Upper GI Diseases Flashcards
2 functions of medications of upper GI Diseases
eliminate formed acid (antacids)
reduce acid secretion
medicines which reduce acid secretion (2)
H2 receptor blockers
proton pump inhibitors
how do antacids work
Covert acid to salt
Adsorb that
Depend on what is in can poison with too high magnesium levels
what cell makes acid in GI
parietal cell
what is the secreting portion of parietal cell
proton pump
how can parietal cell be inhiited
by proton pump inhibitor
- stops acid production
3 triggers for acid production on parietal cell
histamine H2 recpetor
gastrin
ACh (cholinergic)
Gastrin
local hormone caused by stomach stretch
when is ACh released and thus detected by parietal cells
in anticipation of food - salivation
how many pathways do you need to block to stop acid secretion by parietal cells
all 3
what do you need to block to stop acid being made
proton pump at top of parietal cell
other 3 pathways trigger acid to be made
role of H2 receptor antagonists
Reduce acid production by preventing histamine activation of acid production
- Revolution for medicine, used to be surgical treatment only
Limited benefit as alternative pathways still operative
-Acetylcholine, Gastrin
cimetidine
H2 receptor antagonist
Original H2 blocker
Many drug interactions
Not fully effective
ranitidine
H2 receptor antangonist
Not any more effective
Safer in clinical use
Licensed for over the counter sale
examples of proton pump inhibitors
Omeprazole
Lansoprazole
Pantoprazole
all end in prazole
what are more effective clinically - proton pump inhibitors of H2 receptor antagonists
proton pump inhibitors
- acid secretion completely stopped
dyspepsia
indigestion
causes of dyspepsia
diet
medicine side effect
3 classes of upper GI disease
Oral diseases
Oesophageal disease
Gastric disease
3 main commonly seen of oral diseases
Recurrent oral ulceration
Lichen planus
Orofacial granuomatsis
minor apthae
Form of recurrent oral ulcers
Get anywhere in gut including mouth
Driven by immune system
Last for 2 weeks and then go away and heal
Less than 1cm
major apthae
More than 1cm in size
3 months to heal
Scar when heal
Can be nuisance but can be significant pain to patient
herpetiform apthae
Lots of small ulcers around mouth
Don’t get on keratinised mucosa
Dorsal of tongue
Will on underside of tongue, masticatory mucosa etc
orofacial granulomatosis
Blockage of lymphatics
- Move from venules into tissues
Drains through lymphatics back into circulation
Get blocked up by giant granulomatous cells
Cannot be easily phagocytosed and removed
Chunky and when get washed into lymphatics - blocked by giant cell granuloma
- Build up, tissue puffy and swollen
Peri-oral and intraoral swelling
Can be temporary or permanent
Any age
Reason for happening is unclear
Psychological issue
- Cosmetic, no physical harm
Intraoral swelling
- Fixed tether hold tissue - so swelling between tethers
- Cobble stoning
- Blobs separated by fissure
Ulcerations and fistula of fissures
- Holes forming between tissues e.g. bowel
Can be a nuisance to very disfiguring - range
main effect of orofacial granulomatosis
Psychological issue
- Cosmetic, no physical harm
how to examine the mouth
by eye
can see subtle changes
to examine the inside of gut use
endoscopy
endoscopy
use to examine inside of gut
Not flexible - Rigid glass rods - Can steer them round borders Pocket at far end - Grab bits of tissue
oesophagus
Joining between gut and mouth
where does embryonic gut begin down the oesphagus
2/3 way down
- head and skin above is ectoderm
change of mucosa in embryonic gut part of oesophagus
stratified squamous to simple columnar
musculature in embryonic gut part of oesophagus
Muscular tube with peristalsis down - active process
Grab and propel down with contraction behind
3 oesophageal disorders
dysphagia
dysmotility disorders
GORD
dysphagia
compression
Cannot get food bolus down beyond a blockage in oesophagus
can be localised by patient or barium meal
dysmotility of oesphagus can be due to
fibrosis or neuromuscular duyfacunction
fibrosis dysmotility of oesophagus
common with acid reflux
recurrent irriation of oesophagus with acid reflux
change into fibrosis tissue - not stretch, oesophagus becomes non-muscular
Have to by pass oesophagus to get into stomach
neuromuscular dysmotility of oesophagus
‘Nerves in muscle no longer working
Ability to tell muscles to tell contract as was impaired
duration of dysphagia
varies
can be intermittent or constant
potential causes of dysphagiea
‘functional’
- Anxiety, nerves not functioning properly
- Brain interference
dysmotility
external compression
- squamous cell carcinoma
anatomical location of oesophagus
Runs from bottom of larynx - Down through thorax - Above diaphragm towards left side - Stomach muscle sphincter of oesophagus All 3 help keep things in stomach
3 main causes of GORD
- defective lower oesophageal sphincter
- impaired lower clearing
- impaired gastric emptying
problem in stomach contents not exiting into duodenum
- pressure build up
- acid back into oesophagus
effect of GORD
ulceration, inflammation, metaplasia
damaging to oesophageal lining – columnar to squamous epithelium
metaplasia
squamous cell carcinoma risk
GORD Signs and symptoms
epigastric burning
- worse lying down, bending, pregnancy
dysphagia
- oesophagitis, stricture, dysmotility
- damage to muscular tissue at bottom of oesophagus – more fibrous
GI bleeding
Severe pain - mimics MI!
- Oesophogeal muscle spasm
- Antacid can help with pain
barrett’s oesophagus
Recurrent acid reflux into lower part of the oesophagus
- Inflamed metaplastic lower third of oesophagus
Metaplasia of the oesophageal lining to Gastric type mucosa
Associated with malignant change
- adenocarcinoma – higher risk
how to treat barrett’s oesophagus if becomes malignant
part of oesophagus resected
how can proton pump inhibitors reduce risk of barrett’s oesophagus
- stop acid
- stop reflux
- reduce risk
hiatus hernia
Part of stomach is in THORAX
- Moved through the diaphragm
- When diaphragm contacts see part of stomach in thorax
Easy for acid to get into oesophagus
Symptoms can be similar to GORD
Commoner in women
2 types of hiatus hernia
Rolling (or paraesophageal) hiatus hernia
- Area is not connected to bottom of oesophagus
- Permanently stay there
- Sealed off when diaphragm contracts
Sliding Hiatus hernia
- More common
- get GORD
GORD Management
Stop smoking - improves sphincter
Lose weight & avoid triggering activity
antacids
- symptomatically – use as and when
H2 blockers & PPI’s
- ranitidine & omeprazole
- reduce acid formation
increase GI motility & gastric emptying
- encourage stomach to empty quicker
peptic ulcer disease PUD
ANY acid affected site
- oesophagus, stomach, duodenum
Hole forming in stomach wall
- Progress through whole width of stomach wall into peritoneal cavity
Acid protection removed in an area
- Burn hole through connective tissue
- lining should protect stomach
Potential for perforation
- Acidic content in stomach out
Degree of inflammation
3 causes of peptic ulcer disease
High acid secretion - duodenal
Normal acid secretion - stomach
- Mucous on surface of stomach not functioning properly (reduced resistance)
drugs - NSAIDS, Steroids
what normally happens when acid food suspension enters duodenum
neutralised by duodenal secretions
PUD outwith stomach is commonly
too much acid secretion
hormone related (gastrin)
PUD within stomach is due to
damaged lining
• Steroid - inhibit mucous
• Bacterial infection grow in stomach lining and acid in contact with tissue
what happens if PUD interacts with small artery
vomit has blood in it
2 reasons for PUD
- excessive acid
- normal acid but reduced protection
excessive acid PUD causes
oesophageal, duodenal ulcers
unknown Trigger for secretion
normal acid PUD has
reduced protective barrier
helicobacter pylori involvement
helicobacter pyrlori
bacteria found in stomach
Metabolise
- Make CO2 and waste products
- Detect in blood
- Endoscopy and biopsy of stomach can see
Gradually disrupt mucous barrier
- Ulceration and bleeding
- Inflammation
action of helicobacter pylori
Gradually disrupt mucous barrier
- Ulceration and bleeding
- Inflammation
effects of helicobacter pylori
Irritation
- Immune system not able to remove
- Annoys immune system
- Keeps grumbling away
- Leads to developing a malignancy
Gastric Ulcers
Chronic gastric wall inflammation
- Lymphoma of the stomach
Mucosal associated lymphoid lesion
- Peyer’s patches
- Present all the way through gut
- Irritant develop a lymphoma of lymphoid tissue
how to treat helicobacter pylori infection
Gastric lymphoma can be treated by treating the Helicobacter pylori
ELIMINATE with TRIPLE THERAPY - 2 antibiotics - 1 proton pump inhibitor Get rid and will be OK Lymphoma recede with bacteria
PUD Signs and symptoms
Asymptomatic!
Epigastric burning pain
- worse before/just after meals
- worse at night
- relieved by food, alkali & vomiting
usually NO physical signs
- only when complications, e.g. bleed, perf.
PUD Investigations (4)
Endoscopy
- oesphagus, stomach & duodenum
Radiology
- barium meal
Anaemia
- F.B.C and faecal occult blood test (FOB’s)
H. pylori
- breath, antibodies, mucosa
4 local PUD Complication
Perforation
Haemorrhage
Stricture
Malignancy
systemic PUD complication
anaemia
medical PUD treatment
Stop smoking
Small regular meals – easier to manage
Eradication therapy
Ulcer healing drugs
- Proton pump inhibits
- Remove acid
reasons for medical treatment of PUD
Reversible problem
Lifestyle changes
H.pylori present – take away = reverse
reason for surgical PUD treatment
Stricture
Acute bleed
Perforation
Malignancy
surgical PUD treatment
Endoscope
Surgical repair
- Gastrectomy
Vagotomy
why is decrease in PUD treatment success with age
Older age less chance of surviving operation
Death rate going up as less surgery when young and fit
2 actions of medication in upper GI diseases
reduce acid secretion
improve mucosal barrier
2 medicines which reduce acid secretions of upper GI
H2 receptor blockers
Proton pump inhibitors
ways in which medicines improve the mucosal barrier in upper GI
Eliminate helicobacter
Inhibit prostaglandin removal
- NSAID use encourages this – avoid
- Reduce steroid use
what is triple therapy
For elimination of Helicobacter pylori
Two week course of:
- Two antibiotics (Amoxycillin and Metronidazole
- Proton Pump Inhibitor
omeprazole)
bilroth 1
surgical PUD management
Remove part where stomach ulcers occur Smaller stomach Stop slow feed of food out drops straight to duodenum - Dumping syndrome - blood rush to intestine Hypertensive effect
bilroth 2
surgical PUD management
Join smaller hole from duodenum to stomach
Smaller outflow
Duodenum secretions earlier
Highly selective vagotomy
surgical PUD management
Sever ACh nerve that goes to stomach
Pick of branches ot parital cells
Reduce gastric acid secretion without causing motility problems
- Trunk vagotomy will cause stasis problems in bottom of stomach
Reduce secretion
