GC068 Indigestion And ‘heartburn’
Indigestion (dyspepsia) and heartburn are upper gastrointestinal symptoms characterized by epigastric discomfort, bloating, and a retrosternal burning sensation typically caused by gastric acid reflux or impaired digestion.
Indigestion and “Heartburn”
This lecture, delivered by Dr. Mak Lung-Yi (QMH / HKU), covers four interconnected topics spanning the upper GI tract, from the most common presentations to the rarest [1]:
- Approach to indigestion (dyspepsia) and heartburn (GERD)
- Approach to nausea and vomiting
- Overview of gastric motility problems — focusing on gastroparesis
- Overview of benign esophageal lesions
The unifying clinical thread: a patient walks in saying "I have heartburn" or "I keep vomiting." Your job is to distinguish physiological from pathological, organic from functional, and benign from sinister — all while being cost-effective. The exam loves testing the definitions, the diagnostic approach (especially the PPI test, 24-hr pH monitoring, and when to scope), the pharmacology of anti-emetics and prokinetics, and the classification of benign esophageal lesions.
Part 1: Approach to Indigestion and Heartburn
Heartburn typically refers to GERD: a burning feeling rising from the stomach or lower chest up towards the neck. May include acid regurgitation, sour stomach, bitter belching, waterbrash. [1]
Indigestion / Dyspepsia is pain or discomfort centered in the upper abdomen. May include epigastric pain/burning, postprandial fullness, early satiety, epigastric bloating. Sometimes patients confusingly refer to heartburn or regurgitation as "indigestion." [1]
Why this matters from first principles: Heartburn implies an esophageal problem (acid going up through an incompetent barrier). Dyspepsia implies a gastroduodenal problem (the stomach or duodenum is irritated, obstructed, or dysmotile). But there is significant symptom overlap — this is explicitly stated on the slides as an "area of controversy" [1].
| Feature | Heartburn (GERD) | Dyspepsia |
|---|---|---|
| Direction | Rising from stomach → neck | Centred in upper abdomen |
| Key symptom | Burning, acid regurgitation, waterbrash | Epigastric pain, fullness, early satiety |
| Timing | Within 1 hr of eating; supine; ↑ intra-abdominal pressure | Variable; postprandial or fasting |
| Overlap | GERD patients can have dyspepsia | Dyspepsia patients can describe "heartburn" |
Regurgitation is defined as the effortless return of gastric contents upward — key word is "effortless" — distinguishing it from vomiting which is forceful [1].
High Yield
The lecture explicitly notes the overlap between GERD (32%), dyspepsia (14%), and NCCP (16%), with 8% having all three (Wong WM, AP&T 2003). Exam questions may present mixed symptoms and ask you to identify the predominant syndrome.
1.2 Gastro-Esophageal Reflux Disease (GERD)
GERD is the condition in which the reflux of gastric contents into the esophagus results in symptoms and/or complications. Gastroesophageal reflux (GER) itself is physiological — it becomes a disease only when it causes symptoms or mucosal damage. [1]
This is a crucial conceptual point: everyone refluxes to some degree after meals. It becomes GERD when reflux causes troublesome symptoms and/or complications; symptom frequency alone is not a universal diagnostic cut-off [21].
GERD is a spectrum of disease resulting from imbalance between anti-reflux barriers vs. aggravating factors. [1]
Anti-reflux barriers (why they prevent reflux):
| Barrier | Mechanism |
|---|---|
| LES (resting pressure ~10 mmHg) | Tonic contraction creates a high-pressure zone; intra-abdominal location means abdominal pressure compresses it shut [1] |
| Diaphragmatic hiatus (crural muscle + phrenoesophageal ligaments) | External "pinch" on the esophagus during inspiration reinforces LES [1] |
| Angle of His (oblique entry of esophagus into stomach) | Creates a flap valve: when gastric pressure rises, the sharp angle on the greater curvature side compresses the esophageal opening shut [1] |
Aggravating factors (why reflux increases):
| Factor | Explanation |
|---|---|
| tLESR (transient LES relaxation) | The single most important mechanism in most GERD patients. Stimulated by proximal gastric distension (large meal, swallowed air). The LES relaxes inappropriately for 10-60 seconds, allowing reflux [1] |
| Hiatus hernia | Proximal stomach herniates above the diaphragm → LES loses its intra-abdominal location → loses the reinforcing "pinch" of the crural muscle → ↑ reflux episodes and ↓ acid clearance [1] [4] |
| Impaired esophageal emptying/peristalsis | Normally, secondary peristalsis clears refluxed acid. If peristalsis is weak (e.g., scleroderma), acid dwell time ↑ → more mucosal damage [1] |
| Hypotensive LES (post-POEM) | POEM (per-oral endoscopic myotomy for achalasia) deliberately disrupts LES → high rate of post-procedure GERD [1] |
| Acid pocket | Post-meal, an area of unbuffered acid sits on top of the food bolus near the cardia; if LES opens, this acid preferentially refluxes [1] |
| Excessive gastric acid | Hypergastrinaemia from Hp-positive antral gastritis (G-cells spared), post-Hp eradication in corpus-predominant gastritis (parietal cells recover but G-cell drive persists temporarily), Zollinger-Ellison syndrome (gastrinoma), or delayed gastric emptying [1] |
Exam Trap
Hiatus hernia is an important mechanical risk factor for GERD, but it is neither necessary nor sufficient: many patients with a hiatus hernia have no GERD, and many patients with GERD have no hernia. In an exam answer, describe how separation of the LES from the diaphragmatic crura weakens the anti-reflux barrier rather than using an absolute “cause/not a cause” statement [21].
Typical GERD symptoms: post-prandial (especially after large meals); triggered by spicy food, citrus, fat, chocolates, alcohol; worsened in supine or right decubitus posture. [1]
Why right decubitus worsens GERD: lying on the right side positions the gastric fundus (acid pocket) above the GEJ, facilitating reflux. Left lateral decubitus keeps the acid pool below the GEJ.
Atypical chest pain — this is NCCP (non-cardiac chest pain). Important to exclude cardiac causes first [1].
Extra-esophageal symptoms: asthma, chronic cough, sleep disturbance, laryngo-pharyngeal reflux, hoarseness of voice, throat tightness, dental erosion. [1]
Why extra-esophageal symptoms occur: Acid can microaspirate into the larynx/tracheobronchial tree (direct contact theory), or vagal reflex from acid in the distal esophagus triggers bronchospasm (reflex theory). This explains why some GERD patients present first to ENT or Respiratory.
Do Not Over-Attribute Extra-Esophageal Symptoms
These symptoms are non-specific and may coexist with reflux without being caused by it. Exclude cardiac disease for chest pain and assess common pulmonary, ENT, allergic, and medication-related causes of cough, asthma, or hoarseness before attributing them to GERD. Objective reflux testing is preferred when the diagnosis is uncertain, especially if typical heartburn/regurgitation is absent [21] [22].
Endoscopic classification: erosive vs. non-erosive [1]
Complications: esophagitis, esophageal ulcer and stricture, Barrett's esophagus, adenocarcinoma of esophagus [1]
The cascade: chronic acid exposure → inflammation (esophagitis) → ulceration → scarring and stricture → intestinal metaplasia (Barrett's) → dysplasia → adenocarcinoma. This is the dreaded long-term complication that drives surveillance programmes.
| Associated Conditions | DDx of GERD |
|---|---|
| Pregnancy (30-80%) — progesterone relaxes LES + growing uterus ↑ intra-abdominal pressure [1] | Achalasia — failure of LES relaxation (opposite mechanism!) but can mimic with regurgitation |
| NG tube — splints the LES open [1] | Zenker's diverticulum — regurgitation of undigested food, halitosis |
| Scleroderma (38% erosive disease) — fibrosis of esophageal smooth muscle → ↓ peristalsis + ↓ LES tone [1] | Gastroparesis — nausea, vomiting, early satiety |
| MEN — associated with Zollinger-Ellison (MEN1) [1] | Angina pectoris — must always exclude cardiac chest pain |
| Obesity [1] | Other causes of esophagitis: pill-induced, infective (Candida, HSV, CMV in immunosuppressed), radiation, eosinophilic |
1.3 Diagnosis of GERD
The lecture presents a hierarchy from subjective to objective, emphasizing cost-effectiveness [1]:
A once-daily PPI trial for 8 weeks can be considered as an initial step in patients with classic heartburn/regurgitation and no alarm features. Symptom response supports acid-mediated disease but is not sufficiently specific to prove GERD [21].
Why this works: If symptoms resolve with acid suppression, the diagnosis of acid-related disease is supported. It is both diagnostic and therapeutic. The 8-week duration matters because some patients with erosive esophagitis need the full course for healing.
Why to take PPI 30-60 min before meals: PPIs are prodrugs that require an acidic environment to be activated. They irreversibly bind to H+/K+ ATPase (proton pumps) that are actively secreting acid. Meals stimulate proton pump activity via gastrin/vagal/histamine pathways. If you take PPI with an empty stomach and no meal follows, fewer pumps are active → less drug effect [1].
Chinese (Cantonese) GERDQ — validated 7-question questionnaire assessing frequency and severity of heartburn, acidity in stomach, acid regurgitation, and use of antacids. [1]
The slide teaches the historical catheter criterion of distal esophageal pH < 4 for ≥4.2% of the recording and the DeMeester composite score [1]. Current Lyon 2.0 interpretation prioritizes acid exposure time (AET): AET > 6% is conclusive evidence for GERD, AET < 4% is physiologic evidence against GERD, and 4–6% is inconclusive and requires supportive evidence. With prolonged wireless pH monitoring, AET > 6% on at least 2 days is diagnostic [23].
| Parameter | Detail |
|---|---|
| Sensitivity for erosive GERD | ~90% [1] |
| Sensitivity for NERD | Much lower [1] |
| Catheter type | 2 antimony pH electrodes [1] |
| Newer technology | BRAVO™ catheter-free capsule — transmits pH via radio frequency; more comfortable [1] |
| Combined impedance-pH | Detects liquid/gas movement, direction, and acid versus weakly acidic/non-acid reflux; symptom-event markers permit association analysis [1] |
Why pH 4.0 threshold? Below pH 4, pepsin is activated and causes mucosal injury. This is the physiological basis for the DeMeester threshold.
How to read the impedance-pH diagram: a swallowed bolus produces sequential impedance changes moving down the catheter; reflux produces sequential changes moving up from distal to proximal sensors. The pH channel then classifies the event by acidity. Test off PPI when GERD is unproven; test on optimized PPI when GERD is already objectively established but symptoms persist [24].
Role of endoscopy in GERD: [1]
- Diagnosing erosive GERD (~30% of all GERD; i.e. 70% GERD is NERD) — Normal endoscopy does NOT exclude GERD
- Look for cause — hiatus hernia, EoE, antral gastritis, associated PUD
- Look for complications — strictures, Barrett's, adenocarcinoma
- Alarm symptoms: weight loss, dysphagia, odynophagia, GI bleeding
Key Exam Fact
~70% of GERD is NERD (non-erosive reflux disease). A normal endoscopy does NOT exclude GERD. This is a very commonly tested concept. Only 20-60% of patients with abnormal esophageal pH have visible esophagitis on endoscopy [1].
| Grade | Description |
|---|---|
| A | ≥1 mucosal break confined to folds, ≤5 mm long [1] |
| B | ≥1 mucosal break confined to folds, > 5 mm long [1] |
| C | ≥1 mucosal break continuous between tops of ≥2 folds, < 75% circumference [1] |
| D | ≥1 mucosal break continuous between tops of ≥2 folds, ≥75% circumference [1] |
Visual recognition: grades A and B remain confined to individual mucosal folds (≤5 mm versus > 5 mm). Grade C bridges the tops of folds but involves < 75% of the circumference; grade D is circumferential or near-circumferential (≥75%). The endoscopic photographs progress from isolated linear breaks to confluent disease [1].
Why this classification matters: LA grade C/D = severe erosive esophagitis → requires long-term maintenance PPI therapy [1]. LA A/B may be managed with on-demand or intermittent therapy.
1.4 Management of GERD
Confirm diagnosis, relieve symptoms, reassure patients, heal esophagitis, improve quality of life, prevent long-term complications. [1]
Lifestyle advice should be targeted, not a universal prohibition list [21]:
- Weight loss (if obese)
- Elevate head of bed (gravity assists acid clearance)
- Avoid late meals / lying down within 2-3 hours of eating
- Avoid foods only when they reproducibly trigger that patient's symptoms
- Smoking cessation
- Prefer left lateral sleep and avoid right lateral decubitus for nocturnal symptoms
| Drug Class | Role | Key Points |
|---|---|---|
| Antacids | On-demand symptom relief | Little evidence for sustained benefit [1] |
| H2 Receptor Antagonists (H2RA) | Main role: add-on therapy for bedtime breakthrough GERD despite PPI | Tachyphylaxis develops — effect wanes with chronic use [1] |
| Proton Pump Inhibitors (PPI) | Superior relief of heartburn/regurgitation + healing of esophagitis cf. H2RA | Take 30-60 min before meal; try to discontinue long-term therapy if possible [1] |
PPI Maintenance Therapy Indications: [1]
- Long-term: Erosive esophagitis LA grade C/D, peptic stricture, Barrett's esophagus
- On-demand/intermittent: NERD patients with severe symptoms responsive to PPI
No role: Baclofen, prokinetics, sucralfate (except sucralfate during pregnancy). [1]
High Yield - PPI Side Effects (Directly Tested in 2022 MCQ Q40)
Known effects: fundic gland polyps (mostly benign), acute interstitial nephritis [1].
Association studies (many, but NO cause-and-effect confirmed): intestinal infections, pneumonia, gastric cancer, osteoporosis-related fractures, CKD, stroke, dementia, hepatic encephalopathy, hypomagnesemia [1].
Current interpretation: observational associations do not establish causation. High-quality data have not shown a significant increase in most proposed adverse outcomes, although a small intestinal-infection signal remains. Do not stop an indicated PPI solely because of these associations [21] [25].
Bottom line: review and document the indication, use the lowest effective dose, and step down when no chronic indication remains. Patients with complicated GERD (severe erosive esophagitis, ulcer, peptic stricture) generally should not have therapy withdrawn. Routine extra calcium/vitamin D, bone-density testing, B12 testing, or creatinine monitoring is not recommended in otherwise low-risk patients [21] [25].
Historical exam note: the 2022 local MCQ expected C. Enteric infections [18]. Preserve that as past-paper context, but use the current indication-based counselling above in clinical practice.
Possible actions for refractory GERD: [1]
- Optimize PPI dose, timing, compliance
- Try switching class of PPI (different CYP2C19 metabolism profiles)
- Add nocturnal H2RA for night-time symptoms
- Add Alginate (e.g. Gaviscon) for post-dinner symptoms
- 24-hour pH monitoring ± impedance study
- Anti-reflux surgery (only after confirmed with objective testing)
- Esophageal manometry
- Repeat OGD after OFF PPI for 2-4 weeks (drug holiday) to look for erosive esophagitis and obtain esophageal biopsies for EoE — 1-8% of refractory GERD [1]
The slide's differential is worth using before escalating treatment: persistent symptoms may reflect insufficient acid suppression, weakly acidic/non-acid reflux, reflux hypersensitivity, or a non-GERD disorder such as delayed gastric emptying, achalasia, eosinophilic esophagitis, aerophagia/supragastric belching, rumination, or a functional disorder [1].
Why switch PPI class? PPIs are metabolized by CYP2C19 (and to a lesser extent CYP3A4). Genetic polymorphisms in CYP2C19 mean some patients are "rapid metabolizers" who break down certain PPIs too quickly → inadequate acid suppression. Switching to a PPI less dependent on CYP2C19 (e.g., rabeprazole) may improve response.
Why biopsy for EoE? Eosinophilic esophagitis mimics GERD with heartburn and dysphagia but does not respond to PPI (or only partially responds). Diagnosis requires ≥15 eosinophils/HPF on esophageal biopsy. Must take PPI holiday before biopsy to avoid PPI-responsive esophageal eosinophilia being mistaken for EoE.
Anti-reflux surgery options: [1]
- Laparoscopic fundoplication (Nissen) — wraps gastric fundus around distal esophagus to augment LES
- Magnetic sphincter augmentation (MSA) - LINX — ring of magnetic beads placed around LES
- Trans-oral incisionless fundoplication (TIF)
What the procedure diagrams show: Nissen fundoplication creates a gastric-fundus wrap around the distal esophagus; LINX beads separate during swallowing and re-approximate to augment the LES after the bolus passes; TIF places transoral fasteners to recreate the gastroesophageal flap valve [1].
Pre-op evaluation: [1]
- Confirm GERD diagnosis
- Confirm symptoms are at least partially PPI-responsive
- Exclude contraindications (e.g., achalasia — you would make achalasia worse by adding a fundoplication)
Drawbacks: [1]
- Surgical risks (~4%)
- Recurrence of GERD post-op (~20% long-term)
- Post-operative dysphagia / gas bloat / inability to belch (Nissen-specific complications [5])
1.5 Uninvestigated Dyspepsia — The Algorithm
Most prevalent causes: peptic ulcer disease, Hp infection, functional dyspepsia [1] Significant organic causes to exclude: malignancy of upper GIT, hepato-pancreatic-biliary causes [1]
Current ACG/CAG guidance uses age ≥60 as the routine endoscopy threshold. In patients under 60, an alarm feature does not automatically mandate endoscopy; investigate case by case according to the feature, severity, background risk, and local pathway [26].
Two approaches (may be sequential): [1]
- Test (for Hp) and Treat — non-invasive Hp testing (urea breath test or stool antigen), if positive → eradication therapy
- Empirical anti-secretory drug (PPI trial)
If no response or recurrence → may eventually need upper endoscopy [1]
Laboratory tests (CBC, LRFT, TFT): cost-effectiveness not established [1]
One or more bothersome symptoms—postprandial fullness, early satiation, epigastric pain, or epigastric burning—with no structural disease likely to explain them. Rome IV requires symptoms for the last 3 months with onset at least 6 months before diagnosis [1].
Note: presence of H. pylori does NOT exclude FD. Eradication of Hp CAN relieve symptoms in some FD patients. [1]
ROME IV criteria divide FD into: [1]
- Post-prandial distress syndrome (PDS) — bothersome postprandial fullness or early satiation on ≥3 days/week
- Epigastric pain syndrome (EPS) — bothersome epigastric pain or burning on ≥1 day/week
The subtypes overlap and should not be treated as a rigid drug-selection rule. A practical sequence is H. pylori test-and-treat → PPI → low-dose tricyclic antidepressant → prokinetic, with psychological therapy for selected persistent cases [26].
Part 2: Approach to Nausea and Vomiting
Nausea → retching → vomiting: a progression leading to the emetic reflex, but they may occur separately. [1]
| Term | Definition |
|---|---|
| Nausea | An unpleasant subjective sensation as a feeling of impending vomiting in the epigastrium or throat [1] |
| Retching | Spasmodic abortive respiratory movement with glottis closed [1] |
| Vomiting | Forceful, coordinated reflex expelling gastric/intestinal content through the mouth; distinguish this from deliberately self-induced vomiting [1] |
| Regurgitation | Effortless reflux of gastric contents into esophagus; NOT associated with forceful ejection [1] |
Exam Trap: Vomiting vs. Regurgitation
If an exam question describes "effortless" return of food — that is regurgitation (think GERD, achalasia, Zenker's diverticulum). If it describes "forceful" ejection with retching — that is vomiting (think mechanical obstruction, raised ICP, metabolic causes). This distinction is tested in history-taking scenarios.
Emetic center: located in the medulla (dorsal portion of the lateral reticular formation) — the solitary nucleus [1]
Afferent pathways (what triggers vomiting):
| Source | Examples |
|---|---|
| GI tract | Pharynx, stomach, small intestine, bile duct, peritoneum [1] |
| Non-digestive organs | Heart (AMI), testicles [1] |
| CNS | Cerebellum, vestibular system, brainstem, chemoreceptor trigger zone (CTZ) [1] |
The CTZ (area postrema) lies outside the blood-brain barrier, allowing it to detect circulating emetogenic substances (drugs, toxins, metabolites like urea).
How the pathway diagram fits together: vagal/sympathetic visceral afferents, the vestibular system, cortex/limbic inputs, and the area postrema converge on the medullary emetic network. The CTZ is rich in D2 and 5-HT3 receptors, explaining why dopamine and serotonin antagonists work; vestibular input explains the value of H1/antimuscarinic drugs in motion-related symptoms [1].
Efferent pathway (what happens during vomiting): [1]
- Cerebral cortex activation (you become aware)
- Stomach: antral relaxation + inhibition of intestinal peristalsis
- Intercostal muscles and diaphragm: spasmodic contraction + closure of glottis
- Brisk muscular contraction, relaxation of LES, forceful retrograde peristalsis of jejunum
- ± Hypersalivation, cardiac arrhythmia
The lecture divides causes into GIT and Non-GIT. Bowel sounds can be a supporting clue, but are variable and examiner-dependent: normal or quiet sounds do not exclude mechanical obstruction, and imaging should not be delayed when obstruction or perforation is suspected.
| Category | Causes | Bowel Sounds |
|---|---|---|
| Mechanical obstruction | GOO, SBIO, SMA syndrome | ↑ |
| Motility disorder | Paralytic ileus, gastroparesis, colonic pseudo-obstruction, achalasia | ↓ / Normal |
| Hepato-biliary-pancreatic | Acute hepatitis, acute cholecystitis, acute pancreatitis | ↓ / Normal |
| Bowel inflammation | Acute mesenteric ischemia, gastroenteritis | ↓ |
| Pharyngeal irritation | — | Normal |
| Eating disorder | Bulimia, anorexia nervosa | ↓ / Normal |
| Peritoneal irritation | Peritonitis, carcinomatosis | — |
| CNS/PNS | Raised ICP, CNS infection, acute stroke, vestibular, migraine | — |
| Cardiac | AMI, heart failure | — |
| Systemic/Metabolic | DKA, Addisonian crisis, hypoNa, uraemia | — |
| Drugs | Chemotherapy, metformin, colchicine, levodopa, anticonvulsants, antibiotics, narcotics, digoxin | — |
| Hormonal | Hyperestrogenemia (pregnancy, OCPs) | — |
| Other | Alcohol abuse | — |
Key history elements: [1]
- Onset: acute (< 1 week) vs. chronic
- Timing: empty stomach vs. post-prandial
- Nature of vomitus: total undigested vs. acidic vs. bilious
- Preceding nausea: absence of nausea or projectile vomiting may raise concern for a neurological cause, but neither is reliable or localising; use associated headache, focal deficits, altered consciousness, or papilloedema to guide urgent neurological assessment
- Constitutional symptoms
- Associated GI symptoms: abdominal pain, jaundice, diarrhea, hematemesis
- Associated CNS/vestibular/cardiac symptoms
- LMP for females (always!)
- PMH: DM (medication? DKA? Gastroparesis?), stroke, MI, psychiatric history
- Drug history
- Surgical history: abdominal surgery → adhesive SBIO
Why "nature of vomitus" matters:
- Undigested food → esophageal cause (Zenker's, achalasia) or very proximal obstruction
- Acidic (partially digested) → gastric cause
- Bilious (green/yellow) → obstruction DISTAL to ampulla of Vater (i.e., beyond D2)
- Feculent → distal small bowel or colonic obstruction
General exam: [1]
- Vitals: hypovolaemic shock?
- Hydration status: capillary refill, mucous membrane, skin turgor, body weight, urine output
- Acidotic breathing (Kussmaul — metabolic acidosis)
- Jaundice? Uraemic complexion?
- Russell's sign (callused knuckles — self-induced vomiting in eating disorders)
Abdominal exam: [1]
- Inspection: distension, surgical scars, hernia
- Palpation: peritoneal signs, Murphy's sign, mass
- Percussion: characterize mass, shifting dullness
- Auscultation: bowel sounds are supportive only; integrate them with distension, tenderness/peritonism, hernias, scars, and imaging
Targeted exam based on history: [1]
- Cardiovascular exam (if cardiac cause suspected)
- Neurological + fundoscopy (if CNS cause suspected — papilloedema in raised ICP)
Investigations (underlined = complications OF vomiting; not underlined = causes): [1]
Order tests according to the history, examination, illness severity, and pregnancy potential—not as an indiscriminate panel.
| Investigation | Looking For |
|---|---|
| Urinary pregnancy test | Pregnancy (always in women of childbearing age) |
| CBC | Leukocytosis, reactive thrombocytosis, anaemia |
| LFT, GGT | Hepato-biliary causes, hypoalbuminaemia |
| Amylase ± lipase | Acute pancreatitis, IO, bowel ischemia, perforated gut |
| RFT, CaPO4 | Cr↑, Ca↑, electrolyte disturbances (K↓, Na↓ or Na↑), AKI |
| Random glucose | DKA |
| Ketone | DKA |
| Venous blood gas | Metabolic acidosis OR metabolic alkalosis (from vomiting: loss of HCl → hypochloraemic hypokalaemic metabolic alkalosis) |
| Serum ethanol | Alcohol intoxication |
| ECG | U wave, flat T wave, long QTc (from hypokalaemia), myocardial ischemia |
| Cardiac enzymes | AMI |
| CXR | Aspiration pneumonia (complication), perforated viscus (free air), Boerhaave's syndrome (pneumomediastinum) |
| AXR | Dilated small/large bowel, gastric distension |
| Imaging | USG/CT abdomen; CT brain |
Radiograph atlas from the slide: centrally dilated loops with valvulae conniventes crossing the full width suggest small-bowel obstruction; haustrated peripheral dilation suggests large bowel; multiple air-fluid levels support obstruction; a massively dilated “coffee-bean” loop suggests volvulus; and free subdiaphragmatic gas suggests perforation. These are pattern-recognition clues, not standalone diagnoses—CT is often needed to identify the level, cause, ischemia, or perforation [1].
Boerhaave's Syndrome
Boerhaave's syndrome = spontaneous esophageal perforation from forceful vomiting. Look for Mackler's triad: vomiting + lower thoracic pain + subcutaneous emphysema. CXR shows pneumomediastinum. This is a surgical emergency.
Detailed history + physical examination → narrow DDx → then: [1]
- Upper GI endoscopy
- Contrast studies
- Gastric emptying study
- CT/MR enterography
- Referrals (neurology, psychiatry)
5 steps: [1]
- Fluid rehydration (chart I/O)
- Correction of electrolyte disturbance
- Nutritional support (enteral preferred over parenteral)
- Pharmacological therapy
- Look for and treat underlying cause
Anti-emetic Pharmacology (High Yield)
| Drug Class | Examples | Mechanism | Side Effects |
|---|---|---|---|
| Dopamine D2 antagonist | Metoclopramide (Maxolon) 10 mg q8h IV/PO | Central anti-emetic + peripheral prokinetic (5HT4 agonist) | Somnolence, extrapyramidal effects [1] |
| Domperidone 10 mg TDS PO only | Peripheral D2 antagonist (crosses BBB poorly) | Less extrapyramidal S/E, risk of ↑QTc [1] | |
| Both can increase prolactin [1] | |||
| Antihistamines / Antimuscarinics | Diphenhydramine; antimuscarinics are a separate class | H1 or muscarinic blockade, especially useful for vestibular pathways | Drowsiness; anticholinergic effects. Check the specific drug—important cautions include angle-closure glaucoma and urinary retention; asthma is not a class contraindication |
| Serotonin 5HT3 antagonist | Ondansetron | Blocks 5HT3 at CTZ and vagal afferents | Well tolerated; may cause constipation, headache |
| NK1 receptor antagonist | Aprepitant | Blocks substance P at emetic center | Used mainly for chemotherapy-induced N/V |
| Motilin receptor agonist | Erythromycin IV (3 mg/kg q8h) | Mimics motilin → stimulates gastric motility | Long QTc; more specific for gastroparesis [1] |
Exam Pearls: Metoclopramide vs. Domperidone
Metoclopramide has DUAL action: central anti-emetic (D2 antagonist) + peripheral prokinetic (5HT4 agonist). It crosses the BBB → more extrapyramidal side effects. Domperidone crosses BBB poorly → fewer CNS side effects but still raises prolactin (acts on pituitary, which is outside BBB). Both prolong QTc. Domperidone is oral only [1].
Part 3: Gastroparesis
Gastroparesis is a syndrome of: [1]
- Delayed gastric emptying
- In the absence of mechanical obstruction
- Cardinal symptoms: early satiety, postprandial fullness, nausea, vomiting, PPI-refractory GERD
- Less specific: bloating, upper abdominal pain
Prevalence: [1]
- Type 1 DM: 5-40%
- Type 2 DM: 1-20%
- Non-diabetic controls: 0.2% → 'Idiopathic gastroparesis'
Interstitial Cells of Cajal (ICC) = pacemaker cells derived from c-Kit positive mesenchymal cell precursors. Located on the greater curvature between fundus and proximal corpus. Generate slow waves at ~3 cycles per minute.* [1]
Depletion of ICCs in the corpus-antrum is the key pathological finding in gastroparesis [1].
What the pacemaker diagram shows: the slow wave begins in the proximal stomach along the greater curvature and propagates distally through an ICC network coupled by gap junctions to smooth muscle. Loss or dysfunction of the corpus-antral ICC network disrupts coordinated antral contractions and gastric emptying [1].
Why diabetes causes gastroparesis: Chronic hyperglycaemia → autonomic neuropathy (vagal nerve damage) → loss of excitatory neural input to ICC + smooth muscle → impaired gastric accommodation and antral contractions. Additionally, hyperglycaemia itself acutely slows gastric emptying (reversible component).
| Causes | Triggering Factors | DDx |
|---|---|---|
| DM, Idiopathic, Thyroid dysfunction, Neurological (Parkinsonism, amyloidosis, paraneoplastic), Post-surgical (vagotomy, fundoplication, bariatric), Autoimmune (scleroderma), Medications (GLP-1 agonist, narcotics, anticholinergics, cyclosporine) [1] | Infection (post-viral), Hyperglycaemia, Ischemia, Electrolyte disturbance [1] | Cyclic vomiting syndrome, Rumination syndrome, Eating disorders, Cannabinoid misuse [1] |
GLP-1 Agonists and Gastroparesis
GLP-1 receptor agonists (e.g., semaglutide, liraglutide) delay gastric emptying and may mimic or worsen gastroparesis symptoms. Review the timing of symptoms and medications before assigning an irreversible diagnostic label.
Step 1: Exclude gastric outlet obstruction → endoscopy ± cross-sectional imaging [1] Step 2: Scintigraphy → gastric emptying study (solid meal) [1] Step 3: Look for secondary causes → review history, CBC, RG, LRFT, CaPO4, TFT, blood gas [1] Step 4: Prepare for pharmacological treatment → ECG (baseline QTc before prokinetics) [1] Step 5: Nutritional support → enteral route preferred (post-pyloric feeding) over parenteral [1]
Retained gastric contents on endoscopy may support delayed emptying, but are not by themselves diagnostic; fasting adequacy, obstruction, and medications must be considered before confirmation with a standardized emptying test [27].
Gastric Emptying Study (Scintigraphy) — Key Details:
Precautions: [1]
- Withhold drugs affecting gastric motility for 48-72 hours: narcotic opioids, anticholinergics, metoclopramide, macrolides, domperidone
- Control glucose to < 15 mmol/L (hyperglycaemia slows emptying and invalidates test)
- Solid phase meal: 99mTc sulfur colloid-labeled egg sandwich (or EggBeaters with jam + toast + water)
- Standard imaging at 0, 1, 2, and 4 hours
- Normal: < 10% retention at 4 hours [1]
Reading the scintigraphy images: the radiolabelled meal should progressively leave the stomach and appear in small bowel during the 4-hour sequence. The normal examples have only 1–9% gastric retention at 4 hours, whereas the delayed example retains 82%. Diagnose from the quantified standardized study—not from one frame or symptoms alone [1] [27].
| Agent | Dose | Mechanism | Key Side Effects / Notes |
|---|---|---|---|
| Metoclopramide | 10 mg TDS PO or q8h IV (individualize dose) | D2 antagonist (central + peripheral) + 5HT4 agonist | Extrapyramidal effects and potentially irreversible tardive dyskinesia; use the lowest effective dose for the shortest duration and avoid treatment beyond 12 weeks except rare cases where benefit outweighs risk [28] |
| Domperidone | 10 mg TDS PO (where locally available) | D2 antagonist (peripheral predominant) | Less CNS toxicity, but hyperprolactinaemia and QT prolongation/ventricular arrhythmia risk; avoid in known conduction disease or significant cardiac disease and with QT-prolonging/CYP3A4-inhibiting drugs; follow local ECG/electrolyte protocol [29] |
| Erythromycin | 3 mg/kg q8h IV | Motilin receptor agonist | Prolongs QTc; tachyphylaxis (motilin receptor downregulation) [1] |
| Gastric electrical stimulation | Device implant | Electrical pacing | Marginal benefit — mainly in diabetic gastroparesis [1] |
| G-POEM | Endoscopic procedure | Pyloromyotomy | Modest benefit [1] |
No use: intra-pyloric botulinum toxin injection [1]
Nutritional support hierarchy: [1]
- NG tube for decompression; NJ tube for temporary feeding (post-pyloric preferred)
- PEG-J (percutaneous endoscopic gastrostomy with jejunal extension)
- Jejunostomy ± gastrostomy for venting
Part 4: Benign Esophageal Lesions
Mostly asymptomatic, incidentally found during endoscopy for other reasons. Rare, prevalence ≤ 0.5%. [1]
Epithelial lesions vs. sub-epithelial lesions. Endoscopic ultrasound (EUS) is helpful for sub-epithelial lesions. Biopsies may be helpful sometimes. [1]
EUS layer anatomy (exam favourite):
- A (superficial mucosa/luminal interface) — hyperechoic
- B (deep mucosa, including muscularis mucosae) — hypoechoic
- C (submucosa) — hyperechoic
- D (muscularis propria) — hypoechoic
- E (adventitia) — hyperechoic
Mnemonic: alternate echogenicity starting with bright at the luminal surface. The slide's cross-section and EUS image align A→E from lumen outward; layer of origin narrows the differential and guides tissue acquisition [1].
| Condition | Incidence | Key Points |
|---|---|---|
| Heterotopic gastric mucosa | 0.1-10% | Must differentiate from Barrett's esophagus (heterotopic = congenital island of gastric mucosa, usually in cervical esophagus; Barrett's = metaplasia at distal esophagus from chronic acid exposure) [1] |
| Squamous cell papilloma | 0.01-0.45% | Hypothesis: chronic mucosal irritation, HPV infection [1] |
| Xanthoma | Unknown | Ectopic xanthoma in GIT (stomach 75%, esophagus 12%, duodenum 12%). NOT necessarily associated with hypercholesterolaemia. Hypothesis: focal mucosal damage → lipids from broken-down cell membranes captured by interstitial histiocytes [1] |
| Acanthosis glycogenes | Unknown | Glycogen accumulation in squamous epithelium; no clinical significance [1] |
Endoscopic appearance atlas: an inlet patch is a discrete salmon-coloured island in the proximal/cervical esophagus, separate from the gastroesophageal junction; squamous papilloma is a small pale exophytic/warty nodule; xanthoma appears yellow-white and granular; glycogenic acanthosis produces multiple oval, slightly raised grey-white plaques [1]. Appearance suggests a diagnosis, but histology is required when the lesion is atypical or clinically consequential.
| Condition | Frequency | Layer of Origin | Key Points |
|---|---|---|---|
| Leiomyoma | Most common benign esophageal neoplasm (2/3 of all tumors) | Muscularis propria | Can cause dysphagia; malignant transformation rare [1] |
| Granular cell tumor | 2nd most common | Submucosa (Schwann cell origin) | 1-3% can be malignant [1] |
| Hemangioma | 0.04% | Vascular | Red-blue compressible vascular-appearing bump; differentiate from esophageal varices and do not blindly biopsy a suspected vascular lesion [1] |
| Neuroendocrine tumor (historically “carcinoid”) | Rare (more common in small bowel, stomach) | Mucosa/submucosa | Smooth polypoid lesion; chromogranin and synaptophysin positive; may be functional [1] |
| GIST | Extremely rare in esophagus (most common in stomach/SI) | ICC origin, usually muscularis propria | Often a hypoechoic muscle-layer mass; commonly KIT/CD117 positive; has a risk continuum for malignant behaviour based on site, size, mitotic rate, and rupture [1] |
Leiomyoma vs. GIST
Both can appear as smooth subepithelial bulges arising from the muscularis propria. EUS defines the layer and morphology but may not reliably distinguish them; a muscularis-propria lesion generally requires EUS-guided tissue acquisition when the result will change management. Immunohistochemistry then distinguishes leiomyoma from GIST. Manage GIST according to its graded malignant-risk profile rather than assuming identical behaviour in every lesion [1] [30].
Appear as tortuous, dilated blue veins running along the long axis of the esophagus [1]. The photographs progress from small/minimally raised columns to medium and large columns occupying increasing luminal circumference. Varices are portal-systemic collaterals with major bleeding risk, not benign neoplasms; do not biopsy. The slide's small/medium/large grading is descriptive and historical.
| Condition | Key Features |
|---|---|
| Zenker's diverticulum | Pharyngeal pouch; posterior herniation through Killian's dehiscence above the cricopharyngeus. The barium swallow shows a posterior contrast-filled pouch. Think regurgitation of undigested food, halitosis, dysphagia, cough/aspiration—not primary vomiting [1] |
| Paterson-Brown Kelly syndrome (= Plummer-Vinson syndrome) | Triad: dysphagia + iron deficiency anaemia + esophageal webs. On barium swallow, a cervical web is a thin shelf-like indentation/narrowing. It is associated with increased upper aerodigestive squamous-cancer risk [1] |
Exam Intelligence
| Year/Paper | Relevant Question | Key Concept |
|---|---|---|
| 2022 MCQ Q40 [18] | Long-term PPI side effects | Historical slide answer: enteric infections; current counselling emphasizes association versus causation and ongoing indication |
| 2016 SAQ Q6 [17] | Barrett's esophagus from chronic GERD | Predisposing factors, staging investigations, standard treatment |
| 2018 Minicase [19] | Epigastric pain → perforation | Background of chronic dyspepsia + NSAIDs/migraine meds → perforated PUD workup |
| Trap | Correct Answer |
|---|---|
| "GERD is caused by hiatus hernia" | Hiatus hernia is a mechanical risk factor, but neither necessary nor sufficient |
| "Normal OGD excludes GERD" | 70% of GERD is NERD — normal OGD does NOT exclude GERD |
| "PPI causes osteoporosis/dementia" | Observational association does not establish causation; review indication instead of stopping an indicated PPI because of theoretical harms |
| "Botulinum toxin injection is useful for gastroparesis" | No — intra-pyloric botulinum toxin injection has NO demonstrated benefit |
| "Domperidone can be given IV" | Domperidone is oral only |
| "Metoclopramide is only a prokinetic" | It is ALSO a central anti-emetic (D2 antagonist at CTZ) |
Q: Name the anti-reflux barriers. → "LES (resting pressure ~10 mmHg, intra-abdominal location); diaphragmatic hiatus (crural muscle + phrenoesophageal ligaments); angle of His (oblique esophago-gastric junction creating flap valve effect)."
Q: How is ambulatory reflux monitoring interpreted? → "The lecture's historical catheter threshold is pH < 4 for ≥4.2% of recording time. Current Lyon 2.0 interpretation uses AET: > 6% supports GERD, < 4% is physiologic evidence against GERD, and 4–6% is inconclusive; impedance adds event composition, direction, and symptom association."
Q: Describe the management algorithm for uninvestigated dyspepsia in a 45-year-old. → "No alarm symptoms and age < 60: test for H. pylori (UBT or stool antigen). If positive → eradicate. If negative or persistent symptoms post-eradication → empirical PPI trial. If still symptomatic → OGD."
High Yield Summary
-
GERD
- = reflux causing symptoms/complications.
- Anti-reflux barriers: LES, diaphragmatic hiatus, angle of His.
- Aggravating: tLESR, hiatus hernia, impaired peristalsis, acid pocket. A normal OGD does not exclude GERD.
- Diagnosis: an 8-week PPI trial may support but does not prove GERD. Ambulatory reflux monitoring provides objective evidence; OGD assesses alarms, alternative diagnoses, and complications.
- LA classification A-D.
- Treatment: lifestyle → PPI (30-60 min pre-meal) → H2RA add-on → surgery.
- PPI safety: review the indication and use the lowest effective dose; do not stop an indicated PPI because of unproven observational associations.
- Maintenance PPI: important for LA C/D, peptic stricture, and other established chronic indications.
-
Dyspepsia
- If age < 60 → test-and-treat H. pylori → empirical PPI; consider endoscopy and further therapy according to response, alarm features, and risk. Functional dyspepsia requires compatible Rome IV symptoms without explanatory structural disease; PDS and EPS can overlap.
-
Vomiting
- emetic centre in medulla.
- Check pregnancy testing when relevant; target electrolytes, ECG, and imaging to the presentation and severity.
- Anti-emetics: metoclopramide (D2 + 5HT4), domperidone (oral only, less CNS), ondansetron (5HT3), erythromycin (motilin agonist, for gastroparesis).
-
Gastroparesis
- delayed emptying + no obstruction. ICC depletion. Scintigraphy: < 10% retention at 4 hr = normal. Treat: metoclopramide, domperidone, erythromycin. No botulinum toxin.
-
Benign esophageal lesions
- Leiomyoma (most common, usually muscularis propria). GIST often expresses KIT/CD117 and has a graded malignant-risk profile. Zenker's diverticulum is a posterior pharyngeal pouch; Plummer-Vinson syndrome combines dysphagia, iron-deficiency anaemia, and esophageal webs.
Active Recall - Lecture Notes
[1] Lecture slides: GC 068. Indigestion and 'heartburn'.pdf (all pages) [2] Senior notes: Block A - Indigestion and 'heartburn': nausea and vomiting; gastric motility problems; benign esophageal lesions.pdf [3] Senior notes: Ryan Ho GI.pdf (pages 57, 63, 75, 94) [4] Senior notes: Maksim Medicine Notes.pdf (page 122) [5] Senior notes: Maksim Surgery Notes.pdf (page 57) [6] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (page 676) [7] Senior notes: Block A - Introduction to GI_Hepatology investigations (LFT, Endoscopy).pdf (pages 19, 21) [8] Senior notes: Block A - Coffee ground vomitus tarry stool upper GI bleeding.pdf (pages 5, 30) [9] Senior notes: Block A - Gastroenterology Interactive Tutorial.pdf (page 1) [10] Senior notes: Block A - Gastrointestinal Data Interpretation.pdf (page 2) [11] Senior notes: Adrian Lui Pediatrics Notes.pdf (page 253) [12] Senior notes: Ryan Ho Cardiology.pdf (pages 54, 56) [13] Senior notes: Ryan Ho Fundamentals.pdf (page 268) [14] Senior notes: Block A - Chronic diarrhoea_ irritable bowel syndrome and inflammatory bowel disease.pdf (page 1) [15] Senior notes: Block A - I am overweight, doctor_ obesity; Hyperlipidaemia.pdf (page 6) [16] Senior notes: Block A - Pallor_ diagnosis of anaemia; nutritional anaemia; anaemia of systemic diseases.pdf (page 10) [17] Past papers: 2016 Fourth Summative SAQ.pdf (page 3, Q6) [18] Past papers: 2022 Fourth Summative MCQ.pdf (page 15, Q40) [19] Past papers: 2018 Fourth Summative Minicase.pdf (page 9) [20] Medicine Lecture Slides: Gastroenterology - Two cases of dyspepsia.pdf (page 13) [21] Katz PO, Dunbar KB, Schnoll-Sussman FH, et al. ACG Clinical Guideline for the Diagnosis and Management of Gastroesophageal Reflux Disease. Am J Gastroenterol. 2022;117:27-56. https://pmc.ncbi.nlm.nih.gov/articles/PMC8754510/ [22] American Gastroenterological Association. Diagnosis and management of extraesophageal gastroesophageal reflux disease (GERD). https://gastro.org/clinical-guidance/diagnosis-and-management-of-extraesophageal-gastroesophageal-reflux-disease-gerd/ [23] Gyawali CP, Yadlapati R, Fass R, et al. Updates to the modern diagnosis of GERD: Lyon consensus 2.0. Gut. 2024;73:361-371. https://pmc.ncbi.nlm.nih.gov/articles/PMC10846564/ [24] Yadlapati R, Kahrilas PJ, Fox MR, et al. ACG Clinical Guidelines: Clinical Use of Esophageal Physiologic Testing. Am J Gastroenterol. 2022;117:1412-1428. https://pmc.ncbi.nlm.nih.gov/articles/PMC9468980/ [25] Targownik LE, Fisher DA, Saini SD. AGA Clinical Practice Update on De-Prescribing of Proton Pump Inhibitors: Expert Review. Gastroenterology. 2022;162:1334-1342. https://gastro.org/clinical-guidance/de-prescribing-proton-pump-inhibitors-ppis/ [26] Moayyedi PM, Lacy BE, Andrews CN, Enns RA, Howden CW, Vakil N. ACG and CAG Clinical Guideline: Management of Dyspepsia. Am J Gastroenterol. 2017;112:988-1013. https://pubmed.ncbi.nlm.nih.gov/28631728/ [27] Camilleri M, Chedid V, Ford AC, et al. ACG Clinical Guideline: Gastroparesis. Am J Gastroenterol. 2022;117:1197-1220. https://pmc.ncbi.nlm.nih.gov/articles/PMC9373497/ [28] US Food and Drug Administration. Reglan (metoclopramide) prescribing information. 2026. https://www.accessdata.fda.gov/drugsatfda_docs/label/2026/017854s071lbl.pdf [29] European Medicines Agency. Domperidone-containing medicines: referral and risk-minimisation recommendations. https://www.ema.europa.eu/en/medicines/human/referrals/domperidone-containing-medicines [30] American Gastroenterological Association. Management of subepithelial lesions encountered during routine endoscopy. 2022. https://gastro.org/clinical-guidance/management-of-subepithelial-lesions-sel-encountered-during-routine-endoscopy/
GC067 I Keep On Bumping Into People On My Side
Homonymous hemianopia is the loss of vision in the same half of the visual field in both eyes, typically caused by a lesion in the contralateral optic tract, lateral geniculate nucleus, optic radiation, or occipital cortex, leading patients to collide with objects or people on their blind side.
GC069 Inherited Cardiac Conditions
Inherited cardiac conditions are a group of genetically determined disorders affecting the heart's structure, rhythm, or function—including cardiomyopathies, channelopathies, and familial aortopathies—that predispose affected individuals to arrhythmias, heart failure, and sudden cardiac death.