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1/33

FAILURE TO THRIVE( FTT )

=2=

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2/33

MALDIGESTION

DISORDERS

INTRALUMINALMEMBRANE

INTRACELLULAR-GASTER

-PANCREAS

-LIVER

-GUT ENTEROKINASE(trypsinogen trypsin)

- MALTASE

- LACTASE

- SUCRASE

- GLUCOAMYLASE

PEPTIDASE

LIPASE

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3/33

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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4/33

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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5/33

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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6/33

CLASSIFICATION OF MALABSORPTION

1.SUBSTRACTS

2.SELECTIVE/GENERALIZED

3.OBTAINEDCONGENITAL

--- ACQUIRED

4.PATHOPHYSIOLOGY

5.PATHOGENESE & ETIOLOGY

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7/33

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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9/33

CARBOHYDRATE

1. INTRALUMINAL ENZYME :AMYLASE

2. BRUSH BORDER ENZYME

OLIGO/DISACHARIDASE3. ABSORPTION

4. COLONIC BACTERIA

GLUCOSE

FRUCTOSE

GALACTOSE

SCFA

COLON NUTRITION

7/30/2019 GIS 2-K6 FTT ( II )

10/33

BOWEL NUTRITION

SMALL

INTESTINE

COLON

70% INTRALUMINAL

30% INTRAVASAL

45% INTRALUMINAL

55% INTRAVASAL

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11/33

TRYGLYCERIDE

FATTY ACID GLYCEROL

SHORTCHAIN FATTY

ACID (SCFA)

MEDIUM CHAIN FATTY ACID(MCFA)

LONG CHAIN FATTY ACID

(LCFA)

C12

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12/33

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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13/33

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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14/33

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

7/30/2019 GIS 2-K6 FTT ( II )

15/33

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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16/33

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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17/33

MALABSORPTION

ACUTE CHRONIC DEF. ABD.

DISTENSION

DEHYDRATION

- PERSISTENT DIARRHOEA

- FAILURE TO THRIVE

AVITAMINOSIS

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18/33

TREATMENT OF MALABSORPTION

1. ETIOLOGY-INFECTION

-ENZYMS

2. DIET

3. SUPPORTIVE- WATER & ELECTROLYTES

- VITAMIN & MINERAL- PREVENTION OF

MALNOURISHED

PREDIGESTED FORMULA

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19/33

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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20/33

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

7/30/2019 GIS 2-K6 FTT ( II )

24/33

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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25/33

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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26/33

Stools pH & clini test

Screening Test

Only drunk lactose

Fast intestinal transit time

Fresh stools

Incomplete degradation of lactose

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27/33

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

7/30/2019 GIS 2-K6 FTT ( II )

29/33

COWS MILK PROTEIN INTOLERANCE

-SMALL BABY

-DIARRHOEA

-ENTEROPATHY

Lact. Intol. CMPI

>>> >

(-) (+)

1.FREQ.

2.Extra GI Tract

manifestation

3.Phenomenon DOSE DEPENDENT DOSE INDEPEN.

7/30/2019 GIS 2-K6 FTT ( II )

30/33

30

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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32/33

PROTEIN LOSING

ENTEROPATHY

MUCOSAL

DAMAGE

INFLAMMATION

NONINFLAMMATION

LYMPH OBSTR.

LYMPHANGIECTASIA

CHD*

*Congenital Heart Disease

7/30/2019 GIS 2-K6 FTT ( II )

33/33

DIAGNOSTIC OF PROTEIN LOSING

ENTEROPATHY

1. ISOTOP

2. FECAL 1- ANTITRYPSIN