Vitamin D deficiency remains the most common cause of Osteomalacia & rickets.
My first presentation prepared by me as a first year family medicine board resident. 😊
Bone physiology, OSTEOPOROSIS, Pagets Disease, HyperparathyoidismKaushal Kafle
A brief introduction to bone physiology, with more focus on Osteoporosis and its recent updates. Small tail topics include hyperparathyroidism and pagets disease.
Rickets - Bony manifestation of altered Vit. D, Calcium, and phosphorus metabolism
- Rickets – child;
- Osteomalacia – adult form
there is an inability to mineralize chondroid and osteoid
- lack of available calcium or phosphorus (or both) for mineralization of newly formed osteoid
- osseous changes in both adults and children
--- Definition - a defect in mineralization of osteoid matrix caused by inadequate calcium and phosphate deposition prior to closure of physis.
- Clinical features arise from un-mineralized matrix at the growth plate.
- less mineralized bone per unit volume of bone
- classic changes of rickets will typically occur in children younger than 6-7 years of age
-- Pathophysiology of Rickets
- Vitamin D => increase the absorption of calcium from intestine
PTH => mobilizes calcium from bone and increases urinary excretion of phosphate
Calcitonin => inhibits bone resorption
CLINICAL FEATURES
Head:
Craniotabes — softening of cranial bones. also seen in osteogenesis imperfect, hydrocephalus and syphilis
Frontal bossing
Delayed dentition and tooth caries
Delayed closure of fontanel
Craniosynostosis.
Chest
Rachitic rosary — widening of osteochondral junction
Harrison’s groove — occurs due to pulling of softened ribs in inspiration by diaphragm. Softened ribs also predispose to atelectasis and pneumonia because of decreased air entry
Pectus carinatum (pigeon breast)
Spine
Scoliosis (uncommon)
Kyphosis (rachitic cat back)
Accentuation of lumbar lordosis
Limbs and Joints
Bone pain and tenderness
Coxa vara
Genu valgum or varum
Windswept deformity
Bowing of tibia, femur, radius and ulna
Widening of wrist, elbow, knee and ankle because of enlargement of ends of long bones
Rachitic saber shins
Sausage like enlargement of ends of phalanges and metacarpals, with regular constrictions corresponding of the joints string of pearls deformity
Double malleoli sign
General
Failure to thrive
Protuberant abdomen
Apathy, listlessness and irritability
Proximal muscle weakness
Ligament laxity
Symptoms of hypocalcemia—tetany, seizures and stridor due to laryngeal spasm
Bilateral lamellar cataract (Vitamin D deficiency in early infancy).
RADIOLOGICAL SIGNS
Generalized osteopenia
Bowing deformities of the long bones, femur and tibia
Widening of the growth plate
Cupping or flaring of the metaphysis
Radiographic findings in vitamin D resistant rickets
similar to those in infantile rickets
Bowing deformities and shortening of the long bones => more pronounced in early rickets
More common in distal ends of radius and ulna (more so in ulna)
Changes in the shaft appear a few weeks later than metaphysis.
The epiphysis is cloudy and indistinct and periosteum is thick.
The shaft shows diffuse rarefaction, thin cortices with coarse texture of spongiosa.
Umbau zones (Looser’s zones) => sharply defined radiolucent transverse zones
-- Findings of healing rickets:
Earliest finding => reappearance of the provisional zone of calcification, which gradually thickens
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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2. RICKETS AND OSTEOMALACIA
• Inadequate bone
mineralization.
• Excessive
unmineralized
osteoid.
• Osteomalacia adult
version of rickets.
• In rickets epiphyseal
involvement.
Different expression of
same disease
3.
4. Pathophysiology
• Deficiency of vit-D
• Hypocalcemia
• PTH secretion
• Plasma Ca
• Plasma P
• Bone resorption
• Bone formation for
compensation, lack of
Ca&P
• Rickets/osteomalacia
5. Epiphyseal Plate Abnormalities
• Resting & proliferative
zone not affected.
• zone of maturation:
irregularly distributed
cells.
• hypertrophic cells are
irregularly distributed
and the intervening
matrix bars cannot be
identified.
6. Cont..
NORMAL RICKETS
• honey comb
pattern vascular
growth distorted.
• Increase cartilage
cells and
unmineralized
matrix increase
length& width of
bones.
• Joint weight
produce “cupping”
18. Osteomalacia and osteoporosis
osteomalacia osteoporosis
unwell well
Generalized chronic ache Pain only after fracture
Muscle weak Muscle normal
Loosers zone No Loosers zone
Alkaline phosphatase
increased
Normal
Serum phosphorus
decreased
Normal
Ca X P < 2.4mmol/l >2.4 mmol/l
19. Treatment
• Vitamin –D deficiency rickets:
• Correction of cause of vitamin D deficiency:
adequate dietary supply, sun light exposer.
• 15000μg or 600,000 IU Vit D3 orally or IM
with calcium supplement.
• If healing occurs continue with 400 IU-1000
IU of Vit D3/day however elderly people
require 2000 IU/day vitamin D3.
• In Intestinal malabsorption: 50,000-100,000
IU vit D3/day with calcium supplements.
20. Renal tubular rickets & osteomalacia
• 3 pathophysiological mechanisms:
1. increase clearance of PO4 by the PCT
(hypophosphatemic rickets).
2. A failure in the production of H⁺ and its
substitution for fixed base in the DCT, (renal
tubular acidosis).
3. A failure in the conversion of 25-hydroxy
vitamin D to1, 25-dihydroxy vitamin D.
4. Combined lesion of both tubules which causes
the Fanconi group of rickets and osteomalacia.
21. Proximal tubular ricketic and
osteomalacic syndromes:
1.VDRR/hypophosphatemic rickets
or phosphate diabetes.
• +ve family history, X-linked
dominant.
• bony deformities present.
• Markedly reduced PO4, normal
serum calcium, No secondary
hyperparathyroidism, No Myopathy.
• Oral Neutral phosphate 1-4 gm/day
• Calcitriol (1, 25-DHCC) 2-
5µgm/kg/day)
22. 2.VDRR with Glycosuria
• less common than classic VDRR.
• abnormal resorptive mechanism for both
inorganic phosphate and glucose.
• Serum phosphate less, glycosuria.
• No evidence for genetic transmission.
• Diabetes not necessary to present.
• Vit-D= 0.5-1.5 mg/day(20,000-60,000 IU/day).
• Ca = 1gm/day
• Neutral Phosphates = 1.5 – 6 mg/day.
23. 3. Proximal Fanconi Syndrome
• defective reabsorption of phosphate, glucose,
and many amino acids.
• Autosomal recessive transmission.
• more florid, severe rachitic lesions and
pathological fractures.
• Later develop ch. Liver disease.
• Low serum po4, normal serum amino acid,
aminoaciduria.
• Vit-D=0.6 – 1mg/day(25,000-40,000 IU/day).
• Ca = 1gm/day and neutral phosphate=1-3g/d.
24. 4.Late onset VDRR/Hypophosphatemia.
• Normal in childhood, occurs early adulthood.
• Rare but one cause of unexplained bone loss,
joint pain in adults.
• No genetic error found.
• PTH responsible for phosphate leak rather
than tubular defect.
• Dramatic respond to vit-D(0.5-1.5 mg/day),
Ca(1gm/day), neutral phosphate(1-
3mg/day).
25. Proximal and Distal Renal Tubular
Rachitic and Osteomalacic Syndromes:
• Defective reabsorption in both PCT &
DCT.
• impaired reabsorption of water, fixed
base, protein, and bicarbonate.
• Results in acidosis, dehydration,
hyperproteinemia
• Four syndromes have been identified
in this group:
26. 1. proximal and distal Fanconi syndrome
(Debre De Toni Fanconi syndrome)
• Autosomal recessive transmission.
• Genetic swan neck deformity of renal tubule.
• Very severe hypophosphatemic ricket.
• Multiple # in few months of life.
• serum Ca, P, Na&K, Alk. Phos. Academia.
• Urine Pᴴ alkaline, glycosuria, amino aciduria.
• Vit-D=0.6 – 1mg/day(25,000-40,000 IU/day).
• Ca = 1gm/day and neutral phosphate=1-3g/d.
• Alkalizing solution, k- supplement.
27. 2. Lignac-Fanconi syndrome
• cystinosis, cystine storage disease.
• Cystine deposited through out the soft tissue.
• Autosomal recessive transmission.
• serum Ca, P, Na&K, Alk. Phos. Academia.
• Urine Pᴴ alkaline, glycosuria, amino aciduria.
• Vit-D=0.6 – 1mg/day(25,000-40,000 IU/day).
• Ca = 1gm/day and neutral phosphate=1-3g/d.
• Alkalizing solution, k- supplement.
28.
29. Renal Osteodystrophy:
• includes rickets or Osteomalacia, osteitis fibrosa
cystica, osteoporosis, osteosclerosis, and
metastatic calcification.
• Pathophysiology:
1. interferes with the conversion of 25-OH vitamin-
D to 1 ,25-dihydroxy vitamin-D.
2. Increase PTH secretion.
3. Hypocalcemia, hypocalciuric,
hyperphosphatemia.
4. Metastatic calcifications( arteries, cornea,).
30. Clinical features
• Growth impairment.
• Classic sign of rickets present.
• Ricketic rosary, Harrisons sulcus >
Craniotabes, Frontal bossing.
• Bowing and other deformity present.
• Wrist, ankle enlargement present.
• Epiphyseal separation.
• Arterial ,corneal calcification.
31. X- RAYS:
• Slipped capital femoral& humeral
epiphysis.
• Metaphyseal fracture.
• Cystic lesion in mandible.
• Soft tissue calcification(vessels, tendon)
• Subperiosteal erosion of bone (brown
tumors)
• Rugger- jercy spine.
34. Unusual Forms of Rickets and
Osteomalacia:
• Rickets and Osteomalacia Associated with
Benign Bone and Soft Tissue Tumors:
• hyposphatemic VDR Osteomalacia.
• Hemangioma of bone, giant-cell tumor,
reparative giant-cell granuloma, NOF,
Cavernous Hemangioma of the thigh, and
“ossifying mesenchymal tumor "of the
larynx.
• Tertiary hyperparathyroidism.
• Ectopic vit-D antagonist secretion.
35. Rickets and Osteomalacia Associated
with Anticonvulsant Therapy:
• 15% epileptic patient with long term anti epileptic
drugs( hydantoin, Phenobarbital).
• stimulation of hepatic microsomal P-450
enzymatic activity.
• An important syndrome to produce iatrogenic
cycle.
• usually responds well to vitamin D.
36. Vitamin-D dependent rickets and
osteomalacia
Type-I(pseudo vit-D deficient) Type-2 vit-D dependent
•Autosomal recessive
•Deficiency of 1ᾳ
hydroxylase.
•Severe ricketic syndrome.
•Secondary
hyperparathyroidism.
•Multiple #, Myopathy.
•Life time treatment with
1-OH vit-D.
•Autosomal recessive.
•Defect in vit-D receptors
in target cells.
•Adults and children
affected.
•Not responds to vit-D.
•Parenteral calcium is
needed.
37.
38. Orthopaedic Measures:
• Needed in established long bone
deformity.
• Surgery should be done after correction
of metabolic disorder.
• Very early stage different braces are used
accompanying systemic treatment.
• Surgery for deformity correction, may
need multiple surgery.