Category Archives: Endo

The Menstrual Cycle

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The menstrual cycle. What more of a classic drawing can you get? Though it has been done a million times over, here’s the Sketchy Medicine version of the classic hormonal interplay that allows for the endometrial lining to build up, shed, build up, shed, build up, shed…

The nice thing is the the pituitary hormones are aptly named so that FSH (follicle stimulating hormone) stimulates the follicle to grow and LH (luteinizing hormone) causes ovulation (the infamous LH surge) and subsequent corpus luteum development.

Meanwhile the developing follicle secretes estradiol which stimulates the proliferative phase of the cycle. Then the corpus luteum secretes estradiol and progesterone to kick things into high gear for the secretory phase.

You can now passively study this all the time (and keep your own notes) on a notebook or a mug. Nothing says “mmm, coffee” like the hormonal phases of the female reproductive system.

Calcium homeostasis, parathyroid and vitamin D

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Calcium homeostasis is largely controlled by the parathyroid glands (tucked away underneath the thyroid). I’ve included a little bit of the vitamin D synthesis pathway as well, though D3 (the form that is absorbed in the intestines) is also synthesized in the skin as long as you’re getting a little bit of sunlight.

Hypercalcemia

  1. Hyperparathyroidism: usually an adenoma
  2. Malignancy: PTH-related peptide released by tumor (squamous cell, renal, breast, bladder)
  3. Vitamin D excess: granulomas (sarcoidosis, TB, Wegener’s)
  4. Increased bone turnover: hyperthyroidism, Paget’s
  5. Familial hypocalcuric hypercalcemia: mutation in the calcium-sensing receptor in parathyroid and kidney

Hypocalcemia

  1. Hypoparathyroidism: sporadic, caused by thyroid surgery, Wilson’s, hypomagnesemia
  2. Pseudo-Hypoparathyroidism: PTH end-organ resistance
  3. Vitamin D deficiency: no sunlight, GI disease
  4. Chronic renal failure: decreased 1,25(OH)D production, increased phosphate
  5. Calcium sequestration: acute phosphate increase

Insulin Regimens and Dosing

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Insulin dosing has to be one of the most (seemingly) unnecessarily complicated dosings in medicine. Not only are there 4 ways to dose it (BID, QID with rapid, QID with fast, QID with extended-release) there are three different companies, all naming their insulins slightly differently. But how can you remember whether to give Humalog, Humulin N, Humulin R, NovoRapid, Novolin Toronto, NPH, Lantus, or some combination of the above?

This is a master illustration to help organize insulin dosing and amounts.

Total Daily Dose

0.3 – 0.6 units/kg
Start low, titrate up

BID (conventional therapy)

2/3 : 1/3 rule
2/3 breakfast : 1/3 supper
2/3 long : 1/3 fast

QID (with either Rapid or Fast-acting and either long or extended)

Breakfast: 20-25% long, 15-20% rapid
Lunch: 15-20% rapid
Supper: 15-20% rapid
Bedtime: 25-30% long

Thyroid hormone differential

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As with all of the pituitary axises, the thyroid one is a little confusing when people talk about it but really quite simple when it’s drawn out.

Hypothalamus -> Pituitary -> TSH -> Thyroid -> T4 & T3

Free T4 is what normally gets measured to determine if someone is hypo- or hyperthyroid, but if you are just doing a basic screening test, you only need to measure TSH.

In the image, black represents the gland not functioning, while red is it going wild and crazy. remember that primary is the END ORGAND (in this case the thyroid).

Things in flux simply means that you’ve measured someone’s levels while things were in the midst of a change. This is because T3 and T4 levels can change fairly quickly, but it takes a while for the pituitary to catch up. This can happen either in the case of one of the glands ceasing to function or the person has recently started medication to correct thyroid hormone levels and the thyroid has changed but the pituitary hasn’t.