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5 Human Diseases > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

what medication is used in upper GI disease? (3)

A

antacids
H2 receptor blockers
proton pump inhibitors

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2
Q

how do antacids help upper GI disease?

A

alkaline that forms a salt with stomach acid neutralising it

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3
Q

how do H2 receptor blockers help upper GI disease?

A

Prevent histamine activation of acid production, limited benefit as other pathways still operate (acetylcholine, gastrin)

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4
Q

how do proton pump inhibitors help upper GI disease?

A

reduce the amount of acid produced in the stomach

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5
Q

what can be used to look at the upper GI?

A

endoscopy

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6
Q

what is GORD -> gastro-oesophageal reflux disease commonly known as?

A

heartburn

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7
Q

what are the 3 main causes of GORD?

A

Defective lower oesophageal sphincter -> not able to shut gastric contents away from oesophagus

Impaired lower clearing -> oesophagus isn’t emptying properly into the stomach

Impaired gastric emptying: if the stomach is full of food it will eventually go back into the oesophagus causing gastric contents and acid to pass back into the oesophagus

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8
Q

what are the signs and symptoms of GORD?

A

Epigastric burning - worse lying down, bending, pregnancy

Dysphagia - difficulty swallowing

GI bleeding

Severe pain - mimics MI so can be differential diagnosis if ECG and troponin normal

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9
Q

what can GORD lead to?

A

Ulceration
inflammation
metaplasia
Barrett’s oesophagus

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10
Q

what is Barrett’s oesophagus? malignant?

A

acid in the oesophagus is left, causing a change in the oesophageal epithelium from the normal squamous epithelium to epithelium that more related to the gastric mucosa

Potentially malignant lesion -> adenocarcinoma at the bottom of the oesophagus

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11
Q

what is the management of GORD?

A

Stop smoking - improves sphincter

Lose weight and avoid triggering activity -> fat puts pressure on stomach

Medical management
- Antacids
- H2 blockers and proton pump inhibitors

Increase GI motility and gastric emptying -> prevents backfill of stomach into oesophagus

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12
Q

what is hiatus hernia?

A

Part of the stomach is in the thorax above the diaphragm

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13
Q

what are the symptoms of hiatus hernia?

A

Symptoms similar to GORD as easier for gastric contents to enter the oesophagus

  • Epigastric burning - worse lying down, bending, pregnancy
  • Dysphagia
  • GI bleeding
  • Severe pain
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14
Q

what is a sliding hiatus hernia?

A

hiatus hernia can move up and down through the diaphragmatic hole but does so together with the oesophagus

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15
Q

what is a rolling hiatus hernia?

A

oesophagus and hernia may behave independently

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16
Q

peptic ulcers affect what sites?

A

any site where acid should or shouldn’t be there -> oesophagus, stomach, duodenum

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17
Q

generally peptic ulcers are caused by what two things?

A

High acid secretion that passes into the duodenum that can’t neutralise them properly

Normal acid secretion that overcomes the barriers of the stomach

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18
Q

peptic ulcers can be caused by Normal acid secretion that overcomes the barriers of the stomach. how does this occur? cause?

A

Reduced protective barrier of the stomach lining

helicobacter pylori

drugs - NSAIDs and steroids

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19
Q

how is peptic ulcer caused by hepilobacter pylori treated?

A

triple therapy
2 antibiotics, 1 proton pump inhibitor

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20
Q

name 3 types of peptic ulcer

A

bleeding
perforated
gastric

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21
Q

what is a bleeding peptic ulcer?

A

Where it destroys a vessel wall causing bleeding

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22
Q

what is a perforated peptic ulcer

A

Where acid burns through into the peritoneum

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23
Q

what is a gastric ulcer?

A

○ Peptic ulcer in the stomach
Histologically ulcer has gone through the lining and submucosa into the gastric tissues where it has eroded into an artery causing gastric bleeding

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24
Q

what are the signs and symptoms of a peptic ulcer?

A

Asymptomatic

Epigastric burning pain -> worse just before/after meals, night

No physical signs -> only when complications e.g. bleed, perforation

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25
Q

name 4 investigations for peptic ulcer

A

endoscopy
radiology
anaemia - full blood count
H.pylori test

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26
Q

a local complication of peptic ulcer disease is perforation, what is this?

A

Escape of gastric contents into peritoneum -> can be fatal

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27
Q

a local complication of peptic ulcer disease is haemorrhage, what is this?

A

Erosion of ulcer into blood vessel causing bleeding into the stomach

Brown granular vomit

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28
Q

a local complication of peptic ulcer disease is stricture, what is this?

A

Chronic ulceration heals by secondary intention as a scar that contracts reducing the size of the stomach exit

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29
Q

a local complication of peptic ulcer disease is malignancy, what is the risk factor for this?

A

Helicobacter pylori

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30
Q

what is a systemic complication from peptic ulcer disease?

A

anaemia

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31
Q

what is the medical treatment for peptic ulcer disease?

A

stop smoking
small regular meals
H.pylori triple therapy
ulcer healing drugs - proton pump inhibitors

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32
Q

name 3 surgical treatments for peptic ulcer disease

A

endoscope
gastrectomy
vagotomy

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33
Q

how does a vagotomy help peptic ulcer disease?

A

reduces the acid producing trigger by branching the vagal nerve trunk

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34
Q

what is a gastrectomy?

A

remove part of the stomach

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35
Q

what are the 2 types of gastrectomy?

A

bilroth 1 and 2

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36
Q

what is a bilroth 1 gastrectomy?

A

Remove part of stomach containing the ulcer

Attach top of duodenum to remaining part of the stomach

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37
Q

what is a bilroth 2 gastrectomy?

A

Remove part of the stomach containing the ulcer

Attach the remaining portion of the stomach further down the duodenum

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38
Q

what medications for upper GI disease reduce acid secretion?

A

H2 receptor blockers (histamine)

proton pump inhibitors

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39
Q

what medications for upper GI disease improve mucosal barrier?

A

Eliminate H.pylori

Inhibit prostaglandin removal
- Prostaglandins can increase the resistance of the gastric mucosa
- Avoid NSAIDs and reduce steroid use

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40
Q

where is the small bowel?

A

From the duodenum to the ileocecal junction

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41
Q

what is the function of the small bowel?

A

absorption

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42
Q

coeliac disease is
Sensitivity of ? component of ? in the ? bowel causing an ? reaction

Involves both ? and ?? in the destruction of ? tissue (? atrophy)

As ? changes take place the villi are ? (villus atrophy) decreasing the ?? of the duodenum for ??

A

a-gliadin
gluten
small
immune

antibodies
T cells
villus
villous

inflammatory
lost
surface area
food absorption

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43
Q

name 3 causes of coeliac disease

A

Genetic
Environmental trigger
Consumption of gluten

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44
Q

what effects does coeliac disease have on the body? 6

A

Weight loss

Diarrhoea

oral aphthae - group of small ulcers

Tongue papillary loss

Malabsorption issues

  • Iron, folate, vitamin B12, fat
45
Q

what investigations are done for coeliac disease? 4

A

Autoantibody test
- TTG or anti-gliadin/endomyseal antibodies

Jejunal biopsy

Faecal fat
- Increased if malabsorption

Haematinics -> ferritin, folate, Vit B12
- Can be reduced which suggests malabsorption
- Done if patient presents with ulcer to detect malabsorption

46
Q

what is the management of coeliac disease?

A

If don’t eat gluten then jejunum and symptoms return to normal

47
Q

what skin disease is linked to coeliac disease?

A

dermatitis herpetiformis

48
Q

what is dermatitis herpetiformis?

A

Ulceration and blisters on the skin and oral mucosa

Will go away if pt is gluten free

49
Q

what is pernicious anaemia?

A

Vitamin B12 deficiency due to diet or absorption issue

50
Q

Vitamin B12 has a complex absorption process -> only absorbed in the ?? with help from ??

A

terminal ileum
intrinsic factor

51
Q

name 4 causes of pernicious anaemia

A

Lack of vitamin B12 in diet

Disease of gastric parietal cells

Inflammatory bowel disease of the terminal ileum -> Chron’s

Bowel cancer at ileocecal junction

52
Q

how is pernicious anaemia diagnosed?

A

Schilling test uses radioisotopes to determine whether there is an absorption problem

antibodies against the parietal cells and intrinsic factor have superseded schilling test

53
Q

how is pernicious anaemia treated?

A

Diet with vitamin B12

Vitamin B12 supplements

IM vitamin B12 injections if absorption not possible

54
Q

irritable bowel disease covers what 2 main disease?

A

ulcerative colitis
Crohn’s disease

55
Q

what is the term is used if unsure whether a pt has ulcerative colitis or Crohn’s disease?

A

intermediate colitis

56
Q

ulcerative colitis and Crohn’s disease are very similar but differ in clinical presentation. name one way they differ

A

ulcerative colitis has bloody diarrhoea

Crohn’s disease has watery diarrhoea

57
Q

what 3 groups are involved in the pathogenesis of IBD?

A

genetic predisposition

mucosal immune system

environmental triggers

58
Q

Pathogenesis of IBD:
Genetic predisposition

?? on chromosome ? encodes a protein involved in ??. Mutation in this gene is found in 10-20% of Caucasian pt’s with ??

A

NOD 2
16
bacterial recognition
Crohn’s disease

59
Q

pathogenesis of IBD
Mucosal immune system
Innate immune system

? junctions to regulate ?permeability

Mucus layer containing ?helps to ? the epithelial layer

Defensives (proteins) can be activated ? or in response to ??.

? gene contributes significantly to this normal mucosal defence

A

tight
epithelial

bacteria
protect

constitutionally
abnormal bacteria

NOD2

60
Q

pathogenesis of IBD
Adaptive immunity

?? cells which are part of the first line defence but there is also ? that are critical in developing adaptive immune response

Many types of T lymphocyte
- ? tends to be more of an inflammatory and disease promoting
- ? keep the inflammatory T cells in check

Crohn’s disease have over-activation of effector T cells ?

Ulcerative colitis have a ?? response and get introduction of ??? cells

A

antigen presenting
t lymphocytes

TH1
TH2

TH1

mixed TH1/TH2
natural killer T

61
Q

name 2 environmental triggers for IBD

A

smoking
NSAIDs

62
Q

how does smoking affect IBD - ulcerative colitis and Crohn’s

A

aggravates Crohn’s - narrowing of small bowel and colon which causes them to have obstructive GI symptoms, and can increase symptoms of nausea and vomiting

Protects against ulcerative colitis

63
Q

what is ulcerative colitis?

A

Inflammation of colon of unknown aetiology affecting the rectum and progresses proximally

64
Q

symptoms of ulcerative colitis 4

A

Diarrhoea and bleeding

Problems defecating and urinating

65
Q

what in the pt history indicates risk of ulcerative colitis?

A

Recent travel

Antibiotics

NSAIDs

Family history

Smoking

66
Q

what investigations (generally) are taken for ulcerative colitis? 4

A

blood test
abdominal x-ray
endoscopy (biopsy)
histology of biopsies

67
Q

what blood tests are taken to investigate ulcerative colitis?

A

C-reactive protein - rise in response to inflammation

Albumin - negative acute phase reactant - low albumin indicated inflammation

Platelets - thrombocytosis indirect marker - low platelets

68
Q

what could be seen in an endoscopy for ulcerative colitis?

A

Loss of vessel pattern, granular mucosa, contact bleeding

Pseudo polyps

69
Q

what is seen when investigating the histology of ulcerative colitis?

A

Lose goblet cells and get expansion of crypts that can lead to abscess formation

Only affects the mucosal layer

70
Q

what is Crohn’s disease?

A

chronic inflammation affecting any region of the GI tract from the anus to the mouth

71
Q

how does Crohn’s disease differ from ulcerative colitis?

A

transmural inflammation - fistulas (abnormal connections) between different parts of the small bowel, it can also cause stretching or narrowing to occur

histologically - cobblestone appearance in Crohn’s but pseudopolyps in ulcerative colitis

72
Q

symptoms of Crohn’s disease are determined by what?

A

the site of the disease

73
Q

symptoms of Crohn’s disease?

A

Weight loss
abdominal pain, watery diarrhoea and perianal involvement

Mouth ulcers, swollen lips, angular cheilitis

74
Q

mouth specific symptoms of Crohn’s disease

A

Mouth ulcers, swollen lips, angular cheilitis

75
Q

what blood tests are done for Crohn’s disease

A

CRP, albumin, platelets, B12, ferritin, FBC

If last section of small bowel is affected then B12 will be affected, this will affect ability to absorb iron so ferritin may be low

76
Q

oral manifestations of IBD

A

Ulcers that are deep, aggressive and don’t respond to treatment

Tend to have poorer oral hygiene and have predisposition to dental caries

Oral manifestations and abnormal bowel troubles can be a sign of a flare so refer them to secondary care

77
Q

what lifestyle advice is given to manage IBD

A

Avoid smoking as it aggravates Crohn’s, worse disease outcome and rapid recurrence post-surgery

Diet - > balanced and healthy
- Stricturing/fistulating Crohn’s -> low fibre, elemental diet, strict gut rest (parenteral nutrition)

78
Q

what drugs are used for an acute flare of ulcerative colitis?

A

steroids

Anti-inflammatory

Rapid remission of acute flares

Short course of high dose initially - need vitamin D3 supplements

Not a long term maintenance therapy

79
Q

what drugs are used for maintenance of ulcerative colitis?

A

5-ASA (mesalazine)
immunosuppressants
biologics
jack inhibitors

80
Q

what drugs are used for an acute flare of Crohn’s disease?

A

steroids

Anti-inflammatory

Rapid remission of acute flares

Short course of high dose initially - need vitamin D3 supplements

Not a long term maintenance therapy

81
Q

what drugs are used for maintenance of Crohn’s disease?

A

immunosuppressants
biologics

82
Q

biologics mechanism of action on IBD

Infliximab/adalimumab -> blocks ?? pathway and promotes ? of activated ??, has a ? affect

Ustekinimab -> blocks ?? - proinflammatory pathways to try and regulate the activation of the immune system within the ??
- If pt are needing any extractions or extensive work done get in touch with secondary care for advise

Vedolizumab -> ? specific biologic, stops the activated cells moving ? the ??

A

TNF alpha
apoptosis
T cells
systemic

IL 12/23
bowel wall

gut
into
gut wall

83
Q

jack inhibitors mechanism of action on IBD

Impacts on the expression of ? that drive the inflammatory process.

? are messenger molecules that once activated are used to ? the inflammatory process

When cytokine hits the target JAK ? it so you cant get the movement of other molecules into the ? of the cell to ? the expression of the cytokine ?
Tofacitinib, Upacitinib, Filgotinib

A

cytokines

cytokines
propagate

blocks
nucleus
promote
genes

84
Q

understand

Surgery for IBD

Emergency - failure to respond to medical therapy, small bowel obstruction, abscess, fistulae

Elective - failure to respond to medical therapy, dysplasia of colon mucosa

A
85
Q

understand

Therapy pyramid for IBD drugs
- Steroids if required
- 5-ASA (UC)
- Immunosuppression
- Biologics
- JAK inhibitors

A
86
Q

why does bowel cancer generally mean colonic cancer?

A

tumours are possible within the small intestine but are unusual and more likely to be a lymphoma.

87
Q

Bowel cancer screening programme in the UK from what age?

A

50

88
Q

symptoms of bowel cancer

A

No symptoms until the tumour completely blocks the bowel and the pt presents with obstruction

Bleeding from the tumour can lead to anaemia and rectal blood loss

89
Q

what is the medical name of colon cancer?

A

colonic carcinoma

90
Q

Aetiology of colonic carcinoma

Most arise from polyps in the surface of the lumen, these will grow and progress into tumours

If the polyps are removed cancer will not develop

Bowel cancer screening (endoscopy) aims to detect polyps before they are cancers. If polyps found screening reduced from every 5yrs to 2yrs

Polyps often bleed due to irritation and trauma from bowel contents passing

Polyps take 5 years to develop to malignancy

A

polyps
lumen
tumours

cancer

endoscopy
before
5yrs
2yrs

bleed
irritation
trauma
contents

5yrs

91
Q

aetiological factors for bowel cancer 7

A

Diet -> low fibre, high fat, high meat, low veg

Smoking

Alcohol

Low exercise

Genetics - P53

Ulcerative colitis

Intestinal polyps

92
Q

what is intestinal polyposis?

A

Genetic tendency to form a lot of polyps in the bowel which are each at a risk of developing cancer

93
Q

name the condition when intestinal polyposis occurs in the small intestine?

A

Peutz-Jehgers syndrome

94
Q

oral manifestation of peutz-jehgers syndrome

A

Pt gets perioral melanosis but gets polyps in the small intestine

95
Q

name 2 conditions where intestinal polyposis occurs in the large intestine

A

Gardiner’s syndrome
Cowden’s syndrome

96
Q

oral manifestation of cowden’s syndrome

A

Mucosal polyposis where polyps are present throughout the mouth as well as throughout the bowel. Mouth polyps do not develop into oral cancer

97
Q

how is colon cancer staged?

A

according to level of invasion into the bowel wall

Dukes classification

98
Q

list the Dukes classification

A

A submucosal
B muscularis
C lymph nodes
D liver

99
Q

how is colon cancer treated? 3

A

Surgery
- Removal of colon with cancer resulting in a stoma and colostomy bag

Radiotherapy

Chemotherapy

100
Q

how is colon cancer screened?

A

FiT test - faecal immunochemical test
- every 2 years if negative
- If positive endoscopy

101
Q

dental erosion / NCTSL can be caused by acidic diet, GORD and excessive vomiting (bulimia, morning sickness)

what is the most common sites for dental erosion?

A

palatal surface of upper anteriors

102
Q

oral manifestations of coeliac disease are due to nutritional deficiencies from malabsorption

name 3 oral manifestations

A

Oral Aphthous ulceration - ovoid, creamy centre, erythematous or halo border

Glossitis - tongue depapillation

Angular cheilitis - deficiency in iron, folate or vit B12

103
Q

oral stigmata of crohn’s disease

A

Facial/labial swelling - most common sign

Ulceration - aphthous or linear common in buccal sulci

Mucosal tags

Cobblestone mucosa - due to granulomatous inflammation and oedema of tissues

Staghorning - raised submandibular ducts due to tissue swelling

Angular cheilitis

Perioral dermatitis

Inflammatory gingivitis - inflammation far exceeds the area expected from gingivitis

104
Q

what is orofacial granulomatous?

A

Chronic inflammation of the orofacial region characterised by non-caseating granulomas on histopathology

105
Q

what is the cause of orofacial granulomatous?

A

Unsure of cause but most likely due to hypersensitivity to preservatives in food

106
Q

clinical presentation of orofacial granulomatous

A

Similar presentation to oral Crohn’s disease but absence of GI involvement

107
Q

what distinguishes orofacial granulomatous and oral Crohn’s?

A

If linear ulceration, scarring and elevated inflammatory marker in blood test oral Crohn’s disease is more likely

108
Q

ulcerative colitis oral manifestations

A

Oral manifestations are rare

Aphthous ulceration

Angular cheilitis

Glossitis

Pyostomatitis Vegetans
Micro-abscesses and pustules which burst leading to ulceration. Cobble stoning and raised exophytic growths (vegetations) can also occur

5 Human Diseases (16 decks)

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