Gastric Trichobezoar
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? Bezoars are concretions of undigestible matter that accumulate inthe stomach.
? Trichobezoars, (hairbal s) composed of hair, occur most commonly
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in young women who swal ow their hair
? Phytobezoars are composed of vegetable matter
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? Most commonly, bezoars produce obstructive symptoms, but theymay cause ulceration and bleeding.
? Diagnosis is suggested by upper GI series and confirmed by
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endoscopy.
? Treatment options include enzyme therapy (papain, cel ulase, or
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acetylcysteine), endoscopic disruption and removal, or surgicalremoval
Trichobezoar forming cast of stomach and duodenum removed from a young female
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Gastric Lymphoma? Gastric lymphomas general y account for about 4% of gastric
malignancies.
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? Over half of patients with non-Hodgkin's lymphoma have
involvement of the GI tract.
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? Stomach is the most common site of primary GI lymphoma, andover 95% are non-Hodgkin's type.
? Most are B-cel type, thought to arise in mucosa-associated
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lymphoid tissue (MALT).
? In populations with a high incidence of gastric lymphoma, there is a
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high incidence of H. pylori infection; patients with gastric lymphomaalso usual y have H. pylori infection.
? Low-grade MALT lymphoma, essential y a monoclonal proliferation of B
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cel s, arises from a background of chronic gastritis associated with H.pylori.
? These relatively innocuous tumors then undergo degeneration to high-
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grade lymphoma.
? Remarkably, when the H. pylori is eradicated and the gastritis
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improves, the low-grade MALT lymphoma often disappears.? Thus low-grade MALT lymphoma is not a surgical lesion.
? Careful follow-up is necessary.
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? High-grade gastric lymphoma require aggressive oncologic treatment for cure
? Systemic symptoms such as fever, weight loss, and night sweats occur in about
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50% of patients? The tumors may bleed and/or obstruct.
? Lymphadenopathy and/or organomegaly suggest systemic disease.
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? Diagnosis is by endoscopy and biopsy.
? Primary lymphoma is usual y nodular with enlarged gastric folds.
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? Diffusely infiltrative process akin to linitis plastica is more suggestive of secondarygastric involvement by lymphoma.
? EUS; CT scanning of the chest, abdomen, and pelvis; and bone marrow biopsy.
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? Treatment is with primary chemotherapy and radiation without surgery
Liver
Anatomy: Embryology
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? The earliest appearance of the liver primordium occurs
on Day 22 after conception.
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? It appears at the superior intestinal portal, caudal andventral to the heart.
? By Day 24 hepatic diverticulum grows into the
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transverse septum that contains the vitelline and
umbilical veins
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? By Day 51, the intrahepatic veins attain thenormal adult distribution and segmentation
? By the ninth week, the liver embraces as much
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as 10% of body volume
Relative size of the left and right lobes of the liver in the foetus
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? largest solid organ of the body
? Weight: adult male ranges from 1.4 kg to 1.8 kg
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adult female from 1.2 kg to 1.4 kg? wedge-shaped
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Diaphragmatic aspect of the liver
Diagram of the posterior aspect of the liver
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? Anatomic & nonanatomic factors responsible for the
fixation of the liver at the right upper quadrant of the
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abdomen:
Anatomic
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? Inferior vena cava? Suprahepatic veins
? Several ligaments such as the round ligament and coronary
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ligament? Peritoneal folds
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Nonanatomic
? Positive intraabdominal pressure
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Parasagittal section through the upper abdomen showing the potential rightsuprahepatic and sub hepatic spaces
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The umbilical fissure separates the anatomic left lobe (segments 2 and 3) from theright lobe (segments 4-8)
The middle hepatic vein runs within the main portal fissure (Cantlie's line), which
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separates the left liver (segments 2 to 4) from the right liver (segments 5 to 8)
Vascular Distribution
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? Hepatic artery? Portal vein
? About one-fourth of the blood and one-half the oxygen come
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by way of the hepatic artery.? Remainder is carried by the portal vein
? Blood from these two sources mingles in the blood sinusoids
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of the liver parenchyma and is drained by tributaries of thehepatic veins
? These veins open into the inferior vena cava
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Intrahepatic distribution of the hepatic artery
Survival of a liver segment following arterial
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ligation is the result of all the following:
? Increased extraction of oxygen from portal venous
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blood? Extrahepatic collateral circulation
? Intrahepatic collateral circulation formed in response
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to the ligation
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Intrahepatic distribution of the hepatic portal vein
Intrahepatic distribution of the bile ducts
Lymphatics
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? The liver sinusoids have an endothelial lining composed of flattened
squamous cel s and stel ate macrophages (Kupffer cel s)
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? This endothelial layer is separated from the surroundinghepatocytes by a narrow perivascular space (of Disse) partial y fil ed
by microvil i of the hepatocytes
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? The perivascular space of Disse is the source of lymph produced by
the liver
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? The lymphatics of the liver are usual y divided into superficial or subcapsular and deep or portal systems
Nerve Supply
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? The sympathetic fibres arise from thoracic spinal cord
segments 7 to 10
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? The parasympathetic efferent fibres arise from thehepatic division of the anterior and posterior vagal
trunks
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The phrenic nerve supply via its C3, 4, 5 roots is probably
the basis of shoulder pain in biliary colic
Investigations
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? Serum Liver Tests
Parenchymal
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(hepatocytes)AST, ALT
Canalicular
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(biliary)
ALP, 5'NT, GGT, bilirubin
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SyntheticINR, factors V and VII, bilirubin,
function and
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metabolism
albumin
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? Radiologic Evaluation of the Liver? Ultrasound
? Computed Tomography Scan
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? Magnetic Resonance Imaging
? Positron Emission Tomography
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? Angiography? Percutaneous Biopsy
? Diagnostic Laparoscopy
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