Aside from the very informative jewels of knowledge u simply throw at us during ur vids... i really enjoy watching them..u have an intelligence to be super witty and funny with the most straight face.. love ya❤
Pretty sure that’s a typo by Nbme … should say Costovertebral, nbme don’t know what they talking bout sometimes as well but I bet it’s a typo. Imma email them and ask for my $60 bank back cause I ain’t paying that much dough fo stale bread. Good content as usual Mailman! Always delivering the dope 🔥
I took NBME and this was there. Thank you. Please make a video on gestational diabetic mother giving birth to a big baby and baby goes to hypoglycemia immediately vs 18 hours after delivery. All NBMEs step1 ask tricky questions about mechanism comparing insulin vs glucose etc.
If it's any help, I don't think it's too difficult a topic to explain once you have your basics down: Diabetes = Insulin (deficiency or resistance is irrelevant) cannot uptake glucose in body, leaving the patient with HIGH serum glucose, even in a physiologically hypoglycemic state. Remember that in these questions, it's the mother that has diabetes, not the baby. Surprisingly, this is an easy thing to forget in exam settings. |- Maternal hyperglycemia (while fetus is in utero) --> Glucose crosses the placenta --> fetal hyperglycemia --> Fetal beta-cell hyperplasia -> hyperinsulinemia |- Immediately after birth (umbilical cord cut): Hyperinsulinemia --> Hypoglycemia (more insulin than glucose, all the glucose gets taken up and the body still wants more because there's still free insulin in the bloodstream) + Decreased gluconeogenesis -> body won't produce more glucose to satisfy what the body wants. End result: Immediate hypoglycemia |- 18+ hours after birth: Baby already has beta-cell hyperplasia --> Baby's pancreas will produce and secrete way more insulin than a normal baby --> Hyperinsulinemia. Just like before, insulin>glucose means all the glucose is taken up but body still needs more + Increased insulin = Decreased glucagon --> Decreased gluconeogenesis So now we have a situation where the body needs more glucose but has also shut down any way to generate that glucose endogenously. End result: Hypoglycemia Summary: |- Maternal diabetes leads to elevated glucose in the fetus. Fetus adapts to chronically elevated glucose. All these adaptations work against the fetus once it's birthed. Bonus points (I don’t think I’ve seen these on the NBME): Now that you understood this, you can also plot out the other neonatal complications of gestational diabetes. |- Fetal hyperglycemia and hyperinsulinemia while in utero cause the macrosomia => big body for baby (insulin acts as a growth factor) |- Fetal hyperglycemia and hyperinsulinemia while in utero decreases surfactant production --> NRDS after birth |- High insulin means the fetus is always in an anabolic state. Once the fetal body can't take in any more glucose, the excess glucose will be turned into glycogen. Now the fetus has a bunch of glycogen it won't ever need (because the mother is always hyperglycemic therefore the fetus is always hyperglycemic), so it needs to be kept SOMEWHERE, yet another cause of organomegaly (because macrosomia will also contribute to organomegaly) Glycogen can deposit in the interventricular septum of the heart --> Hypertrophic Cardiomyopathy And if you're thinking "doesn't this sound like Cori disease (T. 3 glycogen storage disease)?" then yeah, it's because this is functionally Cori disease but the fetus doesn't use glycogen debrancher enzyme, not because the fetus doesn't have it. |- The fetus also has increased metabolic demand from always being in an anabolic state. This will lead to hypoxemia in the in utero fetus pretty quickly, to which the body will adapt by increasing erythropoiesis --> Polycythemia |- And since this was constantly asked on my in-house exams, I'll mention it just in case: Hyperglycemia --> Hyperkalemia Fetal hyperglycemia --/ /--> Baby will be born hyperkalemic Once the hypoglycemia kicks in (Again, Insulin>Glucose), insulin results in shifting potassium into the cells, leading to hypokalemia in the baby.
Mehlman HY Repro/Obgyn PDF: mehlmanmedical.com/hy-obgyn-repro
Mehlman HY Renal PDF: mehlmanmedical.com/hy-renal/
Aside from the very informative jewels of knowledge u simply throw at us during ur vids... i really enjoy watching them..u have an intelligence to be super witty and funny with the most straight face.. love ya❤
Only mike makes you get it right and yet still learn so much
Finally you're back at teaching...
Thank you!! 🖐️🖐️
Pretty sure that’s a typo by Nbme … should say Costovertebral, nbme don’t know what they talking bout sometimes as well but I bet it’s a typo. Imma email them and ask for my $60 bank back cause I ain’t paying that much dough fo stale bread.
Good content as usual Mailman! Always delivering the dope 🔥
You might be right
I took NBME and this was there. Thank you.
Please make a video on gestational diabetic mother giving birth to a big baby and baby goes to hypoglycemia immediately vs 18 hours after delivery. All NBMEs step1 ask tricky questions about mechanism comparing insulin vs glucose etc.
If it's any help, I don't think it's too difficult a topic to explain once you have your basics down:
Diabetes = Insulin (deficiency or resistance is irrelevant) cannot uptake glucose in body, leaving the patient with HIGH serum glucose, even in a physiologically hypoglycemic state.
Remember that in these questions, it's the mother that has diabetes, not the baby. Surprisingly, this is an easy thing to forget in exam settings.
|- Maternal hyperglycemia (while fetus is in utero) --> Glucose crosses the placenta --> fetal hyperglycemia --> Fetal beta-cell hyperplasia -> hyperinsulinemia
|- Immediately after birth (umbilical cord cut):
Hyperinsulinemia --> Hypoglycemia (more insulin than glucose, all the glucose gets taken up and the body still wants more because there's still free insulin in the bloodstream) + Decreased gluconeogenesis -> body won't produce more glucose to satisfy what the body wants.
End result: Immediate hypoglycemia
|- 18+ hours after birth:
Baby already has beta-cell hyperplasia --> Baby's pancreas will produce and secrete way more insulin than a normal baby --> Hyperinsulinemia.
Just like before, insulin>glucose means all the glucose is taken up but body still needs more + Increased insulin = Decreased glucagon --> Decreased gluconeogenesis
So now we have a situation where the body needs more glucose but has also shut down any way to generate that glucose endogenously.
End result: Hypoglycemia
Summary:
|- Maternal diabetes leads to elevated glucose in the fetus. Fetus adapts to chronically elevated glucose. All these adaptations work against the fetus once it's birthed.
Bonus points (I don’t think I’ve seen these on the NBME):
Now that you understood this, you can also plot out the other neonatal complications of gestational diabetes.
|- Fetal hyperglycemia and hyperinsulinemia while in utero cause the macrosomia => big body for baby (insulin acts as a growth factor)
|- Fetal hyperglycemia and hyperinsulinemia while in utero decreases surfactant production --> NRDS after birth
|- High insulin means the fetus is always in an anabolic state. Once the fetal body can't take in any more glucose, the excess glucose will be turned into glycogen.
Now the fetus has a bunch of glycogen it won't ever need (because the mother is always hyperglycemic therefore the fetus is always hyperglycemic), so it needs to be kept SOMEWHERE, yet another cause of organomegaly (because macrosomia will also contribute to organomegaly)
Glycogen can deposit in the interventricular septum of the heart --> Hypertrophic Cardiomyopathy
And if you're thinking "doesn't this sound like Cori disease (T. 3 glycogen storage disease)?" then yeah, it's because this is functionally Cori disease but the fetus doesn't use glycogen debrancher enzyme, not because the fetus doesn't have it.
|- The fetus also has increased metabolic demand from always being in an anabolic state. This will lead to hypoxemia in the in utero fetus pretty quickly, to which the body will adapt by increasing erythropoiesis --> Polycythemia
|- And since this was constantly asked on my in-house exams, I'll mention it just in case:
Hyperglycemia --> Hyperkalemia
Fetal hyperglycemia --/ /--> Baby will be born hyperkalemic
Once the hypoglycemia kicks in (Again, Insulin>Glucose), insulin results in shifting potassium into the cells, leading to hypokalemia in the baby.
Amazing ...Pdf pathology ???
The smizeee in the camera between answer choices thoughhh !!
Great,thanks
Arigatou maan I got it right. Gonna go for 80uworld today
Thank you very much.
CLEAN
Ooo daddy