Achalasia:
Botulinum injections are most effective of all the options for relieving a lower oesophageal sphincter restriction which leads to achalasia.
Nifedipine, nitrates or sildenafil can also be used, but are less effective.
Surgically, Heller’s oesophageal myotomy is the best treatment option, it can be done via an abdominal incision or laparascopically.
BCS is a good mnemonic for Barrett's dysplasia.
Barrett's Columnar replaces Squamous in Barrett’s oesophagus.
This is also known as small intestinal (columnar) metaplasia.
There is increased risk of oesophageal adenocarcinoma.
Nitrates, caffeine and alcohol can help relieve symptoms by relaxing lower oesophageal tone.
Not all patients with GORD should undergo an OGD (should be considered if GI bleeding or symptoms of dysphagia occur).
Oesophagitis is present in half of GORD patients.
Oesophageal manometry or oesophageal motility study measures the strength of the lower oesophageal sphincter. This would rule out achalasia.
A Mallory-Weiss tear occurs in the mucous membrane typically in the lower oesophagus.
Mallory-Weiss tears are usually caused by forceful or prolonged vomiting or coughing.
They may also be caused by epileptic convulsions.
The tear may be followed by vomiting bright red blood or by passing blood in the stool.
The incidence is 4 in 100,000 people. Achlorhydria (absence of gastric acid secretion) can be caused by immune destruction to the stomach wall, malnutrition and marijuana use. The pentagastrin testis used as a diagnostic aid for evaluation of gastric acid secretory function
Coxsackie, mumps, ECHO and hepatitis viruses as well as hypothermia can cause acute pancreatitis.
The following are poor prognostic indicators in acute pancreatitis:
Calcium < 2.0 (hypocalcaemia rather than hypercalcaemia as a consequence) WCC > 15
Urea >16
ALT >200
PaO2 <8
Age > 55 years
Glucose > 10
Chronic Pancreatitis
Cullen's sign (periumbilical discolouration) can be present
Grey Turner's sign (flank discoloration) can be present
Purtscher's retinopathy (ischaemic areas in the retina) can be present
lack of digestive enzymes leads to steatorrhoea In chronic pancreatitis,
trypsin secretion is reduced. Trypsin is required in the processing of dietary B12 which enables absorption and hence B12 deficiency is the most likely.
Result from dilated veins in the walls of the lower part of the esophagus and sometimes the upper part of the stomach.
are a life-threatening complication of portal hypertension.
Tests to visualize the varices include EGD (esophagogastroduodenoscopy).
symptoms are
1) Signs of chronic liver disease or cirrhosis
2) Low blood pressure
3) Rapid heart rate
4)Bloody or black stool on rectal exam
Tests to visualize the varices include EGD (esophagogastroduodenoscopy).
manage persistent varices with medical and procedural therapies:
1) endoscopic therapy
2) balloon tamponade
3) the transjugular intrahepatic portosystemic shunt (TIPS) procedure
4) Octreotide and vasopressin are medications that may be used to decrease portal blood flow and slow bleeding.
5) Emergency surgery may rarely be used to treat patients if other therapy fails
Bleeding esophageal varices are a serious complication of liver disease and carry a poor prognosis.
Liver transplantation should be considered.
Complication
1) Recurrence of bleeding after treatment
2) Hypovolemic shock
3) Esophageal stricture after surgery or endoscopic therapy
4) Worsening encephalopathy (confusion)
5) Infection (pneumonia, blood stream infection, peritonitis
Prevention
Treatment of the underlying causes of liver disease may prevent bleeding.
1.Gastroesophageal Acid Reflux Disease (GERD, acid reflux ) is injury to the esophagus that develops from chronic exposure of the esophagus to acid coming up from the stomach (acid reflux).
2.In contrast, heartburn is the symptom of acid in the esophagus, characterized by a burning discomfort behind the breastbone (sternum).
3.Patients that have heartburn symptoms more than once a week are at risk of developing GERD (acid reflux).
4.A hiatal hernia is usually asymptomatic, but the presence of a hiatal hernia is a risk factor for development of GERD (acid reflux).
5.Trouble swallowing Dysphagia requires immediate medical attention Vomiting blood or partially digested blood (looks like coffee grounds) requires immediate medical attention as does digested blood in the stools.
6.Edema and basal hyperplasia (non-specific inflammatory changes) Lymphocytic inflammation (non-specific) Neutrophilic inflammation (usually either acid reflux or Helicobacter gastritis) Eosinophilic inflammation (usually due to acid reflux) Goblet cell intestinal metaplasia or Barretts esophagus.
7.Zollinger-Ellison syndrome can present with increased gastric acidity due to gastrin production.
8.Treatment Avoiding aggravating factors The rubric “lifestyle modifications” is the term physicians use when recommending non-pharmaceutical treatments for GERD.
9.Avoid eating for 2 hours before bedtime and elevate the head of the bed on 6 inch blocks.
10.Drug treatment A number of drugs are registered for the treatment of GERD, and they are amongst the most often prescribed forms of medication is most Western countries.
11.The upper part of the stomach is wrapped around the LES to strengthen the sphincter and prevent acid reflux and to repair a hiatal hernia.
The term "functional" is generally applied to disorders described by symptoms when no organic explanation is detected using common diagnostic procedures
Functional esophageal disorders
Globus - a sensation of a lump, something stuck, or a tightness in the throat
Rumination syndrome - effortless regurgitation of recently swallowed food
Functional chest pain - the feeling of chest pain, presumably of esophageal origin (can be confused with cardiac pain which must be examined)
Functional heartburn - persistent burning sensation in the absence of gastroesophageal reflux disease (GERD), a motility disorder, or a structural explanation
Functional dysphagia - the sensation of difficulty swallowing
Functional gastroduodenal disorders:
Functional dyspepsia - pain or discomfort located in the upper abdomen
Aerophagia - repetitive air swallowing or ingesting air and belching
Functional vomiting - recurrent vomiting in the absence of all known medical and psychiatric causes
Functional bowel disorders and abdominal pain:
Irritable bowel syndrome (IBS) - a group of bowel disorders characterized by abdominal discomfort or pain associated with defecation or a change in bowel habit
Functional abdominal bloating - a group of functional bowel disorders dominated by a feeling of abdominal fullness or bloating
Functional constipation - a group of functional disorders characterized by persistent difficult, infrequent, or seemingly incomplete defecation
Functional diarrhea - continuous or recurrent passage of loose or watery stools without abdominal pain
Functional abdominal pain - continuous or frequently recurrent abdominal pain, either not or infrequently related to gut function, and associated with some loss of daily activities
Functional disorders of the biliary tract and pancreas:
Gall bladder dysfunction - characterized by episodes of severe steady pain
accompanied by decreased gall bladder emptying
Sphincter of Oddi dysfunction - a motility disorder characterized by severe steady pain with no structural abnormalities that explain the symptoms. It sometimes occurs following gall bladder removal, but also may occur with an intact gall bladder.
Functional disorders of the anus and rectum
Functional fecal incontinence - recurrent uncontrolled passage of fecal material where no structural or neurological cause is evident
Functional anorectal pain - Levator ani syndrome is a dull ache in the rectum that lasts for hours to days. Proctalgia fugax is an infrequent sudden, severe pain in the anal area of short duration
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"Motility" is a term used to describe the contraction of the muscles that mix and propel contents in the gastrointestinal tract. The gastrointestinal tract is divided into four distinct parts that are separated by sphincter muscles; these four regions have distinctly different functions to perform and different patterns of motility (contractions). They are the esophagus (carries food to the stomach), stomach (mixes food with digestive enzymes and grinds it down into a more-or-less liquid form), small intestine (absorbs nutrients), and colon (reabsorbs water and eliminates indigestible food residues). Abnormal motility or abnormal sensitivity in any part of the gastrointestinal tract can cause characteristic symptoms.(3)
Abnormal motility patterns in the small intestine can lead to symptoms of intestinal obstruction. Symptoms of bloating, pain, nausea, and vomiting can result either from weak contractions or from disorganized (unsynchronized) contractions.
Small bowel bacterial overgrowth
Too many bacteria in the upper part of the small intestine may lead to symptoms of bloating, pain, and diarrhea. Symptoms occur immediately after eating because the bacteria in the intestine begin to consume the food in the small intestine before it can be absorbed. Small bowel bacterial overgrowth is a result of abnormal motility in the small intestine.
Constipation
The symptoms of constipation are infrequent bowel movements [usually less than 3 per week], passage of hard stools, and sometimes difficulty in passing stools. One motility problem that can lead to constipation is a decrease in the number of high amplitude propagating contractions [slow transit] in the large intestine. The test used to detect this is a transit time (Sitzmark) study.
Outlet obstruction type constipation (pelvic floor dyssynergia)
The external anal sphincter, which is part of the pelvic floor normally stays tightly closed to prevent leakage. When you try to have a bowel movement, however, this sphincter has to open to allow the fecal material to come out. Some people have trouble relaxing the sphincter muscle when they are straining to have a bowel movement, or they may actually squeeze the sphincter more tightly shut when straining. This produces symptoms of constipation.
Diarrhea
The symptoms of diarrhea are frequent, loose or watery stools, and a subjective sense of urgency. An excessive number of high amplitude propagating contractions [rapid transit] can be a cause of diarrhea; it reduces the amount of time food residues remain in the large intestine for water to be reabsorbed. Changes in the motility of the small intestine may also occur, but there is little information available on this.
Fecal incontinence
Fecal incontinence means involuntary passage of fecal material in someone over the age of 4 years. The most common causes are (a) weakness of the anal sphincter muscles; (b) loss of sensation for rectal fullness; (c) constipation, in which the rectum fills up and overflows; and (d) stiff rectum, in which the fecal material is forced through the rectum so quickly that there is no time to prevent incontinence by squeezing the sphincter muscles. Diarrhea can also lead to fecal incontinence.
Hirschsprung's disease
There are actually two anal sphincter muscles: an internal anal sphincter that is part of the intestines, and an external anal sphincter that is part of the pelvic floor muscles. The internal anal sphincter normally stays closed to prevent the leakage of gas or liquid from the rectum, but when the rectum fills up with gas or fecal material, a reflex causes it to open to allow the bowel movement to pass through. The nerves that this reflex depends on are sometimes missing at birth, with the result that the internal anal sphincter stays tightly closed and bowel movements cannot occur. This congenital (birth) defect is called Hirschsprung's disease.
Gastroparesis
Gastroparesis is a disorder in which the stomach takes too long to empty its contents. Gastroparesis is most often a complication of type 1 diabetes. At least 20 percent of people with type 1 diabetes develop gastroparesis. It also occurs in people with type 2 diabetes, although less often. Symptoms of gastroparesis are nausea, vomiting, an early feeling of fullness when eating, weight loss, abdominal bloating, abdominal discomfort. These symptoms may be mild or severe, depending on the person. In most cases treatment does not cure gastroparesis -- it is usually a chronic condition. However, treatment does help manage the condition.
Achalasia
Achalasia is an esophageal motility disorder. It is diagnosed when there is a complete lack of peristalsis within the body of the esophagus. The lower esophageal sphincter does not relax to allow food to enter the stomach. Symptoms are difficulty swallowing both liquids and solids. Many people also have associated regurgitation, vomiting, weight loss, and atypical chest discomfort.
In hemochromatosis, the commonest mutation is C282Y. It is found in approximately 90% of cases.
The mutation is on chromosome 6, affecting the HFE gene.
There is an increased incidence in males.
The serum Fe is elevated (> 300 mg/dL).
The serum transferrin saturation is a sensitive parameter of increased Fe and merits evaluation when > 50%.
The serum ferritin is increased ferritin of >1000 μmol/l is suggestive (normal <200).
Urinary Fe excretion is markedly increased (> 2 mg/24 h) by the chelating drug deferoxamine (500 to 1000 mg IM based on the size of the patient), and this has been used as a diagnostic test.
In addition, when the Fe content in the liver is significantly increased, an MRI may reflect this change. Liver biopsy had been the gold standard in diagnosis; it now serves only to provide evidence of fibrosis (cirrhosis). Gene assay (Homozygosity C282y mutations) is the also an excellent diagnostic test.
Venesection is preferred therapy . Treatment consists of bi-weekly venesection removing approximately 500 ml per week. Desferrioxamine infusion (another iron chelator) can also be used.
Iron infiltrates the parathyroid glands and can cause hypoparathyroidism. In haemochromatosis , joint deposition of iron occurs, causing arthropathy. Increased iron deposition in the skin stimulates increased melanin production. Haemochromatosis is a recognised cause of restrictive cardiomyopathy. Cardiac damage is commonly seen with ferritin >2,000 ng/l
Wilson disease : The abnormal gene is the ATP7B gene on chromosome 13. It is autosomal recessive. Kayser-Fleischer rings are often seen on slit lamp, but not always. The best test is hepatic copper concentration (> 250 μg /g of dry weight). . Typically there is low serum copper levels but high urine excretion of copper. There is low liver production of caeruloplasmin (< 20 mg/dl) in 95% of patients. Copper deposits can occur in the liver and kidney, hence affecting vitamin D metabolism leading to osteomalacia/osteopenic changes.
Non-alcoholic steatohepatitis (NASH) is a form of liver disease resembling alcoholic liver disease in a patient who does not consume significant amounts of alcohol. The natural course is relatively benign, but liver cirrhosis. together with all its sequelae, may develop; sometimes liver transplantation is indicated. NASH is associated increased prevalence of Insulin resistance/type 2 diabetes. There may also be lipid abnormalities and increased iron stores.
Abdominal tenderness is found in more than 50% of patients with Spontaneous Bacterial Peritonitis. Findings on the abdominal examination can range from mild tenderness to overt rebound and guarding. Traditionally, three fourths of SBP infections are caused by aerobic gram-negative organisms (50% of these being Escherichia coli), and one fourth of these infections are due to aerobic gram-positive organisms ( streptococcal species).
An ascitic fluid neutrophil count of > 250 cells/mL and ascites lactate level of >25 mg/dL are the single best predictors of SBP. A combination of an aminoglycoside and ampicillin or cefotaxime can be used.
Budd-Chiari syndrome is thrombosis of the hepatic vein, the major vein that leavesthe liver. Most patients have an underlying thrombotic tendency. About 10% have polycythemia vera, and about 10% have been on the OCP. The most common symptoms in Budd-Chiari syndrome are hepatomegaly, abdominal pain, ascites and jaundice.
Child's Pugh classification includes bilirubin, prothrombin tine, encephalopathy scores, ascites and albumin to measure the severity of liver disease.
Somatostatin its derivative, octreotide, and terlipressin are often used for emergency treatment of bleeding oesophageal varices in patients with cirrhosis of the liver.
Beta blockers (nadolol), nitrates, vasopressin analogues and somatostatin analogues can also be used for reducing rebleeding in oesophageal varices
Wernicke encephalopathy is a neurologic disorder of acute onset caused by a thiamine deficiency. The condition is characterized by ocular abnormalities, ataxia, and a global confusional state. Wernicke encephalopathy results from a deficiency in vitamin B-1 (ie, thiamine). The episode may have been precipitated by intravenous dextrose administration which exhausted his vitamin B reserves. B vitamins should be administered to all alcoholic patients requiring dextrose.
The main features of Korsakoff’s psychosis is short term memory loss and subsequent compensatory confabulation by patient. Other symptoms may include delirium, anxiety, depression, confusion, delusions and insomnia. The treatment is with intravenous thiamine.
Hepatorenal syndrome (HRS) is the development of renal dysfunction in patients with severe liver disease (acute or chronic) in the absence of any other identifiable causes of renal Pathology
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