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GI tract > Gastric disease > Flashcards

Gastric disease Flashcards

1
Q

What is dyspepsia?

A
  • A complex of upper GI symptoms which are typically present for 4+ weeks
  • Includes upper abdominal discomfort, heartburn, acid reflux, nausea and/or vomiting
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2
Q

What are the symptoms of gastro-oesophageal reflux disease?

A
  • Heartburn
  • Acidic taste (potential dental erosion)
  • Cough and sore throat
  • Can be asymptomatic
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3
Q

What are the risk factors for GORD?

A
  • Anything that causes increased intra-abdominal pressure
  • Obesity
  • Pregnancy
  • Lower oesophageal sphincter dysfunction
  • Hiatus hernia
  • Delayed gastric emptying
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4
Q

What is a hiatus hernia?

A
  • Lower oesophageal sphincter herniates through diaphragm and ends up in thorax
  • Lose crura muscles acting as a sling
  • Not everyone with a hiatus hernia suffers from reflux
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5
Q

Outline the mechanism of the lower oesophageal sphincter

A
  • Muscular elements include intrinsic smooth muscles and diaphragm
  • Normally contracted - only relax when food passes into stomach
  • Right crus of diaphragm forms circular loop to close oesophagus off when pressure in stomach increases
  • Oesophagus enters stomach at an acute angle
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6
Q

What are the complications of GORD?

A
  • Oesophagitis
  • Ulceration
  • Haemorrhage
  • Strictures (can cause dysphagia)
  • Metaplastic changes
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7
Q

What is Barrett’s oesophagus?

A
  • Reversible metaplastic change
  • Stratified squamous epithelia of oesophagus changes to columnar epithelium of stomach
  • Increased risk of dysplasia and adenocarcinoma
  • Need regular endoscopies to check for further changes
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8
Q

What lifestyle management is given to someone with GORD?

A
  • Weight loss
  • Avoid trigger foods
  • Eat smaller meals
  • Don’t eat then sleep
  • Decrease alcohol and coffee consumption
  • Stop smoking
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9
Q

Which drugs might be prescribed for someone with GORD?

A
  • Proton pump inhibitors for symptom relief and healing of inflammation
  • H2 receptor antagonists
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10
Q

What is the last resort treatment of GORD?

A
  • Surgery - fundoplication
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11
Q

What is gastritis?

A
  • Inflammation of the stomach mucosa
  • Inflammatory cells such as neutrophils invade lamina propria
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12
Q

What are the symptoms of gastritis?

A
  • Pain
  • Nausea
  • Vomiting
  • Haemorrhage
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13
Q

What are the causes of acute gastritis?

A
  • NSAIDs
  • High alcohol consumption
  • Chemotherapy
  • Bile reflux
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14
Q

What are the causes of chronic gastritis?

A
  • Infection with H pylori
  • Autoimmune
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15
Q

What pathological changes occur with acute gastritis?

A
  • Epithelial damage
  • Some epithelial hyperplasia
  • Vasodilation - gives ‘angry looking’ appearance
  • Neutrophil response
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16
Q

What pathological changes occur with acute gastritis?

A
  • Lymphocyte response in lamina propria
  • Glandular atrophy of gastric glands
  • Fibrotic changes
  • Metaplastic changes
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17
Q

Why does autoimmune chronic gastritis lead to anaemia?

A
  • Antibodies to parietal cells
  • Atrophy of parietal cells
  • Decreased acid production and decreased intrinsic factor production
  • Decreased absorption of vitamin B12 in ileum
  • Leads to megaloblastic anaemia because vitamin B can’t be made in the body - it has to be absorbed
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18
Q

Why does death of parietal cells lead to gastritis?

A
  • Body of stomach atrophies
19
Q

What are the symptoms of chronic gastritis caused by an autoimmune condition?

A
  • Anaemia
  • Neurological symptoms
  • Anorexia (loss of appetite)
  • Glossitis
20
Q

Describe the properties of an H-pylori bacterium

A
  • Helix shape
  • Gram negative
  • Microaerophilic (needs only a little O2 - stomach has prefect level)
21
Q

How does H pylori infect people?

A
  • Faeco-oral
    -Oral-oral
  • Navigates + adheres to mucosa/epithelial lining of stomach
22
Q

What are some of the key features of H. pylori?

A
  • Flagellae
  • Chemotaxis allows bacterium to find areas of lower acidity in stomach
  • Adhesins allow bacteria to fix to gastric epithelia and resist peristalsis
23
Q

How does H. pylori produce ammonia?

A
  • H. pylori contain urease enzyme that converts urea + water to CO2 + ammonia
  • Ammonia de-acidifies local environment so bacteria can survive
  • Ammonia toxic to epithelial cells
  • Cells get damaged
24
Q

Why does H. pylori cause gastritis?

A
  • Produces ammonia
  • Produces mucinase - damages mucus layer
  • Produces protease and lipase that breakdown structure of stomach
  • Cytotoxin associated gene A
  • Produces a protein that is inserted into stomach epithelium
  • Generates a huge inflammatory response by stimulating interleukin B
25
Q

How does H pylori cause damage in the stomach antrum?

A
  • Antrum is where G cells are located
  • Causes over-activity of G cells
  • Increases gastrin production
  • Increases number of parietal cells
  • Increases acid production
  • Chyme leaving stomach is more acidic
  • Duodenum damaged
  • Epithelium of duodenum changes to gastric epithelium
  • Can lead to colonisation of duodenum
  • Ulceration of duodenum
26
Q

How does H pylori cause damage in the stomach body and/or fundus?

A
  • Atrophy of parietal cells
  • Precursor to dysplastic changes
  • Increases risks of stomach cancer
27
Q

What happens if H.pylori colonises the stomach antrum and body?

A
  • Asymptomatic infection
28
Q

How do we diagnose H. pylori?

A
  • Urea breath test
  • Patients ingest urea enriched with C13
  • If H. pylori present, this urea is broken down into CO2 and ammonia
  • C13 isotope is present in exhaled CO2
  • Also stool antigen test and endoscopy with biopsy
29
Q

How is H. pylori eradicated?

A
  • Proton pump inhibitor
  • And 2 antibiotics (e.g. clarithromycin and metronidazole)
  • Side effects include diarrhoea and nausea
  • Check after 7 days using urea breath test
  • Treat for up to 14 days
30
Q

What is peptic ulcer disease?

A
  • Defect in the gastric or duodenal mucosa that extends through the muscularis mucosa
31
Q

What are the common sites of peptic ulcer disease?

A
  • Lesser curve and antrum of stomach
  • Most commonly found in duodenum
32
Q

Compare gastric and duodenal ulcers

A

gastric: duodenal
- Incidence = 1:3
- Age = increased: up to 35 years
- Social class = low: irrelevant
- Blood group = A:O
- Acid levels = normal/low: normal/high
- H. pylori = ~70%: 95-100%

33
Q

Why is there increased incidence of duodenal ulcers with elevated acid levels?

A
  • Overwhelms ability of small intestine to neutralise chyme
34
Q

What are the defences of the stomach?

A
  • Mucus layer
  • Bicarbonate secretion
  • Mucosal blood flow
  • Prostaglandins
  • Epithelial renewal
35
Q

What are risk factors for peptic ulcer disease?

A
  • H. pylori
  • NSAIDs (decrease prostaglandin synthesis)
  • Smoking (contributes to relapse)
  • Massive physiological stress
36
Q

What is the difference between acute and chronic ulcers?

A
  • Acute ulcers develop as part of acute gastritis
  • Chronic ulcers occur at mucosal junctions
37
Q

Outline the morphology of peptic ulcer disease

A
  • Most are <2cm
  • Necrotic tissue found at base or ulcer
  • Muscularis externa is replaced by scar tissue
  • Ulceration can perforate wall of gut and cause peritonitis
  • Scar tissue can narrow stomach lumen if ulceration is repeated
  • Can lead to pyloric stenosis which causes extensive vomiting
38
Q

What happens if an ulcer erodes into a blood vessel?

A
  • Can erode into gastroduodenal artery
  • Stomach fills up with blood
  • Massive haematemesis
39
Q

What is a sign of a relatively slow upper GI bleed?

A
  • Malaena
  • Haem component of blood is oxidised as it passes through GI tract
40
Q

What are the symptoms of peptic ulcer disease?

A
  • Epigastric pain leading to back pain following meals
  • Pain at night (duodenal ulcers)
  • Haematemesis/Malaena
  • Early satiety
  • Weight loss
41
Q

How is peptic ulcer disease managed if it’s due to H. pylori?

A
  • Proton pump inhibitors
  • 2x antibiotics
  • Eradicate H. pylori to promote ulcer healing
42
Q

How is peptic ulcer disease managed if it’s not caused by H. pylori?

A
  • Stop exacerbating medications
43
Q

How do we treat active bleeding caused by peptic ulcer disease?

A
  • Adrenaline injections
  • Cautery
  • Possible clip application

GI tract (23 decks)

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