Advertisement - Members don't see this ad
A 6 year-old girl is brought to the physician by her mother because of a 2-week history of increased thirst and a 3-kg weight loss. Her mother says that the patient is constantly drinking water. She is at 75th percentile for height and 50th percentile for weight. Physical examination shows tachypnea and dehydration. Laboratory examination shows hyperglycemia, metabolic acidosis and ketonemia. if a biopsy specimen were obtained from this patient's pancreas, which of the following findings in islet cells would now be most likely?
A: basement membrane thickening of capillaries
B: cellular necrosis and lymphocyte infiltration
C: Decrease in mass and deposition of amyloid
D: large beta cell and nuclei
E: marked atrophy and fibrosis
----------------
I put E. Extended feedback says it's wrong. Other forums say it's B.
My reasoning:
1) Despite lymphocytic infiltration obviously occurring with type-I DM, I would think that since the beta-cells are destroyed by the immune system, it would be APOPTOSIS, not necrosis. Since when are the cells necrotic? That just seemed wrong. I would think we'd get CD8+ induced apoptosis secondary to glutamic acid decarboxylase being displayed on MHC-I, either that or auto-antibodies merely binding the GAD.
2) The other thing is that I believe having heard/read somewhere that glucose levels don't actually begin to elevate until somewhere around 90% of the islet cells are already destroyed. So for this kid to already be in DKA means that his beta-cells have to already virtually be gone, so I'd think the lymphocytic infiltrative phase is long-passed. If they asked about what process "gave rise" to his current Sx, that's totally different.
3) Final sentence of the question says, "which of the following findings in islet cells would now be most likely?" This implies that they are acknowledging the chronology of the beta-cell degradation, such that lymphocytic infiltration with APOPTOSIS had occurred early, but NOW fibrosis and atrophy have ensued, with the atrophy occurring secondary to exhaustive hypertrophy.
----------
Please help.............
BS question quite frankly.
A: basement membrane thickening of capillaries
B: cellular necrosis and lymphocyte infiltration
C: Decrease in mass and deposition of amyloid
D: large beta cell and nuclei
E: marked atrophy and fibrosis
----------------
I put E. Extended feedback says it's wrong. Other forums say it's B.
My reasoning:
1) Despite lymphocytic infiltration obviously occurring with type-I DM, I would think that since the beta-cells are destroyed by the immune system, it would be APOPTOSIS, not necrosis. Since when are the cells necrotic? That just seemed wrong. I would think we'd get CD8+ induced apoptosis secondary to glutamic acid decarboxylase being displayed on MHC-I, either that or auto-antibodies merely binding the GAD.
2) The other thing is that I believe having heard/read somewhere that glucose levels don't actually begin to elevate until somewhere around 90% of the islet cells are already destroyed. So for this kid to already be in DKA means that his beta-cells have to already virtually be gone, so I'd think the lymphocytic infiltrative phase is long-passed. If they asked about what process "gave rise" to his current Sx, that's totally different.
3) Final sentence of the question says, "which of the following findings in islet cells would now be most likely?" This implies that they are acknowledging the chronology of the beta-cell degradation, such that lymphocytic infiltration with APOPTOSIS had occurred early, but NOW fibrosis and atrophy have ensued, with the atrophy occurring secondary to exhaustive hypertrophy.
----------
Please help.............
BS question quite frankly.
Last edited:
