GI Disease

Disease of teeth gums and aveolar structure

• dental carries “ tooth degradation due to mineral dissolution

• gingivitis : inflammation of soft tissue around teeth

• periodontitis : inflammation affecting tooth supporting structure

• odontogenic cyst and tumours

Infection diseases of oral mucosa

• herpetic stomatitis (cold sores) : Caused by HSV 1 causing lesions of vesicles, bullas or shallow ulceration (heal in 3-4 wks)

• oral candidiasis (thrush) : from dimorphic fungus called candida albicans, appears as gray white plaques that can be scrapped off

• Hairy leukoplakia : caused by EBV w white patches of fluffy hyperkeratosis on lateral border (cant be scrapped off)

Possible reactive disease of oral mucosa (4)

• frictional keratosis: thickened epithelium

• Irritation fibroma : nodule of fibrous tissue

• Epulis (pyogenic granuloma : nodule of granulation tissue in gingival

• Peripheral giant cell granuloma : fibrous tissue +vessel + giant cell

Canker sore characteristic

• small painful ulcer w shaklow grey necrotic base

• hyperemic/erythematous rim

• assoc w coeliac, ibd and bechets

Glossitis characteristics

• beefy red tongue

• papillae atrophy w mucosal thinning

• occurs in nutrient deficiency (iron and b vitamins)

potentially precancerous condition of oral mucosa

• leukoplakia : hyperleratosis + hyperplasia of squamous epithelium

• erythroplakia : think, loss of differentiation, transparent (greater risk of malignancy)

invasive scc histopathplogy (5)

• ragged groups/islamds

• cohesive cells

• intercellular bridges

• abundant eosinophilic keratin

• ±keratin pearls

Oral manifestation in disease (5)

• infectious : scarlet fever (strawberry tongue), measles (koplik spots), infectious mononucleosis

• immune : perisistent canker sore in coeliac and ibd

• skin : lichen planis, blisters, SJS

• deficiency: glossitis

• iatrogenic : mucositis, GVHD

What are mucoceles

• salivary gland lesion

• due toductal blockage / rupture w saliba leakage

• tx is by excision

Sialadenitis types

• acute : either bacterial (unilateral) or viral (bilateral from mumos)

• Chronic sialadenitis : inflammation, radiation, gvhd, dental carries

Benign salivary gland tumours

• pleomorphic adenoma : discrete w many ct due to translocation

• Warthins tumour : well encapsulated tumour w double layer of eosinophilic epithelial cell w lymphocyte in the middle

both commonly at parotids

Malignant salivary gland tumours (3)

• mucoepidermoid carcinoma ; well defined capsule w cord/sheet arrangement of squamous/mucous cells

• Adenoid cystic carcinoma : small tumour cells w scant cytoplasm (protein secreted into ct) + cribriform patterns . though slow, may be unpredictable

• acinic cell carcinoma : resembles normal salivary serous acinar cells

Infective gastroenteritis virus and bacteria involved

• norovirus, (rotavirus + adenovirus for children only)

• campylobacter, shigella (salmonella, vtec for adults only)

What is diarrhoea and types

>2 epsiodes of loose or liquid stool in 24hrs (stool that takes shape of cup)

classified into 3

• acute : less than or equal to 14

• persistent : >14 days

• chronic : >30mdays

Bristol stool chart

• type 1 (hard lumps like maltesers) → type 7 ( liquid)

• diarrhoea is type 6 or 7

Lab dx of viral gastroenteritis

• EM

• antigen detection : lateral flow or elisa

• multiplex pcr : all 3 nori, rota, adeno, others

Viral gastroenteritis

• common, mostly children <5

• seasonal

Management of viral gastroenteritis

• supportive : rehydration , electrolyte + feeding in children

• Hand hygeine

• isolation

• vaccination(norovirus)

Rotavirus characteristics (4)

• Reovirus (DS RNA)

• Multiple serotypes with less antigenic variance

• transmitted via faecal oral

• survive on fomites

• summer peak

Rotavirus pathogenesis

• infects enterocyte in small bowel causing cell destruction

• fluid moves inti intestinal lumen → loss of fluid in faeces

• Lose ability to digest food but fusion and repair of villous architecture follows

• also secretory diarrhoea due to enterotoxin NSP4

NB NO BLOOD IN STOOL

Rotavirus Sx

• incubation period around 48 hours

• diarrhoea, vomit, fever, dehydration

• self limiting

Norovirus characteristic (4)

• SRSV (ss rna)

• Multiple genotypes with many antigenic variance in short time

• peaks in cold weather

• maybe sporadic but also outbreaks (in healthcare, cruise ship etc)

NB if outbreak isolate until Asx afetr 48 hrs

Norovirus transmission and pathogenesis

• faecal oral, airborne, food w low infectious dose (<100)

• Prolonged shedding w 1-2 incubation

• poorly understood but thought to blunt villi in jejunum wo damaging cells → transient malabsorption

Clinical features of norovirus

• n & v

• diarrhoea

• cramps

• 2-3 days

Adenovirus features

• DS virus

• cause gastroenteritis (40,41) Resp infection, eye infectiom, myocarditis cystitis

Campylobacter type, transmission, pathogenesis

• C jejuni, c.coli, c foetus

• isolated from faeces to raw/undercooked

• ingestion on bacilli, attached to gi epthelium

Dx Sx Tx

• GNB in charcoal based selective media, PCR

• prodromal illness, abdominal pain, diarrhoea, n&v, GBS

• rehydration, amr when worsening sx immunocompromised (macrolide or fluoroquinolone)

Salmonellae types and subtypes

• enteric fever : typhoid and paratyphoid

• non typhoidal salmonellae : `s. enteritidis, s. typhimuriium

enteric fever pathogenesis

• ingestion of bacilli

• penetrate Small intestine → proliferate submucisa (peyers patch hypertrophy)

• perforation of intestinal wall → disseminate to res

Enteric fever Sx

inisidious onse w vague sx

fever, chills, relative bradycardia

rose spots

hepatosplenomegaly, perforation

enteric fever dx tx

Dx : blood culture ± faeces culture

tx : rehydration], amr (3rd gen cephalosporin)

prevention : sanitation, hygeine, vaccination

non typhoidal salmonellosis (transmission, dx, sx, tx)

• contaminated food, person to oerson , in faeces

• PCR, selective media (SSA). serotyping

• diarrhoea(rarely bacteraemia, edocarditis)

• rehydration, Antimicrobial pnlh in severe illness or high risk pt

VTEC epi, transmissiom

summer peak

extreme abew but usually sporadic

cattle main reservoir, animal contact

vtec pathogenesis

• low knfective dose

• ingestion of bacilli attach to large intestinal epithelium

• secrte bacterial proteins and verotoxin

VTEC dx sx tx

• PCR, CULTURE (Sorbitol macconkey)

• diarrhoea, vomit, fever. HUS

• rehydration as abx not good

Shigellosis what and epi

• bacillary dysentry by S. dysenteriae

• MSM, faecal oral

• AMR

Shigellosis pathogenesis

• ingestion of bacilli (low infective dose)

• adhere to m cells of peyers batch of latge bowel

• spread, knflammed, release toxin/ enterotoxin

Shigellosis sx dx tx

• abd cramp, fever, bloody diarrhoea, HUS\

• PCR, CULTURE (SSA)

• TX rehydrate, ABX only in immunocompromised