Upper GI Flashcards

1
Q

What 6 symptoms combined can be described as dyspepsia

A
Epigastric pain/ burning
Early satiety
Belching
Bloating
Nausea 
Discomfort in upper abdomen
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2
Q

Where can peptic ulcer disease occur?

A

Stomach (20%) or duodenum (80%)

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3
Q

Name 4 symptoms of Peptic Ulcer disease

A

Epigastric pain related to eating
Early satiety
Nausea and vomiting
Anorexia and weight loss

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4
Q

Name 3 signs of peptic ulcer disease

A

Epigastric tenderness
Pointing sign
Signs and symptoms of blood loss/ anaemia

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5
Q

Give 2 ways to differentiate duodenal and gastric ulcers

A

Pain:

  • Duodenal 2-3 hours after eating. Awakens patients at night.
  • Gastric shortly after eating

Weight change:

  • Duodenal over-eat, weight gain
  • Gastric: avoid eating, weight loss.
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6
Q

Name 4 things that can cause a peptic ulcer

A
  • H. Pylori
  • Gastric acid
  • Pepsin
  • NSAIDs
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7
Q

Name 8 risk factors for peptic ulcer disease

A
  • H. Pylori
  • Smoking
  • NSAIDs
  • Bisphosphonates
  • Head trauma: can lead to cushing ulcer
  • Age
    Burns- can lead to curling ulcer
  • Zollinger Ellison syndrome
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8
Q

What is the basic mechanism of action of NSAIDs?

What effect does this have on GI mucosa?

A

Inhibition of COX 1 and COX 2 suppresses prostaglandin synthesis.

Barrier properties of GI mucosa impaired, reduction of gastric mucosal blood flow also.

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9
Q

Describe 2 investigations for H. Pylori.

What gram stain is H. Pylori?

A
  • 13c Urea breath test: ingest 13c urea. Measure 13-CO2 in breath using mass spectrometry (H. Pylori produces urease)
  • Stool antigen test

Gram negative flagellate.

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10
Q

What is the management for H. Pylori?

A

1 week Triple therapy:

  • PPI
  • Clarithromycin
  • Amoxicillin or Metronidazole
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11
Q

What is Zollinger-Ellison syndrome?

What condition may it be a part of?

A

Gastrin secreting neuroendocrine tumour in pancreas.
(gastronoma). 0.1-1% of all duodenal ulcers.

May be part of Multiple Endocrine Neoplasia 1 (MEN1)

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12
Q

What are the 3 pathophysiological steps of Zollinger- Ellison syndrome

A
  1. Hypergastrinaemia
  2. Hypertrophy of gastric mucosa and stimulation of acid secreting cells.
  3. Damaged mucosa and Ulceration

+ Malabsorption due to damage of GI mucosa
+ inactivation of pancreatic enzymes.

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13
Q

When should you consider Zollinger- Ellison Syndrome?

A
  • Multiple ulcers refractory to treatment.

- Family history of MEN1

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14
Q

Name 3 investigations for Zollinger-Ellison syndrome.

A
  • Fasting serum gastrin
  • Serum calcium
  • Gastric acid secretory tests, stimulation tests, imaging.
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15
Q

Name 2 management steps for Zollinger- Ellison syndrome.

A
  • PPI

- Surgical resection of tumour.

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16
Q

What is a Cushing ulcer?

What is a Curling ulcer?

A
  • Raised ICP stimulates vagus nerve after head injury- leads to gastric acid secretion.
  • Reduced plasma volume following sever burn injury leads to ischaemia and necrosis of gastric mucosa..
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17
Q

Name 2 investigations for PUD under 55.

Name 3 investigations for PUD over 55, or red flag symptoms.

A

Under 55:

  • Breath test/ stool antigen
  • FBC, stool occult blood, serum gastrin.

Over 55 - suspect malignancy:

  • UGI endoscopy
  • Histology + biopsy, urease testing
  • Repeat endoscopy after 6-8 weeks.
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18
Q

For management of PUD, name 3 risk factor modifications.

Name 2 pharmacological management steps.

A

RFM:

  • Diet
  • Smoking
  • NSAIDs and bisphpsphonates

Pharm.

  • H. pylori positive: triple therapy
  • H. pylori negative: PPI (-oprazole) or H2 (-tidine) antagonist
  • May need to treat anaemia
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19
Q

How do you manage a bleeding peptic ulcer? 3 steps.

A
  • Endoscopy (+/- therapy e.g. adrenaline)
  • IV PPI e.g. omeprazole
  • Triple therapy if H. Pylori.
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20
Q

How do you manage a perforated peptic ulcer? 3 steps.

A
  • NBM
  • IV antibiotics
  • Surgery
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21
Q

What is the relation between PUD and gastric outlet obstruction?

A
  • Active ulcer causes inflammation and oedema/ scarring
  • Blocked outflow causes full stomach of gastric juice and ingested food.
  • This causes vomiting without pain.
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22
Q

Name two complications of a perforated ulcer.

A
  • Pneumoperitoneum- air under diaphragm.

- Peritonitis.

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23
Q

Name 4 symptoms of gastric cancer.

A
  • Epigastric pain
  • Nausea/ vomiting (+/- blood)
  • Anorexia
  • Weight loss
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24
Q

Name 3 risk factors for gastric cancer:

A
  • Smoking
  • H. Pylori
  • Chronic gastritis and therefore PUD.
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25
Q

Name 3 signs of gastric cancer.

A
  • Palpable epigastric mass
  • Virchow’s node/ Troisier’s sign - lymphadenopathy in left supraclavicular fossa.
  • Sister Mary Joseph node- metastatic node on umbilicus

Both nodes suggestive of metastatic abdominal cancer

26
Q

Name 2 investigations for gastric cancer.

A
  • endoscopy

- biopsy and histology.

27
Q

Give 3 oesophageal (typical) symptoms of GORD

A

Heartburn
Regurgitation: return of gastro-oesophageal contents to pharynx.
Dysphagia (difficulty swallowing), sensation food is stuck retrosternally.

28
Q

Give 4 Extra-oesophageal signs of GORD

A
  • Coughing/ wheezing
  • Hoarseness, sore throat
  • Noncardiac chest pain
  • Enamel erosion or other dental manifestations
29
Q

What are the risk factors for GORD relating to:

  • Increase Intra-abdominal pressure (2).
  • Lower oesophageal sphincter hypotension (3)
  • Gastric hypersecretion (3).
A

Raised IAP:

  • Obesity
  • Pregnancy

LOS hypotension:

  • Drugs: anti-muscarinics, CCBs, nitrates, smoking.
  • Treatment of achalasia
  • Hiatus hernia

Gastric hyper secretion:

  • Diet
  • Smoking
  • Zollinger- Ellison syndrome
30
Q

What is a hiatus hernia and what does it predispose to?

How does patient present?

A

Portion of stomach prolapses through diaphragmatic oesophageal hiatus, predisposing to reflux/ worsening of existing reflux.

Patient presents with symptoms of GORD (most hiatus hernias are asymptomatic)

31
Q

Name 4 risk factors for hiatus hernia

A
  • Muscle weakening/ lack of elasticity with age.
  • Pregnancy
  • Obesity
  • Abdominal ascites
32
Q

Name 3 investigations for a hiatus hernia, with most important first.

A
  • Barium swallow
  • Chest X-ray
  • Endoscopy

BS may show:

  • out pouching of barium at lower end of oesophagus
  • Wide hiatus through which gastric folds are seen in continuum with those in stomach.
  • Free reflux of barium.
  • Distinguish sliding and paraoesophagheal hernia.
33
Q

Name 3 management steps for a hiatus hernia.

A
  • Conservative: risk factor modification- change diet, loose weight, stop smoking.
  • Pharmacological: PPI.
  • Surgery: Nissen fundoplication.
34
Q

What are the two main complications for hiatus hernia?

A
  • GORD

- Paraoesophageal hernia incarceration (blood supply gets cut off)

35
Q

What is the list of investigations for GORD in order?

A
Clinical diagnosis =>
Trial of PPI =>
UGI endoscopy =>
Biopsy =>
Consider other tests
36
Q

What is the management of GORD

  • Conservative (3)
  • Pharmacological (1)
  • Surgical (2)
A

Conservative:

  • Diet
  • Sleep
  • Stop smoking/ drugs

Pharmacological:
- PPI or H2 antagonist

Surgical:

  • Nissen fundoplication (for hiatus hernia)
  • Endoluminal gastroplication
37
Q

How many times is risk of oesophageal cancer increased by Barret’s oesophagus?

What type of cancer can it become?

A

11 times increased risk of oesophageal cancer.

Adenocarcinoma.

Requires regular surveillance- endoscopy and biopsy.

38
Q

What is the management for Barret’s oesophagus with high grade dysplasia? 2 steps

A
  • Radiofrequency ablation

- PPI

39
Q

What is the management for Barret’s oesophagus with nodule(s)? 2 steps

A
  • Endoscopic mucosal resection

- PPI

40
Q

What are two symptoms and two red flags of oesophageal cancer?

A
  • Progressive dysphagia from solids to liquids
  • Burning chest pain

Red flags:

  • Weight loss
  • Anaemia
41
Q

Differentiate oesophageal adenocarcinoma and squamous cell cancer by location and risk factors.

A

Adenocarcinoma:

  • Lower third
  • Barret’s oesophagus

Squamous cell:

  • Middle third
  • Smoking, alcohol, nitrosamines/ nitrates (Chinese, Iranian and South African diets)
42
Q

What are the purposes of endoscopy and CT in oesophageal cancer.

A
  • UGI endoscopy and biopsy to diagnose/ grade/

- CT to stage cancer.

43
Q

What are the 4 domains of dysphagia classification?

Name one condition from each domain

A

High dysphagia
Low dysphagia
Functional
Structural

  • High functional: Stroke, Parkinson’s (neuromuscular disease)
  • Low functional: Achalasia
  • High structural: cancer, pharyngeal pouch.
  • Low structural: cancer, plummer-vinson syndrome.
44
Q

Give 4 symptoms of achalasia

A

Dysphagia- solids and liquids
Regurgitation
Dyspepsia
Weight loss

45
Q

Give the aetiology of Achalasia (2 points).

A
  • Absence of oesophageal peristalsis
  • Failure of lower oesophageal sphincter to relax

‘reverse GORD’

46
Q

Give 4 investigations for dysphagia and their purposes

A
  • Barium swallow:
    Avoid perforation on endoscopy, suspect achalasia.
  • Endoscopy: low dysphagia, first line
  • Videofluroscopy: High dysphagia, SALT to modify swallow technique.
  • Manometry: Assess pressure of LOS and wave of peristalsis in rest of oesophagus. Useful for achalasia, oesophageal spasm, motility disorders.
47
Q

Give the pathophysiology of achalasia.

What would you see in Barium swallow?

Which disease has identical pathophysiology?

A
  • Absence of ganglion cells in myenteric plexus
  • Peristalsis
    Failure of LOS to relax.

Birds beak on barium swallow.

Chagas disease results in identical pathophysiology.

48
Q

Differentiate oesophageal cancer and achalasia by:

  • Age
  • onset
  • Structural/ functional
  • Progressive/ intermittent
  • Presence of red flags.
  • 1st line investigation
A
Cancer vs achalasia
Old vs young
New onset vs long term
Structural vs functional
Progressive vs intermittent
Red flags vs no red flags
UGI endoscopy vs barium swallow
49
Q

Name 2 neurological causes of dysphagia and 4 clues.

A

Stroke, parkinson’s.

  • Coughing immediately on swallow
  • Choking
  • Slow eating
  • Early dysphagia for liquids
50
Q

What is Plummer-Vinson syndrome a combination of?

A

Oesophageal webs and Iron deficiency anaemia-
- Cheilosis
- atrophic glossitis
Koilonychia.

51
Q

What acronym is used for the signs of limited cutaneous scleroderma? What does it stand for?

A

CREST:

  • Calcinosis- calcium deposits in skin.
  • Raynaud’s
  • Esophageal dysfunction- acid reflux, motility dysfunction.
  • Sclerodactyly- thickening and tightening of skin on fingers
  • Telangiectasia
52
Q

What sign is seen on barium swallow in Limited cutaneous scleroderma (CREST)?

A

Corkscrew oesophagus

53
Q

When can Mallory-Weiss tears occur?

Where do they occur?

What does it look like in vomit?

A
  • After any event raising intragastric pressure, particularly vomiting.
  • After episode of sever vomiting, e.g. alcohol, bulimia
  • Usually seen as blood streaked in vomit
  • Episode of vomit always precedes bleeding
  • Occur at Gastro-oesophageal junction.
54
Q

What investigation is used to diagnose Mallory-Weiss tears?

How long do tears take resolve?

A

Endoscopy

24-48 hours

55
Q

What is Boerhaave syndrome?

What investigations are used to diagnose Boerhaave syndrome? What will be seen?

What is Mackler’s triad?

A

A full tear in the oesophageal wall as a complication of a Mallory-Weiss tear, 35% mortality. Surgical management.

Diagnosis by CXR/ CT shows pneumomediastinum.

Chest pain, vomiting, subcutaneous emphysema.

56
Q

What is an oesophageal varix and where does it occur?

What is it a consequence of?

A

An extremely dilated vein in sub-mucosa of lower third of oesophagus.

Consequence of portal hypertension due to cirrhosis.

57
Q

Give 3 presenting features of a ruptured oesophageal varix.

A
  • Extreme haematemesis
  • unconscious or in shock
  • Melaena if minor bleed.
58
Q

Give 3 factors promoting rupture of oesophageal varies.

A
  • Cirrhosis, reduced clotting factors, increased bleeding risk
  • Cirrhosis, extra hepatic blood shunting, portal hypertension.
  • Continued alcohol use, oesophageal irritation.
59
Q

Oesophageal varices: what would you see in these investigations:

  • FBC
  • LFT
  • U&E
A

All signs of alcoholism/ cirrhosis.

  • FBC: Macrocytic anaemia, reduced platelets.
  • LFTS: raised GGT, bilirubin, decreased albumin.
  • U&Es: raised urea.
60
Q

What drug is used to reduce portal hypertension in a patient with ruptured oesophageal varices?

What investigation is first line?

What treatment is first line?

A
  • Terlipressin
  • Endoscopy
  • Band ligation

It is an emergency, ABCDE approach necessary.

61
Q

What picture of emesis is expected from ruptured peptic ulcer?

What other blood related sign?

A
  • Coffee ground emesis

- Melaena