About me

Hello guys!!! =D
I am Vinayak, the newest author here.

I would start this mini-autobiography by expressing my gratitude to the coordination of all those zillion coincidences which ended up as me writing for this blog. :)

I have written a few articles for this awesome blog till now but this one took me the most time and brains. It is always challenging to write or say about oneself, it's like being honest without being truthful.

I belong to a very small town in Odisha situated alongside its border with Jharkhand; and like all towns situated at the border, it's pretty backward. I currently live in Mumbai, I first visited this city when I was seven years old to visit my grandfather who was admitted in JJ Hospital, at that time I never would have thought that it would be the same hospital I would become a doctor in many years later. From that moment, it was my dream to live in this city one day, and now everyday I wake up I am happy because I am living my dream! :)

"I believe that imagination is stronger than knowledge, that dreams are more powerful than facts, that hope always tiumphs over experience, that laughter is the only cure for grief and that love is stronger than death." This is my favorite quote. I also believe that "mistakes" should not be frowned upon and berated, that your evolution as a person, as a student, as a family member, as a professional is the result of a "trillion mistakes". One should be so confident about his failures that he is able to fail at the time and place of his own choosing.

As you can gather from the above article, I aspire to be a philosophical writer one day. :D

That'll be all for now! I hope one day I can come back to this article and add another paragraph about living the dream I have right now. :) Thanks IkaN for giving me this oppurtunity!

-VM

Cephalosporins : A mnemonic to get you out of the Cepho-pocalypse

Hello Everyone !
I have with me today a somewhat easy way to remember the Cephalosporins. To rescue you of the Cepha-pocalypse, if you will. Rid you of your Cepha-problems with some Cepha-lutions. (Had to say that. Sorry for the Cephalameness ;;) .)

So the 1st Generation are 3 drugs .
Remember : ZoLeDrox:
So add cef everywhere now
CefaZoline
CephaLexine
CephaDroxil

Now the 2nd Generation.
Remember : ChloroFuro carbons
So CefaChlor And Cefuroxime
(2nd is the least imp generation. So to hell with it. )

The 3rd Generation  is the most important.
So first the Parenteral  ones.
Remember:
Cef (Pronounce Saif like Saif Ali Khan)  Opera (like Oprah Winfrey)
Taxi me
Cefti(Like Safety) ke liye
Axe and
Cefta ke liye not even a
Dime (like the money dime)

So add Cef to Opera and Taxi-me to get Cefoperazone And Cefotaxime.
And further add Cefti / Cefta to the next two respectively to get :
Ceftriaxone
And Ceftazidime
So that gives you 4 Parenteral drugs.  Cefoperazone Cefotaxime Ceftriaxone Ceftazidime.

Now Oral ones.
(Whenever I think of 'Oral' - Denaerys Targaryean comes to my mind. God knows the reason for this Ceph-oral Problems ;;) )

Remember : Denaerys Xi (pronounce Chi) Beauty
Add Cef related prefixes to each of the 3 words to get your drugs.
Cefdinir  Cefixime And Ceftibuten.

And That, friends, is the story of the Cephalosporins. Now there's 4th and 5th generations too. But doing them all together can lead to a Cepha-tastrophe. ;;) That's all this time. Hope you found this helpful. Let me know what other topics you'll would like to learn in an easier way.
Bye :)

~A.P.Burkholderia

Membranous glomerulonephritis notes

Hey!
This post is on membranous glomerulonephritis :D

Carbohydrate Loading

I learnt this concept today while going through Harper's. This is especially for the fitness enthusiasts, since learning it can help you to build up your stamina better.

Energy for Muscle Contraction

Let us start by subdividing muscle fibers into two types: Type I (Slow twitch, Oxidative) and Type II (Fast twitch, Glycolytic).

Step 2 CK: Abdominal aortic aneurysm notes

Hey, here are my notes :)

Role of Glucocorticoids in Developmental events

Glucocorticoids in the fetus are either of maternal origin or syntheiszed from placental progesterone in the fetal adrenal cortex(which lacks zona reticularis). Glucocorticoids are essential for a lot of developmental events, but three of them are most important which goes as follows.

Erythropoietin therapy

Here are some important things you should know about erythropoietin therapy.

It is used in patients on dialysis.

Resistance to erythropoietin is most commonly due to iron deficiency.

Adverse effects are associated with rapid rise in hematocrit and hemoglobin - Hypertension, Thrombosis.

Other side effects are: Headache, flu like symptoms, red cell aplasia.

Did you know?

Erythropoietin was the first human hematopoietic growth factor to be isolated.

Erythropoietin was originally purified from urine of patients with severe anemia.

It is banned by the International Olympics Committee.

That's all!
-IkaN

Gap Junctions and Connexin Mutations

Let's start with a brief description of Gap Junctions. Take two empty cardboard boxes, assume they are cells. Bore a hole in each one of them and then enter a small straw in it. Then arrange the two boxes(cells) in such a way that the two straws are aligned perfectly with each other and that their cavities form a continuous column, so that if you pour water in one box it should completely go into the other one without even a single drop falling in between them.

Causes of priapism

Hello lovely medical students!

Priapism is persistent, painful erection that develops without sexual simulation.

Here are a few causes of priapism:

Prazosin
(Mnemonic: PRazosin causes PRiapism)

Trazodone
(Mnemonic: Trazodone causes a boner - TrazoBone)

Perineal or genital trauma

Neurogenic lesions

Sickle cell disease and leukemia

Always check medications first, since it is often drug induced.

That's all!
-IkaN

Medicowesome on Telegram

It's like the broadcast list on Whatsapp

https://t.me/medicowesome

Nephrotoxic antimicrobials

Hello! In this post, I'll be talking about nephrotoxic antimicrobials.

Let's start with Aminoglycosides!

Aminoglycoside toxicity manifests in the form of tubular necrosis.

Did you know AKI due to Aminoglycosides manifest 5-7 days after therapy even after the drug has been discontinued? :O

Aminoglycosides accumulate in the renal cortex and cause non oliguric AKI. Hypomagnesemia is a common finding.

Amphotericin B also causes tubular necrosis. It binds to tubular membrane cholesterol and introduces pores. Clinical findings include polyuria, hypomagnesemia, hypocalcemia and NAGMA.

Mnemonic for nephrotoxic drugs: Drugs with A!

Aminoglycosides
Amphotericin B 
Antivirals like acyclovir, tenofovir, cidofovir, foscarnet, pentamidine.
(Cause tubular toxicity)

Antibiotics like penicillin, cephalosporins, quinolones, sulfonamides, rifampin.
(Cause acute interstitial nephritis)

Remember, in acute interstitial nephritis, WBCs, WBC casts and urine eosinophils will be seen. However, in AKI, the urine sediment will show granular casts.

That's all!
The predominant feeling I have is that if gratitude (=
-IkaN

Pathophysiology of Absence Seizures

Currently, the best understood of the primary generalized seizures is the Absence Seizure(also called Petit Mal seizure).

So we will focus on it. In contrast to secondary generalized seizures, where synchronicity begins in a specific foci in the brain within an aggregate of neurons and then spreads to the entire brain; the primary generalized seizures arises from central brain regions like Thalamus and then spreads rapidly to both hemishpheres.

To understand the pathophysiology of absence seizures, we first have to be acquainted with the physiology of slow-wave(Stage 3) sleep; since they both have similar EEG reading patterns; i.e., the 3-per-second spike-and-wave activity.

In the awake state, the thalamocortical circuits are in "transmission" mode, whereby incoming sensory informations are faithfully transmitted to the cerebral cortex. Whereas in slow-wave sleep, these circuits are in"burst" mode, because of the bursting activity of a unqiue, dendritic T-type Calcium channel in the thalamus which alters the incoming sensory signals in such a way that the output signals to the cortex have an oscillatory firing rate; but no sensory information is transmitted to the cortex. Something similar happens in Absence Seizure.

In absence seizure, there is abnormal, abrupt activation of this T-type calcium channel in the awake state. This has been postulated to be due to hyperpolarizaion of relay cells in thalamus which in turn is due to increased GABAergic input from the reticular nuclei. 

Hence, drugs that block T-type calcium channels (Ethosuximide, Valproate, Lamotrigine, Clonazepam) are used in the treatment of these seizures while Barbiturates which augment the GABAergic activity in the reticulothalamic relay circuits exacerbate the condition. 

-VM