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.
Just like everybody knows that Andrew Garfield is the best-looking Spider-Man ever, everybody knows what PTH does.
Obviously! Your local supermarket worker knows it! Your angry ex-partner who’s now filing for asset claims from you knows it! The door-knocking salesperson you try to hide from by pretending you’re not at home when they try to pester you knows it!
Parathyroid hormone, affectionately referred to as PTH, is renowned for its action of freeing calcium from bones. But does it do this through osteoclasts directly? After all, osteoclasts eat bone and osteoblasts build bone.
The answer is…
No.
NO.
NO!
PTH indirectly stimulates osteoclasts to resorb bone. Mind-blowingly, it does this through osteoblasts.
Let’s learn about a good friend: ACE inhibitors!
Renin (from those pesky organs called kidneys) turns angiotensinogen (also known as renin substrate) into angiotensin I.
ACE (whose full title is angiotensin-converting enzyme) turns angiotensin I into angiotensin II.
Angiotensin II has numerous magical properties: vasoconstriction, stimulating aldosterone release and more…so magical!
Angiotensin II normally clears bradykinin. When ACE inhibitors block that, bradykinin builds up and makes the person cough.
Aldosterone retains sodium and kicks out potassium. Take that, distal kidney parts! That’s where it acts.
Spironolactone, a medication well-known for its alluring gynaecomastia properties, is an aldosterone antagonist. It’s a potassium-sparing diuretic, which means it helps pass more urine without destroying the person’s blood potassium level to low, low amounts.
Let’s return to aldosterone itself, however. Aldosterone is like a vindictive, electrolyte-discriminating landlord that takes in sodium but evicts potassium from the rental property. It’s the excessively muscly security guard who stops that drunken, disorderly potassium from trying to enter the blood club.
Given the above, inhibition of aldosterone causes the opposite of its normal effects: not ejecting as much potassium from the system. Too much potassium is in the nightclub of your blood! That means hyperkalaemia!
Therefore, anything that stops the triggering of aldosterone creates a risk of hyperkalaemia.
But an ACE inhibitor stops angiotensin II from being formed! And that indirectly reduces the triggering of aldosterone that otherwise would have occurred! Hyperkalaemia might ensue! Chaos everywhere!
That explains one of the potential side effects of ACE inhibitors.
If an ACE inhibitor triggers this, the patient can be switched to an ARB, which is an angiotensin II receptor blocker. It achieves a similar effect without as much risk of the side effects of ACE inhibitors.
Well, well, well, ACE inhibitors. We’ve figured you out now!
Milk is famous because it comes from animal breasts and is widely touted as a source of calcium.
In the body, calcium is primarily stored in bones and teeth, because it’s good to have a regulated amount circulating in the blood. You know, to avoid things going wrong.
Hypercalcaemia means too much calcium in the blood.
Parathyroid hormone (PTH) is a substance released from the parathyroid glands, which are 4 tiny structures located behind the thyroid gland.
Let’s analyse this, like language-obsessed…language obsessors. Real poetic, yes.
Para: beside.
Thyroid: thyroid.
Gland: a bunch of cells that collectively secretes things.
Yet another medical acronym!
Why is PTH important?
Because PTH liberates calcium from bones into blood.
In political terms, PTH is the Joan Of Arc freeing the oppressed French calcium from the English occupation of bone.
But if there’s too much or too little PTH, the blood calcium level can be thrown off.
And yes, if your PTH is burnt at the stake, things will also not be good.
More PTH ==> more calcium release from bones ==> blood calcium level goes up.
Less PTH ==> less calcium release from bones ==> blood calcium level goes down.
What are the ways in which blood calcium levels can be elevated? There are 2 main ones.
Fake PTH
Most commonly, some cancers involve the release of PTH-related protein, a substance similar to PTH that isn’t PTH.
On investigation, endogenous PTH will be low, due to endocrine suppression. From blood tests, expect high PTH-related protein and low actual PTH; your body thinks there is enough PTH around, so it stops making as much. The fake PTH isn’t measurable according to normal PTH tests.
Real PTH
More uncommonly, a cancer can abnormally make its own PTH.
On investigation, endogenous PTH will be high, due to excessive production. Your parathyroids again stop making PTH because there’s too much already, but the extra PTH is measurable in blood because it’s actual PTH…even if it doesn’t come from the right place.
Bones
If cancer spreads to bone, it can induce calcium release that way. The blood calcium level goes up.
Intestines
Cancer can make extra vitamin D, a substance that normally encourages intestinal calcium absorption.
If too much calcium is absorbed from the intestines, the blood calcium level rises.
