This document summarizes alterations in calcium metabolism, including hypercalcemia and hypocalcemia. Hypercalcemia is defined as elevated serum calcium levels and can be caused by increased bone resorption, as seen in primary hyperparathyroidism, or increased intestinal calcium absorption. Hypocalcemia is defined as low serum calcium levels and can be caused by calcium exiting the blood compartment, or by decreased calcium flow from intestines or bones into the blood, as seen in hypoparathyroidism. The document outlines the clinical presentations, diagnostic evaluations, and treatments for hypercalcemia and hypocalcemia.
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.
Tumor Lysis Syndrome
The most common disease-related emergency encountered by physicians caring for children or adults with hematologic cancers
When tumor cells release their contents into the bloodstream, either spontaneously or in response to therapy-
leading to the characteristic findings of
hyperuricemia, hyperkalemia, hyperphosphatemia, and
hypocalcemia
Electrolyte and metabolic disturbances- progress to clinical toxic effects- including
-renal insufficiency,
-cardiac arrhythmias,
-seizures, and
-death due to multiorgan failure
Laboratory tumor lysis syndrome : Requires that two or more of the metabolic abnormalities occur within 3 days before or up to 7 days after the initiation of therapy
Clinical tumor lysis syndrome: Laboratory tumor lysis syndrome is accompanied by an increased creatinine level, seizures, cardiac dysrhythmia, or death.
IN MALIGNANCIES
–high proliferative rate,
–large tumor burden,
–high sensitivity to treatment-
Initiation of cytotoxic chemotherapy,
Cytolytic antibody therapy,
Radiation therapy,
Sometimes glucocorticoid therapy alone
Rapid lysis of tumor cells!!!!!
Releases massive quantities of intracellular contents:
K+ , phosphate, and nucleic acids
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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.
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.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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.
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
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
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.
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
- 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
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
1. UNIVERSIDAD TECNICA DE MACHALA
ACADEMIC UNIT OF CHEMICAL
SCIENCES AND HEALTH
MEDICINE SCHOOL
ENGLISH
ALTERATIONS OF
CALCIUM
METABOLISM
STUDENTS
William Cruz
Kevin Herrera
TEACHER:
Mgs. Barreto Huilcapi Lina Maribel
CLASS:
EIGHTH SEMESTER ‘’A’’
Machala, El Oro
2018
ALTERATIONS OF CALCIUM METABOLISM
2. HYPERCALCEMIA
Definition.- The serum concentration of total calcium in the normal limits of 8.5
to 10.5 mg / dL. In patients with higher figures, pseudohypercalcemia should first
be ruled out, in which the elevations of total serum calcium are due to an increase
in the concentration of calcium transport proteins (albumin or a paraprotein).
Etiology.- The most important sources of calcium intake are the intestine and
bone, and it is useful to classify hypercalcemias according to these two origins.
More than 90% of cases of hypercalcemia are due to neoplasms or primary
hyperparathyroidism
a) Hypercalcemia due to increased bone resorption: It occurs in primary
hyperparathyroidism where 80% -85% of cases are due to a single
adenoma of the parathyroids, in 15% to diffuse hyperplasia and in 1% -3
% of patients with parathyroid carcinoma, likewise in secondary
hyperparathyroidism that appears in chronic renal failure. In the most
severe cases, a nodular hyperplasia of the parathyroid glands develops,
with monoclonality; that usually produces hypercalcemia and finally is
observed in the hypercalcemia associated with neoplasms. 10% -20% of
patients with neoplasia develop hypercalcemia, usually in the late stages of
the disease, and the diagnosis is usually evident. The neoplasms that most
commonly produce hypercalcemia are breast cancer, lung cancer and
multiple myeloma. In the context of a neoplasia, hypercalcemia can occur
by three distinct mechanisms: osteolytic metastases with local release of
cytokines such as IL-1, and TNF-a, release into the circulation by the
tumor of the PTH-related protein (PTHrP) , and production of calcitriol by
the tumor. Hypercalcemia is the most common cause of non-metastatic
solid tumors, malignant humoral hypercalcemia, caused by the release of
PTHrP.
b) Hypercalcemia due to increased intestinal calcium absorption:
association with lower renal calcium excretion, vitamin D poisoning,
sarcoidosis and other granulomatosis.
3. Clinical Table.- Anorexia and constipation are usually the first digestive
manifestations, followed by nausea and vomiting. In hypercalcemic individuals,
and particularly in primary hyperparathyroidism, there is an increased incidence
of peptic ulcer and pancreatitis, may be associated with high blood pressure with
high plasma renin. The shortening of the QT interval is the most characteristic
electrocardiographic sign of hypercalcemia. Serious cases add drowsiness,
confusion and coma.
Treatment.- They are dehydrated as a consequence of a decrease in urinary
concentration capacity and losses of another origin (vomiting and others).
This conditions a decrease in the filtrate that decreases the excretion of calcium,
with which the hypercalcemia is perpetuated. Therefore, the expansion of
extracellular volume through the infusion of isotonic saline should be the first step
in the treatment of hypercalcemia. It usually begins with 200-500 mL / h if the
cardiac reserve of the patient allows it, to maintain a diuresis of 100-150 mL / h.
The use of loop diuretics (furosemide 20-40 mg / 4-6 h) produces an increase in
the renal excretion of sodium and calcium; thiazides should not be used, since
they increase distal calcium reabsorption.
General measures such as withdrawing calcium and drugs that elevate calcemia,
maintain good oral hydration, promote mobility, and avoid the use of sedatives
and analgesics that worsen mental confusion, are mandatory.
HYPOCALCEMIA
It is defined as a decrease in calcium concentrations below 8.5 mg / dl (2.1 mmol /
L) in the absence of hypoalbuminemia. Whenever they persist, the determination
of ionic calcium concentrations should be used; a figure lower than 4.2 mg / dL
(1.05 mmol / L) indicates hypocalcemia.
Etiology.- It can be by:
a) Calcium exit from the blood compartment or intravascular ligament:
In hyperphosphatemia, phosphocalcic complexes are formed and deposited
in soft tissues, leading to hypocalcemia. The most common clinical
4. situations are renal failure, administration of phosphate (i.v. or enemas),
rhabdomyolysis and tumor lysis syndrome, it also appears during the acute
phase of pancreatitis although it has not yet been fully clarified.
Exceptionally, osteoblastic metastases, hungry bone syndrome and
administration of calcium chelators (EDTA, citrates, lactate, foscarnet).
b) Decrease in the flow of calcium from the intestine or bone to the
plasma: It may be due to hypoparathyroidism after surgery of the
parathyroid or neck and by irradiation or infiltration of the parathyroids.
Idiopathic hypoparathyroidism can occur in the context of a familial
autoimmune poly glandular syndrome type 1. Also in severe
hypomagnesemia and marked hypermagnesemia, in sepsis, large burns, in
pseudohypoparathyroidism and patients with primary or tertiary
hyperparathyroidism treated with calcimetics also they can develop
hypocalcemia; or another cause may be for hypovitaminosis D.
Vitamin D deficiency causes hypocalcemia and secondary hyperpathoidism,
through a decrease in intestinal calcium absorption, insufficient insolation in the
context of a deficit diet, malabsorptive syndromes, surgical intervention of the
upper digestive tract, hepatobiliary disease, renal failure and consumption of
anticonvulsants (difelhydantoin and barbiturates).
Clinical picture: Tetany is observed, produced by an increase in neuromuscular
irritability. It begins with circumoral and acrosal paresthesias to continue with
muscular spasms that end with carpedal spasm, Chevostek sign and Trosseau sign.
Acute intense hypocalcemia when it can cause seizures, papilledema, mental
retardation and dementia. A variety of extrapyramidal disorders, ectodermal
alterations, cataracts and lengthening of the QT interval on the ECG can occur.
Diagnosis: Once the presence of true hypocalcemia is established, the clinical
history itself will determine its cause in most cases. The determination of
creatinine, phosphorus and hypomagnesemia concentrations all cause
hypocalcemia. When in this context the diagnosis is not reached, it is necessary to
resort to the determination of PTH concentrations and the percentage of tubular
reabsorption of phosphorus (% RTP).
5. Treatment: In acute hypocalcemia, symptomatic or with calcemia figures lower
than 7 mg / dl, calcium will be administered i.v. If the situation is emergency,
initially use 10 ampoules of 10 mL of 10% calcium gluconate diluted in 100-250
mL of glucose solution at 5% for a period of at least 10-15 min and if the situation
does not is emergency, is infused 1-2 m / kg of weight and hour of calcium
element. If there is hyperphosphoremia, the calcium calcium oral calcium intake
of choice is calcium carbonate. When a hypoglycemia is suspected, a blood
sample should be taken for confirmation, and magnesium sulfate infused until the
results are available. In chronic hypocalcemia, an attempt should be made to
elevate calcemia to concentrations that are in the limit under normal conditions to
prevent an increase in the filtered calcium load that only produces hypercalciuria,
and in the long term, nephrolithiasis and nephrocalcinosis. The treatment is based
on the supply of calcium supplements orally and vitamin D. Calcium will be
administered in the form of lactate, gluconate or calcium carbonate, at a dose of 1-
2 g. of calcium element per day.
BIBLIOGRAPHIC REFERENCE:
A, Torres Ramírez "Alterations of calcium, phosphorus and magnesium
metabolism" In: Farreras Valenti - C. Rozman. Internal Medicine XVIII. Elsevier
Edition Spain (Barcelona) 2012 p. 787-796