GI & Hepatology JC074: Indigestion And "Heartburn": Nausea And Vomiting, Gasteric Motility Problems, Benign Oesophageal Lesions Flashcards
N+V
Vomiting:
- Nausea + Autonomic symptoms e.g. salivation —> **Forceful abdominal + thoracic muscle contraction associated with retching (coordinated)
- involves **Emetic centre to coordinate the actions
- **need to differentiate Acute vs Chronic vomiting (cutoff: **1 month)
Regurgitation:
- Sudden, **effortless return of small amount of gastric contents into pharynx / mouth
- **No Emetic centre involved
Rumination:
- Repetitive, effortless regurgitation of recently ingested food into mouth —> re-chewing / re-swallowing / expulsion
- Seen in ***psychiatric conditions
- Difficult to treat in clinical practice
Acute vomiting
Causes:
1. Abdominal
- **Intestinal obstruction
- Pseudo-obstruction
- **Acute pancreatitis
- ***Acute cholecystitis
- Infections
- ***GE - ***Toxins
- Staph aureus
- Bacillus cereus - Metabolic
- Renal failure
- Ketoacidosis
- ***Addison’s disease - ***CNS disorders
- Vestibular disorders
- Pregnancy
-
Drugs (most common cause)
- Narcotics
- Digitalis
- Chemotherapy
Investigations:
1. Abdominal pain
- **Amylase / Lipase (pancreatitis)
- **Erect / Supine AXR (obstruction: mechanical / pseudo —> Coiled spring sign (dilated air-filled SB in intussusception), String-of-pearls sign (bubbles trapped in bowel, gas not resorbed quickly enough due to obstruction))
- ***USG (cholecystitis)
- CT, MRI
- Fever, Diarrhoea, Food poisoning
- Stool tests - Abnormal mental status (CNS causes)
- CT, MRI - ***Review all drugs taken (drug most common cause of acute vomiting)
Chronic vomiting
Causes:
1. Gastric
- **Mechanical: Peptic ulcers, **Gastric cancer, **Gastric lymphoma, Pancreatic disease, Crohn’s
- **Functional: ***Gastroparesis (DM, scleroderma, metabolic, idiopathic), Drugs, After gastrectomy, Post-viral Functional dyspepsia, Anorexia nervosa, Eosinophilic esophagitis
-
**Small bowel dysmotility / **Intestinal pseudo-obstruction
- Drugs, Scleroderma, ***Diabetic gastroparesis (∵ damage to vagus nerve), Amyloidosis, Jejunal diverticulosis, Small bowel myopathy, Neuropathy - ***Psychogenic vomiting
- After emotional stress - ***Bulimia nervosa (eating disorder characterised by binge eating followed by purging)
- CNS disorders
- Drugs
- **Chemotherapy: Methotrexate, Tamoxifen, Azathioprine
- **OC pills
- Recreational drugs: Marijuana - Metabolic
- **Hyperthyroidism
- **Addison’s disease - Idiopathic
Complications of vomiting
- ***HypoK
- Dehydration
- ***Metabolic alkalosis
- Injury e.g. ***Mallory-Weiss tear
- ***Boerhaave syndrome (esophageal rupture)
Investigations for Gastric emptying
- ***Barium X-ray imaging
- ***CT, MRI for change in gastric volume
- Scintigraphy (radiolabelled isotope meal / drink)
- ***Real time USG
- ***Gastric impedance
- Breath tests (with 13C Octanoic acid)
Drugs for treating N+V
- ***Antihistamines: Dimenhydrinate, Promethazine, Meclizine, Cyclizine (for vestibular / motion sickness)
- ***Anticholinergic: Scopolamine (for vestibular / motion sickness)
- ***Phenothiazine (Typical antipsychotics): Prochlorperazine, Chlorpromazine
- Haloperidol
- ***Dopaminergic antagonist: Metoclopramide, Domperidone
- ***Serotonin receptor antagonist: Ondansetron
- Cisapride, Molsapride, Itopride
- Erythromycin
GERD
Develops when reflux of stomach contents causes **troublesome symptoms / complications
- **some GER is physiological (e.g. after meals), but are rare + most don’t cause symptoms / complications
Mechanism:
1. **Ineffective clearance of esophagus + gastric **dysmotility
2. **Defective LES (normally contracted at its natural state, if more lax / normal strength but transient relaxation (pathological) —> GERD)
(3. Hiatus hernia —> Tortuosity + Mechanical obstruction + Volvulus of herniated stomach
4. Acid pockets
5. **Increased intra-abdominal pressure (obesity, tight garment))
Epidemiology:
Disease of the West:
- more Hiatus hernia
- higher BMI
- 18% symptoms >= once per week (3.7% in HK)
- ↑ incidence in HK
Symptoms:
Typical
1. Heartburn + Acid regurgitation into mouth / pharynx
2. **Reflux chest pain syndrome (Non-cardiac chest pain)
3. **Acid feeling in stomach, dysphagia, waterbrash (↑ salivation due to indigestion)
Extra-esophageal symptoms
1. **Asthma, Chronic cough
2. Sleep disturbance
3. Laryngo-pharyngeal reflux
4. **Hoarseness of voice
5. Throat tightness (globus sensation)
6. ***Dental erosion
Complications:
1. **Esophagitis (Los Angeles classification)
2. **Esophageal ulcer
3. **Esophageal stricture
4. **Barrett’s esophagus
5. Adenocarcinoma of esophagus
NB: Overlap between GERD, Non-cardiac chest pain (NCCP), Dyspepsia!!!
Factors associated with GERD
More likely to be Cause of GERD:
Genetic:
- Parental family history
- GI disease / symptoms in immediate family
Demographic:
- Pregnancy
- Age
- ***BMI
- Education level
Behaviour:
- **Smoking
- **Alcohol
- ***Drug: Anticholinergic, Aspirin, NSAID
- Oral contraceptive, HRT (negatively associated)
- Coffee (negatively associated)
More likely to be Effect of GERD:
Comorbidity
- Dysphagia
- Dyspepsia
- Asthma
- Cough
- Hoarseness
- Angina
- Laryngitis
- Otitis
- Sinusitis
- Chest pain
- Anxiety / Depression
Classification of GERD based on endoscopy
- GERD without erosive esophagitis (60-80% of GERD patients)
- ***Non-erosive reflux disease (NERD)
- nothing to see on endoscopy - GERD with erosive esophagitis (20-35%)
- GERD with Barrett’s esophagus (1-5%)
Diagnosis of GERD
- ***PPI test
- give standard PPI for 1-4 weeks —> respond —> diagnose as clinical GERD
- PPI empirical trial can be considered as initial diagnostic step in patients with the disease spectrum of GERD
- diagnostic + therapeutic
- accurate + cost-effective in patients with symptoms suggestive of GERD, NCCP - Validated Chinese GERD questionnaire
- 7 questions
- frequency, severity of heartburn
- frequency, severity of feeling of acidity in stomach
- frequency, severity of acid regurgitation
- frequency of use of antacids
- score >=12: GERD -
**24 hour esophageal pH monitoring
- gold standard
- sensitivity in GERD with esophagitis (~90%), but in NERD **much lower
- expensive, not widely available, unpleasant to patient
- catheter with 2 antimony pH electrode, portable pH recorder, pH sensor —> 5cm above LES
- study is abnormal if total % of time with pH **<4 is >=4.2% / 6% in **distal esophagus
- patient need to record meal time (see relationship with meal), time of supine position
—> after meal: can be physiological
—> other times: can be pathological depending on duration
- ***Demeester score
- newer system: Catheter-free pH system (BRAVO pH capsule) —> transmit pH data to a pager worn by patient
—> advantages: wireless, convenient, can be placed during endoscopy, 48 hours recording, potentially >1 capsule can be placed at various levels, more specific + directed placement
—> disadvantages: if it is not acidic reflux but reflux of air, liquid, bolus, bile —> no pH change —> need to use Multichannel Intraluminal Impedance (MII) monitoring - Upper endoscopy / OGD / Gastroscopy
- useful in diagnosing **erosive GERD
- erosive esophagitis with known GERD (only 30% have something to see)
- but poor test for GERD (poor sensitivity) —> ∵ >50% have no esophagitis (NERD) —> normal endoscopy findings does **not exclude GERD
- invasive, expensive, uncomfortable
- only do when want to see other things e.g. H. pylori status, peptic ulcers
Types of GER
- Acidic reflux (most common)
- Bile (Duodeno-gastro-esophageal reflux)
- Bolus of food
- Liquid
- Air
If patient has other types of reflux other than acidic reflux —> pH monitoring is NOT useful
Multichannel Intraluminal Impedance (MII) monitoring
Measurement of resistance of electric conductivity during bolus movement inside esophagus
Air: high resistance
Liquid bolus: low resistance
Food: intermediate resistance
—> Impedance changes can be seen
Advantage:
- can detect ***ALL types of reflux (acidic / non-acidic)
Indication:
- reflux symptoms persist ***despite adequate acid suppression
- NERD with normal acid study
- visualise + characterise bolus antegrade + retrograde movement within esophagus (useful in rumination / regurgitation)
Applications:
1. Esophageal function test
- Swallow challenge
- Combined MII + ***manometry
- GERD monitoring
- Acid + Non-acid reflux monitoring
- Combined MII + ***pH monitoring
Aims of treatment of GERD
- ***Confirm diagnosis of reflux disease
- **Relief of reflux symptoms
- Reassurance of patients
- Healing of esophagitis if present
- Improve QOL
- ***Prevent long term complications (Barrett’s esophagus, Stricture, Adenocarcinoma of esophagus)
Treatment options in GERD
- Lifestyle modification
- smoking cessation
- **reduce weight
- **small meals, reduce fat (slow down gastric emptying)
- **allow time from dinner to bed (allow time for gastric emptying)
- **elevate head to bed
- ***avoid reflux-promoting agents e.g. alcohol, coffee (not evidence based)
- consider alternatives to reflux-promoting drugs e.g. Theophylline, Anticholinergics - Medication
- **PPI (standard dose BD **4-8 weeks) (taper down to H2 antagonist due to risk of gastric cancer (SpC FM))
- H2 receptor antagonists
- **Antacids
- **Prokinetics: Metoclopramide, Cisapride - Endoscopic therapy (experimental)
- Surgery (***Nissen fundoplication)
- young patients with Grade C / D GERD with complications associated with GERD
2 Choices of initial therapy
Traditional step-up:
Antacids —> H2 blocker —> PPI
- weeks to symptoms control
- slow esophagitis healing
- diagnostic uncertainty
- higher total drug cost
- higher consultation cost
High-level step down:
***Daily standard dose PPI
- symptom control <1 week
- rapid esophagitis healing
- diagnostic confirmation
- lower total drug cost
- lower consultation cost
General recommendations:
Initial therapy for esophagitis:
- Start with PPI —> trial of step down of intensity of therapy
- Most effective initial therapy —> also most cost effective
- ascending level of efficacy from H2 antagonist to PPI
Why are some patients difficult to treat even with PPI?
- Inappropriate advice on PPI
- **Nocturnal symptoms
- **Extra-esophageal manifestations (respond poorly to PPI)
Rmb:
- After treating with PPI —> only neutralise acid but not reflux —> patient will still have reflux (instead of acid just liquid / bolus / air)
