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!
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