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

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!
!

Part 2 mcq & emq recollection

Please post all the questions u can remember from part 2
Exam here

A few are as below

here is another valuable compilation of files

Here is another zip compilation of files my colleagues and i used for the exam
in this zip file contains a compilation off all the important rcog guidelines and tog guidelines so you dont have to download one by one . Also a compilation of all busy sprs osce, essays and notes.

sample osce:

Audit

Design an audit for the following protocol.
You are not expected to criticize the protocol.

Post dates protocol

Criteria for referral

Women seen in antenatal clinic at 40 weeks
Assessment in Day assessment unit from 41 weeks

All patients should be given a daily kick chart
If <10 movements between 9am to 9pm then patient should contact the Labour Ward to arrange CTG

Follow-up should then be arranged in the DAU

41-42 weeks
Twice weekly CTGs
Biophysical profile weekly
Check date for induction of labour at 42 weeks

>42 weeks
Admit
Record summary of findings, symptoms etc on a page(s) inserted in the antenatal in-patient part of the patient’s maternity notes booklet


The candidate needs to cover the following 5 areas of discussion and can be prompted by a specific question if he/she does not mention them spontaneously

Describe the key components of an audit
Which patients should have been managed by this protocol in the given time period
Would a x% sample be sufficient
Determine method of establishing whether each element in the protocol was followed for each patient
Ascertain the outcome
Analyse data including quantifying missing data
Consider sampling bias
See which items in the protocol had significant failures of compliance and try to assess why this occurred

Feed results back to departmental staff
Sensitively
Consider confidentiality
What reactions might be expected

Consider if organization changes are needed to facilitate/improve compliance
Resource implications
How to achieve consistent implementation

Consider if any elements of protocol require modification
Recent research data/College guidelines
Are pregnancy outcomes in line with national/regional norms
Has there been criticism of protocol by user groups

Decide when audit should be repeated
How long will it take for organizational/protocol changes to be implemented
If protocol is changed a second audit may not be comparable


Topic

Standard setting – literature search
RCOG/NICE guidelines
DOH guidelines
Previous audit (departmental/other hospital)
If no standard – may have to set own standard
(Mention recognized well-known standards if available e.g. National sentinel caesarean section audit)

Planning
Form audit team (stake-holders, user groups)
Involve audit department (especially to trace notes)
Decide whether retrospective or prospective
Design proforma
Data collection on structure, process, outcome?
Sample size (usually 50-100 cases)
Who to include?
Length (usually 3-6 months)
Audit team meeting to discuss proforma – any changes, improvement

Data collection
Who to collect?
Where to store? (Data protection act)
Use excel to store data

Data analysis
Results – whether standards achieved or not (are standards achieved in line with the standard set?)
If not achieved, what is the reasons

Analyse data including quantifying missing data
Consider sampling bias

Make recommendations if any, on:
Structure
Process
Outcome

Disseminate results
May need to be sensitive
May need to consider confidentiality
Audit meeting, departmental meeting, notice boards
Use power point
What reactions might be expected

Implement change
Barriers – resources (manpower, financial), individual “stubbornness”
Protocol revision/modification?
Any elements of the protocol
Any recent data/College guidelines
Any criticism of protocol by user groups/stake holders

Complete the audit cycle by reauditing
Allow some time for changes to take effect (? 6 months)
Is the audit proforma still applicable
If applicable - May need to change/review the audit protocol
If not applicable – need to do a new audit (i.e. especially after changing the protocol, a second audit (reaudit) may not be comparable)


Audit on a protocol
Given a protocol
How would you audit to see whether this protocol has been adhered to in your department? E.g. Protocol for management of 3rd and 4th degree perineal tear

Important : Then the standard is your protocol!!! You aspect it to be adhered 100%!
Audit to find out whether the staff is compliant to the protocol or are there any deficiencies.
If there are any deficiencies, then need to implement changes


Audit on e.g. excessive and unnecessary IOL in the department

Start by asking:
Is the rates really high?
Reasons if it is high
Who decides for IOL
Is the consultant involved in decision making
Who does the IOL

Compilation of important TOG and RCOG guidelines and busy spr osce,essay,notes

STOLEN questions MRCOG part 2

I have sat for the mrcog part 2 papers
Ive spent 250 pounds on the exam
250 pounds on busy spr website
250 pounds onexamination.com website
Have compiled the questions if any one wants to buy them email me or click the button below and i will sell u them at fraction of the price
I also have the past papers downloadedable version with answers from lulu.com also ill sell it to you for much less
The exam mostly came out questions from the past papers . Lulu.com is selling them by the name of the author which i believe is an imposter of the real khaldoun sharif from Birmingham. It is an illegal copy of the rcog press passpapers in a downloadable format but the answers they provide are all wrong. I have a copy of all the corrected answers and i will provide them together with your purchase.
I am willing to give all i have in a zip format busy sprs emq,onexamination mcqs and emqs, lulu pastpapers, and correct answers .
Tips for the exam-
Any advice to read the rcog guidelines and all the tog guidelines is a stupid advice because the human mind cannot retain so much information. And for example during this exam malaria in pregnancy only produce one emq question which was is mefloquine contraindicated in pregnancy - true of false and visitors from a malaria endemic country should continue prophylaxis for 8 weeks- true or false! Now this is a very small print stuff and stupid to read the whole guideline . Like finding and remembering the position of a needle in a haystack. My friends and i are compiling all the questions we remember and i will include it in your purchase. Mean all the emqs And mcqs in the march 2011 mrcog part 2 exam.
My advise on passing the exam .. Read as minimal as u can and only important things
Past papers -most useful all questions were similar just addition of new stems in the questions
Busyspr- only emqs useful and i have the full collection . All the options in the emq were exactly the same as the exam paper
On examination - useless
Reading tog - useless , better read my notes instead eg .u dont need to read the whole article on tog on botulinum toxin with urge incontinence if you knew that only one question came out in the mcqs that ask is botulinum toxin used in failed conservative management of urge incontinence dun waste your time
Rcog guidelines dont read everything . Read my compilation of the rcog bank to direct you to what is important and will coming out in the exam .

sample as below

Options for Questions 1-1
A Antihypertensive treatment B Insert central venous pressure line
C Intravenous magnesium sulphate D Measure serum aspartate transaminase immediately
E Measure serum magnesium F Transfer to intensive treatment unit
G Monitor patellar reflex every 15 minutes H Provide a fluid challenge with colloids
I Provide intravenous Hartmann's solution at the rate of 85ml per hour J Calculate the mean arterial blood pressure
K Immediate dose of 10ml 10% calcium gluconate intravenously L Carry out visual field assessment


Instrunctions:For each patient described below choose the single most appropriate initial treatment option from the list. Each option may be used once, more than once, or not at all.
Explanation
CVP is high and the woman is anuric with markedly raised serum urea = renal failure. Risk of multi-system organ failure and ITU treatment indicated

Respiratory depression suggestive of magnesium toxicity: 10% calcium gluconate

Question 1 A 20-year-old primigravida delivered a live infant 24 hours previously. She has developed severe gestational proteinuric hypertension. Treatment with intravenous magnesium was required. Her fluid balance is satisfactory and serum urea, electrolytes and clotting profile are all normal. Her respiratory rate falls to 6 per minute and she is drowsy but rousable. K(Correct answer: K)



Options for Questions 2-2
A Intravenous labetalol B Immediate delivery by caesarean section
C Intravenous magnesium sulphate D Measure serum aspartate transaminase immediately
E Measure FBC and clotting profile F Blood transfusion
G Immediate induction of labour H Provide a fluid challenge with colloids
I Antihypertensive treatment J Administer iv phenytoin
K Measure 24h urine protein excretion L Arrange in-utero transfer to tertiary centre


Instrunctions:For each patient described below choose the single most appropriate management option from the list. Each option may be used once, more than once, or not at all.
Explanation
Delivery indicated but need results from FBC and clotting profile before proceeding

BP not controlled by oral therapy: iv therapy therefore necessary

Question 2 A 35 year old woman remains in hospital 4 days after induction of labour and spontaneous vaginal delivery at 36 weeks gestation. She had developed severe gestational proteinuric hypertension and hypertension has been difficult to control post-partum. Her BP is 170/110 on oral oxyprenolol, nifedipine and captopril. She complains of a severe headache and her BP 15 minutes later is 180/110. Her blood tests taken earlier in the day are normal. A(Correct answer: A)
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