MET3 Revision - Gastroenterology II COPY Flashcards
Which anatomical point distinguishes between an upper and lower GI bleeding? [1]
Ligament of Treitz:
- Proximal: upper GI
- Distal: lower GI
State the causes of upper GI bleeds [5]
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%
State the causes of lower GI bleeds [5]
Diverticular disease (30%)
* Haemorrhoids (14%)
* Mesenteric Ischaemia (12%)
* Colitis (9%)
* Cancer (6%)
* Rectal ulcers (6%)
* Angiodysplasia (3%)
* Radiation (3%)
* Drugs
* Other
What is this cause of upper GI bleeding? [1]
Gastritis
What is the most common cause of portal HTN worldwide? [1]
Schistomiasis
What is a mallory weiss tear? [1]
Describe typical presentation [1]
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
Describe pathophysiology is diverticular disease causing lower GI bleeding? [1]
How does diverticular disease lead to lower GI bleeding? [1]
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
What are causes of diverticular disease? [6]
- Constipation
- Genetics
- Obesity
- NSAIDs
- Low fibre diet
- Muscle spasm
State 5 causes of haemorrhoids [5]
- Straining (in bowel movement)
- Sitting for long periods
- Chronic diarrhoea or constipation
- Overweight / obese
- Pregnancy
Describe how colonic cancer develops [3]
- polyps;
- larger polyp (severe dysplasia)
- adenocarcinoma
State 4 reasons that cause colitis which in turn causes lower GI bleeding [4]
Ishcaemic colitis: in distal transverse colon / descending colons - position as watershed area between SMA & IMA can lead to bleeding
IBD
Infection
NSAIDs
When taking a history for upper GI bleed, what should you investigate? [3]
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)
What are the different classes of blood loss? (% and volume lost?) [4]
Class 1:
- 10-15%
- 750mls
Class 2:
- 15-30%
- 1.5L
Class 3:
- 30-40%
- 2L
Class 4:
- >40%
- 3L
Describe the symptoms that classify each class of shock with regards to blood loss? [4]
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
Which cannulae are wide bore? [4]
- 14G (300ml/min)
- 16G (150 ml/min)
- 17G
- 18G (75ml/min)
What are possible complications of massive blood transfusion [5]
- 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
Which blood tests would you suggest for investigating upper GI bleed? [7]
- 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
How do you optimise clotting:
- What levels should: platelets [1] and INR [1] be above/below? [2]
- Drug management? [2]
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
What drugs might be prescribed if have an upper GI bleed? [2]
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.
Specific treatment for variceal bleeding? [2]
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
Name the scoring system used to determine if risk of re-bleeding [1]
Which scores result in outpatient endoscopy [1]
Blatchford score
< 2: low risk - outpatient endoscopy
> 6: endoscopic Rx
Name another score (other than Blatchford score) for upper GI blleds [1]
What is important to note about this score [1]
Rockall score: needs endoscopic diagnosis to calculate full score
Describe management of high risk, actively bleeding ulcer [4]
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}}
Describe the endoscopic management of varices [3]
Band ligation
Injection sclerotherapy (glue)
Sengestaken blakemore tube: compresses varices
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}
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
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
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
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.
The NICE clinical knowledge summaries (updated January 2021) suggest management of uncomplicated diverticulitis 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
Describe the presentation of diverticulosis [3]
Diverticulosis may cause lower left abdominal pain that relieved by defecation, constipation or rectal bleeding
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
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)
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
Which drug classes are a risk factor for upper GI bleeds? [5]
NSAIDs
Aspirin
Steroids
Thrombolytics
Anticoagulants
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.
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)
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
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
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
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.
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
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.
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
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
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
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
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.
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}
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
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