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Year 3 - primary care + medicine > Gastro > Flashcards

Gastro Flashcards

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
Q

What are some causes of an upper GI bleed?

A
  • peptic ulcers
  • mallory-weiss tear (tear in the oesophageal mucosa)
  • oesophageal varies ( secondary to portal hypertension in liver cirrhosis)
  • stomach caners
26
Q

How does an upper GI bleed present?

A
  • haematemesis - vomiting blood
  • coffee ground vomit
  • melaena ( black-tar like greasy stools containing digested blood)
  • may be haemodynamically unstable
27
Q

When do mallory-weiss tears tend to occur?

A
  • after heavy retching or vomiting
    E.g. binge drinking, bulimia, gastroenteritis or hyperemesis gravidarum
28
Q

What scoring system is used to estimate the risk of an upper GI bleeds?

A

Glasgow-blatchford bleeding score

29
Q

What does the glasgow-blatchford bleeding score do?

A

Estimates the risk of a patient having an upper GI bleed

30
Q

What is the rockall score used fir?

A

Used after endoscopy to estimate the risk of rebleeding and mortality.

31
Q

How can upper GI bleeds be managed?

A
  • 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
Q

What is IBS?

A

A functional disorder causing abdominal pain and intestinal symptoms.

33
Q

What are the key symptoms of IBS?

A
  • abdominal pain
  • diarrhoea or constipation (or may fluctuate)
  • bloating
  • worse after eating
  • improved by opening bowels
  • passing mucus

Can cause mental health issues.

34
Q

What can worsen the symptoms of IBS?

A
  • anxiety
  • depression
  • stress
  • sleep disturbance
  • illness
  • medications
  • certain foods
  • caffeine
  • alcohol
35
Q

What are some differentials for IBS?

A
  • bowel cancer
  • IBD
  • coeliac disease
  • ovarian cancer
  • pancreatic cancer
36
Q

How is IBS diagnosed?

A
  • 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
Q

How is IBS managed?

A

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
Q

What is coeliac disease?

A

An autoimmune condition that is triggered by eating gluten and can cause inflammation of the small intestine issues such as malabsorption.

39
Q

What antibodies are related to coeliacs disease?

A
  • Anti- tissue transglutaminase antibodies (anti TTG)
  • Anti-endomysial antibodies (anti-EMA)
40
Q

What is the effect of coeliac disease on the small bowel?

A

Causes inflammation which leads to villous atrophy and crypt hypertrophy

41
Q

What genes are associated with coeliacs disease?

A

HLA-DQ2
HLA-DQ8

42
Q

How does coeliac disease present?

A

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
Q

How is coeliac disease diagnosed?

A

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
Q

What will be seen in a biopsy of someone with coeliac disease?

A
  • crypt hyperplasia
  • villous atrophy
45
Q

How is coeliacs disease managed?

A

Lifelong gluten free diet

46
Q

What are complications of coeliacs if not managed?

A
  • nutritional deficiencies
  • anaemia
  • osteoporosis
  • hyposplenism (+ immunosuppression)
  • ulcerative jejunitis
  • enteropathy associated T cell lymphoma (EATL)
  • non hodgkins lympoma
  • small bowel adenocarcinoma
47
Q

What is alpha-1 antitrypsin deficiency?

A

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
Q

What organs are mainly affected by alpha-1-antitrypsin deficiency and how?

A
  • Lungs - COPD and bronchiectasis
  • Liver - dysfunction, fibrosis and cirrhosis
49
Q

What is the inheritance pattern of alpha-1-antitrypsin deficiency?

A

Co-dominant pattern *disease severity results from the combination of both copies of the gene)

50
Q

What gene causes alpha-1-antitrypsin deficiency?

A

SERPINA1 gene on chromosome 14

51
Q

How is alpha-1-antitrypsin deficiency diagnosed?

A
  • low serum alpha-1-antitrypsin
  • genetic testing
  • High-resolution CT thorax
  • pulmonary function tests
  • liver biopsy
52
Q

What will liver biopsy show in alpha-1-antitrypsin deficiency?

A

Acid-Schiff positive staining globules in hepatocytes

53
Q

How is alpha-1-antitrypsin deficiency managed?

A
  • stop smoking - as accelerates emphysema
  • symptomatic management (e.g. of COPD)
  • organ transplant
  • monitor for complications (hepatocellular carcinoma)
  • screen family members
54
Q

What is Wilson’s disease?

A

Genetic condition where there is excessive accumulation of copper in the body tissues.

55
Q

What is the inheritance pattern of Wilson’s disease?

A

Autosomal recessive

56
Q

What organs are commonly affected by Wilson’s disease?

A
  • Liver
  • Brain and neurological system
57
Q

What are the features of Wilson’s disease?

A
  • 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
Q

What is a sign found in Wilson’s disease?

A

Kayser-Fleischer rings - deposition of copper in the cornea - brown circles around the iris

59
Q

How is Wilson’s disease diagnosed?

A
  • 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
Q

How is Wilson’s disease managed?

A

Copper chelation using
- penicillamine
- trientine

Can also consider liver transplantation

Year 3 - primary care + medicine (20 decks)

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