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yb_26
I also picked decreased inhibin.
may be it was one of the "experimental questions", which are not even counted on the real exam
+ 2019-07-17T04:06:24Z
artist90
Inceased FSH will lead to spermatogenesis and spermiogenesis NOT Increase in Testosterone which is causing increased Height of this pt
+1 2019-07-18T11:15:19Z
artist90
Inhibin B only has negative feeback on FSH not GnRH. see the diagram on the topic of semineferous tubules in FA. Testosterone has a negative feedback on BOTH LH and GnRH
+1 2019-07-18T11:52:13Z
usmile1
Kind of like how nocturnal pulsatile GNRH release occurs during sleep to stimulate growth (FA page327), the same thing happens for puberty. Pg 325 in FA, "pulsatile GnRH leads to puberty and fertility." It doesn't explicitly state during sleep, but pulsatile release of GnRH leading to pulsatile release of LH and FSH will lead to puberty. Puberty starts in the brain, its onset really has nothing to do with decreased inhibin levels which happens in the testes. hope that makes sense!
+ 2019-09-04T17:18:28Z
yb_26
I also picked decreased inhibin.
may be it was one of the "experimental questions", which are not even counted on the real exam
+ 2019-07-17T04:06:24Z
artist90
Inceased FSH will lead to spermatogenesis and spermiogenesis NOT Increase in Testosterone which is causing increased Height of this pt
+1 2019-07-18T11:15:19Z
artist90
Inhibin B only has negative feeback on FSH not GnRH. see the diagram on the topic of semineferous tubules in FA. Testosterone has a negative feedback on BOTH LH and GnRH
+1 2019-07-18T11:52:13Z
usmile1
Kind of like how nocturnal pulsatile GNRH release occurs during sleep to stimulate growth (FA page327), the same thing happens for puberty. Pg 325 in FA, "pulsatile GnRH leads to puberty and fertility." It doesn't explicitly state during sleep, but pulsatile release of GnRH leading to pulsatile release of LH and FSH will lead to puberty. Puberty starts in the brain, its onset really has nothing to do with decreased inhibin levels which happens in the testes. hope that makes sense!
+ 2019-09-04T17:18:28Z
artist90
VEINS: 1-Intercostal veins drain into Azygous vein which drains into SVC BUT some blood from this Azygous vein is also draining into BATSONS VERTEBRAL VENOUS PLEXUS how the breast cancer metastasizes to vertebral column.
2-Internal thoracic(mammary) vein drains directly into Brachiocephalic vein.
3-Lateral thoracic vein drains into Axillary vein which drains into Subclavian vein which drains into Brachiocephalic vein.
ARTERIES ARE DIFFERENT:
Subclavian artery----branches into---Internal thoracic(mammary) artery---Intercostal arteries. Internal thoracic artey is used for CABG if there is 1 vessel block.
+5 2019-07-17T14:22:56Z
lsmarshall
Summary of metabolic issues relating to hyperammonemia
+3 2019-05-28T21:34:34Z
seagull
i'm leaning towards Ornithine transcarbamylase deficiency.
+2 2019-06-08T00:35:27Z
notadoctor
Not sure why this isn't considered a mitochondrial disorder since the issue is Ornithine transcarbamylase deficiency in the mitochondria?
+1 2019-06-23T00:48:30Z
charcot_bouchard
if it was mitochondrial disorder no one would escape
+1 2019-06-26T06:52:30Z
wowo
figure in OTC deficiency, they might have to explicitly mention the orotic aciduria AND typically presents earlier, around 24-48hrs of life after they've fed (at least per BB)
+ also per BB, propionic acidemia and MM acidemia have an onset of weeks to months and lead to build up of organic acids --> acidemia in addition to hyperammonemia (not sure why, but several aa enter the TCA cycle via propionyl CoA --> methylmalonyl CoA --> succinyl CoA, but now this is defunct d/t enzyme deficiencies...?). Anywho, propionic acidemia described on FA2019 p85, but doesn't list hyperammonemia
+1 2019-06-27T23:57:23Z
artist90
i think it cannot be Ornithine transcarbamylase deficiency bc it is XR disease. this pt has a healthy 2yr old brother which rules out X-linked recessive disease correct me if i m wrong
+ 2019-07-16T15:40:09Z
artist90
it is 100% Propionic acidemia Uworld Q-id: 1340. it is an exact copy question of uworld. i got it wrong bc i forgot these are organic acids. But i am still confused on 2 things
1-how does acidosis cause Hypoglycemia and Ketosis.
2-why is Ammonia elevated in these pts bc urea cycle will be fine?
+ 2019-07-16T16:12:29Z
yb_26
1) hyperammonemia is seen in all urea cycle disorders except arginase deficiency
2) organic acids directly inhibit urea cycle => hyperammonemia (from UWorld)
+ 2019-07-20T21:37:15Z
yex
According to UW, there is another question # 1341. This one refers to methylmalonic acidemia (ORGANIC ACIDEMIA). HYPOGLYCEMIA results from overall increased metabolic rate leading to increased glucose utilization and direct toxic (-) of gluconeogenesis by organic acids. The presence of hypoglycemia leads to increased free fatty acid metabolism that produces KETONES, resulting in a further anion gap met acidocis. Finally, organic acids also directly (-) the urea cycle, leading to HYPERAMMONEMIA.
+5 2019-08-23T03:05:27Z
lsmarshall
Summary of metabolic issues relating to hyperammonemia
+3 2019-05-28T21:34:34Z
seagull
i'm leaning towards Ornithine transcarbamylase deficiency.
+2 2019-06-08T00:35:27Z
notadoctor
Not sure why this isn't considered a mitochondrial disorder since the issue is Ornithine transcarbamylase deficiency in the mitochondria?
+1 2019-06-23T00:48:30Z
charcot_bouchard
if it was mitochondrial disorder no one would escape
+1 2019-06-26T06:52:30Z
wowo
figure in OTC deficiency, they might have to explicitly mention the orotic aciduria AND typically presents earlier, around 24-48hrs of life after they've fed (at least per BB)
+ also per BB, propionic acidemia and MM acidemia have an onset of weeks to months and lead to build up of organic acids --> acidemia in addition to hyperammonemia (not sure why, but several aa enter the TCA cycle via propionyl CoA --> methylmalonyl CoA --> succinyl CoA, but now this is defunct d/t enzyme deficiencies...?). Anywho, propionic acidemia described on FA2019 p85, but doesn't list hyperammonemia
+1 2019-06-27T23:57:23Z
artist90
i think it cannot be Ornithine transcarbamylase deficiency bc it is XR disease. this pt has a healthy 2yr old brother which rules out X-linked recessive disease correct me if i m wrong
+ 2019-07-16T15:40:09Z
artist90
it is 100% Propionic acidemia Uworld Q-id: 1340. it is an exact copy question of uworld. i got it wrong bc i forgot these are organic acids. But i am still confused on 2 things
1-how does acidosis cause Hypoglycemia and Ketosis.
2-why is Ammonia elevated in these pts bc urea cycle will be fine?
+ 2019-07-16T16:12:29Z
yb_26
1) hyperammonemia is seen in all urea cycle disorders except arginase deficiency
2) organic acids directly inhibit urea cycle => hyperammonemia (from UWorld)
+ 2019-07-20T21:37:15Z
yex
According to UW, there is another question # 1341. This one refers to methylmalonic acidemia (ORGANIC ACIDEMIA). HYPOGLYCEMIA results from overall increased metabolic rate leading to increased glucose utilization and direct toxic (-) of gluconeogenesis by organic acids. The presence of hypoglycemia leads to increased free fatty acid metabolism that produces KETONES, resulting in a further anion gap met acidocis. Finally, organic acids also directly (-) the urea cycle, leading to HYPERAMMONEMIA.
+5 2019-08-23T03:05:27Z
mousie
http://www.sparknotes.com/biology/cellreproduction/cellcycle/section3/page/2/
+2 2019-06-02T17:59:14Z
fahmed14
Cyclins help regulate cell cycle phases. They help with checkpoints before progression to the next phase of a cell cycle. Therefore the checkpoint before mitosis would be in G2 and probably where mitotic specific cyclins are synthesized
+5 2019-06-16T19:43:17Z
shayan
if its a metaplasia, then how it be normal ? I mean Metaplasia is not normal?
+ 2019-07-15T15:26:50Z
artist90
i got it confused bc the question stated that there was a mass in one lobe of lung and i didn't knew that squamous metaplasia also presents as a mass in lung. i missed that on biopsy they were clearly stating squamous metaplasia.
+3 2019-07-16T12:24:43Z
Does anyone have a good explanation for why decreased levels of inhibin is wrong? From my understanding, inhibin and activin work together, in that inhibin binds and blocks activin leading to decreased feedback on hypothalamus and activin increases FSH and GnRH production.. thus, if you decrease inhibin then you would have increased activin which would lead to increased GnRH and FSH, right? I found one article talking about it in regards to puberty, but it seems to be a hypothesis/not confirmed at this point... is that why? But still... how do I rule it out on a test?