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BDS2 BAMS > Upper GI Diseases > Flashcards

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
Q

main effect of orofacial granulomatosis

A

Psychological issue

- Cosmetic, no physical harm

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26
Q

how to examine the mouth

A

by eye

can see subtle changes

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27
Q

to examine the inside of gut use

A

endoscopy

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28
Q

endoscopy

A

use to examine inside of gut

Not flexible 
- Rigid glass rods 
- Can steer them round borders 
 Pocket at far end 
- Grab bits of tissue
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29
Q

oesophagus

A

Joining between gut and mouth

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30
Q

where does embryonic gut begin down the oesphagus

A

2/3 way down

- head and skin above is ectoderm

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31
Q

change of mucosa in embryonic gut part of oesophagus

A

stratified squamous to simple columnar

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32
Q

musculature in embryonic gut part of oesophagus

A

Muscular tube with peristalsis down - active process

Grab and propel down with contraction behind

33
Q

3 oesophageal disorders

A

dysphagia

dysmotility disorders

GORD

34
Q

dysphagia

A

compression

Cannot get food bolus down beyond a blockage in oesophagus

can be localised by patient or barium meal

35
Q

dysmotility of oesphagus can be due to

A

fibrosis or neuromuscular duyfacunction

36
Q

fibrosis dysmotility of oesophagus

A

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
Q

neuromuscular dysmotility of oesophagus

A

‘Nerves in muscle no longer working

Ability to tell muscles to tell contract as was impaired

38
Q

duration of dysphagia

A

varies

can be intermittent or constant

39
Q

potential causes of dysphagiea

A

‘functional’

  • Anxiety, nerves not functioning properly
  • Brain interference

dysmotility

external compression
- squamous cell carcinoma

40
Q

anatomical location of oesophagus

A 
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
Q

3 main causes of GORD

A
  • 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
Q

effect of GORD

A

ulceration, inflammation, metaplasia

damaging to oesophageal lining – columnar to squamous epithelium

metaplasia

squamous cell carcinoma risk

43
Q

GORD Signs and symptoms

A

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
Q

barrett’s oesophagus

A

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
Q

how to treat barrett’s oesophagus if becomes malignant

A

part of oesophagus resected

46
Q

how can proton pump inhibitors reduce risk of barrett’s oesophagus

A
  • stop acid
  • stop reflux
  • reduce risk
47
Q

hiatus hernia

A

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
Q

2 types of hiatus hernia

A

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
Q

GORD Management

A

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
Q

peptic ulcer disease PUD

A

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
Q

3 causes of peptic ulcer disease

A

High acid secretion - duodenal

Normal acid secretion - stomach
- Mucous on surface of stomach not functioning properly (reduced resistance)

drugs - NSAIDS, Steroids

52
Q

what normally happens when acid food suspension enters duodenum

A

neutralised by duodenal secretions

53
Q

PUD outwith stomach is commonly

A

too much acid secretion

hormone related (gastrin)

54
Q

PUD within stomach is due to

A

damaged lining
• Steroid - inhibit mucous
• Bacterial infection grow in stomach lining and acid in contact with tissue

55
Q

what happens if PUD interacts with small artery

A

vomit has blood in it

56
Q

2 reasons for PUD

A
  • excessive acid

- normal acid but reduced protection

57
Q

excessive acid PUD causes

A

oesophageal, duodenal ulcers

unknown Trigger for secretion

58
Q

normal acid PUD has

A

reduced protective barrier

helicobacter pylori involvement

59
Q

helicobacter pyrlori

A

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
Q

action of helicobacter pylori

A

Gradually disrupt mucous barrier

  • Ulceration and bleeding
  • Inflammation
61
Q

effects of helicobacter pylori

A

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
Q

how to treat helicobacter pylori infection

A

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
Q

PUD Signs and symptoms

A

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
Q

PUD Investigations (4)

A

Endoscopy
- oesphagus, stomach & duodenum

Radiology
- barium meal

Anaemia
- F.B.C and faecal occult blood test (FOB’s)

H. pylori
- breath, antibodies, mucosa

65
Q

4 local PUD Complication

A

Perforation
Haemorrhage
Stricture
Malignancy

66
Q

systemic PUD complication

A

anaemia

67
Q

medical PUD treatment

A

Stop smoking

Small regular meals – easier to manage

Eradication therapy

Ulcer healing drugs

  • Proton pump inhibits
  • Remove acid
68
Q

reasons for medical treatment of PUD

A

Reversible problem

Lifestyle changes

H.pylori present – take away = reverse

69
Q

reason for surgical PUD treatment

A

Stricture

Acute bleed

Perforation

Malignancy

70
Q

surgical PUD treatment

A

Endoscope

Surgical repair
- Gastrectomy

Vagotomy

71
Q

why is decrease in PUD treatment success with age

A

Older age less chance of surviving operation

Death rate going up as less surgery when young and fit

72
Q

2 actions of medication in upper GI diseases

A

reduce acid secretion

improve mucosal barrier

73
Q

2 medicines which reduce acid secretions of upper GI

A

H2 receptor blockers

Proton pump inhibitors

74
Q

ways in which medicines improve the mucosal barrier in upper GI

A

Eliminate helicobacter

Inhibit prostaglandin removal

  • NSAID use encourages this – avoid
  • Reduce steroid use
75
Q

what is triple therapy

A

For elimination of Helicobacter pylori

Two week course of:
- Two antibiotics (Amoxycillin and Metronidazole
- Proton Pump Inhibitor
omeprazole)

76
Q

bilroth 1

A

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
Q

bilroth 2

A

surgical PUD management

Join smaller hole from duodenum to stomach
Smaller outflow
Duodenum secretions earlier

78
Q

Highly selective vagotomy

A

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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