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BDS2 - GIT system > Upper GI Disease > Flashcards

Upper GI Disease Flashcards

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1
Q

where does the gastrointestinal tract start

A

half way down the oesophagus

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2
Q

is the head part of the GI tract

A

no

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3
Q

what is GI disease split between

A
  • diseases affecting the tube the food goes down

- the actual gut

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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)
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5
Q

what do antacids do?

A

change acids to salts

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6
Q

what do proton pump inhibitors do

A

acts on the proton pump

stops you being able to make acid

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7
Q

in the proton pump, what is acid

A

an ion of hydrogen

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8
Q

what are the triggers for making acid

A
  • acetylcholine
    = neurological trigger
  • gastrin
    = local hormone with stomach being stretched
  • histamine
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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

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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
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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
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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

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13
Q

what does dyspepsia mean

A

indigestion

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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

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15
Q

name upper GI diseases

A
  • oral disease
  • oesophageal disease
  • gastric disease
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16
Q

what are common things in oral diseases to see

A
  • recurrent oral ulceration
  • lichen planus
  • orofacial granulomas
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17
Q

name 3 types of oral ulcerations

A

minor aphthae
major aphthae
herpetiform aphthae

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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
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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

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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

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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)

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22
Q

what are giant cells

A

macrophages fused together

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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

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24
Q

what is an EGD

A

esophagogastroduodenoscopy

also called an upper endoscopy

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25
Q

how can you look inside the gut

A

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

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26
Q

what do oesophageal disorders usually involve

A

mucosa and musculature changes

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27
Q

name oesophageal disorders

A
  • dysphagia
  • dysmotility disorders
  • Gastro-oesophageal reflux disease
28
Q

what does it mean when dysphagia is caused by compression

A

squamous carcinoma in the lungs can compress the oesophagus

does not allow food to pass down through and causes problems with swallowing

29
Q

what can be the cause of problems with swallowing

A
  • 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
Q

what can be the reason for dymotility disorders

A
  • 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
Q

what is GORD

A

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
Q

where is the oesophagus found

A

runs from bottom of larynx / pharynx

passes through the diaphragm

33
Q

what are the 3 main causes of GORD

A
  • 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
Q

what are the effects caused by GORD

A
  • ulceration
  • inflammation
  • metaplasia (change from columnar epithelium to squamous - risk of squamous cell carcinoma)
35
Q

what are the signs and symptoms of GORD

A
  • 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
Q

what is barrett’s oesophagus

A
  • 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
Q

what does barrett’s oesophagus look like

A
  • red
  • inflamed
  • metaplastic
38
Q

how can you treat barrett’s oesophagus

A
  • proton pump inhibitors
    = stops acid reflux
    = stops progression of cancer
39
Q

what is a hiatus hernia

A
  • 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
Q

what are the symptoms of hiatus hernia

A

similar to GORD

41
Q

who is hiatus hernia more commonly found in

A

women

42
Q

what is a sliding hiatus hernia

A

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
Q

what is a rolling (or paraoesophageal) hiatus hernia

A

a true herniation of the stomach into a peritoneal sac in the mediastinum

permanently sealed here

tends not to give GORD

44
Q

how is GORD managed

A
  • 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
Q

what is PUD

A

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
Q

where does PUD affect

A

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
Q

what are the causes of PUD

A
  • high acid secretion (duodenal)
  • normal acid secretion (stomach but reduced resistance to the acid)
  • drugs = NSAIDs, steroids (interfere with the stomach)
48
Q

what age group are peptic ulcers more commonly found

A

in over 45 year olds

49
Q

how can PUD occur in the duodenum

A

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
Q

how can NSAIDs and steroids cause PUD

A

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
Q

what can happen if the ulcer erodes into a muscular artery

A

bleed into ulcer into stomach
lose a lot of blood through gastric bleeds
patient may present vomiting blood / blood pressure fall

52
Q

where is mostly affected by excessive acid in PUD

A
  • oesophagus

- duodenum

53
Q

what happens in PUD with a normal acid secretion

A

there is a reduced protective barrier
helicobacter pylori involvement
medicines interfere

54
Q

what are helicobacter pylori

A

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
Q

what part of the stomach does helicobacter pylori infect

A

the lower part of the stomach, antrum

56
Q

what does helicobacter pylori cause inflammation of

A

the gastric mucosa (gastritis)
often asymptomatic
causes loss of barrier from surface and will end up with an ulcer and a bleed

57
Q

what are the effects of helicobacter pylori

A
  • gastric ulcers

- chronic gastric wall inflammation (lymphoma of the stomach)

58
Q

how can helicobacter pylori be eliminated

A

triple therapy
(treat the bacteria, dont treat the tumour as the lymphoma will go away by itself)
- 2 antibiotics
- 1 proton pump inhibitor

59
Q

what are the signs and symptoms of PUD

A
  • 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
Q

what investigations can be done for PUD

A
  • 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
Q

what are the local and systemic complications of PUD

A 
- local 
> perforation
> haemorrhage 
> stricture
> malignancy (helicobacter pylori)
  • systemic
    > anaemia (low level bleeds cause low level irritation)
62
Q

how can PUD be treated

A 
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
Q

explain the types of medications used in the upper GI disease treatment

A
  • 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
Q

what is triple therapy for the elimination of helicobacter pylori

A

core treatment

2 week course of
- 2 antibiotics
> amoxycillin
> metronidazole

  • proton pump inhibitor
    > omeprazole
65
Q

what is bilroth 1

A

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
Q

what is bilroth 2

A

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
Q

what is highly selective vagotomy

A

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

BDS2 - GIT system (5 decks)

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