Instead of having a number of separate posts, I’m going to answer three questions here

I am a little bit overwhelmed seeing the additional 31 page document that requires memorizing several new concepts including a multi-step equation problem to calculate IV fluid orders. Would these equations be provided to us on the TBL tomorrow? Is this more of a prep for how your material will be tested on the final exam? 

No need to memorize any equations, all equations that you need for the TBL will be provided to you. Same with the exam for the renal section.

I very much enjoyed your lecture on renal disorders, and wanted to clarify some confusion I had about Tea and Toast syndrome.

This is where my head is at:

Low solute load leads to decreased medullary interstitium gradient, which makes it more difficult for water to be reabsorbed (against said gradient) effectively.

This is where I need clarification:

I believe urine output is low in this condition, but I am having trouble with the cause-and-effect system, given that you said ADH is low. I am wondering if the kidneys are actively reabsorbing water to prevent excess water loss, or if they are actively trying to concentrate the urine. My assumption would be that reabsorbing more water would contribute to further hyponatremia by dilution.

Tea and toast syndrome

Yes the kidney is unable to make the large quantity of low osmolar urine it needs to correct the hyponatremia. In most cases of hyponatremia this is because of pesky ADH, but in tea and toast ADH is appropriately suppressed. But the kidney only makes a small amount of dilute urine due to lack of solute. 

Urine osmolality can only drop to a minimum of 50 mmol/l (higher in an aging or damaged kidney). So if the patient is only eating 100 mmol of solute a day (tea and toast) then the maximum urine volume would be 2 liters.

Does this make sense?

The medullary interstitial is irrelevant because, in the absence of ADH, the tubules are locked and the tubular fluid is never exposed to that osmotic temptation. 

last question

I have a question regarding the cause for the release of ADH in Hypervolemic Hyponatremia. I understand how in Hypovolemic Hyponatremia there is a release of ADH to allow for water reabsorption which helps to improve the decrease in volume (please correct me if that is incorrect),

Nailed it

but I do not understand why in Hypervolemic Hyponatremia there is release of ADH.

So I mention in the lecture that ADH has two masters, one is osmolality, increased serum osmolality stimulates ADH. This is operational in true hyponatremia since these patients have decreased osmolality. The other master is perfusion. In hypervolemia, think about heart failure, there is decreased perfusion of the baroreceptors of the kidney and aortic arch. This triggers a release of ADH. When ADH binds to V1 receptors in the vasculature it causes vasoconstriction (hence the other name for ADH, vasopressin), increasing blood pressure and improving perfusion (or at least this is what it hopes to do). When ADH hits the V2 receptors in the medullary collecting (and cortical) collecting duct it will trigger an increase in water reabsorption (through the insertion of aquaporin channels into the apical membrane, making the collecting tubule permeable to water).

Is this not exacerbating the excess volume, as increased ADH would cause increased water reabsorption and thus increase volume? 

Yes, this may in fact be a maladaptive response.  However a trial called EVEREST looked at pharmacologically blocking ADH with a drug called tolvaptan and it did not improve heart failure outcomes 😩

Further, is both result in decreased urine output and decreased urine sodium, how are the two differentiated? Are they differentiated simply by their causes?

YES!