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FAILURE TO THRIVE

( FTT )
=2=
MALDIGESTION

DISORDERS

INTRALUMINAL INTRACELLULARE
MEMBRANE •PEPTIDASE
-GASTER - MALTASE •LIPASE
-PANCREAS - LACTASE
-LIVER - SUCRASE
-GUT  ENTEROKINASE - GLUCOAMYLASE
(trypsinogen trypsin)
MUCOSAL INJURY

ENTEROCYTE TIGHT JUNCTION


-LUMINAL MEMBRANE
-INTRACELL / CYTOPLASMA
-BASOLAT. MEMBRANE
-SECRETION 
-BASAL MEMBRANE
-MACROMOLECULAR ABSORPTION
INTERCELLULER SPACE

LAMINA PROPRIA
SENSITIZATION
-BLOOD/LYMPH VESSELS
Causes of mucosal injury
1. 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
ABS-BIKA FKUSU 4
Consequences of mucosal injury

1. Diarrhoea
2. Malabsorption
3. Protein losing enteropathy
4. Sensitization  macro moleculer absorption
5. Necrotizing Enterocolitis

ABS-BIKA FKUSU 5
CLASSIFICATION OF MALABSORPTION

1.SUBSTRACTS

2.SELECTIVE/GENERALIZED

3.OBTAINED –CONGENITAL
--- ACQUIRED

4.PATHOPHYSIOLOGY

5.PATHOGENESE & ETIOLOGY


CARBOHYDRATE

FAT

PROTEIN

SUBSTRACT WATER & ELECTROLYTES


VITAMIN

MIXED OR GENERALIZED
II

PAN MALABSORPTION
Congenital & genetic

Bacterial overgrowth
Pathogenese
Bile acid def.
& etiology
sensitization

nutritional

Drug induced
CARBOHYDRATE
1. INTRALUMINAL ENZYME :
AMYLASE
2. BRUSH BORDER ENZYME
OLIGO/DISACHARIDASE
3. ABSORPTION •GLUCOSE
•FRUCTOSE
•GALACTOSE

4. COLONIC BACTERIA SCFA

COLON NUTRITION
BOWEL NUTRITION

COLON SMALL
INTESTINE

70% INTRALUMINAL 45% INTRALUMINAL


30% INTRAVASAL 55% INTRAVASAL
TRYGLYCERIDE

FATTY ACID GLYCEROL

SHORTCHAIN FATTY LONG CHAIN FATTY ACID


ACID (SCFA) (LCFA)

MEDIUM CHAIN FATTY ACID


(MCFA)
C<6 C>12

C=6-8(12)
DIGESTION & ABSORPTION OF
FAT
1.EMULSIFICATION
2.LIPOLYSIS LIPASE
3.MICELLE BILE SALT
4.ENTER INTO MUCOSE
5.RE-ESTERIFICATION
6.CHYLOMICRON
7.BLOOD/LYMPH VESSELS
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
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
LIPIODOL ABSORPTION TEST

LIPIODOL FAT+IODINE

Drink of 5-10 mL

BLOOD

URINE + AMYLUM 1%

DILUTION 1:1
1:2
1:8 (+) N
DIGESTION &
ABSORPTION OF
PROTEIN
1.INTRALUMINAL DIGESTION (HCL, PEPSIN)
2.ACTIVATED PANCREATIC ENZYMES BY
ENTEROKINASE
3.PROTEOLYSIS PEPTIDE & AMINO ACIDS
4.MUCOSE  INTRACELLULER DIGESTION
5.PORTAL VEIN
MALABSORPTION

ACUTE CHRONIC DEF. ABD.


DISTENSION

AVITAMINOSIS
DEHYDRATION

- PERSISTENT DIARRHOEA
- FAILURE TO THRIVE
TREATMENT OF MALABSORPTION
1. ETIOLOGY
-INFECTION
-ENZYMS
2. DIET
PREDIGESTED FORMULA

3. SUPPORTIVE
- WATER & ELECTROLYTES
- VITAMIN & MINERAL
- PREVENTION OF
MALNOURISHED
MALABSORPTION SYNDROME

1. LACTOSE INTOLERANCE
2. COW’S MILK PROTEIN INTOLERANCE
3. PCM
4. CHOLESTASIS
5. PARASITIC INFESTATION
6. ANTIBIOTICS
7. POST ENTERITIS MALABSORPTION
Lactose Intolerance
Terminology
 Lactase Defisiency :
Low / absence activity of lactase  enzyme
assay
 Laktose Malabsorption :
Failure of the small intestine to absorb lactose
 conformity with the test
 Lactose Intolerance : clinical
symptoms/signs
LACTOSE

The Primary Carbohydrate Of


Mammals Milk

Breast Milk Sea Lion Milk


Cow Milk
(7 %) (0 %)
(4 %)
Glucose &
LACTOSE
Galactose
Lactase
• In outer of brush border
• Smallest amount
• No adaptive enzyms
Developmental

Primary Congenital alactasia

Late onset hypolactasia


LACTASE
Defisiency

Secondary Mucosal damage eg 


rotavirus diarrhoea
UNABSORBED LACTOSE

OSMOTIC ACTION
H2
COLON FERMEN GASES CO2
TATION
CH4

ABSORBED WATER LACTOSE SHORT CHAIN FATTY ACID

COLONIC L - LACTATE
SALVAGE

• OSMOTIC DIARRHOEA
• REDUCTION SUBSTANCE (LACTOSE)  CLINITEST
• LACTIC ACID  stools pH  LACMUS
DIAGNOSTIC OF LACTOSE INTOLERANCE

Lactose tolerance test


+
Lactose malabsorption test
a. Stools pH & clini test
b. Lactose loading test
c. Breath hydrogen test
Stools pH & clini test

Screening Test

• Only drunk lactose


• Fast intestinal transit time
• Fresh stools
• Incomplete degradation of lactose
Breath
hydrogen
test

•Night fasting
•Doses of lactose : 2 gr/kgBW (max. 50 gr) in
concentration of solution 20 %
•Samples are then collected every 30 minutes
for 3 hours to determine H2 concentration in
expired air
• Malabsorption : > 20 ppm greater than fasting
level
TREATMENT

LACTOSE INTOLERANCE

Primary Secondary

Breast milk continued


1. Low/free lactose
2. Premature
Breast milk (-) ??
- Breast milk (+): continued
- Breast milk (-) : lactose lowered
+ glucose polymer
COW’S MILK PROTEIN INTOLERANCE
-SMALL BABY
-DIARRHOEA
-ENTEROPATHY

Lact. Intol. CMPI


1.FREQ. >>> >
2.Extra GI Tract (-) (+)
manifestation
3.Phenomenon DOSE DEPENDENT DOSE INDEPEN.
Goldman Criteria
1. Remission of symptoms after
elimination of cow milk from the diet
2. Relapse within 48 hours of beginning
a milk challenge
3. Positive reaction to 3 such challenges
(similar onset, duration, and clinical
features)

30
BIOPSY

MUCOSAL
DAMAGE

PERMEABILITY

-Dxylose absorption test


-L/M excretion ratio
-Polyethylen glycol abs. test
PROTEIN
LOSING
ENTEROPATHY
INFLAMMATION

MUCOSAL
DAMAGE

PROTEIN LOSING NONINFLAMMATION


ENTEROPATHY

LYMPHANGIECTASIA

LYMPH OBSTR.

CHD*

*Congenital Heart Disease


DIAGNOSTIC OF PROTEIN LOSING
ENTEROPATHY

1. ISOTOP
2. FECAL α1- ANTITRYPSIN

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