Potassium is the most abundant cation in the human body, located mainly intracellularly. Serum potassium levels are tightly regulated between 3.5-5 mEq/L through hormones like insulin and mechanisms in the kidneys and digestive tract. Alterations in potassium levels can cause neuromuscular and cardiac issues due to potassium's role in cell excitability. Hypokalemia is a serum potassium below 3.5 mEq/L and can be caused by excessive losses or intracellular shifts, presenting as muscle weakness. Hyperkalemia, above 5 mEq/L, is more serious as it can cause fatal arrhythmias and is due to excess intake or intracellular shifts, initially showing peaked T waves on ECG.
Magnesium is a very important ion in the body, crucial to over 300 reactions.
Its disorders are underdiagnosed and can help improve healthcare if appropriately treated
10.01.08: Potassium and Magnesium HomeostasisOpen.Michigan
Slideshow is from the University of Michigan Medical School's M2 Renal sequence
View additional course materials on Open.Michigan:
openmi.ch/med-M2Renal
Magnesium is a very important ion in the body, crucial to over 300 reactions.
Its disorders are underdiagnosed and can help improve healthcare if appropriately treated
10.01.08: Potassium and Magnesium HomeostasisOpen.Michigan
Slideshow is from the University of Michigan Medical School's M2 Renal sequence
View additional course materials on Open.Michigan:
openmi.ch/med-M2Renal
A simple presentation on hypokalemia. The most common electrolyte disorder in the Critical Care practice.The presentation is based on a mortality and morbidity case report and discussion. It covers all the basic aspects of understanding the causes of hypokalemia in ICU and its management. Target audience are residents ICU and ER but all health care workers can benefit.
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.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
- 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
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
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
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
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
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.
1. UNIVERSIDAD TECNICA DE MACHALA
ACADEMIC UNIT OF CHEMICAL
SCIENCES AND HEALTH
MEDICINE SCHOOL
ENGLISH
ALTERATIONS OF
POTASSIUM
METABOLISM
STUDENTS
William Cruz
Kevin Herrera
TEACHER:
Mgs. Barreto Huilcapi Lina Maribel
CLASS:
EIGHTH SEMESTER ‘’A’’
Machala, El Oro
2018
2. ALTERATIONS OF POTASSIUM METABOLISM
Physiological considerations.- Potassium is the most abundant cation in the human
organism, with a total of 4000 mEq (4000 mmol). Located mostly (98%) in the
intracellular space and only 60 mEq are in the extracellular. The serum potassium
concentration is maintained between 3.5-5 mEq / L (3.5-5 mmol / L).
Rapid regulation.- The force retaining potassium inside the cell is the
transmembrane negative charge, maintained by the Na-K-ATPase pump of the cell
membrane, which exchanges three sodium ions for two of potassium ions. Insulin and
catecholamines are the two main hormones that regulate the entry of potassium into
the cell through the activation of the Na-K-ATPase pump.
The alteration of the extracellular pH influences the transcellular distribution of
potassium. A pH decrease of 0.1 U produces an increase of about 0.5 mEq / L (0.5
mmol / L) in the serum potassium and a rise in pH of 0.1 U induces a similar
reduction.
Slow regulation.- The intake of potassium in the diet is variable and requires
mechanisms that regulate homeostasis. The kidney removes 90-95% of the potassium
ingested in the diet, and the rest is eliminated by the digestive tract. Renal adaptation
to sustained potassium overload is relatively slow and needs 6-12 h to normalize
serum potassium levels, while the kidney's response to dietary potassium restriction is
still slower and is not fully activated until after After 7-10 days. Even then, urinary
potassium losses are usually greater than 20 mEq / day.
Potassium and neuromuscular excitability. - Involved in the activation
mechanisms of excitable tissues, such as the heart, skeletal muscle and smooth
muscle. The main clinical manifestations associated with potassium disorders are
secondary to alterations in transmembrane electrical phenomena in excitable tissues
that result in cardiac conduction disorders and neuromuscular function.
HYPOKALEMIA
3. Concept.- Hypokalemia is considered to be serum potassium levels below 3.5 mEq /
L (3.5 mmol / L). Hypokalemia should be differentiated from the potassium deficit.
Etiology.- The majority of hypokalemia are usually due to excessive intestinal and /
or renal losses or to the massive entry of potassium into the cell. The renal losses of
potassium differ in three groups of different clinical entities:
a) hypokalemia with arterial hypertension.
b) hypokalemia with normotension arterial
c) drug-induced hypokalemia.
WITHIN EACH ONE WE FIND:
Hypokalemia associated with arterial hypertension: Primary
aldosteronism, vasculorrenal hypertension, 11-b-hydroxysteroid
dehydrogenase deficiency, Cushing's syndrome, congenital adrenal
hyperplasia, Liddle's syndrome and familial hypokalemic periodic paralysis.
Hypokalemia with normal blood pressure: Kidney tubular acidosis types I
(distal) and II (proximal) and Bartter syndrome (hereditary).
Drug-induced hypokalemia: loop diuretics (furosemide, bumetanide),
thiazides, indapamide, mannitol and acetazolamide; the mineralocorticoids
and glucocorticoids; carbenicillin and other penicillins; amphotericin B; the
aminoglycosides, cisplatin, foscarnet and alcohol.
Clinical picture.- With muscle potassium concentrations between 2 and 2.5 mEq / L
(2 and 2.5 mmol / L) muscle weakness appears. The arreflexica paralysis appears in
situations of severe hypokalemia as well as constipation, paralytic ileus and
respiratory failure. In the heart, hypokalemia produces electrophysiological disorders:
flattening of T waves and the appearance of U waves. Severe hypokalemia (serum
potassium below 2 mEq / L [2 mmol / L]) inhibits the reabsorption of chlorine in the
ascending portion of the loop of Henle and causes urinary losses of this, with
hypochloremic metabolic alkalosis. Chronic hypokalemia can develop vacuolization
of the proximal tubule and interstitial fibrosis.
Treatment.- Consists of the administration of potassium salts, in addition to
correcting the disorder responsible for hypokalemia. If there are digestive disorders or
4. neuromuscular manifestations, especially cardiac, administration by intravenous route
is advisable; the total amount of potassium administered in a day will be less than 200
mEq. For oral administration, organic potassium salts, such as gluconate or citrate,
are more convenient.
HYPERKALEMIA
Concept.- Defined by serum potassium levels greater than 5 mEq / L (5mmol / L), it
is the most serious of the electrolyte alterations, due to the risk of causing fatal
ventricular arrhythmias quickly. Before any hyperkalemia, the first thing is to rule out
the existence of a pseudohyperkalemia.
Etiology.- The true hyperkalemia is produced by a positive balance of potassium
(defect of elimination or excess of contribution) or by a rapid exit of potassium from
the intracellular space to the extracellular one.
Clinical picture.- It manifests in the form of neuromuscular and cardiac alterations.
Paresthesias, muscle weakness, flaccid paralysis and respiratory arrest can occur in
the neuromuscular system. The initial electrocardiographic alteration associated with
hyperkalemia is the appearance of peaked T waves, which emerge with K
concentrations of 6.5 mEq / L.
Treatment.- Severe hyperkalemia with electrocardiographic alterations constitutes a
critical situation, requiring immediate treatment such as: myocardial stabilization,
transfer of potassium from the extracellular to the intracellular space and the
elimination of potassium from the body by diuretics.
a) Myocardial stabilization.- the administration of calcium gluconate i.v (10-30
mL of a 20% solution in a min) does not modify the serum potassium but
improves the ECG immediately.
b) Transfer of potassium from the extracellular space to the intracellular space.-
(insulin, B2-agonists and sodium bicarbonate). Insulin is the fastest way to
decrease serum potassium; its effect is observed 15 minutes after
administration. B2-agonists administered by inhalation or i.v produce a rapid
entry of potassium into the cell, allowing transient control of hyperkalemia.
5. Sodium bicarbonate, at a rate of 40-150 mEq via i.v, passes potassium into the
cells in an interval of 3-4 h.
c) Elimination of potassium from the organism by diuretics - especially those of
asa (furosemide) increase the urinary excretion of potassium in patients with
preserved renal function. Hemodialysis or peritoneal dialysis are effective
methods of eliminating body potassium and correcting hyperkalemia.
BIBLIOGRAPHIC REFERENCE:
Campistol Plana, J., "Alterations of potassium metabolism", Farreras, V. Rozman, C,
Internal Medicine, Barcelona-Spain, Elsevier, 2016, Vol. 1, p., 782-787