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GI AND SURGERY > UPPER GI BLEEDING > Flashcards

UPPER GI BLEEDING Flashcards

1
Q

What are the main signs of upper GI bleeds?

A

Haematemesis/coffee-ground vomit
Meleana
Haematochezia (only in context of profuse upper GI haemorrhage)
Haemodynamic instability - hypotension, tachycardia, syncope
Symptoms related to underlying pathology e.g. pain/jaundice etc

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2
Q

Whats the epidemiology and mortality of upper GI bleeds?

A

1 in 1,000 per year
1:2 males:females
Mortality 7-10%

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3
Q

What are causes of upper GI bleeds?

A

Varices (10-20%) - oesophageal or gastric
Gastric and duodenal ulcers (50%)
Mallory-Weiss tear (5-10%)
Oesophagitis (2-5%)
Gastritis
Duodenitis
Diverticulum
Aortoduodenal fistula
Arteriovenous malformation
Neoplasms stomach/duodenum/oesophagus
Trauma from recent surgeries and interventions

Less common:
Swallowed blood e.g. posterior nose bleed
Bleeding disorders
Aortoenteric fistula
Hereditary haemorrhagic telangiectasia
Gastric natural vascular ectasia
Dieulafoys lesion

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4
Q

What scoring system is used for suspected upper GI bleed?

A

Glasgow-blatchford scale
It helps clinicians decide whether pt can be managed as an outpatient or not

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5
Q

Outline the Glasgow-blatchford scaling system?

A

It asks about…
Hb
BUN
Systolic BP
Sex
HR >100
Melena present
Recent syncope
Hepatic disease history
Cardiac failure present

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6
Q

How do we interpret the Glasgow-blatchford score?

A

A score greater than 0 suggests a high risk GI bleed that is likely to require medical intervention
A score =/>6 is associated with a >50% risk of needing an intervention

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7
Q

Why does urea rise in upper GI bleeds?

A

Blood in the GIT gets broken down/digested and one of the products is urea

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8
Q

What is the Rockall score?

A

A scoring system used after endoscopy
It determines the severity of GI bleeding and what the re bleeding and mortality risk

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9
Q

What is in the Rockall scoring system?

A

Age <60, 60-79, =/>80
No shock, tachycardia, hypotension
Comorbidities (higher risk if renal failure, liver failure or disseminated malignancy)
Diagnosis of Mallory-Weiss tear, no lesion identified, all other diagnosis or maliganncy of upper GIT
Major stigmata of recent haemorrhage (none, dark spot, blood in upper GIT, adherent clot, visible/spurting vessel)

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10
Q

What are the risk factors for upper GI bleeds?

A

NSAID use
Anticoagulant use
Alcohol abuse
Chronic liver disease
CKD
Advancing age
Previous PUD or H.pylori infection

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11
Q

How do we formally risk assess pt with acute upper GI bleeding?

A

The blatchford score at first assessment
Full Rockall score after endoscopy

(Early discharge for pt with a pre-endoscopy Blatchford score of 0)

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12
Q

When should pt with acute upper GI bleeds have an endoscopy?

A

Immediately after resuscitation
Within 24 hours of admission if not severe

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13
Q

What proportion of pt with an acute upper GI bleed will stop bleeding spontaneously within 48 hours?

A

85%

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14
Q

How are upper GI bleeds investigated?

A

Upper GI endoscopy as soon as patient is stabilised
Obs
ECG
Monitor urine output
FBC, VBG, U&E, coag, LFT, clotting, Group and save with cross match
Chest X-ray
PR

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15
Q

Why is NSAID use a risk factor for upper GI bleeds?

A

NSAIDs inhibit the synthesis of prostaglandins, which are gastroprotective.
Prostaglandins work by inhibiting enterochromaffin-like cells, which are involved in the secretion of histamine. Histamine stimulates parietal cells to secrete hydrochloric acid. Therefore, inhibition of prostaglandins leads to excessive HCl secretion and damage to the underlying mucosa.

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16
Q

why does alcohol abuse increase risk of upper GI bleed?

A

It can cause Mallory-Weiss tears

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17
Q

why does chronic liver disease put you at risk for an upper GI bleed?

A

Portal hypertension can lead to gastrooesophageal varices or gastropathy

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18
Q

How are upper GI bleeds managed?

A

A-E approach
Bloods (FBC, U&E, INR, LFT, group+crossmatch)
IV access x2 large-bore
IV Crystalloid fluids
Blood transfuse if necessary. Give oxygen therapy
Platelet transfusion if necessary
Endoscopy
Drugs - stop Anticoagulation and NSAIDs (be wary about stopping platelets - risk of thrombosis)

Arrange surgery if bleeding persists

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19
Q

How can you remember what is in the Rockall scoring system?

A

ABCDE
Age
Blood pressure
Comorbidity
Diagnosis
Endoscopic findings

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20
Q

What are the indications for blood transfusion when managing an acute GI bleed?

A

Shock - pallor, cold nose, systolic BP <100, >100bpm)
Hb <100g/L

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21
Q

What is the half life of rivaroxaban (normal renal function)?

A

5-9 hrs

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22
Q

What is the half life of apixaban (normal renal function)?

A

8-15 hrs

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23
Q

What is the half life of dabigatran (normal renal function)?

A

12-14 hrs

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24
Q

What is the half life of edoxaban (normal renal function)?

A

10-14 hrs

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25
Q

In what proportion of cases of upper GI bleeds can endoscopy detect the cause of haemorrhage?

A

In 80% or more

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26
Q

What are the indications for platelet transfusion when managing an acute GI bleed?

A

Those who are actively bleeding and have a Plt count of <50x109/L

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27
Q

How do you manage non-varices bleeding?

A

Endoscopic - mechanical methods e.g. clips, thermal coagulation with adrenaline, fibrin/thrombin with adrenalin
PPI after endoscopy (DONT GIVE BEFORE)

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28
Q

How do you manage variceal bleeding?

A

ABC:
correct clotting: FFP, vitamin K

vasoactive agents: terlipressin (octreotide may also be used although there is some evidence that terlipressin has a greater effect on reducing mortality)
prophylactic IV antibiotics (quinolones) have been shown to reduce mortality in patients with liver cirrhosis.
both terlipressin and antibiotics should be given before endoscopy in patients with suspected variceal haemorrhage

endoscopic variceal band ligation (second line is endoscopic sclerotherapy)
Sengstaken-Blakemore tube if uncontrolled haemorrhage
Transjugular Intrahepatic Portosystemic Shunt (TIPSS) if above measures fail

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29
Q

What are the complications of GI bleeding?

A

Respiratory distress
MI
Infection
Shock
Death

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30
Q

What are oesophageal varices?

A

Abnormally dilated submucosal veins in the wall of the oesophagus that lie within the anastomoses of the systemic and portal circulation

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31
Q

What causes oesophageal varices?

A

Oesophageal varices occur secondary to portal hypertension most commonly secondary to chronic liver disease / cirrhosis
Increases in portal pressure lead to the development of a collateral circulation to overcome the obstruction to flow in the portal system.
The lower end of the oesophagus forms an important ‘portacaval anastomosis’ which allows the flow of venous blood from the portal system to the systemic circulation - extra blood causes oesophageal/gastric vessels to expand and swell

Other causes: thrombosis in portal vein, schistosomiasis and budd-chiari syndrome

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32
Q

What are Mallory Weiss tears?

A

Longitudinal mucosal lacerations in the distal esophagus and proximal stomach

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33
Q

What is Boerhaaves syndrome?

A

a spontaneous perforation of the esophagus that results from a sudden increase in intraesophageal pressure combined with negative intrathoracic pressure (eg, severe straining or vomiting)

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34
Q

What causes Mallory-Weiss tears?

A

Sudden increases in intra-obdimanl pressure e.g. coughing, retching,m alcoholic dry heaves

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35
Q

Where do Mallory-Weiss tears tend to occur?

A

At the gastro-oesophageal junction

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36
Q

Whats the prognosis of mallory-Weiss tears?

A

They are generally small bleeds and self-limiting in the absence even of blotting abnormalities or anti-coags
Presentation with haemorrhagic shock is possible but rare!

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37
Q

Whats the most common underlyign cause for oesophageal varices?

A

Alcohol-related liver disease

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38
Q

What is a gastric/duodenal ulceration?

A

A breach in the epithelium of the gastric or duodenal mucosa respectively, that penetrates the muscularis mucosa

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39
Q

What is peptic ulcer disease?

A

An umbrella term for the development of gastric and duodenal ulcers

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40
Q

Which type of ulcer in PUD is more common?

A

Duodenal ulcers 2-3 times more likely

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41
Q

What are the risk factors for PUD?

A

H.pylori infection
Drugs
Smoking
Alcohol consumption
Stress
Zollinger-Ellison syndrome (rare)

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42
Q

How does an h.pylori infection increase the risk of PUD?

A

H.pylori colonise the gastric antrum causing persistent low-grade inflammation which can damage the epithelial lining. This can cause destruction of the normal gastric mucosal barrier which promotes the development of ulcerations and others complications

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43
Q

What proportion of cases of PUD in those not taking NSAIDs are associated with an H.pylori infection?

A

90% of those with a duodenal ulcer and 70-80% of those with a gastric ulcer

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44
Q

What drugs can be a risk factor for PUD?

A

NSAIDs
Aspirin
Bisphosphonates
Corticosteroids
Potassium supplements
SSRIs
Recreational drugs e.g. crack cocaine

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45
Q

How do NSAIDs increase the risk of PUD?

A

NSAIDs inhibit COX-1 which reduces the production of mucosal protective prostaglandins

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46
Q

How do stress/alcohol/coffee/smoking/spicy foods increase the risk of PUD?

A

They increase HCL production

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47
Q

Whats the incidence of ulcers in chronic NSAID users?

A

20%
4 fold increase

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48
Q

How does Zollinger-Ellison syndrome increase the risk of PUD?

A

Zollinger-Ellison syndrome occurs secondary to hypersecreting gastrinoma within the pancreas
Hypergastrinarmia = multiple peptic ulcers

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49
Q

Where are duodenal ulcers typically found?

A

In the duodenal cap

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50
Q

Where are gastric ulcers commonly found?

A

On the lesser curvature but can be found in any part of the stomach
Most commonly in gastric antrum because its least acidic

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51
Q

What proportion of the adult population do duodenal ulcers affect?

A

10%

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52
Q

Why is PUD more prevalent in developing companies?

A

Due to high H.pylori infection rates

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53
Q

What is helicobacter pylori?

A

A slow-growing spiral gram-negative flagellate ureatase-producing bacterium
It colonises the mucous layer in the gastric antrum and duodenum

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54
Q

Outline the epidemiology of H.pylori?

A

80-90% of population in developing countries
20-50% in developed countries

Infection rates are highest in low-income groups
Infection is usually acquired in childhoos

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55
Q

How is H.pylori transmitted?

A

Faecal oral or oral-oral

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56
Q

What proportion of those infected with H.pylori will develop PUD?

A

15%

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57
Q

What factors allow H.pylori to survive within the stomach/duodenum?

A

Pathophysiology
Helicobacter pylori has 2 main mechanisms to survice in the acidic gastric environment:
chemotaxis away from low pH areas, using its flagella to burrow into the mucous lining to reach the epithelial cells underneath
secretes urease → urea converted to ammonia → alkalinization of acidic environment (buffers H+) → increased bacterial survival
pathogenesis mechanism:
Helicobacter pylori releases bacterial cytotoxins (e.g. CagA toxin) → disruption of gastric mucosa

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58
Q

What are the possible complications of a H.pylori infection?

A

Inflammation - antral gastritis or gastric intestinal metaplasia
PUD
Gastric cancer

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59
Q

What are the characteristics features of peptic ulcer disease?

A

Recurrent, burning epigastric pain
Pain may be relived by antacids
Dyspepsia
Nausea
Vomiting is infrequent but can relive the pain
Anorexia and weight loss may occur (particularly in GU)
May be symptomaless

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60
Q

Patients with PUD may present acutely with what features?

A

Features of an acute upper GI bleed - haematemesis, melaena, shock
Perforation - acute severe abdo pain and tenderness, gaurding, features of shock

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61
Q

What proportion of peptic ulcers are asymptomatic?

A

70%

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62
Q

What are the differences in presentation for gastric vs duodenal ulcers?

A

Eating worsens the pain of gastric ulcers and improves the pain of duodenal ulcers (but painful when hungry)

Pain of DU is typically at night as well as in the day
Anorexia and weight loss are more common with GU

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63
Q

Who do the NICE guidelines suggest a referral for urgent upper oesophago-gastro-duodenoscopy?

A

New onset dysphagia
>55 with weight loss and upper abdo pain/reflux/dyspepsia
New onset dyspepsia refractory after PPI treatment

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64
Q

How long after eating does the pain from duodenal ulcers tend to worsen?

A

2-4 hours after

65
Q

What is Zollinger-Ellison syndrome?

A

A rare condition where 1 or more tumours develop in the pancreas of small intestine = gastrinoma
A triad of severe PUD, gastric acid hypersecretion and gastrinoma (pancreatic or duodenal tumours)

66
Q

How is H.pylori infection tested for?

A

Carbon-13 urea breath test or stool antigen test
Lab serological testing if above can’t be done

67
Q

Whats the serological test done for testing for the presence of H.pylori?

A

enzyme linked immunosorbent assay to detect serum H. pylori–specific immunoglobulin G and immunoglobulin A antibodies

68
Q

What is the 13 c-ureabreath test?

A

Patients swallow urea labelled with non-radioactive carbon-13. 10–30 minutes later, the detection of isotope-labelled CO2 in exhaled breath indicates that the urea was split; this indicates that urease is present in the stomach, and hence that H. pylori bacteria are present.

69
Q

How should you investigate suspected PUD?

A

Test for h.pylori with urea breath test or stool test
ECG to rule out cardiac cause
FBC (may show IDA)
LFTs (rule out biliary pathology and gallstone)
Upper GI endoscopy
All identified gastric ulcers should be biopsies

70
Q

Whats the stool antigen test for H.pylori?

A

It assess faeces for the presenc of H,pylori antigen

71
Q

What invasive tests can be done to investigate H.pylori?

A

Urease test (also known as CLO test)
Histology
Culture

72
Q

What is important to ensure prior to any H.pylori tests?

A

Patients should stop any current medical therapy for 2 weeks prior (especially PPIs) to reduce the risk of false negatives

73
Q

What should you do if a pt you are investigating for proven PUD tests negative for H.,pylori infection?

A

Full dose PPI therapy for 4-8 weeks depending on clinical judgment

74
Q

How should you manage someone with confirmed gastric/duodenal ulcer who tests positive for H.pylori infection and takes NSAIDs chronically? I.e. H.pylori infection + ulcer + NSAID use

A

prescribe full-dose PPI therapy for 2 months, then prescribe first-line eradication therapy after completion of PPI therapy.

75
Q

Whats the first line H.Pylori eradication regimen?

A

PPI with a combination of antibiotics and in some cases bismuth in cases of eradication failure

PPI - lansoprazome, omeprazole, esomeprazole or pantoprazole or rabeprazole
Antibiotics - 7 day triple therapy regimen of amoxicillin and PPI and clarithfrocmycin (or metronadazole)

76
Q

Why should smoking be stopped in PUD?

A

prescribe full-dose PPI therapy for 2 months, then prescribe first-line eradication therapy after completion of PPI therapy.

77
Q

What follow up does a pt with gastric or duodenal ulcer need?

A

Re-endoscopied at 6 weeks to confirm mucosal healing and exclude an underlying gastric cancer
Repeat biopsies may be necessary

Duodenal ulcers do not routinely require this follow-up endoscopy

78
Q

Whats the 1st line eradication for H.pylori in someone with a penicillin allergic?

A

Triple therapy with PPI, clarithromycin and metronidazole

79
Q

When is specialists referral warranted in patients with H.pylori infection?

A

When the disease has not responded to second-line therapy or there are unexplained symptoms.

80
Q

What conservative management can pt with PUD be given?

A

Smoking cessation
Weight loss
Reduction in alcohol consumption
Avoidance/cessation of NSAIDs where possible

81
Q

What are the complications of PUD?

A

Haemorrhage
Perforation
Gastric outlet obstruction

82
Q

Which ulcers perforate more commonly?

A

Duodenal ulcers - perf into the peritoneal cavity of lesser sac

83
Q

Whats the mortality of a peptic ulcer disease-related perforation?

A

Up to 20%

84
Q

What are the symptoms of a peptic ulcer disease-related perforation?

A

Sudden epigastric pain later becoming more generalised
Syncope

85
Q

How do we investigate a PUD related perforation?

A

Plain x-ray erect chest
As 75% of pt will have free air under the diaphragm

86
Q

How are PUD-related perforations treated?

A

Laparoscopic surgery to close the perforation and drain the abdomen
In elderly and very sick pt instead conservative management may be used - nasogastric suction, IV fluids and antibiotics

87
Q

Whats the most common complication of PUD?

A

Acute bleeding

88
Q

Outline the pathology behind a haemorrhage secondary to PUD?

A

Typically its a posterior duodenal ulcer eroding through into the gastroduodenal artery. However many occur secondary to erosions through smaller-sized blood vessels within the submucosa.

89
Q

Whats the mortality of a PUD-related haemorrhage?

A

5-10%

90
Q

Whats the presentation of a PUD-related haemorrhage?

A

Haematemesis
Meleana
Hypotension and tachycardia

91
Q

How is a haemorrhage secondary to PUD managed?

A

ABC approach as with any upper GI haemorrhage
IV PPI
Endoscopic intervention

In 10% of pt endoscopic intervention fails so they may need an urgent interventional angiography with transarterial embolisation, or surgery.

92
Q

What is a gastric outlet obstruction?

A

a mechanical obstruction of the proximal gastrointestinal tract, occurring at some level between the gastric pylorus and the proximal duodenum, resulting in an inability in the stomach to empty.

93
Q

How can PUD cause gastric outlet obstruction?

A

There may be an active ulcer with surrounding oedema
OR
The healing of an ulcer has been followed by scarring

94
Q

What are the most common causes of gastric outlet obstructions?

A

Crohn’s disease
External compression from a pancreatic carcinoma

Others:
PUD
Gastric cancer or small bowel cancer
Iatrogenic - anastaomotic structure following gastrectomy
Bouveret syndrome
Gastric bezoar

95
Q

What is the presentation of gastric outflow obstruction?

A

Vomiting without pain - infrequent, projectile and large in volume. Vomitus contains particles of previous meals. Occurs post-prandial
May have epigastric pain, early satiety and nausea

Dehydrated and often hypovolaemic - tachycardia, hypotensive and oliguric
Tender and distended upper abdomen
Succession splash on auscultation

96
Q

What is bouveret sundrome?

A

a gastric outlet obstruction secondary to a gallstone impacted at the pylorus or proximal duodenum. It occurs in patients with a cholecystoduodenal fistula, typically developing from episodes of recurrent cholecystitis.

97
Q

Whats the main differential for gastric outflow obstruction?

A

Gastroparesis
Similar clinical features but its caused by a neuromuscular dysfunction rather than a mechanical obstruction present - differentiated by endoscopy/CT

98
Q

What metabolic abnormality can severe or persistent vomiting cause?

A

Hypokalaemia metabolic alkalosis

99
Q

What should you check for/rule out if the pt has recurrent ulcers?

A

H,pylori
Zollinger-Ellison syndrome
Malignancy

100
Q

What is dumping syndrome?

A

Nausea and distension associated with sweating, fainting and palpitations
These sympotms occur in pt following a gastrectomy or gastroenterostomy and is caused by the dumping of food into the jejunum
This occurrence causes a shift of fluid from the intravascular component to the intestinal lumen, which results in cardiovascular symptoms, release of several gastrointestinal and pancreatic hormones and late postprandial hypoglycemia. Early dumping symptoms comprise both gastrointestinal and vasomotor symptoms. Late dumping symptoms are the result of reactive hypoglycemia

101
Q

What are the long-term complication sof a gastric surgery?

A

Dumping syndrome
Diarrhoea
Nutritional complications - IDA< folate deficiency, vit B12 and weight loss

102
Q

What are H.pylori associated diseases?

A

PUD
Gastric adenocarcinoma (distal!)
Gastric B-cell lymphoma (70% of pt with this have H.pylori)

103
Q

What is gastroparesis?

A

Delayed gastric emptying causing nausea, vomiting, early satiety, fullness, bloating and upper abdominal pain.

104
Q

What can cause gastroparesis?

A

diabetes
• amyloidosis
• scleroderma
• parkinsonism
• multiple sclerosis
• stress
• medications (tricyclic antidepressants, dopamine agonists, calcium-channel blockers, octreotide, cyclosporine, glucagon-like peptide agonists, phenothiazines)
• post-surgical
• idiopathic.

105
Q

How is gastroparesis investigated?

A

OGD to rule out mechanical obstruction + CT/MRI or barium meal if needed
Scintigraphy

106
Q

What is scintigraphy?

A

also known as a gamma scan
Radioisotopes attached to drugs travel to a specific organ or tissue and are taken internally and the emitted gamma radiation is captured by external detectors to form 2D images in a similar process to the capture of x-ray images

107
Q

What is gastrooduodenal manometer?

A

a test of the pressure changes that occur within the stomach and upper intestine during digestion
It can help differentiate between myopathic and neuropathic causes of gastroparesis

108
Q

How is gastroparesis managed?

A

Relief of symptos
Correct nutritional deficiencies
Pro-motility agents - metoclopramide, domperidone
Gastric pacemark insertion
Frequent, small, low-fibre meals

109
Q

What is oesophagitis?

A

inflammation of the oesophagus

110
Q

What are the common symptoms of oeosphagitis?

A

Dysphagia
Odynophagia
Food impaction
Retrosternal pain
Heart burn/acid reflux

111
Q

What is gastritis?

A

Inflammation of the mucosa of the stomach

112
Q

What are the typical symptoms of gatsritis?

A

Indigestion
Abdominal pain
Nausea and vomiitng
Bloating
Loss of appetite
Burping and flatulence

113
Q

What is Duodenitis?

A

Inflammation of the mucosa of the duodenum

114
Q

What are the common symptoms of Duodenitis?

A

Early satiety
Flatulance and bloating
Nausea and vomiting
Abdo cramps
Indigestion

115
Q

What is oesophageal diverticulum?

A

a pouch that protrudes outward in a weak portion of the esophageal lining

116
Q

What is Zenker’s diverticulum?

A

Aka hypopharyngeal diverticulum or pharyngeal pouch
Posterior herniation of oesophageal mucosa into Killian’s triangle
It’s actually a pseudodiverticulum since the Zenkers pouch contains only oesophageal mucosa and submucosa

117
Q

What is Killian’s triangle?

A

an area of least resistance situated above the cricopharyngeus muscle and below the inferior pharyngeal constrictor muscle

118
Q

What is oesophageal diverticulitis?

A

Inflammation or infection of diverticula in oesophagus

119
Q

What is an aorto-enteric fistula?

A

a direct communication between the aorta and the GI tract

120
Q

How are Aortoenteric fistula classified?

A

can be classified into primary and secondary types according to the presence or absence of a prior history of aortic surgery

121
Q

What is an Aortoduodenal fistula?

A

an abnormal communication between the infrarenal aorta and duodenum involving the 3rd part of the duodenum in two-thirds of cases and the 4th part in one-third of cases

122
Q

What is an Arteriovenous malformation?

A

Abnormal connection between an artery and a vein - capillary bed doesn’t form so the arteries are connected directly to the veins = high pressure causes arteries to dilate and veins to fibrose

123
Q

What is hereditary hemorrhagic telangiectasia?

A

A rare autosomal dominant disorder involving the components inbolved in blood vessel development
Causes recurrent epistaxis and chronic GI bleeding

124
Q

What are Dieulafoy’s lesions?

A

A condition characterized by a large tortuous arteriole most commonly in the stomach submucosa that erodes and bleeds.
It can present in any part of the gastrointestinal tract.
It can cause gastric hemorrhage but is relatively uncommon

125
Q

Whats the prophylactic management of variceal bleeding?

A

propranolol: reduced rebleeding and mortality compared to placebo
Offer endoscopic variceal band ligation for the primary prevention of bleeding for people with cirrhosis who have medium to large oesophageal varices - every 2 weeks until all varices have been eradicated (give PPI alongside to prevent EVL-induced ulceration

126
Q

Whats the MOA of terlipressin?

A

It’s a vasopressin analogue

It causes splanchnic vasoconstriction, thereby causing a reduction in portal pressure and variceal bleeding

127
Q

Whats the investigation of choice for a suspected perforated peptic ulcer?

A

Erect chest x-ray

128
Q

Why are IV antibiotics given prophylactically before endoscopy when managed oesophageal varices?

A

can prevent infection and improve mortality in cirrhotic patients.

129
Q

What is an OGD?

A

oesophago-gastro-duodenoscopy

130
Q

What is a Sengstaken-Blakemore tube?

A

a medical device inserted through the nose or mouth and used occasionally in the management of upper gastrointestinal hemorrhage due to esophageal varices
a red tube with three ports on one end and two balloons on the other. One balloon goes into your stomach and is filled with air using one port. The other balloon sits in your esophagus and is inflated with the second port. The third port, called the gastric suction port, suctions fluid and air out of your stomach.‌

131
Q

How should you manage a patient with ongoing acute bleeding despite repeated endoscopic therapy?

A

Laparotomy and surgical exploration

132
Q

What are the symptoms of Zenkers diverticulum?

A

dysphagia
regurgitation
aspiration
neck swelling which gurgles on palpation
halitosis

133
Q

How do you investigate zenkers diverticulum?

A

barium swallow combined with dynamic video fluoroscopy

134
Q

Should you prescribe PPIs for upper GI bleeds?

A

Not until after the endoscopy as it can mask the site of bleeding

135
Q

Whats the definition of an upper GI bleed?

A

a haemorrhage with an origin proximal to the ligament of Treitz

136
Q

Whats the mortality rate of upper GI bleeds?

A

10% in outpatients
30% in inpatients

137
Q

How much blood have you lost if you are experiencing postural hypotension?

A

20 mmHg drop in systolic blood pressure or a 10 mmHg drop in diastolic blood pressure.
10% blood loss

138
Q

When should a pt have a blood transfusion?

A

Hb <80g/dL

139
Q

What is within the GBS score?

A

Blood urea level
HB level
Systolic bp
Pulse >100
Melaena
Syncope
Hepatic disease
Cardiac failure

140
Q

What is used to calculate the Rockall score?

A

Age
Shock
Comorbidities
Diagnosis
Major stigmata of recent hemorrhage

141
Q

Outline class 1 hypovolaemic shock?

A

<750ml of blood loss (0-15%)
HR <100
Normotensive
Norm resp rate
Slightly anxious

142
Q

Outline class 2 hypovolaemic shock?

A

750-1500ml blood loss (15-30%)
HR >100
Normotensive
20-30 RR
Mildly anxious

143
Q

Outline class 3 hypovolaemic shock?

A

1500-2000ml blood loss (30-40%)
HR >120
Decrease bp
30-40 RR
Anxious and confused

144
Q

Outline class 4 hypovolaemic shock?

A

> 2000ml blood loss (>40%)
HR >140
Decreased bp
35 RR
Confused and lethargic

145
Q

Why are upper GI bleeds increasing in incidence?

A

Elderly, increased use of drugs, increased alcohol use, NASH cirrhosis and more nterventions e.g. ERCP

146
Q

Which ulcers (gastric/duodenal) are more likely to be maligannt?

A

Gastric

147
Q

What causes acute haemorrhagic gastritis?

A

H pylori infections
NSAIDs and aspirin
Alcohol abuse
Stress and unwell e.g. after surgery

148
Q

What are the 2 most common causes of upper GI bleeding?

A
  1. PUD
  2. Oesophageal varices
149
Q

Whats the most likely cause of an upper GI bleed in a pt with vascular comorbidities?

A

Fistula

150
Q

Why do you need antibiotics in upper GI bleed?

A

Likely to develop bacterial infections e.g. through aspiration pneumonia

151
Q

How does terlipressin work in managing variceal bleedS?

A

Synthetic analogue of vasopressin which reduces portal blood flow hence variceal bleeds

152
Q

What surgery can be done for varices?

A

Banding

153
Q

Why do you need adrenaline injections to manage varices as well as the banding/clips?

A

Not sure

154
Q

What is a transjugular intrahepatic portosystemic shunt (TIPS)?

A

a procedure that involves inserting a stent to connect the portal vein to the hepatic vein which has a lower pressure. This relieves the pressure of blood flowing through the diseased liver and can help stop bleeding and fluid back up.

155
Q

How are oesophageal varices staged?

A

According to size

Grade 1 - small, straight oesophageal varices
Grade 2 - enlarged, tortuous oesophageal varices occupying <1/3rd of the lumen
Grade 3 - large coil shaped oesophageal varices occupying >1/3rd of the lumen

156
Q

Whats the Mackler triad for Boerhaave syndrome?

A

vomiting, thoracic pain, subcutaneous emphysema

157
Q

Who does Boerhaave syndrome typically affect?

A

Middle aged men with a background of alcohol abuse

158
Q

Whats the moa of PPIs?

A

Irreversible blockade of H+/K+ ATPase of gastric parietal cell

159
Q

What are the adverse effects of PPIs?

A

hyponatraemia
Rare - hypomagnasaemia (more common after 1 year of treatment)
osteoporosis → increased risk of fractures
microscopic colitis
increased risk of C. difficile infections

GI AND SURGERY (31 decks)

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