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MBBS IV - Junior Clerkship WCS > JC74 (Medicine) - Gastric motility problems, Benign esophageal lesions > Flashcards

JC74 (Medicine) - Gastric motility problems, Benign esophageal lesions Flashcards

1
Q

GERD

  • Definition
  • Pathophysiology
A

Definition: condition which develops when the reflux of stomach contents causes troublesome symptoms and/or complications

Pathophysiology:

  1. 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
  2. Acid damage: mucosa expose to gastric content
  3. Chronic inflammation: complications e.g. esophagitis, strictures, Barret’s esophagus…etc
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2
Q

Physiological mechanisms against acid reflux?

A

Lower esophageal sphincter

Esophageal hiatus in crus of diaphragm

Oblique entrance of esophagus into stomach with Sharp angle on greater curvature (Angle of His)&raquo_space; forms a flap/ valve

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3
Q

Aggravating factors of esophageal reflux

A

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

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4
Q

Clinical manifestations of GERD

A

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
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5
Q

Complications of GERD

A

→ Odynophagia due to oesophagitis and ulcers

→ Dysphagia due to strictures

→ Barrett’s oesophagus

→ Adenocarcinoma

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6
Q

Factors that lower LES tone

A

→ Genetic determinants
→ Hiatus hernia
→ Diet/environment: alcohol, caffeine, smoking
→ Drugs (that cause sm relaxation), eg. NSAIDs, CCB, BB, nitrates, α-blocker, theophylline, anticholinergic

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7
Q

Ddx GERD

A

Achalasia

Zenker’s diverticulum

Gastroparesis

Angina pectoris

Causes of dyspepsia and esophagitis

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8
Q

Conditions most commonly associated with GERD

A

Pregnancy, Obesity

Long-term NG tube usage

Scleroderma (erosive GERD)

Multiple endocrine neoplasia (MEN)

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9
Q

Clinical classification of GERD

A

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%)

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10
Q

Diagnostic tests for GERD (5)

A

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

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11
Q

First diagnostic test for suspected GERD and NCCP (non-cardiac chest pain)

A

Proton pump inhibitor test

PPI empirical trail for 8 weeks
Symptoms improve = positive for GERD

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12
Q

ODG for GERD

  • Indications
  • Diagnostic of which conditions/ Role
A

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

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13
Q

24h esophageal pH monitoring test

  • Indication
  • Test cut-off for Dx
A

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

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14
Q

24h esophageal pH test

  • Modalities
  • Advantages
  • Disadvantages
A

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
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15
Q

Comparative advantages between 2 modalities for esophageal pH monitoring

A

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&raquo_space; detects acid and non-acid reflux
  • Better dx of NERD
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16
Q

Endoscopy for GERD

  • Normal endoscopic finding can Dx GERD, True or False
A

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

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17
Q

Clinical classification for esophagitis

A

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

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18
Q

Esophageal manometry

  • Indications
  • Function
A

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
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19
Q

Management options for GERD

  • Lifestyle modifications
A

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

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20
Q

Medical management options for GERD

Indication for each option

A

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)

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21
Q

PPI therapy for GERD

  • Indications for maintenance therapy
  • Risks of long-term use
A

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

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22
Q

Medical management options for GERD

  • list examples of each class of drug
A

→ Antacids: Triact, magnesium / aluminum hydroxide
→ H2RA: cimetidine, raniditine, famotidine
→ PPI: omeprazole, lansoprazole, esomeprazole

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23
Q

Management of refractory GERD

Modifications to existing treatment? Investigations?

A
  1. Optimize PPI: dose, timing, compliance; switch class of PPI
  2. Add-on therapy:
    - Nocturnal H2RA for night-time symptoms
    - Alginate for post-dinner symptoms
  3. Find cause:
    - Early upper endoscopy if red-flag symptoms
    - 24h pH monitoring and impedance study
    - Esophageal manometry
  4. Definitive surgery
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24
Q

Surgical treatment options for GERD

Indications

Pre-op checks

A

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
25
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
26
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)
27
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
28
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
29
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)
30
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
31
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)
32
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
33
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 ```
34
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
35
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
36
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
37
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
38
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
39
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
40
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
41
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
42
Acute and chronic causes of vomiting - Metabolic causes
Acute and chronic: - Pregnancy - Alcoholism - Endocrine – DKA, Addison’s disease - Uraemia - Drugs – narcotics, digitalis, chemo
43
Outline key history taking questions for vomiting
1. Confirm vomiting, diff. regurgitation 2. Characterize vomiting - Duration, number - Timing: delayed =GOO, gastroparesis, Early morning = pregnancy... - Vomitus: undigested, old, bilious, blood, feculent 3. Any preceding nausea: projectile vomit = direct stimulation of emetic center 4. Associated GI S/S: pain, distension, diarrhea, TOCC 5. Associated CNS/ vestibular S/S: e.g. vertigo ,gait instability 6. LMP and pregnancy 7. PMH and constitutional symptoms for malignancy: DM, stroke, MI, Gastroparesis 8. Surgical: abdomen, adhesion
44
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
45
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
46
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
47
Acute vomiting Management options
1. Fluid rehydration + correct electrolyte disturbance 2. Nutritional support (enteral preferred) 3. Medical: - Antihistamines, anti-muscarinic agents - Anticholinergics - Dopamine antagonists - Serotoninergic agents - Erythromycin (prokinetic use) 4. Find underlying cause
48
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)
49
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
50
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
51
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
52
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
53
Trigger factors for gastroparesis
Infection (e.g. post-viral) Hyperglycaemia Ischemia Electrolyte disturbance
54
Ddx gastroparesis
Cyclic vomiting syndrome Rumination syndrome Eating disorders Cannabinoid misuse
55
First-line investigation for gastroparesis Immediate management options
1. Endoscopy +/- imaging: r/o Gastric outlet obstruction 2. Scintigraphy: gastric emptying study 3. Look for secondary causes 4. Serology: CBC, LRFT, CaPO4, TFT, Blood gas Management: Nutritional support: enteral preferred NG decompression, PEG-J/ Jejunostomy/ Gastrostomy for decompression
56
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
57
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
58
List 4 benign epithelial lesions in esophagus
Heterotopic gastric mucosa Squamous cell papilloma Xanthoma Acanthosis glycogens
59
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)

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