Bankart's and Hill Sach's lesion mnemonic

These two lesions occuring in relation with shoulder dislocation can stump someone if asked in an MCQ as to which lesion is specifically related to which structure.

Remember the sentence-

" Sacks of money are deposited in a bank"

In a similar way, the head of humerus is 'deposited' (articulates within) the glenoid cavity.

Thus,
Hill Sach's lesion occurs on the humeral head.
Bankart's lesion occurs on the anterior glenoid labrum.

Now, how to remember whether is it the anterior or the posterior labrum?
Remember that anterior dislocation of the humeral head is the commonest occurence. That will leave no confusion.

That's all!

-Sushrut Dongargaonkar

How to interpret a Chest X-ray.

Hello everybody, so today's post will be a little long so kindly bear with me.

I hope that this post helps you and makes interpretation of an x-ray less daunting and more fun.

So let's get started.
Step 1:
Always place the x-ray in a such a way so that it seems you are facing the patient.

So naturally this is only possible with AP(Anteroposterior) and PA (Posteroanterior) views.

The technicians mark the X-ray indicating the side but chest x-rays are sort of independent of side markers due to the position of the left ventricle and the aortic knuckle.

Step 2:
To interpret a chest x-ray you need to think in layers as in from outside-in or from inside-out, with one type of structure at a time.
Do a targeted search rather than just staring at the radiograph, an abnormality is unlikely to strike unless you look for it in a planned manner.
Your eyes should scan each part of the film and one should always look twice in the regions where mistakes are more likely, like the Apices in a PA view and the region over the spine in a lateral view.

Step 3:
Scan the whole radiograph in a sequence:

Identify AP or PA view.
Check for side markers.
Radiographic exposure.
Check for integrity of bony cage.
Begin with lung Apices.
Upper middle and lower zones.
Check the Cardiophrenic angles.
Mediastinal structures.
Soft tissues.

Step 4:

Then Detect the lesion : Where is the lesion and what structures are affected by it. Starting with

Trachea and Bronchi:
Position,shift and deviation.

Mediastinal Lines:
Paratracheal stripes: visible or lost.
Aortopulmonary Window: Fullness or normal.
Paraspinal Lines: bulging or normal.

Hilum and Cardiac prominences, and see cardiogenic or mediastinal cause for the prominence.

Lungs :
Check for the Lung Volumes, Right or left lung densities,Diffuse lung abnormalities.
Whether the lesion is Pulmonary or Extrapulmonary. If pulmonary whether it is focal or diffuse.

Pleura and Fissures : Check for pleural effusion and pleural based masses.

Bones :
Focal injuries
Rib fractures, Notching.
Shoulder girdle and clavicles .

Step 5:
Directed search in an apparently normal chest x-ray.

Lungs :
See the Hidden lung areas like retrocardiac and retroclavicular areas.
Also check for Pulmonary Embolism.

Mediastinum :  Check for the Posterior mediastinal masses and hilar masses.

Step 6:
Describe the Lesion :
Location and Extent of the lesion.
Characteristics in the form of :
Shape
Homogeneity
Calcification
Necrosis
Associated features of trachea, lungs fissures etc.

Step 7:
In the end.
Put up a provisional diagnosis.
Differentiate from the closer/similar diagnoses.
Put up a final diagnosis.
A breif description on the Management.

Viola! We are through our way describing a chest x-ray!

Reading any radiograph has its learning curve and the more we see the more we learn.

Try and describe all the radiographs you see hence forth in the manner mentioned above or anyway you like it but follow a definite protocol and don't miss any important points.

I hope this post was helpful.

Let's Learn Together!
-Medha.

A neonate with cyanotic heart disease (Case #2)

A 3 day old new born is found to have cyanosis. On examination, a II/IV holosystolic murmur is heard. CXR shows decreased pulmonary vascular markings and cardiomegaly. ECG shows tall P waves and left axis deviation. Diagnosis?

Similar to the case we discussed last time (A neonate with cyanotic heart disease #1), let's narrow our differential.

Step 2 CK: Immunization schedule in the US mnemonic

Hey!

I did not create the mnemonic, I just created the table to put it all together for quick revision :)

Why some people hate cheese!

Hello everybody!

So today let's learn a bit about how our brain circuits work.

Some people hate cheese. Like seriously?
How can you miss the warm fussy feeling you get while eating warm molten cheese in a Fondue!

Well some people might not feel any bit of it and rather feel disgusted when presented with cheese.( I feel bad for them )

Anyway let's see how these things work.

Why aversive to cheese per say? 

Cheese is the food that most frequently triggers aversion. 

 Among those with an aversion to cheese, 20% say they are intolerant to lactose. In 50% of cases, at least one of their family members does not like cheese either. These stats suggested that there is a genetic origin to this aversion, which might be related to lactose intolerance.

To find out what happens in the brain,  people who like cheese and who do not were selected and participated in a functional magnetic resonance imaging (fMRI) study. 

They observed that the ventral pallidum which is activated in people who are hungry was totally inactive in people who had an aversion to cheese but was active for all other food types. Also the Globus Pallidus and Substantia Nigra part ( the reward circuit) was more active in people who had aversion to cheese than in those who do. 

So in conclusion, the areas of reward centres of our brain the Globus Pallidus and Substantia Nigra have two types of neurons with complementary activity , one relating to the rewarding aspect of food and other to it's aversive nature.

So now we have a breif idea as to how the brains are wired differently and how we all our special in our own ways!

Let's learn Together!

-Medha.

Femoral Nerve Mnemonic

Hello Everyone,
Lets discuss Femoral nerve today. Doesn't femoral nerve sound feminine? Also I am writing this post on Mothers Day, what a coincidence!

Root value: L2-L4
   (Ladies work 24 hours.)

Motor innervation:
It innervates following muscles:

• Anterior division branches innervates
•   Sartorius 
•   Illiacus
•   Pectineus 
• Posterior division branches (innervates Quadriceps femoris)
•   Rectus femoris 
•   Vastus medialis 
•   Vastus lateralis 
•   Vastus intermedius 

How to remember it? @_@
Queens hardly get time to SIP coffee  ^_^


Sensory innervation:

Anterior division branches provides sensation to anteromedial asepct of the thigh, consists of 2 branches:

• Medial cutaneous nerve of thigh 
• Intermediate cutaneous nerve

Posterior division:

• Saphenous nerve : provides sensation to anteromedial aspect of lower leg.
• Infrapatellar branches to knee :pierces the sartorius and fasica lata medial to the knee, and provides cutaneous innervation to the skin anteriorly over the patella.

How to remember it? @_@

MISs is Insensitive to pain. ^_^

Wish you Happy Mothers Day : )

That's all

Thank you,

Chaitanya Inge

Monteggia and Galeazzi fracture mnemonic

One can get confused on hours end as to what fracture is related to what bone. Hope this mnemonic comes in handy!

1. MUFC( Manchester united fan club)

- Monteggia upper ulnar fracture
With radial head dislocation

2. GFR low(Glomerular filtration rate)

- Galeazzi fracture radial, lower
With distal radio ulnar subluxation

That's all!

-Sushrut Dongargaonkar

Laughter Disorders - It might not be funny!

Hello everybody!

So today I am going to share some information on how laughter has a dark side too.

There are a lot of laughter related disorders and this gets the scientists more Intrigued to understand the neurocircuitry involved in laughter.The actual neural basis of laughter is still not very well known and what we do know about it largely comes from pathological clinical cases.

 So laughter can be classified,
 ranging from genuine and spontaneous to simulated (fake), stimulated (tickling), induced (by drugs) or even pathological.

Some of the laughter related disorders are:

1) Pseudobulbar affect : identified by Charles Darwin, It is characterised by frequent, involuntary and uncontrollable outbursts of laughing and crying. It arises due to disconnection of the descending pathways between the frontal lobes and brainstem.

Some disorders associated with the condition are : Traumatic brain injury, Alzheimer's, Parkinson's Disease, Multiple sclerosis and Most importantly Stroke.

2) Gelatophobia : Fear of being mocked at. It may lead to social ineptness to severe​ depression. It is thought to arise from negative early life experiences if being teased, ridiculed.

Imagining shows us that people who suffer from this condition have poor brain wiring and poor connections between frontal and medial temporal brain areas.

On the continum Gelatophilia is the joy of being laughed at and another related condition Katagelasticism is joy of laughing at others.

3) A twisted sense of humor and laughing at inappropriate times is thought to be an early sign of demetia.

4) Gelastic seizures : rare type of seizure that involves a sudden burst of energy, usually in the form of laughing. Mainly associated with Hypothalamic Hamartoma.

5) Angelman Syndrome : It's a chromosomal disorder affecting the Central Nervous  System.They laugh frequently due to heightened stimulation of parts of Brain involved in laughter.

So these were some pathologies and conditions of abnormal laughter.Do share if you know of any such conditions I may have missed.

So long as there are no underlying illnesses laughter is still the best medicine!

Let's Learn Together!

-Medha.

Fact of the day : Loss of Olfaction is a prodrome of neurodegeneration

Hey Awesomites

Loss of the sense of smell is one of the first warning signs of neurodegenerative diseases such as Alzheimer's, Parkinson's and other diseases associated with dementia.

One of the common link evidenced in some studies is the damage to neurotransmitter and neuromodulator receptors ( particularly acetylcholine ) in the frontal part of brain.

Also, one of the pathogenic hallmarks of AD, the Neurofibrillary Tangles ( NFTs ) have been found in olfactory bulb, olfactory tract, the transentorhinal and entorhinal cortex, anterior olfactory nuclei and amygdale. The number of NFTs within these areas have been positively correlated with the disease progression.

Thus, olfactory testing at the 'right time' is essential to detect the presence of disease process in its 'preclinical phase' itself. It could help in the differential diagnosis of several neurodegenerative diseases. Early diagnostic interventions such as smell testing, brain imaging procedures like functional MRI and PET scan, olfactory epithelium biopsy, using radioactive neurochemicals help in evaluation.

The anosmic symptoms are much more common in old patients of more than 65 years of age.


Thats all
- Jaskunwar Singh

Research update : Genetic locus of Anorexia nervosa revealed

Hey Awesomites

A Research landmark study led by UN school of medicine has found the first genetic locus for the perplexing illness, anorexia nervosa. Previously it was known that this eating disorder runs in families with genetic and environmental factors both playing their role and there is ten - fold risk in first -degree relatives, but no particular association with a genetic locus was provided.

Thought to be associated with psychiatric disorders like neuroticism and schizophrenia, it has also been positively correlated with underlying metabolic abnormalities including body - mass index (BMI) and insulin - glucose metabolism. Genome - wide association studies ( GWAS ) have revealed a significant locus for anorexia nervosa on chromosome 12, in a region previously shown to be associated with type -1 diabetes mellitus and autoimmune disorders. This means that this eating disorder shares common roots with metabolic and psychiatric traits !!

These results may help in reconceptualizing the underlying aetiology and pathogenesis of such a lethal disorder and also coming up with new treatment interventions to cure the disease.


Thats all
- Jaskunwar Singh

Treatment of erythema migrans in early Lymes disease

Hi.

Like the title suggests, this post is on treatment of erythema migrans in early Lymes disease.

For non pregnant adults and children ≥8 years of age with early Lyme disease: Doxycycline, amoxicillin, or cefuroxime axetil.

Why is doxycycline preferred for most patients with early localized Lyme disease?

Because it is effective against both Lyme disease and human granulocytic anaplasmosis.

Children <8 years of age or pregnant women with early localized Lyme disease: Amoxicillin or cefuroxime axetil.

Doxycycline is not recommended for children under the age of eight years or for pregnant or lactating women. 

Why?

Because of severe adverse effects, including teratogenicity, permanent yellowish-brown teeth discoloration after in utero exposure and in children under 8 years of age and more rarely fatal hepatotoxicity reported in pregnant women.

That's all!
-IkaN

Dwarfism vs Cretinism

Hello Everyone,
   How do we differentiate between dwarfism and cretinism?
Just remember GIRL

G- Growth- Reduced in both
I- IQ- Normal in pituitary dwarfism and decreased in cretenism
R-Reproduction-Absent or delayed puberty in both
L-Limbs- Proportionate in Dwarfs and Disproportionate in cretins.
                (C follows D)(cretins have disproportionate limbs)

What are features seen in a cretin?
Remember 5P's

1. Pot-bellied
2. Pale
3. Puffy-faced child
4. Protruding umbilicus
5. Protuberant tongue

That's all,
Thank you,
Chaitanya Inge

Authors' diary: Cerebellar tumor location and associated symptoms

Hello!

In 2013, I wrote this anatomy mnemonic on parts of the cerebellum and their functions.

I was tested this fact in a question today and I got it right. Yaay! :D

The question asked about a tumor, expected to know the most common location of the tumor and then expected you to know the symptoms caused due to it's location. Ooooh!

Anyway, lemme summarize what you should know:

Medulloblastomas usually occur in the vermis and spare the cerebellar hemispheres - They are more likely to cause truncal ataxia.

Pilocytic astrocytomas occur in the cerebellar hemispheres - They are more likely to cause intention tremors.

Added by VM:
An ependymoma can also cause truncal ataxia just like medulloblastoma. Ependymoma can be differentiated by it's location, again. Being more common on the floor of fourth ventricle, it will irritate area postrema and cause vomiting. It can also cause CN 7, CN 10 and CN 12 palsies. 

It's funny how in your preclinical years, all you ask is, "WHY DO I HAVE TO LEARN THIS?" 
And in your clinical years, you are always like - I wish I took my first and second year seriously! :P

-IkaN

Treatment of restless leg syndrome mnemonic + notes

Hello!

This is a loooooong post on the treatment of restless leg syndrome. (Bear with me!)

Those who are just here for the mnemonic 

Mechanism of action of gabapentin and pregabalin

Gabapentin binds to which of the following receptors?
1. GABAA receptors
2. GABAB receptors
3. alpa2delta subunit of voltage-sensitive Ca2+ channels
4. NMDA receptors

Akathisia vs Restless legs syndrome

Hey guys, Ikan posted a clinical vignette based on this differentiation. So I did a little digging.

Both Akathisia and RLS can be caused due to antipsychotics, Akathisia goes more with typical ones and RLS with atypical ones.

Besides RLS has some other characteristic features:

1. Associated with dysesthesia originating in legs whereas in case of akathisia patient feels like it's originating in the central core of the body.

2. RLS has evening-predominance, it disturbs sleep of the patient as the patient jerks his legs during sleep which might be noted by his gf or wife.

3. There is positive family history in RLS.

4. RLS can be induced by other centrally acting drugs like Diphenhydramine, Citalopram, Clonazepam etc if there is a positive family history.

Treatment:

First intervention should always be reduction of dose of antipsychotics.

While RLS responds well to dopamine agonists like Pramipexol and Ropinirole, Akathisia responds well to Mirtazapine, a tetracyclic antidepressant. Although withdrawing the causative drug works the best.
According to latest clinical trial reports, The first line treatment of akathisia is propranolol, second line is Benztropine​ and if these doesn't work we resort to benzodiazepines.

That's all! You never stop learning.

-VM

Abdominal Aorta Mnemonic

Hello Everyone,
Lets discuss abdominal aorta.
Its a game of odd numbers. Following branches are present:

• 3 Anterior
• 3 Lateral visceral
• 3 Terminal
• 5 Lateral Abdominal

3 Anterior branches single include:

• Coeliac Trunk (T12)
• Superior Mesenteric Artery (L1)
• Inferior Mesenteric Artery (L3)

3 paired lateral Visceral:

•  Middle Suprarenal(L1)
• Renal (between L1 and L2)
• Gonadal (L2)

5 paired lateral abdominal

• 4 Lumbar arteries (respectively at L1 L2 L3 L4)
• Inferior phrenic (T12)

3 Terminal

• 2 Common Illiac (L4)
• Median Sacral (L4)

How to remember it? @_@
Counter Strike Is MR GLIC's Mastery. ^_^

Fun Facts:

• There are 3 suprarenal arteries ( again a odd number). The superior branch is derived from the inferior phrenic artery, the middle branch originates directly from the aorta, and the inferior branch comes off the renal artery.

• The fifth lumbar arteries on either side arise from the median sacral artery. 

     Click Here to see a beautiful flowchart submitted to us.

That's all,

Thank you 

Chaitanya Inge

Fact of the day : Testosterone administration impairs 'cognitive reflection' in men

Hey Awesomites

You must have tried solving brain teasers at some point of time.. right? Ok so how many of you tried to solve it right at that instant ( sensing your gut reaction ), but guessed it wrong? If so, you might be having loads of testosterone in your veins!

X-Linked Dominant Disorders.

Hello everybody!

Let's learn a quick way to remember a few important X-linked Dominant Disorders.

The mnemonic goes like:

All Hypo Pigmented Rats Have Resistant Rickets.

All - Alport Syndrome.
Hypo - Familial Hypophosphatemia.
Pigmented - Incontinentia Pigmenti.
Rats - Rett Syndrome.
Resistant​ Rickets - Vit.D Resistant Rickets.

X linked dominant disorders are rare pattern of inheritance.

All affected males will transmit it to all their daughters and all affected females will transmit the disease to 50% of her sons/daughters.

If you have another mnemonic on the same do share.

Let's learn Together!
-Medha.

Marfan syndrome - High Yield Information.

Hello everybody,
lets today briefly revise all the high yield points on Marfan syndrome.

Marfan syndrome is an example of structural protein disorder and with autosomal dominant inheritance, lets see what exactly goes wrong in this condition.

Etiopathogenesis:

There is a missense mutation seen in the fibrillin-1 gene located on the chromosome no.15.
So to understand the condition better, lets understand a bit about fibrillin.

Fibrillin forms the glycoprotein component of cellular microfibrils and also provides a scaffold for the elastin deposition.
Abundant fibrillin is found in the connective tissues of the aorta,ligaments and the eye, these are the structures predominantly affected in the disorder too.

The defective fibrillin leads to defective microfibril assembly intracellularly and reduced elasticity in connective tissues.
 Defective fibrillin also leads to decreased TGF-beta(Transforming growth factor ) sequestration, and excess of TGF-B hampers normal vascular smooth muscle development and matrix production.

Morphological Features:

1) Skeletal changes:
    Tall stature with long extremities.
     Long tapering fingers and toes.(Arachnodactyly)
     Hyperextensibility.
     Dolicocephaly.
     Kyphosis ans scoliosis.
     Pectus excavatum or Pigeon breast deformity.

2) Cardiovascular changes:
     Aortic regurgitation: Due to aortic cystic medial degeneration leading to valvular ring dilatation & valvular incompetence. Most threatening valvular lesion.
     Mitral valve prolapse : Most common valvular lesion.
     Aortic Dissections are the most common cause of death in these patients.

3) Occular changes:
    Ectopia Lentis: bilateral superotemporal dislocation of lenses.
    Retinal Detachment : due to increased axial length of the globe.

Diagnosis:

Currently Revised Ghent Criteria is used for the diagnosis of Marfan syndrome.
It considers:
Family history,
Cardinal Clinical Signs in absence of family history,
Presence or absence of Fibrillin Mutation.

so that's all on marfans syndrome.

Fun Fact:
We all have been hearing about some famous personalities with Marfan syndrome like Abraham Lincon and Michael Phelps, but Tutankhamen the 11th pharoh of 18th Egyptian Dynasty was diagnosed to be suffering from Marfan's Syndrome by a series of CT scans and DNA tests carried out on his MUMMY!

Do post any other interesting facts you know about Marfan's Syndrome.

Let's Learn Together!
-Medha!

Fact of the day: Psychiatric effects of steroids

Did you know corticosteroid therapy can cause depression, mania, psychosis, and delirium?

Why?

The mechanism by which the corticosteroid induces symptoms such as mania, depression, and psychosis is not clear.

The administration of prednisone is associated with decreased levels of corticotrophin, norepinephrine, and beta-endorphin in the cerebrospinal fluid. Furthermore, corticosteroids induce an increased release of glutamate that induces neuronal toxicity due to accumulation effect.

-IkaN