Ischial Spines - Important Obstetric Landmark.

Hello There!

So let's enlist few important points in relation to the ischial spines.

Ischial spines can be generally be palpated at about a finger-length into the vagina, at 4 & 8o'clock.
They are felt as bony prominences and their palpation may cause a little discomfort to the patient.

These spines serve as a landmark for:

1) Engagement of Fetal Head.(Most commonly used for determining the Fetal Station during labor.
Ischial spines are considered as Station0)
2) Internal Rotation of the fetal head.
3) Pudendal Nerve Block.
4) External os.
5) Obstetric Curve (J shaped) takes forward curve at this level.
6) Insertion of levator Ani.
7) Plane of least pelvic dimension.
8) Ring pessary is kept at the level of ischial spines.

These are the few things I know about at the level of the Ischial spines.
Do let me know some additional points you know of, to add to the list.

Let's learn Together!
-Medha.

Umbilical Cord Knots.

Hello everybody!

Recently during my Ob-Gyn internship while delivering the placenta, the Umbilical cord that I held, was very lumpy bumpy. Little knowing about the reason at that moment, I came home found out the reason.
Let's see how the Umbilical cord can get knotty sometimes.

So there are two types of knots seen in the cord.
1)True Umbilical Knots
2)False Umbilical Knots.

True Knots :
These are noted after delivery. 

The umbilical vessels, are protected by the thick myxomatous Wharton jelly, and can rarely be occluded completely. The jelly protects the vessels and the fetal blood supply, as there is only flattening or dissipation of Wharton jelly when a Knot is formed.
Due to the knot some amount of venous congestion distal to it and some  partially or completely occlusive vascular thrombi may also be observed.

A true knot is formed when a loop of cord slips over the infant’s head or shoulders during delivery.
If the knot is pulled tightly it can cause fetal demise due to restriction of the circulation in the cord. 

The True Knots can occur due to:
1)A long cord, 
2)Large amounts of amniotic fluid
3)A small infant,
4)An overactive fetus
5)As a result of external version. 

(All the above causes lead to increased fetal movements in utero)

However the fetal mortality rate associated with true knots is low.

False Knots:
In the cord the blood vessels are longer than the cord and are often folded on themselves producing nodulations on  the surface of the cord. These nodulations are lumps and bumps I saw!
These have been termed as false knots.

So guys the next time you see a lumpy bumpy cord, unlike me, you now know the reason.
That's​ all, on the Umbilical cord and it's knots.

Let's learn Together!
-Medha.

Laryngomalacia vs tracheomalacia mnemonic

Laryngomalacia casuses inspiratory stridor.

Tracheomalacia causes expiratory stridor.

Terson Syndrome.

Hello everybody!

In this post let's quickly learn about Terson Syndrome.

So what is it?
This Syndrome is a combination of intraocular and subarachnoid haemorrhage secondary to aneurysmal rupture, most commonly arising from the anterior communicating artery.

Terson Syndrome along with other bleeding disorders is included amongst the Systemic causes of vitreous hemorrhage!

Intraocular haemorrhage is also seen to occur with:
1)Subdural haematoma
2)Acute elevation of intracranial pressure

The mechanism of intraocular bleeding:

There is increase in cavernous sinus pressure due to the subarachnoid/subdural hemorrhage leading to stasis in the retinal veins. This stasis in the retinal veins leads to increased intraluminal pressure in the veins making them susceptible to bleed.

The haemorrhage is often Bilateral.
Typically intraretinal and/or preretinal. With this hemorrhage there is a possibility of it leaking in the vitreous.

The vitreous haemorrhage usually resolves in a few months and the long-term, the visual prognosis is good.

I hope you guys found it useful. Do let me know about some neuro-opthalmology syndromes you know about.

Let's learn Together!
-Medha.

Innate Cellular Anti-retroviral Mechanisms

This post will focus on the mechanism by which a cell fights against HIV, mainly by interfering with its life cycle. There are only 3 such mechanisms discovered and elucidated till date.

As it says on the post, these are innate mechanisms most of which are upregulated by Interferons (alpha and gamma).The adaptive immune system is mostly ineffective against retroviruses. How? Earlier the most accepted hypothesis was that this is because of error-prone Reverse trancriptase which makes a lot of errors while forming the proviral ds DNA, hence causing hypermutations(mainly G to A) resuting in change in the viral antigenic domains. This is true for both HIV and HBV. 

1. APOBEC3G: The full form is Apolipoprotein B mRNA editing enzyme and catalytic polypeptide like 3g which you will easily forget and you should. It is basically a cytidine deaminase which acts on the negative cDNA strand and converts dC into dU; hence converting G into A in the positive strand. These hypermutations ultimately lead to failure of viral replication by unknown processes. So the latest most accepted hypothesis explaining the G to A hypermutations in virion DNA is this. This is more effective against HBV than HIV, guess why? Its because HIV-1 has Vif (Viral Infectivity Factor) that inactivates APOBEC3G.

2. TRIM5: This is the reason why Rhesus monkeys are innately resistant to HIV. Its an awesome protein in my opinion. What it does is as soon as the viral nucleocapsid enters the cell, it forms a cage around it and cause it to "uncoat" prematurely hence inactivating the reverse transcriptase and other enzymes present within the capsid. Then it performs a Kamikaze!

It ubiquitinates itself (auto-ubiquitination); hence causing its own proteasomal degradation and destroying the viral proteins in the process as collateral damage.

3. Tetherin: Now this is a case of Stockholm Syndrome! Tetherin are proteins that tethers or chains the virion to the cell membrane, hence preventing its release from the cell. The cell is not letting the virus leave her. So that when the cell dies either by apoptosis or inflammatory processes, the virions die with it. <3

Unfortunately however cool these may appear, these are mostly ineffective and hence the standard microbiology textbooks choose to ignore these proteins. Hopefully in future, drugs will be designed to make them more effective. :)

That's all!

-VM

Cerebellum and Motor learning!

Hello everybody!
Let's today learn about cerebellum and how amazing it is.

So all of us know that walking, swimming or typing needs conscious effort while being learnt for the first time, but after learning, one can continue these activities mechanically without having to think about them.

After learning, the responsibility for these activities seems to shift more and more to the cerebellum leaving the cerebral cortex free for other tasks.

That is why a child who is learning to walk has to put all his mind into it. Any distraction may make him fall. But as adults we can multitask along with walking.

Let's see how this happens.
There is evidence that cerebellar circuits can undergo functional changes as a result of experience.
The climbing fibres play an important role in this process. (bring information only from the inferior olivary nuclei, and establish excitatory synapses with Purkinje cells)
In a new situation, the climbing fibre activity is high, and it tends to reduce mossy fibre activity.
(Mossy fiber excitation not only stimulates Specific Purkinge cells but also inhibits the neighbouring Purkinge Cells.)
On repeated exposure to stimulus while learning, the mossy fibre response gets stabilized at the low level without an increase in the climbing fibre activity and the Cerebellar efferents perform the function semiautonomously on stabilized afferent input.

Thus Cerebellar learning may spare the cerebral cortex in the learnt movements.

I hope this was informative.

Let's learn together!
-Medha.

Drug: Evolocumab

This post will be on Evolocumab, a monoclonal antibody drug recently approved by FDA for use in refractory cases of Primary Hyperlipidemia and Homozygous(Not used in heterozygous) Familial Hypercholesterolemia alongwith Statins and appropriate diet and lifestyle modifications. 

Mechanism of Action:

As you know, LDL-Cholesterol is the bad cholesterol which is cleared by hepatocytes via surface LDL-receptors. These receptors are catabolized in hepatocytes by the enzyme proprotein convertase subtilisin/kexin subtype 9, fondly called PCSK9.

This enzyme is inhibited by Evolocumab, hence decreasing the intracellular clearance of LDL-R, thereby increasing the clearance of LDL-C from the body.

And Statins also help in raising the expression of LDL-R in hepatocytes by inhibiting HMG-CoA Reductase, hence decreasing cholesterol synthesis forcing the hepatocyte to extract more cholesterol from the blood.

The most common adverse effect is Nasopharyngitis which is easily manageable. And the black box warning is Hypersensitivity Reaction.

Look out for new drugs and ever-changing treatment and management guidelines and try to stay updated! :)

-VM

Medicowesome secret project: Let's talk about unhappiness

What is the "Let's talk" project? How can I talk about mental illnesses?

Medicowesome secret project: Let's talk about depression

What is the "Let's talk" project? How can I talk about mental illnesses?

Thalamus.

Helloooo everybody!
 let's quickly learn a few basics and beyond in today's post on Thalamus.

So thalamus is nothing but a collection of neurons which are organized well-defined nuclear masses.

The nuclei have confusing names and are difficult to remember too.

But from a functional point of view they are divisible into four groups to keep our lives simple.

1) Specific Sensory Nuclei
2) Association Nuclei
3) Nonspecific Nuclei
4) Motor Nuclei.

Specific Sensory Nuclei :These receive all sensory afferents. The arrangement of fibres is topographic and so is their projection to the somatosensory cortex. 

Corresponding to the thalamocortical projection fibres, there are also corticothalamic fibres which provide feedback information to the relay nuclei.

Let us now see how the sensory relay nuclei work.

A specific sensory stimulus activates neurons in the sensory relay nucleus.
                           
The thalamic nuclei activate some thalamic interneurons as well as an area in the sensory cortex. Activated sensory cortex also sends impulses back to the thalamic relay nucleus, thereby modulating the thalamic output.

In short, the sensory relay nuclei really do not act as simple relays.  They process the sensory signal by local intrathalamic circuits and descending corticothalamic  fibres before sending it to the sensory cortex.

Association Nuclei :
These help achieve integration of different types of sensory information.

Nonspecific​ Nuclei:
These also receive sensory information but project to the cortex in a diffuse manner.  Therefore they seem to be involved in the arousal induced by sensory stimuli.
They also project to the limbic system, thereby suggesting their involvement in the emotional impact of sensory stimuli.

Motor Nuclei :
They relay and process messages from the basal ganglia and cerebellum to the motor and premotor cortex.

All nuclear groups have to and fro connections with the cerebral cortex. Thus the thalamus and cortex function as one functional entity, the thalamocortical​ system.

Possibly the thalamus prepares a crude blue pint of the  final product achieved by the cortex.

The global involvement of the thalamus in central nervous function is revealed when its function is impaired, as in the thalamic syndrome.

Let's now quickly learn about Thalamic Syndrome.

Level of lesion : Posteroventral thalamus.

Etiology: Thrombosis of  Posterolateral branch of the posterior cerebral artery.

Manifestations :

1) Impairment of discrimination in sensory perception,
2) Hypotonia, muscular weakness and incoordination,
3) Volatile emotions, pleasant or unpleasant. 

After a few weeks to months, partial recovery may occur.

The sensations, regardless of the nature of the stimulus, may be very painful. 

The symptoms are thought to arise partly because the medial nuclei of the thalamus are spared by the lesion. 

 The medial nuclei are the nonspecific nuclei which receive major projections from pain  fibres.Hence the dominance of pain among the sensations. 

Well that's all on Thalamus,Hope it was helpful!

Let's learn Together!
-Medha.

Medicowesome secret project: Let's talk about seeking help

What is the "Let's talk" project? How can I talk about mental illnesses?

Medicowesome secret project: Let's talk about low self esteem

What is the "Let's talk" project? How can I talk about depression?

Treatment of migraine headaches mnemonic

Hello! Here's a short post on treatment of migraines!

Treatment of acute migraine attacks mnemonic: NSAiDs

N: NSAIDS like Naproxen, S, Aspirin, Ibuprofen, Diclofenac

S: Sumatriptan (And other Triptans such as rizatriptan, eletriptan, almotriptan, zolmitriptan, naratriptan, and frovatriptan)

AiDs: Antiemetic/dopamine receptor antagonists: Chlorpromazine, prochlorperazine, and metoclopramide

Ds: Dihydroergotamine and ergot derivatives

Prophylaxis of migraine mnemonic: ABC

Antidepressants: Amitriptyline and venlafaxine

Beta blockers: Metoprolol, propranolol, and timolol

AntiConvulsants: Valproate and topiramate

Calcium channel blockers (less effective): Verapamil, Flunarizine

That's all!
-IkaN