Top 10 series: Everolimus

Post MI complications mnemonic

Hey Awesomites!

Complications due to an attack of myocardial infarction mnemonic: DARTH VADER (I loved his character in Star wars you know :p )

D- Dressler's syndrome
A- Arrhythmia
R- Rupture
T- Tamponade
H- Heart failure
V- Valvular defects
A- Aneurysm
D- Death!
E- Embolism
R- Recurrence


That's all
- Jaskunwar Singh

Cushing's Reflex in Meningitis : Mnemonic and Explanation

Hello everyone !
Another short post on a very important triad. Cushing's!

Cushing's reflex
It occurs in response to raised Intracranial Pressure (ICP/ICT)

Mnemonic : 

HIB

H - Hypertension
I   - Irregular Breathing
B - Bradycardia

Mechanism :
So just imagine :
Due to some reason you develop an increase in the ICT.
We know that blood flows from High Pressure to Low Pressure. Generally , the CSF pressure is lower than the BP.
However after a point , the ICT is bound to become equal to or even more than the systemic BP!
If that happens , the blood flow to the brain is decreased and the Brain can get ischemic (cause the Cranial pressure would be higher. So the body won't be able to pump the blood into it.)

Thus, in order to compensate for this , the sympathetic system is activated. The body's peripheral vessels undergo constriction to raise the BP. This would keep them at a higher pressure than the Cranium thus keeping the blood flow intact for a while at least. This causes the Systemic Hypertension.

In a way it's the last ditch effort to save the brain!
Due to sympathetic stimulation the respiratory centers get stimulated too and it's all weird so it causes Irregular Respiration.

Now you'd expect Tachycardia when there is so many Sympathetic juices flowing through your body.
But no. Things aren't as simple as that.

The aortic baroreceptors sense the increased BP and end up decreasing the Heart Rate. Resulting in Bradycardia. So in a way that's the 2nd phase of this Reflex!

The Reflex serves as a marker of raised ICT as that is the event that puts the whole cycle into place.
This generally occurs as the body's last resort to restore blood to the brain.
What a wonderful Homeostatic mechanism !!

Hope this helped !
Stay awesome !

Reynolds pentads

Hello readers ! Today's blog is sweet and simple.

Reynolds pentads are collection of signs and symptoms appearing when there is obstructive cholangitis -infection of bile duct usually caused by bacteria .Following are the diagnostic features of the reynolds pentads with simple  mnemonic.
   RJ -FHC.
R-Right upper quadrant pain .
J-Jaundice .
F-Fever .
H-Hypotension.
C-Confusion .

By the way the first three diagnostic features are also called as Charcot's triad so we can also say Reynolds traid is combination of charcot's triad with low blood pressure and mental confusion .

Stay awesome:)

~Ojas

Neonatal reflexes mnemonic

Hey Awesomites!

Here's a mnemonic for the reflexes seen in neonates and infants: GRASPMEN

G- Grasp reflex/ Glabellar tap
R- Rooting reflex (to assist breastfeeding)
A- Automatic walking reflex
S- Suckling reflex (during breastfeeding)
P- Plantar Reflex
M- Moro's reflex
E- Extrusion reflex
N- Neck (tonic reflex)

That's all
- Jaskunwar Singh

Tuberculosis : Ocular Manifestations

Hello everyone !
This is a short post about the manifestations of Tuberculosis in the eye.

TB is associated with a lot of findings in the eye.
We can classify them as :
1. Disease related.
2. Therapy related.

Let's look at the first one.

1. Disease related :

A. Extra Ocular structures -

    I. Appendages :
       Eyelid - Lupus Vulgaris. Lid granuloma.
       Lacrimal apparatus - TB Dacryoadenitis. Dacryocystitis.
      
    II. Orbit :
         Orbital Cellulitis.
         Orbital Pseudotumor.

B. Ocular manifestations -
    
     I. Conjunctiva -
         Phlyctenular Conjunctivitis - due to hypersensitivity to Tuberculin. Seen as intense itching , discharge , redness and nodules.

     II. Cornea -
          Interstitial Keratitis

     III. Uvea -
          Granulomatous uveitis ( Chronic anterior Uveitis ). Shows Mutton Fat appearance.

          Choroiditis - Choroid Tubercles - classic of TB Uveitis. Tuberculoma may be seen. Miliary choroid nodules may be seen.

      IV. Retina -
            Eale's disease - may be a result of Hypersensitivity to Tuberculin. Although causality is not established clearly.
           Sub retinal Tubercles.

2. Therapy Related :

       A. Ethambutol - may cause Optic Neuritis - generally retrobulbar type. With Color Blindness.

      B. INH - Isoniazid can cause retrobulbar optic neuritis, although this is much rarer.

     C. Immune Reconstitution Inflammatory Syndrome - When a person recuperates from TB /HIV his immune system may become hyperactive and show Immunologically mediated uveitis.

Hope this helps !
Happy studying.
Stay awesome. 

~A.P.Burkholderia

Nodule at the Limbus : Mnemonic

Hello everyone !
Here's a way to remember the D/D's of Nodules at the Limbus.

Mnemonic :
Please Please Please ! Eat Spicy MCDonald's Tortilla.

Please - Pterygium.
Please - Pinguecula.
Please - Phlycten.
Eat - Episcleritis.
Spicy - Scleritis.
M - Melanoma. 
C -  Choristoma
Donald - Dermoid.
Tortilla - Trachoma. Tranta spots.

1. Out of these Pterygium , Pinguecula and Phlyctens are Conjunctival lesions.
Pterygium is a fold of conjunctiva that encroaches towards the pupil.
It can be vascular and nodule like. Can cause Foreign body sensation and decreased vision if it covers the pupil.
It may also cause Diplopia and a Squint due to its traction over the eye.
A pinguecula is milky like nodular swelling of the conjunctiva.
A Phlycten is a lesion in Phlyctenular Conjunctivitis which is an allergic or Hypersensitivity response to Tuberculin or staph Antigens. There is intense itching , discharge and nodules in the eye - called Phlyctens.

2. The lesions of Episcleritis and Scleritis are similar. They're both associated with systemic disease like Rheumatoid Arthritis , SLE, Sarcoidosis etc.
Scleritis is a more severe one of the two. There's marked redness and congestion of the eye along with multiple vascular nodules. The eye is very inflamed. There is intense pain and watering. It needs urgent treatment. It may causes various types of staphylomas.
Episcleritis is a more benign form. There is intense itching , nodular vascularity and discharge with some amount of congestion.

3. Tumors like Choristoma , Dermoid tumor and Melanoma mainly arise from the uvea. They're not very common.

4. Trachoma : presence of lesions in trachoma at the nodule may be prominent. You may also get 'Horner Tranta spots' in Vernal Keratoconjunctivitis which is an allergic Conjunctivitis.

Hope this helped !
Stay awesome !
Happy Studying!

How to check for the Pupils : Clinical Pearl

Hello everyone !
This is a post about how to look for a normal pupil while doing an ophthalmological examination.
So here goes :

1. The Setting.
- Relax the Patient
- Take the patient to a semi dark room.
- Make the patient Fixate on a distant point to eliminate any error that Accomodation may produce.
- Place an obstruction between the two eyes.
- Always shine your torch laterally and bring it in only from the sides to avoid light shining directly on the other eye.

2. The Parameters.
Look for the following in the pupils :
- Size
- Shape  ( for eg. You may get a Festooned pupil on adding your Mydriasis if the patient has adhesions)
- Number ( for eg. You may get Poly Coria which causes Diplopia )
- Location  ( for eg. You may get Corectopia)

3. Reaction to light.
- Unless you've met the criteria above ( The setting) , you cannot say 'Direct and indirect reflex present' .
So unless you're in a semi dark room (and the other 3 criteria mentioned above) you would plainly shine the torch and look for constriction. This plainly shows the pupils are reactive to light.

4. Light Reflexes.   
- Check for your direct and consentual (indirect) reflexes in both your eyes after meeting the listed Criteria in the *Setting* !

Hope this helps !
Happy studying !
Stay aweosme.

~A.P.Burkholderia

Argyll Robertson Pupil : Mnemonic

Hello everyone ! I'm back with a short and sweet post on Argyll Robertson Pupil.

Mnemonic for Argyll Robertson  Pupil (ARP) :
ARP Accomodation reflex present
PRA Pupillary reflex absent.

It's seen in conditions like Neurosyphilis for which it is extremely specific. 
You could also see it in some form of strokes or Diabetic Neuropathy.

Another similar Pupillary reaction is Aedes pupil. The difference is Aedes is a  dilated pupil while Argyll's is constricted. How to remember this ?
Mnemonic : AeDes.
So Aedes is tonically Dilated.

Hope this helped !
Stay aweosme.
Thanks.

Treatment of Narcolepsy

Hey Awesomites!
This is the last post of the four-post series on Narcolepsy. So let's begin.

Diagnosis of Narcolepsy

Hello friends!!

This is the third one in the four-post series on Narcolepsy. Let's commence.

Diagnosing a not so common disorder, that too neurological is quite tricky. The greatest difficulty is separating it from the normal daytime and postprandial sleepiness of most people. Admit it, most of us feel like sleeping in the afternoon period after lunch, especially while reclining in the sofa, while watching television or in the theatres watching matinee shows. :p  

What distinguishes the typical narcoleptic attack from commonplace postprandial drowsiness and napping is the frequent occurrence of the former(2 to 6 times everyday), their irresistibility, and their occurrence in unusual situations, as while eating, standing, or carrying on a conversation.

Excessive daytime sleepiness can also be present with heart failure, hypothyroidism, use of antihistaminics, alcohol intake, head trauma, certain brain tumours like craniopharyngioma etc.

 

Overnight polysomnography followed by a standardized multiple sleep latency test can exclude other causes of excessive daytime sleepiness like obstructive sleep apnea. In the test, the patient is given 5 opportunities to nap at 2 hour intervals in a day

. 

If there are more than 2 Sleep-onset REM periods and a mean sleep latency of less than 8 minutes, it strongly suggests narcolepsy. 

Actually, in Narcolepsy, there is characteristic reversal in the order of the two states of sleep, with REM (rather than NREM) phase occurring  at the onset of sleep attacks. And the sleep latency is nothing but the interval between the point when an individual tries to sleep and the point of onset of sleep with the respective EEG patterns.

Measurement of hypocretin(orexin) levels in the CSF may help establish the diagnosis; a level lower than 110pg/ml is diagnostic of narcolepsy.

Cataplexy must also be distinguished from syncope, drop attacks and atonic seizures. In atonic seizures, there is temporary loss of consciousness, while in narcolepsy consciousness is perfectly preserved. 

That's all! Do go through the other posts in this series.

Role of Orexins in Narcolepsy
Clinical features of Narcolepsy
Treatment of Narcolepsy

-VM

Clinical Features of Narcolepsy

Hello friends!!

This is the second one in the four-post series on Narcolepsy. So let's begin.

Narcolepsy is not just a disorder in which the patient sleeps a lot, believe it or not the number of hours in a day spent in sleep by the narcoleptic is no greater than that of a normal individual!!

Narcolepsy is characterized by the classic tetrad of excessive daytime sleepiness, cataplexy, hypnagogic hallucinations and sleep paralysis. There is also a disorder of REM sleep. So let us try to understand these major clinical features.

The essential disorder is one of frequent attacks of irresistible sleepiness several times a day, usually after meals or while sitting in class or in other boring and sedentary situations. Now let us try to picturize the patient.

The eyes close, the muscles relax, breathing deepens slightly and it seems that the individual is dozing. A noise, a touch or even the cessation of lecturer’s voice is enough to awaken the patient. So the periods of sleep rarely last longer than 15min unless the patient is reclining, or if he is in an appropriately comfortable situation to sleep. At the conclusion of the nap, the patient feels somewhat refreshed.

Cataplexy refers to a sudden loss of muscle tone brought on by strong emotion- that is, circumstances in which hearty laughter or, more rarely, excitement, surprise, anger, intense athletic activity. So you can basically “tickle” a Narcoleptic into a Cataplectic state. 

The patient’s head will fall forward, jaw will drop, knees will buckle with sinking to the ground – all with perfect preservation of consciousness (scary, right?). Most attacks of cataplexy are partial, eg., only dropping of the jaw or weakening of the knees.

In about half the patients, there is hypnagogic hallucination and sleep paralysis. Please do not confuse sleep paralysis with cataplexy; sleep paralysis is brief loss of control(not tone) of voluntary muscles that occurs during the period of falling asleep or less often when awakening.

There are two terms which we should know, hypnagogic and hypnopompic. Hypnagogic or predormital refers to the period of falling asleep while hypnopompic or postdormital refers to the period of awakening. Sometimes there may be vivid and terrifying hallucinations with or before the onset of sleep paralysis, which may be visual, auditory, vestibular or somatic, called hypnagogic hallucinations.

That's all. Do go through the other posts in this series.

Role of Orexins in Narcolepsy
Diagnosis of Narcolepsy
Treatment of Narcolepsy

-VM 

Role of Hypocretins/Orexins in Narcolepsy

Hello friends!!

This is the first of the four-post series on Narcolepsy.

So let's start. The hypocretins were thought in the past to regulate feeding behaviour and energy metabolism, the word “orexin” is derived from the Greek word for appetite. But later through animal experimentation it was found that in mice, inactivation of two hypocretin receptors reproduces Narcolepsy.

First of all, let us learn that monoaminergic neuronal projections from Tuberomammilary nucleus(histaminergic), Locus Ceruleus(noradrenergic) and the Raphe nucleus(serotonergic) inhibit the Ventrolateral Preoptic Nucleus(VLPO) of hypothalamus.

To put it simply, the transition between sleep and waking is determined by the state of activity of the VLPO. Now imagine a see-saw, on one side we have all these nuclei wanting the person to wake up and on the other side we have VLPO forcing the person to sleep. Whoever gets heavier, metaphorically speaking, chooses the person’s state. 

So what’s the role of orexin/hypocretin ? We can say that it enables a smooth transition between wakefulness to sleep by reinforcing the monoaminergic firing from those three nuclei; hence it indirectly inhibits the VLPO. Hence if we remove orexin from the picture, the person will fall asleep immediately without being able to control; and roughly this is what occurs in Narcolepsy. 

That's all. Do go through the subsequent posts in this series.

Clinical features of Narcolepsy
Diagnosis of Narcolepsy
Treatment of Narcolepsy

-VM