finding in liver in acute hepatitis is presence
of baloon cells
viii.
The appropriate diagnostic imaging studies (eg, ultrasound,
computed tomography) can be done if the differential
diagnosis favors gallbladder disease, biliary obstruction, or
liver abscess.
71.
72.
Hepatitis A
The most prevalent of the five viruses
RNA virus, a member of the picornavirus family.
It is heat stable
Highly contagious.
Transmission is by person-to-person contact through the fecal-oral route
Mean incubation period for HAV is about 3 wks
Infectivity: incubation to 2 wks after jaundice
73.
CLINICAL MANIFESTATIONS.
Only acute hepatitis; no chronic state
Resembles viral gastroenteritis
Abrupt onset of anorexia, nausea, malaise, vomiting, and jaundice.
The duration of illness is 714 days
Regional lymph nodes and the spleen may be enlarged
ulceration of the gastrointestinal tract can occur
Rare possibilities: Acute pancreatitis, myocarditis, nephritis, arthritis &
vasculitis
74.
DIAGNOSIS
1. By antibodies to HAV: anti-HAV Ig M radioimmunoassay
2. Viral particles in stool.
3. A viral polymerase chain reaction (PCR)
75.
COMPLICATIONS
1. most patients achieve full recovery
2. Acute liver failure
3. prolonged cholestatic syndrome
4. Pruritus
5. fat malabsorption
76.
TREATMENT
1. No specific treatment
2. Most children are asymptomatic or only mildly symptomatic.

3. Supportive treatment consists of intravenous hydration as needed and

antipruritic agents and fat-soluble vitamins
4. Serial monitoring for signs of acute liver failure and early referral to a
transplantation center can be lifesaving
77.
PREVENTION
1.
Patients are contagious for 2 wk before and about 7 days after the
onset of jaundice and should be excluded from school, child care, or work
during this period.
2.
Careful handwashing is necessary, particularly after changing diapers
and before preparing or serving food.
3.
In hospital settings, contact and standard precautions are recommended
for 1 wk after onset of symptoms.
4.
Vaccine.
1. Inactivated, highly immunogenic, and safe HAV vaccines available
2. 2 doses over 1 year at 6-12 interwals
5.
Immunoglobulin (Ig): IV < 2 weeks after expossure for
1. Household and sexual contacts of HAV cases;
2. Newborn infants of HAV-infected mothers;
3. Child-care center staff, employees, children,
4. Outbreaks in institutions and hospitals
78.
PROGNOSIS
1. The prognosis is excellent, with no long-term sequelae.
2. The only feared complication is ALF.
3. HAV infection remains a cause of major morbidity, however, and has a
high socioeconomic impact during epidemics and in endemic areas.
79.
80.
HEPATITIS B
1. DNA viruses of Hepadnaviridae family
2. Important components:
a. Hepatitis B surface antigen (HBsAg),
b. Hepatitis B core antigen (HBcAg),
c. Hepatitis B e antigen (HBeAg), derived from HBcAg
81.
EPIDEMIOLOGY
1. Two billion people worldwide have been infected
2. Important occupational hazard for health workers
3. Transmission by blood exposure and sexual contact and vertical
4. Hbv has eight genotypes (ah).
5. The incubation period ranges from 45 to 160 days, with a mean of
about 120 days.
6. Chronic hbv infection, defined as being positive for hbsag for >6 mo
7. Chronic infection is associated with the development of chronic liver
disease, as well as hepatocellular carcinoma
82.
PATHOGENESIS
1. injury predominantly by immune-mediated processes
2. Less cytopathic effect
3. Immune-mediated mechanisms are also involved in the extrahepatic
conditions

83.
CLINICAL MANIFESTATIONS
1. Prodrome marked by arthralgia or skin lesions, including urticarial,
purpuric, macular, or maculopapular rashes
2. Jaundice, in 25% of infected individuals, usually begins 8 wk after
exposure and lasts for 4 wk
3. Recovery in most people
4. 10% become chronic carriers
5. The liver is enlarged and tender
6. Splenomegaly and lymphadenopathy are common.
7. Clinical signs of altered sensorium and hyper-reflexivity mark the onset of
encephalopathy and ALF
84.
DIAGNOSIS.
1. HBs Ag is the 1st serologic marker of infection
2. Anti-hbc Ig M also increase in acute phase
3. Anti-hbc Ig G, appears months later and persists for years
4. The development of anti-HBe marks improvement
5. Anti-HBs marks serologic recovery and protection
85.
COMPLICATIONS
1. ALF with coagulopathy, encephalopathy, and cerebral edema
2. HBV infection can also result in:
1. Chronic hepatitis,
2. Cirrhosis,
3. End-stage liver disease
4. Primary hepatocellular carcinoma.
86.
TREATMENT
1. No available medical therapy is successful in the majority of persons
infected with HBV.
2. Interferon--2b (IFN-2b) and lamivudine are the current therapies for
treatment of chronic hepatitis B in adults older than 18 yr of age with
compensated liver disease and HBV replication.
3. IFN-2b also has been used in children, with long-term eradication rates
similar to the 25% rate reported in adults.
4. Recombinant interferons have immunomodulatory and antiviral effects
whereas lamivudine, a nucleoside analog, inhibits the viral enzyme
reverse transcriptase.
5. Liver transplantation also has been used to treat patients with end-stage
HBV infection
6. Peginterferon-2, adefovir dipivoxil and entecavir are approved for use
only in adults
87.
PREVENTION
88.UNIVERSAL
89.
90. Schedule
PROPHYLAXIS
91.Infants of
HBsAg-negative
women
94.Children and

92.
0

93.Birth, 12, 6
18 mo

95.

96.0, 1, and 6

adolescents
(1119 yr)
97.Infants of
HBsAg (+)
women

0
98.
0

mo
99.Birth 1 and 6
mo & 0.5 mL
HBIG

100.
101. Extra hepatic manifestation of Hepatitis B:
1. Immune-mediated mechanisms are involved in the extrahepatic conditions
2. Circulating immune complexes containing HBsAg can occur in patients
who may develop :
a. Polyarteritis nodosa,
b. Membranous or membranoproliferative glomerulonephritis,
c. Polymyalgia rheumatica,
d. Leukocytoclastic vasculitis,
e. Guillain-Barr syndrome.
3. The illness may also be preceded in a few children by a serum sicknesslike prodrome marked by:
a. Arthralgia
b. Skin lesions, including urticarial, purpuric, macular, or
maculopapular rashes.
c. Papular acrodermatitis, the Gianotti-Crosti syndrome
4.Other extrahepatic conditions associated with HBV infections in children can
include aplastic anemia.
102.
HEPATITIS C
1. Transfusion-related non-A, non-B hepatitis
2. Single- stranded RNA virus, classified as a separate genus within the
Flaviviridae family
3. Mild and insidious in onset
4. Causes chronic infection
5. Progress to cirrhosis, liver failure, and, occasionally, primary
hepatocellular carcinoma (HCC) within 2030 yr of the acute infection.
6. Diagnosis: aniti HCV antibody; PCR
7. Treatment:
1. Effective therapy to prevent the progression of HCV infection to
cirrhosis, liver failure, or hepatocellular cancer is not yet
available for the majority of patients.
2. Monotherapy with IFN-2b has resulted in sustained response in
10-15% of patients, defined as having normal ALT levels and
negative PCR results 6 mo after completion of therapy.
3. Combination therapy with interferon and ribavirin has yielded
sustained response in about one third of patients and is now
considered first-line therapy.
4. Future treatment strategies are likely to include development of
more effective protease and helicase inhibitors and drugs that
can disrupt the HCV RNA genome.
103.
HEPATITIS D
1. The smallest known animal virus,

2.
3.
4.
5.

It cannot produce infection without a concurrent hbv infection.

The 36 nm diameter virus is incapable of making its own coat protein;
Its outer coat is composed of excess hbsag from hbv.
The inner core of the virus is single-stranded circular RNA that expresses
the HDV antigen.
6. Transmission as HBV infection (co-infection), or those already infected
with HBV (super-infection).
7. Disease more severe than those of the other hepatotropic viruses
8. chronic hepatitis & acute liver failure are common
9. Diagnosis: IgM antibody to HDV
10.The treatment:
1. HDV superinfection of a person who has chronic HBV infection is
more common
2. Treatment is to as per management of HBV and is mostly based
on controlling and treating HBV
104.
HEPATITIS E
1. RNA virus ; a non-enveloped calicivirus
2. Transmission is fecal-oral
3. infection is similar to HAV but is often more severe
4. ALF in pregnant women
5. Diag: IgM and IgG assays
6. HEV is associated with a high prevalence of death in pregnant women.
7. No specific treatment or prevention are available
8. Child is to be manages as in Hepatitis A
9. Vaccine not effective; pooled immunoglobulin can be given
105.
106. PORTAL HYPERTENSION
107. Definition:
1. Portal hypertension, defined as an elevation of portal pressure >1012
mm Hg. The normal portal venous pressure is 7 mm Hg
108. Causes
1. Portal hypertension is most commonly a result of cirrhosis.
2. Etiology:
109.
Prehepatic causes
1. Umbilical infection (omphalitis)
2. Catheterization of the umbilical vein
3. Portal vein thrombosis due to neonatal dehydration and systemic
infection.
4. Primary sclerosing cholangitis.
5. Hypercoagulable states such as deficiencies of factor V Leiden, protein
C, or protein S.
6. Rare anomalies: agenesis, atresia, stenosis portal vein.
110.
The intrahepatic causes
1. Chronic hepatitis,
2. Congenital hepatic fibrosis
3. Schistosomiasis
4. Infiltration with malignant cells

5. Idiopathic form of portal hypertension

6. Cirrhosis liver & its cause:
1. Biliary atresia,
2. Autoimmune hepatitis,
3. Chronic viral hepatitis,
4. Metabolic liver disease such as 1-antitrypsin deficiency,
5. Wilson disease,
6. Glycogen storage disease type iv,
7. Hereditary fructose intolerance,
8. Cystic fibrosis.
9. Non alcoholic fatly liver disease
111.
Posthepatic:
1. The Budd-Chiari syndrome; obstruction to hepatic vein due to
thrombosis from hypercoagulable states
2. Metastatic neoplasms,
3. Collagen vascular disease,
4. Veno occlusive disease:
1. Cytotoxic drugs before bone marrow transplant;
2. Herbal tea
112.
PATHOPHYSIOLOGY
1. Obstruction to portal blood flow
2. Porto systemic shunt by collaterals
3. Hepatocellular dysfunction
4. Increase in plasma volume
5. Congestive gastropathy- gastric varices
6. Haemorrhoids
113.
CLINICAL MANIFESTATIONS
1. Variable hepatosplenomegaly: enlarged slightly or shrunken
2.

Digital clubbing occurs in 1015% of cases.

3. Pretibial edema due to hypoproteinemia.

4.

In biliary cirrhosis, patients often have jaundice, dark urine, pruritus,

hepatomegaly, and sometimes xanthomas

5. Bleeding from esophageal varices is the most common presentation;

hematemesis or with melena during intercurrent illness.
6. Growth retardation
7. Ascites in patients with intrahepatic causes
8. Collateral vessels carrying blood from the portal to systemic circulation
in the periumbilical region
9. Splenomegaly, with hypersplenism
9. Signs of Liver failure:

a. PRURITUS. Intense generalized itching, often with skin excoriation,

can occur in patients with cholestasis (conjugated
hyperbilirubinemia).
b. SPIDER ANGIOMAS: most prominent on the face and chest;
reflective of altered estrogen metabolism
c. PALMAR ERYTHEMA: This may be due to vasodilation and
increased blood flow.
d. XANTHOMAS: deposition of lipid in the dermis and subcutaneous
tissue.
e. ENDOCRINE ABNORMALITIES: reflect alterations in hepatic
synthetic, storage, and metabolic functions.eg. amenorrhea,
infertility, gynecomastia etc
f.

Hepatorenal syndrome (HRS) is defined as functional renal

failure in patients with end-stage liver disease. The pathophysiology
of HRS is poorly defined, but the hallmark is intense renal
vasoconstriction

g. Hepatopulmonary syndrome is characterized by the typical triad

of hypoxemia, intrapulmonary vascular dilations, and liver disease.
114. DIAGNOSIS
1. Ultrasonography:
a. presence of esophageal varices
b. cavernous transformation of the portal vein
c. Reversal of portal vein bloodflow
2. Selective arteriography of the celiac axis, superior mesenteric artery, and
splenic vein
3. CT scan similar to ultrasonography
115. TREATMENT
1. No specific treatment for cirrhosis
2. Bleeding managed by:
a. fluid resuscitation, initially in the form of crystalloid infusion
b. replacement of red blood cells
c. Correction of coagulopathy by administration of vitamin K
d. the infusion of platelets or fresh frozen plasma
e. A nasogastric tube to monitor for ongoing bleeding.
f. An H2 receptor blocker such as ranitidine should be given
intravenously to reduce bleeding from gastric erosions.
g. Vasopressin bolus of 0.33 U/kg over 20 min, followed by a
continued infusion of 0.2 U/1.73 m2/min
h. Nitroglycerin, usually given as a portion of a skin patch, has also
been used to decrease portal pressure

i.
j.

3.
4.
1.
2.
3.
4.
5.
6.
7.
8.
1.
2.
3.
4.
5.
6.
7.
1.
2.
3.
4.
5.

Endoscopic sclerosis or elastic band ligation of esophageal varices

Sengstaken-blakemore tube can be placed to stop hemorrhage by
mechanically compressing esophageal and gastric varices.
k. Portacaval, mesocaval or distal splenorenal shunt procedures
l. Transjugular intrahepatic portosystemic shunt (TIPS), in which a
stent is placed between the right hepatic vein and the right or left
branch of the portal vein
blockers such as propranolol act by lowering cardiac output and portal
perfusion in adults
Liver transplantation
116. Ascites
Clinical examination (fluid wave, shifting dullness), abdominal
ultrasonography.
Sodium restriction (12 mEq/kg/d), spironolactone (35 mg/kg/d),
furosemide (12 mg/kg/d),
intravenous albumin (0.51 g/kg per dose),
paracentesis,
peritoneovenous (LeVeen) shunt,
TIPS, surgical portosystemic shunt,
OLT- orthotopic liver transplantation
117. Hepatic encephalopathy
Abnormal neurologic examination, elevated plasma ammonia
Protein restriction (0.51 g/kg/d),
intravenous glucose (68 mg/kg/min),
neomycin (24 g/m2 BSA PO in four doses),
rifaximin (200 mg three times a day in children > 12 hry),
lactulose (1 mL/kg per dose [up to 30 mL] every 46 h PO),
Plasmapheresis, hemodialysis, OLT.
118. Hypersplenism
Low WBC count, platelets, hemoglobin. Splenomegaly
No intervention, partial splenic embolization, surgical portosystemic shunt,
TIPS, OLT. Splenectomy may worsen variceal bleeding.
PROGNOSIS
intrahepatic disease has a poor prognosis
Patients with progressive liver disease and significant esophageal varices
ultimately require liver transplantation.
119.