mk pg slide failure to thrive
TRANSCRIPT
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FAILURE TO THRIVE( FTT)
Atan Baas SinuhajiSub Division of Pediatrics Gastroentero-HepatologyDepartment of ChildHealth,School of MedicineUniversity of Sumatera Utara/Adam Malik Hospital
Medan
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GROWTH
Increase in themass of body tissues
ABSABS--BIKA FKUSUBIKA FKUSU 22
Anthropometric measurement
HeadCircumference
BodyLenght
BodyWeight
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DevelopmentDevelopment
ABSABS--BIKA FKUSUBIKA FKUSU 33
SkillSkill
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Anthropometric asessment
At the spesific time Repeated visit
44
Poor Poor
Malnutrition F T T
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Table 1. WATER LOW’S CLASSIFICATIONTable 1. WATER LOW’S CLASSIFICATION
NORMAL WASTING STUNTE
EIGHT/ AGE %100 70 70
EIGHT/ HEIGHT %
EIGHT/ AGE %
100
100
70
100
100
87
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F.T.T
SUBOPTIMAL OF GROWTH
REPEATED VISIT
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Malnutrition isMalnutrition isthe sine qua non ofthe sine qua non of
ABSABS--BIKA FKUSUBIKA FKUSU 88
the failure to thriv the failure to thriv
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MALNUTRITION
GENETIC
FTT
99
PSYCHOSOCIAL
Malnutrition : inadequate nutrients
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CALORI / NUTRIENTSCALORI / NUTRIENTS
Intake
Stools Absorption
1010
Utilization
BasalMetabolism
Peripheral Utilization
Growth
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IMPAIRED OFPERIPHERAL
UTILIZATION
BASAL UTILIZATION
NUTRIENTS
MALABSORPTION
INTAKE
1111
NUTRITIONINADEQUATE
MALNUTRITION
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Etiology of growth disordersEtiology of growth disorders
1.1. Inadequate intake ofInadequate intake of
calories/nutrientscalories/nutrients2.2. Excessive calories/nutrientsExcessive calories/nutrients
losseslosses
4.4. Impaired of peripheralImpaired of peripheral
utilizationutilization – – Chronic infectionChronic infection
– – MalignancyMalignancy
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– –
– –MalabsorptionMalabsorption
3.3. Basal metabolismBasal metabolism
– – Fever Fever
– –HyperthyroideaHyperthyroidea
– – HyperkinesiaHyperkinesia
– – InfectionInfection
– –Congenital heartCongenital heartdiseasesdiseases
– – AnemiaAnemia
– –
Inborn errorsInborn errors – – HormonalHormonal
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FTT CAUSED
BY BOWELDYSFUNCTION
INADEQUATE
CALORY INTAKE-QUALITY
-IGNORANCE
-ANOREXIA
EXCESSIVECALORY LOSS -VOMITING
-MALABSORPTIO
-PROTEIN LOSIN
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ENTEROPATHY
INCREASED
NEED - FEVER
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DISORDER OF DIGESTION
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MALDIGESTION
MALABSORPTION
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MALABSORPTION
FAILURE OF THE DIGESTIVESUBSTRACTS ACROSS LUMEN INTO
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MUCOSE
VESSELSBLOOD
LYMPH
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MALABSORPTION
1.MALDIGESTION
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.3.PERISTALSIS
4. ABSORPTION AREA- SHORT GUT
- MUCOSAL INJURY
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MALDIGESTION
DISORDERS
INTRALUMINAL INTRACELLULAR
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-GASTER-PANCREAS
-LIVER-GUT →→→→ ENTEROKINASE
(trypsinogen trypsin)
- MALTASE
- LACTASE- SUCRASE- GLUCOAMYLASE
•PEPTIDASE•LIPASE
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Causes ofCauses of mumuccosaosal injuryl injury
1. Mucosal compromised
Malnutrition
Folic acid Deficiency
Iron Deficiency
Antioxidant Deficiency
ABSABS--BIKA FKUSUBIKA FKUSU 1919
Viral (rotavirus) Bacteria overgrowth
Antibiotica ( e.g. Neomycine )
3. Immunological disorder SIgA Deficiency
4. Parasitic Infestation
Giardiasis
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Consequences ofConsequences of mumuccosaosallinjuryinjury
1.1. DiarDiarrhorhoeeaa
2.2. MalabsorpMalabsorpttiionon
ABSABS--BIKA FKUSUBIKA FKUSU 2020
3.3. PProteinrotein losing enteropathylosing enteropathy4.4. SensitiSensitizzaattiionon mamaccroro molemolecculeruler absorptionabsorption
5.5.NNeeccrotirotizing Enterocolitiszing Enterocolitis
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CLASSIFICATION OF MALABSORPTION
1.SUBSTRACTS
2.SELETIVE/GENERALIZED
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3.OBTAINED –CONGENITAL--- ACQUIRED
4.PATHOPHYSIOLOGY
5.PATHOGENESE & ETIOLOGY
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CARBOHYDRATE
FAT
PROTEIN
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SUBSTRACT
VITAMIN
MIXED OR GENERALIZEDI I
PAN MALABSORPTION
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Pathogenese& etiology
Congenital & genetic
Bacterial overgrowth
Bile acid def.
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sensitization
nutritional
Drug induced
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CARBOHYDRATE1. INTRALUMINAL ENZYME :
AMYLASE
2. BRUSH BORDER ENZYMEOLIGO/DISACHARIDASE
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3. ABSORPTION
4. COLONIC BACTERIA
•GLUCOSE
•FRUCTOSE
•GALACTOSE
SCFA
COLON NUTRITION
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BOWEL NUTRITION
SMALLINTESTINE
COLON
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70% INTRALUMINAL30% INTRAVASAL
45% INTRALUMINAL55% INTRAVASAL
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TRYGLYCERIDE
FATTY ACID GLYCEROL
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SHORTCHAIN FATTYACID (SCFA)
MEDIUM CHAIN FATTY ACID
(MCFA)
LONG CHAIN FATTY ACID(LCFA)
C<6
C=6-8(12)
C>12
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DIGESTION & ABSORPTION OFFAT
1.EMULSIFICATION
2.LIPOLYSIS LIPASE
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.
4.ENTER INTO MUCOSE
5.RE-ESTERIFICATION
6.CHYLOMICRON
7.BLOOD/LYMPH VESSELS
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MCT(MEDIUM CHAINTRIGLYCERIDE)
C=6-8(12)
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1.LIPASE 70%
2.NO BILE SALT
3.NO REESTERIFICATION
4.NO CHYLOMICRON FORMATION
5.PORTAL VEIN
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DIAGNOSTIC OF FAT
MALABSORPTION1. MICROSCOPIC
2. FLOATING TEST (ROSSIPAL)
3. LIPIODOL ABSORPTION TEST
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4. SERUM CAROTEN
5. FAT BALANCE (VAN DE KAMER)6. STEATOCRITE
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LIPIODOL ABSORPTION TEST
LIPIODOL FAT+IODINE
Drink of 5-10 mL
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BLOOD
URINE + AMYLUM 1%
DILUTION 1:1
1:2
1:8 (+) N
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DIGESTION &ABSORPTION OF
PROTEIN1.INTRALUMINAL DIGESTION (HCL, PEPSIN)
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2.ACTIVATED PANCREATIC ENZYMES BYENTEROKINASE
3.PROTEOLYSIS→→→→
PEPTIDE & AMINO ACIDS4.MUCOSE →→→→ INTRACELLULER DIGESTION
5.PORTAL VEIN
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MALABSORPTION
ACUTE CHRONIC DEF. ABD.
DISTENSION
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DEHYDRATION
- PERSISTENT DIARRHOEA- FAILURE TO THRIVE
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TREATMENT OF MALABSORPTION1. ETIOLOGY
-INFECTION
-ENZYMS
2. DIETPREDIGESTED FORMULA
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3. SUPPORTIVE- WATER & ELECTROLYTES- VITAMIN & MINERAL
- PREVENTION OFMALNOURISHED
MALABSORPTION SYNDROME
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MALABSORPTION SYNDROME
1. LACTOSE INTOLERANCE
2. COW’S MILK PROTEIN INTOLERANCE3. PCM
3434
4. CHOLESTASIS
5. PARASITIC INFESTATION
6. ANTIBIOTICS
7. POST ENTERITIS MALABSORPTION
L t I t lL t I t l
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TerminologyTerminology
Lactose IntoleranceLactose Intolerance
Lactase Defisiency :Lactase Defisiency :Lactase Defisiency :Lactase Defisiency :Lactase Defisiency :Lactase Defisiency :Lactase Defisiency :Lactase Defisiency :
Low / absence activity of lactaseLow / absence activity of lactaseLow / absence activity of lactaseLow / absence activity of lactaseLow / absence activity of lactaseLow / absence activity of lactaseLow / absence activity of lactaseLow / absence activity of lactase →→→→→→→→ enzyme assay enzyme assay enzyme assay enzyme assay enzyme assay enzyme assay enzyme assay enzyme assay
Laktose Malabsorption :Laktose Malabsorption :Laktose Malabsorption :Laktose Malabsorption :Laktose Malabsorption :Laktose Malabsorption :Laktose Malabsorption :Laktose Malabsorption :Failure of the small intestine to absorb lactoseFailure of the small intestine to absorb lactoseFailure of the small intestine to absorb lactoseFailure of the small intestine to absorb lactoseFailure of the small intestine to absorb lactoseFailure of the small intestine to absorb lactoseFailure of the small intestine to absorb lactoseFailure of the small intestine to absorb lactose
3535
conformity with the testconformity with the testconformity with the testconformity with the testconformity with the testconformity with the testconformity with the testconformity with the test
Lactose Intolerance :Lactose Intolerance :Lactose Intolerance :Lactose Intolerance :Lactose Intolerance :Lactose Intolerance :Lactose Intolerance :Lactose Intolerance : clinicalclinicalclinicalclinicalclinicalclinicalclinicalclinical
symptoms/signssymptoms/signssymptoms/signssymptoms/signssymptoms/signssymptoms/signssymptoms/signssymptoms/signs
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LACTOSE
The Primary Carbohydrate Of
Mammals Milk
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Breast Milk(7 %) Cow Milk(4 %)
Sea Lion Milk(0 %)
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LACTOSELACTOSEGlucose &Glucose &
GalactoseGalactoseLactaseLactase••
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•• Smallest amountSmallest amount
•• No adaptive enzymsNo adaptive enzyms
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PrimaryPrimary
DevelopmentalDevelopmental
Congenital alactasiaCongenital alactasia
Late onset hypolactasiaLate onset hypolactasia
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DefisiencyDefisiency
SecondarySecondary
Mucosal damage egMucosal damage eg →→
rotavirus diarrhoearotavirus diarrhoea
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UNABSORBED LACTOSEUNABSORBED LACTOSE
OSMOTICOSMOTICOSMOTICOSMOTICOSMOTICOSMOTICOSMOTICOSMOTIC ACTIONACTIONACTIONACTIONACTIONACTIONACTIONACTION
COLONCOLONCOLONCOLONCOLONCOLONCOLONCOLON
WATERWATERWATERWATERWATERWATERWATERWATER LACTOSELACTOSELACTOSELACTOSELACTOSELACTOSELACTOSELACTOSEABSORBEDABSORBEDABSORBEDABSORBEDABSORBEDABSORBEDABSORBEDABSORBED
FERMENFERMENFERMENFERMENFERMENFERMENFERMENFERMEN
TATIONTATIONTATIONTATIONTATIONTATIONTATIONTATION
GASESGASES
SHORT CHAIN FATTY ACIDSHORT CHAIN FATTY ACID
HH22
COCO22
CHCH44
3939
COLONICCOLONICCOLONICCOLONICCOLONICCOLONICCOLONICCOLONIC
SALVAGESALVAGESALVAGESALVAGESALVAGESALVAGESALVAGESALVAGE
•• OSMOTIC DIARRHOEAOSMOTIC DIARRHOEAOSMOTIC DIARRHOEAOSMOTIC DIARRHOEAOSMOTIC DIARRHOEAOSMOTIC DIARRHOEAOSMOTIC DIARRHOEAOSMOTIC DIARRHOEA
•• REDUCTION SUBSTANCE (LACTOSE)REDUCTION SUBSTANCE (LACTOSE)REDUCTION SUBSTANCE (LACTOSE)REDUCTION SUBSTANCE (LACTOSE)REDUCTION SUBSTANCE (LACTOSE)REDUCTION SUBSTANCE (LACTOSE)REDUCTION SUBSTANCE (LACTOSE)REDUCTION SUBSTANCE (LACTOSE) →→→→→→→→ CLINITESTCLINITESTCLINITESTCLINITESTCLINITESTCLINITESTCLINITESTCLINITEST
•• LACTAT ACIDLACTAT ACIDLACTAT ACIDLACTAT ACIDLACTAT ACIDLACTAT ACIDLACTAT ACIDLACTAT ACID →→→→→→→→ stools pHstools pHstools pHstools pHstools pHstools pHstools pHstools pH →→→→→→→→ LACMUSLACMUSLACMUSLACMUSLACMUSLACMUSLACMUSLACMUS
LL - - LACTATE LACTATE
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DIAGNOSTIC OF LACTOSE INTOLERANCEDIAGNOSTIC OF LACTOSE INTOLERANCE
Lactose tolerance testLactose tolerance test
++
4040
ac ose ma a sorp on esac ose ma a sorp on esa.a. Stools pH & clini testStools pH & clini test
b.b. Lactose loading testLactose loading test
c. Breath hydrogen testc. Breath hydrogen test
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Stools pH & clini testStools pH & clini test
Screening TestScreening Test
4141
• Only drunk lactose
• Fast intestinal transit time• Fresh stools
• Incomplete degradation of lactose
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BreathBreathhydrogenhydrogen
testtest
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••Night fastingNight fasting
••Doses of lactose : 2Doses of lactose : 2 gr gr//kgBWkgBW (max. 50(max. 50
gr gr) in concentration of solution 20 %) in concentration of solution 20 %
••Samples are then collected every 30Samples are then collected every 30
minutes for 3 hours to determine Hminutes for 3 hours to determine H22
concentration in expired air concentration in expired air
••MalabsorptionMalabsorption : > 20: > 20 ppmppm greatergreaterthan fastin levelthan fastin level
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TREATMENTTREATMENT
LACTOSE INTOLERANCELACTOSE INTOLERANCE
Primary Secondary
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1.1.Low/free lactoseLow/free lactose
2.2.PrematurePremature
-- Breast milk (+): continuedBreast milk (+): continued
-- Breast milk (Breast milk (--) : lactose lowered) : lactose lowered
+ glucose polymer + glucose polymer
Breast milk continued
Breast milk (Breast milk (--)) ????
COW’S MILK PROTEIN INTOLERANCE
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COW S MILK PROTEIN INTOLERANCE
-SMALL BABY
-DIARRHOEA
-ENTEROPATHY
Lact. Intol. CMPI
4444
>>> >
(-) (+)
1.FREQ.
2.Extra GI Tractmanifestation
3.Phenomenon DOSE DEPENDENT DOSE INDEPEN.
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Goldman CriteriaGoldman Criteria1.1. Remission of symptoms after eliminationRemission of symptoms after elimination
of cow milk from the dietof cow milk from the diet2.2. Relapse within 48 hours of beginning aRelapse within 48 hours of beginning a
4545
3.3. Positive reaction to 3 such challengesPositive reaction to 3 such challenges(similar onset, duration, and clinical(similar onset, duration, and clinical
features)features)
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MUCOSAL
DAMAGE
BIOPSY
PERMEABILITY
4646
PROTEIN
LOSINGENTEROPATHY
-Dxylose absorption test
-L/M excretion ratio
-Polyethylen glycol abs. test
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PROTEIN LOSINGENTEROPATHY
MUCOSALDAMAGE
INFLAMMATION
NONINFLAMMATION
4747
LYMPH OBSTR.
LYMPHANGIECTASIA
CHD*
*Congenital Heart Disease