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

Pathophysiology of Secondary Generalized Seizures

To understand the pathophysiology of seizures in brief, lets take the following case.

“Two brothers, Ram and Shyam were playing chess. When all of  a sudden Ram noticed that his 40-year old brother seemed to be daydreaming  and seemed to be confused and having a petrified stare for about 20 seconds. Then suddenly his right hand began to bend into an awkward position and then to shake. The shaking grew worse, progressing gradually from the hand to the arm and then to the entire right side of the body. Then his body stiffened for about 15 seconds, followed by shaking movements of all four limbs that lasted another 30 seconds or so. Then he became limp and unconscious.”

1. Now here Rob first showed the symptoms of daydreaming, confusion and petrified stare, this is known as Aura. Since its a behavioural disturbance, we can guess that the foci of this seizure activity is in the temporal lobe(hippocampus, amygdala etc).

2. So there is abnormal synchronous electrical activity(ASET) somewhere in the temporal lobe which could have been due to any pathology like tumour, tuberculoma, stroke, viral encephalitis, neurocysticercosis etc.

3. It took the seizure activity 20 seconds to override the Surround inhibition  of the temporal lobe and then spread to the neighbouring areas.

4. Next there is contraction of muscles followed by shaking first in his right hand, then arm, then the complete right side. This means now the abnormal synchronous electrical activity(ASET) has spread to the left motor cortex and progressively involved the entire homunculus.

5. Next this tonic-clonic activity involves the entire body. This means that ASET has spread to the contralateral hemishphere via corpus callosum and other commissures and that it has involved Thalamus, which is the gateway to the entire cerebral cortex. Now since it is bilateral, we can call it a Generalized seizure.

6. Lets learn the mechanism of Tonic-Clonic seizure(Grand Mal seizure) activity.

A: First there is sudden inhibition of all GABAergic activity leading to overriding       of the Surround Inhibition, causing contraction of both agonist and antagonist group of muscles, referred to as the Tonic phase.

B: Then the GABA-mediated inhibition is gradually restored and while increasing it starts      oscillating with the excitatory activity mediated by Glutamate via its NMDA and AMPA receptors. If this oscillation involves the motor cortex, there is shaking movements, referred to as Clonic phase.

C: Ultimately the GABA-mediated inhibition prevails, resulting in all the muscles               becoming flaccid and the patient becomes unconscious until normal brain function is restored.   

-VM