can Gonadotrophs “hyperplasia” rather than hypertrophy?
Yellow nodules (cholesterol deposits) on the achilles tendons have a very high association with Type II familial dyslipidemia, or familial hypercholesterolemia. This is caused most often by a defect in the LDL receptor function. (FA2020 p94)
Yellow nodules (cholesterol deposits) on the achilles tendons have a very high association with Type II familial dyslipidemia, or familial hypercholesterolemia. This is caused most often by a defect in the LDL receptor function. (FA2020 p94)
This woman is showing signs of HELLP syndrome (Hemolysis, elevated liver enzymes, low platelets) [FA2020 p643] HELLP can lead to DIC.
A blood smear will show schistocytes.
HELLP syndrome is a manifestation of severe preeclamspia (hypertension after 20 weeks with either proteinuria or end-organ dysfunction).
Question describes the genetic concept of uniparental disomy ( inheriting both genes/ alleles from one parent )
Most cases of uniparental disomy will give a normal phenotype but in cases when imprinting is involved ( natural silencing of genes ) , abnormalities may occur . * Take for example the two most commonly cited examples of this situation
Prader -Willi and Angelman syndrome
In Prader Willi - normally the gene derived from mother(at that specific locus ) is silenced and it is the paternal allele which is functional. If the paternal gene becomes deleted , all you end up with a is the mothers silenced/nonfunctional allele . Alternatively if both genes are maternally derived ( Uniparental Disomy ) , you end up with 2 nonfunctional/silenced genes
The same thing occurs for angelman just vice-versa
CYP's are highly polymorphic genes, so it's likely that there are 4 different alleles in the 2 parents, making for 4 possible different combinations in the offspring and a 25% chance of each one occurring.
Agreed that the question is a bit nit-picky because it requires you to know that CYP is a polymorphic gene. However you can back into the reasoning by combining 2 ideas: CYP's function is drug metabolism + there is a wide spectrum of how quickly patients metabolize drugs (ie fast, medium, slow acetylators). From there you can make the wide arrange of phenotypes must mean that there is a wide number of alleles.
The way I got this was first based off the MRI, it's definitely not the stomach, as it's no where near the stomach. Going off that, the duodenum comes right off the stomach, leading me to also cross that out. Then from the stem it said LEFT MIDabdominal pain, allowing me to cross out appendix (also no fever) and therefore cecum as well. Only remaining choice you're left with is jejunum!