GP-gastro Flashcards

1
Q
  • GORD definition
A

Gastro-oesophageal reflux disease (GORD) is where acid from the stomach flows through the lower oesophageal sphincter and into the oesophagus, where it irritates the lining and causes symptoms.

The oesophagus has a squamous epithelial lining that makes it more sensitive to the effects of stomach acid. The stomach has a columnar epithelial lining that is more protected against stomach acid.

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1
Q

GORD causes and triggers

A

Certain factors can exacerbate or worsen the symptoms of GORD:

Greasy and spicy foods
Coffee and tea
Alcohol
Non-steroidal anti-inflammatory drugs
Stress
Smoking
Obesity
Hiatus hernia

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2
Q

GORD presentation

A

Dyspepsia is a non-specific term used to describe indigestion. It covers the symptoms of GORD:

Heartburn
Acid regurgitation
Retrosternal or epigastric pain
Bloating
Nocturnal cough
Hoarse voice

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3
Q

Key red flags to screen for in GORD and nice guidelines for cancer referral

A
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4
Q
  • Investigations in GORD
A

Indications for upper GI endoscopy:
age > 55 years
symptoms > 4 weeks or persistent symptoms despite treatment
dysphagia
relapsing symptoms
weight loss

If endoscopy is negative consider 24-hr oesophageal pH monitoring (the gold standard test for diagnosis)

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5
Q

Indications for upper GI endoscopy

A

age > 55 years
symptoms > 4 weeks or persistent symptoms despite treatment
dysphagia
relapsing symptoms
weight loss

extras:
anemia
Melaena/haematemesis

Proton pump inhibitors should be stopped 2 weeks before an upper GI endoscopy

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6
Q

what is an OGD?
it can be used to assess for:

A

An oesophago-gastro-duodenoscopy (OGD) involves inserting a camera through the mouth down to the oesophagus, stomach and duodenum. It can be used to assess for:

Gastritis
Peptic ulcers
Upper gastrointestinal bleeding
Oesophageal varices (in liver cirrhosis)
Barretts oesophagus
Oesophageal stricture
Malignancy of the oesophagus or stomach

Patients with evidence of upper gastrointestinal bleeding (e.g., melaena or coffee ground vomiting) need admission and urgent endoscopy.

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7
Q

GORD management

A
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8
Q

We offer a test for H. pylori to:
how can we test for H.pylori?

A
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9
Q

The H. pylori eradication regime involves

A

triple therapy with a proton pump inhibitor (e.g., omeprazole) plus two antibiotics (e.g., amoxicillin and clarithromycin) for 7 days. Routine re-testing is not necessary after treatment.

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10
Q
  • Key important complication of GORD
A

Barrett’s oesophagus

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11
Q

Barret’s oesophagus definition, pathophysiology and treatment

A
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12
Q

What is Zollinger-Ellison syndrome

A
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13
Q

Coeliac disease definition and associated conditions

A

Coeliac disease is an autoimmune condition triggered by eating gluten. It can develop at any age and is thought to be caused by genetic and environmental factors. There is a link with other autoimmune conditions, particularly type 1 diabetes and thyroid disease.

TOM TIP: Remember for your exams that we test all new cases of type 1 diabetes and autoimmune thyroid disease for coeliac disease, even if they do not have symptoms.

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14
Q

pathophysiology of coeliac disease

A

It is associated with certain human leukocyte antigen (HLA) genotypes:

HLA-DQ2
HLA-DQ8

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15
Q

There are three antibodies related to coeliacs:

A
  • Anti-tissue transglutaminase antibodies (anti-TTG)
  • Anti-endomysial antibodies (anti-EMA)
  • Anti-deamidated gliadin peptide antibodies (anti-DGP)
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16
Q

Coeliac disease affects which part of the bowel the most? What is the name of the process it causes?

A

Inflammation affects the small bowel, particularly the jejunum. The surface of the small intestine is covered in projections called villi, which increase the surface area and help with nutrient absorption. Coeliac disease causes atrophy of the intestinal villi, resulting in malabsorption.

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17
Q

Coeliac disease is associated with certain human leukocyte antigen (HLA) genotypes:

A

HLA-DQ2
HLA-DQ8

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18
Q

Presentation of coeliac

A
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19
Q

Diagnosis and investigations in coeliac

A
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20
Q

biopsy findings in coeliac

A
  • crypt hyperplasia
  • villous atrophy
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21
Q

first line blood tests in coeliac disease

A
  • Total immunoglobulin A levels (to exclude IgA deficiency)
  • Anti-tissue transglutaminase antibodies (anti-TTG)
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22
Q

management of coeliac disease

A

A lifelong gluten-free diet should completely resolve the symptoms. Dietician input may be helpful. Relapse will occur upon consuming gluten. Coeliac antibodies may help monitor the disease.

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23
Q

complications of coeliac disease

A

If someone with coeliac disease continues eating gluten, even in tiny amounts, it can lead to:

  • Nutritional deficiencies
  • Anaemia
  • Osteoporosis
  • Hyposplenism (with immunodeficiency, particularly to encapsulated bacteria such as Streptococcus pneumoniae)
  • Ulcerative jejunitis
  • Enteropathy-associated T-cell lymphoma (EATL)
  • Non-Hodgkin lymphoma
  • Small bowel adenocarcinoma
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24
Q

diverticulum vs diverticulosis vs diverticulitis

A
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25
Q

pathophysiology of diverticular disease

A

sigmoid colon most affected

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26
Q
  • The most commonly affected section of the bowel in diverticular disease is
A

sigmoid colon
However, it can affect the entire large intestine in some patients. Small bowel diverticula are also possible but much less common.

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27
Q

risk factors for diverticular disease

A

increased age.
Low fibre diets,
obesity and
the use of NSAIDs are risk factors
The use of NSAIDs increases the risk of diverticular haemorrhage.

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28
Q

Investigations/diagnosis of diverticular disease
severity classification name and components

A
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29
Q

Symptoms of diverticular disease

A

Constipation
Left lower quadrant abdominal pain
Possible rectal bleeding
Physical examination may be normal or may demonstrate tenderness in the left lower quadrant on digital rectal examination.

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30
Q

Management of diverticular disease

A

Management is with increased fibre in the diet and bulk-forming laxatives (e.g.,** ispaghula husk**). Stimulant laxatives (e.g., Senna) should be avoided. Surgery to remove the affected area may be required where there are significant symptoms.

31
Q

Complications of diverticular disease and their management

A

Diverticulitis
Haemorrhage
Development of fistula
Perforation and faecal peritonitis
Perforation and development of abscess
Development of diverticular phlegmon

32
Q

Signs and symptoms of diverticulitis

A

Palpable abdominal mass (if an abscess has formed)
Raised inflammatory markers (e.g., CRP) and white blood cells
Diffuse abdominal tenderness suggestive of perforation or generalised peritonitis.

33
Q

Investigations for diverticulitis

A
34
Q

management of diverticulitis

A
35
Q

Complications for diverticulitis

A

Perforation
Peritonitis
Peridiverticular abscess
Large haemorrhage requiring blood transfusions
Fistula (e.g., between the colon and the bladder or vagina)
Ileus / obstruction

36
Q

Differentials to diverticular disease

A
37
Q

IBD definition, causes and typical age of presentation

A

Inflammatory bowel disease involves recurrent episodes of inflammation in the gastrointestinal tract. The two main types are ulcerative colitis and Crohn’s disease. They are associated with periods of exacerbation and remission.

Inflammatory bowel disease is thought to be caused by a combination of factors related to genetics, environment and the gut microbiome. The typical patient presents in their 20s.

38
Q

The general presenting features of inflammatory bowel disease are:

A

Diarrhoea
Abdominal pain
Rectal bleeding
Fatigue
Weight loss

39
Q

Differentiating features of Crohn’s

A
40
Q

Differentiating features of ulcerative colitis

A
41
Q

Many associated conditions can occur in patients with inflammatory bowel disease:

A
42
Q

‘extra-intestinal’ features of inflammatory bowel disease are

A
43
Q

Investigations in IBD

A
44
Q

General presentation for UC

A
45
Q

Investigation findings in UC

A
46
Q

General Chron’s presentation

A
47
Q

Chron’s pathology

A
48
Q

UC management

A
49
Q

Chron’s management

A
50
Q

Chron’s investigations results

A

raised inflammatory markers
increased faecal calprotectin
anaemia
low vitamin B12 and vitamin D

Bloods
C-reactive protein correlates well with disease activity

Endoscopy
colonoscopy is the investigation of choice
features suggest of Crohn’s include deep ulcers, skip lesions

Histology
inflammation in all layers from mucosa to serosa
goblet cells
granulomas

Small bowel enema
high sensitivity and specificity for examination of the terminal ileum
strictures: ‘Kantor’s string sign’
proximal bowel dilation
‘rose thorn’ ulcers
fistulae

51
Q

Flares of ulcerative colitis are usually classified as either mild, moderate or severe:

A
52
Q

Most ulcerative colitis flares occur without an identifiable trigger. However, a number of factors are often linked:

A

stress
medications
NSAIDs
antibiotics
cessation of smoking

53
Q

Cronh’s complications

A
  • fistulae, abscess and strictures
  • small bowel cancer (standard incidence ratio = 40)
  • colorectal cancer (standard incidence ratio = 2, i.e. less than the risk associated with ulcerative colitis)
  • osteoporosis
54
Q

Inducing remission in UC

A
55
Q

maintaning remission in UC

A
56
Q

General points and inducing remission in Cronh’s

A
57
Q

Maintaining remission in Crohn’s

A
  • stopping smoking is a priority
  • azathioprine or mercaptopurine is used first-line to maintain remission

+TPMT activity should be assessed before starting
* methotrexate is used second-line

58
Q

Surgical management in Crohn’s

A
59
Q

IBS cause, epidemiology

A
60
Q

IBS symptoms

A
61
Q

Symptoms of IBS can be triggered or worsened by:

A

Anxiety
Depression
Stress
Sleep disturbance
Illness
Medications
Certain foods
Caffeine
Alcohol

62
Q

Differentials to IBS

A

Bowel cancer
Inflammatory bowel disease
Coeliac disease
Ovarian cancer (often presents with vague symptoms, particularly bloating in women over 50 years)
Pancreatic cancer

63
Q

Investigations can be used to assess for underlying differentials (normal in IBS):

A
  • Full blood count for anaemia
  • Inflammatory markers (e.g., ESR and CRP)
  • Coeliac serology (e.g., anti-TTG antibodies)
  • Faecal calprotectin for inflammatory bowel disease
  • CA125 for ovarian cancer
64
Q

Red flags to screen for in IBS

A

rectal bleeding
unexplained/unintentional weight loss
family history of bowel or ovarian cancer
onset after 60 years of age

65
Q

IBS management

A
66
Q

IBS lifestyle management

A
  • Drinking enough fluids
  • Regular small meals
  • Adjusting fibre intake according to symptoms (more fibre if predominantly constipated, less with diarrhoea/bloating)
  • Limit caffeine, alcohol and fatty foods
  • Low FODMAP diet, guided by a dietician
  • Probiotic supplements may be considered over-the-counter (discontinuing after 12 weeks if there is no benefit)
  • Reduce stress where possible
  • Regular exercise
67
Q

First-line medications for IBS

A

First-line medications depend on the symptoms:

Loperamide for diarrhoea
Bulk-forming laxatives (e.g., ispaghula husk) for constipation (lactulose can cause bloating and is avoided)
Antispasmodics for cramps (e.g., mebeverine, alverine, hyoscine butylbromide or peppermint oil)

There is only weak evidence for the benefit of using antispasmodic medications, and they may cause side effects.

Linaclotide is a specialist secretory drug for constipation in IBS when first-line laxatives are inadequate.

68
Q

Other management options for IBS include where symptoms remain uncontrolled:

A

Low-dose tricyclic antidepressants (e.g., amitriptyline)
SSRI antidepressants
Cognitive behavioural therapy (CBT)
Specialist referral for further management

69
Q

investigation of choice for suspected perianal fistulae in patients with Crohn’s

A

MRI is the investigation of choice for suspected perianal fistulae in patients with Crohn’s

70
Q

first line medication for diarrhea in IBS

A

Loperamide

71
Q

First line medication for constipation in IBS

A

laxatives but avoid lactulose

For patients with constipation who are not responding to conventional laxatives linaclotide may be considered, if:
* optimal or maximum tolerated doses of previous laxatives from different classes have not helped and
* they have had constipation for at least 12 months

72
Q

In a mild-moderate flare of distal ulcerative colitis, the first-line treatment is

A

In a mild-moderate flare of distal ulcerative colitis, the first-line treatment is topical (rectal) aminosalicylates

73
Q

What is generally used to induce remission of Crohn’s disease

A

Glucocorticoids (oral, topical or intravenous) are generally used to induce remission of Crohn’s disease

74
Q

If a mild-moderate flare of distal ulcerative colitis doesn’t respond to topical (rectal) aminosalicylates then…

A

If a mild-moderate flare of distal ulcerative colitis doesn’t respond to topical (rectal) aminosalicylates then oral aminosalicylates should be added

e.g.on topical mesalazine already –> add oral mesalazine

75
Q

Coeliac disease increases the risk of which type of cancer?

A

Coeliac disease increases the risk of developing enteropathy-associated T cell lymphoma in areas of the small intestine afflicted by the disease’s intense inflammation