This document discusses the approach to diagnosing and treating hypercalcemia. It reviews calcium metabolism and the role of parathyroid hormone. Symptoms of hypercalcemia are described for the neurological, gastrointestinal, skeletal, renal, and cardiovascular systems. Causes of hypercalcemia include primary hyperparathyroidism, malignancy, granulomatous diseases, vitamin D toxicity, and certain drugs. The diagnostic approach involves measuring PTH, phosphorus, vitamin D, and PTH-rP levels. Treatment options aim to increase calcium excretion or decrease bone resorption/absorption and include IV fluids, calcitonin, bisphosphonates, glucocorticoids, loop diuretics, and dial
Hypercalcaemia is a common disorder we doctors from all faculties face in day to day clinical practice. This was a presentation done by me to give you an update regarding hypercalcaemia and it's management.
This lecture is based on National guidelines(Sri Lanka) and guidelines by NHS UK. all the materials used to prepare the lecture are trusted and high in quality. also the books referred are internationally recognized. both hyper and hypokalemia management included in the lecture. lecture is free and you can even download. i kept no copy rights. i appreciate your support, comments and suggestions. also i would be grateful if you can make these lectures popular. wishing your success.
Calcium,magnesium,phosphate and chloride imbalances Jyothi Swaroop
Calcium,magnesium,phosphate and chloride imbalances
Their treatment,my main reference is Eric strong's lectures in youtube,and some of the websites.Hope everyone finding Serum electrolytes find atleast some use of it .
Thank you
Calcium,magnesium,phosphate and chloride imbalances jyothiswaroopb1
i could make best of me ,by collecting information from mainly Eric's strongs medical lectures in youtube and from many websites .
Hope you guys may find any important information.
Thank you
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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.
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Similar to Hypercalcemia- Approach to the Diagnosis Palak Choksi.pptx
Hypercalcaemia is a common disorder we doctors from all faculties face in day to day clinical practice. This was a presentation done by me to give you an update regarding hypercalcaemia and it's management.
This lecture is based on National guidelines(Sri Lanka) and guidelines by NHS UK. all the materials used to prepare the lecture are trusted and high in quality. also the books referred are internationally recognized. both hyper and hypokalemia management included in the lecture. lecture is free and you can even download. i kept no copy rights. i appreciate your support, comments and suggestions. also i would be grateful if you can make these lectures popular. wishing your success.
Calcium,magnesium,phosphate and chloride imbalances Jyothi Swaroop
Calcium,magnesium,phosphate and chloride imbalances
Their treatment,my main reference is Eric strong's lectures in youtube,and some of the websites.Hope everyone finding Serum electrolytes find atleast some use of it .
Thank you
Calcium,magnesium,phosphate and chloride imbalances jyothiswaroopb1
i could make best of me ,by collecting information from mainly Eric's strongs medical lectures in youtube and from many websites .
Hope you guys may find any important information.
Thank you
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
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 .
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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
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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
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
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.
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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
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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.
3. Intended Learning Outcomes
–Review calcium metabolism
–Describe symptoms of hypercalcemia
–Review the etiology of hypercalcemia
–Discuss the treatments for
hypercalcemia
–Conclusions
4. Intended Learning Outcomes
–Review calcium metabolism
–Describe symptoms of hypercalcemia
–Review the etiology of hypercalcemia
–Discuss the treatments for
hypercalcemia
–Conclusions
5. Calcium metabolism
• Absorption from GI tract is by passive diffusion
and active transport
• Most of the calcium is reabsorbed by the kidney
– net loss is about 2%
• Calcium is controlled by both PTH and
calcitonin
7. Calcium
• Total calcium
- Free (ionized) calcium (50%)
- Protein bound calcium (40%)
- Calcium complexed with organic and inorganic
molecules (10%)
8. Role of albumin
High albumin states (volume depletion or
multiple myeloma) may lead to
pseudohypercalcemia.
Low albumin states like malnutrition, total
serum calcium may appear low while
ionized calcium is again not very affected.
Ca2+= serum Ca2+ + 0.8 x [normal alb-patient alb]
9. Intended Learning Outcomes
–Review calcium metabolism
–Describe symptoms of hypercalcemia
–Review the etiology of hypercalcemia
–Discuss the treatments for
hypercalcemia
–Conclusions
11. Renal (stones)
• Polyuria
• Renal insufficiency (rarely seen in mild disease,
although in severe cases may cause a reversible
drop in GFR)
• Nephrolithiasis
• Nephrogenic DI
13. Neuro-psychiatric (Groans)
• Depression
• Anxiety
• Cognitive dysfunction
• Lethargy, confusion, stupor, and coma may
occur in patients with severe hypercalcemia
• More likely to occur in the elderly and in those
with rapidly rising calcium concentrations
15. Cardiovascular
• Increases myocardial contractility and irritability
• Shortened QT interval
• Prolonged PR
• Wide QRS complexes
• Calcium deposition in coronary arteries and
myocardial fibers
• Hypertension
16. Intended Learning Outcomes
–Review calcium metabolism
–Describe symptoms of hypercalcemia
–Review the etiology of hypercalcemia
–Discuss the treatments for
hypercalcemia
–Conclusions
21. Medications
> 10.3 mg% I-PTH
High/Normal PTH
Low
Vit D Toxicity
Milk-Alkali
Cancers/
Lymphoma
Low PTHrP
Approaching the diagnosis
22. Case
• 40/ W noted to have mild elevations in
serum calcium on routine testing.
Calcium at the last two visits is 10.4-
10.6 mg/dL.
• She is relatively asymptomatic.
• You obtain labs:
• PTH:
• 120
23.
24. Case
• 40/ W asymptomatic hypercalcemia
• You obtain labs:
• PTH: 120
• Phos: 2.0
• Vitamin D (25OHD): 40
• Creatinine: 1.0
• Albumin: 4.0
• Likely diagnosis: ?
25. Medications
> 10.3 mg% I-PTH
High/Normal PTH
Low
Vit D Toxicity
Milk-Alkali
Cancers/
Lymphoma
Low PTHrP
Approaching the diagnosis
26. Case
• 40/ W noted to have mild elevations in serum calcium on
routine testing. Calcium at the last two visits is 10.4-10.6
mg/dL.
• She is relatively asymptomatic.
• You obtain labs:
• PTH: 120
• Phos: 2.0
• Vitamin D (25OHD): 40
• Creatinine: 1.0
• Albumin: 4.0
• Likely diagnosis: Primary hyperparathyroidism
27. Primary Hyperparathyroidism
• Most common cause in the outpatient setting
• Renal calculi seen in 15-20%
• Classic bone disease (brown tumors, osteitis
fibrosa cystica, subperiosteal resorption) is
rarely seen
• Increased risk for vertebral fractures
28. Familial Hypocalciuric
Hypercalcemia (FHH)
• Rare, autosomal dominant condition
• caused by an inactivating disorder of calcium-
sensing receptors (CaSR)
• PTH normal to mildly elevated, mild hypercalcemia
• Fractional excretion of calcium is lower than 1%,
despite hypercalcemia.
• Genetic testing is not often required
• ClCa/ClCr= (Uca X SCr) X (Sca X UCr)
• A ratio of 0.01 or less is typically with FHH
29. Case
• 70/M with history of renal cell carcinoma. Calcium
levels are noted to be recently elevated at 13.0
mg/dL.
• You obtain labs:
- PTH: 23
- Phos: 2.1
- Vitamin D: 40
- Creatinine: 1.0
- Albumin 3.6
- PTH-rP: 1.0 (High)
30. > 10.3 mg% I-PTH
Low PTHrP
Low
Vit D Toxicity
Milk-Alkali
Cancers/
Lymphoma
High/Normal PTH
Approaching the diagnosis
31. Case
• 70/M with history of renal cell carcinoma. Calcium
levels are noted to be recently elevated at 13.0 mg/dL.
• You obtain labs:
- PTH: 23
- Phos: 2.1
- Vitamin D: 40
- Creatinine: 1.0
- Albumin 3.6
- PTH-rp: 1.0 (High)
- Likely diagnosis: Hypercalcemia of malignancy
32. Humoral Hypercalcemia of
Malignancy
• Usually have obvious malignant disease
• Most common cause for inpatient
hypercalcemia
• PTH is low, PTH-rP is elevated
• Associated with localized bone destruction
33. Case
• 51/M presents with fatigue and trouble concentrating with a
5-lb weight loss. Calcium levels are noted to be recently
elevated at 13.0 mg/dL.
• You obtain labs:
- PTH: 17
- Phos: 3.0
- CXR: Hilar lymphadenopathy
24 hour urine calcium is elevated
- Vitamin D: 27, Creatinine is normal
- DHVD: 110
- Likely diagnosis: Hypercalcemia due to granulomatous
disease
34. Hypercalcemia associated with
granulomatous diseases
• Sarcoidosis is most commonly associated
although can occur in any granulomatous
disease
• Increased activation of 1α hydroxylase that
converts 25OHD to 1,25(OH)2D
35. Intended Learning Outcomes
–Review calcium metabolism
–Describe symptoms of hypercalcemia
–Review the etiology of hypercalcemia
–Discuss the treatments for
hypercalcemia
–Conclusions
36. Treatment
• Asymptomatic or mildly symptomatic patients do
not require immediate treatment
• Chronic hypercalcemia with no symptoms 12-14
mg/dl can be monitored as well
• > 14 mg/dl needs treatment even if asymptomatic
37. Treatment
• Correction of dehydration/volume depletion
• Correction of any electrolyte abnormalities
• Discontinuation of medications that may cause
calcium elevation
• Reduction of dietary calcium in states of
intestinal hyperabsorption (vitamin D
intoxication and milk alkali)
• Weight bearing or mobilization
38. The Four Rx Modalities
I.V. Saline
Hydration &
Diuresis
Gluco-
Corticoids
Anti-
resorptives
Calcitonin
I.M/S.C.
39. • Agents that decrease the release of calcium from
bone or increase the uptake of calcium into bone
• Agents that increased urinary excretion of
calcium
• Agents that reduce intestinal absorption of
calcium
Treatment
40. • IV fluids
Depending on clinical status
200-300 ml/hour to maintain UO of 100-150
ml/hour
Dehydration can make hypercalcemia worse by
impairing the renal excretion of calcium
Treatment
41. Salmon Calcitonin
• IM or SQ injections at dose of 4 IU/kg
• At 6-12 hour intervals
• Modest reductions and low toxicity profile
• Vitamin D intoxication and immobilization
• Acts quickly
• Escape phenomenon may develop in 48 hours
42. Bisphosphonates
• Inhibit release of calcium by interfering with
osteoclast mediated bone resorption
• More potent than saline and calcitonin
• Can be used for hypercalcemia of any cause
• Max effect seen in 2-4 days
• Also used to prevent hypercalcemia and skeletal
events in malignancy
43. Bisphosphonates
• Pamidronate 60 or 90 mg IV over 2-4 hours
• Zoledronic acid (ZA) 4 mg over 15 minutes
• ZA preferred due to quicker infusion time
• Side effects (low grade fever, myalgias,
osteonecrosis of the jaw, atypical fractures)
45. • Agents that decrease the release of calcium from
bone or increase the uptake of calcium into bone
• Agents that increased urinary excretion of
calcium
• Agents that reduce intestinal absorption of
calcium
Treatment
46. Loop diuretics
• WITH SALINE
• Correct volume depletion first!
• 80-120 mg every 2-6 hours
• Monitor lytes, large losses of K and Mg
• Fallen out of favor:
1) Better drugs
2) Frequent monitoring of lytes
48. • Agents that decrease the release of calcium from
bone or increase the uptake of calcium into bone
• Agents that increased urinary excretion of
calcium
• Agents that reduce intestinal absorption of
calcium
Treatment
49. Glucocorticoids
• Vitamin D intoxication or endogenous
production of calcitriol (sarcoidosis, TB)
• Prednisone 20-40 mg
• Lowers calcium in 2-5 days
50. Intended Learning Outcomes
–Review calcium metabolism
–Describe symptoms of hypercalcemia
–Review the etiology of hypercalcemia
–Discuss the treatments for
hypercalcemia
–Conclusions
51. Conclusion
• Most common cause of hypercalcemia in the
outpatient setting is primary
hyperparathyroidism
• Most common cause of hypercalcemia in the
inpatient setting is malignancy
• Establishing the cause is important for treatment
decisions
Calcium is important for a number of intracellular reactions including muscle contraction, nerve cell activity, release of hormone through the process of exocytosis and activation of several enzymes, blood coagulation and structural integrity of teeth and bone. 99% of the body calcium is in the bones in the form of hydroxyapatite cyrstals. The next largest pool is the intracellular calcium. Smallest pool is in the ECF. Regulation of calcium involves the control of calcium movement between ECF, bone, GI tract and kidneys.
Kidney serves as a route for excretion
Actual % may vary with health and disease
80% is albumin bound
Mild hypercalcemia: Asymptomatic
Non specific symptoms
Gastrointestinal symptoms are probably related to the depressive action of hypercalcemia on the autonomic nervous system and resulting smooth-muscle hypotonicity
Calcium between 12-14 mg/dl maybe well tolerated if elevated chronically
Acute rises: polyuria, polydipsia, dehydration, anorexia, nausea, muscle weakness, and changes in sensorium
PHPT – most common cause in the ambulatory setting
PHPT – most common cause in the ambulatory setting
PHPT – most common cause in the ambulatory setting
The underlying pathophysiology of HPT is caused by excessive secretion of parathyroid hormone (PTH), which leads to increased bone resorption by osteoclasts, increased intestinal calcium absorption, and increased renal tubular calcium reabsorption. The consequent hypercalcemia is also often accompanied by low-normal or decreased serum phosphate levels because PTH inhibits proximal tubular phosphate reabsorption.
Hypercalcemia of malignancy: 30% of individuals with cancer develop hypercalcemia– typically late in the disease course. Calcium levels are generally higher
Hypercalcemia of malignancy: 30% of individuals with cancer develop hypercalcemia– typically late in the disease course. Calcium levels are generally higher
Usually, this term is applied to patients with excessive tumoral production of PTH-related peptide (PTHrP).
The predominant mechanism for the development of hypercalcemia and hypercalciuria is increased intestinal absorption of calcium induced by elevated calcitriol levels,
Activity of this enzyme is under negative feedback control in normal tissues. However, in granulomatous disorders, normal feedback inhibition is abolished, probably by the effects of interferon gamma.
Cautious use when EGFR 35 or less
ONJ: Limited relevance when used for management of acute hypercalcemia