GI - 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
Q

Surgical treatment for GERD

Drawbacks/ complications

A
  • 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
Q

Ddx non-cardiac chest pain

A

→ 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
Q

Approach to non-cardiac chest pain

- Investigations and workup?

A

→ 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
Q

Dyspepsia

Definition
Gastrointestinal causes: most common, must not miss ddx?

A

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
Q

Dyspepsia

Non-GI causes

A

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
Q

Alarming/ red-flag features in dyspepsia

A

(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
Q

First-line investigation and treatment for dyspepsia

A

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
Q

Outline history taking for dyspepsia (check)

A

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
Q

Functional dyspepsia

  • Definition
  • Diagnostic criteria
A

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
Q

Functional dyspepsia

Clinical features and major clinical subtypes

A

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
Q

Functional Dyspepsia

Management options

A

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
Q

Differentiate vomiting, regurgitation and rumination

A

□ 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
Q

Stimuli that activate vomiting centre in medulla

A

□ 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
Q

Vomiting reflex

Afferent and efferent pathways and target organs

A

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
Q

Acute and chronic causes of vomiting

- Stomach casues

A

Acute:

  • Food poisoning – S. aureus, Bacillus cereus
  • Gastroenteritis
  • GOO

Chronic:

  • Mechanical (GOO) – PUD, CA stomach, lymphoma, CA pancreas
  • Functional (motility) – gastroparesis, functional dyspepsia
40
Q

Acute and chronic causes of vomiting

  • Visceral causes
A

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
Q

Acute and chronic causes of vomiting

Neurological causes

A

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
Q

Acute and chronic causes of vomiting

  • Metabolic causes
A

Acute and chronic:

  • Pregnancy
  • Alcoholism
  • Endocrine – DKA, Addison’s disease
  • Uraemia
  • Drugs – narcotics, digitalis, chemo
43
Q

Outline key history taking questions for vomiting

A
  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
Q

Outline P/E and specific features for vomiting

A

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
Q

First-line investigations for acute vomiting

A
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
Q

List imaging investigations for chronic vomiting

A

□ 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
Q

Acute vomiting

Management options

A
  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
Q

List all drug options for acute vomiting

A

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
Q

Gastroparesis

Definition
Major clinical subtypes
Pathogenesis

A

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
Q

List motor functions of the stomach

A

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
Q

Neural control of stomach contraction

A

Migrating myoelectric complex (MMC) from stomach to ileum: maintains constant frequency of muscle contraction

Neural/ hormonal stimuli control smooth muscle contraction force

52
Q

Causes of gastroparesis

A

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
Q

Trigger factors for gastroparesis

A

Infection (e.g. post-viral)
Hyperglycaemia
Ischemia
Electrolyte disturbance

54
Q

Ddx gastroparesis

A

Cyclic vomiting syndrome

Rumination syndrome

Eating disorders

Cannabinoid misuse

55
Q

First-line investigation for gastroparesis

Immediate management options

A
  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
Q

Gastric emptying study/ scintigraphy

  • Pre-op checks
  • Procedure
A

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
Q

Treatment options for gastroparesis

A

Prokinetics: Metoclopramide, Domperidone, Erythromycin
Long QT syndrome S/E

Gastric electrical stimulation (DM)

Gastric peroral endoscopic myotomy (G-POEM) *** most useful

58
Q

List 4 benign epithelial lesions in esophagus

A

Heterotopic gastric mucosa
Squamous cell papilloma
Xanthoma
Acanthosis glycogens

59
Q

List 5 benign sub-epithelial lesions in esophagus

A

Leimyoma

Granular cell tumor (Schwann cells, malignant potential)

Hemangioma

Carcinoid tumor (chromogranin/ synaptophysin +ve, hormone secreting)

GIST (from ICC, malignant potential)