Sunday, April 30, 2017

Medicowesome secret project: Earth day poem

Collier's Sign

Hey guys!

Collier’s sign (“posterior fossa stare,” “tucked lid” sign) is elevation and retraction of the upper eyelids, baring the sclera above the cornea, with the eyes in the primary position or looking upward.

This may be seen with upper dorsal midbrain supranuclear lesions (e.g., Parinaud’s syndrome). There may be accompanying paralysis of vertical gaze (especially upgaze) and light-near pupil-
lary dissociation.

The sign is thought to reflect damage to the posterior commissure levator palpebrae superioris inhibitory fibers; causing overactivity of this muscle.

-VM

Hydatid cyst mnemonic

Here's a mini mnemonic on hydatid cyst. Caused by E. Granulosus.

H - Hepatic cysts common
Y -
D - Dogs are definitive host
A - Albendazole treatment (Remember, anaphylaxis risk if aspirated)
T -
I -
D -

C - Calcification (eggshell calcification)
Y -
S -
T -

That's all!
-IkaN

Phencyclidine intoxication mnemonic

A combative, agitated, psychotic patient with multi directional nystagmus, tachycardia and hypertension. 

Yup. You guessed it right. It's PCP intoxication. 

Here's a mnemonic 

Melanoma marker mnemonic

The immunohistological marker for melanoma is HMB 45.

You can remember it by remembering the gorilla named 'Harambe' (HaraMBe) of Cincinnati zoo who was in the news as he unfortunately had to be put down because a child entered his enclosure.

You can correlate melanoma's black pigment with that of Harambe's black fur.

That's​ all!

- Sushrut Dongargaonkar


Chronic granulomatous disease mnemonic

Chronic granulomatous disease mnemonic

CGD - GRANULES!
G - chronic Granulomatous disease
R - Rhodamine (Dihydrorhodamine abnormal flow cytometry)
R - ROS, Respiratory burst decreased
A - Abscess / Granulomas
N - Nitroblue tetrazolium dye test
N - NADPH oxidase defective

Catalase positive organisms mnemonic: CATALASE!
Candida
Aspergillus
Tuberculosis
Listeria
Staphylococcus aureus
Serratia
pSeudomonas
E coli

That's all!

-IkaN

Deglutition

Hello Everyone!
 Today lets discuss deglutition. Human's love this process :) .

1.What is Deglutition?
Process by which food  moves from mouth into stomach.

2.What are the different stages?
Oral
Pharyngeal
Oesophageal

3.Is it voluntary?

No, Only the Oral stage is voluntary.

4.What is the oral stage?

Bolus is pushed by the tongue into the Oropharynx.

What is the pharyngeal stage?
It is a involuntary stage. Here bolus moves from pharynx to oesophagus. Bolus has got 4 paths in pharynx
Back in mouth: This is prevented by position of tongue against soft palate.
Upward into nasopharynx: Prevented by elevation of soft palate.
Forward into larynx: Prevented as follows(Only if you don’t talk while swallowing food :P

  • Approximation of vocal cords
  • Forward and upward movement of vocal cords
  • Backward movements of epiglottis to seal opening of larynx
  • This causes Deglutition Apnea
Enters the Oesophagus:

  • Pharyngoesophageal sphincter relaxes.
  • Also upward movement of larynx stretches opening of oesophagus.




What is Oesophageal Stage?

Food from oesophagus enters the stomach.Peristaltic waves aid in this process.Two types of Waves are seen:
Primary peristaltic contractions
Secondary peristaltic contractions


What is the role of lower oesophageal sphincter(LES)?

It undergoes Receptive Relaxation. i.e. it relaxes only upon entry of bolus. Otherwise it is constricted.We have 2 clinical conditions associated with it:

1.Achlasia cardia : Failure of sphincter to relax during swallowing. Causes accumulation of food in oesophagus.

2.Gastroesophageal Reflex disease(GERD): Due to incompetence of LES. Acidic content from stomach regurgitates back into pharynx.


That's all,
Thank you,
Chaitanya Inge



Friday, April 28, 2017

Mnemonic for Sulci And Gyri of the cerebrum

Hello everyone,
  Memorising sulci and gyri of the cerebrum consists of two parts:

  1. Memorising the names of the sulci and gyri
  2. Memorising the locations
Today I will help you with the first part. Please bear with me, it will be a lengthy one.
Lets start with Superolateral surface
We have 4 regions on superolateral surface. They are

  1. Frontal 
  2. Parietal
  3. Temporal
  4. Occipital
Trick for superolateral surface revolves around 3 letters, they are: PSI

Frontal
Sulci- PSI      Gyri- PSIM
Sulci:
  1. Precentral 
  2. Superior frontal
  3. Inferior frontal
Gyri

  1. Precentral
  2. Superior Frontal
  3. Inferior frontal
  4. Middle frontal 
Temporal
Sulci:SI  Gyri: SMI
  Names of Sulci are:
  1. Superior Temporal
  2. Inferior Temoral
Gyri

  1. Superior Temporal
  2. Middle Temporal
  3. Inferior Temporal



Parietal
Sulci: PI Gyri: PSI
Sulci
  1. Postcentral
  2. Intraparietal
Gyri

  1. Post central 
  2. Superior Parietal
  3. Inferior Parietal
For occipital. Remember a simple mnemonic : Sulci- SaLLTy C    Gyri- Gisa.
Sulci
SaLLTy C
  1. Superior and Inferior Polar
  2. Lunate
  3. Lateral Occipital
  4. Transverse Occipital
  5. Calcarine
And the gyri
GISA
  1. Gyrus descendens
  2. Inferior Occipital
  3. Superior Occipital
  4. Arcus parieto-occipitalis.
So that completes the superolateral surface.
Now moving on to Medial Surface
  Here's the mnemonic CAPS. Men wear CAPs.  
Now  it goes like this Sulci- CCCAPPS. Gyri- Men wear CCaPPPPs
Sulci 
  1. Calcarine
  2. Callosal 
  3. Cingulate
  4. Anterior parolfactory
  5. Posterior Parolfactory
  6. Parieto-Occipital
  7. Suprasplenial or subparietal
Gyri
  1. Median frontal
  2. Cuneus
  3. Cingulate
  4. Paraterminal
  5. Paraolfactory
  6. Paracentral
  7. Precuneus
Finally moving to the Inferior Surface
 Here's the mnemonic
     when Cars HOORns  PeoPle LAugh LoudLy on boys playing GaMMes on streets!

Sulci (red coloured in mnemonic)



  1. Collateral
  2. H shaped orbital sulci
  3. Olfactory
  4. Occipitotemporal
  5. Rhinal

Gyri(purpled coloured in mnemonic

  1. Parahippocampal
  2. Posterior Orbital
  3. Lateral orbital
  4. Anterior Orbital
  5. Lingual
  6. Lateral Occipitotemporal
  7. Gyrus rectus
  8. Median Occipitotemporal
  9. Medial Orbital
Lets hope it will make memorising these things a bit easier.

That's all,
Thankyou,
Chaitanya Inge

Blood Supply And Nerve Supply of the Scalp



 Hello Everyone!
                Today we will discuss blood supply and nerve supply of the scalp. Just too many nerves and arteries out there. But there is a way out.
     First let us talk about nerves.

Nerve Supply:
  1.  Sensory
  2. Motor
Sensory:
Here's the trick
 In front of the auricle we have 4 nerves, and all are branches of trigeminal nerve.They are:
  1. Supratrochlear (Opthalmic division)
  2. Supraorbital  (Opthalmic division)
  3. Zygomaticotemporal (Maxillary division)
  4. Auriculotemporal (Mandibular division)
The remaining 4 are located behind the auricle. They are very simple to remember:
GaLeO Go To
  1. Great Auricular(C2,C3)
  2. Lesser Occipital(C2)
  3. Greater Occipital(C2)
  4. Third Occipital(C3)
Motor Supply:
In front of auricle: Temporal branch of facial nerve
Behind the auricle: Posterior auricular branch of facial nerve







Nerve supply of the Scalp 

Coming to the  Blood Supply:
  1. Arterial supply:
    1. Supratrochlear
    2. Supraorbital
    3. Superficial Temporal
    4. Posterior Auricular
    5. Occipital

  1. Venous Drainage: Common, thats simple. Names corresponds to arteries.
    • But there's a twist. The superficial temporal along with maxillary vein wants to drain in external as well as internal jugular. So they form retro mandibular vein whose course is pretty clear in diagram.



Blood Supply of the Scalp

That's all,
-Chaitanya Inge 



Thursday, April 27, 2017

How to draw midbrain sections and lesions (Fun mnemonic diagrams)

Hello everyone!

Brain sections are super hard to remember, I imagine them as monsters and this is how I draw them:

Paraneoplastic Dermatoses - Bazex Syndrome.

Hello everybody,

So to continue our series on cutaneous manifestations of internal malignancies
Let's quickly learn about Bazex Syndrome.

Bazex syndrome — acrokeratosis
paraneoplastica is a paraneoplastic phenomenon associated with squamous cell carcinoma of the upper digestive tract.

Presents more commonly in Males and over the age of 40.

Presentation: Erythematous to violaceous psoriasiform plaques predominantly located in acral areas (especially the fingers, toes, nose, and helices).

Nail dystrophy, palmoplantar keratoderma, and alopecia are common.

In most patients, manifestations of Bazex syndrome precede the diagnosis of malignancy or the malignancy is diagnosed concurrently.

The lesions of Bazex syndrome are usually resistant to targeted therapies, but treatment of the neoplasm usually leads to resolution of the cutaneous findings, although not always.

Let's learn together!
-Medha!

Wednesday, April 26, 2017

Medicowesome secret project: Journey of Medicowesome

Medicowesome secret project: Avoidant personality disorder

Medicowesome secret project: Panic disorder

Medicowesome secret project: A prayer for medicowesomites

Exam Prep Hacks -Tips for a lazy person

Hola everyone!

This post is for those people who really struggle during exam time, not because they can't understand studies or are stressed, but for someone who is really lazy and no amount of stress can change that (believe me I'm one of those :P)

So if you're someone who puts on their best game forward during exams and becomes a ninja  - this post is not for you! :P

Okay, so you know your exams are just around the corner and you have shit loads of syllabus to complete and you know there will be last minute panic yet you do not make a strategy and  "go with the flow", completely regret it later and are desperate to change this.

Understand that this post won't make you active all of a sudden, this post is all about embracing your laziness and turning into an asset and to rock your exams always without being under constant stress ;)

Let's get down to the basics then.

1. Always set rewards for yourself.
Sitting continuously for 5-6 hours IS JUST NOT POSSIBLE. Your concentration span is of a fly and you get distracted very easily, so instead of setting a target of studying for 5-6 hours continuously and then being disappointed later, make short targets. Like finishing one or two topics in one sitting and then maybe watching an episode of friends or going out for a walk. This way you feel like you've "earned" the break and will keep you motivated.

2. JUST SWITCH OFF YOUR PHONE.
Let's face it. Our phone's are the greatest source of distraction. Be it a whatsapp text, facebook notification or instagram post, we are constantly checking our phones. Either turn the internet off or put it on do not disturb mode, check the phones during your breaks.

3. Exercise!!!
Okay yes I get it, how is exercise gonna help me study? Remember endorphins- feel good hormones? Yeah well, they are secreted whenever we exercise. Exercise also help increase the blood flow and makes us more active. So, go for a walk for 20 min, skip in your room or dance, Whatever keeps you going, believe me, it's really gonna help. Will increase your concentration too!

4. Coffee.
I do not need to explain this. This is like a godsent drink!!  Everyone swears by it, but honestly, whatever will help you stay up.

5. Make realistic targets.
DO NOT set your goals according to others. Forget how your roommate is studying, how the lights of the topper of your class is always turned on. You know yourself the best. Do what suits you. Set targets for yourself. Setting targets according to others will just leave you disappointed and demotivated. It's a vicious cycle. Don't do it.

6. Select a time best suited for you.
Decide if you're a morning or a night person. And stick to that. Again, do not follow others. If you're a morning person, sleep well in time and wake up as early you can. If you're a night owl, prolong your study for as late as you can. Push yourself a little. Lol, just a little though :P

7. Sleep is your best friend.
Haha. Sleep to your rescue. It has been documented that sleep is very important to convert your short term memory to long term memory, so don't shy away taking those naps! :P Lack of sleep will cause dark circles too :P
But obviously not too long, 4-5 hours is adequate during exam time :P

8. Good diet.
Last but the most important part. Keep yourself hydrated and try to have a healthy diet, something which isn't too heavy. Heavy or oily food will just make you sleepy, tired and of course gain weight. Keep drinking water and fluids. Your brain needs food to function!

Hope all these things help you guys in acing your exams!
So the next time someone calls you lazy, Be Proud ;)

Ashita Kohli

Tuesday, April 25, 2017

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

Submissions : External Carotid Artery branches mnemonic

Hello

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

Superior Thyroid - Anterior branch
Ascending Pharyngeal - Medial
Lingual - Anterior
Facial - Anterior
Occipital - Posterior
Posterior auricular - Posterior
Maxillary - terminal
Superficial Temporal - terminal




Submitted by - Chaitanya Inge

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

Monday, April 24, 2017

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

Medicowesome secret project: Heart art

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

Medicowesome secret project: Let's talk about finding love

Medicowesome secret project: Earth Day

Sunday, April 23, 2017

'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

Saturday, April 22, 2017

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.

     1The 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.

Friday, April 21, 2017

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

Thursday, April 20, 2017

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

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

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

Wednesday, April 19, 2017

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 - dependant 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.

Tuesday, April 18, 2017

Hypersensitivity types mnemonics

Hypersensitivity types are:

Type 1 RTA pathophysiology, notes and mnemonics

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
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