Do the following things, in this order of priority.
A simple acronym solves everything. The point is not to let the patient DIE.
Behold! It is 500-1000g annually.
If you want to change your future for the better: sleep enough, eat healthy food and don’t be a sloth.
And maybe fidget to burn more energy, so you can eat more food.
Food is great.
Bras haven’t been proven to be useful. One argument is that it’s more of a personal preference or even a fashion statement.
There isn’t much research on this front. But based on the limited evidence out there, bras are more likely to be harmful if they’re the wrong fit. The nudists win again.
DKA can lead to AKI.
DKA can lead to lactic acidosis, which can be associated with thiamine deficiency.
Thiamine deficiency less commonly involves vomiting, which can stain clothing. The nudists win again.
Lipase is more specific for pancreatic disorders than amylase.
Lipase has a p in it. So does pancreas.
Amylase has nothing.
It’s magic!
The hypothalamus releases GnRH.
This stimulates the anterior pituitary gland to release FSH and LH, which act on the testes.
FSH triggers spermatogenesis from Sertoli cells.
LH triggers testosterone production from Leydig cells.
To control things for homeostasis, Sertoli cells release inhibin to dampen the release of FSH and LH from the anterior pituitary gland.
Testosterone gives negative feedback to the anterior pituitary gland and the hypothalamus.
Breast cancer can be oestrogen-sensitive, so a treatment target for such types is to inhibit oestrogen.
In premenopausal women, selective oestrogen receptor modulators, more conveniently called SERMs, include tamoxifen. This particular medication acts as an oestrogen receptor antagonist at the breast but an oestrogen receptor agonist at the uterus, which is why it minority increases the risk of endometrial cancer.
In postmenopausal women, aromatase inhibitors are an option. These interrupt the production of oestrogen by suppressing the action of the enzyme aromatase. Anastrazole and letrozole are the names to know here; they’re non-steroidal, reversible binders of aromatase from the third generation of aromatase inhibitors.
Why are aromatase inhibitors less effective in premenopausal women? Premenopausal women have a large quantity of aromatase in the ovary. Note that ovarian aromatase is sensitive to changes in the gonadotropin LH, which is produced by the pituitary gland. If aromatase is suppressed with an aromatase inhibitor, gonadotropins increase in response, according to the usual feedback pattern, which stimulates more ovarian aromatase. This makes aromatase inhibitors less proficient at inhibiting oestrogen production in the ovary in such a group.
Diabetes mellitus is a disease of not enough insulin. It’s a story of pancreatic insufficiency when it comes to insulin.
In Type 1, there’s no insulin produced. This is an absolute insulin deficiency.
In Type 2, the gradually failing pancreas doesn’t produce enough insulin to meet the body’s increased requirements; in certain people, the body is a needy thing that becomes less and less sensitive to insulin over time, so more is needed of it. This is a relative insulin deficiency.
If diabetic ketoacidosis is a crisis characterised by a lack of insulin, why is it that both intravenous glucose and insulin are part of the treatment?
This is because DKA has two big issues:
Treatment with insulin corrects both of these. However, the hyperglycaemia resolves first. IV glucose gives more time to allow the insulin to keep suppressing ketones, thus addressing the acidosis as well.
