Upper gastrointestinal tract Flashcards

1
Q

Define hiatus hernia with regard to anatomical type

A

Hiatus herniae allow part of the stomach into the thoracic cavity. They are usually asymptomatic.

The two types are:

  • Sliding hiatus hernia:
    • The gasto-oesophageal junction slides through the hiatus to lie above the diaphragm
    • Occurs in 30% of adults over 50
  • Para-oesophageal/rolling hernia
    • A small part of the fundus rolls up through the hernia alongside the oesophagus, but the sphincter remains competent below the diaphragm
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2
Q

What are the anatomical and physiological factors predisposing gastro-oesphageal reflux disease (GORD)?

A

Anatomical:

  • Hiatus hernia

Physiological:

  • Raised IAP (pregnancy/obesity)
  • Large meals, eaten late at night
  • Smoking
  • High caffeinated drink intake
  • High fatty foor intake
  • Drugs (anticholinergics, nitrates, tricyclics and calcium channel blockers)
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3
Q

Name the 3 typical symptoms of GORD

A
  1. Heartburn/indigestion
    • Aka ‘dyspepsia’
    • Worse on bending/lying down, when drinking hot liquids or alcohol
    • Relieved by antacids
    • May experience odynophagia (pain when swallowing)
  2. Regurgitation of food/acid
    • Passive process (not like vomiting)
    • More common when bending/lying
    • Aspiration may occur
  3. Waterbrash
    • ​Sudden filling of the mouth with dilute saliva
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4
Q

What investigations are used to confirm a diagnosis of GORD?

A
  • GORD can generally be diagnosed clinically without further investigations

Although:

  • Endoscopy is able to establish malicious causes and consquency of GORD such as malignancy, hiatus hernia, oesophagitis and Barrett’s oesophagus.
  • Barium swallow/meal can diagnose any anatomical problems such as hiatus hernia
  • 24 hour luminal pH monitoring and manometry (measures competence of sphincter) to diagnose GORD if endoscopy is normal
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5
Q

All patient with GORD should be treated empirically with a PPI unless there are any red flag symptoms that would indicate a need for endoscopy.

What are those red flag symptoms?

(not an objective)

A

ALARM55

  • Anaemia (iron deficiency)
  • Loss of weight
  • Anorexia
  • Recent onset, progressive symptoms
  • Melaena or haematemesi
  • Swallowing difficulties
  • 55 years of age or older
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6
Q

What is the difference between dysphagia and odynophagia?

A

Dysphagia is difficulty swallowing

Odynophagia is pain upon swallowing

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7
Q

What are the common causes of dysphagia?

A
  • Diseases of the mouth tongue:
    • E.g. tonsillitis
  • Neuromuscular disorders:
    • Myasthenia gravis
    • Motor neurone disease
    • Bulbar palsy
  • Oesophageal motility disorders:
    • Achalasia (lower esophageal sphincter fails to open during swalling)
    • Scleroderma (an autoimmune, rheumatic, and chronic disease that affects the body by hardening connective tissue)
    • Diabetes mellitus
  • Extrinsic pressure:
    • Goitre
    • Lymph nodes
    • Enlarged left atrium
  • Intrinsic lesion:
    • Forgein body
    • Benign/malignant stricture
    • Pharyngeal pouch
    • Oesophageal web (Plummer-Vinson syndrome)
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8
Q

What are the main investigations for dysphagia?

A

Establishing time course and differences in passage of liquids and solids can help narrow down DDx.

Is it oropharngeal dysphagia (difficulty initiating swallow +/- choking/aspiration) or oesophageal dysphagia (food ‘sticks’ after swallowing, +/- regurgitation)?

Endoscopy and barium swallow are the main investigations.

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9
Q

What is the typical history of a patient with a malignant lesion of the oesophagus? (who and symptoms)

A
  • Generally occur in over 60s, although becoming more common in younger age groups

Symptoms:

  • Progressive dysphagia, starting with solids and progressing to liquids and eventually difficulty swallowing saliva
  • Weight loss and anorexia
  • Retrosternal chest pain
  • Coughing/aspiration
  • Occasional lymphadenopathy
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10
Q

Describe the pathology of oesophageal malignancy

(location and type)

A
  • Most are now in the lower third
  • Most are adenocarcinomas and the remainders are mainly squamous cell carcinomas

Adenocarcinoma:

  • Increasing incidence, arise from areas of epithelial metaplasia in the lower oesophagus (Barrett’s oesophagus-refers to an abnormal change (metaplasia) in the cells of the lower portion of the esophagus. It is characterized by the replacement of the normal stratified squamous epithelium lining of the esophagus by simple columnar epithelium with goblet cells - usually caused by GORD)
  • Risk factors are thus those related to GORD

Squamous cell carcinoma:

  • Mainly occur in heavy smoking and drinking males
  • Usually present late when the tumour is early enough to compromise the lumen and cause dysphagia
  • Regional lymph node spread is early and common
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11
Q

What are the main causes of peptic ulcer disease?

A
  • Helicobacter Pylori infection (90% duodenal, 70% gastric ulcers)
  • NSAIDs (around 30% of ulcers)
  • Zollinger-Ellison syndrome (excessive acid secretion due to non-insulin secreting islet cell tumour of pancreas secreting gastrin-like hormone, often leading to excessive ulceration)

Other risk factors: are smoking, coffee cosumption, and hepatic/renal failure

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12
Q

How does H. Pylori cause peptic ulceration?

A
  • H. Pylori produces gastritis, mainly in the gastric antrum, leading to activation of an inflammatory infiltrate
  • There is also increased acid secretion in the presence of H. Pylori (increased gastrin and decreased somatostatin), and abnormal mucus production, leading to epitheal damage
  • H. pylori is also causally associated with duodenal ulcers
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13
Q

How does smoking cause peptic ulceration?

A
  • Impairs gastric mucosal healing
  • Nicotine increases acid secretion
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14
Q

How do NSAIDs cause peptic ulceration?

A
  • NSAIDs inhibit cyclo-oxygenase enzymes, which has anti-inflammatory properties as the COX-2 isoform normally causes inflammatory prostaglandin synthesis
  • Adverse GI effects generally occur due to inhibition of COX-1 in the stomach, which is responsible for synthesis of prostaglandins that inhibit acid secretion and protect the mucosa

(given PPIs can diminish gastric damage caused by these agents)

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15
Q

What are symptoms of a peptic ulcer?

A
  • Epigastric pain, related to food intake, relieved by antacids
    • Pain classically relieved by eating in duodenal ulcers
    • Worse on eating in gastric ulcers
  • Nausea
  • Anorexia and weight loss
  • Haematemesis/melaena ( dark sticky faeces containing partly digested blood)
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16
Q

What are the difference between duodenal and gastric ulcers?

A

Duodenal:

  • 4x commoner than gastric ulcers, with 90% within 2cm of the pylorus
  • Pain is at night and before meals, relieved by eating food or drinking milk
  • Alcohol intake is a risk factor

Gastric:

  • occur in older patients (>55), mainly on the lesser curve of the stomach
  • Pain is worse on eating, and relieved by antacids
17
Q

How would you investigate peptic ulcer disease?

A
  • Urgent oesophago-gastro-duodenoscopy (OGD) if fir ALARMS55 critieria
    • Multiple biopsies taken from rim/base (histology/H. pylori) as well as brushings (cytology)
  • No investigation needed if <55, no ALARM symptoms and resolves on antacids
  • If symptoms persist on treatment, investigate for H.Pylori (13C urea breath test)
18
Q

What are the common causes of upper GI bleeding?

A
  • Peptic ulceration (40%)
  • Gastroduodenal erosions (15%)
  • Oesophagitis (15%)
  • Mallory-Weiss syndrome (tears at the gastro-oesophageal junction due to violent vomiting - 15%)
  • Varices (10%) - dilated veins in the oesophagus
  • Upper GI malignancy (1%)
19
Q

What are the symptoms of upper GI bleeding?

What are the signs?

A

Symptoms:

  • Haematemesis
  • Malaena (blood altered by bacteria thus tarry stools)
  • Haematochezia (unaltered PR blood, can rarely occur in massive upper GI bleeds)
  • Abdominal pain

Signs will be of any underlying cause, and of shock

Chronic GI blood loss presents with sign/symptoms of iron-deficient anaemia - kolionychia, angular stomatitis, brittle nail/hair. Fatigue, weakness, headaches, cardiovascular symptoms. Pallor, tachycardia.

20
Q

What are the risk factors for gastric cancer?

A
  • H. Pylori infection leading to metaplasia
  • High salt/nitrate (red meat) diet
  • Smoking
  • Genetic factors - blood group A/HNPCC, Japanese heritage
  • Pernicious anaemia
  • Adenomatous polyps (benign (noncancerous) growths)
  • Low socio-economic status
21
Q

What are symptoms and signs that would suggest gastric cancer?

A

Symptoms:

  • Often non-specific
  • Epigastric pain, as with gastric peptic ulcer
  • Nausea and vomiting (vomiting is frequent if the tumour is near the fundus)
  • Dysphagia (if the tumour is near the fundus)
  • Anorexia/weight loss

Signs:

  • Palpable epigastric mass (50%)
  • Large left supraclavicular node (Virchow’s)
  • Hepatomegaly, jaundice & ascites
  • Acanthosis nigricans (brown to black, poorly defined, velvety hyperpigmentation of the skin. It is usually found in body folds)
22
Q

Describe the classification of morphology of gastric cancers

A

Gastric adenocarcinomas, which make up over 90% of gastric neoplasms, may be classified as:

  • Intestinal (Type 1)
    • well to moderately differentiated glandular (tubular) structures, with multiple lumens.
    • Often associated with HPylori, and may be polypoid (presents earlier with bleeding and easier to resect) or ulcerative (the most common form, has a raised edge and a necrotic base)
  • Diffuse (Type 2)
    • poorly cohesive “signet ring” cells (keep mucous inside), linitus plastica (leather bottle stomach), and infiltration (worse prognosis).
    • The tightening and thickening of the mucosa causes a reduction in stomach capacity.
23
Q

Describe the natural history of gastric cancer

A
  • Most occur in the antrum
  • Metastases are local by direct invasion of abdominal viscera, lympathic (Virchow’s) and then to the liver by portal dissemination
  • Transcoelomic spread may cause peritoneal seedings, including bilateral ovarian ‘Krukenberg’ tumours (name for any secondary ovarian tumour)
24
Q

List diagnostic methods used to investigate patients with suspected gastric neoplasia

Staging?

A

Diagnosis:

  • Oesophageal-gastric-duodenal endoscopy and multiple edge biopsy

Staging:

  • Endoscopic USS and CT for staging
25
Q

Define the term ‘acute abdomen’

A
  • An emergency surgical condition caused by damage to one or more of the abdominal organs due to injury or disease
26
Q

Identify the the cardinal symptoms of the acute abdomen and the pain patterns

A

Inflammatory

  • Constant pain
  • Raised temperature, pulse and leucocytosis
  • Pertionitis gives localised pain (due to somatic innervation), worse on movement, coughing or inspiration
  • Often assoicated with guarding (reflex contraction of abdominal muscles on examination of the inflammed area) and rigidity (increased tone at rest)

Obstructive:

  • Colicky pain, patients often agitated
  • May become constant with superimposed inflammation

Referred visceral pain (generally midline)

  • Fore-gut (oesophagus to D2) pain is referred to the upper abdomen
  • Mid-gut (D2 to transverse colon) pain is referred to the middle abdomen
  • Hind-gut is referred to the lower abdomen
27
Q

What are the differential diagnosis of the acute abdomen?

A

Abdominal Viscera:

  • Acute appendicitis
  • Meckel’s diverticulitis
  • Intestinal obstruction
  • Perforated viscus (acute sever pain and shock)
  • Acute pancreatitis
  • Acute cholecystitis/cholangitis
  • Renal calculi
  • The acute scrotum
  • Inflammatory bowel disease

Vascular causes:

  • AAA
  • Mesenteric thrombosis/embolus

Medical causes:

  • GORD
  • Referred pain from pneumonia/MI/UTI/pyelonephritis

Gynae causes:

  • Ruptured ectopic, torted/ruptured ovarian cysts, salpingitis ect.
28
Q

What investigations would be done to further define a cause for an acute abdomen?

A
  • FBC, U&Es, LFTs, CRP, Amylase & ABG
  • Pregnancy test
  • Urinalysis
  • Erect CXR/AXR
  • USS/CT
29
Q

What is the management for a pateint with an acute abdomen?

A

ABCDE: IV Fluids, Oxygen, Analgesia.

Insert catheter for fluid balance, NG tube for drain/feeding (patient should be kept NBM).

History and examination should be undertaken

Certain presentations require urgent laparotomy:

  • Rupture of an organ (spleen/aorta/eptopic)
  • Peritonitis (perforated ulcer, diverticulum, appendix or gallbladder)
  • Pancreatitis can mimic these so check amylase/lipase