ABDOMINAL...
Transcript of ABDOMINAL...
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