Thursday, March 31, 2011
Thursday, August 12, 2010
Thursday, August 05, 2010
Just had a mum come into surgery requesting OT referral for her daughter,aged 6. Apparently, teachers at school say her daughter has Mixed Dominance problem. When asked which specifically, she says it is difficulty crossing over righ and left hand dominance.
For me, i never thought being ambidextrous was a problem but apparently it shows that at the neuronal level the brain is still trying to organize itself!.
An interesting article below sheds some light on the matter:
JOURNAL OF THE NATIONAL ACADEMY FOR CHILD DEVELOPMENT
1987, Volume 7, No. 1
Learning Disabilities and Organization
Robert J. Doman, Jr.
The term "neurological organization" means that the brain can take in and store information in an orderly and "organized" fashion. A child lacking in complete neurological organization is to some degree neurologically dysorganized. To a large extent, this is an environmental or inherited problem as opposed to the organic dysorganization found in a child suffering from a brain injury.
The first step in detecting neurological dysorganization is to evaluate the child against the developmental profile and to have him tested to rule out the possibility of an organic problem.
NACD's evaluation of these children begins by determining the organization at the brain level of the pons. This is ascertained while viewing the child's ability to crawl on his stomach. The child should be able to crawl on his stomach in what is termed a "cross pattern" without receiving specific instruction. Cross-pattern crawling is forward movement where the child extends his right arm and pulls up his left leg, pushing and pulling with the right arm and left leg. He then alternates his movement so that he is pushing and pulling with the left arm and right leg. If the child crawls in what is called a homolateral pattern (which is pushing and pulling with the right arm and right leg, and then the left arm and left leg) he is exhibiting a degree of dysorganization at that level. If the child crawls without a pattern or in a manner where he is extending both arms forward and pulling both legs up, he is also reflecting dysorganization in the pons area of the brain.
Advancing to the mid-brain, organization or dysorganization can be assessed by examining the child's ability to creep on his hands and knees. Remember, you crawl before you creep. Crawling is on the stomach, and creeping is on the hands and knees. The child should also creep in a cross pattern. Properly, the child's hands should be extended flat on the floor with fingers pointing forward. Ideally, the child should be looking forward at the extended hand. Again, if the child creeps in a homologous (bunny hop) or a homolateral pattern (right arm and right leg) he is exhibiting a degree of dysorganization. In assessing your child's ability to creep, it is necessary that you have him creep at various speeds, with varied amounts of starting and stopping. A child properly organized at this level should never go into the homolateral pattern or homologous pattern.
Progressing up into the lower cortex area of the brain, you may evaluate organization by viewing the child's ability to walk. Instruct the child to walk across the room while he points at his feet, and assess whether he is walking in a homolateral pattern or a cross pattern. You may wish to demonstrate to the child what you intend him to do, then have him mimic your actions. Have the child follow your instructions while starting and stopping his movement several times. Any hesitation he displays about which hand to point is an indication of dysorganization. He should be pointing opposite hand to opposite foot, and should not walk in a homolateral pattern. There are many children who lack this cross-pattern function, and they reflect coordination problems to a certain extent. Coordinated gross motor action culminates in a cross pattern whether it's bowling, doing a basketball lay-up, or throwing a baseball pitch. A child who lacks complete organization will display a loss of coordination to some degree. Interestingly, there is the rare child who is neurologically dysorganized but has good coordination. Such children generally have other inefficiencies, particularly mixed dominance.
Neurological organization culminates at the top cortical level of the brain. This organization is the establishment of cortical-hemispheric dominance. This is the establishment of a dominant hemisphere, or side. A completely organized child should be right-handed, right-footed, right-eared, and right-eyed, or left-handed, left-footed, and so on.
To assess your child's dominance, begin by evaluating the function of his hands. You can find out if he has a dominant hand, as this will be the hand he writes with, throws a ball with, etc. These functions should all be done with the same hand. If a child writes with one hand and throws a ball with the opposite hand, he obviously is displaying mixed dominance. Assessment of foot dominance is essentially done by using the same method, observing which foot the child kicks with, hops with, etc.
To assess auditory dominance, have the child put his ear next to the door and attempt to listen to conversation that is emanating from the other side. Speak very softly so that the child leans toward you. The child will turn his head to either the right or left so that the dominant ear is closest to the source of the sound.
Assessment of visual dominance is accomplished at what is called near point and far point, using vision as close as three feet and at a further distance. To assess the child at a distance, have him point his finger toward your finger while you extend your arm and point your finger toward the child. If you sight along your finger to his finger, you can find out which eye he is using. You may wish to have him alternate his extended arm from right to left to double check your findings. Also have the child look into a telescope or kaleidoscope, as he will invariably use the dominant eye.
At near point place a one-eighth inch dot on a piece of paper and put another paper with a one-eighth inch hole in the center on top. Line up the hole with the dot so that the child can see the dot by looking through the hole on the top piece of paper. Have the child grasp the paper with the hole in both hands and slowly move the paper up to his eye, watching the dot the entire time. Again, watch which eye the child brings the paper to, as it will invariably be the dominant eye.
A completely organized child will have a dominant hand, foot, ear, and eye, which will be all on the same side. If the child lacks complete dominance in any area or does not exhibit dominance on the same side, it's a reflection of a degree of neurological dysorganization.
If the child lacks a controlling hemisphere of the brain organization is lacking because the influx of information to the brain is not occurring correctly. For instance, a child may take visual information through his right eye and store it in his left hemisphere. When a child neglects to take in information from one side and place it in one hemisphere he is not establishing firm pathways into the brain. The child cannot efficiently process that information. You might view the dysorganization as a room filled with filing cabinets. If he is properly organized all of the files are in alphabetical order and he can place a piece of information in and extract it efficiently. A dysorganized child's files are not alphabetized, and he may absorb the information but when he attempts to retrieve it he may be unable to do so. These children are classically the ones who study for a test one night, only to fail when they go in to take it. They took in the information but lost it when they attempted to retrieve it. When you place these children under any type of stress, the system immediately begins falling apart, and their function diminishes. Often these children neglect to remember a homework assignment from the previous night, yet they can remember what color dress mother wore on Christmas two years previously. These individuals are not lacking innate intelligence. They just cannot properly take in information, assimilate it, process it, and bring it back out again.
For me, i never thought being ambidextrous was a problem but apparently it shows that at the neuronal level the brain is still trying to organize itself!.
An interesting article below sheds some light on the matter:
JOURNAL OF THE NATIONAL ACADEMY FOR CHILD DEVELOPMENT
1987, Volume 7, No. 1
Learning Disabilities and Organization
Robert J. Doman, Jr.
The term "neurological organization" means that the brain can take in and store information in an orderly and "organized" fashion. A child lacking in complete neurological organization is to some degree neurologically dysorganized. To a large extent, this is an environmental or inherited problem as opposed to the organic dysorganization found in a child suffering from a brain injury.
The first step in detecting neurological dysorganization is to evaluate the child against the developmental profile and to have him tested to rule out the possibility of an organic problem.
NACD's evaluation of these children begins by determining the organization at the brain level of the pons. This is ascertained while viewing the child's ability to crawl on his stomach. The child should be able to crawl on his stomach in what is termed a "cross pattern" without receiving specific instruction. Cross-pattern crawling is forward movement where the child extends his right arm and pulls up his left leg, pushing and pulling with the right arm and left leg. He then alternates his movement so that he is pushing and pulling with the left arm and right leg. If the child crawls in what is called a homolateral pattern (which is pushing and pulling with the right arm and right leg, and then the left arm and left leg) he is exhibiting a degree of dysorganization at that level. If the child crawls without a pattern or in a manner where he is extending both arms forward and pulling both legs up, he is also reflecting dysorganization in the pons area of the brain.
Advancing to the mid-brain, organization or dysorganization can be assessed by examining the child's ability to creep on his hands and knees. Remember, you crawl before you creep. Crawling is on the stomach, and creeping is on the hands and knees. The child should also creep in a cross pattern. Properly, the child's hands should be extended flat on the floor with fingers pointing forward. Ideally, the child should be looking forward at the extended hand. Again, if the child creeps in a homologous (bunny hop) or a homolateral pattern (right arm and right leg) he is exhibiting a degree of dysorganization. In assessing your child's ability to creep, it is necessary that you have him creep at various speeds, with varied amounts of starting and stopping. A child properly organized at this level should never go into the homolateral pattern or homologous pattern.
Progressing up into the lower cortex area of the brain, you may evaluate organization by viewing the child's ability to walk. Instruct the child to walk across the room while he points at his feet, and assess whether he is walking in a homolateral pattern or a cross pattern. You may wish to demonstrate to the child what you intend him to do, then have him mimic your actions. Have the child follow your instructions while starting and stopping his movement several times. Any hesitation he displays about which hand to point is an indication of dysorganization. He should be pointing opposite hand to opposite foot, and should not walk in a homolateral pattern. There are many children who lack this cross-pattern function, and they reflect coordination problems to a certain extent. Coordinated gross motor action culminates in a cross pattern whether it's bowling, doing a basketball lay-up, or throwing a baseball pitch. A child who lacks complete organization will display a loss of coordination to some degree. Interestingly, there is the rare child who is neurologically dysorganized but has good coordination. Such children generally have other inefficiencies, particularly mixed dominance.
Neurological organization culminates at the top cortical level of the brain. This organization is the establishment of cortical-hemispheric dominance. This is the establishment of a dominant hemisphere, or side. A completely organized child should be right-handed, right-footed, right-eared, and right-eyed, or left-handed, left-footed, and so on.
To assess your child's dominance, begin by evaluating the function of his hands. You can find out if he has a dominant hand, as this will be the hand he writes with, throws a ball with, etc. These functions should all be done with the same hand. If a child writes with one hand and throws a ball with the opposite hand, he obviously is displaying mixed dominance. Assessment of foot dominance is essentially done by using the same method, observing which foot the child kicks with, hops with, etc.
To assess auditory dominance, have the child put his ear next to the door and attempt to listen to conversation that is emanating from the other side. Speak very softly so that the child leans toward you. The child will turn his head to either the right or left so that the dominant ear is closest to the source of the sound.
Assessment of visual dominance is accomplished at what is called near point and far point, using vision as close as three feet and at a further distance. To assess the child at a distance, have him point his finger toward your finger while you extend your arm and point your finger toward the child. If you sight along your finger to his finger, you can find out which eye he is using. You may wish to have him alternate his extended arm from right to left to double check your findings. Also have the child look into a telescope or kaleidoscope, as he will invariably use the dominant eye.
At near point place a one-eighth inch dot on a piece of paper and put another paper with a one-eighth inch hole in the center on top. Line up the hole with the dot so that the child can see the dot by looking through the hole on the top piece of paper. Have the child grasp the paper with the hole in both hands and slowly move the paper up to his eye, watching the dot the entire time. Again, watch which eye the child brings the paper to, as it will invariably be the dominant eye.
A completely organized child will have a dominant hand, foot, ear, and eye, which will be all on the same side. If the child lacks complete dominance in any area or does not exhibit dominance on the same side, it's a reflection of a degree of neurological dysorganization.
If the child lacks a controlling hemisphere of the brain organization is lacking because the influx of information to the brain is not occurring correctly. For instance, a child may take visual information through his right eye and store it in his left hemisphere. When a child neglects to take in information from one side and place it in one hemisphere he is not establishing firm pathways into the brain. The child cannot efficiently process that information. You might view the dysorganization as a room filled with filing cabinets. If he is properly organized all of the files are in alphabetical order and he can place a piece of information in and extract it efficiently. A dysorganized child's files are not alphabetized, and he may absorb the information but when he attempts to retrieve it he may be unable to do so. These children are classically the ones who study for a test one night, only to fail when they go in to take it. They took in the information but lost it when they attempted to retrieve it. When you place these children under any type of stress, the system immediately begins falling apart, and their function diminishes. Often these children neglect to remember a homework assignment from the previous night, yet they can remember what color dress mother wore on Christmas two years previously. These individuals are not lacking innate intelligence. They just cannot properly take in information, assimilate it, process it, and bring it back out again.
Thursday, December 24, 2009
Government of Western Australia
Department of Health
Public Health
Dear Colleague
BonSoy soy milk: information for Medical Practitioners
5 Key points for Medical Practitioners
BonSoy soy milk has been withdrawn from the marketplace following detection of
1.
high levels of iodine in this product. This product should not be consumed.
Several adult cases in NSW have been diagnosed with thyroid conditions
2.
believed to be associated with consumption of BonSoy soy milk.
In addition, a newborn has been diagnosed with hypothyroidism secondary to
3.
iodine excess following maternal consumption of BonSoy during the pregnancy.
Doctors should be alert to seek information about BonSoy soy milk consumption
4.
by any persons presenting or who have presented in the past months with
thyroid conditions.
Medical practitioners should report all suspected cases of thyroid disease where
5.
BonSoy soy milk is involved to the Communicable Diseases Control Directorate
during business hours on tel. 9388 4999 or fax 9388 4848.
BonSoy is a soy milk product distributed nationally in Australia. Tests have shown it to
contain extremely high levels of iodine and consumption has been linked to clinical
thyrotoxicosis and, less commonly, hypothyroidism. Iodine crosses the placenta and may
cause foetal and neonatal hypothyroidism which can cause developmental problems in the
newborn.
Exceeding the safe upper limit for iodine intake may occur when 30ml is consumed per day
by an adult, or 5ml for a child.
Recommended levels of Iodine
The recommended daily intake for iodine depends on age and life stage:
• Younger children (1 to 8 years) – 90µg
• Older children (9 to 13 years, boys and girls) – 120µg
• Adolescents (14 to 18 years) – 150µg
• Men – 150µg
• Women – 150µg
• Pregnancy and breastfeeding – 220µg and 270µg respectively.
The recommended safe upper limit for iodine is:
• Young children (1 to 3 years) – 200µg
• Older children and Adolescents (14 years) – 900µg
• Adults – 1,100µg
Signs and Symptoms excessive iodine intake
Excessive iodine can lead to hyperthyroidism or, less commonly in adults, hypothyroidism.
Infants appear more susceptible to hypothyroidism following excessive iodine exposure.
The commonest symptoms of hyperthyroidism are palpitations, fatigue and weight loss.
Hypothyroidism is often insidious and, in mild cases, may only be detected on routine
screening but it can cause fatigue, weight gain and mental clouding.
Medical Management
• Patients should be advised not to consume the product and to dispose of it either
down the drain or in the garbage bin.
• Iodine has a half life of approximately 30 days.
• When a patient presents with a history of prolonged BonSoy soy milk consumption
together with symptoms or signs listed above, Medical Practitioners should consider
measurement of TSH. If the TSH is abnormal, proceed to measurement of the
urinary iodine level (normal range in children 100-500 ug/L) and thyroid antibodies
and consider referral to an endocrinologist or at least try to obtain phone
consultation with an endocrinologist. There is no need to measure the urinary iodine
level if the TSH is normal (Normal range 0.3-4.0 mU/L, can vary between
laboratories) as stopping the ingestion of the milk will return the body’s iodine levels
to normal within a few weeks.
• Advice to patients who report they have drunk the milk and are pregnant: see your
GP or obstetrician for a TSH measurement. The baby may also need additional TSH
and free T4 measurement after birth (but this is usually routinely done with the
Guthrie heelprick test); If the TSH is abnormal, then thyroid ultrasound and thyroid
scan are indicated. The effect of the high iodine levels will be to block synthesis of
thyroid hormones causing hypothyroidism which in the neonatal period could cause
a permanent loss of cognitive function.
• Suspected cases should be reported during business hours to the Communicable
Disease Control Directorate on 9388 4999, fax number 9388 4848.
Advice for the general public about the recall of BonSoy soy milk product and a fact
sheet about iodine is available on the Food Standards Australia and New Zealand
website: http://www.foodstandards.gov.au/
Thank you for your support in this matter.
Yours sincerely
Dr Tarun Weeramanthri
Chief Health Officer
Department of Health
Department of Health
Public Health
Dear Colleague
BonSoy soy milk: information for Medical Practitioners
5 Key points for Medical Practitioners
BonSoy soy milk has been withdrawn from the marketplace following detection of
1.
high levels of iodine in this product. This product should not be consumed.
Several adult cases in NSW have been diagnosed with thyroid conditions
2.
believed to be associated with consumption of BonSoy soy milk.
In addition, a newborn has been diagnosed with hypothyroidism secondary to
3.
iodine excess following maternal consumption of BonSoy during the pregnancy.
Doctors should be alert to seek information about BonSoy soy milk consumption
4.
by any persons presenting or who have presented in the past months with
thyroid conditions.
Medical practitioners should report all suspected cases of thyroid disease where
5.
BonSoy soy milk is involved to the Communicable Diseases Control Directorate
during business hours on tel. 9388 4999 or fax 9388 4848.
BonSoy is a soy milk product distributed nationally in Australia. Tests have shown it to
contain extremely high levels of iodine and consumption has been linked to clinical
thyrotoxicosis and, less commonly, hypothyroidism. Iodine crosses the placenta and may
cause foetal and neonatal hypothyroidism which can cause developmental problems in the
newborn.
Exceeding the safe upper limit for iodine intake may occur when 30ml is consumed per day
by an adult, or 5ml for a child.
Recommended levels of Iodine
The recommended daily intake for iodine depends on age and life stage:
• Younger children (1 to 8 years) – 90µg
• Older children (9 to 13 years, boys and girls) – 120µg
• Adolescents (14 to 18 years) – 150µg
• Men – 150µg
• Women – 150µg
• Pregnancy and breastfeeding – 220µg and 270µg respectively.
The recommended safe upper limit for iodine is:
• Young children (1 to 3 years) – 200µg
• Older children and Adolescents (14 years) – 900µg
• Adults – 1,100µg
Signs and Symptoms excessive iodine intake
Excessive iodine can lead to hyperthyroidism or, less commonly in adults, hypothyroidism.
Infants appear more susceptible to hypothyroidism following excessive iodine exposure.
The commonest symptoms of hyperthyroidism are palpitations, fatigue and weight loss.
Hypothyroidism is often insidious and, in mild cases, may only be detected on routine
screening but it can cause fatigue, weight gain and mental clouding.
Medical Management
• Patients should be advised not to consume the product and to dispose of it either
down the drain or in the garbage bin.
• Iodine has a half life of approximately 30 days.
• When a patient presents with a history of prolonged BonSoy soy milk consumption
together with symptoms or signs listed above, Medical Practitioners should consider
measurement of TSH. If the TSH is abnormal, proceed to measurement of the
urinary iodine level (normal range in children 100-500 ug/L) and thyroid antibodies
and consider referral to an endocrinologist or at least try to obtain phone
consultation with an endocrinologist. There is no need to measure the urinary iodine
level if the TSH is normal (Normal range 0.3-4.0 mU/L, can vary between
laboratories) as stopping the ingestion of the milk will return the body’s iodine levels
to normal within a few weeks.
• Advice to patients who report they have drunk the milk and are pregnant: see your
GP or obstetrician for a TSH measurement. The baby may also need additional TSH
and free T4 measurement after birth (but this is usually routinely done with the
Guthrie heelprick test); If the TSH is abnormal, then thyroid ultrasound and thyroid
scan are indicated. The effect of the high iodine levels will be to block synthesis of
thyroid hormones causing hypothyroidism which in the neonatal period could cause
a permanent loss of cognitive function.
• Suspected cases should be reported during business hours to the Communicable
Disease Control Directorate on 9388 4999, fax number 9388 4848.
Advice for the general public about the recall of BonSoy soy milk product and a fact
sheet about iodine is available on the Food Standards Australia and New Zealand
website: http://www.foodstandards.gov.au/
Thank you for your support in this matter.
Yours sincerely
Dr Tarun Weeramanthri
Chief Health Officer
Department of Health
Tuesday, December 15, 2009
PLEASE note scheduling changes for the following OTC Cough and Cold medicines for children aged 2-12 years old:
1. Anthistamines: Brompheniramine, Chlorpheniramine (PIRITON), Dexchlorpheniramine, Diphendyramine (BENADRYL), Doxylamine, Pheniramine, Promethazine (Phenergan), and Triprolidine.
2. Antitussives: Codeine, Dextromethorphan, Dihydrocodeine, Pentoxyverine and Pholdodine.
3. Expectorants/mucolytics: Ammonium chloride, Bromhexine, Guaifenesin, Ipecacuanha, Senega and Ammonia.
4. Decongestants: Oxymetazoline, Phenylephrine, Pseudoephedrine and Xylometazoline.
Regulatory authorities for 5 countries: Australia, USA, UK, Canada and New Zealand have conduct safety and efficacy reviews of these medicines for children under 2 years old and concluded they should not be given to children in that age group.
The TGA (Australia) proposes that:
* OTC cough and cold should NOT be used ofr children <6 years old and only for children between 6-12 years old on the advice of doctors and pharmacists.
1. Anthistamines: Brompheniramine, Chlorpheniramine (PIRITON), Dexchlorpheniramine, Diphendyramine (BENADRYL), Doxylamine, Pheniramine, Promethazine (Phenergan), and Triprolidine.
2. Antitussives: Codeine, Dextromethorphan, Dihydrocodeine, Pentoxyverine and Pholdodine.
3. Expectorants/mucolytics: Ammonium chloride, Bromhexine, Guaifenesin, Ipecacuanha, Senega and Ammonia.
4. Decongestants: Oxymetazoline, Phenylephrine, Pseudoephedrine and Xylometazoline.
Regulatory authorities for 5 countries: Australia, USA, UK, Canada and New Zealand have conduct safety and efficacy reviews of these medicines for children under 2 years old and concluded they should not be given to children in that age group.
The TGA (Australia) proposes that:
* OTC cough and cold should NOT be used ofr children <6 years old and only for children between 6-12 years old on the advice of doctors and pharmacists.
Monday, December 14, 2009
It is definitely good to be back in KL,albeit for a very short visit.
For friends who were interested in doing the MRCGP as an alternative to the Fellowship exams;please take note.
For the MRCGP Int, i was just informed last week that the RACGP Assessment Unit in Melbourne have no idea how to "assess" it. Apparently between June 23rd (when i sat for my AKT exam of the FRACGP as part of the specialist pathway) and now, they have changed theri minds yet again and do not think it is "equivalent"
I wrote to the RCGP UK and UK PMETB and apparently with the MRCGP Int you can actually apply under the CESR pathway to obtain a certificate equal to the CCT. Please see the quote below regarding the process you need to go through:
In the first instance, you will need to pass the General Medical Council’s PLAB test before you can apply for a license to practice in the UK. In order to practice in the UK as a substantive Consultant, you must also be registered on the GMC’s Specialist register.
Please see link below for more information regarding the PLAB test:
http://www.gmc-uk.org/doctors/plab.asp
Furthermore, in order to be registered on the GMC’s specialist register you will need to get the Certificate of Eligibility for Specialist Registration (CESR) award from PMETB.
This will ascertain whether your training abroad matches the UK standard. After being awarded a CESR, you will be eligible for specialist registration.
Below is a link with more information and Frequently Asked Questions (FAQs) about the equivalence routes to the specialist register and GP registers.
http://www.pmetb.org.uk/index.php?id=961
It is a bit fairer as the pathwya is clear and they do not change it every minute like the RACGP in Australia.
For instance take a look at this letter they sent in March 2009:
Further to our correspondence, we acknowledge your desire to undertake the RACGP assessment in March 2009. As you are aware, in July 2008 the RACGP Specialist Pathway (SP) was introduced as a tailored program for international medical graduates (IMGs) wanting to work in Australian general practice. This pathway is intended for IMGs who do not have Australian medical registration.
According to your application, you have already been granted medical registration in Australia, hence you were notified that enrolment in the RACGP assessment could not take place unless you met the enrolment eligibility criteria for the practice eligible route. We identified that this may have created an obstacle with the medical board, as your registration was conditional pending the undertaking of the RACGP Applied Knowledge test (AKT). Hence we offered you the opportunity to enter into the Specialist Pathway which will enable you to sit the AKT without meeting your GP experience time requirements. Please see 'The Assessment Handbook for Candidates- eligibility for Assessment' http://www.racgp.org.au/assessmenthandbook.
The policy still remains the same; that you either continue down the practice eligible route and fulfil the GP experience time requirements or enter into the SP. Due to the difficulty this presents to you, the RACGP are reconsidering this policy and a review is underway. As you can appreciate, this review may take some months before an outcome is published. We are aware of the time constraints you are under hence we propose a short term solution to your current situation.
We have made arrangements for a special sitting of the AKT on 23 June 09 in Sydney. We anticipate that by the time your results are released, we will be better positioned to advise you of what is required to proceed with the final exam segments and eventually achieving the Fellowship of the RACGP.
However this has changed AGAIN and now they switched me to a Practice Based Assessment!.
For friends who were interested in doing the MRCGP as an alternative to the Fellowship exams;please take note.
For the MRCGP Int, i was just informed last week that the RACGP Assessment Unit in Melbourne have no idea how to "assess" it. Apparently between June 23rd (when i sat for my AKT exam of the FRACGP as part of the specialist pathway) and now, they have changed theri minds yet again and do not think it is "equivalent"
I wrote to the RCGP UK and UK PMETB and apparently with the MRCGP Int you can actually apply under the CESR pathway to obtain a certificate equal to the CCT. Please see the quote below regarding the process you need to go through:
In the first instance, you will need to pass the General Medical Council’s PLAB test before you can apply for a license to practice in the UK. In order to practice in the UK as a substantive Consultant, you must also be registered on the GMC’s Specialist register.
Please see link below for more information regarding the PLAB test:
http://www.gmc-uk.org/doctors/plab.asp
Furthermore, in order to be registered on the GMC’s specialist register you will need to get the Certificate of Eligibility for Specialist Registration (CESR) award from PMETB.
This will ascertain whether your training abroad matches the UK standard. After being awarded a CESR, you will be eligible for specialist registration.
Below is a link with more information and Frequently Asked Questions (FAQs) about the equivalence routes to the specialist register and GP registers.
http://www.pmetb.org.uk/index.php?id=961
It is a bit fairer as the pathwya is clear and they do not change it every minute like the RACGP in Australia.
For instance take a look at this letter they sent in March 2009:
Further to our correspondence, we acknowledge your desire to undertake the RACGP assessment in March 2009. As you are aware, in July 2008 the RACGP Specialist Pathway (SP) was introduced as a tailored program for international medical graduates (IMGs) wanting to work in Australian general practice. This pathway is intended for IMGs who do not have Australian medical registration.
According to your application, you have already been granted medical registration in Australia, hence you were notified that enrolment in the RACGP assessment could not take place unless you met the enrolment eligibility criteria for the practice eligible route. We identified that this may have created an obstacle with the medical board, as your registration was conditional pending the undertaking of the RACGP Applied Knowledge test (AKT). Hence we offered you the opportunity to enter into the Specialist Pathway which will enable you to sit the AKT without meeting your GP experience time requirements. Please see 'The Assessment Handbook for Candidates- eligibility for Assessment' http://www.racgp.org.au/assessmenthandbook.
The policy still remains the same; that you either continue down the practice eligible route and fulfil the GP experience time requirements or enter into the SP. Due to the difficulty this presents to you, the RACGP are reconsidering this policy and a review is underway. As you can appreciate, this review may take some months before an outcome is published. We are aware of the time constraints you are under hence we propose a short term solution to your current situation.
We have made arrangements for a special sitting of the AKT on 23 June 09 in Sydney. We anticipate that by the time your results are released, we will be better positioned to advise you of what is required to proceed with the final exam segments and eventually achieving the Fellowship of the RACGP.
However this has changed AGAIN and now they switched me to a Practice Based Assessment!.
Latent Autoimmune Diabetes in Adults (LADA) is a slow progressive form of Type 1 Diabetes.
* autoimmune destruction of pancreatic B-islet cells leading to an absolute insuloin deficiency within 2-6 years.
* Distinguished from Type 2 DM by presence of Islet autoantibodies especially to Glutamic Acid Decraboxylase (GAD)
TYPE 2 DM:
* progressive deterioration in glucose tolerance caused by insullin sensitivity and insulin secretion defects.
* Risk factors are: Obesity, hypertension, dyslipidemia and insulin resistance; a strong family history is also a risk factor.
TYPE 1 DM:
* absolute deficiency in Insulin secretion, and usually arises in children aged 15 years or younger.
* 13% of all diabetes in Australia
* Specific autoimmune destruction of insulin producing B-cell in pancreas leading to a dependency in insulin replacement.
* Serological markers for this autoimmune process include: Islet cell cytoplasmic autoantibodies (ICA), autoantibodies to to GAD and insulin or to the tyrosine phosphate IA2.
Patients with LADA:
* more likely to be symptomatic
* poor glycemic control
* existence of other autoantibodies (GAD)
* present clinically as osmeone with Type 2 DM, do not require insulin immediately after diagnosis and may be overweight.
* UKPDS 1997: one in 10 adults aged 25-65 years with Presumed Type 2 DM actually had GAD antibodies.
* autoimmune destruction of pancreatic B-islet cells leading to an absolute insuloin deficiency within 2-6 years.
* Distinguished from Type 2 DM by presence of Islet autoantibodies especially to Glutamic Acid Decraboxylase (GAD)
TYPE 2 DM:
* progressive deterioration in glucose tolerance caused by insullin sensitivity and insulin secretion defects.
* Risk factors are: Obesity, hypertension, dyslipidemia and insulin resistance; a strong family history is also a risk factor.
TYPE 1 DM:
* absolute deficiency in Insulin secretion, and usually arises in children aged 15 years or younger.
* 13% of all diabetes in Australia
* Specific autoimmune destruction of insulin producing B-cell in pancreas leading to a dependency in insulin replacement.
* Serological markers for this autoimmune process include: Islet cell cytoplasmic autoantibodies (ICA), autoantibodies to to GAD and insulin or to the tyrosine phosphate IA2.
Patients with LADA:
* more likely to be symptomatic
* poor glycemic control
* existence of other autoantibodies (GAD)
* present clinically as osmeone with Type 2 DM, do not require insulin immediately after diagnosis and may be overweight.
* UKPDS 1997: one in 10 adults aged 25-65 years with Presumed Type 2 DM actually had GAD antibodies.
SUMMARIZED FROM AUSTRALIAN DOCTOR DIABETES SUPPLEMENT NOV 2009
8 different classes of medications are now available for treatment of diabetes:
1. GLP-1 and DPP-IV
2. insulin 1921
3. Sulfonylureas:stimulate insulin release 1946
4. Metformin:reduced hepatic glucose production and insulin resistance 1957
5. Acarbose: reduces carbohydrate digestion 1995
6. Thiazolidinediones "glitazones": reduce insulin resistance 1997
7. Repaglinide: short term insulin stimulation 1997
8. Exenatide GLP-1 Analogue 2005
9. Sitagliptin DPP-IV inhibitor enhances GLP-1 action 2006
GLP-1 resembles the structure of glucagon but has an OPPOSITE physiological effect:
1. PROMOTES insulin secretion
2. INHIBITS glucagon release
3. REDUCES circulating glucagon levels
GLP-1 is released from the gut wall in response to food. it is degraded very rapidly by enzyme dipeptidyl peptidase-IV (DPP-IV)
New GLP-1 based therapies are: Exenatide an INJECTABLE GLP-1 analogue or mimetic, DPP-IV INHIBITORS such as sitagliptin which slow degradation of GLP-1 and boosts its effects.
LOW RISK HYPOGLYCEMIA FROM TREATMENT AS EFFECT of GLP-1 DECLINES as blood glucose levels fall.
EXENATIDE
developed from exendin-4 compound of Gila monster salivary gland.
In clinical trials: S/c EXENATIDE BID decreased HBA1C by 0.8-0.9% and associated with INCREASED SATIETY, REDUCED APPETITE, WEIGHT LOSS and low rate of hypoglycemia.
side effects"nausea, sweating, vomiting, dizziness,
weight loss 2.5kg at 12 momths using exenatide compared to 2.9kf weight gain with insulin.
PROF DRUCKER from Banting and Best Diabetes Centre in Toronto recommends: EARLY combination therapy with METFORMIN and Sitagliptin.
METFORMIN ALSO STIMULATES GLP-1 SECRETION!
GLP-1 is also CARDIOPROTECTIVE.
Sitagliptin is indicated in Australia for combination therapy woth metformin, sulfonylureas and thiazolinedinediones.
Consensus recommendations from American Diabetes Association and European Association the Study of Diabetes (Diabetes Care 2009;32:193-203):
* Tier 1 medications with well-established safety records and efficacy are diet, eexrcise, metformin, insulin and sulfonylureas.
* Tier-2 less 'well validated" are pioglitazone and GLP-1 agonist exenatide. Useful if recurrent hypoglycemia or for promotion of weight loss.
* Other therapy includes: acarbose, repaglinide, DPP-IV inhibitors such as sitagliptin.
8 different classes of medications are now available for treatment of diabetes:
1. GLP-1 and DPP-IV
2. insulin 1921
3. Sulfonylureas:stimulate insulin release 1946
4. Metformin:reduced hepatic glucose production and insulin resistance 1957
5. Acarbose: reduces carbohydrate digestion 1995
6. Thiazolidinediones "glitazones": reduce insulin resistance 1997
7. Repaglinide: short term insulin stimulation 1997
8. Exenatide GLP-1 Analogue 2005
9. Sitagliptin DPP-IV inhibitor enhances GLP-1 action 2006
GLP-1 resembles the structure of glucagon but has an OPPOSITE physiological effect:
1. PROMOTES insulin secretion
2. INHIBITS glucagon release
3. REDUCES circulating glucagon levels
GLP-1 is released from the gut wall in response to food. it is degraded very rapidly by enzyme dipeptidyl peptidase-IV (DPP-IV)
New GLP-1 based therapies are: Exenatide an INJECTABLE GLP-1 analogue or mimetic, DPP-IV INHIBITORS such as sitagliptin which slow degradation of GLP-1 and boosts its effects.
LOW RISK HYPOGLYCEMIA FROM TREATMENT AS EFFECT of GLP-1 DECLINES as blood glucose levels fall.
EXENATIDE
developed from exendin-4 compound of Gila monster salivary gland.
In clinical trials: S/c EXENATIDE BID decreased HBA1C by 0.8-0.9% and associated with INCREASED SATIETY, REDUCED APPETITE, WEIGHT LOSS and low rate of hypoglycemia.
side effects"nausea, sweating, vomiting, dizziness,
weight loss 2.5kg at 12 momths using exenatide compared to 2.9kf weight gain with insulin.
PROF DRUCKER from Banting and Best Diabetes Centre in Toronto recommends: EARLY combination therapy with METFORMIN and Sitagliptin.
METFORMIN ALSO STIMULATES GLP-1 SECRETION!
GLP-1 is also CARDIOPROTECTIVE.
Sitagliptin is indicated in Australia for combination therapy woth metformin, sulfonylureas and thiazolinedinediones.
Consensus recommendations from American Diabetes Association and European Association the Study of Diabetes (Diabetes Care 2009;32:193-203):
* Tier 1 medications with well-established safety records and efficacy are diet, eexrcise, metformin, insulin and sulfonylureas.
* Tier-2 less 'well validated" are pioglitazone and GLP-1 agonist exenatide. Useful if recurrent hypoglycemia or for promotion of weight loss.
* Other therapy includes: acarbose, repaglinide, DPP-IV inhibitors such as sitagliptin.
CHANGING CONCEPTS TYPE 1 & 2 DIABETES.
Summarized from Australian Doctor Supplement November 2009
Prof Len Harrison at IMR Melbourne reviewed links between "diabetogenic" environment and causes and classification of diabetes (Nature Reviews Endocrinology 2009;5:483-89).
* increasing numbers children,adolescents and adults have BOTH autoimmunity against beta cells (typical of Type I DM) AND Insulin resistance (classical of Type 2 DM)
* =DOUBLE DIABETES=Latent autoimmune diabetes in youth, latent autoimmune diabetes in adults and type 1.5 diabetes
* likely environment that fosters expressions of genes once posed only a low risk.
ENVIRONMENTAL CHANGES PROMOTING DIABETES:
1. Increased total intake of food:high fat, trans fatty acids, fructose, low fibre
2. Changes in exposure to pathogens (hygiene hypothesis)
3. Low levels Vitamin D as hormone as well as Vitamin assoc with increased risk Type 1&2 DM.
4. Heating and cooling of buildings has reduced need to expend energy to thermoregulate.
5. Shorter periods of sleep tend to increase weight gain.
POSSIBLE INTERVENTIONS:
1. healthy diet and exercise
2. normalizing sleep
3. re-acquaint with temperatures outside thermoneutral zone
4. vitamin D therapy serum levels >70ng/ml target
5. EARLY use METFORMIN and THIAZOLINEDIONES which might preserve beta cell function in type 2 and even type 1 DM.
6. PREVENTION IS ONLY SUSTAINABLE APPROACH
Protecting beta cells:
* 80% of beta cells have been destroyed by the time a patient presents with Type 1 DM, 60% when presenting with Type 2 DM.
* METFORMIN, STIGAGLIPTIN, THIAZONELINEDIONES might slow rate decline of beta cells.
CLASSIFICATION DIABETES (American diabetes association)
* >50 types!!Type 1 DM 10%
* Type 2 DM
* Gestational DM (5% all Aussie women), 13% women aged 45-49 and higher in Aboriginals, torres straits islanders and south Asian women.
Summarized from Australian Doctor Supplement November 2009
Prof Len Harrison at IMR Melbourne reviewed links between "diabetogenic" environment and causes and classification of diabetes (Nature Reviews Endocrinology 2009;5:483-89).
* increasing numbers children,adolescents and adults have BOTH autoimmunity against beta cells (typical of Type I DM) AND Insulin resistance (classical of Type 2 DM)
* =DOUBLE DIABETES=Latent autoimmune diabetes in youth, latent autoimmune diabetes in adults and type 1.5 diabetes
* likely environment that fosters expressions of genes once posed only a low risk.
ENVIRONMENTAL CHANGES PROMOTING DIABETES:
1. Increased total intake of food:high fat, trans fatty acids, fructose, low fibre
2. Changes in exposure to pathogens (hygiene hypothesis)
3. Low levels Vitamin D as hormone as well as Vitamin assoc with increased risk Type 1&2 DM.
4. Heating and cooling of buildings has reduced need to expend energy to thermoregulate.
5. Shorter periods of sleep tend to increase weight gain.
POSSIBLE INTERVENTIONS:
1. healthy diet and exercise
2. normalizing sleep
3. re-acquaint with temperatures outside thermoneutral zone
4. vitamin D therapy serum levels >70ng/ml target
5. EARLY use METFORMIN and THIAZOLINEDIONES which might preserve beta cell function in type 2 and even type 1 DM.
6. PREVENTION IS ONLY SUSTAINABLE APPROACH
Protecting beta cells:
* 80% of beta cells have been destroyed by the time a patient presents with Type 1 DM, 60% when presenting with Type 2 DM.
* METFORMIN, STIGAGLIPTIN, THIAZONELINEDIONES might slow rate decline of beta cells.
CLASSIFICATION DIABETES (American diabetes association)
* >50 types!!Type 1 DM 10%
* Type 2 DM
* Gestational DM (5% all Aussie women), 13% women aged 45-49 and higher in Aboriginals, torres straits islanders and south Asian women.
TREATMENT TARGETS FOR DIABETES
UKPDS Study 1998
* looked at patients with newly diagnosed DM assigned intensive control with METFORMIN, Sulfonylurea or insulin or conventional treatment with diet alone.
* Median HbA1C of 7.0-7.9% only achieved.
* only half achieved target 7.0% even after intensive treatment.
* better control lead to 12% reduction in all diabetes endpoints ESP. microvascular events.
* MI and all-cause mortality reduced in obese patients treated with MTF as firstline.
ACCORD STUDY 2008
* 10,000 patients, average age 62 years with longstanding disease and had established CVD or increased risk
* randomised to intensive therapy to reach HBA1C 6.0% or conventional therapy 7.0-7.9%
Trial stopped: all-cause MORTALITY INCREASED with INTENSIVE glucose lowering ( 5.0% vs 4.0%)
-->reasons for death unknown
AUSTRALIAN TREATMENT TARGETS
* general target: <7.0%
* Diabetes if short duration (10 years in younger patients/<20 years in older patients and no cardiovascular disease)
* + require lifestyle modification=<6.0%
* +require antidiabetics other than MTF and insulin=<6.5%
* requiring insulin =<7.0%
* Pregnancy or planning pregnancy=<6.0%
* Diabetes of longer duration or clinical cardiovascular disease=<7.0%
* Recurrent severe hypoglycemia or hypoglycemia unawareness <8.0%
HBA1C vs estimated average glucose (mmol/L)
* 5% = 5.4mmol/L
* 6% =7.0mmol/L
* 7%=8.6 mmol/L
* 8%=10.2 mmol/L
* 9%=11.8 mmol/L
* 10%= 13.4 mmol/L
* 11%=14.9 mmol/L
* 12%=16.5 mmol/L
DATA FROM DIABETES CARE;2008; 1473-1478.
UKPDS Study 1998
* looked at patients with newly diagnosed DM assigned intensive control with METFORMIN, Sulfonylurea or insulin or conventional treatment with diet alone.
* Median HbA1C of 7.0-7.9% only achieved.
* only half achieved target 7.0% even after intensive treatment.
* better control lead to 12% reduction in all diabetes endpoints ESP. microvascular events.
* MI and all-cause mortality reduced in obese patients treated with MTF as firstline.
ACCORD STUDY 2008
* 10,000 patients, average age 62 years with longstanding disease and had established CVD or increased risk
* randomised to intensive therapy to reach HBA1C 6.0% or conventional therapy 7.0-7.9%
Trial stopped: all-cause MORTALITY INCREASED with INTENSIVE glucose lowering ( 5.0% vs 4.0%)
-->reasons for death unknown
AUSTRALIAN TREATMENT TARGETS
* general target: <7.0%
* Diabetes if short duration (10 years in younger patients/<20 years in older patients and no cardiovascular disease)
* + require lifestyle modification=<6.0%
* +require antidiabetics other than MTF and insulin=<6.5%
* requiring insulin =<7.0%
* Pregnancy or planning pregnancy=<6.0%
* Diabetes of longer duration or clinical cardiovascular disease=<7.0%
* Recurrent severe hypoglycemia or hypoglycemia unawareness <8.0%
HBA1C vs estimated average glucose (mmol/L)
* 5% = 5.4mmol/L
* 6% =7.0mmol/L
* 7%=8.6 mmol/L
* 8%=10.2 mmol/L
* 9%=11.8 mmol/L
* 10%= 13.4 mmol/L
* 11%=14.9 mmol/L
* 12%=16.5 mmol/L
DATA FROM DIABETES CARE;2008; 1473-1478.
Thursday, May 29, 2008
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