Lab 1: Presentation 1 Flashcards

1
Q

What does melena mean?

A

Black stool as a result of an upper GI bleed

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2
Q

At what stage of the GI tract if there was a bleed it would be black and why is it black?

A

A bleed before the jejunum will be black in the stool (melena)

It is black because it has been partially digested

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3
Q

What should be done initially when a patient is in heamorrhagic shock?

A

Give fluids by intervenous injection to increase the blood pressure.

Sample the blood to determine haemoglobin levels (to show if blood needs to be give)

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4
Q

What is the normal haemoglobin levels for a female and male?

A

Female: 110

Male: 130

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5
Q

What are the two ways to stop the bleeding for a peptic ulcer?

A
  1. Inject with adrenaline as it is a vasoconstrictor
  2. Coagulate the area with a heat probe
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6
Q
A
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7
Q

What is the pH of gastric juice?

A

1.5-3.5

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8
Q

What are these?

A

Gastric pits and Gastric glands

Can be one gastric pit and multiple gastric glands

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9
Q

What are the two types of gastric glands that are found in the stomach?

A

Oxyntic and pyloric glands

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10
Q

What region of the stomach are the oxyntic glands found?

A

The fundus and body of the stomach

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11
Q

What region of the stomach are pyloric glands found?

A

In the pyloric antrum

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12
Q

What are the differences between a oxyntic and pyloric gland?

A

Oxyntic:

Found in the fundus and the body

More parietal cells

High secretion of hydrochloric acid and intrinsic factor

Pyloric:

Found in the pyloric antrum

Less parietal and more G cells

High secretion of gastrin

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13
Q

What are the components of gastric juice?

A

Hydrochloric acid (secreted by parietal cells)

Pepsin (secreted in the form of pepsinogen by chief cells)

Mucin (large glycoprotein, which is a structural component of mucus)

Intrinsic factor (secreted by parietal cells)

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14
Q

When the pH begins to fall what gets secreted?

A

Somatostatin from D cells

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15
Q

What cells does the vagus nerve innervate?

A

ACh (released by the vagus nerve) inhibits D cells, stimulates G cells and parietal cells

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16
Q

What receptor does ACh innervate on the parietal cell?

A

M3 receptor

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17
Q

What receptor does the gastrin innervate on the parietal cell?

A

CCK 2 receptor

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18
Q

What cells does the ACh innervate?

A

Inhibits D cells

Stimualtes parietal cells

Stimulates G cells

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19
Q

Name these receptors?

A
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20
Q

Name these cells?

A
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21
Q

What does gastrin do?

A

Stimulates ECL cells to produce histamine

Stimulates parietal cells to produce acid

22
Q

What does ACh do in the gastric secretion process?

A

Stimulates G cell to produce gastrin

Stimulates parietal cell to produce acid

23
Q

What does somatostatin do in the gastric secretion process?

A

Secreted by the D cells

Inhibits parietal cell acid secretion

Inhibits ECL cell histamine secretion

24
Q

What does histamine do in the acid secretion process?

A

Stimulates parietal cell to produce acid via H2 receptor

Inhibits D cells somatostatin secretion, thus stimulates acid secretion

25
Q

What are the 3 functions of the gastric acid?

A

Aids digestion- converts pepsinogen to pepsin

Absorption of iron, vitamin B12 and calcium

Antimicrobial

26
Q

What is the main defence against the gastric acid in the stomach? Why is it such a good defence

A

The gastric mucus is the main defence

Physical and chemical barrier

Chemical: its rich in bicarbonate which neutralises the hydrochloric acid

27
Q

Give examples of too much attack causes that results in peptic ulcer disease?

A

Zollinger Ellison Syndrome- benign gastric producing tumour

H.pylori infection

28
Q

Which cyclooxygenase is important in mucus production?

29
Q

Why are NSAIDs so dangerous in the stomach?

A

NSAIDS are non selective inhibitors of COX1 and COX2

COX1 is important for the production of mucus, hence NSAIDs are dangerous and it lowers this protective barrier from the gastric acid

30
Q

Give examples of too little defense causes that results in peptic ulcer disease?

A

Non steroidal anti-inflammatory drugs aka NSAIDs

Stress” ulceration

H.pylori infection

31
Q

How does the H.pylori result in peptic ulcer disease?

Is it too much attack or too little defense?

Why?

A

Both attack and defense

Attack: Blocks D cells, limiting in the inhibition of parietal cells and it secretes ammonia which neutralises the acid. Triggering more acid production

Defense: causes chronic inflammation of the lining

32
Q

What are “stress” ulceration?

A

It is when an ulceration results in a patient who is under a lot of physiological stress e.g. surgery.

33
Q

What does a peptic ulcer look like in an endoscope?

A

Looks similar to a mouth ulcer

White circular shape on the lining

34
Q

What are some complications of peptic ulcer disease?

A

Perforation

Bleeding

Penetration

Gastric outlet blockage

35
Q

What is the main cause of peptic ulcer disease?

36
Q

Describe the difference in the outcome of H.pylori as a result of geographical design?

A

Asia

H.pylori predominately results in pangastritis

Pangastritis: Atrophy of the parietal cells leading to hypochlorhydria (low levels of acid). Increasing the risk of gastric cancer. Effects the entire stomach lining.

West

H.pylori predominately results in antral predominant gastritis

Antral predominant gastritis: Excessive acid production but does not cause atrophy. Found in the antrum.

37
Q

What is the main cause of duodenal ulcers?

A

Usually are a result of acid hypersection from the stomach.

The acid moves into the duodenum when chyme travels through.

38
Q

How does H.pylori live in the stomach?

A

It metabolises urea via urease, into ammonia. Ammonia is an alkaline which is secreted around the H.pylori creating a buffer zone , as the ammonia neutralises the acid.

39
Q

What are the 5 ways to detect Helicobacter pylori ?

A

Serological (blood) test

Stool test

Urea breathe test

Barium swallow

Biopsy urease test

40
Q

What are the pros and cons of the blood test to detect Helicobacter pylori?

A

The test detects IgG antibodies

85% sensitive

Can only be used once

41
Q

Describe the urea breathe test for detecting Helicobacter pylori?

A

Patient ingests 13C-Urea (isotope 13 for Carbon)

If H. pylori is present they will convert the 13C-urea into 13CO2 and ammonia

Test the levels of 13CO2

42
Q

Describe how the barium swallow test can be used to detect H.pylori?

A

Ingests barium

If a peptic ulcer is present, it will be filled with barium

Can be seen on an X-ray

43
Q

Describe the biopsy urease test (also known as rapid urease test) to detect Helicobacter pylori?

A

A biopsy is taken

The biopsy is added to a substrate that contains urea and phenol red (hence the red colour)

If H.pylori is present, it will convert the urea into ammonia, and this will increase the pH.

This causes a colour change from red to yellow- positive indication of H.pylori

44
Q

What colour is the rapid urease test initially and after a positive result?

A

Initially it is yellow

Positive result, red

45
Q

What are the 4 treatments for peptic ulcer disease?

A
  1. Eradication therapy- antibiotics
  2. Medication
  3. Lifestyle changes
  4. Surgical treatment
46
Q

Describe the medications available to test peptic ulcer disease?

A

H2 receptor antagonist

Proton pump inhibitors

47
Q

Give an example of a H2 receptor antagonist?

A

Ranitidine

48
Q

Give an example of a proton pump inhibitor?

A

Omeprazole

49
Q

Describe the way H2 receptor antagonist works in reducing acid secretion?

A

Competitive and reversibility bind to the H2 receptor on the parietal cells

Histamine released by the ECL cell bind to the H2 receptor. Hence the H2 receptor antagonist reduces the histamine effect

Reduces acid secretion

50
Q

What are some cons of the H2 receptor antagonist?

A

Interacts with other drugs

“Drug holidays” are required- this is when you have to take breaks when taking a medication because you become tolerant

51
Q

Describe the mechanism of action for proton pump inhibitors?

A

Taken orally

Absorbed in the small intestine

It inhibits the potassium/hydrogen ion pump located on the apical membrane of the parietal cell

52
Q

What are some cons of the proton pump inhibitors?

A

Slight increase in the risk of food poison

Rebound acid hypersecretion- when PPI are stopped, there is an increase in acid secretion (higher than it was prior to PPI)