Classification and causes of hyponatremia mnemonics + notes

Hi!

Classification and causes of hyponatremia mnemonics + notes:

1. Hyponatremia with low osmolality :

     (i) reduced effective blood volume

              (A) increased ECF volume -

                               - Edematous kidney (nephrotic syndrome)

                               - Cirrhosis of liver

                               - Failure of heart

              (B) REduced ECF volume -

                                - Renal loss of Na ( Diuretics, Ketonuria, Addison's disease)

                                - Extrarenal loss of Na ( sweating, diarrhea, vomiting, peritonitis, pancreatitis)

    (ii) Normal/ increased EBV

                - Inadequate ADH syndrome

                - Constant thirst

                - Renal failure (chronic)

2. Hyponatremia with raised osmolality :

( H & M)

- Hyperglycemia 

- Mannitol administration 

Note -

- Hyponatremia per se does not produce any significant clinical features. The low osmolality that it causes is responsible for various features.

- Slow correction of hypotonicity produces gradual rise in osmolality without any significant risk. But rapid correction of hyponatremia produces loss of brain water resulting in brain damage!

- The rate of correction should be around 0.6 mEq/L/hr. In severely symptomatic patients, total correction in a day should not exceed 8-10 mEq/L/hr.

That's all

Hope it helps

- Jaskunwar Singh

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Hello friends, Let's talk about Aurora kinases today.... Aurora sounds so beautiful, right ?

Aurora kinases represent serine threonine kinases with instrumental role in cell division.

Specifically, Aurora kinase A is required for duplication and separation of centromere, and Aurora B is required for attachment of microtubules to centromere.

They are often over expressed in tumors resulting in defective cytokinesis during cell division, eventually causing aneuploidy and driving the carcinogenesis.

Now, it really gets interesting; usually when functioning of microtubules are perturbed say by paclitaxel, then spindle check point inhibitor is activated leading to cell demise by upregulation of P53, PUMA and other mediators.

But in case of Aurora kinase inhibition, cells keep on dividing especially in case of P53 mutated cells. Since centromeres will not segregate, it ultimately leads to tetraploid genome and four centromeres in a cell, causing catastrophic mitosis in subsequent cell cycle effectively tearing apart the genome.

They are significant because often when other tyrosine kinase inhibitors targeting EGFR, VEGFR, FGFR are used, tumors over express Aurora kinases, there by over riding the inhibition mediated by tyrosine kinase inhibitors.... So targeting them is key to maintain remission in patients already on kinase inhibitors.

Few examples of drugs in trials: Monastrol, Hesperidin.

It's called Aurora because of the similarity between the appearance of microtubule spindles during cell division and Aurora Borealis.

Pretty Majestic, right?

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What does cryoprecipitate contain? 
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