​Kembara Xtra - Medicine - Gastritis

​Kembara Xtra - Medicine - Gastritis  
Inflammation of the mucosa lining the stomach can be categorized according to its time course.
- In acute cases, neutrophilic infiltration might be seen on the histology
On histology, chronic cases show a combination of mononuclear cells, lymphocytes, and macrophages.
Among the many subtypes of gastritis are:
– Erosive gastritis – Mucosal damage caused by a noxious agent (particularly nonsteroidal anti-inflammatory medications [NSAIDs] or alcohol) – Vascular congestion brought on by portal hypertension (HTN) or gastric antral vascular ectasia (GAVE)
– Hemorrhagic gastritis (stress ulceration) – A reaction to protracted reflux exposure to biliary and pancreatic fluid – Reflux gastritis (a form of gastritis caused by reflux)
 A response to a disturbance in the hemodynamic state (for example, hypovolemia or hypoxia [shock]). Patients admitted to the intensive care unit (ICU) frequently have this condition, especially after suffering serious burns or trauma.
- Gastritis due to an infectious agent
 Acute and/or chronic: Helicobacter pylori infection (the most common cause of gastritis); Viral infection (reaction to systemic infection); caused by cytomegalovirus or Epstein-Barr virus; Phlegmonous gastritis: a rapidly progressive and frequently fatal bacterial infection of the gastric wall; – Atrophic gastritis; Metaplastic atrophic gastritis: autoimmune primary (per
Granulomatous disease, often known as sarcoidosis or Crohn disease
Considerations Regarding the Aged
Infection with H. pylori is common in those older than 60 years of age.
Considerations Relating to Children
Gastritis affects newborns and young children quite seldom; nevertheless, its incidence rises with advancing age. H. pylori infection is the most common cause of gastritis in children and adolescents.



 The most common age group is old people, but people of all ages in adulthood are affected.
Despite the fact that autoimmune gastritis affects more women than men, the predominant gender is male.
In the United States, the incidence ranges from 1.8 million to 2.1 million visits each year.


Prevalence
People who were born before 1950 have a higher risk of developing gastritis.
Comparatively, only about 20% of persons under the age of 40 are infected with H. pylori, whereas over 50% of people over the age of 60 have the infection.
In 2018, it was discovered that approximately 27% of adults in the United States were infected with H. pylori.
The incidence of infection is significantly higher among members of underrepresented groups and immigrants.
- Higher incidence in those with lower socioeconomic status

Causes and effects: etiology and pathophysiology 

Toxic substances are responsible for the loss of the mucosal barrier that protects the stomach, which leaves the underlying epithelial tissue vulnerable to damage.
Infections: Helicobacter pylori (the most prevalent cause), Staphylococcus aureus exotoxins, and viral infections (including Epstein-Barr virus and human cytomegalovirus)
Alcohol, which causes cell DNA damage and subsequent pyroptosis; aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), which inhibit protective prostaglandin synthesis; bile reflux and pancreatic enzyme reflux; portal hypertensive gastropathy, which causes erosion; emotional stress, which causes cortisol production; Crohn's disease-related gastritis, which causes focally enhanced gastritis with histiocytes, lymphocytes, and granul
Genetics
There is a divergence of opinion concerning genomic research between the association of toll-like receptor 1 (TLR1) generating inflammation in H. pylori–infected gastric mucosa. This inflammation is caused by H. pylori.
There is a need for additional investigation.

Age greater than 60 years old; exposure to potentially toxic medications or chemicals (such as alcohol or nonsteroidal anti-inflammatory drugs; NSAIDs); hypovolemia; hypoxia (shock); burns; brain injury; and a complex postoperative course are all risk factors.
Autoimmune illnesses (thyroiditis and type 1 diabetes mellitus, Addison disease, vitiligo, erosive oral lichen planus) Family history of H. pylori and/or stomach cancer Tobacco use Radiation, chemotherapy, ischemia, pernicious anemia, gastric mucosal atrophy Tobacco use Autoimmune diseases (thyroiditis and type 1 diabetic mellitus, erosive oral lichen

Prevention 
Patients with hypovolemia or hypoxia (particularly ICU patients) should get prophylaxis with H2 receptor antagonists, PPIs, prostaglandins, or sucralfate. Harmful medicines or chemical agents, alcohol, and tobacco should be avoided.
Patients diagnosed with idiopathic thrombocytopenic purpura (ITP), patients on long-term NSAID therapy, and patients from endemic locations should all be tested for H. pylori and treated with antibiotics if the bacteria is found to be present.


Conditions that are associated with it include: peptic ulcer of the stomach or duodenum; primary (pernicious) anemia; atrophic gastritis; portal hypertension; and hepatic failure.
Lymphoma of the mucosa-associated lymphoid tissue (also known as MALT).

History of the Presenting Symptoms Epigastric discomfort, which is frequently made worse by eating; burning epigastric pain; anorexia; nausea, with or without vomiting; Significant bleeding is uncommon, with the exception of hemorrhagic gastritis.
Hiccups, belching, bloating or abdominal fullness, unintentional weight loss, generalized fatigue due to iron-deficiency anemia, neurologic symptoms related to vitamin B12 deficiency if atrophic gastritis, history of smoking, consumption of alcohol, NSAID use, radiotherapy, gallbladder disorders, autoimmune disorders, IBD, vasculitis, or eosinophilic gastrointestinal (GI) disorders; can be 


The Patient's Clinical Examination 

 Examine for stigmata of persistent alcohol addiction. Mild epigastric discomfort. May have heme-positive stool. Vital signs to determine hemodynamic stability. Abdominal exam is often normal. Mild epigastric tenderness. May have heme-positive stool.
If the patient is anemic, they may have a pale complexion and a slowdown of their capillary refill.

Differential Diagnosis Abdominal pain that is functional (dyspepsia) Peptic ulcer disease, viral gastroenteritis Cholecystitis Gastric cancer in the elderly Pancreatic illness (inflammation vs. tumor)

Results From the Laboratory 

Initial Tests (lab, imaging)
typical or typical
● Evaluate for iron deficient anemia.
Stool testing for the presence of fecal H. pylori antigen has a diagnostic accuracy of 95% and a sensitivity of 95%; it can be used for both diagnosis and eradication.
The 13C-urea breath test has a specificity and sensitivity of 95% for detecting H. pylori.
H. pylori serology using serum IgG is a cost-effective method with a sensitivity of 85% and a specificity of 79%.
- If there is evidence of colonization or previous infections, the test is positive; it cannot be used to determine whether or not the infection has been eradicated.
Patients with autoimmune chronic gastritis may have antibodies to intrinsic factor or parietal cells (the latter being the most sensitive biomarker), elevated serum fasting gastrin level, elevated serum pepsinogen I (PGI) level, and elevated PGI to PGII ratio. Patients with pernicious anemia may have macrocytic anemia with low serum vitamin B12 levels and intrinsic factor autoantibodies. Gastric acid analysis may be abnormal but is not a reliable indicator of gastriti
Medications that could influence the results of lab tests: Antibiotics, proton pump inhibitors (PPIs), and other medications containing bismuth may alter the urea breath test for H. pylori.
- Stop using proton pump inhibitors (PPIs) for a period of 14 days, H2 receptor antagonists for a period of 24 hours, and antibiotics for a period of 28 days before undergoing stool or breath testing.


Additional Examinations, as well as Other Important Factors
Endoscopy to check for H. pylori: get a tissue for culture; perform polymerase chain reaction (PCR); histology with H&E plus second staining; perform fast urease testing

Diagnostic Methods and Other Procedures
Gastroscopy with biopsy is the first-line treatment in the following situations: – Patients older than 50 years who are experiencing new symptoms
- A decrease in body mass, prolonged vomiting, or gastrointestinal bleeding
Take into consideration patients under the age of 50 who test negative for H. pylori.
If there is a poor response to the initial treatment, several gastric biopsies in both the body and the antrum are indicated to be performed. In order to get the most accurate diagnosis possible, patients need to stop taking PPIs two weeks before their endoscopy.
Interpretation of Test Results: Acute or chronic inflammatory infiltration in gastric mucosa, frequently accompanied by deformation or erosion of surrounding epithelium; presence of H. pylori frequently confirmed. There is a possibility of ulcers or bleeding being present.
Cytological samples taken from the antrum and the body of the stomach

Treatment for H. pylori is necessary if one want to experience symptomatic relief.
If the patient is unable to accept oral consumption, parenteral hydration and electrolyte supplements should be administered, and NSAID use should be stopped.
Complete abstinence from alcoholic beverages; quitting smoking
Endoscopy for patients who have not shown improvement despite treatment

First and Foremost, Medication
Antacids should be taken in liquid form, 30 milliliters one hour after meals and before going to bed.
Oral H2 receptor antagonists such as cimetidine (Tagamet) 300 mg every six hours, famotidine (Pepcid) 20 mg twice day, or nizatidine (Axid) 150 mg twice daily have not been found to be demonstrably more effective than antacids.
Sucralfate (Carafate): 1 g every four to six hours on an empty stomach; the rationale for this recommendation is unclear, although it has been shown to be useful in practice.

● Prostaglandins (misoprostol [Cytotec]): can help allay
gastric mucosal injury; dosage 100 to 200 μg QID
● PPIs if no response to antacids or H2 receptor blockers
(e.g., omeprazole 20 mg daily or BID or esomeprazole 20
mg daily or BID)
● Treatment will depend on penicillin allergy and previous
macrolide exposure or clarithromycin resistance of >15%.
– Clarithromycin triple therapy (also known as CTT) consists of a short course (14 days) of amoxicillin 1 g BID, standard-dose PPI BID (omeprazole 20 mg BID, etc.), and clarithromycin 500 mg BID.
If you have an allergy to PCN, you should switch to metronidazole 500 mg TID instead of amoxicillin. According to current meta-analyses, this results with a 75–80 percent eradication rate.
PPI (omeprazole 20 mg) BID plus bismuth salicylate (Pepto-Bismol) 30 mL liquid or 2 tablets QID plus metronidazole 250 mg QID plus tetracycline 500 mg QID for 10 to 14 days 75%–90% eradication
 Use as a first therapy in regions where the prevalence of clarithromycin resistance is greater than 15%.
Take into consideration patients who are allergic to penicillin.
○ Alternative: Pylera combination tablet (bismuth subcitrate, metronidazole, and tetracycline) ● H. pylori therapy failure: Alter your treatment plan and stay away from clarithromycin (unless susceptibility may be shown through resistance testing):
- Between 7 and 14 days of the BQTConsider administering levofloxacin 250 mg BID, amoxicillin 1 g BID, and a standard-dose PPI BID for a period of 14 days to patients who have experienced two previous failures.
– Consider using levofloxacin quadruple therapy on patients who are allergic to penicillin. This treatment consists of levofloxacin 500 mg QD, omeprazole QD 40 mg, nitazoxanide 500 mg BID, and doxycycline 100 mg QD for a period of 7 to 10 days.
The severity of gastritis and peptic ulcers may be reduced, and the progression toward atrophic gastritis and gastric adenocarcinoma may be slowed by the use of probiotics in patients who are known to have symptomatic H. pylori infection (4).[A]
- Probiotics alone likely do not eradicate H. pylori.
- Examples of possible dosage regimens taken during clinical tests:  14 days of treatment with Bifidobacterium spp. BID
Indications to avoid use include hypersensitivity.
Bismuth has the potential to make feces appear dark in color.

Things to Think About When Expecting
Antacids containing magnesium trisilicate and sodium carbonate should be avoided, and women who have hyperemesis gravidarum (HG) have a higher risk of being infected with the H. pylori bacteria. Treatment can be deferred until after birth. Testing for H. pylori on a routine basis is not suggested for people who have HG.


Surgical Methods and Operations 

Except in the cases of phlegmonous gastritis or gastritis with high-grade dysplasia, surgical intervention is typically not required when treating gastritis.


Alternative Medicine 

Because of their powerful anti-inflammatory qualities, cranberries, garlic, curcumin, ginger, and Pistacia gum have been suggested in some research as having the potential to prevent or lessen the severity of an H. pylori infection.

Admission Prophylaxis for patients in the Intensive Care Unit Hemorrhagic gastritis


In general, there are no limitations on the follow-up.
Verify that the H. pylori infection has been eradicated at least 4 weeks after treatment.
Monitoring of the Patient
If the gastritis was severe or there was a poor response to treatment, you should think about getting a second endoscopy after six weeks.
It is not currently recommended to perform surveillance endoscopy on patients who have mild to moderate atrophic gastritis at this time. Patients diagnosed with severe atrophic gastritis should undergo endoscopy with biopsy sampling at regular intervals not to exceed three years.
It is recommended that patients with confirmed high-grade dysplasia undergo surgical or endoscopic resection. Surveillance may be suspended when two or more endoscopies are negative for dysplasia. Twenty-five percent of patients with high-grade dysplasia may progress to adenocarcinoma within a year, although this number is strongly influenced by geography, ethnicity, race, and family history.

Diet

The intensity of symptoms will determine the dietary limits (such as eating meals that are bland, light, and soft). In general, you should stay away from things like coffee, foods that are spicy, alcohol, peppermint, carbonated beverages, and foods that are high in fat content.

Patient Education Ceasing smoking; cutting back on alcohol use; making dietary adjustments Relaxation therapy; avoiding nonsteroidal anti-inflammatory drugs (NSAIDs).

Even with treatment, the mortality rate for phlegmonous gastritis ranges between 40 and 50 percent.
In the event that the H. pylori infection returns, you will need to undergo another round of therapy.

Complications 

• Bleeding as a result of significant mucosal erosion or ulceration • Obstruction of the gastric outlet as a result of edema, which prevents an appropriate movement of food from the stomach to the small intestine.
Clearing H. pylori before the development of chronic gastritis may prevent the development of gastric cancer. Chronic autoimmune gastritis has an increased risk for the development of gastric neuroendocrine tumors and adenocarcinoma due to dysplasia. Gastric intestinal metaplasia puts a patient at a 10-fold increased risk of developing gastric cancer.

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