Friday, March 31, 2017

Ion-exchange resins and Laxatives

In my last post on Hyperkalemia, I asked this question that why do we give laxatives with ion-exchange resins, eg. Sodium polystyrene sulfonate.

The reason is that if there is constipation due to Hyperkalemia or any other condition we are treating, besides these ion-exchange resins can themselves cause constipation; these resins will be stuck in the colon and the ion to which it is bound to will be reabsorbed into the circulation hence foiling the whole agenda.


Difference between polysaccharide vaccines and conjugated vaccines

Polysaccharides are strings of sugars. Some bacteria, such as Streptococcus pneumoniae and Neisseria meningitidis, have large amounts of polysaccharide on their surface, which encapsulate the bacteria. The polysaccharide capsules protect the bacteria from the host’s immune system and can make the bacteria more virulent. 

Polysaccharide vaccines are poorly immunogenic. They produce low affinity antibodies (which do not bind well to the antigen) and, because they do not elicit T-cell responses, immune memory does not develop. 

The new generation conjugate vaccines contain carrier proteins that are chemically attached to the polysaccharide antigens. Attaching relatively non-immunogenic polysaccharides to the highly immunogenic carrier proteins means that by activating a T-cell response, conjugate vaccines induce both high-affinity antibodies against the polysaccharide, and immune memory.

So in conclusion:

Polysaccharide vaccine - T cell independent B cell response

Conjugate vaccine -  Carrier proteins - T cell dependent B cell response

CT (Like a CT scan?)
ConjugaTe has a T cell response

That's all! 

Trastuzumab notes + mnemonic

Trastuzumab (Herceptin) is a humanized monoclonal antibody directed against the extracellular domain of the tyrosine kinase receptor HER2.

ARDS pathophysiology Q&A

In Acute Respiratory Distress Syndrome (ARDS), what happens to the following parameters? (Increase / decrease / normal) 

Pulmonary artery pressure
Pulmonary capillary wedge pressure
A-a gradient (Alveolar-arterial gradient)
PaO2 / FiO2

Answers given below!

Thursday, March 30, 2017

Medicowesome secret project: Cyclothymia

Fact of the day : Neuroticism and creative thinking

Hey Awesomites

While the medial prefrontal cortex is a part of the brain that shows high levels of activity in the neurotics, innovation of new ideas is also something the frontal areas of our ( mainly right ) brain function for.

There is often a preponderance to generation of self - generated thoughts and a perception of threat appraisal when there is no such actual external stimulus. The neurotics tend to 'create' situations of threat in their mind and respond accordingly, but they also come up with creative ideas to find solutions to such 'internal' problems by overthinking and overactivating their thought - provoking areas of brain. They also have oversensitive amygdalae, that is concerned with panic attacks, excess fear and anxiety.

Thats all
- Jaskunwar Singh

Did you know? Sir Isaac Newton suffered from bouts of depression and once had a mental breakdown. Inspite of that he made use of his creative mind and formulated laws of gravity, and fathomed several mathematical theories.

Sunday, March 26, 2017

Pregnancy risks related to hypertension

Important for multiple choice questions (=

Post partum hemorrhage
Placental abruption
Gestational diabetes

Preterm delivery
Growth restriction (Asymmetric IUGR, Head spared, Head abdominal ratio increased)
Still birth


Friday, March 24, 2017

Calcium Gluconate in Hyperkalemia

Hey guys!!

In this post I will try to explain why Calcium gluconate is the first line drug in managing hyperkalemia.

First of all, please form a mental image of normal cardiac action potential with the-
1- Very steep phase 0 caused by Na+ influx,
[Note: Vmax is the rate of build-up of membrane potential in phase 0]

2- A short, sharp phase 1 caused by K+ efflux via Transient outward K+ channel
( and some books say Cl- influx)

3- Phase 2 plateau phase caused by Ca2+ influx and K+ efflux via slow delayed rectifier channels.

4- And finally, the downsloping, not so steep repolarization phase caused by K+ efflux via Ikr (Rapid delayed rectifier channels) and also a few other channels which you can afford to forget.

Now what changes Hyperkalemia bring in this sequence of normal action potential?

1. Initially it increases myocardial excitability by raising the RMP from -90mv to approx -75mv; hence bringing it closer to the threshold potential. This is coz of the K+ concentration gradient alteration.

2. But as Hyperkalemia progresses, it causes myocardial depression by decreasing Vmax, essentially slowing down phase 0, hence causing increase in QRS complex duration. This is because the no of Na+ channels activated decreases if RMP becomes less negative.

3. Conversely, it increases the rate of Repolarization, hence causing shortening of QT interval. This is because of a strange reason. The Ikr which I have mentioned above becomes more active if the extracellular K+ levels are high.

Now that we know what happens in Hyperkalemia, let us learn how calcium gluconate amends these changes.

1. It makes the threshold potential become less negative, thereby restoring the normal difference between it and RMP. Myocardial excitability amended!

2. It increases Vmax. Myocardial depression amended!

3. It acts on the SA node and AV node and increases their automaticity further rectifying myocardial depression.

A word of caution! In patients having Hyperkalemia due to digitalis toxicity, hypercalcemia can potentially kill the patient. So in such conditions we use calcium gluconate cautiously only if-
1. There is loss of P waves
2. Widened QRS complex.

Other treatment modalities:

1. Insulin with Dextrose
2. Beta-2 Agonists​ like Albuterol

Both 1 and 2 work by increasing the activity of Na+-K+ ATPase.

3. Bicarbonate. It will cause increased pH which will increase the activity of H+-K+ exchangers.

4. Haemodialysis if it's readily available

5. Ion exchange resins like Sodium Polystyrene Sulfonate along with a laxative like Sorbitol.

A question for you guys, Why is it recommended to give a laxative with an ion exchange resin? ;)


Thursday, March 23, 2017

Education - a vaccine for violence


We are often so engulfed with racks of books to study and revise for exams that some might even go unrevised or untouched !! Many a times we notice poor children roaming on the streets and asking for coins and notes that are not of much value in their life. These children need education and proper guidance to re - track their life routes and help them fulfil their dreams. Poverty and lack of education in life makes such people feel helpless and force them to use illegal ways to fill their pockets.

" Brian was a poor boy. Born to a poor family, he worked all day to help his parents earn some money. Wearing a half - torn  white - turned - black tee and a faded brownish - black shorts, the eight -year old roamed here and there on the roads while holding some beautiful soft toys for being sold to the so-called 'high class' passers - by. Little did he know why was he doing all that. He was just told that he has to give the toys to some people and in return, he would get something called 'money'.

Then one day, he saw other boys of his age, carrying bags full of books and going to school. Fully energized, cheerful and in high spirits, they went on to their place. And Brian just saw them going. At that moment, he decided to change his life for the better. :)

Brian squandered his bag of toys on the roadside and started searching for a book store. A few hours passed but he couldn't find one. He knew nothing about shops, places, or any people around. He felt lone. It was a new place for him. He felt suffocated in the rising shades of darkness. The sun was getting closer to the horizon. The street lights scattered blue on the dusty road. He felt helpless and tired. Unable to get back to his home, he just slept on the footpath. Not even one eye focused on him inspite of busy streets and the flux of vehicles on the roads.

It was 8 in the morning. Seeing him still there and crying, an old man came up to him. Brian couldn't respond to any of his questions. The old man gave him some food to eat, and then took him to his house. There the little boy saw a library of books - just what he was finding since so long. He got overjoyed and went on to reach the shelves. The old man felt his curiosity to study. He asked the boy if he goes to school.

Brian told him his story after which the old man decided to help the little boy. He got him admitted to a reputed school. He gave him all he could. Books, clothes, food, shelter and work so that the little boy could help his family. And so now the boy was not poor any more. He got the treasure of his life - the books. :) "

In view of the Dhule incident a few days back, it is unethical and unacceptable for parents and relatives to demonstrate any act of physical and mental abuse towards a doctor if a patient with head injury cannot be saved due to the unfortunate circumstances such as the patient being brought late to the hospital and shortage of staff and equipment. These factors attract the need to shift the patient to a higher centre for provision of better treatment facilities and medical care.

The poor prefer to visit government hospitals and clinics because it suits their pockets. Referring the patient to a higher centre means more expensive and more delay in treatment. But that absolutely does not mean you argue with and abuse the doctor to force the treatment which cannot be done !!

Education is a key component to ensure that the person who has met with an accident and severely injured is immediately brought under medical care and treated successfully with suitable measures to save the life.

We, as responsible and educated citizens of the country must take steps to help the poor children and give them their weapons to fulfil dreams which seemed impossible to them. :)

That's all
- Jaskunwar Singh

Fact of the day: Histoplasmosis can present like sarcoidosis

Patients with histoplasmosis who have hilar lymphadenopathy, arthralgias, and erythema nodosum can be mistakenly given the diagnosis of sarcoidosis (“pseudosarcoidosis.”)

Steroids mistakenly given for sarcoidosis can cause acute exacerbation of histoplasmosis.

Tuesday, March 21, 2017

Brainstem Syndromes-Pons!

Hellooo people!

After travelling from the Midbrain  I we have reached  the Pons.. which literally means a Bridge... So .... Let's study the important eponymous Pontine syndromes today...

1) Millard-Gubler Syndrome:
Lesion location:Pons
Structures affected: CN VII ,Corticospinal tracts!!
Clinical features: Ipsilateral peripheral facial palsy; contralateral hemiparesis ,CN VI not involved

Foville's Syndrome(Raymond-Foville) :
Lesion location:Pons
Structures affected:CN VII; lateral gaze center; Corticospinal tracts.
Clinical features • Ipsilateral facial palsy and horizontal gaze palsy; contralateral hemiparesis

Raymond's (Yelloly, Landry) Syndrome: Lesion Location: Pons
Structures affected: CN VI; Corticospinal tracts
Clinical Features: Ipsilateral abducens palsy; contralateral hemiparesis ,it is  often lumped with Foville's syndrome.

There are other Pontine syndromes ...And an Anatomical classification of them makes them easy to understand !

I shall in the next post put up the respective syndromes along with associated diagrams..

Till then... Study Well Guys!
Also I would like to say... Medicine is not just science and theory but also an art to be understood.... So we all need to have the artists eyes and spot out the subtle presentations of the  diseases in our patients and treat them with all our hearts!


Monday, March 20, 2017

Fact of the day: High maternal cortisol good for foetal brain

Hey Awesomites

Neurodevelopment attained in the foetal period is greater than in any other period of an individual's life. Foetal exposure to "optimal levels" of maternal cortisol in third trimester has been linked to better cognitive and functional performance in the child.

Maternal cortisol acts on its receptors present in amygdala, hippocampus and the pre - frontal cortex ( PFC ) in high amounts. This hormone influences various stages of neurodevelopment including neurogenesis, axonal development, and myelination of nerve fibres and thus it leads to increased cortical thickness in frontal part of the brain and increased brain maturity.
Source )

Thats all
- Jaskunwar Singh

Brutons disease (X linked agammaglobulinemia) mnemonic

Guess who made a new video?

Saturday, March 18, 2017

Differentials of Unilateral Central Scotoma

Hey, guys this post will be on the differential diagnosis of "Blurred Vision in one eye" due to a central scotoma.

So a central scotoma can be usually due to retrobulbar neuritis(inflammation of the optic nerve) or optic nerve compression.

Now when you have detected a central scotomata in one eye it is essential to do the confrontation test in the other eye also. If in the other eye you detect a defect in upper temporal field, a superior temporal quandrantonopia; it is higly likely that this is a case of optic nerve compression.

How so? Well refer the attached pic with the illustrated diagram and I am sure you will understand. :)


Friday, March 17, 2017

Studying made simple: Ocular signs of thyrotoxicosis

Hey Awesomites

I read about ocular signs seen in patients with thyrotoxicosis. On googling and partly my work, studying these signs has become so simple to remember. -

Lhermitte's sign Variants!


Well we all know about the Lhermitte’s sign... The famous Barber's Chair sign!

For the people who are reading for the first time... Lhermitte's sign  is a sensation of tingling or electric shocks running down the back and legs on flexion of the neck.

Some other actions giving rise to similar sensations are:  Neck rotation, arm abduction, coughing ,Yawning 

It is common in multiple sclerosis, and other demyelinating diseases  but can occur with other conditions involving the cervical spinal cord.

But...Some variants to Lhermitte’s sign have also been described.

1) Delayed typical Lhermitte phenomenon can follow contusion of the spinal cord from neck trauma.

2) Reverse Lhermitte phenomenon
Paresthesias induced by neck extension have been described in extrinsic compression of the cervical spinal cord.

3) Inverse Lhermitte's sign:
Upward moving paresthesias with neck   flexion have been described in myelopathy from nitrous oxide inhalation.

I hope this was informative!


Brainstem syndromes-Midbrain!

Here we shall review three syndromes in the Midbrain occuring majorly due to a vascular event.
Weber's Syndrome:
Lesion Location: Midbrain base
Structures involved :CN III fibers; cerebral peduncle
Features: Ipsilateral CN III palsy; contralateral hemiparesis

(The image showing the involved 3 nerve and the crus! The lesion is anterior—in the cerebral peduncle—in  Weber’s syndrome, causing hemiparesis.)

Claude's Syndrome:
Lesion location :Midbrain tegmentum
Structures involved: CN III fibers; red nucleus; SCP
Clinical features: Ipsilateral CN III palsy; contralateral ataxia and tremor (“rubral tremor”)

(The sky blue line depicts the sup. Cerebellar peduncle! Lesion is more posterior—in the tegmentum—in Claude’s syndrome, causing hemiataxia.)

Benedikt's Syndrome:
Lesion location: Midbrain tegmentum
Structures involved: CN III fibers; red nucleus; CST (corticospinal tract)SCP(superior cerebellar peduncle)
Clinical features:
•Ipsilateral CN III palsy; contralateral hemiparesis with ataxia, hyperkinesia and tremor “rubral tremor

(The blue fibers being the sup. Cerebellar peduncle. In Benedikt’s syndrome, the lesion is more extensive, involving both the tegmentum and the peduncle, causing hemiparesis with tremor and ataxia of the involved limbs)

These three midbrain syndromes are variations on a theme.
Benedikt’s is essentially  Weber’s + Claude’s.

Because the fascicles of cranial nerve (CN) III are scattered in their course through the midbrain, the third nerve palsy in any of these syndromes may be partial.

Last on the list....
 Nothnagel's Syndrome mainly due to neoplasms ...affecting the Midbrain tectum involving Ipsilateral or bilateral CN 3 causes Oculomotor palsies; ataxia.

We finish Alll the midbrain syndromes !!!!!😎

Hope it helps!


Facts and Fallacies: Vitamin D link to cancer

Hey Awesomites

Vitamin D has been shown beneficial for a variety of disorders and diseases. Recent studies now suggest that those deficient in vitamin D are at a  higher risk of developing cancer compared to those with adequate levels.

Brainstem Syndromes!

So let's get done with all the important brainstem syndromes once and for all !
I would be writing on all of them one by one...
Also ...I will try and incorporate many of my diagrams to help you guys make it seem less daunting...
Starting from the Midbrain the first syndrome is..
(The image shows the level of the lesion)

1):Parinaud's Syndrome
Lesion location:Midbrain dorsum ,superior  collicculi.
Structures involved: Quadrigeminal plate region; pretectum; periaqueductal gray matter
Etiology: •Due to mass lesion in the region of the posterior third ventricle, most often pinealoma, or due to midbrain infarction.
Clinical features:
•Impaired upgaze as centre for upward gaze is affected
convergence retraction nystagmus;
Argyll Robertson pupil :dilated pupils with light near dissociation.

A closer look at the structures involved .

I hope it helped !Also do share your Neuroanatomy diagrams and and more information on Parinaud Syndrome.

Have a nice day!


Thursday, March 16, 2017

How I remember the duration of symptoms for Generalized anxiety disorder (GAD) required for diagnosis

The symptoms of generalized anxiety disorder should be present for at least 6 months. For me, it's hard to remember the duration of the symptoms in psychiatry. So I mnemonic-ify them :D

I remember G6PD, and say G6AD instead!

For those who don't know what GAD is here is the DSM V criteria for diagnosis of Generalized Anxiety Disorder...

Transposition of Great Arteries!


So I have divided the post into two parts - A short summary for those who don't have the time to read everything (#TLDR) and a nice long explanation for those who want to read everything :)
Let's start with TLDR.

Buzz words for congenital syphilis!

Following are some important signs and buzzwords that are testable ...And high yeild for entrances.

Olympian Brow: Bony prominence of the forehead caused by persistent or recurrent periostitis

Clavicular or Higoumenakia sign:Unilateral or bilateral thickening of the sternoclavicular third of the clavicle

Saber shins :Anterior bowing of the midportion of the tibia

Scaphoid scapula :Convexity along the medial border of the scapula

Hutchinson teeth:Peg-shaped upper central incisors; they erupt during 6th yr of life with abnormal enamel, resulting in a notch along the biting surface

Mulberry molars :Abnormal 1st lower (6 yr) molars characterized by small biting surface and excessive number of cusps

Saddle nose :Depression of the nasal root, a result of syphilitic rhinitis destroying adjacent bone and cartilage

Rhagades:Linear scars that extend in a spoke-like pattern from previous mucocutaneous fissures of the mouth, anus, and genitalia

Juvenile paresis :Latent meningovascular infection; it is rare and typically occurs during adolescence with behavioral changes, focal seizures, or loss of intellectual function

Juvenile tabes : Rare spinal cord involvement and cardiovascular involvement with aortitis

Hutchinson triad :Hutchinson teeth, interstitial keratitis, and 8th nerve deafness

Clutton joint :Unilateral or bilateral painless joint swelling (usually involving knees) from synovitis with sterile synovial fluid; spontaneous remission usually occurs after several weeks

Interstitial keratitis: Manifests with intense photophobia and lacrimation, followed within weeks or months by corneal opacification and complete blindness

8th nerve deafness: May be unilateral or bilateral, appears at any age, manifests initially as vertigo and high-tone hearing loss, and progresses to permanent deafness.

Well all these are late manifestations of congenital syphilis occuring after 2 years of life.
It is important to recognise these signs clinically and also on the exams...


Pathophysiology of myopathy caused during hypothyroidism and hyperthyroidism

Hello awesomites! Today's topic of discussion is - Myopathy in thyroid disease.
Interestingly, it is caused by both, hypothyroidism as well as hyperthyroidism.

What is myopathy?
It is a disease of muscle tissue where, ultimately, muscles get weak and are unable to perform work due to deficiency of ATP.

Why is there myopathy in hyperthyroidism?
The thyroid hormone is a catabolic hormone. Hyperthyroidism increases energy expenditure, glucose turnover, lipolysis, and protein breakdown (proteolysis). But here is the catch - Hyperthyroidism increases whole-body protein turnover and breakdown before any measurable changes in energy expenditure or glucose and fat metabolism, suggesting that amino acid and protein metabolism is an early and primary target for thyroid hormone action in humans. It was therefore concluded that the thyroid-hormone concentration may be an important factor in regulating muscle proteolysis. The altered protein metabolism causes myopathy.

Then, one may ask, why myopathy in hypothyroidism? Less thyroid hormone should lead to less protein breakdown, shouldn't it?

Well, this is a good question! Slightly complex and tricky to answer though. 

In hypothyroidism, there is abnormal glycogenolysis, defective mitochondrial oxidative metabolism and triglyceride storage.

Abnormal glycogenolysis and triglyceride storage: Less glucose is released and utilised because of this. The body starts using more proteins usually derived from muscles leading to myopathy.

Mitochondrial oxidative metabolism defect: Thyroid hormone is responsible for activation of bc1 complex also known as complex 3 & succinate dehydrogenase. Less activation of bc1 leads to less formation of ATP from glucose.... So again, the body switches to proteins from muscles as a source of energy!

That's all!
Stay cool :)

Medicowesome secret project: Exam time

Medicowesome secret project: Embryo – Male or female?

Medicowesome secret project: Ghrelin

Medicowesome secret project: Biostatistics

Wednesday, March 15, 2017

Fact of the day: Regulate brain activity with your type of music

Hey Awesomites

Which genre or type of music do you like the most? Well, it surely has to do a lot with the functioning of our brain. Some of you may like slow music while others like to rock n roll on the floor while listening to their favourite beats. I am more of the latter type too, depending on the mood. ;p

Saturday, March 11, 2017

Fact of the day: Paradoxical undressing in fatal hypothermia

Hypothermia causes paradoxical undressing.

This typically occurs during moderate to severe hypothermia, as the person becomes disoriented, confused, and combative. They may begin discarding their clothing, which, in turn, increases the rate of heat loss. It is estimated that twenty to fifty percent of hypothermia related deaths are due to paradoxical undressing.

Why does this happen?

Friday, March 10, 2017

Fact of the day: Psychosomatic symptoms love to travel

Hey Awesomites

Yes, you read it right. The symptoms of psychosomatic disorders flit from one body part to another, and just too easily and quickly ( they love to travel a lot ;p ) . Just as one symptom is discovered, it disappears and another one emerges in some other part of the body.

The psychosomatic symptoms have been linked to a chameleon. Every time a medicine tries to pin them down,  they become something different.

That's all
- Jaskunwar Singh

The colours of a chameleon are not more numerous and inconstant than the varieties of the hypochondriac and hysteric disease.
 - Robert Whytt

NYHA Classification Mnemonic

Hey guys, this post will help you to remember the definitions of the four NYHA classes.

So first just remember two phrases-
"Patient with a heart disease" and "in ordinary or accustomed activities". For convenience I will use letters A and B to refer to these phrases respectively. Now I will just fill in the gap between them.

1. NYHA Class I:
A--- will not get dyspnea ---B.

2. NYHA Class II:
A--- will get dyspnea ---B.

3. NYHA Class III:
A--- will get dyspnea in less than ---B.

4. NYHA Class IV:
A--- will get dyspnea at rest.

This system of classification has its flaws since the definition of "ordinary and accustomed activities" is entirely subjective. Like for example if a rich businessman gets breathless after walking 1 km, you may label him as NYHA Class II, but the same case in a hard working labourer will have to be labelled as NYHA Class III.

And another thing that NYHA has recently clarified NYHA Class III a bit further, it has included self-care activities in it's spectrum. As a supposition, if a 56 year old male person gets breathless while shaving or bathing then it is NYHA Class III.


Authors' diary: Medicowesome secret project

We initially introduced the secret project very mysteriously and kept the details highly confidential just for fun! Let me tell you more about it...

Thursday, March 9, 2017

Grave's ophthalmopathy features mnemonic

Hey Awesomites

Grave's disease, a common cause of primary hyperthyroidism causes some epic features of ophthalmopathy apart from lid retraction and lid lag. Mnemonic: EPIC

E- Exophthalmos
P- Periorbital Edema
I- Involvement of ocular muscles (diplopia)
C- Conjunctival irritation and chemosis

- Jaskunwar Singh

Amiodarone- induced thyroid dysfunctions


Amiodarone, a potent class III anti- arrhythmic drug is contraindicated in thyroid patients or those with subclinical disease. The reason lies in the pharmacokinetic profile of this drug.

The drug has a structural resemblance to triiodothyronine (T3) and thyroxine (T4). In the body, it is metabolized by dealkylation to Desethylamiodarone (DEA), the intrathyroidal concentration of which is higher than the parent drug.

Normal daily recommended intake of iodine for adults is approx. 0.15mg (150mcg).  Each 200mg tablet of amiodarone contains about 74.4mg of iodine with 7.4mg (10%) being released as free form. This is roughly 50- fold higher than the normal. Therefore, total body stores may remain increased for upto 9 months after stopping the drug.

High iodine content of this drug inhibits  local type-1 5'- deiodinase activity (blocking conversion of T4 to T3) and type- II 5'- deiodinase activity in the pituitary. As a result, TSH is increased initially (mild elevation) and then return to normal or may even decrease in euthyroid patients after weeks, while T4 is normal or raised, and T3 levels decrease.

The increased delivery and uptake of iodine by the thyroid gland may cause increase in hormone production and release, a condition called type-1 Amiodarone- induced thyrotoxicosis (AIT) . In other cases, excessive thyroid tissue destruction due to destructive thyroiditis may lead to type-2 Amiodarone- induced thyrotoxicosis. These are hyperthyroid states!!
Discontinuation of the drug is recommended, if not, then high doses of thioamides and corticosteroids may work in AITs.

Amiodarone may also cause hypothyroidism (AIH) in  patients depending upon the iodine status of individuals and prior thyroid disease. Wolff- chaikoff effect is shown by thyroid cells due to failure of thyroid hormonogenesis. Levothyroxine is the drug of choice.

Thats all
- Jaskunwar Singh

Wednesday, March 8, 2017

Fact of the day: Burning the heart to ashes

An interesting fact about heart I read today:

The heart is resilient, literally. When a body is burnt, the heart is the last organ to oxidize. While the rest of the body can catch flame like a polyester sheet on campfire, it takes hours to burn the heart to ash because it's deep inside!

That's all!

Did you know? According to Hindu mythology, when Arjuna cremated the body of Lord Krishna, his whole body turned into ashes, except his heart which was still burning. Arjuna washed the ashes and burning heart into the river.

- Jaskunwar Singh

Munchausen's syndrome


"Psychosomatic disorders are conditions in which a person suffers from significant physical symptoms (causing real distress and disability), that is out of proportion to that which can be explained by medical tests and physical examinations."

Karl Friedrich Von Munchausen, the "Baron of Lies" gave his name to the syndrome. Munchausen's syndrome (now more correctly called factitious disorder in DSM- 5 classification of somatic symptom and related disorders ) refers to patients who imitate illness (may be in an exaggerated form ) for medical attention and care and may even expose themselves to life- threatening operations, amputations, unnecessary medications and toxic treatments.

Lets take an example: A woman presents to hospital with a headache and a dilated pupil. On investigations, scans were normal and no other systemic abnormality seen. Then, a nurse walks into her room and finds the patient self- administering dilating eye drops into the affected eye.

The person has an awareness of the lies they are telling but they surely do it to seek medical care and attention, being unaware of their own motivation and uncontrolled behavior.

Upto one- third of patients in neurology ward suffer from psychosomatic illness and most often, an emotional cause is suspected.

Thats all
- Jaskunwar Singh

Parinauds syndrome notes, mnemonic and a video

Parinauds syndrome notes + mnemonic + video!

Is it okay to wish a man "Happy Women's Day"?

Hello awesomites!

Happy women's day to everyone - Male and female!

Tuesday, March 7, 2017

Study group discussion: PGE and congenital heart diseases

We had a discussion on this question on our study group today :)

PGE causes clinical worsening in an infant with?
A. PS without VSD
B. Hypoplastic left heart syndrome
C. Obstructive TAPVC
D. Obstruction in Aorta

Let's work this out - choice by choice!

Acute intermittent porphyria mnemonic

Acute intermittent porphria - AIP - That's the mnemonic!

Asbestosis and Silicosis mnemonics

Here are a few mnemonics to help you not mix these conditions up!

Monday, March 6, 2017

Hyperthermia in Pontine Haemorrhage

Hey guys!

This post will be focused on the pathophysiology of Hyperthermia in Pontine Haemorrhage( which may manifest as the Locked-in Syndrome, remember that super-awesome House episode? <3 )

1. First try the easy simple reason. Hypothalamus has been basically cut off from the body below pons and there has been Haemorrhage. Therefore, there will be a Sympathetic outflow causing peripheral vasoconstriction. Meanwhile the internal visceral organs are still functioning and consequently producing heat. So without hypothalamus, the body's ability to produce heat has transcended it's ability to lose heat.

2. The next reason is a bit "cooler", literally. Our body hates Hypothermia more than Hyperthermia, thanks to evolution. (Ice Age!!!) Now there is no central thermoregulation but peripheral one is still intact. And the peripheral thermoreceptors are much more sensitive to lower temperatures or basically cold environment. Once again, without the Hypothalamus, the body is defending itself too vigorously against Hypothermia as to contribute ironically to Hyperthermia.

3. This reason is the only one which you should know since this will explain how Baclofen, a GABA-B Agonist works to treat this Hyperthermia. Remember the Medial Forebrain Bundle, it connects Hypothalamus to a lot of structures, one of them being Nucleus Raphe in the Pontine reticular formation. This is a very crucial portal in control of Sympathetic nervous system outflow by Hypothalamus. Simply speaking, if the body is hot, Hypothalamus will send inhibitory (GABAergic and Dopaminergic) signals to this nucleus and if the body is cold, it will send excitatory (Glutaminergic and Serotonergic) signals. And apparently this connection is lost in Pontine Haemorrhage, so we substitute it with a drug.

P.S. Now you can guess how Bromocriptine and Apomorphine cause Hypothermia. :)


Fact of the day: Blood coagulopathies in Familial Hypercholesterolemia


It is known since long that familial hypercholesterolemia is associated with increased risk of cardiovascular disease as a consequence of atherosclerotic plaques in blood vessels. But Its NOT due  to high cholesterol levels in blood !!

The cause of such consequences lies in genetics. Genetic aberrations in patients with FH include variations in Prothrombin gene which increases coagulation and clot formation. This ultimately blocks the arteries by forming plaques!

Heart patients with FH also have higher concentrations of Fibrinogen and Factor VIII in their blood in addition to other factors, compared to healthy ones.

People with familial hypercholesterolemia tend to live a longer life than those with low cholesterol levels, suggesting a minor role of high cholesterol in pathogenesis of the disease.

However, cholesterol is still associated with other systemic diseases, though recently LDL has been considered 'good' too!

That's all
- Jaskunwar Singh

Sunday, March 5, 2017

Fact of the day: Proton pump inhibitors and osteoporosis

Chronic PPI usage is associated with an increase occurrence of bone fractures, at present, the likely mechanism of this affect, is not at all clear.

The assumed mechanism is that long-term PPI use leads to decreased intestinal absorption of calcium resulting in negative calcium balance, increased osteoporosis, development of secondary hyperparathyroidism, increased bone loss and increased fractures.

An acidic environment in the stomach facilitates the release of ionzed calcium from insoluble calcium salts, and the calcium solubilization is thought to be important for calcium absorption. 

That's all!
Happy studying!

Saturday, March 4, 2017

Facts and Fallacies: Almonds for Migraine


Some people who suffer from migraine are found to be deficient in magnesium and certain  vitamins. This proves to be one of the factor for causing such attacks!

Almonds are rich in magnesium and vitamin B2 ( riboflavin ) and contain salicin, an anti-  inflammatory agent and ingredient in aspirin. So 10- 12 almonds a day, equivalent to 2 aspirins helps in preventing acute attacks of migraine.

However, for those who are allergic to salicin, almonds may even trigger migraine attacks! Therefore prior testing is important in such cases.

Many recent updates and drugs have become available to treat the attacks but no single one is effective in long- term. For those deficient in magnesium and allergic to salicin,  infuse magnesium sulfate solution i.v.  over 3- 5 minutes.

That's all
- Jaskunwar Singh

Thursday, March 2, 2017

The story of Medicowesome (With Q&A)

Here's the video to the many questions people have asked me till date:
How did Medicowesome start? How do you manage blogging and studying? etc etc.

Pediatric milestones mnemonic

Another awesome video by Shilika!

Fact of the day: Multi- vitamin supplements beneficial for schizophrenics


Recent studies suggest that high- doses of vitamin B help in reducing the symptoms of schizophrenic patients and those with other neuropsychological disorders, when added to the normal treatment in early stages. (Source)

- Jaskunwar Singh

Wednesday, March 1, 2017