Podcast
Questions and Answers
What is a common characteristic of pain due to pressure on nerves?
What is a common characteristic of pain due to pressure on nerves?
- Dull and persistent
- Burning and radiating
- Numbness and tingling (correct)
- Throbbing and pulsating
How is pain of non-inflammatory origin typically related to activity?
How is pain of non-inflammatory origin typically related to activity?
- It improves with increased activity
- The less you do, the worse it gets
- It remains constant regardless of activity level
- The more you do, the worse it gets (correct)
What type of pain is often present at rest as well as on use, and tends to vary unpredictably?
What type of pain is often present at rest as well as on use, and tends to vary unpredictably?
- Bone-related pain
- Nerve-related pain
- Muscle-related pain
- Pain caused by inflammation (correct)
Which type of arthritis is associated with prolonged morning stiffness that may last for several hours?
Which type of arthritis is associated with prolonged morning stiffness that may last for several hours?
What can joint swelling, especially if intermittent, indicate?
What can joint swelling, especially if intermittent, indicate?
What type of arthritis tends to cause localised stiffness that may be short-lasting but can recur after sitting for short periods?
What type of arthritis tends to cause localised stiffness that may be short-lasting but can recur after sitting for short periods?
What is a common complaint associated with ankle swelling?
What is a common complaint associated with ankle swelling?
What type of pain is severe bone pain often suggestive of?
What type of pain is severe bone pain often suggestive of?
What does intermittent joint swelling sometimes feel like according to patients?
What does intermittent joint swelling sometimes feel like according to patients?
What type of pain tends to be relieved by rest?
What type of pain tends to be relieved by rest?
Which symptom is more associated with inflammatory joint conditions like rheumatoid arthritis (RA)?
Which symptom is more associated with inflammatory joint conditions like rheumatoid arthritis (RA)?
What distinguishes non-inflammatory conditions like osteoarthritis (OA) from inflammatory joint conditions?
What distinguishes non-inflammatory conditions like osteoarthritis (OA) from inflammatory joint conditions?
In the shoulder, where is pain from the acromioclavicular joint usually felt?
In the shoulder, where is pain from the acromioclavicular joint usually felt?
Where is pain from the glenohumeral joint or rotator cuff usually felt in the shoulder?
Where is pain from the glenohumeral joint or rotator cuff usually felt in the shoulder?
What type of pain is associated with tennis elbow?
What type of pain is associated with tennis elbow?
What does it mean if a patient localizes their pain accurately to the affected joint?
What does it mean if a patient localizes their pain accurately to the affected joint?
What distinguishes inflammatory and non-inflammatory musculoskeletal conditions based on symptoms?
What distinguishes inflammatory and non-inflammatory musculoskeletal conditions based on symptoms?
Where might pain from the knee be felt, other than in the knee itself?
Where might pain from the knee be felt, other than in the knee itself?
What type of pain is associated with irritation of a nerve, such as in sciatica?
What type of pain is associated with irritation of a nerve, such as in sciatica?
What distinguishes pain from inflammatory joint conditions like rheumatoid arthritis (RA) from non-inflammatory conditions like osteoarthritis (OA)?
What distinguishes pain from inflammatory joint conditions like rheumatoid arthritis (RA) from non-inflammatory conditions like osteoarthritis (OA)?
Where might pain due to irritation of a nerve be felt?
Where might pain due to irritation of a nerve be felt?
Which of the following is a key feature of psoriatic arthritis?
Which of the following is a key feature of psoriatic arthritis?
What is a common feature of several rheumatological diseases?
What is a common feature of several rheumatological diseases?
What is a key component of history taking in exploring a patient's concerns and expectations?
What is a key component of history taking in exploring a patient's concerns and expectations?
What does signposting involve in a history taking context?
What does signposting involve in a history taking context?
What should be assessed when asking about medical conditions?
What should be assessed when asking about medical conditions?
'Intravenous drug use is a risk factor for which condition?'
'Intravenous drug use is a risk factor for which condition?'
'When should joint swelling and fever prompt urgent review and investigation?'
'When should joint swelling and fever prompt urgent review and investigation?'
What is an effective approach to history taking at the start of consultations?
What is an effective approach to history taking at the start of consultations?
What is the purpose of closed questions in history taking?
What is the purpose of closed questions in history taking?
Why is it important to demonstrate general communication skills during history taking?
Why is it important to demonstrate general communication skills during history taking?
What is an important initial step before proceeding with history taking in an OSCE setting?
What is an important initial step before proceeding with history taking in an OSCE setting?
How does using open questions contribute to effective history taking?
How does using open questions contribute to effective history taking?
Why is it important not to forget general communication skills during history taking?
Why is it important not to forget general communication skills during history taking?
What does gaining consent before proceeding with history taking indicate?
What does gaining consent before proceeding with history taking indicate?
Why should closed questions be used during history taking?
Why should closed questions be used during history taking?
What should be done before proceeding with history taking?
What should be done before proceeding with history taking?
Why is it important to facilitate patients to expand on their presenting complaint if required?
Why is it important to facilitate patients to expand on their presenting complaint if required?
What is the process of skeletal change known as?
What is the process of skeletal change known as?
Who developed the law that describes the nature of bone remodeling regarding stresses?
Who developed the law that describes the nature of bone remodeling regarding stresses?
Which cells are responsible for the resorption and deposition phases of bone remodeling?
Which cells are responsible for the resorption and deposition phases of bone remodeling?
What dictates how the integrity of the bone is altered in response to forces applied?
What dictates how the integrity of the bone is altered in response to forces applied?
Which cells are influenced directly or indirectly by hormonal signals in bone remodeling?
Which cells are influenced directly or indirectly by hormonal signals in bone remodeling?
What did Julius Wolff's law state about bones adapting to mechanical loading?
What did Julius Wolff's law state about bones adapting to mechanical loading?
What contributes metabolically to the body's balance of calcium and phosphorus?
What contributes metabolically to the body's balance of calcium and phosphorus?
Which marker is specific to bone formation?
Which marker is specific to bone formation?
What is the primary cause of osteoporosis?
What is the primary cause of osteoporosis?
Which condition is characterized by abnormal bone resorption and irregular osteoblastic response?
Which condition is characterized by abnormal bone resorption and irregular osteoblastic response?
What is the function of bisphosphonates in treating osteoporosis?
What is the function of bisphosphonates in treating osteoporosis?
What is the characteristic feature of osteopetrosis?
What is the characteristic feature of osteopetrosis?
What imaging technique is used for bone scintigraphy?
What imaging technique is used for bone scintigraphy?
What does dual-energy X-ray absorptiometry (DEXA) measure?
What does dual-energy X-ray absorptiometry (DEXA) measure?
Which medication inhibits osteoclast activity and increases the renal excretion of calcium?
Which medication inhibits osteoclast activity and increases the renal excretion of calcium?
What is the mechanism of action of Denosumab?
What is the mechanism of action of Denosumab?
Which medication has agonist activity in bone and antagonist activity in other tissues?
Which medication has agonist activity in bone and antagonist activity in other tissues?
Why are non-nitrogen-containing bisphosphonates no longer typically prescribed?
Why are non-nitrogen-containing bisphosphonates no longer typically prescribed?
What is the primary effect of Raloxifene in bone?
What is the primary effect of Raloxifene in bone?
Which medication decreases the activity and survival of osteoclasts by inhibiting the RANK-RANKL interaction?
Which medication decreases the activity and survival of osteoclasts by inhibiting the RANK-RANKL interaction?
What cell lineage do osteoblasts and osteoclasts derive from?
What cell lineage do osteoblasts and osteoclasts derive from?
What is the role of osteocytes in bone remodeling?
What is the role of osteocytes in bone remodeling?
Which hormone acts to increase calcium levels in the bloodstream?
Which hormone acts to increase calcium levels in the bloodstream?
What effect do glucocorticoids have on bone formation?
What effect do glucocorticoids have on bone formation?
What is the consequence of estrogen deficiency on bone remodeling?
What is the consequence of estrogen deficiency on bone remodeling?
What is the function of Calcitonin in bone remodeling?
What is the function of Calcitonin in bone remodeling?
Which type of joint is typically lined with hyaline cartilage and has a wedge of fibrocartilage joining the bones?
Which type of joint is typically lined with hyaline cartilage and has a wedge of fibrocartilage joining the bones?
What contributes to joint stability?
What contributes to joint stability?
Which joint type permits the greatest movement?
Which joint type permits the greatest movement?
What is an example of a fibrous joint?
What is an example of a fibrous joint?
What is the primary gender demographic affected by rheumatoid arthritis (RA)?
What is the primary gender demographic affected by rheumatoid arthritis (RA)?
What is the key improvement index for desirable outcomes in RA?
What is the key improvement index for desirable outcomes in RA?
What is the optimal therapeutic window for early symptoms of RA?
What is the optimal therapeutic window for early symptoms of RA?
What are the clinical manifestations of symmetrical joint involvement in RA?
What are the clinical manifestations of symmetrical joint involvement in RA?
Which cytokines involved in RA can promote osteoclastogenesis and suppress bone formation?
Which cytokines involved in RA can promote osteoclastogenesis and suppress bone formation?
What is the cornerstone in RA treatment, acting through various mechanisms including folate antagonism and downregulation of adhesion molecules?
What is the cornerstone in RA treatment, acting through various mechanisms including folate antagonism and downregulation of adhesion molecules?
What might contribute to bone loss in RA by targeting osteoclasts?
What might contribute to bone loss in RA by targeting osteoclasts?
What is a known side effect of Methotrexate (MTX) interaction with other drugs?
What is a known side effect of Methotrexate (MTX) interaction with other drugs?
Which organs are affected by RA, leading to sarcopenia among other conditions?
Which organs are affected by RA, leading to sarcopenia among other conditions?
What is a potential consequence of destruction of subchondral bone in weight-bearing joints?
What is a potential consequence of destruction of subchondral bone in weight-bearing joints?
Which cells are activated in the articular joints due to early cartilage damage in RA?
Which cells are activated in the articular joints due to early cartilage damage in RA?
What is a potential effect of cytokines involved in RA on cardiovascular health?
What is a potential effect of cytokines involved in RA on cardiovascular health?
What is the primary mechanism through which Methotrexate (MTX) acts as a cornerstone in RA treatment?
What is the primary mechanism through which Methotrexate (MTX) acts as a cornerstone in RA treatment?
Which autoimmune mechanisms may contribute to bone loss in RA?
Which autoimmune mechanisms may contribute to bone loss in RA?
What is the route of administration for Methotrexate (MTX) in RA treatment?
What is the route of administration for Methotrexate (MTX) in RA treatment?
Which scale is used for measuring disease activity in rheumatoid arthritis?
Which scale is used for measuring disease activity in rheumatoid arthritis?
What is the primary aim of treatment for rheumatoid arthritis?
What is the primary aim of treatment for rheumatoid arthritis?
Which genetic factors are major risk factors for rheumatoid arthritis?
Which genetic factors are major risk factors for rheumatoid arthritis?
What may trigger ACPA production in rheumatoid arthritis?
What may trigger ACPA production in rheumatoid arthritis?
What has gained attention in recent years due to its effectiveness in attenuating disease activity in rheumatoid arthritis?
What has gained attention in recent years due to its effectiveness in attenuating disease activity in rheumatoid arthritis?
What type of drugs are available for rheumatoid arthritis treatment?
What type of drugs are available for rheumatoid arthritis treatment?
What is the routine starting dose of Leflunomide for the initial 3 days?
What is the routine starting dose of Leflunomide for the initial 3 days?
Which adverse effect is commonly associated with Sulfasalazine?
Which adverse effect is commonly associated with Sulfasalazine?
What is the primary mechanism of action of Hydroxychloroquine in reducing joint inflammation in RA patients?
What is the primary mechanism of action of Hydroxychloroquine in reducing joint inflammation in RA patients?
What do biological DMARDs (bDMARDs) target in the treatment of RA?
What do biological DMARDs (bDMARDs) target in the treatment of RA?
What is the proposed role of TNF-α in mediating local bone destruction in inflammatory musculoskeletal diseases?
What is the proposed role of TNF-α in mediating local bone destruction in inflammatory musculoskeletal diseases?
What is the primary adverse effect associated with Leflunomide that may require dose reduction?
What is the primary adverse effect associated with Leflunomide that may require dose reduction?
What is the potential risk associated with long duration and high dose use of Hydroxychloroquine?
What is the potential risk associated with long duration and high dose use of Hydroxychloroquine?
What are the metabolites of Sulfasalazine?
What are the metabolites of Sulfasalazine?
What is the primary role of TNF-α in inflammatory musculoskeletal diseases?
What is the primary role of TNF-α in inflammatory musculoskeletal diseases?
Which infectious agent is associated with higher rates in RA patients, leading to neutrophil hyper citrullination and release of citrullinated autoantigens in the gums?
Which infectious agent is associated with higher rates in RA patients, leading to neutrophil hyper citrullination and release of citrullinated autoantigens in the gums?
Which factor has been shown to lower the risk of ACPA production and prevent RA onset?
Which factor has been shown to lower the risk of ACPA production and prevent RA onset?
What is the primary cause of cartilage damage in RA?
What is the primary cause of cartilage damage in RA?
Which infectious agent can affect ACPA-producing B cells and impaired EBV control is observed in RA?
Which infectious agent can affect ACPA-producing B cells and impaired EBV control is observed in RA?
What plays a role in smoking and genotype interaction in ANPA-positive RA?
What plays a role in smoking and genotype interaction in ANPA-positive RA?
What is linked to RA through their ability to trigger autoimmune responses and contribute to citrullinated autoantigens production?
What is linked to RA through their ability to trigger autoimmune responses and contribute to citrullinated autoantigens production?
What has been implicated in RA pathology, but the association with ACPA is not well established?
What has been implicated in RA pathology, but the association with ACPA is not well established?
What leads to hyperplastic synovium, which produces inflammatory cytokines and proteinases that perpetuate joint destruction in RA?
What leads to hyperplastic synovium, which produces inflammatory cytokines and proteinases that perpetuate joint destruction in RA?
What causes major cartilage damage by degrading type II collagen and glycosaminoglycans?
What causes major cartilage damage by degrading type II collagen and glycosaminoglycans?
What contributes to joint destruction in RA by targeting osteoclasts?
What contributes to joint destruction in RA by targeting osteoclasts?
Which type of psoriatic arthritis primarily affects the DIP joints?
Which type of psoriatic arthritis primarily affects the DIP joints?
What is the most common form of psoriatic arthritis that presents similarly to rheumatoid arthritis?
What is the most common form of psoriatic arthritis that presents similarly to rheumatoid arthritis?
Which form of psoriatic arthritis involves back stiffness and pain, primarily affecting the axial skeleton?
Which form of psoriatic arthritis involves back stiffness and pain, primarily affecting the axial skeleton?
What is the most severe form of psoriatic arthritis that affects the phalanges (the bones of the fingers and toes)?
What is the most severe form of psoriatic arthritis that affects the phalanges (the bones of the fingers and toes)?
Which characteristic x-ray finding is associated with arthritis mutilans in psoriatic arthritis?
Which characteristic x-ray finding is associated with arthritis mutilans in psoriatic arthritis?
What is the Psoriasis Epidemiological Screening Tool (PEST) used for?
What is the Psoriasis Epidemiological Screening Tool (PEST) used for?
Which joints does psoriatic arthritis tend to affect, distinguishing it from rheumatoid arthritis?
Which joints does psoriatic arthritis tend to affect, distinguishing it from rheumatoid arthritis?
What is the recommended approach for managing psoriatic arthritis?
What is the recommended approach for managing psoriatic arthritis?
What is the most commonly affected joint in gout?
What is the most commonly affected joint in gout?
What is the characteristic appearance of monosodium urate crystals under polarised light?
What is the characteristic appearance of monosodium urate crystals under polarised light?
What is the critical differential diagnosis for gout presentation?
What is the critical differential diagnosis for gout presentation?
Where are gouty tophi typically seen?
Where are gouty tophi typically seen?
What is the management for acute flares of gout?
What is the management for acute flares of gout?
What is the primary prophylactic treatment for gout after an acute attack has resolved?
What is the primary prophylactic treatment for gout after an acute attack has resolved?
What lifestyle changes can help reduce the risk of gout?
What lifestyle changes can help reduce the risk of gout?
When should prophylaxis for gout be initiated?
When should prophylaxis for gout be initiated?
What is the recommended duration for continuing antibiotics in the treatment of joint infections?
What is the recommended duration for continuing antibiotics in the treatment of joint infections?
What is the purpose of joint aspiration before starting antibiotics in the treatment of joint infections?
What is the purpose of joint aspiration before starting antibiotics in the treatment of joint infections?
What is the recommended initial route of administration for antibiotics in the treatment of joint infections?
What is the recommended initial route of administration for antibiotics in the treatment of joint infections?
What is the mortality rate associated with septic arthritis?
What is the mortality rate associated with septic arthritis?
In which type of surgery is infection more likely to occur?
In which type of surgery is infection more likely to occur?
Which bacterium is the most common causative organism for septic arthritis?
Which bacterium is the most common causative organism for septic arthritis?
What should be considered in a young patient presenting with a single acutely swollen joint until proven otherwise?
What should be considered in a young patient presenting with a single acutely swollen joint until proven otherwise?
What is the main factor governing the type of bone healing achieved at the fracture site?
What is the main factor governing the type of bone healing achieved at the fracture site?
What is the primary difference between primary and secondary bone healing?
What is the primary difference between primary and secondary bone healing?
What kind of mechanical strain achieves primary bone healing?
What kind of mechanical strain achieves primary bone healing?
Which fixation modality achieves a mechanical strain between 2-10% for secondary bone healing?
Which fixation modality achieves a mechanical strain between 2-10% for secondary bone healing?
What is the process by which mesenchymal tissue is converted directly to bone, with no cartilage intermediate?
What is the process by which mesenchymal tissue is converted directly to bone, with no cartilage intermediate?
What is the name given for the process of conversion of cartilage to bone?
What is the name given for the process of conversion of cartilage to bone?
What stimulates bone formation on the compression side and osteoclasts on the tension side?
What stimulates bone formation on the compression side and osteoclasts on the tension side?
What inhibits the activation of osteoclast precursor cells by occupying the binding site of RANK?
What inhibits the activation of osteoclast precursor cells by occupying the binding site of RANK?
What results in osteoclasts differentiation and activation by interacting with RANK expressed by osteoclasts?
What results in osteoclasts differentiation and activation by interacting with RANK expressed by osteoclasts?
What occurs at the junction of maturing chondrocytes and newly forming bone?
What occurs at the junction of maturing chondrocytes and newly forming bone?
Which type of bone ultimately replaces the center of the callus during coupled remodeling?
Which type of bone ultimately replaces the center of the callus during coupled remodeling?
What occurs during forming a bony callus when newly formed collagen-rich cartilaginous callus gets replaced by immature bone?
What occurs during forming a bony callus when newly formed collagen-rich cartilaginous callus gets replaced by immature bone?
What is the primary bone healing phase where stem cells are recruited and differentiated, leading to cartilaginous callus formation and primary bone formation?
What is the primary bone healing phase where stem cells are recruited and differentiated, leading to cartilaginous callus formation and primary bone formation?
Which phase of fracture healing provides provisional stability, triggers an inflammatory response, and initiates fibrocartilaginous callus formation?
Which phase of fracture healing provides provisional stability, triggers an inflammatory response, and initiates fibrocartilaginous callus formation?
What is the crucial step in fracture healing where disrupted blood vessels cause clotting and provide a temporary frame for subsequent healing?
What is the crucial step in fracture healing where disrupted blood vessels cause clotting and provide a temporary frame for subsequent healing?
Which cells are involved in concurrent angiogenesis during fracture healing, resulting in the mineralization of the extracellular matrix and chondrocyte apoptosis?
Which cells are involved in concurrent angiogenesis during fracture healing, resulting in the mineralization of the extracellular matrix and chondrocyte apoptosis?
What phase of bone fracture healing involves the interaction of signaling pathways to differentiate the appendicular skeleton for months to years after clinical union?
What phase of bone fracture healing involves the interaction of signaling pathways to differentiate the appendicular skeleton for months to years after clinical union?
What is the mechanical strain percentage range for secondary bone healing?
What is the mechanical strain percentage range for secondary bone healing?
Which type of bone healing is characterized by mechanical strain greater than 10%?
Which type of bone healing is characterized by mechanical strain greater than 10%?
What is the primary purpose of granulation tissue formation during fracture healing?
What is the primary purpose of granulation tissue formation during fracture healing?
Which cells are involved in laying down woven bone and calcifying the cartilaginous callus during fracture healing?
Which cells are involved in laying down woven bone and calcifying the cartilaginous callus during fracture healing?
What continues for months to years after clinical union, involving the interaction of signaling pathways to differentiate the appendicular skeleton?
What continues for months to years after clinical union, involving the interaction of signaling pathways to differentiate the appendicular skeleton?
What occurs concurrently with anabolic phase during fracture healing, resulting in mineralization of extracellular matrix and chondrocyte apoptosis?
What occurs concurrently with anabolic phase during fracture healing, resulting in mineralization of extracellular matrix and chondrocyte apoptosis?
Which medication is a selective estrogen receptor modulator combined with conjugated estrogen approved by the FDA for osteoporosis prevention but not for treatment?
Which medication is a selective estrogen receptor modulator combined with conjugated estrogen approved by the FDA for osteoporosis prevention but not for treatment?
What is the primary function of teriparatide in osteoporosis treatment?
What is the primary function of teriparatide in osteoporosis treatment?
Which medication inhibits farnesyl pyrophosphate synthase, leading to inhibition of osteoclast resorption and induction of osteocyte apoptosis?
Which medication inhibits farnesyl pyrophosphate synthase, leading to inhibition of osteoclast resorption and induction of osteocyte apoptosis?
What is the mechanism of action of denosumab in treating osteoporosis?
What is the mechanism of action of denosumab in treating osteoporosis?
What is the recommended first-line therapy for men with osteoporosis?
What is the recommended first-line therapy for men with osteoporosis?
What is the most common cause of nutritional rickets?
What is the most common cause of nutritional rickets?
Which medication can impair vitamin D metabolism and result in rickets?
Which medication can impair vitamin D metabolism and result in rickets?
What type of rickets may result from poor calcium absorption in children with malabsorption syndromes?
What type of rickets may result from poor calcium absorption in children with malabsorption syndromes?
What stimulates the secretion of parathyroid hormone (PTH) in calcipenic rickets?
What stimulates the secretion of parathyroid hormone (PTH) in calcipenic rickets?
What is the recommended daily vitamin D supplementation for pregnant women to prevent rickets in their offsprings?
What is the recommended daily vitamin D supplementation for pregnant women to prevent rickets in their offsprings?
What is the recommended daily oral vitamin D supplementation for breastfed infants and infants who consume less than 500 mL of fortified formula per day in the first year of their life?
What is the recommended daily oral vitamin D supplementation for breastfed infants and infants who consume less than 500 mL of fortified formula per day in the first year of their life?
What is the recommended daily vitamin D supplementation for high-risk groups for vitamin D deficiency beyond infancy?
What is the recommended daily vitamin D supplementation for high-risk groups for vitamin D deficiency beyond infancy?
What is the treatment for vitamin D-dependent rickets type I A (VDDR1A) and vitamin D-dependent rickets type I B (VDDR1B)?
What is the treatment for vitamin D-dependent rickets type I A (VDDR1A) and vitamin D-dependent rickets type I B (VDDR1B)?
What is the treatment for vitamin D-dependent rickets type II A (VDDR2A) and vitamin D-dependent rickets type II B (VDDR2B)?
What is the treatment for vitamin D-dependent rickets type II A (VDDR2A) and vitamin D-dependent rickets type II B (VDDR2B)?
What is the long term management for familial hypophosphatemic rickets?
What is the long term management for familial hypophosphatemic rickets?
What was the effect of a nationwide program in Turkey that introduced free vitamin D drops (400 IU/day) to children less than three years?
What was the effect of a nationwide program in Turkey that introduced free vitamin D drops (400 IU/day) to children less than three years?
What was the recommendation for residents located higher than 55th attitudes in Canada regarding daily maintenance doses of Vitamin D?
What was the recommendation for residents located higher than 55th attitudes in Canada regarding daily maintenance doses of Vitamin D?
Which serum 25-hydroxyvitamin D level is defined as insufficiency?
Which serum 25-hydroxyvitamin D level is defined as insufficiency?
What is the recommended dose of vitamin D for infants in single-dose therapy (stoss therapy)?
What is the recommended dose of vitamin D for infants in single-dose therapy (stoss therapy)?
What is the recommended daily dose of vitamin D for children aged 1-12 months in multiple doses therapy?
What is the recommended daily dose of vitamin D for children aged 1-12 months in multiple doses therapy?
Which biochemical abnormality may persist longer after the initiation of rickets treatment?
Which biochemical abnormality may persist longer after the initiation of rickets treatment?
In which type of rickets are serum calcium and PTH levels usually normal?
In which type of rickets are serum calcium and PTH levels usually normal?
What radiological change is the earliest sign of rickets?
What radiological change is the earliest sign of rickets?
Bone pain improves within two weeks after treatment initiation refers to which age group?
Bone pain improves within two weeks after treatment initiation refers to which age group?
What is the primary cause of rickets?
What is the primary cause of rickets?
What is the most common reason for limited sun exposure leading to vitamin D deficiency?
What is the most common reason for limited sun exposure leading to vitamin D deficiency?
Which region has the highest prevalence of rickets?
Which region has the highest prevalence of rickets?
What is necessary for normal mineralization in the context of rickets?
What is necessary for normal mineralization in the context of rickets?
Which factor contributes to the high incidence of rickets in Alaska?
Which factor contributes to the high incidence of rickets in Alaska?
What leads to hypophosphatemia and accumulation of hypertrophic chondrocytes in rickets?
What leads to hypophosphatemia and accumulation of hypertrophic chondrocytes in rickets?
What does evaluation for rickets typically include?
What does evaluation for rickets typically include?
What is a contributing factor to decreased prevalence of rickets in developed countries?
What is a contributing factor to decreased prevalence of rickets in developed countries?
What are the primary sources of vitamin D for normal mineralization in rickets?
What are the primary sources of vitamin D for normal mineralization in rickets?
Which of the following is a characteristic of FGF-23-independent hypophosphatemic rickets?
Which of the following is a characteristic of FGF-23-independent hypophosphatemic rickets?
What is the main cause of rickets worldwide in older infants and toddlers?
What is the main cause of rickets worldwide in older infants and toddlers?
What can predispose babies to rickets and hypocalcemia?
What can predispose babies to rickets and hypocalcemia?
What type of rickets is characterized by defects in vitamin D synthesis, vitamin D receptor, or vitamin D-VDR interactions?
What type of rickets is characterized by defects in vitamin D synthesis, vitamin D receptor, or vitamin D-VDR interactions?
What is a risk factor for nutritional vitamin D deficiency?
What is a risk factor for nutritional vitamin D deficiency?
What can lead to internalization of phosphate co-transporters in renal tubules?
What can lead to internalization of phosphate co-transporters in renal tubules?
What characterizes calcipenic rickets and phosphopenic rickets?
What characterizes calcipenic rickets and phosphopenic rickets?
What causes inhibited mineralization rickets?
What causes inhibited mineralization rickets?
What leads to increased renal phosphate loss?
What leads to increased renal phosphate loss?
What is the main cause of fibroblast growth factor 23 (FGF23)?
What is the main cause of fibroblast growth factor 23 (FGF23)?
What type of mutations cause end-organ resistance to the active form of vitamin D?
What type of mutations cause end-organ resistance to the active form of vitamin D?
What is the recommended analgesic for mild pain?
What is the recommended analgesic for mild pain?
What type of pain are NSAIDs particularly effective for?
What type of pain are NSAIDs particularly effective for?
For which conditions should strong opioids like morphine be reserved?
For which conditions should strong opioids like morphine be reserved?
Which type of pain is mild opioids such as codeine beneficial for?
Which type of pain is mild opioids such as codeine beneficial for?
For what conditions should strong opioids such as morphine, fentanyl, and pethidine be reserved?
For what conditions should strong opioids such as morphine, fentanyl, and pethidine be reserved?
What is a more suitable alternative pain management technique for pain of neuropathic origin or of a longer duration?
What is a more suitable alternative pain management technique for pain of neuropathic origin or of a longer duration?
What is the primary role of calcitonin in calcium homeostasis?
What is the primary role of calcitonin in calcium homeostasis?
Which condition is NOT a symptom of hypercalcemia?
Which condition is NOT a symptom of hypercalcemia?
What is a potential cause of hypercalcemia?
What is a potential cause of hypercalcemia?
Which medication can contribute to hypercalcemia by increasing renal reabsorption of calcium?
Which medication can contribute to hypercalcemia by increasing renal reabsorption of calcium?
Which hormone is secreted by the thyroid glands to regulate the amount of calcium in the blood?
Which hormone is secreted by the thyroid glands to regulate the amount of calcium in the blood?
What is the main function of calcitriol (vitamin D) in relation to calcium?
What is the main function of calcitriol (vitamin D) in relation to calcium?
What happens when levels of calcitriol become excessive?
What happens when levels of calcitriol become excessive?
What stimulates chief cells in the parathyroid gland to secrete additional parathyroid hormone (PTH)?
What stimulates chief cells in the parathyroid gland to secrete additional parathyroid hormone (PTH)?
What is the main function of calcitriol (vitamin D) in regulating serum calcium?
What is the main function of calcitriol (vitamin D) in regulating serum calcium?
How does parathyroid hormone (PTH) raise blood calcium levels?
How does parathyroid hormone (PTH) raise blood calcium levels?
What is the consequence of excessive levels of calcitriol (vitamin D)?
What is the consequence of excessive levels of calcitriol (vitamin D)?
Where is calcitonin secreted from?
Where is calcitonin secreted from?
What is the role of calcitonin in calcium homeostasis?
What is the role of calcitonin in calcium homeostasis?
What are the symptoms of hypercalcemia when levels exceed 3mmol/L?
What are the symptoms of hypercalcemia when levels exceed 3mmol/L?
What can cause hypercalcaemia?
What can cause hypercalcaemia?
How do thiazide diuretics contribute to hypercalcaemia?
How do thiazide diuretics contribute to hypercalcaemia?
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Study Notes
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Bone remodeling begins in fetal life and involves two cell lineages: osteoblasts and osteoclasts.
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Osteoblasts derive from mesenchymal stem cells and contribute to bone growth.
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Osteoclasts originate from hematopoietic lineage in bone marrow and cause bone resorption.
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Fusion of osteoblast and osteoclast precursors forms multinucleated osteoclast, which attaches to bone surface and commences resorption by breaking down bone matrix (hydroxyapatite and organic material).
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Mononuclear macrophage lineage cells may conduct a "reversal" phase, depositing organic material and releasing growth factors to initiate bone deposition.
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Differentiation of mesenchymal precursors fills "Howship lacunae" with new collagen and minerals.
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Osteocytes, the most abundant cell type in mature bone, are situated in bone matrix and play a role in bone remodeling by transmitting signals regarding bone stress and regulating fluid flow.
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Parathyroid Hormone (PTH) is a polypeptide hormone secreted by parathyroid glands and acts to increase calcium levels in bloodstream by influencing bone and kidney and indirectly acting on intestines via vitamin D.
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Estrogen deficiency leads to increased bone remodeling and decreased bone mass, potentially due to blocking production and action of interleukin-6 and osteoclast survival thriving in its deficiency.
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Calcitonin is a polypeptide hormone released from thyroid C cells in response to high calcium levels and inhibits bone resorption.
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Growth Hormone (GH) is a peptide hormone secreted by pituitary gland and acts directly and indirectly through insulin-like growth factors to stimulate bone formation and resorption.
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Glucocorticoids decrease bone formation and cause osteoblast cell death, favoring osteoclast survival.
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Hormones such as Thyroid-stimulating hormone (TSH), thyroxine (T4), and triiodothyronine (T3) stimulate bone growth and elongation at epiphyseal plates.
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Hypothyroidism and hyperthyroidism result in low and high rates of bone turnover, respectively, due to effect on number and activity level of osteoblasts and osteoclasts.
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RA treatment outcomes and disease progression depend on patient awareness, timely diagnosis, and physician capability.
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Poorly controlled or severe RA may lead to extra-articular manifestations such as keratitis, pulmonary granulomas, pericarditis/pleuritis, small vessel vasculitis, and other non-specific symptoms.
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There is no cure for RA and treatment aims to achieve a low disease activity state (LDAS).
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Composite scales for measuring disease activity include DAS-28, SDAI, and CDAI.
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NSAIDs and corticosteroids are often used to relieve stiffness and pain but do not prevent disease progression.
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DMARDs have gained attention in recent years due to their effectiveness in attenuating disease activity and delaying joint deformity.
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Traditional synthetic drugs, biological DMARDs, and novel potential small molecules are available for RA treatment.
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HLA-DR, especially HLA-DR1 and HLA-DR4, and PTPN22 are major genetic risk factors for RA. ACPA production is associated with these genes and with environmental factors.
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ACPA can be detected before joint symptoms and may be triggered by lung exposure to noxious agents and ER-Golgi transport disruptions.
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The role of the environment in gene-environment interaction and its impact on ACPA production is an ongoing area of research.
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Genetic and environmental factors influence RA susceptibility and outcomes differently in men and women.
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Familial factors and twin studies suggest that the risk of developing RA is increased in first-degree relatives of RA patients.
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The environment plays a significant role in ACPA production and may act as a triggering factor in RA development.
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Mutations in the coatomer subunit α gene can disrupt ER-Golgi transport and lead to hereditary autoimmune-mediated lung disease and arthritis.
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Smoking and the HLA-DR SE gene interaction can cause immune reactions to citrullinated proteins in RA.
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DNA methylation plays a role in smoking and genotype interaction in ANPA-positive RA.
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Three infectious agents, Porphyromonas gingivalis (P. gingivalis), Aggregatibacter actinomycetemcomitans (Aa), and Epstein-Barr virus (EBV), are linked to RA through their ability to trigger autoimmune responses and contribute to citrullinated autoantigens production.
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Aa infection is associated with higher rates in RA patients, leading to neutrophil hyper citrullination and release of citrullinated autoantigens in the gums.
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P. gingivalis and ACPAs can promote each other's production through different mechanisms: PAD and Rgps of P. gingivalis, and NETosis induced by ACPAs.
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EBV can affect ACPA-producing B cells and impaired EBV control is observed in RA.
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Dysbiosis in RA patients, particularly in the intestinal tract, is linked to the pathogenesis of RA through multiple molecular mechanisms.
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Omega-3 fatty acids have been shown to lower the risk of ACPA production and prevent RA onset.
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Hormonal levels have been implicated in RA pathology, but the association with ACPA is not well established.
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The loss of contact inhibition in FLS leads to hyperplastic synovium, which produces inflammatory cytokines and proteinases, such as MMPs and TIMPs, that perpetuate joint destruction in RA.
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Hyperplastic synovium causes cartilage damage through directed adhesion and invasion, resulting in joint-space narrowing on radiography.
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Major cartilage damage is caused by MMPs, such as membrane-type I MMP, that degrade type II collagen and glycosaminoglycans.
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Cartilage does not have enough regenerative potential, and under the influence of synovial cytokines and reactive nitrogen intermediates, chondrocytes undergo apoptosis, leading to cartilage degradation.
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Bone healing: primary (mechanical strain <2%), secondary (mechanical strain 2-10%), and non-union or delayed union (mechanical strain >10%)
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Bone fracture healing: intricate process to restore bone to pre-injury state and composition, involves hematoma formation, granulation tissue formation, callus formation, and bone remodeling
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Fracture healing starts with an anabolic phase, where stem cells are recruited and differentiated, leading to cartilaginous callus formation and primary bone formation
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Concurrently, angiogenesis occurs, where cells involved are recruited and differentiated, resulting in the mineralization of the extracellular matrix and chondrocyte apoptosis
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Hematoma formation is a crucial step, where disrupted blood vessels cause clotting and provide a temporary frame for subsequent healing, and MSCs are recruited
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Granulation tissue formation provides provisional stability, triggers an inflammatory response, and initiates fibrocartilaginous callus formation
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Callus formation involves the action of various cells, including fibroblasts, osteoblasts, and osteoclasts, to lay down woven bone and calcify the cartilaginous callus
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Bone remodeling continues for months to years after clinical union, involving the interaction of signaling pathways to differentiate the appendicular skeleton.
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Women with osteoporosis should begin treatment with risedronate, alendronate, zoledronic acid, or denosumab to reduce the risk of both vertebral and non-vertebral fractures.
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Bazedoxifene, a selective estrogen receptor modulator combined with conjugated estrogen, is approved by the FDA for osteoporosis prevention but not for treatment.
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Men should be offered bisphosphonates as the first-line therapy.
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Teriparatide can be used in patients who cannot tolerate bisphosphonates.
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Medications, such as raloxifene and ibandronate, which only reduce vertebral fractures, are reserved for patients who cannot tolerate previous medications.
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Combination therapy of teriparatide and a bisphosphonate or teriparatide and denosumab can be considered for patients with severe osteoporosis and hip and vertebral fractures.
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There are no randomized studies regarding monitoring of treatment with follow-up dual X-ray absorptiometry scans, but several studies show that women had reduced fractures with treatment independent of follow-up bone mineral density.
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Agents like teriparatide and hormonal-based therapy require immediate follow-up treatment with another agent upon stopping the medication, or bone mass is rapidly lost.
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There is ongoing debate about the most beneficial bisphosphonate treatment regimen, with studies underway to determine the benefits of drug holidays after five years of therapy or continuous therapy.
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Pharmacotherapy agents work through either anti-resorptive or anabolic means and include bisphosphonates, hormone replacement therapy, selective estrogen receptor modulators, teriparatide, and RANKL inhibitors.
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Bisphosphonates, particularly nitrogen-containing compounds, inhibit farnesyl pyrophosphate synthase, inhibiting osteoclast resorption and inducing osteocyte apoptosis.
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Common bisphosphonates include alendronate, risedronate, and zoledronic acid, and they reduce the rate of hip, spine, and wrist fractures significantly.
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Hormonal-based therapy, such as conjugated estrogen-progestin hormone replacement therapy and estrogen-only replacement therapy, can also be used for osteoporosis treatment, but with caution due to the risk of adverse effects.
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Teriparatide is a recombinant form of parathyroid hormone that stimulates osteoblasts to produce more bone, and is now FDA-approved for osteoporosis treatment in males and females.
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Denosumab is a monoclonal IgG2 that targets RANKL and inhibits its ability to bind to RANK, inhibiting osteoclast activation.
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Patients on bisphosphonates for any length of time and presenting with mild thigh discomfort should undergo a thorough workup, including education on the risks of thigh discomfort, full-length femur and hip radiographs, discontinuation of bisphosphonates, and referral to an orthopedic surgeon.
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Osteoporosis is a significant public health issue, affecting millions of elderly individuals, and is best managed by an interprofessional team of healthcare workers.
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Patient education is vital, including urging patients to modify their lifestyle and remain compliant with medications, quitting smoking and alcohol, and following a calcium-rich diet and taking vitamin D supplements.
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The outcomes of osteoporosis are poor, with over 250,000 hip fractures occurring each year and high mortality rates, loss of independence, and poor quality of life.
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Secondary complications, such as pressure sores, deep vein thrombosis, and nosocomial infections, are common in patients with osteoporosis.
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Limited sun exposure can lead to vitamin D deficiency and rickets despite year-round sunlight, due to clothing, indoor living, skin color, diet, pollution, or sunscreen use.
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Prevalence of rickets is higher in developing countries, especially in Africa, Middle East, and Asia, with rates of 10% to 70%.
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Developed countries saw a decrease in rickets with dietary supplementation, improved air quality, and public awareness.
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Incidence rates vary widely: 2.9/100,000 eventually 24.1/100,000 in the US, 10.5/100,000 for children under 3 in New Zealand, and 3.8/100,000 in Turkey.
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Rickets is most common in Alaska due to higher latitudes and lowest sunlight.
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Rickets is a bone disease caused by defects in the osteoid mineralization process, which results in abnormal growth of the cartilaginous growth plate.
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Vitamin D is necessary for normal mineralization; it can be obtained through diet or UVB exposure.
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Low serum calcium and phosphate levels can cause increased parathyroid hormone (PTH), which leads to hypophosphatemia and accumulation of hypertrophic chondrocytes.
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Evaluation includes serum alkaline phosphatase (ALP), which is high due to phosphate deficiency and increased osteoblastic activity, and serum 25-hydroxyvitamin D level, which is typically low in vitamin D deficiency.
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Secondary hyperparathyroidism can lead to internalization of phosphate co-transporters in renal tubules, resulting in renal phosphate loss and hypophosphatemia.
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Phosphopenic rickets is caused by chronic low serum phosphate levels due to impaired intestinal absorption or increased renal loss.
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Phosphate deficiency is rare in healthy individuals due to abundance in food.
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Premature children can experience osteopenia of prematurity from dietary phosphate deficiency.
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Fibroblast growth factor 23 (FGF23) increases renal phosphate loss and decreases reabsorption.
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Mutations causing inactivation of sodium-dependent phosphate transporters in the kidneys can lead to increased urinary phosphate loss.
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Both calcipenic rickets and phosphopenic ricks are characterized by hypophosphatemia and rachitic bone changes.
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Inhibited mineralization rickets occurs due to defects in growth plate mineralization with normal calcium and phosphate levels.
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Genetic causes of rickets are classified into vitamin D-dependent (calcipenic) and congenital hypophosphatemic types.
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Vitamin D-dependent rickets (VDDR): caused by defects in vitamin D synthesis, vitamin D receptor, or vitamin D-VDR interactions.
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VDR mutations in VDDR2A cause end-organ resistance to the active form of vitamin D.
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FGF-23-dependent hypophosphatemic rickets: characterized by an abnormality in phosphatonin regulation of phosphate homeostasis.
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FGF-23-independent hypophosphatemic rickets: characterized by a pathology in the renal tubules causing phosphate transport defects.
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Vitamin D deficiency is the main cause of rickets worldwide in older infants and toddlers.
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Risk factors for nutritional vitamin D deficiency include prolonged exclusive breastfeeding, excessive juice consumption, and inadequate intake of vitamin D fortified foods.
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Vitamin D deficiency in pregnant mothers can predispose their babies to rickets and hypocalcemia.
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Vitamin D deficiency and rickets are more common in higher latitudes due to reduced UVB radiation.
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