Post MRCS Part B

So I finally sat the OSCE on thursday and it was a very passable exam although I think I screwed up 2-3 of the stations and thus may lead to my failing the exam. However, results aren't till the end of June so I can still try and be mindlessly optimistic.

Anyway, for all those considering sitting the exam this winter (which will very likely include my self), I shall endeavour to give you as many tips and advise as necessary using my experiences. Over the next few weeks, I shall blog about the format of the exam, the level of detail questioning required as well as books, courses and other revision aids.

Firstly, the exam involves 18 stations in addition to two 10 minute rest stations whereby you sit by yourself in a cubicle and one twenty minute rest station separating the exam in two and during which everyone who has sat the same stations gathers and has tea. Of the 18 stations these are divided as follows:

1) Anatomy and pathology:
1x speciality anatomy station
2x generic anatomy stations
1x generic pathology station

2) Communication skills:
2x history on speciality topics
1x generic history
1x explain something to patient/relative (also has a 9 minute prep station whereby you read the notes)
1x communicate with a colleague over the phone (also has a prep station whereby you have 9 minutes to read notes and prepare)

3)Clinical skills and patient safety:
3x speciality topics- physical exam
1x generic system- physical exam
2x procedure e.g gloving/cannulation/blood cultures/excision of lesion

4)Critical care and physiology
1x manned station with imaging/results for interpretation
1x 2 manned station with a scenario and viva on critical care
1x manned station and viva on physiology and critical care

Ok so that's me done for now but watch this space for further info in the coming days and weeks.

Amel

Question 2

2. The vertebral artery is the most important branch of the subclavian artery. It ascends through the upper six cervical foramina to enter the foramen magnum where it joins with the vertebral artery from the opposite side to form the basilar artery anterior to the pons. Which structure divides the subclavian artery into three parts?
a. Pectoralis minor
b. Teres Major
c. Scalenus Anterior
d. Scalenus medius
e. First rib

Answer to previous question

1. A 40 year old male motorbike rider is brought into the A&E department following a collision with a lorry. An urgent laparotomy reveals a severely damaged spleen, and pancreas. Major arterial supply to the pancreas is derived from the…..
a. Left gastric artery
b. Splenic artery
c. Right gastric artery
d. Hepatic artery
e. Gastroduodenal artery

Answer: Splenic artery

Major blood supply to the pancreatic body is derived from the arteria pancreatca magna (aka greater pancreatic artery). It is a branch off the splenic artery as it travels superior to the pancreas towards the splenic hilum. Prior to entering the splenic hilum, the splenic artery gives off approximately 6 pairs of short gastric arteries, and forms the left gastroepiploic artery which anastomoses with the right gastroepiploic/gastro-omental (branch of the gastroduodenal artery) to supply the greater curvature of the stomach and the omentum.

The arterial supply to the head of the pancreas is derived from superior (branch of the gastroduodenal artery), and inferior (branch of the superior mesenteric artery) pancreaticoduodenal artery.

Left gastric artery supplies the distal oesophagus, and anastomoses with the right gastric artery (branch of the common hepatic) to supply the short curvature of the stomach.

Hepatic artery arises from the common hepatic artery distal to the origin of the gastroduodenal artery and right gastric artery. Hepatic artery ascends to the left of the common bile duct and anterior to the portal vein to enter the portahepatis; where it divides into left and right to supply the respective lobes of liver. The right hepatic artery gives off the cystic artery which supplies the gall bladder.

MRCS Part A approaches

MRCS part A is about a week away, and about the time when panic spreads like wildfire amongst candidates. Our plans to get the website up and running by this month has hit major setbacks due to various work commitments, however rest assured we are working hard on it. 

As a taster; I will be posting one question a day for the next week only till the website becomes online. The questions are of course written by me, and various sources have been consulted to ensure upto date answers are given. What you will see is that the explanation i shall give to the questions are not like the ones you are used to in other questions banks, but they will have complete explanations to explain why one answer is more correct than the other. Please leave feedbacks, as this will help us improve our standards and formats. 

Anatomy

1. A 40 year old male motorbike rider is brought into the A&E department following a collision with a lorry. An urgent laparotomy reveals a severely damaged spleen, and pancreas.  Major arterial supply to the pancreas is derived from the…..

1. Left gastric artery

2. Splenic artery
3. Right gastric artery
4. Hepatic artery
5. Gastroduodenal artery

The answer will be posted tomorrow. Good luck

Romesh

Basic surgical skills course

Apologies for delay in postings. Completed the basic surgical skills course at Queen Elizabeth hospital last week. It was the first time the course has been trialled to run over 2 days outside the Royal College of Surgeons (normally 2.5 days). This of course meant earlier start (8am), late finish (1800), and shorter lunch break (30mins). Of course any surgical doctors will agree the above timetable almost feels like a holiday.

The course content was not altered in anyway,and there were plenty of time allowed to complete all the tasks. At the end of the course, 100% of participants preferred the 2 day course over the 2.5 days as it meant less annual leave/study leave were required to complete the course.

Having completed a similar course as an undergraduate (instructed by Mr Paraskeva at Imperial college), i found it relatively straightforward course, and it greatly helps if the candidates are familiar with the 'Reef knot'.

I particularly enjoyed the 'debridement of necrotic tissue' part of the course, as well as stacking the sugar cubes using laparascopic instruments in a box trainer. I was slightly dissapointed with my 'tower of 8', as the 9th cube slipped from the grasper and then  ricochet off the sidewall and flattened my hard work.

Although the basic surgical skills course deals a low blow to the bank balance (currently ranging from £650-£700), If the 2 day course is implemented it might mean a reduction in cost. However, the course it self uses up a lot of resources including many consultant's time who have to give up their clinic/theatre list in order to tutor the trainees.

In summary, a very useful and a thoroughly enjoyable course that is not just for surgeons, but for any medical professionals who perform minor surgery (GP, Dermatologist, A&E etc).

The courses are usually very popular, and sell out months in advance, so i recommend contacting centres at the earliest oppurtunity to reserve your place.

Please visit the royal college of surgeons website for more information regarding the course http://www.rcseng.ac.uk/education/courses/basic_surgical_skills.html?searchterm=bss

Romesh

Physiology of The Respiratory System III: Blood flow, Gas exchange and the regulation of Ventilation

Thank you for still sticking with us, I know respiratory physiology isn't everyone's cup of tea but it is essential to know the basics as they frequently come up in exams. So in this final blog on the matter, I'll give an overview of the important concepts goerning blood flow, gas exchange and reglation.

Blood Flow
A good understanding of pulmonary anatomy will be useful to tackle this bit. Pulmonary blood flow is regulated by levels of pCO2 and pO2. Hypoxia or hypercapnia result in vasoconstriction which allows blood to be diverted to better oxygenated areas (this is called hypoxic vasoconstriction). Flow is determined by perfusion pressure and resistance. The three pressures that determine blood flow in the lung are:

1. Hydrostatic pressure in the pulmonary arterioles
2. Pressure in the pulmonary veins
3. Pressure of air in the alveoli

The blood flow in the lung can be divided into zones:

1. Zone 1: this is the apex of the lung. Blood flow is low in this region as alveolar pressure is similar to pressure  in the pulmonary arterioles so smaller vessles become compressed. 
2. Zone 2: here the pressure in the arterioles is higher than alveolar pressure so blood flow is better.
3. Zone 3: The pressure in the arterioles is at its greatest in comparison with the pressure in the alveoli thus blood flow is highest here. This area corresponds with the bases and explain why vasculitic disease affects the bases.

Ventilation and Perfusion
The ventilation to perfusion ratio varies through out the lung and depends on the pressure in the arterioles:

• V/Q = infinity in alveoli that are ventilated but not perfused.
• V/Q = zero in alveoli that are perfused but not entilated.
• At the apex, V/Q = 3 which means that the alveoli are ventilated better than they are perfused. Whilst at the bases V/Q = 0.6 which indicates that the alveoli are perfused better than ventilated. 
• The ideal V/Q is found 2/3 of the way up the lungs.

 Gas Exchange
The diffusion of gases is affected by:

1. Pressure gradient: this is the partial pressure and involves the flow of air from an area of high pressure to lower pressure
2. Diffusion coefficient: this is the ease with which a gas can diffuse and is determined by its solubility in water as well as molecular weight.
3. Tissue factors: the tissue at site of diffusion should have a large surface area and short diffusion distance.

Sysemic venous blood is pumped into the pulmonary arteries from the right ventricle. This blood has a pO2 of 5.3 kPa and pCO2 of 6 kPa whereas alveolar pO2 is 13.7 and pCO2 is 5.3.  Thus oxygen will diffuse into the bood as it has a lower partial pressure whilst carbon dioxide will diffuse into the alveoli. This results in oxygenated blood transported back to the heart via the pulmonary veins. Physiological shunting (passage of blood through the lungs without going through the alveoli) occurs as bronchial blood mixes with the oxygenated blood therefore the partial pressure of oxygen in systemic blood is lowered to 13kPA. Pathological causes of shunting include pneumonia, ASD, VSD and Patent ductus arteriosus.

Oxygen is predominantly transported by haemoglobin and only a miniscule amount is dissolved. The oxygen dissociation curve shows the relationship between the partial pressure of oxygen and the concentration of oxygen in the blood. The position of the curve is altered by several factors:

1. Right shift decreases oxygen affinity thus oxygen is released at higher partial pressure. This is caused by raised temperature, increase in levels of 2,3-diphosphoglycerate (2,3-DPG) and increased H+. Right shift of the dissociation curve is called the Bohr effect.
2. Left shift increases oxygen affinity and thus oxygen is released at lower partial pressure. 

Foetal Haemoglobin and Myoglobin
Adult Hb has two alpha and two beta chains whilst foetal Hb has two gamma chains as well as two alpha. The change in globin chain results in greater affinity for oxygen thus allowing the foetus to extractblood from the maternal circulation. The curve for HbF is to the left of adult Hb as there is greater affinity for oxygen. Myoglobin has an even greater affinity for oxygen and so its curve is even further to the left as it is an oxygen storage molecule which only releases O2 when the partial pressure has dropped significantly. The function of myoglobin is to provide additional oxygen during anaerobic respiration.


Carbon Dioxide
CO2 is transported in three ways:

1. Carbamino groups which are formed between CO2 and proteins/peptides. 
2. Dissoved
3. HCO3- makes up arund 70% of transported carbon dioxide. It forms when carbon dioxide diffuses into red blood cells and reacts with water to give carbonic acid which dissocites to H+ and HCO3-. The H+ binds haemoglobin and the bicarbonate diffuses into the plasma. The reverse of this process occurs in the alveoli (bicarb diffuses into the cell to produce CO2 which can be expired).

The CO2 dissociation curve differs from that of oxygen as it has no plateau phase as blood can not become saturated with CO2, carbon dioxide is far more soluble than oxygen and the normal rnge for CO2 is narower (5.3-6kPa). The curve is influenced by partial pressure of oxygen thus the amount of CO2 carried increases as oxygen levels fall (this is called the Haldane effect).

Regulation

• Neurological: this occurs via the medulla oblongata, Pons, cerebral cortex and Limbic system. In the medulla inspiratory neurons rhythmically fire action potentials which stimulate the diaphragm and external intercostals to contract this is followed by intervening periods of inactivity when expiration occurs. Expiratory neurons in the medulla are inacive during quietrespiration but during increased respiration fire action potentials to stimulate the internal intercostals and abdo muscles to contract thus producing forced expiration. In the pons, the apneustic centre prolongs inspiration and reslts in short expiratory efforts whilst the pneumotaxic centre inhibits inspiritory neurons to shorten inspiration. Neither of these centres are essential for respiration. The cerebral cortex can override neurons in the medulla to increase ventilation or reduce it/hold breath. Finally, in extreme emotional states, the limbic system may influence respiration.
• Chemical: central and peripheral chemoreceptors monitor changes in arterial PCO2, pH and PO2. Central chemoreceptors are found in the CNS close to the resp centre in the medulla and are especially sensitive to changes in pCO2. As CO2 diffuses into the blood in the brain, it reacts with water to give H+ which causes a fall in pH. This fall stimulates the central chemoreceptors which increases the resp rate in an attempt to blow off CO2. The opposite occurs with low CO2. Peripheral chemoreceptors are located in the carotid bodies and are less important than central chemoreceptors. They respond to changes in arterial pH and low levels of pO2. Thus a fall in arterial pH due to metabolic acidosis will stimulate respiration and thus lower the level of CO2 to bring pH back to normal. The response to low oxygen is only seen when pO2 is less than 8kPa. The importance of this mechanism is witnessed in chronic lung disease whereby persistently elevated carbon dioxide levels cause the patient to become accustomed to it and thus lose the effect low pCO2 has on chemoreceptors. Thus they rely on low levels of pO2 to stimulate respiration and is called the hypoxic drive. 

Hypoxia, hypoxaemia and respiratory failure
Hypoxia is a reduction of oxygen in the tissues and is classified as:

1. Hypoxic hypoxia: due to low arterial pO2 and caused by high altitude, PE, hypoventilation, lung fibrosis and pulmonary oedema.
2. Anaemic hypoxia: decrease in amount of haemoglobin which leads to a decrease in oxygen and is due to haemorrhage, reduced red cell production, haemolysis and carbon monoxide poisoning.
3. Stagnant hypoxia: due to low blood flow which maybe due to vasoconstriction or reduced cardiac output.
4. Histotoxic hypoxia:  this occurs when the enzymes involved in cellular respiration become poisoned and thus are unable to use oxygen. The main cause of this is cyanide poisoning.

Hypoxaemia is a reduction in the concentration of oxygen in arterial blood. It is caused by:

1. Hypoventilation: this may result from CNS depression, trauma, neuromuscular disorders and chest wall deformity. It may be treated using oxygen therapy.
2. Impaired diffusion: this can be caused by asbestosis, sarcoidosis and ARDS. It maybe treated by oxygen therapy.
3. Shunt: this is not improved by oxygen therapy.
4. V/Q mismatch: this usually occurs in chronic lung disease and results in mismath between ventilation and perfusion.
5. Reduction in inspired Oxygen tension

Respiratory failure is present if PaO2<8kPa and is subdivided into:

• Type I: PaCO2 < 6kPa and is due to ventilation-perfusion mismatching. The PaCO2 is normal or low as the increase in ventilatory rate results in compensation by remaining alveoli for any increase in CO2. Causes of Type I resp failure include pneumothorax, pneumonia, contusion, PE and ARDS.
• Type II: PaCO2 > 6kPa. This is largelydue to hypoventilation and caused by COAD, neuromuscular disorders, airway obstruction, central respiratory depression and chest wall deformity.

Well that's it for respiratory physilogy, hope it was useful.

Amel

Physiology of The Respiratory System II: Lung Function Tests

The assessment of lung volumes is important in dignosing respiratory disease and monitoring progression. Spirometry is used to measure lung volumes. It is important to know the definition of each lung volume in order to be able to intepret spirometry findings and their relevance:

• Tidal Volume (TV): air breathed in and exhaled during quite respiration
• Inspiratory reserve volume (IRV): maximum volume of air that can be inspired on top of normal inspiration
• Expiratory reserve volume (ERV): maximum amount of air that can be forcefully expired after normal expiration
• Functional residual capacity (FRC): volume of gas left in the lungs after expiration during normal breathing. This can be determined using the helium dilution method. This involves the patient breathing normally from a spirometerfilled with a known volume of helium and air thus as they breath in and out, the helium is diluted into the air that is left in the lungs 

FRC = (initial helium concentration of spirometer) x Volume/(final helium concentration) 

• Residual volume (RV): volume remaining after maximal expiration. It can't be measured directly but is calculated as RV= FRC - ERV
• Total lung capacity (TLC): the sum of all volumes plus the residual volume
• Vital capacity (VC):volume of air expelled from maximal inspiration to maximal expiration

Dead space
The concept of dead space is important to grasp as this is the volume of air which does not take part in gas exchange. The are two types:

1. Anatomical: the volume of gas which does not mix with air in the alveoli. It can be determined using Fowler's method. This involves the patient breathing through a tube connected to a nitrogen analyser. The patient initial takes a single breath of pure oygen, holds their breath for several seconds and breathes out. This will determine deadspace as only the alveoli will have maximal concentrations of nitrogen whilst the higher up airways will have purer concentrations of oxygen as they did not participate in gas exchange. Thus if a curve is drawn, air initially expired will not have nitrogen as it is part of the anatomical deadspace whilst nitrogen concentrations will increase as alveolar air is expired.
2. Physiological: this is the volume of gas that reaches the alveoli but due to a lack of perfusion does not take part in gs echange. It can be determined using the Bohr equation

Volume of deadspace= Volume expired CO2(1-(Fraction of expired CO2/Fraction of alveolar CO2))

Alveolar Ventilation rate
This is the rate at which gas exchange occurs in the alveoli.
Alveolar ventilation rate= (TV-dead space) x Respiratory rate

Peak Expiratory Flow rate
This is a cheap and simple test that can be performed at the bedside. A patient is asked to take a maximal inspiration and then blow out as fast as possible into the peak flow meter. It is useful in assessing the severity of asthma attacks and monitoring treatment.

Closing Capacity
This is the volume of the lungs at which airways at the base of the lung start to close. It is normally 10% of vital capacity and can be assessed by getting the patient to breath a maximal inspiration of 100% O2 then expiring fully through a nitrogen analyser. A graph can be plotted which will show 4 phases:

1. Pure dead space is exhaled so its 100% oxygen
2. a mixture of deadspace and alveolar gas (increasing concentration of nitrogen)
3. pure alveolar gas (reaches a plateu)
4. abrupt increase in nitrogen as airways at the base of the lung close and therefore not participating in gas exchange so the expired air is coming from the apex which has received less oxygen thus the nitrogen is more concentrated.

 Factors that affect the closing capacity include increasing age, supine position and anaesthesia which increase it.

Diffusion Capacity
This tests the diffusion capacity of the alveolar membrane and pulmonary vasculature. It is measured by inhaling small amounts of carbon monoxide and measuring its levels in the blood.Diffusion capacity is most commonly reduced in pulmonary oedema (as diffusion distance is increased) and emphysema (causes loss of alveolar surface area).

Flow-Volume and Volume-Time Curves
These can be plotted using spirometry results and are important because certain pathological processes such as obstructive lung disease cause typical curves.

Well that's it for now from me. Watch out for the third and final respiratory physiology tutorial. By the way if there are any specific topics you'd like us to cover/discuss just leave a comment/send an email and we'll get on to it.

Amel