The Basics : Deviated Nasal Septum

Hello

Deviated Nasal Septum - "Abnormal and asymmetrical alignment of the nasal septum that results in acute nasal obstruction and other symptoms of upper respiratory tract."

AETIOLOGY -

1. Trauma : Abnormal pressure ( lateral or frontal ) applied to nasal septum results in its deviation to one side or another.
- The lateral blow may cause displacement of septal cartilage from the vomerine groove and maxillary crest.

Groove on which septal cartilage sits ( encircled ) - lateral view
Diagram by IkaN.

- Frontal blow causes crushing injuries to the nose, usually occurs in sportspersons especially the boxers.

2. Developmental anomalies : Palate forms the base of nasal septum. Highly arched palate, cleft palate or lip, and dental abnormalities can all lead to deviation of the septum.

3. Racial factors : Caucasians have more incidence of DNS.

4. Hereditary : Familial predisposition.


TYPES of DNS -

1. Anterior dislocation : dislocation of nasal septum into one of the chambers. ( unilateral nasal obstruction )
2. C - shaped dislocation : simple curve to one side with compensatory hypertrophy of turbinates in other side. It causes unilateral nasal obstruction.
3. S - shaped deformity : causes bilateral nasal obstruction
4. Spurs : shelf - like projections may lead to headache and epistaxis. ( unilateral obstruction )
5. Thickening : due to septal hematoma

CLINICAL FEATURES of DNS mnemonic

TREATMENT - Only required if the symptoms are severe. The procedures are to be done once the patient is more than 17 years old.

- Septoplasty : The most deviated parts of nasal septum are removed and rest of the parts are surgically corrected and repositioned.

- Submucous resection ( SMR ) : Mucoperiosteal and mucoperichondral flaps that overlie one side of the septum are lifted. Most of the septum is removed and flaps repositioned.

Thats all
Hope this helped :)

- Jaskunwar Singh

External Carotid Artery branches mnemonic

Hello

External Carotid Artery branches mnemonic - Seven Angry Ladies Fighting Over PMS

Cranial nerve III damage (Oculomotor nerve damage mnemonic)

Hello!

The CN III has both motor (central) and parasympathetic (peripheral) components.

Which fibers get affected in diabetes?
Which would lead to loss of pupillary light reflex?
Which fibers are compressed first?
Which would cause the down and out pupil?

Don't know? Check the video out!

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.