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Gastroenterology > Oesophageal Diseases > Flashcards

Oesophageal Diseases Flashcards

1
Q

What are the following 3 different forms of chemical signalling and examples

A
  1. Paracrine: a cell targets a nearby cell
    Eg: somatostatin - inhibits gastrin, GH
  2. Autocrine: a cell targets itself
    eg: insulin growth factor, gastrin - acid secretion
  3. Endocrine: cell targets a distant cell through the bloodstream
    Eg: insulin, gastrin (acid secretion)
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2
Q

What is the function of Cholecystokinin

A

Cholecystokinin stimulates the gallbladder to contract and release stored bile into the intestine. It also stimulates the secretion of pancreatic juice and may induce satiety.

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3
Q

Side effects of PPI

A 
- Cancer
Causes hypergastrinaemia where high gastrin levels are associated with CRC 
- Pneumonia
- Gastroenteritis
- Osteoporosis
- Low Mg 
- Can increase C diff

PPIs inhibit acid secretion, leading antral G cells to release gastrin, causing hypergastrinemia.

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4
Q

Causes of hypergatrinaemia

A
  • Prolonged acid inhibition - PPI or H2RA
  • Atrophic gastritis - pernicious anaemia, h pylori
  • Vagotomy/small bowel resection
  • Gastrin secreting tumours
  • Renal failure
  • Hypercalcaemia
  • Hyperlipidemia
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5
Q

What are the 2 forms of dysphagia?

A

Oropharyngeal Dysphagia
- Oropharyngeal dysphagia are unable to initiate the swallowing process despite several attempts to swallow.
- Unable to get food from oral cavity into oesophagus
- Causes: stroke, dementia, neurological disorders
- Ix: modified barium swallow, speech path
Key Symptoms of Oropharyngeal Dysphagia
- delayed/absent swallow initiation
- nasal regurg
- deglutitive cough
- need for repetitive swallows

Esophageal Dysphagia
- Problem is getting food down the esophagus
- Causes
Mechanical - strictures, cancer
Dysmotility - achalasia, spasm, scleroderma
Both - eosinophilic esophagitis
- Ix: gastroscopy, barium swallow, manopmetry

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6
Q

What are features of Zenker diverticulum?

A
  • A Zenker’s diverticulum, also pharyngeal pouch, is a diverticulum of the mucosa of the human pharynx

Clinical Features (due to food being stuck in the pouch)
- Regurgitation of
undigested food hours after eating
- Gurgling noise in the neck
- Dysphagia
- Halitosis, smelly breath, as stagnant food is digested by microorganisms
- Cervical webs are seen associated in 50% of patients with this condition.

  • The initial test of choice for evaluation of oropharyngeal dysphagia is a modified barium swallow,
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7
Q

What does esophageal dysphagia to solid or liquids mean?

A

Esophageal dysphagia to solid foods suggests mechanical
obstruction
- Dysphagia to liquids or both solids and liquids suggests a motility disorder.
- Upper endoscopy is the most appropriate test for esophageal dysphagia; it allows for both diagnostic intervention (biopsies and inspection) and therapeutic intervention (dilation).

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8
Q

What are luminal causes of esophageal obstruction?

A

Luminal causes of obstruction may include benign strictures, malignancy, esophageal webs (may be associated with iron deficiency anaemia), or a Schatzki ring

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9
Q

What are causes of odynophagia?

A

The most common causes of odynophagia are:

  • caustic ingestion
  • pill-induced damage
  • infection with Candida, herpesvirus, or cytomegalovirus
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10
Q

Features of achalasia

A
  • Motility disorder of the oesophagus that results in aperistalsis and INADEQUATE RELAXATION of the LOWER esophageal sphincter (LES).

Pathophysiology: Failure of oesophageal peristalsis and of relaxation of the lower oesophageal sphincter (LOS) due to degenerative loss of ganglia from Auerbach’s plexus

Clinical Features

  • Dysphagia to both solids + liquids
  • Regurgitation of undigested bland food and saliva
  • Weight loss, chest pain, heart burn
  • Does not respond to PPI
  • Aspiration

Ix:

  • Barium swallow: dilation of the oesophagus and narrowing of the gastroesophageal junction - “bird beak” appearance
  • Manometry: most sensitive test to demonstrate incomplete LES relaxation and peristalsis
  • Upper Endoscopy: used to exclude mechanical obstruction, will show retained food + saliva (not that useful but obligatory)
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11
Q

What are causes of secondary achalasia?

A

Caused by extrinsic compression after fundoplication or gastric band weight loss surgery or mass

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12
Q

Treatment for achalasia

A
  • Treatment is directed at lowering LES pressure and alleviating symptoms
  • 1st line: POEM (peroral endoscopic myotomy)
  • Non Surgical/2nd line: Endoscopic pneumatic dilation of LOS, main complication is perforation
    Mortality low, quick procedure, 80-90% response, low recurrence
  • Surgical: Laparoscopic surgical myotomy leading to disruption of the circular muscle fibres
  • Can also try endoscopic injection of botulin toxin which inhibits acetylcholine release, leading to LES relaxation but normally used for patients who cannot tolerate other definitive treatment

For those that are not candidates for endoscopy:
PHARMCOTHERAPY
- Calcium channel blockers - nifedipine
- Long acting nitrates

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13
Q

What is a rare complication of achalasia?

A

There is an associated risk of squamous cell esophageal
cancer in patients who have had achalasia for more than 10
years. Given the very low incidence of malignancy, endoscopic surveillance has not been widely recommended in these patients.

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14
Q

The manometric feature most characteristic of achalasia is:
A. lack of peristalsis in the oesophageal body.
B. high resting tone of the lower oesophageal sphincter.
C. failure of lower oesophageal sphincter relaxation with
swallowing.
D. poor propagation of oesophageal contraction waves.
E. diffuse spasm in the oesophageal body.

A

C. failure of lower oesophageal sphincter relaxation with

swallowing.

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15
Q

What is the most common cause of infectious oesophagitis?

A

Candida - fluconazole
Others include:
- HSV : acyclovir
- CMV: ganciclovir, valganciclovir

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16
Q

What medications cause pill induced esophagitis?

A
  • Aledronate
  • Quinidine
  • Tetracycline
  • Doxycycline
  • Potassium chloride
  • Ferrous sulfate
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17
Q

Features of eosinophilic esophagitis

A
  • Defined as esophageal squamous mucosal inflammation caused by eosinophilic infiltration.
  • The classic presentation of EoE is an atopic man in
    the third decade of life with solid-food dysphagia and food impactions requiring removal by endoscopy.
  • EoE has been associated with food allergies, asthma, and eczema.

Symptoms:

  • Dysphagia
  • Classically - young male patient, present with food bolus obstruction, hx of atopy

Ix:

  • Upper endoscopy: concentric rings, “corrugated iron” and longitudinal furrows
  • Esophageal biopsies: > 15 eosinophils per high-power field.
  • PPI trial: Patients with esophageal eosinophilia should undergo an 8-week trial of a PPI; clinical response to the PPI trial indicates GERD-associated eosinophilia rather than EoE.
  • If esophageal eosinophilia is still present on repeat endoscopy, this confirms a diagnosis of EoE.
18
Q

Risk factors for eosinophilic esophagitis and clinical features

A

Risk Factors

  • Allergies/ asthma: suffering from food/ environmental allergies or atopic dermatitis and asthma increases the risk of diagnosis
  • Male sex
  • Family history of eosinophilic oesophagitis or allergies
  • Caucasian race
  • Age between 30-50
  • Coexisting autoimmune disease e.g. coeliac disease
Clinical Features 
Patients typically present with a subacute onset of:
- dysphagia
- food impaction (55%)
- Chest pain
- Heartburn and refractory "GERD"
- regurgitation/ vomiting
- anorexia
19
Q

Treatment for eosinophilic esophagitis

A
  1. PPI Trial - 85% effective
  2. Dietary Modifications
    - Elemental diet (involves taking an amino acid mixture for six weeks)
    - 6 food elimination diet (involves avoiding foods commonly associated with allergy e.g. nuts, soy, egg, seafood, wheat, dairy)
    - Targeted elimination diet
  3. Topical steroids e.g. fluticasone - this requires the patient to swallow solutions of the steroid to line the oesophagus - risk of thrush

Oral steroid (budesonide) +/- immunosuppression

  1. Oesophageal dilatation: 56% of patients require this at some point in their treatment to reduce the symptoms associated with oesophageal strictures
  2. New medication: Dupilimumab IL4/13 monoclonal antibody inhibitor
20
Q

Complications of eosinophilic esophagitis

A
  • Strictures of the oesophagus (56%)
  • Impaction: 55% of patients experience this, and 38% of these require endoscopic removal of the impaction
  • Mallory-Weiss tears
21
Q

What are complications of GERD?

A

Complications of GERD include:

  • erosive esophagitis
  • stricture
  • Barrett esophagus, and
  • esophageal cancer
22
Q

Treatment for GERD

A
  • Proton pump inhibitor therapy is superior to H2 blockers for treatment of gastroesophageal reflux disease.
  • In patients with gastroesophageal reflux disease, indications
    for antireflux surgery include patient preference
    to stop taking medication, medication side effects, large
    hiatal hernia, and refractory symptoms despite maximal
    medical therapy - fundoplication or bariatric surgery
23
Q

Risk factors for GERD

A
  • Age
  • Obesity (central)
  • Hiatus hernia
  • Pregnancy
  • Specific conditions: scleroderma, asthma
  • Smoking (Alcohol)
  • NEGATIVE – H. pylori
24
Q

Medications that may aggravate GERD

A

Medications that may aggravate reflux symptoms

Impairment of LOS function

  • Beta agonists
  • Theophylline
  • Anticholinergics
  • TCAs
  • Progesterone
  • Alpha antagonists
  • Diazepam
  • Calcium channel blockers

Damage the oesophageal mucosa

  • Aspirin and other NSAIDs
  • Doxycycline
  • Quinidine
  • Bisphosphanates
25
Q

What is the histological change of barrett’s oesophagus?

A

BE is classified as a premalignant condition that could progress to esophageal cancer.
- Results from CHRONIC REFLUX AND ACID EXPOSURE - normally takes 10 years to occur

  • METAPLASIA of the DISTAL OESPHAGEAL MUCOSA - consists of change in the normal squamous lining of the LOWER oesophagus to the COLUMNAR epithelium (metaplasia).
  • Categorised into short segment (<3cm) or long segment (>3cm)
  • Intestinal metaplasia –> low grade dysplasia –> high grade dysplasia –> invasive adenocarcinoma
  • Malignancy risk is higher with LONG SEGEMENT Barett’s
26
Q

Risk factors and protective factors for Barret’s oesophagus

A

Risk Factors

  • Older age
  • Male
  • White ethnicity
  • GERD
  • hiatal hernia
  • High BMI
  • Smoking

Protective Factors

  • Moderate wine consumption
  • Diet rich in fruits and vegetables

BE is a consequence of GERO whether or not patients
experience clinical symptoms.

27
Q

Treatment of Barrett Oesophagus

A
  • Treatment to remove Barrett esophagus is recommended for patients with confirmed HIGH-grade dysplasia and can be done with endoscopic therapies that include radiofrequency ablation, photodynamic therapy,
    or endoscopic mucosal resection

Lifelong PPI to heal inflammation - no RCT evidence though

NO DYSPLASIA

  • If no dysplasia - surveillance endoscopy 3 years
  • If dysplasia follow protocol for low/high

LOW GRADE DYSPLASIA
- LGD: surveillance endoscopy 1 year - now you would treat with ?endoscopic mucosal resection - ANY DYSPLASIA = TREAT

HIGH GRADE DYSPLASIA 
 Treat:
- Endoscopic mucosal resection 
- Endoscopic submucosal dissection 
- Radiofrequency ablation (first line but can cause strictures)
- Surgery

Estimated Cancer RIsk
Barrets: 0.2%/year
Low grade dysplasia: 0.7%/year
High grade dysplasia: 7%/year

28
Q

What are the most common types of esophageal cancer?

A

The most common types are squamous cell carcinoma (SCC) and adenocarcinoma

29
Q

Risk factors associated with esophageal cancer

A 
RF associated with SCC (proximal): mainly smoking, alcohol
- Tobacco and alcohol
use
- Caustic injury
- Achalasia
- Past thoracic radiation
- Nutritional deficiencies (zinc, selenium)
- Poor socioeconomic status,
- Poor oral hygiene,
- HPV

Adenocarcinoma RF (distal): mainly Barrett’s oesophagus, obesity, absence of H pylori

  • GERD
  • BE
  • obesity
  • tobacco use
  • past thoracic radiation
  • diet low in fruits and vegetables
  • increased age, male sex, .
30
Q

Clinical manifestation of esophageal cancer and Ix

A
  • The most common clinical manifestation of esophageal cancer is solid-food dysphagia but can be asymptomatic.
  • Weight loss. anorexia.
    and anemia (secondary to gastroinlestimli bleeding).
  • Upper endoscopy with biopsy is the preferred initial diagnostic test.
  • SCC is located in the PROXIMAL esophagus (thinking smoking, achalasia)
  • Adenocarcinoma is usually found in the DISTAL esophagus. (think reflux and BE)
31
Q

Gastroesophageal varices

  • What hepatic venous gradient (HVPG) is required for formation and bleeding
  • Surveillance required
A
  • Venous collaterals that form in the presence of portal hypertension
  • Hepatic venous pressure gradient (HVPG) >12mmHg required for formation
  • HVPG >18mmHg before bleed occurs

Surveillance

  • Endoscopy: usually at diagnosis of cirrhosis/portal htn
  • If no/small varices (grade 1): repeat in 1-2 years
  • If large varices (grade 2/3): primary prophylaxis with beta blockade or variceal band ligation
32
Q

Primary and secondary prophylaxis for gastroesophageal varices

A

Primary Prophylaxis (to prevent it from occurring): non-selective BB or variceal banding
- Non-selective BB: propranolol, carvedilol
Decreases risk of first bleed by 50%
Goal is to reduce resting pulse by 25%
- Banding - normally >grade 2 varices
No difference between 2 modalities in terms of mortality/prevention of bleeding, trend towards better outcomes for banding

Secondary Prophylaxis (to prevent relapse - has happened previously)

  • Beta blockers AND band ligation (if tolerated)
  • TIPSS if recurrent bleeding
  • Liver transplant
33
Q

Abx in variceal haemorrhage

A 
In acute bleed - need to give abx (eg: ceftriaxone)
Abx in variceal haemorrhage reduces:
- Mortality 
- Re- bleeding
- Infection
34
Q

What interventions can be done for uncontrolled variceal haemorrhage?

A

Sengstaken Blakemore/Linton tube

  • Tamponade bleeding as a temporising measure
  • Repeat endoscopy in 24 hours

Danis Stent
- Large self expanding metal stent endoscopically placed

Porto-systemic Shunt

  • TIPSS
  • Surgical
35
Q 
The most common precipitant of Oesophageal squamous cell carcinoma is:
A. Smoking 
B. Achalasia
C. Barrett’s Oesophagus
D. Low fibre diet 
E. Reflux Oesophagitis
A

A. Smoking

Adenocarinoma is related to reflux and barrets esophagus

36
Q

For obstructed bile ducts, what investigation would you do?

A
  • CT cholangiogram can only be done if bilirubin < 50

- If bili >50 then the answer would be MRCP

37
Q

GERD pathogenesis and RF

A

Pathogenesis: transient relaxation of the lower oesophageal sphincter

RF

  • Obesity
  • Alcohol
  • Hiatus hernia
  • Smoking
  • Drugs: bisphosphonates, pill esophagitis
38
Q

First investigation for ampulla lesion

A

The ampulla, or ampulla of vater, is where the pancreatic duct and bile duct join together to drain into the duodenum,

  • EUS
39
Q

What should you think of when you have a pancreatic lesion?

A
  • Do EUS + biopsy

- Think also of IgG4 disease

40
Q

What are contraindication to TIPPs?

A

Hepatic encephalopathy
Occluded portal vein

Absolute contraindications to TIPS placement include

  • severe pulmonary hypertension (mean pulmonary pressure > 45 mm Hg)
  • severe tricuspid regurgitation
  • congestive heart failure
  • severe liver failure
  • polycystic liver disease
  • uncontrolled systemic infection/sepsis
  • unrelieved biliary obstruction

Portal vein thrombosis - relative contraindication

41
Q

SE of PPI

A

Most evidence for:
Acute interstitial nephritis
Hypomagnesaemia

Gastroenterology (11 decks)

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