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 :)