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BAMS Bds2 > GI Medicine > Flashcards

GI Medicine Flashcards

1
Q

Upper GI disease

A

-Gastro-Oesophageal Reflux Disease (GORD)
-Peptic Ulcer Disease (PUD)

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2
Q

What are the components of the Upper GI tract?

A

Mouth
Pharynx
Oesophagus
Stomach
Small intestine (duodenum)

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3
Q

Function of GI tract

A

Ingestion of food
Digestion of food
Nutrient absorption
Anal canal

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4
Q

What are the components of the Lower GI tract?

A

Small intestine (jejunum, ileum)
Colon (caecum, ascending, transverse, descending, sigmoid)
Rectum
Anus

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5
Q

Which parts of the GI tract are involved in the ingestion of food?

A

Mouth and pharynx.

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6
Q

What components aid in the digestion of food in the GI tract?

A

Teeth, saliva, stomach acid, stomach enzymes, bile, and pancreatic enzymes.

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7
Q

Where does nutrient absorption occur in the GI tract?

A

Small intestine and colon.

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8
Q

What part of the GI tract is responsible for excretion of waste products?

A

Anal canal.

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9
Q

What are the four layers of the GI tract?

A

Mucosa, submucosa, muscularis externa, and adventitia/serosa.

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10
Q

What is the fibromuscular tube in the GI tract that transports food from the pharynx to the stomach?

A

Oesophagus

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11
Q

What process moves food through the oesophagus to the stomach?

A

Peristalsis

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12
Q

What is the function of sphincters in the GI tract?

A

To prevent the reflux of the food bolus and stomach contents.

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13
Q

What are the two types of digestion that occur in the stomach?

A

Chemical digestion (HCl acid, pepsin, lipase) and mechanical digestion.

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14
Q

What substances are absorbed by the stomach?

A

Vitamin B12 (via parietal cells), alcohol, and water.

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15
Q

Which endocrine hormones are secreted by the stomach, and what are their functions?

A

-Gastrin (stimulates HCl secretion)
-CCK (stimulates the gall bladder).

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16
Q

What do chief cells in the stomach produce?

A

Pepsin

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17
Q

What do parietal cells in the stomach produce?

A

HCl and intrinsic factor

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18
Q

What is the function of mucus cells in the stomach?

A

Mucus

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19
Q

What does GORD stand for?

A

Gastro-oesophageal reflux disease

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20
Q

What percentage of the population is affected by GORD?

A

10-30%

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21
Q

What happens in GORD?

A

Acid and stomach contents flow through the lower oesophageal sphincter (LOS) into the oesophagus.

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22
Q

What are the causes of GORD?

A

Laxity of LOS)
Increased gastric pressure
Delayed gastric emptying

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23
Q

What are the consequences of gastric acid irritating the oesophageal mucosa?

A

-Symptoms of irritation
-Metaplasia of oesophageal epithelium (Barrett’s oesophagus, a precancerous condition)

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24
Q

What are the common symptoms/signs of GORD?

A

Dyspepsia (indigestion or “heartburn”)
Epigastric pain
Bloating
Nausea/vomiting
Vocal hoarseness
Dental erosion

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25
Q

What are the risk factors for GORD?

A

Stress and anxiety
Smoking
Alcohol consumption
Trigger foods (e.g., coffee, chocolate, fatty meals)
Obesity
NSAIDs (non-steroidal anti-inflammatory drugs)
Pregnancy
Lying flat after a large meal

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26
Q

What are the management strategies for upper GI conditions?

A

-Lifestyle changes:
Weight loss
Stopping smoking
Reducing alcohol
Eating smaller meals
-Medications:
Antacids
Proton pump inhibitors (e.g., omeprazole)
H2 receptor antagonists (e.g., ranitidine)
Surgery in extreme cases

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26
Q

What are the red flag features in GI disease that warrant a GP referral for upper GI endoscopy (OGD)?

A

Unexplained weight loss
Loss of appetite
Dysphagia (difficulty swallowing)
Vomiting blood
Rectal bleeding or blood in stool
Unexplained iron deficiency anaemia

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26
Q

What is the role of antacids in the medical management of GORD, and how do they work?

A

Role: Provides symptomatic relief.
Mechanism: Creates a foam on the surface of gastric acid and neutralizes pH.
Example: Gaviscon.

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27
Q

How do proton pump inhibitors (PPIs) work in the treatment of GORD?

A

Mechanism: Inhibit the proton pump (H⁺) of parietal cells, reducing the production of HCl (gastric acid).
Examples: Omeprazole, lansoprazole.

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28
Q

What is the mechanism of action of H2 receptor antagonists in managing GORD?

A

Mechanism: Bind to H2 receptors on parietal cells, preventing the binding of histamine and the stimulation of parietal cells to produce gastric acid.
Examples: Ranitidine, famotidine.

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29
Q

What is Barrett’s oesophagus, and what are its causes and risks?

A

Definition: A complication of GORD involving metaplasia of the oesophageal epithelium at the gastro-oesophageal junction.
Cause: Prolonged exposure to gastric acid, leading to the transformation of squamous epithelium into columnar epithelium.
Risk: Malignant potential, increasing the risk of oesophageal adenocarcinoma.

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30
Q

What are the dental implications of GORD?

A

Erosion:
Acid softens tooth structure and causes loss of tooth tissue.
Affects palatal and labial aspects of upper teeth and occlusal surfaces of lower teeth.
Restorations may “stand proud” due to surrounding tooth erosion.
Symptoms:
Burning mouth symptoms.
Taste disturbance (dysgeusia).
Significance:
Dentists may be the first to detect GORD through these oral signs.

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31
Q

What are the two main types of oesophageal cancer, and what are their causes?

A

Upper 2/3 of oesophagus: Squamous cell carcinoma
Risk factors: Smoking and alcohol.
Lower 1/3 of oesophagus: Adenocarcinoma
Associated with Barrett

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32
Q

What is peptic ulcer disease and how does it occur?

A

Definition: Ulceration of the mucosa in the stomach, duodenum, or oesophagus (rarer).
Cause: Lack of mucus production disrupts the protective coating against gastric juices (acidic), leading to mucosal damage.

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33
Q

What are the key risk factors for peptic ulcer disease that disrupt the mucus barrier?

A

NSAIDs (due to topical effects and COX-1 inhibition).
Helicobacter pylori infection.

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34
Q

What are the risk factors for increased stomach acid production in peptic ulcer disease?

A

Stress.
Caffeine.
Smoking and alcohol.
Spicy foods.

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35
Q

What are the common symptoms of peptic ulcer disease (PUD)?

A

Dyspepsia.
Epigastric pain (often related to meals).
Nausea and vomiting (rarely with blood).

36
Q

What are the potential complications of peptic ulcer disease (PUD)?

A

Bleeding (can be life-threatening)
Anaemia
Perforation of stomach / duodenum
Stricture
Stomach cancer

37
Q

What is Helicobacter pylori (H. pylori), and how does it survive in the stomach?

A

Definition: A bacteria that can live in the stomach (~40% of people).
Survival Mechanisms:
Burrows into the gastric mucosa using flagella.
Produces ammonia to neutralize surrounding acid.
Effect: Toxins produced by H. pylori cause mucosal damage leading to ulcers.

38
Q

Why is H. pylori commonly tested for in patients presenting with dyspepsia symptoms?

A

H. pylori is a major cause of peptic ulcer disease, and its identification helps guide treatment.

39
Q

How is H. pylori tested?

A

Breath test: Detects urea breakdown by H. pylori.
Stool antigen test: Detects H. pylori antigens.

40
Q

What is the 7-day eradication therapy for H. pylori?

A
  1. Proton pump inhibitor (e.g. omeprazole, lansoprazole).
  2. Amoxicillin.
  3. Clarithromycin or metronidazole.
    Also known as triple therapy.
41
Q

How do NSAIDs work and what pathways do they inhibit?

A

Inhibit the formation of prostaglandins via the COX enzyme pathway.
COX-1: Prostaglandins help maintain gastric mucosal integrity and platelet aggregation.
COX-2: Prostaglandins drive pain and inflammation.

42
Q

What are the key management strategies for peptic ulcer disease (PUD)?

A

Lifestyle measures – stress, caffeine, smoking, alcohol,
Stopping NSAIDs
Eradication of H. pylori
Long-term PPI

43
Q

What are the dental implications of peptic ulcer disease (PUD) related to NSAIDs?

A

Avoid use due to their impact on gastric mucosal protection.

44
Q

What are the shared risk factors between PUD and oral cancer?

A

Smoking and alcohol.

45
Q

Lower GI disease

A

Coeliac disease
Inflammatory bowel disease
Bowel cancer

46
Q

What is coeliac disease and how is it triggered?

A

An autoimmune disease triggered by the ingestion of gluten (barley, rye, wheat).
Trigger: Gluten peptides cause an immune response that damages the small intestine.

47
Q

What is the typical age range for diagnosing coeliac disease?

A

Commonly diagnosed: Age 30-40 years.
Can be diagnosed at any age: Affects approximately 1% of the UK population.

48
Q

Which autoimmune diseases are commonly linked with coeliac disease?

A

Type 1 diabetes (T1DM).
Hypothyroidism.

49
Q

What is the pathophysiology of coeliac disease?

A

Loss of immune tolerance to gluten.
Production of autoantibodies (e.g., anti-tTG) targeting epithelial cells of the small intestine.
Inflammation of the intestinal wall leads to gut symptoms and malabsorption.

50
Q

Which autoantibodies are commonly associated with coeliac disease?

A

Anti-tTG (anti-tissue transglutaminase antibodies).

51
Q

How does inflammation in coeliac disease affect the mucosa of the small intestine?

A

Inflammation leads to atrophy of villi (finger-like projections).
Reduced surface area for nutrient absorption.

52
Q

What are the common symptoms of coeliac disease?

A

Abdominal pain
Bloating
Diarrhoea
Nausea and vomiting
Weight loss
Fatigue
Recurrent oral ulcers
Children – failure to thrive

53
Q

What are the key nutrients commonly malabsorbed in coeliac disease?

A

Iron
Folic acid
Vitamin B12
Calcium
Vitamin D
Fat

54
Q

What is the key investigation required for diagnosing coeliac disease?

A

Patient must continue eating gluten when being investigated.
1.Blood tests:
Anti-tTG antibody (tissue transglutaminase) – first line.
EMA (endomysial antibody) – second line.
2. Endoscopy + duodenal biopsy – gold standard for confirming coeliac disease.

55
Q

What are the classic findings on a duodenal biopsy in coeliac disease?

A

Villous atrophy.
Crypt hyperplasia.

56
Q

What is the main management approach for coeliac disease?

A

Gluten-free diet (barley, rye, wheat)
Correct nutritional deficiencies (iron, folate, B12, calcium, vitamin D).

57
Q

How does a gluten-free diet impact coeliac disease?

A

Improves symptoms.
Reverses histological changes.
Reduces lymphoma risk.

58
Q

What are the common complications of coeliac disease?

A

Nutritional deficiencies (iron, folate, B12, calcium, vitamin D).
Anaemia.
Osteoporosis.
Dermatitis herpetiformis.
Lymphoma of the small intestine (due to chronic inflammation and villous atrophy).

59
Q

What is dermatitis herpetiformis and how does it relate to coeliac disease?

A

A skin condition caused by autoantibodies (IgA) being deposited in the skin.
Associated with coeliac disease.

60
Q

What are the dental implications of coeliac disease, especially in children?

A

Tooth development: Enamel hypoplasia, delayed eruption.
Haematinic malabsorption can lead to recurrent oral ulceration.
Glossitis: Atrophic due to iron deficiency.
Oral dysaesthesia (altered sensation).
Angular cheilitis
Candidal infections

61
Q

What characterizes inflammatory bowel disease (IBD)?

A

Recurrent episodes of inflammation in the gastrointestinal tract.
Exacerbation and remission cycles.
Two main types:
Crohn’s disease.
Ulcerative colitis.
Unknown cause:
Immunologically driven, genetic susceptibility, gut microbiome, and psychosocial factors (stress, trauma).

62
Q

What are the common symptoms shared by both Crohn’s disease and ulcerative colitis?

A

Weight loss.
Fatigue.
Abdominal pain.
(Bloody) diarrhoea.
Rectal bleeding.

63
Q

What is Crohn’s disease and how is it characterized?

A

Inflammation of the GI tract wall.
Can involve any part of the GI tract (mouth to anus).
Most commonly affects the ileo-caecal region and perianal areas.
Transmural inflammation: Affects all layers of the GI wall.
Skip lesions: Areas of inflammation separated by normal tissue.

64
Q

What is the pathophysiology of Crohn’s disease?

A

Trigger
Inflammatory infiltrate (CD4, CD8, B cells, monocytes)
Ulceration of mucosa
Invasion of deeper mucosal layers
Formation of granulomas
Formation of crypt abscesses

65
Q

What role do granulomas play in Crohn’s disease?

A

They attempt to isolate and contain the inflammatory process, leading to tissue damage.

66
Q

What are the key investigations for diagnosing Crohn’s disease?

A

Blood tests:
FBC (for anaemia and inflammation).
Haematinics (to check for nutrient deficiencies).
CRP (inflammatory marker).
Anti-tTG antibody (to exclude coeliac disease).
Faecal calprotectin: Stool sample analysed to detect gut inflammation.
Colonoscopy + biopsy:
Classic biopsy findings:
Transmural inflammation.
Granulomas (non-caseating).
Crypt abscesses.

67
Q

What is the management approach for Crohn’s disease?

A

Complex, specialist-led, multidisciplinary team (MDT) approach.
Inducing remission:
Corticosteroids (oral prednisolone, IV hydrocortisone).
Maintenance:
Azathioprine.
Mercaptopurine.
Methotrexate.
Biologics (e.g., infliximab).
Surgery:
Up to 80% of patients
Resection of persistently inflamed bowel (ileostomy/colostomy common).

68
Q

What are common complications of Crohn’s disease?

A

Fistula formation.
Severe abdominal infections.
Anaemia (due to malabsorption of iron, folate, B12).
Orofacial involvement (up to 60%).

69
Q

What are common orofacial manifestations of Crohn’s disease?

A

Buccal oedema.
Cobblestoning (mucosal irregularities).
Linear, sulcal ulceration (long, narrow ulcers).
Mucosal tags (excess tissue around ulcerations).
Lip fissuring.

70
Q

What is Orofacial Granulomatosis (OFG)?

A

A heterogeneous group of conditions leading to orofacial swelling.
Granulomatous inflammation present.
Significant overlap with Crohn’s disease.

71
Q

What is ulcerative colitis and how does it differ from Crohn’s disease?

A

Inflammation limited to the colon and rectum.
Superficial mucosa affected only, unlike Crohn’s disease which involves all layers.
Continuous inflammation that starts at the rectum and progresses proximally (moving upward).

72
Q

What is the pathophysiology of ulcerative colitis?

A

Trigger: Genetic, environmental, previous GI infections, smoking may be protective.
Leaky gut epithelial barrier.
Antigens activate mucosal immune cells.
Dysregulated immune response.
Ulceration of gut mucosa.
Formation of crypt abscesses.

73
Q

What are the key investigations for diagnosing ulcerative colitis?

A

Blood tests:
FBC (for anaemia).
Haematinics (to check for nutrient deficiencies).
CRP (inflammatory marker).
Anti-tTG antibody (to exclude coeliac disease).
Faecal calprotectin: Stool sample analysed for gut inflammation.
Colonoscopy + biopsy:

74
Q

What are the key histological findings in ulcerative colitis on biopsy?

A

No inflammation beyond submucosa
Widespread ulceration
Crypt abscesses
No granulomas

75
Q

What is the management approach for ulcerative colitis?

A

Complex, specialist-led, multidisciplinary team (MDT) approach.
Inducing remission:
Mild/moderate: Rectal or oral mesalazine (5-ASA).
Severe: IV hydrocortisone.
Maintenance:
Rectal mesalazine.
Azathioprine.
Mercaptopurine.
Surgery:
Only 10% of patients require surgery.
Panproctocolectomy is curative (removal of the entire large bowel and rectum).

76
Q

What are the complications of ulcerative colitis?

A

Toxic megacolon – risk of sepsis and death.
Bleeding (haemorrhage).
Bowel cancer (increased risk).
Primary sclerosing cholangitis – bile duct scarring.
Red eye conditions (episcleritis, anterior uveitis).

77
Q

What are the dental implications of inflammatory bowel disease (IBD)?

A

Orofacial features of Crohn’s disease (CD):
Buccal oedema- Linear, sulcal ulcers- Mucosal tags- Buccal cobblestoning- Lip fissure.
Malabsorption:
Haematinic deficiencies (iron, folate, B12) → recurrent oral ulceration.
Stomatitis gangrenosum (1% of patients) – ulcer with necrotic borders.
Drug-related:
Corticosteroids → candidosis.
Methotrexate → oral ulceration.

78
Q

What are the risk factors for bowel cancer (colorectal cancer)?

A

Non-modifiable:
Age >50.
Family history.
Inflammatory bowel disease (UC).
Intestinal polyps.

Modifiable:
Dietary red meat.
Low dietary fibre.
Obesity.
Smoking.
Alcohol consumption.
Not engaging with screening.

79
Q

What is the most common type of bowel cancer?

A

Adenocarcinoma.

80
Q

What are common symptoms and signs of bowel cancer?

A

Change in bowel habits (constipation, diarrhoea, tenesmus).
Bleeding (in stool or on wiping).
Unexplained weight loss.
Iron deficiency anaemia.
Abdominal mass.
Abdominal pain/discomfort.

81
Q

What is the investigation for diagnosing bowel cancer?

A

Colonoscopy + biopsy (gold standard)
Staging CT scan (chest, abdomen and pelvis – to look for metastasis)

82
Q

Who is involved in the multi-disciplinary team (MDT) meeting for cancer management?

A

Surgeons / radiologists / pathologists / oncologists / nurse specialists

83
Q

What does the TNM staging system evaluate in cancer?

A

Tumour size.
Nodal involvement.
Distant metastases.

84
Q

What are the main management options for cancer?

A

Surgery.
Chemotherapy.
Radiotherapy.
Palliative care

85
Q

What factors influence the decision-making for cancer management?

A

Stage of cancer.
Grade of cancer.
Medical history.
Performance status (patient’s fitness).
Patient and family wishes.

86
Q

What is the bowel cancer screening program in Scotland?

A

Every 2 years for men and women aged 50-74.

87
Q

What does the FIT (faecal immunohistochemical test) identify in bowel cancer screening?

A

FIT identifies and quantifies haemoglobin in stool.

88
Q

What happens if the FIT test results are abnormal?

A

An abnormal FIT result leads to a colonoscopy for further investigation.

89
Q

What are the dental implications of bowel cancer?

A

Anaemia as a presenting symptom – dentists can identify and refer patients.
Effects of cancer treatment (chemo-/radiotherapy)

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