Gastric Secretion LAB Flashcards

1
Q

what is the main diagnosis for H.pylori

A

C-urea breath test

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2
Q

describe the sequence of events which occur to C-urea once it enters the patients stomach

A

normal carbon- 12
breath test- enriched Carbon 14

If H.pylori present in stomach, urease enzyme secreted which then reacts with C and causes CO2 and ammonia production.

enriched CO2 = H.pylori present
not enriched CO2 = H.pylori not present

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3
Q

what are the other diagnosis techniques available

A

Blood test (serology for antibody IgG)
Stool test
Histological Biopsy
Endoscopy

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4
Q

what are the contents of gastric juice

A

Hydrochloric acid
Pepsin
Mucin
Intrinsic factor

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5
Q

what controls gastric acid secretion

A

Acetylcholine (neuronal – parasympathetic)
cephalic phase
Histamine (ECL cell – paracrine)

Gastrin (G cell – endocrine)
in response to high pH-gastric phase
Somatostatin (D cell – endocrine)
IN RESPONSE TO LOW pH – INTESTINAL PHASE

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6
Q

Describe gastric secretion

A

ACh stimulates G cell to produce gastrin
ACh stimulates parietal cell to produce acid

Gastrin stimulates ECL cell to produce histamine
Gastrin stimulates parietal cell to produce acid

Somatostatin inhibits parietal cell acid secretion
Somatostatin inhibits ECL cell histamine secretion

Histamine stimulates acid secretion by acting on parietal cell via H2 receptor
Histamine stimulates acid secretion by acting on D cell via H3 receptor to inhibit somatostatin production

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7
Q

list 3 physiological functions of gastric acid

A

Digestion (pepsinogen -> pepsin)
Absorption (Fe, Ca2+, viatmin B12)
Antimicrobial

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8
Q

what is the pH of HCl in gastric acid

A

pH 0.8

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9
Q

What protects gastric epithelium from damage by gastric acid

A

Mucous neck cells

produce mucous that protects the stomach from HCl

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10
Q

describe Zollinger Ellison Syndrome

A

Disease in which tumors cause the stomach to produce too much acid, resulting in peptic ulcers.

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11
Q

What is the main cause of peptic ulcer disease

A

H.Pylori

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12
Q

What are the adverse effect of PPI

A

Reduction in Gastric Acid Output
- Reduced nutrient absorption (iron, calcium and vit B12)
- Reduced gastric antimicrobial function (risk of enteric infections)
Increase in serum gastrin Levels (osteoporosis)

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13
Q

what normally prevents gastric acid from refluxing into oesophagus

A

lower oesophageal sphincter

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14
Q

what is the normal resting pressure of the LOS and how do u measure that

A

2-3 mmHg

manometry

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15
Q

what lifestyle factors may produce GORD and what is the mechanism of the effect

A

increased BMI, obesity
pregnancy
–> increased pressure on stomach so weakens the LOS muscles

smoking
alcohol
coffee/chocolate
stress
--> may relax LOS muscles
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16
Q

what drugs can be used for management of GORD and how do they work

A

1) Histamine 2- receptor antagonist (e.g. Zantac)
competitively inhibits the H2 receptor on the parietal cell -> inhibiting acid secretion
2) PPIs- weak bases (e.g. Lansoprazole)
Acts on the final common pathway- irreversibly binds to and blocks the proton pump  inhibiting acid secretion from the parietal cells

17
Q

What is the role of surgery in the management of reflux disease

A

Vagotomy: (surgery uncommon nowadays)
This was the treatment before drugs were introduced
involves cutting the vagus nerve. Thus, ennervating the stomach-> no peristalsis so food is emptied very slowly after the surgery.
High risk of gastric cancer after surgery

18
Q

what is the treatment for peptic ulcers

A
  • triple therapy involving proton pump inhibitors and two of the three antibiotics (Amoxycillin, Clarithromycin and Metronidazole).

The triple therapy is taken for a week.