Acute pancreatitis

ACUTE PACREATITIS 

Its an acute inflammatory process caused by the effects of enzymes released from the pancreatic acini . There are numerous aetiological factors .

The pancreas is a super gland behind the breadbasket and close to the duodenum—the first part of the diminutive intestine. The pancreas secretes digestive juices, or enzymes, into the duodenum through a tube titled the pancreatic duct. Pancreatic enzymes join with bile—a liquefied produced in the liver and stored in the gallbladder—to digest food. The pancreas also releases the hormones insulin and glucagon into the bloodstream. These hormones help the body regulate the glucose it takes from food for energy.

PATHOGENESIS of acute pancreatitis is obscureb,but two main mechanism may be involved 

1.DUCT OBSTRUCTION __ this may lead to reflux of bile into the pancreatic ducts causing injury .Alternatively increased intraductal pressure may damage the pancreatic acini ,leading to leakage of pancreatic enzymes which may further damage the pancrease .

2.DIRECT ACINAR DAMAGE __ this may be caused by viruses ,bateria ,drugs or trauma .

The appearance of the pancrease in acute pancreatitis may be explained by release of pancreatic enzymes. Protease release causes widespread destruction of the pancrease and increases further enzyme release ,with consequent further damage.Release of lipase causing fat necrosis resulting in characteristic yellowish-white flecks on the pancrease ,mesentry and omentum .Often with calcium deposition.Other enzymes ,e.g. elastase ,destroy blood vessels ,leading to haemmorrhage within the pancrease and haemmorrhagic exudate into the peritoneum .Haemmorrhage may be extensive ,leading to acute haemmorrhagic pancreatitis.

BIOCHEMICAL CHANGES increased serum amylase. Amylase is released from the damaged acini and enters the blood stream .The serum amylase is released in the acute phase ( 24 - 48  h) but later falls to normal .Occasionally with acute haemmorrhagic pancreatitis the destruction of pancreatic acini is so swift and complete that the serum amylase may not be raised by th time the patient reaches hospital. Hypocalcaemia ,this arises become of deposition of calcium in areas of fat necrosis .Hyperglycemia ,this occurs because of associated damage to the pancreatic islets .Abnomal liver function tests may occur , especially raised bilirubin and alkaline phosphatase due to mild obstruction of the bile ducts by oedema .

Sudden, unceasing discompose in the upper part of the abdomen is a hallmark of acute pancreatitis, though other medical conditions crapper also cause this type of pain. The discompose may wrap around your upper body and involve the back in a band-like pattern. The discompose typically lasts days and is ofttimes relieved by leaning forward. Some grouping hit only slight abdominal tenderness and in 5 to 10 percent of people, there is no discompose at all.

In grouping with gallstone pancreatitis, gallbladder discompose may become before pancreatic pain. Gallbladder discompose (referred to as biliary colic) occurs in the right upper abdomen, extending to the back and right shoulder. The discompose gradually increases in intensity, is constant, and may be attended by sickness and vomiting. Gallbladder discompose ofttimes follows a meal.

In grouping with alcoholic pancreatitis, the symptoms of acute pancreatitis ofttimes become digit to three days after an alcohol binge or after stopping drinking. Pain is attended by sickness and regurgitation in most people. In severe cases, the initial symptom may be shock or coma. 

Other conditions that have been linked to pancreatitis are:

Damage to the ducts or pancreas during surgery
High murder levels of a fat titled triglycerides (hypertriglyceridemia)
Injury to the pancreas from an accident
Blockage of the pancreatic duct or common bile duct, the tubes that pipage enzymes from the pancreas 

Diagnosing accent pancreatitis is often difficult because of the deep location of the pancreas. The student will likely visit one or more of the mass tests:

•Abdominal ultrasound. Sound waves are dispatched toward the pancreas finished a handheld device that a technician glides over the abdomen. The good waves bounce soured the pancreas, gallbladder, liver, and other organs, and their echoes make electrical impulses that create a picture—called a sonogram—on a recording monitor. If gallstones are causing inflammation, the good waves will also bounce soured them, showing their location.

•Computerized picturing (CT) scan. The CT construe is a noninvasive x ray that produces three-dimensional pictures of parts of the body. The person lies on a table that slides into a donut-shaped machine. The effort may exhibit gallstones and the extent of alteration to the pancreas.

•Endoscopic ultrasound (EUS). After spraying a solution to numb the patient’s throat, the student inserts an endoscope—a thin, flexible, aflame tube—down the throat, finished the stomach, and into the small intestine. The student turns on an ultrasound adhesion to the scope that produces good waves to create seeable images of the pancreas and bile ducts.

•Magnetic kinship cholangiopancreatography (MRCP). MRCP uses attractable kinship imaging, a noninvasive effort that produces cross-section images of parts of the body. After being lightly sedated, the patient lies in a cylinder-like plaything for the test. The technician injects dye into the patient’s veins that helps exhibit the pancreas, gallbladder, and pancreatic and bile ducts.

 

Treatment of pancreatitis

Treating pancreatitis

IT OCCURS SUDDENLY AND SUBSIDE IN FEW DAYS IF TREATS PROPERLY.

EACH YEAR ABOUT 210,000  PEOPLE IN THE US ARE ADMITTED TO THE HOSPITAL WITH ACUTE PANCREATITIS.

TREATMENT

The goals of communication of accent pancreatitis are to alleviate pancreatic inflammation and to correct the inexplicit cause. Treatment commonly requires hospitalisation for at small a few days."Treatment of accent pancreatitis"

BED REST
SUPPORTIVE INTRAVENOUS THERAPY  restore adequate blood volume as soon as possible e.g by physiological saline .A careful fluid balance chart should be kept ,with appropiate allowance made for insensible loss .Daily serum electrolyte estimations are made ,together with acid-base studies.Full water replacement is given by intravenous route .Calories are given as glucose .Na ,K ,and Cl are given in appropriate amounts .ca deficiency, if develops , is treated by Ca gluconate IV

NASOGASTRIC ASPIRATION   continuous suction removes gastric HCl from entering duodenum,that suppressing hormonal stimulation of exocrine secretions of pancrease .It also brings relief from persistent nausea and vomiting.

PAIN RELIEF  
Originally it was thought that analgesia should not be provided by morphine because it haw drive symptom of the musculus of Oddi and exacerbate the pain, so the drug of choice was meperidine. However, due to lack of effectualness and risk of toxicity of meperidine, more recent studies hit institute morphine the analgesic of choice. Meperidine haw ease be utilised by some practitioners in more secondary cases, or where morphine is contraindicated.

PROPHYLACTIC ANTIBIOTICS  given as a prophylactic against infection of necrotic retroperitoneal tissue ,and also against bronchopneumonia .A  broad spectrum antibiotic ,e.g. cefoperazone should  be given for 3-5 days.

EDOSCOPIC SPHINCTEROTOMY gallstone pancreatitis will be improved ,if a stone is obstructing the ampulla of vater .

Surgical options for pussy necrosis include:

• Minimally intrusive management - necrosectomy through small incision in wound (left flank) or breadbasket
• Conventional management - necrosectomy with ultimate drainage
• Closed management - necrosectomy with closed continuous postoperative lavage
• Open management - necrosectomy with planned staged reoperations at definite intervals (up to 20+ reoperations in some cases)

COMPLICATIONS include : Pancreatic Pseudocyst __  this is a localized collection of fluid in the lesser sac of peritoneum. Pancreatic Abscess , Stress induced gastric erosion with haemate mesis or melena .Acute renal failure  ,Toxic psychosis ,Multiple organ failure ,chronic pancreatitis .

PROGNOSIS  the overall mortality is between 10 % and 20 % .With severe haemmorrhagic pancreatitis the mortality rate reaches 50 % .The usual cause of mortality is multiple organ failure .

Acute pancreatitis
Sign and symptoms
Causes
Patophysiology
Diagnosis

Cholecystitis acute

INCIDENCE RATE APPROXIMATELY SAME IN WORLDWIDE

5 TO !0 % MORTALITY OCCURS IN PATIENTS OLDER THAN 60 YEARS.

ACUTE CHOLECYSTITIS : is an inflammation of the gall bladder ,and is usually associated with stones. Occasionally it occurs without stones,i.e. acalculous cholecystitis.The later may be due to infection with E coli .Clostridia,or rarely Salmonella typhi. Acalculous cholecystitis may occur after prolonged starvation or total parenteral nutrition. Stasis is probably a contributing factor in the latter conditions .

The gall bladder becomes oedematous ,with mucosal ulceration ,and a fibrinopurulent exudate .Acute inflammatory cells infiltrate the wall . Even in the presence of thrombosis of the cystic artery ,gangrene is rare ,as the gall bladder gains a blood supply directly from the liver via the gall bladder bed .However ,gangrene does occasionally occur with perforation of the gall bladder ,resulting in generalised bile peritonitis or a localised abscess depending on whether the gall bladder has been walled off by adhesions or not .An empyema of the gall bladder may also result, suppuration occuring within the gall bladder and the gall bladder becoming distended with pus. Occasionally the gall bladder may fistulate into the duodenum.

Factors that haw initiate the inflammatory process include the manufacture of inflammatory mediators (eg, lysolecithin and prostaglandins); an increase in intraluminal pressure in association with compromise of the murder supply; and chemical botheration by bile acids. 

90 % calculous and 10 % acalculous, Acalculous cholecystitis associated with higher complication rate and associated with acute illness ( i.e. burns ,trauma, major surgery ) ,fasting ,hyperalimentation leading to gall bladder stasis ,vasculitis ,carcinoma of gall bladder or common bile duct ,some gall bladder infections ( Leptospira ,Streptococcus,Parasitic ,etc.) but in >50% of cases an underlying explanation is not found.

In patients who hit emphysematous cholecystitis, ischemia of the gall bladder surround is followed by infection with gas-forming organisms that display pedal in the bladder lumen, in the gall bladder wall, or both. In 30-50% of patients, preexisting diabetes mellitus is present; the male-to-female ratio is 5:1.1 Gas haw be confined to the gall bladder; however, in 20% of cases, pedal is also seen in the rest of biliary tree. Gallstones are not inform in 30-50% of cases, and the mortality rate is 15%.1  There is a predisposition for gangrene formation and perforation, but clinical symptoms are mild; much symptoms can be deceptive. Emphysematous cholecystitis haw occur after chemoembolization performed as palliation for hepatocellular carcinoma; after fat embolism during aortography; and after gall bladder hypoperfusion during viscus resuscitation.

CLINICAL FINDINGS

Acute cholecystitis usually occurs with correct upper quadrant discompose and tenderness. The abdominal discompose increases with time. The place of discompose is usually the correct subcostal region, though the discompose haw begin in the epigastrium or the mitt upper quadrant and then shift to the correct subcostal region to the area of the gallbladder  inflammation. Referred discompose to the correct shoulder or the interscapular region haw be experienced. Approximately greater than half of patients hit had preceding attacks of similar discompose that spontaneously resolved. Anorexia, nausea, and vomiting haw occur, but vomiting is seldom severe. Most patients are symptom and hit no leukocytosis.

When feverishness occurs, the patient's temperature is seldom higher than 38°C. Chills are unusual; their proximity suggests a case of complicated cholecystitis (abscess or associated cholangitis).

In some patients with acute cholecystitis  hit mild jaundice, which haw be related to ordinary hepatic edema, bile duct edema, or both, or to the proximity of calculi within the common bile duct.1 In most patients, improvement occurs within 24 hours after hospitalization, and signs and symptoms gradually subside. Persistent pain, feverishness and leukocytosis, chills, and more nonindulgent localized or generalized compassionateness haw indicate complicated disease, much as abscess manufacture or GB perforation. The utilization of empyema of the GB haw display systemic toxicity, and it haw be predictive of GB perforation.

Acute acalculous cholecystitis  is difficult to diagnose clinically. It often occurs in children  and in patients who are critically ill or who hit fresh undergone pronounce from nonindulgent trauma, burns, or surgery. Predisposing factors allow prolonged fasting, immobility, and hemodynamic instability. Often, these patients cannot impart pain; however, fever, jaundice, vomiting, abdominal tenderness, leukocytosis, and hyperbilirubinemia are highly suggestive findings.

In approximately 1/3rd of patients, a distended, tender gall bladder haw be palpable as a distinct mass. This is an important clinical finding and haw confirm the diagnosis.

LABORATORY TEST Shows mild leukocytosis ,serum bilirubin alkaline phosphatase and AST may be mildly elevated.

DIAGNOSTIC INVESTIGATIONS

CHEST AND PLAIN ABDOMINAL X-RAYS it can help to exclude other causes ,and show radio-opaque stones .

ORAL CHOLECYSTOGRAPHY it is unreliable during acute attack , and is postponed until patients has recovered.

ULTRASONOGRAPHY confirm the diagnosis.

RADIOISOTOPE SCANNING confirm the diagnosis .

TREATMENT

CONSERVATIVE TREATMENR FOLLOWED BY CHOLECYSTECTOMY 

No oral intake ,nasogastric suction .IV fluids and electrolytes ,analgesia ( mepridine or NSAIDS ). and antibiotics ( ureidopenicillins ,ampicillin sulbactam ,third generation cephalosporins ,anaerobic coverage should be added if gangerous or emphysematous cholecystitis is suspected , consider combination with aminoglycosides in diabetic patient or others with signs of gram-negative sepsis.Acute symptoms will resolve in 70% of patients.

SURGERY  Optimal timing of surgery depends on patients stabilization and should be performed as soon as feasible. Urgent cholecystectomy is appropriate in most patients with a suspected or confirmed complication. Delayed surgery is reserved for patients with high risk of emergent surgery and where the diagnosis is in doubt.

Recurrent symptoms are common in patients with acute cholecystitis who are treated expectantly; most patients need elective cholecystectomy.

Percutaneous cholecystostomy is a minimally invasive procedure that can goodness patients with serious comorbidity who are at broad venture from major surgery. Percutaneous cholecystostomy can be performed at the bedside low local drug and is suitable for patients in qualifier care units and those with burns. It is the expressed treatment in patients with acalculous cholecystitis , or it may be used as a temporising measure—to pipage pussy bile and retard the requirement for expressed treatment.

Treatments for ulcerative colitis

TREATMENT

Both medications and surgery have been used to treat ulcerative colitis. However, surgery is reserved for those with severe rousing and life-threatening complications. There is no medication that can cure ulcerative colitis. Patients with ulcerative redness will typically undergo periods of relapse (worsening of inflammation) followed by periods of remission (resolution of inflammation) lasting months to years. 

During relapses, symptoms of abdominal pain, diarrhea, and rectal injury worsen. During remissions, these symptoms subside. Remissions usually occur because of communication with medications or surgery, but occasionally they occur spontaneously, that is, without some treatment.

Medications treating ulcerative redness allow 1) anti-inflammatory agents such as 5-ASA compounds, systemic corticosteroids, topical corticosteroids, and 2) immunomodulators.

Anti-inflammatory medications that modification intestinal rousing are analogous to arthritis medications that modification render rousing (arthritis). The anti-inflammatory medications that are used in the communication of ulcerative redness are:

Immunomodulators are medications that suppress the body's insusceptible system either by reaction the cells that are responsible for immunity, or by interfering with proteins that are important in promoting inflammation. Immunomodulators increasingly are becoming important treatments for patients with severe ulcerative redness who do not move adequately to anti-inflammatory agents. Examples of immunomodulators allow 6-mercaptopurine (6-MP), azathioprine (Imuran), methotrexate (Rheumatrex, Trexall), cyclosporine (Gengraf, Neoral).

SURGERY

If fasting and lifestyle changes, drug therapy or other treatments don't assuage your signs and symptoms, your doctor may propose surgery.
Surgery can often decimate ulcerative colitis. But that usually means removing your whole colon and rectum (proctocolectomy). In the past, after this surgery you would dress a small bag over an opening in your cavum (ileostomy) to collect stool. But a procedure titled ileoanal anastomosis eliminates the need to dress a bag. Instead, your doc constructs a pouch from the modify of your small intestine. The pouch is then attached directly to your anus. This allows you to expel squander more normally, although you may hit more-frequent viscus movements that are soft or watery because you no individual hit your colon to absorb water.

If you hit surgery, communicate your doctor whether an ileostomy or an ileoanal pouch is correct for you. Between 25 and 40 proportionality of people with ulcerative colitis eventually need surgery.

COMPLICATIONS 


These include toxic dilatation .haemmorrhage ,stricture and perforation .Carcinomas may occur ,the overall incidence being around 2% .However ,in patients who have had the disease for over 25 years this rises to 10 %.Factors associated with higher risk inclde onset in childhood , a severe first attack ,total colonic involvement ,and contineuos rather that intermittent symptoms .Extracolonic complications include seronegative arthritis ( sacroilitis ,ankylosing spondylitis) sclerosing cholangitis ,cirrhosis ,pericholangitis ,iritis uveitis ,episcleritis erythema nodosum ,pyodera gangrenosum ,and apthous stomatitis .Rarely , systemic amloidosis may occur.

ULCERATIVE COLITIS 

CAUSES

SYMPTOMS

DIAGNOSIS

TREATMENT

SURGERY

COMPLICATIONS

Ulcerative colitis diagnosis

DIAGNOSTIC INVESTIGATIONS 

Many tests are utilised to diagnose ulcerative colitis. A fleshly communicating and medical history are usually the first step.Blood tests haw be done to check for anemia, which could indicate injury in the colon or rectum, or they haw uncover a high white murder radiophone count, which is a sign of rousing somewhere in the body

.

A crap distribution can also reveal white murder cells, whose presence indicates ulcerative redness or inflammatory disease. In addition, a crap distribution allows the student to detect injury or infection in the colon or rectum caused by bacteria, a virus, or parasites.

A colonoscopy or endoscopy are the most accurate methods for making a diagnosis of ulcerative redness and ruling-out another doable conditions, much as Crohn’s disease, diverticular disease, or cancer. For both tests, the student inserts an endoscope—a long, flexible, aflame tube adjoining to a computer and TV monitor—into the arsehole to wager the exclusive of the colon and rectum. The student will be healthy to wager some inflammation, bleeding, or ulcers on the colon wall. During the exam, the student haw do a biopsy, which involves attractive a distribution of tissue from the covering of the colon to view with a microscope.

A colonoscopy or endoscopy are the most accurate methods for making a diagnosis of ulcerative redness and ruling-out another doable conditions, much as Crohn’s disease, diverticular disease, or cancer. For both tests, the student inserts an endoscope—a long, flexible, aflame tube adjoining to a computer and TV monitor—into the arsehole to wager the exclusive of the colon and rectum. The student will be healthy to wager some inflammation, bleeding, or ulcers on the colon wall. During the exam, the student haw do a biopsy, which involves attractive a distribution of tissue from the covering of the colon to view with a microscope.

A colonoscopy or endoscopy are the most accurate methods for making a diagnosis of ulcerative redness and ruling-out another doable conditions, much as Crohn’s disease, diverticular disease, or cancer. For both tests, the student inserts an endoscope—a long, flexible, aflame tube adjoining to a computer and TV monitor—into the arsehole to wager the exclusive of the colon and rectum. The student will be healthy to wager some inflammation, bleeding, or ulcers on the colon wall. During the exam, the student haw do a biopsy, which involves attractive a distribution of tissue from the covering of the colon to view with a microscope.

Sometimes x rays much as a barium enema or CT scans are also utilised to diagnose ulcerative redness or its complications.

ULCERATIVE COLITIS 

CAUSES

SYMPTOMS

TREATMENT

SURGERY

COMPLICATIONS

Disease ulcerative colitis

AROUND 100,000 HAVE THIS DISASE IN UK

CURRENT HYPOTHESIS ,

HIGHER CONCORDANCE RATE IN MONOZYGOTIC TWINS

ULCERATIVE COLITIS 

Ulcerative colitis is a inflammatory disease which involves the whole part of the colon .The inflammation is initially confined to the mucosa and nearly always involves the rectum .extending to involve the distal or whole colon.In severe cases the inflammation may extend into the muscle coats .Acute complications include toxic dilatation , haemorrhage and perforation .

AETIOLOGY 

The cause of ulcerative colitis is not known.Current hypotheses includes immunological ,dietary and genetic factors .Familial clustering occurs . There is an association with HLA-DR2.Other evidence of a genetic role includes a higher concordance rate in monozygotic twins  ,and increased prevalence in certain ethnic groups and an association with disease that are known to have a genetic predisposition .e.g ankylosing spondylitis and sclerosing cholangitis . Immunological mechanism may be important .Under normal circumtances the mucosal immune system is tolernt of luminal forign antigens and this is dependent upon the relationship between colonic epithelium and suppressor T cells .

Changes in epithelial cell antigen presentation consequent upon an acquired expression of class II major histocompatibility mlecules activate helper T lymphocytes and induce a sustained mucosal immune reaction .Antigens from gut flora may be responsible for this .This may explain the well-known triggering of ulcerative colitis by enteric infections. Dietary factors may also provide a triggering factor.

MORPHOLOGY ulcerative colitis is a diffuse inflammatory disease confined initially to the mucosa.Unlike Crohn's disease it is confined to the large intestine and is continuous in its distribution.In some cases it is confined to the rectum ( proctitis ) ,or to the rectosigmoid (distal proctitis ).

Abcesses form in the crypts of Lieberkuhn ,penetrate the superficial mucosa ,spread horizontally and cause the overlying mucosa to slough.The margins of the ulcers are raised as mucosal tags that project into the lumen ( inflammatory pseudopolyps ) Except in the most seere forms the muscle layers are spared .Occasionally the last few centimeters o the terminal ileum is ulcerated ,i.e the so called condition of 'backwash ' ileitis .

CLINICAL FEATURES  More common in women ,aged 3rd ,4th and 2nd decade ,in that order .

SYMPTOMS

IN CHRONIC TYPE initially watery diarrhea occuring day and night ,in a person of previously normal bowel habit.Later a rectal discharge of mucus ,sometimes blood stained and purulent is very common .Severe bloody diarrhea upto 20 times daily may occur .pain is unusual ,initially,relases and remissions.

IN ACUTE FULMINATING TYPE

Incessant diarrhea containing blood ,mucus and pus .fever Abdominal distension ( due to toxic dilatation of colon ) ,Abdominal pain

SIGNS

IN CHRONIC TYPE depending upon severity of attacks dehydration ,Anemia

IN ACUTE FULMINATING TYPE pyrexia ,100-102 F .dehydration ,anemia and abdominal distension.

ULCERATIVE COLITIS 

CAUSES

SYMPTOMS

DIAGNOSIS

TREATMENT

SURGERY

COMPLICATIONS

Gall stones(cholelithiasis)-Gall bladder problems common in women eat high fibre diet for prevention

PATHOLOGICAL CONDITIONS OF THE GALL BLADDER ARE COMMON SURGICAL PROBLEMS....

GALL STONES ( CHOLELITHIASIS )

In medicine, gallstones (choleliths) are crystalline bodies formed within the embody by increment or concretion of normal or deviant bile components.In 80% of patients gall stones are composed predominantly of cholesterol with smaller amounts of calcium salts and bile pigments . They are referred to as mixed stones , are usually multiple with a faceted surface , and have a characteristic laminated surface on cross section. Only about 10 % of them contain sufficient calcium to be visible on a plain X-ray .Pure cholestrol stones form less than 10% of stones .They are usually solitary ( the cholestrol " solitaire " ) up to 5 cm in diameter ,and have a characteristic radial arrangement of crystals on cross section . Cholestrol stones usually form in bile which is supersaturated with cholestrol. When bile contains more cholestrol than can be solublised in the bile- acid -lecithin micelles ,crystals of cholestrol form in the bile .

The greater the concentration of bile acids and lecithin in bile ,the greater is the amount of cholestrol that can be contained in the mixed micelles .Lecithin is important because lecithin - cholestrol mixed micelles can solubilise more cholestrol than can micelles of bile acids alone .Following Crohn's disease of the terminal ileum or ileal resection thebile salt pool is reduced because of lack of absorption of bile salts ,and the liver can not make good the losses .

Such patients are prone to cholestrol stones. Oestrogen increases the hepatic synthesis of cholestrol ,and this may explain why females of child - bearing age have a higher incidence of cholestrol stones . A high animal fat ,low fibre diet is also associated with cholestrol stones because of excretion in bile of the excess cholestrol absobed from the gut.Clofibrate , a cholestrol-lowering agent ,has been implicated in cholestrol stone formation ,because it increases excretion of cholestrol in the bile . Decreased gall bladder motility probably plays a rle in aetiology of gall stones .

Cholestrol and other substances which form the nuclei for gall stone formation must remain in the gall bladder long enough for crystal growth to occur .Stasis occurs during pregnancy due to the smooth muscle relaxing effect of progesterone.Motility of the gall bladder is also decreased during starvation and total parenteral nutrition , due to decreased stimulation of the gall bladder by CCK.Stones may also form after vagotomy ,because of lack of vagal potentiation of CCK.Bile pigment stones account for about 10 % of stones in the UK.The major constituent is the calcium salt of unconjugated bilirubin.

They are associated with chronic haemolytic disease where there is breakdown of red cells with release of excessive bilirubin.Pure pigment stones occur in sickle cell disease , thalassaemia and hereditary spherocytosis .Pigment stones are found in the Far East ,where they are associated with biliary tract infection with E.coli and Bacteroides fragilis ,These organism produce beta-glucuronidase which splits bilirubin diglucuronide and releses free bilirubin.The latter combines with calcium to form the relatively insoluble calcium bilirubinate.

PATHOLOGICAL CONSEQUENCES OF GALL STONES ARE :

• Inflammation of the gall bladder ,acute cholecystitis ,chronic cholecystitis ,acute on chronic cholecystitis
• obstructive jaundice due to impaction of a stone at the lower end of the common bile duct : secondary biliary cirrhosis may result .
• ascending cholengitis
• empyema of the gall bladder.
• mucocele
• gall stone ileus __ a fistula occurs between the gall bladder and duodenum ,and a large stone enters the small bowel ,causing obstruction .usually at the terminal ileum .
• pancreatitis ,usually associated with multiple small stones .
• carcinoma of gall bladder .
• perforation of the gall bladder .
  

Medicines titled chenodeoxycholic acids (CDCA) or ursodeoxycholic acid (UDCA, ursodiol) may be given in preventive form to dissolve cholesterin gallstones. However, they may take 2 eld or longer to work, and the stones may return after communication ends.

Rarely, chemicals are passed into the gallbladder finished a catheter. The chemical apace dissolves cholesterin stones. This communication is not used rattling often, because it is difficult to perform, the chemicals can be toxic, and the gallstones may return.

Cholecystectomy (gallbladder removal) has a 99% chance of eliminating the recurrence of cholelithiasis. Only symptomatic patients staleness be indicated to surgery. The lack of a gall bladder does not seem to have any perverse consequences in some people. However, there is a momentous assets of the population — between 5 and 40% — who amend a information called postcholecystectomy syndrome which haw drive gastrointestinal painfulness and persistent discompose in the upper right abdomen. In addition, as some as 20% of patients amend chronic diarrhea.

Electrohydraulic damper wave lithotripsy (ESWL) of the gallbladder has also been utilised for selected patients who cannot have surgery. Because gallstones often become backwards in many patients, this treatment is not utilised very often any more.

Test for appendicitis -Pinch-an-inch test

PINCH-AN-INCH TEST FOR APPENDICITIS

Its a prospective comparative assesment of two physical exam technique for evaluating patients with doubtable appendicitis.Rebound tenderness is a widely acclimated assay address for patients with doubtable appendicitis.but it can be absolutely uncomfortable.an another analysis for peritonitis is termed THE PINCH-AN-INCH TEST.

This address call two patients who presented with balmy belly affliction who subsequently were begin to accept appendicitis.In both patients classic peritoneal signs were absent but the compression an inch analysis was positive.the accomplished physicians bedside analytic assay remains the most critical component for rapidly anecdotic peritonitis.Although rebound tenderness is a broadly acclimated examination.It is afflictive and may be inaccurate.

To perform the pinch-an-inch test,a bend of belly derma over McBurney's point is grasped and animated abroad from the peritoneum.The derma is recoil back briskly against the peritoneum.If the patient has added affliction if the derma bend strikes the peritoneum, the analysis is absolute and peritonitis apparently is present.

As an added feature,if the affliction seems boundless just during the antecedent compression phase,the patient may accept a actual low affliction threshold,a factor that can be taken into account when deciding if the patient has a surgical abdomen.We anecdotally accept begin the analysis to be appreciably accessible for the appraisal of appendicitis.

Delayed analysis of acute appendicitis can advance to cogent morbidity.However recent technological advances in radiological imaging, the alert analysis of acute appendicitis can be difficult.Indeed,some experts accept that overreliance on imaging at the amount of the bedside assay may in fact access appendicitis accompanying morbitity.Arguably,both of these patients ability accept been bigger served by undergoing surgery directly without the delay of of CT imaging.Therefore analysis efforts should be directed against developing and acceptance bigger bedside assesment of peritonitis.

One important admonition to clinicians is the actuality that patients with appendicitis may in fact accept hyperesthesia over McBurney's point,and an boundless affliction acknowledgment to he compression appearance should not be absolved out of the hand.

The technique potencially allows for a added objective and reproducible physical assay than rebound tenderness which requires the examiners abjure his easily rapidly abundant to break advanced of the accustomed natural recoil of the belly wall.Rebound tenderness as well requires that the physicians does not added abase his easily in a form of backswing.Pinch an inch in contrasr allows for a added accelerated and reproducible absolution of tension.

In an accomplishment to advance patient's abundance during the belly assay we developed an alternating address for detecting peritonitis.we appellation this pinch-an-inch,we accept that compression an inch after-effects in less affliction than rebound tenderness.while not compromising effectiveness.

We achievement that our pinch-an-inch assay address may eventually action a added adequate and authentic another to classic rebound tenderness.Toward this effort,we will conduct a -to-be abstraction to appraise its accurateness and about abundance in diagnosing appendicitis.
several studies have shown it to be quite accurate in the evaluation of the appendicitis so its use should not be stoped.

Intestinal pain - Acute intussusception if you avoid can lead to death

What Could Happen If You Avoid The TREATMENT ?

IT Will Get So Extreme.........Lead To DEATH

ACUTE INTUSSUSCEPTION :

INTUSSUSCEPTION is an invagination of size of intestine ( intussuscepiens ) into the immediate portion of bowl ( intussusceptum ) and  most of cases occur in children during the first 5 decades of life. This can often result in an obstructio .The part that prolapse into the other is called the INTUSSUSCEPTUM and the part that recieves it is called INTUSSUSCEPIENS.

In some of children with intussuscetion , an anatomic predisposing condition . Such as Meckle's diverticulum , Burkitt lymphoma, or hamartomatous polyps ,can be found .And in most of the cases are associated with hyperplastic lymphoid tissue.suggesting an infectious causes ,which is not confirmed in most of the cases.By using serology and virus isolation from fecal and pharyngeal swabs.Adeno virus , Rotavirus ,Enterovirus , Human herpes virus  ,Cytomegalovirus and Epstien-barr-virus.some bacterial agents can also involved in this condition include Yersinia ,enterocolitis and salmonella typhimurium and candida albican .

TYPES

Ileocolic  ( 77 % ) 

Ileoileocolic ( 12 % ) 

Ileoileal (5 % ) 

Colocolic ( 2 % ) 

Multiple (! % ) 

Retrograde ( 0.2 % )

Others  ( 2.8 % ) .

CLINICAL FEATURES :

SYMPTOMS

• Sudden paroxymsm of abdominal pain ,with drawing up of legs and screaming  :each attack lasts a few minutes and recur about every 15 minutes.
• Facial pallor 
• Vomiting
• Listleness and somewhat drawn between the attacks .
• Stool : intially normal later  blood and mucus are evacuated called  "red currant jelly stool " 
• when not relieved upto 24-36 hours

        a . Pain becomes contineous

          b. Abdomen distends

          c. Vomiting becomes copious

          d. Absolute intestinal obstruction follows

SIGNS

• A lump is felt ,which may harden on palpation .
• PR examination : if intussuscetion has travelled far enough ,its apex ( a conical ) mass will be felt .
• When not relieved ,upto 24 - 36 hours  

         a . Dehydration

         b . Abdominal distension

         c . Abdominal guarding , tenderness and rebound tenderness if gangrene has occured.

DIAGNOSTIC INVESTIGATIONS :

INTUSSUSCEPTION is often suspected based on history and physical examination , including observation of Dance's sign .Per rectal examination is particularly helpful in children as part of thintussusceptum may be felt by the finger .A definite  diagnosis often requires confirmation by diagnostis imaging modalities .

ULTRASOUND is today considered the imaging advanced technology of choice for diagnosis and exclusion of intussusception due to its high accuracy and lack of radiation.A target like mass ,usually around 3 cm in diameter confirm the diagnosis.

PLAIN ABDOMINAL X-RAY
Revealed increased gas shadow in small intestine and at times absence of cecal gas shadow .

X-RAY WITH BARIUM ENEMA :
Reveal characteristic " claw sign " in ileocolic intussusception .

TREATMENT :

The condition is not usually immediately life threatning.The intussusception can be treated with either a barium or water soluble contrast enema or an air contrast enema .which both confirms the diagnosis of intussusception, and inmost cases successfully reduce it . The success rate is over 80% .Therefore approximately 5 - 10 % of these recur within 24 hours .If it cannot be reduced by an enema or if the intestine is damaged , then surgical reduction is necessary.

PRELIMINARY TREATMENT 


Gastric aspiration should be carried out and contiued during and after operation.
Give IV dextrose - saline solution.

REDUCTION OF INTUSSUSCEPTION
REDUCTION BY HYDROSTATIC PRESSURE


OPERATIVE REDUCTION :


Abdomen is opened through a right lower paramedian incision .First part of reduction is accomplished by squeezing lower part of sausag like mass ,and little intussusception is reduced.Last part is most difficult to reduce and should br withdrawn and gently compressed in a warm saline soaked pack,to

lessen the edema.
After reduction if a specific cause is revealed appropriate treatment is carried out ,eg Meckle's diverticulum.

PROGNOSIS :

The outlook for intussusception is excellent .when treated immediately .but when untreated it can lead to death within 2-5 days .Quick treatment can avoid this surgery .Prolonged intussusception can lead to ischemia and necrosis and it requires surgical resection.

AFTER TREATMENT


Gastric aspiration should be continued for 12-24 hours
Dextrose-saline is given IV or SC with hyaluronidase.
On 2nd day ,gastric tube is removed and sips of water are given.
Few hours later ,feeding is commenced with mother's milk ( if infant is still being breast-fed ).

COMPLICATIONS:

Intestinal obstruction
Gangrene