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Year 3 > Case 19 - Upper GI Diseases > Flashcards

Case 19 - Upper GI Diseases Flashcards

1
Q

What is Barrett’s Oesophagus?

A

A pre-malignant condition where there is a change of the normal epithelium of the esophagus
Not all cases will go on to become malignant, but gives a higher risk (x50) of oesophageal cancer

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2
Q

What is the pathophysiology of Barrett’s Oesophagus?

A

Normal oesophageal epithelium is squamous epithelium
Barrett’s is a change to glandular epithelium, like that of the stomach
Dysplasia is when there are abnormal cell types present - when dysplasia is present, this leads to a very high risk of cancer

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3
Q

RFs for Barrett’s Oesophagus

A 
Male
Smoker
Increasing age
GORD
Hiatus hernia
Central obesity
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4
Q

Diagnosis and screening for Barrett’s Oesophagus?

A

Should screen anyone with persistent GORD (>5y) or that affects ADL with any 3 of:

  • Over 50
  • White
  • Male
  • Smoker
  • Obese

Then, OGD done to assess the oesophageal lining - will see pink streaks of different cells in the normal epithelium
Can then biopsy to determine if there’s any evidence of dysplasia - stain for p53 overexpression

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5
Q

When should Barrett’s be monitored?

A

When there are streaks of Barrett’s more than 3cm, should have 3-5 yearly OGD to monitor and treat the GORD Sx

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6
Q

What is the management for Barrett’s Oesophagus?

A

When there is any evidence of dysplasia, treat
Otherwise surveillance and PPIs/H2 receptor antagonists to treat the GORD

Endoscopic resection of the mucosa - nodular areas, can stage Ca. Can cause strictures
Radiofrequency ablation - for flat areas. Can cause post-op chest pain and strictures
Cryotherapy - for those who have had failed ablation. May have post-op chest pain and strictures
Surgery - when the neoplasia involves the submucosa the risk of lymph node involvement becomes greater than surgery

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7
Q

What is dysphagia?

A

Inability to swallow food and/or liquids comfortably
Can be due to a variety of causes:

Neuromuscular - neuro=stroke, Parkinsons
Muscular=myaesthenia gravis, muscular dystrophy
Weakened muscles = in elderly

Narrowing - Mass of any kind - oesophageal, throat etc
Scars or rings formed in oesophagus e.g. from GORD

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8
Q

Symptoms of dysphagia and their likely aetiologies

A

When there is a struggle with solids and foods, suggests a neuromuscular aetiology/achalsia

When liquids can pass easily, progressive dysphagia for solids, suggests some kind of obstructive cause/stricture

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9
Q

History for dysphagia?

A 
Weight loss
Vomiting/haematemesis
Change in bowels/malaena
Any pain
Sx of anaemia

PMHx - any previous upper GI investigations
Medications, why, when
NSAIDs
Previous abdo surgery

FHx of strokes etc

SHx - smoker/drinker

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10
Q

Examination for dysphagia

A 
Note body habitus, jaundice, pallor etc
Abdo exam
oral inspection for candida/dry mouth
Should see if there is a lump on swallowing or sticking tongue out
Any lymphadenopathy
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11
Q

Investigations for dysphagia?

A

BTs - anaemia, U and E, LFTs
OGD +/- biopsy

Prep - No food 6 hours before, only clear liquids, NBM 2 hours before. stop anticoagulants

During - telescope test, use numbing spray at the back of the throat and potentially a sedative. If anything is found, we will take a biopsy

After - must be accompanied for 24hrs if had the sedative

Risks - pain, infection, bleeding, perforation

Alternatives - can do swallow studies, but none will give us as good a view of the tract as OGD

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12
Q

Treatment for dysphagia

A

Proper sitting position when eating can help
Physiotherapy to re-train the swallowing muscles
Soft/liquid only diet can be helpful
Surgery
Tube feeding

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13
Q

Complications of dysphagia

A

Aspiration - aspiration pneumonia etc
Choking
Malnutrition

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14
Q

What is odynophagia?

A

Pain on swallowing- can be associated with masses, ulcers, GORD etc.

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15
Q

What is the epidemiology of oesophageal cancer?

A

Often only found when symptomatic and therefore in its later stages
On the increase, and increasing in younger people
Smoking and alcohol have a syndergistic effect
Most are squamous cell/adenoarcinoma

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16
Q

RFs for oesophageal cancer

A 
Smoker
Excess alcohol
GORD
Poor diet
Folate deficiency
High BMI and reflux
17
Q

2WW guidelines for oesophageal cancer

A 
Should refer for an urgent OGD-
Anyone with dysphagia 
>55y with:
-upper abdo pain
-reflux
-dyspepsia

Non-urgent OGD for others

18
Q

Investigations for oesophageal cancer

A 
FBC - WCC, Hb
U and E for contrast tolerance and chemo tolerance
LFTs
CRP
OGD +/- biopsy
Staging CT/PET
19
Q

Staging of oesophageal cancer

A

T1 - in the submucosa
T2 - in the muscularis
T3 - in the adventitia
T4 - in the adventitia, potentially spreading to adventitia of other organs (T4b) or into other organs (T4b)

20
Q

Treatment of oesophageal cancer

A

Should determine if resectable by using endoscopic USS
No, lymph node involvement and a small tumour can be operated on straight away
In larger tumours or if there are nodes - chemo first then re-evaluate
T4 straight to palliative

21
Q

What are the types of hernia?

A

Named after location - inguinal, umbilical etc.
Direct inguinal is when there is a weakness in the abdominal wall and the contents spill out into the inguinal canal
Indirect is when there is no rupture of the abdominal wall, but the abdominal contents enter the inguinal canal through deep inguinal ring, and can extend down to the scrotum in men

Strangulation is when the blood supply to the hernia is cut off - surgical emergency

22
Q

How are hernias treated?

A

Open or laparoscopic surgery
Try laparoscopic for a small hernia in an otherwise fit and healthy person - fewer risks, smaller scar and less healing time
Use open if it’s a large hernia of if there’s likely to be adhesions, or if closed has been unsuccessful

23
Q

Haematemesis history

A 
Duration and Frequency ie. quantity
Volume
Colour of blood
Clots
Sx of shock
Any retching
Hx of GI bleed or ulcers
NSAID use
Anticoagulants/antiplatelets
Weight loss
Alcohol/smoking
Contact with ill people?
24
Q

What is a Mallory-Weiss tear?

A

A small tear in the oesophageal lining usually after extended period of sickness or retching
More common in younger people
Often self-resolves, but need scope and clipping if GBS above 1
Due to:
-Self-enforced vomiting
-Pregnancy
-Alcoholic binge

25
Q

What are oesophageal varices?

A

Due to liver failure etc.
Due to venous back flow the veins become inflamed in the oesophagus and can tear - can be fatal amounts of blood lost
Would treat with terlipressin, which reduces the amount of blood flow through the splanchnic vessels, meaning the varices are less likely to tear
Fluid resuscitaton
Prophylactic Abx
If they do tear, need urgent band ligation
Sengstaken tube - balloon

26
Q

Normal stomach physiology

A

Cells -
Parietal cells - Make HCl. Stimulated by PNS and gastrin
ECL cells - Make histamine, which then stimulates the chief cells. Also stimulated by PNS
Chief cells - Make pepsinogen, converted to pepsin by HCl
G cells in antrum make gastrin which activates parietal cells
D cells in the duodenum make somatostatin, which decreases the activation of Chief cells
Mucin cells - make alkaline mucus to protect other cells

27
Q

Symptoms of peptic ulcers

A

Burning/gnawing epigastric pain, worse on lying flat
Pain associated with eating - better for duodenal ulcers, worse for gastric
Indigestion
Heartburn
Loss of appetite
Weight loss
N and V

Perforation:
Malaena
Haematemesis
Sudden sharp epigastric pain

28
Q

Differentials for peptic ulcers

A

Non-ulcer dyspepsia
Gastritis
Pancreatitis
Gall stones

29
Q

RFs for peptic ulcers

A 
Alcohol
FHx
Stress
Smoking
NSAID use
Hypersecretory syndromes e.g. Zollinger Ellison syndrome
30
Q

How does H. Pylori act to cause ulcers?

A

It is a gram negative organism that is capable of living in acidic environments
Lives in many people, but becomes active to cause an ulcer in a few
It can burrow through the mucus layer of the stomach, exposing the epithelium to the acidic environment of the stomach, leading to ulcer formation
Increases gastrin and acid production

31
Q

How do you treat H. Pylori?

A

Test for it with urea breath test, stool antigen, or found on blood test

Should commence triple therapy - amoxicillin, clarithro/metronidazole, PPI for 7 days
In quadruple therapy, add a bismuth compound and a tetracycline to metronidazole and PPI

32
Q

How do NSAIDs cause ulcers?

A

They directly reduce epithelial repair, and induce epithelial damage
Reduction in COX activity reduces prostaglandin production an dtherefore the pretective inflammatory mechanisms
Leaves the epithelium vulnerable to the acidic environement of teh stomach

33
Q

Treatment for NSAID-related ulcers?

A

Stop NSAID use

Use a PPI for 4-8 weeks and see if symptoms have resolved

34
Q

Other medications associated with GI bleeding?

A 
Aspirin - should take PPI if at high risk of ulceration
Warfarin
SSRIs
GCC
Potassium channel activators
35
Q

Complications of a peptic ulcer?

A

Gastric outlet obstruction
Bleeding
Perforation

36
Q

How do you treat a bleeding peptic ulcer?

A

The ulcer can burrow through the arteries surrounding the stomach - normally the gastroduodenal and left gastric arteries
This can lead to large amounts of bleeding
Would do OGD and either:
Clip and use adrenaline
Thermal coagulation and use adrenaline
Fibrin/thrombin with adrenaline

37
Q

What are scoring systems for upper GI bleeds?

A

Glasgow-Blatchford score - looks at obs and blood tests to assess prognosis of upper GI bleeds
Don’t need endoscopy to score

Rockall score - based on OGD findings and demographics to come up with prognosis
3+ is severe risk of re-bleed

38
Q

What is a perforated peptic ulcer?

A

When ulcer erodes through stomach lining

Stomach fluids and air enter the peritoneal cavity > peritonitis

39
Q

What is gastric outlet obstruction?

A

If the ulcer is at the antrum it can stop the progression of food through the gastric outlet, this can lead to discomfort and post-prandial vomiting
Can be due to gastric Ca or pancreatic Ca

Year 3 (23 decks)

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