Chronic Gastritis Flashcards
What is chronic gastritis
A chronic stomach disease pathological base of which are dystrophy, inflammation, disregeneration of gastric mucosa with atrophy as the result of these events
Etiology of Chronic gastritis
- Exogenous
- Endogenous
- infection
Exogenous-food i.e quality and quantity
- mechanical or professional i.e heat,steams,acids,dusts,foreign bodies
- chemical and drug consumption i.e alcohol,NSAIDS,potassium
Endogenous- metabolic and endocrine disorders, tissue hypoxia,food allergy etc
Infection -H.pylori, syphillis, histoplasmosis, schistosomiasis
Also due to sarcoidosis, chrohns disease(how)
Pathogenesis of chronic gastritis
- For helicobacter infection, due to its virulence(4factors)-flagella
-urease
-adhesion
-toxins
This will lead to erosion (how)of the mucosal layer by Interleukin release and PMNs infiltration and inflammation occurs
2.For other factors i.e overeating will cause stomach distension, increase in amount of HCL causing erosion then inflammation
Classification(9)?
1.By the type of gastritis
I. Non-atrophic
II. Atrophic
- Autoimmune
- Multifocal
Special forms
- Chemical
- Radiation induced
- Lymphocytic
- non infectional
- Eosinophilic
- Other infection
- Collagenous
- By Etiology
- Pathogenesis(Type A,B,C).
- Morphologic-superficial
- atrophic gastritis of different severity grade
- Remodelling(metaplasia)gastritis-a.gut metaplasia
b. glands pylorisation
c. atrophic hypertrophic gastritis
- Hypertrophic
- By Etiology
- By localisation-diffuse(pan gastritis)
- focal(antral, pyloroduodenal)
- fundal(rare) - Functional -with normal or moderately increased secretion
- with secretion insufficiency of different degrees from initial to histamine resistant achlorhydiac and achylia - Special forms-rigid antrum gastritis
- hypertrophic gastritis (Menentries), polipous gastritis
- erosive hermorrhagic - Clinical course-
- By phase -exacerbation, remission,recovering exacerbation.
- By stage-compensation,subcompensation,decompensation
- Concomittant gastritis-Addisons burmer anemia
- Gastric cancer
- mediogastral ulcers
What is the clinical picture of chronic gastritis?
Represented by syndromes, depends on localisation
- Stomach dyspepsia
- pain in epigastrium
- Intestinal dyspepsia
- Asthenoneurotic syndrome
- pain
- gastric dispepsy
- general symptoms-rare e.g weight loss, increased appetite to piquant(spicy) food, hypotonia
- Damping syndrome may be present
- Objective
- Secondary gut dispepsy
What are the Pathogenetic types of chronic gastritis?
There are three types namely
- Type A
- Type B
- Type C
Type A C.G, Etiology, pathogenesis, treatment,prophylaxis
Etiology- autoimmune disease predisposition e.g DM,addisons disease,Hashimotos autoimmune thyroiditis
Localisation -fundus or body of stomach
Pathogenesis- loss of parietal cells
Due to absence of acid secretion it leads to gastrin release resulting in hypergastrenemia and hyperplasia of gastrin producing G cells
Lack of intrinsic factor disables VitB12 absorption leading to B12 deficiency and megaloblastic or pernicious anemia.
Autoimmune ABs directed against parietal cells attach and destroy them causing decrease HCL production causing achlorydia, causing hypergastrenemia >1000pg/ml.
May induce small, multicentral carcinoid tumours
Clinical picture;
Criteria(MIC)
- morphology
- localisation
- inflammatory reactions(weakly expressed)- why ?
- epithelium development-primary
- Erosion-rare - Immunologic
- Infectious factor HP- absent
- ABs to HP are absent
- ABs to intrinsic factor are present - Clinical
- Bright gastrinemia-present
- Hypoacidity is present
- B12deficiency anemia is present
- Combination with ulcer - present
- Malignization is rare
- rapid progression i.e especially in patients over 50 and the ones with severe mucus affection
- Incase of affection of stomach body affection progression is more but in antral more stable disease is seen.
Treatment
- Diet
- During exacerbation (2-3 weeks treatment of inflammation by natural means e.g flowers of chamomile,plantain leaves
- Symptomatic e.g pain ( prokinetic-spasmolytics, Peripheral Group B2 dopineminegic antagonist e.g Motiluim 10mg 4 times a day, 3 times 30 minutes before eating and once before sleeping
- Stomach function correction -stimulation(Limontar)
- replacing (acid pepsin intake - Pancreatic secretion ( if symptoms are present)- Creon
- Anabolics i.eRetaboli 25 to 50 mg every 3 to 4 weeks or I.v infusion of amino acid mixtures e.g Alvesin incase of marked protein metabolism disturbance
Prevention
- Limit amount of food per every meal
- Less fatty,spicy food
Type B C.G, Etiology, Pathogenesis,Treatment
Etiology- Bacterial i.e H.pylori bacteria
Gram negative bacteria
Clinical picture(MIC) 1. Morphology Localisation- Antrum Inflammatory reaction-strongly marked Epithelium atrophy development-secondary Erosion-frequently
2.Immunologic
Infectious factor HP present
Antibodies to HP present
Antibodies to parietal cells and intrinsic factor are absent
3.Clinical Bright gastrenemia is absent Hypoacidity Any type of secretion B12 deficiency absent Combination with ulcer in 100% cases Malignization is frequent
Treatment
Duration 7-14 days
Eradication or etiology
1st line- Omez 20mg , twice a day
-Clarythromycin 250mg ; twice a day
- Amoxicillin 500gx 4 or 1000x2 with eating
-Metronidazole 400-500mg twice while eating
2nd line- combination
-Denol(240x2 )+ Metronidazole (400x3)+Amoxicillin(500x3)
Or Denol+ Clarythromycin+ Amoxicillin
3rd line- Omeprazol e.gOmez 20mg twice a day
RanitidineH2 histamine receptor blocker
Tetracycline
2.Cytoprotectors e.g in exacerbation
Sucralfat(1g 3 times a day)
Binds with proteins of affected mucosa and forms protective
- Antacids e.g phospalugel. 1-2packs 40mins before meals or an hr after it
- Peripheral cholinolytics incase of secretion with pain e.g metacin
Prophylaxis
1probiotics
2.Food
2.
Type C C.G, etiology, Pathogenesis, treatment, prophylaxis
Etiology- Chemical
- Reflux gastritis
-maybe due to Stomach resection
Bile components e.g lysolecitin, bile acidsrefluxes to stomach,why?
-maybe failure of pyloric sphincter function
-there is toxic affection of the mucosa, lipid affection of epitheliocytes, mucus bicarbonate barrier destroying
2.Iatrogenic affection
Rare
Causedby NSAIDS with antral part affection ,how?
Block COX1 enzyme and reduce production of prostaglandins in the stomach
By irritation of gastric mucosa, weaken resistance to acid
Treatment
PPi e.g omeprazole
Food,stop smoking
What is the diagnosis for Chronic gastritis?
Clinical symptoms according to subjective data
Predominance of dyspeptic syndromes
Physical exam e.g palpation of abdomen
Laboratory and instrumental diagnosis
- Endoscopic examination (in suspected H.Pylori-associated gastritis –w ith biopsy and
investigation aimed on HP search)
- Confirms diagnosis
- Confirms HP presence (biopsy)
- Diagnosis of erosive gastritis: 2 types of erosions: flat ones “bleeding tears” or elevated,
with necrosis focus in center (variolomorphic gastritis), more often lymphocytic origin is
proved by histological investigation
- Diagnosis of Menentries disease – mucosa is folded, looks like brain section Endocopic criteria of gastritis:
- marked diffuse oedema
- marked diffuse hyperemia
- haemorrhages
- vulnerability of the mucosa
- trend to bleeding of the mucosa
- flat or elevated erosions
- changes of the vessels (may be either smoothed and hardly seen or marked) - atrophy
- smoothed or hypertrophic folds
- presence of H.Pylori (biopsy)
Special stains to identify H pylori, such as Warthin-Starry, Giemsa, or Genta stain are used to identify H.Pylori. - Gastric secretion st
Basic (1 hour of investiga-
tion)
Healthy males 3.3+0.3 mmol/hour (0-9)
Healthy females 2.3+0.21 (0-7) Atrophic gastritis 0.75+0.03
Histamine –stimulated acid production (2nd hour)
11.5+0.9 (6.25-26)
8.5+0.6 (4.5-20)
1.36+0.05
Antral gastritis may lead to mild increase of secretion due to G-cells activation- pH-metry through naso gastric tube
- Serum IgG antibodies to H pylori are detectable by (Microbiological)ELISA, and kits are commercially(
- Noninvasive 14C- and 13C-urea breath tests. Because these urease breath tests indi- cate active infection, they may become the tests of choice for noninvasive screening for H pylori infection or for verifying eradication after antibacterial therapy.
- immunological test (blood) for H.Pylori antibodies presence evaluation – 2 times
- blood analysis (haemogram)
- serum proteins and protein fractions
- Urineanalysis
- coprogram (cytology, test for occult bleeding)
- ultrasonic examination of the abdominal organs
Additional exam
Screening method for gastritis with marked atrophy and for gastric cancer in regions with high incidence of these diseases: measuring serum levels of the pepsinogen I–to– pepsinogen II ratio. Pepsinogen I (PGA, PGI) ; level of PGA in the serum decreases as loss of gastric chief cells during gastric atrophy occurs, resulting in a decreased PGI/PGII ratio. However, the sensitivity and specificity of the assay is relatively low, with 84.6% and 73.5% values, respectively, reported in a recent study.
- For autoimmune gastritis: Antiparietal and anti-intrinsic Castle’s Factor (IF) - antibodies in the serum
Diagnosis formulas
1. Chronic B gastritis, exacerbation, with moderate atrophic changes and secretion insuffi- ciency, HP ++++
2. Erosive gastritis, exacerbation. Stomach bleeding (date) HP +++
3. Chronic A gastritis, remisiion. HP (-). Addison-Birmer’s anaemia (date). Diffuse stomach
corpus polyposis.
Differential diagnosis. Aims of diagnostic measurements:
1. Confirm presence of gastritis (clinical syndromes+endoscopy+secretion investiga- tion+HP). Differential diagnosis with non-ulcer dyspepsia, cancer, peptic ulcer
2. Investigation of the other digestive system organs to reveal their affection (usually gastri- tis is not isolated disease).
3. To determine is gastritis the main or concomitant disease
Clinical course: fluctuating, with exacerbations and remission, the first ones being usually
- ECG
What is the diagnosis for Chronic gastritis?
Clinical symptoms according to subjective data
Predominance of dyspeptic syndromes
Physical exam e.g palpation of abdomen
What is the diagnosis for Chronic gastritis?
Clinical symptoms according to subjective data
Predominance of dyspeptic syndromes
Physical exam e.g palpation of abdomen
- Endoscopic examination (in suspected H.Pylori-associated gastritis –w ith biopsy and
investigation aimed on HP search)
- Confirms diagnosis
- Confirms HP presence (biopsy)
- Diagnosis of erosive gastritis: 2 types of erosions: flat ones “bleeding tears” or elevated,
with necrosis focus in center (variolomorphic gastritis), more often lymphocytic origin is
proved by histological investigation
- Diagnosis of Menentries disease – mucosa is folded, looks like brain section Endocopic criteria of gastritis:
- marked diffuse oedema
- marked diffuse hyperemia
- haemorrhages
- vulnerability of the mucosa
- trend to bleeding of the mucosa
- flat or elevated erosions
- changes of the vessels (may be either smoothed and hardly seen or marked) - atrophy
- smoothed or hypertrophic folds
- presence of H.Pylori (biopsy)
Special stains to identify H pylori, such as Warthin-Starry, Giemsa, or Genta stain are used to identify H.Pylori. - Gastric secretion st
Basic (1 hour of investiga-
tion)
Healthy males 3.3+0.3 mmol/hour (0-9)
Healthy females 2.3+0.21 (0-7) Atrophic gastritis 0.75+0.03
Histamine –stimulated acid production (2nd hour)
11.5+0.9 (6.25-26)
8.5+0.6 (4.5-20)
1.36+0.05
Antral gastritis may lead to mild increase of secretion due to G-cells activation- pH-metry
- Serum IgG antibodies to H pylori are detectable by ELISA, and kits are commercially
available. Highly sensitive, these tests do not necessarily denote ongoing, active infec- tion. At least, performed 2 times. After successful H pylori eradication with antibiotics, antibody levels decline slowly over 6–12 months but may remain positive. - Noninvasive 14C- and 13C-urea breath tests. Because these urease breath tests indi- cate active infection, they may become the tests of choice for noninvasive screening for H pylori infection or for verifying eradication after antibacterial therapy.
- immunological test (blood) for H.Pylori antibodies presence evaluation – 2 time
- blood analysis (haemogram)
- serum proteins and protein fractions
- urinanalsis
- coprogram (cytology, test for occult bleeding)
- ultrasonic examination of the abdominal organs
- ECG
Addional methods of diagnosis
Screening method for gastritis with marked atrophy and for gastric cancer in regions with high incidence of these diseases: measuring serum levels of the pepsinogen I–to– pepsinogen II ratio. Pepsinogen I (PGA, PGI) ; level of PGA in the serum decreases as loss of gastric chief cells during gastric atrophy occurs, resulting in a decreased PGI/PGII ratio. However, the sensitivity and specificity of the assay is relatively low, with 84.6% and 73.5% values, respectively, reported in a recent study.
- For autoimmune gastritis: Antiparietal and anti-intrinsic Castle’s Factor (IF) - antibodies in the serum
Diagnosis formulas
