This document discusses several metabolic bone diseases including hyperparathyroidism, Paget's disease, and rickets. It provides details on:
- The processes of bone remodeling and how disorders can disrupt mineralization or formation/resorption, leading to conditions like rickets.
- Hyperparathyroidism, which can be primary due to parathyroid adenomas, secondary due to hypocalcemia, or tertiary if secondary is longstanding. This causes high calcium and affects bones, kidneys, and other organs.
- Paget's disease, which involves abnormal bone remodeling from viral infection, leading to deformity, fractures, and other complications. It typically involves the pelvis, spine,
Acute and Chronic Osteomyelitis - Infection of BoneRahul Singh
Acute and Chronic Osteomyelitis - Infection of Bone
http://essentialinspiration4u.blogspot.com
Osteomyelitis is defined as an acute or chronic inflammatory process of bone, bone marrow and its structure secondary to infection with micro organisms.
Duration , Mechanism & Host response.
Duration - Acute / Subacute / Chronic
Mechanism - Heamatogenous (tonsil , lungs , ear/ GIT) - Exogenous (injection , open fractures)
Host response - Pyogenic / Granulomatous
Introduction of bacteria from :
Outside through a wound or continuity from a neighboring soft tissue infection
Hematogenous spread from a pre existing focus (most common route of infection)
Acute and Chronic Osteomyelitis - Infection of BoneRahul Singh
Acute and Chronic Osteomyelitis - Infection of Bone
http://essentialinspiration4u.blogspot.com
Osteomyelitis is defined as an acute or chronic inflammatory process of bone, bone marrow and its structure secondary to infection with micro organisms.
Duration , Mechanism & Host response.
Duration - Acute / Subacute / Chronic
Mechanism - Heamatogenous (tonsil , lungs , ear/ GIT) - Exogenous (injection , open fractures)
Host response - Pyogenic / Granulomatous
Introduction of bacteria from :
Outside through a wound or continuity from a neighboring soft tissue infection
Hematogenous spread from a pre existing focus (most common route of infection)
This presentation is about Parathyroid Disorders which are hypo and hyperparathyroidism and their relationship to teeth and oral cavity including oral and dental manifestation of these disorders , and correct management patients seeking dental care with these disorders.
This presentation (in English) made at ONCOTRANS in Besançon on Friday 3rd 2017 reviews the potential for TGF-beta inhibition in hepatocellular carcinoma based on preclinical and clinical data.
Hyperparahyroidsm is an endocrinal disorder majorly affecting the parathyroid glands which secrete parathyroid hormone and calcitonin.
A condition characterised by excessive secretion of calcium in blood and Bone resorption and inanbility to metabolise calcium in blood.
Hypercalcaemia certainly possesses some diagnostic challenges
Cases are too different in ways of presentation and management do need a lot of things to be checked out. This is merely an approach for such patients.
Antimicrobial stewardship to prevent antimicrobial resistanceGovindRankawat1
India is among the nations with the highest burden of bacterial infections.
India is one of the largest consumers of antibiotics worldwide.
India carries one of the largest burdens of drug‑resistant pathogens worldwide.
Highest burden of multidrug‑resistant tuberculosis,
Alarmingly high resistance among Gram‑negative and Gram‑positive bacteria even to newer antimicrobials such as carbapenems.
NDM‑1 ( New Delhi Metallo Beta lactamase 1, an enzyme which inactivates majority of Beta lactam antibiotics including carbapenems) was reported in 2008
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the 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 lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
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. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
DISSERTATION on NEW DRUG DISCOVERY AND DEVELOPMENT STAGES OF DRUG DISCOVERYNEHA GUPTA
The process of drug discovery and development is a complex and multi-step endeavor aimed at bringing new pharmaceutical drugs to market. It begins with identifying and validating a biological target, such as a protein, gene, or RNA, that is associated with a disease. This step involves understanding the target's role in the disease and confirming that modulating it can have therapeutic effects. The next stage, hit identification, employs high-throughput screening (HTS) and other methods to find compounds that interact with the target. Computational techniques may also be used to identify potential hits from large compound libraries.
Following hit identification, the hits are optimized to improve their efficacy, selectivity, and pharmacokinetic properties, resulting in lead compounds. These leads undergo further refinement to enhance their potency, reduce toxicity, and improve drug-like characteristics, creating drug candidates suitable for preclinical testing. In the preclinical development phase, drug candidates are tested in vitro (in cell cultures) and in vivo (in animal models) to evaluate their safety, efficacy, pharmacokinetics, and pharmacodynamics. Toxicology studies are conducted to assess potential risks.
Before clinical trials can begin, an Investigational New Drug (IND) application must be submitted to regulatory authorities. This application includes data from preclinical studies and plans for clinical trials. Clinical development involves human trials in three phases: Phase I tests the drug's safety and dosage in a small group of healthy volunteers, Phase II assesses the drug's efficacy and side effects in a larger group of patients with the target disease, and Phase III confirms the drug's efficacy and monitors adverse reactions in a large population, often compared to existing treatments.
After successful clinical trials, a New Drug Application (NDA) is submitted to regulatory authorities for approval, including all data from preclinical and clinical studies, as well as proposed labeling and manufacturing information. Regulatory authorities then review the NDA to ensure the drug is safe, effective, and of high quality, potentially requiring additional studies. Finally, after a drug is approved and marketed, it undergoes post-marketing surveillance, which includes continuous monitoring for long-term safety and effectiveness, pharmacovigilance, and reporting of any adverse effects.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
2. • Calcium and Phosphate ion regulation
• Vitamin D metabolism and absorption
• Effects of active vitamin D
• PTH (primary, secondary, tertiary)
• Paget’s disease (classification, clinical
manifestations, treatment)
• Rickets (classification, clinical
manifestations, treatment)
3. Bone remodeling (bone metabolism)
• A lifelong process where
mature bone tissue is removed from the
skeleton (a process called
bone resorption) and new bone tissue
is formed (a process called ossification
or new bone formation).
4. Bone remodeling occurs in
four steps:
1. Activation,
2. Osteoclast resorption,
3. Surface preparation,
4. Building new bone
tissue.
5. Metabolic Bone Disorders
• Metabolic bone diseases are disorders of bone
strength, usually caused by abnormalities of
minerals (such as calcium or phosphorus),
vitamin D, bone mass or bone structure.
• At times occur because bone formation and
remodelling is not prioritized if the materials are
required more urgently somewhere else (e.g.
muscle contraction and coagulation).
6. Calcium and Phosphate
regulation
• Following two are responsible for the regulation
and supply of calcium and phosphate for the bone
formation:
1. Active Vitamin D (1,25, Dihydrocholecalciferol)
2. Parathyroid Hormone
10. 1,25-dihydroxycholecalciferol
• Increases absorption of calcium from intestines.
• Increase absorption of phosphate from the intestines.
• Decreases calcium excretion in the kidney.
• PTH production supression.
• Regulates Osteoblast function.
• Facilitate PTH induced Osteoclast function.
OVER ALL:
• Increases calcium in blood.
• Increases PO4 in blood.
• Aids bone formation.
12. Parathyroid Hormone
• Increases renal reabsorption of calcium.
• Releases calcium from skeletal stores.
• Increases the bone resorption of calcium.
• Decreases renal reabsorption of phosphate.
• Increases the bone resorption of phosphate.
OVER ALL:
• Increases serum calcium levels.
• Bone resroption (chronic continuous excess).
13.
14. Hyperparathyroidism
• Hyperparathyroidism is overactivity of the parathyroid glands resulting
in excess production of parathyroid hormone (PTH). The parathyroid
hormone regulates calcium and phosphate levels and helps to maintain
these levels.
15. Primary hyperparathyroidism
• Primary hyperparathyroidism causes hypercalcemia (elevated
blood calcium levels) through the excessive secretion
of parathyroid hormone (PTH), usually by an adenoma (benign
tumors) of the parathyroid glands. It is the commonest cause of
elevated calcium levels.
16. • “Stones" refers to kidney stones, nephrocalcinosis, and diabetes
insipidus (polyuria and polydipsia). These can ultimately lead
to renal failure.
• "Bones" The classic bone disease in hyperparathyroidism
is osteitis fibrosa cystica, which results in pain and sometimes
pathological fractures. Other bone diseases associated with
hyperparathyroidism are osteoporosis, osteomalacia,
and arthritis.
• "Abdominal groans”
of constipation, indigestion, nausea and vomiting.
Hypercalcemia can lead to peptic ulcers and acute pancreatitis.
The peptic ulcers can be an effect of increased gastric
acid secretion by hypercalcemia.
17. • "Psychiatric moans" lethargy, fatigue, depression, memory loss,
psychosis, ataxia, delirium, and coma.
• "Thrones" refers to polyuria and constipation
• Left ventricular hypertrophy.
• Other signs include proximal muscle weakness, itching, and band
keratopathy of the eyes.
18.
19. • Labs: Serum calcium levels are elevated, and the parathyroid
hormone level is abnormally high compared with an expected
low level in response to the high calcium. A relatively elevated
parathyroid hormone has been estimated to have a sensitivity of
60%-80% and a specificity of approximately 90% for primary
hyperparathyroidism. Serum phosphorus will decrease.
• Imaging: radio labeled technitium 99m remains in adenomas.
• Treatment: usually surgical removal of the gland(s) containing
adenomas, but medication may also be required.
20. The brown tumor is a
bone lesion that arises in
settings of
excess osteoclast activity,
such
as hyperparathyroidism.
21. Secondary hyperparathyroidism
• Secondary hyperparathyroidism refers to the excessive
secretion of parathyroid hormone (PTH) by
the parathyroid glands in response
to hypocalcemia (low blood calcium levels) and associated
hypertrophy of the glands. This disorder is especially seen
in patients with chronic renal failure.
• Clinical features: Bone and joint pain are common, as
are limb deformities. The elevated PTH has also
pleiotropic effects on blood, immune system and
neurological system.
22. • Labs: The PTH is elevated due to decreased levels of
calcium or 1,25-dihydroxy-vitamin D3. It is usually seen in
cases of chronic renal disease or defective calcium
receptors on the surface of parathyroid glands. Serum
phosphorus will increase.
• Treatment: If the underlying cause of the
hypocalcemia can be addressed, the
hyperparathyroidism will resolve.
• In patients with chronic renal failure, treatment
consists of dietary restriction of phosphorus,
supplements with an active form of vitamin D such
as calcitriol, Hectorol, Zemplar(paricalcitol), etc.
and phosphate binders which can be divided into
calcium-based and non-calcium based.
23. Subperiosteal resorption
Thirty year-old patient with
chronic renal failure and
elevated parathyroid
hormone.
Subperiosteal resorption is
most evident on the radial
sides of proximal and
middle phalanges.
Note the shaggy outer
cortical surface in the mid-to-
distal shaft of the middle
finger proximal phalanx.
24. Tertiary hyperparathyroidisim
• Tertiary hyperparathyroidism is a state of excessive secretion of parathyroid
hormone (PTH) after a long period of secondary hyperparathyroidism and
resulting in hypercalcemia. It reflects development of autonomous (unregulated)
parathyroid function following a period of persistent parathyroid stimulation.
• Serum calcium increases. PTH levels are increased. Serum phosphorus remains
increased.
• The basis of treatment is still prevention in chronic renal failure, starting
medication and dietary restrictions long before dialysis treatment is
initiated. Cinacalcet has greatly reduced the number of patients who ultimately
require surgery for secondary hyperparathyroidism; however, 5% of patients do
not respond to medical therapy.
• When secondary hyperparathyroidism is corrected and the parathyroid
glands remain hyperfunctioning, it becomes tertiary hyperparathyroidism. The
treatment of choice is surgical removal of three and one half parathyroid glands.
25.
26. Paget’s disease of the bone
• Paget Disease of Bone, or osteitis deformans, is a
condition of older individuals characterized by progressive
skeletal deformation due to problems in bone resorption
and remodeling. Likely due to a viral infection, it stimulates
an increase in osteoclast activity. This leads to increased
bone resorption coupled with abnormal and excessive
bone remodeling.
• It is relatively common and can affect up to 4% of
individuals over 40 and up to 11% over the age of
80 1. There may a slight male predilection.
27. Clinical features
• Paget Disease is often asymptomatic and may take
months to years to diagnose. Skeletal bone deformity and
enlargement may be the first presentation.
• localised pain and tenderness
• increased focal temperature due to hyperaemia (due
to hypervascularity)
• increased bone size: historically changing hat size
was a give-away
• bowing deformities
• kyphosis of the spine
• decreased range of motion
28. Stages
There are three stages classically described (but is part of
continuous spectrum)
• lytic (incipient active): predominated by osteoclastic activity
• mixed (active): osteoblastic as well as osteoclastic activity
• sclerotic/blastic (late inactive)
Markers
• serum alkaline phopatase (ALP) elevated
• urine hydroxyproline increase
Imaging
• Xray (skull, pelvis, humerus, femur)
• CT scan (Vertebrae, Skull)
• MRI
• Bone Scan
29. Complications
• osseous weakening resulting in deformity and fractures
• arthritis
• neural compression
– deafness is the most common complication
– cranial nerve paresis may occur
– basilar invagination may occur in advanced cases
with hydrocephalus orbrainstem compression
• secondary development of tumours (e.g. osteosarcoma: ≈1%
of cases), which is often highly resistant to treatment
• high output congestive cardiac failure
• hyperparathyroidism (~10%)
Treatment
• Calcitonin – Inhibits osteoclast formation.
• Bisphosphonates – Induces apoptosis of osteoclasts.
30. Sites of involvement
• Usually polyostotic and asymmetric
– Pelvis (75%) most common, followed by:
• Lumbar spine
• Thoracic spine
• Proximal femur
• Calvarium
• Scapula
• Distal femur
• Proximal tibia
• Proximal humerus
31. This 92 year-old male patient
presented for assessment of
acute hemiparesis.
An incidental finding was
marked thickening of the
calvarium.
The diploic space is widened
and there are ill-defined sclerotic
and lucent areas throughout.
The cortex is thickened and
irregular.
The findings probably
correspond to the “cotton wool
spots” seen on plain films in the
later stages of Paget’s disease.
33. Bone scan
demonstrates
intense uptake
involving several
lower thoracic
vertebrae, L3, right
hemipelvis, sacrum,
left proximal femur
and right knee.
There is expansion
and bowing of the
involved femur.
34. There is osseous
expansion,
coarsened
trabeculae,
thickened
cortex, and
increased density of
the right 5th rib.
35. Paget disease of the
distal femur in an 80
year old male
characterized by
cortical thickening
and coarsened bony
trabeculae.
There is mild loss of
medial tibiofemoral
compartment joint
space without
secondary
degenerative
features.
36. Lateral radiograph of the
tibia in a patient with
Paget sarcoma reveals a
destructive bone-forming
mass in the proximal tibia
(osteosarcoma).
37. Blade of grass
sign (candle flame
appearance) in lytic
phase Paget's
disease of bone.
38. Rickets
• Rickets is the softening and weakening of bones in
children, usually because of an extreme and prolonged
vitamin D deficiency.
• Vitamin D promotes the absorption of calcium and
phosphorus from the gastrointestinal tract. A deficiency of
vitamin D makes it difficult to maintain proper calcium and
phosphorus levels in bones, which can cause rickets.
• If a vitamin D or calcium deficiency causes rickets, adding
vitamin D or calcium to the diet generally corrects any
resulting bone problems for your child. Rickets due to a
genetic condition may require additional medications or
other treatment. Some skeletal deformities caused by
rickets may need corrective surgery.
39.
40. Signs and symptoms of rickets may include:
• Bone pain or tenderness
– Arms, Legs, Pelvis, Spine
• Dental deformities
• Impaired growth
• Increased bone fractures
• Muscle cramps
• Short stature (adults less than 5 feet tall)
• Skeletal deformities
– Asymmetrical or odd-shaped skull
– Bowlegs
– Bumps in the ribcage (rachitic rosary)
– Breastbone pushed forward (pigeon chest)
– Pelvic deformities
– Spine deformities (spine curves abnormally,
including scoliosis or kyphosis)
41. Risk factors
• Age Children 3 to 36 months old are most at risk of rickets
because their skeletons are growing so rapidly.
• Dark skin Dark skin doesn't react as strongly to sunshine as
does lighter colored skin, so it produces less vitamin D.
• Northern latitudes Children who live in geographical
locations where there is less sunshine are at higher risk of
rickets.
• Premature birth Babies born before their due dates are more
likely to develop rickets.
• Anti-seizure medications. Certain types of anti-seizure
medications appear to interfere with the body's ability to use
vitamin D.
• Exclusive breast-feeding Breast milk doesn't contain
enough vitamin D to prevent rickets. Babies who are
exclusively breast-fed should receive vitamin D drops.
45. Complications
• If left untreated, rickets may lead to:
• Failure to grow
• Abnormally curved spine
• Skeletal deformities
• Dental defects
• Seizures
Labs
• Serum calcium may show low levels of calcium,
serum phosphorus may be low, and serum alkaline
phosphatase may be high from bones or changes in
the shape or structure of the bones. This can show
enlarged limbs and joints.
• Bone biopsy is rarely performed but will confirm rickets.
46. Treatment
• Replacing calcium, phosphorus, or vitamin D that is
lacking will eliminate most symptoms of rickets.
Dietary sources of vitamin D include fish, liver, and
processed milk.
• Exposure to moderate amounts of sunlight is
encouraged. If rickets is caused by a metabolic
problem, a prescription for vitamin D supplements
may be needed.
• 400 international units (IU) of vitamin D a day for
infants and children.
• Positioning or bracing may be used to reduce or
prevent deformities. Some skeletal deformities may
require corrective surgery.
47. Blount's disease is a growth disorder of the tibia (shin bone) that causes the
lower leg to angle inward, resembling a bowleg.
It is also known as "tibia vara".[1]
Photos of a child with Blount's
Disease in a brace.
48. • In surgical correction of Blount’s disease, the pediatric orthopedist
performs an osteotomy, cutting the tibia and fibula as close to the
growth plate as possible and realigning the bones. Following the
procedure, the surgeon places a fixator on the leg to maintain
proper alignment during healing.