Mnemonic : Deviated Nasal Septum clinical features

Hey Awesomites

The clinical features ( s/s ) that are presented by a patient with DNS are : NOSE MASH

NO - Nasal Obstruction
S - Septal cartilage and bone deformity
E - Epistaxis

M - Middle Ear infection
A - Anosmia
S - Sinusitis
H - Headache


- Jaskunwar Singh

C Peptide levels : An Overview

Hello everyone!So I ended up uttering 'C peptide' recently in my Medicine Viva and my professor screwed me over it.
(Clearly I didn't C it through :'D )
So I thought of doing a brief summary on it.
Here goes.

1. What is C peptide ?
- When pro- insulin is cleaved , it gives insulin and C peptide.
- C peptide in general has a longer half life than insulin and is easier to detect.
- The pathway is something like this :

Pre proinsulin produced in Rough Endoplasmic Reticulum of Pancreas --> Transported to the Golgi apparatus and cleaved to form Proinsulin -->  Packed into secretory granules --> In these granules proinsulin is converted to : Insulin and C peptide. 

- Traditionally it is said to have no intrinsic activity but recent studies say it might have anti oxidant and anti inflammatory properties.   

2. What does it indicate ?
- So , its presence indicates presence of Insulin in the body in a proportionate amount.
- Hence in a case of Hypoglycemia if C peptide levels are high, it's likely to be due to increased endogenous Insulin levels.

3. C peptide levels increased in -
- Insulinoma
- Sulfonylurea induced Hypoglycemia ( As they are Insulin Secretagogues)
- Type 2 Diabetes Mellitus ( Hyperinsulinism due to resistance)
- Insulin Resistance states like Obesity , PCOS , Cushing's.

4. C peptide levels reduced in -
- Type 1 Diabetes as Insulin secretion is reduced
- Latent Autoimmune Diabetes of Adult (LADA )
- Factitious hypoglycemia - Due to excess exogenous Insulin administration.
- Hypoglycemia due IGF secreting tumors.

So if you get a patient with Hypoglycemia with elevated insulin levels , C peptide levels help you decide if due to exogenous Insulin , or Endogenous Insulin  ( Sulfonylurea induced or Insulinoma).

Hope this helped !
Stay awesome.
Happy studying!
~ A.P Burkholderia.

The Basics : Middle Ear

Hey Awesomites

In this post, I will be talking about the middle ear structures and its relations with its neighbors ( just a summary ).

The Middle Ear is an air filled and bilaterally compressed/ concaved cavity lined by mucous membrane located in between the external and internal parts of ear. It is divided into:
- Epitympanum or the Attic ( 6mm ) - lies  above pars tensa and medial to pars flaccida
- Mesotympanum ( 2mm ) - lies opposite to pars tensa
- Hypotympanum ( 4mm ) - lies below the level of pars tensa

BOUNDARIES of the middle ear ( homologous to structure of a cube ) :-

Roof : Tegmen tympani - a thin bony plate that is a part of petrous part of temporal bone, separates the middle ear cleft from middle cranial fossa.
- Infection in the middle ear may spread superiorly and lead to formation of abscess in the meninges ( especially Extradural abscess ), meningitis or if severe, it may even lead to abscess formation in the temporal lobe.

Floor : Jugular bulb - The middle ear cavity is separated from jugular bulb by a thin piece of bone that if deficient may lead to formation of a layer of fibrotic tissue and mucous membrane in between. The contents of jugular bulb are:
- Internal Jugular vein
- Glossopharyngeal nerve ( IX )
- Vagus ( X )
- Accessory nerve ( XI )

The tympanic branch of glossopharyngeal nerve enters the middle ear at the junction of the floor and medial wall to play an important role in formation of tympanic plexus.

Anterior wall : The upper part of the narrow anterior wall has two openings or tunnels for - ( mnemonic : TEA )
- Canal for Tensor tympani muscle
- Pharyngotympanic ( or Eustachian ) tube

The lower part of anterior wall is separated from the Internal Carotid Artery by a thin plate of bone. The ICA is surrounded by a plexus of sympathetic nerves that enter middle ear through openings in this bony plate to form tympanic plexus.

Posterior wall : Posteriorly, it is related to middle ear cleft ( Aditus, Antrum and mastoid air cells )
- Infection in this region may spread posteriorly into the sigmoid sinus ( in posterior cranial fossa ) and cause thrombophlebitis !!

Medial wall : Medially the middle ear cavity is related to the promontory, oval and round window

Lateral wall : Tympanic membrane separates the middle ear from the external ear.

A brief about the functions of middle ear:
On the incoming of sound waves, the tympanic membrane oscillates and these oscillations are sensed by the strongly attached and faithful middle ear ossicle, the Malleus. The sound energy is transmitted as such by the ossicles ( Malleus - Incus - Stapes ) to the internal ear for further processing.

The major function of these ossicles is amplification of sound waves - Tympanic membrane is 17 times larger than the oval window - So that means the sound energy is picked up by the larger area ( TM ) and impinged over a much smaller area ( oval window ) thus amplifying it 17 times.

In addition, the lever action of the ossicular chain is approx. 1.3 units. Thus the intensity ( force ) of sound waves/ vibrations changes ( increased by ~20 times ) and not the frequency !! If the sound waves are not amplified ( in case OC is removed ), the Air Conduction would be lost. So BC > AC and thus hearing would then be poor.


Thats all
Hope this helped :)
Stay Awesome!

- Jaskunwar Singh

Craniopharyngioma mnemonic

The C's of Craniopharyngioma

Children

Calcification
Cholesterol crystals
Cyst formation

Central diabetes insipidus

Compresses chiasm, can't C (see, because butemporal hemianopia)

CR: CRAniopharyngioma RAthkes pouch remnant

Yup. That's all!

-IkaN

Medicowesome secret project: Organ series

What is the secret project? How can I participate?

Medicowesome secret project: Heart art

What is the secret project? How can I participate?

Medicowesome secret project: Let's talk about depression in medical professionals

What is the "Let's talk" project? How can I talk about mental illnesses?

Medicowesome secret project: Let's talk about finding love

What is the "Let's talk" project? How can I talk about mental illnesses?

Medicowesome secret project: Earth Day

'A' wave in JVP : Mnemonic and explanation

Hi everyone. So JVP is one of the most theoretical clinical signs I've ever studied. And though parts of it are logical , I find it tedious to memorize all causes for a particular finding.
So I've prepared a Mnemonic for prominent a waves.
Here goes.

The A wave is a positive wave of the JVP.
It represents the Right Atrial pressure during systole.

Causes of a prominent a wave
Remember :
CRePT's

C - Cor Pulmonale
R - Right heart Failure
P - Pulmonary stenosis
T - Tricuspid stenosis
S - The S tells you it's Stenosis for P and T.

The a wave essentially represents the pressure in the Right atrium during systole.
So any condition that causes this pressure to increase would cause a prominent A wave.

Cor Pulmonale and RVF are basically congestion in RV causing elevation of pressure in the RV.
This means the atrium needs to pump with greater force into the Ventricle for the venous return to enter the Ventricle. This increases the RA pressure causing prominent a wave.

Pulmonary Stenosis leads to accumulation of blood in the RV and this follows a similar fate as the above mentioned causes.

Tricuspid stenosis causes obstruction to the flow of blood from RA to RV. Thus accentuating the pressure in the RA.

That's the Prominent a wave for you !

~~~~~~~~~~~
Now there's something called the Cannon a wave.
These represents contraction of the RA against a closed Tricuspid valve.
The causes of this include -
A- V dissociation.
Heart blocks.
Ventricular arrhythmias - V tach , Ventricular premature complexes and Ventricular pacing.
~~~~~~~~~~~
The a wave would be absent in Atrial fibrillation as the atrium is functionally not pumping at all , and just vibrating.

These are the a wave findings for you !
Hope this helped
Stay awesome.
~ A.P. Burkholderia

Number needed to treat and number needed to harm mnemonic

Hello!

Number needed to treat = 1 / Absolute risk reduction

Mnemonic: TARR - Treat Absolute Risk Reduction

Number needed to harm = 1 / Attributable risk

Mnemonic: HARM - Harm Attributable Risk M

That's all
-IkaN

The Basics : Lateral wall of Nasal cavity

Hey Awesomites

In this post, I will be talking about the anatomical structures in the lateral wall of the nasal cavity. 

Clubbing : Why it occurs.

Hi everyone !
This is a short post on why clubbing happens.
So it's simple !
It's cause people like to go out and get drunk. 
Just kidding. Here goes.

1. What is clubbing ?
- It's the bulbous enlargement of the terminal digits​ and the nail bed.

2. What are its causes ?
- Symmetrical clubbing can occur due to a host of causes.
- To summarize :
  A. Respiratory
   : Lung  cancer
   : Suppurative lung conditions like   

     Bronchiectasis , lung abscess and Chronic TB.
    : Pulmonary  Fibrosis

   B. Cardiac
   -  Cyanotic heart disease
   - Eisenmenger Syndrome
   - Infective endocarditis

    C. GIT
     -  Inflammatory bowel disease
     -  Cirrhosis - esp Biliary

     D. Endocrine
     -  Thyroid Acropachy
     -   Acromegaly

3. Why does it occur 

So I've spent a lot of time researching theories on how clubbing occurs. And let me tell you in the start itself, they're not clear on why it occurs.
But what makes sense to me , I want to share with you'll! And it was an absolute pain to find something convincing enough. So just stick with me here ;;) 

So the crux of clubbing lies in vasodilation of the digital vessels causing proliferation of the tissue there in.
The most widely accepted theory right now is the megakaryocyte theory.

So in the figure above , the left side in white shows the normal course of a megakaryocyte through the blood. 

In altered  cardiorespiratory conditions , these large platelets either bypass the Pulmonary circulation owing to the shunting produced due to Heart defects or the lung parenchyma itself proves to be less to purify the blood of the platelets.

 This causes these giant platelets to go lodge into the digital circulation causing release of cytokines like Platelet derived growth factor (PDGF) and TGF beta amongst others. These GF's cause vasodilation and in return , nail bed proliferation and collagen deposition.

How do we explain the Clubbing in GI causes ?
IBD - especially Crohn disease seen to have thrombocytosis eventually which may aggravate the PDGF.
In cirrhosis of liver , especially biliary , pulmonary arteriovenous shunting is observed. This could result in the megakaryocyte entrapment as explained.

Another theory suggests inflammation triggers a vagal response causing Vasodilator effects. ( Neurogenic).

Other theories -
Hypoxia induced
Reduced ferritin related
Neurogenic
Humoral - various PG's and other humoral molecules.

The most widely accepted theory is the Megakaryocyte theory.

Hope this satisfied you ! 
Thank you.
Stay awesome. 

~A.P.Burkholderia

Preparing for NEET - Part 2

Hello everyone.

So now for my part 2 post on NEET PG prep, I will provide you with a seventh month schedule, but before that let’s  talk about the pros and cons of joining classes and how to deal with studies if you don’t join one.

Now in my earlier post I did mention that classes will help YOU with only 20% of the entire prep that also with sustained proper attention in the 12 hour class with proper notes and revision.

     1. The biggest thing you achieve by attending class is that the professors don’t beat around the bush, they give you point to point details and explain the things which they know by experience that the students are bound to screw up the most.

This is not something you can’t achieve by your own.  If you can get your hand on any class notes, then that’s enough, just thoroughly read that book, be regular in solving mcq’s and discuss your issues in group chats or with your study buddies. This does take care of it plus you gain a lot more, because here you are actively seeking answers and not being spoon fed like in classes

If you don’t have any class notes and our reading standard books, I suggest only read the bold lines, don’t read anything else. If you clearly don’t know anything about a particular topic then only read it in depth.

2. Weekly test series and grand test with ranking. This is beneficial only if you stick to the schedule, sadly I feel only 3 out of 10 students are regular at these exams. Also even if you don’t join the regular course, you can just join the test series, which I feel is a great option .

The bad point is that sometimes students feel torn between their own study speed, the subjects they want to study first and the test series schedule. Sometimes the test series just overwhelms you a lot cause every week you need to prepare for a different subject.  This has happened to me, and I feel that if I hadn’t join the test series to begin with, maybe I  wouldn’t have been so confused as to whether what to study and what to revise.

So it’s very important that you all know your own study patterns and your comfort. Don’t do things just because everyone else is doing it.  Chart down your schedule, and once you start with it, stick to it. Don’t listen to people and try doing things their way, you are your own person and you are awesome.

NOW for the study schedule.  This way of prep is bold and ridiculous. Its exhausting and It will demand that you trust the process, but it will work. It was taught to me by one of my friend. Its esp for the ones who haven’t joined any classes.

·         This first phase is for you to grab onto all the possible books on mcq’s you can for the last ten year mcq’s. And then you go crazy, just solve the mcq. Don’t read the explanations. Just solve and solve, just  reading the answers. Thats it. This whole process should take you a month at the max of rigorous solving.

·         Take a break..chill out for a couple of days

·         Phase two. repeat the phase one, now I  have tried this. And by experience I will tell you this is when it gets tough, monotonous and downright stupid but keep going at it. This will take you two months max.

·         Breaktime

·         Phase three is when you repeat it all over again, but now you will see the difference. You will love solving cause now the answers will flow out of you. Cause you have just learned 30.000 important one liners of all the 20 subjects. This process will take you 20 days.

·         Phase four is when you read and solve your doubts, read any damn book you want. Search for pictures, make your own picture library.

Remember 75% mcq are repeats, so this plan is made in a way that you learn all of those 75% first

You need to solve atleast all the mcq a minimum of five times to score a decent rank

Your speed of solving should reach 300 questions in one hour with atleast 65- 70% right.

These above are your goals after you are done with phase four

Irrespective you choose to follow this plan or any of the tips in my part 1 post, or if you choose to modify it according to you. Remember the most important thing is that you have to be consistent and do smart studies and not study like a dog. Have your wits about yourself and don’t  waste your time on reading unnecessary details.

Thank you

Sakkan

Authors' diary: Homemade cheap DIY alternatives for a smartphone camera stand

This video is from the authors diary!
In this video, I show how I keep my camera stable while shooting videos of my notes / whiteboard.
I use paper cups and books as my camera stand.

Types of abortion: Explanation and mnemonic

Hello!
This video is on the types of abortion.

Paraneoplastic Dermatoses - Tripe Palm.

Hello everybody,

So from today onwards, I will cover a series of cutaneous manifestations of internal malignancies starting with the first one called Tripe Palm.

               (Image courtesy-Google)

(The palmar ridges are accentuated and resemble to the stomach mucosa of a ruminant-tripe.)

Tripe palm (also known as acanthosis palmaris and acquired pachydermatoglyphia) is a velvety thickening of the palms with a ridged or rugose appearance.

The term is derived from its resemblance to the stomach mucosa of ruminants (tripe).

It is associated with gastric or lung cancer.

In some cases, tripe palm is the initial presenting feature of the underlying malignancy.

Improvement of tripe palm occurrs in one-third of patients after beginning treatment for malignancy.

Hope it was helpful.

Let's learn Together!
-Medha.

Nail Changes in Medicine : A Summary

Hi everyone. Just a list of changes you can see in the nails in different systemic Diseases. So let's get nailed ;)

1. Clubbing -
Loss of angle between the nail and the nail fold - More soft and bulbous nail.
Typically indicates Cardio Pulmonary function disturbance :
--> Cardiac conditions like Cyanotic heart disease, Infective endocarditis and Atrial myxoma.
--> Respiratory conditions :
Neoplastic like CA lung ( Esp. Squamous cell CA) , Mesothelioma.
Infective like Bronchiectasis , Abscess , Empyema.
(Non cardiorespiratory causes = Inflammatory bowel disease, Biliary Cirrhois.
Thyroid Acropachy , Acromegaly. )

2. Koilonychia -
Spoon shaped nails.
Strongly indicative of Iron Deficiency anemia or Fungal nail infection.

3. Onycholysis -
Destruction of nail. 
Seen in Psoriasis , Hyperthyroid and Fungal nail infection.

4. Chronic Paronychia -
Inflammation of nail fold. May have swollen nail and discharge with throbbing pain. May occur due to frequent nail biting.

5. Cyanosis -
Can be looked for in nail bed. We have a post on this already.

6. Beau line -
Transverse furrows from temporary arrest of nail growth due to increased stress.
Nails grow at 0.1 mm/d , so furrow distance from the cuticle can be used to time the attack. Can be seen in Malaria , Typhus , Rheumatic fever , Kawasaki.

7. Mees line -
White transverse bands in Arsenic poisoning / Renal failure.

8. Muerhcke's line - 
White parallel lines without furrowing on the nail.
Seen in Hypoalbuminemia.

9. Terry's nails -
Proximal portion of nail is white / pink , tip is reddish brown.
Seen in cirrhosis , CRF

10. Splinter hemorrhage -
Longitudinal Hemorrhage streaks under the nail seen in Infective endocarditis.

What a fun way to get nailed down 😂 Happy studying !
Stay awesome.

~ A.P.Burkholderia.

Drug Induced Edema : Mnemonic

Hi everyone. Here's a short post highlighting drugs causing edema.

Remember : SWOLLEN

S - Steroids
W (V) - Vasodilator drugs
O - Oral Hypoglycemic drug - Glitazones
L - CycLosporine
L
E - Endocrine - Growth Hormone
N - NSAIDs

1. Steroids -
Due to the Mineralocorticoid action of reabsorbing the Sodium from the kidneys, they act as volume expanders.

2. Vasodilator drugs -
Especially CCB's like Amlodipine  are known to cause this. Other Vasodilator drugs used for hypertension can also cause edema like Alpha Methyl dopa, Hydralazine, etc

3. Oral Hypoglycemic drug : Glitazones -
The Glitazones act on the PPAR gamma receptors. These receptors are also present in the kidneys and vascular system. They somehow modulate the kidneys to reabsorb Na+ and also act on the level of blood vessels via PPAR receptors.
This is one of the reasons why they are c/i in Heart failure and Liver cirrhosis ( as they cause fluid overload).

4. Cyclosporine -
Reduces the GFR , thus more fluid retention.

5. Growth hormone. I don't understand why. Do tell me if you find out !

6. NSAIDs -
NSAIDs inhibit PG synthesis in kidneys causing renal vasoconstriction and this reducing the GFR.
This causes excess fluid accumulation eventually causing edema.

That's all!
Happy studying. Stay awesome. :)

~ A.P.Burkholderia

Adult ADHD : A Clinical Overview

Hey Awesomites

Attention - Deficit Hyperactivity Disorder ( ADHD ) is a mental health disorder that usually occurs in childhood and continues into adulthood. The symptoms in adults may not be as clear as in children. In India, there are more than 10 million cases of adult ADHD per year.

In adults, the symptoms of hyperactivity may decrease, but the characteristic features of decreased attention span, mood swings, impulsive behavior, difficulty in communication and language skills, restlessness may still continue to appear.

Now lets talk about the signs. The WHO has lately released a set of six questions to test the adults for signs of ADHD - Adult Self - Report Scale Screener (ASRS) is a self - screening questionnaire that you can use to determine if you might have ADHD. The answers to these questions predict the people suffering from this disorder and is a simple way of screening :

1. How often do you have difficulty in concentrating on what the other person is saying to you, directly as well as indirectly ?

2. How often do you leave your seat when you are in a group or meetings in which you are expected to remain seated?

3. How often do you have difficulty in unwinding and relaxing when you have time to yourself ?

4. When you are in a conversation, how often do you find yourself finishing sentences of the people you are talking to before they can finish them themselves?

5. How often do you put things off until the last minute?

6. How often do you depend on others to keep your life in order and attend to details?

- The answers to these set of questions can be 'never', 'rarely', 'sometimes', 'often', or 'very often'.
- If the answer to four of the six questions is 'sometimes', 'often' or 'very often' , the person may be considered to have ADHD!

Note that this is a simple way of screening the people for signs of ADHD, and not the diagnostic criteria.


Thats all
- Jaskunwar Singh

Croup mnemonic

If croup crops up in the exam, here are some high yield points you should know:

Croup CROPS!

Corticosteroids
Racemic epinephrine
Oxygen

Parainfluenza virus

Seal barking cough
Stridor
Subglottic stenosis
Steeple sign

#TLDR
Parainfluenza virus type 1 is the most common cause of croup.

The onset of symptoms in laryngotracheitis is gradual, beginning with nasal irritation, congestion, and coryza. Fever, hoarseness, barking cough, and stridor usually develop during the next 12 to 48 hours. 

In children with croup, a posterior-anterior chest radiograph demonstrates subglottic narrowing, commonly called the "steeple sign" 

Children with croup are treated with dexamethasone, nebulized epinephrine and humidified oxygen depending on severity.

Remember, intubation is rarely required in croup, so think of other etiologies if the patient needs intubation.

That's all!
-IkaN

Edge of an ulcer : An overview

Hello

An overview on how edge of an ulcer appears with characteristic identification features depending on the underlying causes: (SPURE)

Sloping edge - Venous ulcer, also seen in traumatic cases. It is red - purplish in color and consists of new healing epithelium. ( spreading type )

Punched out edge - Arterial and Neuropathic ulcer. Edges are punched out at right angles. ( non spreading type )

Undermined edge - Decubitus and Tuberculous ulcer. It spreads rapidly to destroy the surrounding tissue !!

Rolling back - Basal cell Ca. It is characterised by raised, pearly white beaded edge with central necrotic tissue.

Everted edge - Squamous cell Ca. It is a rapidly growing invasive ulcer with heaped up and everted edges.

Thats all
Hope this helps :)

- Jaskunwar Singh

Submission: Internal Illiac artery branches mnemonic

submitted by Mayank Kesharwani

Submission: Direction of growing end of bone, opposite to direction of nutrient artery

submitted by: Mayank Kesharwani

Upper limb joints types mnemonic

Hey Awesomites

From proximal to distal, the joints and its types are:

Shoulder joint - Ball and socket type
Elbow joint - Hinge joint
Radio carpal ( wrist ) joint - Ellipsoidal and biaxial type
Carpo metacarpal joint - Saddle joint
Metacarpo phalyngeal joint - Ellipsoidal ( condylar ) joint
Interphalyngeal joint - Hinge joint

Mnemonic to remember the types, from proximal to distal : BaSu ( Ball and Socket ) writes Hindi ( hinge ) in elliptics ( Ellipsoidal ) but is sadly (Saddle ) condemned ( Condylar ) without hinges .


Thats all
- Jaskunwar Singh

Submission ( notes and mnemonic ) by Mayank Kesharwani - ( PS: This is a Hindi Urdu mnemonic )
Bhaiya Hum ESE Hain

Bhaiya - Ball and Socket joint
Hum - Hinge joint
E - Ellipsoidal
S - Saddle
E - Ellipsoidal
Hain - Hinge

Thanks Mayank for sharing :)

Submissions : Tonsillar Bed mnemonic

Hello

Tonsillar bed mnemonic ( from within outwards ) :

P(b) S S B(p)

Pharyngo Basilar fascia
Superior constrictor
Styloglossus
Bucco pharngeal fascia

- Submitted by Mayank Kesharwani

Submissions : Important vertebral levels

Hello

Important vertebral levels for bifurcations:
- Common carotid artery bifurcation - C4 vertebra
- Tracheal bifurcation - T4 ( may ascend or descend upto two vertebrae higher or lower with breathing )
- Abdominal Aorta bifurcation - L4

Important vertebral levels for formations:
- Cricoid cartilage-  C5- C6
- Thoracic duct crosses right to left - T5 ( and enters left IJV )
- Inferior Vena Cava formation - L5 ( from two common iliac veins )

Submitted by Mayank Kesharwani

Submissions: Rolando fracture mnemonic

Hello

TATA truck ROLLS on wheels

The shape of this fracrure is T- shaped or Y ( bent- T ) shaped, which resembles the sign of the Tata motors truck, and Roll is for "Rolando fracture"

Mnemonic submitted by Mayank Kesharwani

Diagram by Jaskunwar Singh 

Medicowesome secret project: Let's talk about unpleasant changes

What is the "Let's talk" project? How can I talk about mental illnesses?

Medicowesome secret project: Let's talk about providing psychological support

What is the "Let's talk" project? How can I talk about mental illnesses?

Bartonella henselae and Pasteurella multocida infection mnemonic

Hello!

Sometimes I confuse the clinical manifestations of these two cat related diseases - Cat scratch disease caused by Bartonella henselae and Pasteurella multocida infection caused by cat bites. 

I probably wouldn't have confused these two in my step 1 days, but the older you get, the more confusing rare diseases become,

Sooo... Mnemonic!

Preparing for NEET: Part 1

Hello folks,

This is a common post requested as to how to prepare for NEET PG exams.
And as to whether joining classes is really required to get a decent rank.

So today I will share with you a study schedule told to me by my professor. Which takes around 7 month hardcore prep.

Now for a general approach to it
1. Classes are not essential. Classes add only 20% to the entire PG prep of yours.. That's with like max optimum attention and taking down notes vigorously.

2. Don't read standard books. The competition is so high, that the publishers end up increasing the number of pages. Just to make the book more appealing. Reading those books is a waste of your time cause they repeat the explanations over and over again with unnecessary details which will make you take a month atleast to finish a subject like obstetrics.
The only decent book I found was modit khanna for medicine, like the initial pages of high yield notes and the questions and not the explanations. Don't read the explanations unless the answer is not known to you through the high yeild section.

3. Try getting your hands on class notes. Be it DAMS, Bhatia or IAMS. They are all amazing and to the point. And that's what is needed.

4. Get the NEET PG question booklet, by Arvind Arora. A minimum of last five years questions of NEET is a must to solve.

5. Never sit with a pen and a paper or a marker during your first read for any subject. You will end up marking the whole book and write unnecessary notes  and wasting a lot of precious time. Save it for your second and third read or when you are confident enough that you know the flow of the subject and now just need to focus on details.

6. While reading if you have any doubts make a point to jot it down and find answers before sleeping or at the end of the week. But do solve them. Cause at the end just before exams these are the doubts that trouble you the most.

7. You need to score only a 75% aggregate to score a decent rank. Like to be in the top 3000. That is very much possible with a 7 month smart prep. For the the fight in between the top 3000 see the next para

8. Imagine yourself after a 24hr emergency duty, back to back and just next day you have to write theory paper of your uni exam.That's a near about situation of how mind stressed you are before neet.
Like it's 20 subjects..and you need to shift your focus from ophthalmology to psm in a matter of seconds. If you can't do that and if you waste your time even like an extra 5 mins on one question then you will be compromising the tail questions and that's when the stress gets to you. You keep looking at the timer and boom you black out.

A solution to this is you need to train your brain to deal with this situation. I have an aggregate of tips from medicowesome authors to deal with this.

- Solve the grand test. Just don't stick to one subject solving be as varied as possible. Like your best shot is solving 100 random questions every day doesn't matter if you know only 5subjects out of the 20, you only need to train your brain to deal with it.

- Solve the questions after an on call or after a very stressful day, give yourself the taste of it. So that your brain will be able to switch attentions during exams.

I feel the battle between the top 3000 rankers all comes down to who switched their attention between questions the fastest. The knowledge is the same it all matters that whether you were able to use it to your best or not.

9. Follow medicowesome :D
A bit cheeky but seriously it helps. Every now and then try reading the various posts. It will help you to condition your brain to all the subjects piece by piece.

10. A lot of questions are photo based. Try making your own picture library like jot down the things of pics you want to search for and look for it at the end of the day or the week end.

11. We don't promote apps and stuff but I would seriously advice downloading the pg prep app from Google play. It has stats to show your progress, daily exams, a 55 thousand question bank, photo questions, subject wise and grand test questions. It is amazing. Go ahead download it if you haven't and stick to it.

12. Have a way to destress yourself during the prep. Like be it running , movie, at a cafe or a novel.
Pg prep is a monotonous dumb thing to do , let's not lie to our selves -_-
You need to keep your engine at a steady pace so that you are able to fast track during the last month before your exam.
Like I personally read manga :D
Weekly updates were my solace and paradise. That's the way I treated myself after I had completed my schedule for the week.

I will upload a seven month prep schedule in part 2.

- Sakkan

Myopic Shift : Explanation

Hi everyone ! So this is a short post on the Second Sight or the Myopic Shift seen in Cataract.

So in people who  have a hypermetropic / presbyopic power , tend to experience a reduction in their refractive errors when Cataract starts to develop. This is called Myopic Shift or Second sight.
This​ occurs most commonly in nuclear cataracts. Now why this occurs is , the lens in early stages of Cataract undergoes sclerosis. That increases the Power of the lens ( this increases the refractive index).
Thus it makes the lens slightly more Powerful , or Convex. Due to this it acts as a correction for Hyperopia/ Presbyopia (Where the error was due to a weaker lens. )
This transient Myopic nature of the eye is called the Myopic Shift.
It does go away when the Cataract progresses as the sclerosis begins to reduce refractive surface in the lens.

Hope this helped! Stay awesome  !
Happy Studying :)

~ A.P.Burkholderia

Infants of Diabetic Mothers (IDM) : A clinical overview

Hello

With the prevalence of insulin - dependent diabetes mellitus and maternal hyperglycemia, serious consequences to the ingrowing foetus may occur during its organogenesis. Lets have a quick review of the clinical problems in the infants of diabetic mothers ( IDM ) with some lame mnemonics :p -

GENERAL BUILT :
- Macrosomia ( birth weight >4,000 gm ) resulting in difficult labor and complications such as traumatic asphyxia, shoulder dystocia, BP injury, etc.
- Large for gestational age

CONGENITAL ANOMALIES :-

1. CARDIOVASCULAR - mnemonic : CASTeD
- Cyanotic heart disease
- Asymmetric septal hypertrophy ( resulating in small LV )
- Septal defects ( VSD, ASD )
- Transposition of blood vessels
- Decreased cardiac output ( due to perinatal asphyxia and metabolic acidosis )

2. SKELETAL AND CNS -
- Caudal regression syndrome
- Mental retardation

3. NEURAL TUBE DEFECTS - mnemonic : HAM

- Holoprosencephaly

- Anencephaly

- Meningomyelocoele

4. RENAL and GENITOURINARY - mnemonic : HURT

- Hydronephrosis

- Urethral dysplasia

- Renal agenesis

- Thrombosis of renal vein

( patient presents with flank mass, intermittent hematuria, and thrombocytopenia )

5. GASTROINTESTINAL - mnemonic : GAS

- Gastrointestinal obstruction ( due to duodenal atresia )

- Anorectal malformations

- Small left colon syndrome

6. RESPIRATORY -
- Hyaline membrane disease ( Infantile RDS )
- Persistent Pulmonary Hypertension

7. METABOLIC changes -

- Hyperbilirubinemia ( due to polycythemia )

- Hypoglycemia occurs 30 - 90 mins post delivery which may take several days to resolve. Rebound hypoglycemia may occur in response to rapid, large boluses of glucose ( 10-15 mg/kg/min ).

- Hypocalcemia ( levels <7 mg/dL ) occurs within hours to days after birth due to a delay in PTH synthesis after birth, often accompanied with Hypomagnesemia.


Thats all
Hope this helps :)

- Jaskunwar Singh

Mnemonico diagnostico : Risk approach to Antenatal cases

Hello

'High - risk' antenatal cases contribute to 70 - 80% of perinatal morbidity and mortality rates. The screening and diagnostic tests to evaluate and identify such cases is a must so as to provide special care to the mother - child duo. Risk approach for antenatal cases according to WHO includes : ( mnemonic - RISK APPROACH )

Prader-Willi syndrome and Angelman syndrome mnemonic

Hello! Let me start with the mnemonic and then I'll explain these syndromes in detail.

Hypersensitivity types mnemonics

Hypersensitivity types are:

Type 1 RTA pathophysiology, notes and mnemonic

Hello! This post is on type 1 renal tubular acidosis.

What causes Type 1 RTA?
Defective H+ ion secretion in the distal tubule.
Impairment in H+ ions secretion result in an inability to acidify the pH beyond 5.5 (Used in the diagnosis of type 1 RTA)


The plasma bicarbonate is significantly reduced and may fall below 10 meq/L.
These patients tend to have urinary K+ wasting and hypokalemia (thought to be due to increased potassium secretion by distal tubular cells in the setting of diminished H+ ion secretion.)

What type of RTA is associated with an enhanced chance if nephrolithiasis?
Distal or type 1 RTA can cause nephrocalcinosis / calcium oxalate kidney stones.
Mnemonic: ONE predisposes to stONEs

Pathophysiology: Hypercalciuria, hyperphosphatemia, nephrolithiasis (calcium phosphate stones) and nephrocalcinosis are frequently associated with untreated type 1 RTA. The hypercalciuria is thought to be due to:
1) increased calcium phosphate release from bone as a result of bone buffering of excess acid and
2) reduction in tubular calcium reabsorption secondary to chronic acidosis.
The hypercalciuria, alkaline urine, and reduced excretion of citrate in the urine (which normally prevents calcium crystallization) promote the precipitation of calcium phosphate and stone formation.

Which conditions are associated with type 1 RTA?
diStal RTA is associated with the 3 S's:
Sjogren's
SLE

Sickle cell anemia

Treatment: Bicarbonate administration

That's all!
-IkaN

Mnemonico diagnostico : Vitamin D deficient Rickets

Hey Awesomites

The clinical features specific for Rickets due to vitamin D deficiency are : Vit D BHP RICKETS

V - Visceroptosis ( due to ligament laxity )
D - DEXA scan / low bone Density
B - Bossing of skull
H - Harrison's groove
P - Ping pong ball sensation
R - Rachitic rosary
I - Iron deficiency and other anemias
C - Coxa vara
K - Kyphosis
E - Eruption of teeth ( delayed )
T - Thoracolumbar ( Lordosis )
S - Sternum and ribs protrusion ( Pigeon chest )


Thats all
- Jaskunwar Singh

Difference between Duodenal and Gastric Ulcer

Hello everyone, let’s talk about the ever confusing difference between Duodenal and Gastric Ulcer. Both the ulcers are a type of Peptic Ulcer which occurs due the action of acid resulting in the damage of alimentary mucosa. The main cause for both of them could be infection with H. pylori or intake of NSAIDs.

Mnemonico diagnostico : Klinefelter's syndrome

Hey Awesomites

Criteria for diagnosis of Klinefelter's syndrome in males mnemonic : KLINEFELTER

K - (K) Cryptorchidism
L - Leydig cells hypertrophy
I - Increased gonadotrophins
N - Negative/ Positive chromatism (aberrations)
E - Elongated legs
F - Failure of secondary sexual characters
E - Eunuchoidism
L - Late pubic hair
T - Testicular failure
E - Erectile dysfunction / Elbow deformities
R - Retardation (mental)


Thats all
- Jaskunwar Singh

Non Contraceptive uses of the Condom

Hi everyone. So we know what we use a condom for generally :p
But there are a few non Contraceptive uses for this magical device that prevents babies :').

So here goes -

1. Prevention of STD's.
2. Can be used in Balloon Tamponade to control PPH.
3. Used to cover the USG probe inserted into the female tract.
4. Can be used as a mould for the vagina during Vulvoplasty.
5. Women with Anti Sperm antibodies during the initial phase. (Controversial).

So that's about it.
We know no 5 more reasons to use condoms !
Go get em ; )
Happy studying.
Stay awesome.

~ A.P.Burkholderia

How to remember Hepatitis B is associated with membranous glomerulonephritis

Writing this post because I confused it with focal segmental glomerulonephritis yesterday.

Hepatitis B is associated with membranous glomerulonephritis.

Mnemonic: Happy memory - Heppy membory - Hepatitis B Membranous nephropathy :D

That's all!
-IkaN

Bromocriptine : Utility Review

Hi everyone ! Here's a brief review on the drug Bromocriptine which happens to be one of my favorite drugs. So here goes.

- Bromocriptine is a Dopaminergic agonist , specifically acting on the D2 Receptors.

- It is a very widely used drug , with various and multi systemic uses.

Uses :

1. Parkinson's disease.
- Bromocriptine and other D2 agonists like Rotigotine , Ropinirole and Pramipexole can be used to treat Parkinsonism.
- They act by providing a sort of  replacement for the depleted dopamine in the circuits of the basal ganglia.
- They are quite effective , especially in case of L Dopa resistance , or deterioration of symptoms when on L dopa.

2. Neuroleptic Malignant Syndrome.
- NMS is perhaps caused by D2 blockade due to drugs like Haloperidol and Fluphenazine.
- Thus it makes sense if you give this D2 agonist to treat this disorder.

3. Hyperprolactinemia.
- Dopamine acts as a Prolactin Inhibitory Factor (PIF) at the Hypthalamo-Pituitary level.
- In cases of Hyperprolactinemia where there is gynecomastia and galactorrhea,  giving D2 agonists counteracts the elevated prolactin levels.
- Thus it's useful in Anti psychotic/ Metoclopramide induced Hyperprolactinemia.
- Can be used in Ovulation induction due to elevated prolactin by a Pituitary adenoma.

4. Diabetes Mellitus.
- Bromocriptine modulates the Dopaminergic discharge at the Hypothalamus level.
- This modulates the circadian rhythm and resets the abnormal metabolic drive of the Hypothalamus and reduces the insulin resistance.
- The specific Quick Release formulation is used for this indication.
- It may be used in conjunction with Insulin and does not cause hypoglycemia.
- It cannot however be used for DKA

5. Acromegaly.
- Inhibits the excess Growth Hormone secretion by acting at the Hypothalamus level.

Hope this helped !
Happy studying and stay awesome!
~ A.P.Burkholderia

Neuroleptic Malignant Syndrome : A Crisp Overview

Hi everyone ! So I recently saw a patient who possibly had Neuroleptic malignant syndrome. So I though I would do a post on it !

1. The Syndrome -

NMS is an idiosyncratic reaction to Anti psychotic drugs. It causes a host of symptoms like Rigidity , Hyperpyrexia and altered consciousness.

2. The Etiology -

- All Antipsychotic drugs can cause NMS. But most commonly implicated are Haloperidol, Fluphenazine and Chlorpromazine.
- Especially at risk are those taking Depot preparations.
- Even lithium in high doses can precipitate this.
- Atypical Antipsychotic drugs have a lower propensity to cause this.

3. The Pathophysiology -
- Although largely speculative , the cause is said to be the dopaminergic blockade by the anti psychotic drugs.
- Blockade of D2 in Hypothalamus is responsible for the Behavioral and Temperature changes.
- Blockade of D2 in the basal ganglia ( nigro striatal pathway) causes the Rigidity.
- increased muscular activity can cause muscle break down.

4. The Clinical Features - 

- generally within 4-10 days after starting the Antipsychotic drug. But can even occur years later.
- Hyperthermia ( Hypothalamus is conked off )
- Lead pipe Rigidity ( Basal ganglia are screwed)
- Altered mental state - delirious.
- Sweating/ Diaphoresis  ( compensation for high temp)
- Tachycardia
- Dyspnea
- Urinary incontinence
- Dysphagia
- Pallor.

Symptoms develop over a period of 24-72 hours.

5. Tests -
- Creatine Phosphokinase (CPK MM) is raised
- Leukocytosis
- Low Iron
- Deranged LFT and LDH

( Can be used to differentiate from serotonin syndrome)

- Diagnosis requires Hyperthermia + Rigidity +   2  other features ( including riased leukocytes and CK MM)

6. Management -
- ABCD
- Ventilatory support if needed
- stop Antipsychotic drugs.
- Anti pyrectics . Ice packs. Cooling blankets.
- BDZ
- Specific -->
Dantrolene - Muscle relaxant and Hyperthermia management. 400 mg/D.

- Bromocriptine - D2 agonist.

- ECT may be needed.

Hope this was helpful ! Happy studying and Stay awesome.

~ A.P.Burkholderia

Reversible Causes of Dementia : Mnemonic

Hi everyone ! This is a short post on causes of dementia that can be corrected. This is very important as most causes other than these have no available treatment ! (One Reversible cause of dementia is the Demeantor's kiss ;;) Treat using  Expectro Patronum)

So the medically treatable causes include the following.

Remember : ABCD2E

- Alcoholism
- Vitamin B deficiency - Thiamine / Niacin /B12
- CNS infections - HIV , Chronic Meningoencephalitis , Whipple Disease, Neurosyphilis.
- Depression
- Drug induced
- Endocrine - Thyroid disturbances

Let's look at how these can be corrected medically.
- A = Alcohol abuse. May be a result of Alcoholic delirium/ Wernicke-Korsakoff syndrome. So the management would include giving Thiamine to the patient , and alcohol withdrawal using Disulfiram ans other anti craving drugs like Ondansetron, Acamprosate, Topiramate and Naltrexone.

- Vitamin B Deficiency = Thiamine deficiency we've seen above.
Niacin Deficiency causes 3 D's - Diarrhea , Dermatitis and Dementia. So treat that using Niacin.
B12 Deficiency and possibly folic acid can also cause Dementia.

- CNS Infections = They cause transient cognitive changes that are reversible on treating the disease.

- Depression = may cause depressive pseudodementia or even true dementia. (pseudo dementia = no confabulation or impaired recent memory)

- Drug induced = Chronic use of drugs like BDZ , Opiates and TCA's.

- Endocrine = Hypothyroidism is notorious to cause Dementia.

~~~~~~~~~~~~~~~~~~~~~~~

The surgically correctable causes are below.
Remember = T2 H2

- Tumors  (esp frontal lobe tumors )
- Trauma (Subdural Hematoma)
- Normal Pressure Hydrocephalus (NPH)
- Hydrocephalus

- Tumors are resected surgically.
-  For the hydrocephalus group , ventriculo peritoneal shunting is performed.
- NPH = Triad of symptoms showing Gait disturbances , Urinary incontinence and Dementia. (GUD)

Hope this post helped you and didn't leave you too demented. !  If it did, have some chocolate like Lupin would offer ;;)
Happy studying.
Stay awesome.

~ A.P.Burkholderia

Fact of the day: Nightmares are a warning for serious mental problems

Hello

Not one or two, but frequent nightmares are major caveats for underlying serious mental problems. Rapid Eye Movement sleep disorder is a rare disorder that causes the person to act violently during dreamy state. This may be a warning sign for major neurologic disorders like Parkinson's and neurodegenerative diseases like Alzheimer's !!

Night owls are more likely to have frequent sleep and mood disturbances than the early sleepers. Evidences suggest people suffering from nightmares and related sleep disorders are more likely to have suicidal tendencies than those not, in addition to other contributing factors.


- Jaskunwar Singh

Drugs causing hyperkalemia mnemonic

Hello!

I modified the K BANK mnemonic and added more to it to cover a few more drugs.

The mnemonic for drugs causing hyperkalemia is: K BANK Digs, cycles, sucks, self help (Sulf hep!)

K - Potassium sparing diuretics (Obviously!)

B - Non selective beta blockers

A - ACEI, ARBs

N - NSAIDs

K - Potassium supplements

Digs - Digoxin

Cycles - Cyclosporine

Sucks - Succinylcholine

Sulf - Sulfonamides, Trimethoprim

Hep - Heparin

That's all!

-IkaN

Direct acting cholinomimetic agonist mnemonic

Hi everyone, 

Here's the mnemonic for direct acting cholinomimetic drugs: ABC VPN

Nerve fibres : A clinico-physiological approach.

Hello everyone. So I've not been active at all lately , cause Final Year ! Pretty depressing 🙄. Anyway. Here's a post about the nerves and what we need to know for clinical application!

Nerves

So Erlanger and Gasser classified the nerves into A, B and C based on Myelination and size.

So you have :
A
(Which has Alpha , Beta , Gamma , Delta fibres )
B
C

Out of these , the first 3 : 
A - Alpha , Beta , Gamma = Large fibres which are largely Myelinated.

And next 3 :
A - Delta , B , C = Small fibres which are not Myelinated as much.

How I remember these fibres is as per evolutionary significance.
The least Myelinated fibres , which are the smallest are the ones all living creatures need. As we progress from C to B to A , we continue to gather more and more well developed and specialised fibres.

C -
The smallest fibres.
Least Myelinated.
Most basic fibres and most primitive from an evolutionary stand point !
Control sensations of Dull Pain and Temperature (Heat)

B -
Small fibres.
Low Myelination.
Next most Basic Instinct - Urination.
Controls your Autonomic nervous system.
Remember- B = Bladder

A Delta -
Moderately Small fibres.
Lower Myelination than other A fibres.
Responsible for sensation of Sharp pain and Temperature ( Cold )

Thus to summarize the small fibres -

We have C , B and A Delta.
Out of these
C and A Delta control Pain and Temperature
( where C controls Dull pain and Heat ; A Delta controls Sharp pain and Cold )
And B controls Bladder /ANS.

(How to remember A Delta vs C.
C is more primitive. Hence controls Dull pain. Sharp pain is a little more specialized and hence is controlled by the relatively more modern fibre - the A Delta)

Coming to the large fibres.

We progress from A gamma to A beta to A alpha.

A Gamma :
Large but smaller then Alpha and beta.
Myelinated but not as much as alpha and beta.
Responsible for muscle tone.
Remember : A Gamma = Gamma motor neuron which is responsible for tone.

A Beta :
Very large.
Well Myelinated.
Responsible for modern sensations like Fine touch, Pressure and Vibration.

A Alpha :
Largest.
Most Myelinated.
Responsible for Muscle Contraction and Most modern sense - Proprioception.
It's the Bomb of the fibres hence responsible for muscle contraction.

Thus , demyelinating diseases like Guillian Barre syndrome and CIDP would affect the fibres that are used to being Myelinated.
So your presentation in these diseases would generally involve loss of:
A Alpha - Motor + Proprioception
A Beta -  Modern sensations of fine touch and vibration.
A Gamma - Tone

And Axonal Polyneuropathic Diseases like Metabolic or Post infectious ones would involve loss and abnormalities of -
A Delta - Sharp Pain and Cold
B - ANS
C - Dull pain and Heat.

Hope this was helpful !
Happy studying !
Stay awesome.

~ A.P. Burkholderia