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GI > s4. gastric diseases > Flashcards

s4. gastric diseases Flashcards

1
Q

what is dyspepsia

A

a complex of upper GI tract symptoms which are present for 4 or more weeks
- including upper abdominal discomfort, heartburn, acid reflux, nausea/ vom

e.g. GORD, gastritis, PUD

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2
Q

symptoms of GORD (Gastro-oesophageal reflux disease)

A

heart burn/ chest pain
acidic taste
cough/ sore throat
asymptomatic

reflux of contents into oesophagus

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3
Q

risk factors for GORD

A 
anything increasing intra abdominal pressure e.g. 
-obesity
-pregnancy
-lower oesophageal 
sphincter(LOS) dysfunction
-hiatus hernia
-delayed gastric emptying
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4
Q

what is hiatus hernia

A

when LOS herniates through diaphragm into thorax> loses mechanisms like the crural muscles acting as a sling around it > distorted anatomy therefore less useful as a sphincter.

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5
Q

describe the mechanism of LOS

A

intrinsic muscles > help contract and close
only relaxes when detects food coming down oesophagus

  • muscular element of diaphragm - oesophagus pierces through so D muscle is kinda wrapped around oesophagus> right crus > pulls tighter when pressure increases
  • acute angle that oesophagus joins stomach
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6
Q

complications of GORD

A

Oesophagitis- irritation

ulcerations -deeper erosion through muscularis mucosa

bleeding / haemorrhage > anaemia

fibrous strictures> make it hard to swallow=dysphagia
(scar tissue in oesophag)

Barrett’s oesophagus

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7
Q

what is Barrett’s oesophagus

problem?

A

metaplastic change in the normal epithelia in lower oesophagus (stratified squamous) into gastric columnar epithelia
> repeated exposure of stomach contents causes adaptive change
> reversible

problem- can become dysplastic. risk of oesophageal cancer is higher
adenocarinoma>glandular cancer in oesophagus.

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8
Q

lifestyle management of GORD?

A
  • weight loss to dec obesity
  • avoid trigger foods
  • eat smaller meals
  • don’t eat them sleep
  • sit up in bed
  • reduce alcohol and caffeine
  • stop smoking (less evidence)
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9
Q

drug treatment of GORD

A

proton pump inhibitors
> provide relief from symptoms
> heal the inflammation

H2 receptor antagonists (blockers) > added if PPI not effective

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10
Q

surgical intervention of GORD name and describe

A

fundoplication > funds of stomach wrapped round lower oesophagus to help with sphincter mechanism

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11
Q

what is gastritis?

symptoms?

A

inflammation of stomach mucosa

symptoms:
pain 
nausaea
vomiting
haemorrhage

endoscopic appearance- angry and inflamed

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12
Q

acute vs chronic gastritis causes

A

acute

  • heavy use of NSAIDs
  • alcohol
  • chaemotherapy
  • bile reflux

chronic

  • H pylori bacteria
  • autoimmune

acute can go onto be chronic

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13
Q

what is bile reflux

A

bile delivered to duodenum usually but if it goes back into stomach through pyloric sphincter , causes chemical injury to stomach

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14
Q

pathological changes seen in acute gastritis

A
  • epithelial damage
  • epithelial hyperplasia
  • vasodilation ‘angry looking’
  • neutrophil response
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15
Q

pathological changes in chronic gastritis/ longlasting stimulus

A
  • lymphocyte/plasma cells found in lamina propria
  • glandular atrophy
  • fibrosis of lamina propria
  • metaplastic changes
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16
Q

describe autoimmune chronic gastritis

A 
antibodies to parietal cells
>lose parietal cells
> dec acid production
> dec intrinsic factor
> dec absorption of B12

-atrophy of body of stomach> renders defence system less effective

17
Q

where is B12 absorbed with intrinsic factor

A

ileum

18
Q

complications of AUTOimmune chronic gastritis

A
  • megaloblastic anaemia (lack of B12 disturbs DNA synthesis)
  • neurological symptoms
  • anorexia (loss of appetite)
  • glossitis = inflammation of tongue
19
Q

describe Helicobacter Pylori bacteria

A
  • helix shape
  • gram negative
  • microaerophilic (needs some o2 but not lots> stomach ideal condition)
  • enters GI tract vua faeco oral or oral oral route.
20
Q

what are the important features of Helicobacter Pylori and how do these aid its survival?

A
  • flagella > can move and advance
  • chemotaxis > find areas of lower acidity in stomach (e.g. surface of epithelia under mucosal layer)
  • adhesins> adhere to epithelial lining so aren’t washed away can resist peristalsis
  • own urease enzyme > converts urea into CO2 and NH4
    > de-acidifyies outer membrane creating an env to thrive and survive
21
Q

how does Helicobacter pylori cause gastritis?

A
  • produced NH4> damage stomach epithelia
  • produce cytotoxin associated gene A (CAG A) causes inflammatory response IL8 of stomach epithelia > inc stomach cancer risk

-produce Vacuolating toxin A (Vac A)> inc paracellular permeability
>toxic to stomach epithelial cells

22
Q

compare the presence of H pylori in antrum of stomach vs in body of stomach

A

antrum:
- overactivity of gastrin > produce more acid
> makes chyme more acidic. damage duodenum. change in duodenum epithelial cells > colonisation of H pylori in duodenum > ulcers

body: /fundus
cause atrophy and inc cancer risk

*when in both places usually asymptomatic

23
Q

what investigations are used to determine diagnosis of Helicobacter pylori?

A

Urease breath test-
Ingest C13 isotope of gastric urea> if H. P present, broken down into NH4 and CO2> C13 isotope detected when exhale.

Stool antigen test

endoscopy with biopsy

24
Q

how do we eradicate helicobacter pylori colony?

A

drugs:
proton pump inhibitor AND 2x Abx (usually Clarithromycin and Metronidazole)

side effects: diarrhoea, nausea

7 days
> check success with urease breath test

25
Q

what is peptic ulcer disease?

A

defect in the gastric or duodenal mucosa that extends through the muscular mucosa

26
Q

common sites of peptic ulcer

A

First part of duodenum
lesser curve of stomach

  • can occur anywhere in stomach tho
27
Q

describe the layers beyond epithelia (that ulceration could pass through)

A 
epithelia
lamina propria
muscular mucosa
sub mucosa
muscular externa
28
Q

compare gastric and duodenal ulcers

A 
gastric:
less common 1:3 ratio
incidence increases with age (only up until 35 with duodenal)
social class bias (none with duo)
blood group A
normal/low acid levels

duodenal
blood group O
normal/high acid levels
almost 100% due to Helicobacter pylori

29
Q

how do NSAIDS affect stomach defences?

A

DECREASE prostaglandins so less stimulation of blood flow

30
Q

risk factors for peptic ulcer disease

A
  • H. Pylori
  • NSAIDS
  • smoking > contributes to relapse of ulcer
  • massive physiological stress e.g. extensive burns
31
Q

difference between acute and chronic ulcers

A

acute
- develop as part of acute gastritis
> transient. healing.

chronic
- occur at mucosal junctions e.g. where Antrim meets body/ small int.

32
Q

implications of ulceration through muscular externae

A

muscularis externae replaced by scar tissue
> can narrow stomach lumen (pyloric stenosis)
> excessive vomitting

perforate gut wall and cause leakage into peritoneal cavity > peritonitis
/ erosion into adjacent structures e.g. liver/ pancreas

33
Q

complications if duodenal ulcer erodes posteriorly?

A

erosion into blood vessels - Gastroduodenal artery or splenic artery
- stomach/duodenum fill with blood
> haematemesis (vom blood)
> melana (black tarry stools)

34
Q

what is melana

A

indicative of slow upper GI bleed
haem component oxidised when pass through GI tract
> produce black tarry stools

35
Q

symptoms of peptic ulcer disease PUD

A
  • Epigastric pain, back pain > following meals
  • pain at night > duodenal ulcers
  • haematemesis
  • melana
  • early satiety > from scar tissue. can’t expand as much so get full quicker
  • weight loss
36
Q

how does pain present differently following a meal with duodenal and gastric ulcers?

A

duodenal:
food initially makes it better as LOS contracts
> transiently
> pain when chyme leaves

gastric
food makes it immediately worse

37
Q

management of PUD when no active bleeding

A
  • investigate H. pylori presence
  • eradicate H. pylori via PPI, 2x abx (usually Clarithromycin and Metronidazole)
    > promotes ulcer healing

if no H. pylori > stop taking exacerbating medications e.g. NSAIDs

38
Q

management of PUD when ACTIVE bleeding

A

endoscopic treatments
- adrenaline injected at base of ulcer and cautery

if perforated > open surgery

GI (14 decks)

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