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GI disease Flashcards

1
Q

What is dyspepsia?

A

A complex of upper GI tract symptoms, typically present for 4 OR MORE WEEKS. Including upper abdo discomfort, nausea, heartburn, acid reflux +/- vomitting

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2
Q

What is gastro-oesophageal reflux disease?

A

Reflux of stomach contents into oesophagus/pharynx

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3
Q

Symptoms of GORD

A

Heart burn - chest pain
Acidic taste (dental erosion?)
Cough

BUT Asymptomatic sometimes

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4
Q

Risk factors for GORD

A

Increase in intrabdominal pressure:
Obesity
Pregnancy
LOS dysfunction
Hiatus hernia
Delayed gastric emptying - increase pressure in stomach

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5
Q

What is a hiatus hernia?

A

When the lower oesophageal sphincter (which is usually in abdomen), herniates through to thorax.

Loses crural muscle, distort anatomy and does not work as well

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6
Q

3 parts of LOS which prevent GORD

A

Muscular elements - intrinsic and diaphragm

Right crus of diaphragm forms muscular ring around oesophagus, when IAP increases it pinches

Angle is acute that oesphagus enters stomach

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7
Q

Which is more effective pyloris or LOS?

A

PYLORIC - very muscular

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8
Q

Complications of GORD

A

Oesophagitis
Ulceration
Haemorrhage
Strictures (narrowing due to fibrosis, repeated insult forms scar tissue)
Metaplastic changes

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9
Q

What is oesophagitis?

A

Inflammation of epithelia of oesophagus +/- bleeding

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10
Q

What is ulceration of oesophagus?

A

Erosion that is deeper than muscularis mucosae

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11
Q

Explain barrett’s oesophagus

A

Normal epithelia in oesophagus is stratified squamous
If oesophagus is exposed to acid repeatedly it changes to gastric columnar to cope with stress - metaplasia
This is reversible but there is increased risk of dysplasia to adenocarcinoma

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12
Q

Cancer caused by barrets oesophagus

A

Adenocarcinoma - glandular cancer

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13
Q

What is the usual only cancer which could develop in oesophagus?

A

squamous cell carcinoma - oesophagus is stratified squamous usually

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14
Q

Cell change in barretts oesophagus

A

Stratified squamous to gastric columnar

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15
Q

Lifestyle management of GORD

A

Weight loss
Avoid trigger foods
Eat smaller meals
Don’t eat then sleep
Decrease alcohol and caffeine
Stop smoking

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16
Q

Drug management of GORD

A

Proton pump inhibitors these allow for symptom relief and heal inflammation

H2 receptor antagonists - stop histamine from binding to parietal cell, decrease acid production

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17
Q

What surgery is available for GORD?

A

Fundoplication

Fundus of stomach is wrapped around the back of oesphagus

Secured with sutures, keeps below diaphragm

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18
Q

What is gastritis?

A

Inflammation of the stomach mucosa

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19
Q

Symptoms of gastritis

A

Pain
Nausea
Vomiting
Haemorrhage

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20
Q

Endoscopic appearance of gastritis

A

Red, angry inflamed stomach lining

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21
Q

Histology of gastritis

A

Neutrophils invading lamina propria

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22
Q

Acute gastritis causes (4)

A
  1. NSAIDS
  2. ++ Alcohol
  3. Chemotherapy
  4. Bile reflux - stomach not used to chemical injury of bile
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23
Q

Chronic gastritis causes

A
  1. Infection with helicobacter pylori
  2. Autoimmune
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24
Q

Acute pathological changes of gastritis (4)

A

Epithelial damage
Some hyperplasia
Vasodilation - angry, inflamed red surface
Neutrophil response (to LP)

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25
Q

Chronic pathological changes of gastritis (4)

A

Lymphocyte response
Glandular atrophy (within gastric pits)
Fibrotic changes
Metaplasia

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26
Q

What is the problem with autoimmune gastritis?

A

Antibodies develop to parietal cells
Loss of parietal cells - loss of acid and intrinsic factor

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27
Q

What else do parietal cells produce other than acid?

A

Intrinsic factor

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28
Q

What happens if intrinsic factor is lost due to destruction of parietal cells?

A

Absorption of B12 is reduced in ileum (usually uses intrinsic factor) = B12 deficiency/pernicious anaemia

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29
Q

What happens to the stomach as a result of this autoimmune attack on parietal cells?

A

Atrophy of body of the stomach

30
Q

Symptoms of chronic autoimmune gastritis

A

Anaemia - megaloblastic (slow DNA replication and synthesis means cytoplasm is large)

Neurological symptoms

Anorexia

Glossitis - smooth red inflamed tongue

31
Q

How many people are infected with H.pylori?

A

50% of the population
usually asymptomatic, may have some microbiome benefits

32
Q

What conditions does H-pyloris cause?

A

Chronic gastritis
Peptic ulcer disease

33
Q

How is h-pylori transmitted?

A

Faeco-oral route
or oral oral

34
Q

Characteristics of H-pylori

A

Helix
Gram-ve
Microaerophilic - need low O2 not as high at atmosphere (stomach best)

35
Q

What are some features/upgrades of H-pylori?

A

Flagella - move and allow adherence to epithelia of stomach

Chemotaxis - finds lower acidity regions, eg under mucous layer

Adhesins - stick to epithelia surface mucous cells, dont get washed away during peristalsis

36
Q

What does H-pylori have inside it?

A

Its own cytoplasmic Urease

37
Q

What does the urease in H-pylori do?

A

Urease converts the urea in stomach to CO2 and ammonia

38
Q

Problem with H-pylori producing ammonia

A

De-acidifies environment - increases pH, allowing bacteria to survive and thrive

Ammonia is toxic to epithelia

(ammonia is basic)

39
Q

What are the 4 things that -pylori expresses/has which causes gastritis?

A

Cytotoxin associated gene A - expresses protein

Vacuolating toxin A - secretes this protein

Ammonia production

Secretes mucinase, protease and lipase (damages mucous layer)

40
Q

What does cytotoxin associated gene A do?

A

Expresses protein that is inserted into epithelia causing inflammatory response

This stimulates IL8 - can cause cancer

41
Q

What does vacuolating toxin A do?

A

Increases paracellular permeability of stomach epithelia

Toxic

42
Q

What is the problem with Cag A (cytotoxin associated gene A)?

A

Causes inflammation chronically
Increase risk of stomach cancer

43
Q

What happens if H-pylori colonises the antrum part of the stomach?

A

Causes overactivity of G cells
Increase gastrin

44
Q

What does increase in gastrin mean for antrum?

A

Increase HCl production from parietal cells
Chyme is then VERY acidic
Damages duodenum epithelia - can then colonise here

45
Q

What can happen if h-pylori colonise and damage duodenum?

A

Can get duodenal ulcer

46
Q

What happens if h-pylori colonises the stomach body (+/- fundus)?

A

Usually asymptomatic
Atrophy of parietal cells
= precursor for dysplasia
Increases stomach cancer risk

47
Q

3 ways which H-pylori can be diagnosed

A

Urea breath test
Stool antigen test
Endoscopy with biopsy

48
Q

2 isotopes of carbon present in gastric urea

A

C12 - majority 99%
C13 - only 1%

49
Q

Explain urea breath test

A

Pt ingests urea enriched with C13 (usually only 1% in normal gastric urea)

H-pylori urease breaks this down into ammonia and CO2 if present

Breath test can detect isotope C13 in CO2 exhaled if it has been broken down

(eg if C13 is detected in high conc in exhaled CO2, H-pylori is present)

50
Q

How to eradicate H-pylori from Pt

A

Proton pump inhibitor
2 x antibiotics (esp with clarithromycin and metronidazole)

For 7 days usually

51
Q

How to check success of eradication

A

Another urea breath test

52
Q

SE of eradication meds for H-pylori

A

Nausea
Diarrhoea

53
Q

What is peptic ulcer disease?

A

Defect in the gastric or duodenal mucosa that extends through the muscularis mucosae

54
Q

2 places where peptic ulcers occur

A

First part of duodenum - MOST COMMON

Lesser curve (or antrum) of stomach

55
Q

Gastric vs duodenal ulcers

A

3x more likely to get duodenal

Increase incidence with age for gastric ulcer, only increase incidence up until 35 for duodenal

Gastric affects lower social class

Gastric affects group A, duodenal affects group O blood

Acid levels are normal/low in gastric (barrier problem), normal/high in duodenal

H-pylori causes 70% of gastric, 95-100% in duodenal (increased acidity of chyme)

56
Q

Stomach defenses

A

Mucus layer
HCO3 secretion
Mucosal blood flow
Prostaglandins
Epithelial renewal

57
Q

Problem with NSAIDS

A

Inhibit prostaglandins
Decrease mucosal blood flow, cannot repair cells or take away extra acid

58
Q

Risk factors for peptic ulcer

A

H-pylori
NSAIDs - affect prostaglandin synthesis
Smoking - relapse ulcer but nor original cause
Physiological stress - MASSIVE

59
Q

How do acute ulcers form?

A

Part of acute gastritis

60
Q

Where do chronic ulcers occur?

A

At mucosal junctions (between antrum and body at lesser curve or at antrum to duodenum)

61
Q

Describe the morphology of peptic ulcer disease?

A

Base of ulcer contains necrotic tissue, when invades tissue around it is replaced by scar tissue

62
Q

What can happen is repeated ulceration occurs?

A

Stomach lumen can narrow or cause pyloric stenosis as scar tissue and fibrosis occurs

Or can get peritonitis (inflammation of peritoneal cavity)

63
Q

How does ulceration cause peritonitis?

A

Repeated ulceration = ulceration can go through wall and cause opening into peritoneal cavity

64
Q

What else can ulcers do to nearby structures?

A

Erode adjacent structures eg liver and pancreas

65
Q

What happens when ulcers erode into blood vessels?

A

Haematemesis - vomiting of blood

Malaena - black tarry stools from oxidised Hb as it goes through GI tract

66
Q

What arteries can be eroded by peptic ulcers?

A

Gastro-duodenal artery - posterior to duodenum, large artery

RARELY - splenic artery

67
Q

Where does a bleed occur to cause malaena?

A

Upper GI - Hb is oxidised as it travels through and turns blood black

68
Q

What do we usually do around ulcers?

A

Biopsy to ensure no malignancy

69
Q

Symptoms of peptic ulcer disease

A

Epigastric pain, back pain following meals

Pain at night - duodenal ulcers

Bleeding can cause malaena or haematemesis

Early satiety - scar tissue prevents expansion of stomach

Weight loss - reluctant to eat

70
Q

Why does pain at night suggest duodenal ulcer?

A

It was said that food initally made duodenal ulcers feel relieved as presence of food causes pyloric sphincter to contract meaning no acid chyme could irritate ulcer.
Usually would then get pain later after food (1hr)

Whereas gastric usually gives immediate pain

71
Q

Management of PUD - no active bleeding

A

Are they H-pylori +ve or -ve

If +ve, eradicate pylori - this promotes ulcer healing (via PPI and 2x abx)

When -ve:
Then stop any exacerbating meds (eg NSAIDs)

72
Q

Management of PUD if actively bleeding

A

Adrenaline injected around base of ulcer using endoscopy

Cautery - burning to close perforation +/- clips

Then test for h-pylori and follow steps for non-active bleeding

GI (32 decks)

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