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Upper GI Diseases Flashcards

1
Q

2 functions of medications of upper GI Diseases

A

eliminate formed acid (antacids)

reduce acid secretion

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2
Q

medicines which reduce acid secretion (2)

A

H2 receptor blockers

proton pump inhibitors

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3
Q

how do antacids work

A

Covert acid to salt

Adsorb that

Depend on what is in can poison with too high magnesium levels

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4
Q

what cell makes acid in GI

A

parietal cell

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5
Q

what is the secreting portion of parietal cell

A

proton pump

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6
Q

how can parietal cell be inhiited

A

by proton pump inhibitor

- stops acid production

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7
Q

3 triggers for acid production on parietal cell

A

histamine H2 recpetor

gastrin

ACh (cholinergic)

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8
Q

Gastrin

A

local hormone caused by stomach stretch

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9
Q

when is ACh released and thus detected by parietal cells

A

in anticipation of food - salivation

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10
Q

how many pathways do you need to block to stop acid secretion by parietal cells

A

all 3

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11
Q

what do you need to block to stop acid being made

A

proton pump at top of parietal cell

other 3 pathways trigger acid to be made

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12
Q

role of H2 receptor antagonists

A

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

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13
Q

cimetidine

A

H2 receptor antagonist

Original H2 blocker
Many drug interactions
Not fully effective

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14
Q

ranitidine

A

H2 receptor antangonist

Not any more effective
Safer in clinical use
Licensed for over the counter sale

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15
Q

examples of proton pump inhibitors

A

Omeprazole
Lansoprazole
Pantoprazole

all end in prazole

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16
Q

what are more effective clinically - proton pump inhibitors of H2 receptor antagonists

A

proton pump inhibitors

- acid secretion completely stopped

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17
Q

dyspepsia

A

indigestion

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18
Q

causes of dyspepsia

A

diet

medicine side effect

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19
Q

3 classes of upper GI disease

A

Oral diseases
Oesophageal disease
Gastric disease

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20
Q

3 main commonly seen of oral diseases

A

Recurrent oral ulceration
Lichen planus
Orofacial granuomatsis

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21
Q

minor apthae

A

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

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22
Q

major apthae

A

More than 1cm in size

3 months to heal

Scar when heal

Can be nuisance but can be significant pain to patient

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23
Q

herpetiform apthae

A

Lots of small ulcers around mouth

Don’t get on keratinised mucosa

Dorsal of tongue

Will on underside of tongue, masticatory mucosa etc

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24
Q

orofacial granulomatosis

A

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

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25
main effect of orofacial granulomatosis
Psychological issue | - Cosmetic, no physical harm
26
how to examine the mouth
by eye | can see subtle changes
27
to examine the inside of gut use
endoscopy
28
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 ```
29
oesophagus
Joining between gut and mouth
30
where does embryonic gut begin down the oesphagus
2/3 way down | - head and skin above is ectoderm
31
change of mucosa in embryonic gut part of oesophagus
stratified squamous to simple columnar
32
musculature in embryonic gut part of oesophagus
Muscular tube with peristalsis down - active process Grab and propel down with contraction behind
33
3 oesophageal disorders
dysphagia dysmotility disorders GORD
34
dysphagia
compression Cannot get food bolus down beyond a blockage in oesophagus can be localised by patient or barium meal
35
dysmotility of oesphagus can be due to
fibrosis or neuromuscular duyfacunction
36
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
37
neuromuscular dysmotility of oesophagus
'Nerves in muscle no longer working Ability to tell muscles to tell contract as was impaired
38
duration of dysphagia
varies can be intermittent or constant
39
potential causes of dysphagiea
‘functional’ - Anxiety, nerves not functioning properly - Brain interference dysmotility external compression - squamous cell carcinoma
40
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 ```
41
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
42
effect of GORD
ulceration, inflammation, metaplasia damaging to oesophageal lining – columnar to squamous epithelium metaplasia squamous cell carcinoma risk
43
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
44
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
45
how to treat barrett's oesophagus if becomes malignant
part of oesophagus resected
46
how can proton pump inhibitors reduce risk of barrett's oesophagus
* stop acid * stop reflux * reduce risk
47
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
48
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
49
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
50
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
51
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
52
what normally happens when acid food suspension enters duodenum
neutralised by duodenal secretions
53
PUD outwith stomach is commonly
too much acid secretion hormone related (gastrin)
54
PUD within stomach is due to
damaged lining • Steroid - inhibit mucous • Bacterial infection grow in stomach lining and acid in contact with tissue
55
what happens if PUD interacts with small artery
vomit has blood in it
56
2 reasons for PUD
- excessive acid | - normal acid but reduced protection
57
excessive acid PUD causes
oesophageal, duodenal ulcers | unknown Trigger for secretion
58
normal acid PUD has
reduced protective barrier helicobacter pylori involvement
59
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
60
action of helicobacter pylori
Gradually disrupt mucous barrier - Ulceration and bleeding - Inflammation
61
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
62
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 ```
63
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.
64
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
65
4 local PUD Complication
Perforation Haemorrhage Stricture Malignancy
66
systemic PUD complication
anaemia
67
medical PUD treatment
Stop smoking Small regular meals – easier to manage Eradication therapy Ulcer healing drugs - Proton pump inhibits - Remove acid
68
reasons for medical treatment of PUD
Reversible problem Lifestyle changes H.pylori present – take away = reverse
69
reason for surgical PUD treatment
Stricture Acute bleed Perforation Malignancy
70
surgical PUD treatment
Endoscope Surgical repair - Gastrectomy Vagotomy
71
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
72
2 actions of medication in upper GI diseases
reduce acid secretion improve mucosal barrier
73
2 medicines which reduce acid secretions of upper GI
H2 receptor blockers Proton pump inhibitors
74
ways in which medicines improve the mucosal barrier in upper GI
Eliminate helicobacter Inhibit prostaglandin removal - NSAID use encourages this – avoid - Reduce steroid use
75
what is triple therapy
For elimination of Helicobacter pylori | Two week course of: - Two antibiotics (Amoxycillin and Metronidazole - Proton Pump Inhibitor omeprazole)
76
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 ```
77
bilroth 2
surgical PUD management Join smaller hole from duodenum to stomach Smaller outflow Duodenum secretions earlier
78
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

BDS2 BAMS (54 decks)

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