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Diseases of human systems > Upper GI tract > Flashcards

Upper GI tract Flashcards

1
Q

What does GORD stand for

A

Gastro-Oesophageal reflux disease

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2
Q

What does PUD stand for

A

Peptic ulcer disease

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3
Q

What does the upper GI tract consist of

A

Mouth
Pharynx
Oesophagus
Stomach
Small intestine (duodenum)

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4
Q

What makes up the lower GI tract

A

Small intestine (jejunum, ileum)
Colon (all of it)
Rectum
Anus

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5
Q

What are the sections of the colon

A

Caecum
Ascending
Transverse
Desecending
Sigmoid

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6
Q

What are the 4 layers of the GI trac

A

Mucosa​

Submucosa​

Muscularis externa​

Adventitia/serosa

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7
Q

Does the whole GI tract have the same 4 layers

A

Yes

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8
Q

What is the function of the GI tract

A

Ingestion and digestion of food
Nutrient absorption
Excretion of waste products

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9
Q

What sphincters are found in the oesophagus

A

Upper oesophageal
Lower oesophageal

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10
Q

What is the purpose of sphincters in the oesophagus

A

Aim to prevent the reflux of food bolus and stomach contents

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11
Q

What is the function of the oesophagus

A

Fibromuscular tube​

Transports food pharynx to stomach​

Peristalsis​

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12
Q

What substrates aid with digestion

A

HCl acid, pepsin, lipase

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13
Q

What substrates aid in absorption

A

B12 (parietal cells)​

Alcohol​

Water

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14
Q

What cells are found in the stomach

A

Chief cells – produce pepsin​

Parietal cells – HCl, intrinsic factor​

Mucus cells - mucus

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15
Q

What is the function of the stomach

A

Digestion
Absorption
Endocrine

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16
Q

Where is gastrin and CCK found

A

In the stomach

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17
Q

What is the function of gastrin

A

Regulates stomach acidity

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18
Q

What does CCK do

A

Stimulates the digestion of fat and protein

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19
Q

How prevelant is GORD

A

10-30% of the population have it

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20
Q

What is the pathology of GORD

A

Acid and stomach contents flow through LOS and into oesophagus​

Laxity of LOS​

Increased gastric pressure​

Delayed gastric emptying

Gastric acid irritates oesophageal mucosa

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21
Q

What is Barrett’s oesophagus

A

Complication of GORD​

Metaplasia of oesophageal epithelium at gastro-oesophageal junction​

squamous epithelium -> columnar epithelium

Malignant potential - oesophageal cancer (adenocarcinoma)​

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22
Q

What are the signs/symptoms of GORD

A

Dyspepsia = indigestion (“heartburn”)​

Epigastric pain​

Bloating​

Nausea/vomiting​

Vocal hoarseness​

Dental erosion*

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23
Q

What are the risk factors associated with GORD

A

Stress/anxiety​

Smoking​

Alcohol​

Trigger foods (coffee, chocolate, fatty meals)​

Obesity​

NSAIDs​

Pregnancy​

Lying flat after large meal

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24
Q

How is GORD diagnosed

A

Via an upper GI endoscopy (OGD)

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25
Q

What are the red flag features for GI disease

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

How is GORD managed

A

Lifestyle changes – e.g. weight loss, stopping smoking, reduce alcohol, smaller meals​

Antacids ​

Proton pump inhibitors (omeprazole)​

H2 receptor antagonist (ranitidine)​

Surgery in extreme cases

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27
Q

What do antacids do

A

Example - gaviscon
Creates a “foam” on surface of gastric acid, neutralises pH​
Provides symptomatic relief

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28
Q

What are some examples of proton pump inhibitors

A

omeprazole, lansoprazole

29
Q

What do proton pump inhibitors do

A

Inhibits the proton pump (H+) of parietal cells, thereby reducing production of HCl (gastric acid)

30
Q

What are some histamine receptor antagonists

A

ranitidine, famotidine

31
Q

What do H2/histamine receptor antagonists do

A

Binds to H2 receptors on parietal cells, preventing the binding of histamine – thereby preventing the stimulation of parietal cells to produce gastric acid

32
Q

What causes GORD

A

Prolonged exposure to acid causes squamous epithelium -> columnar epithelium​

33
Q

What are the dental implications of GORD

A

Erosion​
-Effect of acid – softens tooth structure​
-Loss of tooth tissue​
-Palatal and labial aspects of upper teeth and occlusal surfaces of lower teeth​
-Restorations “stand proud”

“Burning mouth” symptoms

Taste disturbance​
-Dysgeusia

34
Q

When treating erosion what guidelines can dentists consult

A

Royal college of surgeons of england
Clinical guidelines for dental erosion (2021)

35
Q

How can dentalerosion be prevented from progressing

A

Dietary counselling​

Management of GORD​

Management of vomiting​

Dental prevention

36
Q

What are the types of possible causes of erosion

A

Extrrinsic
Intrinsic

37
Q

What are the types of oesophageal cancer

A

Upper 2/3 – squamous cell carcinoma​
-Smoking and alcohol​

Lower 1/3 – adenocarcinoma​
-Barret’s oesophagus**

38
Q

What are the causes of squamous cell carcinoma in the oesophagus

A

Smoking and alcohol

39
Q

How is oesophageal cancer managed

A

MDT decision​

Chemo/radiotherapy​

Surgery​

Palliative

40
Q

Why does peptic ulcer disease occur

A

The usual mucus production within the stomach/duodenum/oesophagus is less or none leaving the mucosa exposed/unprotected and allows for ulceration

41
Q

What are the risk factors of PUD

A

Disrupt mucus barrier:
NSAIDS (topical and cox-1 inhibition)
Helicobacter pylori

All increase acid production:
Stress​
Caffeine ​
Smoking and alcohol​
Spicy foods

42
Q

What medication could cause peptic ulcer disease

A

NSAIDs (topical and cox-1 inhibition) as they disrupt the mucus barrier

43
Q

What are the symptoms of PUD

A

Dyspepsia​

Epigastric pain (around meals)​

Nausea and vomiting (rarely blood)

44
Q

What complications may arise from PUD

A

Bleeding (can be life-threatening)​

Anaemia​

Perforation of stomach / duodenum​

Stricture​

Stomach cancer

45
Q

What is stricture

A

Abnormal narrowing in a passage in the body

46
Q

What is Helicobacter Pylori

A

Bacteria that can live in stomach (~ 40% of people)​

Able to avoid acidic environment by burrowing into gastric mucosa (flagella)

Also produces ammonia to neutralise surrounding acid

47
Q

How does Helicobacter Pylori disrupt the mucus barrier

A

Toxins produced by H. Pylori cause mucosal damage -> ulcer

48
Q

How does stomach bacteria survive in the acidic conditions

A

Able to avoid acidic environment by burrowing into gastric mucosa (flagella)​

Also produces ammonia to neutralise surrounding acid​

49
Q

How many people have Helicobacter Pylori in their stomachs

A

Around 40%

50
Q

What are the tests for Helicobacter Pylori

A

Breath test (look for ammonia)
Stool antigeb=n

51
Q

How is Helicobacter Pylori treated/eradicated

A

1) Proton pump inhibitor (e.g. omeprazole, lansoprazole)​

2) Amoxicillin​

3) Clarithromycin or metronidazole​

Also known as “triple therapy”

52
Q

What is triple therapy

A

The treatment to get rid of Helicobacter Pylori

Proton pump inhibitor (e.g. omeprazole, lansoprazole)​

Amoxicillin​

Clarithromycin or metronidazole

53
Q

What are some NSAIDS

A

ibuprofen, aspirin, diclofenac, naproxen

54
Q

How do NSAIDS work

A

NSAIDs work by inhibiting the formation of prostaglandins via COX enzyme pathway​

COX-1 = prostaglandins help with gastric mucosal integrity and platelet aggregation​

COX-2 = prostaglandins drive pain and inflammation

55
Q

How do NSAIDS decide which COX pathway to inhibit

A

They vary in how selective they are

56
Q

What NSAIDS are COX-2 seletive

A

Celecoxib

57
Q

What are the side effects of COX-2 selective NSAIDS

A

Increased risk of CV events
Decrease risk of GI side effects

58
Q

What are some semiselective NSAIDS

A

Meloxicam
Diclofenac
Etodolac
Piroxicam

59
Q

What are the affects of semiselective NSAIDS

A

Use with caution in patients at increased risk of CV

60
Q

What does semiselective mean

A

Increase affinity for COX-2 but still retain activity for COX-1

61
Q

What are the dental implications of PUD

A

Avoid use of NSAIDS
Risk factors with oral cancer (smoking/alcohol)

62
Q

How is PUD diagnosed

A

Endoscopy

63
Q

How is PUD managed

A

Lifestyle measures – stress, caffeine, smoking, alcohol, ​

Stopping NSAIDs*​

Eradication of H. pylori *​

Long-term PPI (Proton Pump Inhibitors)

64
Q

How selective is ibuprofen and naproxen

A

Non-selective NSAIDS

65
Q

What does a Non-selective NSAID increase the risk of

A

GI side effects and reduces risk of CV events compared to selective

66
Q

What is an example of anirreversible nonselective NSAID

A

Aspirin

67
Q

What are the benefits of a non-selective NSAID

A

Decreased risk of CV events

68
Q

What makes an NSAID more prone to GI side effects

A

Decreased selectivity

Diseases of human systems (7 decks)

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