CMS neurology form 2 question on fibromuscular dysplasia with paresis, occulomotor palsy

Disclaimer: This is an CMS neurology form 2 question for step 2 CK. If you are planning to take USMLE step 2 CK in the future, I would recommend that you DO NOT read this post because it will bias your assessments.

CMS neurology form 2 question on headache, seizures, urinary incontinence, broad based gait

Disclaimer: This is an CMS neurology form 2 question for step 2 CK. If you are planning to take USMLE step 2 CK in the future, I would recommend that you DO NOT read this post because it will bias your assessments.

NBME 7 question on intoxication

Disclaimer: This is an NBME form 7 question for step 2 CK. If you are planning to take USMLE step 2 CK in the future, I would recommend that you DO NOT read this post because it will bias your assessments.

Fact of the day : Pinenes for refreshing your Airways

Hello

Did you know? One of the reasons your lungs feel refreshed ( increased mental focus and energy ) when you walk through the shades of beautiful pine forest is because of an anti - inflammatory compound called alpha -Pinene, that is found in conifers. It is used as a bronchodilator in the treatment of asthma and is abundantly present in marijuana.

- Jaskunwar Singh

Pill induced esophagitis mnemonic

Pill induced esophagitis is caused by a pill! :D

Causes of pill induced esophagitis mnemonic: A PILL.

Aspirin
Alendronate
Antibiotics like tetracycline, clindamycin

Potassium chloride
Iron
Less water
Lying down immediately

Interesting anatomy correlation:
The most common sites of injury are the proximal esophagus near the compression from the aortic arch and the distal esophagus in patients with left atrial enlargement.

The typical endoscopic appearance of pill-induced esophageal injury is a discrete ulcer with relatively normal surrounding mucosa.

That's all!
-IkaN

Motor nuclei in the brainstem : An overview

Hi everyone. Just thought of doing an overview of the various motor nuclei of cranial nerves in the brain stem.

So we can classify the motor nuclei into 3 groups -

1. Somatic motor efferent - 4
2. Branchial motor efferent - 4
3. Visceral motor efferent - 4

Now how are these classified ?

1. Somatic Motor Efferent

- In the embryological stage , there are certain precursors to muscle and skin segment groups called 'Somites'. These are processes of the paraxial mesoderm.
- Sach somite gives rise to a particular set of muscles called its myotome. 

- There 4 such important somite groups -->

A. Pre otic somites = 3.
So this is simple.
There are 3 pre otic somites giving rise to distinct groups of extraocular muscles supplied by their own cranial nerve.

Somite 1  =
Muscles -
All Extra ocular muscles except Lateral Rectus and Superior oblique.
Nerve -
Oculomotor nerve (III)
Nucleus -
Oculomotor nucleus in the Upper Midbrain.

Somite 2  =
Muscles -
Superior oblique.
Nerve -
Trochlear nerve (IV)
Nucleus -
Trochlear motor nucleus in the Lower Midbrain.

Somite 3  =
Muscles -
Lateral Rectus.
Nerve -
Abducent nerve (VI)
Nucleus -
Abducent motor nucleus in the Pons.

(I'm sure you remember the popular mnemonic - LR6 SO4)

B. Occipital somites

Muscles -
All muscles of the tongue except Palatoglossus
Nerve -
Hypoglossal I'm nerve (XII)
Nucleus -
Hypoglossal nucleus in the Medulla.

Since these nuclei represent the motor innervation to the derivatives of Somites , they're called Somatic Motor or General Somatic Efferent (GSE) Fibres. 

2. Branchial Motor Efferent - 

- In the embryological stage , there are various branchial or Pharyngeal arches that give rise to muscles , bones and cartilage supplied by a particular nerve of that arch.

- Each nucleus that supplies the muscles from such a Branchial arch is called Branchiomotor Efferent or Special Visceral Efferent. (SVE) 

- There are 4 such important arches - 

A. 1st Pharyngeal arch (mandibular arch)

Muscles -
All muscles of mastication + TT (Tensor tympani + Tensor veli Palatini) + Digastric anterior belly. ( And Meckel cartilage)
Nerve -
Mandibular branch of Trigeminal
Nucleus - 

Trigeminal motor nucleus in Pons 

B. 2nd Pharyngeal arch (hyoid arch) 

Muscles -
All muscles of facial expressions + Stapedius + Digastric posterior belly.  ( And Reichter cartilage)
Nerve -
Facial nerve (VII)
Nucleus - 

Facial motor nucleus in Pons 

C. 3rd Pharyngeal arch

Muscles -
Stylopharyngeus

(And the hyoid bone funnily.)
Nerve -
Glossopharyngeal nerve (IX)
Nucleus - 

Nucleus Ambiguus in Medulla

D. 4th and 6th Pharyngeal arches

Muscles -
- All muscles of  Soft palate ( except Tensor veli which is up in the 1st arch) by the 4th. + cricothyroid muscle of Larynx. 

- All muscles of Larynx by the 6th except cricothyroid which is by the 4th. 

(All laryngeal cartilage as well)
Nerve -
4th arch - Superior laryngeal nerve of the Vagus.(X)

6th arch - Recurrent laryngeal nerve of the Vagus (X)
Nucleus - 

Nucleus Ambiguus of Medulla 

Now there's another Motor nucleus - The Accessory nerve. It supplies Trapezius and Sternomastoid muscles but it's doubtful if it's Branchial or Somatic. 

3. Visceral Motor Efferent - General. 

- These nuclei are parasympathetic and stimulate a particular gland to secrete or a ganglion to function. 

- These are called Secretomotor or General Visceral Efferent Fibres 

Again , there are 4 of these. 

A. Ciliary ganglion 

Function mediated by - 
Sphincter pupillae - Constricts pupil 

(Mnemonic = Remember C and C - Cholinergic Constricts )
Nerve -
Oculomotor nerve
Nucleus - 

Edinger Westphal in Midbrain 

B. Pterygopalatine ganglion 

Function mediated by - 
Lacrimal glands, nasal mucosal, sinuses mucosal glands and pharynx mucosal - Secretomotor. 

Nerve -
Facial nerve  (Greater Petrosal)
Nucleus - 

Superior salivatory nucleus - Pons. 

C. Submandibular ganglion 

Function mediated by - 
Submandibular glands , sublingual glands - Secretomotor.

Nerve -
Facial nerve  (Chorda tympani)
Nucleus - 

Superior salivatory nucleus - Pons. 

D. Otic ganglion 

Function mediated by - 
Parotid gland

Nerve -
Glosspharyngeal nerve  (Lesser Petrosal)
Nucleus - 

Inferior salivatory nucleus - Pons. 

The Vagus nerve has the largest parasympathetic discharge and supplies a lot of visceral with this input in the guy as well.

Hope this helps you to re-orient yourself to neuroanatomy and grasp the roles of various brainstem structures ! 

Happy studying ! 

~ A.P.Burkholderia

Lacunar strokes : An Overview

      Hi everyone ! Here's a short post on Lacunar infarcts. Credits to IkaN without whom IKant have done this post. Haha ;;) here goes.

- A Lacunar infarct is an infarction occurring    in the deep penetrating branches supplying the deep subcortical structures - Mainly the Internal capsule and parts of thalamus. 

- These are some of the most common infarctions seen. 

- Causes of lacunar infarction include Hypertensive bleeds and Microthrombi. 

- So these infarcts can present as one of the following​ Syndromes --> 

1. Pure Motor 

2. Pure Sensory 

3. Combined Sensorimotor 

4. Ataxic 

5. Dysarthria- Clumsy hand syndrome. 

- The illustrations I've drawn below clearly depict the syndromes , their anatomical localization and the arteries commonly involved. 

- The commonest of the lot is the Pure Motor type of stroke that affects mainly the Internal capsule containing the motor corticospinal fibres. Since a multitude of Fibres is concentrated very judciously in the Internal capsule , the hemiplegia resulting from this type is a 'Dense' or total hemiplegia affecting both upper and lower limbs in equal measure. 

(click on the image to see them in better resolution ) 

- The management is much like the other strokes - 

1. Airway Breathing Circulation to be established. 

2. Check Blood sugar and BP.

3. Send for an emergency Non contrast CT scan to rule out hemorrhage. 

4. If within 3-4.5 hours and absence of hemorrhage = Thrombolyse. 

5. If hemorrhage - BP control and ICT management.

6. If beyond 4.5 hours = Symptomatic and Palliative care and treat risk factors.

- I hope all of these Syndromes are clear to you now !

 Let me know if you'll have any doubts. 

Happy Studying ! 

Stay awesome.

~ A.P.Burkholderia

Fact of the day: Marchiafava-Bignami disease

Marchiafava-Bignami disease is a rare disorder of demyelination or necrosis of the corpus callosum and adjacent subcortical white matter that occurs predominantly in malnourished alcoholics. Dementia, spasticity, dysarthria, and inability to walk may present as an acute, subacute or chronic condition.

Lesions appear as hypodense areas in portions of the corpus callosum on CT and as discrete or confluent areas of decreased T1 signal and increased T2 signal on MRI. Alcohol abusers without liver disease, amnesia, or cognitive dysfunction show thinning of the corpus callosum at autopsy and on MRI, suggesting that alcohol or malnutrition damages the corpus callosum commonly in the absence of the necrotic lesions of Marchiafava-Bignami disease.

Interesting, isn't it?
-IkaN

High ankle and low ankle sprain mnemonic

Hello!

High ankle and low ankle sprain

Atrial fibrillation begets Atrial fibrillation: Explanation

Hi ! Short post on pathophysiology of Atrial Fibrillation!

- Atrial Fibrillation is a fairly common disorder of rhythm, where the atria begin to beat at random , irregular and very high rates. Like 300-600 beats / min !
- Some of these MANY contractions get transmitted to the ventricles causing an Irregular , yet High , Ventricular rate - around 100-160 per minute or even higher.

Now how this occurs is a very interesting yet much-ignored mechanism.

- Due to some pre existing factors like Rheumatic heart disease , Myocardial ischemia or Thyroid abnormalities among many others, the atria get electrically irritated and begin to fire on their own.

- These ectopic foci are common along the opening of the pulmonary veins = called the pulmonary sleeve.
This area of hyperactivity and automaticity begins to fire from the left Atrium creating a wavefront of abnormal impulses.

- Say one of these myocytes becomes ectopic one day and produces an abnormal wavefront. This wavefront progresses across the atrium and in turn stimulates the other Atrial myocytes to inturn fire ectopically -- causing formation of multiple Daughter ectopic foci.

- These daughter ectopic foci produce daughter wavelets that then propagate through the atria , in turn producing more duaghter wavefronts.

- Eventually there are A LOT of Atrial foci causing multiple wavelets to produce multiple electrical wavefronts.

- Thus A-Fib causes multiple wavefronts which in turn cause more wavefronts eventually propogating A fib as a positive feedback mechanism​.

- In the long term, due to this constant irregular beating there is fibrosis and electrophysiological remodelling making the atrium more irritable and automatic.

Thus A-Fib begets A-Fib!

Hope you liked this !
Happy Studying !
Stay awesome.
~A.P.Burkholderia

Mitral Regurgitation Begets Mitral Regurgitation : Explanation

Hi everyone  ,just a short explanation of the famous phrase 'MR begets MR'.
Here goes.

- Mitral Regurgitation is a disease where the mitral valve is incompetent or insufficient and leaks or pukes when it should be shut. (Rather like a blithering idiot who keeps talking at the wrong time. =}. )

- So it allows the blood to puke back into the Left Atrium from the Ventricle during systole.

- So assume - 100 ml of blood would flow into LV from the LA normally which the LV would pump into the Aorta.

- Now because of the weird and incompetent valve , the LV can pump only like 70 ml into the Aorta and the rest of the 30 ml goes back into the LA.

- So now the LA volume is 30 ml + 100 ml
And it'll pour in 130 ml into the LV.

- So effectively, the LV has an overload of volume in it and over a period of time it would undergo Dilatational changes and increase in size.

- As the Ventricle increases in size , the mitral valve apparatus is stretched all the more.

-This is because the mitral valve is attached to the Ventricular myocardial tissue directly at the annulus as well as via the papillary muscles. Both of these are stretched. 

- The stretching causes further increase in MR. This causes further volume overload. Which causes further MR.

- Thus it is like a positive feedback response and a vicious cycle is formed.

This phenomenon is referred to as ' MR begets MR' which means MR basically causes Ventricular changes which stretch the heart and cause more MR which continues the cycle further.

Hope this helped !
Happy studying !
~ A.P. Burkholderia

Microbiology of Actinomyces vs Nocardia mnemonic

Hello! Let's go back to Microbiology today.

Nocardia typically appear as delicate filamentous gram-positive branching rods that appear similar to Actinomyces species.

Nocardia can usually be differentiated from Actinomyces by acid-fast staining, as Nocardia typically exhibit varying degrees of acid fastness due to the mycolic acid content of the cell wall.

Another useful clue is that Nocardia grow under aerobic conditions, whereas Actinomyces grow under anaerobic conditions.

How to remember this? Remember one mnemonic, the other one is the other one. Okay?

So let's start with nocardia.
nocarDIA. nocarDICA. ACID fast!
noCARDIA. Heart needs oxygen. Aerobic organism.

Therefore, the other one, Actinomyces is anaerobic, non acid fast.

Treatment mnemonic: PANT
Penicillin Actinomyces
Nocardia TMP-SMX

That's all!
-IkaN

Tay-Sachs disease notes and mnemonic

Hello!

Tay-Sachs disease is an autosomal recessive, neurodegenerative disease.

Plasma Proteins Mnemonic

Hello Everyone,
 Lets discuss plasma proteins.

1.How do we classify them?

• They are classified into Albumin, Globulin and Fibrinogen.
• Globulins are further classified into Alpha , Beta Globulins and Gamma Globulin.
• Alpha Globulin is further divided into Alpha 1 and Alpha 2 Globulins.

Memorising the examples of them is simple. 

Examples of Beta Globulins can be remembered as follows:

         B PTH

B-Beta Lipoproteins(LDL)

P-Plasminogen

T-Transferrin

H-Hemopexin

Interesting Fact:

Acute-phase proteins are a class of proteins whose plasma concentrations increase (positive acute-phase proteins) or decrease (negative acute-phase proteins) in response to inflammation. This response is called the acute-phase reaction.

• Positive acute-phase proteins increase in inflammation e.g., C-reactive protein, mannose-binding protein, complement factors, ferritin, ceruloplasmin, serum amyloid A and haptoglobin.
• Negative acute-phase proteins decrease in inflammation. Examples include albumin, transferrin, transthyretin, retinol-binding protein, antithrombin, transcortin. 

Thats all,

Thank you,

Chaitanya Inge

No cyanosis in cyanide poisoning. Why?

I was reading about cyanide poisoning today and saw "Cherry red skin" in the clinical manifestations. I know that carbon monoxide poisoning causes a cherry red color to blood. But why cyanide?

The curiosity lead to this post.

In normal cellular metabolism, most adenosine triphosphate (ATP) is generated from oxidative phosphorylation. .

Cyanide avidly binds to the ferric ion (Fe3+) of cytochrome oxidase a3, inhibiting this final enzyme in the mitochondrial cytochrome complex. When this enzyme's activity is blocked, oxidative phosphorylation ceases. The cell must then switch to anaerobic metabolism of glucose to generate ATP.

Anaerobic metabolism leads to the formation of lactic acid and the development of metabolic acidosis. Hydrogen ions produced by ATP hydrolysis are no longer consumed in aerobic ATP production, exacerbating this acidosis. Serum bicarbonate decreases as it buffers excess acid, leading to an increased anion gap.

Despite an ample oxygen supply, cells cannot utilize oxygen because of their poisoned electron transport chain. This functional (or "histotoxic”) hypoxia is particularly deleterious to the cardiovascular and central nervous systems (especially the basal ganglia).

Because of the decreased utilization of oxygen by tissues, the venous oxyhemoglobin concentration will be high, making venous blood appear bright red.

Therefore, despite hypotension, apnea, and/or bradycardia, the patient does not usually appear cyanotic in the setting of cyanide poisoning.

Clinical features:
Central nervous system toxicity is the most prominent in cyanide toxicity – Headache, anxiety, confusion, vertigo, coma, seizures.

Which should you suspect cyanide poisoning?
Victims of fires
Reported ingestions
Treatment with sodium nitroprusside

Antidote:
Hydroxocobalamin
Sodium thiosulfate
Nitrites (to induce methemoglobinemia)

That's all!
-IkaN

CT scans and role of Contrast enhancement

Contrast enhancement and it's role in CT scan
The concept of Contrast enhancement in radiology is not new and it has been in practice even before the Advent of CT scans.
CT scan as a modality of imaging was invented by a British engineer Godfrey Hounsfield in the year 1972.

Purpose of Contrast enhancement

Contrast enhancement is a method of exaggerating  the visible difference between adjacent structures on scan by administrating contrast agents.The term Contrast enhancement in CT scan includes usage of radio opaque substances for better visualization of the anatomic structures as well as better localization and characterization of the pathologies, better differentiation of the pathology from the normal surrounding structures.

Principle of Contrast enhancement

The diffusion of contrast agents from the blood stream to the body tissue is physiologically limited. In pathologies such as cancer, blood vessels grow (angioneogenesis) with increased leaking of contrast agents resulting in lesions much more visible on Contrast enhanced scans.
In CNS, contrast diffusion is limited by Blood brain barrier. Disruption of BBB lead to enhancement after administration of contrast agents.

Indications of Non Contrast CT (NCCT )
For detection of
1.Stones in kidney,ureter, cbd
2.Calcification
3. Fat in various tumors
4. Head injury
5. Acute hemorrhage
6. Stroke
7. SAH


CECT

The pathologic lesions show enhancement or attenuation depending upon the phase of contrast enhancement. So if you are looking for a particular pathology,it is important to know in which phase of CECT to look for.
For that purpose,I've enumerated the phase in which CT scan is done and can be recorded.

1. Non enhanced phase (NECT)
Uses are same as those of Ncct. Many a times this scan is done before administration of the dye to compare pre and post contrast enhancement study.
Calcification, fat in tumors, inflammation and infarction can be seen in this phase well.

2. Early arterial phase (15-20 secs post injection)
When contrast is still in the arteries, it has not enhanced the organs.
This phase is useful to look for vascular abnormalities such as aneurysms, vascular stenosis, etc

3. Late arterial phase (35-40 secs post injection)
Sometimes known as arterial phase.
All the structures that get their blood supply from arteries will show optimal enhancement in this phase.

4. Hepatic or late portal phase (70-80 secs post injection)
Liver parenchyma enhance trough blood supply by portal vein and some enhancement of hepatic veins.

5. Nephrogenic phase (100 secs post injection)
This is when all of the renal parenchyma including medulla enhances. Particularly helpful for small renal cell carcinoma which are otherwise missed.

6. Delayed phase (6-10 mins post injection) called as wash out phase or equilibrium phase
Washout of contrast in all abdominal structures except for fibrotic tissues which become relatively more dense in this phase.

Factors affecting CECT
The timings depend on
1. Organs to be scanned and focussed
2. Type of CT machine available, number of slice
3. Amount of contrast given depending upon the body weight of the patient
4. Injection rate of the contrast
5. Route by which contrast given. (Mainly IV but can be oral,rectal too)

Lesions / pathologies visualized on CECT
1. Liver tumors
Due to it's dual blood supply, 80% by portal vein and 20% by hepatic artery normal parenchymal enhancement maximally in hepatic phase . On the contrary, all all liver tumors are supplied 100% by hepatic artery. So hyper vascular tumors are best seen in late arterial phase. Hypovascular tumors on the other hand are better seen in hepatic phase.
2. Fibrotic lesions
Fibrotic lesions like cholangiocarcinoma and fibrotic mets hold contrast much longer than normal parenchyma hence best seen in delayed phase.
3. Pancreatic tumors most of them being hypovascular are seen best in late arterial phase. In cases of acute pancreatitis, late arterial phase best detects necrosis. Remember chronic pancreatitis can be very well appreciated on NCCT due to calcification.
4. Anastomosis leakage 
CECT done in post op patients to check anastomosis leakage. Oral contrast play a role here for check scans done in post op bowel anastomosis.

5. Pulmonary embolism - 
Good quality scans are required to delineate the emboli in the pulmonary vasculature.
6.CT angiography 
For vascular studies.

Dr. Shil Pill

Coccidioidomycosis mnemonic

Coccidioidomycosis is caused by Coccidioides immitis!

Diabetes insipidus and water deprivation test

In this video I talk about pyschogenic polydipsia, central diabetes insipidus, nephrogenic diabetes inspidius, water deprivation test :)

Theophylline toxicity mnemonic

Theophylline's effects arise from antagonism of adenosine receptors and indirect adrenergic activity.

It is used as a bronchodilator for patients with asthma or chronic obstructive pulmonary disease.

Chest x-ray - Left Lung.

Hello everybody!

Let's see the image correlations of the left lung today.

The left lung has an apical lobe ,lingula and a basal lobe.

Apical lobe has 2 segments: Anterior and posterior.
Lingula : The tongue like extension and the alleged counterpart of the middle lobe has 2 parts to it : Superior and Inferior.
Basal lobe has 4 segments namely : Superior, Posterior, Medial, Lateral.

Carefully observe how the identification of these segments differs while seeing an X-ray.

Apical lobe:

Basal Lobe:

So that's it with the interpretation of lung fields on X-rays!

Hope this is helpful!

-Medha.

“PILL” Esophagitis.

Hello!

Let's review a very common preventable condition of pill/drug induced esophagitis. 

It is occurs due to prolonged contact of the esophageal mucosa with a medication, which acts like the damaging agent.

Medications implicated in
“pill”esophagitis are :
Tetracycline
Potassium chloride
Ferrous sulfate
Nonsteroidal antiinflammatory drugs
Alendronate. 

Most often the offending tablet is ingested at bedtime with inadequate  water, this leads to prolonged contact  u of the drug with the esophageal mucosa leading to focal damage and esophagitis.

This causes acute discomfort followed  by progressive retrosternal pain,  odynophagia, and dysphagia.

Endoscopy reveals a focal lesion localized to one of the anatomic narrowed regions of the esophagus or an unsuspected pathologic narrowing. 

Treatment is supportive.
Antacids, topical anesthetics, bland or  liquid diets are often used.

Let's Learn Together!
-Medha.

Flow volume loop notes and mnemonics

Here are my notes on the flow volume loops!

Flow volume loop explanation video and mnemonic

Hello!

I explain the flow volume loops seen in obstructive lung diseases, restrictive lung diseases, intrathoracic and extrathoracic - fixed variable obstruction in this video with mnemonics! :)

Chest X-ray - Right Lung!

Hello everybody!
So today let's go through the Right lung segments as seen on a Chest x-ray with the help of images.

This will help us identify the exact location of the pathology and the possible etiology for the same.

So the Right lung has 3 lobes.
Upper
Middle
Lower.

Let's start with the right UPPER LOBE.
It has 3 segments.

Now moving to the MIDDLE LOBE .
It has 2 segments Medial and Lateral.

Moving to the LOWER LOBES.

It has 5 segments.

Superior Basal

Lateral Basal

Antero Basal

Medial Basal

Posterior Basal.

(3D CT Images courtesy - CU medicine Hong Kong)

So well I hope this helps to correlate the various Bronchopulmonary segments while interpreting a Chest x-ray!

Let's Learn Together!

-Medha.

Difference between cauda equina syndrome and conus medullaris (with mnemonics)

Let's differentiate Cauda equina syndrome (CES) from conus medullaris today!
With mnemonics because they make life easier! (And because it is the IkaN style of doing things)

Ischioanal fossa (Fun Mnemonic Diagrams)

Hello Everyone,
Lets discuss Ischioanal fossa. I remember it as a Rocket!!
How to draw it?

Draw a rocket

Add 2 wings !!

Draw 2 snakes underneath the wings

                                             

Color it up.

And Label it.

That's all,

Thank you,

Chaitanya Inge

Methamphetamine intoxication mnemonic

Hello!

This post is about crystal meth.

Aortic stenosis murmur explained

In this video I talk about:

The systolic crescendo decrescendo murmur of AS
Early vs late systolic murmur - Which is more severe?
Why there is a soft S2 and paradoxical splitting of the second heart sound in AS?

And mnemonics! Yaay! :D

Cortisol and eosinophils

Today, I forgot the relationship between cortisol and esosinophils. Completely screwed up a practice question because I couldn't remember it.

Now I made a mnemonic to remember this :D

Mnemonic: In hypERcortisolism, Eosinophils Reduce.

Why do corticosteroids cause eosionopenia? Why does hypocortisolism cause an increase in eosinophil count?

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