This document provides guidelines for the management of hypokalemia according to NICE guidelines. It defines hypokalemia as a serum potassium level below 3.5 mmol/L. The major causes are decreased intake, increased losses through the kidneys or GI tract, and shifts in distribution. Treatment involves identifying and correcting the underlying cause, monitoring for magnesium deficiency, and replacing potassium orally or intravenously depending on the severity. Close monitoring of serum potassium levels, ECG, renal function, and for side effects is important when replacing potassium.
Hypoglycemia is characterized by a reduction in plasma glucose concentration to
a level that may induce symptoms or signs such as confusion, loss of consciousness,
seizures, or death.
A feeling of hunger, sweating, shakiness, and weakness may also be present
. This
condition typically arises from abnormalities in the mechanisms involved in
glucose homeostasis.
The most common cause of hypoglycemia is medications used to treat diabetes
mellitus such as insulin and sulfonylureas.
Hypoglycemia is characterized by a reduction in plasma glucose concentration to
a level that may induce symptoms or signs such as confusion, loss of consciousness,
seizures, or death.
A feeling of hunger, sweating, shakiness, and weakness may also be present
. This
condition typically arises from abnormalities in the mechanisms involved in
glucose homeostasis.
The most common cause of hypoglycemia is medications used to treat diabetes
mellitus such as insulin and sulfonylureas.
This lecture is based on National guidelines(Sri Lanka) and guidelines by NHS UK. all the materials used to prepare the lecture are trusted and high in quality. also the books referred are internationally recognized. both hyper and hypokalemia management included in the lecture. lecture is free and you can even download. i kept no copy rights. i appreciate your support, comments and suggestions. also i would be grateful if you can make these lectures popular. wishing your success.
Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria.
This lecture is based on National guidelines(Sri Lanka) and guidelines by NHS UK. all the materials used to prepare the lecture are trusted and high in quality. also the books referred are internationally recognized. both hyper and hypokalemia management included in the lecture. lecture is free and you can even download. i kept no copy rights. i appreciate your support, comments and suggestions. also i would be grateful if you can make these lectures popular. wishing your success.
Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria.
Electrolytes are an integral component of human physiology and homeostasis.
Management of hypo and hyperkalemia is difficult in most of the hospital settings
In this ppt we have explained it in a simplified manner
Pharmacology of drugs acting on Renal System.pdfAFFIFA HUSSAIN
Diuretics also known as water pills increases the excretion of water and electrolytes (Na+) in
urine.
Natriuresis – large amount of sodium excreted in urine due to the action of kidneys.
Promoted by – ventricular and atrial natriuretic as well as calcitonin.
Inhibited by chemicals such as aldosterone. The drugs which increases sodium excretion are
known as natriuretic.
Diuresis – increased or excessive production of urine. The drugs which enhances the excretion
of water without loss of electrolyte is called as aquaretic.
- 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
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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
263778731218 Abortion Clinic /Pills In Harare ,ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group of receptionists, nurses, and physicians have worked together as a teamof receptionists, nurses, and physicians have worked together as a team wwww.lisywomensclinic.co.za/
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
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Title: Sense of 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
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
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
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
1. Management of Hypokalemia
according to NICE Guidelines
By/Sadek Al-Rokh
Consultant Acute medicine & Endocrinology and Diabetes (East
Sussex trust NHS - UK).
MRCP (UK).
SCE Acute medicine of the royal college of physicians .
SCE Endocrine and diabetes of the royal college of physicians.
European board in Endocrine and diabetes.
2. Definition of Hypokalaemia
Hypokalaemia is defined as a serum potassium concentration of
less than 3.5 mmol/L.
Severe hypokalaemia is a concentration of less than 2.5 mmol/L.
3. Causes of hypokalaemia
- There are three major mechanisms by which hypokalaemia can occur:
Decreased intake: inadequate dietary potassium intake such as
alcoholism, anorexia.
Increased losses (renal and gastrointestinal losses):
Renal: Diuretic therapy (loop or thiazide diuretics)*, urinary loss in congestive
heart failure, primary or secondary hyperaldosteronism, Cushing’s syndrome, large
doses of corticosteroids .
Gastrointestinal : Prolonged diarrhoea**, vomiting**, excessive use of laxatives.
Shifts in distribution : Metabolic alkalosis, re-feeding, magnesium
depletion, certain drugs such as theophylline, insulin, B2-agonists).
4. Causes of hypokalaemia
Drugs that can cause hypokalaemia:
Thiazide diuretics (e.g. bendroflumethiazide) and loop diuretics (e.g. furosemide).
Beta-agonists (e.g. salbutamol, terbutaline) .
Insulin treatment (e.g. in the treatment of diabetic ketoacidosis).
Corticosteroids (e.g. fludrocortisone, hydrocortisone) .
Proton pump inhibitors (e.g. omeprazole).
High-dose penicillins.,Amphotericin, cisplatin.
Aminoglycosides (e.g. amikacin, gentamicin)
Caffeine, theophylline, Adrenaline, pseudoephedrine.
5. Causes of hypokalemic metabolic acidosis
1. With low Blood Pressure:
- Genetic diseases
Bartter syndrome
Gitelman's syndrome
Autosomal dominant hypocalcemia with hypercalciuria (ADHH)
- Acquired diseases
Diuretic use
Vomiting
2. With high Blood pressure:
- Genetic disease :
Liddle Syndrome
11-beta-HSdehydrogenase inactivating mutation
- Acquired diseases :
Conn disease
Cushing’s disease/tumor of the adrenals
Chronic administration of corticosteroid
Natural licorice abuse
6. Causes of hypokalemic metabolic acidosis
Diarrhea
Type 1 Classical Distal renal tubular acidosis (RTA)
-2nd to Sjögren's syndrome and lupus sickle cell anemia,
hyperparathyroidism, hyperthyroidism, chronic active
hepatitis, primary biliary cirrhosis.
Type 2 Proximal renal tubular acidosis (RTA)
-2nd to Fanconi's syndrome, Wilson disease, multiple
myeloma, cystinosis.
7. Signs and Symptoms of hypokalemia
- Manifestations of hypokalaemia depend upon the severity of potassium
depletion :
3.0 – 3.5mmol/L : Usually asymptomatic, but symptoms may include
arrhythmias*, weakness, constipation, nausea, muscle cramps and fatigue. ECG
changes may include a flat or inverted T wave, ST segment depression and prominent U
waves.
2.5 – < 3.5 : As above, but more pronounced. Muscle necrosis and arrhythmias
can occur in patients with underlying cardiac problems.
< 2.5 : Cardiac arrhythmias, paralysis of legs and respiratory muscles,
rhabdomyolysis, ileus, myoglobinuria, acute renal failure.
* N B : In patients with ischaemic heart disease, heart failure, or left
ventricular hypertrophy, even mild hypokalaemia increases the
likelihood of arrhythmias.
9. Treatment of hypokalemia
General guidance :
The underlying cause of hypokalaemia should be identified and
corrected before potassium supplementation. In particular, consider
potential drug causes and check magnesium concentration.
It has been demonstrated that there is an association between
potassium and magnesium deficiencies. A patient with a low potassium
concentration should have their magnesium concentration checked, as
it can be very difficult to correct hypokalaemia in the presence of
hypomagnesaemia.
The normal daily requirement of potassium of 50-100mmol (1 mmol/kg)
per day also needs to be considered when supplementing potassium if
there is no other intake.
10. Treatment of hypokalemia
1- Oral potassium administration
Indication:
Asymptomatic mild hypokalaemia (3.0 – 3.5 mmol/L)
Asymptomatic moderate hypokalaemia (2.5 – 2.9 mmol/L)
Table 1: Oral potassium preparation suitable for use:
Preparation Route Contents of 1 tablet
(mmol) Potassium /
Chloride
Dose
Sando- K Oral 12 / 8 2 tablets three times a
day. Total dose = 72
mmol/day
11. Treatment of hypokalemia
1- Oral potassium administration
Monitor serum potassium concentration daily, especially in patients with
cardiovascular disease or those taking digoxin.
Dose and duration of treatment depends on the existing potassium deficit and
whether there are continuing losses. Larger doses may be required in patients with
digitoxicity or diabetic ketoacidosis. Specialist advice should be sought in such
situations.
Side-effects include abdominal discomfort, diarrhoea, nausea and vomiting.
If gastric irritation occurs, Sando-K should be given with or after food.
Excessive doses can lead to hyperkalaemia.
12. Treatment of hypokalemia
2- Intravenous potassium administration
Indications:
Symptomatic hypokalaemia.
Severe hypokalaemia <2.5 MMOL/L.
Patients unable to tolerate oral therapy, or those in whom the oral route is inappropriate (e.g.
if not absorbing).
Table 2: Suggested initial doses for intravenous replacement therapy (assuming
normal renal function):
Serum potassium
concentrations
Suggested IV replacement Serum potassium
monitoring
2.5-3.4 mmol/L (e.g. if
patient unable to take
potassium orally)
20 - 40 mmol potassium
chloride in 1 litre sodium
chloride 0.9% over at least 8
hours.
- Monitor after 24 hours.
- Repeat infusion if
appropriate.
- Switch to oral
management as soon as
practical.
< 2.5 mmol/L or patient
symptomatic
40 mmol potassium chloride in
1 litre sodium chloride 0.9%
over 6 hours.
- Monitor after 6 hours and
repeat infusion if
appropriate.
13. Treatment of hypokalemia
2- Intravenous potassium administration
Initial potassium replacement therapy should not involve glucose infusions, as glucose
may cause a further decrease in the plasma-potassium concentration. This will unmask
the intracellular deficit, which will indicate that further replacement is required.
The rate of administration should not exceed 10mmol/hour, unless in emergencies,
where 20mmol/hour can be given for short periods with close, cardiac monitoring,
including continuous ECG monitoring.
40mmol/L is usually recommended as the maximum concentration for peripheral
infusion.
In this hospital, the most concentrated preparation available is 80mmol/L (40mmol in
500mLs). This can be given peripherally in exceptional circumstances only – e.g. in
severely fluid restricted patients. It should be advised that this is infused into a large
vein with close monitoring of the injection site.
High concentrations of potassium can cause serious cardiotoxicity; it is therefore
recommended that concentrations exceeding 40mmol/L be administered with caution
and with close cardiac monitoring, including continuous ECG monitoring.
The maximum dose that can be given in 24 hours is 3mmol/kg (assuming normal renal
function). Care needs to be taken to avoid fluid overload.
14. Treatment of hypokalemia
3- Monitoring during intravenous replacement
Urea and electrolytes, with special attention to the following:
Potassium concentration must be closely monitored during replacement.
Failure to correct hypokalaemia despite appropriate treatment may be due to underlying
hypomagnesaemia, which may require magnesium supplementation.
Chloride Potassium depletion is frequently associated with chloride depletion and with metabolic
alkalosis. Regular monitoring of acid-base balance is essential and a continuing metabolic alkalosis is
an indicator of potassium deficiency.
Renal function:
Potassium is excreted renaly, and accumulation can occur in patients with poor kidney function.
Replace potassium with extreme caution in patients with severe renal impairment and monitor
frequently. Seek specialist advice from the renal team.
Lower doses of replacement therapy are required for patients with renal disease.
ECG and blood pressure:
ECG monitoring is essential when potassium is given intravenously; periodic evaluation is
recommended with oral supplementation.
ECG monitoring is particularly important in patients with cardiac disease and in those receiving digoxin.
Correction of hypokalaemia may lower blood pressure.
15. Treatment of hypokalemia
4- Injection site
Extravasation may cause tissue damage due to high osmolarity and low
pH.
Monitor for local pain and phlebitis, particularly at higher
concentrations.
5- Adverse effects of potassium replacement.
Excessive doses of potassium may lead to the development of
hyperkalaemia, particularly in patients with renal impairment Symptoms
include:
Cardiovascular (cardiac arrhythmias, heart block, cardiac arrest)
Musculoskeletal (muscle weakness, paralysis).
Neurological (paraesthesia of the extremities, confusion).
Pain, phlebitis or serious injury following intravenous administration.
16. Treatment of hypokalemia
6- Interactions
- Potassium supplements should be used with caution in patients receiving drugs that
increase serum potassium concentrations. These include :
Potassium-sparing diuretics (e.g. spironolactone, amiloride,
triamterene, coamilofruse, co-amilozide).
ACE inhibitors (e.g. ramipril, lisinopril, captopril)
Angiotensin II receptor antagonists (e.g. irbesartan, losartan,
candesartan)
Tacrolimus.
Ciclosporin.
Drugs that contain potassium, such as the potassium salts of
penicillin. Please note also the potential potassium content of other
intravenously administered drugs.