Pediatric Gastroenterology, Hepatology and Nutrition Fellowship
7. PEDIATRIC GASTROENTEROLOGY
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Transcript of 7. PEDIATRIC GASTROENTEROLOGY
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PEDIATRICPEDIATRIC
GASTROENTEROLOGYGASTROENTEROLOGY
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GENERAL POINTS
1 month age: preference for sweet & salty foods
4 month age: Interest in solids increases6 month age: Recommended to begin solids
First few months of life: Oral & pharyngeal movements necessary for
swallowing solids develop
Meconium: Dark, viscous material that is normally passed within the first 48
hrs of life
Transition stools: Green-brown stools passed after beginning of feeding
followed by yellow brown milk stools after 4-5 days
If white grey obstructed jaundice
4 6 month age: Pancreatic amylase secretion
Length of Esophagus
At birth: 8-10 cm
2-3 years: 16-20 cm
Adult: 25 cm
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LES normally relaxes to vent swallowed air & to permit physiologic reflux
episodes
Physiologic GE reflux resolves in 80% infants by 6 months of age
Stomach volume
1-3 month: 90-150 ml
1 year: 250-300 ml
5 year: 700-850 ml
Adult: 2000 ml
Acid secretion low at birth & increases dramatically by 24 hr
Length of Small IntestineAt birth: 270 cm
4 years: 450-550 cm (adult length)
MMC occurs less often in neonates
Fat absorption is less efficient
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Liver is palpable 1-2 cm below costal margin at birth
Riedel lobe: thin projection of the right lobe
Newborn are relatively intolerant of prolonged fasting (d/t decreased
ketogenesis)Fatty acid oxidation provides a major source of energy in early life
13th week of gestation: Pancreas can be identified
16th week of gestation: Immature zymogen granules in primitive acini
20th week of gestation: Mature zymogen granules containing amylase,
trypsinogen, & lipase
8th week of gestation: Glucagon
12-16th week of gestation: Islet of langerhans appear
Although, amylase & lipase are present in pancreas early in gestation,
secretion is low in infants (adult levels reached by 1 year of life)
Low levels are partially compensated by salivary amylase & lingual lipase
This is the cause of diarrhea in infants fed on formulas high in glucose & fats
(fat & glucose intolerance)
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VOMITINGVOMITING
BiliousBilious == GIGI obstructionobstructionBloodBlood ((HemetemesisHemetemesis)) == UpperUpper GIGI bleedbleed (MCC(MCC PortalPortal
HTNHTN;; othersothers GastricGastric ulcer)ulcer)
FeverFever == GastroenteritisGastroenteritis (MCC(MCC ofof vomitingvomiting inin infancy)infancy)
EmesisEmesis onlyonly (no(no nausea)nausea) == GERDGERD
UndigestedUndigested foodfood == Achalasia Achalasia (relieved(relieved onon feedingfeeding ininproppedpropped upup position)position)
ProjectileProjectile emesisemesis == PyloricPyloric stenosisstenosis,, AntralAntral web,web, AnnularAnnular
pancreaspancreasTenseTense fontanellefontanelle == increasedincreased ICPICP
OlderOlder adolescentadolescent femalefemale == pregnancy,pregnancy, migranemigrane,, bulemiabulemia
SoonSoon afterafter birthbirth == EsophagealEsophageal atresiaatresia
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ACUTE ABDOMINAL PAINACUTE ABDOMINAL PAIN
TraumaTrauma == perforation,perforation, hemorrhage,hemorrhage, musculoskeletalmusculoskeletal injury,injury,
pancreatitispancreatitis
BiliousBilious vomitingvomiting == obstructionobstruction
PeritonitisPeritonitis == appendicitis,appendicitis, cholecystitischolecystitis,, PIDPID
AdolescentAdolescent femalefemale == PID,PID, pregnancy,pregnancy, ovulatoryovulatory painpain
CurrantCurrant jellyjelly stoolstool == intussusceptionintussusception ((11stst && MCMC symptomsymptom isis
abdominalabdominal pain)pain)
MelanaMelana == upperupper GIGI bleedbleed
NonNon--specificspecific == gastroenteritis,gastroenteritis, UTI,UTI, pneumonia,pneumonia, functionalfunctional
abdominalabdominal painpain
MCC of abdominal pain in children = Worm colic
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TRACHEOESOPHAGEAL FISTULATRACHEOESOPHAGEAL FISTULA
AND ESOPHAGEAL ATRESIAAND ESOPHAGEAL ATRESIA
11//40004000 birthsbirths
9090%% tracheosophagealtracheosophageal abnormalitiesabnormalities presentpresent asas blindblind
upperupper esophagealesophageal pouchpouch withwith aa fistulafistula betweenbetween aa lowerlower
esophagealesophageal segmentsegment andand thethe lowerlower portionportion ofof thethetracheatrachea
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11//33 ofof patientspatients willwill havehave otherother congenitalcongenital abnormalitiesabnormalities(VACTERL(V ACTERL VVertebral,ertebral, AAnalnal atresiaatresia,, CCardiac,ardiac,TTracheoracheoEEsophegealsophegeal fistula,fistula, RRenal,enal, andand LLimbimb abnormalities)abnormalities)
EsophagealEsophageal atresiaatresia withoutwithout TEFTEF == excessiveexcessive secretionssecretions
TEFTEF withoutwithout esophagealesophageal atresiaatresia (H(H--type)type) == chokingchoking duringduring
feedingfeeding
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EsophagealEsophageal atresiaatresia withwith distaldistal TEFTEF
diagnoseddiagnosed byby placingplacing NGTNGT
(unable(unable toto advanceadvance intointo
stomach)stomach)
CXRCXR willwill showshow coiledcoiled tubetube andand nono
airair inin stomachstomach
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FOREIGN BODY INGESTIONFOREIGN BODY INGESTION
MostMost cancan bebe diagnoseddiagnosed withwith CXRCXR ((9090%% areare radiopaqueradiopaque))CoinsCoins inin thethe coronalcoronal planeplane == esophagusesophagus
CoinsCoins inin sagittalsagittal planeplane == tracheatrachea
EndoscopyEndoscopy usuallyusually neededneeded forfor removalremoval andand evaluationevaluation
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CONGENITAL PYLORIC STENOSISCONGENITAL PYLORIC STENOSIS
11//200200 -- 11//750750 livelive birthsbirths
CommonestCommonest surgicalsurgical disorderdisorder ofof thethe stomachstomach duringduring infancyinfancy
66 timestimes moremore commoncommon inin malesmales
PresentsPresents betweenbetween 33 wkswks && 22 mthsmths
NonNon--bilious,bilious, projectileprojectile vomitingvomiting
WeightWeight lossloss
O/EO/E:: VisibleVisible peristalsisperistalsis;; MassMass abdomenabdomen
HypochloremicHypochloremic hypokalemichypokalemic alkalosisalkalosis ifif notnot noticednoticed earlyearly
IxIx:: BariumBarium mealmeal:: StringString signsign ororDoubleDouble tracktrack signsign
PyloromyotomyPyloromyotomy forfor treatmenttreatment
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Age group: INFANTS (6-11 months)
Intermittent colicky pain (1st & MC symptom) + Vomiting +
Bloody mucus stools after abdominal pain (Currant jelly)
It is the MCC of intestinal obstruction in children
(MCC of acute intestinal obstruction in neonates DUODENAL
ATRESIA)
H/o URTI, change of milk formula, or vaccination
O/E: Sausage shaped mass in the RUQ
Empty right iliac fossa
INTUSSUSCEPTIONINTUSSUSCEPTION
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IxOC: Barium enema (both diagnostic & therapeutic)
CI to enemai. Symptoms > 24 hrsii. Air fluid levels on plain abdominal X ray (evidence ofobstruction)iii. USG showing intestinal ischemia
If enema not therapeutic, do laparotomy
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DUODENAL ATRESIADUODENAL ATRESIA
50% of all intestinal50% of all intestinal atresiasatresiasAssociated with multiple anomalies (GI, cardiac,Associated with multiple anomalies (GI, cardiac, anorectalanorectal, or, or
esophageal)esophageal)
40% have40% have trisomytrisomy 2121
Classic doubleClassic double--bubble signbubble sign
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MECKEL DIVERTICULUMMECKEL DIVERTICULUM
MCCMCC ofoflowerlower GIGI bleedingbleeding inin childrenchildren
EctopicEctopic tissuetissue isis commoncommon ((8080%% beingbeing gastricgastric inin originorigin andand55%% ofof pancreatic)pancreatic)
RuleRule ofof 22ss 22%% ofof populationpopulation
22 feetfeet fromfrom ileocecalileocecal junctionjunction
22 inchesinches inin lengthlength
22 cmcm inin diameterdiameter
22::11 malemale::femalefemale ratioratio UsuallyUsually asymptomaticasymptomatic beforebefore 22 yearsyears ofof ageage
DiagnosisDiagnosis isis usuallyusually mademade byby MeckelMeckel scanscan (ectopic(ectopic tissue)tissue)
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LACTASE DEFICIENCYLACTASE DEFICIENCY
CommonCommon disorderdisorder afterafter ageage 22
CongenitalCongenital (rare)(rare)
AcquiredAcquired (Viral/Bacterial(Viral/Bacterial gastroenteritisgastroenteritis MCC)MCC)
AcidicAcidic stoolsstools (pH(pH > 00..55%% ofofreducingreducing substancesubstance inin freshfresh stoolsstools
BreathBreath hydrogenhydrogen testtest isis diagnosticdiagnostic testtest
EndoscopicEndoscopic biopsybiopsy withwith measurementmeasurement ofof mucosalmucosal enzymeenzyme
activityactivity isis thethe goldgold standardstandard
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ARTIDiarrheaMalariaMeaslesHIVPrenatal Disordersothers
18 %
25 %
23 %
4 % 5 %
10 %
15 %
Causes of death in children < 5yr
DIARRHEA
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MCC of under 5 mortality in INDIA
Definition: Passage of watery stools 3 in 24 hrs OR a recent
change in consistency of stools
TYPES
1. Acute watery diarrhea (diarrhea for < 14 days)
2. Dysentery (Acute bloody diarrhea)3. Persistent diarrhea (starts acutely & lasts for 2 wks-2 months)
4. Chronic diarrhea (diarrhea for > 2 months)
4. Diarrhea with severe malnutrition
Sequele of diarrhea
Dehydration (MC cause of death)
Malnutrition
Infections
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MC infective cause of diarrhea inchildren is ROTAVIRUS, followedby ETEC
CAUSES OF ACUTE DIARRHEA
Viral
Rotavirus (MC),
Adenovirus,
Astrovirus,
Coxsackie virus,
Echovirus
Bacteria
E. coli (ETEC),Salmonella,
Campylobacter,
Yersinia enterocolitica,
Clostridium difficile,
Shigella,Vibrio cholerae (Cholera)
Parasites
Giardia,
Cryptosporidium parvum,
Entamoeba histolytica
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DYSENTRY
Presence of blood and pus in the stools, abdominal cramps and
fever
Gross blood in the stools is the most reliable sign
Causes: Shigella
EHEC
EIEC
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Total Body water = 60% of body weight
20 % (1/3 rd) as ECF
40% (2/3 rd) as ICF
5% (1/4th of ECF) = Plasma volume
15% (3/4th of ECF) = Interstitial fluid (ISF)
ECF = Relatively rich in Sodium with lower potassium
Diarrheal losses come from ECF
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Loss of water from the body reduction in the volume of ECF
Sodium is a major osmotic determinant of ECF
In 50% of cases, the concentration of sodium in the ECFremains nearly normal (ISONATREMIC DEHYDRATION)
In 45-50% cases, excessive sodium may be lost in the stools
relative decline in the serum and ECF sodium level hyponatremia fall in osmolality of ECF movement of waterfrom the ECF to ICF further shrinkage of the alreadyreduced ECF volumes (HYPONATREMIC DEHYDRATION)
In about 5% of diarrhea cases (especially if the child has beengiven fluids with more salts), serum sodium levels may beelevated the osmotic pressure of ECF become higher Shiftof water from ICF to ECF (HYPERNATREMICDEHYDRATION)
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Diarrhea stools contain large amounts of potassium
HYPOKALEMIA, if diarrhea persists
Hypokalemia is more pronounced in children with severe
malnutrition
Intestinal secretions are alkaline bicarbonate is lost in diarrheal
stools METABOLIC ACIDOSIS
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SIGNS OF DEHYDRATION
1. LOSS OF SKIN TURGOR
Impaired skin elsticity (On pinching, it takes a few seconds forthe skin fold to return to normal)
Lost in Iso- & Hyponatremic dehydration
May be masked in Hypernatremic dehydration
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2. HYPOTENSION
Results from a decline in the blood volume
- Cold extremities
- Thin, thready pulse
- Reflex tachycardia
- Decreased Urine output (good indicator of the severity of
illness)
- Depressed fontanel
- Sunken eyes,
- Dry tongue
Functional ability of the kidney of infants is not fully developed
as compared to older children cannot regulate the metabolic
derangements
Chronic decreased perfusion of the kidneys may lead to Renal
failure
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3. SIGNS OF HYPOKALEMIA
Abdominal distension
Paralytic ileus and
Hypotonia of muscles
ECG: U waves, ST depression and flat T waves
4. KUSSUMAULS BREATHING
OTHER CLINICAL FEATURES
Child becomes IRRITABLE, POOR FEEDING
NAUSEA/VOMITING + FEVER (Infective diarrhea)WEIGHT LOSS
ASSOCIATED INFECTIONS (Pneumonia, OM)
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INVESTIGATIONS & NUTRITIONAL ASSESSMENT
Weight for Age: BEST PARAMETER to assess nutritional status(acute malnutrition)
Stool microscopy & culture
Serum electrolytes
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MANAGEMENT
ORAL REHYDRATION THERAPY1. Home made solution
2. WHO-ORS
3. Food based solutions (Rice water with Salt)
4. Lassi, Kanji, Coconut water, Dal soup
WHO-ORS is ordinarily used for all types of diarrhea at all ages
ORS should be given with a teaspoon or in small sips from a cup
A child with profuse vomiting is more likely to retain the fluid if it
is consumed in small sips rather than large gulps
Large gulps often induces gastrocolic reflex
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WHO ORS
Ingredients in grams/liter
(Old WHO-ORS)
(New low osmolarity ORS)
Concentration in mmol/L
(Old WHO-ORS)
(New low osmolarity ORS)
Sodium chloride: 3.5 (2.9) Sodium: 90 (75)
Trisodium citrate dehydrate:2.9 (2.9)
Potassium: 20 (20)
Potassium chloride: 1.5 (1.2) Chloride: 80 (65)
Glucose, anhydrous: 20 (13.5) Citrate*: 10 (10)
Water:- 1 L (1 L) Glucose: 111 (75)
New ORS was designed to prevent hypernatremia seen with the
use of old ORS in neonates & very young infants with immature
kidney functions
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ASSESSMENT OF SEVERITY OF DEHYDRATION
Severe dehydration
Child is Lethargic, unconscious
Very dry tongue (palpation)Drinks poorly (or not able to drink)
Very sunken eyes with absent tears
(Dry eyes)
Signs of dehydration
Skin goes back very slowly after
pinchingTreatment: Use Plan C urgently
No dehydration
Child is alertMoist tongue
Drinks normally (not thirsty)
Normal eyes with tears
No signs of dehydration
Skin goes back quickly after
pinchingTreatment: Plan A
Some dehydration
Child is Irritable
Dry tongue
Drinks eagerly (thirsty)
Sunken eyes with absent tears
Signs of dehydration
Skin goes back slowly after
pinching
Treatment: Plan B
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PLAN A
Give ORS & food based solution at home
Mother asked to visit health center
i. If the child does not get better in 3 days, or
ii. If the child develops any of the following danger signs:
a. many watery stools
b. repeated vomiting
c. marked thirst
d. eating or drinking poorlye. fever, and
f. blood in stool
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PLAN B
All cases to be treated in Health center or Hospital
Rehydration therapy: Correction of the existing water &electrolyte deficit Give 75 ml/kg of ORS in the first 4 hours
Maintenance therapy: Replacement of ongoing losses due tocontinuing diarrhea to prevent recurrence of dehydration
Begins when signs of dehydration disappear (usually within 4hrs)
ORS should be administered in volume equal to diarrhea losses(10-20mL/Kg for each liquid stool)
ORS is administered in this manner till diarrhea stops
Breast feeding continued during rehydration
If the child continues to have some dehydration after 4 hours,repeat another 4 hours treatment with ORS solution (as inrehydration therapy) and start to offer feeds, milk and
breastfeed frequently
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PLAN C
All cases to be treated in Health center or Hospital
Start IV fluids immediately (Best: Ringers lactate with 5% D)If RL not available, use 0.9% Normal saline
Give 100 mL/kg
< 1 yr: First give 30 ml/kg in 1 hr# followed by 70 ml/kg in 5 hrs
1-5 yr: First give 30 ml/kg in hr# followed by 70 ml/kg in 2 hr# Repeat if pulse is weak or not detectable
All children should be started on some ORS solution (about 5
mL/kg/hr) when they can drink without difficulty during the time
they are getting IV fluids
If unable to give IVF immediately start rehydration with ORS
using NGT at 20 mL/kg/hr (total of 120 mL/kg)
If the child is improving but still shows signs of some dehydration,
discontinue IV treatment and shift to Plan B
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DRUG THERAPY
Antibiotics (Cotrimoxazole or Ampicillin X 5 days) should be
used only for infectious agents such as Shigella, Vibrio
cholerae, Entamoeba histolytica and Giardia
Zinc supplements
Anti-motility agents may cause distension of abdomen and other
undesirable side effects of opiates
They can be dangerous (even fatal) . So dont use them !
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CAUSES OF CHRONIC PERSISTENT DIARRHEA
Giardia lamblia
Cryptosporidium parvum
EPEC
Any enteropathogen in an immunocompromised host
Damage to the intestine by an enteropathogenMilk allergy
Malabsorption syndromes
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VIRAL HEPATITIS
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VIRAL infections that can involve the liver include
Hepatitis viruses
IMN
CMV
YELLOW FEVER
RUBELLA (In children & immuno-suppressed patients)
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HEPATITIS A
MC type of viral hepatitis
Agent: Single stranded RNA, non-enveloped, PicornavirusIt is also called as RELAPSING HEPATITIS
HAV does NOT cause chronic hepatitis or a carrier state
Fulminant hepatitis is RARE
Incubation period 15-45 days
Spread by feco-oral route (ingestion of contaminated waterand foods)
Virus is shed in the faeces for 2-3 weeks before & 1 weekafter the onset of jaundice
Disease is MAXIMALLY INFECTIOUS just before the onset of
jaundiceHAV viremia is transient thus, blood borne transmission of
HAV occurs only rarely (donated blood is not specificallyscreened for HAV)
Prognosis Excellent
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Diagnosis
Anti-HAV IgM antibodies (appears at the onset of symptoms)
(persists for 6-12 months)(Diagnosis of acute illness)
Anti-HAV IgG antibodies (confers immunity life long
protective antibody)
(can be detected for years)
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HEPATITIS B
Agent:HBV - Hepadnaviridae family
It has a double stranded circular DNA having 3200nucleotidesIt is spherical & double layered (DANE PARTICLE)
Enveloped
Incubation period 30-190 days
Can produceAcute hepatitis with resolution
Non-progressive chronic hepatitis (no cirrhosis)
Progressive hepatitis (with cirrhosis)
Fulminant hepatitis
An asymptomatic carrier stateHepatocellular carcinoma
Patients with chronic hepatitis represent carriers
HBV remains in the blood up to & during active episodes ofacute & chronic hepatitis (unlike HAV)
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Types of proteins (antigens) synthesized from genome
HBsAg Envelop glycoprotein (Australian antigen)
HBeAg Protein associated with active viral replication
HBcAg Nucleocapsid core protein; it remains in the
hepatocyte for the assembly of complete virions
HBxAg Modulates gene transcription of viral as well as host
genes (viral replication, hepatocyte cell cycle check points);
plays a key role in the development of HCC in HBV infected
patients
DNA polymerase
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SEROLOGICAL DIAGNOSIS
Sequence of appearance of serum markers
HBsAg > HBeAg > IgM-AntiHBc > AntiHBe > IgG-AntiHBc >AntiHBs
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HBsAg Appears before the onset of symptoms
Peaks during overt disease
Declines to undetectable levels by 3-6 months
(Persistence for more than 6 months indicateschronic infection)
HBcAg It is sequestered within HBsAg coat, thus, it isnot detectable in the serum
HBeAg It is a qualitative marker for HBV replication &infectivity
It appears in the serum transiently
Subsides with the disappearance of jaundice
Persistence of this in serum beyond first 3months indicates chronic infection
HBV DNA is the quantitative marker of HBVreplication & infectivity
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AntiHBs It is the protective antibody
Appears after the disappearance of HBsAg
Occasionally, a gap may separate the
disappearance of HBsAg & the appearance of
AntiHBs Gap or window period
AntiHBc It implies that the acute infection has peaked &
the disease is on the wane
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HEPATITIS CAgent:Enveloped, Single stranded RNA Flavivirus
Incubation period: 15-190 days
Responsible for 70-90% of post transfusion hepatitis
Has a high rate of progression to chronic disease or eventualCIRRHOSIS as compared with HBV
It has a high predisposition to HCC
Elevated titers of IgG anti HCV antibodies occurring after anacute infection DOES NOT confer immunity (in contrast toHAV & HBV) Thus no immunity is produced after acuteHCV infection
Serum markers are HCV RNA, IgM-AntiHCV, IgG-AntiHCV
In chronic infection, a characteristic clinical feature isEPISODIC elevations in serum transaminases withintervening normal periods
So, PERSISTENT INFECTION & CHRONIC HEPATITIS arehallmarks of HCV infection
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HEPATITIS DIt is caused by HDV (DELTA agent or virus)
It is an incomplete RNA particle enclosed in a shell of HBsAg
Unable to replicate on its own, thus, activated by the presenceof HBV (dependent on genetic information provided byHBV)
Co-infection Infection of HDV & HBV occurring together
Leads to RECOVERY 90%
FULMINANT HEPATITIS 5%CIRRHOSIS (Rarely)
Super-infection Infection of an already HBV infected person
Leads to CHRONIC HEPATITIS (CIRRHOSIS) 80%
FULMINANT HEPATITIS 10%
ACUTE SEVERE HEPATITIS 15%HDV is absolutely dependent on HBsAg & thus, during
infection is determined by duration of HBV infection
Most commonly associated with IV drug abusers
Diagnosis HDV RNA, IgM & IgG AntiHDV antibodies
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HEPATITIS E
Most common cause of hepatitis EPIDEMICS in india
Agent: Unenveloped single stranded RNA calcivirus
A characteristic feature of the infection is the high mortality
rate among PREGNANT WOMEN (~ 20%)
NOT associated with chronic disease or persistent viremia
Diagnosis HEV RNA & HEV particles in stool
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CLINICO-PATHOLOGIC SYNDROMES
1. CARRIER STATE
Best seen for HBV
Also seen with HCV
Normal Liver
2. ASYMPTOMATIC INFECTION
No symptoms at all
Detected accidentally by the presence of elevated serum
transaminasesSee with HBV
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3. ACUTE HEPATITIS
Can be caused by all types of hepatitis virus
Has 4 phases
i. An incubation period
ii. Symptomatic pre-icteric phase (non-specific symptoms)
Seen in about 10% cases with HBV
Serum sickness like syndrome (fever, arthralgia)
iii. Icteric phase
MC with HAV
Seen 50% cases with HBV
Never seen in cases with HCV
iv. Convalescence
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4. CHRONIC HEPATITIS
It is either continuing or relapsing hepatic disease for> 6
months
5. FULMINANT HEPATITIS
When hepatic insufficiency progresses from onset of
symptoms to hepatic encephalopathy WITHIN 2-3
WEEKSCan be induced by all viral types
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TREATMENT
HBV
- Lamuvidine
- IFN
Chronic HBV IFN OR Lamivudine
Acute HBV IFN only
Detection of HBeAg warrants the use of IFN (But is given
only after confirming the replication by doing HBV DNAbecause one has to be absolutely sure before starting asit is very expensive)
IFN given in acute hepatitis reduces the progression tochronic hepatitis
HCV
Acute IFN
Chronic IFN + Ribavirin