ABDOMINAL DISTENTION

OROR

MASSES

Atan Baas SinuhajiSub Division of Pediatrics Gastroentero-Hepatology

Department of ChildHealth,School of MedicineUniversity of Sumatera Utara/Adam Malik Hospital

Medan

ABDOMINAL

DISTENTION

ABDOMINAL

WALL

PCM

PRUNE BELLY

SYNDR.

OBESITY

DISTENTION

ABDOMINAL

CONTENT

GASES

FLUIDS

ABD. MASS

PRUNE BELLY SYNDROME

= EAGLE BARRET SYNDROME

= TRIAD SYNDROME

- DEFICIENT ABDOMINAL MUSCLE

- URINARY TRACT ABNORMALITY

UROPATHY NON OBSTRUCTIVE

- CRYPTORCHIDISM

GASES

OUT PERFORATION

PNEUMOPERITONEUMBOWEL

IN

OBSTRUCTION

MALABSORPTION

AEROPHAGIA

BOWEL OBSTRUCTION :

1. MECHANICAL/PARALYTIC

2. INCOMPLETE/COMPLETE2. INCOMPLETE/COMPLETE

3. CONGENITAL/ACQUIRED

OBSTRUCTION

MECHANICAL SIMPLE

STRANGULATION

VASCULAR

COMPROMISE

PARALYTIC

= ILEUS

=INTESTINAL PSEUDOOBSTRUCTION

ILEUS

ACUTE

SPASMOLYTIC

HYPOKALEMIA

PNEUMONIA

ILEUS

CHRONIC MUSCLE & NEURON

(CHRONIC INTESTINAL PSEUDO

OBSTRUCTION)

OBSTRUCTION

ACCUMULATION OF

BOWEL CONTENTS

OVERGROWTH

MICROORG.GUT CIRCULATION

MICROORG.GUT CIRCULATION

MUCOSAL DAMAGE

ENTEROCOLITIS

SEPSIS

ABD.MASS

ABD. CAVITY

PELVIC

RETROPERITONEAL

-KIDNEYS : -WILM’S TUMOR

-NEUROBLASTOMA

-CYSTE

-PANCREAS

PANCREATIC CYST

TRUE PSEUDO

DELINEATED BY EPITHELIAL WALL DELINEATED BY FIBROUS WALL

PANCRATITIS FAIL TO RESOLVE

RESECTIONDRAINAGE

OVARIAL CYST

HEMATOCOLPOS

TUBOOVARIAN ABSCESS

FETUS

PELVICTUBOOVARIAN ABSCESS

TERATOMA

IN

ABD. CAV.

WORMS > 100

FECAL IMPACTION

TUMOR

FOREIGN BODY

APP. ABSCESSGUT

OUTTUMOR

- KISTA MESENTERIUM

ORGANOMEGALY

TUMORS OF THE GUT

1.POLYPS

2.HEMANGIOMA

3.LEIOMYOMA

4.CARCINOMA

5.LIMPHOSARCOMA

6.CARCINOID:

- CHRONIC DIARRHOEA

- VASOMOTOR

- BRONCHOCONSTRICTION

POLYP

Any mass projecting into lumen of GI Tract

Neoplastic Non neoplastic

=Benigna adenoma=Malignant carcinoma

=Juvenile=Inflammatory=Hyperplastic

POLYPS OF THE GUT

FAMILIALJUVENILE

ADENOMA

PREMALIGNANT

HAMARTOMA

INTESTINAL JUVENILE POLYPS

NON SYNDROMIC SYNDROMIC

SOLITARY

AMPUTATED

EXTRAINTESTINAL FEATURES

(-) (+)

JPS = BRRS= CS

INTESTINAL JUVENILE POLYPS

NONSYNDROMIC JUVENILE POLYPOSIS SYNDROME( JPS )

PREMALIGNANTNON MALIGNANT

JUVENILE POLYPOSIS SYNDROME

-≥ 5 JUVENILE POLYPS OF THE COLON OR RECTUM-≥ 5 JUVENILE POLYPS OF THE COLON OR RECTUM-JUVENILE POLYPS IN OTHER PARTS OF GI TRACT OR-ANY NUMBER OF JUVENILE POLYPS AND A POSITIVE FAMILY HISTORY

BANNAYAN RILEY RUCULCABA SYNDROME( BRRS )

ADDITIONAL FEATURES= MENTAL RETARDASI= MENTAL RETARDASI= MACROCEPHALY= LIPOMATOSIS= HEMANGIOMAS AND= GENITAL PIGMENTATION

COWDEN SYNDROME( CS )

ADDITIONAL PATHOGNOMONIC FEATURES OFMUCOCUTANEOUSLESION (FACIAL TRICHILEMMOMA,ORAL FIBROMA,ACRAL KERATOSIS)AND ASSOCIATED TUMOR OF THE THYROID, BREAST AND ENDOMETRIUM

DIAGNOSIS OF POLYPS

INVASIVE NONINVASIVE

ENDOSCOPY MATRIX METALLOPROTEINASES IN URINE

MMP(MATRIX METALLOPROTEINASE)

VEGF(VASCULAR ENDOTHELIAL GROWTH FACTOR)

ANGIOGENESIS

PHYSIOLOGICAL PATHOLOGICAL

-DEVELOPMENT-TISSUE REPAIR-REPRODUCTION

-TUMOR GROWTH-METASTASIS

GROWTH

ANGIOGENESIS

MMP(+) IN URINE

Table 1 Lower Gastrointestinal surveillance strategies

Recomendations by Howe et Recommendations by Dunlop

From age 15 or ealier if symptoms:Do full blood examination andendoscopy

From age 15-18 or earlier if symptomsInterval 1-2 years

endoscopy

If normal,repeat 3 yearlyIf polyps are found,removeand screen annually untilpolyps free ,then 3 yearly

Gene carriers or affected continuesurveillance until age 70

Table 2 Upper gastrointestinal surveillance strategies

Recommendation by Howe et al

Recommendation by Dunlop

Recommendation by Sayed et al

Contemporaneously withcolonoscopy

From age 25 Frequency :SMAD4+ patients :1-3 yearly

Biliary and/or pancreatic duct bruishings recommended if elevated amylase or abnormalliver function test

Frequency :1-2yearly contemporaneouslywith colonoscopy

Mutation negative orBMPR1A+ patients :5 yearly

HEPATOMEGALY

1. INFLAMMATION HEPATITIS

2. CONGESTION : DECOMPENSATION,

CONTRICTIVE PERICARDITIS

3. BLOOD DISORDERS :

HEMOLYSIS : THALASSEMIA

MALIGNANCY : LEUKEMIA

4. TUMORS :CHOLEDOCHAL CYST

HEPATOMA

5. METABOLIC DISORDERS : FATTY LIVER

FATTY LIVER

1. NUTRITIONAL : OBESITY, KWASHIORKOR

2. DRUGS : ESTROGEN, STEROID

3. INTOXICATION : ALCOHOL

4. ALTERATION OF GI ANATOMY :

JEJUNOILEAL BY PASSJEJUNOILEAL BY PASS

5. OCCUPATIONAL EXPOSURE :

HYDROCARBON

6. METABOLISM : A – ß LIPOPROTEINEMIA

PATHOGENESIS

1.PERIPHERAL

MOBILIZ. OF

FATTY ACID

4. IMPAIRED SYNTHESIS

& EXCRETION VLDL (

VERY LOW DENSITY

2. HEPATIC SYNTHESIS

OF FATTY ACID 3. HEPATIC CATABOLISM OF

FATTY ACID

LIPOPROTEIN) FROM

THE LIVER

FATTY LIVER

HEPATIC STEATOSIS

INFLAMATION

ALCOHOLICNON ALCOHOLIC

NON INFLAMATION

(BENIGNA STEATOSIS)NON ALCOHOLIC

STEATOHEPATITIS

(NASH)

8-20 %

PROGRESIVE FIBROSIS

(10-50 % OF NASH)

CIRRHOSIS (10% OF NASH)

FIBROSIS (-)

NO INCREASED MORTALITY

NO INCREASED

MORTALITY

HEPATIC STEATOSIS

NASH ALC. HEPATITIS

ALT > AST

2 : 1

AST > ALT

2 : 1

ALT = SGPT

ALANINE AMINO TRANSFERASE= SERUM GLUTAMATE PYRUVATE TRANSAMINASSE

AST=SGOT

ASPARTAT AMINO TRANSFERASE = SERUM GLUTAMIC OXALOACETAT

TRANSAMINASE

FLUIDS

IN OUT

BOWEL

IN OUT

OBSTRUCTION ASCITES

PORTAL HYPERTENSION

-HEART FAILURE

-CIRRHOSIS

HYDROSTATIC PRESS.

LOSS

- NEPHROTIC SYND.

INTAKE

- PCM SYNTHESIS

- HEPATIC CIRRHOSIS

ONCOTIC PRESS.

ASCITES

PERMEABILITY

-DHF

-PERITONITIS TBC

-PERITONEAL TUMOR

LYMPH

OBSTRUCTION