Friday, June 23, 2017

Lymphedema - High yeild Information.

Hello there!
So today in the surgery OPD I happened to see a case of Lymphedema feet ,and hence thought of reviewing some important points on same.

So, Congenital lymphedema may involve a single lower extremity, multiple limbs, the genitalia, or the face. 

The edema typically develops before 2 years of age and may be associated with specific hereditary syndromes -Turner syndrome,Milroy syndrome, Klippel-Trenaunay-Weber syndrome.

 Lymphedema praecox is the most common form of primary lymphedema, accounting for 94% of cases. 

Lymphedema praecox is far more common in women, with the gender ratio favoring women 10:1. 

The onset is during childhood or the teenage years, and the swelling involves the foot and calf. 

Lymphedema tarda is uncommon, accounting for <10% of cases of primary lymphedema. The onset of edema is after 35 years of age. 

Secondary lymphedema is far more common than primary lymphedema. Secondary lymphedema develops as a result of lymphatic obstruction or disruption.

 Other causes of secondary lymphedema include radiation therapy, trauma, infection, and malignancy. 

Globally, filariasis (caused by Wuchereria bancroftiBrugia malayi, and Brugia timori) is the most common cause of secondary lymphedema.

Hope It helps.
Let's Learn Together!

Pathophysiology and Radiologic patterns of Atelectasis

Hey guys!

This post will be on the classification of Atelectasis based on its pathophysiology and a brief overview of its radiology patterns. 

Let us deal with the radiology aspects first:

1. Opacification of airless lobe and displacement of fissures,

2. displacement of hilar and cardiomediastinal structures toward the side of collapse,

3. narrowing of the ipsilateral intercostal spaces,

4. elevation of the ipsilateral hemidiaphragm,

5. compensatory hyperinflation and hyperlucency of the remaining aerated lung and

6. obscuration or desilhouetting of the structures adjacent to the collapsed lung (eg, diaphragm and heart borders).

Google the Chest X ray scans for atelectasis to consolidate the above points.

Now the lengthy part, The Pathophysiology. Let us start with active or obstructive atelectasis. 

1. Active/Obstructive Atelectasis.

Obstructive atelectasis is a consequence of blockage of an airway. Air retained in the alveoli distal to the occlusion is absorbed into the pulmonary capillary blood since the pressure of gases in the blood plasma (PvO2) is lower than that in the alveoli. For this reason, it is also called absorptive atelectasis. This causes the affected regions to become totally gasless and then collapse. 
Obstruction of a segmental bronchus is less likely to result in segmental atelectasis than obstruction of a lobar bronchus is to produce lobar atelectasis. This difference is because of collateral ventilation between bronchopulmonary segments within a lobe. 
Collateral ventilation occurs via the age-old physiologic adaptive process of recruitment and distension of neighbouring bronchioles. But three are three other players here, or brothers as I like to call them. A small anecdote to remember these three brothers:
Once there was a priest named Kohn who decided to help out a fellow bronchopulmonary segment in aeration. Brother Kohn being eldest and hence weak could only manage to dig a pore. His work was carried on by Brother Boren who bored (as his name suggests) and made this pore into a fenestration. There was still some work left. And for that Brother Boren asked the help of the engineer Brother Lambert. Brother Lambert, after much hard work was eventually able to dig up a canal all the way upto the neighbouring segment so that they can share the aeration bestowed upon them by Lord Almighty!
So we have three distinct collateral connections: 1. Pores of Kohn, 2. Fenestrations of Boren and 3. Canals of Lambert.
So you need to defeat these three if you want to cause obstructive atelectasis.
Let's dig a bit deeper into Fenestrations of Boren. These collateral channels are extensively prominent in an emphysematous lung. Now take a case of a 60 year old male smoker with emphysema who has now developed small cell carcinoma. Suppose there is a tumor mass obstructing the right bronchus, this patient will take a lot of time to develop obstructive atelectasis in the right lung because of the presence of extensive network of fenestrations of Boren. Hence, this patient will become symptomatic late and thereby will be diagnosed late. Blessing or Curse!
One more thing, it has been observed that atelectasis occurs more rapidly in patients on oxygen therapy. Why? There is a simple reason behind this. Oxygen is more soluble than nitrogen in water, when you give inhalational O2 with a FiO2 take 50%, you are altering the partial pressures of gases in the alveoli, Nitrogen which was 79% will fall down to below 50% and O2 which was 20% will rise upto 50%. Hence overall solubility rises, this elevates the tendency and spontaneity of gases diffusing into the blood plasma.

Honestly speaking, rest of the causes are nowhere as important as the one mentioned above so let us try to ace them quickly. 
2. Nonobstructive Atelectasis

A. Relaxation (ie, passive) atelectasis ensues when contact between the parietal and visceral pleurae is eliminated. While this is usually due to a pleural effusion or pneumothorax, a large emphysematous bulla can have a similar effect. In this case, the residual physiologic elastic recoil of normal lung parenchyma allows the normal lung to collapse away from the chest wall with consequent loss of volume.
The middle and lower lobes may shrink more than the upper lobe in the presence of a pleural effusion, while the upper lobe may be affected more by a pneumothorax.

B. Adhesive atelectasis is a consequence of alveolar instability due, in part, to surfactant deficiency or dysfunction. As its name suggests, the alveoli walls will collapse into the alveolar space sticking with each other. In the normal lung, surfactant reduces the surface tension of alveoli and decreases the tendency of alveoli to collapse. Decreased production or inactivation of surfactant leads to alveolar instability and collapse. Adhesive atelectasis is a major problem in respiratory distress syndrome of premature infants(IRDS), acute respiratory distress syndrome (ARDS) in adults, acute radiation pneumonia, and posttraumatic lung contusion.

C. Cicatrization (ie, cicatricial atelectasis) results from diminution of lung volume due to severe parenchymal scarring. Common underlying etiologies include granulomatous disease (eg, sarcoidosis), necrotizing pneumonia, and radiation pneumonia.
D. Acceleration Atelectasis- This type of atelectasis has been described in pilots subjected to very high, vertical accelerative forces between 5G and 9G: at 5G, up to 50 percent of pulmonary airways are distorted and closed due to gravitational forces. The atelectasis is exacerbated by breathing a high fractional concentration of oxygen. Decreases in vital capacity are a reflection of this type of atelectasis in pilots. Acceleration atelectasis can cause symptoms like chest pain, coughing, and dyspnea.
E. Rounded atelectasis (also called folded lung, Blesovsky’s syndrome, or atelectatic pseudotumor) is a distinct form of atelectasis associated with pleural disease, particularly following asbestos exposure and in India following pleural tuberculosis. Asbestosis is associated with pleural plaques and diffuse pleural thickening while pleural TB will have pleural thickening alongwith pleural effusion which eventually resolves with or without organization and pleural septations(Harbingers of Fibrothorax). 
In this condition, there is a subpleural mass mainly in the middle or lower lobes from which bronchi and blood vessels arise and they form a structure like a comet tail which traverses through the underlying atelectatic lung parenchyma to join at the hilum. Some un-astronomical sources compare this to a Vacuum Cleaner, with the dirt box as the subpleural mass and the hose as the comet tail. 

P.S. Blesovsky's Syndrome is not the only syndrome connected to pneumoconiosis, there is also Caplan's syndrome(Rheumatoid pneumoconiosis); which has a well-known mnemonic CAPlaN;
C- Coal workers' pneumoconiosis
A- Rheumatoid Arthritis
PlaN- Pulmonary nodule

That's all! 

Thursday, June 22, 2017

Pills of knowledge in Ophthalm- Nodal cataract

The condition where 'day blindness' is present is a cataract at the nodal point. Nodal point of the eye is where the rays of light pass through the lens without any refraction, usually at the centre of the lens. Thus, during the day, especially when out in the sun, the pupil contracts and the light has to pass through the cataractous area, causing diminution of vision.

Immunotherapy for Prostate cancer

Hey Awesomites

Immunotherapy is now an emerging and much promising intervention in the treatment of prostate cancer, apart from the traditional cancer treatments - chemotherapy, radiation and surgery.

Research Update - The Multitasking Brain.

Hello there!
So you must be probably Studying (I assume and if not,you better be!)with your Cellphone besides you,
And you hear the Pinggg!!!
Aha.. GOTHAM needs you!! You shift your focus from the task of studying to the task of on your cellphone,and simultaneously thinking about how good you are at multitasking!
 Well don't pat your Backs yettt.
Although “multitasking” is a popular buzzword, research shows that only 2% of the population actually multitasks efficiently.
Most of us just shift back and forth between different tasks, a process that requires our brains to refocus time and time again — and reduces overall productivity by a whopping 40%.

 Told ya! No need to pat your backs,for decreasing your efficiency. So the next time your Read ,you only Read.

New Tel Aviv University research identifies a brain mechanism that enables more efficient multitasking. 

The key to this is “reactivating the learned memory,” a process that allows a person to more efficiently learn or engage in two tasks in close conjunction.

How does this work???

Starts with - Training the brain.

“When we learn a new task, we have great 
difficulty performing it and learning something else at the same time.

This is due to interference between the two tasks, which compete for the same brain resources.

The research demonstrates that - By pairing the brief reactivation of the original memory with the exposure to a new memory, long-term immunity to future interference was created.

For example- researchers first taught student volunteers to perform a sequence of motor finger movements with Right hand. 
After acquiring this learned motor memory, the memory was reactivated on a different day, during which the participants were required to briefly do some task with their Left hand — with an addition of brief exposure to the same learned motor task being performed by the Right hand.
By utilizing the memory reactivation paradigm, the subjects were able to perform the two tasks without interference.

So well we now have an overview of how the brains circuits are intimately connected and how they can still constantly evolve.

Hope this was helpful.

With this I finish the blog and my cup of tea!!
So much for Multitasking! 

Let's Learn Together.
-Medha 😊

Wednesday, June 21, 2017

Hematuria: A clinical pearl

Hey Awesomites

Hematuria (blood in urine) may be microscopic or macroscopic/ gross.

The American Urological Association (AUA) defines microscopic hematuria as 3 red blood cells/ high - power field on microscopic examination of the centrifuged urine specimen in two of the three freshly voided, clean- catch, midstream urine samples.

Gross/ visible hematuria can result from as little as 1mL of blood in 1L of urine, and therefore, the color of urine does not necessarily reflect the degree of blood loss.

Now lets have a brief review of the clinical presentation of hematuria on the basis of its source -

- A glomerular source of bleeding (nephronal/ glomerular hematuria) usually results in persistent microscopic hematuria that may be with/ without intermittent periods of gross hematuria.

- Total hematuria (present throughout the void) indicates bleeding of bladder/ upper tract origin.

- If renal sources of hematuria are present, the blood is equally dispersed throughout the urine stream  and does not clot.

In cases of clotting, its localisation is a must to evaluate the underlying cause:

- Hematuria/ clots at the beginning of the urine stream ( initial hematuria ) is a symptom of a urethral cause.

Terminal hematuria occurring at the end of stream may be caused due to either prostatic, bladder, or trigonal source of bleeding.

Thats all
- Jaskunwar Singh

Grossing the thyroid and differentials to be considered

Thyroidectomy is often received for lesions found suspicious on FNA or in cases where goitrous enlargement causes clinical symptoms of obstruction. Hemi includes the lobe and the isthmus, lobectomy only the lobe, while near total includes almost the entire thyroid except a small part of the thyroid left behind.
The following key factors should be described of the received specimen:

1. Type of the specimen
2. Dimensions of all the lobes
3. Size- If enlargement seen, is it diffuse or focal
4. Colour- Brown ( Normal); yellowish white/ beefy red/ mahogany brown
5. Consistency of the lesion - cystic ( single or multiple; bilateral or unilateral lobe involvement); solid; solid- cystic
6. Relation of the lesion to the adjacent thyroid
7. Surface of the thyroid - Smooth/ infiltrated - hemorrhagic irregular areas
8. Whether received intact or in pieces due to extensive extrathyroidal adhesions ( Reidel thyroiditis)

Serotonin receptor agonist and antagonist notes

1. 5-HT 1A receptor :- 
Partial agonists of this receptor are BusPIRONE,
These are useful as anti-anxiety drugs.

2. 5-HT 1B/1D receptor :-
Agonists at this receptors are sumaTRIPTAN, NataTRIPTAN.
These are useful for the treatment of acute migraine attacks.

3. 5-HT 2A/2C receptor :-
Antagonists are clozapine and risperidone.
These are used as atypical antipsychotic agents.

4. 5-HT 3 receptor :-
Antagonists are ondanSETRON, graniSETRON, tropiSETRON.
These agents are used in chemotherapy induced vomiting.

5. 5-HT 4 receptor :-
Agonists on this receptors are cisaPRIDE, 
These are useful in the treatment of GERD.

-Upasana Y. :)

mPFC activation in depression: The Associations

Hey Awesomites

I had talked about how people with neuroticism also have an advantage of being creative in a previous post.
Lets now know the basis of this in brief -

Sinus of Morgagni- Contents

There occurs a gap in the pharyngeal wall between the base of the skull and superior constrictor muscle called as Sinus of Morgagni. This space is closed by the pharyngeobasilar fascia.

Contents- (mnemonic PLATE)

1. Palatine branch of ascending pharyngeal artery
2. Levator palati muscle
3. Ascending palatine artery
4. Tensor vetli palatini
5. Eustatian tube

In nasopharyngeal carcinoma, the tumor may extend laterally and involve this sinus involving the mandibular nerve. This produces a triad of symptoms known as Trotter's Triad. 
These symptoms are:
1) Conductive deafness 
2) Ipsilateral immobility of the soft palate
3) Trigeminal Neuralgia

Hope that helped!
Ashita Kohli

Zenker's Diverticulum

Zenker's Diverticulum is a posterior pulsion diverticulum which occurs through the Killian's Dehiscence.

Killian's Dehiscence is a potential gap between the oblique and transverse fibres of the inferior constrictor muscle. It is also known as the gateway of tears as it is a potential site of perforation during oesophagoscopy. 

Zenker's diverticulum occurs due to the outpouching of the pharyngeal mucosa at the site of Killian's dehiscence.
There is incoordination between the descending peristaltic wave and the cricopharyngeus muscle at the upper oesophageal spincter which leades to high intra luminal pressure and the mucosal herniation through the weak area of Killian's Dehiscence.

It is not a true diverticulum as it has just the herniation of the pharyngeal mucosa. ( A true diverticulum has all the layers of the oesophageal wall)

It is usually seen in elderly above the age of 60.


1. The most common symptom is Dysphagia, which is intermittent initially and later becomes progressive.
2. Halitosis ( ie. bad breath, well ofcourse because food can get trapped in this pouch)
3. Regurgitation of food and cough.
4. There maybe regurgling sounds in the neck, gurgling sensation on palpation is known as Boyce sign.

Malignancies may develop in 0.5-1% cases.

Diagnosis- Barium Swallow and videofluoroscopy

1. Endoscopic stapling of the diverticulo esophageal sphincter.
2. In patients not fit for major surgeries, Dohlman's surgery may be done.

Hope that helped!
Ashita Kohli

Waldeyer's Ring

Waldeyer's Ring is an aggregation of lymphoid tissue seen in the subepithelial lining of pharynx guarding the nasopharynx and oropharynx in the form of a ring.

The ring is bounded by-

1. Palatine Tonsils ( also called as Faucial Tonsil)- Situated in between the anterior and posterior pillars on each side of oropharynx
2. Adenoids (aka Lushka's Tonsil)- Lies at the junction of roof and posterior wall of nasopharynx
3. Tubal Tonsils ( aka Gerlach's Tonsil)- Lies in the fossa of rosenmuller behind the eustatian tube opening
4. Lateral Pharyngeal Band and Nodules

Hope that helped!
Ashita Kohli

Rhinolalia Aperta

Rhinolalia Aperta is a speech disorder which involves hypernasality in voice.
The defect is seen in the failure of the nasopharynx to cut off from oropharynx.

Some fibres of palatopharyngeus muscle make the posterior pillar, go posteriorly in the posterior wall of nasopharynx and along with the lower fibres of the superior constrictor muscle forms a ridge known as the Passavant's Ridge

During swallowing and speaking the passavant's ridge closes the nasopharyngeal isthmus.
When this doesn't happen (eg- cleft lip, paralysis of palate) it leads to nasal regurgitation of food and nasal tone in speech known as Rhinolalia Aperta.


1. In children with cleft palate, special exercises can help in strengthening the muscles so as to reduce the nasality in voice.

2. Surgery- Posterior Pharyngeal Flap
                   Sphincter Pharyngeoplasty

Hope this helps!
Ashita Kohli 

Tuesday, June 20, 2017

Differentials of lower limb ulceration: Venous, arterial or neuropathic?


Q. Today, in our OPD, a 45 year old diabetic Male, farmer by profession presented with an ulcer on left lateral malleolus.
He had a history of edema in lower limb associated with an itching 2 years ago. Since 6 months he got a non-healing ulcer on left lateral malleolus.

On examination:-
Pigmentation of skin, eczema lipodermatosclerosis, atrophied Blanche are present and dilated veins on the medial aspect of left lower limb.

My question is how to differentiate whether the ulcer is due to neuropathy, venous stasis or obliteration of artery.

Why do the above doubt arise?
Because venous ulcer are commonly found at the lower third of the leg usually on the medial side and even on the foot.


(I) to rule out neuropathy,
1. Ask whether he feel the ground and pebble while walking barefoot
2. Test for the pain sensation, whether it is intact or not.

(II) Venous ulcer have characteristic findings. History is utmost important. They are shallow and flat. The edge is sloping and purple blue color.
The floor: - appears pink due to presence of granulation tissue. If it is a chronic ulcer there is more white fibrous tissue. Most important is A FAINT BLUE RIM of advancing epithelium may be seen at the margin.

(III) To check for arterial obliteration

1. Feel the dorsal pedis pulsation.
2. Ask for claudication also.

Conclusion: - It was venous ulcer.

Then why did it appear on the lateral side? Remember! On inspection dilated veins were found on the medial side.

Before answering the above question. Let us ask why is it most common on medial side?

There are more perforating veins on the medial side means more pressure in that area. But that doesn't mean lateral side is spared .There is some rise in pressure on lateral side also. The only thing that precipitated this was “Trauma”. Due to more itching on lateral side, he traumatised that area .It was initially small in size, non-healing ulcer which is gradually increasing in the size.

Found this great article on the lower limb ulcers.

Take care:)
-Upasana Y.

Authors diary: Tip for solving multiple choice questions

So this random tip comes from a fun conversation that I was having with my study partner today.

Baclofen for treatment of alcohol dependence


Recent evidence suggest that the gamma-aminobutyric acid-B receptor agonist baclofen is a promising agent for the treatment of alcoholism.


Baclofen produces an effortless decrease or suppression of alcohol craving. It decreases alcohol consumption including in those with poor motivation. The drug causes few side effects and does not add to the intoxication effect of alcohol.

It benefits patients with alcohol dependence (even those who are still in precontemplation stage of motivation!)

Research has shown that baclofen reduces withdrawal symptoms of alcohol and is safe in those with liver impairment.

Although further studies that compare long-term alcohol-related outcome of baclofen with established drugs such as naltrexone and disulfiram are needed.

Interesting, isn't it?


More than what you know about vitamins!

Hello! :)

These were the questions asked during my pharmacology vivas. And I found it fascinating after studying. I have never studied these points about vitamins before! 

Q. Which vitamin deficiency is related with lowering of seizure threshold?

Ans. Pyridoxine Vitamin B6. 

Why? As it is associated with synthesis of neurotransmitter GABA. Therefore, it is indicated during isoniazid induced convulsions. :)

Q. Why laropiprant (20mg) + Niacin (1g) is used in combination?

Ans. Nicotinic acid (a derivative) results in flushing of face.

Why? Vasodilation of cutaneous vessels.

Therefore, we combine it with specific anti-flushing drug called laropiprant.

Q. In hyperemesis gravidarum, what do you give for associated Wernicke's encephalopathy following hyperemesis? 

Ans. I thought of anti-emetics at first but the answer is vitamin B1. (Wernicke's encephalopathy doesn't always result from alcohol :P )

That's for today.
Take care. :)
-Upasana Y.

Lacunar infarction notes + mnemonic

Lacunar infarcts are small (0.2 to 15 mm in diameter) noncortical infarcts caused by occlusion of a single penetrating branch of a large cerebral artery.

Lipohyalinosis of the penetrating arteries. (Mnemonic: L for Lipohyalinosis, L for Lacunar)
Microatheroma of the origin of the penetrating arteries.
Lacunar stroke is usually related to a chronic vasculopathy associated with systemic hypertension.

Clinical features:
Penetrating artery occlusions usually cause symptoms that develop over a short period of time, typically minutes to hours. However, a stuttering course may ensue, as with large artery thrombosis, and symptoms sometimes evolve over several days.

As a general rule, lacunar syndromes lack findings such as aphasia, agnosia, neglect, apraxia, or hemianopsia (so-called "cortical" signs). Monoplegia, stupor, coma, loss of consciousness, and seizures also are typically absent.

These syndromes are common :
● Pure motor hemiparesis
● Pure sensory stroke
● Ataxic hemiparesis
● Sensorimotor stroke
● Dysarthria-clumsy hand syndrome

Pure motor hemiparesis: Characterized by weakness involving the face, arm, and leg on one side of the body in the absence of "cortical" signs (aphasia, agnosia, neglect, apraxia, or hemianopsia) or sensory deficit.

Artery / structure involved: Posterior limb of the internal capsule.

Mnemonic: PM - Pure Motor, Posterior limb of internal capsule.

Pure sensory stroke: Numbness of the face, arm, and leg on one side of the body in the absence of motor deficit or "cortical" signs.

Artery / structure involved: Thalamogeniculate branches of the posterior cerebral artery (Ventral posterolateral and ventral posteromedial nuclei)

Mnemonic: MIST
Motor - Internal capsule
Sensory - Thalamus

Ataxic hemiparesis: Ipsilateral weakness and limb ataxia that is out of proportion to the motor deficit. Some patients may exhibit dysarthria, nystagmus, and gait deviation towards the affected side. As with other lacunar syndromes, the above-mentioned "cortical" signs are absent.

Artery / structure involved:  Fibres of the fronto-ponto-cerebellar system in the internal capsule / corona radiata.

Sensorimotor stroke: Characterized by weakness and numbness of the face, arm, and leg on one side of the body in the absence of the aforementioned "cortical" signs.

Artery / structure involved: Sensorimotor strokes arise from infarcts involving the posterolateral thalamus and posterior limb of the internal capsule. The exact vascular anatomy is debated. 

Dysarthria-clumsy hand syndrome: Facial weakness, dysarthria, dysphagia, and slight weakness and clumsiness of one hand are characteristic. There are no sensory deficits or "cortical" signs.

Artery / structure involved: Lacunar infarctions of the anterior limb of the internal capsule, genu of the internal capsule, or corona radiata.

Intravenous alteplase (recombinant tissue-type plasminogen activator or rt-PA) improves outcomes for patients with ischemic stroke in general if administered within 4.5 hours of symptom onset. The available evidence suggests that intravenous thrombolysis is beneficial for patients with lacunar stroke. Most patients with acute ischemic stroke who are not eligible for thrombolytic therapy should be treated with aspirin.

That's all!

Monday, June 19, 2017

Changes in glomerular dynamics mnemonic

Hello everyone!

If you forgot the afferent - efferent stuff from step 1, I have a mnemonic.

Remember ACE ID, PDA ANC.

Step 2 CK: Management of thromboembolic stroke

Here are my notes. The most simplified version you'll get. 

That's all!

So I've been questioned the most about the last point, regarding heparin. Here's the source and reading material:

There are additional situations of high thrombotic risk after ischemic stroke where anticoagulation may be beneficial but for which there are little or no data. These include mechanical heart valves, carotid artery dissection, and large artery atherosclerotic stenosis.

Drugs used to lower BP acutely in severe preeclampsia mnemonic

Drugs used to lower blood pressure acutely in severe preeclampsia (Maternal hypertensive crisis) mnemonic

"Lower Hypertension Now"

Labetalol iv preferred (Avoid in bradycardia)

Hydralazine iv

Nifedipine oral

That's all!

Sunday, June 18, 2017

Micturition and Neurological diseases

Here, presenting you a detailed description of Pathologies of Bladder in Neurology. I believe this is the best resource on this topic available online for free. :)

Diaphragmatic hernia : Mnemonic and Review

Here's a short post on the key points about Congenital Diaphragmatic Hernia.

So there's deficiency in the diaphragm during development causing abdominal contents to budge into the Thorax.

There are 2 main types -->

1. Bochdalek.

2. Morgagni.

Now out of these 2, Bochdalek is commoner.
(It's hard to remember the word Bochdalek. I struggle with it every day. )

You can memorize it by realising that it rhymes with ' Scotch da Lake '
(Which means a lake of scotch in Punjabi)

Key points about Bochdalek -

- Back  - Located posteriorly
- Big - Bigger than the Morgagni form
- Bad - Poor prognosis
- Bag and Mask Contra indicated. 

Also realise - Bochdalek
So it's got an L in it. L = Left. So it's more common on the left side. These hernia classically cause a scaphoid abdomen and Mediastinal shift to the opposite side.

Morgagni can be remembered by the opposite of the BBB
So it's
- Not on the back - Anteriorly
- Not Big - Small sized.
- Not as Bad - Prognosis is alright.

Also realise - Morgagni
It's got an R in it = Right. So it's more common on the right side. And it contains the Transverse colon generally.

So that's all !
Happy studying! 
Stay awesome !

~ A.P.Burkholderia 

Croup : Review of key points

Here's a short Mnemonic/Review of Important facts about Croup - Acute Tracheobronchitis !

Remember :

C - Common respiratory disease
R - Respiratory viruses like Parainfluenza
O - Oxygen Treatment (Humidified)
U - Ugly Cough - Barking / Seal like cough
P - Prodrome of illness followed by Inspiratory Stridor
S - Steeple sign on X Ray

It's helpful to remember Acute EPIGLOTTITIS as the complete opposite of CROUPS using similar ideas.

- Not as common.
- Caused by Bacteria generally (Strep , Hib)
- Oxygen Therapy + AntiBiotics
- Ugly - Sniffing dog like position + Drooling
- Prodrome not particularly, but Stormy acute onset.
- Shows Thumb print appearance on X Ray.

Hope this helped !
Happy Studying !
Stay awesome.

~ A.P.Burkholderia

CMS neuro form 2: Question on numbness, tingling and decreased grip strength

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.

A 52 year old man presents with a 1 month history of numbness and tingling of the ring and small fingers of his right hand that radiates to his palm. His symptoms are not constant and exacerbated at night. He has a 2 week history of decreased grip strength and wasting of the small muscles in his right hand. He has not had neck or arm pain. 4 months ago, he was diagnosed with pancreatic cancer, since then, he underwent Whipple procedure and is currently receiving chemotherapy with gemcitabline. Since his diagnosis, he has had significant fatigue and an 18 kg weight loss. He is 173 tall and weighs 54kg. BMI is 18. His temp is 37, pulse is 95, and BP is 120/79. There is wasting of the interosseous muscles on the right. Muscle strength is 3/5 in the right interosseous and hypothenar muscles and flexor digitorum profundus of the ring and small fingers. It is full elsewhere. Deep tendon reflexes are 2+ throughous. Babinski sign is absent. Sensation to pinprick and temperature is decreased over the ulnar aspect of the palm and dorsum of the hand ring and small fingers; proprioception is intact. The remainder of the neurologic exam shows no abnormalities. Which of the following is the cause of his symptoms?

A. C8 nerve root infiltration by tumor

B. Cervical disc herniation

C. Chemotherpay neurotoxicity

D. Ulnar nerve compression

E. Vit B12 deficiency

Confusing answer choices: C8 root infiltration by tumor infiltration vs ulnar nerve compression.

The weakness pattern given is conforming to ulnar nerve rather than C8 myotomes. Root pain is generally present in radiculopathies. Also, in C8 radiculopathy, sensory and motor involvement will be more extensive. Triceps reflex would be affected in C8 radiculopathy.

Obvious incorrect answer choices:

Cobalamin deficiency is a generalized peripheral neuropathy. Vibration sense is one of the earliest to go.

Chemotherapy induced neuropathy also is generalized polyneuropathy and has preponderance of sensory symptoms.

The absence of neck pain makes the possility of cervical spondolysis less likely. Also, cervical spondylosis is most common in C5 C6 though it can rarely occur in C7 C8.

Doubt: Why is there no loss of proprioceptive sensation?

Please note that the author of this question has said that there is decreased senstion and not complete anesthesia.

Thus, patient can percieve vibration (present or absent) while testing and feel the decreased sensation of pinprick, temperature by comparison with the normal area.

Generally, when we do vibration test with a tuning fork, all we ask the patient is can he feel it and we ask the patient to indicate when the vibrations stop. But in pinprick, we ask the patient to compare with a normal sensation in a normal area.

Extra: In ulnar nerve compression, Froment's sign, tests for palsy of the ulnar nerve, specifically, the action of adductor pollicis. It isn't mentioned in this question but worth knowing.

This was explained by a Medicowesomites (Upsana's) professor. Thank you, Dr Pankaj Kumar for taking the time and explaining this question and the doubt in such detail. Also, thank you for letting me make a few edits and publish this. It'll be helpful to a lot of students!


Differentiating C8 radiculopathy from ulnar neuropathy

Hello. This is a very short post (because I am super busy studying)

It's on differentiating C8 radiculopathy from Ulnar neuropathy based on a question I solved the other day. How would you differentiate the two in clinical practice?

C8 radiculopathy:
- Thumb abduction weakness: abductor pollicis brevis (C8, T1)

- Triceps affected (C6, C7, C8)

- Radiculopathies are often painful.

Ulnar neuropathy:
- Hand intrinsics (C8, T1) affected:
Palmar and dorsal interossei
Lumbricals III & IV
Abductor/opponens/flexor digiti minimi

- Basically, all hand intrinsics except for the median-supplied "LOAF" muscles (lumbricals I & II, opponens/ abductor/flexor pollicis brevis)

- Triceps not affected.

- Focal neuropathies aren't painful.

Conclusion: The ulnar nerve innervates all intrinsic hand muscles, except the abductor and flexor pollicis brevis, opponens pollicis, and lateral two lumbricals, which are innervated by C8 and T1 via the median nerve which helps differentiating the ulnar neuropathy from C8 radiculopathy.

That's all!

Pills of knowledge in Ophthalm- Anterior ciliary artery

The point where the anterior ciliary artery pierces the sclera is often marked by a pigment. This is of particular importance while cauterization as in a bid to make everything look neat and shiny, the pigmented part shouldn't be cauterized as it will cause necrosis of the structures supplied by the artery. 

Saturday, June 17, 2017

Effects of Angiotensin-II on GFR

So this is a highly confusing topic. No matter how many times you read it, some amount of doubt is always there in your mind. So an advice to the readers, bookmark this post because you will be needing to read it more than once to get the drift.

First of all, let us review the effects of Angiotensin II on Glomerulus.

It constricts both the afferent and efferent arterioles but preferentially increases efferent resistance. Why? 3 reasons:

1. Efferent arterioles have a smaller diameter in their basal state.

2. Ang II stimulates the release of vasodilator NO from the afferent arteriole.

3. Ang II minimizes vasoconstriction at the afferent arteriole via the stimulation of Ang II type 2 (AT-2) receptors, which result in vasodilatation through a CYP450 dependent pathway.

The net effect of preferential rise in efferent arteriolar resistance is that the glomerular pressure is increased or stabilized(in hypoperfusion states), which helps to maintain or increase GFR. But in the long run, lots of fluid have been filtered out leaving behind the proteins which raise the colloid osmotic pressure, eventually enough to overrule the hydrostatic pressure and hence it leads to decrease in GFR.

Ang II also reduces GFR by causing constriction of the mesangial cells which reduces the effective surface area for filtration. 


Pills of knowledge in Ophthalmology- Squint and refractive errors

1.A refractive error should be thoroughly assessed prior to surgical squint correction or the squint may recur.

2. Divergent squint occurs in myopes as the divergent system of muscles is more active during far vision. So, the far vision in myopes being hampered, the eyes try to diverge more.

3. Same goes for hypermetropes. They end up with a convergent squint if left uncorrected.

-That's all!

Sushrut Dongargaonkar

Differentiating peroneal neuropathy, sciatic nerve injury and L5 radiculopathy

This post is on differentiating weak dorsiflexion of foot - I made a little algorithm on it. (I'll add images later)

If there's weakness in foot dorsiflexion, check plantar flexion and inversion.

If plantar flexion and inversion is normal: Peroneal neuropathy.

If plantar flexion and inversion is weak: Check hip movements.

If weakness at hip joint: S5 radiculopathy.
If no weakness at hip joint: Sciatic nerve compression.

You can differentiate based on sensory levels and reflexes too but this is easier.

Peroneal nerve supplies the dorsiflexors and evertors of the foot. There will be no weakness in plantar flexion and inversion in peroneal nerve injury.

Hip abduction is an action of Gluteus medius and minimus muscles. These are Superior gluteal nerve innervated muscles. This nerve arises from L4, L5 and S1 roots . If there is hip abduction deficit with foot drop, it means pathology at the radicular ( root) level. 

Here's the reading material.

Common peroneal neuropathy presentation:
- Acute foot drop (difficulty dorsiflexing the foot against resistance or gravity).
- Patients describe the foot as limp; there is a tendency to trip over it unless they compensate by flexing the hip higher when walking, producing what is called a "steppage" gait.
- Patients may also complain of paresthesias and/or sensory loss over the dorsum of the foot and lateral shin.
- Examination typically reveals weakness in foot dorsiflexion and foot eversion (deep and superficial peroneal nerve-innervated, respectively), with normal inversion and plantar flexion (posterior tibial nerve).
- Sensory disturbance is confined to the dorsum of the foot, including the web space between digits 1 and 2 and the lateral shin.
- Reflexes are normal.

Sciatic nerve injury presentation:
- Weakness affecting most of the lower leg musculature, including the hamstrings.
- Hip flexion, extension, abduction and adduction, and knee extension are normal.
- Sensory loss involves the entire peroneal, tibial, and sural territories.
- In the lower leg, however, the medial calf and arch of the foot may be spared secondary to innervation by the preserved saphenous nerve (a branch of the femoral nerve). Sensation is also spared above the knee both anteriorly and posteriorly.
- The knee jerk is normal, but the ankle jerk is unobtainable.

L5 radiculopathy presentation:
- Back pain that radiates down the lateral aspect of the leg into the foot.
- On examination, strength can be reduced in foot dorsiflexion, toe extension, foot inversion, and foot eversion.
- Mild weakness in leg abduction may also be evident in severe cases due to involvement of gluteus minimus and medius. Atrophy may be subtle; it is most readily observed in extensor digitorum brevis.
- Sensory loss is confined to the lateral shin and dorsum of the foot.
- Reflexes are generally normal.

That's all!

Friday, June 16, 2017

Alvarado Score Parameters Mnemonic ; For Appendicitis

Alvarado score is one of the most famous scores to clinically diagnose Appendicitis. Without further adieu let us delve into it.

            Anorexia or ketones in urine           - 1 
            Leukocytosis >10,000                      -2  
            Vomiting/Nausea                             -1
     migrAtory pain to right iliac fossa            -1
           Rebound tenderness                         -1
 temperAture above 37.3 celsius                 -1
      tenDerness in right iliac fossa              -2
   neutrOphilia >70%                                 -1

Of these the second parameter from above and second parameter from below have 2 points credited for each. Every other parameter is credited with 1 point each.

The overall aggregate comes out of 10, which the highest possible score for Alvarado score.

If, the aggregate is,

<3 - Low risk for appendicitis
4-6 - Mid risk for appedicitis
>=7 - High risk for appendicitis

In some hospitals where a differential count is difficult to find, use a modified score with 9.

That's all guys, if you find any mistake let me know.

With love,

P.S. - yayyy.....missed me much awesomites? I was away from the blog for the last 6 months from posting, because I had very disastrous scores for surgery in my university and I didn't feel worthy enough to write for you guys. (So my activity was largely concentrated in the Whatsapp Medicowesome groups, and the Author's page.) Anyways, I had to take a remedial exam for Surgery 2 weeks ago. And BAAM!!!!.....the results were released today, and yayyyyy.....I passed surgery! :)

I must thank all my Medicowesome admin/author collegues for tolerating my rants and, help me to push through the hellish scary time together. Thanks everyone. Finally I'm through it, and I'm back to writing for you all guys. So thought to start the first post after returning, with a General Surgery Diagnosing score with the help of Schwartz Textbook of Surgery.

See ya soon peepz! :)

Thursday, June 15, 2017

Pills of knowledge in Ophthalm- Posterior staphyloma

A posterior staphyloma is common because the durability of the layers of the eye where the optic nerve enters the eye is lesser in comparison.

-That's all!

Sushrut Dongargaonkar

Pills of knowledge in Ophthalm- Moxifloxacin

Moxifloxacin is the preferred antibiotic in Ophthalmic surgeries and pathologies because it gets concentrated into the anterior chamber and the aqueous.

That's all!

-Sushrut Dongargaonkar

EMG and NCS - Review

Hello there!

Today we'll see some important points on Electromyography (EMG) and Nerve conduction studies (NCS).

EMG evaluates abnormal electrical activity in muscles, and NCS investigates how electricity flows through a nerve.

They help to locate and determine the causes of diseases that affect muscles and peripheral nerves.

In EMG, a small needle is inserted into a muscle, to measure its electrical activity. In NCS, electrodes are placed on the skin overlying a nerve, and other recording electrodes are attached at a different point over the same nerve and a small shock is applied, and the electrical impulse is recorded​.

Understanding the terminologies and results of these tests-

 Amplitude: The electrical signal is represented as a wave, and the amplitude is its height.

ConductionVelocity (CV): The conduction velocity describes the speed at which the electrical impulse travels along the nerve.D

Duration This describes the width of an electrical wave.

ConductionBlock: The diminution of signal across an anatomical region such as the wrist. This suggests nerve entrapment.

So when a nerve stimulates a muscle to contract, there is a brief burst of electrical activity called a motor unit action potential (MUP).

Some of the abnormal responses seen are:

1)Fibrillations & positive sharp waves on the monitor seen in diseases of peripheral nerves.

Muscles sometimes start having spontaneous activity on their own.

2)Fasciculations: Sometimes the abnormality causes visible muscle twitches.

3)Abnormally large MUPS : These are seen If a nerve has been injured and then regrows.

 On regeneration the nerve tends to branch out to include a wider area of the muscle and hence we get large motor unit potentials on the screen.

4) Abnormally small MUPS: When they're  abnormally small or brief it suggests the presence of a disease of a muscle (a myopathy) where the muscle is unable to contract to and fails to provide the normal amplitude of the wave.

5)"Recruitment pattern":  As a muscle is contracted, nerve fibers signal more and more bits of muscle (called motor units) to join in and help. 

In a neuropathic disorder, the amplitude of different motor units is strong, but there are fewer of them because the nerve is unable to connect to as many units.

 In myopathies, the number of motor units is normal, but the amplitude is smaller

You may never come across an actual EMG for an interpretation,but it is always good to know the investigation.

The interpretation of EMG and NCSs is not always straightforward and may not always lead to just one possible diagnosis — but the tests can reduce the number of diagnostic possibilities.

Hope this was helpful!

Let's Learn Together!


New TB Risk Factor

People with low levels of vitamin A who live with individuals who were sick with tuberculosis were 10 times more likely to develop the disease than people with high levels of the nutrient, according to research led by investigators at Harvard Medical School.

Vit A rich foods: Liver, fish, hard-boiled egg(not omelette), cheese, butter, cheddar etc

And now some vegetables: Sweet potato, Carrot, Squash, Spinach, Lettuce

Some fruits: Mango, Papaya, Guava, Watermelon, Apricot, Passion fruit

Another reason to love Mango!


Research update: Statins may increase risk of Parkinsons' disease

Hey Awesomites

A new research by neuroscientists has updated our knowledge about the association between high cholesterol levels in people and prevalence of neurodegenerative diseases such as the Parkinson's.

Mind - wandering : How your body reacts to it?

Hey Awesomites

First lets have a word about mind - wandering.. "Mind- wandering (or task-unrelated thoughts) is an experience of thoughts which are totally unrelated to the task you are doing right now, especially when it demands attention. It involves activities such as reading, driving, attending lectures, etc."

Wednesday, June 14, 2017

Dibucaine Number.

Hello !
Let's see what this Dibucaine number is.

So Dibucaine is a local anesthetic.

Dibucaine inhibits 80% of the normal Pseudocholinesterase enzyme and 20% of the Atypical enzyme.

The number is determined by measuring the percentage of Pseudocholinesterase enzyme that remains unchanged in the blood of individuals administered a standard dose of Dibucaine intravenously.

Normal Dibucaine number is 70-80% i.e 70-80%of normal enzyme is inhibited by Dibucaine.
If there is a point mutation in the enzyme making it a Atypical Pseudocholinesterase then Dibucaine will not be able to inhibit it and the number will decrease.

This number is used to measure the activity of Atypical Pseudocholinesterase,and to assess the likely hood of prolonged apnea after succinylcholine administration.

Sodium Fluoride can also be used in place of Dibucaine.

If you know more on it Add to this information.

Let's learn Together!

Monday, June 12, 2017

Contraindications for Noninvasive Ventilation Mnemonic

Hey guys

This is one of my rare mnemonic posts. I don't post much on this coz most of my mnemonics are kinda personal if not socially inappropriate :p

So Noninvasive ventilation, imagine having a mask on ur face, all air tight, almost strangulating and as if this isn't enough, with multiple tiny outlets giving jets of air which are titillating your highly itchable nasal area.

Unpleasant, right?

Talking of unpleasant, you do remember Hitler, right?
He GAAASED the Jews, since that's not a possibility for us since we all love Zuckerberg let's think about something on a similar note.

"GAAAS the HOEs"

G- GI bleeding
A- Aspiration
A- Angina( including MI)
A- Arrest( Cardiac and Respiratory)
S- Surgery on ur face

H- Haemodynamic instability
O- Obstruction ( in upper airway)
E- Encephalopathy ( Severe)
S- _____

I've left the last one blank for the reader to fill up. Hint: It has something to do with​ obstruction of the lower airways.

Hope this is helpful!


Sunday, June 11, 2017

Study Group Discussion: Salisbury Phenomenon

Whats Salisbury effect?

It's a very interesting phenomenon.

It states that when coronary collaterals develop in the face of myocardial ischemia, they improve the blood supply. However they physically restrict left ventricular dilation and thereby raise LVEDP(LV end diastolic pressure) and reduce LV compliance.
This is because they act like tendrils/scaffold which prevent ventricular dilation.

Nice one!


Ductus Arteriosus : Review of Key Points

Hi everyone ! Just a short review on Ductus Arteriosus.

- Ductus Arteriosus is basically a communication between the Pulmonary trunk and the Systemic Aorta.
- This communication is between pulmonary trunk and the end of Arch of aorta. Just after the Brachiocephalic trunk , and Left Common carotid and Subclavian have branched off.
- In embryonic life this communication helps transport blood from RV- Pulmonary artery to the Systemic circulation.

So ,
Remember :
Prostaglandins Persist

-Prostaglandins, especially PGE1 , act on the Ductal muscle tissue and keep it Open.
-So the Ductus arteriosus stays open.

-This is important in certain Duct dependent lesions
- Duct dependent heart lesions are those which need the presence of an Open ductus to receive blood in systemic / Pulmonary circulation.

- For example -->
✓ Duct dependent lesions for Systemic Circulation are those that cause obstruction to the Left side heart to pump blood into the aorta. These include :

- Coarctation of Aorta ( especially pre Ductal ) : Here there is a constriction of the aorta just before the ductus Arteriosus. So , a persistent Ductus would transport blood from pulmonary circulation into the systemic. 
If ductus gets closed , there would be minimal blood flow to the Lower limbs and abdomen.

- Critical Aortic stenosis.
- Left side Hypoplastic heart.


✓ Duct dependent lesions for pulmonary circulation
-These are lesions where pulmonary blood flow would be severely reduced due to some RV- Outflow tract Abnormality and the only source to the lungs would be through the ductus shunting some blood from aorta into the pulmonary vein.

- These include : 

- Critical Pulmonary Stenosis
- Hypoplastic Right heart syndrome
- Tetrology of Fallot
- Tricuspid Atresia
- Ebstein Anomaly


So. We've seen in what conditions we'd like to keep the Ductus Arteriosus open / persistent.
Normally this Ductus closes functionally within 24 hours of birth. And anatomically between 10 and 14 days post natally.

If this persists on its own for a long time it causes a Congenital Heart Disease called Patent Ductus Arteriosus.
This defect is characterised by shunting of blood into the pulmonary trunk constantly during systole and diastole causing a Continuous murmur.

To close this ductus , we could try using Indomethacin / Ibuprofen especially in preterm children.
These drugs inhibit Prostaglandin synthesis , thus causing Ductus Smooth muscle to constrict and eventually close.

So that's all about the ductus !

Happy studying !
And Stay Awesome !

~ A.P.Burkholderia

Saturday, June 10, 2017

Jaundice Syndromes : Mnemonic

Hey everyone. Just a short post on how to remember the Jaundice Syndromes.


Remember :
(As in the CGI special effects in movies.)

C - Criggler Najjar Syndrome
G - Gilbert Syndrome
I  - Indirect Jaundice ( Unconjugated Bilirubin).

So this would make Dublin Johnson and Rotor Syndromes Direct Jaundice.

Another useful fact :
All are inherited as Autosomal recessive trait except Gilbert and Criggler Najjar 1.

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

Lowe syndrome mnemonic

Lowe Syndrome (Oculocerebrorenal dystrophy) mnemonic

Think of Lowe = Love and it'll make sense.

Lowe makes you blind (cataracts, glaucoma)

Lowe makes you HAPpy (High Alkaline Phosphatase along with normal calcium, low phosphate)

Lowe messes with your head (intellectual disability)

LoveR - Renal defects (proximal tubular acidosis, aminoaciduria, and low-molecular-weight proteinuria)

Lowes syndrome is a cause of Fanconi syndrome.

That's all!


Renal Cell Carcinoma Etiology : Summary

Hi everyone. Here's a short summary of the causes for Renal cell carcinoma !

Renal Cell Carcinoma ( or RCC) is a common tumor of the kidneys and is essentially an Adenocarcinoma.
It's quite often called as the 'great mimic' as it is relatively hard to diagnose.

Here's the list of causes of this tumor.

Remember :
CCCC or C4

C = Cigarette smoking and Tobacco usage.
C = Chronic Kidney Disease / Cystic (Acquired) Disease of kidneys.
C = Cadmium, Asbestos and other occupational Exposures.
C = Cancer Syndromes.
Important Cancer Syndromes =

- Von Hippel Lindau Syndrome :
3p mutation in VHL Gene which is a tumor suppressor --> Tumors seen include Cerebellar and Retinal Hemangioblastomas , Pheochromocytoma, RCC (Clear type) and various other Cystic tumors.

- Tuberous Sclerosis

- Birt Hogg Dube Syndrome : Associated with various weird skin changes and chromophobe type RCC.
Skin changes include --> Tumors of Hair disc (Tricho-discoma) , Tumors of Hair follicle - Fibrofolliculoma and Acrochordons ( skin tags).

- Hereditary Papillary Cancer : Associated with MET Gene mutations

- Hereditary Leiomyomatosis with RCC : Associated with multiple Fibroids in the uterus.

That's​ all for today!
Hope this helped.
Happy Studying !
And, as always , Stay awesome !

~ A.P.Burkholderia

Friday, June 9, 2017

Step 2 CK: Differentiating ileus from SBO

Hello! Short post.

SBO: Small bowel obstruction.

Both: Nausea, vomiting, abdominal distension

Ileus: Hypoactive bowel sounds
Dull and constant pain
Dilated bowel but no air fluid levels

SBO: Initially hyperactive, later hypoactive
Colicky abdominal pain
Air fluid levels seen

That's all!
Back to studying.

Thursday, June 8, 2017

Neuroblastoma mnemonic


The term neuroblastoma is commonly used to refer to a spectrum of neuroblastic tumors (including neuroblastomas, ganglioneuroblastomas, and ganglioneuromas) that arise from primitive sympathetic ganglion cells and, like paragangliomas and pheochromocytomas, have the capacity to synthesize and secrete catecholamines.

Remember the N myc mnemonic for neuroblastoma :

N - Neuroblastoma, N myc gene
M - Crosses midline (differentiates from Wilms)
MY - MYoclonus (Opoclonus myoclonus)
C - Calcifications in tumor present
C - Catecholamine secretion

You can also remember "High BP" for additional findings seen in neuroblastoma:

Horner syndrome
Heterochromia iridis (different colors of the iris or portions of the iris)
Homovanillic acid and vanillylmandelic acid elevated in urine
Bombesin positive
Back pain
Bone pain
Beckwith-wiedemann syndrome association
Posterior mediastinum or retroPeritoneal mass
Purple skin lesions
Periorbital ecchymoses

That's all!

Wednesday, June 7, 2017

Doyne's macular degeneration

So, the other day the head of my department asked us about Doyne's maculopathy. Couldn't find rest until I searched it up on Google. Here what it is in short-

1. Accumulation of material between
the Bruch's membrane and the retinal pigment epithelium.

2. This results into the formation of a drusen, which is a radially localised
white, large one which spreads over

3. The cause is a mutation in the
EFEMP1 gene,on chromosome
2p16, inherited as an autosomal
dominant trait which results in the
formation of a misfolded protein
which is poorly secreted as well.

4. All this results into a gradual loss of

5. Photodynamic therapy forms the
mode of treatment for subfoveal nets which may also occur in the disease.

It is also known as 'Honeycomb retinopathy'

That's all!

-Sushrut Dongargaonkar

Tuesday, June 6, 2017

The Romberg's Test.

Today's review is on Rombergs test.

Romberg/Brauch-Romberg sign:
In cases where the proprioception is disturbed, patient may be able to stand with eyes open but sways or falls with eyes closed.

Romberg described this test, in patients with tabes dorsalis where the Dorsal Columns are damaged.
Well he did not state that the feet should be placed together; it was added later.. Nor did he comment on where the arms were to be positioned.

It is just a common practice to have the patient hold the arms outstretched in front, in order to check simultaneously for pronator drift or to perform finger-to-nose testing; it is not what the original test was.

The Romberg sign is often misunderstood and misinterpreted. 

The essential finding is a difference between standing balance with eyes open and closed. To test this function, the patient must have a stable stance, eyes open and then demonstrate a decrease in balance with eyes closed, when visual input is eliminated.
This is the time patient must rely on proprioception to maintain balance.

The Romberg sign is used primarily as a test of proprioceptive, not cerebellar, function, patients with cerebellar disease, particularly disorders of the vestibulocerebellum or spinocerebellum, may have some increase in instability with eyes closed, but not usually to the degree seen with impaired proprioception.

A patient with an acute unilateral vestibulopathy may fall toward the side of the lesion when standing with eyes closed.

Additional Manuevers for this Sign.

1) Ropper's Refined Rombergs Test :
Turning the head side to side eliminates vestibular clues and increases the reliance on proprioception.

2) The Sharpened Romberg Test :
It is done by having the patient stand in tandem position with eyes open and closed; the limits of normality for this variation are conjectural.

Hope this was helpful!

Let's Learn Together!

MCQ Pointers - Pityriasis Versicolor.


If you see some of the below "pointer" words in MCQs the ans would most likely be pointing towards Pityriasis Versicolor.

-Acquired lesions.
-Hypopigmented small macules coalescing to form Patches classically on the chest (m/c),back,face.
-Perifollicular (around hair follicles) distribution.
-Fine scaling on lesions which becomes prominent on scratching - Scratch sign+.
-Pale yellow fluorescence of the lesions on Wood's lamp examination.

Finally the classic - Indicating the causative organism : Malasessia.
Spaghetti and meat balls appearance or Banana and Grapes appearance on KOH mount.

Lemme know more of pointers you know about.
Let's Learn Together!

Step 2 CK: Psychiatry tip for possible depression questions


Whenever I come across a possible major depression question, I write SIGECAPS (full form at the end of the post) down and strike out the alphabets as and when I come across the symptoms.

For example, weight loss - strike out A for appetite change, fatigue because staying up at night - strike out S for sleep change, E for loss of energy.

Then re-read the stem and see for symptoms I missed out due to twisted wording (she stopped singing a month ago - strike out I for loss of interest)

It REALLY helps in figuring out 5/9 SIGECAPS for diagnosis of MDD because if you are not actively looking for the symptoms in the question stem, you'll miss them out. Also, if you are not counting, you might wrongly over diagnose MDD.

Writing it down also saves time because you don't have to keep re-reading the stem over and over.

It also helps getting the count right because if you have already striked out an alphabet, you can't strike it out again. So you won't get the count wrong for possible rephrasing of the same symptom in the question stem. (patient says she has lost appetite, there is weight loss - it is one alphabet in SIGECAPS, so you can't strike A out again - you will get the symptom count right!)

That's all!

I've read so many comments by students in forums where people get MDD wrong just because they didn't see the obvious 5/9 SIGECAPS. Don't miss it out guys, it's very easy to diagnose with this trick! :)
Hope that helps!


For those who don't know what SIGECAPS stands for :

S: Sleep changes: Increase during day or decreased sleep at night

I: Interest (loss): of interest in activities that used to interest them

G: Guilt (worthless): Devalue themselves, feel guilty

E: Energy (lack): common presenting symptom (fatigue) 

C: Cognition / Concentration: Reduced cognition &/or difficulty concentrating

A: Appetite (weight loss): Usually declined, occasionally increased

P: Psychomotor: Agitation (anxiety) or retardations (lethargic)

S: Suicide / preoccupation with death

Originally when a physician would write a prescription, the abbreviation “SIG” would be written which was to mean directions. The "E" CAPS was to remind the prescriber to write “Energy” capsules for depression (antidepressants).

Hence:  SIG:  E. CAPS

GLP-1 analogues mnemonics


Mechanism of action of GLP 1 analogues
- Increase glucose dependent insulin release
- Decrease glucagon release

Exenatide, leraglutide

Mnemonic: They secrete a tide of insulin dependent on glucose.

Adverse effects: Pancreatitis
Mnemonic: Tides causes titis

That's all!

Monday, June 5, 2017

Motor Neurone Disease : Why and How to rule it out.

Hi everyone ! Here's a short post on How and why to rule out Motor Neuron diseases.

Motor Neurone Disease includes a group of conditions where the Motor Neurons of your body begin to degenerate.
If these neurons are located above the level of the Alpha motor neuron of spinal cord , the result is UMN lesions , like Primary Lateral Sclerosis.
If the degeneration occurs in the Alpha motor neurons themselves , the result is LMN type paralysis, like Spinal Muscular Atrophy..
A combination of the two - UMN + LMN features as seen in - Amyotrophic Lateral Sclerosis.

Now a few set of conditions are used as a way to exclude to MND.
MND itself isn't very common , and carries an extremely poor prognosis. Treatment options are extremely limited. So it's important to rule it out whenever you come across a Paraplegia , Quadriplegia, Bulbar or Pseudobulbar palsy patient .

An MND has No COBS.
C - No Cognitive changes
O - No Ocular motility involvement till late.
B - No Bladder bowel involvement till late.
S - No Sensory involvement.

There are a few exceptions to this -
Cognitive changes can be present if it's associated with Fronto temporal dementia. A lot of the familial cases are associated with this.

Behavorial changes can also be seen in a Pseudobulbar palsy patient. (More on that some other day !)

Sensory involvement may be seen in Hereditary spastic paraplegia - a variant of MND.

So that's all !
Happy studying !
Stay awesome !

~ A.P.Burkholderia.

Sunday, June 4, 2017

Clonus - A review.

Hello everybody!
Let's review Clonus breifly today.

So what is it?
It is a series of rhythmic involuntary muscular contractions induced by the sudden passive stretching of a muscle or tendon.

Clonus occurs most frequently at the ankle, knee, and wrist, occasionally elsewhere.

The important Clonus that we all frequently examine is the Ankle Clonus so let's see that in detail here.

Ankle clonus is a series of rhythmic alternating flexions and extensions of the ankle.

How to do it?
The leg and foot should be well relaxed, the knee and ankle in moderate flexion, and the foot slightly everted.
The examiner supports the leg, with one hand under the knee or the calf, grasps the foot from below with the other hand, and quickly dorsiflexes the foot while maintaining slight pressure on the sole at the end of the movement.
A single tap on the tendon to elicit the ankle jerk may occasionally provoke clonus.

Unsustained clonus fades away after a few beats; sustained clonus persists as long as the examiner continues to hold slight dorsiflexion pressure on the foot.

Unsustained (transient) symmetric ankle clonus may occur in normal individuals with physiologically fast Deep Tendon Reflexes. Nonorganic clonus occurs rarely. False clonus (pseudoclonus) in psychogenic disorders is poorly sustained and irregular in rate, rhythm, and excursion.

Sustained clonus is never normal. In severe spasticity, clonus may occur spontaneously or with the slightest stimulus. At the ankle, true clonus can usually be stopped by sharp passive plantar flexion  of the foot or the great toe; false clonus is not altered by such a maneuver

Part one - For ankle clonus, the sudden stretch of the gastrosoleus muscle elicits a contraction essentially analogous to a stretch reflex that causes a contraction with resultant plantar flexion of the foot. The foot goes down. 
Part two - This contraction increases tension in the Golgi tendon organs in the gastrosoleus tendon, sending a volley of impulses via the Ib fibers that then inhibit the contraction of the gastrosoleus and facilitate contraction of its antagonist, the tibialis anterior muscle.  The foot goes up. 
This in turn passively stretches the gastrosoleus, and the cycle is repeated.

A simpler explanation is alternating stretch reflexes.

A few other Clonus' seen are :

1) Patellar clonus :
It consists of a series of rhythmic up-and-down movements of the patella. It may be elicited if the examiner grasps the patella between index finger and thumb and executes a sudden, sharp, downward thrust, holding downward pressure at the end of the movement. 

The leg should be extended and relaxed. Patellar clonus may appear when eliciting the patellar or suprapatellar reflex.

2) Wrist Clonus :
It is produced by a sudden passive extension of the wrist or fingers.

3) Jaw Clonus occurs occasionally.

So that's all about clonus.
Hope it was helpful!

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