This document discusses various fluid and electrolyte imbalances in the human body. It covers topics like:
- Types of fluid compartments and their normal volumes and electrolyte contents
- Causes, features, and treatment of dehydration, hypovolaemia, hypervolemia, and fluid overload
- Causes, features, and management of various electrolyte imbalances including hyponatremia, hypernatremia, hypokalemia, hyperkalemia, and hypomagnesemia
- Importance of slow correction and monitoring in treating electrolyte abnormalities to avoid complications
It provides a comprehensive overview of fluid and electrolyte physiology and disturbances.
This slide share includes definition,indications,dehydration status,types of fluids,when to administer which fluid,how to calculate the fluid to be administered and how to monitor fluid therapy.Hope its helpful.
This slide share includes definition,indications,dehydration status,types of fluids,when to administer which fluid,how to calculate the fluid to be administered and how to monitor fluid therapy.Hope its helpful.
THIS SEMINAR GIVES THE BASIC OVERVIEW THAT HOW YOU CAN MANAGE THE PATIENT WHO COMES TO YOU A FLUID AND ELECTROLYTE IMBALANCE . AND BASIC MECHANISM OF HOMEOSTASTIS
THIS SEMINAR GIVES THE BASIC OVERVIEW THAT HOW YOU CAN MANAGE THE PATIENT WHO COMES TO YOU A FLUID AND ELECTROLYTE IMBALANCE . AND BASIC MECHANISM OF HOMEOSTASTIS
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
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.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
- 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
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.
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.
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
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.
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.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
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.
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.
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
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
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
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journey
Fluids & Electrolytes
1. Prof. M.C.Bansal.
MBBS;MS. FICOG. MICOG.
Founder Principal & Controller,
Jhalawar Medical college , Jalawar.
Ex.Principal&Controller;
Mahatma Gandhi Medical College,sitapura , Jaipur.
2. Total body water is 60% in male, 50% in female i.e. 30
litres
Inraceullar fluid (ICF) –20 litres water (2/3).
Extracellular fluid (ICF)– 10 litres water (1/3).
>Plasma –2.2 litres (1/4).
> Interstitial fluid – 7.5 litres (3/4).
EcF volume and Osmalality regulation is controlled by 3
hormones –aldosterone, ADH Atrial natriuretic
hormoneION ICF ECF
Sodium 10mml/L 140mml/L
Potassium 150mml/L 4.5mml/L
Chloride Traces 105mml/L
3.
4.
5.
6.
7.
8.
9.
10. It is decrease in whole body fluid volume
which includes both exta and intracellular fluid
loss.
Extracellular fluid loss is more important and
has to be assessed .
This fluid loss may be :
>Isotonic –Water and salt loss leading to
Hypovolaemia.
> Hypotonic – only water loss with minimal
electrolyte loss; leading to dehydration.
11. Isotonic Volume Depletion
Occurs due to diarrhea, vomiting and excess
dieresis.
> Fluid loss is only of ECF compartment and so
immediate reduction in intravascular volume
results leading to hypovolaemia and fall in BP.
> decreased Tissue perfusion.
features Dry tongue , rapid pulse, cold clammy
skin , sunken eyes , decreased BP, oliguria , raised
blood urea and decreased urinary sodium.
Hypovolaemia –Mild (<2l), Moderate (2-3L) ; severe
( > 3l ) fluid loss.
12. Hypotonic Fluid loss
> i.e. only water loss , occurs due to decreased
intake of water and diabetes insipidus .
> It causes dehydration and appropriate and
decrease in total body water in all fluid
compartments ( 2/3rd ICF , 1/3rd ECF ).
>As ECF loss is less ---intravascular fluids loss is
also less hence Fall in BP is also less .
Features severe thirst , confusion,
convulsions( due to hypernatraemia ), BP
relatively normal .
Dehydration : mild (weight loss 5%), moderate
(10%) , severe (15% ).
13. Evaluation is done by estimation of serum
Na+, urinary Na+ and blood urea .
Isotonic volume depletion is corrected by o.9%
normal saline infusion ,
Pure water depletion is corrected by more
water in take / IV 5% dextrose infusion .
Monitoring fluid therapy by skin and tongue
examination, weight gain pulse, BP, urine
output , CVP and PCWP.
14. Water & Salt excess
occurs in CCF , Cirrhosis, nephrotic syndrome ,
hypoproteinaemia, renal failure , excessive
saline infusion.
Water Intoxication
TCRE, excess infusion of 5% dextrose only,
SIADH secretion, Psychogenic polydypsia.
It is managed by stopping fluid infusion or
procedure (TCRE), fluid restriction and treating
the cause.
15. Excessive amount of intravenous dextrose(5%).
Bowel Wash by plane water in place of normal
saline.
In TCRE (TUR in urology ) hydro dissection in
tumour surgery , when excessive fluid Plane
water or glycine is used for uterine distension.
In syndrome of inappropriate Anti diuretic
hormone secretion which is commonly
associated with lobar pneumonia, empyema ,
oat cell carcinoma and head injury .
16. Drowsiness , weakness.
Convulsions , coma.
Nausea and vomiting.
Passage of dilute urine.
Distended neck veins.
Gain in body weight .
Circulatory over load –tachycardia, pulmonary
edema, hypertension and pedal edema.
Bilateral basal crepitations , ascites.
Raised CVP, PCWP.
17. Investigations
>Haematocrit and sodium level (will show fall in
level)
> Low Potassium and Low blood urea.ECG< X-ray
Chest.
Treatment
>Water and salt restriction and observation .
> Monitoring in ICU.
> Management of fluid and electrolyte balance as per
serum electrolyte reports.
> Infusion of( ½) hypotonic saline.
Administration of diuretics and hypertonic saline
should be avoided as it may de arrange serum
electrolytes which may lead to neuronal demylation
and FATL OUTCOME.
18. ECF Loss
> Here only ECF loss occurs , ICF remains Normal.
> It is seen in diarrhoea , vomiting, intestinal
obstruction / fistula.
> Normal Saline infusion = to calculated ECF loss.
ECF excess
Only ECF Excess ,ICF remains normal.
It occurs when excessive infusion of saline with
impaired excretion as in renal diseases.
Raised JVP , cardiac failure and peripheral edema.
Treatment is fluid restriction and diuretics like
frusamide.
19.
20. Definition
> Serum Sodium level is < 130mEq/L
> Severe degree hyponatraemia, when serum
sodium level < 100 mEq/L in acute type and in
chronic type serum sodium level <115 is taken
as reference value.
< May be due to water over loading (dilution)
or sodium loss.
21. Acute—presents as neurological manifestations.
Chronic – cause pontine myelonlysis , presents as behavioral
changes , weakness and central nerve palsies.
Other types may be
(a) hypervolaemic Hyponatraemia –Rapid absorption of fluid occurs
leading to dilution and decreased Na+ concentration. Decreased
osmalality results in migration of ECF in to ICF compartment and
hence patient develops cerebral and pulmonary edema ., causing
convulsions and respiratory symptoms.
-Urinary Na+ conc. Is 15 mmol/L.
-fluid restriction ,hypertonic saline (double strength) infusion and
loop diuratics like frusamide injection are the main lines of
management.
- Monitoring is done by Serum Na= estimation and its correction till
it reaches above the level of 125mmol/L .
- correction should be slow and gradual at the rate of 2mEq/L /Hr
and up to 20 mEq/L in 24 hours. Serum Na+ estimation should be
done at 4 hourly interval .
- Rapid correction may lead to irreversible myelinlysis of pontine .
- Over correction should always be avoided.
22. (b) Hypovolumaemic hyponatraemia –
- Hypovolaemic as in dirrhoea and vomiting ,
hyponatraemic as urinary Na= level is <
20mmol/L.
- Due to forced diuresis and renal causes water is
lost and urinary Na+ level is more than
20mmol/L.
- It may be due to over correction of
hypovolaemia by only dextrose / hypotonic fluid.
- condition is treated by using Isotonic
fluid(normal saline ) therapy.
23. (c) Normovolaemic Hyponatraemia—
- It may be due to renal failure or Syndrome
of inappropriate ADH secretion
- Mild cases fluid restriction (1 litre /day )
will raise the Na+ level .
- In severe cases Vasopressin antagonist (
Demeclocyclin) will increase the diluting
ability of kidney . And Na+ level will improve.
24. ( d) Pseudo-hyponatraemia –
- Plasma osmalality is mainly achieved by Na+ but small
portion of it i.e. 25% is due to other solutes like glucose ,
proteins, urea and lipids which do not move out easily from
vascular compartment, in IC / EC Spaces.
- When concentration of this substances increase , the Na+
level will fall causing Pseudo hyponatraemia.
Correction of increased element will correct the Na+ level.
Causes
- Intestinal obstruction,
-intestinal fistula,
-gastric outlet obstruction with excess of vomiting ,
-prolonged Ryle’s tube aspiration,
-Severe diarrhoea due viral cause –in colitis and cororectal polyposis,
-SIADH,
-Immediate after surgery / trauma Na+ depletion occurs .
-stroke etc.
26. Serum electrolytes --- Low serum Na= Level.
Urinary Na+ level low,
Sodium deficit =
( 125- present Na+ ) X body weight in Kg X 0.6.
27. In acute cases --IV infusion of normal saline to
achieve slow and gradual correction of serum
Na+ level at the rate of 2mEq/L / hr.
Maximum 20mEq/L in 24 hrs. monitor Na=
Level at 4 hrs interval.
In chronic Case--< 1mEq/L/Hr and should
not exceed > 10mEq/l in 24 hrs.
Hypertonic saline 1.6 % or 3% can be used in
acute severe cases with caution of too early and
rapid correction is associated with myelinlysis
of pontine.
Cause is also treated simultaneously.
Type of Saline fluid NaCl content
0,9% normal saline /L 154mEq/L
3% hypertonic Saline 500 mEq/L
28.
29. Serum Na+ level >150mEq/L., is taken as
hypernatraemia.
Causes
>Renal Dysfunction.
>Cardiac Failure.
>Drug induced like NSAID , Corticosteroids.
>Excess infusion of hypertonic saline /intra amniotic
hypertonic saline previously used for mid trimester
MTP.
> excess of normal saline infusion causes overloading
in circulating salt and water. It is due to when water
deficit present in initial stage..
30. (A) Euvolaemic ( pure water loss ):
- It is due to decreased water intake as in coma,
bedridden people , post operative patients when iv
therapy has been stoped but pt does not take reqired
amount of water, patient in high fever leading to
external loss of water. It can also occur in diabetes
incipidus / chronic renal failure as renal loss of only
water.
( B ) -Hypovolaemic:
-( Among loss of water and Na= but water is more lost
than Na+.) as in cases of vomiting ,diarrhoea , more
undue sweating ( extra renal ) , osmotic diuresis by
high concentration glucose/ mannitol infusion (renal ).
( C ) Hyper volaemic :
- (Both water and Na+ gain But Na= gain is more than
water.) as seen in more salt intake, excess steroids , Na
HCo3/ hyper tonic saline infusion ( salt gain )
31. Pitting edema.
Puffiness of face .
Increased urination .
Often dilated jugular vein.
Features of pulmonary Edema.
32. Investigations
>Serum Electrolytes.
> Plasma and Urinary osmolality.
> Renal Function Test.
> Haematocrit.
Treatment
>Restriction of saline , Na+.
> Correction should be slow and gradual –
Initial infusion of normal saline ,then infusion of ½
strength (0.4.5% ) saline later with 5% dextrose ;
otherwise cerebral edema and hyperglycaemia can
develop.
> oral / nasogastric administration of water / other
fluids as condition improves.
33.
34. Serum Potassium level < 3.5 mEq/L is leveled as
hypokalaemia.( normal range –4.0 to 4.5 mEq /L)
1.Sudden onset It occurs in diabetic coma cases
treated with insulin and saline infusion ; as insulin
causes influx of K+ in the cells and saline (containing
NO K+) dilutes its concentration in serum.
2. Gradual onset
Diarrhoea of any cause,
ulcerative colitis,
gastric aspiration / vomiting,
After trauma or surgery ,
duodenal fistula/ileostomy ,
insulin therapy ,
poisoning ,
beta blockers ,
prolong diuretic therapy etc.
35. Slurred speech.
Muscular hypotonia (physical sign).
Depressed reflexes.
Paralytic Ileus.
Weakness of respiratory muscles.
Cardiac arrhythmias.
Inability to produce concentrated urine.
Nocturia and polyuria.
36. ECG– shows prolonged QT interval, depression of
ST segment , inversion of T wave and prominent
U wave.
Often hypokalaemia is associated with alkalosis.
Serum potassium < 3.5 mEq/L.
Treatment
> oral potassium 2gm ;6hrly , 15 ml K Cl
syrup(2ommol of K)
> Iv K CL 40mmol?L in5% dextrose / normal saline
slowly , often under ECG monitoring . Maximum
dose / hr is 20 mmol .
>Hypocalaemic alkalosis if present should be
treated carefully by iv Potassium .
37.
38. Normal serum K+ level ranges from 4.0 to 4.5
mEq/L
Hyperkalaemia menifests when serum K+
exceeds 6.0 mEq/L
39. Causes
Renal Failure.
Rapid infusion of potassium.
Transfusion of stored blood –K+ diffuse out of stored RBC.
Diabetic Ketoacidosis .
Adrenal Insufficiency.
Potassium sparing drugs like diuretic therapy
(spironolactone), beta blockers , cyclosperine .
Massive tissue destruction ,burns , trauma, tumor necrosis,
crush injury –intra cellular K+ is released in blood.
In vitro haemolysis, thrombocytosis , torniquet application
exercise cause pseudo hyperkalaemia.
Familial hyperkalaemic periodic paralysis.
Note Hyperkalaemia is dangerous state can result in cardiac
arrest.
40. (A) Investigations
> High serum potassium level.
> Peak T wave on ECG.
( B ) Treatment
> IV infusion of 50 ml of 50% glucose with 10 units of
soluble insulin , slowly .
>Infusion of 10% cal gloconate IV ( cardio protection)
> CaCl2 is given Iv in severe cases as calcium in this form
is immediately released without hepatic metabolism.
> Dieresis using Frusemide –causes K+ excretion.
> Haemolysis / dialisis when required.
> continuous ECG monitoring ,
> Salbutamol / Albuterol nebulisation
> IV Sodium bicarbonate –shifts K+ in to cells – 50- 100 ml
slowly over 10 minutes in 7.5% concentration .
41.
42. It is rare: serum magnesium level >
2.5mEq/L(normal level is 1.5- 2.5mEq/L ).
Intracellular magnesium is more 26mEq/L ( 2nd
more higher element).
Mg is mainly deposited in bones.
It is a co- factor for many enzymes necessary
for phosphorylation of glucose in cell and ATP
utilization in muscle fibers.
Daily dietary of Mg is 0.4 gram.
It is reabsorbed well in proximal renal tubules.
43. Advanced renal failure, patient treated with Mg containing
antacids.
Diabetic ketoacidosis .
Over dose of Mg SO4 in treatment of PIH / Eclampsia.
Clinical features
> Loss of tendon reflex.
> Flaccid quadriplegia.
>Neuromuscular depression.
> Respiratory depression– muscle paralysis.
> Hypotension.
> renal out put decreased ; oligourea and anurea.
Monitoring urine out put should not go down < 3o ml in one
hour. Knee jerk, planter reflex should not depress.
Keep watch on respiration Rate. Serum Mg estimation .
Management next dose to be given after checking , respiratory
rate, urinary output and reflexes .
- I V inj. Ca gluconate / CaCl2 in 10% concentration, 10-20 ml
slowly over 20-30 minutes.
44.
45. Serum MG < 1.5mEq/L
Causes Malnutrition , chronic alcoholism,
large GI fluid loss; patient on parenteral fluid
therapy for along time.
Clinical Features
hyper reflexia, muscle spasm , parasthesia ,
tetany, it mimics hypo calcaemia associated
with hypokalaemia.
Treatment 2 gm ( 16mEq /L ) of MgSO4 given
IV slowly in 10 minutes. Later maintenance
dose of 1mEq /kg / day is infused as slow IV
drip.
46.
47. Normal pH( - log of H+ ) is 7.36 – 7.44
When H+ increases pH decrases.
Factors which Control pH
.> Buffer System –
Bicarbonate Buffer
Protein Buffer
Phosphate Buffer
> Renal Control Of pH
> Respiratory Control of pH
48. Acid – is a substance that dissociates Waterto
release hydrogen Ion .
Base – is a substance that takes hydrogen Ion
Buffer – is combination of weak acid and
conjugate base.
These buffers maintain the H+ concentration in
blood with in a fine limit / range .
Buffers are 1. Intra cellular .
2. Extracellular.
49. Extra Cellular Buffer – Bicarbonate / Carbonic
acid , phosphate buffer and Plasma Protein
buffer arte extracellular natural buffers
.Bicarbonate / carbonic Acid buffer is most
important as carbonic acid level in blood is
regulated by lungs which removes excess of
Co2 gas. , while bicarbonate pare is contrilled
by Kidney.
Intra Cellular Buffer – Haemoglobin and other
protein inside cell are playing major role of
intra cellular Buffer.
Acidosis---When pH of blood is < 7.35 .
Alkalosis ---- when pH is more > 7.45 .
50. H+ (nmol/L ) = K x H2Co3m mol /L
_____________
HCO3m mol/L
or K x d PCO2
__________
HCO3 m mol/L
Here K is coefficien a constant factor =800( for H2 CO3 / HCO3
buffer )
Carbonic acid (H2CO3) is solubility coefficient of CO2 in blood (d)
multiplied by partial pressure of CO2 (pCO2) d is 0.03ml/mmHg
/ ml blood .
pCO2 is 40 mmHg .
H2CO3 = d pCO2 = 0.03 x 40 ==1.2ml .
Normal blood Bicarbonate (HCO3) level is 24 m mol /L
So H+ is 800 x 1.2 devided by 24 = 40m mol / L
51. It is used to find out pH of blood using
Logrithm .
Negetive log of K (800 for carbonic buffer ) is
called as pKa . It is 6.1 for H2CO3 / HCO#
buffer system.
pH = pKa + log HCO3 / H2CO3 means
6,1 + log 24 devided by 1.2 = 6.1 + log 20 =
6.1 + 1.3 = 7.4
52.
53. Primary base excess . E.g. HCO3 . A standard
bicarbonate above 27m mol /L.
Causes
1. Repeated vomiting as in pyloric stenosis . Here
hypokalaemic alkalosis develop due to loss of K+
and acid in vomit .
2. Excess alkali intake e.g. antacid .
3. Cortisol excess due to over ingestion /injection
or cushing’ syndrome.
Clinical Features 1.Chine strokes breathing in
period of apnoea of 5-30 seconds.
2.Tetany due to alkalosis ---latent tetany revealed
by Trousseau’s sign .
54. Investigations
Serum electrolytes.
Arterial blood gas analysis.
Treatment
Normal saline or double strength saline IV with
slow IV infusion of KCl 40 m mom/L under ECG
monitoring .
pH < 7.7 causes life threatening alkalosis and
requires rapid correction by infusing dilute HCl
acid or Ammonium chloride with careful
monitoring
55. Arterial PCO2 is below normal(45mmHg).
Causes
1. Hyperventilation during anaesthesia, severe
pain , hyper pyrexia , head injury .
2. High altitude.
3. encephalitis , hypothalamic tumors ,
salicylates over dose / poisoning , Liver
cirrhosis.
4. Hysteria.
56. Clinical Features and Management
1. Headache , tingling , circum oral
anaesthesia ,tightness in chest ,tetany and
Arrhythmias are the features.
2.Low PaCO2 , low HCO3, High alkaline Ph .
3. It can be acute or chronic.
4. It is managed by O2 therapy , treating the
cause and tab Aceozolamide in high altitude.
5. respiratory depression is treated by CO2.
58. - It is state of excess acid / base deficit .
A standard Bicarbonate below 21 m mol /L.
Causes
a. Diabetic Ketoacidosis.
b. Starvation.
c. Hypoxia—CO2 accumulation.
d. Renal efficiency .
e. cardiac arrest ---Hypoxia.
f. Excessive exercise --- Lactic acid over production .
g. Intestinal strengulation , here anion gap is
increased.
59. Loss of base causing metabolic acidosis
a, Diarrhoea.
b, Ulcerative Colitis .
c, Gastrocolic Fistula .
d, Intestinal Fistula .
e, Uretero-sigmoidostomy done for urinary
diversion --- results in Hyperchoraemic –
Hypokalaemic acidosis , anion gap is normal
60. Clinical Features
a, Rapid, deep, noisy breathing – air hunger; known as
KUssMaul’s Breathing.
Cold clammy skin , Tachycardia, right heart strain , altered level
of consciousness.
Cardiac Arrhythmia , hypotension .
Anorexia, vomiting , muscle weakness.
Ph < 7.2 A dangeorus and life threatening level.
capillary stassis.
Strongly acidic Urine.
Low standard HCO3.
Base deficit.
Evaluation --. Do Arterial blood gas analysis. , showing Low
HCO3 level . Low Ph , anion Gap , Urinary anion Gap which is
zero or positive ,
Note __ U A G become negative in metabolic acidosis due to GI
cause as there is increased NH4Cl excretion .
If it is due to renal orgion UAG will be positive .
61. Treatment
> correction oh hypoxia.
> 50M ML OF 8,4 % Sodium bicarbonate iv infusion –
NAHCO3 requirement in m Eq/L = Body weight in Kg X base deficit
X 0.3
>Correction of Electrolytes.
> Specific Treatment for acidosis depends on
.Type A (Shock , Respiratory , CO/ Cynide Poisoning , Anaemia )
. Type B ( Diabetic , hepatic , toxins / drugs .)
It needs only careful use of NaHCO3 in severe cases.
Dicholoroacetate therapy will stimulate Pyruvate Dehydrogenase
enzymes to reduce Lactate.
> Specific treatment is needed to start in cases of diabetic Ketoacidosis ,
Alcoholic acidosis , Salicylates poisoning and Renal cause .
Astrup Formula
Total base deficit / exceesve = Base deficit / excess X Body Wt In KG X
0.3
62. It is feature of respiratory insufficiency to breath out CO2 as
in respiratory failure ; resulting in High PCO2 and fall in
pH.
Causes
> During or after anasthesia .
> Chronic Bronchitis , obstructive lung disease, Emphysema.
> diseases of Thoracic cage.
> Upper abdominal surgery / disease3 decreasing abdomino
–thoracic respiration .
> Respiratory air ways obstruction .
> Myesthenia Gravis,
> Poliomyelits causing paralysis of respiratory muscles to
variable extend.
> Stroke, infection , obesity, Hypoventilation.
63. Clinical Features
> Dyspnoea, confusion , psychosis ,
Hallucinations , sleep disturbances, tremors ,
jerks and personality changes .
> CNS changes are more common and severe
in Respiratory acidosis than in metabolic
acidosis . As in respiratory acidosis lipid
soluble C)2 crosses brain barrier easily than
HCO3.
64. Treatment
> O2 Therapy ; ventilator support .
> O2 therapy should not be used in chronic
hypercapnoea unless it is realy indicated as
Hypoxia induced respiratory stimulation may
be decreased as more CO2 is washed out at
faster rate.
> Alkali therapy is also not started unless pH is
< 7.15. 0r there is severe bronchospasm .
65. It is a calculated estimation of the undetermined or
unmeasured ANIONS in blood .
ANION GAP = ( Na+ + K+ ) – ( HCO3- + Cl - ).
e.g. Total ANION – total Cation in blood
Normal anion gap is 10-16m mol /L.
Important unmeasured are +ve charged proteins ,
phosphate , sulphate and organic acids .
Important unmeasured Cations –Ve charged CA and
Mg.
Albumin is main component of Anion Gap .
When albumin level in blood decreases by 1 gm /
dl –anion gap decreases by 2m Eq /L .
66. Increased Anion Gap Is seen In Normal Anion Gap Is seen in
Metabolic acidosis due to
Ketoacidosis.
Diuarrhoea.
Lactic acidosis. GIT Fistula .
Poisoning ( CO / salicylates/
cynide
Hyper chloraemic acidosis .
Renal Failure
68. Osmolality of a solution is assessed by the
amount of solute dissolved in a solvent like
water measured in weight (Kg).
Osmolality of a solution is assessed by amount
of solute dissolved in solvent like water
measured in volume (litre) .
Normal plasma is 285 mOsm / Kg (275 -295 ).
69. * Plasma Crystalliod osmolality --2 Methods
a. Osmolality of plasma = 0.54/1.86 X 1o rase to power 3
mOsmol / Kg.
It is based on the fact that solution of 1mOsmol/ Kg
freezes at -1.86 degree Centigrade ; where as plasma freezes
at -0.54 degree Centigrade .
b . Osmolality of plasma= 2X(Na) +( Glucose mg%/18)
+ ( Blood urea mg % /6)
It is based on the concentration of major solutes ( Na , glucose
and urea) in plasma. Na+ contributes maximum in plasma
osmolality.
*Colloidal Osmotic Pressure It is difference in plasma
osmotic pressure and interstitial fluid pressure = 25 mmHg.
This is mainly due to concentration of Albumin in plasma.
Plasma proteins do not go out of capillary wall and do not
enter in interstitial compartment.
70. Indications
> For rapid restoration of fluid and electrolite
deficit as in dehydration as in cases of diarrhoa,
vomiting , burns, Haemorrhagic shock and sepsis.
> Total parentral nutrition.
> anaphylaxis, cardiac arrest , hypoxia.
> Post operative period .
> for maintenance , replacement of loss or as a
special fluid.
Advantage Controlled , accurate , adjustable,
rapid , predictable and specfic in terms of solutes
and solvent as per need of clinical situation.
71. Needs Hospitalisation : costaly ; needs to
practice universal aseptic measures.
Fluid over load; pulmonary edema; cardiac
failure .
Infection , thrombophlebitis ,
haematoma;cellulitis ion local area.
Pyogenic infection , air embolism , bacteraemia
.
Discomfort , poor acceptance by patient and
relatives.
72. Daily requirement > Na –100mEq ; K– 60mEq ; Ca –
5mEQ ; Mg 1mEq.
Crystalloid Solutions(fluids)
.
Name of
fluid
NA + mEq/L K+ mEq/l Cl- mEQ /L Lactate
(HCO3)mEq
/L
Ca+ mEq/L
Normal
Saline
154 - - - -
Ringer
lactate
130 4 109 28 3
Dextrose
Saline
5% dextrose
Isolyte P
Isolyte G
Isolyte M
73. Colloids are large molecules which shift the
fluid (solvent/ Water ) from interstitial
compartment to intravascular compartment.,
used as plasma volume expanders.
name Na K Cl Ca bicarbo
nate
Molecula
r size
Remar
ks