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GI Term 4 > 4.2-Gastric & Peptic Ulcer Disease > Flashcards

4.2-Gastric & Peptic Ulcer Disease Flashcards

1
Q

What are the normal secretory components of the stomach?

A
  • Upper 2/3s; parietal cells secrete HCl and intrinsic factor and chief cells secrete pepsinogen
  • Lower 1/3 secretes bicarbonate-rich mucus (mucus cells)+ gastrin from G cels
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2
Q

Name some common symptoms of gastritis and PUD?

A
  • dyspepsia
  • anorexia
  • nausea/vomiting
  • haematemesis; vomiting blood
  • melaena; black tarry stools
  • GERD
  • acid brash
  • retrosternal pain
  • epigastric abdominal pain
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3
Q

Define gastritis? What is an ulcer and how does it form?

A
  • mucosal inflammation leading to:
  • mucosal breakdown leading to
  • peptic ulcer disease (duodenal and gastric ulcers)
  • mucosal layer breaks down from fissure to erosion to ulcer ie exposed tissue
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4
Q

State the pathogenesis of ulcer disease

A
  • acid
  • diet; spicy foods/ coffee
  • alcohol
  • H. pylori
  • NSAIDS
  • Zollinger-Ellison syndrome; gastrin secreting tumour of the pancreas
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5
Q

What is Helicobacter pylori?

A
  • major causative factor of PUD
  • motile, flagellated ; adheres to gastric mucosa
  • spiral cocbacillus
  • microaerophilic; o2 is dangerous to it so must survive without it
  • urease producing
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6
Q

Describe the importance of the urease reaction in HP?

A

uses chemotaxis to avoid areas of low pH

  • UREASE: neutralises acid in its environment by producing large amounts of urease which breaks down urea to CO2 and NH3
  • NH3 then utilises stomach acid to NH4+ ie neutralises the acid
  • urease is highly immunogenic ie causes local inflammation which RESULTS IN chronic infection
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7
Q

How does HP damage the stomach/ duodenal linings?

A
  • the ammonia produced to regulate pH is toxic to epithelial cells,
  • so are HP proteins EG proteases, vacuolating cytotoxin A (VacA)
  • they damage the epithelial cells, disrupts tight junctions and cause apoptosis
  • Cytotoxin associated gene CagA can also cause inflammation+ carcinogenic
    *
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8
Q

How can HP be diagnosed?

A
  • UREA BREATH TEST
  • Blood test for antibodies
  • Stool test; check for an antibody against any antigens of HP
  • endoscopy to see if there is a peptic ulcer
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9
Q

Describe the varied phenotype of HP ie how does it affect different people ie manifest itself?

A
  • gastritis only
  • intermittent gastric ulcers
  • intermittent duodenal ulcers
  • gastric cancer
  • MALT lymphoma
    *
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10
Q

What conditions are associated with the different locations of HP?

A

1) Antrum only - duodenal ulcer
2) Antrum and body-asymptomatic
3) Body only- gastric ulcer leading to dysplasia in mucosa and cancer

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11
Q

Why do duodenal ulcers result from HP colonising the antrum only?

A
  • Because the antrum is closer to the duodenum
  • a large amount of acid goes into the duodenum from the antrum, when it should normally be neutralised at this stage
  • Metaplasia occurs in the duodenal lining
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12
Q

What is dysplasia ( in context of gastric ulcers and cancer)?

A

presence of an abnormal type of tissue which can preceed cancer development stage

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13
Q

Why does HP colonize different areas?

A
  • The localisation of colonisation of HP , which affects the location of the ulcer, depends on the acidity of the stomach ie depends on the individual normal production of acid
  • in people producing lots of acid: HP colonises away from acidic area in the pyloric antrum to avoid acidic parietal cells near fundus
  • in people producing less acid: could be because of meds eg PPI Omeprazole
  • inflammatory response caused by bacteria colonizing near the antrum, induces G cells to secrete gastrin which sitmulates parietal cells in fundus to secrete acid
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14
Q

Why is a bacterium that only colonises gastric mucosa, implicated in duodenal ulceration?

A
  • If HP is in the antrum, near the duodenum,
  • then the G cells in the antrum will produce more gastrin; this stimulates HCl production
  • Therefore there is increased HCl production from parietal cells into the antrum
  • Increased HCl from the antrum passes straight into the duodenum
  • causes gastric metaplasia; favourable environment for HP
  • therefore allows HP to colonise duodenum ie duodenitis and ulceration
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15
Q

How do NSAIDS cause PUD?

A
  • gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins
  1. NSAIDS which are COX1 inhibitors therefore prevent production of these prostaglandins . COX1 inhibitors are worse than COX2 inhibitors
  2. COX-2 selective anti-inflammatories eg CELECOXIB preferentially inhibit cox-2

this is less essential in the gastric mucosa and roughly halve the risk of NSAID-related gastric ulceration

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16
Q

Summarise briefly the mechanism of prostaglandins

A
  • Prostaglandins stimulate mucus and bicarbonate production
  • they also cause vasodilation of nearby blood vessels, this increases blood flow
  • this increases epithelial cell growth which inhibits acid secretion
17
Q

How are HP and NSAIDS linked together in causing ulcers?

A
  • HP and NSAIDS are synergistic
  • ie if you have HP and you take NSAIDS, your risk of ulcers increases highly
  • Ulcers and GI bleeds happen in people> 65 years on NSAIDS/ aspirin
  • THEREFORE give PPIs ( to decrease acid secretions from parietal cells) for eldery NSAID patients (BUT PPIs have side effects on the liver so monitor with blood tests)
18
Q

How does presentation of ulcers in different places vary?

A

1) Gastric Ulcers: ​ -pain while eating

  • heart burn if higher up in the antrum
  • extra gastrin production; can get reflex

2)Duodenal ulcers: -pain is relieved by eating but returns after

-eg wake up in the middle of the night hungry and with pain ie need food to relieve pain

3) Pyloric Sphincter: if you have a peptic ulcer here, it can erode blood vessels

-causes a PYLORIC OBSTRUCTION because of pyloric ulcers close to the pyloric sphincter

you can vomiting and difficulty digesting your food

19
Q

What are the endoscopic findings of PUD?

A

ulcers which are lifelong may initially asymptomatic BUT over time, they erode away and affect blood vessels

therefore cause bleeding and rarely; perforation

  • you can also get SQUIRTING ULCERS:
  • Ulcer erodes into artery
  • blood squirts out ie heavy bleed is an emergency!
  • if a slight bleed; you only get malaena
  • if a TINY bleed; you get some anaemia
20
Q

Name 5 main causes of upper GI bleeds?

A
  • Peptic ulcers
  • Gatroduodenal erosions
  • Oesophagitis
  • Mallory Weiss tear; persistent vomiting over 24 hours causes a tear in stomach from stress of vomiting ]
  • Oesophageal varices
21
Q

Describe the appearance of a clean gastric ulcer

A
  • nice rolled edges
  • mucosa is normal till sloughy base
  • flat based pigmented spot ie low rebleeding risks
22
Q

What is the appearance of a duodenal bulb ulcer?

A

caused by increased acid secretion

23
Q

Describe the endoscopic appearance of oesophaeal varices?

A
  • higher up
  • normal mucosa on the ends
  • varices are lacerated and filled with blood
    *
24
Q

What are symptoms and signs of an upper GI bleed? ( eg varices)

How would you treat if it was a medical emergency?

A
  • haematemesis (can be altered)
  • malaena
  • increased blood loss
  • normally a medical emergency because of fear of patient getting shock
  • diziness eg postural hypotension/fainting
  • cool and clammy, delayed CRT
  • hypotension/ tachycardia ie shock
  • low JVP

Treatment:

  • immediate blood transfusion
  • stop warfarin if patient uses it ( bc this would exacerbate bleeds)
25
Q

State important key history points in a patient w upper GI bleed?

A
  • Previous peptic ulceration/ upper GI symptoms
  • current meds eg OTC analgesics
  • Bleeding disorders+ meds eg warfarin, clopidogrel, asparin
  • alcohol intake ( gastritis)
26
Q

How to detect if a GI bleed is causing SHOCK?

A

Things to consider:

  • cold and clammy
  • delayed CRT
  • tachycardic
  • systolic BP< 100mmHg ( if so, give crystalloid solution eg saline, then send for an endoscopy, to diagnose and treat)
  • postural drop; common in younger patients w HIGH BLOOD LOSS
  • urine output< 30 ml/hour
27
Q

What prognostic markers are used in GI bleeds?

A

BLATCHFORD SCORE: helps to risk stratisfy patients

  • check for Hb
  • blood urea
  • SBP
  • tachycardia
  • malaena

if 0 signs, then can early discharged with OPD endoscopy

A score, 4-:low probability of urgent endoscopy

GBS> 0; High risk of GI bleed⇒needs medical intervion ie transfusion, endoscopy, surgery

28
Q

Name 5 techniques of endoscopic management of bleeding?

A

1) Injection sclerotherapy: inject material into substance to seal it off

2) Diathermy: burning the vessel

3) Variceal ligation: for oesophageal varices; not for ulcer treatment

4) Laser therapy

5) Endoscopic clipping: good for detecting a large vessel that needs to be closed off

-only useful if you can PINPOINT where the bleed is

29
Q

Name 3 pre-endoscopy therapeutics? ie medicines to stabilise the patient

A

1) PPIs: reduces acid-dependent protease clot lysis

  • reduces high-stigmata and need for intervention
  • no clear reduction in mortality, surgery, rebleeding

2) Antifibrinolytics eg tranexamic acid

3) Prokinetics eg Metaclopramide

  • stimulate contraction of smooth muscle+ reduce abdominal discomfort+ tighten oesophageal sphincter
  • reduce need for repeat OGD
30
Q

What is HEMOSPRAY?

A

-at the end of the endoscope, you spray this into the bleeding area; a blend of powder+ developed for endoscopic haemostasis ie forms a mechanical barrier over the bleeding site

31
Q

Describe the on-going management of UGIB?

A

1) Stop NSAIDS, aspirin (give w PPIs), clopidogrel- short term
2) Give COX2 inhibitors to Rheumatology pts instead of COX1
3) If previous ulcer and due to start NSAID, eradicate HP

32
Q

How does perforation occur?

A
  • If you do not treat gastric ulcers
  • Medical emergency; when patient is upright, the air will rise and sit on top of diaphragm; gas can escape and leak out into stomach+ needs immediate intervention

GI Term 4 (7 decks)

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