Question

This a very important assessment so if you are not sure of the answer please let someone else answer the question, in order for me to understand.

Compare LH production in Alan, Charles, David, Jackson, Robert and Stan.

Bill is most likely suffering from one of two possible genetic mutations that effect his reproductive endocrine system. Describe what the two most likely genetic mutations are that he is suffering from and describe the easiest therapeutic way without genetic testing that you could determine which mutation he is actually suffering from.

As a future reproductive endocrinologist you are working with the following patients: Alan is 45 years of age. His weight and BMI are all ideal for his age. A year ago he was diagnosed with aggressive prostate cancer, and he elected to be castrated. He weigh his body fat content is normal. Bill is a 24 year old. You are trying to diagnose a genetic mutation that he has. He weighs 178 lbs and his body fat content is normal. His testicular volume is very low for his age. Adrenal gland steroidogenesis is normal. His testosterone, estradiol and DHT levels are within in the normal range. Charles is a 23 years old marathon runner with very high adiponectin levels. His daily caloric intake does not meet his daily energy expenditures about 20% of the time. David is a 23 year old steroid abuser that is taking a 100% effective aromatase inhibitor along with hCG. He weighs 185 lbs and his body fat content is normal. Frank is 30 years of age. He has extremely elevated leptin and resistin levels and very low adiponectin levels. Jackson, is 23 years old. He suffers from severe asthma and takes a daily lipoxygenase inhibitor. He weighs 180 pounds and has a body fat content equal to Alan and Bill. Robert is 52 years of age. Feeling that he was losing his edge, a month ago he started applying a GnRH cream to his upper arms that he buys of the internet shop that sells supplements. He has the same BMI and body weight and body fat content as Jackson. Stan is 9 years old and has undiagnosed mutation in his adrenal 21 hydroxylase enzyme. He has started a precocious puberty. His BMI and body fat levels are normal for his age. s 185 lbs and

Answer 1

*Alan is 45 years of age. His weight and BMI are all ideals for his age. A year ago he was diagnosed with aggressive prostate cancer, and he elected to be castrated. He weighs 185lbs and his body fat content is normal,

Here we can see the case is elected for castration that means is nothing but gonadectomy, that means the surgical removal of testicles

. Luteinizing Hormone leads to the production of testosterone by acting on the Leydig cells between the seminiferous tubules, and at the same time induces the synthesis of androgen-binding protein by acting on the Sertoli cells within the seminiferous tubules.. Here there is an imbalance in LH surge and production that results in the increased testosterone production thus results in aggravation of prostate cancer, thus he elected for castration.

*Bill is a 24-year-old. You are trying to diagnose a genetic mutation that he has. He weighs 178lbs and his fat content is normal. His testicular volume is very low for his age. Adrenal gland steroidogenesis is normal. His testosterone, estradiol and DHT levels are within the normal range.

Follicular stimulating hormone receptor mutations

In other FSHR mutations occurred, amino acid 189 alanine is replaced by valine (Ala189Val), but muscularization and testosterone concentrations are as usual; FSH and LH levels are slightly increased,

Androgen and Defects of Androgen Receptors mutation, the mutations that do not draw the expressions of genes in the target cells are sterile in large.

*Charles 23-year-old marathon runner with very high adiponectin levels. His daily caloric intake does not meet his daily energy expenditure about 20% of the time.

Testosterone is a sex hormone that plays important roles in the body. In men, it also helps in maintaining bone mass, fat distribution, muscle mass, and strength A small amount of circulating testosterone is converted to estradiol, a form of estrogen. Here, in this case, his caloric intake does not meet his daily expenditure may be due to the decline in LH production.

*Frank is 30 years of age. He has extremely elevated leptin and resistin levels and very low adiponectin levels

characterized by the metabolic disorders that result in reproductive dysfunction may lead to infertility and variation in LH levels.

*Jackson is 23 years old, he suffers from severe asthma and takes a daily lipoxygenase inhibitor. He weighs 180 pounds and has a body fat content equal to Alan and Bill.

Adipokines, factors produced by adipose tissue, may be proinflammatory (such as leptin and resistin) or anti-inflammatory (such as adiponectin). Effects of these adipokines on the lungs have the potential to evoke or exacerbate asthma.

*Robert is 52 years of age. Feeling that he was losing his edge, a month ago he started applying a GnRH cream to his upper arms that he buys of the internet shop that sells supplements. He has the same BMI and body fat content as Jackson.

Gonadotropin hormone-releasing hormone (GnRH) is the key regulator of the reproductive axis. Its pulsatile secretion determines the pattern of secretion of the gonadotropins follicle stimulating hormone and luteinizing hormone, which then regulates both the endocrine function and gamete maturation in the gonads. I think here the case is having low LH level.

*Stan is 9 years old and has an undiagnosed mutation in his adrenal 21 hydroxylase enzyme. He has started precocious puberty. His BMI and body fat levels are normal for his age

21-hydroxylase deficiency is an inherited disorder that affects the adrenal glands. The adrenal glands are located on top of the kidneys and produce a variety of hormones that regulate many essential functions in the body. In people with a 21-hydroxylase deficiency, the adrenal glands produce excess androgens, which are male sex hormones.

Too much testosterone can lead to precocious puberty and result in infertility and as well as a decrease in the activation of LH