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
What are the 3 functions of the gastric acid?
Aids digestion- converts pepsinogen to pepsin Absorption of iron, vitamin B12 and calcium Antimicrobial
26
What is the main defence against the gastric acid in the stomach? Why is it such a good defence
The **gastric** **mucus** is the main defence Physical and chemical barrier Chemical: its rich in bicarbonate which neutralises the hydrochloric acid
27
Give examples of too much attack causes that results in peptic ulcer disease?
Zollinger Ellison Syndrome- benign gastric producing tumour *H.pylori* infection
28
Which cyclooxygenase is important in mucus production?
COX-1
29
Why are NSAIDs so dangerous in the stomach?
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
Give examples of too little defense causes that results in peptic ulcer disease?
Non steroidal anti-inflammatory drugs aka NSAIDs "*Stress"* ulceration *H.pylori* infection
31
How does the *H.pylori* result in peptic ulcer disease? Is it too much attack or too little defense? Why?
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
What are *"stress"* ulceration?
It is when an ulceration results in a patient who is under a lot of physiological stress e.g. surgery.
33
What does a peptic ulcer look like in an endoscope?
Looks similar to a mouth ulcer White circular shape on the lining
34
What are some complications of peptic ulcer disease?
Perforation Bleeding Penetration Gastric outlet blockage
35
What is the main cause of peptic ulcer disease?
*H.pylori*
36
Describe the difference in the outcome of *H.pylori* as a result of geographical design?
_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
What is the main cause of duodenal ulcers?
Usually are a result of acid hypersection from the stomach. The acid moves into the duodenum when chyme travels through.
38
How does *H.pylori* live in the stomach?
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
What are the 5 ways to detect *Helicobacter pylori* ?
Serological (blood) test Stool test Urea breathe test Barium swallow Biopsy urease test
40
What are the pros and cons of the blood test to detect *Helicobacter pylori*?
The test detects IgG antibodies 85% sensitive Can only be used once
41
Describe the urea breathe test for detecting *Helicobacter pylori?*
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
Describe how the barium swallow test can be used to detect *H.pylori?*
Ingests barium If a peptic ulcer is present, it will be filled with barium Can be seen on an X-ray
43
Describe the biopsy urease test (also known as rapid urease test) to detect *Helicobacter* *pylori?*
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
What colour is the rapid urease test initially and after a positive result?
Initially it is yellow Positive result, red
45
What are the 4 treatments for peptic ulcer disease?
1. Eradication therapy- antibiotics 2. Medication 3. Lifestyle changes 4. Surgical treatment
46
Describe the medications available to test peptic ulcer disease?
H2 receptor antagonist Proton pump inhibitors
47
Give an example of a H2 receptor antagonist?
Ranitidine
48
Give an example of a proton pump inhibitor?
Omeprazole
49
Describe the way H2 receptor antagonist works in reducing acid secretion?
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
What are some cons of the H2 receptor antagonist?
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
Describe the mechanism of action for proton pump inhibitors?
Taken orally Absorbed in the small intestine It inhibits the potassium/hydrogen ion pump located on the apical membrane of the parietal cell
52
What are some cons of the proton pump inhibitors?
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)