Tuesday, 31 December 2013

Anatomy

1. Incudo malleal joint is an examle of? A saddle joint
2. Stem cell in hair follicles? Bulge
3. Largest branch of vertebral artery?  Post inf cerebellar
4. Labrynthine artery is a branch of? Basilar Artery
5. Damage to nervous tissue is repaired by? Neuroglia
6. Corpus Striatum consists of? Caudate nucleus + lenticular nucleus
7. Charcots artery is a branch ? Middle cerebral artery
8. Tonsils are derived from? 2nd branchial pouch
9. Foramen spinosum transmits?  Middle meningial artery, mandibular nerve
10. Common carotid artery usually bifurcates at? C4

Hernias

Different Types of Hernia -
Gibbon's hernia- hernia with hydrocele
Berger's hernia - hernia in Pouch of
Douglas
Grynfelt/s hernia- Upper lumbar triangle hernia
Petit's hernia - Lower lumbar triangle hernia
Cloquet's hernia- hernia through pecteineal fascia
Narath's hernia - behind femoral artery
Hesselbach's hernia - lateral to femoral artery
Serofini's hernia - behind femoral vessels
Laugier's hernia - through lacunar ligament
Tealse's hernia - in front of femoral vessels
Richter's hernia - part of circumference of bowel wall is gangrenous
Littre's hernia - hernia with Meckels's
Diverticulum
Sliding hernia - Posterior wall of sac
is formed by colon or bladder
Maydl's hernia - 'w' hernia
Phantom hernia - Localised muscle
buldge following muscular paralysis
Spigelian hernia - through spigelian fascia
Obturator hernia - through obturator
foramen
Femoral hernia - hernia medial to femoral vein
Beclard's hernia - femoral hernia
through saphenous opening

Anatomy Mnemonics

Contents of broad ligament is : BROAD
B – Bundle (ovarian neurovascular bundle)
R – Round ligament
O – Ovarian ligament
A – Artefacts (vestigial structures)
D – Duct (oviduct)

Mnemonic for tributaries of External jugular vein is : PAST
PAST stands for :
P – Posterior external jugular vein
A – Anterior jugular vein
S – Suprascapular vein
T – Transverse cervical vein

Remnants
Ductus arteriosus - ligamentum arteriosus
Ductus venosus - ligamentum venosus
Urachus (allantois)  - mediaN umbilical ligament
Left umbilical vein - ligamentum teres of liver
Right umbilical vein  - disappear
Vitello intestinal duct - meckel diverticulum
UmbilicaL arteries - mediaL umbilical ligament .
Wolfian duct in female - gartner duct
Wolfian tubule in female - paraoophoron n eoophoron
Left anterior cardinal vein - oblique vein of marshall.

Mnemonic for Structures passing through foramen ovale of skull is : OVALE
OVALE stands for:
O – Otic ganglion (Does not pass through it, but lies inferior to it)
V – V3 cranial nerve
A – Accessory meningeal artery
L – Lesser petrosal nerve
E – Emissary vein

Mnemonic for the nerves supplying the scalp is: GLASS
GLASS stands for:
G – Greater occipital/ Greater auricular
L – Lesser occipital
A – Auriculotemporal
S – Supratrochlear
S – Supraorbital

Monday, 30 December 2013

One liners

Bucharts classificatin for ? Mesothelioma
Figure of 8 brain is seen in?Lissencephaly
Figure of 8 sign in orthopedics: Acetabular Retroversion
Figure of 8 splint? Clavicular fracture
Empty delta sign is seen in? Superior sagital sinus thrombosis
In sheehans syndrome: Empty sella sign
Goldenhar syndrome: Oculo auriculo vertebral dysplasia
Swimmer's shoulder aka Impingement syndrome
Pointing index can be seen in supracondylar
Adenosine used topically for woundhealing deficiencies, n in diabetics
Golden hair - arsenic poisoning
Straddle fracture: B/L # of superior and inferior pubic rami. Ass with bulbous urethral and extraperitoneal rupture of bladder
 Crescent: # of iliac wing with sacroiliac disruption
Chopart #? # dislocation thru intertarsal joint
 Wilson osteotomy? Congenital coxa vara
Wilson approach? Juvenile angiofibroma
 Bumper #: Depressed communited # of lateral condyle of tibia
Coleman sign: Seen in # Mandible, hematoma in the floor of mouth if # of body occurs

Human Herpes virus

Human Herpesvirus (HHV) classification

Type Synonym Subfamily Pathophysiology
# HHV-1 Herpes simplex virus-1 (HSV-1) α (Alpha) --Oral and/or genital herpes (predominantly orofacial)

#HHV-2 Herpes simplex virus-2 (HSV-2)
- Oral and/or genital herpes (predominantly genital)

#HHV-3 Varicella zoster virus(VZV)
- Chickenpox and Shingles

#HHV-4 Ebstein barr virus (EBV), lymphocryptovirus γ (Gamma)
-Infectious mononucleosis,Burkitt's lymphoma, CNS lymphoma in AIDS patients, post-transplant lymphoproliferative syndrome (PTLD), nasopharyngeal carcinoma.

#HHV-5 cytomegalovirus (CMV) β (Beta) -Infectious mononucleosis-like syndrome, retinitis, etc.

# HHV-6, -7 roseolo virus β Sixth disease- (roseola infantum or exanthem subitum)

#HHV-8

Kaposi's sarcoma-associated herpesvirus (KSHV), a type of 
-Kaposi's sarcoma, primary effusion lymphoma, some types of multicentric Castleman's disease

ENT

-irwin moore sign seem in chronic tonsillitis.
Pressure on the anterior pillar results in expression of pus from tonsillar crypts.

-primary elevators of larynx
= stylopharyngeus
= salpingopharyngeus
= palatopharyngeus
= thyrohyoid

-secondary elevators of larynx
= mylohyoid
= digastric
= stylohyoid
= geniohyoid

-TB larynx
=earliest symptom is weakness of voice

= first sign is impairment of adduction
=mouse nibbled appearance also seen

-WALDEYER RING

INNER RING
= ADENOIDS
= TUBAL TONSIL
= LINGUAL TONSILS
= PALATINE TONSILS

OUTER RING
= RETROPHARYNGEAL LYMPH NODE
=JUGULODIGASTRIC NODE
=SUBMANDIBULAR LN
= SUBMENTAL LN

-Broyle's ligament = ligament connecting both vocal cords at the anterior commisure to the thyroid gland

-Galen's anastomosis = anastomosis between superior and recurrent laryngeal nerve

-most common type of laryngeal ca  glottic ca

-hoarseness early symptom in glottic ca.
( late feature in supraglottic and subglottic ca)

- earliest symptom of subglottic ca  stridor and laryngeal obstruction

-Early nodal mets occurs in supraglottic ca

Drugs and Adverse effects

Drugs specific adverse effect :::

Vanishing bile duct syndome -- chlorpromazine

Coronary steal phenomena -- dipyridamole and isoflurane

Toxic ambylopia --- ethambutol

Fatal myocarditis ---clozapine

Idiosyncratic hepatic necrosis in infant --sodium valproate

Pseudo porphyria -- piroxicam

Amotivational syndrome-- marijuana

Fetal aplasia cutis -- carbimazole/methimazole in pregnancy

Drug induced mysthenia gravis-- d- penicilamine

Salt and pepper fundus -- thioridazine

Blue halo effect -- sidenafil

Calciphylaxis -- warfarin use in hemodylasis pt

Livedo reticularis -- amantidine

DRESS ie drug related eosinophila and systemic symptoms -- allopurinol

Pseudolymphoma syndrome -- anticonvulsants

Delayed bone marrow suppresion --nitrosourea anticancer drugs

Predisposition to listeria infection -- fludarabine

FSGS --heroin

Peripheral neuropathy resembling motor neuron disease -- dapsone

Vacuolar myopathy -- vincristine

Acute hepatic necrosis in pregnancy -- tetracycline

Cytokine release syndrome --muromonab cd3

Hand foot syndrome -- capcitabine

Hemorragic cystitis -- ifosfamide

Haemolytic uremic syndrome -- mitomycine c

Periods for Vertical Transmission of Diseases

congenital Varicella: First trimester

Congenital Rubella: First trimester

Congenital Parvovirus: Second Trimester

congenital syphilis: Third trimester

Congenital Toxoplasmosis: Third trimester

Congenital Hepatitis B: Third trimester

congenital CMV: Third trimester

Congenita HIV During delivery

congenital Hepatitis C During delivery

Congenital Herpes: During delivery

Sunday, 29 December 2013

Nerve palsies

Erb’s palsy
-Policeman tip deformity .(Porter's tip deformity)

Nerve of bell (Long thoracic nerve) palsy -Winging of scapula

Median Nerve Palsy (Labours nerve)
-Pointing index
-Bendiction test
-Pen test (tests abductor pollicis brevis)
-Oschner clasp test
-Opposition of thumb lost
-Ape thumb deformity

Ulnar nerve palsy (Musician nerve)
-Book test (froment sign),
-Card test (PAD) — Palmar interossei
-lgawa’s test (DAB) — Dorsal interossei

Radial nerve palsy
-Wrist drop,
(Finger drop and Thumb drop Specifically in posterior interosseous
nerve (PIN) injury)

Common peroneal nerve palsy (Lateral popliteal nerve palsy) or sciatic nerve palsy
-Foot drop(complete)

Lung Sounds: Differential Diagnosis

Rales(crackles)
-Simulated by rolling hair near ear between two fingers.
-Best heard on inspiration in lower bases.
-Unrelieved by coughing.
-Associated with bronchitis, CHE and pneumonia.

Wheezes
-High—pitched, squeaky sound.
-Best heard on expiration over all lung fields.
-Unrelieved by coughing.
-Associated with asthma, bronchitis, CHF, and emphysema.

Rhonchi
-Coarse, harsh, loud gurgling.
-Best heard on expiration over bronchi and trachea.
-Often relieved by coughing.
-Associated with bronchitis and pneumonia.

Stridor
-Harsh, high—pitched, audible sound.
-Easily heard without stethoscope during inspiration and expiration.

Saturday, 28 December 2013

Prolapse Treatment

For young nulliparous women with 2' or 3' uterovaginal prolapse
-Abdominal sing operation Cervicopexy (eg. Purandare, shirodkar, Khanna)

For a parous women in early weeks of pregnancy
-Ring pessary in the first trimester of pregnancy.

For a parous women in pregnancy with 2° or 3° prolapse at 28 weeks.
-Ring pessary till child birth and few weeks after and then Fothergirs repair.

For < 40 years multipara, desirous of retaining menstrual function and reproductive function with 2° or 3° prolapse.
-Fothergill's repair

For women > 40 years completed family size
-Mayoward's vaginal hysterectomy (with ant. Colporrhaphy and posterior colpoperineorrhaphy) with pelvic floor repair

For elderly menopause patient with advanced prolapse
-Lefort's repair

For enterocele
-Moscowitz repair

For vault prolapse
-Right sacrospinous colpopexy (in o and elderly not fit for abdominal surgery).
transvaginal
-Transabdominal sacral colpopexy using Mersilene mesh extraperitoneally in patient fit for abdominal surgery).
Congenital prolapse of uterus/ Nulliparous prolapse without cystocele:
- Purandare's cervicopeoy

Cracking exams

Posted by Dr. Savinay Kapur in his Facebook Wall

Hello folks. When I was preparing for Post Graduate exams, I felt the need for some proper guidance as to how to go about reading, what to read, from where to read and so on and so forth. I would constantly bug my seniors, teachers at my coaching institutes and practically anyone else I could get my hands on for the same! I have repeatedly been asked the same ever since I cleared the November 2012 PG entrances. My personal belief is that everybody reads, but the difference between those who get selected and those who don’t is that the former know what to read and how to read it. So this is my attempt at making things a little simpler for those who are preparing for Post Graduate entrances.

First, a small little introduction is in order- I’m Dr. Savinay Kapur and my ranks in the November 2012 entrances were 41st in AIIMS and 5th in PGI. I am currently pursuing M.D. Radiodiagnosis at PGIMER, Chandigarh. I graduated from AIIMS and completed my internship in December 2012. I fared pretty okay in my professional exams and the MBBS entrances as well and had the honour of being part of the team that represented North India at the IAP National Pediatrics quiz and the team which won the Medillectual quiz at MAMC and AIIMS in 2012.

I'm no one to preach but I hope to be useful to at least some people who can complete the herculean task of reading this! I hope I don’t end up offending anyone and if I may add- reader discretion is advised!

The most important message that I want to convey is that there is NO SINGLE PATH TO CRACKING ENTRANCE EXAMS. I've interacted with many toppers and most of them had followed regimes which were quite different from each other. So just don't follow any one blindly including me. Many people are interested in knowing how much time we need to study for getting a good rank. I think that’s a redundant question. Please remember that the amount of time one needs to read, remember and learn what they’ve read, depends on the individual. There is no universal constant for the amount of time that you need to put in. Your aim should be to give your one hundred percent and you yourself will have to introspect and judge if you are doing that or not. Having said that, you can’t sit in oblivion and be aloof from the outside world. After all, your performance will be evaluated only in comparison to that of your peers.  So the best way of knowing whether you’re on the right path or not is by looking at your ranks in the various GRAND TESTS.
Give all GRAND TESTS: The one thing that I've found common in all methodologies followed by people who got good ranks is that they started giving Grand tests pretty early and gave all grand tests including those of DBMCI, DAMS and IAMS. The best time to start would be right at the beginning of final year. Keep giving them even if you aren't getting good ranks. Try to compete with yourself and read all explanations. This helps in two ways; one is that you know whether you are doing the right thing, and second, the questions asked are pretty relevant and focused to current patterns and trends. So with every test, aim at reading at least 8-10 topics which have been asked in the exam from reference text books. This way you end up reading and revising some very high yield and you’ll probably end up remembering these discrete topics better as you have read these topics in isolation from similar confusing topics
Try to discuss things in GROUPS. The more you discuss, the more you will remember.
Form as many MNEMONICS as you can. However while doing so, try to make ones that are either relevant to the topic for which you are making the mnemonic or are so bizarre that you'll remember them for the bizarreness quotient. Also visual cues in the form of small little diagrams or drawings or flow charts help. Try making them in your book next to the text. It's easier to remember pictures than it is to remember the text
You'll get selected if you're FOCUSED. By focus I don't mean staying tense all the time thinking about what will happen in the exam. By being focused I mean getting away from the multitude of distractions and constantly reminding yourself that your sole aim is to clear the PG exam with flying colors.
Don't dismiss entrances as being just determined by luck. I agree that luck does play a role, but so does hard work. The proof lies in the fact that the top 100 in AIIMS as well as PGI are almost the same. There might be exceptions but from what I've seen, people who have been dedicated and hardworking, have got through.
I can assure you that most MCQ books have answered a number of questions incorrectly, including AA. Given that a large number of questions are repeated, it makes sense to correct those answers. You’ll only know if a given question is right or wrong if you’ve read well earlier. Don’t hesitate to check the answer if you have the slightest doubt that you’ve read something else in the book. Laziness at this point in time can cost you very, very dearly.
8. Another similar matter, very close to the heart of all of us and something we all are very emotional about- THE CONTROVERSIAL QUESTIONS!!
There is an order which you should follow while selecting answers to controversial questions

1. Ask the AIIMS professor who is likely to have made that question, this is for AIIMSonians as we guys know the favourites of almost every professor.
2. Ask any AIIMS professor of that subject.
3. Ask an AIIMS student if they've been told about it in college.
4. Try and search reference books but only standard reference books.
Plus don't try and infer stuff from any book. Only rely on a certain book if it gives the exact same line as is asked. Don't extrapolate things which are written to find a particular answer. Most questions are asked directly from stuff written in a particular book or journal. You just have to find the right reference.

5. If you can resist the temptation, the simplest thing to do is to go with the answers your coaching teachers tell you.
If you are still not satisfied with the answer or can’t find one, relax. The probability of that same question figuring in the exam are slim. Moreover, the probability of the answer you find now matching with the answer given in the key are even more remote.

6. If your rank in the Grand tests is within 100 then refer to online articles. Only rely on those journals which have a very high impact factor like NEJM, Lancet and the likes. Again, don’t extrapolate the things you read. Search for statements that match perfectly with what has been asked.
If your rank in the Grand tests isn’t within the top 100, you are better off not wasting time and effort in search of that all elusive answer. Read the rest of the topics rather than going after such controversial questions. You have two options if the question does appear in the exam- Chant Jai Mata Di and mark the answer or Leave the question in the paper.

9. How many questions to mark in the exam- It depends on the negative marking, the number of questions in that exam and your own caliber. If the negative marking is 1/3, mark the question if you can eliminate 1 option. If the negative marking is ¼, I suggest you attempt all questions. If the number of questions is 200 or less, scores will be more closely placed and there will be more people with same marks, so you are better off not attempting questions where you can’t eliminate 1 or 2 options. If your rank is within 100 in the grand tests, go with your gut feeling even if you can’t eliminate any option. If your rank is from 100-500, mark according to the negative marking. If your rank is beyond 500, I’d advise you to mark only if you have eliminated 2 options. But this is just my point of view, opinions may vary.

For PGI, you have to put your gut feeling to good use. Marking around 525-575 questions seems to be wise. So you can’t hold back as much as people probably tell you to do. Try to mark things that you think are correct or have read even if you aren’t a 100% sure. The seats are very limited, so if you mark less than 500, I don’t think you are giving yourself a good enough chance of qualifying.

10. TIME MANAGEMENT in the exam- It’s a very common problem that people are able to finish mock tests in time but when it comes to the real exam, everything goes haywire and people end up marking the last 50 questions in 15 minutes. That can be well and truly be disastrous. My personal approach always used to be to aim at finishing a certain number of questions every half hour. This way you can pace your exam pretty well and increase/ decrease your speed accordingly. The size of each block would obviously depend on the total number of questions in the exam.

I hope that covers most of the general stuff that I wanted to share with everyone. For the ease of the readers, I've divided the rest of the note into a few sections. Please read the section you currently fit in, though it might not be such a bad idea to read the rest of them as well, because I’ve wasted a lot of time and effort in writing those too :-P

SECTION A- For MBBS Students in 1st year to Pre-final year:

READ YOUR TEXT BOOKS WELL- Though this sounds dumb and boring but this is the only way which can assure you of a good rank. Read standard text books.
MCQ books will only supplement your preparations; they can't substitute standard text books. After you've read your standard text book WELL and feel you remember most of the stuff, only then go on to the MCQ books. When you read MCQ books, you can’t really remember new stuff, you can just reinforce and add on a few finer points to what you’ve already read. If most of it is alien, you won't remember anything you read. So use them only if you know the theory/ the basics pretty well and want to fill in the gaps.
Attend postings and classes- This holds true esp. for AIIMSonians. Most of what is taught in our lectures is asked in the exam. So it is a very good idea to hear things right from the horse’s mouth. Most of the so called “controversial questions” are discussed in those lectures and you know that these very people set the questions. So blindly follow what you hear in class, don’t bother reading weird references or listening to explanations from teachers of any coaching institute.
Relax and party whenever you can. It is never a good idea to read, read and read without enjoying life. You won’t get this time back ever again so make the most of it.
Differentiate between text books and reference books- Text books are the books to be read from 1st line to last line with special emphasis on “marked” topics. Try to read the whole book like a novel but remember the stuff marked by your seniors. Don’t try and remember the whole book.


SECTION B- FOR MBBS FINAL YEAR STUDENTS

Final year as such is a stressful period for all of us. Don't try to do anything special or spectacular. Heroics in general are best avoided in final year. Read your textbooks well.
If you haven't read Harrison even once then it might not be a great idea to start reading it now. Instead of trying to read the entire Harrison I'd personally recommend you to read those topics only, which are being asked repeatedly. Now the question is how do you select those topics? Simply read the questions from AA and Manoj Chaudhary given under medicine and read those topics retrospectively. I'm pretty sure this will help you in your professional exams as well as PG entrances. I had read different topics from different books including CMDT, Harrison, Kundu, PJ Mehta and George Matthew. You have to mix and match. But I know for a fact that if you read Harrison well, as in you are confident enough to be able to quote stuff from there when asked something, your odds of getting selected go up pretty substantially.
For OBG I had read Dutta for Obs and Shaws for Gyne. Plus the Johns Hopkins manual is an excellent read and highly recommended for those topics which are undergoing rapid changes in terms of guidelines and where protocols are universally applicable like oncology. In case of any confusion you can refer to Williams.
For surgery I myself was and still am confused as to what to do. I think for NEET, Bailey should be your go to book. But do read Schwartz/Sabiston for topics recently asked in AIIMS and All India just like Harrison is to be read for corresponding Medicine topics. A bonus point- Read M.L Saha for your practicals, that book rocks!
Pediatrics has to be read from Ghai and Ghai alone. Don't bother reading Nelson. If you really love to read then as I've told you above, read the commonly asked topics or topics which are controversial from Nelson.


SECTION C- For Interns:


OK, so you've passed the final year and are now, an over-zealous intern brimming with enthusiasm. But somewhere deep down inside, you know that the euphoria of passing the final year is soon going to die down and will be replaced by the fear of the unknown.
First take a break for some time. But don't lose focus! Remember that you have to start studying soon. You will want to keep telling yourself that you've just passed final year and you deserve a longer break. But if you keep delaying things, you'll soon realise that you've fallen behind and can't cope up now and that you must start thinking of preparing for the next year’s exam. Trust me it does not take that much time to fall behind. There creeps in a fear that there is too much to do and too less time. You soon land up in depression because you have so much to study and there seems to be so less hope; have to work in a hostile environment with odd hours, the patients hate you for being a blood sucker, the residents hate you because you keep disappearing; your parents keep reminding you that this is it, the exam your future wrests on; your friends might start looking at you as competition, best avoided. All in all, not the best time of your life!

From there on it’s a vicious cycle of not studying --> getting poor ranks --> getting depressed --> not studying. That is to be avoided. So start early.

Read for your T & Ds.
During internship it might be difficult to spare time for reading. But remember that it is the only time you're going to be getting for that topic(s). So however you do it, from wherever you do it, try and finish that topic(s) within the stipulated time. If you’re short on time, do only the questions and answers or read your notes or anything that you've read before and/or believe that you will be able to read again in the future. The point is that a certain subject, if ignored, will keep haunting you. Even if you try reading it later on, it’ll seem so much like a burden that you’ll end up pushing it under the carpet and ultimately that topic will not be read again, ever. This happened to me with Ophthalmology. There was such a fear psychosis of that subject that I could never read it. No matter how hard I tried, I just couldn’t understand what was happening. Finally I ended up leaving it altogether and hardly marked any Ophtha question correctly in the exam.

Remember, only the things you read multiple times are the things you'll be able to retain in the long run.

There are different kinds of facts
                 i.          Some, you read once and you just remember.
                ii.          Some, you read multiple times and you remember
               iii.          Some, no matter how many times you read, you tend to forget.
i. In the first category fall things that you've read about in class 11 and 12 maybe or are very basic. Plus some  topics you’ve read very well during your MBBS. Anything that you have read more than a month ago and have been able to remember it in any test is most probably in that Hard Disk of yours. You don't need to worry about them now.

ii. Majority of the topics fall in the second category. These are things which someone has asked you and you get a feeling as that answer is stuck somewhere and you just can’t retrieve it or else you've marked them incorrectly in a test because you can't remember what you read. These are things you should either read in more detail or note them down in a notebook for revision or do both.

iii. Into the third category fall numerical values, numbers and years and that sort of things. Things you can't remember even a week after you've read them. These should constitute your last minute revision notes; not the ones in the second category.
A subset of this category are things that aren't numbers or figures but things that you haven't ever understood and hence can never remember. If you can't remember stuff that doesn’t have to do with numbers then you need some kind of association to remember it.  Read it from someplace else, maybe from a few different sources. Try the internet. Look for articles on wiki relating to that. You'll surely find enough interesting cues that will serve as trigger points in your memory which will help you remember better.

SECTION D- FOR POST INTERNS:


Quite frankly I shouldn't be commenting on something that I haven’t experienced first hand. However what I feel is a lot of people think that at this stage they just need to sit down with question banks and previous years’ papers. I highly doubt that is the right way of going about things. I believe that you should ask yourself if most concepts of MBBS are clear to you or not. If they are and you feel comfortable reading most explanations then go ahead doing only previous years’ question papers. However if you feel that you haven't really read most of the topics that are being asked or if the explanations seem gibberish to you, I think you need to read those topics from textbooks to clear your concepts. That will help convert information from category ii/iii to category i.

The ultimate aim should not be to read but to remember, like I've already said.
I think I've conveyed most of the things that I wanted to. If there are still any doubts please inbox me. I will try to get back to you if I think I can help you with something.

Before I end, I would just like to thank the people without whom I couldn’t have achieved whatever little I have. My parents have been my biggest support and I owe everything to them. I’d also like to thank my grandparents, without their wishes I don’t think any of this would’ve been possible. Next in line is my brother, Pranay Kapur, my guide and friend in the darkest of times, my cousins and, my bhuas, and everybody else who have always been there whenever I’ve needed them. My friends Hameed, Aakanksha, Ankita and Veronica who always believed in me and were always there to motivate me and help me selflessly, even if it meant sacrificing their own precious time, thanks for being there people, I know how lucky I am to have you guys around. A big thanks to all my seniors for all there help and affection esp. Dudes, Khera babu and APS, thanks a lot yaar. Finally thanks to all my teachers, at AIIMS and at DBMCI and DAMS esp. Dr. Apurv Mehra and Dr. Sumer Sethi for being the mentors that I needed and for being available even a day before the exams.
To be honest I don’t think the ones close to me how much I value them and care about them, but I genuinely love each one of you. Thanks everyone :)

I’ll leave you with a list of books read by me-


Anatomy
TEXTBOOKS
BDC for gross anatomy
I.B. Singh for histology 
Langman for embryology
Snell’s neuroanatomy

REFERENCE BOOKS
Snell’s
Greys
Di Fiores for histology


Physiology
TEXTBOOKS
Bijlani and *Ganong*

REFERENCE BOOK
Guyton

Biochemistry
TEXTBOOKS
Harper’s, Lippincott

Pathology
*Robbins Robbins and Robbins*

Microbiology
Ananthnarayan for everything
*Jawetz*- for immunology and virology
Paniker- parasitology
AIIMS notes

Forensic medicine
Pass the Professional exam somehow and then simply read Sumit Seth

Pharmacology
TEXTBOOKS
KDT, Katzung (Both are complimentary, keep KDT as your base book and just browse through Katzung like a story book)
REFERENCE:
FDA Drug information


CCM
K.Park
USMLE High Yield Biostatistics
Policies and Programmes by D.K. Taneja

ENT
Dhingra

Ophtha
Not the right person to guide.

Skin
Neena Khanna

Anesthesia
Ajay Yadav

Radiology
Dr. Sumer Sethi’s book

Psychiatry
Neeraj Ahuja, Harrison

Orthopaedics
Dr. Apurv Mehra’s notes


* are the books which I found most useful and recommend as must reads even if you are a post intern.
I've already mentioned the books for major subjects of final year in the text above.

Best of luck to everyone who has had the courage and determination to read this Ramayana of sorts. I hope you achieve what you want to in life and even more! May the force be with you :-D "

Inclusion Bodies

Intracytoplasmic eosinophilic-

Negri bodies in Rabies
Guarnieri bodies in Small pox
Henderson-Peterson bodies in Molluscum contagiosum

Intranuclear acidophilic-

Cowdry type A in Herpes simplex virus and Varicella zoster virus and Torres bodies in Yellow fever
Cowdry type B in Polio

Intranuclear basophilic-

Cowdry type B in Adenovirus

"owl eyes" in cytomegalovirus

Both intranuclear and intracytoplasmic-

Warthin finkeldey bodies in Measles

Tests

-Spurling test-to assess cervical root disorder.

-Adson's test-for thoracic outlet syndrome.

-Wright test-for thoracic outlet syndrome.

-Neer test-to test for impingement of supraspinatus tendon.

-Hawkin's test-to test for impingement of supraspinatus tendon.

-Empty can test-to test for rotator cuff injury.

-Sulcus test-to test for inferior glenohumeral instability.

-Relocation test-to assess anterior glenohumeral instability.

-Push off test-to test for subscapularis muscle injury.

-Speed's test-to assess bicep tendon instability.

Surgical Sutures

Absorbable natural sutures
Collagen
Plain surgical gut
Fast-absorbing surgical gut
Chromic surgical gut
Absorbable synthetic sutures
Polyglactin 910 (Vicryl)
Polycaprolate (Dexon II)
Poliglecaprone 25 (Monocryl)
Polysorb
Polydioxanone (PDS II)
Maxon
V-Loc
Absorbable monofilament sutures
Caprosyn
Absorbable multifilament sutures
Nonabsorbable natural sutures
Surgical silk
Surgical cotton
Surgical steel
Nonabsorbable synthetic sutures
Nylon
Polyester fiber (Mersilene/Surgidac [uncoated] and
Ethibond/Ti-cron [coated])
Polybutester Suture (Novafil)
Coated Polybutester Suture (Vascufil)
Polypropylene (Prolene)
Surgipro II

Friday, 27 December 2013

Cataracts

►Nulcear cataract: Hemeralopia + Index Myopia + Second sight
►Cortical cataract: Night blindness
►Posterior Subcapsular: Maximum visual handicap because PSC is closest to the nodal point + Near vision impaired.
►Myotonic dystrophy: Blue dot cortical cataract and posterior subcapsular cataract / Christmas Tree Cataract.
►Wilson’s disease: Green sunflower cataract (copper) anterior or posterior subcapsular.
►Atopic dermatitis: Blue dot cortical cataract and posterior subcapsular cataract.
►Hypocalcemia: Discrete white cortical opacities.
►Diabetes mellitus: Snowflake opacities located in anterior and posterior subcapsular cortex.
►Acute onset diabetes: Cortical wedges caused by lens fiber swelling.
►Down’s syndrome: Snowflake opacities located in anterior and posterior subcapsular cortex.

Temperature curves

1. Febris continua - permanent fever. Fluctuate between morning and evening temperature do not exceed 1 °С. Such temperature curve is observed on the first period of abdominal typhus, crupose pneumonia.

2. Febris remittens - indulgence fever. Fluctuate between morning and evening temperature exceeds 1-2 °С. Such type of curve observes due to viral infections, sepsis, in second half of abdominal typhus.

3. Febris intermittens. It is alternating fever. It is characterized that by the rising periods of temperature (paroxysmuses) right alternate with the periods of normal temperature (apirrhexions). Temperature of the body rises to the level of 40 °С and higher, holds for a few hours, goes down to the norm and rises again. This fever type is observed in the malaria. The paroxysmuses can arise every fourth day (febris quartana), every third day (febris tertiana) or daily (febris quotidiana). Periodicity of the temperature rise depends on duration of development cycle of malarial Plasmodium. Paroxysmuses coincide in course of the time of erythrocytes destruction   (after completion of cycle).

4. Febris hectica. It is exhausting fever. Daily fluctuation of it is equal 3-4 °С and more. Sometimes temperature goes down below the norm. Such fever is typical for sepsis, tuberculosis, malignant tumors.

5. Febris inverse. It is inverted fever. Maximum of the temperature is observed in the morning, temperature decreases in the evening, sometimes to normal range. It is typical for sepsis and serious types of tuberculosis.

6. Febris recurrens. It is recurrent fever. There are periods of rising temperature (5-8 days) and normal level of temperature (nonfever periods). Example is recurrent typhus, malaria.

7. Febris undulans. It is undulating fever. There is slow increasing of body’s temperature during some term after that there its decreasing with period of normal temperature. It is typical for brucellosis.

8. Febris irregularis. It is irregular fever (atypical). It is characterize by nonright and different daily fluctuations of the temperature. It is typical for chronic bronchitis, chronic cholycystites, rheumatism and leucosis.

Anesthesia Facts

Dioscorides-used the term anaesthesia
Oliver wendell holmes-1846 termed anesthesiology
William.T.G.Morton-demonstrated general anaesthetic effects of ether(oct 16 1846 world ether day)
Carl koller- 1884 introduced cocaine as ophthalmic anaesthetic
Niemann-1860 introduced cocaine as local anaesthetic
Joseph priestley- produced nitrous oxide 1772
Horace walls-1844 demonstrated use of nitrous oxide in tooth extraction
Robert liston-dec21 1846 performed first surgery under ether anaesthesia
August bier-1898 first spinal anaesthesia
Simpson-first to use chloroform
John lundy-1934 first to use i.v. anaesthetic thiopentone
Ferdinand cathelin-1901-caudal epidural anaesthesia
Fidel pages-1921-lumbar epidural anaesthesia
Alexander wood-1855-invented needle & syringe
Harold griffith-1942 used curare
Lofgren-1943 introduced lignocaine
John lundy & Ralph waters- coined balanced anaesthesia
Domino&corsen-first used ketamine
Bovet-synthesised succinylcholine
Edmund gaske boyle-1917 boyle's machine
Ivan magill-first endo tracheal intubation
Stanlers rowbothon-first nasal intubation

Thursday, 26 December 2013

Avascular Necrosis


  • Ahlback disease - medial femoral condyle = SONK
  • Brailsford disease - head of radius
  • Buchman disease - iliac crest
  • Burns disease - distal ulna
  • Caffey disease - entire carpus or intercondylar spines of tibia
  • Dias disease - trochlear of the talus
  • Dietrich disease - head of metacarpals
  • Freiberg infraction - head of second metatarsal
  • Friedrich disease - medial clavicle
  • Hass disease - humeral head
  • Iselin disease - base of 5th metatarsal
  • Kienbock disease - lunate
  • Kohler disease - patella or navicular (children)
  • Kummel disease - vertebral body
  • Legg-Calvé-Perthes disease - femoral head
  • Liffert-Arkin disease - distal tibia
  • Mandi disease - greater trochanter
  • Mauclaire's disease - metacarpal heads
  • Milch disease - ischial apophysis
  • Mueller-Weiss disease - navicular (adult)
  • Panner disease - capitellum of humerus
  • Pierson disease - symphysis pubis
  • Preiser disease - scaphoid
  • Sever disease - calcaneal ephiphysis
  • Thiemann disease - base of phalanges
  • Van Neck-Odelberg disease - ischiopubic synchondrosis

FIBRILLAR COLLAGEN

Type 1- osteogenesis imperfecta, ehlers danlos syndrome(arthrochalasias type)
Type 2-achondroplasia type 2, spondyloepiphyseal dysplasias
Type 3- vascular EDS
Type 5- classical EDS
Type 9-stickler syndrome
BASEMENT MEMBRANE COLLAGEN
Type 4- alport's
OTHER COLLAGENS
Type 6- bethlem myopathy
Type 7-dystrophic epidermolysis bullosa
Type 9- multiple epiphyseal dysplasias

Christmas tree appearances in medicine

[1] Christmas tree pattern = A descriptive term for the multiplanar appearance of a high resolution 3-D MR Fourier transform reconstruction of the normal human endolympatic duct and system.
[2] Christmas disease = Hemophilia B.
[3] Pityriasis rosea= Christmas tree rash.
[4] Neurogenic bladder = The appearances has been described as a "Christmas tree" of pine cone bladder.
[5] Leak from paraspinal spaces into systemic circulation = Christmas Tree Sign.
[6] Christmas tree cataract = Nearly 100% of patients with myotonic dystrophy have a cataract. It is an opacity that radiates from the center of the lens like Christmas tree branches. It may impair vision.
[7] Peut zeghers polyp = "Christmas tree" appearance at low power under microscope.
[8] The transciptionally active DNA has a "Christmas tree-like appearance" on electron microscopic pictures.

Grades of Lymphoedema

Grade 1 (mild edema): Lymphedema involves the distal parts such as a forearm
and hand or a lower leg andbfoot. The difference in circumference is less than 4 cm, and other tissue changes are not yet present.
Grade 2 (moderate edema): Lymphedema involves an entire limb or corresponding
quadrant of the trunk. Difference in circumference is more than 4 but less than
6 cm. Tissue changes, such as pitting, are apparent. The patient may experience erysipelas.
Grade 3a (severe edema): Lymphedema is present in one limb and its associated
trunk quadrant. The difference in circumference is greater than 6 centimeters.
Significant skin alterations, such as cornification or keratosis, cysts and/or fistulae, are present. Additionally, the patient may experience repeated attacks
of erysipelas.
Grade 3b (massive edema): The same symptoms as grade 3a, except two or more
extremities are affected. Grade 4 (gigantic edema): Also known as elephantiasis, in this stage of lymphedema, the affected extremities are huge due to almost complete
blockage of the lymph channels. Elephantiasis may also affect the head and face.

Wednesday, 25 December 2013

All Criterias and Classifications

-Mcneal classi- Prostate
-Cohen wood classif- Lactic acidosis
-Scoreten Prognostic Score- Toxic Epidermal Necrolysis
- Modified Bell’s Staging Criteria for Necrotizing Enterocolitis
-Tiles classification- Hypovolemic shock
-Seddon amd Sunderland classi-Nerve injury
-Ozen criteria-PAN
-Ikeda classi- Alopecia areata
-Weibels classification-Tracheobraonchial divisions
-Heath Edwards classification: grading of histopath changes occuring in small pulm arterioles and mascular arteries in eisenmenger synd
-Castellvi-- lumboscaral transitional vertebrae(LSTV)
-Bigliani-Acromian morphological type classif
-Ruynon-Atypical mycobacteria
-Reese elworth classification for
retinoblastoma
-Breslow and clark classification
for melanoma
-Gilbert-Open hernia repain
-Nyhus-Lap hernia repair
-Halls criteria : Downs syndrome
-Dukes criteria: Infective Endocarditis/Heart failure
-Duke staging : colon cancer
-Butchers criteria :mesothelioma
-Bismuth classification: tumors of hepatic ductal system
-Nazers Index: Wilsons disz
-Ghent criteria-Marfan syndrome
-NADA's criteria: ASD assesment of child fo parameters
checked in Nazer index
-Pagets Index : Abruptio placentae
-Quetlet index: BMI -wt in kg/ht in meter square
-Ponderial Index: ht in cm/cube root of body wt in kgs
-Brocas index : Ht in cms-100
-Corpulence index : Actual wt/desired wt
-GCS/Ransons criteria/APACHE score: Pancreatitis
-Ennekings staging : Bone tumors
-Mc Donald's criteria: Multiple Sclerosis
-Durie salmon system of staging: Multiple myeloma
-Lights criteria: pleural effusion
-GOLD's criteria :COPD
-wells criteria: pulmonary embolism
-Epworths criteria : Sleep apnea
-Framminghams criteria/Boston's criteria: CHF
-OKUDA staging : HCC
-Child's Turcott pug score/MELD/ PELD- Cirrhosis of liver
-Milans crjteria: for liver transplant in HCC
-KINGS GEORGE CRT- ORTHOTOPIC LIVER TRANSPLANTATION
-FAB: Leukemias
-Glisson's staging: Prostrate
-Bosniak classification- Renal cyst
-Robson's staging : RCC
-Jackson's ataging :Penile Carcinoma
-Chang staging: Medulloblastoma
-Evan's stagng: Neuroblastoma
-Shimada Staging- Neuroblastoma
-Larren's classification: Gastric Ca
-Amsel's criteria: bacterial vaginosis
-Mallampati scoring: for intubation
-Forrest classification: Peptic ulcer bleed
-Rockall scoring: Adverse out come after GI bleed
-Glasgow Blatchford score : UGI
bleed for medical intervention
-Hess & Hunt Scale: subarachnoid hemorrhage
-Rule of wallace/Rule of 9: Burns
-Rotterdam's criteria : PCOS
-Stanford classification: Aortic dissection
-Waterlow-classification- Malnutrition in child
-Asbury criteria fr gullain barre syndrome
-Sapparos criteria fr ApLas
-Gilliam classification: Cutaneous manifestation of SLE
-Rifle criteria : renalfailure
-Todani classification: bile duct cysts
-Nealon classification : pancreatic pseudocyst
-D'Egidio classification:: pancreatic pseudocyst
-Galassi classification: arachnoid cysts
-BRADFORD HILL CRITERIA - CAUSAL RELATIONSHIP
-LORBERS CRITERIA- SELECTIVE SURGERIES IN NEURAL TUBE DEFECT
-HAAGENSENS CRITERIA- INOPERABILITY OF BREAST CANCER
Few Important CLASSIFICATIONS used in ENT--
-Sade classification: Retraction of pars tensa
-Toss classification : Retraction of pars flaccida
-Antoni classification:Acoustic neuroma
-Derlacki classification: Congenital cholesteatoma
-Levenson criteria- Cong. Cholesteatoma
-Nelson classification: CSOM
-Austin classification-Csom myringoplasty
-Savic classification-Reinke Oedema
-Shea classification :Meniere’s disease
-Isshika classification:Thyroplasty
-Wullstein classification :Tympanoplasty
-Fisch classification:Glomus tumours and Angiofibromas also
-Ohngren/Lederman:Maxillary sinus carcinoma
-The Myer-Cotton staging:  Subglottic stenosis
-The McCaffrey system classification: laryngotracheal stenosis.
-Paradise criteria-Recurrent tonsillitis so criteria for Tonsilloadenoidectomy in children
**
-Balthazar score-
Ct criteria for acute pancreatitis
-TIGAR-O Classification- Chronic pancreatitis
-RIPASA score: acute appendicitis
-Mantrles criteria/Alvarado score: Appendicitis
-Tzanakis score: acute appendicitis
-Ohmann score:  acute appendicitis
-Lintula score: acute appendicitis
-Samuel Score: pediatrics- acute appendicitis.
-Fenyo-Lindberg scoring system: pregnancy- acute appendicitis
**
-judet - acetabular #
-park n weber- ankle injury
-LEEFORDT's classification : facial #
-Mansons classification: Radial head #
-Neer's classification: supracondylar# femur
-Gartland's classification: Supracondylar # Humerus
-Waldvogel classification system Osteomyelitis
-ACR-euler criteria - joint involvement in RA
-Mirels classification- Pathological #(Risk)
-Wilke classification- Tmj Dislocation
[[-Wiltse is spondylolisthesis]]
-Delben and colonna classi-#femure in children
**
-Poelman and mcelin  criteria- for Cervical Pregnancy
-Rubins criteria- Cervical Preganancy
-Studifort criteria: Abdominal Pregnancy
-Spigelberg criteria- Ovarian Pregnency
**
-Ann Arbours classifiacation-Hodgkin's lymphoma
--Rye classification: Hodgkins lymphoma
--Hasenclever scoring fr prognosis in hodgkin lymphomas
- REAL classification for non- Hodgkin’s lymphoma
-RAI & BINET staging-CLL

Receptors of GABA and their Drugs

GABA REC ( CL - Channl)

GABA A SITE
-AGONIST. gaba. Muscimol
-Antagonist bicuculine     ( Competive)

BZD SITE
-AGONIST. BZD
-Antagonist flumazenil(competitve)
-Inv agonistbeta carboline

PICROTOXIN SITE
-Agonist barbiturate

Tuesday, 24 December 2013

Pathology Bodies

PATHOLOGY BODIES
1) Asteroid bodies - Sporotrichosis
2) Councilman bodies - Yellow fever
3) Torres bodies - Yellow fever
4) Leishman’s Donovan’s bodies - Kala Azar
5) Halberstaedter -Prowazek’s bodies - Trachoma
6) Miyagava's bodies - Lymphogranuloma
venereum
7) Levinthal-Cole-Lillie bodies – Psittacosis
Negri bodies (intracytoplasmic, intra neuron,
hippocampus) - Rabies
9) Guarnieri's bodies - Vaccinia (intracytoplasmic)
10) Bollinger's bodies - Fowl pox (intracytoplasmic)
11) Henderson-Peterson's bodies - Molluscum
contagiosum
12) Cowdry type-A bodies - Yellow fever, Herpes virus infection
13) Cowdry type-B bodies - Adenovirus, Poliovirus(code-BAP)
14) Aschoff's bodies - Rheumatic fever
15) Russell’s bodies - Multiple myeloma
( Intranuclear )
16) Schaumann’s/Conchoids bodies (calcium & iron complexes) - Sarcoidosis & Berylliosis
17) Asteroid bodies (eosinophilic inclusions) -Sarcoidosis
18) Call-Exner bodies - Granulosa cell tumor of ovary
19) Verocay bodies - Neurilemmoma
20) Civatte’s (colloid) bodies - Lichen planus
21) Michaelis-Guttmann's bodies - Malakoplakia
22) Lewy bodies - Parkinson's disease
23) Lafora bodies - Familial myoclonus
24) Hirano bodies - Alzheimer’s disease
25) Weibel-Palade bodies - storage organelles of von Willebrand’s factor in platelets & endothelium
26) Pappenheimer bodies – non heme iron
pigments in siderocyte
27) Howell-Jelly bodies - splenectomy ,
Megaloblastic Anaemia, Hemolytic anaemia
28) Hectoid bodies - Sickle cell anemia
29) Heinz bodies - thalassemia
30) Döhle bodies - cytoplasmic inclusion bodies in neutrophils seen in bacterial infection
31) Histiocytosis-X(HX)(Birbeck's granules) -
Histiocytosis-X
32) Gamma-Gandy bodies - Congestive
splenomegaly
33) Mallory's bodies - hyaline inclusions in
hepatocytes seen in alcoholic, indian childhood cirrhosis etc...
34) Apoptotic bodies - membrane bound spherical structures in Apoptosis
35) Psammoma bodies - dystrophic calcification in meningioma, papillary serous cystadenoma of ovary
& papillary carcinoma of thyroid, papillary type of RCC.
36) LE bodies (hematoxylin bodies) - SLE
37) Dumbbell shaped Asbestos bodies - asbestos fibres coated with glycoprotein & hemosiderin.
stained with Prussian blue stain
38) Luys body - subthalamic nucleus
39) Davidson’s body - sex chromatin in neutrophils(dumbbell shaped)
40) Herring bodies - pars nervosa of pituitary gland
41) Donovan body - Granuloma inguinale
42) Nissl’s bodies - cytoplasmic inclusions in
neurons
43) Moser’s bodies - Typhus fever
44) Lipschütz' bodies - intra nuclear inclusions in herpes simplex infection
45) Zebra bodies - cytoplasmic inclusions in
schwann cell degeneration
46) Babes-Ernest metachromatic granules -
Diphtheria
47) Reilly’s bodies - Hurler's syndrome
48) Gamma-Favre bodies - LGV
49) Winkler's & Ross's bodies - Syphilis
50) Sandström’s bodies - Parathyroid gland
51. Councilman Bodies = HEP B ( dying
hepatocytes )
52. Feruginous Bodies = Asbestosis
53. Heinz BODIES = G6PD DEF
54. Pick BODIES = PICKS D/S
55. Creola BODIES = Asthma
56. Odland BODIES = Keratinosome
57. Rushton BODIES = Odontogenic CYSTS
58. Zebra BODIES = Metachromatic Leukodystrophy,
Niemann Pick's Disease.
59. Brachy Wächter Bodies = Infective Endocarditis
60. Globoid bodies = Krabbes disease
61. Alder - Reilly Bodies = coarse azurophilic
granules in the leukocytes in ALDER - REILLY
SYNDROME.
62. Bodies Of Arantius = aortic valve nodules
63. Verocay Bodies = schwannoma
64. Balbiani's Bodies = yolk nucleus
65. Bamboo Bodies = asbestos bodies
66. Brassy Body = dark shrunken blood corpuscle found in MALARIA
67. Coccoid X Bodies = psittacosis
68. Cytoid Bodies = in degenerated retinal.N fibres. seen in cotton wool spots
69. Harting Bodies = calcospherite in the cerebral capillaries
70. Body Of Highmore = mediastinum testis
71. Masson Bodies = rheumatic pneumonia
72. Mott Bodies = multiple myeloma
73. Donnes Bodies = colostrum corpuscles
74. Oken's Body = mesonephros
75. Paschen Bodies = variola or vaccinia
76. Schiller Duval's Bodies = ENDODERMAL SINUS TUMOUR
77. Residual Bodies = SARCOID AND SARCOID LIKE GRANULOMAS
78. Body Of Highmore = medullary carcinoma of testis
79. Odland Bodies = Flegel’s Disease (i.e
hyperkeratosis lenticularis perstans)
80. Red Neurons = Apoptosis

Monday, 23 December 2013

Stains

SPECIAL STAIN REVIEW:---• HEMATOLOGY STAINS:
1) ROMANOWSKY STAIN:
routine stain for peripheral smear
examination
it’s a family of stain consisting of
1) Giemsa ( best and most commonly used)
2) leishman
3) wright
4) jenner
it can stain( apart from normal cells):
a) reticulocytes ( but non specific)
b) howell jolly bodies
c) basophilic stippling
d) cabot rings
BUT NOT FOR ---heinz bodies

2) HEINZ- BODIES
By supravital staining---methyl violet and crystal violet

3) RETICULOCYTES:
Specific stains are SUPRAVITAL STAINS
BEST –brilliant CRESYL BLUE
ALSO used are---NEW METHYLENE BLUE

• 1) HEMATOXYLIN stain:
Blue and basic
Stains NEGATIVELY CHARGED substances e.g.
DNA and RNA
Nucleus stained

2) EOSIN :
Pink and acidic
Stains POSITIVELY CHARGED structures e.g.
mitochondria
Cytoplasm is stained

• 3) Oil red O stain:
fat/lipid (on frozen section)
other stains for lipid /fat are:
a) Sudan black B
b) Sudan IV
c) Annexin V
d) Osmium teroxide

• 4) PAS Stain :
a) Glycogen
b) Fungus and amoeba
c) Basement membrane
d) Lymphoblast (BLOCK LIKE POSITIVITY)
e) Erythroblast (DIFFUSELY POSITIVE)

• 5) CALCIUM STAINS :
a) Von kossa
b) Alizarin red
c) Calcein

• 6) PERL’S PRUSSIAN BLUE :
Iron/hemosiderin

• 7) FUNGUS STAINS:
a) Gomori’s methenamine silver stains ---
(best fungal stain; stains both live and dead fungus)
b) PAS stain----only live fungus staining

• AMYLOID STAINS:
a) Lugol’s iodine—gross specimen
b) Hematoxylin and eosin
c) Methyl violet
d) Crystal violet
e) Thioflavin T
f) Toluidine blue
g) PAS
h) Alcian blue
i) CONGO RED STAIN--- pink/red under
ordinary light
And APPLE –GREEN BIREFRINGERENCE on
POLARISED MICROSCOPY(DIAGNOSTIC)

• 9) ALCIAN BLUE STAIN;
Mucin and mucosubstances
• ACID FAST yh
Mycobacterium

11) FONTANA MASSON:
Melanin and Argentaffin cells

12) MASSON’s TRICHROME STAINS:
Collagen and connective tissue

13) VERHOFF-VON-GIESON (VVG):
Elastic fibres ( other stain---ORCEIN stain)

14) TOLUIDINE BLUE: Mast cells

15) LUXOL FAST BLUE: Myelin

16) BIELSCHOWSKY STAIN:
(uses silver stain)
Neurofibrillary tangles and neuritic plaques

IPC - Criminal Laws

  Definition of rape - 375
• Punishment of rape - 376
• Unnatural sexual offence - 377
• Definition of perjury - 191
• Punishment of perjury - 193
• Murder - 302 • Attempt to murder - 307
• Chievous injury - 320
• Dowry death - 304 B
• Criminal negligence by doctor - 304 A
• Criminal responsibility of insane - 84
• Request of arrested person for medical examination - Sec. S3
• Negligence of father towards son - 317
• Criminal abortion - 312
• Magistrate inquest - Sec. 176 (1) Cr Pc.
• A person below 12 year can't give consent - 89
• A child below 7 year is not capable of committing offence - 82
• Police inquest - See 174 Cr Pc.
• Powers of magistrate - Sec. 29 Cr. Pc.
• Cognizable offence - Sec. 2 (n) Cr. Pc. & Sec. 40
IPC.
• Any act done by child under 7 year is not offence - Sec. 82 IPC.
• Issuing/signing false certificate is punishable
under-See.197 .

Dermatology

Beau's lines (Palpable horizontal deep grooves & ridges on nail)- Trauma, coronary occlusion, infection, Malnutrition, chemotherapy, psoriasis, diabetes, KAWASAKI DISEASE(after a few months of onset)
Muehrcke's nails (Hypopigmented lines on nail. Neither any groove nor any ridge is palpable.)- Chemotherapy, Nephrotic syndrome.

Axillary freckles-NF type 1
Café au lait spots- NF type 1
Lisch nodules(Iris)-NF type 1
Buttonhole invagination- NF type 1
Dennie-Morgan fold- Atopic dermatitis
Koebner phenomenon- Psoriasis, Lichen planus, Vitiligo, Pityriasis rubra pilaris
Wickham's striae- Lichen planus
Pterygium of nail- Lichen planus
(Cicatrical alopecia, Koebner phenomenon;
Bucca mucosa involvement)
Pin prick itching- Pityriasis versicolor
Sun fungus- Pityriasis Versicolor
Nickolsky's sign- Toxic epidermal necrolysis & Pemphigus vulgaris Row of
Tombstone appearance- Pemphigus vulgaris
Acantholysis- Pemphigus vulgaris
( Pemphigus-Intraepidermal blisters, Buccal mucosa involved.
Pemphigoid-- Subepidermal blisters, Mucosa not involved)

Target lesion- Erythema multiforme  Bull's eye- Erythema multiforme
Iris lesion- Erythema multiforme
Diascopy (vitropression) distinguish between erythma &papule    seen in
Papules in sarcoidosis , tuberculosis (apple jelly nodules )  other granulomas
Darrier's sign -urticeria pigmentosa (cutanous mastocytosis )
Grattage sign psoroasis
Auspitz's sign - psoriasis
Candle grease sign- Psoriasis
Burkley's membrane- Psoriasis
Warnoff ring- Psoriasis
Micro-munro abscess- Psoriasis
Silvery scales- Psoriasis
Onycholysis- Psoriasis
Herald patch- Pityriasis rosea
Christmas tree pattern- Pityriasis rosea

Sunday, 22 December 2013

Embryology of Eye- Derivatives

1.Surface Ectoderm
-Crystalline lens.
-Epithelium-cornea,conjuntiva,eyelids,lacrimal appartus
-LACRIMAL GLAND.
2.Neural Ectoderm
-RETINA and PIGMENT LAYER
-Epithelial layers of ciliary body and Iris
-SPHINCTER N DILATOR PUPILLAE
-OPTIC NERVE
-Melanocytes
-Secondary Vitreous
-Ciliary Zonules
3.Paraxial Mesoderm
-Primary vitreous
-Sclera
-Ciliary muscles
-Sheaths of optic nerve
-Extraocular muscles
-Upper n medial walls of orbit
-Connective tissue of orbit n upper eyelid
4.Visceral mesoderm of maxillary process
-Lower n lateral walls of orbit
-Connective tissue of lower eyelid.

INDIAN CHILDHOOD CIRRHOSIS

  • incidence decreasing in India ,Sri lanka
  • affects 1-3 yrs age group
  • >1 children in family affected
  • growth retardation
  • ascites
  • liver-- enlarged, firm, sharp edges, fine granular surface, grainy leathery appearance, mallory hyaline
  • cells are strongly+ive for Copper on orcein stain
  • excess copper intake from utensils responsible
  • may be ass. with genetic defect also
  • fine creeping fibrosis---- pericellular fibrosis
  • no nodule formation
  • scanty inflammatory infilterate
  • Cu chiefly concentrated in lysosomes as CuSO4 aggregates
  • also scattered Cu in cytoplasm
  • orcein/rhodamine staining +++ ive
  • ceruloplasmin NOT decreased
  • serum Cu, urinary Cu,hair Cu ------ increased
what are sources of Cu in ICC?
  • lack of maternal Breast feeding
  • top feeds--animal milk
  • brass / Cu utensils
  • genetic----- often  ass. with viral hepatitis

Treatment
  • D-penicillamine
  • Prednisolone
  • i.m. Gamma globulin

Physiology

Physiology Updates:
Heart receives <5% (4.7%) of cardiac output at rest
• Coronary blood flow is 250mL/min at rest- this can increase by 200-300% (500- 750mL/min)
• In terms of per 100g/ min, coronary blood flow- 84mL/100g/min (blood flow in resting skeletal muscle is 3- 4mL/100g/min; increases to 50 to 80mL/100g/min during exercise)
• Heart is a hard working organ (”thank God”), needs a lot of oxygen!
• Basal oxygen consumption (ref Ganong pg 550
24th edi)- 2mL/100g/min (much more than the oxygen consumption by resting skeletal muscle,
which is 0.2mL/100g/min)
• Oxygen consumption by a beating heart-
9mL/100g/min
• At rest heart extracts 70-80% of the oxygen
from each unit of blood delivered to it (“heart is the organ with maximum oxygen extraction at rest”).
So whenever there is an increase in oxygen
demand coronary blood flow will also show an increase.

Bio Weapons

Key Features of Biologic Agents Used as Bioweapons
1. High morbidity and mortality rates
2. Potential for person-to-person spread
3. Low infective dose and highly infectious by aerosol
4. Lack of rapid diagnostic capability
5. Lack of universally available effective vaccine
6. Potential to cause anxiety
7. Availability of pathogen and feasibility of production
8. Environmental stability
9. Database of prior research and development
10. Potential to be "weaponized 

CDC Category A, B, and C Agents 

Category A
 Anthrax (Bacillus anthracis)
 Botulism (Clostridium botulinum toxin)
 Plague (Yersinia pestis)
 Smallpox (Variola major)
 Tularemia (Francisella tularensis)
 Viral hemorrhagic fevers
 Arenaviruses: Lassa, New World (Machupo, Junin, Guanarito, and Sabia)
 Bunyaviridae: Crimean-Congo, Rift Valley
 Filoviridae: Ebola, Marburg
Category B
 Brucellosis (Brucella spp.)
 Epsilon toxin of Clostridium perfringens
 Food safety threats (e.g., Salmonella spp., Escherichia coli
 0157:H7, Shigella)
 Glanders (Burkholderia mallei)
 Melioidosis (B. pseudomallei)
 Psittacosis (Chlamydophila psittaci)
 Q fever (Coxiella burnetii)
 Ricin toxin from Ricinus communis (castor beans)
 Staphylococcal enterotoxin B
 Typhus fever (Rickettsia prowazekii)
 Viral encephalitis [alphaviruses (e.g., Venezuelan, eastern, and western equine encephalitis)]
 Water safety threats (e.g., Vibrio cholerae, Cryptosporidium parvum)
Category C
 Emerging infectious diseases threats such as Nipah, hantavirus, SARS coronavirus, and pandemic influenza

MEDICAL DISORDERS DURING PREGNANCY

A) Valvular Heart
a) MS
* Most common valvular disease causing death in pregnancy.
* Sudden death if hypovolemia occurs.
* Prone for Tachyarrythmias.
* Digoxin, Beta blockers.
* Treatment-Balloon mitral valvulotomy
b) AS
* Well tolerated.
* Decrease in systemic vascular resistance reduces risk of cardiac failure.
B) Congenital Heart Disease
* Increase risk of congenital cardiac disease in newborn
*ASD/VSD- well Tolerated
C) SVT
* Common
* Adenosine, can be used
* Electrocardioversion – well Tolerated in pregnancy
D) Peripartum Cardiomyopathy
* Uncommon.
* Most recover.
* May progress to DCM.
* Can recur in next pregnancy.
E) Marfans
* High risk of maternal mortality.
* Aortic root diameter < 40mm – favourable prognosis.
* Beta Blockers.
*15% of pregnant women develop a major cardiovascular manifestation during pregnancy.
*Ehlers-Danlos syndrome (EDS) - associated with premature labor, and in type IV EDS, there is increased risk of uterine rupture.(18th edition)
F) PHT
* Primary PHT is a contraindication. (AIIMS 2009), [AI 2010***]
* Vaginal delivery is less stressfull than CS.
*Eisenmenger syndrome - maternal and fetal death occur frequently.
G) DVT
* Hypercoaggulable state.
*Associated with an increase in procoagulants such as factors V and VII, and a decrease in anticoagulant activity, including proteins C and S.(18th edition)
* More common in left leg (compression of lt. iliac vein).
* 25% with DVT have factor V leiden mutation
* Prothrombin G20210A mutation (homo, hetero zygos).
* Methylene Tetrahydrofolate reductase C677T mutation (homozygotes)..
* Trt – LMWH
Warfarin
- 1st Trimester – chondrodysplasia punctata
- 2nd, 3rd Trimester – foetal optic atrophy.
- mental retardation.
- not contraindicated in breast feeding.
H) Obesity
*An increased risk of stillbirth, congenital fetal malformations, gestational diabetes, preeclampsia, urinary tract infections, and post-date deliveries.
*Following bariatric surgery, women should delay conception for one year.(18TH EDITION)
I)Hematologic disease
* Physiologic anemia.
* Thrombocytopenia-immune thrombocytopenia, thrombotic thrombocytopenic purpura(18TH EDITION), and preeclampsia-Benign gestational Thrombocytopenia (common)- also associated with the development of DIC, including retention of a dead fetus, sepsis, abruptio placenta, and amniotic fluid embolism.
* Disseminated intravascular coagulation (DIC)- characterized by thrombocytopenia, prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT), elevated fibrin degradation products, and a low fibrinogen concentration.(18TH EDITION)
J)HELLP
- A severe preeclampsia.
- Hemolysis.
- Elevated liver enzymes.
- Low platelet.
* Mild preeclampsia – conservative.
* Severe preeclampsia – Delivery.
* Drugs
- Labetol, Hydralazine, Ca channel blockers
- To avoid ACEI, ARBs in 2nd & 3rd Trimester- develop oligohydramnios, caused by decreased fetal renal function.
K) Hyperthyroidism
* 2 per 1000.
* Well Tolerated.
* Severe – spontaneous abortion.
* Treatment
-Propylthiouracil (choice) - can be associated with liver failure.(18TH EDITION)
-Methimazole (crosses placenta more).
-Can cause aplasia cutis.
-propylthiouracil in the first trimester and methimazole thereafter(18TH EDITION)
-KI, Beta blockers.
-Radio Iodine contraindicated.
*Easiest to control in 3rd Trimester & most difficult to treat in 1st trimester*
Hypothyroidism
* Thyroxine requirement increases as early as 5th wk by 30%.
* Increase the thyroxine dose by 30% as soon as pregnancy is diagnosed.

Shelf life

Shelf life (whole blood / red cells ) in :
1) ACD( acidified citrate dextrose) = 21 days
(> 70% transfused cells viable after 24 hours)
2) CPD( Citrate phosphate dextrose) = 28 days
3) Citrate Phosphate Dextrose Adenine (CPDA) = 35 days
4) SAGM ( Saline Adenine Glucose Mannitol)= 42 days
• Whole blood:
Storage temp.= 2-6 0c
1 unit raises Hb by ---1gm/dl and haematocrit by 3%.

Anesthesia

PRESERVATIVES

  • Halothane:0.01%thymol
  • Ketamine:Benzethonium chloride
  • Thiopentone:Anhydrous sodium carbonate(6%)&nitrogen gas
  • Ether:Propyl galate/ hydroquinone/ diphenylamine



  1. Post-op shivering: pethidine, pentazocine
  2. inhalational anaesthetic that boils at room temp:desflurane
  3. inhalational anaesthetic that causes coronary steal:isoflurane
  4. anaesthesia of choice in hemorrhagic shock:cyclopropane
  5. associated with post anaesthetic chills:halothane
  6. agent of choice for cerebral protection:thiopentone
  7. abnormal spike discharges in epileptic pts:methohexitone
  8. thalamoneocortical junction is the primary site of action for:ketamine
  9. steroid anaesthetic:althesin, minaxolone
  10. anti-analgesic anaesthetic agent:thiopentone

Criterias

1.Halls criteria : Downs syndrome
2.Dukes criteria:Endocarditis/Heart failure
3.Butcherscriteria :mesothelioma
4.Ann Arbours classifiacation :Hodgki.s lymphoma
5.Bismuth classification: tumorsof hepatic ductal system
6.Nazers Index: Wilsons disz
7.Pagets Index : Abruptioplacentae
8.Quetlet index: BMI -wt in kg/ht in meter square
9.Ponderial Index: ht in cm/cube root of body wt in kgs
10.Brocas index : Ht in cms-100
11.Corpulence index : Actual wt/ desired wt
12.Milans crjteria: for liver transplant in HCC
13.Mayers n cottons grading system: Subglottic stenosis
14.Spaldings criteria: abdominal pregnancy 15.GCS/Ransons criteria/APACHE score:
Pancreatitis
16.Ennekings staging : Bone tumors
17.Mc Donald's criteria: Multiple Sclerosis 18.Epworths criteria : Sleep apnea 19.Framminghams criteria/Boston's criteria: CHF
20.Durie salmon system of staging: Multiple myeloma
21.Lights criteria: pleural effusion
22.GOLD's criteria :COPD
23.OKUDA staging : HCC
24.Child's Turcott pug score/MELD/PELD- Cirrhosis

Laryngeal pseudosulcus

Laryngeal pseudosulcus is subglottic edema seen in some new borns.
Laryngeal pseudosulcus is d/t------- reflux induced laryngitis (pharyngoesophageal reflux) in the pediatric patients.
Edema along the undersurface of the vocal fold from the anterior to the posterior commissure
It is a common endoscopic finding of EER (extraesophageal reflux).
By contrast, true sulcus vocalis involves the free edge of the fold and terminates at the vocal process.
Major laryngeal findings in chronic laryngitis associated with EER are seen in the posterior larynx.
Posterior laryngitis is manifested by edema, increased vascularity and erythema of the posterior commissure, and arytenoids.
Chronic irritation can result in a thickening of the posterior laryngeal mucosa with hyperkeratosis, which is also called pachydermia laryngeus. This posterior mucosal thickening with increased granularity and rough cobblestone appearance is described as “granular mucositis.”
Increased mucus formation and thickness, along with mucus stranding and pooling, may result from chronic irritation and alterations of mucociliary flow. Laryngeal ulceration, granuloma formation, scarring, and stenosis may indicate more severe EER.
Erythema of the posterior larynx is the most prevalent sign
Erythema of posterior larynx----- sign which is most reversible with treatment of EER.
More severe inflammation or longer duration of symptoms is associated with increasing vascularity and erythema extending into the remainder of the larynx and supraglottis. Posterior glottic mucosal thickening is the second most common findings.

Saturday, 21 December 2013

X - Ray finding chest

Heart and blood vessels
1. Flake shaped / pear shaped / Leath - bottle /money bag shaped heart - Pericardial effussion
2. Boot shaped heart / Coer - en - sabot - Fallot's tetralogy
3. Box - shaped appearence - Tricuspid atresia
4. Jug handled appearence - primary pulmonary artery hypertension
5. '3' appearence - Coarctation of aorta
6. Egg on side appearence - Trans position of great vessels
7. Egg in cup appearence - Constrictive pericarditis
8. Snow man heart - TAPVC (Total Anomalus Pulmonary Venus Connection )
9. Figure of '8' - TAPVC ( Total Anomalus Pulmonary Venus Connection )
10 . Cottage leaf apeearence - TAPVC
11. Perecardial calcification - Constrictive perecarditis
12 . Calcification in heart wall - is seen in - Carcinoid syndrome
13 . Calcification of ascending aorta - Atherosclerosis , syphilis
14 . Hilar dance on fluroscopy - Atreal septal defect
15 . X -ray finding in 'Ebstein's anomaly - Pulmonary oligaemia
16 . Posterior displacement of trachea - seen in - Aneurysm of Aorta
17 . Oblitaration of left border of heart (PA viewchest ) - is - suggestive of - Linguler pathology(Left lung )
18 . Bat wing's appearence - Pulmonary oedema
19 . Pruned tree appearance (of pulmonary circulation ) - Pulmonary artery hypertension
Lungs -
1. Ground glass appearence - Hyaline membrane disease
2. Solitary pulmonary mass lession - > 4 cms is - most commonly due to - Broncheal adenoma
3 . Honey comb appearance - Cystic fibrosis , cystic bronchiactasis , collagen disorders - Rheumatoid arthritis , scleroderma
Pneumoconiosis , tuberculosis , histyocytosis ,intersticial lung disease , sarcoidosis
drugs - Bleomycin , Busulphan , melphalan ,
cyclophosphamide
4. Meniscus sign / crescent sign (mobile mass in pulmonary cavity ) is most commonly seen in - Asperglloma (fungal ball lession )
5. Egg cell calcification - sillicosis , sercoidosis , coal - minors pneumoconiosis , lymphoma following radiotherapy
6. Pop corn calcification / craggy popcorn calcification - Pulmonary hemartoma
7. Plural calcification - commonest cause is - tuberculosis (Asbestosis )
8. Diaphragmatic plura calcification - is due to -Asbestosis -
9. Calcification in a pulmonary metastasis - most common cause is - Osteosercoma
10 . Coin shadow in the lung (single ) - With calcification - Epidermoid carcinoma
11. For radiologically evedent plural effussion - The minimal amount of plural fluid that should be present is - 250 ml .
12 . Plethoric lung field seen in - L - R shunt (VSD ,PDA , ASD )
13 .Oligemic lung fields - Pulmonary atresia , stenosis , Ebstein's anomaly
14 . Peri hilar fluffy opacities - seen in Pulmonary venous hypertension.

Ribs
1. Superior surface notch of ribs - seen in - - Hyperparathyroidism , neurofibromatosis , connective tissue disorder
2. Inferior surface notch of ribs - seen in - Coarctation of Aorta , SVC obstruction , chest wall
AV fistula AV thrombosis , Aortic thrombosis
3. Unilateral obstruction - seen in - Coarctation of left subclavian artery , subclavian artery block , Blacklock Taussig operation
Others
Displacement of Tracheal shadow - most common cause is - Thyroid swelling
Watery lily sign - Ruptured hydatid cyst

PAX Genes

PAX (PAIRED BOX) GENES
• PAX-2 → “renal-coloboma” syndrome
• PAX-3 → Waardenburg syndrome (white forelocks of hair; eye colors don’t match)
• PAX-5 → lymphoplasmacytoid lymphoma
• PAX-6 → aniridia and Wilms’ syndrome
• PAX-8 → follicular thyroid carcinoma
• PAX-9 → congenital absence of teeth

Friday, 20 December 2013

Paediatrics

Microcephaly : > 3 SD below mean
Macrocephaly : > 2 SD above mean
Newborn Head circumference - 35 cm , By 2year sge - it reaches 48cm (i.e 90% of adult head circumference is achieved in 2yr)
Meningitis
1st 2 months - E.Coli (MC)
2months - 12 years - Pneumococcal and Neisseria.
95% Meningitis in child - affects 1month - 5years age group.
Most common causes :
Sporadic encephalitis - Herpes
Epidemic encephalitis - Arbovirus
Viral encephalitis - Enterovirus (also MC
meningoencephalitis)
Brainstem encephalitis - Rabies
Viral encephalitis : causes
1. Enterovirus (80%)
2. Arbovirus
3. Herpes
4. Mumps

Poisons

Ideal suicide poison = Cyanide
Ideal homicide poison = Thallium, fluoride compounds.
Commonly used homicidal poisons: Arsenic, aconite
Commonly used suicidal poisons: Endrine, Opium, Barbiturates, Organophosphorus  compounds.
Poison resembling cholera = Arsenic
Poison resembling tetanus = Strychnine
Poison resembling natural death = Thallium
Poison resembling fading measles = Arsenic
Poison resembling thyrotoxicosis = Bi-nitro compounds.

Cardiac markers for MI

Things you should know about
Cardiac markers for MI:
1)... Myoglobin first comes and first goes (rises first, disappears first)
2)...LDH is called "lazy enzyme" because it comes late, and goes late (rises after 24 hours and remain till
14 days)
3)...Trop-I has the greatest sensitivity and specificity.
4)...The investigation of choice within first hour of MI is "CKMB"
5)..."CKMB" is useful for confirmation of reinfarction as this enzyme disappears after 72 hours of MI. So, if a patient comes after 72 hours of initial infarction, and you are suspecting a reinfarction, go for "CKMB".
- Myoglobin disappears after 24 to 48 hours.
- CKMB disappears after 72 hours.
- Trop I disappears after 7 - 10 days.
- LDH disappears after 14 days.
Scenerio 1: CKMB of patient is normal. Trop-I is raised. He is 3 - 10 days post MI patient.
Scenerio 2: CKMB and trop - I of patient is normal. LDH is raised. He is 10 - 14 days MI patient.

Immunoglobulin

1.Ig that crosses the placenta ?
Answer:IgG
2.Ig present in milk?
Ans:Ig G & Ig A
3.Ig in seromucinous glands?
Ans:Ig G & Ig A
4.Ig in primary immune response?
Ans:IgM
5.Ig in secondary immune response?
Ans:IgG
6.Ig wid maxm molecular weight?
Ans:IgM
7.Ig wid maximum sedimentation rate?
Ans:IgM
8.Ig wid minimum sedimentation coefficient?
Ans:Ig G
9.Blood group antibodies belong to which type of Ig?
ans:IgM
10.Rheumatoid factor belongs to which type of Ig?
ans:IgM(antibody against Fc fragment of Ig G)
11.Ig that is heat labile?
ans:IgE
12.Ig mediating d prausnitz kustner reaction?
Ans:IgE
13.Ig appearing 1st in life?
Ans:IgM
14.homocytotropism is seen in which Ig?
ans:IgE
15.Ig wid maxm serum concentration?
Ans:IgG
16.Ig wid minimum serum concentration?
Ans:IgE
17.Ig wid longest half life?
Ans:IgG
18.Ig wid shortest halflife?
Ans:IgE
19.Ig wid maxm synthesis per day?
Ans:IgA
20.Ig wid minimum synthesis per day?
Ans:IgE
21.Ig responsible for hypersensitivity pneumonitis?
Ans:IgG
22.binary exposure to an antigen results in suden increase in?
ans:IgG
23.Ig to fix complements via clasical pathway?
Ans:IgG1 & IgM
24.Ig to fix complements via alternate pathway?
Ans:Ig A,Ig D,IgG4

Neuro

Multiple sclerosis is the most common cause of an isolated sixth cranial nerve palsy due to a plaque in the brainstem.

The closest nerve to the eighth cranial nerve is the facial nerve; however, after the acoustic nerve, the most common nerve to be affected is the trigeminal nerve. There is a relative loss of higher tones in nerve deafness whereas lower tones are lost in middle ear deafness.

The most common presenting symptom of a posterior fossa mass is headache related to mass effect, or obstruction of cerebrospinal fluid (CSF) pathways.

Pilocytic astrocytomas (PAs) are the most common pediatric cerebellar neoplasm and occur at a mean age of 7 to 8 years.

The most common genetic anomaly in medulloblastoma is isochromosome 17q. The most common genetic alteration in ependymoma is loss of chromosome 22;

Hemangioblastomas are the most common posterior fossa lesion in adults but are rarer in the pediatric population.

Spinal cord ependymomas are the most frequent SCIMTs in adult patients.

Spinal cord astrocytomas represent more than 80% of the SCIMTs in children,43 and in adults astrocytomas are the second most common type of tumor.

Lens of the Eye : Overview

Lens of the eye is formed from –
a) Surface ectoderm
b) Mesoderm
c) Endoderm
d) None of the above
Where Do Lenses Come From?

The vertebrate eye develops from a diverse collection of embryonic sources through a complex set of inductive events [6]. Whereas the neural retina is derived from the diencephalon and is a part of the brain, the lens comes from surface ectoderm and the iris and ciliary body arise primarily from the neural crest. Mapping the genes known to play a role in mouse eye development, for example, shows that some of these genes are present on every chromosome [6]. The apparent patchwork assembly of the eye makes it all the more surprising that common developmental programs seem to produce comparable outcomes across a broad phylogenetic divide .

Could we use the composition of lenses to gain insight into eye evolution?

Vertebrate lenses are formed from modified epithelial cells that contain high concentrations of soluble proteins known as crystallins because they are packed in a highly organized fashion. It is the change in relative concentration of these proteins from the periphery to the center of vertebrate lenses that produces the refractive index gradient necessary for a lens to be useful to the animal. In fact, the identity of the proteins seems not to be important since the crystallin proteins are not more transparent than others. Instead, the distribution of protein concentration as a function of radius is the key to a successful lens. Thus, the challenge in understanding lens evolution lies in discovering how the distribution of proteins within a lens is established and maintained.

Of the eleven lens crystallins now known, only three, alpha-, beta- and gamma-crystallins, are common to all vertebrates. In fact, until recently, all crystallins were thought to be unique to lens tissue and to have evolved for this special function. However, despite their apparently specialist role, most of the crystallins are neither structural proteins nor lens specific. There are two major groups of lens crystallins, those present in all vertebrates and those specific to a particular taxon. For example, in crocodiles and some bird species, the glycolytic enzyme lactate dehydrogenase B is a major protein in the lens. Indeed, 4 of the 8 taxon-specific crystallins are identical to metabolic enzymes and products of the same genes, suggesting these products share a gene.

Why might enzymes be recruited to make vertebrate lenses?

Perhaps the robust regulation of enzyme production is advantageous for producing sufficient protein for a lens, but there is not much beyond speculation to support this notion. There may be some deeper reason, however, because this molecular opportunism seemed such a good idea, that certain invertebrates, e.g. mollusks, independently evolved the same strategy . Squids have lenses whose protein content is nearly entirely the enzyme glutathione S-transferase. The common strategy of constructing lenses from different proteins seems to be a convergent evolutionary solution. This convergence of molecular strategy suggests that enzymes as lenses may have a functional meaning, or that it is easy to get lens cells to make a lot of enzyme, or there may be other as yet not understood reasons.

Eyes: Convergence or Homology?

Have the structural similarities among eyes resulted from evolutionary convergence due to similar selective pressures (analogous) or from descent from a common ancestor (homologous)? This distinction is particularly hard to draw when comparing eyes because the physical laws governing light greatly restrict the construction of eyes. Similar eye structures may have arisen in unrelated animals simply because of constraints imposed by light.
The most commonly cited example of evolutionary convergence are the eyes of squids and fish. Both of these are 'camera-type' eyes, in which an image is formed on the photosensitive retinal layer at the back. Moreover, both have evolved a spherical lens with an exquisitely constructed gradient of refractive index that allows good focus despite their spherical shape. In addition, both types of eyes use the same light-sensitive molecule, opsin, to convert photons into neural energy. However, the fish retina is inverted, meaning the light-sensing cells are at the very back of the eye (inverse) while those in squid are at the front of the retina (everse). Moreover, the parts of the eyes of fish and squid arise from very different embryological sources during development, suggesting different origins for these eye types.


Paired eyes in the three major phyla, vertebrates, arthropods and mollusks (fig. 4), have long been considered to be classic examples of evolutionary convergence. At the macroscopic level, this must be true since they arise from different tissues and have evolved radically different solutions to the common problem of collecting and focusing light. However, as discussed above, opsin has a significant DNA sequence homology across all phyla. Remarkably, recent work by Gehring and Ikeo has shown that features of ocular development in different phyla can be coordinated by a homologous 'master' gene, Pax-6. That a single gene could trigger construction of an animal's eye in diverse species led to their proposal that eyes are monophyletic, i.e. evolved only once. This is an interesting hypothesis that goes against all the previous suggestions of multiple (i.e. polyphyletic) origins for eyes. There are several reasons why this hypothesis seems difficult to support. It is well known that Pax-6 organizes other structures besides eyes and is even necessary for the onset of various actions outside the nervous system. Also, other genes can cause development of eyes [reviewed in 10]. Whether eyes are monophyletic or not, the work of Gehring and his colleagues has stimulated a great deal of new work on eye evolution, which is a good thing in itself.


Clearly, eyes have common molecular constituents whether they be opsins, Pax-6, or others. Yet, homology at the molecular level of organization does not predict homology at the organ or organismic level. Molecules are not eyes.

Conclusions

Eyes exist in a variety of shapes, sizes, optical designs and locations on the body, but they all provide similar information about wavelength and intensity of light to their owners. Different tissues have been recruited to build lenses and retinas across the phyla. In contrast, all eyes share the same mechanism of absorbing photons, i.e. the opsin-chromophore combination has been conserved across phylogeny. Despite new findings yielded by powerful molecular techniques, all evidence still suggests that eyes have a polyphyletic origin, with the caveat that they contain homologous molecules responsible for many structural, functional and even developmental features (fig. 5). Given a growing list of homologous gene sequences amongst molecules in the eye across vast phylogenetic distances, the challenge is now to discover what makes the eyes of Drosophila, squid and mouse so different. Since strictly homologous developmental processes must produce homologous structures, key elements responsible for the development of nonhomologous eyes remain missing. Understanding what makes eyes different may be a bigger challenge than finding what they have in common.

10 Weirdest Medical Syndromes

1.Sexsomnia is a disorder in which people participate in sexual acts (either solo or with a partner) while sound asleep. It is classed as one of many parasomnias, which also include things like sleep-walking and talking. Though this is a relatively new syndrome (officially identified in 2003) it has already been accepted as a defense against some alleged rape cases.

2.Trimethylaminuria is a rare metabolic disorder that causes a defect in the normal production of a specific enzyme. Long story short, when the body can't break down trimethylamine during food digestion, the compound builds up and is released in the person's sweat, urine, and breath, giving off a strong fishy body odor. 


The odor varies from person to person; in one, it will just smell like terrible body odor, but in most people it gives off a noticeable pungent fish odor


3.Exploding Head Syndrome is a parasomnia disorder that causes sufferers to hear loud, explosion-like noises that seem to originate from within their own head. The "explosions" usually occur right after the victim has fallen asleep and sound like a roar, gunshot, loud voices or screams, a ringing noise, or the sound of electrical buzzing. 


While victims of this syndrome aren't physically injured, they tend to experience fear and anxiety after such attacks. There is no known cause or cure for this condition, though it has been linked to stress and fatigue and often vanishes without treatment.

4.Foreign accent syndrome (FAS) is a speech disorder that is often a side effect of severe brain injury, such as stroke or head trauma. FAS causes sudden changes in speech patterns, intonation and pronunciation so that the victim suddenly starts speaking with a "foreign" accent. FAS typically develops within one or two years after the injury and is often incurable.

5.Non-24 is a chronic circadian rhythm sleep disorder defined as "a chronic steady pattern comprising one-to-two-hour daily delays in sleep onset and wake times in an individual living in society." The pattern of delay persists "around the clock," taking several weeks to complete one cycle. This disruption of the body clock causes cyclical bouts of nighttime sleeplessness and excessive daytime fatigue and napping. 


It is a neurological sleep disorder that has been traced to genetic abnormalities that affect specific factors in the brain. While anyone can be diagnosed with Non-24, the disorder affects proportionately more totally blind individuals than sighted.

6.People who suffer from Genital Retraction Syndrome (GRS) are overcome by the fear that their external genitals (and the breasts, for women) are shrinking and/or retracting into the body to the point of complete disappearance. GRS is a mental condition prevalent in cultures that are often without sufficient medical resources and who attribute the condition to voodoo, witchcraft, or superstition. In Asia and Africa there have been widespread instances of this syndrome called "Penis Panics."

7.Gourmand syndrome is a rare condition that sometimes occurs in people who sustain injuries to the right frontal lobe. These people develop a new, post-injury passion for gourmet food. Lesions or injuries to this specific portion of the brain cause an intense preoccupation with food and a preference for fine eating. 

The condition is considered "benign" or not harmful, but it sounds pretty painful for the wallet.

8.People who suffer from Cotard's Syndrome have the delusional belief that they are dead, do not exist, are putrefying, or have lost their blood or internal organs. There may also be sensory hallucinations, for instance, they might think that they smell of rotting flesh. The disorder tends to occur intermittently rather than being chronic and may be a feature of mood disorder, schizophrenia or organic disorders

9.Since the main symptoms of this lifestyle syndrome are forgetfulness and lack of concentration, we're pretty sure we all have it. According to researchers: “Forgetfulness is an ordinary part of getting older but anecdotal evidence suggests that it is now affecting people earlier in life as a result of busy work and home lives, and so-called 'information overload' from the various media channels we consume today,” lead researcher Dr. Alan Wade said. 


The recommended treatment is a drug called memantine, which is also used to treat Alzheimer's Disease

10.Moebius syndrome is a rare neurological disorder that is present at birth. People with the condition are unable to move their faces (they can't smile, frown, ^*&^*, grimace or blink their eyes) and are unable to move their eyes from side to side. There may be skeletal problems as well, causing hand/feet anomalies such as club feet. Respiratory problems, speech and swallowing disorders, visual impairments, sensory processing disorder, sleep disorders, and weak upper body strength may also be present. Approximately 30% of children with Moebius syndrome are on the autism spectrum.