NBME 23 Impaired release of glucagon (NBME Answers)

Retired NBME 23 Answers

nbme23/Block 3/Question#18 (reveal difficulty score)
A patient with a 20-year history of type 1 ...
Impaired release of glucagon 🔍 / 📺 / 🌳 / 📖
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+10 upvote downvote
submitted by ∗moxomonkey(20)

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glucagon secretion is inhibited by hyperglycemia, somatostatin and insulin FA2019 - 325

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an1 Insulin inhibits glycogen phosphorylase via protein kinase A and up-regulates glycogen synthase. A is wrong, glycogen increases with insulin use. Insulin may reduce catelcholamines itself, but nothing is indicated about receptor reduction. Again with C, no indication of receptors affected. E may be seen with insulin resistance possible? That’s a DM2 issue, not DM1. +

adong This is true but I think there's more to it because the hypoglycemia is prolonged. UW QID 19224 covers this and the two important takeaways are that patients with longstanding T1DM are more susceptible to hypoglycemia bc 1) exogenous insulin is not subject to the same negative feedback that endogenous insulin is and will still be absorbed even if blood sugar low and 2) extended type 1 DM can damage pancreatic alpha cells that release glucagon. Just thought I would include this in case you come across a similar question testing a slightly different concept. +2

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submitted by ∗keycompany(351)

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Type I Diabetes is characterized as the destruction of pancreatic islets (specifically beta cells) by T-cells. The most likely cause for hypoglycemia following insulin administration, therefore, is the destruction of alpha cells that surround the beta cells. This would cause decreased levels of circulating glucagon.

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titanesxvi I think rather that high insulin is going to block the release of glucagon +6

mdmikek89 No, his answer is more correct. Obviously insulin will decrease glucagon release, but it says PROLONGED. So if I give a rapid acting insulin, serum glucose decreases, the insulin degrades...no rise in glucagon. The alpha cells are destroyed as well. This is the how I came to the answer and the best explanation. +3

melanoma https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402257/ +

melanoma the answer is not correct +1

melanoma his answer +1

prolific_pygophilic I actually think this has some merit. I believe there is a U world question that talks about how very long history of T1DM (20 years in this patient) can progress to destruction of alpha cells and hence impaired release of glucagon and episodes of hypoglycemia. Thats how I reasoned it. The first answer is also possible. +1

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submitted by ∗mcl(671)

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According to this paper, insulin inhibits alpha cells from releasing glucagon. This is the relevant figure from the paper.

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medpsychosis There are three ways that Glucagon secretion is stimulated: +(1) a stimulatory effect of low glucose directly on the alpha cell, +(2) withdrawal of an inhibitory effect of adjacent beta cells, and +(3) a stimulatory effect of autonomic activation. The response of Glucagon to hypoglycemia is diminished in T1Diabetes. Hence in this pt, the impaired release of Glucagon allows for prolonged Hypoglycemia. Reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3005043/ +9

xmen FA 2019 p 324 insulin decrease glucagon release +

xmen FA 2019 p 325 Glucagon Secreted in response to hypoglycemia. Inh ibited by insu lin, hyperg lycem ia, and somatostatin. +

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submitted by ∗imgdoc(183)

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Couple of Uworld questions on this, but basically Type 1 diabetics have a CD4+ T cell response to their pancreatic islets, which target beta cells in the pancreas. This leads to almost absent insulin secretion in these patients. OVERTIME, the autoimmune reaction to the beta cells causes damage to alpha cells in the pancreas, leading to a decreased ability to increase serum glucose levels appropriately as a counter balance to insulin.

The reason it wasn't related to catecholamine based increase in glycogen phosphorylase is because GLUCAGON is the primary hormone responsible for increasing glucose levels, not catecholamines.

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imgdoc alpha cells secrete glucagon, just FYI. +

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submitted by ∗criovoly(17)

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Insulin decreases the level of blood glucose and Glucagon increases levels of blood glucose. They both counter block each other. If insulin is high glucagon will be inhibited, and when glucagon is high insulin will be inhibited. FA 2018 page 76.

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dermetfak won’t glucagon stimulate insulin release? https://www.researchgate.net/figure/Paracrine-interactions-between-islet-cells-Insulin-secreted-by-b-cells-acts-as-a-prime_fig4_221914949 +1

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