gis 2-k6 ftt ( ii )
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7/30/2019 GIS 2-K6 FTT ( II )
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FAILURE TO THRIVE( FTT )
=2=
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MALDIGESTION
DISORDERS
INTRALUMINALMEMBRANE
INTRACELLULAR-GASTER
-PANCREAS
-LIVER
-GUT ENTEROKINASE(trypsinogen trypsin)
- MALTASE
- LACTASE
- SUCRASE
- GLUCOAMYLASE
PEPTIDASE
LIPASE
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MUCOSAL INJURY
ENTEROCYTE
-LUMINAL MEMBRANE-INTRACELL / CYTOPLASMA
-BASOLAT. MEMBRANE
-BASAL MEMBRANE
INTERCELLULER SPACE
LAMINA PROPRIA
-BLOOD/LYMPH VESSELS
TIGHT JUNCTION
-SECRETION
-MACROMOLECULAR ABSORPTION
SENSITIZATION
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ABS-BIKA FKUSU 4
Causes of mucosal injury1. Mucosal compromised
Malnutrition
Folic acid Deficiency
Iron Deficiency
Antioxidant Deficiency
2. Infection
Viral (rotavirus)
Bacteria overgrowth
Antibiotica ( e.g. Neomycine )
3. Immunological disorder
SIgA Deficiency
4. Parasitic Infestation
Giardiasis
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ABS-BIKA FKUSU 5
Consequences of mucosal injury
1. Diarrhoea
2. Malabsorption3. Protein losing enteropathy
4. Sensitization macro moleculer absorption
5. Necrotizing Enterocolitis
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CLASSIFICATION OF MALABSORPTION
1.SUBSTRACTS
2.SELECTIVE/GENERALIZED
3.OBTAINEDCONGENITAL
--- ACQUIRED
4.PATHOPHYSIOLOGY
5.PATHOGENESE & ETIOLOGY
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SUBSTRACT
CARBOHYDRATE
FAT
PROTEIN
WATER & ELECTROLYTES
VITAMIN
MIXED OR GENERALIZED
I I
PAN MALABSORPTION
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Pathogenese
& etiology
Congenital & genetic
Bacterial overgrowth
Bile acid def.
sensitization
nutritional
Drug induced
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CARBOHYDRATE
1. INTRALUMINAL ENZYME :AMYLASE
2. BRUSH BORDER ENZYME
OLIGO/DISACHARIDASE3. ABSORPTION
4. COLONIC BACTERIA
GLUCOSE
FRUCTOSE
GALACTOSE
SCFA
COLON NUTRITION
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BOWEL NUTRITION
SMALL
INTESTINE
COLON
70% INTRALUMINAL
30% INTRAVASAL
45% INTRALUMINAL
55% INTRAVASAL
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TRYGLYCERIDE
FATTY ACID GLYCEROL
SHORTCHAIN FATTY
ACID (SCFA)
MEDIUM CHAIN FATTY ACID(MCFA)
LONG CHAIN FATTY ACID
(LCFA)
C12
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DIGESTION & ABSORPTION OF
FAT1.EMULSIFICATION
2.LIPOLYSIS LIPASE
3.MICELLE BILE SALT
4.ENTER INTO MUCOSE
5.RE-ESTERIFICATION
6.CHYLOMICRON
7.BLOOD/LYMPH VESSELS
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MCT(MEDIUM CHAIN
TRIGLYCERIDE)
C=6-8(12)
1.LIPASE 70%
2.NO BILE SALT
3.NO REESTERIFICATION
4.NO CHYLOMICRON FORMATION
5.PORTAL VEIN
G OS C O
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DIAGNOSTIC OF FAT
MALABSORPTION
1. MICROSCOPIC
2. FLOATING TEST (ROSSIPAL)
3. LIPIODOL ABSORPTION TEST
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
BLOOD
URINE + AMYLUM 1%
DILUTION 1:1
1:2
1:8 (+) N
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DIGESTION &
ABSORPTION OFPROTEIN
1.INTRALUMINAL DIGESTION (HCL, PEPSIN)
2.ACTIVATED PANCREATIC ENZYMES BY
ENTEROKINASE
3.PROTEOLYSIS PEPTIDE & AMINO ACIDS4.MUCOSE INTRACELLULER DIGESTION
5.PORTAL VEIN
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MALABSORPTION
ACUTE CHRONIC DEF. ABD.
DISTENSION
DEHYDRATION
- PERSISTENT DIARRHOEA
- FAILURE TO THRIVE
AVITAMINOSIS
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TREATMENT OF MALABSORPTION
1. ETIOLOGY-INFECTION
-ENZYMS
2. DIET
3. SUPPORTIVE- WATER & ELECTROLYTES
- VITAMIN & MINERAL- PREVENTION OF
MALNOURISHED
PREDIGESTED FORMULA
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MALABSORPTION SYNDROME
1. LACTOSE INTOLERANCE2. COWS MILK PROTEIN INTOLERANCE
3. PCM
4. CHOLESTASIS
5. PARASITIC INFESTATION
6. ANTIBIOTICS
7. POST ENTERITIS MALABSORPTION
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Terminology
Lactose Intolerance
Lactase Defisiency :Low / absence activity of lactase enzymeassay
Laktose Malabsorption :Failure of the small intestine to absorb lactose conformity with the test
Lactose Intolerance : clinicalsymptoms/signs
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LACTOSE
The Primary Carbohydrate Of
Mammals Milk
Breast Milk(7 %)
Cow Milk
(4 %)
Sea Lion Milk(0 %)
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LACTOSEGlucose &Galactose
Lactase In outer of brush border Smallest amount
No adaptive enzyms
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LACTASE
Defisiency
Secondary
Primary
Mucosal damage eg rotavirus diarrhoea
Developmental
Congenital alactasia
Late onset hypolactasia
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UNABSORBED LACTOSE
OSMOTIC ACTION
COLON
COLONICSALVAGE
OSMOTIC DIARRHOEA REDUCTION SUBSTANCE (LACTOSE) CLINITEST LACTIC ACID stools pH LACMUS
WATER LACTOSEBSORBED
FERMENTATION
GASES
SHORT CHAIN FATTY ACID
L - LACTATE
H2
CO2
CH4
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DIAGNOSTIC OF LACTOSE INTOLERANCE
Lactose tolerance test
+Lactose malabsorption test
a. Stools pH & clini test
b. Lactose loading test
c. Breath hydrogen test
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Stools pH & clini test
Screening Test
Only drunk lactose
Fast intestinal transit time
Fresh stools
Incomplete degradation of lactose
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Breath
hydrogentest
Night fasting
Doses of lactose : 2 gr/kgBW (max. 50 gr) in
concentration of solution 20 %
Samples are then collected every 30 minutesfor 3 hours to determine H2 concentration in
expired air
Malabsorption : > 20 ppm greater than fasting
level
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TREATMENT
LACTOSE INTOLERANCE
Primary Secondary
1.Low/free lactose
2.Premature
- Breast milk (+): continued
- Breast milk (-) : lactose lowered
+ glucose polymer
Breast milk continued
Breast milk (-) ??
COWS MILK PROTEIN INTOLERANCE
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COWS MILK PROTEIN INTOLERANCE
-SMALL BABY
-DIARRHOEA
-ENTEROPATHY
Lact. Intol. CMPI
>>> >
(-) (+)
1.FREQ.
2.Extra GI Tract
manifestation
3.Phenomenon DOSE DEPENDENT DOSE INDEPEN.
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Goldman Criteria
1. Remission of symptoms afterelimination of cow milk from the diet
2. Relapse within 48 hours of beginninga milk challenge
3. Positive reaction to 3 such challenges
(similar onset, duration, and clinicalfeatures)
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MUCOSAL
DAMAGE
PROTEINLOSING
ENTEROPATHY
BIOPSY
PERMEABILITY
-Dxylose absorption test
-L/M excretion ratio
-Polyethylen glycol abs. test
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PROTEIN LOSING
ENTEROPATHY
MUCOSAL
DAMAGE
INFLAMMATION
NONINFLAMMATION
LYMPH OBSTR.
LYMPHANGIECTASIA
CHD*
*Congenital Heart Disease
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DIAGNOSTIC OF PROTEIN LOSING
ENTEROPATHY
1. ISOTOP
2. FECAL 1- ANTITRYPSIN
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