LIVER BILIARY TRACT 3 Hepato cytes lobules

BILE SECRETION

Normal adult produces 250 to 1100 ml. bile per day.

*  Vagal stimulation increase secretion

*  Stimulation of splanchnic nerves results in decreased bile

   flow

*  Bile  salts  are   very   effective   choleretics   (stimulate

   secretion).

Biliary Secretion

Lobules of the hepatocytes are the source of hepatic bile secretion. Blood flow to the hepatocytes comes from brahches of both the portal vein and the hepatic artery. Blood from the portal vein flows through sinusoids past the hepatocyte to the central vein where it drains into the hepatic veins and inferior vena cava. Only one layer of hepatocutes separates the sinusoids.

Bile is a solution of both organic and inorganic compounds.

The hepatocyte secretes two primary bile acids, cholic acid and chenodeoxycholic acid. These are synthesized in the hepatocyte from cholesterol and recycled through the enterohepatic circulation to conserve bile salts. Primary bile acids, are converted to secondary bile acid (deoxycholic acid and lithocholic acid) when in contact with bacteria in the GIT

Purpose of secretion of bile acids is to allow for the formation of micelles. Micelles are formed and the, bile acid form the outer layer with the fats in the centre so that they will be more soluble in the aqueous medium. The emulsion then move down the gastrointestinal tract and allow lipids that are ingested to freely move in and out of the micelles so that they can be presented to the enterocytes for absorption.

The pigment of bile give it its color, is bilirubin. Bilirubin is derived from the degradation of hemoglobin in the reticuloendothelial system. Because bilirubin itself is not soluble. It is conjugated primarily with glucuronide and occasionally with sulfate. Circulating bilirubin is bound to albumen from which it dissociates at the hepatocyte on the portal venous membrane. It enters the bile canaliculus as bilirubin diglucuronide.

The bile acids, are synthesized or reused by the hepatocutes as they are presented as conjugated and unconjugated bile acids from the portal circulation. The liver produces approximately 500 to 1000 ml of bile per day.

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LIVER BILIART TRACT 2 Physiology Jaundice

2. PHYSIOLOGY

JAUNDICE

The  bile  pigment  bilirubin  is  formed  from  haemoglobin  and

myoglobin breakdown when the red blood cells are destroyed by the

reticuloendothelial system Fig. Above.

*  The iron and globin are separated

*  The  haem  ring  is transformed into biliverdin  and  this  is

   reduced to bilirubin which is yellow

*  Bilirubin  combines  with albumin and is  transported  to  the

   hepatic parenchymal cell

*  This complex gives the indirect van den Berg diazo reaction

*  In  the hepatic parenchymal cell, the albumin is  removed  and

   the  bilirubin  is conjugated with glucuronic acid to  form  a

   diglucuronide which is water soluble and is excreted into  the

   bile canaliculi

*  This  substance  gives  an immediate  diazo  reaction  (direct

   reaction)

*  The  conjugated bilirubin is excreted via the bile ducts  into

   the intestine.

*  It  is acted upon by intestinal bacteria converting it into  a

   colourless urobilinogen and the coloured urobilin

*  Fecal excretion is on an average of 100 to 200 mg.

*  Some  of  the urobilinogen is reabsorbed and  returns  to  the

   liver to be excreted in the urine.

*  Normally  there is less than 1.2 mg of  indirect-reacting  and

   0.3 mg. of direct reacting bilirubin per 100 ml. of serum.

*  Jaundice  is apparent when the serum bilirubin  level  exceeds

   2mg/100 ml.

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LIVER & BILIARY TRACT 1 Anatomy

LIVER AND THE BILIARY SYSTEM

1. ANATOMY

The  liver  lies  under  cover of the lower  ribs  in  the  right

hypochondrium and epigastrium and weighs 1200-1600 gms.

*  In an obese adult, the liver is impalpable

*  In  a  thin adult, the lower edge of the liver may be  felt  a

   fingers  breadth below the costal margin, as  the  contracting

   diaphragm  pushes  down  the  liver  at  the  end  of  a  deep

   inspiration.

The segmental division is to the right of the falciform  ligament

in the line with the fossa for the inferior vena cava Fig. 17.1

*  The  right  lobe  is  divided into  an  anterior  segment  and

   posterior segment.

*  The left lobe is divided by the falciform ligament into medial

   and lateral segments.

*  The right anterior and posterior segmental ducts join to  form

   right hepatic.

*  The  left  medial  and lateral ducts join  to  form  the  left

   hepatic duct.

*  Both  join to form the common hepatic which is joined  by  the

   cystic duct to form the common bile duct.

*  The  common  bile  ducts sescends along the  right  margin  of

   hepatoduodenal ligament to the right of the hepatic artery and

   anterior to the protal vein.

*  This supraduodenal portion continues behind the first  portion

   of the duodenum as retroduodenal portion and eventually enters

   the wall of the duodenum to empty into Ampulla of Vater.

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6 Unusual stomach tumours LIniti Plastica lymphoma leiomyosarcoma

This  is one type of gastric cancer. Most type of gastric  cancer produce  an ulcer or a mass on the mucosa. These can be  detected with   a  barium  or  endoscopy.  

Some  cancers  show   only   an infiltration  of  the  wall  of the  stomach.  

The  wall  becomes inelastic  and  on barium study show a narrow stomach  is  called leather bottle stomach.

This lesion is called linitis plastica.

 LYMPHOMA

It   may  as  the  only  lesion(primary)  or  as  a  part  of   widespread

lymphoma.

Anorexia and weight loss are prominant symptoms.

Diagnosis is by endoscope biopsy

Radiation  is the treatment of choice where stomach is  the  only

site of the lesion with a 85% 5 year survival

10. LIEMYOSARCOMA

They  originate from the muscle wall. Usually present  late  when

they have grown to a large size.

Treatment

Is  by surgical resection.  They do not respond to  radiation  or

chemotherapy.

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5 Gastric Carcinoma presentation treatment

8. GASTRIC CANCER

Incidence  of Gastric cancer, by contrast with tumours  of  other

organs,  has  been  decreasing during  recent  decades.   In  age

adjusted  mortality  rate  from  gastric  cancer  in  the   white

population fell from 29 to 3-6/100000.

Gastric  cancer  has  become  more  prevalent  in  Japan,  Chile, 

Iceland, Finland and the Scandinvian countries.

Countries  with  more  gastric  cancer can  also  have  a  higher

incidence of benign gastric ulcer .

8.1 ETIOLOGY

Although  the  cause of gastric cancer  remains  unkown,  several

clues may eventually clarify its etiology.

8.1.1 ATROPHIC GASTRITIS

Patients with gastric ulcer often have a diffuse pangastritis.

a  similar  type of chronic gastritis often  accompanies  gastric

cercinomas.    These  atrophic  changes  apparently   cause   the

Achlorhydria usually accompanying this condition.

8.1.2 DIET

Cabbage  is  the  only dietary factor  correlating  with  gastric

cancer.   This  vegetable  is a stable diet  of  countries  where

gastric  cancer  is common.  Countries with a high  incidence  of

gastic cancer also have a high consumption of fish.  Others  have

incriminated the salty and spicy foods.

8.2 SYMPTOMS

In  the early stages the disease is symptomless.  Later  patients

present with :

*  Vague indigestion

*  Fullness after meals

*  Pain epigastrium not reduced by anything

*  Loss of weight

*  Anaemia

Diagnosis is by

*  Barium studies

*  Fibro endoscopy

8.3 TREATMENT

Surgery  by radical gastrectomy in early mucosal lesions can  aim

for a cure .

The incision is upper midline or bilateral subcostal for a  total

gastrectomy   and  thoroabdominal  incision  may   be   required. 

Identify the lesion and assess its operatibility.

The stomach is freed by ligating its arteries as close to them as

their origins to include the draining lymph glands.  The  greater

omesutum and spleen are removed with the stomach.

The  jejunim is mobilised to anaetoma with the  oesophagus.   The

cut end of duodenum is closed.

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