lots of talking about salt

Yesterday we talked about approach to diagnosis of Hyponatremia

See the previous post on this : HERE

Also: take a lot at a review on hyponatremia.

Its important to note that volume depletion should results in HYPERnatremia. Hypovolemic hyponatremia is a result of replacing your loss with hypo-osmolar fluid (ie water or juice)

A special thanks to Dr. Amna Ahmed for reviewing the treatment of hyponatremia this morning as well as discussing HYPERnatremia.

HERE is a review on hypernatremia.

Acetaminophen TOX

Today we talked about a case from the weekend who was admitted with overdose of tylenol and effexor.

At time of presentations, there were not acute symptoms of an OD, but after being admitted the patients liver enzymes dramatically increased to >6000 and INR rose to 3.8.

When liver enzymes are over 1000, always consider tylenol as one of the causes (the others include shock liver, autoimmune, viral hepatitis, and wilsons- although wilsons typically a chronic problem)

Acetaminophen pathway requires glutathione for  the toxic metabolite (napq) to be metabolized. When glutathione runs out you are left with liver toxicity. NAC repeats it.

See this article for a good summary of acetaminophen pathway and treatment.

At presentation: high risk features include: pH <7.3. As well, elevated INR, encephaolopaty, Cr>300, high bili and  hypoglycaemia are predictors of fulminent liver failure.

another cause of hypercalcemia

Welcome new clerks!!

I hope you will have a chance to look at the attachments here to complement your exposure at the hospial.


We started off this week with a case of serious hypercalcemia (3.78!!, normal albumin)  that was managed with fluids, pamidronate, calcitriol .. and was still high in the morning.
See the previous post on hypercalcemia HERE.

Along with the : CALCIUM,
there was RENAL FAILURE, ANEMIA, BONY PAIN.
thus very suggestive of Multiple myeloma. 

Multiple Myeloma is a hematologic malignancy that arises from a single clone of plasma cells producing a monoclonal immunoglobulin (usually IgG or IgA). 

A lot of the clinical features arise from the proliferation of these cells, and the immunoglobulins which are released.

Renal disease: there are MANY causes such as: 1) light chain or cast nephropathy,  2)amyloidosis, 3)light chain deposition disease, 4)Fanconi’s syndrome (proximal tubular dysfunction), and 5)hypercalcemia with acute renal failure. Less commonly, one might see 6)heavy chain deposition disease, 7)cryoglobulinemia, 8)uric acid nephropathy and 9)renal plasma cell invasion.

Anemia:  due to plasma cells proliferating, displacing the normal bone marrow. 

Bone Pain: secondary to lytic lesions or pathologic fractures. (increased osteoclast and decreased osteoblast activity because of cytokine RANKL)

Recurrent Infection: secondary to hypogammaglobulinemia and impaired plasma cell function. (most commonly: Pneumonia and pyelonephritis)

For more information, here is a Review on MM.

a very high TSH

Friday morning we chatted about an elderly patient who presented with hallucinations and was found to have a very high TSH (98).

In hypo and hyperthyroidism it is important to consider that elderly patients may have atypical or apathetic presentations so TSH should be ordered because thyroid disorders are systemic and often have very non specific symptoms

For a good article on thyroid related emergencies see my previous post.

Here is an odd cause of severe hypothyroidism and myxedema coma

Here is a prospective study on the starting dose for treating hypothyroidism. These results — plus common sense — suggest that slow titration probably is unnecessary for young healthy patients but is prudent for older patients or those at risk for coronary ischemia.

hemoptysis

I would like to thank our special guest Dr. Jade Coyne for teaching MR today about hemoptysis.

Here is a guide to managing massiv hemoptysis.

See you tomorrow.

etoh withdrawal

Hope everyone had a nice long weekend.




We started off the short week talking about alcohol withdrawal.




There are key clinical manifestations that depend on timing since last drink:

Early: (6-36h)
"Minor" - headache, diaphoresis, tachycardia, nausea/vomiting

Seizures can occur early (even with high ETOH levels)--->this is not a good sign
(remember etoh seizure are NOT focal, if recur -its within 6 hours, short, self resolving with minimal post ictal)

12-24h:
hallucinations

48-96h
Delerium tremen (all of the above PLUS autonomic instability-fever, HTN, tachy)


TREATMENT:
Benzo (long acting)
Vitamins
Supportive care

Here is a link to NEJM article outline withdrawal.

hypertensive urgency

Today we talked about a case of hypertensive URGENCY.

We reviewed sthe differnence of Urgency (no end organ damage, should lower soon) vs Emergency (end organ damage present-->must lower soon now)

In general, aim for a decrease in MAP (not SBP) by no more than 20-25% within 2 hours, or a DBP brought down to 110ish. 

EXCEPTIONS: stroke- less rapid lowering; dissection- more rapid lowering

HERE is a good resource for management from CHEST.

Have a lovely long weekend!

A