This document discusses calcium imbalances, including hypercalcemia and hypocalcemia. It begins with introducing calcium, its functions, and homeostasis. Hypercalcemia is defined as a calcium level above 10.5 mg/dL and can be caused by primary hyperparathyroidism, malignancy, or excessive vitamin D and calcium supplementation. Clinical features of hypercalcemia include neurological, cardiovascular, and renal symptoms. Treatment involves rehydration, bisphosphonates, calcitonin, surgery for severe cases. Hypocalcemia is a calcium level below 8.5 mg/dL and can result from vitamin D deficiency, kidney disease, or certain drugs. Symptoms include numbness and tetany. Treatment focuses on calcium and
MULTIPLE MYELOMA -HEMATOLOGIC MALIGNANCY-DISEASE OF BONE MARROW - PLASMA CELL DISORDER
PATHOLOGY, .CLINICAL FEATURES , AND ITS MANAGMENT REFERENCE HARRISON
It is a neoplasm of B-cell lineage; proliferation of the cells forms a monoclonal population of plasma cells and produces a single type of Ig/Ig fragment.
MULTIPLE MYELOMA -HEMATOLOGIC MALIGNANCY-DISEASE OF BONE MARROW - PLASMA CELL DISORDER
PATHOLOGY, .CLINICAL FEATURES , AND ITS MANAGMENT REFERENCE HARRISON
It is a neoplasm of B-cell lineage; proliferation of the cells forms a monoclonal population of plasma cells and produces a single type of Ig/Ig fragment.
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.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
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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.
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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
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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.
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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Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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2. GENRAL OBJECTIVE : AT the end of the presentation we would understand about
the calcium imbalances and their management.
SPECIFIC OBJECTIVE :
Introduction to calcium its function and homeostasis .
Define hypercalcaemia, hypocalcaemia and its causes.
Explaining clinical features and diagnostic evaluations of calcium
imbalances .
Describing the detailed management of calcium imbalances.
Summarization of calcium imbalances.
Conclusion of topic.
References.
3. INTRODUCTION
Calcium is the most abundant metal and the fifth-most abundant element in the human body.Calcium is positively
charged ion (cation) which is 99% in bones and teeth, 1% in intracellular and 0.1% in extracellular fluid( blood and
interstitium)
Functions of calcium
1.Biochemical functions 1. Development of bones and teeth : Calcium, along with phosphate, is required for the formation
and physical strength of skeletal tissue.
2. 2. Muscle contraction : Ca2+ interacts with troponin C to trigger muscle contraction. Calcium also activates ATPase,
increases the interaction between actin and myosin.
3. Blood coagulation : Several reactions in the cascade of blood clotting process are dependent on Ca2+(factor IV ).
4. Nerve transmission: Ca2+ is necessary for the transmission of nerve impulse.
5. Membrane integrity and permeability : Ca2+ influences the membrane structure and transport of water and several ions
across it.
6. Activation of enzymes : Ca2+ is needed for the direct activation of enzymes such as lipase (pancreatic), ATPase and
succinate dehydrogenase
8. Calcium as intracellular messenger
9. Release of hormones
10. Action on heart : Ca2+ acts on myocardium and prolongs systole
6. HYPERCALCEMIA
Hypercalcemia is a total serum calcium concentration of > 10.5 mg/dL (> 2.62 mmol/L)
or ionized (free) calcium concentration of > 5.25 mg/dL (> 1.31 mmol/L).
Hypercalcemia affects 0.5% to 1% of the general population
ETIOLOGY
1. primary hyperparathyroidism: Primary hyperparathyroidism results from the
excessive secretion of PTH and typically produces frank hypercalcemia. Primary
hyperparathyroidism is approximately 2 to 3 times more common in women than in
men.
2. malignancy-associated hypercalcemia: It is most common in squamous cell
carcinoma of the lung, head, and neck, renal cell carcinoma, breast ca
3. Calcium & Vitamin D (Hypervitaminosis –D) over Supplementation
4. Sarcoidosis and Other granulomatous disorders
5. Cancer, multiple myeloma, and lymphoma, sarcoidosis.
6. Thyrotoxicosis, Adrenal Insufficiency.
7. 7. ENDOCRINE TUMORS: pheochromocytoma (may be associated with MEN-2), VIPomas.
8. Thiazide Diuretics & Indapamide
9. Hypervitaminosis A
10.Milk Alkali Syndrome (Rare nowadays)
11.Immobilization
12.Acute Renal Failure due to rhabdomyolyses
CLASSIFICATION OF HYPERCALCEMIA
According to level of corrected total serum calcium value hypercalcemia can be classified into:
1. Mild Hypercalcemia (>10.5 mg/dL to less than 12 mg/dL)
2. Moderate Hypercalcemia (Corrected Ca Level 12 to 14 mg/dL)
3. Severe Hypercalcemia (A level greater than 14 mg/Dl)
8. CLINICAL FEATURES
Central nervous system effects: Lethargy, depression, psychosis, ataxia, stupor,
and coma
Neuromuscular effects: Weakness, proximal myopathy, and hypertonia
Cardiovascular effects: Hypertension, bradycardia (and eventually asystole), a
shortened QT interval (ECG)
Renal effects: Stones, decreased GFR, polyuria, nephrocalcinosis;
Gastrointestinal effects: Nausea, vomiting, constipation and anorexia
Eye findings such as band keratopathy
Systemic metastatic calcification.
PNEUMONIC:
9. DIAGNOSTIC EVALUATIONS:
General Investigations:
S. Calcium Level
S. PO4 Level
S. Alkaline phosphate
S. Parathyroid level
S. Vitamin-D level
S. Total protein, S. Albumin
ECG
Specific Investigations: Varies according to cause.
10. TREATMENT MODALITIES
mild hypercalcemia
Patients with asymptomatic or mildly symptomatic hypercalcemia (calcium
<12 mg/dL) do not require immediate treatment.
However, they should be advised to avoid factors that can aggravate
hypercalcemia, including thiazide diuretics, volume depletion, prolonged
bed rest or inactivity, and a high calcium diet (>1000 mg/day).
Adequate hydration (at least six to eight glasses of water per day) is
recommended to minimize the risk of nephrolithiasis.
11. MODERATE HYPERCALCEMIA
In these patients, treatment with saline hydration and bisphosphonates.
SEVERE HYPERCALCEMIA
Patients with calcium >14 mg/dL (3.5 mmol/L) require more aggressive therapy.
Volume expansion with isotonic saline at an initial rate of 200 to 300 mL/hour to
maintain the urine output at 100 to 150 mL/hour. To maintain rehydration therapy.
loop diuretics can be given for calcium excretion.
Administration of salmon calcitonin (4 IU/kg) and repeat measurement of serum
calcium in after 6 hours. It can be repeated every 6 to 12 hours (4 to 8 IU/kg).
The concurrent administration of zoledronic acid(biphosphate) (ZA; 4 mg
intravenously [IV] over 15 minutes) or pamidronate (60 to 90 mg over two hours),
preferably ZA because it is superior to pamidronate in reversing hypercalcemia
to malignancy.
To increase GI excretion calcium patient can also be put on glucocorticoids
calcitriol production by the activated mononuclear cells in the lung and lymph nodes
12. Hemodialysis should be considered, in addition to the above treatments, in patients who have serum calcium concentrations in the
range of 18 to 20 mg/dL (4.5 to 5 mmol/L) and neurologic symptoms but a stable circulation or in those with severe hypercalcemia
complicated by renal failure.
Surgical management:
parathyroidectomy: removal of parathyroid gland.
13. Nursing responsibility
Provide safety measures and institute seizure precautions, if appropriate.
Give prescribed I.V. solution; ensure patent I.V. access.
Expect to administer I.V. normal saline for severe hypercalcemia at an initial rate of 200 to 300 mL/hour,
and then adjust to maintain urine output at 100 to 150 mL /hour.
Ensure readily available access to a bathroom if the patient is receiving I.V. saline.
Assess for signs and symptoms of fluid overload.
Assess for flu-like symptoms if the patient is receiving I.V. bisphosphonates.
Administer I.M. or subcutaneous calcitonin every 12 hours, if ordered.
Auscultate heart and lung sounds, noting signs and symptoms of heart failure.
Institute continuous cardiac monitoring if patient exhibits ECG changes.
Obtain specimens for laboratory testing, including serum calcium levels.
Assess for signs and symptoms of hypocalcemia secondary to treatment.
Assess level of orientation and note any changes.
Prepare the patient and family for surgery, if indicated.
14. Hypocalcaemia
A decrease in the calcium levels below 8.5mg/dl is termed hypocalcemia,if serum protein is normal OR Ionized calcium <
4.5mg/dL
Etiology
• Vitamin D deficiency
• Chronic renal failure
• Magnesium deficiency
• Alcoholism
• Biphosphonate therapy - drugs used to treat high blood calcium levels or pills used to treat osteoporosis.
• Certain types of leukemia or blood disorders
• A complication of chemotherapy, tumor lysis syndrome, occurs when body breaks down tumor cells rapidly, after
chemotherapy. This may cause hypocalcemia, hyperkalemia,hyperuricemia, and other electrolyte abnormalities.
• Drugs such as diuretics, estrogens replacement therapy, fluorides, glucose, insulin, excessive laxative use, and
magnesium.
• Certain things in diet, like caffeine, phosphates (found in soda pop), and certain antibiotics may make it difficult for
to absorb calcium.
15. Pathophysiology
Decrease in extracellular Ca2*
The membrane potential on the outside becomes less negative
Less amount of depolarisation is required to initiate action potential
Increased excitability of muscle and nerve tissue
16. Clinical features
"CATs go numb" - convulsions, arrhythmias, tetany, and numbness in the hands and feet and
around the mouth.
Integumentary : Petechiae purpura paresthesias, tingling or 'pins and needles' sensation in and
around the mouth and lips, and in the extremities of the hands and feet.
Muscoskeletal : Carpopedal and generalized tetany
Trousseau sign (eliciting carpal spasm by inflating the blood pressure cuff and maintaining the cuff
pressure above systolic)
Chvostek's sign (tapping of the inferior portion of the zygomatic bone will produce facial spasms)
Tendon reflexes are hyperactive
Cardiovascular system: Effects on cardiac output
• Negative chronotropic effect, or a decrease in heart rate.
• Negative inotropic effect, or a decrease in contractility
iintermittent QT prolongation,
17. Diagnostic evaluation
History collection and physical examination
S. Calcium and Phosphate levels
• S. Albumin
• S. & Urinary Creatinine (for renal disease)
• PTH levels in serum
• Parathyroid antibodies (present in idiopathic hypoparathyroidism)
•Vitamin D serum level (low inVitamin D def.)
• Magnesium level
• X-rays of metacarpals (showing short 4th metacarpals which occur in pseudo
hypoparathyroidism)
• ECG
18. management
1. Dependent on the underlying cause and severity
2. Administration of calcium alone is only transiently effective.
3. Mild/moderate asymptomatic cases: Often adequate to increase dietary
calcium by 1000 mg/day
Aim to keep serum Ca between 8-8.5mg/dl
Oral Calcium supplements
• Active preparations ofVitamin D • 1,25-dihydroxyvitamin D (Calcitriol)
• 1-α-hydroxyvitamin D (Alfacalcidiol)
@ 50 nanograms/kg (Max ~2 micrograms/day
Severe Symptomatic: • IV 10% Calcium Gluconate 10 ml over 10 minutes •
Continuous IV infusion of Calcium Gluconate @ 0.1 mmol/kg over 24 hours .
19. SUMMARY
Hypercalcemia is an elevated serum ionized calcium or total calcium concentration,
corrected for albumin. There are five major differential diagnostic techniques of
hypercalcemia by: (1) endocrine diseases, (2) malignancy, (3) granulomatous diseases, (4)
drug induced and (5) miscellaneous. The most common etiology in hospitalized patients is
malignancy, and in ambulatory patients it is primary hyperparathyroidism. These two
diagnostic categories account for more than 90% of cases of hypercalcemia. The clinical
findings of hypercalcemia are also mentioned— such as neuromuscular manifestations,
cardiovascular manifestations, renal manifestations, and so on. The laboratory testing
guided by the history and physical status of the patient are important to establish the correct
diagnosis and the severity of illness. The proposed treatments of hypercalcemia includes:
dialysis against a low-calcium bath, use of calcitonin, hydrate with normal saline infusion,
measures to rapidly reduce the serum calcium, and use of glucocorticoids.
20. Hypocalcemia can occur acutely over minutes to hours or chronically
over weeks to months. Correspondingly, the signs and symptoms of
hypocalcemia can develop acutely or chronically and can be life-
threatening. The clinical manifestations of hypocalcemia are due to the
increased neuromuscular tingling in the extremities and around the
mouth. Chvostek’s and Trousseau’s signs can be elicited. When severe,
tetany, convulsions, laryngospasm and bronchospasm can occur.
Hypocalcemia symptoms are a result of both the absolute level of serum
calcium and the rate of change in serum calcium concentration.
Management consists of calcium supplementation and identifying and
treating the underlying cause.
21. CONCLUSION
I concluded that hypercalcemia and hypocalcemia can be serious if left untreated. It is
therefore important that patients with cancer are closely monitored and receive adequate
prevention and treatment measures to maintain normal blood calcium levels.Even the
normal individual should also adequate sunlight for vitamin D and due to their lifestyle busy
schedule if not possible then go for the investigation of vitamin D and start supplement after
concerning to physician.
22. REFRENCES
1. Suzanne C. smeltzer, Bare, Janice L. Hinkle. “Text book of medical-surgical Nursing”,11th
edition,2009.Wottess kluwer Pvt Ltd, New Delhi, page No :301-352
2. Joyce M.Black, Jane Hokanson Hawks, "Medical surgical Nursing, Clinical management
for positive outcomes”,7th edition,Volume I, 2005, saunders publication, Missouri, Page
No:205-244
3. Helen Hakreader, Mary Ann Hogen, “Fundamentals of Nursing,Caring and Clinical
Judgement”,3rd edition, 2009, saunders an imprint of Elsevier, Missouri, page No :613-663
4. Williams S.Linda,Paula D.Hopper, Understanding Medical Surgical Nursing, 2nd Edition,
Jaypee publishers Page No :60-68
5. Lewis et al,”Medical Surgical Nursing”, Mosby first printed in India 2007, Page no 84-97
6. Nightingale nursing times volume X Issue 7, 2003, Page no:14-17 7. The Nursing journal
of India,Vol XVIX, Jan 1992,Page no:21-25
6. www. Wikipedia.com