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Gastrointestinal > Gastric Disease > Flashcards

Gastric Disease Flashcards

1
Q

What is dyspepsia?

A
  • A complex of upper GI tract symptoms which are present for 4+ weeks
  • including upper abdominal discomfort, heartburn, acid reflux, N+V
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2
Q

Symptoms of gastro-oesophageal reflux disease

A
  • heart burn
  • acidic taste > dental erosion
  • cough
  • asymptomatic
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3
Q

What are the risk factors of gastro-oesophageal reflux disease?

A

increased intra abdominal pressure

  • obesity
  • pregnancy
  • lower oesophageal dysfunction
  • hiatus hernia
  • delayed gastric emptying
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4
Q

What is a hiatus hernia?

A

Lower oesophageal sphincter herniates through diaphragm into thorax

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5
Q

What are the complications of gastric oesophageal reflux disease?

A
  • oesophagitis
  • ulceration
  • haemorrhage > anaemia
  • strictures > dysphagia
  • metaplastic changes > Barrett’s oesophagus
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6
Q

What is gastric oesophageal reflux disease?

A

Reflux of stomach contents into the oesophagus

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7
Q

What is Barrett’s oesophagus?

A
  • Reversible change of stratified squamous epithelia into gastric columnar
  • due to repeated exposure of gastric contents
    .
  • risk of adenocarcinoma due to increased risk of dysplasia
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8
Q

Lifestyle management of gastric oesophageal reflux disease

A
  • weight loss
  • avoid trigger foods
  • eat smaller meals
  • don’t eat right before sleep
  • decrease alcohol, caffeine (+smoking)
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9
Q

Drug management of gastric oesophageal reflux disease

A
  • proton pump inhibitors > symptom relief + healing inflammation
  • H2 receptor antagonists
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10
Q

Surgical management of gastric oesophageal reflux disease

A
  • Fundoplication
  • fundus of stomach wrapped around oesophagus
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11
Q

What is gastritis?

A
  • Inflammation of stomach mucosa
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12
Q

Symptoms of gastritis

A

Pain
Nausea
Vomiting
Haemorrhage

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13
Q

Causes of acute gastritis

A

NSAIDs
Excessive alcohol
Chemotherapy
Bile reflux

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14
Q

Causes of chronic gastritis

A

Infection of H pylori
Autoimmune

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15
Q

Changes in acute gastritis

A
  • epithelial damage
  • epithelial hyperplasia
  • vasodilation ’angry looking’
  • neutrophil response
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16
Q

Changes in chronic gastritis

A
  • lymphocyte response
  • glandular atrophy
  • fibrotic changes
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17
Q

Outline autoimmune chronic gastritis

A
  • antibodies damage parietal cells
  • decreased acid production
  • decreased intrinsic factor > reduced B12 absorption in terminal ileum
  • atrophy of stomach body > gastritis
18
Q

Symptoms of autoimmune gastritis

A
  • Megaloblastic anaemia
  • neurological symptoms
  • anorexia + loss of appetite
  • glossitis
19
Q

Why does Helicobacter pylori cause gastritis?

A
  • H pylori produces ammonia > damage to cells
  • cytotoxin associated gene A > expresses protein into stomach epithelia > stimulates interleukin 8 > inflammation > ^ stomach cancer risk
  • vacuolating toxin A: protein which increases paracellular permeability + toxin
  • secretes mucinases > damages mucus layer
20
Q

Describe Helicobacter pylori

A
  • gram negative bacteria
  • helix shape
  • microaerophilic > needs some O2
  • faecal-oral / oral-oral
    features:
  • produces urease > produces ammonia from urea
  • flagellae for movement
  • chemotaxis to find area of lower acididty
  • adhesions > adhere to gastric epithelium > resists peristalsis
21
Q

Consequence of H pylori in stomach antrum

A
  • stimulates G cells to release gastrin
  • ^ number of parietal cells + acid secretion
  • ^ pH of chyme > damages duodenum > ulceration
22
Q

Consequences of H pylori in stomach body or fundus

A
  • atrophy of parietal cells
  • increases risk of stomach cancer
23
Q

Diagnosis of H pylori

A
  • urease breath test
  • stool antigen test
  • endoscopy with biopsy
24
Q

Outline urease breath test for H pylori

A
  • patient injects urea enriched with carbon 13
  • if H pylori is present, urea > CO2 + ammonia
  • C13 isotope can be detected in CO2 on expiration
25
Q

Treatment for H pylori

A

Proton pump inhibitor + 2 antibiotics
e.g. Lansoprazole + clarithromycin + metronidazole/amoxicillin

  • check if successful with urease breath test
26
Q

What is peptic ulcer disease?

A

Defect in the gastric or duodenal mucosa that extends through the musclaris mucosa

27
Q

Where does peptic ulcer disease occur in the stomach?

A

Lesser curve (most common)
Antrum

28
Q

Compare gastric vs duodenal ulcers:
- incidence
- age
- social class
- blood group
- acid levels
- H pylori

A

Gastric
- incidence: v
- age: increases with age
- social class: higher in lower
- blood group: A
- acid levels: normal/low
- H pylori: 70%

Duodenal

  • incidence: x3 as common as gastric
  • age: increases with age up to 35
  • social class: X
  • blood group: O
  • acid levels: normal/high
  • H pylori: almost 100%
29
Q

Risk factors for peptic ulcer disease

A
  • H pylori
  • NSAIDS > decrease prostaglandin synthesis
  • smoking > contributes to relapse of ulcer
  • massive physiological stress
30
Q

Where do chronic ulcers normally occur?

A

Mucosal junctions

31
Q

What is malaena?

A
  • Black stool due to slow upper GI tract bleed
  • Haem component is oxidised
32
Q

Symptoms of peptic ulcer disease

A
  • epigastric pain: burning/gnawing pain
  • pain at night
  • haematemesis
  • malaena
  • early satiety due to scar tissue
  • weight loss
33
Q

What is haematemesis?

A

Vomiting blood

34
Q

Management of peptic ulcer disease with no active bleeding

A

H pylori present
- eradicate H pylori > proton pump inhibitor + 2 antibiotics

H pylori absent
- stop NSAIDs

35
Q

Management of peptic ulcer disease with active bleeding

A
  • adrenaline injection
  • cauterisation
  • test for H pylori after stopping bleeding
36
Q

Where are peptic ulcers most likely to occur?

A

Duodenum

37
Q

What blood vessel can be damaged by peptic ulcer disease and cause internal bleeding?

A

Gastroduodenal artery

38
Q

What part of the stomach is most prone to ulceration?

A

Lesser curve

39
Q

How does H pylori produce ammonia?

A
  • produces urease
    .
  • catalyses urea +CO2 > ammonia + CO2
40
Q

How does H pylori resists peristalsis?

A

Forms adhesions to gastric epithelium

Gastrointestinal (28 decks)

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