Friday, May 8, 2009

When Is Season 2 Of Huntik Starting?

Welcome!

Welcome to the Blog dedicated to the management of cholangitis ...
First Blog that discusses in detail this neglected disease in the literature yet its share of serious life-threatening complications ...

This site is an initiative of DR.BOUDEN MED ANIS who wished to share his graduation thesis done in collaboration with MED DR.AOUADI YACINE under the supervision of DR.MLBENKHALIFA (Assistant Professor of Surgery General)
I hope you enjoy browsing through the blog, and please let me know your comments and suggestions, and thank you for reporting any Error ...


Regards!
Yanis

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BILIARY PHYSIOLOGY


The gallbladder stores and concentrates bile (10 times) until it is required in the small intestine. During the process of concentration, water and ions are absorbed through the lining of the gallbladder.

When the small intestine needs of bile, the smooth muscle wall of the gallbladder to contract and push the bile into the cystic duct, common bile duct and small intestine.

When the small intestine is empty, a valve located around the ampulla hepatopancreatic called sphincter of the hepatopancreatic bulb (sphincter of Oddi), closes and causes the bile accumulated up to the cystic duct 'to the gallbladder to be stored [29].


Bile



Liver cells secrete daily from 800 to 1000 ml of bile, liquid yellow, brown or olive green, has a pH between 7.6 and 8.6.

Bile is mainly composed of water and bile acids, bile salts, cholesterol, phospholipid called lecithin, bile pigments and several ions. Bile is both a product of excretion and intestinal secretion.


Bile is secreted continuously by the liver, then stored in the gallbladder which concentrated.
Upon digestion, bile is sent by the gallbladder into the duodenum through the bile duct.

Its role is to promote the absorption of fat by bile salts it contains. It still consists of water, mucin, minerals, pigments from the dégradation de l’hémoglobine et du cholestérol.

Les sels biliaires



Les sels biliaires, qui sont des sels de sodium et de potassium des acides biliaires (principalement l’acide cholique et l’acide chénodésoxycholique), jouent un rôle dans l’émulsification, la dégradation de volumineux globules de graisses en une suspension de fines gouttelettes graisseuses et dans l’absorption des graisses Après leur digestion.

Les fines gouttelettes de graisse présentent une très grande surface pour l’action de la lipase pancréatique nécessaire à une digestion rapide des graisses. Le cholestérol est rendu soluble dans la bile par les sels biliaires et la lécithine.


Le principal pigment biliaire est la bilirubine. Lorsque les globules rouges se dégradent, le fer, la globine et la bilirubine (dérivée de l’hème) sont libérés. Le fer et la globine sont recyclés, mais une partie de la bilirubine est excrétée dans les canaux biliaires. La bilirubine est ensuite dégradée dans les intestins. L’un de ses produits de dégradation, l’urobilinogène, donne aux fèces leur couleur brune habituelle.


Les sels biliaires sont des molécules à structure stéroïdienne synthétisées par les hépatocytes at the expense of cholesterol under control of a single enzyme: the cholesterol - 7 - hydrolase.


normal humans, the major bile acids, cholic and chénodeoxycholique are combined with two amino acids: glycine and taurine.
as conjugates, bile salts are secreted into bile by the hepatocyte cells.

regulation of bile secretion



bile secretion is regulated by nervous and hormonal factors. Vagal stimulation of the liver may increase more than twice the normal rate of bile production. Secretin, a hormone that stimulates production of pancreatic juice rich in bicarbonate ions (HCO3-), also stimulates the secretion of bile rich in HCO3-by liver cells.

The increase in blood flow to the liver leads to a certain point,
increasing bile secretion.

Finally, the presence of large amounts of bile salts in the blood also increases the rate of bile production.

Cholecystokinin (CCK), a hormone that stimulates production of pancreatic juice rich in digestive enzymes, also stimulates the contraction of the gallbladder biliaire. La bile ainsi comprimée passe de la vésicule biliaire au canal cholédoque.

Par ailleurs, la cholécystokinine provoque le relâchement du sphincter de l’ampoule hépato-pancréatique de Vater, favorisant ainsi l’écoulement de la bile dans le duodénum.


Wednesday, May 6, 2009

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PEDICLE THE LIVER LIVER PHYSIOLOGY

Il forme grossièrement une tige courte et trapue, de 4 cm de long, limitée en bas par le duodénum et en haut par le hile hépatique. Il est contenu dans le bord droit du petit épiploon[38].


The elements of the hepatic pedicle are

The portal vein

She was born behind the pancreas, common trunk splénomésaraïque venous and superior mesenteric vein. It is a large vein, 15 mm in diameter, its pedicle portion goes to D1 hilum where it bifurcates into two right and left portal branches. Through it all the venous blood passes through the digestive "filter" liver. The hepatic artery

Pédicule Hépatique
It arises from the celiac trunk and bifurcates at the foot of the hepatic pedicle gastroduodenal artery and hepatic artery, then she climbs into the hepatic hilum and will give two terminal branches, which are the right and left hepatic arteries.

The hepatic duct, which receives on its right edge of the cystic duct and the bile duct becomes lower.




Lymphatics

They fall into two channels: one to the right of the hepatic pedicle, large, with the ganglion Quenu, the other to the left edge, hail.

nerves

They are 3 shots: one in front of the hepatic pedicle (anterior plexus of Latarjet) the other behind (posterior plexus) and the gastro-hepatic nerve, from the X left, who joined the pedicle very top to the hilum (sometimes called plexus Burge)


The overall order of the elements of front to back, is always

- Bladder

-

artery - vein



reports of hepatic pedicle

The entire hepatic pedicle is encased in layers of the lesser omentum.
- the left is the lesser omentum and distance, the lesser curvature.

- Right , the cystic duct and gallbladder.

- Back , the hepatic pedicle forms the anterior edge of the foramen of Winslow which opens onto the rear cavity of lesser sac. Further back is the inferior vena cava.

- Forward is the anterior abdominal wall.



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Tank blood

Receives about 1500 ml / min (PV = 1100 ml / min and AH = 400 ml / min)
always contains 450 ml (10% blood volume). Can s'expandre (1.5 l) in heart failure.

Role immune

- Lymphatics

- Liver Macrophages (Kupffer cells)

metabolic function

Carbohydrate metabolism: important role in maintaining blood glucose:


- Storage of glucose as glycogen .

- Release of glucose from glycogen (glycogenolysis).

- Synthesis of glucose from amino acids and fatty acids (gluconeogenesis).

Lipid metabolism:


- Fatty acid oxidation (energy production).

- Synthesis of lipoprotein (lipid transport).

- Synthesis of cholesterol (adrenal hormones, ovarian and testicular).

- Conversion of glucose to fat and protein (storage).
protein metabolism:

- deamination and transamination.

- Synthesis of urea (ammonia removal).

- Synthesis of nearly 90% of plasma proteins (albumin ,...).

Extras


- Storage of certain vitamins: Vitamin A + + +, D, B12.

- Synthesis of some coagulation factors:

- Dependent on Vitamin K: II, VII, IX, X.

- independent of vitamin K: V.

- Storage of free iron in the hemoglobin content (related to ferritin).

- Metabolism of certain drugs and hormones.

Formation of bile

Formation de la bile
It is continuously secreted by the liver and is stored in the gallbladder which normally sends in the duodenum and intermittently during digestion. The order of the gallbladder is nervous and humoral.

Bile consists of:


- Water.

- Mucin.

- Minerals.

- Cholesterol.

- bile pigments.



Its role is to assist in the digestion of fats and the role of alkalinization of the chyme.




Detoxification of endogenous toxins and exogenous

- Endogenous: hormones.

- Exogenous: alcohol and drugs.

- Role of conjugation: bilirubin + Glucuronic acid => water solubility.

Role metabolic

on proteins: synthesizes plasma proteins (albumin and glabuline) and coagulation factors (fibrinogen).


on lipids: synthesizes cholesterol (bile composition).


on carbohydrates:

- glycogenesis: production of glycogen.

- Glycogenolysis: conversion into glucose.

- gluconeogenesis: fabricationde glycogen with amino acids.
In the liver, there are enzymes: ASAT, ALAT that allow these changes, if these enzymes increase is synonymous cytolysis.

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Epidemiology of cholangitis


FREQUENCY:

France is estimated that 3 to 4 million people are carriers of gallstones.
they become symptomatic from 100,000 to 200,000 people each year, and is made more than 70,000
cholecystectomies per year.
Its main complications (which occur in about 20% of cases) are
acute cholecystitis (25% of them), cholangitis (21%) acute pancreatitis (7%). Thus, complicated gallstone
represents more than 20 000 new cases per year for 4% of the population
.

SEX:

It is 02 times higher in women with a sex ratio of 0.55, indeed, as the main cause of cholangitis is
gallstones, women are more often affected than Rights:
hormones promote stone formation. Pregnancy is particularly conducive to
lithogenesis.

AGE:

The average age is between 50 and 60.

THE RACE: Since

cholangitis is most often associated with gallstones, risk factors are often the same
So, in effect, the frequency is higher among people of northern Europe,
among Hispanics and Native Americans (Indians). Some populations of South Asia, in which
intestinal parasites are common, are often affected, and
inhabitants of the Far East. Africans and Americans are less affected


OTHER RISK FACTORS:


- Obesity: if weight> 20% of ideal weight.
- Diet: high-calorie diet rich in polyunsaturated fatty acids, preventive effect of a diet rich in fiber.
- Drugs: The Estrogens, Progestogens, Octreotide ...
- intestinal diseases: Crohn's Disease , resection of the terminal ileum.
- Mucoviscidose.

Tuesday, May 5, 2009

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JUNCTION choledocho ulcer

the sphincter of Oddi



The choledocho-duodenal junction is always on the inner edge of the duodenum, but to varying degrees.

Classically bile duct after crossing obliquely the duodenal wall, ending in the middle of the second duodenum, in the back of the posterior and internal surfaces, 3 or 4 cm from the pylorus at the large caruncle .

Sphincter d'Oddi

The anastomosis of the bile duct into the duodenum is common with the termination of the MPD and they lead together in a small cavity, the ampulla, which opens into the large caruncle. In fact, the light bulb, very variable in size, is not constant.
The pancreatic duct can jump higher or lower in the terminal segment of the bile duct, although no mention of Vater. Finally, the two channels can be thrown separately into the duodenum, close to one another.
A lack of pancreatic duct was sometimes observed, the pancreatic secretion is then fully discharged by the duct of Santorini.
The exit of the bile duct and pancreatic duct is provided with a sphincter: the sphincter of Oddi, which normally opposes reflux of duodenal contents in hepato-pancreatic channel.
The projection of the sphincter duodénum forme la papille duodénale, recouverte d’un capuchon muqueux, comparé à un «phimosis» muqueux. L’orifice papillaire lui-même est très petit, le plus souvent de la dimension d’une tête d’épingle. Sur le vivant, il est difficile à voir du fait de l’importance et de la mobilité des villosités de la muqueuse duodénale.


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Anatomy Liver

Le foie est la plus volumineuse des glandes annexes du tube digestif. Il est doué de fonctions métaboliques complexes et indispensables à la vie, et est situé à la partie supérieure et droite de la abdominal cavity in the upper abdomen, under the right diaphragmatic dome [9], [29].

Foie-localisation
Its lower boundary runs along the bottom edge of the chest that is, it normally does not extend beyond the costal margin.
It is the largest of the viscera. It weighs 1.5 kilograms itself, which must be added about 0.5 kg of blood from the living, He is smooth, firm consistency, color red brown, consisting of a friable parenchyma surrounded by a thin fibrous capsule: the capsule of Glisson ;
- It is conventional to describe three sides to the liver: upper, inferior and posterior:


- The upper surface is diaphragmatic and is convex.


- The underside is visceral and has three grooves H that determine four lobes:

- right lobe;

- left lobe;

- caudate lobe;

- coded lobe or lobes Spiegel (bottom).
Foie-Face inférieure

Each lobe is divided into one or more segments, and the liver is made up entirely of 08 segments, each being subject to proper vascularization.
- The back is nearly vertical and mold on the anterior vena cava (but never completely surrounds the liver the vena cava) and the convexity of the spine

Vascularization is Double:


hepatic artery: nutritional circulation of the liver, it is from the celiac trunk.


Portal vein: functional traffic: Drainage of venous blood from the digestive tract containing the nutrients absorbed from the intestinal mucosa and that will be transported to the liver cells to be processed and stored = the portal system.

We will come back at the " Hepatic Pedicle .

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The gallbladder


The gallbladder is a pear-shaped bag, along 8 to 10 cm wide and 3 or 4 cm. Its capacity is about 50 ml (1-2 ml / g body weight).

It lies in the cystic fossa, located on the underside of the right lobe of the liver, adjacent to the caudate lobe and caudate lobe separated by tracts that lead to the hilum of the liver.
It is divided into several parts:


- Bottom: Rounded, responds to the notch of the anterior cystic liver, the gallbladder is full when it reaches the parietal peritoneum near the anterior end of the 9th costal cartilage.
- The body : Whose upper side adheres to the liver and whose underside is covered by the parietal peritoneum.


- The infundibulum.
- Col. : Long 2 cm is angled forward and right with the body and form an acute angle open forward.
The cystic duct

He was born at the neck of the gallbladder and a path S to reach the hepatic duct. The cystic duct is often moniliforme in its upper part where the light is occupied by the valves of Heister, kind of braces that are opposed to the folding of the channel, and thus allow the bile to reach the gallbladder, regardless pressure. It is smooth in its distal part.
Its caliber increases from the gallbladder (2 or 3 mm) to its terminal portion (3 or 5 mm). Its average length is 2 to 3 cm, can reach 6 cm when it flows directly into the duodenum. Its mode of termination is variable.
The cystic short address in general the hepatic duct close to the hilum, at right angles. Normally the cystic duct attaches itself to the right edge of the bile duct that runs up to their entrances into it.

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accessory bile duct bile duct


It originates in the liver hilum of the junction of right and left hepatic ducts. Its formation is highly variable. It can be straight. More often it makes an arc accentuated himself up at the hilum and in the form of an elongated S. Sometimes she has an angular path. When the angle is very pronounced light may seem narrow.

hepatic ducts


Conventionally, the left and right hepatic ducts emerge from the liver at the hilum and immediately merge to form the hepatic duct that comes from 0.75 to 1.5 cm below the liver.
The left hepatic duct, because of its greater obliquity, is generally longer than the right. The latter is very short and does not exist in 38% of cases. It is then replaced by the 2 channels sectoral rights, paramedian and lateral, which are directly involved in the formation of the main junction.
A number of channels intra-hilar biliary accessories often drain directly into the confluence of the main left and right channels.

the common hepatic duct

The hepatic duct descends along the free edge of the lesser omentum to the foramen of Winslow. At a variable it converges with the cystic duct and gives rise to the bile duct. He has averaged 2 to 3.5 cm long, with extreme dimensions 1 to 5 cm. Its diameter varies from 0.4 to 1.5 cm with an average width of 0.8 cm.

the bile duct



The bile duct descends into the peritoneal layer hepato-duodenal and passes behind the duodenum and the first head of the pancreas. At this level it bends to the right to empty into the duodenum. The bile
be buried on a variable length in the pancreatic head where he dug a deep groove that covers the pancreatic tissue more or less completely backwards.

In its retro-duodenal portion, the duct may be in contact with the duodenum or not be separated by 2 cm of pancreatic tissue. The length of the duct varies depending on the level of the confluence with the cystic duct. It is an average of 5 cm with extreme numbers of 1.5 to 9 cm. The diameter
normal bile duct does not exceed 10 to 12 mm, judged on radiographies.Le diameter of the bile duct increases with age. There is no correlation between the size of the bile duct and the weight and size of individuals.
In its final part, just before its drainage into the duodenum, the bile duct has an inner diameter that tapers sometimes brutally, as is clearly seen on radiographs. The end portion has a length of 11 to 27 mm (16 in average). It is the sphincter of Oddi.

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PATHOPHYSIOLOGY Cholangitis

In most cases cholangitis is the result of a complete or incomplete obstruction on serving the CBD, but in some cases much more rare it occurs comparison of patients with CBD free [16].

cholangitis WITH OBSTRUCTION OF THE CBD

Three elements are involved in their development:

- A complete or incomplete obstruction of the bile duct.

- The penetration of pathogens into the CBD.

- factors promoting the spread of the root canal infection.


Injury of the CBD

is complete or incomplete obstruction of pathogens is essential. Stasis and dilatation of the CBD are the consequence of obstruction and contribute to the development of infection.


penetration of germs in the CBD

The multiplicity of channels offered reflects their possible interaction and ignorance of the exact mechanism.

ductal upward track:
remains the most commonly accepted, but it was discussed. It is reflux of enteric and stasis upstream allows them to multiply.

Thus the origin of intestinal bacteria isolated is a compelling argument in favor of this hypothesis. But the relative sterility of the duodenum is an objection to this theory.


hematogenously:
It has been suggested that the portal route involves the passage of intestinal bacteria in portal blood and their return to the hepatic bile after treatment, but this mode of penetration of germs seems very questionable.

the direct route:
This mode of infection of the bile duct is present, less often involved.
It is the result of a traumatic biliary tract infections, mainly instrumental endoscopic maneuvers, and any surgery on the hepatobiliary sphere.


Dissemination of infection


Is done in two ways:


Local Propagation: From
infection directly responsible for biliary abscess formation at the walls of the bile ducts or hepatic parenchyma.

Broadcast:
Infectious process is done through blood, this blood-borne hypertension is facilitated by the CBD in relation to prevailing the existence of the obstacle.

Thus several studies have demonstrated the existence of reflux cholangioveineux bacteria on an obstructed bile duct under pressure just higher than that of the hepatobiliary secretion.

Moreover, whatever the mode of spread of infectious process, terrain plays a facilitating role. Thus, cholangitis develops in a more severe in immunocompromised patients (treatment with corticosteroids and immunosuppressants), and elderly patients or carriers of multiple defects.



cholangitis TRACK FREE BILE


gastrointestinal reflux in VB

It seems that the reflux isolé ne puisse entraîner qu'exceptionnellement des angiocholites. Il s'observe dans la plus part des cas opérés après anastomose bilio-digestive, le plus souvent cholédoco-duodénale.

De plus l'exploration chirurgicale ou endoscopique des anastomoses bilio-digestives cholédoco-duodénales à permis de constater la relative fréquence des débris alimentaires stagnants dans la VBP.

Les angiocholites au cours d'une infection siégeant en dehors de la VBP, il s'agit d'un problème encore mal élucidé.

However, in cases of suppurative cholecystitis, intrahepatic abscess or primary or working in the context of a sepsis, intraoperative bilicultures can show pre ; presence of an infection of the bile duct with normal bile duct. The hypothesis of Oddi spasm associated reaction could be considered.

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Introduction to the History of cholangitis


The activity of a general surgeon is dominated by biliary surgery.

Indeed, several studies around the world can show that 25% of surgeries at the hospital level are interventions for gallstone disease.

On the other hand, the prevalence of gallstone disease as it represents the most common cause of cholangitis is estimated between 15 and 25 % of the adult population.


Thus biliary disease and more accurately because of cholangitis is a mortality, bed occupancy in hospitals and increased health costs.


Indeed, cholangitis is a complication of biliary lithiasis especially as it requires multidisciplinary care (medical and surgical) to be specific and tailored .

Interest of the question ...

The interest we take in this condition is based on the frequency of cholangitis and its severity represented by the high mortality rate.

other hand, the concept of cholangitis, which highlights the affections of their bile purely surgical field and opens the door to an area where many medical and surgical clinical features, therapeutic and I ; biological entangled me.

Indeed, the indication of operative cholangitis is unambiguous, the time of surgery remains a topic of discussion, as patients are operated variable within the hospital for immediate emergency and up to several weeks in the delayed emergency.



For all these reasons it seemed useful to conduct a retrospective study at the University Hospital of Annaba (Algeria) on cholangitis, allowing a diagnostic approach as well as tea
peutic.

This study will, hopefully, contribute to a better management of cholangitis CHU Annaba

L'angiocholite

(«angio-» du grec aggeion signifiant: vaisseau ou conduit, «chol(é)-» du grec kholè signifiant: bille et le suffixe «-ite» du grec itis servant à désigner une inflammation)
[25]correspond littéralement à une inflammation des voies biliaires .

En pratique le terme angiocholite est utilisé pour désigner un syndrome clinique qui, dans sa forme typique de l’angiocholite aigue lithiasique, associe une douleur de l’hypochondre droit, une fièvre and jaundice. It reflects an infection of the bile and an acute inflammatory condition of the walls of the bile ducts.


But the definition of cholangitis varies schools:

Indeed, the French school emphasizes the definition of bacteriological affection, describing and cholangitis as an acute bacterial infection of the bile ducts inside and outside the liver, gallbladder excluded. So they opt for the concept of cholangitis sans obstacle


En revanche les anglo-saxons la définissent comme étant une infection de la bile associée obligatoirement à un obstacle lithiasique des voies biliaires dans 90% des cas.


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cholangitis

Cette maladie est reconnue depuis 1877 , quand CHARCOT en donna la première description, en rapportant la triade symptomatique associant :

  • Douleurs de l'hypochondre droit ;
  • Fièvre avec frissons ;
  • Et Ictère.

In 1903 : ROGERS After noting, in autopsy studies, the relationship between suppurative cholangitis, obstruction of the biliary tract and abscess hey , Hepatic, tried first, unsuccessfully surgical decompression of the bile duct (CBD) in a patient who had a
acute obstructive suppurative.

In 1940 : CUTLER and ZOLLINGER : insisted on the need for early surgical intervention.

In 1945 : GRANT reported 03 cases of acute suppurative cholangitis secondary to a gallstone obstruction of the bile duct. Patients survived after decompression
VBP, the same year CAROLI created the concept of cholangitis urémigène. In 1947

: COLE described cases of suppurative cholangitis on obstruction of the CBD in relation to calculations, a cancer of the pancreas head and stenosis. In 1959

: CAROLI and ANDRE clarify the concept of cholangitis urémigène emphasizing the need for anatomical and clinical correlation: Triad of Charcot and obstacles on the VBP


- On the same date REYNOLDS and Dargan USA individualize the Hyper-complicated acute septic characterized: In terms of clinical signs of nervous type of mental confusion, lethargy and the onset of septic shock.
A purulent bile under pressure in the presence of complete obstruction of the CBD They intitulent this form of "acute obstructive cholangitis.


- Thereafter the term adopted by the Anglo-Saxon authors to describe these forms hyper-tank is that of "acute obstructive suppurative cholangitis »

- Depuis la première description du traitement chirurgical par ROGERS , en 1903 et jusqu'en 1969 quelques rares publications sont relevées dans la littérature.

- Ces dernières années, malgré la persistance d'aspects encore mal connus dans la pathogénie, un certains nombres de progrès ont été réalisés, dans la connaissance de cette maladie dans le domaine du diagnostic et de la thérapeutique :

- Dans le domaine diagnosis must include the contribution of some interesting new techniques of biliary opacification (VB) and especially the contribution of ultrasonography in the exploration of the liver and VB in an emergency.

- On the therapeutic (treatment), greater control of preoperative resuscitation techniques (eg hemodialysis), facilitated by the use of new antibiotics more effective on the bladder infection represent the single most interesting. Their goal is to facilitate the processing
surgery.


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LIVER HISTOLOGY

Architecture liver [34]


branching pedicle within segments leads to portal areas constituésd'une branch artery hey ; hepatic, a branch of the portal vein and a bile duct or two. Several portal areas that define a center lobe centrilobular vein.

Blood passes from the portal to centrilobular vein within the liver parenchyma. Liver parenchyma consists of hepatocytes arranged in single cell spans tense area periportal to centrilobular area and separated from each other by sinusoids.


Liver Cells

There are parenchymal cell (hepatocyte) and sinusoidal cells (endothelial cells, Kupffer and stellate cell of the liver).


Hepatocyte: The hepatocyte has a dual polarity. His face is sinusoidal in intimate contact with the portal blood through the endothelial cell. This is an area of intense exchanges where the cell draws the elements necessary for its synthesis activities (lipids, proteins and carbohydrates) and catabolism (xenobiotic hormones ...) and dumps the product of these activities. His face

delineates the biliary canaliculus biliary own space without walls defined by the decline of the membranes of two adjacent hepatocytes. Bile secreted by the fireplace in the hepatocyte canalicular system and is then collected in juxta-portal ductules that drain into the bile duct of the portal.

endothelial cells: endothelial cell limits the sinusoid and prevents blood from s'imiscer in the space of Disse while allowing its pore system, the e exchange between plasma and hepatocyte.

Kupffer Cell: He is a resident macrophage, located inside the sinusoid, is to act as "purifying" the blood sinusoidal impurities not adopted by the intestinal wall (bacterial endotoxins, viral particles or mineral ...).

liver stellate cells: (CET also called Ito cells or perisinusoidal cell). Located in the space of Disse, the ETC's functions (1) the storage of vitamin A and (2) synthesis la matrice extracellulaire hépatique.

HISTOLOGIE DE LA VESICULE BILIAIRE [29]



La vésicule biliaire possède un revêtement séreux et une couche de tissu sous-séreux conjonctif au-dessous de laquelle se trouve :

La couche musculaire : Celle-ci est constituée par un filet irrégulier de fibres lisses longitudinales, obliques et transversales, mélangées à des fibres élastiques et collagènes.

A l'intersection du col de la vésicule et du canal cystique, there in 75% of muscle thickening that would play the role of cervical vesicle sphincter: the "sphincter" of Liitkens, was the subject of much debate.

"There is no muscularis mucosa.

mucosa: forms numerous folds divided themselves into smaller folds. Most wrinkles disappear when the gallbladder is very distended.

epithelium: is made of high-span of cells. If they are devoid of striated border, study these cells in phase contrast microscopy and ultramicroscopy showed the existence of fine microvilli sometimes containing fat.

mucosa contains no glands, except in the neck region where it is in the lamina propria and in the layer périmusculaire simple tubulo-alveolar glands with epithelial cuboï and clear of, secreting mucus.

HISTOLOGY OF THE BILE DUCT [29]

Includes two tunics: mucosa tunic and elastic more or less rich in muscular fibers.

mucosa: is made of a columnar epithelium without villi, but having kind of columns. It contains numerous mucous glands, which may extend to the adventitia.

The elastic tunic: is composed of collagen fibers and elastic fibers. The muscle fibers are rare and only longitudinal. These muscle fibers become abundant at the lower end of the bile duct at the sphincter of Oddi.


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FORMS OF CLINICAL cholangitis Cholangitis

asymptomatic asymptomatic

The discovery when it operates (during surgery) for gallstones (cholecystectomy), in this case can evolve cholangitis sue a less evocative, the discovery is obviously more difficult especially in the absence of previous biliary known [8].


crude form LATENT OR

It is rare mais possible. Il y a peu de signes cliniques, existe surtout chez le vieillard. Cependant même latente, cette angiocholite impliquera un geste rapide car des complications risquent d'être très brutales.

Les angiocholites latentes peuvent s’extérioriser brutalement, lors d’une poussée aigue d’une maladie lithiasique, ou dans diverse circonstances :

- Opacification instrumentale des voies biliaires.

- Sphincterotomie endoscopique.

- Endoscopie cholédocienne.

- Explorations manométriques peropératoires.


FORMES SYMPTOMATIQUES

- Forms purely painful.

- Pure febrile forms.

- Forms icteric pure.


COMPLICATED SHAPE: "The acute cholangitis icterus UREMIGENE"

- fortunately rare, but still fear it achieves a typical picture of cholangitis but is, in the hours and the maximum in few days, accompanied by a severe septic shock who goes largely to the forefront, combining a very short period of time renal organic. Age above 70 is an additional factor of gravity. Clinically

:

jaundice is a very fast installation and becomes very intense, "said" flamboyant. "

- Signs of toxic shock-infectives.

- And the rapid installation of a renal organic (oliguria).

- Sometimes disorders of consciousness (delirium). Biologically

:

- Thrombocytopenia \u0026lt;150,000 mm3.

- Direct bilirubin that can be> 400 mmoles / l.

- Increased blood urea> 20 mmol / l and creatinine> 110 mmol / l.

- Hyperkalemia dangerous above 6 mEq / l.

- acidosis (retention of H + that are not eliminated).

is an emergency treatment will require unblocking the bile duct and possibly hemodialysis.



Customized Stick Wars



Infection des voies biliaires n’est jamais primitive. Elle se rencontre en cas de stase biliaire secondaire à un obstacle incomplet des voies biliaires extra hépatiques, plus rarement dans les affections des voies biliaires intra hépatiques et en cas de reflux du liquide duodénal dans les voies biliaires.

Et malgré la grande diversité des affections pouvant conduire à une angiocholite, l’étiologie est dominée incontestablement par la lithiase biliaire [4][41].



LES OBSTACLES INCOMPLETS DE LA VOIE BILIAIRE PRINCIPALE


Gallstones

Conceivably, for there to be precipitation, it was necessary that there be a fault with the solubilizer, bile salts, or an excess of the substance to dissolve cholesterol.

This imbalance could have a foodborne because, in fact, cholelithiasis is much more common in Europe and the Far East. But it is certain that these dietary factors are not the only ones involved. There are probably circumstances where the rate of salt Bile is insufficient.

endocrine factors could cause such an alteration, the stone is more common in women and appears to be particularly favored by pregnancies.

But in some cases, although different, the stone is due to an excess of bilirubin, resulting from hemolysis: these are pigment stones.

Gallstones represents the main etiology of cholangitis, it is due to a single calculation or multiple stones, they will promote infection.


cholelithiasis

It lithiasis of the bile duct, most commonly due to calculations (calculation of the low - choledochal choledochal or ballast) is a frequent complication ; quente of lithiasis of the gallbladder, it can still occur without any vesicular disease.

It is clinically characterized by Charcot's triad: pain, fever, with such a prominent symptom obstructive jaundice . The general condition is good at first, then eventually deteriorate. The


cholelithiasis is complicated:



- Liver failure and the resulting biliary cirrhosis.


- The suppurative cholangitis: big suppuration of the entire biliary tree, which can create a true septicemia with renal disease (cholangitis urémigène).


inflammatory strictures of the bile duct Main

mostly due to surgical trauma, usually during a cholecystectomy. The wound during surgery is unknown in most cases.

These are usually short strictures who sit at the junction of cystic duct - common hepatic duct. These strictures

post traumatic cause cholangitis in 64% of cases, either in the immediate postoperative period or after several months or one year of intervention.


Tumor of the ampulla of Vater


Papillitis stenosing


Pédiculite





DISORDERS OF BILIARY LIVER INTRA

They are rare but must ê ; be known because they cause stasis and biliary infection.


Caroli Disease

dysgenesis is a congenital intrahepatic bile duct, head of multifocal cystic dilatation, it is associated in most cases with hepatic fibrosis.

More rarely, absence of hepatic fibrosis, the disease is so often localized to a portion of the liver and may be accompanied by other congenital malformations of the bile duct (choledochal cyst ).

disease acquired and not congenital. Clinically it may be asymptomatic and discovered incidentally, bulletin recurrent cholangitis start between 5 and 30 years.



biliary papillomatosis

It is a condition characterized by papillary hyperplasia in continuous sheets of the mucosa of the bile ducts. Cancerous degeneration is common, it is considered rare cause of cholangitis.


The intrahepatic gallstones are seldom

purveyors of cholangitis, besides the existence of the latter, in this case is discussed.


reflux of duodenal fluid in the biliary

It can be spontaneous, without any apparent stasis and be due to:


fistula Spontaneous bilio-digestive

They are usually progressive complications of lithiasis biliary-duodenal fistula cholecysto are most frequent, but often less complicated than cholangitis cholecysto-colic fistula. The risk of cholangitis appears to be related mainly to the gene flow of bile.


Can be due to some surgical

Such as sphincterotomy and choledocho-duodenal anastomoses that are responsible for reflux into the bile ducts and cholangitis.


PARASITIC

In general they are associated with cholelithiasis:

Some parasites " fluke Fasciola hepatica in ", " Ascaris " create a barrier intraductal.


Other parasites that tells "the alveolar echinococcosis " or hydatid cyst, are responsible for compression. Note the possible migration of vesicles, girls or membranous debris in the bile duct, evidence of a cracking of the cyst.

Note the special case of cholangitis Far East mostly due to a fluke in " clonochis sinensis " cholangitis in this case is due to inflammatory stricture of intrahepatic bile ducts with inflammation of the parasite.

The prognosis is usually bleak cholangitis.


RECURRENT PRIMARY

Cholangitis is a disease of unknown etiology, met in the Far East, usually associated with intrahepatic lithiasis, more rarely a parasitic " Clonorchis sinensis .


CAUSES CANCER: It

a less common cause is mainly cites: cancer of the pancreatic head, ampulla of Vater, cancer of the bile duct or common hepatic duct. The prognosis of this type is particularly acute cholangitis.


The odditis sclerosus-CHRONIC PANCREATITIS

constitute rare causes of cholangitis.


Cholangitis IATROGENIC

They are rare, and they are the price of progress in the techniques of opacification of bile ducts, as well as in non-surgical methods intervention on the bile duct.


The T-tube cholangiography: cholangitis is caused by venous reflux cholangio promoted by intracanal pressures greater than 25 cm of water.

cholangiography transparietal: The
cholangitis is caused by a dual mechanism:

- Increased intraductal pressure during injection of contrast.

- Sowing the seeds by direct blood bile during transhepatic puncture.

The endoscopic retrograde cholangiopancreatography:
Two conditions seem necessary to cause cholangitis, following an ERCP

- Getting overpressure bile previously infected.

- Existence of a prior biliary obstruction.


The Mirizzi syndrome

Mirizzi syndrome is a rare complication of cholelithiasis in connection with an extrinsic compression of the bile duct by a stone impacted in the infundibulum or in the cystic duct [36].


OTHER CAUSES

They may be foreign, including foodborne, which are sometimes responsible for cholangitis.