Gastrointestinal Medicine - 1 Flashcards

1
Q

What medications are used for upper GI diseases and what do they do?

A

Antacids
- elimate acid via neutralising by forming a salt

H2 receptor blocks
- block histamine

PPI (proton pump inhibitors)
- reduce PP acid release

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2
Q

How do H2 receptor antagonists work and why are they limited in benefit?

what are examples?

A
  • Reduce acid production by preventing histamine activation of acid production
  • Limited benefit as alternative pathways still operative through Acetylcholine, Gastrin
  • Ranitidine
  • Cimetidine (many drug interactions)
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3
Q

What are the 3 triggers for parietal cells to secrete acid?

how can stimulation be stopped

A

ACh (vagus nerve via surgery)
Gastrin
Histamine (H2 blockers)

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4
Q

What are examples of PPI?

A

omeprazole
lansoprazole
pantoprazole
any prazole ending

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5
Q

Why are oral diseases not part of the GI tract?

A

they are embryologically not part of the GI tract
oral tissues develop from invaginations of the ectoderm as the head grew to accommodate the brain

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6
Q

What are the types of endoscopy?

A

esophagogastroduodenoscopy
- flexible scope with light and small forceps for biopsy passed through the GI

capsule endoscopy
- takes photos of the GI as it passes through when swallowing

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6
Q

What can cause dysphagia?

A

external compression
dysmotility disorder - fibrosis
neruromuscular dysfunction

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7
Q

What can cause compression and what structures can be compressed?

A

tumours/aneurysm
lung/aorta/trachea/cervical spine

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8
Q

What are examples of fibrosis and what do they cause?

A

scleroderma (elastic tissue is replaced by fibrous tissue)

acid related fibrosis (GORD) causing chronic inflammation

they cause loss of specalised tissue that aids in swallowing

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9
Q

What are examples of neuromusular dysfunction?

A

parkinsons disease
diabetes mellitus
achalasia (nerve does not form properly)

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10
Q

Why is the dysphagia localised well by the patient?

A

the oesophagus is highly innervated

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11
Q

What are the 3 main causes of GORD?

A
  • defective lower oesophageal sphincter
  • impaired lower clearing
  • impaired gastric emptying
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12
Q

What are the effects of GORD?

A
  • ulceration, inflammation, metaplasia (Gastric)
  • Barrett’s Oesphagitis
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13
Q

What is the metaplasia that GORD can cause?

A

from simple squamous epithlium to gastric (simple columnar)

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14
Q

What are GORD signs and symptoms?

A
  • Heartburn
  • Acid reflux
  • Chest pain
  • Dysphagia
  • GI bleeding
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15
Q

How cause GI bleeding diagnosed?

A

fecal occult blood tests

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16
Q

What is a hiatus hernia?

A

part of stomach is in thorax
similar symptoms to GORD

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17
Q

How can GORD be managed via lifestyle?

A
  • Stop smoking and excess caffeine - improves sphincter
  • Lose weight & avoid triggering activity - fat can cause pressure onto stomach forcing acid up, bending can also force acid up
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18
Q

What medications can manage GORD?

A
  • antacids
  • H2 blockers & PPI’s
  • ranitidine & omeprazole
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19
Q

What are the causes of PUD (peptic ulcer disease)?

in duodenum and stomach

A
  • High acid secretion - duodenal
  • Normal acid secretion - stomach (NSAIDS, steroids, H-pylori)
20
Q

What major issues can peptic ulcers cause?

A

ulcer can erode into artery causing bleeding or perforate the peritoneum causing peritonitis

21
Q

What can be causing excessive acid production?

A

Gastrinomas are neuroendocrine tumors characterized by the secretion of gastrin with resultant excessive gastric acid production

22
Q

What is the bacterium that causes PUD?

A

H. pylori
infects the lower part of the stomach antrum

23
Q

What does H.pylori cause?

A

gastric ulcers through loss of mucus barrier which allows acid in stomach to get to gastric wall

chronic inflammation of the gastric mucosa

lymphoma

24
Q

How is H.pylori eliminated?

A

TRIPLE THERAPY
* 2 antibiotics
* 1 proton pump inhibitor

25
Q

What are PUD signs and symptoms?

A
  • Burning stomach pain
  • Indigestion
  • Acid reflux
  • Blood in vomit or stool (serious - means perforation)
26
Q

How can PUD be investigated?

A
  • Endoscopy
  • Radiology - barium meal
  • F.B.C (anemia) and faecal occult blood test (FOB’s) (GI bleeding)
  • H. pylori - breath, antibodies, mucosa
27
Q

What are the complications of PUD?

A
  • perforation
  • haemorrhage (coffee grounds)
  • stricture
  • malignancy
  • anaemia
28
Q

What is treatment of PUD?

A
  • Antibiotics (to kill H. pylori)
  • Medications to reduce stomach acid (PPIs or H2 blockers)
  • Lifestyle changes (quit smoking, limit alcohol)
29
Q

How can the mucosal barrier be improved?

A
  • Eliminate Helicobacter
  • Reduce NSAID (irritant)
  • Reduce steroid use (weaken barrier)
30
Q

What is triple therapy?

A

For elimination of Helicobacter pylori
Two week course of:
Two antibiotics
Amoxycillin, Metronidazole
Proton Pump Inhibitor
Omeprazole

31
Q

What are the three surgeries available for PUD?

A

Bilroth 1 - top half of stomach is reconnected to duodeum, removes part of stomach and sphincter

Bilroth 2 - top half of stomach reconnected to jejunum bypassing duodeum

Highly selective vagotomy

32
Q

What are the diseases found in small bowel?

A
  • Coeliac Disease
  • Pernicious Anaemia
  • Crohn’s Disease
  • Infections
  • Tumours
33
Q

Why is the duodeum most affected by PUD?

A

due to gastric emptying and bile/pancreatic secretions

34
Q

What is the cause of coeliac disease?

A

Sensitivity to α-gliaden component of Gluten - causing a reactive change in the small bowel

35
Q

What is the aetiology of coelic disease?

A
  • Genetic susecptibility
  • Environmental trigger
36
Q

What happens in coeliac disease at the enterocytes?

A

gluten consumed

alpha -gliaden passes through enterocytes and causes an immune reaction

t-cells damage mucosal tissue causing villous atrophy

37
Q

What is loss of projections called and what does it lead to?

A

Subtotal villous atrophy of the jejunum > decreased surface area > decreased absorption

38
Q

What are classic symptoms of coeliac disease?

A
  • Weight loss
  • Weakness
  • Abdominal pain/swelling
  • Diarrhoea
  • Canker sore
  • Tongue papillary loss
  • Steatorrhoea
  • Dysphagia - plummer vinson syndrome caused by loss of iron
39
Q

How can coeliac disease be investigated?

A
  • Autoantibody Test - TTG, anti-gliadin antibodies
  • Jejunal Biopsy
  • Faecal Fat – increased if malabsorbtion
  • Haematinics – B12, Folate, Ferritin
40
Q

Why is a serum TTG not very accurate?

A

delivers many false positives

41
Q

What is the outcome of a gluten free diet for coeliacs?

A
  • Reversal of jejunal atrophy
  • Improved well-being
  • Reduced risk of lymphoma
42
Q

What skin disease is associated with coeliac disease?

what does it do

A

Dermatitis Herpetiformis

skin/oral conditon (granular IgA deposits) that causes itching, blistering and ulcers

43
Q

What is pernicious anaemia?

A

failure of body to absorb vit B12

44
Q

Why is vit b12 complex during absorption?

A
  • Needs intrinsic factor from Gastric parietal cells and R protein in saliva
  • Needs functioning of a discrete area of the Terminal Ilium – this is the ONLY vit B12 absorption site in the bowel
45
Q

What are the possible tests for pernicious anaemia?

A

serology
blood tests

46
Q

What causes pernicious anaemia?

A
  • Lack of Vitamin B12 in the diet
  • Disease of Gastric parietal cells (autoimmune found in diabetes)
  • IBD at terminal end
  • Bowel cancer
47
Q

What can vit B12 deficiency lead to?

A

permanent neurological damage
bone marrow production damage