Therapeutics in Sickle Cell Anemia

Apart from Hydroxyurea, Analgesics and vasodilators like phosphodiesterase inhibitors, certain tantalizing novel drugs have been approved for Sickle cell anemia.... Let's take a closer look at them.

(1) Voxelotor (HbS polymerization inhibitor) binds covalently to N-terminal valine of alpha chain of HbS (around 30% of HbS in individual cell) stabilizing it's oxygenated form and causing left ward shift of dissociation curve without impairing oxygen delivery to tissues.

Consistently reduces hemolysis and viscosity with in 2 weeks of administration... FIRST EVER therapy targeting core defect.

Benign vs Malignant pulmonary calcifications mnemonic

A nice mnemonic to differentiate benign and malignant pulmonary calcifications is:

Malignant calcifications are ***SuPER bad*** :P
S: Spiculated
P: Punctate
E: Eccentric
R: Reticular

I use those 3 starts (***) to remind me of punctate.(vs the other P of Popcorn in the benign lesions)

Bening ones are the rest:
Popcorn, laminated, concentric and diffuse homogeneous

-Murad

NB: these calcification types suggest benign vs malignant lesions and are not diagnostic per se.

Check the other amazing mnemonic by Drashtant in the comments section below  :)

Inferior wall MI treatment mnemonic

Inferior wall MI is different than other MIs . It is associated with sinus bradycardias and AV block.

Lower back pain notes

Hello!

Here are my quick and dirty notes on Low back pain (LBP) mostly seen in ambulatory medicine! I will not be going into evidence-based medicine (EBM) physical examination (PE) findings but I have put a quick note for conditions you can test on PE so you can look them up.

Hepatorenal Syndrome: An Overview

Hello good folks! Let's discuss HepatoRenal Syndrome (HRS) in brief.

Cirrhosis + Ascites + Renal Failure = HRS, after excluding other causes of kidney damage.

How common is HRS?
1 in 10 patients of advanced cirrhosis or acute liver failure develop HRS.

How does HRS happen?
Abnormal haemodynamics, that's how. Pathogen, faulty immune system and mesenteric angiogenesis result in splanchnic and systemic vasodilation but renal vasoconstriction. Other factors maybe contributory.

Types and management
Type 1: Rapidly progressive, median survival about 2 weeks. Haemodialysis may be required.

Type 2: Slowly progressive, median survival about 6 months. Transjugular Intrahepatic Portosystemic Shunt (TIPS) maybe required.

Liver and/or kidney transplant maybe considered for both types.



Thanks for reading.
- Ashish Singh.

Dihydropyridine vs non-Dihydropyridine CCBs mnemonic

Dihydropyridine vs non-Dihydropyridine CCBs were always a struggle to me because they are both CCBs but at the same time they have some differences.

I hope that the following mnemonic will help in reminding you which one is Dihydro and which one is not :D :

The mnemonic (remember DIE HARD movie and Bruce Willis)

I am a DIe Hard FAN

DIHydropyridine CCBs:
FAN
F- felodipine
A- amlodipine
N- nicardipine

So non-Dihydropyridine CCBs are Verapamil and Dilitazem.

The original FAN mnemonic was posted here:
http://woanchyi818.blogspot.com/2015/03/calcium-channel-blockers-ccbs.html

good luck :)

Murad

Topical vs Oral antifungal mnemonic

Hey my friends, a common question in qbanks is when to use topical vs oral antifungals in Tinea infections.
Well, you can use the following mnemonic:

Tinea CAPitis => Imagine a CAP covering your head/scalp so you need a systemic treatment => Oral treatment (eg: Terbinafine) to reach it.
Scientifically, the systemic/oral treatment is needed to reach the hair shaft.

Tinea Corporis: Since Tinea Capitis is the oral one, Tinea Corporis is the topical one :)


Murad :)

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

Attrition

In simple words, Attrition is the loss of tooth structure occlusally due to excessive forces by the occluding teeth, grinding of teeth, deep bite.

Aurora kinases

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?

Submitted by Kirtan Patolia 

Risk factors for puerperal sepsis mnemonic

Hi!

Risk factors for puerperal sepsis mnemonic:
PUERPERAL SEPSIS

Maternal complications of diabetes in pregnancy mnemonic

Hi!

Maternal complications of Diabetes in pregnancy mnemonic:
PREGNANCy

JVP documentation

Hi everyone!

Someone questioned on how to document JVP. Just saying JVP is 8 cm is not enough - Say what is your reference for better documentation :)