Saturday, February 24, 2018
Tumor lysis syndrome and rhabdomyolysis: Why does calcium decrease?
Friday, February 23, 2018
HPV vaccines
HPV infection can cause:
1.Gardasil (6,11,16,18)
2.Cervarix (16,18)
3.Gardasil 9
No, it is for both boys and girls.
Then what is that 9-11 years or 11-12 years criteria?
Actually most of the vaccination programme for adolescent is in that age group. So to avoid that extra visit it has been scheduled so.
It is not required because such cases are either already exposed or already infected.
In <14 years -2 doses is needed to mount same immunity.
Wednesday, February 21, 2018
Thiamine and Beri-Beri: A Summary
- Vitamin B1 is Thiamine.
- Peripheral neuropathy in dry beri-beri is symmetric, sensorimotor, distal > proximal and non-inflammatory demyelinating type.
- Wernicke's syndrome is reversible early while Korsakoff psychosis is reversible in only 20% cases.
- Wernicke-Korsakoff syndrome has typical damage to dorsomedial nucleus of thalamus and mamillary bodies.
- Clinical manifestations of B1 deficiency is worsened by glucose load! As seen in pathophysiology, excess of glucose with relative or absolute deficiency of B1 - as TPP - causes diversion from the preferred PDH pathway (linked to TCA), to the LDH pathway causing life-threatening lactic acidosis. Hence, in a patient with alcohol intoxication/ chronic alcoholism a B1+glucose cocktail is given as they usually are deficient in B1.
- Diagnostic - Blood or RBC transketolase activity and increase after intramuscular B1 administration
- Supportive - Blood thiamine, pyruvate and lactate levels
Sunday, February 18, 2018
Cushing's Syndrome: A Quick Review
Etiologic classification:
- Pituitary Cushing's is Cushing's disease.
- ACTH dependence simply means if raised ACTH is the cause of raised cortisol.
- Feedback loop, more correctly negative feedback loop, implies if cortisol level influences ACTH level inversely. Ectopic Cushing's is caused my malignant cells that continuously proliferate and hence, continuously make ACTH, regardless of cortisol levels.
- Therapeutic administration of ACTH hormone for long periods can cause ACTH-dependent Cushing's. However, they are exceedingly rare (and hence, omitted from the whiteboard for simplicity).
(MCC= Most Common Cause ; B/L= Bilateral ; U/L=Unilateral)
Clinical Features:
CUSHINGOID
Ulcers (peptic)
Striae, Skin thinning & bruising
Hypertension, Hyperglycemia, Hirsutism
Immunosuppression, Infections
Necrosis (Avascular) of femoral head, Neuropsychiatric symptoms
Glucose intolerance, Growth retardation
Osteoporosis, Obesity
Impotence and menstrual abnormalities
Diabetes
Diagnosis:
High dose DXM or CRH don't bother ACTH or cortisol levels in Ectopic Cushing's as they're out of the feedback loop.
Other tests include:
- 24 hour urinalysis
- Midnight salivary cortisol
- 9 am cortisol
- Overnight low-dose DXM suppression test
- B/L inferior petrosal sinus sampling
- Electrolytes and routine CBC
- Iatrogenic: Withdraw steroids slowly.
- Pituitary: Trans-sphenoidal resection OR radical hypophysectomy, less commonly
- Adrenal: Surgical resection with post-op prednisolone OR medically treat with Metyrapone or Aminoglutethimide.
- Ectopic: Chemotherapy and Radiotherapy for small cell lung cancer OR surgical resection for carcinoids.
Schizophrenia First Rank Criteria : Mnemonic
Kurt Schneider laid down the First Rank Symptoms of Schizophrenia.
They're tedious to remember but we need to know them for MCQs and entrance tests!
So here goes :
Mnemonic :
ABDS VV (Very Vella)
A = Audible Thoughts (Echo de la Penses)
B = Broadcasting Thoughts + Insertion/Withdrawal of Thoughts
D = Delusional Perception
S = Somatic Passivity
V = Volition absent (Avolition)
V = Voices speaking / Arguing
That's all !
Few contributions to Schizophrenia :
The word was Coined by : Bleuler
Demence Praecoxe : Morel
Dementia Praecox : Kraeplin
1st rank symptoms : Schneider
Bleuler also gave the 4 A's of Schizophrenia !
They are Avolition, Autism , Ambivalence and flat affect.
Hope this was a good list for you !
Happy studying !
Stay awesome !
~ A.P. Burkholderia
The Oedipus Complex
The Oedipus Complex has been an ever popular Freudian concept.
Here's a summary of Psychosexual development as per Freud and the Oedipus Complex concept.
I insist you put up with this incestuous concept :p
So Freud was an extraordinary Psychoanalyst and gave the stages of 'Psycho Sexual Development' in his book 'Interpretation of Dreams'.
There Are 4 stages of Psychosexual development in Freud's opinion that all of us pass through to reach the mature stage eventually.
The 4 stages are :
1. Oral
2. Anal
3. Phallic
Latent period
4. Genital
Remember -
Mnemonic : On A PG break.
If one fails to break through any of these stages , it is said he'd develop specific psychiatric illnesses.
It's important for a child to go through these stages without 'fixation' over any of those.
For example Oral stage fixation Makes you SAD
Schizophrenia
Anxiety
Dependent Personality disorder.
Anal Stage fixation makes you an 'Anal' person.
So you're likely to develop Obsessive Compulsive disorder or Obsessive Compulsive Personality (Ankanastic Personality)
Phallic Stage Fixation is "complex."
So in previous stages , it's been obvious what the object of gratification has been (Mouth and Anus respectively).
This one's slightly more "complex".
So as per Freudian theory , Boys would be sexually fixated on their Mothers, viewing their Fathers as a threat ;
This is called the 'Oedipus Complex'.
And also have Castration anxiety.
The theory says similarly Girls would be sexually fixated on their Fathers , viewing their mothers as a threat ;
This is called the 'Elektra Complex'.
And have Penis Envy.
The Oedipus Complex :
So this stems from the Greek story where Oedipus marries his own mother unkowningly , after he kills his father.
King Laius was the king of Greek city Thebes. He and his wife Jocasta bore a child : Oedipus.
The problem is some Seer prophesized that this child would kill him. And so he sent away his child, who was found and raised in another city by another King. Years later he returned to Thebes and quarreled with an old man and ended up killing him.
After a while he was told that the King had been killed , and that he could take charge of the town if he defeats the Sphinx. He did so, and won the hand of the King's wife Jacosta as well.
Years later he found out the King was actually his Father , and his Wife was his mother.
Here's where the 'Oedipus Complex' gets its name from.
Electra Complex
Stems from another Greek story.
Electra was the daughter of Agamemnon, whose wife killed him.
Electra then avenged her father's death by killing her mother.
(Talk about Daddy's lil girl ;;) )
Another complex is 'Pharoah Complex' where siblings are fixated sexually on each other.
Fixation in Phallic phase leads to Paraphilias and Hysteria.
Hope this wasn't overly disturbing !
Happy studying !
Stay awesome.
~ A.P. Burkholderia
Saturday, February 17, 2018
Kallman syndrome mnemonic
Kallman Syndrome (also known as Olfactogenital dysplasia/syndrome or anosmic idiopathic hypogonadotropic hypogonadism)
Let's get down with the mnemonics!
'Kallman' kinda rhymes with 'Tallman', right? Well, "man" for it's more common in boys and Tall these individuals are of normal or even increased height (Tall).
The other features are:
K - kinda looks like an X so it's X-linked
K also sounds like C for Colorblindness
A - anosmia
L - lip (cleft lip and cleft palate)
N - nerve deafness
A - ataxia (cerebellar ataxia)
M - midline defects (cleft palate, cleft lip)
Other important points are:
- The defect is in the KAL gene which codes for the protein anosmin.
- It can be due to autosomal dominant or recessive inheritance.
That's all!
Stay awesome
This post is written by Nikhil as part of the MSGAI.
Friday, February 16, 2018
How to write ERAS CV for the USMLE match and FAQs about the application
Immunomodulators mnemonic
Let's work out an interesting way of remembering a few Immunomodulators and Chemotherapeutic agents today!
These mnemonics were submitted to us by Mikey.
1. SIRolimus
Is it nephrotoxic? Does it cause pancytopenia?
- Kidney SIRvives. It causes panSIRtopenia
2. MycophenolATE side effects:
- M: Marrow suppression
- ATE: for GI effects: Nausea, cramping and abdominal pain
3. What do you use Azathioprine for?
- *Auto*thioprine - *Auto*immune conditions, as well as Rheumatoid Arthritis, Crohn's disease and glomerulonephritis
4. What is the MOA of Basiliximab and what are it's side effects?
- It is an IL- 2R monoclonal antibody
5. What is the MOA of Trastuzumab and what is it used for? it's side effect?
- It is a therapeutic antiobody againts HER2/neu receptor
Tuesday, February 13, 2018
Advice for interview season: Being street smart
Akshay Vacchani wrote these tips and tricks for interview season. He told me, "I didn't know all of this, it's what experiences taught me."
I think it's helpful to read it after you've submitted your application.
After 15th September, download mymail application:
I found this app fastest one to download ERAS email and notify you with earliest possible time with distinct notification sound.
(Gmail wasn't refreshing new emails that quickly, I think least time duration was 15 minutes and I didn't like Gmail app.)
Be ready to respond quickly to the programs as in some date may fill out quickly, so fast notification and quick response to program, along with keeping google calendar open either in your tablet or phone will help you easily choose date and organize them based on their locations.
Once you get an interview....
Organize dates of program wisely.
Use Google calendar and use some special color for program's interview day. Use different color code for different works like flights or airbnb check in time, etc.
Use Google reminders to respond to any email or phone call important for these all procedures.
Use google map and save all program locations and your hotel or Airbnb rooms, give them stars or label them as you like. This will definitely help you to plan all stuffs and may help you to save money with better planning.
Before the interview:
Make a different folders for each program in your google drive, copy and paste all ERAS info, any program related info, place where you are leaving, flight info into different docs.
Why? So that you can have access to all from one place, especially, in case of emergency. (No network or device lost or something.)
Day before the interview...
Check weather info in advance.
Sometimes you may not have access to Internet because of bad connection. Make a shortcut of Google maps (travelling to hospital from your place).
If you are going to book a cab, you can also book Lyft or Uber in one day advanced for particular time in the morning, I would definitely suggest that.
Bus recommendation:
Use Greyhound instead of megabus because of wonderful facility of waiting station with restrooms even in mid size city. I had to wait in 0 F° outside for Megabus, and the bus was delayed, which may not go well for you sometime.
For Greyhound, I would suggest you to book a flexible ticket especially using discount coupons on festivals if you sure about your departing and arriving city. You can always change date, have priority boarding or full refund.
Flight recommendation: Southwest
For flight, I would definitely suggest to book Southwest, even if you don't have luggage.
Booking in advanced, you can get it for cheaper price, always use refund money for other flight, always modify or cancel.
And best thing, you can get change flight time with no extra money even at last minute.
You call them, tell your flight is delayed and there is any slight chance of change in estimated time of departure, (if there is more than 1 hour, then for sure), you can ask for early flight whatever time you want, and no any extra fees.
Monday, February 12, 2018
Hemiplegia Evaluation : Case-related Clinical Pearls
Here's a couple of special pointers for a CNS Case with the Viva Questions asked commonly !
General Examination (In addition to what you would routinely mention)
- GCS / MMSE depending on status of the patient
- Regular Temperature, Pulse , Respiratory Rate and Blood Pressure.
(Pulse could have irregularly irregular rhythm which indicates Atrial Fibrillation. Very strong Etiological clue)
(Blood pressure is super important : to be brought down rapidly if Hemorrhagic suspected and to be brought down below 185/110 of planning to Thrombolyse.
Do not reduce to very low levels too rapidly to prevent damage to the Ischemic penumbra)
- Carotid Bruit : indicates Carotid artery stenosis due to Atherosclerosis. Before palpating for the carotid pulse always auscultate to rule out a Thrombus as you may dislodge it when you press it.
- Signs of Hyperlipidemia :
Xanthoma , Xanthelesma , Arcus Senilis , Locomotor Brachii
- Check for Bed Sores - will find in long term Hemiplegics
- Check for an Indwelling Catheter.
- Neurocutaneous markers :
(Cafe au lait for Neurofibromatosis , Shahgreen patches , Ash leaf macules for Tuberous Sclerosis, Port wine stain for Sturge Weber Syndrome)
After this perform the routine neurological examination.
_______________________________________
Specific Questions that can be asked on Hemiplegia , and we must be aware of for exams (and for life) :
1. Elicit :
Tone
Power
Any deep tendon reflex (Commonly Biceps , Triceps , Knee , Ankle)
Clonus
Plantar Reflex (Babinski)
Glabellar tap
Jaw jerk
Facial Movements (7th nerve )
Gag reflex (Never forget to check for gag - it decides whether Ryles tube is needed or not and is super important to prevent Aspirations).
Extra Ocular movements
Tongue examination
2. Viva Questions :
A. Plegia vs Paresis?
Total paralysis = Plegia
Incomplete paralysis / Weakness = Paresis
B. What is Hemiplegia, Quadriplegia, Diplegia , Monoplegia , Cruciate Hemiplegia?
Diplegia = All 4 limbs involved but Lower Limb involved more than the upper.
Cruciate Hemiplegia= Upper limb of one side and lower limb of the other.
(I'm sure you know the others )
Complete Hemiplegia is when Facial involvement is present as well.
C. Hemiplegia vs Paraplegia site of lesions?
Hemiplegia is brainstem and above upto the cortex.
Paraplegia is spinal cord and below - upto the nerve.
(Paraplegia = Both lower limbs )
D. Rigidity vs Spasticity
- Lead pipe and Cogwheel Rigidity in Extra Pyramidal lesions like Parkinson's
- Clasp Knife Spasticity in UMN pyramidal tract lesion
E. UMN vs LMN lesions
(What is UMN ? What is LMN?)
F. Root values for all reflexes ?
(Deep + Superficial)
G. Plantar reflex components? What is a positive Babinski Sign? (5 components)
H. Causes of Babinksi positive other than Pyramidal tract lesions ?
(Deep sleep , Infancy , Coma.)
I. Alternatives to Elicit Babinski :
Gordon = Squeeze the Calves
Shaefer = Squeeze Tendoachilles
Oppenheim = Slide the knuckles down the tibial shaft
Chaddock = Strike along the medial aspect of the malleolus.
Hoffman Sign in Upperlimb
J. What is Jendrassik's maneuver ? What's its use?
K. Grades of Power ? (Should be pit pat)
L. Grades of Reflexes ? (In terms of + ++ +++ and ++++)
M. Causes of Hypo and Hypertonia?
Remember : Cerebellar disease causes Hypotonia
N. Clonus definition ?
O. What is Spinal Shock ?
P. Importance of aphasia ?
Wernicke vs Broca with area numbers ?
Conduction aphasia ?
How are these different from dysarthria?
Q. Know your blood supply : Anterior vs Posterior Circulation
- Middle Cerebral Artery - Superior vs Inferior Branch how to distinguish?
- Features of MCA territory stroke ?
R. Know Brainstem Syndromes names - the Crossed Hemiplegias.
Weber , Claude , Benedikt in Midbrain
Milliard Gubler and Foville in Pons
Medial and Lateral medullary Syndrome in Medulla.
S. Frontal lobe lesion features ! Especially Frontal release signs can be asked - Palmar grasp , Palmomental reflex , glabellar tap.
What is Gegenhalten phenomenon?
T. Then if you answer some of these they'll ask Management!
In that Basic Routine Ix. Don't forget Bloor Sugars and ECG.
NCCT best initial (Non contrast CT Scan)
Diffusion weighted MRI is very accurate for localisation!
U. Thrombolysis can ask everything about !
rTPA 0.9 mg/kg
CONTRA INDICATIONS and Indications.
V. BP control in stroke - Which agents ? Target BP ? How to Reduce?
W. Raised ICT management?
X. What drugs would the patient be on life long ?
Aspirin and Statins
Y. Neuroprotective agents , name a few?
Citicholine , Piracetam , Adavarone
Hope this was a good list !
Do message on the Medicowesome Group or comment down below if any answers are needed or you have doubts !
Happy studying!
Stay awesome.
~ A.P. Burkholderia.
Hemiplegia History-taking : Case-related Clinical Pearls
Hi everyone !
Just a short summary of what not to miss in your case taking of a Hemiplegia case - on the Boards or the Wards ! Here goes.
In the History of Present Illness
- Ask Onset - Time of onset very imp. And sudden or gradual. (To decide Ischemic or Hemorrhagic)
- Progress - If maximal at onset -- likely embolic. If progressive gradually -- Thrombotic stroke. If rapidly progressive -- Hemorrhagic stroke.
- Hemiplegia / Paresis - what position was pt in ;
Upper Limb (UL) more than Lower Limb (LL) or equal.
(ASK FOR PROXIMAL AND DISTAL MUSCLE INVOLVEMENT IN EACH LIMB)
( Proximal UL = Raise hands above head to take an object/Comb hair ;
Distal UL = Button Tee shirt or Eat food.
Proximal LL = Get up from Squatting position
Distal LL = Walking).
- Ask for facial deviation ; Drooling of food after feeding ? -- Facial palsy
- Hemianaesthesia - ask for sensory loss or paraesthesias.
- The Episode -->
• Seizures ? Urinary / faecal incontinence? - suggests increased severity / Cortical involvement
•Speech disturbances ?
- Likely cortical lesion if Aphasia ; or dysarthria due to UMN lesions
•Symptoms of cranial nerves --> Vision changes, Diplopia , Facial sensations , repeated aspiration of food , tongue problems. ( Localise the lesion to Brainstem)
• Gets better for a while and then Symptoms re appear - Lucid interval of extradural Hemorrhage
• Preceded by headache, vomiting , photophobia ?
( Meningitis/ SAH or PCA stroke) (Thunderclap headache in SAH)
• Any h/o Alcoholism / Trauma - Could be Subdural Hemorrhage
Always rule out a simple Syncopal episode and a plain Seizure.
In the Past History :
- H/O similar episodes - how were they treated and what were the residual deficits.
- H/O similar episodes that spontaneously resolved - TIA's
- H/O Other occlusive events - Myocardial Infarction, Peripheral Vascular Disease , Pulmonary embolism
- Ask h/o heart disease - Skipped beats for Atrial Fibrillation and other Valvular problems.
_________________________________________
What is expected out of the history-taking for Stroke :
1. What is the topographic distribution of weakness -
Hemiplegia / Monoplegia / Quadriplegia / Diplegia
2. Is the likely Etiology a vascular event in the Cerebral Circulation?
(From : typical elderly to middle aged presentation in a Hypertensive , Diabetic patient with sudden onset Focal Neurological deficit).
3. If fairly certain that this is Vascular : is it Thrombotic , Embolic or Hemorrhagic ?
4. What is the possible site of lesion in terms of :
A. Structure(s) involved
B. Vessel involved
Quick Rules of Thumb for diagnosis of CVA on history
<> Thrombotic Strokes have an insiduous onset , are progressive in their deficit but gradually , and may occur during earlier hours of the day.
<> Embolic Strokes have a sudden onset and are non progressive - Maximal deficit at onset ; May have History of Atrial Fibrillation or Valvular Heart disease and may have H/O recurrent emboli.
<> Hemorrhagic strokes are sudden in onset , very rapidly progressive and may be Preceded by Thunderclap headache in Subarachnoid Hemorrhage. Almost invariably the patient is hypertensive.
<> RISS = Rapidly Improving Stroke Symptoms are a feature of TIA (Transient Ischemic Attack) - generally resolving within about an hour , but the technical definition is the Deficit relieving in 24 hours or lesser.
<> Diabetic patients on Insulin must be watched out for Hypoglycemia which is highly common.
<> If no focal deficits and just a 'Confused' state of the patient or Diffuse CNS features must prompt a search for Electrolyte imbalance especially in the elderly for a Metabolic Encephalopathy.
<> Hypertensive Encephalopathy must be suspected if the patient is an Uncontrolled Hypertensive and has headaches and evidence of End organ damage.
<> Todd's palsy must be suspected in a young man who has recurrent attacks of 'Apparent Paresis' that occurs after some form of a seizure - it's a post ictal confused state.
<> Acephalgic Migraine is a rare form of Migraine where the headache is absent. So the patient would experience an Aura , go through non ache features of migraine and then followed by post migraine weakness.
The weakness can be perceived as a stroke.
Hope this was helpful !
Will be doing another one on stuff not to miss on examination and the questions asked generally!
Happy studying !
Stay Awesome !
~ A.P.Burkholderia
Saturday, February 10, 2018
Neurology Nuggets : Trigeminal neuralgia in Multiple Sclerosis.
Hello everybody!
A short nugget to start your Day with.
Let's see the reason behind the occurrence of Trigeminal Neuralgia in Multiple Sclerosis.
Multiple Sclerosis is basically a disorder of oligodendrocytes - derived Myelin which leads to blocks of varied degrees in Nerve impulse conduction.
The Trigeminal nerve is myelinated by Schwann cells, like rest of the Peripheral nervous System.
But still we see a high frequency of Trigeminal Neuralgia in Multiple Sclerosis.
The reason for this is-
*The trigeminal nerve is ensheathed by oligodendrocytes - derived myelin, rather than Schwan cells - derived myelin for upto 7mm after it leaves the Brainstem.*
This explains the high frequency of Trigeminal Neuralgia in Multiple Sclerosis which is a disorder of oligodendrocyte myelin.
Let's Learn Together!
-Medha Vyas.
Friday, February 9, 2018
My NEET experience
I could start off by mentioning how daunting it is to study for this particular exam, but I don’t think I need to. Nearly everyone, from their own experience or that of others has known and feared the NEET preparation. 19 subjects, 10 months, and in my case, the year of internship. Weekdays were spent running around the wards, weekends, trying to stay awake in 10-12 hour long classes. This was essentially 2017 for me.
It took me a while to get used to the amount of work and studying, both of which were never ending. The first week was like being thrown headfirst into a deep pool without knowing how to swim! Several coin sized haematomas later, I finally learnt the basics of what an intern was supposed to do.
Then came the first class of the year. If having 500 students in the batch wasn’t intimidating enough, the teacher more than made up for it. And so began my journey of fear, hurtling towards the NEET with no idea how to brake. Things became clearer in retrospect, as they should, for that is what retrospection is for. I wonder if I have had a calmer, even happier year if not for the constant weekly badgering. That being said, I knew I would have never stood a chance if not for the highly concise and valuable course material given to us by our classes.
In the weeks that followed, I managed to juggle both my duties with difficulty, not quite succeeding at doing justice to either. Nevertheless, I was happy, probably because the gravity of the situation hadn’t quite caught up with me.
‘There’s always a next year’, I thought to myself every time the dark thoughts about the exam loomed nearby.
Now, this blissful ignorance was beneficial in some ways, because it allowed me to adapt to and deal with the various perks of my job. The daunting working hours of the heavier departments, being constantly exposed to blood and bodily fluids and being in a frightful sense of awareness about the the hazards they carried, being addressed as ‘sister’ while my male colleagues had the privilege of being ‘doctor saab’ and the eventual satisfaction that came with staring a patient down till they squirmed and called me ‘doctor’, to name a few.
Reality caught up with me sometime around July, and brought with it a portion of self esteem issues and demotivation, much to my dismay. Try as I might, I just couldn’t rid myself of the notion that I would falter and fail. The previous mantra of ‘there’s always a next year’ didn’t seem comforting anymore, not when I saw my batchmates grinding it out everyday in the library. I tried to buck up my pace but kept zoning out, distracted by the very thing I was supposed to focus on. This mental inertia lasted for almost 2 months, relapsing and remitting, for lack of better words.
It spilled over to aspects of my life other than studying. I began to lose interest in work. It didn’t help that I was posted in Surgery, which is one of the more trying postings with shifts running upto 30 hours on emergency days. Imagine being an intern in surgery and not wanting to learn suturing. That is how demotivated I had become and that is how worthless I felt.
In the midst of this, there was a marathon 3 day session from our classes. Maybe it was the 42 hours worth of lectures that finally pushed me off the edge, but I ended up having one of the worst breakdowns of my life on the last day of the marathon session.
Thankfully, crying it out is something that has always made me feel better and this time was no exception. “Where there’s tears, there’s hope.” the Twelfth Doctor had said, and I truly realised the significance of that simple but powerful statement that day.
After that, I made a vow to pull up my socks and put in every effort towards my goal. Regret is a terrible thing, and nothing hurts more than knowing one could have done better. I made a list of the subjects I was not good at, and allotted more hours to them. I signed up for a series of mock tests which helped me keep track of my progress. I split the remainder of my time into revision sessions of 15-20 days, as per the advice of my extremely helpful seniors. When I was actively doing all the things, it was easier to put the crippling self doubt to the back of my mind, and assure myself that I was doing everything I possibly could.
Did I falter every now and then? Of course I did. My mock test scores had reached a plateau I couldn’t seem to overcome. There were times when I couldn’t remember the simplest of things that would lead to gross errors, at times simply because I did not read the question properly. This was more distressing than it should have been, mainly because I was functioning on such low levels of self esteem, and tended to be very harsh with myself for making errors.
With time, I realised this attitude was getting me nowhere. However, changing something that is so deeply ingrained in yourself is easier said than done. Nevertheless, I tried my best to build up my confidence by working on my weaker subjects, cutting myself some slack, and when things got difficult, confiding in my parents and friends and basking in their endless love and support. I also pampered myself with my favourite Murakami novels and endless mugs of tea. It didn’t make the stress go away, but it certainly made it more bearable.
Before I knew it, my time was up and it was time for the exam. I went in, promising myself that no matter what happened, I would not be drawn into the pit of self loathing I had escaped from. Surprisingly, I didn’t need to be. The weeks after the exam passed in a blur and then the results arrived, when I was on a train to Gwalior. My mother’s excited phone call rang through the sleeping compartment at 5am and I could barely stop smiling when I heard that I’d sailed through, and with a good score to boot!
I could hear the relief and pure joy in my mother’s voice, and then the tears fell, for what it had cost to get here. Back then it was almost impossible to believe, but in the end, it was worth it. Every extra hour, every missed question, every mediocre mock test, every stepping stone that had eventually paved the way for this.
If I had a few words of advice for the next batch of students preparing for the NEET, it’d be this. Surround yourself with people who love and support. Keep encouraging yourself and don’t be too hard on yourself when you make mistakes. Don’t ever withhold the things you love as a twisted form of positive reinforcement. It never works and ends up being a punishment for something you haven’t even done wrong. Be nice to yourself. You’re doing your best. Have faith and never stop believing in what you can achieve!
- Written by Aditi
Aditi decided to write the emotional aspect of NEET which very few students address. Hope it is helpful and relatable to those beginning the journey :)
Thursday, February 8, 2018
Opportunistic infections in AIDS
AIDS is a retroviral disease caused by HIV. It is characterized by the triad of immunosuppression associated with:
1) Opportunistic infections.
2) Secondary neoplasms.
3) Neurological manifestation.
Opportunistic infections seen are:
1) Bacterial infections:
MANS.
M-M.tuberculosis
A-Atypical mycobacterial infections
N-Nocardiosis
S-Salmonella
M.tuberculosis is the most common infection with HIV in India.
2) Viral infection:
H.C. verma of John Cunningham.
H-Herpes simplex virus
C-Cytomegalovirus
V-Varicella zoster virus
John Cunningham -JC virus causing progressive multifocal leukoencephalopahty.
3) Fungal infections:
H P computers creates crossword
H-Histoplasmosis
P-Pneumocystis jiroveci
computers-Cryptococcosis
creates-Coccidiomycosis
crosswords-Candidiasis
Candidiasis is the most common fungal infection of AIDS in India
Pneumocystis jiroveci is the most common fungal infection of AIDS in world.
4) Protozoal infection:
CITy
C-Cryptosporidium
I-Isosporidium
T-Toxoplasmosis
-Demotional bloke.
Tuesday, February 6, 2018
Monday, February 5, 2018
USMLE Step 3 - My two cents by Dr. B
My name is Dr. B and I have recently finished my Step 3 - results aren’t out yet, but I hope I can stay as just the author of this article and not have to read it once more. Fingers crossed!!
Pearls on polyps
Sunday, February 4, 2018
Headaches : Fun Facts
Here's just a list of fun facts about headaches :p
You might find some of them lame but hey, I can write whatever interests me - this is My-Graine you see ! (Sorry about that, had to crack that graine up since it's mine ;;) )
1. Coffee is actually an Anti Migraine substance ! It helps in vasodilation of cerebral vessels since it contains Caffeine and Theobromine (Compare : Theophylline) which are PDE Inhibitors.
There are drugs that combine Caffeine with Aspirin for this purpose ! Who would've thought ! Surprisingly, through mysterious mechanisms , Caffeine may Trigger migraine in few people.
(Go figure.)
2. Telcagepant is a novel drug being tried for treatment of Migraines. It's a CGRP Antagonist - Calcitonin Gene Related Peptide - Which is said to be a molecular mediator for Migraine headaches.
3. Constipation was said to cause headache. There's no evidence to prove this but old timers might still prescribe laxatives to treat headache.
4. Oxygen therapy helps treat Cluster headache !
5. Migraines may sometimes occur without headache ! Yeah , who would've thought.
So the patient would experience all other symptoms : Aura , Photo-phonophobia with vomiting and nausea , a mild headache And the post headache weakness !
It may actually become a stroke mimic at times as the weakness is pretty severe.
It's called "Acephalgic migraine"
6. Bickerstaff Migraine is a type of migraine where brainstem features are prominent. Also called Basilar migraine.
7. Tension type headache is the most common type of Primary headache ! But it may not have anything to do with being stressed at all.
8. People with cluster headaches may get so worked up and agitated they may actually want to bang their head and beg you to kill them , it's so severe ! (Talk about banging your head against a wall?)
9. There is a type of headache called 'Analgesic Overuse Headache'. The person with a known headache disorder begins to abuse NSAIDs to such an extent that taking the NSAID causes the headache ! So the solution is simple right ? STOP the NSAID?! BUT NO. IT'S NOT AS SIMPLE.
There is a sort of Physical dependence on it. And the withdrawal period is also characterized by headaches for a couple of of days/ weeks till the headaches finally stop. (What a pain!)
10. A subarachnoid Hemorrhage may be preceded by a series of minor headaches called 'Sentinel Headaches'. They can be warning signs in a known hypertensive and must be taken seriously.
That's all!
Hope this helps.
Happy Studying!
Stay awesome!
~ A.P.Burkholderia
Headache : Clinical Overview of Primary Headache Disorders
Preceded by an Aura - in the form of halos / fortification Spectra / floaters etc.
2 . Tension type headache
NO nausea vomiting ; may have photo and phonophobia. Not as rapidly progressive as migraine headaches.
Ipsilateral miosis , conjunctival injection , chemosis , rhinorrhea , sweating over forehead.
Patient may become agitated and restless.
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Happy Treating !
Stay awesome !