oral-gast

 EMBED Package 
Diseases Of the MouthOral Ulceration and
Oral Infection:Causes:Aphthous Ulcer: Idiopathic, and PremenestrualInfection: Fungal(as Candidiasis),Viral(as Herpes simplex), Bacterial(as Vincents stomatitis, Syphilis).Gastrointestinal Diseases: Crohns disease, Celiac Disease.Dermatological: Lichen planus, Pemphigus, Pemphigoid.Systemic Dis.:Behcet syndrome,Systemic Lupus Erythematosus(SLE).Drugs: Hypersensitivity(as Steven jonson synd.), Cytotoxic drugs.Neoplasia:Carcinoma(as Squamous cell), Kaposi sarcoma,Leukemia.Aphthous Ulceration: Occur and is recurrent in up to 30%of population.Def: Recurrent painful superficial ulceration that occur any where inthe mouth, self limiting, and usually of unknown aetiology.particularly common in women prior to menstruation, Management: Symptomatic relief by local anesthetic, To help healinglocal steroid (as triamcinolone 0.1% in orabase)or cholinesalicylate 8.7% gel, is useful.In severe , persistent and large sized ulcers consider the:Special types of Aphthous ulceration: Persistent & Deep, in HIV/AIDS.It may be the presenting symptom in Behcets disease.Similar less painful lesion in Reiters syndrome & SLELesions with Crohns disease exhibit granuloma reaction.Lesions with Celiac disease may remit by glutein free diet.Other causes of Ulceration may be considered in atypical lesions & may need biopsy.Vincent's Angina (V.Stomatitis): Invasion of the mucous membrane by Borreliavincenti and other commensals of the mouth, when oral hygiene ispoor and host resistance is low as in malnutrition, debility and AIDS.Characterized by Deep painful sloughing ulcers with halitosis & fever.loss of interdental papillae, ulcerated gingiva, enlarged LN.Management: hydrogen peroxide local mouthwash, Broad spectrum AB.Candidiasis of the mouth: Proliferation of Candida Albicans(a normal commensalof the mouth) in Babies (Thrush), In debilitated patients, Diabetics, Immune-suppressed (as AIDS),& those on corticosteroids or broad spectrum Antibiotics or cytotoxic drugs.Clinically: Thrush is seen as white patches any where in the mouth sometimes painful swollowing & dysphagia.creamy & reveal raw bleeding area on scrap.Sometimes Erythematous in type(painful red flat area).or a nonremovable white patch (candidal leukoplakia).Candidal Angular Cheilitis is a sore fissure at mouth angleManagement: correction of predisposing factors, Nystatin (or Amphotericin) suspension or lozengesFor resistant cases & immune-suppressed ,oral fluconazole.Salivary Glands Pathology: Parotitis (viral-Mumps, Bacterial- Post operative inf.)Parotid swelling: Parotitis, Calculi, Tumours, Sjogren's synd., Sarcoid.Oral Medicine in the Elderly: Baseline salivary flow drops(40% feel dry mouth).Chewing power and olfactory and Gustatory sensations decline.Root caries are common, Gm-ve bacteremia & septicemia may occur.GastritisIs a Histological term , Acute or Chronic, depending on inflammatory cells type.Acute Gastritisneutrophilic infiltrates, Erosive & sometimes hemorrhagic.Causes: Drugs(commoest)as NSAID & Aspirin, Iron, AlcoholSevere physiological stress as in Burns, major operationscar accidents and severe infection.Infective, as the Acute H.pylori phase, viral as H.simplex inAIDS, Bacterial as phlegmonous (rare).Clinically: Often Asymptomatic, or Anorexia,nausea,vomiting,sometimes upper GI bleeding(hematemesis and melena).Diagnosis, usually clinical, May need Endoscopy to exclude PU & Ca.Management: Heals spontaneously(days or weeks for regeneration)Prevention is more important for the high risk groups.Short term therapy with Antacid, or Antisecretory Drugs.Upper GI bleeding need special urgent care and admissioneven blood transfusion & other measures.Chronic GastritisLymphocytic and Plasma cell infiltrates, commoest due to H.Pylori.Presentation: usually Asymptomatic, but may cause Dyspeptic sympt.With H.pyloi type,patients may present with PU diseaseWith Autoimmune type Anemia (pernicious)may be found.Histological stages of Chronic Gastritis:1.Superficial, limited to lamina propria2.Atrophic gastritis, deeper infiltration and glandular destruction.3. Gastric atrophy, paucity in inflammatory cells, loss of glands withthin mucosa and on endoscopy; visible underlying vessels.Classification according to cause: 1. Chronic nonspecific gastritisH.pylori type (commonest)Autoimmune type(pernicious Anemia (PA))Postgastrectomy(Biliary gastritis)2.Chronic specific gastritis (rare)Infectious(T.B, CMV)Lymphocytic&Eosinophilic gastritisGranulomatous,Crohns,Sarcoid dis.Classification according to site: 1. Type A gastritis,less common,Autoimmune,sprae antrum2.Type B gastritis,more common,H.Pylori,Antral to Body.Autoimmune Chronic Gastritis: Result from Autoimmune activity againest parietal cells.with circulating antiparietal cell(>90%inPA)and anti-intrinsic factor antibody(40%).With severe degree of gastritis loss of intrinsic factor secretion cause PA.Other organ specific autoimmunity may be there as Vitilligo, Thyroid diseases.Achlorhydria, hypergastrinemia, are common with increased risk of Gastric Cancer.Chronic Helicobacter pylori Gastritis: is the commonest, Antral predominant gastritis,With years cause pangastritis (up to 100% in people above 70 year of age.subsequent metaplasia has been observed & considered independent risk for Ca.Also associated with development of low grade B cell lymphoma (Respond to AB90% of DU and 70% of GU patients are infected with H. Pylori.Helicobacter PyloriBacteriology:gram -ve rod, non invasive &live in the depth of the mucus,flagellated S shapedto survive in the stomach,multitude of proteins are secreted to determine pathog.As Urease that split urea to ammonia to live in its alkaline cloud, other factors asVacuolating cytotoxins(VacA),Cytotoxin associated gene(cagA),Adhesin,Porins,And Phospholipases and outer membrane protein(Hop protein) affect its virulencePathogenesis:release of the different cytokines provoke the inflammatory response (antral)lead to depletion of somatostatin(D Cells) and increased Gastrin release(G Cells)this increase acid secretion which in the minority of patients with high Parietalcell mass is exaggerated and lead to Duodenal Ulcer.Gastritis may lower gastric mucosal resistance causing Gasrtric Ulcer.in 1% it leads to pangastritis, and hypochlorhydria stimulate bacterial proliferationleading to accumulation of mutagenic nitrites from dietary nitrates predisposingto gastric cancer. Also chronic T cell stimulation from the inflammatory cytokinesand promote for B cell and mucosa associated Lymphomas(respond to Eradication)Epidemiology: In the industrial world its prevalence rises with age (50% by the age of 50 year)In the underdeveloped world it start in children and >90% are infected by adult lifeThe majority of colonized people are healthy, minority are symptomatic/diseased90% of DU and 70% of GU patients are infected, its incidence is higher in gastric carcinoma patients (like wise Ca incidence is 3-6 folds higher in seropositive pts.it is probable that different H.pylori related diseases are due to strain difference.Diagnosis: Invasive & non invasive methods gives variable sensitivity (healthy false +ve) andvariable specificity (diseased false -ve), you need a sensitive and specific test.1.Non invasive: A.Serology: Rapid,Useful in pop.survey, lower sen.&sp.(old&new)B.Urea breath, C14 or C13 labled (expensive technology) but very sen. & spec.2.Invasive(Endoscopy & Antral biopsy):A.Histology, Sen.&sp.,need days to read.B.Rapid Urase test,cheap&specific, but less sensitive.C.Microbiology culture & antibiot.sen, Gold standard, slow & lack sen.overall, best is breath test,Eradication of H.pylori: will be discussed with peptic ulcer disease.