This document discusses hyponatremia and hypernatremia. It begins by explaining sodium regulation and the physiological basis of serum sodium concentration. It then defines and describes the types and causes of hyponatremia, including hypovolemic, euvolemic, and hypervolemic hyponatremia as well as pseudo hyponatremia. Specific conditions like SIADH are explained in detail. The clinical features, diagnosis, and treatment of hyponatremia are outlined. Hypernatremia is also defined and the causes of net water loss and hypertonic sodium gain are listed. The clinical features of hypernatremia are said to be predominantly neurologic.
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.
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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.
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
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 Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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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.
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
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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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
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2. SODIUM REGULATION:PHYSIOLOGICAL
BASIS
Most prevalent cation in ECF(normal level of around 135- 145
mmol/L).
Intracellular concentration of around 10mmol/L.
Responsible for 90% of total osmolality of ECF.
Major function of sodium is to maintain ECF volume and thus BP.
In normal individuals, the kidney strives to achieve Na+ balance –
that is, to have Na+ excretion equal to Na+ ingestion.
The long-term control of BP is achieved by the excretion or retention
of Na+ (and hence plasma volume) in the kidney.
5. HYPONATREMIA
Definition: Plasma Na+ concentration <135 mEq/L.
Due to a relative excess of water in relation to sodium.
Can result from excessive loss of sodium from excessive sweating,
vomiting, diarrhoea, burns, and diuretics.
It is a very common disorder, occurring in up to 22% of hospitalized
patients.
Result of an increase in circulating ADH and/or increased renal
sensitivity to ADH, combined with any intake of free water.
7. Hypovolemic Hyponatremia
Patient dehydrated; reduction in total body sodium > reduction in total
body water.
NON RENAL LOSSES ( Urinary Sodium excretion < 20 mEq/L)-
Vomiting, Diarrhea, Third space losses, Pancreatitis, Burns.
RENAL LOSSES (Urinary Sodium excretion > 20 mEq/L)- The renal
causes of hypovolemic hyponatremia share an inappropriate loss of
Na+-Cl– in the urine.
Volume depletion and an increase in circulating ADH.
Causes: Reflux nephropathy, recovery phase of ATN,
diuretics,mineralocorticoid deficiency, osmotic diuresis, ketonuria.ria.
8. Euvolemic Hyponatremia
Patient has a normal store of sodium but an excess of total body water.
The most common form seen in hospitalized patients.
The most common cause Inappropriate administration of hypotonic
fluid.
The syndrome of inappropriate antidiuresis is the most common
condition causing euvolemic hyponatremia.
Other causes :Glucocorticoid therapy , stress, hypothyroidism.
9. SIADH
Most common cause of euvolemic hyponatremia.
The secretion of ADH is not inhibited by either low serum osmolality or
expanded intravascular volume.
Child with SIADH is unable to excrete water. This
results in dilution of the serum sodium and hyponatremia.
Kidney increases sodium excretion in an effort to decrease
intravascular volume to normal; thus, the patient has a mild decrease in
body sodium.
10. Diagnostic Criteria for SIADH
Absence of:
Renal, adrenal, or thyroid insufficiency
Heart failure, nephrotic syndrome, or cirrhosis
Diuretic ingestion
Dehydration
Urine osmolality >100 mOsm/kg (usually > plasma)
Serum osmolality <280 mOsm/kg and serum sodium <135 mEq/L
Urine sodium >30 mEq/L
Reversal of “sodium wasting” and correction of hyponatremia with
water restriction
11.
12. Hypervolemic Hyponatremia
Increase in total body water > increase in total body sodium.
Patients are edematous.
RENAL CAUSES(urinary sodium > 20mEq/L): Acute or Chronic renal
failure.
NON RENAL CAUSES(urinary sodium < 20mEq/L): CHF, Cirrhosis,
Nephrotic syndrome.
13. Psuedo hyponatremia
Normal Osmolarity
Due to a measurement error which can result when the solid phase
of plasma (that due to lipid and protein) is increased.
Typically caused by hypertriglyceridaemia or paraproteinaemia.
14. Psuedo hyponatremia….
High Osmolarity: Translocational hyponatraemia
Occurs when an osmotically active solute that cannot cross the cell
membrane is present in the plasma.
In case of insulinopaenic diabetic patient, glucose cannot enter cells
and hence water is displaced across the cell membrane, dehydrating
the cells and “diluting” the sodium in the serum.
This is also the cause of hyponatraemia seen in the TURP syndrome, in
which glycine is inadvertently infused to the same effect.
15. CLINICAL FEATURES
Severity of symptoms depends upon the severity of hyponatremia and
the rate at which the sodium concentration is lowered.
Acute: develops in 48 hours or less. Subjected to more severe degrees
of cerebral edema.
Chronic: develops over 48 hours and brain edema is less and is well
tolerated.
The signs and symptoms are due to increase in volume of ICF and
increase in volume of brain cells rather than decrease in serum sodium.
17. DIAGNOSIS
History and physical examination- to identify hypovolemic
hyponatremia (diarrhoea, vomitting, burns).
Radiologic imaging - to assess whether patient has a pulmonary or
CNS cause for hyponatremia.
18. DIAGNOSIS….
Laboratory tests- Provide important initial clue in the differential
diagnosis
1. Plasma Osmolality
2. Urine Osmolality
3. Urine Sodium concentration
4. Uric acid level
5. Serum potassium
6. Serum glucose
19.
20. TREATMENT
Individualized considering etiology, rate of development, severity and
clinical signs and symptoms.
Hyponatremia which developed quickly needs to be treated fast
whereas slow developing hyponatremia should be corrected slowly.
GOALS of THERAPY:
1. To raise the plasma sodium concentration at a slow rate.
2. To replace sodium or potassium deficit or both.
3. To correct underlying etiology.
BASIC PRINCIPLES OF CORRECTION:
Rapid correction is indicated in acute (<48hours) symptomatic or
severe hyponatremia.(serum Na <120 mEq/L).
In chronic cases patients are at little risk, however rapid correction can
lead to demyelination. Use slower acting therapies like water
restriction.
21. Hypovolemic hyponatremia will respond to intravenous hydration with
isotonic normal saline, with a rapid reduction in circulating AVP and a brisk
water diuresis.
Diuretics induced hyponatremia is treated with saline and potassium
supplementation.
Hypervolemic hyponatremia responds to salt, water restriction (intake
< urine output), and loop diuretics .
Euvolemic hyponatremia will respond to successful treatment of the
underlying cause, with an increase in plasma Na+ concentration.
Regardless of the initial rate of correction, chosen acute treatment is
stopped once-
1. patient’s symptoms are abolished
2. A safe plasma sodium ( >125 mEq/L) is achieved.
22. SPECIFIC THERAPY:
1. Removal of responsible drugs- diuretics, chlorproamide etc
2. Management of physical stress or post operative pain.
3. Specific treatment of underlying cause.
4. Vasopressin antagonists (vaptans) highly effective in treating SIADH
and hypervolemic hyponatremia, reliably increasing plasma Na+
concentration as a result of their aquaretic effects (augmentation of free-
water clearance). Most of these agents specifically antagonize the V2
vasopressin receptor.
TO CALCULATE NEED OF REPLACEMENT SODIUM CONTAINING FLUID:
0.9% saline (154mEq/L) and 3% NaCl- hypertonic saline (513 mEq/L) are
the only two routinely used I.V. fluids . However 0.9% NS is not used to
correct hyponatremia in SIADH
23. Symptomatic Hyponatremia
GOAL : Quickly raise the sodium level but only as much as necessary to
ensure that the pt has normal respiration , seizure free and is alert.
Initial therapy – with 3% NaCl @ 4-6 ml/kg over 30-60 mints.
If no clinical improvement –another 3-4 ml/kg
Therapy stopped once child is asymptomatic or serum sodium is 125 meq/lit
Once pt is asymptomatic, remaining deficit corrected by NS.
Total body sodium defict is approximated as :
Na+ deficit(meq/lit)=(130 - serum Na+) x 0.6 x BW(kg)
Rate of rise of serum should not exceed 0.5-1 meq/lit/hr.
Rate of rise of sodium can be predicted as follows:
Rise of serum Na+/lit of fluid infused=(Inf Na+ - plasma Na+)/(0.6 x BW+ 1)
24. Asymptomatic or Chronic Hyponatremia
Rate of correction should be comparatively slow .
<8–10 mM in the first 24 h and <18 mM in the first 48 h
SIADH
Response to isotonic saline is different in the SIADH
In hypovolemia both the sodium and water are retained
Sodium handling is intact in SIADH
Administered sodium will be excreted in the urine, while some of
the water may be retained possibly worsening the hyponatremia
Water restriction
0.5-1 liter/day
Salt tablets
Demeclocycline
Inhibits the effects of ADH
Onset of action may require up to one week
25. HYPERNATREMIA
Defined as an increase in the plasma Na+ concentration to >145 mM.
Considerably less common than hyponatremia.
Associated with mortality rates as high as 40–60%.
Caused by a relative deficit of water in relation to sodium which can
result from
1. Net water loss: Accounts for majority of cases
Pure water loss
Hypotonic fluid loss
2. Hypertonic gain: Results from iatrogenic sodium loading
26. Causes of Hypernatremia
Net water loss
Pure water loss
Unreplaced insensible losses (dermal and respiratory)
Hypodipsia
Neurogenic diabetes insipidus
Post-traumatic
tumors, cysts, histiocytosis, tuberculosis, sarcoidosis
Idiopathic
aneurysms, meningitis, encephalitis, Guillain-Barre´
syndrome
Congenital nephrogenic diabetes insipidus
Acquired nephrogenic diabetes insipidus
Renal disease (e.g. medullary cystic disease)
Hypercalcemia or hypokalemia
Drugs (lithium, methoxyflurane, amphotericin B, vasopressin V2-receptor
antagonists)
27. Hypotonic fluid loss
Renal causes
Loop diuretics
Osmotic diuresis (glucose, urea, mannitol)
Post obstructive diuresis
Polyuric phase of acute tubular necrosis
Gastrointestinal causes
Vomiting
Nasogastric drainage
Entero cutaneous fistula
Diarrhea
Use of osmotic cathartic agents (e.g., lactulose)
Cutaneous causes
Burns
Excessive sweating
28. Hypertonic sodium gain
Hypertonic sodium bicarbonate infusion
Ingestion of sodium chloride
Ingestion of sea water
Hypertonic sodium chloride infusion
Primary hyper-aldosteronism
Cushing’s syndrome
29.
30. Clinical Features
The symptoms of hypernatremia are predominantly neurologic.
Altered mental status is the most common manifestation, ranging from
mild confusion and lethargy to deep coma.
The sudden shrinkage of brain cells in acute hypernatremia may lead to
parenchymal or subarachnoid haemorrhages and/or subdural
hematomas.
Osmotic damage to muscle membranes also can lead to hypernatremic
rhabdomyolysis.
31. DIAGNOSIS
HISTORY AND PHYSICAL EXAMINATION:
History Should focus on the presence / absence of thirst, polyuria,
and/or an extrarenal source for water loss, such as diarrhoea.
The physical examination should include a detailed neurologic
exam and an assessment of the ECFV; patients may be
hypovolemic, with reduced JVP and orthostasis.
Accurate documentation of daily fluid intake and daily urine output.
LAB INVESTIGATIONS:
Measurement of serum and urine osmolality in addition to urine
electrolytes.
- The appropriate response to hypernatremia and a serum
osmolality >295 mosmol/kg is an increase in circulating ADH and the
excretion of low volumes (<500 mL/d) of maximally concentrated urine,
i.e., urine with osmolality >800 mosmol/kg
32. MANAGEMENT
A two-pronged approach:
Addressing the underlying cause.
Correcting the prevailing hypertonicity.
RATE OF CORRECTION:
Hypernatremia that developed over a period of hours (accidental
loading)
Rapid correction improves prognosis without cerebral edema.
Reducing Na+ by 1 mmol/L/hr appropriate.
Hypernatremia of prolonged or unknown duration
A slow pace of correction prudent.
Maximum rate 0.5 mmol/L/hr to prevent cerebral edema.
A targeted fall in Na+ of 10 mmol/L/24 hr,
33. Goal of Treatment
Reduce serum sodium concentration to 145 mmol/L.
Make allowance for ongoing obligatory or incidental losses of hypotonic
fluids that will aggravate the hypernatremia.
In patients with seizures, prompt anticonvulsant therapy and adequate
ventilation.
Administration of Fluids
Water ideally should be administered by mouth or by nasogastric tube
as the most direct way to provide free water, i.e., water without
electrolytes.
Alternatively, patients can receive free water in dextrose-containing IV
solutions such as 5% dextrose.
34. Hypernatremia with ECF volume contraction: Isotonic
saline is given initially till ECF vol is restored. Subsequently water
deficit can be replaced with water by mouth or I.V. 5% dextrose or
0.45% NaCl
Hypernatremia with increased ECF volume: Since
hypernatremia is secondary to solute administration, it can be rapidly
corrected .
Patients are volume overloaded- loop diuretic is given along with
water to remove excess sodium