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? ;)

-VM

Education - a vaccine for violence

Hello

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.

Fact of the day: Ferritin is an inflammatory disease marker

Ferritin is an acute phase reactant.

Serum ferritin arises from damaged cells, and is thus a marker of cellular damage.

Medicowesome secret project: Hemispheres of the brain

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An overview of the NEET PG entrance exam

AN OVERVIEW OF THE NEET PG ENTRANCE EXAM
by Dr. Prateek Charuchandra Joshi (DNB AIR 291, MH state rank 51)

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!

-Medha!

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

Hello! 

Guess who made a new video?

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. :)

-VM

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!

Helloooo....

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!

-Medha!😊

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!

-Medha😊

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!

-Medha!

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!

Hello!

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...

-Medha.

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 :)

~Ojas

Medicowesome secret project: Exam time

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Medicowesome secret project: Embryo – Male or female?

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