HY lecture notes:
If USMLE asks you how to decrease risk of type II diabetes mellitus the most – low-carbohydrate diet or low-calorie diet – what’s the answer? –> Low-calorie diet is correct. High BMI is the risk factor is why.
Diabetes insipidus –> low urine osmolality + high serum sodium.
Central –> decreased ADH (can be due to head trauma); Tx with desmopressin.
Nephrogenic –> decreased sensitivity of the kidney to ADH (ADH levels are high in the blood); can be due to lithium, demeclocycline, hypercalcemia; Tx with NSAID + thiazide diuretic. The NSAID will decrease renal blood flow by inhibiting prostaglandin synthesis (decreased opportunity for filtration by the kidney, so less chance for fluid loss); for the thiazide, the distal Na loss will cause the PCT to compensate by increasing Na reabsorption, and water follows sodium — less fluid loss overall compared to not being on the diuretic; in someone who doesn’t have DI, the thiazide will of course cause net fluid loss, not retention.
In states of severe dehydration and shock, lactic acidosis can be seen –> decreased oxygen delivery –> increased anaerobic respiration at tissues –> increased lactic acid –> decreased serum bicarb. Not just limited to DI, but any type of shock on the USMLE (hypovolemic, septic, cardiogenic, etc.), you can get low bicarb, and the reason is frequently lactic acidosis for this reason. This is really HY on 2CK in particular.
SIADH –> high urine osmolality + low serum sodium.
Classically caused by small cell lung cancer ectopic ADH secretion; can also be caused by head trauma (similar to central DI).
Cannot do surgery for small cell lung cancer; chemotherapy (treating underlying condition) may help; otherwise ADH receptor antagonists such as conivaptan and tolvaptan can be used.
Psychogenic polydipsia –> low urine osmolality + low serum sodium
Person is drinking too much.
For SIADH, DI, and PP, fluid restriction is done as the first step in diagnosis – i.e., see how their urine + serum change when you withhold fluid.
In DI, fluid restriction won’t cause a decrease in urinary output; the patient will still be polyuric + serum sodium will stay elevated.
In SIADH, fluid restriction won’t cause serum sodium to go – i.e., ADH remains elevated, so excess free water reabsorption persists.
In PP, the patient is physiologically normal, so fluid restriction will both decrease urinary output as well as increase serum sodium.
Addison disease = primary hypoadrenalism –> adrenal cortex is unable to adequately make aldosterone AND cortisol (both are low).
High ACTH + hyperpigmentation (low cortisol –> decreased negative feedback at hypothalamus + anterior pituitary –> increased POMC, which is the precursor to both ACTH and alpha-MSH –> the latter causes hyperpigmentation) + high potassium + low sodium + low bicarb + low pH.
Therefore Addison = high potassium + low sodium + low bicarb + low pH in a patient with high ACTH and hyperpigmentation.
Aldosterone normally reabsorbs sodium in the cortical collecting duct and secretes potassium and protons; so low aldosterone –> high potassium + low sodium + low bicarb + low pH.
Low cortisol causes chronic fatigue syndrome.
The combination of low cortisol + low aldosterone –> low blood pressure in fatigued patient.
Diagnose Addison with ACTH stimulation test –> patient will already have been measured to have high ACTH; if we give more ACTH (exogenous ACTH) and cortisol fails to rise appreciably, a Dx of Addison is made.
Treat with fludrocortisone (very similar to aldosterone structurally, but also takes care of low cortisol).
Waterhouse friderichsen syndrome may be a cause of Addison –> meningococcal septicemia followed by bilateral hemorrhagic infarction of the adrenal cortices. After giving normal saline for the low BP, must give hydrocortisone to compensate for the low cortisol.
Cortisol normally helps maintain blood pressure by upregulating alpha-1 receptor expression on arterioles –> permits norepinephrine + epinephrine to bind and constrict the vasculature –> if low cortisol, then NE + E simply can’t do their job and BP is low.
Secondary hypoadrenalism –> caused by low ACTH –> only cortisol is low; aldosterone is normal or elevated.
Because ACTH is low, there’s no hyperpigmentation (POMC is also low because the anterior pituitary lacks synthesis capacity).
In secondary hypoadrenalism, the adrenal gland itself is functioning fine (i.e., there’s nothing wrong with the actual adrenal parenchyma; the problem is merely ACTH isn’t there to stimulate it), aldosterone will be normal or slightly elevated because RAAS is still intact.
This means potassium is not elevated like it is in Addison. And if aldosterone is elevated, it’s not at the level where potassium secretion is in excess; there’s merely an increased basal secretion (i.e., you won’t get full-blown hypersecretion causing hypokalemia; the emphasis is merely that one’s baseline aldosterone would be slightly increased).
I make this point because there’s an NBME Q for Step 1 where, in Sheehan syndrome, the arrows they wanted were ↓ prolactin, ↓ TSH, ↓ ACTH, and ↑ aldosterone. Sheehan syndrome is ischemic infarction of the anterior pituitary following postpartum hemorrhage, where there is pan-hyposecretion by the anterior pituitary.
So for secondary, potassium is normal, sodium is normal, bicarb is normal, pH is normal in a patient with low ACTH and no hyperpigmentation.
Tx with hydrocortisone. Fludrocortisone isn’t needed because aldosterone is intact.
In patients with adrenal insufficiency, they cannot mount a stress response (i.e., they cannot secrete cortisol in response to trauma, surgery, illness, etc.) and can experience hypotensive episodes. After giving fluids, give hydrocortisone (same as we talked about above for WFS).
USMLE also wants you to be aware that “autoimmune diseases go together.” Meaning, if the vignette is hinting at a presentation like Addison disease, they might also throw in that the patient has a history of autoimmune thyroiditis, or has a sibling who has rheumatoid arthritis, etc.
