Oral Cavity and Gastrointestinal Tract

What are Aphthous ulcers (Canker sores)?

Solitary or multiple painful recurrent lesions of the oral mucosa; shallow hyperemic ulcerations covered by thin exudate and surrounded by erythem

Aphthous ulcer treatment & cause

resolve spontaneously in 7-10 days; cause unknown; increased prevalence in celiac disease, IBD, and Behçet disease

most common fungal infection of the oral cavity

candidiasis

Oral candidiasis (thrush)

White, curdlike pseudomembranes that can be scraped off, revealing an erythematous base; caused by Candida albicans

3 types of oral candidiasis

Pseudomembranous (thrush)

Erythematous

Hyperplastic

trt of candidiasis

nystatin

HSV1 vs HSV2

1: oral lesions

2: genital lesions

HSV1 sx

lymphadenopathy, fever, anorexia

causes of HSV1 reactivation

trauma, allergies, UV light, URI, pregnancy, mesntruation, excessive exposure to heat or cold

cells of HSV2 infection

ballooned with large eosinophilic intranuclear inclusion

adjacent cells fuse to form large mutlinucleated polykaryons

MC oral cavity cancer

squamous cell carcinoma (95%)

when is SCC often diagnosed?

late stages

field cancerization

exposure to carcinogens results in multiple primary tumors developed independently

• associated with squamous cell carcinoma

where are SCC HPV associated lesions found?

tonsillar crypts, base of tongue, oropharynx?

do HPV + or HPV - tumors have a better prognosis?

HPV +

atresia

thin, non canalized cord replaces a segment of esophagus

mechanical obstruction

atresia is often associated with what abnormality?

a fistula connecting upper and lower esophageal pouches

MC cause of esophageal stenosis

inflammation and scarring

causes of esophageal stenosis

gerd, irradiation, caustic injury

progressive esophageal stenosis can lead to what difficulty?

swallowing liquids (starts as solids)

achalsia

failure of the lower esophagus sphincter (LES) muscle to relax

*functional obstruction

achalsia triad of causes

incomplete LES relaxation

increased LES tone

esophageal aperistalsis

*LES = lower esophageal sphincter

primary achalasia

idiopathic failure of distal esophageal inhibitory neurons

secondary achalasia

Chagas disease caused by Trypanosoma cruzi can cause (secondary) achalasia

mallory weiss syndrome

tear of distal esophagus from retching in alcoholic or bulimic or hyperemesis gravidarum

sx of mallory weiss syndrome

painless hematemesis

dx of mallory weiss syndrome

endoscopy

trt of mallory weiss syndrome

epi injection or thermal coagulation if not self-limited

is mallory-weiss or boerhaave syndrome more severe?

boerhaave syndrome

boerhaave syndrome

spontaneous esophageal rupture due to forceful vomiting, severe pain

mediastinal crunch; variety of sound including loud crackles and clicking or gurgling sounds; associated with mediastinal emphysema

hamman sign - in Boerhaave syndrome

diagnosis of boerhaave syndrome

CXR: mediastinal widening

contrast esophagram: definitive diagnostic study

trt of boerhaave syndrome

surgery if needed

mallory-weiss vs boeerhave locations

mallory-weiss : submucosa, mucosa, RIGHT posterolateral wall of the GE junction, linear lacerations

boerhaave: full thickness tear (transmural), LEFT posterolateral wall of distal esophagus

stratified squamous mucosa of the esophagus may be damaged by a variety of irritants including alcohol, corrosive acids or alkalis, excessively hot fluids, and heavy smoking. May present with pain with swallowing.

chemical esophagitis

odynophagia casues

pill-induced

infectious esophagitis (especially immunocompromised)

MCC of esophagitis

GERD

pathogenesis of GERD

decrease in LES tone or increase of abdominal pressure

delayed gastric emptying

increased gastric volume

GERD histology (normal vs significant diease)

hyperemia

significant disease: eosinophils in squamous mucosa followed by neutrophils

GERD sx

heartburn

regurgitation

dysphagia (NOT odynophagia)

overproduction of saliva

cough

hiccups

wheezing

GERD management

lifestyle

H2 blockers

PPI

endoscopy (if over 45, PPIP failed, bleeding, dysphagia, weight loss NSAIDS)

Eosinophilic esophagitis sx and trt

symptoms include food impaction, GERD-like symptoms, feeding intolerance, dysphagia;

treat with dietary restriction (e.g., milk/soy) and topical/systemic corticosteroids.

Eosinophilic esophagitis cardinal histology

epithelial infiltration by large numbers of eosinophils superficially and away from GE junction; patients often atopic;

Barrett esophagus pathophysiology

Replacement of normal squamous epithelium with metaplastic columnar epithelium (intestinal metaplasia with goblet cells) in distal esophagus due to long-standing reflux; intestinal metaplasia shows goblet cells.

What is the progression of the epithelium in Barrett Esophagus?

progression sequence: metaplasia → dysplasia → adenocarcinoma

What is the pathogenesis of Barret Esophagus?

• prolonged and recurrent acid reflux attack causes inflammation leading ulceration of squamous cells

• Healing occurs that change the cells

• acidic pH in the distal esophagus from reflux differentiate the cells into columnar epithelial

Stomach protective layers

Surface foveolar mucin protects epithelium;

rich vascular supply delivers oxygen and bicarbonate and washes away acid;

gastric mucosa renews every 2-6 days.

Acute gastritis sx

transient mucosal inflammation

sx: dyspepsia, n/v

severe: erosion, ulcer, hemorrhage, melena

Acute gastritis causes

nsaids, etoh, smoking,, bisphosphonates, chemo, salmonellosis, trauma

Chronic gastritis cause & patho

Helicobacter pylori = S-shaped gram-negative rod

secretes enzymes/toxins causing mucosal damage

neutrophils recruited and contribute to injury

Peptic ulcer disease (PUD) cause

H. pylori

2nd is NSAIDS

*smoking and alcohol will exacerbate the disease and delay healing

Peptic ulcer disease (PUD) - duodenal or gastric more common?

duodenal ulcers occur more often than gastric (5x)

ages of PUD

typical age ranges: duodenal 30-55, gastric 55-70;

sx of PUD gastric vs duodenal

symptoms: dyspepsia, burning/gnawing pain radiating to back; gastric pain worse postprandial

duodenal pain often relieved by food.

most common cause of non-hemorrhagic GI bleed

PUD

what do PUD ulcers look like?

sharply punched out, round

MC malignancy of the stomach

Gastric adenocarcinoma

Gastric adenocarcinoma epidemology

Epidemiology varies by geography (higher in Chile, Japan, E Europe), lower socioeconomic

gastric adenoma pathogenesis

CDH1 mutation

familial

• loss of E-cadherom function

familial adenomatous polyposis

• APC/TP53 gene

H.pylori

• IL-1 beta

EBV

• proximal stomach

• TP53 mutation

Small and large intestines — obstruction types

herniation, adhesions, volvulus, intussusception, neoplasm

Small bowel obstruction (SBO) Most common cause

adhesions (prior surgery)

Small bowel obstruction symptoms and trt

N/V, abdominal pain, distention; findings: high-pitched tinkling bowel sounds early, silent late; KUB shows air-fluid levels;

treatment: NG tube, bowel rest, surgery if not resolved in 24 hr.

Large bowel obstruction Most common cause

neoplasm

what is Hirschsprung disease?

Congenital aganglionic megacolon caused by absence of Meissner and Auerbach autonomic plexuses in a bowel segment causing inability or difficulty to pass stool

Hirschsprung disease sx and trt

presents with constipation, vomiting, failure to thrive, delayed passage of meconium; diagnosis via barium enema and confirmed with rectal biopsy;

treatment = resection of affected bowel.

Hirschsprung disease is associated with what disorder

Down Syndrome

Volvulus

Twisting of bowel on itself

volvulus is mc where?

most commonly sigmoid colon;

volvulus sx and trt

causes crampy abdominal pain, N/V, tympany; diagnosis with abdominal x-ray showing distention;

treatment = endoscopic decompression or surgery if unresolved.

Intussusception usually happens in

children

Intussusception

Telescoping of intestine into distal segment

intussusception is associated with what illness?

rotavirus

intussusception diagnosis and trt

children diagnosed and treated with barium or air enema (diagnostic + therapeutic);

adults often require CT diagnosis and surgery.

intussusception CT sign

bulls seye

what is celiac disease?

Immune-mediated enteropathy triggered by gluten ingestion

Celiac disease pathogenesis

gliadin deamidated by tissue transglutaminase interacts with HLA-DQ2/DQ8 → CD4+ T cell activation and cytokine-mediated tissue damage

symptoms: weight loss, chronic diarrhea, iron deficiency anemia, failure to thrive in children; labs show malabsorption (Fe, Ca, Vit D, B12), IgA endomysial antibody positive.

Celiac disease sx and lab findings

symptoms: weight loss, chronic diarrhea, iron deficiency anemia, failure to thrive in children;

labs show malabsorption (Fe, Ca, Vit D, B12), IgA endomysial antibody positive.

Celiac disease associated dz

DDM, thyroiditis, Sjögren;

Celiac disease — extraintestinal sx

Dermatitis herpetiformis (pruritic papulovesicles on extensor surfaces) occurs in <10% but almost all with the skin disorder have celiac

Celiac disease causes an increased risk of what cancer?

enteropathy-associated T-cell lymphoma.

Celiac disease diagnosis and management

Diagnosis via serology (anti-tTG, endomysial antibodies) and duodenal biopsy (villous atrophy, crypt hyperplasia); treatment = strict gluten-free diet, nutrition support, involvement of dietician, avoidance of barley/rye/oats/wheat and cross-contamination; corticosteroids (e.g., budesonide) or prednisone may be used in refractory cases.

Inflammatory bowel disease (IBD)

Chronic idiopathic relapsing disorders (Crohn disease and ulcerative colitis) with interplay of genetics, microbiota, epithelial dysfunction, and mucosal immune responses

Is Inflammatory bowel disease (IBD) an autoimmune dz?

Crohn's and UC are not considered classic autoimmune diseases but involve dysregulated mucosal immunity.

IBD pathogenesis

Activated T cells drive disease progression; mucosal immunity and MALT (IgA) dysregulation; environmental triggers (microbes, diet) in genetically susceptible individuals; NOD2 mutation associated with Crohn disease (but <10% with mutation develop disease).

where can crohns occur?

May affect any GI segment, most commonly terminal ileum, ileocecal valve, cecum;

Crohn disease hallmarks

transmural inflammation with creeping fat, serosal reaction, ulcers, strictures, skip lesions, cobblestoning; noncaseating granulomas in ~35% of cases.

Crohn disease — clinical features

Abdominal pain, weight loss, fever, diarrhea, perianal fistulas, arthralgias, iritis/uveitis, sacroilitis, migratory polyarthritis, erythema nodosum, iron deficiency/hematochezia possible.

where does UC occur?

Continuous mucosal disease starting at rectum and extending proximally

Ulcerative colitis hallmarks

superficial mucosal inflammation limited to mucosa and submucosa; broad-based ulcers, pseudopolyps (mucosal bridges), granulomas typically absent.

megacolon typically occurs where

transverses colon

sx of toxic megacolon

leukocytosis, fever, emergency (perf risk)

Ulcerative colitis — clinical features

Bloody diarrhea, lower abdominal cramps relieved by defecation

Diverticulosis

Outpouchings of colonic mucosa/submucosa (false diverticula) through muscularis

how does Diverticulosis develop?

develops under conditions of elevated intraluminal pressure; taeniae coli anatomy contributes to focal weakness.

Diverticulosis usually occurs where and in who?

sigmoid colon, >80

Diverticulitis

Occurs in 15-20% of patients with diverticulosis when a diverticulum undergoes microperforation and inflammation

Diverticulitis sx and trt

LLQ pain, fever, leukocytosis; CT for diagnosis if not resolving with conservative therapy; avoid barium/colonoscopy in acute phase.

Diverticulitis complications

May lead to abscess, microperforation, peritonitis; outpatient treatment possible for mild disease