Upper GI diseases Flashcards
Pt X has pain chest pain immediately with/after food? What is their diagnosis?
GORD
Pt D has pain between meals/ at night - this is relieved by eating. What is their diagnosis?
Gastritis or Duodenal Ulcer
Pt G has pain in the upper abdomen immediately with/after food. What is their diagnosis?
Gastritis or Gastric Ulcer
What drugs lower lower sphincter (LOS)pressure, resulting in GORD?
NSAIDS, Bisophosphonates, Clindamycin, Clotrimazole, Doxycycline, Potassium, Theophylline, Tetracycline
How can H.Pylori cause a duodenal ulcer?
1) The bacteria burrows under the mucosa, which means they colonise beneath the mucus later in the antrum.
2) This causes chronic inflammation
3)Decreasing somatostatin
4) Gastric production is increased meaning more stomach acid
5) H.Pylori like acid
6) Chronic inflammation in he duodemin,
7) H.Pylori relocates to the duodemin
8) Local protection reduced
9) Ulcer formation
How can H.Pylori cause gastric cancer?
1) Causes gastritis
2) Cells are damaged
3) Increase in acid production
4) Decreased mucosa
5) Long term results in gastric ulcer
6) Gastric cancer
What is the function of somatostatin in the GI tract?
It is a negative feedback loop due to the contents in the duodenum, which signals acid production to slow/stop.
What is the function of Histamine through the H2 receptor in the GI Tract?
To stimulate ECL cells by gastric and the vagus nerve.
What is the function of gastrin through the G receptor?
Causes distension because of the stomach contents.
What does the Acetylcholine M3 receptors on the vagus nerve respond to?
Thought, sight, taste or smell.
What cells produce acid and what stimulates this?
Parietal cells, stimulated by: Vagus nerve, Gastrin, Histamine, Somatostatin
What is gastric cryoprotection?
This prevents the stomach from self-digesting. It is a thin layer above the mucosa surface. It decreases blood flow and the necrosis of the mucosa is protected as there is an increase in H+ conc. This is altered within shock/critically ill patients, stress ulcers can form.
Why are PPI’s so good?
Highly specific mechanism
*Works regardless to acid stimuli
*Drug is inactive at body pH, needs canniculi pH of 2 to be active
*Target is only at the canniculi - as this is where they are protonated
*Reacts fast - Cascade reaction
What are the red flats with patients presenting with Upper GI symptoms?
45+ with new/changed symptoms
Continuous symptoms
No response to treatment for 4 weeks
Weight loss appetite loss
Any signs of Anaemia
Pain when exercising
Dysphagia
Pregnant/BF
Blood in stool or vomit
Child
Mass present
Severe pain
What is the MOA of PPI’s?
1) orally taken and enter systemic circulation as they are lipophillic and neutral
2) Reach parietal cell and flow into canniculus, metabolism occurs in low pH of canniculi and becomes charged
3) Cascade reaction, PPI transformed into active species
4) Disulfide bond with cysteine residue on proton pump
=Irreversible inhibition of pump, no protons can be transported into the canniculus
