Acute Cholecystitis is a condition characterized by acute abdominal pain, fever and positive Murphy’s sign due to inflammation of the Gall bladder.

What causes the Acute Cholecystitis?

1. Gallstone, Ninety percent of cases involve stones in the cystic duct (i.e., calculous Cholecystitis)
2. Non Calculous includes:

• Severely ill patients with nothing by mouth since long time
• Burn Patients
• Trauma
• Post surgical patients
• Pregnancy
• Infection
• Drugs (especially hormonal therapy in women)
• Diabetes mellitus

What is the pathophysiolgy of acute Cholecystitis?

In calculous Cholecystitis there is obstruction of cystic ducts due to gall stone leading to biliary colic. If the cystic duct remains obstructed, the Gall stone wall distends and the gallbladder wall then becomes inflamed and edematous. In most common cases the gall stone dislodges and the inflammation gradually resolve but in some and severe cases there is ischemia and necrosis of the gall bladder wall.

What are the signs and symptoms of acute Cholecystitis?

• Biliary colic (right upper quadrant abdominal pain)
• Fever
• Nausea and vomiting
• Anorexia
• Tenderness or rebound tenderness
• Guarding and rigidity
• Jaundice
• Murphy’s sign positive, ie Inspiration arrest of during deep palpation of the right upper quadrant)

What are the complications of Acute Cholecystitis?

1. Emphysematous Cholecystitis
2. Empyema of gall bladder
3. Acute cholangitis
4. Acute pancreatitis

What is the differential diagnosis of acute Cholecystitis?

• Appendicitis
• Perforated peptic ulcer
• Acute pancreatitis
• Bowel obstruction
• Acute pyelonephritis
• Myocardial infraction
• Pneumonia right lower lobe

How to diagnosed acute Cholecystitis?

Diagnosis relies on patient’s history, physical examination, Radiological examination and Laboratory studies.

Laboratory studies shows leukocytosis (increased WBC count), Liver function tests; including serum bilirubin, alkaline phosphatase, alanine transaminase (ALT), asparate transaminase (AST) and serum amylase also may be abnormal.

Diagnostic Imaging includes:

• Ultrasound: it is the most commonly used test for diagnosis acute Cholecystitis with the sensitivity and specificity of 84% and 99% respectively.
• Radionuclide cholescintigraphy: Biliary radionuclide scanning is used less frequently but may be helpful in atypical cases. No filling of the gallbladder with the radiotracer (99m Tc-HIDA) after 4 hours indicates an obstructed cystic duct with a sensitivity and specificity of 95%.
• Computed tomography (CT): Nowadays CT   is performed frequently in patient with abdominal pain, but is less sensitivity than ultrasound for acute Cholecystitis.

How to managed acute Cholecystitis?

• After the diagnosis of acute Cholecystitis hospitalized the patients and managed with giving iv fluid, parenteral antibiotic (eg. Piperacillin/ tazobactam) and analgesic.
• Patients with acute Cholecystitis should have gone cholecystectomy as definitive treatment. Cholecystectomy may perform in either an early (2 to 3 days of symptoms) or a delayed (6 to 10 weeks after initial medical therapy).
• Tube cholecystectomy should be performed in patients who have acute Cholecystitis and who are failing systemic therapy but are not candidates for cholecystectomy because of severity of illness or concomitant medical problems.

What is the prognosis of acute Cholecystitis?

After the proper treatment of acute Cholecystitis prognosis is excellent.

References:

• Sabiston textbook of surgery 18th edition
• Bailey and love, surgery 25th edition
• www.sciencedirect.com
• The Washington manual of surgery, 5th edition.
• emedicine.medscape.com

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Zollinger-Ellison syndrome is  one of the severe cause of peptic ulcer disease (PUD) due to pancreatic adenoma gastrin-mediated gastric acid hypersecrection. ZES may occur at the age of 50 with a part of an autosomal dominant familial syndrome called multiple endocrine neoplasia type 1(MEN type1). Rarely, adenomas are located in the stomach and duodenum .50-60% is malignant, 10% are multiple and 30% or cases are associated with MEN type 1.

What is the pathophysiolgy of Zollinger-Ellison syndrome?

Zollinger-Ellison syndrome is caused by gastrinomas (tumor) which release the gastrin hormone.  Gastrin resulting in excess gastric acid secretion. The excess acid cause many ulcers in the stomach and duodenum.

What are the symptoms of ZES?

1. Burning abdominal pain especially in the epigastric region.
2. Diarrhea and weight loss in 40% of patients
3. Nausea and vomiting
4. Gastro intestinal bleeding
5. History of Nephrolithiasis, hyperparathyroidism, and gastrinoma also may be present if ZES is due to MEN type 1.

How to diagnosed Zollinger-Ellison syndrome?

ZES should be considered in any patients present with

1. PUD refractory to treatment for helicobacter pylori and convention dose of H2 blocker or omeprazole.
2. Recurrent, multiple, or atypically located peptic ulcer.
3. Peptic Ulcer disease with diarrhea.

Diagnosis is confirmed by lab test, endoscopy and imaging studies.

Lab tests:

1. A fasting serum gastric level of 100 pg/ml of greater and a basal gastric acid output (BAO) of 15 mEq/hour.
2. Increased gastrin levels (>200 pg/mL over base line) in response to a secretin stimulation test.

Endoscopy: Endoscopy shows multiple ulcers in stomach and duodenum.

Imaging studies: Imaging studies includes angiograph, ultrasonography and computerized tomography (CT).

How to managed Zollinger-Ellison syndrome?

A patient of ZES is managed with H2-histamine receptor antagonist like (cimentidine) or Omeprazole.  Surgical removal of tumor is the only cure of ZES. If a gastrinoma cannot be localized intraoperative, a parietal cell vagotomy may be preformed. Surgical debulking of metastatic or unrespectable primary gastrinoma and patients with ZES and MEN 1 facilitates medical treatment and prolongs life expectancy.

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Acute fatty liver of pregnancy (AFLP) is a rare and potentially fatal complication that typically occurs in the last trimester or early postpartum period usually from unknown pathogenesis but has been linked to an abnormalits in fetal fatty acid metabolism. This abnormality is a deficiency in the LCHAD (long-chain 3-hydroxyacyl-coenzyme A dehydrogenase) enzyme.

Clinical manifestation usually manifests in the third trimester (35 to 36 weeks of gestation) but some cases occur with a rage of 28 to 40 weeks. Patients usually present with nonspecific symptoms such as anorexia, nausea, vomiting, malaise, fatigue, headache and abdominal pain. On physical examination, patients are febrile and jaundiced. Tenderness in the right upper abdomen usually present. In a severe form of disease, patient may present with multiple organ failure (renal, cardiac failure, GI bleeding) and some women also present with the symptoms of pre-eclampsia, eclampsia or HELLP syndrome.

On laboratory finding, patients will often have an elevated white blood count, but a normal hemoglobulin level. Thrombocytopenia may be present. Liver function tests shows elevated prothrombin and partial thromboplastic times, low fibrogen levels and elevated serum AST, ALT, ALP.

The diagnosis of acute fatty liver of pregnancy is challenging task for clinician because of the nonspecific clinical presentation which may mimic conditions such as acute viral hepatic, pre-eclampsia, HEELP syndrome. Ultrasound, CT, MRI may be used to diagnose this disease. Liver biopsy is the gold standard for diagnosed AFLP.

Early diagnosis, prompt delivery and intensive supportive care are the main stay in the management of AFLP. First patients are stabilized with intravenous fluid or blood products. After the mother is stabilized, delivery of the fetus is the next step. Liver transplantation may be the option for severe liver failure patients.

The mortality from AFLP is approximately 18% and deaths are usually secondary to sepsis, renal failure, circulatory collapse, pancreatitis or gastrointestinal bleeding.

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1. HELLP Syndrome

G proteins functions as key transducers of information across cell membranes by coupling receptors to effectors such as adenylyl cyclase (AC) or phospholipase C.They are part of a large family of proteins that bind and hydrolyze guanosine triphosphate (GPT) as part of an “on” and “off” switching mechanism. G proteins are heterotrimers, consisting of Gα, Gβ, and G­ɣ subunits, each of which is encoded by a different gene.

Some strains of bacteria have developed toxins that can modify the activity of the α subunit of G proteins, resulting in disease. For example, cholera toxin produced by the microorganism that causes cholera, vibrio cholerae causes ADP ribosylation of the stimulatory (Gαs) subunit of G proteins. This modification abolishes the GTPase activity of Gαs and results in an αs subunit that is always in the “on” or active state. Thus, cholera toxin results in continuous stimulation of AC. The main cells affected by this bacterial toxin are the epithelial cells of the intestinal tract, and the excessive production of cAMP causes them to secrete chloride ions and water. This causes severe diarrhea and dehydration and may result death.

Another toxin, Pertussis toxin, is produced by Bordatella Pertussis bacteria and causes whooping cough. The Pertussis toxin alters the activity of Gαi by ADP ribosylation. This modification inhibits the function of the αi subunit by preventing association with activated receptors. Thus, the αi subunit remains GDP-bound and in an “off” state, unable to inhibit the activity of AC. The molecular mechanism by which Pertussis toxin cause whooping cough is not understood.

The understanding of the actions of cholera and pertusis toxins highlights the important of normal G-protein function and illustrate that dysfunction of this signaling pathway can cause acute disease. In the years since the discovery of these proteins, there has been an explosion of information of G proteins and several chronic human diseases have been linked to genetic mutations that cause abnormal function or expression of G proteins. These mutations can occur either in the G proteins themselves or in the receptors to which they are coupled.

Mutations in G protein-coupled receptors (GPCRs) can result in the receptor being in an active conformation in the absence of ligand binding. This would result in sustained stimulation of G proteins. Mutations of G- protein subunits can result in either constitutive activation (e.g., continuous stimulation of effectors such as AC) or loss of activity (e.g., loss of cAMP production).

Many factors influence the observed manifestations resulting from defective G-protein signaling. These include the specific GPCRs and the G proteins that associate with them, their complex patterns of expression in different tissues, and whether the mutation is germ-line or somatic. Mutation of a ubiquitously expression GPCR or G protein results in widespread manifestations, while mutation of a GPCR or G protein with restricted expression will result in more focused manifestations.

Somatic mutation of Gαs during embryogenesis can result in the deregulated activation of this G protein and is the source of several diseases that have multiple pleiotropic or local manifestations, depending on when the mutation occurs. For example, early somatic mutation of Gαs and its overactivity can lead to McCune-Albright syndrome (MAS). The consequences of the mutant Gαs in MAS are manifested many ways, with the most common being a triad of features that includes polyostotic (affecting many bones) fibrous dysplasia, café-au-lait skin hyperpigmentation, and precocious puberty. A later mutation of Gαs can result in a more restricted focal syndrome, such as monostotic (affecting a single bone) fibrous dysplasia.

The complexity of the involvement of GPRS of G proteins in the pathogenesis of many human diseases is beginning to be appreciated, but already this information underscores the critical important of understating the molecule events involved hormone signaling to that rational therapeutic interventions can be designed.

References:

• Harrison’s Principles of Internal Medicine, 17th edition.
• Davidson’s Principles and Practice of Medicine, 20th Edition
• Medical physiology, Lippincott Williams & Wilkins 3rd edition.

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Ulcerative lesions of the gastroduodenal area are classified as peptic ulcer diseases. Peptic ulcer disease is associated with a high rate of recurrence. The saying, “no acid, no ulcer”, has withstood test of the time and still accepted by most physicians and researcher are generally true. One possible cause of gastric and duodenal ulcers is reduced mucosal defense mechanisms. Human and animal data, however, have demonstrated that duodenal ulcers do not occur with reduced mucosal defense mechanism alone but also require the presence of sufficient amounts of acid. In one study, patients suffering from duodenal ulcer had a significantly increased mean number of gastric parietal cells and appeared to have increased sensitivity to gastrin when compared with healthy subjects. Although the reason is unknown, the stomach emptying rate may be greatly increased in duodenal ulcer patients. Another abnormality in duodenal ulcer patients is decreased inhibition of gastrin release by acid and a reduced rate of duodenal bicarbonate secretion. It should be emphasized, however, that a significant number of patients with duodenal ulcer do not have excessive secretion of acid.

An exciting development in the field of peptic ulcer disease is the finding of a possible correlation between Helicobacter pylori (H.pylori) infection and the incidence of gastric and duodenal ulcers. The role of H.pylori infection in the genesis of peptic ulcer is unclear, but in a significant number of patients, eradication of the bacteria reduces the rate of ulcer recurrence. H.pylori produces large quantities of the enzyme urease, which hydrolyzes urea to produced ammonia. The ammonia neutralizes acid in the stomach, protecting the bacteria for the injurious effects of hydrochloric acid.

Although the mechanism has not been elucidated, the presence of H.pylori in the stomach enhances the secretion of gastrin by the gastric mucosa. Whether increased gastrin release by the presence of H.pylori is responsible for the increased recurrence of gastric and duodenal ulcers in patients has yet to be proven. It has been demonstrated That H2 receptor blockers (cimentidine and ranitidine) have no effect on H.pylori infection. In contrast, omeprazole (an inhibitor of the H+/K+-ATPase) appears to be bacteriostatic. A combination therapy using omeprazole 20 mg  twice a day plus metronidazole 500mg two times a day or Amoxicillin 1 gm two times a day and clarithromycin 500mg twice a day  appears to be effective in the eradication of H.pylori in 50 to 80% of patients with peptic ulcer disease, resulting in a significant reduction of duodenal ulcer recurrence.

References:

1. Medical physiology, Lippincott Williams & Wilkins 3rd edi.
2. Harrison’s Principles of Internal Medicine, 17th edition.
3. Davidson’s Principles and Practice of Medicine, 20th Edition
4. www.aafp.org

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The 10^th leading cause of death in the world wide is the chronic irreversible liver damage, characterized by replacement of normal liver tissue by fibrosis, scar tissue and regeneration of noramal liver tissue form nodules or lump in the liver leading to progressive loss of normal liver function.

Causes:

• Alcohol abuse
• Chronic hepatitis B ,C and D
• Fatty liver
• Cystic fibrosis
• Glycogen storage disease
• Alpha 1  antitrypsin deficiency deficiency
• Chronic Bile Duct Blockage
• Wilson’s Disease and Hemochromatosis
• Drugs and Toxins
• Autoimmune Hepatitis

Pathology :

The pathology of cirrhosis is formation of scar tissue that replaces normal liver parenchyma and blocking the portal blood flow. During scar formation normal parenchyma is damages that lead to activation of the stellate cell, formation of contractile myofroblast and obstructs blood flow. Additionally in cirrhosis there is disturbs the balance between matrix metalloproteinase and its inhibitors (TIMP 1 and 2) cause matrix breakdown and replacement by connective tissue-secreted matrix.

Finally entire liver is replaced by scar tissue.

Sign and symptoms:

1. Alopecia( hair loss)\
2. The person may experience fatigue, weakness, and exhaustion. Loss of appetite is usual, often with nausea and weight loss.
3. Palmer erythema (Red palm)
4. Muscle wasting
5. Spidernavie ( Spider like blood vessels appear in the skin)
6. Parotid gland enlargement
7. Enlarge Men breasts( gynecomastia) and Testicular atrophy( shrunken testes)
8. Spleen enlarges
9. Fluid accumulate in the abdomen (ascite)

Diagnosis:

Diagnosis relies on history, physical examination, blood tests, ultrasound and CT scan and if still unable to diagnose Liver biopsy is needed.

Complication:

• Portal hypertension and its consequence
• Bleeding problem
• Hepatic encephalopathy
• Kidney failure
• Diabetes
• Increased risk of infections
• Liver cancer

Treatment:

There is no cure for this disease but treatment of symptoms and sings and minimize the damage to liver cells and reduces complications.

1. Stop alcohol for alcoholic patient
2. Restricting salt and water
3. not to use unnecessary drugs
4. Use of diuretic
5. Decreasing dietary protein and using of laxatives
6. Antiviral drugs Like interferon
7. Steroid for autoimmune disease
8. Management of bleeding varices by injected sclerosing agents, banding, occasionally TIPPS and surgery is necessary to prevent bleeding.
9. Liver transplant is the standard treatment of selected patient.

Prognosis:

Cirrhosis is usually progressive even with medication and abstinence for alcohol can prolonged the life but who are having difficult abstaining alcohol, ascite and encephalopathy are dramatically impact a patient prognosis.

Conclusion:

Liver cirrhosis is a common problem world wide. Early diagnosis can be done to prevent complications .various treatment is available but there is no cure.

Ongoing medical research promise major advance in treating this disease in near future.

Reference:

1. gicare.com
2. ehow.com
3. digestive.niddk.nih.gov
4. medicinenet.com
5. webmd.com
6. www.merck.com
7. healthscout.com
8. en.wikipedia.org

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1. Infertility

Dieulafoy, s lesion, a large dilated tortuous aberrant sub mucosal arteriole mostly located in the lesser curvature of the stomach wall which erodes and bleeds.It is relatively uncommon but potentially fatal cause of gastrointestinal bleeding.

Patients with Dieulafoy, s almost always presents with massive pain less upper gastrointestinal bleeding, homodynamic instability and shock.Diagnosis of Dieulafoy, s lesion is difficult, so repeated endoscopy may improve diagnostic afford, especially during active bleeding, If repeated endoscopy couldn’t diagnosed then angiography may be useful.

The treatment of this lesion consists of bipolar electrocoagulation, monopolar electrocoagulation, heater probe, sclerotherapy, laser photocoagulation, epinephrine injection and surgery is done for both therapeutic and diagnostic  Point of view.

If patient is managed as early as possible, it achieves very good long-term results.

Sources:

1.PMID: 1748038 [PubMed - indexed for MEDLINE]

2.G. Dieulafoy. Exulceratio simplex: Leçons 1-3. In: G. Dieulafoy, editor: Clinique medicale de l’Hotel Dieu de Paris. Paris, Masson et Cie: 1898:1-38.

3.  www.ncbi.nlm.nih.gov/pmc/articles/PMC149361/

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what is the mechanism of ursodeoxycholic acid in dissolution of bile stone??

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