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Metabolic Bone Diseases for Orthopaedic Exams
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Metabolic Bone Diseases for Orthopaedic Exams
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Segment:0 .
Mason today, giving us a talk on metabolic bone disorders. Now, Mr tuberosity is a senior registrar at the Countess of Chester Hospital. Now own metabolic bone disorders is a very important topic for the assessment of RCS exam. It's very easy to get tripped over, so please, please pay attention, then hopefully break it down nicely.
Simple before you so it will protect you. Well, get you well prepared for the exam. Now also as well. Potential good sources for knowledge of the exam for metabolic bone diseases does include. Are Fox concise orthopedic notebook? So please, please get. You can get this on Amazon as a download as well.
So I do recommend it. OK so without further ado, I will pass you on to Mr Peabody. OK oh, hi, David. Thank you for the kind introduction. Hi, good evening, everyone. I'll start my screen share. Yep right. So good evening, everyone, as David has rightly said, it is not one of the most comfortable topics when it comes to your exit exam.
So hopefully this talk today will the ease in your preparation does not would be very relevant for a clinical practice, but yeah, this should be sufficient enough for clearing the hurdle of a fuss. Yes Yeah. No no disclosures to begin with. And as we know, this part of orthopedics would be very relevant for both your x and y examination as well.
So to begin with on your wiwa table, your examiner might ask, can you tell me about the normal bone metabolism? I can't emphasize enough here that you will need to draw and speak together. I would, I say the vitamin D enters into the body by a foot and skin. It is hydroxyl by level by 25 hydroxylase. It is then acted upon from the kidney and is made into an active form of vitamin d, which is the 125 hydroxy collect from this active form of vitamin D brings about calcium and phosphorus absorption from the gut, which in turn increases the calcium level in the blood.
What are the other ways by which the calcium level increases in the blood? The one is by calcium and phosphorus resorption from the bone. And the calcium reabsorption from the kidney. Both of these are regulated by parathyroid hormone, which is in turn secreted by petrel glands. So this I calcium level in the body act by a negative feedback mechanism and suppresses the uptake in the clinical context of hypercalcemia.
So that is what would be relevant here. So having known the background of your normal bone metabolism, we would start with. Sorry osteoporosis, when it comes to definition, a WHO is very clear about how to define how I define osteoporosis. It's a skeletal disease characterized by age related decrease in bone mass per unit volume with a disrupted microarchitecture.
Consequently, there is increasing bone fragility and susceptibility to. Low trauma fractures can be. Tell me what a score is, you will be handed over a prop like this showing a bone mineral density, showing the scores on the right side and the age on the x-axis. A Peace Corps is essentially a number of standard deviations above or below the mean bone mineral density for a sex and race match healthy population.
It can be used as a guide, whether a patient is osteopathic or osteoporotic and whether they need to commence a treatment in the context and background of the T score. Z-score is a similar test score, which is a number of standard deviations above or below the mean BMD for sex and race, but for an age matched population. So for a 70-year-old patient, will be compared with a standard 70 year population for that particular cohort.
This definition would be very useful in your wider context and what was revising the Earth example? On on the background of Austria, discord and said score osteopenia is defined as L to 2L four lumbar density of 1 2, 1 2.4 standard deviation below the peak bone mass of a 25 individual, while osteoporosis is lumbar density, which is more than 2.5 standard deviation below the peak bone mass of a 25-year-old individual.
So what are the risk factors when it comes to osteoporosis, as we can't emphasize enough and then it's an exam of structure and how well you articulate it, so have headings in mind. Risk factors can be primary. Secondary primary are genetic, hormonal and mental and dietary, while secondary are for the person with underlying medical conditions on long standing drugs, or it can be also classified as type I and type Ii.
The type 1 osteoporosis happens is very common around the menopause, when there is a reduced levels of estrogen, while a type Ii is age related, which happens 10 to 15 years later and essentially due to poor calcium absorption and a low turnover. Investigation wise, you need to know about plane access. The fact that a 30% bone loss is required to manifest osteoporosis during my exam when I had this examiner took me directly to the DEXA scan.
However, it is worthwhile knowing about the different parameters, which involves a blood test involving FVC bone profile, prostate specific antigen myeloma, screen use of alkaline phosphatase and 24 hour urinary calcium, which which then brings about to the meat of the diagnosis, which involves Texas can, which in a sense is a gold standard for diagnosis and management of osteoporosis. And essentially, it measures an actual bone density, which is a mineral surface area of the bone.
How does it act? So in short, it's a twin X-ray beam, which are passed through the target of interest in which would be lumbar bone or proximal femur. And the emerging strength is measured into access, and that gives you a rough estimate of the Texas skin. I want a way that is accurate. The patient exposed to not a significant amount of radiation.
It's quick and simple to perform. The British Orthopedic Association laid down some guidelines for a patient who is less than 75 and one insufficiency fracture. They are sent for a DEXA scan. However, if you are having a patient with more than 75 and one insufficiency. No need for a Texas scan, you can straight away go ahead with treatment.
Which brings us to the next question. What are the indications? When would you send a patient or refer for a DEXA scan when there is a radiographic evidence of osteopenia? The BMI less than 19 and maternal history of hip fracture and another important algorithm in this context is the FRAX tool, which is quite again, often. Often the exam.
It's an algorithm for 10 years, absolute fracture given by the World Health Organization. It is based on a combination of independent clinical risk factors and BMD measured by the DEXA scan. The only caveat to this is if the clinical risk factors, even with the background of higher BMD, shows more at risk for a fragility fracture than someone who has a low BMD without a risk factor. So they lay more emphasis on patients with the risk factors for osteoporosis.
Of having had this background, how would you treat a patient osteoporosis? The treatment guidelines given by nice are preventive and treatment, everyone should be given a lifestyle modification advice, nutritional advice, exercise program and falls prevention for the genetic population. If treatment can be roughly into one which prevents your bone loss and one which stimulates the bone formation.
A calcium and vitamin D are, in a sense, having had known the mechanism reduces the bone resorption recommended. Daily allowance is 100 to 500 milligrams of calcium and vitamin D is 1,000 international units. The most commonly asked drugs in the treatment would be a bisphosphonate which inhibits osteoclast, and the studies have shown that the hip fracture rate is reduced by 50% As a clinician, the cautionary measure the chances of chronic kidney disease suffer Kendrick fracture, which which are prevented by a bisphosphonate holiday in patients taking long, long term and a rare incidence of osteonecrosis of jaw.
When it comes to mechanism of action of bas status, it is divided into some having nitrogen and without the nitrogen non nitrogen containing are not that common. They act by causing apoptosis, by accumulation of ATP metabolites within the cells, while the one nitrogen containing inhibit the production of cholesterol, which in turn interferes with the cell membrane. Examples of this nitrogen containing are the one which is commonly used by metronidazole Allen internet and abandon it to name a few.
Apart from this bisphosphonates that one needs to know about the second line and third line of drugs used for the treatment of osteoporosis, which includes some which are selective estrogen receptor modulators. Estrogen therapy, which would be very sex specific. Kelce trial and calcitonin. Of the other mechanism by which support is treatable, stimulating bone formation, the role of physical activity can be enhanced can be kind to emphasize enough.
While the other is teriparatide, which is a recombinant parathyroid hormone, the way it acts is by increasing the bone formation and microarchitecture and reducing the incidence of vertebral and non vertebral fractures. The other relevant metabolic bone disorders is osteoporosis, which is a marble bone disease. It would be easier to break this down. When you compare all the different metabolic disorders into suitable headings, which which would be useful when it comes to revising for this exam.
So in a sense, to know what it is, it is an increased bone sclerosis followed with loss of medial epicondyle. Why does it happen to impair osteoclast function? A genetic background wise? Most of the patients in clinical practice autosomal dominant because autosomal recessive can be infantile malignant variant. They are benign form and autosomal dominant give a residual of a lifelong risk of fractures that heal poorly.
Well, they also known the autism dominant, also known as Albert Schoenberg disease, and histologically, the osteoclast here like the raffel border, which impairs the action radiology wise. There is an increase in bone density. You have white cortices, a narrow canal. So as an orthopedic surgeon, you need to have an additional set of instrument as a bone is really hard.
To him, quite often ask and important is the pageot's, so know what it is. It is an imbalance between your osteoblasts and the osteoclast activity is opposite of what we discussed in the osteoporosis. Epidemiology, while it has been seen traditionally in the mining communities in the Lancashire population. There has been some evidence of viral etiology to it with measles.
Breaking down the path of a president, it will be worthwhile knowing the mnemonic as slap, which the disease process in a sense starts in the light phase, where there is increased. It starts with increasing the osteoclast size and the number, which leads to increase bone resorption. It is followed by the compensatory active phase, which is the attempt of the body to compensate the light egawa that is 40 times increase in the bone activity.
However, the end result is a disorganized woven bone. So you have various sclerosis and relate to osteopenia, along with increased blood flow and fibrous tissue formation. Resultantly, it turns out to do a burnt-out out phase when you are left with a dense mosaic pattern of bone with little cellular activity. Here, the matrix is brittle and the fracture healing is elsewhere.
It's quite slower. So clinically, most of them remain asymptomatic and are picked up quite late. You have bone pain quite unrelated to the activities and you have secondary osteoarthritis, which might be picked up when the sees her orthopedic surgeon or a primary care physician or any young lady, they can come with deformities. You can have pathological fractures.
No compression spinal tenodesis can result in come with a record of aquela from the medical background. They have a high incidence of high output cardiac failure and the later on there's a 30% increased risk of osteosarcoma when compared to the normal population. Investigation why the blood parameters for this page would be raised serum alkaline phosphatase, which is a marker of osteoblasts acid phosphatase, which is a marker of osteoclast and urine parameters.
How do you recognize this pathology early in your disease process wherein there will be light tick physis in the bone? Classical sign described, which is quite insecure, might be relevant for it would be a candle flame area of neurosis and metaphysics, also known as a flame or arrow sign. Later on in the burnt out and the faith, you have thick and sclerotic coats and there is lots of cortical material differentiation with vibrant bones and booing of.
The long medullary. So treatment as an orthopedic surgeon, what do you need to know and what to know for the exam? So when we are planning elective orthopedic surgery, this like arthroplasty or spinal stenosis, nerve entrapment and the treatment is required for prevention of fractures. Up to bisphosphonates are a mainstay of medical management. When would you do it and why would you do it?
So the guidelines are you start two to three months before your planned elective surgery. What is the rationale? You don't want to operate on a patient who is in the active phase of the disease. You want to convert the lytic face to the point out phase and. What pitfalls are also normalize the bone turnover, which makes the elective surgery easy.
You would do a standard operation, as you would do for a patient, including RF osteotomy or arthroplasty. So some factors when it comes to planning arthroplasty, like elective surgery for a patient would for a patient of pageot's, you would essentially divide into either surgeon factor, patient factor anesthetist factor and you would do pre-op bloods, including to the aco, which for, as we know about the high incidence of higher cardiac failure surgeon factor.
It's a complex case of need of MDT for pre-op deformity analysis, planning osteotomy involving the rheumatologist or the physician, including for the timing of the surgery. Intra operatively you would need to order an extra set of Remmers cemented would be good in the case of bleeding and hemostasis, and as a patient factor, the needs to counsel about the risk of underlying delay and use a cell salvage for excessive bleeding.
The other way to pick it or to structure this, an example would be either depending on timing of surgery, planning for surgery, pre-op factors, internal factors, postal factors. This would be the same as what we just discussed in the last slides. What does the evidence say for pageot's, assuming it's a challenging operation for day one orthopedic surgeon? So, yeah, MDT approach.
Long leg films, if the hospital doesn't have them, it isn't necessarily have a CT scan ground have the AP and the lateral views. Some recent evidence suggest use of uncommitted implants, as there had been reports of increased incidents of aseptic loosening with segmented implants. However, it is not beyond the doubt and these results are in. There are not enough to give convincing evidence, but worthwhile knowing about them.
As we touched upon the malignant sarcoma, a stage that is 30% higher risk, it happens in the one to 6% of all patients with pageot's. It is more common in the diffuse polyols traject variants. The prognosis with this background is very poor. Having having discussed the osteoporosis, the other question would be about Australasia.
What is a difference between the two and how would you find on biochemical testing? So having studied the osteoporosis, Oster militia is an adult form of rickets that occurs as a result of impaired or deficient mineralization. It is a sense a quality problem as opposed to a quantity problem in an osteoporosis and biochemical testing in osteoporosis.
A no, the normal urine in the serum calcium and phosphate are low and the alkaline phosphatase elevated. The caveat here would be unless hypo phosphatase is the cause, which is difficult for anyone to remember. Having said, editable, the adult form of records, it's mainly due to dietary deficiency of vitamin D or calcium. It leads to a being a quality problem that leads to impaired mineralization of bone matrix and as like an osteoporosis, it leads to weakened bone and increase the risk of pathology fragility fractures.
Serum calcium and phosphate are low in biochemical parameters and alkaline phosphatase is elevated. Of under the juvenile form of this rickets, which affects it, is an important mineralization of the cartilage matrix in the growth phase, and it affects the zone of provisional calcification in the hypertrophic zone of the physis.
Clinical features are generalized features and head-to-toe features for a patient less than 18 months will present with failure to thrive restlessness, hypotonia and a waddling gait. Well, the local features are from head to toe would be a delayed closure of fontanel of frontal and parietal pausing the grocery, which is the prominence at the cost to control junction. Harrison, sulcus, pigeon chest pot, belly and a cock, or guess it would be worthwhile mentioning, if you get this, you would be expected to know the reason for each of them.
Well, for the clinical feature of Oscar nominations, more incidents on set than rickets, the bone pain initially is vague and non-specific, and you can present with proximal muscle weakness. Well, radiology for as many classical features, which involves the physical widening, metaphyseal cupping and decreased bone density. Which can be very apparent in the wrist, X-rays or the X-rays.
We're also Malaysia this they have characteristic loser zones, which in a sense, is because of the stress on the compression side of the bone. And you have Milkman's Zulu fractures, in which because of impaired mineralization, the fractures have United but not mineralized. Some this would be relevant for the part one for the forces, which are the vitamin D resistant cricket, so it's uncommon, but it's the most common heritable version of rickets wherein it presents that one to two years.
And because of the dominant mutation, x-linked domination. Sorry exclaimed a mutation of a gene that is inability of renal tubules to absorb phosphate and resultant have rickets. Then another variant of vitamin D dependent, which is again rare, but clinical features, there are more severe if we go back into the mechanism of bone metabolism. The type 2 is where in the intracellular act intracellular receptor, that is where the mutation happens.
And in type one, the mutation of the renal 25 one hydroxyl is the last step before the formation of active form of vitamin D. A perennial austere dystrophies, another which was very difficult as an orthopedic surgeon to understand. I've tried to make it simple here. This is essentially a spectrum of disease seen in patients with chronic diseases, and it's characterized by bone deficiency due to electrolyte and endocrine abnormalities.
What you have here is a hypercalcemia because of the chronic renal disease damage, kidney cannot convert into its active form. And because of inability to excrete the phosphate tamia that is result in hyperparathyroidism and uranium because of the background of the chronic renal failure. You have two forms of austere dystrophy, the one with high bone turnover, which is a high. The mechanism of it is damage to the multiples because of the renal pathology of wherein vitamin D is affected.
Decreased calcium absorption, which which leads to a negative feedback loop, increase parathyroid hormone and bone turnover. The other one. So we end up with a low serum calcium explanatory hormone and ectopic calcium deposition. The other variant is a low bone turnover variety for renal dystrophy, where because of metals like aluminium, there is renal damage and where BPH releases inhibit, inhibited and you have resulted or Malaysia.
So two types the high bone turnover and the low bone turnover. A we to summarize, we will include a short description about and the hypercalcemia. The hypercalcemia you won't be expected to treat them, but it would be worthwhile knowing the clinical features of the popular saying is bone stones, groans and moons, wherein bones is for pain following excessive bone resorption stones is a renal calculi and with you grown, so will be your gastrointestinal nausea, vomiting, constipation and pains and moons will be the one for patients seen as manifestation, having lethargy and disorientation.
Well, closet of them can be akin. Structure wide malignancy, endocrine or genetic, AJ due to long standing steroids, vitamin D intoxication and metabolic disorders like sarcoidosis. Hypercalcemia again, it is worthwhile knowing the acute and the chronic features, you won't be expected to treat this pathologies. So they present with neuromuscular irritability, which can present a caustic sign through the sign, which is neuromuscular under the carpet spasm following low muscularity and epidural anesthesia.
On an ECG perimeter, there will be a prolonged interval if this persist for a long time in chronically. Patients can have cataract fungal infection. Well, so that would, in a sense, describe and conclude the talk. As I said, it's no matter meant to be an exhaustive lecture for treating a patient with metabolic bone disorder, but this would, in a sense, help to clear the FARC as a short seller about hypo for.
It is a rarer variant of metabolic bone disease, which is characterized by generalized impairment of bone mineralization. It is clinically, it presents similar to rickets, but with abnormal dentition blood parameters, while there is low level alkaline phosphatase, which results in decreased synthesis of inorganic phosphate necessary for bone formation. So that said, my main lecture was done from this book, which we as a group contributed and would be worthwhile reading about it.
Thank you. Thank you very much, Reihan. So that was a brilliant talk. It went through quite good detail about the key metabolic bone diseases that come up regularly in the exam. It also is interesting how it reminded me how everything is connected. So we discussed basic science advisor table we had.
We had osteoporosis, which can quite happily turn up on the trauma, the trauma table, talking about fragility fractures. Then you had adult pathology with had this disease, and then you also had as well rickets. So the pediatric table pediatrics. The key thing is it crosses all boundaries. So with any basic science topic, you have to think, where else will this turn up in the exam?
It's not just going to be limited to the basic science table, and a very good way of doing well in the basic science table is attributing any basic science topic to a clinical picture and vice versa. If you have a clinical picture and you can break it down into the basic science, you can, you're going to do do well with the examiners. OK, yeah, very well, explained David. That it very well.
Now, just to reassure everyone. This through a few people did join later. This has been recorded and will show up on their physis and mental website. So please, please do go through this again, even if you were here at the beginning. It's really important, and I had went through it in very, very well and made it very easy and explainable. OK, now we have got one volunteer for the vyver.
Segment:0 .
Mason today, giving us a talk on metabolic bone disorders. Now, Mr tuberosity is a senior registrar at the Countess of Chester Hospital. Now own metabolic bone disorders is a very important topic for the assessment of RCS exam. It's very easy to get tripped over, so please, please pay attention, then hopefully break it down nicely.
Simple before you so it will protect you. Well, get you well prepared for the exam. Now also as well. Potential good sources for knowledge of the exam for metabolic bone diseases does include. Are Fox concise orthopedic notebook? So please, please get. You can get this on Amazon as a download as well.
So I do recommend it. OK so without further ado, I will pass you on to Mr Peabody. OK oh, hi, David. Thank you for the kind introduction. Hi, good evening, everyone. I'll start my screen share. Yep right. So good evening, everyone, as David has rightly said, it is not one of the most comfortable topics when it comes to your exit exam.
So hopefully this talk today will the ease in your preparation does not would be very relevant for a clinical practice, but yeah, this should be sufficient enough for clearing the hurdle of a fuss. Yes Yeah. No no disclosures to begin with. And as we know, this part of orthopedics would be very relevant for both your x and y examination as well.
So to begin with on your wiwa table, your examiner might ask, can you tell me about the normal bone metabolism? I can't emphasize enough here that you will need to draw and speak together. I would, I say the vitamin D enters into the body by a foot and skin. It is hydroxyl by level by 25 hydroxylase. It is then acted upon from the kidney and is made into an active form of vitamin d, which is the 125 hydroxy collect from this active form of vitamin D brings about calcium and phosphorus absorption from the gut, which in turn increases the calcium level in the blood.
What are the other ways by which the calcium level increases in the blood? The one is by calcium and phosphorus resorption from the bone. And the calcium reabsorption from the kidney. Both of these are regulated by parathyroid hormone, which is in turn secreted by petrel glands. So this I calcium level in the body act by a negative feedback mechanism and suppresses the uptake in the clinical context of hypercalcemia.
So that is what would be relevant here. So having known the background of your normal bone metabolism, we would start with. Sorry osteoporosis, when it comes to definition, a WHO is very clear about how to define how I define osteoporosis. It's a skeletal disease characterized by age related decrease in bone mass per unit volume with a disrupted microarchitecture.
Consequently, there is increasing bone fragility and susceptibility to. Low trauma fractures can be. Tell me what a score is, you will be handed over a prop like this showing a bone mineral density, showing the scores on the right side and the age on the x-axis. A Peace Corps is essentially a number of standard deviations above or below the mean bone mineral density for a sex and race match healthy population.
It can be used as a guide, whether a patient is osteopathic or osteoporotic and whether they need to commence a treatment in the context and background of the T score. Z-score is a similar test score, which is a number of standard deviations above or below the mean BMD for sex and race, but for an age matched population. So for a 70-year-old patient, will be compared with a standard 70 year population for that particular cohort.
This definition would be very useful in your wider context and what was revising the Earth example? On on the background of Austria, discord and said score osteopenia is defined as L to 2L four lumbar density of 1 2, 1 2.4 standard deviation below the peak bone mass of a 25 individual, while osteoporosis is lumbar density, which is more than 2.5 standard deviation below the peak bone mass of a 25-year-old individual.
So what are the risk factors when it comes to osteoporosis, as we can't emphasize enough and then it's an exam of structure and how well you articulate it, so have headings in mind. Risk factors can be primary. Secondary primary are genetic, hormonal and mental and dietary, while secondary are for the person with underlying medical conditions on long standing drugs, or it can be also classified as type I and type Ii.
The type 1 osteoporosis happens is very common around the menopause, when there is a reduced levels of estrogen, while a type Ii is age related, which happens 10 to 15 years later and essentially due to poor calcium absorption and a low turnover. Investigation wise, you need to know about plane access. The fact that a 30% bone loss is required to manifest osteoporosis during my exam when I had this examiner took me directly to the DEXA scan.
However, it is worthwhile knowing about the different parameters, which involves a blood test involving FVC bone profile, prostate specific antigen myeloma, screen use of alkaline phosphatase and 24 hour urinary calcium, which which then brings about to the meat of the diagnosis, which involves Texas can, which in a sense is a gold standard for diagnosis and management of osteoporosis. And essentially, it measures an actual bone density, which is a mineral surface area of the bone.
How does it act? So in short, it's a twin X-ray beam, which are passed through the target of interest in which would be lumbar bone or proximal femur. And the emerging strength is measured into access, and that gives you a rough estimate of the Texas skin. I want a way that is accurate. The patient exposed to not a significant amount of radiation.
It's quick and simple to perform. The British Orthopedic Association laid down some guidelines for a patient who is less than 75 and one insufficiency fracture. They are sent for a DEXA scan. However, if you are having a patient with more than 75 and one insufficiency. No need for a Texas scan, you can straight away go ahead with treatment.
Which brings us to the next question. What are the indications? When would you send a patient or refer for a DEXA scan when there is a radiographic evidence of osteopenia? The BMI less than 19 and maternal history of hip fracture and another important algorithm in this context is the FRAX tool, which is quite again, often. Often the exam.
It's an algorithm for 10 years, absolute fracture given by the World Health Organization. It is based on a combination of independent clinical risk factors and BMD measured by the DEXA scan. The only caveat to this is if the clinical risk factors, even with the background of higher BMD, shows more at risk for a fragility fracture than someone who has a low BMD without a risk factor. So they lay more emphasis on patients with the risk factors for osteoporosis.
Of having had this background, how would you treat a patient osteoporosis? The treatment guidelines given by nice are preventive and treatment, everyone should be given a lifestyle modification advice, nutritional advice, exercise program and falls prevention for the genetic population. If treatment can be roughly into one which prevents your bone loss and one which stimulates the bone formation.
A calcium and vitamin D are, in a sense, having had known the mechanism reduces the bone resorption recommended. Daily allowance is 100 to 500 milligrams of calcium and vitamin D is 1,000 international units. The most commonly asked drugs in the treatment would be a bisphosphonate which inhibits osteoclast, and the studies have shown that the hip fracture rate is reduced by 50% As a clinician, the cautionary measure the chances of chronic kidney disease suffer Kendrick fracture, which which are prevented by a bisphosphonate holiday in patients taking long, long term and a rare incidence of osteonecrosis of jaw.
When it comes to mechanism of action of bas status, it is divided into some having nitrogen and without the nitrogen non nitrogen containing are not that common. They act by causing apoptosis, by accumulation of ATP metabolites within the cells, while the one nitrogen containing inhibit the production of cholesterol, which in turn interferes with the cell membrane. Examples of this nitrogen containing are the one which is commonly used by metronidazole Allen internet and abandon it to name a few.
Apart from this bisphosphonates that one needs to know about the second line and third line of drugs used for the treatment of osteoporosis, which includes some which are selective estrogen receptor modulators. Estrogen therapy, which would be very sex specific. Kelce trial and calcitonin. Of the other mechanism by which support is treatable, stimulating bone formation, the role of physical activity can be enhanced can be kind to emphasize enough.
While the other is teriparatide, which is a recombinant parathyroid hormone, the way it acts is by increasing the bone formation and microarchitecture and reducing the incidence of vertebral and non vertebral fractures. The other relevant metabolic bone disorders is osteoporosis, which is a marble bone disease. It would be easier to break this down. When you compare all the different metabolic disorders into suitable headings, which which would be useful when it comes to revising for this exam.
So in a sense, to know what it is, it is an increased bone sclerosis followed with loss of medial epicondyle. Why does it happen to impair osteoclast function? A genetic background wise? Most of the patients in clinical practice autosomal dominant because autosomal recessive can be infantile malignant variant. They are benign form and autosomal dominant give a residual of a lifelong risk of fractures that heal poorly.
Well, they also known the autism dominant, also known as Albert Schoenberg disease, and histologically, the osteoclast here like the raffel border, which impairs the action radiology wise. There is an increase in bone density. You have white cortices, a narrow canal. So as an orthopedic surgeon, you need to have an additional set of instrument as a bone is really hard.
To him, quite often ask and important is the pageot's, so know what it is. It is an imbalance between your osteoblasts and the osteoclast activity is opposite of what we discussed in the osteoporosis. Epidemiology, while it has been seen traditionally in the mining communities in the Lancashire population. There has been some evidence of viral etiology to it with measles.
Breaking down the path of a president, it will be worthwhile knowing the mnemonic as slap, which the disease process in a sense starts in the light phase, where there is increased. It starts with increasing the osteoclast size and the number, which leads to increase bone resorption. It is followed by the compensatory active phase, which is the attempt of the body to compensate the light egawa that is 40 times increase in the bone activity.
However, the end result is a disorganized woven bone. So you have various sclerosis and relate to osteopenia, along with increased blood flow and fibrous tissue formation. Resultantly, it turns out to do a burnt-out out phase when you are left with a dense mosaic pattern of bone with little cellular activity. Here, the matrix is brittle and the fracture healing is elsewhere.
It's quite slower. So clinically, most of them remain asymptomatic and are picked up quite late. You have bone pain quite unrelated to the activities and you have secondary osteoarthritis, which might be picked up when the sees her orthopedic surgeon or a primary care physician or any young lady, they can come with deformities. You can have pathological fractures.
No compression spinal tenodesis can result in come with a record of aquela from the medical background. They have a high incidence of high output cardiac failure and the later on there's a 30% increased risk of osteosarcoma when compared to the normal population. Investigation why the blood parameters for this page would be raised serum alkaline phosphatase, which is a marker of osteoblasts acid phosphatase, which is a marker of osteoclast and urine parameters.
How do you recognize this pathology early in your disease process wherein there will be light tick physis in the bone? Classical sign described, which is quite insecure, might be relevant for it would be a candle flame area of neurosis and metaphysics, also known as a flame or arrow sign. Later on in the burnt out and the faith, you have thick and sclerotic coats and there is lots of cortical material differentiation with vibrant bones and booing of.
The long medullary. So treatment as an orthopedic surgeon, what do you need to know and what to know for the exam? So when we are planning elective orthopedic surgery, this like arthroplasty or spinal stenosis, nerve entrapment and the treatment is required for prevention of fractures. Up to bisphosphonates are a mainstay of medical management. When would you do it and why would you do it?
So the guidelines are you start two to three months before your planned elective surgery. What is the rationale? You don't want to operate on a patient who is in the active phase of the disease. You want to convert the lytic face to the point out phase and. What pitfalls are also normalize the bone turnover, which makes the elective surgery easy.
You would do a standard operation, as you would do for a patient, including RF osteotomy or arthroplasty. So some factors when it comes to planning arthroplasty, like elective surgery for a patient would for a patient of pageot's, you would essentially divide into either surgeon factor, patient factor anesthetist factor and you would do pre-op bloods, including to the aco, which for, as we know about the high incidence of higher cardiac failure surgeon factor.
It's a complex case of need of MDT for pre-op deformity analysis, planning osteotomy involving the rheumatologist or the physician, including for the timing of the surgery. Intra operatively you would need to order an extra set of Remmers cemented would be good in the case of bleeding and hemostasis, and as a patient factor, the needs to counsel about the risk of underlying delay and use a cell salvage for excessive bleeding.
The other way to pick it or to structure this, an example would be either depending on timing of surgery, planning for surgery, pre-op factors, internal factors, postal factors. This would be the same as what we just discussed in the last slides. What does the evidence say for pageot's, assuming it's a challenging operation for day one orthopedic surgeon? So, yeah, MDT approach.
Long leg films, if the hospital doesn't have them, it isn't necessarily have a CT scan ground have the AP and the lateral views. Some recent evidence suggest use of uncommitted implants, as there had been reports of increased incidents of aseptic loosening with segmented implants. However, it is not beyond the doubt and these results are in. There are not enough to give convincing evidence, but worthwhile knowing about them.
As we touched upon the malignant sarcoma, a stage that is 30% higher risk, it happens in the one to 6% of all patients with pageot's. It is more common in the diffuse polyols traject variants. The prognosis with this background is very poor. Having having discussed the osteoporosis, the other question would be about Australasia.
What is a difference between the two and how would you find on biochemical testing? So having studied the osteoporosis, Oster militia is an adult form of rickets that occurs as a result of impaired or deficient mineralization. It is a sense a quality problem as opposed to a quantity problem in an osteoporosis and biochemical testing in osteoporosis.
A no, the normal urine in the serum calcium and phosphate are low and the alkaline phosphatase elevated. The caveat here would be unless hypo phosphatase is the cause, which is difficult for anyone to remember. Having said, editable, the adult form of records, it's mainly due to dietary deficiency of vitamin D or calcium. It leads to a being a quality problem that leads to impaired mineralization of bone matrix and as like an osteoporosis, it leads to weakened bone and increase the risk of pathology fragility fractures.
Serum calcium and phosphate are low in biochemical parameters and alkaline phosphatase is elevated. Of under the juvenile form of this rickets, which affects it, is an important mineralization of the cartilage matrix in the growth phase, and it affects the zone of provisional calcification in the hypertrophic zone of the physis.
Clinical features are generalized features and head-to-toe features for a patient less than 18 months will present with failure to thrive restlessness, hypotonia and a waddling gait. Well, the local features are from head to toe would be a delayed closure of fontanel of frontal and parietal pausing the grocery, which is the prominence at the cost to control junction. Harrison, sulcus, pigeon chest pot, belly and a cock, or guess it would be worthwhile mentioning, if you get this, you would be expected to know the reason for each of them.
Well, for the clinical feature of Oscar nominations, more incidents on set than rickets, the bone pain initially is vague and non-specific, and you can present with proximal muscle weakness. Well, radiology for as many classical features, which involves the physical widening, metaphyseal cupping and decreased bone density. Which can be very apparent in the wrist, X-rays or the X-rays.
We're also Malaysia this they have characteristic loser zones, which in a sense, is because of the stress on the compression side of the bone. And you have Milkman's Zulu fractures, in which because of impaired mineralization, the fractures have United but not mineralized. Some this would be relevant for the part one for the forces, which are the vitamin D resistant cricket, so it's uncommon, but it's the most common heritable version of rickets wherein it presents that one to two years.
And because of the dominant mutation, x-linked domination. Sorry exclaimed a mutation of a gene that is inability of renal tubules to absorb phosphate and resultant have rickets. Then another variant of vitamin D dependent, which is again rare, but clinical features, there are more severe if we go back into the mechanism of bone metabolism. The type 2 is where in the intracellular act intracellular receptor, that is where the mutation happens.
And in type one, the mutation of the renal 25 one hydroxyl is the last step before the formation of active form of vitamin D. A perennial austere dystrophies, another which was very difficult as an orthopedic surgeon to understand. I've tried to make it simple here. This is essentially a spectrum of disease seen in patients with chronic diseases, and it's characterized by bone deficiency due to electrolyte and endocrine abnormalities.
What you have here is a hypercalcemia because of the chronic renal disease damage, kidney cannot convert into its active form. And because of inability to excrete the phosphate tamia that is result in hyperparathyroidism and uranium because of the background of the chronic renal failure. You have two forms of austere dystrophy, the one with high bone turnover, which is a high. The mechanism of it is damage to the multiples because of the renal pathology of wherein vitamin D is affected.
Decreased calcium absorption, which which leads to a negative feedback loop, increase parathyroid hormone and bone turnover. The other one. So we end up with a low serum calcium explanatory hormone and ectopic calcium deposition. The other variant is a low bone turnover variety for renal dystrophy, where because of metals like aluminium, there is renal damage and where BPH releases inhibit, inhibited and you have resulted or Malaysia.
So two types the high bone turnover and the low bone turnover. A we to summarize, we will include a short description about and the hypercalcemia. The hypercalcemia you won't be expected to treat them, but it would be worthwhile knowing the clinical features of the popular saying is bone stones, groans and moons, wherein bones is for pain following excessive bone resorption stones is a renal calculi and with you grown, so will be your gastrointestinal nausea, vomiting, constipation and pains and moons will be the one for patients seen as manifestation, having lethargy and disorientation.
Well, closet of them can be akin. Structure wide malignancy, endocrine or genetic, AJ due to long standing steroids, vitamin D intoxication and metabolic disorders like sarcoidosis. Hypercalcemia again, it is worthwhile knowing the acute and the chronic features, you won't be expected to treat this pathologies. So they present with neuromuscular irritability, which can present a caustic sign through the sign, which is neuromuscular under the carpet spasm following low muscularity and epidural anesthesia.
On an ECG perimeter, there will be a prolonged interval if this persist for a long time in chronically. Patients can have cataract fungal infection. Well, so that would, in a sense, describe and conclude the talk. As I said, it's no matter meant to be an exhaustive lecture for treating a patient with metabolic bone disorder, but this would, in a sense, help to clear the FARC as a short seller about hypo for.
It is a rarer variant of metabolic bone disease, which is characterized by generalized impairment of bone mineralization. It is clinically, it presents similar to rickets, but with abnormal dentition blood parameters, while there is low level alkaline phosphatase, which results in decreased synthesis of inorganic phosphate necessary for bone formation. So that said, my main lecture was done from this book, which we as a group contributed and would be worthwhile reading about it.
Thank you. Thank you very much, Reihan. So that was a brilliant talk. It went through quite good detail about the key metabolic bone diseases that come up regularly in the exam. It also is interesting how it reminded me how everything is connected. So we discussed basic science advisor table we had.
We had osteoporosis, which can quite happily turn up on the trauma, the trauma table, talking about fragility fractures. Then you had adult pathology with had this disease, and then you also had as well rickets. So the pediatric table pediatrics. The key thing is it crosses all boundaries. So with any basic science topic, you have to think, where else will this turn up in the exam?
It's not just going to be limited to the basic science table, and a very good way of doing well in the basic science table is attributing any basic science topic to a clinical picture and vice versa. If you have a clinical picture and you can break it down into the basic science, you can, you're going to do do well with the examiners. OK, yeah, very well, explained David. That it very well.
Now, just to reassure everyone. This through a few people did join later. This has been recorded and will show up on their physis and mental website. So please, please do go through this again, even if you were here at the beginning. It's really important, and I had went through it in very, very well and made it very easy and explainable. OK, now we have got one volunteer for the vyver.
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