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Medicine Phase 2a GI > Causes of Upper GI Bleeding > Flashcards

Causes of Upper GI Bleeding Flashcards

1
Q

Causes of upper GI bleeding

A

Mallory-weiss tear
Oesophago-gastric varices
Peptic ulcer

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2
Q

What is a Mallory-Weiss tear

A

This is a linear mucosal tear occurring at the oesophagogastric junction and
produced by a sudden increase in intra-abdominal pressure
Lead to bleeding

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3
Q

Clinical presentation of Mallory-Weiss tear

A

Bout of retching or vomiting -> Haemetesis

Others: Syncope, light headedness, dizziness

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4
Q

Pathophysiology of Mallory-Weiss tear

A

Sudden increased intragastric pressure within the non-distensible lower oesophagus can cause tearing of the mucosa.
Blood then enters the oesophagus and is vomited out

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5
Q

Aetiology of Mallory-Weiss tear

A

Trauma from frequent cough, vomit, retching or even hiccuping
RF: Excessive alcohol consumption; NSAIDs

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6
Q

Epidemiology of Mallory-Weiss tear

A

2-8% all Upper GI bleeding
Bulimics and alcoholics
Males aged 20-50

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7
Q

Diagnosis of Mallory-Weiss tear

Differentials

A

*Endoscopy (confirms)
Differential diagnosis:
Gastroenteritis; peptic ulcer; oesophageal varices

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8
Q

Treatment of Mallory-Weiss tear

A

Resuscitation
Maintain airway, high flow oxygen, correct fluid losses
Identify co-morbidities
Tear tends to heal rapidly

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9
Q

Complications of Mallory-Weiss tear

A

Hypovolaemic shock (and death)
Rebleeding
MI
Such bleeding rare

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10
Q

What are Oesophago-Gastric varices

A

Dilated veins at the junction between the portal and systemic venous systems leading to variceal haemorrhage

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11
Q

Clinical presentation of Oesophago-Gastric varices

A

Haematemesis
Liver disease
Pallor
Shock (low BP/ high HR)

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12
Q

Pathophysiology of Oesophago-Gastric varices

A

Liver disease leads to high pressure in the portal veins -> veins at the junction with systemic venous system distend (varices).
This causes damage and can lead to bleeding from the varices into the oesophagus -> Haematemesis

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13
Q

Aetiology of Oesophago-Gastric varices

A

Portal hypertension

Majority of patients with oesophageal varices have chronic liver disease

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14
Q

Epidemiology of Oesophago-Gastric varices

A

10-20% of all Upper GI bleeding

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15
Q

Diagnosis of Oesophago-Gastric varices

A

Endoscopy

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16
Q

Treatment of Oesophago-Gastric varices

A 
Resuscitation
Maintain airway
Treat shock
other:
Vasoactive drugs
Endoscopic band ligation
Antibiotics as prophylaxis
Can obturate with glue like substance
17
Q

Complications of Oesophago-Gastric varices

A

70% chance of rebleeding

Significant risk of death

18
Q

What is a peptic ulcer

A

Break in the GI mucosa in or adjacent to acid bearing area

19
Q

Types of peptic ulcer

A

Gastric

Duodenal

20
Q

What % of Gastric peptic ulcer is H.pylori associated with?

A

80%

21
Q

What % of Duodenal peptic ulcer cases is H.pylori associated with?

A

95%

22
Q

Where in stomach can H.pylori be found

A

Mucus layer

23
Q

Clinical presentation of peptic ulcer

A

Burning epigastric pain. Nausea, heartburn, and flatulence. Occasionally painless haemorrhage.
(Not vomiting)

24
Q

Difference in clinical presentation between duodenal and gastric peptic ulcer

A

Duodenalmore pain when the patient is hungry, and at night.

25
Q

Pathophysiology of peptic ulcer

A

Depending on the aetiology, a reduction in protective prostaglandins or an increase in gastric acid secretions causes the acidic contents of the stomach/duodenum to break down the mucosa. Pain varies with the acid level of the area affecting the ulcer. H. pylori can infect mucosa following this damage -> further damage through inflammation and proteases.

26
Q

**Aetiology of peptic ulcer

A

H. pylori, Bile Regurgitation, Ischaemia of mucus producing cells and NSAIDs.
H. pylori: Increased gastric acid secretions. Disruption of mucous protective layer. Reduced duodenal bicarbonate production
NSAIDs (Ibuprofen): Inhibit cycloxygenase-1 which inhibits production of prostaglandins needed for mucous production and provide mucosal protection in the upper GI - thus mucousal damage.
Ischaemia, reducing blood flow to mucus secreting cells, therefore less mucus secreted and so acid of stomach destroys these cells and over time causes ulceration.
Bile regurgitation

27
Q

Epidemiology of peptic ulcers

A

50% of all Upper GI bleeding

Duodenal 2-3x more common than gastric

28
Q

*Diagnosis of peptic ulcers

A 
Testing for H.pylori: Urea breath test, serology or stool antigen test
Alternatively endoscopy (but more invasive)
29
Q

Treatment of peptic ulcers

A 
Avoid NSAIDs
Cessation of smoking
Eradication of H.pylori through 2 antibiotics and PPI
->Triple therapy: 
Lansoprazole (PPI)
Clarithromycin
Metronidazole or Amoxicillin
Antacids also helpful
30
Q

Complications of peptic ulcers

A

Can cause upper GI bleed

Peritonitis if continues to grow

31
Q

Prevention of bleeding from vatical haemorrhage

A
  • Non-selective B-blockade e.g. PROPRANOLOL to reduce resting pulse rate to decrease portal pressure
  • Variceal banding repeatedly (to obliterate varices)
  • Liver transplant - best option when there is poor liver function
32
Q

Initial management of bleeding from variceal haemorrhage

A
  • Resuscitate until haemodynamically stable
  • If anaemic then BLOOD TRANSFUSION aiming to get Hb to 80g/L
  • Correct clotting abnormalities -> administer VITAMIN K and PLATELET TRANSFUSION
  • Vasopressin -> IV TERLIPRESSIN -> to cause vasoconstriction, (use IV SOMATOSTATIN if terlipressin is contraindicated e.g. in ischaemic heart disease)
  • Prophylactic antibiotics to treat and prevent infection as well as reduce early rebleeding and mortality e.g. CEPHALOSPORIN
  • Variceal banding
  • Ballon tamponade to reduce bleeding by placing pressure on varice if banding fails
33
Q

What is variceal banding

A

where a band is put around varice using an endoscope, after a few days the banded varix degenerates and falls off leaving a scar

34
Q

How do NSAIDs cause mucosal damage

A

NSAIDs inhibit cyclooxygenase-1 which inhibits the production of prostaglandins needed for mucous production, leading to mucosal damage

35
Q

Medical treatment of oesophageal varices

A

Beta blocker to reduce CO -> reduce portal pressure
Nitrate to reduce portal pressure
Terlipressin – analogue of ADH -> reduce portal pressure

36
Q

Surgical treatment of oesophageal varices

A

Band ligation

Transjugular intrahepatic portosystemic shunt (TIPSS)

Medicine Phase 2a GI (35 decks)

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