Upper GI Disorders - Oesophagus, Stomach, Pancreas Flashcards

1
Q

Anatomy of the oesophagus and gastro-oesohageal junction

A

Upper third → striated muscle, vagal motor innervation

Lower two thirds → smooth muscle, continuous with stomach. Vagal parasympathetic innervation

Oesophageal motility

Upper oesophageal sphincter relaxation → brief as bolus passes through

Relaxation of the oesophageal body and LOS → nitric oxide, VIP. LOS relaxes to intragastric pressure

Coordinated contraction of smooth muscle of the oesophagus → acetylcholine

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2
Q

Risk factors for gastro-oesophageal reflux

A
  • Age
  • Obesity
  • Hiatus hernia
  • Pregnancy
  • Specific conditions → scleroderma, asthma
  • Smoking, alcohol

H. pylori protective

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3
Q

Complication of reflux disease

A

Ulceration/bleeding

Stricture/Schatzki ring

Barrett’s oesophagus

Adenocarcinoma of oesophagus

Extra-intestinal manifestations - pharyngeal reflux

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4
Q

Epidemiology of reflux disease, symptoms, and symptoms of complications

A
  • Common - 40% ever
  • West>East, developed > developing
  • Symptoms not a predictor of oesophagitis - severity of heartburn similar in patients with different grades of oesophagitis

Symptoms

Heartburn, regurgitation

Nonspecific → nausea, epigastric pain, respiratory (cough, worsening asthma), ENT, dental, chest pain, sleep disturbance

Symptoms of complications

Dysphagia - oesophagitis, stricturing, malignancy

Haemetemesis

Weight loss

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5
Q

Diagnosis of GORD

A

Clinical diagnosis

Endoscopy only if atypical symptoms, poor response to treatment, red flags → 50% endoscopy negative

PH/impedence studies

Endoscopy

Severity of oesophagitis - Los Angeles A→ D

Presence of hiatus hernia

Presence of Barrett’s

Presence of other conditions that may mimic or exacerbate reflux symptoms

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6
Q

Management of GORD

A
  • Lifestyle → lose weight, avoid fatty/spicy food, avoid late meals, elevate head of bed, antacids, avoid alcohol, citrus fruits may also aggravate
  • PPIs - start high dose then titrate down
  • H2 receptor antagonists (PPIs more effective in terms of healed eosophagitis)
  • Prokinetics
  • ?Trial of TCA

Medications that may aggravate GORD

Impaired LES function → beta agonists, theophylline, anticholinergics, TCAs, calcium channel blockers, progesterone, alpha adrenergic antagonists, diazepam

Damage to oesophageal mucosa → aspirin, NSAIDs, doxycycline, quinidine, bisphosphonates

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7
Q

Inidications for surgery and options in GORD

A
  • Failed medical management
  • Medication non-compliance

Fundoplication - laparoscopic or open

  • Side effects → ++flatus, limited period of dysphagia
  • Occasional → severe dysphagia, gas bloat, inability to belch, vomit. Paraoesophageal hernia
  • Failure with time
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8
Q

Notes on Barrett’s oesophagus - definition, epidemiology

A
  • Metaplasia of variable distance of lower oesophagus to mucosa of cardia, gastric or intestinal type
  • Increases with age - 1-2% population, 10% reflux patients
  • Risks:
    • Male
    • Caucasian
    • Severe reflux symptoms → prevalence increases with duration of reflux symptoms
  • Increased incidence of oesophageal adenocarcinoma → lesions >3cm associated with higher risk
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9
Q

Screening and management of Barrett’s oesophagus

A

Screening

  • No proven benefit but if found needs biopsy confirmation → best taken after healing (inflammatory changes interfere with assessment of dysplasia)

Management

  • Management of oesophagitis and symptoms
  • Manage risk of malignancy → surveillance programme
    • No dysplasia → 3-5 years
    • Low grade → 6 month
    • High grade → see below

High grade dysplasia

  • Mucosal ablation combined with PPI can elimate macroscopic Barrett’s (submucosal islands may persist)
  • Reduced incidence of oesophageal adenocarcinoma (in high grade group only)
  • If young and multifocal disease may need to consider oesophagectomy (1-20% mortality however, risk and benefit needs to be balanced)
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10
Q

Manifestations of coeliac disease

A

Iron deficiency

Osteoporosis

Hypocalcaemia

Late menarche, early menopause, miscarriages, secondary amenorrhoea, infertilty, preterm delivery and low birth weight

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11
Q

Notes on primary biliary cirrhosis

A
  • Most common presenting symptom fatigue and pruritus
  • Presence of symptoms worsens prognosis - 50% asymptomatic
  • Positive antimitochondrial antibody
  • No role for treatment if normal LFTs
  • Ursodeoxycholic acid used in treatment
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12
Q

Mechanism of aspirin/NSAID induced peptic ulcer disease

A
  • COX 2 inhibition → decreased prostaglandins
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13
Q

Notes on gastrinomas/Zollinger-Ellison syndrome

A
  • Diagnosed with secretin stimulation test → differentiate patients with gastrinomas from other causes of hypergastrinaemia (e.g. in the setting of gastrin < 10 times ULN, and gastric pH ≤2
  • Secretin stimulates release of gastrin by gastrinoma cells, patients with ZES tumours → dramatic rise in serum gastrin. Normal gastric G cells inhibited by secretin
  • Should not be performed on patients on PPI therapy → false negative up to 20%, false positive up to 40%
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14
Q

Notes on achalasia - symptoms and investigations

A
  • Incomplete LOS relaxation → Oesophageal aperistalsis → replaced by undulating “common cavity” pressure waves due to ineffective contractions
  • Loss of inhibitory neurotransmission → ?autoimmune precipitated by viral infection
  • Heterogeneous condition
  • Symptoms → dysphagia (solids & liquids, progressive +/- weight loss), regurgitation (postural → night), chest discomfort/pain (may simulate heartburn)
  • Endoscopy → food in oesophagus, tight LOS, dilated oesophagus, done to exclude stricturing lesions
  • CXR → Lack of gastric air bubble, retrocardiac fluid level
  • Barium swallow → birds beak, holdup in dilated oesophagus, aperistalsis
  • Manometry → most sensitive, imcomplete LOS relaxation
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15
Q

Management of achalasia

A
  • Medications → GTN, calcium channel antagonists (generally not effective)
  • Balloon dilation → controlled rupture of LOS, 3-5% perforation rate, variable success rate
  • Botox → injected into LOS, 70% success, needs repeating after 3-6 months
  • Myotomy → surgical division of LOS, laparoscopic. Highly effective, low morbidity.
  • POEM (per oral endoscopic myotomy), PEG, oesophagectomy other options
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16
Q

Notes on acute pnacreatitis

A

Amylase

  • Half life 10 hours
  • >3x ULN sensitivity of 67-83%, specificity 85-98%
  • Low in: alcoholics, hypertriglyceridaemia
  • High in: DKA, ARF, parotid disease, malignancy, other

Lipase

  • Peaks at 24 hours, returns to normal in 8-14 days
  • High inL renal failure, DU, DKA, HIV, coeliac disease, other
  • Mild = no organ failure
  • Moderately severe = > 48 hours organ failure or local/systemic complications
  • Severe = persistent organ failure
17
Q

Complications of acute pancreatitis

A

Acute peripancreatic fluid collection

  • Extra-pancreatic, no wall
  • No necrosis or solid material

Psuedocysts

  • Mature fluid collections outside the pancreas at least four weeks out
  • Well defined wall
  • No necrosis or solid material

Acute necrotic collection

  • Adjacent to or involving the pancreas
  • No wall
  • Liquid and solid material

Walled off pancreatic necrosis

  • Mature encapsulated necrosis with solid and liquid elements
  • Intra- or intrapancreatic
18
Q

Notes on chronic pancreatitis

A
  • Progressive fibroinflammatory process → permanent structural damage and impairment of exocrine or endocrine function
  • Complications → psuedocyts (10%), bile duct or duodenial obstruction (5-10%), pancreatic ascites, splenic vein thrombosis and psuedoaneursyms
  • Differs from acute pancreatitis:
    • May be asymptomatic over long periods
    • Enzymes tend to be normal
    • Patchy focal disease with fibrosis

Causes

  • Alcohol
  • Genetic - CFTR, SPINK1
  • Ductal obstruction (stone, trauma, psuedocyst)
  • Tropical pancreatitis
  • Autoimmune pancreatitis
  • Systemic diseases → SLE, hyperparathyroidism
  • Idiopathic
19
Q

Features of chronic pancreatitis and treatment

A

Features

  • Abdominal pain
  • Pancreatic insufficiency
    • Exocrine (>90% pancreas lost)
    • Endocrine (increased risk of hypoglycaemia due to loss of alpha cells)

Diagnosis difficult - lab tests and imaging can be normal

MRI best imaging modality

Dx strongly suggested by pancreatic calcification, steatorrhoea, and DM

Faecal elastase most sensitive and specific lab test

Selective genetic testing - CFTR, SPINK1, PRSS 1

Treatment

  • Pain management
    • Stop alcohol, smoking
    • Hydration, small meals
    • Analgesia - opiates, NSAIDs, pregabalin, endoscopic therapy, coeliac plexus block, surgery
  • Correction of pancreatic insufficiency
    • Lw fat diet
    • Enzyme supplementation
    • Medium chain triglycerides
20
Q

Notes on autoimmune pancreatitis

A
  • Rare
  • Painless jaundice
  • Clinically and radiologically difficult to distinguish from pancreatic cancer
  • Dramatic response to glucocorticoids
  • Untreated can → pancreatic failure