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Year 3 - primary care + medicine > Gastro > Flashcards

Gastro Flashcards

(60 cards)

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1
Q

What is GORD?

A

Where gastric acid from the stomach flows through the lower oesophageal sphincter, into the oesophagus, where it irritates the lining, hence causing symptoms.

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2
Q

What is the oesophagus more sensitive to stomach acid?

A
  • squamous epithelial lining
  • whereas stomach has columnar
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3
Q

What can trigger / exacerbate GORD?

A
  • greasy and spicy foods
  • tea and coffee
  • alcohol
  • NSAIDs
  • stress
  • smoking
  • obesity
  • hiatus hernia
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4
Q

How does GORD present?

A

Dyspepsia (non specific term for indigestion)
- heartburn
- acid regurgitation
- retrosternal or epigastric pain
- bloating
- nocturnal cough
- hoarse voice

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5
Q

What are red flag symptoms for upper GI cancer?

A
  • Dysphagia (difficulty swallowing) at any age
    Aged > 55 with GORD +
  • weight loss
  • upper abdo pain
  • reflux
  • treatment resistant dyspepsia
  • nausea and vomiting
  • Upper abdo mass on palpation
  • anaemia
  • thombocythaemia
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6
Q

What is a hiatus hernia?

A

Herniation of the stomach up through the diaphragm

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7
Q

How is GORD managed?

A
  • lifestyle changes - minimise triggers. Weight loss, avoid smokings, smaller meals.
  • review medications - e.g. stop NSAIDs
  • antacids can be used short term
  • PPIs
  • test for H. pylori and treat if + (needs 2 weeks prior without a PPI to be accurate)
  • surgery if severe - laparoscopic fundoplication
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8
Q

What is Helicobacter pylori?

A

Gram negative aerobic bacteria that can live in the stomach and cause damage to its lining

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9
Q

What damage can H. Pylori cause?

A
  • gastritis
  • ulceration
  • increased risk of stomach cancer
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10
Q

What investigations can be done for H. pylori?

A
  • stool antigen test
  • urea breath test
  • H. pylori antibody blood test
  • rapid urease test during endoscopy
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11
Q

How is H. pylori eradicated?

A

Triple therapy
- PPI
- 2x abx - normally amoxicillin + clarithromycin for 7 days.

( metronidazole if penicillin allergic)

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12
Q

What is Barrett’s oesophagus?

A

Metaplastic change of the lower oesophageal epithelial cells from squamous to columnar due to chronic acid reflux

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13
Q

What are the complications of Barrett’s oesophagus?

A
  • can develop into oesophageal adenocarcinoma
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14
Q

How is barrett’s oesophagus managed?

A
  • endoscopic monitoring
  • PPI
  • endoscopic ablation can be done
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15
Q

What is Zollinger-ellison syndrome?

A

Rare condition where duodenal or pancreatic tumours secrete excess gastrin (known as gastrinomas - often associated with MEN1) which then stimulated excess acid secretion - causing severe dyspepsia, peptic ulcers and diarrhea.

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16
Q

What are peptic ulcers?

A

ulceration of the mucosa of either the stomach (gastric) or proximal duodenum

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17
Q

Which type of peptic ulcers are the most common?

A

Duodenal

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18
Q

What are some risk factors for peptic ulcers?

A

Factors that disrupt the mucus barrier
- H. pylori infection
- NSAIDs

Factors that increase stomach acid
- stress
- alcohol
- caffeine
- smoking
- spicy foods

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19
Q

What medications increase the risk of bleeding from a peptic ulcer?

A
  • NSAIDs
  • Aspirin
  • Anticoags e.g. DOACs
  • steroids
  • SSRIs
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20
Q

How do peptic ulcers present?

A
  • epigastric pain
  • nausea and vomiting
  • dyspepsia
  • signs of upper GI bleeding - e.g. haematemesis, anaemia
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21
Q

How can you tell the difference between gastric and duodenal ulcers?

A

Eating tends to worsen the pain of gastric ulcers initially , whereas it improves duodenal ulcers initially followed by pain 2-3 hours later.

  • Also patients with gastric ulcer tend to be losing weight due to fear of pain on eating
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22
Q

How can peptic ulcers be diagnosed?

A

During endoscopy
- a H.pylori test can also be done as well as a biopsy

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23
Q

How are peptic ulcers managed?

A
  • stop NSAIDs / any contributing medications
  • treat H. pylori infection
  • PPI
  • endoscopies are often repeated at 4-8 weeks to ensure it heals
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24
Q

What are some complications of peptic ulcers?

A
  • bleeding
  • perforation
  • scarring and strictures can cause gastric outlet obstruction
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25
What are some causes of an upper GI bleed?
- peptic ulcers - mallory-weiss tear (tear in the oesophageal mucosa) - oesophageal varies ( secondary to portal hypertension in liver cirrhosis) - stomach caners
26
How does an upper GI bleed present?
- haematemesis - vomiting blood - coffee ground vomit - melaena ( black-tar like greasy stools containing digested blood) - may be haemodynamically unstable
27
When do mallory-weiss tears tend to occur?
- after heavy retching or vomiting E.g. binge drinking, bulimia, gastroenteritis or hyperemesis gravidarum
28
What scoring system is used to estimate the risk of an upper GI bleeds?
Glasgow-blatchford bleeding score
29
What does the glasgow-blatchford bleeding score do?
Estimates the risk of a patient having an upper GI bleed
30
What is the rockall score used fir?
Used after endoscopy to estimate the risk of rebleeding and mortality.
31
How can upper GI bleeds be managed?
- OGD done to diagnose and treat the source of bleeding - if variceal is suspected - give terlipressin + broad spec abx. Then on endoscopy band ligation can be done. - non variceal - can use clips, thermal coagulation etc.
32
What is IBS?
A functional disorder causing abdominal pain and intestinal symptoms.
33
What are the key symptoms of IBS?
- abdominal pain - diarrhoea or constipation (or may fluctuate) - bloating - worse after eating - improved by opening bowels - passing mucus Can cause mental health issues.
34
What can worsen the symptoms of IBS?
- anxiety - depression - stress - sleep disturbance - illness - medications - certain foods - caffeine - alcohol
35
What are some differentials for IBS?
- bowel cancer - IBD - coeliac disease - ovarian cancer - pancreatic cancer
36
How is IBS diagnosed?
- hx and examination - rule out other conditions ( all results should be normal in IBS) - FBC - inflammatory markers - coeliac serology (anti-TTG antibodies) - faecal calprotectin ( for IBD) - CA125 ( for ovarian cancer)
37
How is IBS managed?
Lifestyle advice - drinking enough fluids - regular small meals - adjust fibre intake - limit alcohol, caffiene + fatty foods - probiotic supplements may help - regular exercise - reduce stress Medications - for diarrhoea - loperamide - for constipation - bulk forming laxatives such as ispaghula husk - for cramps - antispasmodics - e.g. hyoscine butylbromide
38
What is coeliac disease?
An autoimmune condition that is triggered by eating gluten and can cause inflammation of the small intestine issues such as malabsorption.
39
What antibodies are related to coeliacs disease?
- Anti- tissue transglutaminase antibodies (anti TTG) - Anti-endomysial antibodies (anti-EMA)
40
What is the effect of coeliac disease on the small bowel?
Causes inflammation which leads to villous atrophy and crypt hypertrophy
41
What genes are associated with coeliacs disease?
HLA-DQ2 HLA-DQ8
42
How does coeliac disease present?
Often asymptomatic and goes undiagnosed initially Symptoms - failure to thrive in young children - diarrhoea - bloating - fatigue - weight loss - mouth ulcers - dermatitis herpetiformis (itchy, blistering rash typically on the abdomen) - anaemia may occur secondary to malabsorption of iron, B12 or folate
43
How is coeliac disease diagnosed?
Blood tests - Total IgA (as anti-TTG is IgA so would come back negative if total IgA is low) - anti-TTG ** patient must be eating gluten whilst being investigated** Endoscopy and jejunal/duodenal biopsy
44
What will be seen in a biopsy of someone with coeliac disease?
- crypt hyperplasia - villous atrophy
45
How is coeliacs disease managed?
Lifelong gluten free diet
46
What are complications of coeliacs if not managed?
- nutritional deficiencies - anaemia - osteoporosis - hyposplenism (+ immunosuppression) - ulcerative jejunitis - enteropathy associated T cell lymphoma (EATL) - non hodgkins lympoma - small bowel adenocarcinoma
47
What is alpha-1 antitrypsin deficiency?
A genetic condition caused by low levels of alpha-1-antitrypsin. This normally inhibits proteases - particularly neutrophil elastase which attacks liver and lung tissue.
48
What organs are mainly affected by alpha-1-antitrypsin deficiency and how?
- Lungs - COPD and bronchiectasis - Liver - dysfunction, fibrosis and cirrhosis
49
What is the inheritance pattern of alpha-1-antitrypsin deficiency?
Co-dominant pattern *disease severity results from the combination of both copies of the gene)
50
What gene causes alpha-1-antitrypsin deficiency?
SERPINA1 gene on chromosome 14
51
How is alpha-1-antitrypsin deficiency diagnosed?
- low serum alpha-1-antitrypsin - genetic testing - High-resolution CT thorax - pulmonary function tests - liver biopsy
52
What will liver biopsy show in alpha-1-antitrypsin deficiency?
Acid-Schiff positive staining globules in hepatocytes
53
How is alpha-1-antitrypsin deficiency managed?
- stop smoking - as accelerates emphysema - symptomatic management (e.g. of COPD) - organ transplant - monitor for complications (hepatocellular carcinoma) - screen family members
54
What is Wilson's disease?
Genetic condition where there is excessive accumulation of copper in the body tissues.
55
What is the inheritance pattern of Wilson's disease?
Autosomal recessive
56
What organs are commonly affected by Wilson's disease?
- Liver - Brain and neurological system
57
What are the features of Wilson's disease?
- Hepatic problems - chronic hepatitis and liver cirrhosis - Neuro - dysarthria (difficulty speaking), dystonia and parkinsonism - psych - ranges from mild depression to psychosis - Haemolytic anaemia - Renal tubular damage and acidosis - Osteopenia - Kayser-Fleischer rings
58
What is a sign found in Wilson's disease?
Kayser-Fleischer rings - deposition of copper in the cornea - brown circles around the iris
59
How is Wilson's disease diagnosed?
- serum caeruloplasmin ( protein that carries copper in the blood) = low - serum copper = low - 24 hr urine copper assay = high - liver biopsy = gold standard - genetic testing - brain MRI may show a double panda sign (in midbrain and pons)
60
How is Wilson's disease managed?
Copper chelation using - penicillamine - trientine Can also consider liver transplantation

Year 3 - primary care + medicine (20 decks)

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