Upper GI Disease Flashcards
(67 cards)
1
Q
where does the gastrointestinal tract start
A
half way down the oesophagus
2
Q
is the head part of the GI tract
A
no
3
Q
what is GI disease split between
A
- diseases affecting the tube the food goes down
- the actual gut
4
Q
what medications are involved in upper GI diseases
A
- eliminate formed acid
= antacids - reduce acid secretions
= H2 receptor blockers
= proton pump inhibitors (commonly used now a days)
5
Q
what do antacids do?
A
change acids to salts
6
Q
what do proton pump inhibitors do
A
acts on the proton pump
stops you being able to make acid
7
Q
in the proton pump, what is acid
A
an ion of hydrogen
8
Q
what are the triggers for making acid
A
- acetylcholine
= neurological trigger - gastrin
= local hormone with stomach being stretched - histamine
9
Q
how can you stop the triggers for making acid
A
need to block all 3 triggers individually
unless you block all 3 triggers there will be an acid secretion
simpler to use the proton pump inhibitors and stop the proton pump
10
Q
what do H2 receptor antagonists do
A
(helpful but not the solution)
- reduce acid production by preventing histamine activation of acid production
- limited benefit as acetylcholine and gastrin pathways still work
11
Q
name 2 H2 receptor antagonists
A
- cimetidine
> original H2 blocker
> many drug interactions
> not fully effective
- ranitidine > not any more effective > safer in clinical use > licensed for over the counter sale > helps with heart burn
12
Q
name proton pump inhibitors
A
- omeprazole
- lansoprazole
- pantoprazole
end in ‘prazole’
basically all the same drug but tweaked for different clinical action ie different duration lengths
much more effective clinically
13
Q
what does dyspepsia mean
A
indigestion
14
Q
why would a patient taking steroids to treat COPD take proton pump inhibitor drug as well
A
to reduce the chances of ulceration occurring in the stomach
15
Q
name upper GI diseases
A
- oral disease
- oesophageal disease
- gastric disease
16
Q
what are common things in oral diseases to see
A
- recurrent oral ulceration
- lichen planus
- orofacial granulomas
17
Q
name 3 types of oral ulcerations
A
minor aphthae
major aphthae
herpetiform aphthae
18
Q
what are minor aphthae
A
these come and go they are driven by the immune system probably last 2 weeks then heal less than 1 cm in size annoying
19
Q
what are major aphthae
A
can take 3 months to heal
larger than 1 cm in size
can leave scars / a mark on tissues
20
Q
what are herpetiform aphthae
A
lots and lots of small ulcers
wont find these on the dorsum of the tongue or on the attached gingiva
21
Q
what is the cause of orofacial granulomatosis
A
blockage of lymphatics by multinucleate giant cells
these giant cells wash into lymphatics and sits over them blocking them so only a little liquid can pass through instead of all the liquid (like a tea bag blocking a drain)
fluid still enters lymphatics so the tissue gets puffy and swells
causes swelling of tissues inside the mouth (characteristic . = swelling of cheek mucosa)
22
Q
what are giant cells
A
macrophages fused together
23
Q
when can OFG happen and why does it
A
the reason it happens is not clear
can happen at any age
can be temporary or permanent
24
Q
what is an EGD
A
esophagogastroduodenoscopy
also called an upper endoscopy
25
how can you look inside the gut
using an endoscope
= a flexible tube which can be steered into the GI tract
= the tube can travel long distance through the gut
helps with seeing and managing problems
26
what do oesophageal disorders usually involve
mucosa and musculature changes
27
name oesophageal disorders
- dysphagia
- dysmotility disorders
- Gastro-oesophageal reflux disease
28
what does it mean when dysphagia is caused by compression
squamous carcinoma in the lungs can compress the oesophagus
| does not allow food to pass down through and causes problems with swallowing
29
what can be the cause of problems with swallowing
- can be because of a blockage
- can be a problem with the muscles not working properly
- can be function, caused by the way things work, brain tries to involve itself where it shouldn't
- may be dysmotility
- may be external compression
30
what can be the reason for dymotility disorders
- fibrosis
- neuromuscular dysfunction (nerves and muscles don't work anymore - nerves cannot signal to the muscles in the oesophagus to contract etc - this is needed as swallowing is an active process caused by the muscles propelling food down the oesophagus [peristalsis])
31
what is GORD
gastro-oesophageal reflux disease
also known as heart burn or acid reflux
the oesophagus is being burned from the inside by acid = very common
muscular tissue goes through chronic repair and healing so the oesophagus becomes more non-muscular
may need to by pass this area to get food into the stomach
32
where is the oesophagus found
runs from bottom of larynx / pharynx
| passes through the diaphragm
33
what are the 3 main causes of GORD
- defective lower oesophageal sphincter
- impaired lower clearing
- impaired gastric emptying (problem with the stomach, when you eat and fill your stomach the contents are not leaving the stomach quickly enough and this builds up when you eat again causing the pressure in the stomach to build up and forces the contents up into the oesophagus
34
what are the effects caused by GORD
- ulceration
- inflammation
- metaplasia (change from columnar epithelium to squamous - risk of squamous cell carcinoma)
35
what are the signs and symptoms of GORD
- epigastric burning
> worse lying down
> bending (puts more pressure on the abdomen)
> during pregnancy
```
- dysphagia
> damage to muscular tissue in oesophagus making it more fibrous
> oesophagitis
> stricture
> dysmotility
```
- GI bleeding
> acid irritate lining so it becomes inflamed and encourages bleeding
- severe pain = mimics MI
> oesophageal muscle spasm
> can feel like a heart attack
36
what is barrett's oesophagus
- recurrent acid reflux into lower part of the oesophagus
- metaplasia of the oesophageal lining to gastric type mucosa
- associated with malignant change (adenocarcinoma)
= high risk of developing carcinoma
37
what does barrett's oesophagus look like
- red
- inflamed
- metaplastic
38
how can you treat barrett's oesophagus
- proton pump inhibitors
= stops acid reflux
= stops progression of cancer
39
what is a hiatus hernia
- part of stomach is in thorax (moved through the diaphragm, when diaphragm contracts it seals part of stomach in thorax and this allows acid to move into the oesophagus)
40
what are the symptoms of hiatus hernia
similar to GORD
41
who is hiatus hernia more commonly found in
women
42
what is a sliding hiatus hernia
when the junction between the oesophagus and the stomach, as well as a portion of the stomach itself, slides up above the diaphragm
more common
moves up and down depending on what is going on in the stomach
causes GORD
43
what is a rolling (or paraoesophageal) hiatus hernia
a true herniation of the stomach into a peritoneal sac in the mediastinum
permanently sealed here
tends not to give GORD
44
how is GORD managed
- stop smoking (improves sphincter)
- lose weight and avoid triggering activity
- anatacids
- H2 blockers and PPIs (rantidine and omeprazole, preventative treatment, doesnt stop the reflux but stops there being acid for the reflux )
- increase GI motility and gastric emptying ( encouraging stomach to empty faster so pressure cannot build up in stomach)
45
what is PUD
peptic ulcer disease
(acid associated ulceration)
effectively a hole forming in the stomach (or whatever site) wall and it has the potential to progress the whole way into the periotoneum cavity
ulcer is kind of like a pothole in the road
the acid protection is removed so the acid can digest the stomach wall and may cause complete perforation
this means the acidic contents of the stomach can enter the periotenum and cause disease (high degree of inflammation)
46
where does PUD affect
any acid affected site
- oesophagus
- stomach (should not be having ulcers due to acid here as the stomach lining should be able to resist the low pH but something goes wrong to compromise its resistance)
- duodenum
47
what are the causes of PUD
- high acid secretion (duodenal)
- normal acid secretion (stomach but reduced resistance to the acid)
- drugs = NSAIDs, steroids (interfere with the stomach)
48
what age group are peptic ulcers more commonly found
in over 45 year olds
49
how can PUD occur in the duodenum
usually alkaline secretions mix with the acidic contents leaving the stomach and are able to neutralise the acid
if more acid leaves the stomach than is anticipated then there is not enough alkaline secretions to neutralise it
the duodenum is not protected against acid and acid can burn through the wall of the duodenum
the walls of the duodenum are thinner than the walls of the stomach so it takes less acid to perforate it
50
how can NSAIDs and steroids cause PUD
they inhibit the formation of mucous so the mucous layer (usually protects the stomach from acid) is disrupted which allows the acid to come into contact with the tissue in the wall of the stomach and then start digesting this tissue
51
what can happen if the ulcer erodes into a muscular artery
bleed into ulcer into stomach
lose a lot of blood through gastric bleeds
patient may present vomiting blood / blood pressure fall
52
where is mostly affected by excessive acid in PUD
- oesophagus
| - duodenum
53
what happens in PUD with a normal acid secretion
there is a reduced protective barrier
helicobacter pylori involvement
medicines interfere
54
what are helicobacter pylori
bacteria living in the stomach
they metabolise and produce CO2 and waste products and these can be measured and detected in the blood as proof that these bacteria live here
these bacteria can gradually disrupt the mucous barrier of the stomach (causing PUD)
55
what part of the stomach does helicobacter pylori infect
the lower part of the stomach, antrum
56
what does helicobacter pylori cause inflammation of
the gastric mucosa (gastritis)
often asymptomatic
causes loss of barrier from surface and will end up with an ulcer and a bleed
57
what are the effects of helicobacter pylori
- gastric ulcers
| - chronic gastric wall inflammation (lymphoma of the stomach)
58
how can helicobacter pylori be eliminated
triple therapy
(treat the bacteria, dont treat the tumour as the lymphoma will go away by itself)
- 2 antibiotics
- 1 proton pump inhibitor
59
what are the signs and symptoms of PUD
- asymptomatic
- epigastric burning pain
> worse before or after meals
> worse at night
> worse lying down
> relieved by food, alkali and vomiting (so eating can sometimes make it better)
- usually not physical signs only when there are complications like a bleed or perforation
60
what investigations can be done for PUD
- endoscopy
> oesophagus
> stomach
> duodenum
- radiology
> barium meal
> not always very helpful
- anaemia
> full blood count (FBC) and faecal occult blood tests (FOB's)
> bleeding from an ulcer can cause chronic iron deficiency anaemia
> good way for looking for blood in the stomach is by testing stools
- helicobacter pylori
> breath = look for waste products of the bacteria
> antibodies
> mucosa
61
what are the local and systemic complications of PUD
```
- local
> perforation
> haemorrhage
> stricture
> malignancy (helicobacter pylori)
```
- systemic
> anaemia (low level bleeds cause low level irritation)
62
how can PUD be treated
```
1. medical
> reversible problem (remove cause and problem goes away)
> lifestyle changes
> helicobacter pylori present
- sop smoking
- small regular meals
- eradication therapy
- ulcer healing drugs (PPI to remove the acid secretion)
```
```
2. surgical
> stricture
> acute bleed
> perforation
> malignancy
- endoscope
- surgical reapir = gastrectomy
- vagotomy
```
63
explain the types of medications used in the upper GI disease treatment
- reduce acid secretions
> H2 receptor blockers
> proton pump inhibitors
- improve mucosal barrier
> eliminate helicobacter
> inhibit prostaglandin removal (NSAID encourages this so avoid this and reduce steroid use)
64
what is triple therapy for the elimination of helicobacter pylori
core treatment
2 week course of
- 2 antibiotics
> amoxycillin
> metronidazole
- proton pump inhibitor
> omeprazole
65
what is bilroth 1
lower part of the stomach is removed and the duodenum is reconnected to the top half of the stomach
leaves you with a smaller stomach so you dont eat as much
food drops straight through to the duodenum and this also causes problems
66
what is bilroth 2
lower part of the stomach is removed
the end of the duodenum next to the stomach is sewn up
the top part of the stomach is reconnected to the small bowel
joins a smaller hole
allows for bowel secretion further up to join on
pictures explain it better
67
what is highly selective vagotomy
a surgical option
either
- cut the vagus nerve directly
> this causes problems with motility so it is not done
- cut selective branches of the vagus nerve that go to the parietal cells
> can reduce gastric acid secretion
> doesnt cause motility issues
> can be done
