Chronic kidney disease-mineral bone disorder (CKD-MBD) is a common complication in chronic kidney disease caused by reduced kidney function and mineral metabolism abnormalities. This leads to high phosphate, activation of parathyroid hormone, and bone abnormalities from renal osteodystrophy to vascular calcification. Treatment focuses on controlling phosphate levels through binders like sevelamer and cinacalcet to reduce parathyroid hormone in order to prevent bone disease and fractures while minimizing cardiovascular risks.
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- Recorded videos of this lecture:
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https://youtu.be/AtiaKPIdzAQ
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https://youtu.be/2cwyPcRDGEY
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Presentation given to our fellowship program about diabetic kidney disease.
2022 update discussing SGLT2i, MRA (e.g. finerenone), health economics and beyond
Infectious diseases are the second most common cause of death in end-stage renal disease (ESRD) patients. Patients with ESRD are at high risk for several infections, due to exposure to blood products and frequent dialysis. The increased susceptibility to infections among these patients is indicative of a complex and varied state of immunodeficiency manifested by abnormal phagocytosis, T and B lymphocytes abnormalities and impaired response to T cell dependent pathogens such as hepatitis B and influenza viruses. These immunologic abnormalities are complicated by the use of immunosuppressive drugs used to treat and control underlying disease and exacerbated by nutritional deficiency and the dialysis procedure. Though many of these infections can be prevented by appropriate vaccination, the usual schedules of vaccination may be less effective.
The aim of this paper is to review the studies on the use of vaccines in ESRD patients
and summarize the vaccines required in this population.
Diagnosis, Evaluation, Prevention and Treatment of CKD-MBDAbdullah Ansari
Introduction and definition of CKD–MBD
Diagnosis of CKD–MBD: biochemical abnormalities
Diagnosis of CKD–MBD: bone
Diagnosis of CKD–MBD: vascular calcification
Treatment of CKD–MBD targeted at serum phosphorus and serum calcium
Treatment of abnormal PTH levels in CKD–MBD
Treatment of bone with bisphosphonates, other osteoporosis medications and growth hormone
Evaluation and treatment of kidney transplant bone disease
Presentation given to our fellowship program about diabetic kidney disease.
2022 update discussing SGLT2i, MRA (e.g. finerenone), health economics and beyond
Infectious diseases are the second most common cause of death in end-stage renal disease (ESRD) patients. Patients with ESRD are at high risk for several infections, due to exposure to blood products and frequent dialysis. The increased susceptibility to infections among these patients is indicative of a complex and varied state of immunodeficiency manifested by abnormal phagocytosis, T and B lymphocytes abnormalities and impaired response to T cell dependent pathogens such as hepatitis B and influenza viruses. These immunologic abnormalities are complicated by the use of immunosuppressive drugs used to treat and control underlying disease and exacerbated by nutritional deficiency and the dialysis procedure. Though many of these infections can be prevented by appropriate vaccination, the usual schedules of vaccination may be less effective.
The aim of this paper is to review the studies on the use of vaccines in ESRD patients
and summarize the vaccines required in this population.
Diagnosis, Evaluation, Prevention and Treatment of CKD-MBDAbdullah Ansari
Introduction and definition of CKD–MBD
Diagnosis of CKD–MBD: biochemical abnormalities
Diagnosis of CKD–MBD: bone
Diagnosis of CKD–MBD: vascular calcification
Treatment of CKD–MBD targeted at serum phosphorus and serum calcium
Treatment of abnormal PTH levels in CKD–MBD
Treatment of bone with bisphosphonates, other osteoporosis medications and growth hormone
Evaluation and treatment of kidney transplant bone disease
a precise presentation over CKD made for house officers/medical interns . It focuses over signs and symptoms and in-hospital management of resulting problems , material taken majorly from medscape, CMDT and oxford hand book
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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
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- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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.
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
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
3. CKD-MBD
Chronic kidney disease–mineral and bone disorder (CKD-
MBD) is a common complication of chronic kidney disease
and is a part of broad spectrum disorders of mineral
metabolism.
4.
5.
6.
7.
8. Pathogenesis of CKD MBD
Reduced glomerular filtration of phosphate leads to phosphate retention
Hyperphosphataemia as a result of phosphate retention usually becoming
clinically evident at stage 4–5 CKD.
Reduced renal mass leads to reduced activity of 1 -hydroxylase in the renal
tubule and thus failure to increase calcitriol production when required.
However, circulating calcitriol concentrations begin to fall at stage 3 CKD either
as a direct result of phosphate retention or as a secondary effect via FGF-23
stimulation.
Ann Clin Biochem 2012; 49: 432–440
9. PATHOGENESIS OF CKD-MBD
Lowered calcitriol leads to reduced calcium absorption from the gut and
proximal tubule, thus causing a tendency to hypocalcaemia which is
counteracted by increased PTH production and secretion.
The net effect is secondary hyperparathyroidism (i.e. abnormally high PTH
concentrations as an appropriate response to hypocalcaemia), which further
aggravates hyperphosphataemia (positive feedback).
Ann Clin Biochem 2012; 49: 432–440
10. Consequences of CKD-
MBD
A. Renal osteodystrophy
B. Hyperphosphatemia
C. Cardiovascular calcification
D. Extraskeletal calcification
E. Endocrine disturbances
F. Neurobehavioral changes
G. Compromised immune system
H. Altered erythropoiesis
11. BONE FRACTURES DUE
TO CKD MBD
If left uncorrected, the secondary hyperparathyroidism leads to
increased mobilization of calcium from bone with bone weakening and a
tendency to fracture.
The risk of fracture is increased in patients who have had longer
exposure to dialysis.
Ann Clin Biochem 2012; 49: 432–440
12. BONE DISEASE DUE TO
CKD
HIGH BONE TURNOVER DISEASE: Osteitis fibrosa.
LOW BONE TURNOVER DISEASE: Osteomalacia
Adynamic bone disease
Ann Clin Biochem 2012; 49: 432–440
13.
14. VASCULAR
CALCIFICATIONS
In CKD-MBD, there is a greater proportion of
calcification in the arterial media which causes
vascular stiffness and hypertension.
Calciphylaxis is a condition where small cutaneous
blood vessels become calcified, leading to acute,
painful necrosis and ulceration of the skin. It is
strongly associated with the presence of CKD-MBD
Ann Clin Biochem 2012; 49: 432–440
15. SECONDARY
HYPERPARATHYROIDISM
Secondary hyperparathyroidism (HPT) in patients with chronic kidney
disease (CKD) is a progressive disease, associated with increases in
parathyroid hormone (PTH) levels and derangements in calcium and
phosphorus metabolism.
Increased PTH stimulates osteoclastic activity resulting in cortical bone
resorption and marrow fibrosis.
16.
17. TERTIARY
HYPERPARATHYROIDISM
Parathyroid glands gradually undergo hypertrophy and become less
responsive to modulatory influences.
In late CKD, therefore, PTH production may become autonomous (so-
called tertiary hyperparathyroidism) with acceleration of bone
destruction and vascular calcification.
Ann Clin Biochem 2012; 49: 432–440
21. The KDOQI guidelines recommend against PTH levels below 150 pg/ml
in CKD stage 5 in order to mitigate the risk of adynamic bone disease.
Lower the PTH, greater the survival.
22. HYPERPHOSPHATASEMIA
High serum alkaline phosphatase level in CKD patients is usually (esp. if > 120 U/L)
associated with poor survival in hemodialysis patients
Whereas serum alkaline phosphatase used to be a traditional measure for the
management of kidney bone disease, in recent years it appeared to have fallen
out of favor, probably since the KDOQI guidelines did not include it in its
recommendations, nor did they suggest any cutoff levels or target ranges for it
Alkaline phosphatase can be effectively lowered by both active vitamin D products
and calcimimetics
Lower serum alkaline phosphatase the better is the response of dialysis patients to
ESAs during anemia management.
Kidney Int Suppl. 2010 August ; (117): S10–S21
23. Martin K J , González E A JASN 2007;18:875-885
28. PHOSPHATE BINDERS
The administration of agents to bind phosphate in food is usually
required as CKD progresses.
Agents containing calcium are inexpensive and well tolerated, but these
may contribute to vascular calcification.
Non-calcium-containing phosphate binders (lanthanum and sevelamer)
have the advantage of reducing calcium intake and thus slowing vascular
calcification.
31. Sevelamer: Calcium-free,
aluminium-free phosphate binders
Sevelamer was approved by the US Food and Drug Administration
(FDA) in 1998.
Sevelamer is completely resistant to digestive degradation and,
therefore, not absorbed from the GI tract.
Sevelamer carbonate tablets are a phosphate binder indicated for the
control of serum phosphorus in adults with chronic kidney disease on
dialysis
32. MECHANISM OF ACTION
By binding phosphate in the gastrointestinal tract and decreasing
absorption, sevelamer carbonate lowers the phosphate concentration
in the serum (serum phosphorus).
35. SEVELAMER HYDROCHLORIDE
VS. SEVELAMER CARBONATE
Sevelamer hydrochloride is an ion-exchange resin that reduces serum
phosphorus concentrations. & produces favorable lipid profile effects and
does not cause hypercalcemia.
However, reported drawbacks of this agent are metabolic acidosis, high
pill burden, and a relatively low affinity and selectivity for phosphate
anions.
36. SEVELAMER HYDROCHLORIDE
VS. SEVELAMER CARBONATE
Sevelamer carbonate is a new buffered formulation that does not
increase the risk of metabolic acidosis.
It does not decrease serum bicarbonate levels, it may be more
appropriate for patients at risk for metabolic acidosis who require
phosphate binders that do not contain calcium or aluminum.
38. DOSAGE AND
ADMINISTRATION
Starting dose of sevelamer carbonate tablets is 800 mg (if serum
phosphorus level > 5.5 and < 7.5 mg/dL) or 1600 mg (> 7.5 mg/dl)
administered orally three times per day with meals.
Titrate by 800 mg per meal in two week intervals for adult patients
as needed to obtain serum phosphorus target.
For adult patients switching from Sevelamer Hydrochloride tablets
to sevelamer carbonate tablets or powder, use the same dose.
40. SUMMARY
It does not increase calcium load and is associated with fewer
hypercalcaemic episodes than calcium-based agents.
Reduces the tendency to soft tissue calcification and renal damage
Attenuates the progression of coronary and aortic calcification in
haemodialysis patients.
Nephron Clin Pract 2005;99:c1–c7
41. SUMMARY
Reduces total and LDL, while increasing HDL, cholesterol.
Sevelamer is commonly initially used over lanthanum, although equally
effective in lowering Phosphate, as the long-term data on safety of
Lanthanum are more limited.
Nephron Clin Pract 2005;99:c1–c7
42. CALCINOMIMETIC
AGENTS
Calcium-sensing receptor (CaSR) is a G protein–coupled receptor identified
as an essential molecule for the regulation of PTH secretion by
extracellular calcium (Ca).
Binding of extracellular Ca inhibits PTH secretion
Calcimimetics are agents that increase the sensitivity of the calcium-
sensing receptor (CaSR) in the parathyroid gland to calcium, regulating
PTH secretion and the gland hyperplasia.
43. Cinacalcet: mechanism of
action
The calcium-sensing receptor on the surface of
the chief cell of the parathyroid gland is the
principal regulator of PTH secretion.
Cinacalcet directly lowers PTH levels by
increasing the sensitivity of the calcium-sensing
receptor(CaSR) to extracellular calcium.
The reduction in PTH is associated with a
concomitant decrease in serum calcium levels.
45. DOSAGE AND
ADMINISTRATION
30 mg once daily with food or shortly after a meal.
Serum calcium and serum phosphorus should be measured within 1 week and PTH
should be measured 1 to 4 weeks after initiation or dose adjustment of Cinacalcet.
Cinacalcet should be titrated no more frequently than every 2 to 4 weeks through
sequential doses of 60, 90, 120, and 180 mg once daily to target iPTH consistent
with the NKF-K/DOQI recommendation for CKD patients on dialysis of 150-300
pg/mL.
PTH levels should be assessed no earlier than 12 hours after dosing with
Cinacalcet.
46. ADJUVANT WITH VITAMIN D
ANALOGUES
Treatment is associated with hypocalcaemia, hyperphosphataemia and an
increased requirement for calcium supplements.
The long-term consequences of these effects are unknown, thus the use of
cinacalcet is recommended only in patients with CKD stage 5.
They generally used to adjunct treatment with vitamin D analogues where the
latter have not sufficiently suppressed PTH production
47.
48. SUMMARY
Lowered PTH and reduced bone turnover and tissue fibrosis among most dialysis
patients with sHPT.
40-50% (250-350 pg/ml) serum PTH, a 5-8% (0.5-0.8 mg/dl) serum calcium and 5-
10% (0.2-1.0 mg/dl) serum phosphorous reduction is expected when cinacalcet is
administered
Reduces the rate of parathyroidectomy, fracture, and hospitalization due to
cardiovascular events
Cinacalcet HCl and Concurrent Low-dose Vitamin D Improves Treatment of
Secondary Hyperparathyroidism in Dialysis Patients Compared with Vitamin D Alone
Editor's Notes
FGF-23 is a circulating peptide that plays a key role in the control of serum phosphate concentrations.
FGF-23 is a circulating peptide that plays a key role in the control of serum phosphate concentrations.
Similar to PTH, FGF-23 has phosphaturic properties, but it also inhibits 1-α hydroxylation and, hence, may aggravate calcitriol deficiency leading to further PTH production and release.
FGF-23 is a circulating peptide that plays a key role in the control of serum phosphate concentrations.
Klotho, a transmembrane protein produced by osteocytes, is required for FGF-23 receptor activation
Fetuin-A has been noted as a vascular calcification inhibitor and is associated with mortality in HD patients. a prospective study including 57 HD patients
[28]. After phosphate binder was changed from calcium-containing binder to Sevelamer hydrochloride, serum fetuin-A level significantly increased (+21%).