This document discusses sodium metabolism and hyponatremia. It begins by explaining that sodium is the primary determinant of extracellular fluid osmolality and plays a key role in determining water distribution between intracellular and extracellular compartments. It then describes sodium absorption, excretion, and regulation by the kidneys and hormones like aldosterone, ANP, and ADH. The document classifies and explains various causes of hyponatremia including pseudohyponatremia, true hypotonic hyponatremia based on volume status, cerebral salt wasting syndrome, and SIADH. Clinical features of hyponatremia vary based on its severity and speed of onset.
Sodium metabolism and its clinical applicationsrohini sane
A comprehensive presentation on Sodium Metabolism and its clinical significance for MBBS, BDS, B Pharm & Biotechnology students to facilitate self- study.
Sodium metabolism and its clinical applicationsrohini sane
A comprehensive presentation on Sodium Metabolism and its clinical significance for MBBS, BDS, B Pharm & Biotechnology students to facilitate self- study.
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
fourth important cation , Second most abundant cation in intracellular fluid after K+., co- factor for more than 300 enzymes , functions of magnesium,Mg-ATP substrate , Mg-GTP substrate, ATP metabolism, muscle contraction and relaxation,normal neurological function and release of neurotransmitters are Mg dependent, green leafy vegetables are particularly rich in magnesium. Absorption in intestine and re absorption in Kidney .Paracellular -Claudin-16/-19, TRPM 6/ 7. Factor affecting for absorption and res absorption ,Action potential conduction in nodal tissue. Neuromuscular Irritability,As Constituent of Bones and Teeth: Hypomagnesemia Causes of Hypomagnesemia -Decreased intake, Redistribution from extracellular to intracellular, Increased losses -Renal Gastrointestinal. hypermagnesemia. sing and symptom of Mg deficiency, familial hypomagnesemia . Hypomagnesemia clinical manifestation, endocrinological manifestation , biochemical manifestation, method of estimations , calmagite , methylbule, Xylidyl blue, forzaman dye, enzymatic method, Magnesium Tolerance Test
Magnesium is a very important ion in the body, crucial to over 300 reactions.
Its disorders are underdiagnosed and can help improve healthcare if appropriately treated
It is the review research based topic of presentation on most important body's serum electrolytes "potassium". it is really a very useful effort to collecting the data material from such a many different websites and pages as i gave references in the end of this presentation.
Gout is a chronic inflammatory disease in which monosodium urate crystal precipitate in joints, soft tissues and cartilage. it is due to increase uric acid level in blood. Gout characterized by red, hot, tender and pain. Presence of MSU crystals (needle shape) in aspirated synovial fluid confirm Gout.
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
fourth important cation , Second most abundant cation in intracellular fluid after K+., co- factor for more than 300 enzymes , functions of magnesium,Mg-ATP substrate , Mg-GTP substrate, ATP metabolism, muscle contraction and relaxation,normal neurological function and release of neurotransmitters are Mg dependent, green leafy vegetables are particularly rich in magnesium. Absorption in intestine and re absorption in Kidney .Paracellular -Claudin-16/-19, TRPM 6/ 7. Factor affecting for absorption and res absorption ,Action potential conduction in nodal tissue. Neuromuscular Irritability,As Constituent of Bones and Teeth: Hypomagnesemia Causes of Hypomagnesemia -Decreased intake, Redistribution from extracellular to intracellular, Increased losses -Renal Gastrointestinal. hypermagnesemia. sing and symptom of Mg deficiency, familial hypomagnesemia . Hypomagnesemia clinical manifestation, endocrinological manifestation , biochemical manifestation, method of estimations , calmagite , methylbule, Xylidyl blue, forzaman dye, enzymatic method, Magnesium Tolerance Test
Magnesium is a very important ion in the body, crucial to over 300 reactions.
Its disorders are underdiagnosed and can help improve healthcare if appropriately treated
It is the review research based topic of presentation on most important body's serum electrolytes "potassium". it is really a very useful effort to collecting the data material from such a many different websites and pages as i gave references in the end of this presentation.
Gout is a chronic inflammatory disease in which monosodium urate crystal precipitate in joints, soft tissues and cartilage. it is due to increase uric acid level in blood. Gout characterized by red, hot, tender and pain. Presence of MSU crystals (needle shape) in aspirated synovial fluid confirm Gout.
Water and electrolytes especially sodium are closely associated in their regulation in the body. Both are tightly regulated as a tilt of one may result in serious consequences to an individual.
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
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.
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.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
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The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
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 .
Early Life and Career
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
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
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
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
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- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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2. SODIUM AND WATER
• Water is the most abundant constituents of body , comprising 50% of
body weight in women and 60% in men
• Total Body water is distributed into two major compartments; 55-75%
is intracellular(ICF) and 25-45% is extracellular(ECF)……ECF is further
subdivided in intravascular(Plasma) and extravascular(interstitial)
space in ratio 1:3
• Sodium is the most abundant ion of extracellular compartment and is
the primary determinant of osmolality of ECF
• Normal plasma level of Na+ is 135-145 mEq/L
• Normal plasma osmolality is 275-295 mOsm/kg
4. PHYSIOLOGY
• OSMOLARITY: It is no of osmoles per litre of solution . Affected by
volume of various solutes and temperature of solution
• OSMOLALITY: It is no of osmoles per kg of solvent and is independent
of temperature or solutes
• Effective solute are impermeable to cell membrane ,i.e Na, mannitol
and contribute to osmolality of the compartment it is in
• Ineffective solute are freely permeable to cell membrane ,..urea ,
ethanol
• Glucose is ineffective solute in physiological state but in high conc it
becomes effective solutes
• Osmolality of plasma = 2[Na+] + [Glucose]/18 + [ BUN ]/2.8
5. SODIUM METABOLISM
• normal plasma level is 135-145 mEq/L
• Sodium intake- normal Indian diet contains 11g per day which is more
than WHO recommendation of 5g per day
• Functions of sodium
i. Sodium and its attendant anions(Cl and HCO3) account for 90_95% of
osmotic pressure in ECF
ii. It determines membrane potential and neuromuscular excitability
iii. Acid base balance , various enzymatic activity
• Total sodium in body is distributed in two pools
i. Exchangeabale pools- in ECF and ICF
ii. Non-exchangeable pool 40% of na+ is bound to polyanionic proteoglycans
in bone,cartilage,skin etc
6. SODIUM ABSORPTION
• It occurs via two mechanism
1. Freely permeable across the interstitial cell
2. Symport with glucose and amino acids
• It is main determinant of Na+ balance
1. KIDNEYS most efficient and well regulated, elimination if intake and vice
versa ….doesn’t eliminate if there is no sodium intake
2. GASTROINTESTINAL <10% of sodium is lost in feces
3. Sweat glands-insensible loss
SODIUM EXCRETION
7. SODIUM HANDLING OF KIDNEY
• Sodium is reabsorbed at 3 main regions in nephron
A. PCT about 2/3rd of sodium is reabsorbed Sodium
passes along an electrochemical gradient (passive
transport) from the lumen into the tubular cell,
together with water and chloride which also diffuse
passively.
B. TALH around 25-30% is reabsorbed via apical Na-K-
2Cl symporter and Na-H antiporter.
C. DCT In the distal convoluted tubule sodium is
transported against an electrochemical gradient by
sodium-chloride symporters.
D. Some sodium reabsorption occurs in cortical and medullary
collecting ducts
8. REGULATION OF WATER AND SODIUM
EXCRETION
• Circulating level of aldosterone-
• Circulating ANP and other Natriuretic hormones
• Intrarenal level of angiotensin II,PGE
• Tubular secretion of K+ and H+
• ADH and its activity
9. ALDOSTERONE
• IT upregulates and activates basolateral Na+/k+ pumps
• Also upregulates epithelial sodium channels ( ENaCs) in
collecting duct and colon
• Upregulates expression of Na+ CL- cotransporter in DCT
• Factors stimulating release of aldosterone
i. Angiotensin II
ii. Decrease sodium level in ECF
iii. Increase potassium level in ECF
This Photo by Unknown Author is licensed under CC BY
RAAS
10. ATRIAL NATRIURETIC PEPTIDE
• Released from atrium in response to increased atrial stretch via
mechanoreceptors
• Effects
i. Dilates renal blood vessels- increases GFR
ii. Inhibits reabsorption of Na+ from CD
iii. Inhibits release of renin , aldosterone and ADH
iv. Endogenous antagonist of angiotensin II
• Increases excretion of both water and sodium
11. INTRARENAL HORMONES
• Angiotensin II
It stimulates Na+ reabsorption in PCT
Release of Aldosterone from ZG of adrenal cortex
Vasoconstriction of arterioles
• Prostaglandins causes natriuresis by inhibition of ENaCs
12. Antidiuretic hormone(ADH)/Vasopressin/arginine
vasopressin(AVP)
• Produced in Hypothalamus and released via posterior pituitary
• Effect on kidney
1. Increase water permeability of CT, cortical collecting
duct(CCT), outer and inner medullary collecting duct
(OMCD & IMCD) via insertion of aquaporin-2 channels
2. Increase permeability of inner medullary CT to urea and
thus water with it
3. Increase Na+ absorption across loop of henle, adding to
increase water absorption in DCT and CT
• Factors causing secretion
i. Increase serum osmolality(most important)
ii. Angiotensin II
14. HYPONATREMIA
• It is defined as serum sodium concentration of less than 135 mEq/L
• Joint European guideline classify Hyponatremia in adults as
Mild 130-134 mEq/L
Moderate 125-129 mEq/L
Profound <125 mEq/L
• Hyponatremia have been also classified according to volume status
i. Hypovolemic hyponatremia…….decrease in total body water with greater
decrease in total body sodium
ii. Euvolemic hyponatremia….normal body sodium with increase in total body
water
iii. Hypervolemic hyponatremia….increase in total body sodium with greater
increase in total body water
15. HYPONATREMIA CAUSES
1. Pseudo hyponatremia-
a) Normal plasma osmolality(Isotonic hyponatremia)- normal plasma water is
around 92-94% this water fraction falls in increase of fats and proteins, thus
measured sodium is low
• Hyperlipidemia
• Hyperproteinemia
• Post transurethral resection of prostrate/bladder
b) Increased plasma osmolality(hypertonic hyponatremia)- it is due to
presence of osmotically active molecules in serum resulting in water shift
from ICF to ECF causing dilution of Na+
• Hyperglycemia each 100mg/dl causes 1.6-2.4 mEq/L decrease in Na+
• Mannitol
16. TRUE HYPONATREMIA (hypotonic hyponatremia)
• Based on volume status hyponatremia is classified as
1. HYPOVOLEMIC HYPONATREMIA- there is decrease in TBW with greater
decrease in total body Na+
Primary Na+ loss
RENAL LOSS U(Na+) >20
i. Mineralocorticoid deficiency
ii. Diuretic excess
iii. Osmotic diuresis
iv. Cerebral salt wasting synfrome
EXTRARENAL LOSS U(Na+) <20
i. Burns
ii. Pancreatitis
iii. Diarrhoea and vomitting
17. 2. EUVOLEMIC HYPONATREMIA-normal to low Na+ with increase in
TBW, it is associated with nonosmotic and non-volume related ADH
secretion seen in
i. Glucocorticoid deficiency
ii. Drugs
iii. SIADH
iv. Stress ,surgery
v. Hypothyroidism
vi. Beer potomania
18. 3. HYPERVOLEMIC HYPONATREMIA- increase in Na+ with greater
increase in TBW decrease Na+ concentration
the causative disorder can be differentiated by urinary Na+
Na+ Avid state U(Na+) < 20
i. Liver cirrhosis
ii. Nephrotic Syndrome
iii. Cardiac failure
Renal cause U(Na+) >20
i. Acute or Chronic renal failure
20. CLINICAL FEATURES
• HISTORY
Exercise associated hyponatremia(in Hot climate and ingestion of fluids)
Medical history of OTC drugs(antipsycotic,antiepileptic,antidepressants)
Dieatry history (salt,protein,water and parentral fluid in hospital case)
• Symptoms varies from Nausea/malaise (mild) to lethargy,seizure (very
low <115 mEq/L
• Gradual fall in Na+ is well tolerated
• Clinical manifestations of hyponatremia results from osmotic water
shifting to ICF……causing
i. Cerebral edematentorial herniationbrainstem compression Death
ii. Non cardiogenic pulmonary edema normocapneic respiratory failure
21. Clinical features cont…..
• Bad prognosis- underlying neurological or metabolic disorder
• Few common symptoms are
i. Stupor/altered sensorium
ii. Anorexia/nausea/vomitting
iii. Lethargy
iv. Decrease tendon reflex
v. Limb weakness
vi. Orthostatic hypotension
vii. Seizure/headache
viii. Stomach cramps
22. • Premenopausal women are prone to developing cerebral edema in
association with hyponatremia due to inhibition of Na-k ATPase by
estrogen and progesterone, may also be caused by hypothalamic and
pituitary infarction
• Hyponatremia in cortisol deficiency occurs due to hypersecretion of
ADH
• Beer potomania The low solute content of beer, and suppressive
effect of alcohol on proteolysis result in reduced solute delivery to the
kidney. The presence of inadequate solute in the kidney eventually
causes dilutional hyponatremia secondary to reduced clearance of
excess fluid from the body
•
23. CEREBRAL SALT WASTING
• It is a rare salt wasting disorder secondary to intracranial pathology as
SAH, Meningitis, carcinoma, post neurosurgery/intervention
• Damage to sympathetic neural input to kidney
• Signs and symptoms are
i. polyuria, defined as over three liters of urine output over 24 hours in an
adult)
ii. high amounts of sodium in the urine
iii. low blood sodium concentration
iv. excessive thirst (polydipsia)
v. extreme salt cravings
vi. dysfunction of the autonomic nervous system (dysautonomia), and
dehydration
24. • CSWS is a diagnosis of exclusion and is difficult to distinguish from the
SIADH, The main clinical difference is that of total fluid status of the
patient: CSWS leads to a relative or overt low blood volume, whereas
SIADH is normal or high blood volume (due to water reabsorption via
the V2 receptor).Urine output is classically low in SIADH and elevated
in CSWS
• CSWS occurs within the 1st week after brain injury and spontaneously
resolves in 2–4 weeks, can last for months or years.
• CSWS is treated by replacing the urinary losses of water and Na+ with
hydration and sodium replacement.
• The mineralocorticoid medication fludrocortisone can also improve
the low sodium level
25. SIADH- Syndrome of inappropriate ADH secretion
• Marked by continued secretion or activity of ADH, despite normal or
increased plasma volume
• Water retention ,hyponatremia , hypoosmolality and high urine
osmolality is hallmark feature
• Signs and symptoms
Depend on rate and severity of hyponatremia
Signs of AVP secretion…chronic pain ,pulmonary or CNS symptoms or drug
use
• Investigations
Serum Na+, K+,Cl-, HCO3, Cr, BUN, Uric acid, blood glucose
Serum osmolality
Urine osmolality
26. Diagnosis of SIADH – barter-schwartz criteria 1967
• Hyponatremia with hypoosmolality
• Continued renal Na+ excretion
• Urine less than maximum diluted
• Absence of signs of volume depletion
• Absence of other cause of hyponatremia-mineralocorticoid deficiency
hypothyroidism ,CHF ,CLD ,ESRD , drugs
• Correction of hyponatremia with fluid restriction
27. WORKUP
• Three essential test to differentiate cause of hyponatremia
i. Urine osmolality-Impaired water clearance(>100mOsm/kg) Vs primary
polydipsia
ii. Serum osmolality- True vs pseudohyponatremia
iii. Urinary sodium concentration- hyponatremia secondary to hypovolemia
{U(Na+)<25 mEq/L} vs SIADH {U(Na+) >20-40 mEq/L}
• Ancilary test
i. Serum uric acid SIADH and CSW (autocorrection with Na+ correction in
SIADH)
ii. TSH and Serum Cortisol
iii. Serum albumin, Triglycerides, Blood glucose, Serum K+
iv. ECG
28. • Imaging
i. Head CT in suspected CSW
ii. Chest CT or Xray in selected case of SIADH
30. Management
Hypovolemic hyponatyremia most common
• Acute hyponatremia <48hrs- can be corrected rapidly than chronic
hyponatremia > 48hrs duration
• In pseudohyponatremia (isotonic and hypertonic ) treat underlying
diseases
• Infuse saline to correct hypovolemia decrease activity of AVP
• Replace K+ if due to diuretic use
31. Hypervolemic Hyponatremia
• Salt and fluid restriction
• Loop diuretics with salt tablets
• Correct underlying condition
• V2 antagonist may be considered
Euvolemic Hyponatremia
• Asymptomatic- fluid restriction <1 litre/day
Severe symptomatic hyponatremia 3% NaCl can be used
32. OSMOTIC DEMYELINATION SYNDROME
• During chronic hyponatremia—efflux of organic osmolytes(Cr,Betaine,
taurine)
• While rapidly correcting hyponatremia (>10mmol/L/day) there is re
accumulation of organic osmolytes causing degenerative loss of
oligodendrocyte
• Rapid correction of hyponatremia causes disruption of BBB adding to
demyelinosis
• Risk factor for developing ODS
i. Alcoholism,malnutrition
ii. Neurological symptoms (seizure,stupor,coma)
iii. Metabolic underlying cause
iv. Chronic hyponatremia
33. Type of lesion in ODS
1. Pontine-
i. occurs 2-3 days after overcorrection of hyponatremia
ii. Presents as paraparesis, Quadriparesis ,dysphagia ,dysarthia, diplopia and
locked in syndrome
2. Extrapontine
i. Lesion could be cerebellum, LGB, thalamus, Putamen, Cerebral cortex
ii. Signs and symptoms are ataxia, mutism, parkinsonism, dystonia and
catatonia
34. Guideline
Joint European clinical practice guideline on diagnosis and treatment of hyponatremia
• Three parameters determine treatment guidelines
i. Patient’s volume status
ii. Duration and severity of hyponatremia
iii. Severity of clinical symptoms
• Acute/chronic severely symptomatic hyponatremia
i. Promptly infuse 150ml 3% NaCl IV over 20 min repeat max 3 times, check
Na+ before repeating
ii. If patient improves with 5mmol/L increase in 1st hour
a. Limit increase in Na+ by 10mmol/L in 24hr and 8mmol/L in next any 24 hrs
b. Check Na+ 6 hourly
iii. If no improvement
a. Control increase infusion @ 1mmol/L /hr
b. Stop if Na+ 130mEq/l or condition improves or total increase is 10mmol/L
c. Check Na+ 4 hourly till hypertonic saline is being used
35. • Acute hyponatremia with mild or moderate symptoms
i. Rule out error of measurement
ii. water restriction and stop hyponatremia causing drugs
iii. Workup for cause
iv. If acute decrease of Na exceeds 10mmol/L may infuse a single infusion of 150ml 3%NaCl
over 20min
v. Recheck Na+ after 4hrs
• In chronic hyponatremia with mild or moderate symptoms
i. Stop non-essentials fluids medications provoking hyponatremia
ii. In moderate to profound hyponatremia avoid increase of serum Na >10mmol/L in 1st 24hrs
and >8mmol/L in next every 24hrs to prevent ODS
36. • Hypervolemic hyponatremia
i. Treatment of underlying cause ,correction of hypokalemia
ii. Fluid restriction to prevent further fluid overload
iii. AVP antagonist as vaptans are highly effective in HF, liver disease
beside SIADH (max duration 1-2 mnths)
iv. Therapy with vaptans should be initiated in hospital setting with
liberalisation of fluid intake >2litre/day with close monitoring of
plasma Na+
Tolvaptan V2antagonist- oral
Conviptan iv use V1a/V2 antagonist
37. For patient with SIADH
i. In moderate to profound hyponatremia consider fluid restriction as
first line treatment
ii. In moderate or profound hyponatremia, solute intake @ 0.25-0.50
g/kg per day with low dose loop diuretics (furosemide 20mg twice
daily) as second line of treatment
iii. In moderate and profound hyponatremia demeclocycline, Vaptans,
lithium is not advised
iv. Demeclocycline a potent inhibitor of principal cell,used in cases
where Na doesn’t increase with furosemide and salt tablets,
nephrotoxic(decrease GFR) and also avoided in liver disease
38. Hypovolemic hyponatremia
i. Restore ECF with 0.9% NaCl or a balanced crystalloid at 0.5-
0.1ml/kg/hr
ii. If hemodynamicly unstable rapid fluid resuscitation
iii. The traditional approach is to calculate Na+ deficit
Na+ deficit = 0.6 * BW* (target Na+ -plasma Na ) and replenish at fixed rate
iv. Na+ should be monitored every2-3 hrs during treatment
v. IV loop diuretics helps in relieve from symptoms due to acute
pulmonary edema
39. • If hyponatremia is corrected too rapidly consider
i. Promptly lower Na if increase is >10mmol/L in 1st 24hrs or >8mmol/L in any
24hrs thereafter
ii. Discontinue the active treatment
iii. Consider infusion of 10ml/kg of electrolyte free water over 1hr with strict
monitoring of urine output and fluid balance
iv. Consult to consider to add desmopressin 2mcg,not to be repeated before
8hrs
41. HYPERNATREMIA
• It is defined as plasma Na+ concentration > 145 mEq/L
• Less common than hyponatremia but with mortality 40-60%
42. CAUSES
• Inadequate water Intake
i. Impaired thirst
ii. Decrease access to fluid (elderly with mental illness)
iii. Increase insensible loss
• Increase water loss
i. GI Loss- vomiting, diarrhoea(secretory and viral gastroenteritis)
ii. Renal loss- Central diabetes insipidus, osmotic diuresis(hypercalcemia, hyperglycemia )
Nephrogenic DI
• Excessive sodium
i. Iatrogenic- hypertonic saline, NaHCO3 tablets
ii. Mineralocorticoid excess- cushing, primary aldosteronism, ectopic ACTH
iii. Peritoneal dialysis- loss of water> loss of sodium
• Drugs/medication- alcohol, lithium, phenytoin, sulfonylurea, colchicine
44. Clinical signs of hyponatremic states related to
serum osmolality
• Osmolality (mOsm/kg) Manifestations
i. 350-375
ii. 375-400
iii. 400-430
iv. > 430
Restlessness, irritability
Ataxia, tremulousness
Hyperreflexia, twitching, spasticity
Seizures and Death
45. • Most hyponatremia in emergency is related to severe volume loss
• In healthy patients, hypovolemia causes conservation of free water by
kidney
i. low Urine output (<20ml/hr) with
ii. high osmolality (>1000 mOsm/kg water)
• Diabetes Insipidus
i. Failure of central or peripheral ADH response NDI
ii. Urine osmolality is low(200-300 mOsm/kg)
iii. Urinary [Na+] 60-100mEq/kg
iv. Large urine volume >50ml/kg/day
46. WORKUP
• History- diarrhoea, thirst, polyuria
• Documentation of Input Output in hospitalised cases
• Laborotary investigation
Serum and urine osmolality
Urine Electrolytes
• DI requires measurement of urine osmolality to DDAVP
• AVP assay to differentiate between Central DI and NDI
In pregnancy drawn in Vial containing 1,10- phenthroline
Inhibits placental vasopressinase
48. Treatment
• Withdraw causative agent- hyperglycemia, hypercalcemia ,hypokalemia, diarrhoea
• Correct slowly to avoid cerebral edema by correcting “free water
deficit over 48 hrs or max @ 10 mmol/day
• In acute hypernatremia(<48hrs) can correct rapidly @ 1mmol/hr
• Oral route is preferred for volume correction
• IV fluid
i. Treat initially with 0.45% saline
ii. Then with D5W (preferred)
49. Treatment
• Additional drugs – mostly used in chronic management of polyuria
DDAVP(artificial AVP) desmopressin – oral, intranasal, Iv
Amiloride (2.5-10 mg/d) in Lithium induced NDI
NSAIDS inhits intrarenal PGE
Thiazides reduces polyuria in NDI
51. GUIDELINES
• Society of endocrinology guideline for diabetes insipidus
i. In CDI with unconsciousness check volume status every 12 hourly and daily
maintenance of Input-Output chart, daily Na+
ii. Measure Na+ every 4 hourly during fluid resuscitation and later at least 12
hourly
iii. In patient with High Urine Output and low urine osmolality consider
desmopressin (DDAVP)
iv. First goal is fluid optimization then asses for DDAVP therapy
v. Correction rate in acute symptomatic hypernatremia @ 5mmol/L in 1st hour
if asymptomatic rate @ 0.5 mmol/hr
vi. Maximum rate of correction in 24hrs is 10mmol/L
52. TAKE HOME MESSAGE
• History of duration of hypo/hypernatremia is very important in
management
• Rate of correction in hyponatremia should keep in mind risk of ODS
• CSW Vs SIADH (intracranial pathology) can be differentiated with
urine Na+ increased in SIADH
• V2 antagonist-vaptans should be initiated in hospital setting with
liberalisation of fluid intake >2litre/day
• Regular monitoring of serum Na+ is essential for proper management
in both hypo/hypernatremia
• Central DI and NDI can be differentiated with response to DDAVP and
AVP assay(falls in central DI)