How to pass the international MRCGP OSCE cheat sheet

The OSCEs are standardized stations where specific history, examination and thinking skills are going to be assessed. The RCGP have provided for the international MRCGP five main areas or domains that are being tested for in the OSCEs. These are probably as equally applicable to the nMRCGP CSA section as well. To make life easier and, God Willing, help you pass try and learn what I call trigger phrases, these will trigger the examiner to record a tick in the particular domain that they are assessing you during the exam. If you do it well and have practiced, practiced and practiced then you should get a high score. One thing I recommend strongly is putting yourself under test conditions and get someone who has experience with the MRCGP to mark you, and video yourself and marl yourself and see how you can improve your technique and the flow of the consultation. In the following table I have listed a natural flow for a consultation and the key trigger phrases that you need to adopt. Of course your trigger phrase may be different to the one table but make sure it is triggering the right OSCE domain. All the best with your exams!

Patient consultation setting:

Introduce yourself

Verbal
Hi, I am doctor Abc.

Body language
Smile, nod, lean forward slightly to show interest but look professional

OSCE Domains
A: courtesy consideration

Take a history

Again nod you head and look as you are interested in what the patient has to say, look at the patient not anywhere else! Listen carefully Encourage the patient. You mentioned Listen for the cues, Hunt for the hidden diagnosis (pain/ walking the role playing if the history is nebulous or difficulty/ patients will give psychiatric. If the patient dizziness / thirst/ them and expect provides a problem assess chest discomfort / you to pick them their iedas by asking them breathing up! Remember the what they think is the cause, problems etc), can patients will be they might think eczema is you tell me a bit talking in contagious hence they are not more about it? laymans going out in which case you Is there anything language. can address their worries or else on your The actors will try correct through education mind? Are you and look their ideas. If after 1 minute worried about uncomfortable or you can see they are anything else? hesitate this is a rambling and they pause this [Concerns] What cue to a hidden is probably a heart sink do you think is agenda, they may

How can I help you today?

A: Full focused history

B: sensitivity to patient, facilitates free expression of ICE (ideas, concerns and expectations) C: Good communication skills E: Considers implications for the patient and others.

patient and you need to ask what their expectations are so you can work out what they want you to do?

You have a diagnosis in mind, think is anything serious, ask the important questions, red flags, things that will sift important from less important. Think red flags: Upper GI: weight loss, dysphagia. Lower GI: Change in bowel habits >6w Resp: Weight loss, sweating at night, cough >2 weeks. Cauda equine lesion: weaknes, bladder bowel control loss, pain raditing to tip of toe etc. Check the NICE fast track referral guidelines! Ask the socio-economic impact of the problem. Examine appropriately, dont do a full exam, concentrate on the bits you need, and dont miss postural hypotension if they are dizzy!

causing it? [Ideas]. What would you like me to do for you today? What would you like to see happen today? [Expectations] Back pain: Do you have numbness in between your legs. Any problems with passing urine such as difficulty controlling it? Clarify difficult questions. Is this affecting your life or work? Do you find it difficult to deal with the children?

avoid eye contact or say something like There was something else but its not important.

Use your fingers to demonstrate what you mean by in between. Try and use body language to help your questions.

A: takes a history sufficient to exclude a serious condition.

Diagnosis Make your diagnosis, and add 2 differentials if appropriate. If the diagnosis is obvious just state it and do not add differentials unless the patient asks could it be anything else. Dont forget to rule out any concerns that patient had said at the beginning. Dont forget to assess for understanding at the end by asking for any questions.

I would like to examine your back / hands is that okay? I will need you to (mention what you need them to do) Let me explain what I think, From what you have said and the exam I think you have A or B or C. I think A is likely but we will need to do some tests to work out if it is A or B or C. Let me explain what A is You mentioned

Pause after asking permission! Demonstrate the exam procedure if simple with your own body, i.e. position your hands etc.

A: Examines patient appropriately and efficiently.

C: Offers clear explanation of symptoms and diagnosis to the patient.

Management Start with the least expensive (show correct resource management), and offer a couple of options quickly explain the pros and cons of each and then hand over to the patient. Be prepared to negotiate i.e. I want CBT and medication say we have limited resources and we should try one and then the other

Summarise and Safety Net. Health promote tag this on here.

you were worried about skin cancer, I can reassure you that this is not related to skin cancer but is eczema. Do you have any questions? For the depression we can use talking therapies or medications or herbal therapies. Talking therapies work as well but take time, tablets work quickly while herbal remedies can work but can also be unpredictable. What would you like to do? Let me summarise so I am sure I have explained things well: You have depression. Well treat it with an anti-depressant which is one tablet per day. I would like to review in one week to see how you are getting along. If you have any problems dont hesitate to come back and see on the on call doctors or if it out of hours one of the out of hours services. Just one more thing I would like to add: have you had your cervical smear /

C: Negotiates management of patient. Involves them in decision. D: Treats and investigates appropriately, offers range of options, safe prescribing.

You could write down basic points on a sheet of paper and give them to the patient. Your prescriptions will be assessed so write fully and

do you smoke? (if they say yes) Could we please talk more about this, could you book an appointment in the next few weeks whenever is convenient?

MRCGP case list

If you have come across this page after Googling MRCGP cases or having asked me a question on the website then welcome. I have been asked this question many times and have often wondered what is the best way of tackling the question. My standard answer was to not prepare for specific cases and to think in general and to develop the skills set that the RCGP is looking for. But having thought about this more I have come to a slightly different conclusion: I feel a list of cases are actually extremely useful to the vast majority of candidates and videos of seeing good and bad candidates would be a very good way of preparing. But why did I change my mind? Most learners I suspect, sorry no evidence for this apart from my observations, need to have a real-life model which they then internalise and build up their own internal theoretical framework. The RCGP I think does not quite believe this or is worried that giving away a list of cases will render their exam ineffective and hence keep talking about confidentiality of the cases that doctors have seen. I think they are mistaken and should re-visit this frame of mind. So just give me the case list I hear you complain. Well it is a bit like the holy grail or the secret ingredient of Coca-cola as long as you have difficulty getting this secret list of cases you will keep searching and you will value it highly. This makes the MRCGP exam more highly valued whether that is an intended or unintended consequence I will leave you to conclude. I have found a list of cases but think just giving them will not be that useful without a full write up. So I have decided to set up a wiki to provide a collaborative document for people who have done the MRCGP to share their information. If you would like to collaborate please send me your email and some information about yourself and I will (God willing) add you on as a collaborator on the website. If you have not got enough time to read a huge case list then concetrate on the basic areas: 1. Paediatric case (Poor schooling, not growing well, bullying) 2. Elderly case (Deafness, dry eyes, falls, dizziness) 3. Chronic disease case (DM, IHD)

Womens health case (Contraception, PMB) Mens health (ED, LUTS) Infectious disease Case (TB, Pneumonia) Psychiatry case (Depression, GAD or OCD) Bad news (Cancer) Difficult patient (I want screening, I want my partner to be sterlised, Complain about your colleague etc.) 10. Drug problems (EOH, Side effects, hidden agenda) 11. Neuro (CTS, CVA) 12. MSK (Back, shoulder, knee, carpal tunnel, OA) 13. Skin (Eczema, psoriasis, fungal infection) 14. GI (IBS, change of bowel habit) 15. Resp (Asthma, COPD) 16. Joker (anything) 4. 5. 6. 7. 8. 9. If you stick to the basic method given here of asking questions getting information, exploring idea and addressing patients ICE then you should be able to deal with category 16. If you still want to read a list of cases then it will God willing be here: http://sites.google.com/site/mrcgpcases/ (

Ethics mnemonic iMRCGP ABCDE

In the i/nMRCGP you may get a patient that presents an ethical dilemma. The patient who has had a stroke and is now not fit to drive, should you breach your confidentiality and tell the authorities or not? A male patient who has come for a vasectomy because his female partner would like him to have one, they have one child. Is the patient acting autonomously, should you recommend this to the patient and so on. When dealing with these patients it is good to have a framework to hang your questons on and the outcome of your consultation. A simple menmonic is the following one: ABCDE which stands for: A Autonomy: Is the patient acting because s/he wants to do it or is someone else pushing them into this action? Are you being forced to act because of the patient demand (Give me this drug doctor! Response: You have the right to ask for the medication but I as a doctor have the right based on my professional judgement to prescribe or not, to force me would be to breach my autonomy) B Beneficence: i.e. do good and not harm. I could give just refer the patient for his vasectomy but has he thoought about if the marriage goes wrong and he starts a new relationship that the vasectomy is very difficult to reverse and he may not have children in the future? If I agree to prescribe this drug to this patient then will this set a trend in the future i.e. harming other doctors and the doctor patient realtionship. If I prescribe the most expensive drug always first am I causing harm to society and the exchequer? C Confidentiality Mother comes to speak about son, who is 19 an adult. You have to maintain confidentiality. You could breach it with the permission of the other i.e. son happy to talk about his case with his mother, but if you sense this is difficult what do you do? Stick

to keeping confidentiality in the abscence of permission. If two patients come together, you can always ask one to step out of the room for a short while, take permission from the other or ask any potentially embarassing questions: i.e. have you had sexual partners etc. D Duty : Duty of care to the patient, yourself (you do not have to be at the back and call of someone and you can let them know that there are certain procedures and hours and these should be followed), staff (sticking to general guidelines or working practices in your surgery), and society (resources, not misuring them etc.) E Equity Being equal with your resources between patients.

Should pregnant mothers be vaccinated against influenza? Should pregnant mothers be vaccinated against influenza?
This is currently a recommendation in the USA and Canada across all trimesters, but the uptake of this vaccine in the USA is only 16% indicating reluctance amongst pregnant ladies and health professionals. I must admit to being one of the reluctant health professionals and decided to read up on the matter. An article in the Lancet Infectious Diseases reviewing influenza vaccine in pregnancy by Mak et al in January 2008 provided a very good summary of the data concerning this topic so far. It was titled Influenza vaccination in pregnancy: current evidence and selected national policies I have summarised the article in a Q & A format with my own comments in italics.

1. How many pregnant women are exposed to influenza?

11%, as worked out by a four fold increase in antibody titres.

2. Does it cause increased mortality in pregnant mothers?

a. When comparing deaths in influenza season (1989-90) to non-influenza season (1985-6) there were 8 pregnant ladies who died in the influenza season compared to 2 in the noninfluenza season. This has been criticised by two other authors DrAyoub and Yazbak, who cite a 17 year study examining 38,151 pregnant ladies and not recording a single maternal death. This study itself has been criticised as it relied on patient interviews and recall and was thought to be underpowered. Another criticism of the above data is that the causes of deaths are not recorded though it does provide important information if the deaths are truly attributable to influenza. Further, I wonder whether this trend is held up with other years during the influenza and non-influenza season no mention of this is made here.

3. What degree of morbidity is associated with influenza?

a. Comparing the peri-influenza season to the influenza season from 1974-93 there was an excess rate of admission due to cardio-respiratory illness in hospitalised pregnant women. The excess rates per 10,000 were x3 x6 x10 for first, second and third trimesters respectively. Compared to non-pregnant women who had a rate of 1.91. This data was based on Medicaid data, which has a greater representation of lower socioeconomic groups and increased smokers. Again the data was examining hospital admission and not identifying influenza per se, but it could be argued that comparing this to a similar time in the year should cancel out the possibility of confounders (i.e. other respiratory infections which also occur at an increased rate during winter seasons). b. Data from Nova Scotia and a higher socio-economic group did not correlate with the figures given above. The excess rate of hospital admissions comparing a influenza and noninfluenza season were 1.1 (-0.1 to 2.3), 0.4 (-1.1 to 1.9) and 2.0 (-0.3 to 4.3) for the three trimesters when comparing pregnant to non-pregnant women. All the data sets had a range which extended across 0 implying that it was within the range of error rendering these results non-significant. An alternative conclusion is tht women from a high socio-economic background are not disadvantaged by influenza infection during pregnancy. c. Other data from Washington US HMO databases looked for the incidence of influenza like illnesses and the excess rates of consultations between pregnant and non-pregnant ladies. The excess rates of consultation were: 5.8, 9.8, 14.1 and 11 for the three successive trimesters and post-partum. Only 5.4 % of these consultations were classed as severe. Consultations marked as influenza-like illness are likely to be a poor surrogate marker for influenza. The data also mirrors the data from Tenesse Medicaid data (3a) and makes you wonder what the socioeconomic group was. d. Data from Oregon examined the number of outpatient visits for acute respiratory diseases in pregnant v non-pregnant women across four years 1975/6/8/9. In 1978 when a previously non-circulating strain H1N1 resurfaced the excess rate of medical visits by pregnant women was 48. No excess was shown for pregnant women during the other years of the study when H3N2 was predominant. Again influenza is being bunched together with other respiratory diseases which detracts from this data set. Acute respiratory diseases included all the following: influenza, pneumonia, URTI and respiratory symptoms. Bearing the above point, it seems pregnant ladies during years of pandemics where new strains are circulating may be at more risk than non-pregnant ladies. The converse also holds true, pregnant ladies during normal seasonal influenza are not at increased risk.

4. What are the effects on pregnancy outcomes?

a. From 1998-2002 6,277,508 hospital admissions for pregnant women were examined. Rates of women with influenza or respiratory illness were 2.3% v 1.2% in influenza v noninfluenza season. Respiratory disease was associated with the following higher odds (respiratory illness v non-respiratory illness): Preterm delivery 4.08, Fetal Distress 2.48, C section 3.91. This data does not differentiate between pneumonia and influenza. It is more plausible to assume that pneumonia was more strongly associated with adverse peri-natal outcomes.

5. Are women with co-morbidities more at risk?

a. Pregnant ladies with co-morbidities had 3.2 greater rate of respiratory illness than women without co-morbidities during defined influenza months. Again this study is using respiratory illness rather than influenza.

b. There was 10 fold increased rate of admissions of asthmatic pregnant women v nonasthmatic pregnant women during an influenza season. Again this looks at a surrogate marker rather than influenza. c. Novo Scotia 1990-2002 Pregnant ladies with one or more co-morbidities, compared influenza attributable hospital admissions between pregnant mothers with and without influenza. 3.9 (-6.4 to 14), 6.7 (-4.1 to 17) and 35.6 (21 to 50) in the three trimesters. The results are only significant in the third trimester, and again the influenza attributable hospital admissions is imprecise.

6. Are women at more risk during pandemics?

a. 1918-19 20 million died. In a mail survey 1350 women were diagnosed with influenza. Fatality rate was 27% but in the pneumonia subgroup it was 54%. Case fatality in nonpregnant ladies was 32% in a series of patients admitted at the same time with pneumonia. In 1957-8 12/103 people who died were pregnant and all had fulminant haemorrhagic pulmonary oedema. The two patient sets were not age and sex matched. In contrast to 1918 and 1957 in the 1968 9 pandemic there is an absence of evidence of increased risk of morbidity or mortality in pregnant women.

7. Can maternal infection harm the fetus?

a. There are 1 or 2 case reports of in-utero infection of the fetus. But no IgMAb in cord sera in 138 infants whose mothers had confirmed serological infection with influenza. IgM cannot cross the placenta so demonstration of it implies intra-uterine infection. This clearly contradicts the two case reports above. b. Cluster of 12 deaths in 3 weeks in a family practice. 8 spontaneous abortions and 4 still births, expected rate 12/year. Evidence of serological exposure to Influenza A during pregnancy in all 12 mothers. But a single cluster is poor evidence as clusters can and do occur due to random chance. c. 50-100% cases causes a temperature >37.8 lasting 3-5 days with a range of 38-40 C. No evidence to link pyrexia of the mother with congenital abnormalities. d. One seroepidemiological study has provided evidence of a higher risk of adult schizophrenia if maternal influenza exposure occurred in the first half of pregnancy. Schizophrenia has been extensively studied and associated with a multiplicity of factors both genetic and environmental. The multiplicity of associated factors usually through epidemiological studies will forever be plagued by the problem of confounders. Further given the fact that influenza virus does not cross the placenta(apart from two isolated case reports) the biological plausibility of such an association is suspect.

8. What is the risk in the neonatal stage?

a. 5.7% of children in a study examining 2797 children presenting to selected clinics had a positive nasal/throat swab for influenza. Implying it is a significant problem. b. Lab confirmed hospital admission due to influenza per 1000 are : 0-5m 4.5, 6-23m 0.9, 2459m 0.3. Implying that there are signifcant rates of morbidity especially in the first 6 months of life enough to cause hospital admission. c. The rate of influenza in non-hospitalised young children is looked at, children who are 05m had the lowest annual rates of outpatient visits with lab confirmed influenza. While those who were 6-23m had the highest rates. There were no differences in these rates inside or outside the influenza season.

The implication from studies (a) and (b) is that neonates will be afforded protection during the first 6 months of life by vaccinating pregnant mothers. But if study (c) is taken into account the event rate, in a group more reflective of the population as a whole, is lower in the age group (0-6 months) hence the early benefits are mitigated especially as the half-life of IgG is only 45 days.

9a. What is the immunological efficacy of the vaccine in pregnancy?

a. 3-4 weeks post vaccination pregnant and non-pregnant ladies have the same titre of circulating antibodies. b. IgG is transmitted across the placenta when mother are immunised, with an 87-99% transfer of IgG occurring. the t1/2 is 43-53 days which is the same as natural antibodies. There is no difference if vaccination occurred in T2 or T3.

9b. What is the clinical efficacy of the vaccine in pregnancy?

a. Inactive vaccine, in non-pregnant recipients, according to Cochrane prevents 67% of serologically confirmed cases and 25% of clinically apparent cases. It is argued that using only recent better studies this figure is higher. b. A RCT in Bangladesh assessed the prevention of febrile illness if pregnant ladies were immunised in T3, the percentage of febrile illness prevented were 25% (4-46%). Protection of infants was around 61% based on figures from the Bangladesh study. c. Texas Study looked at children under 6m of age born to immunised mothers. They were less likely to have medically attended respiratory illness during 2004/5 influenza season compared to babies born to non-immunised pregnant women (10.9% v 31% p<0.001) d. Epidemiological studies followed 39 mother-infant pairs in 1978/9 influenza season. Mothers were infected when pregnant and there was NO reduction in the rate of clinically apparent serologically proven acute infection in infants, but there was evidence to suggest respiratory illness was milder and delayed in onset. e. Retrospective studies from 1997-2002 in the USA did NOT find a reduction in the incidence of medically attended respiratory illness in either immunised mother or infants. It is said these studies were underpowered as the overall rate of influenza was lower than predicted. Study (a) talks about the general efficacy of the vaccine at 67%. The only study which had clearly identified and relevant outcome measure is (b). The one other study (c) in support of clinical efficacy of the vaccine used attended respiratory illness as an outcome measure which is an unclear outcome measure. Study (d) followed pregnant mothers infected by influenza when pregnant, which could be argued as having a highly effective form of immunization and this turned out to be a negative study. Study (e) looking over a much longer period of time are also negative. The evidence to argue for a clear clinical benefit is limited and contradictory.

10. How safe is the vaccine in pregnant women?

a. 650 mothers were vaccinated in the USA at T1 with Influenza trivalent inactivated vaccine/ IPV/ T Toxoid and diphtheria. They were followed up for 7 years and no association was found with minor or major malformations.

b. In another study 2991 mothers were vaccinated in T 1/2/3 with a follow up of 1 year for malignancies or increased cancer mortality at 4 years, no significant associations were found. c. 1976-77 study looked at 41 mothers vaccinated in T1 and compared them to nonvaccinated mothers. The infants were followed upto 8 weeks for evidence of neurodevelopmental problems and no association was found. A side effect rate of <3% was found to the mothers (fever, headache, and myalgia). d. 1998-2003 A Texas study, looked at 252 vaccinated pregnant mothers and compared them non-vaccinated mothers and looked at the hospitalization rate of infants 6 months after their birth. No significant association was found. e. 2004-5 A study looked at 1006 vaccinated pregnant mothers and compared them to 1495 unvaccinated pregnant mothers and no serious event in pregnancy was found. f. 1976 Study examined 45 pregnant mothers vaccinated in T3, no side effects noted. The safety studies are clearly positive and encouraging, but are limited by the number of women in each study and the limited duration of follow up or non-specific outcomes in many.

11. Are there any other risks that should be considered?

a. Fetal hypoxia can occur as a result of anaphylaxis. b. The vaccines contain thiomersal (sodium ethylmercurithiosalicylate a mercury containing compound). It is a component of the inactivated influenza vaccine. Studies in children looking at any causal association with neurodevelopmental disorders have proven to be negative. These have followed children up to 7 years. The US Institute of Medicine said in 2001 that there is biological plausibility of neurodevelopmental disorders occurring as a result of thiomersal. This decision was reversed in 2004 when they rejected causality as a result of the review of the cumulative paediatric exposure to thiomersal containing vaccines. The European Medical Agency has agreed with them. c. The WHO states there is no evidence of the lack of safety of vaccines containing thiomersal but noted that there was a lack of safety data for pre-term and malnourished infants. d. The UK health department recommend thiomersal free vaccines for pregnant women but if only thiomersal containing vaccines are available any theoretical e. 1994-2004 Yellow Card database: This is a passive reporting system. There are 1366 adverse reports concerning influenza vaccine. 8 of these were in pregnant ladies. 7 had the vaccine in T1. 6 of the mothers had asthma, diabetes or pleurisy. 2 had other vaccines at the same time. 4 had other treatments as well. The adverse outcomes that were reported were as follows: 1 stillbirth, 3 spontaneous abortions, 3 fetal growth retardations of which 2 were premature deliveries, 1 urinary tract anomaly which resolved by birth (thought to be an ultrasound error) There are no studies looking at the effect of thiomesal per se on human fetal development. Thiomersal free vaccines are offered to women in the UK and are available in the USA. The Yellow card data is definitely concerning and the authors have given it little weight arguing that due the nature of its collection interpretation of the results is difficult. It is worth remembering that the Yellow Card scheme was partly founded to pick up rare but

serious adverse associations with drugs such as Thalidomide. Where association is weak but positive the power of a study to pick up such an association may not be possible to perform and therefore any link will technically lie unproven. The Yellow Card data while difficult to interpret cannot be wholly ignored.

12. Which countries or bodies recommend vaccinating pregnant mothers?

a. WHO : Influenza vaccine in pregnancy is considerd safe and recommended for all pregnant women in the influenza season. b. USA: Practiced since the 1950s. ACIP recommended it in 2004 for all trimesters. Only 16% take up. c. Canada: 07-08 vaccine in all trimesters. d. Australia: T2/3 recommended e. UK: Any trimester if co-morbidities rpesent. f. Germany: Does not routinely recommend influenza vaccine. They note that safety evidence is incomplete but no teratogenic effect has been clearly identified. The German statement on the incomplete data on the safety of the vaccine speaks volumes.

Summary
(1,2) Pregnant women are exposed to the influenza virus, but the case for their increased mortality is based on inadequate data. (3) As for an increased morbidity most of the cited studies are looking at non-specific outcome measures such as consultations, or admissions to hospital for cardio-respiratory disease and are thus limited. Though of note are the increased incidence in lower socio-economic groups and when new strains of the influenza virus are seen circulating. This is most pronounced in the third trimester. (4) While the odds ratios for adverse pregnancy outcomes is significantly positive with respiratory disease inside and outside of the influenza season it is limited again by the non-specific nature of the outcome measures. (5) For women with co-morbidities the rates of admission are more pronounced in the influenza season vs the non-influenza season but suffer from the same imprecision in outcome measures. (6) Pregnant women seem to have a much higher mortality if affected by pneumonia during a pandemic, but again this data is not consistent across al pandemics. (7) There is scant data of any quality to claim an adverse effect on the fetus during maternal infection by the influenza virus. (8) The presumed benefits of maternal vaccination to neonates is potentially present but has to be balanced by the fact that vast majority of infants are not affected by influenza in the primary care setting. (9a) The vaccine is immunologically effective but the evidence of its clinical benefit to the infant post-birth is unclear. (10) The safety studies to date are limited to either 7 years or measuring unclear outcomes, hence the lack of a significant result should be viewed with caution. (11) The Yellow Card data while difficult to interpret cannot be wholly ignored. Finally the German statement on the incomplete data on the safety of the vaccine speaks volumes.

So what would I do?

I am not convinced about the whole sale recommendation of influenza vaccination of pregnant women primarily due to the incomplete safety data. The benefits of the vaccine are

probable but small and the harms while improbable and serious. Weighing the two up the pendulum would swing towards giving it especially in the case of pregnant, from a low socioeconomic background with the background of a circulating pandemic with a new strain, in which case I would give the vaccine at the end of T2. And the pendulum swings back to the opposite corner if the pregnant mother is from a relatively high socio-economic background in the absence of a pandemic or a newly circulating strain of the influenza virus. As for the cases in between these two poles the decision is to be made on an individual clinical basis. But to my mind the first Hippocratic principle of Do no harm would make the absence of vaccination my preferred choice. Abbreviations Used T1 Trimester 1 T2 Trimester 2 T3 Trimester 3 Ads by Google

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Posted in Vaccinations | Tags: efficacy of influenza vaccine, Fetal risk from influenza, immunisation against influenza in pregnant mothers, Neonatal risk from influenza, pregnant mothers, risk of pregnant mothers in pandemics, safety of the influenza vaccine, Yellow Card data influenza vaccine Is sertraline safe in breast feeding? How to pass the international MRCGP OSCE cheat sheet

Is sertraline safe in breast feeding?

One of my colleagues and I had a PUN/DEN moment today. A PUN is a Patient Unmet Need while a DEN is a Doctors Educational Need. This are rather fancy abbreviations for questions that come to us in daily clinical practice. A quick discussion with colleagues or a search on websites will bring a resolution to the problem in most cases. These questions if compiled somewhere are a good source of directed learning and education. The answer to our question was not quite as clear as we initially expected. According to Epocrates online it is safe in lactation. According to rxlist.com It is not known whether, and if so in what amount, sertraline or its metabolites are excreted in human milk. And finally to confuse matters according to drugs.com Sertraline passes into breast milk. Side effects have been reported in a baby exposed during nursing. Before taking this medicine, make sure your doctor knows if you are nursing your baby. For a final clinically weightted answer rather than an avoid being sued legal answer we went to emedicine.com which said the following:

yWomen who plan to breastfeed must be informed that all psychotropic medications, including antidepressants, are secreted into breast milk. Concentrations in breast milk vary widely. yData on the use of tricyclic antidepressants, fluoxetine, sertraline, and paroxetine during breastfeeding are encouraging, and serum antidepressant levels in the breastfed infant are either low or undetectable. Reports of toxicity in breastfed infants are rare, although the long-term effects of exposure to trace amounts of medication are not known.

We discussed the case and it transpired the mother had only fed her child once as she was afraid of the package insert. We felt it was in the patiets best interests and her childs that she continue breast feeding and consider the likelihood of any adverse outcome due to the sertraline as very low

Pigmented Purpuric Dermatitis

I came across a male patient with these odd purpuric lesions which where pigmented on his legs. This was 3 months after starting Metformin for diabetes. Not too sure what was going on I sent him to see our dermatologist and a diagnosis of Pigmented Purpuric Dermatitis was

made. In essence it is a capillaritis with T cell inflitration of unknown origin. If the medication is suspected stopping it for many months is recommended. They can dissapear in time or just hang around for many years. Steroids are not useful except for any itching. They look like this (courtesy of Derm Net) and you can read more about it here. Ads by Google

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Bacterial vs viral & antibiotic duration

HbA1c and all that!

Just when I thought life was simple, I am starting to understand that HbA1c is not quite what it is meant to be. First of all it is a dying breed and will be replaced by a new number which is no longer a percentage (Ref):

HbA1c-DCCT (%) 4.020

HbA1c-IFCC (mmol/mol)

hyare they doing this? Because now we are using a more accurate measure of glycosylation of Hb by looking at a single Valine on of the Hb chains rather than using a biological assay which included glycosylation of other things as well as Hb (but UKPDS used this biological test! So is validity true?) And then I started spotting HbA1c and FG & 2HPP discrepancies: So I needed to add a bit more to my HbA1c rudimentary knowledge: turns out the 120 day is not quite an accurate picture. The previous 30 days has a 50% impact on the HbA1c while the days 90-120 (before the test) only have a 10-20% effect on it. (http://www.endocrinetoday.com/view.aspx?rid=61106) . So the fresher your RBCs are and the worse your recent sugars are the higher your HbA1c will be even though the MPG (Mean Plasma Glucose) may be unchanged. (MPGs can be worked out by 7 measurements per day super snazzy glucose meters that sample your glucose automatically). So does the average life cycle of a red blood cell differ by ethnicity / genetic profile? From the anecdotal lack of complications in my diabetics with HbA1cs off the Richter scale (1015%) the answer sees to be yes at least in Saudi Arabia. Does BTS (Beta Thallasemia Trait) have an effect? Potentially depending on the assay it seems is a possibility. (Ref) Vitamin B12: Yes no yes again? Should we be checking Vitamin B12 once a year? Read this case report which argues for a yes: Report of Metformin induced B12 deficiency and neuropathy. And then finally to cap it all off statins can increase your risk of diabetes by 9%! This is the result of a meta-analysis published in the Lancet in Feb 2010. (Read more here). In short if you are low risk then it may not be a good idea, for moderate to high risk and if your old it works out as follows: Results further revealed that treatment of 255 patients with statins for four years would result in one extra case of diabetes. But, for 1 mmol/L reduction in LDL concentration, the same 255 patients could expect to experience five fewer major coronary events, such as coronary heart disease death or nonfatal myocardial infarction. Hope you are good at statistics and risk analysis and perhaps a bit of Bayes theorem

Should I take Vitamin C or E?

The Physicians Health Study II has reported in the Journal of the American Medical Association the effect of taking Vitamin C and E as supplements to prevent CVD after an eight year follow up using a RCT trial design. It wont be a surprise to many physicians to find out that it had absolutely no effect on these outcome measures and on the other hand it did throw up a concerning result. The concerning result was the increased incidence of haemorrhagic strokes for those taking Vitamin E. Though total mortality outcomes are equivalent in Vitamin C or E v placebo groups there was hazard ratio of 1.74 for haemorrhagic stroke for Vitamin E v placebo with a p value of 0.04 (significant). I dont recommend vitamin C or E for my patients for the purpose of primary prevention and / or general purpose well being and would put patients off taking Vitamin E in particular without any compelling reason

Dyspepsia and meals linked?

Came across what sounded like an interesting article from the title Functional Dyspepsia Usually Worsened by Meal Intake it is reviewed by Medscape as part of their CME series for doctors (link). The study tried to work out the time course of symptoms post-meal and came up with the conclusion that there is a temporal link between meals and symptoms. The symptoms occurred in the following order about 15 minutes after the meal fullness, bloating, nausea, belching and lastly epigastric pain. Functional dyspepsia is striclty speaking an endocsopic diagnosis where there is no underlying pathology noted on endoscopy to account for findings. At first glance this study seems a bit inane. But it provides valuable corroboration for an intuitive conclsuion that most family doctors have i.e. there is a link between dyspepsia and meals. This might seem like an obviously true statement but as illustrated by the NICE guidelines on dyspepsia the evidence linking lifestyle measures and types of meals to dyspepsia is contradictory at best and non-existant at worse. This study provides evidence of causality of symptoms to meals. It confirms my own observations on the relationship between meals, types of meals and functional dyspepsia

By how much does SLE increase CVD risk?

Bismillah, alhamdulillah Doing the medication refills today I saw a patient on a statin aged 38y. I wondered why she was taking a statin and looked for any history of CVD in the notes but found none. She does not have the classic courier risk factors of DHL i.e. diabetes or hypertension or lipidemia reaching a level high enough to justify statins. So I revised the notes again and saw that she had SLE. This led to a question in my mind. How much does SLE increase the risk of CVD disease?

Having been recently introduced to the Trip Database I used it to try and quickly search for an answer and came up with the paper whose abstract is included at the bottom. It looked at the Nurses Health Study and concluded that SLE doubled (relatively speaking) the risk of CVD. Using the Pubmed link there was a free link to an editorial in one of the Arthritis Journals and this gave some further additional insight which was worth reading. My take home points:
y y y

CVD risk is doubled if you have SLE. SLE has a bimodal mortality pattern: mortlaity is raised soon after diagnosis and later on in life Try and minimise steroid usage because of the CVD risk.

Dementia
Bismillah, alhamdulillah. Heard a nice podcast from the BBC on Dementia. Take home points:
y y y y y

35 million have it world wide. Singing and music may help but patients point out it is contact with others that matters. Goa psychiatrist, DrAmit Dias, has a new idea: Sangath Dementia Project with a community outreach project for dementia. Angst of relatives who promised to keep their elderly relatives at home but who need to send them to an institution. Simple ideas from Dementia House: lighting should be increased as yellowing of the cornea causes difficulty in depth perception. Long life bulbs decrease in their luminosity with time and need regular changing! A telephone where the quick dial buttons have pictures of relatives rather than names. Infra red sensor connected near the bed and to an in-house pager, if they wake up at night someone can come to assist them. A little door opening audio prompt that says Dont forget your keys. A clock that gives the time, the date, the day, the month and the time of day as in evening or morning and the year.

Posted in Geriatrics | Tags: dementia, Dementia and lighting, Dementian House, DrAmit Dias, Patient Tips for dementia, Sangath Dementia Project Palliative care in the NHS the USA effect Negative drug trials

ome more relevant quotes from Medscape 2010 s review. Watchout for NDM-1 export from India NDM, a gene that makes bacteria impervious to many antibiotics, is spreading worldwide. The gene evolved in India but is widespread in Pakistan and Bangladesh as well. Its been isolated all across the United Kingdom, prompting a national alert. Its also popped up in the United States, Canada, Sweden, Australia, and the Netherlands. A Swedish patient of Indian origin who got a urinary tract infection while visiting New Delhi was found to be infected with NDM-carrying bacteria. Reseachers dubbed the new bug NDM-1. 4 million people have been born through IVF. Robert Edwards was awarded the 2010 Nobel prize for his work in IVF. I wonder how may fertilised embryos had to be terminated to get this research right. Robert Edwards, PhD, was awarded the 2010 Nobel Prize in medicine or physiology, for his work in developing vitro fertilization (IVF). About 4 million people were born over the past 32 years using IVF. ADHD more genetic causality unearthed New research provides the first direct evidence that attention-deficit/hyperactivity disorder (ADHD) is genetic. In a study published online September 30 in The Lancet, investigators from the University of Cardiff, United Kingdom, say their findings suggest ADHD should be classified as a neurodevelopmental and not a behavioral disorder.

Do PPIs cancel Clopidogrel benefits?

A Canadian based population study looked at patients who had an MI, were given Clopidogrel +/- a PPI. They found giving a PPI (omeprazole, lansoperazole, rabeprazole ) that inhibits Cytochrome p450 2C19 is associated with a OR of 1.4 of a recurrent MI in the first 30 days following an MI. Pantoprazole did not have this association and is the single PPI that does not inhibit CYP 450 2C19. This effect was not noted with H2 antagonists. Clopidogrel is a pro-drug converted to its active form by the enzyme CYP 450 2C19. This enzyme which sits inside hepatic cells in the mitochondira and the endoplasmic reticulum busily adds an extra oxygen to the molecules its processes. The interesting thing is according to the wikipedia entry 15-20% of Asians have poor CYP 450 2C19 activity! So will it change my practice? Probably early days yet, populations studies are open to errors, everyone will call for a RCT (especially the companies that make PPIs), and pantoprazole is a sensible choce at least for the first 30 days while we try and work out whether this study is replicated by others. The other important question is: are 15 -20% of Asians with poor CYP 450 2C19 activity benefiting from Clopidogrel?