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MBBS VI - SpC - Medicine > GI - Dysphagia, GERD, Esophageal Cancer > Flashcards

GI - Dysphagia, GERD, Esophageal Cancer Flashcards

1
Q

Define Dysphagia, Oropharyngeal dysphagia and Esophageal dysphagia

A

Dysphagia: difficulty in swallowing, Failure to clear good and drink through upper digestive tract into stomach at appropriate rate

Oropharyngeal dysphagia

  • Difficulty with initial phases of swallowing, from mouth to esophagus
  • Usually functional (i.e. due to neuromuscular diseases)

Esophageal dysphagia

  • failure of peristaltic delivery of food through oesophagus
  • Can be functional or mechanical
  • Sensation of food or liquid obstructed in passage from mouth to stomach
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2
Q

Define 3 physiological phases of swallowing

A

Oral phase
Oropharyngeal phase
Esophageal phase

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3
Q

Describe oral phase of swallowing

A

Oral phase: voluntary, striated muscles

→ Mastication of solid to form food bolus
→ Tongue movement to achieve glossopalatal seal → push food bolus or fluid against hard palate

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4
Q

Describe oropharyngeal phase of swallowing

A

Oropharyngeal phase: involuntary

→ Activation of mechanoreceptors of pharynx → initiation of swallowing reflex

→ Soft palate elevates (levator veli palatini) → nasal cavity closed off

→ Larynx elevates (suprahyoid muscles) → larynx closed off (by epiglottis)

→ Pharyngeal muscles contract → food bolus delivered from pharynx into oesophagus

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5
Q

Describe esophageal phase of swallowing

A

Oesophageal phase: involuntary
→ Peristaltic movement of muscularis propria
→ food bolus delivered into stomach

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6
Q

Neurological control of swallowing

A
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7
Q

3 key questions for suspected dysphagia

A
  1. Is it real dysphagia? Globus hystericus or Odynophagia?
  2. Oropharyngeal or Esophageal dysphagia?
  3. Mechanical/ anatomical or Functional motility problem?
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8
Q

Causes of oropharyngeal dysphagia

  • Functional?
  • Mechanical?
  • Iatrogenic?
A

Functional:
- Diseases of CNS:
Bulbar palsy, pseudobulbar palsy, Parkinson’s disease
- Diseases of motor neurones:
Motor neuron disease, peripheral neuropathy, poliomyelitis, syphilis
- Diseases of NMJ/muscles:
Myasthenia gravis, myopathies (muscular dystrophy, polymyositis, dermatomyositis)

Mechanical:
- Mural causes:
Pharyngeal pouch, oropharyngeal tumours, strictures
- Extramural causes:
Goitre, lymphadenopathy, cervical osteophytes, retropharyngeal abscess

Iatrogenic:
- Radiotherapy causing salivary gland atrophy

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9
Q

Causes of esophageal dysphagia

A

Primary motility disorders:
Achalasia, diffuse oesophageal spasm, nutcracker oesophagus, hypertensive LES

Secondary motility disorders:
Diabetic neuropathy, scleroderma, Sjogren’s syndrome, multiple sclerosis

Intraluminal causes:
Foreign bodies (fishbone commonest), lower oesophageal rings, oesophageal webs

Mural causes:
Oesophageal/cardia tumours, oesophagitis, strictures

Extramural causes:
Anterior mediastinal masses, CA lung, TB, cardiovascula

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10
Q

Esophagitis:

Causes

A

Peptic: acid reflux
Post-radiation
Chemical

Infectious:
Healthy: Candida albicans, HSV
HIV: fungal, viral (esp CMV), mycobacteria, protozoan, ulcers

Drugs:
tetracyclines, NSAIDs, KCl, alendronate

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11
Q

Extramural causes of esophageal dysphagia

A

Anterior mediastinal masses (thyroid, thymus, teratoma, terrible lymphoma)
CA lung
TB

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12
Q

S/S of oropharyngeal dysphagia

A
  • Difficulty in initiating swallowing
  • Nasal regurgitation, choking and weak cough
  • Halitosis
  • Recurrent aspiration pneumonia
  • A/w other neurological signs:
     Nasal speech (soft palate paralysis)
     Drooling of saliva, dysarthria
     Dysphonia
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13
Q

S/S esophageal dysphagia

A

C/O food getting stuck in throat or chest

Region localized is poorly correlated with exact site of abnormality
 Retrosternal: usually corresponds to site
 Suprasternal: commonly referred from below

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14
Q

Differentiate mechanical vs functional cause of dysphagia

  • Onset
  • Progression
  • Solid and fluid swallowing
  • Variation with temp.
  • Intermittent causes
  • Progressive causes
A
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15
Q

Explain why pharyngeal pouch can cause halitosis

A

Zenker diverticulum/ Pharyngeal pouch

Outpouching arise from the Kilian Dehiscence between thyro- and cricopharyngeus

Cricopharyngeal (CP) muscle fails to relax during swallowing + Incoordination of swallowing within pharynx → herniation through cricopharyngeus muscle
→ formation of a pouch

> > Easy to lodge food there and causing dysphagia and foul smell

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16
Q

Ddx intermittent mechanical dysphagia

A

Webs and rings

  • hiatus hernia (97%) and eosinophilic oesophagitis
  • Plummer-Vinson syndrome, Zenker’s diverticulum, bullous dermatological disease and GVHD

Esophagitis

CVS causes (rare)

  • Dysphagia lusoria due to aberrant right subclavian artery
  • Dysphagia aortica due to thoracic aorta aneurysm
  • Dysphagia megalatriensis due to LA dilatation
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17
Q

Ddx progressive mechanical dysphagia

A

Benign strictures

  • Reflux: acid regurgitation, heartburn
  • Post-RT strictures
  • Previous oesophagitis

CA oesophagus, cardia of stomach
- RFs of CA oesophagus, eg. chronic GERD, smoking, FHx

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18
Q

Ddx Functional esophageal dysphagia

A

Achalasia

  • progressive dysphagia
  • regurgitation of undigested food/saliva
  • Must exclude pseudoachalasia due to carcinoma infiltrating myenteric plexus

Other motility disorder:

  • intermittent, non-progressive dysphagia
  • Hypertensive disorders, eg. diffuse oesophageal spasm, nutcracker oesophagus

Scleroderma/ Systemic sclerosis

  • a/w heartburn (GERD symptom) and progressive dysphagia
  • Look for systemic features: Calcinosis, Raynaud’s phenomenon, Esophageal dysmotility, Sclerodactyly, Telangiectasia
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19
Q

Ddx Odynophagia and dysphagia

A

□ Oesophagitis: drug-induced, radiation, infectious, reflux
□ Caustic ingestion
□ Late CA oesophagus

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20
Q

Specific investigations for dysphagia

A

Video fluoroscopy swallowing study (VFSS)

Barium swallow

Upper Endoscopy

Fiberoptic endoscopic evaluation of swallowing (FEES)

High resolution manometry (HRM)

Endoluminal Functional Lumen Imaging Probe (EndoFLIP)

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21
Q

Outline different types of Primary esophageal motility disorders

A

Achalasia
- Hypertensive LES + hypoperistalsis

Hypercontracting oesophagus

  • Hypertensive LES
  • Nutcracker/jackhammer oesophagus
  • Hypertensive peristalsis

Hypocontracting oesophagus

  • Hypotensive LES
  • Ineffective oesophageal motility (IEM)

Dyscoordinated motility
- Diffuse oesophageal spasm

22
Q

Outline different types of secondary esophageal motility disorders

A

Systemic sclerosis
- Hypotensive LES + distal hypoperistalsis + normal proximal oesophagus and UES

Chagas’ disease
- Hypertensive LES + hypoperistalsis (= idiopathic achalasia)

DM neuropathy

Sjogren’s syndrome

23
Q

Management options for esophageal motility disorders

A

□ Antispasmodics: CCB, nitrates, anticholinergics

□ Surgical options:
→ Endoscopic pneumatic dilatation
→ Surgical or minimally invasive myotomy
→ Intrasphincteric injection of botox

□ Psychological Mx:
→ Benzodiazepines, anxiolytics, antidepressants
→ Psychological and behavioural therapies
→ Reassurance

24
Q

Achalasia

  • Characteristic features
  • Demographics
A

characterized by
□ Hypertonic LES
□ Failure of LES to relax in swallowing
□ Hypoperistalsis: failure of propagation of oesophageal contraction → progressive dilatation of oesophagus

Demographics: M:F ≈ 1:1, age infancy to 9th decade (but majority 20-40y)

25
Q

Causes of Achalasia

A

□ Primary (idiopathic): HLA-DQw1 and HSV-1 infection

□ Secondary: Chagas’ disease, infiltrative (amyloidosis, sarcoidosis), paraneoplastic (CA lung, cholangiocarcinoma)

□ (Pseudoachalasia): OGJ cancer → mechanical obstruction + infiltration of nerve plexus

26
Q

Pathophysiology of idiopathic achalasia

A

Normal innervation by
→ Excitatory (cholinergic) motor neurones
→ Inhibitory (nitric oxide) motor neurones

Early: loss of inhibitory neurones → ↑basal LES pressure + failure of LES relaxation during swallowing

Later: loss of excitatory neurones → oesophageal hypo/aperistalsis

27
Q

Clinical features of Achalasia

Complications of achalasia

A

□ Progressive dysphagia:
→ Initially intermittent, gradually worsens
→ Worse for solids, eased by drinking liquids, by standing and moving around after eating

□ Regurgitation: immediately after meals

□ Cough: esp when recumbent

□ chest pain due to oesophageal spasms (may not resolve even after treatment)

□ Recurrent aspiration pneumonia/bronchitis in late stages

Complications:
□ SCC of oesophagus (28× risk)
□ Food stasis may result in erosions or candida oesophagitis

28
Q

Manometric subtypes of achalasia

Function of sub-typing

A

therapeutic and prognostic significance

□ Type I (classic): impaired LES relaxation + no oesophageal body pressurization
□ Type II (compressive): impaired LES relaxation + oesophageal compression
□ Type III (spastic): impaired LES relaxation + spastic oesophageal contractions

29
Q

Investigations and typical findings for achalasia

A

OGD + Biopsy: mainly to r/o pseudoachalasia
→ Dilated oesophagus with stasis of food and secretions (frothy)
→ LES appears tight

CXR:
→ Widened mediastinum with air-fluid level
→ Absence of gastric air bubble

Barium swallow: bird’s beak / rat’s tail appearance
→ Tapered narrowing of lower oesophagus
→ Dilated proximal oesophagus + air-fluid level in late stage
→ Obstruction often relieved by drinking more fluid

High-resolution manometry: for definitive diagnosis
→ Aperistalsis with low-amplitude simultaneous oesophageal body contraction
→ Hypertensive LES (>45mmHg) + pressurized oeso body
→ Failure of LES relaxation (>8mmHg) with swallowing

30
Q

List treatment options for different manometry subtypes of achalasia

A

Pneumatic dilatation / surgery for type I/II
POEM for type III

Options:
- Endoscopic pneumatic dilatation: Dilatation of LES using endoscopically placed balloon

  • Surgical myotomy (Heller’s operation) + partial fundoplication: Laparoscopic or open cutting of LES fibers + reduce GERD symptoms
  • Peroral endoscopic myotomy (POEM): endoscopic diathermy of LES muscles
  • Endoscopic botox injection, Nitrates / CCB if failed botox
  • Oesophagectomy in end-stage
31
Q

Diffuse esophageal spasm

  • Clinical presentation
  • Investigations and typical findings
  • Management
A

Clinical presentation:
□ Late middle age
□ Episodic chest pain (may mimic angina)
□ Sometimes a/w transient dysphagia or occur in response to gastroesophageal reflux

Ix:
Manometry:
→ Simultaneous contraction of oesophageal body
→ Intact LES relaxation**
Barium swallow: cockscrew appearance**
→ Due to simultaneous contractions of circular muscle of oesophageal body

Mx:
□ PPI when gastroesophageal reflux is present
□ Oral/sublingual nitrates or nifedipine to relieve attacks of pain

32
Q

Zenker’s diverticulum

  • Pathogenesis
  • S/S
  • Ix
  • Tx
A

Pathology:
□ Cricopharyngeus and thyropharyngeus do not overlap → physiological weak spot
□ Incoordination of swallowing within pharynx → herniation through cricopharyngeus muscle → formation of a pouch

S/S:
□ asymptomatic
□ long Hx of halitosis and recurrent sore throats
□ Regurgitation: food without acid/bitter taste
□ Dysphagia if pressing on oesophagus
□ ± neck swelling

Ix:
□ Barium swallow: visualizes pouch, incoordination of swallowing ± pulmonary aspiration
□ C/I endoscopy: risk of perforation!!

Mx:
□ Surgical myotomy ± resection of pouchq

33
Q

Medications that cause esophageal ulceration?

A

Pills that lodge in esophageal wall can cause erosions:

NSAIDs
Tetracyclines
Potassium chloride
Alendronate

34
Q

GERD

  • Pathophysiology
  • Complications
A

Reflux: reflux of gastric content into lower oesophagus due to
→ Incompetent LES (hiatus hernia or dietary factors)
→ Increased intra-abdominal pressure due to obesity, tight garments, large meal, pregnancy
→ Gastric dysmotility: gastric emptying often delayed

Acid damage: mucosal inflammation due to exposure to acidic gastric content
→ Gastric content: acid, pepsin, bile
→ Ineffective oesophageal clearance

Chronic inflammation causes complications 
→ Oesophagitis
→ Strictures
→ Barrett’s oesophagus
→ Adenocarcinoma
35
Q

Risk factors of GERD

A

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

High intra-abdominal pressure: pregnancy, chronic cough, obesity, constipation

36
Q

Clinical presentation of GERD

A

Heartburn and regurgitation
- characteristically posturally aggravated

Water brash: reflex salivary gland stimulation as acid enters throat

Odynophagia due to oesophagitis and ulcers

Dysphagia due to strictures

Extra-oesophageal symptoms

  • Laryngo-pharyngeal reflux (LPR)
  • Asthma
  • Recurrent chest infections
  • Dental erosions
  • Sleep disturbances

(large overlap between GERD, NCCP and dyspepsia)

37
Q

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%)

38
Q

Diagnosis of GERD

A

Non-invasive tests for clinical diagnosis
→ Clinical symptomatology ± diagnostic questionnaire
→ Proton pump inhibitor test (PPI test)

OGD

24h oesophageal impedance pH testing: GERD symptoms refractory to treatment

Manometry

39
Q

Management of GERD

A
  1. 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)
  2. Medication:
    → Acid-reducing agents: antacids, H2RA, PPI
    → Prokinetics: metoclopramide, cisapride
  3. Surgery, eg. Nissen fundoplication
40
Q

Esophageal cancer

  • 2 main histological subtypes
  • Prevalence and demographics
A

Gender: M (9.9/100k) >F (2.3/100k)

Asian population, SCC > adenocarcinoma
Western population, adenocarcinoma > SCC

Incidence of SCC decreasing: less smoking
Incidence of Adenocarcinoma increasing: due to ↑obesity, ↑GERD

41
Q

Risk factors for SCC esophagus

A

Age >60y, male gender, FHx
Genetics: Peutz-Jegher syndrome, PTEN
Race: African, Asians

Smoking + alcohol**

Diet:
↓fresh vegetables/fruit
↑hot soup, beverages
↑pickles, salted fish (nitrosamines)
↓micronutrients, eg. β-carotene, folate, vitamin C/E, selenium

Oesophageal diseases
 Achalasia
 Caustic injuries/strictures
 Others, eg. Plummer-Vinson syndrome, diverticula, webs

H&N cancers: field cancerization by similar RFs

HPV infection

42
Q

Risk factors for esophageal adenocarcinoma

A

Age >60y, male gender, FHx

Race: Caucasians

Smoking (NOT alcohol)

Obesity and metabolic syndrome

Oesophageal diseases

  • Chronic GERD
  • Barrett’s oesophagus (40×)
43
Q

Compare SCC and adenocarcinoma of esophagus

  • Site
  • Pathogenesis
  • Metastasis propensities
  • Malignant behavior
A

SCC:

  • Middle 1/3 esophagus
  • Carcinoma-in-situ&raquo_space; invasive SC
  • Early invasion of submucosal wall, intrathoracic LN, trachea and aorta
  • Early metastasis (30% at presentation): liver, bone, lung

Adenocarcinoma:

  • Distal 1/3 esophagus, near EGJ
  • Chronic GERD&raquo_space; Barrett’s esophagus&raquo_space; dysplastic changes&raquo_space; invasive adenocarcinoma
  • Early LN invasion (lower abdominal LN)
  • Late metastasis to intra-abdominal organs
44
Q

Why does esophageal cancer carry poor prognosis?

A

□ Late presentation with early spread of disease
□ Anatomically deep-seated with important surrounding structures
□ Typically occur in elderly population with comorbid diseases

45
Q

Clinical presentation of esophageal cancer

A

Asymptomatic/non-specific for early stage disease

Progressive painless dysphagia, especially solids

Odynophagia: late extra-oesophageal involvement

Regurgitation

Systemic S/S:

  • Weight loss
  • Anaemia

Local invasion:

  • Profuse UGIB from vascular invasion
  • Recurrent pneumonia/ intractable cough from tracheobronchial fistula
  • Hoarseness from RLN invasion

Systemic metastatic S/S
- Bone, Liver, Lungs, Brain, LN …etc

46
Q

First-line investigations, staging Ix and expected findings for esophageal cancer

A

OGD + biopsy:
- Appearance: large mucosal mass pathognomonic

Barium swallow: irregular stricture with shouldering

Staging Ix:

  1. Endoscopic ultrasound (EUS) for T/N (locoregional) staging
  2. PET-CT for M (systemic) ± T/N staging
  3. Bronchoscopy for airway involvement
  4. Laryngoscopy
47
Q

Management of esophageal cancers:

  • Early cancer
  • Superficial cancers
  • Resectable local cancers
  • Unresectable cancer
A

Early: Endoscopic Tx

  • Endoscopic mucosal resection (EMR)
  • Endoscopic submucosal dissection (ESD)
  • ± adjuvant: photodynamic therapy (PDT), RFA

Superficial: Esophagectomy only

Resectable/ locally advanced: Resection + neoadjuvant chemo/RT + adjuvant chemo/RT (if adenocarcinoma)

Unresectable: Palliative chemo/RT

chemo/RT:
→ Cisplatin + 5-FU + RT for SCC
→ Carboplatin + paclitaxel + RT for adenocarcinoma

48
Q

Esophagectomy

Phases/ number of areas operated on
Fields of LN dissection

A

Phase, i.e. number of areas operated on

  • I: oesophagogastrectomy, transhiatal
  • II: Lewis-Tanner operation (most common)
  • III: McKeown operation

Field of LN dissection:

  • II: thorax + abdomen
  • III: thorax + abdomen + neck**
49
Q

Esophagectomy

  • Choices of conduits
  • Route of anastomosis
  • Approaches
A

→ Conduit: stomach, colon, jejunum

→ Route of anastomosis: orthotopic, retrosternal, subcutaneous (rare)

→ Approach: open, VATs, totally minimally invasive, robotic

50
Q

Complications of esophagectomy

A

CVS: post-oesophagectomy AF, acute MI, VTE

Pulmonary: atelectasis, pneumonia, ARDS, sputum retention

Surrounding structure injury:

  • RLN injury → hoarseness
  • Tracheo-bronchial injury → can lead to fistula formation

Anastomotic complications:

  • Anastomotic leak leading to mediastinitis
  • Anastomotic strictures due to healed anastomotic leaks
  • Conduit ischaemia

Chylothorax due to thoracic duct damage

Hiatal herniation of bowel

Post-esophageal GERD

MBBS VI - SpC - Medicine (80 decks)

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