cbd oil for duodenitis

How your gut could be causing inflammation

A growing area of research suggests that an imbalance in gut bacteria could be causing inflammation. What does this mean for your health – and what can you do about it?

Inflammation is a vital part of our immune response – without it we would not heal. What’s less helpful is chronic, low-level inflammation that can spread throughout the body.

Some experts now believe our gut could be a source of chronic inflammation, but there is a way you can help bring your body back into balance.

Why is inflammation a problem?

Inflammation is a feature of old age, but it’s also associated with many autoimmune diseases as well as weight gain, insulin resistance, poor energy, sleep and libido, reduced brain function and depression.

Inflammation is identified by inflammatory markers in the blood including interleukin-6 (IL-6) tumor necrosis factor-α (TNF-α) and C-reactive protein (CRP). 1

The gut-inflammation connection

Rebalance your gut bacteria

In the future, we may be able to address specific microbial imbalances with targeted ‘friendly’ bacteria medicines. Until then, we can try to mitigate chronic inflammation by improving our gut health with diet and lifestyle changes designed to boost the number and diversity of our gut microbes.

This means reducing stress, keeping active and aiming for a balanced, diverse diet based on whole foods. Eat an abundance of fruit and vegetables in a rainbow of colours. Fill up on lean protein, healthy fats, a range of wholegrains, legumes and pulses, nuts and seeds. And avoid or limit processed foods, artificial ingredients and refined sugars.

Feed the microbes in your gut with fibre-rich foods such as bananas, asparagus, onions, garlic, leeks, oats. And replenish the microbes with naturally beneficial bacteria found in fermented foods like natural yoghurt, miso, kefir, sauerkraut, kimchi, other pickled vegetables, kombucha, and aged cheese.

It can be useful to include naturally anti-inflammatory, calming ingredients in your cooking too. Look for recipes that use the spice turmeric (active ingredient curcumin), ginger, and oregano.

You may also want to take a broad-spectrum beneficial bacteria supplement, and anti-inflammatory omega-3 essential fatty acids.

Cbd oil for duodenitis

Video Endoscopic Sequence 1 of 4.

This is the case of a 73-year-old woman who, in a routine endoscopy, Finds this image of the duodenal bulb, prior to this endoscopy, the gallbladder is not found in an abdominal ultrasound, there had been a previous medical history 30 years ago. in a small hospital was hospitalized for 22 days apparently due to biliar lithiasis, but patient did not accept surgery.

Fistula between gall bladder and gastrointestinal tractus occurs anywhere for example stomach, duodenum, and colon. Results of inflammatory reaction adhesion may be occur and between two organs and gall stone’s pressure may be contribute this process. After that fistula occurs. Fistula’s size is ranging from a few millimeters to centimeters. Malignant tumors can cause fistula too.

For more endoscopic details download the video clips by clicking on the endoscopic images. All endoscopic images shown in this Atlas contain video clips.

Video Endoscopic Sequence 2 of 4.

Cholecystoduodenal fistula: an uncommon endoscopic diagnosis

A biliary enteric fistula is a rare complication associated with inflammation, ischemia and eventually necrosis of the gallbladder wall. It is common mainly in elderly women. Its most common form is the cholecystoduodenal fistula, which can lead to a gastric obstruction case known as the Bouveret syndrome. Early diagnosis is essential as it is a high mortality entity, and an early endoscopic approach could allow endoscopic stone extraction avoiding invasive surgery, especially in elderly patients with high comorbidity.

Video Endoscopic Sequence 3 of 4.

In the video clips, bile that emerges from this fistula is seen

There is no clinical syndrome that is characteristic of internal biliary fistula with the exception of gallstone obstruction of the intestinal tract.

S Video Endoscopic Sequence 4 of 4.

The incidence of cholecystoduodenal fistula reported in the medical literature. It is a rare complication of gallstones and its diagnosis is difficult due to its nonspecific symptomatology. It should be contemplated in elderly patients that have a contracted gallbladder with numerous adhesions.

Video Endoscopic Sequence 1 of 6.

A 25-year-old male patient underwent endoscopy of the upper gastrointestinal tract due to the fact that for three months he had had untreatable vomiting, sialorrhea, dizziness and weight loss of more than 30 pounds. In the leukogram, it revealed WBC count 8600 with 10% of eosinophils. He had been hospitalized for 22 days in in a national hospital without being able to eat any food.

Endoscopy found the duodenum with edema, erythema and some tissue thickening, multiple biopsies are taken. In the gastric fundus, there is thick liquid of green color that sometimes is observed in paralytic ilium.

Eosinophilic gastroenteritis (EGE) is a rare gastrointestinal disease characterized by crampy generalized abdominal pain, nausea, vomiting, diarrhea, gastrointestinal bleeding and weight loss or various combinations of the above symptoms. The etiology of the disease remains unknown. It is usually encountered in patients with a history of atopy. The disease may involve any part of the gastrointestinal tract, but the stomach and the small intestine are the most common sites involved. Isolated eosinophilic esophagitis or colitis may occu.

Video Endoscopic Sequence 2 of 6.

Eosinophilic gastroenteritis (EGE) represents one member within the spectrum of diseases collectively referred to as eosinophilic gastrointestinal disorders (EGIDs), which includes eosinophilic esophagitis (EoE), gastritis, enteritis, and colitis. EGE is less common than EoE and involves a different site of disease, but otherwise shares many common features with EoE. The clinical manifestations of EGE are protean and can vary from nausea and vomiting to protein losing enteropathy or even bowel obstruction requiring surgery. Although systemic corticosteroids are an effective treatment for EGE, their use over the chronic course of the disease results in substantial corticosteroid toxicity. Accordingly, there is a great need for improved therapies for these patients.

Video Endoscopic Sequence 3 of 6.

The disease can affect patients of any age, but case series have noted a dominance of presentations starting in the third through fifth decade. As the prevalence of EoE has increased and there is an overall greater appreciation of EGID, it is likely that a second peak of incidence in the first decade of life will become better appreciated. As with EoE, there is a clear male predominance. An electronic survey sent to North American Allergists and Pediatric Gastroenterologists indicate prevalence for EGE of 22–28 per 100,000 persons. Although no large longitudinal study has been performed, EGE is largely understood to be a chronic disease with few remissions after the first year.

The clinical features of EGE are protean and are related to the organs, tissue layers affected, and the intensity of eosinophilic inflammation. Some patients present with dominant gastric or duodenal disease, whereas others have involvement of both organs. Dominant gastric disease often presents with nausea, vomiting and early satiety. In contrast, dominant duodenal disease may present with malabsorption and protein losing enteropathy. Both forms of EGE often have crampy abdominal pain and bloating as additional features. Because jejunal and ileal biopsies are not routinely obtained on endoscopy, it is not known how much these gut segments contribute to disease. Patients can variably present with either diarrhea or constipation.

Video Endoscopic Sequence 4 of 6.

Duodenal biopsy showing intense areas of eosinophilic inflammation.

Video Endoscopic Sequence 5 of 6.

Duodenal biopsy showing intense areas of eosinophilic inflammation.

In addition to the varying distribution of eosinophils along the length of the GI tract, multiple reports have cited EGE subtypes based on differing depth of eosinophilic infiltration. The 3 well-described subtypes include dominant involvement of the mucosal, muscularis, and subserosal layers, respectively. Whether these actually represent different diseases or simply different presentations of the same disease is not known. The prevalence of each subtype is unknown because of reporting and referral biases. For example, surgical series report a predominance of muscularis disease with obstruction, whereas medical series primarily describe patients with mucosal involvement. Serosal disease is associated with eosinophilic ascites, but it is not known whether this reflects isolated serosal involvement or simply intense transmural eosinophilic inflammation.

In addition to the common presentations noted above, EGE can present with a variety of unusual manifestations. Patients may have gastric ulcer disease as a feature of their EGE. Typically these ulcers do not respond well to PPI therapy, but do respond to either topical or systemic corticosteroids. There is a case report of ulcer disease responding to an elemental diet

Video Endoscopic Sequence 6 of 6.

In contrast to EoE, stricture formation is not a common feature of EGE. That said, a subset of perhaps 5–10% of EGE patients do have clinically significant strictures at some point. Such cases will typically present as an acute bowel obstruction with nausea, vomiting, crampy abdominal pain and bloating. Such bowel obstructions appear to be a combination of both mechanical obstruction due to structuring as well as functional obstruction due to inflammation, edema, and decreased GI motility. Most of the time these obstructions are reversible with corticosteroid treatment, suggesting that in many cases there is a functional component that can be reversed with treatment. As such, clinically stable EGE patients presenting with bowel obstruction should generally first be treated with parenteral corticosteroid therapy, such as methyl prednisolone 1–2 mg/kg/day and carefully observed.

Video Endoscopic Sequence 1 of 2.

Metastasis from lung adenocarcinoma to second portion of the duodenum.

A 71-year-old male, presented with bleeding from the upper gastrointestinal tract, this mass is compatible with metastasis and a primary tumor is found in the thoracic tac.

Video Endoscopic Sequence 2 of 2.

Metastasis from lung adenocarcinoma to second portion of the duodenum.

Video Endoscopic Sequence 1 of 1.

An 88-year-old male, who underwent endoscopy of the upper digestive tract due to a dyspeptic syndrome, signs of chronic atrophic gastritis and multiple duodenal lipomas are found.

Lipomas of the gastrointestinal tract are rare. Duodenal lipomas are incidental and mostly asymptomatic. Tumours may produce symptoms of abdominal pain and discomfort or cause bleeding due to ulceration or intestinal obstruction due to intussusception. Review of cases published in last 67 years indicate that duodenal lipomas are rare to occur but commonly found in second part, they may be seen in third and fourth part of duodenum which may be missed on endoscopy. They can be multiple and may present as severe UGI bleeding which could be managed surgically. Though CT is diagnostic, histopathology confirms the diagnosis which shows lipomatous lesion composed of mature adipose arranged in lobules.

Video Endoscopic Sequence 1 of 1.

Ectopic opening of the common bile duct (CBD) into The Duodenal Bulb.

Small hole of which bile emerges at anterior wall of duodenal bulb.

The GI tract is an extremely rare congenital anomaly. The clinical implications and frequency of this anomaly are not clearly known.

Although an ectopic opening of the CBD is rare, it may be associated with severe pancreaticobiliary disorders. Endoscopists should be aware of this anomaly and know what to do in case they encounter the condition. Small hole of which bile emerges at anterior wall of duodenal bulb.

An ectopic opening of the common bile duct in the duodenal bulb is an extremely rare anomaly and one that should not be dismissed as just a benign congenital variant because it is associated with recurrent duodenal ulcer, biliary pain, choledocholithiasis, and recurrent cholangitis. Caution must be exercised before diagnosing such ectopia because duodenal ulcer also can cause a choledochoduodenal fistula. To make the diagnosis of ectopic common bile duct, there must be no evidence of a papillary structure in the lower duodenum. A good history, thoughtful endoscopy, and good pancreaticobiliary imaging is key to proper diagnosis.

See in the Gastric Ulcer3 Chapter an ulcero the pre-piloric antrum with probably ectopic opening of CBD.

Video Endoscopic Sequence 1 of 5.

Endoscopy of Salmonella Enteritis.

Multiple Duodenal Erosions due to Acute Gastroenteritis Gastrointestinal infections secondary to Salmonella Enteritis.

This is the case of a 42 year-old woman with acute diarrhea, (loose watery stools) fever chills, nausea and vomiting and acute abdominal pain with diffuse nonfocal abdominal tenderness, patient was hospitalized management with intravenous fluids and broad spectrum antibiotics.

Video Endoscopic Sequence 2 of 5.

Duodenal Involvement in Salmonella

Gastroenteritis usually starts 12 to 48 h after ingestion of organisms, with nausea and cramping abdominal pain followed by diarrhea, fever, and sometimes vomiting. Usually the stool is watery but may be a pastelike semisolid. Rarely, mucus or blood is present. The disease is usually mild, lasting 1 to 4 days. Occasionally, a more severe, protracted illness occurs.

If the infection is more severe, a disruption of the intestinal mucosa can occur with necrosis and ulceration, non-typhoidal salmonella.

In rare cases, Salmonella infection mimics inflammatory bowel disease or pseudoappendicitis.

Video Endoscopic Sequence 3 of 5.

Prognosis of patients with simple gastroenteritis is excellent except for very young infants or patients with debilitating diseases.

The prognosis for Salmonella meningitis or endocarditis is poor.

Salmonella infection most commonly begins with ingestion of bacteria in contaminated food or water. However, direct contact with animal and human carriers has also been implicated. Reptile and amphibian carriers are the most commonly recognized sources of direct contact Studies involving healthy human volunteers required a median dose of 1 million bacteria to produce disease. However, point outbreaks suggest as few as 200 bacteria may produce nontyphoid gastroenteritis.

Video Endoscopic Sequence 4 of 5.

Salmonella organisms are gram-negative bacilli in the family Enterobacteriaceae. Differences in lipopolysaccharide (LPS) and flagellar structure generate the antigenic variation that is reflected in the more than 2,000 known serotypes. The principal reservoirs for nontyphoidal Salmonella organisms are poultry, livestock, reptiles, and pets. The mode of transmission is ingestion of foods of animal origin, including poultry, red meats, unpasteurized milk, and eggs that have been contaminated by infected animals or an infected human. Contact with infected reptiles, such as iguanas, pet turtles, and tortoises, and ingestion of contaminated water are other modes of transmission.

Video Endoscopic Sequence 5 of 5.

Salmonella syndromes can be divided into gastroenteritis, enteric fever, bacteremia, localized infection, and a chronic carrier state.

Video Endoscopic Sequence 1 of 3.

Unusual Long Mass of the Duodenum

Incidentally we find this rather long mass with smooth texture. Apparently could correspond to a hyperplastic polyp.

Although this image I’ve seen described elsewhere as Brunoma, personally I do not agree with this term for this picture

Video Endoscopic Sequence 2 of 3.

With the polypectomy snare we pass this mass through the pylorus.

Video Endoscopic Sequence 3 of 3.

Another aspect of this mass.

Video Endoscopic Sequence 1 of 4.

A 58 year-old female who came from the republic of Guatemala with your husband who is thorax surgeon. She has this small sessile lesion at the duodenal bulb.

Video Endoscopic Sequence 2 of 4.

The tip of this small sessile lesion suggest an early ulceration that is typical for this tumor. In the duodenum, a small submucosal nodule located in the duodenal bulb is typical. In the Ileum, they aregenerally larger and may ulcerate. Most common in middle-aged patients. Duodenal carcinoids may cause obstruction or symptoms due to peptide secretion. Distal small bowel carcinoids cause obstructive symptoms such as abdominal pain, vomiting due to kinking from mesenteric involvement. Ulcerated ileal carcinoids cause acute, episodic, or occult gastrointestinal bleeding.

Video Endoscopic Sequence 3 of 4.

In addition to the described carcinoide in the duodenum Patient had this mass.
Antral nodule with typically central depression and intact overlying, antral mucosa.

Sequence 4 of 4.

The histopatologic study of the above case. Carcinoid tumor is a term applied to low-grade neuroendocrine tumors. They are composed of uniform cells with ampholilic cytoplasm, round nuclei, and inconspicuous nucleoli and arranged in nest, ribbons, cords, glands, and trabeculae Mitotic figures are scarce. More aggresive atypical or intermediate grade carcinoid tumors have increased numbers of mitotic figures and sometimes areas of necrosis.

Video Endoscopic Sequence 1 of 7.

Intestinal lymphangiectasia is characterized by a focal dilatation of intestinal mucocal and submucosal lymphatic ducts and may induce protein-losing enteropathy, steatorrhea, lymphocytopenia, chylous ascites, hypocalcemia, etc. Since transient “functional” duodenal lymphangiectasia (DL) was firstly described in healthy volunteers after nasogastric olive oil infusion, there were several reports describing endoscopic evidence of DL in patients without clinical evidence of malabsorption.

Video Endoscopic Sequence 2 of 7.

At eleven o”clock, the pappilla of Vater.

Video Endoscopic Sequence 3 of 7.

Endoscopy of Duodenal Lactocele

The nature of white submucosal areas as was at first
uncertain: on biopsy chyle was released indicating dilated
lacteals or a lactocele.

White tips to the intestinal villi are commonly seen but
even after histological examination the cause is not always
clear. Often this is due to endoscopically visible normal
filled lacteals as shown. Recent ingestion of fat-containing
fluids or food is the likely explanation in most cases.
It may in some patients be associated with obstruction to
lymphatic flow.

DL without evidence of clinically significant malabsorption
is not infrequently found during routine upper endoscopies.

Video Endoscopic Sequence 4 of 7.

Endoscopy of Duodenal Lactocele

On biopsy chyle was released indicating dilated lacteals or
a lactocele.

Video Endoscopic Sequence 5 of 7.

Chyle was released

Intestinal lymphangiectasia can present as malabsorption
and protein-losing enteropathy.

Video Endoscopic Sequence 6 of 7.

The histopathological appearances of lymphangiectasia
with endotheliumlined lymphatics is shown.

Click on the image to enlarge in a new windows.

Video Endoscopic Sequence 7 of 7.

Section shows lakes of ectatic lymphatic vessels within the
lamina propria of the small intestine.

Click on the image to enlarge in a new windows.

Video Endoscopic Sequence 1 of 2.

Endoscopy of duodenal lactocele

Video Endoscopic Sequence 2 of 2.

Endoscopy of duodenal lactocele

On biopsy chyle was released indicating dilated lacteals or a lactocele.

Pancreatic Cancer that Infiltrates the Duodenal Wall.

The cat scan showed a tumor of the head, this nodule is in the second part of the duodenum that was proven to be by biopsies adenocarcinoma.

Among cancers of the gastrointestinal tract, it is the third
most common malignancy and the fifth leading cause of
cancer-related mortality. The disease is difficult to
diagnose in its early stages, and most patients have
incurable disease by the time they present with symptoms.
The overall 5-year survival rate for this disease is less
than 5%.

Mycobacterium Avium Complex of the Duodenum.

Endoscopically Mycobacterium Avium and
Mycobacterium Tuberculosis infection can be suspected
by the presence of tiny, punctate white nodules or exudate.
Both illnesses can cause ulcers, bleeding, diarrhea, and
Mycobacterium Avium Complex infection occurs in the
small intestine in patient with HIV disease, typically
presents with weight loss, fever, diarrhea and abdominal
paint. The duodenum is most commonly involved in 90% of
the cases.

Video Endoscopic Sequence 1 of 4.

Extensive neoplasia of the head of pancreas that invades
the duodenal bulb and causes pancreato duodenal fistula.
The patient had gastrojejunum anastomosis in a public
hospital. See that anastomosis.

Video Endoscopic Sequence 2 of 4.

The gastric antrum is observed deformed.

Video Endoscopic Sequence 3 of 4.

The neoplasia is observed ulcerated and necrotic.

Video Endoscopic Sequence 4 of 4.

The fistula is observed below and to the posterior wall
the pancreatic segment is observed into the fistula.

Infiltrating Pancreatic Cancer into the Duodenal Bulb

Post bulbar Adenocarcinoma.

A 20 year-old female that undergone open cholecystectomy
due to choledocolitiasis a T-Tube was placed.
A choledoscopy was performed 6 week after surgery
through the fistula.

Video Endoscopic Sequence 1 of 4.

Brun ner’s Gland Adenoma

Brunner’s gland adenoma (BGA) of the duodenum appear
to be nodular hyperplasia of the normal Brunner’s gland
with an unusual admixture of normal tissues, including
ducts, adipose tissue and lymphoid tissue.

Overgrowth of Brunner’s gland forming a tumour larger
than 1cm in size in diameter is referred to as BGA and less
than 1cm as Brunner’s gland hyperplasia.

The etiology of Brunner’s gland adenoma remains obscure.
Concurrent H. pylori infection is very common in patients
with Brunner’s gland adenoma. However, the role of H.
pylori infection in the pathogenesis and development of
Brunner’s gland hyperplasia remains unclear.

Video Endoscopic Sequence 2 of 4.

Endoscopy of Brunner’s Gland Adenoma

Normal Brunner’s glands are found in the highest concentration in the proximal duodenum and found normally extending to the proximal jejunum. These glands secrete a viscous alkaline fluid that is thought to protect the duodenal mucosa from the effects of gastric acid. This fluid also contains a glycoprotein that binds to the mucosa to further protect it. Brunner’s glands also secrete enterogastrone, a hormone that inhibits gastric acid secretion. The precise etiology of Brunner’s gland hyperplasia has not been completely elucidated. One theory is that the glands are stimulated to proliferate by increased acid production. However, no studies have confirmed this hypothesis.

Brunner’s gland adenomas are rare duodenal lesions that can present with hemorrhage or signs and symptoms of obstruction. They are not true adenomas, but are actually hamartomas with little to no malignant potential. These lesions should be treated with endoscopic polypectomy if possible, but surgical resection is an acceptable option.

Video Endoscopic Sequence 3 of 4.

Brunner’s glands consist of submucosal mucin-secreting
glands located exclusively in the duodenum. They extend
from the pylorus distally for a variable distance, usually at
the first and second portions of the duodenum, and less
frequently, stopping at the third and fourth portions.
Brunner’s glands secrete an alkaline fluid composed of
viscous mucin, whose function appears to protect the
duodenal epithelium from acid chyme of the stomach.
It is a tumor without malignant predisposition. The
malignant type is rare.

Video Endoscopic Sequence 4 of 4.

Las glándulas de Brunner, localizadas en la submucosa y
las capas profundas de la mucosa del duodeno, son más
numerosas en la primera porción del duodeno, y su número
decrece progresivamente en la segunda, tercera y cuarta
porción. Debido a su localización profunda, la proliferación
de las glándulas de Brunner dan como resultado una masa
submucosa. Histologicamente, las glándulas de Brunner
son las glándulas submucosas acinotubulares ramificadas,
revestidas por grandes células que muestran el citoplasma
tejido ligeramente con la tinción de hematoxilina-eosina.
Cambios quisticos pueden ocurrir dentro del acini y la
atipia celular no está presente por lo general.