GI question

[LuckiestOne]

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After fasting, a patient has no gastric acid secretion
when chewing and no receptive relaxation of the
proximal stomach when swallowing. Which of the
following best explains these findings?


(A) Absence of antral G cells
(B) Absence of chief cells
(C) Increased concentration of secretin
(D) Increased concentration of somatostatin
(E) Vagally denervated stomach

Another pretty confusing question, let's have a discussion on it. What do you guys think the answer is and please provide explanation, thanks!

 

[Phloston]

Failure of relaxation [of anything] should immediately make you think of VIP. VIP, however, doesn't act directly. It acts via increasing somatostatin, so right away, we can eliminate choice D, because if somatostatin were present, we'd get relaxation.

VIP secretion is increased by vagal stimulation, as is HCl secretion.

ACh, histamine and gastrin all act synergistically to stimulate HCl secretion. If ANY ONE of those are deficient, HCl secretion greatly decreases. So I'd say lack of vagal stimulation is decreasing both HCl and VIP secretion, particularly since we know VIP secretion is mediated by vagal stimulation.

Chief cells secrete pepsinogen and are irrelevant here.

Increased secretin and the absence of G-cells could explain the decreased HCl, but neither would explain the decreased receptive relaxation, so both are eliminated via the same reasoning.

So I'd go with choice E.

 

[Chirurg]

After fasting, a patient has no gastric acid secretion
when chewing and no receptive relaxation of the
proximal stomach when swallowing. Which of the
following best explains these findings?


(A) Absence of antral G cells
(B) Absence of chief cells
(C) Increased concentration of secretin
(D) Increased concentration of somatostatin
(E) Vagally denervated stomach

Another pretty confusing question, let's have a discussion on it. What do you guys think the answer is and please provide explanation, thanks!

where is this question from? I think it's a good question.
it asks whether you understand the concept of the cephalic phase of digestion which is vagally mediated. so I would go with denervated stomach.
note: there is no mention of further compromise in secretory function once the food hits the stomach, so the other choices are distractors.

 

[LuckiestOne]

Failure of relaxation [of anything] should immediately make you think of VIP. VIP, however, doesn't act directly. It acts via increasing somatostatin, so right away, we can eliminate choice D, because if somatostatin were present, we'd get relaxation.

VIP secretion is increased by vagal stimulation, as is HCl secretion.

ACh, histamine and gastrin all act synergistically to stimulate HCl secretion. If ANY ONE of those are deficient, HCl secretion greatly decreases. So I'd say lack of vagal stimulation is decreasing both HCl and VIP secretion, particularly since we know VIP secretion is mediated by vagal stimulation.

Chief cells secrete pepsinogen and are irrelevant here.

Increased secretin and the absence of G-cells could explain the decreased HCl, but neither would explain the decreased receptive relaxation, so both are eliminated via the same reasoning.

So I'd go with choice E.

Thanks Phloston. I thought the same thing but I was wondering why fasting would cause vagal nerve denervation. It's not like he went through a vagectomy...

 

[Suncrusher]

Thanks Phloston. I thought the same thing but I was wondering why fasting would cause vagal nerve denervation. It's not like he went through a vagectomy...

It's E imo too, and it's not that fasting caused the vagal denervation--the patient already had vagal denervation and experienced those symptoms in the fasting state to make the question less complex (i.e. no one can argue that things he just ate or that hormones that were released due to things he just ate are what caused the symptoms). It's just to make answering the question go even faster.

 

[Cozenboy]

Where is that q from?