MET3 Revision - Gastroenterology II COPY Flashcards

(51 cards)

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
Describe the endoscopic management of varices [3]
Band ligation Injection sclerotherapy (glue) Sengestaken blakemore tube: compresses varices
26
What is this endoscopic tx for oesophageal variceal bleeding? [1] Explain how it works [2]
**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
Explain post-endoscopical / medical therapy for ulcers: [3]
**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
Describe post-endoscopic treatment of varices [4]
- 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
When would you use interventional radiology or red cell scanning with GI bleeds? [2] Describe the procedures [2]
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
What is the most common cause of small bowel bleeding? [1]
**Angiodysplasia**: abnormal, tortuous, dilated small blood vessel in the mucosal and submucosal layers of the GI tract.
31
The NICE clinical knowledge summaries (updated January 2021) suggest management of uncomplicated diverticu**litis** in primary care with.. [4]
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
Describe the presentation of diverticulosis [3]
Diverticulosis may cause **lower left abdominal pain** that **relieved by defecation**, **constipation** or **rectal bleeding**
33
How do you manage diverticulosis? [2]
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
Describe management plan for upper bleeds [6]
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
A patient has suspected bleeding varices. What two drugs should you prescribe? [2] Is this before or after endoscopy? [1]
**Terlipressin** & Antibiotics (**Ceftriaxone**) **BEFORE** **endoscopy**
36
Which drug classes are a risk factor for upper GI bleeds? [5]
NSAIDs Aspirin Steroids Thrombolytics Anticoagulants
37
Describe pathophysiology of PUD [2]
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
Risk factors for PUD? [6]
**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
State for duodenal or gastric ulcers the following: - % related to H.pylori - Weight loss is more likely - If malignant
**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
Describe management of PUD [4]
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
Why do NSAIDs increase chance of gastric related ulcers? [1]
**Inhibition of COX-1** in the gastrointestinal tract leads to a reduction of prostaglandin secretion and its cytoprotective effects in gastric mucosa
42
Describe the different pathways for duodenal and gastric ulcer pathways
**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
Describe the managment for patients who have recurrent peptic ulcers [3]
**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
When should barium radiography be used for investigating POD? [1]
Barium radiography should be reserved for **patients who are unable or unwilling to undergo endoscopy**, and it is not routinely recommended.
45
Describe the presentation of the complications of significant peptic ulcerations [4]
**Haematemesis** (vomiting blood) **Coffee ground vomiting** **Melaena** (black, tarry stools) **Fall** in **haemoglobin** on a **full blood count**
46
Where is the most common place for duodenal ulceration?
**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
Investigations for perforated peptic ulcer? [5]
**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
Describe the treatment pathway for the initial resuscitation of perforated peptic ulcer disease [4]
**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 ## Footnote 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
After initial resuscitation, describe the operative management for PPUs [3]
**Operative**: - Closure of perforation < 2 cm ulcer - Resection of lesion > 2cm ulcer - Use piece of omentum to cover}
50
Describe the post-op management of PPUs [2]
**Upper endoscopy:** - ID cause of perforation & healing of ulcer - Biopsy for H. pylori **H.pylori eradication:** - triiple therapy for 10-14 days
51
Describe what is meant by Zollinger-Ellison syndrome [1] It is made from a triad of which three causes? [3]
**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