Oculocardiac Reflex

Oculocardiac Reflex/Aschner phenomenon.

This is one of the trigeminovagal reflexes produced on digital massage of eye. Digital massaging of the eyeball is done to lower intraocular pressure after producing a retrobulbar or a peribulbar block. But rarely....this event is followed by cardiac depression, asystole and even death. The afferent is by the ophthalmic division of trigeminal nerve which relays in the visceral motor nucleus of the vagus nerve. The efferent is carried by the parasympathetic vagus nerve to the heart. It is most commonly seen in pediatric cases during squint surgery.
It is not seen very commonly in adults and in other surgeries as the procedure would involve just one eye and massaging of this eye is not sufficient to produce bradycardia normally.

Treatment: atropine or glycopyrrolate . Cardiopulmonary resuscitation might be needed in severe cases.

Bulbar and Psuedobulbar palsy : Overview

Here's a short overview of Bulbar and Pseudobulbar palsy !

If there is a lesion is at the level of Medulla - affecting the motor neurons : The nuclei of the cranial nerves -  you get LMN Palsy features - Flaccid paralysis of 9 10 11 12 Cranial nerves. This is called a 'Bulbar palsy' as the bulb (Medulla) is involved in isolation.

Now , essentially when the fibres supplying the motor neurons of the bulb (your Medulla)  are affected themselves - that is any neurons above the nucleus of the nerve - it's a UMN lesion. So you get 9 10 11 12 UMN palsy - Spastic paralysis.
This would be Pseudo-bulbar as same CN involved but lesion is above the Medulla

So Pseudobulbar you'd have a hyper active gag reflex while it'll be absent in Bulbar.(Mediated by 9th cranial nerve).

You'd have a Hot potato like speech in Pseudobulbar as your vocal muscles of larynx and tongue are spastic. - (10th and Cranial 11th. )

While you'd see a nasal twang in Bulbar (also called Donald duck speech)
As your soft palate doesn't abut against the nasal cavity (due to LMN flaccid paralysis). Also causing nasal Regurgitation of food in Bulbar.

So they both essentially present with 9 10 features and some of the 11 12. Hence one is Pseudo and the other is true Bulbar.

Psuedobulbar would also have emotional problems. Called Pseudobulbar affect (as the higher fibres are involved - lesions are generally multiple infarcts in the cortex).

A few important causes : 

Psuedobulbar palsy :

- Vascular = B/L Frontal lobe lesion , B/L Pontine stroke , Vascular dementia = Multi infarct dementia.

- Central Pontine Myelinolysis

- Degenerative = Multiple sclerosis  , Motor neuron disease

- Cerebral Palsy

_________________________________
Bulbar palsy :

- Guillian Barre Syndrome

- Polio

- Motor neuron Disease

- B/L Medullary infarction

Hoping this helped !
Happy studying guys !
And stay awesome !!

~ A.P.Burkholderia.

Myopathies series - Part 1

Hello :)

Before starting with the series, I will post on the basics you need to know for myopathies.

Q. What do you mean by muscular dystrophy and myopathy?

A. I found that following definition from Harrison is simple.

Skeletal muscle disease myopathies, are disorder with structural changes or functional impairment of muscle.

Muscular dystrophy refers to a group of hereditary progressive diseases with unique phenotypic and genetic features.

Do you know glycogen storage diseases?

Yes! But why do you need to mention it here? Because, skeletal muscles are the store house of glycogen. It gets converted into glucose-6-phosphate (Note:- Never in glucose unlike liver. Why? Otherwise glucose will move out from the myocyte to blood. And myocytes will fail to utilize their own stored glycogen. That is why muscle lack an enzyme called glucose-6-phosphatase.)

There are some glycogen storage disease which will lead to myopathies.

For now remember that myopathies have different way of presentation. 

Muscle weakness is one of the clinical feature.

The muscle weakness can either be 1. Intermittent or 2. Persistent.

If there is energy deficiency in muscle, it will become weak.

Today, we are focusing mainly on skeletal muscle energy metabolism.

Glycogen storage disease are described in the Roman numerals. Not all glycogen storage disease lead to myopathies. Some glycogen storage disease lead to myopathies is mentioned in the diagram.

 More is coming up.:) 

-Upasana Y.  

Pathophysiology of laboratory findings in tumor lysis syndrome

Which of the following electrolysi abnormalities will you see in tumor lysis syndrome?
Answer either high, normal or low for each of these - calcium, phosphate, potassium, uric acid.

Answers:
Labs in tumor lysis syndrome -
Hypocalcemia 
Hyperuricemia
Hyperphosphatemia
Hyperkalemia

Why?

When cancer cells lyse, they release potassium, phosphorus, and nucleic acids, which are metabolized into hypoxanthine, then xanthine, and finally uric acid. 

This leads to:

Hyperkalemia can cause serious — and occasionally fatal — dysrhythmias.

Hyperphosphatemia can cause secondary hypocalcemia, leading to neuromuscular irritability (tetany), dysrhythmia, and seizure, and can also precipitate as calcium phosphate crystals in various organs (e.g., the kidneys, where these crystals can cause acute kidney injury).

Uric acid can induce acute kidney injury not only by intrarenal crystallization but also by crystal-independent mechanisms, such as renal vaso-constriction, impaired autoregulation, decreased renal blood flow, oxidation, and inflammation.

Crystal-induced tissue injury occurs in the tumor lysis syndrome when calcium phosphate, uric acid, and xanthine precipitate in renal tubules and cause inflammation and obstruction.

That's all!

-IkaN

Causes of microcytic erythrocytosis

A high RBC count combined with a low mean volume is seen in:

1. Thalassemia minor, either alpha or beta
2. Polycythemia vera with iron deficiency
3. Secondary polycythemia (hypoxia) with incidental iron deficiency.

Differentiating thalassemia minor from polycythemia vera:

The RBC size distribution curves reliably distinguish between thalassemia minor and polycythemia with iron deficiency.

RDW is elevated in iron deficiency. It is normal in thalassemia minor.

That's all!

-IkaN

Type 2 RTA pathophysiology, notes and mnemonic

Hello! This post is on type 2 renal tubular acidosis.

What causes Type 2 RTA?
Defect in proximal bicarbonate reabsorption - resulting in a hypokalemic hyperchloremic metabolic acidosis.

The defect in proximal reabsorption of filtered HCO3-  in effect leads to decreased proximal NaCl reabsorption and a tendency for salt wasting. This causes hyperaldosteronism -  leading to increased K secretion by the distal nephrons.

Staphylococcal Scalded Skin Syndrome vs Bullous Impetigo

How do you differentiate Staphylococcal Scalded Skin Syndrome (SSSS) from Bullous Impetigo (BI)?

The exfoliative toxins are restricted to the area of infection in BI. In SSSS, infection is diffuse.

In BI, bacteria can be cultured from the blister contents. Cultures from blisters are negative in SSSS.

Blood cultures are usually negative in SSSS (positive in BI).

In SSSS, Nikolsky sign is positive. It is negative in BI.

In BI, patients are usually not ill appearing.

That's all!
-IkaN

Pills of knowledge in Ophthalm- squint and frontal eye field

Mentally challenged people may have a squint as the frontal eye field in the brain cortex is involved in ocular movements as well. It also may explain why somebody's eyes go crazy when they're starting into nothingness.

That's all!

-Sushrut Dongargaonkar

Settings for mechanical ventilation

These are my quick and dirty notes to help ventilator settings related questions on the USMLE.

Treponemal and nontreponemal tests for syphilis (notes + mnemonic)

Nontreponemal tests include:

Rapid plasma reagin (RPR)
Venereal Disease Research Laboratory (VDRL)
Toluidine Red Unheated Serum Test (TRUST) 

Mnemonic:
Do not trust VDRL rapidly.

Features of non treponemal tests:

They are based upon the reactivity of serum from infected patients to a cardiolipin-cholesterol-lecithin antigen. 

Used for initial syphilis screening due to their relatively low cost, ease of performance, and ability to be quantified for the purpose of following response to therapy.

Specific treponemal tests include:

Fluorescent treponemal antibody absorption (FTA-ABS)
Microhemagglutination test for antibodies to T. pallidum (MHA-TP)
T. pallidum particle agglutination assay (TPPA)
T. pallidum enzyme immunoassay (TP-EIA)
Chemiluminescence immunoassay (CIA)

Features of treponemal tests:

Treponemal tests have been more complex and expensive to perform than nontreponemal tests. Thus, they have traditionally been used as confirmatory tests for syphilis when the nontreponemal tests are reactive.

Treponemal tests are qualitative only and are reported as "reactive" or "nonreactive" 

Once a patient has a positive treponemal test, this test usually remains positive for life. Thus, these tests are generally not useful for confirming a diagnosis of syphilis in a patient with prior treated disease.

That's all!
-IkaN

Postural variations in pulmonary edema and embolism

Hey Awesomites

Patients with pulmonary edema prefer to be in an upright position, while those with pulmonary embolism prefer flat position.


This is because in cases of edema, there is excess fluid accumulation in lungs, which limits respiratory movements. In upright position, the fluid will settle down and thus it lowers the pressure in pulmonary vessels which makes it easier to breathe.

On the other hand, in case of pulmonary embolism, the patient  is placed in left lateral decubitus (durant maneouver) and Trendelenburg position immediately. The air embolus moves through the right side of heart to enter into the lungs. But in Durant's maneouvre and Trendelenburg position, the embolus gets trapped in the apex of the heart and so does not get transported through pulm arteries to enter the lungs.
Check this link for more detail on venous emboli management


Thats all
- Jaskunwar Singh

New drug launched for Sickle Cell Disease

Heyy guys, I have taken this post from Medscape. Nonetheless, awareness about this new drug should be spread.

The US Food and Drug Administration (FDA) has approved L-glutamine oral powder (Endari, Emmaus Medical Inc) to reduce severe complications of sickle cell disease in patients aged 5 years and older with the disorder. This is the first approval for the rare disorder in almost 20 years.

"Endari is the first treatment approved for patients with sickle cell disease in almost 20 years," Richard Pazdur, MD, acting director of the Office of Hematology and Oncology Products in the FDA's Center for Drug Evaluation and Research and director of the FDA's Oncology Center of Excellence, said in an FDA news release. "Until now, only one other drug was approved for patients living with this serious, debilitating condition."

The decision follows consideration of data from a randomized trial of patients aged 5 to 58 years who had suffered two or more sickle cell pain crises within the 12 months before enrollment in the trial. The researchers randomly assigned patients to receive L-glutamine or placebo. Treatment was evaluated during a 48-week period.

Those who received L-glutamine experienced fewer hospital visits for pain crises that resulted in treatment with parenteral narcotics or ketorolac, on average, compared with those who received placebo (median three vs median four), fewer sickle cell pain hospitalizations (median two vs median three), and fewer hospitalized days (median 6.5 days vs median 11 days).

Those who were given L-glutamine also experienced fewer episodes of acute chest syndrome — a life-threatening sickle cell disease complication — compared with those who were given placebo (8.6% vs 23.1%).

Frequent adverse events include constipation, nausea, headache, abdominal pain, cough, extremity pain, back pain, and chest pain.

L-glutamine received orphan drug designation for sickle cell disease. The FDA's Office of Orphan Products Development (OOPD) is intended to incentivize the development of drugs for rare diseases. Development of this drug was supported in part by the OOPD Grants Program, which provides grants to conduct clinical studies on safety and effectiveness of treatments for rare diseases or conditions.

Approximately 100,000 people in the United States have sickle cell disease, according to the National Institutes of Health. The disease primarily affects African Americans, Latinos, and other minority groups. The average life expectancy for those with sickle cell disease in the United States is 40 to 60 years.

-VM

Parkinson's disease associated with melanoma: Research update

Hey Awesomites

Patients with movement disorder such as the Parkinson's are at four-fold higher risk for malignant melanoma, and vice versa. This is likely due to mutual genetic, environmental and pathogenic ( immune system ) abnormalities and factors that they both share, as suggested by a research study at Mayo clinic.
( Source )

- Jaskunwar Singh

Causes of dilated cardiomyopathy mnemonic

Hi awesomites!

Here's a short note on causes Dilated cardiomyopathy.

It's mostly idiopathic.

Other causes are:

1. G enetic Mutation
2. Myocarditis

3.  Alcohol  abuse
4.  Drugs
5.  Pregnancy
6.  Hemochromatosis

Mnemonic.  GMM ADPH

That's all :)
 
H@Mid

Why do newborns have a higher heart rate?

Hey guys!

Have y'll ever wondered why do babies have heart rates as high as 160s?

Answer:
Babies have a high proportion of Body Surface Area to heart than that in adults. Therefore, in order to maintain adequate blood flow, baby's "li'l heart" has to pump more often to cover the "large Body Surface Area"!

I hope y'll find this interesting!

Till then, stay awesome!

-Rippie

Nasal Encephalocele vs Nasal Glioma

Both nasal encephalocele and nasal gliomas are congenital conditions in which there is herniation of glial tissues and meninges into the nasal cavity through the foramen cecum.

Both the masses are seen in the nasal cavity as bluish masses with nasal obstruction.

Nasal gliomas have no communication to the brain as the communication gets detached after the fusion of cranial bones in late IUL. Gliomas are firm and non compressible mass.

Encephalocele also presents as nasal mass with obstruction. The swelling increases in size in response to coughing. Most common site is occipital and then frontal.

Bilateral compression of the internal jugular vein also leads to the increase in the size of mass called as Frustenberg Test.
Frustenberg test is positive in encephalocele and negative in gliomas.

Investigation of choice for both is MRI.

Hope this helps!
Ashita Kohli

External Cephalic Version : An overview

Here's a short review on basics of External Cephalic Version.

So this Procedure is basically manipulating the baby externally to come in a favorable cephalic presentation.

Its indications need are limited and mainly include -
Breech Presentation and Transverse Lie.

The most important thing to remember is when not to do an ECV.

You can remember these contraindications as :

ABCDEF

A - Ante partum hemorrhage ( Previa and Abruptio.) It can result in detachment and more Accidental Hemorrhage (Abruption).

B - Bad Obstetric History

C -
Contracted Pelvis - ECV can cause fetal Hypoxia if the pelvis is small already

Congenital uterine Abnormalities - like bicornuate etc as can cause uterine rupture.

D - Dual Pregnancy (Twins/ Multifetal pregnancy).

E - Eclampsia PIH.

F - Fluid - Oligohydramnios

2 other C/I are important to remember -

Previous Cesarean section ( Uterine rupture chances are high).

Rh Incompatibility.

The best time for doing an ECV is around 36-38 weeks. It's easiest to perform the maneuver before 36 weeks but the fetus undergoes a lot of spontaneous movements before 36 weeks and may come back to being Breech.

Beyond 40 weeks best to avoid it as liquor reduces in amount and can cause cord compression amongst other things.

Another pre requisite is having the uterus relaxed. So it may be done in OT set up where anesthesia like Halothane can be used as a uterine relaxant. (Not so sure about the last part as some PG resident in college told us this. :P)

Hope this helps.
Happy Studying !
And as always ,
Stay Awesome !

~ A.P.Burkholderia.

Pancreatic cysts

The take home message for differentiating pancreatic cysts are-

1. When you see no epithelial lining to the cyst on microscopy, think of a pseudocyst
2. When you see a multilocular cyst with a central scar, think of a serous cystadenoma; if it is absent, think of a mucinious cystadenoma. Both are " NOT" connected to the main pancreatic ductal system
3. When you see a sizable (more than 1cm) growth within the pancreatic duct, think of IPMN!

That's it!

Mnemonic- Causes of saddle nose

Saddle nose is a nasal deformity due depressed nasal dorsum which may be bony, cartilaginous or may involve both.

Causes- HOT SALT

H- Hematoma
O- Operative (during SMR)
T- Trauma
S- Syphilis
A- Abscess
L- Leprosy
T- Tuberculosis

Hope this helps!
Ashita Kohli

Mikulciz Disease- Rhinoscleroma

Mikulciz disease aka Rhinoscleroma is a chronic granulomatous disease commencing in the nose and extending into the nasopharynx, oropharynx, larynx, trachea and bronchi

This disease may occur in either or the sexes at any age.

Causative organism- Klebsiella rhinoscleromatis (gram negative Frisch bacillius)

Three stages-

1. Atrophic Stage-
This stage typically resembles atrophic rhinitis and presents with nasal discharge which is purulent and foul smelling with nasal crusting.

2. Granulomatous Stage-
This is a proliferative stage. Characterised by granulomatous reaction and presence of mikulciz cells.
Presents as painless nodules in the nasal mucosa.
The subdermal infiltration into the lower part of external nose and upper lip gives a Woody feel to the nose.
There may occur broadening of the nose with thickened skin- Hebra nose

3. Cicatricial Stage-
There occurs fibrotic adhesions and fibrosis of nose, nasopharynx and oropharynx.
The fibrotic deformity of nose is known as- Taper nose.

Most common symptoms-
Nasal discharge and crusting> nasal deformity> epistaxis

Diagnosis-
Diagnosis can be done histopathologically which shows mikulciz cells and Russell bodies in the submucosa which is characteristic of rhinoscleroma.
Mikulciz cells are foam cells with central nucleus and vacuolated cytoplasm containing bacteria.
Russell bodies are eosinophilic inclusion bodies seen in the cytoplasm.

Treatment-
Streptomycin (2g/day) + teracycline (2g/day) for 4-6 weeks

Hope this helps!
Ashita Kohli

Polycythemia in newborn notes

Polycythemia in newborns

Definition: Venous hematocrit of 65%

Clinical manifestations:
Ruddy, plethoric skin.

CNS - Lethargy, hypotonia, tremulousness, irritability.

Seizures.

Hypoglycemia, hypocalcemia, hyperbilirubinemia.

GI - Vomiting, distension, NEC.

Kidney - Renal vein thrombosis, acute renal failure.

Cardiopulmonary - Respiratory distress syndrome, congestive heart failure.

Treatment: Partial exchange transfusion.

That's all!
Remember the association with infants of diabetic mothers.
-IkaN

REM, NREM and dream content recall mnemonic

My friend had difficulty remembering whether dreams can be recalled from REM sleep or NREM sleep.

I have a mnemonic!

REM REMembers nightmares.

Similarly, NREM does Not REMember night terrors.

That's all!
The North remembers.
-IkaN

Ultrasonography in Acute Appendicitis

Hey Awesomites

Ultrasonography ( graded compression technique ) is the investigation of choice in cases of acute appendicitis.

Antiarrhythmic drugs: Classification, Mechanism of Action and ECG changes

Hello guys, this is a much important topic especially in Emergency Medicine. And before going through this post, if you may, brush up your concepts of cardiac action potential.

A quick recap: Imagine a non-pacemaker AP with a flat phase 4, phase 0 upstroke, then a phase 1 downward notch, then phase 2 plateau phase, phase 3 downstroke slow at first, rapid later. Now the channels.
Phase 0- Na+ channels in the open state, it is inactivated in all other phases.
Phase 1- Transient-outward K+ channels
Phase 2- L type Ca2+ channels and Slow K+ channels (IKs)
Phase 3- Delayed rectifier K+ channels; Slow K+ channels(IKs) to Rapid K+ channels(IKr) and finally ultrarapid K+ channels(IKur).
Phase 4- Inward rectifier K+ channels(IKi)


First, Classification:

We have the Vaughan-Williams classification, the Sicilian gambit which is the most accepted albeit with some significant limitations which will be discussed later.

Class I: 
These are the Na+ channel blockers and "membrane stabilizers". So, they reduce slope of phase 0 and hence the peak of action potential. And they all prolong effective refractory period(ERP).  Because of subtle differences in its members, they are further classified as three subclasses.
             
IA:
It has moderate efficacy, i.e., it moderately reduces the slope of phase 0. And now look at the letter A, it is pointing upwards. That is coz it increases APD (Action Potential Duration) and ERP(Effective refractory period) both since it blocks IKr channels which are a part of delayed rectifier K+ channels involved in repolarization phase 3, so they prolong both QRS(ventricular depolarization) and QT intervals(Due to increased APD).

Note: This class of drugs have a cumulative effect. They block Na+ channels in the open state during phase 0 and then dissociates from them slowly and incompletely during the diastolic period after QRS complex so that in next beat, some Na+ channels are already blocked from the previous beat. So the QRS prolongation will rise with each beat. And this effect will be exaggerated at higher rates since diastolic period will shorten and more no of Na+ channels will be stuck with drugs.

Hence, in a way, it attacks more strongly if the rate is uncontrollably higher.

Eg. Quinidine, Procainamide, Disopyramide


IB:
It has low efficacy, it weakly reduces the slope of phase 0. Unlike the above class, it decreases APD. On the ECG, it slightly shortens QT interval and have little effect on QRS complex although both are considered therapeutically irrelevant.
Now why does it shorten APD? In the quick AP recap above I lied a bit, in phase 2 plateau phase the depolarizing Ca2+ channels are helped by residual(still open) depolarizing Na+ channels which are blocked by these drugs, so the repolarizing K+ channels dominate earlier and shorten phase 2.

IA vs IB:

IA is like a friend who attaches to you quickly and then doesn't like to leave you. Wheareas, IB is like a friend who takes his good time to attach but then leaves you quickly.
So based on this, unlike IA, IB blocks both open and inactivated Na+ channels, but they do it so slowly that they miss most of the open Na+ channels in phase 0 (the reason behind them producing little changes in QRS complex) and their real effect starts after phase 0 when they block the inactivated Na+ channels and prolong ERP. They detach relatively quickly so they show less cumulative blocking effect, but at higher rates when the diastolic repolarization phase is so short that even these fast-detaching fellas fail to detach and remain stuck on producing cumulative blocking effect beat after beat.

Another question, why are IB drugs not effective in tackling down Atrial arrhythmias?

2 reasons:
1.Unlike ventricular myocyte AP, atrial myocyte AP has a very short plateau phase and APD and as stated above phase 2 is where IB drugs exert their major effect.
2. IB drugs have negligible effect on normal cardiac cells, they mainly show their effect on ischaemic cells. And atrial myocytes by virtue of their less thickness, less demand and adequate blood supply rarely become ischaemic.

Eg., Lidocaine, Phenytoin, Mexiletine


IC: 
It is very strong, it significantly reduces the slope of phase 0. But coz its C, it doesn't Care about APD and ERP, so no effect. On the ECG, it prolongs QRS complex significantly and shows cumulative blocking effect in a very similar way to IA drugs.

Eg., Flecainide, Propafenone, Moricizine


Class II: These are Beta-blockers. They prolong phase 4 of AP, which reduces the automaticity and hence controls rate as well as conduction. On ECG, they prolong PR interval.

Class III: These are K+ channel blockers. They prolong phase 3 of AP, so it delays repolarization and prolongs APD and ERP.
Eg., Amiodarone, Dronedarone, Dofetilide, Sotalol, Ibutilide

Class IV: The Ca2+ channel blockers or more specifically the L-type Ca2+ channel blockers. In SA node and AV node, it prolongs both phase 0 and 4, so controls the rate. In myocardial cells, it prolongs phase 2 of AP, so it impedes conduction.  On ECG, they prolong PR interval.
Eg., Verapamil, Diltiazem

Class V: Variable Mechanism; including Magnesium Sulfate, Adenosine, Digoxin, Atropine.

The major drawback of this classification is that some drugs like Amiodarone have overlapping features of other classes.

Mnemonic by iKan :) -

Remember, VeraPamil has P in the name so PR interval is Prolonged.

(Cain) from Flecainide sounds like Quain, Q is for QRS interval prolongation.

That's all!
My next post will be on what, why and how of indications of anti-arrhythmics. Stay tuned! :)

-VM

Fact of the day: Sleep Apnea linked with Acute Gout attacks

Hey Awesomites

Those who suffer from sleep apnea are usually overweight, and so may be those with acute gout exacerbations.

In addition to lower body temperature and nighttime dehydration, hypoxic patients of sleep apnea are at upto 50% higher risk of having acute attacks of gout at night. This is due to excess tissue damage and cell breakdown, both of which increase uric acid levels that may accumulate in joints to cause exacerbations !!

- Jaskunwar Singh

Eagle Syndrome

Eagles Syndrome also known as Styalgia is due to elongated process or calcification of the styohyoid ligament.

Symptoms-
1. Pain in tonsillar fossa and upper neck which radiates to upper neck which gets aggrevated during swallowing.
2. Dysphagia

Diagnosis-
1. Transoral palpitation of the styloid process in tonsillar fossa.
2. X Ray of lateral view of skull or AP view with open mouth.

Treatment-
Many people may remain asymptomatic and do not need treatment.

Symptomatic patients may need excisition of styloid process by transoral or cervical approach.

Hope this helps!
Ashita Kohli

Fact of the Day : Pantaloon Hernia

So this is just a very interesting fun fact.

When a person has a Direct Inguinal Hernia along with an Indirect Inguinal hernia , the person is said to have a Dual / Pantaloon/ Romberg / Saddle bag hernia.

Tried a lot to find out why the name is 'Pantaloon'. Pantaloon = Saggy pants or a Foolish old man. So take your pick !

That's all!
Happy studying!
Stay Awesome.
~ A.P.Burkholderia

Placenta Previa : Why it occurs.

Here's a short discussion post on Placenta Previa Etiology.

So Placenta Previa is a dangerous condition that presents with bleeding after 28 weeks up to the 1st stage of labour. (So it could so happen that the baby needs to tear it open and come out - as it may cover the Os. Hence Previa , where Previa means 'In front of'. Of course the reality being that the placenta gets compressed and results in fetal Hypoxia along with bleeding ).

The main pathology is that the Placental gets abberantly deposited / implanted in the lower uterine segment in stead of the upper.

This could be due to :
1. Decidual area being defective in the upper segment (Due to maternal age , Multiparity, Curretage or Cesearan section in the past).
2. Large placenta - due to which some part may encroach over the lower segment. (Multiple pregnancy, Smoking etc).

Here's a way to remember the risk / etiological factors for this condition.

Risk Factors for Placenta Previa -

Mnemonic : M4 C3

M - Maternal Age - Decidua becomes weaker with age so the placenta ends up encroaching over the lower segment.
M - Multiparity (Similar reason. Especially in a grand multi para)
M - Multifetal pregnancy (Twins etc. There's less space in the fundal area hence gets lodged in the lower segment)
M - Maternal Serum AFP (Indicates high/persistent Chorionic activity - essentially invades into more and more of the Endometrium.)

C - Curretage - in the past if done , damages the uterine layer making the upper segment defective.
C - Caeserean sections in the past / other operations on the Endometrium/myometrium - Makes the uterus defective.
C - Cigarette smoking - causes Hypoxia to the baby leading to Placental Hypertrophy - larger placenta occupies larger area and may encroach downwards.

Hope this helped !
Stay Awesome and
Happy Studying !
~ A.P.Burkholderia

Step 2 CK: Algorithm for management of Atrial Fibrillation and Atrial Flutter

A patient presents with palpitations and irregular pulse-- What would you do next? The clock is ticking away.. and you might need to answer your multiple choice question!

This is a classic presentation of Atrial fibrillation - Palpitations and irregular pulse.
Next step in diagnosis: Do an EKG first--> if it does not show A.fib --> the next step depends on the patient's location --> If inpatient-> order Telemetry monitoring
If outpatient--> order Holter monitoring.

Now, once the diagnosis has been made, what they want you to know is the next best step in management.
The answer to this will depend on the HEMODYNAMIC status of the patient.
Patient can be either STABLE or UNSTABLE.
Now, what defines being UNSTABLE is any of the following:
* systolic blood pressure <90
* C.H.F.
* confusion
* chest pain

Once you know the status, follow the chart below.

Happy Doctors' Day!

-- Rajavee Panchal & Vikramjeet Kakade

Fact of the day: The link between Alzheimer's and Cancer

Hey Awesomites

People with a history of cancer are less likely  to suffer from Alzheimer's in the advanced age, while those with Alzheimer's disease are less likely to get cancer.
( Source )

- Jaskunwar Singh

Hemineglect mnemonic + clock drawing

Hemineglect - where is the lesion ? Which side is neglected?

Mnemonic: Hemineg-left. Left side is neglected. 

Lesion located in the right parietal lobe (non dominant lobe).

Interesting fact: Right-brain-damaged (RBD) individuals with spatial neglect often depict an object with left-sided features absent on drawing.

Usually, the patient is asked to draw a clock.

The drawing of patients with hemineglect contain empty space on the left, as if the clock were covered by an opaque semicircle.

However, this metaphoric occlusion frequently leaves the rim of the clock unaffected. The circular outline is rarely compromised in neglect patients’ clock drawings and is almost always the first feature produced in the task.

Interesting, isn't it?

-IkaN

Torn meniscus and inability to extend the knee

Doubt: Why does torn meniscus present with inability to extend the knee? I don't understand the anatomy correlation.

If there is complete tear, the meniscus (a piece of it) gets dislodged. It gets stuck in the knee joint.

This causes:
Inability to extend the knee.
Pain on extension of the knee.

Why is it called "bucket handle"?

A bucket handle meniscus tear represents a complete tear of the mensicus support or the ligament that holds the meniscus in place. This allows the meniscus to flop over like the handle on a bucket.  When the meniscus flips over it becomes stuck in the middle of the knee joint, you lose the ability to fully straighten the knee then you have a “locked knee”.

Explained by Dr. Mustufa Poonawala

The meaning of valgus (with doubt + mnemonic)

Meaning of valgus: A deformity involving oblique displacement of part of a limb away from the midline.

Doubt: Why is genu valgum knock knees? The knees (genu) are displaced towards the midline!

Answer: It's not the knees we consider during the deformity... It's the relationship of distal part with the proximal part at a joint.

Mnemonic: L in vaLgum is for Lateral displacement.

(Conversely, varuM is medial displacement.)

That's all!
Hate the inaccurate naming.
-IkaN

Study group discussion: Queckenstedt Sign

Suppose there is an obstruction to cerebral venous drainage in the left side, and u r doing an LP with manometry. If u occlude the left internal jugular vein, there will be no change in pressure but if u do it on the right side, there will be increase in csf pressure.

Response of Vagus to Systemic Injury.

Hello!

Let's learn/revise.

The vagus nerve exerts several homeostatic influences, including enhancing gut motility, reducing heart rate, and regulating inflammation.

Central to this pathway is the understanding of neurally controlled anti-inflammatory pathways of the vagus nerve.

This neurally mediated anti-inflammatory pathway allows for a rapid response to inflammatory stimuli and also for the potential regulation of early proinflammatory mediator release, specifically tumor necrosis factor (TNF).

Vagus nerve activity in the presence of systemic inflammation may inhibit cytokine activity and reduce injury from disease processes such as pancreatitis, ischemia and reperfusion, and hemorrhagic shock.
This activity is primarily mediated through nicotinic acetylcholine receptors on immune mediator cells such as tissue macrophages.

Furthermore, enhanced inflammatory profiles are observed after vagotomy, during stress conditions. 

Let's learn Together!
-Medha.

Greenish discoloration of Urine

The common causes of greenish discolouration of urine are :

(1) Phenol containing compounds: Promethazine, Propofol, Thymol,
(2) Dyes: Indigo-blue, Indigo carmine, Carbolic acid, Flavin derivatives,
(3 Biliverdin (in cases of long standing obstructive jaundice),
(4) Amitryptyline (anti-depressant),
(5) Pseudomonas infection,
(6) Cemetidine,
(7) Indomethacin,
(8) Methylene blue (bluish )

CerebelloPontine Angle Syndrome

13th and 14th Cranial Nerves.

13th and 14th cranial nerves

Congenital Corneal Opacities

Congenital Corneal Opacities

Rhinosporidium seeberi

Rhinosporidium seeberi

Hilton's law

Hilton's law.

The nerve which supplies a muscle of a joint, will also supply the joint and the overlying skin.
Conversely, any nerve that is innervating a joint will also supply the muscles of the joint and the overlying skin.

In humans, we find only 2 exceptions to this general rule:

1) Buccal branch of Mandibular nerve as we all know, pierces the Buccinator muscle. But it doesn't supply the muscle. The innervation of Buccinator is by the Buccal branch of Facial nerve.
2) Sciatic nerve in the Gluteal region....is very closely related to the Pyriformis muscle.... And may occasionally send a fibre that pierces the muscle. But it doesn't supply it. Pyriformis is supplied directly by the sacral plexus(the nerve to pyriformis).

Mithil Jagannath.
Medicowesome 2017.

Vasculitis Classification : A way out

Here's my way out of the necrotising vasculitis. Pan intended ;;).

So depending on the size of the vessel involved you can classify it as -

1. Large Vessel Vasculitis
2. Medium Vessel Vasculitis
3. Small Vessel Vasculitis

For the first two Remember :

TT PK

So Large vessel = TT
Takayasu Arteritis
Temporal Arteritis (Giant cell Arteritis)

And Medium Vessel = PK
Polyarteritis Nodosa
Kawasaki disease

Now Small Vessel Vasculitis can be classified further. It can be positive for a particular antibody called ANCA or it can be negative. This antibody is purely an association and not a causative one.

ANCA Negative : HCC

H - Henoch Schonlein Purpura
C - Cryoglobulinemia related
C - Cutaneous Leukocyto-angiitis

(Think of crying babies.
Cry = Cryoglobulinemia related Vasculitis
And another baby related Vasculitis​ is HSP).

Now ANCA positive Vasculitis can be either c-ANCA or p-ANCA depending on what part it stains.

Remember - WC
(Like Western commode)
Wegner's is c-ANCA.

Remember - PCM
p-ANCA in Churg Strauss and Microscopic Poly-angiitis.

Please note - The names of Wegner's and Churg Strauss have been changed to Granulomatosis with Polyangiitis , and Eosniophilic GPA respectively. This is said  to be because the scientist Wegener had been discovered to be possibly related to some Nazi war time activities and this opportunity was made the most of to also take a step towards  a more pathology-specific name-calling by altering the honorific name given to the disease.

That's all!
Happy studying.
And Stay Awesome !

~ A.P.Burkholderia.

Pills of knowledge in Ophthalm- Retinal haemorrhages

1. Flame shaped haemorrhages are seen when they occur in the superficial layers of the retina because the blood can spread as tight junctions are not present there.

2.Dots and blots show up into the deeper layers because the space to spread for the blood is relatively lesser.

That's all!

Sushrut Dongargaonkar

Step 2 CK: The algorithm to Management of Ventricular Tachycardia

Did you ever find it time consuming and confusing to answer the multiple choice questions about the "what will you do next" questions for different heart rhythm disorders?
Well, we did too. So, we are going to post some algorithms in subsequent posts, which will make it easier and save you some time in the preparation. They will guide your thoughts during those timed multiple choice questions.

Ventricular Tachycardia: It's a type of ventricular arrhythmia. The EKG is a must have diagnostic test. Look for wide-QRS-complexes. If the EKG is inconclusive--> telemetry monitoring should be done. If the questions asks, what is the most accurate test to diagnose this patient with V.Tach--> its Electrophysiologic studies.

Now, read very carefully the last line of the question as to what the question is demanding; it could be the next step in management or the test for a definite diagnosis.
The next (VERY IMPORTANT) step is to look at the vital signs and understand if the patient is hemodynamically unstable
(LOOK FOR :
               *IS THE B.P. LOW?
               *IS THERE CHEST PAIN?
               *CHECK THE Respiratory Rate- does the patient complain of shortness of breath/dyspnea,
               *LOOK FOR HIS MENTAL STATUS- is the patient confused/has altered mental status?                    *LOOK FOR SIGNS/SYMPTOMS OF CHF.
If any of these are present--categorize the patient as Hemodynamically Unstable.

And then, follow the chart below for management questions.

- Vikramjeet Kakade & Rajavee Panchal

We all wanna help others; but do we help ourselves?

{This might be quite a descriptive post. So read this if you don't have exams upcoming recently}

As a Medical student, or a doctor we all are opting for a profession of care for people. But often we forget that the people who need care includes ourselves too.
How should we take care of ourselves.
1. One should take care of one's self.
2. One should take care of one's colleagues.

Do you eat well? Do you sleep enough? Are you spending time with your family? All these fall into such a level about taking care of your ownself.
As medical students we have long weeks and short sleeps. Let's admit, still we don't have enough time.

1. First of all, don't forget to,

EAT WELL. Food is essential for your sustenance. Eat nutritious food. Not just starch and sugary food. Opt for some fruits, yoghurt and more veges.
Our professor said it is better to get yourself a multivitamin complex if you feel like you are running out of enough nutritious food.

SLEEP WELL. Sleep is one of the most important aspects of your daily life. You probably cant sleep 6hrs straight. But get some decent sleep at least for 4hrs. And if you are taking a powernap, try taking it in multiplies of 90mins. I saw it recently in an article 90mins(180/270 etc) of nap improves your ability to wake up fresh as it is appox 1 sleep cycle.

EXERCISE WELL. You dont have hop into University gym and run on those treadmills for your dear life, but obvio try taking a stroll with your friends in the ground, or get a brisk walk to market instead of getting a taxi or riding there.

RELAX WELL. We surely don't have time to sit on a sedan chair and reflect on life or get a bikini/short picnic to the nearest beach when we have an Internal Medicine exam 3 days away. But surely you have time to go grab a coffee and enjoy it without looking at your jumbled up notes. (They aren't much readable anyways 😜jk...), Sit on a short wall and swing your legs like you remember all the drug regimes of the world. Look at the sky from the terrace and try to find a constellation or two that you learned in Grade school. Listen to a song that uplifts you or soothe you depending on your mood. Sketch something (personal secret : I sketch my crushes when I'm stressed 😜). Do something that makes you feel good. Meditation or yoga or something are good too. If spa, manicure pedicure, massage works for you, by all means go for it too.

CHECK-UPS. What is the last time you checked if you have enough Hgb count? Get your personal body checkups. You are only riding that Car, don't forget to check the oil and water levels too. Even a Benz or a BMW can wreck havoc if they don't have enough care. Get yourself done a teethscaling.

ENVIRONMENT. Look at your desk. Does it look like that you just performed an exocism there? 😂 Clean it up yo! Clean your desk. Your room. Keep some airfreshners, keep stuff that motivate you surrounding you. Not things that make you feel like "I'll rather live in the library!". 😜 Get enough Oxygen into your place and for all the love for Zeus, don't get into a room without enough ventilation.

MENTAL HEALTH. Almost every university provides free mental health counselling to its students. What was the last time you used it? Last time I had stress issues with my Neurology final exams, I went to meet a guidance counsellor. She totally listened to me and made me feel good. And another time when I felt like I'm losing my interest and the passion, I talked to my psychiatry professor.I think you should talk to someone qualified about it. And never think talking to a psychiatrist or a counsellor is a bad thing. In the long run it will help you heaps.

2. How to take care of your colleagues.

Ok we don't even have time for ourselves. I agree. But please don't leave those who are around you.

We all are in the same journey. Look out for them. Check if they ate their meals. If they forgot their attendance. Check if they are okay. If their relationships are going well. If they are performing fine in exam. Look out for people around you. Close friends are the first people are recognize depression and anxiety in a person before it attains to clinical levels. If you notice a difference talk to them. Or lead them to talk to someone qualified about it.

If someone is losing marks and failing exams offer to help them. If they ask for support never refuse.

Be a good person to others, this way you will be a good doctor too.

That's it for now folks. Enjoy and always take care of yourselves and others around you.

With love,

Jay

Mnemonico diagnostico: Opacities that may be confused with renal calculus

Hey Awesomites

Mnemonic for opacities on a plain abdominal radiograph that may be confused with renal calculus:
TOP GAME

Tubercular calcified lesions in the kidney
Ossified tip of 12th rib
Phleboliths (calcifications in the wall of pelvic veins)

Gall stones
Appendicular/ Adrenal gland concretions
Mesenteric lymph node calcifications
External (foreign) bodies in alimentary canal (ex., cyclopenthiazide)


Thats all
- Jaskunwar Singh

Answer is not always antibiotics!

Clinical vignette:
Young, non smoker, female comes with complaints of sore throath, dry cough, nasal congestion for 10 days. Now, she feels better however she coughs out yellowish expectoration.
There are scattered wheezes and crackles that clear with coughing.
You've ordered relevant labs and meanwhile the patient asks you if she would need antibiotics. What would your next step be?

Answer: Symptomatic management.
Reason: Since there is a history of preceding viral infection and her current situation indicated Acute Bronchitis, the expectant management would be fairly Symptomatic!
Infact, there are articles that state that giving antibiotics could worsen the patient condition! Also, judicious use of antibiotics can help prevent antibiotic resistance.

Let's fight antibiotic resistance!

Stay awesome!
-Rippie

FENO in asthma: routine clinical testing

Hey Awesomites

One of the additional tests for determining the present status of airways in asthmatics is the measurement of Fraction of Nitric Oxide in Expired air (FENO).

The levels of Nitric oxide are elevated in the presence of inflammation in the airways, that is eosinophilic in nature.

In children <12 years, normal FENO is usually less than 36 ppb. However, in case of allergic inflammation of airways, the levels rise to >50 ppb.

Note that FENO is not diagnostic, but a test for independent prediction of exacerbations in asthmatic patients and is now done routinely in clinical practice, as approved by US- FDA.

Thats all
- Jaskunwar Singh

My Elective experience

Hey guys,

I was off blogging for a while for obvious reasons and I apologise for that. But, hey! Let me share the reason behind it :D
I was off to the States for my Clinical Electives at Mayo Clinic and Cleveland Clinic, so I'm going to briefly write about Electives in this post.

Overview of US Clinical Experience:

A) HANDS-ON Clinical Experience:
- One to one patient contact, can elicit history, perform physical examinations, write notes, suggest plan of care, have full access to patient records
- Considered better as what can be better than hands-on!
- Can be done only before a Medical Student graduates. ( Therefore, you can't do electives if you're already a Doctor -_-)

1. Sub-Internship equivalent to a 4th year US Medical Student
2. Clinical electives are equivalent to a 3rd year US Medical Student
3. Clerkship (This typically is for US Medical students; not applicable to IMGs)
4. Externships

B) NOT HANDS-ON Clinical Experience:
- You only get to observe (hence, Limited role in patient care)
- Can be done while you're a Medical Student or even after you graduate
- Controversial if it can be considered as USCE?

C) RESEARCH ELECTIVE:
- Usually, longer the elective, the better it is! (Increases yield of getting a fruitful publication out of it.
- No outlined criteria, eligibility varies from place to place.

Now,
I typically like to classify Clinical Electives into: (Although, others may classify them based on different criteria, I believe, classifying this way is logical in terms of expenses majorly)
1. USMLE Step 1 required
2. USMLE Step 1 NOT required
[I shall soon write a separate blog on this, pre requisites for elective application and rough expenses soon, so stay tuned as always :D]

About my elective experience:

I had given my USMLE Step 1 while I was in Third year. So, when I got into Fourth year I applied to Universities that had USMLE Step 1 criteria.
As now a days, getting electives is becoming more and more competitive, along with my friends, I applied to IMG friendly elective places well in advance  (about 10 months prior for a few places). This also meant that we had to wait for a long time to get our acceptances as they don't send out acceptances until 3-1 month prior to your elective start date.

Fortunately, I got accepted at Mayo Clinic, Rochester for Infectious Diseases elective and at Cleveland Clinic, Ohio for Endocrinology elective! Yippie!! (Big thank you to Ikan for guiding me with the application process)

Both, Mayo Clinic and Cleveland Clinic are amazing places to work at! (And if you don't already know, Mayo Clinic has been ranked no.1 and Cleveland Clinic has been ranked no.2 on U.S. News and World Report's Honor Roll :D)

What to do while you're there?

- Be professional, dress professionally, follow code and conduct of your Hospital or Clinic.
- Take histories, perform physical examinations as required, write patient notes, suggest plan of action and so on...
- Volunteer for case presentations/ talks
- If you find an interesting case while you're rotating there, discuss with your residents/ fellows/ attendings if you can submit it to a journal or present it at any conference.
- If you're interested in research, talk to your attending and try to get involved in one.
- Most importantly, As an IMG, it is crucial for us to get A Strong Letter of Recommendation. If you've been working hard, I am sure, most attendings would agree to write you a Strong LoR! Hurray!

Also, once you are done with your elective, in the following week or so, it is good to write your attendings a courtesy/ Thank you email, so that they know you really learnt during your elective!

Stay awesome!
-Rippie

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 bancrofti, Brugia malayi, and Brugia timori) is the most common cause of secondary lymphedema.

Hope It helps.
Let's Learn Together!
-Medha.