What is the difference? : Meconium vs. Meconium Ileus

Hey Folks, Jay here!

Meconium is the very first stool ("poop") of a Neonate. This is mainly composed of the material that it ingested during its intrauterine life. This can include, amniotic fluid, mucus, bile, intestinal epithelium cells, lanugo and water.

Classical Findings of RDS Infant!

Hi awesomites, Jay here! This is a short description on Classical clinical findings of a Neonatal Respiratory Distress Syndrome(RDS or NRDS) infant.

Scarlet fever notes and mnemonic

Hello. How are you awesomites?

Let's talk about scarlet fever today!

Scarlet fever, also known as scarlatina, is characterize by exudative pharyngitis, fever and scarlatiniform rash.

It's caused by erythrogenic toxin producing GABHS (Group A Beta Hemolytic Streptococci)

Characterized by:
- Fever, headache
- Sore throat, circumoral pallor
- Sandpaper rash (Pinpoint, erythematous blanchable papules), erythema trunk, pastia lines
- Lymphadenopathy

Diagnosis:
- Rapid antigen detection test is specific, but not sensitive.
- If it is negative, do throat culture.
- Elevated ASO, DNAse maybe seen.

Treatment:
- Treatment as long as 9 days after the onset of symptoms prevents rheumatic fever.
- Oral penicillin, amoxicillin for 10 days.
- Cephalosporins, macrolides are alternatives. (Penicillin resistant group A staphylococcus doesn't exist.)
- If adherence problem, intramuscular benzathine penicillin G.

That's all!
The only fever I have is for Scarlett Johansson =P
-IkaN

Erythroblastosis fetalis (HDNF)

It is a condition that develops when Rh-negative women is pregnant with Rh-positive baby .
It causes phagocytosis of the fetus's RBC's (Baby inherits Rh positive antigen from father ).
As mother is Rh-negative , exposure to fetus's antigen causes development of anti-Rh agglutinins .
These agglutinins(mostly IgG antibody ) diffuse through the placenta and enters fetus blood cells and leads to phagocytosis of the RBCs ,which leads to release of hemoglobin into blood !Then fetus's macrophages converts the hemoglobin into bilirubin ,which causes baby skin to become yellow(jaundiced).Although the severe form of anemia is responsible for many deaths of infants ,many children who barely survive the anemia exhibit permanent mental impairment , because of precipitation of bilirubin in the neuronal cells  ,causing destruction of many cells , condition known as Kernicterus

It usually doesn't affect the first child ,since sensitization occurs during parturition.However ,if Rh-negative mother was sensitized earlier with Rh antigen then first child can get affected .

Treatment:
1)One treatment of HDNF is to replace the neonate's blood with Rh-negative blood .About 400ml of Rh negative blood is infused over a period of 1.5 or more  hours ,while neonate's own blood is removed,the process may be repeated several times during the first week of life ,to prevent Kernicterus .

Prevention:
Anti-D antibody is administered to the expectant mother ,starting at 28-30 weeks of gestation.The anti -D antibody is also administered to Rh-negative women who deliver Rh -positive babies to prevent sensitization of the mothers to the D antigen .This greatly reduces the risk of developing large amounts of D antibodies during second pregnancy !

~ojas

DON'T use Perfumes to test Olfactory nerve!!! But why?

Hi folks,

Our Neurology professor said not to use Perfumes to test Olfactory nerve in Cranial nerve testing. But why?

The updated Glasgow Coma Scale

Hi Awesomites,

The Glasgow coma scale or GCS as we know it has changed since its inception in 1974.

So lets go!

Main differences are 

• We no longer use the term "Pain", but "Pressure"
• We no longer recommend "Sternal Rub", but "Trapezius Pinch" or "Supraorbital notch pressure" or careful "Fingertip pressure"(Peripheral stimulation)
• "To speech" is changed to "To Sound"
• "To pain" is changed to "To pressure"
• "Inappropriate speech" is changed to "Words"
• "Incomprehensible speech" is changed to "Sounds"
• Flexion is defined two way now as "Normal flexion" and "Abnormal flexion"

The differences between 1974 and 2014 updates are as follows.

You can read more details on the update, in this link. Download the pdf in the page which is the original paper.

Thanks,

With love,

Jay :) 

Anatomy of the larynx: Cartilages

Here's an awesome video on the anatomy of the larynx by A. P. Burkholderia!

Isn't he just awesome? :D

Beta HCG notes

Where is beta HCG produced? 

Syncytiotrophoblast.

Step 2 CK: Goodpastures syndrome notes

Hello!
Here's a short post on Goodpastures syndrome!

Cocaine in the brain - "The Addiction"

Hey Awesomites!

Here I will be talking about a social problem amongst the youngsters - “Addiction to cocaine”. 

Menstrual cycle and related problems

Here are some common menstural complaints that I studied today during my posting that I would like to share with you. There are many more though. Comment if you think I have missed out on something!

Contrast induced nephropathy notes

Features of contrast induced nephropathy

- Due to iodinated contrast agents (Other agents that cause AKI: Gadolinium for MRI, sodium phosphate solutions as purgatives)
- Prevented by use of non ionic contrast agents, IV hydration, acetyl cysteine.
- Serum Creatinine rises 24-48 hours after exposure. Resolves in a week.
- FeNa low, benign urinary sediment.
- Risk increases in CKD, Diabetic nephropathy, multiple myeloma.

Brachial plexus mnemonic

This was probably the most important answer you must have encountered during your 1st year.

Here are tricks to remember Brachial Plexus!

Analgesic nephropathy notes

Analgesic nephropathy

Characterized by:
Renal insufficiency
Papillary necrosis

Due to:
Toxic drug levels in inner medulla
Causes chronic tubulointerstitial damage
Results from papillary ischemia due to vasoconstriction of medullary blood vessels (vasa recta)

Caused by:
Phenacetin containing preparations
Aspirin
Caffeine

Symptoms:
Polyuria (Due to impaired concentrating ability)
NAGMA (Due to tubular damage)
Hematuria (Due to sloughed necrotic papilla)
Sterile pyuria and WBC casts may also be seen
Ureteric colic, obstruction (Due to sloughed necrotic papilla)

At increased risk of:
Premature aging
Atherosclerotic vascular disease
Urinary tract cancer

That's all!
-IkaN

Radial nerve mnemonic

I am gonna put radial nerve in the simplest form mostly including mnemonics how to learn it's huge muscles supply!

Remember when you were in 1st year and how these nerves used to test your patience?! Let's make it easy.

-Nerve root: C5-T1

-Sensory nerve supply:
Skin of dorsal surface of forearm
Lateral side of the dorsal part of palm
Lateral 3 & 1/2 digits

-Motor nerve supply:
(It supplies extensor compartment)
Here is mnemonic
S: Supinator.
I: Extensor indices.
D: Extensor Digitorum.
B: Brachioradialis.
A: Anconeus.
T: Triceps.
C: Extensor carpi radialis longus.
C: Extensor carpi radialis brevis .
A: Anconeus.
P: Extensor pollicis brevis.
P: Extensor pollicis Longus.
CU: Extensor carpi ulnaries.
ED: Extensor digiti minimi.

So mnemonic is
SID (C)CAP(P) (Read it as cap!) BAT Cu-ed.

Remember:
Cu = Extensor carpi ulnaris (Supplied by radial nerve not ulnar nerve as it is extensor muscle)

~ Ojas

Treatment of TTP mnemonic

Safia made a mnemonic of TTP and sent it to Medicowesome, hoping it would help someone. So sweet!

Treatment of TTP: CART
C: corticosteroids
A: asprin
R: rituximab
T: transfusion

In emergency situations, transfuse blood first!

Thanks Safia.

-IkaN

Cranial nerves type mnemonics

Here is one of the mnemonics which I made to remember types of cranial nerves
1)Olfactory  -Sensory
2)Optic.  -Sensory
3)Occulomotor-Motor
4)Pathetic(Trochlear)-Motor
5) Trigeminal-Mixed
6)Abducens-Motor
7)Facial-Mixed
8) Auditory-Sensory
9) Glossopharyngeal-Mixed
10)Vagus-Mixed
11)Spinal accessory-Motor
12) Hypoglossal-motor

"Some say marry money but my brother says beautiful bride matters more!"

S-Sensory ;M-Motor ;B-Both (Mixed)

~Ojas

Contraindications of thrombolytic therapy

BISHOPS

B = Bleeding disorder .
I = Intracranial Hemorrhage.
S = Stroke past 3 months .
H = Head injury past 3 months .
O =Oesophageal varices.
P = Pregnancy.
S =Surgery.

Made by: Khushboo shaikh
Written by: Ojas gite

Step 2 CK: Mortality benefit in Congestive Heart Failure (CHF)

Another USMLE Step 2 CK important topic :D

Things that have a mortality benefit in CHF mnemonic: "ABCDES"
A: ACEI and ARBS
B: Beta blockers
CD: implantable Cardiac Defibirillator
E: Epelerenone
S: Spironolactone

Reading material from UpToDate! =)

T wave Inversion Mnemonic

In this post, I'll be sharing a mnemonic to remember the causes of T wave inversion.

Cleft lip and palate

Hi friends,

Here's a quick way to remember the cause of Cleft lip and Cleft palate.

LMN
Cleft Lip - failure of fusion of Maxillary and median Nasal prominences!

PPP
Cleft Palate - failure of fusion of two Palatine Processes!

That's all!

-Rippie

Alport syndrome notes

Alport syndrome notes

If we were parts of the ECG, you'd be the QT segment, cutie!

I know it isn't Valentine's day, but hey, do we need a day to be all lovey dovey and flirty? xD

Hypercalcemia and hypocalcemia - ECG

Hey!

Hypocalcaemia causes QTc prolongation primarily by prolonging the ST segment.

In hypercalcemia, the ST segment is short.

And since I am a mnemonic queen:

Prinzmetal's angina notes

Hello!

Here are my notes on Prinzmetal's angina:

1. Ischemic pain at rest.
2. Diagnosed by transient ST elevation.
3. Nitrates and calcium channel blockers are used for treatment.

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

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