G18 - Disorders of the esophagus and the stomach Flashcards
(61 cards)
1
Q
Basic anatomy and function of esophagus
A
anatomy:
- length: 25cm
- tubular organ
- parts: cervical, middle and supracardial
- physiological narrowings: cricopharyngeal constriction, aortic constriction, inferior esophageal sphincter
function:
- propulsion of bolus into the stomach
- interferes with acid content regurgitation
2
Q
What are the general symptoms of esophageal diseases?
A
- epigastric pyrosis (heartburn)
- regurgitation
- dysphagia, odynophagia
- (non-cardiac) chest pain
3
Q
What are the examination methods for esophageal diseases?
A
- lab parameters
- barium swallow
- upper GI endoscopy
- examinations of motility (manometry)
- impedance
4
Q
What are the congenital diseases of the esophagus?
A
- atresia
- tracheoesophageal fistula
- congenital stenosis
- doubled esophagus
- esophageal ring
5
Q
Prevalence and risk factors of esophageal congenital diseases
A
- 1/3000-4000
- 50% is associated other developmental alterations (spine, airways, kidneys)
- genetical factors and intrauterine environmental factors
6
Q
What is esophageal diverticulum?
A
- an outpouching of the esophageal mucosa
- acquired, predominantly in adulthood
7
Q
Classification of esophageal diverticula by site of occurence
A
- hypopharyngeal (Zenker)
- epiphrenic
- middle third
8
Q
Classification of esophageal diverticula by mechanism of formation
A
- pulsion diverticula
- traction diverticula
9
Q
Classification of esophageal diverticula by wall thickness
A
- true diverticula: contains all three esophageal layers
- false diverticula: herniation of the mucosa and submucosa through muscular layer
10
Q
Zenker’s diverticulum
A
- pharyngoesophageal diverticulum
- occurs in older women
- pulsion diverticulum
- false diverticulum
11
Q
Midesophageal diverticulum
A
- could be formed due to pulling from fibrous adhesions following lymph node infections (usually TB)
- true diverticulum
- may form from increased intraluminal pressure and be a pulsion diverticula
12
Q
Epiphrenic diverticulum
A
- location is usually distal esophagus on lateral esophageal wall (right > left)
- often associated with hiatal hernia
- pulsion diverticulum
- false diverticulum
13
Q
What is pulsion diverticula?
A
- increased intraluminal pressure
- secondary to motility disturbances such as achalasia
- location: proximal and distal esophagus
- example: Zenker’s is most common
14
Q
What is traction diverticula?
A
- extrinsic inflammation retracts or pulls bowel wall outwards
- not as common
- location: mid-esophagus
15
Q
What are the symptoms of esophageal diverticula?
A
- dysphagia
- regurgitation
- cough
- halitosis (bad breath)
16
Q
What is the therapy for esophageal diverticula?
A
- no therapy for small and asymptomatic diverticula
- endoscopic stapling for large and symptomatic diverticula
- esophagomyotomy
- pouch resection
17
Q
What is hiatal hernia?
A
a part of the stomach pushes out through the opening in the diaphragm, into the chest cavity
Types:
- sliding
- paraesophageal
- mixed
18
Q
What are the symptoms of hiatal hernia?
A
- no symptoms
- dysphagia
- non-cardiac chest pain
19
Q
How is hiatal hernia diagnosed and treated?
A
Diagnosis:
- endoscopy
- X-ray/CT
Therapy:
- lifestyle changes
- surgical (laparoscopy): nissen fundoplication surgery
20
Q
What is GERD?
A
- gastroesophageal reflux disease
- complex motility disorder: dysfunction of LES + decreased esophageal clearance + prolonged gastric emptying
- the reflux of gastric contents causes adverse symptoms or complications
21
Q
What is the Montreal classification of GERD?
A
esophageal syndromes
- symptomatic: 1) typical reflux syndrome; 2) reflux chest pain syndrome
- with esophageal injury: 1) reflux esophagitis; 2) reflux stricture; 3) barrett’s esophagus; 4) esophageal adenocarcinoma
extraesophageal syndromes
- established associations: 1) reflux cough syndrome; 2) reflux laryngitis syndrome; 3) reflux asthma syndrome; 4) reflux dental erosion syndrome
- proposed associations: 1) pharyngitis; 2) sinusitis; 3) idiopathic pulmonary fibrosis; 4) recurrent otitis media
22
Q
What are the phenotypes of GERD?
A
- NERD: non-erosive reflux disease (60%)
- erosions in distal esophagus - ERD: erosive reflux disease (35%)
- normal esophagus, abnormal pH - Barrett-esophagus (5%)
- intestinal metaplasia/dysplasia
23
Q
What is physiologic and pathologic reflux?
A
- physiologic typically occurs posprandially, is short-lived and asymptomatic
- pathologic can have nocturnal episodes, disturbing sleep
24
Q
What are the symptoms and complications of GERD?
A
- NCCP (non-cardiac chest pain)
- dysphagia, odynophagia
- coughing, hoarseness, dyspnea
- throat pain, recurrent pneumonia, asthma bronchiale, caries, otalgia, increased salivation, sleep disturbance
complications: stenosis, ulcer, bleeding, adonocarcinoma
25
How is GERD diagnosed?
according to clinical symptoms
- typical symptoms: empirical PPI-test (2 wks)
- chest pain: exclude cardiac origin before PPI therapy
- atypical extraesophageal symptoms: increased PPI dose for 8-12 wks
- alarming symptoms: endoscopy, barium swallow
- ambulatory 24 hour monitoring in case its unresponsive to treatment
26
What is the Los Angeles classification of ERD?
- **A:** <5mm
- **B:** in the edge of folds, >5mm
- **C:** b/w folds, <75% lumen circumference
- **D:** b/w folds, >75% circumference
27
What are the recommended lifestyle changes for GERD?
- decrease body weight, stop smoking
- elevated head in bed
- avoid eating 2-3 hours before sleep
- eliminate triggering foods, eat small meals
28
What is the treatment of GERD in case of typical symptoms?
- 8 wks PPI therapy
- standard dose: 1/day 30-60mins before meal
- insufficient response: 2/day or another PPI
- no response: endoscopy for further investigation
29
What drugs are used to treat GERD?
- **H2-receptor antagonist:**
- decreases secretions of gastric parietal cells
- **prokinetics (+baclofen):**
- increases release of Ach by enteric system, D2 antagonism, muscarinic receptor sensitization of smooth mm. of GI system
- Baclofen = GABAb agonist (inhibits TLESR)
- in case of small stomach, poor compliance, delayed gastric emptying, intestinal dysmotility
- **sucralfate:**
- binds positively charged proteins in exudes to form thick viscous substance that protects mucosa from pepsin, peptic acid and bile acids
- during pregnancy
- **alginates:**
- forms a physical barrier by making a raft in acid pockets (precipitates into a gel in the presence of gastric acid)
- in case of GERD, LA-A, pregnancy
30
When is surgery indicated for GERD?
- long-term PPI
- PPI-dependent
- ineffective PPI
- extraesophageal/airway symptoms
31
What are the treatment interventions for GERD?
- Nissen fundoplication: 62% require medication after 10 yrs
- endoscopic procedures: GEJ suturing, radiofrequency energy
- possible endoscopic complications: bleeding, aspiration, perforation, mediastinitis
32
What are motility disorders of the GI?
- hyper/hypo contractile esophagus
- cricopharyngeal disorder
- diffuse esophageal spasms
- achalasia
symptoms: dysphagia, chest pain
diagnosis: X-ray, manometry
therapy: medication, surgery
33
What is diffuse esophageal spasm?
- **"corkscrew sign"** in endoscopy
- **therapy:** CCB, nitrates, surgery (long esophagomyotomy + antireflux procedures)
- simultaneous onset or too rapid production of contractions (repetitive: 6/sec, increased amplitude, decreased LESR
34
What is achalasia?
- increased LES pressure, decreased LES relaxation, w/ peristalsis dysfunction (neurogenic degeneration of mesenteric plexus)
- **symptoms:** dysphagia of solids and fluids; chest pain; difficulty belching; passive regurgitation
- **diagnosis:** X-ray, manometry, endoscopy (possibly CT, EUS), barrium swallow
- inflammation can lead to Chaga's disease (South Africa)
- **therapy:** pneumatic dilation, Heller (LES) myotomy, Botulinum injection, nitrates, CCB, POEM (peroral endoscopic myotomy)
35
What is esophageal candidiasis?
- fungal infection
- usually in immunosuppressed population
- **symptoms:** hematemesis, odynophagia, dysphagia, vomiting/nausea, or asymptomatic
- white plaques along esophageal mucosa
- diagnosis by endoscopy
- **treatment:** amphotericin B (per os), imidazole
36
What are the esophageal viral infections?
- HSV, HPV, EBV, VZV, CMV
- **symptoms:** hematemesis, vomiting, odynophagia, nausea (HSV)
- **antiviral therapy:** acyclovir, gancyclovir, foscarnet, fancyclovir
- common in immunosuppressed individuals
37
What is Mallory-Weis syndrome?
- longitudinal tear in esophageal mucosa, doesn't affect the wall
- due to bulimia or alcoholism (forceful vomiting)
- **symptoms:** hematemesis from esophageal vasculature
- **therapy:** conservative, endoscopical, surgical (cauterization)
38
What is Boerhaave Syndrome?
- esophageal tear that penetrates wall
- **complications:** mediastinal crepitation (air in mediastinum), subcutaneous emphysema, eventually shock
- **symptoms:** chest pain worsened after vomiting, odynophagia, dyspnea, cyanosis
- **treatment:** iv. fluids, antibiotics
39
What are the functions of the stomach?
- temporary storage of food for enzymes to break it down (ie. pepsin)
- mechanical break down
- chemical break down (pepsin breaks down protein into peptides)
- limited absorption
- preparation of iron for absorption; secretion of intrinsic factors for B12 absorption
- defence against microbes
- regulation of gastric contents to duodenum
40
What is gastritis?
**acute**
- symptoms: epigastric pain, nausea, vomiting, fever
- causes: HP, viruses, bacterial infections
**chronic**
- usually asymptomatic
- autoimmune atrophic gastritis (Type A), HP gastritis (Type B)
41
Classification of gastritis by histology
- atrophic
- non-atrophic
- metaplasia
42
Classification of gastritis by localization
- antrum
- corpus
- multiple sites
43
Classification of gastritis by etiology
- infection
- autoimmune
- systemic disease
44
What is type A gastritis?
- mostly in elderly women
- antibodies against parietal cells
45
What is type B gastritis?
- antrum/corpus predominant
- precancerous
46
What is helicobacter pylori?
- spiral-shape, gram negative bacteria
- most prevalent GI infection (50%), increases in elderly
47
What are the clinical outcomes of helicobacter pylori?
- >85% asymptomatic chronic gastritis
- 15-20% chronic atrophic gastritis w/ intestinal metaplasia or gastric/duodenal ulcer
- <1% gastric cancer, MALT lymphoma
48
What are the methods of diagnosing HP?
**invasive biopsy**
- bacterial culture for susceptibility test to antibiotics and antibiotic resistance
- histology (gold standard!!)
- urease test, antrum biopsy
**non-invasive**
- serology
- locally produced antibodies
- PCR
- HP antigen test
- urea breath test (control): done 3-5 days after therapy
49
What is the treatment for HP in case of clarithromycin resistance?
(>20% prevalence)
1. quadruple bismuth = PPI + bismuth + tetracycline + metronidazole
2. PPI + levofloxacin/amoxycillin
3. based on culture
50
What is the treatment for HP in case of low clarithromycin resistance?
(<20% prevalence)
1. PPI + clarithromycin + metronidazole (or quadruple bismuth)
2. quadruple bismuth (or PPI + levofloxacin/amoxicillin)
3. based on culture
51
What is gastropathy?
changes to gastric mucosa without inflammation
1. reactive/chemical: drugs, NSAIDs, biliary reflux, alcohol
2. hemorrhagic: subepithelial hemorrhage, erosions, stress
3. vascular: injury to vessels, portal hypertensive gastropathy
4. hypertrophic: thickening of mucosal folds (Zollinger-Ellison)
52
What is the prevalence of peptic ulcer disease?
- duodenal ulcers are 5x > gastric ulcers
- men:women ratio
- 3.5:1 (duodenal)
- 1:1 (gastric)
- 90% duodenal ulcers are HP +ve, 80% gastric ulcers are HP +ve
53
What is the pathogenesis of peptic ulcer disease?
- HP: urease converts urea into NH3 → alkaline condition → increased bacterial colonization/survival thus damaging cells and mucosal barrier
- increased gastric acid secretions by parietal cells
- dysfunction of protective mechanisms (decreased mucous secretion)
- hyperpepsinogenemia
- smoking, alcohol, ischemia, stress
54
What are the causes of peptic ulcer disease?
1. HP
2. NSAID:
- COX1 and COX2 inhibition → decreased prostaglandins → erosion of mucosa
- dose/duration dependent
3. other: Zollinger Ellison, Crohn's, irradiation, sarcoidosis, myeloproliferative disease
55
What are the complications caused by peptic ulcer disease?
bleeding, perforation, dyspepsia (indigestion → pain after eating), nausea, vomiting, GI reflux, bloating and stenosis
56
What is the drug therapy for peptic ulcer disease?
- antacids
- PPI
- prostaglandins
- H2R antagonists
- sucralfate
57
What are the surgical interventions for peptic ulcer disease?
- vagatomy: decreased vagal stimulus to parietal cells
- antrectomy
- Billroth's I. or II. (partial gastrectomy)
58
What is the etiology of gastroparesis?
- idiopathic, DM
- surgery
- anorexia nervosa
- metabolic
- radiation
59
What are the symptoms of gastroparesis?
early satiety, weight loss, nausea, vomiting, epigastric pain, discomfort
60
What is the therapy for gastroparesis?
- medication: prokinetics, erythromycin, metoclopramide, antiemetics
- electric stimulus by pacemaker
- diet: small amounts of food, less insoluble starch
- surgical: feeding jejunostomy, complete/partial gastrectomy
61
Overview of gastric cancer
- intestinal: more prevalent in men, in older age
- diffuse/infiltrative: more prevalent in young age with worse prognosis
- symptoms: weight loss, abdominal pain, nausea, vomiting, early satiety, dysphagia, occult GI bleeding, metastasis, ascites
