Search This Blog

Sunday, October 28, 2012

Crash Course short cut to passing MRCOG part 2

This is my newest promotion of my materials in this purchase you get all you need to memorize to pass the exam. It contains Corrected answers and explanations to the past papers. Explanations hand written by myself and each and every true false answers rechecked on pubmed,google,emedicine and journals, etc for the latest updated answers for the past papers.This is most important because everywhere else the answers provided are 30-40% wrong , for example the one selling on lulu.com! completely rubbish. This one is 100% correct and it took me 1 and half years to compile this . Real emq questions that appeared in previous exams. And a compilation of all questions mcq,emq, essay in the recent years And valuable gurantee scoring technique for passing the essays.
I have cut down the price of this from 3800USD to 1200USD as now i have decided to provide everything on the site along with this purchase. I will continue to add files to these files. Please keep in touch by email after purchase , i will list all my buyers of this file down to a mailing list that i will be given new additional goodies for free over time. to buy my whole compilation which will give u the best chance at passing mrcog click on the link below after payment u will be automatically be redirected to oronjo.com to download my materials

shortcut to passing mrcog part 2 . Crash course of only the things you require to pass.


thanks i know what your going through this is the hardest exam and obstacle you will ever encounter in your life but its well worth it trust me because im already there good luck another tip when talking to patients when breaking bad news during osce never say u understand what they are going through the actors are instructed to shout at u and say how could u ever understand its never happened to you!!! i learned this through the hard and embarassing way instead say i cant even begin to imagine what position u are in right now , it must be hard for you !!

Thursday, January 26, 2012

EMQ past year 2008-2011

These are emq questions that appeared in the exam between 2007-2010. I paid a lot of money to get these from a pakistani guy who sat the exam 5 times and has passed his theory every single time but failed his OSCE. He has given up since. Now how the hell did he do that? Same way how 90% of whites passed. As opposed to asians who are unexposed. Cos HE KNEW WHAT CAME OUT in the exam. However you cannot cheat the examiners when it comes to OSCE's. But what U need NOW is to pass this paper where 90% asians fail and give yourself a better chance with a 75% pass rate for the OSCE's. These questions are photos taken with an Iphone. Some are a bit blurry but most are extremely clear i suppose under the pressure and stress of taking these photos...

sample





2008 EMQ click below







Past EMQ 2009 click below







past emq 2010 click below




Monday, January 2, 2012

latest REAL past mrcog exam questions March and September 2011

these are the real exact questions that came out in march and september 2011. Recollected from the exam. Written down immediately by my friends and i right after both exams.These questions are new questions in the RCOG bank and never seen before . Having seen these questions i can assure you that you will never had come across these questions in any other book . Now how are you going to get the right answer if you have never seen such questions before?? As i said , the only way to pass this hardest exam with the highest suicide rates in the world, is to know what is coming out for the exam. Knowledge of O&G is to broad. Your brain is like a book shelf. If you overload it with new books, the older ones will drop off! You cannot remember everything as knowledge in O&G is so broad. Its like an ocean of fishes,You need to have seen those fishes before to recognise them. Now the exam has only a few fishes that you need to know. How are you going to remember those fishes when you have filled your limited brain with every single species in the ocean??? Stop kidding yourself. Be sensible . You cannot study everything. In fact you shouldnt. You need to study just what is coming out to score.

This download consist of the mcq and emq's that came out during March and September 2011 exam.
for a limited time i will send u everything on site after you purchase these (email me after purchase or include request in paypal comment)

latest exam past paper march & september 2011
latest exam past paper march & september 2011


past paper 2 course . first ever explained and corrected answers

I found out why so many people keep on failing this exam. Its because the answers available to the past papers are at least 40 % wrong . I have corrected these answers and add on references and detailed explanations so you don't need to spend a year looking for these answers like i did.
Do you know that every question published in the past papers was based on a particular study ? And how many questions are there in all these papers??
The only way to pass this hardest exam in the world with the highest number of suicides is to KNOW WHAT IS COMING OUT IN THE EXAM.

so here is a preview of whats in the book

March 1997
?Achondroplasia:
1. Is the most common lethal chondrodysplasia. (F)
2. Can be excluded by a normal femur length measured by
ultrasound at 18 weeks of pregnancy. (F)
3. Is associated with polyhydramnios. (T)
4. Is not associated with mental retardation. (F)

It is not the most common lethal condrodysplasia. Usually intelligence is normal but in some cases it is associated with mental retardation




?Phenytoin:
1. Is best administered by intramuscular injection. (F)
2. Has a short biological half life. (F)
3. Is rapidly absorbed from intestinal tract. (T)
4. Is metabolized by the liver. (T)
5. is rapidly absorbed in the GI tract (T)
6. associated with hirsutism (T)
7. Toxicity with ataxia (T)
8. long plasma half life (T)
9. Effective for petit mal epilepsy (F)

Phenytoin toxicity include ataxia, vomiting , arrythmias and has a half life of 22 hours.




?Neonatal jaundice appearing on the 3rd day and still present at
2 weeks of age may be due to:
1. Haemolytic disease of the newborn due to rhesus
incompatibility. (F)
2. Galactosaemia. (T)
3. Phenylketonuria. (T)
4. Neonatal hyperthyroidism. (F)

NEONATAL JAUNDICE
________________________________________
NEONATAL JAUNDICE
? Occurs when serum bilirubin > 80 micromol/L
? Bilirubin is formed from the breakdown of heme, bound to albumin and transported to the liver where it is conjugated by the enzyme glucuronyl transferase and excreted in bile. Conjugated bilirubin is water soluble
? About 0.1% of unconjugated bilirubin is unbound and available to cross the blood-brain barrier
? There is transient immaturity of the glucuronyl transferase system in the neonate, especially in the pre-term neonate
? Jaundice progresses from face to feet
? Prolonged unconjugated hyperbilirubinaemia may occur in the breast-fed neonate
Physiological
? Transient rise in serum bilirubin in all neonates, 30-50% of term neonates are jaundiced - unconjugated
? Peak concentration on day 3 in term neonate and day 5 in pre-term. Cleared by day 10. Does not present within the first 24h of life
? Caused by high haematocrit, shorter life-span of red cells, immature hepatic enzymes and increased entero-hepatic circulation
OTHER CAUSES OF UNCONJUGATED HYPERBILIRUBINAEMIA
? Increased incidence with prematurity, bruising, instrumental delivery (RCTs show no difference in need for phototherapy between ventouse and forceps delivery), breastfeeding, polycythaemia
? Urinary tract infection, Hypothyroidism Galactosaemia, Fructosaemia cause prolonged unconjugated hyperbilirubinaemia
? Cold stress, respiratory distress syndrome or respiratory failure and neonatal hypoglycemia contribute to pathological levels of bilirubin by interfering with albumin binding of bilirubin
? Oxytocin and other drugs such as diazepam, sulphonamides, steroids, and salicylates compete with bilirubin for binding sites, rendering elimination difficult and are associated with increased risk of neonatal jaundice
Haemolytic
? Caused by Rhesus disease, ABO haemolytic disease of glucose-6-phosphate dehydrogenase deficiency, hereditary spherocytosis, pyruvate kinase deficiency, polycythaemia, TTTS, haemoglobinopathies
? Usually presents in the first 24h of birth
? Unconjugated bilirubin crosses the blood - brain barrier causing kernicterus - basal ganglia involved, athetoid cerebral palsy + deafness Fits / Opisthotonus / neonatal death
? Risk of kernicterus increased in extreme prematurity, sepsis and acidosis
? Jaundice is treated by phototherapy or exchange transfusion - decision should be based on unconjugated bilirubin concentration rather than total bilirubin concentration
Jaundice is pathological if
? Conjugated
? Marked jaundice (bilirubin > 250-300micro mol/L)
? Prolonged (>10 days term / 14 days pre-term infant)
? Occurs in first 24h
? Associated with other illness
Worldwide, Glucose-6-phosphate dehydrogenase deficiency is the most important cause of pathological jaundice - X-linked recessive.
CAUSES OF CONJUGATED HYPER-BILIRUBINAEMIA
? Sepsis - hepatitis caused by CMV, toxoplasmosis, herpes, syphilis, rubella
? Biliary atresia
? Cystic fibrosis
? alpha-1antitrypsin deficiency
? Choledochal cyst
? Prolonged TPN
Conjugated bilirubin does not cross the blood-brain barrier and therefore does not pose a risk of kernicterus




?Analysis of a sample of amniotic fluid obtained by
amniocentesis assists in the diagnosis of:
1. Tay - Sachs disease. (T)
2. Congenital adrenal hyperplasia. (T)
3. Spina bifida occulta. (F)
4. Oesophogeal atresia. (F)

Amniocentensis cannot diagnose neural tube defects
There are two types of NTDs: open, which are more common, and closed. Open NTDs occur when the brain and/or spinal cord are exposed at birth through a defect in the skull or vertebrae (back bones). Examples of open NTDs are anencephaly, encephaloceles, hydranencephaly, iniencephaly, schizencephaly,and spina bifida. Rarer types of NTDs are called closed NTDs. Closed NTDs occur when the spinal defect is covered by skin. Common examples of closed NTDs are lipomyelomeningocele, lipomeningocele, and tethered cord.




The following disease are inherited as autosomal recessive
traits:

1. Pseudohypertrophic (Duchenne) muscular dystrophy. (F) - xlinked recessive
2. Cystic fibrosis. (T) - Autosomal recessive
3. Haemophilia. (F) - X-linked
4. Phenylketonuria. (T) -autosomal recessive
5. Congenital spherocytosis. (F) -autosomal dominant



Factors predisposing to maternal pulmonary aspiration of
gastric contents during labour include:

1. An increase in gastric motility. (F)
2. The effect of progesterone on the cardiac sphincter. (T)
3. Epidural analgesia. (F)
4. The use of muscle relaxant. (T)

This is just common sense


past papers mrcog part 2 corrected answers , explanations and references to the explanations. Also some tips to score >60% without any knowledge!
!