Diseases of the upper GI tract,epigastric pain

Dr. Hajnal Székely

Esophagus

• 25 cm long

• tubular

• Propulsion of bolus into the stomach

• Interferes with acid content regurgitation

• Cervical, middle, supracardial part

• 3 physiological narowings

• Epiphrenic ampulle

• 2 sphincters

Symptoms of esophageal diseases

• Epigastric pyrosis, heartburn

• Regurgitation

• Dysphagia, odynophiagia

• Chest pain (non-cardiac)

Examination methods

• Laboratory parameters

• Barium swallow

• Upper GI endoscopy

• Examinations of motility - manometry

• Impedance

Congenital diseases

1/3000-4000 ; Genetical factors + intrauterin enviromental factors

50%-associated with other developmental alterations (spine, airways, kidneys)

Atresia

Tracheooesophageal fistula

Congenital stenosis

Doubled esophagus

Esophageal ring

Esophageal diverticula

• Aquired, occur predominantly in adulthood

• Classified according to: site of occurence:

• Hypopharyngeal – Zenker

• Epiphrenic

• Middle third

Esophageal diverticulaclassified according to mechanism of formation

According to wall thickness: true or false

Th.: esophagomyotomyPouch resection

Hiatal herniaInsufficiency of the LES +

Longitudinal contr. of the esoph.+

Increased intraabdominal pressure

Types: sliding - paraoesophageal-mixed

No sy. – dysphagia – NCCP

Imaging:

rtg/endoscopy

Th.: lifestyle

Surgical –laparosc.

GERD – Montreal classification

GERD – complex motility disorder

• main patogenetical factor: dysphunction of LES + decreased esophagealclearence + prolonged gastric emptying

• Agressive factors:

• Gastric acid + pepsin

• Duodenogastric reflux:

• Conj., deconj. bile acids, tripsin

GERD

GERD

GERD -symptomsHeartburn, acid regurgitation –

25% once / mo., 12% once /w., 5% daily sy.

NCCP –non cardiac chest pain

Dysphagia, odynophagia

Coughing, hoarsenedd, dypsnea

Extraoesophageal sy.:

persistent couhing, pharyngeal dysphagia,

throat pain, rec. pneumonia, asthma bronchiale, caries, otalgia, increased salivation, globus pharyngeus, sleep disturbance

Complications: stenosis, ulcer, bleeding

Barrett’s oesophagus,

adenocarcinoma

GERD

GERD - examinations

GERD – th.

Barrett esophagus

risk factors:long GERD historyage >50ymale gendercaucasioan rassobesitypositive family history

Barrett esophagus

BE - treatment

Esophagectomy:

• 3-10% mortality

• 45% morbidity

• Patients operative risk

• Focality of dyspl.

• Local endosc. +

• Surgical expertise

• EMR

• ESD

• RFA

Eosinophilic esophagitis - EE

• allergen-driven inflammation of the esophagus;

• P:30/100.000

• Young (21-31y)

• male patients (65-70%)

• 40-50% atopic diseases: asthma, food allergy,

• rhinitis all., rhinoconj., dermatitis

• Sy.: children – nausea, abd. pain, eating dist.

• Young – dysphagia, food impaction

• Elderly- + regurgitation, heartburn

Dg.based on histological examination of upper and lower esoph. biopsies (6) after initial treatment with PPPIs for 6–8 weeks.

Th.:Identification of the underlying food / airborne allergen –directs dietary advice.six-food elimination diet - can be tried if specific allergens cannot be identified.

Pharmacologic th: topical corticosteroids and leukotriene antagonistsEsophageal dilation - associated strictures, rings Safe- perforation rate of less than 1% effective - dysphagia improving for up to 1–2 years in over 90%

Motility disorders• Cricopharyngeal disorder

• Diffuse esophageal spasm

• Hypo /

• hypercontractile esophagus

(„nutcracker”)

Sy.: dysphagia, chest pain

Dg.: rtg., manometry

Th.:medication

surgery

• Inability of LES relaxation-

• dysphagia for both solids and liquids.

• difficulty belching, chest pain ,

• passive regurgitation of undigested food,

• aspiration, dyspepsia

• Dg.:rtg., manometry, endoscopy

• (CT, EUS)

Sec.- gastric tu. infiltr the esoph.

lymphoma, irradiation, Chagas’s., -kór, neuropathiás, idült in intestinal pseudoobstruction

Achalasia

AchalasiaISDN - ↓LES pressure-90 min. (66%)

Nifedipine – 30-40%, >60 min.

Botulinum toxin ˧ Ach release, 90%,

60% -1y., repeat

Dilation – 60-95%, 5y: 60%, perf.: 1-13%

Heller myotomy

POEM

Infective diseases of the esophagus

Candidiasis – present in healthy population

Causes oesophagitis:

Immunsuppr, states –

Tx, AIDS, haematological diseases, tumors, DM)

Sy.:asymptomatic, odynophagia-dysphagia, nausea / vomiting, haematemesis

Complications: stenosis, bleeding, perforation

Dg.: endoscopy

Th.: po. imidazol, amphotericin B journals.plos.org

Viral infections

HSV, CMV, VZV, EBV, HIV, HPV

Immunszuppressed patients

Odynophagia, chest pain, nausea, vomiting(haematemesis)

Dg.: endoscopy

Th.: antiviral th.

laccylovir, gancyclovir, foscarnet, fancyclovir

HSV

www.medscape.com

Infective diseases of the esophagus

Bacterial infections - Esophagitis caused by bacteria of physiological flora

Mycobacterium

Other : syphilis, diphteria, Nocardia

Parasitic infections -Chagas disease

Pill esophagitis

Infective diseases of the esophagus

Boerhaave-sy.

Esophageal tear

Chest pain – worsened by swalow, breathing

Subcutan emphysema, mediastinal crepitatio… shock

Chest X-ray, CT, Swallow with gastrographin

Th.:

Conservative - carentia, iv. fluid, AB

Surgery

radiopaedia.org

Mallory-Weiss sy

Consequence of retch, forced vomiting

Tear of the mucosa at the esophagogastric transition

Dg.: Endoscopy

Th.:

Conservative

Endoscopical

Surgicalwww.msdmanuals.com

www.statpearls.com

Functional diseases

Globus pharyngeus

Rumination

Functional heartburn

Functional chest pain

Functional dysphagia

Sy.- variable,

Long lasting

No alarm sy.

ROME criteria

Stomach

Gastritis

Inflammation of the gastric mucosa confirmed by histology

Time interval: acut / chronic

Histological signs: activity – atrophy – non-atrophic -metaplasia-specific forms

Anatomical localisation: antrum-corpus-multiple sites - pangastritis

Etiology: infetion – autoimmune – systemic diseases

Gastritis

Acut

H. pylori

Other bacteria

Viruses

Parasites

Fundal infections

Chronic

Autoimmune atrophic gastritis – type A

H. pylori gastritis - type B

Other types of chr. gastritis

Other infective agents

Granulomatosus gastritis

Lymphocytic gastritis

Collagenous gastritis

Eosinophil gastritis

Gastritis cystica profunda

GVH-gastritis

Allergic gastritis

Gastritis

Acut gastritis: asympt., sy.: epigastric pain, nausea, vomiting, fever

Chr. gastritis: asymp.

Type A (autoimmune gastritis, autoimmune metaplastic atrophic gastritis, diffusecorpus predominant atrophic gastritis):

Elderly women,

Antibodies against parietal cells

+other ai. diseases - anaemia perniciosa, 1DM, Hashimoto-thyreoiditis, hyperplastic + us adenomatosus polyps, endocrine tumors-carcinoma, praecancerosus állapot!

Type B - (H. pylori): non-atrophic

Acut gastritiswww.gastrointestinalatlas.com

medtube.netchr gastritis

erosiv gastritiswww.msdmanuals.com

atrophic gastritis

www.sciencephoto.com

Spiral, G-, in the mucus coating the mucosa / epithelium1983 –Marshall and WarrenMost prevalent GI tract bact.- 50%

Virulence of the Hp.cytotoxin assoc. gene A (CagA)vacuolating cytotoxin A (vacA)

Host geneticsEnviromental factors

Hp

Hp.1. Invasive – biopsy samples

*Histology - gold standard, sens: 90-95%, spec: 95-98%

*Culture - 4-7 d., sens: 90-95% (100%), spec: 80-90%, scientific puroses – AB resistance

*Urease test - Quick, simple, sens/spec: 85-95%, 95-100%, antrum biopsy –culture – bicarb., NH3 – change of colour

2. Non-invasive

*Serology – locally produced antibodies – IgA – sens: 60-80%, Syst. antibodies – sens., spec.: 95%

*PCR - gingiva, stool, gastric juice, biopsy forceps, sens.:100%, scientificpurposes

*UBT – controll of succes of erad., sens: 85-955, spec: 95-98%

*Hp. antigen examination – stool, Elisa, sens.:85-98%, spec:90-96%, multiple samples, -20 C

controll of succesfull erad. – 3-5 d after th.

Hp. eradication2x1 PPI+4x120mg bismuth-subsalicylate +3x500mg metronidazol+4x500mg tetracyclin

2x1 PPI+ clarithromycin (2x500 mg)+ amoxicillin (2x1 gr) / metronidazol (3x500 mg)

2x1PPI+2x250-500 mg levofloxacin2x1g amoxycillin

Sequential:2x1 PPI+2x1g amoxycillin 5 days,than2x1 PPI+2x500 mg clarithromycin+2x500 mg tinidazol 5 days

Gastropathy

Changes of gastric mucosa without inflammation

Reactive, chemical: drugs, NSAID, biliary reflux, alcohol consumption

Haemorrhagic: subepithelialis haemorrh., erosions, stress factors (phisical, termal, shock, sepsis, CNS injury)

Vascular: injury of vessels in the gastric mucosa

Gastric antral vascular ectasy (GAVE)

Portal hypertensive gastropathy

Hypertrophic:

Thickening of mucosal folds., giant folds

Menetrier disease

Zollinger-Ellison-sy.

Peptic ulcer disease

10% lifetime chance of ulcer form.

DU: 90%, GU:80% Hp. pos.

• Eradication-recurr. <5%/y.

Def.: ulcers caused by gastric acid activated pepsin- depth:musc. mucosaePatogenesis:

oGastric acid hypersecretionoNervous system dysphunction: cholinerg hypersen, parasympatic dominancy → gastric acid↑, pepsin↑

ohyperpepsinogenaemia: sign of H. pylori infection

oGenetic factors: O blood group, non-secretory state, HLA-B12 Ag, inherited hyperpepsinogenaemia

oEnviromental factors: (co-factors): osmoking, alcohol, eating habits, NSAID usage, oischaemia, stress (critically ill: severe burns, trauma, MOF)

DU> GU 5xDU: male: female – 3.5:1GU: 1:1GU: more common in elderlySy.: abd. pain, nausea, vomiting

1. H. pylori positive ulcers: 70-90% of DU, 30-60% of GU

PUD

PUD

PUD

PPI, eradication of Hp.Endos. th.Surgery - complications

Gastroparesis

Altered gastric emptying, > 3 mo., no mechanical obstruction

Female / male: 4:1

Causes:

Idiopathic

Diabetes mellitus

Connective tissue diseases: scleroderma, polymyositis/dermatomyositis, amyloidosis, SLE

Postoperative: gastrectomy, vagotomy, gastric resection, Nissen fundoplication

Diseases of the esophagus:GERD, achalasia

Endocrine diseases: hypo-hyperthyreosis, Addison’s

Metabolic causes: chr. Liver – kidney disorders

Neuromuscula diseases: Parkinson’s, head injury, stroke, brain tu.

Malignancies: paraneoplastic sy., leukaemia

Infections: HIV, Chagasdiseases

Anorexia nervosa

Radiation

Gastroparesis

Sy.: early satiety, nausea, vomiting, epigastric pain, dyscomphort, loss of weight

99mTc-scintigraphy

Th.:

Diet: small amounts of meal, diet containing less unsoluble starch

Medication: prokinetics, erythromycin, metoclopramid, antiemetic drugs

Electric stimulation of the stomach -pacemaker

Surgical - feeding jejunostomy, complete or partial gastric resection)

www.cureus.com

Rare organic diseases

Inherited – duplication, stenosis, obstruction

Chr. infections (syphilis, TBC, fungal infections, anthrax)

Besoar

Diverticuli

Eosinophil gastroenteritis

besoarwww.bing.co

m

diverticulagastrolab.net

Functional disordersCommon – prev.: may be as high as 25-50%

Patomechanism: multifactorial, complex – not fully understood

(altered motility, chemical effect, hypersensitivity of afferent sensory nerves, CNS perception alterations)

Functional dyspepsia

Eructation

Funct. vomiting, cyclic vomiting sy.

Rumination sy.

Rome IV criteria

Functional disorders

Physical exam., „rutin” lab data, abdominal US (gastroscopy)

Funct. disorder – probable if:

<45 y

Ongoing sy.without progression

Godd apetite, no loss of weight

Normal blood count (no anaemia)

No psysical signs with exam. (no palpable abd .mass)

Negative family history (no malignancies within the family)

NO ALARM symptoms

Th.: symptomatic

Gastric cancer

Gastric cancer – endoscopy, staging

Treatment options