JC74 (Medicine) - Gastric motility problems, Benign esophageal lesions Flashcards
GERD
- Definition
- Pathophysiology
Definition: condition which develops when the reflux of stomach contents causes troublesome symptoms and/or complications
Pathophysiology:
- Imbalance between anti-reflux barriers and aggravating factors
- Anti-reflux barriers: e.g. LES, Hiatus, Oblique entrance of esophagus into stomach
- Aggravating factors: e.g. LES relaxation, Hiatus hernia, imported emptying…etc - Acid damage: mucosa expose to gastric content
- Chronic inflammation: complications e.g. esophagitis, strictures, Barret’s esophagus…etc
Physiological mechanisms against acid reflux?
Lower esophageal sphincter
Esophageal hiatus in crus of diaphragm
Oblique entrance of esophagus into stomach with Sharp angle on greater curvature (Angle of His)»_space; forms a flap/ valve
Aggravating factors of esophageal reflux
Transient LES relaxation after meal/ proximal gastric distension
Incompetent LES due to hiatus hernia or diet (fat, alcohol, chocolate, spicy food…)
Hypotensive LES after POEM surgery
Impaired esophageal emptying/ peristalsis or gastric dysmotility
Increase intra-abdominal pressure: obesity, large meal, pregnancy…
Excessive gastric acid production: e.g. H. pylori antral gastritis, Zollinger Ellison syndrome
Clinical manifestations of GERD
Heartburn sensation and acid regurgitation
- Post-prandial
- Supine or right decubitus position
- a/w water brash
Typical chest pain
Extra-esophageal symptoms: → Laryngo-pharyngeal reflux (LPR) with - Chronic cough - Hoarseness - Throat tightness → Asthma (correlated with GERD, reason unknown) → Recurrent chest infections → Dental erosion → Sleep disturbance
Complications of GERD
→ Odynophagia due to oesophagitis and ulcers
→ Dysphagia due to strictures
→ Barrett’s oesophagus
→ Adenocarcinoma
Factors that lower LES tone
→ Genetic determinants
→ Hiatus hernia
→ Diet/environment: alcohol, caffeine, smoking
→ Drugs (that cause sm relaxation), eg. NSAIDs, CCB, BB, nitrates, α-blocker, theophylline, anticholinergic
Ddx GERD
Achalasia
Zenker’s diverticulum
Gastroparesis
Angina pectoris
Causes of dyspepsia and esophagitis
Conditions most commonly associated with GERD
Pregnancy, Obesity
Long-term NG tube usage
Scleroderma (erosive GERD)
Multiple endocrine neoplasia (MEN)
Clinical classification of GERD
Montreal Classification
□ Non-erosive reflux disease (NERD) (60-80%):
→ Typical GERD symptoms but normal oesophageal mucosa with OGD
□ GERD with erosive oesophagitis (20-35%)
□ GERD with Barrett’s oesophagitis (1-5%)
Diagnostic tests for GERD (5)
Proton pump inhibitor test (first-line)
Diagnostic questionnaire: Frequency and severity of heartburn, acidity in stomach, acid regurgitation and use of antacids, >12 marks = GERD
24h Esophageal pH monitoring: Portable pH sensor and recorder/ Catheter-free pH system (BRAVO)/ Combined Multichannel Impedance and pH catheter
Upper endoscopy
Manometry: LES abnormalities
First diagnostic test for suspected GERD and NCCP (non-cardiac chest pain)
Proton pump inhibitor test
PPI empirical trail for 8 weeks
Symptoms improve = positive for GERD
ODG for GERD
- Indications
- Diagnostic of which conditions/ Role
Indications:
→ Diagnosis uncertain: atypical symptomatology or refractory to Tx
→ Alarming features suggestive of complications or malignancy
- Eg. dysphagia, odynophagia, GI bleeding, anaemia, weight loss, recurrent vomiting
→ Screening for complications if high-risk or clinically likely (eg. severe symptoms)
Role of OGD:
→ Diagnosis of erosive GERD
→ Detect complications, eg. strictures, Barrett’s oesophagus
→ Find underlying cause, eg antral gastritis, hiatus hernia
24h esophageal pH monitoring test
- Indication
- Test cut-off for Dx
Indication:
- Diagnosis of GERD refractory to treatment
Cut-off: total percentage time with pH <4.0 is over 4.2% is the distal esophagus; DeMeester score >14.72 (95th %ile) from frequency of reflux episodes and time required for
oesophagus to clear acid
24h esophageal pH test
- Modalities
- Advantages
- Disadvantages
Modalities:
- Antimony probe with portable pH recorder
- Catheter-free pH monitoring capsule with portable pH recorder
- Combined multichannel impedance and pH catheter
Advantages:
- Gold standard in GERD dx: High sensitivity for GERD
Disadvantages:
- Low sensitivity for NERD (non-erosive)
- Unpleasant procedure
- Not freely available
Comparative advantages between 2 modalities for esophageal pH monitoring
Capsule/ BRAVO system:
- Wireless, more convenient, less uncomfortable
- Placed during endoscopy > more specific and directed placement
- Offers 48h recording time
- Multiple capsules placed for more data
Multichannel intraluminal impedance (MII)
- Detects impedance between ring electrodes + pH monitoring»_space; detects acid and non-acid reflux
- Better dx of NERD
Endoscopy for GERD
- Normal endoscopic finding can Dx GERD, True or False
False
Endoscopy can Dx erosive GERD (30%), but cannot cover non-erosive GERD (70%)
Endoscopy can be normal in NERD even with abnormal esophageal pH
Clinical classification for esophagitis
LA classification of oesophagitis:
→ Grade A: ≥1 isolated mucosal breaks ≤5mm long not extending between tops of 2 mucosal folds
→ Grade B: ≥1 isolated mucosal breaks >5mm long not extending between tops of 2 mucosal folds
→ Grade C: ≥1 mucosal breaks bridging tops of folds but involving <75% of circumference
→ Grade D: ≥1 mucosal breaks briding tops of folds and involving >75% of circumference
Esophageal manometry
- Indications
- Function
Indication:
→ Symptoms suggestive of oesophageal motility disorder, eg. dysphagia, regurgitation
→ Prior to surgical therapy to r/o oesophageal motility disorder
Role: assess oesophageal motility to → R/o oesophageal motility disorder → Assess LES function: - Transient LES relaxation (TLESRs) - Hypotensive LES
Management options for GERD
- Lifestyle modifications
Lifestyle modification:
□ Stop smoking and drinking
□ Reduce weight
□ Elevate head of bed + avoid tight clothing
□ Diet changes:
→ Eat small meals, avoid late meals
→ Avoid reflux-promoting agents, eg. alcohol, coffee, chocolate etc (not evidence-based)
□ Drug changes: consider alternatives to reflux-promoting drugs, eg. theophylline, anticholinergics
Medical management options for GERD
Indication for each option
Acid-reducing agents: antacids, H2RA, PPI
- Antacids: symptoms management
- H2RA: add-on therapy for bedtime breakthrough GERD symptoms despite PPI; Tachyphylaxis
- PPI ***: symptom management, superior relief of heartburn/ regurgitation, healing esophagitis
(Prokinetics: metoclopramide, cisapride, sucralfate, baclofen have no role anymore)
PPI therapy for GERD
- Indications for maintenance therapy
- Risks of long-term use
Indication:
Long-term maintenance: Erosive esophagitis (LA grade C/D), Peptic stricture, Barrett’s esophagus
Intermittent maintenance: NERD patient with severe GERD symptoms, responsive to PPI
Risks:
Causative: Clostridium difficile infection***
Associative: Pneumonia, gastric cancer, OP, CKD, Stroke, Dementia…etc
Medical management options for GERD
- list examples of each class of drug
→ Antacids: Triact, magnesium / aluminum hydroxide
→ H2RA: cimetidine, raniditine, famotidine
→ PPI: omeprazole, lansoprazole, esomeprazole
Management of refractory GERD
Modifications to existing treatment? Investigations?
- Optimize PPI: dose, timing, compliance; switch class of PPI
- Add-on therapy:
- Nocturnal H2RA for night-time symptoms
- Alginate for post-dinner symptoms - Find cause:
- Early upper endoscopy if red-flag symptoms
- 24h pH monitoring and impedance study
- Esophageal manometry - Definitive surgery
Surgical treatment options for GERD
Indications
Pre-op checks
Anti-reflux surgery:
- Laparoscopic (Nissen or partial) fundoplication
- Trans-oral incisionless fundoplication
- Magnetic sphincter augmentation
Indications:
→ Failure of medical Tx: compliance issue, PPI non-responders (10-30%), pt preference
→ Persistent regurgitation symptoms despite medications
→ Severe reflux oesophagitis or other complications
Pre-op checks:
- Confirm dx of GERD
- Confirm symptoms are responsive to PPI
- Exclude contraindications for esophageal surgery e.g. achalasia, severe strictures…etc
Surgical treatment for GERD
Drawbacks/ complications
- Limited to PPI-responsive GERD
- Surgical risks: bleeding, infection, GA…etc
- Recurrence of GERD post-op (20% long-term)
- Post-op complications: Dysphagia, Gas bloat, Inability to belch…etc
Ddx non-cardiac chest pain
→ Cardiac: coronary spasm, microvascular angina etc.
→ Pulmonary
→ Musculoskeletal: costochondritis, Tietze’s syndrome, chest wall pain syndrome
→ Psychological: psychogenic, panic disorder
→ Oesophageal: GERD (most common, 50% NCCP), motility disorder (nutcracker/jackhammer oesophagus, achalasia, non-specific oesophageal spasm)
Approach to non-cardiac chest pain
- Investigations and workup?
→ Full cardiac workup to r/o cardiac chest pain first
→ PPI test: PPI standard dose BD 4-8w for GERD
→ 24h oesophageal monitoring if PPI test negative
→ Manometry for motility disorder if 24h –ve
Dyspepsia
Definition
Gastrointestinal causes: most common, must not miss ddx?
Dyspepsia: chronic or recurrent pain or discomfort centred in upper abdomen
Most common GI causes:
- Peptic ulcer disease; H. pylori infection
- Functional dyspepsia
- GERD
Must-not-miss:
- Gastroesophageal cancer/ abdominal cancers
- Bowel ischemia due to celiac artery compression
- Hepatobiliary: biliary pain, pancreatic or HBP diseases
Dyspepsia
Non-GI causes
Drug-induced dyspepsia: NSAIDs, steroids, oral antibiotics, iron, digoxin, metronidazole, alendronate, slow K…
Abdominal wall pain
Functional dyspepsia
Electrolyte disturbances, eg. hyperCa, hyperK
Thyroid and parathyroid diseases
Chronic renal failure
Coronary artery disease (basal myocardial ischaemia)
Alarming/ red-flag features in dyspepsia
(1) Age >60y
(2) Unintentional weight loss
(3) Dysphagia or odynophagia
(4) Unexplained Fe def anaemia
(5) Persistent vomiting
(6) UGIB
(7) Palpable mass or LNs
(8) FHx for UGI cancers
First-line investigation and treatment for dyspepsia
Pt >60 years old or any alarming features of malignancy:
- Early endoscopy
Pt <60 years old without alarming features of malignancy:
- H.pylori test and treatment
- Empirical PPI +/- TCA or prokinetics
- Psychotherapy (last-line)
Outline history taking for dyspepsia (check)
Characterize dyspepsia
Find underlying cause:
- PUD risk factors, S/S
- GERD risk factors, S/S
- Biliary pain r/o
- Drug-induced dyspepsia
- Thyroid or parathyroid diseases
- Pancreatic pathologies
Alarming features for malignancies
Functional dyspepsia
- Definition
- Diagnostic criteria
Functional dyspepsia (FD): dyspepsia in the absence of detectable organic diseases
ROME IV criteria: - Post-prandial fullness (3 days per week) - Early satiety (3 days per week) - Epigastric pain (1 day per week) - Epigastric burn (1 day per week) AND No evidence of structural disease
Functional dyspepsia
Clinical features and major clinical subtypes
Postprandial distress syndrome (‘dysmotility-like’):
→ postprandial fullness
→ early satiation
Epigastric pain syndrome (‘ulcer-like’):
→ epigastric pain or burning
→ NOT necessarily related to meals
→ NOT related to defecation/passing flatus
Other features: morning symptoms characteristic, ± psychiatric comorbidities, eg. anxiety, depression
Functional Dyspepsia
Management options
Dietary changes: avoid known precipitants, low fat diet, ↓FODMAPs, ↓lactose
HP eradication empirical therapy
Empirical PPI +/- H2RA
Simeticone (Mylicon): anti-foaming agent for symptoms of belching
Antidepressants: TCAs (eg. amitriptyline) and SSRIs (eg. escitalopram)
Prokinetics, eg. metoclopramide for refractory cases
Differentiate vomiting, regurgitation and rumination
□ Vomiting: forcible involuntary expulsion of stomach content through mouth
→ Preceded by nausea and autonomic symptoms (eg. salivation)
□ Regurgitation: sudden, effortless return of small amount of gastric content into pharynx/mouth
→ No preceding autonomic symptoms
□ Rumination: repetitive effortless regurgitation of recently ingested food into mouth
→ ± re-chewing and re-swallowing or expulsion
Stimuli that activate vomiting centre in medulla
□ Visceral afferents at GI mucosa (mAChR, H1, D2, 5HT3) detecting visceral stimuli
□ Chemoreceptor trigger zone at 4th ventricle (D2, 5HT3) detecting chemical stimuli
□ Cerebellum and vestibulocochlear nerve (H1, mAChR) detecting vestibular stimuli
□ Higher centers detecting pain, emotional, repulsive sights/smell stimuli
Vomiting reflex
Afferent and efferent pathways and target organs
Afferent:
Vagal nerve and sympathetic fibers
Integration:
Vomiting centre in medulla oblongata
Efferent:
Cranial nerve to upper GIT: stomach antral relaxation and inhibit intestinal peristalsis, relaxation of LES, forceful retrograde peristalsis at jejunum
Spinal nerve to diaphragm and abdominal muscles: spasmodic contraction + close glottis
Cerebral cortex
Sympathetic output: cardiac arrhythmia, brisk muscle contraction
Acute and chronic causes of vomiting
- Stomach casues
Acute:
- Food poisoning – S. aureus, Bacillus cereus
- Gastroenteritis
- GOO
Chronic:
- Mechanical (GOO) – PUD, CA stomach, lymphoma, CA pancreas
- Functional (motility) – gastroparesis, functional dyspepsia
Acute and chronic causes of vomiting
- Visceral causes
Acute:
- SB obstruction
- Acute abdomen – acute appendicitis, cholecystitis, pancreatitis
- Hepatitis
Chronic:
- Small bowel dysmotility (pseudo-obstruction) – drugs, scleroderma, DM, amyloidosis, jejunal diverticulosis, SB myopathy/neuropathy
Acute and chronic causes of vomiting
Neurological causes
Acute:
- CNS disorders – meningitis, migraine, ↑ICP
- Vestibular disorders – vestibular neuronitis
- Psychogenic – after stress
Chronic:
- CNS disorders - ↑ICP
- Psychogenic – psychogenic (after stress), bulimia nervosa
- Cyclical vomiting syndrome
Acute and chronic causes of vomiting
- Metabolic causes
Acute and chronic:
- Pregnancy
- Alcoholism
- Endocrine – DKA, Addison’s disease
- Uraemia
- Drugs – narcotics, digitalis, chemo
Outline key history taking questions for vomiting
- Confirm vomiting, diff. regurgitation
- Characterize vomiting
- Duration, number
- Timing: delayed =GOO, gastroparesis, Early morning = pregnancy…
- Vomitus: undigested, old, bilious, blood, feculent - Any preceding nausea: projectile vomit = direct stimulation of emetic center
- Associated GI S/S: pain, distension, diarrhea, TOCC
- Associated CNS/ vestibular S/S: e.g. vertigo ,gait instability
- LMP and pregnancy
- PMH and constitutional symptoms for malignancy: DM, stroke, MI, Gastroparesis
- Surgical: abdomen, adhesion
Outline P/E and specific features for vomiting
General:
- Vitals: hypovolemic shock
- Hydration
- Acidotic breathing
- Uremia
- Russel’s sign (callused knuckles of hand, Bulimia/ eating disorder)
Abdominal: full
Targeted: Neurological, fundi, cardiovascular
First-line investigations for acute vomiting
For abdominal pain, work up for □ Amylase for pancreatitis □ Erect/supine AXR for pneumoperitoneum (perforation), obstruction □ USG for cholecystitis and cholangitis □ CT/MRI as indicated
For fever/diarrhea, workup for food poisoning
□ Stool for microscopy (RBC, WBC) and rapid GI panel (for eg. coronavirus, E. coli)
Complications of vomiting
□ CBC for anaemia, leukocytosis
□ RFT for hydration status, electrolyte disturbance
□ ABG for metabolic alkalosis
List imaging investigations for chronic vomiting
□ Upper endoscopy
□ Gastric emptying scan: 99mTc-DTPA meal/drink to visualize gastric emptying via scintigraphy
→ Gold standard for gastric emptying
□ Barium/ Contrast studies
□ CT/MRI enterography
□ Real-time ultrasound
Acute vomiting
Management options
- Fluid rehydration + correct electrolyte disturbance
- Nutritional support (enteral preferred)
- Medical:
- Antihistamines, anti-muscarinic agents
- Anticholinergics
- Dopamine antagonists
- Serotoninergic agents
- Erythromycin (prokinetic use) - Find underlying cause
List all drug options for acute vomiting
Antihistamines: dimenhydrinate, promethazine, meclizine, cyclizine
□ Useful for vestibular causes eg. motion sickness
Anticholinergics: scopolamine
□ Useful for vestibular causes eg. motion sickness
Dopamine antagonists:
□ Phenothiazines: prochlorperazine, chlorpromazine
□ Haloperidol
□ D2 blocker: metoclopramide, domperidone
Serotoninergic agents:
□ 5HT3 blocker: ondansetron
□ 5HT4 agonist: cisapride, molsapride, itopride (prokinetic)
Erythromycin (prokinetic)
Gastroparesis
Definition
Major clinical subtypes
Pathogenesis
Delayed gastric emptying, In absence of mechanical obstruction
with Cardinal symptoms of early satiety, post-prandial fullness, nausea, vomiting, PPI-refractory GERD
60% - Type 1 and Type 2 DM - ‘ Diabetic gastroparesis’
0.2% - ‘Non-diabetic gastroparesis’
Pathogenesis:
DEPLETION OF INTERSTITIAL CELLS OF CAJAL (ICC) in the corpus-antrum > disrupts gastric myoelectrical activity from the pacemaker region in greater curvature
List motor functions of the stomach
Storage: by Receptive Relaxation of proximal stomach under vagovagal reflex
Mixing and grinding ingested food with gastric juice: by Antral peristalsis against closed pylorus; retropulsion
Controlled emptying: by pylorus sphincter tone under neural and hormonal control
Neural control of stomach contraction
Migrating myoelectric complex (MMC) from stomach to ileum: maintains constant frequency of muscle contraction
Neural/ hormonal stimuli control smooth muscle contraction force
Causes of gastroparesis
Factors affecting gastric plexus and neural control:
DM
Thyroid dysfunction
Neurological disease: PD, amyloidosis…
Iatrogenic: vagotomy, fundoplication, bariatric surgery…
Autoimmune: scleroderma
Medication: GLP-1 agonist, narcotics, anti-cholinergics, cyclosporine
Trigger factors for gastroparesis
Infection (e.g. post-viral)
Hyperglycaemia
Ischemia
Electrolyte disturbance
Ddx gastroparesis
Cyclic vomiting syndrome
Rumination syndrome
Eating disorders
Cannabinoid misuse
First-line investigation for gastroparesis
Immediate management options
- Endoscopy +/- imaging: r/o Gastric outlet obstruction
- Scintigraphy: gastric emptying study
- Look for secondary causes
- Serology: CBC, LRFT, CaPO4, TFT, Blood gas
Management:
Nutritional support: enteral preferred
NG decompression, PEG-J/ Jejunostomy/ Gastrostomy for decompression
Gastric emptying study/ scintigraphy
- Pre-op checks
- Procedure
Pre-op:
- withhold drugs that affect gastric motility for 2-3 days
- Control glucose under 15mmol/L
Procedure:
99m-Tc sulfur-colloid labeled Egg sandwich as test meal / EggBeaters
Standard imaging at 0,1,2,4 hours
Normal result: <10% retention at 4 hours
Treatment options for gastroparesis
Prokinetics: Metoclopramide, Domperidone, Erythromycin
Long QT syndrome S/E
Gastric electrical stimulation (DM)
Gastric peroral endoscopic myotomy (G-POEM) *** most useful
List 4 benign epithelial lesions in esophagus
Heterotopic gastric mucosa
Squamous cell papilloma
Xanthoma
Acanthosis glycogens
List 5 benign sub-epithelial lesions in esophagus
Leimyoma
Granular cell tumor (Schwann cells, malignant potential)
Hemangioma
Carcinoid tumor (chromogranin/ synaptophysin +ve, hormone secreting)
GIST (from ICC, malignant potential)
