Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Diseases of human systems > Upper GI tract > Flashcards

Upper GI tract Flashcards

1
Q

What does GORD stand for

A

Gastro-Oesophageal reflux disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does PUD stand for

A

Peptic ulcer disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does the upper GI tract consist of

A

Mouth
Pharynx
Oesophagus
Stomach
Small intestine (duodenum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What makes up the lower GI tract

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the sections of the colon

A

Caecum
Ascending
Transverse
Desecending
Sigmoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 4 layers of the GI trac

A

Mucosa​

Submucosa​

Muscularis externa​

Adventitia/serosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Does the whole GI tract have the same 4 layers

A

Yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the function of the GI tract

A

Ingestion and digestion of food
Nutrient absorption
Excretion of waste products

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What sphincters are found in the oesophagus

A

Upper oesophageal
Lower oesophageal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the purpose of sphincters in the oesophagus

A

Aim to prevent the reflux of food bolus and stomach contents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the function of the oesophagus

A

Fibromuscular tube​

Transports food pharynx to stomach​

Peristalsis​

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What substrates aid with digestion

A

HCl acid, pepsin, lipase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What substrates aid in absorption

A

B12 (parietal cells)​

Alcohol​

Water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What cells are found in the stomach

A

Chief cells – produce pepsin​

Parietal cells – HCl, intrinsic factor​

Mucus cells - mucus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the function of the stomach

A

Digestion
Absorption
Endocrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Where is gastrin and CCK found

A

In the stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the function of gastrin

A

Regulates stomach acidity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does CCK do

A

Stimulates the digestion of fat and protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How prevelant is GORD

A

10-30% of the population have it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)​

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the signs/symptoms of GORD

A

Dyspepsia = indigestion (“heartburn”)​

Epigastric pain​

Bloating​

Nausea/vomiting​

Vocal hoarseness​

Dental erosion*

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How is GORD diagnosed

A

Via an upper GI endoscopy (OGD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are the red flag features for GI disease
Unexplained weight loss​ Loss of appetite​ Dysphagia (difficulty swallowing)​ Vomiting blood​ Rectal bleeding or blood in stool​ Unexplained iron deficiency anaemia
26
How is GORD managed
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
27
What do antacids do
Example - gaviscon Creates a “foam” on surface of gastric acid, neutralises pH​ Provides symptomatic relief
28
What are some examples of proton pump inhibitors
omeprazole, lansoprazole
29
What do proton pump inhibitors do
Inhibits the proton pump (H+) of parietal cells, thereby reducing production of HCl (gastric acid)
30
What are some histamine receptor antagonists
ranitidine, famotidine
31
What do H2/histamine receptor antagonists do
Binds to H2 receptors on parietal cells, preventing the binding of histamine – thereby preventing the stimulation of parietal cells to produce gastric acid
32
What causes GORD
Prolonged exposure to acid causes squamous epithelium -> columnar epithelium​
33
What are the dental implications of GORD
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
When treating erosion what guidelines can dentists consult
Royal college of surgeons of england Clinical guidelines for dental erosion (2021)
35
How can dentalerosion be prevented from progressing
Dietary counselling​ Management of GORD​ Management of vomiting​ Dental prevention
36
What are the types of possible causes of erosion
Extrrinsic Intrinsic
37
What are the types of oesophageal cancer
Upper 2/3 – squamous cell carcinoma​ -Smoking and alcohol​ Lower 1/3 – adenocarcinoma​ -Barret’s oesophagus**
38
What are the causes of squamous cell carcinoma in the oesophagus
Smoking and alcohol
39
How is oesophageal cancer managed
MDT decision​ Chemo/radiotherapy​ Surgery​ Palliative
40
Why does peptic ulcer disease occur
The usual mucus production within the stomach/duodenum/oesophagus is less or none leaving the mucosa exposed/unprotected and allows for ulceration
41
What are the risk factors of PUD
Disrupt mucus barrier: NSAIDS (topical and cox-1 inhibition) Helicobacter pylori All increase acid production: Stress​ Caffeine ​ Smoking and alcohol​ Spicy foods
42
What medication could cause peptic ulcer disease
NSAIDs (topical and cox-1 inhibition) as they disrupt the mucus barrier
43
What are the symptoms of PUD
Dyspepsia​ Epigastric pain (around meals)​ Nausea and vomiting (rarely blood)
44
What complications may arise from PUD
Bleeding (can be life-threatening)​ Anaemia​ Perforation of stomach / duodenum​ Stricture​ Stomach cancer
45
What is stricture
Abnormal narrowing in a passage in the body
46
What is Helicobacter Pylori
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
How does Helicobacter Pylori disrupt the mucus barrier
Toxins produced by H. Pylori cause mucosal damage -> ulcer
48
How does stomach bacteria survive in the acidic conditions
Able to avoid acidic environment by burrowing into gastric mucosa (flagella)​ Also produces ammonia to neutralise surrounding acid​
49
How many people have Helicobacter Pylori in their stomachs
Around 40%
50
What are the tests for Helicobacter Pylori
Breath test (look for ammonia) Stool antigeb=n
51
How is Helicobacter Pylori treated/eradicated
1) Proton pump inhibitor (e.g. omeprazole, lansoprazole)​ 2) Amoxicillin​ 3) Clarithromycin or metronidazole​ Also known as “triple therapy”
52
What is triple therapy
The treatment to get rid of Helicobacter Pylori Proton pump inhibitor (e.g. omeprazole, lansoprazole)​ Amoxicillin​ Clarithromycin or metronidazole
53
What are some NSAIDS
ibuprofen, aspirin, diclofenac, naproxen
54
How do NSAIDS work
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
How do NSAIDS decide which COX pathway to inhibit
They vary in how selective they are
56
What NSAIDS are COX-2 seletive
Celecoxib
57
What are the side effects of COX-2 selective NSAIDS
Increased risk of CV events Decrease risk of GI side effects
58
What are some semiselective NSAIDS
Meloxicam Diclofenac Etodolac Piroxicam
59
What are the affects of semiselective NSAIDS
Use with caution in patients at increased risk of CV
60
What does semiselective mean
Increase affinity for COX-2 but still retain activity for COX-1
61
What are the dental implications of PUD
Avoid use of NSAIDS Risk factors with oral cancer (smoking/alcohol)
62
How is PUD diagnosed
Endoscopy
63
How is PUD managed
Lifestyle measures – stress, caffeine, smoking, alcohol, ​ Stopping NSAIDs*​ Eradication of H. pylori *​ Long-term PPI (Proton Pump Inhibitors)
64
How selective is ibuprofen and naproxen
Non-selective NSAIDS
65
What does a Non-selective NSAID increase the risk of
GI side effects and reduces risk of CV events compared to selective
66
What is an example of anirreversible nonselective NSAID
Aspirin
67
What are the benefits of a non-selective NSAID
Decreased risk of CV events
68
What makes an NSAID more prone to GI side effects
Decreased selectivity

Diseases of human systems (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions