MET3 Revision - Gastroenterology II COPY Flashcards

1
Q
A
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2
Q

Which anatomical point distinguishes between an upper and lower GI bleeding? [1]

A

Ligament of Treitz:
- Proximal: upper GI
- Distal: lower GI

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3
Q

State the causes of upper GI bleeds [5]

A

Peptic Ulcer Disease – 44%
Oesophagitis - 28%
Gastritis/Erosions – 26%
Erosive Duodenitis – 15%
Varices – 13%
Portal Hypertensive gastropathy – 7&
Malignancy - 5%
Mallory Weiss Tear – 5%
Vascular Malformation – 3%

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4
Q

State the causes of lower GI bleeds [5]

A

Diverticular disease (30%)
* Haemorrhoids (14%)
* Mesenteric Ischaemia (12%)
* Colitis (9%)
* Cancer (6%)
* Rectal ulcers (6%)
* Angiodysplasia (3%)
* Radiation (3%)
* Drugs
* Other

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5
Q

What is this cause of upper GI bleeding? [1]

A

Gastritis

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6
Q

What is the most common cause of portal HTN worldwide? [1]

A

Schistomiasis

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7
Q

What is a mallory weiss tear? [1]

Describe typical presentation [1]

A

Forceful vomiting / retching causing a mucosal tear in the oesophagus causing subsequent bleeding

First bout of vomiting has no bleeding (prior to tear)
Second + bout of vomiting has bleeding

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8
Q

Describe pathophysiology is diverticular disease causing lower GI bleeding? [1]

How does diverticular disease lead to lower GI bleeding? [1]

A

Diverticular disease:
- a condition where small pouches (called diverticula) form in the lining of your bowel and push out through your bowel wall due to high intra-luminal pressure
-

Diverticulae lie adjacent to mesenteric blood flow and because they cause decreased thickness of colonic thickness; increases chance of bleeding

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9
Q

What are causes of diverticular disease? [6]

A
  • Constipation
  • Genetics
  • Obesity
  • NSAIDs
  • Low fibre diet
  • Muscle spasm
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10
Q

State 5 causes of haemorrhoids [5]

A
  • Straining (in bowel movement)
  • Sitting for long periods
  • Chronic diarrhoea or constipation
  • Overweight / obese
  • Pregnancy
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11
Q

Describe how colonic cancer develops [3]

A
  1. polyps;
  2. larger polyp (severe dysplasia)
  3. adenocarcinoma
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12
Q

State 4 reasons that cause colitis which in turn causes lower GI bleeding [4]

A

Ishcaemic colitis: in distal transverse colon / descending colons - position as watershed area between SMA & IMA can lead to bleeding

IBD

Infection

NSAIDs

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13
Q

When taking a history for upper GI bleed, what should you investigate? [3]

A

History:
- Determine if upper or lower GI bleed: haematemesis?

Systemic symptoms of blood loss?
- Dizzyness
- Palpitations
- Chest pain

Risk factors?
- Drugs
- Chronic liver disease (portal HTN?); IHD (anticoagulants); CKD (poorer prognosis)

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14
Q

What are the different classes of blood loss? (% and volume lost?) [4]

A

Class 1:
- 10-15%
- 750mls

Class 2:
- 15-30%
- 1.5L

Class 3:
- 30-40%
- 2L

Class 4:
- >40%
- 3L

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15
Q

Describe the symptoms that classify each class of shock with regards to blood loss? [4]

A

Class 1:
- no clinical signs

Class 2:
- postural hypotension
- generalised vasoconstriction

Class 3:
- Hypotension
- Tachycardia over 120
- Tachyopnea

Class 4:
- Marked hypotension
- Marked tachycardia
- marked tachyopnea
- Comatose

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16
Q

Which cannulae are wide bore? [4]

A
  • 14G (300ml/min)
  • 16G (150 ml/min)
  • 17G
  • 18G (75ml/min)
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17
Q

What are possible complications of massive blood transfusion [5]

A

- Fluid overload

  • Electrolyte / Acid-Base disturbance
  • Transfusing products devoid of clotting factors (consider giving additional platelets)
  • Hypothermia (blood transfused is cold)

Repeated transfusions:
- Iron overload

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18
Q

Which blood tests would you suggest for investigating upper GI bleed? [7]

A
  • Blood gas: contains Hb and lactate levels
  • FBC: Hb and clotting levels
  • U&E: kidney function
  • LFTs
  • Coagulation screen
  • Cross match (to find a compatible samples for transfusion)
    OR
  • Group and save (instruct transfusion lab to find blood group of patient and save serum of sample sent for later cross match
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19
Q

How do you optimise clotting:

  • What levels should: platelets [1] and INR [1] be above/below? [2]
  • Drug management? [2]
A

Platelets: > 50
INR: < 1.5

Do not give any anti-coagulants the Ptx may be on (warfarin, clopidogrel, aspirin, DOAC)
Reverse warfarin with vitamin K

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20
Q

What drugs might be prescribed if have an upper GI bleed? [2]

A

PPI:
- Decrease lesions identified at endoscopy level; but no difference in transfusion, surgery or mortality
- NICE does not rec. PPI before endoscopy

Tranexamic acid?
- improves clotting in area of GI bleeding, but may improve clotting with poor vascular blood flow & cause CAD.

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21
Q

Specific treatment for variceal bleeding? [2]

A

Terlipressin:
- causes mesenteric and splachnic vasoconstriction
- contraindicated in IHD

Antibiotics:
- cephalosporin; quinolone; augmentin
- reduces liklihood of sepsis, which decreases portal pressure
- treat chest infection if aspiratio has occurred.

NOTE: Propanolol is prophylaxis

22
Q

Name the scoring system used to determine if risk of re-bleeding [1]
Which scores result in outpatient endoscopy [1]

A

Blatchford score
< 2: low risk - outpatient endoscopy
> 6: endoscopic Rx

23
Q

Name another score (other than Blatchford score) for upper GI blleds [1]
What is important to note about this score [1]

A

Rockall score: needs endoscopic diagnosis to calculate full score

24
Q

Describe management of high risk, actively bleeding ulcer [4]

A

Adrenaline:
- vasoconstriction
- causes local tamponade of blood vessels

Clip: closes bleeding

Diathermy: (therapeutic treatment that uses electric currents (radio and sound waves) to generate heat in layers of your skin below the surface)

Haemospray: powder in endoscope; promotes clotting}}

25
Q

Describe the endoscopic management of varices [3]

A

Band ligation

Injection sclerotherapy (glue)

Sengestaken blakemore tube: compresses varices

26
Q

What is this endoscopic tx for oesophageal variceal bleeding? [1]
Explain how it works [2]

A

Sengstaken-Blakemore Tube [1]
Tube into stomach; inflate balloon; pull up agaisnt fundus of stomach; compresses varices so that blood can’t flow into varices}

27
Q

Explain post-endoscopical / medical therapy for ulcers: [3]

A

PPIs:
- allow ulcers to heal
- increase gastric pH; improves clotting ability (low pH activates pepsin which inactivates platelets)
- some patients will need continous infusion for 72hrs

H. pylori eradication (triple therapy: 1xPPI; 2xantibiotics)

Reassess of OGD

28
Q

Describe post-endoscopic treatment of varices [4]

A
  • Beta blockers (reduce portal pressure: carvedilol; propanolol)
  • Sequential banding procedures (close future varices)
  • TIPPS: blood from portal vein goes straight from liver into systemic system (reduces pressure)
  • Liver transplant
29
Q

When would you use interventional radiology or red cell scanning with GI bleeds? [2]

Describe the procedures [2]

A

If endoscopy fails / too unwell to have endoscopy

Interventional radiology:
- CT angiogram: IDs bleeding vessel
- Angiography: embolise the vessel

Surgery:
- If have uncontrolled bleeding
- Failed 2x endoscopic treatment

30
Q

What is the most common cause of small bowel bleeding? [1]

A

Angiodysplasia: abnormal, tortuous, dilated small blood vessel in the mucosal and submucosal layers of the GI tract.

31
Q

The NICE clinical knowledge summaries (updated January 2021) suggest management of uncomplicated diverticulitis in primary care with.. [4]

A

The NICE clinical knowledge summaries (updated January 2021) suggest management of uncomplicated diverticulitis in primary care with:

  • Oral co-amoxiclav (at least 5 days)
  • Analgesia (avoiding NSAIDs and opiates, if possible)
  • Only taking clear liquids (avoiding solid food) until symptoms improve (usually 2-3 days)
  • Follow-up within 2 days to review symptoms
32
Q

Describe the presentation of diverticulosis [3]

A

Diverticulosis may cause lower left abdominal pain that relieved by defecation, constipation or rectal bleeding

33
Q

How do you manage diverticulosis? [2]

A

Management is with increased fibre in the diet and bulk-forming laxatives (e.g., ispaghula husk). Stimulant laxatives (e.g., Senna) should be avoided

34
Q

Describe management plan for upper bleeds [6]

A

The initial management can be remembered with the ABATED mnemonic:

A – ABCDE approach to immediate resuscitation
B – Bloods
A – Access (ideally 2 x large bore cannula)
T – Transfusions are required
E – Endoscopy (within 24 hours)
D – Drugs (stop anticoagulants and NSAIDs)

35
Q

A patient has suspected bleeding varices. What two drugs should you prescribe? [2]
Is this before or after endoscopy? [1]

A

Terlipressin & Antibiotics (Ceftriaxone)
BEFORE endoscopy

36
Q

Which drug classes are a risk factor for upper GI bleeds? [5]

A

NSAIDs
Aspirin
Steroids
Thrombolytics
Anticoagulants

37
Q

Describe pathophysiology of PUD [2]

A

The mucosa lining inner lining of the stomach and duodenum secretes bicarbonate into this mucus coating to neutralise stomach acid & digestive enzymes

Disruption of the mucus barrier or increase stomach acid increase the risk of mucosal ulceration.

38
Q

Risk factors for PUD? [6]

A

Helicobacter pylori is associated with the majority of peptic ulcers:
- 95% of duodenal ulcers
- 75% of gastric ulcers

Drugs:
- NSAIDs
- SSRIs
- corticosteroids
- bisphosphonates

Zollinger-Ellison syndrome (duodenal or pancreatic tumour secretes excessive quantities of gastrin - stimulates acid secretion in the stomach)

39
Q

State for duodenal or gastric ulcers the following:

  • % related to H.pylori
  • Weight loss is more likely
  • If malignant
A

Duodenal:
- 95/99% related to H.pylori
- Not malignant (most cases)
- Weight loss less likely

Gastric:
- Weight loss likely (pain on eating)
- 60/70% related to H.pylori
- NSAIDs significant cuase
- 5-10% malignant

40
Q

Describe management of PUD [4]

A

PPI:
- lansoprazole
- omeprazole

Treat H.pylori using triple therapy (x2 antibiotics; x1 PPI)

Stop NSAIDs

Confirm eradicaiton using endoscopy and / or faecal antigen or urea breath test

41
Q

Why do NSAIDs increase chance of gastric related ulcers? [1]

A

Inhibition of COX-1 in the gastrointestinal tract leads to a reduction of prostaglandin secretion and its cytoprotective effects in gastric mucosa

42
Q

Describe the different pathways for duodenal and gastric ulcer pathways

A

Duodenal ulcer pathway;
antral gastritis, increased acid secretion which causes gastric metaplasia in the duodenal and leads to a duodenal ulcer

Gastric ulcer pathway:
corpus gastritis – inflammation in the body of the stomach, decreased acid secretion which causes gastric atrophy and predisposes you to dysplasia/neoplasia.

43
Q

Describe the managment for patients who have recurrent peptic ulcers [3]

A

Reducing the NSAID dose & substituting the NSAID with paracetamol

If symptoms recur after initial treatment: offer a PPI at the lowest dose possible to control symptoms:
* esomeprazole
* lansoprazole
* omeprazole

Offer H2 antagonist therapy if there is an inadequate response to a PPI:
- famotidine
- nizatidine

BMJ Best Practise

44
Q

When should barium radiography be used for investigating POD? [1]

A

Barium radiography should be reserved for patients who are unable or unwilling to undergo endoscopy, and it is not routinely recommended.

45
Q

Describe the presentation of the complications of significant peptic ulcerations [4]

A

Haematemesis (vomiting blood)
Coffee ground vomiting
Melaena (black, tarry stools)
Fall in haemoglobin on a full blood count

46
Q

Where is the most common place for duodenal ulceration?

A

Duodenal ulcers occur most frequently in the first portion of the duodenum (over 95%), with approximately 90% located within 3 cm of the pylorus and are usually less than or equal to 1 cm in diameter

47
Q

Investigations for perforated peptic ulcer? [5]

A

Bloods:
- Leukocytes present
- Anaemia

U & E:
- Significant bleeding may alter electrolytes
- Urea may be raised: digested blood is protein source

Liver function: useful to rule out biliary pathology

XR:
- upright XR if acute upper abdominal pain
- See free air presence

CT scan: if not seen on XR, but clinical presentation suggests

48
Q

Describe the treatment pathway for the initial resuscitation of perforated peptic ulcer disease [4]

A

IV fluids

Nasogastric tube insertion:
- reduces amount of gastric fluids in GIT AND allows nill by mouth

IV PPI
- loading and maintence doses
- enhance sealing of perforation

Antibiotics:
- stop sepsis due to leaking of fluids into peritoneum

Use one of the following methods to achieve haemostatic control of an actively bleeding ulcer via endoscopy:

A mechanical method (e.g., clips) with adrenaline (epinephrine)

Thermal coagulation with adrenaline

Fibrin or thrombin with adrenaline.

49
Q

After initial resuscitation, describe the operative management for PPUs [3]

A

Operative:
- Closure of perforation < 2 cm ulcer
- Resection of lesion > 2cm ulcer
- Use piece of omentum to cover}

50
Q

Describe the post-op management of PPUs [2]

A

Upper endoscopy:
- ID cause of perforation & healing of ulcer
- Biopsy for H. pylori

H.pylori eradication:
- triiple therapy for 10-14 days

51
Q

Describe what is meant by Zollinger-Ellison syndrome [1]

It is made from a triad of which three causes? [3]

A

Zollinger-Ellison syndrome (ZES) is a condition caused by a gastrin-secreting tumour that causes hypersecretion of gastric acid leading to ulcer disease.

Triad:
1) gastric acid hypersecretion, sustained by:
2) fasting serum hypergastrinemia causing:
3) peptic ulcer disease and diarrhea